Causes of Upper GI Bleeding Flashcards
Causes of upper GI bleeding
Mallory-weiss tear
Oesophago-gastric varices
Peptic ulcer
What is a Mallory-Weiss tear
This is a linear mucosal tear occurring at the oesophagogastric junction and
produced by a sudden increase in intra-abdominal pressure
Lead to bleeding
Clinical presentation of Mallory-Weiss tear
Bout of retching or vomiting -> Haemetesis
Others: Syncope, light headedness, dizziness
Pathophysiology of Mallory-Weiss tear
Sudden increased intragastric pressure within the non-distensible lower oesophagus can cause tearing of the mucosa.
Blood then enters the oesophagus and is vomited out
Aetiology of Mallory-Weiss tear
Trauma from frequent cough, vomit, retching or even hiccuping
RF: Excessive alcohol consumption; NSAIDs
Epidemiology of Mallory-Weiss tear
2-8% all Upper GI bleeding
Bulimics and alcoholics
Males aged 20-50
Diagnosis of Mallory-Weiss tear
Differentials
*Endoscopy (confirms)
Differential diagnosis:
Gastroenteritis; peptic ulcer; oesophageal varices
Treatment of Mallory-Weiss tear
Resuscitation
Maintain airway, high flow oxygen, correct fluid losses
Identify co-morbidities
Tear tends to heal rapidly
Complications of Mallory-Weiss tear
Hypovolaemic shock (and death)
Rebleeding
MI
Such bleeding rare
What are Oesophago-Gastric varices
Dilated veins at the junction between the portal and systemic venous systems leading to variceal haemorrhage
Clinical presentation of Oesophago-Gastric varices
Haematemesis
Liver disease
Pallor
Shock (low BP/ high HR)
Pathophysiology of Oesophago-Gastric varices
Liver disease leads to high pressure in the portal veins -> veins at the junction with systemic venous system distend (varices).
This causes damage and can lead to bleeding from the varices into the oesophagus -> Haematemesis
Aetiology of Oesophago-Gastric varices
Portal hypertension
Majority of patients with oesophageal varices have chronic liver disease
Epidemiology of Oesophago-Gastric varices
10-20% of all Upper GI bleeding
Diagnosis of Oesophago-Gastric varices
Endoscopy
Treatment of Oesophago-Gastric varices
Resuscitation Maintain airway Treat shock other: Vasoactive drugs Endoscopic band ligation Antibiotics as prophylaxis Can obturate with glue like substance
Complications of Oesophago-Gastric varices
70% chance of rebleeding
Significant risk of death
What is a peptic ulcer
Break in the GI mucosa in or adjacent to acid bearing area
Types of peptic ulcer
Gastric
Duodenal
What % of Gastric peptic ulcer is H.pylori associated with?
80%
What % of Duodenal peptic ulcer cases is H.pylori associated with?
95%
Where in stomach can H.pylori be found
Mucus layer
Clinical presentation of peptic ulcer
Burning epigastric pain. Nausea, heartburn, and flatulence. Occasionally painless haemorrhage.
(Not vomiting)
Difference in clinical presentation between duodenal and gastric peptic ulcer
Duodenalmore pain when the patient is hungry, and at night.
Pathophysiology of peptic ulcer
Depending on the aetiology, a reduction in protective prostaglandins or an increase in gastric acid secretions causes the acidic contents of the stomach/duodenum to break down the mucosa. Pain varies with the acid level of the area affecting the ulcer. H. pylori can infect mucosa following this damage -> further damage through inflammation and proteases.
**Aetiology of peptic ulcer
H. pylori, Bile Regurgitation, Ischaemia of mucus producing cells and NSAIDs.
H. pylori: Increased gastric acid secretions. Disruption of mucous protective layer. Reduced duodenal bicarbonate production
NSAIDs (Ibuprofen): Inhibit cycloxygenase-1 which inhibits production of prostaglandins needed for mucous production and provide mucosal protection in the upper GI - thus mucousal damage.
Ischaemia, reducing blood flow to mucus secreting cells, therefore less mucus secreted and so acid of stomach destroys these cells and over time causes ulceration.
Bile regurgitation
Epidemiology of peptic ulcers
50% of all Upper GI bleeding
Duodenal 2-3x more common than gastric
*Diagnosis of peptic ulcers
Testing for H.pylori: Urea breath test, serology or stool antigen test Alternatively endoscopy (but more invasive)
Treatment of peptic ulcers
Avoid NSAIDs Cessation of smoking Eradication of H.pylori through 2 antibiotics and PPI ->Triple therapy: Lansoprazole (PPI) Clarithromycin Metronidazole or Amoxicillin Antacids also helpful
Complications of peptic ulcers
Can cause upper GI bleed
Peritonitis if continues to grow
Prevention of bleeding from vatical haemorrhage
- Non-selective B-blockade e.g. PROPRANOLOL to reduce resting pulse rate to decrease portal pressure
- Variceal banding repeatedly (to obliterate varices)
- Liver transplant - best option when there is poor liver function
Initial management of bleeding from variceal haemorrhage
- Resuscitate until haemodynamically stable
- If anaemic then BLOOD TRANSFUSION aiming to get Hb to 80g/L
- Correct clotting abnormalities -> administer VITAMIN K and PLATELET TRANSFUSION
- Vasopressin -> IV TERLIPRESSIN -> to cause vasoconstriction, (use IV SOMATOSTATIN if terlipressin is contraindicated e.g. in ischaemic heart disease)
- Prophylactic antibiotics to treat and prevent infection as well as reduce early rebleeding and mortality e.g. CEPHALOSPORIN
- Variceal banding
- Ballon tamponade to reduce bleeding by placing pressure on varice if banding fails
What is variceal banding
where a band is put around varice using an endoscope, after a few days the banded varix degenerates and falls off leaving a scar
How do NSAIDs cause mucosal damage
NSAIDs inhibit cyclooxygenase-1 which inhibits the production of prostaglandins needed for mucous production, leading to mucosal damage
Medical treatment of oesophageal varices
Beta blocker to reduce CO -> reduce portal pressure
Nitrate to reduce portal pressure
Terlipressin – analogue of ADH -> reduce portal pressure
Surgical treatment of oesophageal varices
Band ligation
Transjugular intrahepatic portosystemic shunt (TIPSS)
