Gastroenterology training and education

Discuss portal pressure?

Portal venous pressure is determined by the product of portal venous flow and the resistance to outflow from the portal venous system:

Portal pressure = Portal venous flow x portal venous outflow resistance

It is usually caused by an increase in resistance in the portal-hepatic vascular bed due to obstruction to flow, which in the vast majority of patients is related to cirrhosis.

However, a variety of disorders can cause portal hypertension in the absence of cirrhosis, a condition referred to as “noncirrhotic portal hypertension.”

In both the above cases the PH is because of increased resistance, but rarely PH can result because of increased portal flow in normal resistance, e.g. splanchnic AF fistula

Discuss portal vein anatomy?

• Splenic vein joins with short gastric vessels to form the main Splenic vein
• Inferior mesenteric vein joins Splenic vein in its medial third and left gastric vein joins the confluence of Splenic vein and SMV
• Splenic vein joins the superior mesenteric vein to form the portal vein
• portal vein bifurcates into right and left branches
• umbilical vein joins the bifurcation of the above
• Portal blood flow is 1200ml/mt and it carries 72% of the oxygen content of the liver and the 75% of the total blood flow ( hepatic artery carries 400ml/mt = 25%)

Discuss the normal pressure and flows?

Hepatic vein pressure= 4mm Hg
Portal vein pressure= 7mm Hg
Hepatic artery pressure = 100 mm Hg

Hepatic vein flow = 1600ml/mt
Portal vein flow = 1200ml/mt
Hepatic artery flow = 400ml/mt

Portal pressure is 7 mm Hg (remember this is an average value – but absolute in nature rather than below)
Portal hypertension is defined by a hepatic venous pressure gradient (HVPG) greater than 5 mmHg.

When the portal circulation is obstructed, whether it is within or outside the liver, a remarkable collateral circulation develops to carry portal blood into the systemic circulation veins.

Collaterals usually imply PH although occasionally if the collateral circulation is very extensive portal pressure may fall.
Conversely PH of short duration can exist without a demonstrable collateral circulation

Haemodynamic of PH
Normally 100% of portal blood flow is recoverable from hepatic veins whereas in cirrhosis only 13% goes to hepatic vein and rest reaches the systemic circulation through the collaterals
Discuss portal pressure studies?

• A balloon catheter is introduced into femoral or internal jugular vein under fluoroscopic control
• first catheter tip is wedged into a tributary of hepatic vein and balloon is inflated = Wedged hepatic venous pressure= WHVP
• Then it is withdrawn into the hepatic vein = Free Hepatic Venous Pressure= FHVP
• Normal uncorrected portal pressure is 5-10mm Hg and is influenced by the intra-abdominal pressure and central venous filling pressure.
• In order to eliminate the contribution of intra-abdominal pressure and central venous pressure and thus express portal pressure as the intrinsic pressure difference between the portal and systemic venous compartments portal pressure is usually expressed as a portal pressure gradient
• So Hepatic Venous Pressure Gradient = HVPG= WHVP- FHVP= 7-4=3
• PH is defined as HVPG > 5
• Risk of GIB when HVPG > 12

	FHVP	WHVP	HV-PG
Pre-sinusoidal Eg. Schistosomiasis/ NCPF	Normal	Normal	Normal
Sinusoidal Eg. Cirrhosis	Normal	High	High
Post- sinusoidal Eg. Budd Chiari	High	High	Normal

Discuss the causes of portal hypertension?

Causes of presinusoidal portal hypertension – associated with relatively normal hepatocellular function and consequently if patient suffers a haemorrhage from varices liver failure is rarely a consequence in contrast patients with the intra-hepatic type frequently develop liver failure after bleeding

• Extrahepatic portal vein obstruction – Particularly prominent gastric varices – supplied by short gastric veins
• Lesions in surrounding structures: pancreatitis, tumour, biliary tract disease
• Lesions of vessel wall: phlebitis-pylephlebitis, omphalitis
• Hypercoagulable state
• Segmental portal hypertension
• Intrahepatic portal vein obstruction
• Schistosomiasis- later mixed presinusoidal and sinusoidal
• Noncirrhotic portal fibrosis
• Early Primary biliary cirrhosis – later mixed presinusoidal and sinusoidal
• Early Sclerosing cholangitis – early – later mixed presinusoidal and sinusoidal
• Sarcoidosis
• Myeloproliferative disease- later mixed presinusoidal and sinusoidal
• Congenital hepatic fibrosis
• Hepatic arterioportal fistula
• Non Obstructive causes – increased blood flow
• Splanchnic arteriovenous fistula
• Idiopathic tropical splenomegaly – Splenomegaly may cause portal hypertension because of hyperdynamic portal blood flow arising from the enlarged spleen.
• Splenomegaly (eg, lymphoma, Gaucher’s disease)

Causes of Sinusoidal portal hypertension

• Cirrhosis – secondary to chronic hepatitis
• Noncirrhotic cause
• Acute hepatitis – alcoholic hepatitis
• FHF
• Vitamin A toxicity
• Arsenic poisoning – both pre-sinusoidal and sinusoidal
• Vinyl chloride toxicity – both pre-sinusoidal and sinusoidal
• Secondary syphilis
• Nodular regenerative hyperplasia

Causes of post sinusoidal portal hypertension

• Intra-hepatic
• Venoocclusive disease (VOD)
• Budd-Chiari syndrome (hepatic vein thrombosis)

• Extra-hepatic
• IVC obstruction- web/thrombus
• Constrictive pericarditis
• Restrictive cardiomyopathy
• Tricuspid regurgitation
• Severe right heart failure

Discuss the mechanism of increased resistance in sinusoidal portal hypertension?

• Hepatocyte swelling
• Collagen deposition in space of Disse
• Loss of intersinusoidal anastomoses
• Compression by regenerative nodules and fibrosis

As a general rule, the clinical consequences of portal hypertension are similar regardless of the cause or site of obstruction. However, several pathophysiologic changes are related to specific types and causes of portal hypertension, which may influence their clinical presentation and therapy.

Liver Cirrhosis: pic shows destruction and fibrosis in centre, with remaining nodules of more normal liver at bottom right and top left. Note the irregular whorls of fibrosis around the nodules.