A man of 45 consults his general practitioner (GP) with a 6-month history of reduced appetite and weight loss

A man of 45 consults his general practitioner (GP) with a 6-month history of reduced
appetite and weight loss, from 78 to 71 kg. During the last 3 months he has had intermittent
nausea, especially in the mornings, and in the last 3 months the morning nausea has
been accompanied by vomiting on several occasions. For 1 month he has noted swelling
of his ankles. Despite his weight loss he has recently noticed his trousers getting tighter.
He has had no abdominal pain. He has no relevant past history and knows no family
history as he was adopted. He takes no medication. From the age of 18 he has smoked
5–6 cigarettes daily and drunk 15–20 units of alcohol per week. He has been a chef all his
working life, without exception in fashionable restaurants. He now lives alone as his wife
left him 1 year ago.
He has plethoric features. There is pitting oedema of his ankles. He appears to have lost
weight from his limbs, but not his trunk. He has nine spider naevi on his upper trunk. His
pulse is normal and the rate is 92/min. His jugular venous pressure (JVP) is not raised and
his blood pressure is 146/84 mmHg. The cardiovascular and respiratory systems are normal.
The abdomen is distended. He has no palpable masses but there is shifting dullness
and a fluid thrill.

This man has abnormal liver function tests which indicate hepatic failure; the hypoproteinaemia
has caused the ascites and ankle swelling. The number of spider naevi is more
than the accepted normal of three. The cause is likely to be alcohol as it is a common
cause of this problem, he is at increased risk through his work in the catering business. His
symptoms of morning nausea and vomiting are typical, and this would account for his
cushingoid appearance (alcohol increases adrenocorticotrophic hormone (ACTH) secretion)
and the macrocytsis on the blood film (due to dietary folate deficiency and a direct
toxic action on the bone marrow by alcohol). However his alcohol intake is too low to be
consistent with the diagnosis of alcoholic liver disease. When the provisional diagnosis is
discussed with him though, he eventually admits that his alcohol intake has been at least
40–50 units per week for the last 20 years and has increased further during the last year
after his marriage had ended, the reason for this being his drinking.
The slight reductions in the sodium and urea reflect a chronic reduced intake of salt and
protein; the rise in bilirubin is insufficient to cause jaundice.
Further investigations are the measurement of hepatitis viral serology, which was negative,
and an ultrasound of the abdomen. This showed a slight reduction in liver size, and
an increase in splenic length of 2–3 cm. There was no evidence of a hepatoma. These findings
indicate that portal hypertension has developed. A liver biopsy, performed to confirm
the diagnosis, assess the degree of histological damage and exclude other pathology,
showed changes of cirrhosis.
The crucial aim in management is to impress upon the patient the necessity to stop drinking
alcohol, in view of the degree of liver damage, the presumed portal hypertension and
the risk of oesophageal varices and bleeding, and to effect this by his attending an alcohol
addiction unit. In the short term he should also improve his diet to increase his protein
intake. Diuretics could be used to reduce his oedema, but it should be remembered
that they could cause postural hypotension more easily against this background.
His attendance at the addiction unit was fitful, he continued to drink heavily and he died
3 years later as a result of a second bleed from oesophageal varices.