5 MedBear GS Notes 2020

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MedBear General Surgery Notes
FOREWORD
Welcome to the new and improved version of MedBear!
For future versions of MedBear, the MedBear team hopes to build a shared collaborative learning platform for medical students
through continual input from our readers on areas for improvement. We hope that MedBear will serve as a one-stop General
Surgery resource guide, supplemented with reliable and up-to-date information on clinical practices, research and tips, so as to
support medical students during their preparation for the MBBS General Surgery.
We envision this to be a student-led resource for students to create locally relevant surgical education content. Medical students
of the future must be able to synthesise widely available medical knowledge, critically analyse data to see its relevance to local
context. Instead of passively learning through self-directed reading, we hope that students can come together to participate and
collaborate in surgical education. The online notes are meant to be up-to-date, concise and progressive.
Of course, in-person learning activities in the wards, OT and clinics are undeniably important to build a strong foundation and
understanding of GS. Hence, MedBear should only serve as a guide to supplement clinical learning to help students maximise
their learning during GS postings in the hospitals and synthesise the new knowledge learnt.
If you spot any errors in MedBear, have comments on areas for improvement, have any questions requiring clarification, or have
resources to contribute to MedBear, please contact us at https://tinyurl.com/askmedbear or askmedbear@gmail.com.
Alternatively, feel free to leave comments within the online document. We value all your feedback and appreciate your
contributions. If you are keen to submit new topics, interesting case write-ups, images or videos, the editorial team will give
acknowledgement to all contributors.
We believe that knowledge with collaboration will lead to wisdom. The editorial team wishes you all the best in your learning
experience and looks forward to receiving your feedback and contributions.
Yours Sincerely,
The MedBear team (2020)
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Foreword_Last Updated 8th June 2020
CONTENTS PAGE
Foreword 2
Contents Page 3
1. Trauma 8
Approach to Trauma & Advanced Trauma Life Support (ATLS, 10th Edition, 2018) 8
Abdominal Trauma 17
Cardiothoracic Trauma 23
Musculoskeletal Trauma 28
Neurosurgical Trauma 32
Neck & Facial Trauma 36
Burns 38
2. Surgical Critical Care 42
Acid-Base & Electrolytes 42
Acute Respiratory Distress Syndrome 44
Disseminated Intravascular Coagulation (DIC) 46
Fluids & Electrolytes 48
Nutrition 52
Shock 57
Sepsis 61
Pre-operative Management 66
Post-Operative Complications 69
Local Anaesthesia 77
3. Acute Abdomen 78
Approach To Acute Abdomen 78
Intestinal Obstruction 85
Acute Appendicitis 94
4. Oesophagus 99
Anatomy of the Oesophagus 99
Approach to Dysphagia 101
Achalasia 106
Gastroesophageal Reflux Disease (GERD) 108
Barrett’s Oesophagus 114
Oesophageal Cancer 117
Gastro-Oesophageal Junctional (GEJ) Tumour 124
Hiatus Hernia 125
Oesophageal Perforation 127
5. Stomach 129
Anatomy & Physiology of the Stomach 129
Approach to Bleeding Upper GIT 131
Variceal Bleeding 139
Peptic Ulcer Disease 142
Gastric Cancer 152
Gastric Lymphoma 164
Gastrointestinal Stromal Tumour (GIST) 165
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Contents Page_Last Updated 3rd June 2020
Obesity 167
6. Colorectal 169
Approach to Lower Bleeding Gastrointestinal Tract 169
Ischaemic Colitis 175
Colon Carcinoma 178
Rectal Cancer 192
Colonoscopy & Colorectal Polyps 199
Stoma Principles 207
Diverticular Disease 213
7. Small Bowel, IBD 217
Anatomy of the Small Bowel 217
Small Bowel Cancer 218
Enteric Fistula 219
Meckel’s Diverticulum 220
Inflammatory Bowel Disease 222
Crohn’s Disease 224
Ulcerative Colitis 227
8. Anal 230
Haemorrhoids 230
Anal Fissures 234
Anal Fistula 235
Anorectal Abscess 238
Anal Intraepithelial neoplasia 239
Anal Malignancies 240
Pilonidal Sinus 242
9. Liver 243
Surgical Anatomy of the liver 243
Portal Hypertension 246
Ascites 248
Approach to Hepatomegaly 250
Liver Haemangioma 253
Focal Nodular Hyperplasia (FNH) 254
Hepatic Adenoma 255
Hepatic Cysts 256
Hepatocellular Carcinoma 258
Secondary Liver Malignancy (Non-Colorectal) 268
Hepatic Abscess (Pyogenic) 269
Hepatic Abscess (Amoebic) 271
10. Pancreas & Spleen 272
Anatomy of the Pancreas 272
Acute Pancreatitis 275
Chronic Pancreatitis 286
Pancreatic Cancer 290
Pancreatic Neuroendocrine Tumour (PNETs) 298
Cystic Neoplasm Of the Pancreas 300
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Spleen 302
Splenic Cyst & Abscess 302
Approach To Enlarged Spleen (Splenomegaly) 302
11. Biliary System 304
Anatomy & Physiology of the Biliary System 304
Approach to Jaundice 307
Cholelithiasis 316
Acute Calculous Cholecystitis 324
Acute Acalculous Cholecystitis 327
Mirizzi’s Syndrome 332
Cholangitis 333
Choledochal Cyst 337
Gallbladder Carcinoma 339
Cholangiocarcinoma 341
12. Breast 344
Anatomy of the Breast 344
Approach to Nipple Discharge 347
Approach to Breast Lump 349
Breast Cancer 359
Breast Cancer Management by Tumour Stage 370
Uncommon Presentations of Breast Cancer 374
Gynaecomastia 376
13. Endocrine, Head & Neck 377
Anatomy of the Neck 377
Approach to Neck Masses 379
Causes of Midline Mass 382
Causes of Anterior Triangle Mass 384
Causes of Posterior Triangle Mass 387
Cervical Lymphadenopathy 388
Anatomy of the Salivary Glands 390
Sialolithiasis 392
Salivary Gland Tumours (Parotid) 393
Approach to Solitary Thyroid Nodule 402
Thyroid Cancers 409
Multiple Endocrine Neoplasia (MEN) 416
Thyroiditis 417
Thyroid Storm 419
Parathyroid 420
Hyperparathyroidism 421
Hypercalcemia 423
Adrenal Tumours 425
Functional Hormone Secreting Adrenal Tumours 427
14. Urology 430
Approach to Gross Haematuria 430
Renal Cell Carcinoma 435
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Urolithiasis 441
Bladder Cancer 446
Approach to Acute Urinary Retention 449
Prostatic Cancer 453
Benign Prostate Hyperplasia (BPH) 457
Approach to scrotal swellings & Pain 462
Testicular Torsion (A Surgical Emergency) 464
Scrotal Abscess 465
Fournier Gangrene 465
Epididymal Cyst 465
Varicocele 466
Hydrocele 466
Testicular Tumour 468
15. Vascular 470
Anatomy of Arteries of the Lower Limb 470
Peripheral Arterial Disease - Lower Extremities Arterial Disease (LEAD) 471
Acute Limb Ischemia 487
Carotid Disease 492
Arteriovenous (AV) Access 493
Aneurysm 496
Aortic Dissection 498
Abdominal Aortic Aneurysm 501
Anatomy of the Venous System of the Lower Limb 505
Chronic venous insufficiency 506
Varicose Vein 508
Venous Ulcers 511
16. Hernia 512
Anatomy of Hernias 512
Inguinal Hernia 515
Approach to Groin Swelling 520
Femoral Hernia 522
Umbilical / Paraumbilical Hernia 524
Incisional Hernia 525
17. Others 528
Skin & Wound Healing 528
Skin Cancers 530
Squamous Cell Carcinoma 531
Basal Cell Carcinoma 533
Malignant Melanoma 536
Approach To Lumps & Bumps 539
Lipoma 540
Sebaceous cyst 541
Ganglion 542
Neurofibroma 544
Dermoid Cyst 545
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Seborrheic Keratosis 546

Pyogenic Granuloma 547
Papilloma 548
Kerathocanthoma 549
Keloid (Hypertrophic Scar) 549
Fibrosarcoma 550
Pyoderma Gangrenosum 550
Radiotherapy Marks 551
Drains 552
Nasogastric Tube 554
Chest Tube 555
Urinary Catheterization 558
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1. TRAUMA
APPROACH TO TRAUMA & ADVANCED TRAUMA LIFE SUPPORT (ATLS, 10TH EDITION, 2018)
INTRODUCTION
The main principles in approaching trauma is to treat the greatest threat to life first with definitive diagnosis being less important. Time
is very important in the management of trauma with emphasis on the “golden hour”. This refers to the period of time followin g a
traumatic injury during which there is the highest likelihood that prompt medical and surgical treatment will prevent trauma related
mortality. About 30% of all in hospital trauma deaths occur within the first hour of injury, and 3 in 4 in hospital trauma deaths occur
within the first 48 hours.1
To reduce trauma-related mortality, emphasis is made on prevention of the lethal triad of death. This involves prevention of
hypothermia, coagulopathy and acidosis.
EPIDEMIOLOGY
Trauma Death (Trimodal Distribution) - Trunkey et. al (1983)2

Deaths Timing Location Cause Intervention
Traumatic brain injury (TBI), high spinal
Immediate (50%) Minutes Scene cord injury, Massive haemorrhage Injury Prevention
(great vessel disruption)
Head injury, haemorrhage (i.e. liver,
Improved Access to
Early (30%) Hours Hospital splenic lacerations), haemothorax,
Trauma Care.
ruptured viscus, pelvic fractures
Improved Resuscitation
Late (20%) Weeks Hospital Sepsis, Multiple organ failure (MOF)
/ Critical Care
With improvement in trauma surgery, the classic trimodal distribution of trauma related death is being challenged. While the
percentage of immediate deaths (60%) remained unchanged, early deaths (30%) occurred much earlier (median 52 vs. 120
minutes) and the late peak (10%) has dramatically decreased secondary to improved clinical care.
In Singapore, the leading cause of trauma related admissions are road traffic accidents and falls. Uncontrolled hemorrhage is the
leading cause of early death.
1 World J Surg. 2007 Nov;31(11):2092-103.

2 Sci Am. 1983 Aug;249(2):28-35.
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1. Trauma_Last Updated 3rd June 2020
PATHOPHYSIOLOGY
Mechanism of the lethal triad of death in trauma

The causes of each facet of the lethal triad is multifactorial, and they reinforce each other leading to a vicious cycle if there is no
intervention. Traumatic injuries lead to severe haemorrhage resulting in hypovolemic shock and reduced tissue perfusion. Reduced
tissue perfusion causes tissues to switch to alternative sources of energy (anaerobic respiration) with the increased production of
lactate as a by-product resulting in lactic acidosis. Acidosis contributes to the failure to clot. As hemostasis is impaired, further
bleeding occurs which results in further tissue hypoperfusion and hypothermia. Hypothermia impairs platelet aggregation and
decreases the function of coagulation factor. Trauma itself can also lead to coagulopathy via dilution, depletion and disseminated
intravascular coagulopathy. Patients are at risk of spiralling into a vicious cycle of hypothermia, acidosis and coagulopathy resulting
in worsening hemorrhage and death.
CLINICAL PRESENTATION
In a tertiary hospital, general surgeons are involved in the management of seriously injured trauma patients from the moment they
arrive in the emergency department. The on-duty general surgery team will be trauma activated to the emergency department. The
general surgeon is the team leader in the situation and he has to make decisions on the necessary investigations, involvement of
other sub-speciality teams (i.e. orthopedics, neurosurgery, intensivist, anesthetist) and decide on the patient’s disposition. The
management of trauma patients follow a systemic flow as guided by ATLS principles.
Trauma Management
1. Preparation and Triage
2. Primary survey (ABCDE), Resuscitation & Adjuncts
3. Secondary survey (head to toe evaluation & patient history) & Adjuncts
4. Continued post-resuscitation monitoring & re-evaluation
5. Definitive care
PREPARATION AND TRIAGE

Prior to the arrival of the trauma patient, the ED trauma team leader briefs the team of their roles
and responsibility. The ED team is gowned with personal protective equipment (PPE) while
anticipating the arrival of the trauma patient. The P1 area of the emergency department is
prepared (i.e. airway equipment, intravenous equipment)
The ED team is the main team resuscitating the patient. When the general surgeon arrives at
the P1 the first priority is to understand the time of injury and the mechanism of injury.
Subsequently, the evaluation follows a systematic process of Primary Survey and Secondary Survey.
Mechanism of injury which are deemed high risks includes:

- Fall – greater than 6meters (2 stories)
- Motor Vehicle Accident – intrusion > 30cm on occupant side, intrusion > 45 cm on any side, ejection (partial or complete) from
vehicle, death in the same passenger compartment
- Car vs. Pedestrian / Cyclist – thrown, run over, > 32km/hr
- Motorcycle Accident – > 32 km/hr
PRIMARY SURVEY (A B C D E), RESUSCITATION AND TRIAGE

Ask the patient for his name and what has happened? – Appropriate response suggest no major airway compromise (ability to speak
clearly), breathing is not severely compromised (ability to generate air movement to permit speech) and there is no major decrease in
level of consciousness (alert enough to describe what happened) – brief assessment of ABCD
[A] - Airway Assessment with Restriction of Cervical Spine
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- Airway Assessment – is this a compromised airway?

▪ Inspection for facial, mandibular, tracheal fractures (i.e. hoarseness, subcutaneous emphysema, palpable fracture)
▪ Burns with inhalational injuries
▪ Obtunded patients
- Airway Assessment – is the airway obstructed or at risk of impending obstruction?
▪ Obtunded (hypercarbia), Anxiety / Belligerent (hypoxia), Cyanosis (prolonged hypoxia)
▪ Abnormal Sounds – stridor, grunting / gurgling
- Predicting a difficult airway

▪ C-spine injury, severe arthritis of the c-spine
▪ Maxillofacial / Mandibular Trauma
▪ Obesity
▪ LEMON – look externally, 3-3-2 rule*, Mallampati, Obstruction, Neck Mobility
- How to establish a patent airway?

▪ Simple Suctioning – clear airway of foreign bodies and secretions
▪ Chin lift & Jaw Thrust – displace tongue anteriorly from the pharyngeal inlet
▪ Airway adjuncts – Nasopharyngeal airway / Oropharyngeal (guedel) airway
▪ Extraglottic Devices – Laryngeal Mask Airway
▪ Establish a definitive airway if have doubt about patient’s ability to maintain airway integrity
o Tracheal Intubation with drug assisted intubation (adjuncts – cricoid pressure, bougie, video laryngoscope)
o Needle Cricothyroidectomy with jet insufflation of the airway
o Surgical Cricothyroidotomy
o Emergent tracheostomy
- Definition of definitive airway

▪ Tube placed in the trachea with the cuff inflated below the vocal cords, the tube is connected to an oxygen enriched assisted
ventilation and the airway secured in place with appropriate stabilization methods
▪
- Indication for definitive airway
▪ Patency and Protection of Airway – impending airway obstruction (i.e. inhalational injuries, complex facial fractures,
retropharyngeal hematoma, airway bleeding, chemical injury to mouth, nares, hypopharynx, injuries to neck with expanding
hematoma, reduced GCS < 8)
▪ Breathing – respiratory insufficiency with need for ventilation
▪ Difficult clinical course – i.e. anaphylaxis or airway/breathing compromise
- In a multi-system trauma patient assume cervical spine injury till proven otherwise
▪ Put on c-spine collar, prevent excessive movement of the cervical spine
▪ Presence of paraplegia, quadriplegia, sensory loss on chest / abdomen – suspect spinal instability
▪ NEXUS C-Spine Clearance – sensitivity: 90.7% & specificity 36.8% for C-spine injury
o No focal Neurological deficit
o No Spinal (posterior or midline cervical) tenderness
o Normal level of Alertness (altered alertness level – i.e. GCS ≤ 14, not oriented to time, place, person)
o No evidence of Intoxication
o No painful Distracting injuries (i.e. long bone fractures, visceral injury, lae laceration, degloving injury)
▪ Canadian C-spine Rule – sensitivity: 99.4%, specificity: 45.1% for C-spine injury
EXTRA INFORMATION
Sizing of airway adjuncts
- Nasopharyngeal airway: From nares to tragus of ear
- Oropharyngeal airway: From angle of mouth to angle of jaw
Orotracheal intubation using Drug Assisted Intubation (DAI) / Rapid-sequence induction (RSI)
- Pre-oxygenate patient with 100% oxygen
- In-line cervical spine restriction with anterior portion of cervical collar removed
- Drugs – short-acting induction agent (i.e. etomidate 0.3mg/kg IV) and paralytic agent administered immediately after (succinylcholine 1-
1.25mg/kg IV or rocuronium 0.6-0.85mg/kg IV)
- Sellick Manoeuvre (cricoid pressure) to prevent aspiration
- ETT tube inserted through vocal cords and adequacy of ventilation is assessed (ETT sits 2cm above carina) - confirm placement with CXR
- Maintain with inhalational anaesthetic
Cricothyroidotomy
- Involves the median cricothyroid ligament – thickened anterior portion of the cricothyroid membrane that runs between the cricoid and thyroid
cartilage. In adults, cricothyroidotomy remains the standard of care (esp. patients with tracheal trauma or tumour). In patients < 12,
tracheostomy is preferred over cricothyroidotomy in view of high risk of tracheal stenosis or cricoid injury
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Tracheostomy
- Placed through the 2 nd or 3rd tracheal ring. A tracheal flap of Bjork may also be fashioned although less commonly due to risk of stenosis
- Damage to 1st tracheal ring causes subglottic stenosis & lower placement increases the risk of tracheal-innominate fistula (patients presents
with haemoptysis)
[B] - Breathing
- Assessment of adequacy of ventilation

▪ Exposure of neck & chest – assess jugular venous distention, trachea position, chest wall excursion (symmetry and
asymmetry, determine rate & depth of respiration)
▪ Inspect and palpate the neck and chest for distended neck veins, tracheal deviation, unilateral and bilateral chest
movements, use of accessory muscles and any signs of injury (i.e. flail chest)
▪ Auscultate chest bilaterally: if there are unequal breath sounds, percuss the chest for presence of dullness or hyper-
resonance to determine hemothorax or pneumothorax
- Assessment of adequacy of oxygenation

▪ Pulse Oximeter – measure patient oxygen saturation and gauge peripheral perfusion
▪ Arterial Blood Gas
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- Life-threatening conditions that require immediate attention and treatment

▪ Airway Obstruction – i.e. Tracheobronchial Disruption
▪ Tracheobronchial Tree Injury – will require placement of definitive airway (with fibre-optic assistance)
▪ Tension Pneumothorax
o Patients should be assessed clinically for pneumothorax even prior to CXR. If a patient requires intubation, there is a
risk of converting a simple pneumothorax into tension pneumothorax.
o Immediate management of PTX involves insertion of a large bore 14G IV catheter at the 4th or 5th intercostal space in
the mid-axillary line or at the 2nd intercostal space in the midclavicular line followed by tube thoracostomy within the
triangle of safety – mid-axillary line, lateral border of pectoralis major, upper border of the 5th rib)
▪ Open pneumothorax
o Immediate management of open PTX involves application of a 3-sided occlusive dressing to create a flutter-valve (if
taped on 4 sides can convert an open PTX to tension PTX) followed by operative closure of chest wall defect and
placement of chest tube remote from the wound
▪ Massive Hemothorax (>1500ml or > 200ml in 2-4 hours) – will require tube thoracostomy (28 to 32Fr) +/- thoracotomy
▪ Cardiac Tamponade – will required pericardiocentesis followed by definitive operative repair (i.e. pericardiotomy)
- Management of Ventilation
▪ Ventilate with bag-valve-mask (with airway adjuncts)
▪ Mechanical ventilation for intubated patients - minute ventilation controlled by adjusting respiratory rate and tidal volume
▪ Tube thoracostomy (Chest Tube Insertion) in event of pneumothorax and/or hemothorax
- Management of Oxygenation
▪ High concentration of oxygen via mask-reservoir device (i.e. Non-rebreather Mask)
▪ Attach an end-tidal CO2 (ETCO2)* monitoring device to the endo-tracheal tube (ETT)
▪ Monitor saturation with pulse oximeter and Arterial Blood Gas (ABG) readings
* ETCO2 best determinant of esophageal vs. tracheal intubation – sudden rise: alveolar hypoventilation (increase TV / RR), malignant hyperthermia,
pneumothorax, mucus plug, faulty equipment. Sudden drop: disconnection from ventilator, kink of ETT, pulmonary embolism, significant hypotension,
CO2 embolism
[C] - Circulation (Hemorrhage Control & Replacement of Intravascular Volume)
Hypotension (SBP <90) following trauma is considered haemorrhagic in origin till proven otherwise. Physiologic response to
blood loss varies between individuals. Patients who are elderly may not show a normal tachycardia response, especially so if they are
on beta-blockers. In younger patients or children who have abundant physiological reverse, they may demonstrate few signs even
during severe hypovolemia
In event that hemorrhage is excluded, other causes of non-haemorrhagic shock includes cardiogenic shock, cardiac tamponade,
tension pneumothorax, neurogenic shock, septic shock
- Assessment of organ perfusion

▪ Level of consciousness (i.e. altered consciousness – reduced cerebral perfusion)
▪ Pulse Rate and Character (i.e. is the pulse rate rapid & thready), assess pulses (i.e. femoral [BP ≥ 70] / carotid [BP ≥ 60])
▪ Blood Pressure (aim for permissive hypotension)
▪ Skin Perfusion (i.e. ashen & grey facial skin with pale extremities ~ blood loss ≥ 30%)
▪ Urinary Output (aim ≥ 0.5-1.0ml/kg/hr)
- Apply ECG monitor / Pulse Oximeter / Automated BP cuff

▪ Dysrhythmias: consider cardiac tamponade / cardiac contusion
▪ PEA: consider treatable causes (5Hs and 5Ts)
o 5Hs – hypovolemia, hypoxia, H+ (acidosis), hyper/hypokalemia, hypothermia
o 5Ts – toxicity (drug overdose), tamponade (cardiac), tension pneumothorax, thrombosis: coronary (AMI),
thromboembolic: pulmonary (PE)
▪ Bradycardia, aberrant conduction, ventricular ectopic: ?hypoxia / hypo-perfusion
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- Massive blood loss in trauma setting can occur in 5 sites - on the floor and 4 more
▪ External (on the floor),
▪ Chest
▪ Abdomen
▪ Pelvis & Retroperitoneum
▪ Around long bone fractures (i.e. femur)
- Management (Haemorrhage Control)

▪ External Haemorrhage – control with direct compression / arterial tourniquet / hemostatic dressings (i.e. celox)
▪ Internal Haemorrhage (i.e. chest, abdomen, pelvis & retroperitoneum, long bones) – control with chest decompression,
application of pelvic binder (i.e. T-POD), application of extremity splints
- Management (Replacement of Intravascular Volume)

▪ Insert 2 large bore (14G / 16 G) peripheral IV catheter (antecubital veins). In event that intravenous access is not difficult
an alternative is to use intraosseous access (i.e. EZ-IO device) – sites: proximal humeral, proximal tibial, distal tibial
▪ Bloods are taken simultaneously. The blood draw includes full blood count (FBC), Group Cross Match (GXM), Renal Panel,
Coagulation Screen (PT/PTT/INR), Lactate (+/- Blood Toxicology).
▪ Arterial Blood Gas (ABG) is taken and run through iSTAT analyser machine
▪ Initiate IV fluid therapy with warmed crystalloids – 1L of crystalloids

o Rapid Responder
o Transient Responder – likely to require blood and/or definitive intervention (operative / angioembolization)
o Non-Responder – highly likely to require Massive Blood Transfusion / O type blood and definitive intervention
▪ Activation of Massive Blood Transfusion Protocol

o Transfusion of blood during massive blood transfusion is performed with the 1:1:1 ratio [fresh frozen plasma, platelets
and RBCs] in setting of trauma – PROPPR study
o In the setting of uncontrolled haemorrhage, perform damage control resuscitation
▪ Damage Control Resuscitation3

o Permissive hypotension – allows organ perfusion rather than normotension
o Early use of blood products over crystalloid
o Compressive / Haemostatic dressings / devices
o IV Tranexamic acid4 – IV 1g over 10mins within 3 hours followed by 1g over 8 hours
o Prevention of acidosis and hypothermia (i.e. limit crystalloid to prevent dilutional coagulopathy, run warmed fluids)
o Definitive Intervention (i.e. surgical or angioembolization)
[D] - Disability (Neurological Evaluation) - Glasgow Coma Scale
- GCS 13-15 (Mild Traumatic Brain Injury), GCS 9-12 (Moderate TBI), GCS ≤ 8 (Severe TBI)
- For patients with mild traumatic brain injury with GCS scores between 13-15, use Canadian CT Head Rule to decide which
patients can be cleared without the need for a CT brain.
- For any patients with GCS ≤ 8, they should be intubated to protect the airway prior to performing CT imaging. Patient's pupils
must also be examined (size, equality and reaction to light).

- For patients with depressed GCS, early neurosurgical consult is warranted.
- For adults with moderate TBI (GCS < 13) or any evidence of intracranial bleeding on CT scan, use of tranexamic acid within 3
hours of injury reduced head related injury related death. (CRASH 3 trial)5
3 Mil Med. 2018 Sep 1;183(suppl_2):36-43.

4 Health Technol Assess. 2013 Mar;17(10):1-79. [Landmark Trial –CRASH-2]
5 Lancet. 2019 Nov 9;394(10210):1687-1688. (CRASH 3 Trial)
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Assessment of GCS Score (must know)

Original Revised Score Original Revised Score
Eye Opening (E) Eye Opening (E) Verbal Response (V) Verbal Response (V)
- Spontaneous - Spontaneous 4 - Oriented - Oriented 5
- To Speech - To Sound 3 - Confused Conversation - Confused 4
- To Pain - To Pressure 2 - Inappropriate Words - Words 3
- None - None 1 - Incomprehensible - Sounds 2
- Non-Testable NT Sounds - None 1
- None - Non-Testable NT
Original Revised Score
Best Motor Response (M) Best Motor Response (M)
- Obeys Command - Obeys Command 6
- Localizes Pain - Localizing 5
- Flexion withdrawal to pain - Normal Flexion 4
- Abnormal Flexion (Decorticate) - Abnormal Flexion 3
- Extension(Decerebrate) - Extension 2
None (Flaccid) - None (Flaccid) 1
- Non-Testable NT
[E] - Exposure
For trauma patients to be examined properly, full exposure is required. Completely undress the patient by cutting off clothing while
maintaining patient’s dignity and minimizing heat loss. (this is usually done simultaneously with the patient's arrival to the emergency
department) Look for visible or palpable injuries. Proceed to secondary survey.
Trauma Adjuncts
- Trauma X-Ray Series – Portable Chest-XR & Pelvic XR.
▪ Chest XR can be used to guide need for chest tube (i.e. pneumothorax, hemothorax) and assess placement of ETT tube
▪ Pelvic XR can be used to guide need for pelvic binder (i.e. open book pelvic fracture)
- FAST scan
▪ Positive FAST = detection of intraperitoneal fluid on any of the three abdominal windows or detection of pericardial fluid on
the cardiac window (if a window is not well visualized, FAST is inadequate and not negative). It is a rapid, reproducible,
portable and non-invasive bedside test to detect fluid in the abdomen or pericardium (≥ 100ml and more typically 500ml of
peritoneal fluid, sensitivity: 60-95%)

▪ Ultrasonography evaluation of four windows: Subxiphoid: Pericardium, RUQ: Perihepatic Space (i.e. Morrison’s Pouch or
hepatorenal recess), LUQ: Perisplenic Region (splenorenal recess) & Pelvis: rectovesical pouch in males & rectouterine
(Pouch of Douglas) and vesicouterine pouches in females
▪ E-FAST, include unsound of lung for detection of pneumothorax
- Insertion of Indwelling Urinary Catheter (IDC) – assess for gross haematuria (know the contraindications for IDC insertion)*
- Computed Tomography
▪ In the setting of trauma, a pan-scan refers to performing a CT Brain, C-Spine, Thorax, Abdomen & Pelvis.
▪ The clinical decision to proceed with a CT scan for seriously injured trauma patients is based on many factors such as
hemodynamics, mechanism of injury, glasgow coma score, initial blood test (i.e. base excess, lactate), clinical suspicion of
injury (i.e. traumatic brain injury, spinal injury, pelvic fractures etc.)
▪ In general, most seriously injured trauma patients will have a pan-scan performed for them.
- Others:
▪ ECG – assessment of arrhythmias, unexplained tachycardia, AF, PVCs, ST changes (i.e. blunt cardiac injury)
▪ Gastric tube (decompress stomach to reduce risk of aspiration) – NG tube** vs. OG tube**
▪ Hypothermia prevention – “hot air” heating blankets, infusion of warmed IV fluids
* Urinary Catheter insertion is contraindicated with blood at urethral meatus, scrotal hematoma, perineal ecchymosis/hematoma
** NG tube is contraindicated with CSF rhinorrhoea / otorrhea, periorbital ecchymosis, midface instability, hemotympanum (po ssibility of cribriform
plate (base of skull) fracture, consider inserting OG tube instead)
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SECONDARY SURVEY
A complete head-to-toe examination to inventory all injuries sustained in the trauma after primary survey. An AMPLE history is taken
from the patient. This includes Allergies, Medications, Past Illnesses / Pregnancy, Last meal, Events/environment related to the
injury.
Complete head-to-toe examination
- Head
▪ Scalp – lacerations, depressed / open skull fractures
▪ Eyes – ocular entrapment (assess mobility), visual acuity, pupillary size and reactivity, haemorrhage of conjunctiva
▪ Basilar skull fracture – CSF otorrhea, rhinorrhoea, racoon eyes (periorbital ecchymosis) & battle’s sign (mastoid ecchymosis,
a/w facial nerve injury)
▪ Temporal skull fracture – can injure CN 7 & 8, commonly a/w lateral skull or orbital blows
▪ Complete neurological examination – cranial nerves
- Maxillofacial *frequently missed injuries*

▪ Any bony tenderness, crepitus or discontinuity, any palpable deformity
▪ Mid-facial fractures – check by grasping maxilla and attempting to move it
▪ Mandibular fracture – check for mucosal violation and abnormal dental occlusion
▪ Inspect for septal hematoma
▪ Oral/dental examination
▪ Caution: potential airway obstruction in maxillofacial injury, for patients with suspected cribriform plate fracture with CSF
rhinorrhoea do not insert NG tube. Instead, use orogastric tube to decompress stomach
- Neck (r/o cervical spine, vascular, airway or aerodigestive tract injuries)

▪ Keep on c-collar till C-spine cleared
▪ Inspect – blunt and penetrating injuries, tracheal deviation, use of accessory breathing muscles (any hoarseness of voice,
stridor, dysphonia), neurological deficits
▪ Palpate – tenderness, deformity, swelling (i.e. expanding hematoma), crepitus (bony crepitus or subcutaneous
emphysema) and tracheal deviation
▪ Auscultate – carotid arteries bruit
▪ Any dysphagia
- Chest
▪ Inspect – blunt and penetrating injuries, use of accessory breathing muscles, bilateral symmetrical respiratory excursion
▪ Palpate – chest compression / fractures, subcutaneous emphysema
▪ Percuss – hyperresonance (pneumothorax) or dullness (hemothorax)
▪ Auscultate – quality / location of breath sounds (and also heart sounds)
o Check EtCO2, O2 sats, and ABG to ensure adequate ventilation and oxygenation
▪ Any thoracoabdominal injuries (i.e. along costal margin) – potential for missed diagrammatic injuries, small bowel injury
o Evaluate with diagnostic laparoscopy (CT does not reliably detect small diaphragmatic injuries) if patient
hemodynamically stable without indication for laparotomy (alternative is to do DPL, rarely done)
- Abdomen (r/o intra-abdominal injury rather than characterise its exact nature)
▪ Inspect – blunt and penetrating injuries (“seat-belt sign”), bruises
▪ Palpate – signs of peritonism, suspect liver / spleen injuries if have lower rib fractures
- Pelvis
▪ Assess Pelvis stability – pelvic compression (palpate iliac wings once), repeated manipulation of a fractured pelvis can
aggravate haemorrhage
▪ Apply pelvic binder over level of greater trochanter
▪ Pelvic fracture – ecchymosis over iliac wings, pubis, labia or scrotum, pain on palpation, mobility of the pelvis
▪ External Genitalia, any blood, lacerations
▪ Urinary Injuries: urethral blood, scrotal hematoma, contusions, hematomas, laceration
15
- Musculoskeletal System
▪ Upper Limbs (r/o soft tissue, vascular, orthopaedics, neurological injuries)
▪ Ask patient which is their dominant hand
o Inspect – contusion, deformities, abrasions / lacerations, active bleed, hematoma (take photo of injuries)
o Palpate – neurovascular (radial pulses bilaterally), subcutaneous air
o Neurological examination – Tone / Power / Reflex & Sensation
▪ Lower Limbs (r/o soft tissue, vascular, orthopaedics, neurological injuries)

o Inspect – contusion, deformities, abrasions / lacerations, active bleed, hematoma (take photo of injuries), pallor (acute
limb ischemia)
o Palpate – neurovascular (radial pulses), subcutaneous air
o Neurological examination – Tone / Power / Reflex & Sensation
o Assess for risk of compartment syndrome – beware of typical areas (eg. tibia/fibula, ankle), pain out of proportion to
injury, pain worsened on passive stretch of muscle of the respective compartment
- Spine
▪ Back – log-roll patient
o Inspect – wounds and hematomas
o Palpate – vertebral step-off / step deformity or spinal tenderness*
o Keep on spinal nursing if unable to clear spine (presence of spinal tenderness)
▪ DRE: Sphincter tone, rectal blood, pelvic fracture (may feel fragments of bone), rectal wall integrity, high-riding prostate*
o High riding prostate no longer assessed as it is deemed to be unreliable
* Patients with spinal tenderness should undergo CT evaluation for diagnosis of bony injuries. If no fracture is found but spinal tenderness persists, can
consider MRI spine to identify ligamentous or soft tissue injury
- Neurological System
▪ Frequent re-evaluation – i.e. GCS score, pupillary size and response
▪ Prevent secondary brain injury
▪ Imaging as indicated
▪ Early neurosurgical consult
▪ Protection of spinal cord is required at all times until a spine injury is excluded
Concluding Remarks
- Have a high index of suspicion for injuries to avoid missing them (frequent re-evaluation)
- Isolated intracranial injuries do not cause shock (unless brainstem is injured) – look for other causes
- Rapidly recognise when patient is deteriorating (continuous monitoring)
- Any rapid decompensating by the patient should initiate a return to the primary survey
- In penetrating trauma, all entry and exiting wounds must be accounted for
- IV analgesia as appropriate for pain management
16
ABDOMINAL TRAUMA
All penetrating injuries below the nipple line should be suspected of entering the abdominal cavity. Multi-trauma patients with
hypotension are assumed to have intra-abdominal injuries till proven otherwise.
Types of Intra-abdominal injury in Blunt Trauma

- Solid organ injury: spleen, liver – bleeding (may be quite massive)
- Hollow viscus injury with rupture
- Vascular injury with bleeding
Indication for Trauma Exploratory Laparotomy

1. Evisceration, stab wounds with implement in-situ, gunshot wounds traversing abdominal cavity
2. Any penetrating injury to the abdomen with haemodynamic instability or peritoneal irritation
3. Obvious or strongly suspected intra-abdominal injury with shock or difficulty in stabilising haemodynamics
4. Obvious signs of peritoneal irritation
5. Rectal exam reveals fresh blood
6. Persistent fresh blood aspirated from nasogastric tube (oropharyngeal injuries excluded as source of bleeding)
7. X-ray evidence of pneumoperitoneum or diaphragmatic rupture
INVESTIGATIONS
- The first line investigation performed in the trauma resuscitation is a FAST scan.
▪ If the patient is hemodynamically unstable despite initial fluid resuscitation with positive or equivocal FAST scan, suspect
for active intra-abdominal bleeding as cause of hypotension, patient should be brought to the operating theatre.
▪ If the patient is hemodynamically stable with negative or equivocal FAST, proceed with trauma CT scan.
- Patient must be hemodynamically stable prior to transfer to the CT scan room
Focused Assessment with Sonography in Trauma (FAST)

- Positive FAST = detection of intraperitoneal fluid on any of the three abdominal window or detection of pericardial fluid on the
cardiac window (if a window not well visualized, FAST is inadequate)
- Rapid, reproducible, portable and non-invasive bedside test to detect fluid in the abdomen or
pericardium (≥ 100ml and more typically 500ml of peritoneal fluid, sensitivity: 60-95%)
- FAST evaluates 4 main region (e-FAST evaluates 4 main region + lungs)
1. Subxiphoid: Pericardium
2. RUQ: Perihepatic Space (hepatorenal recess)
3. LUQ: Perisplenic Region (splenorenal recess)
4. Pelvis: Pouch of Douglas (suprapubic window)
5. Lungs: bilateral anterior thoracic sonography – detect pneumothorax (absence of pleural
sliding in patients with PTX)
- Advantages: early operative determination, non-invasive, rapid, no need for transport out of
resuscitation area
- Disadvantages: operator dependent, bowel gas and subcutaneous air distort images, can miss diaphragm, bowel and
pancreatic injury, does not completely assess retroperitoneal structure, body habitus can limit image clarity
Computer Tomography Scan

- Only suitable for hemodynamically stable patient as can be time consuming
- In the trauma setting, a pan-CT scan refers to performing a CT brain, C-spine, thorax, abdomen and pelvis. However, depending
on the nature of the injury, a targeted CT scan can be performed.
- Advantages: anatomic diagnosis, non-invasive, visualize retroperitoneal, bony and soft tissue structures, visualize extra-luminal
free air, able to identify injuries that can be managed nonoperatively
- Disadvantages: time consuming, not sensitive for bowel injury, diaphragmatic injury, require transportation from resuscitation
area, use of IV contrast, radiation exposure, higher cost
- CT can miss GI, diaphragmatic and pancreatic injuries, In the absence of hepatic or splenic injuries, the presence of free fluid in
the abdominal cavity suggest injury to the GI tract and/or its mesentery, patients may require for early operative intervention if
clinically indicated (i.e. hemodynamically unstable, peritonitic abdomen)
17
EXTRA INFORMATION
Diagnostic Peritoneal Lavage (DPL)

- Used to be done previously when access to CT scanners were not readily available for trauma patients
- Sensitivity of 97-98% with a 1% complication rate
- Useful in hypotensive, unstable patient with multiple injuries as a means of excluding intra-abdominal bleeding
- Involves an incision in the midline, infra-umbilical, dissection down to peritoneum, a catheter is placed and 1 litre of N/S is run into the peritoneal
cavity, bag is then planed on floor and allowed to fill
- All patients undergoing DPL require abdominal decompression via NG tube and indwelling catheter insertion
- Absolute Contraindication: indication for laparotomy already exists
- Positive DPL in setting of blunt abdominal trauma and (penetrating trauma) → proceed to OT
▪ Lavage fluid appear in chest drain or urinary catheter
▪ Frank blood (>10ml) or any enteric contents (i.e. bile of faeces)
▪ RBC >100,000 per mm 3 (penetrating: > 10,000 RBC)
▪ WBC >500 per mm 3 (penetrating: > 50 WBC)
▪ Amylase of >175U/ml
COMPLICATIONS
Abdominal Compartment Syndrome (ACS)

- Definition: intra-abdominal hypertension sufficient to produce physiological deterioration leading to end-organ dysfunction
- Causes of ACS
▪ Primary – intra-abdominal injury, damage control laparotomy, bleeding pelvic fractures, massive retroperitoneal hematoma,
failed non-operative management of solid organ injury
▪ Secondary (causes originating from outside the abdomen) – sepsis, massive fluid resuscitation, major burns
- Classification of IAP via Bladder Pressure Measurement [normal IAP ~ 5-7mmHg]

▪ I: 12-15mmHg,
▪ II: 16-20mmHg,
▪ III: 21-25mmHg,
▪ IV: >25mmHg
- Clinical outcomes
▪ ↑renal vascular resistance: renal malperfusion, oliguria
▪ ↓ venous return (IVC compression): ↓CO, ↓SV ↑SVR leading to extremity & splanchnic ischemia
▪ ↑intrathoracic pressure (diaphragmatic splinting): hypoxemia (↑CVP, ↓compliance, ↑airway pressure, ↓tidal volumes)
▪ ↑intracranial pressure
- Management
▪ Improve abdominal wall compliance (i.e. sedation, NMB, analgesia),
▪ Evacuate intra-luminal contents (i.e. NG decompression, rectal decompression, prokinetic agents),
▪ Evacuate abdominal fluid collections (i.e. percutaneous drainage),
▪ Correct positive fluid balance (i.e. avoid excessive fluid resuscitation, diuretics, haemodialysis),
▪ Organ support
▪ Aim to keep Abdominal Perfusion Pressure (APP) > 50-60mmHg to maintain visceral and splanchnic perfusion (APP =
MAP - IAP)
▪ Patients with grade III / IV IAP with evidence of new organ dysfunction not responsive to non-operative mx, proceed to
decompressive laparotomy
18
Liver Trauma (AAST Liver Injury Scale)

- Most common injury in blunt trauma (some texts say spleen)
Grade I II III IV V
Subcapsular Hematoma
< 10% 10-50% > 50% or ruptured
(% of total surface area)
Parenchymal Laceration Juxtahepatic venous

< 1cm 1-3cm > 3cm Active hepatic
(depth) injury involving retro-
hemorrhage with
hepatic vena cava and
Intraparenchymal extension into the
< 10cm > 10cm central major hepatic
Hematoma (diameter) peritoneum
veins
25-75% lobar > 75% lobar
Vessels involved in Capsular tea identified
parenchymal parenchymal
laceration intra-operatively
disruption disruption
Management
- Conservative vs. Angioembolization vs. Operative Intervention
▪ Is the patient hemodynamically stable? – if hemodynamically unstable with high grade liver injury (i.e. liver likely source of
bleed and hemorrhagic shock) → operate
▪ Is there an active arterial bleeder seen on CT scans? – if hemodynamically stable with active blush seen → consider
angioembolization (evaluate for risk of contrast allergy, creatine function, asthma)
▪ If patient is hemodynamically stable with no active blush on CT scan → consiervative management (involves serial FBC,
close monitoring of vitals, serial abdominal examination)
EXTRA INFORMATION
Operative Management of Liver Trauma

- Exploratory Laparotomy + Evacuation of Blood
- Packing with penny towel + Perihepatic packing
- Ligamentum teres is then clamped, divided and ligated and falciform ligament is divided close to the abdominal wall
- Mobilization of the liver – right and left triangular ligament + coronary ligament
- Pringle manoeuvre (clamp portal triad, occludes hepatic artery and portal vein) – used when persistent bleeding despite
perihepatic packing (but does not stop bleeding from hepatic veins or retrohepatic vena cava)
- Total vascular exclusion – clamp vena cava above and below the liver
Pringle Manoeuvre
Splenic Trauma (AAST Spleen Injury Scale)

Grade I II III IV V
Subcapsular Hematoma > 50% or expanding or

< 10% 10-50%
(% of total surface area) ruptured
Parenchymal Laceration Completely shattered

< 1cm 1-3cm > 3cm
(depth) spleen
Intraparenchymal ≥ 5cm or expanding or

< 5cm Segmental or
Hematoma (diameter) ruptured hilar ( ≥ 25% hilar devascularization
Vessels involved in Not involving Involved trabecular devascularization)
laceration trabecular vessels vessels
19
Investigations
- In the hemodynamically normal blunt abdominal trauma patient without peritonitis, an abdominal CT scan with intravenous
contrast should be performed to identify and assess the severity of injury to the spleen
Management6
- Selective non-operative management (NOM) ~ 85%
▪ Criteria for NOM – hemodynamically stable, no active contrast extravasation, no blush (usually for grade I to III)
▪ Requires (1) monitored care, (2) serial Hb check, (3) watch for abdominal pain, left shoulder pain, fever
▪ Risk of NOM failure: advanced age (>55), High ISS (> 15-25), Moderate to Severe Splenic Injury (AAST ≥ 3 ), GCS score
(<12), need for blood transfusion > 2pRBC, cirrhotic patients, on anticoagulation
▪ Of patients who failed NOM, 75% will fail within 48 hours, 93% fail within 1 week.
▪ Use of LMWH – early use (<3days) does not increase the failure rate of NOM of splenic laceration
- Splenic Artery Angiography & Embolization

▪ Usually for higher grade blunt splenic injury (i.e. AAST IV / V), presence of vascular injury on CT, hemodynamically stable
- Operative
▪ For patients with diffuse peritonitis or are hemodynamically unstable after blunt abdominal trauma → laparotomy
▪ Spleen salvage (i.e. hemostatic agents, splenorrhaphy) vs. Splenectomy (usually choice)
▪ Post-splenectomy immunization against encapsulated bacteria – Pneumococcus, Haemophilus influenza B and
Meningococcus
EXTRA INFORMATION
Operative Management of Splenectomy

- Lesser Sac entered by removing the omentum from the transverse colon
- Splenic flexure of the colon is mobilized by dividing the splenocolic ligament
- Short gastric arteries ligated (gastrosplenic ligament, only vascular ligament)
- Spleen mobilized out of the retroperitoneum (retracted medially, peritoneal attachments proceeding from inferior pole to
superior pole, ligaments (i.e. spleno-renal ligament (inferior pole) and spleno-phrenic (superior pole)) divided.
- Spleen rotates medially and anteriorly
- Dividing of the splenic artery and vein
6 J Trauma. 2005 Mar;58(3):492-8.
20
EXTRA INFORMATION
Duodenal Trauma
- 2nd portion of duodenum – most common site of injury, can also get tears near ligament of Treitz
- Start early total parenteral nutrition (TPN) – reduce septic complications
- If at laparotomy (suspect duodenal injury) – perform Kocher Maneuver and open lesser sac through the omentum – check
for hematoma, bile, gastric fluid, fat necrosis
Kocher Maneuver
- Kocher maneuver allow inspection of the duodenum, pancreas, and other retroperitoneal structures
- If there is a high suspicion of duodenal or pancreatic injury due to a missile or highly associated injuries, each of the
steps described below should be performed to mobilize and examine the retroperitoneum.
- Perform a Kocher maneuver by dissecting the lateral peritoneal attachments of the duodenum to expose the first, second, and
third portion of the duodenum, and the head and neck of the pancreas.
- Divide the gastrocolic ligament to allow entry into the lesser sac and inspection of the posterior aspect of the first portion of the
duodenum, the medial aspect of the second portion of the duodenum, and the anterior surface of the pancreas.
- Divide the retroperitoneum inferior to the pancreas to inspect the posterior pancreas after mobilizing and lifting the inferior edge
of the pancreas.
- Expose the third portion of the duodenum with a right medial visceral rotation.
- Mobilize the ligament of Treitz to expose the fourth portion of the duodenum and pancreas.
Small Bowel Trauma

- Occurs in ~ 1% of blunt abdominal trauma patient
- Patients with operation delayed more than 24 hours have increased mortality
- Diagnosis – certain characteristic physical examination and CT findings
▪ Chance fracture (L2) a/w 52% risk of small bowel injuries
▪ Intra-abdominal fluid not a/w solid organ injury, bowel wall thickening or mesenteric hematoma
▪ Abdominal seat belt sign
▪ KIV repeat CTAP in 8-12 hours to re-evaluate
- If suspicious, exploratory laparotomy is indicated
Renal Trauma
- Haematuria is the best indicator
- Indication for operation
▪ Ongoing haemorrhage with hemodynamic instability
▪ Major collecting system disruption, non-resolving urine extravasation, severe haematuria
Bladder Trauma
- Gross haematuria is the best indicator (95% a/w pelvic fracture)
21
- Extra-peritoneal bladder rupture (~60%): IDC after a negative retrograde urethrogram*, keep for ~ 14 days
- Intraperitoneal bladder rupture (~30%): surgical repair + IDC
▪ Repaired in a standard two-layer closure with running slowly absorbable suture – 1st layer incorporates mucosa and
muscularis and 2nd layer incorporates muscularis and overlying serosa
Urethral Trauma
- Haematuria or blood at meatus is the best indicator. high riding prostate also suggestive of urethral trauma
- Fracture patterns – pubic diastasis or fracture of inferior pubic ramus
- Retrograde urethrogram (RUG) is the best test
- Indication for re-alignment – stable patient with complete or partial urethral disruption
- Complications – stricture (rates higher in suprapubic cystostomy as compared to re-alignment procedures), urinary / sexual
dysfunction
- Contraindication to IDC insertion, proceed to insert SPC
▪ Blood at urinary meatus
▪ Scrotal hematoma
▪ High riding prostate on DRE
Retroperitoneal Hematoma
- Classified into 3 zones: central (zone 1), lateral (zone 2) and pelvic (zone 3)
▪ Zone 1: highest risk of vascular injury, investigate with surgery unless small and stable
▪ Zone 2: 2nd most common site of retroperitoneal haemorrhage, a/w renal injuries
▪ Zone 3: Most common site of retroperitoneal haemorrhage, a/w pelvic fractures
- Management
▪ Zone 1 Injuries → surgery
▪ Zone 2 & 3 → can observe if hemodynamically stable
▪ For all penetrating injuries → surgery
22
CARDIOTHORACIC TRAUMA
There are 5 clinical scenarios in chest trauma where bedside procedures are lifesaving: cardiac tamponade, airway obstruction, flail
chest, hemothorax, and pneumothorax.
CARDIAC TAMPONADE
High index of suspicion required
Clinical features
- Chest trauma and hypotension
- Beck’s triad (hypotension, muffled heart sounds, distended neck veins) – only in 50% of cases as hypovolemia may prevent neck
vein distension; muffled heart sounds least reliable
- Pulseless electrical activity
- Kussmaul’s signs (jugular venous distension during inspiration, pulsus paradoxus)
▪ Pulsus paradoxus = exaggerated (>10mmHg) reduction of the arterial pressure brought on by inspiration – common finding
in patients with large pericardial effusion causing tamponade
Diagnostic clues
- Enlarged cardiac shadow in CXR (globular heart – very rarely seen)
- Small ECG voltages, electrical alternans = alternation of QRS complex amplitude or axis between beats.
- 2DE – separation of pericardial layers detected (fluid exceeds 15-35ml); early diastolic collapse of RV wall (tamponade)
Management
- Aggressive fluid resuscitation – helps maintain cardiac output and buys time.
- Pericardiocentesis: 2D-echo guided or ECG lead-guided (Stop inserting needle when an abrupt change in the ECG waveform is
noted. If the ECG waveform shows an injury pattern (ST segment elevation), slowly withdraw the needle until the pattern returns
to normal, as this change in waveform suggests that the spinal needle is in direct contact with the myocardium)
- Resuscitative thoracotomy – for patients with SBP <60mmHg, patients with isolated cardiac injury have the greatest benefit
compared to blunt trauma
23
Cardiac Tamponade Investigation Findings
*ACC/AHA definition for low QRS voltage is amplitude <5mm in standard limb leads or <10mm in precordial leads
ECG showing electrical alternans:
24
AIRWAY OBSTRUCTION
Due to laryngeal injury or posterior/fracture dislocation of SCJ
Diagnostic Clues (for laryngeal trauma)

- Hoarseness
- Subcutaneous Emphysema
- Palpable Fracture
Management:
- Definitive airway – ETT, tracheostomy, cricothyroidotomy
FLAIL CHEST
2 or more contiguous ribs are fractured at 2 or more points
Diagnostic Clues
- Paradoxical movement of the chest wall
- Respiratory distress (hypoxemia due to underlying pulmonary contusion*, contributed to by pain with restricted chest wall
movement)
- External evidence of chest trauma (bruising etc)
- Pain with respiratory effort
Management:
- Ensure adequate oxygenation and ventilation
- Judicious fluid therapy (avoid fluid overload)
- Adequate intravenous analgesia
- KIV mechanical ventilation in high-risk patients: shock, severe head injury, previous pulmonary disease, fracture of >8 ribs, age >
65, >3 associated injuries
- Rib stabilization – improved chest wall deformity (proven) ± ?↓time on ventilator, ?↑pulmonary function, ?↓pain, ?↑QOL [best
indicated for patient with significant flail segment with chest wall deformity and unable to wean off mechanical ventilation in a
short period of time]
*Pulmonary Contusion – develops over the first 24 hours. CXR: irregular, non-lobar opacification of the pulmonary parenchyma
MASSIVE HEMOTHORAX
blood >1500mls or on-going haemorrhage of more than 200ml / hr over 2-4 hours
Diagnostic Clues
- No breath sounds
- Dullness to percussion
- Shock
- Flat Neck Veins (a/w hypotension) or Distended Neck Veins (a/w tension haemothorax)
Management:
- Resuscitation: Ensure adequate oxygenation, establish 2 large bore IV access and fluid resuscitation / type-specific blood
transfusion, correction of coagulopathy
- Decompression of Chest Cavity: Chest tube insertion in the triangle of safety
- Operative Intervention: Indication for thoracotomy: evacuation of > 1500ml upon chest tube insertion, >200ml/hr for 2 to 4 hours,
clinically unstable patient or patient with persistent need for blood transfusion (colour of blood is a poor indicator) or in patients
with retained haemothorax (manage with VATS)
- Retained / incompletely drained haemothorax, risk of progression to a post-traumatic empyema and eventual fibrothorax
- Majority of haemothorax is evacuated within 3 – 4 days, if chest tube output still high (with 2 well-placed chest tubes) investigate
for retained haemothorax 🡪 video-assisted thoracoscopic surgery (VATS)
25
PNEUMOTHORAX (TENSION/ OPEN)
Tension pneumothorax
develops when air is trapped in the pleural cavity under positive pressure, displacing mediastinal structures and compromising
cardiopulmonary function
Mechanism: One-way valve effect in the defect of the pleura allows air to enter the pleural cavity but not escape, leading to a buildup
of positive pressure.
- Clinical diagnosis (CXR will only delay treatment) – signs: hypotension, ± neck vein distension (may be flat due to hypotension),
severe respiratory distress, deviated trachea, subcutaneous emphysema
- Hypotension qualifies pneumothorax as tension pneumothorax (hemodynamic instability)
- Mechanism of obstructive shock: Decreased venous return caused by compression of the relatively thin walls of the atria impairs
cardiac function. The inferior vena cava is thought to be the first to kink and restrict blood flow back to the heart. It is most evident
in trauma patients who may be hypovolemic with reduced venous blood return to the heart.
Management
- Needle thoracotomy: 14G needle at the 4th / 5th intercostal space in the mid-axillary line OR at the 2nd intercostal space in
the midclavicular line [temporizing measure]
- Followed by tube thoracotomy at the 5 th IC space between the anterior and mid-axillary line. (triangle of safety: lateral border of
the pectoralis major medially, a line just anterior to the mid-axillary line laterally, and the upper border of the fifth rib inferiorly)*
Tension Pneumothorax
Open pneumothorax
- Chest wall defect with equilibration between intrathoracic and atmospheric pressure (sucking chest wound)
- Cover defect with sterile dressing, taped down on 3 sides to produce a flutter-valve effect which let air out but not back in
- Taping the dressing on all 4 sides converts an open pneumothorax into a tension pneumothorax!
- Insert chest tube (not through the wound) - refer to topic on chest tube
BLUNT CARDIAC INJURY
Clinical features
- Persistent tachycardia
- Rhythm disturbances
- Associated with sternal fractures
- Can lead to cardiac tamponade, cardiogenic shock – secondary to atrial or RV rupture
Diagnostic clues
- Perform ECG – monitor with telemetry for 24 hours for dysrhythmias if abnormal ECG (normal ECG has a NPV of 95%)
- Troponin I + ECG – if both normal (NPV of 100%), patient can be safely discharged
- If hemodynamically unstable or have persistent new arrhythmias – perform echocardiogram (look for RWMA, valvular dysfunction,
chordae rupture, pericardial fluid, diminished EF)
26
EXTRA INFORMATION
EMERGENCY THORACOTOMY7
Thoracotomy occurring immediately at site of injury, emergency department or operating room as an integral part of resuscitation
process – survival is between 4 to 33% (determinants: mechanism of injury [i.e. blunt vs. penetrating], location of injury [i.e.
cardiac vs. great vessels / pulmonary hilar], and presence of vital signs)
Aims of performing thoracotomy

▪ Control of haemorrhage (i.e. cardiac wounds, great vessel, pulmonary & hilar injuries)
▪ Release of cardiac tamponade
▪ Internal or open cardiac massage
▪ Cross-clamping of descending thoracic aorta (to enhance coronary and cerebral perfusion & to reduce sub-diaphragmatic
bleeding)
▪ Treatment of air embolism*
* Suspect Air Embolism in patients with penetrating thoracic injury, who is hemodynamically stable but experiences arrest aft er being intubated and
placed on positive pressure ventilation – management: place patient in Trendelenburg position & perform emergency thoracotomy followed by cross-
clamping of pulmonary hilum on the side of injury to prevent further introduction of air. Air is aspirated from left ventricle
Factors associated with increases success

▪ Sings of life in ED
▪ Penetrating thoracic injury (~9-12% survival, 1-2% for cardiac arrest following blunt trauma)
▪ Stab Wounds (as compared to GSW)
▪ Thoracic Injuries (as opposed to abdominal injuries)
Indications
▪ Penetrating thoracic injury arriving with PEA
- Previous witnessed cardiac activity
- Unresponsive hypotension (SBP<70) despite resuscitation
▪ Blunt thoracic injury
- Rapid exsanguination from chest tube (> 1500ml)
- Unresponsive hypotension (SBP < 70) despite resuscitation
Relative indications
- Penetrating thoracic injury with traumatic arrest without previously without previously witnessed cardiac activity
- Penetrating non-thoracic injury (e.g. Abdominal, peripheral) with traumatic arrest with previously witnessed cardiac activity
(pre-hospital or in-hospital)
- Blunt thoracic injuries with traumatic arrest with previously witnessed cardiac activity (pre-hospital or in-hospital)
Contraindication
▪ Blunt thoracic injury with PEA
▪ Penetrating abdominal trauma without witnessed cardiac activity
▪ Non-traumatic cardiac arrest
▪ Severe head injury
▪ Severe multisystem Injury
▪ Improperly trained team / lack of equipment
7 Injury, Int. J. Care Injured (2006) 37, 1—19
27
MUSCULOSKELETAL TRAUMA
GENERAL POINTS
- Extremity trauma tends not to be life-threatening, but occult blood loss can occur in large volume – i.e. pelvic # (up to 3L), femoral
shaft # (2L)
- Patients with bilateral femur fractures are at higher risk for significant blood loss, pulmonary complications, multiple organ failure
and death
- Need to have high level of suspicion and treat with urgency
- Look out for any tachycardia, early signs of shock → prepare to resuscitate patient
ASSESSMENT OF THE EXTREMITY

- Perfusion: colour, pulses, skin temperature, capillary refill
- Viability of the limb
- Neurological assessment
- Wounds – open or closed injury; abrasion over a fracture is considered open fracture
- Soft tissue assessment
- Deformity
- Abnormal joint mobility – ligamentous injury around joint; in knee, highly likely that popliteal artery is injured as well
Things to consider
- Is pulselessness due to shock?
- Arterial or venous compromise?*
- Is there compartment syndrome** (clinical diagnosis, with intra-compartmental pressure as an adjunct)
- Any pre-existing vascular disease?
- Duration? Peripheral nerves and muscle can survive for ~ 4 hours under ischemic conditions, at 6 hours
results in variable return of function and at 8 hours leads to irreversible nerve and muscle damage
Physical examination
- Any limb deformity (can result in kinking of vessels)?
- Any joint instability (joint dislocation can result in an intimal tear in the major vessel running across it, with
thrombosis and occlusion)?
- Skin colour/temperature
- Post-reduction tibial pulse in knee dislocation – if still absent, do an urgent angiogram
* Vascular Injury
- Hard Signs – active bleeding, pulse deficit, expanding or pulsatile hematoma, distal ischemia, bruit, thrill →
go to OR for exploration / on-table angiography

- Soft Signs – proximity to vasculature, significant hematoma, associated nerve injury, API < 0.9
- Consider fasciotomy if ischemia > 4-6 hours (prevents compartment syndrome)
THE PULSELESS **High Risk for compartment syndrome

EXTREMITY - Fractures – tibial diaphyseal #, distal radius #, radius / ulnar diaphyseal #
- Prolonged ischemia
- Presence of shock
- Combined arterial and venous injury
- Massive soft tissue or crush injury
- In paediatric age group – open fracture
Fasciotomy
- Occurs secondary to increased pressure in the enclosed fascial space
- Causes: muscle edema from direct trauma to extremity or reperfusion after vascular injuries
- Clinica features: 6Ps (pain out of proportion to injury, pallor, paralysis, paresthesia, pulselessness,
poikilothermia), pain with passive stretch, tight compartment, increasing analgesia requirements
- Indications for fasciotomy
▪ Absolute compartment pressure > 30mmHg
▪ < 30mmHg pressure difference between compartment pressure and diastolic pressure
▪ > 6 hour of ischemic time
▪ Combined arterial and venous injuries
EXTRA INFORMATION
Fasciotomy Steps
28
- 2 incision approach (antero-lateral incision & posteromedial incision) to release 4 compartments

▪ Anterolateral incision is centered halfway between the fibular shaft and tibia, once the fascia is
identified, a transverse incision is made to identify and anterior (1) and lateral (2) & the superficial
fibular nerve
▪ Posteromedial incision is made 2cm posterior to tibial shaft and used to identify the superficial (3)
and deep (4) posterior compartment & the saphenous nerve and vein
Types
- Open: laceration, abrasion
- Crushing
- Degloving: open or closed
- Closed
Wound care
SOFT TISSUE
- Swabs of the wounds for culture and sensitivity
INJURIES
- IV antibiotic prophylaxis
- Tetanus toxoid cover
- Photograph wound
- Betadine (povidone-iodine) dressing
- In OT: generous debridement, irrigation (within 4-8 hours, especially in open fractures), fracture
stabilisation
- Leave wound OPEN
- Recognise fracture and/or dislocation
- Complete neurovascular examination of the limb involved before reduction
- Appropriate X-rays (at least 2 planes) including joint above & below
- Analgesia
- Correction of deformity
- Temporary immobilisation – backslab, malleable splint
MANAGEMENT
- Neurovascular examination; examine for compartment syndrome
OF FRACTURES
- Repeat imaging of the limb to check for correct placement (especially in dislocations)
- Circulation chart
- Complications: Fat embolism (a/w long bone fracture) – presents with acute dyspnoea, petechiae (neck
and axilla) and altered mental status – treat with respiratory support, Avascular necrosis (with femoral #)
- Blood Loss Estimates: Pelvic # (> 1000mls), Femur # (800 – 1000mls), Tibial # (300 – 500mls), Rib
Fractures (100 – 200mls)
29
PELVIC FRACTURE
Anatomy: Closed compartment of two innominate bones connected anteriorly at the pubic symphysis and posteriorly to the sacrum
at the sacroiliac joints.
Tile classification
A Stable With an unstable pelvic fracture, the internal volume of the pelvis increases
B Rotationally Unstable making it possible for the patient’s entire blood volume to accumulate within the
C Vertically & Rotationally Unstable retroperitoneal space without much self-tamponade effect.
Management of pelvic fractures

- Exclude other sites of haemorrhage (i.e. thoracic cavity, retroperitoneal tissue, bony fractures, abdominal cavity)
- Evaluate for genitourinary and abdominal injuries
- Reducing and stabilising the disrupted pelvic ring using pelvic binders or pelvic sheet wrap (temporizing measure)
- Stabilization can be achieved initially with external fixation (EF), usually for open book fractures (see below)
- Advanced haemostasis: Pelvic angiography with embolization or operative intervention with preperitoneal packing (PPP) + EF
- May need colostomy for open pelvic fractures with rectal tears and perineal laceration
Unstable Pelvic Fracture. (A) Pelvic X-Ray on arrival. (B) Displacement is reduced by external fixators. Surgical packing is seen within the pelvic
cavity. (C) Displacement is reduced by internal fixators.
EXTRA INFORMATION
Preperitoneal Packing
PPP involves creating a lower midline incision above the pubis extending towards the umbilicus, which is then depended till the
preperitoneal space is reached. The bladder is retracted away from the fracture, and three large laparotomy pads are packed in
the retroperitoneal space on each side of the bladder to tamponade bleeding vessels.
OPEN FRACTURE
Definition: a fracture with direct communication to the external environment
Gustilo-Andersen classification (INTRA-OPERATIVE classification, although some features can be derived before)
Type I ≤1cm AND clean
Type II 1-10cm AND no extensive soft tissue injury, moderate contamination, no periosteal stripping
Extensive soft tissue injury, contamination & periosteal stripping but adequate soft tissue coverage of bone OR > 10cm,
Type IIIA
high-energy trauma
Extensive soft tissue loss, contamination with periosteal stripping and exposure of bone which requires replacement of
Type IIIB
exposed bone with a free flap for coverage
Type IIIC Extensive soft tissue loss, contamination with periosteal stripping and arterial injury requiring repair
30
Management of open fractures

- Stabilise patient – trauma survey and resuscitation
- May need to tourniquet limb if bleeding refractory (Life over Limb)
- IV broad-spectrum antibiotics & updated tetanus prophylaxis
▪ Type I & II: 1st gen cephalosporin (i.e. cefazolin) – if allergic use clindamycin – dose based on patient’s weight
▪ Type III: 1st gen cephalosporin + aminoglycoside (i.e. gentamicin)
▪ Wounds with soil, standing water – broad spectrum coverage with piperacillin-tazobactam (gm + & gm – coverage)
- Pain relief and analgesia
- Photograph Wound
- Cover the wound with sterile saline-soaked dressing/gauze
- Temporary immobilisation and splinting
- Appropriate X-rays
- NBM
- Pre-op investigations: FBC, U/E/Cr, PT/PTT, GXM, ECG, CXR
- Arrange for emergency operation
- Angiogram if needed
Surgery involves
- Aggressive debridement and irrigation with low-pressure saline lavage
▪ Bony fragments without soft-tissue attachment can be removed
▪ Type I: 3L, Type II: 6L, Type III: 9L
- Fracture Stabilization – usually external fixation (with eventual internal fixation after wound closure)
- Staged debridement and irrigation – Q24-48hrs as indicated
- Early soft tissue coverage or wound closure
EXTRA INFORMATION
Fat Embolism Syndrome

Results when embolic marrow fat macroglobules damage small vessel perfusion leading to endothelial damage in pulmonary
capillary beds. Risk factors includes (1) Long bone #: note that the risk is esp high w femoral shaft # and concomitant head injury,
(2) Risk if higher w non-operative therapy but is also higher w overzealous reaming of femoral canal, (3) Multiple trauma w major
visceral injuries and blood loss (incidence may be as high as 5-10%). Cause of death on 3rd day after pelvic # is often due to fat
embolism.
Clinical Presentation: Symptoms usually begin 24-48 hrs after injury, diagnosis based on Gurd’s diagnostic criteria: 1 major +
4 minor criteria + fat microglobulinemia must be present to formally diagnose fat embolism syndrome
Major criteria Minor criteria

1. Axillary or subconjunctival petechiae 1. Tachycardia (> 110 bpm)
2. Hypoxaemia (PaO2 < 60 mmHg; FiO2 = 0.4 2. Tachypnea
3. CNS depression/ AMS disproportionate to hypoxaemia 3. Hypotension
4. Pulmonary edema 4. Renal dysfunction
5. Jaundice
6. Pyrexia (> 38.5°C)
7. Emboli present in the retina on fundoscopy
8. Fat present in urine
9. A sudden unexplainable drop in haematocrit or platelet values
10. Increasing ESR
11. Fat globules present in sputum
31
NEUROSURGICAL TRAUMA
PATHOPHYSIOLOGY
The CNS & its contents (brain, CSF, blood) are enclosed in a rigid space whose total volume tends to remain
constant whereby increase in the volume of one component will elevate the intracranial pressure
Cerebral perfusion pressure = Mean arterial pressure – Intracranial pressure
‘When an intracranial mass is introduced, compensation must occur by a reciprocal decrease in the
Monroe volume of venous blood and CSF’
Kellie
doctrine Compensatory mechanisms:
- Hyperventilation → vasoconstriction of cerebral vessels due to decrease in pCO 2 resulting in decreased blood
volume
- However, excessive hyperventilation will also compromise perfusion and result in infarction
- CSF pushed into spinal canal (but limited volume available)
- Hence, removal of any reversible cause of raised ICP will improve cerebral perfusion
Early: gradual dilation, sluggish response to light ipsilateral to the lesion
Late: dilatation of ipsilateral pupil and non-reactive to light
Very Late: bilateral pupil dilation and fixation
Fixed
dilated Pathophysiology
pupil - Constrictor fibres to the pupil run in the oculomotor nerve, which exits the brainstem at the upper midbrain
- Due to raised ICP, it would cause the uncus to herniate and compress on the midbrain leading to compression
of the third nerve
- Thus a fixed dilated pupil occurs on the side of the compression
A triad of
- Hypertension
- Irregular breathing (Cheyne-Stokes breathing) – cyclic pattern in which apnoea is followed by gradual ↑ then ↓
tidal volumes (the pattern of breathing may be different depending on extent of brain stem injur)
- Bradycardia
Cushing’s
From Monroe-Kellie, increase in MAP maintains cerebral perfusion pressure when ICP is raised.
reflex
Increase in mean arterial pressure achieved by sympathetic overdrive:

(late px of
a) Increased heart rate
brain stem
b) Increased contractility
dysfunctio
c) Increased vasoconstriction – increased total peripheral resistance
n)
(a) and (b) increase cardiac output which increases BP; (c) increases BP
- Baroreceptors detect abnormally raised BP and try to decrease it by triggering a parasympathetic response via
vagus nerve + Direct distortion of vagus nerve due to raised ICP leading to decrease in heart rate (reflex
bradycardia)
- Distortion and/or increased pressure of brainstem (controls involuntary breathing) leading to irregular breathing
and/or apnoea
32
- Temporary neuronal dysfunction following nonoperative head trauma (CT: normal)
- Colorado grading system – [1] HI with confusion, [2] HI with amnesia, [3] HI with LOC
Concussion
- Second-impact syndrome: brain more vulnerable to injury 1-2wks after concussion
▪ Examples of this include athletes in rugby, boxing etc
- Bruise of the brain – breakdown of small vessels and extravasation of blood into brain
- Repeat CT Brain in 24 hours – contusion may enlarge or progress to frank hematoma
Contusion
- Contre-coup injury: contusion occurring in brain tissue opposite site of impact
▪ In particular, frontal lobe and temporal poles are vulnerable to this kind of injury
Extradural Lens-shaped (lentiform) haematoma: between skull & dura
haemorrhage - Pathology: laceration of middle meningeal artery due to temporal bone # – operative
(EDH) for significant neurological degeneration or mass effect (>0.5cm), open craniotomy
with clot evacuation (better prognosis than SDH)
- Classic 3-stage presentation: LOC followed by ‘lucid interval’ and eventual rapid
deterioration
▪ Lucid interval due to temporary slowing of bleed due to vasospasm of bleeding
vessels
- Transtentorial (Uncal) Herniation from EDH / SDH
▪ Ipsilateral oculomotor (3rd) nerve – fixed and dilated pupil
▪ Posterior cerebral artery – ipsilateral infarction of the occipital lobe
- Conservative – clot volume <30cm3, max thickness <1.5cm & GCS >8 (criteria may
not always apply and is patient and presentation dependent)
Subdural Crescent-shaped (lunate) haematoma: between dura & arachnoid
haemorrhage
(SDH) Acute SDH: high-speed acceleration / deceleration trauma which shears small bridging
(emissary) veins
- More severe than EDH (usually due to nature of injury that causes SDH to occur –
associated with higher impact, thus brain has other injuries) – (i.e. shaken baby
syndrome, in which similar shearing forces classically cause intra- and pre-retinal
haemorrhages)
- Pathology: underlying brain damage in addition to expanding SOL – worse functional
recovery prognosis
- Surgery – thickness >1cm, midline shift >5mm, GCS ↓ >2pts (craniotomy/ craniectomy
Intracranial
haemorrhage and evacuation of SDH)
Chronic SDH: present in elderly and alcoholics days to weeks after initial HI – can
cause focal neurological deficits, AMS, metabolic abnormalities and/or seizures
- If chronic SDH (>1cm) or symptomatic = stop anticoagulants / antiplatelets, reverse
effect by FPP, PT complex, factor Vii, platelet transfusion, observe and monitor, once
resolve = burr-hole drainage
Subarachnoid Star-shaped appearance (fissure and CSF cistern around base of brain)
haemorrhage - Causes:
(SAH) ▪ Traumatic: Head Injury (usually will give SAH at the site of impact and not at
the basal cisterns)
▪ Atraumatic: rupture of a cerebral aneurysm*, vascular malformation**,
intracerebral hematoma into subarachnoid space
- Can present with LOC, focal neurological symptoms, symptoms of meningeal irritation
(i.e. nuchal rigidity, photophobia, headache, papilledema, seizure)
- High clinical suspicion but negative CT Brain – do Lumbar Puncture (most sensitive
after 12 hours of symptom onset)
- LP with xanthochromia and high RBC (~100,000/ml) which do not decrease btw
tubes 1 & 4 = SAH
- Xanthochromia more specific, to differentiate between true SAH and traumatic tap
- SAH +ve require four-vessel cerebral angiography within 24 hours to assess cerebral
vasculature and other vascular malformations
Intraparenchym - a/w HTN bleed or AVMs (often affect temporal lobe)
al haemorrhage - Surgery – if there is evidence of mass effect and increasing drowsiness/ neurological
(IPH) deficits
- Damage to axons due to rotational acceleration and then deceleration
- A major cause of unconsciousness and persistent vegetative state after head trauma
Diffuse axonal
- If severe will see punctate haemorrhages at the grey-white border (corpus callosum, brain stem are
injury
common areas)
- Maximal effects at corpus callosum and dorsolateral midbrain
Hypoxic / Cytotoxic (cellular)
33
- Decreased blood supply (oxygenation) → loss of function of Na-K pump as ATP decreases → increased
intracellular sodium → cellular swelling

- Conventionally thought to be resistant to any known medical treatment
Interstitial
Cerebral
oedema - Impaired absorption of CSF → increases in transependymal CSF flow → acute hydrocephalus
(3 types) - Also not responsive to steroid administration, and its response to osmotherapy is debatable
Vasogenic
- Breakdown of blood-brain barrier → proteins enter interstitial space → oedema
- Seen in TBI, neoplasms, and inflammatory conditions
- This oedema subtype is responsive to both steroid administration and osmotherapy
MANAGEMENT
Assessment: 3 important parameters: ABCs, GCS, pupil size
- Most common
- Indications for admission:
▪ Persistent headache and/or vomiting
▪ CSF leak
Minor
▪ Neurological deficit
Traumatic
▪ Skull fracture
Brain Injury
▪ History of loss of consciousness
(GCS >13)
▪ Amnesia
- In ward: NBM, IV drip (no dextrose saline!), no sedation, monitor GCS
- If pt deteriorates, proceed to CT scan, exclude metabolic causes (e.g. hypoglycaemia) and do septic workup
(exclude sepsis)
Mod. TBI - All will be CT-scanned at ED → NES will operate if any indication to do so
(GCS 8 - 13) - In ward: as per mild head injury
Must scan to look for reversible causes of raised ICP but stabilise patient first
Screen for other life-threatening injuries (likely to be multi-trauma patient)
Management of ICP – to maintain CPP and prevent cerebral oedema

- Medical – osmosis diuresis, loop diuretics NOT steroids, stress ulcer prophylaxis with PPI
- Surgical – CSF diversion, decompression, removal of mass effect
- Raise head of bed (30deg) – improves venous drainage but could decrease BP to the head
- Intubate and hyperventilate (aim PaCO2 to 35mmHg) – hyperventilation reduces PaCO2 which causes
cerebral vasoconstriction. Aggressive and prolonged hyperventilation can result in cerebral ischemia – use
only in moderation (i.e. PaCO2 ~ 35mmHg) and for a limited time.
Severe TBI - IV mannitol (1g/kg) – hypertonic solution – decrease brain volume by decreasing overall water content,
reduce blood volume by vasoconstriction and reduce CSF volume by decreasing water content. Can also
ICP ~ (<20 improve cerebral perfusion by decreasing viscosity
mmHg is ▪ Complications: fluid and electrolyte imbalance (dilutional hyponatremia, metabolic acidosis,
considered hyperaemia), pulmonary oedema, rebound cerebral oedema
normal) – - IV 3% Normal Saline – 100ml (6-8Hr PRN) – preferred for hypotensive patient as hypertonic saline is not a
sustained diuretic
ICP >20mm
Hg can Achieve haemodynamic stability
injure the - Check for long bone fractures
brain - FAST for bleeding into abdominal cavity
- ABG to detect acidosis
- Keep monitoring patient and re-investigate where appropriate
Operate if reversible cause found

- Craniectomy (i.e. bone flap not replaced) or craniotomy (bone flap replaced after blood evacuated) [Burr
hole usually not big enough to drain an acute bleed]
- Evacuate clot
- Insert endo-ventricular drain (EVD) if there is hydrocephalus
Total sedation after operation, ward in ICU

- Prevents patient from struggling which will raise ICP
Depressed - Can leave alone unless depression is greater than the thickness of the skull bone
skull # - Seizure prophylaxis
34
Compound - There is through-and-through skin laceration over the fracture

depressed - Always explore to ensure underlying dura is intact, and repair if dura is torn (since meningitis can occur with a
fracture torn dura)
EXTRA INFORMATION
Relative Indications for Surgical Evacuation

- Neurologic symptoms 20 mass lesion, midline shift > 5-10mm
- Elevated ICP refractory to medical management
▪ Transtentorial (Uncal) herniation – temporal lesion push uncus medially compressing midbrain, occurs when there is
rapidly expanding lesion in the supratentorial parenchyma (i.e. intracranial haemorrhage)
- CN 3 compression: fixed and dilated pupil (down & out eye), ptosis
- Posterior Cerebral Artery (PCA) occlusion leading to occipital infarct
- Brainstem: respiratory paralysis and death
▪ Subfalcine (Cingulate) herniation – push cingulate gyrus under falx cerebri, usually caused by SOL
- Anterior Cerebral Artery (ACA) occlusion leading to medial frontal and parietal infarct
▪ Tonsillar herniation – through foramen magnum, affect brainstem
Cerebral Aneurysm & Arteriovenous Malformation
Cerebral Aneurysm – 85% arise from anterior circulation (carotid) and 15% from posterior circulation (vertebrobasilar) – treatment:
craniotomy with microsurgical dissection and clipping of aneurysm neck OR endovascular coiling – post-procedure, potential
complications (1) vasospasm – monitor GCS, monitor with TCDs, prevention with nimodipine (i.e. 60mg q4h x 21days) and induced
HTN, (2) seizures – prevention with Keppra, (3) increased ICP – monitor with ICP monitors / cerebral pulse oximeter, treatment is
either medical (i.e. mannitol / 3% saline) or surgical
Arteriovenous Malformations – treatment: microsurgical excision, endovascular embolization or stereotactic radiosurgery (delay
definitive therapy 3-4weeks post-haemorrhage
35
NECK & FACIAL TRAUMA
NECK TRAUMA
- Penetrating neck trauma (i.e. deep to platysma) – risk of vascular injuries, tracheal injuries and oesophageal injuries. Rarely
thoracic duct injury can occur (injury to zone 1 or 2 on left side)
- Blunt trauma to the neck – evaluate integrity of cervical spine
- Investigation of choice – CT angiography
- Historically, the management of asymptomatic patients was dependent on the zone of injury. Zone 2 underwent mandatory
surgical exploration while zone 1 and 3 were evaluated more selectively (zone 1 & 3 had difficult access and exposure with
vascular control being challenging) – currently indication for mandatory exploration is based on symptoms (no more mandatory
exploration for zone 2 injuries)
Associated Injuries
Symptoms
Vascular Active haemorrhage, expanding hematoma, vascular bruit & pulse deficit
Asymptomatic and may result in leakage of saliva, subcutaneous emphysema, bleeding from the oesophageal
Oesophageal
inlet, and ultimately neck or mediastinal abscess
Airway Subcutaneous emphysema, hoarseness, stridor, and respiratory distress
Nerve Cranial nerve deficits or hemiparesis
Zones of the Neck

Anatomical
Assessment (Asymptomatic) Assessment (Symptomatic*) Structures at risk
Boundaries
Proximal Common Carotid Arteries
Vertebral and Subclavian Arteries
CT Angio neck and thorax Surgical exploration
From clavicles Trachea
(assess vascular injuries)
Zone 1 to cricoid Recurrent Laryngeal Nerve & Vagus
Barium Swallow or OGD Consider angiography KIV
cartilage Nerve
(work-up within 24 hours) angioembolization for vascular injury
Oesophagus
Thoracic Duct
Carotid Arteries
Jugular and vertebral veins,
From cricoid
Either mandatory exploration pharynx, and larynx
cartilage to Urgent surgical exploration is
Zone 2 or directed evaluation and Proximal trachea
angle of the indicated
serial examinations Recurrent Laryngeal Nerve & Vagus
mandible
Nerve
Spinal Cord
Limited operative accessibility (may
Extracranial carotid and vertebral arteries
From angle of require craniotomy +/-
Jugular Veins
the mandible to CT Angio Brain & neck mandibulotomy)
Zone 3 Spinal Cord
the base of (assess vascular injuries)
Cranial Nerves 9 – 12
skull Consider angiography KIV
Sympathetic Trunk
angioembolization for vascular injury
* Symptomatic (hard signs): expanding hematoma, pulsating bleeding, airway compromise, wound bubbling, subcutaneous emphysema, stridor,
hoarseness, overt evidence of aerodigestive injuries, difficulty or pain when swallowing secretion, neurological deficit s
36
EXTRA INFORMATION
Tripod Fractures / Zygomaticomaxillary complex / Malar Fractures

- Sustained with direct blunt trauma to zygomatic buttress of the face
- 4 stability point of the zygoma
▪ Temporal bone at the zygomatic arch
▪ Frontal bone at the frontozygomatic suture
▪ Maxilla at the medial inferior orbital rim
▪ Zygomaticomaxillary buttress
Common Physical Findings: numbness / paresthesia (CN V), depression of the zygomatic eminence, ocular dystopia, lateral canthal
ptosis, enophthalmos, palpable fractures at the inferior and lateral orbital rims
LeFort-type fractures of the mid-face

- Le Fort I – transverse fracture through the maxilla above the roots of the teeth
- Le Fort II – pyramid shaped fracture through the nasal bridge, lacrimal bones, orbital floor and rim and maxilla
- Le Fort III (craniofacial dissociation) – fracture through bridge of nose, extend posteriorly along medial wall, floor, then lateral
orbital wall and then the zygomatic arch + intranasally fracture extend through to the base of the sphenoid
Classical signs in midface #: subconjunctival haemorrhage, malocclusion, mid-face numbness, facial ecchymosis / hematoma,
ocular signs/symptoms and mobility of maxillary complex
Orbital Floor Blowout Fractures

- Due to transient increase in intra-orbital pressure with subsequent blowout fracture of the floor
- Complications – (1) entrapment of inferior rectus muscle leading to double vision with eye movement, (2) disruption of
infraorbital branch V2 leading to anterior cheek and maxillary tooth numbness
37
BURNS
DEFINITION
Burns are skin damage caused by pathological excess of energy within tissue. This can be caused by thermal, chemical, electrical,
radiation energy. The extent of injury is determined by the nature of agent, length of exposure, body part involved and depth of the
burn.
Burns assessment depends on location of burns, depth of burn and extent of burns. Also patients must be assessed for presence of
inhalation injury which is a major cause of death.
Inhalational Injury
- History: mechanism (i.e. exposure to flame, smoke, chemicals), timing, duration of exposure, location where burns occurred
(i.e. enclose area), any hoarseness of voice, any loss of consciousness
- Examination: soot in the mouth / nose, perioral burns, singed nasal hairs, facial burns, wheezing, carbonaceous sputum
▪ Supra-glottic injury – hoarseness, pharyngeal erythema, oedema, dyspnoea
▪ Infra-glottic – AMS secondary to hypoxia
- Nasopharyngoscopy Assessment
▪ Can evaluate extent of inhalation injury, presence of laryngeal edema
EXTRA INFORMATION
Carbon Monoxide Poisoning

Suspect CO poisoning if a/w unexpected neurological symptoms (i.e. headache, confusion, coma), SOB, chest pain. Blood CO
measurement > 9-10%. Carbon monoxide binds to haemoglobin with much higher affinity than oxygen. This prevents oxygen
binding to haemoglobin, carboxyhemoglobin increases. This also reduces oxygen unloading from haemoglobin in the tissues
which causes a leftward shift of the Hb-oxygen dissociation curve. Treatment with 100% O2 therapy – reduce ½ life from 250 min
in room-air to 40-60min with 100% FiO2 (the affinity of CO for Hb is 200 – 250 times more than that of oxygen).
Cyanide Poisoning
Suspect Cyanide poisoning if a/w persistent lactic acidosis (> 10mmol/L) or ST elevation. Requires a high degree of suspicion
(burns exposure with combustion of nitrogen containing polymers such as silk, wool, paper, nylon PVC). Treatment with sodium
nitrate, sodium thiosulphate and hydroxocobalamin. (see video)
Other Types of Burn Injuries

- Electrical – need cardiac monitoring and test renal function
▪ Risk of cardiac arrhythmias, compartment syndrome with concurrent rhabdomyolysis, myonecrosis induced AKI – cardiac
monitoring
▪ Maintain urine o/p 75-100ml/hr to minimize myoglobin precipitation
- Chemical Burns – removal of toxic substance and copious irrigation with water (≥ 30mins)
▪ Hydrofluoric Acid – topical calcium gluconate on wound + IV calcium gluconate (risk of hypocalcaemia as fluoride ion binds
calcium)
▪ Alkali – penetrates deeply secondary to liquefactive necrosis (more severe burn)
▪ Acid – coagulative necrosis limits depth
- Powder Burns (i.e. concrete powder) – wipe away before irrigation (avoid activating the aluminium hydroxide with water)
- Lighting Burns – cardiopulmonary arrest secondary to electrical paralysis of brainstem
38
CLASSIFICATION OF BURNS
3 main components: location of burns, depth of burns and extent of burns
Location of Burns
- Limbs (may affect long-term function)
- Special Area → face, hands, feet, genitalia/perineum
- Circumferential burns wounds (may lead to neurovascular compromise)
Depth Description Prognosis

1st (epidermis) – painful, erythema that blanches Symptoms subside over 2-3 days, epithelium peels at
(superficial) with pressure, no blisters day 4.
Superficial (spares skin appendages) – Heal within 2- 3 weeks via stem cells from skin
painful, erythematous and moist, blanchess appendages without hypertrophic scarring. May have
2nd
with pressure, blistering, intact sensation pigmentation problems
(partial thickness)
Deep (loss of skin appendages) – blistering, Heals in 3-9 weeks, hypertrophic scarring common
decreased sensation, no cap refill, treated with excision and skin grafting, joint contractures
(entire dermis and adnexal structures) – If nil intervention – demarcate and separate over days to
3rd
blistering absent, insensate, leathery weeks, circumferential burn can lead to compartment
(full thickness)
consistency, thrombosed vessels can be seen syndrome, likely require skin grafting
4th
Down to bone, into adjacent muscle tissue,
(underlying soft- Can lead to myoglobinuria, renal failure
tendon
tissue involved)
Extent Description
head 9%, back 18%, chest 18%, arm 18% legs 36% perineum 1%
Adults
[Patient’s palm to estimate injury (palm = 1%)]
Children
(child) – head 18%, back 18%, chest 18%, arms 18% legs 28%
(age < 3yrs)
* Superficial (first-degree) burns not included in calculation
Minor: ≤15% TBSA, Moderate: 15-25% TBSA, Severe: ≥25% TBSA
39
BURNS MANAGEMENT
Initial Evaluation
- Initial evaluation is based on ATLS principles
- Consider early intubation for patients with history of being trapped in enclosed space (> 10mins), present
Airway &
1 unconscious, presence of facial burns, singed nasal hair, carbonaceous sputum, soot in mouth and with
Breathing
signs of respiratory distress
- Administer supplemental oxygen, ensuring saturation > 90%
- IV access with large bore cannulas for fluid resuscitation
- Parkland Formula (used for burns ≥ 20%): 4ml x weight (kg) x %TBSA burn in 24 hours
▪ Lactated Ringer’s in first 24 hours
▪ Fluid resuscitation beings at the time of injury (½ in 1st 8hr and ½ in next 16hrs)
▪ Target Urine Output – 0.5ml/kg/hr in adults, 1 ml/kg/hr in children, 1.5ml/kg/hr for electrical injuries
2 Circulation - In ATLS 2018, suggested fluid regimen is 2ml/kg/%TBSA in adult patients with burns, 3ml/kg/%TBSA in
paediatric burn patients and 4ml/kg/%TBSA in patients with electrical burns
- There exists many other adult burns resuscitation formulas. Ultimately, the goal is for fluid resuscitation
to preserve organ perfusion and preserve urine output.
-
- For patients with < 15-20% TBSA without inhalational injury, burns are usually not enough to initiate the
SIRS, patients can be rehydrated via oral route with IV fluid supplementation.
- Initial Investigations: ABG, CXR, Assessment of Carboxyhemoglobin Levels
Initial
3 - Biochemical Investigations: FBC, Renal Panel, PT/INR/APTT, GXM
Investigations
- Serum lactate levels during the first 48 hours is an independent factor for mortality after major burns
- No prophylactic antibiotics – (promote development of fungal infection and resistant organism)
- Analgesia (i.e. IV morphine)
- Tetanus vaccination (IM ATT)
- Insertion of Urinary Catheter
- Stress ulcer prophylaxis (i.e. IV PPI)
- Transfusion as needed
4 Adjuncts
- Administer Anxiolytics (i.e. BZD) as required
- Nutrition – early enteral feeding for patients with burns > 20% TBSA
▪ Curreri Formula: 25kcal/kg/day + 40kcal/%TBSA/day
▪ 1.5-2g/kg/day of protein with additional glutamine supplementation
▪ Avoidance of Hyperglycaemia – OHGA +/- intensive insulin therapy
- Topical Treatment – silver sulfadiazine, silver nitrate, mafenide acetate
- Indication for transfer to burn centre:
▪ For patients < 10 or > 50, partial thickness burns > 10% TBSA
▪ For adult patients, partial thickness burns >15- 20% TBSA
Transfer to
5 ▪ Burns in special area(i.e. face, hands, feets, genitalia, perineum, major joints)
Burns Centre
▪ Electrical burns (i.e. lightning injury), Chemical Burns
▪ Presence of inhalational injury
▪ Patients who require surgery
Surgical - Surgical Intervention (Escharotomies ± Split-Thickness Skin Graft) – for constricting, circumferential deep
6
Intervention burns (compartment syndrome)
40
COMPLICATIONS IN BURNS
- Respiratory – pneumonia (due to impaired mucociliary transport and bacterial clearance), ARDS, pulmonary oedema
- Renal Failure – ATN 20 to hypo-perfusion, circulating myoglobin producing rhabdomyolysis
- Catheter-related bloodstream infection (SIRS → multi-organ failure)
- Wound Infection (> 105 organism) – Pseudomonas, Staph, E.coli and Enterobacter (HSV – most common viral infection in burn
wounds)
- Gastric ulceration (curling ulcer)
- Eyes – corneal abrasion, ectopia (contraction of burned adnexa), symblepharon (eyelid stuck to conjunctiva)
- Hypothermia
- Electrolyte disturbances – can result in seizures
- DVT / PE – give routine prophylaxis
- Hypertrophic burn scars – secondary to increased neovascularity
- Abdominal compartment syndrome – increased airway pressure with hypoventilation, decreased urine output and hemodynamic
compromise (secondary to massive resuscitation)
- Marjolin’s ulcer – chronic non-healing burn wound
EXTRA INFORMATION
Burn Wound Infection

- Silver Sulfadiazine (Silvadene) can cause neutropenia & thrombocytopenia (limited eschar penetration)
▪ Ineffective against some pseudomonas, effective for candida
- Silver Nitrate can cause electrolyte imbalances (i.e. hypoNa+, hypoCl-, hypoCa2+, hypoK+) & rarely methemoglobinemia*
(limited eschar penetration)
▪ Ineffective against some pseudomonas species and GPC
▪ Can cause discolouration
- Mafenide Sodium (Sulfamylon) can cause metabolic acidosis (due to carbonic anhydrase inhibition)
▪ Painful application
▪ Good eschar penetration; good for burns overlying cartilage
▪ Broad spectrum against pseudomonas and GNRs
* Contraindicated in G6PD patients. Treatment = increase supplemental oxygenation and administration of methylene blue
PROGNOSIS
- Major predictor of mortality = age + TBSA + inhalational injury [BAUX score]8
▪ 50% mortality if age + %TBSA = 110 or
▪ 50% mortality if inhalation injury + age + %TBSA = 100
- Other factors – coexisting trauma, pneumonia
8 National Burn Repository 2011 report, American Burn Association
41
2. SURGICAL CRITICAL CARE

ACID-BASE & ELECTROLYTES
Organ system involved in regulating acid-base balance – (1) respiratory system, control of pCO2 through alteration in alveolar
ventilation, (2) Kidney, control of [HCO3-] for long-term control, (3) Blood, through buffering by plasma proteins and Hb, (4) Bone, H+
may exchange with cations from bone mineral, (5) Liver, may generate HCO3- and NH4- (ammonia) by glutamine metabolism.
Carbon Dioxide Transportation – 3 ways

- Bicarbonate ion (HCO3-) – 85-90%
▪ Carbonic acid-bicarbonate system [Dissolved CO2 + H2O ↔ H2CO3 ↔ HCO3- + H+]
▪ Catalysed by carbonic anhydrase
▪ H+ generated binds with haemoglobin molecule
▪ HCO3- generated diffuse out of the red cell (able to penetrate red cell membrane unlike H +) and to maintain electrical
neutrality chloride (Cl-) enters [chloride shift]
- Carb-amino compound – 5-10%
▪ CO2 binds with terminal amine groups of plasma protein (i.e. haemoglobin)
▪ The addition of CO2 and H+ reduced oxygen affinity [right shift in oxygen dissociation curve] hence , more O 2 released to
the tissue where it is needed
- Dissolved in solution – 5%
▪ CO2 is 24x more water soluble than oxygen (1% of oxygen is dissolved in plasma)
▪ CO2 never reaches saturation point, hence blood saturation is not expressed as a % of a total level
Normal ABG results

- pH: 7.38-7.42 (7.40)
- PaCO2: 35-44 mmHg (40mmHg)
- PaO2: 75-100mmHg
- HCO3–: 22-26 mmol/L (24mmHg)
- Base Deficit/Excess*: -2 to +2 mmol/L
*amount of acid / alkali required to restore 1L of blood to normal pH at pCO 2 of 40mmHg and at 37deg.
Approach to ABG interpretations

1. What is the pH?
2. Is the primary disorder respiratory or metabolic
3. Calculate the Serum Anion Gap
4. Identify the compensatory process (if one is present)
5. Identify if this is a mixed picture (in the assessment of HAGMA use delta ratio to determine if a mixed picture is present)
pH & Primary Disorder

Expected change occurs in the same direction in 1 o metabolic disorder and in the opposite direction in 1 o respiratory disorders
If pH is normal, check for balanced acid base disorder:

[HCO3] < 20 PCO2 < 35 Metabolic acidosis + Respiratory alkalosis
[HCO3] > 24 PCO2 > 45 Metabolic alkalosis + Respiratory acidosis
[HCO3] & PCO2 normal AG > 11 HAGMA + metabolic alkalosis
[HCO3] & PCO2 normal AG normal Normal (unlikely NAGMA + metabolic alkalosis)
Serum Anion gap = (Na+) – (Cl- + HCO3-)

- Normal = 3-11 mmol/L
- Hypoalbuminemia: anion gap decrease in 2.5 mmol/L for every decrease in 10g/L of serum [albumin]
- Elevated anion gap = HAGMA even in the presence of a normal pH / [HCO3]
Compensatory Process
- The body does not fully compensate the primary acid-base disorder
- Pace of compensation varies depending on whether it is respiratory or metabolic compensation
Henderson-Hasselbalch Equation: pH = 6.1 + log10 [(HCO3–) / (0.03 x PaCO2)]

(This also implies: pH = constant + (kidney function / lung function)
42
2. Surgical Critical Care_Last Updated 3 rd June 2020
↓ [HCO3] 1 mmol/L = ↓ PCO2 1.2 mmHg
Expected PCO2 = (1.5 x [HCO3]) + 8 ±2 mmHg [Winters Formula]

▪ PCO2 < expected (concurrent respiratory alkalosis)
▪ PCO2 > expected (concurrent respiratory acidosis)
Metabolic Acidosis 𝐴𝐺 𝐴𝐺 − 12
Delta ratio = = 24 − 𝐻𝐶𝑂3−
𝐻𝐶𝑂3−
< 0.4: hyperchloremic NAGMA

0.4-0.8: combined HAGMA and NAGMA
1.0-2.0: pure HAGMA (lactic acidosis ~1.6, DKA ratio ~1.0 due to urine ketone loss)
> 2.0: concurrent metabolic alkalosis
↑ [HCO3] 1 mmol/L = ↑PCO2 0.7 mmHg
Metabolic Alkalosis Expected PCO2 = (0.7 x [HCO3]) + 21 mmHg

▪ PCO2 < expected (concurrent respiratory alkalosis)
▪ PCO2 > expected (concurrent respiratory acidosis)
Acute: ↑PCO2 10 mmHg = ↑[HCO3] 1 mmol/L [pH expected to fall by 0.08]
Respiratory Acidosis
Chronic: ↑ PCO2 10 mmHg = ↑ [HCO3] 4 mmol/L
Acute: ↓ PCO2 10 mmHg = ↓ [HCO3] 2 mmol/L

Respiratory Alkalosis
Chronic: ↓ PCO2 10mmHg = ↓ [HCO3] 5 mmol/L
Underlying Aetiology
Respiratory Acidosis (respiratory depression) Respiratory Alkalosis (hyperventilation)
- CNS depression – head injury, drugs (i.e. opiates), coma, CVA, - Stimulation of respiratory centre – high altitude, pneumonia,
encephalitis pulmonary embolism, pulmonary oedema, fever, head injury
- NM disorders – MG, GBS - Increased alveolar gas exchange – hyperventilation (i.e. hysteria,
- Skeletal Disease – AS, flail chest, kyphoscoliosis pain, anxiety), artificial ventilation
- Artificial Ventilation
- Impaired Gaseous Exchange – pneumonia, ARDS, obstructive
airway disease, pulmonary contusions
Metabolic Acidosis (see below) Metabolic Alkalosis

- Excessive production of H+ – DKA, lactic acidosis*, ingestion of Excess loss of H+ – vomiting, NG aspirate, gastric fistula, diuretic
-
toxins, septicaemia, starvation therapy**
- Impaired excretion of H+ – acute / chronic RF - Excess Intake of base – antacids (i.e. milk-alkali syndrome)
- Excess loss of base – diarrhoea, intestinal, biliary, pancreatic - Volume Contraction (vomiting, over-diuresis, ascites) – contraction
fistula, renal tubular acidosis, alkalosis***
- Cushing’s syndrome, Conn’s syndrome
- Usually either GI losses or diuretic therapy
* Lactic Acidosis: in surgical patients with lactic acidosis, lactate is produced in presence of hypoxia from inadequate tissue perfusion, tre atment,
therefore, is to restore perfusion with volume resuscitation rather than exogenous bicarbonate
** Loop Diuretics & Metabolic Alkalosis: In surgical patients, post-operative patients experience hyperaldosteronism (stress-induced stimulation of the
RAAS). With loop diuretics, increased Na delivery to the distal tubule (together with hyperaldosteronism) leads to exchange for K+ and H+. H+ is
preferentially secreted leading to metabolic alkalosis.
*** Contraction alkalosis: loss of free water around a fixed quantity of bicarbonate leads to its increased concentration (usually due to oedematou s
patients treated with diuretic therapy)
High Anion Gap Metabolic Acidosis (HAGMA) – MUDPILERS Normal Anion Gap Metabolic Acidosis (NAGMA) – HARDUP
- Methanol - Hyperchloremic Acidosis – rapid administration of 0.9% NaCl
- Uremia - Acetazolamide (Carbonic Anhydrase Inhibitors) / Addison’s Disease
- DKA - Renal Tubular Acidosis
- Propylene Glycol / Paraldehyde / Paracetamol - Diarrhoea, vomiting, ileostomies, fistulas
- Iron / Isoniazid - Ureteroenterostomy
- Lactic Acidosis (Sepsis, Ischemia, Short Gut, Propofol) - Pancreatic Enterostomies (pancreatic fistula)
- Ethylene Glycol
- Rhabdomyolysis / Renal Failure Usually either GI losses or renal losses – urine pH is high if renal
- Salicylates causes and low if GI causes
43
ACUTE RESPIRATORY DISTRESS SYNDROME
DEFINITION
Syndrome of acute respiratory failure with formation of non-cardiogenic pulmonary oedema leading to reduced lung compliance and
hypoxemia which is refractory to oxygen therapy
RISK FACTORS
- Direct Pulmonary Insults: aspiration, pneumonia, smoke inhalation, fat embolism, burns, severe trauma – i.e. bilateral lung
contusion, blast injury
- Indirect Pulmonary Insult: sepsis, polytrauma, fat embolism, massive transfusion, DIC, acute pancreatitis, cardiopulmonary
bypass, burns
PATHOGENESIS9
- Inflammatory / Exudative Stage [injury, inflammation, oedema]
▪ Characterized by diffuse alveolar damage, Alveoli lined by waxy hyaline membrane
- Proliferative Stage (7-10days) [organization and repair]
▪ Proliferation of type II alveolar cells, resolution of pulmonary oedema, increase in local fibroblast population
- Fibrotic Stage [healing, repair with fibrosis, recovery ± pulmonary hypertension]
▪ Obliteration of normal lung architecture, diffuse fibrosis and cyst formation
DIAGNOSTIC CRITERIA (BERLIN CLASSIFICATION)

- Acute (onset) – within 7 days of a known clinical insult
- Respiratory failure not fully explained by cardiac failure or fluid overload
- Diagnostic Imaging – bilateral opacities present on CXR / CT
- Severity (PaO2 / FiO2) – mild ARDS (200-300), moderate ARDS (100-200), severe (<100) with a PEEP of 5 cmH2O
Pathological Effects
- Ventilation / Perfusion (V/Q) Mismatch
- Alteration in function of surfactant
- Increased Pulmonary Vascular Resistance (PVR)
- Decreased compliance
- Decreased Functional Residual Capacity (FRC)
MANAGEMENT
Aim to achieve appropriate arterial oxygen tension & adequate perfusion of vital organs
- Management of initial predisposing insult
- Supportive Care – i.e. nutritional support (i.e. enteral feeding), use of sedative / NMB, DVT prophylaxis, Stress ulcer Prophylaxis,
optimize BSL control
- Strict control of fluid resuscitation to prevent worsening of pulmonary oedema
- Management of Hypoxia
▪ Supplemental Oxygenation – mechanical ventilation (see below) or CPAP
▪ If mechanical ventilation continues > 7 days, consider tracheostomy
9 Surgical Critical Care Vivas (Mazyar Kanani) – Pg. 30
44
- Mechanical Ventilation
▪ Use high FiO2
▪ Low tidal volume / lung protective ventilation (4-8ml/kg ideal body weight), less likely to generate alveolar overdistension,
hence ↓ventilator associated barotrauma, however usually lead to permissive hypercarbia, improve survival
▪ High positive end-expiratory pressure (PEEP) – 10-20cm H2O, leads to expansion of partially collapsed alveoli & recruitment
(re-expansion) of collapsed alveoli – improves oxygenation
▪ Inverse ratio ventilation, length of inspiratory phase increased
▪ Prone ventilation
EXTRA INFORMATION
Ventilation Settings
- Tidal Volume = volume of air in each breath (8-12 cm3 /kg)
- Rate = Number of breaths delivered per min
- FiO2 = Amount of O2 delivered (N = 40%; the higher it is, the more O2 damage to the lungs)
- PEEP = positive end-expiratory pressure (opens alveoli that would otherwise collapse in expiration)
▪ Normal: 3 – 5 cmH2O (physiologic PEEP)
▪ Therapeutic PEEP can go up to 10 – 35 cmH2O (but too high impedes venous return to the heart)
* decrease pCO2 – ↑minute ventilation
** increase pO2 – ↑PEEP, ↑FiO2
Physiological effects of increased PEEP

- Respiratory: ↑Functional Residual Capacity^ (FRC), ↓intrapulmonary shunting, improved compliance
- Cardiovascular: ↓ venous return (sec to ↑ intrathoracic pressure), ventricular dysfunction (sec to ↑ pulmonary vascular
resistance causing ↑ RV afterload)
- Renal: ↓ urine output (sec to ↓ renal perfusion), water retention, sodium retention [renal dysfx & electrolyte imbalance]
- Neurological: ↑ intracranial pressure
Functional Residual Capacity (FRC)

FRC: lung volume at the end of normal exhalation, where the inward elastic recoil of the lung approximates the outward elastic
recoil of the chest. FRC is also the point where PVR is at its lowest.
45
DISSEMINATED INTRAVASCULAR COAGULATION (DIC)
DEFINITION
Systemic processing producing both thrombosis and haemorrhage (widespread activation of clotting leads to deficiency of clotting
factors resulting in bleeding)
RISK FACTOR (“STOP Making New Thrombi”)

- Sepsis (gram negative) – by releasing endotoxins
- Trauma
- Obstetrics Complications – i.e. abruption placenta, amniotic fluid embolism
- Pancreatitis (acute)
- Acute Myeloid Leukaemia: AML-M3 (promyelocytic leukemia)
- Malignancy
- Nephrotic Syndrome
- Transfusion
- Others – liver failure, vascular abnormalities (i.e. large aortic aneurysm), snake bites, transplant rejection, burns
PATHOPHYSIOLOGY
- Massive intravascular activation of coagulation (i.e. thrombin) that overwhelms control mechanisms thrombosis in
microvasculature
▪ Fibrin deposition in microcirculation
o Secondary fibrinolysis (due to release of tPA): ↑FDP and bleeding
o Intravascular fibrin strands cause mechanical shearing of RBC leads to MAHA
o Ischemic organ damage (due to thrombotic manifestations)
▪ Acute consumption of coagulation factors and platelets worsens bleeding
- Leads to multiple organ failures
46
INVESTIGATION AND DIAGNOSTIC CRITERIA

- ↓Platelets, ↑FDP/D-dimer, ↑PT/↑PTT, ↓fibrinogen* (consumed)
- ↑LDH, ↓factors V and VIII, ↓haptoglobin, (+) schistocytes (intravascular haemolysis), microangiopathic haemolytic anaemia
(seen on PBF)
- ISTH Diagnostic Scoring system10 – Does patient have an underlying disorder known to be a/w DIVC, if yes proceed to scoring
▪ Platelet count – > 100 x 109/L (0), < 100 x 109/L (1), < 50 x 109/L (2),
▪ FDP (i.e. D-dimer, fibrin degradation product) – no increase (0), moderate increase (2), strong increase (3)
▪ Prolonged PT – <3sec (0), > 3sec (1), >6sec (2)
▪ Fibrinogen Level – >1.0g/L (0), < 1.0g/L (1)
- If score ≥ 5, suggest overt DIVC, repeat score daily
* Fibrinogen is also an acute phase reactant, hence, will be elevated due to underlying inflammatory conditions. Therefore, a normal (57%) / (elevated)
level can occur, although, a low fibrinogen level is more consistent with the consumptive process of DIVC
MANAGEMENT
- Treat underlying process
- Plasma & Platelets – FFP (active bleeding, high risk of bleeding), fibrinogen concentrate / cryoprecipitate** (aim: fibrinogen >
100mg/dL)
- Anticoagulants – LMWH (for non-bleeding patients, prophylaxis for venous thrombosis), ± Continuous infusion of UFH
(thrombosis predominates, yet high risk of bleeding)
- Anticoagulant factor concentrates – recombinant human activated protein C
- Anti-fibrinolytic therapy (i.e. ε-Aminocaproic acid, Tranexamic Acid) – Not recommended
** Cryoprecipitate – contains fibrinogen, factor 8, factor 13 & vWF
10 Br J Haematol. 2009 Apr;145(1):24-33 [Important Paper]
47
FLUIDS & ELECTROLYTES
Goals of Fluid management

The aim of fluid management is the avoidance of shock or inadequate end-organ perfusion as poor perfusion may lead to hypoxia
and irreversible end-organ damage
Body composition11
- Total body water (TBW) = 60% body weight in adult males*
▪ Intracellular Fluid = 2/3 of TBW → largest proportion in skeletal muscle mass
▪ Extracellular Fluid = 1/3 of TBW (or about 20% of body weight)
- Interstitial Space = 3/4 of ECF
- Intravascular Volume = 1/4 of ECF (of TBW or 5% of body weight)
- 3rd Space (potential space) = pathological expansion of the interstitial space via a capillary leak in response to injury and illness.
The shift of fluid between the intravascular space and the 3 rd space is important in the evaluation of surgical patients
*approx. 50% in adult females, 80% in infants which decrease to 65% by 1 year of age – estimate should be adjusted downward by
10% for obese individuals and upwards by 10% in malnourished individuals
Intravascular Volume Control

- Osmoreceptors (located in hypothalamus)
▪ Detect changes in fluid osmolality and drive changes through thirst and diuresis through the kidney (i.e. ADH secretion)
- Baroreceptors (sensory receptors, located in aortic arch and carotid sinuses)
▪ Modulate volume in response to changes in pressure and circulating volume
▪ Activity inhibits the vasomotor centre (VMC) in medulla (i.e. fall in BP leads to vasoconstriction)
Principles of Fluid Management

Fluids required are based on 3 factors, patient’s maintenance requirement (4-2-1 or 100-50-20 principle), patient’s fluid deficit prior to
institution of fluids (usually an estimation), and anticipated fluid losses (requires strict input/output charting).
Maintenance Fluid Requirement Prior Fluid Deficit On-going/ anticipated losses

Holliday-Segar nomogram: Estimated Deficits Blood: trauma / surgery / BGIT
1st 10 kg – 100 ml/kg/day (4ml/kg/hr) Based on history and PE
2nd 10 kg – 50 ml/kg/day (2ml/kg/hr) (weight x % dehydration = __/L) Gastrointestinal: NG aspirates, vomiting,
> 20 kg – 20 ml/kg/day (1ml/kg/hr) fistula, stoma, surgical drains*, diarrhoea,
Mild (thirsty) ~ 3% intraluminal (i.e. IO, paralytic ileus)
↑10% fluids for every 1°C above 37°C Mod (tachycardia) ~ 6%
Severe (hypotensive) ~ 9% 3rd space: inflammation (i.e. acute
pancreatitis, peritonitis, septicaemia),
↑fluids: burns, sweating, tachypnoea More relevant in paediatric population SJS/TENs, burns
↓fluids: oliguric RF, oedematous states,
hypothyroidism, SIADH
Daily Gastrointestinal Absorption & Secretions12

Absorbed Secreted / Ingested Na K Cl HCO3
1.5L saliva secreted
Mouth / Saliva Nothing 10 20-30 15 50
+/- 2-3L fluid ingested
Lipid-soluble compounds,
Stomach 1-2L secreted 60-90 10-30 100-130 0
i.e. alcohol
Biliary / Absorbs water and
300-800ml secreted 135-145 5-10 90-110 30-40
Gallbladder concentrate bile
Pancreas Nothing 600-800ml secreted 135-145 5-10 70-90 95-115
Small Bowel 8 - 9L fluid absorbed 2 - 3L secreted 120-140 5-10 90-120 30-40
Large Bowel 1L of fluid absorbed 100ml excreted 60 30 40 0
* GI losses should be replaced ml for ml
Parenteral Solutions
Components of regularly used IV fluids

D/S Lactated Pre-Mix
0.9% N/S ½ D/S 3% N/S Gelatin
(D5 NS) Ringers (KCL in 5%
11 Greenfield’s Surgery Scientific Principles and Practice 5th Edition (pg190)

12 Schwartzs Principle of Surgery 10th Edition (pg: 69)
48
dextrose and
0.33 NaCL)
Na+ 154mEq/L 154mEq/L 77mEq/L 130mEq/L 56mEq/L 513mEq/L 154mEq/L
Cl- 154mEq/L 154mEq/L 77mEq/L 109mEq/L 76mEq/L 513mEq/L 120mEq/L
K+ 4mEq/L 20mEq/L
Ca2+ 2.7mEq/L
50g/L 25g/L Lactate 50g/L
Others 40g/L gelatin
dextrose dextrose 28meq/L dextrose
Crystalloids
- 0.9% N/S – infusion of large volumes can lead to total body sodium overload and hyperchloremia
which can result in hyperchloremic metabolic acidosis
▪ Following correction of fluid deficit, less concentrated saline is more appropriate to replace
on-going fluid losses
Normal Saline*
- 0.45%/0.33%/0.2% N/S – Fluids are hypoosmotic and hypotonic, rapid infusion can result in RBC
lysis, hence, 5% dextrose is usually added to increase tonicity
- 3% N/S – hypertonic saline solution: for replacing sodium deficit in patients with symptomatic
hyponatremia (i.e. seizures) or to decrease ICP (monitor Na level)
- Used to replace fluid with the ionic composition of plasma (i.e. GI losses) – physiological fluid
Lactated Ringer
- Used for fluid resuscitation and/or replacement of existing fluid deficit
(Hartmann’s solution)
- Risk of hyponatremia with extended use and in patients with impaired renal function
Sterofundin
- Glucose is rapidly metabolized by the liver and remaining water will distribute itself across all
5% Dextrose (D5W) components with little fluid remaining within blood space. Hence, not for fluid resuscitation!!
- Excess 5% dextrose water have risk of hyponatremia
*0.9% N/S (isotonic) – does not remain within the intravascular space but will diffuse into the interstitial space (throughout ECF) but
the sodium it carriers will not enter the ICF due to active sodium extrusion from the cells hence, this leads to immediate expansion of
intravascular volume. In contrast, for D5W, once glucose is metabolized, remaining water would initially dilute ECF relative to ICF and
water would be equally distributed throughout the body, as such, do not use D5W for fluid resuscitation!
Colloids
Hetastarch - Benefit of promoting retention of fluids in the intravascular space
(HES)
- Fallen out of favour, HES use in septic patients a/w ↑risk of bleeding complications, AKI, mortality
Dextran
- Increase plasma oncotic pressure which retards movement of water into interstitial space (oedema)
▪ Albumin 5% solution = 50mg/ml (given in 250 or 500ml)
▪ Albumin 20% solution = 200mg/ml (given in 100ml)
- Can be used as a volume expanding resuscitation fluid (after bolus of crystalloid fluids) – i.e. 250mls of
Albumin 5% albumin
- There is a 1:3 ratio of albumin to crystalloid to achieve the same intravascular volume expansion
- Hence, can be used for patients at risk for fluid overload (i.e. heart failure, ESRF)
- Albumin showed to induce renal failure and impair pulmonary function when used for resuscitation in
hemorrhagic shock13
Succinylated gelatin – i.e. gelofusine
Gelatin Urea crossed lined gelatin – i.e. haemaccel
Risks – allergic reactions, renal impairment
**Precaution with colloids – coagulopathy (dextran, gelatin, starch) can interfere with platelet adhesion and vWF, interaction with blood
transfusion (Haemaccel can cause blood to clot if infused into the same cannula), immunologic reaction, transmission of disease, risk
of worsening oedema
49
Daily Electrolytes Requirements

For a 70kg Individual / day Primary Location Normal Serum Values
Na+ 1-2 mmol/kg/day ~ 140 mmol / day Extracellular Fluid (ECF) 135-145mmol/L
K+ 0.5-1mmol/kg/day ~ 70 mmol/day Intracellular Fluid (ICF) 3.5-5.0mmol/L
(for ions with a ±1 charge: 1 mEq = 1 mmol | for ions with a ±2 charge: 1 mEq = ½ mmol)
Effects of potassium and calcium ions on heart function

HyperK+ paralyses the heart in diastole while HyperCa 2+ paralyses the heart in systole – potassium decreases the resting
membrane potential in the cardiac muscle fibre hence the intensity of the action potential also decreases resulting in weaker cardiac
contractions. Conversely, calcium ion initiates the cardiac contractile process resulting in spastic contractions
Hyperkalemia
- ECG features: tall tented T waves, prolonged PR interval, widened QRS, sine wave pattern
▪ Hemolysis of blood sample, excessive oral/IV therapy, tissue necrosis (crush injury, burns),
▪ Metabolic acidosis,
▪ Renal failure, drugs (i.e. spironolactone)
- Hyperkalemia Management
▪ PO resonium 15gm TDS
▪ IV D50%/Insulin (10 units of insulin with 50mls D50%) +/- IV calcium gluconate
Hypokalemia
- Causes
▪ NBM with inappropriate IV therapy,
▪ Drugs (i.e. diuretics such as lasix, insulin, salbutamol),
▪ Renal losses, Magnesium depletion (a/w with increased renal K excretion)
▪ GI losses (i.e. vomiting & diarrhoea)
- ECG features: increased QT interval, ST depression, T wave inversion, U waves
- Hypokalemia Management
▪ 15mls Mist KCL = 20mmol | 600mg Span K = 8 mmol
▪ IV KCL 1 cycle = 10 mmol (on average, this will increase serum K by ~0.1mmol)
▪ If IV KCL were to be given at a faster rate than 10mmol/hr (i.e. higher concentration), patients will require administration
via a central line with cardiac monitoring (HD or ICU setting)
Hypernatremia Management
- Presents with altered mental status, lethargy, seizure, coma, evidence of dehydration
- Causes – usually due to unreplaced water loss
▪ Renal losses (i.e. diuretics) or GI losses (i.e. vomiting, diarrhoea)
▪ Diabetes Insipidus (in severe brain injury) → can be central (deficient in ADH) or nephrogenic (renal resistance to ADH
- DO NOT correct sodium more than 12mmol/day as risk of cerebral edema
Hyponatremia Management
- Presents with altered mental status, nausea, lethargy, seizure, coma
- Causess
▪ Common postoperatively due to excessive fluid retention (increase ADH)
▪ Hypovolemic Hyponatremia – renal and/or GI losses
▪ Euvolemic Hyponatremia – SIADH, hypothyroidism,
▪ Hypervolemic Hyponatremia – cirrhosis, congestive heart failure, renal failure
- DO NOT correct sodium > 12mmol/day as risk of osmotic demyelination syndrome (central pontine myelinolysis)
▪ Symptomatic Patients (i.e. neurological symptoms) correct no more than 1mEq/L/hr,
▪ Asymptomatic hyponatremia correct no more than 0.5mEq/L/hr
Equations (patients with hypovolemic hyponatremia)

1. TBW = weight (kg) x correction factor (i.e. women = 0.5, males = 0.6, children = 0.6)
2. Sodium deficit = TBW x (desired serum Na – actual serum Na)
3. Δ serum Na per L infusate = [(infusate Na – serum Na) / (TBW + 1)]
Equation (patients with hypernatremia)

1. Free water deficit (in L) = TBW x [(actual serum Na / 140) – 1]
CASE SCENARIO
60yr man, 70kg, presented with 2/7 hx of vomiting and abdominal pain, Noted to have bilious vomit of ~ 1L while at ED
Vitals on arrival to ED: Temp: 37.2 BP: 90/60, HR: 120.
50
Amount of fluids to replace:

- Maintenance / day: 2.5L [(100 x 10) + (50 x 10) + (20 x 50)
- Prior Losses: subjective assessment ~ 2L
- On-going Losses: 1L
Rate of fluid administration

- Run 1-2L fast and then reassess response – can use lactated ringers
- Assessment of response based on patient vitals (BP & HR), urine output (at least 0.5ml/kg/hr) & biochemically (i.e. normalization
of lactate / base deficit)
- Will need to monitor strict I/O charting (i.e. catheterize patient for strict urine o/p, chart volume of vomitus, chart volum e of
nasogastric tubes, drains) – fluid losses needs to be replaced
Choice of IV fluids
- Check electrolytes (i.e. Renal Panel, Ca/Mg/Phos) and replace accordingly (on top of maintenance requirements)
▪ 1L 0.9% N/S = daily sodium requirement met (~150mmol/L)
▪ Divided doses of K = K requirements are met (~ 70mmol/L)
▪ D5 (Dextrose 5%) = 50g of dextrose in 1L (isotonic, 200kcal; 1g glucose = 4kcal)
- Can use a mixture of 0.9% N/S & D5 + potassium in divided doses
- Now, use Pre-Mix (i.e. 3.5L / 24 hours) which would add up to ~ 196 mmol of Na + and ~ 70 mmol of K+
EXTRA INFORMATION
Effect of Renin Aldosterone System (with hypovolemia)

- Aldosterone acts on distal convoluted tubule (i.e. principle cells) to reabsorb water by upregulating Na/K ATPase on the
membrane (Na reabsorbed and K secreted)
51
NUTRITION
Nutritional support may supplement normal feeding, or completely replace normal feeding
Benefits of nutritional support

- Preservation of nutritional status
- Prevention of complications of protein malnutrition
- Decrease postoperative complications – i.e. delayed wound healing, risk of infections
Nutritional support should be considered for:

- Patients already with malnutrition (i.e. surgery / trauma / sepsis)
- Patients at risk of malnutrition
▪ Depleted reserves
▪ Poor oral intake for > 5 days
▪ Impaired bowel function
▪ Critical illness
▪ Need for prolonged bowel rest
- Malnourished Patients
▪ BMI < 18.5
▪ Unintentional weight loss > 10% BW within last 3 – 6 months
▪ BMI < 20 and unintentional weight loss > 5% within last 3 – 6 months
▪ Poor absorptive capacity, high nutrient losses, increased catabolic rate
Clinical Assessment
- Dietary History
- Significant LOW (5% in the last month or 10% over 6 months) or current body weight 80-
History
85% (or less) of ideal body weight
- Beware of patients who present with ascites / oedema
- Evidence of muscle wasting → thenar and temporal muscles
- Depletion of subcutaneous fat → loose or flabby skin
Physical Examination - Peripheral oedema and/or ascites → due to hypo-proteinemia
- Features of vitamin deficiency → nail and mucosal changes

- Ecchymosis and easy bruising
- Easy to detect >15% loss
- Weight for Height comparison
- BMI < 19 or > 10% decrease
Anthropometric - Triceps-skinfold
Measurements - Mid-arm muscle circumference
- Urinary Creatinine height index
- Others : bioelectric impedance / hand grip dynamometry
- Serum albumin: < 35g/L (half-life: 14-20days)
- Serum prealbumin: mild (10-17mg/dl), moderate (5-10mg/dL) and severe (<5mg/dL) –
Laboratory half-life 2-3 days
Investigations - Serum transferrin: <200mg/dL (half-life: 10days)
- Others: total lymphocyte count <1800/mm3, Skin anergy testing, test reflecting specific
nutritional deficit – i.e. prothrombin time, U/E/Cr, LFT
Daily Caloric Requirements

- 2000 – 2500 kcal/day = 20% protein (0.8-1g protein/kg/day), 30% fat, 50% carbohydrates
Caloric Contents:
- Glucose: 4 kcal/g
- Dextrose: 3.4kcal/g
- Protein 4 kcal/g
- Fats: 9 kcal/g
- Alcohol: 7 kcal/g
52
REFEEDING SYNDROME14
Potentially fatal medical condition, a result of fluid and electrolyte shifts during nutritional rehabilitation of malnourished patients
Pathophysiology
- Glucose cause rapid rise in insulin: trigger cellular uptake of PO 4+ (K+ & Mg2+)*
- Starvation: thiamine & mineral deficiency: exacerbated by onset of anabolic processes
- Renal reabsorption of sodium increases (secondary to insulin): fluid retention, exacerbate pulmonary edema, CHF
* increase use of phosphate to produce ATP and 2,3 DPG.
Clinical Manifestation
- Electrolyte Deficiencies such as hypoPO4+, hypoK+, hypoMg2+
- Thiamine Deficiencies
- Volume Overload
Medical Complications
- Cardiovascular: heart failure, arrhythmias, peripheral oedema
- Respiratory: impaired respiratory function leading to dyspnoea, respiratory failure
- Gastrointestinal: constipation / diarrhoea, elevated LFTs
- Muscular: impaired contractility, myalgia, tetany, rhabdomyolysis
- Neurological: tremor, paraesthesia, delirium, seizures
Risk factors
- Reduced Intake – i.e. prolonged fasting or low energy diet / Marasmus
▪ Dysphagia (stroke patients, oesophageal cancer patients etc.)
▪ High-stress patient unfed for >7 days
▪ Anorexia nervosa, Depression, Chronic Alcoholism
- Reduced absorption – i.e. malabsorptive syndromes
▪ Inflammatory Bowel Disease
▪ Chronic Pancreatitis
▪ Short Gut Syndrome
- Increased Metabolic Demands
▪ Post-operative patients
▪ Oncology Patients
- Others – lowered physiological reserves
▪ Elderly patients (multiple comorbid, decreased physiological reserve)
▪ Uncontrolled DM (electrolyte depletion, diuresis)
▪ LT user of antacids (Mg2+ & Al salts bind PO4+) or diuretics (loss of electrolytes)
Prevention and Management

- Identification of high-risk individuals: ≥2 of the following:
▪ BMI < 18.5
▪ Unintentional weight loss >10% in past 3-6 months
▪ Little or no nutritional intake for > 5 days
▪ History of alcohol misuse, drugs (i.e. insulin, chemotherapy, antacids, diuretics)
- Nutritional replenishment commence after correction of electrolyte abnormalities (check electrolyte after restarting feeding)
- Vitamin supplementation started with re-feeding and continued for at least 10 days
- NICE guidelines – refeeding is started at no more than 50% of estimated energy requirements – rate can be increased if no
refeeding problems detected clinically or biochemically
- Refeed at lower rate (10-15kcal/kg/day)15
14 BMJ. 2008 Jun 28;336(7659):1495-8

15The Absite Review 4th Edition – Chapter 10, Pg 38
53
ENTERAL FEEDING
Provision of nutritional requirements via non-invasive or invasive methods with standard formulation or disease-specific formulations
Choice of feeding regimen

- Allow lowest possible hourly feeding rate (i.e. 10ml/hr) better GI tolerance
- Better control of blood glucose due to continuous CBH input
Continuous
- When post-pyloric feeding is required, continuous feeding is often better tolerated than
intermittent
- Daytime feeds may reduce aspiration risk if it is difficult to maintain 30deg elevation overnight
Intermittent
- More physiological (daytime feeding)
- Patient must have competent oesophageal sphincter – minimize aspiration risk
Bolus
- Physiological similar to typical eating pattern
Advantages
- Maintains the GIT cyto-architecture and mucosal integrity, absorptive function and normal microbial flora, reduce risk of bacterial
translocation
- More physiological, ↓complications, gut mucosa preserved, no bacterial translocation,
- Cheaper
Indications
- Nutritional support is needed
- Problem with swallowing – i.e. stroke or oesophageal obstruction (require tube feeding)
- Proximal small intestine intact & functional (functional GIT but unable to sustain an adequate oral diet)
- Stimulation of secretory function does not worsen the condition being treated (e.g. small bowel fistula)
Contraindications
- Complete small bowel obstruction
- Ileus
- Proximal small intestinal fistula, high o/p enterocutaneous fistula
Types of Feeding Tubes

Non-Invasive - Nasogastric Tubes
(tubes inserted down - Orogastric Tubes
upper GIT, following - Naso-jejunal Tubes (when gastric emptying is a problem), either via radiological guidance or
normal anatomy) endoscopic guidance
- Gastrostomy Tubes
Invasive
i. Percutaneous endoscopic gastrostomy (PEG) used for feeding, drainage and/or
(require invasive
prevention of volvulus (rare, fix stomach to abdominal wall)
procedure for
ii. Open Gastrostomy
insertion)
- Feeding Jejunostomy Tubes
Types of Oral Feeds

- Ensure (protein 9 gram /serving)
- Ensure Plus (highly concentrated in calories 1.5 cal/ml & protein 13 g/serving)
- Glucerna (for DM patients: ↓ carbohydrates, modified fat)
- Pulmocare (for COPD patients: high calorie, low carb to help ↓ CO2 production)
- Novasource Renal (for renal patients: low protein & nitrogen content)
Complications of enteral feeding

Gastrointestinal - Nausea, vomiting, diarrhoea
- Malposition of feeding tube – displacement and catheter migration
Mechanical
- Sinusitis, Ulcerations / Erosions, Tube Blockage
- Refeeding syndrome (i.e. hypoPO4, hypoMg, hypoK)
Metabolic
- Hyperglycemia – reduced glucose tolerance of the critically ill
- Aspiration Pneumonia
Infectious
- Infection around a gastrostomy or jejunostomy wound (i.e. PEG / feeding J site)
54
PARENTERAL NUTRITION
Provision of all nutritional requirements by the intravenous route
Advantages / Disadvantages:
- Allow greater caloric intake BUT more expensive & have more complications
Types of Parenteral Nutrition:

- Given through peripheral vein
Peripheral
- Short-term use
Parenteral
- Low caloric requirements
Nutrition
- Needs large amount of fluids
- Need venous access to a large central line, risk of thrombophlebitis due to
Central (Total) concentrated dextrose content if given through peripheral veins
Parental Nutrition - Long peripheral line (i.e. PICC), subclavian approach, internal jugular approach,
external jugular approach (i.e. CVP line)
Indication for TPN

- Obstruction of GIT proximal small bowel obstruction not immediately relieved (i.e.
secondary to carcinomatosis peritonei)
- Short bowel syndrome:
Abnormal gut i. Temporary (before adaptation) in patients who undergo significant SB
function resection
ii. Permanent in < 1m of functional small intestine
- Intestinal fistula / Enterocutaneous fistula
- Refractory inflammatory bowel disease of the GIT (e.g. Crohn’s, UC)
- Cannot consume adequate amounts of nutrients via enteral feeding – Inability to use
Others
the GIT: pancreatitis with pseudocysts/abscess (only if enteral nutrition not tolerated)
Stopping TPN: aim to stop when enteral feeding can restart, wean slowly to avoid hypoglycemia
Complications
- Related to insertion of line: pneumothorax, air embolism, arterial injury, bleeding,,
Mechanical catheter misplacement, catheter embolism, thoracic duct injury
- Related to catheter in situ: venous thrombosis and catheter occlusion
- Electrolyte abnormalities: check U/E/Cr, acid-base abnormalities,
- Hyperlipidaemia
Metabolic
- Hyper/hypoglycemia
- Hepatic complications: cholestatic jaundice, acalculous cholecystitis – check LFTs
- Insertion site Infection
- Catheter / Line Infection
Infectious
- Secondary contamination / risk of bacterial / fungal (i.e. candida) translocation, risk of
septicaemia / candidemia
Effects of Electrolytes Derangement
Phosphate
- Hypophosphatemia (intra-cellular processes and structural integrity of cell membrane)
▪ Confusion
▪ Convulsion
▪ Muscle Weakness – can lead to diaphragmatic weakness
▪ Left shift of oxyhaemoglobin curve – decrease oxygen delivery to tissue (↓in 2,3 DPG)
- Hyperphosphatemia – Usually asymptomatic and no treatment is required
Magnesium
- Necessary for muscle and nerve function also needed for normal PTH secretion
- Replace Mg when hypoK or hypoCa co-exists with hypoMg
Potassium
- Hypokalaemia
▪ Fatigue and lethargy with eventual muscle weakness
▪ ECG: flattened T wave → appearance of U wave depressed ST segment
- Hyperkalaemia
▪ Sudden cardiac arrhythmias with cardiac arrest
55
▪ ECG: peaked T waves → prolonged PR interval → loss of P waves → widened QRS → sine wave pattern
56
EXTRA INFORMATION
Steps to Ordering TPN

- Maintenance requirements based on body weight
Determine Total
- Add on-going losses based on I/O charts
Fluid Volume
- Add insensible fluid losses, add 10% for every 1deg rise in temperature
- Based on total energy expenditure (TEE)
Determine Non-N
- Resting Energy Expenditure (REE): 25 to 30kcal/kg/day (Schofield equation)
Caloric Needs
- Harris Benedict Equation = REE based on weight, height, age and gender
determine how much
fat and CBH to give - TEE = REE + Stress Factor + Activity Factor
- Fats (25-30% of calories) and Carbohydrates (70-75% of calories)
- based on calorie: nitrogen ratio
- The ratio of 150 kcal : 1g nitrogen in stressful condition promotes anabolism, and 250-300 Kcal :1gm N is adequate
for normal body maintenance (1gN = 6.25g protein)
- Based on degree of stress and body weight
Determine Protein i. non-stress: 0.8g-1.0g/kg/day
Requirements ii. mild stress 1.0-1.2g / kg / day
iii. moderate stress: 1.3-1.75g/kg/day
iv. severe stress 2-2.5g/kg/day
- Based on nitrogen balance: aim for positive balance of 1.5-2g/kg/day

Electrolyte Requirements
- Na+ → 1-2mmol/kg/day (or 60-120 meq/day)
- K+ → 0.5-1 mmol/kg/day (or 30-60meq/day)
- Mg2+ → 0.35-0.45 meq/kg/day (or 10-20meq/day)
- Ca2+ → 0.2-0.3 meq/kq/day (or 10-15meq/day)

Determine
- PO42- → 20-30mmol/day
Electrolyte and
Trace element
requirements Trace Elements
- Commercial preparations exist to provide RDA
- Zn → 2-4mg/day
- Cr → 10-15ug/day
- Cu → 0.3-0.5mg/day
- Mn → 0.4-0.8 mg/day
- Vitamins → give 2-3x that of oral intake

Determine need for - 1 ampoule MultiVit per bag of TPN
additives - MultiVit does not include Vitamin K (can give 1mg/day or 5-10mg/week)
- Mediations needed (ie. Insulin)
SHOCK
57
DEFINITION
Inadequate tissue oxygenation and organ perfusion to meet metabolic demands leading to eventual global cellular hypoxia.
Hypotension: SBP < 90mmH or MAP < 60mmHg or reduction in SBP > 30mmHg from baseline
PATHOPHYSIOLOGY
- MAP ∝ CO x SVR | MAP = 2/3 DBP + 1/3 SBP
- Cardiac Output (CO) = SV x HR = MAP-MVP / TPR
▪ Stroke Volume (SV) ∝ preload, afterload and myocardial contractility
- MAP ∝ HR, preload, afterload, contractility
- Cardiac Index (CI) = CO / BSA (normal range: 2.6 – 4.2L/min/m2) – < 1.8 = cardiogenic shock
Stroke volume (SV) = LV end diastolic volume – LV end systolic volume [EF = stroke volume / LV end diastolic volume]
Preload: end diastolic length of cardiac myocytes ∝ end-diastolic volume (EDV) and filling pressure
Afterload: resistance against ventricular contraction (SVR)
Systemic hypotension leads to release of catecholamines, aldosterone, renin and cortisol which act together to ↑HR, preload, afterload
and contractility.
- Inadequate tissue perfusion
▪ Skin – cold, pale, decreased capillary refill
▪ Renal – decreased urine output (<0.5ml/kg/hr)
▪ CNS – anxiety, confusion, lethargy
- Increased sympathetic tone
▪ Tachycardia
▪ Narrowed Pulse Pressure
Classes of Shock
Class 1 2 3 4
Blood Loss (%) < 15 15-30 30-40 >40
Blood Loss (ml) < 750 750–1500 1500–2000 > 2000
Normal
Heart Rate (bpm) >100 >120 >140
(<100)
SBP – N SBP – ↓ SBP – ↓↓
Blood Pressure Normal
DBP – ↑ DBP – ↓ DBP – ↓↓
Pulse Pressure Normal or Increased Decreased Decreased Decreased
Normal ↑ ↑↑ ↑↑↑
Respiratory Rate
(14-20) (20-30) (30-40) (>35)
Urine Output Normal ↓ Oliguria Anuria

(ml/hr) (>30) (20-30) (5-15) (<5)
Mental State Minimal Anxiety Mild Anxiety Confusion Lethargy

Base Deficit 0 to -2 -2 to -6 -6 to -10 ≤ -10
Massive Transfusion
Fluid Replacement Monitor / Crystalloid Crystalloid Crystalloid + Blood
Protocol
*The first noticeable change in systemic BP is a drop in pulse pressure, increased SVR in response to decreasing preload pred ominantly increases the
diastolic BP resulting in an overall decrease in pulse pressure
** Narrowed pulse pressure = less than 25% of systolic value
- Stage 1: Normal BP as compensated by increased systemic vascular resistance

- Stage 2: ↑HR, postural hypotension, ± sweating / anxiety – partially compensated by increased SVR
- Stage 3: Systolic BP <100 mmHg, ↑HR, ↑ RR, altered mental state (confusion)
- Stage 4: Very low BP, ↓ HR, weak pulse pressure, depressed mental state, urine output negligible
In severely anaemic patients, there is systemic vasodilation and widening of pulse pressure (SVR falls and PP widens).
CLASSIFICATION [Hypodynamic vs. Hyperdynamic/Distributive]
58
Shock Classification Causes Sign & Symptoms Investigations

Acute Hemorrhage (usually at least 20%) – BGIT Pallor FBC
Trauma Cold clammy skin (reflex U/E/Cr
Dehydration – burns vasoconstriction) PT/PTT
Hypovolemic
Severe GE ↑diastolic pressure (initial alteration) GXM
Loss of circulating
Cardiac
blood volume ↓JVP
Others: acute pancreatitis, ruptured AAA, ruptured ectopic Enzymes
(hypodynamic)
pregnancy, ruptured HCC ↓CVP, CO, ↑SVR ABG
↑HR
AMI / abnormal ventricular wall motion Pallor Cardiac
Acute cardiac arrhythmias Cold clammy skin (reflex enzymes
Cardiac Trauma vasoconstriction) ECG
Cardiac Tamponade* ↑JVP TTE
Cardiogenic
Intrinsic cardiac failure ↑CVP, PCWP & SVR
Others: Valvular Stenosis, Regurgitation or Rupture, CXR
(hypodynamic)
Ischemia, Cardiomyopathy, AVSD, viral myocarditis ↓SvO2, CO
* decreased ventricular filling due to fluid in pericardial sac ↑HR

around heart (TTE: impaired diastolic filling of RA)
Tension Pneumothorax** ↑JVP D-dimer
Cardiac Tamponade CTPA
Pulmonary Embolism
Obstructive
impaired venous return ** Tension pneumothorax = air enters pleural space → flap
(hypodynamic) valve mechanism prevents escapes → increased
intrapleural pressure → lung collapse → mediastinal shift →
impaired in venous return → decreased cardiac output

Spinal Injury Warm skin (peripheral vasodilation) Normal
Head Injury ↓JVP
CT / MRI
↓ CVP, CO, SVR Spine
Neurogenic ***Interruption of sympathetic chain with unopposed vagal
(distributive) N/↓ HR (relative bradycardia)
tone → lack of sympathetic tone → decreased SVR →
Loss of symp. tone*** Neurological deficit
pooling of blood in extremities → hypotension DRE: lax anal tone
Infections – sepsis Fever, Rigor FBC

Warm skin (peripheral vasodilation) Blood C/S
↑HR CRP
Septic ProCal
(distributive) ↓ CVP, ↑CO, ↓SVR
↓JVP CXR
UFEME
Urine c/s
Bites / Stings Fever, rigors
Anaphylactic
Allergens – Drugs / Food Warm skin (peripheral vasodilation)
(distributive)
a/w angioedema, bronchospasm
Withdrawal of exogenous steroids Fever Glucose
Relative or absolute adrenal insufficiency (in setting of Severe lethargy U/E/Cr
Hypo-adrenal concomitant illness) – i.e. exogenous steroids, Confusion, syncope Thyroid
(distributive) hypopituitarism Psychosis Screen
Severe vomiting / diarrhoea 8am Cortisol
↓ CVP, CO, SVR
59
MANAGEMENT
Principles: Assess early, intervene promptly, and review frequently

Aim: ensure adequate delivery of oxygen to the peripheral tissues by optimizing Sa0 2, Hb concentration and Cardiac Output*
- SaO2 – maximized in acute setting, check with pulse oximetry
- [Hb] – transfusion trigger of 7 g/dL
- CO – HR and SV (CO ~ 4-8L / min, cardiac index ~ 2.5-4L / min)
*Cardiac output: 25% of CO goes to kidney, 15% goes to brain, and 5% goes to heart
Endpoint of resuscitation16
- Normalization of BP, HR, Urine Output
- Serum markers – lactate (<2 mmol/L), base deficit (between -2 and +2) & gastric mucosal pH (7.30 – 7.35) are more
appropriate end-points: aim for normalization within 24hours
General Management
- Narrowed Pulse Pressure, Postural Hypotension
Recognize - Tachycardia
early features
- Hypotension: SBP <90mmH or MAP <60mmHg or ↓ in SBP >30mmHg from baseline
of shock
- Assess hypotensive patients early
Airway - Maintain airway, consider intubation if necessary
Breathing - 100% O2 via non-rebreather mask
- 2 large bore IV catheter (start fluid resuscitation)
- Raise Legs
- Intravenous crystalloids +/- colloids (i.e albumin) +/- blood
Circulation
- ± Inotropic support
▪ IV dopamine 5-10μg/kg/min
▪ IV norepinephrine 5-20μg/kg/min (esp. for septic shock)
- Vitals – HR, BP, SpO2, RR, Temperature – continuous pulse oximeter
- Monitor Urine Output
Monitoring
- Clinical – peripheries, capillary refill time
- May require HD support with intra-arterial line for BP monitoring
- Tension Pneumothorax – emergent decompression
Evaluate Life-
- Cardiac Tamponade – Start IV fluid bolus with 500ml N/S and/or IV dopamine infusion 5 ug/kg/min and prepare for
Threatening
pericardiocentesis
Causes
- AAA – examine abdomen for any pulsatile mass
- History – current symptoms (trauma, infective), past medical hx (IHD, medications), recent operation (i.e. re-bleeding)
Identify
- Examination – vitals, urine output, systemic review, PR exam
Underlying
Causes - Investigations (as indicated) – FBC, GXM, PT/PTT, U/E/Cr, Cardiac Screen (enzymes + ECG), ABG, CXR, Septic Work-up
(Blood Culture, Inflammatory Markers – i.e. CRP)
*Inform Senior Early*
EXTRA INFORMATION
Spinal Shock vs. Neurogenic Shock

- Spinal shock is a state of transient physiological reflex depression of cord function below the level of injury a/w loss of sensorimotor functions
▪ Spinal shock has increased in BP due to the release of catecholamines followed by hypotension, flaccid paralysis and bladder/ bowel
paralysis noted.
▪ These symptoms last several hours to days until the reflex arcs below level of injury begin to function again – bulbocavernosus reflex
▪ Spinal shock is not true shock
- Neurogenic shock describes the hemodynamic changes resulting from a sudden loss of autonomic tone
▪ May require vasopressors (i.e. phenylepinephrine) if BP does not respond to fluid challenge
▪ Early administration of IV high dose methyl-prednisolone (30 mg/kg over 1 st hour, followed by 5.4mg/kg/h for next 23 hr) – indicated
for non-penetrating spinal cord within 8 hour of injury
16 J Trauma. 1998 May;44(5):908-14.
60
SEPSIS17
DEFINITION
Sepsis if a systemic, deleterious host response to infection leading to organ dysfunction.
Background
- Sepsis is the primary cause of death from infection especially if not recognized and treated promptly
- Sepsis is a syndrome shaped by pathogen factors and host factors (i.e. sex, race, age, co-morbidities) – sepsis involves
dysregulated host response with or without organ dysfunction
- Sepsis-induced organ dysfunction may be occult; therefore, its presence should be considered in any patients presenting with
infection
Clinical Definition of Sepsis Syndrome18

- Sepsis is a life threatening, systemic, deleterious host response to infection leading to organ dysfunction.
▪ Infection +
▪ Organ dysfunction as defined as a change in total SOFA score ≥ 2 consequent to the infection
- A SOFA score ≥ 2 reflects an overall mortality risk of ~ 10%
- Septic shock is sepsis with fluid resistant hypotension requiring vasopressors to maintain MAP ≥ 65 and having a serum lactate >
2mmol/L despite adequate volume resuscitation
▪ Subset of sepsis where underlying circulatory and cellular / metabolic abnormalities are profound enough to substantially
increase mortality ~ 40%
PATHOPHYSIOLOGY
Phases of Septic Shock

- Rescue
▪ Lifesaving measures to treat the underlying cause of shock
▪ Prompt administration of intravenous crystalloid (i.e. 30ml/kg)
▪ Aim to obtain a minimal acceptable blood pressure / cardiac output
- Optimization
▪ Optimize and maintain tissue perfusion and oxygen availability (organ rescue)
▪ Optimize cardiac output, lactate levels
▪ Repeated assessment of intravascular fluid status and determination of further fluid administration
- Stabilization
▪ Provide organ support
▪ Maintain intravascular volume, replace ongoing fluid losses (aim for zero or negative fluid balance)
▪ Avoid iatrogenic harm with unnecessary fluid administration (minimize complications
- De-escalation
▪ Aim for organ recovery
▪ Weaning from vasopressors
▪ Mobilize fluid accumulated, aim for negative fluid balance
17 Crit Care Med. 2013 Feb;41(2):580-637

18 JAMA. 2016 Feb 23;315(8):801-10. [Landmark paper]
61
DIAGNOSTIC CRITERIA
Sequential Organ Failure Assessment (SOFA) Score
qSOFA Score (if ≥ 2, to further investigate for organ dysfunction, initiate / escalate therapy as appropriate
1. RR ≥ 22/min
2. Altered mentation
3. SBP ≤ 100
National Early Warning Score (NEWS)

- NEWS score ≥ 5 has sensitivity of sepsis of 79%
Diagnostic Criteria for SIRS ≥ 2 of the following present (no longer used as criteria for sepsis)
1. Temp > 38 or < 36oC
2. HR > 90bpm
3. RR > 20 breaths/min OR PaCO2 < 32mmHg
4. WCC > 12000/mm3, < 4000/mm3,or >10% immature forms
Note: immunocompromised patients can be septic without eliciting an inflammatory response

* Most potent stimulus for SIRS = endotoxin (lipopolysaccharide-lipid A) – potent stimulator of TNF
62
MANAGEMENT
The management of sepsis is based on the surviving sepsis campaign (2016). The initial management is based on the implementation
of a sepsis bundle which should be initiated in the first 3-6 hours from diagnosis of sepsis (3 hour bundle). In 2018, the updated
guidelines recommend for these bundles to be implemented within 1 hour of sepsis recognition (1 hour bundle). At present,
controversies are still present between the timing of implementation of the sepsis bundle. (NEJM Case Vignette)
In the UK, the sepsis bundle is referred to as Sepsis 6 which consists of 3 diagnostic and 3 therapeutic interventions.
Sepsis 6 Bundle
1 Give Oxygen Aim to keep saturations > 94%
Give 500mls IV crystalloids fast
2 Give IV Fluids
If hypotensive / lactate > 2mmol/l or AKI, can give up to 30ml/kg
3 Take Blood cultures Consider Source Control (inform surgeon / radiologist if needed)
Increased lactate represents tissue hypoxia. If initial lactate is elevated > 2mmol/L it
4 Measure Lactate Levels
should be remeasured with 2-4 hours to guide resuscitation
5 Give IV Antibiotics
6 Measure Urine Output Insert urinary catheter and aim for urine output > 0.5ml/kg/hr
Initial Management of Septic Patient

Upon recognition of a septic patient, I will institute early goal directed therapy. My initial management will be based upon the Sepsis
6 bundle. I would ensure that the patient is given oxygen to maintain oxygen saturations of > 94%. I would set 2 large bore IV plugs
and commence IV fluid resuscitation with an initial bolus of 500mls of IV Hartmans. More importantly, I would obtain an Arterial
Blood Gas and Lactate measurement. The lactate value can help guide fluid therapy. Also, I would take blood cultures and
administer broad spectrum antibiotics. I will also insert a urinary catheter to aid in the measurement of urine output.
Blood investigations such as FBC, Renal Panel, PT/INR/APTT LFT, CRP, Procalcitonin will also be performed as clinically required.
I will escalate the patient to my senior early as well as the patient may require imaging to identify the source of sepsis, closer
monitoring in the high-dependency or intensive care unit and use of vasopressors if he remains persistently hypotensive.
63
EXTRA INFORMATION
Surviving Sepsis 2016 Guidelines19

Initial Resuscitation & Infection Issues
GOALS THINGS TO DO
- IV fluid replacement (IV 500mls crystalloids or

- Target resuscitation to normalize lactate
Initial Resuscitation administer 30ml/kg crystalloid for hypotension or
- Urine output ≥ 0.5ml/kg/hr
(golden 6 hours – lactate ≥4mmol/L within the 1st 3 hours)
early goal directed - MAP ≥ 65mmHg
- Measure lactate level KIV re-measure if initial value
therapy) - SVC O2 saturations (Scvo2 = 70%)
is elevated (>2 mmol/L)
- CVP 8-12mmHg
- Insert Urinary Catheter (aim for ≥ 0.5ml/kg/hr)
- Recommend routine screening of dangerously ill

Screening for sepsis
patients to allow implementation of sepsis bundle
- Blood culture (Aerobic & Anaerobic)
- Obtain blood cultures before anti-microbial initiated
- For patients with intravascular catheter in place for >
(aerobic & anaerobic) in patients with suspected
Diagnosis
sepsis or septic shock before administration of 48 hours (i.e. CVP line, PICC) → obtain 1 set of culture
antibiotics
of catheter line
- Administer empirical broad-spectrum Ab within 1

- Administer within the first hour of recognition of
hour of sepsis recognition
septic shock / severe sepsis
- Daily assessment for de-escalate antibiotics depending
Antimicrobial Therapy - Antibiotics should not to be used in patients with
on blood culture results and clinical response
severe inflammatory states determined to be of non-
(procalcitonin can also be used to support shortening
infectious cause (i.e. severe pancreatitis, burns)
duration of antibiotics)
- Imaging studies performed to confirm potential source
- Diagnose infective source within first 6-12hours and
of infection and implement early source control
emergent source control carried out – if patient is
Source Control - If line sepsis suspected, prompt removal of
severely septic intervene with least invasive effective
intravascular access device should be performed after
option (percutaneous rather than surgery)
other vascular access has been established
Hemodynamic support and adjunctive therapy

GOALS THINGS TO DO
- Crystalloid is the initial fluid of choice KIV IV albumin
- After initial resuscitation, additional fluid guided by
Fluid Therapy - DON’T USE hydroxyethyl starches (HES) – absence of
frequent reassessment & normalization of lactate
clear benefit with colloids
- Target MAP of 65mmHg in patients with septic shock - Insert arterial catheter (IA line) + CVP when using
requiring vasopressors vasopressor
Vasopressor - Dopamine is alternative to norepinephrine - Norepinephrine (NE) is the initial vasopressor of choice
- Phenylephrine is not recommended as initial therapy – - If a second agent is required, vasopressin (up to
used for salvage therapy 0.03U/min) or epinephrine can be used.
- Use of IV hydrocortisone 200mg / day only in specific
- If adequate fluid resuscitation and vasopressor is able
scenarios (i.e. hypotension despite adequate fluid
Corticosteroids to restore hemodynamic stability – no role for
resuscitation and vasopressor therapy or adrenal
corticosteroids
dysfunction )
- For patients with sepsis related ARDS, target a tidal - Conservative fluid strategy for patients with establish
sepsis-induced ARDS
Ventilator volume of 6ml/kg of predicted body weight and a
- Elevate head 30-45 degree (limit aspiration risk &
plateau pressure of ≤ 30cm H20 reduce development of VAP)
Supportive therapy
GOALS THINGS TO DO
- Target Hb 7.0 – 9.0 g/dL in adults
- Administer platelets if counts <10,000/mm 3 or if patient - RBC transfusion if Hb <7.0
at risk of bleeding and counts <20,000mm 3 or patients - Platelet transfusion (depending on clinical scenario)
Blood Products
is actively bleeding, planned for surgery or invasive - Don’t use FFP to correct clotting abnormalities in
procedures and counts < 50,000/mm 3 absence of bleeding or planned invasive procedure
-
- Monitor blood glucose every 1-2 hours till glucose level
Glucose Control - Target upper blood glucose of ≤ 10mmol/L
and insulin infusion is stable, then q 4hourly
19 Intensive Care Med. 2017 Mar;43(3):304-377.
64
- KIV start insulin infusion when 2 consecutive blood

glucose >10mmol/L
- Enteral feeding (i.e. trophic feeds) +/- IV dextrose
- Aim for early initiation of enteral nutrition who can be
Nutrition containing drip
fed enterally (instead of parenteral nutrition)
- +/- prokinetic agents if have feeding intolerance
- Renal Replacement Therapy: consider for patients with sepsis with AKI
- Stress Ulcer Prophylaxis: IV PPI for patients with sepsis or septic shock with risk factors for GI bleeding
Others
- DVT Prophylaxis: Consider starting SC clexane for DVT prophylaxis
- Establish goals of care
Commonly used Inotropes 20

Drug Alpha-1 Beta-1 Beta-2 DA Dose
Dopamine (low)* - ++ - +++ 3-5 mcg/kg/min
Dopamine (high) ++ ++ - +++ 5-20 mcg/kg/min
40 – 100 mcg/dose every 1-2min
Phenylephrine**
++ - - - For patient with low BP and high HR
(50mcg/ml)
Can have reflex bradycardia
3-5mg each dose titrate to effect
Ephedrine
++ ++ + - For patients with low BP and low HR
(30mg/ml)
Rapid onset, DOA: 1 hour
Epinephrine (low) - ++ ++ -
0.05 – 2 mcg/kg/min
Epinephrine (high) ++ ++ + -
Norepinephrine ++ + - - 1-20 mcg/minute
* At low dose, dopamine causes renal and mesenteric vasodilation causing diuresis and natriuresis (no evidence for renal prot ective activity)
** Phenylephrine – pure alpha-adrenergic agonist (potent vasoconstrictor) – can cause reflex bradycardia
20 Sabiston Textbook of Surgery 19 th Edition (Chapter 23, Surgical critical care) – pg 572
65
PRE-OPERATIVE MANAGEMENT
Routine Preoperative preparation / investigations

- Fasting: GA / RA: > 6 hours for milk / food, >2 hours for clear fluids, LA + Sedation: minimum 4 hour fasting
- ASA 1 patients & < 50yr: no investigation,
- > 50yr: FBC, RP, PT/INR/APTT, ± GXM (if expected blood loss or low Hb), ECG, CXR + indicated investigations
- In the absence of new clinical changes, blood test are valid for 3/12, ECG 6/12 and CXR 1yr
- Patients listed for elective surgeries should be referred to the anesthesia outpatient clinic for pre-op assessment
Pre-Anaesthetic Assessment
Organ System Specific Pointers
- Age, Height, Weight, BMI
- Drug Allergies (minor vs. life-threatening), anaesthetic implications
- What is the planned operation
General - Previous anaesthetic history and its complication, if any
▪ Airway – easy / difficult ventilation / intubation, ETT / LMA size, larynx grade
▪ Post-op Nausea & Vomiting (PONV)
▪ Previous complications (i.e. malignant hyperthermia)
- Screening for:
▪ HTN (adequacy of control)
▪ Ischemic Heart Disease (assess effort tolerance, threshold: 4METs – i.e. 2 flight of stairs, light housework)
▪ Congestive Cardiac Failure (assess for PND, orthopnoea)
Cardiovascular ▪ Cardiac Arrhythmias
▪ Recent cardiac stents (see below)
- Permanent pacemaker (PPM) or Automated Implantable Cardiac Defibrillator (AICD)
- Revised Lee’s Cardiac Risk Index (see below)
- Investigations: ECG (any IHD, arrhythmias) ± TTE ± Stress Echo ± Myocardial Perfusion Scan
- Screen for:
▪ Chronic respiratory disease (i.e. asthma / COPD) → administer inhalers prior to operation
▪ Control, frequency of exacerbation, previous hospitalization,
▪ Review inhalers
Respiratory ▪ Smoking – 6-7x increased risk of respiratory complications → stop smoking 4-6 weeks prior to operation
▪ Obstructive Sleep Apnoea
▪ STOP-BANG screening criteria (i.e. Snoring, Tired in the day, Observed apnoea during sleep, high Blood
pressure, BMI > 35, Age > 50, Neck circumference > 40cm, Gender male)
▪ Active URTI – postpone surgery for 2 weeks after URTI ends (risk of bronchospasm, laryngospasm, hypoxia)
- Investigations: CXR ± Lung Function Test ± Sleep Study
- Screen for:
▪ Risk for aspiration – i.e. GERD, trauma, pregnancy
Gastrointestinal ▪ History of gastritis – impacts NSAIDs use
▪ Hepatic risk – Child-Pugh Classification, MELD score
▪ Nutritional Assessment – any need for dietician review preoperatively
- Screen for
▪ Diabetes Mellitus
▪ T1DM – refer endocrine
Endocrine ▪ Adequacy of control (i.e. HbA1c), any end organ complications
▪ Thyroid Disease
▪ Hyper / hypothyroidism
▪ Large (retrosternal) goitre: review scans – airway / vascular compression
- Screen for
Renal
▪ Chronic Renal Failure (dialysis or non-dialysis dependent) – needs dialysis 1 day before surgery
- Screen for
Musculoskeletal
▪ Rheumatoid Arthritis as its complications – i.e. Atlanto-axial subluxation, cardiac / respiratory involvement
- Anaemic patients undergoing elective major surgical procedures will benefit from non-transfusion based preoperative
Haematological optimization (i.e. IV iron, PO iron, EPO)
- Arrange for autologous blood transfusion if indicated
EXTRA INFORMATION
Cardiac Stents
- DAPT for 4-6 weeks (bare metal stent) and 6-12 months (drug-eluting stent)
- Perioperative death, MI, stent thrombosis as high as 30% within the first month
- Indication for stent placement (i.e. stable angina vs. ACS) predicts perioperative cardiac complications more than stent type deployed
Revised Lee Cardiac Index

- Each of the six risk factors was assigned one point. Risk of major cardiac event
- 0 point = 0.4%, (1 point = 0.9% (low) 2 points = 6.6% (intermediate) ≥ 3 points = 11% (high)
- Age > 70 also known to increase cardiac risk
66
- Risk of myocardial infarction is highest during the 1 st 72 hours (plaque destabilization)

- Pre-operative statins should be considered for all intermediate and high risk patients
- High Risk Surgeries (i.e. intraperitoneal (i.e. laparoscopic or open), Intrathoracic (i.e. open aortic
Nature of Surgery
surgery, endovascular aortic aneurysm repair), Lower Limb Revascularization)
- History of MI
- History of positive exercise test
Ischemic Heart Disease - Current chest pain due to myocardial ischemia
- Use of nitrate therapy
- ECG with pathological Q waves
- Pulmonary Edema, bilateral crepitations, S3 gallop
Congestive Heart Failure - Paroxysmal nocturnal dyspnoea
- CXR showing pulmonary vascular redistribution
Cerebrovascular Disease - Prior TIA or stroke
Insulin dependent Diabetes Mellitus - Patients with DM on insulin have higher cardiac risk
Chronic Kidney Disease - Pre-op Cr >177umol/L (2mg/dL ) leads to high cardiac risk
Medication History
Types of Drugs Specific Pointers
- Document type of allergic reaction – any anaphylaxis
Drug Allergy - May require preoperative steroids (i.e. 30mg prednisolone ON and OM prior to surgery or IV hydrocortisone 200mg prior
to surgery) – i.e. contrast allergy for patients going for procedures that requires use of contrast
- Indication for antiplatelet – any recent MI/CVA, any stents
- Antiplatelet agents needs to be discontinued for 5-7 days before surgery for restoration of platelet function
Antiplatelets - Operation specific
▪ Endovascular procedures (i.e. angioplasty, fistuloplasty, EVAR) – can usually continue with DAPT
▪ Cholecystectomy – can usually continue on SAPT (i.e. aspirin)
- Low Risk of thromboembolization (i.e. non-valvular AF w/o hx of stroke/TIA, stroke >3/12 without AF): stop warfarin
Anti-coagulants 5-7 days prior to surgery
(recommendation - High-Risk TE: stop warfarin and bridge with clexane 1mg/kg/BD (stop 24 hours prior to surgery) or IV heparin (stop 6
varies from hours prior to surgery)
hospital)
- Recheck INR prior to surgery – if ≥ 1.5 discuss with consultant in-charge
- Taken up to the day of surgery (i.e. anti-HTN, statins, thyroid meds, antibiotics) – serve with sips of water
Medication for - Usually withhold taking ACE-I / ARB on morning of surgery as it can cause refractory intraoperative hypotension
chronic disease
- Continue beta-blockers – abrupt discontinuation is a/w ↑perioperative cardiac risk
- Patients currently on BB should continue the medication throughout the perioperative period – rebound after abrupt
discontinuation of medication is a/w increased perioperative cardiac events
Beta-Blockers
- BB decreases perioperative death only in high cardiac risk patients – BB should be started as early as possible in the
pre-operative period, minimum over a 2-week period
Supplements (i.e. - Awareness of interaction with anaesthesia
herbal and TCMs) - Supplements to be discontinued 1-2 weeks before surgery – potential interaction with coagulation and anaesthesia
- Prolonged corticosteroid use a/w increased complications (i.e. anastomotic leaks, wound infections)
- Consider perioperative steroid supplementation in patients who take ≥ 20mg of prednisolone for 3 weeks or longer
- Current recommendation involves maintaining patient on chronic steroid supplementation prior to surgery with addition
of intraoperative dosing in unexplained clinical deterioration,
- No published prospective trials have demonstrated benefit to treating steroid dependent patients with supra-physiological
“stress dose” of steroids compared with continuing their preoperative dose
Uptodate Recommendation
Degree of
Corticosteroid Use Definition Glucocorticoid dose
Surgical Stress
Take the usual morning steroid dose. No extra supplementation
Mild Local Anaesthesia, <1 hour
is required
I.e. total joint replacement, Take the usual morning steroid dose. Give 50mg IV
Moderate segmental colectomy, open hydrocortisone prior to procedure nad 25mg hydrocortisone q8h
cholecystectomy for 24 hours. Resume usually dose thereafter
Take the usual morning steroid dose. Give 100mg of IV
hydrocortisone before induction of anesthesia nad 50mg
Major I.e. esophagectomy, CABG
hydrocortisone q8h for 24 hours. Taper dose by half per day to
maintenance levels.
67
Management of medical problems in surgical patients

T2DM Perioperative Management
- Omit all OHGA and scheduled insulin on morning of procedure
Short duration NBM ▪ If DM medications were given, or long-active insulin was given in last 24 hours, start IV dextrose containing drip
(NBM from 12MN) - Omit the T2DM SCSI on morning of procedure
- Check POCT glucose at 8am
- Omit all OHGA and scheduled insulin on morning of procedure
Short duration NBM ▪ If DM medications were given, or long-active insulin was given in last 24 hours, start IV dextrose containing drip
(NBM after - Administer the T2DM SCSI for breakfast
breakfast) - Start the T2DM 4hrly NBM SCSI after breakfast
- Check POCT glucose pre-breakfast and 4hourly thereafter
- Monitor POCT blood glucose 4 hourly
- Stop OHGAs and scheduled insulin
- Start IV dextrose containing drip
- Consider starting basal insulin if blood glucose is > 14 mmol/L
▪ If not previously on basal insulin, start at 0.2 units / kg / body weight
Long duration NBM ▪ Give as SC NPH in 2 divided doses 12 hourly (omit NPH if BG is < 4.0)
▪ Start NPH 8-12 hours after the last dose of OHGA/scheduled insulin (24 hours after glargine)
- Order the T2DM 4 hourly SCSI
- If NBM is prolonged > 24 hours, review BG trend daily
▪ Increase basal insulin by 10-20% every 1 - 2 days if BG is consistently > 14 mmol/L
▪ Review nutritional needs if NBM is prolonged > 48 hours
- Monitor POCT BG TDS-premeal + 10pm
When full diet is - Resume usual DM medications with next meal if no contraindication (reduce dose by 25-50% if oral intake is anticipated
resumed to decrease)
- Change SCSI BG from 4 hourly to TDS-premeal
Others
Long-Term Steroids - IV hydrocortisone before and after operation till patient can resume oral intake
- Pre-op: arrange for CXR and Lung Function Test ± baseline ABG
COPD - Chest Physiotherapy – breathing exercise – pre-op and post-op
- Smokers – encouraged to stop smoking 4-6weeks prior to surgery
- Pharmacological prophylaxis (i.e. LMWH or low-dose unfractionated heparin)
- Thromboembolic deterrent (TED) stockings
DVT / PE - Intermittent pneumatic calf compression
- Early Mobilization
- For cancer patients (high risk of post-op thrombosis), there is benefit of perioperative anticoagulant prophylaxis21
Anemia - Pre-operative correction of mild anaemia without transfusion reduces perioperative morbidity and mortality
- Magnetic deactivation pre-op & device interrogation before d/c from recovery room
Implantable - If dual function, program device to an asynchronous pacing mode
cardioverter - Bipolar is preferred
defibrillator (ICD) - If using monopolar, avoid using within 15 cm of device – use minimal power setting with grounding pad near site of
operation
21 Chest. 2004 Sep;126(3 Suppl):338S-400S.
68
POST -OPERATIVE COMPLICATIONS22
COMMON POSTOPERATIVE COMPLICATIONS
Immediate (1st few hours post-op)

- Hemorrhage (primary / reactionary hemorrhage) – may require return to operative theatre to re-explore wound
- Heart: Acute Myocardial Infarction
- Infection Disease: Septic Shock from bacteremia (post-instrumentation – i.e. post percutaneous cholecystostomy / post
percutaneous drainage of liver abscess, post-ERCP for cholangitis, post-PCN for hydronephrosis)
Early (1st 24-48 hours post-operation)

- Bleeding (reactionary hemorrhage)
- Lung: Basal Atelectasis (collapse of alveoli) & Increased bronchial secretion – commonest cause of fever in first 24-48 hours
(Mx: chest physiotherapy, incentive spirometry, adequate analgesia, early mobilization)
- Heart: Acute Myocardial Infarction (Type 1 / Type 2), Arrhythmias (i.e. atrial fibrillation), pulmonary embolism
- Renal Function: oliguria, acute renal impairment, acute urinary retention
- CNS: altered mental state / post-op confusion
- Delayed recognition of operative complication – bile leak, delayed detection of enterotomy
Late (between 48 hours to 1 month post-op)

- Bleeding (secondary hemorrhage) – often a result of infection
- Infection Disease – hospital acquired pneumonia, aspiration pneumonia, urinary tract infection (UTI)
- Thrombotic Complications – deep vein thrombosis / pulmonary embolism
- Postoperative paralytic ileus (requiring NGT decompression)
- Electrolyte derangements / Refeeding Syndrome
- CNS: altered mental state / post-op confusion
- Surgical Site Infection – superficial, deep, organ space (can lead to sepsis / septic shock)
- Anastomotic Complications – anastomotic leak (can lead to sepsis / septic shock)
- Wound complications – wound / fascia dehiscence (can lead to burst abdomen, incisional hernia in future)
- Post-operative adhesions – resulting in adhesion colic, intestinal obstruction
CLASSIFICATION OF POST-OPERATIVE COMPLICATIONS
Clavien-Dindo Classification
- Emphasis is placed on clavien classification grade 3 and above. These complications will be presented and discussed at the
weekly morbidity and mortality meeting.
- Any deviation from the normal postoperative course without the need for pharmacological treatment or
surgical or endoscopic and radiological intervention
Grade I
- Acceptable drugs are anti-emetics, antipyretics, analgesia, diuretics, electrolyte replacement
- This grade also includes wound infection opened at bedside
- Require pharmacological treatment with drugs other than those allowed for grade I complications
Grade II
- Blood transfusion, antibiotics and total parenteral nutrition are included
- Require surgical, endoscopic or radiological intervention
Grade III - IIIA – intervention under regional / local anesthesia
- IIIB – intervention under general anesthesia (i.e. re-operation)
- Life-threatening complications requiring ICU management
Grade IV - IVA – single organ dysfunction (including dialysis)
- IVB – multi-organ dysfunction
Grade V - Death
22 The Washington Manual of Surgery, Chapter 38 (pg. 880)
69
Post-op Altered Mental State

- Vitals Monitoring
▪ Hypoxia can result in metal state suppression and agitation
▪ Hypotension, Arrhythmias
- Investigations
▪ POCT glucose measurement
▪ ECG – new-onset arrhythmias or myocardial infarction
▪ Bloods – FBC, Electrolytes, ABG +/- GXM
▪ Imaging – CT Brain TRO intracranial haemorrhage
- Medications
▪ Naloxone – reasonable trial dose if suspect excessive narcotic agents
Post-op Oliguria
FeNa (fractional excretion of sodium) = (urine Na / Urine Cr) / (serum Na / serum Cr) = (urine Na x plasma Cr / plasma Na x urine
Cr) x 100 [FeNa is the comparison of sodium and creatinine ratio in urine and blood] use to determine the underlying cause.
- Pre-renal Causes
▪ Renal Hypoperfusion
- Decrease intravascular volume (i.e. hemorrhage, GI losses, third spacing of fluids)
- Low cardiac output (i.e. cardiogenic shock, heart failure)
- Change in vascular resistance (i.e. use of vasopressors, septic shock, renal artery stenosis)
▪ Lab Values = U/Cr ratio > 100:1, FENa <1%, urine Na <20mEq/24hr, urine osm >500mOsm
- Renal Causes
▪ Acute Tubular Necrosis (i.e. nephrotoxic drugs, ischemia)
▪ Acute Interstitial Nephritis
▪ Lab Values = U/Cr ratio <40:1, FENa > 2-3%, urine Na > 40mEq/24hr, urine osm <350
- Post-Renal Causes
▪ Post-renal obstruction (i.e. BPH, blocked urinary catheter)
- Others
▪ Pain (i.e. after hernia surgery) leading to acute urinary retention (usually on the b/g of BPH)
▪ Abdominal Compartment Syndrome (ACS)
Post-op Oliguria (based on postoperative days)

- Post-op Day 0
▪ Pre-renal causes – hypotension from bleeding, dehydration (i.e. fluid losses from surgery)
▪ Post-renal causes – obstructed IDC
- Post-op Day 1-2
▪ Pre-renal causes – dehydration / GI losses (i.e. third spacing of fluids), bleeding resulting in hypovolemia
▪ Renal causes – nephrotoxic drugs, acute tubular necrosis
- Post-op Day 3-10
▪ Pre-renal causes – ?early sign of sepsis, inadequate hydration
▪ Others – SIADH (euvolemic patient, Serum Osm < 275mOsm/kg, Urine Osm > 100mOSm/kg, Urine Na Excretion >
40mmol/L, Serum Na < 135mmol/L)
EXTRA INFORMATION
Indication for Dialysis

- Fluid overload, Metabolic acidosis, Hyperkalaemia, Poisoning, Uremic encephalopathy, Uremic coagulopathy
- Intermittent HD – best for patients requiring rapid metabolic control (i.e. hyperkalaemia)
- Continuous Renal Replacement Therapy (CRRT) – best for patients with hemodynamically instability, volume overload, head
trauma, increased ICP or hepatic encephalopathy
70
Post-op Hypotension
- Surgical – rule out postoperative hemorrhage
- Cardiac – rule out myocardial infarction, cardiac arrhythmias, heart failure
- Lungs – rule out pulmonary embolism (massive PE present with hypotension, tachycardia and desaturation)
- GI – rule out dehydration (assess intake & output charts)
- Infectious Disease – rule out sepsis / septic shock (can be from lungs (i.e. HAP), intra-abdominal (i.e organ space abscess,
anastomotic leak), urinary (i.e. UTI), wound infection)
- Drugs – rule out iatrogenic causes (i.e. anti-hypertensive medications, anesthetics drugs)
- CNS – vasovagal causes
- Others – adrenal insufficiency, anaphylaxis (i.e. drugs)
Post-op Hemorrhage
- Primary
▪ Damage to blood vessels/vascular organs (primary haemorrhage)
▪ Unrecognized bleeding after skin closure
- Reactionary (< 24 hours)
▪ Occurs when increase BP after surgery leads to bleeding (i.e. missed vessel, slipped ligature)
▪ High risk for patients on antiplatelets / anticoagulants (failure of coagulation)
- Secondary (few days later)
▪ Usually due to infection leading to erosion of vessels at the operation site
Post-op Tachycardia
- Sinus Tachycardia (<120)
▪ Post-operative pain / Agitation (i.e. for acute retention of urine)
▪ Atelectasis
▪ Hypovolemia / Anemia
▪ Electrolytes Derangement
▪ Sepsis with fever spike
▪ Thyrotoxicosis / Hyperthyroidism
- Sinus Tachycardia (>120)
▪ Pulmonary Embolism
▪ Supraventricular Tachycardia
- Non-sinus tachycardia
▪ Atrial Fibrillation
Management of Atrial Fibrillation in Surgical Patients

- Confirm presence of AF with ECG (vs. sinus tachycardia or supraventricular tachycardia)
- Is the patient hemodynamically stable or unstable. If unstable require cardioversion
- Maintain airway, give oxygen
- Assess what is the underlying cause – sepsis (investigate cause, start antibiotics), electrolytes derangements, thyrotoxicosis,
coronary artery disease / heart failure
- Check & Correct Electrolytes – keep K > 4 and Mg > 1
- Rate Control – ABCD (amiodarone, beta-blockers, calcium channel blockers, digoxin)
▪ If patient have heart failure or low BP (be cautious with using beta blockers)
▪ Digoxin use will require a loading dose (i.e. IV digoxin 250mcg then 62.5mcg daily)
- Escalate patient to senior and/or cardiology consultation to clarify dose of medication if unsure
- Patients may need to be brought down to high dependency for closer monitoring (i.e. intra-arterial line for BP monitoring)
- Assess patient’s CHADsVASc score – discuss with patient regarding long-term anticoagulation
71
Poor Wound Healing

- Patient Factors: Poor Blood Supply, Malnutrition, Smoker, Diabetes, Radiotherapy, Drugs (i.e. steroids)
- Wound Factors: Wound Infections, Poor Wound Care
- Surgical Factors: Technical Reasons – wound closure under tension
Surgical Site Infection

- Infection occurring within 30 days of an operation or within 1 year if an implant is in place
- Superficial Incisional SSI / Deep Incisional SSI / Organ Space SSI
- Risk Factors for Surgical Site Wound Infection (SSI) – patient factors, procedural factors and perioperative factors
▪ Patient factors – age, obesity, smoking (↑2x), DM, malnutrition, HLD, immunosuppression status
▪ Perioperative factors
- Parenteral Antimicrobial Prophylaxis: administer within 30-60mins before the incision and re-dose if operative duration
is > 2 half-lives of the drug or if there is excessive blood loss, prophylaxis should be discontinued within 24 hours of
end of surgery
- Maintain perioperative normothermia, Maintain perioperative glycaemic control (<11.1)
- Antiseptic Prophylaxis – advise patient to shower with soap / antiseptic agent at least 1 night prior to surgery, intra-op
skin preparation with alcohol based agent
- Not associated with SSI
▪ Choice of skin preparation (i.e. chlorhexidine based vs iodine based)
▪ Application of antimicrobial agent (i.e. ointment) to surgical incision
▪ Administrating high concentrated oxygen
▪ Removing hair from surgical site
Wound Class Definition Examples SSI Rates23 Prophylactic Antibiotics
Elective Hernia Repair, Breast Surgery, No Antibiotics unless special
Clean No entry into hollow-viscus Varicose Vein Surgery, Lipoma Excision, < 2% indications (i.e. heart valvular
Thyroidectomy disease, other infection)
Controlled entry into hollow viscus Cholecystectomy without spillage,
Clean Antibiotics Required
without gross spillage or Hysterectomy, Appendectomy, Colorectal < 8%
Contaminated (<24 hours)
contamination Surgery
Penetrating Abdominal Injury, Open #,

Open accidental wounds, Controlled Animal or Human Bites, Enterotomy
Contaminated entry into hollow viscus with gross during bowel obstruction, ~ 15% Antibiotics Required
spillage and contamination cholecystectomy with spillage, Colorectal
Surgery
Open accidental wound with
devitalized tissue, Contaminated Perforated Diverticulitis, Feculent
Dirty > 25% Antibiotics Required
wound with existing infection, Peritonitis, Amputations
perforated viscus
Post-op Fever
- Day 0-2*
▪ Basal Atelectasis (will need aggressive chest physio)
▪ Drug Fever (i.e. malignant hyperthermia), blood transfusion
▪ Others – Prior Trauma (SIRS reaction)
- Day 3-7
▪ Wind – atelectasis / pneumonia
▪ Water – UTI (esp. if catheterized), IV line infection
▪ Walk – DVT / PE
▪ Wound – i.e. surgical site infection, intra-abdominal infection (usually occur in day 5-7), anastomotic leak
▪ Wonder Drug – Drug Fever
- Day > 7
▪ Surgical Site Infection
▪ Drug Fever
* in general, do not perform blood culture for patients who spike fever on POD 1
23 from “revision guide for surgical trainees” (2nd Edition)
72
DEEP VEIN THROMBOSIS / PULMONARY EMBOLISM

DVT in deep calf veins: 5-10% risk of PE while that in iliofemoral veins: 50-60% risk of PE
RISK FACTORS [Virchow Triad]

- Stasis: bed rest, inactivity, CHF, CVA within 3/12, air travel >6hrs
- Endothelial Injury: trauma, surgery, prior DVT, inflammation
- Thrombophilia: anti-protein C resistance, protein C/S deficiency, APS, prothrombin gene mutation, hyperhomocysteinemia,
OCP, HRT, Tamoxifen,
- Others – malignancy (active), history of thrombosis
Deep Vein Thrombosis

- Mild fever – Post-Op fever (day 5-7)
- Calf warmth, tender, swelling, erythema, venous distention, pitting oedema
- Phlegmasia Alba Dolens: swelling, pitting oedema, pallor, tenderness
- Phlegmasia Cerulea Dolens: massively swollen blue leg with pain and oedema, compresses arterial inflow leading to venous
gangrene
- Homan’s sign: calf pain on dorsiflexion, seen in <5% of patients
- Others: seizures, syncope, new-onset atrial fibrillation
- In pregnant patients – look for thromboembolism in uncommon sites (i.e. pelvic veins, upper extremities)
EXTRA INFORMATION
Pretest Probability for Deep Vein Thrombosis (Well’s Criteria)

- High Probability: ≥ 3 – treat as suspected DVT and perform compression U/S
- Moderate Probability: 1 or 2 – treat as suspected DVT and perform compression U/S
- Low Probability: ≤0 – D-dimer test
Clinical features Score
Active cancer (treatment on-going or within the previous 6 months or palliative) 1
Paralysis, paresis, or recent plaster immobilization of the lower extremities 1
Recently bedridden for more than 3 days or major surgery, within 4 weeks 1
Localized tenderness along the distribution of the deep venous system 1
Entire leg was swollen 1
Calf swelling > 3 cm compared to the ASX leg (measured below tibial tuberosity) 1
Pitting oedema (greater in the symptomatic leg) 1
Collateral superficial veins (non varicose) 1
Alternative diagnosis as likely or more likely than that of deep venous thrombosis -2
Pulmonary Embolism
- Dyspnoea (73%), pleuritic chest pain (66%), cough (37%), haemoptysis* (13%)
- ↑RR (>70%), crackles (51%), ↑HR (30%), fever, cyanosis
- MASSIVE PE: syncope, hypotension, PEA, CCF (↑JVP, S3)
* haemoptysis is rare because of dual circulation – bronchial and pulmonary
INVESTIGATIONS
DVT → Duplex ultrasound: 95% sensitivity and specificity for symptomatic DVT
Pulmonary Embolism (PE) – diagnostic studies

- Chest x-ray: usually normal (classical findings listed below are rarely seen)
▪ Atelectasis, Pleural effusion (transudate or exudate), Raised hemi-diaphragm,
▪ Hampton hump: late sign, wedge shaped infiltrate with apex towards the hilum,
▪ Westermark sign: dilatation of the pulmonary vessels proximal to the embolism, with collapse of the distal vessels (oligemia)
- ECG24
▪ T wave inversion in V1-V4 (most common abnormality; quoted: 68%)
24 CHEST 1997; 111:537-43
73
▪ Sinus tachycardia, AF rhythm , Signs of RV strain: Right axis deviation, P pulmonale, RBBB
▪ Rarely will have the classical S1Q3T3 feature
- ABG: hypoxemia, hypocapnia, respiratory alkalosis [elevated A-a gradient]
- D-Dimer: YEARS Study Group25
▪ Suspect PE: (1) clinical signs of DVT, (2) haemoptysis, (3) Is PE the top suspect
▪ If 0 YEARS items & D-dimer ≥ 1.0mcg/ml: proceed with CTPA
▪ If 0 YEARS items & D-dimer < 1.0mcg/ml: PE excluded
▪ If ≥1 YEARS items & D-dimer ≥ 0.5mcg/ml: proceed with CTPA
▪ If ≥1 YEARS items & D-dimer < 0.5mcg/ml: PE excluded
- If PE is not your top suspect, do CTPA if D-dimer ≥ 1.0mcg/ml. If PE is your top suspect, do CTPA if D-dimer ≥ 0.5 mcg/ml
- CT pulmonary angiogram (gold standard), look for filling defects in pulmonary artery
- Echocardiogram (for patient’s too unstable to travel)
EXTRA INFORMATION
A-a gradient
A-a gradient = PAO2 – PaO2
PAO2 (from alveolar gas equation) = F iO2 x (PATM – PH2O) – PACO2 / 0.8 | estimated 150 – 1.25 x PACO2
PaO2 (from ABG) = average 75 – 100mmHg
FiO2 ~ 0.21
PATM ~ 760mmHg
PH2O ~ 47mmHg
PACO2 ~ PaCO2 (arterial CO2 – get from ABG)
Respiratory Quotient ~ 0.8
5 causes of hypoxemia
1. V/Q mismatch (i.e. PE, CHF, ARDS, atelectasis) – elevated A-a gradient
2. Shunt (i.e. PFO, ASP, pulmonary AVMs) – elevated A-a gradient
3. Alveolar hypoventilation (i.e. ILD, environmental lung disease) – elevated A-a gradient
4. Hypoventilation (i.e. COPD, CNS dysfunction, neuromuscular disease) – depressed A-a gradient
5. Low FiO2 (i.e. high altitude) – depressed A-a gradient
25 Lancet. 2017 Jul 15;390(10091):289-297. [Important Paper]
74
MANAGEMENT
Non-pharmacological
- Use of pneumatic calf pumps intra-operatively and postoperatively (or TED stockings)
- Early, aggressive ambulation post-surgery
Pharmacological
- Unfractionated heparin or LMWH
- Warfarin
- Novel Oral Anticoagulation (NOAC)
Unfractionated heparin (onset: IV = immediate, SC = 30min, ½ life: 1-2hrs)

- Potentiates effect of antithrombin III, inactivates thrombin (PTT increases)
- Efficacy monitored using aPTT
- Antidote: protamine sulphate
- Side effects: heparin-induced thrombocytopenia and thrombosis (HITT, type 2) – occurs 4-10 days after exposure (immune
mediated, suspect when platelet count < 100,000 or drop by > 50% from baseline) → predispose to thrombosis (STOP heparin!
& start another anticoagulant – i.e. direct thrombin inhibitor (DTI) – i.e. argatroban / Bivalirudin / Lepirudin*
LMWH (Clexane/Enoxaparin) (onset: as above, ½ life: 4-5hrs)

- Potentiates effect of anti-factor 10a (not reflected by PTT)
- More predictable dose-effect relationship
- Reversibility by protamine sulphate limited (60% reversal)
- Excretion exclusively renal, require dose reduction in patients with renal failure
Warfarin (Vitamin K antagonist) – long-term (onset: 2-4days, goal INR 2-3)

- Antagonise Vitamin K recycling → inhibits synthesis of factors II, VII, IX, X, Protein C / S (3-5 days)
- Start with heparin for ≥ 5 days, stop heparin when target INR reached
- Antidote: vitamin K, FFP, Factor IX complex, PCC
▪ Prothrombin Complex Concentrate (PCC) – mixture of vitamin K dependent protein (II, VII, IX, X, Protein C / S) → reliably
reduces INR to < 1.3 in 62% of patients treated with PCC within 30mins (compared to 10% of patients with FFP)
- Have potential for drug – drug interactions (via the cytochrome P450 (CYP) metabolic pathway)
▪ Warfarin effects increased with concomitant intake of macrolides, quinolones, metronidazole, bactrim
▪ Warfarin effects decreased with intake of anticonvulsants, rifampicin, chronic alcohol, St John’s Wort
- Dietary restriction (low vitamin K diet)
- Rare but important – warfarin induced skin necrosis (WISN) – can induce a paradoxical transient hypercoagulable state in
first few days, (especially in patients with protein C deficiency, have shorter ½ life), increase risk of thrombosis and skin necrosis.
(risk of WISN increased in setting of HITT)
New Oral Anticoagulants (NOAC)

- Direct Thrombin Inhibitors – argatroban, dabigatran | antidote: Idarucizumab
▪ Argatroban is cleared by the hepatobiliary system.
▪ Dabigatran is cleared by the kidneys (contraindicated if eGFR < 30ml/min)
- Factor Xa inhibitors – rivaroXaban,, apiXaban | antidote: PCC, andexanet-alfa (phase III trials)
- Benefit of once daily oral therapy
Surgical
- IVC filter – Indications (risk of PE after IVC filter is 0.7 to 4.0%)
▪ Anticoagulation contraindicated
▪ Occurrence of PE in the presence of adequate anticoagulation
Treatment options for PE

- Supplemental oxygen, intubation, mechanical ventilation
- Anticoagulation – LMWH
- Thrombolysis – TPA 100mg over 2 hours (for large, proximal PE + hemodynamic compromise)
- Surgical/ catheter embolectomy
- Thrombectomy (for large, proximal PE + hemodynamic compromise + CI to lysis)
75
EXTRA INFORMATION
Choice of Treatment
- Pregnant Patients – LMWH (potential for other agents to cross placenta)
- Cancer Patients – LMWH
- Renal Disease with CrCl < 30ml/min – VKA (NOACs and LMWH are contraindicated in severe renal disease)
- Liver Disease with coagulopathy – LMWH (NOAC contraindicated if INR raised due to liver disease, VKA difficult to titrate)
- Patients with epidural catheter – UFH may be started 1 hour after catheter removal, LMWH may be started 4 hours after
catheter removal (patients with PE)
Long Term Treatment for DVT / PE

- 1st unprovoked proximal DVT or PE: long term anticoagulation (minimum 3 months)
- 1st unprovoked distal DVT or PE: 3 months
▪ Isolated distal DVT (asymptomatic) – serial imaging for 2 weeks, anticoagulation if thrombus extends
▪ Isolated distal DVT (symptomatic, risk of extension) – anticoagulate
- For provoked (i.e. surgery) DVT / PE: anticoagulation for 3 months
- For cancer associated DVT / PE: extended therapy (lifelong) – preference (LMWH)
- For pregnancy associated DVT / PE: anticoagulation with LMWH for duration of pregnancy and for at least 6 weeks postnatally
(total of at least 3 months of treatment)
▪ Postpartum warfarin or heparin (UFH, LMWH) are not contraindicated in breastfeeding
Upper Limb DVT

- Primary (20%): venous thoracic outlet syndrome or effort related thrombosis
- Secondary (80%): thrombosis from an indwelling central venous catheter, pacemaker or defibrillator
- Complications with UL DVT is less as compared to LL DVT
▪ PE risks: 6% vs 15-30%
▪ Recurrence at 12 months: 2-5% vs 10%
▪ Post-thrombotic syndrome: 5% vs 56%
- Treatment
▪ Anticoagulation with clexane or heparin followed by warfarin for 3 to 6 months
▪ If DVT is secondary to indwelling catheter – catheter can be left in place (if functional)
76
LOCAL ANAESTHESIA
Local Anesthesia can be classified as amides (double i) or esters (single i) – usually injected into the subcutaneous layer to block
pain transmission from the free nerve endings located in the epidermal and dermal layers
Physiology
- Reversibly block sodium channel within nerve fibres hence prevent transmission of pain signals by disrupting depolarization of
the nerves
- LA (i.e. lidocaine) comes in HCO3- buffer to keep it unionized so it can cross the lipophilic membrane to act on sodium channel,
however, in acidic medium, it gets ionized and can no longer cross the membrane to effectively block nerve conduction
- Pain fibres (unmyelinated) as compared to afferent fibres (for touch / temperature / muscle contraction) 🡪 relief of pain without
muscle paralysis
Choice of Anaesthetic
- Lidocaine WITHOUT epinephrine = 4mg/kg (0.4ml/kg of lidocaine 1%) – max dose 300mg
▪ Onset – 2-5mins, Duration – 30mins to 2 hours
- Lidocaine WITH epinephrine = 7mg/kg^ (0.7ml/kg of lidocaine 1%) – max dose 500mg
▪ Onset – 2-5mins, Duration – 60mins to 3 hours
▪ Avoided for digital anaesthesia in patients with peripheral arterial disease
- Bupivacaine (Marcaine) WITHOUT epinephrine = 2mg/kg (0.8ml/kg of bupivacaine 0.25%), max dose 175mg
- Bupivacaine (Marcaine) WITH epinephrine = 3mg/kg (1.2ml/kg of bupivacaine 0.25%), max dose 225mg
▪ Onset – 5-10mins, Duration – up to 6 hours
^ Vasoconstriction caused by epinephrine limits the initial serum peak concentration
Complications
- Allergic Reaction – contact dermatitis, urticaria, anaphylaxis
- Central Nervous System – perioral numbness (early), tingling of lips, metallic taste, tinnitus, agitation (i.e. tremors, shivering,
muscle twitching), tonic-clonic seizures (esp. with bupivacaine toxicity) – which can progress to drowsiness/sedation, respiratory
depression
▪ Treatment of seizures – intravenous BZD (i.e. midazolam)
- Cardiovascular – bradycardia, ↓myocardial contractility, AV block, vasodilatation, arrhythmias
▪ Treatment of cardiac arrhythmia – IV fat emulsion
77
3. ACUTE ABDOMEN
APPROACH TO ACUTE ABDOMEN
DEFINITION
The presence of an abdominal pathology which if left untreated (<72 hours) will result in patient morbidity and mortality26
- Sudden onset of severe abdominal pain (new pain or an increase in chronic pain) is the hallmark of the acute abdomen
- Most common general surgical problem presenting to the emergency department
- Abdominal Pain arising from intra-abdominal pathology originates in the peritoneum (visceral and parietal layer)
- A transition from visceral to somatic pain indicates extension of the underlying process
Visceral Parietal Referred Pain

Bilaterally by the autonomic nervous Results from central neural pathways
Unilaterally via spinal somatic nerves
Innervation system (sympathetic and that are common to the somatic nerves
that also supply abdominal wall
parasympathetic) and visceral organs
Irritation of the parietal peritoneum –
Predisposing Stretch (distension, pressure, traction), inflammatory cause (i.e. peritonitis) or (i.e. biliary tract pain referred to right
Factors Inflammation, Ischemia mechanical cause (i.e. surgical inferior scapular area)
incision)
Embryologic origin of the affected organ
Well-localized pain though distant from
Site of Pain determines location of visceral pain in the Well-localized pain
the involved organ
abdominal midline* (poorly localized)
Character of Pain Dull, cramping or burning Sharp, severe Produces symptoms not signs
* Organs transmit sympathetic sensory afferent to both side of the spinal cord
History
Evaluation of abdominal pain can be via the SOCRATES (site, onset, character, radiation, associated symptoms, timing, exacerbating
and relieving factors, severity).
Patient’s Bio-data
- Age: older patients ↑ risk of AAA, mesenteric ischemia, atypical presentations of AMI, colon cancer
- Women of childbearing age: possibility of pregnancy!
Presenting Complaint
- Onset & Duration of Pain
▪ Seconds to Minutes – infarction (AMI, mesenteric ischmia), ruptured (AAA, HCC, ectopic pregnancy), perforation (perforated
viscus)
▪ Minutes to Hour – inflammation (Pancreatitis, Diverticulitis), colic (Biliary colic, Ureteral colic, Small Bowel Obstruction),
Ischemia (Strangulated Intestinal Obstruction / Hernia, Volvulus)
▪ Several Hours – inflammation (Acute appendicitis, chronic pancreatitis, IBD, peptic ulcer disease), obstruction (Non-
strangulated Bowel Obstruction)
- Character of Pain
▪ Colicky Pain: waxing and waning pain which occur secondary to hyper-peristalsis of smooth muscle against a mechanical
site of obstruction. Exception: biliary colic – constant, intense pain that lasts for 30min to several hrs.
▪ Sharp Persistent Severe Pain – infective or inflammatory process
▪ Burning Pain – ulcer
▪ Tearing Pain – aortic dissection
- Radiation of Pain
▪ Back – Pancreatitis, AAA, Aortic Dissection
▪ Shoulder Tip or Angle of Scapula
- Right – Cholecystitis, Liver Abscess, Subphrenic Abscess, Perihepatitis (Fitz Hugh Curtis syndrome)
- Left – Splenic Abscess, Subphrenic Abscess
▪ Loin to Groin – Renal Colic (begin in patient’s back and radiate to the ipsilateral groin)
▪ Flank – Pyelonephritis, Retroperitoneal Hematoma, AAA
- Associated Symptoms
▪ Systemic
- Fever or chills – suggest inflammatory or infectious process
26 Acute Care Surgery (L.D. Britt, A.B. Peitzman, P.S. Barie, G.J. Jurkovich)
78
3. Acute Abdomen_Last Updated 3rd June 2020
- Anorexia – very non-specific symptoms

- Weight loss – any other constitutional symptoms suggestive of underlying malignancy
▪ Cardiac / Lung symptoms (dyspnea, cough, chest pain)
▪ GI symptoms
- Nausea & Vomiting – vomiting before suggest ?GE, vomiting after suggest ongoing inflammatory process
- Bilious Vomit – suggest process distal to the duodenum
- Hematemesis – suggest peptic ulcer, esophagitis
- Abdominal distension – obstruction, ascites
- Diarrhoea – GE/food poisoning, colitis
▪ Jaundice – acute cholangitis, choledocholithiasis, hepatitis,
▪ Urinary symptoms (dysuria, frequency, urgency, hematuria)
▪ O&G-related symptoms (vaginal bleeding, abnormal vaginal discharge, menstrual changes)
- Time Course of Pain (any pattern)
- Exacerbating and Relieving Factors

▪ After meals – gastric ulcer pain worsens with food, duodenal ulcer pain improves, biliary colic worsens after fatty meal
▪ Pancreatitis – pain improves with sitting upright and leaning forward
▪ Diffuse Peritonitis – hallmark: pain worse with movement improved by lying still
▪ Renal Colic – hallmark: writing in pain, unable to keep still, loin to groin pain
▪ Intestinal Obstruction – visceral pain relieved after vomiting (abdominal pain, distention, vomiting, obstipation)
- Severity of Pain (pain score 1 to 10) → pain out of proportion to examination findings – suspect mesenteric ischemia
Past Medical/Surgical History

- Medical conditions may precipitate intra-abdominal pathology
- Risk Factors for Abdominal Vascular Disease (AAA / Mesenteric Ischemia)
▪ Peripheral Vascular Disease
▪ Coronary Artery Disease / Atrial Fibrillation
- Risk Factor for Bowel Obstruction / Perforation
▪ History of Cancer
▪ History of Peptic Ulcer Disease
- Exclusion of extra-abdominal causes of abdominal pain
▪ Myocardial Ischemia / Lower Lobe Pneumonia
- Exclusion of gynaecological causes of abdominal pain
▪ Last Menstrual Period – if suspect ectopic pregnancy
- Previous surgery – ↑ risk of IO
- Orthopaedic conditions – use of painkillers
Drug History
- Risk Factors for complications of Peptic Ulcer Disease (any NSAIDs* ingestion (eg aspirin, ibuprofen))
- Risk factors for constipation (i.e. anticholinergics – antihistamines, antispasmodics, antidepressants, antipsychotics)
- Other important medications of note
▪ Beta blockers, corticosteroids – may mask symptoms and signs
▪ Antibiotics – mask pain caused by peritonitis, prolonged antibiotics may lead to pseudomembranous colitis (PMC) caused
by clostridium difficile
▪ Opioid Analgesia – even if administered prior to PE, it is not a/w decrease in diagnostic accuracy27
Social History
Family History
Systemic Review
27 Ann Emerg Med. 2006 Aug;48(2):150-60
79
Physical Examination
Aim to evaluate the presence or absence of peritonitis – i.e. guarding, rebound tenderness, pain on coughing.
General Appearance
- Lying motionless (Diffuse Peritonitis)
- Restless, writhing in pain, knees curled up (Ureteric Colic, Intestinal Colic)
- Bending Forward (Pancreatitis)
Vital Signs + Peripheral Signs

- Hemodynamic Instability – r/o life threatening causes of abdominal pain
- Fever – suggests inflammatory (i.e. pancreatitis) or infective (i.e. appendicitis, cholecystitis, cholangitis, pneumonia) pathology
▪ Older/immunocompromised pts may not be able to mount fever
- Peripheral signs: jaundice, pallor, peripheral vasoconstriction, hydration status
Abdominal Examination
- Inspection (from the foot of the bed)
▪ Distension, Surgical Scars, Bulging Masses, Area of erythema, Pulsations, Peristalsis
- Palpation (patient in supine position, eyes fixed on patient’s eye)
▪ Where is the tenderness located? Which quadrant?
▪ Peritoneal Signs – rebound tenderness, guarding, board-like rigidity
▪ Any palpable masses
▪ Hernias – incisional, umbilical, inguinal, femoral
▪ Pain out of proportion to PE findings – suggest mesenteric ischemia
- Assess for Renal punch
- Percussion
▪ Dullness over bladder – acute retention of urine
▪ Tympanic sounds over distended bowel – intestinal obstruction
- Auscultation
▪ Absence of bowel sounds – possibly ileus from diffuse peritonitis
▪ High-pitched tinkling bowel sounds – suggestive of obstruction
▪ Bruit – AAA
- Rectal Examination – DRE (any PR bleeding, any masses)
- Pelvic Examination – PV + bimanual examination
- Testicular Examination
Cardiorespiratory Examination
- Any signs of pleurisy, AMI, basal pneumonia
- AF – ↑ risk of mesenteric ischemia
Others
- Evidence of coagulopathy
Classical signs in patients with abdominal pain

Sign Findings Association
Cullen’s Bluish Periumbilical Discoloration
Retroperitoneal Haemorrhage
Grey Turner’s Discolouration of the flanks
Murphy’s Inspiratory Arrest with continuous palpation of gallbladder Acute Cholecystitis
Mc Burney’s Tenderness, 1/3 distance from ASIS to umbilicus on R. side
Psoas Hyperextension of R hip causes abdominal pain Appendicitis
Obturator Internal Rotation of flexed right hip cause abdominal pain (Psoas – retrocecal; obturator – pelvic)
Rovsing’s RLQ pain with palpation of the left lower quadrant
80
DIFFERENTIAL DIAGNOSIS
Common causes of Acute Abdominal Pain28

- Non-specific abdominal pain (NASP) (35%)
- Acute appendicitis (17%), Intestinal Obstruction (15%), Urological causes, Gallstone disease, Colonic diverticular disease,
Abdominal Trauma, Perforated peptic ulcer, Pancreatitis
- O&G conditions (i.e. PID, ovarian cyst, Endometriosis, Mittelschmerz)
- Others – ruptured AAA, inflammatory bowel disease, mesenteric ischemia, medical causes (i.e. MI, lobar pneumonia)
Rare causes of Acute Abdominal Pain

- Omental Infarct (torsion of omentum around its vascular pedicle or thrombosis or vasculitis of the omental vessel)
- Omental Cyst (asymptomatic abdominal mass) – freely moving intra-abdominal mass
- Sclerosing Mesenteritis (inflammatory and fibrotic process involving the intestinal mesentery) – conservative Mx
- Mesenteric Cyst (asymptomatic or abdominal pain secondary to compressive effect / torsion of cyst)
- Epiploic appendagitis (benign and self-limiting inflammation of epiploic appendages)
- Rectus Sheath Hematoma (palpable abdominal mass that remains unchanged with contraction of rectus muscle) – usually
conservatively managed with reversal of anticoagulation and regular FBC checks.
Life Threatening Causes of Acute Abdominal Pain29

If patients present with acute abdomen with hypotension, consider the following, ruptured AAA, ruptured HCC, ruptured ectopic
pregnancy, ruptured spleen, ruptured splenic artery aneurysm.
1. Perforated Viscus (i.e. perforated peptic ulcer most common)

▪ Can presents to A&E 2-3 days after onset of epigastric pain
▪ Suspected in individuals with hx of PUD symptoms and who develop sudden onset of severe, diffuse abdominal pain
▪ Others causes includes:
- Perforated oesophagus (Boerhaave syndrome)
- Perforated bowel (ischemic bowel, toxic megacolon, diverticulitis)
2. Ruptured HCC
3. Ruptured Abdominal aortic aneurysm (AAA) or Aortic Dissection
▪ Risk Factors: advanced age (>60 years). COPD, pulmonary disease, PVD, HTN, smoking and family history
▪ Hallmark: pulsatile epigastric mass, if ruptured, exsanguinating haemorrhage, unstable hypotension
4. Mesenteric Ischemia (i.e. ischemic bowel / ischemic colitis)
▪ Risk Factors: advanced age, ATH, low cardiac o/p state, cardiac arrhythmias (i.e. AF), severe cardiac valvular disease,
recent AMI, intra-abdominal malignancy
▪ Strangulated Bowel (i.e. strangulated hernia)
▪ Hallmark: acute onset of severe periumbilical abdominal pain out of proportion to findings on physical examination
5. Severe Hemorrhagic Pancreatitis
6. Splenic Rupture (i.e. secondary to EBV, leukemia, trauma)
7. Medical Conditions (i.e. diabetic ketoacidosis, acute MI, Addison’s Disease (Addisonian crisis)
8. Obstetric Conditions – Women of childbearing age with abdomen pain should get a UPT!
▪ Ruptured Ectopic Pregnancy
▪ Placental Abruption
▪ Ovarian Torsion
Red Flag Signs & Symptoms for Acute Abdominal Pain

History Pain Characteristics PE Findings
- Age >65 - Sudden onset - Tense or rigid abdomen
- Immunocompromised (eg HIV) - Maximal at onset - Involuntary guarding
- Alcoholism – risk of pancreatitis, cirrhosis, hepatitis - Pain then subsequent vomiting - Signs of shock
- CVS disease (eg IHD, hypertension, PVD, AF) - Constant pain of < 2 days
- Major comorbidities (eg cancer, diverticulosis, gallstones, IBD,
pancreatitis, renal failure)
- Prior surgery of recent GI instrumentation – risk of obstruction,
perforation
- Early pregnancy – risk of ectopic pregnancy
Differential Diagnosis based on site of Acute Abdominal Pain
28 Core topics in General & Emergency Surgery, A Companion to Specialist Surgical Practice (5 th edition) – pg. 84
29 uptodate: Evaluation of the adult with abdominal pain in the emergency department
81
RIGHT UPPER QUADRANT EPIGASTRIC LEFT UPPER QUADRANT

- Biliary: biliary colic, acute cholecystitis, - Pancreas: Pancreatitis - Spleen: splenomegaly, splenic infarct,
acute cholangitis, sphincter of Oddi - GI: PUD, GERD, gastritis, functional splenic abscess, splenic rupture
dysfunction dyspepsia, gastroparesis/GOO - Thoracic: pneumonia, AMI
- Hepatic: acute hepatitis, perihepatitis - Thoracic: AMI, pericarditis, ruptured aortic - Others: pancreatitis, PUD, gastritis,
(Fitz-Hugh-Curtis syndrome), liver aneurysm diverticulitis
abscess, Budd-Chiari syndrome, portal
vein thrombosis
- Thoracic: pneumonia, subphrenic
abscess, pulmonary embolism, empyema
- Others: pancreatitis, PUD, appendicitis
RIGHT FLANK PERIUMBILICAL LEFT FLANK
- Biliary (see RUQ) - GI: acute appendicitis (early), GE, IO - Spleen (see LUQ)
- Urological: - Others: ruptured aortic aneurysm, pancreatitis - Urological (see right flank)
- Infection: pyelonephritis, abscess
- Obstruction: hydronephrosis, DIFFUSE
nephrolithiasis, ureteral obstruction - Intestinal obstruction
- Cancer: RCC, TCC renal pelvis, - Viscera perforation
bladder Ca - Mesenteric ischemia
- Others: PKD, renal cyst, - IBD: ulcerative colitis, Crohn disease
angiomyolipoma, infarction - Infection: viral GE, food poisoning, colitis
- Peritonitis: SBP (in advanced liver disease),
peritoneal dialysis pts
- Malignancy: CRC, Gastric CA, pancreatic CA
- Ketoacidosis: diabetic, alcoholic
- Adrenal insufficiency
- Irritable bowel syndrome
- Constipation
- Diverticulosis
- Intolerance: coeliac disease, lactose
intolerance
RIGHT ILIAC FOSSA HYPOGASTRIC LEFT ILIAC FOSSA
- GI: acute appendicitis, terminal ileitis, - Urogenital: acute urinary retention, - GI: diverticulitis (Caucasian pts), inguinal
diverticulitis (Asian pts), Meckel’s cystitis/UTI, testicular torsion hernia, constipation
diverticulum, mesenteric adenitis, inguinal - O&G: ectopic pregnancy, pregnancy - Urological (see RIF)
hernia complications, PID, fibroid complications, - O&G (see RIF)
- Urological: urolithiasis, pyelonephritis adenomyosis, endometriosis, endometritis, - Ortho:
- O&G: ovarian cyst rupture, ovarian ovarian hyperstimulation, ovarian Ca - Infection: hip septic arthritis, TB
torsion, Mittelschmerz (ovulatory pain), hip
ectopic pregnancy, salpingitis - Degeneration: OA hip
- Ortho (see LIF) - Inflammation: RA hip, ankylosing
spondylitis, Reiter’s syndrome
- Infiltration: primary bone tumour
(hip), mets to hip
- Destruction: # of NOF/pubic rami
- Radiation: back pathologies
(referred pain)
- Paediatric: transient synovitis,
Perthes’ disease, SCFE
82
INVESTIGATIONS
Haematological Investigations
- Full Blood Count
▪ Haemoglobin (Hb) – signs of anemia or occult bleeding, in acute bleeds due to hemoconcentration, Hb can be falsely
elevated – correlate with other parameters
▪ Mean Corpuscular Volume (MCV) – can be low if have iron deficiency secondary to GI blood loss
▪ Haematocrit (Hct) – low haematocrit can be due to occult blood loss
▪ White Blood Cell (WBC) – infectious source present (older/immunocompromised pts may have normal WBC counts)
▪ Left Shift on the differential – indicate presence of an inflammatory source
- Fingerpick/serum glucose – to r/o DKA
- Urea Electrolyte Creatinine (U/E/Cr)
▪ Hypokalemic, Hypochloremic and Metabolic Alkalosis – prolonged vomiting and severe volume depletion (gastric outlet
obstruction) – a/w high urea and creatinine if patient is dehydrated
▪ Low Serum Bicarbonate or Metabolic Acidosis – ?general tissue hypo-perfusion (intestinal ischemia)
▪ HypoK+ / HypoCa2+ can cause ileus, third spacing can also cause electrolyte imbalance
▪ Cr – for suitability of contrast scans*
- Liver Function Test (LFTs) – Hepatitis vs. obstructive vs. mixed picture
- Pancreatic Enzymes (amylase and lipase)
▪ Serum amylase peaks at 6-24 hours (if > 3x normal limits) suggestive of acute pancreatitis.
▪ Serum lipase more sensitive and specific for pancreatitis
▪ Amylase can also be raised in perforated viscus, IO, ischemic bowel, ectopic pregnancy
- Cardiac Enzymes (CK/CKMB/Trop T), ECG – r/o ACS
- Lactic Acid Level (consideration of intestinal ischemia) / ABG
▪ Serum lactate as an indicator of tissue hypoxia (suggestive of mesenteric ischemia or worsening sepsis)
- Urinalysis – UFEME / UC9
▪ Assess urological causes of abdominal pain
- Urine Pregnancy Test (b-Human chorionic gonadotropin)
- In woman (with UPT +) with abdominal pain or vaginal bleeding, findings of serum beta-hCG < 1500mIU/ml is associated with a
higher risk of ectopic pregnancy30
- GXM / PT/PTT – if surgery required
Radiological Investigations
- Erect Chest X-Ray – look for free air under the diaphragm (diff dx: Chilaiditi syndrome – transposition of transverse colon between
diaphragm and liver)
- Supine Abdominal X-Ray or KUB
▪ Free air distribution throughout SB (jejunum – valvulae conniventes) and LB (haustrations)
▪ Coffee Bean Sign (‘bent inner tube’ – indicative of sigmoid volvulus)
▪ Calcifications – most urinary stones are radio-opaque (90%), only 15% of gallstones are calcified
▪ Sentinel Loop in acute pancreatitis / other inflammatory conditions
▪ “Stack of coins” appearance, “string of beads” sign, air-fluid levels – intestinal obstruction
▪ Rigler’s sign – intra-abdominal free air
▪ KUB – can look for rectal gas (beware of the presence of colonic gas following DRE)
- Erect/left lateral decubitus Abdominal X-Ray (not routine) – look for air-fluid level
- Ultrasonography
▪ Operator dependent
▪ Useful for AAA, gallbladder disease, trauma (FAST), renal and O&G conditions.
▪ Acute Cholecystitis – diagnosed via (1) thickened gallbladder wall (>3mm), (2) pericholecystic fluid, (3) stone impacted at
neck of gallbladder and (4) sonographic murphy’s sign. US can detect up to 95% of gallstones
- Computed Tomography (CT)
▪ Evaluate acute mesenteric ischemia and GI bleeding with CT angiography
▪ Useful for evaluating retroperitoneal structures (suspected leaking AAA) and undifferentiated abdominal pain
- Magnetic Resonance Imaging (MRI)
▪ Greatest application in pregnant women with acute abdominal and pelvic pain
30 Acad Emerg Med. 2003 Feb;10(2):119-26
83
INVESTIGATIONS
Aim to decide – (a) early operation required, (b) early operation not required, (c) early operation uncertain
- History & Physical Examination

- Adequate Resuscitation
▪ Vitals monitoring
▪ IV hydration
▪ Monitor fluid balance – strict I/O, ± insertion of urinary catheter
▪ ± Insertion of nasogastric tube (if suspect intestinal obstruction)
▪ Evaluate if need closer monitoring (i.e. IA line)
- Adequate Analgesia – Paracetamol 1mg 6H (PRN) & Tramadol 50mg 8H (PRN) – good to give opiate analgesia*
- NBM if pending further diagnostic tests to evaluate if need early operation
- Further diagnostic tests (as required)
▪ Serial abdominal examination – useful for abdo pain of unclear etiology
▪ FBC / RP1 / LFT / Amylase / UFEME should be performed in A/E
▪ Trending of inflammatory markers (i.e. TW) – higher discriminatory power
▪ ± ABG, Lactate (trend more useful than single value)
▪ ± erect CXR (initial test for suspected perforation)
▪ ± supine AXR (suspected intestinal obstruction, perforation)
▪ ± CT AP with contrast (does it affect decision to operate – i.e. intestinal obstruction in virgin abdomen, underlying peritonism
with suspicion of perforation)
▪ ± US HBS (for suspected acute biliary disease)
▪ ± Diagnostic laparoscopy
- Treat underlying aetiology
▪ IV broad spectrum antibiotics (i.e. IV rocephin 2gm OM & IV flagyl 500mg TDS) if septic / diagnosis confirmed (i.e.
cholecystitis, acute appendicitis, acute diverticulitis, liver abscess, cholangitis, suspected cholangitis (with pancreatitis),
perforated viscus)
- Inform senior, OT, HD or ICU early if necessary and/or if in doubt
84
INTESTINAL OBSTRUCTION
DEFINITION
Intestinal obstruction occurs when normal flow of intestinal contents is interrupted. It can be classified pathologically into mechanical
obstruction (dynamic) or function obstruction (adynamic)
“Small bowel obstruction is more common than large bowel. The most common causes of small bowel obstruction are adhesions,
hernia, strictures and cancers. The most common causes for large bowel obstruction are cancers, cancers, cancers, diverticular
disease or volvulus”
PATHOPHYSIOLOGY
Range of clinical manifestation of bowel obstruction – simple obstruction > bowel ischemia > gangrenous bowel > perforation
- Characterized by collapse of bowel distal to obstruction with proximal dilatation

▪ Gas Accumulation: significant overgrowth of both aerobic and anaerobic organisms & from swallowed air
(gas composition – O2 , CO2 , H2S & N2)
▪ Fluid Accumulation: impaired absorption from gut leading to sequestration of fluid into the bowel lumen (risk of
dehydration and electrolyte imbalance)
- If obstruction is not resolved (i.e. strangulated bowel), proximal bowel dilation increases which compromises venous return.
- This leads to increased capillary pressure with resulting compromised arterial supply leading to bowel ischemia
▪ Bowel undergoes hemorrhagic infarction (risk of bacterial translocation into peritoneal cavity) which put it as risk of
▪ Bowel perforation leading to peritonitis, sepsis and eventual septic shock
The aim of the history and examination is to determine the likelihood of the patient having intestinal obstruction and to determine the
level of obstruction. Also, consideration must be given for potential complications such as bowel ischemia and/or perforation.
History (4 cardinal symptoms)

- Visceral pain secondary to distention – colicky in nature
Pain - Centred on the umbilicus (small bowel) or lower abdomen (large bowel)
- Progression to more focal, constant pain → need to rule out complications (i.e. perforation / peritonitis)
- Ask if projectile, bilious or faecal stained

- Quantify amount of vomitus (assess hydration)
- Time and load of vomitus can determine if obstruction is proximal or distal
Vomiting
▪ Proximal Small Bowel Obstruction: greenish blue, bile stained (obstruction distal to ampulla of vater)
▪ Distal Small Bowel Obstruction: brown and increasingly foul smelling (feculent = thick brown foul)
▪ Large Bowel: uncommon to have vomiting esp. if competent ileocecal valve, usually late symptom
- Prominent feature in large bowel or distal small bowel obstruction
Abdominal
- Usually not seen in proximal small bowel obstruction, esp. if patient is vomiting
Distention
- Large Bowel closed loop obstruction: RIF bulge that is hyper-resonant
Constipation / - Constipation: no bowel output but still passing flatus, Obstipation: no bowel output and no flatus passed
Obstipation - Ask patient about NORMAL BOWEL OUTPUT FREQUENCY
Other pertinent history

- Associated symptoms eg GI bleeding
- Previous pelvic or abdominal surgeries or irradiation & any complications from surgeries
- Previous admission for intestinal obstruction
- History of hernias
- History of GI disorders (eg intra-abdominal inflammation, IBD, gallstone disease)
- Risk factors for ischaemic bowel: atherosclerotic, heart disease, atrial fibrillation, previous stroke
- Suspicion of malignancy: LOW, LOA, Previous Cancer, Family history of cancer (any previous colonoscopy)
- Drug history (i.e. loperamide)
History suggestive of complications

- Worsening abdominal pain, pain out of proportion to examination
- Fever
- GI bleeding (i.e. altered blood)
85
- Vitals: Is the patient stable? Any fever? (sepsis) Hypotension, tachycardia/AF? (dehydration – hallmark of SBIO)
- General inspection: Abdominal distension? Cachexia? Confusion?
- Peripheries: Look for signs of dehydration e.g. capillary refill, dry tongue, palpate lymph nodes (i.e. virchow’s node)
- Abdomen:
▪ Any abdominal distension?
▪ Scars from previous abdominal surgery?
▪ Visible peristalsis? – severe obstruction
▪ Signs of peritonitis: guarding, tenderness, rebound tenderness?
▪ Any palpable abdominal masses?
▪ Any hernia – incisional hernia, inguinal, femoral (assess for reducibility)
▪ Bowel sounds: initially hyperactive, later may be sluggish or absent, tinkling BS: small bowel obstruction
▪ Succussion splash + epigastric tenderness: gastric outlet obstruction
- DRE: any intraluminal mass, any impacted stools, blood
The causes for intestinal obstruction can be divided into mechanical (peristalsis working against a mechanical obstruction) of
functional (absence of peristalsis without obstruction)
Mechanical Causes
- Intussusception (small bowel neoplasm usually as lead point)
- Impaction (severe constipation) – i.e. bed-ridden patients (8%)
- Bezoars (tricho- / phyto- / pharmaco-, eg PICA syndrome)
Intra-luminal
- Gallstone ‘ileus’
- Foreign Body (ingested / iatrogenic)
- Parasites (ascaris lumbricoides, strongyloides stercoralis)
- Malignancy (15%)
- Strictures
▪ Malignant Stricture,
Intra-mural ▪ Inflammatory Strictures (TB / Crohn’s, diverticulitis, radiation colitis)
▪ Anastomotic stricture post-op
▪ Ischemic stricture (PAD, aortic surgery, colon resection)
- Congenital malformations, atresia
- Intraperitoneal bands and adhesions (40%)
▪ Risk Factors: previous surgery, diverticulitis, peritonitis, Crohn disease, endometriosis (open adnexal
operations have highest rate of adhesion related admissions)
Extra-mural - Hernia (12%)
- Volvulus – sigmoid / cecum (more commonly sigmoid)
- Peritoneal carcinomatosis (i.e. from ovarian, gastric cancer)
- Superior Mesenteric Artery (SMA) Syndrome (secondary to rapid weight loss)
EXTRA INFORMATION
SMA Syndrome
Classically occurs in a young patient presenting with abdominal pain, nausea and vomiting. Pathophysiology: rapid weight loss
leading to loss of duodenal fat pad resulting in narrowing of aorto-mesenteric angle and obstruction of duodenum as it passes
under the SMA (angle < 25 degree). Treatment: medical (i.e. bowel rest, gastric decompression, nutritional support (i.e. enteral
with NJFT or IV TPN), surgical (i.e. duodenojejunostomy). Other predisposing factors: scoliosis correction surgery (arteries are
stretched), congenital ligament of treitz abnormality
Functional Causes
86
- Paralytic Ileus
▪ Hypo-mobility w/o obstruction leading to accumulation of gas & fluids with associated distention,
vomiting, absence of bowel sounds and obstipation
▪ DDx: mechanical/pseudo: hypo/absent BS as opposed to high-pitched tinkling
Causes of paralytic ileus

- Physiologic ileus spontaneously resolves within 2-3 days, usually self-limiting
- Clinically significant if:
- Ileus that persists for more than 72 hours following surgery
Post-operative
- No bowel sounds on auscultation
(most common)
- No passage of flatus
Absent
- Abdominal distention becomes more marked and tympanic
Peristalsis
- Pain is not a feature
Infection - Intra-abdominal sepsis (may give rise to localised or generalised ileus)
Infraction - Ischemic Bowel
- Retroperitoneal hematoma
- Intra-abdominal inflammation/peritonitis, biliary/renal colic
Reflex Ileus
- Trauma: (#ribs/spine/HI)
- Spinal Cord injury above T5 level
- Metabolic: hypoK/ hypoMg/ hypoNa, uraemia
- Metabolic Acidosis (i.e. DKA)
Metabolic
- Hypothyroidism
- Drugs: opiate-induced, antacids, TCA
- Recurrent obstruction (usually colon) that occurs in the absence of a mechanical cause or acute intra-
abdominal disease
Causes of Pseudo-Obstruction
Pseudo- Acute Colonic
- Toxic Megacolon (see below)
Obstruction Pseudo
- Ogilvie Syndrome (see below)
Obstruction
Chronic Colonic - Hirschsprung Disease
Pseudo - Paraneoplastic immune mediated – small cell Lung CA
Obstruction - Infection – Chagas’ Disease (American trypanosomiasis by T. cruzi)
EXTRA INFORMATION
Toxic Megacolon
Potentially lethal complication of inflammatory bowel disease (IBD) or infectious
colitis that is characterized by total or segmental non-obstructive colonic dilatation
plus systemic toxicity. Patients can present with severe bloody diarrhoea, altered
sensorium, tachycardia, fever, postural hypotension, lower abdominal distention
and tenderness ± localized or generalised peritonitis.
Diagnostic Criteria
- Radiological evidence of colonic distention PLUS (≥ 3 of the followings)
▪ Fever > 38deg
▪ HR > 120bpm
▪ Neutrophil > 10,500 / micoL
▪ Anaemia
▪ PLUS ≥ one of the following – 5a. Dehydration, 5b. Altered sensorium, 5c.
Electrolyte disturbance, 5d. Hypotension
OGILVIE SYNDROME (Colonic Pseudo-obstruction) – acute gross dilatation of the colon (predominantly cecum (> 10cm) right and
transverse colon) without a mechanical cause
Pathogenesis:
Unknown, probably due to impairment of the autonomic nervous system a/w underlying disease in 95% of patients 31
Trauma Fractures
31 Dis Colon Rectum. 1986 Mar;29(3):203-10.
87
Electrolytes hypoCa, hypoNa, hypoK, hypoMg, & hypoPO4

Calcium channel antagonist, narcotics, anticholinergic, TCAs,
Drugs
steroids
Infections Pneumonia / Sepsis
Cardiac MI / Heart Failure
Obstetric / Gynaecologic C-section / NVD, Spinal anaesthesia during childbirth
Retroperitoneal Pathology Malignancy / Haemorrhage
Surgery Pelvic, abdominal, orthopaedics
Metabolic, Cancer
Others Respiratory failure, Renal failure,
Neurological conditions
Clinical Features:
- Nausea, vomiting, abdominal pain, constipation and paradoxically diarrhoea
- Abdominal Distention always present
- Diagnosis of exclusion – made after excluding toxic megacolon or mechanical obstruction
Treatment (conservative):
- Treat underlying condition
- Review medications (stop drugs that can contribute to ileus) – as above
- Supportive Therapy (NBM, NGT, Rectal Tube, IVF)
- Strict I/O charting (± IDC)
- Check and replace electrolyte abnormalities + check thyroid function test
- Stool culture / OCP / C-diff (if having diarrhoea)
- Serial P/E
- Daily AXR
- KIV gastrografin to ensure no mechanical cause of obstruction
Failure of conservative therapy: Caecal diameter* > 12 cm and when the distention has been present for greater than 6 days.32 Or
failure to resolve within 24-48hours of conservative therapy
- Conservative therapy is successful in majority of patients – neostigmine at the onset is not indicated
- (2nd line) Neostigmine
- (3rd line ) Colonoscopy decompression – risk of perforation ~ 3%
- (if suspect ischemia, perforation / peritonitis) surgical intervention – mortality risk ~ 40%
▪ If cecal diameter > 12cm, risk of ischemia and perforation increases, if symptoms > 6 days, risk of perforation increases
▪ If bowel viable: decompressive cecostomy tube
▪ If ischemic / perforated: bowel resection
*The Law of Laplace states: tension ∝ pressure x radius. In a long pliable tube, the site of largest diameter requires the least pressure
to distend. Hence, in a patient suffering a distal large bowel obstruction, in the setting of a competent ileocecal valve, the cecum is
the most common site of perforation.
32 Gastrointest Endosc Clin N Am. 2007 Apr;17(2):341-60, vi-vii.
88
CLASSIFICATIONS
A. Anatomical: small bowel (high / low) vs. large bowel
B. Clinical: acute vs. chronic vs. acute on chronic vs. subacute
C. Pathological: Simple Obstruction vs. Closed Loop Obstruction
Anatomical Classification
- Vomiting occurs early and is profuse with rapid dehydration
High
Small Bowel - Distention is minimal
Obstruction - Pain is predominant with central distention
Low
- Multiple central fluid level seen on AXR
- Pain is mild and vomiting and dehydration are late
Large Bowel - Distention is early and pronounced
Obstruction - Proximal colon & cecum distended (competent ileocecal valve)
- Present with constipation / obstipation
Clinical Classification
- Usually in small bowel obstruction
Acute
- Presents with sudden onset of colicky central abdominal pain, distention, vomiting and constipation
Chronic - Usually seen in large bowel obstruction with lower abdominal colic and constipation followed by distention
Acute on
- Short history of distention and vomiting against a backdrop of pain and constipation
Chronic
- Incomplete obstruction
Sub-acute
- Recurrent attacks of colic relieved by passing flatus or faeces
Pathological Classification
Simple Loop Parital - One obstructive point, symptoms not as severe, may still be passing flatus
Obstruction Complete - One obstructive point, marked symptoms of nausea, vomiting, distention and constipation
- Obstruction at 2 points forming a loop of grossly distended bowel – at risk for perforation
- Causes of Closed Loop Obstruction
▪ Obstructing Large Bowel Lesion (i.e. colonic tumour, bowel stricture) with competent
ileocaecal valve
▪ Peritoneal Carcinomatosis with obstruction at 2 points
▪ Sigmoid Volvulus with competent ileocaecal valve
Closed Loop Obstruction ▪ Herniation of Bowel
- Clinical Presentation of Large Bowel Closed Loop Obstruction (i.e. obstructed tumour with
competent ileocaecal valve) → patients present with RIF pain, guarding, tenderness, absence
of dilated small bowels

- Closed loop obstruction is a surgical emergency
89
INVESTIGATIONS
Biochemical
- FBC: leukocytosis with left shift may indicate complications
- U/E/Cr: any dehydration/electrolyte imbalances due to (or acute renal failure from dehydration)
- ABG: acidosis from bowel ischemia or alkalosis due to vomiting (more for pyloric stenosis in children)
- Lactate (trend): surrogate measurement for anaerobic respiration, important if suspecting of ischemic bowel
- Inflammatory markers – CRP, procalcitonin
- Blood cultures (if fever, tachycardia, hypotension)
- Amylase – ? acute pancreatitis (AXR may just show small bowel dilatation)
Imaging
- Erect CXR: free air under diaphragm, any aspiration pneumonia
- AXR or XR KUB
▪ Erect AXR: air fluid levels
- In general ≥ 5 fluid levels are diagnostic of intestinal obstruction
- In the small bowel – number of air fluid levels is directly proportional to the degree of obstruction and to its site (more
number = distal lesion)
▪ Supine AXR: look for small or large bowel dilatation on radiograph
- Duodenum: C-shaped
- Jejunum: dilated small bowel >3cm is abnormal, centrally located multiple dilated gas filled bowel, stack of coins
appearance (plicae circulares / valvulae conniventes) – completely pass across width of the bowel, regularly spaced
- Distal Ileum: Featureless
- Colon: dilatation of the caecum >9cm or the colon >6cm is abnormal, peripherally located, incomplete bands
(haustrations due to presence of taenia coli) – spaced irregularly, do not cross whole diameter of the bowel
- Assess for complications: Rigler’s Sign / double-wall sign → pneumoperitoneum. Thumb-print sign / pneumatosis
intestinalis → ischemic bowel

▪ XR KUB (extends to the pubic symphysis)
- Able to look for rectal gas – r/o if it is a complete IO (note: if patient just got PR may have presence of rectal gas)
Special Considerations on X-Rays

- Sigmoid Volvulus: massive colonic distention with dilated loop of bowel running diagonally across the abdomen from right to
left (COFFEE BEAN SIGN), gastrografin enema shows bird’s beak
- Caecal Volvulus: gas filled ileum and ± distended caecum – no longer in RIF – rotation can occur around ileocolic blood
vessels and vascular impairment occur early (risk of colonic closed loop obstruction with higher risk of ischemia)
- Gallstone Ileus: Look for aerobilia (occurs in cholecystoduodenal fistula), SBIO & ectopic gallstone (Rigler Triad)
Left picture – Sigmoid Volvulus | Middle pictures – Caecal Volvulus | Right Picture – Gallstone Ileus
- Sigmoid volvulus – redundant sigmoid colon with an elongated narrow mesocolon (result in large mobile loop of colon),
common in older, institutionalized patients with neurological disorders and chronic constipation → loop pointing to RUQ
- Caecal volvulus – usually congenital (incomplete peritoneal fixation of right colon) → loop pointing to LUQ
▪ 2 variants based on character of caecal twisting (axial torsion type vs. cecal bascule type)
▪ Unlike sigmoid volvulus, cecal volvulus cannot be detorted endoscopically
▪ Tx33: Right hemicolectomy with ileocolic anastomosis (simple detorsion and cecopexy a/w high rates of recurrence)
- CT abdomen & pelvis

▪ Almost always performed for patient with intestinal obstruction in a virgin abdomen
33 Schwartz’s Principle of Surgery 10 th Edition – pg. 1220
90
▪ Able to identify transition point, severity of obstruction, any fecalization in small bowel proximal to transition, closed-loop
obstruction
▪ Able to identify complications – pneumoperitoneum, ischemic bowel (no bowel wall enhancement), necrotic bowel
(pneumatosis intestinalis)
▪ Target sign – intussusception
▪ Whirl sign – rotation of SB mesentery in volvulus
▪ Air in distal bowel with no transition point – paralytic ileus
- Water soluble (i.e. gastrografin) contrast (meal & follow-through) – for small bowel obstruction
▪ Hypertonic water-soluble contrast agent that is both diagnostic and therapeutic*
▪ Useful to differentiate between patients who will settle with non-operative management vs. those who will require surgery
▪ Appearance of water soluble contrast in the colon on AXR within 24 hours predicts resolution of adhesive small bowel
obstruction (sensitivity 97%, specificity 96%)34
▪ This reduces duration of hospital stay for patients with adhesive small bowel obstruction that do not require surgery
EXTRA INFORMATION
Gastrografin Mechanism of Action

Water soluble contrast promotes peristalsis less irritating to peritoneum in event of perforation. Attracts fluid from the bowel wall
into the lumen which potentially decreases the edema of the bowel wall. By shifting fluid into the bowel lumen it also increases
the pressure gradient across an obstructive site. Also it dilutes the bowel contents hence assisting its passage through a
narrowed lumen.
Predicting Risk of Strangulated Small Bowel Obstruction

- Small bowel intestinal obstruction confirmed by CT scan (excluding incarcerated abdominal wall hernia, postoperative ileus,
IBD, peritoneal carcinomatosis)35
- Scoring System (each 1 point)
▪ Abdominal guarding – OR: 5.04
▪ History of pain > 4 days – OR: 18.18
▪ CRP ≥ 75 – OR: 19.91
▪ TW ≥ 10 – OR: 3.03
▪ ≥ 500ml of free intra-abdominal fluid – OR: 7.15

▪ Reduced wall contrast enhancement on CT – OR: 4.87
- Interpretation: ≥4 points = 100% need for bowel resection, 3 points = 67.7 need for bowel resection (sensitivity 67.7 & specificity
90.8%)
Predictors of Intestinal Complications (high risk features)

- Onset of fever and ↑TW (>15) with localized abdominal tenderness
- ↑amylase, ↑lactate, metabolic acidosis a/w intestinal ischemia

- CT Scan with IV contrast
▪ Diagnosticate underlying case – hernia, mass, inflammatory lesion, intussusception, malignant vs. benign obstruction,
volvulus
▪ Assess potential complications (strangulation) – bowel wall thickening, poor bowel wall enhancement, mesenteric
haziness
34 Cochrane Database Syst Rev. 2007 Jul 18;(3):CD004651. [Important Paper]

35 Br J Surg. 2010 Jul;97(7):1119-25. [Important Paper]
91
Complications on X-Rays
- Rigler Signs / Double Wall Sign (Extraluminal Free Air)
▪ Blue arrows = falciform ligament, made visible by a free air in the peritoneal cavity
▪ Red arrows = both sides of the wall of the stomach (Rigler's sign), a sign of free air
▪ Yellow arrow points to a skin fold
- Thumb-printing (ischemic bowel),
- Left Pipe Colon (seen in inflammatory bowel condition, i.e. ulcerative colitis),
- Pneumoastosis Intestinalis (Bowel ischemia with necrosis)
▪ Can also be identified in Neutropenic Enterocolitis / Typhlitis – but not a surgical indication here.
▪ Neutropenic Enterocolitis – transmural inflammation of the cecum. Associated with use of cytotoxic drugs and other
immunomodulating agents. Patients present with non-specific symptoms of fever, abdominal pain, nausea, vomiting,
diarrhoea, hematochezia, low WBC with absolute neutrophil counts < 500cells/mm 3. Initial treatment: intravenous broad
spectrum antibiotics. Surgical intervention for patients who present with bowel perforation.
ACUTE MANAGEMENT
Rule out surgical emergencies

- Ischaemic bowel with bowel necrosis – pneumatosis intestinalis
- Perforation/peritonitis
- Obstructed and strangulated abdominal hernia
- Volvulus (caecal, stomach)
- Closed-loop obstruction (competent ileocecal valve)
Initial Management
1. ABCs: breathing (ventilation / oxygenation) – may be affected due to splinting of the diaphragm – give supplemental oxygen
2. Keep NBM – 70% recover with bowel rest and decompression
3. NG tube insertion
▪ Large bore NG tube (small diameter easy to get blocked up)
▪ Either passive with 4 hourly aspirates or low-intermittent suction (preferred for patients with expected high NG output)
4. IV fluid rehydration (i.e. Hartman’s) – account of maintenance + deficit + ongoing losses)
5. Urinary catheterization to monitor urine output
▪ Assess the hydration status – patient may be hypotensive (resuscitate, monitor vitals), aim for >0.5ml/kg/hr
6. Correct electrolyte abnormalities
▪ Correct acidosis, replace electrolytes as guided by investigations
▪ Do renal panel – look at urea and creatinine (>100:1 = prerenal dehydration, < 40:1 suggest intrinsic renal damage)
7. ± Prophylactic broad-spectrum antibiotics
▪ Preemptively prevents bacterial flora translocation (not usually given unless suspect ischemic bowel or bowel perforation)
▪ If required, use 3rd generation cephalosporin and metronidazole (IV Rocephin 1g 12H + Metronidazole 500mg 8H)
▪ If have raised TW – r/o bacterial infections
8. ± IA line and/or CVP for monitoring monitoring
▪ Assess dynamically as a response to fluid challenge
▪ CVP trend more impt than isolated pressure measurements in assessing volume status
92
Definitive Management (based on underlying cause)
1. Ischaemic bowel: Exploratory laparotomy with bowel resection if bowel is non-viable (gangrenous or necrotic)
2. Bowel Perforation: Exploratory laparotomy: resect lesion & perforated bowel with generous peritoneal lavage (i.e. 10L of wash)
3. Closed loop obstruction from left sided tumour: Colonic Stenting vs. Emergency Laparotomy +/- stoma
4. Obstructed Inguinal / Femoral hernia: Exploratory Laparotomy +/- bowel resection if ischemic bowel is present
5. Intussusception
▪ Children: usually due to hypertrophic Peyer’s patches. Administer air or barium enema: watch intussusception reduce on
fluoroscopy
▪ Elderly: usually a/w malignant pathological lead point (i.e. polyp, cancer) in 30-50% of the cases. Barium enema unlikely
to work, or if works recurrence rate is high, therefore surgery is 1st line treatment
6. Caecal Volvulus: Right hemi-colectomy with primary ileocolic anastomosis is the surgical procedure of choice (caecal volvulus
almost never able to be detorsed endoscopically)
7. Sigmoid Volvulus
▪ Non-surgical/ conservative:
o Placement of Rectal Flatus Tube (large bore urinary catheter (i.e. 3 way IDC) decompression (gown up, use 3 way
IDC – 1st port (spigot), 2nd port (attach to urinary bag), insert lubricated soft rectal tube into anus)
o Gentle flexible sigmoidoscopy decompression (recur in 50%)
▪ Surgical:
o Sigmoid colectomy with primary anastomosis – performed if the divided bowel ends are viable, peritoneal
contamination is not evident, and the patient is hemodynamically stable
o Sigmoid colectomy with end colostomy (Hartman’s procedure) – if bowel ischemia is present
o Sigmoid colectomy & formation of double barrel colostomy (Paul-Mikulicz procedure) with future re-anastomosis
o Sigmoidopexy: fix sigmoid to posterior abdominal wall (rarely done as high risk of recurrence)
8. Adhesive Small Bowel Obstruction
▪ Most patients with adhesive SBIO can resolve with non-operative therapy within 24 to 72 hours (70-90%)
▪ Selected patients for conservative management: partial obstruction, no signs of peritonitis, no high risk CT scan findings
(i.e. free fluid, mesenteric edema, de-vascularized bowel, small bowel faeces signs)
o NGT insertion to low intermittent suction
o IV fluids
o Correcting electrolytes
o Serial abdominal examination
▪ Water Soluble Contrast (i.e. Gastrografin)
o Can be attempted after an attempt of initial non-operative management of 48 hours
o Gastrografin accurately predicts need for surgery and reduce hospital stay, but does not affect recurrence rates
o After 72 hours (i.e. 3 days) of non-operative management – water soluble contrast study or surgery is recommended
o Contrast given through NGT – if it reaches colon in 4-24hrs – majority will resolve with non-operative management
(99%), if contrast fail to reach colon, obstruction will not resolve without surgery in 90% of patients 36
o But gastrografin study does not reduce the need for surgical intervention (studies not powered to show this)
▪ Surgical intervention if development of complications or IO not resolved after 3-5 days
9. Non-adhesive small bowel obstruction (without indications for surgery)
▪ IBD – corticosteroids / immuno-modulatory drugs
▪ Anti-helminthic therapy for parasitic infection
▪ Radiation enteritis – damaged bowel has higher risk of anastomotic leak so surgery is avoided. If op needed, prefer
intestinal bypass to resection.
▪ Early post-op SBIO secondary to adhesions – avoid surgery as new adhesions are dense and hypervascular. Withhold
surgery for longer than non-postop SBIO
10. Post-op paralytic ileus (>3 days post-op)
▪ Supportive management: drip & suck, wait for peristalsis to restart
▪ Oral gastrografin: hyperosmotic, causes intraluminal osmosis, can re-establish peristalsis
▪ Prokinetics agents: erythromycin (motilin agonist), metoclopramide
36 Current Surgical Therapy (11th Edition) – pg. 112
93
ACUTE APPENDICITIS
DEFINITION
Acute appendicitis is one of the most common causes of lower abdominal pain. The lifetime risk of appendicitis is ~16% and lifetime
risk of appendectomy is ~10%37. It is most frequently seen in the 2nd to 3 rd decade of life with slight male predominance of 1.4:1, The
rate of misdiagnosis is ~ 22.2% in females nad 9.3% in males.
ANATOMY
- Blind muscular tube (6 to 9 cm) with mucosal, submucosal, muscularis and serosa layers
- Appendix participates in secretion of immunoglobulins – i.e. IgA. Lymphoid tissue atrophies with age.
- Appendix location
▪ Retrocaecal position (75%)
▪ Pelvic (21%), Subcaecal (1.5%), Paracaecal (2%)
▪ Constant base of appendix – at confluence of 3 taeniae coli, fuse to form outer longitudinal muscle coat of the appendix
- Meso-appendix contents
▪ Appendicular artery (branch of the ileocolic artery branch of SMA) – end artery, hence thrombosis leads to gangrenous
appendicitis
▪ Lymphatic channels (empty to ileocaecal lymph nodes)
▪ Adults – laden with fats, children – transparent
AETIOLOGY
- Changes in dietary habits – decrease dietary fibre and increased refined carbohydrates
- Bacterial infection secondary to obstruction of appendiceal lumen
▪ Faecoliths: calcium salts & faecal debris collect around nidus of faecal material within appendix
▪ Lymphoid hyperplasia: a/w inflammatory (Crohn’s) & infective dz (GE, URTI, IMS, measles)
▪ Less common causes: parasitic worm, TB, tumour of caecum or the appendix, unknown
- Hyperplasia – most common cause in children, following a viral illness
- Faecolith – most common cause in adults
PATHOLOGY
- Obstruction → distension by mucus → increased luminal and intramural pressure → thrombosis and occlusion of blood supply,
stasis of lymphatic flow → ischemia (periumbilical abdominal pain) → necrosis → bacterial overgrowth and invasion (polymicrobial
– E coli, Bacteroides fragilis, Peptostreptococcus, Pseudomonas) → fibropurulent reaction on serosa → irritation of parietal
peritoneum (localised pain at McBurney’s point)

- Suppurative (i.e. pus filled), gangrenous (i.e. hemorrhagic ulceration and necrosis in the wall), or perforated (may be a/w located
peri-appendiceal mass/abscess or generalized peritonitis)*
- Midpoint of antimesenteric border most likely to perforate
37 J Epidemiol. 2010; 20(2): 97–105.
94
History
- Anorexia (~75%)
▪ Useful and constant clinical feature especially in children
- Abdominal Pain (a/w migration – umbilicus to RIF)
▪ Visceral discomfort (poorly localised, mid-gut) in response to appendiceal inflammation and obstruction, after 4-6hours (up
to 12hr) presents with localization of pain to RIF
▪ Somatic pain (intense, localised) in response to progressive inflammation and irritation of parietal peritoneum in RIF
▪ Symptoms & location of pain may differ depending on appendix location
- Nausea and Vomiting
▪ Almost always occur after pain
▪ If vomiting precedes pain, diagnosis is questioned (?intestinal obstruction)
- Diarrhoea / Constipation (little differential diagnostic value)
- Sequence of symptoms in >95% of patients – anorexia followed by abdominal pain, in turn by vomiting. Fever comes later.
- History taking MUST also be performed to rule out other differential diagnosis depending on clinical suspicion
Vitals
- Temp: low grade fever, rarely increased by >1°C (in children if >38.5°C – ?mesenteric adenitis)
- Heart Rate: normal or slightly elevated
- Early signs are often subtle
- Mc-Burney point (1/3 distance from right ASIS to umbilicus): localised point of maximal tenderness,
- Signs of localized peritonism
▪ Rebound tenderness
▪ Voluntary Guarding (early), Involuntary, true reflex rigidity (late)
- Cutaneous hyperesthesia – spinal nerve of right T10, T11 and T12 (uncommon)
Signs to elicit
- Rovsing sign: RIF pain with deep palpation of the LIF (indirect tenderness, sign of right-sided local peritoneal irritation)
- Psoas sign: RIF pain with passive right hip flexion (inflamed retrocaecal appendix irritates stretched iliopsoas muscle)
- Obturator sign: RIF pain with internal rotation of a flexed right hip (inflamed pelvic appendix irritates obturator internus muscle)
- Cough sign: RIF pain on coughing (localized peritonitis)
Considerations
- Retrocaecal: tenderness most marked in right flank and/or RUQ
- Pelvic: DRE: pain in suprapubic area, rectal tenderness and history of diarrhoea
- Infants/children may present with inflamed hemi-scrotum due to migration of pus through patent processus vaginalis – often
mistaken for acute testicular torsion
DIFFERENTIAL DIAGNOSES
Paediatric Male Adults Female Adults Elderly
Acute Gastroenteritis Acute Gastroenteritis Urine Tract Infection Caecal Diverticulitis
Acute Mesenteric Adenitis* Caecal Diverticulitis Ectopic Pregnancy Colonic Carcinoma
Meckel’s Diverticulitis Meckel’s Diverticulitis Pelvic Inflammatory Disease*** Malignancy (i.e. carcinoid)
Intussusception Terminal Ileitis (i.e. Crohn’s, UC) Mittelschmerz Pain
Malignancy (i.e. carcinoid) Ovarian Torsion
Omental Infarct** Ruptured Ovarian Cyst
Urological Causes (i.e. renal calculi, Others: Intestinal Obstruction,
Constipation
testicular torsion, epididymo-orchitis) Perforated PUD
* During surgery find enlarged mesenteric lymph nodes and a normal appendix (i.e. Yersinia enterocolitica)
** Omental Infarct – if clinically stable – manage conservatively with NSAIDs and observation (no need antibiotics), if diagnosis is unclear or prog ressive /
severe symptoms – diagnostic laparoscopy with resection of infarcted omentum
*** Fitz-Hugh Curtis Syndrome – transperitoneal spread of PID leading to RUQ pain due to perihepatic adhesions
INVESTIGATIONS38
The most common imaging utilized in a patient suspected with acute appendicitis is to perform a contrasted computer tomography of
the abdomen and pelvis (CTAP). However, in pregnant patients, imaging choice is between MRI or abdominal ultrasound.
Diagnosis
38 World J Emerg Surg. 2020 Apr 15;15(1):27.
95
- Clinical Scoring System

▪ Alvarado Score [MANTRELS] - see below
▪ Other Scoring System: Adult Appendicitis Score39 (Finland), RIPASA Score40 (Brunei), Appendicitis Inflammatory Score
- The use of clinical score helps with excluding AA and identifying intermediate patients who require further imaging.
Migratory RIF pain 1 point - Alvarado ≤ 3 = no imaging, unlikely appendicitis
Symptoms Anorexia 1 point - Alvarado 4-6 = recommend CT scan
Nausea and/or Vomiting 1 point - Alvarado ≥ 7 = surgical consultation
Tenderness (RIF) 2 points
Rebound Tenderness 1 point Alvarado ≤ 5 good to r/o admission for appendicitis (sensitivity: 99% overall,
Signs
96% males, 99% females, 99% children)
↑ Temperature (> 37.3°C) 1 point
At ≥ 7 (specificity: 81% overall, 57% males, 73% female, 76% children) –
Leukocytosis > 10,000 2 points
score is well calibrated in males, inconsistent in children, over-predicts in
Laboratory
Left Shift of Neutrophils 1 point females41
- FBC: TW ranges from 10–18 (higher in gangrenous/perforated appendix), TW<13.5 = predictor of negative appendectomy 42
- U/E/Cr: ensure creatinine not deranged
- CT AP:
▪ Enlarged appendix >6 mm
▪ Thickened appendix wall >2mm with enhancement – target sign (fluid-filled hypoechoic lumen surrounded by echogenic
mucosa and submucosa)
▪ Periappendiceal fat stranding
▪ Presence of appendicolith (is an independent predictor for operation and failure of nonoperative management)
▪ To rule out other etiologies & look for complications (i.e. abscess, perforation)
- MRI Abdomen – recommended for pregnant patients with suspected appendicitis
Rule out differential causes and assess complications

- UFEME (r/o UTI, may have pyuria & haematuria)
- Pregnancy Test (B-HCG) – r/o ectopic pregnancy
- CRP
- Blood Cultures
- Erect CXR – r/o perforation (free air under diaphragm), r/o lobar pneumonia at right lung base
- Supine AXR (limited value, unless want to rule out other pathology (i.e. urolithiasis)
- Abdominal U/S: diagnostic modality in paediatrics and pregnant patients – look for (1) Non-compressible appendix ≥ 6mm in AP
direction (2) Thickening of appendiceal wall & (3) Periappendiceal fluid – however, if inconclusive will require MRI to rule out
appendicitis
- MRI Abdomen – if available, this will be the preferred imaging modality for pregnant patients.
Other investigations
- PT/PTT, GXM, (usually not necessary for laparoscopic appendectomy)
- LFT / Amylase / Lactate / ABG (depending on clinical suspicious of alternative diagnosis)
- ECG (required pre-operatively)
39 BMC Gastroenterol. 2014 Jun 26;14:114

40 Singapore Med J. 2011 May;52(5):340-5.
41 BMC Med. 2011 Dec 28;9:139
42 Hong Kong Med J. 2010 Feb;16(1):12-7
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MANAGEMENT
- NBM, IV hydration, correct electrolyte abnormalities
- IV antibiotics (cephalosporin and metronidazole)
- Symptomatic relief: antiemetics, analgesia (opioid analgesia does not mask signs of peritonism)
- Definitive treatment: laparoscopic appendectomy keep in view
▪ Risk of progression to rupture with treatment delay – children <5 & adults >65 have highest rates of perforation (45 and
51%)
▪ Short, in-hospital delay up to 24hrs is safe in uncomplicated acute appendicitis (does not increase complications / perforation
rate)
▪ Appendectomy vs. Antibiotics treatment (see below): surgery remains gold standard
▪ For non-perforated, uncomplicated appendicitis, antibiotics can be stopped post-operatively
- Intraperitoneal cultures – definite for patients who are immunocompromised
- Non-operative management of complicated appendicitis (appendiceal abscess / phlegmon): Ochsner Sherren Regime
▪ Omentum wraps around inflamed appendix containing inflammatory process (phlegmon)
▪ Immediate appendectomy a/w higher complication rates, treat conservatively with antibiotics if patient remains is
hemodynamically stable and non-peritonitic
▪ May benefit from percutaneous drainage of appendiceal abscess
▪ Symptomatic patients (during clinic visit) → inflammatory markers, CT scan or diagnostic laparoscopy
▪ Asymptomatic patients (during clinic visit) → consider colonoscopy vs. interval appendectomy
EXTRA INFORMATION
Appendectomy vs. Antibiotics

The antibiotic first strategy can be considered in selected patients with uncomplicated appendicitis with absence of appendicolith. However, patients
must be warned about the risk of treatment failure ~ 8% during initial hospitalization and a 20% risk of needing a second hos pitalization within the
first year of diagnosis. The risk of recurrence at 5 years is up to 39%. The current recommendation is still for appendectomy for patients diagnosed
with acute appendicitis.
Role of Interval Appendectomy

The role of interval appendectomy is questionable – retrospective review of 32938 patients where 1012 patients (3%) were treated with initial non-
operative treatment. 148 (15%) had interval appendectomy and 864 (85%) did not. At a median follow-up of 4 years only 39 patients (5%) had
symptoms of recurrent appendicitis. Given such low recurrence rate, routine interval appendectomy was deemed not justifiable 43. However, adult
patients with complicated AA treated with interval appendectomy can be diagnosed with appendiceal neoplasm in ~ 11% of ca ses.
Suggestion for colonoscopy to rule out underlying malignancy (i.e. perforated CRC), especially in patients over the age of 40 .
COMPLICATIONS
- Haemorrhage: intra-abdominal, abdominal wall hematoma
- Infection / Sepsis: surgical site infection, abscess (intra-abd, appendiceal stump, pelvic, scrotal)
- Risk of conversion to open surgery ~ 10% (~3.5% for uncomplicated appendicitis, 18% for complicated appendicitis)
- Risk of limited bowel resection (i.e. limited right hemicolectomy) ~ 1%
- Paralytic Ileus as with any abdominal surgery
- Local (stump): retained faecolith, stump appendicitis, leak, fistula
- Late: adhesions leading to small bowel obstruction (~1% in 30 years)
43 Arch Surg. 2005 Sep;140(9):897-901.
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EXTRA INFORMATION
Appendicitis in Pregnancy
- Negative appendectomy rate ~27%
- Investigations: MRI Abdomen vs ultrasound
- Rates of foetal loss 3.4% (simple), 12.1% (complicated) and 7.3% (negative)
- Peritonitis increases risk of preterm labour and preterm delivery
- Risk of early delivery is 7% (incidence is higher in patients with complex appendicitis than those with
negative appendectomy / simple appendicitis)44
- IV Roc/Flagyl (Class B) – safe to give if suspicion of appendicitis in pregnancy
- Laparoscopic appendectomy is safe and effective procedure during pregnancy
Appendiceal Carcinoids45
- Majority discovered retrospective from histology
- 10% involves base, majority located in the tip
- Mortality is strongly a/w size – (1) 1cm ~ 5% 5-yr mortality, (2) ≥ 2cm ~ 29.5% 5yr mortality
- Indication for further management: (1) size > 2cm, (2) lymphovascular invasion, (3) invasion of
mesoappendix, (4) higher grade tumours (i.e. intermediate / high), (5) mixed histology (i.e. goblet cell
carcinoid / adenocarcinoma), (6) undetermined size
- Management:
▪ < 1cm: appendectomy
▪ ≥ 1cm and < 2cm
o Located at tip or mid appendix → appendectomy

o Location at base, invasion of mesoappendix, metastases → Right hemicolectomy
o Goblet cell histology → Right hemicolectomy
▪ ≥ 2cm: Right hemicolectomy (30% of pts will have +ve LN)

- No role for adjuvant chemotherapy or immunotherapy
Appendiceal Lymphoma
- If confined to the appendix → appendectomy
- If tumour extends beyond the appendix onto the caecum or mesentery → right hemicolectomy
- Post-operative staging is required before initiating adjuvant therapy (adjuvant therapy is not indicated for lymphoma con fined to the appendix)
Pseudomyxoma peritonei
- Mucinous ascites arising from rupture appendiceal or ovarian adenocarcinoma. Peritoneal cavity filled with tenacious semi sol id mucus and
large, loculated cystic masses
- Epidemiology: age: 40 – 50 years, equal frequency between males and females
- Classification (most are due to ruptured low grade appendiceal tumours)
▪ Low Grade Mucinous Adenocarcinoma / Disseminated peritoneal Adenomucinosis (DPAM)
▪ High Grade Mucinous Adenocarcinoma / Peritoneal Mucinous Carcinomatosis (PMCA)
- Clinical Presentation: most commonly present with suspected appendicitis and non-specific abdominal distention, New hernia, ascites,
abdominal distention with non-shifting dullness, palpable abdominal mass, non-specific abdominal pain or incidental diagnosis during
laparotomy
- Investigations: CEA / CA 125 (females) + Computer tomography scan of thorax, abdomen and pelvis
- Management:
▪ Drainage of mucus and intra-peritoneal fluid
▪ Omentectomy, peritonectomy, resection of involved organs, appendectomy
▪ ± right hemicolectomy (for appendiceal adenocarcinoma) or TAHBSO (for ovarian cancer)
▪ Heated intraperitoneal chemotherapy (HIPEC)
- Prognosis: with cytoreductive surgery & HIPEC – 55% 10 year survival rate
44 Schwartzs Principle of Surgery 9th Edition (pg: 2043, pdf version)

45 Pancreas. 2010 Aug;39(6):753-66. (NANETS consensus)
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4. OESOPHAGUS
ANATOMY OF THE OESOPHAGUS
ANATOMY
The oesophagus extends from the lower border of cricoid cartilage (C6) from the oropharynx and continues into the cardiac orifice of
the stomach. From the Upper Esophageal Sphincter (UES) to the Lower Esophageal Sphincter (LES), it is 25cm and divided into 3
main parts – cervical (~5cm), thoracic (~18cm) and abdominal (~1-2cm). It then passes through the oesophageal hiatus in the right
crus of the diaphragm at T10 and ends at oesophagogastric junction
UES = cricopharyngeus: at lower border of cricoid cartilage (≈C6, 15cm from incisors)
- Cricopharyngeus muscle. most common site of oesophageal perforation
- N: recurrent laryngeal nerve
Follows thoracic kyphosis of vertebral column

- Broncho-aortic constriction: arch of aorta (≈22.5cm from incisors), left main bronchus (≈27.5cm from incisors)
LES = “physiological” sphincter due to zone of high pressure within right crus of diaphragm: at T10 (≈40 cm from incisors)
- Diaphragmatic fibres loop around oesophagus at OGJ (oesophageal hiatus): contracts when ↑IAP (cough, sneeze)
- Angle of His at OGJ (acts as valve) – acute angle acts as a valve
- Mucosal folds in the lower oesophagus acts as a valve
- Closure of sphincter is under vagal control, the hormone gastrin & motilin causes the sphincter to contract (secretin, CCK,
somatostatin and glucagon causes it to relax)
- Intra-abdominal pressure being higher than intrathoracic pressure
3 narrow points along the course of the oesophagus

1. (UES) – Cricopharyngeus sphincter (15cm from incisors)
2. Aortic Arch and left main bronchus crosses the oesophagus (25cm from incisors)
3. Where the oesophagus pierces through the diaphragm, the LES is situated at this level (40cm from incisors)
Upper 1/3 Middle 1/3 Lower 1/3

Muscularis Propria striated muscle striated and smooth muscle smooth muscle
Oesophageal branches of the aorta
Oesophageal branches of left gastric artery
Blood Supply Inferior thyroid artery Bronchial arteries (i.e. right bronchial, superior
Inferior Phrenic Artery
left bronchial & inferior left bronchial artery)
Left gastric vein*
Venous Return Brachiocephalic veins Azygos veins
(tributary of portal vein)
Nodes along L. Gastric Vessels;
Lymph Drainage Deep Cervical Nodes Superior and Posterior Mediastinal Nodes
Celiac Nodes
* A porto-systemic anastomosis exists at the lower oesophagus thus leading to formation of varices in portal HTN
- Parasympathetic via the vagus nerves that have synaptic connections to the myenteric (Auerbach’s) plexus. Meissner’s
submucosal plexus is sparse in the oesophagus + indirect contribution from recurrent laryngeal nerve
- Sympathetic via middle cervical ganglion proximally and upper 4 thoracic ganglia distally
Histology (from outside to inside)

- Adventitia – Most of oesophagus lined by adventitia, only short segment of intra-abdominal oesophagus lined by serosa
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4. Oesophagus_Last Updated 3rd June 2020
- Muscularis Propria – upper 1/3 is skeletal, lower 1/3 is smooth, middle 1/3 is mixed – responsible for peristalsis
▪ Outer Longitudinal Layer of Muscularis Propria (between the layers contains the myenteric plexus (Auerbach’s plexus
– has synaptic connections with the vagus nerve)
▪ Inner Circular layer of Muscularis Propria (thicker than the outer longitudinal layer, helical in shape (peristalsis of
oesophagus assumes a wormlike drive)
- Submucosa – contains submucosal plexus (Meissner’s Plexus – sparse in the esophagus)
- Mucosa – non-keratinized stratified squamous epithelium
SURGICAL ANATOMY
Mediastinum: Right Lateral View & Vagal supply to Stomach
Course of the Left Recurrent Laryngeal Nerve

- Emerges from vagus nerve at level of arch of the aorta (T4) – travels inferior then posterior to aortic arch (hook around arch of
aorta deep to the ligamentum arteriosum)
- Ascends to the trachea via the trachea-esophageal groove
- Passes deep to the inferior border of the inferior pharyngeal constrictor muscle
Course of the Azygos Vein

- Formed by the union of the ascending lumbar veins and right subcostal (T12) veins
- Transverse through the diaphragm via the aortic opening (T12)
- Ascends in the posterior mediastinum before arching over the right main bronchus joining the SVC at the root of the right lung
Course of the Thoracic Duct

- Commence at the cisterna chyli between Abdominal aorta (AA) and right crus of diaphragm
- Passes upwards through aortic opening (12)
- Ascends behind oesophagus inclining to the left at the level of T5
- At the root of the neck, it arches laterally lying between carotid sheath and vertebral artery to enter junction between left internal
jugular vein and left subclavian vein
- Virchow’s node therefore lies between the 2 heads of the SCM
Course of the Vagus Nerve

- Exits from the medulla oblongata and leaves the skull through the jugular foramen – where it has the superior (jugular) ganglion
and inferior (nodose) ganglion (vagus nerve is joined by CN XI just below the inferior ganglion)
- Descends vertically within the carotid sheath (posterior to CCA & IJV)
- Right vagus cross anterior to right subclavian artery, descends on right side of trachea, behind the hilum of the right lung
- Left vagus cross anterior to the left subclavian artery, descend on left side of aortic arch, posterior to left phrenic nerve, course
behind hilum of left lung
- Both vagus forms the oesophageal plexus which give rise to the anterior and posterior gastric vagus
▪ Right Vagus: travels on posterior portion of stomach, forms celiac plexus (distribution to intestines and pancreas), gives off
posterior nerve of Latarjet (1st gastric branch of the posterior vagus nerve known as Criminal nerve of Grassi)
▪ Left Vagus: travels on anterior portion of stomach, large hepatic branch (distribution to liver and biliary tree), gives off
anterior nerve of latarjet
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APPROACH TO DYSPHAGIA
DEFINITION
Dysphagia: sensation of difficulty in or abnormal swallowing → “Oropharyngeal” vs “Oesophageal” (ref History)
Odynophagia: pain with swallowing
Globus pharyngeus*: Sensation of a lump in the throat that doesn’t go away ≠dysphagia
*Patients may c/o persistent clearing of the throat, chronic cough, hoarseness and phlegm. Usually idiopathic (functional disorder i.e. no structural
pathology). May be a/w GERD, sinusitis, post-nasal drip, cricopharyngeal spasm, osteophytosis, goitre, FB, anxiety (96% patients report exacerbation
of symptoms during times of emotional intensity). Management: Reassurance, vocal hygiene (avoid smoking, alcohol, caffeine)
CLASSIFICATION
In each anatomic region the dysphagia can be caused by neuromuscular dysfunction (impaired physiology of swallowing) or
mechanical obstruction to the lumen
Oropharyngeal Dysphagia Oesophageal Dysphagia

Neuromuscular diseases: Neuromuscular diseases:
Central Causes Primary Motility Disorder
Brain/brainstem: stroke, tumour, trauma Achalasia / Vigorous Achalasia
Others: Parkinson’s disease, Cerebral Palsy Spastic Motility Disorders
Peripheral Causes - Diffuse oesophageal spasm(i)
Myasthenia gravis - Nutcracker/Jackhammer oesophagus(i)
Motor Neuron Disease (i.e. ALS) - Hypertensive lower oesophageal sphincter
Peripheral neuropathy Secondary Motility Disorder
Skeletal Muscle Disease (i.e. myopathies) Muscular Scleroderma (Systemic Sclerosis)(ii)
Dystrophy (myotonic dystrophy) Multiple Sclerosis
Polymyositis, Dermatomyositis Sjogren’s Syndrome
Post infectious Diabetic Neuropathy
Poliomyelitis
Syphilis Obstructive lesions:
Intra-luminal Causes
Mechanical lesions: Oesophageal webs (e.g. Plummer-Vinson)(iii)
Intra-luminal Causes Lower oesophageal rings (Schatzki’s ring) (iv)
Oesophageal webs Foreign bodies (e.g. fish bone)
Intra-mural Causes Intra-mural Causes
Oropharyngeal Tumour Tumour
Inflammatory masses e.g. abscess Strictures:
Pharyngeal pouch (Zenker’s diverticulum) (vi) - Peptic (reflux oesophagitis)
Extraluminal Causes - Radiation
Anterior Mediastinal masses – 4Ts: thyroid, thymus, teratoma, - Chemical (caustic ingestion)
terrible lymphoma) - Medication
- Malignant
Others: - Eosinophilic oesophagitis(v)
Inadequate mastication: poor dentition, mucosal lesions (e.g. Extraluminal Causes
ulcers) Anterior Mediastinal masses – 4Ts: thyroid (goitre with
Inadequate saliva: anticholinergics, antihistaminergic, Sjogren retrosternal extension), thymus, teratoma, terrible lymphoma
Bronchogenic Carcinoma
Very rare causes: CVS abnormalities
- Thoracic aorta aneurysm (dysphagia aortica)
- Aberrant R subclavian artery (dysphagia lusoria)
- Left atrial dilatation (dysphagia megalatriensis)
- Congenital
- Osteophyte
101
EXTRA INFORMATION
(i) Spastic Motility Disorder: patients present with odynophagia, chest pain & less dysphagia (differential diagnosis: AMI) – treat with CCB, nitrates.
Nutcracker Oesophagus – increased resting lower oesophageal pressure + mean distal oesophageal peristaltic amplitude of >180mmHg.
Diffuse Oesophageal Spasm – normal resting lower oesophageal pressure + high intensity disorganized contractions
(ii) Scleroderma: smooth muscle atrophy leading to normal peristalsis in the proximal striated oesophagus with absent peristalsis in the distal smooth
muscle portion. The LES is progressively weakened as the disease advances. Risk of GERD and esophagitis with stricture format ion. Barium Swallow:
dilated esophagus, stomach, duodenum or a hiatal hernia with distal oesophageal stricture and proximal dilatation. Management: PPI, antacid,
elevation of head in bed, dilatation of strictures. (if recurrent dilatation required) – Surgical option: Partial (Toupet) fundoplication (Oesophageal
shortening may require a Collis gastroplasty in combination with a partial fundoplication)
(iii) Plummer-Vinson Syndrome: triad of postcricoid dysphagia, Fe deficiency anemia and cervical oesophageal webs
- a/w glossitis + angular cheilitis, koilonychia, splenomegaly, enlarged thyroid, in middle aged women
- Pathophysiology: unknown -?iron/nutritional deficiency, genetics, autoimmune
- Complication: oesophageal or pharyngeal squamous cell carcinoma (SCC)
- Tx: dilatation, Iron supplements; screening for oral cancers
(iv) Schatzki’s Ring: It is a thin submucosal circumferential ring located at the squamocolumnar junction, proximal to the LES. It leads to intermittent
dysphagia during hurried ingestion of solid food, without pain. Little is known about the natural progression of this disease. a/w sliding hiatal hernia.
Management: (if symptomatic without reflux) – treat with dilatation of ring and PPI, (if symptomatic with reflux and defective LES) – anti-reflux
procedure to avoid repeated dilatation, (if asymptomatic) – observation
(v) Eosinophilic oesophagitis: allergic inflammation (“asthma” of the oesophagus). Endoscopic findings – stacked circular rings, proximal strictures,
linear furrows, whitish papules, small calibre oesophagus. Dx: OGD with oesophageal biopsy.
(vi) Zenker Diverticulum: outpouching of pharyngeal mucosa between 2 parts of the inferior pharyngeal constrictor muscle (i.e . thyropharyngeus &
cricopharyngeus) – patients present with halitosis, difficulty initiating swallowing & regurgitation.
HISTORY:
1. Characterizing Dysphagia
▪ Duration: when did it start, acute vs. chronic
▪ Is it progressive? (solid vs. liquid)
2. Establish if there is odynophagia (pain with swallowing)46

Causes of Odynophagia
- Chemical Oesophagitis (i.e. caustic Ingestion – acid / alkali)
- Drug-Induced Oesophagitis: bisphosphonates (alendronate, risedronate), NSAIDs, antibiotics (e.g. doxycycline*), zidovudine, KCl (s low
release), Quinidine, Iron Sulfate, Vitamin C
- Radiation Oesophagitis
- Infectious Oesophagitis
▪ Immunocompetent – Candida Albicans, HSV
▪ Immunodeficient – Fungal (candida albicans, histoplasmosis), Viral (HSV, CMV, HIV, EBV), Mycobacteria (TB, mycobacterium avium-
complex), Protozoan (cryptosporidium, pneumocystis carinii), Ulcers (aphthous ulcers)
- Severe ulcerative Esophagitis secondary to GERD
- Oesophageal Carcinoma (pain occurs late)
* consider drug esophagitis in a young patient who is taking medication for acne with acute onset of odynophagia
3. Which phase of swallowing is affected (oropharyngeal vs. oesophageal dysphagia)

▪ Oropharyngeal
- Presenting complaint is usually of difficulty in initiating swallowing
- May be associated with choking, coughing, nasal regurgitation, food spillage, drooling, dysarthria
- Voice may sound nasal (bulbar palsy)
- Cause of oropharyngeal dysphagia is usually neuromuscular rather than mechanical; stroke most common cause
▪ Oesophageal
- Presenting complaint is that of food “getting stuck” in the throat or chest (retrosternal discomfort)
- Localisation of the symptom often does not always correspond to actual site of pathology
- Can be due to either neuromuscular dysfunction or mechanical obstruction
4. Differentiating obstructive from function (neuromuscular dysfunction) causes – (a) solids, liquids, or both? (b)
progressive or intermittent?
Solids > Liquid (mechanical)

- Patient complains of more difficulty swallowing solids than liquids – happens with narrowed oesophageal lumen
- May have regurgitation of undigested food
46 Chapter 6: Dysphagia, odynophagia, heartburn, and other esophageal symptoms (Joel E. Richter)
102
- Recent onset dysphagia that is progressively and rapidly worsening, with LOW → high suspicion of oesophageal cancer
- Red flag symptoms: dysphagia, LOW/LOA, GI bleeding, (iron deficiency) anaemia, nausea/vomiting, age > 40-45
- Dysphagia that progressively worsens gradually over longer time → suspect peptic strictures
- Intermittent/non-progressive symptoms → suggestive of webs, rings
Liquids > Solids (neuromuscular disorder)

- Patient complains of more trouble swallowing fluids than solids, or both
- Dysphagia more long-standing, slowly progressive → achalasia (beware of pseudoachalasia from malignancy)
- Intermittent or non-progressive symptoms → suggest diffuse oesophageal spasm, nutcracker oesophagus

- May have history of stroke, neuromuscular disease
5. History of predisposing conditions (Risk Factors)

▪ Reflux symptoms e.g. retrosternal burning pain (heartburn), sour fluid reflux into mouth (acid brash), excessive salivation
(water brash), postural aggravation on lying down [Reflux Oesophagitis, Peptic Strictures]
▪ Caustic chemical ingestion in the past [Chemical Oesophagitis]
▪ Smoking, chronic alcohol intake
▪ Symptoms of systemic disease e.g. stroke (focal neurological deficits), myopathies, limited cutaneous systemic sclerosis
(CREST – calcinosis, Raynaud’s, oesophageal dysmotility, sclerodactyly, and telangiectasia), diabetes mellitus
▪ Medication history: [Pill-induced Oesophagitis]
▪ Previous laryngeal / oesophageal / gastric surgery [Strictures 2º surgery]
▪ Previous radiation for head & neck tumour [Strictures 2º Radiation]
6. Complications
▪ Symptoms of aspiration pneumonia – fever, cough, shortness of breath esp. at night
▪ Malnutrition / Low BMI
Summary of Differential Diagnosis
103
1. General condition
▪ Patient’s level of alertness and cognitive status (impact safety of swallowing)
▪ Vitals: the patient may be hypovolemic from vomiting/decreased intake
▪ Nutrition: presence of cachexia
▪ Dehydration (mucous membranes, skin turgor, etc.)
▪ Conjunctival pallor: bleeding from tumour, oesophagitis ulcerations, or associated with P-V syndrome
▪ Scleral icterus: metastases to liver
2. Disease / Causes
▪ Neuro Examination (esp. CN V, VII-XII, PD features, myopathy)
▪ Inspect for any neck masses
▪ Bedside Swallowing Test (any choking / coughing on swallowing ?oropharyngeal dysfunction)
▪ Scars/marks over the chest and abdomen suggesting previous surgery, radiation
▪ Palpable mass in abdomen (not likely)
▪ PR examination for melaena
3. Complications of disease
▪ Signs of pneumonia: patient febrile, may be toxic, lung crepitations, decreased air entry usually over right lower lobe
▪ Signs of Metastatic Disease: Cervical lymphadenopathy (i.e. Virchow’s), Hepatomegaly, Ascites
4. Does patients have any ongoing treatment

▪ Tube feeding through NG tube, gastrostomy/jejunostomy – if aspirates seen, what is the colour?
▪ Total Parenteral Nutrition (TPN)
INVESTIGATIONS
Diagnostic
1. Oesophagogastroduodenoscopy (OGD)
▪ Advantage is direct visualisation of the lesion, ability to take tissue biopsy (esp. useful in malignancy), and therapeutic
(stopping bleeding from a tumour, stenting the lumen, etc.)
2. Barium swallow
▪ Advantage of barium swallow is that it is less invasive than OGD, especially when suspecting webs, diverticula in the
oesophagus where OGD may cause perforation; however if the patient is at high risk of aspiration, barium swallow is
dangerous.
- Done in prone-oblique position to eliminate effect of gravity
- Can also ask pt to swallow food eg bread to demonstrate subtle abnormalities
▪ Visualisation of obstructive lesions:
- Shouldering of a stricture (benign strictures form a smoother contour whereas malignant strictures form a more right-
angled contour)
- Bird’s beak / Rat’s Tail sign of achalasia
▪ Visualisation of pharyngeal pouch or oesophageal diverticulum
▪ Diffuse oesophageal spasm gives a corkscrew/rosary bead appearance
Achalasia Oesophageal Diverticulum Stricture Carcinoma Spasm
104
4. Oesophageal Manometry
▪ Indications: non-diagnostic OGD, patients with suspicion of motility disorder
▪ Assess motor function of the UES, oesophageal body and LES
▪ Achalasia: increased LES pressure, failure of LES to relax, no peristalsis
▪ Diffuse oesophageal spasm: frequent strong non-peristaltic unorganized contractions, normal LES
▪ Nutcracker oesophagus: high amplitude peristaltic contractions, normal LES
▪ Scleroderma: low LES pressure and aperistalsis
5. Video-fluoroscopic examination of swallowing (VFES) – using barium or flexible-endoscopic examination of swallowing (FEES)
▪ Used to assess oropharyngeal dysphagia (neuromuscular causes) by looking for penetration and aspiration of various
consistencies of food during swallowing
▪ VFES limited to cervical oesophagus (unable to r/o distal oesophageal lesions)
Supportive
1. Blood investigations:
▪ Full blood count – Low Hb (anemia from chronic blood loss / Plummer Vinson), High TW (aspiration pneumonia)
▪ U/E/Cr – electrolyte disturbances from vomiting, poor oral intake; raised creatinine and urea in dehydration (creatinine will
be raised more than urea if patient has pre-renal failure from dehydration), low urea in malnutrition
▪ Low phosphate – risk of refeeding syndrome during treatment
▪ LFTs – low albumin with nutritional deprivation
2. CXR
▪ Consolidation (aspiration pneumonia)
▪ Any tracheal deviation / masses compressing on oesophagus
3. 24-hour pH probe monitoring

▪ If patient complains of reflux symptoms and non-diagnostic OGD (see topic on GERD)
105
ACHALASIA
DEFINITION
Achalasia is defined as a failure of the lower esophageal sphincter to relax appropriately with swallowing. In addition to failure of
relaxation there is aperistalsis of the oesophagus and increase in LES tone.
EPIDEMIOLOGY
- Rare (1 in 100,000) but most common primary oesophageal dysmotility
- Typically presents in the ages 25-60.
PATHOPHYSIOLOGY
- Aperistalsis of the oesophagus (progressive degeneration in the ganglia of Auerbach’s plexus)
- Increased LES tone/pressure (hypertensive LES)
- Failure of LES to relax with swallowing
CAUSES
- Primary Achalasia: idiopathic (idiopathic neuronal inflammation/degeneration)
- Secondary Achalasia: Chagas Disease* (caused by Trypanosoma cruzi via bite of a Reduviid bug), diabetic autonomic
neuropathy, lesions of dorsal motor nuclei (polio or surgical ablation), eosinophilic esophagitis
- Differential diagnosis – pseudo-achalasia: malignancy (i.e. gastric adenocarcinoma), strictures
* Chagas disease a/w megacolon, megaesophagus, dilated cardiomyopathy and cardiac failure – treatment: nifurtimox
- Progressive gradual dysphagia (99%) to solids and liquids, immediate regurgitation of saliva / undigested food after meals (>70%),
aspiration (10%), nocturnal cough, mild weight loss (due to poor nutritional input) and retrosternal chest pain (due to oesophageal
spasm)
- In pseudo-achalasia: advanced age at symptoms onset (>60yr), short duration of symptoms (<6mth), rapid weight loss, difficulty
advancing endoscope through the GEJ of a non-dilated oesophagus47
- Eckardt scoring (commonly used) – (1) weight loss, (2) dysphagia, (3) retrosternal pain, (4) regurgitation
Complications48
- Stasis of food can lead to friability , erosions and/or candida esophagitis
- Increased risk oesophageal squamous cell carcinoma (0-140x normal population) – usually occurs >10years after diagnosis
- Predisposition to Barrett’s metaplasia and oesophageal adenocarcinoma (see below)
INVESTIGATIONS
- Oesophageal Manometry (for definitive diagnosis) – characterized by:
▪ Lack of progressive peristalsis (aperistalsis/ disorganised peristalsis)
▪ Abnormally high basal resting pressures at the LES
▪ Incomplete LES relaxation on swallowing
- Barium swallow
▪ “Bird’s beak” tapering of distal oesophagus with proximal dilatation (not specific)
▪ Late: severely dilated oesophagus that takes on the contortion of a “sigmoid” shape
▪ Disorganised peristalsis
- OGD to rule out mechanical stricture and malignancy (at esophagogastric junction)
- CXR: a widened mediastinum with an air-fluid level and large amounts of retained food and fluid in the dilated oesophagus with
absence of gastric air bubble
- EUS: useful for characterizing tumours of the distal oesophagus and cardia (differentiate with pseudo-achalasia)
- CT Thorax/Abdomen: to rule out malignancies
47 Am J Gastroenterol. 1994 Nov;89(11):2014-8.

48 Scand J Gastroenterol Suppl. 2006;(243):7-10
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MANAGEMENT / TREATMENT
Lifestyle
- Eat when sitting up
- Don’t lie down after eating
- Eat slowly
- Antacids/H2 receptor antagonists
Medical Therapy (aim: decreased LES tone)

- CCB (nifedipine)/nitrates (nitroglycerine)
- Endoscopic injection of botulinum toxin type A
▪ Blocks Ach release from nerve terminals
▪ Short duration of effect (6-9 months), successful in 50% of cases, high relapse rates
▪ Indicated for elderly patients who are high risk for invasive procedures, poor surgical candidates
Endoscopic Treatment
- Pneumatic balloon dilatation
▪ 65-70% of patients improve, 40% response rate at 5 years
▪ Equally effective as cardiomyotomy but needs to be done repeatedly
▪ First choice non-surgical treatment
▪ Risks: perforation with dilatation (3-5%), recurrence of symptoms common
- Per-Oral Endoscopic Myotomy (POEM)

▪ Endoluminal myotomy via the oesophageal mucosa to reach the hypertrophied muscles of the LES
▪ Not combined with an anti-reflux procedure – risk of significant post-procedural reflux
▪ Long-term outcomes still pending
Surgical Treatment
- Laparoscopic Heller esophagomyotomy (myotomy of lower oesophagus) with anterior 180-degree partial (Dor) fundoplication
(reduce postoperative reflux)*
▪ Excellent results in 90-98% of pts
▪ Dissection is carried out at least 5cm onto the oesophagus and 2cm on the stomach
▪ Pre-op predictive factor for success: elevated resting LES pressure >30mmHg
▪ Risks: bleeding, infection, oesophageal perforation
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GASTROESOPHAGEAL REFLUX DISEASE (GERD)
DEFINITION
Reflux of stomach contents causes distressing/troublesome symptoms and/or complications (physiologic reflux occurs postprandially
and is asymptomatic/transient)
EPIDEMIOLOGY49
Prevalence of GERD and its related complications in Asia is reported to be increasing (~ 10%) though still lower than that in the
Western countries (10-30% of the Western population affected by weekly symptoms). Indians more commonly report reflux symptoms
and are more commonly diagnosed with endoscopic esophagitis as compared to Chinese or Malays
RISK FACTORS
- Inefficient oesophageal clearance of refluxed material – oesophageal motility disorders eg scleroderma
- Fixed gastric outlet obstruction / Functional delayed gastric emptying – eating habits eg lying down after heavy meal
- Increased gastric acid secretion
- Inappropriate relaxation of LES (decreased tone) – alcohol, smoking, caffeine (not proven)
- Hiatal hernia (functional decrease in LES tone)
- Increased intra-abdominal pressure – obesity, pregnancy, chronic cough, tight garments, large meal
- Drugs (smooth muscle relaxation) – NSAIDs, CCB, beta blockers, nitrates, alpha blockers, theophylline, anticholinergics
PATHOPHYSIOLOGY
- LES is the primary anti-reflux mechanism
- Gastro-oesophageal continence is maintained by:
▪ Lower oesophageal sphincter (LES)
▪ Angle of His
▪ Diaphragmatic crus
▪ Pressure difference between oesophagus and intra-abdominal stomach
- Defective LES and/or increased abdominal pressure (resulting in shortening of the LES) leads to reflux of acidic gastric contents
into the lower oesophagus resulting in acid-induced mucosal damage
- Acid incites inflammation in the lower oesophagus – extent of inflammation increases with duration of contact with acid
- Chronic inflammation results in complications of GERD – eg oesophagitis, ulcers, strictures, Barrett’s oesophagus,
adenocarcinoma
CLASSIFICATIONS
49 J Gastroenterol. 2010 Aug;45(8):808-15.
108
- History is important as most patients with reflux are seen in the primary setting with no facilities for detailed investigations
- Esophageal-related symptoms: heartburn + acid regurgitation >90% specificity but low sensitivity
▪ Heartburn – post-prandial retrosternal burning sensation, aggravated by lying flat, may be relieved by antacid. Significant if
≥2 days/week.
▪ Regurgitation – acid brash with small amounts of undigested food
▪ Posturally aggravated (lying flat) sub-sternal or epigastric burning pain / discomfort that is readily relieved by antacid
▪ Dysphagia – reflux oesophagitis / stricture formation in chronic GERD, r/o malignant cause
▪ Odynophagia –suspect oesophageal ulcer in chronic GERD
▪ Chest / epigastric pain – resolves spontaneously or with antacids, r/o dangerous causes
▪ Globus sensation
▪ Water brash / hypersalivation – not common, foaming at the mouth in response to reflux
- Extra-oesophageal symptoms:
▪ Chronic cough, hoarseness – irritation of larynx
▪ Wheezing – aspiration and bronchial reactivity
▪ Recurrent otitis media
- Atypical Symptoms: Chest Pain (non-cardiac), Chronic Cough, Dysphagia, Dyspepsia, Epigastric Pain, Effortless Emesis,
Hoarseness, Recurrent Otitis Media
Complications
- 20% of patients with GERD get Benign Peptic Strictures or Columnar-lined Barrett oesophagus
- Reflux with respiratory complications (i.e. recurrent pneumonia) or reflux with throat symptoms (i.e. halitosis, chronic cough,
chronic laryngitis, chronic sinusitis)
- Less common complications include acute or chronic bleeding
- New onset odynophagia (in setting of chronic GERD) – indicates progression to erosive esophagitis and formation of ulcer
- Malignancy (adenocarcinoma arising from Barrett’s oesophagus) – see below
INVESTIGATIONS
1. Oesophagogastroduodenoscopy (OGD)
▪ Cannot actually diagnose reflux
▪ Good for evaluation of esophagitis, Barrett changes (take biopsy specimens) and ruling out malignancy and other aetiologies
▪ May see a hiatal hernia which is associated with reflux (though not all patients with hiatus hernia will have reflux)
Indications for OGD in patients with GERD

Alarm Features (suspicious for malignancy) Screening for Barrett’s in patients with risk factors
- New onset dyspepsia ≥ 60 yo - Chronic GERD (at least 5-10 years)
- GI bleeding, iron deficiency anemia - Demographic: age ≥ 50, male, Caucasian

- Anorexia, unexplained LOW >5% - Obesity
- Dysphagia, odynophagia - Hiatal hernia
- Persistent vomiting - Nocturnal reflux
- Family history of GI malignancy - Past or current smoker
- Abnormalities seen on other imaging study - Family history of Barrett’s oesophagus and/or
- Persistence / recurrence of symptoms despite appropriate adenocarcinoma
medical therapy / post-antireflux procedure
Grading of Oesophagitis: helps guide management
Los Angeles classification

Grade A – ≥1 mucosal break ≤5mm long
Grade B – ≥1 mucosal break >5mm long, but not continuous between the tops of adjacent mucosal folds
Grade C – ≥1 mucosal break that is continuous between the tops of adjacent mucosal folds, but involving <75% of circumference
Grade D – mucosal break that involves ≥75% of luminal circumference
Savary-Miller classification
Grade I – Isolated erythematous or erythematous-exudative erosion, covering a single mucosal fold
Grade II – Multiple erosions covering several mucosal folds partly confluent but never circumferential
Grade III – Circumferential erosive and exudative lesions
Grade IV – Chronic complications of ulcers and/or strictures
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Grade V – Barrett’s oesophagus (histologically confirmed columnar cell epithelization)
2. Ambulatory 24hour oesophageal pH probe

▪ Gold standard to confirm diagnosis of GERD and can be used to monitor adequacy of treatment
▪ Diagnosis based on the percentage of time in 24hrs the pH reading is below 4
▪ A DeMeester score is derived based on frequency of reflux episodes and time required for oesophagus to clear the acid
EXTRA INFORMATION
Measurement technique
- Transnasal antimony probe most commonly used; alternative is the Bravo capsule (a wireless capsule that is temporarily
attached to the oesophageal wall)
- The probe is placed 5cm above the manometrically-determined upper limit of the LES (for the wired probe), or 6cm above the
endoscopically-determined squamocolumnar junction (for the wireless capsule)
3. Manometry
▪ Defines the location and function of the LES for placement of pH probe
▪ Helps to exclude oesophageal motility disorder
▪ Helps to evaluate peristaltic function before anti-reflux surgery
▪ Manometrically abnormal LES:
- (1) pressure < 6mmHg
- (2) overall length < 2cm and
- (3) an abdominal length of < 1cm
- Patients with one or more of these abnormal values have 90% chance of having reflux
4. Barium swallow and follow-through

▪ Not of much value in diagnosing reflux (low sensitivity and specificity)
▪ Can document the presence or absence of hiatus hernia, presence of oesophageal stricture and ulcers
▪ Hiatal hernias are a/w reflux (but not all patients with hiatal hernia will have reflux)
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MANAGEMENT
Lifestyle
1. Overweight patients
▪ Encourage weight loss – regular exercise program
▪ Avoid tight-fitting garments
2. Sleeping Alterations
▪ Elevate head (6-8 inches) when sleeping
▪ Encourage not to lie down to sleep within an hour of eating
▪ Avoid meals 2-3 hrs before bedtime
3. Dietary Alterations
▪ Avoid fatty foods, alcohol, caffeine, spicy food or anything that worsens symptoms
▪ Remain upright after meals or walk after eating
▪ Avoid excessive eating, eat smaller, more frequent meals
4. Smoking and alcohol intake cessation
5. Drugs – change or reduce dose of drugs that exacerbate reflux
Medication (aim: lower gastric acidity or enhance oesophageal/gastric clearance)

1. Acid suppression therapy
▪ Proton pump inhibitors (i.e. omeprazole 40mg OM) – for esophagitis. Irreversibly bind to H-K-ATPase pump.
- Side Effects of long-term PPI: increased incidence of community acquired pneumonia, interstitial nephritis
(omeprazole/lansoprazole), visual disturbances (pantoprazole/omeprazole) & fundal gastric polyp (regress with
cessation of omeprazole), clostridium difficile infection (no correlation with small bowel bacterial overgrowth)
- Reassess symptoms in 8 weeks and consider tapering & stopping PPIs if asymptomatic for 8 weeks and no severe
erosive oesophagitis/Barrett’s
▪ H2-receptor antagonists (i.e. ranitidine, famotidine) – inhibit histamine 2 receptors on parietal cells. Only for short-term
use in mild GERD can cause tachyphylaxis or tolerance. (cimetidine is a potent CYP450 inhibitor – generally avoided)
- Can be used in pregnant patients (instead of PPI)
2. Adjunct agents
▪ Antacids (i.e. gaviscon*, MMT) – don’t prevent GERD. Use PRN to relieve symptoms. Can use in pregnancy (but avoid
those containing NaHCO3 and Mg trisilicate)
▪ Surface agents i.e. sucralfate – adhere to the mucosal surface to protect and promote healing. Short duration of action,
limited efficacy. Can use for GERD in pregnancy.
▪ Sodium alginate – polysaccharide derived from seaweed forms floating viscous gum in the stomach to neutralise
postprandial acid in the proximal stomach. Can be used as adjunct therapy in refractory GERD.
* Gaviscon contains antacids and alginate
3. Prokinetics –↑LES tone,↑antrum contraction,↑bowel peristalsis

▪ Metoclopramide (dopaminergic antagonist)
▪ Domperidone
Surgical
Indications
- Persistence of reflux symptoms despite maximal medical therapy (PPIs)
- Manometric evidence of a defective LES
- Compliance problems – patient does not want to be on medication for life
- Severe symptoms or progressive disease (i.e. oesophagitis with frank ulceration or stricture)
- Complications of reflux oesophagitis – respiratory complications, Barrett’s oesophagus
Surgery versus conservative treatment

- Surgery has higher rates of cure and better long-term results
- No need to adhere to strict lifestyle and diet change as well as long-term medications
- Disadvantage of surgery is the associated morbidity and mortality
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EXTRA INFORMATION
Goals of Surgery
- Restore pressure of LES to level twice the resting gastric pressure and its length to at least 3cm
- Ensure adequate length of the distal esophageal sphincter (>2cm) in the positive pressure environment of the abdomen
- Ensure the reconstructed cardia is able to relax on swallowing
- Fundoplication should not increases resistance of the relaxed sphincter to a level that exceeds the peristaltic power of the
oesophagus (too tight will lead to dysphagia)
- Fundoplication placed in the abdomen without undue tension and maintained there by approximating the crura of the
diaphragm above the repair
Fundoplication is the mainstay of surgical therapy

- Can be done via open (trans-abdominal) or laparoscopic surgery (most laparoscopic now). The original fundoplication is a 360
degree (total) wrap, but since then, many modification has been performed
▪ Nissen fundoplication (introduced by Rudolf Nissen in 1956) – a 360 degree (total) wrap of the gastric fundus around the
gastro-oesophageal junction (10-year recurrence free > 90%)
▪ Partial fundoplication can also be done in patients where oesophageal motility is poor or the oesophagus is foreshortened;
anterior 90 degrees, anterior 180 deg, posterior 270 deg (Toupet) fundoplication are various options
- Total or partial fundoplication have similar 5 year similar rates of patient satisfaction, esophagitis, and post-operative use of PPI.
Partial fundoplication has lower rates of post-op dysphagia and gas related symptoms. Total fundoplication more effective at
controlled pot-op reflux symptoms (i.e. heartburn)50
Other Treatments for GERD

- Augmentation of the lower oesophageal sphincter using interlinked titanium beads with magnetic cores – LINX reflux
management system (approved by FDA in 2012)
- Electrical stimulation of the lower oesophageal sphincter
- Endoscopic therapies – inferior to laparoscopic fundoplication
Management of stricture
- Rule out malignant cause of stricture by taking biopsy
- Dilatation (variety of means available – balloon, dilators, etc.)
- Treatment of underlying reflux
- If resistant to dilatation, resection and reconstruction
50 ANZ J Surg. 2012 Jan-Feb;82(1-2):17-22.
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COMPLICATIONS
Nissen Fundoplication
- Mortality Rate (< 0.1%)
- Intraoperative Complications
▪ Perforation – oesophageal or gastric (i.e. avulsion injury of the gastric cardia)
▪ Pneumothorax – due to injury to left pleural membrane during retro-esophageal dissection
▪ Haemorrhage – vascular injuries to IVC, left hepatic vein and AA
- Early Postoperative
▪ Dysphagia – due to over-tightening of hiatus during hiatal hernia repair and excessive peri-hiatal scar tissue formation
▪ “Gas bloat syndrome” – patient experiences difficulty burping gas that is swallowed (self-limiting within 2-4weeks)
- Migration of Fundoplications
▪ Para-esophageal hiatus hernia – Intrathoracic migration of the fundoplication (present with substernal pain), minimize by
routinely repairing hiatus hernia and avoid excessive lifting / straining 1 month after surgery
▪ “Slipped-Nissen” occurs when the wrap slides down, the GE junction retracts into the chest, and the stomach is partitioned;
usually due to a foreshortened oesophagus unrecognised in the first operation
▪ Excessively loose or short wrap – reflux recurs (failure of treatment)
- Others: Bi-lobed Stomach
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BARRETT’S OESOPHAGUS
DEFINITION
Metaplastic columnar epithelium with gastric / intestinal features (≥1cm above GOJ) replaces normal stratified squamous epithelium.
US guidelines require biopsy confirmation of IM while UK guidelines require histological confirmation with or without features of IM.
EPIDEMIOLOGY
- Prevalence 1.3% in Asia (more common amongst whites)
- >50 years old (typically diagnosed at ~55 years old), males > females (4:1)
- Diagnosed in 10-15% of patients with esophagitis, persistent symptomatic GERD
CAUSES / RISK FACTORS

- Associated with long-term acid reflux (i.e. GERD > 5yr), adaptation mechanism where intestinal epithelium withstands exposure
to acidic reflux better than oesophageal epithelium (especially if diagnosed erosive oesophagitis / peptic stricture)
- Age (>50), Males, Smoking, Central obesity, Caucasian, family history of Barrett oesophagus / oesophageal adenocarcinoma
(genetic and environmental risk factors)
- Presence of hiatal hernia associated with 80% of cases of Barrett oesophagus
PATHOPHYSIOLOGY
- Characterized by intestinal metaplasia: oesophageal squamous mucosa (stratified squamous epithelium (SSE) converted to
mucus-secreting columnar epithelium with goblet cells)
- Gastroesophageal Junction (GEJ / EGJ) – proximal end of gastric longitudinal mucosal folds is the endoscopic landmark of
the mucosal GEJ51 or distal end of the oesophageal palisading vessels 52
- In healthy patients, the Squamocolumnar Junction (SCJ, Z line) is at the same level as the mucosal GEJ. It is a serrated zigzag
line, hence known as the Z-line.
CLINICAL PRESENTATION53
- Barrett’s itself is asymptomatic but patients often have history of long standing GERD
- Patients with long standing gastric reflux and endoscopically proven Barrett reported these symptoms: dysphagia (75%),
heartburn (50%), bleeding (25%)
Complications
- Oesophageal ulcers and its resultant complications (4Bs: bleed, burrow, burst, block)
- Ulcers penetrate the metaplastic columnar epithelium in a manner similar to that seen in gastric ulcers
- Oesophageal scarring and strictures
- Increased risk of development of dysplasia and adenocarcinoma (40x)
▪ Higher risk in men, older patients and long segment Barrett’s mucosa
▪ Non-dysplastic BE → adenocarcinoma ~ 0.33% / year
▪ LGD → adenocarcinoma ~ 0.7% / year
▪ HGD → adenocarcinoma ~ 7% / year

▪ Persistent of high grade dysplasia require therapeutic intervention
INVESTIGATIONS
- Diagnosed on endoscopy and histology
▪ Normal SSE (A) → pale-pink (pearly grey white) and smooth (note: SCJ / Z-line represents the normal GEJ where the
squamous mucosa of the oesophagus and columnar mucosa of the stomach meets)
▪ Barrett Oesophagus (B, C & D) → extension of salmon coloured mucosa into tubular oesophagus ≥ 1cm proximal to GEJ
(with histological confirmation of intestinal metaplasia with goblet cells*) – SCJ is shifted proximally from the GEJ. The
mucosa between the SCJ and GEJ is termed the columnar lined oesophagus
* At least 8 random biopsies should be obtained – 4-quadrant biopsies every 2 cm. If short (12cm) segment, then obtain at least 4
biopsies per cm of circumferential BE
51 Gastroenterology. 2004;127(1):310–330
52 Best Pract Res Clin Gastroenterol. 2008;22(4):569-83.
53 Ann Surg. 1983 Oct;198(4):554-65.
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OGD + Biopsy (sensi 82%, spec 81%): long- vs short-segment (length ≥3cm vs <3cm)
D
- 3cm used as the cut-off between short and long segment Barrett’s Oesophagus
- Indications: (multiple risk factors) ≥50 years old, male, white race, central obesity, smoking, chronic GERD, hiatal hernia, 1º FHx
Barrett oesophagus/oesophageal adenocarcinoma

- Prague C&M Criteria: measure depth during OGD withdrawal (ensure OGD is straight to measure length accurately)
▪ Circumferential extent: GOJ - circ extent of columnar epi
▪ Maximum extent: GOJ - max extent of columnar epi
- Biopsy Barrett region: 4 quadrant biopsy per 2cm, or 1cm (if mucosal irregularities)
▪ Gastric cardia-type mucosa
▪ Atrophic gastric fundic-type mucosa
▪ Specialised intestinal metaplasia: goblet cells, gastric foveolar-type cells, small intestinal-like cells, colonic-like columnar
cells, ± endocrine/Paneth cells
115
MANAGEMENT / TREATMENT
1. Treatment of underlying reflux
▪ Lifestyle changes, acid suppression (PPIs: omeprazole→ titrate from 20mg OD to 40mg BD), surgery (similar principle to
treatment of GERD)
▪ Elimination of reflux may halt progression of disease, heal ulceration and prevent stricture formation, improve symptoms
however, it is not shown to decrease risk of cancer, still requires endoscopic surveillance
2. Chemoprevention
▪ High dose PPI (omeprazole 40mg BD) + Aspirin, improves outcomes in patients with BE, all-cause mortality, oesophageal
adenocarcinoma & high grade dysplasia – AspECT trial54 (not currently practiced in Singapore)
▪ Aspirin only useful if patients are not on NSIADs
▪ Benefit seen when patient on high dose PPI and aspirin for > 5 years (i.e. 8-9 years)
3. Endoscopic surveillance
Chronic, longstanding GERD or multiple risk factors Screening endoscopy recommended
(i.e. males with chronic (> 5 years) GERD symptoms
(weekly or more), age ≥ 50 , white, central obesity,
smoking, 1st degree relative with BE or oesophageal

adenocarcinoma )
Established Barrett’s with no dysplasia Confirmed on repeat biopsy (Repeat OGD with biopsy within 6 months, if negative
(0.2-0.5%/yr risk of progression to cancer) repeat, once every 3 years)
Low grade dysplasia (LGD) Endoscopic eradication vs. intense surveillance
(0.5-0.7%/yr risk of progression to cancer) Yearly OGD and biopsy till no dysplasia on 2 consecutive biopsy then repeat OGD
every 3 years
High grade dysplasia (HGD) / CIS Treated with endoscopic therapy or surgery (see below)
(4-8%/yr risk of progression to cancer) If patient not keen for either, intensive surveillance (q3 months for at least one year)
with multiple large capacity biopsy specimen to detect cancer development
Indeterminate dysplasia with evidence of acute Repeat OGD and biopsy after 8 weeks of effective acid suppression therapy. If still
inflammation indefinite, repeat OGD In 12 months
Adenocarcinoma Refer to Chapter on Esophageal Cancer
4. Treatment of high-grade dysplasia

▪ Endoscopic Mucosal Resection (EMR), Endoscopic Submucosal Dissection (ESD): for localized HGD, nodular lesion
▪ Endoscopic radiofrequency ablation (for non-nodular lesions, circumferential ablation device, HALO): complete eradication
success rates at 12 months for low-grade dysplasia (90.5%) and high grade dysplasia (81.0%) 55 and associated risk
reduction in disease progression
▪ Esophagectomy: definitive treatment to remove all dysplasia with cure rates ~100%, but a/w high morbidity and mortality
A = Barrett’s Oesophagus, D = Post Endoscopic Radiofrequency Ablation
54 Lancet . 2018 Aug 4;392(10145):400-408.

55 N Engl J Med. 2009 May 28;360(22):2277-88
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OESOPHAGEAL CANCER
Malignancy of the oesophagus, most commonly squamous cell carcinoma (SCC) and adenocarcinoma (AC)
EPIDEMIOLOGY56
- 10th most common cause of cancer death (2/3 are non-operable), age (>60 years old), males > females
- Oesophageal SCC: incidence 3.85 per 100,000 in males and 0.81 per 100,000 in females | generally decreasing due to declining
prevalence of smoking
- Oesophageal AC: incidence 0.5 per 100,000 in males | increasing due to rising prevalence of GERD/obesity (especially Western
countries)
RISK FACTORS
Age (> 60), Gender (male), Family History are also risk factors
RF for Squamous Cell Carcinoma (SCC) RF for Adenocarcinoma

Race: African / American
Race: whites
“Oesophageal belt” (countries with high prevalence): China, Africa
Males : Females ( 2-10 : 1) Males : Females ( 4-7 : 1)
Alcohol and Smoking Smoking
Hot beverages (i.e. hot tea) or
Nutritional Deficiencies (i.e. lack of fresh vegetables and fruits Obesity (predispose to hiatus hernia and reflux)
Betel (Areca) nut chewing (Women – BMI > 30, Males – BMI > 25)
Ingestion of nitrosamines
Achalasia
Others: Plummer-Vinson Syndrome, Oesophageal diverticula (i.e. Chronic GERD which leads to Barrett’s Metaplasia
Zenker Diverticulum) and webs, Caustic oesophageal injuries, HPV Barrett Oesophagus (40x)
infection, previous radiotherapy
PATHOLOGY
There are 2 main subtypes of esophageal cancer to consider, squamous cell carcinoma and adenocarcinoma.
Squamous Cell Carcinoma

- SCC can arise anywhere in the oesophagus but typically found in the middle third of oesophagus (ratio for U:M:L → 1:5:2)
- 60% shows exophytic or fungating growth, 25% ulcerative and 15% infiltrative
- SCC: (multi-step process) → dysplasia (low vs. high grade) → carcinoma in situ (full-thickness dysplasia) → invasive SCC →
metastatic disease (plentiful submucosal lymphatics present in oesophageal wall which permits tumour cell infiltration above
and below level of apparent tumour).
Adenocarcinoma
- Adenocarcinoma typically occurs in distal third oesophagus
- It is a malignant epithelial tumour with glandular differentiation that usually arise in the background of chronic GERD and Barrett
oesophagus. This eventually leads to intestinal metaplasia, dysplasia and then invasive adenocarcinoma.
Most patients with early-stage disease are asymptomatic or may have symptoms of reflux, non-specific i.e. retrosternal discomfort,
“indigestion”. However, approximately 50% of patients have unresectable lesions or distant metastasis on presentation.
1. Rapidly progressive dysphagia (first and most common presentation) – fluid and soft food better tolerated than hard/bulky food
2. Odynophagia (20%): pain develops late, usually due to extra-esophageal involvement
3. Weight loss: secondary to reduced appetite, malnutrition and active cancer
4. Regurgitation of saliva or undigested food (without gastric acid): secondary to tumour disrupting normal peristalsis and causing
esophageal obstruction (risk of aspiration pneumonia)
5. Anemia (with or without melena/frank hematemesis – bleeding is usually occult): tumour surface may be fragile and bleed
56 Am J Gastroenterol. 2006 Jul;101(7):1430-6.
117
Features suggestive of complicated oesophageal cancer

1. Locally Advanced
▪ Bleeding (hematemesis, melena, Fe-deficiency anemia): chronic (from tumour), acute (rare: invasion aorta, pulmonary
arteries, bronchial arteries)
▪ Obstructive (malnutrition, aspiration pneumonia)
▪ Hoarseness suggestive for RLN invasion (secondary nodal metastasis, rarely by primary tumour): left > right (vocal cord
paralysis)
▪ Horner’s Syndrome suggestive for brachial plexus invasion
▪ Respiratory (cough, fever or aspiration pneumonia) suggestive for tracheo-oesophageal fistula
2. Systemic: SCC typically spreads intra-thoracic, AC usually spreads intra-abdominally (e.g. liver, peritoneum)
▪ Nodal → supraclavicular LN,, gastric/celiac LN (assess on imaging)
▪ Bone → Persistent back / bone pain, pathological #, hypercalcemia
▪ Liver → RHC pain, LOW, Jaundice, Ascites
▪ Lung → Haemoptysis, cough, SOB, pleural effusion
▪ Others → adrenals, cutaneous, muscle, brain (RARE)
Modes of Spread
- Direct extension into surrounding structures (pericardium, trachea → risk of tracheoesophageal fistula),
- Lymphatic (along submucosal lymphatic channels)
- Haematogenous – commonly to liver, lung, adrenal gland and kidney
INVESTIGATIONS
Establishing Diagnosis
1. Esophagogastroduodenoscopy (OGD) and biopsy
▪ Findings: circumferential, ulcerative, sloughy, partially-obstructing lesion with contact bleeding
▪ Allows biopsy of the lesion for confirmatory histological diagnosis, measurement of tumour location (distance from incisors,
tumour location (epicentre), local extent), check stomach for synchronous lesions (impt as stomach is needed for gastric
conduit in subsequent oesophagectomy), lumen diameter (risk of impending obstruction) and presence or absence of
barrett's esophagus
2. Barium swallow (non-invasive)

▪ Can assess for tumour complications (i.e. tracheo-oesophageal fistula) and can show proximal dilatation, mucosal
irregularity and annular constrictions
▪ Diagnostic accuracy rate of ~ 70%
▪ Less commonly performed (OGD firstline)
118
Staging
1. CT TAP +/- CT Neck

▪ Modality of choice for staging distant metastasis, If proximal tumour, include CT neck
▪ Can be used for T, N, and M staging
- Nodes > 10mm are considered to be metastatic
- Nodal involvement outside area of resection (i.e. supraclavicular or paraaortic lymph nodes – M1 disease) –
contraindication to esophagectomy
▪ CT Thorax
- Presence of any lung metastases
- Aspiration pneumonia – pleural effusion, collapse, consolidation
- Pleural and/or pericardial effusion
- Tracheal deviation or extrinsic compression of tracheobronchial system
- Widened superior mediastinum in an upper oesophageal tumour
- Raised hemi-diaphragm with phrenic nerve involvement
- Any chronic respiratory conditions
2. Endoscopic ultrasound (EUS) +/- FNA

▪ EUS combines endoscopy with high frequency ultrasound within the oesophageal lumen which allows for high resolution
image of the tumour, the oesophageal wall and adjacent structures
▪ EUS is good for T staging of small tumours (determine depth of wall invasion), and N staging (identify malignant (>10mm,
sharp borders, hypoechoic, homogenous) lymph nodes)
▪ Role in early stage esophageal cancer, if endoscopic resection is feasible
3. Positron Emission Tomography with integrated CT Scan (PET/CT)*

▪ Essential, most useful test to r/o distant metastatic disease57 (identified in ~20% if patients who are free of metastases
on CT / EUS to prevent unnecessary high morbidity surgery)
▪ Essential staging investigation in identification of distant metastases not evident on CT
▪ Can also be used for assessing recurrence or re-staging after neoadjuvant therapy
** Mechanism: malignant tumours exhibit an increased rate of glycolysis hence accumulate more glucose than normal cells (glyc olytic catabolism) →
preferential uptake within tumour tissue in fasted patients. PET scan uses the glucose analogue 18-FDG. 18-FDG transported from blood into cells via
GLUT 1. In the cells, FDG is phosphorylated by hexokinase to form FDG-6-phosphate which is trapped within the cell.
4. Surgical Laparoscopic Staging (most beneficial for patients with adenocarcinoma) (controversial)
▪ For patients with distal esophageal tumour who appear free of distant metastases on CT scan (T3-T4)
▪ Can r/o occult liver metastasis and peritoneal carcinomatosis not evident on CT scan
▪ Peritoneal lavage also performed at time of laparoscopy
Complications of Disease
1. Blood Tests
▪ FBC: low hemoglobin (anemia from chronic blood loss), raised TW (? aspiration pneumonia)
▪ U/E/Cr: electrolyte derangement for vomiting, poor oral intake
▪ LFTs: low albumin with nutritional deprivation
2. Rigid Bronchoscopy with biopsy and brush cytology
▪ For patients with supracarinal primary tumours and suspicion of airway involvement (trachea-oesophageal fistula)
▪ Patients with tracheo-oesophageal fistula are not for surgery. For palliative care (survival ~6 months)
3. Laryngoscopy: assess vocal cord paralysis
Pre-operative Investigations
1. Blood Tests – FBC, RP, LFT, PT/INR/APTT, GXM
2. Cardiac Investigations – ECG, 2D Echogram
3. Respiratory Investigations – Lung Function Test: determine ability to tolerate single lung ventilation during operation
57 uptodate: Management of locally advanced unresectable esophageal cancer
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CLINICAL TNM “CTNM” STAGING (AJCC 8TH EDITION)58
Tis Carcinoma in situ / High Grade Dysplasia

Tumour invades submucosal
T1 (a) lamina propria or muscularis mucosae – can aim for endoscopic resection
(b) submucosa – at risk of nodal spread
T T2 Tumour invades muscularis propria
T3 Tumour invades adventitia
Tumour invades adjacent structures
T4 (a) invading pleura, pericardium or diaphragm – still resectable
(b) invading aorta, vertebral body, trachea – unresectable
No No regional node mets
N1 = 1-2 regional LN
N
N1-3 N2 = 3-6 regional LN
N3 = 7 or more regional LN
M0 No distant metastasis
M
M1 Distant metastasis
(NOTE: the staging differs between SCC and AC. For example, T4aN1 is Stage IVA for SCC, but Stage III for AC.)
(NOTE: there is a different staging for pathology “pTNM” and post-neoadjuvant therapy “ypTNM”)
58 J Thorac Oncol. 2017 Jan;12(1):36-42.
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MANAGEMENT
Treatment of esophageal cancer involves a multimodal approach involving surgery +/- chemotherapy +/- radiotherapy. The exceptions
are for early disease (T1N0) which can be managed with endoscopic resection and for metastatic disease for which treatment is
palliative.
Approach to selection of treatment modality

- Stage of Oesophageal Cancer
▪ Very early tumours (Tis, T1a) → endoscopic submucosal dissection (ESD) – see below
▪ Tumour confined to oesophagus (T1b, T2) → controversial can either do upfront surgery or neoadjuvant chemoRT
(adenocarcinoma) → at present, current staging modalities are not reliable to confidently stage tumours clinically as T2
▪ Locally advanced tumours (T3-4, N1-3) → multimodal therapy with neoadjuvant chemoRT or neoadjuvant chemotherapy
followed by surgical resection

- Upfront esophagectomy has high rates of recurrence and low 5 year survival, hence multi-modality therapy preferred
- Depending on histology, SCC and Adenocarcinoma have different sensitivities to radiotherapy
▪ Metastatic Disease (M1) → palliative treatment (endoscopic methods to treat malignant dysphagia or fistulous disease)
▪ Malignant dysphagia (M1) → expandable oesophageal stent or RT (for GEJ cancer, as stents leads to severe GERD)
Feeding in oesophageal obstruction

- Feeding via PO route is preferred unless the passage is obstructed (i.e. risk of aspiration)
- If still able to pass NG tube around tumour, then feed via NG (but also consider complications with long-term NG placement e.g.
erosions around nasal area, sinusitis); consider PEG placement* for long-term feeding if able to get scope around tumour
- If unable to pass tube or scope around tumour, consider total parenteral nutrition or open gastrostomy
- Relief of obstruction via endoscopic stenting and/or radiotherapy helps to enable oral feeding, but most techniques are not long-
lasting and dysphagia will return with tumour growth
Endoscopic Therapy for Localized Disease

- Endoscopic Submucosal Dissection (ESD)
▪ Advocated for early cancers such as T1a (mucosa)
▪ T1a tumours have 1-5% chance of LN spread as compared to T1b tumours (involve submucosa) which have 17-20% risk
of LN spread
▪ ESD better than EMR in terms of recurrence rates, curative rates with equivalent rates of complications (perforation, stricture,
bleeding)
Neoadjuvant Therapy
- Long-term survival advantage with the use of trimodal therapy with neoadjuvant chemoradiotherapy followed by surgery in the
treatment of oesophageal cancer as compared to surgery alone
- Varying sensitivities between SCC and Adenocarcinoma with radiotherapy hence different centres have different neoadjuvant
approaches
- Some centres practice neoadjuvant chemoRT for SCC and neoadjuvant or peri-operative chemotherapy (i.e. chemotherapy
before and after surgery) for adenocarcinoma
121
Surgery
- Transthoracic Esophagectomy
▪ Ivor Lewis (2-stages) which involves gastric mobilisation (first stage, done through upper midline abdominal incision),
oesophagectomy, extended lymphadenectomy and intra-thoracic esophagogastric anastomosis (second stage, through
right posterolateral thoracotomy)
▪ McKeown (3-stages) which involves right posterolateral thoracotomy or thoracoscopy, then abdominal (via laparotomy)
and then cervical portion (for cervical esophagogastric anastomosis via left neck incision)
▪ Minimally invasive esophagectomy (MIE)* – can be total MIE, hybrid MIE or robotic MIE
- Trans-hiatal Esophagectomy
▪ Two incisions – one in the abdomen (via upper midline laparotomy) and one in the neck (left neck incision)
▪ Avoids thoracotomy and involves a cervical esophagogastric anastomosis
▪ Blunt esophagectomy(removal of oesophagus), gastric mobilisation with creation of neo-oesophagus* (gastric conduit) and
cervical esophagogastrostomy (translocation of the stomach)
▪ Less morbidity than Ivor-Lewis as the chest is not opened
▪ The colon or jejunum can also be used if the stomach is not a suitable conduit
*MIE have similar oncological outcomes with benefits of MIE including shorter LOS, reduced pain, reduced pulmonary and postoperative
complications. No difference in relation to anastomosis outcomes. In an event where thoracoscopic esophagectomy cannot be s afely performed, a
hybrid MIE with a laparoscopic gastric mobilization still yields the benefits of MIE surgery.
EXTRA INFORMATION
Important considerations between the 2 approaches59
Transthoracic Trans-hiatal
Approach via right or left chest via abdomen

better visualization finger dissection
Surgical factors allow better LN clearance, LN yield higher (+8) no nodal clearance, LN yield lower
intrathoracic anastomosis neck anastomosis
Patient factors For middle ⅓ and/or bulky tumour For lower ⅓ and/or smaller tumours
Anastomotic Leak lower (10.6%) Anastomotic Leak higher (16.9%)

Vocal cord Paralysis lower (5.6%) Vocal cord Paralysis higher (10.9%)
Complications
Pulmonary complications Higher (35.7%) Pulmonary Complications Lower (28.0%)
Wound Infection Higher (10.1%) Wound infection Lower (6.4%)
Longer LOS Shorter LOS (-4 days)
Outcomes 30 days mortality (10.6%) 30 days mortality (7.2%)
5 year survival same* (26.6%) 5 year survival same* (25.8%)
Management Post-esophagectomy60
- Analgesia – IV or epidural (i.e. morphine or bupivacaine)
- Gastrointestinal
▪ NBM – 5 to 7 days
▪ Jejunostomy feeding tube – placed during surgery and start feeding on POD 2-3
▪ NG tube on low level intermittent suction
▪ Gastrografin swallow – day 5 to 7 to check for anastomotic leak before initiating oral intake, can also add blue dye to check
for leakage of dye into chest tube suggesting anastomotic leak
▪ Escalation of feeds as tolerated – aim for 6 to 8 small frequent meals each day
- Prevention of complications
▪ Early mobilization (SOOB from POD 1)
▪ Aggressive Pulmonary Rehabilitation (i.e. incentive spirometry, chest physiotherapy)
59 Ann Surg. 2011 Dec;254(6):894-906.

60 Crit Care Nurse. 2004 Feb;24(1):16-29
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Palliative treatment (aim: relief obstruction and dysphagia) – median survival of 4 months
- Indication
▪ Metastatic oesophageal cancer (M1)
▪ Cancer with invasion of adjacent organs (T4b)
▪ Aortic oesophageal fistula (~100% lethal)
- > 50% of patients at presentation is only suitable for palliative treatment
- Nutritional support with percutaneous endoscopic gastrostomy (PEG) or jejunostomy tube (PEJ)
- 2 arms of treatment (local treatment - treat dysphagia, and systemic treatment)
Local Treatment
- Endoscopic Intraluminal Prosthesis
▪ Mostly only pureed diet tolerated
▪ Self-expanding metal stents (i.e. SEMS, uncovered metal stent) preferred over plastic stents
▪ Procedural related mortality ~ 1-2%, early complication rates ~ up to 30%
- Risk of perforation, malposition, incomplete stent expansion, migration of stent (1%), obstruction of tube by food,
tumour ingrowth or overgrowth
- Pyloric stents may be used as first line treatment in patients with poor prognosis requiring palliation of gastric outlet
obstruction. If patient is fit with longer life expectancy, can consider gastro-jejunostomy
- External Beam Radiotherapy (EBRT)

▪ Compared to stenting, EBRT have slower relief of dysphagia, but is effective for patients whose tumour are bleeding
▪ Palliation of dysphagia is successful temporarily in 80% of patients but rarely provide relief for longer than several months
▪ Usually given in combination with palliative chemotherapy
Systemic Therapy
- Chemotherapy
- Targeted Therapy → herceptin (for patients with Her-2 overexpression)
COMPLICATIONS
- Cardiovascular Complications: post-esophagectomy atrial fibrillation, AMI / VTE
- Pulmonary Complications: atelectasis, pneumonia, ARDS
- Oesophageal anastomosis complications: anastomotic leak and resultant mediastinitis (chest anastomosis), anastomotic
strictures secondary to healed anastomotic leaks, conduit Ischemia
- Gastric Outlet Obstruction (transected vagal nerve)
- Other local traumatic complications: chylothorax (can be low or high volume), bleeding, injury to recurrent laryngeal nerve
▪ Low volume chylothorax (<500ml/day), manage conservatively (i.e. enteral intake with medium chain TG, NBM with parental
nutrition ±octreotide), if chylothorax persists – consider talc pleurodesis
▪ High volume chylothorax (>1000ml/day), thoracic duct embolization or thoracic duct ligation or talc pleurodesis
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GASTRO-OESOPHAGEAL JUNCTIONAL (GEJ) TUMOUR
DEFINITION
GEJ tumours are defined as tumours with the epicentre arising from distal 5cm of oesophagus, the GEJ or the cardia of the stomach
(within 5cm of the GEJ) with extension into the GEJ or oesophagus
CLASSIFICATION (SIEWERT)
- Type 1 – distal oesophagus (within 1-5cm above anatomic GEJ)
- Type 2 – cardia (within 1cm above and 2cm below GEJ)
- Type 3 – sub-cardial (2-5cm below GEJ)
TREATMENT / MANAGEMENT61
- Rationale for aggressive neo-adjuvant therapy → improve overall survival
▪ Eradication of micro-metastatic disease
▪ Downsizing tumour to improve rates of R0 resections
▪ Better tolerance of intensive therapy prior to surgery
▪ Adjustment of treatment based upon response
- Perioperative chemotherapy (Europe) or Perioperative chemo-radiotherapy (USA)

▪ For patients with ≥T2 tumour and LN positive loco-regional disease
Treatment Approach
- Type 1 – treat as per oesophageal cancer (esophagectomy)
- Type 3 – treat as per gastric cancer (total gastrectomy or proximal gastrectomy [possible if stage 1])
- Type 2 – debatable*
▪ Total gastrectomy + distal esophagectomy
▪ Esophagectomy + proximal gastrectomy
* determining factors – extent of oesophageal involvement (if <2-3cm: extended gastrectomy, if >2-3cm: esophagectomy), mediastinal
nodal involvement, T staging, patient’s fitness for operation
61 Oncologist. 2015 Feb;20(2):134-42
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HIATUS HERNIA
- Asymptomatic
- GERD symptoms
- Obstructive symptoms – transient obstruction of the GEJ (i.e. dysphagia, regurgitation), obstruction of distal stomach (i.e. nausea,
vomiting, palpitation, shortness of breath, dyspnoea, chest pain & early satiety)
- Cameron ulcers leading to bleeding and chronic iron deficiency anemia
- Acute gastric volvulus: Gastric Ischemia – septic shock, epigastric pain, multi-organ failure
- Borchardt’s triad – epigastric or chest pain, retching without vomiting and inability to pass a nasogastric tube
CLASSIFICATION
Type 1 – Sliding hernia Type 2 – Classic paraesophageal hernia (rolling)
- Most common - Only gastric fundus is displaced
- Only GEJ is displaced - Cardio-oesophageal junction is intact but fundus of stomach rolls
- Upper stomach and lower oesophagus slide upwards into chest
up through the hiatus in front of the oesophagus → patient
through the lax hiatus when the patients lies down → patient
experiences epigastric discomfort, flatulence, dysphagia,
experiences oesophagitis with heartburn, bleeding, eventually
heartburn, but no regurgitation
stricture formation - Can also have iron deficiency anemia in 50% of patients
- Cameron lesions – linear gastric erosions in patients with
paraesophageal hernia that can be a/w severe acute or chronic
occult GI bleeding)
Management:
- Observation vs surgical repair – dependent on symptoms
- Transthoracic vs transabdominal approach, open vs laparoscopic
repair – Preferred: lap transabdominal approach with repair of
paraesophageal hernia, cruroplasty and fundoplication
- Primary suture repair vs mesh repair – primary suture repair a/w
recurrence rates of 20-30% (mostly asymptomatic)
- Biologic mesh vs prosthetic mesh – prosthetic mesh has lower
recurrence rates (risk of erosion/stricture formation ~2%)
Type 3 – Mixed paraesophageal hernia (combined sliding-rolling) Type 4 – Giant hernia

- Both GEJ and gastric fundus are displaced - Presence of an additional organ within the hernia sac
- Upward dislocation of both the cardia and the gastric fundus - Eg colon (usually transverse), omentum, spleen
- Management: repair of hiatal hernia and fundoplication
EXTRA INFORMATION
INVESTIGATIONS
- CXR: retrocardiac air–fluid level and often a second one below the diaphragm
- Barium Swallow: shortened oesophagus
125
- CTAP: presence of stomach within the chest

- OGD: to identify presence of any gastric ischemia, ulceration or erosions
COMPLICATIONS
- Gastrointestinal Bleeding
- Iron Deficiency Anemia
- Gastric Volvulus – rotation of stomach more than 180 degrees around a fixed axis of rotation which leads to gastric necrosis,
perforation, severe sepsis and multi-organ failure
▪ Anatomical Classification – (a) organoaxial (longitudinal) axis which leads to gastric strangulation, (b) mesenteroaxial
(transverse) which leads to intermittent gastric obstruction
▪ Presentation – severe epigastric pain, retching and inability to vomit, inability to pass a nasogastric tube, severe chest
pain (incarcerated segment within the chest)
▪ Management – urgent NG decompression, aggressive IV fluid resuscitation, surgical repair
MANAGEMENT
- All symptomatic type II–IV hernia should be repaired, especially in patients with obstructive symptoms or previous gastric
volvulus
- Initial Management
▪ Insertion of NG tube for gastric decompression
▪ Prompt IV fluid resuscitation
- Surgery
▪ Complete excision of hernia sac
▪ Assessment of adequate intra-abdominal oesophageal length and management of short oesophagus
▪ Creating the antireflux barrier → fundoplication (Nissen or Toupet)
▪ Repair of diaphragmatic hiatus
▪ Anterior Gastropexy – to secure stomach within abdomen
- Post-operative complications: recurrence of hiatus hernia
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OESOPHAGEAL PERFORATION
A true surgical emergency (mortality 10-40%) – most commonly at left lateral wall of oesophagus 3-5cm above GEJ
RISK FACTORS
- Iatrogenic (i.e. instrumentation of oesophagus, OGD, trans-oesophageal echocardiogram, pneumatic dilatation, placement of
intra-oesophageal tubes, traumatic intubation)
- Spontaneous perforation (Boerhaave’s Syndrome), often barogenic trauma after severe vomiting,
▪ characterized by Mackler’s triad: vomiting, chest pain and subcutaneous emphysema
- Foreign body perforation
- Caustic ingestion
- Blunt / Penetrating trauma
- Pain – cervical area / substernal area
- Cervical crepitation / swelling (subcutaneous emphysema)
- Fever (after instrumentation of the oesophagus)
- Hartmann’s sign – mediastinal crunching on auscultation (pneumomediastinum)
- Stony dullness on percussion over intercostal space (pleural effusion)
- Medical: myocardial infarction, pericarditis, pneumothorax, pneumonia, mallory-weiss tear
- Suriglca: acute pancreatitis, peritonitis, aortic aneurysm (dissection), mesenteric ischemia, perforated peptic ulcer
DIAGNOSIS / INVESTIGATIONS
- CXR: pleural effusion, pneumomediastinum, subcutaneous emphysema, hydropneumothorax, collapse / consolidation
▪ Distal oesophageal rupture lead to left sided pleural effusion
▪ Mid-thoracic rupture lead to right sided pleural effusion (more likely)
- Computer Tomography Thorax, Abdomen & Pelvis (imaging of choice) + oral contrast
- Contrast esophagram (i.e. gastrografin, patients in right lateral decubitus position), look for contrast extravasation
MANAGEMENT62
Aim for sepsis control & elimination of on-going contamination of mediastinum, chemical pleuritis, peritonitis
General
- NBM + Resuscitation + IV fluids with monitoring of urine output
- Broad-spectrum antibiotics – coverage of UGI pathogens +/- Antifungals
- IV PPI
- NGT (placed under endoscopic or radiological guidance) - to decompress the stomach
- Early escalation of care, early referral to HD/ICU
- Enteral feeding assess (NJ feeding tube or feeding jejunostomy)
- Chest tube, if have significant pleural effusion – food debris / purulent discharge can establish diagnosis of rupture
- OGD – diagnostic & therapeutic (i.e. KIV stent placement)
▪ Stenting contraindicated in long tears (>6cm), delayed presentation due to substantial tissue necrosis (>24hrs), proximal
oesophagus (posterior pharynx) and distal oesophagus / GEJ (distal flare will not attach to stomach)
▪ Stenting is useful in setting of malignancy
Non-operative Management (selected situations – Cameron’s Criteria)

- Contained perforation within the mediastinum with good drainage into oesophagus (on contrast swallow)
- Symptoms should be mild, no symptoms of mediastinitis
- No solid food contamination of mediastinal or pleural space
- Minimal evidence of clinical sepsis
- Treatment: NBM, IV Abx +/- antifungals, IV PPI (decrease acid secretion)
62 Thorac Surg Clin. 2011 Nov;21(4):541-55.
127
Operative Management for Non-contained Perforation

- < 24 hours (80-90% survival) → primary closure with drains + longitudinal myotomy +/- muscle flap
- > 48 hours with extensive contamination (< 50% survival)
▪ Neck → place drains, no esophagectomy
▪ Thorax → resection of diseased portion of oesophagus with end cervical esophagostomy or exclusion and diversion (i.e.
cervical esophagostomy, staple across distal esophagus, mediastinal washout, place chest tubes)
▪ Gastric replacement of esophagus when patient recovers
EXTRA INFORMATION
Endoscopic Description of Caustic Injuries (Zagar Classification)63

- Grade 0: normal mucosa
- Grade I: edema and erythema of the mucosa
- Grade IIA: Hemorrhage, esrsions, blisters, superficial ulcers
- Grade IIB: Circumferential Lesions
- Grade IIIA: focal deep gray or brownish black ulcers
- Grade IIIB: extensive deep gray or brownish-lack ulcers
- Grade IV: Perforation
63 World J Gastrointest Pharmacol Ther. 2017 May 6; 8(2): 90–98
128
5. STOMACH
ANATOMY & PHYSIOLOGY OF THE STOMACH
Stomach Glands
Location Cells Hormone Function
Cardia Mucus secreting
Pepsinogen - Pepsinogen converted to Pepsin by low pH in stomach lumen
Chief Cells
(secretory granule) - Initiate proteolysis
Fundus HCl (H+)
- Histamine, Gastrin and Acetylcholine → increases HCl secretion
& Parietal Cells & Intrinsic Factor
Body (IF) - IF binds B12, re-absorbed in terminal ileum
Enterochromaffin
Histamine
-like cells (ECL)
Mucus & HCO3- - Protects stomach
Stimulated by acid in duodenum
Antrum Somatostatin
D cells - Inhibits gastrin, insulin, secretion, glucagon
& (great inhibitor)
- Inhibits biliary and pancreatic output
Pylorus Stimulated by gastric distention, amino-acid & Ach, calcium, EtoH
G cells Gastrin
- ↑HCl, intrinsic factor and pepsinogen secretion
Brunner Gland Alkaline mucus
Stimulated by amino acids and fatty acid chains
Cholecystokinin - Contract gallbladder
I cells - Relax sphincter of oddi
(CCK)
- ↑pancreatic enzyme secretion
K cells
Gastric Inhibitory Stimulated by glucose and fatty acids
(duodenum &
Peptide (GIP) - Stimulate insulin secretion
jejunum)
M cells Motilin - ↑intestinal motility (erythromycin acts on this receptor)
Duodenum
- ↑pancreatic bicarbonate secretion
- Inhibits gastrin release & HCL release
S cells Secretin
- High flow – ↑HCO3- & ↓Cl-
- Low flow – ↓HCO3- & ↑Cl-

- Activates trypsinogen (zymogen) to its active form trypsin (once
activated, trypsin can activate more trypsinogen to trypsin)
Enterokinase
Others - Trypsin activates other pancreatic digestive enzymes (i.e.
(Enteropeptidase)
chymotrypsinogen to chymotrypsin, proelastase to elastase,
procarboxypeptidase to carboxypeptidase and prolipase to lipase)
129
5. Stomach_Last Updated 3rd June 2020
Blood Supply of the Stomach
Junction of pylorus with duodenum – marked by a constriction externally and by a constant vein (of Mayo)
130
APPROACH TO BLEEDING UPPER GIT
DEFINITION
Upper Gastrointestinal Tract Bleeding (UBGIT) is defined as bleeding that occurs proximal to the ligament of Treitz. The ligament of
Treitz is the suspensory muscle of the duodenum that connects the DJ flexure to the connective tissue surrounding the celiac axis
and SMA .
Patients commonly present with hematemesis (vomiting of red blood or coffee-ground vomitus) and/or melena. Patients can present
with hemorrhagic shock, hence, initial assessment begins with the assessment of the hemodynamic status of the patient.
There is a spectrum of presentation which corresponds to the rate of bleeding. Patients who present with hematemesis of bright red
blood have a faster rate of bleeding as compared to a patient with coffee ground vomitus. Similarly, patients who present with
passage of dark red blood (frank PR bleeding) have a faster rate of bleeding as compared to a patient with melena. The passage of
dark red blood may indicate a massive UBGIT which is masquerading as PR bleed.
Factors that are predictive for UBGIT64 includes patient-reported history of melena (LR: 5.1-5.9), melenic stool on examination (LR:
25), blood or coffee grounds detected during NG lavage (LR: 9.6) and ratio of BUN to Serum Cr > 30 (LR: 7.5). The presence of blood
clots in the stool made an UBGIT less likely (LR: 0.05)
History & Examination
1. Nature of bleeding (is this haemoptysis or UBGIT)
Haemoptysis
- Bloody expectoration from the larynx, trachea, bronchi and the lungs
- Patient will describe a sensation in their throat followed with the abrupt expectoration of blood (frothy and bright red)
Hematemesis (red blood or coffee-ground emesis)

- Vomited blood might be mixed with food particles
- Colour of vomitus depends on contact time with HCl acid from stomach (red → brown)
- Fresh red blood suggest moderate to severe bleeding
- Coffee grounds vomitus is altered blood due to gastric acid, suggest limited bleeding
Hematemesis Haemoptysis
Not associated with cough Associated with Cough
Not Frothy Frothy
Darker Red (altered by gastric acid) Bright Red (aerated)
Melena Present Melena Absent
Melena
- Passage of altered blood (black tarry stool) that originate proximal to the ligament of Treitz (90%) – types of melena:
● Fresh melena – jet black with sheen, tarry, non-particulate, almost liquid in consistency (suggest fairly acute bleeding)
● Stale melena – black-grey, dull, mixed with normal stool, occasionally particulate (suggest bleed which stopped followed
with melena)
- Ddx: Iron stool – greenish hue on rubbing between gloved fingers, particulate. if gloved finger is stirred in a cup of water, melena
will “dissolve” completely with no sedimentation and turn the water black, but iron stool will have sedimentation and turn the water
green
Frank PR bleeding
- Very brisk upper GI bleed which can present as frank PR bleeding as blood passes down so fast it doesn’t get altered
- In the presence of hemodynamic instability, this indicates severe bleeding
2. Determine Etiology (variceal vs. non-variceal bleed)
Variceal Bleeding
- Any previous variceal bleed, ask patient if he/she goes for regular banding or OGD screening and banding
- Any history of chronic liver disease, ask for risk factors (i.e. alcohol ingestion, hepatitis B/C, any regular follow-up for liver disease
– AFP, U/S HBS)
64 JAMA. 2012 Mar;307(10):1072-9.
131
Non-Variceal Bleeding
- Peptic Ulcer Disease (most common cause)
● History of dyspepsia, previous H. pylori infections, previous endoscopy (OGD) performed
● Drug History – NSAIDs, antiplatelets, steroids, anticoagulants, TCM
● Secondary to cirrhosis-induced hypergastrinemia from decreased hepatic metabolism of GI hormones
- Stress Ulcer
● Curling ulcer – large acute ulcer in the duodenum (cx from burns) – can cause mucosal ischemia
● Cushing’s ulcer – gastric ulcer produced by elevated ICP (i.e. head trauma) – vagal stimulation leads to increased Ach &
H+ production
- Mallory-Weiss tear
● Diagnosis requires a high index of suspicion
● Characterized by arterial bleeding (hematemesis or melena – depending on volume), secondary to violent retching following
alcoholic binge (rapid increase of intra-abdominal and intraluminal gastric pressure).
● This leads to one or more longitudinal fissures in the mucosa of the herniated stomach at the GEJ
● Majority of bleed with stop spontaneously with non-operative management (decompress stomach and give antiemetics)
- Dieulafoy’s Disease – AVM of the gastric fundus

● Presents with massive or recurrent bleeding coming from an area of apparently normal gastric mucosa.
● Characterized by a large tortuous arteriole in the submucosal that bleeds
● More common in males, with multiple comorbid (i.e. HTN, IHD, ESRF, DM)
● Suspect in patients presenting with BGIT with no history of alcohol abuse or NSAIDs use
- Malignancy (gastric / oesophageal carcinoma)

● Early lesions: asymptomatic, epigastric pain, dyspepsia
● Intermediate lesions: anemia, melena, hematemesis, early satiety, dysphagia, nausea/vomiting, bloatedness
● Late lesions: loss of appetite, loss of weight, palpable epigastric mass, obstructive jaundice (mets to liver)
- Gastric Antral Vascular Ectasia

● Dilated mucosal blood vessels that often contain thrombi in the lamina propria (predominantly affects distal stomach),
appears as longitudinal linear red streaks on the antrum mucosa (i.e. watermelon stomach)
● More common in elderly women with chronic occult GI blood loss
● Associated with autoimmune connective tissue disorder and/or chronic liver disease
3. Quantify the amount of bleeding

- If the patient presents with haematemesis, ask how much blood vomited, Cup? Bowl?
- When patients have hematemesis, there can by up to 1.5L of blood in the stomach (bleeding more than pylorus can empty)
- Is patient symptomatic from BGIT, any symptoms of chest pain, shortness of breath
- Gauge percentage of blood loss
● 15-30% 🡪 class 2 – Narrowed Pulse Pressure, Resting Tachycardia, Postural Hypotension
● 30-40% 🡪 class 3 – Supine Hypotension, marked tachypnoea, confused, anxious
● > 40% 🡪 class 4 – Minimal urine output, markedly depressed or lethargic
132
4. Comorbidities
- Ask about other significant medical history, of importance is cardiac history, renal history
● Presence of IHD/CCF will predispose patients to fluid overload during resuscitation
● Presence of ESRF will predispose patients to fluid overload during resuscitation
- Ask about other significant medication history

● Presence of antiplatelets, anticoagulants, novel oral anticoagulants (should be stopped in acute bleed)
● Presence of anti-hypertensive medications (should be stopped in acute bleed), Beta-blockers can mask tachycardic
response
● Is patient previously on any proton pump inhibitors or H2 antagonist
Clinical Examination
1. Vital Signs (most important)

- Assess hemodynamic stability – blood pressure, heart rate, oxygen saturation
2. Confirm UBGIT
- DRE for melenic stool (differentiate from Fe-laden stools)
- If NGT in-situ, can aspirate on NGT
3. Determine Etiology
- Variceal Bleed: look for stigmata of chronic liver disease, jaundice
- Non-variceal bleed
4. Look for complications

- Signs of Anemia
● Face – (i) conjunctival pallor (ii) pallor of mucous membrane
● Cardiac Auscultation – short systolic flow murmur at aortic area (rarely assessed)
● Pulse – (i) tachycardia (ii) bounding (iii) collapsing pulse
● Hands – pallor of palmar creases
- Urine output – is patient clinically dehydrated
- Lungs: auscultate for any aspiration pneumonia
- Exclude peritonism – contraindication for endoscopy (ensure no abdominal guarding / rigidity)
Diagnostic Studies
133
Variceal Bleed
- Oesophageal
- Gastric
- Duodenum
Non-variceal Bleed
Oesophagus Gastric Duodenum Others
Esophagitis Peptic Ulcer Disease Peptic Ulcer Disease Aorto-enteric fistula*
Mallory Weiss Tear Erosive Gastritis Lymphoma Dissecting Aneurysm
Oesophageal Cancer Stomach Cancer HOP cancer, CholangioCa,
Periampullary Cancer
Boerhaave Syndrome Dieulafoy’s Lesion HCC
Trauma (OGD / NGT) AVM (i.e. GAVE) Trauma (ERCP with
AVM (i.e. angiodysplasia)
Trauma (OGD / NGT) sphincterotomy)
* Especially if have recent history of AAA repair in last 6 -12 months
Others
- Bleeding from other sources: Haemoptysis, nasopharyngeal bleeding
MANAGEMENT
Patients' hemodynamic status must be immediately assessed. Fluid resuscitation is the first step in the management. Once the patient
is stabilized he can be transferred for further investigations to determine the cause of the bleeding. Escalate to seniors early if the
patient is hemodynamically unstable.
1. Fluid Resuscitation
- Assessment begins with Airway, Breathing & Circulation
- If patients can respond logically, his airway and breathing is intact. Logical responses also suggest good cerebral perfusion. If
airway or breathing is affected, consider early intubation to protect the airway from risk of aspiration pneumonia
- Circulation: even if patient appears to be hemodynamically stable, he may be in class 1 hypovolemic shock, management should
be pre-emptive
● Nasal Prongs (supplemental O2 to increase O2 carrying capacity)
● IV cannula: 2 large bore 18G catheter inserted at the antecubital fossa
● IV cannula sizes: 14G – orange, 16G – grey, 18G, green, 20G, pink, 22G, Blue, 24G – yellow
● Bloods should also be taken for investigations: GXM, FBC, U/E/Cr, PT/PTT/INR, LFT, Trop I
○ GXM: needed prior to ordering of cross-matched bloods
○ FBC: assessment of hemoglobin level (compare against the baseline), assessment of platelet level (any risk of bleeding)
○ U/E/Cr: assessment of urea level (isolated uremia suggestive of UBGIT), assessment of creatinine or eGFR (may
require contrasted scans to investigate bleeding)
○ PT/PTT/INR: assessment of degree of coagulopathy (especially important for patients on anticoagulants)
○ LFTs: deranged in patients with chronic liver disease, suggestive of possible variceal etiology
○ Trop I: patients are at risk of developing T2MI with severe blood loss
○ ABG/Lactate: useful in patients presenting with hemodynamic instability / hypovolemic shock
● ECG to rule out cardiac event
- Circulation: if patient is hemodynamically unstable

● Fluid resuscitation with crystalloids / ± colloids / packed cells / platelets / FFP
● Run in 1L N/S fast (i.e. over 15 mins) and assess clinical response
○ Responder: sustained improvement clinically & biochemically
○ Transient responder: transfuse blood products, if unavailable, can consider colloids
○ Non-responder: E-bloods (may require massive transfusion protocol)
● Restrictive transfusion strategy to keep Hb > 7g/dL (showed improved outcomes as compared to liberal transfusion strategy
[transfusion when Hb < 9] in patients with acute UBGIT) 65
● May consider platelets if patient has quantitative (i.e. <50k) or qualitative (i.e. on antiplatelets) deficits
● FFP if patient is on anticoagulants or PT/PTT prolonged (+/- IV vitamin K) - refer to protocol
2. Adjuncts
- NG tube if patient is having hematemesis – prevents aspiration, allows gastric lavage prior to OGD (DO NOT insert if suspect
varices) – can also be used to confirm suspicion of UBGIT
- Arterial Line / CVP – for monitoring of hemodynamic status
65 N Engl J Med. 2013 Jan 3;368(1):11-21. [Important Paper]
134
- IDC insertion – monitor I/O balance esp. in elderly or when large amount of fluid resuscitation required, or anticipating surgery
- Intubate if patient having massive uncontrolled active hematemesis or signs of decompensation
- Targets: Keep MAP: > 60mmHg (for end-organ perfusion), urine output > 0.5ml / kg / hr & Hb: ≥ 7 or ≥ 9 (IHD)
3. Early medications
- IV omeprazole 80mg bolus followed by 8mg/hr for 3 days (decreases stomach pH which helps in stabilizing clot formation)
- If suspecting varices – IV somatostatin 250mcg followed by 250 mcg/hr &, IV ceftriaxone 1gm once
- If planning for urgent endoscopy, KIV for IV erythromycin (for gastric emptying)
- Withhold all antiplatelets, anticoagulants,NOAC, NSAIDS, anti-hypertensive
4. Urgent esophagogastroduodenoscopy (OGD)
- Indications:
1. Hemodynamic instability despite fluid resuscitation (ensure BP is stable before OGD – requires sedation)
2. Active BGIT, in patients presenting with hematemesis and/or fresh melena
3. Suspected variceal bleed (bleeding can be brisk)
- Risks / Benefits
● Anaesthetic Risk: Risk of Sedation – respiratory depression secondary to airway compromise. CVS risk – AMI, CVA
● Procedural-Related Risk
○ Bleeding and Perforation (1 in 10,000)
○ Failure of endoscopic haemostasis
○ Failure of complete scope – standard OGD scope to D2
● Benefits: OGD will help to diagnose the source of bleeding, enable therapeutic procedures to be carried out and allows for
prognostication of re-bleeding
- Patients whose condition does not stabilize after initial resuscitation (i.e. hypovolemic shock), proceed for urgent endoscopy.
- However, if patients are high risk (i.e Glasgow–Blatchford score of ≥ 12) but hemodynamically stable, endoscopy performed
within 6 hours after GI consultation was not associated with lower 30-day mortality than endoscopy performed between 6 and 24
hours after consultation.66
66 Timing of Endoscopy for Acute Upper Gastrointestinal Bleeding [await pubmed link]
135
- Confirms UBGIT & identify source of bleeding,

- Biopsy of gastric mucosa (+ CLO test* if ulcer) – All gastric ulcers should be biopsied (6 bites) – risk of underlying
Diagnostic
malignancy & would require f/u scope in 6 weeks to document ulcer healing (in setting of active bleeding, may
not be able to perform endoscopic biopsy)
- Injectable – adrenaline, sclerotherapy, procoagulants
- Thermal – heat/diathermy, Argon Plasma Coagulation (APC)
- Mechanical – hemoclips,, endoscopic variceal ligation (EVL)
- Varices: (i) Band ligation/sclerotherapy, (ii) glue

- Non-variceal: (i) HaemoClip, (ii) Injection of adrenaline (1:10,000), (iii) APC (heater probe)
Principle: Dual modality better than single (as less risk of recurrent bleed and mortality). Patients usually undergo
Adrenaline Injection + HaemoClip/Heater probe
Therapeutic
NEWER ADVANCES
- Haemostatic Spray – non-contact, highly adsorptive proprietary mineral blend (powder) which forms a
mechanical plug that adhere to bleed site and activates clotting cascade
- Over-The-Scope-Clip* (OTSC) – for (1) recurrent post-EMR duodenal bleeding (failed adrenaline injection,
bipolar coagulation, through-the-scope (TTS) clips) and (2) rescue therapy
- Endoscopic Suturing – for marginal and peptic ulcers, direct vessel ligation (acute lesions), lesion closure
(fibrotic ulcers), prophylactic closure of large EMR/ESD defects
- Endoscopic stigmata of recent haemorrhage – forest classification
Prognostic
SUBSEQUENT MANAGEMENT
Patient are to receive 80mg bolus IV PPI followed by continuous infusion of 8mg / hr of IV PPI for 72 hours (thereafter revert to
oral PPI) to reduce rate of recurrent bleeding, shortened length of hospitalization, decreased need for endoscopic re-treatment and
blood transfusion67
For duodenal ulcer bleeding, presume this is related to H. Pylori infection. Treatment involves triple therapy with omeprazole 20mg
BD (for 6 weeks), amoxicillin 1g BD, clarithromycin 500mg BD for 10-14 days followed by urea breath test at clinics.
Scoring systems are available to guide clinicians on the risk of re-bleeding. This includes the Rockall and Glasgow Blatchford Bleeding
Score.
Management of Re-bleeding
- Repeat OGD and re-attempt endoscopic haemostasis
- If failure of endoscopic haemostasis
● Surgery: normally have 2 goals: curative and decrease acid component, but mortality and morbidity risk is high so better to
keep surgery short thus rather than decreasing acid component, patient is placed on life-long PPI
● Radiological Intervention: CT mesenteric angiogram OR mesenteric angiogram KIV embolization
○ CT: non-invasive, require contrast (risk of nephropathy)
○ Mesenteric Angiogram: catheterize through femoral artery(risk of puncture), require contrast, if negative can be due to
low blood flow rate 🡪 KIV prop up BP but risk of further bleed (clinical judgment call)
67 N Engl J Med 2000; 343:310-316. Effect of intravenous omeprazole on recurrent bleeding after endoscopic treatment of bleeding peptic ulcers. [Landmark Paper]
136
Blatchford Scoring System: only clinical and laboratory factors, no endoscopic component
> 6 is associated with greater than 50% chance of needing an intervention
More commonly used than Rockall score as it does not require OGD. In ED setting, can treat as outpatient if score = 0
AIMS 65 Scoring System: prognosticate inpatient mortality rates

Albumin <30g/L 1 point = 1% mortality
INR > 1.5 2 points = 3% mortality
Altered Mental States (GCS < 14) 3 points = 9% mortality
Systolic BP <90mmHg 4 points = 15% mortality
Age > 65 5 points = 25% mortality
137
MASSIVE BLOOD TRANSFUSION

Transfusion equalling the patient’s blood volume within 24 hours
Complications of Massive Blood Transfusion68

Lethal triad – acidosis, hypothermia and coagulopathy a/w high mortality rates
Complications Features Minimize Risks

- 10% decrease in coagulation factor activity with each 1°C drop in - Warm room & patient
1 Hypothermia temperature - Warm all IV fluids & blood
- Decrease ability to form stable clots products
- 1:1:1 approach (FFP : platelets :
Coagulopathy &
2 - Dilutional and consumptive coagulopathy & thrombocytopenia RBC)
Thrombocytopenia
- Re-Factor VII as needed
- HypoK+ & HyperK+ (underlying renal insufficiency)
- HypoCa2+ (citrate* binding ionized calcium)
3 Electrolytes - Monitor and correct accordingly
- Hypo Mg2+ (citrate binding to mg and large volumes of mg deficient
fluids)
- Citrate metabolized to bicarbonate 🡪 metabolic alkalosis
- If severe metabolic acidosis,
4 Acid-Base Disorders - Metabolic acidosis 🡪 due to inadequate tissue perfusion (and not blood
consider sodium bicarbonate
product)
- TRALI – acute lung injury that occurs within 6 hours of transfusion
Transfusion Related - Minimize transfusion once
5 - Massive blood transfusion a/w development and increased mortality in
Acute Lung Injury bleeding controlled
ARDS
- Fluid overload leading to acute pulmonary edema – transfusion
associated circulatory overload
- Infection – bacterial / viral**
6 Others
- Allergic Reaction / Anaphylaxis
- Acute Febrile Haemolytic Reaction***
- Non-haemolytic febrile transfusion risk****
* Blood is anti-coagulated with sodium citrate & citric acid, citrate toxicity: metabolic alkalosis, hypocalcaemia
** Hep B (1 in 205,000), Hep C (1 in 1.8 million), HIV (1 in 1.9 million)
*** Acute haemolytic transfusion reaction is an antibody-mediated (type II) hypersensitivity reaction caused by anti-ABO antibodies
that bind antigens on transfused donor erythrocytes. Subsequent complement activation results in erythrocyte lysis, vasodilation, and
symptoms of shock. Common findings include fever, hypotension, chest and back pain, and haemoglobinuria
**** Most common cause of febrile reaction post-transfusion: febrile non-haemolytic transfusion reaction (FNHTR) – caused by
antibodies directed against donor leukocytes and HLA antigens
68 Chest. 2010 Jan;137(1):209-20.
138
VARICEAL BLEEDING69
Gastroesophageal varices are the most clinically important collaterals because their rupture results in potentially fatal hematemesis .
The dilated submucosal veins in the lower third of oesophageal is formed by the portocaval anastomosis between the left gastric
vein and esophageal branches of azygos vein.
RISK FACTORS
- Prevalence of gastroesophageal varies increases in Child’s Score (A: 40%, C: 85%)
- Strongest predictor for development of varices in patients with cirrhosis is the hepatic venous pressure gradient of > 10mmHg
- Most important predictor of haemorrhage is the size of varices, other predictors includes decompensated cirrhosis and
endoscopic stigmata of recent haemorrhage (see below)
- Variceal bleeding associated with mortality of at least 20% at 6 weeks
WHEN TO SUSPECT VARICEAL SOURCE IN UBGIT

- Any previous variceal bleed – ask patient whether he/she goes for regular banding or OGD screening and banding
- Any history of chronic liver disease – ask for risk factors (i.e. alcohol ingestion, hepatitis B/C)
- Any stigmata of chronic liver disease
MANAGEMENT
1. Active Variceal Bleed

2. Prophylaxis
3. Chronic management
I. ACTIVE VARICEAL BLEED – MANAGEMENT
Hemodynamically Unstable Patient

1. Resuscitate (manage in critical care area)
▪ Maintain airway – KIV intubation If patient has altered mental state (encephalopathy) or hematemesis is copious
▪ Breathing – supplemental high flow oxygen, maintain Sp02 >94%
▪ Establish 2 or more large bore peripheral IV lines
▪ Monitoring – Vitals, ECG, pulse oximeter, urine output (IDC)
▪ Labs – GXM (4units), FBC, U/E/Cr, PT/PTT, ±LFT, ±Cardiac Enzymes
▪ Infuse fluids – 1L crystalloid fast and reassess parameters
▪ ICU bed and facilities should be made available
Note: DO NOT insert NG tube if oesophageal varices is suspected – worsen variceal bleed
Note: Under-resuscitate in variceal bleed as blood volume expansion increases portal venous pressure in patients with cirrhosis which may sustain active
bleed or precipitate further bleeding – initiate blood transfusion if Hb <7g/dL with goal of maintaining level ≥ 7 g/dL (for patients likely to suffer from
adverse events in setting of significant anemia – i.e. unstable CAD can keep Hb ≥ 9 g/dL)
Note: alcohol withdrawal should be anticipated
2. Pharmacological Management
▪ IV broad-spectrum Ab 7 days – (ciprofloxacin 500mg bd or ceftriaxone 1g / day)
▪ IV somatostatin (250ug bolus then 250ug/h infusion) or IV octreotide (50mcg bolus then 50mcg/hour) for 3-5days
▪ IV omeprazole 80mg bolus + 8mg/hr for 3 days
▪ IV Vitamin K (10mg) – should be given routinely to cirrhotic with coagulopathy
▪ ± IV Terlipressin (2mg Q6H) (synthetic vasopressin) is the vasoactive drug of choice with a 34% mortality relative risk
reduction (CI in patients with IHD)
▪ ± Recombinant activated factor VII (rFVIIa) – for correcting PT in cirrhotic
Note: Infection is a strong prognostic indicator in acute bleed – use of Ab reduces risk of spontaneous bacterial peritonitis (SBP), re-bleeding and
mortality
Note: IV somatostatin/octreotide – Not given in ulcer bleed; mode of action is as a splanchnic vasoconstrictor which decreases portal blood flow and
hence portal pressures which decrease variceal bleeding. Also, it acts indirectly to inhibit secretion of gut hormones that increase portal blood flow –
somatostatin decreases gastric acid and pepsin secretion but there is no proven benefit of it in the management of active non -variceal GI bleed
69 Hepatology. 2007 Sep;46(3):922-38.
139
3. Management of severe variceal bleeding (balloon tamponade)

▪ Protect the airway before inserting the SB tube .
▪ Sengstaken-Blakemore (SB) tube (maximum 24 hours – temporary deflate after 12 hours to prevent pressure necrosis) in
patients with uncontrollable bleeding for whom a more definitive therapy is planned (i.e. TIPS or endoscopic therapy)
▪ Consists of (1) gastric balloon (2) oesophageal balloon (3) gastric opening (4) oesophageal opening
- 200ml of fluid in gastric balloon
- Traction on SB tube with 1kg weight (i.e. 2 x 500mls normal saline packets) – gastric balloon compress GEJ
- Oesophageal balloon with air – keep Pa 25-45 mmHg – use lowest pressure to stop bleeding
EXTRA INFORMATION
Sengstaken-Blakemore (SB) tube
4. Definitive Management (endoscopy and TIPS)
Endoscopy
- Confirms diagnosis and institute definitive management
- Sclerotherapy (into bleeding varies or overlying mucosa)
▪ Induce inflammation and fibrosis
▪ Controls bleeding in 70% after 1st injection and 85%after a second
- Variceal band ligation – ligation is superior to sclerotherapy in initial control of bleeding and a/w fewer adverse effects70
Bleeding Gastric Varices

- Gastric varices along lesser curve – manage as per extension of oesophageal varices
- Gastric varices along greater curve – evaluate splenic vein patency – if patent, manage with endoscopic gastric variceal obturation
using N-butyl-cyanoacrylate, if unavailable / failure – consider TIPSS
TIPSS (Transjugular Intrahepatic Porto-Systemic Shunt)

- Indications: protracted bleeding, progression of coagulopathy, visceral hypo-perfusion, refractory ascites
- Involves radiologically guided intra-hepatic placement of a stent between branches of the portal and hepatic venous circulation
(i.e. intra-hepatic right portal vein and right hepatic vein) – acute decompression of portal pressure thus controlling refractory
variceal bleed
- Needle track is dilated until a portal pressure gradient of ≤ 12mmHg is achieved
- TIPSS is not a good long-term preventive strategy
70 Semin Liver Dis. 1999;19(4):439-55.
140
EXTRA INFORMATION
Emergency Shunt surgery

- Risk of more frequent encephalopathy and higher mortality (can be extrapolated to TIPS because its physiology is the same as that of surgical
shunts (i.e. divert blood away from liver)
- Selective
▪ Proximal splenorenal shunt (splenectomy with end-to-side anastomosis of portal side of splenic vein to left renal vein)
▪ Distal splenorenal shunt (Warren-Zeppa shunt – splenic vein divided and splenic side anastomosed end-to-side to left renal vein)
- Non-selective
▪ Portacaval shunts (joining portal vein to IVC) – side-to-side, end-to-side
▪ Mesocaval shunts (joining superior mesenteric vein to IVC)
Salvage Haemostatic Surgery (esophagogastric devascularization) – rarely done (i.e. Sugiura Surgery)
II. PROPHYLAXIS OF VARICEAL BLEEDING 71

1. Secondary prophylaxis of variceal bleeding
▪ Patients with cirrhosis who survive an episode of active variceal bleed should receive therapy to prevent recurrent
▪ Best option is combination of:
- Band ligation (3 weekly ligation until completely obliterated) &
- Non-selective beta-blockers (Propranolol unless CI)
2. Primary prophylaxis of variceal bleeding

▪ Prevention of variceal haemorrhage in patients who have never bled (reduce bleeding risk by 30-45%)
▪ Indications: Large varices (grade 3) or medium varices (grade 2) with endoscopic red signs or Child’s C cirrhosis
▪ Best option is:
- Non-selective beta-blockers (Propranolol & Nadolol) – reduce risk of bleeding and slow progression of small varices
into larger ones (block ß1 receptor – decrease cardiac o/p, block ß2 receptor – produce splanchnic vasoconstriction
and reduce portal flow and portal pressure)
▪ If contraindicated to BB – long acting nitrates (isosorbide mononitrate)
▪ Insufficient evidence to support treatment of patients with small varices
▪ No evidence for prophylaxis with BB in patients with cirrhosis without varices
Predictors of variceal haemorrhage:

1 Site: GEJ varices (thinnest coat of supporting tissue) are at highest risk of rupture and bleeding
2 Size:
▪ Grade 1: Small straight varices not disappearing with insufflation
▪ Grade 2: Enlarged tortuous varices that occupy less than one-third of the lumen
▪ Grade 3: Large varices that occupy more than one-third of the lumen
3 Child’s score – patients with higher Child’s score have higher risk
4 Red signs – Endoscopic Stigmata of Recent Haemorrhage (ESRH)
▪ Red wale marks (longitudinal red streaks)
▪ Cherry red spots (flat discrete spots)
▪ Hematocystic spots (raised discrete spots – resemble “blood blisters”)
▪ Diffuse erythema
5 Previous variceal haemorrhage
▪ 70% of patients will have further variceal bleeds after an index bleed (risk highest in first 48hours after first bleed
▪ 30% re-bleed within 6 weeks, 30% re-bleed after 6 weeks
III. CHRONIC MANAGEMENT

- Start patient on an ablation regimen (endoscopy with initial ligation/sclerotherapy and subsequent endoscopic monitoring and
repeated ligation/sclerotherapy as required to completely ablate varices)
- If patient bleeds again – failed ablation – consider shunt surgery (as above)
- LT propranolol + PPI – Acid suppressive therapy is theorized to improve the stability of clot
71 Clinical Practice Guidelines (May 2007) - Management Of Acute Variceal Bleeding
141
PEPTIC ULCER DISEASE
DEFINITION
Peptic ulcers refers to acid peptic injury of the digestive tract resulting in defects in the mucosa that extends through the muscularis
mucosae into the submucosal, and often into the muscularis propria or deeper. Most are round, sharply demarcated punched out
craters 2-4cm in diameter.
EPIDEMIOLOGY
- Remitting and relapsing lesions, often diagnosed in middle-aged to older adults
- Incidence = 100 per 100,000 per year
- M:F ratio for duodenal ulcers = 3:1 , M:F ratio for gastric ulcer ~ 1:1
- Lifetime prevalence for PUD = 5-10% – gastric ulcer patients are older than duodenal ulcer patients
- Overall mortality: 7-10% – mostly due to ulcer bleeding especially in elderly with significant comorbidities
RISK FACTORS
- 50-60% of population are positive for H. pylori by age 21
- About 10-20% of infected patients develop an ulcer
Helicobacter Pylori - Gastric ulcer 20 to H. pylori infection tend to occur on lesser curvature72
Infection - a/w 85% of duodenal ulcers & 68% of gastric ulcers73
- H. pylori exerts inhibitory effect on D cells (decreased level of somatostatin) leads to hypergastrinemia
and acid hypersecretion
- 8-fold increase in risk of duodenal ulcers
NSAID - 40-fold increase in risk of gastric ulcer (more often on greater curvature)
(including aspirin) - Chronic use of NSAID increase risk of upper BGIT about 4-folds & PUD by 5-folds74
- Dose-dependent relationships: ulcers do not recur when NSAIDs discontinued
- 2x increased risk compared to non-smokers (impairs mucosal blood flow and healing, or provide
Smoking
favourable milieu for H. pylori)
- Zollinger Ellison Syndrome (ZES), Antral G-cell hyperfunction/hyperplasia
- Previous Peptic Ulcer
- Psychological Stress , Head Trauma (i.e. Cushing Ulcer), Burns (i.e. Curling Ulcer)
Others
- Alcohol, alcoholic cirrhosis a/w with higher incidence of PUD
- Other Drugs: corticosteroids (high dose + frequent use delay healing of lesion rather than causing de novo
ulceration), anticoagulant (increased risk of bleed)
LOCATION OF PEPTIC ULCER

- Duodenum – proximal (75%)
- Stomach – lesser curvature, antrum (20%), greater curve*
- Stomal ulcer – at the stoma of a gastroenterostomy
- Oesophagus
- Meckel’s Diverticulum – specifically when it possess ectopic gastric mucosa
- Multi-sites (i.e. Distal duodenum, jejunum, stomach, proximal duodenum), suspect Zollinger Ellison Syndrome (see pancreatic
endocrine tumours)
* Giant ulcers (> 3cm) along the greater curvature have a higher likelihood of underlying malignancy. Only 10% of benign ulcers are
located along the greater curve
72 Endoscopy. 1996 Feb;28(2):229-33.

73 Singapore Med J. 2000 Oct;41(10):478-81.
74 Schwartz’s Principle of Surgery 10 th Edition – pg. 1057
142
PATHOPHYSIOLOGY
- Ulcer development depends on imbalance between acid secretion and the mucosal protective factors
▪ Aggressive factors: gastric acid activity, pepsin activity, H. Pylori & NSAIDs
- HCl secreted by parietal cells (see below)
- Pepsinogen secreted by chief cells – pepsinogen converted to pepsin by HCl
▪ Protective mechanisms:
- Mucus secretion
- Bicarbonate secretion into mucus
- Robust mucosal blood flow to remove protons
- Epithelial regenerative capacity (i.e. cell renewal)
- Prostaglandin secretion by mucosa to maintain blood flow
- Duodenal ulcers due to excessive acid & pepsin secretion that overwhelms (impaired) mucosal defences (hence epigastric
pain experienced when hungry, which is relieved by food)
- NSAIDs impair mucosal prostaglandin synthesis (through non-selective COX inhibition)

▪ PGs are important for (1) mucin production, (2) mucosal bicarbonate secretion, (3) maintaining mucosal blood flow and (4)
inhibiting gastric acid secretion
- Helicobacter Pylori
▪ H pylori produces urease which creates an alkaline environment allowing it to survival in the stomach
▪ H pylori expresses adhesins which facilitate attachment of bacterial to the gastric epithelium
▪ H. Pylori secrete toxins which results in inflammation and host tissue damage
▪ Inhibitory effect on antral D cells (↓ somatostatin) leading to hypergastrinemia
▪ Increased acid secretion results in gastric metaplasia in duodenum. H.pylori colonization in duodenum decreases
duodenum bicarbonate secretion and increased inflammation resulting in duodenal ulceration
▪ Without eradication of Helicobacter Pylori, complete mucosal healing occurs in < 0.5%
Gastric Acid Secretion

Gastric acid secretion by the parietal cell is stimulated by histamine (ECL cells), gastrin (G cells) or ACH (vagal nerve stimulation)
which in turn activates H+K+ATPase which leads to secretion of Hydrochloric Acid (HCL)
- Major site of parietal cells and hence HCl production is in the gastric fundus and body
- Major site of gastrin & somatostatin production is in the pyloric antrum
- Smaller division of the vagus nerve (anterior nerves of Latarjet) supply the pyloric region and are responsible for relaxation
of the pylorus to allow emptying
ACH & gastrin = activates phospholipase (PIP → DAG + IP 3 to ↑Ca), Ca-calmodulin activates phosphorylase kinase to ↑H
Histamine = activates adenylate cyclase which activates cAMP which activates protein kinase A to ↑H+
Inhibitor of parietal cells: somatostatin, prostaglandins (PGE1), secretin and CCK
H+K+ATPase is inhibited by PPI
143
1. Incidentally detected on OGD
2. Symptoms of dyspepsia
- Epigastric pain that is burning in quality and non-radiating
(a) Ulcer-like dyspepsia: burning, gnawing, intermittent epigastric pain
▪ Duodenal ulcer: pain 2-3hrs after a meal and at night, 2/3 complains of pain that awakens them from sleep
▪ Gastric ulcer: pain occurs / exacerbated with food intake, patient avoid food and presents with weight loss (unlike
duodenal ulcers)
(b) Dysmotility-like dyspepsia: non-painful discomfort (upper abdomen), a/w upper abdominal fullness, nausea, vomiting
early satiety, bloating, belching
(c) Unspecified dyspepsia
3. Bleed
- Mild and chronic: iron deficiency anemia, FOBT +ve
- Severe and acute: haematemesis (coffee-grounds vomitus) or melena
4. Perforation
- Clinical manifestation can be divided into 3 phases
▪ Within 2 hours – epigastric pain, tachycardia, cool extremities
▪ 2 – 12 hours – generalized abdominal pain, worse on movement, abdominal rigidity, involuntary guarding, right lower
quadrant tenderness (fluid tracking along right para-colic gutter)
▪ > 12 hrs – abdominal distention, fever, hypotension, circulatory collapse
- Sudden onset of epigastric pain – patient able to recall exact timing
- No relieving factors
- Erect CXR will show free air under diaphragm
▪ 70% of PPU has free gas under diaphragm
▪ 70% of free gas under diaphragm is caused by PPU
▪ 100% failure if you cannot identify this in exams
- When diagnosis in doubt – severe peritoneal signs with no free air
▪ Repeat CXR or decubitus AXR
▪ Urgent CT abdomen with contrast
▪ Urgent Barium contrast meal with follow through (if no CT)
5. Obstruction (uncommon presentation for gastric ulcers)

- Can be due to benign peptic strictures
144
INVESTIGATIONS
Oesophagogastroduodenoscopy (3 indications)
(a) Diagnosis
▪ Confirmation of Peptic Ulcer Disease (PUD) – note location of ulcer
▪ Biopsy to rule out malignancy (usually 6 bites) – especially if s/s (gastric ulcers, weight loss, anemia, obstruction) or
appearance of ulcer (associated mass, folds around ulcer) are present
▪ Biopsy rapid urease testing (CLOtest)* – antral biopsy for H. pylori → biopsy tissue placed into a medium containing urea
and an indicator such as phenol red. The urease produced by H. pylori hydrolyses urea to ammonia, which raises the pH
of the medium, and changes the colour of the specimen from yellow (NEGATIVE) to red (POSITIVE) depending on the
test kit.
▪ Endoscopic biopsy is the most accurate diagnostic method for H. pylori (low sensitivity during acute upper GI bleeding)
*Biopsy rapid urease testing (CLOtest = Campylobacter-Like Organism) → test ability of H. pylori to secrete urease enzyme which
cleaves urea to liberate ammonia and bicarbonate (↑pH)
Forrest Classification
Forrest grade (endoscopic stigmata) Prevalence Bleeding risk
1A Spurting (arterial) 100%
18%
1B Non-spurting, ooze (venous) 55% (17-100%)
2A Non-bleeding ulcer with visible vessel 17% 43% (8-81%)
2B Non-bleeding ulcer with adherent clot 17% 22% (14-36%)
2C Ulcer with haematin-covered base (flat base) 20% 10% (0-13%)
3 Ulcer with clean base 42% 5% (0-10%)
(b) Therapeutic
▪ Injection with adrenaline (1:10,000 dilute to 10ml - continue with N/S if need more) or absolute alcohol – tamponade effect
is the most effective. Also vasoconstrictive effect for adrenaline (inject around ulcer, 4 quadrants)
▪ Thermal Coagulation (Heater probe = thermal / Argon plasma)
▪ Haemostatic clipping (endo-clip)
▪ Novel Modalities: hemo-spray, over the scope clip (OTSC), over-stitch
Principle: Dual modality better than single (as less risk of recurrent bleed and mortality), usually Adrenaline Injection + Clip/Heater
probe (No study proves superiority of either therapy)
145
Post-endotherapy:
- IV PPI 80mg followed by infusion of 8mg/hr for 72 hours should be given to patients with ulcers with active bleeding, non-bleeding
visible vessel or an adherent clot (i.e. Forrest 1A, 1B, 2A, 2B)
- Monitor for re-bleed by monitoring of hemodynamics & trending of Hb
- Diet individualised: NBM or clear feeds for high risk patients, soft diet / DOC for low risk patients (i.e. ulcer with clean base)
- Routine second-look OGD (within 16-24hours of initial endoscopy) is not recommended
- Second-look OGD for high-risk patients – i.e. primary haemostasis uncertain, initial evaluation incomplete, recurrent bleed
- Oralise PPI after 3/7 infusion (if worried, can give IV bolus PPI BD)
- TCU 1/12 at clinic
(c) Prognostication of bleeding risk (in UBGIT)

▪ Forrest classification75 (or endoscopic stigmata of recent haemorrhage – ESRH)
▪ For patients (Forrest Ia, Ib, IIa and IIb) after successful endoscopic treatment: 76
i. High risk of re-bleeding = initial Hb ≤ 9g / dL, endoscopist with < 2 years of therapeutic experience, need for > 15cc
of epinephrine, chronic renal disease, liver cirrhosis, unstable patient with hypotension and ulcer size >2cm
ii. High risk of mortality = initial active spurting bleeding, re-bleeding
EXTRA INFORMATION
Investigations for assessment of Helicobacter Pylori

- Invasive: Endoscopic Biopsy, Endoscopic Culture, Endoscopic CLO test (rapid urease test)
- Non-invasive:
▪ Urea Breath Test (UBT)
▪ Stool Antigen Test
▪ Serologic Testing (IgG and IgA ELISA tests)
In clinical practice, Endoscopic CLO test is the most common way in which HP is being detected. Urea Breath Test done 6 weeks
later is used to assess for eradication of HP.
Urea Breath Test
OTHER INVESTIGATIONS
- Fasting Serum Gastrin: screen for Gastrinoma (Zollinger-Ellison Syndrome)
- Serum Calcium: screen for Multiple Endocrine Neoplasia (MEN)
- Barium Meal: less invasive but unable to accurately define mucosal pathology or distinguishing benign from malignant ulcer.
75 Lancet. 1974 Aug 17;2(7877):394-7.

76 Clin Endosc. 2011 December; 44(2): 93–100.
146
MANAGEMENT
Uncomplicated Peptic Ulcer Disease

- Medical Therapy & Lifestyle Modifications
▪ Smoking & Alcohol Cessation
▪ Proton Pump Inhibitor (PPI) for 4-6 weeks
▪ NSAID-associated PUD → discontinue offending medication and initiate antisecretory therapy
▪ H. Pylori Eradication
- Repeat Endoscopy to document ulcer healing (for gastric ulcers)
▪ Re-scope in 6 weeks to document gastric ulcer healing, If ulcer still present, biopsy ulcer again (taken at margin of ulcers,
to rule out gastric cancer) and also do antral biopsy for rapid urease test – CLOtest (to confirm eradication of H. pylori)
EXTRA INFORMATION
Side Effects of Omeprazole

- ↑incidence of community acquired pneumonia (does not affect HAP)
- ↑ risk of C-diff colitis (esp. in elderly)
H. Pylori Eradication
- First line triple therapy: omeprazole 40mg BD, amoxicillin 1g BD, clarithromycin 500mg BD for 10-14 days
- In penicillin-allergic patients: substitute amoxicillin with metronidazole 400mg BD
- For patients with Peptic Ulcers & HP positive: treat with triple therapy, then continue omeprazole BD dosing for another 4
weeks and plan for UBT at the next clinic visit.
- Document eradication by urea breath test (UBT), usually performed 6-8 weeks post-diagnosis (note that patients should have
stopped omeprazole for 2 weeks prior to UBT)
- Treatment failure occurs in up to 20%, treat with quadruple therapy: colloidal bismuth subcitrate 120mg QDS, tetracycline
500mg QDS, metronidazole 400mg BD, omeprazole 20mg BD for 7-14 day
- Surgical Treatment (Acid-Reducing Operations) for Uncomplicated PUD (rarely performed due to widespread use of PPI)
▪ Truncal Vagotomy – division of anterior and posterior nerves at level of the distal esophagus
▪ Selective Vagotomy – division of the anterior vagus nerve (after its branch to liver & gallbladder) and division of posterior
vagus (after its branch to the pancreas and small intestine)
▪ Highly Selective Vagotomy – division of anterior vagus nerve with preservation of the Latarjet/s nerve
- Surgical Treatment (Non-Healing Gastric Ulcers) - uncommon presentation

▪ Wedge Excision
▪ Antrectomy with inclusion of ulcer, depending on ulcer location
▪ Total Gastrectomy (for ulcers in proximal half of the stomach)
▪ Concurrent acid-reducing operation (vagotomy) is reserved for acid hyper-secreting patients or patient who are known to
have refractory PUD despite maximal medical management (rare)
147
EXTRA INFORMATION
Vagotomy Options
Procedure Remarks
Truncal vagotomy: decreases “functional” parietal cell mass, reduce the responsiveness of “functional” parietal cells to
gastrin / histamine – acid output drops by 90% despite increase in basal and postprandial gastrin 77
Truncal vagotomy: ↓ acid secretion, ↑liquid emptying* and ↓solid emptying (transected nerve of Latarjet) therefore
Truncal vagotomy* must combine with pyloroplasty, incise pylorus longitudinally through mucosal later then suture the incision transversely
with pyloroplasty (see below)78 – prevent stenosis / GOO
Pyloroplasty: Heineke-Mikulicz pyloroplasty (see below)
Diarrhoea (40%) – most common problem following vagotomy, caused by sustained MMCs (migrating motor complex)
forcing bile acids into the colon
Truncal vagotomy*
Truncal vagotomy with antrectomy yields maximal acid suppression with lowest ulcer recurrence rate (1-2%) but
with antrectomy
carries highest post-operative morbidity (5-15%) and mortality rates (1-2%)
and Billroth 1 /2 or
(G cells that secrete gastrin are mainly located in the antrum) – hence antrectomy helpful for ulcer disease
Roux-en-Y
HSV has lowest postoperative morbidity and mortality but is technically challenging to perform with a high recurrence
Highly selective
rate (5 to 15%), selecting only branches that supply peptic cells. Does not require drainage as nerves of latarjet that
vagotomy* (HSV)
supply pyloric sphincter are not affected
* assessing vagotomy, assess peripheral pancreatic polypeptide levels in response to sham feeding – a 50% increase in pancreatic polypeptide levels
within 30mins of sham feeding suggest vagal integrity
77 Gastroenterology. 1986 Apr;90(4):1001-7.

78 Surgical Talk Revision in Surgery (2nd Edition) p118
148
Complicated Peptic Ulcer Disease

4 main complications can occur: Bleed, Burst (perforation), Block (Obstruction), Burrow
Bleeding Peptic Ulcer Disease

- Leading cause of death due to PUD a/w 5-15% mortality
- Institute fluid resuscitation +/- blood products, adjuncts for monitoring, escalate patient to senior
- Pharmacological: IV omeprazole 80mg bolus dose + 8mg / hour for 3 days – for prevention of PUD re-bleeding79
▪ Increase Intra-gastric pH (less acidic environment) ↓ risk of platelet disaggregation and helps maintain clotting thus
preventing re-bleeding – i.e. pH = 6.0 disaggregation = 77%, pH = 7.3 disaggregation = 0%

- Endoscopic: Upper endoscopy is the preferred therapy for treatment of bleeding ulcer
▪ For patients whose condition did not stabilize after initial resuscitation, they have to proceed for emergency endoscopy.
▪ However, if they stabilize, (although high risk, Glasgow–Blatchford score of ≥ 12), endoscopy can be performed within 6-24
hours later.80
- Endoscopic Therapy: Dual Method is preferred for treatment of bleeding PUD
▪ Endoscopic Injection of epinephrine – tamponade & vasoconstrictive effect
▪ Thermal: Heater Probe – coaptive effect – compress till sealing of vessels
▪ Mechanical: Hemo-clip / Hemo-spray
- For patients who fail endoscopic hemostasis, consider angioembolization or surgical intervention
- CT Mesenteric Angiogram +/- Angioembolization

▪ Celiac and superior mesenteric angiogram performed, selective cannulation of the bleeding vessel followed by
angiographic coiling from a distal to proximal manner would be done till extravasation ceased
▪ TAE vs. Salvage Surgery81 – In patients with ulcer bleeding after failed endoscopic haemostasis, TAE reduces the need
for surgery without increasing the overall mortality and is associated with fewer complications.
- Surgical Indications for Bleeding Peptic Ulcer

▪ Hemodynamically unstable despite vigorous resuscitation > 6 units transfusion
▪ Failure of endoscopic haemostasis
▪ Repeated episodes of bleeding after initial stabilization (up to 2 attempts at obtaining endoscopic haemostasis)
▪ Hemorrhagic shock a/w recurrent haemorrhage
▪ Continued slow bleed with transfusion requirement ≥ 3 units / day
EXTRA INFORMATION
Bleeding Duodenal Ulcer

- Longitudinal duodenotomy distal to the pyloric ring (1cm distal to pylorus and extending 2cm into the duodenum)
- Stomach & duodenum cleared of blood and clots using suctioning
- 3 point ligation (oversewing/under-running) of gastroduodenal artery
▪ Bleeding DU usually located at posterior duodenal bulb within 2cm of the pylorus typically erode into gastroduodenal artery
▪ superior to ulcer (GDA), inferior (GDA) and posterior-medial (transverse pancreatic branch of the GDA)
- Post-operative H. Pylori eradication
Bleeding Gastric Ulcer

- Biopsy followed by oversewing the bleeding vessels or wedge excision of the ulcer
- Bleeding GU usually located at lesser curvature
79 N Engl J Med. 2000 Aug 3;343(5):310-6. (same as earlier reference)

80 Timing of Endoscopy for Acute Upper Gastrointestinal Bleeding [await pubmed link]
81 Gastrointest Endosc. 2011 May;73(5):900-8
149
Perforated Peptic Ulcer Disease

- Patients present with sudden acute onset of severe abdominal pain, generalized peritonitis (contents spill into abdominal
cavity) or localized peritonitis (perforation walled off by omentum or adjacent structures preventing peritoneal contamination)
- More common in elderly patients on chronic NSAID therapy
- Finding of free air under the diaphragm present in most cases
Initial Management:
- NBM + IV fluid resuscitation
- IV PPI 40mg BD dosing
- Blood cultures + IV broad spectrum antibiotics (IV Roc/Flagyl)
- IV Analgesia
- Strict I/O charting: insert urinary catheter ± CVP line
- Inform senior, OT, HD or ICU early if necessary
Non-operative Management:
- While majority of patients will require surgical intervention, there remains a specific subgroup of patient who could undergo
non-operative management (patients with sealed perforation)
▪ Hemodynamically stable, not peritonitic
▪ Onset of symptoms within 24 hours
▪ < 70 years of age
- Non-operative management involves close monitoring of hemodynamic status, serial abdominal examination, intravenous
antibiotics, keep patient nil-by-mouth, NG tube decompression, administration of PPI and eventual water-soluble contrast
imaging to ensure that the perforation has sealed
- Prompt operative intervention if no improvement of symptoms within 12 hours or clinical deterioration
Surgical Management
- Open exploratory laparotomy or diagnostic laparoscopy to identify the site of perforation
- Send peritoneal fluid for cultures
- Perforated Duodenal Ulcers (usually located at anterior wall of D1 just distal to the pylorus)
▪ Simple Ulcer Closure (for duodenal perforation < 5mm) vs. Ulcer Closure + Omental Patch Repair
▪ Usually, omental patch repair will be performed, this involves a patch of omentum secured in a tension free fashion over
the defect with absorbable sutures placed into the sero-mucular layer adjacent to the ulcer
- Perforated Gastric Ulcers
▪ Biopsy of ulcer edges and omental patch repair
▪ Simple wedge resection (ulcerectomy), eliminate perforation and exclude malignancy
▪ If perforation too large for 1 0 repair ( > 2.0cm) or suspected malignancy → Partial gastrectomy (Billroth II)
▪ Post-operatively, will require endoscopic confirmation of ulcer healing (13% of ulcers are malignant)
- Extensive peritoneal lavage with 10L of warmed saline
- Air-leak test with intra-operative OGD
- Placement of Drains
Prognosis
- Mortality 6 – 14%, Morbidity up to 63% (in patients > 70 years, mortality ~ 40%)
- Age, pre-operative hypotension, delay in surgery (>24hr), major medical comorbid leads to worse outcome
EXTRA INFORMATION
Predictor of Mortality
- BOEY score: time since ulcer perforation (< 24hr vs > 24hr), pre-operative BP (< 100mmHg or > 100mmHg) & presence of
systemic illness (mortality range from 0, 10%, 45.5% and 100%)
- Peptic Ulcer Perforation (PULP) score: Age (i.e. ≥ 65), comorbid (i.e. malignancy or liver cirrhosis), time from perforation
to admission ≥ 24 hours, use of steroids, hypotension, renal impairment (i.e. serum creatinine > 130umol/l) and ASA score
help predict mortality. A score of ≥ 8 put the patient at high risk (i.e. > 25%) of mortality within 30 days.
- In clinical setting, we commonly use the P-POSSUM score as a predictor for morbidity and mortality in emergency surgeries
150
Obstructed Peptic Ulcer Disease

- Due to fibrosis and scarring of the pylorus from chronic PUD
- Need to biopsy ulcer to rule out malignancy
- (rare) – patient presents with recurrent vomiting of poorly digested food, dehydration, hypochloremic, hypokalemic metabolic
alkalosis (Gastric Outlet Obstruction)
- Initial Management
▪ Correction of volume and electrolytes
▪ NG Insertion with Low Intermittent Suction
▪ IV PPI
▪ OGD (evaluate nature of obstruction)
- Definitive Management
▪ Endoscopic hydrostatic balloon dilation
▪ Surgical Intervention (for patients with persistent obstruction / recurrent obstruction
1. High selective vagotomy with gastrojejunostomy (GJ)
2. Antrectomy and Vagotomy with Billroth 1 or 2 reconstruction
Penetrating Peptic Ulcer Disease

- PUD may erode through entire thickness of gastric / duodenal wall into adjacent abdominal organs (i.e. pancreas, bile ducts,
liver, small / large intestines)
- Patients present with acute onset of pancreatitis, cholangitis, diarrhoea of undigested food
- Surgery not recommended
151
GASTRIC CANCER
EPIDEMIOLOGY82
- 7th most common cancer in males and 8th most common in females in Singapore
- 4th leading cause of cancer related mortality in males and 5th in females in Singapore
- Ethnic: Gastric Cancer more common among Chinese > Indian > Malays
- Gender: Gastric Cancer more common in Males > Females
- ASR of Gastric Cancer: 11.8 / 100,000 in Males and 7.0/ 100,000 in Females
- Lifetime risk for stomach cancer in Chinese Males: 1 in 50
- Large geographical variation – increase prevalence across Asia (Korea / Japan / China) and Eastern Europe
- Overall incidence slowly decreasing but sharp increase in cancer of the gastric cardia / GE junction in western countries (related
to increased incidence of GERD)
RISK FACTORS
1. Infection – Helicobacter Pylori / EBV virus
▪ Ask patient about past infection, whether he has been on triple therapy, previous endoscopic procedures and its results
▪ Lead to chronic active pan-gastritis > atrophic gastritis > intestinal metaplasia* > dysplasia – eradication of H. Pylori leads
to regression of intestinal metaplasia and improvement in atrophic gastritis
▪ H. Pylori with cyototoxin associated gene A (cagA)
▪ 3-6x increased risk of developing gastric cancer
2. Environmental
▪ Diet: preserved foods (nitrosamines – canned food), smoked foods (high salt)
▪ Smoking: 2x increased risk of gastric cancer (intestinal cancer of distal stomach)
▪ Low socioeconomic status: poor refrigeration of food and diet a/w increased risk
▪ Aspirin, Fresh Fruits & Vegetables, Selenium & Vitamin C & E are protective factors
▪ Alcohol – no effect
3. Genetic
▪ Family History: 2-3x increased risk in siblings / offspring of patients with gastric CA
▪ Mutations in E-cadherin: present in 50% of diffuse (infiltrative) type cancer
▪ FAP / HNPCC
▪ Hereditary (familial) diffuse gastric cancer (HDGC): a/w germline mutation of E-cadherin (CDH 1 gene), early onset,
highly penetrant, diffuse gastric carcinoma
- Prophylactic Gastrectomy should be considered
- Common among New Zealanders, Autosomal Dominance syndrome
▪ Blood Group A
4. Significant Past Medical History

▪ Barrett Oesophagus – increased risk of gastroesophageal junctional tumour
▪ Previous diagnosis of gastric polyps (adenomatous gastric polyp)
▪ Previous diagnosis of gastric ulcer (patients with history of duodenal ulcers are at decreased risk for gastric cancer)
▪ Previous Gastric Resection (i.e. Partial Gastrectomy) – allow reflux of bile induces chronic gastritis – significant if surgery >
7 years ago
▪ Chronic Atrophic Gastritis** (most common premalignant lesion)
- Menetrier’s Disease (hyperplastic hypersecretory gastropathy (mucous cell hyperplasia), glandular atrophy) – ↑rugal
folds, ↓acid production, protein losing enteropathy

- Pernicious Anaemia – risk of gastric cancer in the long term
* Metaplasia: reversible replacement of one fully differentiated cell type with another differentiated type – adaptive change in
response to injury, irradiation or altered cell function
** Gastric bacteria convert nitrate into nitrite – proven carcinogen
82 Trends in Cancer Incidence in Singapore 2008-2012 (data report are as of 7th June 2013)
152
PATHOLOGY
Endoscopic Classification (Boormann’s)

- Type 1 – polypoid (not ulcerated) – bulk of tumour intra-luminal
- Type 2 – excavating / fungating (ulcerated) – bulk of tumour intra-luminal
- Type 3 – ulcerative – bulk of tumour in wall of stomach
- Type 4 – diffuse thickening / scirrhous / linitis plastica – infiltrate entire thickness of the stomach
Distribution of Gastric Cancer

Gastric carcinomas are located as follows – pylorus and antrum (50 – 60%), cardia (25%), remainder in the body and fundus. The
lesser curvature is involved in (40%) and the greater curvature in (12%). Favoured location for gastric carcinoma is the lesser
curvature of the antropyloric region. (40% distal | 30% middle | 30% proximal)
Histological Classification
Adenocarcinomas (95%)
- From mucous producing cells in the gastric mucosa
- Lauren classification (divide into 2 main subtypes or mixed):
(a) Intestinal (expanding) type (53%) – papillary, tubular, mucinous
- More common in elderly males and in the distal stomach (more likely to cause GOO)
- a/w chronic atrophic gastritis, severe intestinal metaplasia and dysplasia
- Less aggressive
- Haematogenous spread to distal organs
(b) Diffuse (infiltrative) type (33%) – signet ring cell, undifferentiated
- More common in younger patients, females and in the proximal stomach
- a/w invasive growth pattern and rapid submucosal spread, linitis plastica
- Late presentation, worse overall prognosis (signet ring cell a/w poor prognosis)
- Transmural and Lymphatic spread with early metastases are more common (peritoneal recurrence is more common)
(c) Unclassified / Mixed (14%)
- HER2 overexpression has also been reported in 13-30% of patients – potential survival improvement with treatment with
trastuzumab
Non-adenocarcinoma (5%)
- Gastric Neuroendocrine Tumours (Carcinoids) → derived from enterochromaffin-like (ECL) cells
▪ Gastric NET Type 1 (70-80%) – a/w hypergastrinemia (due to chronic atrophic gastritis)
▪ Gastric NET Type 2 (5%) – a/w MEN1, Zollinger Ellison Syndrome
▪ Gastric NET Type 3 (15-20%) – sporadic
- Gastric Lymphoma (B cell lymphoma, extranodal MALT type) → derived from lymphocytes in gastric mucosa
- Mesenchymal Tumours of the GIT
▪ Gastrointestinal Stromal Tumour (GIST) → derived for Interstitial cells of Cajal, express c-KIT or PDGFRA
▪ Leiomyoma / Leiomyosarcoma → derived from smooth muscle and express actin & desmin
153
There exists a wide spectrum of clinical presentation depending of the stage of the tumour at presentation.
History
- Age of Patient + Risk Factor Assessment (as above)
- Asymptomatic
▪ Detected incidentally on OGD – no gastric cancer screening in Singapore (present in Japan / Korea)
- Symptoms that are non-specific (early)

▪ Intermittent Dyspepsia (required high index of suspicion) – for patients age > 40 with new onset dyspepsia, consider OGD
▪ Abdominal Bloatedenss
- Symptoms suggestive of locally advanced disease

▪ Persistent Dyspepsia
▪ Anemia (iron deficiency anemia)
▪ Hematemesis or Melena
▪ Dysphagia (cardia tumour)
▪ Gastric Outlet Obstruction (antrum/pyloric tumour) – early satiety, nausea, vomiting
▪ Intestinal Obstruction (carcinomatosis peritonei)
▪ Malnourished
- Symptoms suggestive of local complications

▪ Acute abdominal pain (perforated gastric cancer)
▪ Active hematemesis (bleeding gastric cancer)
- Symptoms suggestive of distant metastatic

▪ Constitutional Symptoms – loss of weight and loss of appetite
▪ SOB – pleural effusion (metastatic disease)
▪ Bone Pain (metastatic disease)
▪ LL swelling (i.e. Deep Vein Thrombosis)
- General Inspection
▪ Hydration status of patients? (for patients who presents with nausea, vomiting)
▪ Is the patient cachectic?
▪ Is the patient anemic?
- Abdominal Examination
▪ Soft non-tender, no palpable mass (early disease)
▪ Mild epigastric tenderness (early disease)
▪ Palpable epigastric mass (intermediate to late disease)
▪ Positive Succussion Splash (intermediate to late disease)
▪ Ascites (late)
▪ Hepatomegaly (late)
▪ DRE: presence of melena (ongoing upper BGIT)
- Others
▪ Respiratory Examination
▪ Enlarged Left supravicular lymph node (Virchow’s Node)
▪ Trousseau’s syndrome (thrombophlebitis)
▪ Deep Vein Thrombosis – effects of the tumour on thrombotic and haemostatic mechanisms u
Complications
- Bleeding: Fe deficiency anemia, melena, hematemesis
- Gastric outlet obstruction: vomiting, dehydration, biochemical abnormalities (hypokalemic, hypochloremic metabolic alkalosis),
aspiration ± pneumonia), increase risk of aspiration pneumonia
- Intestinal obstruction: from carcinomatosis peritonei
- Malnutrition: cachexia
- Perforation: acute abdomen
154
Gastric Outlet Obstruction Causes

- Extraluminal obstruction (i.e. pancreatic pseudocyst causing obstruction)
- Mural obstruction (i.e. gastric malignancy, periampullary tumours, peptic ulcer disease causing strictures)
- Intraluminal obstruction (i.e. gallstones (Bouveret’s), bezoars)
Gastric Outlet Obstruction Pathophysiology

GOO presents as hypokalemic, hypochloremic, metabolic alkalosis with paradoxical aciduria
With vomiting K+, Cl-, Na+ and H2O are lost from the body (hypochloremic metabolic alkalosis). Initially urine has low chloride and
high bicarbonate content to compensate for gastric losses of HCl (urine alkaline). With continued dehydration, intravascular
hypovolemia sensed by JGA leads to the activation of the RAAS. Aldosterone leads to sodium and water reabsorption in exchange
for potassium and hydrogen ion (Na+/K+ ATPase). Hence, urine becomes paradoxically acidic and hypokalaemia ensues.
HypoCl & HypoNa+ – (1) loss from vomitus, (2) ADH conserves water
HypoK+ – (1) loss from vomitus, (2) aldosterone effect on distal tubule, secrete K in exchange for Na
Alkalosis – (1) loss of H+ from vomitus, (2) with hypok+, K+ shifts out of cell and H+ shifts into cell (intracellular shift to maintain
electrical neutrality)
Aciduria – (1) aldosterone effect on distal tubule
Modes of Spread
- Local Spread (direct extension to neighbouring organs) – i.e. gastric antrum cancer spread
(a) Pancreas
(b) Transverse colon
(c) Duodenum
- Lymphatic Spread
(a) Local lymphatic spread to perigastric lymph nodes, further spread follow the arterial supply (i.e. nodes along the branches
of the celiac artery: left gastric artery, common hepatic artery and splenic artery), further spread to para-aortic nodes
(b) Enlarged Left Supraclavicular nodes (Virchow’s node)
- Haematogenous Spread
(a) Hepatosplenomegaly with ascites and jaundice (liver)
(b) Lungs
(c) Rarely: Bony Tenderness (bone), Neurological Deficits (brain) (usually these organs are not worked up for metastasis)
- Trans-coelomic Spread (Peritoneal Seeding)
(a) Seeding to the omentum, parietal peritoneum, leading to peritoneal carcinomatosis (can lead to small bowel intestinal
obstruction [multiple sites], hydronephrosis)
(b) Infiltration of the umbilicus (Sister Mary Joseph’s node)
(c) Enlarged ovaries on PE (Krukenberg’s tumour)
(d) Fullness in pelvic cul-de-sac (Blumer’s shelf = shelf-like tumour of ant rectal wall, rectal mass ddx tuberculous peritonitis
INVESTIGATIONS
- Assessment of tumour (i.e. location, size, morphology, extent) – Boorman Classification
- Assess for any complications (i.e. tumour bleeding, tumour causing obstructioN)
- Assess for any helicobacter pylori (i.e. CLO test)
- Allow for biopsies of suspicious lesions (biopsy the edges/margins of the ulcers, at least
OGD + Biopsy
6-8 bites)
- Advancement in OGD – magnifying OGD with narrow-band imaging (NBI)
Establish the - Signs of early gastric CA with NBI – (VSD) irregular micro-vascular pattern, irregular
Diagnosis micro-surface pattern, well demarcated border
Barium Swallow → Non-invasive but Limited Diagnostic Value (unable to perform histological assessment)
- Useful for linitis plastica (↓distensibility, “leather-flask” appearance more obvious)
Histology → confirm adenocarcinoma (Lauren Classification) or non-adenocarcinoma tumours, tumour

differentiation, can also assess for HER2 overexpression (15-30%)
- CT performed with oral ingestion of effervescent granules – for gastric distention
Staging - Accurate for T staging but limited in detecting organ invasion (i.e. direct invasion of
Investigations pancreas, liver & colon) – difficulty in differentiating between inflammatory adhesions
Computer
with fibrosis, edema or tumour invasion.
Tomography (CT
(divide to local - Limited accuracy for N staging – small nodes (<5mm) may contain metastatic disease,
TAP) with Gastric
& systemic - Limited accuracy for assessing distant metastasis – good for haematogenous spread to
Protocol
staging) distant organs (i.e. most commonly liver mets), but limited value in detecting trans-
coelomic spread and presence of peritoneal seeding. Can have a role in detect
metastatic disease in the form of malignant ascites but not always accurate
155
(1st test to do - CT Thorax is important for gastric cardia tumour

is to exclude - Useful in early stage gastric cancer
mets) - Superior to CT in delineating depth of tumour invasion (gold standard for T staging) and
Endoscopic
identifying perigastric & celiac lymphadenopathy (>5mm) – N staging
Ultrasound
- Depth of tumour invasion (T staging) is an important prognostic factor
- Addition of FNA for suspicious node increases accuracy to ~100%
Positron emission
- Combines spatial resolution of CT with contrast resolution of PET
tomography
- Role is not established in gastric cancer
(PET)
- Can detect radiologically occult peritoneal metastases
- Routine use can detect small volume peritoneal and liver metastasis in 20-30% of
Staging patients believed to have local-regional disease (upstage)
Laparoscopy - Risk factors: patients with GEJ lesions, diffuse gastric tumour, poorly differentiated
cancer, age < 70, patients with preoperative imaging that revealed lymphadenopathy >
1cm and T3 or T4 tumour
Peritoneal - Positive peritoneal lavage – independent poor prognostic factor83 (peritoneal metastasis
Cytology is refractory to systemic chemotherapy)
Supportive FBC - Any Anemia (Iron Deficiency Anemia)
Investigation U/E/Cr - Biochemical abnormalities a/w gastric outlet obstruction
to assess for - Albumin as a marker of nutritional status
complications LFT
- Unlikely to get deranged LFTs unless widespread liver metastases
STAGING (TMN)84
- Tumour arising at the esophagogastric junction (EGJ), or arising in the stomach 5cm or less from the EG junction and cross the
EG junction are staged as oesophageal carcinoma (TNM system)
- Gastric cancer TNM staging for distal stomach tumours and for tumours arising in the proximal 5cm but not crossing the EGJ
T0 No evidence of primary tumour T N M
Tis Carcinoma in situ: intraepithelial tumour w/o invasion of the lamina propria Stage 0 Tis 0 0
Tumour invades Stage 1A 1 0 0
T1 (a) lamina propria, muscularis mucosae, or 2 0 0
(b) submucosa Stage 1B
1 1 0
T2 Tumour invades muscularis propria 3 0 0
T
Tumour penetrates subserosa connective tissue – include those extending into Stage 2A 2 1 0
T3
gastrocolic or gastrohepatic ligaments, or into greater or lesser omentum 1 2 0
Tumour invades 4a 0 0
(a) serosa (visceral peritoneum) or
T4 3 1 0
(b) adjacent structures (i.e. spleen, transverse colon, liver, diaphragm, pancreas, Stage 2B
2 2 0
abdominal wall, adrenal gland, SI and retroperitoneum)
1 3 0
N0 No regional LN metastasis
4a 1 0
N1 Metastasis in 1-2 regional LN
Stage 3A 3 2 0
N N2 Metastasis in 3-6 regional LN
2 3 0
N3 Metastasis in 7 or more regional LN
4b 0/1 0
Mo No Metastatic spread to distant organs
Stage 3B 4a 2 0
Distant Metastasis or Positive Peritoneal Cytology
3 3 0
M 4b 2/3 0
M1 Stage 3C
4a 3 0
Stage 4 Any T Any N M1
MANAGEMENT85
83 Gastric Cancer. 2005;8(4):228-37. – SGH data

84 Ann Surg Oncol. 2010 Dec;17(12)3077-9
85 Gastric Cancer. 2017 Jan;20(1):1-19. [Important Paper]
156
CURATIVE INTENTION
Patient’s case would be discussed at multidisciplinary tumour board (MDTB)
Endoscopic Resection
- Curative for early gastric cancer (gastric cancer defined as superficial to muscularis propria (T1a) regardless of LN status)
- Endoscopic Resection Indication: early gastric cancer with minimal risk of lymph node metastasis
- Endoscopic mucosal resection (EMR) or Endoscopic submucosal dissection (ESD)
▪ EMR: lesion together with surrounding mucosa is lifted by submucosal injection of saline and removed by high frequency
steel snare
▪ ESD: mucosa surrounding the lesion is circumferentially incised using a high frequency electric knife and submucosal layer
is dissected from the proper muscle layer
Pre-operative
- Nutritional Support
▪ Assess – history (significant weight loss = 10% drop in last 12 months), clinical exam (BMI < 18.5kg/m 2), labs (i.e. serum
albumin <35g/L)
▪ Pre-operative nutritional support significantly improves morbidity and mortality in the malnourished surgical patient, give for
at least 7 days to have clinical benefit, route: enteral or parenteral, estimated nutritional requirements = 20-35kcal/kg/day
- Neoadjuvant Chemotherapy (see below)
Management Principle:
- Extent of Gastric Resection – achieve negative margins (in general ≥5 cm, but dependent on tumour T staging) ± intraop frozen
section
▪ Early Gastric Cancer (T1a, UL(-), size ≤2cm) – Endoscopic Resection

▪ Everything else – Surgical Management (Laparoscopic / Robotic / Open) – trials ongoing comparing between Lap vs. Open
(KLASS-01 / KLASS-02)
▪ ± En-bloc resection of structures involved by local invasion
- Extent of Lymph Node Dissection (i.e. D1, D1+, D2 etc.) – see below
- Reconstruction after Gastrectomy – see below
- Adjuvant Chemotherapy – see below
Extent of Gastric Resection:

- Standard Gastrectomy: Resection of at least two-third of the stomach with a D2 lymph node dissection
- Non-Standard Gastrectomy (modified): extent of gastrectomy and/or lymphadenectomy is reduced (i.e. D1, D1(+) etc.)
compared to standard surgery. (extended): gastrectomy with combined resection of adjacent involved organs and/or extended
lymphadenectomy exceeding D2
EXTRA INFORMATION
Types of Gastrectomy
157
- Total Gastrectomy: total resection of the stomach, including cardia and pylorus – treatment of choice for proximal tumour,
diffuse-type tumours, cardio-oesophageal junction tumour & pancreatic invasion by gastric tumour
- Distal Gastrectomy: resection including the pylorus, cardia is preserved – treatment of choice for distal gastric tumours
- Pylorus Preserving Gastrectomy (PPG): resection preserving the upper third of the stomach, and the pylorus along with a
portion of the natrum
- Proximal Gastrectomy: resection includes the cardia, (esophagogastric junction). Pylorus is preserved. – potential treatment
for early proximal gastric tumours (instead of total gastrectomy) – ongoing KLASS-05 trial comparing laparoscopic proximal
gastrectomy and laparoscopic total gastrectomy for upper third early (confined to mucosa / submucosa, size < 5cm) gastric
cancer
Selection of Gastrectomy
- cN(+) or T2-T4a tumours → total or distal gastrectomy (distal if satisfactory proximal margins can be achieved)
- Pancreatic Invasion → total gastrectomy +/- pancreatico-splenectomy
- cT1N0 → PPG (for middle gastric tumour >4cm proximal to pylorus), proximal gastrectomy (where more than ½ of stomach
can be preserved)
Extent of Lymphadenectomy
- More than 15 resected lymph nodes are required for adequate staging
- cT1N0 tumours → D1 or D1(+) lymphadenectomy
▪ cT1a tumour that do not meet criteria for EMR/ESD and cT1bN0 tumours (differentiated, <1.5cm) – suitable for D1
▪ Every other cT1 tumours – D1(+)
- cN+ or cT2-T4 tumours → D2 lymphadenectomy – removal of perigastric nodes (D1) and nodes along left gastric artery, common
hepatic artery, celiac trunk, splenic artery and splenic hilum (D2 resection – i.e. clearance of major arterial trunks) – spleen
preserving
158
EXTRA INFORMATION
Lymph Node Stations86

▪ Total Gastrectomy – D1: 1 – 7 | D1(+): D1 + 8a, 9 & 11p | D2: D1 + 8a, 9, 10, 11p, 11d, 12a
▪ Distal Gastrectomy – D1: 1, 3, 4sb, 4d, 5, 6, 7 | D1(+): D1 + 8a, 9 | D2: D1 + 8a, 9, 11p, 12a
▪ Proximal Gastrectomy – D1: 1, 2, 3a, 4sa, 4sb, 7 | D1(+): D1 + 8a, 9, 11p
Station Station
1 LN along Right Paracardial 7 LN along Left Gastric Artery
LN along Anterior Superior part of Common Hepatic
2 LN along Left Paracardial 8a
Artery
3 LN along Lesser Curvature 8p LN along Posterior part of Common Hepatic Artery
4sa LN along Greater Curvature (along Short Gastric Artery) 9 LN around the Celiac Artery
LN along Greater Curvature (along Left Gastroepiploic
4sb 10 LN around Splenic Hilar
Artery)
LN along Greater Curvature (along the 2 nd part and distal
4d 11p LN along the Proximal Splenic Artery
branch of the Right Gastroepiploic Artery)
LN along the Suprapyloric (along 1 st branch and proximal
5 11d LN along the Distal Splenic Artery
branch of Right Gastric Artery)
LN along the Infrapyloric (along proximal part of Right
6 12a LN along Hepatoduodenal (along Proper Hepatic Artery)
Gastroepiploic Artery)
12p LN along Hepatoduodenal (behind Portal Vein)
12b LN along Hepatoduodenal (along bile duct)
Lymph Node Stations 1 to 6 are located left and right of the stomach (perigastric)
Lymph Node Stations 7 to 9 are centrally located from anterior to posterior
Lymph Node Station 10 to 12 are peripherally located in a clockwise fashion
86 World J Gastroenterol. 2016 Mar 14;22(10):2875-93.
159
Reconstruction
- Considerations are tumour location, remnant stomach size, operative risk
- Options
▪ Billroth I (end-to-end gastroduodenostomy) – more physiological, but potentially increased biliary reflux into stomach, better
for small tumour located distally with large amount of remnant stomach
▪ Billroth II/Polya (gastrojejunostomy) – no protection against biliary reflux into stomach, easy to perform, 1 anastomosis, can
still access duodenal papilla in future (i.e. for biliary intervention)
▪ Roux-En-Y esophagojejunostomy – preferred option after total gastrectomy, preferred if small amount of remnant stomach,
no biliary reflux post-op, unable to access duodenal papilla in future
▪ Double-Tract Reconstruction87 (for proximal gastrectomy)
Chemotherapy / Radiotherapy
- Most common side effect of chemo: nausea, vomiting, neutropenia, anorexia
- HER2 testing – can use trastuzumab-containing regimen
Neoadjuvant Therapy – survival benefits in European trials & potential for increasing resectability rates – down-staging
- MAGIC TRIAL88 (UK) – significant improvements in 5 year survival rates in patient with gastric or GEJ cancer → chemotherapy
regimen: 5FU, epirubicin, cisplatin (3 pre-operative cycles followed by 3 post-operative cycles)
- FLOT4 TRIAL 89 (Germany) – compared a perioperative docetaxel-based triple regimen with an anthracycline based triple
regimen (previously standard of care) in resectable gastric and GEJ cancer → chemotherapy regimen: docetaxel, 5-FU,
leucovorin, oxaliplatin (4 pre-operatively cycles followed by 4 post-operative cycles, 14 days cycle)
Adjuvant Therapy – aim to start within 8 weeks

- CLASSIC TRIAL 90 (South Korea, China) – adjuvant capecitabine & oxaliplatin (8 cycles chemotherapy, 21 days cycle), for
patients with stage 2, 3a/3b who had D2 surgery and achieved R0 resection → increased 3 year disease free survival (74% vs.
59%)
- Chemoradiotherapy (controversial): for patients who have not undergone an adequate D2 lymph node dissection. ChemoRT +
Chemotherapy remains an option for patient who have node-positive disease
Palliative Intention
- For patients with unequivocal evidence of incurability – i.e. haematogenous metastases, involvement of the distant peritoneum, N4
level nodal disease (para-aortic and paracolic region) and disease beyond N4 level nodes and fixation to structures that cannot be
removed
- If patients have single non-curable factor (i.e. metastatic disease) – chemotherapy without surgery (no role for surgery) as survival
same between chemotherapy and surgery (REGATTA TRIAL91)
▪ Painful Bony Mets – External Beam Radiotherapy (EBRT)
▪ Bleeding – transcatheter embolization (catheter up femoral artery), external beam radiation (delayed effect – 2-3 weeks
before radiation kills enough cancer cell for bleeding to stop) or palliative gastrectomy
▪ Obstruction – Self-expandable metal stents (SEMS) vs. palliative gastrojejunostomy (GJJ)
- SEMS – shorter hospital stay, earlier resumption of oral intake
- GJJ – longer patency,
87 Gast Cancer. 2014;17(3):562-70.

88 N Engl J Med. 2006 Jul 6;355(1):11-20. [Landmark Paper] – MAGIC TRIAL
89 Lancet Oncol. 2016 Dec;17(12):1697-1708. [Landmark Paper] – FLOT4 TRIAL
90 Lancet. 2012 Jan 28;379(9813):315-21. [Landmark Paper] – CLASSIC TRIAL
91 Lancet Oncol . 2016 Mar;17(3):309-318. – REGATTA TRIAL
160
- GJJ recommended for use in patients with good performance status (ECOG 1-2) & with both ascites and
carcinomatosis peritonei. SEMS for patients with poor ECOG performance or patient with neither ascites nor
carcinomatosis92
▪ Perforation – require surgery
Post-operative
- Feeding
▪ NBM till POD 2-3 followed by escalation of feeds
▪ Advise small, frequent meals with nutritional supplementation (high calories and protein)
▪ IM Vitamin B12 injection to circumvent loss of IF and Fe-tablets for Fe deficiency anaemia
▪ Aim discharge in 7 days for uncomplicated cases
- Identify complications (see below), Adjuvant Chemotherapy (see above)
COMPLICATIONS (GASTRECTOMY)
Early
- Haemorrhage
▪ Reactionary bleeding (within first 24 hours, may require re-operation)
▪ Secondary bleeding (due to intra-abdominal infection following anastomotic leak or pancreatic fistula) possible
pseudoaneurysm formation* (i.e. splenic artery pseudoaneurysm) – radiological intervention
- Anastomotic leak (day 5-7) – tachycardia is an early sign (mostly occur at esophagojejunostomy)
▪ Early leak – present as septic episode or contaminated drain discharge
▪ Delayed leak – can treat conservatively if patient not septic (radiologically guided drainage if septic)
- Duodenal Stump Leak / Blowout – due to progressive afferent limb dilation from kink/volvulus (day 5-7)
- Pancreatic Fistula (can occur even without pancreatic resection)
* A small amount of bleed can precede massive haemorrhage (herald bleed)
Late
- Early satiety → advise patient to have small frequent meals
- Gastroesophageal reflux leading to esophagitis → common for proximal gastrectomy

- Dumping syndromes
▪ Sigstad Scoring System (score > 7 is suggestive of dumping syndrome)
▪ Pathophysiology: With meal, rapid gastric emptying leading to:
- Hyperosmolar jejunal chyme which increases intraluminal fluid sequestration and decreased blood volume
(hypotension, tachycardia, palpitations, dizziness) & abdominal bloating (diarrhoea, cramping, nausea)
- Inappropriate gut hormone release → vasomotor and GI symptoms
- Rapid glucose absorption → reactive hyperinsulinemia → hypoglycaemia (faintness, severe hunger, dizziness, cold
sweating)
▪ Early dumping syndrome (within 30 mins) → rapid filling of the proximal small intestine with hypertonic food resulting in
fluid being drawn into the gut by osmosis (rapid fluid shift + complex neurohumoral response), treat by eating small frequent
meals with low carbohydrates and high protein/fat ± somatostatin / octreotide (i.e. SC 50mg 30min before meals)
▪ Late dumping syndrome (within 2-3 hours) → rapid inflow of carbohydrates into jejunum induce hyper-insulinemia follow
by hypoglycemia (reactive hyperinsulinemia) → treat by decreasing carbohydrate load in main meals and take small amounts
of carbohydrate between main meals ± acarbose / somatostatin
92 Gastrointest Endosc. 2015 Feb;81(2):321-32.
161
- Nutritional deficiency
▪ Need to supplement with B12 injections, Vitamin D and Iron
▪ Fat malabsorption leads to decrease in absorption of fat soluble vitamins (Vit A,D,E,K) + decreased calcium absorption after
gastrectomy → all post-menopausal women and all patient > 70 should be replaced with oral calcium and vitamin D
▪ Iron deficiency – mixed picture
- B12 binds to IF and gets absorbed in the ileum – Loss of intrinsic factor (secreted by parietal cells), → B12 deficiency
(megaloblastic anemia, clinically apparent only after 24 months) → Treat: IM Vitamin B12 1mg q3 monthly
- Iron absorption in duodenum & upper jejunum – Decreased acid production leads to decreased conversion of iron from
Fe3+ to Fe2+ by gastric acid → malabsorption due to reduced gastric acid and bypassed duodenum → Treat: Oral Fe
supplement
- Loop Syndromes (Afferent Loop Syndrome)

▪ Occurs in Billroth II reconstruction
▪ Mechanical obstruction of the afferent jejunal loop due to kinking, anastomotic narrowing, or adhesions → postprandial
epigastric pain with nausea, non-bilious vomiting

▪ Can be complicated by duodenal stump blowout in the early postoperative period and postoperative obstructive jaundice,
ascending cholangitis, and pancreatitis due to transmission of high pressures back to the biliopancreatic ductal system
▪ Can be decreased by doing Roux-en-Y surgery (but may still occur)
- Retained antrum syndrome

▪ Not enough antrum removed leads to increased acidity in residual stomach, with formation of marginal ulcers on the jejunal
side of the anastomosis
- Intestinal hurry → Inadequate reservoir function leads to poor digestion may have phytobezoar formation
- Biliary/intestinal reflux into stomach (bile reflux gastritis)
▪ Postprandial epigastric pain a/w nausea / vomiting; pain not relieved with vomiting
▪ More common in patients who underwent Billroth 2 procedure as compared to patients who underwent Roux-En-Y
- Post-splenectomy complications (see spleen topic)
- Recurrence of gastric cancer
162
PROGNOSIS
- Follow-up (NCCN guidelines): TCU 3-6/12 x1-2years, then 6-12/12 for 3-5yrs then annually
- Labs, CT and OGD as clinically indicated
- Iron supplementation and Vitamin B12 (prevention of nutritional deficiency, especially after total gastrectomy)
- Upper Endoscopy as clinically indicated (for patients with partial or subtotal gastrectomy)
- CT TAP every 6 to 12 months for 1 st 2 years then annually
- 5yr survival rates for curative surgery is higher in Japan (50-75%) compared to the West (25%)
- The 5-year overall survival rates of patients with pathological stage IA, IB, II, IIIA, IIIB, and IV disease were 91.5%, 83.6%, 70.6%,
53.6%, 34.8%, and 16.4% respectively.93
93 Gastric Cancer. 2018 Jan;21(1):144-154.
163
GASTRIC LYMPHOMA
DEFINITION
GI lymphoma is the most common form or extranodal lymphoma – involves the stomach in 60-75% of cases
HISTOLOGY TYPES
- Marginal zone B cell lymphoma of the mucosal associated lymphoid tissue (MALT) ~50%
- Diffuse large B cell lymphoma (DLBCL)
- Other: Mantle cell lymphoma, Follicular lymphoma, Peripheral T cell lymphoma
RISK FACTORS
- Helicobacter Pylori Infection – implicated in MALT lymphoma
- Autoimmune Disease – i.e. rheumatoid arthritis, Sjogren syndrome, SLE
- Immunodeficiency (i.e. HIV) & Immunosuppression
- Usually poorly specific – vague dyspepsia, epigastric pain to less frequently gastrointestinal bleeding or persistent vomiting
- Systemic B symptoms – fever, night sweats
STAGING – ANN ARBOR MODIFIED SYSTEM94

- Stage I – involvement of mucosa to infiltration of neighbouring organs
- Stage II – regional lymph nodes / intra-abdominal distant lymph nodes
- Stage III – involvement of extra-abdominal lymph nodes
- Stage IV – infiltration of distant / extra-gastrointestinal organs, bone marrow involvement
MANAGEMENT
- Rule out systemic involvement – CT TAP, EUS, Bone Marrow Biopsy
- The first line treatment of all low grade gastric MALT lymphoma is H. Pylori eradication therapy
▪ In H. pylori negative lymphoma / t(11;18)-positive lymphoma / lymph node involvement that has failed H. pylori eradication
therapy → consider external beam radiation therapy and / or chemotherapy
- For high grade (aggressive) MALT → treat with External Beam RT + Chemotherapy
- Surgery – restricted to complications – i.e. bleeding / perforation
94 Gut. 2011 Jun;60(6):747-58.
164
GASTROINTESTINAL STROMAL TUMOUR (GIST)
DEFINITION
GIST is the most common mesenchymal soft tissue sarcoma of the GI tract which arises from the Interstitial cell of Cajal. They are
generally positive for CD117 (c-kit) on immunohistochemistry. CD 117 is a transmembrane tyrosine kinase receptor.
- Incidental on OGD or imaging (i.e. CTAP) in an asymptomatic patient
▪ Location: stomach (60%), jejunum and ileum (30%), duodenum (5%), rectum (2-3%), colon (1-2%), oesophagus (<1%)
▪ Metastases – usually intra-abdominal involving peritoneum and liver
- Symptomatic – abdominal pain, abdominal mass, dysphagia, upper BGIT, acute abdomen (i.e. rupture)
- Syndromes a/w GIST: Carney Triad, NF-1
DIAGNOSIS95
- Macroscopic: well circumscribed, fleshy, pink or tan-white mass
- Immunohistochemical (IHC) staining: CD117 (c-kit) positive
- Molecular Characterization: KIT mutations (75-80% with exon 11 most common, exon 9), PDGFRA mutations (10%, exon 18),
wild type tumours (10-15%)
STAGING - MIETTINEN CLASSIFICATION96

Size (cm) Mitotic Index (50 HPF*) Site Rupture Tumour Genotype
< 2 cm ≤ 5 mitosis Any
Very low Risk
2 – 5 cm ≤ 5 mitosis Gastric
5.1 – 10 cm ≤ 5 mitosis Gastric KIT exon 9 &

Low-Risk PDGFRA exon 18
2 – 5 cm ≤ 5 mitosis Intestinal mutations, likely to
develop resistance
> 10 cm ≤ 5 mitosis Gastric Capsule rupture
to imatinib
Intermediate Risk indicates high-risk
5.1 – 10 cm ≤ 5 mitosis Intestinal
2 – 5 cm > 5 mitosis Gastric (in clinical practice,
tumour genotype is
2 – 5 cm > 5 mitosis Intestinal
rarely tested for)
> 10 cm ≤ 5 mitosis Intestinal
High-Risk
5.1 – 10 cm > 5 mitosis Any
> 10 cm > 5 mitosis Any
* 50 HPF = 5mm2 optical fields used by Miettinen (usually in practice 50 HPF = 10mm 2)
INVESTIGATIONS
- CT-AP (first-line): well circumscribed exoluminal masses, with contrast show heterogeneous enhancement with necrotic-
hemorrhagic areas or degenerative components
▪ Evaluate for metastasis via (1) loco-regional infiltration, (2) haematogenous to liver, omentum and peritoneal cavity
- OGD: features of high risk GIST: size, irregular borders, echogenicity, central cystic spaces, presence of lymph nodes
- EUS +/- FNA (for histology)
- Pre-op FDG-PET – establish any early metastases and establish baseline metabolic activity
- Histology via CT guided or endoscopic guided biopsy ( patients with unresectable disease, considering neoadjuvant therapy)
▪ Spindle cell type (70%), epithelioid cell type (20%) or mixture of both
95 Cancer Res Treat. 2016 Oct;48(4):1155-1166.

96 Cancer Chemother Pharmacol. 2014 Nov;74(5):883-98.
165
MANAGEMENT
Localized Disease (Resectable)
- For GIST < 2cm, manage with active surveillance, re-image in 6-12 months
- For GIST > 2cm, operate with complete surgical resection with negative margins (R0 resection)
▪ Extended anatomic resection & lymphadenectomy not required
▪ Avoidance of tumour rupture
- Postoperative Management
▪ For high risk GIST tumours – adjuvant Imatinib at least 36 months (KIV genotyping for KIT / PDGFRA exon mutation)
▪ For patients with positive margin (R1 resection) – adjuvant Imatinib (no benefit with re-excision to clear margins)
▪ For low-risk GIST tumour – adjuvant therapy is not indicated
Locally Advanced (Borderline Resectable)

- Neoadjuvant therapy with imatinib 400mg/day (Gleevec) – selective inhibitor of KIT protein tyrosine kinase
▪ 60% will respond to treatment with Imatinib. Repeat staging scan after 6 months of therapy as 60% of patients can attain
R0 resection (post-op, continue adjuvant Imatinib for at least 36 months)
▪ If have disease progression, KIV for dose escalation to 800mg/day or use of second line agent (i.e. sunitinib (Sutent))
▪ Side effects of imatinib: gastrointestinal (i.e. nausea / diarrhoea), periorbital oedema, fluid retention, muscle cramps, fatigue,
GI bleed (i.e. rapid tumour necrosis) , contraindicated in pregnancy
Metastatic GIST
- Neoadjuvant therapy with imatinib (Gleevec) – selective inhibitor of KIT protein tyrosine kinase
- Re-evaluate tumour size in 3-6 months, KIV for surgical resection
- Surgical resection of residual metastatic disease responding to Imatinib sensitive GIST lead to prolonged progression free
survival (reduce tumour burden and remove resistant tumour cells)
FOLLOW-UP & PROGNOSIS

- High / Intermediate risk: post-op CTAP every 3-4 months for 1st 3 years then every 6 months until 5 years then annually
- Low / Very low risk: post-operative surveillance with CTAP every 6 months for 1 st 5 years
- High Risk = 45% recurrence free survival at 5 years
- Intermediate Risk = 80% RFS at 5 years
- Low Risk = 95% RFS at 5 years
166
OBESITY
DEFINITION
Obesity is a complex disease, multifactorial in origin associated with multiple comorbidities and increased risk of cardiovascular
mortality. It currently is the second leading cause of preventable death in the USA.
RISK FACTORS
- Genetics: children of 2 obese parents – 80-90% change of developing obesity, 2x higher risk of obesity among twins
▪ Reduced metabolic activity – reduced thermogenic response to meals
▪ Difference in intra-luminal bacterial composition
- Environmental: diet, culture
CLASSIFICATION (WHO)
Classification Cut-off BMI Asian Population (intervention levels)
Normal Range 18.5 – 24.9 23.0
Pre-obese (overweight) 25.0 – 29.9 27.5
Obese Class I (obesity) 30.0 – 34.9 32.5
Obese Class II (severe obesity) 35.0 – 39.9 37.5
Obese Class III (morbid obesity) ≥40.0 ≥40.0
- Take a complete history on patient’s diet, exercise, previous attempts at weight loss, any previous trial of pharmacological therapy
or surgical intervention
- Assessment of Metabolic Complications
▪ Cardiovascular Disease (obesity paradox – obese patients with established CVD have better prognosis than thin leaner
patients with same CVD)
▪ T2DM / HLD
▪ Associated comorbidities – HTN/HLD/T2DM, cardiac arrhythmias, right side heart failure, OSA, GERD, cholelithiasis,
asthma, depression, degenerative joint disease,
INVESTIGATIONS
- Blood – HbA1c / Fasting Glucose / Insulin, Lipid Panel, Vit D / Thyroid Screen / PTH, FBC / U/E/Cr, Uric Acid, LFT, Fe Panel /
Vitamin B12 / Folate, Cortisol, C-peptide
- Imaging – Bone Mineral Density (BMD), US HBS, OGD, CXR
- Others – ECG, ± sleep study
MANAGEMENT
Individualized weight loss strategy – aim for loss of 5-10% of baseline weight over 6 months
- 7% weight loss & ≥150m of exercise: 58% reduction in incidence of T2DM 98 (more effective than tx with metformin)
- 1kg weight loss: ~0.5% reduction in LDL,
Lifestyle intervention
- Diet modification (i.e. caloric restriction – achieve weight loss)
- Physical activity (i.e. aerobic exercise 30-45min/ day – maintenance of weight)
- Behavioural therapy (i.e. self-monitoring with food / activity logs, frequent self-weighing)
Pharmacological therapy – orlistat, phentermine/topiramate and lorcaserin,
Surgical Intervention
- Indications: BMI ≥ 40.0 kg/m 2 or BMI ≥ 35.0 kg/m2 with obesity related comorbid conditions who have not responded to lifestyle
intervention
- Multiple surgical options are available99, the 2 most common are vertical sleeve gastrectomy & gastric bypass
- Percentage Excess Weight Loss (i.e. (baseline weight - follow-up weight) / (baseline weight - ideal weight for BMI 25) x 100%)
97 J Cardiopulm Rehabil Prev. 2015 Mar-Apr;35(2):81-92.

98 N Engl J Med 2002; 346:393-403
99 Obes Surg . 2019 Jul;29(Suppl 4):309-345
167
EXTRA INFORMATION
Laparoscopic Sleeve Gastrectomy (LSG)

- It involves tubularization the stomach removing the hormonally active gastric fundus
- In sleeve gastrectomy, faster gastric emptying leads to rise in satiety hormones
- Outcomes from LSG – 5 year weight loss ~ 58.4%, T2DM resolved in 60.8%
- Complications – gastric leak (2.4%)100, stenosis / stricture (0.7%), bleeding, long-term: intractable GERD, nutritional deficiency
(i.e. vitamin B12, vitamin B1 / thiamine, iron, zinc, niacin (B3), selenium, vitamin A (hair loss / dermatological manifestation),
vitamin D & calcium (osteoporosis)
Roux-En Y Gastric Bypass (GB)

- It involves creation of a small gastric pouch with a roux-en-Y reconstruction.
- Biliopancreatic Limb ~ 30-60cm & Alimentary Limb ~ 75-150cm.
- In Roux-En Y Gastric Bypass, faster delivery to distal ileum give stimulus to entero-endocrine cells (EEC) which feedback to
CNS to increase satiety
- Complications – small bowel obstruction secondary to internal hernia (through the transverse mesocolic defect / Petersen’s
defect) or postoperative adhesions, stenosis at the JJ anastomosis, gallstone disease, marginal ulceration, bleeding
PROGNOSIS
- The weight loss attained between sleeve gastrectomy and gastric bypass is equivalent101
- At 2 years, mean % excess weight loss is ~ 60% for all bariatric procedures
- Absolute mean weight loss is ~ 40kg
Predictor of Long-Term Diabetes Remission after Metabolic Surgery102

Points on ABCD index
Variables
0 1 2 3
Age ≥ 40 < 40
BMI < 27 27 – 34.9 35 – 41.9 ≥ 42
C-peptide <2 2-2.9 3 – 4.9 ≥5

Duration of DM (yr) >8 4–8 1 – 3.9 <1
- Weight Loss is also a predictor of DM remission after metabolic surgery, but it isn’t a pre-operative factor
100 Surg Endosc. 2012 Jun;26(6):1509-15.

101 JAMA. 2018 Jan 16;319(3):241-254.
102 J Gastrointest Surg (2015) 19:1015–1021 [Important Paper]
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6. COLORECTAL
APPROACH TO LOWER BLEEDING GASTROINTESTINAL TRACT
DEFINITION
LBGIT is defined as bleeding that originates from a source distal to the Ligament of Treitz. Majority of the time, LBGIT originates
from the colon with patients presenting with hematochezia. Hematochezia is defined as gross, fresh blood seen either on toilet
paper after defecation or mixed with stools.
Massive LBGIT is defined as bleeding that requires ≥ 3 units of blood over 24 hours or in patients with hemodynamic instability
For patients presenting with PR bleeding, initial evaluation is to determine if the patient is stable to be managed in the outpatient
setting or to be admitted to the hospital for further evaluation. Further history taking and examination will help to narrow down the
underlying cause of the PR bleeding. Unfortunately, even with a detailed history taking and examination, there is a risk of missing
out colonic malignancy if patients do not go for colonoscopic evaluation. As a general rule, all patients with PR bleeding above
the age of 50 should be scheduled for colonoscopy. Based on the clinical presentation, we should learn to identify high-risk
patients who would benefit from undergoing early colonoscopic evaluation.
For patients who are hemodynamically unstable with PR bleeding, further investigation and management will be explained in the
later section.
Presenting Complaint (symptomatology)

- Is this the first episode or has there been recurrent episodes of PR bleeding? If recurrent episodes, does the bleeding “come
& go” or “persist and progress”
▪ Come & Go (self-limiting): suggestive for benign causes of bleeding (i.e. hemorrhoidal bleed, anal fissues)
▪ Persist and Progresses: suggestive for malignant causes (i.e. tumour bleed)
- How was the PR bleeding observed? Was it noticed on wiping, having blood drip into the toilet bowl, frank blood on
defecation?
▪ Noticed on wiping: suggestive for anal fissures (usually have pain as well)
▪ Having blood drip into toilet bowl / blood coating stools: suggestive for hemorrhoidal bleeding
▪ Coating stools: suggests distal bleed
▪ Mixed in with stools: suggests proximal bleed
- What is the colour of the PR bleeding? Frank red blood, maroon coloured blood, melena?
▪ The colour of the blood give suggestion to the anatomical location, the amount and speed of bleeding also affects the
colour – It takes ~14 hours for blood to be broken down within the intestinal lumen; if transit time is < 14 hours the
patient will exhibit hematochezia, and if > 14 hours patient will exhibit melena.
▪ Frank red bleeding: suggestive of blood originating from left colon
▪ Maroon colored bleeding: suggestive of blood originating from right colon (may be mixed with stools)
▪ Melena: suggestive of UBGIT or occasionally from right sided colonic bleed
▪ Ask if stools are foul-smelling, sticky, and as black as hair.
▪ Melena is seen as black tarry stools resulting from oxidation of hematin (altered blood) in the GIT
- How many episodes of PR bleeding? Were there any clots present?

▪ Quantify the severity of PR bleeding (volume and frequency), does this patient need urgent admission and evaluation?
- Associated symptoms such as pain on defecation, multiple episodes of bloody diarrhoea, abdominal pain
▪ Pain on defecation: suggestive of anal fissure, rectal tumours (i.e. tenesmus-- incomplete defecation, recurrent
inclination to defecate, frequently painful), ischemic colitis
▪ Bloody Diarrhoea: suggestive of infective causes, inflammatory bowel disease (diarrhoea mixed with blood & mucus)
▪ Abdominal pain with PR bleed: suggestive of colitis (inflammatory, ischemic, infective)
▪ Passing of mucus
▪ Hematemesis: suggestive of massive UBGIT
- Systemic Review (Red Flags for Malignancy)

▪ Change in bowel habits such as alternating constipation and diarrhoea
▪ Any spurious diarrhoea
▪ Change in stool calibre such as pencil thin stools
▪ Presence of tenesmus, which can be due to rectal tumours, infective colitis, inflammatory colitis and radiation proctitis
▪ Any constitutional symptoms such as loss of weight and appetite
▪ Other risk factors: smoking, diet (i.e. red meat), obesity
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6. Colorectal_Last Updated 3rd June 2020
▪ Additional relevant history for UBGIT if suspected
What is the likely underlying aetiology?

In addition to the points covered above, the following points in history can help give clues to the potential bleeding source.
- Age of the patient

▪ Young patients: suggestive for benign perianal causes such as hemorrhoids, anal fissures, can also be due to
inflammatory bowel disease though uncommon in our local setting (Asians)
▪ Older patients: suggestive for diverticular disease, colorectal malignancy, ischemic colitis
- Past Medical History

▪ Any previous colonoscopy? When was it last done? What were the findings? Was any procedure performed?
▪ Any previous history of colorectal polyps?
▪ Previous hospital admissions for PR bleeding? When was the admission? What was done during the admission? Any
CT imaging, colonoscopy or surgical intervention?
▪ Previous radiation history?
▪ Previous cardiac risk factors such as atrial fibrillation, AMI (risk of ischemic colitis)
- Family History
▪ Any family history of IBD, GI malignancies, cancers
- Social History
▪ Any smoking, alcohol intake, obesity, diet (i.e. red meat), these are known risk factors for CRC
▪ Any recent travel history / positive contact history (infective colitis such as traveller’s diarrhoea, usually a/w fever)
- Medication History
▪ Any recent intake of NSAIDs (NSAIDs induced colitis)
▪ Any anti-platelets, anticoagulants, novel oral anticoagulants (NOACs) → bleeding diathesis
▪ Any antihypertensive medications
▪ Any iron supplementation → dark green stools mimicking melena
Are there any likely complications?

- Potential complications from PR bleeding?
▪ Any symptomatic anemia (i.e. SOB on exertion, postural dizziness, syncope, chest pain, palpitation, lethargy/fatigue),
▪ Any risk of cardiac complications from PR bleeding (i.e. any history of ischemic heart disease which increases patient
risk of acute myocardial infarction)
- Hemodynamic Assessment
▪ Is the patient hemodynamically stable or unstable?
▪ Assess hemodynamic stability – BP (MAP), HR, SpO2, Temperature
▪ Urine output (keep >0.5ml/hr)
▪ Abdominal Examination – any abdominal tenderness, abdominal masses
▪ DRE: examine perianal externally, look for any anal fissures, prolapsed hemorrhoids, thereafter confirm presence of
hematochezia or melena or brown stools, any masses (if paitent has an anal fissure, he will be too tender to allow for
PR examination.
▪ Proctoscopy: can assess if bleeding is due to ano-rectal causes (i.e. low rectal ulcers, hemorrhoidal bleeding) or
bleeding distal to the proctoscope, can assess if bleeding is active (i.e. free flowing +/- clots) or if bleeding has stopped.
▪ +/- NGT insertion – if suspect Upper BGIT, can consider insertion where positive aspirate will indicate UBGIT and need
for OGD. However, absence of blood does not rule out Upper BGIT. (rarely performed)
- Any systemic manifestation of inflammatory bowel disease (joint, liver, eye and skin manifestations)
- Assess for complications

▪ Signs of Anaemia
▪ Face – (i) conjunctival pallor (ii) pallor of mucous membrane
▪ Cardiac Auscultation – short systolic flow murmur at aortic area
▪ Pulse – (i) tachycardia (ii) bounding (iii) collapsing pulse
▪ Hands – pallor of palmar creases
170
Upper GIT (proximal to ligament of Treitz)

- Upper GI bleeding – esophageal, gastric, duodenum
Small Intestine (2-9%)

- [1] Angiodysplasia (50-60%) – more common in elderly
- Meckel’s diverticulum – more common in children
- Small bowel neoplasms (i.e. gastro-intestinal stromal tumours)
- Crohn’s Disease
- Enteritis (inflammatory / infective / radiation / ischemic)
- Aortoduodenal fistula (patients with synthetic vascular graft),
Large Intestine
- Colonic (60-80%)
▪ [2] Diverticular Disease (bleeding diverticulosis) – 20-50%
▪ Colitis
o [3] Infective (i.e. Bacterial / Viral / Parasitic)
o Inflammatory (i.e. UC, CD, Indeterminate IBD)
o Chemical (i.e. NSAIDs use, anti-angina drug (nicorandil))
o Ischaemic: at water-shed area (splenic flexure – 3-9%, recto-sigmoid junction)
o Radiation (i.e. radiation proctitis)
▪ Colonic Carcinoma / Post-polypectomy bleeding

▪ Angiodysplasia* (capillary, cavernous haemangioma) ~ 3-10%
▪ Dieulafoy’s Lesion (most common in stomach – 75%, duodenum – 14%, colon 5%)
▪ Others: Colonic varices, Aorto-colonic fistula, Vasculitis
- Rectal
▪ Rectal Cancer
▪ [4] Anorectal varices
▪ [5] Rectal ulcer / Stercoral ulcer
▪ [6] Solitary Rectal Ulcer Syndrome (SRUS)
- Perianal (4-10%)
▪ Haemorrhoids, anal fissure, anal cancers
Others
- Bleeding after endoscopy procedure (i.e. post-polypectomy bleeding, post-RBL bleeding)
- Bleeding after operation (i.e. staple line bleeding)
171
EXTRA INFORMATION
[1] Angiodysplasia: small AVM composed of clusters of dilated vessels in the mucosa and submucosa. Bleeding more commonly aff ects the right
colon and cecum (80%), small intestine (15%), stomach. Bleeding stops spontaneously but risk of re-bleeding is high
[2] Bleeding Diverticular disease: It is the most common cause of massive acute LGIT, painless hematochezia (maroon or bright red). The
perforating artery adjacent to the colonic diverticulum becomes attenuated and eventually erodes. This leads to arterial bleeding. Majority of the
time, the bleeding stops spontaneously. (risk of re-bleeding ~15%)
[3] Causes of infective colitis includes: E coli, Salmonella, Shigella, Campylobacter jejuni, Entamoeba histolytica, Histopla sma, Cytomegalovirus
[4] Anorectal varice: They are seen in 80% of patients with portal hypertension but are implicated in < 1% of massive GI bleeds
[5] Stercoral Ulcer: a/w hard stools impacted in rectum or rectosigmoid leading to ischemia, necrosis, ulceration and eventua l perforation.
[6] Solitary Rectal Ulcer Syndrome (SRUS): It is a misnomer as the condition is a sequela of both internal rectal prolapse & outlet obstruction
constipation. The lesion is not always solitary (it may be multiple), it is not ulcerative (it may be polypoid / nodular or affecting the erythematous
mucosa only) and is not restricted to the rectum (it may involve the sigmoid colon). Patients present with rectal bleeding, s training during defecation
and a sense of incomplete defecation (tenesmus), and passage of mucus. Histology is crucial for diagnosis, findings of fibromuscular obliteration of
the lamina propria helps to differentiate this condition from IBD / malignancy.
INVESTIGATIONS
Biochemical Investigations
- FBC: keep Hb > 8-10 (know what is the baseline Hb), transfuse platelet if platelet < 50, assess TW if worried about colitis
- U/E/Cr: assessment of renal function (i.e. Cr / eGFR as may need contrasted scans), urea level (tend to be raised in UBGIT)
- PT/PTT: if patient has history of liver disease or on anticoagulants, KIV correct coagulopathy (NUH anticoagulation
guidelines)
- GXM
- Cardiac Enzyme: to rule out cardiac event as a cx
- ABG/Lactate: useful in patients presenting with hemodynamic instability/hypovolemic shock
Colonoscopy
- Endoscopy view is limited in patients with active lower BGIT.
- Able to intubate terminal ileum to identify if bleeding is from small bowel, but unable to visualize rest of small bowel
- More useful in the setting of a hemodynamically stable patient who is able to tolerate adequate bowel preparation
- Diagnostic – able to identify cancer (and biopsy for histology), diverticular disease, angiodysplasia etc.
- Therapeutic advantage: inject vasoconstrictive agents (epinephrine) or applying thermal therapy (laser photocoagulation,
heater probe) to control bleeding and/or mechanical interventions (i.e. endoclips)
Imaging Investigations-- used if hemodynamically unstable. Has the advantage of the ability to diagnose bleeding throughout the
GI tract, including small bowel sources unreachable by colonoscopy. However, it requires active bleeding at the time of the study
to detect the bleeding site.
- CT Mesenteric Angiogram (CTMA)
▪ Contrasted scan that can detect bleeding as low as 0.3 mL/min
▪ When active bleeding is present, it can provide precise anatomical location of bleed in 90% of the time based on where
there is active contrast extravasation in the bowel lumen
▪ Disadv: No therapeutic intervention, radiation exposure, use of IV contrast that risks nephropathy & allergy
- Selective Mesenteric Angiography / Angioembolization
▪ Contrasted procedure that can detect bleeding as low as 0.5 mL/min and provide therapeutic intervention.
▪ Selective mesenteric angiography is usually performed after CTMA diagnoses the presence of an active bleed. The
detection rate of bleeding is significantly higher if selective mesenteric angiography is performed within 90 minutes as
compared to within 150 minutes. (within 150 minutes equates to 2.89 times higher detection rate and within 90 minutes
a/w 8.56 times higher detection rates)
- Radionuclide imaging with technetium 99 m (99mTc-RBC)
▪ Can detect bleeding as low as 0.1 mL/min, but often is unable to localize bleeding accurately (only localises bleeding
to a general area of the abdomen), time consuming and not suitable for patients who are hemodynamically unstable.
▪ Not commonly performed
172
MANAGEMENT
Principle: resuscitation and hemodynamic stabilization, identify site of bleeding, treat accordingly
Resuscitation & Hemodynamic Stabilization

- Keep patient NBM
- ABC: Fast infusion of crystalloids +/- colloids while waiting for whole blood
- Continuous hourly vital signs monitoring
- Input / Output Charting, Stool Charting
- Catheterisation for strict urine output monitoring-- 0.5ml/kg/h
- KIV for NGT insertion if suspicion for Upper BGIT is high
- Decide on patient’s disposition, can he be managed in general ward or require high dependency or ICU care
- KIV insertion of arterial line / central venous line, depending on patient’s hemodynamic status
- Stop all anti-hypertensive medications
- Stop all antiplatelets, anticoagulants and novel oral anticoagulants (NOACs), KIV anticoagulation reversal
- Take bloods for investigation (as above)
Identify site of bleeding

- The first dichotomy is to differentiate if this is an Upper BGIT or Lower BGIT
- For Lower BGIT, clinical examination (DRE / Protoscope) can help reveal if bleeding is from the ano-rectal junction and if
bleeding is active
- For patients who are hemodynamically unstable, a CTMA is the preferred investigation of choice. If an active blush is present,
the patient can proceed to either a selective mesenteric angiography or colonoscopy (depending on the location of the
bleed).
- For patients who are hemodynamically stable and with persistent PR bleeding, a colonoscopy can be performed after
mechanical bowel preparation
- Rarely, surgical intervention is required if the source of bleeding cannot be identified and the patient has persistent lower
BGIT.
Treat accordingly
- Refer to specific sections on the treatment required
- Surgical Intervention can be considered in the following settings:
▪ Continued or recurrent haemorrhage despite non-operative attempts at localization,
▪ On-going hemodynamic instability,
▪ Transfusion requirement > 6-10 units,
▪ Pathological findings requiring surgical intervention
- Aim to have pre-surgical localization of bleed, improve mortality and morbidity

- If bleeding appears to be from colon but cannot be localized – emergency total abdominal collection (TAC) – high mortality
rate (10-30%), re-bleeding rate of < 1%, segmental colectomy have mortality rate 10% with re-bleeding rate of 35-75%
ALGORITHM
In patients with PR bleeding, I will first evaluate the patient's hemodynamic status. If patients are hemodynamically unstable, a clinical judgement
has to be made if the bleeding is from an Upper BGIT or from a Lower BGIT.
Factors that are predictive for Upper BGIT include history of melena, melenic stool on examination, blood or coffee grounds detected during NG
lavage and ratio of BUN to Serum Cr > 30.. The presence of blood clots in the stool made an UBGIT less likely.
If the suspicion of Upper BGIT is high, I would then arrange for an urgent OGD. In the setting of an unstable patient with potentially massive Upper
BGIT, I will aim to perform the OGD in the emergency operating theatre under General Anesthesia to ensure that the patient’s airway is protected.
Second, I will be able to get assistance from anesthesia to help with the resuscitation. Third, I am able to proceed with exp loratory laparotomy
should the need arise if I am unable to stop the bleeding endoscopically.
If the OGD is negative but the patient still has persistent PR bleeding. I will arrange for the patient to undergo a CTMA. The CTMA will allow for
localization of the BGIT and if an active blush is detected with IV contrast entering the bowel lumen, I will proceed to activate the interventional
radiologist (IR) to perform a selective mesenteric angiography for the patient. If the bleed is detected on angiography, angioembolization can be
performed using micro-coils. Following which, the patient will be brought to the ICU for further resuscitation.
If the CTMA is negative, it implies that the bleeding has either stopped or the rate of bleeding is not fast enough. CTMA is able to detect bleeding
rates as low as 0.3ml/min. I will bring the patient to the ICU for further resuscitation. I will proceed with a mechanical bowel preparation and aim for
an early colonoscopy for the patient which has the benefits of diagnosis and therapeutic options. This includes injection wit h adrenaline, thermal
coagulation or mechanical clips. Also, I will attempt to intubate the terminal ileum to rule out the small bowel as the source of bleed.
If colonoscopy is negative but the patient has persistent PR bleeding, further investigation modalities such as radionuclide scan, double balloon
enteroscopy or capsule endoscopy can be attempted.
173
However, if the patient becomes hemodynamically unstable again with a negative CTMA, I may elect to perform an exploratory la parotomy for the
patient. The indications for surgery are persistent or recurrent PR bleeding despite non-operative attempts at localization, hemodynamically
unstable patients and patients who require more than 6 to 10 units of PCT.
174
ISCHAEMIC COLITIS
.
DEFINITION
Ischemic colitis is predominantly a disease of the elderly. It is the most common cause of intestinal ischemia and accounts for ~
1 in 1000 hospital admission
RISK FACTORS
Examples
Occlusive - Mesenteric Artery Emboli – most commonly occur near origin of SMA
Vascular Embolic / Thrombotic Hx - Thrombosis
Disease - Trauma
- Congestive Heart Failure
Recent Hx of - Transient hypotension
Hypotensive Episodes - Shock (i.e. hypovolemic, sepsis)
- Myocardial Infarction
- Chemotherapeutic agents
Medication Hx
- Oral contraceptive pills
(long list)
- Recent Vasopressor use
Surgical Hx - Aorta / Cardiac Surgeries (i.e. aorto-iliac instrumentation, CABG)
Non-occlusive - Acquired or Hereditary thrombophilia
vascular - Deficiency of Protein C/S or antithrombin III
Hypercoagulability Hx
disease - Factor V Leiden mutations
- Antiphospholipid syndrome
- History of Atrial Fibrillation
Cardiovascular Hx
- Atherosclerosis
- Hx of vasculitis, SLE / RA / Wegener Granulomatosis
- Long distance running103
Others - Mechanical factors – i.e. colonic obstruction due to tumours, adhesions,
volvulus, hernia
- Haemodialysis
PATHOPHYSIOLOGY
- Non-occlusive colonic ischemia (95%)
- Embolic and thrombotic arterial occlusion
- Mesenteric vein thrombosis
Arterial supply (Colon & Rectum)

- SMA (L1): Ileocolic, right colic and middle colic arteries
- IMA (L3): Left colic, sigmoid, superior rectal arteries
- Internal Iliac Artery (L4): Middle and inferior rectal arteries
- Marginal Artery of Drummond: a continuous arterial arcade,
running along the distal mesentery near the inner border of the colonic
wall
- Arc of Riolan (meandering mesenteric artery): connects the middle
colic branch of SMA with the left colic branch of the IMA at the root of
the mesentery. (can be absent as an anatomical variant)
Watershed areas
- Right Colon – vulnerable in systemic low flow states (i.e. hypotension from haemorrhage / sepsis, heart failure), also
vulnerable to embolic occlusion (2 reasons: ileocolic is a terminal branch of SMA, straight take-off from SMA (making it
susceptible to embolic occlusion)
- Splenic Flexure – receives blood supply from SMA & IMA
- Rectosigmoid Junction – vulnerable in presence of IMA stenosis with age from atherosclerosis, post-surgery (i.e. IMA ligation)
103 Current Surgical Therapy (11th edition) – pg 169
175
History
- Symptoms are dependent on severity of the ischemia + medical history is critical in diagnosis of ischemic colitis
- Sudden onset of abdominal pain (crampy), not well localized
- Mild hematochezia, starting within 24hr of abdominal pain
- Low-grade fever
- Nausea and vomiting
3 progressive clinical stages have been described:

- Hyperactive phase – severe abdominal pain with passage of bloody, loose stools (blood loss is mild)
- Paralytic phase – pain becomes more continuous and diffuse, abdomen more tender and distended without bowel sounds
- Shock phase – massive fluid, protein and electrolytes start to leak through the damaged gangrenous mucosa. Severe
dehydration with shock and metabolic acidosis may develop
EXTRA INFORMATION
Acute Small Bowel Ischemia vs. Acute Colonic Ischemia
- Vital signs: any hypotension, tachycardia (any AF)
- Abdomen: tenderness over affected colon, any signs of peritonism
- DRE: blood in stools
INVESTIGATIONS
Biochemical
- FBC: leukocytosis >15 in 75%, high Hb/ Hct (due to plasma loss/ hemoconcentration),
- U/E/Cr: assess hydration status, renal function
- ABG: Metabolic acidosis (persistent) – 50%
- Lactate
- PT/PTT: hypercoagulable states (if present, can add Protein C/S, AT III)
- Raised amylase / LDH
- Markers for ischemia – lactate, LDH, amylase level, leucocytes, ALP
176
Imaging
- AXR (supine)
▪ Colonic Dilatation
▪ Thumb-printing (i.e. from submucosal haemorrhage and oedema in the colon) – most common finding, non-specific
▪ Mural thickening
▪ Intramural air/ air in portal venous system (ischemia)
▪ Free air
- CTAP (with contrast) – can localize site of colitis

▪ Segmental pericolonic fat stranding
▪ Thickened bowel wall
▪ Assess for etiology & complications (i.e. transmural ischemia, perfration)
- Occlusion as the underlying etiology: SMA thrombosis or superior mesenteric vein / portal vein thrombosis,
- Transmural Ischemia: intestinal pneumatosis, portal venous gas, lack of bowel wall enhancement
- Perforation: free air
- Endoscopy (gold-standard, i.e. colonoscopy / sigmoidoscopy)

▪ Mild ischemic colitis
- Pale appearing mucosa
- Mucosal edema
- Mucosal erythema
- Petechial haemorrhage
- Single longitudinal ulcer (i.e. single-stripe sign)
▪ Severe ischemic colitis
- Dusky mucosa
- Submucosal haemorrhage
- Hemorrhagic ulceration
- Segmental distribution with abrupt change to normal mucosal in unaffected region
- Histology – inflammatory cell infiltration, mucosal oedema, sloughing, altered crypt morphology, haemorrhage within the
lamina propria
MANAGEMENT
Diverse clinical presentation from mild self-limiting to transmural infarction and necrosis – determine severity (i.e. presence of
peritonitis) and evaluate need for surgical intervention (20% requires surgical intervention)
Non-surgical Management (80%)

- NBM (bowel rest)
- IV analgesia (i.e. IV paracetamol + IV tramadol)
- Aggressive fluid hydration (aim to optimize perfusion to ischemic colon)
- ± NGT decompression – if having nausea / vomiting, dilated bowel loops
- Empirical broad-spectrum antibiotics – colonic ischemia → intestinal epithelial barrier failure → bacterial translocation →
septic complications (i.e. IV ceftriaxone & flagyl)

- serial abdominal examination
- ± limit vasopressor use, optimize cardiac output
- ± endoscopy (to evaluate for worsening ischemia)
Surgical Management (20%)

- Indications (acute): peritonitis, pneumoperitoneum, massive haemorrhage, transmural necrosis (i.e. pneumatosis / portal
venous gas
- Indications (chronic): intractable symptoms >2wks, recurrent sepsis, chronic colitis, ischemic stricture, malnutrition from
protein losing colopathy
- Surgical Intervention
▪ Midline incision, evaluation of small / large intestine for signs of ischemia
▪ ± segmental colonic resection with well-perfused resection margin +/- end ileostomy / colostomy
▪ ± temporary abdominal closure with planned second relook laparotomy in 24 hours (if extensive / patchy involvement)
▪ ± subtotal colectomy & end ileostomy (i.e. if entire colon ischemic)
177
COLON CARCINOMA104
INTRODUCTION
Colorectal cancer is cancer that occurs in the colon (large bowel proximal to the rectum)
EPIDEMIOLOGY105
- Most commonly diagnosed cancer in Singapore
- Ethnic: Colorectal Cancer more common among Chinese
- Gender: Colorectal Cancer more common in Males > Females (number 1 in singaporean males, number 2 in females)
- Stage distribution of colorectal cancer (Stage I: 15.6%, Stage II: 28.3%, Stage III: 31%, Stage IV: 25%) - 2017 data
- Stage distribution of rectal cancer (Stage 1: 21.1%, Stage II: 16.4%, Stage III: 38.8%, Stage IV: 23.8%) - 2017 data
- Peak incidence is 60-70yr (in younger patients, suspect familial syndrome (FAP, HNPCC) or pre-existing inflammatory bowel
disease (UC, CD)
RISK FACTORS106
Increased Risk Protective
- Fruits and Vegetables (hypothesis: increased roughage
- Red / Processed Meat (haem
decreases transit times, which reduces exposure of mucosa to
Diet and N-nitroso compounds)
dietary carcinogens)
- Animal Fat
- High Fibre Grain
- Alcohol
Modifiable - Vitamin Supplements (i.e. folate)
- Smoking (1.5x to 3x)
Lifestyle - Physical Activity
- Obesity
- HRT
Drugs - Aspirin (? mechanism)
- NSAIDs (? mechanism)
Age - Males and females > 50 years old

Ethnicity - Chinese has a higher risk among the races in Singapore
- 1 first-degree relative with CRC a/w RR 2.3x
Family - > 1 first-degree relative with CRC a/w RR 4.3x
History107 - 1 first-degree relative diagnosed with CRC before age 45 years a/w RR 3.9x
*important to ask for age at diagnosis!
- FAP (100% by age 40), attenuated FAP (69% by age 80)
- Lynch Syndrome (40-80% by age 75)
Hereditary CRC
- Peutz-Jeghers Syndrome (39% by age 70),
Syndromes108
- Juvenile Polyposis Syndrome (17-68% by age 60)
- Other: Cowden Syndrome, Cronkhite-Canada have a small increased malignant potential
- Diagnosed with Amsterdam Criteria aka. 3-2-1 rule
a. At least 3 relatives with histologically confirmed colorectal cancer* (1 of whom is a first degree relative
Non-modifiable
of the other 2) – FAP excluded
Familial Cancer b. At least 2 successive generation involved
Syndromes c. At least 1 of the cancer diagnosed before age of 50
(HNPCC)
*These criteria were found to be too strict and were expanded to include the associated non-colorectal cancers (cancer of the
endometrium, small intestine, ureter or renal pelvis); in 1998. These were called the Amsterdam II clinical criteria for families with
Lynch syndrome
- Inflammatory Bowel Syndrome (i.e. Ulcerative Colitis (UC) of more than 10 years duration, or Crohn’s
Disease)
- Past history of colorectal polyp or colorectal cancer (potential for metachronous cancer)
Personal
- Increased risk if have history of large (> 1cm) adenomatous polyps, and polyps with tubulovillous or villous
History
histology, particularly if multiple
- Others: previous pelvic radiation therapy, acromegaly, endocarditis due to streptococcus bovis (a/w colon
cancer – do colonoscopy)
104 Lancet. 2014 Apr 26;383(9927):1490-1502.

105 Annual Registry Report, Trends in Cancer Incidence in Singapore, 2010 – 2014
106 http://www.singaporecancersociety.org.sg/lac-fcco-risk-factors.shtml
107 Am J Gastroenterol 96 (10): 2992-3003, 2001.
108 http://www.cancer.gov/cancertopics/pdq/genetics/colorectal/HealthProfessional/Page3#Section_120
178
PATHOLOGY
Hereditary Colorectal Carcinoma
Molecular Clinical
Histopathology Genetics
Pathway Phenotype
Chromosomal
Innumerable Adenomatous Polyps, Moderately
Instability FAP Germline APC inactivation
differentiated adenocarcinoma
(CIN)
Microsatellite
Mucinous, Poorly Differentiated with Lymphocytic Germline inactivation of MLH1 or MSH2 DNA repair
Instability HNPCC
Infiltrates genes
(MSI)
Sporadic Colorectal Carcinoma

Molecular Clinical
Histopathology Genetics
Pathway Phenotype
Left-sided
Chromosomal Tubular, tubulovillous, and villous adenomas, Somatic inactivation or mutation of multiple genes
predominant
Instability (CIN) Moderately differentiated adenocarcinomas (APC/β-catenin, K-RAS, SMADS, p53)
cancer
Right-sided
Microsatellite No precursor lesions, Sessile serrated adenomas, Somatic inactivation of DNA mis-match repair genes
predominant
Instability (MSI) Large hyperplastic polyps, Mucinous carcinomas (i.e. MLH1 or MSH2)
cancer
(1) APC pathway (adenoma-carcinoma sequence**) or chromosomal instability pathway – 85% of sporadic CRC
This involves a stepwise accumulation of mutations in a series of oncogenes and tumour suppressor genes:
1. Loss of the APC suppressor gene on 5q21 (absent in patients with familial adenomatous polyposis)
2. With the loss of APC, Beta-catenin accumulates and activates the transcription of genes (MYC and cyclin D1) which
promote cell proliferation (APC is required to break down beta-catenin)
3. K-RAS* (12p12) mutation follows the loss of APC – an activating mutation that causes the RAS to keep delivering
mitotic signals and prevent apoptosis, more common in larger lesions, suggesting that it develops later in the
mutagenesis pathway
4. Loss of tumour suppressor gene at 18q21 (SMAD2 and SMAD4) leads to unrestrained cell growth
5. Loss of p53 (17p13) (tumour suppressor gene) occurs late in carcinogenesis (frequently mutated in carcinomas, but
not adenomas, and is thus thought to mark the devt of invasion) → prevents DNA repair / cell apoptosis
The molecular evolution of colon cancer through this pathway occurs through a series of morphologically identifiable stages:
localised epithelial proliferation to small adenoma to large adenoma to more dysplastic adenoma to carcinoma in-situ and finally
to invasive cancer
*K-RAS gene is the most frequently observed activated oncogene in colorectal adenomas and carcinomas (note: mutation of APC is more common
than KRAS, but APC is a tumour suppressor gene). They are a/w advanced stage at presentation and also poor prognosis in node-negative
disease109
** Rationale for adenoma-carcinoma sequence – (1) almost all colon cancer arise within an adenoma, (2) incidence rate of adenoma in colon cancer
resected specimen is ~ 30%, (3) risk of colon cancer increases with increasing number and size of adenoma (4) incidence of colorectal cancer in
patients with FAP is high, (5) risk of cancer in un-resected polyps is 4% after 5 years and 14% after 10 years 110
109 Gut. 2005 Sep;54(9):1283-6.

179
(2) Defects in DNA mismatch repair or microsatellite instability – 15% of sporadic CRC
- Like the APC pathway, there is accumulation of mutations, but without clear identifiable morphologic correlates i.e. no
adenomas
- Due to mutations in one of the five DNA mismatch repair genes (MSH2, MSH6, MLH1, PMS1, PMS2) – deficiency in the
ability to repair mismatched base pairs in DNA that are accidentally introduced during replications, this give rise to HNPCC
- MLH1 are the most commonly involved in sporadic colorectal carcinomas
- Loss of DNA mismatch repair genes results in microsatellite instability which affects coding or promoter regions of genes
involved in cell growth such as the BAX gene (promote apoptosis) and the type II TGF-β receptor (inhibits growth of colonic
epithelial cells)
- Accumulated mutation in these growth regulating genes leads to emergence of colorectal carcinomas
- Tumours that arise from this pathway have a better prognosis than tumours that arise from the APC pathway
Feature Chromosomal Instability Microsatellite Instability

APC, K-RAS*, SMAD2, MSH2, MSH6, MLH1,
Genes Mutated
SMAD4, p53, telomerase TGFβRII, BAX, BRAF
Associated Familial Syndrome Familial Polyposis Coli HNPCC
% of Sporadic Colorectal Cancer 85% 15%
Precursor Lesion Tubular/villous adenoma Sessile serrated adenoma
Mucinous adenocarcinoma
Colorectal Cancer Type Typical adenocarcinoma
(may have signet-ring cells)
Amount of DNA Aneuploid or polyploid Diploid
Typical Location Left-sided Right-sided
Degree of Differentiation Highly Differentiated Poorly Differentiated
Presence of Lymphocytic Infiltration Little Marked
Mucinous Rarely Mucinous Often Mucinous
Relative Prognosis Worse Prognosis Better Prognosis
* Patients with K-RAS mutation are less responsive to epidermal growth factor receptor antibodies (anti-EGFR, i.e. cetuximab or panitumumab)
compared to patients with wild-type K-ras mutation
Distribution of CRC
Most common sites of CRC: sigmoid colon (25%), rectum (21%), cecum (20%), recto-sigmoid junction (20%), transverse colon
(15%), and ascending colon (10%). There can be variation in the sites of the CRC. In general, left sided colon cancers are more
common than right sided cancer.
180
There is a wide variety of clinical presentations for patients diagnosed with colorectal cancer. This can range from asymptomatic
individuals diagnosed via screening colonoscopy, symptomatic individuals who undergo colonoscopy, symptomatic individuals
who present in crisis. Remember that > 50% of patients who are diagnosed with CRC are stage III or IV at diagnosis.
The aim of the clinical history is to ascertain the diagnosis (i.e. is this colorectal cancer or is an alternative diagnosis more likely).
This involves understanding the symptoms that patients present with, identifying red flag symptoms and potential risk factors. In
addition to ascertaining the diagnosis, we should be able to make an educated guess on the location of the tumour (i.e. right
sided or left sided).
Next, we should be able to evaluate for potential complications. This can be related to tumour-related complications such as
tumor perforation, intestinal obstruction or anemia from tumour bleed. We can also ascertain if the tumour is locally advanced
with invasion to bladder / vagina. History taking can sometimes give clues if metastases have occurred, though this is mostly
determined by staging scans. Knowing the complications can enable us to prioritize the necessary treatment for the patients.
For patients with colorectal cancer, the majority of them will be diagnosed via endoscopic evaluation. However, colonoscopy may
not be safe for patients who have tumour complications (i.e. intestinal obstruction). We should also evaluate a patient's fitness
for surgery (i.e. past medical history, effort tolerance).
Symptomatology
- Any abdominal pain (most common ~44%)
- Any PR bleed (hematochezia / melena) – quantify bleeding
- Any symptomatic anemia – decreased effort tolerance, lethargy
- Any changes in bowel habits – in particular rule out these red flags
▪ Alternating constipation and diarrhoea
▪ Spurious diarrhoea* (secondary to obstruction and bacterial degradation)
▪ Diminished stool calibre (pencil thin stool)
▪ Tenesmus (feeling of incomplete defecation, recurrent inclination to defecate, frequently painful)
* Due to obstruction leading to increased peristalsis and intestinal secretion above the level of the obstruction and secondly due to stasis, faecal
material above obstruction undergoes degradation by bacterial and liquefaction → passage of this liquefied stools periodically
- Symptomatic anaemia (iron deficiency anaemia) – usually occult bleeding

Right Sided
- Symptoms of Intestinal Obstruction (small bowel obstruction assuming incompetent ileocaecal valve) - not as common as
(colonic tumour)
left sided tumour as stools are more liquid and colon more spacious on the right side
- Change in bowel habits
Left-sided - Hematochezia
(colonic tumour) - Symptoms of Intestinal Obstruction (large bowel obstruction)
- Tumour perforation (i.e. acute abdomen)
- Tenesmus (due to SOL in rectum)
- Diminished stool calibre (pencil-thin stools)
Left Sided - Mucoid stools (suggests polypoid masses)
(rectal tumour) - Hematochezia
- Change in bowel habits
- Symptoms of Intestinal Obstruction
Risk Factors (modifiable and non-modifiable)

- Significant family history of colorectal cancer, other cancers (sporadic vs familial colorectal cancer - see below)
- Previous colonoscopy and/or FOBT investigations
- Social history → diet, smoking, physical activities
- Drug history & drug allergies
- Significant past medical, surgical, hospitalization History
181
Sporadic vs Familial Colorectal Cancer

Recognition of an individual with inherited colon cancer syndrome (see FAP and HNPCC)
- Diagnosed under the age of 45
- Adenomas >2cm diagnosed under the age of 40
- Multiple primary cancers – either colonic or extracolonic
- ≥ 10 adenomas present over a lifetime in addition to a family history of colon cancer
- Multiple closely related family members who have been diagnosed with colon cancer
- Colon cancer in more than 1 generation
- Clustering of extracolonic cancers in family members (i.e. gastric, breast, thyroid, uterine)
Tumour Complications
- Tumour Bleeding leading to symptomatic anemia
- Tumour Obstruction leading to intestinal obstruction (i.e. abdominal distension, abdominal pain, vomiting, obstipation)
- Tumour Perforation leading to sepsis (i.e. intra-abdominal sepsis with peritonitic abdomen)
- Tumour Fistula leading to fecaluria, pneumaturia, recurrent UTI (recto-bladder fistula), recto-vagina fistula, gastrocolic
fistula may cause faecal vomiting or severe diarrhoea
- Tumour Invasion leading to intractable pain (sacral nerves), lower urinary tract symptoms (trigone of bladder)
Metastatic Symptoms
- Constitutional Symptoms – Loss of Weight (must quantify), Loss of Appetite
- Liver – RHC discomfort, jaundice
- Lungs – SOB (pleural effusion most common), decreased effort tolerance
- Malignant Ascites
- Bone – bone pain, pathological fractures
- Brain – altered mental status
Treatment / Complications of Treatment

- Any surgeries (perianal surgeries, abdominal surgeries)
- Any therapeutic colonoscopy (i.e. polyp resection)
- Any chemotherapy / radiotherapy
PHYSICAL EXAM
1. Vital Signs – Temperature, Blood Pressure, Pulse Rate, RR, Pain Score
2. General Appearance
a. Any signs of altered mental state – alert, orientated to TPP
b. any signs of poor nutritional status – cachexia
c. any signs of anaemia – nailbed pallor, palmar crease pallor, conjunctival pallor
d. any signs of jaundice – scleral icterus, jaundice
3. Abdominal Examination (remember to check hernia orifice)
a. any previous scars – check for incisional hernia
b. any organomegaly (enlarged liver, irregular surface)
c. any tenderness, any masses, abdominal distension (i.e. malignant ascites)
d. any signs suggestive of IO – abdominal distention, abdominal tenderness, tinkling bowel sounds
e. any supraclavicular LN enlargement (Virchow's node)
f. any inguinal LN enlargement (very low rectal tumours, near the dentate line, have a risk of spread to inguinal LN)
4. Digital Rectal Examination
a. Any masses felt
b. Any PR bleeding
c. Is anal tone intact
5. Lung Examination – any pleural effusion, consolidation
6. Cardiac Examination
7. Any bony tenderness
182
MODE OF SPREAD111
1. Direct extension
- Longitudinally, transversely and radially
- Radial spread – may involve ureter, duodenum, muscles of posterior abdominal wall, small intestine, stomach, pelvic
organs or anterior abdominal wall
- Rectal tumours may involve the pelvic organs or side wall
2. Lymphatic
- Progress from paracolic nodes (along main colonic vessels) eventually reaching the para-aortic nodes
- In contrast to rectal disease, it is rare for colonic cancer that has not breached the muscle wall to exhibit LN Mets (~
15% of cases confined to bowel wall will be found to have LN Mets)
3. Haematogenous
- Liver via the portal venous system. ⅓ have liver mets at the time of dx, 50% will develop liver mets eventually.
- 2nd most common site – lungs
- Other sites include ovary, adrenal, bone, brain and kidney
4. Transcoelomic
- Carcinomatosis Peritonei – via subperitoneal lymphatic or viable tumour cells shed from serosal surface
- Malignant ascites (rare)
INVESTIGATIONS
Once the diagnosis is suspected based on history, physical examination, I will perform a colonoscopy to establish the diagnosis
via biopsy and to localize the lesion. Also, colonoscopy can help to rule out synchronous cancer (3% to 5%) and synchronous
polyp (30%). In addition to establishing the histology, I will look for the level of differentiation on the histology report. Following
which, I will proceed to stage the tumour with local as well as systemic staging investigations. Depending on the circumstances,
I would perform supportive investigations to assess for complications. If the patient is suitable for curative surgery, I would proceed
to perform pre-operative investigations.”
Carcinoembryonic antigen level (CEA) – (normal range: 0-2.5mcg/L, in smokers: 0-5mcg/L)

- An oncofetal protein lacks both sensitivity and specificity
- CEA is a useful prognostic and surveillance tumour marker in colorectal cancer (in patients with established disease absolute level
of serum CEA correlates with disease burden)
- Measured preoperatively as a baseline level
- Follow-up after surgery with CEA testing (high = likely recurrence, normal = does not r/o disease recurrence) – 30-40% of all CRC
recurrence, not a/w elevated CEA
- False positive raised CEA: smoking, adjuvant therapy with 5-FU, inflammatory states (i.e. pancreatitis, diverticulitis, cholecystitis
etc.) and cancers (i.e. thyroid, stomach, lung, breast, pancreas, cervix, bladder, kidney etc.)
- For Raised CEA
▪ Determine if patient is a smoker
▪ OGD / Colonoscopy
▪ Consider CT TAP
▪ Consider US thyroid
▪ Mammogram for female patients
Colonoscopy & Double contrast barium & air enema
111 Colorectal Surgery A Companion to Specialist Surgical Practice (5th edition) – pg. 50
183
- Ensure bowel preparation adequate*

- Allow direct visualization (site, size, localization)
- Enables biopsies of suspicious lesions for histological diagnosis
Colonoscopy - Enables detection of synchronous lesions (synchronous polyps in 30%, synchronous cancer in 3 to 5%)
(diagnosticate - Allow for therapeutic procedures (i.e. polypectomy, stenting of obstructed colon)
and therapeutic)
*For patients who present with intestinal obstruction, colonoscopy may not be suitable as the patient will not
Establish the
be able to tolerate PEG intake. For these patients, it is important to get them out of crisis first (i.e. colonic
Diagnosis
stenting vs. surgical intervention)
Histology - Confirm adenocarcinoma, determine level of differentiation (well-differentiated to poorly differentiated)
Other investigative tools:
- CT colonography aka. virtual colonoscopy: needs IV contrast, air and contrast enema, detect tumour that is ≥ 1cm
- Double contrast barium & air enema (need to insert rigid sigmoidoscopy 10-15cm to instil air and contrast, limited diagnostic
value, may miss small lesions and distal lesions): classically see apple core lesion with barium enema (rarely done)
- Thorax: lung Mets – 2nd most common site of Mets in CRC
▪ Isolated lung metastases range from 3.1 to 11.7% in patients with rectal cancer and 1.3-5.9% in
patients with colon cancer112
Computer - Abdominal/Pelvis
Tomography ▪ T Staging – invasion into bladder, ureter, uterus, duodenum (esp. for right-sided colonic tumours)
(Thorax, ▪ Involvement of regional lymph node Mets
Abdominal, ▪ Detect metastatic disease in the form of peritoneal seeding, omental kinking, malignant ascites,
Staging
Pelvis) hydroureter, hydronephrosis, IO (i.e. carcinomatosis peritonei)
Investigation
▪ Hepatic Mets – most common site of Mets in CRC
- Previously, CXR & US HBS was used to identify distant metastasis, but it's no longer utilized as CT TAP is
far more accurate in identifying metastatic lesions
Positron
- Combines spatial resolution of CT with contrast resolution of PET
emission
- Not the 1st line investigation for staging of colorectal cancer
tomography with
- Recommended when surgical resection of metastases is being considered to exclude occult disease
CT (PET-CT)
FBC - Assess Hb levels (assess for iron-deficiency anaemia)
- Biochemical abnormalities a/w 3 rd space losses (intraluminal) or vomiting (i.e. in IO)
U/E/Cr - Cr may be ↑(pre-renal failure) which increases risk of contrast nephropathy
- Hypokalemia – ?villous adenoma (hyper-secretory syndrome)
- Albumin as a marker of nutritional status (< 35 is poor)
Supportive LFT
- Liver Mets (ALP first to be raised)
Investigation
CEA - Important to get a baseline CEA prior to surgical intervention
Acute Setting
Erect and Supine - look for intestinal obstruction (a/w poorer prognosis), any closed loop obstruction (i.e. obstructing tumour
AXR with competent ileocecal valve), colon cut-off sign
Erect CXR - To rule out air under diaphragm (tumour perforation)
GXM / PT/PTT
Preoperative
Cardiac
Investigations - ECG, 2D Echo, Myocardial Perfusion Scan (referral to cardiology as required)
Investigations
112 J Gastrointest Surg. 2009 Apr;13(4):642-8.
184
STAGING
AJCC 8th Edition

TX: primary tumor cannot be assessed
T0: no evidence of primary tumor
Tis: carcinoma in situ, intramucosal carcinoma (involvement of lamina propria with no extension
through muscularis mucosae)
T1: tumor invades submucosa (through muscularis mucosa but not into the muscularis propria)
T2: tumor invades muscularis propria
T
T3: tumor invades through the muscularis propria into the pericolorectal tissues
T4:
T4a: tumor invades through the visceral peritoneum (including gross perforation of the bowel
through tumor and continuous invasion of tumor through areas of inflammation to the surface of
the visceral peritoneum)
T4b: tumor directly invades or adheres to other adjacent organs or structures
NX: regional lymph nodes cannot be assessed

N0: no regional lymph node metastasis
N1: metastasis in 1 - 3 regional lymph nodes
N1a: metastasis in 1 regional lymph node
N1b: metastasis in 2 - 3 regional lymph nodes
N1c: no regional lymph nodes are positive but there are tumor deposits in the subserosa,
N
mesentery or non peritonealized pericolic or perirectal / mesorectal tissues
N2: metastasis in 4 or more regional lymph nodes
N2a: metastasis in 4 - 6 regional lymph nodes
N2b: metastasis in 7 or more regional lymph nodes
* minimum of 12 lymph nodes must be recovered for accurate staging
M0: no distant metastasis by imaging; no evidence of tumor in other sites or organs

M1: distant metastasis
M1a: metastasis confined to 1 organ or site without peritoneal metastasis
M1b: metastasis to 2 or more sites or organs is identified without peritoneal metastasis
M M1c: metastasis to the peritoneal surface is identified alone or with other site or organ
metastases
Duke Staging (Historical)

Original Duke Staging Adapted Duke Staging
A invasion into but not through the bowel wall Limited to mucosa
invasion through the bowel wall but not involving lymph B1: extending into muscularis propria but not penetrating
nodes (70% 5 year survival) through it; nodes not involved
B
B2: penetrating through muscularis propria; nodes not
involved
involvement of lymph nodes (30% 5 year survival) C1: extending into muscularis propria but not penetrating
C through it; nodes involved
C2: penetrating through muscularis propria; nodes involved
D widespread metastases distant metastatic spread
185
MANAGEMENT
Aim for microscopically negative margins; R0 resections
Preoperative management
- Multidisciplinary tumour board meeting – involves medical oncologist, pathologist, radiologist and surgeon
- Pre-operative investigations (see above) & Anaesthesia referral +/- subspeciality referral (i.e. cardiology)
- Mechanical Bowel Preparation (MBP) with PEG
▪ Modification of diet – 3 days low residue diet (reduce frequency and volume of stools – low fibre, reduce food that
increases bowel activity), and one day clear feeds, NBM from 12mn (day of operation)
▪ Contraindicated in GI obstruction, perforation
- +/- Stoma site discussion with stoma care nursing specialist
- Prophylactic intravenous antibiotics
▪ IV ceftriaxone and metronidazole within 30-60 mins of skin incision
- Chest Physiotherapy – incentive spirometry
- DVT Prophylaxis
▪ Subcut Low Molecular Weight Heparin (LMWH) – 40mg OD start on POD 1-2
▪ Anti-embolism (TED) stockings are fitted
▪ Early Ambulation
EXTRA INFORMATION
Enhanced Recovery after Surgery (ERAS) – nurse clinician to speak to patient
- Multi-modal surgical pathway designed to achieve early recovery after surgery. This is achieved by engaging patient with
expectation of care and improving communications among all specialities involves with surgical care (i.e. surgeon, anaesthesia,
nursing care (pre-op, intra-op, post-op), pharmacy, PT/OT, dieticians)
- Standardized pathway for analgesia, nutrition, catheter removal, stoma management, fluids, mobility and exercise, DVT
prophylaxis etc.
- The processes / pathways – reduces hospital length of time, decreases non-surgical complications (i.e. UTI, pneumonia, AMI),
readmission rates are not higher with ERAS. Surgical complications (i.e. re-bleeding, anastomotic leaks, re-operation) has not
improved
- Benefits of Laparoscopic Surgery: 2 day reduction in total hospital stay, reduction in incisional hernia and adhesion obstruction.
Surgical Management for Colon Cancer

The aim of cancer surgery is to optimize oncological outcome while minimizing complication to allow for the best recovery
outcomes. Optimal oncological outcomes involve removal of tumour with its associated lymphovascular package and contiguous
organ involvement.
Surgical Principles
- Complete Mesocolic Excision (CME)113
▪ Dissection in the embryological defined mesocolic plane – includes all mesentery and potentially involved LNs
▪ Central ligation of the vascular pedicle (Minimum number of 12 lymph nodes in resected specimen)
▪ Resection of an adequate length of colon on either side of the tumour (in general 5cm margins)
▪ Bowel continuity restored with a well-vascularized, tension free anastomosis
113 Int J Colorectal Dis. 2014 Apr;29(4):419-28.
186
The selection of the appropriate surgical procedure depends on the location of the primary tumour
- Right Hemicolectomy
▪ For cancer involving the caecum, ascending colon, hepatic flexure
▪ Involves resection of the ileocolic artery, the right colic artery (if present) & right branch of the middle colic artery
▪ Terminal Ileum is transected 10-15cm from IC valve and anastomosis with proximal transverse colon
- Extended Right Hemicolectomy

▪ For cancer involving the mid-transverse colon
▪ Involves resection of the ileocolic artery, the right colic artery (if present) & middle colic artery
▪ Terminal Ileum is transected 10-15cm from IC valve and anastomosis with distal transverse colon
- Left Hemicolectomy
▪ For cancer involving the distal transverse colon, splenic flexure, descending colon, proximal sigmoid colon
▪ Involves resection of the inferior mesenteric artery (IMA)
▪ Requires mobilization of the splenic flexure to ensure tension free anastomosis
- Sigmoid Colectomy
▪ For cancer involving the sigmoid colon
▪ Involves resection of the inferior mesenteric artery (IMA)
- Other Surgical Resections

▪ Subtotal Colectomy: terminal Ileum is transected and is anastomosis with sigmoid colon
▪ Total Abdominal Colectomy: terminal ileum is transected and anastomosis is with rectum (ileorectal anastomosis)
- Hartmann’s Procedure
▪ Hartmann’s Procedure: surgical resection of the (i.e. recto-sigmoid colon) with closure of the rectal stump and
formation of a temporary end colostomy (it is used when immediate anastomosis is not possible) – usually in
emergency settings
▪ Can be performed for benign (i.e. perforated diverticulitis) or malignant conditions (i.e. perforated / obstructed
sigmoid tumour or upper rectal tumour)
Adjuvant Therapy for Colon Cancer

- Stage II → debatable (any high risk features)
- Stage III (node positive) → aim to initiate chemotherapy within 6-8 weeks of surgery, i.e. chemotherapy regimen: 6-month
course of oxaliplatin-based regimen – FOLFOX114 (oxaliplatin + leucovorin (LV) and short-term infusion 5-FU)
114 J Clin Oncol. 2009;27(19):3109. [Important Paper] – MOSAIC trial
187
Surgical Management for Stage IV Colon Cancer (with liver metastases)

- Historically, 2-year overall survival for stage 4 CRC was only 21%, but in the past 2 decades, the 5 year OS increased to
35-40%. In recent years, the 5 yr overall survival has increased to 47-60%
- Synchronously detected colorectal liver metastases: detected at diagnosis or surgery of the primary tumour
- Metachronous colorectal liver metastases: detected after diagnosis or surgery of the primary tumour. Can be early (<12
months) or late (> 12 months)
Management Strategy
- Sandwich Therapy: neoadjuvant chemotherapy, surgical resection followed by adjuvant chemotherapy
- Inclusion of biological agents (i.e. bevacizumab or cetuximab) depending on the RAS and BRAF status
- Surgical Goals – adequate resection of all metastases (margins negative*) with adequate hepatic reserve (at least 2
contiguous hepatic segments, preservation of vascular inflow / outflow and biliary drainage, preserve adequate future liver
remnant (>20% in a healthy liver))115
- Synchronous liver metastases – no difference in mortality and morbidity for staged vs. simultaneous colectomy and
hepatectomy.116
EXTRA INFORMATION
Emergency Management of Colorectal Cancer

- Higher mortality for emergency presentation – 90 days mortality 12.3% for urgent surgery compared to 2.1% for planned
surgery
- 20% of patients with colon cancer presents as an emergency (UK data), obstruction is the most common presentation followed
by bleeding and perforation
- For obstructed right sided cancer
▪ Consider emergency right hemicolectomy +/- stoma vs primary anastomosis
- For obstructed left sided cancer
▪ Emergency Surgery vs. Colonic Stenting
▪ Colonic stenting can be used as a “bridge to surgery”, to allow for optimization of medical status prior to surgery, surgery
will be converted from emergency to elective. Lower rates of stoma creation but evidence for long-term oncological
outcome is suboptimal
▪ If endoscopic stenting fails, will require surgical intervention
Surgical Consideration prior to Surgery for Liver Metastases

- 4 factors to consider prior to surgical resection of liver metastases
▪ Is it oncologically appropriate - ability to perform a R0 resection
▪ Is the resection margin adequate - 1mm margin sufficient
▪ Is there sufficient future liver remnant (FLR) & quality of liver parenchyma - perform ICG retention test (see below)
▪ Is it technically feasible (open vs. lap)
- To increase resectability – (1) portal vein embolization and staged hepatectomy (to achieve compensatory hypertrophy of
remnant liver), (2) portal vein ligation and staged hepatectomy and (3) Association of Liver Partition with Portal vein ligation for
staged hepatectomy (ALPSS)
- Role of liver transplant in CRC liver metastases – controversial, studies with good results have strict patient selection (SECA 1
trial), patients still have high recurrence rates, many countries have lack of deceased donor liver for transplant, ongoing studies
on utility of living donor liver transplant.
- Other alternatives:
▪ Ablation: radiofrequency ablation, microwave ablation
▪ Regional: Treatment: transarterial chemoembolization (TACE), Y-90
ICG retention at 15 mins (Makuuchi decisional algorithm)

- < 10% for trisectionectomy or bisectorectomy
- 10 - 19% for hemihepatectomy, right sided sectorectomy
- 20 - 29% for segmentectomy
- 30-39% for limited resection (i.e. wedge resection)
- > 40% for enucleation
Prognostic Score (Fong) – after resection of colorectal liver metastases (1999)117

- Inclusion Criteria
▪ Fit for major laparotomy
▪ No signs on pre-op imaging of disseminated disease,
115 Dis Colon Rectum 2010; 53: 1080–1092

116 Ann Surg Oncol. 2007;14:3481–3491.
117 Ann Surg. 1999 Sep;230(3):309-18; discussion 318-21.
188
▪ Tumour confined within the liver such that adequate liver parenchyma can be preserved
- Clinical Score Criteria – each criterion assigned one point
▪ Lymph node positive primary tumour
▪ Disease free interval from primary tumour resection to dx of the liver mets <12 months
▪ Number of liver mets in pre-op imaging >1
▪ Pre-op CEA level >200ng/ml
▪ Largest hepatic lesion in pre-op imaging >5cm
- Outcomes
▪ 5 year overall survival: low risk patients: 47% (0 - 2 points) while high risk patients: 24% (3 - 4 points)
▪ 5 year risk of recurrence: low risk patients: 40-60% (0-2 points) while high risk patients: 14-25% (3-5 points)
Surgery in setting of metastatic disease

- Resection of symptomatic primary tumour for palliation (i.e. bleeding, perforation, obstruction)
- Resection of the asymptomatic primary tumour is controversial. At present, there are ongoing prospective randomized
controlled trials (i.e. SYNCHRONOUS, CAIRO 4, GRECCAR 8) assessing impact of primary tumour resection (PTR) in these
patients
Cytoreductive surgery and hyperthermic intraperitoneal chemotherapy (CRS-HIPEC) 118

- Performed for patients with peritoneal mets from GI or gynae cancers.
- 2 components:
▪ CRS: Removal of all macroscopic peritoneal disease.
▪ HIPEC: Targets microscopic disease (lesions <3mm), administered for 60min. A higher dose of chemotherapy can be
delivered with less systemic effects due to the peritoneal-plasma barrier. The higher temperature also synergistically
increases drug penetration.
- For SGH: Post-operative mortality rate is 2%. Overall survival rate for 1, 3 and 5 years after CRS-HIPEC is 91.7%, 59.1%
and 50.9% respectively119.
118 http://www.smj.org.sg/article/cytoreductive-surgery-and-hyperthermic-intraperitoneal-chemotherapy-gastrointestinal-cancers
119 https://www.singhealth.com.sg/patient-care/conditions-treatments/peritoneal-based-malignancies/
189
COMPLICATIONS
- Intraoperative complications → bleeding, injury to surrounding structures (i.e. duodenum, ureter, spleen)
Immediate - Ureteric Injuries usually occur at (1) take-off of the IMA, (2) pelvic brim (during lateral to medial dissection), (3) between the
(<24h) lateral ligament.
- During APR, urethral injury can occur during the deepest portion of the perineal phase (membranous urethral at risk)
- Usual postoperative complications - atelectasis, post-op pneumonia, UTI, DVT / PE, wound infection
▪ Start patient on lung protective measures early (i.e. chest physiotherapy, incentive spirometry, early mobilization)
▪ Start patient on SC clexane for DVT prophylaxis
▪ Remove urinary catheter early
- Bleeding - especially after restarting anticoagulation

- Stoma Complications (i.e. high stoma output, stoma prolapse / retraction)
- Postoperative Ileus
- Anastomotic Leak (most commonly occur between day 5 to 7)
▪ Small bowel and ileocolic anastomosis have lowest reported leak rates (1-3%) and highest rate are for coloanal
Early
anastomosis (10-20%)
(<30 days)
▪ Watch out for tachycardia and raised CRP > 150-200)
▪ Iif free leaks, patient will present with diffuse faecal peritonitis and septic shock
▪ If contained leaks, patients may present later as having prolonged ileus, intra-abdominal abscess or enterocutaneous
fistula
Causes for Anastomotic Leaks

- Patient factors: Low serum albumin (<35), Higher ASA score, Renal disease, Immunosuppressants
- Disease factors: Location of anastomosis
- Surgical factors: Surgical technique (strength layer: submucosa) - aim for tension free, well vascularized anastomosis,
emergency surgery, duration of surgery > 4 hours
- Sexual and Urinary Complications
▪ Impotence & Atonic bladder – damage to mixed parasympathetic and sympathetic periprostatic plexus) can occur in 15-
50% of males (discussed pre-operatively)
▪ Retrograde ejaculation & Bladder dysfunction – injury to hypogastric nerves near sacral promontory
Late
- Anastomotic stricture
(>30 days)
- Anterior Resection Syndrome such as urgency, faecal incontinence, increased bowel frequency, evacuation dysfunction
(worsen patient’s QOL)
- Intestinal Obstruction secondary to adhesion
- Tumour Recurrence
- Radiation Proctitis (consider flexible sigmoidoscopy with APC +/- hydrocortisone for 5 days after procedure)
PROGNOSIS
Stage 5 year observed survival rates – colonic cancer
I 74% 82% (2008 – 2012 – Singapore’s Data)
II A – 67%, B – 59%, C – 37% 70%
III A – 73%*, B – 46%, C – 28% 52%
IV 6% 9%
* Survival was better for some stage III cancers than some stage II cancers, the reasons for this is not clear
High Risk Factors for Recurrence (Stage II)

- Poorly differentiated on histology
- Presence of lymphovascular invasion (LVI), perineural invasion (PNI)
- Close / Indeterminate or positive margins
- Tumour complications (i.e. bowel obstruction, tumour perforation)
- Less than 12 lymph nodes examined
Follow-up
- The goal for close follow-up is to detect resectable recurrence and to improve survival – most recurrences occur within 2 years
of original diagnosis
- Follow-up visits (history and physical exam) with CEA at each visit
- Colonoscopy to identify metachronous CRC → see schedule below
- CT TAP to detect radiological recurrence → see schedule below

- For patients who presented with obstructed tumour (did not have complete colonoscopy pre-operatively), ensure completion
colonoscopy performed
190
For Low Risk Stage II
For High Risk Stage II and Stage III
191
RECTAL CANCER120
DEFINITIONS
Rectal cancer is tumour within 15cm of the anal verge (UK) or within 11-12cm (USA) of the anal verge.
Definition of Anal Verge:

- In the left lateral position, transition between non-hair bearing anal canal with the hair-bearing perianal skin
- Junction between stratified squamous non-keratinizing epithelium (anoderm) & stratified squamous keratinizing epithelium
(cutaneous zone)
Definition of Anorectal Junction:

- Transition between the anal canal and rectum with the puborectalis forming a sling around the posterior aspect
Definition of Rectum
- Segment of large bowel within the true pelvis (below the pelvic brim)
- Part of the large bowel at the 3rd sacral vertebrae represents the top of the rectum
- Intraoperative identification of the fusion of the 2 antimesenteric taenia into an amorphous area where the true rectum begins
ANATOMY
Rectum
- Measures 12 – 15cm long, commencing anterior to the 3 rd segment of the sacrum and ending 2.5cm in-front of the coccyx
where it bends sharply backwards to become the anal canal
- Contains 3 lateral inflexions (each inflexion capped by a valve of Houston)
- Anorectal Junction is the reference point between the anal canal and the rectum
▪ Upper ⅓ (~4cm): covered by peritoneum anteriorly and laterally
▪ Middle ⅓ (~4cm): covered by peritoneum only anteriorly
120 Lancet. 2014 Apr 26;383(9927):1490-1502.
192
▪ Lower ⅓ (~4cm): completely extra-peritoneal, lying below peritoneum reflection

- Blood Supply
▪ Proximal: superior haemorrhoidal artery (superior rectal artery) from IMA
▪ Middle: middle haemorrhoidal artery (middle rectal artery) from hypogastric artery (int. iliac artery)
▪ Distal: inferior haemorrhoidal artery (inferior rectal artery) from pudendal artery (int iliac artery)
Anal Canal
- Measures 2-4cm long and passes downwards and backwards (length variation between genders)
- Surrounded by complex arrangement of sphincter (both internal (smooth) and external (striated) muscle)
- The dentate line (pectinate) divides the upper half (2/3) and lower half (1/3) of the anal canal
Below Dentate Line Above Dentate Line

Embryology Ectoderm Endoderm
Epithelium Stratified Squamous Nonkeratinized Epithelium (SCC) Simple Columnar Epithelium (adenocarcinoma)
Nerves Somatic Innervation (inferior rectal nerve) Autonomic NS (inferior hypogastric plexus)
Venous Systemic Venous System (via middle and inferior
Portal Venous System (via superior rectal vein)
Drainage rectal vein)
Lymph Node Abdominal Nodes
Superficial Inguinal Lymph Node
Drainage (i.e. internal iliac, inferior mesenteric LN)
Internal Sphincter Muscle

- Caudal continuation of rectal circular smooth muscle forms the internal anal sphincter,
- Caudal continuation of outer layer of the rectum, the longitudinal layer of the anal canal forms the medial edge of the inter-
sphincteric space
- Innervation: myenteric plexus & sympathetic & parasympathetic nervous system
- 60-85% of resting anal pressure attributed to internal sphincter muscle, dysfunction leads to passive anal leakage
External Sphincter (3 part sphincter, with pubo-rectalis fused with the deep sphincter)
- Deep and Subcutaneous sphincter – forms ring of muscle
- Superficial sphincter – runs anteriorly from perineal body to coccyx
- Innervation: pudendal nerve (S2-S4)*
Puborectalis Muscle
- Puborectalis and external anal sphincter generate maximal squeeze pressure, dysfunction leads to frank incontinence
- Part of the levator ani muscle group (i.e. puborectalis, pubococcygeus and iliococcygeus)
- Innervation: 4th sacral nerve root ± pudendal nerve*
Course of pudendal nerve

Originates from S2-S4, leaves pelvis via the lower part of the greater sciatic foramen, passes under the pyriformis muscle, cross ischial spine and
sacrospinous ligament enter the ischiorectal fossa through the lesser sciatic foramen. It accompanies the internal pudendal a rtery and pudendal vein
and enters the pudendal (alcock) canal – at the lateral wall of the ischiorectal fossa
Pudendal nerve has 2 branches (1) inferior rectal nerve – innervate external anal sphincter, sensation to perianal skin, (2) perineal nerve – innervate
anterior perineum muscles & sphincter urethrae & gives rise to dorsal nerve of clitoris / penis
193
There is a wide variety of clinical presentations for patients diagnosed with rectal cancer. This can range from asymptomatic
individuals diagnosed via screening colonoscopy, symptomatic individuals who undergo colonoscopy, symptomatic individuals
who present in crisis.
Symptomatology
- Any PR bleed (hematochezia / melena) – quantify bleeding
- Any Tenesmus – feeling of incomplete defecation, passing only small amounts of mucus and loose stools with recurrent
inclination to defecate, frequently painful)
- Any Diminished stool calibre – pencil-thin stools
- Any Mucoid stools (suggests polypoid masses)
- Any Changes in bowel habits – alternating constipation and diarrhoea, spurious diarrhoea)
Assessment of Sphincter Competence

- Any faecal incontinence
- Any neurological conditions affecting faecal continence
- Any previous perianal conditions (i.e. fistula), surgeries & surgical complications
- For females, ask obstetrics history (i.e. childbirth via normal vaginal delivery, birth weight of child, any prolonged labour,
any instrumentations, any episiotomy performed, any peri-anal tears during childbirth)
Local Complications
- Tumour Bleeding leading to symptomatic anemia
- Tumour Fistula leading to fecaluria, pneumaturia, recurrent UTI (recto-bladder fistula), recto-vagina fistula,
- Tumour Perforation leading to sepsis (i.e. intra-abdominal sepsis with peritonitic abdomen)
- Tumour Obstruction leading to intestinal obstruction (i.e. abdominal distension, abdominal pain, vomiting, obstipation)
- Tumour Invasion leading to intractable pain (sacral nerves), lower urinary tract symptoms (trigone of bladder),
hydroureter / hydronephrosis (ureter)
Systemic Complications
- Constitutional Symptoms – Loss of Weight (must quantify), Loss of Appetite
- Liver – RHC discomfort, jaundice
- Lungs – SOB (pleural effusion), decreased effort tolerance
- Bone – bone pain, pathological fractures
- Brain – altered mental status
Physical Examination (Rectal Cancer)
For patients suspected of rectal tumour, clinical examination follows the routine abdominal examination (refer to colon cancer
topic) with particular emphasis on digital rectal examination (DRE). DRE assessment can give guidance on the type of surgery
(sphincter preserving surgery vs. APR) and likelihood of needing neoadjuvant therapy (bulky tumour vs. early stage tumour)
Digital Rectal Examination

- Tumour Localization:
▪ Reference Points: Distance from anal verge (AV) and ano-rectal junction (ARJ)
▪ Which quadrant involved: anteriorly located, posteriorly located, laterally located or circumferential
- Assessment of Tumour Bulk
▪ Tumour dimensions: length of tumour
▪ Tumour morphology: irregular, fungating, ulcerative
▪ Tumour mobility: mobile, adherent, fixed
▪ Tumour lumen (ability to cannulate tumour with finger)
- Assessment of Local Complications
- Assessment of Integrity of Anal Sphincter
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INVESTIGATIONS
For patients with suspected rectal tumour, investigations entails establishing the diagnosis (histological diagnosis). Thereafter,
staging will be divided into local and systemic staging. These investigations also help with tumour localization.
Tumour localization is performed via physical examination (DRE), imaging (MRI) and endoscopy (colonoscopy)
Establishing the Diagnosis

- Flexible Colonoscopy
▪ Allow for direct visualization (localization of tumour, assessment of tumour bulk)
▪ Allow for biopsies for histological diagnosis
▪ Allow for assessment of synchronous lesions (synchronous polyps in 30%, synchronous cancer in 2 to 5%)
▪ Allow for therapeutic procedures (i.e. polypectomy)
- Other investigations tools: rigid sigmoidoscopy, CT colonography, double contrast enema
Local Staging
- MRI Rectum
▪ Superior to CT for delineating T staging & N staging
▪ Reproducible, widely available, can be used for stenotic lesions
▪ Superior to EUS as can assess circumferential resection margin (CRM) refers to the fascia propria and can identify
tumour in relation to peritoneal reflection
- Endorectal Ultrasound
▪ Superior in delineating depth of tumour invasion (especially for early tumours, T1/2)
▪ Can assess local lymph node status
▪ Limitations: operator dependent, must be able to cannulate past tumour
Systemic Staging
- Computer Tomography of the Thorax, Abdomen & Pelvis (CT TAP)
Other Biochemical Investigations

- Full Blood Count
- Renal Panel
- CEA
- Liver Function Tests
STAGING
Refer to the AJCC 8th Edition Staging in Colon Cancer.
195
MANAGEMENT
For patients who do not present in crisis, they should be discussed at multidisciplinary tumour board with a decision for either
preoperative neoadjuvant therapy vs. upfront surgery.
For surgeons, a decision has to be made between sphincter sparing surgery and non-sphincter sparing surgery (i.e. APR). This
decision is based upon tumour localization and assessment of anal sphincter integrity. After surgical intervention, the patient’s
case should be re-discussed at a multidisciplinary tumour board for decision for adjuvant chemotherapy.
Differences between rectal cancer and colon cancer

1. Confinement of pelvis and sphincter making wide excision impossible
2. Proximity to urogenital structures and nerves resulting in impotence in males
3. Dual blood supply (superior rectal artery – from IMA, middle and inferior rectal artery from internal iliac artery) and lymphatic
drainage
4. Transanal accessibility (rectum is defined as within 12-15cm from anal verge)
Neoadjuvant Therapy
- For rectal cancer, neoadjuvant therapy is used for locally advanced rectal cancer. This is defined as stage II (cT3-T4, cN0)
or stage III (any T, cN1-2) invasive adenocarcinoma
- Neoadjuvant therapy is associated with reduced local recurrence as compared to surgery and reduced complications as
compared to postoperative chemoradiotherapy.
- Patients who are in impending obstruction but planned for neoadjuvant therapy can undergo a defunctioning stoma prior to
commencement of neoadjuvant therapy
- Options for Neoadjuvant Therapy
▪ Short-course Radiotherapy (SC-RT)
▪ Long-course Chemo-Radiotherapy (LC-CRT)
▪ Total Neoadjuvant Therapy
EXTRA INFORMATION
Short Course Radiotherapy (SC-RT) vs Long Course Chemoradiotherapy (LC-CRT)

- SCRT (25Gy in 5 days) vs. LCRT (45-50Gy in 25 days + 5FU/capecitabine)
▪ SC-RT can be used in patients with clear circumferential resection margin (CRM), allows for reduced complications,
faster time to surgery and subsequent systemic chemotherapy
▪ LC-RT can be used in patients with large bulky tumors with threatened CRM, presence of multiple mesorectal nodes
(cN2), allows for greater tumour response (tumour shrinkage)
- Both approaches have similar oncological outcomes
- Total Neoadjuvant Therapy

- Recent paradigm shift to consider shifting adjuvant chemotherapy to before surgery, this strategy known as total neoadjuvant
therapy (TNT). The benefits include better treatment compliance, better tolerability of chemotherapy and increased rates of
pCR. Patients who have completed preoperative chemoradiotherapy followed by preoperative FOLFOX can achieve pCR as
high as 38% at time of surgery whereas those given conventional chemoradiotherapy have an expected pCR of only 13% to
17%.121
Surgery for Rectal Cancer (options)

1. Local excision
2. High or Low anterior resection (AR) ± diverting ileostomy
3. Abdominoperineal Resection (APR) with permanent colostomy
Surgical Principles
- Surgical removal of rectal cancer with adequate mural and mesorectal margin.
▪ Mural margins: margin of 5 cm proximally and 2 cm distally is adequate.
▪ Mesorectal margins: margins of 4-5 cm distally.
- Sphincter-sparing versus loss of sphincter

▪ The anal sphincter can be spared if the distal mural margin is > 2cm above the level of the anal sphincter complex,
usually taken to be at the anorectal junction (which is 4cm above the anal verge)
▪ Sphincter-sparing: low anterior resection (anastomosis is below the peritoneal reflection)
▪ Sphincter-sacrificing surgery: abdominoperineal resection (APR) (entire anus and sphincter complex is dissected, with
creation of a permanent end colostomy)
121 J Natl Compr Canc Netw. 2018 Jul;16(7):909-915.
196
▪ Before consideration of either surgery – assessment of patient’s sphincter integrity via history and examination is
required!
Local Excision
- Transanal Excision (full thickness or mucosa) – i.e. Transanal Endoscopic Microsurgery (TEMS) or Transanal Minimally
Invasive Surgery (TAMIS)
- Local excision of any rectal neoplasm should be considered an excisional biopsy as final pathological examination may
reveal an invasive carcinoma that mandates more radical therapy
- Criteria for local excision (not absolute)
▪ Tumour location and size (i.e. < 4cm and < 40% circumference, or < 8cm from anal verge)
▪ Clinical Features (i.e. mobile, T1N0 or T2N0)
▪ Histological Features (i.e. well to mod differentiatedI, no mucinous component)
High or Low Anterior Resection (AR) ± diverting ileostomy

- Anterior Resection: anterior approach to resect the recto-sigmoid colon with a primary anastomosis between descending colon
and rectum
- The terminology “Low” Anterior Resection is used for anastomosis that is performed below the peritoneal reflection
- Total Mesorectal Excision (TME)122 is indicated for low anterior resection
▪ Precise, sharp dissection between the visceral and parietal layers of the endopelvic fascia, ensuring en bloc removal
of the perirectal areolar tissue, including the lateral and circumferential margins of the mesorectal envelope, lymphatics,
and vascular/perineural tumor deposits with the primary rectal cancer, while preserving the autonomic nerves.
▪ Markedly reduces the rates of local recurrence, from 14-45% to 4-7%.
▪ Middle ⅓ and lower ⅓ rectal cancer: Low Anterior Resection (LAR) + TME (gold standard) +/- diverting ileostomy
▪ Upper ⅓: High Anterior Resection + wide mesorectal excision (WME) or subtotal / partial mesorectal excision of at
least 5cm is required for oncological margins
- +/- Diverting ileostomy is usually reserved for low anterior resection

▪ The decision for diverting ileostomy depends on the risks of anastomotic leak which in turn is dependent on patient
factors, tumour factors and surgical factors).
▪ The diversion mitigates against disastrous complications of faecal peritonitis should an anastomotic leak occur
Abdominoperineal Resection (APR) with permanent colostomy

- APR: surgical excision of sigmoid colon, rectum & anal sphincter complex through 2 incision (1) anterior abdominal & (2)
perineum with the creation of an end colostomy +/- reconstruction with myocutaneous flap (i.e. gracilis flap)
- Indication: rectal tumour involving the sphincter complex, inadequate distal margin, patients with anal sphincter incontinence
Adjuvant Chemotherapy
- Stage I = no adjuvant therapy needed
- Stage II & III = adjuvant chemotherapy with FOLFOX
122 J R Soc Med. 1988 Sep;81(9):503-8.
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COMPLICATIONS
Refer to the complications list in Colon Cancer.
Complications of Radiotherapy
- Early Complications – perineal wound breakdown, diarrhoea, proctitis, UTI, small bowel obstruction, venous thrombosis
- Late Complications – effect on anal function
PROGNOSIS
5 year survival rates

Stage 5 year observed survival rates – rectal cancer
I 74%
II A – 65%, B – 52%, C – 32%
III A – 74%*, B – 45%, C – 33%
IV 6%
* Survival was better for some stage III cancers than some stage II cancers, the reasons for this is not clear
Risk factor for local recurrences

- Size of primary tumour
- Involvement of Circumferential Resection Margin (CRM) – main factor!
- Distal location of the tumour (distance to anal verge)
- Extramural Vascular Invasion (EMVI)
- Tumour Differentiation
- Nodal Status
- Extent of Extramural Spread
- Peritoneal Involvement by Tumour
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COLONOSCOPY & COLORECTAL POLYPS
COLONOSCOPY SCREENING
- Why is CRC suitable for screening?
▪ Prevalent and Lethal Disease
▪ Precursor can be detected early (long asymptomatic period – adenoma to carcinoma sequence)
▪ Early detection makes a difference (can institute treatment – i.e. polypectomy)
▪ Safe, effective, cheap test available
▪ Screening Recommendation of colon and rectal cancers, start by age 50yr and stop at 85yr
Complications related to colonic polypectomy

- Bleeding ~0.5% – most stop spontaneously. If persistent, repeat endoscopy and aim to control with clipping
- Perforation ~0.1% (1 in 1000) – may require surgical intervention
- Post-polypectomy syndrome ~0.3% – cautery causes micro-perforation in the colonic wall resulting in bacterial translocation
(patient presents with abdominal pain, fever and abdominal tenderness, CT scan shows fat stranding in the mesentery and
the colonic wall of the polypectomy site is thickened with no pneumoperitoneum) → conservative treatment
Bowel Preparation for Colonoscopy

- Ensure no free perforation or complete bowel obstruction prior to bowel preparation
- Stop Fe-tablets (≥ 5 days prior)
Medication - ± stop anticoagulants (depends on indication and VTE risk)

- ± stop aspirin / clopidogrel, for about 5-7days – tailor to patient’s risk profile
- adjust metformin / insulin as indicated-- want to avoid hypoglycemia in view of diet modification
Diet - Low residue diet 2-5 days prior, then clear liquids 1 day prior, then NBM 6-8hr prior
- Usually use 3-4L PEG in split dose preparation (i.e. 2L PEG at night and 2L PEG at morning or PM
colonoscopy with same day split 2L-2L prep)
Preparation - Alternatives
▪ Low-volume (2L) PEG +/- bisacodyl
▪ Oral Fleet (sodium phosphate) (45ml) – 2 doses separated by 10-12 hours apart +/- bisacodyl
- Metoclopramide (given with PEG)
Adjunct
- ± Fleet enemas
Special Scenarios
- If patients have diverting ileostomy – no need bowel preparation
- Post anterior resection, right hemicolectomy – normal 4L PEG bowel preparation
- Post subtotal colectomy – list for sigmoidoscopy only and fleet enema only, nil PEG
- ESRF patients – 4L PEG is still safe as non-absorbable
Endoscopic Therapy
- Performed for all detected adenomatous polyp during colonoscopy
- Techniques available: removed with biopsy forceps, snare resection (pedunculated polyps), or saline injection to submucosa
so as to elevate polyp then removal by snare resection
- If unable to remove polyps despite these techniques, patient may require more advanced endoscopist to perform endoscopic
submucosal resection (ESR) for polyp removal or surgery (i.e. colonic resection)
199
COLORECTAL POLYPS
A macroscopically visible lesion that results from pathological epithelial elevation of the colonic mucosa. Polyps can be defined by
their endoscopic feature or based on histopathology.
Classification (Paris Classification) – Endoscopic classification
Classification – Histopathological classification

Histopathology Remarks / Malignant Potential
- Most common non-neoplastic polyp in the colon
Normal epithelial cells
Hyperplastic* - Low / No risk malignancy (increased risk with large size
accumulating on the mucosal
(non-neoplastic) (>1cm), right-sided disease, mixed adenoma/hyperplastic
surface.
histology, >20 hyperplastic polyps)
Presence of crypt dilation,
Sessile
irregular branching crypts and - Has premalignant potential
Serrated*
excess serration at base of
Adenoma (SSA)
crypts
Outgrowth composed of
normal mature cells that are - Sporadic / Non-syndromic – not pre-malignant
Hamartomas normally found there, - Familial – higher cancer risk, should undergo regular
(non-neoplastic) originating from below the colonoscopy surveillance
mucosal surface, but growing - a/w Peutz-Jeghers Syndrome
Benign
in a disorganised mass.
Inflammatory
- Inflammatory Polyp (Pseudopolyp)
(non-neoplastic)
- Adenomas are neoplastic polyps, ⅔ of colonic polyps are
Atypical epithelial cells
adenoma with 30-50% of patients having more than 1
accumulating on the mucosal
synchronous adenoma detected during colonoscopy
surface +/- presence of
- 3-5% of patients with adenomas have invasive carcinoma at
cellular atypia
Adenomatous the time of diagnosis.
(neoplastic)
Architecturally can be
- The larger size and greater degree of villous features are
- Tubular (65-85%)
predictive of greater malignancy risk – tubular adenoma (5%
- Tubulovillous (10-25%)
risk), villous adenomas (40% risk), tubulovillous (22% risk),
- Villous (5-10%)
villous adenoma > 4cm (90% risk)
- Further management can either be oservatation with repeat
colonoscopy vs. surgery (i.e. colonic resection)
Adenocarcinoma that invades
- Decision is based on polyp features (favourable vs.
through the muscularis
Malignant Polyp unfavourable features) this depends on depth of invasion,
mucosa into the submucosal
tumour grade, presence of tumour budding, presence of
layer of the bowel wall (T1b)
lymphovascular invasion), resection margin and if resection
was complete or piecemeal.
* Serrated Polyps (i.e. hyperplastic, sessile serrated adenoma)
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EXTRA INFORMATION
Malignant Polyp
- Need for segmental resection is for improved oncological clearance as risk of lymph node metastasis is 8 – 15% (especially if
submucosa is involved)
- Classification based on
▪ Haggitt Level (1 = polyp head, 2 = neck, 3 = stalk, 4 = base / submucosal invasion in a sessile polyp),
▪ Depth of submucosal invasion (i.e. Sm3 → formal resection),
▪ Tumour grade (i.e. well, moderately or poorly differentiated),
▪ Tumour budding (i.e. presence of clusters of malignant cells in submucosa remote from the main site of invasion)
▪ Lymphovascular invasion
- Haggitt level 4 is subdivided into Sm1, Sm2, Sm3
Criteria for good colonoscopy

1. Percentage intubation to cecum (out of 100 colonoscopy performed, caecum reached in ≥97%)
2. Interval cancer rate (≥3years)* (except for hereditary colon cancers)
3. Adenoma detection rate (ADR) (≥30%), Mean withdrawal time > 6mins1 (higher rates of detection of any neoplasia of 28.3%
vs 11.8% for <6min, and advanced neoplasia of 6.4% vs 2.6% for <6min)
Follow-up after Colonoscopy
Benign Polyps
- No polyps / hyperplastic polyps: continue screening as average risk → colonoscopy in 10 years
- 1-2 tubular adenoma, low-grade dysplasia → colonoscopy 5 years
- 3-10 adenoma OR large (1cm adenoma), high grade, villous → colonoscopy in 3 years
- >10 adenomas → repeat colonoscopy within 3 years

- Sessile adenoma that is removed in pieces / large sessile polyp > 2cm → colonoscopy 3-6 months after adenoma removal
1 N Engl J Med. 2006 Dec 14;355(24):2533-41. [Important Paper]
201
COLONOSCOPY SCREENING GUIDELINE
202
ASSOCIATED CONDITIONS
- Up to 30% of colon cancers exhibit familial clustering – autosomal dominant inheritance pattern
- 3-5% a/w high risk inherited colon cancer syndromes, genetic testing is feasible in FAP, MAP, HNPCC, JPS and PJS
- Individuals with a lifetime of 10 polyps should be tested
*Hamartoma – disorganized overgrowth of tissues in their native location
Peutz-Jeghers Syndrome (PJS)

- PJS is an AD condition characterized by multiple gastrointestinal hamartomatous polyps (colon, small intestines and stomach)
and muco-cutaneous pigmentation with melanin spots on the perioral and buccal mucosa.
- Patients with presents with bowel obstruction from intussusception (polyp at apex) or from GI bleeding.
- They are also at significant risk of GI malignancy with a lifetime colorectal cancer risk at 40% (mean age at diagnosis 42-46)
- Increased risk of breast, (most common) pancreatic, lung, uterine and gastric cancers.
- Patients at risk should undergo upper and lower endoscopy every 2 to 3 years (starting from age 8, if no polyp detected at
baseline then repeat at age 18)
Juvenile Polyposis Syndrome (JPS) – “juvenile” refers to type of polyp

- JPS is an AD condition characterized by multiple hamartomatous juvenile polyp in the colon and upper GI tract.
- Juvenile polyps are defined as polyps with abundant lamina propria, absence of smooth muscle and mucous filled cysts
- Individuals diagnosed with JPS have
▪ ≥5 juvenile polyps in the colon and rectum
▪ Juvenile polyps all over the GI tract
▪ Juvenile polyps and a family history of JPS (any one of the three).
- Their lifetime colorectal cancer risk is ~ 40%.
- They are also at risk of extra colonic tumours in the stomach, small intestines, pancreas, lung, breast and uterus.
Ulcerative colitis
- Screening – yearly colonoscopy starting after 10 years of UC (risk increase 1% per year after 10 years of disease)
- Treatment: restorative proctocolectomy with IPAA or Pan-proctocolectomy with end-ileostomy
EXTRA INFORMATION
Cowden Syndrome (multiple hamartoma syndrome)

This is a rare syndrome, inherited in an AD fashion. It is caused by mutation in the PTEN gene and characterized by gastrointestinal
hamartomas and cancer. It also has a high risk of cancer of breast, thyroid, endometrium and cervix, benign fibrocystic breast
disease, non-toxic goitre and benign mucocutaneous lesions (i.e. trichilemmomas)
Cronkite-Canada Syndrome
- GI polyposis a/w alopecia, cutaneous pigmentation, and atrophy of fingernails and toenails
- Diarrhoea (prominent symptom), vomiting, malabsorption and protein-losing enteropathy
203
Familial adenomatous polyposis (FAP)
Familial Adenomatous Polyposis (FAP) is inherited in an autosomal dominant fashion in 1 in 20,000 live births (less common than
HNPCC) and accounts for < 1% of total colorectal cancer burden. It is associated with germline mutation of tumour suppressor gene
APC (5q21-q22), with >80% having a +ve family hx, and the rest due to new mutations in the APC gene. Up to 10 – 30% of patients
with classical FAP do not have APC mutations
Polyps are usually visible on sigmoidoscopy by 15yo. By age 35, 95% of patients have >100 adenomatous polyps, and by age 40,
100% of patients will develop colorectal cancer (occurs 10-20 years after onset of polyposis). If patients have < 100 adenomatous
polyps, consider attenuated FAP.
EXTRA INFORMATION
Variants: Turcot’s / Gardner’s (AD) / attenuated FAP

- Turcot’s – characterized by numerous colonic adenomatous polyps and central nervous system tumours (gliomas)
- Gardner’s – characterized by numerous colonic adenomatous polyps, multiple osteoma (predilection for the mandible),
fibromatosis and epidermal inclusion cysts
- MYH-associated polyposis (MAP) - no identifiable APC mutation. characterized by colorectal adenoma and carcinoma, usually
right sided cancer (100% lifetime risk by age 60), duodenal adenoma, gastric fundic gland polyp, osteomas and dental cyst.
patients do not get desmoid tumours
Extra-intestinal manifestations
This can be classified according to the embryonic origins:
- Ectodermal Origin: epidermoid cysts, pilomatrixoma, tumours of CNS, congenital hypertrophy of retinal pigment epithelium
(CHRPE; present in up to 50% of pts with FAP, and can be used to screen affected families if genetic testing is unavailable)
- Mesodermal Origin: connective tissue (desmoid tumour)*, bone (osteoma, exostosis, sclerosis), dental (supernumerary
teeth, unerupted teeth)
- Endodermal Origin: adenomas and carcinomas of duodenum, stomach, small intestine, biliary tract, thyroid (follicular or
papillary), adrenal cortex (adenoma), hepatoblastoma, fundic gland polyp, Brain Tumour (80% medulloblastoma of the CP
angle of the brain, 70% occur before age 16)
* 1st line treatment with NSAIDs (i.e. sulindac) & Tamoxifen
Diagnosis
Patients should undergo colonoscopy which will characteristically reveal > 100 polyps (disease characterized by the appearance of
hundreds or thousands of adenomatous polyps in the colon), and the dx can be made confidently. If there are no adenomas by 30yo,
FAP is unlikely.
Genetic testing of at-risk family members (screen index case 1 st).
Surveillance2
For patients at risk for FAP (genetic testing not done), recommendation is for yearly colonoscopy from age 12 onwards. Yearly for 10
years then bi-annually for 10 years then every 3 years for 10 years then 3-5 yearly.
EXTRA INFORMATION
OGD Surveillance
OGD surveillance for periampullary cancer should start around 25 to 30 years. Surveillance interval is based on Spigelman
Classification of duodenal polyposis. Duodenal adenoma occurs in all patients with FAP but is severe in only 10% with malignant
change occurring in 5%.
204
Treatment
Patients should be offered prophylactic surgery before colorectal cancer develops (usually before age 25). The available options are
1. Total colectomy with ileorectal anastomosis (TC + IRA) with lifelong surveillance
▪ Advantage of no need for any temporary stoma, but the rectum is left behind and requires regular surveillance
▪ Follow up with surveillance of rectum/pouch is important due to risk of adenomas & carcinomas in the residual bowel (10%
develop malig in 30y follow-up).
2. Restorative proctocolectomy (RPC) with ileal pouch anal anastomosis (IPAA)
▪ Usually requires a temporary stoma
▪ Has a pouch failure rate of ~10%, esp at the stapled anastomosis
▪ Leaves a small cuff of rectal mucosa at the anastomosis, which has a small risk of cancer
3. Total proctocolectomy with end ileostomy (usually performed for patients with very low rectal cancer)
▪ Usually not preferred as young patients want to avoid a permanent stoma
COX2 inhibitors may slow or prevent the development of polyps

For patients with duodenal polyposis (Spigelman IV), can consider prophylactic pancreatico-duodenectomy (whipple’s)
For patients with desmoid tumour, treatment options include NSAIDs, antiestrogen, surgical excision and cytotoxic chemotherapy
Lynch Syndrome (LS) / Hereditary Non-Polyposis Colorectal CA (HNPCC) 3

Lynch Syndrome was first described by Aldred Warthin (1913). Subsequently, Henry Lynch reported 2 large families with hereditary
colorectal cancer (1966).
Lynch Syndrome is inherited in an autosomal dominant fashion and accounts for 1-3% of total colorectal cancer burden. It is
characterized by the development of early onset, colorectal, endometrial (30-50% lifetime risk of endometrial ca), gastric and
genitourinary cancers in individuals with a strong family history of cancer. It is caused by defective DNA mismatch repair genes (MMR):
MSH2 and MLH1 (90%), MSH6 or PMS2 (10%). This results in an 80% lifetime risk of developing colorectal cancer, most in the
proximal colon. Mean age of diagnosis is 45yo.
- Divided into Lynch syndrome I or Lynch syndrome II based on clinical features

▪ Lynch Syndrome type I: familial colon cancer
▪ Lynch Syndrome type II: HNPCC associated with increased risk of cancer of the GI tract and reproductive system (i.e.
endometrial cancer, and also ovarian, gastric, small bowel, hepatobiliary, and renal pelvis/ureter cancers)
Clinical Features
Tumours are usually proximal to the splenic flexure (right sided tumour). They tend to be mucinous, poorly differentiated and of signet
ring appearance with marked infiltration by lymphocytes and lymphoid aggregates at their margins. These tumours tend to arise from
polyps which are commonly flat, with villous histology. The prognosis of these cancers tend to be better than tumours that ar ise
sporadically.
3 Gut. 2013 Jun;62(6):812-23. [Important Paper]
205
Diagnosis (based on the Amsterdam criteria or genetic testing)
- Amsterdam II (incorporates extracolonic malignancies)
▪ 3 or more relatives with HNPCC-associated cancer (i.e. colorectal, endometrial, renal pelvis, small bowel, ureteral cancers),
one of whom is a first-degree relative of the other two (FAP excluded)
▪ 2 generations of the same family affected by cancer
▪ 1 (at least) cancer case diagnosed before age of 50
- Immunohistochemistry of the MMR proteins or DNA MSI
- Risk Factors – for development of adenoma or CRC in LS

▪ Smoking and high BMI increases the risk
▪ Regular aspirin reduces incidence of cancer in LS
Surveillance
- Colonoscopy surveillance reduces the risk of colorectal cancer in Lynch syndrome by 63%. It is recommended that colonoscopy
be performed every 1-2 years from the age 20-25 (or 5 years younger than the youngest affected relative). Surveillance should
continue till 75 years.
- Gynaecological Examination, trans-vaginal u/s, aspiration biopsy from age 35-40, may lead to detection of premalignant disease
and early EC. Benefits of extra-colonic CA surveillance is unknown (i.e. OGD for stomach cancer screening & urine cytology for
urinary tract malignancy) – performed in research setting
Treatment
- For patients with colonic malignancy, surgery involves either segmental colectomy or colectomy with ileorectal anastomosis (IRA).
Segmental colectomy leads to better function but an increased risk of metachronous cancer and need for full colonoscopic
surveillance. The risk of metachronous cancer in the retain rectum is ~ 12% at 12 years. Regular annual endoscopy of the residue
large bowel is required.
- THBSO largely prevents endometrial & ovarian cancer – discuss with patients who have completed their families esp. after the
age of 40
EXTRA INFORMATION
Familial Colorectal Cancer X

- Non-syndromic familial colorectal cancer – colorectal cancer type X involves families who meet Amsterdam criteria but lack
MSI and evidence of germline mutations in DNA mismatch repair genes – accounts for 10-15% of total CRC burden
- Background lifetime risk – 5-6%
- 1 affected first-degree relatives – risk increases 2-3 fold over the background risk
- 2 affected first-degree relatives – risk increases 3-4 folds
- 1 affected first-degree relative with colon cancer before age 50 – risk increase 3-4 folds
- Proposed that moderate risk heritable colon cancers stem from interaction between genetics and environmental triggers
206
STOMA PRINCIPLES
DEFINITION
Artificial opening of a luminal organ into the external environment – may be temporary or permanent, it may be end-on or a loop.
INDICATIONS
1. For input: feeding (Percutaneous endoscopic gastrostomy)
2. For output: decompression/ lavage, defunctioning/ diversion, draining/ exteriorization (urine, faeces)
CLASSIFICATION
- Intestinal Stoma can be small intestine (end or loop), large intestine (end or loop) or small-large intestine (ileo-colic stoma)
▪ Ileo-colic stoma – 2 lumens present (i.e. one lumen leading to ileum and one lumen leading to colon)
- Intestinal Stoma can be classified as end, loop or double barrel

▪ End Stoma – transected end of the intestine is exteriorize and fashioned as a stoma (only 1 lumen)
▪ Loop Stoma – loop of intestine is exteriorized and a stoma is fashioned (2 lumen)
▪ Double Barrel Stoma – intestine is severed and brought out as 2 ends to fashion a stoma (i.e. ileo-colic stoma) (2 lumen
- Stomas can also be classified as temporary or permanent

▪ Temporary
- Decompression – relief of bowel obstruction causing proximal dilatation, i.e. end colostomy or transverse loop
colostomy for obstructed colon tumour (proximal large bowel is decompressed)
- Defunctioning / Diverting – i.e. loop ileostomy after low AR (small bowel contents diverted from large colon)
▪ Permanent
- Absolute – i.e. end colostomy after APR or end ileostomy after panproctocolectomy (where there is no distal bowel
remaining)
- Relative – reversal of stoma is dependent on patient factor, disease factor and surgical factors (many created intestinal
stoma are not eventually reversed)
207
How to decide on placement of stoma

- Over the rectus sheath which reduces risk of prolapse,
- Away from the surgical incision which reduces risk of wound contamination and infection
- Away from skin creases or bony prominences - stoma wafer can be flushed with the skin (gaps between skin and wafer - leakage
of fluid - skin excoriation & infection)
- Away from old surgical scars - reduces risk of hernia
- Sited for easy accessibility i.e. not under a large fold of abdominal fat
- Intra-operatively, avoid tension over the stoma to marked site - causes decreased vascularity of the stoma - risk of stoma necrosis
How to determine what type of stoma

Question Answer Stoma
Left iliac fossa Likely a colostomy
Where is the stoma?
Right iliac fossa Likely an ileostomy
How does the bowel lie in Flush with skin Likely a colostomy
relation to the external skin? Raised spout Ileostomy; less commonly a urostomy
One End colostomy; end ileostomy; urostomy
How many lumens are Two (adjacent) – efferent limb may be difficult to see Loop colostomy; loop ileostomy; end-loop ileostomy
present? Most likely end colostomy with a mucous fistula; double
Two (separate stomas)
barrel stoma; rarely bowel stoma and urostomy
Fully formed stool Colostomy
What are the contents of the
Semisolid or liquid stool Most likely ileostomy; colostomy
stoma bag (don't be afraid to
Urine Urostomy
feel it)?
Mucus Mucous fistula
Ileostomy Colostomy
Location Right Iliac fossa Left Iliac Fossa
Calibre Small Large
Flushed / Protrudes ~3cm ‘spout’ – prevent ileal content (corrosive)
Flushed to the Skin
Key Findings Spouted to contact the skin
Contents Watery greenish ileal output Brown faecal output
Abdominal - Midline laparotomy scar / APR scar
Scars - Can also be laparoscopy scars
- Mucosa (pink and healthy or dusky)
Complications - Overlying skin changes (stoma cx – erythema and excoriations)
- Ask patient to cough to check for parastomal herniation
- *DRE* for patency of anal orifice (determine if temporary or permanent stoma)
- Request to remove face plate to examine the number and patency of lumen
Complete Examination
- Request for I/O chart (especially if ileostomy): exclude high output stoma
- Obtain a psychosexual history
208
How to determine what type of stoma
2 possibilities: permanent end colostomy or temporary end colostomy (to differentiate do a DRE
to check anal canal patency)
Anal Canal Absent → permanent end colostomy, patient most probably has undergone an APR
for low rectal tumour
Anal Canal Present → possible temporary end colostomy, patient has undergone a Hartmann’s
resection for an obstructing rectal tumour

This procedure is most commonly performed to manage carcinoma of the lower rectum or anus,
APR with permanent end
diverticular disease, and rare cases of faecal incontinence that do not respond to medical mx.
colostomy
For example, a very low rectal cancer (distal 1/3) will require resection of the rectum and anus
(APR). The remaining descending and sigmoid colon is mobilised and the cut end brought to the
abdominal surface at an opening about 2 cm across.
This is usually sited in the left iliac fossa. The best site is usually through the lateral edge of the
rectus sheath, 6cm above and medial to the ASIS. (i.e. midway between ASIS and umbilicus)
If the anus, rectum, and a portion of the lower colon have not been removed, as in Hartmann's
Anterior Resection with procedure, two outcomes are possible.
Hartmann's procedure and
temporary end colostomy In the first, the distal, non-functioning part of the colon and the rectum can be stapled or sewn
closed and left inside the abdomen as a rectal stump. The proximal colon is then taken out as an
end colostomy. Because the rectum has not been removed, the urge to have a bowel movement
may occur. Mucus and some old stool, if present, will be passed.
Less commonly, two separate stomas may be created. One stoma is the exit of the functioning
part of the colon through which stool and gas pass. The second stoma opens into the non-
functioning portion of the colon and rectum and is called a mucous fistula. The second stoma
is usually small, flat, pink-red in colour, and moist, and it produces only mucus.
If the colostomy is temporary, a

second operation is needed to
reconnect the two ends.
Loop colostomy (can be

temporary or permanent) A loop colostomy was traditionally created to defunction an inflamed sigmoid in diverticular
disease or to defunction a distal anastomosis. Also, can be indicated for prophylactic
decompression before RT in an obstructing rectal tumour.
A loop of colon is brought to the surface of the body and may be supported on a rod, which is
removed after 5-7 days. The bowel wall is partially cut to produce two openings—of an afferent
limb and an efferent limb. The opening of the afferent limb leads to the functioning part of the
colon, through which stool and gas pass out. The opening of the efferent limb leads into the non-
functioning part of the colon.
The stoma site was usually high on the abdomen above the waistline because the transverse
colon was commonly used. However, currently, loop colostomies are more often fashioned from
the sigmoid colon to defunction the rectum (i.e. in cancer) or anus (i.e. in incontinence).
209
2 possibilities: temporary end ileostomy or permanent end ileostomy (to differentiate do a DRE
to check for anal canal patency)
End ileostomy
No anal canal → permanent end ileostomy, the patient has undergone panproctocolectomy. This
occurs most commonly in severe ulcerative colitis but also in familial polyposis and some cases
of colorectal cancer (i.e. HNPCC). After a panproctocolectomy the ileostomy is permanent.
Anal Canal Present → Temporary end ileostomy. Patient has undergone an emergency subtotal
colectomy, which leaves part of the sigmoid colon and rectum left in place; for acute ulcerative
colitis; acute ischaemic bowel; or neoplastic obstruction of the sigmoid.
EXTRA INFORMATION
Brooke Ileosotmy
The ileum is resected just short of its junction with the caecum, and 6-7 cm of the small bowel
is brought through the abdominal wall, usually in the right iliac fossa. Three or four interrupted
absorbable sutures are placed through the edge of the bowel (90 0 to each other), then through
the serosa, (2cm proximal to the edge), and then through the dermis (Brooke technique).
After the stoma is everted, the mucocutaneous junction is sutured circumferentially with
interrupted absorbable suture.
Loop ileostomy Suspect if ileostomy with 2 adjacent lumens and bag contains greenish liquid contents.
This type of stoma allows for defunctioning of an obstructed colon (in cancer), defunctioning of a
distal anastomosis (after resection and primary anastomosis either as an emergency or after
radiotherapy), or defunctioning of the anus (in incontinence or perineal involvement in Crohn's
disease).
A loop ileostomy has two openings, and most are temporary. Subsequent closure can often be
accomplished without a formal laparotomy.
When the caecum is removed, the surgeon might create a double barrel stoma. In essence, this
Double barrel stoma is an end ileostomy (small bowel) and a mucous fistula (the remaining colon) sited beside each
(i.e. Ileo-colic stoma) other. On examination this will look almost identical to a loop ileostomy; however, closer
inspection will show two separate stomas.
This is a general term for the surgical diversion of the urinary tract. The main reasons for a
urostomy are cancer of the bladder, neuropathic bladder, and resistant urinary incontinence.
Urostomy
(Ileal Conduit) The bladder is usually removed, but this may depend on the underlying condition. Formation of
an ileal conduit is the most common procedure, which constitutes isolation of a segment of ileum.
One end of the ileum is closed and the two ureters are anastomosed to it. Finally, the open end
of the ileum is brought out onto the skin as an everted spout and will look similar to an end
ileostomy. Urine drains almost constantly from the kidneys through the ureters and ileal conduit
into a bag.
Patient may present with hyperchloremic metabolic acidosis and/or less frequently
hypokalemia, hypocalcemia and hypomagnesemia*
210
EXTRA INFORMATION
Principles in Fashioning a Stoma

- Adequate bowel mobilization to ensure proper protruding well vascularized tension free approximation to abdominal wall
- Appropriately sized stoma fascia opening and skin aperture → too large will risk parastomal hernia, too small will risk ischemia,
venous congestion, necrosis, stricture, obstruction

- Ensure correct bowel orientation and mesentery not twisted
- Create peritoneal window over colonic mesentery below stoma and use of stoma rod may decrease risk of stoma retraction
- Closure of all abdominal incisions before maturing stoma to avoid wound contamination
- Ileostomy should be sprouted 2-3cm above abdominal wall to allow output into appliance and not onto skin
- Adequately spaced and snug sutures to abdominal wall dermis to reduce risk of mucocutaneous dehiscence
Stoma Bag System (Single vs 2-piece System)
Single piece systems stick on to a Two-piece systems have a separate base (a flange) that sticks to the skin, and the bag
patient's skin. attaches to this. Bag can be changed without removing the flange.
COMPLICATIONS
Early
- Bleeding
- Stoma Necrosis (stoma appears dusky (grey to black); check by intubating with a glass tube into the stoma to look at colour of
mucosa) → refashion stoma
- Obstruction (faecal impaction → explore with finger, enema / secondary to adhesion – more in ileostomy)
- Leakage → skin erosion, parastomal infection → re-site
- Stoma diarrhoea (high output) → r/o intra-abdominal sepsis, correct water & electrolyte imbalance (hypoNa +, hypoMg2+, hypoK+),
add antimotility agent to thicken output (loperamide ± codeine) – see below
- Peristomal ulceration – if non-healing, ?pyoderma gangrenosum → evaluate for IBD (treat: steroids)
Intermediate
- Prolapse of bowel → refashion/refresh
- Retraction → refashion
Late
- Parastomal hernia (+ve cough impulse) → conservative, 10-30% will require surgery
- Stenosis (unable to pass finger through) → refashion

- Fistulae
- Skin excoriation
- Psychological problem
High Stoma Output4
4 World J Gastroenterol 2001; December 7(6):741-751.
211
- Defined as one producing an effluent volume >1000/ml/day
- Clinically significant when effluent volume > 2000ml/day → cause electrolytes derangements
- Primary cause: loss of normal daily secretions (1.5L saliva, 2-3L gastric juice, 1.5L pancreatico-biliary)
- Other causes of high output (exclude first): intra-abdominal sepsis, infective enteritis (i.e. clostridium difficile), partial / intermittent
bowel obstruction, recurrent disease in the remaining bowel (i.e. Crohn’s disease or irradiation bowel disease), sudden stopping
of drugs (i.e. steroids or opiates), administration of prokinetic drugs (i.e. metoclopramide)
Pathophysiology of Hypokalemia
- Sodium depletion (each L of jejunostomy fluid contains 100mmol/l of Na +) leading to secondary hyperaldosteronism (increase
Na+ reabsorption and concomitantly greater than normal urinary loss of K+ and Mg2+)
- Hypomagnesaemia leading to increase renal potassium excretion
Management5
5 Colorectal Dis. 2011 Feb;13(2):191-7.
212
DIVERTICULAR DISEASE
DEFINITION
- Acquired pseudo-diverticular outpouching of colonic mucosa and submucosal at the antimesenteric side. (Does not involve all 4
layers, hence not true diverticular)
- Diverticulosis coli – presence of acquired pseudo-diverticular within the colon
- Diverticular disease – symptomatic diverticulosis coli
▪ Simple (75%) with no complications
▪ Complicated (25%) with abscess, fistula, obstruction, peritonitis, sepsis
- Diverticulitis – inflammation and infection of diverticula
EPIDEMIOLOGY6
- Prevalence increases with age, 5% at age 40, 30% at age 60, 65% at age 80
- Diverticulosis is symptomatic in 70% of cases, leads to diverticulitis in 15-25% and is associated with bleeding in 5-15%
- Distribution (in Caucasians): sigmoid involvement (95%), involvement of the sigmoid alone (65%), involvement of the entire colon
(7%), not in rectum as taenia coli has fused
▪ Sigmoid colon is most commonly affected owing to decrease luminal diameter and increased luminal pressure (pulsion) –
onset usually in 7th & 8th decade of life
- Risk factors
▪ Diet = lack of dietary fibre or high in red meat / fat
▪ Obesity / lack of physical activity
▪ Genetics = in Caucasian almost always LDD, in Asians / Africans predominant RDD
▪ Others = ADPKD patients on dialysis
- In Singapore – right-sided diverticular disease was more common in all age groups – older patients were more likely to have
LDD as compared to younger patients. Among ethnic groups, Chinese were more likely to have RDD (RDD: peaks in 6 th decade
of life) 7
PATHOGENESIS
1. Increased intraluminal pressure
▪ Forces mucosa and submucosal through areas of weakness in gut wall – occurs in the colon as the muscularis propria layer
is aggregated into 3 bands (taeniae coli)
▪ Associated with lack of dietary fibre
2. Degenerative changes in colonic wall
▪ Usually at point of entry of terminal arterial branches where serosa is weakest
▪ Associated with weakening of collagen structure with age
6 WGO Practice Guidelines Diverticular disease 1 (2007)

7 Colorectal Dis. 2011 Mar;13(3):312-6.
213
1. Acute diverticulitis (due to obstruction of diverticula)
▪ Due to underlying micro/macro perforation of a diverticulum 20 inflammation and focal necrosis (small perforation is walled
off by pericolic fat and mesentery)
▪ Symptoms: LLQ pain, N/V, constipation / diarrhoea, urinary urgency
▪ Signs: Low-grade fever, Localised LLQ tenderness, ±mass (i.e. abscess / phlegmon)
2. Chronic diverticulitis
▪ Recurrent LIF pain, irregular bowel habit, passage of mucus PR
3. Complicated diverticulitis
▪ LGIT haemorrhage – vessel disruption occurs on the mucosal side of the artery → bleeding occur into the lumen instead of
into the peritoneal cavity

- Diverticular bleeding usually occurs in the absence of diverticulitis
- Usually stop spontaneously in ~75% of patients – risk of re-bleeding is ~25% and risk of bleeding after a 3rd episode
is ~50%8
▪ Fistula formation (commonest: colovesical fistula formation) – 2o to pericolic abscess discharging, may present with urinary
symptoms (i.e. UTI). Others – colo-cutaneous, colo-uterine, colo-enteric, colo-vaginal
▪ Perforation – limited spread → phlegmon, further spread but still localized → diverticular abscess, free perforation (rare) →
generalized peritonitis
▪ Bowel obstruction – due to combination of oedema or compression from an abscess or recurrent progressive fibrosis and/or
ustrictures
INVESTIGATIONS
Investigations is ordered based on the initial symptoms (i.e. abdominal pain / PR bleeding), hence, other investigations may be done
if suspecting other differential diagnosis
Biochemical
- FBC – assess TW
- U/E/Cr – assess renal function, suitability for contrasted scan
- CRP (most useful laboratory test for determining the diagnosis and severity of acute diverticulitis – LLQ pain + lack of vomiting
+ raised CRP (>50) – accurate predictor of acute diverticulitis)
- PT/INR/APP – if require intervention (percutaneous or surgery)
- ABG / Lactate – if patient is septic / dehydrated / worry regarding ischemic colitis
Imaging
- CT AP (gold standard in diagnosis and staging severity of diverticulitis)
▪ Localized bowel wall thickening (>4mm)
▪ Fat stranding: ↑ soft tissue density within pericolonic fat 2 0 to inflammation
▪ Presence of colonic diverticula
▪ Complicated Diverticulitis – Pericolonic abscess (fluid collection surrounded by inflammatory changes), Fistula
(extraluminal air collection within other organs – i.e. bladder), Peritonitis (free air)
Hinchey Classification
- Antibiotics, NBM, IV fluids
Pericolic abscess confined by
Stage 1 - KIV percutaneous drainage under radiological guidance (larger abscess, failed antibiotics
the mesocolon
treatment)
Stage 2 Pelvic / retroperitoneal abscess - KIV elective 1 stage surgery – resection of segmental colectomy** with primary anastomosis
Stage 3 Purulent peritonitis -Emergent surgery should be considered
-Type of surgical intervention: single vs. 2-stage operation (i.e. segmental resection* with
Stage 4 Faecal peritonitis primary anastomosis with or without defunctioning ileostomy vs Hartmann’s procedure)
- In Hinchey III – consideration of laparoscopic lavage
* Proximal margins through an area of pliable colon without hypertrophy or inflammation & distal resection margins extend to where the taenia coli
coalesce onto the upper rectum / level of sacral promontory. Recurrent diverticulitis after resection is frequently related to inadequate distal resection
8 Aliment Pharmacol Ther 2010; 32: 466–471
214
MANAGEMENT9
Uncomplicated Diverticulitis
- CT scan proven – uncomplicated diverticulitis
- NBM > clear liquid diet > high fibre low residue diet
- Analgesia
- Antibiotics (10-14days): IV ceftriaxone & metronidazole KIV oralize to augmentin or ciprofloxacin & metronidazole
▪ A trial of non-antibiotic therapy can be considered in immunocompetent patients – based on clinical judgement, with caution
in immunosuppressed patients, those with significant comorbidities, severe signs of sepsis or complicated diverticulitis 10
- Risk of recurrence: 20-40% (similar severity to 1st episode)
- Role of colonoscopy following episode of acute diverticulitis** – definite for patients with high risk features, questionable for
patients with uncomplicated acute diverticulitis with no high risk features (but if patients at screening age for colonoscopy –
proceed with colonoscopy 4-6 weeks after acute episode resolves)
- Prevention of acute diverticulitis recurrence – no role for mesalazine, ?fibre intake (no study performed)
▪ Use of aspirin or NSAIDs should be minimized | (LoE: low)
▪ Encourage weight loss (BMI < 25) and encourage physical activity (>30mins/day) | (LoE: moderate)
▪ Stop Smoking | (LoE: moderate)
** After an episode of acute diverticulitis, risk of finding malignancy on colonoscopy is 1-3%. Higher risk in patients with complicated
diverticulitis (i.e. abscess / perforation)
Complicated Diverticulitis (i.e. perforation, obstruction, abscess or fistula)

- ABC + NBM + Analgesia + IV Antibiotics (as above) + Colonoscopy in 6/52
- Peritonitis: ABC + Antibiotics + Emergency Surgery
▪ Perforation: 2 stage surgery
▪ Obstruction: 1 or 2 stage surgery
▪ Abscess: CT guided drainage ± 1 stage surgery
▪ Fistula (usually sigmoid colon involved): elective 1 stage surgery
- Hinchey I & II
▪ Antibiotics for all abscess as 1st line treatment
▪ CT guided percutaneous drainage for larger abscesses (>4cm), if sepsis not resolving with antibiotics
- Hinchey III/IV diverticulitis

▪ Sigmoid resection and primary anastomosis with or without proximal diversion is preferred over Hartmann’s procedure
▪ Hartmann’s procedure is the preferred option for hemodynamically unstable patients
▪ In unstable patients – damage control surgery can be considered (i.e. resection & temporary abdominal closure)
▪ Laparoscopic lavage can be considered in selected patients – lower stoma rates weighed against higher risk of
complications and re-intervention [for Hinchey III]
Colonic Diverticular Bleeding11

- ABC – resuscitate and stabilize patient
- Colonoscopy – to localize and treat bleeding (i.e. epinephrine injection / cautery)
- Angiography / Embolization – alternative to colonoscopy when bleeding site cannot be identified (to localize and treat bleeding)
▪ Can detect bleeding rates > 0.5ml/min
▪ If blush is detected – patient can undergo angioembolization of the bleeding vessel
- Surgical Intervention (see below)
▪ For patients requiring <4 units of PCT in 24hours, almost all will spontaneously stop bleeding, if patients require >4 units
likelihood of surgery was 60%12
▪ Segmental colectomy (after source of bleeding identified) with restoration of continuity by end-to-end anastomosis (last
resort: subtotal colectomy)
▪ Blind segmental resection is contraindicated
9 uptodate: Treatment of acute diverticulitis

10 JAMA Surg. 2019 Feb 1;154(2):172-173. [Important]
11 uptodate: Colonic diverticular bleeding
12 Ann Surg. 1994 Nov;220(5):653-6.
215
EXTRA INFORMATION
Indication for Surgical Intervention
1. Hinchey III or IV acute diverticulitis

2. Hinchey I or II acute diverticulitis not responding to conservative management (i.e. antibiotics
and percutaneous drainage)
Indications for 3. Obstruction with impending perforation – need to rule out cancer during surgery
emergency operation 4. Emergency bleed
a. Hemodynamically unstable with failure of embolization
b. Need > 4 units of PCT
c. Previous bleed
1. Patients with ?one episode of complicated diverticulitis (who are fit for surgery) – i.e. fistula
(i.e. colovesical, colovaginal, colocutaneous), stricture, persistent diverticulitis
2. Immunocompromised patients (i.e. transplant recipients, patients with chronic disease
affecting immune system) who have had one episode of uncomplicated diverticulitis
Indications for
elective operation Previously indications include (1) recurrent attacks (≥2)*, (2) younger patients (<50yr) – this is no
(i.e. subtotal colectomy, longer recommended

sigmoid colectomy) – Patients with Hinchey Ib / II disease, successfully managed non-operatively during a single episode
wait 4-6 weeks after the of acute diverticulitis – no role for elective resection
attack before operating
* Number of attacks of uncomplicated diverticulitis is not necessarily an overriding factor in defining
the appropriateness of elective surgery. 13 The likelihood of needing emergency surgery is not
affected by the number of previous episodes of uncomplicated diverticulitis – but need to evaluate
abdominal symptoms – if persistent pain, surgery may have a role in improving QoL
Recurrent diverticulitis after surgical treatment

- Incidence ranging from 1% to 10%
- In general, the progression of diverticular disease in the remaining colon is approximately 15%.
- Important factors to be considered in terms of surgery are the adequacy of resection (i.e. degree of proximal resection and level
of distal anastomosis). The use of the rectum as the distal margin decreases the rate of recurrence.
- Differential diagnosis that must be excluded → irritable bowel syndrome, inflammatory bowel disease, and ischemic colitis.
PROGNOSIS
- Likelihood of re-bleeding = 10% in 1st year and 25% at 4 years14
- Among patients with diverticulosis, less than 5% will have 1 st episode of acute diverticulitis, from this 20% will have a 2 nd episode
of acute diverticulitis (within 10 years), from this, 20% will have a 3 rd episode of acute diverticulitis (within 1yr)
- Complications occurs more commonly during the 1 st and 2nd episode of acute diverticulitis
- Advise high fibre diet, weight reduction, exercise, stop smoking
13 Dis Colon Rectum. 2006;49:939–944.

14 Ann Surg. 1994 Nov; 220(5):653-6. (same as earlier reference)
216
7. SMALL BOWEL, IBD
ANATOMY OF THE SMALL BOWEL
ANATOMY
- Arterial arcade increases from 1-2 in the proximal jejunum to 4-5 in the distal ileum
- Layers of the small bowel: mucosa, submucosa, muscularis propria, serosa
▪ Mucosa made up of Epithelial layer, lamina propria & muscularis mucosa
▪ Submucosa is the strongest layer of the small bowel
- Cells found in the small bowel mucosa
▪ Absorptive enterocytes – involved in final digestion step and absorb digested food (transport to lamina propria)
▪ Goblet cells (secrete mucus) – protect surface of intestine with viscous fluid consisting of glycoprotein
▪ Paneth cells (secrete lysozyme, tumour necrosis factor) – protect body against pathogenic microorganisms
▪ Enteroendocrine (EE) cells (produce gastrointestinal hormones)
▪ Stem cells – the epithelial lining of the small intestine (esp. that covering the villi), renews every 5 days
- Duodenum → contains Brunner’s Gland
- Ileum → contains aggregations of lymph nodules called Peyer’s patches (Gut associated lymphatic tissue, GALT) – M cell found
over lymphatic nodules → endocytose and transport antigen from the lumen to lymphoid cells
217
7. Small Bowel, IBD_Last Updated 3 rd June 2020
SMALL BOWEL CANCER
Most common primary malignancy of the small intestine: neuroendocrine tumours.
Most common secondary malignancy of the of the small intestine: metastatic melanoma
SMALL BOWEL NEUROENDOCRINE (CARCINOID) TUMOUR

- Location – most often in ileum, followed by jejunum then duodenum
▪ Hindgut Carcinoid → hematochezia, rarely symptomatic
▪ Midgut Carcinoid → flushing and diarrhoea due to high levels of serotonin secretion (with bulky / metastatic disease), small
bowel obstruction secondary to intense desmoplastic reaction caused by the tumour
▪ Foregut Carcinoid → systemic symptoms, atypical presentation

- Diagnostic Ix: 24hour urine level for serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA)
- Intraoperative findings: fibrosis of mesentery causing obstruction → en-bloc resection including mesentery
- Carcinoid crisis → administer octreotide
EXTRA INFORMATION
Carcinoid Syndrome
- Release of vasoactive substances into systemic circulation; characterized by cutaneous flushing, sweating, bronchospasm,
colicky abdominal pain, diarrhoea, right-sided cardiac valvular fibrosis (carcinoids confined to the GIT typically do not cause
carcinoid syndrome as vasoactive substances undergo ‘first-pass’ effect in liver, hence carcinoid syndrome is strongly
associated with metastatic disease)
- Diagnosis: elevated urinary 5-HIAA (5-hydroxyindoleacetic acid).
- Treatment: octreotide (causes gallbladder sludge) +/- interferon alpha (will usually require cholecystectomy if surgical
intervention is performed)
Small Intestine Lymphoma

- 30% of all GI lymphomas occur in the small intestine
- 3 subgroups:
▪ Immunoproliferative small intestinal disease lymphoma (IPSID): variant of extranodal marginal zone lymphoma of MALT;
secretes alpha heavy chains
▪ Enteropathy-associated T cell lymphoma (EATL): highly associated with gluten-sensitive enteropathy
▪ Others, eg diffuse large B cell, mantle cell, Burkitt, follicular
- Presentation:
▪ IPSID: abdo pain, chronic diarrhea, malabsorption, severe LOW
▪ EATL: acute bleeding, obstruction, perforation
- Ix & Tx: See gastric lymphoma section.
Small Intestine (Other Cancers)

- Leiomyosarcoma
▪ Rare, spread locally and metastasise early via bloodstream.
▪ Arise from leiomyomas, tumours of the smooth muscle that are especially common in the small intestine.
- Adenocarcinomas
▪ Rare compared to rest of GIT, but can occur in small bowel, esp in duodenum.
▪ Usually would have spread to regional LN or liver at presentation.
218
ENTERIC FISTULA15
Enteric / Enterocutaneous fistula is an abnormal connection between two organs (i.e. lumen of GI tract and skin)
- Abdominal discomfort / distention and tenderness
- Nausea / vomiting
- Fever, chills (is patient septic?)
- Enteric contents appear in the surgical wound (is the fistula controlled or uncontrolled?)
CLASSIFICATIONS
- Low output: less than 200ml / day
- Moderate output: 200 – 500ml / day
- High output: more than 500ml / day
Factors Predispose for Non-Closure

- Foreign Body, Radiation, Inflammation (i.e. inflammatory bowel disease) or infection (i.e. tuberculosis), Epithelialization of fistula
tract, Neoplasia, Distal Obstruction, Steroids [FRIENDS}
- High Output Stoma (> 500ml/day), Uncontrolled or Proximal Fistulas
INVESTIGATIONS
- Biochemical – FBC, CRP, U/E/Cr, Ca/Mg/Phos (assessment for sepsis, hydration status, electrolytes abnormalities)
- Radiological – CTAP (assessment for intra-abdominal sepsis, underlying pathology), gastrografin meal/follow-through (delineate
anatomy of the fistula)
MANAGEMENT
It involves a multidisciplinary approach from initial “damage control” and medical management followed by definitive surgical
management. A common acronym in management of ECF is SNAPP. Initial assessment should evaluate if the patient is septic, if the
fistula is controlled and what is the volume of the fistula. Surgical management is usually one of the last steps.
Sepsis
- CT imaging to identify intra-abdominal collections
- Antibiotics – any associated cellulitis / intra-abdominal sepsis (i.e. abscess or peritonitis)
- Percutaneous drainage of intra-abdominal abscess
Nutrition
- Fluid & electrolytes intravenous replacement – the aim is for patients to have no thirst or signs of dehydration
- Nutritional support – enteral or parenteral nutrition
- Reducing intestinal fluid losses (from stoma / fistula) – measure output of fistula
- Review meds – stop prokinetics, start anti-cathartics (i.e. loperamide, diphenoxylate (lomotil), somatostatin analogues (i.e.
octreotide), start high dose PPI to reduce gastric output
Anatomy (definition of fistula anatomy)

- Radiological contrast studies to assess bowel length, site of origin of fistula and anatomy of fistulous tract
- Delineate tract & assess for complications with CT scan (with oral and rectal contrast)
Protection of Skin
- Protect surrounding skin, small bowel output is caustic and can cause excoriation of skin around a stoma
Proposing a procedure to address the fistula / Planned Surgery

- Surgical intervention is usually delayed – definitive surgery should be deferred till nutrition optimization attained, sepsis
eradicated and maturation of adhesions has occurred
- Timing of surgery impacts on mortality rates and ECF recurrence rates. Minimum waiting time is ~ 6 week, though 6-12 months
waiting time is ideal
- Surgical Intervention – adhesiolysis, take down fistula, bowel resection ± anastomosis, ± stoma (if anastomosis is in area of
residual sepsis) ± feeding jejunostomy
15 uptodate: overview of enteric fistulas
219
MECKEL’S DIVERTICULUM
DEFINITION
Blind out-pouching of the antimesenteric aspect of the small intestine (ileum) that has all four layers of the small bowel wall (i.e. true
congenital diverticulum), covered with serosa
EMBRYOLOGY
- It results from incomplete obliteration of the vitelline duct / persistent remnant of the omphalomesenteric duct (connects mid-gut*
to yolk sac in the foetus) – usually obliterated by 7th week
- Vitelline duct abnormalities: presence of vitelline fistula a/w meconium discharge from umbilicus
RULE OF 2s
- 2 inches in length, 2cm wide,
- 2 feet (60cm) from ileocaecal valve
- 2% of the population
▪ No familial predisposition
▪ Increased prevalence in children with malformation of umbilicus, alimentary tract, nervous system, CVS system
- 2:1 (M:F)
- 2-6% becomes symptomatic
▪ Increased risk in (1) presence of ectopic tissue, (2) age <50yrs, (3) diverticulum length >2cm, (4) males, (5) broad based
diverticulum, (6) presence of fibrous bands
▪ < 50% of patients present with symptoms before 2 years of age
- 2 types of ectopic tissue (choristoma*)
▪ Gastric (60%) – gastric acid secretion can produce inflammation, peptic ulceration / bleeding, strictures with subsequent IO
▪ Pancreatic (6%)
▪ May have both types of tissue or other types (i.e. jejunal, colonic, rectal, hepatobiliary)
* Normal tissue in a foreign location

** The midgut loop develop into distal duodenum, jejunum, ileum, proximal 2/3 of transverse colon
*** The artery feeding the Meckel’s diverticulum is long, non-branching, originating from the SMA, transverse the mesentery towards the RLQ where it
terminates
PRESENTATION
- Asymptomatic: incidental finding during abdominal surgery or imaging
- Symptomatic:
▪ Hematochezia / Melena (most common in children): usually massive & painless, due to peptic ulceration
o GI bleeding due to Meckel is rare in adults > 30 years
▪ Intestinal Obstruction (most common presentation in adults):
o Recurrent Intussusception – Meckel’s diverticulum act as the lead point
o Volvulus
o Abdominal Wall Hernia – Littre’s Hernia (at inguinal (50%), femoral (20%))
o Meckel’s Diverticulitis – inflammation results in reduced luminal diameter
▪ Meckel’s Diverticulitis: may present exactly like acute appendicitis
▪ Chronic Peptic Ulceration: pain, although related to food, is felt around the umbilicus (diverticulum is midgut)
▪ Others: umbilical fistula, perforation etc.
▪ Tumour – most commonly carcinoid (76%), adenocarcinoma (11%), GIST (11%)
220
INVESTIGATIONS
Biochemical Investigations: depends on clinical presentation (i.e. intestinal obstruction / lower BGIT / meckel diverticulitis)
Imaging:
- Meckel’s Scan: Technetium-99m pertechnetate scan (detects gastric mucosa)
- Barium studies: small bowel enteroclysis
- CT angiography (for bleeding meckel’s diverticulum) – help detect signs of bleed (0.3ml/min)
- Contrasted CTAP not helpful as hard to distinguish Meckel’s diverticulum from small bowel loops
MANAGEMENT
- Asymptomatic16
▪ Detected on imaging: do not perform elective resection
▪ Detected during surgery: [controversial*]
o Resect in children up to young adulthood
o Resect in adult (<50yrs) – (higher risk for symptoms – age < 50, male gender, diverticulum length > 2cm and ectopic
features within a diverticulum (palpable abnormalities)17 – ?leave in-situ if have broad base and short length
o Do not resect in patients (> 50yrs)
* A systemic review in 2008 found higher early post-operative complication rates in patients undergoing resection of incidental MD vs those in whom it
was left in-situ (5.3% vs. 1.3%). Mortality from MD is very low (0.001%). Number needed to treat to prevent 1 death is 758 patients. Not advisable to
excise incidentally detected Meckel diverticulum in any age group18
- Symptomatic
▪ NBM, IV drip, correct electrolyte imbalance
▪ IO: treat as per small bowel intestinal obstruction algorithm
▪ Bleeding GIT: treat as per BGIT algorithm
▪ Diverticulitis: IV antibiotics + surgical intervention (open or laparoscopic)
o Broad base: wedge ileal resection with anastomosis
o Narrow base: resection of the diverticulum
16 uptodate: Meckel’s diverticulum

17 Ann Surg. 2005 Mar;241(3):529-33. [Important Paper]
18 Ann Surg. 2008 Feb;247(2):276-81
221
INFLAMMATORY BOWEL DISEASE19
DEFINITION
IBD is a chronic, relapsing, often debilitating disease. They are immunologically mediated diseases that arise due to dysregulated
immune response to commensal flora in a genetically susceptible host.
Crohn’s Disease (CD) Ulcerative colitis (UC)

Age Bimodal peaks at 15 – 30 and 50 – 60 years Bimodal peaks at 20 – 40 and 60 – 80 years
Gender Female Predominance Male Predominance

Mutation in CARD15 (NOD2) gene on Chr 16 (in 1/3 of
Genetics patients) – associated with ileal disease location (impairs a/w HLA B-27
innate immune response)
- Family hx – 10x ↑ risk in 1st degree relatives
- Drugs – NSAIDs, OCP, Antibiotics (increased risk) - Drugs – NSAIDs (increased risk)
- Diet – refined sugars, low-fibre diet - Diet – sugar, cola drinks
Risk Factors
- Infections – bacterial / viruses - Smoking (protective – induce remission)
- Smoking (more severe disease) - Appendectomy (protective)
- Appendectomy (increased risk)
- Abdominal pain, diarrhoea - Bloody Diarrhoea
Clinical
- Others: weight loss, fever, anemia, recurrent fistula, - Others: urgency, tenesmus, abdominal pain, fever (if
Presentation
fatigue, intestinal obstruction severe)
- Initial episode of UC20
- Entire GIT anywhere from mouth to anus
▪ 30-50% limited to recto-sigmoid
- Terminal Ileum (35%)
▪ 20-30% left-sided colitis
Bowel - Ileocecal region (40%)
▪ 20% pancolitis
involvement - 20 % have disease confined to colon
- Always affect the rectum (spreads proximally with
- 30% develop perianal disease
decreasing severity)
- Rectum characteristically spared – 40%
- Occasional terminal Ileum involvement (backwash ileitis)
Distribution Skip lesions with normal mucosa between Diffused, continuous
Transmural
Superficial ulceration
Inflammation Chronic Inflammation – lead to non-caseating granulomas
Acute-on-Chronic Inflammation – (non-granulomatous)
(35%) – epithelioid macrophages without central necrosis)
Fistula Frequent Absent / Rare
Fibrosis Marked, Strictures Mild to None
Gut Wall Thickened with narrowed lumen Thin with normal lumen diameter (lead pipe colon)
Macroscopic: extensive shallow ulcers, pseudopolyps and
Macroscopic: cobblestone appearance, deep ulcers and
mucosal bridges (regenerating islands of mucosa amidst
linear fissures +/- aphthous ulcers
shallow ulceration)
Microscopic: transmural inflammation (neutrophils,
Histopathology Microscopic: inflammatory pseudopolyps +/- luminal
lymphocytes, plasma cells and macrophages), non-
narrowing, inflammation limited to mucosal layer (neutrophils,
caseating granulomas, glands are preserved, crypt
plasma cells, eosinophils), crypt architectural distortion (crypt
distortion, irregular villous architecture (in terminal ileum)
abscesses, atrophy), Granulomata is not a feature
Slight increased risk of CRC Substantially ↑ risk of CRC – risk increases 1% per year after
Carcinoma Risk
Increased risk of small bowel lymphoma 10 years of the disease
Associated Ab ASCA: anti-saccharomyces cerevisiae antibodies p-ANCA: perinuclear antineutrophil cytoplasmic Ab

Mayo Score / Disease Activity Index
Severity Harvey Bradshaw severity index Montreal Classification
Modified Truelove and Witts Severity Index
*In 15% of patients with IBD, differentiation between UC and Crohn’s is impossible and these patients are classified as having indeterminate colitis.
EXTRA INFORMATION
Non-caseating Granuloma – sarcoidosis and crohn's disease a/w with non-caseating granulomas, tuberculosis a/w caseating granulomas
Inflammatory Pseudopoylp – extensive ulceration with sparing of mucosa island (common is sigmoid and descending colon)
Cobblestone Appearance – diseased tissue is depressed below level of interspersed spared mucosa
Creeping Fat – circumferential extension of the mesenteric fat around the small and large intestinal serosa, not reaching the antimesenteri c border
Crypt Architecture Distortion – colonic crypts have lost their parallel arrangement and can be branched, atrophy or distorted
Crptitis – presence of neutrophils within crypt epithelium
Crypt Abscess – presence of neutrophils within crypt lumina (more common in UC than CD)
Basal plasmacytosis – presence of plasma cells between the base of the crypt and the muscularis mucosae (early diagnostic feature of UC)
19 PACES for the MRCP 3rd Edition (Tim Hall)

20 uptodate: Clinical manifestations, diagnosis, and prognosis of ulcerative colitis in adults
222
CLINICAL PRESENTATION (Extra-Intestinal Manifestation)
Unrelated to - Sacroiliitis (18% but usually asymptomatic)
Joints
disease - Ankylosing spondylitis (rare)
activity Hands - Clubbing
- Anterior Nongranulomatous Uveitis (up to 10%)
Eyes
- Episcleritis, Iritis, Conjunctivitis
Perioral - Aphthous Ulceration (20% with CD)
Joints - Acute Arthritis – 20x higher incidence, improves with treatment of colonic disease
Systemic - Primary Sclerosing Cholangitis ~5% (UC) – only effective treatment is transplant
Manifestations Related to - Gallstones
disease Liver & biliary - Fatty Change (40-50%) & Liver Cirrhosis (2-5%)
activity tract - Amyloidosis
- Granuloma
- Cholangiocarcinoma – rare complication of long-standing IBD
Kidneys - Ureteric calculi (oxalate in CD, urate in UC)
- Erythema Nodosum (5-10%) – non-ulcerative
Skin
- Pyoderma gangrenosum (more common in UC) – ulcerative
Nutritional Deficiencies, Nutritional Deficiencies,
Complications Malignancy Risk, Malignancy Risk,
Perforation and Peritonitis Toxic Megacolon**
* Around 5% of patients with UC will develop PSC while 75% of patients with PSC are found to have concurrent UC
** Toxic Megacolon: triggered by administration of narcotic, anti-diarrheal, anticholinergic and anti-depressant, NSAID. In severe cases, involvement of
the muscularis propria lead to damage to the nerve plexus, resulting in colonic dysmotility, dilation, and eventual infarctio n and gangrene. Management
involves emergent surgery (abdominal colectomy with end-ileostomy)
MEDICAL MANAGEMENT
Crohn’s Disease (CD) Ulcerative colitis (UC)
Active Maintenance Active Maintenance
Oral prednisolone
5-ASA – high dose
Controlled ileal release 5-ASA
Mild-Mod Smoking cessation mesalazine
budesonide ? appendectomy
Steroids – oral prednisolone
Antibiotics
IV hydrocortisone KIV Antibiotics
Immunotherapy – Immunotherapy –
Mod-Severe Immunotherapy – IV with rectal hydrocortisone
azathioprine / MTX azathioprine, cyclosporine
azathioprine / MTX Surgery*
223
CROHN’S DISEASE
EPIDEMIOLOGY
- Bimodal distribution: affects young in the 2 nd & 3rd decades of life, with the second onset in the 5th & 6th decades of life
- Genetic association – Higher prevalence amongst Ashkenazi Jews & in cooler climates e.g. Scandinavia, UK, Germany, northern
USA
- Abdominal pain, fever, malaise / fatigue, LOW
- Mucus-containing, non-grossly bloody diarrhoea
- Crohn’s fistula
▪ colo-vesical fistula – faeces in urine/ pneumaturia,
▪ colo-ovarian fistula – faeces per vaginal/ PID
- Non-specific systemic: LOW, LOA, fever, fatigue, symptoms of anaemia, chronic malnutrition
- Sites of involvement: terminal ileum, cecum then small bowel then colon and rectum
Clinical Subtypes
1. Active ileal and ileocecal disease – most common
▪ RIF inflammatory mass or abscess formation: constant pain
▪ Small bowel obstruction (strictures): colicky pain + abdominal distention
▪ ± diarrhoea and/or LOW
▪ Damage to ileal mucosa can cause Vit B12 and folate deficiencies
2. Active Crohn’s Colitis
▪ Symptoms are similar to UC but frank bleeding is less common
3. Perianal Crohn’s Disease
▪ Skin Tags
▪ Fissuring (typically located in lateral position), fistula or abscess
▪ Incidence of perianal disease increases with more distal disease presentation
4. Others
▪ CD confined to mouth, stomach, duodenum or rectum only
- Usually normal +/- extra-intestinal manifestations
- Acute severe: fever, tachycardia, tender/distended abdomen
- Complications of Disease
▪ Nutritional Deficiency
▪ RIF mass
▪ Midline laparotomy scar – suggest previous surgery
▪ Perianal enlarged skin tags/ fistula/ abscesses, anal stricture
▪ Extra-intestinal Manifestation: clubbing, perioral aphthous ulceration, erythema nodosum, joint pain, fatty liver
- Complications of treatment (i.e. cushingoid features)
INVESTIGATIONS
- Diagnosis requires endoscopic biopsy and clinicopathological correlation)
- Ultrasound: for diagnosing ileal CD
- Contrast radiographic studies: assess location & extent of disease, look for strictures & fistulae
▪ Barium meal/follow through: small bowel series & enema (cobblestone)
▪ CT scan with oral & IV contrast
▪ MRI
- Endoscopy: look for typical features (i.e. skip lesions of ulcerated erythematous oedematous mucosa, pseudopolyps – see picture)
▪ Colonoscopy with tissue biopsy (non-caseating granulomas)
▪ OGD: upper GIT involvement
▪ Endoanal U/S (EUS): identify fistula tracts
224
MANAGEMENT
Non-Pharmacological
- Trigger Avoidance
▪ NSAIDs and antibiotics
▪ Smoking Cessation – improves maintenance of remission
- Nutrition e.g. TPN (may also aid closure of fistulae)
▪ Elemental Diet (amino acid and glucose)
▪ Polymeric Diets
▪ Vitamin Supplementation (in cases of malabsorption)
Pharmacological
Class Drug Action Remarks
Metronidazole Sepsis or bacterial overgrowth
ANTI-MICROBIAL
Ciprofloxacin Fistulating disease (perianal)
Budesonide*
9mg/day Budesonide is as effective as
CORTICOSTEROIDS Mild to moderately active CD
Prednisolone pred. with fewer s/e & superior to
to induce remission, not to use long-term
40-60mg/day mesalazine and placebo
IV hydrocortisone Severe disease
Sulfasalazine Active colonic disease but not s/e: rash, haemolysis, allergic
SALICYLATES 1g BD maintenance interstitial nephritis
5-Aminosalicylic Acid (5-ASA) Maintenance after surgical
Mesalazine
less beneficial for active CD than for active UC intervention not after medically Not useful in active disease
4g OD
induced remission
Immunotherapy Azathioprine** administered via IV have lasting
Maintaining remission
(IMMUNOMODULATOR) Methotrexate effects
Immunotherapy Infliximab Induction of response,
(BIOLOGICAL THERAPY) remission and maintenance Contraindications (sepsis, TB,
For CD non-responsive to steroids and/or Adalimumab therapy for patients with mod- cancer)
immunomodulators severe CD
* budesonide – have extensive first-pass metabolism in the liver and is a reasonable alternative to patients with active ileitis or right-sided Crohn's disease
(less systemic side effects)
** Immunotherapy (AZA) – onset of action is 6-12weeks, requires concomitant use of steroids
Surgical
- Avoid surgery until absolutely necessary (80% require surgery within 20 years of onset*) & when indicated perform bowel
preserving surgery as repeated bowel resections can lead to short gut syndrome
- Indications :
▪ Disease refractory to medical therapy (common)
▪ Serious complications of medical therapy
▪ Severe bleeding, perforation
▪ Intestinal obstruction due to strictures
▪ Fistulae
▪ Abscesses
▪ Toxic megacolon (failed to respond to medical therapy within 24hours)
▪ Malignancy
* in contrast, only ~ 20% of patients with UC will require surgery
- Elective Surgery
▪ Rectal Sparing – Total colectomy with ileo-rectal anastomosis
▪ Rectum Affected – Pan-proctocolectomy with end ileostomy
▪ Segmental resection of the affected segment (i.e. right hemicolectomy) but a/w higher recurrence rates
- Emergency Surgery (i.e. severe crohn’s colitis, perforation)
225
▪ Total abdominal colectomy with end Ileostomy (removes inflamed intestine with a simple operation that avoids a pelvic
dissection and the risks of an anastomosis)
▪ If small bowel resection is required, margins taken just beyond grossly evident disease
EXTRA INFORMATION
Perianal Disease
- Observe / Medical Therapy if asymptomatic
- Severe Disease – seton / fistulotomy
- Anorectal Vaginal Fistula – rectal advancement flap, possible colostomy
Symptomatic Small Bowel Strictures

- Strictureplasty (save bowel length)
- For long segment stricture (~50cm) consider side to side isoperistaltic enteroenterostomy
Cancer / High Grade Dysplasia / Multifocal Low Grade Dysplasia

- Pan-Proctocolectomy (Preferred to segmental resection as 14-40% will develop metachronous CRC, field change effect)
Surgery in Special Situations

- Incidental finding of IBD or acute ileitis (caused by Yersinia or Campylobacter) in patients with presumed appendicitis who
has normal appendix – remove appendix if cecum not involved (avoids future confounding diagnosis)
Screening for colorectal cancers21 → recommendations applies for both ulcerative colitis and Crohn’s disease
- The duration of disease is a risk factor for the development of colorectal cancer
- American Gastroenterological Association
▪ Colonoscopy after 8 years in patients with pancolitis
▪ Colonoscopy after 15 years in patients with colitis involving only left colon
▪ Repeat colonoscopy every – two years
- British Society of Gastroenterology
▪ Surveillance colonoscopy 10 years after onset of symptoms (done when disease in remission)
▪ Interval depends on severity and additional risk factors
▪ 5 yearly – no active endoscopic / histological inflammation, left-sided colitis, Crohn's colitis involving < 50% of colon
▪ 3 yearly – mildly active inflammation, post-inflammatory polyps, family history of CRC in 1st-degree relative ≥ 50years
old
▪ 1 yearly – moderately active inflammation, stricture in preceding 5 years, primary sclerosing cholangitis, family history
of CRC in 1st-degree relatives ≤ 50 years old

▪ 2-4 random biopsy of specimen every 10cm from entire colon should be sampled – cancer developing in context of UC arise
from area of flat dysplasia
▪ Post-colectomy surveillance colonoscopy – interval as above
21 uptodate: Colorectal cancer surveillance in inflammatory bowel disease
226
ULCERATIVE COLITIS
- Clinical spectrum – inactive phase to low grade active disease to fulminant disease
- Bloody Diarrhoea, lower abdominal pain, urgency, tenesmus
- Severe abdominal pain, bloody diarrhoea & fever consider ?fulminant colitis or toxic megacolon
- Physical findings – non-specific
Mayo Scoring System
Modified Truelove and Witts Severity Index22
- Infection / Infective Colitis (i.e. yersinia, tuberculosis)
- Colitis
▪ Ischemic colitis
▪ Microscopic colitis (watery rather than bloody diarrhoea)
▪ Radiation colitis
▪ Drug-induced colitis – usually due to NSAIDs
- Neoplasm (i.e. colorectal cancer, lymphoma)
- Diverticulitis
- Irritable Bowel Syndrome
- Chronic Pancreatitis and malabsorption
- Others: Celiac Disease, Sarcoidosis, Rectal Mucosal Prolapse
22 World J Gastrointest Pathophysiol. 2014 Nov 15;5(4):579-88.
227
INVESTIGATIONS
Diagnostic
- Endoscopy: look for typical features
▪ Flexible sigmoidoscopy with tissue biopsy: bleeding may occur with contact with a scope.
▪ Rectum is invariably involved
▪ Earliest manifestation = mucosal oedema, result in loss of normal vascular pattern
▪ DO NOT scope patient during acute flare as have high RISK OF PERFORATION
▪ If stricture present on colonoscopy – suspect malignant till proven otherwise
Supportive (looking for complications & assessing severity of disease)

- Blood tests
▪ FBC: anaemia, leukocytosis & thrombocytosis indicate more severe disease
▪ U/E/Cr: hypokalaemia & dehydration in prolonged diarrhoea
▪ LFT: hypoalbuminemia due to poor nutritional intake
▪ CRP, ESR: markers of severity
▪ Biochemical Markers: p-ANCA ↑ in UC, ASCA ↑ in CD
- Radiological
▪ AXR to evaluate colonic calibre (>5.5 cm is abnormal) – in long-standing UC, colon is foreshortened and lacks haustral
marking (lead pipe colon)
▪ CXR to rule out perforation (risk of perforation in acute disease)
228
MANAGEMENT
Medical
- Mild UC – topical anti-inflammatory therapy with 5-ASA enemas
- If there is no improvement, oral 5-ASA can be used as an alternative (combination of oral + enema 5-ASA is more effective)
- Severe UC – topical or oral corticosteroid (acute flares)
- Azathioprine used in patients refractory or dependent on steroids to control symptoms or maintain remission
- IV hydrocortisone is reserved for patients who do not respond to high dose of oral corticosteroids or if patient develops fulminant
colitis
- Severe, refractory UC, especially with perianal involvement – IV infliximab
Class Drug Action Remarks

Steroid suppositories or
distal colitis (topical treatment)
foam enemas
CORTICOSTEROIDS
Oral Prednisolone mild-mod disease
to induce remission, not to use long-term
IV & rectal hydrocortisone
severe disease
400mg OD
Sulfasalazine*
Reduce risk of
SALICYLATES 2g OD Induction and
developing colorectal
5-Aminosalicylic Acid, (5-ASA) Mesalazine** maintenance of remission
cancer
Relapse rate is reduced from 80% to 20% at (suppository or enema)
1 year Useful if have proximal constipation and
Olsalazine***
distal disease
Immunotherapy Azathioprine^ MTX is ineffective in
Maintenance after severe disease
(IMMUNOMODULATOR) Cyclosporine^^ UC unlike CD
Immunotherapy
Induction of response, remission and
(BIOLOGICAL THERAPY)
Infliximab^^^ maintenance therapy for patients with
For UC non-responsive to steroids and/or
severe UC
immunomodulators
Infection – clostridium difficile, shigella,
ANTI-MICROBIAL
salmonella, campylobacter, amoebiasis
EXTRA INFORMATION
* s/e of sulfasalazine – headache, nausea, agranulocytosis, SJS

** s/e mesalazine – nephrotoxicity | refractory distal disease might respond to mesalazine suppositories thrice weekly
*** s/e olsalazine – watery diarrhoea
^ azathioprine – measure thiopurine methyltransferase (TMPT) before initiating azathioprine – identify people at risk of bone marrow suppression
^^ cyclosporine – improvement apparent within 2 weeks of therapy, SE: nephrotoxicity, hirsutism and gum hypertrophy
^^^ Infliximab – although the aetiology of UC differs from that of CD, RCTs have demonstrated that infliximab is also beneficial for the tx of mod-
severe UC in patients who are either intolerant of or refractory to immunosuppressant agents or steroids, or those who are st eroid-dependent.
Surgical
- Indications (emergent)
▪ Acute fulminant colitis with acute abdomen (i.e. toxic megacolon, colon > 5.5cm)
▪ Impending Perforation (i.e. dilatation with thumb-printing or pneumatosis) or free/walled off perforation
▪ Acute fulminant colitis without acute abdomen (i.e. unremitting bloody diarrhoea)
- Indications (elective)
▪ Disease refractory to medical therapy with severe & extensive colitis (most common)
▪ Serious complications of medical therapy
▪ Malignancy – precancerous lesions or prophylactic risk reduction
▪ Debilitating extra-intestinal manifestation – i.e. thromboembolic complications,
- Surgical Options
▪ Emergent Procedure (toxic megacolon) – total abdominal colectomy + ileostomy with preservation or rectum: diseased
rectum left in-situ with resection & IPAA at a later date when the patient has regained health & steroids have been withdrawn
(as rectum is an extraperitoneal organ and dissection/resection takes a long time). Foley catheter used to decompress
rectum for 3-4 days
▪ Emergent Procedure (massive haemorrhage) – subtotal colectomy ± proctectomy (if bleeding from rectal mucosa)
▪ Elective Procedure – Panproctocolectomy with IPAA (ileo-pouch anal anastomosis): standard of care for patients with UC
who ultimately require colectomy. Avoid necessity for long term stoma.
▪ Alternative: Panproctocolectomy + End ileostomy or Pan-proctocolectomy with continent ileal reservoir (Kock pouch)
229
8. ANAL
HAEMORRHOIDS23
DEFINITION
Clusters of vascular tissue (i.e. arterioles, venules, arteriolar-venular connections), smooth muscle (i.e. Treitz muscle), and connective
tissue lined by the normal epithelium of the anal canal
RISK FACTORS
1. Decreased venous return / increase intra-abdominal pressure – pregnancy, prolonged constipation (low fibre diet), straining
2. Increase rectal vein pressure – obesity, prolonged sitting
3. Age – collagen of connective tissue fixing haemorrhoids to the anorectal muscular wall degenerates
* Incidence of haemorrhoidal disease is no greater in patients with portal hypertension than in the general population
PATHOPHYSIOLOGY
- Social
▪ Maintains continence – fibro-vascular cushions engorged during valsalva manoeuvres to aid in occlusion of anal canal
▪ Prevents inadvertent passing of gas – sub-epithelial sensory nerve endings in the fibro-vascular cushions helps discriminate
between solid / liquid and gas in anal canal
- Personal
▪ Painless defecation – engorgement of fibro-vascular cushions ensures dilatation of anoderm without tearing
Internal Hemorrhoids
- The most common presentation of haemorrhoids is rectal bleeding, pain, mucus discharge, pruritus, or prolapse.
- Painless fresh bright red PR bleeding after defecation: coating stools, bright red spotting on the toilet tissue, dripping in the toilet
bowl, not mixed with stools
- PR bleeding comes & go (as compared to CRC which persists and progress)
- Internal hemorrhoids are painless unless thrombosed, prolapsed with edema or strangulated
- Must exclude other causes of PR bleeding (i.e. colorectal cancer, colitis)
External haemorrhoids
- Asymptomatic
- Extreme pain secondary to acute local thrombosis: usually related to a specific event (i.e. after vigorous valsalva manoeuvre
such as physical exertion, straining at bowel movement)
▪ Rupture of vein in external haemorrhoidal plexus leading to tense hematoma formation.
▪ Patients presents as painful perianal subcutaneous nodule
▪ Pain increases / constant for 2-3 days, resolves with spontaneous reabsorption of clot, pressure necrosis of overlying skin,
gradual decompression of clot
▪ Occasionally erode the overlying skin which causes bleeding (pressure necrosis)
EXTRA INFORMATION
Pathophysiology for rectal bleeding and rectal prolapse

- Abnormal swelling of the anal cushions causes dilatation and engorgement of the arteriovenous plexuses. The engorged, thin
& friable anal mucosa is easily traumatized; leading to rectal bleeding that is typically bright red due to high blood oxygen
content within the arteriovenous anastomoses.
- The suspensory muscles get stretched and eventually lead to rectal prolapse. Prolapse leads to soiling and mucus discharge
(triggering pruritus) and predisposes to incarceration and strangulation.
23 Clin Colon Rectal Surg . 2011 Mar;24(1):5-13.
230
8. Anal_Last Updated 3rd June 2020
Complications
- Strangulation and Thrombosis
- Ulceration
- Gangrene
- Portal Pyaemia (septicaemia)
- Perianal sepsis
CLASSIFICATION
External Haemorrhoids Internal Haemorrhoids*
Origin Ectoderm: stratified squamous epithelium Endoderm: columnar epithelium of anal mucosa
Location Below the dentate line On / Above the dentate line
Autonomic nervous system
Innervation Somatic innervation (inferior rectal nerve)
(not sensitive to pin-prick sensation)
Can produce perianal pain by prolapsing and causing
spasm of the sphincter complex around the
May thrombose causing pain and itching,
Pain haemorrhoids,
Secondary scarring may lead to skin tag formation
Can also cause acute pain when incarcerated and
strangulated
Inferior rectal vein → Pudendal veins → Superior rectal vein →
Venous
Drainage Internal Iliac veins → Inferior vena cava Inferior mesenteric vein (Portal venous system)
Rich anastomoses exist between these 2 and middle rectal vein (porto-systemic anastomosis)
* Characteristically lie in the 3, 7 and 11 o’clock position (patient in lithotomy position – left lateral, right anterior & right posterior)
Banov grading for internal haemorrhoids

Grade Description Treatment
I Palpable, non-prolapsing + bleeding Lifestyle*, Stool softeners, Daflon
Above + Non-operative procedures
II Prolapse with straining and defecation, reduce spontaneously ± bleeding
(i.e. rubber-band ligation)
Protrude spontaneously or with straining, require manual reduction ±
III Above ± operative procedures (i.e.
bleeding
Ferguson haemorrhoidectomy, stapled
Chronically prolapsed, irreducible, often with dentate line released from
IV haemorrhoidectomy
internal position ± bleeding
* High-fibre diet, water, good stool habits
231
MANAGEMENT
External Hemorrhoids
- Acute Thrombosis
▪ 24-72 hours – treat by surgical excision (i.e. elliptical excision under LA) of the thrombosed vein outside the muco-cutaneous
junction with the wound left open (as clot is loculated, simple incision and drainage is not effective)
▪ 72 hours (i.e. pain improving, natural reabsorption of clot has started) – treat with non-surgical management, symptomatic
(i.e. sitz bath, stool softener & analgesia)
- External Haemorrhoids – perianal skin tag

▪ Symptomatic (i.e. interfering with anal hygiene) – excise under LA
Internal Hemorrhoids
Exclude other causes of rectal bleeding – i.e. colorectal carcinoma
Conservative:
Grade I - Lifestyle modifications → high fibre diet, adequate fluid intake, avoidance of straining during defecation
No prolapse, just - Medications → stool softener (i.e. lactulose, fybogel), daflon (phlebotonics)
prominent blood
▪ Usual doses: lactulose 10mls TDS PRN, Fybogel 1 sachet OM, daflon with tailing dose (i.e. 2 tabs
vessels
TDS x 4/7 then 2 tabs BD x 3/7 then 2 tabs OM)
- Systemic analgesics
Non-operative Procedure (in addition to conservative measures)
- Rubber band ligation (RBL)
▪ Outpatient treatment, suitable for grade II/III (success rate: 80-100% after 1 session)
▪ Treat each haemorrhoidal complex individually
▪ For grade II haemorrhoids, no difference between RBL and excisional haemorrhoidectomy
▪ Most patient should be able to return to work the day following the ligation procedure
▪ Contraindication – patient on anticoagulant (ASCRS guidelines)24
▪ Complications of RBL:
- Intense pain post-procedure (if placement is too close to dentate line)
- Urinary Retention
- Post-band bleeding (<1%) – occurs 3-7days post-banding (risk of bleeding ~ 25% (warfarin),
7.5% (aspirin or NSAIDs), warn patient that necrotic haemorrhoid would slough off in 3-5 days
with bleeding occurring at that time
- Perianal sepsis (1 in 15,000) – presents with pain, fever and urinary difficulty needs early
recognition and admission for removal of band with debridement of necrotic tissue, IV abx
Grade II - Failure of procedure (rubber band can’t go in, rubber band slips out), new occurrence,
recurrence, a large prolapsing haemorrhoid may require 2-3 repeat ligations 6 weeks apart to
Prolapse upon achieve the desired effects.
bearing down but
spontaneously
reduce
Other Alternatives
- Injection Sclerotherapy → suitable for acutely bleeding grade I/II haemorrhoids, esp. if on anticoagulants,
patients are immunocompromised / coagulopathic
- Infrared Photo-coagulation (IRC) → infrared light energy converted to heat which causes coagulation of the
vessels, tissue destruction and scarring
24 Dis Colon Rectum. 2018 Mar;61(3):284-292.
232
Operative Procedure
- For grade III haemorrhoids, excisional haemorrhoidectomy is superior to RBL,
- Surgical Excision Hemorrhoidectomy or Stapled Hemorrhoidectomy
EXTRA INFORMATION
Surgical Excision Hemorrhoidectomy

- Closed Haemorrhoidectomy (Ferguson) vs Open Haemorrhoidectomy (Milligan-Morgan)
- Under GA, anal canal examined, haemorrhoid cushion identified and excised (external anal skin & anoderm) with an
elliptical incision (dissected off sphincter mechanism), apex of haemorrhoidal plexus ligated (at dentate line) +/- closure
of elliptical defect
- Complications: urinary retention (~10%), bleeding (early – technical error, late [5-7days] – slough of suture line),
infection, sphincter injury leading to incontinence, anal stenosis (excessive excision of the anoderm)
Grade III Stapled Haemorrhoidectomy (Fixation Procedure)

- For uncomplicated 2 nd and 3rd degree internal haemorrhoids
Prolapse upon - Stapled haemorrhoidectomy vs. Conventional haemorrhoidectomy – less operating time (↓11mins), less painful
bearing down
(↓37%), less time off work (↓8.45 days), earlier return to normal activities (↑15.85 days), better wound healing, |
and requires
manual reduction increase in recurrence of haemorrhoids at 1 year, especially among grade IV haemorrhoids (5.7% vs. 1%, OR 3.48),
overall complication rates not significantly different25

- Other complications – faecal incontinence and rectovaginal fistula may result from inaccurate stapler placement
Acute Management of Grade 4 symptomatic haemorrhoids:

- Edema only → reduce size of haemorrhoids and arrange for prompt surgical consultation. Use a
hyperosmolar solution to reduce haemorrhoids size (i.e. gauze with lignocaine gel + cold water +
dextrose solution [or sugar] and daflon), aim to be able to manually reduce haemorrhoids back into anal
canal first before further surgical intervention.
Grade IV
Emergency haemorrhoidectomy for Acute Haemorrhoidal Crisis
- Severe disabling pain, Refractory bleeding,
Prolapsed and
- Gangrene, Necrosis & Ulceration are absolute indications for emergency haemorrhoidectomy
cannot be
manually
reduced
233
ANAL FISSURES
Anal fissure is a split in the anoderm (that is distal to the dentate line)
PATHOPHYSIOLOGY
- Most common aetiology of a primary anal fissure is Trauma (i.e. passage of hard stools)
- 90% occurs in the posterior anal midline and 10% occur anteriorly (but 25% in females), <1% occur off midline
- Tearing pain with defecation
- Severe anal spasm that last for hours after bowel movement
- Hematochezia (bright PR bleed on toilet paper or on surface of stool)
- Perianal pruritus and/or skin irritation
- Chronic anal fissure = symptoms lasting for more than 6-8 weeks
PHYSICAL EXAMINATION
- Acute: superficial tear (usually posteriorly) – if lateral (consider secondary causes
▪ Patients often unable to tolerate DRE / Anal Speculum
- Chronic: hypertrophied with skin tags and/or papillae (4 signs, not related to duration)
▪ Hypertrophic anal papilla (at proximal end, near the dentate line)
▪ Boat shaped – heaped up edges
▪ Exposing muscle internal sphincter
▪ Sentinel skin tag (at distal end of fissure)
SECONDARY ANAL FISSURE

- Crohn’s Disease (fissure in lateral position)
- Extra-pulmonary TB
- Anal Squamous Cell Cancer
- Anorectal Fistula
- Infections – CMV, HSV, HIV, chlamydia and syphilis
MANAGEMENT
- If a/w rectal bleeding: offer colonoscopy
- Atypical fissures: biopsy to rule out additional pathology
- Acute Fissure usually responds to medical treatment while chronic fissures more likely require surgery
- 90% of acute fissure will heal with medical mx because of good blood supply (within 1-2days)
▪ Lifestyle modifications (increase dietary fibre)
▪ Bulking agents & stool softener (i.e. fybogel & lactulose)
▪ Warm sitz baths
▪ Lidocaine (2%) jelly / analgesic cream
▪ Trial with rectogesic BD and lactulose for 2 /12
(if no healing of anal fissure occurs)

- Topical nifedipine / diltiazem ointment x6/52 , equivalent to GTN for efficacy with less adverse events
- GTN ointment: decrease anal resting pressure resulting in increased perfusion of anoderm – up to 30% suffer headache &
recurrence occur in ~50%
- Botulinum toxoid injection
Chronic fissure requires operation

- If they don’t heal, usually due to spasm of internal anal sphincter muscle → surgical management: lateral internal sphincterotomy
(LIS, right or left lateral) (90% successful)
- Recurrence and minor incontinence occur in < 10% of patients
234
ANAL FISTULA
DEFINITION
Anal fistulae are abnormal communications, hollow tracts lined with granulation tissue connecting the primary opening inside the anal
canal to a secondary opening in the perineal skin. They are usually associated with anorectal abscesses (obstruction of ducts leading
to infection).
EPIDEMIOLOGY
- 9 per 100,000/yr. (Western Europe)
- Commonly affect those in the 3rd – 5th decade of life
- Intermittent purulent discharge ± bleeding
- Pain – which increases till temporary relief occurs with pus discharge
Conditions associated with multiple anal fistulas:

- Crohn’s disease
- Unusual Infection (i.e. TB, Actinomycosis, Chlamydia, HIV)
- Systemic disease (i.e DM)
- Hidradenitis suppurativa
- Malignancy
- Radiation
- History of trauma to anal region
- Assess for external opening on perineum seen: may be open, covered in granulation tissue
- Assess for fibrous tract that can be felt underneath skin on DRE
CLASSIFICATION
Goddsall’s Rule
- For fistula within 3cm of the anal verge and posterior to line drawn through ischial spines if
▪ Anterior to transverse anal line: straight radially directed tract into anal canal
▪ Posterior to transverse anal line: curve tract open into anal canal midline posteriorly (at level of dentate line)
- Exception: anterior external opening is >3cm from the anal margin – such fistula usually tack to the posterior midline
Tracts closer to anal verge = simpler, shorter

Tracts further away = trans-sphincteric, long, high tracts
Note: for surgery – patients are sometimes placed in prone jack-kife position (mentally rotate above diagram by 180 deg)
235
Cryptoglandular Theory of Parks (Parks Classification)
Type Diagram Management
Intersphincteric
Fistulotomy
● The common course is via internal
● Division of the internal sphincter alone
sphincter to the intersphincteric space and
usually does not compromise faecal
then to the perineum.
continence
● 70% of all anal fistulae
● Base of the wound is curetted and left
● Other possible tracts include no perineal
open to heal by secondary intention
opening, high blind tract, and high tract to
lower rectum or pelvis.
Low:
Fistulotomy
● For patients who have good pre-op anal
sphincter function
Trans-sphincteric
High / anterior fistulae in women:
(Higher risk for post-fistulotomy incontinence)
● The common course is low via internal &
Conservative approach
external sphincters into the ischiorectal
fossa and then to the perineum.
1. Cutting seton
● Reactive suture / elastic placed through
● Other possible tracts include high tract
the fistula tract
with perineal opening and high blind tract
● Tightening of seton tie sequentially until it
cuts through the fistula tract
2. Partial fistulectomy & endoanal flap

3. Injection of fibrin glue
Supra-sphincteric
● The common course is via intersphincteric

space superiorly to above puborectalis Cutting seton
muscle into ischiorectal fossa and then to
perineum. Endorectal advancement flap
● Other possible tracts include high blind Sphincter reconstruction
tract (i.e. palpable through rectal wall
above dentate line).
● a/w drainage of ischiorectal abscess
Extrasphincteric
Endorectal advancement flap

● The common course is from perianal skin
through levator ani muscles to the rectal
Laparotomy & resection of involved intestinal
wall completely outside the sphincter
segment and curettage of fistula tract (for those
mechanism.
fistulae from more proximal sections of the
colon)
● Not related to sphincter complex
● a/w Crohn’s, CA, recurrent fistulas
236
Anatomy of Ischiorectal Fossa
- Lateral – fascia over obturator internus, pudendal (alcock’s) canal
- Medial – fascia over levator ani and external anal sphincter
- Anterior – urogenital perineum
- Posterior – sacrotuberous ligament covered by gluteus maximus
- Floor – skin and subcutaneous fast
INVESTIGATIONS
- Endoanal U/S (H2O2 aided for hyperechoic effect) – to view course of fistula tract – more accurate than Goodsall’s Rule
- MRI – able to visualise entire pelvis, beyond the sphincter complex (gold standard)
- CT/fistulography (in emergency situation) – for complex fistulas / unusual anatomy
MANAGEMENT
- Puborectalis is the key to future continence
- Low fistula = lay open with fistulotomy or fistulectomy but fistulotomy generally preferred
- High fistula = require 2 stage surgery and options are:
▪ Seton – loose vs. tight , done in extra and supra sphincteric
▪ Endorectal advancement flap can be considered
Fistulotomy (for simple, short tracts) – cut & lay open tract to heal
- A grooved probe is passed from the external to the internal opening and the track laid open over the probe
- Track is curetted to remove granulation tissue, the edges of the wounds are trimmed
- Wound may then be marsupialized
Fistulectomy – core along tract & remove tract entirely

- Coring out of the fistula with a diathermy cautery
Seton – for complex, long, high tracts

- Involves running a surgical-grade cord through the fistula tract so that the cord creates a loop that joins up outside the fistula
- Setons can be tied loosely (long term palliation, temporary measure before surgical treatment) or tightly (cut through tissue inside
the loop while scarring behind the loop)
- Uses
▪ Drain sepsis and allow for identification of the tract at subsequent operation (loosely tied)
▪ Seton as definitive procedure or in whom fibrosis is not desired (i.e. Crohn’s Disease, HIV)
▪ Cutting seton – skin overlying the fistula tract is opened and a seton is placed into the fistula tract and tied snugly – tightened
every 1 to 2 weeks allowing for pressure necrosis to cut through sphincter muscle (rarely used)
Ligation of Intersphincteric Fistula Tract (LIFT)

- Ideal for trans-sphincteric fistula with mature tracts
237
ANORECTAL ABSCESS
Abscess which arises from cryptoglandular infection (blockage of anal crypt) that results in suppuration
PATHOPHYSIOLOGY
- Infection of the anal glands in the anal crypts at the dentate line
- Initial abscess occurs in the intersphincteric space and can then spread:
▪ Superficial to the external sphincter → Perianal space
▪ Through the external sphincter → Ischiorectal space
▪ Deep to the external sphincter → Supra-levator space
- Pain & swelling in the perianal area – classically dull, aching or throbbing, worse on sitting down and with bowel movement
- Fever
- Erythematous, palpable swelling, fluctuant, subcutaneous mass near the anal orifice, indurated tender perianal swelling
- DRE: fullness in posterior anal canal (deep post-natal space abscess), exquisite tenderness (intersphincteric abscess)
ANATOMICAL CLASSIFICATION
- Perianal (60%)
- Ischiorectal (20%)
- Intersphincteric (5%)
- Pelvirectal / Supra-levator (4%)
- Others – submucosal, intermuscular
-
TREATMENT
- EUA & I&D of abscess (send pus for culture) - common bacterial = E.coli, staphylococcus
- Assessment of underlying fistula (~16-30% of patients will have an underlying fistula, 50% in crohn’s patient)
- Document any presence of internal opening – usually can leave alone in the acute setting (work-up subsequently if fistula persists)
- ± Antibiotics – indicated if the patient is (1) immunocompromised, (2) diabetes, (3) extensive cellulitis, (4) valvular heart disease.
(i.e. 5-10 days of augmentin or cipro/flagyl) following I&D associated with 36% lower odds of fistula formation 26
- Post-operatively: analgesia, stool bulking agents and stool softeners, sitz bath, shower spray
EXTRA INFORMATION
- Large Ischiorectal Abscess → multiple counter-incisions and Penrose drains placed between the incisions to allow for drainage
- Intersphincteric Abscess → transverse incision in anal canal (below dentate line posteriorly), plane between internal and external sphincter
exposed, abscess opened to allow drainage
- Supralevator Abscess → Internal Drainage
- Horseshoe Abscess → modified Hanley’s procedure27
COMPLICATIONS
- Sepsis
- Anal Fistula – 40% of patients develop a chronic fistula
26 Am J Surg. 2019 May;217(5):910-917.

27 Tech Coloproctol. 2009 Dec;13(4):301-6.
238
ANAL INTRAEPITHELIAL NEOPLASIA
Multifocal virally induced dysplasia of the perianal or intra anal epidermis which is associated with human papilloma virus (HPV
subtype 6, 11, 16, 18 – more commonly 16)
RISK FACTORS
- HPV infection (16 & 18) – a/w SCC
- HIV
- Anal Intercourse
- Immunocompromised patients
- History of genital intraepithelial neoplasia (VIN, CIN)
- History of extensive anogenital condylomata
GRADES
According to degree of dysplasia on biopsy – lack of keratocyte maturation and extension of proliferative zone from lower third (AINI)
to full thickness of epithelium (AIN III)
- AIN I / Low Grade Squamous Intra-epithelial Lesion (LSIL) : raised, similar to Anal Condylomata but has ability to regress
- AIN II / High Grade Squamous Intraepithelial Lesion (HSIL)
- AIN III / HSIL : 10% will progress to anal carcinoma in 5 years, does not regress
- Symptoms: pruritus, pain, bleeding, discharge
- AIN I lesions: raised, similar to anal condylomata
- AIN III lesions: flat, may be white/grey/brown in colour
- Presence of ulceration will suggest progression to invasive anal carcinoma
TREATMENT
- Patients will require HPV vaccination
- AIN III / HSIL: 6 monthly high resolution anoscopy (HRA) (using acetic acid / lugol iodine) + Local Ablation Therapy.
- Treatment involves topical immunotherapy, laser, cryotherapy, infrared coagulation and/or topical cytotoxic (i.e. 5-FU)
239
ANAL MALIGNANCIES
Anal Cancer is rare and accounts for 2% of all colorectal malignancy. The incidence of anal cancer is increasing.
CLASSIFICATION
- Anal margin (distal to dentate line*) vs. anal canal (proximal to dentate line)
- Perianal vs. intra-anal (cannot be visualized with gentle eversion of buttock)
* Lymphatic drainage distal to dentate line is to inguinal nodes
Over 80% of anal cancers are of squamous in origin (squamous epithelium of anal canal) and 10% are adenocarcinoma (glandular
mucosa of the upper anal canal, the anal glands and ducts)
- Epidermoid Carcinoma – (i.e. SCC most common)

- Adenocarcinoma
- Melanoma (1%) - lesion may mimic a thrombosed external hemorrhoids
- Lymphoma / Sarcoma
RISK FACTORS
- HPV infection (16 & 18) – a/w SCC
- HIV
- Anal Intercourse (33 x increased risk)
- History of genital warts
CLINICAL PRESENTATION (EPIDERMOID CARCINOMA)

- Patients predominantly present with pain and bleeding.
- Up to 25% of patients present with an anal mass.
- A small proportion present with pruritus and discharge.
- Advanced tumours may involve the sphincter mechanism causing faecal incontinence.
- In females, the tumour may invade anteriorly leading to a recto-vaginal fistula.
Clinical examination
- Anal margin tumours will appear as malignant ulcers,
- Anal canal tumours tend to be palpable as irredular indurated tender ulceration.
- Always do DRE to assess for sphincter involvement
Mode of Spread
- Anal canal cancer spreads locally in a cephalad/upwards direction, outwards into the anal sphincter and into the rectovaginal
septum, perineal body, scrotum or vagina.
- Lymph node metastases occur frequently starting from perirectal group then to inguinal, hemorrhoidal and lateral pelvic lymph
nodes. (i.e. 30% inguinal LN spread with tumour size > 5cm)
240
INVESTIGATIONS
- Examination under anesthesia (EUA) with biopsy of the anal mass for histological diagnosis (allows assessment of tumour,
involvement of adjacent structures and nodal involvement)
- MRI of pelvis for loco-regional staging
- CT TAP or PET-CT to stage for metastatic disease
- Biopsy or FNAC of groin nodes (if radical block dissection is contemplated) - although ⅓ of patients will have enlarged inguinal
lymph nodes only 50% will have confirmed metastatic spread
- Stage is based on AJCC TMN staging 7th edition
TREATMENT
- Chemoradiotherapy with 50.4Gy radiotherapy in 28 daily fractions with mitomycin C and 5FU (Nigro protocol).
- For all T2-T4 tumours, prophylactic low dose radiotherapy to clinically uninvolved lymph nodes (reduce risk of recurrence)
- Surgery Indications
● Examination under anesthesia to confirm diagnosis and assess extent of disease involvement,
● Local excision for small T1 (<2cm) tumours,
● Defunctioning stoma prior to commencement of oncological treatment.
● Salvage APR with end colostomy and myocutaneous flap is considered (if disease still present after chemoradiotherapy)
EXTRA INFORMATION
Anal Adenocarcinoma
- Adenocarcinoma within the anal canal are usually extensions of digital rectal cancers.
- Rarely, adenocarcinoma may arise from anal glandula epithelium or develop within a longstanding complex anal fistula
- Treatment for adenocarcinoma: abdominoperineal excision of rectum (APER)
Anal Melanoma
- Melanocytes can be found in the transitional zone of the anal canal
- Presents as blueish black soft mass, mimicking a thrombosed external pile
- Prognosis irrespective of treatment: extremely poor
- Wide local excision is the treatment of choice (APR confers no survival benefit over WLE). As the chance of cure is
minimal, radical surgery as primary surgery should be avoided.
- >5cm unlikely to respond to chemo-radiation, mets to inguinal LN = poor prognostic sign
- Melanoma = 5yr survival ~10%, median survival 18 months after diagnosis
241
PILONIDAL SINUS
Attributed to hair follicle in-growth and subsequent foreign body reaction
PRESENTATION
- Asymptomatic
- Abscess (also known as natal cleft cyst) = pain, swelling, redness
- Carcinoma (0.1% of patients with chronic untreated / recurrent pilonidal sinus) – present as ulcer, rapidly progressing, fungating
margins
RISK FACTORS
- Obesity
- Prolonged sitting
- Lack of exercise
- Greater amounts of hair around buttock region = Ingrown hair and curvature of buttock may increase area of sweat collection
and overlapping of hair to form tracts and cysts
- Positive family history
- Dermoid cyst
- Teratoma
MANAGEMENT
- Conservative – shaving / laser epilation & hygiene, hot compress, antibiotics
- Abscess: I&D, 60% of patient will heal without need for further surgical intervention
- Surgical Treatment of Choice: Wide Excision with flap closure (i.e. Karydakis) +/- hair removal to prevent recurrence
- Recurrent: complete sinus excision with primary closure / healing by secondary intention and obliteration of natal cleft either by
myocutaneous rotational buttock flap or cleft closure
242
9. LIVER
SURGICAL ANATOMY OF THE LIVER
LIVER ANATOMY
Divisions of the Liver

- The anatomical division of the liver lobes is demarcated by the falciform ligament which separate liver into right and left lobes
(left anatomical division: consists of segments II and III)
- The functional division (more practical in surgery) is demarcated by the plane of the gallbladder fossa and inferior vena cava
(Cantlie’s Line or portal fissure, also by the plane in which the middle hepatic vein runs)
* Ligamentum venosum – fibrous remnant of foetal ductus venosus

** Gallbladder lies under segment IV and V
Classification of Liver (Hemi-liver, Section, Sectors & Segments)

- The liver (~1.5kg) can be divided into 2 hemi-liver – right hemiliver (segment V – VIII) & left hemiliver (segment II, III, IV)
- The liver can be divided into 4 main sections (based on hepatic artery & bile duct)
▪ Right anterior section (segment V & VIII),
▪ Right posterior section (segment VI & VII),
▪ Left medial section (segment IV)
▪ Left lateral section (segment II & III) [sectionectomy]
- Alternative 4 main sectors (based on portal vein) – right anterior sector (segment V & VIII), right posterior sector (segment VI &
VII), left medial sector (segment IV & III) and left lateral sector (segment II)
- The liver can be further divided into 8 functional segments (Couinaud segments) that each has their own independent vascular
inflow, outflow, and biliary drainage [segmentectomy]
▪ The segments are divided by one transverse plane and three sagittal planes
▪ Segment I is the caudate lobe (3 sub-segments: spiegel lobe, paracaval, caudate process)
▪ Segments II to VIII are named clockwise
▪ Segment IV – sub-divided into IVa (cephalad) and IVb (caudad)
Ligaments around the Liver
- Bare Area – area on the posterior-superior surface of liver not covered by Glisson’s capsule
243
9. Liver_Last Updated 3rd June 2020
- Liver is held in place by several ligaments – can be divided in a bloodless plane to fully mobilize the liver to facilitate hepatic
resection
▪ Round Ligament (ligamentum teres) – remnant of obliterated umbilical vein
▪ Falciform Ligament – attach liver to anterior abdominal wall, extends to umbilicus (separates left lateral and left medial
segments)
▪ Left and Right Triangular Ligament
▪ Coronary Ligament
▪ Hepatoduodenal Ligament (porta hepatis)
▪ Hepatogastric Ligament
Arterial & Venous Blood Supply through the Liver

- The liver has two blood supplies – portal vein – 75% (confluence of splenic vein and superior mesenteric vein, IMV joins splenic
vein) and hepatic artery proper – 25% (branch of the coeliac trunk)
- The transverse plane is at the level of the main branches of the portal vein and divides the liver into an upper half and a lower
half (portal triad enters segment IV and V)
- The sagittal planes are formed by the three main hepatic veins
▪ Right hepatic vein – drains segment V, VI, VII and VIII (inserts obliquely into the IVC)
▪ Middle hepatic vein – drains segment IV as well as V and VIII
▪ Left hepatic vein – drains segment II and III (left & middle HV form a common trunk (95%) prior to entering IVC)
- Caudate lobe venous drainage is direct to IVC
Hepatic Artery
- Hepatic artery proper most commonly divides into the right and left hepatic artery
- Multiple anatomical variants exist (Michels Classification)
▪ Replaced right hepatic artery from SMA (10-15%)
▪ Replaced (or accessory) left hepatic artery from left gastric artery (3-10%)
▪ Replaced right and replaced left hepatic artery (1-2%)
▪ Completely replaced common hepatic artery from SMA (1-2%)**
Portal Vein
- Portal vein divides into the right and left portal vein branches, right bifurcate to the right posterior (VI & VII) and right anterior (V
& VIII), left have the transverse and umbilical portion (separates segment II from III & IV)
- Multiple anatomical variant exist (i.e. portal vein trifurcation or right anterior branch arising from the left portal vein)
Bile Duct
- Segment V & VIII drain via the right anterior sectoral duct (RASD) running more vertically into the right hepatic duct
- Segment VI and VII drain via the right posterior sectoral duct (RPSD) running more horizontally into the right hepatic duct
- Segmental bile ducts from II to IV unit to form the left hepatic duct
- The left and right hepatic ducts unite to form the common hepatic duct (CHD)
- On cholangiogram, right anterior ducts (RASD) are headed superiorly while right posterior ducts (RPSD) are headed inferiorly
- Multiple anatomical variants exist (i.e. RPSD draining into LHD (15%), RPSD, RASD and LHD forming a trifurcation (11%) etc.)
244
Functions of the Liver (physiology)
- Bile is diverted from liver into the gallbladder due to high tone in the sphincter of Oddi
- CCK stimulates contraction of gallbladder and release of bile into the duodenum
- Bile secretion is governed by 2 factors → enterohepatic circulation and gut hormones (i.e. CCK &
Bile Production
secretin)
- Bile acid important for solubilisation and absorption of fats – lack of bile leads to malabsorption of fats
and fat-soluble vitamins (A, D, E, K)
- Glycogenesis – glucose (delivered via portal vein) forms glycogen (stored)
Carbohydrate
- Glycogenolysis – In starvation, glycogen converted back to glucose
- Gluconeogenesis – In starvation, amino acids converted back to glucose
Protein
- Amino Acid Degradation – amino acids to ammonia then to urea
Metabolic Functions - Lipogenesis – glucose converted to glycerol + FFA forms TG (stored)
- Accumulation of lipid droplets in hepatocytes can lead to hepatic steatosis
Lipid
- Lipolysis – In starvation, TG converted to FFA + glycerol for gluconeogenesis
- Synthesis of lipoproteins and cholesterol
Lactate - Gluconeogenesis (Cori Cycle*) – Lactate → Pyruvate → Glucose
Clotting Factors & - Synthesises plasma proteins (other than immunoglobulin) such as albumin + clotting factors**
Protein Synthesis - Urea synthesized in the liver
- Activation of Vitamin D is a 2-stage hydroxylation process
Vitamin D activation ▪ Liver (first stage) hydroxylation to give 25-hydroxycholecalciferol then
▪ Kidney (second stage) 1,25-hydroxycholecalciferol
Detoxification - Detoxify peptide hormones, steroid hormones, catecholamines, drugs, toxins
- Stores vitamin A,D,E,K,B12
Vitamin &
- Stores iron, copper
Mineral Storage
- Central regulator of Iron Homeostasis – through synthesize of Hepcidin
- Kupffer cells (i.e. liver macrophages) in hepatic sinusoids remove bacteria (i.e. endotoxins
Phagocytosis
(lipopolysaccharides), old RBCs)
Haemopoiesis - In disease states (i.e. chronic haemolysis) extramedullary haematopoiesis can occur
* Cori Cycle: Lactate produced by anaerobic glycolysis in the muscles moves to the liver and is converted to glucose which then returns to the muscle
and is metabolized back to lactate
** all soluble coagulation factors are manufactured in the liver with the exception of factor VIII (endothelium), calcium, platelet factors and
thromboplastin
245
PORTAL HYPERTENSION
DEFINITION
Portal Hypertension is defined as the Hepatic venous pressure gradient (HVPG) ≥ 6mmHg (normal = 3-5mmHg). It is the pressure
gradient between the hepatic and portal vein. This pressure is not routinely measured in clinical practice as it requires an invasive
interventional radiology procedure.
- Portal HTN ≥ 10mmHg – high risk of gastroesophageal varices developing
- Portal HTN ≥ 12mmHg – high risk of variceal bleed and development of ascites
Normal portal flow rate is about 1-1.5L/min
ANATOMY
- Portal veins drain blood for the small intestines, large intestines, stomach, spleen, pancreas and gallbladder.
- The SMV and the splenic vein unite behind the neck of the pancreas to form the portal vein
- The portal trunk divides into 2 lobar veins
▪ Right branch drains the cystic vein
▪ Left branch drains the umbilical and paraumbilical vein (caput medusae in portal HTN)
- The left gastric (coronary) vein with runs along the lesser curvature of the stomach receives distal oesophageal veins
(oesophageal varices in portal HTN)
PATHOPHYSIOLOGY
Portal Hypertension: chronic increase in portal pressure due to mechanical obstruction of the portal venous system. It is almost an
unavoidable consequence of cirrhosis (characterized by bridging fibrosis, regenerative parenchymal nodules & disruption of liver
architecture) and responsible for many complications of CLD (see below)
Cirrhosis (1) architecture distortion (nodules compression sinusoids & active intra-hepatic vasoconstriction [↓NO]), increase in
resistance to portal blood flow, formation of portosystemic collaterals (2) high arterial pressure (splanchnic arteriolar vasodilation) on
low pressure venous system & insufficient portal decompression through collaterals (higher resistance), increased portal blood flow
(hyperdynamic circulation)
Ohm’s Law is V = IR | Poiseuille’s Law R=8hL/pr 4

- Flow (Q) = Change in Pressure (∆P) ÷ Resistance (R)
- Application in vascular flow where P = FR or P = F8hl/pr4
- Decrease portal vascular radius produce a dramatic increase in portal vascular resistance
↑portal pressure gradient (P) = ↑in resistance to portal flow (R) (intrahepatic & collateral) and ↑in portal blood inflow (F)
246
CAUSES OF PORTAL HYPERTENSION
Pre-sinusoidal Sinusoidal Post-sinusoidal
Massive Splenomegaly with consequent Severe right-sided HF
CIRRHOSIS
↑ in splenic vein blood flow (i.e. alcoholic and/or hepatitis B/C) Constrictive Pericarditis
Massive Fatty Change

Portal Vein Thrombosis Hepatic vein thrombosis
Hemochromatosis
(Budd Chiari Syndrome**)
Wilson’s Disease
Splenic Vein Thrombosis
Schistosomiasis IVC thrombosis
Caroli Disease
Congenital Atresia Congenital IVC malformation
Congenital Hepatic Fibrosis
** Budd Chiari = rare thromboembolic disorder of hepatic veins / IVC leading to post-sinusoidal portal HTN. Patient presents with
vague RUQ pain, postprandial bloating, anorexia then ascites, liver failure. Risk factors: prothrombotic states (i.e. MPD, OCP,
coagulopathies) – diagnosed with US/CT or MRI. Treatment: immediate anticoagulation, then percutaneous angioplasty ± stenting,
then TIPS, if all fails consider orthotopic liver transplant
INVESTIGATIONS
- Ultrasound (Liver & Spleen) – radiological findings:
▪ Dilated splenic and superior mesenteric veins ≥ 11mm
▪ Splenomegaly > 12cm
▪ Reduction in portal flow mean velocity <12 cm/second
▪ Dilated portal vein ≥ 13mm
▪ Porto-systemic collaterals – recanalization of the umbilical vein
▪ Other findings: ascites, nodular liver, portal/splenic/SMV thrombosis
COMPLICATIONS (PORTAL HYPERTENSION)

- Ascites
▪ Increased fluid shift (starling’s law) leads to increased lymphatic drainage from liver which overwhelms thoracic duct
capacity , percolation of hepatic lymph into peritoneal cavity
▪ Life-threatening complications: spontaneous bacterial peritonitis (SBP)
- Formation of portosystemic shunts (see below)

- Portal Hypertensive Gastropathy: gastric mucosal friability & dilated blood vessels, patients can present with UBGIT (treat with
BB and nitrates)
- Congestive Splenomegaly
- Hepatic Encephalopathy
▪ Secondary to hyperammonemia (neuro-toxin) exacerbated by portosystemic shunting
Region Name of clinical condition Portal circulation Systemic circulation

Gastro-oesophageal Oesophageal Branch Of Oesophageal Branch Of
Oesophageal Varices
Junction Left Gastric Vein Azygos Vein
Rectal Rectal Varices (Haemorrhoids) Superior Rectal Vein Middle & Inferior Rectal Vein
Paraumbilical Caput Medusae Paraumbilical Veins Superficial Epigastric Veins
Right, Middle Renal, Suprarenal, Paravertebral
Retroperitoneal (No Clinical Name)
& Left Colic Veins & Gonadal Vein
Intrahepatic Patent Ductus Venosus Left Branch Of Portal Vein Inferior Vena Cava
247
ASCITES
PATHOGENESIS (IN CIRRHOTIC PATIENTS)

- Progressive liver cirrhosis leading to obstruction of intra-hepatic vasculature which leads to
- Portal HTN develops resulting in ↑splanchnic NO released which leads to splanchnic vasodilatation
- ↓effective intra-abdominal blood volume – “tank is bigger but less full”
- Renal hypoperfusion which stimulate RAAS leading to ↑vasoconstriction & renal hypoperfusion*
- ↑aldosterone** leading to ↑retention of salt and water
* At risk of hepatorenal syndrome (HRS) 2 0 to altering blood flow and blood vessel tone in the kidneys
** Hence diuretic of choice in treatment of ascites in patients with liver disease is spironolactone (aldosterone antagonist) – which
decrease reabsorption of salt and water
- Progressive abdominal distension ± painless or abdominal discomfort
- a/w weight gain, SOB, early satiety, and dyspnoea
- Fever, abdominal tenderness, and AMS → suspect SBP
- Examine to confirm diagnosis
▪ Abdominal distension
▪ Flank dullness, shifting dullness (pathognomonic) → fluid thrill
▪ Eversion of the umbilicus – also check for hernias
- Examine for likely causes
▪ Peripheral stigmata of chronic liver disease and portal HPT or CLD
▪ Look for signs of hepatic decompensation – confusion or GI bleed
▪ Raised JVP + Peripheral oedema: Right Ventricular Failure (RVF)
▪ Cachexia, cervical lymphadenopathy
▪ Anasarca, think of possible nephrotic syndrome → tell examiner you would like to check urinalysis
SAAG ≥ 1.1g/dL SAAG <1.1g/dL
Liver Cirrhosis (81%) Malignancy: peritoneal carcinomatosis

Liver: Alcoholic Hepatitis, Massive Liver Metastases Infective: peritoneal tuberculosis
Heart: congestive cardiac failure, constrictive pericarditis Inflammation: Pancreatitis, Pancreatic Ascites
Budd-Chiari Syndrome Chylous Ascites^
Portal Vein Thrombosis Serositis
Idiopathic Portal Fibrosis Nephrotic Syndrome
SAAG = serum-ascites albumin gradient, the gradient correlates directly with portal pressure; those whose gradient is ≥ 1.1g/dL have portal HTN and
those with gradient of <1.1g/dL do not (accuracy 97%)
^ milky-appearing peritoneal fluid that is rich in triglycerides, develops when there is a disruption of the lymphatic system seconda ry to traumatic injury
or obstruction (from benign or malignant causes (i.e. lymphoma)
INVESTIGATIONS
- Biochemical – FBC, U/E/Cr, LFT
- Chest X-Ray (assess for pleural effusion) – diaphragmatic channel open up and transmit fluid
- Liver & Spleen Ultrasound / CT scan
- Peritoneal tap
▪ Therapeutic → relief of discomfort & diaphragm splinting from distension
▪ Diagnostic
- colour / appearance – clear, bloody, cloudy, milky
▪ clear / translucent yellow → cirrhosis
▪ bloody malignancy or traumatic paracentesis
▪ turbid / cloudy infection
▪ milky chylous ascites
▪ brown & if ascetic [Br] > serum [Br] ruptured GB or perforated DU
- cell count and differential (FEME)
- albumin – to determine SAAG
- total protein concentration
248
- amylase concentration (pancreatic ascites or bowel perforation)
- Microbiology – gram stain smear, culture (aerobic / anaerobic), cytology
- Others – LDH / TG / Glucose / TB culture / Br / proBNP
TREATMENT
- Conservative
▪ Low salt diet – 2000mg / day or 88mol/day
▪ Fluid restriction – only if serum sodium <125mmol/L
▪ Monitor weight and urine sodium regularly
- Pharmacological
▪ Diuresis – spironolactone ± furosemide
- Typical dose: 100mg spironolactone and 40mg furosemide OM (ratio 10:4) – max 400mg:160mg
- Solely ascites → use spironolactone, if concomitant pedal oedema then add furosemide
- ± Amiloride (if painful gynecomastia due to spironolactone)
▪ Antibiotics – if suspect spontaneous bacterial peritonitis (SBP)
- Fever & Abdominal Pain
- +ve ascitic fluid bacterial c/s
- ↑ ascitic fluid PMN ≥ 250cells/mm 3 (or ascitic fluid WBC > 500cells/mm3)
- IV ceftriaxone or oral quinolones (i.e. ciprofloxacin)
▪ Avoid or use with caution in patients with cirrhosis – propranolol / ACEi / ARBs / NSAIDs
- Therapeutic Paracentesis (i.e. coop-loop for tense ascites) + IV albumin 20% infusion
▪ Site: 2FB above and 2FB lateral to ASIS – perform under aseptic technique, LA, US-guided
▪ Insert a pigtail catheter via seldinger technique and connect to external drain – (i.e. 500ml Q6H into stoma bag)
▪ Administer approximately 8g IV albumin for every 1L of ascitic fluid drained
▪ Albumin infusion prevents paracentesis-induced circulatory dysfunction28 with risk of hypotension, recurrent ascites,
HRS and death – with albumin, large volume of ascites can be drained (i.e. 6-8L)
- Surgical – Liver transplantation and shunts (patients with liver disease)
▪ Transjugular Intrahepatic Porto-Systemic Shunts (TIPSS)
▪ Peritoneovenous shunt (Le Veen or Denver) – complication rates are high, ?impact on survival, ?improvement in QOL
- Treatment of underlying cause if possible
- Liver transplant for cirrhotic liver
EXTRA INFORMATION
Surgery in Cirrhotic Patients

- Umbilical Hernia
▪ Pre-operative control of ascites is essential
▪ Safe elective repair comparable to non-cirrhotic patients can be performed (but try to avoid surgery)
- Abdominal Operation (i.e. colectomy)
▪ High risk for patients especially in setting of advanced cirrhosis, ascites & clinically significant portal HTN (i.e. bleeding
oesophageal varices)
▪ Patients with ‘high’ MELD score (i.e. ≥ 15) – should undergo Transjugular Intrahepatic Portosystemic Shunt (TIPSS) prior
to performing major abdominal operation (wait for 2 -3 weeks after TIPSS) – reduce mortality
28 Hepatology. 2012 Apr;55(4):1172-81.
249
APPROACH TO HEPATOMEGALY
DEFINITION
Hepatomegaly refers to the abnormal enlargement of the liver. Patients can present with RUQ discomfort or palpable RUQ mass.
Majority of liver lesions are incidentally diagnosed during imaging investigations with the majority of the lesions being benign. A
detailed clinical history and examination should be performed.
History
- Symptomatology
▪ Asymptomatic
▪ Abdominal pain, fullness in RUQ, nausea, vomiting,
▪ Infective symptoms (i.e. fever)
▪ Symptoms of anemia (i.e. SOB, chest pain, giddiness etc.)
▪ Symptoms of obstructive jaundice (i.e. tea-coloured urine, pale stools, pruritus)
▪ Symptoms of portal HTN (i.e. any history of hematemesis / melena, abdominal distention from ascites, encephalopathy)
- Differential Diagnosis
▪ Benign Lesions
▪ Malignant Lesions (i.e. risk factors for liver cirrhosis, hepatitis screen, constitutional symptoms)

▪ Any previous surgeries? (i.e. liver / gallbladder surgeries)
▪ Any previous hospitalization history?
▪ Any previous history of any malignancy?
▪ Any previous radiological guided interventions (i.e. liver biopsy, drainage procedures)
▪ Any previous endoscopic procedure (i.e. OGD, ERCP, Colonoscopy)
- Drug History (i.e. OCPs, anabolic steroid use)

- Social History (i.e. alcoholic, smoking)
- Family History
- Travel History
▪ Any palpable organomegaly (i.e. liver, gallbladder, spleen)
i. Palpate and percussion to delineate the borders of the liver (is the liver hard and craggy or smooth enlargement?)
ii. Palpate the spleen, begin from RIF and proceed towards the left subcostal region
▪ Any abdominal tenderness, signs of peritonism
▪ Any abdominal distention, look for any ascites (i.e. fluid thrill, shifting dullness)
▪ Any abdominal scars (i.e. previous surgeries)
▪ Digital Rectal Examination
- Signs of Chronic Liver Disease

▪ Peripheral Signs (i.e. gynaecomastia, clubbing of fingernails, palmar erythema, flapping tremor, scratch marks, scleral
icterus, pallor, foetor hepaticus, lower limb edema)
▪ Abdominal Signs (i.e. presence of spider nevi, ascites, caput medusa)
- Signs of Portal Hypertension

▪ Splenomegaly & Ascites
▪ Caput Medusae
▪ Upper BGIT from esophageal varices (i.e. hematemesis and/or melena)
250
Physiological Riedel’s Lobe, Hyperextended Chest

Bacterial Pyogenic Liver Abscess, Tuberculosis
Infective Viral Hepatitis, EBV, CMV, HIV
Protozoa Malaria, Histoplasmosis, Amoebiasis, Hydatid , Schistosomiasis
Alcoholic Fatty Liver, Cirrhosis
Metabolic Wilson’s Disease, Haemochromatosis, Infiltration – amyloidosis
Malignant Primary / Secondary Solid Tumours, Lymphoma, Leukaemia
Vascular / Cardiac Right Heart Failure (RHF), Tricuspid Regurgitation (pulsatile liver), Budd-Chiari Syndrome
Hepatic Neoplasm
Haemangioma ~ 3-20%
Hepatic Adenoma
Benign Focal nodular Hyperplasia (FNH) ~ 8%
Bile Duct Hamartomas
Cyst – if multiple: familial (polycystic) or non-familial
Hepatocellular Carcinoma (or hepatoma)
Primary Cholangiocarcinoma (only 10% intrahepatic)
Malignant
Hepatic Angiosarcoma*
Secondary Colorectal, stomach, pancreas, breast, urogenital tract, lung
Hepatic Abscess
Pyogenic Abscess
Amoebic Abscess
Hepatic Cyst
Simple Cyst or Polycystic Liver
Non Parasitic Cyst Neoplastic Cyst
Cystic Malignancy
Echinococcal Cysts Cystic Echinococcosis or Alveolar Echinococcosis
Portal Hypertension
Cirrhosis
Intrahepatic Hepatic Fibrosis
Obstruction Hemochromatosis
Wilson’s Disease
Peri-hepatic Congenital Atresia
Obstruction Portal Vein Thrombosis / Portomesenteric venous thrombosis
Budd-Chiari Syndrome (hepatic vein thrombosis)
Post-hepatic Congenital IVC malformation
obstruction IVC thrombosis
Constrictive Pericarditis
* Hepatic Angiosarcoma is a/w exposure to vinyl chloride, arsenic, thorotrast, extremely aggressive tumour with poor prognosis – tumour cells
express CD 31, an endothelial cell marker
251
INVESTIGATIONS
- Biochemical
▪ Full Blood Count – any anemia, signs of infections
▪ Liver Function Test – presence of any hyperbilirubinemia, deranged liver enzymes
▪ PT/INR/APTT
▪ Tumour Markers (i.e. ALP, CEA, CA19-9) – useful if suspicious of malignancy
- Imaging
▪ Ultrasound Liver / Contrast-Enhanced Ultrasound
▪ Computer Tomography (Triphasic Scan – arterial, portal venous and delayed phases)
▪ MRI
- Endoscopy
▪ OGD / Colonoscopy – to rule out gastrointestinal primary tumours
EXTRA INFORMATION
Imaging Features of Common Hepatic Lesions

Lesion Ultrasound CT Scan MRI
Bright on T2-weighted imaging
Well defined smooth walls Water-dense
Simple Cyst ± proteinaceous density if prior
Posterior acoustic enhancement Does not communicate with biliary tree
haemorrhage has occurred
Homogeneously hyperechoic lesion Early peripheral nodular enhancement in
Bright on T2-weighted sequence
Haemangioma acoustic enhancement with sharp arterial phase, centripetal filling in,
(light bulb sign)
margins follows blood pooling
Solitary, well circumscribed Hypervascular enhancement on arterial
Hepatic Distinguished from FNH by presence
heterogeneous mass. phase & Iso/ hypointense on portal
Adenoma of fat; lack of central scar
Can be hypo or hyperechoic venous phase
Early arterial enhancement with
Doppler appearance of central feeding
centrifugal filling and sustained Hyperintense central scar on T2
FNH artery with tortuous spoke-wheel
enhancement in portal venous phase imaging
vascularity
Unenhanced scar may be present
Can be hypoechoic or hyper-echoiec.
Larger HCC are often heterogeneous Hypervascular enhancement on Arterial enhancement with rapid
HCC (liquefaction necrosis and fibrosis). A/w arterial phase and characteristic without +/- persistent rim
venous thrombosis of portal or hepatic portal venous washout enhancement
veins
252
LIVER HAEMANGIOMA
DEFINITION
Liver hemangioma are benign vascular lesions characterized by hamartomatous outgrowths of endothelium made of widened (dilated)
blood vessels rather than true neoplasms. Some of these tumours express oestrogen receptors.
EPIDEMIOLOGY29
- Prevalence 3% to 20%
- Female to male ratio 5-6:1 (middle-aged women)
- Most common benign liver tumour
- Majority diagnosed between 4th to 6th decade of life
PATHOGENESIS
- Vascular malformation that enlarges by ectasia, congenital in origin (poorly understood)
- a/w steroids, pregnancy, OCPs
PRESENTATION
- Usually asymptomatic, found incidentall
- Pain from liver capsule stretch (i.e. Glisson’s capsule – peritoneum that covers the liver) – nonspecific upper abdominal
fullness or vague abdominal pain (larger lesions, > 5cm)
- Mass effects compressing on surrounding organ
- Life-Threatening Haemorrhage – ppt. by needle biopsy (extremely uncommon)
- Congestive Heart failure from large arteriovenous shunt
- Kasabach-Merritt syndrome for large haemangioma – rare consumptive coagulopathy, thrombocytopenia (sequestration of
platelets and clotting factors in a giant haemangioma), treat with urgent resection (rare disease, usually of infants)
DIAGNOSIS
- DO NOT BIOPSY (risk of severe, fatal haemorrhage & low diagnostic yield)
- Imaging Investigations
- Ultrasound (accuracy 70-80%)
▪ Well circumscribed, homogenous, hyperechoic lesion
▪ Compressibility of the lesion is pathognomonic
- Computed tomography (CT) – triphasic CT

▪ Peripheral enhancement in arterial phase, centripetal filling on portal venous phase and retention of contrast on delayed
phase
▪ Contrast enhancement progress towards the centre [peripheral to central enhancement]
▪ Tumours appears brightest and uniformly enhanced in delayed phases
- Gadolinium-enhanced magnetic resonance imaging (MRI)

▪ Hyper-intense on T2-weighted images (“light bulb sign”)
▪ Peripheral nodular enhancement with delayer centripetal filling
TREATMENT
- Majority treated safety with observation (asymptomatic lesions < 4cm)
- For symptomatic or complicated lesions → surgical removal
▪ Enucleation under vascular control (intermittent Pringle manoeuvre)
▪ Formal anatomical resection (i.e. right hepatectomy)
- Large, unresectable lesions → low-dose radiation therapy or embolization
- Spontaneous Rupture (rare) → arterial angioembolization followed by definitive resection
29 The Washington Manual of Surgery (p346)
253
FOCAL NODULAR HYPERPLASIA (FNH) 30
DEFINITION
FNH is a benign tumour, nodular in appearance, characterized by a central stellate scar. It is considered a regenerative process
rather than a tumour resulting from arterial malformation.
EPIDEMIOLOGY / RISK FACTORS

- Second commonest benign liver tumour
- More commonly in females (6-8:1), aged 30 to 50 years
- Associated with arteriovenous malformations (AVMs), hepatic haemangioma, hereditary hemorrhagic telangiectasia
PRESENTATION
- Asymptomatic (incidental on imaging)
- Symptomatic: right upper quadrant pain
- FNH rarely ruptures or bleeds
DIAGNOSIS
▪ Bright homogenous arterial contrast enhancement with hypoattenuating central scar (central artery visualised in 20-30% of
patients)
▪ Isoattenuating in portal venous phase
▪ Delayed phase may show hyperattenuation of central scar
- Sulphur colloid scan – have kupffer cells, will take up sulfur colloid on liver scan
- MRI – central scar is hyperintense on T2 weighted images
TREATMENT
- Conservative Management (asymptomatic patients), FNH is not a precursor of malignancy
- Surgery (symptomatic patients) – liver resection preferred to enucleation as lesions is surrounded by veins)
254
HEPATIC ADENOMA31
DEFINITION
Hepatic adenomas are characterized by benign proliferation of hepatocytes – do not confuse with ’hepatoma’ which refers to HCC

- Female to male ratio 10:1 (found in young women)
- a/w: anabolic steroids, oestrogen & progesterone preparation (i.e. OCP)
PRESENTATION
- Asymptomatic
- Symptomatic: spontaneous rupture and intraperitoneal haemorrhage
▪ Between 25-35% will rupture with nearly 100% of ruptures occurring in lesions >5cm32
▪ 20 – 40% will experience spontaneous bleeding with an 8% risk of death
▪ Require close observation during pregnancy
▪ Others symptoms: abdominal pain, vague symptoms of fullness / discomfort in the RUQ
- Increased risk of malignant transformation (depends on subtype)
DIAGNOSIS
▪ Sharply defined borders
▪ More common in right lobe
▪ Homogenous enhancement during arterial phase with return to isodensity on portal venous and delayed phases (may be
difficult to differentiate from HCC)
- Sulphur colloid scan (cold) – no kupffer cells thus no uptake
- MRI – hypervascular tumour
- Histology – lack bile duct glands and kupffer cells, no true lobules, congested hepatocytes due to glycogen deposition
TREATMENT3334
- Conservative Management
▪ Consider in patients with small, asymptomatic lesions (<4cm) & discontinuation of OCPs
▪ Close observation with repeated imaging and AFP – consider surgery if fails to regress
- Surgical Resection* (for symptomatic lesions, lesions > 4cm-5cm, inability to rule out malignancy, male gender**)
▪ HA carries significant risk of spontaneous rupture with intraperitoneal bleeding (10-25%)
▪ Pregnancy predisposes to rupture – so resection prior to pregnancy is indicated
▪ HA carries risk of malignant transformation to well-differentiated HCC (~5%)**
▪ For patients with acute hemorrhage from HA, proceed to hepatic angioembolization followed by surgery
*Some authors recommend resection of all adenoma in males regardless of size (high risk of malignant transformation)
** Presence of androgen exposure independently influences HCC progression

32 Ann Surg Oncology 2009;16(3):640-648
34 Uptodate: hepatic adenoma
255
HEPATIC CYSTS
DEFINITION
Liver cysts are mostly asymptomatic with majority being incidentally detected on imaging.
CLASSIFICATION
- Nonparasitic Cysts (asymptomatic or symptomatic)
▪ Simple Liver Cysts (5-20%)
▪ Polycystic Liver Disease
▪ Neoplastic Cysts
- Echinococcal Cysts (most common Hydatid cyst)
- Asymptomatic → identified on imaging for other symptoms
- Symptomatic
▪ RUQ tenderness (Stretching of Glisson’s Capsule)
▪ Palpable Hepatomegaly
▪ Bleeding, Infection, Torsion, Rupture
▪ Mass Effect: compression of IVC, cholestasis due to compression of CBD, portal HTN, Gastric Outlet Obstruction
▪ Fistulation into duodenum
EXTRA INFORMATION
Non-parasitic Cysts
Clinical Presentation Management
- Congenital malformation when an aberrant bile duct loses - Asymptomatic: no further treatment
communication with the rest of the biliary tree and becomes - Symptomatic
progressively dilated ▪ Percutaneous aspiration with sclerotherapy
Simple Liver
- Serous cyst fluid (cysts do not communicate with the biliary system). ▪ Laparoscopic “unroofing”or fenestration of
Cyst
Instead, fluid is secreted by epithelial lining of the cyst) the cyst
- Complications: infection, intracystic hemorrhage, pain
- For complex cyst need to rule out neoplasm
- AD inheritance (AD-PLD mutation in Chr19, AD-PKD mutation in - Asymptomatic: no further treatment
Polycystic PKD1 (Chr 16) & PKD 2 (Chr 4). - Symptomatic
Liver - AD PKD with liver cyst: kidney cysts usually precedes liver cyst ▪ Laparoscopic “unroofing” of the cyst
Disease - Extrahepatic Manifestation: Cerebral Aneurysm ▪ Liver resection (with retention of least cystic
area of hepatic parenchyma)
- Cystadenoma - Suspected Cystadenoma
- Cystadenocarcinoma ▪ Formal resection or enucleation
- Intraductal papillary mucinous neoplasm of the bile duct (IPMN-B) - IPMN-B
▪ Surgical resection as up to 90% have high
Neoplastic
- Cystadenoma/ Cystadenocarcinoma are suspected (differentiated grade dysplasia and/or invasive carcinoma
Cysts
from simple cyst) based on imaging features such as internal
septation, mural nodules or projection, thick cystic wall, intracystic
debris, enhancing mural nodules, multilocular architecture
- IPMN-B communicates with the bile ducts which is seen on imaging
- Primary & Secondary Liver Cancer can demonstrate cystic features - For patients suspected with cystic malignancies,
Cystic
proceed with either biopsy or formal hepatic
Malignancy
resection
- Blunt trauma can result in intra-hepatic hematomas or bilomas – - Asymptomatic: no further treatment
develop into traumatic hepatic cyst - Symptomatic
Traumatic - Pseudocyst that lack an epithelial lining ▪ Percutaneous drainage +/- biliary
Cyst decompression (biloma)
▪ Laparoscopic fenestration of cyst +/- suture
ligation of the leaking bile duct (biloma)
256
EXTRA INFORMATION
Parasitic Cysts
Clinical Presentation Management
- Infestation with tapeworm of the genus Echinococcus Cystic Echinococcosis

▪ Cystic Echinococcosis, caused by E. granulosus - Percutaneous treatment of the hydatid cysts with the PAIR
(worldwide) (Puncture, Aspiration, Injection, Re-aspiration) technique
▪ Alveolar Echinococcosis, caused by E. multilocularis ▪ Injection of scolicidal solution(i.e. 95% alcohol or
(north america) hypertonic saline (15-20%))
▪ Risks → anaphylactic shock (spillage of
- Dogs are definitive hosts. Intermediate hosts (goats, sheep,
pigs) are required to complete its life cycle. Humans are echinococcus antigen), secondary echinococcosis,
dead-end hosts. chemical cholangitis, biliary fistula resulting from
- Patients can be asymptomatic for years, they are usually
incidentally detected on imaging. communication with biliary tree
- Infestation leads to hydatid cyst in various organs (i.e.liver,
lung, bone, kidney, spleen, CNS) - Surgery
▪ Radical – pericystectomy (total removal of cyst)
- Diagnosis ▪ Conservative – unroofing of cyst
Hydatid
▪ History of Hydatid Disease
Cysts
▪ Imaging → ultrasound (1st line) – thick wall, - Anti-infective drug treatment (albendazole +/- praziquantel)
- Watch and wait (for inactive silent cysts)
uni/multilocular with peripheral calcifications and
daughter cysts +/- CT and MRI imaging Alveolar Echinococcosis

- Radical Liver Resection vs. Liver Transplantation
▪ Serology → Immunoelectrophoresis or ELISA
▪ High Index of Suspicion
- FBC (elevated TW if cyst has become infected, may have

elevated eosinophils)
- LFTs (elevated bilirubin with elevated ALP suggest for cysto-
biliary communication)
- Classification – Gharbi Classification / WHO working group,

WHO classification
257
HEPATOCELLULAR CARCINOMA3536
EPIDEMIOLOGY
- Annual incidence in Singapore is 18 / 100,000 in males & 4.6 / 100,000 in females
▪ 4th most frequent cancer among males, not in top 10 among females (M:F = 2-3:1)
▪ 3rd most frequent cancer death among males and 4 th among females
- Worldwide: 6th most prevalent cancer and 4th most frequent cause of cancer-related death
- HCC diagnosed mainly in the fifth and sixth decade
- 1o liver cancers are mainly HCCs (85%), with a small proportion of intrahepatic cholangiocarcinoma (6%)
RISK FACTORS
- HCC develops within an established b/g of CLD in 70-90% of all patients
- HBV infection a/w increased risk of HCC because of DNA damage induced by HBV integration, hence, incidence of HCC reduced
with HBV vaccination
- In the setting of cirrhosis, the annual incidence of HCC approaches ~ 2-4%
1. Alcoholic Cirrhosis (5x↑risk)
2. Non-Alcoholic Cirrhosis
- Hepatitis – 70% of HCC
▪ Chronic Hepatitis B – high HBV DNA load, HBeAg positivity increase the risk
▪ Chronic Hepatitis C – accounts for 1/3 of HCC in the USA
- Non-alcoholic Steatohepatitis (NASH)* – 20x ↑risk37 or non-alcoholic fatty liver disease (NALFD)
- Autoimmune
▪ Primary Biliary Cirrhosis (with cirrhosis – i.e. stage 4 PBC, males higher risk)38 – 2-3x ↑risk
▪ Secondary Biliary Cirrhosis
- Chronic obstruction of the biliary tree (secondary to Primary Sclerosing Cholangitis) – usually cause
cholangiocarcinoma but can also cause HCC
- Recurrent infection in the biliary tree – recurrent pyogenic cholangitis
- Recurrent stricture formation (iatrogenic injury) – lead to secondary BC
- Metabolic
▪ Hemochromatosis – increased risk of between 20 to 219x39 (HH patients with HFE gene)
▪ Alpha 1 Antitrypsin Deficiency – 2-3x ↑risk
- Others
▪ Diet – red meat & saturated fats
▪ Aflatoxins B1 (mouldy peanuts / corn / soybeans / aspergillus) – linked with p53 mutation
▪ Diabetes – independent RF for HCC40 – 2-3x ↑risk
▪ Smoking
▪ Alcohol – synergistic effect in individuals with chronic HBV/HCV
- Not Risk Factors – Wilson Disease41 & Primary Biliary Cirrhosis (not proven)
* The yearly cumulative annual incidence of HCC in NASH cirrhosis vs. HCV cirrhosis was 2.6% vs. 4.0% (NASH is a significant risk
factor for development of HCC)
PBC – characterized by inflammation and granulomatous destruction of intrahepatic (interlobular) bile ducts, more common in
middle aged women presenting with pruritus, serology – (+) anti-mitochondrial antibodies
PSC – characterized by segmental inflammation and fibrosing destruction of intrahepatic and extrahepatic bile ducts (concentric
fibrosis around bile ducts with segmental stenosis – onion skin appearance), more common in young males with inflammatory bowel
disease
35 Lancet 2012; 379:1245-55 [Important Paper]

36 N Engl J Med . 2019 Jul 4;381(1):e2. [Important Review Paper]
37 Hepatology. 2010 Jun;51(6):1972-8.
38 Hepatology. 2009 Oct;50(4):1162-8.
39 Genet Med. 2009 May;11(5):307-13.
40 N Engl J Med 2011; 365:1118-27. [Important Paper]
41 J Gastroenterol Hepatol. 2015 Mar;30(3):535-9.
258
PATHOLOGY
- Pathogenesis involves a chronic inflammatory process or on-going hepatocellular damage with high cellular regeneration, leading
to increased rates of genetic mutation (i.e. TERT promoter) in the cells and accumulation of these mutations leading to carcinoma
formation
- Molecular Classification
▪ Proliferative Class → HBV infection, high tumour grade, high AFP, worse clinical outcomes
▪ Non-proliferative Class → HCV infection, alcohol abuse, low tumour grade, low frequency of vascular invasion, better clinical
outcomes
- Histological subtypes:
▪ Non-Fibrolamellar – associated with HBV and cirrhosis
▪ Fibrolamellar (FLC) – associated with younger patients (20-40 years old), equal gender distribution, no association with
hep B or cirrhosis, 70% resectable, good prognosis (5 yr. survival rate >70%)
Liver Cirrhosis
- End-stage of chronic liver disease characterized by 3 main morphological characteristics (1) bridging fibrosis (2) regenerative
parenchymal nodule and (3) disruption of liver architecture
- Patients with cirrhosis are at high risk of developing HCC → recommend 6 monthly US Liver & Serum AFP measurement
- A model to predict (3 month) prognosis in patients with cirrhosis is the Model for End Stage Liver Disease (MELD) score
▪ 3.8 x loge serum Br (mg/dL)
▪ 11.2 x loge INR
▪ 9.6 x loge serum Cr (mg/dL)
▪ 6.4 (constant for liver disease etiology)
- MELD score of 15 = 6% mortality at 3 months

- MELD was originally developed to predict mortality after TIPSS. Now, adapted for use in prioritizing patients awaiting liver
transplantation.
- Also, it has an expanding role in predicting outcomes in patients with liver disease in the non-transplantation setting
▪ With TIPSS best outcomes with score <14 and poor outcomes with score >24
▪ Post-op mortality risk increase by 1% with each MELD point increase up to 20 and by 2% for each MELD point increase
above 20
- In PELD (paediatric end-stage liver disease) – includes age, presence of growth failure & albumin instead of Cr
259
1. Asymptomatic
▪ During screening (ultrasound) for chronic hepatitis B carrier
▪ Incidental finding of liver nodule on imaging (i.e. CT or MRI)
▪ HCC need not present with decompensated chronic liver disease
2. Local signs & symptoms

▪ Upper abdominal pain – dull and persistent (2o to capsular distension) – Hepatomegaly
▪ Early satiety/ vomiting (likely 2o to compression)
▪ Constitutional: LOW, LOA, malaise (80% of patients)
▪ Pyrexia (central tumour necrosis)
▪ Jaundice (5-10%)
- Cholestatic: invasion/compression of intrahepatic ducts or extrahepatic compression by metastatic LN
- Hepatic: a/w pre-existing cirrhosis or acute flare of chronic hepatitis
▪ Budd-Chiari syndrome*: occlusion of the hepatic, intrahepatic or portal vein causing portal hypertension & congestive
hepatopathy which present as ascites
* Most frequently caused by haematological abnormalities – myeloproliferative disorders, polycythaemia vera. Other causes – OCP, collagen vascular
disease, disorder of coagulation cascade (protein C & S)
3. Tumour rupture (<3%)

▪ Severe abdominal pain (peritonism), pallor with shock [ddx: ruptured AAA, ruptured ectopic pregnancy]
- 50% mortality & risk of peritoneal seeding in survivors
- FAST +ve for free fluid in the abdomen, CT may show active contrast extravasation from tumour
4. Features of decompensated chronic liver disease

▪ Worsening liver function (hepatic encephalopathy, jaundice, coagulopathy – purpura, ascites – shifting dullness and fluid
thrill), spontaneous bacterial peritonitis, portal hypertensive bleed
▪ Hepatorenal syndrome in late stages of liver failure
5. Features of Portal Hypertension

▪ Ascites, LL oedema, haematemesis & melena 2 o to bleeding varices
▪ Congestive splenomegaly, secondary hypersplenism (can cause peripheral blood cytopenias), caput medusa, venous hum,
▪ Hepatic encephalopathy
6. Metastases (low incidence of HCC, mortality rarely from Mets)

▪ Bone pain, Dyspnoea
7. Paraneoplastic Syndromes
▪ Hypoglycemia (high metabolic demands of a tumour)
▪ Erythrocytosis (tumour produces erythropoietin)
▪ Hypercalcemia, watery diarrhoea etc.
260
EXTRA INFORMATION
Hepatorenal Syndrome
- HRS is a functional / reversible form of acute renal failure in a patient with advanced liver disease due to cirrhosis (or acute
liver failure, alcoholic hepatitis, metastatic liver disease) in the absence of identifiable renal pathology
- 2 types present
▪ Type 1 = rapid and progressive impairment of renal function, with doubling of initial serum creatine to > 221 in less than
2 weeks [median survival < 2 weeks]
▪ Type 2 = subtle course with serum Cr < 221, patient develops diuretic-resistant ascites [median survival ~ 6 mths]
- Pathophysiology
▪ Advanced Cirrhosis leads to portal hypertension & splanchnic arterial vasodilation
▪ The decreased vascular resistance leads to effective arterial hypovolemia which leads to renal hypoperfusion (sensed
by JGA to activate RAAS leading to constriction of the efferent arterioles in an attempt to improve GFR
▪ There is also progressive intense vasoconstriction of afferent arteriole leading to renal hypoperfusion
▪ Leads to ↓ GFR, ↓ urine o/p (<500ml/day) and ↓ urinary sodium excretion (<10 mEq/L)
- Initial therapy – octreotide, midodrine and vasopressin analogue, often progress to dialysis dependence
- Reversed by liver transplant even after dialysis dependence
Hepatic Encephalopathy
- Causes
▪ BGIT – high nitrogenous waste product for liver to metabolize, can preparate hepatic encephalopathy
▪ Infections – sepsis (i.e. spontaneous bacterial peritonitis, lung infection, urine infection
▪ Drugs – i.e. benzodiazepine, opioids, diuretics
▪ Electrolyte imbalances – i.e. sodium / potassium abnormalities (i.e. vomiting leading to hypokalemia)
▪ Others – i.e. high protein diet, constipation, catabolic state (i.e. surgery / trauma)
- Stages of Hepatic Encephalopathy (West Haven Classification)

▪ Stage 0: Lack of detectable changes in personality or behaviour
▪ Stage 1: Shortened attention span, impaired addition or subtraction, hypersomnia, insomnia or inversion of sleep pattern,
euphoria or depression, asterixis can be detected
▪ Stage 2: Lethargy, inappropriate behaviours, slurred speech, obvious asterixis
▪ Stage 3: Gross disorientation, semi-stupor to stupor, bizarre behaviours
▪ Stage 4: Coma
- Treatment42
▪ Lactulose – titrate to 2-3 stools / day (preventing NH3 uptake by converting it to ammonium)
▪ Low Protein diet (<70g/day)
▪ Branched-chain amino acids
▪ No antibiotics unless for specific infection
▪ Neomycin (get rid of ammonia-producing bacteria from gut)
42 The ABSITE Review (4th Edition) – pg 191
261
INVESTIGATIONS
I would like to perform investigations to obtain the diagnosis of hepatocellular carcinoma. Next, I would like to stage the disease
assessing for tumour burden, assessing for liver function and patient’s performance status. I would also perform investigations to
look for complications of the disease and for pre-operative assessment.
Diagnostic Approach43 [EASL guidelines – 2012]
A. Triphasic CT scan (with arterial and portal venous phase contrast imaging) – GOLD STANDARD
▪ Arterial Phase – early enhancement, lesions are hyper-dense relative to hypo-dense hepatic parenchyma (aorta [& HCC,
bleeds] lights up, IVC and portal vein are dark)
▪ Portal Venous Phase – most CT scans taken at this phase, majority of the contrast flow into portal vein and liver (liver is
bright), tumour will look dull (wash out) – tumour washout defined as hypo-density of a nodule in the delayed phase as
compared with surrounding hepatic parenchyma
▪ Delayed Phase – progressive decrease in contrast intensity of the lesion, scan may show a tumour capsule which is a
specific sign indicating HCC
- Radiological hallmark (HCC): arterial hypervascularity and venous/late phase washout

▪ Metastasis: enhancement in portal venous phase
▪ Haemangioma: capsular enhancement in delayed phase
- HCC has a tendency to invade the portal vein – an enhancing portal vein thrombus
- In a patient with hepatitis B/C and raised AFP, a liver lesion on imaging should be considered HCC until proven otherwise
- CT used to assess for tumour burden (i.e. solitary nodule vs. multiple nodule vs. bi-lobar involvement, macrovascular tumour
invasions, extrahepatic spread) & evidence of portal hypertension
B. Lipiodol contrast CT scan and/or hepatic angiogram with lipiodol

- Lipiodol will be retained in HCC even after many days as the HCC does not contain Kupffer cells to ingest lipiodol
- Hepatic angiogram may reveal abnormal blood vessels within the HCC
- CT scan of the liver weeks after lipiodol ingestion will pick up the areas of tumour (where the pre-lipiodol CT may not have
demonstrated the tumour clearly) – improve sensitivities (often used to evaluate effectiveness of treatment)
C. Alpha-FetoProtein (AFP) and Hepatitis Markers

- AFP has been dropped from the diagnostic scheme
- AFP levels (20 ng/ml) show sensitivity <80% and low specificity [not a good diagnostic test]
- A rise in serum AFP in a patient with cirrhosis should raise concern that HCC has developed
- False +ve: pregnancy, cirrhosis, hepatitis, teratoma, gastric cancer
- Hepatitis Markers to look for carrier status
D. MRI Scan (dynamic, contrast-enhanced)

- Most accurate imaging modality for distinguishing HCC from dysplastic or regenerative nodules in cirrhotic patients
- HCC appears highly intense on T2 images and low-intensity pattern on T1 weighted images
- Used if patient has contrast allergy (contraindication to CT scan)
- Adjunct investigation to be done when CT findings are equivocal
43 J Hepatol. 2012 Apr;56(4):908-43. [Important Paper]
262
E. Ultrasonography
- More often used in screening in setting of liver cirrhosis
- Contrast-enhanced ultrasound for detection of arterial enhancement in HCC
F. Histology
- If required, image-guided percutaneous biopsies used to obtain biopsy – pathological hallmark (HCC): stromal invasion
- Tissue diagnosis is not required before therapeutic intervention if other modalities favour HCC as the diagnosis
- Biopsy have risk of bleeding and needle tract seeding
Staging Studies
Assessment of Liver Function
A. Biochemical Assessment (Child-Pugh Score)

- LFTs + PT/INR/APTT
- (A)lbumin (B)ilirubin (C)oagulation (D)istension (E)ncephalopathy
▪ Class A = 5-6 points (better survival function) → surgical mortality 10%
▪ Class B = 7-9 (still amenable for resection) → surgical mortality 20-30
▪ Class C = 10-15 (not for resection – offer local ablative treatment) → surgical mortality 75-80
- Child Turcotte Pugh (CTP) score was originally developed for risk evaluation of portocaval shunting procedure in patients with
portal HTN. Also, it is used for estimating surgical risk in other intra-abdominal procedures performed in cirrhotic patients.
Points 1 2 3
Albumin (g/L) >35 28-35 <28
Bilirubin (μmoles/L) < 34 35-50 >51
(mg/dL) <2.0 2.0-3.0 >3.0
Coagulopathy (INR) <1.7 1.70- 2.3 >2.3
(PT – sec prolongation) <4.0 4.0-6.0 >6.0
Distension (ascites) None Slight - moderate Severe/refractory
Grade I – II Grade III-IV
Encephalopathy None
(suppressed with medication) (refractory)
Prognostication after Surgery

Child’s A(5-6) B(7-9) C( 10-15)
1 year survival % 100 80 45
85 60 35
2-year survival %
Significant functional Decompensated liver disease,
Disease status Well compensated disease
compromise consider transplant
Maximum resection of 2
Treatment in HCC Resection of up to 4 segments Consider transplant
segments
B. Indocyanine green (ICG) assessment

- Assessment of adequacy of post-resection hepatic function
- Assessing the percentage of ICG remaining in the liver after 15 minutes indicates the level of liver function.
- Normal liver should have < 10% of dye detectable at 15 mins
- Intravenous ICG administered and venous sample taken at 5, 10, 15, 20 minutes
C. CT volumetry / MR volumetry44
- Used to determine Future Liver Remnant (FLR)
- The FLR to standardized liver volume (SLV) is used as an indicator in predicting postoperative liver failure
▪ Normal Liver – FLR ≥ 20% of SLV
▪ Established Cirrhosis – FLR ≥ 40-50% of SLV

- Also have a role in selecting individuals for living donor liver transplantation
Patient’s Performance Status
D. ECOG performance scale

- 0 – fully active
44 Clin Radiol . 2014 Sep;69(9):887-95.
263
- 1 – restricted in physically strenuous activity, otherwise fully ambulatory
- 2 – ADL independent, up and about > 50% of waking hours
- 3 – ADL dependent (can only do limited self-care), confined to bed / chair > 50% of waking hour
- 4 – ADL dependent. Totally confined to bed / chair
Other Investigations
- FBC (low Hb from BGIT, raised TW in SBP, platelet value)
- U/E/Cr (dehydration, 3rd spacing of fluids, use of diuretics for ascites, r/o nephropathy for contrast imaging)
- PT/PTT, LFT
- GXM, ECG
- CXR (if CT thorax not done)
- CT TAP (if suspecting metastatic disease)
- OGD, colonoscopy (if suspecting hepatic lesions are liver metastasis)
MANAGEMENT
Summary of Management Algorithm (based on barcelona clinic liver cancer algorithm

(from N Engl J Med 2019; 380:1450-1462)
264
Summary of Treatment Modalities available for HCC management
- Curative
▪ Surgical Resection (+/- ablation)
▪ Liver Transplantation (Milan Criteria, UCSF criteria)
- Palliative
▪ Local – radiofrequency ablation, microwave ablation, thermal ablation, cryotherapy
▪ Regional – transarterial chemo-embolization (TACE), selective internal radiotherapy (Y-90)
▪ Systemic – Sorafenib / Lenvatinib
- Others – symptomatic treatment
1. CURATIVE SURGERY
- Surgical Resection is the treatment of choice for non-cirrhotic patients with HCC (solitary tumour at early stage (i.e. 0 or A)
- Only about 10-20% of patients with HCC will have disease amenable to surgery
- 5-year survival rates for patients with HCC treated with resection is 60% but with high recurrence rate 70%
1A. Hepatectomy
- For patients with cirrhosis is that there is already a “field-change” effect in the liver, thus a new tumour can still develop in the
remnant liver (high recurrence rates)
- Requires a fine balance between adequate resection margins (~1cm is adequate) and preservation of sufficient functional
liver (Child’s A, no portal HTN) to prevent postoperative liver failure
- Good immediate and short-term results, but not long term due to occurrence of new primaries in the cirrhotic liver
EXTRA INFORMATION
Post-operative Liver Assessment

▪ Vitals Signs & Urine Output
- Temperature (hypothermia, liver responsible for thermoregulation)
- Ensure adequate urine output (i.e. 30-40ml/hr)
▪ Judicious use of fluids
▪ Biochemical – FBC, RP, LFT, PT/INR, ABG, Lactate, Ca/Mg/Phosphate
- FBC (ensure Hb stable)
- LFTs (hyperbilirubinemia, transaminitis, hypoalbuminemia)
- INR (prolongation may develop, give FFP to keep INR < 2.0
- Lactate (hyperlactemia, liver responsible for converting lactate to pyruvate to glucose)
- Phosphate level (hypophosphatemia, phosphate needed for liver regeneration)
▪ POCT blood glucose (hypoglycemia, liver responsible for gluconeogenesis)
▪ Avoid Hepatotoxic Drugs
- May require change of dosage of pain medication (adjusted as ↓ clearance of hepatically metabolized drugs)
▪ Surgical Drain output (may be high due to increase ascitic fluid)
1B. Liver Transplantation

- Definitive treatment as it ‘cures” the underlying disease with replacement of the cirrhotic liver
- Most patients with HCC are not eligible for liver transplant (strict criteria)
▪ Milan criteria for transplantation (5-year survival of 60-80%)
- Single tumour ≤ 5cm, max 3 total tumours with none > 3cm
- No evidence of gross vascular invasion
- No regional nodal or distant metastasis
▪ Expanded Criteria – University of California, San Francisco (UCSF) criteria (5 year survival 60-70%)
- Used in Singapore
- Single tumour <6.5cm, max 3 tumours with none >4.5cm & cumulative tumour size <8cm
- MELD score (see above)
- Due to lack of availability of donor organ, consider “bridging therapy” with RFA, TACE, Y-90 to shrink disease and prevent
progression until donor's liver is available (avoid potential drop-out)
265
EXTRA INFORMATION
Factors affecting resectability
1. Stage of Disease
- Metastatic disease is not suitable for resection &
- Multicentric disease affecting both lobes is a contraindication to hepatectomy
2. Liver function pre-operatively

- Cirrhotic patients have increased risk of postoperative mortality (4-14%) compared to non-cirrhotic patients (0-4%) due to
complications such as liver failure, bleeding and infection
- If patient has cirrhosis, assess Child’s status → Child’s A and good Child’s B can still undergo resection
- Use indocyanine green (ICG) to ascertain extent of resection
▪ < 10% remains after 15 minutes – able to tolerate major liver surgery (normal liver)
▪ ≥ 15% remains after 15 minutes – contraindication for major resection (≥ 3 segments removed)
▪ ≥ 20% remains after 15 minutes – contraindication for resection of ≥ 2 segments

▪ ≥ 30% remains after 15 minutes – contraindication for resection of ≥ 1 segment
▪ ≥ 40% remains after 15 minutes – contraindication for any liver resection (predictor of post-op liver failure)
- CT volumetry (if ICG sub-optimal): residual liver function calculated with a CT liver via a computer programme (assess FLR)
3. Residual liver function postoperatively (i.e. future liver remnant (FLR)

- Dependent on tumour size and how much of the liver it takes up, as tumour is non-functional (a large tumour taking up most
of the liver segments being resected translates to smaller amount of functional liver tissue being resected, while a small tumour
means that more functional tissue is removed with the same resection margins)
- FLR requirements: > 20% of pre-operative liver volume in patients with normal liver, > 30% of pre-operative liver volume in
patients with early disease liver, and >40% in patients with well-compensated cirrhosis
- If insufficient liver volume, portal vein embolization can be performed to the right or left (rare) half of the liver in hope of
obtaining compensatory hypertrophy of the contralateral side. (wait for 3 – 4 weeks before resection to allow for compensatory
hypertrophy to occur
4. Degree of portal hypertension

- Resection of the liver results in worsened portal hypertension since the effective portal venous capillary bed has decreased
leading to increased resistance to flow
5. General fitness for operation
2. PALLIATIVE THERAPY
2A. Local
- Radiofrequency ablation (RFA) – best results for loco-regional strategies [suitable for tumours 2 – 5cm]
▪ Option for patients with early-stage HCC not suitable for resection or transplant
▪ Can also be for downstaging tumours with subsequent liver transplant
▪ A needle electrode is placed in the tumour, destroying tissue by heating it to temp of 60 to 100 deg – coagulative necrosis
▪ Larger tumours (>2.5cm) will require more than one deployment of electrode
- In tumours < 2cm, ethanol ablation and RFA have equivalent outcomes (comparable with surgical resection)
- In tumour > 2cm efficacy of RFA is better than ethanol ablation, however, RFA is inferior to surgical resection
▪ Contraindication – tumour at hilar plate, bile duct unable to tolerate heat and biliary stricture / fistula are potential
complications of thermal injuries
- Percutaneous ethanol injection (PEI)
- Microwave / Thermal Ablation
- Cryotherapy / Cryoablation
2B. Regional
- Trans-arterial chemoembolization (TACE) [best suited for tumours between 5 – 7cm]
▪ Selective intra-arterial administration of chemotherapeutic agents followed by embolization of major tumour artery
▪ Enter from groin (femoral artery) with guide-wire going up to the aorta (look for celiac axis) and then enter hepatic artery
▪ Inject contrast will light up tumour (neovascularization which appears as corkscrew organised vessels)
▪ Adjacent non-tumour liver tissue is protected from TACE (blood supply mainly from portal vein)
▪ Contraindications – portal vein thrombosis, decompensated cirrhosis)
▪ Complications
266
- Fever (secondary to cytokine release as a result of tumour lysis), abdominal pain, nausea, vomiting
- Deranged LFTs – raised ALT and AST (reflection of ischemic hepatitis) – hepatic failure due to infarction of adjacent
normal liver (TACE should not be used for Child’s class C cirrhosis)
- Trans-arterial embolization (TAE)
- Selective Intrahepatic Radiation – Yttrium-90 radioactive beads injected into hepatic artery, irradiating the tumour which induce
tumour necrosis
2C. Systemic
- Limited results – Sorafenib, 200mg BD, (multi-kinase inhibitor) improves median survival and time to radiologic progression by 3
months compared to placebo (10.7 months vs. 7.9 months) – SHARP trial45
- Combining TACE with systemic drugs (i.e. sorafenib) does not improve survival
PROGNOSIS
- Without treatment, HCC has a very poor prognosis with median length of survival of 3 to 6 months after diagnosis
- Even with treatment, estimated 5 year survival is 18% (second most lethal after pancreatic cancer)
45 N Engl J Med. 2008 Jul 24;359(4):378-90.
267
SECONDARY LIVER MALIGNANCY (NON-COLORECTAL)
DEFINITION
Secondary liver malignancy referring to metastatic liver tumors (90%) are more common than primary liver tumors (10%) due to the
dual blood supply of the liver. Of which, colorectal cancer is the most common cause of secondary liver malignancy. Colorectal liver
metastases are detected in 20-25% patients as synchronous lesions and up to 40% as metachronous lesions. Other causes of
secondary liver tumour malignancy can be divided into neuroendocrine and non-neuroendocrine malignancies. For colorectal liver
metastases, refer to the topic on colorectal cancer.
CLASSIFICATION
Neuroendocrine Liver Metastases
- Gastrointestinal origin → Foregut, Midgut, Hindgut
- Pancreatic origin → Functional (i.e. gastrinoma, insulinoma, glucagonoma, VIPoma) or Non-functional
Non-colorectal, Non-neuroendocrine Liver Metastases

- Breast, Melanoma, Urogenital, Testicular, Ovarian, Adrenals, Gastrointestinal (i.e. pancreas, stomach, bile duct) etc.
Metastasis to liver parenchyma Metastasis to porta-hepatis lymph nodes
- Incidentally detected during follow-up - Obstructive Jaundice (i.e. scleral icterus, tea coloured
History - Fullness in RUQ, RHC pain, urine, pale stools)
- Constitutional Symptoms (i.e. LOW / LOA)
Physical - Hard, Irregular, Nodular Hepatomegaly - Jaundice presents early and is proressive
Examination - Jaundice is a late sign - Hepatomegaly may not be present
Investigations - LFTs shows both obstructive and deranged liver enzymes - LFT shows obstructive picture
- Liver failure (extensive metastasis) with ascites and - Biliary Obstruction
coagulopathy
Complications
- Rupture of Liver Tumour
- Infected Liver Metastases with Abscess Formation
INVESTIGATIONS
- Biochemical Investigations: FBC, Renal Panel, LFT, PT/INR/APTT, Relevant Tumour Markers
- CT Liver (Triphasic)
▪ Hypodense on arterial phase (metastases are hypovascular compared to hypervascular HCC; spread via portal vein)
▪ Increasing contrast uptake on portal venous and delayed phases
MANAGEMENT
Patients presenting with metastatic disease to the liver should be discussed at a multidisciplinary tumour board and referred to
medical oncologist. Prognosis is usually guarded once secondary liver metastasis is present as it is a representation of systemic
disseminated disease. Management is usually palliative except in selected cases.
EXTRA INFORMATION
Colorectal Liver Metastases

- Liver Resection is recommended as tumour biology of metastatic colorectal cancer may be more favourable. Secondly, colorectal cancer
spreads to the liver via the portal venous system with the tumour cells entrapped in the liver preventing systemic spread. In contrast, non-
colorectal liver metastasis represents systemic tumour spread hence less favourable prognosis.
Neuroendocrine Liver Metastases

- Hepatic Resection if primary tumour and regional disease are resectable
- While R0 resection is favourable, R0 vs R1/R2 resection did not result in difference in overall survival. Cytoreductive hepat ic resection of at
least 90% volume hepatic resection can be considered for patients who require extensive resection. While R0 resection is a/w lower recurrence,
the overall frequency of recurrence is 60-80% at 5 years and 100% at 10 years. Hence, removal of a large volume of normal liver with extended
resection may limit future therapeutic options.
Non-colorectal, Non-neuroendocrine Liver Metastases

- The role of hepatic resection is not well established, hence, not recommended
- Increasing role in patients with GIST, Breast, Ovarian, Renal & Melanoma
268
HEPATIC ABSCESS (PYOGENIC)
DEFINITION
Pus-filled area in the liver (usually in the right lobe, 2:1)* occurring secondary to other sources of bacterial sepsis – possible organisms
includes: klebsiella, E. coli, proteus vulgaris, streptococcus milleri/faecalis, staphylococcus epidermidis, bacteroides fragilis. Bilateral
involvement in 5%, more often on the right due to anatomical consideration – right receive blood from both the superior mesenteric
and portal veins and right have greater hepatic mass.
RISK FACTORS
- Diabetics (10x ↑ risk), immunocompromised patients
- Underlying hepatobiliary pancreatic disease
- Elderly
PATHOPHYSIOLOGY (5 Routes of Infections)

- Biliary Tree: direct spread of bacterial from biliary system infections (ascending cholangitis, empyema of gallbladder) – 60%
- Portal Vein: Intra-abdominal source – acute appendicitis, diverticulitis, IBD – Crohn’s disease, pancreatitis, pelvic abscess
- Direct trauma: External inoculation – iatrogenic (radiofrequency ablation), traumatic
- Hepatic Artery: spread in sepsis e.g. infective endocarditis
- Adjacent organ infection
- Spiking Fever with chills (90% of patients), daily spiking fever
- Abdominal Pain (RHC pain due to capsular stretch) – 50-75% of patients
- Jaundice, and Hepatomegaly – 50% of patients
- Nonspecific symptoms – anorexia, anemia, weight loss (possible malignancy), pain radiating to shoulder, cough/hiccups
(diaphragmatic irritation), malaise, diaphoresis
INVESTIGATIONS
Biochemical
- FBC (leukocytosis – marker of inflammation)
- CRP / ESR / ± Procalcitonin → trend the values to monitor for treatment response
- LFTs – deranged (marker of severity)
- Renal Panel (urea and Cr – assess hydration status and fitness for contrast CT scan)
- UFEME – check for pyuria
- Blood / Pus Culture – i.e. Klebsiella & E.coli
- Tumour Markers (AFP, CA19-9, CEA – may resemble infected tumour on imaging)
- HbA1c – assess for underlying diabetes mellitus
Imaging
- Chest X-Ray (erect, anterior-posterior) – practical for anyone > 40
▪ Elevation of right hemi-diaphragm
▪ Infiltration at right lung base
▪ Right-sided pleural effusion
- Ultrasound Hepato-biliary System (HBS) – exclude liver tumour
▪ Septations, hypoechoic rim
- CT scanning (definitive diagnosis) – exclude liver tumour (usually first line investigation)
▪ Findings: Irregular lesion with central area of necrosis, air-fluid levels, may be multiloculated.
▪ Rim-enhancing appearance on triphasic CT scan.
Diagnostic
- Percutaneous Drainage + send pus for cultures
▪ Most commonly in local setting (Klebsiella Pneumoniae)
▪ Gram –ve bacilli (i.e. klebsiella) and enterococci suggests biliary tree source
▪ Staphylococcus or Streptococcus milleri suggest haematogenous seeding
- Amoebic serology, PCR Stool ova, cysts and parasites – suspicious for amoebic abscess if patient recovering from
chemotherapy or have recently travelled to an endemic area in the preceding 6 months.
- ± Melioidosis Serology
269
MANAGEMENT
1. Resuscitate if necessary
2. Close monitoring of vitals with strict IO charting
3. Watch for complications – i.e. klebsiella endophthalmitis
▪ Especially in patients with diabetes along with K. pneumoniae induced pyogenic liver abscess complaining of ocular
symptoms = requires prompt eye referral
4. Long-Term Antibiotics +/- via PICC (for abscess < 3cm)

▪ Empirical antibiotics – IV ceftriaxone 1gm 12 hourly + metronidazole 500mg 8 hourly
▪ Change to definitive antibiotics when blood c/s results return
▪ Total duration of 4-6 /52 (IV or oral, count from date of drainage)
5. Drainage
▪ Drainage if >3cm – open, laparoscopic or percutaneous
▪ Anatomical surgical resection can be performed in patients with recalcitrant abscess
6. Colonoscopy
▪ Patients >50yrs with DM & K Pneumoniae PLA (w/o apparent underlying hepatobiliary disease) → colonoscopy to r/o
colonic malignant lesions46

▪ Incidence of GI cancers (i.e. colonic, small intestine, biliary tract & pancreatic) was increased 4.3 fold among patients with
PLA compared with controls47
Percutaneous Drainage Open drainage (OD)

- Radiologically guided - Gold standard of care
- Can be done under LA - Invasive procedure, done under GA
- May require multiple attempts if unable to completely drain - Single procedure
pus (either tube blocked by necrotic tissues or presence of - Not dependent on location
septations)
- Drains are left in place until drainage becomes minimal Indications:
- Concomitant pathology requiring surgery e.g. gallstones
Contraindications: - Multiple abscesses or multiloculated abscess
- Ascites (pus can leak into peritoneal cavity) - Immunocompromised patient
- Uncorrected coagulopathy - Failed percutaneous drainage (tube blocked, or patient not
- Proximity to vital structures getting better)
- Ruptured abscess
Laparoscopic Drainage (LD)
Laparoscopic drainage of liver abscesses may be an alternative to open surgical drainage minimizing the adverse effects of open
surgery and yet maximizing the efficacy of surgical drainage. It is associated with shorter surgery duration, less blood loss, faster
recovery and hence shorter hospital stay compared to OD.
.
46 Colorectal Dis. 2012 Dec;14(12):e794-801.

47 Gastroenterology. 2014 Jan;146(1):129-37.e1.
270
HEPATIC ABSCESS (AMOEBIC)
DEFINITION
Hepatic amoebic abscess is caused by liquefaction necrosis. The cavity is full of blood and liquefied liver tissue (“anchovy sauce”)
EPIDEMIOLOGY
- 7-10 times more frequent in adult men
- Amoebiasis caused by protozoan Entamoeba histolytica (exist as infective cyst stage and a trophozoite stage (cause invasive
disease)) – haematogenous spread from gut (form colonic ulcers) via portal vein (travel hx is IMPT)
- Transmission is faecal-oral (humans are principal host)
- Travellers returning from an endemic area (present within 8-20 weeks)
- Persistent Fever
- Right Upper Quadrant Pain – may be referred to epigastrium, right shoulder
- ± Diarrhoea (suggestive of intestinal amoebiasis) – in <1/3 of patients
- Hepatomegaly and point tenderness over liver – in 50% of patients
- Jaundice – occurs in <10% of patients
- Complications: rupture of abscess causing peritonitis
DIAGNOSIS
- US / CTAP – confirm presence of liver abscess (rounded lesion abutting the liver capsule, without rim enhancement of pyogenic
abscess)
- Serum Antibody Testing – present in > 90% of patients, to confirm causative organism (Entamoeba histolytica)
MANAGEMENT
- Metronidazole (very responsive) – 750mg oral TDS or IV 500mg QDS, 7-10 days (contraindicated in pregnant patients)
- Needle Aspiration (not routinely done) – performed if patient not responsive to antibiotics
▪ Aspirated material – proteinaceous debris and an anchovy paste (fluid of necrotic hepatocytes)
▪ Culture of abscess often sterile, protozoa exist only in peripheral rim
- Intraluminal agents – paromomycin, iodoquinol, diloxanide furoate
COMPLICATIONS
- Bacterial Superinfection
- Erosion into surrounding structures
- Free Rupture into peritoneal cavity
- Complicated case – mortality as high as 20%
271
10. PANCREAS & SPLEEN
ANATOMY OF THE PANCREAS
DEFINITION
Pancreas is a retroperitoneal structure, located behind the stomach, between the duodenum and spleen
EMBRYOLOGY
- Developed from the dorsal and ventral buds (with the bile duct), ventral bud rotates around the 2 nd part of the duodenum (bringing
the bile duct over to the left side of the 2 nd part of the duodenum), majority of main pancreatic duct (duct of Wirsung) from ventral
bud and accessory duct (duct of Santorini) from dorsal bud.
- Main Pancreatic Duct – segment of the dorsal duct proximal to the dorsal-ventral fusion point
- Duct of Wirsung – segment in ventral duct between dorsal-ventral fusion point, terminate at Ampulla of Vater (surrounded by
sphincter of Oddi)
- Duct of Santorini – portion of the dorsal duct distal to the dorsal-ventral fusion point, drains anterior and superior portion of the
head, terminate separately at lesser papilla
ANATOMY48
- Head: lie within c-shaped concavity of duodenum, uncinate process extends to the left behind the superior mesenteric vessels
(SMV)
- Neck: lie in front of the portal vein and overlie origin of SMV
- Body: runs upwards and to the left across the midline
- Tail: passes forward in the splenorenal ligament (vulnerable to damage in splenectomy), anterior to left adrenal gland contacting
hilum of spleen
48 Nat Rev Cancer. 2002 Dec;2(12):897-909.
10. Pancreas & Spleen_Last Updated 3rd June 2020

272
Pancreas is comprised of separate functional units
- Endocrine (consists of specialized cell type organised into compact islet embedded within acinar tissue)
▪ Endocrine Function – Alpha (glucagon), Beta (insulin and amylin), Delta (somatostatin), PP/Gamma (pancreatic
polypeptide), Epsilon (ghrelin)
▪ Alpha cells – located mainly in body / tail (dorsal pancreatic bud) – typical location of glucagonomas
▪ Beta / Delta cells – evenly distributed throughout pancreas
▪ PP cells – located mainly at head / uncinate process* (ventral pancreatic bud) – higher incidence of pancreatogenic DM
after whipples vs. distal pancreatectomy
- Exocrine (consists of acinar cells and duct cells)

▪ Acinar cell
- Synthesize pancreatic protease as inactive proenzymes, stored as intracellular zymogen granules (i.e. trypsinogen &
chymotrypsinogen) → Trypsinogen is activated by Enterokinase (duodenal mucosal cells) to TRYPSIN.
Chymotrypsinogen and additional trypsinogen is activated by trypsin
- Pancreatic amylase & lipase (active) → secrete these digestive enzymes [in response to cholecystokinin (CCK)]
- Others: ribonuclease, deoxyribonuclease, elastase
▪ Epithelial ductal cells – secrete mucus and bicarbonate [in response to secretin] – pH: 8.0-8.5
EXOCRINE PANCREAS
- Protein digestion
▪ Endopeptidase (hydrolyse interior peptide bonds of polypeptides & protein)
- Trypsin*
- Chymotrypsin
- Elastase
▪ Exopeptidase (hydrolyse exterior peptide bonds of polypeptides & protein)
- Carboxypeptidase A
- Carboxypeptidase B
- Fat digestion
▪ Pancreatic Lipase: hydrolyse triglyceride into free fatty acid & 2-monoglycerides
▪ Co-lipase: increases activity of pancreatic lipase
▪ Cholesterol ester hydrolase: cleave cholesterol ester into free cholesterol & fatty acid
▪ Phospholipase A2: hydrolyse phospholipids
- Pancreatic Amylase
- Others – deoxyribonuclease & ribonuclease
* Trypsin (active form), from trypsinogen (inactive form) – enzyme: enterokinase. Trypsin can then auto-activate trypsinogen as well
as activate chymotrypsinogen, pro-elastase & pro-carboxypeptidase
- Physiology of enzyme secretion

▪ Peptide and fatty acid from food trigger release of CCK
▪ CCK induce the release of pancreatic enzymes into the duodenum lumen

273
BLOOD SUPPLY
- Celiac artery give rise to splenic artery* (tail) & superior pancreaticoduodenal artery (head)
▪ Splenic Artery → Dorsal pancreatic artery, Great pancreatic (pancreatica magna) artery & Transverse pancreatic artery
▪ Superior Pancreaticoduodenal Artery (via gastroduodenal artery) → Anterior and Posterior branches (anastomose with
inferior pancreaticoduodenal arteries)
- Superior Mesenteric Artery → inferior pancreaticoduodenal artery** (head)
▪ Inferior Pancreaticoduodenal Artery → Anterior and Posterior branches (collateral circulation)
- Venous drainage (head & uncinated) via the pancreaticoduodenal veins → posterolateral surface of portal vein (there are usually
no anterior venous tributaries and a plane can be developed between the neck of the pancreas and the portal and superior
mesenteric veins during pancreatic resection
* Splenic artery runs superior to pancreatic body while splenic vein runs posterior to pancreatic body
** First branch of the SMA
* Greater omentum derives arterial supply from omental branches from right and left gastroepiploic arteries

274
ACUTE PANCREATITIS49
DEFINITION
Acute pancreatitis is defined as a reversible pancreatic parenchymal damage of varying severity owing to an acute inflammatory
disease of the pancreas. Its clinical presentation is diverse ranging from mild to severe with potentially life threatening conditions.
The diagnosis of acute pancreatitis requires 2 of the following 3 features:

1. Abdominal pain consistent with epigastric pain (acute onset of a persistent, severe, epigastric pain often radiating to the back)
2. Serum lipase / amylase activity of at least 3x greater than the upper limit of normal
3. Characteristic findings of acute pancreatitis on CECT, MRI or trans-abdominal ultrasound
EPIDEMIOLOGY
- In 80% of patients, acute pancreatitis is mild and resolves without serious morbidity – 1% mortality
- The remaining 20% of patients develop a severe form of acute pancreatitis with local and systemic complications associated with
mortality rates as high as 40%50
- Death is bi-modally distributed:
▪ Early: within 1/52; due to severe organ failure
▪ Late: most common cause is infected pancreatic necrosis with resultant sepsis leading to multi-organ failure
RISK FACTORS
- Gallstones & Alcohol are the 2 most common causes for acute pancreatitis which accounts for 60-80% of cases
- Metabolic causes (i.e. hypertriglyceridemia, hypercalcemia), Malignancy (i.e. pancreatic or periampullary tumours), Viral Infection
(i.e. mumps), drugs (i.e. steroids) and iatrogenic (i.e. post-ERCP) accounts for 10% of the cases
Causes of Acute Pancreatitis (I-GET-SMASHED)

1. Idiopathic (15-25%)
2. Gallstones (40-70%)
3. Ethanol (25-35%)
4. Trauma
5. Steroids
6. Mumps and other infections (i.e. mycoplasma, viral hepatitis (i.e. hepatitis B), parasitic infection (i.e. ascaris lumbricoides)
7. Autoimmune (increase in IgG4)
8. Scorpion toxin and other toxins (i.e. organophosphates poisoning)
9. Hypertriglyceridemia, hypercalcaemia(metabolic causes)
10. ERCP (2-5%)
11. Drugs (1-2%) – Antibiotics (i.e. Sulfamethoxazole-trimethoprim, Metronidazole), Immunosuppressive (i.e. Azathioprine) Mood Stabilizers (i.e.
Valproic Acid) Diuretics (Furosemide/Thiazide), ACE inhibitors (i.e. enalapril),
12. Others:: Neoplasm, Congenital (i.e. pancreas divisum), Familial pancreatitis (SPINK1, failure to express normal trypsinogen inhibitor)
PATHOPHYSIOLOGY
- Acute pancreatitis is caused by unregulated activation of trypsin within pancreatic acinar cells, activating pro-enzymes leading to
auto-digestion (liquefactive necrosis of pancreatic parenchyma) and an inflammatory cascade that both amplifies the local
inflammatory response and can result in a progression to SIRS
- Gallstones cause acute pancreatitis due to obstruction of the pancreatic duct causing increased pressure in the pancreatic duct
leading to extravasation of pancreatic juice leading to injury of the gland. Also, interstitial oedema impairs blood flow to the
pancreatic cells resulting in ischaemic cellular injury. This leads to activation of proenzymes which leads to destruction of
pancreatic acinar cells.
- Alcohol causes acute pancreatitis via its direct toxic effects and/or its metabolites on acinar cells which predisposes the gland to
autodigestive injury.51
49 Lancet. 2008 Jan 12;371(9607):143-52 [Important Paper]

50 Nat Clin Pract Gastroenterol Hepatol. 2005 Oct;2(10):473-83.
51 Dig Dis 2005;23:232–240

275
Acute pancreatitis can have a great spectrum of clinical manifestation from mild,self-limiting abdominal pain to presentation with
acute abdomen with shock. Patients can also present without abdominal pain but with symptoms of respiratory failure, confusion or
coma.
- Symptomatology
▪ Acute and constant pain the epigastric area (or RUQ) classically described as a boring sensation that radiates to the back
▪ Patient is unable to get comfortable when lying supine with pain alleviated by sitting up and leaning forward
▪ Pain might last for several days and is a/w nausea and vomiting
- Complications
▪ Respiratory failure (i.e. dyspnoea secondary to diaphragmatic inflammation, pleural effusions or ARDS)
▪ Renal failure (i.e. oliguria)
▪ Gastrointestinal failure (i.e. nausea, vomiting, abdominal bloatedness)
▪ Fever +/- hypotension (SIRS vs. infective complications such as cholangitis)

▪ SIRS response such as tachycardia, tachypnea, fever
▪ Obstructive Jaundice
- Differential Diagnosis
▪ Rule out other differential diagnosis – i.e. gastric causes (PUD, perforated viscus), hepatobiliary causes (hepatitis, GB /
CBD disease) medical causes (AMI, DKA, lower lobe pneumonia)
- If pancreatitis is suspected, aim to ascertain aetiology (risk factors)

▪ Gallstone disease: biliary colic, cholecystitis, CBD stone, cholangitis
▪ Recent alcohol abuse or chronic alcohol abuse
▪ Recent intervention (i.e. ERCP)
▪ Any family history of high cholesterol (i.e. familial hyperlipidemia)
▪ Presence of constitutional symptoms (i.e. LOW / LOA / new onset DM): pancreatic neoplasm
▪ Symptoms of hypercalcemia
▪ Known autoimmune disease (i.e. SLE)
▪ Recent symptoms of mumps (viral fever + bilateral jaw pain/swelling)
▪ Recent change of medications
52 Med Clin North Am. 2006 May;90(3):481-503.

276
Physical signs depends on the severity of the pancreatitis
General Appearance
- Lying motionless (Diffuse Peritonitis) vs. Sitting Up, Leaning Forward (Pancreatitis)
- Need for any supplemental oxygen
- Assess hydration status
- Scleral icterus due to obstructive jaundice from choledocholithiasis or edema of head of pancreas
- Xanthomas (in hyperlipidemic pancreatitis)
- Parotid swelling (in mumps)
- Small red tender nodules on skin and legs – subcutaneous fat necrosis (rare)
Vital Signs
- Temperature: low grade fever (a/w SIRS vs infectious complications)
- Blood Pressure: can present with hypotension (fluid shifts with IV volume becoming markedly depleted)
- Heart Rate: can present with tachycardia
- Respiratory Rate: can present with tachypnea (possible impending ARDS, pleural effusion)
- Oxygen Saturations
- Inspection
▪ Any abdominal distension (due to ileus)
- Palpation
▪ Focal epigastric tenderness
▪ Signs of Peritonism – rebound tenderness, guarding, board-like rigidity (severe pancreatitis, need TRO other causes of
acute abdomen)
▪ Any palpable mass (i.e. pseudocysts, pancreatic phlegmon)
▪ Signs of Hemorrhagic Pancreatitis (severe pancreatitis a/w 40% mortality rate, is usually seen in 1-3% of patients and
usually develops within 48 hours after onset of symptoms, necrosis of blood vessels causes haemorrhage)
1. Grey-Turner Sign (flank ecchymosis)
2. Cullen’s Sign (periumbilical ecchymosis) – see below
3. Fox’s Sign (inguinal ecchymosis)
- Auscultation
▪ Diminished / Absent bowel sounds (paralytic ileus from diffuse peritonitis)
Respiratory Examination (TRO pleural effusion, ARDS)

Request for input/output charts
Cullen Sign: exudates from pancreatic necrotic areas tracking along the falciform ligament and into the retroperitoneal and seen in
the periumbilical region

277
- Peptic ulcer disease

▪ Hx of longstanding epigastric pain that is usually intermittent, no radiation to back
▪ Hx of NSAID use
▪ Hx of H. pylori infection
▪ Normal amylase and lipase
- Choledocholithiasis or cholangitis
▪ Hx of gallstones or biliary manipulation (ERCP)
▪ Elevated ALP, bilirubin
- Cholecystitis
▪ Pain may radiate to right shoulder or back
▪ Murphy’s positive
▪ Mild elevation in amylase, bilirubin
▪ Gallbladder wall edema and pericholecystic stranding on imaging
- Hepatitis
▪ Jaundiced, dark urine, pruritus
▪ Tender hepatomegaly
▪ Marked elevations in AST, ALT, bilirubin
- Perforated viscus
▪ Peritonism signs
▪ May have elevated amylase but unlikely 3x upper limit
▪ Free air on erect CXR
- Intestinal obstruction
▪ May have elevations in amylase and lipase
▪ Hx of prior abdominal surgeries
▪ Look out for surgical scars or hernias
▪ Dilated loops of bowel with air fluid levels on imaging
- Mesenteric ischemia
▪ Pain out of proportion to findings on PE
▪ Risk fx - age, atherosclerosis, cardiac arrhythmias, severe valvular disease, recent MI, intra-abdominal malignancy
▪ May have elevations in amylase and lipase
▪ Focal or segmental bowel wall thickening or intestinal pneumatosis on imaging

278
INVESTIGATIONS
The investigation for acute pancreatitis is divided into investigation for diagnosis, followed by investigation for severity stratification
which will help decide which patients require close monitoring in the high-dependency unit. Lastly, investigations should be
performed to assess for the underlying etiology of the pancreatitis
Diagnostic53
1. Serum amylase (normal = 30-100U/L)
▪ Levels ≥ 3 times the normal upper limit – sensitivity 67% and spec. 99%
▪ Levels rise within a few hours and normalizes in 5 days
▪ Elevation for > 10 days indicate complications (i.e. pseudocysts formation)
▪ Magnitude of elevation not a/w disease severity or prognosis of disease
2. Serum lipase (normal =10-140 U/L)

▪ Levels ≥ 3 times the normal upper limit – sensitivity 82% & spec. 97%
▪ Levels rise within 4-8hours and stays elevated for 8-14days
▪ Useful for patients with delayed presentation of acute pancreatitis
Other causes of elevated serum amylase

- GI source (extra-pancreatic abdominal conditions): Peptic ulcer disease, Intestinal Obstruction, Perforated bowel,
Ischaemic bowel, cholecystitis, cholangitis, appendicitis,
- Non GI sources: Renal Failure, Salivary gland injury or inflammation, Ruptured ectopic pregnancy / Ovarian Cysts / PID,
Diabetic Ketoacidosis (DKA) or any acidosis (ketotic and nonketotic),
- Cancers: pancreatic cancer, prostate, lung, oesophagus, breast, multiple myeloma, pheochromocytoma)
- Complication of pancreatitis: pancreatic pseudocyst, abscess,
Assess severity and Prognosticate disease (based on various scoring criteria)

1. Full Blood Count
▪ Leukocytosis
▪ Haematocrit levels higher than 44% a/w worse prognosis – patients with inadequate fluid resuscitation as evidenced by
persistence of hemoconcentration at 24 hours are at increased risk of developing necrotizing pancreatitis54
2. Renal Panel, Calcium Panel, Glucose
▪ Assessment of hydration status (i.e. urea) and degree of renal impairment
▪ Assessment of hypocalcemia
▪ Assessment of hyperglycemia
3. Liver Function Test
▪ Enzymes (serum AST) – aspartate
▪ Albumin
▪ Lactate Dehydrogenase (serum LDH)
4. ABG
▪ Assess base deficit (negative base excess)
▪ Assess arterial oxygenation
5. C-Reactive Protein (CRP) – best single biochemical marker for risk stratification for acute pancreatitis
▪ >150 mg/L within 48hrs associated with severe pancreatitis
Other Biochemical Investigations

6. ECG / Cardiac Enzymes → rule out possible AMI
7. PT/INR/APTT → needed if patient require subsequent intervention (i.e. ERCP)
8. Lacate → to guide fluid therapy
53 Ann R Coll Surg Engl. 2009 July; 91(5): 381–384.

54 Pancreatology. 2002;2(2):104-7.

279
Radiological Investigations
1. Erect CXR & Supine AXR
▪ Erect CXR may show air under the diaphragm (perforated viscus), pleural effusion, elevated hemidiaphragm, pulmonary
infiltrates; complete whiteout (ARDS)
▪ Supine AXR: look for sentinel loop sign, colon cut-off sign or pancreatic calcification
Sentinel loop sign – a focal area of adynamic ileus close to an intra-abdominal inflammatory process. In acute pancreatitis (LHC –dilated proximal
jejunal loops), acute cholecystitis (RHC), acute appendicitis (RIF)
Colon cut-off sign – distended colon from ascending to mid-transverse with narrowing of the splenic flexure. This results from an inflammatory process
extending from the pancreas into phrenicocolic ligament via transverse mesocolon. Also seen in colorectal cancer, inflammatory bowel disease,
mesenteric ischemia
Pancreatic calcifications – chronic pancreatitis from alcohol abuse, hereditary pancreatitis, cystic fibrosis
2. Hepatobiliary Ultrasound (US HBS)

▪ Diffusely enlarged and hypoechoic pancreas
▪ Gallstones may be visualised in gallbladder or bile duct (dilated extrahepatic / intrahepatic ducts)
▪ Peripancreatic fluid
3. Contrast-Enhanced Computed Tomography (CTAP)

▪ Useful in confirming diagnosis of pancreatitis if haematological results are inconclusive
▪ Useful in severely ill patients with suspicion of necrotizing pancreatitis (only after aggressive volume resuscitation to diminish
risk of contrast-associated nephrotoxicity)
▪ Patients with persisting organ failure, signs of sepsis or deterioration in clinical status 6-10 days after admission – CT
assess local complications such as fluid collections and necrosis
CT Severity Index (Balthazar Score)

- Grades severity of disease according to CT findings
- In 1st 72 hours, necrosis of the pancreatic parenchyma cannot be reliably assessed on CT scan
- Optimal timing is at least 72-96 hours after onset of symptoms
Modified CT severity index

Categories Score Features
0 Normal Pancreas consistent with mild pancreatitis
Intrinsic pancreatic abnormalities (i.e. focal or diffuse enlargement) ±
Pancreatic Inflammation 2
inflammatory changes in peripancreatic fat
4 pancreatic or peripancreatic fluid collection or peripancreatic fat necrosis
Extra-pancreatic ≥ 1 of pleural effusion, ascites, vascular complications, parenchymal cx and

2
Complications or GI involvement
0 None
Pancreatic Necrosis 2 30% or less
4 More than 30%
0-3 8% morbidity & 3% mortality

Morbidity & Mortality Score 4-6 35% morbidity & 6% mortality
7-10 92% morbidity & 17% mortality
4. MRI / MR cholangiopancreatography (MRCP)

▪ Higher sensitivity for diagnosis of early acute pancreatitis as compared with CTAP
▪ Substitute for CT scan in patients allergic to iodinated contrast or in acute renal failure
▪ Good for visualizing cholelithiasis, choledocholithiasis, congenital anomalies of the pancreas and CBD
▪ (secretin-stimulated) MRCP – for idiopathic acute pancreatitis

280
Investigating underlying aetiology
1. Liver Function Test (LFTs)
▪ Elevation of ALP > 150mg/dl (within 48 hours) → gallstone pancreatitis (85%)
▪ Elevation of Br → possible impacted stone in ampulla of Vater
▪ Elevation of AST/ALT → for Ranson and Glasgow scoring system
2. Metabolic Screen (i.e. calcium Panel → hypercalcemia, fasting lipids → hypertriglyceridemia)

3. Autoimmune Screen (i.e. IgG4) - refer patient to gastroenterologist
4. US HBS → assess for possibility of gallstone pancreatitis
▪ Assess for presence of cholelithiaisis or choledocholithiasis (visualize biliary tree) → Dilated CBD, proceed with ERCP to
remove gallstones/Bx tumour, if not dilated, consider MRCP (suspect parenchymal disease)
5. Endoscopic Ultrasonography (EUS) – for idiopathic acute pancreatitis
▪ Assess for occult microlithiasis, neoplasm & chronic pancreatitis
DIAGNOSTIC CRITERIA FOR SEVERITY
Atlanta Classification for Severity55

Mild Moderate Severe
Transient organ failure Persistent organ failure (>48 hours),
No organ failure
(resolves within 48 hours) single or multiple organ failures
Local complications are peripancreatic
fluid collections, pancreatic and
Local complications or exacerbation of
No local or systemic complications peripancreatic necrosis (sterile or
comorbid disease
infected), pseudocyst and walled-off
necrosis (sterile or infected)
Resolves in the first week
Mortality is rare Mortality range from 36-50%
Four categories of acute pancreatitis56

Determinants No Local Complications Severe Local Cx Infected Local Cx
No Organ Failure Mild Moderate Severe
Transient Organ
Moderate Moderate Severe
Failure
Persistent Organ
Severe Severe Critical
Failure
55 Gut. 2013 Jan;62(1):102-11 [Important Paper]

56 Ann Surg. 2012 Dec;256(6):875-80.

281
SCORING SYSTEM FOR ASSESSING SEVERITY OF PANCREATITIS
The choice of scoring system is institution dependent. In NUH, the Glasgow scoring system is commonly used.
(1974) Ranson’s criteria [LEGAL and CAlvin & HOBBES]

Ranson et al. identified 11 objective clinical and laboratory measurements available within 48 hours of admission each of which had
value in predicting severity and could be used as a basis for a predictive scoring system – scoring system for alcoholic aetiology.
Ranson’s criteria prognosticates mortality according to score with patients with a score of ≥ 3 is considered to have severe pancreatitis
On admission – LEGAL Initial 48 hour – Calvin & HOBBES

Serum LDH > 350IU/L Serum Calcium < 2.0mmol/L or 8.0mg/dL
Serum AST > 250 IU/L Haematocrit Fall > 10%
Blood Glucose > 10mmol/L Oxygen (PaO2) < 60mmHg
Age > 55 years BUN (after IV fluid hydration) ≥ 1.8 mmol/L or ≥ 5.0mg/dL
WBC > 16,000 cells / mm 3 Base Deficit (-ve base excess) > 4mEq/L
Sequestration of Fluids >6L
- Mortality: 0-2 (0-2%), 3-4 (15%), 5-6 (50%), ≥7 (70-90%)
- Shortfalls of Ranson’s:
▪ Validated for alcoholic pancreatitis only → revised Ranson’s score was created for gallstone pancreatitis (same parameters
but different cut-off values)

▪ Cumbersome to wait for 48 hours, and difficult to assess for negative fluid balance
(1984) Glasgow (Imrie’s criteria) – PANCREAS

The Glasgow system uses age and 7 laboratory values collected during the first 48 hours following admission for pancreatitis to predict
for severe pancreatitis. It is used for both alcoholic and gallstone pancreatitis.
1. PaO2 <60mmHg
Age >55yrs
2. Neutrophil/WBC >15x109/dL
3. Calcium <2mmol/L
4. Renal (urea) >16mmol/L
Enzymes LDH >600IU/L ≥ 3 criteria = severe
5. or AST/ALT > 200IU/L
Consider management in HDU
6. Albumin <32g/L
Sugar (Glucose ) >10mmol/L
7.
8.
(1989) Acute Physiology and Chronic Health Evaluation II Score (APACHE II)
APACHE II takes into account 12 continuous variables, age of the patient, pre-morbid conditions and the GCS. The major advantage
is that it can be used to monitor a patient’s response to therapy while the Ranson and the Glasgow scales are meant for assessment
at presentation. A score ≥ 8 is a predictor for severe pancreatitis
(1996) Sequential Organ Failure Assessment (SOFA) score
(2006) Systemic Inflammatory Response Syndrome (SIRS)

- Based on Temperature, Heart Rate, Respiratory Rate and WBC
- Persistent SIRS (> 48hr) is a/w MOF and mortality in acute pancreatitis
- Persistent organ failure (> 48hr) is the key determinant of mortality in acute pancreatitis – 25% vs 8% for transient SIRS

282
MANAGEMENT
The management of acute pancreatitis involves supportive treatment, managing of complications and treatment of underlying
aetiology to prevent future recurrence
Supportive Treatment 5758

1. Fluid Resuscitation
▪ Rapid and effective restoration of circulating volume will improve outcomes
▪ Fluid resuscitation with crystalloids (lactated ringer) – (correct fluid losses in the 3rd space)
▪ Biochemical targets – haematocrit 35-44%
▪ Resuscitation guided by urine output (aim >0.5ml/kg/hr), lactate, base deficit, Mixed venous oxygen saturation (SvO2)
2. Monitoring (after resuscitating)

▪ In general ward if mild pancreatitis; HD/ICU monitoring if assessed to be severe (i.e. glasgow score > 3) or presence of
organ dysfunction
▪ Monitor vitals (Temp, BP, HR, RR, SpO2) – may require insertion of intra-arterial line and central venous line (CVP)
▪ KIV insertion of urinary catheter to monitor urine output
▪ KIV monitoring with ABG & Lacate (oxygenation, acid-base status, fluid status)
3. Pain control with analgesia

▪ Use opioid analgesics (tramadol) other than morphine (causes contraction of smooth muscles in sphincter of Oddi)
▪ Do not give NSAIDs as they can worsen pancreatitis & cause renal failure (since there is already decreased renal perfusion
in acute pancreatitis)
4. Nutrition
▪ Enteral nutrition (EN) vs Parenteral Nutrition (PN): EN is superior to PN – maintain integrity of GI barrier thus reduce
bacterial translocation59 & down-regular systemic immune response which reduces organ failure, infections and mortality.
Also gastric colonization by pathogenic bacteria which can increase risk of septic complications is reduced with EN
▪ Early (within 24 hours) vs Delayed Feeding: In mild / moderate pancreatitis, start oral feeding early (no need for
nutritional support). In severe pancreatitis, aim also for early enteral feeding (but may require placement of enteral tube)
▪ NG vs NJ feeding: NG feeding was just as well tolerated as nasojejunal feeding in severe pancreatitis
▪ Prolonged NBM results in poorer recovery due to nutritional debilitation – think about enteral tube feeding; if patients is
unable to tolerate enteral feeding (gastric stasis / ileus) then consider IV TPN
▪ If patient is vomiting, consider antiemetic +/- NGT insertion
5. Antibiotics
▪ Therapeutic role in patients with cholecystitis / cholangitis (coexisting with pancreatitis, patients present with obstructive
jaundice and fever) → IV Rocephin / Flagyl
▪ No evidence for antibiotics prophylaxis in (predicted) severe acute pancreatitis
▪ ?Prophylactic in severe acute pancreatitis to prevent infection of necrosis
▪ No benefit of antibiotics in preventing infection of pancreatic necrosis or mortality was found, except when imipenem
(a beta-lactam) was considered on its own, where a significant decrease in pancreatic infection was found. 60
▪ Others feel that there is no role for routine antibiotics prophylaxis in treatment of necrotizing pancreatitis – withheld till
infection proven with positive cultures
▪ Proven Infection secondary to pancreatic necrosis / pseudocyst, consider using carbapenems, metronidazole,
quinolones (good pancreatic tissue penetration)
6. Support for organ failure – with presence of organ failure, manage patient in surgical HD/ICU
▪ Ventilate with PEEP if hypoxemic (e.g. ARDS)
▪ Dialysis & CVP monitoring if in ARF
▪ Fluid resuscitation & inotropes if hypotensive
57 Gastroenterology. 2018 Mar;154(4):1096-1101. (Initial Management of Acute Pancreatitis, Guidelines)

58 Pancreatology. 2013 Jul-Aug;13(4 Suppl 2)e1-15.
59 World J Emerg Surg. 2014 Feb 10;9(1):15.
60 Cochrane Database Syst Rev. 2010 May 12;(5):CD002941. [Important Paper]

283
Managing Complications
Complications can be divided into local and systemic complications. Local complications can be further divided based on timing of
presentation (< or > 4 weeks) and absence or presence of necrosis. The fluid collections can be sterile or secondarily infected.
Early Local complications61

- Acute peripancreatic fluid collection (30-50%)
▪ Due to increased vascular permeability, 70-80% are asymptomatic and resolve spontaneously
▪ This term only applied to area of peripancreatic fluid seen within the first 4 weeks after onset of interstitial oedematous
pancreatitis and without feature of pseudocyst
- Acute necrotic collection (10-20%) → 30% develops secondary bacterial infection (usually enteric GNR)
▪ A collection containing fluid and necrosis associated with necrotizing pancreatitis, necrosis can involve the pancreatic
parenchyma and/or peri-pancreatic tissue (no contrast uptake on CT)
▪ ? prophylactic antibiotics with imipenem (see above)
▪ Acute necrotic collection can be sterile necrosis or infected (suspect if have gas-bubbles on CT and/or persistent sepsis
and/or progressive clinical deterioration, positive culture may be obtained from FNA or during drainage procedure)
o Sterile necrosis: supportive care (i.e. resuscitation, nutritional support, adjuncts to support organ function)
o Infected necrosis: IV antibiotics (penems) + drainage procedure +/- step-up as required
▪ Step-up Approach (PANTER study)62

o Percutaneous / Endoscopic transgastric drainage >>
o Minimally Invasive Retroperitoneal Pancreatic Necrosectomy (MIRP) or Video Assisted Retroperitoneal Drainage
(VARD) or Endoscopic Transgastric Necrosectomy >>
o Open necrosectomy
Late Local Complications (> 4 weeks)

- Pancreatic Pseudocyst (10-20%)
▪ Presents as persistent pain, mass on examination, persistently ↑amylase or lipase
▪ Pancreatic pseudocyst contains pure pancreatic juice which suggests that there exists a communication with the pancreatic
duct. Duct disruption usually occur with pancreatic necrosis hence most of the time a persistent collection should be termed
as a walled-off pancreatic necrosis (WOPN)
▪ The pancreatic pseudocyst contains a well-defined encapsulated fluid collection (enzymes, blood, necrotic tissue), outside
the pancreas, walled off by a fibrotic wall (inflammatory wall instead of an epithelium lined surface). It develops in the lesser
sac, anterior wall of pseudocyst (posterior aspect of stomach), inferior wall of pseudocyst (transverse mesocolon)
▪ Historically, pseudocyst > 6cm and persistent for > 6 weeks was considered to warrant intervention
▪ Complications associated with pseudocyst
o Fistula formation (duodenum, colon, small bowel, pleura)
o Hemorrhage → angioembolization
o Rupture (pancreatic ascites)
o Obstruction (intestinal, vascular, biliary), gastric outlet obstruction
o Infection (pancreatic abscess)
- Walled-off Pancreatic Necrosis (WOPN)

▪ A mature, encapsulated collection of pancreatic or extra-pancreatic necrosis with a well defined inflammatory wall
▪ Indications for intervention
o Sepsis / Infection (based on radiological features or clinical suspicion)
o Nutritional failure
o Symptomatic: persistent abdominal pain / early satiety / gastric outlet obstruction
o Failure of Resolution
▪ Options for Intervention

o Endoscopic: EUS guided cystogastrostomy (other alternatives includes cystoduodenostomy or cystojejunostomy)
o Laparoscopic Cystogastrostomy (other alternatives includes Roux-En Y cystojejunostomy or cystoduodenostomy)
o Open Surgical Necrosectomy
Other Complications
- Haemorrhage → erosion of arterial pseudoaneurysm secondary to pseudocyst, abscess or necrotizing pancreatitis
- Enteric Fistulation (foregut fistulation leads to clinical improvement, hindgut fistulation results in marked clinical deterioration)
- Venous thrombosis (i.e. splenic vein thrombosis, superior mesenteric or portal vein thrombosis)
61 Pocket Medicine 4th Edition: Pancreatitis – section 3-13

62 N Engl J Med 2010;362:1491-502 [Landmark Paper] – Dutch Pancreatitis Study Group

284
Early Systemic Complications
- Multiple Organ Failure (secondary to uncontrolled SIRS)
▪ Respiratory Failure → Pleural Effusion (exudative)*, ARDS**, may require mechanical ventilation
▪ Renal Failure → fluid overload, electrolyte derangement, anuria, may require dialysis support
▪ Cardiovascular Collapse → hypovolemic shock, may require inotropic support
▪ Gastrointestinal Dysfunction → nausea, vomiting, intolerance of enteral feeding, may require TPN
- Hematological (DIVC)
- Intra-abdominal Hypertension / Abdominal Compartment Syndrome (secondary to pancreatic ascites)
- Metabolic complications → hypocalcemia, hyper/ hypoglycemia
Late Systemic Complications

- Sepsis which can also lead to multiple organ failure
- Vascular complications
▪ Venous Thrombosis (i.e. splenic vein, superior mesenteric vein and portal vein)
▪ Intra-abdominal haemorrhage (erosion of splenic artery / gastroduodenal artery)
Treatment of underlying etiology

- ERCP
▪ Indications – suspect gallstones as the cause of pancreatitis and
o Cholangitis
o Persistent biliary obstruction (i.e. raised bilirubin)
o Evidence of ductal stones on imaging
o Patients contraindicated for surgery (ERCP & sphincterotomy as definitive management)
▪ ERCP algorithm
o Patients with resolving jaundice → observe
o Patients with persistent jaundice but clinically improving → biliary imaging (i.e. EUS / MRCP)
o Patients with persistent jaundice and clinically deteriorating → ERCP and biliary decompression
- Laparoscopic Cholecystectomy
▪ Patients with biliary pancreatitis who do not undergo cholecystectomy have a 40% 6 week recurrence risk
▪ Cholecystectomy can be done in the same admission for patients with mild biliary pancreatitis – PONCHO study63
▪ In patients with severe pancreatitis (presence of acute peripancreatic fluid, acute necrotic collections) there is reluctance to
do the surgery early, as the patient may develop complications that require surgical intervention – better to do all surgery in
the same operation instead of opening the patient twice
- Lifestyle Modification
▪ Avoid alcohol, stop all offending medication & control hyperlipidaemia
▪ Need long-term follow-up to screen for diabetes (higher risk of new-onset DM)
63 Lancet. 2015 Sep 26;386(10000):1261-1268. [Landmark Study]

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CHRONIC PANCREATITIS
INTRODUCTION
Inflammation, fibrosis and loss of acinar and islet cells, which can manifest with pancreatic-type abdominal pain, steatorrhea,
derangements in pancreatic function (exocrine and endocrine insufficiency), and visible pancreatic damage on imaging studies.
CAUSES
- Toxic-metabolic factors (i.e. alcohol (~50%), smoking (usually in combination with alcohol use))
- Hypertriglyceridemia
- Genetic
- Autoimmune – Type 1 (IgG4-related) and type 2
- Recurrent and severe acute pancreatitis – strong risk factor for progression to chronic pancreatitis
- Chronic obstruction of main pancreatic duct by tumours, scars, ductal stones, duodenal wall cysts
- Idiopathic
* Not all patients diagnosed with chronic pancreatitis have a history of recurrent acute pancreatitis
PATHOGENESIS
- Progressive destruction of the pancreas by repeated flare-ups of mild and subclinical types of acute pancreatitis
- Characterized by diffuse scarring and strictures in the pancreatic duct
- The Islet of Langerhans (endocrine function) have a greater resistance to injury than do the exocrine tissues
- Abdominal Pain (upper mid-epigastric pain radiating to the back, worse after eating)
▪ Can last from hours to days
▪ Episodic, more continuous as condition progresses
▪ a/w nausea/vomiting
▪ Cardinal symptom and is present in 85-90% of patients
- Pancreatic insufficiency symptoms (clinically significant deficiencies occur when 90% of pancreas function lost)
▪ Fat malabsorption
- Steatorrhea - loose, greasy, foul-smelling stools that are difficult to flush
- Vitamins ADEK and B12 deficiencies (though rare to have clinical symptoms
▪ Pancreatic diabetes (late)
- Usually requires insulin
- Increased risk of hypoglycemia (as pancreatic alpha cells producing glucagon are also affected)
- Complications (see below)
- Pseudocyst* – occur in 20-38% of patients

▪ Secondarily infected → abscess
▪ Superior mesenteric-portal vein thrombosis OR splenic vein thrombosis (splenomegaly / gastric varices)
▪ Perforate: peritonitis OR intraperitoneal bleeding
- Pancreatic ductal stones
Local ▪ For patients with pain and treated with ESWL/ERCP vs.Surgery (i.e. Puestow Procedure (Longitudinal
1 Roux-En-Y pancreaticojejunostomy))
Complications
- Pancreatic Ascites – fluid sequestration into the peritoneal cavity
- Pancreatico-pleural Fistula – presents as pleural effusion
- Pancreatico-enteric Fistula – presents as sepsis and/or colonic bleeding
- Head of Pancreas Mass (inflammatory mass / pancreatic pseudotumor) → duodenal obstruction, cholestasis –
distal CBD obstruction, daily severe pain (treat surgically)
- Due to transient obstruction from pancreatic inflammation and oedema or from strictures on the intrapancreatic
2 CBD Obstruction
CBD
3 Duodenal Obstruction - Occur due to acute pancreatic inflammation, chronic fibrotic reaction, pancreatic pseudocyst or neoplasm
4 Pancreatic Cancer - Chronic pancreatitis leads to 2-3x higher risk
- Type 1 DM
5 Pancreatic Insufficiency
- Steatorrhoea, Vitamin deficiency, Malnutrition
* Recurrence of pseudocyst after aspiration implies an ongoing communication with the pancreatic duct.

286
- LOW (secondary to anorexia and malabsorption)
- Tenderness of upper abdomen
- Enlarged pancreas is occasionally palpable, especially in thin patients (differential: presence of pseudocyst)
- ± jaundice (secondary to stricture of the common bile duct)
- ± splenomegaly (secondary to thrombosis of the splenic vein)
- ± ascites (secondary to a pancreatic peritoneal fistula)
DIAGNOSIS
- Classic triad of pancreatic calcifications, steatorrhea, DM (but seen together in late, advanced disease only)
- Confirmed if calcifications within pancreas on CT, abnormal pancreatogram with beading of main pancreatic duct or abnormal
secretin pancreatic function test.
- Note: can be difficult to establish secure diagnosis; if significant change in pain pattern or sudden onset of persistent
symptoms, other potential etiologies should be ruled out.
- Pancreatic cancer (most impt differential) → consider if older age, absence of hx of alcohol use, weight loss, protracted flare of
symptoms, onset of significant constitutional symptoms

- Autoimmune pancreatitis, lymphoma, pancreatic endocrine tumours
INVESTIGATIONS
Radiological
- CT, MRI and US
▪ May show calcifications, ductal dilatation, enlarged pancreas, fluid collections
- MRCP
▪ Becoming diagnostic investigation of choice
▪ Demonstrates calcifications and pancreatic duct obstruction consistent with chronic pancreatitis
▪ No radiation risk
- ERCP
▪ Characteristic “chain of lakes” of main pancreatic duct – enlarged > 1.5 times with increased tortuosity
▪ Abnormal side branches – clubbing and dilatation
▪ Can also evaluate pancreatic mass lesions, cytology, delineation of ductal anatomy and can be therapeutic
▪ 3-7% risk of causing acute pancreatitis
▪ As MRCP quality improves, ERCP more reserved for cases with potential need for therapeutic intervention
- Endoscopic Ultrasound (EUS)
▪ Diagnosis of chronic pancreatitis based on Rosemont Criteria
Biochemical
- Pancreatic Secretin Stimulation Test (gold standard but invasive)
▪ Patient is given IV secretin and the pancreatic secretions (released into the duodenum) are aspirated (removed with NGT)
and analysed over a period of about 2 hours → little pancreatic secretion

- Postprandial Pancreatic Polypeptide Hormone
- Pancreatic Endocrine Function – i.e. fasting blood glucose, 2hr post-prandial blood glucose or glucose tolerance test
▪ Abnormal test results in 14 – 65% with early chronic pancreatitis
▪ Abnormal results in 90% of patients when calcifications are present
- 72hr faecal collection for estimation of daily faecal fat
▪ Simple and cheap test for assessing pancreatic function, determine if patient has significant steatorrhea
▪ Limited role in diagnosis of chronic pancreatitis (require high degree of pancreatic insufficiency to have a positive test)
Note: serum amylase and lipase levels are elevated in acute pancreatitis but rarely useful in chronic pancreatitis and are commonly
normal as there is frequently significant fibrosis resulting in decreased abundance of these enzymes within the pancreas

287
MANAGEMENT PRINCIPLES
Patient can be managed via (1) lifestyle modifications (2) medical therapy (3) surgical
- Treat underlying aetiology (eg. stop drinking alcohol and smoking)

- Supportive Treatment
▪ Malabsorption / steatorrhoea: pancreatic enzyme supplements, dietary modification, lipase supplementation, vitamin
supplementation
▪ Diabetes: lifestyle choices, OHGA, Insulin
▪ Pain Relief: narcotics / TCAs
- Treating Complications
▪ Pancreatic Pleural Effusions: tube thoracostomy
▪ Pancreatic Ascites: paracentesis
▪ Ductal Complication: ERCP (i.e. sphincterotomy, stone retrieval (basket/balloon extraction), stenting) +/- pancreatic-ESWL
(if fail then for surgical intervention)
▪ Pseudocyst, aneurysm, fistula, local obstruction: surgical management
Surgery Indications
- Unremitting abdominal pain
- Inability to rule out neoplasm
- Treatment of complications (persistent pseudocyst, pancreatic fistula / ascites, local obstruction [CBD obstruction, duodenum
obstruction, colonic obstruction]
- Variceal haemorrhage secondary to splenic vein thrombosis (need splenectomy)
EXTRA INFORMATION
Choice of Procedure
Principle Procedure Remarks
Duval (1954) Distal pancreatectomy with end-to-end pancreaticojejunostomy ± splenectomy
Drainage
Puestow-Gillesby Distal pancreatectomy with a side-to-side pancreaticojejunostomy ± splenectomy
Preferable for
(1958) - For enlarged ducts >8mm
patients with dilated
Partington-Rochelle
ducts Modification of Puestow – eliminate distal pancreatectomy
(1963)
Duodenum-preserving pancreatic head resection, pancreas transected at pancreatic neck
Combined Duct Beger Procedure
- For normal / small ducts with isolated pancreatic head enlargement
Drainage and
Modification of Beger – pancreatic neck not transected, parenchyma is extensively cored
Resections Frey Procedure
out from head to extent of diseased segment distally, lateral pancreaticojejunostomy
Indication: pancreatitis mainly affects head of the pancreas
Whipple Procedure
Resection - For normal / small ducts with isolated pancreatic head disease
(pancreatectomy) Subtotal / Total
Pancreatectomy
Bilateral thoracoscopic splanchnicectomy or
Nerve Block Celiac Plexus Block
Celiac ganglionectomy
* Puestow leads to early pain relief in 80% but ~ 30% develop recurrent pain within 3-5 years of their procedure
** Whipple’s, Beger and Frey procedures leads to similar pain relief between 1 – 4 years (~80% reports complete or significant pain relief)

288
EXTRA INFORMATION
Duval Procedure Puestow / Partington Rochelle Procedure
Beger Procedure Frey Procedure
Whipple Procedure (pancreaticoduodenectomy)

- En-bloc removal of distal segment of the stomach, duodenum, proximal 15cm of jejunum, head of pancreas, common bile duct,
gallbladder
- Pancreatic and biliary anastomosis placed 45-60 cm proximal to gastrojejunostomy
- Principle: pancreas and duodenum share the same arterial blood supply (gastroduodenal artery) – so both must be removed

289
PANCREATIC CANCER64
DEFINITION
The majority of pancreatic tumours are adenocarcinoma (95%) originating from the exocrine part of the pancreas.
EPIDEMIOLOGY & RISK FACTORS

- 5th in females and 6th in males leading cause of cancer mortality in Singapore
- Leads to estimate 227,000 deaths per years worldwide65
- Very poor prognosis – 80% unresectable at initial diagnosis
- Overall 5-year survival is about 5%, median age at diagnosis is 65 years66
Risk Factors
Smoking* - 2.5x increased risk (risk minimized if stop for ≥ 10yrs)
- Obesity
- High Fat (i.e. saturated fats) Diet
Diet - High Meat Diet
Modifiable - Diet low in Vegetable, Folate, Vitamin C/D
- Alcohol (≥ 9 drinks / day)
- Chlorinated hydrocarbon solvents (industrial carcinogens) – i.e. metal degreasing workers,
Occupational
dry cleaners, workers in paint and varnish industry and textiles industry)
Exposure
- Asbestos
- Family History of Chronic Pancreatitis *

Family History - First-degree relatives with pancreatic tumour (familial pancreatic cancer)* – especially so
with young onset ( < 50 years) pancreatic cancer
- Age (above 60 years)
Age / Gender
- Male Sex
- Chronic Pancreatitis* – 18x increased risk
Personal - Diabetes Mellitus – (preliminary findings suggests metformin could protect against
History pancreatic cancer67)
- IPMN
- Peutz-Jeghers Syndrome
- Li-Fraumeni Syndrome
Non-modifiable - Fanconi Syndrome
- Familial Adenomatous Polyposis
Genetic
- Lynch Syndrome
Predisposition
- Gardner Syndrome
- Multiple Endocrine Neoplasia
- Von Hippel-Lindau Syndrome
- BRCA 1
- Helicobacter Pylori Infection
- Periodontal Disease
Others - Ethnicity: African American
- Blood Group (Non-O blood group)
- Cystic Fibrosis
* Dominant risk factors

- Smoking: 20% of pancreatic tumours attributed to smoking,
- Chronic Pancreatitis: 7-10% of affected individuals have a positive family hx of chronic pancreatitis
- Familial Pancreatic Cancer: with 2 affected family members = 6-9X increased risk of pancreatic cancer over the general
population, with ≥3 first degree relatives have pancreatic cancer = 32x increased risk
64 Lancet. 2011 Aug 13;378(9791):607-20. [Important Paper]

65 Nat Rev Gastroenterol Hepatol 2009;6: 699–708.
66 Cancer Statistics. 2010;60(5):277-300
67 Gastroenterology. 2009 Aug;137(2):482-8.

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PATHOLOGY
- Pancreatic intraepithelial neoplasia (PanIN) to invasive pancreatic carcinoma in a multi-step progression sequence
- Involves progressive genetic mutations
▪ Telomere shortening which contribute to chromosomal instability (early)
▪ Mutational activation of K-RAS oncogene (early)
▪ Inactivation of tumour suppressor genes: p16/CDKN2A, TP53 and SMAD4
- Most common histology is ductal adenocarcinoma (90-95%%)

- Other histological subtypes include adenosquamous carcinoma, squamous cell carcinoma, acinar cell carcinoma* (production of
exocrine enzymes, may cause metastatic fat necrosis due to lipases released into circulation, presents as large tumour (>10cm)),
IPMN with associated invasive carcinoma, serous cystadenocarcinoma undifferentiated (anaplastic) carcinoma,
pancreatoblastoma (rare, found in children 1-15years)
- More favourable prognosis, papillary mucinous cyst adenocarcinoma

- Common sites involved:
▪ Head of Pancreas (60%) – can lead to earlier detection secondary to obstruction of bile duct
▪ Body of Pancreas (15%)
▪ Tail of Pancreas (5%) – usually present late
▪ Entire Pancreas (20%)

291
Early stage pancreatic cancer is usually clinically silent and disease only becomes apparent after the tumour invades the surrounding
tissues or metastasis to distant organs. 80% of patients present with unresectable disease.
A high index of suspicion is needed for diagnosis for pancreatic cancer. Vague epigastric discomfort and presence of constitutional
symptoms (i.e. loss of weight, anorexia) despite normal upper endoscopy should prompt further investigations/
- Symptoms & Signs68

▪ Classical Courvoisier sign (palpable GB in presence of painless obstructive jaundice) ~ 25%
▪ Obstructive Jaundice: tea coloured urine, scleral icterus, pruritus, pale / clay coloured stools
▪ Obstructive Jaundice +/- Pain
- Pain and jaundice ~ 46% (pain due to coeliac/mesenteric plexus invasion)
- Pain ~ 34% (dull constant pain radiating to the back or induced local pancreatitis, pain on initial presentation related to
high incidence of unresectability
- Painless obstructive jaundice ~ 13%
▪ New-onset DM in elderly patients (new onset DM within the year prior to dx is found in 15%, correlation is unclear)
▪ Endoscopy negative epigastric pain

▪ Signs of malabsorption (i.e. steatorrhoea)
▪ LOW and Anorexia ~7%
▪ Nausea / Vomiting (might be related to gastric outlet obstruction)
▪ Upper BGIT (hematemesis and/or melena) – tumour invasion into stomach / duodenum
- Presentation varies with tumour location

▪ Tumours in the head of pancreas, can present earlier with obstructive jaundice
▪ Tumour in body and tail of pancreas, usually present late
- Signs of advanced malignancy

▪ Malignant Pleural Effusion,
▪ Virchow’s node: left supraclavicular node enlargement a/w gastrointestinal malignancy
▪ Trousseau sign: Migratory superficial thrombophlebitis* (paraneoplastic),
▪ Sister Mary Joseph nodule: umbilical metastatic lesion via falciform ligament
▪ Hepatomegaly: underlying liver metastases
▪ Nonbacterial thrombotic (marantic) endocarditis: deposition of sterile platelet thrombi on heart valves
* Hypercoagulability develops because adenocarcinoma produce a thromboplastin like substance capable of causing chronic
intravascular coagulations that can disseminate and migrate
Examination
68 Hepatobiliary and Pancreatic Surgery, A companion to Specialist Surgical Practice, Chapter 15

292
INVESTIGATIONS
Biochemical Investigation
- FBC – looking for any evidence of occult blood loss (NCNC anemia) or sepsis (↑TW)
- U/E/Cr – assess electrolyte abnormalities a/w GOO (vomiting), renal function for scans
- LFTs – confirmation of obstructive jaundice, assess nutritional status (albumin)
- Amylase / Lipase – any ongoing pancreatitis
- PT / INR – evidence of hepatic dysfunction
- Random Glucose Test – assess for any DM
- Carbohydrate Antigen 19-9 (CA19-9), lewis blood group antigen (cell surface glycoprotein)
▪ CA19-9 has poor sensitivity (46 - 86%) and specificity (33-100%) for detecting pancreatic cancer and 4-15% of the general
population do express the antigen, hence have no detectable serum CA19-9 levels (poor screening tool)
▪ Elevated in lung, gastric, colorectal, biliary tract and urothelial cancers
▪ Elevated in pancreatitis, hepatitis, thyroiditis and biliary obstruction
▪ Useful as a marker for tumour recurrence during post-op follow-up
▪ Can act as a prognostic marker
- Preoperative amounts of CA19-9 > 100-200U/ml predicts unresectability and survival69
- Normal perioperative CA19-9 associated with a 5 year survival of 42%
- Lower postoperative CA19-9 at 3 months and before adjuvant chemotherapy were independent favourable prognostic
factors
Radiological Investigation
1. Transabdominal Ultrasound
▪ Initial investigation in a jaundiced patient – higher sensitivity for determining cholelithiasis over CT
▪ CBD dilatation (>7mm; >10mm in post-cholecystectomy patients) + pancreatic duct dilatation (>2mm) is a worrying sign
▪ For lesions >3cm, US has 95% sensitivity
2. Tri-phasic “pancreatic protocol CT Scan” (3-phases – arterial, late arterial and portal venous) and (thin slices – 1-3mm) – most
common staging modality & CT Thorax (for staging)
▪ Allow assessment of primary lesion, its relation to the remainder of the pancreas, peripancreatic vasculature (assessment
of tumour relation to vessels) and determination of resectability
▪ Tumour appears as hypo attenuating indistinct mass (late arterial phase)
▪ Other features to look for: pancreatic atrophy, deformity of the glandular contour, double duct sign, metastatic lesions (i.e.
liver), portal vein or superior mesenteric artery involvement
▪ Double Duct Sign: Simultaneous dilatation of the CBD (intra-pancreatic segment) and the pancreatic duct
▪ Limitations: poor at detecting small liver or peritoneal neoplastic deposits of occult disease
EXTRA INFORMATION
Determination of Resectability
Abutment means < 180 degree contact with vessel & Encasement means > 180 degree contact with vessel
- Resectable: No arterial tumour contact, Minimal venous involvement

- Borderline Resection: Abutment of hepatic artery, or abutment of SMA, tumour causing venous distortion of the SMV/PV axis inc luding
short segment venous occlusion but suitable for reconstruction (sufficient proximal and distal vessel length)
- Unresectable Disease: (1) tumour abutting the celiac axis trunk, (2) encasement of hepatic artery or SMA, (3) encasement of the SMV/PV,
(4) distant mets
3. MRI pancreas with MRCP

▪ Used as an adjunct to CT, useful to visualize the primary tumour and its relationship to biliary and pancreatic ducts & peri-
pancreatic vasculature (assessment of tumour relation to biliary system)
69 Ann Surg Oncol. 2008 Dec;15(12):3512-20.

293
5. Endoscopic ultrasound + FNA biopsy
▪ Tissue diagnosis is used to rule out benign disorders that present with pancreatic enlargement and obstructive jaundice (i.e.
autoimmune pancreatitis, chronic pancreatitis)
▪ In setting of incidental diagnosis of solid pancreatic mass, a tissue diagnosis is essential to establish diagnosis and direct
treatment
▪ A biopsy specimen is not needed when the suspicion of cancer is high as the resection will provide therapeutic benefits and
substantially delaying surgery could set back commencement of effective treatment.
▪ FNA with EUS guidance is preferred to radiologically guided percutaneous needle biopsies as there is less risk of tumour
seeding – histological diagnosis is needed if patients are selected for neoadjuvant therapy.
6. ERCP (KIV stenting)

▪ ERCP can be used to assess obstructive intraductal lesions and to relieve biliary obstruction (i.e. stenting)
▪ ERCP stenting increases risk of post-operative complications in patients with resectable disease (though can be performed
for drainage of biliary obstruction)
7. Staging Laparoscopy
▪ Useful to identify small hepatic or peritoneal deposits, if required, laparoscopic ultrasound can also be use for patient with
suspected vascular invasion and to rule out radiologically occult metastatic disease (i.e. intra-hepatic metastases)
▪ Can be performed immediately before definitive operation or as an interval staging measure, institution dependent
STAGING - AJCC 8th Edition
Clinical staging classifies patients into (1) Local Resectable, (2) Borderline Resectable, (3) Locally Advanced or Unresectable and (4)
Unresectable – metastatic disease (NCCN Guidelines)
Local Resectable Borderline Resectable Locally Advanced Metastatic
Incidence About 10% 10% 30% About 60%
Median 17-23 months
Up to 20 months 8-14 months 4-6 months
Survival70 (20% 5 yr survival)
Stage III with tumour Stage III Stage IV
Stage Stage 0 to IIB
abutment (T4, any N, M0) (any T, any N, M1)
70 Lancet. 2011 Aug 13;378(9791):607-20. (same as earlier reference)

294
MANAGEMENT
Patients with pancreatic cancers are best managed by a multidisciplinary team including oncologists, surgeons, radiologists,
gastroenterologists, radiation oncologists, pathologists, pain management experts, social workers, dieticians and when appropriate
palliative care experts.
Chemotherapy and Radiotherapy

Neoadjuvant chemotherapy
- Used for borderline resectable pancreatic cancer (can down-stage ~ 30% of patients)
- Possibly a/w improvement in survival, however, no study has yet to clearly demonstrate this
- Possibly a/w lower pancreatic leak rates (?reason)
Adjuvant chemotherapy (gemcitabine + oral capecitabine)

- ESPAC-1 (2004, NEJM)71 study – best survival benefit with surgery + chemotherapy (5FU)
- Strong evidence exists that adjuvant therapy increases survival
Adjuvant radiotherapy
- ?benefit of CRT vs. CT, at present adjuvant RT used for margin positive PDAC resection
Surgery – Curative Resection (resectable disease)

Preoperative Biliary Drainage
- For patients with cholangitis or symptomatic liver dysfunction, otherwise no proven benefit
- Should be done prior to initiation of chemo/radiotherapy
Pancreaticoduodenectomy (Whipple Operation)

- Head of pancreas and duodenum share the same arterial supply (gastroduodenal artery), both organs must be removed if the
single blood supply is severed
- Removal of pancreatic head, duodenum, first 15cm of jejunum, CBD, gallbladder, partial gastrectomy
- Consensus panels recommends that PD be done at specialized centres doing at least 15-20 of these operations a year, however,
in general, recurrence rate is still high with overall 5 year survival at about 20% for patients after resection
- Octreotide decreases postoperative complications (i.e. lower incidence of pancreatic fistula and abdominal collection) and
hospital stay (in patients undergoing pancreatic surgery secondary to malignancy)72
- Operative mortality in experienced centres < 5%
Pylorus-preserving Pancreatico-duodenectomy Resection (PPPDR)

- Preserves gastric antrum, pylorus, proximal duodenum (duodenum is transected at least 2cm distal to pylorus)
- Duodenum anastomosis to Jejunum
- Compared to Whipple Procedure73
▪ ↓operating times, ↓intraop blood loss, (theoretical) – prevent reflux of pancreaticobiliary secretion into stomach, decreased
incidence of marginal ulceration, normal gastric acid secretion and hormone release
▪ No difference in in-hospital mortality, overall survival and morbidity, quality of life
71 N Engl J Med . 2004 Mar 18;350(12):1200-10.

72 Cochrane Database Syst Rev. 2010 Feb 17;(2):CD008370.
73 Cochrane Database Syst Rev. 2016 Feb 16;2:CD006053.

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EXTRA INFORMATION
Distal Pancreatectomy +/- splenectomy

- Done for resectable lesions of the body and tail of the pancreas
- Pancreatic neck is dissected from the portal vein and the splenic flexure of the colon is taken down
- When removing the spleen, vaccinate against pneumococci, meningococcal and HiB
- If posterior margins is of concern (i.e. Radical Antegrade Modular Pancreato-splenectomy (RAMPS))
- Spleen Preserving Distal Pancreatectomy (i.e. Kimura or Warshaw Technique)
Definition for Local Resectable Disease (no need biopsy of mass)

- No distant metastases (i.e. liver or peritoneal metastases)
- No extra-regional nodal disease (i.e. no hepatic hilar LN or celiac LN involvement)
- No involvement of IVC, aorta
- Definable tissue plane between tumour and celiac axis, hepatic artery and SMA – tumour does not encase celiac axis or SMA
(cannot involve > 1800 circumference)
- Reconstructable SMV or SMV-portal vein confluence if there is any occlusion, Small segments of PV/SMV (<2cm) can be
resected if needed, hence invasion of PV/SMV does not necessarily denote unresectability
Palliative Management of Pancreatic Cancer

- About 80% of patients are not suitable for curative resection
- Median survival for patients with locally advanced, non-metastatic pancreatic cancer is 8-14 months and for patients with
metastatic pancreatic cancer is 4-6 months
- Palliation of symptoms can be achieved either surgically or endoscopically
- Surgical palliation usually is for (a) obstructive jaundice or (b) upper GI tract obstruction
Surgical Measures
- Surgical bypass of obstruction – Double bypass involving anastomosis (see above)
▪ Stomach and jejunum (gastrojejunostomy)
▪ Biliary system and jejunum (usually hepatico-jejunostomy)
▪ Jejunum and jejunum – essentially a Roux-en-Y loop (entero-enterostomy)
Non-surgical palliative measures

- Palliative chemotherapy (i.e. gemcitabine) / radiotherapy / chemoradiotherapy
- Stenting (see below)
Complications Treatment
- Benefit from endoscopic biliary stenting (plastic or metal stent)
Obstructive Jaundice
- Percutaneous Transhepatic Cholangiography (PTC) Biliary Drainage
- Stents vs surgical bypass (GJ)
- Benefit from duodenal wall stents (wall stent): results in an earlier discharge from hospital and possibly improved survival
Gastric outlet obstruction
compared to gastrojejunostomy (median survival 110.5 days vs. 64 days) 74
(~20% of patients)
- Stents benefits: food intake improved more rapidly, shorter hospital stay, lower costs
- GJ benefits: better long term relief, less major complications, less chance of recurrence of symptoms / re-intervention
- Treat with endoscopic ultrasound or CT guided ablation of the plexus
Pain from coeliac plexus
- Ganglionectomy or direct injection of sclerosing agents
infiltration
- Slow-release morphine (step-wise escalation)
Venous thromboembolism - Prophylaxis is recommended – low molecular weight heparin (i.e. SC clexane)
- Enzyme replacement for steatorrhoea
Others
- Treat DM
74 Surg Endosc. 2002 Feb;16(2):310-2.

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COMPLICATIONS
Complications of Whipple’s operation

- Mortality rate is <4%, with a morbidity rate of up to 20-30% (mostly mild complications)
- Distal pancreatectomy has a higher morbidity and leak rates than PD though mortality rates remains the same
Early complications
- Delayed gastric emptying, subsides with conservative treatment
- Pancreatic fistula – (5-10% have clinically relevant fistulas)
▪ Diagnosed when amylase of drain fluid on or after POD 3 greater than 3x upper limit of normal serum amylase (biochemical
leak)
▪ May require endoscopic or percutaneous drainage
▪ Can lead to sepsis, hemorrhage, organ failure, death if not adequately drained externally – high mortality (20-40%)
▪ Risk factors: Pancreas texture, Underlying Pathology, Pancreatic duct diameter, Intraop blood loss (fistula risk score)
- Wound Infection
Above-listed are the 3 most common complications of PD

- Bleeding – GI haemorrhage, intra-abdominal haemorrhage (pseudoaneurysm of the GDA)
- Marginal ulceration – treat with PPI
- Injury to other organs – liver, kidney, bowel
- Infection – intra-abdominal abscess, peritonitis, sepsis
- Pancreatitis
- Bile leak – Appearance of bile in drain fluid. Leave drain in place until leak stops
- Pseudocyst formation may occur due to anastomotic leaks
Late Complications
- Long-term exocrine insufficiency resulting in malabsorption and steatorrhea
- Gastric stasis with pylorus-preserving Whipple
- Diarrhoea resulting from autonomic nerve injury during lymph node dissection
- Endocrine insufficiency resulting in DM

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PANCREATIC NEUROENDOCRINE TUMOUR (PNETS)
DEFINITION
Rare tumour, with ⅔ representing functional pancreatic endocrine neoplasm. Can have associations with MEN-1 syndrome.
Functional tumours – gastrinoma, insulinoma, glucagonoma, VIPoms, Somatostatinoma
- The presentation is dependent on the functional state of the tumour. For non-functional tumours, symptoms are related to mass
effect or metastatic disease.
- For functional tumours, confirm diagnosis (biochemically) prior to localization (radiologically)
MANAGEMENT
- Resection is curative (including metastatic disease)
- Functional P-NET should be resected – to palliate symptoms from hormonal production
- Non-functional P-NET with metastasis should undergo resection of both primary and metastatic lesion (improve survival)
- Synchronous cholecystectomy should be performed to reduce complications from adjuvant therapy
- Adjuvant therapy is reserved for metastatic disease (i.e. Octreotide – effective for symptoms with gastrinoma, insulinoma)
- Liver 1st site of metastatic spread
PROGNOSIS
- Ki67 (histological proliferation marker) > 2% indicates a higher risk of malignant behaviour in pancreatic neuroendocrine tumours
- 5 year survival ~ 92% (stage 1 disease) to 52% (stage 4 disease)
Gastrinoma
Zollinger-Ellison Syndrome (ZES) is caused by gastrinoma (most common pancreatic islet cell tumors in MEN 1)
Gastrinoma Triangle (Passaro’s Triangle)

- 70-90% of primary gastrinoma located within these boundaries:
- Superiorly = junction of cystic duct and common bile duct
- Inferiorly = junction of the 2nd and 3rd portion of the duodenum
- Medially = junction of the neck and body of pancreas
Clinical Presentation
- Refractory peptic ulcer, secretory diarrhoea (steatorrhoea), esophagitis
with stricture, heartburn, bleeding or perforated ulcer, familial ulcer, peptic
ulcer with hypercalcemia and gastric carcinoid → consider possibility of
underlying gastrinoma
- Epigastric pain, severe esophagitis – GERD, diarrhoea (21%)
- Multiple peptic ulcers – most in typical location (proximal duodenum) but also with atypical ulcer location (distal duodenum,
jejunum) suggestive for gastrinoma
Diagnosis
- Raised fasting serum gastrin* (> 200 or >1000pg/mL (diagnostic)
- Stomach basal acid output > 15mEq/hour
- Secretin stimulation test** – increase gastrin (> 200 pg/ml), normal patients secretin should suppress gastrin release
- Serum calcium & PTH levels – to rule out MEN 1 syndrome
- Somatostatin receptor scintigraphy (SSTR) octreotide scan (gold standard to localize tumour)
* Hypergastrinemia Differential Diagnosis – pernicious anemia, atrophic gastritis, treatment with PPIs, renal failure, G-cell hyperplasia and gastric outlet
obstruction – PPI should be held off for several days prior to gastrin measurement
** Secretin paradoxically stimulates gastrin release from gastrinoma due to abnormal adenylate cyclase activation – used to differentiate patients with
gastrinoma form those with other causes of hypergastrinemia
Management
- Duodenal gastrinoma: full-thickness excision of duodenal wall (may require whipple’s operation)
- Pancreatic gastrinoma: simple enucleation (<2cm) vs. formal pancreatic resection ± HSV (>2cm)
- Debulking can improve symptoms

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Insulinoma
Insulinoma is the most common functional pancreatic endocrine neoplasm originating from the islet of Langerhans – evenly
distributed through head, body and tail of pancreas – incidence 0.4/100,000
- Whipple’s Triad
▪ Symptomatic fasting hypoglycemia (episodes of neuroglycopenic symptoms ± autonomic symptoms)
▪ Documented serum glucose <50mg/dL (2.8 mmol/L)
▪ Symptom relief with administration of glucose
- Neuroglycopenic symptoms – visual change, diplopia, confusion, weakness, seizure, amnesia
- Autonomic symptoms – anxiety, palpitations, trembling, diaphoresis
Diagnosis
- Insulin to glucose (mg/dL) ratio >0.4 after fasting
- Elevated C-peptide levels
- Increased serum proinsulin level (>22 pmol)
- Imaging – CT pancreas (tri-phasic) – most insulinomas are vascular, well seen in arterial phase
- 10% of insulinoma is a/w MEN 1 syndrome – multifocal and higher rates of recurrence
Management
- Surgical exploration with intraoperative ultrasound
▪ Simple Enucleation (<2cm)
▪ Distal Pancreatectomy / Whipple’s – for tumours >2cm
- Medical – diazoxide therapy for management of hypoglycaemia ± octreotide
- Metastatic – 5FU and streptozocin
Glucagonomas (α cell tumour)

- 4Ds: diabetes, dermatitis (necrolytic migratory erythema), deep vein thrombosis & depression
- Rash occurs in 70% and commonly predates other systemic symptoms
- Diagnose with fasting glucose levels & increase plasma glucagon (>1000pg/mL),
- Majority are malignant and located in distal pancreas
VIPomas
- Causes WDHA syndrome: watery diarrhoea, hypoK+ and achlorhydria (WDHA)
- Diagnose with increase VIP levels (>1000 pg/mL), majority malignant and located in distal pancreas
- 10% extra-pancreatic (retroperitoneal / thorax)
Somatostatinomas (δ cell tumour)

- Diabetes, Gallstones & Steatorhoea
▪ Excessive somatostatin inhibits insulin secretion, leading to DM, also inhibit gastrin secretion (leading to hypochlorhydria)
& inhibit cholecystokinin secretion leading to cholestasis resulting in gallstones and steatorrhoea)
- Majority malignant and located in head of pancreas (perform cholecystectomy with pancreatic resection

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CYSTIC NEOPLASM OF THE PANCREAS
CLASSIFICATIONS
Differentials for cystic Pancreatic Mass

- Pancreatic Pseudocyst (see acute pancreatitis)
- Serous Cystadenoma
- Mucinous Cystadenoma & Cystadenocarcinoma (MCNs)
- Intraductal Papillary Mucinous Neoplasm (IPMN)
- Solid Pseudopapillary Tumour
Differential for solid Pancreatic mass

- Pancreatic adenocarcinoma
- Pancreatic neuroendocrine tumours
- Pancreatitis (focal chronic / autoimmune)
- Lymphoma (rare)
Work-up for Asymptomatic Patients with Incidental Pancreatic Cystic Mass 75

- < 2cm – single f/u in 1yr with MRI, if stable then no further f/u, if increase in size then proceed with further work-up
- 2 – 3cm – imaging with MRI/MRCP
▪ Uncharacterized cystic mass – yearly follow-up with MRI
▪ BD-IPMN – f/u q6 monthly for 2 years
▪ Serous cystadenoma – f/u q2yearly
- > 3cm
▪ Serous Cystadenoma – consider resection when ≥ 4cm
▪ Uncharacterized cystic mass or other cystic neoplasm – cyst aspiration, resection depending on comorbid and risk
Serous Cystadenoma
Benign tumour without malignant potential
- ~50% asymptomatic and detected incidentally
- Symptomatic: mild upper abdominal pain, epigastric fullness, weight loss, (if large) – jaundice, gastric outlet obstruction
Management
- Asymptomatic: observe with serial CT scans (must confirm diagnosis)
- Symptomatic: surgical resection (depending on location)
▪ Pancreatic Tail: distal pancreatectomy (no need for splenectomy)
▪ Pancreatic Head / Uncinate: Whipple’s
75 J Am Coll Radiol. 2010 Oct;7(10)754-73.

300
Mucinous Cystadenoma & Cystadenocarcinoma (MCNs)76
- Usually occurs in peri-menopausal females, incidental finding on imaging
- Non-specific symptoms: upper abdominal discomfort, pain, early satiety, LOW
Diagnosis
- Imaging (CT, EUS, MR): cystic lesion, thick walls, may by multi-septated, associated wall calcifications or nodules, commonly
located at body or tail of pancreas, type of liquid aspirated (mucoid)
- Fluid Amylase / Fluid CEA: (>200ng/ml) in the fluid may suggest malignant transformation
- K-RAS: any mutation detected
- Cytology: EUS guided FNA, any mucoid material
- Histology: tall columnar mucinous epithelium surrounded by cellular ovarian-type stroma (+/- atypical cells or adenocarcinoma)
Management
- Usually, open surgical resection required (for large tumours) as important not to rupture cyst
- Whipple’s Operation (head of pancreas lesions)
- Distal Pancreatectomy with splenectomy (ensure vaccination given pre-surgery)
- Prognosis: malignancy reported in 6-36% of mucinous cystadenoma (over 5 yrs), prognosis for mucinous cystadenocarcinoma
is typical to ductal adenocarcinoma of the pancreas
Intraductal Papillary Mucinous Neoplasm (IPMN)77

- Usually in 7th to 8th decade of life, equal gender predisposition
- Abdominal pain or recurrent pancreatitis (secondary to thick mucin obstructing pancreatic duct)
- Leads to weight loss secondary to exocrine insufficiency, steatorrhoea, diabetes
Diagnosis
- Imaging (CT Scan): diffuse dilatation of pancreatic duct, atrophic pancreatic parenchyma (due to
chronic duct obstruction), no calcification, commonly located at head of the pancreas
- ERCP: mucin extruding from ampulla of Vater (fish-mouth / fish-eye sign), presence of mucin within
a dilated duct is diagnostic
Management
- Malignant Transformation is found in main-duct type IPMN in 40-92% of cases78
▪ All main duct IPMN should be resected
▪ 70% of tumour harbour malignancy (invasive or non-invasive) with 45% demonstrating invasive carcinoma
- Malignant Transformation is found in branch-duct type IPMN in 15-25% of cases
▪ <1cm: observe with annual imaging
▪ 1-3cm: EUS-FNA / MRCP / ERCP to r/o high-risk features KIV serial imaging
▪ Symptomatic or ≥3cm: resect
- Prognosis: IPMN with invasive carcinoma (5yr = 60%, 10yr = 50%), better than typical ductal adenocarcinoma
▪ 5 year survival ~ 75% for intestinal type (colloidal) compared with 20% for pancreaticobiliary (tubular) type
EXTRA INFORMATION
Sendai Guidelines
- High-risk features – symptomatic, ≥ 3cm, solid component / mural nodules, dilated main duct (≥ 5mm)
Fukuoka Consensus Guidelines (2015)

- High-risk features – proximal lesion with obstructive jaundice, enhancing nodules, dilated main duct (≥ 10mm)
- Worrisome risk features – size ≥ 3cm, pancreatitis, non-enhancing nodules, thickened enhancing walls, dilated ducts (5 to <10mm), abrupt change
in duct calibre with distal atrophy, lymphadenopathy

- Resection for high-risk groups, surveillance for low-risk groups and EUS for intermediate group (group with worrisome feature)

78 Surgery. 2015 Nov;158(5):1192-202. [Important Paper]

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SPLEEN
Spleen is a retroperitoneal structure
EMBRYOLOGY
- Develops from the mesoderm (dorsal embryonic mesentery) – the mesentery between the spleen and stomach will become the
gastrosplenic ligament, the mesentery between the spleen and dorsal body wall becomes the splenorenal ligament
ANATOMY
- Normal Spleen: 1,3,5 inches (size), 7oz (weight), 9-11 ribs (location)
- Splenomegaly: spleen ≥ 500g and/or ≥ 15cm in length
- Massive splenomegaly: spleen ≥ 1000g and/or ≥ 22cm in length

- Accessory spleen: splenic hilum (54%), pedicle (25%), tail of pancreas (6%), splenic colic ligament (2%), greater omentum
(12%), mesentery (0.5%) & left ovary (0.5%)
- Ligament supports
▪ Splenocolic ligament – colon
▪ Gastrosplenic ligament – stomach (only ligament that is vascular – short gastric arteries)
▪ Splenophrenic ligament – diaphragm
▪ Splenorenal ligament – kidney, adrenal and tail of pancreas
BLOOD SUPPLY
- Splenic Artery
▪ Distributive Type (70%) – short trunk with long branches entering over 75% of medial surface
▪ Magistral Type (30%) – long main trunk with short terminal branches entering 30% of medial surface
- Short gastric vessels
SPLENIC CYST & ABSCESS
Splenic Cyst
Causes includes, parasitic (i.e. echinococcus infection), non-parasitic (i.e. primary (congenital) or secondary (pseudocyst)
Patients can be symptomatic (vague left upper quadrant discomfort) or asymptomatic (incidental findings). Management is usually
conservative. Surgical intervention for symptomatic cyst or cysts >5cm. Options include partial splenectomy (open or laparoscopic)
Splenic Abscess
Causes include haematogenous spread from another septic focus (i.e. endocarditis, diverticulitis, tuberculosis) or trauma to spleen
which makes the organ more susceptible to infection. Splenic abscess can be lethal if not treated appropriately
Management is with IV Antibiotics +/- splenectomy (source control). Percutaneous Drainage a/w high rates of abscess recurrence.
APPROACH TO ENLARGED SPLEEN (SPLENOMEGALY)
- Infection – viral, bacterial, parasitic (i.e. schistosomiasis, malaria), others (i.e tuberculosis)
- Hematological – leukemia, lymphoma
- Portal Hypertension
- Neoplastic – lymphoma, myeloproliferative disorders
- Inflammatory – rheumatoid, systolic lupus, amyloidosis
Indications for splenectomy

- Splenic Trauma / Splenic Rupture
- Splenic Abscess
- Splenic Cyst
- Neoplasm – distal pancreatectomy (pancreatic CA invading to spleen), gastrectomy (gastric cancer invading into spleen)
- Haematological disorders – RBC disorders (spherocytosis, HbSS, thalassemia), WBC disorders (leukemia, myelofibrosis, CML,
CLL), platelets disorders (ITP, Felty’s syndrome)
Preoperative considerations
- Vaccination against encapsulated organisms at least 2 weeks prior or within 7 – 10 days after emergent splenectomy -
Streptococcus pneumoniae, Haemophilus influenzae, and Neisseria meningitidis
- FBC – Optimise hb and platelets count
- PT/INR/APTT - Normalise coagulation profile
Post-operative considerations

302
- Yearly Influenza vaccine
- Vaccinate against pneumococcus, meningococcus C (both repeated every 5 years) and H. influenzae type B (Hib) (repeated
every 10 years)
- +/- Long term oral penicillin prophylaxis (usually in pediatric population)
- Asplenic patients should carry a medical alert and an up-to-date vaccination card
Complications of Splenectomy
- Bleeding – may necessitate conversion to hand-assisted or open procedure
Intra-operatively - Injury to surrounding organs (i.e. tail of pancreas -> pancreatitis/ pancreatic abscess/ pancreatic fistula,
splenic flexure of the transverse colon, greater curve of the stomach ->gastric fistula, diaphragmatic injury)
- Pulmonary Complications – left basal atelectasis, pneumonia and pleural effusion
- Surgical Site Infection (i.e. wound infection, deep/organ space (i.e. subphrenic abscess))
- Vascular Cx: atherothrombosis & venous thrombosis (acute portal vein thrombosis)
Early
- Thrombocytosis: plt count usually peaks after 7-10days (KIV prophylactic aspirin). High risk of DVT.
- Stomach: gastro-paresis, ileus
- Rare: post-splenectomy necrotizing pancreatitis, pulmonary hypertension
- Overwhelming Post-splenectomy Infection (OPSI) → encapsulated bacteria (i.e. strep pneumonia, H.
Influenzae & N. meningitidis), risk of mortality highest in first 2 years*

Late ▪ Polyvalent Pneumococcal Vaccine (Pneumovax) – repeat every 5-7yrs
▪ Meningococcal Vaccine – once
▪ Haemophilus Influenzae Type B conjugate vaccine
▪ Seasonal Influenza Vaccine
Post-splenectomy sepsis syndrome (medical emergency)

- Lifetime risk <1 to 5% (increase risk in children)
- S. pneumonia (#1), N meningitidis, H. Influenza, Group A Strep
- Indication for splenectomy is the most influential determinant of OPSI risk (i.e. highest in patient who undergo splenectomy for
haemolytic disorders or malignancy)
- Children <5 years and adults > 50 years are also at elevated risk
- Patients present with nonspecific flu like symptoms rapidly progressing to fulminant bacteremia septic shock, DIVC, anuria and
death within 12-48hrs – estimated mortality = 0.73 per 1000 patient years – hence need for high index of suspicious and early
empirical treatment
- Vaccinations – 2 weeks before planned elective splenectomy or within 7 – 10 days after emergent splenectomy

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11. BILIARY SYSTEM
ANATOMY & PHYSIOLOGY OF THE BILIARY SYSTEM
ANATOMY
- Gallbladder – divided into 4 anatomical areas: fundus, body, infundibulum & neck
▪ Pear-shaped sac, 7-10cm long, average capacity of 30-50ml (can distend up to 300ml)
▪ Lies beneath segment IV and V
▪ Lined by simple columnar epithelium, it lacks muscularis mucosa and submucosa. The muscularis externa is not
organized into 2 distinct layers. The surface is covered by peritoneal serosa (mesothelium)
- Common Hepatic Duct (~4cm) – fusion of right and left hepatic duct at porta hepatis
- Cystic Duct (~4cm) – variation exists
- Common Bile Duct (~10cm) – diameter (5-10mm), no distinct muscle layer (no peristalsis)
▪ Upper 1/3 (supra-duodenal ~4cm) – edge of hepatoduodenal ligament, right of hepatic artery
▪ Middle 1/3 (retro-duodenal) – curves behind first part of duodenum, diverge laterally
▪ Lower 1/3 (pancreatic) – curves behind head of pancreas, enter 2 nd part of duodenum
- Union of CBD and pancreatic duct:

▪ 70% → duct unite outside duodenal wall
▪ 20% → duct unite within duodenal wall
▪ 10% → ducts exit via separate opening
- Cystic artery – branch of right hepatic artery, found within the hepatocystic triangle ∆
▪ Cystic duct (lateral), common bile duct (medial), liver (superior) – triangle of calot*
- Lymphatics are on the right side of the common bile duct

- Normal Sizes: CBD <8mm (<10mm after cholecystectomy), GB wall <4mm, Pancreatic duct <4mm
11. Biliary System_Last Updated 3rd June 2020

304
EXTRA INFORMATION
Cystic Artery Anatomy79
A – Cystic artery from RHA or aberrant RHA (80-90%)

B – Cystic artery from LHA (2%)
C – Cystic artery from GDA (2%)
D – Illustrate the cystic artery travelling anterior to the CBD
E – Illustrate the cystic artery travelling anterior to the CBD and inferior to cystic duct
F – Short cystic artery, defined as <1cm (9.5%)
G – Multiple cystic arteries (i.e. both from RHA, one from RHA & one from LHA, one from RHA & one from CHA)
Bilirubin Metabolism
79 Surg Radiol Anat. 2016 Jul;38(5):529-39.

305
PHYSIOLOGY (BILIRUBIN METABOLISM)
- RBCs are broken down in the spleen which released Hb which is broken down into heme and globin (globin is broken down into
amino acids and reabsorbed)
- Heme (heme oxygenase) → porphyrin ring and iron
- Porphyrin ring → biliverdin
- Biliverdin (biliverdin reductase) → unconjugated/indirect bilirubin

- Unconjugated Br (released from macrophage) which is water insoluble is then bound to albumin and sent to the liver
- Unconjugated Br conjugated with glucuronic acid (urine diphosphate glucuronosyltransferase) → conjugated / direct bilirubin
- Bilirubin is stored in the gallbladder and excreted in the bile which enters intestines
- Conjugated bilirubin degraded by intestinal bacterial into urobilinogen
▪ 80% excreted in faeces as stercobilin (brown stools)
▪ 10-20% reabsorbed by intestines → 18% taken up by liver via the portal system – enterohepatic circulation of bilirubin
▪ 2% excreted in urine as urobilin (yellow urine)
- Liver can usually cope with an increase in unconjugated bilirubin → patients with haemolysis may therefore be slightly jaundiced
with a normal colour urine and stools.
- Under normal circumstances, tiny amount of urobilinogen is excreted in the urine, in complete biliary obstruction or severe
intrahepatic cholestasis → conjugated bilirubin leaks out and appears in urine giving it a tea-coloured appearance and faeces
take appearance of china clay cause of lack of formation of urobilinogen.
COMPOSITION OF BILE
- Water
- Phospholipids, electrolytes
- Bile salts – cholic acid, chenodeoxycholic acid (reabsorbed in the terminal ileum > portal venous system > liver > secreted back
into bile)
- Bile pigments – conjugated bilirubin
PHYSIOLOGY (FUNCTIONS OF THE GALLBLADDER)

1. Reservoir for bile^ (~50ml)
2. Concentration of bile (5-10x) → active absorption of water, NaCl and HCO 3- by mucous membrane of the gallbladder (prevents
GB from being distended)
3. Secretion of Mucus, with obstruction of the cystic duct have risk of mucocele formation
4. Gallbladder contraction stimulated by cholecystokinin (CCK), mediated by cholinergic vagal neurons (CCK half-life: 2-3 minutes)
* ↑bile excretion – CKK, secretin, vagal input | ↓bile excretion – somatostatin, sympathetic stimulation
** GB lined by columnar epithelium with microvilli (absorption to concentrate bile), no submucosa / goblet cells
^ bile is normally neutral pH but varies with diet, increase in protein shifts bile to become more acidic

306
APPROACH TO JAUNDICE80
DEFINITION
Jaundice is defined as yellow pigmentation of the skin and eyes as a result of excess bilirubin in the circulation, clinically detectable
when levels are >40umol/L (normal: <22umol/L). Obstructive jaundice (post-hepatic) results from biliary obstruction which is
blockage of biliary duct that carries bile from liver to gall-bladder and to the duodenum.
PATHOPHYSIOLOGY
Pathophysiology of Obstructive Jaundice

Increased risk of hepatic dysfunction, renal failure, cardiovascular compromise, coagulopathy & nutritional deficiency.
- Hepatic Dysfunction:
▪ Obstruction of the biliary system leads to increased biliary pressure (from low pressure to high pressure system) reducing
the excretion ability of hepatocytes.
▪ Bile production is reduced.
▪ Secretory, metabolic and synthetic function of the liver is reduced.
▪ Excretory products reflux back into the systemic circulation leading to toxicity. (decreased albumin, clotting factor).
- Renal Failure
▪ Decreased cardiac output leads to decreased renal perfusion.
▪ increased systemic bile salts which leads to diuretic and natriuretic effects causes severe volume depletion.
▪ Increased endotoxin due to decreased hepatic clearance leads to direct parenchymal toxicity.
- Cardiovascular
▪ Decreased cardiac contractility (coupled with decreased total peripheral resistance) makes patients susceptible to
hypotensive shock
- Coaguloapthy
▪ Impaired vitamin K absorption from the gut due to a lack of intestinal bile.
▪ Endotoxin in systemic circulation cause disseminated intravascular coagulation with increased fibrin degradation products
- Nutritional Deficiency
▪ The lack of intestinal bile salts leads to anorexia, decreased absorption of fat and fat soluble vitamins
80 uptodate: Diagnostic approach to the adult with jaundice or asymptomatic hyperbilirubinemia

307
For patients presenting with jaundice, the initial evaluation is to determine if this is a post-hepatic (obstructive) cause or medical
cause of jaundice. For patients with obstructive jaundice, the next step is to differentiate between a benign cause from a malignant
cause.
Presenting Complaint (symptomatology)

- Determine the type of jaundice
▪ Direct hyperbilirubinemia (conjugated): presence of tea coloured urine, pruritus, pale stools
▪ Indirect hyperbilirubinemia (unconjugated): normal coloured urine and stools
- Onset of Jaundice
▪ Is this the first episode?, how long has it been ongoing for?
▪ Episodic or Constant
- Painful or Painless Jaundice

▪ Painless progressive jaundice (more likely underlying malignancy)
- Any associated symptoms

▪ LOW / LOA (underlying malignancy)
▪ Nausea / Vomiting (common , may also be a feature of gastric outlet obstruction with underlying malignancy)
▪ Abdominal bloatedness (possible ileus)
▪ Steatorrhoea – passage of foul-smelling stools which float on water (pancreatic exocrine dysfunction)
▪ New Onset Diabetes (pancreatic endocrine dysfunction)
▪ Shortness of Breath or Lower Limb Edema (underlying hypoalbuminemia)
What is the likely aetiology?

- Pre-hepatic
▪ Previous episodes, sudden onset, precipitating factors (food, drugs, stress), self-resolving nature
▪ Personal/family history of G6PD, family history of jaundice
▪ Symptoms of anaemia
▪ Transfusions, mechanical heart valve replacement, autoimmune conditions, malaria
- Hepatic
▪ Acute viral hepatitis – classic prodromal symptoms – fever, malaise, arthralgia, myalgia, nausea, vomiting
▪ Risk factors for hepatitis – travel history, blood transfusions, IVDA, tatoos, seafood ingestion, sexual contact, family history
of hepatitis, any vaccination history
▪ Chronic liver disease – chronic hepatitis, alcohol abuse, previous liver ultrasound
▪ Drug history
▪ Alcohol History
▪ Autoimmune – rash, red eyes, joint pain (extrahepatic manifestations)
- Post-hepatic
▪ Abdominal pain, stomach distention, pain radiating to back
▪ Underlying Malignancy – LOA/LOW, painless progressive jaundice
▪ History of biliary colic, gallstone disease (i.e. acute cholecystitis, cholangitis)
▪ Previous surgeries (i.e. cholecystectomy, liver resections, etc.), endoscopic procedures (i.e. ERCP)
Are there any likely complications?

- Cholangitis
▪ Charcot triad – fever, jaundice, RUQ pain
▪ Reynold’s Pentad – Charcot triad + septic shock + mental obtundation
- Acute pancreatitis
▪ Sudden onset of epigastric pain with radiation to the back, may be a/w nausea and vomiting
- Portal HTN with Upper BGIT
▪ Hematemesis or melena (portal hypertension and UBGIT)

308
- Vitals: hemodynamically stability, fever
- Assessment of hydration status
- General Inspection: jaundice (scleral icterus, mucous membrane), pallor
▪ A skin discoloration can be mimicked by: (DIET) Consumption of large qty of food containing lycopene or carotene, (DRUG)
Ingestion of drugs such as rifampicin, quinacrine or TCMs, (OTHERS) – dirty sclera due to biological variation, uremia due
to CKD, hemosiderosis due to repeated blood transfusion
- Assessment for stigmata of chronic liver disease

▪ Start from periphery before moving on to the abdomen (i.e. any gynecomastia, clubbing of fingernails, palmar erythema,
flapping tremor of the hands)
▪ Pruritic scratch marks
▪ Bruising (coagulopathy)
▪ Signs of chronic alcoholism – parotidomegaly, Dupuytren’s contractures
- Abdomen
▪ Any scars from previous abdominal surgery
▪ Presence of spider nevi (chronic liver disease), caput medusa (portal venous obstruction)
▪ Tenderness
▪ Generalized distention? (ascites could be due to malnutrition, peritoneal malignancy, or portal HTN)
▪ Hepatomegaly (Could be due to metastatic disease, or primary liver pathology)
▪ Enlarged palpable gallbladder (Recall Courvoisier’s law)
▪ Splenomegaly (Portal hypertension – think pre-hepatic, hepatic, post hepatic)
▪ DRE: Pale stools
- Cardiovascular & Respiratory examination

- Lower Limb – presence of any pedal edema
COURVOISIER’S “LAW”
When the common bile duct is obstructed by a stone, distention of the gallbladder is rare; when the duct is obstructed for some
other reason, distention is common81 “law” is explained by chronicity of obstruction82 – chronically elevated intra-ductal pressure
are more likely to develop with malignant obstruction, gallstones causes obstruction in an intermittent fashion, which is not
consistent enough to produce such a chronic rise in pressure
Basically, in patients with a palpable enlarged gallbladder and painless jaundice, the cause if unlikely to be stones –
malignancy until proven otherwise
Exceptions:
- Mirizzi’s Syndrome- stone in Hartmann’s pouch
- Double Impaction – stones occluding cystic duct and distal CBD
- Oriental cholangiohepatitis – ductal stones form secondary to liver fluke infestation
- Congenital choledochal cyst
- Common hepatic duct obstruction – lymph node at porta hepatis / cholangiocarcinoma
81 Lancet. 1985 Dec 7;2(8467):1293-4.

82 World J Surg. 2009 Apr;33(4):886-91

309
Jaundice can be classified as pre-hepatic (hemolytic), hepatic and post-hepatic (obstructive). A comparative table is placed in a
separate document.
Causes of Obstructive Jaundice

- Commonest causes – Gallstones, Tumour, Hepatitis
- Painful Obstructive Jaundice: Choledocholithiasis (+/- cholangitis), strictures, hepatic causes
- Painless Obstructive Jaundice: Periampullary tumour (see below)
Intrahepatic Extrahepatic
- Hepatitis Intraluminal Mural Extramural
- Drugs
Benign Benign Benign
- Cirrhosis
- Gallstones – CBD stones - Benign Strictures (post- - Mirizzi syndrome
- Primary Biliary
- Parasitic Infestation inflammatory, post-operative, - Chronic Pancreatitis
Cirrhosis (PBC)
(recurrent pyogenic post-instrumentation, pancreatitis) Malignant
cholangitis, clonorchis, - Primary sclerosing cholangitis - Periampullary Tumour
schistosomiasis) - Choledochal cyst - Metastases to the porta hepatis
Malignant (malignant lymph nodes)
- Cholangiocarcinoma (distal)
Choledocholitiasis
- Ask patient about past history of gallstone disease / biliary colic symptoms / previous history of surgery / ERCP
- Suspect choledocholithiasis if jaundice is episodic (recurrent spikes), painful or if u/s shows presence of gallstones – usually if
patient is young and have painful jaundice more likely to be benign causes
Postoperative Jaundice
- Affects 1% of all surgical patients undergoing hepatobiliary procedures
- Differentials: (1) retained CBD stones, (2) post-op biliary leak, (3) injury to CBD +/- stricture formation
Periampullary Tumours
- These are tumours that arise within 2cm of the ampulla of vater in the duodenum.
- Malignancy is suspected when patient is old, jaundice is new onset, painless and progressively worsening
- Ask about constitutional symptoms (i.e. LOA/LOW/malaise) and metastatic symptoms (i.e. SOB, bone pain)
- Pain is a late symptom of pancreatic cancer and tend to be constant and relentless compared to biliary colic which subsides after
a few hours
Tumours Relevant History 5-year Survival

- New onset diabetes + recalcitrant diabetes – ask about diabetic control (is it
Pancreatic Head / well managed with medications!) 15-25%
Uncinate Process - Dull aching pain radiating to the back (if surgically
Adenocarcinoma (85%) - Pseudo GOO (gastric outlet obstruction) – duodenal obstruction (10-15%) curable)
- Worsening steatorrhea
- Present with jaundice, abdominal pain and LOW
Cholangiocarcinoma 20 – 40%
- Age of patient, more common in elderly (requires a high index of suspicion)
- Present with early obstructive jaundice, biliary colic, bleeding or pancreatitis
Ampulla of Vater - Intermittent Jaundice – as a tumour grows, it outgrows its blood supply,
35 – 55%
Adenocarcinoma resulting in central necrosis and tumour sloughing, the lumen re-expands
and jaundice is alleviated
- Patient usually in the 6th to 8th decade of life
- Present with abdominal pain, iron deficiency anaemia*, LOW, nausea &
Duodenal vomiting and obstructive jaundice
40 – 60%
Adenocarcinoma (5%) - Obstructive jaundice + anaemia (chronic GI bleed) → silver stools
(Thomas’s sign) – can occur in any periampullary carcinoma

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Benign Strictures
- Can be Iatrogenic, Inflammatory or Congenital
- Bile duct strictures without a history of pancreatitis or biliary surgery is malignant until proven otherwise
- Most commonly occur following laparoscopic cholecystectomy due to bile duct injuries (i.e. surgical
Iatrogenic Injury inexperience, misplaced clips, excessive use of cautery, excessive dissection around the major ducts
after Surgery resulting in ischemic injury)
- Other surgeries includes: Hepatic resection, Liver transplant
- Endemic to Asian patients of Chinese descent
- Infection with bacteria (i.e. E.coli, Klebsiella, Bacteroides, Enterococcus Faecalis), biliary parasites (i.e.
Ascaris Lumbricoides, clonorchis sinensis & Opisthorchis Viverrini)
- Characterized by:
Oriental ▪ Recurrent bacterial cholangitis
Cholangiohepatitis ▪ a/w intra-hepatic brown pigment stones and
(Recurrent ▪ Intrahepatic biliary obstruction
Pyogenic ▪ Biliary strictures (recurrent cholangitis) leads to further stone formation, hepatic abscess, liver failure
Cholangitis) (secondary biliary cirrhosis)
- Investigations: MRCP (detect obstruction, define strictures and stones)
- Management: extract stones and debris and relieve obstruction
▪ Roux-en-Y hepaticojejunostomy (RYHJ)
▪ Liver resection of involved segment
- Autoimmune cholestatic disorder characterized by progressive fibrous obliteration of the intrahepatic and
extrahepatic bile ducts
- Mean Age of presentation: 30-45, Males > Females (2:1)
- Investigations
▪ Liver biopsy – fibrous obliteration of small bile ducts (also assess degree of liver cirrhosis)
▪ ERCP – multiple dilatation and strictures (beading) of intra & extra-hepatic biliary tree
- Association / Prognosis
▪ PSC affects ~5% of UC patients, and 60-80% of PSC patients suffer from IBD (ulcerative colitis) –
Primary Sclerosing colectomy for colitis makes no difference to the course of PSC
Cholangitis (PSC) ▪ Ridel’s thyroiditis and retroperitoneal fibrosis a/w PSC
▪ PSC is a risk factor for cholangiocarcinoma – affect 10-20% of patients
▪ Leads to portal hypertension and liver failure (median survival 10-12 yrs)
- Management
▪ Biliary Stricture → dilated / stented (ERCP / PTC)
▪ Extra-hepatic / bifurcation strictures → Resection and RYHJ
▪ Advanced liver disease → transplantation (5yr survival ~ 85%)
- Chronic Pancreatitis (accounts for ~ 10% of benign strictures)

- Radiotherapy
- Ampullary stenosis / Sphincter of Oddi Dysfunction (high pressure)
Other Causes
- Ischemic injury
- Choledocholithiasis, Extraluminal compression (i.e. Mirizzi Syndrome) - due to repeated inflammation
- Choledochocal Cyst
Congenital - Biliary Atresia

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Pre-hepatic Jaundice Hepatic Jaundice Post- Jaundice
Jaundice Unconjugated
Unconjugated/conjugated hyperbilirubinemia Conjugated hyperbilirubinemia
/ Skin hyperbilirubinemia
Orange Tint Greenish Tinge
Colour Lemon Yellow
Stool Dark colour (due to increased
Pale stools Pale (no urobilinogen and no stercobilin)
Colour stercobilin)
Urine
Normal Dark (conjugated hyperbilirubinemia) Tea colour (conjugated hyperbilirubinemia)
Colour
No pruritus (no bile Intense Pruritus, presence of scratch marks
Pruritus -
accumulation) (bile accumulation)
Spleen Splenomegaly Normal to Mildly Enlarged -
Total bilirubin raised (often mixed direct/indirect) Total bilirubin raised / Direct bilirubin
Total bilirubin raised
ALT & AST: Raised disproportionate to ALP and GGT raised
Direct bilirubin normal
▪ AST>ALT → toxins (AST in mitochondria) Indirect bilirubin normal
LFTs Indirect bilirubin raised AST & ALT → mildly Elevated
▪ ALT>AST → viral (ALT in cytoplasm)
ALT/AST/ALP/GGT normal
ALP & GGT: Raised (in cholestatic phase) ALP & GGT → elevated > AST & ALT
↑ LDH, ↓ haptoglobin*
Liver Proteins: ↓ serum albumin in chronic liver failure Liver Proteins: Normal
FBC Anemia with Reticulocytosis Low Platelets -
Anorexia
Others ± Enlarged Gallbladder
Hepatic Tenderness
Viral hepatitis serology: Ultrasound HBS:
▪ Acute: Anti-HBc IgM, Anti-HAV IgM ▪ If ducts dilated (>8mm), do
PBF
▪ Chronic: HBsAg, anti-HBs, anti-HCV ERCP/MRCP
Direct Coombs test for
± Prolonged PT/PTT, Prolonged INR (impaired liver fx) ▪ If ducts not dilated, further serologic
autoimmune haemolytic
Autoimmune screen: ANA, anti-dsDNA, AMA testing: Anti-mitochondrial Ab (AMA-
Other anemia
Metabolic screen: Ceruloplasmin, 24 hour urine copper M2 IgG) most specific for PBC, p-
Invx
AFP: malignant aetiology antineutrophil cytoplasmic Ab and
Stool OCP (ova, cysts,
Abdominal U/S: anti-smooth muscle Ab (p-ANCA &
parasites)
anti-SMA) more specific for PSC.
Malaria ▪ Liver surface nodularity,↑ echogenicity in cirrhosis
(ANA may also be positive)
▪ Signs of portal HTN (splenomegaly & ascites) ▪ Consider ERCP, liver biopsy
Infective
▪ Acute Viral Hepatitis (HAV, HBV)
▪ EBV, CMV, Herpes Simplex, TB Intraluminal
Inherited Hemolytic Anemia ▪ Hepatic Abscess ▪ Gallstones
▪ Membrane – hereditary ▪ Parasitic Infestation (i.e. clonorchis
spherocytosis & Autoimmune Hepatitis sinensis, schistosomiasis)
elliptocytosis
▪ Hb synthesis– sickle Drug Induced Hepatitis Mural
cell anemia, ▪ Direct action (metabolite-related) - i.e. phenytoin, ▪ Biliary strictures (post-inflammatory /
thalassemia carbamazepine, Isoniazid, statins, MTX, Paracetamol^ surgery)
▪ Enzyme– G6PD (Transaminases can be > 1000IU/L) ▪ Mirizzi Syndrome (compression of
deficiency, pyruvate ▪ Immunological Reaction - i.e. methyldopa, halothane CHD)
kinase deficiency ▪ PBC (intrahepatic bile ducts)
Liver cirrhosis/chronic liver disease ▪ PSC (intra & extrahepatic)
Causes ▪ Alcoholic Liver Disease
Acquired Hemolytic Anemia ▪ Cholangitis (Charcot’s triad)
▪ Immune – i.e. ▪ Chronic viral hepatitis (HBV, HCV) ▪ Cholangiocarcinoma
transfusion reaction ▪ Metabolic (Wilson’s, hemochromatosis)
▪ Mechanical – i.e. heart ▪ Infiltrative (Sarcoidosis, amyloidosis) Extraluminal
valves ▪ Metastatic Disease ▪ Malignant: Periampullary Tumour
▪ Infective – i.e. malaria ▪ Malignant lymph nodes at the porta
▪ Autoimmune – i.e. SLE Hereditary hyperbilirubinemia** hepatis
▪ Haemolytic uremic Inherited ↓/absent activity of UDPGT (unconjugated hyperBr) ▪ Benign: Chronic Pancreatitis
syndrome ▪ Gilbert’s syndrome (AD)
▪ Drugs (i.e. rifampicin) ▪ Crigler Najjar 1 & 2 (AR) – type 1 more fatal Others
▪ Burns ▪ Choledochal cyst
▪ Poor nutritional state Inherited impaired biliary excretion (conjugated hyperBr) ▪ Biliary atresia
▪ Dubin-Johnson (AR) – deficiency with secretion
▪ Rotor (AR) – deficiency with storage
* haptoglobin: protein that binds free haemoglobin and transfer it to liver
** Hereditary Hyperbilirubinemia
Gilbert Syndrome – mildest form, defective uptake of bilirubin & decreased uridine diphosphate glucuronosyltransferase (UDPGT)
Crigler Najjar Type 1 – most fatal, absence of UDPGT, unable to conjugate bilirubin – requires gene replacement therapy or liver transplant
Crigler Najjar Type 2 – partial deficiency of UDPGT, treatment with phenobarbital
Dubin-Johnson – defect in transport protein (MOAT protein) responsible for excretion of bilirubin glucuronide, black pigmentation of liver
Rotor – Variant of Dubin-Johnson but liver is not pigmented. Similarly, no clinical consequences
^ paracetamol overdose cause liver damage via creation of toxic metabolite by the cytochrome p450 system which overwhelms glu tathione stores, the reactive
intermediate combines with lipid bilayer of hepatocyte causing cellular necrosis (treatment: replace glutathione with sulfhydryl compounds such as acetylcysteine)

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INVESTIGATIONS
Investigations are dependent on the likely underlying cause of the jaundice. Initial investigations involve biochemical assessment to
differentiate between conjugated and unconjugated hyperbilirubinemia. Subsequent investigations are to rule out sepsis (i.e.
cholangitis) and for evaluation of the underlying etiology accounting for the jaundice.
Biochemical Investigation
- FBC (assess for any raised inflammatory markers, anemia, thrombocytopenia)
- U/E/Cr (assess hydration status, assess suitability for contrasted scan)
- LFT – serum albumin, serum bilirubin, direct and indirect bilirubin, ALT/AST, ALP/GGT
- PT/INR/APTT (coagulopathy could be secondary to liver dysfunction and vitamin K malabsorption)
- Serum Amylase (pancreatitis)
- Hepatitis Serology – HBsAg, Anti-HBs, Anti-HCV
- Blood cultures (if septic)
- Tumour Markers – AFP, CA19-9, CEA (if suspect underlying malignancy)
Other Biochemical Investigations (ordered with consultation with medical hepatologist)

- Peripheral Blood Film
- Direct Coombs Test
- Autoimmune screen – anti-dsDNA, ANA, AMA
- Metabolic screen – 24 hour urine copper, ceruloplasmin
- Serum Paracetamol level (if suspect drug overdose)
Interpretation of Liver Function Test

LFT measures the amount of hepatocellular damage, more accurate measure of liver synthetic function is via serum albumin and
prothrombin time (PT)
Hepatocellular Injury – indicated by AST / ALT

- Aspartate Transaminase (AST) found in liver, cardiac & skeletal muscle, kidney, brain, pancreas, lung, RBC – thus less specific
for liver disorder
- Alanine Transaminase (ALT) predominantly found in liver
▪ AST: ALT ratio of >2:1 suggest alcoholic liver disease,
▪ mild elevation = non-alcoholic fatty liver disease, chronic viral infection, medication-induced injury
▪ moderate elevation = acute viral hepatitis
▪ marked elevation (>1000) = ischemic hepatitis, toxic ingestion (i.e. paracetamol), fulminant hepatitis
▪ R factor = ALT / ALP ratio (if > 5, hepatocellular pattern of injury; if < 2, cholestatic pattern of injury; if between 2 and 5,
mixed pattern)
Abnormal Synthetic Function - indicated by serum albumin and prothrombin time / INR
- Albumin (negative acute phase protein) – dependent on nutritional status, renal dysfunction, protein-losing enteropathy,
hormonal disturbances, half-life of 15-20days → not a marker of acute hepatic dysfunction
- Clotting Factors (except factor VIII) → best test of hepatic synthetic function
Cholestasis
- Alkaline Phosphatase (ALP) found in liver (bile duct epithelium, i.e. canalicular membrane), bone, kidney, placenta, malignant
tumours (i.e. bronchial carcinoma) – heat inactivation can separate it into heat labile (bone) and heat stable (liver) [bone burns,
liver lasts], half-life of 7 days, may take several days to normalize even after resolution of biliary obstruction (ALP can also be
elevated in pregnancy and children)
- Y-glutamyl transpeptidase (GGT) – elevation is an early marker, sensitive for hepatobiliary disease though not specific (i.e.
alcohol abuse, pancreatic disease, MI, renal failure, obstructive pulmonary disease)
Obstructive Jaundice
- Raised direct (conjugated) bilirubin > indirect bilirubin
- Raised ALP more than AST and ALT
- Mildly raised liver enzymes (ALT/AST) – biliary backpressure leads to hepatocyte damage
- Urine dipstick – high bilirubin, no urobilinogen

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Imaging Investigations
The aim is to confirm presence of extrahepatic obstruction, determine the level of obstruction and to identify the specific cause of
obstruction. If the underlying cause is due to malignancy, a staging CT scan must be performed.
- Ultrasound HBS (1st line)

▪ Assess for presence of Liver Cirrhosis (increased surface nodularity, increased echogenicity), fatty liver, liver lesions
▪ Assess for presence of any gallbladder stones, any GB complications (i..e cholecystitis)
▪ Assess for presence of intrahepatic and/or extrahepatic ductal dilatation (normal CBD is 5-6mm + 1mm for every 10 years
above 50 years old)
▪ Disadvantages: operator dependent, unable to detect distal CBD lesions (i.e. stone), unable to detect malignancy well,
sensitivity reduced in obsese patients / distended bowel
- CT Abdomen & Pelvis

▪ Useful if suspecting malignancy as cause of obstruction or if suspecting alternative diagnosis
- Magnetic Resonance Cholangiopancreatography (MRCP)

▪ Excellent for visualizing the biliary and pancreatic ducts
▪ Used if US HBS confirms presence of gallstones and LFTs remains deranged, MRCP is a good tool to confirm presence
and location of bile duct stones
- Chest XR
▪ Any pleural effusion, pneumonia, ARDS

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MANAGEMENT
The first step is to ensure the patient is hemodynamically stable by assessment of his airway, breathing and circulation.The patient is
kept nil-by-mouth in anticipation of urgent procedures and will be started on intravenous fluid. If the patient is septic, prompt
administration of broad spectrum IV antibiotics should be given once blood cultures are taken. Depending on the patient’s clinical
status, I may opt for the patient to be monitored in the high dependency unit.
Urgent investigations will be undertaken with further management guided by the underlying causative aetiology.
Brief Summary of Management Options
- Endoscopic Retrograde Cholangiopancreatography (ERCP) 83

▪ Involves the use of an upper endoscopy and fluoroscopy to evaluate the biliary system
▪ Indication – patients with proven CBD stones (on imaging such as MRCP), alternatively, for patients with suspected CBD
stones (i.e. US showing CBD dilatation with deranged LFT), can perform endoscopic ultrasound (EUS) prior and if CBD
stones are detected, proceed to perform ERCP.
▪ Diagnostic – brushing, biopsy, FNA to detect malignancy
▪ Therapeutic – removal of common duct stones with sphincterotomy and/or, relief of biliary obstruction with biliary stent
- Percutaneous Transhepatic Cholangiography (PTC) / Percutaneous Transhepatic Biliary Drainage (PTBD) 84

▪ Involves transhepatic needle insertion into a bile duct for decompression
▪ Indication – Patients who have biliary duct dilatation (on imaging) and are not candidates for ERCP or failed ERCP
▪ Diagnostic – brushing, biopsy to evaluate for malignancy, can assess intra-hepatic ducts
▪ Therapeutic – decompression of biliary system, placement of biliary duct stent
- (1) external drainage → leads to high loss of bile leading to electrolyte imbalances
- (2) internal-external drainage → preferred option (bile can go down duodenum), can subsequently internalize the
drainage if required (usually for malignant strictures)
83 Gastrointest Endosc. 2005 Jul;62(1):1-8

84 uptodate: Percutaneous transhepatic cholangiography

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CHOLELITHIASIS
DEFINITION
Cholelithiasis refers to the presence of gallstones in the gallbladder
EPIDEMIOLOGY
- In the West: 25% of women and 12% of men (by age 60)
- Consistent 2:1 female to male ratio, 1:1 in elderly
PATHOPHYSIOLOGY
Cholesterol Stones (85%)
- Radiolucent, found in gallbladder
- Composed of cholesterol, yellow, finely granular, hard and faceted
- a/w 4Fs – fat (metabolic syndrome), female (3:1 compared to males), forty (age), fertile (estrogenic influence
– pregnancy and OCP use lead to increase uptake and biosynthesis of cholesterol in the liver leading to
increasing biliary cholesterol excretion), family history (1st degree relative have twice the risk)
Formation is due to disruption in the solubility equilibrium of bile

- Increased cholesterol secretion in bile
Cholesterol ▪ Old
Gallstones ▪ Obesity, rapid weight loss
(85%) ▪ Hyperlipidaemia
▪ Oestrogens ↑: female, pregnancy, exogenous administration
- Decreased emptying of the gallbladder

▪ Gallbladder malignancy (important cause to exclude)
▪ Gallbladder hypo-motility (i.e. truncal vagotomy, spinal cord injury)
▪ Pregnancy
▪ Fasting, TPN
Pigment Stones (15%)
- Radiopaque, form in gallbladder
- Composed of calcium salts (calcium bilirubinate, calcium phosphate and calcium carbonate) hard, speculated
and brittle
Black (sterile)
Formation is due to
Gallstones
- Increased secretion of bilirubin conjugates into bile – haemolytic disorders (i.e. G6PD, sickle cell,
(hard)
spherocytosis), cirrhosis, terminal ileal resection (loss of bile salts)
- Gallbladder hypomotility – chronic TPN
- Decreased bilirubin solubilizes, and bile stasis
- Radiopaque, formed in intra & extra-hepatic ducts – primary CBD stones
- Composed of calcium salts (calcium bilirubinate and calcium palmitate) and bacterial cell bodies
- Check for ampullary stenosis, duodenal diverticula, abnormal sphincter of oddi
- Related to recurrent pyogenic cholangitis
Brown
(infected)
Formation is due to
Gallstones
- Infection – Enteric bacteria – i.e. E.coli, Klebsiella which produce beta-glucuronidase, which deconjugates
(soft)
bilirubin with formation of calcium bilirubinate or helminthic infections – i.e. Ascaris Lumbricoides, Clonorchis
Sinensis & Opisthorchis Viverrini)
- Biliary Stasis – i.e. Caroli’s Syndrome, Isolated Choledochal cysts
Mixed - Majority
- Defined as microlithiasis suspended in bile; predisposes to stone formation
- Can be visualised on the ultrasound scan as layering in the biliary tree
Biliary Sludge
- Sludge is a pre-stone condition, but not all sludge becomes stones
- 20% of biliary sludge will disappear, 60% recur, and 10% form stones

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Triangle of Solubility - 3 major component of bile (cholesterol, bile salts & lecithin)
CLINICAL COURSE
Patients can be divided into 3 clinical stages: asymptomatic, symptomatic cholelithiasis and complicated cholelithiasis
Asymptomatic
- Detected on routine imaging studies or incidentally at laparotomy
- 10-25% of patients will become symptomatic after 10-15 years of follow-up (usually present first with biliary colic)
- Once patients have biliary pain -> risk of developing complications is 2-3% per year
- Cumulative incidence of developing severe complications lower in asymptomatic patients compared to those with mild symptoms
Symptomatic
Biliary colic
- Gallbladder contracting in response to hormonal or neural stimulation, forcing a stone against the gallbladder outlet or cystic duct
opening, leading to increased intra-gallbladder pressure
- Site – epigastric (70%) or RHC pain – can be epigastric because embryonically gallbladder is in the midline
- Onset – usually occur within hours of eating a meal often awakening patient from sleep
- Character – not a true colic – waxing-and-waning character but rarely have pain free intervals – basal pain due to inflammation
of ductal epithelium and proximal distention
- Radiation – inferior angle of scapula or tip of right shoulder
- Alleviating – not relieved by squatting, bowel movement, or flatus
- Timing – distinct attacks lasting 30 mins to several hours, often resolves spontaneously by 6 hours (if > 6hrs, suspect
complications such as acute cholecystitis)
- Exacerbating – not worse with movement
- Severity – steady and intense pain
- Associated symptoms (poor predictive value for gallstone disease)
▪ N/V, patient gets better after vomiting
▪ Bloating, abdominal distention
▪ Epigastric or retrosternal burning sensation
▪ Back pain, LUQ pain
- Biliary colic is a herald symptom that indicates risk of further sequelae
- Differential Diagnosis: acute cholecystitis, infectious causes (i.e. hepatitis), inflammatory process (i.e. IBD, PSC), gastritis,
peptic ulcer disease, pancreatitis, renal colic, GERD, inferior AMI, right lower lobe pneumonia
Complicated
In the Gallbladder
- Hydrops of the gallbladder – impacted stone without cholecystitis
- Acute Calculous Cholecystitis – leading to
▪ Acute Gangrenous Cholecystitis^ / empyema of the gallbladder
- Porcelain gallbladder / Chronic Cholecystitis – leading to
▪ Increased risk of GB cancer (chronic inflammation can lead to scarring of the wall, combined with dystrophic calcification
which leads to ‘limey’ bile and transforms the gallbladder into a porcelain-like vessel – associated with GB cancer)

317
- Gallbladder Cancer (0.3 – 1%)
- Mirizzi’s Syndrome (0.1 – 0.7%) – leading to
▪ Obstructive jaundice (rare, gallstone impacted in cystic duct of neck of gallbladder causing compression of the CBD or
common hepatic duct)
In the Common Bile Duct

- Choledocholithiasis – leading to
▪ Obstructive jaundice
▪ Ascending cholangitis
▪ Secondary biliary cirrhosis
▪ Gallstone Pancreatitis
In the Gut
- Cholecystoenteric Fistula Formation – leading to
▪ Intestinal Obstruction / Gallstone Ileus (inflammation of the gallbladder can lead to adhesions with the small bowel which is
converted to a fistula over time whereby large stones can directly enter the small bowel)
- Bouveret Syndrome – leading to
▪ Gastric outlet obstruction – (rare, direct erosion of a large gallstone through the GB into the GIT)
- Gallstone dyspepsia
▪ non-ulcer dyspepsia – fatty food intolerance, dyspepsia and flatulence not due to other causes
^gangrenous gallbladder is rare as even if cystic artery is thrombosed in acute cholecystitis, there is a rich secondary blood supply
from the liver bed
EXTRA INFORMATION
Gallstone Ileus
- Patient presents with triad of gastric / small bowel dilatation, pneumobilia & intraluminal gallstone on CT
- AXR: Rigler’s Triad – distended small bowel loops, air in biliary tree and radiopaque stone in right lower quadrant [rare]
- Most common site of obstruction is terminal ileum (2 feet proximal to ileocecal valve)
▪ Presentationt: unexplained gradual onset of SB obstruction
▪ Investigation: AXR, CTAP, Barium follow through
▪ Small stones (<2-3cm) usually pass spontaneously without problems
▪ If >2.5cm and migrated into gut → impact at terminal ileum (commonest)
- Mortality is 10-15%, mostly in elderly patients in whom gallstone ileus is more common
- Treatment:
▪ Exploratory laparotomy, with enterolithotomy (removal of obstructing gallstone via small bowel enterotomy proximal to
point of obstruction, followed by transverse closure)
▪ Entire bowel searched thoroughly for other stones
▪ ?Cholecystectomy – Performed in the same operation if patient is stable (low risk) and inflammation is not too severe
▪ ? fistula repair

318
INVESTIGATIONS
1. Plain abdominal X-ray (i.e. AXR Supine or XR KUB)

- Pickup rate for gallstones is less than 10% since most stones are radiolucent
2. Ultrasound of the hepatobiliary system (US HBS)

- Investigation of choice for gallstones (92% sensitivity, 99% specificity)
- Even more sensitive than CT scan for stones since CT may miss small stones due to the spacing of the cuts taken
- Features of stone on ultrasound: strong echogenic rim around the stone, with posterior acoustic shadowing
- Bile should appear as black patch in gallbladder; if not homogeneous then likely to have biliary sludge
3. CT scan (CTAP)
- Usually not done to diagnose stones
- Usually done in symptomatic patient where it is uncertain what is the cause of symptoms, looking for other differential
diagnosis (i.e. liver abscess, diverticulitis, perforated peptic ulcer disease)
- Can also be used to detect complications of gallstones (i.e. gangrenous cholecystitis, gallbladder perforation)
4. Magnetic resonance cholangiopancreatography (MRCP)

- MRCP is not the same as MRI liver/pancreas – only selected cuts taken in order to reconstruct the biliary tree & is without
contrast, only T2 images, so the resolution is not as good as MRI
- Comparable to ERCP, and also minimally invasive, preferred to ERCP if patient does not require any therapeutic intervention
that ERCP provides
5. Endoscopic retrograde cholangiopancreatography (ERCP)

- The largest value of ERCP lies in its therapeutic potential (success rates > 90%)
▪ Stone removal (using Fogarty-balloon catheter, or Dormia wire basket)
▪ Sphincterotomy (in order to relieve obstruction or facilitate removal of stone)
▪ Stenting (plastic vs. metal)
- Complications
▪ Specific to procedure: pancreatitis, infection, haemorrhage, perforation
▪ Specific to sedation: hypotension, respiratory depression, nausea, vomiting
6. Percutaneous transhepatic cholangiography (PTC) /biliary drainage (PTBD)

- PTC involves a tube being inserted under radiologic guidance into one of the biliary ducts
- Main indications
▪ Diagnostic: high obstruction not well visualised in ERCP or previous surgery with altered anatomy (i.e. gastrectomy with
Roux-En-Y reconstruction)
▪ Therapeutic: obstructed system that cannot be drained from below
- Mostly for therapeutic rather than diagnostic purposes
- Complications: bleeding (esp. in biliary obs pts due to coagulopathy sec to decreased Vit K);
7. HIDA scan
- No longer used commonly, except in biliary atresia
- Non-invasive nuclear medicine test that will reveal obstruction of biliary system
EXTRA INFORMATION
Gallstone Pancreatitis – suggested diagnostic algorithm

▪ Patient diagnosed with cholelithiasis with normal LFTs → Laparoscopic Cholecystectomy with IOC +/- CBDE vs. post-op ERCP
▪ Patient diagnosed with cholelithiasis, dilated ducts, deranged LFTs → ERCP

▪ Patient diagnosed with cholelithiasis, normal calibre ducts, deranged LFTs (persistently elevated) → EUS / ERCP
▪ Patient diagnosed with cholelithiasis, normal calibre ducts, deranged LFTs (but normalizing) → MRCP vs. EUS / ERCP
Cholangitis – suggested diagnostic algorithm

▪ Patient diagnosed with cholelithiasis, dilated ducts, deranged LFTs → emergent ERCP
▪ Patient diagnosed with cholelithiasis, normal calibre ducts, deranged LFTs (persistently elevated) → EUS / ERCP
▪ Patient diagnosed with cholelithiasis, normal calibre ducts, deranged LFTs (but normalizing) → MRCP vs. EUS / ERCP

319
TREATMENT
Asymptomatic
- No surgery required unless patient has indications for surgery (see above)
- Dietary modifications – avoid fats and large meals
- Expectant management and close follow-up
- Counsel patient about symptoms – biliary colic, acute cholecystitis, obstructive jaundice, etc.
- Indications for surgery
▪ Increased Risk of malignancy – gallstone a/w gallbladder polyp >1cm, gallstone ≥2.5 – 3cm, porcelain gallbladder
▪ Chronic haemolytic disease (i.e. sickle cell anaemia, thalassemia) – 50-60% will develop symptomatic disease
▪ Relative – individuals isolated from medical care for extended period of time, elderly patients with diabetes
Symptomatic
- Indication for surgery – no consensus in selection of patients, certain considerations: (1) abdominal pain with US proven
sludge / stones / cholesterolosis* / adenomyomatosis** (2) recurrent attacks (3) typical biliary colic symptoms (ROME criteria),
(4) pain radiating to the back, (5) positive response to simple analgesics
- Definitive treatment – elective laparoscopic cholecystectomy

▪ Surgery is non-urgent, more importantly, it is deciding which patients should undergo surgery as if the pain is not due to
symptomatic gallstones, post-surgery, patients will still have abdominal pain
▪ Patients have to be counselled that 10-41% of patients post-cholecystectomy for suspected symptomatic gallstones will
continue to have abdominal pain
▪ Suboptimal pain reduction in patients with gallstones and abdominal pain was noted with both usual care (physicians
discretion) and following a restrictive strategy (must meet all criteria as above] for selection for cholecystectomy (37% have
persistent pain) [SECURE Trial]
▪ Hence, symptomatic gallstones might be an epiphenomenon of another condition – rule out other GI causes first (i.e. gastritis
/ esophagitis) prior to surgical intervention
- Non- surgical means of stone treatment – rarely used

▪ Extracorporeal Shockwave lithotripsy
▪ Medical management – chemo-dissolution: ursodeoxycholic***/ chenodeoxycholic acid
*cholesterolosis – accumulation of cholesterol-laden macrophages within mucosa of gallbladder wall (lamina propria), either locally or as polyps →
strawberry gallbladder, clinically insignificant
**adenomyomatosis (cholecystitis glandularis proliferans) – hypertrophic smooth muscle bundles and ingrowth of mucosal glands into the muscle layer
– if symptomatic → cholecystectomy
*** Ursodeoxycholic acid (ursodiol) – drug is concentrated in bile, decreases biliary cholesterol by suppressing hepatic synthesis and secretion of
cholesterol as well as inhibiting its intestinal absorption → decreased cholesterol saturation causes the gradual solubilisat ion of cholesterol from gallstones
Complicated
- Treat complications
- Cholecystectomy to prevent future recurrence

320
Laparoscopic Cholecystectomy
- Hasson Open Technique – pneumoperitoneum established
- Classically, 3 x 5mm ports inserted under direct visualization – subxiphoid, right subcostal area & right flank
- To minimize bile duct injury – “critical view of safety”85 (see below)
▪ Neck of GB dissected off liver bed – i.e. calot’s dissection (start above the Rouviere’s sulcus)
▪ Hepatocystic Triangle (calot triangle) = inferior border of liver superiorly*, cystic duct laterally and the common hepatic duct
medially
▪ The centre of calot triangle contains a lymph node (Lund’s node)
▪ In calot’s original description the cystic artery was the superior border
- ± intraoperative cholangiogram
▪ Cannula inserted into cystic duct and dye is injected under an image intensifier (II)
▪ If cholangiogram is satisfactory, distal cystic duct doubly clipped distally and divided
▪ 5 criteria for a normal cholangiogram
(a) Normal intrahepatic ducts
(b) No filling defects
(c) Smooth common bile duct
(d) No stricture/narrowing of the common bile duct
(e) Good and free flow of contrast into duodenum
- GB dissected from GB bed and removed via umbilicus with the use of an applied medical bag
- GB bed is irrigated and haemostasis checked
- Recovery – 80% of patients discharged within 24 hours, most discharged by POD2
Complications86
- Specific to General Anaesthesia
▪ Stroke, heart attack, death, allergic reaction to anaesthetic agents
- Specific to Procedure
▪ Injury to the bile duct – 0.3% (lap), 0.1% (open)**
▪ Bile leak***
▪ Injury to neighbouring structures (i.e. hepatic artery and small / large bowel)
▪ Un-retrieved gallstone spillage – LT risk of abscess and fistula formation
▪ Retained stones in the CBD – requires subsequent management <5%
▪ Hernia at incision site – esp. in obese patients
▪ ? post-cholecystectomy syndrome
- Related to any surgery
▪ Bleeding, wound infection, DVT, PE
** Intra-op suspicion of bile duct injury should prompt conversion to open laparotomy with sufficient dissection and cholangiography
(routine use of IOC to minimize bile duct injury is not indicated)
*** Duct of Luschka – biliary ducts that can leak after a cholecystectomy – lie in the gallbladder fossa
85 J Hepatobiliary Pancreat Surg (2002) 9:543–547.

86 The Washington Manual of Surgery (6 th edition) – pg. 369

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EXTRA INFORMATION
Critical view of safety

1. Calot triangle is cleared of fat and fibrous tissue
2. Lowest part of the GB is separated from the cystic plate, able to visualize liver bed (segment V) through the window
3. Both cystic duct and cystic artery must be seen entering the gallbladder. (CBD need not be exposed)
Rouviere’s sulcus – sulcus running to the right of the liver hilum anterior to the caudate process usually contains the right portal
triad or its branches. The sulcus was found to indicate the plane of CBD accurately
Anatomy of Bile Duct

The CBD is vascularized by the parabiliary arteries which run adjacent to the bile ducts. The majority of their blood is supplied via
the inferior retroduodenal artery. A minor portion is supplied by the right hepatic artery. By contrast, the intrahepatic bile ducts
are supplied by a rich, nonaxial network of small arteries that are solely derived from the right and left hepatic arteries, known as
the peribiliary vascular plexus.
RASD: right anterior sectoral duct, RPSD: right posterior sectoral duct
Bile Duct Injuries

Incidence during open cholecystectomy ~ 0.1-0.2% and incidence during laparoscopic cholecystectomy ~0.1-0.55%

322
Bile Duct Injuries are classified using the Strasberg Classification for biliary injuries (1995)
A: Leak from cystic duct or small ducts in liver bed
B: Occluded right posterior sectoral duct
C: Bile leak from divided right posterior sectoral duct
D: Lateral injury to the main bile duct without major tissue loss
E1: Transection > 2cm from the confluence
E2: Transection <2cm form the confluence
E3: Transection at the confluence with right and left hepatic duct in communication
E4: Separation of major ducts in the confluence with separation of right and left hepatic ducts
E5: Complete transection of right sectoral duct +/- involvement of common hepatic duct
Risk Factors for Bile Duct Injuries

- Patient Factors – Inflammation (acute or severe chronic), Anatomical Variants (aberrant right hepatic ducts), Disease Factor
(large impacted gallstones)
- Procedure Related Factors – misidentification (CBD misidentified as the cystic duct, or aberrant right hepatic duct misidentified
as cystic duct), technical problems (i.e. tenting injuries, thermal injuries),
- Surgeon Factors – learning curve effect, equipment
- Intra-op (25%) – unexpected bile leakage, abnormal IOC, delayed recognition of anatomy after transection of important
structures
- RUQ pain, fever, elevated LFTs (early presentation) → biloma or biliary peritonitis
- Recurrent cholangitis / Liver cirrhosis (late presentation)
- Cystic duct leak is the most common, followed by leaks from the subvesical ducts of Luschka
▪ Duct of Luschka – accessory biliary ducts that drain sub-segmental areas of liver into the extrahepatic ducts (occurs in
up to 50% of patients)
▪ Treatment of Luschka duct leak (not recognized intra-operatively) = sphincterotomy and trans-ampullary stenting

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ACUTE CALCULOUS CHOLECYSTITIS
DEFINITION
Acute cholecystitis is defined as inflammation of the gallbladder. It is most often caused by gallstones. It is the most common
complication of gallstone disease and usually develops in patients with history of symptomatic gallstones (6-11% of patients over 7-
11 years)
PATHOPHYSIOLOGY
Acute cholecystitis mostly results from obstruction of the cystic duct by gallstone or biliary sludge. This results in increased intraluminal
pressure within the gallbladder which in turn compromise the blood flow and lymphatic drainage within the gallbladder wall leading to
mucosal ischemia and necrosis.
Also, the trauma caused by gallstones stimulates prostaglandin which mediates the inflammation. 50% of cultures are sterile initially.
Eventually, secondary bacterial infection with enteric organism (i.e. E.Coli, Klebsiella) can occur. 87
HISTORY
- RHC pain (inflammation of parietal peritoneum)
▪ Always clarify with patient regarding the duration of symptoms (i.e. how many days of abdominal pain)
▪ Constant, unremitting severe RHC pain (last for hours > 6hrs or days) – due to inflammation spreading to the parietal
peritoneum (less commonly epigastric)
▪ History of fatty food ingestion prior to pain
▪ Radiates to inferior angle of scapula/interscapular region/back
- Associated symptoms
▪ Fever
▪ Nausea / Vomiting
▪ Anorexia
- General – ill-looking, lying still (peritoneal inflammation aggravated by movement)
- Mild jaundice may be present if severe consider other differentials
- Vitals – febrile, tachycardia
- Abdomen
▪ RHC tenderness with guarding
▪ Murphy's sign positive → inspiratory arrest during deep palpation of RUQ (sensitivity 97% but specificity 48%)
▪ Boas's sign – hyperaesthesia below the right scapula
▪ Palpable GB (30%) – omentum wrapping around GB/empyema
87BMJ. 2002 Sep 21;325(7365):639-43.

324
INVESTIGATIONS
Imaging
- CXR, KUB
▪ Radiopaque gallstones, aerobilia (due to fistula)
▪ Exclude lower lobe pneumonia, perf viscus, abnormal right hemidiaphragm/thorax
- Ultrasound HBS (1st line investigation) – features of acute cholecystitis include

▪ Thickened Gallbladder Wall
▪ Sonographic Murphy’s positive
▪ Pericholecystic fluid (oedema of gallbladder wall)
▪ Presence of gallstones in the biliary system
▪ Contracted gallbladder (from chronic gallstone disease)
- CT Abdomen Pelvis – less sensitive than ultrasound in detecting gallstones

▪ Fat stranding around gallbladder not seen on ultrasound but on CT
▪ Thickening of the GB wall, pericholecystic fluid, presence of gallstones, air in GB wall
▪ Exclude complications (i.e. empyema, gangrene, perforation)
▪ Exclude alternative diagnosis (i.e. diverticulitis)
Bloods
- FBC – elevated TW > 18, consider complications (i.e. gangrene, perforation, cholangitis)
- CRP – elevated CRP, consider complicated gallstone disease
- Amylase (i.e. hyperamylasemia, if > 3x upper limit consider possibility of pancreatitis)
- LFT (mild transaminitis) – ALP frequently elevated
- U/E/Cr (dehydration)
- PT/PTT/INR – in preparation if require surgery / percutaneous cholecystostomy
DIAGNOSIS (2013/2018 TOKYO GUIDELINES)
Diagnosis of acute cholecystitis – No single clinical or laboratory finding is sufficient to diagnose or exclude acute cholecystitis
Murphy’s Sign
A Local signs of inflammation
RUQ mass/pain/tenderness
Fever Few studies have addressed procalcitonin in
Systemic signs of
B Elevated CRP acute cholecystitis and at present its value
inflammation
Elevated WBC cannot be used
Imaging findings characteristic of
C Imaging Findings US is recommended as the first choice imaging
acute cholecystitis
Suspected Diagnosis: 1 item in A + 1 item in B | Definite Diagnosis: 1 item in A + 1 item in B + C
EXTRA INFORMATION
Severity of acute cholecystitis

Associated with organ dysfunction Risk factors
- CVS: hypotension requiring dopamine ≥ 5ug/kg - male gender
- older patients (age > 65)
- CNS: decreased level of consciousness
III Severe - ASA > 2
- Respi: p/f ratio < 300
- elevated TW
- Renal: oliguria, creatinine > 2mg/dL (177umol/L)
- elevated CRP
- Hepatic: PT-INR > 1.5
- GB wall thickness > 4mm
- Haematological: platelet < 100,000/mm3
Associated with
- elevated TW > 18K
- palpable tender mass in RUQ
II Moderate - duration of complaints > 72 hrs
- marked local inflammation (gangrenous cholecystitis,
pericholecystic abscess, hepatic abscess, biliary peritonitis,
emphysematous cholecystitis)
I Mild Does not meet criteria of grade III or grade II

325
MANAGEMENT
- Assess the patient’s vitals and resuscitate the patient if needed – IV fluid resuscitation
- Septic workup
- Analgesia
- Empirical intravenous antibiotics* – IV ceftriaxone and metronidazole
▪ Initial inflammation is sterile but secondary infection can occur
▪ Common organisms – E.coli, Klebsiella, Pseudomonas, Enterococcus (possibility of clostridium perfringens in diabetic
patients with necrotic gallbladder)
- NBM – bowel rest
- Careful monitoring for signs of failure of conservative management (peritonism, non-resolving fever/pain)
- Definitive Treatment – laparoscopic cholecystectomy KIV open

▪ Early LC is preferable to delayed LC (early LC a/w shorter hospital stay and fewer complications)
▪ LC should not be offered for patients beyond 7-10 days from onset of symptoms unless symptoms suggestive of worsening
peritonitis or sepsis
▪ For patients beyond 10 days of symptoms → delayed LC is preferred
- Alternative/Immediate Treatment – percutaneous cholecystostomy (trans-peritoneal or trans-hepatic)

▪ Involves percutaneous catheter placement in the gallbladder lumen under image guidance – direct / trans-peritoneal GB
puncture a/w increased risk of dislodgement while trans-hepatic has increased risk of hepatic haemorrhage
▪ Indications: patients who are not fit for surgery (i.e. recent myocardial infarction, recent cardiac operation on DAPT), when
early surgery is difficult due to extensive inflammation, gangrenous gallbladder with thin wall
▪ Bile cultures should be obtained and sent for culture
▪ Keep cholecystostomy tube till mature fistula tract forms (usually within 3 weeks) – KIV contrast tubogram prior to removal
▪ Followed by elective cholecystectomy 4-6 weeks later (modify risk factors)
Timing of cholecystectomy
- Dependent on several factors:
▪ Timing of presentation
▪ Severity of illness
▪ Response to resuscitation and antibiotic therapy
▪ Logistical considerations (availability of OT, surgeon etc.)
- Possibilities available:
▪ Emergency: immediate; in sick patients who are not responding to treatment (uncommon)
▪ Early: within 1 week of onset of symptoms
▪ Delayed/Interval: 6 weeks after symptoms settled
EXTRA INFORMATION
Early vs. Delayed / Interval Cholecystectomy

- Meta-analysis of existing literature shows no significant differences in early versus delayed procedures with regards to
mortality (0%), conversion rates (20.3% vs 23.6% p = 0.47), bile duct injury (0.5% vs 1.4% p = 0.54), collections requiring
intervention, superficial / deep wound infection
- Advantages: Easier to operate as the gallbladder is oedematous, reduced hospital length of stay and fewer loss of working
days – shorter by ~4 days
- Disadvantages: chance of interval complications requiring re-admission (17.5% had recurrent attack, out of this group, 45%
required open conversion, 5% developed cholangitis, 0% had pancreatitis)
Special Situations (i.e. cholecystectomy in patients undergoing peritoneal dialysis)88

- Traditionally thought to be 6 weeks after laparoscopic surgery – but no agreement in the literature
- Alternative is for intermittent PD to start 10 days after surgery and PD restarted after 3 days of intermittent PD
88 Surg Laparosc Endosc Percutan Tech. 2009 Apr;19(2):101-5.

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COMPLICATIONS
1. Hydrops
- Cystic duct obstruction leads to a tense gallbladder filled with mucus (mucocele)
- May lead to gallbladder wall necrosis if pressure exceeds capillary blood pressure
2. Empyema
- If the obstructed gallbladder becomes infected, can be filled with pus due to bacterial infection of the stagnant bile (cystic
duct being obstructed by a stone)
- Patient is usually toxic, requiring urgent surgery
3. Emphysematous Cholecystitis
- Infection with gas forming bacteria (i.e. clostridium, escherichia coli), common in elderly diabetic males
4. Gangrene and perforation

- Localised perforation: localized pericholecystic abscess that is confined by the omentum
- Free perforation: generalised peritonitis and sepsis, requiring emergency laparotomy
- May perforate into the liver leading to hepatic abscess
5. Cholecystoenteric fistula
- Commonly in duodenum, then colon, and stomach; after repeated attacks of cholecystitis
- Usually asymptomatic
- On AXR, aerobilia is seen in 40% of cases
- Symptomatic fistulas should be treated with cholecystectomy and fistula closure
6. Gallstone ileus
- Accounts for less than 3% of intestinal obstruction (though up to 25% of SBIO in patients > 65 years old)
- Pathogenesis: large stone impacts in the neck of the gallbladder, leading to inflammation, pressure necrosis and erosion
into an adjacent hollow viscus (usually due to cholecystoenteric fistula between GB and 2nd portion of duodenum)
Physiological Effects of Cholecystectomy

- Rminal pain & diarrhoea (20 to disturbed micelles formation leading to fat intolerance and malabsorption)
ACUTE ACALCULOUS CHOLECYSTITIS
DEFINITION
Acute inflammation of GB without gallstones, primary pathology is GB distention with bile stasis and ischemia
RISK FACTORS
- Critically ill patients (i.e. prolonged ICU stay)
- Sepsis with hypotension – hypotension leads to formation of viscous bile and GB ischemia, bile may get infected leading to acute
cholecystitis
- Extensive burns, multiple trauma
- Patients on total parenteral nutrition – lead to biliary stasis
- Insidious onset – GB necrosis, gangrene and perforation are frequent at time of diagnosis
- Higher rates of gangrenous cholecystitis (31%) as compared to gallstone induced AC (6%)
INVESTIGATIONS
- US HBS: presence of sludge, GB wall thickening & pericholecystic fluid
MANAGEMENT
- Treatment involves broad-spectrum antibiotics & emergent cholecystectomy.
- If patient is unstable consider percutaneous cholecystostomy followed by +/- interval cholecystectomy
- Mortality rate is high – about 30% (with treatment), up to 70% (untreated)

327
CHOLEDOCHOLITHIASIS
DEFINITION
Presence of gallstones in the CBD (originated from the gallbladder and pass through the cystic duct into the common bile duct)
INCIDENCE
- 5-20% of patients have choledocholithiasis at time of cholecystectomy
- Incidence increases with age
History
- RUQ or epigastric pain (pain often more prolonged than seen with biliary colic)
- Nausea and/or Vomiting
- Obstructive Jaundice – tea-coloured urine, pale stools
- Complications: acute cholangitis & acute pancreatitis
- General – septic looking, jaundice
- Vitals – febrile, hypotension
- Abdomen
▪ RUQ/epigastric tenderness
▪ Palpable GB (more common in malignant CBD obstruction but can occur in choledocholithiasis)
INVESTIGATIONS
Biochemical
- FBC – leukocytosis with left shift (may suggest cholangitis)
- U/E/Cr – dehydration
- LFTs
▪ Early biliary obstruction: ALT/AST elevated
▪ Later: ALP/Serum Br (direct)/GGT more elevated than AST/ALT (cholestatic pattern)
- Serum Amylase – (CBD stone may cause pancreatitis)
Imaging
- Ultrasound HBS (Sensitivity 73%, specificity 91% from meta-analysis of 5 studies)
▪ Gallstones in gallbladder
▪ Gallstones in CBD – ductal stones only visible 50% of the time due to obscuring gas in the duodenum
▪ Dilated CBD – Normal diameter is 6mm at 60 years old with 1mm increase every 10 years (CBD may be larger in patients
on long-term opiates or post-cholecystectomy)
- MRCP (sensitivity of 94%, specificity 95% from meta-analysis of 27 studies)
- EUS (sensitivity of 93%, specificity of 94% from meta-analysis of 13 studies)
- ERCP (sensitivity 80-93%, specificity 99-100%)

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EXTRA INFORMATION
Algorithm for investigations89

- First risk stratify patients into high, intermediate, or low risk based on the table below (ASGE guidelines)
- Next, follow the management algorithm below the table (UpToDate)
- Summary
▪ High risk – 50% probability of CBD stone – pre-op ERCP
▪ Intermediate risk – 10-50% probability of CBD stone
o MRCP/EUS → if positive proceed to ERCP, if negative for CBD stones, proceed to interval cholecystectomy
o Intraop cholangiogram +/- laparoscopic cholecystectomy
● Positive – CBDE (open or laparoscopic) or post-op ERCP
● Negative – continue with laparoscopic cholecystectomy
▪ Low risk – < 10% probability of CBD stone – cholecystectomy
89 Gastrointest Endosc . 2010 Jan;71(1):1-9.

329
MANAGEMENT90
There are currently 2 standard of care approaches (1) ERCP sphincterotomy and stone removal and (2) Common Bile Duct Exploration
(CBDE). In general in our local practice, aim to clear the CBD stones via endoscopy (ERCP) and then proceed with laparoscopic
cholecystectomy.
- Surgery: Laparoscopic Cholecystectomy (LC) +/-intraoperative cholangiography (IOC) +/- Laparoscopic CBD exploration
(LCBDE) +/- open CBD exploration or post-op ERCP
▪ Usually for intermediate risk patients
▪ CBDE done in patients not suitable for ERCP / fail endoscopic clearance of CBD stones
- Large number of stones
- Intrahepatic stones
- Impacted stone
- Dual pathology
- Tortuous duct
- Previous Billroth II (altered anatomy)
- Stone > 2.5cm
▪ Laparoscopic cholecystectomy with intraop cholangiogram, if positive for stones proceed to CBDE (open / laparoscopic) or
post-op ERCP, if negative, then complete laparoscopic cholecystectomy
▪ CBDE options: transcystic CBDE or transcholedochal CBDE
- Endoscopic: ERCP with sphincterotomy and stone removal with Interval LC ± IOC
▪ Indications:
- Pre-op for ductal clearance prior to surgery (i.e. laparoscopic cholecystectomy)
- Patients who are not fit for surgery (ERCP with sphincterotomy as definitive treatment)
- Prior cholecystectomy
- Post-op for ductal clearance if IOC detected CD stones
▪ No significant difference in the mortality and morbidity between LCBDE and ERCP. No significant reduction in the number
of retained stones and failure rates.91 The selection of technique is based on local expertise.
EXTRA INFORMATION
Laparoscopic CBDE
- Trans-cystic approach – better for small CD stones < 9mm, stone in distal CBD
- Trans-choledochotomy – used for patients with larger stones, more proximal stones, failed trans-cystic approach (CBD must be > 7mm)
▪ Primary closure vs Closure over T-tube
CBD exploration
- Cholangiogram or choledochoscopy is performed
▪ Cholangiogram – injection of dye to image ducts
▪ Choledochoscopy – using a scope to visualize large biliary ducts – cannot image higher ducts but can be used to remove stones visualized
in the ducts
▪ Choice depends on site of obstruction and the aetiology
- Removal of stones
▪ Balloon catheter or Dormia wire basket – dredge out stones
▪ Flush out stones
▪ Manual removal with stone-grasping forceps
▪ Lithotripsy
- Biliary stent or T-tube insertion (swelling and oedema of biliary system → obstruction and build-up of bile → higher risk of bile leakage)
- T-tube
▪ T-shaped tube with horizontal limb in CBD and vertical limb leading out to drain bile
▪ "Pressure release valve" as most bile will flow through horizontal limb into distal CBD and only diverted out if there is obs truction to flow
▪ Allows for post-op cholangiogram (POD 9-10) to check for remaining stones before removal – free flow of contrast into duodenum, no residual
stones, no leak of contrast into peritoneum
▪ If normal – release anchoring stitch and exert gentle traction on the tube – tube should slip out gently
▪ If stones present – leave tube in for 4-6 weeks to form a fibrous tract – allows for instrumentation of tract with a scope to remove stones
90 The Washington Manual of Surgery (6 th edition) – pg. 368

91 Cochrane Database Syst Rev. 2013 Sep 3;(9):CD003327.

330
Endoscopic Retrograde Cholangiopancreatography (ERCP) 92
- Evolved from a diagnostic procedure to an almost exclusive therapeutic procedure with introduction of endoscopic
sphincterotomy
- Performed at o/p setting with IV sedation and analgesia, and local anaesthetic spray in throat
- Correct coagulopathy & stop anticoagulants (5 days) if sphincterotomy anticipated
- Ab prophylaxis – suspected biliary obstruction, known pancreatic pseudocyst or ductal leak
- Diagnostic and therapeutic

▪ Diagnostic – brushing, biopsy, FNA to detect malignancy
▪ Therapeutic
- Sphincterotomy (small cut at entry of CBD to duodenum to relieve obstruction/remove stone)
- Stone extraction (balloon catheter or wire basket KIV stent)
- Stricture dilatation (hydrostatic balloon/graduated catheter)
- Stenting (bile duct – decompress bile ducts – helps to prevent cholangitis, pancreatic duct – prevent pancreatitis)
- Complications93 = overall rates (6.85%) – mild-mod: 5.2% | severe: 1.7%

▪ Pancreatitis (3-4%), Necrotizing Pancreatitis (0.7%) – due to irritation of pancreatic duct by injection of contrast, edema
when removing stone (i.e. with balloon trawling)
▪ Infections / Cholangitis (1-2%)
▪ Hemorrhage (1-2%) – due to sphincterotomy
▪ Perforation (0.5% but mortality rate 15%)
▪ CVS and/or analgesia-related (1-2%)
▪ Mortality (0.33%)
EXTRA INFORMATION
Perforation from ERCP (Stapfer Classification)

- Type I – damage to medial or lateral duodenal wall before sphincter cannulation → surgical intervention
- Type II – periampullary, usually as a result of sphincterotomy → surgical intervention
- Type III – guidewire insertion or stone extraction leading to biliary perforation → conservative
- Type IV – retroperitoneal micro-perforation likely due to excessive insufflation → conservative
92 Gastrointest Endosc. 2005 Jul;62(1):1-8

93 Am J Gastroenterol. 2007 Aug;102(8):1781-8.

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MIRIZZI’S SYNDROME
DEFINITION
- Common hepatic duct obstruction secondary to extrinsic compression from an impacted gallstone in the cystic duct or
infundibulum of the gallbladder
- One of the caveats to Courvoisier’s law
EPIDEMIOLOGY
- More common in women (50-75%)
- Occur in 0.0.5-4% of all patients undergoing surgery for cholelithiasis
- Associated with gallbladder cancer (5-28% of patients with Mirizzi syndrome undergoing cholecystectomy had GB cancer)
PATHOPHYSIOLOGY
- Cystic duct is anatomically parallel to common hepatic duct
- Impaction of a stone in the cystic duct or neck of the gallbladder
▪ Mechanical obstruction of CHD by stone
▪ Secondary inflammation
- Intermittent or constant jaundice causing possible recurrent cholangitis and if longstanding secondary biliary cirrhosis
- Impacted gallstone may erode into the CHD or CBD → cholecystohepatic or cholecystocholedochal fistula
- RUQ pain, fever, jaundice, cholangitis
INVESTIGATIONS
- Bloods
▪ FBC – may have leukocytosis (concurrent acute cholecystitis, pancreatitis, or cholangitis)
▪ LFT – usually have elevated bilirubin and ALP/GGT
- Imaging
▪ U/S HBS/CT/MRCP
o Dilatation of biliary system above level of gallbladder neck
o Presence of stone impacted in gallbladder neck
o Abrupt change to normal diameter of common duct below the level of the stone
MANAGEMENT
- Grade 1: attempt laparoscopic cholecystectomy
- Grades 2-4: open cholecystectomy with CBD exploration
EXTRA INFORMATION
Csendes Classification
- Grade I: No fistula; extrinsic compression on CHD
- Grade II: Fistulation into common bile duct with the fistula <1/3 diameter of the CHD
- Grade III: Fistula 1/3 to 2/3 diameter of CHD
- Grade IV: Fistula >2/3 diameter of CHD

332
CHOLANGITIS
DEFINITION
A life-threatening ascending bacterial infection of the biliary tree associated with partial or complete obstruction of the ductal system.
It is described as a clinical syndrome characterized by fever, jaundice, abdominal pain that develops as a result of stasis and infection
in the biliary tract. A delay in treatment can result in multi-organ failure secondary to septicaemia.
AETIOLOGY
- Choledocholithiasis (28-70%) – most common cause
- Benign biliary strictures (PSC, post-infectious, congenital)
- Malignancy (pancreatic, biliary, gallbladder, duodenum)
- Foreign bodies/previous instrumentation (ERCP)
- Others – Mirizzi’s syndrome, cholangitis can occur at same time as acute gallstone pancreatitis
PATHOPHYSIOLOGY
- Bile from gallbladder and bile ducts is usually sterile
- Cholangitis results significant bacterial concentration in bile and biliary obstruction,
- In presence of obstruction, there is an increase in biliary ductal pressure which leads to bacteria organism entering the circulation
system via cholangio-venous reflux
- Typically cultured organisms
▪ Colonic bacteria (gram negative and gram positive) – E.coli, Klebsiella, Enterobacter, Enterococcus
▪ Anaerobes – Bacteroides – mixed infection more common after repeated infections or surgery on biliary tree
- Normal barrier mechanisms (sphincter of Oddi, flushing action of bile) disrupted resulting in entry of bacteria into biliary tract
EXTRA INFORMATION
Entero-hepatic Circulation
- Refers to the cycling of bile salts between the liver and intestine (or bilirubin)
- Bile salts, a primary component of bile, are synthesized and conjugated in the liver and secreted into the biliary system.
- It is temporarily stored in the gallbladder and secreted into the small intestine which helps in fat absorption.
- Most of the bile salts are reabsorbed in the terminal ileum and return to the liver via the portal vein with 95% of bile salts being
re-reabsorbed and the remaining excreted as faecal bile acids
- With biliary obstruction, the entero-hepatic circulation is impaired
History
- Fever, RUQ pain, Jaundice (Charcot's triad), only present in 50-70% of patients
- Hypotension, altered mental state (additional 2 criteria for Reynold's pentad)
- Complications – dehydration, coagulopathies
- General – alert vs AMS, ill-looking, jaundice
- Vitals – febrile, hypotension, tachycardia, tachypnoea (sepsis)
- Abdomen – RUQ tenderness
Complications
- Sepsis or Septic Shock
- Electrolyte abnormality (dehydration)
- Coagulopathy (Vit K)
- Late complications – stricture, liver abscess

333
INVESTIGATIONS
The choice of imaging depends on the clinical scenario and hemodynamics of the patients. In general, US HBS is the investigation
of choice. However, CTAP has the added benefit of excluding other causes of RHC pain and to assess for complications of
cholangitis (i.e. liver abscess). MRCP is excellent in visualizing the biliary system, however, it is a purely diagnostic tool as
compared to EUS/ERCP.
Biochemical
- Blood cultures – septic work-up → isolation of causative organism (i.e. E.coli / Klebsiella)
- FBC – leukocytosis with left shift (+/- CRP & Procalcitonin)
- U/E/Cr – dehydration
- LFT – ALP/GGT >> ALT/AST in cholestatic pattern, elevated bilirubin
- ABG / Lactate – to guide fluid management
- PT/PTT/GXM as pre-procedure assessment
Imaging
- US HBS
▪ CBD dilation
▪ CBD stone
▪ Gallstone
- CT/MRCP/EUS considered (see topic on cholelithiasis)
Others
- ERCP (if high clinical suspicion + abnormal LFTs → proceed straight to ERCP)
DIAGNOSIS
2013/2018 Tokyo Guidelines

334
MANAGEMENT
The main goals of treatment is directed towards treating the biliary infection and obstruction (achieve decompression of biliary tract)
1. Resuscitation – “In view of cholangitis being a surgical emergency, I will like to resuscitate the patient who may be in septic
shock”. Anticipate rapid deterioration.
- Inform seniors
- Obtain good intravenous access and fluid resuscitate as appropriate
- Close monitoring of vitals in HD/ICU
▪ Hourly para + SpO2, Keep MAP > 65mmHg (or to inform doctors if SBP<100mmHg)
▪ Catheterise and watch urine output (hourly urine output) – hepatorenal! (keep >0.5mg/kg/hr)
▪ Insertion of arterial line
▪ +/- CVP line insertion if patient has shock unresponsive to fluid resuscitation (keep 10-12mmHg)
2. Initial investigations (as above, depends on clinical scenario)

- Blood cultures
- FBC, RP, LFT, PT/PTT, GXM
- CRP, Procalcitonin
- ABG / Lactate
3. IV Antibiotics
- IV ceftriaxone and metronidazole; imipenem if the patient is in shock
4. Emergent biliary decompression

- Timing
▪ Usually deferred until 24-48h after admission when patient is stable and/or has improved with systemic antibiotics
▪ Emergency if deteriorating / Abx not improving infection (15%)
- Biliary decompression using ERCP

▪ Endoscopic sphincterotomy +/- stenting (biliary stents) +/- balloon trawling of biliary stones
▪ Success rate 90%
▪ If cause of obstruction can be treated in the same setting (e.g. stones to be removed) then treat the cause also
- Other methods to decompress:

▪ Percutaneous transhepatic drainage (esp. if neoplastic obstruction)
▪ Nasobiliary drainage (rare)
5. Definitive Therapy
- Choices for definitive treatment:
(a) Laparoscopic cholecystectomy +/- intraop cholangiogram, keep in view CBD exploration keep in view Open
(b) ERCP sphincterotomy with removal of biliary stones followed by cholecystectomy

335
EXTRA INFORMATION
Assessment of the severity of Acute Cholangitis

336
CHOLEDOCHAL CYST
DEFINITION
Congenital cystic dilatation of the extrahepatic and/or intrahepatic biliary tree.
RISK FACTORS
▪ Gender – Females (3-8 : 1) Males
▪ Race – Asians (western population ~ 1:100,000)
▪ 90% have anomalous pancreaticobiliary duct junction
PRESENTATION
▪ Most common presentation – non-specific abdominal pain
▪ Episodic RUQ pain, fever, jaundice, cholangitis
▪ Palpable abdominal mass (20%)
▪ Infants presents similar to biliary atresia
CLASSIFICATION (TODANI)
▪ Type 1: fusiform or saccular dilatation of extrahepatic biliary tree (>50%)
▪ Type 2: saccular diverticulum of extrahepatic bile duct (<5%)
▪ Type 3: bile duct dilatation within duodenal wall (choledochoceles) (~5%)
▪ Type 4a: multiple cysts affecting both intrahepatic and extrahepatic ducts
▪ Type 4b: multiple cysts affecting extrahepatic bile ducts only (4a/4b ~5-10%)
▪ Type 5 (caroli disease*): Intrahepatic biliary cysts (~1%)
INVESTIGATION
▪ MRCP / ERCP – to image biliary tree and assess feasibility of surgical resection
MANAGEMENT
▪ Type 1 / 2 / 4 → excision of cyst with cholecystectomy and RYHJ (type 4 – may need additional segmental liver resection)
▪ Type 3 → sphincterotomy is recommended
▪ Type 5 (Caroli Disease) → partial / non-anatomical liver resection or liver transplant
PROGNOSIS
▪ Long term consequence (without surgical intervention) – cholangitis, liver cirrhosis, pancreatitis, malignant transformation (15%
risk of cholangiocarcinoma)
▪ Caroli disease may be a/w chronic hepatic fibrosis, choledochoal cyst and polycystic kidney disease

337
EXTRA INFORMATION
Biliary Atresia
Definition: Fibro-proliferative obliteration of the biliary tree which progresses towards hepatic fibrosis, cirrhosis and End -Stage Liver Failure
Suspect with persistent jaundice >2weeks, a/w other congenital anomalies (~25%). Patients can present with 3 different anatomical variants: (type 1)
– obliteration of CBD, (type 2) – obliteration extending into common hepatic duct, (type 3, ~90%) – obliteration of entire extrahepatic biliary tree
- Investigations:
o LFTs – increased in conjugated bilirubin
o US HBS – triangular cord sign, absence of gallbladder (highly suggestive), also to rule out choledochocal cyst
o HIDA scan (pre-treat with pentobarbital – increase secretion of bile) – no excretion of tracer into intestine
o Liver biopsy
o Intraoperative cholangiogram (gold standard) – hypoplasia of extrahepatic biliary system
- Treatment: Kasai Procedure (hepaticoportojejunostomy) – 1/3 improve, 1/3 need LTX, 1/3 die
- Need to perform Kasai procedure before 60 days of age otherwise get irreversible liver damage
- Prognosis: 10yr survival 50% without transplantation, 67% with transplantation

338
GALLBLADDER CARCINOMA94
EPIDEMIOLOGY
- This is a rare disease but extremely variable by geographical regions and racial groups
▪ Highest incidence in Chileans, American Indians, northern Indians
▪ 2-3 x more common in females with peak incidence in patient’s age 60-70s
▪ Accounts for 2-4% of all malignant GI tumours
▪ Likely related to chronic inflammation
RISK FACTORS
- Cholelithiasis (most impt RF) – up to 95% of patients with GB cancer have gallstones
▪ Larger stones (>3cm) = 10x increased risk
▪ Symptomatic gallstones = higher risk
- Calcified “porcelain” gallbladder – >20% incidence of GB cancer
- Gallbladder Polyps > 10mm
- Chronic Cholecystitis
- Others – Mirizzi’s syndrome95, choledochal cyst, sclerosing cholangitis, exposure to carcinogens (azotulene, nitrosamine)
PATHOLOGY
- Adenocarcinoma (80 - 90%) – papillary (<10%, better outcomes), nodular, tubular
- Tumour spread
▪ Direct tumour invasion → liver parenchyma
▪ Lymphatics* → first to cystic duct node (calot’s) then pericholedochal and hilar nodes, then peripancreatic, duodenal,
periportal, celiac and SMA nodes
▪ Haematogenous (via venous system) → Liver (segment IV & V)
▪ Transcoelomic → seeding in the peritoneal cavity

- Differential Diagnosis – Xanthogranulomatous Cholecystitis**
* the gallbladder lacks a muscularis mucosa and submucosa, with lymphatics present in subserosal layer only – therefore cancer
invading but not extending through the muscular layer have minimal risk of nodal involvement
EXTRA INFORMATION
Xanthogranulomatous Cholecystitis
Rare inflammatory disease of the gallbladder characterized by focal or diffuse inflammatory process, accumulation of lipid laden macrophages, fibrous
tissue and acute and chronic inflammatory cells. It is an active and destructive process with inflammatory processes extending into the gallbladder wall
and adjacent structures.
- Pathogenesis: extravasation of bile into the GB wall from ruptured Rokitansky-Aschoff sinuses or mucosal ulceration
- Clinical Presentation: history of acute cholecystitis with imaging features that mimic gallbladder carcinoma, can also present with obstructive
jaundice or RHC mass.
- Imaging Features: disease process closely mimics gallbladder carcinoma, predictive features on CT imaging includes (1) diffuse GB wall
thickening, (2) continuous mucosal line, (3) intra-mural hypo-attenuated nodule, (4) absence of macroscopic hepatic invasion & (5) absence of
intrahepatic bile duct dilatation.
- Diagnosis: CTAP best imaging modality, pre-op cholangiogram (tro bile duct adenocarcinoma), consider intra-op frozen section.
- Treatment: Open Cholecystectomy (presence of dense fibrosis and possibility of co-existing adenocarcinoma) ± Extended Cholecystectomy
(complete resection of adjacent xanthogranulomatous tissue
94 Nat Rev Cancer. 2004 Sep;4(9):695-706.

95 J Hepatobiliary Pancreat Surg. 2006;13(4):323-6.

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- Asymptomatic – incidental histological finding after cholecystectomy (0.3-1% of patients)
- Early: mimic gallstone inflammation – biliary colic, cholecystitis (RHC pain)
- Late: biliary & stomach obstruction (jaundice, vomiting, LOA, LOW, palpable mass)
INVESTIGATIONS
- US: thickened, irregular GB wall or mass replacing GB ± tumour invasion of the liver, doppler signal in gallbladder mass, enlarged
lymph nodes, dilated biliary tree
- CTAP: required for staging, assessment of local invasion but poor for nodal spread (do prior to definitive surgery)
- MRCP: allows for complete assessment of biliary, vascular, nodal, hepatic and adjacent organ involvement
- Staging laparoscopy is indicated before laparotomy (risk of peritoneal disease is high)
MANAGEMENT
- Counsel patient regarding 1 vs. 2 stage operation
▪ 1 stage: cholecystectomy with intraoperative frozen section KIV extended cholecystectomy ± hepatectomy
▪ 2 stage: simple cholecystectomy then wait for histology to guide further management
- If diagnosis was made after cholecystectomy → review histology on tumour stage and tumour differentiation, review initial
operative notes for any bile spillage → individualized management
▪ If ≥ T2 – suggest for re-operation after ~ 3months if patient clinically fit

▪ Multidisciplinary tumour board discussion on chemotherapy prior to re-operation
Tumour Stage Management Prognosis (5yr)

T1a – invades lamina propria Simple Cholecystectomy
T1 85-100%
T1b – invades muscularis Debatable, simple vs extended cholecystectomy
Invades perimuscular connective Extended Cholecystectomy
T2 >70%
tissue w/o extension beyond serosa (i.e. includes resection of liver segment IVB, V and regional LN dissection*)
Invades serosa and/or invades liver / Extended cholecystectomy + Extended right hepatectomy (segment IV, V, VI,
T3 20-50%
other organs VII, & VIII)
Invades main PV or hepatic artery or
T4
invades ≥ 2 extrahepatic organs
M1 Distant metastases Palliative (i.e. endoscopic / percutaneous biliary stent) 1-3 months
* ½ of the patient (with T2 disease) have nodal disease on pathological examination – patients with lymphadenectomies that recover ≥ 3 nodes have
significant improvement in LT survival compared with patients who have fewer nodes recovered
- No proven effective option for adjuvant RT or chemotherapy

- High incidence of tumour implant in trocar sites when discovered after laparoscopic cholecystectomy (lap approach
contraindicated for gallbladder CA)
- Ensure gallbladder wall not breached during surgery
PROGNOSIS
- Median survival <6/12, 5 year survival = 5% (as most patient dx with unresectable lesion)
- Recurrence – occur in liver, celiac or retro-pancreatic nodes

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CHOLANGIOCARCINOMA96
DEFINITION
Rare malignant tumour that arises from the ductular epithelium of the biliary tree either within the liver or more commonly from the
extrahepatic bile ducts
EPIDEMIOLOGY
- Uncommon Malignancy – 3% of all GI cancers
- Highest incidence of cholangiocarcinoma – in THAILAND – related to widespread parasitic (opisthorchiasis) infestation
- Median age of onset is 65 years, Male preponderance
- Incidence and mortality rates of intrahepatic cholangiocarcinoma are rising and those of extrahepatic cholangiocarcinoma are
declining internationally
- Histology – adenocarcinoma (95%)
RISK FACTORS
- Chronic cholestasis – leading to prolonged inflammation of the biliary epithelium:
▪ Primary sclerosing cholangitis (2/3 of patients with PSC have IBD – UC)
▪ Parasitic infection – Opisthorchis viverrini, Clonorchis sinensis
▪ Hepatolithiasis leading to biliary stasis and recurrent bacterial infections
▪ Liver Cirrhosis
▪ Viral Hepatitis – Hepatitis C / B / HIV
- Congenital biliary tract disorders
▪ Choledochal cysts – cystic dilatations of the bile ducts
▪ Anomalous biliary-pancreatic malformation
▪ Congenital hepatic fibrosis
- Occupation toxin – dioxide, polyvinyl chloride, Thorotrast (thorium dioxide)
- Diabetes
History
- Intrahepatic
▪ Non-specific symptoms – malaise, weight loss, abdominal pain
▪ Incidental finding
- Extrahepatic
▪ Painless progressive obstructive jaundice
▪ Dark urine, pale stools, pruritus
▪ LOW/abdominal pain/fever
▪ May have malaise, fatigue, night sweats
▪ Cholangitis unusual
- Jaundice (90%)
- Hepatomegaly (25-40%)
- RUQ mass (10%)
- Fever (2-14%)
- RUQ tenderness
- Benign Strictures (iatrogenic bile duct injuries, PSC, choledocholithiasis)
- Other carcinomas – GB cancer or metastatic hilar nodal metastases
CLASSIFICATION97
- (A) Anatomical Location
▪ Intrahepatic – within the liver parenchymal (5-10%)
▪ Hilar – upper duct – (60-70%) – location of klatskin tumours* (arise at bifurcation of hepatic ducts)
▪ Extrahepatic – distal CBD – (20-30%)
- (B) Non-hilar Lesions

▪ Mass-forming (nodular)
▪ Periductal (sclerosing) – most frequent (ddx: benign biliary strictures)
96 Lancet. 2005 Oct 8;366(9493):1303-14. [Important Paper]

97 Nat Clin Pract Gastroenterol Hepatol. 2006 Jan;3(1):33-42.

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▪ Intraductal (papillary)
- (C) Hilar Lesions – Bismuth Corlette Classification

▪ Type I: below confluence of hepatic ducts
▪ Type II: tumour reaching confluence
▪ Type IIIA/B: involving common hepatic duct and either right or left hepatic duct
▪ Type IV: multicentric or involving confluence and both hepatic ducts
INVESTIGATIONS
Biochemical
- FBC / RP / PT/INR/APTT
- LFTs → non-specific rise in serum Br, rise in ALP and GGT
- CA 19-9 >100μl/ml (sensitivity – 53%), can also be increased in pancreatic cancer, colorectal cancer, gastric cancer,
gynaecological cancers and cholangitis
- CEA – primarily a tumour marker for colorectal cancer, can be used in cholangioCA workup
Imaging
- Trans-abdominal Ultrasound (US HBS) - first line investigation
▪ Identify biliary duct dilatation
▪ Can localise site of obstruction (i.e. hilar lesions = intrahepatic duct dilatation with normal extrahepatic ducts & distal lesions
= intra and extrahepatic ducts dilated)
- CT (triphasic):
▪ Detect extent of tumour, adjacent lymph nodes and metastatic disease
▪ Assessment of liver volume (guide surgery planning)
- Cholangiography (non-invasive & invasive)
▪ Non-invasive = MRCP, superior to ERCP for assessing tumour anatomy and resectability
▪ Invasive = PTC / ERCP (benefit of cytologic analysis via ductal brushing or FNA)
- Endoscopic ultrasound with FNA: cytologic diagnosis + assess nodal involvement
- PET-CT (cholangiocarcinoma is a FDG avid PET positive disease) - not first line

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MANAGEMENT
Curative Treatment
- A complete surgical resection with histologically negative margins is the only cure
- Only 25% of tumours are resectable
- No proven role for adjuvant chemotherapy or radiotherapy
EXTRA INFORMATION
Surgical Options
- Intrahepatic cholangiocarcinoma: hepatectomy with excision of involved hepatic duct
- Extrahepatic cholangiocarcinoma affecting CBD: resection of the biliary tree and hilar lymphatics
- Hilar (klatskin’s) tumour: bile duct resection with bilateral HJ + caudate lobectomy
- Distal cholangiocarcinoma: pancreatoduodenectomy (Whipple's procedure)
Criteria for unresectability for hilar lesions98

- Vascular Involvement
▪ Hepatic artery involvement
▪ Encasement / occlusion of main portal vein proximal to bifurcation
▪ Bilateral involvement of hepatic arteries or portal venous branches
- Extent of distant spread
▪ Extrahepatic adjacent local invasion
▪ Nodal disease beyond hepatoduodenal ligament
▪ Distant metastases
- Extent of local disease
▪ Bilateral involvement of hepatic ducts to level of secondary biliary radicals
▪ Atrophy of one liver lobe with encasement of contralateral portal vein branch
▪ Atrophy of one liver lobe with contralateral secondary biliary radical involvement
Palliation
- The aims of palliative endoscopic biliary drainage are to
▪ Relieve jaundice and pruritus
▪ Prevention of cholangitis
▪ Avoid liver failure due to progressive biliary obstruction
▪ Enhance the quality of life
- Endoscopic/percutaneous transhepatic biliary stenting with self-expanding metal stents
- Stricture of the main bile duct (Bismuth I lesions) → unilateral stents
- Hilar or Bismuth II-IV strictures → unilateral or bilateral stents

▪ Only 25% of the liver needs to be drained for adequate palliation
▪ Controversial between the use of single or double stents for hilar lesions – no difference showed between either procedure
in terms of procedure-related mortality, late complications and survival99
▪ Plastics stent (last 3-6 months), metal stents (last 6-12 months)
- Other palliative techniques

▪ Percutaneous Transhepatic Cholangiography and biliary drainage
▪ Palliative radiotherapy & chemotherapy
▪ Photodynamic therapy
PROGNOSIS
- Most patients have unresectable disease at presentation and die within 12 months from the effects of cancer cachexia
- 5-year survival rates post-surgery (Intrahepatic cholangiocarcinoma: 8-47% vs. distal cholangiocarcinoma: 20-54%)
- Therapy for recurrent disease is palliation – surgery is no longer recommended
98 Nat Clin Pract Gastroenterol Hepatol. 2006 Jan;3(1):33-42. (same as earlier reference)
99 Gastrointest Endosc 2001; 53: 547–53.

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12. BREAST
ANATOMY OF THE BREAST
BREAST ANATOMY100
The breast is a modified sweat gland that is located between the subcutaneous fat and the fascia of the pectoralis muscle and serratus
anterior muscle. It consists of fat, fibrous tissue & glandular tissue (fat predominant in a non-lactating breast, glandular tissue
predominantly in the outer portion of breast, responsible for cyclical tenderness). It extends from the lateral sternal border to the mid-
axillary line, from the 2nd to the 6th rib. The axillary tail (axillary tail of Spence) pierces the deep fascia and enters the axilla
It consists of 15 – 20 lobules of glandular tissue that drains into a lactiferous duct which converges towards the nipple (and each
becomes dilated to form a lactiferous sinus beneath the areola). The areola is lubricated by the glands of Montgomery (large modified
sebaceous glands)
The suspensory ligament of astley cooper divides the breast lobules into segments. (Cooper Ligament – fibrous septa running from
the subcutaneous tissues to the fascia of the chest wall). In advanced breast carcinoma, dimpling of the skin is due to malignant
infiltration and contraction of the Cooper’s Ligament
Retro-mammary space is the loose areolar tissue that is posterior to the breast and anterior to the pectoralis fascia.
Embryology
The breast arises from the ectodermal and mesodermal origin. The breast begins development in the embryo about 7 to 8 weeks after
conception (arises from the 2 parallel ectodermal thickening – mammary ridges). They form the ‘primary bud’ which divides into many
smaller ‘secondary buds’ that extend into the vascularized connective tissue (mesoderm). During the 3rd trimester, tiny grouping of
cells begin to branch out, laying the foundation for future ducts and milk producing glands (ductal and lobular structures).
100 Atlas of Human Anatomy (6th Edition) – Plate 179 & 414
12. Breast_Last Updated 3rd June 2020

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Vasculature
Arterial supply is via the (1) Internal thoracic artery (via perforating branches), (2) Branches of axillary artery [(2 nd division) lateral
thoracic, thoracoacromial branches and (3rd division) subscapular (thoracodorsal branch)] & the (3) 2 nd to 5th intercostal arteries
Venous drainage is via (1) internal thoracic, (2) axillary vein, (3) lateral thoracic, (4) intercostal veins
Nerves
- Long thoracic nerve – innervate serratus anterior (winged scapula)
- Thoracodorsal nerve – innervates latissimus dorsi (weak arm adduction)
- Median pectoral nerve – innervates pectoralis major and minor
- Lateral pectoral nerve – innervates pectoralis major only
- Intercostobrachial nerve (off 2nd IC nerve) – sensation to medial arm and axilla (can hersect without serious consequences)
Lymphatic drainage
- Axillary nodes – 75% of ipsilateral breast drains to the axillary nodes
▪ 40-50 nodes in 5 groups: anterior, posterior, medial, lateral, apical
▪ Drains into supraclavicular and jugular nodes
- Internal mammary nodes – 20% of drainage from the ipsilateral breast
▪ About 4 nodes per side, with one node in each of the first three interspaces and one in the fifth or sixth interspace
- Inter-pectoral (Rotter’s nodes) – between pectoralis major and pectoralis minor muscles
Anatomic/ Surgical division of axillary nodes into levels I, II and III (relative to pectoralis minor)
Level I: lateral to lateral border of pectoralis minor
Level II: posterior to pectoralis minor and below axillary vein
Level III: medial to medial border pectoralis minor, extending up to apex of axilla
Musculature
- Pectoralis Major
▪ Origin: medial clavicle, sternum, anterior 2-6th ribs, external oblique, rectus abdominis fascia
▪ Insertion: upper humerus, 10cm from humeral head on lateral side of intertubercular sulcus
▪ Blood supply: internal thoracic (mammary) perforators, thoraco-acromial, lateral thoracic, intercostal perforators
▪ Innervation: medial and lateral pectoral nerve
- Pectoralis Minor
▪ Origin: anterolateral surface of 3 rd to 6th ribs
▪ Insertion: coracoid process of scapula
▪ Blood supply: pectoral branch of thoraco-acromial artery and lateral thoracic artery
▪ Innervation: medial pectoral nerve
- Serratus Anterior
▪ Origin: anterolateral aspect of upper 8 th ribs
▪ Insertion: anterior surface of medial aspect of scapula
▪ Blood supply: lateral thoracic artery and branch of thoracodorsal artery
▪ Innervation: long thoracic nerve
- Rectus Abdominis
▪ Origin: pubic line
▪ Insertion: xiphoid process and ribs 5-7
▪ Blood supply: superior and inferior epigastric artery and vein, subcostal & intercostal perforators
▪ Innervation: segmental motor nerve from 7 th to 12th IC nerve
- External Oblique
▪ Origin: lower 8 ribs (5-12)
▪ Insertion: iliac crest, pubic tubercle, linea alba
▪ Blood supply: inferior 8 intercostal arteries

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▪ Innervation: segmental motor nerve from 7th to 12th IC nerve
AXILLA ANATOMY
- Apex: costoclavicular ligament
- Base: skin & axillary fascia
- Anterior: pectoralis major & minor, subclavius muscle (enclosed in clavipectoral fascia)
- Posterior: subscapularis, teres major & latissimus dorsi muscle
- Lateral: intertubercular sulcus
- Medial: ribs & intercostal muscle covered with the serratus anterior muscle
Anatomic Boundaries of axillary dissection (level II dissection)

- Superior border: axillary vein
- Medial border: chest wall (watch for long thoracic nerve)
- Lateral border: skin flap
- Anterior border: pectoralis minor
- Posterior border: latissimus dorsi muscle

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APPROACH TO NIPPLE DISCHARGE
History
1. Is the discharge truly from the nipple?
▪ Exclude eczema, dermatitis or Paget’s disease (common complaint: staining of the bra without obvious nipple discharge)
2. Is the discharge more likely to be pathological?
▪ Nature of discharge – grossly bloody more significant
▪ Unilateral or bilateral discharge – unilateral more significant
▪ Uni-ductal or multi-ductal discharge – uni-ductal more significant
▪ Spontaneous or only on pressing – spontaneous more significant
▪ Persistent or intermittent – persistent more significant
3. Is there any recent pregnancy
▪ Relation to breastfeeding – if discharge present after > 1 yr after stopping breastfeeding more worrisome
4. Is it troubling the patient?
▪ Have the patient sought treatment elsewhere?
Differentiating Paget’s disease from Eczema of the nipple

Paget’s disease Eczema of the nipple
Laterality Unilateral Bilateral
Edges Edges distinct Edges indistinct
Itch / Pruritus Absent Present
Timing Seen in menopausal women Occurs during time of lactation
Vesicles Absent Present (dyshidrotic
eczema)
Nipple Usually destroyed Intact nipple
Underlying lump Usually present No underlying up
Pathological Nipple Discharge

- Discharge: Serous (yellow / clear), sanguineous (bloody), serosanguinous (blood-tinged)
- Patients with bloody nipple discharge has higher risk of breast cancer (~52%) than patients with non-bloody discharge (~19%)101
- High risk for underlying malignancy – if nipple discharge is:
▪ Spontaneous
▪ Uniductal
▪ Persistent (> 2x / week)
▪ Bloody
▪ Age > 50yrs
▪ a/w palpable abnormality
Physiological Nipple Discharge

- Discharge: white or clear, yellow (straw-coloured), green, brown or grey
- Discharge is usually bilateral, involving multiple ducts
101 Breast Cancer Res Treat. 2012 Feb;132(1):9-14.

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Discharge Colour Cause Management
- Commonest cause of bloody nipple discharge in patients 20 to 40 years
- Mammogram: no mass detected due to their small size, clinically difficult to palpate
Intraductal papilloma
- Investigate with ductogram
- Treatment: microdochectomy with pre-op ductogram, major duct excision
- 2 forms: invasive ductal carcinoma or DCIS (pre-invasive lesion)
Grossly bloody (red) Mammary ductal - Unilateral spontaneous discharge = suspicious
carcinoma - Mammogram: DCIS – clustered pleomorphic calcifications IDC – spiculated mass
- Treatment: surgery
- A persistent dominant mass a/w nipple discharge must undergo triple assessment to
Fibrocystic change exclude cancer
- Closer follow up indicated
Ductal papilloma As above
Clear (serous) or
Ductal carcinoma As above
straw-coloured
(yellow) Mammary ductal ectasia - Benign Condition: lactiferous ducts gets dilated along with inflammation and fibrosis
(non-puerperal mastitis) around the ducts
Green, brown, black - Treatment: none, usually self-limiting
Mammary ductal ectasia
(cell debris) - Predisposed to non-puerperal abscess which would require antibiotics ± surgical drainage
- 25% of breast abscesses occurs in non-lactating females
- Lactational Mastitis (swollen, red and tender breast) – usually caused by staphylococcus
aureus (purulent discharge is uncommon), may progress to breast abscess
Purulent, Lactational Mastitis or - Treatment: needle aspiration (± percutaneous drainage) & antibiotics. Can continue
foul-smelling Breast Abscess breastfeeding. Breast abscess < 5cm can be treated with ultrasound localization and
repeated aspirations
- A thick abscess a/w septa may indicate need for surgical drainage
- Follow-up: TRO inflammatory breast cancer (biopsy)
- Any meds that might affect hypothalamic-pituitary axis
▪ Deplete dopamine (i.e. tricyclic antidepressant, methyldopa, benzodiazepines) –
Drug related Dopamine normally inhibits Prolactin
galactorrhoea ▪ Dopamine receptor blocker (i.e. haloperidol; Typical/atypical antipsychotics)
▪ Estrogenic effect (i.e. digitalis)
White - Treatment: medication can be tapered / changed
milky discharge - r/o pituitary prolactinoma (Hx: Bitemporal hemianopia, Signs of increased ICP, Status of
other pituitary hormones eg. Thyroid, Sexual, GH)
Spontaneous
- Measure serum prolactin level & neuroimaging (CT / MRI)
galactorrhoea
- Treatment: Dopamine agonists (bromocriptine/cabergoline) or resection of prolactinoma
(eg. transsphenoidal hypophysectomy)
Lactation - Physiological
- Raw, vesicular or ulcerated lesion that begins on the nipple and spread to the areola
Blood stained Paget Disease
- Mimics eczema of nipple
(spot on bra)
Dermatitis / Eczema - Treatment: short-term course with steroid cream
INVESTIGATION
1. Mammography (≥ 35yrs), U/S or MRI of both breasts to detect any underlying malignancy
2. Histology of biopsied lesion (core biopsy +/- clip placement) – clip is placed to allow subsequent localization during surgery
3. Ductography – duct is cannulated and radiopaque contrast is injected
4. Ductoscopy – 1mm rigid video-scope to perform internal exploration of duct
MANAGEMENT
- Intraductal papilloma – microdochectomy with pre-op ductogram, major duct excision (all retro-areolar ducts transacted and
excised)
- Intraductal carcinoma – appropriate cancer surgery should be planned
- Mastitis or Breast Abscess – antibiotics + incision and drainage for abscess
- Drug induced galactorrhoea – medication can be tapered or changed
- Pituitary prolactinoma – Dopamine agonists (i.e. bromocriptine/cabergoline) or surgical resection (eg. trans-sphenoidal
hypophysectomy)
- Conservative management for most other pathologies unless discharge persists and is troubling patient → microdochectomy of
offending duct

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APPROACH TO BREAST LUMP
DEFINITION
Breast lump is the most common reason for referral to the breast clinic. All patients with a palpable breast lump should undergo triple
assessment. Majority of these patients will have benign breast disease.
“The evaluation of a breast lump is via the TRIPLE ASSESSMENT. This involves history & clinical examination, radiological
assessment with mammogram and/or ultrasound and histopathological assessment. All 3 must be concordant for benign to have >99%
specificity to r/o malignancy.
History
1. History of Lump (apply for any lumps) – Key Questions
- When and how did you first notice the lump?
▪ Site of the lump?
▪ Incidental / self-examination?
▪ Previous Trauma
- How has the lump changed since you first noticed it?
▪ Duration since first noticed
o Any increase in size from first noticed to now?
o Any changes in the nipple e.g. retraction
▪ Overlying skin changes noted:
o Erythema, warmth,
o Dimpling (more prominent hair follicles 2 o to dermal oedema from blocked lymphatics)
o Swelling?
o Any general asymmetry of the breasts noticed?
- What symptoms does it cause you?
▪ Painful or painless?
▪ Nipple discharge? If present, what is the colour and consistency
- Have you got any more or have you had this before?
▪ Single or multiple?
▪ Any other lumps elsewhere – contralateral breast? axilla? neck?
▪ Does it come periodically – (i.e. in relation to menstrual cycle / previous pregnancy)
- What do you think it is?
▪ To assess a patient's anxiety. Patients are usually worried of underlying malignancy
2. Assessment of Cancer Risk – 7 broad categories102

- Age & Gender: age is the most important risk factor for breast cancer development
- Personal history of malignancy: any history of previously treated breast cancer
▪ Increased likelihood of breast cancer in the contralateral breast
▪ In setting of DCIS – invasive cancer arise in ipsilateral breast
- Family history of breast cancer
▪ First degree relatives of breast or gynaecological cancer → 2-3x increased risk with affected first degree relative
(increased if relative had premenopausal onset and/or bilateral breast cancer)

▪ Genetic Predisposition
o 5-10% of all breast cancer, up to 25% of cases in women <30yrs
o Carriers of BRCA 1 or BRCA 2 have lifelong risk of 50-70% of developing breast cancer
o TP53 germline mutation (Li-Fraumeni syndrome)
- Irradiation of breast or chest wall: previous breast disease or Hodgkin lymphoma
- Lifestyle factors: Physical activity (healthy lifestyle), daily alcohol intake, especially before age of 30
- Hormonal factors
▪ Early menarche (<12yr) – increased oestrogen exposure
▪ Late menopause (>55yr) – increased oestrogen exposure (risk increase 2x with menopause after age 55)
▪ Late age of first live childbirth (if 1st birth > age 30, risk increase 2x compared to 1st birth before age of 18)
▪ Nulliparity
▪ Hormone Replacement Therapy
o HRT with estrogen and progesterone for 5yrs leads to ~20% increased risk of developing breast cancer
o Risk of 0.2% at 5yrs, 0.6% at 10yr & 1.2% at 15yr of continuous HRT – risk disappear within 5 years of ceasing
HRT103
102 Sabiston Textbook of Surgery (19 th edition) – pg. 834-836

103 Lancet. 1997 Oct 11;350(9084):1047-59.

349
o Estrogen only formulation (because of previous hysterectomy) – no increased risk
- Proliferative breast disease (on previous breast biopsy)

▪ Lobular Carcinoma in Situ (LCIS)
o Risk ratio of 7-10x, risk ~ 1% / year
o Not a pre-invasive lesion (i.e. LCIS does not progress to ILC)
o Marker of proliferation in the breast
▪ Proliferative epithelial alterations with atypia

o Atypical ductal hyperplasia (ADH) or atypical lobular hyperplasia (ALH)
o ALH have cumulative incidence of breast cancer of 35% at 30 years
o Risk ratio 4-5x & 9-10x with positive family history of breast cancer, risk ~0.5-1%/yr
o Risk increases with multifocality
▪ Proliferative epithelial alterations without atypia (severe hyperplasia)

o Fibrocystic change with hyperplasia greater than usual or mild
o i.e. papilloma, ductal papillomatosis – a/w serous or haemoserous nipple discharge, sclerosing adenosis – a/w
hard rubbery consistency lump, epithelial hyperplasia – a/w microcalcifications on MMG, radial scar
o Risk ratio of 1.3-1.9x
▪ Non-proliferative epithelial alterations

o Fibrocystic change with no, usual or mild hyperplasia, i.e. cysts (blue domed cyst) – a/w multifocality and often
bilateral, apocrine metaplasia, fibrosis
o No increased risk
Risk factors according to extent

Early age at menarche
Late age at menopause
1.5-2.5x risk Late age at first live birth
Prolonged use of hormonal replacement therapy
Family history: one first or second-degree relative diagnosed with breast ca age>50
Pre-malignant breast conditions
- Atypical ductal hyperplasia
- Atypical lobular hyperplasia
5-10x risk Genetic predisposition (special group: frequently present before 40 YO)
- Proven BRCA mutation carriers
- Untested 1st degree relatives of known BRCA mutation carriers
- Strong family history and 20-25% lifetime breast CA risk (risk assessment models)
10-15x risk Strong family history of breast cancer or ovarian cancer suggestive of hereditary predisposition
* 75% of women with breast cancer have no risk factors

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EXTRA INFORMATION
BRCA1 AND BRCA2104

BRCA are tumour suppressor gene a/w 80% of hereditary breast CA but accounts for only 5% of all breast CA. They are autosomal
Dominant inheritance with incomplete penetrance
- BRCA 1 mutation (chromosome 17 q21)^ – lifetime risk (by age 70) of 57% for breast CA & 40% for ovarian CA
- BRCA 2 mutation (chromosome 13 q12.3)^^ – lifetime risk (by age 70) of 49% for breast CA & 18% for ovarian CA
^ Besides breast CA, BRCA1 gene mutation: ↑risk of ovarian, endometrial and prostate cancer
^^ Besides breast CA, BRCA 2 gene mutation: ↑risk of male breast cancer, colon, pancreatic, stomach, gallbladder,
melanoma and prostate cancer
- BRCA 1 tumours tend to be hormone receptor negative (triple negative), high grade and poorly differentiated
- BRCA 2 tumours tend to be hormone receptor positive and well-differentiated
Management
- Prophylactic Mastectomy
- Intensive screening – with MRI
Criteria for referral for genetic counselling

1. Family History
▪ ≥ 2 relatives with breast cancer, one under 50
▪ ≥ 3 relatives with breast cancer, any age

▪ Previously identified BRCA 1 / 2 mutation in the family
▪ Pancreatic cancer with breast and/or ovarian in same side of family
▪ Ashkenazi Jewish ancestry (1-3% incidence)
2. Personal History
▪ Breast cancer diagnosed ≤ 40 years or younger (regardless of tumour subtype)
▪ Ovarian / Fallopian Tube cancer
▪ Male breast cancer
▪ Triple negative breast cancer diagnosed at age ≤ 60 years
104 J Clin Oncol. 2007 Apr 10;25(11):1329-33.

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Preliminaries (HELP)
- Hi: Introduce yourself & ask for permission to examine the breast (for male students, ensure chaperone is present)
- Expose patient adequately from the waist up with exposure of axilla
- Lighting: good
- Position the patient at 45o or sitting position if a bed is not available
Inspection
- General appearance – cachexic, jaundiced, pallor, breathlessness
- Patient’s hands relaxed at her sides – look for:
▪ any asymmetry in the breast contours, any lumps
▪ any scars of previous operation or procedure e.g. punch biopsy
- Look for overlying skin changes
▪ Fixation of skin to the lump
▪ Peau d’orange
▪ Ulcerating, fungating cancerous lump
▪ Retraction of skin – underlying cancerous lump
▪ Erythema
- Look for nipple changes (7 D’s):
▪ Discharge (blood-stained)
▪ Deviation – underlying hard lump
▪ Depression (retraction) – underlying hard lump
▪ Destruction (a/w puckering of nipple) – underlying cancer
▪ Discolouration
▪ Displacement
▪ Dermatitis (eczema-like rash with crusting) – Paget’s Disease
- Ask patient to raise her arms (to accentuate any tethering to the skin → skin dimpling)
- Ask the patient to contract the pectoralis major (push her hands against her hips), may reveal a previously unnoticeable lump
Palpation
- Patient should be lying down at 45 degrees to the horizontal with her ipsilateral hand tucked behind her head – this splays the
breast out so it can be palpated properly
- Start with the normal side first!
- Ask for any pain before starting to palpate
- Use one hand to retract and stabilise the breast and palpate with the other
- Palpate in a systematic manner e.g. quadrant by quadrant (breast tissue is examined using the fingertips)
- Examine the entire breast including the axillary tail
- When the lump is located, check with the patient whether this is the same lump that is of concern to them
- Continue to examine carefully for other lumps (multiple lumps are unlikely malignant, usually fibroadenoma or fibroadenosis)
- Ask patient if she can show you the discharge by expressing it herself (NEVER squeeze the nipple yourself), note if discharge is
from one duct or multiple ducts and if blood is present
Characterise the lump:

- Shape – hemispherical or oval
- Size – measure __cm by __ cm
- Site* – which breast, which quadrant or what o’clock, length (cm) from nipple
- Warmth of overlying skin, Fluctuance
- Tender or non-tender to touch
- Surface – smooth or nodular/irregular
- Margins – regular and smooth, or irregular and ill-defined edge
- Consistency – soft, firm, or hard
- Tethered to the skin – try to pick up the skin above the lump
- Fixation to underlying pectoralis muscle – ask patient to press her hands against her hips to contract the pectoralis major
muscle, then try to move the lump in 2 perpendicular directions, then ask patient to relax and try to move the lump again
- Mobility of lump (mobile in all direction, not mobile)
* Central / sub-areolar tumours are at increased risk for being multi-centric

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Axillary lymph nodes
- Palpate the normal side first
- Rest the patient’s right forearm on your right forearm and use your left hand to palpate the right axilla (vice versa for the left side)
- Palpate gently, slowly, and systematically, covering the five major groups of nodes: anterior, posterior, medial, lateral, and apical
- If any lymph nodes are found to be enlarged, note the number of lymph nodes, their site, size, tenderness, consistency (firm,
hard, matted), mobility. causes of isolated unilateral axillary adenopathy – most commonly due to reactive lymphadenopathy, 25%
due to malignancy, 14% due to lymphoma, 10% due to metastatic carcinoma
- Detection of any palpable axillary lymph nodes affects clinical TNM staging and subsequently management
To complete the examination

- Examine the supraclavicular LNs & cervical LNs
- Examine the lungs for any pleural effusion
- Percuss the spine for bony tenderness
- Examine the abdomen looking for hepatomegaly
- Thank patient and cover up
Differential Diagnosis
The underlying cause of the breast lump varies with age. The lump can be categorized into benign or malignant pathologies. Benign
breast disease can be categorized into congenital abnormalities, aberration of normal breast development and involution, benign
neoplasms and proliferation, breast infection and others.
In premenopausal women in the early reproductive period, breast lumps are usually fibroadenoma, in the later reproductive period,
areas of fibrosis, epithelial hyperplasia, cyst and carcinoma are more common.
Aberration of normal breast development and involution (ANDI)

Age Normal Process Aberration Disease
Lobular Development Fibroadenoma Giant fibroadenoma (> 5cm)

< 25
Stromal Development Juvenile Hypertrophy (Macromastia) Excessive hypertrophy
Nipple Eversion Nipple Inversion Subareolar Abscess
25 - 40 Cyclical activity Cyclical Mastalgia / Cyclical Nodularity (diffuse or Severe mastalgia / nodularity
focal)
Lobular Involution Macrocysts Extensive / Recurrent Cysts
Ductal involution Ductal Ectasia / Nipple Retraction Periductal mastitis

35 - 55
Stromal Involution Sclerosing Lesions Sclerosing Adenosis, Radial Scars,
Complex Sclerosing Lesions
Benign Neoplasm & Proliferation

Proliferative epithelial hyperplasia with atypia Atypical ductal hyperplasia (ADH) or atypical lobular hyperplasia (ALH)
Proliferative epithelial hyperplasia without atypia Intraductal Papillomas (single or multiple)
Breast cysts (blue domed cyst)
Non-proliferative epithelial alterations Apocrine Metaplasia / Papillary Apocrine Change
Mild Epithelial Hyperplasia
Phyllodes Tumour
Others Lipoma
Granular Cell Tumour (originate from schwann cells)

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Others
Lactational Infection
Breast Infection Non-lactational Infection (peripheral or periareolar)
Post-surgical infection
Long-standing T1DM: diabetic mastopathy
Following Trauma: fat necrosis / hematoma
Specific Scenarios Lactating Women: Galactocele
Painless Cord Like Induration: Mondor Disease (thrombosis of superficial veins)
Nipple Lump: Nipple Adenoma
Malignant Breast Lump

Carcinoma In-situ Ductal Carcinoma In-Situ or Lobular Carcinoma In-Situ
Invasive Ductal Carcinoma or Invasive Lobular Carcinoma
Invasive Cancer Inflammatory Breast Cancer
Other Subtypes: Medullary, Mucinous, Tubular, Scirrhotic
Fibroadenoma
- Fibroadenomas arise from terminal duct lobular units, considered an aberration of normal breast development.
- Not neoplastic lesions (do not arise from a single cell, instead they contain a mixture of connective tissue and epithelium and are
affected by hormones in a similar way to normal breast)
- Clinical Presentation:
▪ Patients present with a well-circumscribed, discrete, mobile breast lump of rubbery consistency.
▪ They can be mildly symptomatic such as pain and tenderness or present as an incidental finding.
▪ They are usually solitary but some patients develop multiple fibroadenomas.
▪ May enlarge during pregnancy (increase size and tenderness with estrogen) and involute or calcify after menopause.
▪ Rapid growth of fibroadenoma can occur in adolescence (juvenile fibroadenoma)
- Investigate with ultrasound and +/- core biopsy. (Histology: prominent fibrous tissue compressing epithelial cells, collagen
arranged in swirls and consisting of stromal overgrowth)
- If clinical examination, imaging and histology are concordant, patients can be discharged. Differential diagnosis for fibroadenoma
includes hamartoma and phyllodes tumour.
- Excision is indicated for patients with symptomatic fibroadenoma (pain, enlarging in size). Need to rule out phyllodes tumour.
Phyllodes Tumour (Cystosarcoma Phyllodes) ~ 1% of all breast tumours

- Phyllodes is a fibroepithelial tumour which commonly affects women between 35 – 55 years of age.
- It consists of a large mass of connective tissue and cyst with “leaf-like” lobulations. Increased stromal cellularity, clefts lined by
epithelium, stromal overgrowth with irregular margins.
- It can grow rapidly. Majority are rarely fixed to skin or muscle. Classification: benign, borderline or malignant.
- The tumour spreads via haematogenous route (if any) and rarely spreads to lymph nodes. Local recurrence is common but
distant metastasis is low (more frequent in malignant tumours).
- Treatment: WLE with 1cm-margin for malignant tumour and clear margins for benign or borderline lesions, mastectomy only
necessary for large lesions. No routine role for ALND & chemoradiation. Treatment of metastatic disease has poor outcomes
with lack of response from chemotherapy, radiotherapy or hormonal therapy
Palpable Breast Cysts

Cysts are distended and involuted lobules and are most common in perimenopausal women. It is derived from the terminal duct lobular
unit. A breast cyst can be diagnosed by breast ultrasound and classified as simple, complicated or complex. Simple asymptomatic
cyst should be left alone. Large symptomatic or complex should be aspirated with the fluid sent for cytology (if blood stained). If a
palpable lump is still present after aspiration, further imaging and biopsy are indicated.
Breast Infections
Breast infection can be divided into lactational or non-lactational infection. Examination of the overlying skin should be performed to
assess if the skin is thinned or necrotic. Management involves appropriate antibiotics and early ultrasound to be performed prior to
drainage procedure (i.e. aspiration). Breast infections can be managed with repeated aspiration or limited incision and drainage with
biopsy of the base. Avoid making large incisions. For infection that does not resolve despite antibiotics or in patients with inflammatory
lesions that are solid, breast cancer should be excluded.

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Common Breast Lumps
Type of lump Age Pain Surface / Margins Consistency Mobility
Smooth Soft, Firm (fluid),
30-55 Occasional Not fixed, Mobile
Well defined edges Fluctuant
Asymptomatic cyst: watch & wait, observe
Breast Cyst
Symptomatic cyst: should be aspirated, if not palpable after aspiration TCU 1/12
- If cyst (1) recurs (2) does not resolve completely with aspiration (3) yields bloody aspiration then send patient for
mammogram + ultrasound to r/o intra-cystic tumours
< 30 No Smooth, bosselated Firm, Rubbery Very mobile
- Presents with small, well-defined mobile breast lump
- They may enlarge during pregnancy (increase size and tenderness with estrogen) and involute after menopause
Fibroadenoma
- They have well-circumscribed border on mammogram and u/s
- If < 2cm – can be managed conservatively, if mass is symptomatic, greater than 2 cm, or enlarges, consider excision
- Histology: prominent fibrous tissue of epithelial cells, collagen arranged in swirls and consisting of stromal overgrowth
Smooth
20-55 Occasional Lumpy, Cobblestone Not fixed, Mobile
Well defined edges
- Definition: condition marked by benign changes in breast tissue
Fibrocystic
- Presents with premenstrual breast pain or lump (often bilateral, multifocal)
Breast Change
- Patient suspected of FBC should be re-examined again (preferable on day 10 of the menstrual cycle) – hormonal influence
(FBC) is lowest, mass would have diminished in size \
- A persistent dominant mass must undergo further investigation tro cancer
- Histology: ectatic duct with single or double cell layer
35+ No Irregular Stony hard Tethered or fixed
Cancer
- Histology: mass of epithelial cells invading stroma in a random fashion with suggestion of tubule formation
Investigations
1. Mammography
- Most sensitive breast imaging modalities
- Usually performed in asymptomatic older women (>40YO) [breast tissue in younger women is denser with stroma and
epithelium, resulting in an image without much definition]
- Sensitivity increases with age as dense parenchyma tissue is replaced with fat (fat absorbs little radiation and provides a
contrasting background)
- Rationale: Detection of breast cancers before they become palpable as small tumours are more likely to be early stage
disease, having better prognosis, and are more successfully treated
- 24% mortality reduction associated with an invitation to screening
- Normally, 2 views are done:

▪ Craniocaudal (CC): 70% tumours in lateral quadrant (upper)
▪ Mediolateral oblique (MLO): Look at the axilla on the MLO view for any enlarged lymph nodes, captures the axillary
tail, 80% tumours in oblique milky way
- Additional specialised views: magnification and coned compression; done on request to help magnify areas of abnormality to
further characterize any lesion.
- Malignant Mammographic Findings

▪ Spiculation
▪ Linear, small, thin and/or branching calcifications
▪ Irregular borders
▪ Architecture Distortion
▪ Ductal asymmetry
▪ Asymmetric density
▪ Multiple clusters
- Benign Mammographic Findings

▪ Radial Scar / Complex Sclerosing Lesion (but have risk of upgrade to DCIS / Invasive Cancer)
▪ Fat Necrosis – characteristic oil cyst
▪ Milk of Calcium – characteristic microcalcifications appear discoid on CC view and sickle-shaped on MLO view
Abnormal features:
(a) Microcalcifications (<0.5mm in size)
▪ If calcifications >0.5mm = macrocalcifications; >5/mm2 = cluster
▪ Sole feature of 33% of cancers detected on mammography
▪ Causes: DCIS (microcals in a straight line), invasive cancer, fibrocystic disease (microcals scattered), papilloma
(b) Spiculated mass or stellate lesion with poor outline or comet sign
▪ 95% of spiculated masses on mammography are due to malignancy

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▪ Stellate lesion is a localised distortion of the breast parenchyma without perceptible mass lesion – high chance
of malignancy
▪ Causes: Invasive cancer, radial scar (benign), fat necrosis, abscess, etc.
(c) Architectural distortion (of the contour), tent sign, nipple changes (eg. skin thickening, nipple thickening)
(d) Neo-density or asymmetric density (look for bilateral synchronous ca; satellite lesion)
BI-RADS (Breast Imaging Reporting and Data System) classification

- Category 0: Need additional imaging evaluation
- Category 1: Negative (nothing to comment on, 0.05%, 1 in 2000 risk still present)
- Category 2: Benign – routine screening recommended
- Category 3: Probably benign (<2% malignant) – 6/12 follow-up suggested
- Category 4: Suspicious (2-95% malignant) – core biopsy*
- Category 5: Highly suggestive of malignancy (≥ 95% risk) – core biopsy**
- Category 6: Known biopsy-proven malignancy
* Core Biopsy (BIRAS 4) – malignancy (treat accordingly), non-diagnostic / indeterminate / benign and non-concordant with
mammogram (needle localization and excisional biopsy), benign and concordant with mammogram (6 month follow-up)
** Core Biopsy (BIRADS 5) – malignancy (treat accordingly), non-diagnostic / indeterminate / benign (needle localization and
excisional biopsy)
2. Ultrasound105
- Usually 1st investigation in young patients (<35 years old) or pregnant, lactating patients;
- Younger patients <35yo have dense breasts, better evaluation with ultrasound compared to mammogram
- Sensitivity = 98.4%, Negative Predictive Value = 99.5%, permits imaging rather than biopsy for benign lesions on u/s
- Uses:
▪ Differentiates both palpable and mammographic lesions as either cystic or solid
▪ Subsequent characterization and classification of solid nodules (see below)
▪ Guide procedures e.g. Biopsy, drainage of abscess, aspiration of cyst
▪ Evaluation of a palpable mass with a negative mammogram
▪ Evaluation in mammographically-difficult areas e.g. chest wall, axilla
- Pitfalls:
▪ Operator dependent, non-standardised techniques, poor resolution,
▪ Unable to detect most microcalcifications
- Features of malignancy
▪ Borders = spiculation, microlobulation, angular margins
▪ Internal Calcification
▪ Taller than wide (fir-tree appearance; invasion of fascia)
▪ Central Vascularity / Compressibility (malignant lesions displaced breast tissue w/o change in height)
▪ Hypoechoic nodule / Posterior acoustic shadowing
105 Radiology. 1995 Jul;196(1):123-34.

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- Benign Features
▪ Smooth Margins, well circumscribed
▪ Thin Echogenic Capsule
▪ Ellipsoid Shape (wider than deep)
▪ Macrolobulations
▪ Hyperechogenicity
▪ Anechoic lesion
3. MRI of the breast

- Expensive, but good soft tissue definition without radiation (>90% sensitivity)
- Specificity is significantly lower than mammography
- Annual MRI Screening Indications (adjunct to mammography), should NOT be used as a screening tool for women at normal
risk
- Indications:
▪ Patients whose lifetime risk is > 20 – 25%
▪ First degree relative of BRCA carrier but untested
▪ BRCA mutation
▪ Previous radiation to chest between age 10 – 30years
▪ Li Fraumeni syndrome or Cowden syndrome (& 1 st degree relative)
- Should NOT replace mammography even in abovementioned patients
▪ Some cancers may manifest as microcalcifications which may not show up on MRI
- Other Indications
▪ Nodal disease with occult primary cancers (occur in ~1% of all diagnosed breast cancer)
▪ Multifocal tumours in association with conventional imaging for difficult primaries (i.e. invasive lobular carcinoma)
▪ Assessing response to neoadjuvant chemotherapy (selected patients)
▪ BRCA mutation 1 & 2 (in addition to mammogram) – cannot substitute mammography as screening tool
- In absence of mammographic abnormality, no role to evaluate contralateral breast with MRI prior to breast surgery, although,
MRI has been shown to detect contralateral breast lesion in 3-6% of women diagnosed with breast cancer.
- No role for MRI for patients with history of atypia (i.e. ADH, ALH), history of LCIS, history of cancer
(3) Breast Biopsy
Options available:
Cytology:
- Fine needle aspiration cytology (FNAC) – rarely done (only yield cells and unable to assess tissue architecture/invasion). It has
largely been superseded by core-biopsy.
Histology:
- Core Biopsy (simple punch biopsy, spring loaded core biopsy or Mammotome (Vacuum-assisted biopsy)
- Incisional / Excisional Biopsy
Core biopsy is more invasive and more painful (requires LA). It can be performed via clinical palpation or radiological guided (if the
mass is small or difficult to palpate). Radiological guidance can be via ultrasound or stereotactic (stereotactic mammotome). The risk
of the procedure involves bleeding, pneumothorax (biopsy needle is a spring-loaded firing mechanism, improper angling may result
in puncture of the lung)
Core-biopsy is useful as the tissue specimen obtained can differentiate between invasive and non-invasive disease. Also, it can stain
for ER/PR/Her2 status. On average, 6-8 cores are taken (using the 14G core biopsy) to ensure accurate diagnosis.
For small lesions undergoing core-biopsy, marker clips are increasingly being placed to aid with localization
- The following lesions identified on core biopsy will require excisional biopsy

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▪ ADH – risk of upgrade 15-20%, ADH carries a 4x risk of developing cancer
▪ Lobular Neoplasia (i.e. LCIS, pleomorphic LCIS and ALH)
▪ Radial Scar / Complex Sclerosing Lesion – excision recommended unless lesion is small / completely removed on biopsy
(especially if atypia present) – 20% risk of DCIS / carcinoma
▪ Papillary lesions – a/w papillary DCIS in 10-20%, (if atypia present, upgrade rate increases)
▪ Mucocele like lesions (MLL) – risk of upgrade to mucinous carcinoma ~ 10% (especially if atypia present)
▪ Phyllodes Tumour – core biopsy will report fibroepithelial lesion – excise to determine if this represents Phyllodes

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BREAST CANCER
EPIDEMIOLOGY106
- Most common cancer in females (37.2% of all female cancer in Singapore)
- It has increased about 3 folds from 22.0 / 100,000 in 1973-77 to 62.4 / 100,000 in 2008-12
- Age-standardised incidence 62.4 per 100,000
- Age-specific incidence increases sharply from age 30 and peak at 60-69 then gradually declined after 70
- Lifetime risk in Singapore is 6.45% (1 out of 16 develop breast cancer by age 75)
- Breast Cancer is the leading cause of death among females (2 nd is lung cancer, 3rd is colorectal cancer, 4th is liver cancer)
Stage Distribution of Invasive Breast Cancer in Singapore (2017)
Stage I: 33.9%
Stage II: 39.1%
Stage III: 15.5%
Stage IV: 11.6%
RISK FACTORS
Factors Risk High-Risk Groups
Age 10x Age > 55 years
Genetic Factors 56 - 87% BRCA 1, BRCA2 carriers, TP53 germline mutation

Mammographic Density 4x > 75% of film opaque
Previous Breast Disease 20% ADH / ALH / LCIS

Family History 2-3x Breast cancer in 1st-degree relative (age 50 years or younger)
Hormone Replacement Therapy Current Users
Oral Contraceptive 24% Current Users

Age at menarche Menarche before 12 years old
Age at menopause 2x Menopause after 55 years old

Age at first pregnancy 2x First child > age 30 years or nulliparous (as compared to child < age 20)
Weight BMI > 30 in post-menopausal women

Alcohol Excessive Intake
Breast Feeding Protective
106 Trends in Cancer Incidence in Singapore 2008-2012 (data report are as of 7th June 2013)

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Breast Cancer Screening107,108
- Breast Self Examination (BSE) in the absence of mammography does not reduce mortality from breast cancer 109 however; it
helps improve women’s awareness of their own breast and about breast cancer
- Mammography is a/w with a 20% breast cancer mortality reduction for women aged 40 to 74
- Screening is most effective in detecting early breast cancer in women aged 50-69
Monthly breast self-examination (perform 7-10 days after start of menstruation)

▪
< 40
Normal risk, Should not undergo breast screening with any imaging modality
▪
asymptomatic Annual mammogram*
▪
40-49
Ultrasound and Clinical Breast Exam (CBE) not routinely required
▪
Patients on Bi-annual mammogram
▪
50-69
HRT therapy Ultrasound and CBE not routinely required
▪
> 70 Optional bi-annual mammogram
▪
▪ Monthly BSE
5-10 yrs before the onset of breast disease in youngest family
Increased risk ▪ 6 monthly CBE ± U/S breast ± MRI
member or at age 25-30 yrs for BRCA mutation carrier
▪ Annual mammography
* Relative high incidence of breast cancer for Singaporean women in this age group (40% dx before 50 years)
PATHOPHYSIOLOGY
Carcinoma-in-Situ
Ductal Carcinoma In Situ (DCIS) Lobular Intraepithelial Neoplasia (LIN)
- DCIS is defined as proliferation of malignant ductal - LIN combines lobular carcinoma in-situ (LCIS) and
cells arising from terminal duct-lobular unit, atypical lobular hyperplasia (ALH). Arises from the
confined by basement membrane (BM) with terminal duct-lobular unit.
preservation of myoepithelial cell layer - LCIS if acini is > 50% filled with loosely cohesive
- It is a pre-invasive breast cancer. cells, ALH if < 50%
Definition - Majority of the cases are unicenteric with only 1% - It is not considered as pre-malignant lesion but
showing multicentric disease (separate foci of rather a marker of increased risk ~ 1% per year (7-
tumour found in more than 1 breast quadrant). 10x increased risk), whereby carcinoma can arise
- Positive for E-cadherin in either breast
(immunohistochemistry) - Majority are multicentric and bilateral ~ 90%
- Negative for E-Cadherin
- 80% of patients diagnosed with DCIS are - It is often an incidental finding during breast biopsy
asymptomatic and present as mammographic
abnormalities on screening (fine linear granular - Alternatively, it can be diagnosed coincidentally
Presentation microcalcification). Of these 70% presents as following excision of a coexisting breast lesion (no
microcalcification with no palpable breast lesion. further surgical treatment is necessary)
- DCIS can also present as palpable mass (30%),
Paget’s disease of the nipple or nipple discharge
- 2 major subtypes according to the presence of - 2 major subtypes
absence of comedo necrosis - PLEOMORPHIC: more aggressive
- COMEDO: more aggressive ▪ High risk of upgrade to DCIS or invasive cancer
~25%
Classification - CLASSICAL
107 MOH CPG Feb 2010 – Cancer Screening

108 Sabiston Textbook of Surgery (19 th edition) – pg 832
109 J Natl Cancer Inst 2002;94:1445-57.

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- NON-COMEDO: encompass other subtypes such
as solid, micropapillary, papillary, cribriform,
clinging, neuroendocrine
- DCIS is also classified into low, intermediate and
high nuclear grade
- 10-25% of DCIS have concurrent invasive cancer - Pleomorphic LCIS behaves more like DCIS
- 33% risk of untreated DCIS will progress to IDC - 40% of carcinomas that develop were in-situ
(50% in the ipsilateral breast, 5% in contralateral lesions. Invasive carcinomas that developed were
breast) predominately ductal carcinoma (70%).
- Risk of LN mets <2% - 5% risk of finding synchronous breast cancer at the
- Low recurrence rate time of diagnosis
- Risk Factors for recurrence
▪ Excision margins (margins < 1mm after BCS)
▪ Tumour Grade (i.e. high grade)
Prognosis ▪ Presence of comedo-necrosis
▪ Poorly Differentiated DCIS (histology)
▪ ER / PR –
▪ HER-2 +
▪ Symptomatic at presentation
▪ Tumour size not significant for recurrence
Invasive Breast Carcinoma

Invasive Carcinoma of No Special Type (NST) Classical Special Type
- Previously known as invasive ductal Invasive Lobular Carcinoma (5-10%)
carcinoma, however, these tumour sites of - Typically histological grade 2, hormone status: 93% ER+,
origin are unclear, do not form ‘ducts’ 60% PR+, 0.8% HER2+
hence now commonly referred to as NST. - Higher risk of positive margins (disease is not easily
- Accounts for 50-75% of all lesions assessed on MMG, US and intra-op palpation)
- Hormone Status: 71% ER+, 47% PR+,
18% HER2 + - ILC has a distinctive pattern of metastases. It more
commonly metastasize to the gastrointestinal tract,
gynaecological organs (krukenberg tumour), peritoneum
or retroperitoneum (rather than lung and liver)
Subtypes
Other histological subtypes
- Mucinous (3%): abundance of mucin (favourable
prognosis)
- Tubular (1-2%): small tubule formation (favourable
prognosis)
- Cribriform: (favourable prognosis)
- Medullary (5-7%): smooth borders, ↑lymphocytes
- Scirrhotic: worse prognosis
Inflammatory breast carcinoma (IBC)

- Typical presentation: rapid swelling, ± skin changes (Peau d’orange lymphedema) and nipple depression (retraction),
erythematous swollen breast w/o palpable mass [dermal lymphatic invasion by breast carcinoma]
- Underlying cancer is poorly differentiated and diffusely invades breast parenchyma
- Often mistaken for mastitis (in IBC, true inflammation is absent or minimal)
- Treatment: Multimodal therapy – radio-chemo-hormonal therapy ± surgery
Important Biomakers
- HER-2 positive Breast Cancer
▪ HER 2 over-expressed in ~ 15% of all breast cancer
▪ Previously patients had poor overall outcomes but treatment with anti-HER-2 systemic therapy (i.e. transtuzumab) has
improved survival for patients with both early breast cancer and metastatic disease.
- Triple Negative Breast Cancer (TNBC)

▪ TNBC present in ~ 15% of all breast cancer
▪ In general, patients have a poorer prognosis because of a lack of target for treatment
- Asymptomatic: detected on mammographic screening

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- Symptomatic:
▪ Self-detected painless lump in the breast (>1/3 of patients)
▪ Self-detected painless lumps in the axilla
▪ Nipple changes & overlying skin changes
▪ Nipple discharge
▪ Metastatic
i. Bone: pain, pathological fracture, symptoms of hypercalcemia, neurological symptoms (nerve root compression),
cauda equina syndrome (i.e. leg weakness, bladder / bowel dysfunction)
ii. Liver: pain, jaundice
iii. Lung: breathlessness (metastatic pleural effusion), cough
iv. Brain: headache, seizure, unsteadiness (cerebral metastases), visual disturbance (choroidal metastases)
v. Intra-abdominal: abdominal distention, bowel obstruction, ureteric obstruction
▪ Constitutional Symptoms: LOW, LOA
Features Suggestive of Breast Cancer

- Surface: irregular or nodular
- Edge: poorly defined, (areas more like normal breast tissue in between abnormal areas)
- Consistency: firm / hard
- Nil tenderness, nil fluctuant
- ± tethered to overlying skin or fixed to underlying muscle
- ± nipple involvement / discharge (see above)
- Lymphadenopathy
Modes of Spread
- Local: skin & subcutaneous tissues, underlying ribs and muscle (chest wall)
- Lymphatics: axillary, internal mammary LNs, infraclavicular & supraclavicular LNs
- Haematogenous: lungs/pleura, brain, bone (i.e. spine), liver, adrenals, ovaries

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INVESTIGATIONS
All patients will first undergo triple assessment for evaluation. For patients with early breast cancer, investigation looking for metastatic
disease need not be performed routinely.
Further investigations should be performed for patients with locally advanced breast cancer (LABC). This can be divided into
biochemical and imaging investigations.
Biochemical Investigations: FBC, U/E/Cr, LFT, Calcium Panel, (KIV hepatitis markers if planning for chemotherapy)
Imaging Investigations
- CT Thorax, Abdomen & Pelvis (routinely done)
- Bone scan (whole body) (routinely done)
- MRI whole spine (not routinely done, perform in patients with symptoms of malignant spinal cord compression)
- CT or MRI brain (not routinely done, perform in patients with symptoms of intracranial metastases)
- PET scan
STAGING (8th Edition)

Breast Cancer staging is complicated. It can be performed using anatomical stage, clinical prognostic stage and pathological
prognostic stage. In the AJCC 8th edition, biomarkers (i.e. ER/PR/Her2 status) as well as histological grade will play a role in
determining the final stage. Online resources: Breast Cancer Staging Calculator, AJCC 8th manual
Anatomic TNM Stage

T stage (primary tumour) N stage (lymph node involvement) M stage (distant metastases)
TX: not assessable NX: regional LN not assessable MX: Presence of distant mets not
T0: no evidence of primary tumour N0: no lymph node involvement, isolated tumour cells assessable
Tis (DCIS): Ductal Carcinoma In-Situ M0: no distant mets
Tis (Paget’s): Paget’s disease of nipple (clinical)
cN1: mets to ipsilateral level I, II axillary LN – movable (micro or M1: distant detectable metastasis
T1: Tumour ≤ 20mm macro metastasis) (histologically proven > 0.2mm)
cN2: mets to ipsilateral level I,II axillary LN – fixed / matted OR
- T1mi: Tumour ≤ 1 mm mets to ipsilateral internal mammary (IM) LN in absence of
- T1a: > 1mm but ≤5mm axillary LN
cN3: mets to ipsilateral infraclavicular (level III) lymph nodes,
- T1b: > 5mm but ≤ 10mm ipsilateral internal mammary LN (with level I, II axillary LN),
- T1c: > 10mm but ≤ 20mm ipsilateral supraclavicular LN (with or w/o level I & II axillary LN)
T2: Tumour > 20mm but ≤ 50mm (pathological)

T3: Tumour > 50mm pN1: metastasis in 1 - 3 axillary lymph nodes with at least 1 tumor
T4: Tumour with direct extension to deposit > 2.0 mm
- T4a: chest wall (ribs, intercostal, pN2: metastasis in 4 - 9 axillary lymph nodes with at least 1 tumor
serratus anterior muscle, excluder deposit > 2.0 mm
pectoralis muscle) pN3: metastasis in ≥ 10 axillary lymph nodes with at least 1 tumor
- T4b: skin (Peau d’orange, ulceration,
deposit > 2.0 mm or metastasis to infraclavicular lymph node
satellite skin nodule)
- T4c: T4a + T4b
if post-neoadjuvant therapy use the prefix ‘yp’
- T4d: inflammatory breast cancer
Invasion of dermis does not qualify as T4

363
MANAGEMENT
Management of breast cancer can be divided into local-regional control and systemic therapy. Local-regional control involves
use of surgery and radiotherapy. Surgical management of breast cancer involves breast surgery (breast conserving surgery and
whole breast RT vs mastectomy) and axilla surgery (sentinel lymph node biopsy vs. axillary clearance). Systemic therapy can be
categorized into chemotherapy, hormonal and targeted therapy.
Breast Surgery Management
1. Preparing for operation:

- Anaesthesia workup and necessary imaging.
- Psychological counselling, consent taking, discuss breast reconstruction options (if planning for mastectomy)
2. Breast Conserving Surgery (Wide Local Excision)

- Aim: Removal of tumour with clear margins, while achieving good cosmetic result
- Indications
▪ Most T1, T2 cancers (T3 cancers can be considered in larger breast but consider neoadjuvant chemotherapy first)
▪ Only 1 tumour, not multicentric/ multiple DCIS/ LCIS unless same quadrant
▪ Appropriate tumour size-to-breast ratio (to achieve good cosmetic result)
▪ Patient must agree to post-operative radiotherapy
- Breast conserving therapy (i.e. BCS + post-op RT) have equivalent overall survival as compared to simple mastectomy.
BCT may potentially have higher local recurrence in the long-term.
- Factors affecting local recurrence after BCT

▪ Recurrence more common in younger patients (age < 40 years)
▪ Recurrence more common in triple negative breast cancer & HER-2 positive breast cancer
▪ Recurrence more common in grade 3 tumours
▪ Recurrence more common in breast cancer with lympho-vascular invasions
▪ Recurrence more common in patients with involved margins or margin < 1mm (1mm margin is sufficient)
▪ Tumour size does not equate with increase in local recurrence (margins is more important)
3. Mastectomy
- Historically, Halsted Radical Mastectomy which involves total mastectomy, axillary clearance of level I, II & III, & removal
of pectoralis major and minor was performed. However, current evidence suggest for less radical surgery
- Modified Radical Mastectomy (MRM) involves total mastectomy and axillary clearance of level I & II. This is performed for
patients with involved axillary lymph nodes metastases.
- Current recommendation is for simple mastectomy with SLNB KIV axillary clearance (SMAC)
- Alternatives: skin-sparing mastectomy with immediate reconstruction, nipple-sparing mastectomy
- Mastectomy are also performed in the palliative setting for specific indications: symptoms control (bleeding, fungating breast
tumour)
4. Breast reconstruction
- Immediate vs. Delayed → Immediate reconstruction not shown to affect patient outcome adversely – detection of recurrence
not delayed, onset of chemotherapy not changed

- Autologous vs. Implant-Based or Both
▪ Implant-Based (silicon implants) Reconstruction
▪ Latissimus dorsi myocutaneous flaps (LDMF)
▪ Transverse rectus abdominis myocutaneous flaps (TRAM)

364
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if under
Axilla Management
• need artillery clearance .
5. Sentinel Lymph Node Biopsy (SLNB)

- The concept of SLNB is based on the premise that lymph node involvement occurs in a stepwise fashion. The SLN
represents the first draining lymph node, its identification allows for a selective assessment. If negative for tumour cells then
regional lymph nodes are likely free of tumour cells and there is no need to perform an axillary clearance.
- Identification Methods
▪ Use of blue dye (methylene blue, 5-10min before incision) +/- radioactive isotope (technetium-99m sulphur colloid,
20min – 24hr prior) injected intradermal plane in the vicinity of the tumour or sub-areolar area just before surgery
▪ Inform patient that blue dye on breast may be there for up to 4 weeks and that 1 st few days post-op urine colour may
be green = NORMAL
▪ The multiple blue lymphatic ducts converging into the sentinel node – the axillary nodal basin (medial)
▪ During the op, look for the SLN by its blue colour, and/or using a Geiger-Muller counter (gamma probe) to detect the
node with the highest radioactivity.
▪ For patients who use radioactive isotope, after removal of the SLN, background count over 10sec should be less than
10% of nodal count over 10sec
- Dual method gives the highest accuracy, the choice of either method is based on institutional practices, in NUH, dual method
is used based on the rule of 4 (i.e. size + grade > 4)
- Send nodes for frozen section (FS) – [false negative rate: 4-12%]
- When the SLN is negative, SLN alone with no further ALND is safe with similar survival and regional control
- Classification of nodal metastatic disease: (1) macro-metastases (deposit >2mm), (2) micro-metastases (0.2-2mm) – N1mi
and (3) isolated tumour cells (<0.2mm) – N0(i+)
- For patients with micrometastases and isolated tumour cells → no further treatment
- For patients with macro-metastasis → proceed to axillary clearance except in specific circumstances
▪ Previously, patients with positive SLNB would lead to axillary clearance. However, data from trials have suggested that
patients with limited axillary nodal disease do not require axillary clearance.
▪ ACOSOG Z0011 trial110111 – AD is not necessary after SLNB in selected patients (T1/T2, cN0 tumour, undergoing
Breast Conserving Surgery, must have post-op whole breast RT, 1-2 SLN positive, no significant extranodal extension,
receive post-op chemotherapy) → no difference to local recurrence or survival wooly

↳ > } lymph need
t.ve
6. Axillary clearance further
- A positive sentinel lymph node is a/w further axillary disease, earlier disease recurrence and a poorer overall survival rate
- While a standard completion axillary clearance is considered the gold standard for patients with positive SLN metastasis
(micro-metastasis ≥ 0.2mm), management is shifting towards selective surgery
▪ Level I and level II axillary nodes should be removed, Level III axillary nodes to be removed if grossly enlarged
▪ Should remove ≥10 nodes (identified by pathologist)
Adjuvant Radiotherapy*
- Regimen consists: 50Gy in 25 fractions, 1 cycle per day from Monday to Friday over 5/52
- Contraindication – previous RT to breast, severe collagen vascular disease, pregnancy
External beam whole breast radiotherapy (WBRT)

- Reduction in ipsilateral recurrence, however, no reduction in mortality
- Patients with breast conserving surgery should have adjuvant radiotherapy
- Patients with mastectomy – indications: size >5cm, T4 disease, positive surgical margins, ≥4 axillary LN**, chest wall invasion
- Patients who had neoadjuvant chemotherapy (NACT) and mastectomy should undergo RT (reduce local recurrence and disease
free survival)
Axillary Radiotherapy
- Patients with ≥4 pathologically involved nodes should undergo RT to the regional LN (for patients with 1-3 involved nodes, further
discussion with radiotherapy, KIV axillary RT)

- Patients with negative sentinel node after neoadjuvant chemotherapy – consider axillary RT (true axillary status unknown)
110 JAMA. 2011 Feb 9;305(6):569-75.– Z0011 trial

111 JAMA. 2017 Sep 12;318(10):918-926. – Z0011 trial (10 year data)

365
Side effects of radiotherapy:
- Short Term: skin irritation (erythema), tiredness, breast swelling
- Long Term: skin pigmentation, pneumonitis, rib fractures (1%), cardiac toxicity, angiosarcoma, RT-induced cancer (1 in 1000)
- Radiation to axilla – lymphedema, axillary fibrosis
Neoadjuvant Chemotherapy
- Indication: patients who are candidate for adjuvant chemotherapy
- Neoadjuvant vs. Adjuvant chemotherapy are equivalent in terms of OS112
- Advantage of Neoadjuvant Chemotherapy
▪ Allows increased possibility of BCS. Also, limits the area of resection with improved cosmesis for patients who are
candidates for upfront BCS.113
▪ Improved prognostic information (tumour responsiveness to chemotherapy)
o 30-35% achieve complete clinical response (cCR) i.e. tumour is no longer palpable, 40-45% partial responder, 10-15%
stable disease, 3% progressive disease
o 15-20% will achieve complete pathological response* (cPR) i.e. no more tumour cells = good prognosis
o Pathologic complete response is seen most commonly in patients with negative prognostic factor (i.e. age < 40 years,
high grade tumour (Ki67 > 20%), HER-2 positive, triple negative breast cancer (TNBC) – about 40-45% with HER-2
positive, and ~30-40% with triple negative breast cancer have cPR.
- Place a clip into the tumour before starting neoadjuvant therapy to guide surgery in case the tumour disappears; operate
according to pre-op staging (i.e. eventual excision to take into account initial ‘footprint’ of the tumour).
- MRI following neoadjuvant chemotherapy is the best imaging modality to assess extent of disease and suitability for BCS
Adjuvant Chemotherapy114
- Usually either anthracycline based on taxane based
- No indication
▪ HER-2 positive / Triple Negative patients – with pT1a pN0 (cancer < 0.5cm in size)
▪ ER+ PR+ HER-2 negative patients – stage I / II (i.e. LN < 4 positive) – exceptions present (i.e. Luminal B subtype)
- Indications: stage III or Locally Advanced Breast Cancer, HER-2 positive breast cancer, Triple Negative Breast Cancer
- Relative Indications for node negative patients: high risk patients – i.e. high grade tumours, any positive LNs, high Ki67, younger
patients (age < 35), extensive lymphovascular invasion
Side effects of chemotherapy

- Lethargy, tiredness, nausea/vomiting, myelosuppression [requires frequent blood tests], oral mucositis, cardiomyopathy
(anthracyclines) [require 2D echo prior to starting chemotherapy] & peripheral sensory neuropathy (taxanes), increased risk of
infections, GI side effects (i.e. diarrhoea)
112 J Clin Oncol. 1997 Jul;15(7):2483-93

114 Ann Oncol. 2017 Aug 1;28(8):1700-1712. [Important Paper, St Gallen 2017 Expert Consensus]

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EXTRA INFORMATION
Adjuvant Chemotherapy
- Indications
▪ Stage III or Locally Advanced Breast Cancer
▪ Early Breast Cancer – depending on subtype (St Gallen 2017)
1. Luminal A (ER+, HER-2 –, Ki67 low (<14%)), stage III or higher (pT3N1, > pN2 (> 4 positive LN))
2. Luminal B (ER+, HER-2 –, Ki67 high), see relative indications, assess genomic risk scores
3. HER-2 overexpression (ER – HER-2 +), stage pT1b N0 or higher (tumour size ≥ 0.5cm, add anti-HER-2 therapy)
4. Basal like (triple negative, ER/PR/Her-2 negative), stage pT1b N0 or higher (tumour size ≥ 0.5cm)
- Anthracycline based chemotherapy (i.e. doxorubicin / epirubicin)
▪ Typical Regime: 4-6 cycles of FEC (F = 5-fluorouracil, E = epirubicin, C = cyclophosphamide) – i.e. all 3 drugs injected on first day of each
3 week cycle
▪ Side effects (anthracycline) – acute myeloid leukaemia (with high doses), cardiotoxicity (CCF, esp. in older patients)
▪ Anthracycline use in patients with Her-2 + breast cancer comes with higher cardiotoxicity
- Taxanes (i.e. paclitaxel and docetaxel) based chemotherapy
▪ Taxanes used with anthracycline based chemotherapy has no benefit for tumours that are ER + and Her2 – (majority), potential benefit
for patients with HER-2 positive breast cancer and with triple negative breast cancer
- Premenopausal patients tend to have better response to chemotherapy than hormonal therapy (and vice versa for postmenopausal patients)
- Can start about 1 months after breast surgery
- Optimal duration of chemotherapy remains uncertain, usually around 4-6 months
Hormonal therapy
- Mostly used as adjuvant therapy but also as neoadjuvant therapy in locally advanced breast cancer, palliative treatment &
preventive treatment in high risk patients
- For ER/PR +ve will have 90% response
1. Selective estrogen receptor modulators (SERMs): Tamoxifen (20mg daily) / Raloxifene

- Used only in adjuvant setting, decrease in incidence of breast cancer only evident in ER+ breast tumours
- Recent meta-analysis showed for ER+ tumours, tamoxifen for 5 years decreased recurrence rates and breast cancer
mortality rates during the first 15 years by at least a third.115
- 5 years of tamoxifen is recommended for premenopausal and post-menopausal women with ER+ positive breast cancer.
- Extension of treatment to 10 years may be considered (ATLAS trial)
- In high risk premenopausal women, ovarian suppression via medical ablation (i.e. LHRH agonist such as goserelin) or
surgical oophorectomy in combination with hormonal therapy can be considered
- Side effects
▪ Tamoxifen flare – menopausal symptoms (i.e. hot flushes, ↑HR, sweating, fatigue etc.)
▪ Thromboembolic events (1%) – DVT / PE
▪ Endometrial hyperplasia, polyp formation or invasive carcinoma (0.1% per year)
▪ Uterine sarcoma
▪ Cataract Formation
- Raloxifene has a better side effect profile
2. Aromatase inhibitors: Anastrozole, letrozole, exemestane

- Inhibit peripheral conversion of testosterone and androstenedione to oestradiol
115 Lancet. 2011 Aug 27;378(9793):771-84. (Early Breast Cancer Trialists’ Collaborative Group (EBCTCG))

367
- Only suitable for post-menopausal patients – in post-menopausal patients, the primary source of estrogen is from conversion
of androstenedione to estrogen and testosterone to estradiol in peripheral tissues (i.e. breast, skin and adipose tissue by
aromatase) – AI blocks this conversion
- Can be used as neoadjuvant therapy for locally advanced breast cancer for post-menopasual patients (patients who are
poor candidate for chemotherapy, poor performance status)
- Improvement in disease free survival, time to recurrence, contralateral breast cancer, distant recurrence rates with use of
adjuvant Aromatase Inhibitors (compared with 5 years of tamoxifen)
- Side effects:
▪ Musculoskeletal pain – arthralgia, myalgia back pain
▪ Osteoporosis / Fractures (ensure patient do bone mineral density testing) - patient may require bisphosphonates
▪ Hyperlipidaemia
** Estrogen – branching differentiation and duct development

** Progesterone – lobular development of the breast
Summary of Recommendation
- Premenopausal → tamoxifen for 5 years, (for women < 35 years, consider ovarian suppression)
- Post-menopausal → aromatase inhibitors (AI) – i.e. letrozole for 5 years or anastrozole for 5 years
- Women who are menopausal after 5 years of tamoxifen → consider additional AI in high risk patients
Targeted therapy – Herceptin (trastuzumab) [must be given with chemotherapy]

- Targets Her-2/neu (HER2) gene (a type of epidermal growth factor receptor [EGFR] that is overexpressed in 18-20% of IDC,
located on chr 17q12) – encodes for transmembrane tyrosine kinase receptor
- A score of 0/1+ is considered negative (66.7%), a score of 2+ is considered borderline (21.7%) and requires an in-situ
hybridisation test, a score of 3+ is considered positive (11.6%).
- IV administration for 1 year duration, given concurrently with chemotherapy.
- Disease-free survival + Overall survival benefit (reduced risk of death by ~40%)
- Side effects of Herceptin:
▪ Cardiomyopathy (drop in LVEF ~5%, symptomatic CCF ~2%, severe CCF ~ 0.5%)*
▪ Pulmonary toxicity & Infusion reactions & Febrile neutropenia
* worse when given concurrently with anthracyclines

368
COMPLICATIONS
Breast Surgery
- Haemorrhage / Hematoma → postoperative bleeding usually presents within 12 hour of the procedure
- Wound Infection (POD 5-10) – tx promptly with Ab (infection can damage lymphatics further)
- Seroma (likely following axillary clearance) → needle aspiration, ensure seroma resolves prior to RT or chemotherapy
- Intercostal intercostobrachial nerve injury – hyperesthesia of inner arm and lateral chest wall
- Restricted shoulder mobility
- Skin flap necrosis
- Tumour recurrence → skin local recurrence and/or axillary tumour recurrence
Axilla Surgery (Axillary Clearance)

- Post-operative bleeding
- Post-operative seroma formation
- Nerve injury – thoracodorsal nerve (weakness of latissimus muscle, affect adduction / pull-up), intercostobrachial nerve
(numbness to medial arm and axilla), long thoracic nerve (winged scapula), intercostal nerves (paraesthesia)
- Axillary vein thrombosis – early post-op swelling of ipsilateral arm
- Lymphatic fibrosis – painless progressive swelling of ipsilateral arm
- Lymphedema (15-30%)* / Lymphangiosarcoma
- Frozen shoulder – rehabilitate with physical therapy
EXTRA INFORMATION
Lymphedema (15-30%)
- Incidence of lymphedema is 2-4% in SLNB – not exacerbated by physical activity
- Radiation to axilla, UL cellulitis increases this risk, lymphedema increases risk of lymphangiosarcoma (Stewart-Treves syndrome)
- Lymphedema tx: arm PT, pneumatic compression devices and fitted compression sleeves
- Lymphangiosarcoma tx: large resection / amputation of affected limb + neoadjuvant / adjuvant RT ± CT
PROGNOSIS
- Nottingham Prognostic Index116 = [0.2 * S] + N + G
▪ S = Size of Tumour
▪ N = Number of lymph nodes involved
▪ G = Grade of tumour
- Nodal status is the most important prognostic staging factor

- Presence of tumour emboli in lymphovascular spaces a/w poor prognosis. (LVI)
- Hormone Receptor Status
▪ ER(+)/PR(+) = better prognosis, tumour responsive to tamoxifen
- Her2 / Neu (epidermal growth factor receptor)
▪ Overexpression of Her2/Neu is a poor prognostic factor (increased rates of metastases, decreased time to recurrence and
decreased overall survival). However, patients can be treated with anti-HER-2 therapy (i.e. trastuzumab (Herceptin) or
lapatinib (Tykerb)) given with chemotherapy which significantly improves their prognosis
- Triple Negative Breast Cancer (poor prognosis)
- Other tools for risk stratifications
▪ Oncotype Dx: 21 gene real-time PCR assay → a recurrence score between 0 to 100 will be provided (patients who are ER
+, HER2- and LN - early breast cancer and who are intermediate risk for recurrence should be offered gene expression
profiling)
FOLLOW-UP117
- 3 to 6 months for first 3 years, then every 6 to 12 months for next 2 years, then annually thereafter
- Post-treatment MMG should be obtained 1 year after initial MMG and at least 6 months after completion of radiation therapy
- Annual mammogram for contralateral breast (risk of 2nd breast CA is 0.5 to 1% per year)
- Patient at high risk for familial breast cancer → refer for genetic counselling
- Survival data from 2013 to 2017 (5 year survival): Stage I: 100%, Stage II: 89.5%, Stage III: 73.3%, Stage IV: 27.0%
116 Ann R Coll Surg Engl. 2015 Mar;97(2):137-9.

117 J Clin Oncol. 2006; 24:5091-5097.

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BREAST CANCER MANAGEMENT BY TUMOUR STAGE
Surgical management for breast conditions can be categorized as such
- High risk patients (5yr calculated risk of 1.7% or higher) – ADH / LIN (LCIS / ALH)
- Non-invasive (in-situ) Breast Cancer – i.e. DCIS
- Invasive Breast Cancer
▪ Early Breast Cancer (stage 1 & 2)
▪ Locally Advanced Breast Cancer (stage 3 & T3N0)
o Non-inflammatory
o Inflammatory – inflammatory LABC (T4d)
▪ Metastatic Breast Cancer (stage 4)
Atypical Ductal Hyperplasia

- If diagnosed on core biopsy, proceed for excision biopsy or wire localized surgical excision (have 10-20% risk of upgrade to DCIS
or invasive cancer)
- Axillary nodal staging is not recommended
- Margins are irrelevant – no role for repeat excision
- Chemoprophylaxis (only for ER+ cancer)
- Prophylactic Mastectomy: consider for women with deleterious mutation in BRCA 1 or BRCA 2
Lobular Intraepithelial Neoplasia (Lobular Carcinoma in Situ & Atypical Lobular Hyperplasia)
- LCIS (>50 % lobular involvement) and atypical lobular hyperplasia (<50% lobular involvement)
- LCIS is not itself pre‐cancerous, it is simply a marker of a susceptible field, it is usually not clinically and radiographically
detectable
- 7-10 x increased risk of invasive cancer in either breast
- If diagnosed on core biopsy proceed for excision biopsy or wire localized surgical excision (have risk of upgrade to DCIS / invasive
cancer in up to 25% of patients, especially for pleomorphic LCIS)
- If diagnosed on coincidentally following excision of a coexisting breast lesion (no further surgical treatment, even if margins are
involved, margins are irrelevant, disease is diffuse (unlike DCIS) – no role for repeat excision
EXTRA INFORMATION
Management of LCIS
- Lifelong close surveillance* – annual mammogram and PE
- Chemoprophylaxis with tamoxifen for 5 years**
- Bilateral Total Mastectomies*** (for selected high-risk patients)
*Close surveillance for normal-risk patient undergoing screening mammogram, fewer than 4 loci of LCIS on core biopsy, no high risk features
**NSABP P-1 shows that tamoxifen produces a 56% reduction in the risk of developing subsequent invasive cancer in patients with LCIS
***Consideration for prophylactic mastectomy: LCIS with family history of BRCA + gene, (+) high patient anxiety, poor assess for follow-up
examination, patient’s preference, difficult lesion to follow on an exam or with a mammogram

370
Ductal Carcinoma in Situ (DCIS)
- Accounts for 20% of screen-detected cancers with invasive carcinoma found on definitive excision in up to 15-20% of patients
- Surgical excision
▪ Breast Conserving Surgery with wire-needle localization to identify the area to be excised with intra-op XR of specimen to
ensure all suspicious microcalcifications are removed (treatment of choice!)
▪ Total (simple) mastectomy ± immediate reconstruction
o indications: radiotherapy contraindicated, multicentric lesions, larger area for DCIS (arbitrary > 4cm)
o Offer mastectomy for patients with margins positive following BCS where re-excision is deemed not suitable
- Management of Axilla
▪ SLNB is generally not indicated, however, it can be performed for selected high risk patients (i.e.comedonecrosis
morphology, high nuclear grade, DCIS > 4-5cm, palpable breast lesion)
▪ SLNB should be performed in patients with DCIS undergoing mastectomy (SLNB cannot be performed post-mastectomy if
an occult invasive cancer* is found, patient will require axillary clearance)
- Assessment of excision margins

▪ This involves intraoperative assessment via X-ray to ensure all suspicious microcalcification are excised and based on
histological assessment
o Histological margins of 1-2mm margin is adequate (wider margins do not reduce local recurrence, positive margins
increases local recurrence)
o Margins > 10mm (without adjuvant RT) a/w local recurrence rate 14% at 12 years118 (previously reported at 3% over
8 years)119 – hence in patients with lumpectomy with wide margins can achieve similar local recurrence rates with
patients who underwent lumpectomy with radiotherapy. (this is no longer practised)
▪ If margins are inadequate (i.e. close <1mm margins or involved on histology), patients should undergo re-excision
- Adjuvant therapy
▪ +/- Adjuvant radiation
o Indications: patients with DCIS treated with breast conserving surgery
o Decrease local recurrence rates, No survival benefits
▪ +/- Hormonal Therapy (adjuvant tamoxifen or aromatase inhibitors)

o Indication: benefit found for ER-positive DCIS
o Tamoxifen – ↓RR by 37% over 5 years and ↓risk of developing contralateral breast cancer
o Survival benefits were restricted to ER-positive DCIS (↓RR by 42%)120
EXTRA INFORMATION
Specific scenarios
- LCIS / ADH found on margin → no need for re-excision (no increased risk of local recurrence)
- Young patients: involved margins have greatest impact on local recurrence in younger women → re-excision
- Extensive in-situ component with positive margins (i.e. ≥ 25% of tumour is non-invasive and it is also present in breast tissue surrounding the
invasive cancer) → re-excision to reduce local recurrence
The risk factors for recurrence of DCIS involves:

- Involved or close margins (<1mm)
- High tumour grade
- Presence of comedo necrosis
- Poorly differentiated histological type
- Young age of diagnosis (<40yrs)
- Hormonal Status (i.e. ER/PR negative, HER-2 positive)
- Genomic tests – i.e. oncotype Dx DCIS
Most recurrence represents residue disease and incomplete excision. Tumour size is not related to recurrence of DCIS
118 Am J Surg. 2006 Oct;192(4):420-2.

119 N Engl J Med. 1999 May 13;340(19):1455-61.
120 J Clin Oncol. 2012 Apr 20;30(12):1268-73.

371
Stage 1 and Stage 2 Early Stage Breast Cancer
- Curative Intent – clear surgically with adequate margins (no ink on tumour)121
- BCT with adjuvant whole breast radiotherapy is superior to mastectomy without radiotherapy 122
- Breast Conservation Therapy (BCT) with Sentinel Lymph Node Biopsy (SLNB)
▪ Aim for microscopically disease free margins (≥ 1mm) around the carcinoma at all radial margins
▪ Optimal margin widths in the neoadjuvant setting are unknown, in general, ensure tumour free margins123124
▪ Neoadjuvant chemotherapy or hormonal therapy – aim to reduce size of tumour
- Non-Conservative Therapy – Mastectomy

▪ Simple Mastectomy with SLNB KIV Axillary Clearance (SMAC) aka ‘modified radical mastectomy (MRM)’
▪ Alternatives: skin-sparing mastectomy with immediate reconstruction, nipple-sparing mastectomy
- Management of Axilla
▪ ACSOG Z0011 study125: T1 or T2 invasive breast cancer with no palpable lymphadenopathy undergoing BCT with SLNB
found to have 1-2 positive sentinel lymph nodes → no difference in 5-year & 10-years, overall disease survival or disease-
free survival (between no further axillary specific treatment vs. completion ALND) 126
▪ Post-op, these patients require whole breast radiation and adjuvant systemic therapy
▪ Criteria to avoid ALND: breast-conserving therapy, post-op whole breast RT, clinically T1 or T2 and cN0 tumour, no
neoadjuvant chemotherapy, 1 or 2 positive SLNs
▪ Not applicable for patients who have ≥3 positive SLNs, matted nodes, gross extra-nodal disease, received neoadjuvant
hormonal / chemotherapy, undergoing mastectomy
▪ If no SLN identified or if many suspicious nodes identified, proceed with axillary nodal dissection
- Adjuvant Therapy (node-positive patients)

▪ Adjuvant radiation – required component after BCT (decreases local recurrence from 30% to <7% at 5 years)
▪ Adjuvant Chemotherapy (in general, for all node-positive patients, any number of nodes)
▪ Adjuvant Hormonal Therapy for at least 5 years (for ER/±PR positive tumours)
▪ Adjuvant Trastuzumab – IV monthly for 1 year concurrently with chemotherapy (for HER-2 positive tumours)
- Adjuvant Therapy (node-negative patients)

▪ Individualized approach (see above section on adjuvant chemotherapy)
- Prognosis for local recurrence (breast-conserving therapy)

▪ Patients at increased risk of local recurrence after BCS – young age at diagnosis (<40yrs), HER-2 positive, triple negative,
presence of lymphovascular invasion, tumour grade, margin status (involved or < 1mm),
▪ Multifocal breast cancer, size of breast cancer, invasive lobular vs. ductal carcinoma and partial breast RT are NOT
associated with increased local recurrence
Stage 3 Locally Advanced Breast Cancer (LABC)
Non-inflammatory LABC
LABC is defined as stage III breast tumours, breast tumours > 5cm with regional lymphadenopathy, tumour of any size with direct
extension to chest wall or skin or presence of regional lymphadenopathy regardless of tumour stage. LABC can be categorized into
operable and inoperable disease.
LABC is defined as T3,T4, N2,N3 breast cancer. It can include non-inflammatory and inflammatory breast cancers. Loco-regional and
systemic staging should be performed in all patients with LABC
- Neoadjuvant Therapy
▪ Neoadjuvant Chemotherapy (anthracycline and/or taxane based) – downstage tumour, improves survival & predicts tumour
response to adjuvant therapy
121 Cancer. 2018 Apr 1;124(7):1335-1341.

122 Br J Surg. 2018 Jun 21. doi: 10.1002/bjs.10889. [Epub ahead of print]
123 Eur J Surg Oncol. 2016 Jul;42(7):986-93.
124 Ann Surg Oncol. 2018 Nov;25(12):3541-3547.
125 JAMA. 2011 Feb 9;305(6):569-75. [Landmark Paper] – Z0011 Trial
126 JAMA. 2017 Sep 12;318(10):918-926.

372
▪ +/- Neoadjuvant Herceptin (i.e. trastuzumab) for HER2+ breast cancer
▪ Neoadjuvant Endocrine Therapy (i.e. aromatase inhibitors) for ER + / PR + breast cancer (i.e. aromatase inhibitors (i.e.
anastrozole / letrozole) for ~ 9 months for post-menopausal women)
o Indicated for post-menopasual patients with hormone sensitive breast cancer and who have a poor performance status
- Surgical Excision
▪ For most patients, simple mastectomy will be the standard surgical approach.
▪ Patients who received neoadjuvant chemotherapy and can be converted to BCT candidates with no difference in overall
outcome survival
▪ Indication for mastectomy
o Extensive malignant microcalcifications
o Multicentric tumours
o Extensive skin invasion
o Persistent skin edema after neoadjuvant therapy
o Residual size is not amenable to BCS
- Axilla Management (clinically node positive)

▪ Axillance clearance is the usual standard of care, however, recent evidence suggest that SLNB can be offered to patients
with LABC with negative axilla at presentation
▪ Axillary Clearance: requires level I and II axillary dissection with at least 10 lymph nodes for evaluation. Take level III only if
gross disease is apparent
- Adjuvant Radiation + Systemic Therapy (CT, HT, TT) – individualized

- Complications related to LABC → malodorous, fungating wounds
EXTRA INFORMATION
Axilla Management after neoadjuvant chemotherapy

- For patients who convert from node positive to node negative after neoadjuvant chemotherapy (controversial), can opt to
perform SLNB (using dual method), if have ≥3 LN examined and noted to be negative, no further treatment (regardless of
initial axilla LN status), 1-2 LN examined is inadequate – St Gallen (2017)
- If pre-chemotherapy nodes are positive and then convert to negative on SLNB → consider post-op axillary RT
Inflammatory LABC (T4d)

- Investigate with skin punch biopsy (differentiate inflammatory breast cancer with mastitis)
- Has dermal lymphatic invasion, causes peau d’orange lymphedema (no role for SLNB)
- Approximately 60% have nodal mets & 30% have distant mets at time of diagnosis
- Aggressive multimodal therapy – 5yr survival is ~ 40%
- Neoadjuvant chemotherapy then surgery (i.e. SMAC ) then adjuvant chemotherapy and radiotherapy
Stage 4 Metastatic Breast Cancer

- Intention: Palliative, aim for disease control, maintain QoL
- Role of Surgery: for local control – toilet mastectomy for fungating, bleeding primary tumour
- Systemic Therapy is the mainstay of treatment – Chemotherapy, Hormonal Therapy, Targeted Therapy
- Palliative Radiotherapy for symptoms control (i.e. painful bone metastases)
- Bone is the most common site for distant metastasis – spread through batson's plexus (valveless vertebral veins) – direct
metastases to the spine.
- Occurrence of brain metastases (BM) a/w poor prognosis with 1yr survival of 20% and impaired quality of life (breast cancer is
2nd most common cause of BM after lung cancer)127
127 Breast. 2013 Oct;22(5):993-8

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UNCOMMON PRESENTATIONS OF BREAST CANCER
Paget’s Disease of the Breast

- Erythema and eczematous change of the nipple (not the areola) with crusting exudates, may develop into erosions and
ulcerations, clinically resembles eczema
- Extension of DCIS along ducts within the epithelial layer to the area under the skin over the nipple
Paget’s Disease Eczema

Breast Affected Unilateral Bilateral
Long-Term Effect Destroys the Nipple Does not destroy the nipple
Associated with underlying DCIS or invasive
Associated with Not associated with underlying lump
carcinoma (85-88%)
Steroids a/w dramatic improvement
- Pathogenesis
▪ Malignant cells invade across the epithelial-epidermal junction and enter the epidermis of the nipple, breaking the normal
epidermal barrier thus allowing fluid to be extruded onto the nipple
▪ Pathological Hallmark: malignant, intraepithelial adenocarcinoma cells (Paget cells) occurring singly or in small groups within
the epidermis of the nipple
▪ Often associated with underlying ductal carcinoma in situ (DCIS) or invasive carcinoma in 85-88% of cases often w/o
associated breast mass or mammographic abnormality
- Investigations
▪ Mammography (bilateral)
▪ Breast MRI (if have –ve PE & mammography, ultrasound), if MRI +ve, require confirmatory biopsy
▪ Punch biopsy or full-thickness wedge biopsy of the nipple
▪ 90% of paget’s cell are HER-2 positive, more commonly they are high grade and ER negative
- Prognosis of the underlying cancer is not altered by the presence of Paget’s disease of the nipple
▪ Palpable mass: most have IDC & axillary nodal involvement with 5yr survival of 37-43%
▪ No palpable mass: most have DCIS with excellent 5yr survival of 90-100%
- Treatment should be planned according to underlying cancer if found

▪ Simple Mastectomy & SLNB
▪ Breast Conserving Therapy & SLNB & RT (complete resection of the nipple-areola complex followed by whole breast RT)

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EXTRA INFORMATION
Male Breast Cancer

- Risk factors: Klinefelter syndrome (20-50x), testicular abnormalities, cirrhosis, obesity, familial predisposition, BRCA 2
- Male Breast Cancer, usually ductal, majority are ER+ → simple mastectomy + SLNB +/- AC
- Metastatic disease: if hormone positive → tamoxifen, if hormone negative → chemotherapy
Positive Axillary LN metastases without a known primary cancer (Occult Breast Cancer)
- This represents < 1% of all operable breast cancer.
- Primary breast tumour not present on physical examination, ultrasound or mammogram
- Differential diagnosis: lymphoma, melanoma, lung, ovarian, thyroid, neuroendocrine tumours
- Patients should undergo imaging work-up to evaluate primary cancer (i.e. mammography, ultrasound +/- breast MRI if both
are negative)
- Patients should also undergo evaluation of metastatic disease (i.e. CT TAP & Bone Scan)
- Management: axillary clearance +/- whole breast RT or mastectomy
Treatment of Breast Cancer in pregnancy

- 1st Trimester & 2nd Trimester: modified radical mastectomy (MRM) or Mastectomy + SLNB (using radiolabeled colloid*) ± AD
- 3rd Trimester: if late, can perform BCS + SLNB (using radiolabeled colloid) ± AD and post-partum RT (if not, MRM)
- Chemotherapy is ideally started after 1st trimester
- Hormonal therapy is not recommended during pregnancy
* Isosulfan blue classified as category C (possible teratogen) – for pregnant patients use radiolabeled colloid for SLNB

375
GYNAECOMASTIA
DEFINITION
It is defined as the benign enlargement of male breast tissue which most commonly occurs in adolescent and older age groups.
Microscopically, it is characterized by ductal epithelial hyperplasia, ductal elongation and branching, proliferation of peri-ductal
fibroblasts and increase in vascularity in the involved tissue.
CAUSES
- Oestrogens
- Spironolactone – aldosterone antagonist, have significantly anti-androgenic effects
- Cimetidine
- Digitalis
- Tricyclic Antidepressants
- Cannabis
Drugs
- Anabolic Steroid Abuse
- Amphetamines
- Antifungal –azoles (systemic) – i.e. fluconazole, ketoconazole
- Cyproterone
- Griseofulvin
- Bicalutamide (Casodex) – for prostate cancer treatment
- Liver Failure
- Renal Failure
Organ Failure
- Testicular failure (cryptorchidism, torsion, orchitis)
- Hyperthyroidism
- Neonates
Physiological - Puberty
- Old Age
Idiopathic
Nutrition - Malnutrition
- Klinefelter Syndrome → increased risk of male breast cancer (20-50x)
G – hypoGonadism
- Agenesis
- Carcinoma of the male breast

- Testicular Tumours
Neoplasm
- Bronchial Carcinoma (inappropriate secretion of hormones)
- Prolactinoma
Others - Pseudo-gynecomastia
INVESTIGATIONS
- Biochemical: U/E/Cr, LFT, TFT, Testosterone, LH/FSH, Oestradiol, prolactin, α-FP, ß-HCG
- Imaging:
▪ Mammography (for patients age > 40 years)
▪ Ultrasound breast (if lump is present)
▪ Testicular ultrasound (if PE shows a testicular mass)
- Histology: core-biopsy (if lump is present)
MANAGEMENT
- Conservative management → Tamoxifen (10mg for 3-6/12) – reduction of pain and breast enlargement
- Surgical excision

376
13. ENDOCRINE, HEAD & NECK
ANATOMY OF THE NECK
Anterior & Posterior Triangles of the Neck

- The anterior triangle is bounded by the lower border of the mandible superiorly, the midline anteriorly, and the anterior border
of the SCM posteriorly – contains the carotid sheath
▪ The anterior triangle is further divided into muscular, carotid, submandibular and submental
- The posterior triangle is bounded by the posterior border of the sternocleidomastoid anteriorly, the anterior border of the
trapezius posteriorly, and the clavicle inferiorly – contains the spinal accessory nerve
▪ The posterior triangle is further divided into occipital and subclavian triangles.
Midline Bony Landmarks

- Hyoid Bone – C3
- Notch of the thyroid cartilage – C4
- Cricothyroid ligament
- Cricoid Cartilage – c6
- Tracheal Rings – 2nd and 3rd rings
- Suprasternal Notch – T2/3
Musculature
- Supra-hyoid Muscles
▪ Digastric (anterior & posterior belly)
▪ Mylohyoid – paired, sheet-like muscle
▪ Stylohyoid
▪ Geniohyoid**
- Infra-hyoid Muscles
▪ Omohyoid* (superior and inferior belly) – from scapula to hyoid bone –
innervated by ansa cervicalis
▪ Sternohyoid*
▪ Sternothyroid*
▪ Thyrohyoid**
* supplied by ansa cervicalis (C1-C3)

** supplied by C1 spinal nerve via the hypoglossal nerve
13. Endocrine, Head & Neck_Last Updated 3rd June 2020

377
Arteries
- Vertebral artery arises from the subclavian artery
- Common Carotid Arteries (CCA) have no side branches and terminate at upper border of thyroid cartilage – C4 into the
external and internal carotid
▪ Right CCA – begins from bifurcation of brachiocephalic artery behind right sternoclavicular joint (SCJ)
▪ Left CCA – begins from aortic arch, right of left subclavian artery, passes behind the left SCJ
▪ Both ascend up in the neck within the carotid fascia sheath – contains (1) common carotid, (2) internal jugular vein and
(3) vagus nerve. In addition, the (4) cervical sympathetic chain ascend immediately posterior to the carotid sheath
- External Carotid Artery (ECA) –
▪ Branches – superior thyroid artery, ascending pharyngeal artery, lingual artery, facial artery, occipital artery, posterior
auricular artery, maxillary artery and superficial temporal artery (Some Anatomists Like Freaking Out Poor Medical
Students)
- Internal Carotid Artery (ICA) – enters the carotid canal in the petrous temporal bone, give off ophthalmic artery
Veins
- Internal jugular vein – runs from the lobule of the ear to the medial end of the clavicle, lies between 2 heads of the SCM
▪ Tributaries – inferior petrosal sinus, pharyngeal, common facial, lingual veins, superior and middle thyroid vein and +/-
occipital vein
- The IJV unites with the subclavian vein behind the sternoclavicular joint giving rise to the right brachiocephalic vein.
- This joins the left BC vein posterior to the right 1 st costal cartilage to form the SVC, pierce pericardium at the 2 nd costal
cartilage and enters the right atrium at the 3 rd costal cartilage.
EXTRA INFORMATION
Embryology of Pharyngeal (Branchial) Arches

Skeletal / Cartilage
Arch Nerve* (neural ectoderm) Artery (Aortic Arch Mesoderm) Muscle (mesoderm)
(Neural Crest)
Muscles of mastication (Masseter,
Temporalis, Lateral & Medial Pterygoid) Maxilla
(V) Trigeminal: Maxillary Artery Digastric (anterior belly) Mandible
1
mandibular nerve & External Carotid Artery Mylohyoid Incus
Tensor Tympani Malleus
Tensor Veli Palantini
Muscle of facial expression Stapes
Digastric (posterior belly) Styloid Process
2 (VII) Facial Stapedial Artery & Hyoid Artery
Stylohyoid Lesser horn and upper
Stapedius body of hyoid bone
Common Carotid Artery Greater horn and lower
3 (IX) Glossopharyngeal Stylopharyngeus Muscle
& Internal Carotid Artery body of hyoid bone
(X) Vagus: superior Cricothyroid Muscle
Left – Aortic Arch
4 laryngeal nerve, Soft palate Thyroid Cartilage
Right – Right Subclavian Artery
pharyngeal branches Pharynx Muscle
(X) Vagus: recurrent Right and left Pulmonary Artery Intrinsic Muscle of Larynx (except All other laryngeal
6
laryngeal nerve Ductus Arteriosus (left arch) cricothyroid muscle) cartilage
* Nerves are not derived from pharyngeal arch; they grow into the arch

378
APPROACH TO NECK MASSES
DEFINITION
Neck masses can be subdivided according to the triangle they occur in as there are pathologies peculiar to each triangle. They
can either be located in the anterior triangle, posterior triangle or midline. In general, enlarged lymph nodes are the most common
cause of a lump in the neck, regardless of location
History
- Age (older age higher likelihood of malignancy)
- Risk Factors for Malignancy: smoking, alcohol, betel nut
- About the lump
▪ Location, onset, duration, drainage (?branchial cyst), associated symptoms, lumps elsewhere
▪ Pain: inflammatory > CA
▪ Growth pattern / rate of growth (if over days = infection / inflammatory / haemorrhage into cyst, if months = cancer)
- Local symptoms – intra-oral diseases (i.e. tooth decay, oral/tongue ulcer, and tonsillitis)
- Red flags for malignancy – Persistent mass, hoarseness, dysphagia, odynophagia
- PMHx – prior malignancy, prior tuberculosis (treated?), previous head/neck surgery, previous radiation exposure
- Social history – travel and contact history, sexual history for HIV, oral sex
- Constitutional symptoms
▪ Fever, malaise, arthralgia, myalgia (viral prodrome)
▪ Night sweats, low-grade fever (TB, B symptoms of lymphoma)
▪ Loss of appetite, loss of weight (chronic infection, malignancy)
Inspection
- General Inspection: cachexia, smoker,
- Assessment of Mass – location, site, size
- Size, shape, surface: erythema, discharging sinus (multiple lymph node enlargements with discharging sinuses can be TB
or actinomycosis; sulphur granules seen in actinomycosis)
Palpate
- Assessment of Mass – tenderness, consistency (hard, matted nodes are suspicious for malignancy), mobility/fixed)
- Symmetry to contralateral neck
- Pulsatile (?carotid body tumour)
- Movement with swallowing vs. sticking out of tongue (? thyroglossal cyst)
- Examine LN stations systematically (i.e. submental, then submandibular, preauricular, postauricular, along anterior border
of sternocleidomastoid, supraclavicular (i.e. vicrhow’s node), posterior triangle, lastly occipital)
- Assessment of neurological function (i.e. facial symmetry (CN VII), voice (CN X), function of SCM and Trapezius (CN XI),
tongue deviation (CN XII)
To complete the examination:

- Examine skin, face, neck, scalp and external auditory canal
- Examine dentition (dental infection can lead to cervical lymphadenopathy)
- Examination of the thyroid gland & major salivary glands
- Full respiratory and abdominal examination especially if supraclavicular lymph node (i.e. virchow’s node) found
- Breast examination in female patient
- Examination of lymphoreticular system – other lymph node groups (i.e. axillary, inguinal), liver, spleen
- Formal ENT clearance of upper aero-digestive tract (UADT) especially looking at the post-nasal space for nasopharyngeal
carcinoma (NPC being the most common cancer causing enlarged cervical lymph nodes

379
In childrens, most neck masses are inflammatory or congenital, however, in adults majority are likely malignant
Rule of 80s (for patients > 40 years old)

- 80% of non-thyroid neck masses in adults are neoplastic
- 80% of neoplastic masses are malignant
- 80% of malignancies are squamous cell carcinoma
- 80% of malignant masses are metastatic
- 80% of metastases are from primary sites above the level of the clavicle
Midline
1. Submental lymph node
2. Thyroglossal cyst
3. Pyramidal lobe of thyroid / Thyroid nodule in the isthmus
4. Sublingual dermoid cyst
5. Plunging ranula (retention cyst of the sublingual)
6. Rarely, hyoid pathology e.g. bursa
Anterior triangle
1. Lymph node – along anterior border of sternocleidomastoid (levels II, III, IV)
2. Thyroid Nodule
3. Submandibular gland mass (see later section on Salivary gland swellings)
4. Branchial cyst + fistula
5. Chemodectoma (carotid body tumour)
6. Carotid aneurysm
7. Pharyngeal pouch
8. Laryngocoele (rare; an air-filled, compressible structure seen in glass-blowers)
Posterior triangle
1. Lymph node – level V
2. Cystic hygroma
3. Cervical Rib
4. Brachial plexus neuroma/schwannoma
Cervical Lymph Nodes Location

380
INVESTIGATIONS
Similar to breast lumps → Neck masses warrant a triple assessment
- Clinical examination
- Imaging → Usually CT neck with contrast
- Histology → Usually FNAC (as opposed to core biopsy in breast)

- Endoscopy
Biochemical
- FBC, U/E/Cr
- Thyroid Function (i.e. TSH / T4)
- +/- Calcium Panel
- +/- calcitonin (medullary thyroid cancer)
Imaging
- Initial imaging of choice is CT face & neck with contrast (MRI as an acceptable alternative)
- CT Thorax, Abdomen, Pelvis (to evaluate for primary site)
- +/- Ultrasound if evaluating for thyroid / parathyroid masses or for congenital neck masses
- PET-CT as a diagnostic tool in head and neck cancer is controversial (potential to identify primary site)
Panendoscopy (Triple Endoscopy)

- Flexible Nasopharyngoscopy (evaluate nasal cavity, nasopharynx, oropharynx, hypopharynx and glottis) - evaluate UADT
- Bronchoscopy
- Esophagogastroscopy
Histology
- Fine needle aspiration (for solitary neck mass that is suspicious for a metastatic lymph node)
▪ Able to accurately diagnose malignancy (adenocarcinoma / squamous cell carcinoma), tuberculosis
- Excisional biopsy can be performed if lymphoma is suspected (to be done after FNAC)
▪ Do not do excision Bx first as it can compromise resection later if LN Mets are from H&N CA because LN Mets counted
as locally advanced disease (still resectable)
EXTRA INFORMATION
Further Investigations according to FNAC results
Adenocarcinoma
- CT neck/thorax/abd/pelvis
- OGD / Colonoscopy
- Bilateral mammogram (female patients)
- If primary lesion found, this represents stage 4 disease
Squamous Cell Carcinoma (SCC)

- CT head / neck +/- thorax (?lung cancer)
- Panendoscopy of the upper aerodigestive tract (i.e. direct laryngoscopy, esophagoscopy, nasopharyngoscopy and
bronchoscopy)
- Biopsies of the nasopharynx, base of tongue, pyriform sinus, tonsil
Lymphoma
- Excisional lymph node biopsy
- CT neck/thorax/abd/pelvis
- Bone marrow biopsy (stage 4 disease)
- Stage disease – number of nodal groups / which side of diaphragm
- Chemotherapy (CHOP)
Infective/Inflammatory
- Treat underlying condition
- +/- Toxoplasma, HIV, EBV

381
CAUSES OF MIDLINE MASS
Approach:
- Move with swallowing? – divides thyroglossal cyst and thyroid nodule from other causes
- If it moves with swallowing, does it move with tongue protrusion – thyroglossal cyst moves with protrusion but a thyroid
nodule / superficial dermoid cyst, does not
Thyroglossal cyst
Definition: Congenital cyst of epithelial remnants of the thyroglossal tract

Epidemiology: Equal in males and females. Occurs mostly in children and adolescents (2/3 are diagnosed in 1 st 3 decades, 50%
diagnosed by age 10)
Pathology: A cystic expansion of the remnant thyroglossal tract – failure of the thyroglossal duct to obliterate after embryologic
descent of the thyroid from the foramen cecum at the base of the tongue to low anterior neck (normally duct disappears at 5 – 8
weeks gestation)
Features:
- Smooth, rounded, cystic lump. 75% are in the midline while 25% are slightly to the left or right.
- Usually asymptomatic but may become infected (i.e. oral flora – staph aureus, staph epidermidis, haemophilus influenza)
with sinus formation and seropurulent discharge (occurs with incision or rupture of cyst)
▪ If infected: directed antibiotics coverage, avoid incision and drainage (risk seeding cells outside the cyst which
increases risk of recurrence), wait for 3 months for inflammation to resolve prior to definitive operation
- Located anywhere from base of tongue to behind sternum – A & B – lingual (rare), C & D – adjacent to hyoid bone (common),
E & F – suprasternal fossa (rare)
Histology:
- Cyst lined by pseudostratified ciliated columnar epithelium and squamous epithelium, with heterotopic thyroid tissue (~20%)
- If malignancy occurs (rare, <1%, CA of the thyroglossal duct), it is usually a papillary carcinoma (~90%).
Investigation / Treatment:
- Pre-op TFT
- CT neck with contrast – confirms diagnosis (well circumscribed lesion with homogenous fluid attenuation surrounded by a
thin enhancing rim) and identifies normal orthotopic thyroid tissue
- U/S thyroid and thyroglossal cyst – well-defined, thin-walled, hypoechoic mass with posterior acoustic enhancement in
midline
- Sistrunk Operation – en bloc cystectomy, include its tract upward to the base of the tongue and resection of the central
portion of the hyoid bone (to minimize recurrence, 2-5%)
▪ Risk factors for recurrence128 – simple cyst excision (38-70%), intra-operative cyst rupture, presence of cutaneous
component secondary to infection & post-operative wound infection
128 Ashcraft’s Pediatric Surgery 6th Edition – pg. 1030

382
Dermoid cyst
Small non-tender mobile subcutaneous lump, may be fluctuant, skin-coloured or bluish
Pathology:
- Can be congenital or acquired.
▪ Congenital – developmental inclusion of epidermis along lines of fusion of skin dermatomes (seen in younger patients,
present since birth). Locations include:
o medial & lateral ends of the eyebrows (internal & external angular dermoid cysts)
o midline of the nose (nasal dermoid cysts)
o midline of the neck and trunk
▪ Acquired – due to forced inclusion of skin into subcutaneous tissue following an injury, usually on fingers. Seen in older
patients, no previous history of mass, history of trauma to the area (may have associated scar).
Histology:
- Cyst lined by epidermis, with evidence of adnexal structures such as hair follicles, sebaceous glands and sweat glands –
cystic teratoma
Management:
- Imaging investigations (e.g. XR, U/S, CT) are important especially for cysts on the skull as they can communicate with
cerebrospinal fluid.
- Complete surgical excision of the cyst, preferably in one piece w/o spillage of cyst contents
Plunging ranula
Pathology:
- A pseudocyst associated with the sublingual glands and submandibular ducts.
- Ranulas can be congenital or acquired after oral trauma
▪ Congenital: secondary to an imperforate salivary duct or ostial adhesions
▪ Acquired: trauma to sublingual gland leading to mucus extravasation and formation of a pseudocyst (mucus escape
reaction)
- Simple Ranula: confined to floor of the mouth
- Plunging Ranula: a large ranula can present as a neck mass if it extends through the mylohyoid musculature of the floor of
the mouth
Treatment:
- Complete resection if possible, often in continuity with the associated sublingual gland (but often difficult due to close
association with the lingual nerve and submandibular duct).
- If complete resection is not possible, marsupialisation and suturing of the pseudocyst wall to the oral mucosa may be
effective.

383
CAUSES OF ANTERIOR TRIANGLE MASS
Branchial (Pharyngeal) cyst and/or fistula

Second branchial cleft anomalies are the most common abnormality, followed by first branchial cleft abnormalities
Third & fourth branchial anomalies are rare, usually occur on left side
Epidemiology:
- Affects both sexes equally, usually in young adults in their 20s
Pathology:
- Failure of fusion of the embryonic 2nd and/or 3rd branchial arches (failure of obliteration of the 2nd branchial cleft)
- All branchial cleft/groove (II, III, IV) are obliterated except for branchial cleft/groove I which give rise to the epithelial lining
of the external auditory meatus
- It is lined by squamous epithelium
Features:
- Located close to the parotid gland, sinus persist as the external auditory canal (1st branchial cleft anomaly)
- Occurs anterior to the upper or middle third of the sternocleidomastoid muscle (2nd branchial cleft anomaly)
- Smooth firm swelling, ovoid in shape, with its long axis running downwards and forwards
- May be fluctuant, usually not transilluminable (due to desquamated epithelial cell contents)
- Look for fistula in this area – a branchial fistula will run between tonsillar fossa and the anterior neck, passing between the
external and internal carotid arteries
- FNA of the cyst will yield opalescent fluid with cholesterol crystals under microscopy
- May be complicated by recurrent infections – purulent discharge, fixation to surrounding structures
- Usually occur on the left side of the neck and may present as suppurative thyroiditis (3rd / 4th branchial cleft anomaly) –
tract travel through or in proximity to upper left lobe of the thyroid gland (left hemi thyroidectomy performed with sinus tr act
excision)
Management:
- If fistula present, perform fistulogram to delineate course.
- Surgical excision of the cyst where possible.
- If the fistula/sinus present, inject Bonney’s blue dye into the tract prior to surgery to allow accurate surgical excision.
- Treatment of infection with antibiotics
- Complications: cyst recurrence; chronic discharging sinus
Clefts / Grooves = Ectoderm, Arches = Mesoderm & Neural Crest, Pouches = Endoderm

384
Embryology of Pharyngeal (Branchial) Pouches
Pouches Endoderm Nerve (neural ectoderm)
1 Auditory Tube, Middle Ear, Mastoid Antrum, Inner layer of Tympanic Membrane (V) Trigeminal: mandibular nerve
2 Middle ear, Palatine tonsils (VII) Facial
Dorsal wings – Inferior parathyroid glands
3 (IX) Glossopharyngeal
Ventral wings – Thymus
Superior parathyroid glands and Parafollicular C cells of the thyroid gland (X) Vagus: superior laryngeal nerve, pharyngeal
4
Musculature and cartilage of larynx branches
6 Musculature and cartilage of the larynx (X) Vagus: recurrent laryngeal nerve
Chemodectoma (Carotid Body Tumour)

Pathology:
- Defined as a tumour of the paraganglion cells (paraganglioma) of the carotid body
- Located at the bifurcation of the common carotid artery (into the internal and external carotids)
- They are usually benign, but locally invasive
- Risk of malignancy is 10%, with metastasis to local lymph nodes, no histopathological features for malignancy, thus
malignant nature can only be diagnosed by presence of metastasis
Features:
- Solid, non-painful mass at the level of the hyoid bone (where the bifurcation is – level II of the neck) – be gentle during
palpation as pressure on the carotid body can cause vasovagal syncope.
- Mass is pulsatile but not expansile, due to transmitted pulsation from carotids.
- Due to close a/w carotid arteries, lump can be moved side to side but not up and down.
- May be bilateral
- If suspecting aneurysm, listen for bruit, look for signs of Horner’s syndrome, and examine the rest of the peripheral vascular
system.
Differentials and investigation:

- Main differential is carotid artery aneurysm; an aneurysm can occur at any level but carotid body tumour occurs at the level
of the hyoid bone.
- DO NOT PERFORM FNAC
- CT and/or MRI can be used to delineate tumour anatomy in relation to surrounding structures; CT reveals homogenous
mass with intense enhancement following IV contrast administration.
- Angiography is the gold standard investigation – hypervascular mass displacing the bifurcation. May also show vessel
compromise by tumour invasion and undetected synchronous tumours.
Treatment:
- Rule out associated syndromes (i.e. pheochromocytoma) in the pre-op preparation!
- Surgical excision with preoperative embolization (reduces bleeding and complications, and facilitates resection); any
enlarged ipsilateral lymph nodes are also removed due to the small possibility of malignancy
- Radiotherapy is an effective alternative for patients who are unfit for surgery or whose tumours are too large.

385
Pharyngeal pouch (also called Zenker’s diverticulum)
Pathology:
- False diverticulum that develops in elderly, males > females, 2-3:1
- A herniation of the pharyngeal mucosa (pulsion diverticulum) between 2 parts of the inferior pharyngeal constrictor –
thyropharyngeus & cricopharyngeus – weak area situated posteriorly (Killian’s Dehiscence)
- Caused by failure of the cricopharyngeus to relax
Features
- Occurs in older patients, males > females (2-3:1)
- A cystic swelling low down in the anterior triangle, usually on the left
- Halitosis, regurgitation of undigested food with coughing, upper oesophageal dysphagia, hoarseness, weight loss,
squelching sound on deep palpation
- Complications: chest infection (due to chronic aspiration); diverticular neoplasm/squamous cell carcinoma (<1%)
Diagnosis: barium swallow (best seen in lateral view), oesophageal manometry

(Endoscopy and NGT are contraindicated as risk of developing perforation of the pharynx is high)
EXTRA INFORMATION
Treatment
- Leave it alone if small and asymptomatic
- Minimally invasive treatment: endoscopic cricothyroid myotomy
- Surgical: cricopharyngeal myotomy + diverticulectomy or diverticulopexy
▪ Left cervical incision along anterior border of left SCM
▪ Myotomy, extend cephalad dividing 1-2cm of inferior constrictor muscle and caudad dividing 4-5cm of cricopharyngeal
muscle and cervical oesophagus
▪ If a diverticulum is present and is large enough to persist after a myotomy
▪ Diverticulopexy → diverticulum sutured in inverted position to the prevertebral fascia
▪ Diverticulectomy (if diverticulum is excessively large so that it would be redundant if suspended, thickened wall) → base
of pouch crossed with a linear stapler and amputated, test with water-soluble contrast esophagogram on POD 1
▪ Complications: fistula, stenosis, abscess, hematoma, recurrent nerve injury, difficulty in phonation, Horner's syndrome
(diverticulopexy – lower risk of stenosis / fistula but risk of malignancy remains)

386
CAUSES OF POSTERIOR TRIANGLE MASS
Cystic hygroma
Pathology: A cystic hygroma is a congenital cystic lymphatic malformation found in the posterior triangle of the neck, probably
formed during coalescence of primitive lymph elements. It consists of thin-walled, single or multiple interconnecting or separate
cysts which insinuate themselves widely into the tissues at the root of the neck.
Features:
- 50-65% present at birth, but occasionally may present later in childhood or adulthood (usually present in 1 st 2 years of life)
- Lobulated cystic swelling that is soft, fluctuant, and compressible, located in the posterior triangle of neck
- Other locations – axilla, groin, mediastinum
- Classically “brilliantly transilluminable”
- A large cyst may extend deeply into the retropharyngeal space
Complications:
- Cystic hygroma seen on prenatal ultrasound in the 1st trimester suggests chromosomal abnormality (i.e. trisomy 21) or other
structural abnormalities (i.e. congenital heart anomalies)
- May obstruct delivery
- Compressive problems after delivery – respiratory, swallowing
- Can become infected with staph / strep
Management:
- Radiological investigations e.g. CXR, CT to delineate extent of cyst
- Non-surgical treatment – aspiration and injection of sclerosant (usually unsuccessful)
- Surgical excision – partial (to alleviate symptoms) or complete
Cervical Rib
Features:
- Usually more symptoms than signs as it causes thoracic outlet syndrome* (compression of the trunks of the brachial plexus
(usually C8/T1), subclavian artery and/or subclavian vein)
- Compression between the scalene triangle (anterior and middle scalene muscle and first ribs)
- A hard mass in the posterior triangle at the root of the neck
- Symptoms/signs:
▪ Arterial: pallor, gangrene or necrosis of the tips of the fingers
▪ Venous: oedema, cyanosis
▪ Neurological: complaints of radicular symptoms (pain, paraesthesia), wasting of the small muscles of the hand
- Adson’s test can be done – ask patient to extend neck and rotate it towards side of symptoms, radial pulse will be diminished,
occasionally with reproduction of radicular symptoms in the limb
- Diagnosis by CXR
Neuroma/Schwannoma
Features:
- Slow growing tumour arising from peripheral neural structures of the neck (i.e. brachial plexus*, cervical plexus, vagus nerve,
phrenic nerve, etc. → the trunks of the brachial plexus traverse the posterior triangle of the neck
- Fusiform, is mobile in plane perpendicular to axis of nerve but not parallel (mobile in 1 plane)
- Usually benign
- May be Tinnel’s positive – tap on the mass for any paraesthesia occurring in distribution of the nerve
- DO NOT PERFORM FNA – excruciatingly painful

387
CERVICAL LYMPHADENOPATHY
ANATOMY
CLASSIFICATION
The cervical LN basin is divided into seven levels
- The SCM divides LN levels II,III, IV & levels V
- The Hyoid Bone (C3) and Cricoid Cartilage (C6) divides LN levels II, III and IV
- The spinal accessory nerve divides LN level IIA & IIB
Lymph Node Level Anatomical Boundaries129

IA Submental - Bordered by anterior belly of digastric muscle, hyoid bone & midline
IB Submandibular - Bordered by anterior and posterior belly of digastric muscle, stylohyoid muscle and the inferior border of the mandible
- Skull base superiorly, hyoid bone inferiorly, stylohyoid muscle medially, posterior aspect of SCM laterally
IIA
Upper jugular - IIA is anterior the spinal accessory nerve
IIB - IIB is posterior to the spinal accessory nerve
- Hyoid bone superiorly, cricoid cartilage inferiorly, lateral aspect of sternohyoid muscle medially and posterior
III Mid jugular
aspect of SCM laterally
- Cricoid cartilage superiorly, clavicle inferiorly, lateral aspect of sternohyoid muscle medially and posterior aspect
IV Lower jugular
of SCM laterally
- Convergence of SCM and trapezius muscle superiorly, clavicle inferiorly, posterior border of SCM medially, anterior
VA Posterior Triangle
border to trapezius muscle laterally
VB Supraclavicular - VB is area inferior to cricoid cartilage
Central - Trachea-esophageal groove, nonpalpable – hyoid bone superiorly, suprasternal notch inferiorly, common carotid
VI
Compartment arteries laterally (i.e. lateral borders at carotid sheath)
Superior
VII - Upper border of sternum superiorly, aortic arch inferiorly and common carotid arteries laterally
Mediastinum
Spinal Accessory Nerve

- Exits the skull via the jugular foramen (with CN 9 and 10), passes anterior to the jugular vein
- Enters posterior SCM and exits posteriorly in the vicinity of Erb point (1.5cm superior / cephalad to Erb point)
- Found in the level of Va (posterior triangle) and courses superiorly into level II (separates level IIa & IIb)
Drainage
- Oral cavity and oropharynx → levels I, II, III
- Thyroid & larynx → levels II – VI (thyroid malignancy first spread to level VI nodes)
- Nasopharynx (NPC) → II – V (usually upper neck – level II and high-level V)
129 Head and Neck Cancer: A Multidisciplinary Approach – pg. 183 Table 10.1

388
* Bacteria: Streptococcus, Staphylococcus, Klebsiella (from intraoral pathology e.g. dental abscess, tonsillitis)
** Inflammatory: Kikuchi’s (necrotising lymphadenitis occurring in young females, presenting as painful cervical lymphadenopathy)
EXTRA INFORMATION
Neck Dissection – Surgical Options
Radical Neck Dissection (Crile)

- Removal of Level I to V of cervical lymphatics
- Removal of Spinal Accessory Nerve (CN XI), Internal Jugular Vein & Sternocleidomastoid Muscle – high morbidity
Modified Radical Neck Dissection (MRND)

- Removal of Level I to V of cervical lymphatics
- Preservation of SCM and/or IJV and/or Spinal Accessory Nerve
▪ Type I: preserve SAN
▪ Type II: preserve SAN and IJV
▪ Type III: preserve SAN, IJV and SCM
Selective Neck Dissection (SND)

- Preservation of selected cervical lymphatics component (as primary site drain lymphatics in a predictable pattern)
▪ Lateral Neck Dissection → removal of LN levels II to IV with preservation of SAN, IJV, SCM
▪ Postero-lateral Neck Dissection → removal of LN levels II to V, sub-occipital, retroauricular with preservation of SAN, IJV, SCM
▪ Modified Lateral Neck Dissection → removal of LN levels II to V with preservation of SAN, IJV, SCM
Central Neck Dissection

- Resection of lymph nodes and fibrous fatty tissue within level VI
- Superiorly: hyoid bone, Inferiorly: thoracic inlet, Laterally: carotid sheath, Medially: tracheal midline
Complications from Radical Neck Dissection

- Carotid blowout – risk factors: infection, irradiation. Mx: resuscitate, apply constant pressure all the way to the OT!
- Chylous fistula / Chyle leak* – leads to electrolyte disturbances, hypovolemia, hypoalbuminemia, coagulopathy. Mx: nutritional modifications
(strict fat-free diet / medium chain TG), adequate drainage, SC octreotide 100mcg q8H. Consider surgical ligation of thoracic duct or embolization
if failed non-operative management with persistent high volume (> 500mls)
- Haematoma – bring back to OT to find source of bleeding and stop it
- Nerve Injury – vagus (vocal cord paralysis), cervical sympathetic chain (Horner’s), mandibular branch of facial nerve (lower lip weakness),
cranial nerve XI – test strength of ipsilateral SCM and trapezius muscle on POD 1
- Salivary Fistula / Wound Infection – risk factors: previous irradiation, upper GI tract opened during surgery with salivary contamination
- Poor healing – usually in irradiated skin; weakest point is the junction of the trifurcate incision

389
ANATOMY OF THE SALIVARY GLANDS
Innervation of the Salivary Glands
SUBMANDIBULAR GLAND
- Consists of a large superficial part and a small deep part that is continuous with one another around the free posterior border
of the mylohyoid
- The deep part of the gland is closely associated with the lingual nerve (with the attached submandibular ganglion) above it,
and the hypoglossal nerve and submandibular duct below it
- Submandibular gland excision – 3 nerve that lie close and potentially can be damaged
▪ Marginal Mandibular Nerve (facial nerve) – weakness of lower lips
▪ Lingual nerve (trigeminal nerve – CNV3) – numbness of tongue
▪ Hypoglossal nerve – weakness of tongue muscles
- Nerve supply: parasympathetic secretomotor supply from lingual nerve carrying postganglionic fibres (facial nerve (chorda
tympani) – CNVII) from the submandibular ganglion (preganglionic fibres in superior salivary nucleus)
- Submandibular duct (of Wharton) arises from supf. part of the gland runs forwards deep to mylohyoid and drains into the
oral cavity at the sublingual papilla just adjacent to the frenulum
- Histology: mixed serous and mucous acini, few ducts – 70% of saliva volume
EXTRA INFORMATION
Submandibular Abscess
- Etiology: periodontal abscess, trauma to oral cavity (i.e. mandibular fracture), URTI, mandibular malignancies, sialadenitis
- Complications: progression to Ludwig angina
- Management:
▪ Early source control with surgical incision and drainage
▪ Broad Spectrum IV Antibiotics (directed against mixed flora of oropharyngeal cavity) – i.e. prevotella, peptostreptococcus,
streptococci, staphylococci, gm negative organisms

390
PAROTID GLAND
- Located between the posterior border of the ramus of the mandible and the mastoid process, wedged between mandible
and SCM
- Surrounded by fibrous capsule – the parotid sheath (thus mumps is painful as the gland swells within a tight envelope)
- Relations – (superior) external auditory meatus and TMJ, (inferior) posterior belly of digastric (anterior) overflows the
mandible with the overlying masseter (medially) styloid process, neurovascular bundle (i.e. IJV, ICA, last 4 CN) and lateral
wall of pharynx
- Important structures that pass through the gland in order from lateral to medial:
▪ Facial nerve and its branches*
▪ Retromandibular vein (junction of maxillary & superficial temporal vein)
▪ External carotid artery (2 terminal branches: maxillary & superficial temporal artery)
- Nerve supply:
▪ Parasympathetic secretomotor supply from auriculotemporal nerve carrying postganglionic fibres (glossopharyngeal
nerve – CN IX) from the otic ganglion (preganglionic fibres from inferior salivary nucleus)
▪ Sensory supply of the gland from auriculotemporal nerve; sensory supply of the capsule from the great auricular nerve.
- Parotid duct (of Stensen):

▪ Runs 5cm across the masseter below zygomatic arch (surface marking: line from intertragic notch to midpoint of
philtrum), pierce the buccinators and drains into the mouth opposite the upper second molar tooth
- Histology: predominantly serous acini, many ducts (other glands have few ducts) – 25% of salvia volume
- Facial Nerve & Parotid:

▪ Emerge from the stylomastoid foramen, winds laterally to the styloid process, (surface marking – intertragic notch of
the ear)* enters the posterior aspect of the parotid gland and bifurcates into a superior and inferior division (motor
branches)
- Superior: temporal and zygomatic branches,
- Inferior: buccal**, mandibular*** and cervical branches
▪ Facial nerve lies deep to the subcutaneous musculoaponeurotic system (SMAS) layer
▪ Branches of the nerve emerge on anterior aspect of the parotid to lie on the masseter then to muscles of the face
* Facial nerve is exposed posteriorly in the wedge-shaped space between the bony canal of the external auditory meatus and the mastoid
process
** Buccal nerve – lies superior to the parotid duct – sometimes can arise from superior division or as a direct branch (facial nerve trifurcation)
*** Marginal mandibular nerve – lies superficial to the retromandibular vein, has no cross-anastomosis hence injury results in paralysis of half of
the lower lips – also lies above the inferior border of the mandible
SUBLINGUAL GLAND
- A small almond-shaped gland located under the mucosa of the floor of the oral cavity
- Each gland has 15 or so ducts, half of which drain into the submandibular duct, the rest draining directly into the oral cavity
- Nerve supply: similar to the submandibular gland
- Histology: predominance of mucous cells, few ducts – 5% of salvia volume

391
SIALOLITHIASIS
EPIDEMIOLOGY
- Stones of the salivary gland that may be impacted within the gland itself or in the duct.
- Usually, occurs in males more than females, and between the ages of 30 and 60.
- 80% of salivary stones occur in the submandibular gland (due to its higher mucus and calcium content with a long duct, and
slow flow of the saliva against gravity); 10% occur in the parotid, 7% sublingual.
- Most submandibular gland stones occur in the duct, while 50% of parotid stones occur in the gland itself.
- 80-95% of submandibular stones are radio-opaque and can be seen on an X-ray of the floor of the mouth, and 60% of
parotid stones are radio-opaque.
- Complete obstruction
▪ Acute pain and swelling of the gland involved at meal times, rapid onset within minutes of starting to eat, resolves about
an hour after the meal.
- Partial obstruction
▪ Occasional symptomatic episodes interspersed by asymptomatic periods of days to weeks, chronically enlarged mass
in the submandibular region
- Can result in sialadenitis, and even abscess formation leading to worsening of symptoms of pain and redness; systemic
symptoms such as fever, chills; purulent discharge from duct opening
- Stone may be palpable along the duct or at the opening of the duct
INVESTIGATIONS
- Non-contrast CT scan – can pick up almost all stones when fine cuts are requested
- Plain X-rays can pick up radio-opaque stones
- Sialogram (rarely done today as it is invasive and technically demanding, and CT is better. Contraindicated in acute
sialadenitis and contrast allergy.)
MANAGEMENTS
- General measures:
▪ Good hydration, soft diet, good oral hygiene
▪ Massage of the gland, milking the duct, application of moist hot towel
▪ Analgesia – NSAIDs such as ibuprofen
▪ Antibiotics if patient has sialadenitis – to cover Staph and Strep e.g. Augmentin
▪ Refer specialist treatment if symptoms persist for several days, or sialadenitis persists despite antibiotic therapy
- Surgical removal
▪ Transoral removal of stones for submandibular duct stones (50% can be removed), less for parotid duct stones
▪ If stones cannot be removed via transoral surgery or is intraglandular, partial gland resection can be performed
- Other options: Lithotripsy, wire basket removal, sialoendoscopy

392
SALIVARY GLAND TUMOURS (PAROTID)
EPIDEMIOLOGY
- 80% occur in the parotid, of which 80% are benign (80% of the benign tumours are pleomorphic adenomas)
- 10% occur in the submandibular, of which 60% are benign (95% pleomorphic adenoma)
- 15% occur in minor salivary glands, of which 50% are benign (all benign tumours are pleomorphic adenomas)
- 0.3% occur in sublingual glands, of which all are malignant
History
- About the lump: onset, duration, progress, associated symptoms e.g. pain
- If pain is present, is it precipitated by food ingestion? (suggestive of sialolithiasis)
- Symptoms of infection e.g. fever, malaise; if considering mumps, ask about testicular pain and swelling (orchitis), abdominal
pain (pancreatitis)
- Any noticed facial asymmetry – incomplete closure of the eye on one side, drooping corner of the mouth, drooling
- Any symptoms of xerostomia (e.g. cannot eat biscuit or bread without water), xerophthalmia
- History of connective tissue disease e.g. rheumatoid arthritis, SLE
Inspect
- Put yourself at the level of the patient’s face and look from front for any asymmetry with an obvious mass on one side –
parotid mass is located between the angle of the jaw and the ear, and lifts the earlobe if large; submandibular mass is
located just under the mandible
- Look for scars – parotidectomy scar runs anteriorly to the ear, below the earlobe and around posteriorly before looping
forward again under the jaw
- Look for fistula/sinus
- Look at the patient’s face for asymmetry (facial nerve palsy)
Palpate from behind

- Ask patient about any pain before starting to palpate
- Palpate the obviously enlarged gland, and always remember to also palpate the contralateral gland for any swelling
- Check for warmth of overlying skin, tenderness, consistency, surface, margins
- Fixation to underlying structures – ask patient to clench the teeth to contract the masseter, then try to move the gland
(parotid)
- Fixation to overlying skin
- Palpate for cervical lymphadenopathy
Other tests
- Facial nerve examination
- Examination of the duct openings
▪ Using a torch and a tongue depressor, examine opposite the second upper molar tooth for the opening of the parotid
duct, and under the tongue for the opening of the submandibular duct.
▪ Look for red inflamed duct opening, discharge (purulent), or any visible stone.
▪ For the parotid duct, can palpate the duct along the masseter for stone, and look for discharge inside the mouth while
palpating
- Palpate the gland openings for stones
- Bimanual palpation of the submandibular gland
Suspicious features of malignancy:

- Hyperaemic hot skin over lump
- Pain
- Fixation to underlying structures or skin
- Hard consistency
- Irregular surface or ill-defined border
- Facial nerve involvement

393
INVESTIGATION
- FNAC (cytology): malignant vs. benign
- CT with contrast (imaging): confirm salivary gland (vs. LN)
▪ esp. parotid – multiple swelling likely LN (DDx Warthin)
- Benign (i.e. Pleomorphic adenoma, Warthin’s, Monomorphic adenoma, Oncocytoma)
- Malignant (i.e. mucoepidermoid, adenoid cystic carcinoma, carcinoma ex-pleomorphic, acinic cell
Neoplasia
adenocarcinoma)
- Lymphoma and leukaemia*
Stones - Sialolithiasis
- Mumps*
Infection/ - Acute sialadenitis
Parenchymal Inflammation - Chronic recurrent sialadenitis
swelling - HIV*
Autoimmune - Sjogren’s syndrome*
Infiltration - Sarcoidosis*
- Alcoholic liver disease
- Diabetes mellitus
Systemic
- Pancreatitis
disease*
- Acromegaly
- Malnutrition
Nodes - Metastatic (i.e. NPC, peri-auricular lesions)
Non- Blood Vessels - AVM, haemangioma
parenchymal Lymphatics - Lymphangiomas
swelling Nerves - Facial schwannoma
Fats - Lipoma
* are conditions in which parotid swelling is bilateral
CLASSIFICATION
Epithelial
Non-epithelial
Adenomas (benign) Carcinomas (malignant)
Pleomorphic adenoma Mucoepidermoid Carcinoma Haemangioma*
Warthin’s tumour Adenoid cystic carcinoma Lymphangioma
Monomorphic Adenoma Carcinoma ex-Pleomorphic Neurofibroma
Oncocytoma Acinic cell Adenocarcinoma Neurilemmoma (schwannoma)
Squamous cell cancer Lipoma
Undifferentiated Sarcoma
Malignant lymphoma
* Most common salivary gland tumour in children

394
Pleomorphic adenoma
Epidemiology
- Most common benign tumour
- 85% occur in the parotid gland
- Equal sex ratio occurs in younger patients less than 50 years old
Histology
Very heterogeneous appearance, containing epithelial cells surrounded by loose stroma with islands of chondromyxoid
(mesenchymal components), and interspersed islands of myoepithelial cells. The tumour appears to be encapsulated, but
histology shows multiple sites of capsular penetration by tumour cells.
Clinical Features
- Slow-growing, painless swelling occurring in the lower pole of the parotid
- Irregular and lobulated surface, texture of cartilage (slightly harder than Warthin’s)
- Does not invade or metastasise
- Chance of malignant transformation if left for 10-15 years (1-6% risk)
- If not completely excised, can recur (recurrence rate of 2%)
Diagnosis by clinical, FNAC, +/- MRI
Treatment – surgical excision

- Blair incision
- Parotid: Superficial parotidectomy, if tumour is deep / large, total parotidectomy with preservation of the facial nerve
- Submandibular: Total gland excision together with adjacent connective tissue, sparing lingual and hypoglossal nerves

395
Warthin’s tumour
Epidemiology
- 2nd most common tumour of the salivary gland
- Only occurs in the parotid gland (10% of parotid tumours) – almost exclusively in the superficial lobe of the parotid gland
- More common in males than females (4:1)
- Occurs in older patients (50 – 70 years)
- Related to cigarette smoking
Histology
- Benign neoplasm (aka papillary cystadenoma lymphomatosum or just adenolymphoma)
- Grossly – bilateral (10%), multifocal (10%), oval/round encapsulated mass containing cystic spaces filled with milky secretion
(mucin)
- Consists cystic spaces lined by two-tiered epithelium, surrounded by dense lymphoid stroma with germinal centres.
Clinical Features
- Slowly enlarging, soft to firm cystic fluctuant swelling in parotid tail
- Invariably benign with no risk of malignant change
- Check for contralateral enlargement
Diagnosis by clinical, FNAC + CT / MRI
Treatment
- Can be left alone if absolutely certain that the entire mass is composed of only Warthin’s tumour cells since there is no
malignant potential
- Superficial parotidectomy if causing trouble to patient
Malignant tumours
Most common malignancies are mucoepidermoid (34%) and adenoid cystic carcinomas (22%) – equal sex ratio, can occur in
any salivary gland, in older patients (usually >60 yrs)
Mucoepidermoid carcinoma is the most common malignant tumour in the parotid, while adenoid cystic carcinoma is the most
common in the submandibular, sublingual and minor salivary glands
Malignant pleomorphic adenoma

- Usually occurs in pre-existing pleomorphic adenoma, rarely de novo
- Worst prognosis of any salivary gland tumour
- 30-70% recurrence and metastasis rate
Treatment
- Parotid
▪ Total parotidectomy with sacrifice of facial nerve if tumour has infiltrated it (may be grafted with great auricular nerve)
▪ Radical neck dissection if neck nodes positive
▪ Postoperative radiotherapy
- Submandibular
▪ Radical excision of gland with lymphatic clearance of submandibular triangle
▪ Radical neck dissection if neck nodes positive
▪ Postoperative radiotherapy

396
COMPLICATIONS
Immediate (intra-operative)
1. Intraoperative facial nerve injury – LMN palsy
▪ Facial Nerve Branches (motor branches) = Temporal, Zygomatic, Buccal, Mandibular, Cervical
▪ Zygomatic: lead to incomplete closure of eye, use ophthalmic drops and eye protection at night
▪ in contrast, submandibular gland surgery can damage the hypoglossal and/or lingual nerves
▪ Incidence of temporary facial nerve dysfunction is around 30 – 60 % (risk increase in patients with sialadenitis & multiple
histology within the same gland)
2. Rupture of capsule of parotid tumour
Early (1 to 30 days)
1. Temporary facial weakness (neuropraxia of facial nerve, occurs in 30-60% of patients but 90% resolves within 1 year)
2. Division of Great Auricular nerve (from cervical plexus) – loss of sensation over preauricular and postauricular skin and
part of the lower posterior ear (i.e. lobular region)
3. Division of Auriculotemporal nerve (branch of trigeminal nerve – CNV3 ) – loss of sensation over upper ear
4. Parotid fistula (~10%) – treat conservatively, ± anticholinergic ± botulinum toxin (majority will resolve)
5. Trismus (inflammation and fibrosis of masseter muscle – usually mild and transient)
6. Wound infection / Wound seroma
7. Haemorrhage / Hematoma
8. Skin flap necrosis (rare)
Late (more than 30 days)

1. Frey’s syndrome (~10%) – gustatory sweating (aberrant regeneration of the severed parasympathetic secretomotor fibres
onto the sympathetic receptors innervating the blood vessels and sweat glands following injury to the auriculotemporal nerve)
– conservative management with topical anticholinergic and botulinum toxin injection (resolves 2 – 4 years after surgery)
2. Hypoesthesia of greater auricular nerve (GAN)
3. Facial synkinesis after facial palsy
4. Recurrent Tumour
5. Cosmetic problems – soft tissue deficit, hypertrophic scar / keloid
EXTRA INFORMATION
Cutaneous branches of the cervical plexus
Greater Auricular Nerve Injury

Leads to numbness of the lower posterior ear and functional deficits such as difficulty shaving or wearing ear-rings. Numbness a/w GAN injuries
usually resolves quickly within a few months. Also look for spinal accessory nerve** that runs deep to the trape zius muscle (red circle = Erb point)
Spinal Accessory Nerve

Passes through the SCM, innervates that muscle and then passes through the posterior triangle of the neck (1.5cm above Erb po int) to innervate
the trapezius muscle and its anterior aspect (approx. 1/3 of the distance along the muscle length from the clavicle) – most commonly injured:
posterior triangle. Presentation: “shoulder syndrome” – shoulder weakness and neuropathic pain. Associated with marked delay in diagnosis.
Management: surgical correction can improve functional outcomes (though some injuries are transient and will improve with time)

397
THYROID EMBRYOLOGY, ANATOMY AND PHYSIOLOGY
EMBRYONIC ORIGINS
Thyroid gland: develop from the endoderm of the primitive foregut at the foramen caecum (midline, junction between anterior
two-thirds and posterior one-third of the tongue and descents down thyroglossal tract into the neck anterior to the hyoid bone and
laryngeal cartilage (thyroid completes its descent in the 7th gestational week)
Parathyroid glands: 2 superior and 2 inferior glands. The inferior parathyroid glands arise from the 3rd pharyngeal pouch (dorsal
wing) – ventral wing becomes the thymus which migrates caudally and medially pulling the parathyroid with it. The superior
parathyroid glands arise from the 4th pharyngeal pouch (dorsal wing)
Pharyngeal pouches: [1st Pouch] epithelial lining of auditory tube and middle ear cavity, [2nd pouch] epithelial lining of palatine
tonsil, [3rd pouch] inferior parathyroid and thymus, [4th pouch] superior parathyroid and calcitonin producing C-cells of thyroid
EXTRA INFORMATION
- Identifying the RLN: BEAHR triangle – bounded by the common carotid artery (laterally), inferior thyroid vessels (superiorly) and the recurrent
laryngeal nerve (inferiorly)
- Tubercles of Zuckerandl (ZT) – most lateral posterior extension of thyroid tissue (rotate medially to find RLN)
- Branches of the external carotid artery (Some Attendings Like Freaking Out Potential Medical Students)
▪ Superior thyroid artery
▪ Ascending pharyngeal artery
▪ Lingual artery
▪ Facial artery
▪ Occipital artery
▪ Posterior auricular artery
▪ Maxillary artery
▪ Superficial temporal artery
PARATHYROID ANATOMY
- Light yellow reddish brown appearance with a fine vascular matrix on the surface supplied by single end artery from the ITA
- Superior PTH located on the posterior part of the upper lobe of the thyroid. Postero-lateral to RLN and superior to ITA
- Inferior PTH are subject to variations, usually found antero-medial to RLN and inferior to ITA

398
THYROID ANATOMY
Structure: 2 lateral lobes joined by an isthmus that lies in front of the 2 nd, 3rd and 4th tracheal rings, anterior to larynx and trachea.
Strap muscles of the neck lie superficial to the thyroid gland. Pyramidal lobe is present in 30% of patients.
A thin layer of connective tissue surrounds the thyroid, part of the fascia layer that invests the trachea. This fascia coalesces with
the thyroid capsule posteriorly (condensation of the deep cervical fascia) forming a suspensory ligament (Berry ligament)
Arterial Blood Supply:

- Superior Thyroid Artery (1st branch from external carotid), adjacent to external branch of superior laryngeal nerve
- Inferior Thyroid Artery (from thyrocervical trunk*, branch of 1 st part of subclavian artery)
▪ Supplies both inferior and superior parathyroid
▪ Thyrocervical trunk – suprascapular artery, transverse cervical artery, ascending cervical artery, inferior thyroid artery
- Thyroid Ima Artery (from brachiocephalic / innominate artery), 5% of patients
Venous Blood Supply:

- Superior Thyroid Vein → Internal Jugular Vein
- Middle Thyroid Vein (single or multiple) → Internal Jugular Vein
- Inferior Thyroid Vein two or three) → Brachiocephalic / Innominate Vein
Nerve Supply:
- External Branch of Superior Laryngeal Nerve – supplies cricothyroid (tense vocal cord) and runs postero-medial to the
STA
▪ If injured leads to inability to produce high pitch sounds along with easy voice fatigability (usually mono-toned voice –
range and power of voice affected)
- Recurrently laryngeal nerve (RLN)* – supplies all intrinsic muscles of the larynx (except for the cricothyroid) and runs
close to the inferior thyroid artery.
▪ Right RLN originates from the right vagus nerve as it crosses anterior to the subclavian artery, the right RLN loops
around the brachiocephalic artery (innominate artery)
▪ Left RLN originates from the left vagus nerve as it crosses anterior to the arch of the aorta, the left RLN loops around
the arch of the aorta
▪ RLN inserts into cricopharyngeus muscle (part of inferior pharyngeal constrictor)
▪ If unilateral damage leads to affected cord lying in the paramedical position (inadequate glottis closure) presents with
weak breathy voice, hoarseness, also sensory loss to larynx inferior to vocal cord
▪ If bilateral damage leads to acute dyspnoea as a result of the paramedical position of both vocal folds which reduce
airway to 2-3mm and which tend to get sucked together on inspiration
- Sympathetic fibres from superior, middle and inferior ganglia

- Parasympathetic from vagus nerve
EXTRA INFORMATION
Non-Recurrent Laryngeal Nerve

- Right non-recurrent laryngeal nerve: 0.6%, seen in setting of aberrant right subclavian artery
- Left non-recurrent laryngeal nerve: 0.04%, seen in setting of situs inversus

399
CLINICAL PHYSIOLOGY
Definitions
- Thyrotoxicosis: biochemical and physiological manifestation of excess excessive circulating free T4 (irrespective of source)
- Hyperthyroidism: thyroid gland over-activity resulting in thyrotoxicosis
▪ TRH from hypothalamus stimulate TSH from anterior pituitary stimulates Thyroid Follicular cells to synthesize T3 & T4
- Euthyroid Sick Syndrome: alterations in patient’s thyroid function test during episodes of critical illness
▪ Acute phase: low serum T3, increased serum reverse T3, normal T4, normal TSH
▪ Chronic phase: low serum T3, low T4, low TSH (Thyroid hormone replacement is not indicated, treatment is directed at
underlying medical illness)
Causes of thyrotoxicosis
Disease Remarks
- Classical triad of complaints
▪ Signs of symptoms of thyrotoxicosis (i.e. AF, heat intolerance, sweating, weight loss)
▪ Diffusely enlarged thyroid gland +/- audible bruit
Graves’ Disease ▪ Exophthalmos
Primary - Thyroid-stimulating IgG antibodies (TSI) are TSH receptor antibody (TRAb) that bind to and
Hyperthyroidism stimulate the TSH receptors >80% positive
- Females affected more frequently than males – peak age of 20 – 40 years old
- Solitary secreting adenoma, usually >3cm to be symptomatic
Toxic Adenoma
- Increased thyroid hormone occurs independently of TSH
Toxic MNG - Prevalence increases with age and iodine deficiency, progressive
TSH-secreting
- TSH detectable despite high FT4 and FT3
pituitary adenoma
Gestational
Secondary - Hyperemesis gravidarum due to high levels of HCG in 1 st trimester which stimulates TSH receptors
thyrotoxicosis
Hyperthyroidism
- Ovarian Teratoma – struma ovarii
Neoplasms - Choriocarcinoma – tumour can produce both HCG and TSH
- Metastatic Thyroid Carcinoma
Sub-acute (de Quervain’s)
- 2nd most common form of thyroiditis – release of large amounts of steroid hormones
- Females affected more frequently than males – peak age 30 – 50 years old
Thyrotoxicosis Destructive
- Present with – odynophagia, firm, tender enlarged neck mass (typically preceded by a viral illness)
without thyroiditis
- Transient hyperthyroidism with eventual hypothyroidism
Hyperthyroidism
- Histology: granulomatous inflammation (multinucleated giant cells) / thyroiditis
Drugs – Amiodarone / Lithium / Interferon-alpha
Others - Excess thyroid hormone ingestion
^ Plummer’s Disease – single toxic nodule (adenoma) on the b/g of a suppressed multinodular goiter (MNG)
EXTRA INFORMATION
Synthesis of thyroid hormone

- IODIDE TRAPPING: TSH receptor (TSHR) bound to TSH stimulates iodide transport into the
thyroid gland by the sodium iodide symporter (NIS)
- IODIDE OXIDATION + ORGANIFICATION: Iodide is oxidised and bound to tyrosine
residues in thyroglobulin (TG) to form iodotyrosine (MIT / DIT)
- COUPLING: MIT and DIT couple to form the hormonally active iodothyronines, T4 and T3.
- T3 and T4 are bound to TG and stored in the colloid in the centre of the follicular unit
- Thyroid peroxidase (TPO) catalyses the oxidation [of iodide], organification/iodination [of
thyroglobulin], and coupling reactions [between 2 iodized tyrosine residues]

400
Antithyroid drugs
Class Drug Actions Remarks
- Methimazole is preferred over PTU except during 1st trimester of pregnancy
Inhibits thyroid peroxidase
and in life-threatening thyroid storm
Carbimazole (TPO)
- PTU not used for 2nd & 3rd trimester due to risk of hepatotoxicity – switch to
Thioamides Propylthiouracil
MMI at start of 2nd trimester1
Methimazole PTU also inhibits peripheral
- Side Effects: agranulocytosis, rash (hypersensitivity reaction), cholestatic
conversion of T4 to T3
jaundice, arthralgia (methimazole: cretinism in newborns, aplastic anemia)
Interferes with organification - When given in large doses after administration of an anti-thyroid medication,
Iodides Lugol’s Solution
and inhibit hormone release iodine can inhibit thyroid hormone release (Wolff-Chaikoff Effect)
Suppress pituitary thyroid
Steroids Hydrocortisone axis and inhibit peripheral - Steroids have rapid action (good for life-threatening thyroid storm)
conversion of T4 to T3
Causes of hypothyroidism
Disease Remarks
- Autoimmune inflammation (dense lymphocytic infiltrate)
- Females affected more frequently than males – peak age of 40 – 65 years old
Hashimoto’s - Presents with hypothyroidism, though initial inflammation may cause transient hyperthyroidism
thyroiditis - Histology: hurthle cells, lymphocytic infiltrates with germinal centre
- Microsomal auto-Ab >90% (anti-thyroglobulin – anti-TG and/or anti-thyroid peroxidase – anti-TPO)
- a/w SLE, RA, Sjogren’s Syndrome, increased risk of non-Hodgkin B cell lymphoma
Autoimmune
- Microsomal autoantibodies are present
(atrophic)
Congenital - Due to maternal hypothyroidism, thyroid agenesis, thyroid dysgenesis
(cretinism) - 6Ps: pot-bellied, pale, puffy-faced, protruding umbilicus, protuberant tongue, poor brain development
Iodine Deficiency - Most common cause of goitre
(Endemic Goitre) - Iodine deficiency can results in nodular goitre, hypothyroidism and cretinism
Primary - Extreme form of hypothyroidism
Hypothyroidism - Seen in elderly females with a history of hypothyroidism, ppt by major surgery / trauma / infection etc.
- Patients develop somnolence, AMS, bradycardia, hypothermia and hypotension (mortality 60%)
Myxedema Coma*
- Investigations: ↓Hb, ↓TW, ↓Na, ↑Cr, ↑LFTs, ↑LDH, ↓glucose, ↓T4, ↑TSH, ↓pH (acidosis)
- Supportive Treatment + avoid active rewarming as it increases O2 consumption and risks hypotension
via peripheral vasodilation
- Iatrogenic – post-thyroidectomy & irradiation (radioactive iodine)
- Drugs –Anti-thyroid drugs, Lithium, Amiodarone, Sulphonylureas
- Neoplasms – infiltration and destruction of the gland secondary to malignant neoplasm
- Thyroiditis
Others
▪ Acute Suppurative Thyroiditis (Infection) – bacterial thyroiditis(i.e. Staph / Strep)
▪ De Quervain’s – preceded by viral URTI, tender thyroid, elevated ESR
▪ Riedel thyroiditis – destruction of thyroid gland by dense fibrosis and fibrosis of surrounding
structures (trachea and esophagus) – a/w retroperitoneal and mediastinal fibrosis
Hypopituitarism
Secondary
Isolated TSH
Hypothyroidism
deficiency
* misnomer as patient exhibits neither non-pitting edema (myxedema) nor coma
EXTRA INFORMATION
Function of Thyroid Hormones (T3 & T4)

System Action
- ↑ HR and cardiac output + ↑B-receptor production – ↑sensitivity to catecholamines (I.e. adrenaline) +
Cardiac
Promotes erythropoiesis + ↓peripheral vascular resistance
- ↑ basal metabolic rate (thermogenic) + ↓ cholesterol production + ↑ catabolism of fatty acids + ↑ absorption
Metabolic
of glucose, gluconeogenesis and glycolysis + ↑synthesis and catabolism of proteins
Respiratory - ↑ ventilation rate
Gastrointestinal - ↑ motility and secretion
CNS - ↑ CNS activity and alertness + Normal neuronal function

Growth and Development - Normal myelination and axonal development + Stimulate skeletal growth + Promote bone mineralization
1 uptodate: Hyperthyroidism during pregnancy: Treatment

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APPROACH TO SOLITARY THYROID NODULE
DEFINITION
It is a discrete and radiologically defined lesion within the thyroid. It may or may not be palpable. The thyroid nodule can lead to local
compressive symptoms, hyperfunctioning status (i.e. hyperthyroidism) or contain an underlying malignancy.
EPIDEMIOLOGY
- Thyroid nodules are detected in up to 50-60% of healthy patients
- Estimated prevalence on the basis of palpation ranges from 3-7%
- Prevalence of cancer from palpable and nonpalpable lesions is similar (5-7%)
- 20-48% of patients with one palpable thyroid nodule (discrete lesions distinct from surrounding thyroid parenchyma) are found
to have additional nodules on u/s investigation
- More common in elderly, women, iodine deficiency and previous radiation exposure
Through history and clinical examination, aim to determine if a patient's neck lump is due to a thyroid nodule. Assess for patient’s
thyroid status (hyperthyroid, hypothyroid or euthyoird), risk of an underlying malignancy (i.e. risk factors, cervical lymph node status)
and presence of local complications (i.e. compressive symptoms).
History
About the LUMP

- Onset (gradual or sudden), duration (rate of growth of neck mass)
- Size (Diffuse or one side predominant? Any sudden increase in size? – malignant growth; ddx includes haemorrhage into necrotic
nodule or cyst, subacute thyroiditis)
- Red Flags – dysphonia, dysphagia, or dyspnoea (see below)
About SYMPTOMATOLOGY
- Most patients with thyroid nodules have few or no symptoms!
History Hyperthyroid Hypothyroid
Hyperactive Tiredness / Lethargy
Easily Irritable Mood changes including depression
General Mood
Insomnia or Anxiety
Depression (elderly)
Weight loss despite increased appetite Weight gain despite decreased appetite
Heat intolerance (preference for cold)
Cold intolerance (preference for warmth)
Other Increased sweating
Symptoms Diarrhoea Constipation
Palpitations, Tremors Bradycardia
Oligomenorrhea and loss of libido Menorrhagia
Hypertension* (due to ↑Peripheral Vascular Resistance)
Cardiovascular
System Bradycardia + ↓ Myocardial Contractility (↓CO)
Hyperlipidaemia* (increase LDL, TG)
* Usually seen in patients with TSH > 10, when treated with levothyroxine → BP, LDL, and TG all decrease
About RISK FACTORS for malignancy

- Age, Gender (females > males),
- Exposure to ionizing radiation (papillary cancer risk ↑3x)
- History of childhood head & neck radiation (i.e. in treatment of lymphoma)
- Family history of thyroid cancer – ~20% of medullary cancers are familial (MEN2a, MEN2b), ~ 5% of papillary cancers
- History of cancer elsewhere – papillary cancer is associated with familial adenomatous polyposis (FAP) & Gardner syndrome
(APC gene), Cowden disease (PTEN gene), Carney Complex (PRKAR1A gene)
- History of autoimmune disease e.g. type I DM, SLE, RA, pernicious anaemia (associations with Graves and Hashimoto’s)

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About COMPLICATIONS OF DISEASE
- Local Complications
▪ Pain – bleeding into cyst can result in sudden increase in size and pain
▪ Compressive Symptoms – difficulty swallowing (i.e. dysphagia, globus sensation, choking sensation), difficulty breathing,
(i.e. subjective dyspnea)
▪ Hoarseness of voice – benign pathologies almost never compress the recurrent laryngeal nerve
- Systemic Complications
▪ High Output Cardiac Failure – ask about dyspnoea, effort tolerance
About previous TREATMENT for any thyroid disease

- Medications e.g. propylthiouracil, carbimazole, propranolol – length, efficacy, side effects
- Radioactive iodine treatment – what was the result? Is the patient receiving replacement?
- Surgery – what kind of surgery, any complications?
- Follow-up – what investigations were done?
Thyroid Gland Examination

Preliminaries
1. Greet Patient and ask for permission to examine (any voice hoarseness – RLN invaded)
2. Position patient and expose adequately – entire neck, sternum and clavicles
3. Inspection from the front
▪ Any swelling?
▪ Any scars? (any transverse incision in a skin crease, 2FB above suprasternal notch)
▪ Any skin changes over the mass?
▪ Any stigmata of hyperthyroidism (i.e. agitation) or hypothyroidism (i.e. bradykinesia)
▪ Check for plethora of face, distended neck veins – may be due to the compressive nature of mass (but rarely seen).
Consider Differential Diagnosis for Thyroid Lump

1. Check if mass moves on swallowing by asking the patient to take a sip of water – “Please take a sip of water and hold it in your
mouth, do not swallow until I tell you to.”
2. Check if mass moves on protruding the tongue – “Please open your jaw slightly. Now, without moving your jaw, please stick your
tongue out and back in again.”
3. Check if mass moves on swallowing or tongue protrusion again with hands palpating thyroid
* A thyroid swelling moves only on swallowing; a thyroglossal cyst will move on both swallowing and protrusion of the tongue
Palpate Thyroid from behind

One side at a time with the opposite hand stabilizing the gland. Gently tilt head forward to relax anterior neck muscles, rest fingers on
the lateral lobe of thyroid (Ask for pain before palpating!)
1. Characteristics of lump and surrounding skin:

▪ Site (anterior triangle)
▪ Size (discrete nodule or multinodular enlargement or diffuse enlargement?)
▪ Consistency (soft, cystic, hard, multinodular?)
▪ Mobility (fixed to skin? Fixed to underlying structures?)
▪ Tenderness
2. Palpate lymph nodes – submental, submandibular, pre/postauricular, down SCM (II, III, IV), supraclavicular, occipital
▪ Hard & clustered (carcinoma)
▪ Thyroid Malignancy most commonly spread to level VI then to levels II to V
3. Feel the carotid pulsation on both sides – are they well felt?
Around the Thyroid

1. Palpate for tracheal deviation
2. Percuss manubrium for signs of any retrosternal extension
3. Auscultate of any neck bruit (using the bell) – specific for Graves’
Assessment of Thyroid Status

Face / Eyes
1. Expression – staring, unblinking (hyperthyroid); lethargic, apathetic (hypothyroid)
2. Complexion – dry, ‘peaches-and-cream’ complexion, loss of outer third of eyebrows (hypothyroid)
3. Eyes
▪ Excessive Sympathetic Activity
- Lid lag (eyelid lags behind eye when patient follows your finger downwards)

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- Lid retraction (sclera visible between upper limbus of iris and upper eyelid)
▪ Graves Disease
- Proptosis (Exophthalmos*) (look from above patient’s head – eye visible over supraorbital ridge, sclera visible
between lower limbus and lower eyelid)
- Ophthalmoplegia** (restriction of eye movements; ask about diplopia!), if patient having fixed gaze have risk of optic
nerve compression (surgical emergency)
- Chemosis (oedema and erythema of conjunctiva) – if present use fluorescein to look for corneal ulceration
* Exophthalmos is reserved for prominence of eyes secondary to thyroid disease

** Infiltrative ophthalmopathy is characterized by edema and infiltration of lymphocytes into the extraocular muscle and connective tissue. Retro-orbital
fibroblasts are then stimulated by cytokines released from infiltrating Th1 cells to produce excessive amounts of glycosaminoglycans resulting
inflammation and accumulation of glycosaminoglycans increases the volume of the retro-orbital tissues
Upper Limb
1. Examine for Proximal myopathy
2. Fine postural tremor – accentuate by placing a sheet of paper on the hands
3. Offer Pemberton’s Sign flushing of face with both hand raised – (1min)
Palm
1. Palms – ↑sweating, palmar erythema (hyperthyroidism), areas of vitiligo (a/w AI disorders, i.e. Graves’ disease)
2. Feel pulse – tachycardia, AF (more in toxic MNG than Graves’), bradycardia (hypothyroidism)
3. Nails – thyroid acropachy (clubbing), onycholysis – plummer’s nail (thyrotoxicosis)
Others
1. Legs for pretibial myxedema* (autoimmune manifestation specific for Graves’ (3%) or hypothyroid)
2. Reflexes (ankle jerk) – slow to relax in hypothyroidism
3. Offer to check thyroid status and ask the patient about compressive symptoms.
* Double Misnomer, elevated lesion occurring on the anterio-lateral aspect of the lower limb and extends to the back of the legs and feets (infiltrative
dermopathy, lesions may be nodular or plaque-like, purplish red or brown and the skin is shiny with a thickened orange peel appearance). The lesion is
thus neither limited to the pretibial area and also seen in hyperthyroidism
Examination findings of Hyperthyroidism or Hypothyroidism
Examination Hyperthyroid Graves Hypothyroid

Thin Obesity
General Alopecia Diffusely enlarged palpable goitre Dry Thin Hair
Inspection Face appears flushed with thyroid bruit ‘Peaches & cream’ complexion
Nervousness Slower Thinking
Proptosis (Exophthalmos)
Lid retraction, lid retraction Loss of outer 1/3 of eye-brows
Eyes Ophthalmoplegia
Bulging Eyes / Unblinking Stare Puffy Eyes
Periorbital edema, Chemosis
Proximal Myopathy Muscle Weakness
Cold peripheries
Warm & Sweaty palms
Carpal Tunnel Syndrome
Upper Limb Tremors
Thyroid Acropachy
Hyperreflexia
Hyporeflexia
Tachycardia at rest ± AF
Bradycardia
Ankle Swelling (heart failure)
Lower Limb Pretibial Myxoedema

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1. Dominant nodule of a multinodular goitre
2. Cyst (simple, colloid, or haemorrhagic)
3. Follicular adenoma
4. Localized forms of thyroiditis (i.e. Hashimoto Thyroiditis)
5. Thyroid Cancer
Clinical features suggesting increased risk of malignant potential

1. History of head and neck ionizing radiation
2. Family history of medullary / papillary thyroid cancer or MEN type 2
3. Male – thyroid nodules less common in male but more likely to be malignant
4. Age <14yrs or >70yrs (majority of nodules which occurs in 3 rd to 6th decades – likely benign)
5. Slow but progressive growth of the nodule (during weeks or months)
6. Firm or hard, solitary or dominant thyroid nodule (which is different from rest of gland)
7. Cervical lymphadenopathy (esp. lateral nodal compartments) → level VI lymph nodes: first nodes that a thyroid malignancy
spreads to; they lie in the tracheo-oesophageal groove and are not palpable.
8. Fixed nodule
9. Compressive symptoms – i.e. tracheal compression (cough and dysphonia), esophageal compression (globus sensation,
dysphagia, choking sensation)
10. Hoarseness (i.e. recurrent laryngeal nerve invasion)
11. Other symptoms of invasion e.g. haemoptysis, stridor, dysphagia, dyspnoea, dysphonia*
* Differentiated thyroid carcinoma rarely cause airway obstruction, vocal cord paralysis or oesophageal symptoms at their clinical
presentation, absence of local symptoms does not r/o malignant tumour
INVESTIGATIONS
1. Thyroid function test (TSH & T4)

▪ Measurement of serum TSH is the best initial laboratory test of thyroid function
▪ ± anti-TSH antibody (TRAb) – if TSH value is below reference
▪ ± anti-thyroid peroxidase antibodies (TPOAb) – if TSH value is above reference
▪ ± anti-thyroglobulin – if suggestive of chronic lymphocytic thyroiditis (Hashimoto) in conjunction with normal serum TPOAb
levels
▪ No role is measuring serum thyroglobulin or calcitonin in the initial assessment of thyroid nodule
2. Ultrasound of thyroid (see below)

▪ For all patients with a palpable thyroid nodule or with clinical risk factors
▪ Advantages:
- Objective measurement of nodule size and characteristics (see below)
- Detection of subclinical / non-palpable nodules – In papillary carcinoma multicentric disease occurs in 15%
- Detection of lymph node enlargement (central & lateral neck)
- Can define consistency of nodule – solid, cystic, or complex
- Can be used to guide FNA biopsy and/or cyst aspiration
▪ Suspicious sonographic features (*a/w thyroid cancers)
- Calcifications – micro*, dense/macro, rim (psammoma bodies 🡪 papillary cancer)
- Vascularity – intra-nodular*, peripheral, absent
- Margins – infiltrative*, spiculated*, well-defined regular
- Echogenicity – hypo*, hyper, iso-…
- Shape – taller than wide*
- Halo – absent*, thin, regular
▪ No u/s feature is independently fully predictive of a malignancy
▪ Standardized reporting indicating – position, shape, size, margins, contents, echogenicity and vascular pattern of the nodule

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EXTRA INFORMATION
Thyroid Nodule Ultrasound Classification System2
3. Fine needle aspiration cytology*

▪ The single most important investigation modality for management of thyroid nodules!
▪ Performed for intermediate or high suspicion nodules > 1cm in size (dependent on ultrasound features)
▪ Best performed under u/s guidance to increase diagnostic accuracy
2 Thyroid. 2016 Jan;26(1):1-133. [ATA guidelines]

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▪ Can be both therapeutic and diagnostic for cyst – chocolate-brown fluid aspirated; feel lump after aspiration to check for
resolution
▪ Cannot differentiate follicular adenoma from follicular carcinoma as the mark of malignant disease is capsular invasion
(FNAC provides limited assessment of architecture) → need to assess the WHOLE capsule for invasion (FNA, Incisional
biopsy or Frozen section cannot be used for diagnosis)
▪ Can be used to sample suspicious LN (i.e. ≥ 8mm)
* Procedure: inject LA, insert 22G needle and apply suction while fanning needle in region of nodule, release suction before pulling out needle, expel
contents onto slide, then fix. Cytologic smears should be interpreted by an experienced on-site cytopathologist and reported based on the BETHESDA
CLASSIFICATION
Bethesda System for Reporting Thyroid Cytopathology (BSRTC)3

Diagnostic Category Examples Malignancy Management
(%)
Repeat FNA with US guidance and on-site cytopathologist
Non-diagnostic / Cyst fluid, blood,
I 1-4 Consider surgery for non-diagnostic solid nodule or growth in
Unsatisfactory clotting artefact
size
Follow-up with clinical examination, US +/- FNA & TSH
measurement for 3 – 5 years
Colloid, - US + FNA in 12 months for high suspicion group
II Benign adenomatous 0-3 - US in 12 – 24 months for intermediate suspicion group
nodules, thyroiditis - US in 24 months for low suspicion group
In nodules with size increase > 50% or symptomatic, repeat FNA
If repeat US/FNA is benign then no further follow-up required
Atypia / Follicular lesion of
Repeat FNA (>60% more diagnostic)
III undetermined significance 5-15
Individualized Mx – surveillance, molecular testing or surgery
(AUS / FLUS)
Follicular neoplasm or
Includes hurthle cell Surgical Lobectomy
IV suspicious for a follicular 15-30
neoplasm Molecular testing (i.e. BRAF mutation) in low suspicion group
neoplasm [indeterminate]
V Suspicious for Malignancy 60-75 Near-total thyroidectomy or surgical lobectomy
Papillary, Medullary,
VI Malignant* 97-99 Near-total thyroidectomy
Anaplastic
* If metastatic tumour rather than a primary thyroid malignancy, surgery may not be indicated
4. Radio-isotope scan (123I or 99mTcO4 (sodium pertechnetate)

▪ For patients with low serum TSH value or an MNG to detect functional autonomy (i.e. identify cold (hypofunctioning) or
indeterminate areas for FNA biopsy and hot area that do not need cytologic evaluation)
▪ Hot nodule: only 1% malignant; but cold or indeterminate nodule: 3-15% malignant
▪ Cold nodule with normal or elevated TSH → proceed to neck ultrasound
▪ 131I is not recommended for routine diagnostic use (its use for evaluation of distant metastases after total thyroidectomy for
differentiated thyroid cancer)
5. Calcitonin Assay
▪ Mandatory for patients with history or clinical suspicion of familial MTC or MEN2
▪ Check calcium level (suspect medullary thyroid cancer)
▪ Calcitonin levels can be increased in pulmonary / pancreatic endocrine tumours, kidney failure, AI thyroid disease,
hypergastrinemia (fr PPI therapy), alcohol, smoking and sepsis
6. Baseline tumour markers (if suspected or confirmed malignancy)

▪ For differentiated thyroid cancer: thyroglobulin
- Thyroglobulin levels have no implication of prognosis
- If pre-operatively thyroglobulin not detected (i.e. patients unable to produce thyroglobulin or have antibodies to
thyroglobulin) = “high risk”, as unable to use thyroglobulin to monitor recurrence post-operatively
▪ For medullary thyroid cancer: calcitonin, carcinoembryonic antigen (CEA) – ask for family history of MEN syndrome
7. CT scan (contrasted or non-contrasted) or MRI

▪ If cervical LN positive (clinically) or FNAC positive 🡪 CT neck
▪ If any evidence of airway deviation, retrosternal goitre, Pemberton’s sign positive, consider non-contrast CT scan
▪ Consider PET/CT only for preoperative staging of malignant nodules with aggressive features
▪ Disadvantage of contrasted CT:
- Large iodine load (in patients with uncontrolled hyperthyroidism, risk of thyroid storm)
- Affects post-op RAI as patients need to be iodine depleted before therapeutic RAI (needs at least 4-8 weeks)
3 Am J Clin Pathol. 2009 Nov;132(5):658-65.

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▪ MRI has same functions as CT but higher cost, also MRI contrast (gadolinium) does not interfere with iodine uptake
▪ CT is useful as post-operative follow-up for assessment of recurrent disease
8. ENT examination of vocal cords

▪ If patient have evidence of change in voice or hoarseness, perform naso-laryngoscopy preoperatively
MANAGEMENT
Indications for surgery (6Cs)

1. Cancer
2. Compressive symptoms (i.e. shortness of breath, dysphagia)
3. Cannot be treated medically - failed medical therapy or unsuitable for medical tx (i.e. Graves Disease)
4. Compliance/cost problems – with long-term medical therapy (but patient may still require long-term therapy after op if he/she
becomes hypothyroid or is still hyperthyroid)
5. Child-bearing – if thioamides are not tolerated because of allergy or agranulocytosis
6. Cosmesis
Types of surgery available

1. Hemithyroidectomy – removal of one lobe of the gland, including the isthmus and the pyramidal lobe
2. Total thyroidectomy – entire gland removed completely
3. Subtotal thyroidectomy (rarely done)
▪ Conventional subtotal thyroidectomy – leave a thumb-sized amount (about 4-6g) of remaining thyroid tissue on both sides
▪ Harley-Dunhill subtotal thyroidectomy – leave a thumb-sized amount only on one side with removal of the rest of the gland
EXTRA INFORMATION
Outcomes for Total versus subtotal thyroidectomy (for hyper functioning thyroid disease)
- Patients post total thyroidectomy will be hypothyroidism, thus the patient will require life-long thyroid replacement and follow-
up → problems with compliance, cost, inconvenience

- Results of subtotal thyroidectomy (at 5 years)
▪ 60-70% euthyroid (do not require medication but still have to be followed up closely)
▪ 16-20% hypothyroid (usually becomes evident within 1 year of surgery)
▪ 8-10% hyperthyroid (% increases proportionately with time → failure of surgical therapy)
- Subtotal thyroidectomy is rarely performed as patients will need to be monitored long-term, an alternative is to perform total
thyroidectomy with post-operative thyroxine replacement (but this is weighed against the benefit of not requiring any
medication)

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THYROID CANCERS4
INTRODUCTION
Thyroid cancers are generally classified into follicular cell derived (i.e. papillary thyroid cancer (PTC), follicular cancer (FC), hurthle
cell variant (HCC) and anaplastic cancer (AC) & non-follicular cell derived (i.e. medullary thyroid cancer (MTC) and thyroid
lymphoma).
They can also be classified into well-differentiated thyroid cancer (WDTC) such as papillary thyroid cancer, follicular cancer and
hurthle cell variant. These slow growing, non-aggressive WDTC accounts for 95% of all thyroid cancer and have excellent 10 year
survival rates
EPIDEMIOLOGY, RISK FACTORS & PATHOPHYSIOLOGY

Papillary Carcinoma Follicular Carcinoma Anaplastic carcinoma Lymphoma Medullary carcinoma
Proportion 75-80% 10% 1-2% 1-5% 5-10%

>50 years (sporadic)
Age 40-50 years 50 - 60 years 60 - 70 years 60 - 80 years
20-30 years (familial)
F:M ratio 3:1 3:1 2-3:1 2:1 1:1
- Ionizing radiation
- Polyposis
syndromes (FAP,
- Ionizing radiation - Long Standing - History of lymphoma
Gardner’s, etc.)
- Iodine deficiency goitre or MALT - Significant family history (familial
- Carney complex,
Risk - Follicular adenoma - History of previous - Hashimoto’s type) – MEN2A / 2B (screen for
Cowden
factors is NOT a risk factor differentiated thyroid thyroiditis (60X pheochromocytoma)
syndrome
- Werner syndrome, cancer (30% of - RET mutation
- McCune Albright ↑risk)
Cowden syndrome anaplastic cancer)
Syndrome (PTC
clear cell)
- Family history (5%)
- Arise from thyroid parafollicular
- Characteristic (1) - FNAC may suggest
- Diagnosis of cancer
Orphan Annie lymphoma but C cells (which produce calcitonin
made on evidence
nuclei, (2) nuclear definitive diagnosis
of capsular or - Small blue round → flushing and diarrhoea
pseudoinclusions requires trucut or
vascular invasion by cells that are highly - Pathology: deposits of acellular
Pathology - Papillary excision biopsy
tumour cells (vs. anaplastic – may amyloid material – altered
architecture with (3) - Multiple subtypes,
follicular adenoma) resemble lymphoma calcitonin collections (shown with
Psammoma bodies almost always non-
- Hurthle cell variant Congo red stain)
- Tall cell variant Hodgkin’s of B-cell
(worse prognosis) - Multicentric C-cell hyperplasia (in
(worse prognosis) type
familial cases)
- Large bulky neck
mass with aggressive
- Sporadic (80%): firm, unilateral
growth - Usually, presents as
nodule (worse prognosis)
- 70% multicentric - Solitary - Multiple metastases rapidly enlarging
- Familial (20%): bilateral,
- Lymphatic spread - Hematologic probably present at goitre with
multicentric tumors (better
Clinical to cervical LNs spread to lung, presentation compressive
prognosis)
Features - LN involvement in bone, brain - Invasion of local symptoms
- Aggressive, spread via local,
80% of disease at - LN involvement in structures leading to - 60-80% aggressive
lymphatic & hematogenous routes
diagnosis (level VI 10% (rare) (respiratory and 30% more
- 95% produce calcitonin,
first) compromise, indolent
- 80% produce CEA
dysphagia, voice
hoarseness)
Bone, Lung Lung, Bone, Brain
Metastatic
(~5% at time of (~ 15% at time of Lung, Bone, Brain Lung, Liver, Bone, Brain
Sites
presentation) presentation)
4 NUHS Lecture Slides – common thyroid disorder in surgery

409
INVESTIGATION & DIAGNOSTIC CRITERIA
Surgical management of thyroid cancer is determined by the histology data obtained from FNAC. (refer to Bethesda criteria)
In addition to FNAC, patients will require thyroid function blood test, tumour markers (i.e. thyroglobulin for WDTC & calcitonin / CEA
for MTC) ultrasound thyroid / neck (to evaluate for enlarged cervical lymph nodes), +/- preoperative laryngeal examination to assess
for vocal cord palsy, +/- evaluation of cervical spine pathology (to allow for appropriate positioning)
Patients do not require preoperative staging CT investigations. Non-contrast CT neck can be performed for patients with large goitre
with impending airway compromise, retrosternal goitres or patients with enlarged cervical LN. Patients with differentiated thyroid
cancer can be assessed for distant organ metastases during subsequent radioactive iodine scan.
STAGING AND CLASSIFICATION

Staging for thyroid cancer is unique as age is a factor in determining stage. TNM staging provides information regarding survival but
does not reliably predict disease recurrence. (age cut-off has increased from 45 to 55years between the AJCC 7th and 8th edition)

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MANAGEMENT
Risk Stratifications
- Patient factors:
▪ Age: < 15 years or >45 years old is high risk (latest AJCC 8th edition uses 55 years old as cut-off)
▪ Gender: male is high risk
- Tumour factors:
▪ Size – nodule >4cm has higher risk
▪ Histology – Tall cell variant (Papillary CA) & Hurthle cell variant (Follicular CA) have worse prognosis
▪ Extrathyroidal extension into surrounding structures
▪ Lymph node or distant metastases
- Various score systems have been formulated to stratify risk:
▪ MACIS – Metastasis, Age, Completeness of resection, Invasion, Size
▪ AMES – Age, Metastasis, Extrathyroidal Extension, Size
- Patients can be divided into three groups:
▪ Low risk – low-risk patient and low-risk disease (i.e. no high-risk features)
▪ Intermediate risk – low-risk patient with high-risk disease, or high-risk patients with low-risk disease
▪ High risk – high-risk patient and high-risk disease
- Risk guides treatment – low-risk patients can undergo hemithyroidectomy without ablative radioiodine therapy post-op, while
high-risk patients undergo total thyroidectomy with post-op ablative RAI treatment; treatment in intermediate risk patients is
tailored to the disease, but usually, it is similar to that in high-risk patients
▪ For DTC > 4cm or DTC with high risk features – consider total thyroidectomy
▪ For DTC 1-4 cm in size – consider surgical lobectomy if uni-focal, no extra thyroidal extension, no cervical LN metastasis.
▪ For DTC < 1cm – consider surgical lobectomy5 (for DTC < 1cm diagnosed after thyroid lobectomy, need for completion
thyroidectomy depends on histology results)
- If post-operatively histology (for surgical lobectomy) suggest high risk features, offer patient completion thyroidectomy (i.e. had
the histology been made available before the initial surgery, total thyroidectomy would have been recommended)
- Thus, risk stratification helps to guide the extent of surgical resection in differentiated thyroid cancer according to the patient’s
disease.
Molecular Testing in Thyroid Cytology

- Current trend is for molecular testing preoperatively to determine tumour biology. Tumour which are deemed higher risk will be
treated with more aggressive treatment
- However, this is limited by high cost ($4000)
- PTC: assess for BRAF mutation (higher incidence of nodal disease, worse prognosis)
- Follicular Cancer: assess for RAS mutation
- Medullary Thyroid Cancer: assess for RET oncogene
Total vs Hemi-thyroidectomy
Advantages of TT
- Evidence for micro-foci of disease and multicentricity of cancer – removal of the entire thyroid decreases risk of recurrence
- Ability to use adjuvant radioiodine to ablate any residual cancer tissue after surgery
- Ability to use radioiodine to detect recurrent disease (normal thyroid picks up iodine better than cancer cells, thus the presence
of the thyroid gland will decrease the ability of RAI to pick up recurrent cancer) and as treatment for recurrence
- Ability to use serum thyroglobulin as a cancer marker for recurrence
Disadvantages of TT
- Risk of bilateral recurrent laryngeal nerve injury and permanent hypoparathyroidism
- Very low incidence of cancer recurrence in residual thyroid – micro-foci probably not clinically significant
- Limited thyroidectomy may spare patients from having to be on lifelong thyroid hormone replacement
5 Thyroid. 2016 Jan;26(1):1-133. [ATA guidelines] (same as earlier reference)

411
Differentiated Thyroid Cancer
Surgical resection
- For suspicious lesion (i.e. hurthle cell cancer / suspicious for follicular cancer) – hemithyroidectomy, trace histology, KIV
completion TT (Intraoperative frozen section unreliable for FC / HCC as unable to determine vascular invasion)
- Hemithyroidectomy / Surgical lobectomy for selected low-risk patients (see below)
- Total thyroidectomy for the majority
- LN clearance
▪ Central compartment clearance (i.e. level 6, trachea-esophageal nodes) – performed for patients with pre-operative or
intraoperative identified central or lateral neck nodes, or prophylactic in high risk patients (i.e. > 45 years, PTC, advanced
primary tumour (T3 or T4), lateral LN involvement)
▪ Lateral neck (levels 2 – 5) – performed for patients with pre-operative or intraoperative identified involved lateral LN
- Identification of RLN, External Branch of SLN and parathyroid glands with their blood supply
- Higher risk of RLN injury if: large thyroid, Graves’ disease, aberrant anatomy (non-recurrent laryngeal nerve), preop neural
invasion, repeat neck surgery
Post-operative Management
- If Total Thyroidectomy performed – PTH, cCa, +/- PO4, +/- Vit D on POD 0 and cCa on POD 1
- Monitor for signs / symptoms of hypocalcaemia, hoarseness of voice or hematoma
- IV antiemetics (i.e. ondansetron / maxolon) + lozenges (i.e. PO difflam)
- POD 1 – start PO T3 10-20mcg TDS for 6 weeks or PO T4 at 2.1mcg/kg/day with thyrogen protocol (if malignant pathology),
start PO T4 at 1.6mcg/kg/day (if benign pathology)
- POD 1 – remove neck drain (if volume < 50mls)
- If patient discharged with T4 – no need blood test for 4-6/52 as it takes at least that time to stabilize
Adjuvant therapy with RAI

- Radioablation (RAI) of metastatic or residual cancer and residual thyroid tissue (75-100mCi of 131I at 4 weeks after TT while
patient is hypothyroid (no replacement of T 4 yet – keep patient in hypothyroid state so any remnant thyroid tissue present would
crave for iodine and take up the RAI)
- Low risk patients: do not require post-op RAI, intermediate risk: consider with lower dose of RAI, high risk: should receive RAI
- LT4 (levothyroxine) to be stopped 4 weeks prior to RAI therapy
- If LT4 has to be stopped for > 4 weeks, LT3 (liothyronine) should be used instead and then stopped 2 weeks prior to RAI (LT3
has a shorter half-life than LT4)
- Advise patient that they will experience hypothyroid symptoms during this “thyroxine withdrawal” period
- Advise patient to have low iodine diet 1 – 2 weeks prior to RAI
Follow-up
- TSH level in first 6 – 12 months
▪ Lifelong long-term suppression of TSH with L-thyroxine to prevent recurrence and improve survival
- Neck ultrasound in first 6 – 12 months then yearly or every few years (depending on risks)
▪ New LN detected >8mm: FNA biopsy + surgical dissection to be considered
- Thyroglobulin as a marker of recurrence. It should be at the lowest at 3-4 weeks post-op (< 1.0 ng/ml a/w favourable prognosis)
- If recurrence suspected clinically on ultrasound or TG elevated, proceed with CT neck
- Radioactive iodine scan to detect recurrence

412
EXTRA INFORMATION
Clinical Response of Differentiated Thyroid Cancer
- Excellent Response – no evidence of disease, negative imaging, TG < 0.2, absent TG antibodies
- Indeterminate – cannot confidently rule out disease, non-specific / negative imaging, TG < 1, absent or declining TG antibodies
- Biochemical Incomplete – no localizable disease but suspicious biochemistry, negative imaging, TG > 1, persistent / rising TG antibodies
- Structural Incomplete – persistent or newly diagnosed disease, positive imaging, any TG, any TG antibodies level
Anaplastic Thyroid Cancer

- Palliative therapy for compressive effects (i.e. chemotherapy to shrink tumors (i.e. doxorubicin + cisplatin), surgical debulking)
- External Beam RT – for patients who are not surgical candidates
- Tracheostomy
- Tumour are not responsive to I131 therapy
- Combination of CT + RT following complete resection may prolong survival
Lymphoma
- Chemoradiotherapy
- R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine and prednisolone)
- 40-60 Gy RT
- 1 cycle of R-CHOP followed by radiation followed by 5 additional cycles of R-CHOP
Medullary Thyroid Cancer

Surgical Resection
- Aggressive resection – total thyroidectomy with level VI nodes (central compartment) clearance (up to 20% of patients with MTC
harbour distant metastases at time of diagnosis)
- Selective Neck Dissection indicated for conically involved ipsilateral cervical lymph nodes
- Sampling of cervical and mediastinal nodes and modified dissection where positive
No good adjuvant therapy

- Use of external beam radiation is controversial
Follow-up
- Thyroxine replacement (not for TSH suppression but to maintain euthyroid state)
- Serum calcitonin and CEA six months after surgery (if normal, considered in remission – 5% 5yr recurrence)
- High calcitonin – screen for residual or metastatic disease, treat surgically, with RT or chemo as appropriate
EXTRA INFORMATION
Adjuvant and Molecular Therapy
- Systemic Chemotherapy
- Multiple Tyrosine Kinase Inhibitors
- Immunotherapy

413
COMPLICATIONS
Immediate (< 24 hours)
1. Haemorrhage with haematoma formation
▪ Haematoma can form superficial to the strap muscles (i.e. sub platysmal plane) or deep to the strap muscles (i.e.
paratracheal space) which can result in acute airway distress – tracheal compression and impairment of the venous and
lymphatic drainage resulting in laryngopharyngeal edema leading to progressive stridor and asphyxiation → patient can die!
▪ Management: Immediate re-exploration, cut horizontal subcuticular stitches and then vertical stitches opposing the strap
muscles to let blood drain out
2. Injury to the Recurrent Laryngeal Nerve – transient (~ 2-11%), permanent injury (> 6months, ~1-2%)
▪ Unilateral injury leads to voice hoarseness, Bilateral injury leading to compromised airway, may require tracheostomy
▪ Mechanism of injury - traction injury (common), transection injury (rare)
▪ If RLN transection injury identified intra-operatively, can perform primary end-to-end re-anastomosis
▪ Intraoperative Nerve Monitor (IONM) is an adjunct to visual nerve identification
3. Injury to the Superior Laryngeal Nerve → nerve injury leads to inability to create high-pitch sounds
4. Tracheomalacia → floppiness of trachea resulting from chronic compression by large goitres (may require intubation)
5. Thyrotoxic Storm → resection of gland can release large amounts of stored thyroid hormone into bloodstream
Intermediate (> 24hr to 1 week)

1. Hypoparathyroidism leading to Hypocalcemia
▪ Etiology: devascularization of the parathyroid hormones, damage to parathyroid hormone
▪ Risk of permanent hypoparathyroidism is 1-4% (only in total or subtotal thyroidectomies); 10-20% of patients may have
temporary hypocalcemia
▪ For patients undergoing total thyroidectomy, check the serum calcium levels & PTH post-operatively
▪ Ask patient for any symptoms and look for signs of hypocalcemia
○ Mnemonic: “CATS go numb” – Convulsion, Arrhythmias, Tetany, Spasm (laryngospasm) and numbness/paraesthesia
(earliest symptom) in oral, perioral and extremities (hands and feet)
○ Tetany – Carpopedal spasm, Chvostek’s Sign (spasm of the facial muscles on tapping the facial nerve) and Trousseau
Sign of Latent Tetany (carpal spasm on inflating BP cuff over arm)
○ Life-threatening complications – laryngospasm and cardiac arrhythmias
▪ ECG – QT prolongation with risk of arrhythmias and going to torsades de pointes
▪ Fast Replacement: IV 10ml of 10% calcium gluconate over 10min (slow bolus)
○ Alternative: IV calcium gluconate 2.3mmol/10ml (10%) injection dilute in N/S 100ml run over 1hr
○ Don’t give bolus as there is a risk that patient will get cardiac arrest (heart stops in systolic state)
▪ Replacement: 1.25g calcium carbonate BD/TDS ± calcitriol 0.5mcg OM/BD (vary between institution)
▪ Replace PO/IV magnesium as well as PO vitamin D
2. Post-op Wound Infection (1-2%)
3. Post-op Seroma formation
4. Chyle Leak (rare, possible with lateral neck dissection)
Late (> 30 days)

1. Hypothyroidism
2. Permanent hypoparathyroidism
3. Hypertrophic scarring or keloid formation
4. Tumour Recurrence
EXTRA INFORMATION
Complications of radioactive iodine therapy
Acute Long-term
Hematologic – Bone Marrow Suppression, Leukaemia (>

Neck pain, swelling, tenderness
1000mCi)
Sialadenitis (50 – 450mCi), taste dysfunction Fertility – testicular damage, spontaneous abortion
Cerebral edema (brain metastases, 200mCi) Pulmonary Fibrosis
Vocal Cord Paralysis Taste Dysfunction

Increased Cancer Risk (Breast Cancer > 1000mCi, gastric
Nausea and Vomiting (50 – 450mCi)
cancer, HCC, lung cancer, bladder cancer)
Bone Marrow Suppression (200mCi) Hypoparathyroidism
PROGNOSIS
Overall Survival (Mortality)
- WDTC (5yrr survival): low-risk patients ~ 95-98%, intermediate risk patients ~ 88%, and high-risk patients ~ 50%

414
- Anaplastic Thyroid Cancer (5yr survival): ~ 5% (median survival is between 3 to 5 months)
- Lymphoma: depends on final histology, stage and treatment
- Medullary Thyroid Cancer (5yr survival): 60-70%
EXTRA INFORMATION
Local Recurrence
- High Risk: gross extrathyroidal extension, incomplete tumour resection, distant metastases or LN > 3cm
- Intermediate Risk: aggressive histology, minor extrathyroidal extension, vascular invasion, > 5 LN involves (0.2-0.3cm)
- Low Risk: intrathyroidal differentiated thyroid cancer, ≤ 5 LN micro-metastases (<0.2 cm)

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MULTIPLE ENDOCRINE NEOPLASIA (MEN)
DEFINITION
A group of inherited diseases resulting in proliferative lesions (hyperplasia, adenomas, carcinomas) of multiple endocrine organs –
derived from APUD cells
FEATURES
- Autosomal dominant inheritance (100% penetrance) – screen family members
- Tumours occur at younger age than sporadic cancers
- Multiple endocrine organs involved, either synchronously or metachronous
- Multifocal tumours in each organ involved
- Tumour usually preceded by asymptomatic stage of endocrine hyperplasia
- More aggressive and higher chance of recurrence compared to sporadic type of tumours in the same organs
MEN 1
- Mutation in the tumour suppressor MEN1 gene leading to non-functional MENIN (located on chromosome 11q13)
- 3 P’s:
▪ Parathyroid (95%) – hyperparathyroidism from hyperplasia of parathyroid glands (multi-gland involvement)
▪ Pancreatic islet cells (30 – 80%) – aggressive pancreatic neuroendocrine tumours (i.e. gastrinoma, insulinoma), multi-
focal, diffuse islet cells hyperplasia → leading cause of death in MEN 1 patients
▪ Pituitary (20 – 65%) – anterior pituitary adenoma (i.e. prolactinoma) or growth hormone secreting tumours
- Can also have other tumours (i.e. foregut carcinoids, adrenal adenoma)
MEN 2
- Activating mutation in the RET proto-oncogene (located on chromosome 10q11.2) which encodes a tyrosine kinase receptor
- The underlying RET mutation results in the heterogeneity of extra-thyroidal clinical manifestations
- Hallmark is medullary thyroid cancer in setting of C-cell hyperplasia (multifocal and bilateral involvement)
MEN-2A (Sipple syndrome)

- Medullary thyroid carcinoma (100%) – diarrhoea most common symptom
- Pheochromocytoma (50%) – often bilateral, need to correct 1 st if simultaneous tumours, must rule out prior to thyroidectomy
- Parathyroid hyperplasia, Hyperparathyroidism (30%)
- Other – Hirschsprung disease (px with abdominal pain, distention, constipation), cutaneous lichen amyloidosis
MEN-2B (William syndrome)* → highest mortality and morbidity

- Medullary thyroid carcinoma* (100%) and Pheochromocytoma (50%) [no parathyroid involvement]
- Characteristic phenotypic appearance
▪ Oral (i.e. multiple mucosal neuromas on the tongue, lips and buccal mucosa, abnormal dental enema),
▪ Ocular (i.e. alacrimia and conjunctival neuroma),
▪ Musculoskeletal (i.e. marfanoid habitus, kyphoscoliosis, pectus deformity)
▪ Others – Gnathism of the mid-face
- Neurocutaneous manifestations – ganglioneuromatosis
- Others – gastrointestinal symptoms (i.e. diarrhoea), megacolon, multiple pseudo-polyps
Familial MTC (FMTC)

- Characterized by MTC in multiple family members with no extrathyroidal manifestations
EXTRA INFORMATION
Screening for MEN 2

- Recommendation for RET testing for at risk members of MEN2 and FMTC families
- Recommendation for RET testing for patients with MTC or pheochromocytoma (or infants with hirschsprung disease)
▪ RET Testing should occur within the first year of life, if positive then plan for total thyroidectomy
- Recommendation for pheochromocytoma screening

416
THYROIDITIS
DEFINITION
Thyroiditis refers to a diverse group of inflammatory disorders that affects the thyroid gland
Form of Thyroiditis Duration of Disease Aetiology Pain Thyroid Fx Management
Chronic lymphocytic
Chronic, progressive Autoimmune Painless Hypothyroid Levothyroxine
thyroiditis (Hashimoto’s )
Subacute lymphocytic
Subacute, transient or
thyroiditis (silent and post- Autoimmune Painless Triphasic Beta-blockers, levothyroxine
progressive
partum)
Subacute granulomatous NSAIDs, prednisolone, beta-
Subacute, transient Viral Painful Triphasic
thyroiditis (de Quervain’s) blockers, levothyroxine
Acute suppurative
Acute Bacterial Painful Euthyroid Antibiotics, Surgical drainage
thyroiditis
Invasive fibrous thyroiditis Painless, Euthyroid /
Chronic, progressive Idiopathic Steroids
(Reidel’s) rarely painful Hypothyroid
Thionamides, steroids, beta-
Acute / subacute, Pharmacologi Hyperthyroid /
Drug-Induced Painless blockers, levothyroxine,
transient or progressive cal Hypothyroid
surgery
Chronic Lymphocytic Thyroiditis (Hashimoto's)

- Most common inflammatory condition of the thyroid gland and most common cause of hypothyroidism
- Characterized by lymphocytic infiltration and follicular destruction of the gland
- 95% female, between age 30-50years
- Asymptomatic, ~ 20% hypothyroidism, ~5% thyrotoxicosis (early phase of disease)
- Diagnosis – (1) PE – Firm, irregular and non-tender goitre (2) biochemical – ↑TSH, ↓T4 ↑TPO antibody
- Management
▪ Levothyroxine ~ 1.6ug/kg/day – recheck TSH 6 weeks after initiation of therapy, then 6- 12 monthly
▪ If persistent hypothyroid symptoms despite TSH in lower ½ of reference range → check FT3 KIV replace
▪ If enlarging goitre / compressive symptoms / suspected malignancy → total thyroidectomy
Subacute Lymphocytic Thyroiditis (silent or post-partum)

- Diagnosis (1) History – triphasic course of self-limiting thyrotoxicosis* (~ 2-4 months), hypothyroidism** (~ 6 months) before
returning to a euthyroid state, (2) PE – goitre, (3) biochemical – ↑TPO antibody and ↑anti-Tg antibody, ESR normal
- Postpartum thyroiditis – development of thyroid dysfunction within 12 months after pregnancy in a previously euthyroid female
- Disease may last for 2-5 months and be recurrent
- Management
▪ Symptoms alleviation (i.e. thyrotoxicosis): beta-blocker therapy
▪ If hypothyroid: levothyroxine – recheck TFT q4-6 weeks
* Due to release of stored hormones

** Depletion of stored hormones
Subacute Granulomatous Thyroiditis (de Quervain’s)

- Most common cause of a painful thyroid gland
- History – URTI preceding development of acute thyroid pain and low-grade fever secondary to viral infection, pain worse with
swallowing, turning of head, radiate to lower jaw, ear, occiput
- Diagnosis (1) History as above, triphasic course – thyrotoxicosis (4-6wks), then hypothyroidism (6mnths), then euthyroid, (2)
biochemical – ↑ESR, normal WBC, evolving TFT, normal anti-TPO antibodies

- Management
▪ Symptoms alleviation: NSAIDs for pain (mean time to resolution of pain, 5 weeks), beta-blockers for thyrotoxicosis,
levothyroxine during period of hypothyroidism

417
Acute Suppurative Thyroiditis
- Bacterial infection (i.e. staph / strep) secondary to lymphovascular spread, direct trauma, persistent pyriform sinus fistula (children)
leading to acute neck swelling, pain and high fever
- Diagnosis (1) history as above, (2) PE – neck swelling, airway distress, compressive abscess (3) biochemical – ↑ESR ↑WBC
normal TFT, screen for HIV, (4) radiological – CT neck: identify any fluid collection, pyriform sinus fistula
- Management
▪ Treatment of infection – broad-spectrum antibiotics then culture directed x 14 days
▪ Source control – surgical incision (if unstable airway), percutaneous drainage (stable patient), with failure of treatment
consider partial / total thyroidectomy
Invasive Fibrous Thyroiditis (Reidel’s)

- Idiopathic disorder characterized by progressive fibrosis and inflammation of thyroid gland and adjacent cervical structures
- Occur 80% in females, mean age of 50yrs
- Diagnosis (1) history – compressive symptoms, neck pain, association with systemic fibrosis (2) PE – hard fixed mass, with
extension to adjacent structures, can cause dyspnoea, hoarseness, dysphagia, restricted neck movements (3) biochemical –
hypothyroidism (4) radiological – ultrasound neck (diffuse hypoechoic, hypo-vascular appearance of extensive fibrosis + carotid
artery encasement)
- Definitive diagnosis → open biopsy to rule out malignancy
- Management
▪ If have compressive symptoms → surgery for debulking
▪ Medical therapy with steroids, if refractory, can trial of tamoxifen or mycophenolate mofetil + prednisolone
Drug-Induced Thyroiditis
- Etiology – amiodarone, lithium, IFN-alpha, IL-2,
▪ Amiodarone type 1 → increased thyroid hormone production from iodine load, Mx – thioamides + potassium perchlorate
▪ Amiodarone type 2 → follicular destruction and release of stored hormones, Mx – steroids

▪ Amiodarone can also induce hypothyroidism due to inhibition of peripheral conversion of T4-T3
▪ Lithium: chronic use usually lead to hypothyroidism

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THYROID STORM
- Manifested by severe tachycardia, fever, confusion, vomiting, mania, coma (see diagnostic criteria below)
- Physical examination may reveal goitre, ophthalmopathy, lid lag, hand tremor, warm moist skin
RISK FACTORS
- Thyroid Surgery (esp. if patient was hyperthyroid prior to surgery)
- Radioiodine
- Withdrawal of drugs
- Acute Illness – i.e. DKA
- Patients usually have untreated and undertreated hyperthyroidism (i.e. Graves Disease)
MANAGEMENT
- Acute management
▪ Intravenous (IV) Fluids + Cooling measures + Electrolyte replacements + Nutritional Support + Glucose
▪ Beta-Blocker to control symptoms and signs → Propranolol 60-80mg orally Q4H
▪ Thionamide to block new hormone synthesis → Propylthiouracil (PTU) – 600mg then 200mg Q4-6H
▪ Iodine solution to block release of thyroid hormones → Lugol’s Solution 10 drops (20 drops/mL, 8mg iodine/drop) (oral)
– administer at least one hour after PTU administration to prevent iodine from being used as substrate for new hormone
synthesis (Wolff-Chaikoff effect*)
▪ Glucocorticoids to reduce T4-T3 conversion → IV hydrocortisone 100mg Q8H
- For definitive therapy → radioiodine therapy or surgery
* Patient given high doses of iodine, which inhibits TSH action on thyroid and inhibits organic coupling of iodide, resulting in less T3 and T4 release
EXTRA INFORMATION
Burch and Wartofsky Scoring System (≥ 45 = highly suggestive, 25-44 = supports dx, <25 = unlikely)
Diagnostic Parameters Scoring / Points Remarks
37.2-37.7 5
37.8-38.2 10
Institute cooling measures – can use antipyretics but
38.3-38.8 15
Temperature avoid aspirin (aspirin – a/w displacement of thyroid
38.9-39.4 20
hormone binding from thyroid binding globulin)
39.4-39.9 25
>40.0 30
99-109 5
110-119 10
Tachycardia 120-129 15
130-139 20
>140 25
Mild (Agitation) 10
Moderate (Delirium / 20 If severely agitated, sedatives (i.e. haloperidol, BZD) can
CNS Effects
Psychosis) be given
Severe (Seizure / Coma) 30
Moderate (Diarrhoea) 10 Nutritional support (i.e. thiamine) + Close monitoring of
Gastrointestinal &
20 glucose levels as glycogen stores are depleted during
Hepatic Dysfunction Severe (Jaundice)
thyroid storm
Mild 5
Congestive Heart Respiratory support (i.e. NIPPV or intubation) as needed
Moderate 10
Failure based on ABG analysis
Severe 15
Absent 0 If a/w hemodynamic instability – manage with
Atrial Fibrillation
Present 10 cardioversion, otherwise use antiarrhythmic therapy
Absent 0
Precipitant History
Present 10

419
PARATHYROID6
INTRODUCTION
Identification of the 1st PTH gland was in 1849 by Sir Richard Own in an Indian Rhinoceros. 80-90% of patients have 4 parathyroid
glands, each roughly 7mm in diameters, 40-50mg. They are known to be yellow to light brown, and are supplied by one or as many
as 3 small arteries usually branches from the inferior thyroid artery. The half-life of PTH is approximately 5 minutes. Histologically –
chief cells interspersed with adipose cells
ANATOMY & EMBRYOLOGY

Superior PTH arises from the 4th branchial / pharyngeal pouch (also give rise to parafollicular C-cells of the thyroid gland
- 1 cm above junction of inferior thyroid artery and RLN (at level of cricoid cartilage) – posterior to RLN
- Most common ectopic site – tracheoesophageal groove7
Inferior PTH arises from the 3rd branchial pouch, dorsal wing (ventral wing give rise to thymus)
- 1 cm below the junction of inferior thyroid artery and RLN (posterolateral aspect of the lower thyroid) – anterior to RLN
- Most common ectopic site – intrathymic (more variable in location, migrates extensively during embryological development)
7 Common Locations of Parathyroid Glands8

A Adherent to the posterior thyroid parenchyma (accepted expected location)
B (Behind) Posterior to the thyroid parenchyma (lies in the tracheoesophageal groove)
C (Caudal) Inferior to the thyroid parenchyma (lies in the tracheoesophageal groove)
D Dangerously close to the recurrent laryngeal nerve
E Externally located gland, not deep in the neck. Easy to resect
F (Fallen) into the thyrothymic ligament. Fun to resect. Retrieved with delivery of superior portion of thymus
G (Gated) into the thyroid parenchyma
PATHOPHYSIOLOGY
PTH acts on bone, kidney and intestine to increase serum ionized calcium concentration and decrease serum phosphate concentration
Parathyroid Hormone is involved in calcium homeostasis*

1. Increase skeletal osteoclastic activity resulting in Ca 2+ release from bone
2. Increase Ca2+ reabsorption from kidney (distal convoluted tubules)
3. Stimulates urinary phosphate excretion (distal convoluted tubules)
4. Increase absorption of Vitamin D
5. Enhances 1-hydroxylation of 25-hydroxyvitamin D which ↑intestinal absorption of Ca 2+ and PO4
* rely on G-protein coupled membrane receptor – sense extracellular calcium levels
Calcitonin (produced by parafollicular C cells) opposes the effects of PTH on calcium

1. Inhibits osteoclastic activity
2. Inhibits Ca2+ reabsorption from the renal tubules
3. Inhibits calcium absorption by the intestines
4. Inhibits phosphate reabsorption by renal tubules (mirrors PTH)

7 Am J Surg. 2006 Mar;191(3):418-23.
8 World J Surg. 2009 Mar;33(3):412-6.

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HYPERPARATHYROIDISM
PRIMARY HYPERPARATHYROIDISM
Definition:
Primary hyperparathyroidism is characterized by elevated or inappropriately normal PTH levels in the presence of hypercalcemia
Epidemiology & Risk Factors

- RF: Females (F:M = 4:1), older age, exposure to low-dose therapeutic radiation, familial predisposition
- Present in almost all patients with MEN 1 and 25% of patients with MEN 2A (commonly present with 4 gland hyperplasia)
Etiology
- Parathyroid adenoma (80%)
- 4-gland hyperplasia (15%)
- Multiple adenomas (4%)
- Parathyroid cancer (1%)
- Classic pentad of symptoms
▪ Kidney stones (20% - 25%) – calcium phosphate / oxalate*, nephrolithiasis (<5%)
▪ Painful bones – osteopenia / osteoporosis**, osteitis fibrosa cystica***
▪ Abdominal groans – peptic ulcer disease, acute pancreatitis, cholelithiasis, constipation
▪ Psychic moans – depression, cognitive dysfunction, psychosis
▪ Fatigue overtones + muscle weakness
- Most patients now are minimally symptomatic or asymptomatic – incidental finding of raised calcium on routine investigations
EXTRA INFORMATION
* PTH increases renal Ca 2+ reabsorption but in setting of primary hyperPTH, serum Ca 2+ concentration increases and the filtered load also
increases eventually overwhelms the reabsorptive capacity of the distal tubules which leads to increased urinary Ca 2+ excretion
** Primary PTH affects cortical bone more than cancellous bone (catabolic effects of PTH more common in femoral neck and distal radius as
compared to lumbar spine)
***osteitis fibrosa cystica resulting from excessive osteoclastic activity. Clinical presentation includes subperiosteal resorption of phalanges (XR
hands), salt and pepper appearance of skull (pepper-pot skull), tapering of distal clavicles, rugger jersey spine (XR spine). It can also be a/w
brown tumour – masses produced by cystic enlargement of bones with area of fibrosis and organized haemorrhage.
Investigation
Biochemical Diagnosis
- ↑total serum Ca2+ (> 10.5mg/dL / 2.62mmol/L)
- ↑PTH or high normal (non-suppressed) PTH
- ↓PO4- (< 2.5mg/dL), Cl- : PO4- > 33
- ↑ALP – increased ALP in bone are a/w increased osteoblastic activity and high bone turnover (i.e. primary hyperPTH)
- 24 hour urinary calcium and creatinine (expect ↑urine Ca 2+ (or normal)) – to rule out familial hypercalcemic hypocalciuria (FHH)
- Mild hyperchloremic metabolic acidosis
Localization Study
- Sestamibi-technetium 99m scan (Tc99mMIBI) with single photon emission CT (SPECT) + ultrasound neck – localize
adenoma (if findings are discordant then consider 4D-CT or MRI)
Others
- Bone Mineral Density Test
- ECG

421
Management
Indication for Surgery

- Symptomatic patients
- Asymptomatic – serum calcium >1.0 mg/dL (above the upper limit of normal), GFR <60ml/min, BMD T-score <-2.5, Age <50yr
The choice of surgery depends on the underlying aetiology of the primary hyperparathyroidism. The choice of focused or bilateral
neck exploration is determined by pre-operative localization studies.
- Single Adenoma (80%) – focused parathyroidectomy with intraoperative PTH monitoring

- Multiple Adenoma (10% in patients >60yr) – surgical resection (bilateral neck exploration)
- Parathyroid Hyperplasia (15%) – total parathyroidectomy and auto-transplantation
- PTH cancer (1%) – En-bloc excision (parathyroidectomy & ipsilateral thyroidectomy) ± lymph nodes
For patients undergoing parathyroid surgery, pre-operatively, a large bore IV cannula should be set to allow for blood taking (pre-op
baseline PTH and intraop PTH at 10mins post excision). Biochemical success refers to a drop of 50% or more in iPTH level from
baseline (Miami Criteria) indicates successful exploration.
For patients who fail to achieve 50% drop in PTH level, consider bilateral neck exploration (i.e. trachea-oesophageal groove, thymus,
within the thyroid, carotid sheath). 4 ways to identify the parathyroid gland, (1) colour (golden yellow / tan, homogeneous colour), (2)
location (found in expected locations), (3) weight (parathyroid sink in saline solution while fat globules float) and (4) presence of
sentinel fat pad
Complications
- Failure to locate diseased parathyroid (1-2%), resulting in persistent hyperparathyroidism (1-5%)
- Neck hematoma (0.3-1%)
- Transient / Permanent VC palsy (RLN injury)
- Hypoparathyroidism (unlikely in focused parathyroidectomy)
- Hypocalcemia due to loss of PTH stimulation and ‘hungry bone syndrome’
Prognosis
The benefit of surgical management of primary hyperparathyroidism includes improvement in renal function, bone density, quality of
life, reduction in cardiovascular events. For there to be a biochemical cure, patients should have normal calcium level 6 months post-
operatively.
EXTRA INFORMATION
Familial Hypocalciuric Hypercalcemia (FHH)

The 2 most common causes of PTH-dependent hypercalcaemia are primary hyperparathyroidism and FHH. To differentiate the 2 conditions,
obtain a urinary calcium level; a low urine calcium level with positive family history suggests FHH, while an elevated urine calcium level suggests
primary hyperparathyroidism. If primary hyperparathyroidism is suspected, proceed to preoperative imaging to localize hyperfunctioning
parathyroid
FHH is an AD condition (chromosome 3) with 100% penetrance. It involves a defect in the PTH receptor in the distal convoluted tub ule of the
kidney causing resorption of calcium (inactivating mutation in the calcium sensing receptor gene (CaSR) gene). Patients will present with lifelong
hypercalcemia not corrected with parathyroidectomy (Ca 2+ generally not that high).
Investigations: ↑Ca2+, normal PTH, ↓24hr urine Ca 2+, (<100mg/24hr), ↓urine Ca:Cr clearance ratio (< 0.01, reference value is 0.6).
Management: No treatment required as patients are mostly asymptomatic
Parathyroid Cancer
PTH cancer is a rare entity that accounts for less than 1% of primary hyperparathyroidism. Patients are usually diagnosed in the 6th - 7th decade.
Patients present with a palpable neck mass (parathyroid gland), dysphagia and choking (30%), hoarseness or vocal cord paralys is (30%) and
dyspnea. Severe bone loss, pathological fractures. Rule of >3: serum calcium > 3mmmol/L and parathyroid gland > 3cm
Investigations: Serum Ca 2+ , ↑↑ PTH (5x normal), ↑ALP

Management: En-bloc excision (parathyroidectomy & ipsilateral hemithyroidectomy) ± lymph nodes
Prognosis: 5% have LN metastases, 33% have distant metastases at presentation (lung most common)
Recurrence: 50%, mortality due to hypercalcemia
SECONDARY HYPERPARATHYROIDISM
Secondary hyperparathyroidism is due to physiological / appropriate secretion of PTH by normal PTH gland in response to
perturbations in calcium homeostasis (i.e. low Ca 2+). There is asymmetrical enlargement and nodular hyperplasia of the PTH glands.
Pathophysiology

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1. CRF leads to impaired absorption of urinary calcium, leading to hypocalcemia and thus stimulating PTH secretion
2. CRF leads to impaired vitamin D activation, with reduced 1-25 dihydroxy-vitamin D there is direct activation of PTH synthesis
3. Hyperphosphatemia (common in renal failure) contributes to hypocalcemia (calcium phosphate) and inhibits renal activation
(hydroxylation) of 25-hydroxyvitamin D
4. PTH resistance to fibroblast growth factor 23
Investigations
- Blood Tests – ALP, Calcium Panel, PTH, TFT, PO4, Vitamin D
+/- Imaging – ultrasound thyroid (r/o concomitant thyroid nodules)
-
Management
- Low-phosphate diet (avoid beer, beef liver, milk, cheese), phosphate binders, calcium supplement, vitamin D, cinacalcet
- 95% do not need surgery
- Surgical Indication: bone pain (most common indication), calciphylaxis, fracture, pruritus, (PTH > 80), patients will require total
parathyroidectomy with autotransplantation (bilateral neck exploration +/- thymectomy) OR subtotal parathyroidectomy
TERTIARY HYPERPARATHYROIDISM
Tertiary hyperparathyroidism occurs with long-term secondary hyperparathyroidism where the parathyroid gland develops
autonomous hypersecretion.
Pathophysiology
Insensitivity of PTH to calcium and skeletal resistance to PTH resulting in PTH hyperplasia & autonomous PTH secretion. This leads
to hypercalcaemia (similar lab values to primary PTH)
Etiology
- Chronic Renal Failure
- Hyperparathyroidism in patients who have had renal transplant
Management
- Surgical Indication: symptomatic patient (bone pain, fractures, etc), calciphylaxis*
- Subtotal or total parathyroidectomy with autotransplantation** and upper thymectomy
EXTRA INFORMATION
*Calciphylaxis develops when circulating calcium and phosphate levels lead to calcium-phosphate precipitation which compromises the
microvasculature. This leads to calcification of cutaneous arterioles with associated subcutaneous tissue inflammation which can lead to
progressive cutaneous ischemia. As such, patients present with painful erythematous skin lesions on the distal extremities / trunk which can
progress to frank gangrene.
** subtotal parathyroidectomy (3 glands) for patients on the renal transplant list. total parathyroidectomy (4 glands) for patients not on the renal
transplant list. Auto-transplantation involves slicing a parathyroid gland in ½ (½ sent for histology and ½ for auto-transplantation), ½ for auto-
transplantation is sectioned/morselized into 1mm x1mm pieces, inserted into sternocleidomastoid or deltoid muscle and stitched up. This
minimizes the chances of graft malfunction.
Biochemical Abnormalities in Hyperparathyroidism

Serum Calcium PTH Vitamin D Phosphate
Primary Hyperparathyroidism ↑ ↑ ↑ ↓
Secondary
N or↓ ↑ ↓ ↑ or ↓
Hyperparathyroidism
Tertiary Hyperparathyroidism ↑ ↑↑ ↓ ↑
Parathyroid Cancer ↑↑ ↑↑ N or ↓
Metastases ↑** ↓ ↓ or N N or ↑
** Hypercalcemia is caused by bone resorption from metastatic tumour deposits which can lead to osteoporosis
HYPERCALCEMIA
Calcium Function
- Intracellular Calcium: Mediator of intra-cellular signals (second messengers in signal transduction) – regulate cell division,
motility, membrane trafficking and secretion
- Extracellular Calcium (10,000 x higher than intracellular levels):
▪ Synaptic transmission in nervous system – Ca2+ ↓ = Na+ permeability ↑and threshold will ↓ thus ↑nerve and muscle
activity,
▪ Muscle contraction – excitation-contraction coupling

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▪ Secretion of other hormones
▪ Coagulation – calcium is an essential blood clotting factor
▪ Bone Formation
Differential Diagnosis for hypercalcemia

- Hyperparathyroidism (Primary, Secondary or Tertiary)
- Malignant Disease – i.e. multiple myeloma
- Granulomatous Disease - i.e. sarcoidosis
- Familial (or acquired) hypocalciuric hypercalcemia
- Exogenous calcium intake (antacid medication)
- Excess intake of Vitamin D
Management
- For asymptomatic / mildly symptomatic patients, advise to avoid thiazide diuretics, lithium carbonate, volume depletion, reduce
prolonged bed rest or inactivity, and a high calcium diet (>1000 mg/day)
- Severe / symptomatic hypercalcaemia (> 3.5mmol/L), patients usually dehydrated

▪ Normal Saline hydration (initial therapy – onset hours) with the aim PU >100ml/hr
▪ Diuresis with Furosemide (increase renal calcium clearance)
▪ Calcitonin (onset: 4-6hrs)
▪ Bisphosphonate – i.e. IV zoledronic acid or pamidronate (onset 24-72hours) – used if due to excessive bone resorption –
i.e. malignancy-related hypercalcemia, hypervitaminosis D
▪ Glucocorticoid (onset 2-5days) – used if due to lymphoma, sarcoidosis or other granulomatous disease
▪ Dialysis with low calcium dialysate fluid (onset: hours)
EXTRA INFORMATION
Pathophysiology of Thiazide
Thiazide (high dose) a/w hypercalcemia, hyponatremia and hypokalemia. Thiazide inhibits the Na+/Cl- cotransporter in
the distal tubule leading to increased excretion of Na and H20 as well as K+ and H+ ions. This also increases distal tubular
Ca2+ reabsorption, which causes both hypercalcemia and hypocalciuria. This increase in serum Ca 2+ will result in appropriate
suppression of parathyroid hormone (PTH) levels.

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ADRENAL TUMOURS
Classified as either functional (hormone-secreting) or silent and as either benign or malignant
ANATOMY
- The cells of the adrenal cortex are derived from mesoderm and cells of the adrenal medulla are derived from neural crest cells
- Located superomedial to the kidney and lateral to the IVC (right) and aorta (left)
- Right Adrenal (triangular) resembles a ‘top hat’ while Left Adrenal (crescentic) resembles a ‘cocked hat’
- Arterial supply: superior (from inferior phrenic), middle (from aorta) and inferior (from renal artery) adrenal artery
- Right adrenal vein drains into IVC
- Left adrenal vein drains into left renal vein*
* Left renal vein can be ligated near IVC as it has adrenal, lumbar and gonadal vein collateral
PHYSIOLOGY (GFR – MGS/ACS)

- Adrenal Cortex ~ 80-90% of adrenal gland
▪ Zona Glomerulosa – Mineralocorticoid (i.e. aldosterone) – primary regulators are circulating levels of ANG II & K+
▪ Zona Fasciculata – Glucocorticoid (i.e. cortisol) – stimulated by ACTH from anterior pituitary / CRH from hypothalamus
▪ Zona Reticularis – Sex Hormones (i.e. androstenedione, DHEA) – stimulated by ACTH from anterior pituitary / CRH from
hypothalamus
- Adrenal Medulla
▪ Chromaffin Cells – produce Catecholamines (i.e. epinephrine and norepinephrine*) – stimulated by preganglionic
sympathetic fibres (Ach release)
- Alpha 1 receptor – Peripheral vasoconstriction | ↑IP3
- Beta 1 receptor – Increase heart rate and contractility | ↑cAMP
- Beta 2 receptor – Relaxation of smooth muscles, vasodilatation, insulin secretion | ↑cAMP
* Norepinephrine stimulates B1 adreno-receptor which utilizes the cAMP signal transduction pathway. Stimulation of these receptors
by norepinephrine causes increase in cAMP concentration within cardiac myocytes
Biosynthetic Pathway of the Adrenal Cortex9
9 FIRSTAID for the USMLE STEP 1 – pg. 312

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ADRENAL INCIDENTALOMA
This is defined as an asymptomatic adrenal mass ≥ 1cm detected on imaging.
Epidemiology – incidence increases with age, 3% at age 50 increasing to 10% in elderly
- Benign (non-secreting): adenoma, nodular hyperplasia, myelolipoma
- Benign (secreting): aldosterone producing (conn’s) tumour, cortisol secreting (cushing) tumour, pheochromocytoma,
- Malignancy (0.1%): adrenal cortical carcinoma (ACC), adrenal metastasis
Investigations
- Evaluate functional status
▪ Aldosterone Secreting Tumours – plasma renin activity, plasma aldosterone concentration & aldosterone / renin ratio
▪ Cortisol Secreting Tumours – serum ACTH, 24 hour urine cortisol or low dose (1mg) dexamethasone suppression test
▪ Pheochromocytoma – 24 hour urine catecholamines and metanephrines or plasma metanephrines
- Evaluate likelihood of malignancy
▪ CT Adrenals (non-contrast or contrast-enhanced)
- Benign – lesion < 4cm, ≤ 10 Hounsfield Unit (HU), Relative washout > 40%, Absolute washout > 60%
▪ Biopsy of Adrenal Nodule (not performed, unless adrenal mass is secondary to metastatic disease and histology is required
to guide subsequent adjuvant therapy)
Management10
- Functional Adrenal Nodule (any size) → surgical resection (i.e. unilateral adrenalectomy)
- Non-functional Adrenal Nodule
▪ > 6cm → surgical resection (i.e. unilateral adrenalectomy)
▪ 4 - 6cm → debatable but most centres will offer surgical resection (any suspicion imaging characteristics)
▪ < 4cm → conservative management
▪ If lesion noted to be increasing in size on follow-up imaging → surgical resection (i.e. unilateral adrenalectomy)
EXTRA INFORMATION
Hounsfield Unit: assessment of tissue density
Contrast (Relative / Absolute) Washout:

- Adenoma takes up contrast rapidly but has rapid loss of contrast.
- Malignant lesions take up contrast rapidly but has a slower washout of contrast medium
- Measurements (1) before injection, (2) at 60sec, and (3) at 10 / 15 mins after contrast injection (assess relative washout)
Follow-up for Adrenal Incidentaloma

- Sub-centimetre lesions (< 1cm) → no further investigations (unless functional adrenal tumour)
- Benign Lesion (Homogenous, ≤ 10HU, < 4cm) → no further imaging required
- Indeterminate Lesion (with negative hormonal work-up) → (1) re-image with another modality (i.e. MRI / CT with contrast, 18F-FDG-PET),
(2) interval imaging in 6 – 12 months or (3) surgery
Adrenocortical Carcinoma (ACC)

- Rare tumour, 60% presents with symptoms of hormone excess
- Measure sex hormones and steroid precursors if imaging suggestive of adrenocortical carcinoma
- CT Features – Large (>6cm) lesion, irregular borders, inhomogeneity, calcification, delayed contrast washout
- More than 90% are > 6cm on presentation, > 40% present with metastatic disease at tumour of diagnosis
- 1 year survival ~ 10%)
- Median survival ~ 22 – 47 months, 5 yr survival for stage I and II tumours are 40 to 60%
Adrenal Metastases
- In setting of other malignancy, 30-75% of adrenal masses may be a metastasis – 1st step involves hormone evaluation for a functional
adrenal mass (i.e. r/o pheochromocytoma)
- CT Features – bilateral disease, irregular borders, heterogeneity, > 20 HU and delayed contrast washout
10 Eur J Endocrinol. 2016 Aug;175(2):G1-G34. [Important Paper]

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FUNCTIONAL HORMONE SECRETING ADRENAL TUMOURS
HYPERALDOSTERONISM
Primary hyperaldosteronism is first described by Jerome Conn in 1955
Aetiology:
- Primary – adrenal hyperplasia – 70%, adenoma (Conn’s Syndrome – 25%), carcinoma – 5% (renin independent)
- Secondary – extra-renal disorders – i.e. RAS, CHF, Cirrhosis, Nephrotic Syndrome (renin dependent)
Clinical Features:
- Hypertension (11% of patients with resistant HTN, refractory to 3 drugs)11
- Hypokalaemia (classically, often normal) – aldosterone increase K+ secretion
- Others – severe muscle weakness, paralysis, paraesthesia, polyuria, polydipsia, metabolic alkalosis, mild hyperNa +
Investigations
Indications
- Patients with hypertension on ≥3 anti-hypertensive meds +/- hypoK +/- adrenal incidentaloma +/- obstructive sleep apnea
- Patients with young onset (< 40 years old) HTN
- Patients with family history of early onset HTN or family history of primary hyperaldosteronism
Screening Tests
- Plasma Renin activity (PRA) – undetectable renin and aldosterone>30 ng/dL = primary aldosteronism
- Plasma Aldosterone concentration (PAC)
- Calculate the Aldosterone : Renin ratio (ARR)
Confirmatory Test
- Salt Suppression Test / Saline Infusion Test (performed for patients with decreased renin and increased aldosterone)
- Imaging → CT Adrenal (detect if unilateral or bilateral disease)
▪ If inconclusive → use adrenal vein sampling to test for lateralisation
Management
- Unilateral Lesion → adrenalectomy
- Bilateral hyperplasia → mineralocorticoid receptor antagonist (i.e. spironolactone or eplerenone)
Adrenal Anatomy
11 Lancet 2008;371:1921

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HYPERCORTISOLISM (CUSHING SYNDROME)
Cushing Syndrome is described by Harvey W. Cushing in 1932
Aetiology:
- Iatrogenic – supraphysiologic doses of exogenous glucocorticoids
- Cushing’s Disease (60-70%) – pituitary adenoma or hyperplasia
- Adrenal Tumour (15-25%) – adrenal hyperplasia (usually bilateral), adenoma or carcinoma
- Ectopic ACTH (5-15%) – Small cell lung cancer (~50%), malignant thymic tumours (~20%),
medullary thyroid cancer, pheochromocytoma, neuroendocrine tumour of pancreas/gut
(carcinoid)
Clinical Manifestations:12
- Nonspecific: glucose intolerance, DM, HTN, obesity, oligomenorrhea, osteoporosis
- More specific: central obesity w/ extremity wasting, dorsocervical fat pads, rounded facies
- Most specific: spontaneous bruising, proximal myopathy, wide striae, hypokalemia
- Others: depression, insomnia, psychosis. Impaired cognition, facial plethora, acne, hirsutism, hyperpigmentation (if ↑ACTH),
fungal skin infection, nephrolithiasis, polyuria
Investigations:
Indications
- Patients with cushing syndrome with adrenal incidentaloma or with clinical features of hypercortisolism (exogenous intake of
glucocorticoids are excluded)
Screening Tests – establish diagnosis of hypercortisolism (require 2 positive tests)

- 24hour urinary free cortisol (UFC)
- Low-dose dexamethasone suppression test* (2 options)
▪ Overnight low-dose DST = 1mg at 11pm with 8am serum cortisol level or
▪ 48hr Low dose DST = 0.5mg q6h x 2d with 24hr UFC
- Late night (11pm) salivary cortisol**
Localization Test – ACTH independent or ACTH dependent

- Serum basal ACTH level – Low (<5pg/ml, ACTH independent) or Normal / High (>20pg/ml, ACTH dependent)
ACTH Independent Test (low ACTH) → proceed with CT/MRI adrenal
ACTH dependent Test (normal / high ACTH) → proceed with high-dose DST or CRH test
- Suppressed 8am cortisol (<5mcg/dL) or suppressed urinary cortisol → proceed with gadolinium enhanced pituitary MRI
▪ Positive → likely Cushing disease* (confirm with CT head / MRI head)
▪ Negative → bilateral inferior petrosal sinus venous sampling (BIPSS)
- Failure of suppression of serum or urinary cortisol → likely ectopic ACTH (search for a source, i.e. small cell lung CA)
* Cushing Disease – mostly micro-adenomas, most tumours can be removed via trans-sphenoidal approach, if unresectable then radiotherapy
Management:
- Cushing Disease → Trans-sphenoidal resection of ACTH producing pituitary tumour
- Ectopic ACTH → Identify source and resection of primary lesion

- Medical Management of Cushing Syndrome → Ketoconazole ((inhibitor of cholesterol desmolase, enzyme that catalyses the 1 st
step in the biosynthesis of adrenocortical steroids)
- Primary Adrenal Hyperplasia → bilateral adrenalectomy
- Cortisol Secreting Adrenocortical Tumour → unilateral adrenalectomy
Complications
- High risk of venous thromboembolism
- Adrenal Insufficiency → require replacement of glucocorticoid and mineralocorticoid
- Risk of wound infection, poor wound healing
12 Pocket Medicine 4th Edition: Cushing’s Syndrome (hypercortisolism) – section 7-7

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PHEOCHROMOCYTOMA
The first successful operation for pheochromocytoma was reported in 1926 by Cesar Roux in Switzerland and CH Mayo in USA
Definition
Catecholamine-secreting tumour that arises from chromaffin cells (adrenal medulla) and/or the sympathetic ganglia (extra-adrenal
/ paraganglionic tissue)
Clinical Features: (5Ps) – symptoms may be constant or intermittent

- Pressure – HTN (frequently episodic) – due to epinephrine secretion
- Palpitation – tachycardia, tremor
- Pain – Headache, Chest Pain – associated with N/V
- Perspiration (profuse)
- Pallor (vasoconstrictive spell)
Rule of 20 (initially classified as 10% but now more likely 20%)

- 20% Malignant
- 20% Children
- 20% Bilateral or multiple
- 20% Multifocal
- 20% Extra-adrenal* – i.e. organ of Zuckerandl at inferior aorta near bifurcation / origin of IMA, bladder dome, along
sympathetic chain, heart, posterior mediastinum, carotid bodies
- 25% Familial (MEN type 2, Von Hippel-Lindau, Neurofibromatosis type 1, Tuberous sclerosis, Sturge-Weber Syndrome)
* In adults, 30-40% of ectopic pheochromocytoma are malignant compared with <10% of adrenal pheochromocytoma
Investigations:
Diagnostic Test
- 24-hour urinary fractionated metanephrines and catecholamines & vanillylmandelic acid (VMA)
- Plasma free metanephrines (stop smoking 4 hours prior) – most sensitive
- Plasma free catecholamines (i.e norepinephrine / epinephrine)
- Clonidine suppression test – failure of catecholamines level to fall suggestive for pheochromocytoma
Localization Test
- CT/MRI Adrenal or MIBG scintigraphy ( 123I-meta-iodo-benzyl-guanidine) or PET
Management:
- Alpha Blockade (i.e. phenoxybenzamine – PO 10mg BD) – 2-4 weeks prior to surgery till BP and symptoms controlled
- Beta Blocker (i.e. propranolol / metoprolol) after complete alpha-adrenergic blockade*** – 1 week prior to surgery
- Calcium Channel Blockers – used as additional therapy if BP not well controlled (aim BP 130/80, HR 60-70)
- IV hydration – 2 days prior to surgery (typically patients are volume contracted)
- Adrenalectomy (Laparoscopic or Open) – ensure minimal tumour manipulation (avoid tumour seeding and HTN crisis)
*** Must not administer before alpha-blockers, avoid unopposed alpha receptor mediated vasoconstriction with risk of malignant hypertension. Started
1 week prior to surgery to minimize risk of cardiac arrhythmias
Complications
- Hypotension (sudden decrease in circulating catecholamines)
- Hypoglycaemia (rebound hyperinsulinemia)

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14. UROLOGY
APPROACH TO GROSS HAEMATURIA13
DEFINITION
- Gross haematuria = visibly bloody or brown urine
▪ Gross haematuria with passage of clots, likely from lower urinary tract source
- Microscopic haematuria = ≥ 3 RBC per high-powered field (in 2 of 3 properly collected (freshly voided, clean-catch, midstream
urine) urinalysis specimens)14
Functions of the urinary system

- Storage and excretion of urine
- Hormone production (i.e. renin, erythropoietin, 1-25-dihydroxycholecalciferol)
- Electrolyte maintenance
- Acid-Base maintenance
- Fluid maintenance
- Questions you want to answer:
▪ What is the underlying aetiology?
▪ What is the time frame? – disease progression / symptomatology
▪ Are there any complications from the disease – local / regional / systemic
▪ Thus far, any treatment instituted for the patients?
▪ Any complications from the treatment?
▪ What are the outstanding issues?
History
1. Is the patient experiencing macroscopic or microscopic haematuria?e
- Haematuria may be visible and reported by the patient (macroscopic haematuria) or invisible and detected on dipstick
(microscopic haematuria)
2. Is this truly pathological gross haematuria?
If patient presents with red/brown urine but have negative dipstick

- Food dye – anthocyanins (beetroot) – red urine
- Drugs – levodopa, senna (orange), rifampicin (orange), phenolphthalein
- Others – porphyria, alkaptonuria, bilirubinuria
Rule out benign causes of haematuria

- Menstruation
- Exercise-induced myoglobinuria (vigorous exercise)
- Sexual Intercourse
- Trauma
* Urinalysis is best obtained when the other causes of bleeding has ceased
If patient present with red urine and have positive dipstick

- Can be true haematuria or false-positives (myoglobinuria or hemoglobinuria)
- Theoretically can centrifuge the urine to determine if the red/brown colour is in the urine sediment (haematuria) or the
supernatant (not haematuria)
13 uptodate: Etiology and evaluation of hematuria in adults

14 Am Fam Physician.2001;63:1145-1154
14. Urology_Last Updated 3rd June 2020

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3. Are there any clues from history to suggest a particular aetiology?
When during urination does blood appear?

- Initial – disease in the urethra, distal to the UG diaphragm
- Terminal – disease near bladder neck or prostatic urethra
- Throughout – disease in the bladder or upper urinary tract
Lower Urinary Tract Symptoms [FUN DISH]

- Storage problem – irritative symptoms: frequency, urgency/urge incontinence, nocturia
▪ Possibly: UTI, stones, bladder tumour
- Voiding problem – obstructive symptoms: terminal dribbling, intermittency/incomplete emptying, poor stream,
straining to pass urine, hesitancy
▪ Possibly: BPH, prostate cancer, urethral stricture
- Others – polyuria, oliguria, urethral discharge
Upper Urinary Tract Symptoms

- Loin pain / tenderness: renal infection, infarction, rarely obstruction and glomerulonephritis
- Severe loin pain with radiation to iliac fossa, groin and genitalia: acute obstruction of the renal pelvis or ureter by
calculus or blood clots
Painful vs. painless haematuria

- Classically, painless gross haematuria in a patient > 35 years-old is the hallmark of malignancy
- Dysuria suggest on-going infection/inflammation
4. Does the haematuria represent extra-glomerular or glomerular bleeding?

▪ Any frothy urine – suggests glomerular bleeding
▪ Any clots present – suggests extra-glomerular bleeding, where heavy focal bleeding sheds sufficient whole blood into the
urine in amounts sufficient to support clot formation, as opposed to glomerular bleeding which is typically a diffuse capillary
process where small amounts of blood are added to relatively large volumes of glomerular filtrate and thus unlikely to form
clots.
▪ What is the colour of the bleeding?
Extraglomerular bleeding Glomerular bleeding

Colour (if macroscopic) Red or pink Red, smoky brown, or "Coca-Cola"
Clots May be present* Absent
Proteinuria May be >500 mg/day
<500 mg/day
(time of onset is impt)** > 2+ on urine dipstick
RBC morphology Normal (isomorphic) Some RBCs are dysmorphic
RBC casts Absent May be present***
* Gross haematuria with the passage of clots indicates a lower urinary tract source (extra-glomerular)
** Proteinuria needs to be assessed temporally with hematuria. If the onset is concurrent and proteinuria is high, it is indicative of glomerular
bleeding, though significant overlap with non-glom bleeding exists. However, if the patient has had previous proteinuria before onset of
hematuria, eg. from CKD, then new onset hematuria should warrant a full evaluation for both extraglom and glomerular causes of hematuria.
*** The presence of red cell casts is diagnostic of glomerulonephritis or vasculitis
5. Severity
▪ Is the haematuria transient or persistent? (1/3 of patients with initial positive urinalysis have transient haematuria)15
▪ Symptoms of anemia – pallor, exertional chest pain, palpitations, SOP, giddiness, fatigue
▪ Any concomitant renal impairment – amount of urine, any fluid overload status
6. Red Flags for malignancy

▪ Male gender
▪ Age (>35yr)
▪ Past or current smoker
▪ Occupational exposure – chemicals or dyes
▪ History of exposure to carcinogenic agents or chemotherapy
▪ History of analgesic abuse
▪ History of gross haematuria, urological disease, irritative urinary symptoms, pelvic radiation, chronic UTI, chronic indwelling
FB
15 Mayo Clin Proc. 2013 Feb;88(2):129-38.

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- Check patient’s vitals – fever (pyelonephritis), HTN (glomerulonephritis)
- Any Signs of Anemia – i.e. conjunctival pallor
- Heart – new murmur (endocarditis)
- Lungs – crackles, rhonchi (? lung and kidney involvement)
- Abd – loin tenderness, renal mass, bruit (renal ischemia), palpable bladder, suprapubic mass
▪ Are the kidneys ballotable, is the bladder percussible?
- Extremities – edema (nephrotic syndrome), rashes (HSP, SLE, vasculitis), joint pain
- Scrotum – varicocele on the left (may have RCC of the left kidney with extension of tumour into renal vein, blocking the testicular
vein at where it drains into the left renal vein)
- External genitalia – blood from urethra, any blood clots, shape of blood clot
- Digital rectal exam – enlarged / nodular prostate (BPH versus cancer)
Aetiology Relevant Significant History
Trauma - Hx of urinary catheterisation, flexible cystoscopy, TURP
- Cystitis, Prostatitis – change in frequency, urgency, nocturia (irritative symptoms), dysuria, urethral discharge
Infection
- Recent travel history – areas endemic for schistosomiasis or tuberculosis (TB)
- Red flags for malignancies, any local-regional complications, metastatic & constitutional symptoms
- Kidney – APKD, RCC, Renal vein thrombosis
Tumours - Ureters –TCC
Post-renal
- Bladder – bladder tumour (i.e. TCC)
- Prostate – Benign Prostate Hyperplasia, Prostatic cancer
BPH - Advanced age presenting with concurrent voiding problems (i.e. hesitancy, dribbling, poor stream)
- Nephrolithiasis (kidney stones)
Stones - Ureterolithiasis (ureter stones) – Unilateral flank pain radiating to the groin
- Cystolithiasis (bladder stones)
Brief screen for glomerulonephritis – usually microscopic but can also be gross
- Goodpasture Syndrome – RPGN (haematuria, proteinuria) and pulmonary haemorrhage (haemoptysis) –
Anti-GBM
absence of skin and eye findings are diagnostic clues
- Wegner’s Granulomatosis – cANCA
- Microscopic Polyangiitis – pANCA
ANCA associated
- Eosinophilic Granulomatosis with Polyangiitis (Churg-Strauss)
vasculitis
- Polyarteritis Nodosa – systemic vasculitis of small and medium sized arteries, affects every organ except
lungs, a/w Hep B in 10-30% of patients, can also present with abdominal pain mimic mesenteric ischemia
- IgA Nephropathy (Berger Disease)* – Young male with episodic gross haematuria, 1-2 days after URTI
(synpharyngitic), (normal C3)
Renal Immune Complex - Acute Post-Strep GN (APSGN) – Young child with fever, malaise, periorbital edema, HTN, smoky urine and
– renal limited
oliguria beginning 2 weeks after a streptococcal pyogenes infection, (low C3, ↑(ASO) Anti-streptolysin-O)
MPGN – variable clinical presentation
-
Immune Complex SLE (esp. type III, IV) – read 2012 SLICC SLE Classification
-
– systemic related HSP – painless palpable purpura, arthritis/arthralgia, abdominal pain, renal disease (a/w IgA nephropathy)
-
vasculitis IE – read Duke’s Criteria
-
Alport’s Syndrome – b/l SNHL + ocular abnormalities + ocular abnormalities (lens and cornea) [assess family
-
Others (usually history]
asymptomatic) - APKD – family history, bilateral flank mass, insidious onset of HTN
- Thin Basement Membrane Disease* – family history
- Bleeding Disorders
Others
- Drugs – i.e. cyclophosphamide – hemorrhagic cystitis
* Most common cause of glomerulonephritis

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INVESTIGATIONS
- Haematuria on repeated urine dipsticks
- Exclude menstruation, infection, trauma → RBC confirmed on urine microscopy, infection absent on culture
- Renal imaging to exclude anatomical bleeding lesions
- If anatomical lesion absent → full assessment and management by nephrologist (i.e. asking qns with regards to features of
significant renal disease, consider possibility of doing renal biopsy)
- Iif anatomical lesion present → full assessment and management by urologist (see below)
Urinalysis = (1) direct visual observation or inspection of urine, (2) urine dipstick, and (3) UFEME
1. Urine dipstick (UC9) – direct counting of RBC/ml of uncentrifuged urine

▪ Tests for: leukocytes, RBC, pH, nitrates, ketones, urobilinogen, glucose, cast, crystals
▪ Gold standard for the detection of microscopic haematuria
▪ Positive dipsticks for blood should get microscopic confirmation (dipsticks are sensitive but not specific, can be true
haematuria or false-positives (myoglobinuria or hemoglobinuria)
▪ If patient presents with red/brown urine but has a negative dipstick, consider other causes:
- Food dye – anthocyanins (beetroot) – red urine
- Drugs – levodopa (red/brown/black), senna (orange), rifampicin (orange), phenolphthalein
- Others – porphyria, alkaptonuria, bilirubinuria
2. Urine Full Examination Microscopic Elements (UFEME)

▪ Test for: WBC/hpf, RBC/hpf, epithelial cell, casts, crystals, other formed elements
▪ Confirm presence of red blood cells and casts
▪ The absence of RBCs / RBC casts despite a +ve dipstick test suggest hemoglobinuria or myoglobinuria
▪ Elevated WBC (pyuria is >5 WBC per hpf), organisms → infection
3. Urine culture and sensitivity

▪ Recommended for exclusion of urinary tract infection prior to evaluation of haematuria
4. Urine cytology for malignant cells

▪ Urine cytology has the greatest sensitivity for carcinoma of the bladder
▪ If malignant or atypical cells are identified, it is recommended to proceed with cystoscopy
5. Urine phase contrast – differentiates glomerular and nonglomerular bleed

▪ Glomerular → casts and dysmorphic RBCs (if associated with protein or renal failure, refer to nephrologist)
▪ Non-glomerular → isomorphic RBCs, proceed with CT urogram + urine cytology + cystoscopy

▪ Not commonly performed
6. Biochemical
▪ FBC – How low is the Hb?, Elevated TW suggest for underlying infection
▪ U/E/Cr – Any renal impairment and electrolyte abn (renal or prerenal dz more likely)
7. Plain KUB
▪ Superiorly, it needs to be above the upper pole of the right kidney (T12), and inferiorly, it needs to show the pubic symphysis
▪ Any kidney, ureteric, bladder stones
8. Ultrasound of the kidneys

▪ Can characterize renal size, mass, presence of any hydronephrosis, renal stones
▪ Lower diagnostic yield as compared to CT urogram
▪ Used for pregnant women
9. Multi-detector CT urogram (CTU) / MR urogram

▪ Recommended for patients with unexplained persistent gross haematuria
▪ Images of the kidney and genitourinary system are obtained in 3 phases
- Non-contrast phase for detection of stones
- Renal parenchymal phase for detection of tumours
- Excretory / Delayed phase
▪ Advantages: Ability to see renal parenchyma tumours (IVU only sees outline)
▪ Disadvantages: Radiation ++ (3 CT scans), contrast allergy, can use MR urogram
10. Intravenous urogram (IVU) or intravenous pyelogram (IVP)

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▪ Distortion of renal OUTLINE and pelvic calyces by RCC, may have specks of calcification
▪ Contrast UPTAKE: present or not (no contrast in obstruction / non-functioning), equal and symmetrical uptake
▪ Configuration of the kidneys eg. Horseshoe kidneys
▪ Stones (filling defect, proximal dilatation, decreased distal passage of contrast) + hydroureter and/or hydronephrosis
▪ Filling defect in bladder due to TCC
▪ Increased residual volume in bladder after micturition due to BPH
Intravenous contrast used to delineate anatomy of the kidneys and urinary system
- Various phases:
▪ Control film – plain KUB (tomogram – zoom into kidneys before contrast)
▪ Nephrogram phase (1 min after contrast) – contrast fills kidney parenchyma so kidneys become more visible 🡪
measure size, outline
▪ Pyelogram phase (3-5 min) – contrast fills calyces & pelvis, can detect dilated calyces/pelvis (hydronephrosis),
any filling defects
▪ Release film (abdominal binder which was placed to slow the flow of contrast into the bladder is released) –
shows ureters, any hydroureter, filling defects → cystogram - any filling defects, abnormal appearance of the
bladder (fir-tree appearance in neurogenic bladder)
▪ Post-micturition – any residual urine in bladder after voiding
- Contraindicated in:
▪ Contrast allergy
▪ Renal impairment (Cr >200)
▪ Patients on metformin (can cause lactic acidosis; patients need to stop metformin 2 days before and after study)
▪ Patients with asthma (given steroids for 3 days before study
▪ Pregnancy: ask LMP
11. Cystoscopy
▪ Recommended for patients with unexplained gross haematuria, passing of blood clots and persistent unexplained
microscopic haematuria
▪ Gold standard for evaluating lower urinary tract
▪ Detection of bladder tumour (IVU may not pick up small tumours <1cm)
▪ Biopsy can be taken at the same time
12. Renal Biopsy

▪ Recommended for patients with glomerular haematuria in the presence of RF for progressive disease such as proteinuria,
elevation in serum Cr concentration and new onset or worsening hypertension
▪ Common findings are (1) normal, (2) IgA nephropathy, (3) thin basement membrane disease, (4) mild nonspecific
glomerular abnormalities and (5) hereditary nephritis (Alport’s syndrome)
▪ NOT INDICATED in patients with persistent isolated non-glomerular haematuria (i.e. no dysmorphic RBC or red cell casts
or proteinuria)

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RENAL CELL CARCINOMA
EPIDEMIOLOGY
- 2-4% of human cancers – Incidence has risen over past 20 years
- Most frequent occurring solid lesion within kidney
- 2:1 male predominance
- Majority present in 5th to 7th decades of life
- Most cases are sporadic, but higher rates seen in families with von Hippel-Lindau disease (VHL) and tuberous sclerosis complex
(TSC)
RISK FACTORS
- Smoking (2x increase in relative risk, and also a/w more advanced disease at presentation)
- Industrial exposure – coke oven workers (cadmium), asbestos, petroleum byproducts
- Prior kidney irradiation
- Family history
▪ Von-Hippel Lindau syndrome (AD) due to mutation of the VHL gene (chr 3p25-26), a/w RCC (40%), renal cysts (75%), cysts
of epididymis and pancreas, cerebellar hemangioblastomas, retinal angiomas and pheochromocytoma (14%)
▪ Hereditary papillary RCC (HPRCC) due to mutation of the MET proto-oncogene on chromosome 7q31 → multifocal bilateral
papillary renal cell carcinomas

- Acquired polycystic kidney disease (secondary to chronic dialysis) – 30x increase in risk, needs yearly ultrasound
PATHOLOGY
- Accounts for 85% of malignant renal tumours in adults
- Malignant tumour arising from the renal tubular epithelium
- Appears well-encapsulated with areas of haemorrhage/necrosis
- Infiltrates locally and by haematogenous spread for metastasis, also direct spread to renal vein and IVC.
- Types of Renal Cell Carcinoma:
Clear Cell Carcinoma Papillary Carcinoma Chromophobe Carcinoma
Accounts for 70-80% 10-15% 5-10%
Proximal tubules Distal tubules Intercalated cells of collecting
Arise from
(often invades renal venous system) (bilateral and multi-focal) tubules
Sporadic or Familial (VHL) MET oncogene
Pathogenesis Loss of multiple chromosomes
Deletion of chromosome 3p Gains of chromosome 7 & 17
Type 1: good
Resistant to chemotherapy and
Prognosis Type 2: poor, a/w advanced stage at Excellent
radiotherapy
presentation.
- Benign
▪ Angiomyolipomas
▪ Renal Cyst – Bosniak classification (septations, calcifications & enhancement) to assess risk
▪ Renal Adenoma / Abscess
▪ Pyelonephritis (acute / chronic)
▪ Renal Oncocytoma – well circumscribed mass with central scar
- Usually unilateral and single, but multiple & bilat oncocytomas can be a/w tuberous sclerosis complex.
- Malignant
▪ Renal Cell Carcinoma
▪ Wilms’ Tumour (nephroblastomas) – typically in children (ages 2 – 4)
▪ Metastasis (lung, breast, GI, prostate, pancreas, melanoma)
▪ Sarcoma
Bosniak classification of renal cysts based on contrast-enhanced CT imaging16
16 "Bosniak classification of renal cysts (illustrations) - Radiopaedia." 26 Dec. 2012, https://radiopaedia.org/cases/bosniak-classification-of-renal-cysts-illustrations.

Accessed 30 May. 2020.

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Type Description Features Workup %
malignant
1 Simple cyst Anechoic, extremely thin walls, no septations, No need for further eval or ~0
no calcifications, no solid components, no monitoring.
contrast enhancement.
2 Minimally May contain thin septa, thin or slight No need for further eval or ~0
complex calcification within cyst wall, but are minimal, monitoring.
with no contrast enhancement.
2F (‘F’ Minimally More complex than Type 2, with increased Requires US/CT/MRI follow up, 5
for complex septa, minimal smooth thickening of wall/septa, around q6/12 (but no strict time
follow (need follow some calcifications, but no measurable contrast frame).
up) up) enhancement, and do not meet criteria of Type
3.
3 Indeterminate Thick, nodular, multiple septa, measurable Partial nephrectomy, or 50

contrast enhancement radiofrequency ablation for poor
surgical candidates.
4 Clearly Solid mass with large cystic/necrotic component Partial or total nephrectomy. ~100
malignant
Initially asymptomatic (may be detected incidentally on imaging studies) – may be incidentally discovered on ultrasound examination
for non-specific symptoms (20%) or features suggesting a paraneoplastic syndrome.
- Symptomatic (local symptoms)

▪ Painless gross haematuria is the most common presenting symptom (50% of cases)-- observed only with tumour invasion
of the collecting system. Severe bleeding can cause clots and lead to ‘colicky’ discomfort.
▪ Historical triad of flank pain, painless haematuria, palpable flank mass (11% of cases), if present, tumour is advanced
- Mass, if present, is firm, homogeneous, non-tender and moves with respiration.
▪ Pathological fracture
▪ Aching loin pain
▪ Episodes of acute pain (from haemorrhage into tumour and sometimes sufficiently serious to present as an emergency)
- Regional Symptoms:
▪ Left varicocele – due to invasion of the left renal vein with tumour and thus obstruction of the left testicular vein at where it
enters the renal vein, and thus fail to empty when the patient is supine.
▪ Extension into IVC can cause (a) lower limb oedema, (b) ascites, (c) liver dysfunction and (d) pulmonary embolism
- Systemic (metastatic) Symptoms

▪ Retroperitoneal lymph nodes (30% have tumour in para-aortic nodes at presentation)
▪ Lungs (cannon-ball mets) / Lymph nodes / Liver / Bones / Brain
- Constitutional Symptoms:
▪ Weight loss, fever – due to tumour necrosis, anemia, and night sweats
- Paraneoplastic syndromes (10-40% of RCC)

▪ Hypertension – due to renin overproduction
▪ Non-metastatic liver dysfunction – Stauffer Syndrome (resolves after tumour removal) → elevation of serum ALP
▪ Hypercalcaemia – due to production of PTH-related protein(PTHrP) / lytic bone mets / increased production of
prostaglandins that promote bone resorption (such patients would respond to NSAIDs)

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▪ Polycythaemia – due to production of erythropoietin (EPO) by the tumour
▪ Cushing Syndrome (corticosteroid synthesis)
▪ Feminization or Masculinization (gonadotropin release)
INVESTIGATIONS
“Evaluation of renal mass requires radiological characterization and assessment for metastatic disease”
Establishing the Diagnosis

1. Imaging – CT Kidneys (alternative, US kidney)
▪ Presumptive diagnosis is made on imaging – a renal parenchymal mass with thickened irregular walls and enhancement
after contrast injection suggests malignancy
▪ CT Kidneys (triphasic) – staging – LN involvement, perinephric extension, Ultrasound of simple renal cyst
renal veins or IVU extension. (Bosniak classification of cystic masses ( I – IV))
▪ Ultrasound – to differentiate cystic from solid renal masses, there are 3 major
criteria: classical cyst will be (i) round and sharply demarcated with smooth
walls, (ii) anechoic, and (iii) strong posterior acoustic enhancement (indicating
good transmission through a cyst). If all 3 criteria are fulfilled, there is no need
for further evaluation. Otherwise, go for CT with contrast.
2. MRI Kidneys
▪ Useful if CT is inconclusive or if contraindication to contrast (eg allergy, poor
renal function)
▪ Most effective in demonstrating presence and extent of renal vein or IVU tumour thrombus
3. Intravenous Urogram (IVU)

▪ Control film gives information regarding position, size and outline of kidneys.
▪ Carcinoma → Mottled central calcification (90% specificity), peripheral calcifications a/w RCC in 10-20% of cases.
▪ Suggestive of renal mass – renal enlargement, displacement of renal pelvis or calyces, irregular renal borders or change in
cortical density.
4. Pathological diagnosis
▪ Historically, percutaneous biopsy not done for resectable lesions due to fears of tumour seeding, however, now the
diagnostic accuracy > 90% with low complication rates (<5%)17
▪ In resectable lesions, a partial or total nephrectomy is often performed, and provides the tissue diagnosis post-operatively
▪ In metastatic lesions, biopsy of the metastatic site is preferred
Staging
1. CT Thorax, Abdomen & Pelvis

▪ Perinephric invasion, adjacent organ invasion
▪ Extension into renal vein, IVC
▪ Retroperitoneal lymph node enlargement
▪ Liver metastases
▪ For lung metastases (cannonball metastases)
2. Bone scan
▪ Indicated in patients with abnormal ALP or bone related complaints with known renal mass
3. MRI with gadaolinium of abdomen and heart

▪ Superior to CT for evaluation of IVC and right atrium involvement
Others
- Urinalysis: Haematuria and proteinuria (significant proteinuria may indicate involvement of renal vein)
- Blood tests: FBC, ESR, RP, Ca/Mg/PO4, LFT (for features suggestive of paraneoplastic syndrome)
STAGING
17 J Urol. 2007 Aug;178(2):379-86.

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18
AJCC 2010 TNM Staging for Renal Cell Carcinoma

Primary Tumour (T Staging) N Staging M Staging
Tx Primary tumour cannot be assessed Nx Mx
T0 No evidence of primary Tumour
T1a Tumour ≤4cm, limited to kidney No No
N0 regional M0 distant
T1b Tumour >4cm but ≤7cm, limited to kidney
LN Mets Mets
T2a Tumour >7cm but ≤10cm, limited to kidney
T2b Tumour > 10cm, limited to kidney
Mets in
T3a Tumour extend into renal veins or perinephric tissues Distant
N1 regional M1
T3b Tumour extends into IVC below diaphragm Mets
LN
T3c Tumour extends into IVC above diaphragm or wall of IVC
T4 Tumour invades beyond Gerota fascia
18 "Renal cell carcinoma | Nature Reviews Disease Primers." 9 Mar. 2017, https://www.nature.com/articles/nrdp20179. Accessed 30 May. 2020.

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MANAGEMENT
Resectable tumours
- Surgery ± Adjuvant Therapy (i.e. IL-2) + Surveillance after resection to detect relapse early
Surgery19
- Laparoscopic versus open methods
- Retroperitoneal versus trans-peritoneal approach
1. Partial nephrectomy: nephron saving, adrenal can be left alone. Requires careful intraoperative examination to exclude
synchronous tumour, otherwise convert to radical nephrectomy.
▪ For tumour ≤7 cm -- T1 disease
▪ For tumours ≤5 cm (T1-T2, N0, M1) both partial and radical nephrectomy provide excellent oncologic results20
▪ For those who need to preserve renal function -- solitary kidney, mult small/bilat tumours, those with or at risk of CKD
2. Total nephrectomy
▪ ≥T2 – primary tumour >7 cm
3. Radical nephrectomy: ligation of renal artery & vein (impt to prevent tumour dissemination at surgery), removal of kidney + Gerota’s
fascia, and occasionally the adrenal gland as well (only if high risk of local invasion of adrenal)
▪ For tumour >7cm
▪ T2 disease -- Gold standard for localised RCC with a normal contralateral kidney, aim for clear margins
▪ In T3/T4 disease, aim for radical nephrectomy and removal of structures affected e.g. adrenal gland + abdominal
lymph nodes ± thrombectomy (involvement of IVC)
▪ For suspected LN involvement
▪ For tumour a/w renal vein or IVC thrombus: also perform thrombectomy
▪ For when there is direct extension into ipsilat adrenal gland: also perform adrenalectomy, also performed for those at risk
of direct extension (includes those with upper pole lesions >4cm or upper-pole non-organ-confined tumour)
Adjuvant chemotherapy
- If patient underwent definitive surgery = no established role for adjuvant therapy
- Currently available cytostatics are ineffective for the treatment of metastasized RCC as response rates are low (5-15%) and most
responses are short lived
Surveillance after resection to detect relapse early21

- Local recurrence with nephron-sparing surgery <6%
- Incidence of contralateral recurrent RCC ~1.2% (reported range: 0.4 – 12.9%)
▪ Tumour stage & ?positive surgical margins – predictors in clear cell RCC
▪ Nuclear grade – predictor in papillary RCC
Patients who cannot undergo resection

- Most small tumours grow slowly and do not become symptomatic or metastasise – reasonable to manage conservatively with
periodic re-evaluation
- Alternatives: (heat) radiofrequency ablation, (freezing) cryotherapy of lesions
Advanced tumours
1. Immunotherapy
▪ High dose interleukin-2 – associated with good results in patients whose tumours respond to treatment, as treatment can
induce long-term remissions without relapse. However, associated with high toxicity and often not tolerable
▪ Cytoreductive nephrectomy performed prior to starting immunotherapy can improve survival (primary tumour acts as an
‘immunologic sink’ of activated immune cells)
2. Molecular targeted therapy

▪ Sorafenib – an inhibitor of tyrosine kinase → blocks intracellular domain of the vascular endothelial growth factor (VEGF)
receptor
▪ Bevacizumab – monoclonal antibody against VEGF
19 uptodate: Definitive surgical management of renal cell carcinoma

20 Eur Urol. 2011 Apr;59(4):543-52. [Important Paper]
21 J Urol. 2005 Feb;173(2):391-4.

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COMPLICATIONS
Nephrectomy Complications
- General anaesthesia – atelectasis, AMI, pulmonary embolism, CVA, pneumonia and thrombophlebitis
- Operative mortality rate is approximately 2%.
▪ Bleeding / Infections
▪ Pleural injuries can result in pneumothorax
▪ Injury neighbouring organs – gastrointestinal organs / major blood vessels
▪ Temporary or permanent renal failure
PROGNOSIS
Stage I (T1N0): >90% 5 year survival
Stage II (T2N0): 75-90%
Stage III (T3N0/N1): 60-70%
Metastatic disease: <10%
EXTRA INFORMATION
Renal Angiomyolipoma
Most common benign tumour of the kidney and composed of blood vessels, smooth muscle and fat cells
Risk Factors
- Can be sporadic or a/w tuberous sclerosis complex (TSC) or pulmonary lymphangioleiomyomatosis (LAM)
▪ TSC is present in about 10% of patients with clinically dx renal AML
▪ TSC-associated AML are often multiple and affect both kidneys
CLINICAL FEATURES
- Most patients with sporadic AML are asymptomatic and usually are incidentally detected on renal imaging
- Complications: Retroperitoneal haemorrhage, Haematuria, Renal impairment
INVESTIGATION
- Imaging Studies – ultrasound, CT, MRI kidneys
▪ Demonstration of fat in the tumour
o Hypoechogenic on U/S
o Low attenuation value on CT
o Bright on T1 images and dark on T2 images on MRI
- Biopsy – image guided percutaneous needle biopsy as alternative to surgical exploration
Management
- Mostly conservative management → repeat imaging studies – yearly to r/o rapid tumour growth
- AML ≤ 3cm and growing → Radiofrequency ablation or Cryoablation

- AML >4cm and with high vascularity – prophylactic surgery to prevent haemorrhage
▪ Nephron-sparing surgery
▪ Selective renal arterial embolization
▪ Radical nephrectomy KIV tumour thrombectomy

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UROLITHIASIS
EPIDEMIOLOGY
- Urinary calculi occur in 1-5% of the population
- Stones may form in the kidney or the bladder – 90% of the calculi are radio-opaque
- 50% of patients with previous urinary calculi have a recurrence within 10 years
RISK FACTORS
- Diet – low fluid, low calcium, high oxalate (spinach, rhubarb), high protein, high sodium, high fructose
- Dehydration – low urine volume
Modifiable
- Massive ingestion of vitamin D or Vitamin C (calcium oxalate stones)
- Milk-Alkali Syndrome – triad:f hyperCa 2+, metabolic alkalosis and AKI, due to repeated ingestion of Ca 2+ & absorbable alkali
- Age (majority occur during the 4 th – 6th decade of life)
- Gender (M:F – 3:1)
- Cystinuria – inherited AR disease
- Inborn error of purine metabolism
Non-modifiable
- Distal renal tubular acidosis (type 1) – hypocitraturia + alkaline urine
- Crohn Disease – hyperoxaluria
- Hyperparathyroidism – primary hyperPTH – hyperCa2+
- Gout – hyperuricosuria
ANATOMY OF THE URETER

- Each ureter is 25cm long and approximately 3mm in diameter
- The ureter is a hollow muscular tube which commences at the renal pelvis, runs on the anterior surface of the psoas major muscle
and terminates at its entry into the bladder
- Plain radiograph:
▪ Ureter exits from renal pelvis (L1 on left, L1/L2 junction on the right)
▪ Runs along tips of the transverse process / medial edge of psoas major
▪ Crosses in front of the sacroiliac joint (at bifurcation of common iliac arteries)
▪ Runs laterally on the pelvic wall towards the ischial spine
▪ Curves anterior-medially to enter the bladder through the back at the vesicoureteric junction
- Points of constriction
▪ Pelvic-ureteric junction (PUJ)
▪ Pelvic brim (near bifurcation of the common iliac arteries)
▪ Veisco-ureteric junction (VUJ) – entry to the bladder
CLASSIFICATION OF CALCULI
Morphology X-Ray Pathogenesis Clinical Features
‘mulberry’ stones
Alkaline urine Causes symptoms when comparatively small owing
Calcium Oxalate (75%) covered with sharp Radiopaque
Hypocitraturia to their sharp surface
projections
Calcium Phosphate Wedge-shaped prism
Radiopaque Alkaline Urine
(10%) (urine crystal)
Struvite Stones (5-10%) Smooth and dirty white Forms staghorn calculus
[Magnesium, Caused by infection with urease (+) bugs (i.e.
Radiopaque Alkaline urine
Ammonium, Coffin Lid Proteus mirabilis, Staphylococcus Saprophyticus,
Calcium Phosphate] (urine crystal) Klebsiella) that hydrolyse urea to ammonia
Hard, smooth, faceted Risk Factor: dehydration, acidic pH
and light brown in colour Strong a/w hyperuricemia (i.e. gout / tumour lysis
Urate Stones (5%) Radiolucent Acid urine
Rhomboid / Rosettes syndrome / Lesch-Nyhan*) or disease with high cell
(urine crystals) turnover (i.e. leukaemia)
Hereditary (AR) in which cystine reabsorbing PCT
Usually multiple stones Radiolucent / transporter loses function leading to cystinuria.
Acid urine /
Cystine Stones (1-2%) Hexagonal Poorly Transporter defect results in poor reabsorption of
metabolic origins
(urine crystal) Radiopaque Ornithine, Lysine & Arginine. Usually, it starts in
childhood. Can form staghorn calculi
Xanthine (rare) Due to inborn error
RARE
Pyruvate Stones (rare) of metabolism
* Lesch-Nyhan Syndrome (XLR): deficiency of the enzyme hypoxanthine-guanine phosphoribosyl-transferase (HGPRT) resulting in hyperuricemia and hyperuricosuria leading to
gout, renal impairment, neurological signs (i.e. intellectual disability, self-mutilating behaviours in boys)
PATHOLOGY
- Cause of stone formation (1) super-saturation (2) infection (3) drugs
- Most important cause of stone formation is urine becoming supersaturated wrt. stone-forming salts, such that they exceed their
solubility, precipitate out of solution and form crystals
▪ Crystals may flow out with urine or become retained in the kidney at anchoring sites that promote growth and aggregation
leading to stone formation
- Urinary tract infections can also cause infection stones – struvite stones (magnesium ammonium phosphate)
▪ Proteus vulgaris infections (urea-splitting bacteria) splits urea into ammonium, generating alkaline urine

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▪ More common in women (more prone to UTI)
▪ Proteus, Pseudomonas, Klebsiella (note: E. Coli is not capable of splitting urea therefore not a/w struvite stones)
- Drug-induced stone – medication or their metabolites can precipitate in urine causing stone formation
- Bacteria can also form nidi for the formation of any kind of stone
Pain
- Typically begins in the early morning and intensifies over 15-30min.
- Develops in paroxysms and related to movement of stones in the ureter
- Obstruction – at pelvic-ureteric junction, in the ureter, at bladder neck (rarely at ext. urethral meatus)
- Ulceration – of calyces, pelvic mucosa or bladder which can lead to haematuria
- Chronic Infection – lead to pyelonephritis, pyonephrosis, urosepsis, kidney failure
Renal stones
- Most often asymptomatic unless the stone gets lodged in the pelviureteric junction (PUJ) causing hydronephrosis and subsequent
infection → pyonephrosis
- Vague flank pain may occur
- Small stones are commonest, but large-branched staghorn calculi may occur and completely fill the pelvis and calyces – if bilateral
kidneys affected leading to chronic renal failure
Ureteric stones
- Even small stones can cause severe symptoms as the ureter is narrow
- Classic ureteric colic pain – severe, intermittent loin-to-groin pain (± to ipsilateral testis/labia)
- Haematuria – gross or microscopic (occur in 95% of patients)
- Can cause upper urinary tract infection (i.e. fever, pain)
- Stone at VUJ – frequency, urgency, dysuria can result
Bladder stones
- May originate in the kidney with enlargement in the bladder – phosphate encrustation OR
- Formed primarily in the bladder
- May be asymptomatic
- Can cause irritative urinary symptoms – frequency, urgency
- Haematuria
- If infection is present – dysuria, fever, etc.
- In treating of bladder stones, also treat underlying cause – i.e. treating BPH if it is causing urinary retention and hence precipitating
stone formation

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History
Chronology of stone events

- Age of 1st stone presentation
- Number and size of stones
- Spontaneous passage vs. need for intervention
- Symptoms during the past episodes
Stone formation (systemic disease / underlying metabolic disorder)

- Crohn’s
- Gout – uric acid stones
- Renal tubular acidosis (type 1, distal) – failure of H+ excretion, alkaline urine 🡪 predispose to stone formation
- Hyperparathyroidism 🡪 leads to hypercalcemia 🡪 calcium precipitates in tubules forming stones
- Metastatic cancer, paraneoplastic syndrome
- Hyperthyroidism
Stone formation (family, drug, social hx)

- Family history of stones
- Intake of medications that increase risk of stone formation – antacids, salicylic acid, anti-viral (acyclovir, indinavir*)
- Occupation hx
- Diet – high protein and sodium intake increase risk of stone formation
* Indinavir (Protease Inhibitor) – drug precipitate out in the kidney tubules, needs contrast to be identified on CT scan
- In ureteric colic, symptoms are often out of proportion to signs – no guarding, rebound
- If the patient has pyelonephritis, renal punch may be positive
- Otherwise unremarkable examination
INVESTIGATIONS
1. Hematological
▪ Full Blood Count – mild leukocytosis (↑WBC)
▪ U/E/Cr
▪ Serum Ca (if raised do PTH)
▪ LFTs (albumin)
▪ +/- Serum Uric Acid
2. Urine tests – dipstick, UFEME, urine culture/sensitivity, 24 hr urine collection

▪ 24 hr urine collection of the metabolic profile 🡪 Ca2+, Na+, Oxylate, Uric Acid, PO4-, Mg2+
▪ Hematuria – microscopic or gross
▪ Pyuria, micro-organisms (UTI)
▪ pH of urine (acidic vs. alkaline stones)
3. KUB X-Ray
▪ May be able to see radio-opaque stone (90% of renal stones are radio-opaque) – differentiate with radio-lucent stones (i.e.
urate stones 20 gout)
▪ Look at kidney size, any renal stones
▪ Trace path of ureter along tips of transverse processes, across sacroiliac joint, and medially into bladder, looking for ureteric
stones & bladder stones
▪ Usually for follow-up and recurrence screening
4. CT Scan
▪ CT KUB (non-contrast)
▪ If other diagnosis is concerning (i.e. appendicitis) can perform CTAP with both non-contrast and contrast in same setting
▪ Replaced IVU as the diagnostic test of choice in the acute setting to evaluate for stones
▪ CT Urogram (tri-phasic) – contrast to identify masses, abscess and tumour
▪ No contrast – any stones, gross abnormalities
▪ Medullary – any cysts, parenchyma abnormalities
▪ Delayed phase – any filling defects
▪ Evaluate anatomy and reflects renal function
5. Ultrasound of kidney or bladder

▪ Any evidence of kidney stones or complication of stones – i.e. hydronephrosis
▪ Choice for patients with contrast allergies and pregnant females

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▪ Features of stone: echogenic rim, posterior acoustic shadowing
6. MAG-3 renogram
▪ If pyelonephritis present due to stone obstruction, it is valuable to measure the renal function using the MAG-3 renogram
▪ The renogram gives the differential function of each kidney – in normal individuals, the function should be approximately
50% on each side (out of 100% for both kidneys combined)
▪ If one kidney has less than 15% of total renal function, it is not worth salvaging the kidney
7. Intravenous urogram (IVU)

▪ Help visualize uric acid stone (detects radiolucent stones)
▪ Shows dilated urinary system 20 to stone obstruction – hydroureter and/or hydronephrosis
▪ Rough indication of renal function
MANAGEMENT
Principles
- Provision of effective pain control – i.e. IM pethidine, tramadol
- Treatment of any suspected UTI – antibiotics
- Allow for spontaneous passage of stones or decide on active stone removal
▪ Kidney Stones – often asymptomatic – treatment pre-emptive in anticipation of potential complications (observe if <5mm
and monitor for growth, treat if >7mm)
▪ Ureteric Stones – symptomatic – trial of passage if <7mm, otherwise treat
- Treat underlying aetiology of stone formation – i.e. bladder stones sec to BPH tx with TURP
Conservative
- Stones < 5mm can be treated conservatively as 70% will be passed out; only treat if they do not pass out after 4 to 6 weeks,
and/or cause symptoms
- Spontaneous stone passage aided with prescription of narcotic pain medications as well as daily alpha-blocker therapy
(tamsulosin) → improve stone passage by up to 20% (check for postural hypotension when patient is on alpha-blockers)
- High fluid intake
▪ Drink about 2-3L of water/day or till urine clear (a glass of water before sleep is good practice)
- Diet modifications
▪ ↓intake of protein-rich food red meat, animal internal organs – i.e. intestines, liver (for uric acid stones)
▪ ↓ intake of oxalate-rich food – i.e. peanut, spinach, beetroot, strawberries

▪ Coffee and Tea in moderation (for calcium stones)
▪ ↓ intake of sugars (fructose) – i.e. soft drinks, sweets, chocolate
▪ ↑intake of fibre – i.e. fruits, veg, high fibre diet (wholemeal bread, wheat & corn)
▪ ↓ Salt Intake
▪ Normal Calcium Diet
- Medical Therapy – limited, slow process
▪ Calcium stones – thiazide (increase urinary calcium excretion), citrate, low sodium diet
▪ Struvite stones – eradication of underlying infection
▪ Uric acid stones – alkalinizing urine with baking soda or potassium citrate, allopurinol
- Urine should be strained with each void and radio-opaque stones tracked with KUB X-Ray

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Summary of treatment modalities
Location Size Treatment
< 5mm Conservative management unless symptomatic/persistent
5-10mm ESWL
Renal
10-20mm Either ESWL or PCNL
> 20mm PCNL
Upper ureter 5-10mm ESWL
> 10mm URS with lithotripsy
Middle ureter/
URS with lithotripsy
Distal ureter > 5mm
ESWL
< 30mm Cystolitholapaxy
Bladder
> 30mm Open cystolithotomy (also if there are multiple stones)
Surgical intervention
Indications (7s)
- 7s – size, site, symptoms, stasis, stuck, sepsis, social
- Stone complications
▪ Obstructs urine flow, causes urinary tract infection, damages renal tissue or causes significant bleeding, increase in size
- Unlikely to resolve with conservative treatment:
▪ Does not pass after one month, too large to pass spontaneously
Types of treatment available:

1. Extracorporeal shock wave lithotripsy (ESWL)
▪ Calcium oxalate dihydrate, uric acid (may be difficult to target) and struvite stones fragment easily, but calcium oxalate
monohydrate, calcium phosphate and cystine do not
▪ Used for renal stones and upper ureter stones (size <2cm) – not so good for lower system due to difficulty in access
▪ Contraindicated in pregnancy, untreated UTI, low platelets, untreated bleeding diathesis, distal obstruction (i.e. stricture)
▪ Complications (1) procedure-related (2) stone related
1. skin bruising, perinephric/subcapsular haemorrhages, pancreatitis, urosepsis (if stone is infected)
2. incomplete fragmentation
2. Percutaneous nephrolithotomy (PCNL)

▪ Done for renal stones that are too large for ESWL to disintegrate
▪ Contraindicated in uncorrected bleeding diathesis, patients unfit for GA
▪ Complications (1) procedure-related (2) stone related
1. Hydrothorax, haemorrhage, urosepsis, perforation of adjacent organs (rare), urinary fistula
2. incomplete fragmentation
3. Ureterorenoscopy (URS) lithotripsy (Holmium : Yttrium Aluminium Garnet Laser lithotripsy, can also be done by pneumatic drill,
electrohydraulic means)
▪ For stones along the ureter
▪ Risk of urosepsis, strictures, urethral injury, UTI
4. Cystolitholapaxy for bladder stone
5. Open surgery (pyelolithotomy or ureterolithotomy) – rarely done; only if failed other management strategies, altered anatomy,
performing open surgery for another reason anyway, possible indications (1) large staghorn stone, (2) non-functioning kidneys
with stone – to prevent infection and malignant transformation
Adjuncts:
- Double-J stent (or DJ stent) – inserted to stent the urinary system when worried that stone fragments after ESWL may cause
obstruction e.g. when ESWL used for treatment of a large stone; or if system is obstructed, to begin with, may want to stent to
ensure good drainage after surgery
COMPLICATIONS
- Hematoma / Significant Bleeding
- Urinary tract infection
- Ureteric Injury – perforation / ureteric avulsion
- Failure of procedure –i.e. unable to assess stone with URS

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BLADDER CANCER
EPIDEMIOLOGY
- 2nd most common urological CA22 – found in 1.9-10% of patients with microscopic haematuria
- Increasing incidence with age (80% diagnosed in patient >60 years old)
- 10th most frequent cancer in males in Singapore, 4:1 male predominance
- Most commonly (>90%) transitional cell carcinoma (TCC) = urothelial carcinoma
- Squamous cell carcinoma (SCC) seen with relation to schistosomiasis/chronic bladder irritation/untreated bladder
exstrophy/urachal remnant.
- Rhabdomyosarcomas seen in children.
RISK FACTORS
- Exposure to aromatic amines (printing, textile, rubber, cable and plastic industries) – due to 2-
Occupational naphthylamine
- Industrial Chemicals – B-naphthylamine, aniline-containing dyes – synthetic rubber worker
- Cigarette smoking – risk increased 2-3x, and also increases aggressiveness of ca – due to 2-
naphthylamine
- Chronic analgesic abuse (phenacetin)
- Chronic parasitic infection (schistosoma haematobium – cause squamous metaplasia, and then SCC,
Non-occupational
not TCC) – any travel to Egypt / Middle East / Africa
- Chemotherapy – i.e. cyclophosphamide (induces hemorrhagic cystitis, 9x increased risk)
- Chronic cystitis – i.e. pelvic radiation
- Others: males, age >50, personal history of gross haematuria
PATHOPHYSIOLOGY
- TCC is the most common tumour of the bladder (>90%)
▪ Exposure to carcinogenic substances in the urine (eg. tobacco smoke, aniline dyes, printing, rubber processing, pesticides)
leading to FIELD CHANGE EFFECT thus urothelial tumours often occur multifocal
▪ Divided into non-muscle-invasive / superficial (60-75%) or muscle-invasive
- Other types of bladder tumours: adenocarcinoma (1%, arises from remnant of the urachus* in the dome of the bladder),
squamous cell carcinoma (7-9%, due to chronic irritation e.g. long term indwelling catheter or untreated bladder stone)
* A duct between the foetal bladder and umbilicus (i.e. patent urachus, urachal cyst, vesicourachal diverticulum)
- Persistent Painless Haematuria is the most common presenting symptom (90%) – typically gross, painless, intermittent,
occurring throughout the stream
▪ Incidence of bladder ca in gross hematuria: 10-20%
▪ Incidence of bladder ca in microscopic hematuria: 2-5%
- Lower Urinary Tract Symptoms (LUTS)
▪ Irritative symptoms (frequency, dysuria, urgency) suggestive of carcinoma in-situ,
▪ Obstructive symptoms (decreased stream, intermittent voiding, feeling of incomplete voiding, strangury) indicate tumour at
the bladder neck or prostatic urethra, but are less common.
▪ Dysuria – persistent pyuria
- Pain – in locally advanced or metastatic tumour. Flank pain is due to urinary obstruction, suprapubic pain is due to local invasion,
bone pain is due to metastasis.
- Loco-Regional Complications – extension to other organs: fistula formation
▪ Vesico-colic fistula with pneumaturia
▪ Vesico-vaginal fistula with incontinence
- Metastatic Complications
- Constitutional symptoms – LOW, LOA, fatigue
22 "Singapore - Global Cancer Observatory." https://gco.iarc.fr/today/data/factsheets/populations/702-singapore-fact-sheets.pdf. Accessed 31 May. 2020.

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INVESTIGATIONS
Diagnosis
1. Baseline blood investigations
2. Urine cytology for malignant cells
3. Imaging – IVU / CT urogram or Ultrasound KUB to detect synchronous lesions (3% chance of prox. tumour)
4. Flexible cystoscopy or Rigid cystoscopy (cystoscopy is the gold standard for initial dx & staging) KIV transurethral resection of
bladder tumour (TURBT; diagnostic, therapeutic & staging modality)
▪ Describe: exophytic papillary lesion that ± invade the muscular bladder wall (size, number, appearance, location, growth
pattern [papillary or solid], status of uninvolved mucosa)
- Size, stalk and configuration of the cancer can be predictive of muscle invasion
▪ Cystoscopy with cell brushings and biopsy
Staging
1. CT thorax/abdo/pelvis for T, N and M staging (CT thorax for >T2 disease)
2. TURBT with histopathology
3. +/- Bone Scan
Ta Superficial, does not involve lamina propria

Tis Carcinoma-in-situ: “a flat tumour”
T1 Superficial, involves lamina propria (up to muscularis propria)
T2a Superficial involvement of muscularis propria – up to inner half of muscle
T2b Deep involvement of muscularis propria – up to outer half of muscle
T3a Microscopic extension outside bladder (from TURBT specimen)
T3b Macroscopic extension outside bladder
T4a Invasion of prostate, vagina, uterus
T4b Invasion of lateral pelvic walls, abdominal wall Flexible Cystoscopy Photo
Generally can be divided into 2 main groups:

- Superficial tumour (70-80% of patients) – Ta, Tis, T1
- Muscle-invasive tumour (20-30%) – >T2
MANAGEMENT
Superficial tumour (Ta and T1 lesions)

- Primary treatment is TURBT of the tumour
- Intravesical therapy indicated in patients with high risk of tumour recurrence or tumour progression (high grade, multifocality,
multiple recurrences, tumour size >3cm, primary or coexisting carcinoma in-situ, prostatic urethral involvement)
▪ Bacillus Calmette-Guerin (BCG) – 1 instillation per week for 6 weeks
▪ Mitomycin C – single instillation within 24hrs of TURBT – shown to decrease recurrence by 12%23, or weekly/monthly
treatments for up to 2 years
- Follow-up:
▪ 3-monthly cystoscopy for 1 year
▪ 6-monthly cystoscopy for next 4 years
▪ Yearly cystoscopy thereafter
▪ IVU every 2 years Urine cytology with every cystoscopy
23 Eur Urol. 2008 Aug;54(2):303-14.

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Muscle-invasive (≥ T2 or more)
- Radical cystectomy with urinary diversion
▪ Radical cystoprostatectomy with pelvic lymphadenectomy in male – removal of bladder, prostate and possible urethra
▪ Anterior exenteration with pelvic lymphadenectomy in female – removal of bladder, urethra, uterus, cervix and anterior
vaginal wall
▪ Note: about 50% of patients with invasive bladder cancer already have occult metastases at time of surgery
- Ways of diverting urine output

▪ Cutaneous ureterostomy (use ureters to create stoma, but easily stenosed due to small calibre; not continent)
▪ Ileal conduit (a segment of ileum with ureters attached, as a stoma; not continent)
▪ Neobladder construction using ileum (only if urethra not removed; continent, better quality of life, self-image)
▪ Stoma with pouch construction under abdominal wall (not continent)
- Radiotherapy (not as good as surgery)

- Combined modality therapy (‘bladder salvage’ regime) – TUR, platinum-based chemotherapy and external beam radiotherapy
Metastatic
- Chemotherapy
▪ GC (gemcitabine + cisplatin)
▪ MVAC (MTX + vinblastine + doxorubicin + cisplatin)
- Chemotherapy is the treatment of choice for locally advanced or metastatic bladder cancer – both neoadjuvant and adjuvant
chemotherapy benefits patients with advanced bladder cancer who also undergo surgery24
PROGNOSIS
- Non-invasive TCC → 10-20% will progress
▪ Cumulative 70% lifetime risk of tumour recurrence (non-invasive)
- Muscle-invasive – aggressive
▪ >90% mortality within 2yrs in untreated patients,
▪ Survival after cystectomy >50% after 5 yrs, mets usually to lung liver and bones
24 Eur Urol. 2009 Feb;55(2):348-58.

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APPROACH TO ACUTE URINARY RETENTION25
DEFINITION
- Acute Urinary Retention (AUR) is the most common urologic emergency – defined as a sudden and often painful inability to void
despite having a full bladder
- Chronic Urinary Retention – painless retention a/w increased volume of residual urine
EPIDEMIOLOGY
- Incidence ↑ with age – 10% of men >70yrs and 30% of men >80yrs have an episode of AUR
PATHOPHYSIOLOGY 26
- Outflow Obstruction: flow of urine is impeded by mechanical (physical narrowing of urethral channel) and/or dynamic (tension
within and around the urethra) factors
- Neurological Impairment: secondary to disruption of sensory / motor nerve supply to detrusor muscle
- Over-distention: precipitating event results in an acute distended bladder in the setting of an inefficient detrusor muscle
- Medications: usually involving anticholinergic and sympathomimetic drugs
History
Presenting Complaint – confirmation of ARU
- Inability to pass urine
- Suprapubic distention with pain (unlike chronic retention of urine which is painless) – severe!
History of Presenting Complaint

- Characterize current episode of ARU
- Previous history of urinary retention / urinary infection
- Precipitating events – recent surgery, new medications, pelvic trauma, immobilization, alcohol consumption, genitourinary
instrumentations,
History suggestive of aetiology

- BPH → previous hx of voiding / obstructive symptoms [DISH] → Terminal dribbling, intermittency/incomplete emptying, poor
stream, straining to pass urine, hesitancy
- UTI / Acute Prostatitis → fever, dysuria, frequency, urgency, nocturia, haematuria
- Strictures → Previous urethral instrumentation or STD

- Detailed medication history
- Malignancy → constitutional symptoms / gross painless haematuria (i.e. TCC)
- Stones → Previous history of ureteric colic pain or stones
- Spinal Cord Compression → younger patients, history of cancer, presence of back pain or neurological symptoms
- Neurogenic Bladder → Lower limb weakness/paralysis, bowel incontinence, back trauma, history of spinal disease / trauma
Complications
- Infection – symptoms of UTI
- Stone disease (if in the bladder, usually asymptomatic)
- Renal failure (more likely in chronic retention) – vomiting, lethargy, drowsiness
▪ Since duration of obstruction in AUR is short, there is usually insufficient time for a significant elevation in serum creatinine
25 Am Fam Physician. 2008 Mar 1;77(5):643-50.

26 uptodate: acute urinary retention

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- General condition – sallow appearance, scratch marks, pedal oedema, etc (uraemia)
- Abdomen
▪ Palpable bladder – suprapubic palpation (tender)
- Bladder percussible when it contains at least 150ml of urine, palpable when > 200mls
▪ Other pelvic masses – fibroid, gravid uterus, ovarian cyst
▪ Faecal loading
▪ Bilateral enlarged kidneys (hydronephrosis)
- Digital rectal examination

▪ Any saddle anaesthesia
▪ Anal tone
▪ Prostate enlargement – firm and smooth or hard, craggy, irregular, rectal mucosa not mobile?
▪ Faecal impaction
- Neurological examination
▪ LMN paralysis of the lower limbs?
▪ Any sensory level present?
Benign Prostate Hyperplasia – 53%
Prostate Cancer – 7.5%
Faecal impaction / Constipation – 7%
Extraluminal
Pelvic / GI / Retroperitoneal masses – extrinsic bladder neck compression
Pregnancy
Mechanical UV prolapse / Pelvic Organ Prolapse – cystocele / rectocele
Outflow Tumour of the bladder neck (TCC)
Obstruction Intramural Urethritis (UTI) – 2%
Urethral stricture from STD, prev instrumentation – 3.5%
Stones – 2%
Urethral Strictures
Intraluminal
Blood clot – can be due to intra-vesicular bleeding from bladder tumour
Foreign body
Infection Acute prostatitis – usually caused by E. coli / Proteus
Diabetic neuropathy
Peripheral Nerves Radical Pelvic Surgery
Guillain-Barre Syndrome
Neurologic Spinal Cord Trauma
Spinal Cord
Impairment Spinal Stenosis / Transverse myelitis / Spinal Cord hematoma or abscess
Cerebrovascular Disease
Brain Parkinson’s Disease / Multiple Sclerosis / Normal Pressure Hydrocephalus / Shy Drager
Syndrome
Alpha-adrenergic agents – ephedrine, phenylephrine, pseudoephedrine
Sympathomimetic
Beta adrenergic agents – terbutaline
Non-Mechanical Anticholinergic
(Functional) Antihypertensive – Hydralazine / Nifedipine
Cardiac Meds
Antiarrhythmic – Quinidine / Procainamide
Drugs NSAIDs – indomethacin
Pain Medications
Opioid analgesics (morphine, vincristine)
Antihistamines
Antiparkinsonian Levodopa / Bromocriptine
Antidepressants / Antipsychotics
Psychiatric Meds
Carbamazepine*
Others Hormonal agents, Muscle relaxants, Dopamine,
Prolonged immobility
Post-anaesthesia
Others
Post-operative complications – post rectal / gynaecological surgery
Pain / Trauma
* Other adverse effects: bone marrow suppression – anaemia, agranulocytosis, thrombocytopenia, SIADH – leading to hyponatremia

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INVESTIGATIONS
- Bloods/Urine
▪ Urine dipstick, UFEME and culture/sensitivity (UTI, hematuria)
▪ FBC: raised TW (infection)
▪ U/E/Cr: raised creatinine (renal impairment secondary to obstructive nephropathy)
- Imaging
▪ XR KUB for stones, faecal loading
▪ U/S bladder: (1) stones, (2) tumour, (3) intravesical protrusion of prostate (4) residual urine volume
▪ U/S kidney, ureters: hydronephrosis, hydroureter (obstructive complication)
MANAGEMENT
Urinary obstruction + Fever → Admit! (Uro emergency) - urosepsis
Initial Management
- 1st choice: Urethral Catheterisation (14F) – rapid & complete decompression of bladder
▪ (Contraindication: S/S of urethral injury – (a) blood at urethral meatus, (b) high-riding prostate – more relevant in the trauma
setting)
▪ If cannot pass into bladder:
- Enlarged prostate: use thicker (ie. Larger French) catheter (20-22f) (stiffer, easier to pass through)
- Urethral stricture (clue: catheter is stuck quite proximally along the penile urethra / Past Hx of instrumentation – i.e.
TURP /STD) → smaller gauge catheter (10-12F)

▪ Do not push too hard – may cause false passage creation if the obstruction is due to a stricture
- If urethral catheterisation fails, perform suprapubic (SP) catheterisation

▪ Requires distended bladder which pushes the surrounding bowel loops away so that risk of bowel injury is lower
▪ Local anesthetic injected 2 FB above pubic symphysis
▪ Small incision made in the skin and fascia and trocar-type suprapubic tube is inserted – catheter advanced over the trocar
and sutured in place
▪ When a gush of urine is seen, the suprapubic catheter is inserted and secured
▪ SP catheter good for patients expected to require long-term bladder drainage, prevents bladder neck and urethral dilation
– prevents urinary incontinence, avoids risk of urethral strictures

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Subsequent Management
- Treat reversible causes

▪ Stop drugs that may have precipitated ARU – i.e. anticholinergic, antidepressants, antihistamines, opioids
▪ Relieve constipation with fleet enema, lactulose, senna etc.
▪ Treat any urinary tract infection if present
- Anticipate complications
▪ Post-obstructive diuresis: diuresis that persists after decompression of bladder
- Urine output >200ml/hr for 2 hours or more
- Caused by an osmotic diuresis due to retained nitrogenous waste products or temporary renal concentrating defect
- Can result in hypotension and electrolyte abnormalities (hyponatraemia, hypokalemia, hypovolaemia)
- Close monitoring of urine output and fluid/electrolyte status with appropriate replacement and resuscitation
- Fluid replace – 50% of losses with 0.45% normal saline
▪ Haemorrhage ex-vacuo (transient haematuria)

- Bladder mucosal disruption with sudden emptying of greatly distended bladder
- Usually self-limiting, rarely clinically significant
- Drain urine in 500-750ml aliquots, with 15-20min intervals between each
▪ Hypotension
- Secondary to vasovagal response or relief of pelvic venous congestion
- Trial-off catheter (TOC) – attempted before surgical intervention

▪ For men with suspected BPH – start alpha-blocker (i.e. alfuzosin or tamsulosin)
▪ Initial bladder decompression can be followed by a TOC after 1 to 2 days
▪ Post-Void Residual Urine (PVRU) checked with portable ultrasound device (bladder scan)
▪ If patient cannot pass urine and bladder volume >200ml, re-catheterise
▪ When patient passes urine, can perform
- Urodynamic evaluation – is retention directly related to outlet obstruction with concomitant elevation in bladder presser
or due to inefficient bladder muscle
- Bladder scan post-micturition to check residual volume
Failed Trial of void:

- Long-term catheterization
▪ Disadvantages: risk of UTI, urosepsis, trauma, stones, urethral strictures, erosion, prostatitis and potential development of
squamous cell carcinoma
- Clean intermittent self-catheterization:

▪ First-line treatment for UR caused by neurogenic bladder
▪ Advantages: improved rate of spontaneous voiding (pt can PU in btw), decrease complications such as renal failure, upper
urinary tract deterioration and urosepsis
- Transurethral resection of the prostate (TURP – if sec to BPH)

▪ Recommend for elective TURP after 4-6 weeks (> 30 days) following an episode of AUR – reduce intra-operative risk (i.e.
bleeding and infection)

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PROSTATIC CANCER
EPIDEMIOLOGY
- Prostate Cancer is the 3rd commonest cancer and the 6th most frequent cause of cancer death among males in Singapore
- Peak incidence between 60 and 85 years of age
RISK FACTORS
- Advanced age
- Hormonal – growth of tumour can be inhibited by orchidectomy or administration of oestrogens
- Genetic – racial variations in onset and prevalence, family history
▪ Familial Prostate Cancer = 5% of all prostate cancer
- Environmental – industrial chemical exposure, diet containing high animal fat consumption (western diet), Vitamin E, Soy
▪ Low-fat diets lower testosterone levels (vice versa)
PATHOPHYSIOLOGY
- Prostatic Intraepithelial Neoplasia (architecturally benign prostatic acini and ducts lined by atypical cells)
▪ Low-grade PIN (PIN 1): mild dysplasia – no ↑ risk of prostate CA – NOT commented / diagnosed upon
▪ High-grade PIN (PIN 2/3): moderate & severe dysplasia – 30-40% chance of concurrent / subsequent invasive cancer
- Adenocarcinoma (95%)
▪ Arise in the outer parts (peripheral / posterior) of the prostate 70-80% of the time and are thus palpable on DRE and not
resectable by TURP
▪ Only 20% arise from transitional zone
- Others (histologic variants) – ductal adenoCA, mucinous adenoCA, signet cell CA, small cell CA
- Latent (incidental) carcinoma:
▪ Microscopic focus of tumour detected incidentally at histology of prostatectomy specimens removed for BPH
▪ Dormant lesions – metastases in 30% after 10 years
- Clinical (symptomatic) carcinoma:

▪ Can be incidentally picked up on DRE or due to elevated prostate-specific antigen (PSA) level (>100 is highly suggestive)
▪ Urinary symptoms: dysuria, haematuria, hesitancy, dribbling, retention, incontinence
▪ Asymmetrical, hard, irregular, craggy enlargement of prostate palpable PR
▪ Mets especially to bone – pain, pathological fractures, anaemia
▪ Metastatic spread:
o Direct – stromal invasion through the prostatic capsule, urethra, bladder base, seminal vesicles
o Lymphatics – sacral, iliac and para-aortic nodes
o Haematogenous to lung, liver and bones – pelvis, lumbosacral spine, femur
- Complications from Metastatic Disease

▪ Pathological Fractures, Spinal Cord Compression
▪ Ureteral Obstruction, Urethral Obstruction
▪ Extra-skeletal metastases
- DRE: Asymmetric area of induration, or frank hard irregular nodule fixed to pelvic wall
- Percuss spine for any bone pain, pathological #
- Ballot Kidneys – any hydronephrosis
- Examine for lymphedema

453
INVESTIGATIONS
Diagnosis
- Serum PSA level*
▪ > 10ng/ml: biopsy recommended as 67% of patients will have prostate cancer
▪ 4-10ng/ml: biopsy advised, though only 20% will have prostate cancer
▪ < 4ng/ml: majority will have negative biopsies, and yet there are patients with prostate cancer with PSA <4ng/ml
o PSA density (serum PSA / prostate volume): >0.15ng/ml/cc = ↑risk prostate cancer
o PSA velocity: Rate of rise >0.75ng/ml/yr = biopsy as ↑risk prostate cancer
o Free to Total PSA ratio (f/t PSA): f/t PSA <10% = ↑risk prostate cancer
*PSA can be falsely elevated in patient – organ specific but not disease specific
- LT catheter / Recent urethral instrumentation
- UTI / Prostatitis / ARU
- BPH
*PSA can be falsely decreased inpatient – (i.e. drugs = 5-α reductase inhibitors, NSAIDs, Statins)
- Trans-rectal ultrasound (TRUS) with biopsy

▪ Histology of prostate carcinoma is graded by the Gleason score looking at glandular architecture at low magnification
▪ Classically: hypoechoic lesion (30% chance of prostate cancer)
▪ Procedure-related complications – risk of sedation, bleeding (PR bleed, hematochezia, hematospermia), infection,
urosepsis (1% chance of serious infection that require hospital stay – give prophylactic antibiotics (gentamicin))
Staging
- Clinical examination (palpable tumour → T2)
- TRUS biopsy for staging purpose (Gleason Score)
- CT scan of the abdomen and pelvis to assess extent of tumour invasion and nodal status (regional, non-regional) – pelvic
lymphadenopathy
- Bone scan for metastasis – if PSA < 20 chance of mets = 5%
▪ Patients with metastatic disease at presentation have a median 3-year survival
▪ Mets usually spread via the Batson venous plexus to the vertebral column

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Gleason Grading System
- Based upon architectural features of prostate cancer cells (with low power field microscopy), closely correlates with clinical
behaviour → higher score indicates a greater likelihood of having non-organ confined disease, as well as a worse outcome after
treatment of localized disease27

- Tumours graded from 1 to 5, with grade 1 being the most, and grade 5 the least differentiated
- A primary & secondary score are assigned based on the most common and 2 nd most common histological patterns
- Prostate cancer with high Gleason score and/or high PSA (>20) is more likely to have spread (i.e. micro-metastases)28
MANAGEMENT
- Offer treatment if life expectancy is > 10 years
- At 5yr, survival curve not affected between active surveillance or surgical intervention)
- Watchful waiting is possible in elderly (>75yo)
Localised disease (T1/2)

Active Surveillance Watchful Waiting
Aim To Individualised Resection To Avoid Resection
Patient Surgical Fitness Age > 70 or
Characteristics Age 50-80 Life expectancy < 15 years
Tumour T1-T2, Any T stage,
Characteristics Gleason Score 6/7 or less, initial PSA <10 Gleason Score 7 or less, Any PSA
Frequent PSA, DRE PSA testing not important
Monitoring
Repeat Biopsy No repeat biopsy
Indication for Short PSA doubling time, high grade or more
Symptomatic Progression
Treatment extensive cancer on biopsy
Treatment Timing Early Delayed
Treatment Intent Radical Palliative
- Radical prostatectomy (open vs. lap vs. robotic) KIV b/l pelvic lymph node dissection
▪ Surgical procedure to remove the prostate, surround tissue and seminal vesicles
▪ Treatment of choice for patients with life expectancy >10 years
▪ Open – retropubic or perineal approaches
▪ Lymph nodes are removed btw the external iliac vein and obturator vessels bilaterally
▪ Complications – urinary incontinence, erectile dysfunction, lymphocele, rectal / ureteral injury
Locally advanced disease (T3/4) → Radiotherapy with androgen ablation

- Radiotherapy
▪ External beam radiotherapy (EBRT)
▪ Interstitial Bradytherapy
▪ Alpha emitter radiation – Radium-223
▪ Cx: cystitis, prostatitis, bladder over-activity, erectile dysfunction, ERBT users at risk of bladder and GI cancers
27 Am J Surg Pathol. 1994 Aug;18(8):796-803.

28 Schwartzs Principle of Surgery 10th Edition (pg. 1658)

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Metastatic disease → Androgen Deprivation Therapy – to lower serum testosterone
- Surgical Orchiectomy (castration)

▪ Rapidly decreases serum testosterone – a/w improvement in bone pain and disease related symptoms
- Medical Orchiectomy
▪ LHRH / GnRH agonist – i.e. Goserelin (Zoladex®), Leuprolide (lupron®),
o MOA: – initial release of LH and FSH with ↑ in testosterone production from testicular Leydig cells → “flare”
o Initial treatment alone can lead to bone pain, bladder obstruction, hence GnRH agonist usually given with anti-
androgen therapy
o After 1 week, GnRH receptors are down-regulated, ↓ FSH and LH, ↓ serum testosterone (after 3 – 4 weeks)
▪ LHRH / GnRH antagonist – i.e. Degarelix (Firmagon®)
o MOA: – binds to GnRH receptors on pituitary gonadotropin-producing cells, no initial release of FSH and LH
- Anti-androgen – i.e. Bicalutamide (Casodex®)

▪ Combined androgen blockade: prevents disease flare during initiation of GnRH agonist
▪ Steroidal Anti-androgen (i.e. megestrol acetate) – rarely used
- Bisphosphonate Therapy
- Oestrogen therapy (diethylstilbestrol) – historical
EXTRA INFORMATION
Castration-Resistant Prostate Cancer (CRPC)

2 consecutive PSA rises no less than 2 wks apart and/or documented disease progression based on clinical/radiological finding s in patients
with castrate levels of testosterone
- Secondary hormonal manipulation

▪ Androgen Synthesis Inhibitors – Abiraterone Acetate (Zytiga®) – given with prednisolone
o MOA: selectively inhibits P450 17 (CYP 17) α-hydroxylase & cytochrome (C17,20)-lyase, blocks synthesis of androgen in
tumour, testes and adrenals
o AA in post-docetaxel mCRPC patients – AA + Pred vs. Pred alone29 leads to 4 months survival benefit
o AA + pred produces overall survival (25% RR), radiographic progression free survival (16.5 vs. 8.3 months, 57% RR),
significant delays in clinical deterioration (12.3 to 10.9 months), initiation of chemotherapy 25.2 vs. 16.8 months), PSA
progression (11.1 vs. 5.6 months)30
o SE: fluid retention, hypokalemia and hypertension
▪ Androgen Synthesis Inhibitors – Emzalutamide (Xtandi®)
- Other approaches for endocrine resistant disease

▪ Glucocorticoids – prednisone, dexamethasone, hydrocortisone
▪ Progesterone / Estrogen
▪ Adrenal suppressive – ketoconazole, aminoglutethimide
- Chemotherapy – Taxanes
▪ Docetaxel + Prednisone (standard initial regimen)
▪ Cabazitaxel + Prednisolone
▪ Mitoxantrone + Prednisone
PROGNOSIS
15-Year Prostate Cancer-Specific Mortality (PCSM) after Radical Prostatectomy31
Gleason Score 15-Yr PCSM Post-Surgery Histology 15-Yr PCSM
≤6 0.2-1.2% Organ confined disease 0.8-1.5%
3+4 4.2-6.5% Extraprostatic extension 2.9-10%
4+3 6.6-11% Seminal Vesicle Invasion 15-27%
8-10 26-37% Lymph Node Metastasis 22-30%
29 Prostate Cancer Prostatic Dis. 2014 Mar;17(1):34-9.

30 N Engl J Med. 2013 Jan 10;368(2):138-48.
31 J Urol. 2011 Mar;185(3):869-75.

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BENIGN PROSTATE HYPERPLASIA (BPH)
DEFINITION
BPH due to smooth, firm nodular enlargement of periurethral (lateral / middle) lobes which compress the urethra into a vertical slit
EPIDEMIOLOGY
- Affect most men over the age of 50 but only 10% present with symptoms
- Frequency rises with age after the age of 30, reaching 90% in men older than 80
- 25-50% of men with micro/macroscopic evidence of BPH will progress to clinical BPH
▪ Men > 55 yrs old with LUTS
▪ Qmax < 15ml/s
▪ Prostate size > 20g without cancer
PATHOLOGY
- Stromal-epithelial interaction theory
▪ Proliferation of both the epithelial and stromal components of the prostate with resultant enlargement of the gland (ratio of
stroma: epithelial in normal = 2:1. In BPH = 5:1). Commonly occurs in the central zone of the prostate
- Hormones
▪ Major stimulus: dihydrotestosterone (produced from testosterone by 5-alpha reductase) which stimulates prostate growth
and maintenance of size (inducing growth factors and altering the extracellular matrix)
▪ Age-related increases in oestrogen levels may also contribute to BPH by increasing the expression of dihydrotestosterone
receptors on prostatic parenchymal cells
- Stem cell theory
▪ Abnormal maturation and regulation of cell renewal process – increase in size of prostate due to decrease in cell death
- Static and dynamic components of prostatic obstruction
▪ STATIC – includes stromal, epithelial cells and extracellular matrix → androgen ablation, TURP targets this component
▪ DYNAMIC – Obstruction to urine flow contributed by smooth muscles of the prostate. Mediated by alpha-1 receptors in the
prostate stroma, bladder neck and prostatic capsule.
- Severity of symptoms depends on degree of encroachment on prostatic urethra
- Lower urinary tract symptoms (LUTS) obstructive (predominate) >> irritative symptoms (obstruction of the prostatic urethra)
- Irritative symptoms significant for complications of urine retention: UTI, stones
History
Obstructive Irritative
Terminal dribbling / Double voiding (pis-en-deux) Frequency
Intermittency / Incomplete voiding Urgency
Straining to pass urine (strangury) / Weak stream Nocturia
Hesitancy – difficult to start micturition
Prolonged micturition Dysuria*
Urge incontinence
Obstructive S/S predominate Irritative S/S significant for Cx of urine retention: UTI, stones
*dysuria suggests on-going infection / inflammation – not grouped under either irritative or obstructive

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- Cardinal Features
▪ Obstructive S/S – hesitancy, poor stream, terminal dribbling, incomplete voiding
▪ Irritative symptoms – frequency, nocturia
▪ Acute retention of urine / Chronic retention of urine (CRU)
▪ Haematuria – from ruptured dilated bladder neck veins
▪ Occasionally, palpable bladder
- Complications of obstructive uropathy:

▪ Hydroureter with reflux of urine
▪ Hydronephrosis
▪ Pyonephrosis
▪ Pyelonephritis and impaired renal function
▪ Acute urinary retention (previous admissions and IDC)

▪ UTI, Stones Formation: irritative symptoms, haematuria, dysuria
▪ Hydronephrosis, pyelonephritis, renal impairment: loin pain, fever, polyuria/ anuria
▪ Overflow incontinence 2o to CRU with high post-void residual volume in the bladder
▪ Hernia – secondary to chronic straining
▪ Fever (UTI – pyelonephritis from ascending infection)
- Rule out other differentials:

▪ Stricture/ bladder neck contractures: previous instrumentation or STDs causing urethritis / post-TURP
▪ Drug causes: codeine (cough mixture), BB, anticholinergic, TCAs
▪ Chronic constipation
▪ Ca bladder neck/ Ca Prostate: LOW, LOA, bone pain, haematuria
▪ Neurogenic bladder
- Other aspects of history: Social history (effect on lifestyle)

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- Inspection
▪ Vitals: BP for HPT? (CRF) Fever? (UTI) Urine output? (CRF)
▪ Already on IDC? (ARU) Diapers? (incontinence) Haematuria? (UTI, stones)
▪ Sallow? Anaemia? (of CRF/ underlying malignancy) Cachexia (CA)
▪ Hernia repair scar? (hernia)
- Palpation
▪ Check for hernias
▪ Abdominoperineal masses (faecal loading, masses to compress)
▪ Any ballotable kidneys? (Hydronephrosis, Pyelonephritis)
▪ Renal punch? (Pyelonephritis)
▪ Palpable tender bladder in (ARU) non-tender (CRU)
▪ Pedal/ sacral oedema (CRF)
▪ Bony tenderness (tumour)
- Confirm diagnosis and R/O DDx:

▪ DRE → impacted stools and assessment of prostate
▪ prostate (benign features):
1. Smooth, symmetrically enlarged (>3FB), no nodule
2. Median sulcus is intact
3. Firm consistency
4. Rectal mucosal is smooth, not attached to prostate
Complications
- Acute/chronic urinary retention, complicated by bladder stones & recurrent UTI
- Gross haematuria (after excluding other causes)
- Renal impairment secondary to outflow obstruction
- Co-existence of prostate cancer
INVESTIGATIONS
Blood
- FBC: anaemia, raised WBC
- U/E/Cr: dehydration, raised creatinine 🡪 renal impairment due to chronic obstruction
- UFEME, urine c/s
- +/- Urine cytology
- PSA (done 4-6/52 later to avoid false +ves): normal <4
Imaging
- US kidney – hydronephrosis, stones
- US bladder / prostate – PVRU >100ml, bladder stone, measure intravesical prostatic protrusion (IPP), prostate size
- KUB for bladder stone
- Cystoscopy to rule out stones, strictures/ bladder neck obstruction or cancer
- F-V charts for patients with frequency or nocturia as predominant symptoms
- Uroflowmetry (see below)
Uroflowmetry to confirm obstruction to urinary outflow (IMPT!!)

- Normal bell-shaped curve, saw tooth appearance
- Volume voided (>150ml to be valid): too low (falsely low peak flow rate), too high (falsely long duration, increase RU)
- Normal peak flow rate (Qmax) > 15ml/sec
- Total duration ~ 30sec (male), 20sec (female)
- Residual urine ~0ml in young adults, can accept up to 100-200ml in elderly

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Uroflow
- Diagnosticate → Qmax <15ml/s with voided volume > 150ml and RU <150ml
- Prognosticate → Qmax < 10ml/s better outcomes after TURP than those with higher Qmax
- Does not differentiate BOO with detrusor dysfx → requires VUDS (video, urodynamic studies)
- ± urodynamic studies, TRUS with biopsy TRO prostate cancer if PSA >10
MANAGEMENT
- Divided into watchful waiting, medical management, and surgical management
- Objectives: Rapid and sustained relief of symptoms, prevent long-term complications, improve patient’s quality of life
I. Watchful waiting
- Suitable for patients with minimal symptoms, no complications and normal investigations
- Monitor patient’s symptoms and clinical course annually
II. Medical treatment

1. Alpha-blockers (Prazosin, Terazosin, Tamsulosin, Alfuzosin)
▪ 3 days to be effective, 1st line therapy
▪ Treatment of symptoms
- Block α-1 adrenergic receptors in the bladder neck, prostate and urethra
- Result in decreased outflow resistance and decreased bladder instability
- Use of alpha blockers can increase successful trial off catheter (TOC) in men with 1 st episode of spontaneous AUR
and continued use reduced need for BPH surgery during a 6 month treatment period 32
▪ Side Effects: Postural hypo. (esp. if patient is on anti-HTN), dizziness, lethargy, light-headedness
2. 5-alpha reductase inhibitors (Finasteride, Dutasteride)

▪ Reduce prostate size (20%), decreased need for surgery (10-15%)
▪ Takes 3-6 months to be effective and may require long-term maintenance
▪ Treats the disease (not just the symptoms) by inhibiting the conversion of testosterone to dihydrotestosterone by 5-alpha
reductase → reduced prostate size

▪ Proven to decrease need for surgery and acute retention rates
▪ Only effective after 6 /12 (counsel the patient!), and in prostates >40g
▪ PCPT trial (prostate cancer prevention trial33) → finasteride ↓risk of prostate cancer (by 25%) but was associated with
an increased risk of diagnosis of high-grade (6.4% vs. 5.1%) prostate cancer compared with placebo
▪ Side Effects (Finasteride) → ↓libido (erectile dysfunction), ejaculatory dysfunction, impotence, gynaecomastia
32 Urology. 2005 Jan;65(1):83-9; discussion 89-90.

33 N Engl J Med. 2003 Jul 17;349(3):215-24.

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- Combination of Avodart and Tamsulosin (CombAT) study34
▪ Combodart – tamsulosin 0.4mg + dutasteride 0.5mg ($3/tab)
▪ Superior to monotherapy in reducing RR of BPH clinical progression in men with moderate-to-severe LUTS due to BPH and
prostatic enlargement
▪ Not superior to Dutasteride monotherapy at ↓ RR of AUR or BPH related surgery
III. Surgery
Types
- Transurethral resection of prostate (TURP) is the gold standard (aim to widen bladder neck)
- Transurethral incision of the prostate (TUIP): decision made during TURP when the prostate does not appear to be enlarged ,
make small cuts around the bladder neck area to open it up.
- Other techniques: laser prostatectomy, photo-selective vaporization of prostatic tissue (PVP), electro-vaporization (TVP),
transurethral needle ablation of the prostate (TUNA), microwave thermotherapy, open prostatectomy
Indications:
- Failed medical treatment – significant impact on patient’s QOL
- Significant Complications:
▪ Upper Tract Injury – i.e. renal insufficiency, obstructive uropathy, hydronephrosis
▪ Lower Tract injury – i.e. refractory urinary retention, recurrent UTI, bladder decompensation (i.e. high PVRU)
- Recurrent/persistent gross haematuria
- Bladder Calculi – secondary to BPH
Caution: Must rule out neurogenic bladder / detrusor hypotonia before TURP!! → do UDS
1. Insert narrow catheter with pressure gauge at the end into (detrusor pressure = a – b)
▪ Bladder: intravesical pressure
▪ Rectum: intra-abdominal pressure
2. Fill up bladder: look for detrusor contractions
3. Cough when erect: stress incontinence
4. Void: detrusor pressure should be sufficient, good flow (Qmax)
Post-operation: start continuous bladder washout with 22F, 3-way IDC – watch drain colour (assess bleeding) and presence of clots
COMPLICATIONS
- Risk of GA/ spinal analgesia
- Bleeding, infection/ urosepsis
- Local injury causing incontinence (1%), stricture / bladder neck stenosis
- Perforation of the urethra or bladder dome → can form fistula
- Failure of procedure / Recurrence of symptoms (regrowth of prostate)
- Retrograde ejaculation (~40-60%) resulting in ejaculate volume decrease: (incompetent bladder neck)
▪ Penile Erection and Sexual Function not affected after surgery
- TUR syndrome (<1%) = hyponatremia (pseudo-hyponatremia / isotonic hyponatremia)
▪ Symptoms: N/V, confusion, hypertension, visual disturbance, giddiness, seizure
▪ Hyponatremia due to constant irrigation during TURP (glycine used for irrigation – cannot use N/S, as ionic solutions make
diathermy non-functional)
i. Water or 0.9% glycine is used for TURP
ii. Water is hypo-osmotic compared to blood while 0.9% glycine is iso-osmotic to blood
iii. 0.9% glycine preferred because it does not “dilute” the blood
▪ Venous channels opened up during TURP allows the irrigating fluid to enter the circulation – Fluid accumulates +
Hemodilution + HypoNa+ + Change in osmotic pressure
▪ Risk with prolonged operation & high pressure of irrigation, thus op is kept to < 1 hour, and irrigation pressures <60mmHg
▪ Now uncommon as new technology allows isotonic irrigation
34 Eur Urol. 2010 Jan;57(1):123-31.

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APPROACH TO SCROTAL SWELLINGS & PAIN
SCROTAL ANATOMY
- Tunica Vaginalis: potential space that encompasses the anterior two-thirds of the testicle
- Epididymis: positioned posterolateral to the testicle (must be differentiated from an abnormal mass)
- Spermatic Cord: consists of the testicular vessels and the vas deferens, is connected to the base of the epididymi
EMBRYOLOGY
- Testis develops from the mesoderm of the urogenital ridge
- In the 3rd trimester, it descends from the posterior abdominal wall inferiorly towards the deep inguinal ring guided by the fibrous
gubernaculum
- An evagination of the parietal peritoneum and the peritoneal cavity extends into the inguinal canal (processus vaginalis)
- Before birth, processus vaginalis closes, a portion remains patent and surrounds the testis as the tunica vaginalis
Aim: To confirm if swelling is confined to scrotum, establish if testis and epididymis are identifiable & determine transilluminability
Inspect
- Inspect the groin and scrotum: scars and swelling
▪ Groin incisions are usually oblique
▪ Scrotal incisions are usually in the median raphe (easy to miss)
- Assessment of testicular lie (vertical or horizontal)
Palpate
- Ask for any pain; when palpate, look at patient for tenderness
- Palpate one testes at a time
- If palpated any swelling:
▪ Is it tender?
▪ Can you get above the swelling? or is swelling confined to scrotum?
▪ Can you identify the epididymis and testis , is the lump separate or part of them?
▪ Palpate the normal contour of the testis identifying the epididymis and ductus (vas) deferens
▪ If a lump is present – Is it transilluminable?
Offer to
- Transilluminate the swelling if it is likely at hydrocele
- Continue the examine the groin if it is a inguinoscrotal hernia
- Examine the abdomen and groin
▪ Lymph drainage of the testes are to the para-aortic nodes (retroperitoneal) and unless extremely large will not be palpable
▪ Inguinal lymphadenopathy is more likely from a pathology from skin of scrotum and penis (i.e. SSC of penis)

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Cannot get ● Cough impulse, Reducible, Testis palpable, Opaque Hernia
above swelling ● No cough impulse, Not reducible, Testis not palpable, Transilluminable Infantile hydrocoele
Chronic hematocele
Non tender Gumma
Tumour
Testis not definable from Opaque
Torsion
epididymis
Tender Epididymo-orchitis
Acute hematocele
Can get above Transilluminable Hydrocoele

swelling
Non-tender swelling of testis Tumour
Opaque Non-tender swelling of epididymis TB epididymis

Testis definable from
epididymis
Tender Epididymo-Orchitis
Transilluminable Cyst of epididymis

Can you get above the swelling?, Can you identify the testis and the epididymis?, Is the swelling transilluminable?, Is the s welling tender?

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TESTICULAR TORSION (A SURGICAL EMERGENCY)
A true urologic emergency where the testis is rotated on its vascular pedicle resulting in ischemia – irreversible damage after 12hours of ischemia

- Often in peri-pubertal (12-18 yr) age group
- Cryptorchidism (undescended testis)
- Maldescended testis hanging like a bell clapper within the tunica vaginalis
- Clinical Diagnosis – acute abdomen (T10 innervation) & acute onset of testicular pain and swelling (distinct point in time)
a/w nausea & vomiting
- Previous attacks of self-limiting pain; ppt by trauma, cycling, straining, coitus
- No history of voiding complains, dysuria, fever, exposure to STDs
- Swollen and tender scrotum,
- High riding in scrotum with transverse lie
- Absent cremasteric reflex (elicited by stroking inner thigh – in children)
- Negative Prehn Sign – no pain relief with lifting of affected testis (in contrast +ve prehn sign suggests epididymitis)
- Epididymitis
- Torsion of testicular appendage (pea coloured lump through scrotum)
- Strangulated inguinoscrotal hernia
INVESTIGATIONS
- Colour Doppler Ultrasound – help confirm or exclude diagnosis with 95% accuracy (useful when a low suspicion of testicular
torsion exists)
MANAGEMENT
- Emergency exploration if Doppler US –ve for flow or high index of clinical suspicion
▪ Untwisting (lateral) of affected testis and bilateral orchidopexy
▪ Warm up with warm pad to see reperfusion or check with doppler after untwisting [4 hours before ischemia]
▪ More than 80% of testis salvaged if surgery is performed ≤ 6 hours. Rate decreases to <20% if time lapse is > 12 hours 35
▪ If dead, excise and replace with prosthesis
35 Schwartzs Principle of Surgery 10 th Edition (pg. 1662)

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SCROTAL ABSCESS
- History – poor hygiene
- Symptoms of UTI or STD – i.e. frequency, urgency, dysuria, penile discharge
- PE – erythematous and oedematous scrotum
MANAGEMENT
- Analgesia + IV Antibiotics (Augmentin)
- Incision and Drainage with cavity left open and packed (allow wound to granulate from the base preventing a closed space from
forming that becomes secondarily infected)
COMPLICATIONS
- Incomplete drainage leading to persistence of abscess or repeat I&D
- Fournier gangrene (necrotizing fasciitis due to a synergistic poly-microbial infection)
FOURNIER GANGRENE
Necrotizing fasciitis of the perineum and genital region frequently due to a synergistic polymicrobial infection
RISK FACTORS – diabetics, alcoholics, immunocompromised
PATHOPHYSIOLOGY
- Source of infection:
▪ Genitourinary (19%) – urethral stone / stricture / fistulae
▪ Colorectal (21%) – ruptured appendicitis, colonic CA, diverticulitis, perirectal abscess
▪ Dermatological (24%)
▪ Idiopathic (36%)
- Abrupt onset with pruritus, rapidly progressing to edema, erythema and necrosis within hours
- Fever, perineal and scrotal pain and associated indurated tissue
- Edema, erythema of skin of scrotum, phallus and perianal area
- May progress to frank necrosis of skin and subcutaneous tissue
- Crepitus in tissue suggest presence of gas-forming organisms
- Pain out of proportion to physical findings
MANAGEMENT
- Broad spectrum antibiotics cover (against aerobic and anaerobic organisms)
▪ IV penicillin G 4MU q4h, IV clindamycin 900mg q8h, IV ceftazidime 2g 8H [same abx for necrotizing fasciitis]
- Wide debridement with aggressive post-operative support
▪ Testes are often spared (have discrete blood supply)
- If there is damage to external anal sphincter, colostomy may be required
- Tight glucose control and adequate nutrition – important to facilitate wound healing
EPIDIDYMAL CYST
Cyst of the epididymis containing serous liquid.
- Small mass separate from testis (within epididymis); can get above it
- Firm; maybe loculated
- Transilluminable if large cyst
- Often multiple in the head of epididymis
- May occur as a complication of vasectomy (spermatoceles) → spermatocele do not transilluminate
MANAGEMENT
- Conservative [mainstay]
- Surgical: if painful, very large or frequent recurrences (risk: damage and fibrosis of epididymis leading to infertility)

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VARICOCELE
Varicocele = dilatation of veins of the pampiniform plexus of the spermatic cord

- Present in 15-20% of post-pubertal males
- Predominantly occurs in left hemi-scrotum
- Bilateral varicocele occurs in 33% of patients, while unilateral right varicocele are very rare (search for underlying pathology)
- Risk factors: Idiopathic in younger males around puberty, In older men with retroperitoneal disease: need to exclude RCC
PATHOPHYSIOLOGY
- left spermatic vein enters the left renal vein at a perpendicular angle and the intravascular pressure in the left renal vein > right
(compressed btw the aorta and SMA – “nutcracker effect”)
- Therefore, increased pressure in left spermatic vein which can dilate leading to incompetence of the valve leaflets 🡪 retrograde
flow of blood toward testis in the erect position
- Can be asymptomatic or symptomatic (see below)
▪ Dull aching, left scrotal pain – noticeable when standing and relieved by lying down
▪ Testicular atrophy – compare both sides
▪ Decreased fertility
- Best noticed on palpation with the patient standing up
▪ Mass is separate from testis; can get above it
▪ Feels like a bag of worms
▪ Compressible mass above or surrounding the testis
▪ Not transilluminable
CLASSIFICATION
Subclinical (not palpable) Vein larger than 3 mm on ultrasound; Doppler reflux on Valsalva maneuver
Grade I (small) Palpable with Valsalva maneuver only
Grade II (medium) Palpable at rest (without Valsalva maneuver), invisible
Grade III (large) Easily visible
MANAGEMENT
- Conservative: Scrotal Support and NSAIDs
- Surgical:
▪ Trans-femoral angiographic embolization with coil or sclerosant
▪ Surgical Ligation: excise the surrounding dilated veins via high retroperitoneum, inguinal or laparoscopic approach
HYDROCELE
Asymptomatic fluid collection around the testicles (processus vaginalis) that transilluminates
PATHOPHYSIOLOGY
- During descent of the testis from the posterior abdominal wall, it carries a fold of peritoneum (processus vaginalis) – which
normally forms the tunica vaginalis. If this connection does not get obliterated, fluid can accumulate in any part of this peritoneum
derived covering and a hydrocele forms
- Very swollen scrotum; uniformly enlarged
- Cannot define testis well; not separable from testis
- Maybe firm, tense or lax
- Maybe transilluminable if acute (less in chronic hydrocele)
- Can get above the mass; the superficial ring is distinct

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CLASSIFICATION
- Anatomical Classification of Hydroceles
▪ Vaginal hydrocele: only in tunica vaginalis & does not extend into the cord
▪ Hydrocele of the cord
- Mass around the cord; attached distally to the testis
- Difficult to distinguish from irreducible inguino-scrotal hernia – may extend up and beyond
- Traction of the testis causes a hydrocele of the cord to be pulled downwards
▪ Congenital hydrocele
- Patent processus vaginalis filled with peritoneal fluid – sac communicates directly with the peritoneum
- Patients give hx of intermittent scrotal swelling – usually resolves by 1yr of age
▪ Infantile hydrocele
- Situation in between hydrocele of cord and congenital hydrocele
- Processus vaginalis is obliterated at the deep ring and so the hydrocele does not communicate with the abdomen but
remains patent in both cord and scrotum
- Secondary Hydrocele
▪ From testicular tumour
▪ From torsion / trauma
▪ From orchitis (any inflammation)
▪ Following inguinal hernia repair
MANAGEMENT
- Conservaitve
▪ In congenital hydrocele (must differentiate between congenital hernia) – watch and wait, usually, resolves by 1 year of age
– if unresolved by 2.5 to 3 years → surgical closure
▪ Watch & wait or Aspiration [tends to re-accumulate]
▪ Must exclude a 2o cause – ultrasound scrotum
- Surgical
▪ Lord’s plication of the sac - for small sac with thin wall
- Vertical paramedian incision is made
- Layers of the scrotum are divided along the incision to identify the tunica vaginalis (TV) sac-- from superficial to deep:
skin, dartos, external spermatic fascia, cremasteric fascia, internal spermatic fascia
- TV sac is opened, draining the hydrocele fluid out
- TV is bunched up by placing multiple plicating sutures, such that the TV becomes crumpled up around the testis
- Secretions can then be absorbed by the lymphatics and venous system, avoiding reaccumulation of the hydrocele
- Scrotal support to reduce oedema
▪ Jaboulay’s operation to evert the sac - for large sac with thick wall
- Similar to Lord’s plication, except that there is subtotal excision of TV sac (not total as the TV is reflected onto the cord
structures and epididymis posteriorly) with the cut edge of the sac everted and sutured behind the testis, instead of
plication.
COMPLICATIONS
- Haematoma (higher risk for Jaboulay)
- Wound Infection may result in pyelocele (purulent collections)
- Injury to Spermatic Cord

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TESTICULAR TUMOUR
Testicular cancer is the most common solid malignancy in men age 15 – 35yrs

- Lifetime risk: 1 in 500
- RF: cryptorchidism, HIV infection, gonadal dysgenesis (i.e. klinefelter syndrome)
- Asymptomatic enlarging testicular mass / dull ache in one testis in a young man (15-35)
- ± hx of trauma accompanying discovery of mass
- 10% presents with acutely painful testis – usually due to infarct or hemorrhage
- May present as back pain (if para-aortic nodes infiltrated with metastases)
Clinical Examination:
- Inseparable from the testis; distinct from superficial inguinal ring (can ‘get above’ mass)
- Hard, nodular, irregular, non-tender
- Not transilluminable
- Chronic infection with scarring (i.e. orchitis / TB)
- Long standing hydrocele with calcification
INVESTIGATIONS
- No role for percutaneous biopsy – risk of seeding, risk of changing lymphatic drainage
- US scrotum
▪ Seminoma = hypoechoic intratesticular mass
▪ Non-seminoma (i.e. teratoma) = inhomogeneous lesions
- Tumour Markers (monitor effectiveness / response to therapy and screen for recurrence)
▪ LDH (assess tumour burden), AFP, B-HCG
- Staging → CT TAP – assess para-aortic lymph nodes involvement & distant mets
▪ stage 1 = testis lesion, no nodes involved
▪ stage 2 = nodes below diaphragm
▪ stage 3 = nodes above diaphragm
▪ stage 4 = pulmonary and hepatic metastasis
CLASSIFICATION
- Germ cell tumour (90-95%) → most commonly seminomatous tumours
- Sex Cord Stroma Tumors (5-10%)
- Secondary Testicular Tumour → lymphoma, leukemia
Germ Cell Tumors non-seminomatous Seminomatous* (most common)

Embryonal Carcinoma, Choriocarcinoma
Examples Yolk sac tumour (endodermal sinus tumour)
Teratoma, Mixed Germ Cell Tumour (60%)
Age 20-30yr 30-40yr
↑AFP in 70%,↑ B-HCG* in 60% ↑B-HCG

Tumour Markers
(90% for one or the other) (Localized – 10%, metastatic – 25%)
Chemo-Radio Sensitive
Treatment Chemo-Sensitive
Adjuvant EB-RT to para-aortic nodes
(early) (often only 2 cycles of chemotherapy)
± Single dose of carboplatin
Treatment Combination chemotherapy Adjuvant chemotherapy either single dose or
(disseminated) (platinum-based, 4 cycles) combination (platinum-based)
Early Stage Seminoma – 95% cure rate
Variable response to Treatment Highly Responsive to Radiotherapy
Prognosis
Often Metastasize Early Metastasize Late
Excellent Prognosis
* hCG has a structure similar to TSH. Patients with testicular germ cell tumour may develop very high serum hCG concentration which can stimulate TSH
receptors and cause hyperthyroidism [paraneoplastic hyperthyroidism]

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MANAGEMENT
- Fertility & Sperm Banking
- Staging, Radical orchidectomy via inguinal approach ± retroperitoneal lymph node dissection with combination chemotherapy
▪ Not to violate scrotal skin as risk (theoretical) of altering lymphatic drainage of testis
▪ Intra-op, perform early clumping of testicular artery & vein within the spermatic cord before testis is mobilized out of scrotum
to prevent intraoperative seeding of tumour up testicular vein
PROGNOSIS
If no metastases: 5 year survival is 95% after orchidectomy and RT or CT
EXTRA INFORMATION
Nonseminomatous Germ Cell Tumour

- Embryonal Carcinoma – characterized by immature, primitive cells (sheets of immature to anaplastic epithelial cells), present with bulky
mass with hemorrhage and necrosis, AFP are classically elevated
- Choriocarcinoma – a/w widespread metastases at time of diagnosis (i.e. lung & liver), common in males age 15-20 years – present as
small tumour that has extensive hemorrhage and necrosis, gynecomastia, symptoms of hyperthyroidism, (for both serum and urine)
[disordered syncytiotrophoblastic and cytotrophoblastic elements], B-HCG are classically elevated – may lead to hyperthyroidism or
gynecomastia (alpha-subunit of hCG is similar to FSH, LH and TSH)
- Yolk sac tumour (endodermal sinus tumour) – most common germ cell tumour in children (good prognosis), [Schiller-Duval bodies
(glomeruloid structures) pathognomonic], AFP are classically elevated
- Teratoma – present as cystic mass which contains ectodermal, endodermal and mesodermal tissues. Pre-pubertal cases are benign,
adults have malignant potential (malignant in males as opposed to females).
- Mixed Germ Cell Tumour (60%) – germ cell tumours are usually mixed with prognosis based on the worst component.
Sex Cord Stroma Tumors (5-10%) – usually benign

- Leydig cell tumour – bimodal distribution (pre-pubertal and > 50 years , painless testicular mass. 10% malignant, in adults present with
gynecomastia, in children with precocious puberty (due to excessive androgen and estrogen production) – characterized by golden brown
testicular tumour (cholesterol and lipofuscin), large, uniform cells with indistinct cell borders; and pale -staining rod-shaped inclusion
known as crystals of Reinke.
- Sertoli cell tumour – rare, usually benign, a/w gynecomastia – microscopically form cordlike structures resembling seminiferous tubules
- Granulosa cell tumour
Secondary Testicular Tumour

- Lymphoma – a/w bilaterally testicular cancer, arise from metastatic lymphoma to testes, affects males age > 60 years. Most commonly
associated with non-Hodgkin Lymphoma, diffuse large B-cell type
- Leukemia
- Metastatic

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15. VASCULAR
ANATOMY OF ARTERIES OF THE LOWER LIMB
Course of the Femoral Artery

The external iliac artery continues as the femoral artery after crossing the inguinal ligament. The femoral artery divides into 5 branches:
superficial epigastric artery, superficial circumflex artery, superficial external pudendal artery, deep external pudendal artery
and the profunda femoris (or deep femoral)
▪ The profunda femoris arises posterolaterally from femoral artery, 5cm distal to the inguinal ligament – supply the muscle of the
thigh via (3) branches: medial and lateral circumflex femoral arteries and four perforating branches
▪ The superficial femoral artery runs superficially and descends along anterior-medial part of the thigh in the femoral triangle
(superior: inguinal ligament, medially: adductor longus & laterally: sartorius). It exits through the apex of the femoral triangle into
the adductor canal. (posterior: adductor longus and magnus, anterolaterally: vastus medialis, anteromedially: sartorius) . It then
passes through the hiatus in the adductor magnus to reach the popliteal fossa, where it changes its name to become the popliteal
artery.
The popliteal artery passes to lower border of popliteus and divides into (2) branches: anterior tibial artery and the posterior tibial
artery (also called tibioperoneal trunk by some)
▪ The anterior tibial artery gives off small branches which form collaterals with the vessel around the knee and then crosses
into the anterior compartment of the leg (superficial to interosseous membrane) and supplies the muscles there, and then
becomes superficial just above the ankle (between the EHL and TA) where it continues over the dorsum of the foot as the
dorsalis pedis
▪ The posterior tibial artery gives off the peroneal artery (4cm from origin, supplies lateral compartment) and itself supplies the
posterior compartment of the leg and passes posterior to the medial malleolus (between tendon of FDL & FHL) before dividing
into medial and lateral plantar arteries to supply the sole of the foot
Clinical Significance
Important to know the arrangement of the anterior tibial, posterior tibial and peroneal vessels at the trifurcation as you may be asked
to read an angiogram of these vessels. From lateral to medial: Anterior tibial, Peroneal, Posterior tibial
Femoral artery: palpated at the mid-inguinal point (i.e. midway between the pubic symphysis and the anterior superior iliac spine). It
course is marked between the upper 2/3 of line from mid-inguinal point to adductor tubercle. There is a rich anastomosis between
femoral arteries and its branches which is important in the development of collaterals in arteriosclerotic disease. The femoral vein lies
immediately medial to the femoral artery
Popliteal artery: palpated in the lower part of the popliteal fossa (compressed against the upper end of the tibia). Popliteal artery
aneurysm can increase risk of DVT (pressure on vein), pain and nerve palsies (pressure on tibial and common peroneal nerve)
15. Vascular_Last Updated 3rd June 2020

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PERIPHERAL ARTERIAL DISEASE - LOWER EXTREMITIES ARTERIAL DISEASE (LEAD)
DEFINITION36
Peripheral Arterial disease (PADs) includes all arterial diseases other than the coronary arteries and aorta. PADs is the encompassing
term for carotid artery disease, upper-extremity disease, mesenteric artery disease, renal artery disease and lower-extremities arterial
disease (LEAD)
The focus on this topic will be on Lower Extremity Arterial Disease (LEAD), Chronic Limb Ischemia. Acute Limb Ischemia will be
considered in a different section
Intermittent Claudication
Vascular IC, is defined as a reproducible discomfort of a defined group of muscles that is induced by exercise and relieved with rest.
Chronic Limb Threatening Ischemia (CLTI)

CLI is a clinical diagnosis and should be supported by objective testing.
1. Rest pain requiring regular opioid analgesia (e.g. codeine) lasting >2 weeks
AND/OR
2. Gangrene or ulcers over the toes or feet
AND
3. Objective indication of poor vascular supply to the lower limbs
▪ Ankle-brachial pressure index <0.5
▪ Toe pressure index < 0.3
▪ TcPO2 < 30mmhg
* in patients with ischemic ulcers the ankle pressure is typically 50-70mmHg and in patients with ischemic rest pain, it is typically 30-
50mmHg. Toe Pressure should include pressures in diabetic patients (critical level <50mmHg
Ischemic Rest pain: Severe pain in the distal portion of the lower limb (usually toes, foot but may involve more proximal areas
if disease is severe) occurring at rest. In most cases, walking capacity is severely limited or impossible. Rest pain typically
occurs at night due to a lack of blood supply. The patient is not in a dependent position and BP decreases during sleep. The
pain is so severe that it wakes the patient from sleep, he gets better after a short walk around the room. Pain is aggravated or
precipitated by lifting the limb, relieved by dependency of the limb. Many patients sleep with the leg hanging over the side of
the bed to relieve the pain. The pain is not easily controllable with analgesia, hence, patients often require opioids to control
pain
Differential Diagnosis to Ischemic Rest Pain:

- Diabetic Neuropathy, Complex Regional Pain Syndrome, Nerve Root Compression, Peripheral Sensory Neuropathy
(other than diabetic neuropathy), Night Cramps, Buerger’s Disease (thromboangiitis obliterans)
Ischaemic ulcers (most are neuroarthropathy ulcers): This usually arises from minor traumatic wounds with poor healing, they
are often painful. Commonly, they occur on the tips of the toes, bunion area, over the metatarsal heads (ball of the foot), lateral
malleolus (as opposed to venous ulcers that occur over the medial malleolus). The ulcers are usually deep, dry, punctate
(unlike venous ulcers that tend to be superficial, moist, diffuse). Many ulcers may become infected resulting in cellulitis, even
abscess formation, and spread to involve the underlying bone and joints resulting in osteomyelitis, septic arthritis.
36 Eur Heart J. 2018 Mar 1;39(9):763-816.

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Gangrene: This represents cyanotic, anaesthetic tissue associated with or progressing to necrosis. This occurs when arterial
blood supply falls below that which is necessary to meet minimal metabolic requirements. It can either be dry or wet.
EPIDEMIOLOGY AND RISK FACTORS

LEAD usually appear after the age of 50 with an exponential increase after the age of 65 years. This rate reaches ~20% by the age
of 80 years. The prevalence of LEAD ranges from 10-20% of whom ⅓ have symptoms of intermittent claudication (IC).
Patients can present with asymptomatic PAD to limb-threatening chronic limb threatening ischemia (CLTI)
Natural history of lower extremities PAD syndrome37

- For patients with IC, only a quarter of patient will ever significantly deteriorate
▪ symptomatic stabilization due to:
1. Development of collaterals
2. Metabolic adaptation of ischemic muscle
3. Patient alters gait to favour non-ischemic muscle groups
- For patients with IC, predictor of deterioration of PAD (i.e. need for arterial surgery / major amputation) is an ABI of < 0.5
- For patients with low ankle pressure (i.e. 40-60mmHg), risk of progression to severe ischemia or limb loss is 8.5% per year
- For patients with symptomatic LEAD, the prevalence of abdominal aortic aneurysm (AAA) is higher than general population
Risk Factors
- Existing Disease: Diabetes, Coronary Arterial Disease, Previous Stroke / TIA
- Non-modifiable: Age, Gender, Ethnicity, Family History
- Modifiable: Current Smoking & Ex-Smokers (however, for patient who have stopped smoking for > 10 years, the risk is
considerably diminished), Hypertension, Hyperlipidemia & Diabetes (5 x increased risk of amputations), Obesity
37 J Am Coll Cardiol. 2006 Mar 21;47(6):1239-312.

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PATHOPHYSIOLOGY
Peripheral Artery Disease is a systemic atherosclerotic process where there is subintimal accumulation of lipid and fibrous material.
In the lower limb arteries, atherosclerosis and associated thrombosis can lead to diffuse stenosis of the peripheral arteries resulting
in diminished blood supply to the lower limb (imbalance between supply and demand). Endothelial dysfunction, enhanced platelet
activity, dyslipidemia, inflammatory and immunologic factors, and tobacco use contributes to the development of atherosclerosis.
Atherosclerosis forms at the branch point (i.e. proximal bifurcation leading to that vascular bed), bends and tethered segments (i.e.
superficial femoral artery as it passes through Hunter canal). Consequently, the atherosclerotic narrowing of the lower extremities
tend to occur within the aortoiliac, femoropopliteal, tibial-peroneal segments
Less commonly, PAD can be caused by Buerger's disease (aka. thromboangiitis obliterans), vasculitis (i.e. Takayasu arteritis, Bechet's
disease), ergot toxicity and/or vasospasm
EXTRA INFORMATION
Buerger's disease (aka. thromboangiitis obliterans)38
- Progressive non-atherosclerotic segmental inflammatory disease that affects small and medium-sized arteries, veins
and nerves of the upper and lower extremities
- Presentation: Young (20-50) male smokers with foot, leg, arm or hand claudication, progress to calf claudication and
eventually ischemic rest pain & ulceration on toes, feet or fingers
- Investigation: Angiography (all 4 limbs) 🡪 disease confinement to distal circulation, infra-popliteal and distal to brachial
artery, occlusions are segmental and show “skip” lesions with extensive collateralization “cock-screw collaterals”
- Treatment: smoking cessation 🡪 disease remission and amputation avoidance increased
Aortoiliac-Occlusive Disease (AIOD)

AIOD involves occlusion of the abdominal aorta as it transits into the common iliac arteries. Symptomatic patients present with
claudication symptoms involving the hip, proximal thigh muscle, buttocks and calf. Pelvic ischemic can present with erectile
dysfunction. Focal lesions typically present with lower extremities claudication. On examination, patients have reduced femoral
pulses
Leriche's syndrome: occlusion at the bifurcation of the terminal aorta,

- Presentation: Buttock claudication, impotence in men and reduced/absent femoral pulses (and distal pulses), and ± aortoiliac
bruits.
- Treatment: aorto-bifemoral bypass graft
Femoropopliteal Occlusive Disease

Femoropopliteal occlusive Disease affects vasculature between the inguinal ligament and the tibial vessels. The superficial femoral
artery (SFA) and popliteal arteries are most commonly obstructed. The pattern of disease seen frequently in smokers. Symptomatic
patients with IC present with crampy calf pain with walking that occurs at reproducible distance and is relieved by rest. On
examination, patients have decreased / absent popliteal, posterior tibial and dorsalis pedis pulses. ABI can be used to discriminate
between vasculogenic and neurogenic claudication. ,
Tibioperoneal Arterial Occlusive Disease (TPOD)

Tibioperoneal occlusive disease affects the infra-popliteal vessels. Symptomatic patients more commonly present with chronic limb
threatening ischemia (CLTI) as compared to patients with femoropopliteal occlusive disease caused by absence of collateral flow to
the foot. The pattern of disease seen frequently in patients with DM and CKD. On examination, patients have absent posterior tibial
and dorsalis pedis pulse. Absence of hair and shiny skin on lower limb reflect chronic limb ischemia, evidence of ulcerations point to
severe ischemic and potential limb loss.
38 Schwartzs Principle of Surgery 9th Edition (pg.: 1498, pdf version)

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History
1. Age of the patient & occupation
2. Pain of Intermittent Claudication

- Which part of the lower limb does the pain occur in
▪ Stenosis of lower aorta and common iliac: buttock claudication ± impotence
▪ Stenosis of external iliac: thigh claudication
▪ Stenosis of superficial femoral: calf claudication
- Nature of the pain – cramping
- Radiation
- Severity
- Aggravating – muscle pain recurs predictably with exercise/exertion (distal to stenosis)
- Relieving – rest (just standing is sufficient) – quick relief?
- Associated symptoms – i.e. impotence in LeRiche’s
- Duration: When did pain first start
- Progress: has there been worsening pain, increasing areas of lower limb affected, pain on less exertion, development of
rest pain)
- Current claudication distance – fixed or variable
- How have symptoms affected lifestyle, any impaired mobility
Vascular Claudication
Intermittent claudication is defined as a reproducible discomfort of a defined group of muscles that is induced by
exercise and relieved with rest. Usually described as the patient as a cramping, aching pain in the muscle group on exertion
such as walking, and alleviated on stopping (patient does not have to sit down for the pain to go away) – “shop window to
shop window”.
Important to determine the “claudication distance” – within a short period of time the distance is usually fairly constant but
can shorten as the disease progresses. Also, we need to differentiate the various causes: vascular vs. neurogenic vs.
musculoskeletal.
- Calf claudication: affects superficial femoral near to the adductor hiatus, or popliteal artery
- Foot claudication: tibial and peroneal arterial disease, but rarely do patients with claudication due to atherosclerosis get
foot pain alone (more common in Buerger’s)
- Thigh claudication: affects common femoral artery or aortoiliac disease
Neurogenic Claudication secondary to Spinal stenosis

Vascular intermittent claudication needs to be differentiated from neurogenic claudication which can also present as pain in
the lower limb on exertion. The characteristic of neurogenic claudication is “park bench to park bench” where the patient
has to sit down and flex the spine to relieve the pain (pain results from compression of the cord and spinal nerves in spinal
stenosis; extension of the spine further narrows the spinal canal while flexion widens it)
“Claudication distance” of neurogenic claudication is more variable. Patient experiences pain even while standing, hence the
patient prefers to stand in slight flexion posture. Pulses will be absent/diminished in vascular but not in neurogenic
claudication. The patient will usually not experience pain at night, with the patient able to sleep in a lateral decubitus position.
Also, paraesthesia is common in neurogenic claudication.

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3. Rest Pain
- Site – in the least well perfused area (i.e. foot, metatarsophalangeal junction)
▪ Calf pain at night in the absence of foot pain is unlikely ischemic in origin
- Nature – i.e. aching
- Severity – i.e. wakes patient from sleep
- Aggravating factors – raising the limb, lying flat in bed
- Relieving factors – putting limb in a dependent position
▪ i.e. getting up and walking, hanging foot over edge of the bed
- Able to relieve with normal analgesics? Or require opioid analgesia?
- How long has rest pain lasted for requiring opioid analgesia (if > 2 weeks, considered a feature of critical limb ischemia)
4. Any ulcer or gangrene in the lower limb? (is this critical limb ischemia?)
- Ask about onset of ulcer/gangrene
- Progress (stable, or increasing in size, getting worse)
- If ulcer, any preceding trauma? Ill-fitting shoes? Altered sensation in the foot? Does the patient take care to protect his foot?
Pain? Redness/swelling/warmth in surrounding skin? Purulent/foul-smelling discharge from the ulcer?
- If gangrene, is it wet or dry? Redness/swelling/warmth in surrounding skin? Any feeling in the toe involved? Any sensory
changes in the other normal toes, foot, limb?
- Any systemic signs of infection – fever, chills, rigors, malaise
5. Risk factors / Past Medical History

- Current smoker / Ex-smoker (strongest RF; 3-6x risk of IC, higher than the risk for IHD)
- Diabetes mellitus – 2x increase risk, every 1% increase in HbA1c = 26% increase risk of PAD
▪ When was the last ABI? – recommend doing every five years
- Hypertension
- Hyperlipidaemia
- Hyperhomocysteinemia – stronger RF for PAD than CAD
- Coronary Artery Disease + current cardiac symptoms
- Obesity / Sedentary lifestyle
- Stroke / TIA (? carotid disease)
- Family history – i.e. family hx of a first degree relative with an AAA
6. Drug History / Past Medical History

- Medication history: use of antiplatelets (i.e. aspirin / plavix), use of anticoagulants (i.e. warfarin / NOACs)
- Previous vascular interventions (i.e. endovascular or surgical)
- Any allergies to contrast (for angiography)
7. Social history
- Impact on patient’s quality of life – i.e. work and sleep
- Premorbid function and current function
- Social support and home condition (need to climb stairs?)
- Occupation and impact on ability to work

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Clinical Examination39
Examine the patient’s lower limbs in a warm room, with the patient exposed optimally (from the groin to the toes, wearing underwear).
The patient is supine with the bed flat.
Look (Inspect) – most of the pathology will be around the feet and toes!
1. Colour of the lower limb
- Red – vasodilatation of the microcirculation due to tissue ischemia
- White – advanced ischemia
- Purple/blue – excess deoxygenated blood in the tissue
2. Trophic changes
- Loss of hair
- Thickening of the nails
- Dry, shiny skin – autonomic neuropathy
- Small non-healing sores/ulcers – esp. between toes / soles / heels (look at pressure points)
3. Loss of digits / foot – due to previous gangrene / amputation – see below
4. Presence of ulcer (see below)

- Look carefully at the entire lower limb, including the heels and between the toes
- Site of the ulcer
▪ Venous ulcers form at the medial malleolus
▪ Arterial ulcers are more distal (in the least well perfused areas and over the pressure points) – lateral aspect of foot
and lateral malleoli
▪ Neuropathic ulcers form at areas such as the heel and at the metatarsal heads
- Size, shape
- Edges (punched out & well circumscribed – arterial, sloping – venous)
- Base
▪ Depth of the ulcer (can see underlying tendon? Down to bone?)
▪ Appearance of the base – Necrotic? Granulating (beefy-red)? Sloughy?
▪ Any discharge – pus, blood?
- Surrounding skin
▪ Erythema (cellulitis) – there may be an underlying abscess (confirm on palpation)
▪ Blistering, purplish colour (possibility of necrotising fasciitis)
5. Presence of gangrene
- Look between and at the tip of the toes
▪ Wet (infected): moist appearance, gross swelling, blistering, bacterial infection and putrefaction occurs, gangrene
spreads proximally, often occurs in diabetics with decreased sensation and unrecognised trauma, requiring an
emergency surgical debridement of amputation, proximal amputation is required where blood supply is better
▪ Dry (not infected): hard, dry texture, clear demarcation between viable and black necrotic tissue, dead tissue may fall
off (auto-amputation)
- Extent of gangrene – line of demarcation
- Skin blistering may occur
- Differential diagnosis: acral lentiginous melanoma
6. Presence of diabetic skin changes or joint deformities

- Diabetic Dermopathy: atrophic hyper-pigmented skin lesions usually on the shin
- Charcot Joint: chronic progressive destructive neuropathic joint arthropathy secondary to disturbance of sensory innervation
39 Clinical Cases and OSCEs in Surgery (2nd edition) – Case 111 / 118 / 120

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Feel (palpate)
1. Temperature – Warmth of the skin
- Use the dorsum of the fingers of both hands to simultaneously run up the patient’s feet to the shins and thighs bilaterally
- Compare the temperature on both side, if one limb feels cool, feel for the level where the skin becomes warm
2. Capillary Refill Time (normal < 2sec)
- If a toe is blue, check for blanchability (fixed staining = dead toe)
3. Palpating the ulcer if present – any swelling
- Any surrounding tenderness (infection), bogginess of surrounding tissue (may have abscess formation)
- See if any discharge from the ulcer when palpating
Venous Ulcers Ischemic Ulcers Neuropathic Ulcers
Pain Painful Painless
Gaiter region over Heel, metatarsal heads (pressure
Site Tip of toes and pressure area
medial malleolus of the ankle areas)
Can be large (broad base)
Size Varying size, few mm to cm Several cm
Shallow
Regular outline
Shape Variable, usually irregular Regular outline
follows skin contour – ‘punched-out’
Edges Sloping pale purple / brown Punched out clean Clean
Pink granulation tissue, No granulation tissue,
Base Often exposing bone
white fibrous tissue Bone may be exposed
Chronic venous signs
Surrounding Skin Pale / Cyanotic Normal / Red Appearance
(i.e. lipodermatosclerosis)
Temperature May be warmer Cold Foot Dry Warm Foot
Pulses Present Absent Present
Sensation,
Variable Loss
Reflexes
Bone No Bony Deformity Bony Deformity
Local Sensory Loss
Calluses absent / infrequent
Others Presence of callus
Collapsed Vein
Dilated Veins
* Aetiology of DM foot ulcers: (1) neuropathic – 45-60%; (2) ischemic – 10%; (3) mixed neuro-ischemic – 25-45% (correlate clinically)
4. Inguinal Lymph Nodes – especially if LL ulcer looks infected or if considering the differential diagnosis of melanoma
5. Sensation / Paraesthesia
6. Pulses
- Feel the distal pulses and work your way proximally (i.e. DP/PT > Popliteal > Femoral)
- Grading of pulses: 2+ is normal, 1+ is diminished, 0 is not felt
Dorsalis pedis - 1/3 way down a line joining the midpoint of the two malleoli to the 1 st webspace
pulse - Ask patient to point big toe to the sky (demonstrating EHL) – artery lies immediately lateral
Posterior tibial - 1/3 way down a line joining the medial malleolus to the heel
pulse - Examine both posterior tibial pulse simultaneously
- With patient’s knee bend ~ 60 degrees, pulse is best felt by compressing it against the posterior aspect of the tibial
- Examine for possibility of underlying popliteal aneurysm
Popliteal pulse 1. Pulsating mass that does not alter with change in position of the knee
2. 50% are bilateral check contralateral side & 50% have an AAA
3. If distal pulses not felt, ?thrombosed aneurysm
Femoral pulse - Mid-inguinal point (midpoint of the line joining the pubic symphysis to the ASIS), just below the inguinal ligament
Move
1. Any weakness / paralysis
2. Buerger’s test* and assessment of Buerger’s angle (assess 1 limb at a time)
- Get patient to lie as close to the side of the bed as possible
- Holding the heel of the foot, with the patient’s lower limb straightened, slowly lift the LL, looking at the colour of the toes
- Stop when the toes become pale (white)
- Estimate the angle the lower limb makes with the horizontal – this is the Buerger’s angle
▪ Normal lower limb can be raised to 90 degrees without turning white; if the Buerger’s angle is less than 20 degrees,
this indicates chronic ischemia
- There may be venous guttering of the lower limb at this angle as well
- If the patient is lying near the side of the bed, tell the patient that you’re going to put his leg over the edge of the bed before
gently abducting the hip and then letting the leg drop over the edge of the bed
- Look at the leg for reactive hyperaemia (foot turns purple-red)
* holding up the leg induces an ischemic environment and when the patient hangs his legs over the side of the bed there is de pendent rubor secondary
to reactive hyperaemia (autonomic stimulation due to increased acidity in an ischemic environment)

477
Complete the exam
- Examine the rest of the peripheral pulse
- Offer to auscultate over the femoral and popliteal arteries for bruits
- Palpate abdomen for any abdominal aortic aneurysm – expansile pulse above umbilicus (AAA a/w symptomatic LEAD)
- Cardiovascular Examination – atrial fibrillation / murmurs
- Auscultate the neck for any carotid artery stenosis
- Measure the ankle-brachial pressure index (ABPI) on each side
- If suspect neuropathy, assess for proprioception, vibration, pin-prick, monofilament, ankle jerk
AIM TO (1) INDICATE LIMB (2) SEGMENT OF VESSEL DISEASE (3) PRESENTING SYMPTOMS
Patient has Right LL peripheral arterial disease involving the (aorto-iliac / femoral-popliteal or tibial-peroneal) segment with
tissue loss
CLINICAL CLASSIFICATION FOR LEAD40
Fontaine’s Classification (Europe) - Chronic Limb Threatening Ischemia (CLTI)

Stage I: Asymptomatic
Stage IIa: Mild claudication (IC after > 200m of walking)
Stage IIb: Moderate to severe claudication (IC after < 200m of walking)
Stage III: Ischaemic rest pain (rest pain appear especially during the night)
Stage IV: Ischemic ulceration or gangrene
Rutherford Classification (USA) - Chronic Limb Threatening Ischemia (CLTI)

0: asymptomatic
1: mild claudication
2: moderate claudication (the distance that differentiates mild, moderate and severe is not specified)
3: severe claudication
4: ischemic rest pain
5: minor tissue loss (non-healing ulcer, focal gangrene with diffuse pedal ischemia)
6: ulceration or gangrene (major tissue loss extending above trans-metatarsal level, frank gangrene)
Assessment of Severity
The three L’s of peripheral arterial disease:
1. Life – does disease threaten life (e.g. sepsis; other complications of atherosclerosis e.g. stroke, AMI)
2. Limb – will patient lose the limb
3. Lifestyle – is the lifestyle of the patient severely handicapped, does it require intervention
40 J Vasc Surg. 2007 Jan;45 Suppl S:S5-67. [Important Paper]

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INVESTIGATIONS41
1. Ankle-brachial pressure index

- How the ankle-brachial pressure index is done
▪ Brachial pressure is measured with a BP cuff around the arm and a doppler probe at the brachial artery – cuff is
inflated until the arterial signal is obliterated, then slowly deflated until the signal just starts being detected, at which
the pressure is recorded
▪ Ankle pressures measured with the cuff around the calf and the doppler at the dorsalis pedis and posterior tibial
arteries – one reading for each artery
- Interpreting the values

▪ Normal ABI is > 0.9 (can be > 1.0 as ankle pressures tend to be higher than brachial)
▪ ABI between 0.5 - 0.9 – occlusion, often associated with claudication
▪ ABI <0.5: Critical Ischemia Rest pain
▪ if >1.40, suggests non-compressible calcified vessel (i.e. DM / ESRF patients, perform Toe pressures index (TPI)
instead (an abnormal TBI is <0.70)
- Accuracy of the index

▪ ABPI ≤0.9: strongly correlated with all-cause mortality independent of Framingham risk score
▪ ABPI ≤0.9: 95% sens & 99% spec. in detecting angiogram positive disease PAD and is a/w >50% stenosis in one or
more major vessels
▪ ABI ↓by 0.10 associated with ↑10% of major vascular event
- Exercise treadmill testing

▪ For patients with normal ABI at rest in combination with classic symptoms
▪ Measure ABPI before and after patient exercises on a treadmill
▪ If the ABPI falls by >0.2 🡪 claudication
2. Arterial Duplex ultrasound

- 1st line imaging to all people with PAD
- Operator dependent, non-invasive test, limited by difficulty to visualize iliac arteries and extensive calcification may
compromise examination
- Duplex (two modalities): 2D ultrasound (visualize vasculature) and Doppler ultrasound (measures flow and waveforms)
- Normal arterial flow waveform should be triphasic; biphasic and monophasic waves are abnormal
- Can define anatomy of occlusions and also look for relatively good arteries distally for “landing zone” of bypass graft
- Help to determine the TASC classification (see below)
41 N Engl J Med. 2001 May 24;344(21):1608-21.

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3. Basic laboratory investigation
- FBC, U/E/Cr, PT/PTT, septic workup: blood c/s, wound c/s (as indicated)
- C-Reactive Protein – if ↑in asymptomatic patients, higher risk of developing PAD in subsequent 5 years42 (not routine)
4. Transcutaneous Oxygen Pressure (TcPO2)

- Useful in patients with medial calcinosis and incompressible arteries
- Useful to determine wound healing capacity after amputation, if ≤ 10mmHg, wound healing is unlikely, if > 40mmHg, wound
healing is good after minor amputation (if values are between 10-40, perform provocation tests for stratification)
5. CT Angiogram with iodinated contrast

- No significant difference in accuracy between CTA and MRA
- Diffuse calcification may make interpretation difficult
- Able to evaluate the aortoiliac segment - location and distribution of calcified lesions
6. MR Angiogram with contrast (gadolinium)

- Fast, non-invasive outpatient procedure (<15min) with no exposure to ionizing radiation
- Not affected by arterial calcifications
- Tendency to overestimate degree of stenosis can be inaccurate in stented arteries
7. Conventional Angiogram (arteriogram)

- Invasive procedure with its associated risks, hence, perform only if planning intervention e.g. angioplasty, stenting
- Angiogram with digital subtraction – the images of the underlying bone are removed so as to better visualise the arteries,
gold standard for evaluating arterial tree prior to revascularization
- Risks: Bleeding from arterial puncture*, hematoma, femoral pseudo(false)aneurysm, dissection of arteries (or shower emboli)
leading to trash feet, contrast induced nephropathy**, failure of procedure, re-stenosis
- Preparing for angiogram:
▪ Take informed consent from patient – diagnosis, indications, recommendation, benefits, risks, alternatives
▪ Ask about contrast allergy^, asthma, renal disease^^, metformin
▪ Investigations: FBC, PT/INR/APTT, U/E/Cr, GXM
* Arterial puncture above the inguinal ligament increases the risk of retroperitoneal haemorrhage (cannot be controlled with external compression),
patients present with hypotension and ipsilateral flank pain
** Hypertonicity of the agent may produce an intense vasospasm of the afferent arteriole
^ Allergy to Iohexol (omnipaque), premedicate patients with prednisolone 30mg ON and OM or IV hydrocortisone 200mg once + use visipaque instead
^^ Know eGFR, if patients have chronic kidney disease can consider carbon dioxide instead of iodinated contrast (i.e. omnipa que)
DIAGNOSTIC CRITERIA FOR LEAD
42 Eur J Vasc Endovasc Surg. 2007 Jul;34(1):18-22.

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MANAGEMENT
Management of asymptomatic patients43
- Best Medical Therapy (BMT)

▪ Smoking Cessation
▪ Healthy diet and physical exercise
▪ Lipid Control: LDL <1.8 mmol/L or decrease by ≥ 50% if baseline is between 1.8 to 3.5mmol/L – i.e. start statins
▪ HTN control: BP < 140/90mmHg, if DM / CRF BP target < 130/80mmHg – i.e. ACEi
▪ Diabetes Control: HbA1c <7.0%
▪ Single Antiplatelet therapy (SAPT): for symptomatic LEAD patients or those who have undergone revascularization –
clopidogrel is the preferred option (although aspirin is more widely used in clinical practice) , at present there is a lack of
data for DAPT over aspirin alone in reducing CV events in patients with LEAD. (CHARISMA trial) 44
▪ Anticoagulation is given only if there are concomittant indications
- Smoking Cessation* ↓ progression of disease

▪ Doctor’s advice alone = 5% cessation at 5 years
▪ Doctor’s advice + formal cessation program + nicotine replacement = 22% cessation rate at 5 years
▪ (above) + Bupropion (anti-depressant) / Varenicline (nicotinic receptor partial agonist**) = best cessation rates!
▪ Ask patients about the status of smoking at every visit!
* smoking cessation not proven to symptomatically improve symptoms of claudication

** reduces nicotine withdrawal and attenuate the rewarding effects of nicotine
Management of symptomatic (claudication) patients (above plus)
43 Circulation. 2013 Apr 2;127(13):1425-43.

44 N Engl J Med 2006; 354:1706-1717.

481
- Supervised exercise training (SET)
▪ For at least 30-45min at least 3x/week for at least 12 weeks, walk till pain comes, rest 2-3mins, walk again
▪ Keep a walking diary, record daily claudication distance
- Lifelong Antiplatelet Drugs

▪ Aspirin 100mg* or Clopidogrel 75mg** – reduce risk of MI, stroke or vascular death in individuals with symptomatic
atherosclerotic lower limb PAD
▪ Plavix preferred to Aspirin (though aspirin still more widely used)
▪ No benefit of adding warfarin!
* Mechanism of Aspirin – irreversibly inhibits COX-1 & 2 enzymes via acetylation which results in decreased formation of prostaglandin precursors.
Irreversibly inhibits formation of thromboxane A 2 via acetylation of platelet COX thus inhibiting platelet aggregation
** Mechanisms of Clopidogrel – active metabolite irreversibly block P2Y 12 component of ADP receptors on platelet surface which prevent GPIIb/IIIa
receptor complex, thereby reducing platelet aggregation
- Pharmacological agents to decrease walking impairment

▪ Cilostazol (Pletal) – type III PDE inhibitor – inhibits platelet aggregation and cause vasodilatation
▪ Contraindicated in patients with class III or IV Heart Failure
▪ Naftidrofuryl (Praxilene 200mg TDS) – vasodilator (increase mean walking distance by 60%)
▪ Pentoxifylline (not well established)
- Revascularization Therapy (IRONIC trial)

▪ A liberal strategy of invasive endovascular treatment in patients with lifestyle limiting intermittent claudication resulted in
health related quality of life improvement during the first 2 years but this observed benefits was not maintained at 5 years
Management of Chronic Limb Ischemia (endovascular or open revascularization)

Indications
1. Limb salvage, critical limb ischemia (i.e. tissue necrosis, rest pain)
2. Infection
3. Prevention of further peripheral atheroembolization
4. Incapacitating claudication – at least 6 months of conservative treatment first
▪ Monitor claudication distance & ABI – intervene if deteriorating
▪ If parameters improve but then plateau, discuss with patient about acceptance of symptoms, and the risks of intervention
- For patients with chronic threatening limb ischemia (CTLI), early surgical referral is required, if patients are candidates for
revascularization then aim for angiographic evaluation. if patients are not candidate for revascularization then either treat
medically or with amputation (if pain is non-tolerable or patient is septic from limb infection)
Endovascular – Lower Limb Angiography, Angioplasty Keep In View Stenting

- Aortoiliac occlusive disease
▪ Indicated for symptomatic stenosis or occlusive lesions, use the TASC II classification to stratify patients. (see below).
▪ 5-year patency of common and external iliac angioplasty without stenting – common iliac: 70-80% & external iliac: 50-60%
- Infra-inguinal occlusive disease

▪ Involves femoropopliteal occlusive disease & tibioperoneal occlusive disease
▪ Short, focal stenosis (TASC A) are felt to be amenable to endovascular therapy whereas TASC D are best addressed by
open surgical bypass45
▪ The decision for endovascular or surgical procedure is determined by a myriad of factors involving patients surgical risk, life
expectancy, severity of ischemia, anatomical pattern and vein availability.
- Use of Drug Coated Balloon (DCB) or Drug Eluting Stent (DES) has been developed to address the problem of re-stenosis.
▪ Pacitaxel on DCB inhibit neo-intimal growth in the vessel wall
- Post-revascularization, patients to be treated with low dose rivaroxaban (2.5mg BD) + Aspirin (VOYAGER-PAD trial) +/- Plavix
45 The Washington Manual of Surgery (2 nd Edition) – pg. 446

482
Open Surgical Intervention with Bypass grafting
Consider bypass when lesions cannot be treated by angioplasty i.e. lesion extends for long distance through the vessel and/or no
lumen for guide wire to pass through (complete occlusion)
- Aorto-iliac occlusive disease (see below)

▪ Aorto-bifemoral grafting: reported patency up to 95% at 5 years (tx of choice!)
▪ Iliac angioplasty and femoral-femoral crossover bypass (FFB)
▪ Axillo-bifemoral bypass (AxBF)
*Ensure flow to at least 1 internal iliac artery present to prevent vasculogenic impotence and pelvic ischemia – aim to see good back-bleeding
- Infra-inguinal occlusive disease

▪ Above Knee Occlusion (femoropopliteal occlusive disease): femoral-popliteal bypass,
▪ Below Knee Occlusion (tibioperoneal occlusive disease): femoral to anterior / posterior tibial artery
▪ Will needs adequate inflow and outflow (i.e. good “landing zone” for graft distally with best continuous run off to the foot,
hence if vessel is diffusely diseased, difficult to perform bypass)
▪ Conduit used: autogenous veins (i.e. great saphenous vein) > prosthetic conduits (i.e. dacron or ePTFE)
▪ Long-term patency rates are superior to endovascular interventions
** 5-year patency of above knee vein graft is 75%; prosthetic is 40-50%
*** 5-year patency of a below-knee vein graft is 65%; prosthetic is 30%46
Endarterectomy
- To address severe stenosis or occlusion of common femoral and profunda femoris arteries
46 ABSITE Slayer (Vascular, Chapter 24) – pg. 337

483
EXTRA INFORMATION
TASC II Classification for Femoropopliteal Occlusive Disease & Bypass Grafting for Aortoiliac Occlusive Disease

484
Management of Gangrenous Limb
- Infection and Pain Control
- Prompt Revascularization
▪ May require revascularisation interventions before amputation to ensure good healing, or to allow for distal amputation
▪ Do not simply amputate without ensuring good vascular supply to the surgical site, otherwise, the wound will not heal
- Amputation47
▪ Indications (4Ds)
▪ Dead (ischemic): peripheral vascular disease (80-90% of all cases)
▪ Damaged (trauma): unsalvageable limb, burns
▪ Dangerous: Gangrene, ascending sepsis, malignancy (soft tissue / bone)
▪ Damn nuisance (infection/neuropathy): osteomyelitis, necrotizing fasciitis
▪ Level of amputation depends on vascularity of the limb and indication (e.g. if infected, amputate above level of infection)
▪ Arterial duplex ultrasound: occluded SFA and profunda arteries will have high rate of BKA failure
▪ Ankle Pressure: >60mmHg predicts BKA healing in 50-90% of patients
▪ Toe Pressures: utilized if patients have DM
▪ Transcutaneous Oxygen Tension (TcPO2): used if there is edema, obesity, hyperkeratosis
▪ As far as possible try to preserve function of the lower limb
- Types of Amputations
▪ Disarticulation at joint (PIP, DIP)
▪ Ray Amputation (excision of toe and part of the metatarsal)
▪ Transmetatarsal Amputation (TMA)
▪ Lisfranc (tarsometatarsal)
▪ Chopard’s (Midtarsal)
▪ Syme’s (through ankle)
▪ Below Knee Amputation (BKA)
▪ Through Knee (Stokes-Gritti)
▪ Above Knee Amputation (AKA)
▪ Hip disarticulation
▪ Hindquarter amputation (hemipelvectomy)
- Outcome after amputation:

▪ Below Knee Amputation: 90% of patients will eventually be able to walk again, with unilateral BKA energy expenditure
increases by 40% and with bilateral BKA energy expenditure increases by 60-70%
▪ Above Knee Amputation: 50% of patients will eventually be able to walk again
▪ Unilateral AKA will lead to energy expenditure increasing by 100%
47 Clinical Cases and OSCEs in Surgery (2nd Edition) – case 113

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COMPLICATIONS
Complication of Surgical Revascularization

- Morbidity: 20-30% (post-operative cardiac events ~ 5%, pulmonary complications ~ 7%)
▪ Atheroemboli with end organ ischemia
▪ Post-operative hemorrhage
▪ Wound complications - i.e. wound infection, lymphocele, lymphocutaneous fistula
▪ Ischemic colitis (rare)
▪ Pelvic Ischemia (rare)
- Mortality: 1-4%
- Late Complications
▪ Thrombosis
▪ Pseudoaneurysm
▪ Graft Enteric Fistula
Complication of Endovascular Revascularization

- Assess site complications
▪ Pseudoaneurysm
▪ Retroperitoneal Bleeding
▪ Dissection
▪ Atheroembolism
- Procedural complications
▪ Arterial rupture
▪ Dissection, vessel spasm, thrombosis and atheroembolism
- Post-Procedural complications
▪ Contrast induced Nephropathy
▪ Graft Thrombosis (if early require thrombectomy), if occurs within 2 years usually due to neointimal hyperplasia
Complications after amputation:

These patients often have other medical problems (i.e. cardiovascular disease) – hence high risk of mortality – operative mortality
as high as 20% and one-year survival is 50%
- Early complications
▪ Hematoma and wound infection (rare: gas gangrene)
▪ Deep vein thrombosis and pulmonary embolism
▪ Phantom limb pain
▪ Skin necrosis – 20 to poor perfusion of stump – require re-fashioning
▪ Psychological & Social
- Late complications
▪ Osteomyelitis
▪ Stump ulceration – 20 to pressure from prosthesis
▪ Stump neuroma
▪ Fixed Flexion deformity
▪ Difficulty mobilizing
▪ Spurs and osteophytes in underlying bone

486
ACUTE LIMB ISCHEMIA48
DEFINITION
Acute limb ischemia is defined as a sudden decrease in limb perfusion that threatens the viability of the limb (manifested by
ischemic rest pain, ischemic ulcers, and/or gangrene) in patients who present within 2/52 of the acute event (if >2/52, considered
chronic ischemia).
RISK FACTORS
1. Arterial embolism
▪ Most common cause of acute limb ischemia (60-80% of the time)
▪ The most likely source of embolus is the heart (80%), of which 70% is due to atrial fibrillation, 20% due to AMI with LV
mural thrombus, and a small proportion to disease valves, subacute endocarditis and acute bacterial endocarditis
▪ Non-cardiac emboli – arise from arteries where there are atherosclerotic plaques or an aneurysm (the embolic material may
be thrombus or part of a plaque, but atheroemboli are less likely to cause complete arterial occlusion)
▪ Paradoxical embolism – patients have a patent foramen ovale (PFO), whereby embolus from a DVT cross through the atrial
defect to the left side of heart into peripheral circulation
▪ Most common sites where emboli lodge:
- Bifurcation of the femoral artery (most common site)
- Trifurcation of the popliteal artery (next most common site in the lower limb)
- Aortic bifurcation
- External and internal iliac
- Arm (about 20% of emboli)
▪ Emboli usually cause lower limb ischemia
▪ After emboli obstructs the vessel, thrombus can propagate distally (due to stasis of blood) and proximally (due to turbulence
of incoming blood hitting embolus) by derangements in the Virchow’s triad
2. Acute thrombosis
▪ Thrombosis of a previously stenotic but patent artery (atherosclerotic vessel)
▪ Less common cause of acute limb ischemia
▪ When thrombotic occlusion of a vessel does occur, the resulting ischemia is usually less severe than in an embolic occlusion,
because collaterals have had time to form around the chronically stenosed vessel
▪ Other less common causes of acute thrombosis includes arteritides (usually affecting medium-sized arteries), ergotism,
popliteal aneurysm, and hypercoagulable states (notably anti-phospholipid syndrome, heparin-induced thrombocytopenia)
Differentiating between embolic and thrombotic causes

Embolic Thrombotic
Identifiable source Present – AF, recent AMI Less common
Claudication hx Negative Positive
Contralateral pulses present Contralateral pulses diminished
Physical findings
White limb (no blood) Dusky limb (collaterals still supplying limb)
Minimal atherosclerosis, sharp cut-off, few Diffuse atherosclerosis, irregular cut-off, well-developed
Angiography
collaterals collaterals
3. Arterial trauma
▪ Increasing incidence of acute arterial occlusion due to endovascular diagnostic or interventional procedures
▪ Trauma can cause development of an arteriovenous fistula that shunts blood away from the limb
▪ Fracture or dislocations can stretch an artery and cause an intimal tear while the media and adventitia layers are intact
(because they contain elastin and can stretch), a thrombus forms at the site of the tear where underlying thrombogenic
collagen is exposed
▪ Compartment syndrome can result from trauma as well
4. Dissecting aortic aneurysm

▪ As the dissection occur between the intima and media of the aorta, it can cause occlusion of the aortic branches at their
origins
PATHOPHYSIOLOGY
In order of sensitivity to ischemia, the tissues affected are nerves (most sensitive), muscle, skin, and bone (least sensitive); thus early
signs of ischemia involve pain and numbness, and muscle paralysis, as well as skin changes, occur later. The lower limb can survive
about 6 to 8 hours in an ischaemic state before the injury becomes irreversible.
48 N Engl J Med 2012;366:2198-206.

487
The classic 6 P’s of acute limb ischemia: Paraesthesia, Pain, Pallor, Poikilothermia (impaired regulation of body temp), Pulselessness,
Paralysis (order of presentation)
1. Pain Pain Pain Pain Pain Pain

▪ Develops acutely
▪ Starts off in a distal part of the extremity and then progresses proximally, increasing in severity with time
▪ Further progress leads to decrease in pain as the nerves die off from ischemia
▪ Important to ask for any previous claudication pain (10% of claudicants can develop acute ischemia due to thrombosis of
the stenosed vessel)
2. Paraesthesia
▪ Starts off with paraesthesia (develops relatively early in the course of ischemia) and develops to complete loss of sensation
▪ Progression: Light touch > Vibration > Proprioception > (late) Deep pain > Pressure sense
3. Pallor
▪ Assess skin colour, temperature, and capillary refill time
▪ The limb may still be slightly pink though pale, but in severe ischemia, it can be marble-white (especially in embolus where
there are no collaterals)
▪ Other colours:
- Mottling/Marbling (patches of blue on white): deoxygenation of stagnated blood; surrounding areas of pallor are due
to vasoconstriction
- Duskiness: due to deoxygenation of stagnated blood; if there is fixed staining (i.e. does not blanch on pressure) then
the limb is non-viable
- Black: gangrene
▪ The discolouration usually affects a large part of the distal limb (i.e. feet and toes), rarely does it only affect one toe
▪ The site of arterial occlusion is usually one joint above the line of demarcation between normal and ischemic tissue
4. Paralysis – poor prognostic sign

▪ Initial: heavy limb, Late irreversible ischemia: muscle turgidity
▪ Total paralysis occurs late and usually indicates that the limb is non-viable
▪ Intrinsic foot muscles > Leg muscles (toe movement produced by leg muscles → detect late)
▪ Can assess viability of muscle by making a cut – viable muscle will be shiny and twitches in response to flicking, while dead
muscle will be dull and will not twitch
▪ Dangerous to save dead muscle as reperfusion can cause circulation of toxic metabolites
5. Pulselessness
- If able to feel one good pulse (PT or DP), quite unlikely that the limb is ischaemic, but still possible
- If no palpable pulse, assess with a handheld Doppler – there can still be flow without a palpable pulse
- Also feel the pulses on the other limbs – gives a clue as to whether the cause is embolic or thrombotic (see below)
- Acute DVT: Phlegmasia cerulea dolens = painful blue oedema
- Blue toe syndrome: atheroembolism from AAA or more proximal
- Purple toe syndrome: Cx of warfarin therapy
- Venous insufficiency / Venous occlusion
- Acrocyanosis

488
CLASSIFICATION
Rutherford Criteria for Acute Limb Ischemia

Three categories: viable, threatened and non-viable
- Viable: No immediate threat of tissue loss
- Threatened*: Salvageable if re-vascularised promptly
- Non-viable: Limb cannot be salvaged and has to be amputated, no emergency to operate. Patient may require revascularisation
to allow lower amputation or help amputation to heal
* threatened extremities a/w presence of (1) rest pain, (2) sensory loss (3) muscle weakness
Findings Doppler Signal
Stage Description and Prognosis Sensory Muscle Recommendations
Arterial Venous
Loss Weakness
I Limb viable None None Audible Audible
II Limb threatened None None Audible Audible Imaging (i.e. u/s duplex,
Marginally threatened, CTA/MRA) to determine nature
Minimal Often
IIa salvageable if promptly None Audible and extent of occlusion
(toes) Inaudible
treated
Immediately threatened,
> toes, a/w Mild / Usually Imaging & emergency
IIb salvageable with immediate Audible
pain at rest Moderate Inaudible Revascularization
revascularisation
Profound,
Profound,
III Non-viable Paralysis Inaudible Inaudible Amputation after demarcation
aesthetic
(rigour)
INVESTIGATIONS
Biochemical
- FBC, U/E/Cr
- PT/INR/APTT
- GXM
- Trop I (if suspecting AMI with mural thrombus)
Imaging
- Doppler u/s: viable vs. threatened vs. non-viable + level of obstruction
- CXR / ECG
- CT angiogram (but in patients with threatened limb, may instead op to do on-table angiography)
MANAGEMENT
The decrease in perfusion is usually due to sudden cessation of blood supply and nutrients to metabolically active tissues of the limb.
This may be in a setting of already narrowed vessel lumen (acute on chronic ischemia) or in a normal lumen. If adequate collateral
circulation is absent, irreversible changes may appear 4-6hours after onset. Proceed to perform emergent evaluation that defines
anatomical level of obstruction and prompt revascularization (endovascular or surgical)
1. Early anticoagulation
▪ Give IV heparin bolus 3000-5000 units (70 units /kg)
▪ Follow with IV heparin infusion at 1000 units/hour (10-15 units/kg /hr)
▪ Ideal PTT is 2 to 2.5 times normal → avoid clot propagation
2. Measures to improve existing perfusion
▪ Keep foot dependent
▪ Avoid pressure to heel, extremes of temperature
▪ Max tissue oxygenation (O2 supp) – give 100% oxygen
▪ Correct hypotension
3. Surgical emergency requiring active intervention
▪ Emergency thrombectomy / embolectomy
▪ Intra-arterial thrombolysis ± angioplasty
4. KIV fasciotomy to prevent compartment syndrome

489
EXTRA INFORMATION
Heparin Therapy Protocol (Target APTT: 50-75 sec)

- Administer IV heparin bolus dose (70 unit / kg (max 4,000 units)) followed by an infusion of IV heparin at 15 unit/kg/hr
- Check APTT 4-6 hours after initiating therapy (1/2 life of heparin ~60-90min)
- Adjust infusion rate of IV heparin using table below based on APTT
- Protocols may vary between institutions
APTT (sec) Bolus dose Stop Infusion (min) Rate Change (unit / kg / hr) Repeat APTT (hr)
(unit)
< 40 3,000 - ↑2 units / kg / hr 6 hours
40 – 49 - - ↑1 unit / kg / hr 6 hours
50 – 75 - - maintain infusion rate Next day

76 – 85 - - ↓1 unit / kg / hr 12 – 18 hours
86 – 100 - 30 ↓2 unit / kg / hr 6 hours
> 100 - 60 ↓3 unit / kg / hr 4 hours
* If bleeding, repeat APTT and titrate as above (reversal agent = protamine sulfate 1mg/100U of heparin)
Surgical Options
“Aim to restore blood flow as rapidly as possible to a viable or threatened limb”
Open Surgical Revascularization (Emergent Embolectomy)

Usually performed under GA, but can be done under LA but still require anaesthetist to monitor patient as patient may be quite sick
(e.g. AMI), and hyperkalaemia with cardiac arrhythmia can occur after reperfusion
- Involves clamping of the involved artery (i.e. femoral artery) and making an arteriotomy
- A Fogarty balloon catheter (i.e. 4Fr) is inserted into the artery until distal to the clot, then the balloon is inflated to trawl the clot
out of the artery
- Check for forward-bleeding and back-bleeding of the vessel (i.e. free spontaneous flow from proximal and distal ends of the
artery when unclamped)
- Flush with heparinized saline
- Check foot – warm foot with good pulse indicates reperfusion
- Important to monitor ECG for any arrhythmias!
- Closure of arteriotomy with meticulous haemostasis as patient is on heparin
- Post-operatively – look out for complications! (see below)

- Need to convert heparin to warfarin or novel oral anticoagulation (i.e. dabigatran or rivaroxaban)
Intra-arterial catheter-directed thrombolysis ± Angioplasty

- Diagnostic angiogram is done before thrombolysis to locate occlusion
- Thrombolysis catheter inserted into the clot, and the thrombolytic agent (i.e. alteplase – recombinant tissue plasminogen activator
– TPA) is infused → convert plasminogen to plasmin which then degrades fibrin

- Patient will be in HD with thrombolytic infusion for 6 hours (~1000-4000 units per minute)
- Clinical and angiographic examinations are performed during infusion to determine progress
- After 6 hours, repeat angiogram to check for residual clot; if clot remains, adjust catheter and infuse for 6 more hours
- After complete lysis of the clot can do balloon angioplasty/stent
- Takes much longer than embolectomy
- Thrombolysis may be preferred for embolism in a diseased artery, since it may be difficult to trawl out the clot in a diffusely
stenosed vessel – the clot may get caught on a proximal stenosed segment
- Contraindication: recent CVA, active bleeding or recent BGIT, intracranial haemorrhage or vascular brain neoplasm
EXTRA INFORMATION
Surgery versus thrombolysis for initial management of acute limb ischaemia 49

- No evidence in favour of either initial thrombolysis or initial surgery in terms of limb salvage, amputation, death
- Higher incidence of major hemorrhage and distal embolization for thrombolysis group (but less invasive intervention)
49 Cochrane Database Syst Rev . 2018 Aug 10;8(8):CD002784.

490
COMPLICATIONS
- Reperfusion Injury – with re-establishment of arterial flow to ischemic tissue bed
▪ Formation of oxygen free radicals that damage the tissue and cause WCC accumulation
▪ With reperfusion, this ↑ capillary permeability causing local oedema and risk of increasing compartmental HTN
▪ No proven therapy that limits reperfusion injury
- Rhabdomyolysis
▪ Reperfusion release K+, lactic acid, myoglobin, creatinine phosphokinase (increase in PO4 cause deposition of calcium
phosphate on muscle cells results in hypocalcemia)
▪ Correct electrolyte abnormalities – hyperkalemia and hypocalcemia (risk of arrhythmias)
▪ Diuresis patients – aim for urine output 1-2ml/kg/hr
▪ Treatment: aggressive hydration ± IV bicarbonate to alkalinize urine
▪ Patients also at risk of acute renal failure (CK > 5000u/L and/or urine myoglobin >1142nmol/L (>20mg/dL) ↑ risk of ARF)
- Compartment Syndrome
▪ Suspect if pain is out of portion to clinical situation (early sign) or pain with passive stretch.
▪ Compartment Syndrome is a clinical diagnosis based on a high index of clinical suspicion
▪ Highest risk at 4-6 hours after revascularization
▪ Risk Factors: Prolonged ischemia (≥6hr) → delayed reperfusion causes cell membrane damage and leakage of intracellular
ion/proteins/enzymes into the interstitium resulting in swelling of muscle compartments
▪ Investigations are supportive (pressure ≥ 30mmHg or within 30mmHg of diastolic pressure)

▪ Anterior compartment most commonly involved but deep posterior compartment (where tibial nerve is located) is most
functionally devastating
▪ Treatment: emergent four-compartment fasciotomy
EXTRA INFORMATION
Fasciotomy Steps
- 2 incision approach (antero-lateral incision & posteromedial incision) to release 4 compartments
▪ Anterolateral incision is centered halfway between the fibular shaft and tibia, once the fascia is identified, a transverse
incision is made to identify and anterior (1) and lateral (2) & the superficial fibular nerve
▪ Posteromedial incision is made 2cm posterior to tibial shaft and used to identify the superficial (3) and deep (4) posterior
compartment & the saphenous nerve and vein

491
CAROTID DISEASE
DEFINITION
Symptomatic Carotid Stenosis is defined as stenosis in the internal carotid artery leading to symptoms of amaurosis fugax, TIA
and/or ipsilateral ischemic stroke
- Asymptomatic
▪ Carotid bruit (4% at age > 45yr and 12% at age >60yrs)
▪ The presence or absence of a bruit does not correlate with the degree of stenosis
- Symptomatic
▪ Carotid territory: hemi-motor/Hemi-sensory signs, monocular blindness (amaurosis fugax), higher cortical dysfunction (i.e.
dysphagia, visuospatial neglect)
RISK OF STROKE AFTER PRESENTING WITH TIA

- Risk of stroke – 10% within 7 days of index event with ~ 50% occurring within 24 hours.
- Patients with carotid stenosis of 50-99%, stroke risk is doubled to 20%
- Higher the ABCD* score the higher the risk
▪ 0-3 = 2.3% at 7 days → outpatient clinic appointment within 7 days
▪ 4-5 = 5.9% at 7 days → admit and assess within 24 hours
▪ 6-7 = 11.7% at 7 days → admit and assess within 24 hours
* ABCD = Age (i.e. > 60yrs = 1), BP (i.e. systolic > 140 or diastolic > 90 = 1), Clinical (i.e. unilateral weakness = 2, spee ch disturbance only = 1, others
– 0), Duration of symptoms (i.e. > 60mins = 2, 10-59min = 1 < 10min = 0) & Diabetes (1)
MANAGEMENT
Best Medical Therapy

- Optimize BP to < 140/90
- Statin therapy – 25% reduction in major coronary events, stroke, need for revascularization
- Stop smoking, stop alcohol, regular physical activity, diet modification, reduce weight
- Antiplatelet therapy (for symptomatic patients)
Indications for Carotid Endarterectomy

- Symptomatic patients with 70-99% carotid stenosis with life expectancy of at least 5 year
- Symptomatic MALE patients with 50-69% carotid stenosis with life expectancy of at least 5 years
- Asymptomatic patients with high grade (≥ 80%) carotid stenosis or have progression to ≥ 80% stenosis despite intensive medical
therapy
- No role for carotid endarterectomy for asymptomatic patients undergoing general surgery procedures
- Carotid endarterectomy (CEA) greatest benefit in the recently symptomatic (<6 months) with a 70 – 99% carotid stenosis
- Carotid Stenting** – for symptomatic carotid artery stenosis in patients with significant comorbid, high risk for GA
EXTRA INFORMATION
CREST trial50 – among patients with carotid stenosis, the risk of stroke or death were significantly lower with endarterectomy (6.4% stenting vs. 4.7 %
endarterectomy at 4 years, p = 0.03). During the periprocedural period, there was a higher risk of stroke with carotid stenting (4.1% vs. 2.3%, p =
0.01) and a higher risk of myocardial infarction with carotid endarterectomy (1.1 vs. 2.3%, p = 0.03)
50 N Engl J Med. 2010 Jul 1;363(1):11-23. [Important Paper]

492
ARTERIOVENOUS (AV) ACCESS
DEFINITION
Arteriovenous Access is an abnormal connection between an artery and a vein which is surgically created. It can be performed with
or without a prosthesis.
- AV fistula: access created by connecting a native vein to an adjacent artery (autogenous)
- AV graft: uses grafts that are either synthetic or biologic (non-autogenous)
INDICATIONS
Patients with impending renal failure or established renal failure requiring chronic hemodialysis
CLINICAL ASSESSMENT
Prior to creation of AV access
- History
▪ Diagnosis of renal insufficiency* – referred for surgical evaluation 1 year before the anticipated need for dialysis
▪ Indicated when creatinine clearance is < 25mL/min or when serum Cr >4mg/dL (>353.7 umol/L)
- Clinical Examination
▪ Hand Dominance (evaluate non-dominant hand first)
▪ Evaluate forearm – skin condition, pulses, superficial vein condition
▪ Allen’s Test
▪ Patients should protect their forearm veins from venepuncture and IV catheters – avoid potential damage (i.e. stenosis)
which could preclude future use
- Duplex Ultrasound – used for venous mapping and for assessing adequacy for arteries, alternatives:
▪ Contrast venography – evaluate patency and adequacy of venous system
▪ Conventional arteriography – evaluate suspected arterial inflow stenosis or occlusion
CLASSIFICATION
Arteriovenous Fistula (AVF)
- Usually, the radial or brachial artery is used – safest and longest lasting permanent means of vascular access – however –
requires long maturation time (~8 weeks) to provide a flow state adequate to sustain dialysis
▪ Brescia-Cimino fistula (end-end anastomosis between cephalic vein and radial artery)
▪ Gratz fistula (at elbow: anastomosing cephalic vein to brachial artery)
- Advantage of AV fistula (compared to AV graft) → long-term patency
Arteriovenous Graft (AVG)

- AV grafts consists of biologic or synthetic conduit that connects an artery and a vein and is tunnelled under the skin and placed
in a subcutaneous location
- Disadvantages: higher risk of thrombosis – 10x higher than autogenous fistula
- Advantage of AV graft (compared to AV fistula):
▪ Large surface area
▪ Easy cannulation
▪ Short maturation time – requires 2–6 weeks (allows for material to incorporate into surrounding subcutaneous tissue and
for inflammation and oedema to subside)
▪ Easy surgical handling

493
MANAGEMENT
Principles in deciding location of AV access
- Start creation access in non-dominant arm
- Autologous tissue is preferred to prosthesis (i.e. AVF prior to AVG)
- Start as distal as possible and move proximally as access failure occurs. (i.e. forearm before upper arm)
- Requiring imaging to assess adequacy and anatomy of vessels (i.e. size of vessels, any thrombosis)
Recommendation for AV creation

1. Autologous forearm AVF
2. Autologous BC AVF
3. Transposed BB AVF**
▪ Basilic vein usually requires transposition (superficialization) as it lies proximity to median antebrachial cutaneous nerve
and it is usually located deeper within the tissues
4. Upper Arm BC AVG**
** 65-70% of transposed BB AVF are patent at 1-2 years, AVG have patency rate of 50-70% at 1 year
Post-operative Evaluation (prior to starting dialysis)

▪ Wound Condition
▪ Feel for thrill – strong / moderate / weak – absence of which indicates failing or thrombosed AVF (pulsation may indicate
outflow obstruction)
▪ Hand circulation (any steal syndrome)
▪ Abnormal swelling (central vein obstruction)
▪ Evaluate size and configuration of AVF (readiness for cannulation)
- Failure of maturation of AVF at 8 weeks – inform vascular consultant
Post-operative Evaluation (after starting dialysis

- History
▪ Any recent problems with dialysis (look for any memo from dialysis centre)
▪ Thrill, pulsation, skin condition (thinning, erosion, erythema etc.)
▪ Dialysis Flow Chart
▪ Normal Arterial Pressure (Ap) < -150mmHg
▪ Normal Venous Pressure (Vp): < 140 mmHg
▪ Qb – 200-350 ml/min
▪ Access flow >600ml/min
- If no issues, follow-up is 4–6 months for AVF and 3–6 months for AVG with dialysis chart (provide memo to HD centre)
- If have issues with high pressure flow – 1st line: Ultrasound scan (in clinic) → may require endovascular intervention

494
COMPLICATIONS
- Stenosis – which can lead to upstream pseudoaneurysm formation
- Blocked AV Access
- Thrombosis
- Infection – usually with Staphylococcus aureus
- Arterial Steal Syndrome – present with: ischemic pain, neuropathy, ulceration and/or gangrene
- Ischemic monomelic neuropathy (IMN) leading to loss of function of extremity (tx: sacrifice fistula)
- Venous Hypertension – secondary to outflow venous obstruction (intimal hyperplasia)
▪ Present with: skin discolouration and hyperpigmentation, (chronic cases 🡪 ulceration)
- Congestive Cardiac Failure – secondary to increased venous return leading to cardiomegaly and CCF (hyper-circulation) \
EXTRA INFORMATION
Arterial Steal Syndrome

- AV access diverts or steal blood from distal circulation, (occurs in about 1-4% of patients with distal AV access)51
- Treatment: DRIL (distal revascularization with interval ligation) – involves arterial bypass and ligation of the native artery distal
to the mature AV anastomosis
Blocked AV Access
- Assess if the AV assess can be salvageable
▪ If salvageable – optimise patient for surgery
▪ If not salvageable – assess options for temporary dialysis access (ensure that its location will not interfere with next
vascular assess creation site)
Stenosis
- Endovascular treatment with POBA (plain-old balloon angioplasty), DCB (drug-coating balloons) or stents
- Stents used for (1) venous stenosis resistant to angioplasty, (2) thrombosis aiming to compress intraluminal thrombus against
the vessel wall and (3) angioplasty induced rupture
51 Ann Vasc Surg. 2000 Mar;14(2):138-44.

495
ANEURYSM
DEFINITION
A pathological, localized, permanent dilation of an artery to more than 1.5 times its original diameter involving all three layers of its
parent wall
Aneurysm vs. Pseudoaneurysm

- True – involves an intact attenuated vessel where the wall is formed totally by the 3 normal elements (i.e. intima, media and
adventitia). It can be saccular or fusiform.
- False / pseudoaneurysm – a pulsating hematoma, the cavity of which is in direct continuity with the lumen of an artery, where
the wall is formed by the products of the coagulation cascade (pseudocapsule), which is not part of the vessel wall.
▪ The main causes are iatrogenic (i.e. after endovascular procedure), trauma, infections or pancreatitis
▪ The most common presentation is a femoral pseudoaneurysm, followed by visceral pseudoaneurysm and aortic
pseudoaneurysms
CLASSIFICATION
Types of Aneurysm Sub-types Remarks
Saccular - Focal outward bulge (only part of the circumference is involved)
True Aneurysm
Fusiform - Circumferential dilatation
- Congenital defects in media at junction of vessels around the circle of Willis – 90% emerging
from anterior circulation
Congenital Aneurysm Berry
- Most common cause for primary subarachnoid haemorrhage
- Increased incidence in patients with HTN, APKD, Ehlers-Danlos Syndrome
Atheromatous - Commonly affects abdominal aorta, popliteal and femoral artery
- a/w subacute infective endocarditis, any form of bacteraemia (i.e. salmonella or
Mycotic
staphylococcus)
Syphilitic - (rare nowadays) – tend to involve thoracic aorta (esp. arch) – vasa vasorum endarteritis and
(Tertiary) obliteration
- Characterized by rapid development of an intimal flap, which is caused by blood flowing into
Dissecting
the media and forcing the intima and the adventitia apart. This intimal flap separates the true
(aortic
Acquired Aneurysm lumen (the normal pathway of blood flow in the aorta) from a false lumen
dissection)
- Classification into Stanford A & Stanford B (see below)
- Pulsating hematoma
False
- a/w trauma (i.e. stab wounds, IA injections), iatrogenic (i.e. after endovascular procedures)
Charcot- - Location: Basal Ganglia (lenticulostriate vessels), Cerebellum, Thalamus, Pons
Bouchard - Results in Intracerebral haemorrhage causing progressive neurologic deficit
Aneurysm - Increased incidence in patients with chronic HTN
Arteriovenous - Due to trauma or more commonly following formation of an AV fistula for dialysis
COMPLICATIONS OF ANEURYSMS*
- Rupture
- Thrombosis with occlusion – ischemic limbs, renal impairment
- Distal emboli from mural thrombus
- Pressure on adjacent structures – i.e. AAA eroding vertebral bodies, femoral aneurysm pressing on femoral nerve
- Fistula (i.e. aorto-enteric fistula)
*most common complication of aneurysm above inguinal ligament = rupture

*most common complication of aneurysm below inguinal ligament = thrombosis and emboli

496
ANATOMY OF AORTA
(Paired visceral branches)

A – Middle Suprarenal artery (L1)
B – Renal artery (btw L1-L2)
C – Gonadal artery (L2)
(Paired parietal branches)

D – Inferior Phrenic Arteries (T12)
E – 4 Lumbar Arteries (L1 – L4)
F – Common Iliac Arteries (L4)
(Unpaired parietal artery)

G – Median Sacral Artery
- 1 – Left coronary artery
- 2 – Right coronary artery
- 3 – Right brachiocephalic trunk
- 4 – Left internal carotid artery
- 5 – Left subclavian artery → 1st & 2nd posterior intercostal artery from subclavian arteries
- 6 – Posterior intercostals arteries (3rd – 11th)

▪ 1st – 6th anterior IC from internal thoracic artery
▪ 6th – 12th anterior IC musculophrenic artery (from internal thoracic artery)
- 7 – Oesophageal arteries
- 8 – Posterior Mediastinum arteries
- At T12 – aorta, thoracic duct and azygos vein perforate the diaphragm (T10 – oesophagus and vagus, T8 – IVC)
- Abdominal Aorta bifurcate at L4, Trachea bifurcates at T4, Common Carotid bifurcates at C4
EXTRA INFORMATION
Subclavian Steal Syndrome

- Arteriosclerotic stenotic plaque at the origin of the subclavian (proximal to the take-off of the vertebral) allows enough
blood supply to reach the arm for normal activity, but does not allow enough to meet higher demands when the arm is
exercised
- More commonly occurs on the left arm.
- During exercise, the arm sucks blood away from the brain by reversing the flow in the vertebral artery
- Patients present with claudication of arm and posterior neurologic signs (vascular symptoms alone would suggest
thoracic outlet syndrome, but combination with neurologic symptoms identifies subclavian steal) – a/w differences in
pulse pressure between right and left arm
- Treatment: bypass graft from common carotid to subclavian artery distal to the stenosis

497
AORTIC DISSECTION
DEFINITION
Aortic dissection is defined as an abnormal blood flow through a focal defect in the intima into the medial layer separating the layers
of the vessel wall (intima and adventitia separated). The blood returns to the true lumen of the artery distally or ruptures externally.
Risk Factors
- Advanced Age (6th to 7th decade)
- HTN
- Smoking
- Males (4 : 1 ratio)
- Structural abnormalities of the aortic wall
- Collagen Vascular Condition (i.e. Marfan’s syndrome and Ehler-Danlos syndrome)
- Pregnancy
PATHOPHYSIOLOGY
- Aorta originates from the left ventricle and terminates at L4 when it bifurcates into the right and left common iliac arterie s
- Divided into 3 main anatomical regions
▪ Ascending aorta – proximal to brachiocephalic (innominate) trunk
▪ Aortic arch
▪ Descending aorta – distal to left subclavian artery
- Posterior thoracic aorta (above diaphragm)
- Abdominal Aorta (below diaphragm)
- Mechanical Shear Effect – high pressure blood flow on aortic wall leads to intimal tear (ascending aorta and proximal segment
of descending aorta most at risk)
- Aortic Wall Fragility – i.e. hypertension as a pro-inflammatory trigger
(from Nat Rev Dis Primers . 2016 Jul 21;2:16053)
Stanford Classification
- Stanford A – dissection involving the ascending aorta (regardless of site of origin)
- Stanford B – dissection not involving the ascending aorta
DeBakey Classification
- Debakey Type I – originate in the ascending aorta, with involvement of the aortic arch & often descending aorta
- DeBakey Type II – originate in the ascending aorta and confined within it
- DeBakey Type IIIA – originate in the descending aorta, limited to thoracic aorta
- DeBakey Type IIIB – originate in the descending aorta, extends below the diaphragm to involves the abdominal aorta

498
A high index of suspicion is required
History
- Anterior chest pain or back pain (sudden onset, tearing sensation, mimicking myocardial infarction)
- Abdominal Pain – possible mesenteric ischemic
- Syncope – cerebrovascular involvement
- Upper Extremity Symptoms (pain, weakness, paresthesia) – subclavian artery involvement
- Lower Extremity Symptoms – iliac / femoral artery involvement
Examination
- Vitals – severe hypertension or hypotension (aortic rupture)
- Cardiovascular Examination – any aortic regurgitation murmur
- Assessment of upper limb and lower limb neurovascular status – (i.e. peripheral pulses, power, sensation)
Outcomes of Aortic Dissection

- True lumen can be compressed by the false lumen leading to ischemia / malperfusion
- False lumen can become aneurysmal when subject to systemic pressure
- The dissection can propagate retrograde leading to (1) dissection across the coronary ostium leading to inferior myocardial
infarction, (2) dissection across the aortic valve leading to aortic regurgitation, (3) expansion of the perical sac causing cardiac
tamponade & (4) dissection into the carotid arteries resulting in acute stroke
- The dissection can propagate antegrade leading to compromise of (1) visceral perfusion, (2) renal perfusion, (3) distal LL
perfusion
- Myocardial Infarction
- Pulmonary Embolism
- Pericarditis
- Aortic aneurysm without dissection
- Musculoskeletal pain,
- Cholecystitis, GERD, Peptic ulcer disease or Perforating ulcer and Acute pancreatitis
INVESTIGATION
- Biochemical – FBC, U/E/Cr, Trop I, PT/INR/APTT, GXM, ABG/Lactate
- Imaging
▪ ECG* – ST, T wave changes (myocardial infarction or ischemia)
▪ CXR* – widened mediastinum, pleural effusion, abnormal aortic contour
▪ CT Aortogram (gold standard) – see below
▪ 2D Echo – assess for cardiac tamponade, AV regurgitation and cardiac regional wall motion abnormalities (RWMA)
*30-40% will have normal ECG and CXR
Stanford B – ascending aorta not involved Stanford A

499
MANAGEMENT
Acute aortic dissection is a life-threatening condition. Patients should first be dichotomized to either having Stanford A or Stanford B
dissection. The main aim in the management of acute aortic dissection involves reducing the left ventricular pressure while maintaining
adequate distal organ perfusion.
Stanford A (Surgical Emergency)

- Primary Open Surgical Repair – replace ascending aorta +/- aortic valve replacement
Stanford B (Medical Emergency)

- Initial Mx: Intravenous Labetalol (alpha & beta blocker) – controls HR and produce vasodilation – decrease sheer to aorta, aim
for systolic BP of 100 – 120 mmHg, HR < 80
- Assessment of complications (i.e. contained rupture or organ malperfusion syndrome) – require surgery
- Role of endovascular therapy (i.e. TEVAR) for uncomplicated type B dissection is still being evaluated, possibly a/w improved 5-
year aorta-specific survival and delayed disease progression. (INSTEAD-XL Trial)5253
COMPLICATIONS
- Bleeding
- Cardiac Arrhythmias
- Neurological Dysfunction
- Acute Renal Impairment
- Multi-organ Failure
52 Circulation. 2009 Dec 22;120(25):2519-28. [Important Paper]

53 Circ Cardiovasc Interv . 2013 Aug;6(4):407-16. (INSTEAD XL trial)

500
ABDOMINAL AORTIC ANEURYSM54
DEFINITION
- Aortic diameter of >50% larger than normal (normal aorta ~ 2cm)
- A dilatation of < 50% of normal arterial diameter is termed aortic ectasia
- A diameter of ≥ 3cm is used to label for aortic aneurysm
EPIDEMIOLOGY
- 1.7% females and 5% males have aortic diameter of ≥ 3.0cm by age 65
- Most AAA develop below the renal arteries (infra-renal artery)
- Aneurysm disease may extend to the common iliac arteries in 20-25% of patients
- Patients with AAA have 15% risk of having concomitant femoral or a popliteal aneurysm
- Patients are frequently asymptomatic often detected incidentally on abdominal imaging
RISK FACTORS
- Modifiable
▪ Smoking – more than 90% of patients with an aortic aneurysm have been smokers
▪ HTN / HLD
- Non-modifiable
▪ Gender – Males to Females (4:1 ratio)
▪ Family History
▪ Connective tissue disorders
- Marfan's – caused by fibrillin-1-defect (weakening of elastic tissue)
- Ehler-Danlos syndrome type IV – due to abnormal type III pro-collagen
▪ Advanced Age (> 60)
▪ COPD
▪ Hyperhomocysteinemia
- Most commonly found incidentally during physical examination (pulsatile / expansile abdominal mass)
Asymptomatic
or imaging (on US or CT)
- Hypotension → going into shock (feared presentation)
Classical Px - Intense abdominal pain radiating to the back
(ruptured AAA) - Pulsatile abdominal mass
- Rupture usually: Left posterolateral wall, 2-4cm below renal
Local compression - Radicular symptoms in the thigh and groin (nerve root compression)
Symptomatic
(contained rAAA) - GI, urinary obstruction
(rAAA)
Rupture into IVC - Audible abdominal bruit
(aortocaval fistula) - Venous HTN → swollen cyanotic legs, lower GI bleed, haematuria
- Intraluminal thrombus → emboli → acute ischemic limb or mottling of the lower

Distal Embolization
trunk and extremity
- Vital signs – is patient hemodynamically stable
- Visible pulsation over abdomen
- Pulsations and mass in epigastric region felt on deep palpation (video)
- Mass is expansile – when fingers of both hands are placed at the edges on either side of the mass, the fingers are pushed
upwards and outwards
- Auscultate for bruit over the mass
- Check the other arteries – femoral, popliteal – for any aneurysm, and listen for bruits
- Look at the lower limbs for any gangrene, infection, mottling
54 N Engl J Med. 2008 Jan 31;358(5):494-501

501
Upper Abdominal Pain with Shock
- Pale: rAAA, ruptured hepatoma, BGIT, ruptured spleen in trauma, mesenteric bleed
- Not pale: sepsis, pancreatitis, perforated viscus, AMI , pyonephrosis
Risk of Rupture55
Size of Aneurysm Risk of rupture per year Remarks
< 5cm 0.5-5%
5-6cm 3-15% ▪ After an aneurysm ruptures 25% of patients reach the hospital
6-7cm 10-20% alive and only 10% reach the OT alive
7-8cm 20-40% ▪ OT mortality rate for ruptured AAA is >40%
>8cm 30-50%
Higher risk for rupture

- Chronic obstructive pulmonary disease (COPD),
- Female Gender
- AAA morphology (saccular aneurysm)
- Rapid rate of enlargement (> 10% per year)
INVESTIGATIONS
Diagnostic Imaging
- Ultrasound abdomen – to assess size and position (at present, no role of screening in Singapore)
- CT Aortogram / MR aortogram
- Portable Chest X-Ray (look for dissection / mediastinal widening)
Pre-operative investigations
- FBC, UECr, PT/PTT, GXM for 6-8 units of whole blood, ECG
- Echocardiogram / Pulmonary Function Test
MANAGEMENT
Dependent upon clinical context: asymptomatic, symptomatic, or ruptured
Asymptomatic AAA
- For AAA of 4.0 to 5.5cm, no role for surgical repair as it confers no survival benefits, ‘best care’ favours surveillance 56
- Timing of re-evaluation of AAA depends on the initial AAA size and related anatomy57
▪ < 2.6 cm: no further screening
▪ 2.6 – 2.9 cm: re-examine at 5 years
▪ 3.0 – 3.4 cm: re-examine at 3 years
▪ 3.5 – 4.4 cm: re-examine at 1 year
▪ 4.5 – 5.4 cm: re-examine at 6 months
- Medical Management: Smoking cessation & optimize BP / HLD control (statins reduce aneurysmal growth rates) 58,59
- Surgical Options – Open AAA Repair or Endovascular Aneurysm Repair
- Indications for surgery:
▪ Aneurysm > 5.5 cm in largest diameter
▪ Patient fit for surgery (expected mortality rate < 5%)
▪ Increase in diameter of more than 5 mm / 6months or 1 cm / year
▪ Saccular aneurysm (rather than fusiform anatomy, due to higher risk of rupture)
- Patient’s fitness for surgery needs to be properly assessed (optimise cardiovascular function)
- Mortality is <5% in the elective setting (1-3% for high-volume centre), serious morbidity ~10%
55 J Vasc Surg. 2003;37(5):1106

56 Cochrane Database Syst Rev. 2012 Mar 14;(3):CD001835. [Important Paper] (4 trials: UKSAT, ADAM, CAESAR & PIVOTAL)
57 Sabiston Textbook of Surgery 19 th Edition (Chapter 62, The Aorta) – pg. 1699
58 Eur J Vasc Endovasc Surg. 2006 Jul;32(1):21-6.
59 Am J Cardiol. 2006 Jan 15;97(2):279-80.

502
EXTRA INFORMATION
Open Surgery or Endovascular Surgery for patients with AAA ≥5.5cm and are fit for surgery
- Elective endovascular repair for AAA ≥5.5cm a/w lower 30 days mortality and morbidity rate in the EVAR group as
compared to open repair. However, at 4 years, mortality is the same within both groups with higher complications and re-
intervention rates in the EVAR group (EVAR-1 Trial)60

- Beyond 8 years, patients who underwent EVAR have increased mortality (aneurysmal-related, all-cause and interestingly
cancer related mortality) (EVAR-1 Trial at 15 years)61
- Hence, consider endovascular approach for high risk patients & limited life expectancy
Endovascular Surgery or Conservative Management for patients with AAA ≥5.5cm unfit for open surgery
- EVAR showed no difference with conservative management and a/w need for continued surveillance and re-intervention
(EVAR-2 Trial)62
Open Surgery or Endovascular Surgery for patients with ruptured AAA (with AAA feasible for endovascular repair)
- No difference at 30 days mortality with quicker discharge from hospital for the endovascular group. (IMPROVE Trial)63
- Follow-up study showed survival benefit at 3 years. (IMPROVE Trial)64
Symptomatic AAA
- Indications for surgery:
▪ Aneurysm of any size that is painful or tender
▪ Aneurysm of any size that is causing distal embolization
- Surgical Options: Open Surgery or Endovascular Approach
Ruptured AAA
- AAA can rupture anterior into the peritoneal cavity (20%) or posterolaterally into the retroperitoneal space (80%)
▪ Anterior rupture leads to free bleeding into peritoneal cavity (extremely high mortality)
▪ Posterolateral rupture leads to retroperitoneal hematoma (tamponade effect), < 50% reach hospital alive
- High suspicion in unstable hypotensive patient complaining of severe sharp pain radiating to the back; may feel a tender pulsatile
mass in the abdomen
- Surgical options: Open Surgery or Endovascular Approach (if feasible anatomy & access to hybrid theatre available)
Acute Management
1. Stabilise patient – resuscitation with fluid and blood products
▪ Establish 2 large bores IV cannula + Take bloods (i.e. FBC, U/E/Cr, PT/INR/APTT, GXM, ABG/Lactate, ECG, CXR)
▪ Permissive hypotension is advocated for patients with clinical dx rAAA – to maintain a clinically alert patient and sufficient
end-organ perfusion (i.e. systolic BP >70mmHg without reaching normal blood pressure)
▪ 100% O2, continuous ECG and vitals monitoring
▪ KIV for massive blood transfusion
▪ If possible, don’t intubate patient in the EMD as NMB agents will ↓tamponade effect, worsening haemorrhage
2. If hemodynamically stable, i will arrange for a urgent CT aortogram to confirm diagnosis and for pre-operative planning
3. Call for vascular surgeons or cardiothoracic surgeons, senior, OT, ICU/HD immediately
4. Keep NBM GI decompression with NG tube, catheterise ± CVP / IA line
5. Get informed consent for open AAA repair from patient / family emphasize the risk and high mortality rates 50-70%
6. Rapid Transfer to OT for open repair
7. Clean and drape and be ready for midline laparotomy BEFORE induction of anaesthesia
8. Start IV broad spectrum Ab + analgesia (to prevent exacerbation in BP / HR)
60 Lancet. 2005 Jun 25-Jul 1;365(9478):2179-86. (EVAR-1 Trial)

61 Lancet . 2016 Nov 12;388(10058):2366-2374. (EVAR-1 Trial at 15 years)
62 Lancet. 2005 Jun 25-Jul 1;365(9478):2187-92. (EVAR-2 Trial)
63 BMJ . 2014 Jan 13;348:f7661. (IMPROVE Trial - 30 days mortality)
64 BMJ . 2017 Nov 14;359:j4859. (IMPROVE Trial - 3 year mortality)

503
EXTRA INFORMATION
Open Surgical Repair

- Surgeons have to be gowned up with a scalpel in hand, ready to operate before an anaesthetist intubates the patient!
- Usually a midline laparotomy (can have other approaches)
- Proximal and distal control of aorta (i.e. supraceliac clamping, distal vascular clamps on the common iliac arteries)
- Aneurysm sac is opened longitudinally, the surrounding haematoma and mural thrombus within the AAA are removed
- Reconstruction with prosthetic graft
- Assess viability of abdominal viscera prior to closure
Endovascular Repair
- Endograft is a bifurcated (Y-shaped) graft with two branches for the iliac arteries and a main trunk for the proximal aorta.
It is deployed within the aneurysm to form the lumen of the aorta
- It requires adequate “neck” proximally (10-15mm proximal neck) and good landing site distally (20mm iliac landing zone)
COMPLICATIONS
Intra-operatively Early Late
- Bleeding - AMI (50-60% of mortality), - Aortoenteric fistula – graft erode into 3 rd or
- Distal limb micro-embolization (trash - Respiratory (atelectasis, pneumonia), 4th portion of duodenum, herald bleed with
foot) - CVA (20 to hypotension or embolism) hematemesis
- Distal limb arterial thrombosis - Spinal Cord Ischemia – paraplegia - Prosthetic graft infection
- Small or Large Bowel Ischemia - Pseudoaneurysm formation
- Ischemic Colitis (i.e. sigmoid colon) – - Sexual Dysfunction (i.e. infertility,
patient present with bloody diarrhoea retrograde ejaculation)
- Renal Failure - Incisional Hernia
- Mortality
Endovascular Related Complications

- Groin and wound complications – bleeding, hematoma, pseudoaneurysm formation
- Endoleaks
- Aneurysmal sac rupture
- Contrast Induced Nephropathy
- Stent Complications (i.e. graft Infection, stent migration)
EXTRA INFORMATION
Thoracic & Thoracoabdominal Aortic Aneurysm

- Risk Factors: HTN, Bicuspid Aortic Valve, Connective Tissue Disease (i.e. Marfan Syndrome), Tertiary Syphilis
- Classification (Crawford)
▪ I – distal to left subclavian artery to above renal arteries
▪ II – distal to left subclavian artery to below renal arteries
▪ III – from 6th intercostal space to below renal arteries
▪ IV – from 12th intercostal space to iliac bifurcation (total AAA)
▪ V – below 6th intercostal space to just above renal arteries
- Indication for Surgery

▪ Symptomatic patient
▪ Increase in aneurysm diameter of more than 1cm in 1 year
▪ Ascending Aortic Aneurysm ≥ 5.5 cm in largest diameter
▪ Patients with Marfan / Bicuspid aortic valve (or other genetic
mediated disorder), surgery when aneurysm >4.5-5cm (4.5cm
if high risk – i.e. rate of increase >3mm/yr, family history of
dissection, severe AR
▪ Descending Aortic Aneurysm ≥ 6.5 cm in largest diameter (if patient has Marfan, then surgery at 6cm)
- Surgery option: Open Repair vs TEVAR

504
ANATOMY OF THE VENOUS SYSTEM OF THE LOWER LIMB
- The venous drainage of the lower limb is divided into a deep venous system and a superficial venous system separated by the
deep fascia of the lower limb
- The deep venous system is composed of veins corresponding to the arterial supply e.g. anterior and posterior tibial veins,
popliteal vein, femoral vein
- The superficial venous system is composed of two major veins, the great saphenous vein and the small saphenous vein
- Course of the great saphenous vein (GSV):

▪ Arises from the medial side of the dorsal venous arch of the foot
▪ Ascends immediately in front of the medial malleolus* (accompanied by saphenous nerve)
▪ Runs up the leg posteriorly to pass a hand’s breadth behind the medial border of the patella
▪ Ascends obliquely up the medial aspect of the thigh
▪ Pierces the cribriform fascia at the saphenofemoral junction** (SFJ) to drain into the femoral vein at the saphenous opening
(2.5cm inferolateral to the pubic tubercle)
* The relationship of the GSV to the medial malleolus is constant → KIV use for live-saving cannulation (rarely performed(
** The SFJ is the confluence of the (1) GSV (2) superficial epigastric vein (3) superficial circumflex iliac vein and (4) sup erficial external pudendal vein
- Course of the small saphenous vein (SSV):

▪ Arises from the lateral side of the dorsal venous arch of the foot
▪ Passes posterior to the lateral malleolus
▪ Ascends up the midline of the calf
▪ Pierces the deep fascia over the popliteal fossa to drain into the popliteal vein
▪ Accompanied in its course by the sural nerve
- Physiology of venous drainage:

▪ Main mechanism is the calf muscle pump
▪ Contraction of the calf muscles compresses large venous sinuses in the muscles, squeezing the blood into the popliteal
vein and back to the heart
▪ The deep veins have many bicuspid valves to prevent backflow → blood only flows towards the heart
▪ During calf muscle relaxation, the intramuscular veins open and suck blood in from the superficial system through the
communicating veins, thus draining the superficial veins
▪ The superficial system and the deep system communicate through communicating veins that contain valves which allow
only one-way flow of blood from the superficial veins into the deep vein
- Locations of the communicating veins:

▪ Saphenofemoral junction – GSV drains into femoral vein
▪ Hunterian perforator: mid-thigh
▪ Dodd’s perforator: distal thigh
▪ Boyd’s perforator: knee / below the knee – connects GSV to deep vein
▪ Cockett (posterior tibial) perforators: at 5, 10, and 15 cm above the medial malleolus (drain medial lower leg) – connects
the posterior arch vein and the posterior tibial vein

505
CHRONIC VENOUS INSUFFICIENCY
PATHOPHYSIOLOGY
Chronic venous insufficiency develops when there is venous hypertension, which can result from:
- Obstruction to venous flow e.g. tumour compression in the pelvis, pregnancy, deep vein thrombosis
- Dysfunction of venous valves e.g. varicose veins
- Failure of the “venous pump” – dependent on adequate muscle contraction (stroke, muscular weakness can cause failure) as
well as competent venous valves
1. Venous dilatation
▪ Telangiectasias (spider veins or venous stars – intradermal veins) – 0.1-1mm
▪ Reticular veins (slightly larger intermediate veins) – 1-3mm
▪ Varicosities (visible, dilated tortuous superficial veins; formed by main tributaries of the saphenous veins because these
do not have a strong coat of smooth muscle in their walls, unlike the saphenous veins; they are more superficial and not
bound down to the deep fascia) – ≥3mm
▪ Corona phlebectatica (ankle flare) – a network of small dilated venules beneath the lateral and/or medial malleolus with
severe venous hypertension, indicative of advanced venous disease
2. Oedema – pitting: The hallmark of CVI; present in all but the earliest stages
▪ Unilateral oedema worsened by dependency (worse at end of the day) and better with recumbency
3. Skin changes
▪ Hyperpigmentation of the skin over medial lower third of the leg (gaiter area) – due to extravasation with hemosiderin
deposits
▪ Phlegmasia Alba Dolens – caused by obliteration of major deep venous channel (DVT) with relative sparing of collateral
veins, presents with pain, pitting edema and blanching
▪ Phlegmasia Cerulea Dolens – obliteration of major deep venous channels and the collateral veins of the leg,presents with
significant edema, pain, oedematous, cyanotic, arterial insufficiency, venous gangrene
▪ Atrophie Blanche – avascular fibrotic scars (i.e. ivory white areas with hyper-pigmented borders and telangiectasia) , prone
to venous ulceration 20 to poor blood supply
▪ Venous stasis eczema – pruritic, weeping, scaling, with erosion and crusting
▪ Lipodermatosclerosis – a fibrosing panniculitis of the subcutaneous tissue that results in a firm area of tender, indurated,
hyperpigmented skin that is fixed to subcutaneous tissue.
- Results from severe venous hypertension
- Starts in the gaiter area and extends circumferentially to surround the leg
- If severe can result in an “inverted champagne bottle” appearance of the leg with brawny oedema above and below
the area of lipodermatosclerosis
▪ Cellulitis
4. Venous ulcer formation

▪ Typical location is over the medial malleolus
▪ Shallow, flat ulcer with sloping edges; base may be sloughy or granulating, usually quite moist-looking
▪ Surrounding skin will show signs of CVI
▪ In long-standing ulcer SCC can develop (Marjolin’s ulcer) – If ulcer enlarges, becomes painful and malodorous, edge
becomes thickened or raised if inguinal lymph nodes are enlarged
These manifestations can be asymptomatic or associated with symptoms of leg fullness, aching discomfort, heaviness, nocturnal leg
cramps, or bursting pain upon standing.

506
CLASSIFICATION
CEAP Classification for Chronic Venous Insufficiency

507
VARICOSE VEIN
DEFINITION
Varicose veins of the lower limbs: dilated tortuous subcutaneous vein that is ≥3 mm in diameter measured in the upright position.
Varicosity can involve the main axial superficial veins (i.e. GSV & SSV) or any other superficial vein tributaries of the LL. 65
RISK FACTORS
- Age
- Parity
- Occupation – requiring long periods of standing
- Weight
- Posture – crossing legs all the time
- Increased abdominal pressure – constipation, chronic cough, etc.
- Pelvic tumour or other lesion compressing on the deep veins
- Family history: 1 parent (50% risk, both parents (up to 80% risk)
PATHOPHYSIOLOGY
- Inherent weakness in the vein wall, leading to dilation and separation of valve cusps so they become incompetent
- This may be aggravated by obstruction to venous return (as above)
- Causes: Primary or Secondary
Primary Secondary
- Previous DVT (valve destruction by thrombosis
- Valve Incompetence (congenital or degenerative)
- Deep Venous Obstruction
- Multifactorial – may be related to posture and
- Superficial Thrombophlebitis
components and structure of the vein wall
- Increase in flow and pressure 20 AVF
History
- Asymptomatic – varices of cosmetic concern
- Symptomatic:
▪ Nonspecific pain, tingling, aching, burning, muscle cramps, swelling, sensation of throbbing or heaviness, itching skin,
restless leg, leg tiredness, worsen with heat, worsen throughout the course of day (esp. if stand for long periods), relieved
by resting or elevating legs or wearing elastic stockings
- Complications : thrombophlebitis, bleeding, hyperpigmentation, eczema, ulceration
- Ask for past history of DVT & thrombophlebitis, obstetrics history, family history of varicosity or thrombotic disorders
Inspection – Examine patient standing with adequate exposure of the lower limbs
1. Presence of signs of Chronic Venous Insufficiency (CVI)
▪ Pitting Edema (C3),
▪ Skin Pigmentation & Venous Eczema (C4a)
▪ Lipodermatosclerosis & Atrophic Blanche (C4b)
▪ Venous Ulcerations (C5/6)
2. Scars – i.e. previous stab avulsions
3. Look at course of great saphenous vein and short saphenous vein for varicosities
4. Look at the inguinal region for any saphena varix
5. Any signs of infection
Palpate
1. Feel for any dilated varicosities / venous aneurysm
2. Palpate along the course of the saphenous veins and their tributaries to feel any varicosities and for tenderness (may be
more palpable especially in fat legs)
3. Palpate the inguinal region for a saphena varix (compressible lump that refills when released)
4. Do the cough test to feel for reflux at the saphenofemoral junction (2.5 cm below and lateral to the pubic tubercle)
5. Percussion (tap test) – test for valvular incompetence (not a very valuable test) – positive if the distal hand can feel the wave
of blood flowing retrograde after tapping the proximal varicosities
6. Feel the peripheral pulses of LL to exclude any ischemia as the management will involve compression of limbs (ABI >0.8)
7. Feel the inguinal LN – if have presence of venous ulcers
Move
65 J Vasc Surg. 2011 May;53(5 Suppl):2S-48S.

508
1. Ankle Joint – patients with advanced venous disease have decreased mobility in ankle joints
Special tests
Tourniquet test
- Designed to reveal the presence and site of incompetent veins – especially at sites of connection between the superficial and
deep venous system
- Lie the patient down and empty the varicosities & tie a tourniquet just below the SFJ
- Ask the patient to stand up
- Look for filling up of the varicosities above and below the tourniquet
- If the veins dilate above but not below the tourniquet, this indicates that the perforators below the level of the tourniquet are not
incompetent and that the SFJ is incompetent → confirm this by releasing the tourniquet and watching the veins dilate
- If the veins below the tourniquet are dilated on standing, then the incompetent perforator is below the level of the tourniquet
- Repeat the test, placing the tourniquet at different sites
1. Mid-Thigh (just below the Hunterian perforator)
2. Above Knee
3. Below Knee
- The incompetent perforator is located above the level where the tourniquet prevents dilation of the veins in the limb on standing
- The alternative is the triple tourniquet test, where three tourniquets are tied with the patient lying down and then released from
the bottom up to locate the site of insufficiency
Trendelenburg test
- The SFJ is occluded (2.5 cm inferolateral to the pubic tubercle) with the patient lying down
- Get the patient to stand while holding the SFJ occluded
- If varicosities do not fill up, the SFJ is the site of incompetence; if they fill up, there are other sites of perforator valve incompetence
(the SFJ may or may not be incompetent)
Perthes’ test
- Tie a tourniquet around the calf or thigh and ask patient repeatedly stand on tiptoe
- In a person with normal deep venous drainage and competent venous valves in the communicating veins, the superficial veins
should drain into the deep veins
- If the patient’s varicosities remain enlarged then he or she has obstructed deep venous drainage or incompetent valves in the
communicating veins
Completing the examination

- Auscultate over the varicosities for any bruit (indicate arteriovenous malformation)
- Examine the abdomen for any mass that may be causing the varicosities
- Examine the inguinal region for any lymphadenopathy – outflow obstruction
Use of a handheld Doppler probe to detect incompetence

- Doppler probe is placed in the popliteal fossa over small saphenous vein
- Squeeze the calf to empty the veins – should hear a whoosh as blood flows through the small saphenous vein
- When the calf is relaxed there should not be any sound – a second whoosh indicates reflux of blood i.e. there is valvular
incompetence
INVESTIGATIONS
- Venous duplex ultrasound
▪ Indications: Recurrent varicose veins, History of superficial thrombophlebitis or DVT
▪ Can delineate deep and superficial venous systems and locate sites of incompetence
▪ Valve closure time should be assessed, usually within the GSV with times >0.5 sec abnormal
▪ Exclude presence of deep vein thrombosis – stripping is contraindicated
MANAGEMENT
Conservative
1. Lifestyle changes
▪ Decrease amount of time spent standing, postural
▪ Weight loss
▪ If due to job, change job or ask for change to position to stand & walking less
2. Graduated compression stockings, usually grade II → ensure good pulses
3. Medications e.g. Daflon
Surgical
Indications:
1. Complications – CEAP class IV, V, VI, ±III

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2. Symptoms – pain, bleeding, thrombophlebitis, discomfort
3. Cosmesis – large unsightly varicosities
Available modalities:
1. Endovenous laser/radio-frequency ablation of the saphenous vein
▪ Contraindications: saphenous vein thrombosis
▪ Complications: skin burns, DVT, PE, vein perforation & hematoma, superficial thrombophlebitis
2. Ultrasound-guided injection foam sclerotherapy (for VV < 3mm and in telangiectatic vessels)
▪ Sclerosing agent: polidocanol, hypertonic saline, sodium tetradecyl sulfate
▪ Complications: cutaneous necrosis, hyperpigmentation, telangiectatic matting, thrombophlebitis
3. High tie with great saphenous vein stripping, and stab avulsion of varicosities (preferred therapy in large GSV >2cm)
▪ High tie (includes all venous tributaries)
▪ Complications: DVT , saphenous nerve injury (reduce risk by stripping on thigh portion of GSV)

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VENOUS ULCERS
CAUSE – ANY CAUSE OF CHRONIC VENOUS INSUFFICIENCY

- Obstruction to venous flow – thrombosis*
- Incompetent valves – varicose veins, deep vein reflux (post-DVT)**
- Muscle pump failure – stroke, neuromuscular disease
*Thrombosis of the venous system is usually prevented by a nonthrombogenic endothelium (produces endothelial relaxing factor and prostacyclin, which
helps maintain a non-thrombogenic surface through inhibition of platelet aggregation).
** LT complication of DVT include post-phlebitic syndrome, characterized by pain, swelling & ulceration of lower limb
INVESTIGATIONS
1. Exclude infection of the ulcer and other complications
- Blood Test – assess inflammatory markers (TW, CRP)
- Wound swab of the ulcer for gram stain and culture
- X-ray of the area to exclude underlying gas, bone involvement (i.e. osteomyelitis)
2. Venous duplex – assessment of deep (i.e. any thrombosis) & superficial veins (i.e. extent of GSV incompetence)
3. Check for peripheral arterial disease by doing ABPI/TPI – before deciding on compression bandage
4. KIV referral to dermatology to rule out other skin conditions (i.e. vasculitic ulcer, fungal rash etc.)
5. Biopsy venous ulcer if cannot exclude malignant transformation (Marjolin’s ulcer)
MANAGEMENT
Non-surgical
1. 4 layer compression bandage (change 1x/week, 30-40mmHg) – Podiatry
(a) Non-adherent wound dressing over ulcer (e.g. Menolin) followed by wool bandage
(b) Crepe bandage
(c) Blue-line bandage (Elset)
(d) Adhesive bandage (Coban)
Nowadays, 2 layer compression bandage (i.e. UrgoK2) are used – can achieve the same ankle pressure
Ensure that there is no concomitant peripheral arterial disease – check pulses / ABPI prior to compression bandage
2. Analgesia
3. Antibiotics if infected – culture directed
4. Warn patient to avoid trauma to affected area
5. Encourage rest and elevate leg
6. Once healed, (cannot use with ulcer/wound) compression stockings should be fitted and continued for life
Surgical
- +/- Endovenous Ablation
- 2 landmark trials guide surgical treatment principles
- ESCHAR trial 6667 (2004 & 2007): addition of superficial venous surgery to non-surgical therapy does not improve ulcer healing
rates at 24-weeks but reduced ulcer recurrence rates at 12 months by about 20% and increases ulcer-free time (see below)
- EVRA trial 68 (2018): early endovenous ablation (of superficial venous reflux) resulted in faster healing of venous leg ulcers
and more ulcer free time as compared to delayed endovenous ablation
- First, exclude malignancy or other causes of ulcer (biopsy)
- Split skin graft can be considered with excision of dead skin and graft attached to healthy granulation tissue
66 Lancet 2004; 363: 1854–59 [Important Paper]

67 BMJ 2007 Jul 14;335(7610):83. [Important Paper]
68 N Engl J Med. 2018 May 31;378(22):2105-2114. [Important Paper]

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16. HERNIA
ANATOMY OF HERNIAS69
DEFINITION
An abnormal protrusion of a viscus through an abnormal opening in the wall of the cavity in which it is normally contained. It can be
due to congenital or acquired causes. They can be described as reducible, incarcerated or strangulated. It consist of 3 parts, neck,
body and sac
TYPES OF HERNIA
A. Inguinal (96%): indirect (2/3), direct or pantaloon (direct & indirect)
B. Femoral (4%)
C. Abdominal Wall Hernia
1. Incisional Hernia: hernia through sites of previous incisions
2. Umbilical / Paraumbilical Hernia [see later section]
3. Epigastric Hernia: hernia through the linea alba above the umbilicus (i.e. extra-peritoneal fat)
▪ Frequently in athletically active young males who present with epigastric pain
4. Richter Hernia: hernia involving only part of bowel (rather than entire circumference) – knuckle of bowel is strangulated but
lumen is patent
5. Spigelian Hernia: herniation of linea semilunaris
6. Lumbar Hernia: occur in Petit triangle (lower lumbar) or Grynfeltt triangle (upper lumbar)
7. Obturator Hernia: herniation through the obturator canal a/w:
▪ Frequent in elderly lady who is thin (i.e. little old lady hernia)
▪ Presents as intestinal obstruction
▪ Howship-Romberg Sign / obturator neuralgia – pain in medial thigh extending to knee caused by hernia compression
of the obturator nerve
▪ Loss of adductor reflex
D. Internal Hernia
1. Mesocolic (paraduodenal) Hernia: small bowel herniate behind mesocolon
2. Sliding Hernia: herniation of posterior peritoneum with underlying retroperitoneal structures (i.e. caecum, sigmoid, bladder,
ovaries/fallopian tubes)
3. Littre Hernia: Hernia that contains a Meckel’s diverticulum
4. Amyand’s Hernia: hernia that contain the appendix
E. Parastomal Hernia
ANATOMY OF ANTERIOR ABDOMINAL WALL
6 Layer Construct of the Anterior Abdominal Wall

1. Skin & Subcutaneous Tissue
2. Superficial Fascia – composed of 2 distinct layers (mainly in the trunk)
a. Camper’s fascia – superficial fatty layer (continuous with superficial fat of the rest of the body)
b. Scarpa’s fascia – deep fibrous layer (attaches to the fascia lata of the thigh and is continuous with dartos fascia of
scrotum and penis and colles’ fascia of perineum)
3. Myofascial (see below)
a. Abdominal Wall Muscles
b. Fascial Interface
c. Rectus Sheath
4. Transversalis Fascia
5. Extra-peritoneal Fat
6. Parietal Peritoneum
69 Hernia. 2018; 22(1): 1–165. [Important Paper]
16. Hernia_Last Updated 3rd June 2020

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Abdominal Wall Muscles
▪ Rectus Abdominis
o Origin: pubic line (superior ramus of pubic bone), insertion: xiphoid process and 5-7th costal cartilages
o 3 intersection points at umbilicus, xiphoid and point ½ between the two
o Nerve: thoracoabdominal nerves (anterior rami of T7-11 intercostal nerves)
▪ External Oblique
o Origin: lower 8 ribs (5-12) , insertion: iliac crest, pubic crest, linea alba
o Orientation: infero-medially
o Nerve: thoracoabdominal nerves (T7-11)+ subcostal nerve (T12)
▪ Internal Oblique
o Origin: lumbar fascia, iliac crest & inguinal ligament, insertion: costal margin, aponeurosis of rectus sheath, conjoint
tendon to pubic crest and pectineal line
o Orientation: supero-medially
o Nerve: thoracoabdominal (T7-11) + subcostal (T12) + ilioinguinal nerve (L1)
▪ Transversus Abdominis
o Origin: costal margin, lumbar fascia, anterior iliac crest, inguinal ligament, insertion: aponeurosis of rectus sheath,
conjoint tendon to pubic crest and pectineal line
o Orientation: horizontal
o Nerve: thoracoabdominal (T7-11) + subcostal (T12) + ilioinguinal nerve
▪ Pyramidalis
o Functionally insignificant triangular muscle
Fascial Interface
▪ Linea Alba
o Midline decussation of anterior rectus sheath
o Runs vertically from xiphoid process to pubis
▪ Linea semilunaris
o Fascial adherences that defines the lateral border of the rectus
Rectus Sheath
▪ Arcuate line: about halfway between umbilicus and pubic crest
o Lower limit of posterior rectus sheath
o Where inferior epigastric vessels (from external iliac vessels) perforate rectus abdominis and continue upwards (between
RA and posterior rectus sheath) to anastomose with superior epigastric vessels (from internal thoracic vessels)
▪ Above arcuate line
o Anterior rectus sheath (aponeurosis of EO and anterior leaf of IO)
o Posterior rectus sheath (posterior leaf of the IO aponeurosis, TA muscle and transversalis fascia)
▪ Below arcuate line
o Anterior rectus sheath (aponeurosis of EO, IO and TA),
o Posterior rectus sheath is deficient (transversalis fascia only)

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EXTRA INFORMATION
Blood Supply of the Anterior Abdominal Wall
▪ Zone I – area between xiphoid and pubic symphysis, bordered by lateral

edges of rectus muscles → supplied by the deep superior epigastric (br. of
the internal thoracic/mammary) and deep inferior epigastric (DIEA)
(medial br. Of the external iliac) which collateralize within the middle 3 rd of
the rectus near the umbilicus
▪ Zone II – area between ASIS to pubic symphysis and paired groin creases,
overlaps inferior aspect of zone 1 → supplied by both DIEA perforators &
3 arteries that originate from the common femoral artery – superficial
circumflex femoral artery, superficial inferior epigastric artery &
external pudendal artery
▪ Zone III – area superior to zone II and lateral to the lateral border of the
rectus abdominis → supplied by both thoracic intercostal perforators from
T7-T12 & first lumbar neurovascular pedicle
- General Inspection: obesity (BMI), any previous abdominal scars, any prominent bulge on neck flexion, cough impulse
- Location: occurs at congenital or acquitted weak spots in the abdominal wall
- Reducibility: is the hernia reducible, incarcerated or strangulated
i. Reducible: hernia sac can be manually reduced back into the abdomen with manual pressure or on lying down
ii. Incarcerated: hernia sac cannot be manipulated back into the abdomen
iii. Strangulated: vascular supply to the contents contained within the hernia sac is compromised leading to ischemia and
gangrenous tissue
- Size of hernia defect/neck, narrow neck suggest a higher risk of incarceration and strangulation
- Any overlying skin changes over the hernia
- Any loss of abdominal domain
INVESTIGATIONS
- Ultrasound – for diagnosing patients with vague swelling or possible hernia. Performed with valsalva maneuver to detect the
presence of a hernia
- CT / MRI – can be used for further evaluation if ultrasound is negative or non-diagnostic.
MANAGEMENT
Hernia is a clinical condition that requires surgical intervention. The principle of abdominal hernia surgery involves (1) identification
of hernia sac, (2) reducing the contents of the hernia sac back into the abdominal cavity +/- removal of non-viable tissue/bowel, (3)
excision and closure of the sac (4) repair of the abdominal wall defect.
In the majority of cases, the abdominal wall repair involves the use of a mesh. Abdominal mesh can be sites in different locations,
namely (A) Onlay, (B) Inlay, (C) Sublay (retrorectus), (D) Pre-peritoneal & (E) Underlay (Intraperitoneal)

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INGUINAL HERNIA
DEFINITION
An inguinal hernia involves the abnormal protrusion of omentum or bowel through the inguinal canal. It can be either an indirect or
direct inguinal hernia or combination of both (pantaloon hernia).
The inguinal canal is a 4-6cm long oblique passage along the lower anterior abdominal wall, above the inguinal ligament. In males,
it allows for the passage of the spermatic cord, testicular and cremasteric vessels into the scrotum. The canal consists of 2 openings,
the deep inguinal ring (a defect in transversalis fascia which is located 2cm above midpoint of inguinal ligament) and the superficial
inguinal ring (a triangular defect in the aponeuroses of the external oblique, located above (~1cm) and medial to the pubic tubercle)
The indirect inguinal hernia (takes the longer route) travels through the deep inguinal ring (lateral to the inferior epigastric vessels),
down the inguinal canal on the outer side of the spermatic cord and emerges from the superficial inguinal ring to descending into the
scrotum.
The direct inguinal hernia (takes the shorter route) comes out directly forward through the weak posterior wall of the inguinal canal.
As such, the neck of the direct hernia is medial to the inferior epigastric vessels. The hernia travels through the Hesselbach’s triangle
ANATOMY
IMPORTANT LANDMARKS
Inguinal Ligament: located between the ASIS and Pubic Tubercle
Deep Inguinal Ring: midpoint of inguinal ligament
Femoral Pulse: mid inguinal point, which is located between the ASIS and Pubic Symphysis
Indirect Inguinal Hernia: neck arises lateral to the inferior epigastric vessels
Direct Inguinal Hernia: neck arises medial to the inferior epigastric vessels (via Hesselbach’s triangle)
Boundaries of the Inguinal Canal

- Anterior Wall: External Oblique Aponeurosis (reinforced in the lateral 1/3 by IO muscle)
- Posterior Wall: Transversalis Fascia (reinforced in the medial 1/3 by the conjoint tendon)
- Roof: Arching fibres of the IO and TA before they merge as the conjoint tendon
- Floor: Inguinal Ligament and Lacunar Ligament medially
Contents of the Spermatic Cord

External spermatic fascia: derived from external oblique
Layers Cremasteric fascia & muscle: derived from internal oblique
Internal spermatic fascia: derived from transversalis fascia
Testicular Vein (Pampiniform Venous Plexus)
Veins Veins of the Vas Deferens
Cremasteric Vein
Testicular artery (branch of abdominal aorta)
Artery Artery to the vas deferens (branch of inferior vesical artery from internal iliac artery)
Cremasteric artery (branch of inferior epigastric artery)
Ilioinguinal Nerve (strictly speaking, on and not in the cord)
Nerves Sympathetic Fibres / Autonomic Nerves (T10)
Nerve to Cremaster (genital branch of genitofemoral nerve*)
Remains of Processus Vaginalis
Vas Deferens (or round ligament of the uterus in females)
Others
Lymphatics
* innervates skin lateral side of scrotum and labia and motor to the cremaster muscle

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Boundaries of the Hesselbach’s triangle
- Laterally → inferior epigastric artery (arise from external iliac artery)
- Medially → lateral border of rectus abdominis,
- Inferiorly → inguinal ligament
- Floor → transversalis fascia
Anatomy of Inguinal Ligament

The inguinal ligament is the inferior most edge of the external oblique aponeurosis (reflected posteriorly between the ASIS and the
pubic tubercle). Below the ASIS, the external oblique muscle is wholly aponeurotic. The anterior-inferior fibres of insertion of the
external oblique aponeurosis fold on themselves to form the inguinal ligament.
Lacunar Ligament is a triangular extension of the inguinal ligament before its insertion upon the pubic tubercle

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- The true incidence and prevalence of inguinal hernia worldwide is unknown
- Male : Female ratio is > 10:1
- Lifetime prevalence – 27-43% in males and 3-6% in females
- 2/3 of inguinal hernia are indirect
- Bilateral hernia are 4x more common in direct hernia than in indirect hernia
- 1 in 2 males who develop an inguinal hernia will present bilateral hernia or develop a contralateral hernia (always check
contralateral side)
- 10% of inguinal hernia are at risk of incarceration, a smaller proportion may become strangulated
Risk Factors for Inguinal Hernia

The causes for hernia are multifactorial but can usually be due to anatomical reasons (i.e. persistence of a patent processus vaginalis)
or collagen disorders.
Gender – 8-10x more common in males

Age – peak prevalence at 5 years (indirect), and at 70-80 years (direct)
Collagen metabolism – diminished collage type I to type III ratio
HIGH
Obesity – inversely correlated with inguinal hernia incidence
Prostatectomy history – especially open radical prostatectomy
Inheritance – 1st degree relative diagnosed with inguinal hernia
Rare Connective Tissue Disorders – Ehlers-Danlos
MODERATE
Increased Systemic levels of matrix metalloproteinase
Chronic Constipation
LOW Social-occupational factors
Smoking – inversely correlated with inguinal hernia incidence
VERY LOW Pulmonary Disease – COPD and chronic cough
Diagnosis
- Clinical Presentation:
▪ Intermittent bulge in the groin related to exertion or long periods of standing
▪ Pain in the groin without bulge (ddx: epididymitis, testicular pain, endometriosis)
▪ Lying flat almost always results in symptoms improvement
▪ A purposeful Valsalva manoeuvre can reproduce the symptoms (i.e. unilateral discomfort) and/or the presence of a bulge
▪ Incarcerated Inguinal Hernia will present with pain + abdominal distention + nausea + vomiting
- Radiological Evaluation:
▪ Dynamic Ultrasound (with Valsalva, to accentuate small hernia) – if clinical findings is inconclusive
▪ AXR (supine) if suspect intestinal obstruction secondary to obstructed inguinal hernia
▪ CT AP if diagnosis is in doubt.
Complications
Reducible → Irreducible / Incarcerated → Obstructed → Strangulated
- Irreducible/ Incarcerated: contents of hernia sac cannot be replaced into abdomen

▪ If during surgery, the incarcerated hernia drops back into the abdomen, may need to explore through pre-peritoneal incision
by opening the peritoneum vs. diagnostic laparoscopy
- Obstructed: loop of bowel trapped in hernia sac such that its lumen, but not blood supply, is obstructed (no ischemia hence
patients are not unduly tender, but they present with IO)
- Strangulated: blood supply cut off, impending ischemic bowel; ~4-6hrs to gangrene.
▪ Acutely tender with signs and symptoms of Intestinal Obstruction
▪ Exception: Richter’s hernia where there is a segment of bowel trapped & ischaemic but the lumen is patent hence patients
do not have signs and symptoms of intestinal obstruction
▪ No need for CT scan, patient should be listed for emergency surgery (P1) → NBM, IV drip, NG tube on low-intermittent
suction, IV antibiotics, pre-op investigations as required, emergent surgery

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Clinical differences between indirect and direct inguinal hernia:
Indirect Hernia Direct Hernia
Neck lies lateral to inferior epigastric artery, Neck lies medial to inferior epigastric artery,
out of Hesselbach’s triangle within Hesselbach’s triangle
Reduces upwards, laterally and backwards Reduces upwards and straight backwards
Controlled after reduction by pressure over the deep ring Controlled after reduction by pressure over the superficial ring
May descend down the scrotum Usually does not descend down the scrotum
May cause strangulation at superficial ring (narrow) Rarely causes strangulation due to wide hernia neck
Does not readily reduce on lying down Readily reduces on lying down
MANAGEMENT
Non-surgical / Watchful Waiting
- Males with asymptomatic or minimally symptomatic inguinal hernia have low complication risks (incarceration / strangulation) –
watchful waiting is acceptable70
- Hernia Truss: for compression of reducible hernia at deep ring (not routine)
Surgical:
- Principles: reduce bowel, ± excise hernia sac, reinforce posterior wall
- Offer to patients who are physically fit for surgery and to patients with symptomatic hernia
▪ Elective Surgery for symptomatic hernia
▪ Emergency Surgery (P1) if suspect strangulation to prevent any ischemic bowel or bowel perforation
Open Inguinal Hernia Repair (with mesh / without mesh)

- Herniotomy (removal of hernia sac only) – done in kids, rarely in adults
- Herniorrhaphy (herniotomy + repair of posterior wall of inguinal canal)
- Hernioplasty (reinforcement of the posterior inguinal canal wall with a synthetic mesh)
▪ Lichtenstein tension-free mesh repair (anchor mesh medial to pubic tubercle and along inguinal ligament)
EXTRA INFORMATION
Types of Herniorrhaphy
- Shouldice repair: 2 continuous back & forth sutures – layered closure (1) transversalis fascia to flap of internal oblique and transversus
abdominis, (2) external oblique to internal oblique fascia
- Bassini Repair: suture conjoint tendon to the inguinal ligament from pubic tubercle to the deep ring
- McVay Repair: suture conjoint tendon to cooper’s (pectineal) ligament (close femoral space as well) then to inguinal ligament (poupart)
Laparo-endoscopic Inguinal Hernia Repair (intraperitoneal or extraperitoneal)

- Totally extra-peritoneal (TEP) repair
- Trans-abdominal preperitoneal (TAPP) repair
Indications: bilateral inguinal hernia, recurrent hernia after open anterior approach
- In these approach, the myopectineal orifice is approached posteriorly and allows
for inguinal, femoral and obturator hernia repairs to be performed simultaneously
- Laparo-endoscopic techniques have less chronic pain and a faster recovery time
than open mesh repair
Laparoscopic vs. Open Repair71

- Laparoscopic approach a/w shorter length of hospital stay and faster return to
normal activity (+/- less chronic pain)
- Long learning curve with laparoscopic surgery (~250 cases), during initial phase of
learning curve, risk of recurrence tends to be higher ~10%
- When compared between surgeons who are highly experienced, risk of recurrence
was similar between open (6.7%) and laparoscopic repair (6.6%)72
70 JAMA. 2006 Jan 18;295(3):285-92.

71 N Engl J Med. 2004 Apr 29;350(18):1819-27.
72 Br J Surg. 2005 Sep;92(9):1085-91.

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Intra-operative Classification (European Hernia Society, EHS guidelines)
EHS System Primary / Recurrent

0 1 2 3 X
Lateral (L)
Medial (M)
Femoral (F)
Postoperative monitoring
- Look out for any of the early complications especially ARU, scrotal hematoma
- Early mobilization
- Advise on heavy lifting (controversial) – some surgeons put no limitations immediately post-op
- Treat any medical conditions to avoid increased abdominal pressure (i.e. coughing, constipation, difficulty PU)
COMPLICATIONS
Complication rates are higher in older patients and in patients who undergo hernia surgery in an emergency setting. In the emergency
Surgery, the reported mortality rate is 5% for patients aged 70-79 and 6.5% for patients > 80. In contrast, in elective Surgery the
mortality rate is 0.64% for patients aged 70-79 and 0.74% for patients > 80.
Early
- Acute Retention of Urine – a/w increased age, may require IDC insertion post-op
- Hematoma (~5%) – groin / scrotal hematoma (fewer hematoma in the endoscopic group as compared to open)
- Seromas (~1-2%) – treat conservatively (risk factors – large scrotal hernia, coagulopathy and congestive liver failure)
- Nerve Injury – i.e. ilioinguinal nerve [open], lateral femoral cutaneous nerve [laparoscopic], patients complain of paraesthesia /
post-operative pain in the upper lateral thigh
- Wound Infection (<2%)** / mesh infection
Late
- Chronic (> 3 months) postoperative groin pain (~10-12%), 1-3% have severe debilitating chronic pain (avoid mesh fixation to the
pubic bone)
- Injury to Vas Deferens (infertility)
- Recurrence (~5%) – from inadequate ring and posterior wall closure***,
- Ischaemic orchitis from thrombosis of pampiniform plexus which drains from the testes
- Testicular atrophy from testicular artery damage
- Meshoma – folding of mesh
** Hernia surgery is classified as a clean operation (wound class) – wound infection 1.4% in open repair and 1% in laparoscopic repair
*** Occurs at floor of inguinal canal near pubic tubercle – tension on suture line the greatest (if occur, usually within first 2 years)

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APPROACH TO GROIN SWELLING
DEFINITION
A swelling in the inguinal region. Most commonly due to an inguinal hernia but consider other differentials as well.
Physical Examination for Inguinal Hernia - 5 Questions to Answer

1. Is this an inguinal-scrotal swelling or a groin lump?
2. Is this likely to be an inguinal hernia or a femoral hernia
3. Is the hernia reducible or irreducible
4. Is the hernia likely to be direct or an indirect hernia
5. Are there any predisposing factors
- Don gloves, introduce and explain your intention, expose the patient adequately, use clothes peg / ask patient to hold shirt up
- Stand patient up, must always examine both sides
- Mr X is a pleasant gentleman who presents with a (location) sided groin / inguinoscrotal swelling.
Inspect
- Inspect as per a lump: (if unable to see, ask the patient)
▪ Is the lump above or below the inguinal ligament? Any scrotal lump?
▪ Estimate the dimensions of the lump
▪ Any skin changes? Previous scars? (look hard, don’t miss a scar!) → is this a recurrent hernia
▪ Any lump on the other side?
- Sir, could you turn your head to the left and cough?, Look for visible cough impulse
- Sir, is there any pain over the groin area? I am going to feel the lump.
Palpate
- Aim to answer the questions (as listed above)
▪ Are you able to get above the lump?
▪ Are you able to feel testis?
▪ Lump: consistency, fluctuant, size, temperature, any tenderness?
▪ Landmark for the pubic tubercle (show that inguinal hernia neck is above and medial to the PT as compared to femoral
hernia which is located inferiorly and laterally to the pubic tubercle)
▪ Landmark the deep inguinal ring (2cm superior to midpoint of inguinal ligament), occlude the deep ring
▪ Sir, could you turn your head to the left and cough again? Feel for palpable cough impulse (bilaterally?)
- Sir, could you reduce the lump for me?
▪ Reducibility: The point of reduction is “above and medial to the PT” (superficial ring) - not easy to perform while standing
▪ Incarcerated (irreducible): The patient is unable to reduce the lump.
Lay the patient supine (Inspect & Palpate)

- Reduce the hernia if patient has not done so
- Locate the deep inguinal ring & keep pressure on deep ring (use right hand for right sided hernia and left hand for left sided
hernia), ask patient to sit up & support his pelvis, then swing his legs over the bed and stand up
With patient standing:

- Sir, could you turn your head to the left and cough?
▪ If remains reduced – indirect hernia,
▪ If not, direct hernia. (poor accuracy)
▪ If hernia appears slightly and on removal of compression appear even more fully then consider if it is a pantaloon hernia
- Remove pressure & watch: hernia slide obliquely (indirect) or project forward (direct)
- KIV auscultate for bowel sounds (not routinely done in clinical practice)
Offer:
- Abdominal exam: any scars, masses, distention, ascites, distended bladder, other abdominal hernias
- DRE for BPH, impacted stools
- Respiratory exam for COPD
- Ask patient for history of smoking, chronic cough, any heavy lifting (occupation), difficulty passing stools (constipation), difficulty
passing urine (BPH), previous abdominal / inguinal surgeries
Femoral Hernia
Hernia
Inguinal Hernia
Vascular Femoral Artery Aneurysm

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Saphenous Varix
Hematoma
Inguinal Lymphadenopathy
Lymphatics
Lymphoma
Sebaceous Cyst / Lipoma
Hidradenitis suppurativa
Soft Tissue Groin Abscess – look for multiple puncture holes (r/o infected pseudoaneurysm)
/ Bone Psoas Abscess
Muscle / Soft Tissue Tumour – Rhabdomyosarcoma
Bone Tumour
Nerves Femoral Neuroma
Varicocele
Cord Lipoma (retroperitoneal fat that has herniated through the deep inguinal ring)
Others
Undescended Testes / Ectopic Testis
Hydrocele of the spermatic cord (young boys)
Approach to Inguinal Lymphadenopathy

Assess for local-regional causes as well as for systemic lymphadenopathy
- Legs – any infection / malignancy (i.e. acral lentiginous melanoma – at nail beds,
open wounds)
- Examine Perineum – scrotum / penis / clitoris / vulva
Local-Regional - Per Vagina Exam – lower third drain to superficial inguinal lymph nodes
- PR Exam – lower ½ of anal canal drain to superficial inguinal nodes
- Abdominal wall (below umbilicus)
- Back (below iliac crest)
- Check contralateral inguinal nodes
- Cervical Nodes
Systemic
- Axillary Nodes
- Abdomen – for Hepatosplenomegaly

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FEMORAL HERNIA
EPIDEMIOLOGY
- Uncommon – 2-4% of all groin hernia
- 70% occur in women (pelvis is wider and the canal is therefore larger)
- 25% of femoral hernia gets complicated by incarceration or strangulation
- Rarely put up for exams as it is operated quickly
ANATOMY
*NAVEL = Nerve, Artery, Vein, Empty Space (where the femoral hernia sac is), Lymphatics
Anatomy of the Femoral Sheath

- The femoral sheath (anterior wall arises from transversalis fascia and posterior wall from fascia covering the iliacus) contains –
femoral vessels and lymphatics below the inguinal ligament – ends 4cm inferior to inguinal ligament.
▪ Medial Compartment = Femoral Canal which carries lymphatics, Lymph Node of Cloquet & Adipose Tissue
▪ Intermediate Compartment = Femoral Vein
▪ Lateral Compartment = Femoral Artery
Femoral Canal – 2 main functions

- The superior opening of the femoral canal is known as the femoral ring.
- Dead space for extension of the distended femoral vein
- Lymphatic pathway from LL to external iliac nodes
Boundaries of the femoral ring:

- Anterior = inguinal ligament
- Posterior = pectineal ligament (of Astley Cooper) which runs along pectineal line of the superior pubic ramus
- Medial = lacunar ligament
- Lateral = femoral vein
- Femoral hernia size is limited (as compared to inguinal hernia) as the hernia cannot extend anteriorly, posteriorly or medially.
Can only expand laterally compressing on femoral vein
Boundaries of the Femoral Triangle

- Superior = inguinal ligament
- Medial = medial border of adductor longus
- Lateral = medial border of Sartorius
- Floor = iliacus, psoas tendon, pectineus, adductor longus
- Roof = superficial fascia (LN & great saphenous vein)

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- Femoral hernia: marble-shaped lump in the upper thigh just below the inguinal ligament and medial to femoral artery
▪ At risk for being irreducible; narrow neck, hence risk of strangulation is high
▪ Usually does not have a cough impulse
- Incarcerated Femoral Hernia presents as a firm tender mass
Differences between an inguinal and a femoral hernia

Inguinal Hernia Femoral Hernia
Appear through superficial ring Appears through femoral canal
Superior and medial to pubic tubercle Inferior and lateral to pubic tubercle
Usually reducible Usually not reducible
Expansile cough impulse usually present Expansile cough impulse usually absent
Low risk of strangulation High risk of strangulation
- Skin/ soft tissue: lipoma, sebaceous cyst, sarcoma
- Vascular masses: saphena varix, femoral aneurysm
- Nerve: neuroma of femoral nerve
- Lymph nodes
- Hernia: inguinal hernia, obturator hernia
- Other: psoas bursa, psoas abscess, ectopic testis, hematoma
INVESTIGATIONS
In the acute setting with worry of obstructed or strangulated small bowel, imaging of choice will be a contrasted CT AP
MANAGEMENT
Femoral Hernia Repair can be approached via laparoscopic or open repair. The laparoscopic approach for femoral hernia is similar
to that for inguinal hernia (i.e. TAPP approach). For open repair, classically 3 approaches are considered.
- Infrainguinal Approach (Lockwood) – used for elective femoral hernia

- Trans-inguinal Approach (Lothiessen) – can repair both inguinal and femoral hernia
- Supra-inguinal Approach (McEvedy) – used when suspecting strangulated hernia (can enter peritoneum)
▪ Modified McEvedy – transverse incision 2 FB above the inguinal ligament
- Mesh repair is usually preferred unless contraindication exists (i.e. ischemic bowel with perforation)
COMPLICATIONS
- Similar to Inguinal Hernia Repair (see above)
- Specific: femoral vein susceptible to injury (femoral vein forms the lateral border of the femoral canal

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UMBILICAL / PARAUMBILICAL HERNIA7374
DEFINITION
Umbilical hernia defined as a primary hernia with the centre of defect in the middle in the centre of the umbilical ring. It can be classified
as small (0-1cm), medium (1-4cm) and large (>4cm).

True Umbilical Hernia Paraumbilical Hernia
Location Occur through the umbilical scar Occur around the umbilical scar
Common in Africa or Afircan-orgin people (8x) Uncommon before 35-40 yrs old, Common in
Epidemiology Common in infants and children (20% of adults
newborn) 5x more common in females
Acquired Pregnancy,obesity, liver ascites* Pregnancy,obesity, liver ascites*
Causes (stretching of linea alba fibres) Usually occurs above the umbilical cicatrix
Complications As per any other hernia, there is a risk to be incarcerated, lead to bowel obstruction or strangulation
* Liver cirrhosis and ascites are not absolute contraindication – elective repair is safe and should be performed. Post-operative management of ascites
is important to minimize complications and recurrence
History
- Intermittent abdominal pain, colic from intermittent intestinal obstruction
- Risk Factors: smoking, drugs (i.e. steroids)
- Inspect – body habitus, BMI, abdominal scars, prominence of bulge with neck flexion, associated ulceration, peristalsis through
the skin, visible cough impulse
- Palpate – size of defect, reducibility, cough impulse
Issues of concern
- Narrow neck of hernia sac → higher risk of strangulation/ infarction – should repair
- Fistula formation (i.e. enterocutaneous fistula) with discharge of contents may occur
MANAGEMENT
- Defects < 1cm – primary surgical repair
- Defect >1cm & ≤ 4cm – open repair with mesh (with 3cm overlap) → sublay mesh repair (lowest recurrence)
- Defect > 4cm – consider laparoscopic repair
▪ Laparoscopic intraperitoneal on-lay mesh (IPOM) +/- closure of defect (IPOM ‘plus’)
▪ If Laparoscopic Mesh Repair used, aim for 5cm overlap
- Mayo’s ‘vest over pants’ operation – hardly used in view of mesh repair
COMPLICATIONS
- Injury to visceral contents (within incarcerated hernia sac) – if bowel injured and repaired performed, do not use mesh
▪ In emergency setting, if field is contaminated, avoid using mesh
- Seroma / Hematoma
- Wound Infection (smoking cessation 4-6 weeks and weight loss to BMI < 35 to reduce risk of Surgical Site Infection)
- Recurrence – with mesh (1-3%), without mesh (10-30%)
▪ Most common cause of recurrence is the mesh area to defect ratio
73 Br J Surg . 2020 Feb;107(3):171-190.

74 Clinical Cases and SOCEs in Surgery (2nd Edition) – Case 48, pg. 79-80

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INCISIONAL HERNIA
DEFINITION
Extrusion of the peritoneum & abdominal contents through a weak scar or accidental wound on the abdominal wall. They consist of a
hernia orifice and peritoneum sac.
Principles of Surgical Incision

Incisions are made based on:
- Accessibility – shortest distance to disease process
- Morbidity – avoidance of important structures eg nerves, vessels, muscles
- Cosmetic Reasons – Langer’s lines: Skin lines of approximately equal tension
▪ Associated with the distribution of collagen and elastic fibres in the skin and are predominantly transverse
▪ Therefore transverse incisions parallel to Langer’s lines have less tension and heal with a narrower, more cosmetic scar
▪ Also hiding of scars in skin creases
- Surgeon’s Preference
- Extendability (for surgeries that turn out to be difficult)
Classical Abdominal Imaging

- Midline – bloodless and rapid entry into peritoneal cavity (via linea alba)
- Paramedian (lateral and parallel to midline) – on suturing the peritoneum, the rectus slips back overlying the peritoneal incision
- Subcostal / Kocher (midline & parallel to costal margin) – right for biliary system (eg cholecystectomy), left for spleen
- Gridiron / Muscle Splitting (perpendicular to the spinoumbilical line [between right ASIS & umbilicus] at Mc Burney’s point) –
abdominal wall musculature is left undamaged
- Lanz – transverse incision made at Mc Burney’s point
- Roof Top – epigastric (eg esophagectomy, gastrectomy, hepatic resection, liver transplant) / bilateral surgeries (eg bilateral
adrenalectomy)
- Small incisions – drain sites, laparoscopic surgery port sites

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RISK FACTORS
- Patient Factors: age, malnutrition, chronic disease (ESRF, CLD, Malignancy), steroids, DM (predispose to infections), morbid
obesity, ↑ abdominal pressure chronic cough, obstructive uropathy, constipation, connective tissue abnormalities (patients
undergoing surgery for AAA)

- Surgical Factors: wrong suture material used, wrong technique – i.e. too small bites*, emergency surgery higher risk compared
to elective surgery
- Disease Factors: wound infection, wound breakdown, postoperative complications requiring reoperation
- History: details of surgical intervention, any postoperative complications, any pain, reducibility, patients’s comorbids
- Scars are incisional hernias until proven otherwise. Always check for cough impulse
- Physical examination similar to abdominal examination +
▪ Inspect – body habitus, abdominal scars (i.e. multiple surgeries), prominence of bulge with neck flexion, peristalsis through
the skin, visible cough impulse
▪ Palpable – tenderness, size of defect, reducibility, cough impulse
- Type of defects in incisional hernia: small defect (<2cm), large defects (>2cm), multiple defects (swiss cheese pattern), very large
defect with loss of abdominal domain
- Complications – i.e. intestinal obstruction, incarceration, strangulation, skin excoriation, persistent pain (similar to most hernia)
- Diastasis Recti (separation of the two rectus abdominis muscles by an abnormal distance)
▪ A cosmetic condition with no associated morbidity or mortality
▪ Diastasis of this muscle can occur in newborns, pregnant women (esp. multiparous women) and obese patients
▪ Clinical Presentation: appears as a ridge down the midline of the abdomen, (i.e. xiphoid process to umbilicus) which
becomes prominent with straining and may disappear when abdominal muscles are relaxed
▪ Management: No treatment needed – not a true hernia (as no fascial defect) and therefore no risk of incarceration or
strangulation. Weight loss and exercise often advised

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MANAGEMENT
Pre-operative management
- Weight loss
- Nutrition optimization
- Treatment of chronic conditions (i.e. chronic cough, BPH, chronic constipation)
Surgical Repair
- Primary Repair with mesh repair is the gold standard for patients with incisional hernias (lowest recurrence rate)
▪ Location of Mesh
- Onlay (superficial to fascial defect) – high risk of recurrence (30%), not recommended
- Sublay (Retrorectus) – recommended
- Underlay (Intra-peritoneum)
▪ Open vs. Laparoscopic Repair (i.e. Laparoscopic Intraperitoneal Mesh Repair (IPOM))
- Laparoscopic Repair benefits – lower risk of wound infection rate, shorter hospital stay, better abdominal wall function
(recurrence rate benefits remains controversial)
- For very large defects, may require component separation as well mesh repair
COMPLICATIONS
- Wound Infection / Mesh Infection
- Seroma Formation
- Hernia Recurrence
- Wound Sinus
- Enterocutaneous Fistula (rare)
EXTRA INFORMATION
Jenkin’s Rule
Traditional teaching suggests that for laparotomy wounds that are closed continuous, the length of suture should be four
times the length of the incision and bites should be taken 1cm from the wound edge at 1cm interval. However, current
evidence suggests that taking smaller bites (5-8mm) will instead lead to lower risk of SSI and incisional hernia rates.75
(Millbourne)
75 Arch Surg. 2009 Nov;144(11):1056-9.

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17. OTHERS
SKIN & WOUND HEALING
Layers of the skin (superficial to deep)

- Epidermis
▪ Stratum granulosum
▪ Stratum spinosum
▪ Stratum basale (germinal layer where cell division occurs)
- Dermis
▪ Consists of dense interlacing collagen fibers whose orientation determines the Langer’s lines (lines of tension; parallel
surgical incisions minimise scarring)
- Hypodermis
▪ Loose fibrofatty tissue → loosely connected to the superficial fascia → skin is mobile over deeper structures (except palms
& soles)
▪ Skin appendages: sweat glands, hair follicles + sebaceous glands
Sites of skin lesions
Source: Essential Surgery 5th edition chapter 46 pg 564
17. Others_Last Updated 3rd June 2020

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Phases of Wound Healing
-Transient vasoconstriction (for about 5-10min),
-Platelet aggregation and activation of coagulation cascade (injured cells release factor III [thromboplastin, tissue
Haemostasis factor] – fibrin clot forms
& Inflammation - Vasodilation occurs – supplies cells and substrate for further wound repair
[1day to 6days] - Neutrophils (PMN) – peaking at 24-48hrs [dominant cell type – days 0 to 2]
- Macrophages* – peaking at 48-96hrs [dominant cell type – days 3 to 4] – important in activation of cell proliferation
- Epithelialization – day 1 – proliferation & migration of epithelial cells adjacent to wound
- Fibroblast appear and initiate collagen synthesis (begins 3-5 days after injury)
o Collagen molecule contains 2 unique amino acid – hydroxyproline** & hydroxylysine
Proliferation
o The hydroxylation that forms these – requires ascorbic acid (vitamin C), alpha-ketoglutarate, ferrous ion &
[3days to 3wks]
oxygen, and occurs in the endoplasmic reticulum
- Angiogenesis – induced by endothelial cells, give wound pink / purplish red appearance
- Organization of collagen bundle – Early Matrix (i.e. fibronectin and collagen type 3), next matrix (i.e.
glycosaminoglycan and proteoglycans), final matrix (i.e. collagen type 1)
Maturation
o Type III collagen – predominate for days 1-2
& Remodelling
o Type I collagen – predominate by days 3-4
[3wks to 1yr]
- Tensile Strength: wk1 (3%), wk3 (30%, max collage accumulation), wk8 (80%, cross-linkage improve tensile
strength)
* Macrophage activity – phagocytosis, debridement, cell recruitment and activation, matrix synthesis and angiogenesis
** Hydroxyproline is found almost exclusively in collagen – marker of quantity of collagen tissue
Factors affecting Wound Healing76
Wound Factors
- Wound infection
- Wound ischaemia (hypoxia): secondary to fibrosis, pressure, poor arterial inflow, poor venous outflow, smoking, radiation, edema,
vasculitis
- Tissue trauma, devitalisation, foreign body: crush injury produces worse scars
- Anatomical area: areas that are poorly vascularised and over major joints are likely to heal poorly. Scarring over major joints can
cause contractures.
Patient Factors
- Age: younger people heal better but may have worse scarring due to skin elasticity and recoil which produces more tension.
- Smoking (Nicotine is a potent vasoconstrictor – reduce erythrocytes, macrophages and fibroblast )
- Diabetes Mellitus – glucose > 11.1 or HbA1c > 8.5
▪ Accumulation of sorbitol, increased dermal vascular permeability and glycosylation results in decreased dermal fibroblast
within wound
- Drugs / Chemotherapy / Radiotherapy
▪ Steroids – inhibit macrophages, PMNs and collagen synthesis by fibroblast; decrease wound tensile strength as well, also
inhibits epithelization and contraction (increased risk of wound infections) – Vitamin A (25,000 IU qds) counteracts effects
of steroids on wound healing
▪ Chemotherapy – global suppression of bone marrow, inhibition of inflammatory phase of wound healing, fibroblast collagen
production and decreased ability to fend off infection
▪ Radiotherapy – micro-vascular damage leading to inadequate oxygenation of tissue
- Albumin <30 – risk factor for poor wound healing
- Malnutrition – brief (days) preoperative illness or reduced nutrient intake in period immediately preceding the operative
intervention will demonstrate impaired fibroplasias
- Vitamin C deficiency (vitamin C is required for conversion of proline and lysine to hydroxyproline and hydroxylysine)
Surgical Factors
- Aseptic technique
- Wound edge eversion
- Tension free closure
- Minimisation of tissue trauma: atraumatic technique, debridement of necrotic tissue, removal of foreign bodies
- Prompt removal of skin sutures: to avoid leaving permanent suture marks
76 The Absite Review 4th Edition – Chapter 14, pg. 54

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SKIN CANCERS
Lifetime risk is 1 in 5 with more than 97% being non-melanocytic skin cancers (NMSC) (white population). BCC is 4-5x more common than SCC.
Primary modifiable risk factor = UV exposure
History taking
- Site, size, shape, number of lesions, pain, colour, change over time, etc
▪ Similar previous lesions (eg BCC)
▪ Concurrent disorders, eg DM (predisposes to infx and affects surgical mx)
▪ Previous surgical tx or trauma to that area (eg implantation dermoid, chronic inflammatory response to foreign body)
- Family History: eg NF
- Social History:
▪ Occupation: exposure to carcinogens (i.e. lubricating oils & SCC), outdoor work (increases risk of all types of skin CA)
▪ Travel: eg tropical ulcers, Madura foot, TB ulcers
- Systemic Review: LOW & LOA (suggests ca)
Physical examination
1. Lump
▪ Size, shape, surface (smooth/irregular/exophytic)
- Epidermal lesions have surface abnormalities, while deeper lesions have normal epidermis overlying.
- Punctum: lesion arises from epidermal appendage (i.e. epidermal cyst)
▪ Margins: Regular (i.e. cystic or encapsulated) or Irregular (i.e. malignant)
▪ Tethering:
- To underlying structures → origin from deeper structures (eg ganglion)
- To overlying epidermis → derived from skin appendage
▪ Consistency:
- Soft: lipoma, fluid filled cysts (cysts are fluctuant, unless filled with semisolid material (i.e. epidermal cyst) or tense
(i.e. small ganglion)
- Hard: malig
- Bony hard: gouty tophi, exostoses
▪ Pulsatility
▪ Emptying & refilling: vascular lesions blanch and refill
▪ Transilluminable: cysts (filled with clear fluid)
▪ Warmth: inflammation
2. Tenderness
▪ Malignant lesions tend to be painless
3. Ulceration (loss of epidermal integrity)
▪ Tumours and keratoacanthomas tend to ulcerate 2’ central necrosis
- Benign: only slightly raised margin 2’ inflamm edema, with base lying deep to level of normal skin
- Malig: solid mass of proliferating epidermal cells, which develops central necrosis → margins elevated & rolled
▪ Arterial/venous insufficiency, chronic infection, trauma
▪ Malignant ulcers: expand indefinitely. May go through cycles of breakdown & healing (often with bleeding)
4. Colour
▪ Normal: lesion is deep to skin
▪ Red/purple: increased vascularity → blanchable; distinguish from purpura which is not blanchable
- Arterial blood (red): Campbell de Morgan spots, strawberry naevi
- Venous (darker): port-wine stain
▪ Deeply pigmented
- Benign nevi, if hairy, almost never malignant
- Malignant melanoma: Darkening is suspicious of malig change, rarely, there are amelanotic melanomas
5. Multiple, recurrent
▪ NF
▪ Dercum’s disease: recurrent lipomata
▪ Viral warts: can appear in crops
▪ Malignant melanoma: superficial spreading, satellite lesions (via dermal lymphatics)
6. Site
▪ Anatomical
▪ Due to exposure to RF, eg sunlight → solar keratoses, BCC of hands & face
7. Systemic
▪ Enlarged LN for mets or possible primary malig elsewhere resulting in skin mets
▪ Soles of feet for malig melanoma

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SQUAMOUS CELL CARCINOMA
DEFINITION
Tumors that originate from the cells of the epidermis forming superficial keratinous squamous layer
EPIDEMIOLOGY
- Peak incidence at age 60, elderly males
- More common on sun-exposed skin (head, neck, arms, hands, trunk), developing from pre-existing solar keratosis
- SCC usually on lower lip – may present as a non-healing ulcer over many years
- BCC usually on upper lip – presents as pearly nodule with telangiectasia
- Biopsy is diagnostic, surgical excision is curative and metastasis is rare
RISK FACTORS
Non-modifiable
- Xeroderma pigmentosum – AR inheritance
- Oculocutaneous albinism – AR disorder of melanin biosynthesis
- Fair complexion
- Advanced Age
Acquired
- UV Exposure (intermittent, intense sun exposure, esp. in childhood / adolescence)
- Proximity to Equator
- Immunosuppression – AIDS, organ transplant
- Carcinogens (arsenics, hydrocarbon)
- Ionizing Radiation
- Chronic inflammation: i.e. chronic ulcer (old burns, chronic venous ulcers), margin of osteomyelitic sinuses
Premalignant Condition
- Actinic Keratosis
- Bowen Disease

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LESIONS ASSOCIATED WITH SQUAMOUS CELL CARCINOMA (SCC)
Types Features Photo
- SqCC arising in long-standing benign ulcer / scar

Marjolin - Commonest ulcer: venous ulcer
Ulcer - Commonest scar: burns
- Very similar in appearance to classic SqCC, but may not be so florid
- Intraepidermal carcinoma
- Very slowly growing, may progress to SqCC
- Red, scaly irregular plaque on the trunk, if on the penis, vulva or oral
Bowen
cavity = Erythroplasia of Queyrat
Disease
- a/w visceral malignancies in 5-7 yrs time esp if area of skin has not been
(SCC in
exposed to the sun
situ)
- Microscopically: Epidermis (Atypical keratinocytes) & basal layer is
intact
- Treatment: excision (SqCC will grow eventually)
- Premalignant lesion(marker of chronic sun damage) that can progress to
SCC
- Multiple yellow-grey to brown scaly macules/papules, small, hard, flat,
well-demarcated, with erythematous base, begins with thickening of skin
- On sun-exposed skin of elderly patients, fair-skinned ppl living in
Solar tropical/subtropical regions are predisposed (eg Australia)
(actinic) - 25% may undergo change to SCC
keratosis - Microscopically: hyperkeratosis, atypical dividing cells in prickle cell
layer (irregular acanthosis), focal parakeratosis, basal layer atypical only
(vs atypia in whole epidermis in SCC), dermal changes consistent with
solar elastosis
- Treatment: Non-surgical: cryotherapy, topical chemotherapy (5-FU) or
Surgical: curettage of affected skin
History & Physical Examination

- Usually has been growing for 1 – 2 months before being noticed
- Begins as small nodules on skin, as enlargement occurs, centre undergoes necrosis, sloughs with nodule turing into ulcer
▪ Round nodule or circular ulcer or irregular/ exophytic/ fungating/ cauliflower-like mass
▪ Painless
▪ Central ulceration – ulcer initially circular with prominent everted edges, bleeding (more common with SCC vs. BCC),
serous exudation
▪ Necrotic Tumour, may be covered with coagulated blood
▪ Granulation tissue tends to be pale, unhealthy
▪ Deep tissue may be exposed – depth variable, can be very deep in soft tissues – assess for pain and mobility
▪ Can have copious, bloody, purulent, foul smelling discharge
▪ Lymphadenopathy (5% at time of presentation) – infection vs. metastases
▪ Distant mets are uncommon
- Complications: Infection & bleeding (massive / fatal if erosion into large vessel)
MANAGEMENT
- Confirm dx with biopsy (histology: nests of atypical keratinocytes invading dermis, formation of keratin pearls and intercellular
bridges (desmosomes))
- Wide-excision with 1 cm margin
- Eyes, ears, nasolabial fold lesions: Moh’s chemosurgery (histological assessment of margins & electrodessication)
- Radiotherapy (if unresectable, nodal spread) & block dissection of regional lymph nodes (if involved)
- Annual review for 5y after successful tx.

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BASAL CELL CARCINOMA
DEFINITION
Tumour that originates from the pluripotent epithelial cells of epidermis and hair follicles (basal keratinocytes) at the dermoepidermal
junction
EPIDEMIOLOGY
- Most common skin cancer (4 – 5X more than SCC)
- Rates increased with age and in males
- Risk of subsequent BCC after initial diagnosis of NMSC is high (7 to 33%)
- Risk of metastasis low (0.0029% to 0.55%)
- Pathogenesis: Sonic Hedgehog (SHH) pathway, proto-oncogene on chr 9q22.3 and/or mutation in p53 and RAS genes
RISK FACTORS
Non-modifiable
- Nevoid basal cell syndrome (Gorlin’s syndrome) – AD inheritance
- Xeroderma pigmentosum – AR inheritance
▪ Mutation in any of the 8 genes involved in the repair of UV-induced DNA damage → intolerance to UV rays
▪ Have early-onset pigmentary skin changes, SCC & BCC develop at ave 9yo
- Epidermolysis Bullosa
- Advanced Age
- Fitzpatrick Skin type I and II
- Oculocutaneous albinism - AR inheritance
- Fair skin, light coloured eyes, red hair, high number of past sunburns, northern European ancestry
Acquired
- Proximity to Equator
- Immunosuppression – AIDS, organ transplant
- Carcinogens (arsenics, hydrocarbon)
- Ionizing Radiation, eg for facial acne, psoriasis, tinea capitis, with latency period of devt of 20y, limited to within radiation field
Premalignant Condition
- Naevus sebaceous of Jadassohn – well circumscribed hairless yellowish plaque that become verrucous and nodular at puberty
→ 10-15% risk of BCC transformation
CLASSIFICATION
6 Identifiable Subtypes

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- Most common
- Well-defined borders, flesh-coloured, pearly nodule,
Nodular
telangiectasia
(50-75%)
- May have central ulcer surrounded by rolled border (Rodent Ulcer)
- 90% occur on head
Micro-nodular
- Small rounded nodule the size of hair bulbs
(15%)
- Well-circumscribed, scaly, pink-to-red macule, patch, thin papule or

plaque
- Crust or a thin rolled border with fine translucent small papules
Superficial spreading
- Spontaneous regression can occur, leaving areas atrophic &
(9-15%)
hypopigmented
- Favour the trunk and extremities
- Often mistaken for infection or eczema
- “enlarging scar” with no history of trauma
- Shiny, smooth, scar-like, indurated plaques / depressions
Morpheaform - Ill-defined borders and frequently, there is associated atrophy
(sclerosing / fibrosing - Exhibits subclinical spread with the potential for extensive local
destruction, High incidence of + margins
- Most aggressive, rarely ulcerates
Pigmented - In the local population – incidence probably much higher

(6%) - Often confused with melanoma
Infiltrative
- Opaque yellow-white colour, blends with surrounding skin
(7%)
- History & Physical Examination (with dermatoscopy)
▪ Most arise on the upper part of the face
▪ Present early as lesions are very visible
- Biopsy – excisional, incisional, shave and/or punch biopsy

▪ Important to incorporate full depth of lesion
▪ Histology: basaloid cells with a palisading growth pattern

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MANAGEMENT
Goal: remove the tumour with preservation of function and cosmesis
Choice of treatment: depends on high / low risk – dictates risk of recurrence
- Imiquimod 5% (Aldara) or 5-FU

Medical
▪ For multiple, low risk superficial BCC and SCC in-situ
- Primary surgical excision (+/- intraop frozen section)
▪ 4mm margin for small primary BCC (<2cm) on face or other low risk lesions
▪ Systemic review (2010) – 3mm margin equally effective
Surgical
▪ 10mm for primary resection of high risk larger tumours on trunk or extremities
Excision
- Moh’s surgery
▪ Sequential horizontal excision till all margins free of tumour
▪ Cure rates 99% for primary tumour with significant tissue conservation
- Electrodessication & Curettage (ED & C)
▪ Superficial Ablation combined with surgical scraping with curettage
▪ Traditional Approach: 3 rounds of ED &C
▪ For low risk tumours
Destructive ▪ 3 caveats – don’t use in hair-bearing sites, don’t use if tumour reach subcutaneous layer (surgical
excision required), don’t use if high risk features (see histology results, KIV additional therapy)
- Cryosurgery
- Laser phototherapy (CO2 laser)
- Photodynamic therapy (PDT)
- Radiotherapy
▪ For tumours with perineural involvement, positive tissue margins, LN positive
Adjuvant
▪ Surgery contraindicated
Therapy
▪ Avoid nose or ear as cartilage is susceptible to RT and may undergo necrosis
- Immunotherapy (i.e. vismodegib (hedgehog pathway inhibitor) – tx metastatic and locally advanced BCC)
EXTRA INFORMATION
High-risk vs Low-risk BCC

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MALIGNANT MELANOMA
DEFINITION
Tumour that originate from melanocytes (neuroectodermal origin, neural crest cells in basal layer of epidermis)
PATHOGENESIS
- Often driven by activating mutation in BRAF kinase. S-100 tumour marker
- Stepwise Progression
▪ Radial Growth (confined to epidermis)
▪ Pagetoid Spread (extend along epidermis, into stratum corneum)
▪ Micro-invasive Radial Growth (dermal extension)
▪ Vertical Growth (invasion of the subcutaneous layer)
RISK FACTORS
Non-modifiable
- Familial atypical multiple mole melanoma (FAMMM) syndrome – p16 tumour suppressor gene, CDKN2A, chromosome 9
- Familial BK mole syndrome (~ 100% risk of melanoma)
- Atypical Nevi / large congenital naevi
- High nevus count
- Light skinned race
- Xeroderma pigmentosum
- Age (50% occur in patient >50yr)
Acquired
▪ Short periods of intense sun exposure causing blistering sunburn is a more impt RF for malig melanoma than a cumulative
sun effect for other skin malignancy
▪ Strong sunlight: suppress general immunological response, including immunological tumour surveillance → MM can appear
on parts of skin not exposed to sunlight, eg soles of feet

- Prior melanoma

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Features of pigmented skin lesion suspicious of malignancy, always remember ABCDE
A. Asymmetry – angulation, indentation, notching, ulceration, bleeding

B. Bleeding & Borders (late) – irregular
C. Change in: colour, size, shape, surface, number (early)
▪ Surface: Loss of normal surface markings (i.e. skin creases) around lesion, skin may become rough / scaly
▪ Size: Growth of newly-formed / long-standing mole, increase in edge, width, thickness
▪ Colour: Becoming darker, Halo of brown discolouration in skin around the lesion, patchy colour change (black, to blue-
purple due to ↑ vascularity), occasionally colourless: no melanin production

▪ Number: Satellite nodules of tumour around the lesion (lateral spread cia dermal lymphatics)
D. Diameter >6mm
E. Elevation & Evolving over time (flat plaque to a nodule)
- Hematogenous spread: occurs later, involving lung, liver, bone, brain

▪ Lung most common location for distant melanoma metastases
▪ Most common metastases to small bowel – melanoma
CLASSIFICATION

- Most common
- Asymmetry and colour variegation, patches of regression, flat
Superficial
- Red zones: areas of vessel ectasia and inflammation
Spreading
- White and grey regions 🡪 amelanotic or regressed foci
(75%)
- Predilection for the back in men and lower extremities in women
- Usually arise in pre-existing pigmented naevi
- Usually darkly pigmented, pedunculated or polypoid nodule

- Rarely, they may be amelanotic (5%)
Nodular
- Most aggressive – likely to have metastasized at time of diagnosis
(15-30%)
- Vertical Growth 1st (worse prognosis)
- Arise de novo in normal skin
- Arise in sun damaged areas of skin in older individuals, on face & neck
- Freckle-like tan-brown macule, enlarges (>3cm)and develops darker or
lighter asymmetric foci and raised areas, which signify dermal invasion.
Lentigo-maligna - Radial growth 1st prior to dermal invasion
melanoma - 5% of intra-epidermal lesion progress to become clinically palpable →
dermal invasion and transformation into lentigo maligna melanoma

- Low metastatic potential but are locally invasive.
- In the local population – incidence probably much higher

- Dark brown to black, unevenly pigmented patch, >3cm
Acral-
- Occurs on palms, soles or under nails
Lentiginous
- Longitudinal brown or black band of the proximal nail fold (Hutchinson’s
sign) ± onychodystrophy
- Mucosal Melanomas – commonly in nasal cavity, then oral cavity

(aggressive)
- Ocular Melanomas -- arises from uveal melanocytes. Can metastasise
to the liver years after treatment of primary lesion.
Others - Desmoplastic Melanoma – amelanotic, pale, fleshy nodule – resemble a
scar
- Melanoma of the head and neck have a more aggressive course than
melanoma of the trunk / extremities. 26% of mucosal melanoma presents
with metastatic disease in regional nodes at time of diagnosis.

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INVESTIGATIONS
- Biopsy – excision with clinically negative margins or incisional
- Small lesions should be removed by excisional bx, while larger lesions sampled by incision bx
▪ Histology: Histological presence of melanin is diagnostic, but amelanotic lesions need to be diagnosed by
immunohistochemical tests. Melanomas that exhibit marked lymphocytic infiltration on histo a/w better prognosis
STAGING77
- Breslow thickness – measure tumour thickness in (mm)
▪ Measured from granular layer of epidermis (stratum granulosum) to deepest point of invasion
▪ More useful for prognosis than Clark’s levels, correlating well with the likelihood of regional and distant mets.
- Clark’s level – determined by anatomical invasion through skin layers
Other Staging System

- AJCC TMN staging classification
▪ T – (T1) <1mm, (T2) >1-2mm, (T3) >2-4mm, (4) >4mm, (a) no ulceration, (b) with ulceration
▪ N – (N1) one node, (N2) 2-3 nodes, (N3) ≥ 4 nodes, matted
▪ M – (M1a) mets to skin, (M1b) mets to lungs, (M1c) mets to distant non-CNS site, (M1d) mets to CNS
MANAGEMENT
- Wide Local Excision +/- Sentinel Lymph Node Biopsy +/- Lymph Node Dissection
▪ Keep muscular fascia intact – breach leads to increase incidence of LN metastases
▪ Excision Margins, based on thickness / tumour depth
o In-situ: 0.5 – 1cm margin (European recommend 0.5cm)
o < 1.0mm: 1cm margin
o 1.01 – 2.0mm: 1-2cm margin (European recommend 1cm)
o >2.0mm: 2cm margins
▪ Always need to resect clinically positive lymph nodes
▪ Sentinel lymph node biopsy
o Indications: melanomas with a Breslow depth > 0.75mm (for tumour < 0.75mm, relative indications include presence
of ulcerations, mitotic rate ≥ 1mm 2
- Immunotherapy / Interferon Therapy for Advanced Disease

- Resected stage III melanomas: high dose interferon-alpha or weekly Peg Interferon (IFN)
- Metastatic Melanoma: Targeted Therapy and/or Immunotherapy: BRAF inhibitors (i.e. vemurafenib, dabrafenib), Ipilimumab
(CTLA-4 inhibitor)
- Unresectable Isolated limb perfusion or Radiotherapy
PROGNOSIS
10 year survival
- Depth (Breslow thickness)
▪ ≤ 1.0mm: 92%
▪ 1.01 – 2.0mm: 80%
▪ 2.01 – 4.0mm: 63%
▪ >4.0mm: 50%
- Presence of ulceration is a poor prognostic marker, increasing risk of mets (included in T staging)
- Mitotic count (5yr & 10yr)
- Lymph Node Involvement – once involved = stage 3 and above (5yr)
▪ Stage 3 = 45%, <45% if more than 3 nodes involved
▪ Stage 4 = 10%
- BRAF mutation and PD-L1 expression are good prognostic marker (targeted therapies and immunotherapies available)
- Site of primary: scalp lesions tend to recur locally
77 Essentials of Plastic Surgery (2 nd Edition) – pg. 187-188

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APPROACH TO LUMPS & BUMPS
Permission: Introduce yourself

Position: Ensure patient (and you) are comfortable
Exposure: Expose area to be examined fully
Remember: Compare with other side if applicable
Inspection
- Number: solitary / multiple
- Size
- Site: take reference from bony points
- Shape / Symmetry: Hemispherical, Round, Exophytic
- Scars
- Colour & skin changes? – Sinuses, discharge, Ulceration, Erythema /
cellulitis
Palpation (ask patient: Is area painful?)

- Overlying skin temperature
- Tenderness
- Surface: Smooth/ Irregular/ Rough
- Margins clearly defined?
- Consistency: Hard > Firm > Tense > Soft
- Mobility: Fully mobile in all directions?, Fixed and immobile?, Mobile only
in certain directions?
- Relations to surrounding tissues – Move lump in 2 perpendicular planes
▪ Attached to skin? Muscle / tendon / bone?
▪ If appears to be attached to muscle: ask patient to tense muscle;
Reassess mobility in the 2 planes
- Intramuscular or below the muscle, it will disappear.
- Above the muscle it will be more prominent.
- Fixed to muscle, it will become less mobile.
- Fluctuant? (for small / medium lumps)
▪ Paget’s sign: Rest 2 fingers on opposite sides of lump, press down on middle of lump if +ve: Feel fingers moving apart
Special tests
- Transillumination [only for large lumps; Use pen torch on one side]
- Pulsatility (only for some sites, e.g. Neck, abdomen) – place finger on opposite sides of lump
▪ Expansile: fingers pushed apart
▪ Transmitted: Fingers pushed in same direction (usually upwards)
- Slip sign – if lipoma is suspected – tends to slip away from the examining finger on gentle pressure
- Compressibility / reducibility [if AVM, haemangioma, hernia suspected]
▪ Compressible: Disappears on pressure, reappears on release (AVM)
▪ Reducible: Disappears on pressure, reappears with opposing force (hernia)
- Auscultation – only for certain sites / lesions (e.g. neck, abdomen, etc.)
Request – “I would like to complete my examination by…”

- Examine the draining LNs
- If sebaceous cyst / lipoma – “Looking for other lumps elsewhere”
- Ganglion – “Looking for other lumps elsewhere” + “Asking for hand dominance” + “Taking an occupational history”

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LIPOMA
Inspection
- Can be single, often multiple
- Usually at neck, trunk
- Hemispherical – may appear lobulated
- Scars, Implies recurrent lipoma
Palpation
- Smooth or lobulated on firm pressure – bulging between strands of fibrous
tissue)
- Soft / firm (depending on nature of fat)
- Well defined edges (may not be regular; series of curves corresponding to each
lobule
- Pseudo-fluctuance if large – lipomas are not liquid; but fat maybe more liquid
- Mobile in all directions (if subcutaneous)
- Positive slip sign; No transillumination / thrill
- Usually in the subcutaneous tissue. [check attachment skin & muscle]
Definition: Benign tumour consisting of mature fat cells (distended with fat from over-activity)
- Malignant change does not occur
- Liposarcomas arise de novo; occur in older age (deeper tissues – retroperitoneal, deep tissues of thigh, subscapular)
- Liposarcoma classification
▪ Well-differentiated
▪ Myxoid, round cell (poorly differentiated myxoid)
▪ Pleomorphic liposarcoma
Clinical features
- Can occur at all ages (not common in children)
- Slow-growing, never regress
- May be multiple: lipomatosis (multiple continuous lipomata)
▪ Occur in buttocks / neck
▪ Can cause distortion of subcutaneous tissues.
Treatment
- Non-surgical – watch & wait
- Surgical – If patient wants it removed (Pain / peripheral neuropathy – Dercum’s disease, Cosmesis)
▪ Can be removed under LA
▪ Nuchal lipomas (back of the neck): extremely fibrous septae: difficult to excise
▪ If close to joint: LA may not be possible (may communicate with joint)
Variants of lipomas / syndromes associated with lipomas

- Adiposis dolorosa (Dercum’s disease)
▪ Multiple painful lipomas in limbs, sometimes trunk
▪ Associated with peripheral neuropathy
▪ Angiolipomas: prominent vascular component
- Hibernomas: brown fat cells
- Cowden’s disease – a/w: Thyroid cancer, Lipomas, Palmoplantar keratoses, Multiple facial papules, Oral papillomatosis
- Bannayan-Zonana syndrome – rare AD dz: lipomas with macrocephaly and haemangiomas, intestinal polyps

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SEBACEOUS CYST
Inspection
- Usually solitary (can be multiple)
- Hemispherical
- Site: face, trunk, back, neck, scalp, shoulders (none on palms / soles)
- Variable size ; few mm to 4-5 cm
- May have bluish discolouration
- Punctum in apex: in 50%
- May exhibit plastic deformation on palpation
Palpation
- Normal Temperature, non-tender (unless inflamed)
- Smooth surface
- Well-defined margins (lies in subcutaneous fat)
- Tense consistency, may stretch overlying skin ( plastic deformation)
- Non fluctuant, not transilluminable
- Attached to skin, not attached to deeper structures, mobile in all directions
Background Information
- Considered to be similar to epidermoid cyst, more accurate terminology: pilar / trichilemmal cysts
- 2 histological types:
▪ Epidermal cyst: from infundibular portions of hair follicles
▪ Trichilemmal cyst: from hair follicle epithelium (most common on scalp), frequently multiple (AD inheritance)
- Arise from infundibular parts of hair follicles
- Definition: Distension of sebaceous glands with sebum from blockage of opening
- Clinical features
▪ Occur in all age groups, rarely present before adolescence
▪ Slow growing,– may appear suddenly at adolescence
▪ May become infected: acutely painful, sudden increase in size
▪ May spontaneously discharge contents through punctum, regress
▪ Point of fixation & discharge along a hair follicle
▪ Point gets pulled inwards on enlargement of the mass – creates punctum
- Sebaceous horn may form from hardening of slow discharge from wide punctum
▪ Sebum slowly exudes, dries and hardens into conical spike
▪ Sebum usually washed away – horn results only if overlying skin not washed
▪ Can be pulled out of skin
▪ Treatment: excision / curettage along with base + histological assessment
Complications
- Infection (±discharge)
- Ulceration
- Calcification (trichilemmal cyst) (may lead to cyst hardening)
- Sebaceous horn formation, [hardening of a slow discharge of sebum from a large, central punctum.]
- Malignant change (rare)

541
Treatment
- Non-surgical: leave alone (if small, asymptomatic).
- Surgical
▪ Complete excision of cyst and contents under LA.
▪ Prevention of recurrence: by removal of elliptical portion of skin containing punctum along the lines of Langers.
▪ If at the angle of jaw, be careful of the facial nerve during operation. Damage to the zygomatic branch can cause eye
ulceration.
- If lump is increasing in size, what to exclude? Malignancies: SCC, BCC
Cock’s peculiar tumour (complication)

- Proliferating trichilemmal cysts that can grow to large size, ulcerate
▪ May become infected, open, granulating & edematous
▪ Boggy, painful, discharging swelling
▪ solitary, 90% occur in scalp
- often mistaken for SCC scalp; Angry, malignant-looking (malignant transformation rare)
▪ Heaping up of granulation tissue from the lining of the cyst
▪ Burst through skin, giving everted appearance
▪ Regional lymphadenopathy may be present
Gardner’s syndrome (If multiple lumps found)

- Genetic disorder associated with:
▪ Multiple osteomas of skull & epidermal cysts
▪ Adenomatous polyposis of large bowel & CRCs
▪ Desmoid tumours (intra-abdominal)
▪ Thyroid cancers
GANGLION
Inspection
- Single; may have overlying scar [recurrent mass]
- Hemispherical, flattened,
- Near joint capsules, tendon sheaths (90% on wrist,
hand – ventral / dorsal)
- Variable (0.5 – 6 cm)
Palpation
- Normal temperature, non-tender
- Smooth surface with Well-defined margins
- May be multilocular
- Soft & fluctuant if large > firm consistency if small
- Weakly transilluminant. (gelatinous material)
- Mobility:
▪ Should assess mobility in 2 perpendicular
planes, then with underlying muscles tensed
(less mobile when tensed)
▪ Not attached to overlying skin (mobile over it)
▪ Attached to fibrous structures of origin [to joint
capsule, tendon sheath, intra-muscular septum, fixed when tensed]
- Reducibility: may slip between deep structures when pressed (appears falsely reduce into joint)
Request
- Other similar lumps
- Ask which hand is dominant (may affect management), Occupation

542
Definition
- Cystic myxomatous degeneration related to synovial lined cavity [joint capsule or tendon sheath]
- Origin controversial: pockets of synovium communicating with joint, tendon sheath / degeneration of mucoid fibrous tissue
Site:
- Can occur anywhere in body
- Common in areas of fibrous tissue (e.g. around joints, esp. Dorsal > Volar wrist @ scapholunate joint)
- Most common soft-tissue mass in the hand
Types:
- Simple
- Compound – chronic inflammation distends tendon sheath above and below the flexor retinaculum, r/o TB / RA
- Occult
- Interosseous
Clinical features
- Majority between 20 and 60 years (rare in children)
- Grow slowly over months / years
- Non painful
Differentials
- Bursae (soft)
- Cystic protrusion of synovial cavity in OA (joint will be abnormal)
- Benign giant cell tumours of flexor shealth (Pigmented VilloNodular Synovitis)
- Lipoma
- Sebaceous cyst
Treatment
- Non-surgical
▪ Watch & wait, usually may disappear after a few months.
▪ Aspiration + 3/52 of immobilisation (successful in 30-50%). High chance of recurrence 6-12/12 later.
- Surgical → Complete excision to include neck of ganglion at site of origin. Along the lines of Langers.
Complications
- Wound complications: Scar, haematoma, infection
- Recurrence <10%
- Damage to adjacent neurovascular structures.
- Stiffness & Contractures

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NEUROFIBROMA
Inspection
- Often multiple
- Anywhere in skin, subcutaneous tissues, e.g. forearm
- Spherical / Pedunculated / Fusiform (long axes lie along length of
limb)
- Rarely more than few cm
- Comment on any café-au-lait spots
Palpation
- Normal temp., Non-tender
- Smooth, Well-defined
- Soft/ fleshy, rubbery consistency
- Non-fluctuant
- If in subcutaneous tissue: mobile within it
- Move most freely perpendicular to course of nerve
Request
- Look for other similar lesions & other manifestations of NF-1: café-
au-lait spots, axillary freckling, lisch nodules, optic glioma
- Measure the BP (HPT 2o to pheochromocytoma, CoA, RAS)
- Examination of cranial nerve VII & VIII (acoustic neuroma)
Sporadic Neurofibroma
- Benign tumour containing mixture of elements from peripheral nerves: Neural (ectodermal) & Fibrous (mesodermal)
- Often multiple
History
- Any age (but usually adult)
- Symptoms: usually cause no discomfort, rarely disfiguring
- If related to nerve trunk, may be tender
- Patient may get tingling sensations in distribution of nerve
Histology
- Schwann cells: appear as bundles of elongated wavy spindle cells
- Collagen fibrils, myxoid material
- Often not encapsulated (unlike neurilemmomas)
Complications of Neurofibroma
- Pressure effects: spinal cord, nerve root compression
- Deafness: involvement of VIII
- Neurofibrosarcoma (only in NF-1): 5-13 %
- Intra-abdominal effects: obstruction, chronic GI bleeding
- Skeletal changes: kyphoscoliosis, cystic changes, pseudoarthrosis

544
Treatment (single neurofibroma)
- Non-surgical: leave alone if asymptomatic, patient agreeable
- Surgical: indicated only if malignancy suspected
▪ Local re-growth common (cannot be surgically detached from underlying nerve)
Neurofibromatosis I (Von Recklinghausen's disease)

- AD, neurocutaneous syndrome; incidence 1 in 3000 births; chr 17q11.2
- NIH diagnostic criteria78 for NF 1 (≥ 2 of the following clinical features)
▪ Fibroma ≥2 NF or ≥1 plexiform NF
▪ Iris hamartomas ≥ 2 (Lisch Nodules)

▪ Bone: sphenoid dysplasia, pseudoarthrosis
▪ Relatives – 1st degree (parent, sibling or offspring)
▪ Optic glioma
▪ Macules ≥6 café au-lait macules of >5mm in prepubertal individuals & >15mm post-puberta
▪ Axillary freckling or Inguinal freckling
- Neurofibroma of all sizes (few mm to large subcutaneous nodules), related differently to skin
▪ Within skin
▪ Tethered to skin
▪ Pedunculated
- Complications79 of NF1
▪ Learning Problems
▪ Plexiform Neurofibroma
▪ Epilepsy = CNS tumour, optic glioma, spinal NF
▪ Aqueduct stenosis
▪ Orthopedics = scoliosis, pseudoarthrosis of tibial and fibula, vertical scalloping, sphenoid wing dysplasia
▪ Malignancy = MPNSTs, pelvic rhabdomyosarcomas
▪ Other Cancers = GI neurofibromas, pheochromocytomas, duodenal carcinoid, glomus tumour of nail bed
▪ Vascular = renal artery stenosis, cerebrovascular disease
DERMOID CYST
Inspection
- Usually single
- Ovoid / spherical
- Site:
▪ Congenital, 1-2 cm usually
- Along lines of fusion of ophthalmic & maxillofacial processes
- Inner & outer ends of upper eyebrow
▪ Acquired, 0.5-1 cm usually
- Beneath skin likely to be injured e.g. fingers
- Scars often present
Palpation
- Not warm, maybe tender if infected
- Smooth surface, Well-defined margins
- Consistency
▪ Congenital: Soft (not tense / hard)
▪ Acquired: Hard & tense (sometimes stony hard)
- Fluctuant (if large)

- Mobile over deeper tissues
▪ Deep to skin, in subcutaneous tissue
- Congenital: Not attached to skin or underlying structures
- Acquired: may be tethered to scar
78 uptodate: Neurofibromatosis type 1 (NF1): Pathogenesis, clinical features, and diagnosis

79 PACES for the MRCP 3rd Edition (Tim Hall) – pg: 626

545
- A dermoid cyst is a cyst deep to the skin, lined by skin
- 2 different methods of formation:
▪ Congenital: Accident during antenatal development
▪ Acquired: Implantation of skin into subcutaneous tissue by injury
Clinical features
- Congenital (suspect if in child, young adult)
▪ Formed intra-utero, when skin dermatomes fuse
▪ Occur at any point in mid-line, common in neck / face / nose
▪ May be seen at birth
▪ Distends a few years later, becomes obvious; few symptoms other than cosmetic problems
▪ Rarely infected
- Acquired – Implantation dermoid (suspect if in adult – Browse pg 60)
▪ Develop when piece of skin survives after being forcibly implanted into subcutaneous tissue
▪ Often by injury: cut, stab, etc.
▪ Symptoms: small, tense lump, painful and tender (in areas subjected to repeated trauma), local effects (e.g. problems with
grip / touch if on finger), rarely infected
Differentials – sebaceous cyst (look for old injury, presence of scar near cyst: more likely dermoid)
Treatment
- Congenital – surgical treatment; complete excision, full extent should first be established with X-ray / CT (midline cysts may
communicate with CSF; must exclude bony defect)
- Acquired – complete excision of cyst
SEBORRHEIC KERATOSIS
Inspection
- Often multiple
- Any part of skin; most found on back & fac
- Round / ova
- Light brown → blac
- “stuck on appearance”; appears wart
- Varying size; Few mm to 2-3 c
- Distinct margins
Palpation
- No warmth, no tenderness
- Rough surface (sometimes papilliferous)
- More firm than surrounding skin
- Attached to skin
- Special tests – may be picked off gently – reveals patch of pale-pink skin, 1-2 surface capillaries (DON’T DO THIS IN EXAM)
Request to look for similar lesions elsewhere

546
- Benign outgrowth of basal layer of epidermis
- Raised above the level of normal epidermis
- Microscopy:
▪ Hyperkeratosis (thickening of keratin layer)
▪ Acanthosis (thickening of prickle cell layer)
▪ Hyperplasia of variably pigmented basaloid cells
Clinical features
- Occur in both sexes
- More common in elderly people
- Begin as a patch,
▪ Increases in area, size over months / years
▪ May not increase in thickness
▪ May suddenly fall off: leave pale-pink patch of skin
Complications:
- May become disfiguring, catch on clothes
- May get infected (may imitate SCC, pyogenic granuloma)
- Seldom bleeds (may cause it to change colour to brown)
Leser-Trelat sign: Sudden onset of multiple seborrhoeic keratoses may imply visceral malignancy
Treatment
- Non-surgical – can be left alone as it is benign
- Surgical – for cosmetic reasons, etc.
▪ Superficial shaving (lies above level of normal epidermis) or Cautery
PYOGENIC GRANULOMA
Inspection
- Single; usu < 1 cm, bright red
- May be blood-encrusted or Ulceration
- Hemispherical; may be sessile / pedunculated
- Likely sites to be injured, e.g. hands, face
- Bright red; long-standing lesions may be skin-coloured
- May have sinuses, associated serous / purulent discharge, Erythema / cellulitis
Palpation – request to palpate: may bleed easily

- May be slightly tender
- May bleed easily on palpation
- Well-defined edges
- Soft, fleshy consistency
- Confined to skin
- Slightly compressible (vascular origin)
Request
- Take history for previous injury
- Rate of growth of lump? (rapid growth in few days)
Background Information – Neither pyogenic nor a granuloma!

- Rapidly-growing capillary haemangioma, usually less than 1 cm
- Occur commonly after injury:
▪ Small capillary loops develop in healing wound, form granulation tissue
▪ When capillary loops grow too vigorously, form protruding mass, epithelization
▪ Mass form called pyogenic granuloma (surface often ulcerated, infected)

547
Clinical features
- Uncommon in children
- May have history of minor injury, chronic infection (e.g. paronychia)
- Rapidly-growing lump on skin,
- Bleeds easily, discharges serous / purulent fluid
- Bleeding, pain stops once lump epithelises
- Once nodule is completely covered, begins to shrink (rarely disappears completely)
Treatment
- Surgical
▪ Curettage with diathermy of the bas
▪ Complete excision biopsy
▪ if recurrent; malignancy e.g. amelanotic melanoma has to be excluded
- Non-surgical
▪ Regression is uncommon: surgical treatment best option
▪ Silver nitrate cautery is possible
PAPILLOMA
Inspection
- Single / multiple
- Variable: from raised plaque to pedunculated polyp
- Site: Neck, trunk, face, anus (anywhere on skin)
- Variable
- Flesh-coloured
Palpation
- Not warm, non-tender
- Variable: smooth to papilliferous
- Soft, not compressible
- Arises from skin
Request
- Similar lumps elsewhere
- Ask for associated conditions: pregnancy, diabetes, intestinal polyposis
- An overgrowth of all layers of the skin with central vascular core
- Not a neoplasm, but a hamartoma (skin tag is a more accurate term)
- Increasingly common with age – may be congenital
Clinical features
- Catches on clothes, rubs against other body parts
- May resemble carcinoma if granulation is excessive
- Complications:
▪ May become red, swollen, and ulcerate
▪ May become infected
▪ May be infected (contains all skin components – sebaceous glands, etc.)
Treatment
- Excision – diathermy, scissors (bleeding from central vascular core controlled using single suture / diathermy)

548
KERATHOCANTHOMA
Inspection
- Often found on face
- Usually solitary;1 – 2 cm in diameter
- Hemispherical or conical, with central crater
- Normal skin colour
Palpation
- Firm and rubbery (central core is hard)
- Confined to skin, freely mobile over subcutaneous tissues
Background information
- Benign overgrowth of hair follicle cells with a central plug of keratin
- Complain of rapidly-growing lump in skin
- Not painful, but can be unsightly
- Takes 2 – 4 weeks to grow, regresses in 2 – 3 months
▪ Central slough appears,
▪ Surrounding skin retracts to form puckered scar
- Cause is unknown (may be self-limiting benign neoplasm or post-viral infection)
- Treatment:
▪ Conservative if asymptomatic
▪ Surgical excision of lesion with histology to r/o SqCC
KELOID (HYPERTROPHIC SCAR)
Healing by primary intention – 3 stages:

- Tissue defect filled by blood / fibrin
- Replacement by collagen and fibrous tissue
- Organisation of fibrous tissue to maximise wound strength
Wounds prone to hypertrophic / keloid scar

- Most surgical scars have thin lines, but tissue response may be excessive leading to
hypertrophic / keloid scar
- Infection, Trauma, Burns, Tension
- Susceptible areas: across flexion areas, earlobes, chest, neck, shoulder
Hypertrophic scar
- Any age – common 8-20 years,
- Excessive amount of fibrous tissue, but confined to scar (between skin edges)
- Located across flexor surfaces, skin creases
- Common, especially if infection / excessive tension
- Only enlarge for 2-3 months, then regress spontaneously
- Do not recur if excised and causative factor eliminated
Keloid scar
- Puberty to 30 years, F>M, black, hispanic more likely
- Hypertrophy and overgrowth extend beyond original wound
- Located at earlobes, chin, neck, shoulder, chest
- Due to local release of fibroblast growth factors
- Continue to enlarge 6-12/12 after initial injury
- May be tender, unsightly
- Will recur unless special measures taken
Treatment (recurrence can be as high as 55%)

- Non-surgical: mechanical pressure therapy – topical silicone gel sheets (day and night for 1 year), Intralesional steroid, LA
injections: e.g. triamcinolone with lignocaine
- Surgical: revision of scar by direct suturing, skin grafting (avoid excessive tension)

549
FIBROSARCOMA
Inspection
- Single; Usually limbs (but can be anywhere)
- Spherical or hemispherical
- If large, vascular: may make skin shiny & pink
- May have: sinuses & discharge, ulceration, erythema / cellulitis
Palpation
- Usually feel warmer (abnormal blood supply)
- May be tender
- Smooth surface (may be bosselated – covered with knobs)
- Well-defined margins (indistinct if fast-growing, invasive)
- Firm / hard consistency (rarely stony hard; do not ossify)
- Usually fixed
- May pulsate, have audible bruit, palpable thrill (may be very vascular)
Request to test for distal neurological status (for invasion of nerve)
- Fibrosarcoma is one of the commonest mesodermal soft tissue malignant tumours
- Pure benign fibroma is very rare
- More common in elderly (but can occur any age)
- Common complaints – growth: disfigurement, interference with range of motion, pain, weakness (infiltration of other structures)
- Low sensitivity towards radiotherapy and chemotherapy
- High rates of tumour recurrence
PYODERMA GANGRENOSUM
Inspect
- Ulcer with a necrotic base
- Irregular bluish red overhanging edges
- a/w surrounding erythematous plaques with pustules
Request to examine for evidence of inflammatory bowel disease, RA
- More common in males
- Pyoderma gangrenosum is associated with:
▪ IBD
▪ RA
▪ Myeloproliferative disorders: PRV, myeloma
▪ Autoimmune hepatitis
Differential diagnosis:
- Autoimmune: rheumatoid vasculitis
- Infectious: tertiary syphilis, amoebiasis
- Iatrogenic: warfarin necrosis
- Others: Behcet’s disease
Treatment:
- Non-surgical: treat underlying condition, saline cleansing, high dose oral or intralesional steroids.
- KIV cyclosporine & antibiotics
- Surgical: serial allograft followed by autologous skin graft or muscle flap coverage when necessary

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RADIOTHERAPY MARKS
Assessment of underlying disease

- Cachexia,
- Mastectomy scar/ wide excision scar → suggest breast cancer
- obvious skin cancer,
- Clubbing & other signs of chest disease →suggest lung cancer
- Suprapubic mass → suggest pelvic tumour
- Neck swellings with cranial nerve palsies → head and neck tumour
Assessment of the radiotherapy:

- Site of radiation
- Shape: usually well defined borders
- Features of active RT: Indian ink marks, skin markings, erythema, desquamation
- Features of previous RT: telangiectasia, hyperpigmentation
- High energy X-rays interact with tissue to release electrons that cause local damage to DNA in adjacent cells via an oxygen
dependent mechanism.
- Damage is usually irreparable, and normal cells have greater ability to repopulate than tumour cells in this setting
- If reparable, manifests as chromosomal abnormalities
Radiotherapy affects cells with:

- Rapid turnover: Skin (epidermal layers), small intestine, bone marrow stem cells
- Limited replicative ability: spinal cord, gonads
Complications:
- Early:
▪ General: malaise, fatigue, LOA, N/V
▪ Skin changes & temporary hair loss
▪ Bone marrow suppression, esp. if to long bone and pelvis
▪ GI: diarrhea
- Late:
▪ Skin changes
▪ Heart: IHD
▪ Lung: pneumonitis, pulmonary fibrosis
▪ Blood Vessels: radiation arteritis, esp to carotids 🡪 necrosis, distal ischaemia and vessel rupture
▪ CNS: spinal cord myelopathy
▪ Uro: bladder fibrosis, Renal impairment (depletion of tubular cells)
▪ Abdo: IO 2o to strictures & adhesions,
▪ Genital: infertility
▪ Endocrine: hypothyroidism
▪ Eye: cataracts
▪ Increase incidence of future cancers
- Haematogenous malignancy, e.g. leukemia
- Solid tumours: Thyroid cancers
- Breast cancers
Minimalising of side effects of radiotherapy:

- Lead shields to eyes, gonads and thyroid
- Dose fractionation (to allow recovery of normal cells)
- Prior chemotherapy (increase sensitivity of tumour cells)
- Regional hypothermia
- Radiolabeled antibody to deliver local radiation to tumour

551
DRAINS
DRAIN FUNCTIONS
- Evacuate collections of pus, blood or fluids (e.g. lymph), removes potential source of infection
- Drain potential collections
- Allow early detection of anastomotic leaks or haemorrhage
- Leave tract for potential collections to drain after removal
TYPES OF DRAINS
- Drains are often made from inert silastic material (induce minimal tissue reaction)
- They induce minimal tissue reaction
Open Active
Active drains require suction

(i.e. Jackson-Pratt Drain, Redivac Drain, T-tube)
Have expandable chambers to create low-pressure suction
Used when small – mod amts of drainage are expected or
when passive drainage system won't provide adequate
Corrugated drain, Yeates drain, Penrose drain drainage
Drain fluid collects in gauze pad or stoma bag Tubing of the low-pressure active drainage system is placed
Easier to drain infected collections through a separate puncture wound or the tube may exit the
edge of the surgical wound
If the tubing isn't sutured in place, it could become dislodged
If a portion of the tube is pulled outside the skin, an air leak will
cause the chamber to fill with air & it won't drain properly.
Closed Passive
Passive drains rely on gravity
Consist of tubes draining into a bag or bottle
Passive drains have no suction
They include chest and abdominal drains
Works by differential pressure (body cavities and the exterior)
The risk of infection is reduced
Used when a mod – large amt of drainage is expected

552
Blake Drain
Redivac Drain Jackson-Pratt Drain (JP) Drain Penrose Drain
Redivac Drain Bottle has a green vacuum indicator which if compress indicates that suction is intact and if not indicates that suction is lost
Blake Drain has 4 channels that provide greater tissue contact area than regular perforated drains (minimize blockage)
Penrose Drain is used for passive drainage
CARE OF TUBES:
- Prevent Infection, maintain meticulous skin care and aseptic technique around the insertion site
- Prevent blockage of the drain, do not allow bottles to fill up
- Prevent slippage by securing drain carefully to skin, refix as required
- Never hold a drainage collection device higher than the tube insertion site to prevent the drainage from flowing backward into
the patient
- Note amount of drainage daily
COMPLICATIONS
- Bleeding / Infection
- Tissue damage by mechanical pressure or suction
- Drain failure → blocked/slipped/kinked
- Incisional hernia occurs when drain inserted through an incision wound site (create a separate incision site for drain)
REMOVAL OF DRAINS
- A drain is removed as soon as it is no longer required. The following are general guidelines:
▪ Drains put in to cover perioperative bleeding and haematoma formation, can come out after 24— 48 hours.
▪ Where a drain has been put in to drain an infection (abscess), remove it when fever settles or when there is evidence of
complete drainage
▪ Decreasing drainage trend (i.e. < 50mls)
▪ When the operating surgeons says so

553
NASOGASTRIC TUBE
INDICATIONS
- Diagnostic: Bleeding from the upper gastrointestinal tract, haematemesis
- Decompression
▪ Therapeutic (i.e. intestinal obstruction, gastric outlet obstruction)
▪ Preventive (i.e. expected ileus after a major abdominal surgery, decompress stomach /
duodenal stump after gastric surgery)
▪ Intra-operative (i.e. prevent stomach from obstructing operative field)
- Nutrition: Enteral Nutrition (i.e. patient are unable to take orally)
- Lavage: Poisoning
CONTRAINDICATIONS
- Base of Skull Fracture
- Esophageal Tears
PRE-PROCEDURE
1. Gather equipment.
2. Don non-sterile gloves.
3. Explain the procedure to the patient and show equipment.
4. If possible, sit patient upright with head forward for optimal neck/stomach alignment. Otherwise, prop the patient up at 45 °.
5. Deflate the endotracheal tube or tracheostomy cuff
6. Determine the size of the nasogastric tube required (usually 14 – 16Fr). If aspirating (i.e. patient with intestinal obstruction), use
as large a tube as possible to reduce the risk of blocking during use; if feeding, a smaller tube may be used (eg. 10-12Fr) because
it is more comfortable in the long term.
PROCEDURE
1. Estimate the length of the tube to be inserted: from the bridge of the nose to the tragus of the ear to the point halfway between
the xiphisternum and the navel. Mark the measured length with a marker or note the distance.
2. Examine nostrils for deformity/obstructions (eg. choanal stenosis) to determine best side for insertion. Select the largest nostril
for insertion.
3. Lubricate tube.
4. Introduce the tube through the nostril horizontally in, passing the tube along the floor of the nose. Resistance may be felt as tip
reaches the nasopharynx, which is the most uncomfortable part of the procedure. In the operation theatre, when the patient is
under general anesthesia, the McGill’s forceps may be used to guide the tube down.
5. Instruct the patient to swallow (you may offer ice chips/water if not contraindicated) and advance the tube as the patient swallows.
Swallowing of small sips of water may enhance passage of tube into esophagus.
6. Continue to advance the tube down the esophagus. There should not be resistance. If resistance is met, rotate the tube slowly
with downward advancement towards the closer ear. Do not force the tube down against resistance as this may form a false
passage.
7. Withdraw the tube immediately if changes occur in the patient's respiratory status, if the tube coils in the mouth, or if the patient
begins to cough or turns pretty colors.
8. Advance the tube until the mark is reached (approximately 50-60cm). Stop.
9. Check for correct placement by attaching a syringe to the free end of the tube and aspirating a sample of gastric contents to test
with litmus, auscultating the epigastrium while injecting air through the tube, or obtaining an x-ray to verify placement before
instilling any feedings/medications or if you have concerns about the placement of the tube.
10. Secure the tube with adhesive tape.
11. If for suction, remove the syringe from the free end of the tube; connect to suction; set machine on type of suction and pres sure
as prescribed.
12. Document the reason for the tube insertion, type & size of tube, the nature and amount of aspirate, the type of suction and
pressure setting if for suction, the nature and amount of drainage, and the effectiveness of the intervention.
COMPLICATIONS
- Risk of insertion of tube into trachea
- Technical: traumatic insertion, risk of perforation to pharynx / oesophagus
- Respiratory: risk of aspiration pneumonia
- Gastrointestinal: gastric / esophageal erosion, pressure necrosis, bleeding
- Loss of Fluids & Electrolytes: loss of sodium, potassium, chloride and hydrogen ion
- Dry Mouth: due to mouth breathing

554
CHEST TUBE
Chest tubes are inserted to drain blood, fluid, or air and allow full expansion of the lungs. The tube is placed between the ribs and into
the space pleural space.
The area where the tube will be inserted is anesthetized locally. The patient may also be sedated. The chest tube is inserted through
an incision between the ribs into the chest and is connected to a bottle or canister that contains sterile water (underwater seal). Chest
tube will transverse through the skin, serratus anterior muscle, intercostal (external, internal, innermost) muscles, and parietal pleura
to reach the pleura cavity Suction is attached to the system to encourage drainage. A suture and adhesive tape is used to keep the
tube in place.
The chest tube usually remains in place until the X-rays show that all the blood, fluid, or air has drained from the chest and the lung
has fully re-expanded. When the chest tube is no longer needed, it can be easily removed, usually without the need for medications
to sedate or numb the patient. Antibiotics may be used to prevent or treat infection.
INDICATIONS
1. Pneumothorax.
2. Hemothorax.
3. Drainage of pleural effusion.
4. Chylothorax
5. Drainage of empyema/lung abscesses
6. Prophylactic placement of chest tubes in a patient with suspected chest trauma before transport to specialized trauma center
CONTRAINDICATIONS
1. Infection over insertion site
2. Uncontrolled bleeding diathesis/coagulopathy
MATERIALS
1. Iodine & alcohol swabs for skin prep
2. Sterile drapes & gloves
3. Scalpel blade & handle
4. Clamp
5. Silk Suture & Prolene Sutures
6. Needle holder
7. Petrolatum-impregnated gauze
8. Sterile gauze
9. Tape
10. Suction apparatus (Pleuravac)/underwater seal apparatus
11. Chest tube (size depends on clinical setting, 24,28,32Fr)
12. 1% lignocaine with epinephrine, 10 cc syringe, 25- & 22-g needles
PRE-PROCEDURE PATIENT EDUCATION

1. Obtain informed consent
2. Inform the patient of the possibility of major complications and their treatment
3. Explain the major steps of the procedure, and necessity for repeated chest radiographs
4. Keep patient on continuous monitoring

555
PROCEDURE
1. Determine the site of insertion. Locate the triangle of safety; bounded by the lateral border of the pectoris major, 5th or 6th
intercostal space, imaginary vertical line between the anterior and mid axillary lines.
2. Surgically prepare and drape the chest at the predetermined site of the tube insertion.
3. Locally anaesthetized the skin and rib periosteum.
4. Make a 2-3cm transverse incision at the predetermined site and bluntly dissect through the subcutaneous tissues, just over the
top of the rib.
5. Puncture the parietal pleura with the tip of a clamp and put a gloved finger into the incision to avoid injury to other organs and to
clear any adhesions, clots, etc.
6. Select a 24–28Fr chest tube (pneumothorax) or 32Fr chest tube (hemopneumothorax),
7. Clamp the proximal end of the chest tube and advance the tube into the pleural space to the desired length.
8. For pneumothorax, direct the chest tube upwards to apex, if hemothorax then toward base.
9. Look for fogging of the chest tube with expiration or listen to air movement.
10. Connect the end of the chest tube to an underwater seal apparatus. (ensure the underwater seal is below the level of the patient)
11. Suture the tube in place (anchored with silk 2/0 and purse string with prolene 2/0)
12. Apply a dressing and tape the tube to the chest.
13. Do a chest X ray
14. Obtain arterial blood gas values and/or institute pulse oximetry monitoring as necessary.
COMPLICATIONS
Damage to structures:
- Laceration or puncture of the intrathoracic and/or abdominal organs, all of which can be prevented by using the finger technique
before inserting the chest tube.
- Damage to the intercostals nerve, artery or vein.
- Subcutaneous emphysema, usually at tube site.
Equipment:
- Incorrect intrathoracic or extrathoracic tube position.
- Chest tube kinking, clogging or dislodging from the chest wall or disconnection from the underwater seal apparatus.
- Anaphylactic or allergic reaction to surgical preparation or anaesthesia.
Failure:
- Introduction of pleural infection.
- Persistent pneumothorax
- Recurrence of pneumothorax upon removal of the chest tube.
- Lungs fail to expand due to plugged bronchus; bronchoscopy required.
Recovery from the chest tube insertion and removal is usually complete, with only a small scar. The patient will stay in the hospital
until the chest tube is removed. While the chest tube is in place, the nursing staff will carefully check for possible air leaks, breathing
difficulties, and need for additional oxygen. Frequent deep breathing and coughing is necessary to help re-expand the lung, assist
with drainage, and prevent normal fluids from collecting in the lungs.

556
Underwater Seal Apparatus

557
URINARY CATHETERIZATION
INDICATIONS FOR SHORT-TERM CATHETERISATION

1. Relief of acute retention of urine, e.g. benign prostatic hypertrophy, bladder outflow obstruction.
2. Bladder washout, e.g. blood clots causing acute retention of urine.
3. Cystourethrogram
4. Administration of intravesical drugs
5. As an adjunctive measure pre/post-operatively
a) Pre-operatively:
(i) To drain the bladder so as to improve access to the pelvis in urologic or pelvic surgery.
(ii) To allow accurate measurement of urine output in major surgery.
b) Post-operatively:
(i) To relieve acute urinary retention because post –op pain results in failure of the sphincter to relax.
6. Urinary output monitoring, e.g. in patients with hypovolemic shock or the critically ill.
INDICATIONS FOR LONG-TERM INDWELLING CATHETERIZATION

1. Refractory bladder outlet obstruction.
2. Chronic retention of urine, eg. neurogenic bladder.
3. Incontinence, e.g. in palliative care of terminally ill or patient’s preference.
CONTRAINDICATIONS
1. Presence of urethral injury, suspected by:
a) blood from the meatus,
b) scrotal haematoma,
c) pelvic fracture, or
d) high-riding prostate (on digital rectal examination
PROCEDURE80
1. Know indications, contraindications and complications associated with urinary catheterization
2. Prepare requisites, position procedure trolley appropriately
3. Check patient’s identity using 2 identifiers
4. Obtain verbal consent. Have a chaperone if performing the procedure on a member of the opposite sex.
5. Observe aseptic technique during procedure – perform hand wash
6. Open the sterile pack, catheter, urinary bag and lignocaine aseptically
7. Use chlorhexidine onto swabs (for cleansing)
8. Don sterile gloves
9. Test the integrity of the catheter balloon with STERILE WATER
10. Place catheter into kidney dish and apply lignocaine gel on the catheter
11. Using the chlorhexidine soaked swabs, clean in one direction away from glans along shaft
12. Drape the penis and retract foreskin and clean urethra meatus (in females: retract labia majora and swab perineum)
13. Inject lignocaine gel into the urethra (in females: apply lignocaine gel to catheter tip)
14. Wait for 3-4min (ideally) before inserting the catheter.
15. Communicate, provide reassurance and monitor patient throughout procedure
16. Place the tray containing the catheter on the drape
17. Hold penile shaft in 60-90 degree position and insert catheter gently into meatus (in females: expose external urethral orifice)
18. If resistance is felt, increase traction on the penis slightly and apply steady gentle pressure on catheter
19. Advance catheter till the bifurcation point when urine flows out
20. Slowly inflate the balloon with STERILE WATER (usually 10ml),(inflating the balloon should be painless)
21. Withdraw catheter gently till resistance is felt (snug against bladder neck)
22. Connect catheter to urine bag
23. Reposition foreskin (males). Secure catheter on lower abdomen with tape.
24. Ensure the urine bag is below the level of bladder and urine flow is unobstructed
25. Clean up area and WASH HANDS BEFORE LEAVING
26. Document catheterization date, type of catheter used, amount of water in balloon, patient’s response to procedure
“Urinary catheter __Fr inserted under aseptic technique. Balloon was filled with 10ml sterile water. Clear / light-yellow / dark-yellow /
tea-coloured / bloody urine __ml drained. Atraumatic insertion, patient tolerated procedure well. SIGN.”
COMPLICATIONS
1. Infection
2. Stricture formation
3. Creation of a false passage due to wrong technique of insertion.
4. Occasionally, irritation of the bladder may cause severe bladder spasms.
80 TTSH Urinary Catheterization of Male Patient (Skills Performance Checklist)

558

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1

MedBear General Surgery Notes

Welcome to the new and improved version of MedBear!

Seborrheic Keratosis 546

Trauma Death (Trimodal Distribution) - Trunkey et. al (1983)2

1 World J Surg. 2007 Nov;31(11):2092-103.

Mechanism of the lethal triad of death in trauma

PREPARATION AND TRIAGE

Mechanism of injury which are deemed high risks includes:

PRIMARY SURVEY (A B C D E), RESUSCITATION AND TRIAGE

[A] - Airway Assessment with Restriction of Cervical Spine

- Airway Assessment – is this a compromised airway?

- Predicting a difficult airway

- How to establish a patent airway?

- Definition of definitive airway

- Assessment of adequacy of ventilation

- Assessment of adequacy of oxygenation

- Life-threatening conditions that require immediate attention and treatment

[C] - Circulation (Hemorrhage Control & Replacement of Intravascular Volume)

- Assessment of organ perfusion

▪ Urinary Output (aim ≥ 0.5-1.0ml/kg/hr)

- Apply ECG monitor / Pulse Oximeter / Automated BP cuff

- Management (Haemorrhage Control)

- Management (Replacement of Intravascular Volume)

▪ Initiate IV fluid therapy with warmed crystalloids – 1L of crystalloids

▪ Activation of Massive Blood Transfusion Protocol

▪ Damage Control Resuscitation3

[D] - Disability (Neurological Evaluation) - Glasgow Coma Scale

must also be examined (size, equality and reaction to light).

3 Mil Med. 2018 Sep 1;183(suppl_2):36-43.

Assessment of GCS Score (must know)

peritoneal fluid, sensitivity: 60-95%)

Complete head-to-toe examination

- Maxillofacial *frequently missed injuries*

- Neck (r/o cervical spine, vascular, airway or aerodigestive tract injuries)

▪ Lower Limbs (r/o soft tissue, vascular, orthopaedics, neurological injuries)

Types of Intra-abdominal injury in Blunt Trauma

Indication for Trauma Exploratory Laparotomy

Focused Assessment with Sonography in Trauma (FAST)

Computer Tomography Scan

Diagnostic Peritoneal Lavage (DPL)

Abdominal Compartment Syndrome (ACS)

- Classification of IAP via Bladder Pressure Measurement [normal IAP ~ 5-7mmHg]

Liver Trauma (AAST Liver Injury Scale)

Parenchymal Laceration Juxtahepatic venous

bleed and hemorrhagic shock) → operate

angioembolization (evaluate for risk of contrast allergy, creatine function, asthma)

Operative Management of Liver Trauma

Splenic Trauma (AAST Spleen Injury Scale)

Subcapsular Hematoma > 50% or expanding or

Parenchymal Laceration Completely shattered

Intraparenchymal ≥ 5cm or expanding or

- Splenic Artery Angiography & Embolization

Operative Management of Splenectomy

6 J Trauma. 2005 Mar;58(3):492-8.

Small Bowel Trauma

▪ Zone 2 & 3 → can observe if hemodynamically stable

▪ For all penetrating injuries → surgery

Cardiac Tamponade Investigation Findings

Diagnostic Clues (for laryngeal trauma)

short period of time]

PNEUMOTHORAX (TENSION/ OPEN)

BLUNT CARDIAC INJURY

Aims of performing thoracotomy

- Maxillofacial frequently missed injuries