GASTROINTESTINAL

BLEEDING

NUR JASHIMAH IDAYU JAMALUDINTAN LAY TENG

MOHD HANAFI RAMLEE

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CONTENTS

• Anatomy• Definition• Epidemiology• Clinical features• Aetiology• History & Examination• Investigation• Management

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• FOREGUTAbdominal esophagus

• MIDGUT Major duodenal papilla • HINDGUT Junction B/w prox 2/3 and distal 1/3 of tranverse colon

Major duodenal papilla

Junction B/w prox. 2/3 and distal 1/3

of tranverse colon.

Midway of anal canal

ANATOMY OF GIT

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ARTERIAL SUPPLY

• Mostly by anterior branch of abdominal aorta

Celiac trunk - Foregut

• left gastic artery

• splenic artery

• common hepatic artery

Superior Mesenteric

Artery - Midgut• inferior

pancreaticoduodenal artery

• jejunal and ileal arteries

• middle colic artery

• right colic artery

• ileocolic artery

Inferior Mesenteric

Artery - Hindgut

• sigmoid arteries

• superior rectal artery

• Left colic artery

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PORTAL VEIN

Union of splenic vein and sup. Mesentric

vein• Tributaries ; -right and left

gastric veins -cystic veins -para umbilical veins• Portal vein drains to

inferior vena cava (systemic system) through hepatic vein

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PORTAL-SYSTEMIC ANASTOMOSES• Lower 3rd of esophagus

Left gastric veinAzygos vein

• Anal canalSuperior rectal veinInferior rectal vein

• Umbilicus Paraumbilical veinSuperficial vein of

anterior abdominal wall• Bare area of liver

Vein in liverDiaphragmatic/

phrenic vein• Retroperitoneal organs

Colic veinLumbar/renal vein

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INTRODUCTION

• Gastrointestinal bleeding describe every form of haemorrhage in the GIT, from the pharynx to the rectum.

• Can be divided into 2 clinical syndromes:-- upper GI bleed (pharynx to ligament of Treitz)- lower GI bleed (ligament of Treitz to rectum)

LIGAMENT OF TREITZ

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UPPER GASTROINTESTINAL BLEEDING

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EPIDEMIOLOGY

• Upper GI bleed remains a major medical problem.

• About 75% of patient presenting to the emergency room with GI bleeding have an upper source.

• In-hospital mortality of 5% can be expected.

• The most common cause are peptic ulcer, erosions, Mallory-Weiss tear & esophageal varices.

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CLINICAL FEATURES

• Haematemesis : vomiting of blood whether fresh and red or digested and black.

• Melaena : passage of loose, black tarry stools with a characteristic foul smell.

• Coffee ground vomiting : blood clot in the vomitus.

• Hematochezia : passage of bright red blood per rectum (if the haemorrhage is severe).

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CLINICAL FEATURES

• Haematemesis without malaena is generally due to lesions proximal to the ligament of Treitz, since blood entering the GIT below the duodenum rarely enters the stomach.

• Malaena without haematemesis is usually due to lesions distal to the pylorus

• Approximately 60mL of blood is required to produced a single black stool.

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AETIOLOGY

Oesophagus-Oesophageal varices-Oesophageal CA-Reflux oesophagitis-Mallory-Weiss syndrome

-Haemophilia-Leukemia-Thrombocytopenia-Anti-coagulant therapy

Stomach-Gastric ulcer-Erosive gastritis-Gastric CA-gastric lymphoma-gastric leiomyoma-Dielafoy’s syndrome

Duodenum-Duodenal ulcer-Duodenitis-Periampullary tumour-Aorto-duodenal fistula

LOCAL

GENERAL

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OESOPHAGEAL VARICES• Abnormal dilatation of

subepithelial and submucosal veins due to increased venous pressure from portal hypertension (collateral exist between portal system and azygous vein via lower oesophageal venous plexus).

• Most commonly : lower esophagus.14/81

Esophageal varices: a view of the everted

esophagus and gastroesophageal junction, showing

dilated submucosal veins (varices).

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OESOPHAGEAL VARICES: PORTAL HYPERTENSION

PRE HEPATIC• Portal

vein thrombosis

• Splenic vein thrombosis

INTRA HEPATIC

• Cirrhosis• Schistos

omiasis• Sarcoido

sis• Myelopro

liferative disorder

• Congenital hepatic fibrosis

POST HEPATIC

• Budd-chiari syndrome

• Right heart failure

• Constrictive pericarditis

• Veno-occlusive disease

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OESOPHAGEAL VARICES: PATHOPHYSIOLOGY

Portal venous hypertension

Resistance to flow in portal venous system

Pressure

Portal systemic shunting(Abnormal venous communication between portal system

and systemic venous circulation)

Appearing of large submucosal veins at lower end of oesophagus and gastric fundus

Haemorrhage due to intravariceal pressure17/81

OESOPHAGEAL VARICES• Sudden onset• Painless• Large volume of blood• Dark red• History of (alcoholic) liver

disease• Physical findings of portal

hypertension – ascites, splenomegaly

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OESOPHAGEAL VARICES• Management

- blood transfusion- endoscopic variceal injection with sclerosant or banding.- sengstaken tube

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MALLORY-WEISS TEAR• Longitudinal tears at the

oesophagogastric junction.• may occur after any event that provokes

a sudden rise in intragastric pressure or gastric prolapse into the esophagus.

Clinical features:- An episode of haematemesis

following retching or vomiting.- melaena- hematochezia- syncope- abdominal pain.

Precipitating factors:- hiatus hernia- retching & vomiting- straining- hiccuping- coughing- blunt abdominal trauma - cardiopulmonary resuscitation 20/81

MALLORY-WEISS TEAR: MANAGEMENT

- Bleeding from MWTs stops spontaneously in 80-90% of patients - A contact thermal modality, such as multipolar electrocoagulation (MPEC) or heater probe, with or without epinephrine injection, is typically used to treat an actively bleeding - Epinephrine injection -reduces or stops bleeding via a mechanism of vasoconstriction and tamponade - Endoscopic band ligation - Endoscopic hemoclipping

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ESOPHAGEAL CANCER• 8th most common cancer seen

throughout the world.• 40% occur in the middle 3rd of

the oesophagus and are squamous carcinomas.

• adenoCA (45%) occur in the lower 3rd of the oesophagus and at the cardia.

• Tumours of the upper 3rd are rare (15%) 22/81

ESOPHAGEAL CANCER

-more common in men.-risk factor:

- tobacco smoking- heavy alcohol intake- plummer-vinson syndrome- achalasia- coeliac disease- tylosis- diet deficient in vitamins

high dietary carotenoids & vitamin C possibly decrease the risk.

- arise in the columnar lined epithelium of the lower

oesophagus.- risk factor:

- long-standing GORD- barrett’s

oesophagus- tobacco smoking

ADENOCARCINOMASQUAMUS CELL CARCINOMA

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ESOPHAGEAL CANCER: CLINICAL FEATURES

1) Dysphagia- progressive & unrelenting- initially there is difficulty in swallowing solids, but eventually dysphagia for liquids also occur.

2) Odynophagia- retrosternal pain on swallowing.

3) Regurgitation4) Aspiration pneumonitis5) Weight loss6) Anorexia7) Anemia8) Lassitude

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ESOPHAGEAL CANCER: TNM STAGING

1. Tumour confined to submucosa2. Tumour extends into muscularis propria3. Tumours extend outside muscle layer4. Tumour invades adjacent structures

5. Lymph node metastases to paraoesophageal, cardia or left gastric regions.

o. No other metastatic spread1. Lymph node metastases to all other areas.

Metastases to liver, lung, brain, bone, etc.

T

N

M

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PEPTIC ULCER• gastric ulcer & duodenal

ulcer• Caused by imbalance

between secretion of acid and pepsin, and mucosal defence mechanism.

-Helicobacter pylori infection-Zollinger-ellison syndrome-NSAIDs-others: stress, smoking,alcohol, steroid

- epigastric pain- haematemesis- Melaena- heartburn

AETIOLOGY

SIGNS & SYMPTOMS

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PEPTIC ULCER: PATHOGENESIS

Predisposing factors including H.pylori infection of mucosa

Acid-pepsin attack and/or breach of mucosal protection

Acute inflammation resolution

Destruction of mucosa

Mucosal ulceration mucosal regeneration

Extension through submucosal & muscular layers causing deep ulceration

Perforation erosion of major granulation tissue blood vessel formed & attemps repair

Peritonitis massive haemorrhage chronic & relapsing

ulceration27/81

Feature Gastric ulcer Duodenal ulcer

Onset Soon after eating 2-3 hours after eating

Relieving factor vomiting Eating

Precipitating factor

eating Missing a meal, anxiety, stress

Duration of attack

A few weeks A month or two

PEPTIC ULCER

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PEPTIC ULCER: COMPLICATION

• Haemorrhage- posterior duodenal ulcer erode the gastroduodenal artery- lesser curve gastric ulcers erode the left gastric artery

• Perforation- generalized peritonitis- signs of peritonitis

• Pyloric obstruction- profuse vomiting, LOW, dehydrated, weakness, constipation

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PEPTIC ULCER: TREATMENT

• Antacid – aluminium/Mg hydroxide, Mg Trisiclate• Mucosal protective agents – sucralfate• Prostaglandin analogues – misoprostol• H2 receptor antagonist – cimetidine & ranitidine• Proton pump inhibitor – omeprazole & lansoprazole

• H.pylori eradication- triple

therapy :metronidazole,amoxycilin,erythromycin

• surgery should be done if -failed medical treatment-vagotomy, gastrectomy, pyloroplasty 30/81

EROSIVE GASTRITIS

• Acute mucosal inflammatory process

• Accompanied by hemorrhage into the mucosa and sloughing of the superficial epithelium (erosion).

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EROSIVE GASTRITIS: AETIOLOGY

- NSAIDs- alcohol- smoking- chemotherapy- uraemia- stress - ischaemia and shock- suicide attempts - mechanical trauma- distal gastrectomy

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EROSIVE GASTRITIS: CLINICAL FEATURES

- asymptomatic- epigastric pain with nausea & vomiting- haematemesis and melaena- fatal blood loss

It is one of the major causes of haemetemesis, particularly in alcoholic!

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GASTRIC CANCER

- adenomatous polyps- leiomyoma- neurogenic tumour- fibromata- lipoma

- gastric adenocarcinoma (90%)- lymphomas- smooth muscle tumour

BENIGN GASTRIC NEOPLASM

GASTRIC CARCINOMA

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GASTRIC CANCER

• 60-80 years age group.• Male:female , 2:1

- diet- H.pylori infection- gastric polyps- gastroenterostomy- chronic gastric ulcer disease- chronic atrophic gastritis- intestinal metaplasia- gastric dysplasia- host factors

AETIOLOGICAL FACTOR

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GASTRIC CANCER: TNM STAGING

T1 tumour extends to lamina propria or submucosa.

T2 tumour extend into muscleT3 tumour extend into serosaT4 tumour invades adjacent structures

N0 no lymph node involvementN1 fewer than 7 lymph node involved by tumourN2 7-15 lymph node involved by tumourN3 more than 15 lymph node involved by tumour

M0 no metastasesM1 metastases present

T

N

M

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GASTRIC CANCER

Early signs -Indigestion -Flatulence -DyspepsiaLate signs - LOW -anemia -dysphagia -vomiting -epigastric/back pain - epigastric mass -sign of metastases (jaundice, ascites, diarrhoea, intestinal obstruction)

• Radical total gastrectomy• Palliative resection• Palliative bypass

CLINICAL FEATURESTREATMENT

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DIEULAFOY’S DISEASE

• Rare – erosion of mucosa overlying artery in stomach causes necrosis arterial wall & resultant hemorrhage.

• Gastric arterial venous abnormality

• covered by normal mucosa

• profuse bleeding coming from an area of apparently normal mucosa.

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DUODENITIS

- aspirin, - NSAIDs- high acid secretion

- Symptoms are similar to peptic ulcer disease

- stomach pain- bleeding from the intestine- nausea & vomiting- LOA- intestinal obstruction(rare)

AETIOLOGY

CLINICAL FEATURE

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DUODENITIS

- endoscopy, may

be some redness and nodules in the wall of the small intestine.

- Sometimes, it can be more severe and there may be shallow, eroded areas in the wall of the intestine, along with some bleeding

-stop all medications that can make things worse (aspirin & NSAIDS)

-H2 receptor blockers (ranitidine/cimetidine) or proton pump inhibitors (omeprazole) reduce the acid secretion by the stomach

INVESTIGATION MANAGEMENT

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HISTORY TAKING

- when?- have u vomited blood/passed black tarry stools?- had both haematemesis & malaena?- have u had, bleeding from the nose? Bloody expectoration? A dental extraction?

- what is the color, the appearance of the vomited blood?- red? Dark red? Brown? Black?- ‘coffee ground appearance?- bright red & frothy?- what is the color of the stool? Bright red? Black tarry?

- have u vomited blood only once/several times?- has the bleeding been abrupt/massive?- have u had >1 black, tarry stool within a 24-h period?- for how long have the tarry stools persisted?

MODE OF ONSET

CHARACTER

EXTENT AND RATE

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- retching & severe nonbloody vomiting?- lightheadedness? Nausea? Thirst? Sweating?- faintness when lying down/when standing/syncope?- following the haemorrhage did you have diarrhea?

- aspirin? anticoagulant therapy? iron preparation?- age of the patient?- what is your smoke/alcohol intake?

- have there been similar episode in the past? When? Diagnosis?- were u hospitalized on this occasion? Did u receive a transfusion?- are there any other members of your family who have intestinal disease/bleeding tendency/peptic ulcer/liver disease, History of Malignancy?

OTHER SYMPTOMS

IATROGENIC FACTORS

PREVIOUS EPISODES

FAMILY HISTORY

HISTORY TAKING

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PHYSICAL EXAMINATION:UPPER GI BLEED

Anaemic Bruishing/ Purpura Cachexic Dehydrated Jaundice

Inspection - distension, scar, prominent vein.

Palpation - tenderness, mass/ organomegaly

Percussion - shifting dullness, fluid thrill.

Auscultation - hyperactive bowel sound.

Perianal Skin Lesion Masses Melaena

Supraclavicular LN Cervical LN Axillary LN Inguinal LN

Confusion ( Shock, liver failure….)

Neurological Deficit

GENERAL INSPECTION

ABDOMEN

RECTAL

LYMPH NODES

CNS

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PHYSICAL SIGN

• Clinical shock• Systolic BP < 100mmHg• Pulse rate > 100 bpm• Postural sign: patient place in a

upright position – pulse rate rises 25% or

more- systolic BP alls 20mmHg

or more• Sign of liver disease & portal

hypertension• Sign of GI disease• Sign of bleeding abnormalities• Bloody / black stools on per rectal

examination. 44/81

INVESTIGATIONS

- full blood count – Hb, WCC- liver function test – cirrhosis- coagulation profile- renal profile- RBC morphology- OGDS

- Barium meal / Double-contrast barium meal

- Ultrasound- CT scan

BASELINE INVESTIGATION

IMAGING

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Acute Upper Gastrointestinal Bleed

Resuscitation and Risk Assessment

Routine Blood Test

Endoscopy (within 24 hrs)

Varices Peptic Ulcer No obvious cause

Management Varices

Major SRH Minor SRH Minor Bleed

Major Bleed

Eradicate H.pylori &

Risk Reduction

Endoscopic Treatment

Failure

Surgical

Other colonoscopy or

angiography

OVERVIEW:MANAGEMENT OF UPPER GI BLEED

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RESUSCITATION

• airway and oxygen• Insert 2 large-bore (14-16G) IV cannulate take

blood• IV colloid - crossmatched. • In a dire emergency, give O Rh-ve blood.• haemodynamically stable.• Correct clotting abnormalities• Monitor• Insert urinary catheter and monitor hourly

urine output if shocked.• Consider a CVP line to monitor CVP and guide

fluid replacement.• Organize a CXR, ECG, and check arterial blood

gases in high-risk patient.• Arrange an urgent endoscopy.• Notify surgeon of all severe bleeds on admision.47/81

BLOOD TRANFUSION

– Haemoglobin - May be normal during the acute stages until haemodilution occurs

– Urea and electrolytes - Elevated blood urea suggests severe bleeding

– Cross match for transfusion - Two units of blood are sufficient unless bleeding is extreme.

– If the transfusion is not needed urgently, group the blood and save the serum

– LFT and coagulation profile

1.Systolic BP < 110 mmHg

2.Postural hypotension

3.Pulse > 110/min

4.Haemoglobin <8g/dl

5.Angina or cardiovascular disease with a Haemoglobin <10g/dl

BLOOD TEST INDICATION OF BLOOD TRANSFUSION

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DETECTION & ENDOSCOPIC• Used to detect the site of

bleeding.• May also be used in a therapeutic

capacity (active bleeding from the ulcer, the presence of a visible vessel, adherent clot overlying the ulcer)

• Injection sclerotherapy is used commonly. Other method include the use of heat probes and lasers.

• Angiography in whom endoscopy does not identify the bleeding point. Limitation: can only detect active bleeding of greater than 1mL/min. 49/81

FORREST CLASSIFICATION FOR BLEEDING PEPTIC ULCER

– Ia: Spurting Bleeding– Ib: Non spurting active bleeding– IIa: visible vessel (no active

bleeding)– IIb: Non bleeding ulcer with

overlying clot (no visible vessel)– IIc: Ulcer with hematin covered

base– III: Clean ulcer ground (no clot,

no vessel)

Min

or S

RHM

ajor

SRH

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MANAGEMENT

• H2 receptor antagonist - cimetidine, ranitidine• Proton pump inhibitors – omeprazole, lanzoprazole• H. pylori irradication• Triple regimen – proton pump inhibitor + 2 antibiotics given for 1

week (elimination rate > 90%) e.g. Omeprazol + metronidazole/amoxycillin + clarithromycin

• GU – remove ulcer, gastrin secreting zone – Billroth I gastrectomy• DU – Polya or Billroth II gastrectomy – Vagotomy

MEDICAL

SURGICAL

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UPPER GI BLEED:RISK FACTORS FOR DEATH

1. Advanced AGE2. SHOCK on admission(pulse rate >100 beats/min; systolic

blood pressure < 100mmHg)3. COMORBIDITY (particularly hepatic or renal failure and

disseminated malignancy)4. Diagnosis (worst PROGNOSIS for advanced upper

gastrointestinal malignancy)5. ENDOSCOPIC FINDINGS (active, spurting haemorrhage from

peptic ulcer; non-bleeding visible vessel)6. REBLEEDING (increases mortality 10 fold)

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GASTROINTESTINAL BLEEDING

LOWER

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LOWER GI BLEED: AETIOLOGY

Crohn’s diseaseDiverticula eg:

Meckel’s diverticulum,

Jejujanal diverticulosisBenign neoplasm eg:

Peutz-Jegher’s syndrome

Leiomyoma. Malignant neoplasm eg:

Lymphoma,

Angiodysplasia

Rectal carcinoma and polypsRectal prolapse

Carcinoma of colonPolyps eg:

Familial adenomatous polyposis Diverticular diseaseInflamation

Ischaemic colitisUlcerative colitis

Pseudomembranous colitis Angiodysplasia

HaemorrhoidsFissure-in-anoAnal carcinomaAnal wart

SMALL INTESTINE

RECTUM

COLON

ANUScDNA

PC

PACID

wCHF

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HISTORY TAKING:RECTAL BLEEDING

Blood on its own or streaking the stool:Rectum : polyps or carcinoma, prolapsedAnus : Haemorrhoids, Fissure-in-ano, Anal carcinoma.

Stool mixed with blood:GIT above sigmoid colon. Sigmoid carcinoma or diverticular disease.

Blood separate from the stool:Follows defaecation : Anal condition eg: Haemorrhoids.Blood is passed by itself : Rapidly bleeding carcinoma,

inflammatory bowel disease, diverticulitis, or passed down from high up in the gut.

Blood is on the surface of the stool: suggest a lesion such as polyp or carcinoma further proximally either in the rectum or descending colonBlood on the toilet paper: Fissure-in-ano, Heamorrhoids.Loose, black, tarry, foul smelling stool: from the proximal of DJ flexure

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Bright red/ Fresh blood: Rectum and anus.Dark blood: Upper GIT to above rectum.Drugs eg: iron tablets- appear as greenish black formed stool.

• Discharge apart from blood:--Mucus- irritable bowel syndrome-Copious mucus- villous adenoma, frank cancer of the rectum-Mucus and pus- IBD, diverticular disease

HISTORY TAKING:COLOUR OF BLOOD/DISCHARGE

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Normal bowelIntermittent bouts of constipation interrupted by diarrhoea: Carcinoma or Diverticular disease.Diarrhoea: Inflammatory bowel disease or rectal villous tumour.Tenesmus: Irritable bowel syndrome or abnormal mass of rectum or anal canal (e.g. CA, polyps or thrombosed haemorrhoid)

HISTORY TAKING

ALTER BOWEL HABIT

ANAL PAIN

ITCHINESS

Causes: Allergic, anal warts, anal leak of mucus in haemorrhoid, excessive used of liquid paraffin, generalized disorder. eg: jaundice, diabetes mellitus.

During pregnancy/childbirth: Fissure-in-ano, haemorrhoids.Throbbing, severe pain occur during defaecation: Fissure-in-ano.

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•Previous perianal disease•Inflammatory bowel disease•Peptic ulcer disease•Liver disease•Coagulopathy

HISTORY TAKING

• Laxative agent• Anti-parkinson agent• Anti-coagulant therapy

eg: warfarin• NSAID’s-risk factor of

PUD

• Low fiber diet• Smoking

PREVIOUS HISTORY

•History of malignancy•Familial Adenomatous Polyposis

FAMILY HISTORY

DRUGS HISTORY

SOCIAL HISTORY

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PHYSICAL EXAMINATION:LOWER GI BLEED

Anaemic Bruishing/ Purpura Cachexic Dehydrated Jaundice

Inspection - distension, scar, prominent vein.

Palpation - tenderness, mass/ organomegaly

Percussion - shifting dullness, fluid thrill.

Auscultation - hyperactive bowel sound.

Perianal Skin Lesion Masses Melaena

Supraclavicular LN Cervical LN Axillary LN Inguinal LN

Confusion ( Shock, liver failure….)

Neurological Deficit

GENERAL INSPECTION

ABDOMEN

RECTAL

LYMPH NODES

CNSSAME WITH UPPER GI BLEED

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INVESTIGATION

1. Full Blood Count (FBC)2. BUSE3. Coagulation profile4. Cross-matched (Transfusion)

1. Scintigraphy -Radioactive test using Technetium-99m (99mTc)-

Labelled red cells -diagnose ongoing bleeding at a rate as low as 0.1

mL/min

2. Mesenteric angiography -Can detect bleeding at a rate of more than 0.5 mL/min.

LABORATORY

IMAGING

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IMAGING

3. Helical CT scan• Abdomen and pelvis • Can also be used when routine workup fails to

determine the cause of active GI bleeding • Multiple criteria are used to establish the

bleeding sites: -vascular extravasation of the contrast medium -contrast enhancement of the bowel wall -thickening of the bowel wall -spontaneous hyperdensity of the peribowel fat -vascular dilatations with helical CT.

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IMAGING

4.Colonoscopy• Bleeding slowly or who have already stopped

bleeding.• Biopsy

5.Proctosigmoidoscopy• Exclude an anorectal source of bleeding

6.Oesophagoduodenoscopy (OGDS)• To exclude upper GI bleeding

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IMAGING

7. Double-contrast barium enema

• Elective evaluation of unexplained lower GI bleeding

• Do not use in the acute hemorrhage

phase 8. Small bowel enema• Often valuable in investigation of long-

term, unexplained lower GI bleeding

Example of barium enema study showing ulcerative colitis of the colon

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INTUSSUSCEPTION

• Common in children within 1st year of life

• Symptoms: abdominal pain, red-currant-jelly stool

• Signs: palpable mass at right iliac fossa

• Procedure: Barium enema, laparotomy

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Colorectal polyps

• Adenomatous polyps and adenomas

• Has malignant potential• Morphology: -polypoid and

pedunculated-dome-shaped and sessile

• Histology: -degree of epithelial

dysplasia is highly variable

-carcinoma in situ -early invasive cancer:-

invasion of tumour cells through basement membrane→muscularis mucosa→submucosa

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TYPES OF COLORECTAL POLYPS

1.Tubular adenomas - small pedunculated / sessile lesions

-retain a tubular form similar to normal colonic

mucosa -least potential for malignant transformation

2. Villous adenomas -sessile and frond like lesions -secrete mucus

-more dysplastic -greater potential for malignant change

3. Tubulo-villous adenoma -intermediate between tubular and villous

adenoma -pedunculated, stalk is covered with normal epithelium 66/81

SIGN AND SYMPTOM

• Rectal bleeding• Iron deficiency anaemia• Mucus• Hypokalaemia• Tenesmus• Prolapse• Obstructive symptoms

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FAMILIAL ADENOMATOUS POLYPOSIS

• Autosomal dominant defect in APC gene

• Mid teen years- hundred / more adenomatous polyps

• Average age of 40- colorectal cancer

• Symptoms: -rectal bleeding -diarrhoea • Gardner’s syndrome=

+desmoid tumours + osteomas of mandible & skull

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INVESTIGATION

• Sigmoidoscopy• Colonoscopy -gold standard -visualize, biopsy, remove -disadvantage: full day’s bowel preparation sedation risk of haemorrhage & perforation• CT pneumocolon -elderly / infirm patient -< invasive & not require sedation. -bowel preparation• Double contrast barium enema 69/81

MANAGEMENT

• Subtotal colectomy & ileorectal anastomosis

• Panproctocolectomy & ileotomy / ileal pouch

• Follow-up colonoscopies - an adenomatous polyp is found / a

colorectal cancer has been treated -intervals depend on number, size & pathology of polyps

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ADENOCARCINOMA OF COLON & RECTUM

• Rare < 50 years old, Common > 60 years old

• Common site- sigmoid colon, rectum

• Clinical features: -altered bowel habit &

large bowel obstruction -rectal bleeding -iron deficiency

anaemia -tenesmus -perforation -anorexia & weight loss

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ANGIODYSPLASIA

• 1 or multiple small mucosal or submucosal vascular malformation.

• > 60 years old• Common site : ascending colon

and caecum• Malformations consist of dilated

tortuous submucosal veins• In severe cases, the mucosa is

replaced by massive dilated deformed vessels

• Clinical features: -acute / chronic rectal bleeding -iron deficiency anaemia

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INVESTIGATION

• Colonoscopy -bright red 0.5-1cm diameter

submucosal lesion -small dilated vessels

• Mesenteric angiography

• Radioactive test using technetium-99m –labeled red cells

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MANAGEMENT

• colonoscopic diathermy

• if patient seriously ill→ catheter is placed in the appendix stump and the colon irrigated progradely with saline or water→ on-table colonoscopy carried out and site of bleeding can be confirmed

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ISCHAEMIC COLITIS

• Elderly• Transient ischaemia of a

segment of a large bowel, followed by sloughing of mucosa

• Common site –splenic flexure• Clinical features: -abdominal pain -rectal bleeding ( dark red) -1-3x over 12 hours• Complication- fibrotic sticture

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HAEMORRHOIDS

• M > F• Female- late pregnancy,

puerperium• Supine lithotomy position- 3 ,7,

11 o’clock positions

• Classification: 1st degree : never prolapse 2nd degree: prolapse during

defaecation but return spontaneously

3rd degree : remain prolapse but can be reduced digitally

4th degree : long-standing

prolapse cannot be reduced

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HAEMORRHOIDS: SIGNS & SYMPTOMS

• Rectal bleeding• Perianal irritation & itching• Mucus leakage• Mild incontinence of flatus • Prolapse• Acute pain• Skin tags at anal margin

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ANAL FISSURE

• Longitudinal tear in mucosa & skin of anal canal

• M > F• Common site: midline in posterior

anal margin• Clinical features: - acute pain during defaecation - fresh bleeding at defaecation

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DIVERTICULAR DISEASE• Rare < 40 years old• F > M• Causes: -Chronic lack of dietary fibre -Genetic• Common site: sigmoid colon• Clinical features: -diverticulosis

(asymptomatic) -chronic grumbling

diverticular pain (chronic constipation & episodic diarrhoea)

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MANAGEMENT

1. Vasoconstrictive agents: vasopressin

2. Therapeutic embolization: -Embolic agents: Autologous clot, Gelfoam, polyvinyl alcohol, microcoils,

ethanolamine, and oxidized cellulose

-Selective angiography

3. Endoscopic therapy: -Diathermy / laser coagulation-Short term control of bleeding during resuscitation

• The bleeding point is localized, perform a limited segmental resection of the small or large bowel

• Poor prognostic features: -age over 60 years -chronic history -relapse on full medical

treatment -serious coexisting

medical conditions -> 4 units of blood

transfusion required during resuscitation

MEDICAL SURGICAL

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THANK YOU FOR YOUR aTTENTIONLUNCH TIME !!!

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