A 60-year-old alcoholic was admitted with large-volume, frank haematemesis. On presentation he was hypotensive, tachycardic and obtunded with multiple stigmata of chronic liver disease including a moderate volume of ascites and palpable splenomegaly. Initial phlebotomy revealed a haemoglobin of 6.4 g/dL, INR of 4.5 and bilirubin of 54 μmol/L. Arterial blood gas analysis demonstrated a significant metabolic acidosis and lactate of 11 mmol/L. Large bore intravenous access was established and administration of crystalloid initiated, targeting a systolic blood pressure of 90 mmHg. Urgent cross-match of 10 units of packed red blood cells, clotting products and platelets was requested and the patient was transferred to theatre where upper gastrointestinal tract endoscopy was performed under general anaesthesia. This demonstrated three columns of varices involving the gastro-oesophageal junction. Attempts at banding and injection of sclerosant met with variable success. A Senstaken-Blakemore tube was inserted due to incomplete haemostasis and further attempts at endoscopic therapy abandoned.

The patient was transferred to intensive care. Intravenous cefotaxime and terlipressin were commenced. Further transfusion of clotting products continued as guided by thromboelastography with some slowing of transfusion but red cell requirements persisted at a rate of 1-2 units of blood per hour. At 12 hours, repeat endoscopy was performed – further attempts at sclerotherapy were unsuccessful and transjugular intrahepatic porto-systemic shunting was performed by the interventional radiology team. Upon return to intensive care, a significant reduction in bleeding was noted and both haemodynamic indices and coagulopathy improved over the following 12 hours. A repeat endoscopy demonstrated no evidence of active ongoing bleeding. At this point sedation was stopped; some encephalopathy was evident although this improved in the following 24 hours. Extubation occurred on day 3 after admission and he was discharged to the high-dependency unit at day 5 without significant ongoing acute issues.

Stephen Shepherd

Acute oesophageal variceal haemorrhage is a relatively common complication of cirrhosis of any cause and associated with an in-hospital mortality of up to 50%.(1) Variceal bleeds account for 11% of all gastrointestinal haemorrhages in the United Kingdom with 9% of patients known cirrhotics at presentation(2). Mortality is significantly higher than the non-variceal population.(1,2)

Oesophageal varices reflect the development underlying portal hypertension in cirrhotic liver disease resulting in diversion of portal blood into the systemic circulation via shunts in the distal 2-5 cm of the oesophagus. The cumulative incidence of varices increases with time.(1) Numerous guidelines have been produced regarding the management of this condition.(3-5) The most recent from the National Institute of Health and Clinical Excellence advocates initial resuscitation before secondary treatments are initiated.(3)

Terlipressin and antibiotic therapy should be offered at presentation to all suspected variceal bleeds.(3) The former is a synthetic analogue of vasopressin which has vasocontrictive effects upon both the systemic and portal circulations.(6) It has been shown to have similar efficacy to sclerotherapy and, when combined with endoscopy, reduce transfusion requirements and all cause mortality.(7,8) Octreotide or somatostatin analogues may have similar efficacy.(4,9)

A high rate of (largely Gram negative) bacterial infections have been demonstrated in cirrhotic patients admitted with upper gastrointestinal haemorrhage; mortality is higher than in non-infected patients.1 Antibiotic prophylaxis with a third-generation cephalosporn, extended spectrum β-lactam or quinolone has been shown to reduce mortality.(1,10)

Both endoscopic sclerotherapy and band ligation have been shown to be effective in control of bleeding but when combined with pharmacotherapy, band ligation offers improved outcomes and a better safety profile.(1,4,7,10) Transjugular intrahepatic porto-systemic shunting involves placement of an expandable metal stent across a tract created between a hepatic vein and the portal system. It is often reserved as a rescue therapy in intractable bleeding but may worsen encephalopathy and offers no survival benefit in patients with established organ failure.(4,5) Interestingly, earlier shunting may reduce treatment failure in those considered high-risk, i.e. Childs-Pugh C or Childs-Pugh B with active bleeding.(11,12)

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Lessons Learnt

Earlier administration of both antibiotics and a suitable sphlanchnic vasoconstrictor should have been considered in this case; had administration or terlipressin or similar been achieved, the benefits of attempting sclerosant therapy initially may have been outweighed and the rate of bleeding reduced. Earlier consideration of porto-systemic shunting after failure of the first endoscopy could also have been considered.

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References

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