| ID | 56 |
|---|---|
| Name | PORTAL HYPERTENSION |
| Cause | Causes of Portal hypertension:3 A. Common causes: Prehepatic cause- Portal vein thrombosis (umbilical sepsis, portal pyaemia) Idiopathic portal hypertension Intrahepatic causes- Cirrhosis of liver Chronic hepatitis Schistosomiasis B. Other causes: Prehepatic cause- Umbilical vein transfusion Portal vein thrombosis (from thrombotic diseases, oral contraceptives, pregnancy) Abdominal trauma Biliary surgery Malignant disease of pancreas Pancreatitis Intrahepatic cause- Partial nodular transformation of the liver Cystic liver fibrosis Congenital hepatic fibrosis Myelosclerosis Sarcoidosis Metastatic malignant disease Granulomata Posthepatic causes- Budd-Chiari syndrome Veno-occlusive disease . Right heart failure Constrictive pericarditis |
| Signs Symptoms | |
| Diagnosis | Diagnosis: 1. Laboratory investigations for chronic liver disease (see above). 2. Ultrasonogram of abdominal organs. 3. Endoscopy (diagnostic & therapeutic use for scleropathy). |
| Investigations | |
| Management | Management: 1. Initial management & resuscitation of acute variceal bleeding, please see the management of gastro-intestinal bleeding. 2 Management for ascites- see under cirrhosis. 3. Management for portosystemic encephalopathy- see the management of hepatic encephalopathy under cirrhosis. |
| Introduction | Portal vein, which is formed by the union of the superior mesenteric and splenic veins, drains the greater amount of alimentary blood. The normal pressure in portal vein is about 5-8 mmHg, which creates a very small pressure gradient accross the liver to the hepatic vein. So, any obstruction or impairment in this pathway causes increased portal venous pressure. A rise in pressure of about 10-12 mmHg leads to development of different collaterals and portosystemic shunts. The common sites of shunts are- i. gastro-oesophageal junction, ii. rectal wall, iii. the left renal vein, iv. the diaphragm, v. the retroperitoneum, and vi. anterior abdominal wall through the umbilical vein. Among these, the gastro-oesophageal varices (vessels) are very superficial and tend to rupture & bleed frequently. The rectal veins are also superficial and tend to bleed frequently (about 30%). |
| History | |
| Etiology | |
| Clinical Features | Clinical feature: Clinical presentation of portal hypertension depends on the underlying cause and stage of the disease. In initial stage, portal hypertension may be asymptomarric, but the only evidence is splenomegaly. As the commonst cause of portal hypertension is chronic liver disease e.g cirrhosis, the presenting features include- 1. Features of chronic liver disease - (see above, under cinhosis & hepatitis). 2. Splenomegaly, (hypersplenism is also common & often results thrombocytopenia). 3. Haematemesis &/or melaena or rectal bleeding from gastro-oesophageal and rectal verices 4. Ascites with or without peripheral oedema. 5. Prominent collateral veins visible on the abdominal wall and often radiating veins around the umbilicus (caput medusae). 6. Features of portosystemic encephalopathy (see above under cirrhosis). 7. Fetor hepaticus may result from portosystemic shunting of blood. |
| Preventions | |
| Treatment | |
| Complications | |
| Prognosis | |
| Types | |
| Classification | According to the site of obstruction, portal hypertension can be considered into 3 varieties- 1. Prehepatic- blockage of portal vein before entering liver. 2. Intrahepatic- blockage within the liver. This is again divided into three types- a. Pre-sinusoidal (e.g schistosomiasis), b. Sinusoidal (e.g cirrhosis) & c. Post-sinusoidal (e.g veno-occlusive disease). 3. Posthepatic- blockage of venous drainage outside the liver (rare). |
| Observation | |
| Pathology |
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