Case History

Personal Details:
Mr. A, 48-year-old male, farmer

Presenting Complaints:

• Altered mental status with confusion and drowsiness for 2 days

• Slurred speech and abnormal hand movements noticed by family

• Reduced oral intake and lethargy

History of Presenting Illness:
Mr. A was apparently well until 3 days ago when he developed mild forgetfulness and irritability. Over the next 2 days, his family noticed increasing confusion, disorientation to time and place, and difficulty in speaking clearly. He became drowsy and less responsive. There was no history of seizures or head trauma. His family also noticed flapping tremors (asterixis) when his hands were outstretched.

He had a history of vomiting and abdominal distension for 1 week prior to the onset of neurological symptoms. There was no fever or focal neurological deficits. No history of recent sedative or alcohol intake in the past week.

Past Medical History:

• Diagnosed with chronic liver disease secondary to alcoholic liver disease 4 years ago

• Multiple episodes of ascites managed with diuretics

• No prior episodes of hepatic encephalopathy documented

• No history of diabetes or hypertension

Family History:

• No family history of liver disease or neurological illness

Personal History:

• Chronic alcohol consumption for 15 years, stopped 6 months ago

• Mixed diet, recent reduction in protein intake due to poor appetite

• Non-smoker

• Drug History:

  • On oral spironolactone and propranolol

  • No recent use of sedatives or antibiotics

  • Irregular compliance with lactulose

Socioeconomic History:

• Lives in rural area with moderate access to healthcare

• Supportive family environment

Differential Diagnosis

1. Hepatic Encephalopathy (HE):
   Given the known chronic liver disease, altered mental status, presence of asterixis, and precipitating factors such as vomiting and ascites, hepatic encephalopathy is the most likely diagnosis.

2. Metabolic Encephalopathy:
   Electrolyte imbalances (such as hyponatremia or hypokalemia) or renal failure can cause encephalopathy mimicking HE and should be considered.

3. Wernicke’s Encephalopathy:
   Common in chronic alcoholics, characterized by confusion, ophthalmoplegia, and ataxia. Absence of eye signs makes this less likely but still possible.

4. Infective Encephalopathy:
   Central nervous system infections like meningitis or encephalitis can cause altered sensorium, usually accompanied by fever and focal neurological signs.

5. Intracranial Pathology:
   Stroke, hemorrhage, or brain tumors may present with altered mental status but often have focal neurological deficits.

6. Drug-Induced Encephalopathy:
   Use of sedatives, benzodiazepines, or other CNS depressants can cause similar symptoms.

7. Hypoglycemia:
   Low blood sugar can cause confusion and drowsiness and should be ruled out with bedside glucose testing.

Viva Questions and Answers on Hepatic Encephalopathy

1. What is hepatic encephalopathy?
Hepatic encephalopathy is a reversible neuropsychiatric syndrome occurring in patients with acute or chronic liver disease, characterized by a spectrum of cognitive, psychiatric, and motor disturbances due to impaired hepatic detoxification and accumulation of neurotoxic substances like ammonia134.

2. What are the common clinical features of hepatic encephalopathy?
Symptoms range from subtle cognitive impairment (minimal HE) to overt manifestations including personality changes, confusion, disorientation, asterixis (flapping tremor), somnolence, stupor, and coma. Sleep disturbances and altered behavior are also common134.

3. What are the precipitating factors for hepatic encephalopathy?
Common triggers include gastrointestinal bleeding, infections (e.g., pneumonia, urinary tract infection), electrolyte imbalances, constipation, sedative or opioid use, excessive dietary protein intake, renal failure, and dehydration345.

4. How is hepatic encephalopathy classified?
It is classified into minimal (covert) HE, detectable only by psychometric tests, and overt HE, graded I to IV based on severity:

• Grade I: Mild confusion, euphoria or anxiety

• Grade II: Lethargy, disorientation, asterixis

• Grade III: Somnolence, confusion, incoherent speech

• Grade IV: Coma14.

5. What is the pathophysiology of hepatic encephalopathy?
Impaired liver function and portal-systemic shunting lead to accumulation of ammonia and other neurotoxins in the blood. Ammonia crosses the blood-brain barrier and is metabolized in astrocytes to glutamine, causing astrocyte swelling, cerebral edema, oxidative stress, and neurotransmission disturbances resulting in neurological dysfunction3.

6. How do you diagnose hepatic encephalopathy?
Diagnosis is clinical, based on history and neurological examination. Supportive investigations include elevated serum ammonia (though not always correlating with severity), liver function tests, exclusion of other causes of encephalopathy, and psychometric testing for minimal HE. Imaging and infection screening are also important15.

7. What are the main treatment principles for hepatic encephalopathy?

• Identify and treat precipitating factors

• Reduce blood ammonia levels using lactulose (first-line) and rifaximin

• Supportive care including airway protection if needed

• Nutritional support with adequate protein intake

• Avoid sedatives and CNS depressants5.

8. What is the role of lactulose in hepatic encephalopathy?
Lactulose acidifies the gut lumen, converting ammonia (NH3) to ammonium (NH4+), which is less absorbable. It also acts as a laxative, reducing intestinal transit time and bacterial ammonia production, thereby lowering systemic ammonia levels5.

9. How can you prevent recurrence of hepatic encephalopathy?
Long-term management includes maintenance therapy with lactulose and/or rifaximin, management of portal hypertension, regular screening for precipitating factors, patient and caregiver education, and nutritional counseling5.

10. What other conditions can mimic hepatic encephalopathy?
Differential diagnoses include metabolic encephalopathies (electrolyte imbalances, hypoglycemia), infections (meningitis, encephalitis), intracranial pathology (stroke, tumor), drug-induced sedation, and Wernicke’s encephalopathy34.