A forty-two (42) year old man has been well, apart from a history of alcohol induced liver dysfunction and portal hypertension. He has abstained from alcohol for the past 8 months after being told that it would kill him. After a large haematemesis he presents drowsy, clinically shocked, with a blood pressure of 80 systolic, heart rate of 124 beats/minute, cold and clammy peripheries. He is also clinically jaundiced.
Variceal bleeding is diagnosed and it initially responds to therapy. 48 hours post admission he remains on invasive respiratory support, with weak withdrawal response to pain despite minimal sedation, a persistent coagulopathy, and is inotrope dependent. Serum bilirubin concentration is elevated (100 micromol/L [N 3-20]). He develops a further acute variceal bleed associated with hypotension.
(c) At 6 days there has been no further haematemeses. However he has a Glasgow Coma Score (GCS) of 5, despite no sedation. His serum bilirubin concentration is now 350 micromol/L. Prothrombin time and serum creatinine concentration are twice normal. A CT of the head shows no focal abnormality. What supportive therapies and strategies would you have in place at this stage and why?
Specific strategies to minimise hepatic encephalopathy should have been described if not already done so (including the use of lactulose). Precipitants must be minimised (treatment of infections, avoidance of sedatives, correction of electrolyte abnormalities/hypoxia, avoid alkalosis, limit dietary protein, consider unproven dietary supplements including BCAA etc.). Cautious volume expansion should be considered. Other reversible causes for renal dysfunction and coma should be sought and excluded. Management of ICP may be necessary (and the CT does not exclude cerebral oedema). General supportive care should be considered (eg. physiotherapy, avoidance of line- related problems, family support etc.). Specific treatment may be required for ascites and its effects (drainage, colloid replacement etc).
The college has given us a patient with a combination of several reasons to be encephalopathic; of these, the major one is liver failure -but we are also reminded that the creatinine has doubled.
Specific management of hepatic encephalopathy
Management of the precipitating cause
Supportive management of the encephalopathic patient
Pursuit of other explanations for decreased level of consciousness:
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