Portal hypertension overview: Difference between revisions
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{{Portal hypertension}} | {{Portal hypertension}} | ||
{{CMG}}; {{AE}} | {{CMG}}; {{AE}} | ||
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==Overview== | ==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 vein]]s) of 12 mm Hg or greater. | 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 vein]]s) of 12 mm Hg or greater. | ||
==Overview== | |||
==Historical Perspective== | |||
==Classification== | |||
==Pathophysiology== | ==Pathophysiology== | ||
Many conditions can result in portal hypertension. In North America and Europe, it is usually the result of an intrahepatic block due to [[cirrhosis]] of the [[liver]]. However, in less industrialized parts of the world, climate permitting, the major cause is [[schistosomiasis]]. | |||
==Causes== | |||
Portal venous pressure is determined by portal blood flow and portal vascular resistance. Increased portal vascular resistance is often the main factor responsible for it. The consequences of portal hypertension are due to blood being forced down alternate channels by the increased resistance to flow through the portal system. Due to formation of alternate channels initially some of the portal blood and later most of it is shunted directly to the systemic circulation bypassing the [[liver]]. | Portal venous pressure is determined by portal blood flow and portal vascular resistance. Increased portal vascular resistance is often the main factor responsible for it. The consequences of portal hypertension are due to blood being forced down alternate channels by the increased resistance to flow through the portal system. Due to formation of alternate channels initially some of the portal blood and later most of it is shunted directly to the systemic circulation bypassing the [[liver]]. | ||
== | |||
==Differentiating {{PAGENAME}} from Other Diseases== | |||
==Epidemiology and Demographics== | |||
==Risk Factors== | |||
==Screening== | |||
==Natural History, Complications, and Prognosis== | |||
===Natural History=== | |||
===Complications=== | |||
===Prognosis=== | |||
==Diagnosis== | ==Diagnosis== | ||
===Diagnostic Criteria=== | |||
===History and Symptoms=== | |||
===Physical Examination=== | |||
===Laboratory Findings=== | ===Laboratory Findings=== | ||
[[Liver function test]]s for assessment of severity of the disease. | [[Liver function test]]s for assessment of severity of the disease. | ||
===X Ray=== | ===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. | [[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=== | ===Ultrasound=== | ||
Ultrasonography is useful to note the size of the liver, spleen, portal vein, splenic vein and to look for the presence of collaterals. | Ultrasonography is useful to note the size of the liver, spleen, portal vein, splenic vein and to look for the presence of collaterals. | ||
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==Treatment== | ==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=== | ===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. | 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. | ||
===Surgery=== | |||
===Prevention=== | |||
==References== | ==References== | ||
Revision as of 19:12, 19 July 2016
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
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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.
Overview
Historical Perspective
Classification
Pathophysiology
Many conditions can result in portal hypertension. In North America and Europe, it is usually the result of an intrahepatic block due to cirrhosis of the liver. However, in less industrialized parts of the world, climate permitting, the major cause is schistosomiasis.
Causes
Portal venous pressure is determined by portal blood flow and portal vascular resistance. Increased portal vascular resistance is often the main factor responsible for it. The consequences of portal hypertension are due to blood being forced down alternate channels by the increased resistance to flow through the portal system. Due to formation of alternate channels initially some of the portal blood and later most of it is shunted directly to the systemic circulation bypassing the liver.
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.