Portal hypertension

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Portal hypertension (PH) is technically defined as a pressure gradient of 12 mm Hg or greater. This gradient basically represents backflow pressure created by obstruction of blood flow through the liver as well as an increase of flow into it.


Contents

Etiology of portal hypertension

In cirrhosis, the primary cause of PH, there is an increase in portal vascular resistance that is created by the combined effects of distorted hepatic anatomy and active contraction of elements such as vascular smooth muscle in the intrahepatic veins and myofibroblasts within the liver.

Complicating this increase in resistance is an increase in blood flow through the portal vein. The factors that are responsible for this increase are increased cardiac output, arterial hypotension, and hypervolemia—all essentially a response to a release of endogenous neural and humoral vasodilators.

A classic way of categorizing causes of portal hypertension is anatomic. Prehepatic causes include congenital atresia or stenosis of the portal vein, thrombosis of portal vein, thrombosis of splenic vein, and extrinsic compression, e.g. tumors. Hepatic causes include cirrhosis, acute alcoholic hepatitis, congenital hepatic fibrosis, idiopathic PH (hepatoportal sclerosis), and schistosomiasis. Posthepatic causes include Budd.Chiari syndrome, constrictive pericarditis, and arterial portal venous fistula. [1]


Morbidity with portal hypertension

Portal hypertension has a number of sequelae, but the most serious are esophageal varices. 90% of patients with PH have varices, 30% of these varices bleed, and there is a 30% to 50% mortality rate associated with the first episode of variceal bleeding. [2]


Diagnosing portal hypertension

Radiological studies

When evaluating the nature of PH, abdominal vascular imaging is required to define the portal hemodynamics. The initial study should be a Doppler ultrasound. This reveals general hepatic architecture as well as the portal, splenic, hepatic, and infrahepatic veins, and the inferior vena cava. The study may thus identify any primary extrahepatic causes of PH. If there is a remaining question, CT scanning or MRI may be added to the workup.

Arteriography is still another tool that may be used if there is question about vascular abnormalities. Venography offers direct measurement of vascular pressures. [3]


Clinical presentation

Clinically, PH is often asymptomatic until some event such as a lower GI bleed or esophageal bleed. The most evident symptom of chronic PH is ascites. In general, the clinical presentation for PH is that of a cirrhotic patient (even though cirrhosis may not be the origin of specific case of PH).

This is also true for the individual sequelae of portal hypertension — esophageal varices, ascites, hepatorenal syndrome, and hepatic encephalopathy.

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