What are the components of the triad of portal hypertension and how is it managed?

Portal Hypertension Triad

The classic triad of portal hypertension consists of esophageal/gastric varices, ascites, and splenomegaly with hypersplenism. 1, 2, 3

Components of the Triad

1. Varices (Gastroesophageal)

• Varices develop when hepatic venous pressure gradient (HVPG) reaches ≥10 mmHg (clinically significant portal hypertension) 4, 1
• Present in approximately 50% of cirrhosis patients, with 5-15% developing new or worsening varices annually 5
• Variceal bleeding occurs when portal-systemic gradient exceeds 12 mmHg and carries 30-day mortality of 20% 6
• Risk factors for bleeding include previous gastrointestinal bleeding, large varix size, and red wale marks (longitudinal dilated venules on variceal surface) 1

2. Ascites

• Ascites is the most common complication of portal hypertension, reducing 5-year survival from 80% to 50% 2
• Develops when HVPG reaches ≥10 mmHg 4, 1
• When ascites becomes refractory to conventional medical treatment, 1-year mortality ranges from 20% to 50% 4
• Diagnostic paracentesis with measurement of ascitic fluid albumin/protein, neutrophil count, culture, and amylase should be performed when ascites is present 2

3. Splenomegaly with Hypersplenism

• Splenomegaly leads to reduced blood cell counts (thrombocytopenia, leukopenia, anemia) 2
• Can be detected on abdominal ultrasound along with evaluation of liver appearance and portosystemic collaterals 2

Diagnostic Approach

Gold Standard Measurement

• HVPG measurement is the gold standard for diagnosis and quantification 1, 2
• Normal HVPG: 1-5 mmHg 4, 1
• Portal hypertension: HVPG >5-6 mmHg 4, 1
• Clinically significant portal hypertension (CSPH): HVPG ≥10 mmHg 4, 1
• High mortality risk: HVPG ≥16 mmHg (independently associated with higher mortality in compensated and decompensated cirrhosis) 4, 1

Non-invasive Alternatives

• Transient elastography: 90-96% sensitivity and 48-50% specificity at 15 kPa cutoff 1
• APRI score can be used as blood-based alternative 2
• Abdominal imaging (ultrasound, CT) can identify portosystemic collaterals, splenomegaly, and ascites 2, 7

Management Algorithm

Stage 1: Mild Portal Hypertension (HVPG >5 but <10 mmHg)

• Primary treatment is eliminating the etiological agent (treat underlying liver disease) 8
• Non-selective beta-blockers (NSBBs) are ineffective at this stage 2, 8

Stage 2: CSPH Without Varices (HVPG ≥10 mmHg)

• NSBBs including carvedilol can be considered to prevent clinical decompensation 1, 2
• No specific treatment recommended to prevent varix formation 8
• Goal is preventing decompensation 8

Stage 3: CSPH With Varices (No Prior Bleeding)

• Primary prophylaxis with NSBBs or endoscopic variceal ligation (EVL) 4
• Target HVPG reduction of ≥10% or to <12 mmHg correlates with reduced bleeding risk 4, 2

Stage 4: Acute Variceal Bleeding

• Immediately initiate vasoactive agents (terlipressin, octreotide, or somatostatin) before endoscopy 1, 8
• Combination of vasoactive agents plus endoscopic therapy (sclerotherapy or band ligation) improves hemostasis and reduces 5-day mortality 4, 1
• Endoscopic therapy controls bleeding in up to 85% of patients 6
• For refractory bleeding: TIPS (transjugular intrahepatic portosystemic shunt) 8, 6

Stage 5: Refractory Ascites

• TIPS is recommended for refractory ascites 1, 2
• Large-volume paracentesis with albumin replacement for symptomatic relief 9

Definitive Treatment

• Liver transplantation should be considered for all patients with decompensated cirrhosis 1, 2, 8

Critical Pitfalls to Avoid

• Do not delay vasoactive drug administration while waiting for endoscopy in acute variceal bleeding—early administration facilitates endoscopy and improves outcomes 4, 8
• Do not use NSBBs in mild portal hypertension (HVPG <10 mmHg)—they are ineffective and may cause harm 2, 8
• Do not overlook HVPG ≥16 mmHg—this threshold independently predicts mortality and should prompt aggressive management and transplant evaluation 4, 1
• Hepatorenal syndrome is a frequent and grave complication of refractory ascites requiring prompt recognition 4