It is a neuropsychiatric syndrome secondary to liver disease characterized by unconsciousness.
Etiology:
- Cirrhosis of liver
- Acute fulminant hepatitis
- Biliary cirrhosis
- Surgical portal venous shunt
- Portal hypertension
Precipitating factors
- High protein intake
- Alcohol
- Constipation
- Infection
- Fluid electrolyte imbalance
- GI bleeding
Pathophysiology
Hepatic coma occurs when blood bypass the liver through collateral circulation .as the liver is the main detoxification organ of toxic substance, so toxic substances directly reach the brain. These substances include ammonia, free fatty acids, and false neurotransmitters. These toxic substances are responsible for hepatic encephalopathy.
Clinical features:
Symptoms
Initially there is irritability, confusion, disorientation, slow slurred speech.
Nausea, vomiting, weakness, hiccups, drowsiness.
Hyperventilation and pyrexia.
Signs
Fetor hepaticus (musty sour smell).
Coarse flapping tremors
Hyperreflexia
Bilateral extensor planter response.
Jaundice may be present.
Investigation
Blood complete picture will show increased ESR, WBC and decreased RBC.
Liver biochemistry will show prolonged prothrombin time, increased SGOT, SGPT and bilirubin.
Blood urea will show the renal status.
Blood glucose can exclude the hypoglycemia.
Differential diagnosis.
Dural and subdural hemorrhage
Drunkenness
Wilson’s disease
Hypoglycemia
Diabetes ketoacidosis
Primary psychiatric disorders
Management
Immediate.
Hospitalized the patient
Pass nasogastric tube and insert cannula to maintain I.V line
Identify the precipitating factors and remove them
Catheterize the patient.
Liquid protein free diet.
Give purgatives with enemas.
IV 20 % glucose.
Correct any electrolyte imbalance.
Oral neomycin 1-4 g daily?
Correct ay infection.
Long term
Increase the protein intake slowly
Avoid constipation
Avoid precipitating factors
Avoid sedatives and hypnotics
Use flumazanil (benzodiazepine antagonist)