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Q1: Following the insertion of the Sengstaken tube what additional management would you have instigated?
The Sengstaken tube remains an effective measure for stopping variceal haemorrhage that can not be controlled by other means. However, its use requires expertise and careful aftercare as a number of complications may occur. Initially, only the gastric balloon should be inflated, using 300 ml of air or water. If water is used to inflate the balloon, it is useful to add a small amount of radiographic contrast medium, as this makes radiological checking of the position of the tube easier. Once the balloon is inflated then it should be placed under traction. Traditionally traction has been achieved by suspending a weight to the tube, but this can be uncomfortable and may reduce patient tolerance of the tube. An alternative method of providing traction, that may be better tolerated, is to tape the tube to the patient's forehead under tension. Once the tube is secured then its position should be confirmed with a chest radiograph. Misplacement can lead to severe complications, such as oesophageal perforation. In most cases the inflation of the gastric balloon will result in cessation of haemorrhage. However, if there is continued oesophageal bleeding, which is suggested by the continued ability to aspirate blood from the oesophageal aspiration port, then the oesophageal balloon should be carefully inflated to 30 mm Hg using a manometer to check the pressure. Patients treated with a Sengstaken tube are at risk of developing aspiration pneumonia and should ideally be managed in an intensive care unit, where the airway can be protected if necessary by elective intubation.1 Prolonged use can lead to mucosal ulceration and an attempt should be made to remove the tube after 24 hours. Treatment with a vasoactive drug should also be initiated and this is best done as soon as variceal bleeding is suspected. These drugs, which reduce portal blood pressure by constricting the splanchnic circulation, have, if instigated early, been shown to reduce rebleeding rates after a variceal bleed. Of the drugs available, terlipressin has also been shown to reduce mortality after an episode of bleeding, whereas no improvement in mortality has been documented for octreotide, vasopressin, or somatostatin.2
Q2: What was the cause of the rebleed and what procedure was performed?
The rebleed was due to gastric varices. A transjugular intrahepatic portosystemic shunt (TIPSS) was performed. The radiograph in fig 1 (p 408) shows a portogram, with contrast filling the portal vein and outlining the stent, which has been inserted to create a shunt between the portal and systemic circulation. Bleeding from gastric varices is difficult to control using conventional endoscopic techniques and consequently TIPSS is recommended early in their management.3 TIPSS works by providing a shunt from the portal system into the systemic venous system, thus decompressing the portal system, and reducing portal pressure. Gastric varices can also be treated with direct endoscopic injection of tissue adhesive agents such as cyanoacrylate, but although evidence shows that this is more effective than conventional sclerotherapy, it has not been compared with early TIPSS in a randomised controlled trial.4
Q3: What is the likely cause for the patient becoming drowsy, and how would you manage this?
The patient has developed encephalopathy. This is a complication, which occurs after TIPSS, in around 35% of cases.4Normally the liver metabolises compounds absorbed from the bowel and prevents them from directly entering the systemic circulation (first pass metabolism). However, the TIPSS bypasses the liver and allows ammonium-containing compounds to enter the circulation. When these compounds reach the brain they may act as false neurotransmitters and interfere with cerebral function. Encephalopathy is more commonly a problem in patients with the most severe liver disease, as subsequent metabolism (second pass) is also impaired. Most episodes of encephalopathy after TIPSS are short lived and the patient presented here recovered with treatment after 48 hours. Treatment is with lactulose which works by reducing the amount of ammonium compounds produced by bacteria in the bowel.4 Treatment with a low protein diet can also be used to reduce the amino acid absorbed from the bowel, but this is controversial, as many patients with variceal haemorrhage are already considerably malnourished at presentation. Treatment of encephalopathy should also include assessment for any possible precipitating factors, such as sedating drugs, hypoglycaemia, hyponatraemia, renal failure, further variceal haemorrhage, infection (in particular spontaneous bacterial peritonitis), and subdural haematoma.
Varices are dilated submucosal veins that project into the lumen of the gastrointestinal tract. Ninety per cent occur in the oesophagus with the majority of the remainder occurring in the gastric fundus. They form as a result of raised pressure in the portal vein (portal hypertension). The resulting portosystemic venous pressure gradient leads to varices forming at the sites of anastomoses between the portal and systemic circulation. Portal hypertension is commonly caused by hepatic cirrhosis, but may also arise if there is obstruction to either the posthepatic circulation as in Budd-Chiari syndrome, or to the prehepatic portal circulation as in portal vein thrombosis. In the case discussed here, bleeding oesophageal varices were the presenting feature of chronic hepatitis B infection. Oesophageal varices occur in 30% of compensated and 60% of decompensated cirrhotic patients.1 The mortality from a variceal haemorrhage is 50% after the first bleed and 30% for each subsequent episode.
Initial management of oesophageal variceal haemorrhage is resuscitation and early endotherapy with either sclerotherapy or band ligation. Both techniques are effective at controlling the initial bleed, but band ligation, where the varices are obliterated by strangulation, has been shown to reduce bleed related mortality.5 Both procedures are technically difficult, and even a skilled endoscopist will fail to achieve haemostasis in approximately 10% of cases, in which case a balloon compression device such as a Sengstaken tube should be inserted. Vasoactive drugs have an additive effect to endoscopic treatment and should be instigated at an early stage. TIPSS is recommended when endoscopic therapy has been attempted on two separate occasions.3 The major complications that occur after TIPSS are stent stenosis which occurs in up to 60% of cases, and hepatic encephalopathy which occurs in about 35% of cases. Regular radiological assessment of the stent with Doppler, or venography, is recommended to detect early stenosis, which if present can be treated with dilatation.4
Gastric varices do not respond as well to treatment with conventional endoscopic techniques, such as banding or sclerotherapy, and consequently TIPSS has been advocated early in their management.3 Endoscopic injection of tissue adhesive into the site of bleeding has been proved to reduce bleeding in the majority of cases, and offers an alternative approach. However, complications, which include embolisation of the adhesive, may occur in up to 40% of cases and consequently the use of this technique remains controversial.4
Acute variceal bleeding still carries a high mortality, but it is hoped that new developments in management will lead to improved outcome. The wide range of treatments currently available are likely to be optimally used if patients are managed by a multidisciplinary team, with access to intensive care, skilled endosocopists, and interventional radiologists.
Gastrointestinal haemorrhage due to oesphagogastric varices.
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