Case History

Patient Identification:
Mr. R, a 55-year-old male farmer

Chief Complaint:
Vomiting of blood for the last 8 hours

History of Presenting Illness:
Mr. R presented with sudden onset of multiple episodes of vomiting bright red blood since 8 hours ago. He reports about 3-4 episodes of hematemesis, each approximately 100 ml in volume. He also noticed black tarry stools (melena) once yesterday. He complains of increasing abdominal distension and swelling of both legs for the past 2 months. He has had generalized weakness and easy fatigability for 1 month. There is no history of abdominal pain or trauma preceding hematemesis. He denies fever or jaundice.

Review of Systems:

• General: Fatigue, anorexia, weight loss of 5 kg over 6 months

• Gastrointestinal: Abdominal distension, melena, no jaundice or abdominal pain

• Neurological: No confusion or altered sensorium

• Cardiovascular and respiratory systems: No significant complaints

Past Medical History:
He was diagnosed with chronic liver disease 3 years ago, secondary to chronic hepatitis B infection. He has had multiple episodes of abdominal swelling and was treated with diuretics. Previous endoscopy showed grade 2 esophageal varices. No history of prior variceal bleeding.

Family History:
No family history of liver disease or bleeding disorders.

Personal History:
Chronic alcohol consumption for 20 years, about 60 ml daily, stopped 6 months ago. Non-smoker. No occupational toxin exposure.

Drug History:
He is on regular oral propranolol and spironolactone. No history of NSAIDs or anticoagulant use.

Socioeconomic History

• 4 membered family

• Lives in pucca house

• No overcrowding

• Drinks water from sanitary well

Case Summary

A 55-year-old male with a known history of chronic liver disease secondary to chronic hepatitis B infection presented with sudden onset of multiple episodes of bright red hematemesis over 8 hours, accompanied by melena one day prior. He reported progressive abdominal distension and bilateral leg swelling for 2 months, along with generalized weakness and weight loss. There was no history of fever or jaundice. He had previously been diagnosed with cirrhosis and esophageal varices and was on propranolol and spironolactone.

The clinical picture is consistent with acute variceal hemorrhage secondary to portal hypertension in decompensated chronic liver disease.

Common Viva Questions and Answers on Hematemesis with CLD

1. What is hematemesis?
Hematemesis is the vomiting of blood, which usually indicates upper gastrointestinal bleeding proximal to the ligament of Treitz.

2. What are the common causes of hematemesis in a patient with chronic liver disease?

• Esophageal varices rupture (most common cause)

• Gastric varices

• Portal hypertensive gastropathy

• Peptic ulcer disease (may coexist)

• Mallory-Weiss tear (due to retching)

• Gastric erosions or malignancy (less common)

3. What is the pathophysiology of variceal bleeding in CLD?
Chronic liver disease causes portal hypertension, which leads to the development of portosystemic collateral vessels, including esophageal and gastric varices. Increased portal pressure causes these varices to dilate and their walls to thin, predisposing them to rupture and bleeding.

4. What are the clinical features of variceal bleeding?

• Sudden onset of large volume bright red hematemesis

• Melena or fresh rectal bleeding

• Signs of hypovolemia: dizziness, syncope, tachycardia, hypotension

• Features of chronic liver disease: jaundice, ascites, spider nevi, palmar erythema

• History of alcohol use or viral hepatitis

5. How do you differentiate hematemesis from hemoptysis?

• Hematemesis is vomiting of blood, often mixed with food or gastric contents, usually bright red or coffee-ground in appearance.

• Hemoptysis is coughing up blood, usually frothy and mixed with sputum, often bright red.

• Hematemesis is associated with nausea and retching; hemoptysis is associated with cough and respiratory symptoms.

6. What initial investigations would you order in a patient presenting with hematemesis and suspected CLD?

• Complete blood count (to assess anemia and platelet count)

• Liver function tests (bilirubin, transaminases, albumin)

• Coagulation profile (PT/INR)

• Renal function tests

• Blood grouping and crossmatching

• Upper GI endoscopy (to identify bleeding source)

• Ultrasound abdomen (to assess liver morphology, ascites, splenomegaly)

7. How do you manage acute variceal bleeding in CLD?

• Initial resuscitation with airway protection, oxygen, and intravenous fluids

• Blood transfusion to maintain hemoglobin around 7-8 g/dl

• Correction of coagulopathy if needed (FFP, platelets)

• Vasoactive drugs: octreotide or terlipressin to reduce portal pressure

• Prophylactic antibiotics to prevent infections

• Emergency upper GI endoscopy with band ligation or sclerotherapy

• Consider balloon tamponade or TIPS if bleeding uncontrolled

8. What are the complications of chronic liver disease that predispose to hematemesis?

• Portal hypertension causing varices

• Coagulopathy due to impaired synthesis of clotting factors

• Thrombocytopenia from hypersplenism

• Portal hypertensive gastropathy

• Hepatic encephalopathy and ascites as markers of decompensation

9. What is the role of beta-blockers in CLD patients?
Non-selective beta-blockers (e.g., propranolol) reduce portal pressure by decreasing cardiac output and causing splanchnic vasoconstriction, thereby preventing first variceal bleeding and rebleeding.

10. When would you consider liver transplantation in a patient with CLD?

• Decompensated cirrhosis with recurrent variceal bleeding despite optimal medical/endoscopic therapy

• Hepatorenal syndrome

• Hepatic encephalopathy refractory to treatment

• Hepatocellular carcinoma within transplant criteria

• MELD score indicating poor prognosis