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Oesophageal Varices

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This means varicose veins of the oesophagus. Just like varicose veins in the leg, the veins on the inside of the oesophagus can become enlarged, swollen and tortuous.

These varicosities are caused by excess backpressure in veins, and have a high risk of bleeding, which may be fatal if untreated.

Causes and associated conditions

Cirrhosis

Nearly all cases of oesophageal varices occur in people with liver cirrhosis, which may be due to alcohol abuse, hepatitis C, or primary biliary cirrhosis. Cirrhosis causes scarring in the liver, which slows down the blood flowing through it. This in turn causes blood to dam up in the portal vein (portal hypertension). As this progresses, veins around the bottom of the oesophagus become congested, and start to swell. These veins on the inside of the oesophagus are very thin-walled, and rupture easily. Because they are large and under pressure, the bleeding can be profuse and even life-threatening.

Other causes

Some other causes - all of which involve obstruction to the normal flow of blood - are

  • Congestive heart failure - blood cannot be pumped effectively, so dams up and eventually causes portal hypertension.
  • Budd-Chiari syndrome - rare, and caused by clots obstructing liver veins.
  • Thrombosis of the portal or splenic vein, for instance in pancreas cancer.
  • Bilharzia - an infection common in parts of Africa.
  • Sarcoidosis - an auto-immune disease which can affect the liver.

Symptoms

Portal hypertension of itself causes no symptoms. Nor do oesophageal varices, until they rupture and bleed.

Smaller bleeds - especially over a long period - may go largely unnoticed, as the blood is swallowed. The patient may notice melaena stools (dark, smelly stools due to digested blood) or become anaemic.

Large bleeds are dramatic, and the patient may vomit huge quantities of blood, become dizzy or even lose consciousness due to the shock of blood loss.

Once a bleed has happened, the risk of subsequent bleeds is greatly increased, which are more likely to be fatal. Liver or kidney failure, advanced age and alcohol abuse further increase the risk of repeat bleeds and mortality.

Diagnosis and screening

Patients with cirrhosis should be screened for varices by endoscopy: an instrument with a camera at its tip is passed into the oesophagus, allowing its inside to be seen. Varices can be identified, and their risk of rupture assessed. Any minor bleeding can be treated at the same time.

Treatment

If varices are found during screening, two means of treatment are possible via the endocscope:

  1. Sclerotherapy - injecting a chemical, causing the vein to collapse and stay closed, so that it cannot re-expand with blood; and
  2. Tying off or "banding" the vein.

In emergencies, when the bleed is heavy, a long balloon may be placed in the oesophagus and inflated to press against the veins and stop the bleeding. The patient may need a blood transfusion if blood loss has been heavy. Because cirrhosis affects liver function, the patient may also need to be given clotting factors which the liver can no longer make. Antibiotics are routinely used: if infection is not already present and a cause of the bleed, then it is very likely to set in after the endoscopy.

Treating the underlying cause, the portal hypertension, is difficult. To reduce the risk of bleeds in those known to have varices, non-selective beta blockers (like propanolol) have been shown to be effective. Nitrates are less effective. These drugs lower blood pressure and facilitate blood flow through the liver. Patients with gastric reflux are treated to reduce stomach acid, to prevent corrosion of the varices causing bleeding.

Definitive treatment to reduce portal pressure may include

  • Transjugular intrahepatic portosystemic shunts (TIPS) - a catheter is threaded into the liver via a neck vein, and used to guide the placement of a stent in the liver. This is an expandable mesh tube similar to that used to open heart arteries, but larger. This stent helps the blood flow through the liver, thus reducing the back pressure and the risk of bleeding.
  • Porto-caval shunts : this is risky abdominal surgery and not often undertaken;
  • Spleno-renal shunts: decompress by connecting the spleen and kidney veins; and
  • Liver transplantation is a last resort.

Outcome

Banding and sclerotherapy are effective short-term treatments for mild bleeds. Major bleeds have a high mortality, not only from blood loss, but due to the underlying cirrhosis causing the varices in the first place.

About a third of patients with varices will have a major bleed, and each bleed has a 20 percent mortality risk. Among those who survive and are not treated, only 30-40 percent will survive another two years.

(Dr A G Hall)

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