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  • 0.1% of hospital admissions; but high mortality rate. Up to 10% of people who die in hospital had GI bleeding.
  • High risk:
    • Bleeding because of liver cirrhosis - likely to die because liver is decompensated
    • Bleeding with haemodynamic disorder (e.g. anaemia, cardiovascular disease)
    • Age
  • Sources of bleeding
    1. Peptic ulcers (though now it's curable)
    2. Varices
    3. Mallory-Weiss tears (not a killer)
    4. Gastroduodenal erosions
    5. Erosive oesophagitis
    6. Malignancy
    7. No source identified

Upper GI bleeding - presentation

  • haematemesis
    • bright red blood or brown “coffee grounds” (digested by gastric enzymes)
  • melaena
    • can develop with ~100ml blood loss in upper GIT
    • looks like vegemite
  • bright red blood per rectum (haematochezia) - very rare
    • massive upper GI bleed (>1000ml)
  • iron-deficiency anaemia
    • chronic bleeding, don't eat well due to ulcer
    • top of priority = colon cancer. Anyone over 60 with iron deficiency anaemia should be investigated for colon cancer.


  • Erosions
    • mucosal lesions, focal loss of surface epithelium
    • fast to heal with normal turnover
  • Ulcers
    • Penetrate through muscularis mucosae
    • can continue as far as the peritoneum (perforation) or could penetrate into another organ
    • chronic - repair component

Peptic ulcer disease

remitting and recurring

  • haemorrhage is the most common serious complication of peptic ulcer disease
    • Occurs in 15-20% of patients
    • Accounts for 25% of ulcer deaths
  • What are the other common complications?
    • perforation & peritonitis; 2/3 of deaths
    • bleeding; 1/3 deaths
    • other: malignant transformation,
  • duodenal ulcer is more common than gastric ulcer
    • can result in gastric outlet obstruction & projectile vomiting (due to
      • treatment - Bilroth operation
  • punched-out hole, at the bottom there is necrotic debris. Acid means it doesn't heal. You have acute inflammation on surface, then granulation below it, then fibrosis beneath that. Has a flush edge. Rugae also get flattened (atrophic chronic problem)
    • intestinal metaplasia happens as a result of chronic peptic ulcer; Goblet cells, columnar cells, produce mucus rather than acid
  • culprit: H. pylori - doesn't infect, colonises
    • produces urease enzyme - makes ammonium byproducts, and also the inflammation
      • also makes the pH of the stomach nearby a little alkaline to keep it alive
    • 20% of H. pylori infected people get peptic ulcer
    • if you have the ulcer, you're likely to have bacteria, but not around the other way
    • treatment: antibiotic + proton pump inhibitor (covers both acidity and bacteria people)
  • symptoms on peptic ulcer
    • epigastric pain
      • remember, epigastric pain can be myocardial infarction - so make sure to remember MI as a differential - first do ECG. Peptic ulcer can wait in the queue
    • pain after feeding (duodenal)
    • pain all the time (gastric)
    • early satiety
    • anorexia
    • indigestion, heartburn, reflux
  • Diagnosis of H pylori infection
    • urea breath test - cheap, noninvasive, effective
      • complex instructions
    • Biopsy and rapid urease test
    • Biopsy and microscopic examination
    • Biopsy and culture
    • serology - useful in children
      • stool: look for antigen not antibody (for active infection)

13/14C urea breath test procedure

  1. Expel breath into breath bag/tube Baseline level
  2. Drink 13/14 C-labelled test liquid (containing urea)
  3. Wait for 30 minutes
  4. Expel breath into second breath bag/tube
  5. Measure labeled 13/14CO2

Outcome of 13/14CUBT for H. pylori

  • Helicobacter pylori present
    • Labelled urea hydrolyesed to 13/14CO2
    • Circulates to lungs
    • Expired in breath
    • Detection
  • Biopsy for peptic ulcer disease indicated in:
    • Risk for malignancy (= weight loss, lymphadenopathy, palpable mass)
    • Bleeding - since we have to do endoscopy any way

==A test and treat strategy for H. pylori infection==

  • Uninvestigated persistent dyspepsia who are less than 45 years of age without:
    • bleeding
    • anaemia
    • earlysatiety
    • unexplained weight loss
    • progressivedysphagia(difficulty)
    • Odynophagia (pain)
    • recurrent vomiting
    • family history of gastrointestinal cancer
    • previous esophagogastric malignancy

NSAIDs induced ulcers

  • peptic ulcers in 3-4% of chronic NSAIDs users per year
  • ulcer bleeding or perforation in ~1.5% of chronic users per year
  • ~40% of patients with first episode of NSAIDs-associated upper GI bleed had no warning symptoms
    • Because they're on painkillers
    • Because they have a higher threshold to pain - which is why they're taking painkillers
  • Proactively ask people who are chronically on painkillers - do you have abdominal pain?

NSAIDs -Pathophysiology

  • direct toxicity on epithelium
  • epithelial effects (due to low prostaglandins)
  • low mucin secretion

–  HCO3- secretion –  HCl secretion –  epithelial cell proliferation • reduced blood flow

  • all affect mucosal defense

Locations of ulcers

  • First part of duodenum
  • Stomach antrum
  • Gastroesophageal junction
    • Reflux , Barrett esophagus
  • Margins of gastrojejunostomy - jejunum not equipped for acid
  • Duodenum, stomach and/or jejenum
    • Zollinger-Ellison syndrome: ulcers everywhere. This is a gastrin-producing tumour that increases gastric acid
  • NB - Fundus - mostly ulcerating gastric cancers
  • See pictures of ulcers
    • Second one - source of bleeding, punched-out hole, flattened rugae, metaplastic change
    • Hyperaemic margin
      • Ulcer with heaped up margins - malignancy
    • Take biopsy from the margin
  • Barium meal not done now because of endoscopy
  • Slide: top = lumen, A = intestinal metaplasia, otherwise relatively normal B = base of ulcer - lots of necrotic debris, with neutrophils, fibrin, congested BVs C = granulation tissue (oedema, macrophages, collagen but not well organised) D = scar tissue (organisation). Beneath this is pancreatic glandular tissue - stomach is adherent to the pancreas (perforation through to pancreas). Stars = thick blood vessels. Arteritis obliterans - media gets thicker as the result of the chronic inflammation --> ischaemia, so it contributes to the problem.

Acute gastric erosions

  • mucosal lesions
    • usually do not cause major bleeding
  • causes include:
    • NSAIDs
    • alcohol
    • physiological stress

Stress-related gastric erosions

  • severe medical or surgical illness
    • serious trauma
    • extensive burns (Curling’s ulcer)
    • major intracranial disease
    • sepsis
  • high mortality rate due to underlying illness

These are small but multiple (unlike chronic), and have high mortality rate (other complications), rugae usually intact.

Johnson Classification of peptic ulcers

  • Type I: Ulcer along the body of the stomach, most often along the lesser curvature.
  • Type II: Ulcer in the body in combination with duodenal ulcers. Associated with acid oversecretion.
  • Type III: In the pyloric channel within 3 cm of pylorus. Associated with acid oversecretion.
  • Type IV: Proximal gastroesophageal ulcer
  • Type V: Can occur throughout the stomach. Associated with chronic NSAID use (such as aspirin).

Oesophageal varices

  • Secondary to portal hypertension
    • Pre-hepatic
      • Obstruction of portal vein, splenomegaly
    • Intra-hepatic
      • Liver cirrhosis (most common cause, present in 50% of patients)
        • Alcohol(60%)
        • Viral(10%)
        • Biliary diseases(5%)
        • Hemochromatosis(5%)
        • Cardiac (RHF, pericarditis)
        • Granulomatous inflammations(Schsito,TB,Syphilis)
        • Cryptogenic(10%)
  • Post-hepatic
    • Hepatic vein thrombosis (Budd-Chiari Syndrome)

Portosystemic collaterals

  • Dilated tortuous submucosal and mucosal veins
  • Risk of bleeding with increased size
  • but poor correlation with portosystemic pressure gradient
  • Caput medusae, oesophageal varices, rectal haemorrhoids
  • Main trigger for oeseophageal varices rupture is vomiting, happens with alcohol consumption
    • Varices - tortuous and dilated
    • Coagulopathy due to poor liver synthesis of factors 2, 7, 9, 10
    • Bleeding, swallow the blood, nitrogenous products from product of blood (can't metabolise all the protein) --> hepatic encephalopathy (only just enough liver to keep them going)

==Consequences of cirrhosis==

  • portal hypertension
    • varices
    • splenomegaly
    • ascites
  • hepatic failure
  • hepatocellular carcinoma

Oesophageal varices

  • Blood in gastrointestinal tract --> Acute nitrogenous load --> Hepatic encephalopathy --> Death


  • Give them nitrogylcerine to reduce pressure - vasodilator
  • Band ligation to stop bleeding
  • Sclerotherapy - weld the blood vessel
  • Gastric balloon to pressurise the bleed
  • High pressure - shunting surgery; connect portal vein to IVC, or connect splenic vein to the portal vein (need to remove the spleen)
    • Risk: sepsis. Portal venous system isn't sterile
  • Ultimate treatment: liver transplant

Mallory-Weiss tear

  • longitudinal tear in gastro-oesophageal mucosa
  • usually caused by prolonged forceful vomiting and/or retching
  • commonly seen in alcoholics
  • 80-90%ofpatientsstopbleedingspontaneously
  • makes them panic, but doesn't kill them

Erosive oesophagitis

  • Gastro-oesophageal reflux
  • Chemical injury
    • accidental ingestion in children
    • suicide bids in adults
  • Infective oesophagitis
    • in immunocompromised patients
  • Candida, HSV, CMV


  • Dysphagia
  • Pain on swallowing
  • Complete obstruction from not being able to swallow
  • Upper GI bleeding
  • See Harrison's picture for upper GI bleeding