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Systemic Surgery (GI)

CONTENTS

UPPER GI
1. H pylori 2
2. PU 4
3. Upper GI Bleeding 11
Variceal Bleeding 12
Non Variceal Bleeding: Gastric Erosion 16
Non Variceal Bleeding: Bleeding DU 17
Non Variceal Bleeding: Mallory Weiss Syndrome 19
4. PU Perforation 20
Septic Shock due to DU Perforation 25
GUD 27
Acute Abdomen: Def, Causes 28
5. GOO 29
6. CA Stomach 33
Differential Diagnosis of Mass in Epigastrium 39
7. Troisier’s Sign 40

LOWER GI
8. Differential Diagnosis of Bleeding PR 41
9. Meckel’s Diverticulum 41
10. Colorectal CA 42
11. Intestinal Obstruction 49
Paralytic Ileus 56
12. Intussusception 57
Sign de dance 61
13. Colostomy 63
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H PYLORI

 Gram-negative,
 spiral
 has multiple flagella at one end which make it motile
 exclusively colonises gastric-type epithelium and is only found in the duodenum in association with
patches of gastric metaplasia
 H. pylori is now classed by the World Health Organisation as a class 1 carcinogen
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H. pylori eradication
Treatment is based on a PPI taken simultaneously with two antibiotics (from amoxicillin, clarithromycin
and metronidazole) for at least 7 days.Triple Therapy

Quadruple Therapy
PPI + Bismuth + 2 antibiotics (Metronidazole, Tetracycline) for 10-14 days.

Sequential Therapy
PPI + Amoxicillin for 5 days followed by
PPI + Clarithromycin + Tinidazole for 5 days
Improve Eradication rates especially with clarithromycin resistant strains

Management of Treatment Failure

Rescue Therapy - used for those failing 2 courses of standard treatment
PPI + Amoxicillin + Levofloxacin / Rifabutin for 14 days
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PEPTIC ULCER

Types
According to Duration
 Acute PU - <3months, no fibrosis
 Chronic PU
According to Sites
 DU
 GU
 Stomal Ulcer
 Lower part of Esophagus
 Base of Meckel’s diverticulum
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CAUSES
 H pylori - 90% DU; 70% GU
 NSAID (GU)
 Role of acid (DU)
 Cigarette smoking
 Stress
 Cushing’s ulcer – due to head injury
 Curling’s ulcer – due to severe burns
 Blood group O
 Gastrinoma
 Hypercalcemia
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GASTRIC ULCER DUODENAL ULCER

Site Lesser curve of stomach 1st inch of 1st part of duodenum
(junction of antrum &
body/inscisura angularis)
Prepyloric ulcer
Pyloric Channel ulcer – similar
to DU in etiology
Role of acid Acid secretion may be normal Hyperacidity
Incidence Less common than DU
Peak in low social class &
developing world
Sex Equal sex Male preponderance
Size larger Smaller
Pain Epigastric pain
Gnawing in character
Radiate to back
Nocturnal pain Absent Present
Hunger pain
Food Aggravate the pain Relieve the pain
Vomiting Vomit after food Not vomit
Body weight Weight loss Weight gain
Periodicity Less marked Marked
Complications Bleeding – may erode posteriorly Anterior Ulcer – tends to
into splenic artery. Perforate
Posterior Ulcer – tends to
Perforation penetrate & bleed (penetrate
into GastroDuodenal A)
Chronic Ulcer – marked fibrosis
will lead to Pyloric Stenosis &
GOO
Malignant change Rarely associated No
Any GU should be regarded as
malignant & Needs multiple
biopsies (at least 10 biopsies at
endoscopy)

Clinical Examination: This is usually normal. Epigastric tenderness may be detected on deep palpation.
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MANAGEMENT OF CHRONIC PEPTIC ULCER

Investigations

Upper GI Endoscopy – investigation of choice

■ Endoscopy is the preferred investigation. All GUs must be biopsied.
■ Endoscopy is required in all patients with ‘alarm symptoms’. (Alarm symptoms: Anaemia (iron
deficiency); LOW; anorexia; recent onset/progressive symptoms; melaena/haematemesis; swallowing
difficulty)

Barium Meal XR

GU – ulcer crater
DU – Deformed Duodenal cap & trifoliate appearance
Features of complications – GOO → 3D (Deformed Duodenal cap, Dilated stomach, Delayed gastric
emptying)

Diagnosis of Helicobacter pylori infection

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Treatment

Treatment of Uncomplicated PU

Medical Treatment
H. pylori eradication is the cornerstone of therapy for peptic ulcers, as this will successfully prevent
relapse and eliminate the need for long-term therapy in the majority of patients.
All patients with proven acute or chronic duodenal ulcer disease and those with gastric ulcers who are
H. pylori-positive should be offered eradication as primary therapy.

Drugs to reduce acid:

PPIS, eg lansoprazole 30mg/24h PO for 4 (DU) or 8 (GU) wks.
H2 blockers have a place (ranitidine 300mg each night PO for 8wks).

Lifestyle: Cigarette smoking, aspirin and NSAIDs should be avoided. Alcohol in moderation is not
harmful and no special dietary advice is required.

Surgical Treatment

Operation for GU
 Billroth I Gastrectomy (Distal Partial Gastrectomy & GastroDuodenostomy)
 More proximal GU usually required Billroth II Gastrectomy.

Operation for DU
Vagotomy
 Double truncal vagotomy & drainage by
 Pyloroplasty or
 Gastrojejunostomy
 Selective Vagotomy
 Highly selective Vagotomy
Billroth II Gastrectomy (Distal Partial Gastrectomy & GastroJejunostomy)
GastroJejunostomy alone
Truncal Vagotomy & antrectomy
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Treatment of Complicated PU
 GOO 
 Perforation 
 H&M 
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UPPER GI BLEEDING

CAUSES
 Bleeding PU
 Acute Gastric Erosion
 Ruptured Oesophageal Varices
 Mallory Weiss tear
 Tumor - Cancer stomach
 Vascular malformation
 Blood dyscrasia
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BLEEDING ESOPHAGEAL VARICES

 Varices develop in 30% of COL + Portal Hypertension

 30% of Varices Bleed
 Compared with non-variceal bleeding, higher risk for
 Rebleeding
 Transfusion requirement
 Mortality & hospital stay

Clinical Features
 Haematemesis - If source of bleeding is above gastro-oesophageal sphincter→ Fresh Blood
 Malena ( passage of altered blood per rectum)
 Hematochezia
 Syncope
 Orthostatic Hypotension – indicates ≥ 20% reduction in blood volume
 Shock – indicates ≥ 40% blood loss

MANAGEMENT
Emergency Resuscitation
 Call for help & manage in Team Work Approach
 Secure airway & breathing, give high flow O2
 IV line, IV fluid & Restore circulating blood volume
 Is 1st priority because shock reduces liver blood flow & causes further deterioration in liver
function
 Blood for G&M (crossmatch 4–6 units)

 Coagulopathy needs correction by Vitamin K (10mg IV)or FFP

 Platelet transfusion if platelet count falls <50 x 109/L due to secondary hypersplenism

Focus Assessment
 to confirm Diagnosis & source of bleeding
 History PU
 Alcohol intake, History COL, known varices, signs of chronic liver disease
 Drug History - NSAIDs, anti-coagulants
 Assessment of blood loss, Rockall Score for risk of rebleed & mortality
 Look for evidence of co-morbidity
 Previous Upper GI bleeding & endoscopic findings
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Urgent Investigations & Monitoring

 Urgent investigations include
 FBC (early Hb may be normal because haemodilution has not yet taken place), RBS, Urea
(↑urea out of proportion to creatinine indicative of massive blood meal), Creatinine,
Electrolytes
 LFT, OSPT
 Child Pugh Grading - for severity of liver disease

 Monitor
 Vital signs
 Conscious level
 ECG if age > 50 or known cardiac disease

After successful Resuscitation & getting diagnosis

Reduction of Portal Pressure while waiting for endoscopy
Splanchnic Vasoconstrictor
 Terlipressin 2 mg IV followed by 1-2 mg 6 hourly until bleeding is controlled, for up to 72 hour
TERLIPRESSIN is splanchnic vasoconstrictor,& causes less myocardial ischaemia than Vasopressin
and is more effective than OCTREOTIDE

Arrest Bleeding
Urgent OGD Scopy - Injection SCLEROTHERAPY or BANDING of varices
 Treatment of choice
 Can reduce blood requirements, need for surgery & mortality
 Stops bleeding in 90% of cases
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If bleeding continues, put in Senstaken-Blackmore tube or Minnesota tube

 It may temporarily control the bleeding
 to buy time before operation

Management of Early Rebleeding (Rebleed within 5 days after a single session of therapeutic OGD
Scopy)
 Repeat ENDOSCOPIC THERAPY
 TIPSS for bleeding after 2 sessions of endoscopic therapy within 5 days
 If theses fails or TIPSS is not available- EMERGENCY SURGERY

Emergency Surgery
 Oesophageal Transection & Ligation Of Vessels
 Indications: failure of endoscopic treatment, Rebleeding after initial controlled bledding

Supportive Measures
 Lactulose to prevent HE
 Prophylactic antibiotics before endoscopy

Prevention Of Recurrent Bleeding

 Reduce Portal Pressure: PROPRANOLOL 80-160 mg/day, Elective Porto-Systemic Shunt Surgery,
TIPSS
 Obliterative Varices: ELECTIVE ENDOSCOPIC THERAPY
 SCLEROTHERAPY every 1-2 weeks until varices are obliterated
 BANDING – more effective and less side effects

 LIVER TRANSPLANT - in Child Pugh Grading C

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Management of Upper GI Bleeding due to Gastric Erosion

Erosive gastritis has a variety of causes, especially NSAIDs.

 Resuscitation
 Call for help & manage in Team Work Approach
 Secure airway & breathing,give high flow O2
 IV line, IV fluid & Restore circulating blood volume
 Blood for G&M (crossmatch 4–6 units)

 Urgent investigations include

 FBC (early Hb may be normal because haemodilution has not yet taken place), RBS, Urea
(↑urea out of proportion to creatinine indicative of massive blood meal), Creatinine,
Electrolytes
 Clotting Screen

 Monitor
 Vital signs
 Conscious level
 ECG if age > 50 or known cardiac disease

 Diagnosis: Upper GI endoscopy as soon as possible

 Treatment
 Endoscopic treatment of significant bleeding by
 Injection Sclerotherapy (1:10,000 Adrenaline)
 Heater probes & lasers
 Definitive Treatment
Conservative Treatment is successful in the majority
 PPI - to prevent rebleeding after endoscopy.
 Tranexamic acid
Surgery is necessary for
 Uncontrolled bleeding
 Failed conservative treatment
Surgical options – paritial/total gastrectomy

 Prevention of Recurrence: avoid smoking, NSAIDs & overindulgence of alcohol.

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Management of Upper GI Bleeding due to Bleeding DU

 Resuscitation
 Call for help & manage in Team Work Approach
 Secure airway & breathing, give high flow O2
 IV line, IV fluid & Restore circulating blood volume
 Blood for G&M (crossmatch 4–6 units)

 Urgent investigations include

 FBC (early Hb may be normal because haemodilution has not yet taken place), RBS, Urea
(↑urea out of proportion to creatinine indicative of massive blood meal), Creatinine,
Electrolytes
 Clotting Screen

 Monitor
 Vital signs
 Conscious level
 ECG if age > 50 or known cardiac disease

 Diagnosis: Upper GI endoscopy as soon as possible

 Treatment
 Endoscopic treatment of significant bleeding by
 Injection Sclerotherapy (1:10,000 Adrenaline)
 Definitive Treatment
Conservative Treatment is successful in the majority
 PPI - to prevent rebleeding after endoscopy.
 Tranexamic acid
Surgery is necessary for
 Uncontrolled bleeding
 Failed conservative treatment
 Transfusion requirement ≥6 units within 24 hours
 Warning Signs on Endoscopy: a visible vessel in the ulcer base, a spurting vessel or an
ulcer with a clot in the base
 Elderly patients
Surgical options
 Laprotomy + Duodenotomy + Under-running suture of the bleeder (Gastroduodenal A)
 PG +GJ

Bearing in mind that most patients nowadays are elderly and unfit, the minimum surgery that stops the
bleeding is probably optimal (damage control surgery).

 Prevention of Recurrence
 avoid smoking, NSAIDs & overindulgence of alcohol.
 PPI
 H pylori eradication
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PU PERFORATION

Perforations now occur most commonly in elderly female patients.

NSAIDs appear to be responsible for most of these perforations.

By far the most common site of perforation is the anterior aspect of the duodenum.
However, the anterior or incisural gastric ulcer may perforate and, in addition, gastric ulcers may
perforate into the lesser sac, which can be particularly difficult to diagnose. These patients may not have
obvious peritonitis.

Management

Resuscitation & Analgesia

 Call for help & manage in Team Work Approach
 F & E correction
 Analgesic
 Antibiotics
 Antisecretory drugs

Analgesia should not be withheld for fear of removing the signs of an intra-abdominal catastrophe. In
fact, adequate analgesia makes the clinical signs more obvious.

 Urgent investigations include

 FBC,RBS, Urea, Creatinine, Electrolytes

 Monitor
 Vital signs
 Conscious level
 ECG if age > 50 or known cardiac disease

Diagnosis
 History – PU
 Acute Abdomen – sudden onset of severe and constant pain. This usually begins in the epigastrium,
reaches its maximum intensity quickly and remains severe for many hours. It gradually extends to
involve the whole of the abdomen.
All movement, including respiration, makes the pain worse, causing the patient to lie immobile on
the bed.
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 Features of Peritonitis
3 Stages
 Stage Of Peritonism (Stage Of Chemical Peritonitis)
 Lasts about 3 hour
 Irritation of peritoneum due to leakage of gastric juice into peritoneal cavity
 Pain at site of perforation
 May refer to tip of right shoulder or to RIF (gravitate along right paracolic gutter to RIF)
 Tachycardia, Little changes in Respiration & Temperature
 Abdominal Examination – guarding, tenderness & rebound tenderness present over the
site of perforation

 Stage Of Illusion (Stage Of Reaction)

 3 -6 hours after onset
 Irritant fluid diluted with peritoneal exudates
 Symptoms reduce & patient feels more comfortable
 But Signs are still present
 New features – obliteration of liver dullness & shifting dullness
 PR Examination – tenderness in POD

 Stage Of Bacterial Peritonitis (Stage Of Diffuse Peritonitis)

 > 6 hours, Terminal stage, multiorgan failure & death
 Facies Hippocartica
 Pulse- tachycardia with low volume
 Abdominal distension
 Does not move with respiration (Still Abdomen)
 Board-like rigidity
 Bowel sound – absent (Silent Abdomen)

Atypical presentations

 Elderly patient who is taking NSAIDs will have a less dramatic presentation, perhaps because of the
use of potent anti-inflammatory drugs (steroids).
The board-like rigidity seen in the abdomen of younger patients may also not be observed and a
higher index of suspicion is necessary to make the correct diagnosis.

 In other patients, the leak from the ulcer may not be massive. They may present only with pain in
the epigastrium and right iliac fossa as the fluid may track down the right paracolic gutter
(simulating acute appendicitis)
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 Sometimes perforations will seal owing to the inflammatory response and adhesion within the
abdominal cavity, and so the perforation may be self-limiting.

Investigations

 Erect Chest XR or Plain XR Abdomen (Erect) for GUD

 Free Gas Under Diaphragm (+ in >50%)
 CT – more accurate
 Serum Amylase – to differentiate PU & Pancreatitis
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Treatment

Resuscitaion
 Call for help & manage in Team Work Approach
 Secure airway & breathing,give high flow O2
 IV line, F & E Correction
 Analgesia
 Antisecretory drugs
 Antibiotics
 Monitor – vital signs

Following resuscitation, the treatment is principally surgical.

A. Surgical Treatment

(1st aid surgery)

 Laprotomy &
 DU  Suturing & Omentoplasty of perforation

 GU  Excision (which allows for biopsy), Multiple biopsies followed by simple closure
 Massive DU or GU perforations  Billroth II Gastrectomy with Roux-en-Y reconstruction

 Peritoneal Toilet & Drain

 Post Op Care
 stomach is kept empty postoperatively by nasogastric suction
 Antibiotics
 Antisecretory drugs
 H pylori eradication therapy
 Laprosocpy – can be used
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Role of Definitive Ulcer Surgery

Nowadays, surgery is confined to first-aid measures most commonly, and the peptic ulcer is treated
medically

B. Conservative Treatment
It has a role in
 Small leaks with mild peritonitis
 Already sealed perforation
 Late perforation
 Frail patient

Prevention
 H pylori Eradication therapy
 PPI
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SEPTIC SHOCK due to DU PERFORATION

Management

Resuscitation
Resuscitation should not be delayed by any attempt at definitive diagnosis.

Immediate Resuscitation
 A – ensure patent airway
 B- check adequate oxygenation + )2 to all shocked patients
 C- cardiovascular resuscitation
 Access IV lines with 2 wide bored cannulae
 Blood for G&M and reserve 4-6 units of blood
 Urgent Investigations – FBC, Coagulation Profile

Fluid Resuscitation

Any shock should be considered hypovolemic until proved otherwise.

Fluid resuscitation should be started along with assessment of response.
In actively bleed patient, resuscitation should proceed parallel with surgery.

Type of Fluid – No ideal resuscitation fluid. Blood loss should be replaced by blood.
Amount – Fluid Challenge (Dynamic Fluid Response: Shock status is determined by cardiovascular
response to a fluid bolus (250-500ml over 5-10min) & response is monitored

Monitor
 End point of resuscitation – Vital Signs(Pulse, BP, UO), Base Deficit, lactate, Venous blood O2
 Metabolic Monitoring - ABG

Vasopressor & inotrophic Support

 There must be an adequate preload.
 Vasopressor (Vasopressin, NA, Phenylephrine) are indicated in Distributive Shock (Septic Shock,
Neurogenic Shock)
 Inotroes (Dobutamine) may be required for severe septic shock complicated by myocardial
depression & low cardiac output.
 These agents are not indicated as first line therapy in Hypovolemia.
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Organ Support
Severe cases with organ dysfunction requires admission to ICU for advanced monitoring & organ
support.

Nutrition Support
Shock results in a catabolic state and so nutritional support should be considered early in the course of
the disease

Assessment & Treatment of underlying cause

History – PU
Acute Abdomen – sudden onset of severe and constant pain
Features of Peritonitis
 Stage Of Bacterial Peritonitis (Stage Of Diffuse Peritonitis)
 > 6 hours, Terminal stage, multiorgan failure & death
 Facies Hippocartica
 Pulse- tachycardia with low volume
 Abdominal distension
 Does not move with respiration (Still Abdomen)
 Board-like rigidity
 Bowel sound – absent (Silent Abdomen)

Investigations
 Erect Chest XR or Plain XR Abdomen (Erect) for GUD - Free Gas Under Diaphragm (+ in >50%)
 CT – more accurate

Treatment
Following resuscitation, the treatment is principally surgical.
C. Surgical Treatment
(1st aid surgery)
 Laprotomy &
 Suturing & Omentoplasty of perforation
 Massive DU or GU perforations  Billroth II Gastrectomy with Roux-en-Y reconstruction

 Peritoneal Toilet & Drain

 Post Op Care
 stomach is kept empty postoperatively by nasogastric suction
 Antibiotics
 Antisecretory drugs
 H pylori eradication therapy
 Laprosocpy – can be used

Role of Definitive Ulcer Surgery -Nowadays, surgery is confined to first-aid measures most commonly,
and the peptic ulcer is treated medically

Prevention - H pylori Eradication therapy,PPI

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GUD

Gas under diaphragm (GUD) is a radiological feature.

GUD can be detected by

 Erect Chest XR
 Plain XR Abdomen
 Left lateral decubitus film

Causes
 Perforation of intra-abdominal viscus (Commonest)
 Gas forming organism infection
 Pleura-peritoneal fistula
 Iatrogenic
 Laprotomy (gas may persist up to 4 weeks)
 Laproscopy (carbondioxide rapidly clears within 12 hours)
 Tubal insufflations test

Management
Identify & treat the cause
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Acute Abdomen
Definition
Any condition which gives rise to acute abdominal pain which may or may not require emergency
operation. But the patient requires hospital admission, observation, investigation & treatment.
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GASTRIC OUTLET OBSTRUCTION

Causes
The two common causes of gastric outlet obstruction are
 gastric cancer
 pyloric stenosis secondary to peptic ulceration.

in recent years the most common cause of gastric outlet obstruction has been gastric cancer.
gastric outlet obstruction should be considered malignant until proven otherwise

Clinical Features of GOO

Symptoms
 Vomiting
 More common later in day & when lying down
 Vomiting relieves sensation of fullness
 Vomitus - no bile, undigested or partly digested food matter, food taken
several hours or days previously
 Fullness in epigastrium, Bloating
 Constant dull pain in epigastrium

Signs
 Dehydration
 Visible gastric peristalsis (above umbilicus, from left to right)
 Positive Succussion Splash
 Underlying cause
 History of PU
 Features of CA Stomach
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Metabolic Effects

The metabolic consequences of benign pyloric stenosis are unique.

 The vomiting of hydrochloric acid results in hypochloraemic alkalosis. Initially the sodium and
potassium may be relatively normal, and the urine has a low chloride and high bicarbonate content,
reflecting the primary metabolic abnormality.
 This bicarbonate is excreted along with sodium, and so with time the patient becomes progressively
hyponatraemic and more profoundly dehydrated.
 Because of the dehydration, a phase of sodium retention follows and potassium and hydrogen are
excreted in preference. This results in the urine becoming paradoxically acidic and hypokalaemia
ensues. Alkalosis leads to a lowering in the circulating ionised calcium, and tetany can occur.
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Investigations
 OGD Scopy – Investigation of choice. Biopsy of the area around the pylorus is essential to exclude
malignancy.
 Barium Meal XR
 Chronic DU + GOO  3D 3D (Deformed Duodenal cap, Dilated stomach, Delayed gastric
emptying)

 CA Stomach  Persistent Irregular Filling Defect

(A) Barium meal showing irregular filling defect in the body of the stomach suggestive of carcinoma stomach;
(B) Barium meal showing irregular filling defect in the pylorus suggestive of carcinoma pylorus.

 Urea, Electrolyte
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Treatment

Correct Metabolic Problems

 Rehydration – IV isotonic NS + K+ supplement, Monitor ECG
 Gastric Lavage until stomach is completely emptied. This then allows investigation of the patient
with endoscopy and contrast radiology.
 Gastric antisecretory drugs
 Nutritional support for long standing cases

Treatment of Mechanical Obstruction

Chronic DU
 Early cases may respond to Conservative Treatment because edema around ulcer is diminished
as the ulcer is healed.
 Severe cases with stenosis are treated by Surgery. + Post Op – PPI, H pylori eradication
 Double Truncal Vagotomy + GJ

CA Pylorus – Subtotal Gastrectomy + GJ

Infantile Hypertrophic Pyloric Stenosis – Ramstedt Pyloromyotomy

CA Head of Pancreas - Pylorus Preserving PancreaticoDuodenectomy or Whipple’s Operation for

resectable disease; bypass for non-resectable disease
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CA STOMACH

Pathology
Aetiology
Gastric cancer is a multifactorial disease.

Genetic – P53, HNPCC (lynch’s $), Family history , Blood group A

Environmental
Diet
 Salted foods, preserved foods (Nitroso compounds – Nitrosamine, nitrosamide), Smoked foods
 deficiency of antioxidants
 The aetiology of proximal gastric cancer is associated with obesity and higher socioeconomic status.

Infection : H pylori

Surgery : PU Surgery (particularly those who have had drainage procedures such as Billroth II or Polya
gastrectomy, gastroenterostomy or pyloroplasty, are at approximately four times the
average risk. Presumably duodenogastric reflux and reflux gastritis are related to the increased risk of
malignancy in these patients.)
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Occupation : Dust ingestion

Lifestyle :Alcohol & spirit, Cigarette smoking

Premalignant Conditions
 Gastric polyp (adenoma)
 Pernicious Anemia (Type A Autoimmune gastritis)  Chronic gastritis, Gastric Atrophy
 GU

Site
Lesser Curvature of Antrum - commonest site Worldwide.
Proximal CA – commonest in West. Higher social classes are more affected.

Gross
Early Gastric CA
 limited to mucosa & submucosa with or without lymph node involvement
 This type of cancer is eminently curable,
 5-year survival rates in the region of 90%.

Advanced gastric cancer - involves the muscularis.

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Type I – polypoid (fungating)

Type II – Ulcerated
Type III – UlceroInfiltrative
Type IV – Infilrative ( linitis Plastica / Leather Bottle Stomach )

Histology
Almost all gastric CA are Adenocarcinoma.

Lauren Classification

Intestinal Diffuse
Gross Polypoidal/fungating Ulcerative, infiltrating
Growth pattern Expansile Non-cohesive,infiltrative
Histology differentiation Well differentiated gland Poorly differentiated signet-ring
formation. cells.
Mucin production Limited confined to gland Extensive, prominent in stroma
lumens. around glands.
(colloid carcinoma)
Intestinal metaplasia Almost present Less frequent,arise from
denovo gastric mucus cells

Association with chronic Yes No

gastritis
Risk factors YES Not well defined

Clinical Features
Mean age (yrs) > 50 < 50
Sex (M: F) 2:1 1:1
Decreasing incidence in
Western countries YES NO

Spread
Local Spread – penetration into gastric wall & then to nearby structures (colon, pancreas, Liver).
Lymphatic Spread
 Perigastric nodes, Troisier’s Sign
 Retrograde (downward) spread may occur if the upper lymphatics are blocked.
 Unlike malignancies such as breast cancer, Nodal involvement does not imply systemic
dissemination.
Blood borne Metastases – This occurs first to liver & subsequently to others (Bones, Lungs)
Transperitoneal Spread – Ascites, Omental Cake, Krukenberg’s tumors, Rectal shelves of Blummer,
Sister Mary Joseph’s Nodule (umbilical nodule)
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Management

Diagnosis
Clinical Features

1. Features of Primary Tumor

Early Gastric CA
 Asymptomatic
 Vague dyspepsia (New Dyspepsia after 40)
 Epigastric discomfort

Advanced Gastric CA
“LIONS” + H & M
L - Lump in epigastrium
I - Insidious onset of 3A
 Anaemia (Bleeding - Occult bleeding causes IDA; H & M)
 Anorexia
 Asthenia
O - Obstruction + Perforation
 Ca Antrum - Features of GOO - Bloating and distension after meal, Vomiting
 Ca Cardia - Dysphagia
N - New dyspepsia after 40s

2. Features of Spread
S - Silent & Features of secondaries
 Liver - Jaundice, Hepatomegaly
 Lung - Haemoptysis
 Bone - Bone pain
 Brain - Headache
 Troisier’s Sign

3. Non metastatic Features

 Migratory Thrombophlebitits (Trousseau’s Sign),
 Acanthosis Nigricans, Cushing’s $

Investigations
Investigations for Diagnosis
OGD Scopy: Direct visualization of tumor + Multiple Biopsy
Barium Meal XR
 Persistent Irregular Filling Defect, Shouldering Effect, Dilated Stomach
 Linitis Plastica

Investigations for Staging

 LFT, CT Abdomen & Chest
 Bone Scan, CT (Head)
 Laproscopy
 37

Investigations for Management

FBC, LFT, RFT, ECG, CXR, Grouping & Saving Blood

Treatment
The only treatment modality able to cure is Surgery.

Surgery
Pre-operative
 Neoadjuvant chemotherapy for operable patients
 Opitimizing Lung Function & Nutrition, Booking ICU bed

Operable CA – Curative Surgery

Incurable CA – Palliative Surgery

Evidence of incurability
Hematogenous metastases
N4 node
Fixation to structures that cannot be removed, involvement of distant peritoneum

It is important to note that involvement of another organ per se does not imply incurability, provided
that it can be removed.

Procedure for Operable CA

Total Gastrectomy + reconstruction (Rou-en Y EsophagoJejunostomy)
The whole stomach is removed en bloc, including the greater & lesser omentum.
Controversies exist with regard to extent of lymph node removal D1 vs D2

D1 = tumor resection+ N1 Lymph nodes (Greater and Lesser omentum)

D2 = tumor resection + N2 lymph nodes (Spleen, Body & Tail of Pancreas)
D3 = tumor resection + N3 lymph nodes (Transverse colon, Liver left lobe)
 38

Subtotal Gastrectomy + reconstruction (GJ Billroth II or Rou en Y)

For distal tumors
 39

Palliative Surgery
 Palliative gastrectomy for obstruction or bleeding
 Bypass for nonresecable obstruction (GJ)
 Palliative stenting

Other treatment Options

 Radiotherapy – for bone secondaries
 Chemotherapy – Neoadjuvant, Adjuvant, Palliative (ECF – Epirubicin, Cis-Platinum, 5-FU or its oral
form – capecitabine)

DIFFERENTIAL DIAGNOSIS OF MASS IN EPIGASTRIUM

EXTRA ABDOMINAL
 Epigastric hernia
 Swelling from skin, subcutaneous tissue, muscle

INTRA ABDOMINAL
 CA stomach, GOO
 Enlarged left lobe of liver - CA liver (HCC, metastatic), Liver Abscess
 CA Transverse Colon
 Pancreatic swelling – Pseudo cyst, True Cyst, CA
 Abdominal Aortic Aneurysm
 Lymph nodes
 40

Troisier’s Sign

 Enlarged left clavicular lymph node (Virchow’s node) from metastatic cancer.
 A marker of advanced disease.
 The primary is usually from Upper GI tract (eg: pancreas, stomach)
 Tumor cells reach the nodes via thoracic duct through retrograde lymph flow.





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DIFFERENTIAL DIAGNOSES OF BLEEDING PER RECTUM

Lower GI
 Anus – Hemorrhoids, FIA, CA
 Rectum & Colon – IBD, Rectal polyp or adenoma, Colorectal CA, Angiodysplasia, Diverticular
Disease, Colitis – radiation induced, antibiotic related (pseudomembranous colitis), Ischemic Colitis,
Infectious Colitis
 Small Bowel – Tumors, Meckel’s Diverticulum, polyps

Upper GI
 brisk bleed from PU, varices, tumors

Meckel’s Diverticulum
 42

COLORECTTAL CARCINOMA

Pathology

Aetiology
Genetic
 P53, K-RAS & APC mutation
Familial
 HNPCC (Lynch’s Syndrome) – ADI, 80% risk of CRC
 Familial Adenomatous Polyposis (FAP) - >100 polyps is necessary for diagnosis of FAP, 100% risk of
CRC between 20-40 year of age.

Premalignant
 Previous CRC
 Adenomatous Polyps
 HNPCC
 Chronic active Ulcerative Colitits

Environmental
Diet
 Reduced fiber intake, anti-oxidant deficiency
 High animal fat, Red meat, refined carbohydrate diet

Life style – Smoking, Alcohol

Previous Surgery
 Increased bile secretion following Cholecystectomy
 Ureterosigmoidostomy

Adenoma-Carcinoma sequence is believed to be the causative factor.

Protective factors – Dietary Calcium & NSAID (Aspirin) reduce colorectal adenoma formation.
 43

Gross

The annular variety tends to give rise to obstructive symptoms, whereas the others present more
commonly with bleeding.

Histology
 Adenocarcinoma (Columnar cell Carcinoma)
 Mucinous Adenocarcinoma – 10-15%

Spread

Local Spread

CA Colon – local spread occurs in longitudinal, transverse or radial direction. Circumferential spread
causes IO. Ulcerative type is more commonly associated with invasion.

CA Rectum –This occurs circumferentially. Complete encirclement requires 18 months to 2 years.

Downward spread is rare.

Lymphatic Spread
CA Colon
N1- nodes in the immediate vicinity of bowel wall
N2- nodes along main branches of mesenteric arteries
N3- apical nodes around origin of mesenteric arteries

CA Rectum
Above peritoneal reflection, the lymphatic spread is almost exclusively upwards
Below peritoneal reflection, it is upward as well as laterally along the middle rectal vessels.
Rarely, tumor spreads to inguinal nodes due to involvement of the anal canal.
 44

Blood Spread – liver, lungs, adrenals

Transcoelomic Spread - Ascites, Omental Cake, Krukenberg’s tumors, Rectal shelves of Blummer
 45

Clinical Features

Features of Primary Tumor

CA COLON
Tumours of the left side of the colon usually present with a change in bowel habit or rectal bleeding,
while proximal lesions typically present later, with iron deficiency anaemia or a mass.

CA Caecum & Ascending Colon

 Anemia – severe & unresponsive to treatment
 Mass in RIF
 Intussusception

CA Transverse Colon
 It may be mistaken for Gastric CA (Mass in Epigastrium, Anemia, Asthenia, Anorexia)

CA Left side of colon & Sigmoid Colon

 Increasing IO
 Altered Bowel Habit: Constipation requiring laxatives
 Distention of lower abdomen relieved by passing flatus.
 Lump on abdominal, rectal or bimanual palpation – may be impacted feces or tumor.
 Lower tumors - Tenesmus, passage of mucus & blood
 46

CA RECTUM
 Upper 1/3 - increasing constipation & increasing use of purgatives
- abdominal distension
- lower abdomen pain (colicky)

 Middle 1/3 - sense of incomplete defecation (tenesmus)

- Early morning bloody diarrhea, empty rectum several times a day (Spurious
diarrhoea)
- passage of blood stained mucus (Bloody slime),

 Lower 1/3 - sense of incomplete defecation (tenesmus), purulent and offensive discharge,
Bleeding PR (earliest & most common symptom; Ulcerative types are more prone to bleed.)

PR Examination
 Most tumors can be felt digitally.
 Nodule or ulcer with raised & everted edge, blood or mucopurulent stain on finger withdrawal

Features of Spread
 Enlarged Liver – may be the initial presentation. Weight loss suggests liver metastasis.
 Ascites
 Lung Metastasis
 Pain – due to IO or local penetration

Investigations
Investigations for Diagnosis
CA Colon
Flexible Sigmoidoscopy - It is usually possible to assess the bowel up to the splenic flexure
Colonoscopy
 investigation of choice
 visualization & biopsy, to exclude polyps, synchronous tumor
 mechanical bowel preparation required.
 There is a small risk of perforation (1:1000).

CA Rectum
Proctosigmoidoscopy & Biopsy using Yeoman’s Biopsy Forceps
Colonoscopy – to exclude syndhronous tumors

Double Contrast Barium Enema – when Colonoscopy is CI.

CA appears as
 Persistent/ Constant Irregular Filling Defect + Apple Core Deformity

CT – particularly in elderly when contrast enema are not diagnostic or are CI.

Investigations for Staging

LFT, CT Abdomen & Chest
Bone Scan, CT (Head)
CEA – tumor marker useful for assessing completeness of resection & follow up
 47

Investigations for Management

For fitness of the patient for operation
FBC, LFT, RFT, ECG, CXR, Grouping & Saving Blood

Treatment of CA COLON

Resuscitation for IO

Treatment of Primary Tumor

Options
Surgery – the choice

PreOp Preparation
 Bowel Preparation
Emergency – On table lavage
Elective
 Low residue diet for 5d before surgery
 Fluid only for 48 hours before surgery.
 Mechanical preparation on the day before operation
 Rectal washout (Phosphate Enema)

 Prophylactic Antibiotics
 DVT prophylaxis
 Full pre-operative work up & Informed consent

Operability
Liver secondaries – not contraindication for resection.

Curative Resection – to remove primary tumor & its draining nodes. Radical resection requires at least
5cm distal & proximal clearance.

CA Caecum & Ascending Colon - Right Hemicolectomy

CA Hepatic Flexure - Right Hemicolectomy extended further along the transverse colon and
divide the right branch of the middle colic artery.
CA Transverse Colon - Transverse Colectomy or Extended Right Hemicolectomy
CA Splenic Flexure - Extended right Hemicolectomy, left Hemicolectomy
CA Descending Colon - left Hemicolectomy
CA Upper Sigmoid Colon - left Hemicolectomy down to upper third of Rectum
 48

Palliative Surgery
 Palliative resection
 Palliative bypass
 Palliative stenting – for obstructing lesions
 Colostomy for pelvic colon tumors, Ileostomy for tumors in upper part of left colon.

Advances
 No touch technique (Turnbull) – Early division of major colonic vessels

Lymphovascular ligation before tumour manipulation during colorectal cancer resection is termed
the 'no-touch isolation' technique. It aims to reduce the intra-operative dissemination of colorectal
cancer cells.

 Laproscopic surgery

Radiotherapy
 Adjuvant, Neoadjuvant
 Palliative

Chemotherapy
 Adjuvant (5 FU + Folinic acid/Leucovorin)
 Palliative

Treatment of Spread
Hepatic Metastasis
 Resection if <3 lesions
 They should not be biopsied for fear of tumor dissemination.
 49

INTESTINAL OBSTRUCTION

Types
Dynamic - peristalsis is working against a mechanical obstruction.

Adynamic - there is no mechanical obstruction; peristalsis is absent or inadequate (e.g. paralytic ileus or
pseudo-obstruction).

Clinical Features

DYNAMIC OBSTRUCTION

4 Cardinal Features

Colicky (Intestinal Colic) in nature - severe central griping pain interspersed with periods of little or no
pain
Centered on the umbilicus, occurs every 2–20 minutes (small bowel)
lower abdomen, occurs about every 30 minutes or more (large bowel)
 50

Vomiting
 Frequency
 Amount
 Character
 Taste & Odour of vomitus

Occurs early with SI obstruction, & unusual, late feature of Large bowel obstruction.
Vomitus – greenish blue bile stained (SI) or feculent - thick, brown & foul (Terminal ileal), fecal (LI).

Abdominal distension  central/peripheral

Central distension in SI obstruction, & Peripheral/Supra-pubic with LI obstruction.

Visible peristalsis – step ladder pattern (SI), from right to left above umbilicus (Transverse Colon)

Constipation

Absolute constipation (both feces & flatus) - occurs early in lower large bowel obstructions and late in
high small bowel obstructions.
constipation for feces only in case of partial obstruction.

The consequences of intestinal obstruction are not immediately life-threatening unless there is
superimposed strangulation.
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ADYNAMIC OBSTRUCTION
Paralytic ileus

Pathology

x Changes proximal to the bowel obstruction:

 52

(A) Closed loop obstruction. Here loop of the bowel is obstructed at its point of entry and exit creating closed loop;
(B) Closed loop obstruction of ileo-caecal region.
Necrosis and perforation are both common at obstructed site and over the convex summit of the bowel
content.
 53

Management

Resuscitation
 Gastrointestinal drainage via a nasogastric tube
 Fluid and electrolyte replacement
They are always necessary before attempting the surgical relief of obstruction and are the mainstay
of postoperative management.

Diagnosis
Plain Abdominal XR - Multiple air-fluid levels.

Treatment

Surgical treatment is necessary for most cases of intestinal obstruction but should be delayed until
resuscitation is complete, provided there is no sign of strangulation or evidence of closed-loop
obstruction.
 54

PreOp Preparation
Emergency  On table Lavage
Elective  Bowel Preparation
Colonoscopic decompression, if successful, may convert Emergency into Elective one.

Assessment is directed to:

 the site of the obstruction;
 the nature of the obstruction;
 the viability of the gut.

Surgical Procedure – depends on cause of obstruction

 Adhesion  adhesiolysis
 Intussusception  Manual reduction, resection for gangrene
 Large Gut Obstruction
Right Colon
 Removable lesions: Definitive Surgery (Right Hemicolectomy, Extended Right Hemicolectomy)
 Irremovable lesions – Bypass surgery, Proximal stoma

Left Colon, Sigmoid Colon, RectoSigmoid

 On-table lavage with One-Stage Definitive Surgery
 Definitive Surgery with covering stoma (Colonostomy or Ileostomy) followed by Stoma Closure
later (2 Stage)
 Paul Mikulicz Procedure – both proximal & distal bowels brought out as stoma.

 Hartmann’s Procedure – resection with creation of End Pelvic Colostomy followed by

Reversal of Hartmann’s Procedure)
 55

 Colonostomy alone at initial operation followed by Definitive Surgery, and then Colostomy
closure (3 Stage)

Following relief of obstruction, the viability of the involved bowel should be carefully assessed.

If in doubt, the bowel should be wrapped in hot packs for 10 minutes with increased oxygenation and
then reassessed.
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ADYNAMIC OBSTRUCTION

Paralytic ileus
This may be defined as a state in which there is failure of transmission of peristaltic waves secondary to
neuromuscular failure (i.e. in the myenteric (Auerbach’s) and submucous (Meissner’s) plexuses). The
resultant stasis leads to accumulation of fluid and gas within the bowel, with associated distension,
vomiting, absence of bowel sounds and absolute constipation.

Management
Preventive Measures
 Nasogastric suction
 Restriction of oral intake until bowel sounds return and passage of flatus return
 Maintainace of electrolyte balance particularly potassium

Specific Treatment
 Removal of the cause
 Nasogastric suction (Decompression)
 F & E balance
 Neostigmine – in resistant cases
 Surgery - if ileus is prolong & threatens life.
 57

INTUSSUSCEPTION

Def: Invagination (telescoping) of one segment of the gut within an immediately adjacent segmen.t

Types

 Ileo-Colic = commonest in Children

 Colo-Colic = commonest in Adult

Aetiology
 Idiopathic (primary)
 Secondary to intestinal pathology (Leading points) eg; polyps, Meckel’s Diverticulum

Pathology
An intussusception is composed of three parts
 the entering or inner tube (intussusceptum);
 the returning or middle tube;
 the sheath or outer tube (intussuscipiens).
 The part that advances is the apex, the mass is the intussusceptions and the neck is the junction of
the entering layer with the mass.
 58

Clinical Features

Common in 6–9 months. Commonest cause of intestinal obstruction in infancy.

Common in spring and winter, coinciding with the gastroenteritis and respiratory infections in respective
periods.

 Initial colicky abdominal pain which eventually becomes severe and persistent.
 Vomiting
 Red Currant Jelly Stool

Sudden onset of pain in a male child, with progressive distension of the abdomen, vomiting, with
passage of “redcurrant- jelly” stool. It is usually not found in adult intussusception.

 Sausage-shaped lump with concavity towards the umbilicus

 Depressed RIF compared to LIF, Feeling of Emptiness in RIF (Sidn de dance)
 PR – Blood stained mucus on finger
 59

Features of Complications
 Features of intestinal obstruction with step-ladder peristalsis.
 gangrene and perforation occurs with features of the peritonitis.

Investigations
 Plain XR Abdomen - multiple air fluid levels.
 Barium Enema: Crab or Pencer’s Claw Sign/ Coil Spring Appearance
 USG – Target Sign or pseudokidney sign or bull’s eye sign, which is diagnostic.

Barium enema showing the typical ‘Claw sign’ of intussusception.

 60

Treatment

Resuscitation
 intravenous fluids, broad-spectrum antibiotics and nasogastric drainage

Non-Operative Reduction - In the infant with ileocolic intussusception

 Pneumatic Reduction(air)
 Hydrostatic Reduction,
 Therapeutic Enema (Barium Enema Reduction)

Non-operative reduction is contraindicated if there are signs of peritonitis or perforation, there is a

known pathological lead point or in the presence of profound shock.

Surgery

 Manual Reduction (Milking)

 Resection & Anastomosis – for An irreducible intussusception or one complicated by infarction or a
pathological lead point
 61

SIGN-DE-DANCE

 A classical sign of acute intussusceptions

 It is a feeling of emptiness in RIF due to collapsed caecum because no gas nor intestinal contents
reach the caecum.
 Inspection of abdomen – depressed RIF compared to LIF
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STOMA
 63

COLOSTOMY

It is an artificial opening made in the large bowel to divert feces & flatus to the exterior, where it is
collected in an external appliance.

TYPES
According to site
 Transverse
 Sigmoid
According to duration
 Temporary
 permanent
According to Surgical technique
 loop
 end
 double-barreled

INDICATIONS
TEMPORARY COLOSTOMY
 Congenital – Hirshsprung’s disease, high type imperforate anus
 Trauma – rectal or colonic trauma to prevent fecal peritonitis
 Inflammation – high FIA
 Neoplasia
 Surgery for anorectal incontinence
 Palliation for pelvic cancer
END COLOSTOMY
 Part of APR
 Part of Hartmann’s procedure

Selection of site of Colostomy

The colostomy must be
 Away from bony prominence (ASIS, costal margin)
 Away from old scars & natural skin creases (umbilicus)
 Situated in lateral edge of lateral edge of rectus sheath
Transverse Loop Colostomy – is usually in Right Upper Quadrant (midway between costal margin &
umbilicus)
Permanent End Sigmoid Colostomy – usually at LIF
64
 65

CARE OF COLOSTOMY
 Psychological support
 Care before creation – selection of site, Informed consent
 Care after creation
 Explain about colostomy care
 Prevention of skin excoriation
 Dietary guidance - Avoid food which cause diarrhea, Improve consistency of feces
 Bowel training
 Reduction of odor
 Closure of colostomy for temporary colostomies
 After taking a distal loop colonogram to be sure the distal loop is patent.

COMPLICATIONS
General Complications – Complications of anesthesia & operation
Specific Complications
 Hemorrhage
 Ischaemia & necrosis of distal end
 Stenosis of stoma
 Retraction
 Prolapsed
 Hernia
 Fecal impaction
 Colostomy diarrhea
 Skin complications – excoriation
 Psychological problems
 Social problems
 Complications due to anesthesia & operation