Gastrointestinal · Year 2 · from Gastrointestinal
Case 2: Esophageal Varices and Portal Hypertension
Patient Presentation
Demographics: 52-year-old male
Chief Complaint: Large-volume hematemesis
History of Present Illness: The patient vomited approximately 500 mL of bright red blood 2 hours ago followed by a second episode en route to the hospital. He has known history of alcohol-related cirrhosis but has continued drinking. He notes increasing abdominal girth over the past 2 months and has required increasing doses of diuretics for his "fluid problem."
Past Medical History: Alcoholic cirrhosis diagnosed 3 years ago, portal hypertensive ascites, thrombocytopenia
Social History: Heavy alcohol use (8-10 beers daily for 30 years)
Physical Examination
- Vital Signs: BP 88/52 mmHg, HR 128 bpm, Temperature 36.8C
- General: Pale, diaphoretic male in distress
- HEENT: Icteric sclerae
- Cardiovascular: Tachycardic, weak peripheral pulses
- Abdomen: Distended with shifting dullness (ascites), caput medusae visible, splenomegaly
- Extremities: Palmar erythema, spider angiomata on chest
- Neurologic: Oriented but slow to respond, asterixis present
Workup and Results
- CBC: Hemoglobin 7.2 g/dL, Platelets 68,000
- INR: 2.1
- BMP: Cr 1.8 mg/dL
- Albumin: 2.4 g/dL
- Child-Pugh Score: 11 (Class C)
- MELD Score: 24
- Upper Endoscopy (after resuscitation): Three columns of large esophageal varices with red wale signs; active bleeding from one varix; gastric varices present
Endoscopic image of large esophageal varices with prominent red wale signs (longitudinal red streaks) indicating high risk of bleeding. These portosystemic collaterals form due to portal hypertension redirecting blood flow.
Image Source: Wikimedia Commons, CC BY-SA 3.0
Diagnosis
Acute Variceal Hemorrhage in Decompensated Cirrhosis
Clinical Correlation to Hepatobiliary Anatomy/Physiology
Portal hypertension develops when intrahepatic vascular resistance increases due to cirrhotic architectural distortion. Normal hepatic venous pressure gradient (HVPG) is <5 mmHg; varices form when HVPG exceeds 10 mmHg. The portal vein normally carries nutrient-rich blood from the GI tract to the liver. In portal hypertension, blood is diverted through portosystemic collaterals at sites where the portal and systemic venous systems communicate. Esophageal varices form at the gastroesophageal junction where the left gastric (coronary) vein connects to esophageal veins draining into the azygos system. Other collaterals include caput medusae (paraumbilical veins), hemorrhoids (inferior rectal veins), and splenorenal shunts. The liver's synthetic dysfunction (low albumin, elevated INR) reflects lost hepatocyte mass.
Treatment
- Resuscitation: Two large-bore IVs, crystalloid, restrictive transfusion (target Hgb 7-8 g/dL)
- Vasoactive therapy: Octreotide 50 mcg bolus, then 50 mcg/hr infusion (reduces portal pressure)
- Prophylactic antibiotics: Ceftriaxone 1g IV daily (reduces mortality)
- Urgent endoscopy with band ligation of varices
- PPI therapy after banding
- Consider early TIPS (within 72 hours) given high-risk features
- Secondary prophylaxis: Repeat banding until eradication + non-selective beta-blocker
- Alcohol cessation counseling; liver transplant evaluation