Portal hypertension overview: Difference between revisions
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Portal venous | Life-threatening causes of portal hypertension include [[cirrhosis]], severe [[Portal venous system|portal venous]] obstruction or [[thrombosis]] ([[Budd-Chiari syndrome]]), and [[fulminant hepatic failure]] (e.g., due to [[hepatitis]]). Common causes for portal hypertension include [[alcoholic hepatitis]], [[autoimmune disease]], [[bacterial]] intestinal [[Infection|infections]] (e.g., recurrent [[Escherichia coli|E.coli]] infection), [[chronic hepatitis]], [[cirrhosis]], [[fatty liver]], [[schistosomiasis]], and [[sickle cell disease]]. | ||
==Differentiating {{PAGENAME}} from Other Diseases== | ==Differentiating {{PAGENAME}} from Other Diseases== | ||
Revision as of 17:08, 27 October 2017
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Portal Hypertension Microchapters |
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Portal hypertension overview On the Web |
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Risk calculators and risk factors for Portal hypertension overview |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
Overview
Portal hypertension is hypertension in the portal stem which causes an obstruction in the portal vein and its branches. It is often defined as a portal pressure gradient (the difference in pressure between the portal vein and the hepatic veins) of 12 mm Hg or greater.
Historical Perspective
In 1511, Leonardo da Vinci, Italian Renaissance polymath, first describe the portal hypertension in an illustration in his textbook "De humanis corpore". “... the artery and the vein which go from the spleen to the liver become so large, to block the blood coming from the mesenteric vein; the latter vein dilates and becomes tortuous like a snake, that the liver dries and become like frozen bran, in colour and consistency…”, he mentioned mistakenly the portal hypertension as the outcome of this presentation.
Classification
Based on the etiology, portal hypertension may be classified as pre-hepatic, intra-hepatic, and post-hepatic. Intra-hepatic portal hypertension classified into pre-sinusoidal, sinusoidal, and post-sinusoidal disorders. Based on the function impairment in the liver, portal hypertension may be classified as cirrhotic and non-cirrhotic.
Pathophysiology
The exact pathogenesis in portal hypertension is disturbance in normal physiology of portocaval circulation. The main factors that affect the pressure gradient in blood vessels are blood flow (Q) and vessel radius (r) in a direct and inverse way, respectively. Portal hypertension is related to elevation of portal vasculature resistance. Peripheral vasodilatation is the basis for decreased systemic vascular resistance and mean arterial pressure, plasma volume expansion, elevated splanchnic blood flow, and elevated cardiac index. Fourteen different genes are involved in the pathogenesis of portal hypertension. Homozygous missense mutation in DGUOK gene found to be related with non-cirrhotic portal hypertension. On gross pathology, cirrhotic liver, splenomegaly, and esophageal varices are characteristic findings in portal hypertension. The main microscopic histopathological findings in portal hypertension are related to cirrhosis, esophageal varices, hepatic amyloidosis, and congestive hepatopathy due to heart failure or Budd-Chiari syndrome.
Causes
Life-threatening causes of portal hypertension include cirrhosis, severe portal venous obstruction or thrombosis (Budd-Chiari syndrome), and fulminant hepatic failure (e.g., due to hepatitis). Common causes for portal hypertension include alcoholic hepatitis, autoimmune disease, bacterial intestinal infections (e.g., recurrent E.coli infection), chronic hepatitis, cirrhosis, fatty liver, schistosomiasis, and sickle cell disease.
Differentiating Portal hypertension overview from Other Diseases
Epidemiology and Demographics
Risk Factors
Screening
Natural History, Complications, and Prognosis
Natural History
Complications
Prognosis
Diagnosis
Diagnostic Criteria
History and Symptoms
Physical Examination
Laboratory Findings
Liver function tests for assessment of severity of the disease.
X Ray
Barium swallow is done in the presence of varices where it is seen as filling defects (bag of worms appearance). Barium enema is useful in cases of colonic varices.
Ultrasound
Ultrasonography is useful to note the size of the liver, spleen, portal vein, splenic vein and to look for the presence of collaterals.
Other Imaging Findings
Portal venography is useful in evaluating the patency and the caliber of the portal and splenic veins.
Other Diagnostic Studies
The hepatic venous pressure drainage measurement is the gold standard for measuring portal hypertension. If the pressure is more than 5 mm of Hg, it is considered significant.
Treatment
Endoscopy
Upper gastrointestinal endoscopy is very reliable. It shows the presence of cherry red spots. Proctoscopy is useful in cases of rectal varices.
Medical Therapy
Treatment with a non-selective beta blocker is often commenced once portal hypertension has been diagnosed, and almost always if there has already been bleeding from esophageal varices. Typically, this is done with either propranolol or nadolol. The addition of a nitrate, such as isosorbide mononitrate, to the beta blocker is more effective than using beta blockers alone and may be the preferred regimen in those people with portal hypertension who have already experienced variceal bleeding. In acute or severe complications of the hypertension, such as bleeding varices, intravenous octreotide (a somatostatin analogue) or intravenous terlipressin (an antidiuretic hormone analogue) is commenced to decrease the portal pressure.