Non-reducible rotational head tilt in ankylosing spondylitis.
Authors: M B Finch, B Page, S D Roberts
Journal: BMJ (1983)

Precipitation of hepatic encephalopathy by propranolol in cirrhosisContinuous oral propranolol reduces portal venous pressure in patients with cirrhosis.'A controlled trial in such patients who had bled from varices showed a significantly lower incidence of rebleeding in those given propranolol.2This led to the widespread and en- thusiastic use of propranolol to prevent recurrent variceal haemorrhage in patients with cirrhosis.The beneficial effect of propranolol, how- ever, has so far been demonstrated only in predominantly alcoholic patients who were all in good condition and in whom side effects of propranolol were few.It is not known whether prophylaxis with propranolol reduces the incidence of variceal bleeding in patients with other causes of cirrhosis or more severe liver failure.Complications of treatment with propranolol may be more common in these patients.We report on a patient in whom propranolol given to prevent recurrent variceal bleeding precipitated hepatic encephalo- pathy. Case reportA 69 year old woman presented with bleeding oesophageal varices in 1979.This settled spontaneously without active treatment.She suffered from cryptogenic cirrhosis and insulin dependent diabetes mellitus but remained well until June 1982, when she had a further variceal haemorrhage.This settled after blood transfusion alone.On admission the severity of her liver dysfunction was assessed as Child's grade A. Serum bilirubin concentration was 13 Itmol/l (760 HgllOO ml), serum albumin concentration 37 g/l, and the prothrombin time 14 s (control 13 s); there was no ascites or clinical evidence of hepatic encephalopathy.She was started on propranolol 40 mg twice daily to prevent further variceal bleeding, and her pulse fell from 80 to 62 beats/min.Initially she tolerated propranolol well and was discharged home.Four weeks later, however, she was readmitted with hepatic encephalopathy.She showed typical asterixis, and the mean electroencephalographic frequency (normnal > 8-9 Hz) had fallen from 7 Hz five weeks earlier to 5 Hz.There were no focal neurological signs.She was not feverish, and there was no evidence of gastrointestinal haemorrhage.Plasma urea and electrolyte concentrations were normal, and results of liver function tests were unchanged.Blood glucose concentration was 13-3 mmol/l (240 mg/100 ml) (normal 2-9-4-8 mmol/l (52-86 mg/ 100 ml)).A midstream urine sample grew > 105 Escherichia coli but no pus cells were seen, and treatment with amoxycillin resulted in sterile urine cultures.8 6-Mean elec troencephalographic frequency ( Hz) 4 2 ~~~~~~~~Propranolol 2 -H 0 ,-- -39 0 8 16 24 Days after admissionRelation between propranolol treatment and the mean electroencephalo- graphic frequency.As no obvious cause for the hepatic encephalopathy had been identified propranolol was temporarily stopped in case it was a contributing factor.She was given oral lactulose, magnesium sulphate enemas, and a 40 g protein diet daily.The hepatic encephalopathy disappeared and the mean electroencephalographic frequency rose to 7 5 Hz.Five days later propranolol 40 mg twice daily was started again.Her pulse fell as before, and within 24 hours she was again encephalopathic and the mean electroencephalographic frequency had fallen to 5-7 Hz (figure).Propranolol was withdrawn and the encephalopathy resolved.A further challenge confirmed that propranolol precipitated hepatic encephalopathy in this patient.No other possible precipitating factors were identified at these times.She remained well over the next seven months.long-acting 5-blocking agent.