Gastroenterology Education and CPD for trainees and specialists » Portal

Explanation :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. Main Splenic vein then joins the superior mesenteric vein to form the portal vein. Portal vein bifurcates into right and left branches. Umbilical vein joins the left branch of PV above the bifurcation. 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%).

Explanation :Hepatic vein pressure is 4mm Hg , Portal vein pressure is 7mm Hg. Portal hypertension is defined by a hepatic venous pressure gradient (HVPG) greater than 5 mmHg. 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

Explanation :Hepatic Venous Pressure Gradient = HVPG= WHVP- FHVP. In prehepatic ( Portal vein thrombosis) and intrahepatic presinusoidal (Noncirrhotic portal fibrosis ) PH, the directly measured portal venous pressure (PVP) is always elevated in presence of normal FHVP, WHVP and HVPG. In sinusoidal (Cirrhosis) and intrahepatic post-sinusoidal ( Veno-occlusive disease) PH , the WHVP tends to equal the directly measured PVP and HVPG is increased proportionately. In post-hepatic PH ( eg Budd Chiari syndrome) , the WHVP equals the increased PVP, but as FHVP is also high, the HVPG is usually normal.

Explanation :Portal hypertension leads to congestion of the splanchnic bed leading to formation of vasodilator nitric oxide aided by bacterial translocation and induction by endotoxin. Decreased effective arterial blood volume leads to activation of systemic vasoactive factors, such as the renin-angiotensin-aldosterone system, the sympathetic nervous system, and vasopressin aimed at restoring arterial filling pressure. Non selective beta blocker like oral propranolol in a dose sufficient to reduce resting pulse rate by 25% has shown to reduce portal presssure. Two mechanisms- decrease in cardiac output ( ß1 blockade) and blockade of ß2 fibres on the splanchnic arteries leaving unopposed vasoconstrictor effects. Cardioselective beta blockers like atenolol, bisoprolol and metoprolol lacks the splancnic vasoconstrictor effects. Vasoconstrictor therapy (terlipressin) restricts portal inflow by splanchnic arterial constriction. The earliest ultrasound finding is loss of respiratory variation of the diameter of the PV, followed by sluggish and then reversal of flow in the PV ( from normal hepatopetal to hepatofugal)

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