Clinical Case Scenario (CSE): Abdominal Pain in Chronic Liver Disease

Identifying Data

• Name: Mr. Rajesh Kumar

• Age: 48 years

• Sex: Male

• Occupation: Shopkeeper

• Address: Varanasi, Uttar Pradesh

Chief Complaints

1. Abdominal pain for 3 months

2. Abdominal distension for 2 months

3. Yellowish discoloration of eyes for 1 month

History of Presenting Illness

Mr. Rajesh Kumar was apparently well 3 months ago when he developed a dull aching pain in the right upper abdomen. The pain was insidious in onset, gradually progressive, non-radiating, and persistent throughout the day. It was not related to food intake, and there were no aggravating or relieving factors.

Two months ago, he noticed progressive abdominal distension, which has increased over time. He also reports bilateral pedal swelling for the past 2 weeks.

One month ago, he developed yellowish discoloration of the eyes and skin, which was first noticed by his family members. This was associated with dark-colored urine and pale stools. He also complains of generalized itching.

He gives a history of loss of appetite and significant weight loss over the past 2 months. There is no history of fever, chills, or rigors.

He had two episodes of vomiting blood (hematemesis) in the last 15 days, each episode containing about half a cup of fresh blood, not mixed with food particles. He also noticed black, tarry stools (melena) following these episodes.

For the past week, his family has noticed that he has become forgetful, irritable, and occasionally drowsy during the day.

There is no history of abdominal trauma, chest pain, breathlessness, or urinary complaints.

Past Medical History

• No history of diabetes, hypertension, or tuberculosis.

• No previous surgeries or blood transfusions.

• No known allergies.

Family History

• No family history of liver disease or malignancy.

Personal History

• Alcohol: Consumes country liquor daily, approximately 180 ml/day, for the past 18 years. Last drink was 2 days ago.

• Smoking: Smokes 5-6 bidis/day for 20 years.

• Diet: Mixed diet, poor appetite recently.

• No history of intravenous drug use or high-risk sexual behavior.

• Drug History

  • Not on any regular medications.

  • No history of over-the-counter or herbal medication use.

Socioeconomic History

• Lives in a rented house with wife and two children. Belongs to a lower-middle socioeconomic class.

Review of Systems

• No cough, breathlessness, chest pain, or palpitations.

• No urinary complaints.

• No joint pains or rashes.

Summary

Mr. Rajesh Kumar, a 48-year-old male with a significant history of chronic alcohol intake, presents with chronic right upper abdominal pain, progressive abdominal distension, jaundice, episodes of hematemesis and melena, and recent onset of altered sensorium. The clinical picture is suggestive of decompensated chronic liver disease, likely secondary to alcoholic liver disease, with complications including portal hypertension (ascites, variceal bleed) and hepatic encephalopathy.

1. What are the common causes of chronic liver disease (CLD)?

• Alcohol (most common in many regions)

• Viral hepatitis (B, C, D)

• Non-alcoholic fatty liver disease (NAFLD/NASH), often due to diabetes, obesity, hypertension, and hyperlipidemia

• Genetic causes (e.g., Wilson’s disease, hemochromatosis, cystic fibrosis)

• Autoimmune (primary biliary cholangitis, primary sclerosing cholangitis, autoimmune hepatitis)

• Drugs (e.g., methotrexate, isoniazid, amiodarone, sodium valproate)

• Vascular (Budd-Chiari syndrome)

• Idiopathic/Cryptogenic127

2. What are the main complications of chronic liver disease?

• Variceal bleeding

• Ascites

• Spontaneous bacterial peritonitis

• Hepatic encephalopathy

• Hepatorenal syndrome

• Hepatocellular carcinoma (HCC)1

3. What blood tests are used to assess synthetic liver function?

• Prothrombin time (PT) or INR

• Serum albumin

• Platelet count (as a marker of portal hypertension)1

4. What is hepatic encephalopathy? What causes it?

• Hepatic encephalopathy is a spectrum of neuropsychiatric abnormalities in patients with liver dysfunction, after exclusion of other brain diseases.

• It is mainly caused by the accumulation of neurotoxins (especially ammonia) due to impaired liver detoxification, often precipitated by GI bleeding, infection, constipation, electrolyte imbalances, or sedative drugs68910.

5. What are the clinical grades of hepatic encephalopathy?

• Grade 0: Subclinical (minimal changes in memory, concentration)

• Grade 1: Mild confusion, altered sleep, irritability

• Grade 2: Drowsiness, lethargy, disorientation, personality changes

• Grade 3: Somnolence, gross disorientation, confusion

• Grade 4: Coma10

6. What are the precipitating factors for hepatic encephalopathy?

• Gastrointestinal bleeding

• Infections

• Constipation

• Electrolyte imbalance (especially hypokalemia)

• High protein intake

• Sedative drugs (benzodiazepines, opiates)

• Dehydration or diuretic overuse810

7. What are the signs of portal hypertension?

• Splenomegaly

• Ascites

• Caput medusae

• Esophageal/gastric/rectal varices (history of hematemesis or melena)

• Thrombocytopenia1

8. What are the main causes of ascites in CLD?

• Increased hydrostatic pressure due to portal hypertension

• Decreased oncotic pressure due to hypoalbuminemia

• Renal sodium and water retention1

9. How do you manage hepatic encephalopathy?

• Identify and treat precipitating factors

• Reduce ammonia production (lactulose, rifaximin)

• Protein restriction (in acute setting)

• Correct electrolyte imbalances

• Avoid sedative medications810

10. What is the definitive treatment for end-stage chronic liver disease?

• Liver transplantation is the only curative option for end-stage CLD7.