Notes For My Ho and Mos-1

HOSPITAL PAKAR SULTANAH FATIMAH MUAR
NOTES FOR MY
HOUSE- AND
MEDICAL-
OFFICERS
NORLY SALLEH
TABLE OF CONTENTS
TOPIC PAGE
HEPATOBILIARY
Acute Pancreatitis……………………………………………………………………………………...5
Necrotizing Pancreatitis……………………….............................................................................9
Chronic Pancreatits…………………………………………………………………………………..14
Acute Calculus Cholecystitis………………………………………………………………………...19
Acute Acalculous Cholecystitis................................................................................................21
Common Bile Duct Stone……………………………………………………………………………25
Indications for Open Cholecystectomy……………………………………………………………..27
Adenomyomatosis of Gall Bladder……………………………………………………….…………28
Liver Abscess...........................................................................................................................29
BREAST AND ENDOCRINE
Management of Solitary Thyroid Nodule..................................................................................34
Lymphoedema in Breast Cancer.............................................................................................36
Diagnostic Modalities in Diagnosing Breast Cancer................................................................38
Chronic Granulomatous Mastitis..............................................................................................42
Advanced Breast Cancer.........................................................................................................44
Zometa®……………………………………………………………………………………………….46
UPPER GASTROINTESTINAL TRACT
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Post Gastrectomy Complications.............................................................................................47
COLORECTAL
Carcinoid Tumours...................................................................................................................51
Rectal Prolapse .......................................................................................................................54
Intra-abdominal Abscess.........................................................................................................58
Appendicular Mass/Abscess....................................................................................................62
Toxic Megacolon......................................................................................................................65
Pseudomembranous Colitis.....................................................................................................69
Management of Obstructed Splenic Flexure Tumour..............................................................72
Faecal Incontinence.................................................................................................................77
Fistula In Ano...........................................................................................................................79
Haemorrhoids..........................................................................................................................83
VASCULAR
Management of Leaking Abdominal Aortic Aneurysm.............................................................87
Venous Ulcer...........................................................................................................................92
Assessment and Management of Patient with Critical Limb Ischaemia...................................96
PLASTIC SURGERY
Burns........................................................................................................................................99
PAEDIATRIC SURGERY
Abdominal Wall Defects in Paediatric Patients......................................................................104
Pyloric Stenosis .....................................................................................................................106
Hirschsprung’s Disease.........................................................................................................109
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Necrotizing Enterocolitis (NEC).............................................................................................111
Choledochal Cyst...................................................................................................................114
CARDIOTHORACIC
Flail Chest..............................................................................................................................116
UROLOGY
Benign Prostatic Hyperplasia (BPH)......................................................................................120
Haematuria............................................................................................................................125
Stone Passage…………………………………………………………….………………………..127
PRINCIPLE OF SURGERY
Laparoscopic Surgery............................................................................................................128
Laparotomy Wound Dehiscence............................................................................................131
ARDS.....................................................................................................................................134
TRALI………………………………………………………………………………………….……..136
Post-Operative Pain...............................................................................................................138
Ventilator Associated Pneumonia (VAP)................................................................................141
WHO Guidelines for Safe Surgery..........................................................................................144
Damage Control Surgery (DCS)..............................................................................................146
Evidence-Based Medicine (EBM)...........................................................................................149
Diathermy..............................................................................................................................152
Subcutaneous Emphysema……………………………………………………………………………………………….154
Principle of Intestinal Anastomosis……………………………………………………………………………………156
Norly Salleh Page 4

HEPATOBILIARY
Acute Pancreatitis
Definition
 Acute inflammation of the pancreas which usually lasts for days
Clinical Presentation
History:
 Epigastric pain radiating through to the back

 Associated with nausea or vomiting
 May have a history of recent surgery or procedure (e.g. ERCP)
 May have family of hyperlipidaemia
 There may be previous biliary colic or a binge of alcohol
Physical Findings:
 Epigastric tenderness
 In severe cases: signs of shock: tachycardia, hypotension, cold, clammy extremities,
confusional state
 Tachypnoea
 Severe cases may have Grey Turner sign (bluish discolouration of the flanks) and Cullen sign
(bluish discolouration of the periumbilical area) caused by the retroperitoneal leak of blood
from haemorrhagic pancreatitis
Aetiology
 I- Idiopathic
 G- Gall stone
 E- ERCP
 T- Trauma
 S- Surgery
 M- Mumps/Malignancy
 A- Autoimmune
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 S- Scorpion bite/Snake venom
 H- Hyperlipidaemia/Hypercalcaemia
 E- Ethanol (Alcohol)
 D- Drugs eg frusemide, steroids, H2 blockers
Diagnosis
Clinical signs and symptoms:
 As described above
Biochemicals:
 Serum amylase or lipase levels >3 times the upper limit of normal are diagnostic
 Urine diastase (urine amylase) if symptoms have been present for more than 3 days
Imaging:
 Radiological facilities should be available to permit ultrasound examination of the gall

bladder within 24 hours of diagnosis of acute pancreatitis. It may reveal oedematous
pancreas with peripancreatic fluid, but most of the time pancreas is obscured by the bowel
gases.
 CT scan abdomen may give a better view but is not usually required for diagnosis of acute
pancreatitis. However, patients with persisting organ failure, signs of sepsis, or deterioration
in clinical status 6-10 days after admission will require CT (Grade B recommendation).
CT Severity Index (Balthazar Score) for Acute Pancreatitis
Grade Description
Grade A Normal pancreas
Grade B Focal or diffuse glandular enlargement
Grade C Inflammation involving pancreas and peri-
pancreatic fat
Grade D Single fluid collection or phlegmon
Grade E Two or more fluid collection or the presence of
gas in or nearby the pancreas
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Severity Grading
 Scoring system used commonly: Ranson’s criteria, Modified Glasgow-Imrie criteria, APACHE-
3 (Acute Physiological and Chronic Health Evaluation) scoring system
Ranson’s criteria
 Score at admission and at 48 hours later

 Each criterion given 1 point
 Presence of ≥3 points indicate severe pancreatitis
Criteria at admission (GALAW):
 G: Glucose >11.1 mmol/l

 A: Age >55 years old
 L: LDH >350 iu/l
 A: AST >250 iu/l
 W: WBC >16
Criteria after 48 hours (CHOBBS):
 C: Serum Calcium <2.0 mmol/l

 H: Haematocrit decrease >10%
 O: PaO2 <60 mmHg
 B: Blood urea increase >1.8 mmol/l
 B: Base deficit >4mmol/l
 S: Sequestration of fluid >6 L
Modified Glasgow-Imrie Score
 Scoring is done within 48 hours of admission

 Score ≥3 indicates severity
Abbreviated as PANCREAS:
 P: PaO2 <60 mmHg

 A: Age >55 years old
 N: Neutrophils/WCC >15
 C: Serum Calcium <2.0 mmol/l
 R: RBS >10 mmol/l
 E: Elevated LDH >600 IU/l
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 A: Albumin <32 g/l
 S: Serum urea >16 mmol/l
For APACHE-3 score, score of ≥8 indicates severe pancreatitis.
Management of Acute Pancreatitis
 Management is mainly supportive

 Patients with severe pancreatitis is recommended to be managed in the ICU/HDW setting
 The evidence to enable a recommendation about antibiotic prophylaxis against infection of
pancreatic necrosis is conflicting and difficult to interpret. Some trials show benefit, others do
not. At present there is no consensus on this issue.
 The evidence is not conclusive to support the use of enteral nutrition in all patients with
severe acute pancreatitis. However, if nutritional support is required, the enteral route should
be used if that can be tolerated (Grade A).
 The NGT route for feeding can be used as it appears to be effective in 80% of cases (Grade
B).
 Urgent ERCP should be performed in patients with acute pancreatitis of suspected or proven
gall stone aetiology (or cholangitis, jaundice, dilated CBD present). It is best carried out
within 72 hours.
Complications of Acute Pancreatitis
 Systemic complications: organ failure (respiratory, cardiovascular or renal).

 Local complications: acute peripancreatic fluid collection, pancreatic pseudocyst, acute
necrotic collection, walled-off necrosis, gastric outlet obstruction, splenic or portal vein
thrombosis, colonic necrosis.
Prognosis
 Prognosis based on Ranson’s criteria
Score Mortality (%)

<2 1
3-4 15
5-6 40
>7 100
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HEPATOBILIARY
Necrotizing Pancreatitis
Definition
 Refers to a severe form of acute pancreatitis

 Presence of focal or diffuse pancreatic glandular necrosis
 Associated peri-pancreatic necrosis
 Diagnosis is based on contrast enhanced computed tomography (CECT)
Introduction
 Pancreatic necrosis may be sterile or infected

 The mortality can be as high as 30%
 Death occurs in 2 phases:
o Early (within 2 weeks): due to multi organ failure (MOF)
o Late (after 2 weeks): due to sepsis
History:
 Epigastric pain radiating through to the back

 Associated with nausea, vomiting and fever
 May have a history of recent surgery or procedure (e.g. ERCP)
 May have family of hyperlipidaemia
 There may be previous biliary colic or a binge of alcohol
Physical Findings:
 Fever
 Signs of shock: tachycardia, hypotension, cold, clammy extremities, confusional state
 Tachypnoea
 Abdominal tenderness, distension, guarding and rigidity with diminished or absent bowel
sounds
Norly Salleh Page 9

 Jaundice may be present
 Diminished air entry to lung bases (effusion) on auscultation
 Muscular spasms in the extremities secondary to hypocalcaemia
 Severe cases may have Grey Turner sign (bluish discolouration of the flanks) and Cullen sign
(bluish discolouration of the periumbilical area) caused by the retroperitoneal leak of blood
from haemorrhagic pancreatitis
Management
Diagnosis
Clinical signs and symptoms:
 As described above
Biochemicals:
 Serum amylase or lipase levels >3 times the upper limit of normal are diagnostic
 Urine diastase (urine amylase)
Imaging:
 CT findings: pancreatic oedema, pancreatic necrosis or peri-pancreatic fluid collection

 CECT is the gold standard for the diagnosis of pancreatic necrosis; with an accuracy of >90%
when there is >30% glandular necrosis
CT Severity Index (Balthazar Score) for Acute Pancreatitis
Grade Description
Grade A Normal pancreas
Grade B Focal or diffuse glandular enlargement
Grade C Inflammation involving pancreas and peri-
pancreatic fat
Grade D Single fluid collection or phlegmon
Grade E Two or more fluid collection or the presence of
gas in or nearby the pancreas
Norly Salleh Page 10

Degree of Pancreatic Necrosis (Balthazar Necrosis Score)
Points Description Morbidity (%)

0 points No necrosis 0
2 points Up to 30% necrosis 48
4 points Up to 50% necrosis 75
6 points >50% necrosis 100
Principle of Management
ICU/HDW Care
 All patients with necrotizing pancreatitis need either ICU or HDW care
Supportive Care
 NBM
 NGT: free flow and 4 hourly aspirate
 Pain relief: IV narcotic or epidural
 Fluid resuscitation: use crystalloids or colloids based on CVP or Swan Ganz catheter reading
 Electrolytes correction and replacement
 Proton Pump Inhibitor to prevent stress ulcer
Antibiotics
 Antibiotic prophylaxis for severe acute pancreatitis remains controversial

 The use of antibiotics should be guided by the culture and sensitivity testing
Role of ERCP
 Screening for gallstone causing the pancreatitis can be done by US, CT or MRI/MRCP
 ERCP must be used judiciously in gallstone-related necrotizing pancreatitis
 Should be reserved for patients with biliary obstruction only
 Suspicion is based on raised bilirubin, raised ALP, cholangitis and jaundice
 Sphincterotomy and removal of stones/sludge may be necessary

Nutritional Support
 Preferably enteral feeding via nasojejunal tubing placed beyond the DJ flexure (provided
there is no significant ileus)
 TPN should be avoided because of metabolic and septic complications
Laboratory Monitoring
 FBC, ABG, Renal Profile, Septic Workup need to be done as required
Recognition of Infected Pancreatic Necrosis
 Based on CT- or US-guided FNA for microbiological screening and culture
Debridement of Infected Pancreatic Necrosis
 Operative debridement/necrosectomy is the standard of care and should be undertaken soon

after the confirmation of presence of infected necrosis or the presence of gas bubbles on
imaging
 4 main approaches of surgical debridement:
Conventional Management
o Necrosectomy, drainage, placement of standard surgical drains and reoperation as

required (based on fever, leucocytosis, lack of improvement on imaging studies)
Open or Semi-Open Management
o Necrosectomy with scheduled repeated laparotomies or open packing (abdominal

wound access maintained with zipper for frequent changes of dressing)
Closed Management
o Necrosectomy with extensive intra-operative lavage of pancreatic bed.

o The abdomen is closed with large bore drains for continuous postoperative lavage of
the lesser sac
Minimally Invasive Management
o Necrosectomy through small incision in the left flank/abdomen with or without

laparoscopy
o Also known as minimal access retroperitoneal pancreatic necrosectomy (MARPN)

Percutaneous Drainage/Irrigation
 Large bore catheters are placed into the pancreatic necrosis/lesser sac under radiological
guidance for aggressive irrigation and drainage
Endoscopic Drainage
 Via transgastric or transduodenal catheters

 Nasopancreatic irrigation tubes can be endoscopically placed into the peritoneum for
continuous irrigation
Complication
 Splenic artery pseudoaneurysm

 Haemorrhage from erosion into splenic artery/vein
 Thrombosis of the splenic vein/SMV/portal vein
 Duodenal obstruction
 Pancreatic/bowel fistula
 Stricture/fibrosis in distal bile duct
Conclusion
 Necrotizing pancreatitis is fatal if not managed appropriately and adequately

 Despite the various interventions, morbidity and mortality are significant

HEPATOBILIARY
Chronic Pancreatitis
Definition
 A continuous, prolonged inflammatory process of the pancreas with irreversible morphological

changes of fibrosis and stricture formation (irreversible destruction of pancreas parenchyma
and ductal architecture), resulting in pancreatic exocrine and endocrine insufficiency
(pancreatic failure)
Pathophysiology
 Most patients have previous attacks of acute pancreatitis resulting in inflammatory change
and fibrosis
 4 theories of pancreatic parenchymal destruction:
o Toxic-metabolic: direct effect of alcohol and poor nutrition
o Oxidative stress: high hepatic detoxification enzymes lead to generation of free
radical oxident by-products. This leads to pancreatic damage
o Ductal obstruction and stone formation: an increase in protein secretion with
abnormal form s of protein, combined with an increase in ductal permeability to
calcium, resulting in formation of ‘protein plugs’ and intra-ductal deposition of calcium
o Necrosis-fibrosis: the characteristic fibrosis evolves from the recurrent cycles of
inflammation and necrosis seen after the attacks of acute pancreatitis
 Most likely the pathogenesis is a combination of all the factors
Pathophysiology of Severe Pain in Chronic Pancreatitis
 Increased pressure in the main pancreatic duct

 Parenchymal oedema causing compartment syndrome
 The neuronal inflammatory mediator hypothesis
o Inflammatory mediators are responsible for increased signals along the axons of
pain-sensitive neurons
Incidence
 Male > Female

 Age of onset 35-55 years old
Aetiology
 Main causes (90%): alcohol, idiopathic

 Less common causes (10%):
o Gallstones
o Tropical
o Hypercalcaemia
o Hyperlipidaemia
o Pancreatic tumour
o Pancreatic divisum
o Hereditary pancreatitis
Clinical Feature
History
Abdominal Pain
 Deep, boring epigastric pain, radiates to the back, relieved by sitting upright or ‘jack-knife’
position, pain aggravated by food
Pancreatic Insufficiency
 Steatorrhoea
 Diabetes
 Deficiency of protein and fat
 Thiamine deficiency ± Wernicke’s encephalopathy
Clinical Examination
 Weight loss, malnutrition, anaemic, jaundice, ascites, may have splenomegaly, stigmata of
liver disease
 Chronic pancreatitis predisposes to pancreatic cancer
Differential Diagnosis
 Pancreatic cancer
 Upper GI cancer
 Cholelithiasis

 Irritable bowel syndrome
 Peptic ulceration
 Mesenteric vascular disease
Diagnosis and Investigations
Laboratory Tests
Blood Tests
 Generally unhelpful
 Serum amylase, lipase are usually normal
 LFT may be deranged
 FBC: thrombocytopenia may suggest splenic vein thrombosis
Urine Tests: glucose (TRO DM)
Genetic Sequencing with appropriate counselling for hereditary pancreatitis
Pancreatic Exocrine Function Tests
 Faecal elastase, fat

 Do not differentiate from pancreatic cancer
Imaging
Plain abdominal x-ray: may show pancreatic calcification
U/S abdomen: may show enlargement of pancreas, duct dilatation, pseudocyst, pancreatic stones
CECT:
 Principal investigation
 May show pancreatic atrophy, calcification, main pancreatic duct dilatation, fluid collection
MRCP: secretion stimulation may give functional information
ERCP: used for intervention (stone removal, stricture dilatation, stent insertion)
EUS: investigation of choice ± FNAC
Histology:

 Is the ‘gold standard’ in diagnosis
 There is irregular fibrosis with destruction and loss of exocrine parenchyma
Treatment
Pain
 Opiate analgesia
 Bowel rest and supplement nutrition
 Consider coeliac plexus block
 Consider thoracoscopic splanchnicectomy
Exocrine failure
 Deficiencies in fat, protein, vitamin

 Give pancreatic enzyme supplements e.g. Creon
Endocrine failure
 Needs insulin
 Hypoglycaemia occurs more as a result due to lack of endogenous glucagon
 Higher glucose value should be accepted to avoid hypoglycaemia
Pseudocysts
 Peri-pancreatic fluid collection s that have been present for > 4 weeks
 Can become infected or cause local effect such as biliary obstruction, duodenal obstruction,
gastric compression, pain
 Drainage must be done of any of these features are detected
 Internal drainage is preferable (percutaneous drainage risks of external pancreatic fistula or
infection)
 Endoscopic cyst-gastrostomy, laparoscopic cyst-gastrostomy
 Open surgery: cyst-gastrostomy or cyst-jejunostomy
Biliary Obstruction
 May be due to pseudocyst or pancreatic parenchymal fibrosis affecting the lower CBD
 ERCP + stenting to relieve jaundice in short term
 May need choledochoduodenostomy or choledochojejunostomy
Endoscopic Management of Pancreatic Duct

 Pancreatic ductal stricture can be dilated and stones removed
 Ideally combined with ESWL
Psychological Support
 Especially in alcohol addiction
Open Surgery
 For patients with complications

 Severe intractable pain
 Endoscopically unmanageable pancreatic pseudocysts with ductal pathology
 Internal pancreatic fistulas and pancreatogenic ascites
 Exclusion of cancer despite extensive work up
Type of Operations
 Can be drainage procedure or resection procedure

 Large duct disease (>6mm): drainage procedure
 Small duct disease (<6mm): pancreatic resection
 Types of operation:
o Whipple’s procedure (pancreaticoduodenectomy)
o Beger’s procedure (duodenum preserving pancreatic head resection)
o Frey procedure: lateral pancreatico-jejunostomy with resection of pancreatic head
tissue
o Puestow procedure: lateral pancreatico-jejunostomy
Complications of Chronic Pancreatitis
 Intractable pain
 Pancreatic insufficiency
 Pseudocyst
 Duodenal stenosis, colonic stricture
 Haemorrhage
 Pancreatic cancer
 Pancreatic ascites
 Portal hypertension
 Inflammatory mass at the head of pancreas
 Biliary obstruction
 Pancreatic ductal stricture and stones

HEPATOBILIARY
Acute Calculus Cholecystitis
Introduction
 Acute inflammation of the GB in the presence of cholelithiasis

 Risk factors: female, increasing age, pregnancy, OCP, DM
Pathophysiology
 Occurs most commonly due to blockage of the cystic duct with gall stones
 The blockage causes a buildup of the bile in the gallbladder and increased pressure within the
gallbladder, leading to RUQ pain
 Concentrated bile, pressure and sometimes bacterial infection irritate and damage the
gallbladder wall, causing inflammation and swelling of the gallbladder
 Inflammation and swelling of the gallbladder can reduce normal blood flow to areas of the
gallbladder, which can lead to cell death due to inadequate oxygenation
Clinical features
 The most frequent signs and symptoms are right upper quadrant abdominal pain, nausea,
vomiting, fever, abdominal mass and jaundice
Classifications of cholecystitis
 Acute calculus cholecystitis

 Acute acalculous cholecystitis
 Chronic cholecystitis
 Xanthogranulomatous cholecystitis: may mimic GB cancer
Investigations
Laboratory
 FBC count, liver function tests, and blood culture tests are some of the main laboratory tests
that should be performed

Radiological Examination
 Ultrasound findings suggestive of aacute cholecystitis include gallstones, fluid surround the
gallbladder, gallbladder wall thickening, dilation of the bile duct and sonographic Murphy’s
sign
 CT scan may also be used if complications such as perforation or gangrene are suspected
Management
 Definitive treatment is cholecystectomy. The gold standard is laparoscopic cholecystectomy.

Studies showed that outcomes were better following early removal of the gallbladder,
preferably within the first week.
 For early cholecystectomy, the most common reason for conversion to open surgery is
inflammation obscuring Calot’s triangle. For delayed surgery (after 6 weeks), the most
common reason was fibrotic adhesions.
 Supportive measures are instituted prior to surgery which include fluid resuscitation and
antibiotics targeting enteric organism such as E. Coli and Bacteroides
 Parenteral narcotics can be used for pain control
 In severe cases where patient did not respond to supportive measures but is at high risk for
general anaesthesia, a percutaneous drainage catheter may be inserted into the gallbladder
(percutaneous cholecustostomy tube) by an interventional radiologist. A cholecystectomy
may be warranted if the patient’s condition improves.
Complications
 Gangrene
 Gallbladder rupture
 Empyema
 Fistula formation and gallstone ileus
 Rokitansky-Aschoff sinuses

HEPATOBILIARY
Acute Acalculous Cholecystitis
Introduction
 Inflammation of the GB in the absence of cholelithiasis

 It is uncommon but a very serious disease
 Can occur in persons of any age
 Most commonly observed in the setting of very ill patients
 Occurs in 5-10% of all cases of acute cholecystitis
 In comparison to acute calculous cholecystitis, acute acalculous cholecystitis is associated
with:
o Higher rates of morbidity and mortality
o More common in male
o Higher incidence of gangrene and perforation
Aetiology
 The aetiology of the disease remains obscure and a number of factors have been implicated
 Mainly these can be divided into following groups:
o Depressed motility and starvation: surgery, burns, more than three months of total
parenteral nutrition, mechanical ventilation and trauma
o Decreased blood flow through cystic artery: arteriosclerosis, congestive cardiac
failure, diabetes, shock
o Infection (sepsis)/immunocompromised: AIDS (late manifestation), Candida, cholera,
salmonella, campylobacter
o Obstruction of cystic duct by extrinsic inflammation: lymphadenopathy, metastasis
Pathophysiology
 The precise mechanism is unknown

 The more commonly postulated theories regarding its pathogenesis are bile stasis, sepsis
and ischaemia
 Critically ill patients are more predisposed because of:
o Increased bile viscosity due to fever and dehydration

o Prolonged absence of oral feeding resulting in a decrease or absence of
cholecystokinin-induced gall bladder contraction
Clinical features
 Clinical examination is often not helpful, as many patients are receiving mechanical ventilation
and have decreased mental awareness
 The most frequent signs and symptoms are right upper quadrant abdominal pain, nausea,
vomiting, fever, abdominal mass and jaundice
Investigations
Laboratory
 Biochemical markers are nonspecific

 FBC count, liver function tests, and blood culture tests are some of the main laboratory tests
that should be performed
 Bile culture is negative in 50% of the time due to concurrent antibiotic therapy in these
patients
Radiological Examination
 Ultrasonography and CT abdomen are over 90% specific and sensitive for diagnosing acute
acalculous cholecystitis, while cholescintigraphy is highly sensitive but only 38% specific
 Diagnostic criteria for acute acalculous cholecystitis in CT and US:
o Gall bladder wall thickness greater than or equal to 4 mm
o Pericholecystic fluid
o Subserosal oedema without ascites
o Intramural gas
o Sloughed mucosal membrane
o The sonographic Murphy's sign is strongly positive
o No stones or biliary sludge are visible in the gall bladder
 The colour flow Doppler study demonstrates abnormal and increased arterial blood flow to the
wall of the gall bladder fundus consistent with acute inflammation
 Hepato-biliary scintigraphy with Tc99m-IDA shows non-visualization of the gall bladder with
prompt excretion of radio-pharmaceutical via the common duct into the duodenum.

Treatment
 Best treatment varies, depending on underlying disease and the patient's condition
 When the diagnosis of acalculous cholecystitis is established, options range from conservative
medical therapy to immediate surgical intervention because of the high risk of rapid deterioration
and gallbladder perforation
Percutaneous Transhepatic Cholecystostomy
 Percutaneous transhepatic cholecystostomy is indicated using a pigtail catheter successfully

placed under ultrasonographic and fluoroscopic guidance, particularly in the ill, elderly, or high
risk patients, since he or she is spared open surgery both for diagnosis and treatment
 Percutaneous cholecystostomy is a safe, effective and usually definitive procedure for the
treatment of acute acalculous cholecystitis
Open or Laparoscopic Cholecystectomy
 The historical treatment of choice for acute acalculous cholecystitis has been
cholecystectomy.
 But percutaneous cholecystostomy is now the mainstay of therapy, controlling the disease in
about 85% of patients
 Interval cholecystectomy is usually not indicated after acute acalculous cholecystitis in
survivors if the absence of gallstones is confirmed and the precipitating disorder has been
controlled
Complications
 GB perforation
 Gangrene
 Extrabiliary abscess formation
Mortality
 Acute acalculous cholecystitis: 10-50%

 Acute calculous cholecystitis: 1%

Conclusion
 Acute acalculous cholecystitis is a virulent disease of uncertain aetiology observed most

commonly in critically ill patients
 Early diagnosis is essential to avoid the high rates of associated morbidity and mortality
 The diagnosis is usually made by radiological tests, most often by ultrasonographic
examination of the gall bladder
 Depending on the clinical situation, the gall bladder should either be drained by a surgical or
percutaneous cholecystostomy under local anaesthesia or removed

HEPATOBILIARY
Common Bile Duct Stone
Introduction
 Gall bladder stone is present in 15% of the population (US). The majority of patients are
asymptomatic.
 Common bile duct stone can arise de novo in the bile duct (primary CBD stone), but the
majority is due to migration of stone from the GB (secondary CBD stone).
 Primary stones are more common in south-east Asian populations, have a different
composition to secondary stones, and may be a consequence of biliary infection and stasis
Symptoms
 Sometimes asymptomatic
 When ductal stones do become symptomatic the consequences are often serious and can
include pain, partial or complete biliary obstruction, cholangitis, hepatic abscesses or
pancreatitis.
 Chronic obstruction may also cause secondary biliary cirrhosis and portal hypertension
Diagnosis
 Trans-abdominal ultrasound scanning (USS) is recommended as a preliminary investigation

for CBD stone and can help identify patients who have a high likelihood of ductal stones.
 EUS and MRI are both recommended as being highly effective for confirming the presence of
CBD stone
 When selecting between the two modalities, patient suitability, accessibility and local
expertise are the most important considerations
 Intraoperative cholangiography (IOC) and ERCP are generally considered to be the reference
standards for diagnosis of CBD stone
Management
 Management of CBD stone depends whether the stone is identified pre-operatively, intra-
operatively of post-operatively

Pre-operative Identification of CBD stone
 Management is pre-operative ERCP ± Endoscopic Sphincterotomy (ES)
 If stone is cleared → for laparoscopic cholecystectomy
 If stone remains → 2 choices:
o 1st: Open cholecystectomy + CBD exploration
o 2nd: Laparoscopic Cholecystectomy + Laparoscopic CBD exploration
Intra-operative Identification of CBD stone

 Laparascopic cholecystectomy and laparoscopic CBD exploration
 Laparoscopic Cholecystectomy followed by post-operative ERCP ±ES
 Laparoscopic cholecystectomy converted to open CBD exploration
Post-operative Identification of CBD stone

 ERCP ± ES
Approach to CBD Exploration

 Transcystic or transcholedochal approach
Methods of Clearing CBD Stone

 Irrigation technique
o Give glucagon to relieve the sphincter pressure and then flush with NS or contrast
 Balloon Technique
o Balloon sweep alone, or
o Balloon + choledochoscopy technique
 Basket Technique
 Choledochosope alone technique
 Lithotripsy (electrohydrolic or laser lithotripsy)
 Intra-operative laparoscopic antegrade sphincterotomy
 Surgical Biliary Bypass
 Laparoscopic cholecysto-enterostomy
 Laparoscopic choledocho-duodenostomy
 Laparoscopic choledocho-enterostomy

HEPATOBILIARY
Indications for Open Cholecystectomy
 Laparoscopic Cholecystectomy converted to open due to:

o Unable to identify anatomy
o Dense adhesions, inflammations
o Haemorrhage
o CBD injury
o Other organs injury
 GB cancer
 Cirrhotic patient
 CBD stone
 Large stone
 No expert in doing laparoscopic CBD exploration
 Comorbid: multiple laparotomies or severe COAD
 3rd trimester pregnancy
 As part of another operation e.g. Splenectomy + cholecystectomy in blood disorder patients
 Trauma to GB

HEPATOBILIARY
Adenomyomatosis of Gall Bladder
Introduction
 Acquired, benign, no malignant potential
 Hyperplastic changes of unknown origin
 Involves the GB wall
 Causing: overgrowth of the mucosa, thickening of the muscular wall, formation if intramural
diverticulae of sinus tracts termed Rokitansky-Aschoff Sinuses
 Tumour-like lesion of the GB
 May involve GB in focal, segmental or diffuse manner
 Female to male ratio is 3:1
 Adenomyomatosis is not cholesterolosis. But they are sometimes difficult to differentiate on
ultrasound
Investigations
 Ultrasound: comet-tail artifact (echogenic intramural foci from which emenate v-shaped comet
tail reverberation artifacts are highly specific for adenomayomatosis)
 CT scan of adenomyomatosis reveal a thickened GB wall with the rosary sign
 GB carcinoma
 Cholesterolosis
Management
 Usually requires no treatment
 Usually asymptomatic
 But may be associated with gall stone, biliary inflammation, cholesterolosis
 Cholecystectomy is performed if:
o Symptomatic of biliary colic
o If difficult to distinguish from malignancy

HEPATOBILIARY
Liver Abscess
Introduction
 Liver abscess is a condition with high mortality and morbidity if left untreated
 It usually occur in immunocompromised patients in age >50 years old, but it can also occur in
patients of any age
Aetiology
 Pyogenic (80%)
 Amoebic (10%)
 Others: fungal, TB (10%)
Pyogenic Liver Abscess
Organisms
 Aerobes
o Gram positive: staphylococcus, streptococcus, enterococcus
o Gram negative: E. coli, Klebsiella, B. pseudomallei
 Anaerobes: bacteroides, enterobacter, clostridium
 Most commonly it is due to mixed organisms
Sources of Infection
 Biliary tree: resulting from ascending cholangitis

 Arterial: as part of a general septicaemia
 Portal: from an area of suppuration drained by portal vein e.g. appendicitis, diverticulitis
 Direct spread: from adjacent infection such as subphrenic abscess or acute cholecystitis
 Trauma: followed by secondary haemorrhage and added infection
Clinical Features
 High grade swinging fever

 Chills and rigors
 RHC pain
 Mildly jaundice
 Malaise, anorexia
Risk Factors
 Immunocompromised: RVD positive, IVDU, on chemo

 DM
 Instrumentation e.g. ERCP, biliary stenting
 For melioidosis: farmers, people in contact with soil
On Examination
 Patient looks septic, unwell

 May be dehydrated, mildly jaundice
 RHC tenderness may be present
 Right intercostal tenderness may be present
 May have hepatomegaly
Amoebic Liver Abscess
Organism: entamoeba histolytica (a protozoan)
Pathophysiology
 Faecal-oral route of infection

 Cyst of E. histolytica enters the colon
 Trophozoite is released and then invaded the colonic mucosa
 It enters the portal system into the liver
 Causes liver abscess
Risk Factors
 Poor sanitation, poor hygiene, endemic area
Clinical Features
 Diarrhea, fever, less septic looking if compared to pyogenic liver abscess, younger patient,
jaundice is rare, shorter duration of illness, abdominal pain is more pronounced

Fungal Liver Abscess
Organism: usually candida spp
Risk: prolonged antibiotics usage, prolonged hospitalization, diabetes mellitus
Clinical Features: fever, RHC pain, malaise, anorexia
Investigations for Liver Abscess
Biochemical
 FBC: raised TWC

 RP: raised urea (dehydration), deranged electrolytes (diarrhea in amoebic abscess)
 LFT: may have deranged liver enzymes
 Blood C&S
 Pus C&S: pus in amoebic liver abscess looks like anchovy sauce
 IgM entamoeba histolytica: to rule out amoebic
Imaging
 Ultrasound
o Is usually diagnostic
o To determine the size, site, maturity of the abscess
o To determine the complexity of the abscess (single, multiple, septated, multiloculated)
o Abscess looks hypoechoic and homogenous on ultrasound
o Single abscess is usually amoeba, multiple and small abscesses are usually
secondary to pyogenic causes
 CT scan with iv contrast of the HBS
o May also be useful
o Indications: Complex/septated/multiple/large abscesses, TRO cancer of the liver,
serial ultrasound showed immature abscess, to look for sources and the presence of
other abscesses elsewhere
o CT findings: hypodense lesion with peripheral enhancement
 CXR
o Elevation of right hemidiaphgram
o Right pleural effusion
o Basal pulmonary collapse
o Fluid level below the diaphragm
Treatment

Pyogenic liver abscess
 Resuscitation: correct dehydration, electrolytes imbalance

 IV antibiotics: broad spectrum, empirical to cover anaerobes and aerobes for example iv
cefoperazone 2 g bd and iv metronidazole 500 mg tds for 2 weeks, followed by oral antibiotics
for another 4 weeks (depending on clinical findings and culture results)
 If size of abscesses <3 cm: need antibiotics only
 If size >3 cm: more likely need drainage procedure too
 Drainage of liver abscess can be done percutaneously or open surgically
 Percutaneous drainage is done for single abscess; site not too near major vessels; anterior
abscess
 Abscess can be aspirated or a pigtail catheter can be left in situ
 If needed be, irrigation (under aseptic technique) can be done via the pigtail
 Open surgical drainage is indicated in failed percutaneous drainage, ruptured abscess,
complex abscess, abscess not amenable to percutaneous drainage (near major vessels etc),
giant abscess unlikely to be able to be drained completely by percutaneous method
 Open drainage can be done transperitoneally or extra-peritoneally
 Extra-peritoneal drainage can be done via subcostal incision (for anterior abscess) or via
transpelural approach
 Laparoscopic surgical drainage: for experts only
Amoebic liver abscess
 Resuscitation
 Iv metronidazole 500 mg tds for 7-10 days
 Needle aspiration is done if size >5 cm, unsure of diagnosis, no response to medical
treatment, left sided abscess
 Open surgery is indicated in ruptured abscess
 Amoebic liver abscess may ruptured into the bronchus, ventricle or diaphragm
Fungal liver abscess
 First line treatment is iv fluconazole for 2 weeks

 If not responding, iv amphotericin B
Meiloidosis
 Iv fortum 2 g bd for 2 weeks, then oral bactrim for 4 weeks

 Some authors advocated 20 weeks of oral treatment

Conclusion
 Liver abscess is a condition that needs urgent and prompt management to reduce mortality
and morbidity’
 However in 1/3 of cases, the cause of the abscess is unknown

Management of Solitary Thyroid Nodule
Introduction
 Solitary thyroid nodule occur in 4-7%

 It is usually benign
 It may be associated with goiter (dominant nodule within a multinodular goiter) or in the
presence of a normal gland
History
 Most-likely malignant if:

o In the very young or the very old
o Previous exposure to radiation
o Family history of thyroid malignancy
o Rapid nodule growth
o Pain
o Change of voice
o Compressive symptoms
Physical findings
 Likely to be malignant if firm, irregular surface, fixation to surrounding structures, presence of

enlarged lymph nodes
*Malignancy is unusual in the hyper-functioning thyroid nodule
Investigations
Blood tests: TFT, calcium/albumin, thyroid auto antibody
FNAC:
 Inexpensive, easy
 Results can be: inadequate, benign, malignant, indeterminate

 Adequate sample means: has at least 10 groups of cells with 10 cells per group, obtained
from 2 separated needle passes
 In 20% of cases, inadequate FNA
 If inadequate repeat
 If persistently inadequate, need to manage based on clinical criteria
Ultrasonography:
 May differentiate solid from cystic nodules, show solid components in a cystic nodule, identify
multinodularity, identify associated lymphadenopathy
 Cannot reliably distinguish between benign and malignant lesions
Radionuclide scan:
 Unable to distinguish benign from malignancy

 Only indicated in a patient with a nodule who is thyrotoxic and is considered for surgery
CT/MRI/CXR:
 These are indicated in patients with retrosternal goiter, for assessment of tracheal narrowing
or deviation or, as part of preoperative assessment according to local protocols
Other tests:
 Pulmonary function tests may assist in the assessment of patient with clinical evidence of
airway embarrassment
 Laryngoscopy: this is indicated where the patient has a history of voice change, previous
thyroid surgery or is to be operated on for thyroid malignancy
Indications for surgery in nodular disease
 Cytological features of papillary or medullary cancer of a follicular lesion (adenoma or

carcinoma)
clinical suspicion of malignancy
 Pressure signs or symptoms
 Patient preference: cosmesis/anxiety
 Toxicity
 Progressive enlargement in a retrosternal goiter
 Discomfort in a goiter or associated with its presence

Lymphoedema in Breast Cancer
Definition
 An abnormal collection of lymph in soft tissue (interstitial space)

 There is no cure for lymphoedema
 We can only try to control it
Types of Lymphoedema
 Primary/congenital
 Secondary
o Obstruction
 Infection (filariasis)
 Fibrosis (post radiotherapy)
 Tumour (malignancy e.g. prostate, breast, lymphoma)
o Disruption
 Post trauma
 Post operative (axillary clearance, dissection)
Prophylaxis against Lymphoedema
 Axillary dissection (level 1 and/or 2) vs. axillary clearance (level 1, 2 and 3)

 Sentinel lymph node biopsy vs. axillary dissection
 Surgery or radiotherapy; not both
 Surgery before locally too advanced
Life Long Precaution Post Axillary Dissection/Clearance
 Skin care
o Avoid fluid infusion
o Avoid possible contaminated injuries (e.g. gardening)
 Avoid excessive physical exertion

‘Treatment’ of Lymphoedema
 Moderate exercise
 Massage
o Manual
o Segmental air compression device
o Lympha-press
 Compression garment
 Elevation
 Medication
o Diuretics
o Lymphatic flow stimulant (Daflon)
 Diet (low in sodium e.g. < 2g/day)
Complications of Lymphoedema
 Recurrent cellulitis/lymphagitis
 Cosmesis (thickening/hyperkeratosis/hyperpigmentation)
 Impaired function (heavy & clumpsy)
 Malignancy (lymphangiosarcoma)

Diagnostic Modalities in Diagnosing Breast Cancer
Introduction
 Breast cancer is the most common malignancy to affect woman
Risk factors for developing breast cancer
 Age (increasing risk with increasing age)

 Early menarche (<12 yrs)
 Late menopause (>55 yrs)
 Nulliparous or first child born at > 30 years
 Not breast feeding
 HRT (mainly combined HRT)
 OCP (less risk if stopped after 10 years)
 Family history: account for 10% of breast ca. Two genes involved BRCA 1 and BRCA 2
o BRCA 1 : associated with breast ca, ovarian ca, colon and prostate ca
o BRCA 2 : associated with breast ca, ovarian ca and male breast cancer
 History of radiation to the chest
 Obesity
Modalities to diagnose breast cancer
1. History and Physical Examination

2. Radiology
3. Pathology
Also called as Triple Assessment
History
 Painless lump
 Distorted and asymmetrical breast

- Dimpling/puckering of the skin
- Nipples : discharge, distorted, inverted, destructed
 Axilla mass
 Breast discomfort (rare)
 Symptoms of metastases : lymphoedema, bone pain, SOB, jaundice
Physical Examination
 Palpable lump
 Skin abnormalities
- Tethering (due to Coopers ligament infiltration)

- Direct extend to the skin ( Peau d’orange, ulceration, satellite nodules)
 Nipples abnormalities
 Palpable axillary LN
 Evidence of the metastases
Radiological assessment
Mammography
 Have sensitivity up to 90% in women over the age of 50 years old

 10% are mammographically occult particularly lobular cancers
 Routinely performed for women over the age of 35 years due to increase breast tissue density
 Two view MMG – cranio-caudal/mediolateral oblique
 Features in MMG suggestive of malignancy
 Present of microcalcification – cluster, pleomorphism, spiculation

 Architectural distortion
 Present of mass
 The MMG report can be form of BI-RADS (Breast Imaging Reporting and Data System)-
includes the overall assessment of the likelihood of malignancy
 BI-RADS 0: need further evaluation

 BI-RADS 1: normal mammogram
 BI-RADS 2: benign finding
 BI-RADS 3: probable benign lesion
 BI-RADS 4: suspicious lesion
 BI-RADS 5: highly suggestive of malignancy
 BI-RADS 6: biopsy-proven malignancy
Ultrasound
 Routinely performed for women under the age of 35 yrs

 In addition it also allows accurate image-guided aspiration of breast lesions
 Features in USG suggestive of malignancy
 Mass that is taller than width

 Hypoechogenecity
 Presence of calcification
 Posterior acoustic shadowing
 Speculated contour
Magnetic resonance imaging
 At the current time, MRI is used primarily in selected settings, such as in the identification of
the primary carcinoma in women with breast carcinoma in an axillary node with a normal
mammogram and physical examination.
Pathological Assessment
Core biopsy
 Using trucut or vacuum-assisted mammotome under USG or MMG

 Provide wealth information about a breast lump
 Malignant or benign
 Invasive or in-situ
 Type of cancer
 Grade
 Hormonal status
 Disadvantages – invasive, may cause hematoma
FNAC
 Using 20 G or 23 G needle to obtain the cells and fixed on a glass slide

 Advantages : fast , easy and rapid result
 Disadvantages : high false-negative rate, only cellular interpretation

 Cytological interpretation:
 C1: insufficient or inadequate

 C2: benign/inflammatory
 C3: atypical/probably benign
 C4: suspicious lesion
 C5: malignant
Surgical open biopsy
 Can be excisional biopsy or incisional biopsy

 Indications
 Failure of triple assessment to confirm the breast lesion

 Impalpable mass – hooked wire localization by USG or stereotactic localization
by MMG

Chronic Granulomatous Mastitis (CGM)
Introduction
 Chronic granulomatous mastitis is a rare benign breast condition which is characterized by

granuloma and abscess formation
 It can mimic a breast carcinoma
Histologically
 Predominantly lobular inflammatory disease

 Multinucleated giant cells and epitheliod histiocytes are present around the breast lobules
 Other granulomatous inflammation such as tuberculosis, sarcoidosis, wegener’s

granulomatosis
Aetiology
 The cause is unknown

 Has been speculated to be due to an immune disease, an infectious agent or a local reaction
to chemical reaction
 A primary infectious agent seem unlikely as organism have never been confirmed
histologically or on culture
Clinical Features
 Age 17-42 years old

 Unilateral breast mass, firm, distinct, mostly in subareolar
 May have enlarged lymph node
 May have skin ulceration, nipple inversion, peau d’orange
 secondary infection is a problem and recurrent abscesses
 Requiring drainage is common
 The disease may become inactive after weeks to months
Predisposing Factors
 OCP
 Hyperprolactinaemia
Diagnosis
 From fine needle biopsy

 Clinical and mammogram features may mimic breast cancer
Management
 Anti-inflammatory drugs: prednisolone or methotrexate have been used with varying results
 Prednisolone dosage is as high as 60 mg/day for 3 weeks
 If a localized lesion can be excised with a good cosmetic result, then excision is the best
option
 Otherwise mastectomy is the last option
Conclusion
 CGM is a difficult condition to treat with a 50% recurrence rate

 It at be mistaken as breast carcinoma and fine needle biopsy or core biopsy is needed to
differentiate these two conditions

Advanced Breast Cancer
Introduction
 Advanced breast cancer refers to stage 3 (locally advanced breast cancer) and stage 4
(metastatic breast cancer)
Locally Advanced Breast Cancer
 Stage 3a, 3b, 3c

 With multimodality treatment utilizing a combination of chemotherapy, surgery, radiotherapy
and hormonal therapy, 5-year survival of about 50% possible with local control rates of 80%
 For operable stage 3, the choice is between chemotherapy first or surgery first
 For inoperable stage 3, chemotherapy is given first, and if the tumor remains inoperable after
3 cycles, treatment options are to change to another chemotherapy regime or radiotherapy for
local control
Neoadjuvant Chemotherapy
 Also known as induction chemotherapy. Primary systemic therapy (PST) or pre-operative

chemotherapy
 Response 60-80%, complete pathological response 10%
 No increase in post-operative complications
Advantages of Neoadjuvant Chemotherapy
 Allows assessment of chemosensitivity of the tumour

 Most studies have shown no difference in survival between surgery first or chemotherapy first,
BUT if complete response obtained, prognosis better
 Allows ‘inoperable’ tumour to become operable
 In large stage 2 tumours, may allow breast conservations surgery to become possible
Stage 4 Breast Cancer
 The aim of treatment is palliation of symptoms and prolongation of life

 Local treatment of the breast and axilla depends on the sites of metastasis and whether
symptomatic
 In asymptomatic metastasis or minimal bone metastasis, surgery should still be carried out for
local control and systemic therapy afterwards
in symptomatic metastasis, or where the patient’s quality of life is impaired, systemic treatment
becomes the priority and surgery is indicated for local problems like ulceration and bleeding – the
priority in this situation is palliation of symptoms

ZOMETA® (zoledronic acid)
Introduction
 ZOMETA® (zoledronic acid) 4 mg/5 ml injection is proven treatment that can help reduce and
delay bone complications caused by cancer that has spread to the bone
 ZOMETA® is approved to treat:
 Bone lesions from multiple myeloma, used with anti-cancer medications

 Bone complications from certain metastatic cancers that have spread to the bone –
including breast, lung, and prostate cancer
 Hypercalcaemia of malignancy
Mechanism of action
 Zoledronic acid slows done bone resorption, allowing the bone-forming cells tie to rebuild
normal bone and allowing bone remodeling
 In all cases administration is by intravenous infusion over a minimum of 15 minutes
Side effects
 Can include fatigue, anaemia, muscle aches, fever, swelling in the feet or legs, flu-like
symptoms
 Risk of severe renal impairment: appropriate hydration is important prior to administration.
Zoledronate is rapidly processed via the kidneys; consequently its administration is not
recommended for patietns with reduced renal function or kidney disease
 Rare complication: osteonecrosis of the jaw
Contraindications
 Poor renal function (e.g. creatinine clearance <30ml/min)

 Hypocalcaemia
 Pregnancy
 paralysis

UPPER GASTROINTESTINAL TRACT
Post Gastrectomy Complications
Introduction
 Post gastrectomy syndromes are caused by changes in gastric emptying as a consequence

of gastric operations
 They may occur in up to 20% of patients who undergo gastric surgery
 It depends on extent of resection, disruption of the vagus nerve, status of the pylorus, type of
reconstruction, and presence of mechanical or functional obstruction
 Complications arising post gastrectomy can be divided into early and late complications
Early complications are:
 Anastomotic leak
 Duodenal stump blow up/dehiscence
 Other general complications and complications related to general anaesthesia
Late complications
Nutritional disturbances
 Prolonged iron, folate, vitamin B12, calcium and vitamin D deficiencies can result in anaemia,
neuropathy, dementia and osteomalacia
 These can be prevented with supplementations
Dumping syndrome
 Dumping syndrome can be divided into early dumping and late dumping
Early dumping syndrome:
 Occurs within 30 minutes of eating

 Characterized by nausea, epigastric distress, explosive diarrhea, vasomotor symptoms
(palpitations, flushing, dizziness)
 Caused by rapid fluid shifts in response to the hyperosmolar intestinal load and release of
vasoactive peptides from the gut
 Symptoms are relieved by recumbence or saline infusion
Late dumping syndrome:
 Occurs several hours after eating

 Symptoms are primarily vasomotor: sweating, dizziness, palpitations
 The hormonal response to high simple carbohydrate loads results in hyperinsulinaemia and
reactive hypoglycaemia
 Symptoms are relieved by carbohydrate ingestion
Treatment:
 Mainly conservative
 Meals should be smaller in volume but increased in frequency
 Simple carbohydrate should be avoided
 Use of octreotide can result in relief in symptoms
 In persistent dumping, conversion to a roux-en-y gastrojejunostomy is usually successful
Roux syndrome
 Occur in patients with roux-en-y procedure

 A functional obstruction
 Characterized by chronic abdominal pain, nausea and vomiting
 Symptoms are of delayed gastric emptying
 Motility studies will show propulsive waves toward the stomach in the roux limb
 Treatment: prokinetic agent, acid suppression therapy, surgical treatment if needed (convert
subtotal to total gastrectomy; or resects dilated roux limb and reconstruct another roux limb)
Loop syndromes
 Due to mechanical obstruction

 Can be afferent or efferent loop syndrome
Afferent loop syndrome (ALS):
 May present with an acute, completely obstructed form or with a chronic, partially obstructed
form
 Causes of ALS:
o Kinking in the afferent limb at the gastrojejunostomy
o Entrapment or compression of the afferent loop by adhesions
o Recurrence of cancer at the anastomotic site
o Foreign body in the afferent limb or at the anastomosis

o Bezoars at the afferent limb or at the anastomosis
o Internal herniation
o Volvulus of the intestinal segment
o Presence of enteroliths
 The risk of developing ALS is higher if:
o The jejunal portion of the afferent limb is longer than 30-40 cm in length
o The gastrojejunostomy is placed in the antecolic position instead of the retrocolic
position
o Mesocolic defects are not properly closed after construction of a retrocolic
gastrojejunostomy
 Acute ALS is a surgical emergency
 Symptoms of acute ALS: sudden onset of epigastric pain and/or right or left upper quadrant,
nausea and vomiting (non-bilious), peritonitis and shock (if intestinal perforation or infarction
ensues)
 Symptoms of chronic ALS: abdominal fullness and/or epigastric pain 10-20 minutes post
prandial, projectile bilious vomiting, vomitus usually contains no food, blind loop syndrome
(steatorrhea, diarrhea, Vit B12, iron and folate deficiency due to bacterial overgrowth)
 Physical findings in ALS: an ill-defined mass in RUQ, localized mid epigastric or RUQ
tenderness, peritonitis if necrosis or perforation of bowel wall has occurred, jaundice,
pancreatitis
 The definitive treatment of ALS is reconstructive surgery
Efferent loop syndrome:
 Results from intermittent obstruction of the efferent limb of gastrojejunostomy

 Symptoms: abdominal pain, bilious vomiting
Post-vagotomy diarrhea
 Due to loss of autonomic control of intestinal motility

 The diarrheoa is typically watery and episodic
 Unlike dumping syndrome, the symptoms of diarrhea is not associated with the osmolarity of
meals or the rate of gastric emptying
 Treatment: anti-motility agents, dietary modifications, decrease excessive intake of fluid of
foods that contain lactose
 Symptoms usually improve with time, and surgery is rarely indicated
Alkaline reflux gastritis
 Commonly associated with Billroth II

 Triad of constant (not post-prandial) epigastric pain, nausea and bilious vomiting
 Non-operative therapy consists of frequent meals, antacids, and cholestyramine to bind bile
salts but is usually ineffective
 Surgery to divert bile flow from the gastric mucosa is the only proven treatment
Other complications:
 Recurrent ulceration
 Adenocarcinoma of stomach

COLORECTAL
Carcinoid Tumours
Introduction
 Carcinoid tumours are slow-growing type of neuroendocrine tumour

 It is derived from the primitive stem cells in the gut wall, but can also be found in the lungs,
thymus, liver, bronchus, ovary and kidneys
 It is the most common malignant tumour of the appendix
 All carcinoids are considered to have malignant potentials
 Carcinoid tumours can be divided into foregut, midgut and hindgut carcinoids
Pathophysiology
 The tumour is yellow, tan or gray-brown appearance

 The yellow colour is a result of cholesterol and lipid accumulation within the tumour
 Upon histologic examination, carcinoid tumours have 5 distinctive patterns (STRUM):
1. Solid, nodular and insular cords

2. Trabecular or ribbons with anastomosing features
3. Tubules and glands or Rosette-like patterns
4. Poorly differentiated or atypical patterns, Undifferentiated
5. Mixed patterns
 Immunohistochemically, these tumours have a strong positive reaction to keratin and

neuroendocrine markers
 These include chromogranin and synaptophysin
Products of carcinoid tumours include: 5HT, histamine, kallikrien, gastrin, somatostatin, platelet-
derived growth factor, serotonin, substance P, VIP
 Immunostatin and tumour markers are used for diagnosis
Frequency
 Most common neuroendocrine tumours

 1.5 cases in 100,000 population
History
 Signs and symptoms depend on location of tumour, size of tumour, and the presence of
metastases Most common symptoms of small intestine carcinoid tumour is abdominal pain
 10% of patients will have carcinoid syndrome
 This is usually associated with liver metastases
 However carcinoid tumours arising in the bronchi may be associated with carcinoid syndrome
without liver metastases
 Symptoms of carcinoid syndrome: flushing, diarrhoea, abdominal pain, bronchospasm,
tachycardia Other symptoms of carcinoid tumour may include valvular heart lesions (60% of
patients)
 Patients may get fibrosis in the tricuspid and pulmonary valves
Investigations
 Lab: measure urinary 5HIAA (24 hours), fasting plasma 5 HIAA, measurement of other
peptides e.g. chromogranin, neuropeptide K
 Imaging: may include plain x-ray, upper & lower GI series, CT, MRI, angiography, PET scan,
scintigraphy with MIBG and octreotide, radionuclide imaging with somatostatin analogue,
technetium 99m bone scanning
 Procedures: bronchoscopy, OGDS, colonoscopy; which can be used for diagnosis and biopsy
Treatment
 Surgery is the only curative treatment

 If metastases has occurred or in cases where surgical excision is not suitable, consider
chemotherapy
 Among agents used: 5FU, doxorubicin, cisplatin, interferon alpha, etoposide
 Chemo-embolization of hepatic artery for treatment of metastatic carcinoid tumour has been
widely used
 Octreotide is highly effective in reducing symptoms
 If hepatic metastases is present but resectable, surgical resection is preferred
Complication
 The most serious complication is carcinoid crisis, which is often observed in patients with
foregut tumours and high level of 5 HIAA

Prognosis
 Prognosis is excellent in completely resected localized disease

 Poor prognosis: tumours > 2 cm, positive lymph node, atypical histologic features, 5 or more
liver metastases

COLORECTAL
Rectal Prolapse
Introduction
 Rectal prolapse is a condition wherein the walls of the rectum protrude through the anus and
hence become visible outside the body.
 There are 3 types of rectal prolapse:
1. Full thickness rectal prolapse: the entire rectum protruding through the anus
2. Mucosal prolapse: only the rectal mucosa prolapsing
3. Internal intussusceptions: the rectum collapses but does not exit the anus
Causes
 Conditions with increased intra-abdominal pressure: constipation, diarrhoea, BPH, COPD,

Cystic fibrosis
 Pelvic floor dysfunction: pregnancy, childbirth, previous surgery
 Parasitic infections: amoebiasis, schistosomiasis
 Anatomical features: poor posterior fixation of rectum, redundant rectosigmoid
 Neurologic disorders: multiple sclerosis, spinal tumours
Pathophysiology
 The precise cause of rectal prolapse is not defined

 Associated abnormalities:
In adult: chronic straining with defaecation and constipation, a deep pouch of Douglas, weakness of
the pelvic floor, decreased resting anal sphincter pressure
In children: vertical orientation of the rectum, mobility of the sigmoid colon, relative weakness of
the pelvic floor muscle, mucosa poorly fixed to submucosa, redundant rectal mucosa.
Age

 Although all ages can be affected, peak incidences are observed in the fourth and seventh
decades of life.
 Paediatric patients usually are affected when younger than 3 years, with the peak incidence in
the first year of life.
History
 Constipation
 Faecal incontinence
 Mucus drainage
 Protruding anal mass
 Rectal bleeding
 Protruding rectal mucosa

 Thick concentric mucosal ring
 Sulcus noted between anal canal and rectum
 Solitary rectal ulcer
 Decreased anal sphincter tone
Mortality/Morbidity
 Untreated rectal prolapse can lead to incarceration and strangulation (rare).

 More commonly, increasing difficulties with rectal bleeding (usually minor), ulceration, and
incontinence occur.
Imaging Studies
 A barium enema can assess for concurrent colonic diseases or tumours.

 Defaecography may reveal intussusceptions of proximal colon or pelvic outlet obstruction.
Other Tests
 Colonic transit study

 Anal sphincter manometry (aids in determining the degree of anal sphincter damage)
 Pudendal nerve terminal motor latency (assesses for neurologic injury or dysfunction)
 Ultrasonography
Procedures

 Proctosigmoidoscopy can be an important tool to examine rectal mucosa for ulceration,
inflammation, or other contributing colonic disease.
Treatment
Conservative Approach
 Reduction with gentle digital pressure under sedation or local perianal anaesthesia.
 If significant bowel oedema is present: topical application of granulated sucrose to reduce the
oedema.
 Treat constipation or diarrhoea.
Surgical Approach
 Surgery is generally not performed unless the symptoms of the prolapse have begun to
interfere with daily life or there is presence of complications.
 Two approaches: perineal or abdominal approach.
Abdominal surgery: open or laparoscopically
 Associated with a higher rate of complications and a longer recovery time.

 Results are generally longer lasting.
 Rectopexy and anterior resection are the two most common abdominal surgeries used to
treat rectal prolapsed.
 During rectopexy, the rectum isolated from surrounding tissues, and the sides of the rectum
lifted and fixed to the sacrum with stitches or with a non-absorbable mesh.
 Anterior resection removes the sigmoid colon with primary anastomosis. This straightens the
colon and makes it easier for stool to pass.
 Rectopexy and anterior resection may also be performed in combination and may lead to a
lower rate of prolapse recurrence.
Perineal surgery
 Generally used for older patients who are unlikely to tolerate the abdominal procedure well
Anal encirclement (Thiersch procedure)
 Involves the insertion of a thin circular band of non-absorbable material under the skin of the
anus.
 This narrows the anal opening and prevents the protrusion of the rectum through the opening.
 Does not address the underlying condition.

 Generally reserved for patients who are not good candidates for more invasive surgery.
Delorme Procedure
 Involves the resection of only the mucosa of the prolapsed rectum

 The exposed muscular layer is then folded and stitched up and the cut edges of mucosa
stitched.
Altemeier procedure
 Also called a rectosigmoidectomy

 The prolapsed portion of the rectum is resected and then primary anastomosis done
transanally
STARR (Stapled Transanal Rectal Resection) procedure
 Transanal insertion of a 31mm stapling instrument to resect (full thickness) the lower 5cm of
prolapsing rectum together with any associated rectocoele, intussusceptions or mucosal
prolapse.
 A simultaneous resection and anastomosis is secured with the staple line placed within the
rectum.
 Potential complications include bleeding (primary, reactionary and secondary), perineal
sepsis, rectovaginal fistula, pain.
 50% of patients experience defaecatory urgency early in the postoperative period. The latter
is usually self limiting and usually resolves within three to six months.
Children are treated with linear cauterization
Manchester operation is used for combined pelvic prolapse
Recently, robotic-assisted surgery has been introduced as a treatment option

COLORECTAL
Intra-abdominal Abscess
Introduction
 An intra-abdominal abscess is a localized collection of pus, contained within the peritoneal

cavity
 May be intraperitoneal or retroperitoneal
Intraperitoneal Abscess
 Intraperitoneal abscess can be found in the subphrenic, infracolic, paracolic gutters or pelvis
 The subphrenic spaces are situated between the diaphragm and the liver, one on each side
of the falciform ligament
 Causes of subphrenic abscess: duodenal perforation, acute cholecystitis, pancreatitis,
appendicitis, postoperative complications following gastric, hepatobiliary or splenic surgery
 The infracolic compartment is divided into right and left sides by the small bowel mesentery,
and then further subdivided into the paracolic gutters
 Causes of infracolic and paracolic abscess: GI perforations, IBD, diverticulitis, anastomotic
leak, appendicitis
 The pelvis is the most dependent part of the abdominal cavity, and therefore is the most
common site of intraperitoneal abscesses
 Causes of pelvic abscess: gynaecological infections, appendicitis, colorectal perforation,
anastomotic leak
Extraperitoneal abscesses
 Extraperitoneal abscesses are less common than intraperitoneal abscesses and can be
classified into perinephric or psoas abscesses
 Causes of extraperitoneal abscess: pancreatic abscesses, perforated appendix, posterior
duodenal ulcers, genitourinary tract pathology (pyelonephritis), spinal column pathology
(osteomyelitis, disciitis)
Diagnosis

Microbiology:
 Most yield a mixture of aerobic and anaerobic pathogens

 Common organisms in the upper GIT: aerobic streptococci, enterococci and facultative Gram-
negative bacilli
 Common organisms in the lower GIT: anaerobic Gram-negative bacilli (e.g. Bacteroides
species), anaerobic Gram-positive flora (e.g. streptococci, Clostridia)
 Common organisms in the women with pelvic inflammatory disease: Neisseria gonorrhoeae,
chlamydial species
Presentation:
 Commonly present with non-specific symptoms and signs

 Localized abdominal tenderness, prolonged ileus, systemic inflammatory response syndrome
Imaging
Plain radiographs
 Rarely diagnostic (but often suggestive) of an abscess

 Abdominal X ray: may show air–fluid levels, soft tissue mass, displacement of viscera,
absence of psoas shadow or a localized ileus
 Chest X ray: may show pleural effusions, a raised hemidiaphragm, basilar infiltrates and
atelectasis in a subphrenic or subhepatic abscess
Ultrasound
 Most common method of imaging for suspected intra-abdominal abscesses

 In experienced hands, ultrasound has >90% sensitivity
 Advantages: fast, portable, inexpensive, free from ionizing radiation
 Disadvantages: sensitivity can be significantly decreased by obesity, bowel gas, surgical
dressings and stomas
CT
 More sensitive and specific than ultrasound in the diagnosis of an intra-abdominal abscess
 Allows greater anatomical detail e.g. fluid collections in relation to nearby structures
 Certain characteristics of abscesses can be better defined (e.g. gaseous contents, associated
tumour)
 Contrast enhancement can help to identify anastomotic leaks or fistulas and help plan
appropriate surgery
Radionuclide imaging
 Use leukocytes labelled with gallium- 67 or indium-111

 These agents accumulate in the abscess and are detected as ‘hot spots’ in areas of
inflammation (as well as in tumours)
 False-positive results can occur due to non-infective inflammatory conditions, surgical drains
and incisions
 Lower sensitivity than CT or ultrasound
 Use as adjunct in the diagnosis of intra-abdominal abscesses
 Used in rare cases where intra-abdominal abscesses are suspected, but other imaging
modalities have given negative results
Treatment
 Treatment of the primary cause, adequate drainage and the use of antibiotics are the
principles of treatment.
Antibiotics
 Broad-spectrum antibiotics (i.v.) are started following drainage, and changed when
sensitivities are known
 Patients are monitored clinically and haematologically (white blood count, haemoglobin,
platelets, C-reactive protein, liver function tests)
 Drainage should not be delayed in patients who are systemically unwell with features such as
spiking pyrexia and rigors; after satisfactory drainage, they should be started on broad-
spectrum antibiotics (i.v.) following a blood culture
 A significant clinical improvement should be seen within 24–48 hours.
 Failure of improvement may suggest unsatisfactory drainage, another focus of infection or
organ dysfunction
Percutaneous drainage
 First-line treatment of intra-abdominal abscesses
 CT or ultrasound can be used for guidance

 Can play an important preoperative role: for example, in diverticular and appendiceal
abscesses, it allows the sepsis to resolve, making subsequent surgery safer (and
occasionally obviates the need for surgery)
Open drainage

 Second-line treatment of intra-abdominal abscesses except in certain cases (e.g. pancreatic
abscesses with necrosis, which often need surgical debridement)
 The extraperitoneal approach is the preferred method to minimize the risk of further
contamination of the peritoneal cavity
Laparoscopic drainage
 An alternative to open drainage

 Advantages: decreased morbidity, smaller scars, faster recovery from surgery
 Inadequate drainage may be problematic if laparoscopy does not reveal the full extent of
sepsis
Drainage of pelvic abscesses
 There are many approaches to draining pelvic abscesses:

 Transabdominal Approach: simplest, but is limited by interposed intestine and other pelvic
viscera
 Transgluteal (through the greater sciatic notch), transrectal or transvaginal approach can also
be used

COLORECTAL
Appendicular Mass /Abscess
Introduction
 Acute appendicitis remains the commonest cause of acute abdomen requiring surgical
intervention
 Patients presenting late in the course of acute appendicitis are complicated by the
development of an inflammatory mass in right iliac fossa
 This inflammatory mass is composed of the inflamed appendix, omentum and bowel loops
 It occurs in 2-6% of patients presenting with acute appendicitis
Clinical Features
 Pain: usually present in the RIF

 Tenderness: the mass in the RIF becomes tender not only to touch but to respiratory
movements as well
 Mass in the RIF: There is mass formation in the RIF which is tender to touch
 Paralytic ileus:
 Fever: Fever may be continuous or swinging in nature
 Associated symptoms: Patient may present with difficulty in micturition, frequency of
micturition, acute retention of urine and haematuria. The symptoms are due to presence of
abscess and inflammatory mass near right lower ureter and bladder.
Investigations
 Urine Examination: It is a simple investigation which helps to exclude the renal causes of
urological symptoms in patients with appendicular abscess
 Blood Examination: Haemoglobin percentage is decreased, leucocytes count is raised,
sedimentation rate is raised
 Plain X-ray of the Abdomen: It may show loops of small bowel around the abscess area
(sentinel loop)
 Ultrasound of the Abdomen: The differentiation between appendicular mass and abscess is
easily done with the ultrasound scan. The abdominal ultrasound scan shows a solid mass in
the right iliac fossa as hypoechoic area (fluid collection). The amount of fluid collection varies

with the amount of pus present. The shadow of adherent and distended loops of bowel is also
seen.
 CT scan: It can reliably distinguish phlegmonous inflammation from a liquefied abscess. It can
delineate the full extent of such inflammatory mass.
Management of Appendicular Mass
 Management of an appendiceal mass is controversial with three general approaches usually

employed
Classical Management
 'Classical management' involves initial conservative management with broad spectrum

antibiotics and intravenous fluid until the inflammatory mass resolves
 Patients are offered interval appendicectomy following resolution of symptoms (usually about
4-6 weeks later)
 The reasons for interval appendicectomy is to prevent recurrence of acute appendicitis and to
avoid misdiagnosing an alternative pathology such as malignancy
 Advantages: early appendicectomy is hazardous, time-consuming, may lead to life
threatening complications for example faecal fistula; avoid recurrent appendicitis
Semi Conservative Approach
 The semi-conservative approach involves performing immediate appendicectomy during the

initial admission after resolution of the inflammatory mass
 Advantages: avoids the need for readmission for interval appendicectomy, exclusion of other
pathologies masquerading as an appendix mass (especially if over 40 years old), reduced
hospital stay
 Disadvantages: high complication rate (36%); may lead to dissemination of infection; risk of
intestinal fistula formation; appendiceal mass may be mistaken at surgery for a malignant
tumour (may lead to right hemicolectomy); a malignant mass may be mistakenly under-
treated by appendicectomy
 Current trend shows that early operation is acceptable and associated with low morbidity,
reduced hospital stay, low cost, and increase patient compliance
Entirely Conservative Approach
 Proponents of an entirely conservative approach claim appendicectomy, whether interval

(delayed) or immediate (during initial admission), is unnecessary

 A school of thought argued that after a successful conservative management, interval
appendicectomy is not necessary and can safely be omitted, except in patients with recurrent
symptoms
 In patients above 40 years of age, one must exclude other pathological causes of right iliac
fossa mass by further investigations such as barium enema, colonoscopy and computerized
tomography scan
 A close follow up is needed in this category of patients
 Proponents for this approach argue that:
o Studies have shown that the risk of recurrent acute appendicitis following successful
conservative management is low; between 5% and 14%
o In the minority of patients whose symptoms do recur, this usually occurs within one
year
o Recurrence of appendicitis following conservative management is usually associated
with a milder clinical course amenable to both operative and non-operative
approaches
o There is no accurate method for predicting patients at risk of recurrence
o The conservatively managed group also had the shortest length of hospital stay even
when the recurrences were included
Conclusion
 The selection of methods depends on surgeon’s preference and patient’s condition

 Misdiagnosis of appendiceal tumour or colonic tumour can be disastrous in patients with
appendiceal mass, so we should exercise caution when adopting entirely conservative
approach

COLORECTAL
Toxic Megacolon
Introduction:
 Toxic megacolon is the clinical term for an acute toxic colitis with dilatation of the colon.
 The dilatation can be either total or segmental.
 The hallmarks of toxic megacolon (toxic colitis), a potentially lethal condition, are non-
obstructive colonic dilatation larger than 6 cm and signs of systemic toxicity.
Diagnostic criterion:
 The first criterion is radiographic evidence of colonic dilatation.

 The second criterion is any 3 of the following: fever (>101.5°F), tachycardia (>120 beats/min),
leukocytosis (>10.5 103/μL), or anaemia.
 The third criterion is any 1 of the following: dehydration, altered mental status, electrolyte
abnormality, or hypotension.
Causes:
 Toxic megacolon may complicate ulcerative colitis, crohn’s colitis, pseudomembranous colitis,
radiation colitis, ischaemic colitis, non-specific colitis secondary to chemotherapy and
infective colitis (salmonella, shigella, campylobacter, yersinia)
 Colonic dilatation without systemic toxicity is not toxic megacolon
Pathophysiology:
 Signs and symptoms of acute colitis may be present for as long as 1 week before dilatation
develops.
 Although the risk of toxic megacolon (toxic colitis) increases with the severity of colitis, rapid
tapering or abrupt discontinuation of medications such as steroids, sulfasalazine, and 5-
aminosalicylic acid may precipitate toxaemia and dilatation.
 Medications that negatively impact bowel motility also are implicated in the development of
toxic megacolon. These include, but are not limited to, anticholinergics, antidepressants,
loperamide, and opioids.
 Procedures such as barium enema or colonoscopy may cause distension, may impair blood
supply, or may exacerbate a micro perforation and cause subsequent toxaemia.

 In cases of uncomplicated colitis, the inflammatory response is confined to the mucosa. The
microscopic hallmark of toxic megacolon (toxic colitis) is inflammation extending beyond the
mucosa into the smooth-muscle layers and serosa.
 Neutrophils and macrophages released nitric oxide. NO inhibit smooth muscle tone and this
leads to colonic dilatation.
Incidence:
 5% in severe UC, 0.4 – 3 % in pseudomembranous colitis
Imaging Studies
Plain abdominal radiographs:
 Dilated (>6 cm) transverse colon

 Loss of colonic haustrations
 Possible "thumb printing"
 Presence of intraluminal soft-tissue masses (i.e., pseudopolyps)
 Free intraperitoneal air – Possible finding, best seen on upright chest x-ray or left lateral
decubitus abdominal film
 Avoid barium studies in a patient who is severely toxic. The potential for perforation is
considerable.
Intestinal ultrasonography:
 Complete loss of haustra coli of the colon

 Hypoechoic and thickened bowel walls with irregular internal margins in the sigmoid and
descending colon
 Marked dilation of the transverse colon (>6 cm), a finding that correlated well with the plain X-
ray of the abdomen
 Slight dilation of ileal bowel loops (diameter >18 mm) with increased intraluminal gas and fluid
CT scan
 May identify a local or contained perforation

 CT scan may show classic accordion sign
Endoscopy
 If the diagnosis of toxic megacolon (toxic colitis) is in doubt and the patient's condition is not
toxic or unstable, endoscopy may be attempted by appropriately trained personnel.

 Endoscopy may take the form of flexible sigmoidoscopy or colonoscopy. If clinical concern of
toxic megacolon (toxic colitis) exists, the examination should not progress beyond
sigmoidoscopy, if at all. The scope should only be advanced as far as is needed for
diagnosis. Air insufflations should be a minimal. According to some experts, colonoscopy is
generally justified only if the patient has no or minimal inflammation of the sigmoid or rectum.
 Perforation is an obvious potential complication with this approach.
Medical Care:
 Treatment of toxic megacolon (toxic colitis) includes 3 main goals: (1) reduce colonic
distension to prevent perforation, (2) correct fluid and electrolyte disturbances, and (3) treat
toxaemia and precipitating factors.
 Careful and frequent monitoring of the patient is required, and, initially, CBC counts,
electrolytes, and abdominal radiographs should be checked every 12 hours.
 During the initial resuscitation, fluid replacement, electrolyte repletion, and transfusion should
be aggressive.
 Broad-spectrum intravenous antibiotics with coverage equivalent to ampicillin, gentamicin,
and metronidazole should be initiated.
 All medications that may affect colonic motility must be stopped. These include narcotics,
anti-diarrheal, and anti-cholinergic agents.
 The patient with toxic megacolon (toxic colitis) should be put on bowel rest, and a nasogastric
tube (NGT) or long intestinal tube should be placed to assist with gastrointestinal
decompression.
 The patient should be started on intravenous steroids. Intravenous hydrocortisone is
necessary for patients who are taking corticosteroids or who have been recently treated with
corticosteroids.
 Rolling techniques (knee-elbow and prone) may be performed to assist in redistribution of
colonic gas and decompression.
 If the patient is malnourished, consider parenteral nutrition.
 Some reports indicate that cyclosporin A may be beneficial in the treatment of severe
ulcerative colitis or toxic megacolon (toxic colitis). Data suggest that cyclosporin may provide
an initial response rate of as high as 80%.
Surgical Care:
 Indications for urgent operative intervention include free perforation, massive haemorrhage
(6-8 U packed red blood cells), increasing toxicity, and progression of colonic dilatation.
 If no improvement occurs over 48-72 hours with medical therapy, perform surgical resection.
 Whether to perform a total proctocolectomy or subtotal colectomy with the rectum left behind
is debated.
 The preference in the literature is to perform a subtotal colectomy, because:
o The patient is usually very ill, and not lengthening the operation is prudent if at all
possible;
o It preserves the possibility for an ileal pouch anal anastomosis
o Approximately 50% of patients with Crohn disease have minimal involvement of the
rectum.
o Performance of a total proctocolectomy in a patient who is acutely ill and toxic and on
high-dose steroids would increase the risk of complications, morbidity, and likely
mortality.
 Terminate the resection at the sacral promontory, and perform either a mucus fistula or a
stapled rectal stump. If a stapled rectal stump is performed, keeping a rectal tube in place for
2-3 days may reduce the incidence of rectal stump blowout.

COLORECTAL
Pseudomembranous Colitis (PMC)
Introduction:
 PMC is an acute colitis characterized by the formation of an adherent inflammatory

membrane (pseudomembrane) overlying sites of mucosal injury
 It is a well recognized cause of diarrhea in patients following course of a broad-spectrum
antibiotic therapy
Causes:
 Clostridium difficile infection is the most important infectious cause of PMC

 Rarely PMC can be caused by other aetiologies; e.g. Staph species or enterotoxigenic C.
perfringens, campylobacter species, listeria species, salmonella species
Antibiotic associated with PMC:
 Cephalosporin
 Penicillin
 Clindamycin
 Ampicillin
 Also metronidazole and vancomycin which is used for treatment of PMC
Pathophysiology:
 Clostridium difficile is an anaerobic, toxigenic, spore-forming, gram-positive rod.

 The use of antibiotics alters the normal bowel flora, predisposing to the overgrowth of C
difficile and the production of its toxins.
 PMC results from the inflammatory reaction of the bowel wall to luminal toxins produced by C
difficile.
 Continuation of inflammatory process can lead to formation of pseudomembranes, a mixture
of inflammatory cells, fibrin, and bacterial and cellular components, which exudes from the
bowel mucosa.
 Not all strains of C difficile are toxigenic.
 Toxigenic Clostridium difficile produces 2 similar large molecular weight toxins that disrupt the
barrier function of the colonic mucosa.

 Toxin A is an enterotoxin that binds to receptors in the bowel wall, leading to activation of the
inflammatory cascade and disruption of the intercellular tight junctions, causing fluid
secretion, mucosal injury, oedema, and inflammation.
 Toxin B is the primary cytotoxin responsible for C difficile infection. It appears to act as a
cytoskeletal disruptor, leading to mucosal injury and further activation of the inflammatory
cascade.
 Host factors that increase susceptibility to C difficile –associated diarrhoea
o Age greater than 65 years
o Chronic debilitation or critical illness
o Alteration in gut motility
o Receipt of enteral tube feeds
o Use of proton-pump inhibitors
o Cancer chemotherapeutic agents
o Impaired humoral immunity
o HIV infection
Presentation:
 Ranges from mild self-limited diarrhoea to severe colitis with pseudomembrane formation
complicated by development of toxic megacolon or colonic perforation.
 The classic presentation is cramping abdominal pain with profuse, mucoid, greenish, malodorous
watery stools.
 Other features of infection: leukocytosis, hypoalbuminaemia, faecal leukocytes, positive FOB.
Colonoscopy/Sigmoidoscopy findings:
 Discrete cream to yellow coloured plaques which vary in size 2-20 mm.
 Loosely attached to erythematous bowel wall.
 The pseudomembranes can be easily removed during endoscopy.
 In advanced cases the pseudomembranes are more confluent and linear ulcers develop.
Diagnosis:
 Stool culture of C difficile

 Cytotoxic assay
 ELISA technique to detect the presence of toxin A and/or B
 PCR to detect the presence of toxin A/B
Imaging studies:

 Imaging studies do not aid in confirming the diagnosis of early or mild colitis.
 In patients with severe disease, radiographic studies can aid in detecting complications (e.g.,
toxic dilation, perforation).
 CT scanning of the abdomen can be helpful by revealing the presence of bowel wall oedema
(>4 mm) and inflammation, particularly in cases involving the right colon; however, these
findings are generally nonspecific.
 Barium enema has no role in the diagnosis of early colitis and can be catastrophic in the
setting of dilatation due to toxic megacolon or perforation.
 Toxic megacolon is characterized radiographically by dilation of the transverse colon to
greater than 6 cm and loss of colonic haustrations (possible “thumb printing”).
 Sigmoidoscopy is not routinely used in the diagnosis of PMC because of its invasiveness.
Medical Care:
 Stop the offending agent if possible.

 Provide supportive care for the diarrhoea, including repletion of fluid and electrolyte losses.
 Antiperistaltic agents and opiates should be avoided, as slowing of faecal transit time is
thought to result in extended toxin-associated damage.
 Implement contact isolation precautions (gowns and gloves) to reduce the spread of C difficile
to other hospitalized patients.
 Patients generally respond to 10-14 days of metronidazole or vancomycin therapy; however,
patients with severe colitis or underlying GI conditions (eg, irritable bowel syndrome, lactose
intolerance) may require prolonged courses of therapy.
Surgical Care:
 Surgical intervention is usually indicated for patients whose conditions are complicated by
toxic megacolon with subsequent risk for perforation or existing perforation.

COLORECTAL
Management of Obstructed Splenic Flexure Tumour
Introduction
 25-30% of patients with left-sided colon tumour present as emergency: perforation or

obstruction
 Obstruction carries a high risk of morbidity and mortality
 Splenic flexure tumour is very rare and its account for 2-5% of all colon cancer
 These signs and symptoms may and may not be present

 Symptoms: Constipation, abdominal distension and pain, nausea and vomiting, absence of
flatus
 Signs: abdominal distension, peritonitis, tachycardia, dehydration, electrolytes imbalance
Investigations
Laboratory
 Renal profile: to assess electrolyte imbalance

 Albumin: to assess the nutritional status
 FBC: to assess the presence of infection
 CEA: as tumour marker, may be useful for follow up purposes in the future\
Imaging
 AXR: presence of dilated bowel

 CXR: for pre-operative assessment and to detect lung metastasis
Management
Pre-operatively
 Rehydration

 Correct electrolytes imbalance
 Bowel Decompression by the use of NGT
 Adequate analgesia
 Prophylactic antibiotics: broad-spectrum and covering anaerobes
 CBD and CVP insertion for close monitoring
 Early anesthetics referral
 Oxygen supplementation
 Optimize pre-morbid condition: e.g. diabetic control and blood pressure control
 DVT prophylaxis
 Mark stoma site (may be needed)
Surgery
 Surgery for obstructed splenic flexure tumour can be done as a single-stage, two-stage or
three-stage procedure
 Single stage procedure
o Subtotal colectomy with ileorectal anastomosis, or extended right hemicolectomy with
ileocolic anastomosis, or left hemicolectomy with colo-colic anastomosis
 Two stage procedure

o Hartmann’s procedure followed by closure of Hartmann’s later
 Three stage procedure
o Diverting colostomy, tumour resection, closure of colostomy
Single stage procedure
Subtotal colectomy with ileorectal anastomosis
 Full mobilization of entire colon from caecum to proximal rectum

 Resection of right-sided colon until descending colon
 Ligation of right colic, middle colic, inferior mesenteric arteries and inferior mesenteric vein
Extended right hemicolectomy with ileocolic anastomosis
 Mobilization of right colon until descending colon

 Resection from caecum until part of descending colon
 Ligation of right colic and middle colic arteries
Left hemicolectomy with colo-colic anastomosis
 Mobilization of transverse colon until descending colon

 Resection of distal part of transverse colon until descending colon
 Ligation of left branch of middle colic artery
 The disadvantage of this approach is lack of blood supply in the watershed area can
compromise the anastomosis. Colo-colic anastomosis also heals worse than ileo-colic
anastomosis
*to reduce incidence of sepsis: on table lavage and the creation of defunctioning loop ileostomy
Advantages of single stage operation:
 Relieve obstruction, resects tumour and anastomosis at the same setting

 Avoidance of second operation
 Good quality of life without a stoma
 Total reduction of hospital cost by single admission
Disadvantages of single stage operation:
 Frequent defaecation and the risk of faecal incontinence

 Longer duration of operation
 Have a risk of anastomosis leak
 Anastomosis done at suboptimal condition
Two staged operation
Hartmann’s procedure
 Resection of the tumour with the creation of an end transverse colostomy and the distal
stump is closed and left behind
 Patients need another operation to reverse the Hartmann’s procedure after completing
adjuvant chemotherapy
Advantages of two stage operation:
 Operation can be done faster

 No risk of leaking anastomosis
 Allow time to assess the staging of the disease
 Suitable for unfit patient
Disadvantages of two stage operation:
 Have to go for second operation

 Poor quality of life because of stoma
 Risk of local recurrence, synchronous and metachronous tumour is higher
 Up to 30% of Hartmann’s procedure are never reversed
 10% mortality on reversing the Hartmann’s procedure
Three stage operation
Encompasses diverting colostomy, resection of tumour at a later date and closure of colostomy once
treatment is complete
Advantages of three stage operation:
 Simple initial life-saving operation

 Allow patient to recover before major operation
 Shorter operation time
 Suitable for unstable patient
 Allow decompression of bowel and to assess the extent of the disease with proper staging
Disadvantages of three stage operation:
 Multiple operations
 Increase total hospital cost
 Poor quality of life because of the stoma
 20-50% never had their stoma reversed
 Tumour is not removed in the first setting
Other option:
Endoluminal Stent
 Used for patient who is deemed unfit to undergo surgery or in terminal patient
 Advantages: does not require surgery, can relieve obstruction, operation can be done later as
an elective
*Based on all the options, single stage operation preferably subtotal colectomy or extended right
hemicolectomy is the procedure of choice if the patient is stable and fit for surgery.
*If the patient is elderly and unable to withstand the longer operation time, Hartmann’s procedure is
the procedure of choice.
Post Operative Care
 Adequate analgesia

 Ensure adequate hydration
 Correct electrolytes imbalance
 Prophylactic antibiotics can be given up to 3 doses post operatively
 Wound care and dressing
 Chest and limb physiotherapy
 Early mobilization
 Early enteral feeding
 DVT prophylaxis
 Care of colostomy
 Counselling regarding the diagnosis
Adjuvant Therapy
 The purpose of adjuvant chemotherapy is to reduce local recurrence rate to improve disease
free survival
 Indications for adjuvant chemotherapy in colon cancer are high-risk of stage II and stage III
cancer
 Stage IV cancer patients will be given palliative chemotherapy
 The current case is considered as high risk due to him/her presented as obstruction. So this
patient will need adjuvant chemotherapy
 The chemotherapy used in Mayo’s regime or Degrammont regime. Both are 5FU-based
chemotherapy
 Second-line chemotherapy will be FOLFOX (oxaliplatin-based) regime or FOLFIRI regime
(ironitecan-based)
Follow up
 3monthly follow up with CEA to detect recurrence.

 Colonoscopy within 6 months if not done pre-operatively, and then yearly. If negative, every 3
years colonoscopy
 CT scan abd/pelvis to detect recurrence if CEA is elevated or if patient is symptomatic
 PET scan to detect recurrence

COLORECTAL
Faecal Incontinence
Definition
 Inability to prevent elimination of rectal contents (gas, liquid or solid)
Aetiologies
 Mechanical defect
o Sphincter damage
o Scleroderma affecting the external sphincter
 Neurogenic defect
o E.g. spinal cord injury
 Stool content-related causes
o E.g. diarrhoea, radiation proctitis
Evaluation
 DRE: assess tone, squeeze abnormalities

 Anal manometry: measure resting and squeeze pressure, sphincter length, minimal sensory
volume of rectum
 Pudendal nerve terminal motor latency (PNTML): evaluate sphincter physiology
 EAUS: evaluate sphincter anatomy
Treatment
 Depends on type and severity of the defect

 Neurogenic and minor mechanical sphincter defects
o Dietary fibre to increase stool bulk
o Biofeedback to strengthen muscle and improve early sensation
 Major defects
o Anal sphincter reconstruction
 External sphincter is circularized and then plicated to recreate the perineal
body

o Artificial anal sphincters may be used in patients without a reconstructible native anal
sphincters
o Severe denervation of an intact anal sphincter may be managed with sacral nerve
stimulation, artificial sphincters, or palliative diverting colostomy

COLORECTAL
Fistula In Ano
Introduction
 Fistula means abnormal communication between 2 epithelial surfaces

 Fistula in ano means abnormal communication between the skin and the anus
Risk Factors
 Usually associated with perianal abscess

 Immunocompromised
 Diabetes mellitus
 Crohn’s disease
 May also be associated with TB, malignancy or trauma
Epidemiology
 Male > female, age > 40 years old
Types of Fistula
 Simple fistula
 Complex fistula
o Multiple fistulas
o Fistula with secondary tract
o Fistula with pelvic sepsis
Causes
 Trauma
 Infection (TB/AIDS)
 IBD (Crohn’s)
 Malignancy
 Radiation
 Surgery

 Idiopathic
 Foreign body
Classification of Fistula
Park’s Classification
 Intersphincteric fistula (most common)

 Transphincteric fistula
 Suprasphincteric fistula
 Extrasphincteric fistula (least common)
Presentation
 Discharge per anus

 Anal pain
 Pruritus
 Perianal abscess
 Passage of flatus via tract
 Soiling
Pathophysiology
Cryptoglandular Theory
 Blockage of ducts at the anal crypts leads to gland infection and later abscess formation
 Abscess discharges along the path of least resistance leading to fistula formation
Investigation
 Examination under anaesthesia

o Using probe for example Lockhart mummery probe to define the internal and external
opening
o Can also use H2O2
 EUS
o Use of H2O2 may help to delineate the tract and can identify perianal abscess
o Can assess sphincter
 MRI
o Used for complex tissue to define the anatomy better
 Colonoscopy
o To rule out other pathology
 Fistulogram
o Rarely useful
Goodsall’s Rule
 Says that if we make an imaginary line transversely across the anus, the fistula that opens
anterior to this line will have an internal opening that tract radially
 Posterior fistula will have an internal opening that tract in a curvilinear fashion and opens up
in the midline.
 The exception to this rule is if the opening is > 3 cm away from the anus
Management
1. Treat perianal abscess first if present
 Incision and drainage

 Treatment of fistula at the same setting is not advocated because it is associated with
higher morbidity and incontinence
 Draining seton may be inserted to drain the abscess
2. Antibiotics
 Antibiotics is usually not needed unless there is a presence of sepsis, cellulitis or in

immunocompromised patient or patient with a heart valve
3. Fistulotomy/fistulectomy
 This is laying open the fistula

 In fistulectomy the tract is curetted and excised
 The fistula is then left open to heal by secondary intention
 Recurrence rate is about 4%
 Incontinence rate 45%
4. LIFT
 Ligation of intersphicnteric fistula tract

 Less pain
 Success rate 75%
5. Advancement flap

 Used for complex fistula
 Healing rate 85%
 Incontinence 10%
 Also for recurrent, high or multiple fistulas, impaired continence
6. Role of infliximab in crohn’s fistula
 An heal up to 70% of fistula
7. Use of cutting seton
 Seton is changed and tightened in the office at certain follow up intervals

 It produce immediate fibrosis effect that prevent sphincter retraction
 Recurrence 4-6%
 High incontinence rate up to 65%
8. Fibrin glue
 Obliterates fistula opening and tract
9. In cases where simple fistulotomy will almost certainly result in incontinence, a 3-stage
approach may be considered:
 Colostomy + lay open of fistula

 Repair of sphincter
 Closure of colostomy
Complications of Surgical Procedure
 Incontinence
 Recurrence

COLORECTAL
Haemorrhoids
Introduction
 Dilated veins in the anal cushion

 Affect 4.4 – 36.4% of the general population
Anal Cushions
 3 anal cushions: left lateral, right anterior, right posterior (or classical 3, 7 and 11 o’clock
positions)
 Blood filled
 Gives ‘watertight’ seal to the anal canal
 Vascular filling is thought to contribute between 15-20% of resting anal pressure
Haemorrhoid Theories
Venous Pressure Theory
 Increased local pressure leads to venous dilatation within the anal cushions
Connective Tissue Disorder
 Connective tissue (mainly collagenous) fibres of the submucosa anchor the anal cushion to
the underlying internal sphincter and conjoined longitudinal muscle
 With age, this supportive meshwork degenerates and the anal cushion is displaced caudally,
possibly assisted by straining and the passage of stool
 This may account for the haemorrhoidal prolapsed
*Haemorrhoidal bleeding has the appearance and pH of arterial blood. This is because there is
arteriovenous anastomosis within the submucosa
Classification
Goligher Classification

 1st degree: bleed but do not prolapse
 2nd degree: bleed and prolapsed, but reduced spontaneously after defecation
 3rd degree: need to be reduced manually
 4th degree: permanently prolapsed at the anal verge and cannot be reduced
Treatment
Conservative Treatment
 Reassurance
 Prevention of constipation and straining
 Topical application of creams and ointments to relieve pain and pruritus
Outpatient Treatment
Injection
 Injection sclerotherapy
 For 1st and 2nd degree haemorrhoids
 A small quantity of the sclerosant solution is injected submucosally into the base of the
haemorrhoid → Causing local inflammatory reaction → shrinkage of haemorrhoidal mass →
fixation of the mucosa to the underlying muscle
 E.g. phenol 5% in almond oil
 Advantages: cheap, easily taught, virtually painless, relatively safe
 Disadvantages: high failure rate, need for further treatment, can stop bleeding from
haemorrhoids but is unhelpful in treating prolapsed
 Complications: urinary retention, prostatitis, prostatic abscess, epididymo-orchitis, sepsis
Photocoagulation
 Infrared coagulation technique

 Three areas of coagulation are recommended at the base of the haemorrhoid in a triangular
shape
 Photocoagulation creates a constant depth of necrosis
 This area forms an ulcer, and ultimately a area of mucosal tethering, with associated
shrinkage of the haemorrhoidal mass
 Advantages: safe, effective, relatively non-invasive, avoids the potential complications of
misplaced injections
 Disadvantages: limited by the availability and expense of the equipment
 Larger, prolapsing haemorrhoids may not respond well

Cryotherapy
 Ablates the haemorrhoid mass with a freezing ‘cryoprobe’

 Disadvantages; surgeon has little control over the depth or area of tissue affected → can lead
to pain, bleeding or delayed healing → ulceration → profuse discharge
Banding
 Ligation of haemorrhoidal mass → obliteration of the vessels ‘feeding’ the haemorrhoid →

ulceration → sloughing →healing
 Complications: pain, haemorrhage, pelvic sepsis
Operative Treatment
Open and Closed Haemorrhoidectomy
 Whitehead procedure/total haemorrhoidectomy

o Circumferential excision of the anal cushions, anastomosing the anoderm to the
rectal mucosa
o High risk of complications: excessive blood loss, mucosal ectropion, stricture
formation (whitehead deformity)
 Milligan-Morgan Haemorrhoidectomy
o Open haemorrhoidectomy with preservation of skin bridges between the excised
haemorrhoids to prevent structuring
o Wounds are left to heal by secondary intention
 Ferguson haemorrhoidectomy
o Closed haemorrhoidectomy
o The haemorrhoidal plexus is filleted from the overlying mucosa and wounds are
closed primarily with an absorbable sutures
 Complications of Haemorrhoidectomy
o Pain
o Sepsis
o Stricture
o Urinary retention
o Bleeding (early or delayed)
o Faecal incontinence (transient, permanent)
Doppler-Guided Haemorrhoidal Artery Ligation (DGHAL)
o Superior rectal artery gives off about 5 branches of the haemorrhoidal artery (on
average) reaching he anal cushions
o Doppler signal is used to locate the haemorrhoidal arteries
o Once located, a needle holder is inserted into the lumen of the proctoscope and the
artery ligated with a figure of with absorbable suture in to the submucosa
o The procedure is repeated until no more Doppler signals are identified
o DGHAL both disrupts the arterial inflow an d tethers the mucosa, causing the
haemorrhoid mass to shrink and retract
Stapled Haemorrhoidopexy or PPH (Procedure for Prolapsed Haemorrhoid)
 Reduces prolapsed by a circular stapled mucosectomy 4 cm above the dentate line

 It shortens the prolapsing mucosa (and thus reduces the haemorrhoids)
 It also thought to disrupt the branches of the haemorrhoidal artery which feed the anal
cushions
 But the problems is residual symptoms caused by eternal haemorrhoids an skin tags not dealt
with by the stapled haemorrhoidopexy procedure
 Complication
o Rectal perforation
o Rectovaginal fistula
o Bleeding
o Fournier’s gangrene
 Advantages; less pain, early return to work, less hospital stay

VASCULAR
Management of Leaking Abdominal Aortic Aneurysm
INTRODUCTION
Definition: Aneurysm is an abnormal, focal dilatation of an artery 1.5 times its normal size
Example:
 The normal size of an abdominal aorta is 2 cm, therefore when the size of the aorta reaches 3
cm it is considered to be aneurysmal
 Most cases of abdominal aortic aneurysm (AAA) begin below the renal arteries and end
above the iliac arteries
Risk factors: male, atherosclerosis, smoking, old age, family history of AAA
Causes: degeneration, infection, arteritis, trauma, inherited connective tissue disorder
PATHOPHYSIOLOGY
 AAAs arises as a result of a failure of the major structural proteins of the aorta (elastin and
collagen)
 The inciting factors are not known, but a genetic predisposition clearly exists
 Surgical specimens of AAA reveal inflammation, with infiltration by lymphocytes and
macrophages, thinning of the media and marked loss of elastin
 The combination of proteolytic degradation of aortic wall connective tissue, inflammation and
immune responses, biomechanical wall stress, and molecular genetics represents a dynamic
process that leads to aneurysmal deterioration of aortic tissue
TYPES OF ANEURYSM
 Can be classified according to its shape: fusiform or saccular

 Can be true aneurysm (involving all 3 layers of the vessel wall) or pseudoaneurysm (not
involving all the layers)
 Other types: traumatic aneurysm, mycotic aneurysm, dissecting aneurysm

RISK OF RUPTURE
 Risk of rupture is exponentially related to the aneurysm diameter
Size Annual risk of rupture

5.0 - 5.9 cm 7%
6.0 - 7.0 cm 13%
>7.0 cm 21%
 The frequency of rupture is 4.4 cases per 100,000 persons

 Law of Laplace: tensile strength of the arterial wall is a function of the pressure multiplied by
the radius (T = P x r)
 Other associated risk of rupture: COPD, diastolic hypertension
 Overall mortality of ruptured AAA is 90%
PRESENTATION
 Asymptomatic: in 75% of cases

 Rupture: the most typical manifestation of rupture is abdominal or back pain with a pulsatile
abdominal mass. Other symptoms may include groin pain, syncope, paralysis, or flank mass
 Peripheral embolization
 Acute aortic occlusion: small AAAs may thrombosed, producing acute claudication
 Aortocaval fistulae: AAAs may rupture into the vena cava, producing large arteriovenous
fistulae. In this case, symptoms include tachycardia, congestive heart failure (CHF), leg
swelling, abdominal thrill, machinery-type abdominal bruit, renal failure, and peripheral
ischemia
 Aortoduodenal fistulae: an AAA may rupture into the fourth portion of the duodenum. These
patients may present with a herald upper gastrointestinal bleed followed by an exsanguinating
haemorrhage
Physical examination:
 Abdominal examination includes palpation of the aorta and an estimation of the size of the
aneurysm
 Bruits may indicate the presence of renal or visceral artery stenosis; a thrill is possible with
aortocaval fistulae
 Palpate the peripheral pulses to determine if an associated aneurysm (femoral/popliteal) or
occlusive disease exists
 Flank ecchymosis (Grey Turner sign) represents retroperitoneal haemorrhage

 Transient hypotension should prompt consideration of rupture because this finding can
progress to frank shock over a period of hours
 Temporary loss of consciousness is also a potential symptom of rupture
Radiological examination:
 B-mode ultrasound: used to diagnose and for follow up assessment of size

 CECT: to delineate anatomy
 MRA: has also been used
INDICATIONS FOR INTERVENTION
 Symptomatic aneurysm of any size

 Aneurysm >5.5 cm
 Aneurysm that is increasing in diameter >1cm/year or >0.5 cm/6 months
(UK Small Aneurysm Trial: AAA <5.5 cm were associated with risk of rupture 1% per year.
Operative mortality is 5%. Therefore for AAA <5.5 cm it is recommended for conservative
management with 6-monthly ultrasound to monitor growth)
MANAGEMENT
For elective cases: need to optimize medical conditions (control of BP and other risk factors), stop
smoking, assessment of lung and kidney function, pre-op ECHO
Surgical treatment: either open repair (transabdominal or retroperitoneal) or endovascular repair

(EVAR)
MANAGEMENT OF LEAKING AAA
 90% of patients will die before reaching the hospital

 Those who manage to reach the hospital may be in pain with hypovolaemic shock
 Need to establish at least 2 large-bore intravenous access
 Need to type and crossmatch blood at least 10 units of packed cells, and 1 cycle of DIVC
 Insert a Foley catheter
 Keep SBP 80 - 90 mmHg (permissive hypotension). Studies have shown that keeping
the BP higher may further exacerbate the leaking
 Need to prepare patient for OT stat
 Prepped and draped abdomen whilst patient is awake
 Decompensation can occur with the induction of anaesthesia and loss of abdominal wall
splinting
 Once surgeon is ready only then the patient is intubated
 Incision of choice is midline laparotomy from xiphisternum to suprapubic (can also do
transverse incision across the transpyloric plane)
 Do not give heparin infusion before clamping the aorta as we would normally do for
elective repair
 Use cell saver (autologous blood transfusion) intra-operatively
 May use IV mannitol intra-operatively to prevent renal failure
Postoperative Details
 Fluid shifts are common following aortic surgery.

 Fluid requirements may be high in the first 12 hours, depending on the amount of blood
loss and fluid resuscitation in the operating room.
 Monitor the patient in the surgical intensive care unit for haemodynamic stability,
bleeding, urine output, and peripheral pulses.
 A postoperative electrocardiogram and chest radiograph are needed.
 Prophylactic antibiotics (e.g. Cefazolin at 1 g) are administered for 24 hours.
Follow-up
 The patient is seen in 1-2 weeks for suture or skin staple removal, then yearly thereafter.
COMPLICATIONS OF ANEURYSM REPAIR
 Immediate: haemorrhage, death (5% in elective repair, 50% in emergency repair, visceral
injury
 Early: renal failure, MI, CVA, ischaemic gut, ischaemic foot, spinal cord ischaemia,
pneumonia
 Late: aorto-duodenal fistula, pseudoaneurysm, graft infection
ROLE OF EVAR IN THE TREATMENT OF RUPTURED AAA
 Advantages of EVAR over open repair:

o Safer
o Less invasive alternative to open surgery with the potential to significantly reduce
in-hospital mortality
o May reduce the perioperative mortality
 Disadvantages:
o Not all patients are anatomically suitable for EVAR
o Long-term outcome of EVAR is unknown

o The prerequisite for CT scanning may delay definitive surgery
o Not suitable for patients with haemodynamic instability
o Lack of RCT: most of studies are retrospective, observational and biased
 EVAR as the primary treatment for ruptured AAA is achievable and
appears to be associated with favourable mortality over open repair
with appropriate case selection

VASCULAR
Venous Ulcer
Introduction
 Ulcer is a break in the skin

 Leg ulcer is one of the conditions associated with high morbidity
 Among the causes of leg ulcers are:
o Venous ulcer
o Arterial ulcer
o Neuropathic ulcer
o Diabetic ulcer
o Traumatic ulcer
o Malignant ulcer
o Infective ulcer
Features of Venous Ulcer
 Ulcer edge is irregular

 Base is granulating with exudates
 Skin may be oedematous
 May have skin changes e.g. lipodermatosclerosis, hyperpigmentation
 May be associated with varicose vein
 May have inverted beer bottle leg
Pathophysiology
 Venous ulcer is usually a consequence of chronic venous insufficiency

 Chronic venous insufficiency means that there is a persistent venous hypertension during
exercise as well as during rest
 Venous hypertension is due to blockage of venous flow or reflux disease secondary to faulty
venous valves
 Among the causes are post DVT syndrome and varicose vein
 There are 2 theories associated with venous ulcer: fibrin cuff theory and white cell trapping
theory

 Venous hypertension leads to venous dilatation
 This leads to increased permeability
 As a result, fluid can seep through into the interstitial tissue
 This leads to oedema
 Red blood cell can also seep through into the interstitial tissue and it is later broken down into
haemosiderin and results in hyperpigmentation
 Oedematous tissue later on can undergo fibrosis and thickening resulting in
lipodermatosclerosis
 White cell which is too big to seep through the vein will cause trapping
 It will lead to the release of inflammatory mediators and this can lead to further inflammation
 Fibrin also causes blockage of the venous system causing decrease oxygen and nutrient
going into the tissue
 As a result there is ischaemia and later on develop into ulceration of the skin
Investigation
 Duplex ultrasound: to rule out DVT and venous valve incompetency

 ABSI: need to be done to rule out arterial ulcer
 Hand-held Doppler: to assess all the pulses TRO arterial causes
 Venogram: rarely done
Management
 Conservative
o Reduce weight if obese
o Avoid prolonged standing
o Skin care
o Elevation of leg
o Bed rest
 Graduated compression stocking (GCS)
o Pressure about 18 mmHg at the ankle, 14 mmHg at calf and 4 mmHg at knee
o Grades of GCS:
 Grade 1: 20 mmHg
 Grade 2: 20-30 mmHg
 Grade 3: 30-40 mmHg
 Grade 4: > 40 mmHg
Multilayer bandaging
 Good success rate

 Usually 4 layers
 Clean ulcer, put on Jelonet
o Layer 1: cotton to absorb moisture
o Layer 2: crepe bandage
o Layer 3: compression bandaging; usually done in a figure of 8 manner
o Layer 4: final layer to keep all the layers together
Role of varicose vein surgery
 ESCHAR Trial: compression bandage vs varicose vein surgery

 Surgery was associated with early ulcer healing and decrease recurrent rate
 May consider other varicose vein therapy e.g. sclerotherapy, RFA, laser treatment, SEPS
(subfascial endoscopic perforated surgery)
In non-healing, long-standing ulcer, need to do biopsy to rule out marjolin’s ulcer (squamous cell
carcinoma)
Role of skin grafting
 In clean, non-infected ulcer, skin grafting can be done to assist in healing process
Other methods:
 Hyperbaric oxygen therapy

 Maggot therapy
 These two techniques have been used previously and might help especially in infected ulcer
Differential diagnosis
 Arterial ulcer
 SCC
 Diabetic ulcer
 Neuropathic ulcer
 AVM
 Orthostatic oedema
Classification of Venous Ulcer (CEAP classification)
Clinical signs
C1: Telangiectasia

C2: Oedematous Leg
C3: Varicose vein
C4: Lipodermatosclerosis, hyperpigmentation
C5: Healed ulcer
C6: Active ulceration
Aetiology: congenital, acquired, primary or secondary
Anatomy: deep, superficial or mixed
Pathophysiology: reflux, obstruction or mixed

VASCULAR
Assessment and Management of Patient with Critical Limb Ischaemia (CLI)
Introduction
 Peripheral arterial disease is an important disease causing significant morbidity and mortality
 Limb ischaemia can be acute or chronic
 Chronic limb ischaemia can be divided into intermittent claudication and critical limb
ischaemia
Definition of Critical Limb Ischaemia
 The presence of rest pain requiring maximum analgesia for more than 2 weeks; or the
presence of gangrene or ulcerated foot; or ankle SBP of <50 mmHg or toe pressure <30
mmHg
History
 Rest pain: pain in the foot brought on by going to bed at night and relieved by dangling the
foot out of bed
 May have gangrenous or ulcerated lower limb
Risk Factors
 Smoking, diabetes mellitus, hypertension, hyperlipidaemia, thrombophilia,

hyperhomocystinaemia
 Co-existing vascular disease such as CAD or CVA may be present
 Need to find out the quality of life of the patient, functional status or fitness of the patient
 General examination: BP, PR

 CVS: arrhythmia, murmur, cardiac functional status
 P/A: palpate for AAA
 Pulse: all peripheral pulses should be palpated; present of carotid bruit in the neck, aorta,
femoral, popliteal

 Inspection of lower limb: colour, temperature, muscle atrophy, decreased hair growth
 Hand-held Doppler, ABSI
Imaging
 Duplex ultrasound: non-invasive, no contrast, but operator dependent, difficulty assessing

calcified segment
 MRA: non invasive, no contrast, can get 3D imaging, but not readily available in most centres
and contraindicated in patients with pacemaker, implants etc
 CTA: 3D imaging is possible, but need to use contrast, risk of renal failure and allergy
 Angiography: DSA, gold standard imaging but need to use contrast
Treatment
 Most patients require some form of intervention

 When severe foot infection is present, this needs treating promptly with incision, drainage and
debridement or amputation
 However, if the general condition of the patient appears poor, and the chances of survival
limited due to co-existent pathology, it seems reasonable to treat the patient with analgesia
alone
 If the patient has reasonable quality of life and is likely to survive for more than a few months,
it seems better to attempt revascularization whenever possible
 Patients with fixed flexion deformity and extensive tissue loss usually is managed with
amputation alone
Endovascular Treatment
 Suitable for treatment on 75% of cases

 Need to treat aortoiliac disease first; then only infrainguinal lesion
 Angioplasty and stents are both suitable for aortoiliac disease
 For femoropopliteal disease: angioplasty can be done
 However the use of stent is associated with less successful outcome
Surgical Treatment
 Used for patients who are not suitable for endovascular treatment
 Surgical bypass can be done anatomically or extra-anatomically
 Extra-anatomic bypass is usually reserved for unfit patients
 Autologous vein should be used when possible, due to better patency and resistance to
infection

 Otherwise, grafts that can be used are: Dacron (polyester) or PTFE
 Suprainguinal bypass examples; aortobifemoral bypass, axilllobifemoral bypass
 Infrainguinal bypass examples: femoropopliteal bypass, femorotibial bypass
Non-Interventional Treatment
 Several pharmacological agents have been tried as an alternative to amputation in patients

with non-reconstructable diseases
 Prostacyclin analogue e.g. iloprost; it has anti-platelet, vasodilatory and cytoprotective effect
 Slow release opiate analgesia
 Chemical lumbar sympathectomy
 Dorsal column stimulation
Post Amputation Rehabilitation
 Early rehabilitation
 Use of early walking aid
 Wheelchair and home assessment
 Prosthesis rehabilitation: measurement of first prosthesis can be done at 6-8 weeks from
amputation
 Support for patient and family
Prognosis
 The prognosis for patients with CLI seems poor, as about 25% will die within a year and 50%
within 5 years, mainly from coronary and cerebral vascular disease
Conclusion
 CLI has become a significant problem in the western world

 Many patients can be offered limb salvage but revascularization is often technically
demanding, time-consuming and costly

PLASTIC SURGERY
Burns
Definition
 Tissue injury caused by thermal, radiation, chemical or electrical contact resulting in protein
denaturation, loss of intravascular fluid volume due to increased vascular permeability and
oedema
Pathophysiology of Burns
 Tissue damage → release of vasoactive substance e.g. O2 radicals, prostaglandins,

histamines → increased in capillary permeability → fluid shift to extra vascular compartment
→ oedema
 This leads to decreased in right atrial filling pressures, decreased in cardiac output → shock
 Body’s compensation: tachycardia, increased peripheral resistance
 If it goes uncorrected: decreased cardiac output leads to reduce perfusion of peripheral
tissues & gut → cold, clammy skin, renal failure
Classification
 According to cause: thermal, chemical, electrical, radiation, frostbite, friction (mechanical)

burn
 According to depth of injury:
o 1st degree: epidermis only, red, painful
o 2nd degree: superficial (red, painful), deep (white, discomfort)
o 3rd degree: full thickness (pale, painless)
o 4th degree: muscle involvement
Calculating Size of Burns
 Wallace rule of nines

 Lund-Browder chart
 Using patient’s palm (1%) for estimation
 America Burn Association Burn Severity

Zones of Burn Wounds
 Centre: coagulative necrosis

 Immediate area: zone of stasis
 Further: zone of hyperaemia
Inhalational Burn
 Can cause airway obstruction secondary to reflex laryngospasm, oedema, sloughing of the
mucosa
 Suspect in cases of burn in closed space
 Signs: facial burn, soot in nasopharynx, respiratory distress, coughing up carbonaceous
sputum/soot, hoarseness of voice
Burn Centre Referral Criteria
1. Partial thickness and full thickness burns >10% TBSA in age <10 or >50 years old
2. Partial thickness and full thickness burns >20% in other age group
3. Partial thickness and full thickness burns involving face, genitalia, hands, feet, perineum,
major joints
4. Full thickness burns >5% TBSA
5. Electrical burns
6. Chemical burns
7. Inhalational burns
8. Burns in patients with pre-morbid illness that could complicate management, prolonged the
recovery period, or affect mortality
9. Any burns with concomitant fracture
10. Burn in children admitted to a hospital without qualified personal or equipment for paediatric
case
11. Burn in patients requiring special social, emotional and/or long term rehabilitative support, e.g.
in child abuse cases
Management of Burn
Care at Burn Scene
 Extinguish flame
 Airway management
o 100% via a non-rebreather mask
o If unconscious, intubate
 Assess for other injuries
 Keep warm, NPO, keep patient flat
 Establish 2 large bore branulas
 Give lactated Ringer’s solution running at 1L/hr (in severe burn), otherwise maintenance only
 Transport patient in a clean sheet and blanket
 Small burns may be treated with immediate applications of cool water
Emergency Room Care
 ABC according to ATLS

 CBD, NGT
 Secondary survey
 Give tetanus prophylaxis (no need if last jab <5 years; if >10 years, give booster)
 Calculate BSA
 Pain control: give iv; avoid sc/im; give opioids/NSAIDS
 IV fluid management
o According to Parkland’s Formula: 4ml/kg/TBSA
o Give crystalloids: ringer lactate/Hartmann/normal saline
o Give ½ within 8 hours and another ½ within 16 hours
o Keep urine output >0.5cc/kg/hr
o Other formula available: Brook Army formula, Evans formula
Burn Unit/ICU Care
 Admit to ICU/Burn Unit if severe

 Start PPI or H2 blocker to prevent Curling’s ulcer
 Consider DVT prophylaxis
 Wound care:
o Remove all necrotic tissue and debris

o Rupture blisters except those on palms and soles
o Escharotomy is done if needed
o Can be done without LA
o In extremity with circumferential burn, need to assess these hourly: skin colour,
sensation, capillary refill, peripheral pulses
o Signs indicating poor perfusion: cyanosis, deep tissue pain, progressive parasthesia,
progressive decrease or absence of pulses, sensation of cold extremities
o If initial escharotomy is inadequate, an operative fasciotomy may be needed
 Wound dressing
o Silver sulphadiazine (SSD) can be applied

o Dressing can be:
 Open dressing (no dressing applied e.g. face)
 Exposure dressing: apply soothant e.g. Vaseline
 Occlusive dressing: e.g. for small superficial previously debrided wounds
 Skin grafting
o Artificial skin: can be used, but expensive
o SSG: for burns expected not to heal in 21-30 days
o Full-thickness skin graft: for e.g. grafting across a joint
 Other Considerations
o Upper limb burn: elevate limb to reduce oedema, escharotomy if needed
o Chest burn: escharotomy if needed
Investigation
 FBC, GXM, RP, BUSE, ABG

 Strict I/O
 May need CVP
Nutritional Support
 Preferably enteral
 Burn causes hypermetabolic syndrome
 May need up to 40kcal/kg/day
Physiotherapy
 Chest as well as limb physiotherapy’

 Prevent contracture
 Splint at night
 Encourage movements of limbs to avoid DVT
 Refer occupational therapist
 May need to refer to psychiatrist
Other Considerations
 May need scar revision

 Keloid care
 Pressure garment
 Marjolin ulcer developing in old burn site
Complications of Burns
 Immediate
o Dehydration
o Inhalational injury
o Haemorrhage
o Airway obstruction
o Circulatory collapse
 Early
o Anaemia
o Electrolyte imbalance
o Infection
o ARDS
o Curling’s ulcer
o DVT
 Late
o Keloid
o Hypertrophied scar
o Contracture
o Marjolin’s ulcer

PAEDIATRIC SURGERY
Abdominal Wall Defect in Paediatric Patients
Introduction
 Defects of anterior abdominal wall are usually diagnosed antenatally

 There are 2 distinct defects, namely gastrochisis and omphalocoele
 Both conditions are sporadic with only rare genetic or familial association
Gastrochisis
 Believed to arise from an isolated vascular insult

 Usually occurs to the right of a normal umbilical cord
 In contrast to omphalocoele, there is no membranous sac covering the eviscerated abdominal
organs
 The incidence of associated anomalies is low, but approximately 10% may have intestinal
atresia
Diagnosis is by antenatal ultrasound
Physical examination: abdominal defect to the right of the umbilical cord, no encompassing sac,
and exposed bowel may develop serositis
Management:
 Pre-natal management: delivery should be planned at a tertiary centre with obstetric and
paediatric surgical expertise; delivery at the time of lung maturity may be indicated
 Post-natal management:
 Intravenous fluid: normal saline 20ml/kg bolus, fluid given to achieve urine output of at least
0.5ml/kg/hour
 Heat and fluid losses: can be decreased by covering the exposed bowel with moistened
gauze and then wrapping the bowel with plastic wrap

 Position the neonate in a lateral position to prevent kinking of the bowel and vascular
compromise
 Extension of the fascial defect in the midline for 1 to 2 cm can be done if the bowel mesentery
appears to be compressed by a narrow opening
 Viscera may be reduced primarily, but if this is not possible, viscera are placed in a spring-
loaded or self-made silo, which is secured beneath the fascial edge
 Silo and viscera are gradually reduced over time
 The abdominal wall defect is then repaired in a primary fashion on an elective basis
 Complications: bowel ischaemia, short gut, bowel non-rotation, feeding intolerance
Omphalocoele
 An abdominal wall defect of the umbilical ring in which the intestine protrude through the base
of the umbilical cord and herniate into a sac
 High incidence (50%) of related anomalies (cardiac, chromosomal)
 Diagnosis is by antenatal ultrasound
 Because of the high incidence of related anomalies, the presence of omphalocoele should
direct a thorough search for other birth defects by ultrasonography and ambiocentesis
 Amniotic fluid AFP are elevated
 Physical examination: abdominal wall defect at the base of the umbilical cord, the presence of
a sac covering the herniated viscera, rupture of the sac is infrequent
 Management: care for these patients are the same as gastrochisis
 Due to the presence of other anomalies associated with omphalocoele, the overall prognosis
is significantly worse than that for gastrochisis

PAEDIATRIC SURGERY
Pyloric Stenosis
Introduction
 Pyloric stenosis is a condition whereby there is thickening of the pyloric muscle causing
gastric outlet obstruction
Epidemiology
 Occur in 1 in 400 birth

 Male: female ratio 4:1
 Usually first born male
 May have genetic predisposition
Aetiology
 Unknown, could be congenital or acquired

 Acquired condition is thought to be due to functional hypertrophy that develop in first weeks of
life
Presenting Symptoms
 Usually present between 3 weeks to 3 months of life

 Unusual to present after 6 months
 Projectile, non-bilious vomiting
 Baby is hungry in between the feeds
 May be dehydrated with sunken fontanelle, dry tears and listless
 May hay weight loss
Clinical Examination
 ‘Test feed’ can be given

 There will be palpable olive-shaped mass in the abdomen
Investigations

Blood:
 Low chloride level

 Low potassium level
 High pH
 High haematocrit
 A secondary hyperaldosteronism may develop secondary to the hypovolaemia
 Hb may be low
 On ABG there is hypochloraemic hypokalaemic metabolic alkalosis
 Due to the metabolic alkalosis, the body mat compensate by hypoventilating resulting in
increased PaCO2
AXR:
 Abdominal xray may show dilated stomach with air-fluid level in the stomach
U/S:
 Will show thickened and elongated pylorus

 Length >15 mm and muscle wall >4mm is diagnostic of pyloric stenosis
Management
Resuscitation
 Need to correct dehydration

 Give 20 ml/kg bolus
 Use 1/2NSD5% for maintenance fluid
 Make sure adequate urine output is achieved
 Need to correct electrolytes imbalance
 Need to correct alkalosis
 All these will take about 24-48 hours
Medical Treatment
 Once resuscitated, there is a role of medical treatment. Oral atropine has been used before.
Success rate is about 80-90%. However it is associated with prolonged hospital stay and
may fail.
Surgical Treatment

 Surgical correction with pyloromyotomy gives almost 1100% success rate. This is often done
via Ramstedt’s pyloromyotomy. This can either be done laparoscopically or via open surgical
method. The pyloric muscle is cut longitudinally across from the antrum until duodenum until
mucosa is reached.
Complications of surgery:
 Bowel perforation
 Incomplete pyloromyotomy

PAEDIATRIC SURGERY
Hirschsprung’s Disease
Introduction
 A congenital megacolon caused by malformation in the pelvic parasympathetic system which

results in absence of ganglion cells in Auerbach’s plexus and hypertrophy of associated nerve
trunks
Cause
 Not fully understood

 Thought to result from a defect in the migration of neural crest cells, which are the embryonic
precursors of the intestinal ganglion cells
 Under normal conditions, the neural crest cells migrate into the intestine from cephalad to
caudal
 The length of the aganglionic segment of bowel is determined by the most distal region that
the migrating neural crest cells reach.
 Most cases of aganglionosis involve the rectum and rectosigmoid. In rare instances, total
colonic aganglionnosis may occur
 Patients with Hirschsprung’s disease have an increased frequency of mutations in several
genes, including GDNF, its receptor ret, or its co receptor Gfra-1
Clinical
 Sporadic in 1 in 5000 live births

 Characterized by functional distal intestinal obstruction
 Abdominal distension, failure to pass meconium, bilious emesis
 Some may present with enterocolitis (abdominal distension, tenderness and systemic toxicity)
 On pr examination, forceful propulsion of foul-smelling liquid faeces is typically present, and
represents the accumulation of stool under pressure in an obstructed distal colon.
Initial Treatment
 Rehydration
 Systemic antibiotic
 NGT
 Rectal irrigation
 If not responding: to do defunctioning colostomy
 It is important to ensure that this stoma is in ganglion-containing bowel, which must be
confirmed by frozen section at the time of stoma creation
 Diagnosis
 Rectal biopsy
o Samples of mucosa and submucosa are obtained at 1 cm, 2 cm and 3 cm from the
dentate line
 Histopathology findings
1. Absence of ganglion cells in the myenteric plexus

2. Increased acetylcholinestarase-positive nerve fibres
3. The presence of hypertrophied nerve bundles
 Barium enema
o May demonstrate the location of the transition zone between the dilated ganglionic
colon and the distal constricted aganglionic rectal segments
Treatment
 Surgery
 Multiple stage procedure
o Defunctioning colostomy
o Definitive pull-through operation after the child weighed over 10 kg
 Principles of treatment: resects the aganglionic segment, perform an anastomosis of
ganglionated bowel to either the anus or a cuff of rectal mucosa
 Pull-through procedures:
o Swenson procedure
o Duhamel procedure
o Soave’s procedure
 The main complications of all procedures include post operative enterocolitis, constipation
and anastomotic stricture
If total colonic aganglionosis, the ileum is used for the pull-through segment

PAEDIATRIC SURGERY
Necrotizing Enterocolitis (NEC)
Introduction
 NEC is a condition primarily seen in preterm infants where part of the bowel undergoes
necrosis
Risk Factors
 Prematurity
 Initiation of enteral feeding
 Bacterial infection
 Intestinal ischaemia resulting from birth asphyxia
 Umbilical artery cannulation
 Persistence of a patent ductus arteriosus
 Cyanotic heart disease
 Maternal cocaine abuse
Bacteriology
 Common bacterial isolates from the blood, peritoneal fluid, and stool of infants with advanced
NEC include E. coli, Enterobacter, Klebsiella, and occasionally coagulase negative Staph
species.
Oral prophylaxis with vancomycin or gentamicin reduces the incidence of NEC
NEC may involve single or multiple segments of the intestine, most commonly the terminal ileum
Gross findings of NEC: bowel distension with patchy areas of thinning pneumatosis, gangrene or
frank perforation
Pathogenesis
 Perinatal stress (e.g. respiratory distress syndrome) → Periods of intestinal hypoperfusion →

Periods of reperfusion

 The combination of ischaemia and reperfusion leads to mucosal injury
 The damage intestinal mucosa can then be readily breached by the intestinal flora that
translocate across it → initiate cascade of inflammation → more mucosal injury → NEC
Clinical Manifestations
 Bell Stage I: intolerance to feeding, manifested by vomiting or by finding a large residual

volume from a previous feeding in the stomach at the time of the next feeding
 Bell Stage II: abdominal distension and tenderness, bilious nasogastric aspirated, bloody
stools, may be in sepsis
 Bell Stage III: peritonitis, acidosis, sepsis, DIC, death
AXR findings of NEC
 Pneumatosis intestinalis (represents invasion of the ischaemia mucosa by gas-producing

microbes)
 Presence of ileus
 Presence of portal venous gas
 Dilated loops of bowel
 Paucity of gas
 Pneumoperitoneum (i.e. perforation has occurred)
Treatment
 Stop feeding
 NGT
 Broad-spectrum antibiotics
 May need intubation and ventilation
 TPN
 Stage I Bell:
o NBM, IV antibiotics for 7-10 days, then restart feeding
 Stage II Bell:
o Close observation, if fails to improve after several days of treatment consider
exploratory laparotomy
 Stage III Bell:
o Exploratory laparotomy
o Resects gangrenous/perforated bowel
o Intestinal ends are brought out as stomas
o May need second look laparotomy once stabilizes 24-48 hours later
o Or alternatively drain the peritoneal cavity

o Infants who do not respond to peritoneal drainage alone after 48-72 hours should
undergo laparotomy

PAEDIATRIC SURGERY
Choledochal Cyst
Introduction
 Dilatation of the biliary ductal system

 5 types are described:
o Type I: fusiform dilatation (most common)
o Type II: diverticulum of CBD
o Type III: choledochocoeles; cyst arises from the intraduodenal portion of CBD
o Type IV: A: intra- and extrahepatic dilatation, B: extrahepatic dilatation
o Type V: Caroli’s disease; dilatation of intrahepatic ducts only
Aetiology
 Common channel
 Abnormal pancreatic and biliary duct junction, with the formation of a common channel into
which pancreatic enzymes are created
 This results in weakening of the bile duct wall by gradual enzymatic destruction, leading to
dilatation, inflammation and finally cyst formation
 But not all patients with choledochal cyst demonstrate an anatomic common channel
 Female: male, 4:1

 Symptoms: abdominal pain, mass and jaundice
 If not recognized will lead to cholangitis → cirrhosis → portal hypertension
Diagnosis
 Ultrasound
 CT scan abdomen
 MRI
 ERCP: for patients in whom confusion remains after evaluation by less-invasive imaging
modalities

Treatment
 The cyst wall is composed of fibrous tissue and is devoid of mucosal lining
 Treatment is surgical excision followed by biliary-enteric reconstruction
 Choledochal cyst can lead to the development of a biliary tract malignancy
Complications
 Anastomotic stricture
 Cholangitis
 Intrahepatic stone formation

CARDIOTHORACIC
Flail Chest
Introduction
 Flail chest is a life threatening emergency following a blunt chest trauma.

 Definition of flail chest: Fracture of at least 3 or more consecutive ribs at 2 or more segments.
 A flail chest occurs when a segment of the thoracic cage is separated from the rest of the
chest wall.
 The main significance of a flail chest is that it indicates the presence of an underlying
pulmonary contusion.
Diagnosis
Symptoms:
 Chest wall pain on inspiration or palpation, difficulty in breathing
Signs:
 Paradoxical chest wall movement (in drawing on inspiration and moving outwards on
expiration)
 Tenderness, crepitus, broken ribs felt on palpation of the chest wall
Chest X-Ray:
 The anterior-posterior x-ray view of the chest will identify most significant chest injuries.
 Other injuries associated with broken ribs are pneumothorax, haemothorax and pulmonary
contusion.
Computed Tomography Thorax:
 Computed tomography provides very little further clinical information and is not indicated for
the initial evaluation of chest wall injuries.

Arterial Blood Gas
 Arterial blood gas measurements show the severity of the hypoventilation created by both the
pulmonary contusion and the pain of the rib fractures, and are helpful at baseline to assess
the need for mechanical ventilation and to follow the patient during management.
Pathophysiology
 In flail chest, there is paradoxical movement of the chest as the affected segment does not
move in concert with the rest of the normal lung
 During inspiration, reduced expansion of the lung means less oxygen delivery to alveoli
 Large pulmonary contusions also inhibit gas exchange
 All these will impair oxygen delivery to the tissue and as a result there is hypoxia
 There will also be inadequate carbon dioxide exchange leading to hypercapnia
 Carbon dioxide accumulation may result in acidosis
 There is also a pendulum effect whereby the air from the affected lung will shift to the non-
affected lung like a pendulum due to pressure difference
Management
 Management of chest wall injury is directed towards protecting the underlying lung and
allowing adequate oxygenation, ventilation and pulmonary toilet.
 Initial management should follow the ATLS guideline in trauma where airway, breathing and
circulation is managed as appropriately indicated
Analgesia
 Analgesia is the mainstay of therapy for rib fractures.

 Opioid analgesics are useful, but when used as the sole analgesic agent may require such
high doses that they produce respiratory depression.
 Patient controlled administration of an opioid infusion (PCA) is the best method for
cooperative patients.
 The addition of a non-steroidal anti-inflammatory agent may provide adequate relief.
 The best analgesia for a severe chest wall injury is a continuous epidural infusion of a local
anaesthetic agent (+/- an opioid). This provides complete analgesia allowing normal
inspiration and coughing without the risks of respiratory depression. Epidurals may be placed
in the thoracic or high-lumbar positions.
 For one or two isolated rib fractures, posterior rib blocks may be appropriate. Local
anaesthetic is infiltrated around the intercostal nerve posteriorly. These blocks will last 4-24
hours and will then have to be repeated.

Chest Physiotherapy
 It is imperative that patient is started on chest physiotherapy early

 They should be encouraged to do deep breathing exercise and incentive spirometry
 Saline nebulisers and expectorant medication (for example bisolvon) could be started to
loosen up the mucus in the bronchial tree
Intubation & Ventilation
 Intubation and mechanical ventilation is rarely indicated for chest wall injury alone.
 Where ventilation is necessary it is usually for hypoxia due to underlying pulmonary
contusions.
 Positive pressure ventilation may be required for severe chest wall instability resulting in
inadequate spontaneous ventilation.
 Intubation and ventilation may be required when anaesthesia is necessary to provide
immediate and adequate analgesia and allow further assessment and management.
 Ventilation is usually necessary only until the resolution of the pulmonary contusion.
Chest Tube Insertion
 Patients with rib fractures who receive positive pressure ventilation are at an increased risk of
developing a pneumothorax or tension pneumothorax due to laceration of the lung by the
sharp fracture end.
 Many authors recommend placement of a prophylactic chest tube for all patients with rib
fractures who receive mechanical ventilation.
Rib fracture fixation
 Surgical stabilization of the chest wall is rarely required

 Both external and internal stabilization has been advocated
 In general, operative fixation is most commonly performed in patients requiring a thoracotomy
for other reasons or in cases of gross chest wall deformity.
Complications
 Long term complications include persistent chest wall pain, deformity, and dyspnoea on
exertion
Outcome & Prognosis
 Overall, patients with flail chest have 5-10% reported mortality if they reach the hospital alive.

 Patients who do not need mechanical ventilation do better.
 Most patients do well and return to normal function after 6-12 months.
Conclusion
 Flail chest is a life threatening injury and need to be appropriately managed

UROLOGY
Benign Prostatic Hyperplasia (BPH)
Introduction
 BPH is a common condition affecting men with advancing age

 The incidence of BPH in 50 years old men is 50% and in 80 years old man is 80%
Aetiology
 Thought to be related to:

o Hormones: balance between testosterone, oestrogen, prolactin and growth factors
o Age: the mesenchymal theory that apoptosis of cells is slowed in favour of cell
proliferation with advancing age
Pathophysiology
 Symptoms are related to either the obstructive component of the prostate (obstruction
symptoms) or to the secondary response of the bladder to the outlet resistance (irritative
symptoms)
 Obstruction can wither be due to mechanical obstruction or dynamic obstruction
 Mechanical obstruction may result from intrusion of the prostate into the urethral lumen or
bladder neck
 The dynamic obstruction is due to the increased tone in the prostatic urethra
 The irritative symptoms results from secondary response of the bladder to the increased
outlet resistance
 Bladder outlet obstruction leads to detrusor muscle hypertrophy and hyperplasia
 This leads to decrease in bladder compliance and detrusor muscle instability also occurs
 Irritative symptoms: frequency, urgency, nocturia, dysuria (FUND)

 Obstructive symptoms: hesitancy, incomplete voiding, poor stream, slow flow, straining
(HIPSS)
 Patient may also present with symptoms of complications:

o Acute urinary retention: suprapubic pain, incomplete urination
o Chronic urinary retention: painless
o Signs of UTI: fever, dysuria, frequency
o Pyelonephritis: fever, vomiting, flank pain
o Renal failure: scrotal oedema, leg oedema
 General examination: anaemia (CRF), oedema (ARF), fever (UTI)

 Abdominal examination: full bladder, flank distension
 DRE: normal anal sphincter tone; prostate firm, smooth and enlarge
 Neurological examination: to rule out neurogenic bladder
Investigations
Blood investigations:
 FBC: RaisedTWC to rule out UTI

 BUSE, creatinine
 PSA (normal 0-4 ng/dl)
Urinalysis
 Dipstick TRO UTI

 Microscopy
Urodynamic study
 TRO neurogenic bladder
Uroflow:
 Qmax us the max flow rate in ml/sec

 Qmax 10ml/sec us the cut off for intervention
Imaging
 Abdominal ultrasound
o Size of prostate
o Assessment of upper tract
o Post void urine

 TRUS: TRO prostate cancer
 IVU: if any features of renal failure
 MCU: TRO other causes e.g. stricture, calculi
Assessment of Severity
 The severity of BPH symptoms is assessed by the International Prostate Symptom Score
(IPSS)
 It is a set of questionnaires with maximum mark of 35
 IPSS is used to assess severity of symptoms, monitor progression of symptoms, determine
treatment for patients
Treatment of BPH
Management of patient with AUR
 In patients who come with AUR, the first treatment would be to relieve the urinary retention
either via CBD or SPC
 Then an α1 blocker is started
 We can try trial of void after 2 weeks of therapy
Watchful waiting
 For mild BPH according to IPSS

 No complications from the BPH
 No progression of symptoms
Medical treatment
 α-1 blocker only

o selective: tamsulosisn, alfazocin
o non-selective: doxazocin,, terazocin
o advantages: fast relieve of symptoms
o works in bladder and prostate smooth muscle
o may cause postural hypotension esp. with non-selective type
 5-α reductase inhibitor only
o Example fenesteride, dutasteride
o Inhibits conversion of testosterone to DHT
o Used in large prostate volume
o May take 3-6 months to show improvement
o Will reduce PSA level
o Can cause impotence, retrograde ejaculation, loss of hair
 Combination therapy α-1 blocker and 5-α reductase inhibitor
o These combinations may be continued indefinitely
o However recent studies have shown that stopping the α-1 blocker after 6 months of
combination therapy is feasible
 Phytotherapy
o Saw palmetto berries
o Not proven to be effective
Surgery
 Indication for surgical management:

o Recurrent UTIs
o Renal failure
o Prostatic calculi
o Worsening IPSS
o Qmax < 10m/s
o Failed medical therapy
o Upper tract complications e.g. hydronephrosis
o Patient’s choice
 Surgery can be divided into minimally invasive and invasive
 Minimally invasive
o Intraprostatic stent
o Balloon dilatation
o Laser
o Thermal ablation
o Cryotherapy
o Bladder neck incision
o High intensity focused ultrasound (HIFU)
o Transurethral needle ablation (TUNA)
 Invasive surgery
o Transurethral resection of prostate (TURP)
o Transurethral incision of prostate (TUIP)
o Transurethral laser-induced prostatectomy (TULIP)
o Open prostatectomy:
 Retropubic approach
 Suprapubic approach
 For larger prostate (>75g)
TURP

 Standard of surgery
 Complications
o Early: TURP syndrome, haemorrhage, infection, prostatitis
o Late: retrograde ejaculation, impotence, stricture, recurrence, incontinence

UROLOGY
Haematuria
Definition
 The presence of blood in the urine

 All haematuria should be investigated
Classification
 Microscopic haematuria:
o 2-5 RBC per HPF
 Macroscopic haematuria:
o Gross blood in the urine
o Beware of beetroot, rifampicin, or phenothiazide that can colour the urine
 Dipstick haematuria:
o High sensitivity, low specificity
o All dipstick haematuria should be investigated with microscopy
Causes
 In 60%, no cause is found

 Malignancy: bladder, kidney, ureter, urethra, prostate
 Infection/inflammation: cystitis
 Stone: in bladder, kidney, ureter
 Haematological: caogulopathies
 Nephrological: e.g. nephritic syndrome
 BPH: bleeding from enlarged tortuous veins on the gland
 Post operative: e.g. TURP
 Others: strenuous exercise, chemo/radiotherapy
History
 Age: older age suspect malignancy

 Male: prostate/bladder causes

 Female: ?UTI
 Occupation: dye industry, rubber industry more prone to develop TCC
 Smoking: more prone to develop TCC
 FH
 DH e.g. rifampicin
 Previous radio- or chemotherapy
Examination
 Urine
o Dipstick
o FEME
o C&S
o Cytology
 Blood: FBC, RP, PT/APTT
 Flex/rigid cystoscopy
 US abdomen/pelvis
 IVU
 CT/CTU
 MRI
 24 hours urine collection or renal biopsy (TRO renal cause of haematuria)
Management of Intractable Bleeding of Bladder Tumour
 Angioembolization
 Alum, formalin
 Tumour debulking
 Palliative DXT
 Cystectomy

UROLOGY
Stone Passage
Predictors of passage of stone:
 Size: smaller stone is more likely to pass out

o Size <2mm more likely to pass
o Size 2-6 mm: moderate chances to pass
o Size >6mm: unlikely to pass
 Right stone is more likely to pass
 Position: distal more likely to pass
 Degree of hydronephrosis: less hydronephrosis more likely to pass
Medical Explusive Therapy (MET)
 Only to be used if patient has normal renal function and well-controlled pain
 Usage of alpha blocker e.g. Tamsulosis
 Only used fro distal ureteric stone and stone less than 10 mm
 Give therapy for 1 month
 The use of buscopan for stone expulsion is not supported
 5-10mg of prednisolone for 1 week may help to expel stone
 Oral chemolysis e.g. Ural, is only used for small uric acid stone. Early morning urine ph of
6.5–7.0 is required if chemolysis is planned.
 Allopurinol is used to prevent stone recurrence in uric acid stone
 The use of buscopan to expulse the stone: not supported
 If stone has not been passed after 6 weeks: unlikely it will pass

Laparoscopic Surgery
Introduction
 Also called minimally invasive surgery (MIS) or keyhole surgery

 A modern surgical technique in which operations in the abdomen are performed through small
incisions (usually 0.5-1.5cm) as compared to the larger incisions needed in conventional open
laparotomy
 It uses images displayed on TV monitor for magnification of the surgical elements
Types of surgery that can be done laparoscopically: cholecystectomy, appendicectomy,

adrenalectomy, hernia surgery etc
Advantages of laparoscopic surgery
 Less patient discomfort

 Shorter hospitalization
 Rapid convalescence
 Better cosmetically
Disadvantages of laparoscopic surgery
 Lack of tactile feedback from tissues

 Long learning curve
 Poor depth perception
Contraindications
Absolute contraindications
 Uncorrectable coagulopathy
 Inability to tolerate general anaesthesia
 Decompensated shock
 Patient refusal

Relative contraindications
 Previous abdominal surgery

 Peritonitis
 Pregnancy
 Massive abdominal distension
 Severe cardiopulmonary disease
Techniques for assessing the peritoneal cavity:
 Open technique (Hasson’s)

 Closed technique (veress needle)
Methods to assess whether the position of the port is in the peritoneal cavity or not?
 Elevated pressure – not in-situ

 Low flow – not in-situ
 Machine making noises – not in-situ
 Loss of liver dullness – in-situ
Complications of laparoscopic surgery
Specific
Immediate
 Extra-peritoneal insufflation
 Injury to intra-abdominal viscera or vessels
 Injury to blood vessels at anterior abdominal wall or retroperitoneum
Early
 Shoulder tip pain

 CO2 retention especially in COAD patient
Late
 Incisional hernia, port size metastases
General
Immediate
 Bradycardia
 Inadequate oxygenation secondary to splinting of diaphragm
 Pneumothorax
 Pneumomediastinum
 Gas embolism
Early
 DVT/PE
 Hypothermia
 Nausea and vomiting
Gases used to create pneumoperitoneum: CO2, helium, nitrous oxide, argon
Advantages of using CO2:
 Absorbed by the human body

 Removed by the respiratory system
 Non-flammable
 Odourless
Disadvantages of using CO2:
 Can be retained causing CO2 retention

 Splinting of diaphragm
When to convert to open surgery?
 Failure to progress for example due to dense adhesions, poor exposure

 Surgeon experience is lacking
 Discovery that the disease is not appropriate for minimally invasive methods for example gall
bladder cancer
 Technical problem or instrument malfunction
 Severe bleeding or bowel injury

Laparotomy Wound Dehiscence
Introduction
 Wound dehiscence affects about 2% of mid-line laparotomy wound

 Due to failure of wound-closure technique
 Can be divided into open (burst abdomen and superficial wound dehiscence) and closed
(incisional hernia)
Risk factors for wound dehiscence
 Patient factor: malnutrition, anaemia, jaundice, immunocompromised, steroids, diabetic,

hypoxaemia, smoker, chemotherapy, radiotherapy, obesity, sepsis, uraemia, malignancy
 Surgery factor: closed under tension, no haemostasis, inadequate blood supply, emergency
operation, re-laparotomy
 Disease factor: carcinomatosis, intra-abdominal sepsis, presence of ascites/wound infection
Prevention of wound dehiscence
1. Sound surgical technique
 Appropriate suture material

 Suture length to wound ratio is at least 4:1 (Jenkin’s rule)
 Minimum of 1 cm bites at 1 cm intervals
 Properly laid knots with sufficient throws
 Avoidance of excessive tension
 Restoration of normal anatomy
 Good haemostasis
 Choice of incision
 Selective use of drains
 Minimal tissue dissection
2. Minimize risk of infection

 Ensuring skin is shaved as late as possible
 Adequate skin preparation
 Appropriate use of prophylactic antibiotics for high risk patients and procedure
3. Optimal management of pre-morbid
 Good diabetic control

 Correct anemia/malnutrition
 Stop smoking
 Reduce weight
Management of superficial wound dehiscence
 Can be managed conservatively

 Regular inspection
 Appropriate dressing
 Involve specialist tissue viability nurse
 If infective collection present, drain
 If cellulitis present, to give antibiotics
 May need to remove suture/clips
 May need debridement/de-sloughing
 May need delayed primary closure
Management of complete wound dehiscence/burst abdomen
 A surgical emergency
 Close with sterile dressing first whilst waiting for OT
 Remove previous sutures
 Debride the edges
 May need re-suturing or retention sutures
 Leave skin open
 Need to watch out for abdominal compartment syndrome
 If not able to close (due to loss of domain or unhealthy tissue), use laparostomy
 Can use Bogota/Silo bag, sandwich Opsite dressing, vacuum dressing
Management of incisional hernia
 If wide neck, can treat conservatively with the use of corset and avoid the need for operation
 If the neck of the hernia is small, there is higher risk of strangulation, therefore surgery is
usually indicated

 If overweight, need to reduce weight prior to operation
 Can be repaired in the conventional open method or laparoscopic method
 Laparoscopic repair: apply mesh below the peritoneum layer, defect is not approximated
 Small defects, less than 4 cm: repaired using suture technique (using non-absorbable
material) or Mayo’s repair technique (overlap, 2cm, interrupted & reinforced by
continuous/monofilament suture)
 Large defects, or poor tissue, are best repaired with a synthetic patch/mesh
 The mesh may be applied at 3 levels:
o Inlay: Mesh sutured to the edges of defect without closing the defect, not
recommended unless there is a substantial defect that cannot be closed with other
techniques
o Onlay: Repair the rectus continuously and put mesh on top, make skin flap > 5cm,
mesh size 5cm beyond the margin of the defect in all directions
o Sublay: Repair the peritoneum and posterior rectus sheath then put mesh on top
before closing the anterior rectus sheath

ARDS
Introduction
 Acute respiratory distress syndrome

 Used to be known as adult respiratory distress syndrome, but it was a misnomer as it can
occur in children too
 Typified by many inflammatory insults to the lungs
Definition
 ARDS: PaO2/FiO2 <200

 Acute Lung Injury (ALI): PaO2/FiO2 <300
 The presence of:
o Bilateral pulmonary infiltrates on CXR
o PCWP <18 mmHg
o The absence of left atrial hypertension
o Acute onset
Aetiology
 Alveolar damage
 Endothelial damage causes increased permeability
 Presence of protein exudates in the alveoli
 Resolution can also occur, but usually via pulmonary/alveoli fibrosis
Causes
 Direct injury to the lungs: pulmonary contusion, pneumonia, aspiration pneumonitis, PE, etc
 Indirect injury to the lungs: burns, sepsis, trauma, acute pancreatitits, etc
Clinical features
 Acute respiratory failure

 Presence of hypoxaemia
 Hypoxaaemia intractable to increased O2 supply
 Bilateral pulmonary infiltrates on CXR
 Can lead to pulmonary hypertension and right heart failure
 Mortality 20 - 50%
Characteristics
 Acute lung injury, within 1 week of an apparent insult and with progression of respiratory
symptoms
 Bilateral opacities on chest imaging not explained by other pulmonary pathology
 Respiratory failure not explained by heart failure or volume overload
 Decrease arterial PaO2/FiO2 ratio
o Mild ARDS: 201-300 mmHg
o Moderate ARDS: 101-200 mmHg
o Severe ARDS: <100 mmHg
Management
 Ventilatory and Oxygen support

 PEEP is used in mechanically ventilated patients with ARDS to improve oxygenation
 Avoid over hydration
 Address nutritional support
 Careful fluid balance: better prognosis in patients where PWP is lowered by diuresis or fluid
restriction
 Treat sepsis
 Prone position: might improve oxygenation by relieving atelectasis and improving perfusion

Transfusion Related Acute Lung Injury (TRALI)
Definition
 ALI occurring within 6 hours of completion of transfusion of blood component

 There is no pre-existing acute lung injury
Introduction
 Acute onset, non-cardiogenic pulmonary oedema following transfusion of blood products

 Typically associated with platelets and FFP transfusion
 It is due to the presence of leucocyte antibodies in the transfused plasma
 Incidence is 1 in 5000 transfusion
 Leuko-agglutination and pooling of granulocytes in the recipient’s lung may occur → release
of contents of leucocytes granules → injury to cellular membranes, endothelial surfaces and
potentially lung parenchyma
 ARDS may occur as a result of this phenomenon
 TRALI features: sudden dyspnea, severe hypoxaemia (Sat O2 < 90%), hypotension, fever,
PaO2/FiO2 < 300 mmHg on room air, bilateral infiltrates on CXR
 Usually resolves with supportive care within 48 to 96 hours
 CXR will return to normal within 48 to 96 hours
 TRALI: normal CVP, JVP, PCWP and does not respond to diuretics
Pathophysiology
 ↑ pulmonary vascular permeability

 ↑ protein in the oedema fluid
Treatment
 Supportive
 Oxygen supplementation
 Aggressive respiratory support
 IV fluids
 Vasopressors

 Use of diuretics (which is indicated in transfusion associated circulatory overload) should be
avoided in TRALI
 Corticosteroids can be beneficial
Differential diagnosis
 Transfusion-associated circulatory overload (TACO)

 Cardiogenic oedema
 Anyphylactic transfusion reaction
Mortality
 6-9%

Post Operative Pain
Introduction
 Definition: Pain is unpleasant sensation or emotional experience that is associated with

actual or potential tissue damage
 Types of pain: acute or chronic pain, neuropathic pain, phantom pain, psychogenic pain
Effects of post-operative pain
 Respiratory: reduced cough reflex, inadequate sputum expectorant, atelectasis

 Gastrointestinal: reduced gut motility, nausea, vomiting
 Musculoskeletal: reduced mobility
 Genitourinary: urinary retention
 CVS: increased myocardial O2 consumption, hypoxaemia
Assessment of pain
 Pain is a very subjective subject

 There are multiple ways used to assess pain, for example: visual analogue score (VAS),visual
numerical assessment
Management of pain
 Management of pain can be divided into non-pharmacological and pharmacological methods

 Non-pharmacological method:
o Adequate explanation and reassurance
o TENS (transcutaneous electrical nerve stimulation)
o Hypnosis
o Cold or heat treatment
o Relaxation therapy
o Cognitive behaviour therapy
 Pharmacological method:
o Simple analgesia

 Paracetamol has a weak anti-inflammatory and analgesia effect
 Can be given orally or rectally
 Modulates prostaglandin production in CNS
o NSAIDS
 Inhibits cyclo-oxygenase enzyme
 Reduces prostaglandin, thromboxane, prostacyclin production
 Weak central analgesic effect
 Side effects: GI upset (nausea and vomiting), PUD
 Examples of COX-1 inhibitors are ibuprofen, mefenamic acid
 Example of COX-2 inhibitor is celecoxib
o Opiates
 Can be divided into weak and strong opiates
 Weak opiate example is dihydrocodeine
 Strong opiate examples are morphine and pethidine
 Can be given orally, intramuscularly, subcutaneously, intravenously or
intrathecally
 Side effects are respiratory depression, nausea and vomiting, constipation
 Works on μ receptors
 Can also be given as PCA (patient-control analgesia)
o Local anaesthesia
 For example giving local anaesthetic on wound before closing the skin
 Nerve/plexus blockage
When deciding to give analgesia for post-operative pain, we can use the WHO step ladder
 Step 1: simple analgesia e.g. paracetamol, NSAIDS

 Step 2: weak opiate ± step 1
 Step 3: strong opiate ± step 2
Ways of giving analgesia: oral, iv, im, sc, PCA, epidural, spinal
Gate control theory of pain
 Proposed in 1965
 The idea that physical pain is not a direct result of activation of pain receptor neurons but
rather its perception is modulated by interaction between different neurons
 Both thin (pain) and large diameter (touch, pressure, vibration) nerve fibres carry information
from the site of injury to two destinations on the dorsal horn of spinal cord: transmission
cells that carry the pain signal up to the brain and inhibitory interneuron that impede
transmission cell activity

 Thin fibres impede inhibitory cells and large fibres excites
 The more the large fibre activity relative to thin fibre activity at the inhibitory cell, the less pain
is felt
Pain fibres
 A-α: thicker, carry faster pain sensory, perceived as sharp pain

 C fibre: thinner, dull aching pain, slower transmission
 A-β: carry touch, pressure, vibration sensations

Ventilator Associated Pneumonia (VAP)
Definition
 Pneumonia that develops 48 hours or longer after mechanical ventilation is given by means of
ETT or tracheostomy
 Results from invasion of lower respiratory tract by microorganisms
Epidemiology
 28% of the patient on ventilator

 Incidence increases with the duration of mechanical ventilation
 Mortality 27-76% (esp. with pseudomonas and acinetobacter)
Types
 Can be divided into early onset (within 4 days of duration) or late onset (> 5 days after
admission, usually associated with MDR)
Risk Factors
 Hospitalisation (current) > 5 days

 Hospitalization > 2 days in the preceding 90 days
 Antibiotic use in the previous 90 days
 Residence of nursing home
 Home infusion therapy or wound care
 Long-term dialysis within 30 days
 Immunocompromised
Diagnostic Triad
 Pulmonary infection (fever, purulent secretion, leucotoid)

 Bacteriologic evidence of pulmonary infection

 Radiologic suggestion of pulmonary infection
Reducing Risk of VAP
1. Avoid invasive ventilation - choose non invasive esp. in COAD patients, immunocompromised
patients, respiratory failure
2. Orotracheal and orogastric tubes are preferred over nasal devices
3. Continuous aspiration of subglottic secretions
4. Passive humidifiers or heat moisture exchangers – to reduce colonization of the ventilator
circuit
5. Protocols for sedation and weaning should be applied to reduce the duration of mechanical
ventilation
6. Feeding - avoid semi-recumbent feeding
7. Prevention of stress related bleeding e.g. with PPI, sucralfate
8. Prevention of VTE
9. Use of antibiotics and control of colonization – rinses with oral chlorhexidine
Lab Studies
 Increased WCC
 Blood cultures
 Baseline renal profile and LFT for dosing of antibiotic
 Samples of respiratory secretion from lower tract
o BAL
o Bronchoscopy-guided protection-specimen brush sampling
 Procalcitonins
Imaging
 Portable CXR - Air bronchogram

 Chest CT
 U/S chest
Selection of Antibiotics
 In early onset VAP, no risk factors for MDR:

o Ceftriaxone
o Fluoroquinolones
o Ampicillin-sulbactam
o Ertapenem
 For late onset risk factors or MDR present
o Anti-pseudomonal cephalosporin (e.g. cefipime, ceftazidime)
o Anti-pseudomonal carbapenems (imipenem or meropenem)
o β-lactam/β-lactamase inhibitors (Tazocin) with an anti-pseudomonal fluoroquinolone
(ciprofloxacin) or aminoglycoside plus linozolid or vancomycin
Complications of VAP
 Abscess
 Empyema
 Super infection
 Concomitant infection

WHO Guidelines for Safe Surgery
Introduction
 Complications of surgical care have become a major cause of death and disability worldwide
 WHO guideline for safe surgery was creased to avoid these surgical complications
Objectives for Safe Surgery
1. The team will operate on the correct patient at the correct site
2. The team will use methods known to prevent harm from administration of anaesthetics, while
protecting the patient from pain
3. The team will recognize and effectively prepare from life-threatening los of airway or
respiratory function
4. The team will recognize and effectively prepare for high risk blood loss
5. The team will avoid inducing an allergic or adverse drug reaction for which the patient is
known to be at significant risk
6. The team will consistently use methods known to minimise the risk for surgical site infection
7. The team will prevent inadvertent retention of instruments and sponges in surgical wound
8. The team will secure and accurately identify all surgical specimens
9. The team will effectively communicate and exchange critical information for the safe conduct
of the operations
10. Hospitals and public health systems will establish routine surveillance of surgical capacity,
volume and results
Surgical Safety Checklist
Before Initiation of Anaesthesia
 Has the patient confirmed his/her identity, site, procedure and consent?
 Is the site marked?
 Is the anaesthesia machine and medication checking complete?
 Is the pulse oximeter on the patient and functioning?
 Does the patient have a known allergy?

 Does the patient have a difficult airway/aspiration risk?
 Does the patient have a risk of >500 cc of blood loss (>7 ml/kg in children)?
Before Skin Incision
 Confirm all the team members have introduced themselves by name and role
 Confirm the patient’s name, procedure and where the incision will be made
 Has antibiotic prophylaxis been given in the last 60 minutes?
 Anticipated critical events
 To surgeon: what are the critical or non-routine steps? How long will the case take?
 What is the anticipated blood loss?
 To anaesthetist: are there any patient-specific concerns?
 To nursing team: has sterility (including indicator results) been confirmed?
 Are there equipment issues or any concerns?
 Is essential imaging displayed?
Before Patient Leaves Operating Room
 Nurse verbally confirm

 The name of the procedure
 Completion of instrument, sponge and needle counts
 Specimen labelling (read specimen labels aloud, including patient name)
 Whether there are any equipment problems to be addressed
 Surgeon, anaesthetists and nurse review the key concern for recovery and management of
patient
Conclusion
 The goal of the WHO safe surgery guideline is to improve the safety of surgical care around
the world by defining a core set of safety standards that can be applied in all countries and
settings
 However each country can modify the guideline according to its own needs

Damage Control Surgery (DCS)
Introduction
 Damage control surgery can be regarded as urgent surgical measures to prevent death of
patients while anticipating for more definitive surgery when the patient is more medically
stable
 It is restoration of physiology, and not restoration of anatomy
 In abdominal injury, the concept of DCG is rapid laparotomy, bleeding control, spillage control
and temporary abdominal closure (avoiding tension)
Goals of DCS
 Identification of injury
 Haemorrhage control
 Operation end as soon as possible before establishment of the triad of coagulopathy,
hypothermia and acidosis
 Once established, they form a viscous cycle which is difficult or even impossible to overcome
Hypothermia
 Clinically important if less than 37°C for more than 4 hours

 Can lead to cardiac arrhythmias, decreased cardiac output and decreased systemic vascular
resistance
 Hypothermia induced and exacerbate coagulopathy, therefore further impairing haemostatic
function
Acidosis
 Uncorrected haemorrhagic shock leads to inadequate cellular perfusion, anaerobic

mechanism and the production of lactic acidosis
 Acidosis interferes with clotting mechanism causing more blood loss
Coagulopathy

 Hypothermia, acidosis and massive blood loss lead to coagulopathy
 Patient will continue to bleed even when mechanical control of bleeding achieved
 Platelet dysfunction at low temperature
 Activation of fibrinolytic system
 There will also be haemodilution following massive resuscitation
 All these leads to worsening haemorrhagic shock, hypothermia, acidosis: a vicious cycle
Indications for DCS
 Exsanguinating patient with hypothermia, coagulopathy, haemodynamic instability

 Inability to control bleeding by direct haemostasis
 Inability to close abdomen without tension
 Expected long duration of operation
Phases of DCS
1. Laparotomy/operation in OR
2. Resuscitation in ICU
3. Definitive surgery in OR
Part I
 The principle is to control haemorrhage, control contamination and avoid further injury
 Abdominal/pelvic packing if unable to control bleeding
 Abdominal closure is rapid and temporary
 If there is any doubt about abdominal compartment syndrome, left it open (e.g. with silo bag,
vacuum-pack technique)
Part II
 Begins in ICU
 24-48 hours
 Correction of metabolic acidosis
 Core rewarming: cover patient, dry patient, active rewarming with warm blanket or bair
hugger, use pre-warmed fluid and warm ventilatory gases
 Complete ventilatory support
 Identification of occult injury
 Fluid and blood products therapy
 Initiating specific therapy to reduce complications
o Measurement of intra abdominal pressure

o Peptic ulcer prophylaxis
o Thromboprophylaxis
o Protection of lung ventilation
o Infection control and appropriate antimicrobial
o Early nutritional support (preferably enteral)
 Correction of coagulopathy
o Reverse hypothermia
o Give FFP, platelet, calcium, vitamin K
o Consider recombinant factor VII a
Part III
 Planned reoperation
 Removal of packing, primary repair, end-to-end anastomosis, copious washout, abdominal
closure
 The patient sometimes needs early unplanned re-operation for ongoing haemorrhage,
abdominal compartment syndrome, peritonitis
Complications of DCS
 Abdominal compartment syndrome

 Venous thromboembolism
 Peptic ulceration
 ARDS
 Nosocomial infection
 Wound sepsis
 Wound dehiscence
 Fistula formation
 Nutritional failure
 Critical illness myoneuropathy
Conclusion
 DCS is a significant advance in trauma patient management

 The central principle of DCS is that patients are more likely to die from a triad of
coagulopathy, hypothermia and metabolic acidosis than from a failure to complete operative
repair
 A multidisciplinary approach is needed to optimize outcome

Evidence-Based Medicine (EBM)
Definition
 EBM: the application of the best research evidence in making decisions about the care of
individual patients
 EBP: evidence-based practice; the integration of clinical expertise, patient values, and
the best research evidence into the decision making process for patient care
The Steps in the Evidence-Based Practice Process
 Assessing the patient: a clinical problem or question arises from the care if the patient
STEP 1: ASKING THE CLINICAL QUESTION
 Construct a well built clinical question derived from the case

 Anatomy of good clinical practice is remembered by the mnemonic PICO
 P: patient or problem
 I: intervention, prognostic factor, or exposure
 C: comparison
 O: outcome
STEP 2: ACQUIRING THE EVIDENCE
 Select the appropriate resource (s) and conduct a search

 Choosing the best resource to search is an important decision
 Databases e.g. Pub Med, MEDLINE, Cochrane Library
 Secondary resources: Essential evidence, eMedicine
 Electronic textbooks and libraries: Access Medicine, First Consult MD Consult
 Meta search engines: Sum Search, TRIP Answers
The Ideal Resource
 Located in the clinical setting

 Easy to use
 Fast, reliable connection
 Comprehensive, full text
 Effective search engine
 Provides primary data
Hierarchy of Study Design
 Animal research → Case series/case reports → case control studies → cohort studies →
randomised control trial → systematic review → meta analysis
STEP 3: APPRAISE THE EVIDENCE
 Appraise the evidence for its validity (closeness to the truth) and applicability (usefulness
in clinical practice)
 Key validity issues:
o Were patients randomised?
o Were group allocation concealed?
o Baseline similarities
o Blinding
o Follow-up complete
o Intention –to-treat
o How objective was the outcome measurement?
o Were the statistics used appropriate, and what do they tell you?
STEP 4: APPLYING TH EVIDENCE
 Return to the patient, integrate that evidence with clinical expertise, patient preferences
and apply to practice
Levels of Evidence Scale (US/Canadian Preventive Services Task Force)
 I: Evidence obtained from at least one properly RCT

 II-1: Evidence obtained from well-designed controlled trials without randomization
 II-2: Evidence obtained from well-designed cohort or case-control analytic studies,
preferable from more than one research group
 II-3: Evidence obtained from multiple time series with or without the intervention
 III: Opinions of respected authorities, based on clinical experience, descriptive studies
and case reports, or reports of expert committees
Level of Evidence
 I: Evidence obtained from metal analysis of RCT
IIa: Evidence obtained from RCT
 IIb: Evidence obtained from non-randomised control trial
 IIc: Evidence obtained from quasi-experimental studies
 III: Evidence obtained from cohort studies, case series
 IV: Evidence obtained from expert opinion, observation
Grades of Recommendation
 Grade A: Evidence form large, randomized clinical trials or meta analysis

 Grade B: High quality study of non-randomized cohort who did not receive therapy of
high quality case series
 Grade C: opinions from experts based on arguments from physiology bench research on
first principles

Diathermy
Introduction
 Diathermy is an instrument involving the use of high frequency A.C, electrical current in
surgery as either a cutting modality, or else to cauterize small blood vessels to stop
bleeding
 This technique induces localized tissue burning and damage, the zone of which is
controlled by the frequency and power of the device
 Electrical frequency used by diathermy is in the range of 300 kHz to 3 MHz
Type of Diathermy
 2 types of diathermy: monopolar diathermy, bipolar diathermy

 Monopolar diathermy:
o Electrical plate is placed on patient and acts on indifferent electrode
o Current passes between instrument and indifferent electrode
o Localized heating is produced at tip of electrode
 Bipolar diathermy
o Two electrodes are combined in the instrument (e.g. forceps)
o Current passes between tips and not through patient
Effects of Diathermy
 Coagulation:
o Produced by interrupted pulses of current; square wave form
 Cutting:
o Produced by continuous current; sine wave form
Risks and Complications of Diathermy
 Can interfere with pacemaker function

 Burns especially if spirit-based skin preparation is used
 Channelling effects if used on viscus with narrow pedicle (e.g. penis/testis)

Why is Patient Not Electrocuted?
 An alternating current of low frequency stimulates nerve and muscles and it is this
stimulation which kills someone connected to the mains current
 This effect, which is named after Michael Faraday (Faradism), does not occur when the
frequency is very high
General Hazards of Diathermy
1. Electrocution
 If machine is defective (therefore needs regular servicing)
2. Fire and explosion
 Alcohol-based skin preparations can catch fire if they are allowed to pool on or
under the patient
 Do not use diathermy with explosive gases, including those which may occur
naturally in the colon
3. Neuromuscular stimulation
 Although the high frequency current used for surgical diathermy does not cause
neuromuscular stimulation, the sparks which it induces may invoke secondary
currents which can do so
4. Pacemakers and diathermy
 Diathermy can interfere with pacemaker function
 Modern pacemaker are designed to be inhibited by high frequency interference
 Additional precautions if monopolar diathermy is to be used, the patient ‘s plate
should be sited so that the current path does not pass through the heart or the
pacemaker
 The heartbeat should be monitored throughout the operation
 A defibrillator should be on hand in case a dangerous dysrhythmia develops
through malfunction of the pacemaker
 To avoid these problems: use bipolar diathermy
5. Burns
 More common in monopolar diathermy

Subcutaneous Emphysema
Definition
 Trapped air beneath the skin
Introduction
 Usually occurs on the chest, neck and face

 Has a characteristic crackling feel to the touch (subcutaneous crepitations)
 It is a benign condition
Causes
 Trauma to chest/trachea
 Barotrauma
 Pneumothorax
 Hamman’s syndrome: subcutaneous emphysema occurring with pneumomediastinum
 Blocked/improperly placed chest tube
 Spontaneous rupture of alveoli
 Surgery (known as surgical emphysema)
 Vasalva manoeuvres e.g. giving birth
 Infection
Management
 Simple subcutaneous emphysema (does not compromise respiration)

o Conservative management
o Bed rest
o Oxygenation
o Analgesia
o Antibiotic prophylaxis
o Reassurance
o Close monitoring

 Severe subcutaneous emphysema (respiratory obstruction present)
o Skin incisions on the skin to release the gas
o Chest tube if it is associated with pneumothorax
o Insertion of subcutaneous drains with or without suction
o Tracheostomy
The progression of the condition can be monitored by marking the boundaries with a special
pencil for marking on skin
Macklin effect is a pathophysiological process summed up in three steps: alveolar rupture, air
dissection along broncho-vascular sheaths, and spreading of this pulmonary interstitial
emphysema into the mediastinum

Principle of Intestinal Anastomosis
Introduction
 Intestinal anastomosis is a surgical procedure to establish communication between 2 formerly

distant portions of the intestine. This procedure restores intestinal continuity after removal of
a pathological condition affecting the bowel.
Indications
 Indications for intestinal anastomosis can be broadly divided into 2 categories: restoration of
bowel continuity following resection of diseased bowel and bypass of unresectable diseased
bowel.
Contraindications of Intestinal Anastomosis
 Contraindications to intestinal anastomosis include conditions in which there is high risk of

anastomotic leak, such as the following:
o Severe sepsis
o Poor nutritional status (e.g., severe hypoalbuminemia)
o Disseminated malignancy (multiple peritoneal and serosal deposits, ascites)
o Viability of bowel in doubt
o Faecal contamination or frank peritonitis
o Unhealthy bowel condition: Precludes primary anastomosis
Tenets of Good Intestinal Anastomosis/Halsted’s Rule
 Adequate exposure and access

 Strict aseptic technique
 Gentle handling of the bowel
 Adequate haemostasis
 Approximation of well-vascularized bowel
 Absence of tension at anastomosis (tension-free)
 Good surgical technique
 Avoidance of faecal contamination

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HOSPITAL PAKAR SULTANAH FATIMAH MUAR

Acute Calculus Cholecystitis………………………………………………………………………...19

Acute Acalculous Cholecystitis................................................................................................21

Common Bile Duct Stone……………………………………………………………………………25

Indications for Open Cholecystectomy……………………………………………………………..27

Adenomyomatosis of Gall Bladder……………………………………………………….…………28

BREAST AND ENDOCRINE

Management of Solitary Thyroid Nodule..................................................................................34

Lymphoedema in Breast Cancer.............................................................................................36

Diagnostic Modalities in Diagnosing Breast Cancer................................................................38

Chronic Granulomatous Mastitis..............................................................................................42

Advanced Breast Cancer.........................................................................................................44

UPPER GASTROINTESTINAL TRACT

Norly Salleh Page 2

Rectal Prolapse .......................................................................................................................54

Management of Obstructed Splenic Flexure Tumour..............................................................72

Management of Leaking Abdominal Aortic Aneurysm.............................................................87

Assessment and Management of Patient with Critical Limb Ischaemia...................................96

Abdominal Wall Defects in Paediatric Patients......................................................................104

Pyloric Stenosis .....................................................................................................................106

Norly Salleh Page 3

Benign Prostatic Hyperplasia (BPH)......................................................................................120

Laparotomy Wound Dehiscence............................................................................................131

Ventilator Associated Pneumonia (VAP)................................................................................141

WHO Guidelines for Safe Surgery..........................................................................................144

Damage Control Surgery (DCS)..............................................................................................146

Evidence-Based Medicine (EBM)...........................................................................................149

Principle of Intestinal Anastomosis……………………………………………………………………………………156

Norly Salleh Page 4

 Acute inflammation of the pancreas which usually lasts for days

 Epigastric pain radiating through to the back

Clinical signs and symptoms:

 Radiological facilities should be available to permit ultrasound examination of the gall

CT Severity Index (Balthazar Score) for Acute Pancreatitis

Norly Salleh Page 6

 Score at admission and at 48 hours later

Criteria at admission (GALAW):

 G: Glucose >11.1 mmol/l

Criteria after 48 hours (CHOBBS):

 C: Serum Calcium <2.0 mmol/l

Modified Glasgow-Imrie Score

 Scoring is done within 48 hours of admission

 P: PaO2 <60 mmHg

For APACHE-3 score, score of ≥8 indicates severe pancreatitis.

Management of Acute Pancreatitis

 Management is mainly supportive

Complications of Acute Pancreatitis

 Systemic complications: organ failure (respiratory, cardiovascular or renal).

 Prognosis based on Ranson’s criteria

Score Mortality (%)

Norly Salleh Page 8

 Refers to a severe form of acute pancreatitis

 Pancreatic necrosis may be sterile or infected

 Epigastric pain radiating through to the back

Norly Salleh Page 9

Clinical signs and symptoms:

 CT findings: pancreatic oedema, pancreatic necrosis or peri-pancreatic fluid collection

CT Severity Index (Balthazar Score) for Acute Pancreatitis

Norly Salleh Page 10

Points Description Morbidity (%)

 Antibiotic prophylaxis for severe acute pancreatitis remains controversial

Norly Salleh Page 11

 FBC, ABG, Renal Profile, Septic Workup need to be done as required