Portal pressure
Fibrotic narrowing of portal flow
Also searched as Fibrotic narrowing of portal flow.
You want the pressure low. Every complication downstream is driven by it.
In depth
All the blood from your gut passes through the liver before rejoining the body. Scar tissue narrows that route, and pressure builds behind it. Above 5 mmHg it has a name; above 10 it starts causing the complications. It is the hinge on which everything after cirrhosis turns.
What drives it
Liver scarring increases it.
Verbatim (s1665268123002831, on Baveno vii): 'the development of portal hypertension is the most critical milestone in the natural history of advanced chronic lIVER disease. Portal hypertension is defined as an increase in portal pressure gradient between the portal vein and the inferior vena cava above 5 mmHg. Cirrhosis is by far the most common cause of portal hypertension.' And pmc10311004: 'Cirrhosis transcends various progressive stages from compensation to decompensation driven by the severity of portal hypertension.'.
Tissue scarring increases it.
The pressure begins before cirrhosis does. Baveno VII introduced 'compensated advanced chronic liver disease (cACLD)' precisely because 'cirrhosis implies a pathological (invasive) diagnosis' — the concept 'was put forward based on non-invasive tests that would predict the development of complications of cirrhosis', and Baveno VII 'leveraged the use of liver stiffness measurement to categorize the degree of portal hypertension' (PMC11299547). this edge asserts that advanced fibrosis raises portal pressure before the cirrhosis threshold; the earlier MASLD source notes 'the risk of liver-related complications due to CSPH can already manifest in an earlier stage of MASLD prior to cirrhosis'. PMC11299547
Fluke burden increases it.
Presinusoidal obstruction by egg granulomata raises portal venous pressure. PMID 19825105
What it drives
It increases Abdominal fluid.
Verbatim (pmc11945444): 'ascites is the most common complication from cirrhosis related to portal hypertension and depicts the onset of hepatic decompensation. Ranging from uncomplicated to refractory ascites, the progression carries prognostic value by reflecting the deterioration of underlying cirrhosis and portal hypertension.' scope: a treatment hazard is named in the same source — 'with worsening systemic vasodilation and inflammation when ascites progresses, patients on NSBBs are at risk of hemodynamic collapse leading to renal hypoperfusion and thus hepatorenal syndrome.' not a node here, but named.
It increases Swollen veins.
Verbatim (pmc10311004): 'The downstream effect of increasing portal hypertension severity leads to various pathophysiological pathways, which result in the cardinal complications of cirrhosis, including ascites, variceal hemorrhage, and hepatic encephalopathy.' Baveno VII states 'there is NO indication at present to use NSBBs in patients without CSPH' — the intervention is gated on the pressure, not on the scan.
It increases Mental clarity in liver health.
https://www.merckmanuals.com/professional/hepatic-and-biliary-disorders/approach-to-the-patient-with-liver-disease/portosystemic-encephalopathy — Same source and same sentence as the varices edge — encephalopathy is named as one of the three cardinal complications driven by portal hypertension severity. encephalopathy has both a pressure route (blood bypassing the liver through portosystemic collaterals) and a functional route (failing hepatocytes). This edge carries the pressure route only. Sources:. PMC10311004
It increases Liver decompensation.
10.1016/j.jhep.2021.12.022 — Verbatim (S1665268123002831): 'the appearance of variceal bleeding, ascites, hepatic encephalopathy OR non-obstructive jaundice, herald the onset of decompensated cirrhosis.'. doi 10.1016/j.jhep.2021.12.022
Blends that modulate it
Each blend page names this pathway and carries the study behind its claim.
See it on the map
Open the causal map to follow this pathway upstream and downstream, arrow by arrow, each with its study.