Case-based discussion: 1 History A 65-year-old lady is brought in by ambulance after a 4-hour history of coffee ground vomit. She has a background of severe osteoarthritis of the knees but is otherwise well. On examination, she has a tender epigastrium. Her rectal examination reveals black stool. Observations HR 95, BP 110/80 mmHg, RR 22, SpO2 93%, Temp 37.5 2 (1A) 3 Case history History A 65-year-old lady is brought in by ambulance after a 4-hour history of coffee ground vomit. She has a background of severe osteoarthritis of the knees but is otherwise well. On examination, she has a tender epigastrium. Her rectal examination reveals black stool. Observations: HR 95, BP 110/80 mmHg, RR 22, SpO2 93%, Temp 37.5 Q1 Q2 Q3 Q4 Q5 Q6 What is the most likely cause of this patient’s symptoms? Gastric ulcer Duodenal ulcer Oesophageal ulcer Variceal bleed Mallory-Weiss tear app.bitemedicine.com 4 Explanations Q1 Q2 Q3 Q4 Q5 Q6 What is the most likely cause of this patient’s symptoms? Gastric ulcer Less common than a duodenal ulcer Duodenal ulcer Coffee—ground vomiting, epigastric pain, melaena and likely on NSAIDs (for osteoarthritis) Oesophageal ulcer Less common than a duodenal ulcer and usually a long-standing history of GORD Variceal bleed Would expect features of chronic liver disease and less common than peptic ulcer disease Mallory-Weiss tear Minimal haematemesis, self-limiting, preceding history of wretching/vomiting app.bitemedicine.com 5 Case-based discussion: 1 History A 65-year-old lady is brought in by ambulance after a 4-hour history of coffee ground vomit. She has a background of severe osteoarthritis of the knees but is otherwise well. On examination, she has a tender epigastrium. Her rectal examination reveals black stool. Observations HR 95, BP 110/80 mmHg, RR 22, SpO2 93%, Temp 37.5 6 Introduction Definition • Upper gastrointestinal bleeding refers to bleeding originating proximal to the ligament of Treitz (duodenojejunal junction) Upper Gastrointestinal Epidemiology tract • 70,000 annual hospital admissions in the UK • Non-variceal origin is most common • Mortality rate: 10% Duodenojejunal junction (1B) 7 Aetiology Common • Peptic ulcer disease (26%) • Oesophageal varices (16%) • Oesophagitis (17%) • Mallory-Weiss tear (3%) Uncommon • Boerhaave syndrome • Gastric varices • Arteriovenous malformations • Dieulafoy’s lesions 8 Case history History A 65-year-old lady is brought in by ambulance after a 4-hour history of coffee ground vomit. She has a background of severe osteoarthritis of the knees but is otherwise well. On examination, she has a tender epigastrium. Her rectal examination reveals black stool. Observations: HR 95, BP 110/80 mmHg, RR 22, SpO2 93%, Temp 37.5 Q1 Q2 Q3 Q4 Q5 Q6 Which of the following best describes the bacterium associated with peptic ulcer disease? Gram positive rod Gram negative rod Gram negative spiral Gram positive spiral Gram negative coccus app.bitemedicine.com 9 Explanations Q1 Q2 Q3 Q4 Q5 Q6 Which of the following best describes the bacterium associated with peptic ulcer disease? Gram positive rod Examples include Corynebacterium, Clostridium and Listeria Gram negative rod Examples include Klebsiella, Pseudomonas, Salmonella and E.coli Gram negative spiral Correct description of Helicobacter Pylori Gram positive spiral Spirilla are gram negative, whilst spirochetes are difficult to Gram stain (types of spiral bacteria) Gram negative coccus Examples include Neisseria gonorrhoeae, Haemophilus influenzae and Neisseria meningitidis app.bitemedicine.com 10 Pathophysiology Aetiology Mechanism • H. pylori • Aggressive factors overwhelm protective factors Peptic ulcer disease • NSAIDs • Aggressive: acid, pepsin, H. pylori, NSAIDs • Defensive: bicarbonate layer (2A) (2B) 11 Pathophysiology Bleeding ulcer vs. Perforated ulcer 12 Pathophysiology Aetiology Mechanism • H. pylori • Aggressive factors overwhelm protective factors Peptic ulcer disease • NSAIDs • Aggressive: acid, pepsin, H. pylori, NSAIDs • Defensive: bicarbonate layer Portal hypertension • Liver damage causes portal hypertension Oesophageal varices • Increased resistance • Development of collateral vessels • Increased flow 13 Pathophysiology (2D) (2E) (2C) 14 Pathophysiology (3) 15 Pathophysiology Aetiology Mechanism • H. pylori • Aggressive factors overwhelm protective factors Peptic ulcer disease • NSAIDs • Aggressive: acid, pepsin, H. pylori, NSAIDs • Defensive: bicarbonate layer Portal hypertension • Liver damage causes portal hypertension Oesophageal varices • Increased resistance • Development of collateral vessels • Increased flow • GORD • GORD irritates the oesophagus à inflammation • Medicines e.g. NSAIDs and Oesophagitis doxycycline • Crohn’s disease 16 Pathophysiology Aetiology Mechanism • H. pylori • Aggressive factors overwhelm protective factors Peptic ulcer disease • NSAIDs • Aggressive: acid, pepsin, H. pylori, NSAIDs • Defensive: bicarbonate layer Portal hypertension • Liver damage causes portal hypertension Oesophageal varices • Increased resistance • Development of collateral vessels • Increased flow • GORD • GORD irritates the oesophagus à inflammation • Medicines e.g. NSAIDs and Oesophagitis doxycycline • Crohn’s disease • Straining, coughing, retching • Sudden rise in pressure across the GOJ Mallory-Weiss tear • Often history of alcohol excess • Distention in oesophageal region 17 Pathophysiology Aetiology Mechanism • H. pylori • Aggressive factors overwhelm protective factors Peptic ulcer disease • NSAIDs • Aggressive: acid, pepsin, H. pylori, NSAIDs • Defensive: bicarbonate layer Portal hypertension • Liver damage causes portal hypertension Oesophageal varices • Increased resistance • Development of collateral vessels • Increased flow • GORD • GORD irritates the oesophagus à inflammation • Medicines e.g. NSAIDs and Oesophagitis doxycycline • Crohn’s disease • Straining, coughing, retching • Sudden rise in pressure across the GOJ Mallory-Weiss tear • Most diseases that induce • Distention in oesophageal region vomiting 18 Question Q1 Q2 Q3 Q4 Q5 Q6 Which of the following best explains the pathophysiology of an oesophageal variceal bleed? Increased pressure in the left gastric vein Increased pressure in the middle gastric vein Increased pressure in the azygos vein Increased pressure in the intercostal veins Increased pressure in the coeliac artery app.bitemedicine.com 19 Explanations Q1 Q2 Q3 Q4 Q5 Q6 Which of the following best explains the pathophysiology of an oesophageal variceal bleed? Increased pressure in the left gastric vein Lower 1/3 of the oesophagus drains into portal veins via left gastric vein; portal hypertension à varices Increased pressure in the middle gastric vein This does not exist Increased pressure in the azygos vein The upper oesophagus drains à azygos vein à SVC; not involved in the formation of varices Increased pressure in the intercostal veins These drain the intercostal space and are not involved in the formation of varices Increased pressure in the coeliac artery Varices are engorged veins; the coeliac artery is not involved app.bitemedicine.com 20 Pathophysiology (2) (3) 21 Other causes Aetiology Mechanism • Vomiting • Sudden rise in oesophageal pressure during vomiting causes rupture Boerhaave syndrome • Left posterolateral wall of lower oesophagus most commonly affected 22 Other causes Aetiology Mechanism • Vomiting • Sudden rise in oesophageal pressure during vomiting causes rupture Boerhaave syndrome • Left posterolateral wall of lower oesophagus most commonly affected • Large blood vessels beneath the • Pulsation from large vessel leads gastrointestinal mucosa bleeds to thinning of the mucosa Dieulafoy’s lesions • No abnormality (ulceration or • Vessel becomes exposed erosion) 23 Clinical features Vs. (1B) 24 Clinical features Symptoms Signs Haematemesis Possible abdominal tenderness +/- peritonism • E.g. variceal bleed or Mallory-Weiss tear Coffee-ground vomiting • E.g. peptic ulcer disease or oesophagitis Melaena Shock: e.g tachycardia and hypotension Abdominal pain: e.g. epigastric pain in PUD Chronic liver disease: suggests variceal bleed • Encephalopathy • Scleral icterus • Hepatosplenomegaly Chest pain and SOB: e.g. Boerhaave syndrome Anaemic features: e.g. chronic bleeding tumour 25 Differentials History Clinical findings Initial investigations • Coffee-ground • Epigastric tenderness • Bloods vomitus • Shock if perforated • H. pylori urea breath Peptic ulcer disease • Epigastric pain test • NSAID / steroid use • Erect CXR • Previous ulcers • OGD • Sudden onset, • Signs of chronic liver • Bloods projectile, significant disease • OGD Oesophageal varices haematemesis • Shock • Chronic liver disease 26 Differentials History Clinical findings Initial investigations • Coffee-ground vomitus • Epigastric tenderness • Bloods • Epigastric pain • Shock if perforated • H. pylori urea breath Peptic ulcer disease • NSAID / steroid use test • Previous ulcers • Erect CXR • OGD • Sudden onset, • Signs of chronic liver • Bloods projectile, significant disease • OGD Oesophageal varices haematemesis • Shock • Chronic liver disease • GORD • ’Heartburn’ • Bloods Oesophagitis • Nausea and bloating • OGD • Self-limiting • Epigastric tenderness is • Bloods haematemesis after possible • OGD Mallory-Weiss tear retching/vomiting • Stable • Alcohol excess 27 Differentials History Clinical findings Investigations • Severe • Retrosternal +/- • Bloods retching/vomiting à epigastric pain • CXR and CT chest extreme retrosternal • Subcutaneous pain emphysema Boerhaave syndrome • SOB • Fever • Alcohol