Nausea And Weight Loss In A 45 Year old Alcoholic... Case Study

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

Examination
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

Investigations: 
Haemoglobin = 12.6 g/dL (normal = 13.3–17.7 g/dL)
White cell count = 10.2 × 109/L (normal = 3.9–10.6 × 109/L)
Platelets = 121 × 109/L (normal = 150–440 × 109/L)
Sodium = 131 mmol/L (normal = 135–145 mmol/L)
Potassium = 4.2 mmol/L(normal = 3.5–5.0 mmol/L)
Urea = 2.2 mmol/L (normal = 2.5–6.7 mmol/L)
Creatinine  = 101 μmol/L (normal = 70–120 μmol/L)
Total protein = 48 g/L (normal = 60–80 g/L)
Albumin = 26 g/L (normal = 35–50 g/L)
Bilirubin =  25 mmol/L (normal = 3–17 mmol/L)
Alanine transaminase = 276 IU/L (normal = 5–35 IU/L)
Gamma-glutamyl transaminase = 873 IU/L (normal = 11–51 IU/L)
Alkaline phosphatase = 351 IU/L (normal = 30–300 IU/L)
International normalised ratio (INR) = 1.4 (normal = 0.9–1.2)

Urinalysis: no protein; no blood

• What is the diagnosis?
• How would you manage this patient?


Answer and Discussion:
This man has signs of chronic liver disease with ascites and oedema. The number of spider naevi is more than the accepted normal of three. The most common cause of chronic liver disease is alcohol. He is at increased risk of alcohol misuse because he works in the catering business. His symptoms of morning nausea and vomiting are typical of alcohol misuse.
Chronic alcohol excess would account for his cushingoid appearance due to the increases of adrenocorticotrophic hormone [ACTH] secretion). Macrocytic anaemia can be due to dietary folate deficiency or the direct toxic action of alcohol on the bone marrow. The rise in bilirubin is insufficient to cause jaundice. The low serum albumin and raised international normalised ratio (INR) may be due to impaired synthetic function of clotting factors produced by the liver. Thrombocytopenia may be from platelet sequestration in an enlarged spleen as a result of portal hypertension from liver cirrhosis.
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. His alcohol intake has increased further during the last year after his marriage had ended.

Further investigations include the measurement of hepatitis viral serology, which was negative, and an ultrasound of the abdomen. Ultrasound showed moderate ascites, 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.

The crucial aim in management is to impress upon the patient the necessity to stop drinking alcohol and to affect this by attending an alcohol addiction unit.

• Acute management should include an alcohol withdrawal regimen with diazepam or chlordiazepoxide to reduce the risk of withdrawal seizures.
• Attention needs to be paid to nutrition. 
• Intravenous thiamine should be given to prevent Wernicke’s encephalopathy. 
• Vitamin K is used to correct clotting abnormalities. 
• An ascitic tap should be performed to exclude spontaneous bacterial peritonitis (which maybe asymptomatic). 
• Treatment of ascites includes a low sodium diet and spironolactone.
• Daily weights should be used to measure fluid losses. 
• Therapeutic paracentesis with concomitant albumin infusion can be used if the ascites is diuretic resistant or very uncomfortable. 
• Surveillance endoscopy and banding of oesophageal varices should be considered in this patient, as there is evidence of portal hypertension. 
• If oesophageal varices are present, propranolol can be used to reduce portal hypertension and prevent further variceal formation.

Followup: 
In this patient attendance at the addiction unit was fitful; he continued to drink heavily, and he died 3 years later a result of a second bleed from oesophageal varices

Learning Points In This Case Study

• Patients who drink excessive amounts of alcohol will often disguise this fact in their history

• Alcoholic liver disease has a poor prognosis if the alcohol intake is not terminated.