Upper Gastrointestinal Bleeding: Anthony Alexander University of The West Indies at Mona
Upper Gastrointestinal Bleeding: Anthony Alexander University of The West Indies at Mona
Upper Gastrointestinal Bleeding: Anthony Alexander University of The West Indies at Mona
Bleeding
Anthony Alexander
University of the West Indies at Mona
Overview
Loss of blood from the upper gastrointestinal tract
Clinical spectrum ranging from haematemesis to
circulatory collapse
Occurs at any age
Particularly between the ages of 40-79
Mortality greatest in patients above 60
50-150/100,000 adults/year (US), 50-120/100,000 (UK)
Relevant Anatomy Ligament of
Treitz
•Runs from crus of
diaphragm to DJ
flexure
•Bleeds originating
above this point are
classified as UGIB
Aetiology
Common
Peptic ulcer (35-50%)
Gastritis & gastric erosions (10-20%)
Oesophagitis (10%)
Bleeding varices (2-9%)
Drugs: NSAID, aspirin, steroids, thrombolytics,
anticoagulants
No obvious cause
Aetiology
Less common
Mallory-Weiss tear (5%) & Boorhaave’s
Vascular malformations (5%)
Cancer of oesophagus/duodenum (2%)
Aortoenteric fistula (0.2%)
Pathophysiology
Depends on the aetiology, but…
Most commonly:
Mucosal erosion into blood vessels haemorrhage
Strong association with:
H. pylori: inflammatory effect on gastric mucosa
NSAIDS: ↓COX activity thus impaired mucosal protection
against acid
Alcohol consumption
Pathophysiology
Oesophageal varices
Portal hypertension leads to dilated submucosal
veins in lower oesophagus
Blood that would flow through the portal circulation
is redirected to areas of lower venous pressure
These dilated vessels are susceptible to bleeding
Pathophysiology
Mallory-Weiss tear
Retching against closed LES increased intragastric
pressure
There is now a gradient between intragastric and
intrathoracic pressures
If a shearing force is generated longitudinal
laceration
Presentation
History
Haematemesis
Red with clots with severe bleeding
‘Coffee grounds’ when less
Melaena/Haematochezia
Dark, tarry foul smelling stool
Estimated blood loss and symptoms of hypovolaemia
Pain
Duration
Vomiting/retching
Past Mx Hx: Previous GI bleed, coagulopathy, known liver disease/varices
Comorbidities: cardiovascular, respiratory, hepatic/renal
Past Sx: AAA
Drugs
Social: alcohol consumption
Examination
General
Mucous membranes
Cool, clammy, pale skin
Decreased conscious level
Respiratory distress
Examination
Signs of circulatory compromise
Altered consciousness hepatic encephalopathy
Reduced urine output
Tachycardia
Hypotension (SBP <100 mmHg)
Postural drop in BP (>20 mmHg, systolic)
Examination
Signs of chronic liver disease
Leukonychia
Clubbing
Palmar
Asterixis
Jaundice
Gynaecomastia
Ascites
Spider Naevii
Distended veins
Signs of hepatic encephalopathy
Examination
Abdomen
Distension
Tender epigastrium, tender/enlarged liver, AA
Abdominal scars: aneurysm repair?
Caput medusae, distended veins
Ascites
Rectal
Melaena
Haemathochezia
Management
Secure airway
Sever haematemesis from bleeding varix/ulcer
↓conscious level due to extensive blood loss loss of
airway protective reflexes
May need to intubate
Management:
Secure breathing
Supplemental oxygen
Management
• Secure circulation
2 large bore IV cannulae
CBC
U+E
LFT
Clotting studies
Group and crossmatch
Crystalloid bolus: 2L or 20ml/kg
Blood: type O if necessary
Aspiration pneumonia
Perforation (1% for the first endoscopic therapy, 3% for the second)
Bleeding can be caused by drilling into the vessel with the laser, by
Ileus
Sepsis
Myocardial infarction
Prognosis
10 % die
Summary
UGIB is the most common GI emergency
PUD is the commonest cause
ABC’s, monitoring
PPI’s
Arrange for urgent endoscopy