Upper GI bleed
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Upper GI bleeding is a major complication of Peptic ulcer disease. It occurs in 1/2000 people each year, of which ½ of these cases are due to PUD. Also remember that patients who take long term aspirin not only have increased risk of ulcer, but that they have a reduced platelet count, so if their ulcer bleeds, they are likely to lose more blood.

1/10 people who have a GI bleed will die.


  • Hematemesis – fresh blood in vomit – caused by a bleed anywhere above the jejunum.
  • Melena – altered blood passing from the rectum – i.e. it isn’t fresh. This often has a tar like appearance and a very distinctive smell! Melena is suggestive of an upper GI bleed due to the fact the blood has been altered on travelling through the GIt. It can be caused by a bleed anywhere from the oesophagus to the rectum.
  • Hematemesis and melena together
  • Abdominal discomfort
  • Dizziness
  • Sudden death!
Bleeding from below the duodenal/jejunal junction will virtually never produce haematemesis. The more altered that blood in the stool is, the more likely it is to be from higher up the GIt.
Blood is a good laxative, and it is also likely to cause colicky pain. Chronic bleeding is far more common that acute, and it is likely to produce iron deficiency anaemia.


  • Gastric ulcer – 26%
  • Duodenal ulcer – 23%
  • Oesophagus – 12%
  • Acute gastric erosions – 7%
  • Gastric cancer – 3%
  • Oesophageal varices – 8%
On endoscopy, blood clots appear as little black dots on the sites of the ulcer. The clots are usually digested within ½ an hour, so when clots are present, this suggests continued bleeding. A bleeding ulcer means the ulcer has eroded a blood vessel.
In serious cases, you will actually see the blood spurting from an artery!

Oesophageal bleeding

Oesophagitis is a general term used to describe inflammation of the oesophagus. It is caused mainly by stomach acid. The causes are listed below.
  • GORD – Gastro-oesophageal reflux disease – this will produce small volumes of bright red blood. This condition is chronic mucosal damage caused by acid reflux into the oesophagus. It is often caused by incompetence of the cardia or by problems expelling normal gastric reflux from the oesophagus. This condition often results in Barrett’s oesophagus; a condition where the epithelium of the bottom of the oesophagus changes to be more like that of the stomach as a result of prolonged exposure to acid. It can extend up to 10cm up the oesophagus.
  • Some people use the term hiatus hernia to mean a similar thing to GORD, but infact this is incorrect. A hiatus hernia is a congenital defect present in about 40% of people where part of the stomach extends above the level of the diaphragm. Normally it causes no problems, but it some people it can be a causatory factor in gastric reflux

Mallory-Weiss tear

This will produce larger volumes of bright red blood.This often occurs after a period of prolonged and vigorous retching and vomiting, most commonly often after a period of heavy drinking. The retching is so strong that it tears the oesophageal / gastric junction, causing heavy bleeding. The bleeding will result in haematemesis. Usually it will stop by itself, and these patients will need no further treatment
  • Chemical injury
  • Infection

Oesophageal varices

This will produce large volumes of dark red blood. These are an effect of severe liver disease. In liver disease, the pressure in the portal system will increase greatly. As a result, anywhere where blood can ‘escape’ the portal system and get back to systemic circulation will become overloaded with blood, and the oesophagus as well as the rectum is a place where this can occur. As a result, in liver disease you will get oesophageal and rectal varices. Suspected varices require urgent endoscopy.  If on endoscopy you see the white nipple sign (the varices have an obvious white ‘tip’ a bit like a spot), then this is a sign that the varices have already bled, or are about to bleed. This whiteness is caused by a local weakness in the variceal wall. In some people it may appear red.

  • They are often sudden onset and painless. There will usually be a history of liver disease, and there will be physical signs of portal hypertension.
  • 8% of Upper GI bleeding is due to varices. Varices will develop in 50-60% of cirrhotic patients.
  • Varices carry a mortality rate of 50%, and a re-bleeding rate of 60-70%.

Gastric bleeding

  • Erosive gastritis – small bleed of bright red blood – may often follow NSAID intake or a bout of stress. There will be a history of dyspepsia
  • Gastric ulcer – larger bleed, often painless. The patient may have had previous smaller bleeds – history of PUD.
  • Gastric cancer – usually a small bleedanaemia is common. There will also be weight loss and dyspepsic symptoms.
  • Dieulafoy’s disease – spontaneous large bleed – very rare; accounts for <5% of all gastric bleeds. Often occurs in young people. It is caused by little gastric ‘aneurysms’ that occur during development and then rupture.
  • Gastric ulcers

Duodenal bleeding

  • Duodenal ulcers – usually accompanied by a prominent melena.
  • Artoduodenal fistula –Massive haematemesis and PR bleed –  these are very rare, and are usually a result of a rupture abdominal aortic aneurysm repair. They are nearly always fatal.
There is a scoring system to measure the severity of GI bleeds, known as the Rockall scoring system. This gives a score from 0-8+ and from this score you can predict the likelihood of mortality and re-bleeding. This helps you decide what to do with the patient.
You should never perform endoscopy on a bleeding patient as you could worsen the patient and even kill them. You should wait until you have stabilised the patient first (~24hrs).


  • FBC:  carcinomas, reflux oesophagitis.
  • LFTs:  liver disease (varices).
  • Clotting:  alcohol, bleeding diatheses.
  • OGD:  investigation of choice. High diagnostic accuracy, allows
  • therapeutic manoeuvres also (varices: injection; ulcers:
  • injection/cautery).
  • Angiography:  rare duodenal causes, obscure recurrent bleeds.
  • Barium meal and follow through: useful for patients who are unfit for
  • OGD (respiratory disease) and ?proximal jejunal lesions.


Peptic ulcer – you should act immediately to reduce the amount of acid in the stomach. This will inhibit the action of pepsin, and may encourage the initial bleed to heal by itself if the first 24 hours.
The rest is then exactly the same as you would treat a normal peptic ulcer!
Oesophageal Varices– you should treat the chronic liver disease with non-selective β-blockers to lower the general venous pressure and reduce the risk of variceal bleeding.
  • If the varices present before they have bled, then you can treat them with ‘banding’ whereby youjust stick a little band around the bulging varices and the weakest part of the vein will be cut off from the rest, and will eventually just drop off. This treatment can be done by endoscopy.
  • In acute severe variceal bleeding, where the patient is in immediate danger, you may wish to use a Minnesota tube. This is a tube that is inserted down the oesophagus, into the stomach, and a small bag of air inflated at the bottom with about 300ml of air. This first bag prevents the tube being pulled out of place. There is a second bag that can also be filled with air that sits in the oesophagus. This bag is inflated to around 40mmHg pressure – just above normal venous pressure – and thus this keeps blood in the veins, rather than letting it spurt out into the oesophagus. You must be very careful when inflating the second bag as you can perforate the oesophagus!
  • This is only a temporary solution. It is often very uncomfortable for the patient
Minnesota tube
 Management of an Upper GI bleed: flow chart


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Dr Tom Leach

Dr Tom Leach MBChB DCH EMCert(ACEM) FRACGP currently works as a GP and an Emergency Department CMO in Australia. He is also a Clinical Associate Lecturer at the Australian National University, and is studying for a Masters of Sports Medicine at the University of Queensland. After graduating from his medical degree at the University of Manchester in 2011, Tom completed his Foundation Training at Bolton Royal Hospital, before moving to Australia in 2013. He started almostadoctor whilst a third year medical student in 2009. Read full bio

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