Definition of Portal Hypertension
Portal hypertension is defined as a portal pressure gradient (the difference between the portal vein and the hepatic veins) greater than 5 mm Hg, as measured by the hepatic venous pressure gradient (HVPG). 1
Measurement and Classification
Portal hypertension is most accurately assessed through catheterization of the hepatic vein with determination of the HVPG, which is calculated as:
- HVPG = Wedged (occluded) hepatic venous pressure - Free hepatic venous pressure 1
- Normal HVPG is 3-5 mm Hg 1
Portal hypertension is further classified based on severity:
- Mild portal hypertension: HVPG > 5 but < 10 mm Hg 1
- Clinically significant portal hypertension (CSPH): HVPG ≥ 10 mm Hg 1
Anatomical Classification
Portal hypertension can be classified based on the anatomical location of increased resistance to blood flow:
Prehepatic: Involving splenic, mesenteric, or extrahepatic portal vein (e.g., portal vein thrombosis)
- HVPG measurement is normal 1
Intrahepatic:
- Presinusoidal: Cirrhosis from cholestatic liver disease, schistosomiasis, idiopathic portal hypertension
- Sinusoidal: Most common in Western countries, typically from cirrhosis due to alcohol, hepatitis C, or NASH
- HVPG is elevated in sinusoidal type 1
Posthepatic/Postsinusoidal:
- Sinusoidal obstruction syndrome
- Right heart failure
- HVPG may be normal or elevated depending on specific condition 1
Clinical Significance of HVPG Values
Different HVPG thresholds correlate with specific clinical outcomes:
- HVPG > 10 mm Hg: Complications of portal hypertension become more likely (varices, clinical decompensation) 1
- HVPG > 12 mm Hg: Identifies bleeding risk; reducing HVPG below this threshold is associated with protection from variceal hemorrhage 1
- HVPG > 16 mm Hg: Indicates higher risk of death 1
- HVPG > 20 mm Hg: Predicts failure to control bleeding, early rebleeding, and death during acute variceal hemorrhage 1
Diagnostic Methods
While HVPG measurement is the gold standard for diagnosing portal hypertension, it has limitations:
- Invasive procedure
- Requires specific expertise
- Relatively expensive
- Not available in all centers 1
Therefore, noninvasive methods are increasingly used:
Physical examination:
- Spider nevi
- Visible abdominal portosystemic collaterals
- Note: Absence of physical signs cannot rule out CSPH 1
Laboratory data:
- Low platelet count (most common laboratory sign)
- APRI and FIB-4 scores (though with limited accuracy) 1
Imaging techniques:
- Ultrasound: Presence of portocollateral circulation, recanalized paraumbilical vein, spontaneous splenorenal circulation
- Transient elastography (TE): At 15 kPa, sensitivity 90-96% and specificity 48-50%; at 25 kPa, sensitivity 57-85% and specificity 82-93% 1
- CSPH is highly unlikely at LSM ≤15 kPa and likely at LSM ≥25 kPa 1
Clinical Implications
Understanding portal hypertension is critical because:
- It predicts risk of developing complications in cirrhosis 1
- It guides treatment decisions for preventing variceal bleeding 2
- It helps monitor response to therapy (reduction in HVPG >20% from baseline or to <12 mmHg is considered protective) 2
Portal hypertension management focuses on reducing portal pressure through non-selective beta-blockers and preventing complications such as variceal bleeding, ascites, and hepatic encephalopathy 2.