You already know that haematemesis can be due to gastrointestnal or non-gastrointestinal causes. Moreover, some diseases show up with haematemesis as the primary symptom whereas others only rarely or in their last stages present with this symptom.
It’s much more convenient to go through those diseases first that have this symptom as the primary one and then go through the ones that don’t usually present with haematemesis but possibly can in advanced stages or rare occasions. The gastrointestinal causes are discussed first.
- Esophageal Varices:
What are varices?
In the esophagus, these are pathologically dilated veins which lie in the submucosa. They are dilated due to portal hypertension (which is in turn due to liver cirrhosis, chronic liver diseases, etc). These varices can easily bleed and can cause massive haemorrhage resulting in severe shock or even death if the large bleed is not managed well.
How can we diagnose them?
The patient might have a history of haematemesis as well as liver failure but definitive diagnosis is made by endoscopy since it is not sufficient to assume that liver disease would cause varices which are the cause of the haematemesis. That is because liver disease also causes deficiency of clotting factors which directly causes bleeding within the oesophagus (and at numerous other sites in the body).
Remembering the blood supply of the oesophagus is crucial to understand the pathophysiology. Normally, the oesophagus is drained via the oesophageal veins and the superficial veins located within its mucosa. The former drain into the azygos which directly empties into the superior vena cava whereas the latter drain into the left gastric vein which empties into the portal vein. The superficial veins are usually no more than 1 mm in diameter but when they turn into varices, their diameter reaches 1-2 cm. This is a result of portal hypertension.
So what’s portal hypertension?
It’s easy to say portal hypertension is just raised pressure in the portal system. But what’s the mark where we label the pressure as ‘portal hypertension?’ The portal pressure is about 9 mmHg and that in the inferior vena cava is 2-6 mm Hg, giving us a gradient of 3-7 mm Hg. When the gradient crosses 5 mm Hg, it is said to be portal hypertension. But this pressure is not enough to cause the formation of varices. Varices, in essence, are collaterals that open up due to shunting from the portal system as a result of high pressure. When the portal pressure is above 10 mmHg, the blood has to be redirected to areas of low pressure, a purpose served well by portosystemic anastomoses which are present in the umbilicus, upper anal canal,lower oesophagus, retroperitoneum and the bare areas of the liver.
Cirrhosis is the most common cause of oesophageal varices, however, thrombosis of the splenic vein is also a causative factor (albeit rare) which results in the formation of varices WITHOUT AN INCREASE IN PORTAL PRESSURE. Another common cause of varices is aging which modifies blood vessels, forcing them to get dilated. Therefore, both splenic vein thrombosis and aging cause oesophageal varices without an increase in portal pressure.
Once formed, it is very cumbersome to treat varices. Management in emergency situations aims at mimimizing blood loss, ruling out any predisposing conditions and treating them, maintaining plasma volume and administering antibiotics which work against gram-negative bacteria (such as ceftriaxone or quinolone) since infection by these bacteria occurs either simultaneously or serves as a precipitating factor.
The main therapy is done by endoscopy in which either variceal ligation (banding) or sclerotherapy is done. If bleeding is recurrent, the stengstaken-blakemore tube (which has a balloon that can be dilated once inside the oesophagus, thus pressing on the varices and stopping the bleeding) might have to be used to stop the bleed and stabilize the patient until endoscopy can be attempted again. In terminal cases, a liver transplant is required.
Medical Treatment : A means of prevention
The following are employed to reduce the chances of bleeding in those patients who have already developed varices:
Non-selective Beta-blockers (these decrease cardiac output and block the vasodilating beta receptors of the splanchnic vessels) such as Propranolol (10 mg PO thrice daily) or Nadolol (20 mg PO once daily) are given with nitrates such as isosorbide mononitrate (these decrease resistance and thus lower portal pressures).
- Varices (merckmanuals.com)
- Esophageal Varices (wikipedia.org)
- Alcoholic Liver Disease (addictionts.com)