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==Overview==
==Overview==
Portal vein thrombosis was first discovered by Balfour and Stewart in 1868. In 1868, G201210A mutations were first implicated in the pathogenesis of portal vein thrombosis. In 1945, Allan Whipple, an American surgeon, reported treatment of some cases of the portal hypertension with shunts. He eventually tried shunts between different mesenteric veins. Finally, he found portocaval shunt as the best choice. In 1980s, researchers have observed that endoscopic sclerotherapy is more efficient than surgical shunting in preventing recurrent variceal bleeding. Portal vein thrombosis may be classified according to the extension into 4 groups including confined to the portal vein beyond the confluence of the [[splenic vein]], extended to the [[superior mesenteric vein]], but with patent [[mesenteric]] [[vessels]], extended to the whole [[splanchnic]] venous system, but with large collaterals, and extended to the whole [[splanchnic]] venous system with only fine collaterals. Based on the duration of symptoms, portal vein thrombosis may be classified as either acute or chronic. It is thought that [[vein thrombosis]] is caused by [[Virchow's triad]] which includes reduced portal blood flow, [[hypercoagulable state]], vascular endothelial injury. There are two mechanisms that contribute in loss of portal vein blood flow to liver, [[arterial]] rescue and venous rescue. It is a rapid process and takes a few days to start and 3-5 weeks to complete after portal vein obstruction. Collateral vessel joins to form [[cavernoma]] which connects the proximal and distal part of thrombosed portal vein. Finally, the portal vein becomes fibrosed, thin cord. All these events leads to low systemic vascular resistance and high cardiac output. These are the characterstic findings of hyperkinetic circulation. Portal vein thrombosis may be caused by inherited prothrombotic disorders and acquired thrombophilic disorders. Less common causes of portal vein thrombosis include acquired conditions such as [[cirrhosis]] and[[hepatocellular carcinoma]] and procedures such as abdominal [[surgery]] or surgical injury of the portal vein axis and [[splenectomy]]. *Portal vein thrombosis must be differentiated from other diseases that cause abdominal pain, diarrhea, nausea and vomiting , such as [[Chronic pancreatitis|chronic pancreatitis,]] [[Pancreatic carcinoma]], [[Dumping syndrome]], [[Acute appendicitis]], [[Diverticulitis|acute diverticulitis]], [[Infective colitis]], [[Hepatitis|viral hepatitis]], [[Liver abscess]], [[Mesenteric ischemia]], [[Acute]] [[ischemic colitis]]. The [[incidence]] of portal vein thrombosis in cirrhotic patients is unknown. The [[prevalence]] of portal vein thrombosis is approximately 5000-10,000 per 100,000 in overall cases of portal hypertension in developed counties and 40,000 per 100,000 in developing countries. The overall [[mortality rate]] of portal vein thrombosis is less than 10% except for patients with [[malignancy]] or [[cirrhosis]]. Patients of all age groups may develop portal vein thrombosis. There is no racial predilection to portal vein thrombosis. Portal vein thrombosis affects men and women equally. Common risk factors in the development of portal vein thrombosis include [[cirrhosis]], [[pancreatitis]], [[duodenal ulcer]], [[cholecystitis]], [[Crohn's disease|Crohn’s disease]], [[ulcerative colitis]] and [[cholecystectomy]], [[diverticulitis]] and [[appendicitis]] . Less common risk factors in the development of portal vein thrombosis include [[Oral contraceptive|oral contraceptives]], [[pregnancy]] or [[puerperium]], and [[hyperhomocysteinemia]]. There is insufficient evidence to recommend routine [[screening]] for portal vein thrombosis. If left untreated, patients with portal vein thrombosis may progress to develop portal cavernoma, gastric or [[esophageal varices]]/bleeding, [[hepatic encephalopathy]], [[splenomegaly]], portal biliopathy or cholangiopathy. Depending on the extent of the model for end-stage liver disease score at the time of diagnosis, the prognosis may vary. However, the prognosis is generally regarded as good.


==Historical Perspective==
==Historical Perspective==

Revision as of 18:23, 19 December 2017

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

Overview

Historical Perspective

Portal vein thrombosis was first discovered by Balfour and Stewart in 1868. In 1868, G201210A mutations were first implicated in the pathogenesis of portal vein thrombosis. In 1945, Allan Whipple, an American surgeon, reported treatment of some cases of the portal hypertension with shunts. He eventually tried shunts between different mesenteric veins. Finally, he found portocaval shunt as the best choice. In 1980s, researchers have observed that endoscopic sclerotherapy is more efficient than surgical shunting in preventing recurrent variceal bleeding.

Classification

Pathophysiology

Causes

Differentiating ((Page name)) from Other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications, and Prognosis

Diagnosis

Diagnostic Criteria

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

X-ray

Ultrasound

CT scan

MRI

Other Imaging Findings

Other Diagnostic Studies

Treatment

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