Portal Hypertension Treatment Causes Symptoms by Nurses Note

 Portal Hypertension

What is portal Hypertension?

It is sustained elevation of the portal venous pressure more than 10 mm of Hg. Normal portal venous pressure is 5-10 mmHg. It is also defined as elevation of the hepatic venous pressure gradient (HVPG) >5 mmHg. HVPG is the difference between the wedged hepatic venous pressure (WHVP) and free hepatic venous pressure (FHPV). When HVPG is more than 10 mmHg, porta systemic develop; when it becomes more than 12 mm Hg, risk for variceal bleeding oesophagus varices.

Causes and Symptoms of Portal Hypertension

There is increased portal resistance and altered portal blood of flow. Increased resistance may be presinusoidal, sinusoidal, postsinusoidal.

Presinusoidal 

• Extrahepatic- portal/splenic vein thrombosis.
• Intrahepatic- Schistosomiasis, sarcoidosis, congenital hepatic fibrosis, primary biliary cirrhosis.
• Sinusoidal- Cirrhosis, haemochromatosis, Wilson's disease, non-alcoholic steatohepatitis (NASH).
• Postsinusoidal- Budd-Chiari syndrome, constrictive pericarditis, veno- occlusive disease.

Important Notes: Portal Hypertension

1. Left-sided portal Hypertension (sinistral) can be caused by isolated splenic vein thrombosis, which is often caused by adjacent pancreatitis.
2. A rise in portal pressure stimulates portasystemic circulation.
3. Portal vein carries 75% of blood flow to liver with all nutrients to maintain its integrity and gives 50% oxygen supply to liver. 25% hepatic arterial blood flow gives remaining 50% of oxygen supply to liver.
4. Portal Hypertension causes compensatory portasystemic venous collateral formation, altered intrahepatic circulation and increased splanchnic blood flow. High-pressure portal blood is diverted via coronary (left gastric vein), short gastric and oesophageal veins into azygos venous system.
5. There is dysregulation of compensatory increased hepatic arterial flow response in relation to decreased portal vein flow.
6. 30% of varices patients will bleed; 30% of them will die of bleed; 30% of patients with cirrhosis will develop portal hypertension; 30% of them have variceal bleed in 2 years; 70% of patients who had bleeding once, will rebleed later.
7. Variceal bleed accounts for 7% of upper GI bleed.
8. Small varix is <5 mm in size; large one is >5 mm.

Sites of portasystemic Collateralisation

1. Lower end of oesophagus between left gastric and short gastric veins with azygos vein resulting in oesophageal varices commonest.
2. Umbilicus, between paraumbilical vein and anterior abdominal vein resulting in caput medusae.
3. Lower end of rectum, between superior haemorrhoidal vein resulting in piles.
4. Retroperitoneum.
5. Bare area of the liver.

Presentations

• Triad of portal hypertension
• Oesophageal varices.
• Splenomegaly.
• Ascites.
• Jaundice
• Features of encephalopathy
• Recurrent infection.
• Coagulopathy.
• Hepatorenal syndrome.

General: weakness, tiredness, anorexia, weight loss, abdominal pain, jaundice, oedema, pruritus, spontaneous bleeding and bruises, impotence, muscle cramps, palor, cyanosis, hypotension.

Features of variceal bleeding: anemia, haematemesis, melaena, shock. Bleeding may be from gastric/oesophageal varices or portal gastropathy.

Features of encephalopathy: memory loss, altered behaviour and mental status, asterixis (flapping tremor/liver flap), unconsciousness, foetor hepaticus.

Features of liver cell failure: gynaecomastia, palmar erythema, leuconychia, testicular atrophy, spider angioma, parotid enlargement, cyanosis and tachypnoea.

Ascites and generalised anasarca with oedema scrotum and abdominal wall and limbs. Ascites is a sign of hepatic decompensation.

Decreased urine output features of renal failure: hepato renal syndrome.

Splenomegaly causing hypersplenism: hypersplenism occurs in 30% of cases with features of leucopenia (WBC <4,000/cumm), thrombocytopenia (platelet <1,00,000).

Causes of Portal Hypertension

Prehepatic

• Portal vein or splenic vein thrombosis.
• Hypercoagulable status.
• Periportal inflammation.
• Trauma.
• Extrinsic compression from pancreas, stomach.
• Neonatal umbilicus sepsis.

Hepatic 

• Portal pyaemia
• Alcoholic cirrhosis
• Idieopathic portal Hypertension.
• Primary biliary cirrhosis.
• Schistosomiasis.
• Hepatitis.
• Nodular regenerative hyperplasia.
• Wilson's disease.
• Haemochromatosis.
• Congenital hepatic fibrosis.

Post Hepatic

• Budd-chiari syndrome.
• Constrictive pericarditis.
• Congestive cardiac failure.
• Veno-occlusive disease.

Investigations Portal Hypertension

Blood - Hb% - anaemia is due to bleeding, hypersplenism, nutritional, bone marrow suppression. Pancytopenia shows leucopenia, thrombocytopenia. Counts may be serially repeated during monitoring period. Blood grouping should be done as often patient needs packed cell or FFP transfusion.

Liver function test: usually altered with raised bilirubin. Prothrombin time (INR), activated partial thromboplastin time (APTT) and other coagulation profile should be done as coagulopathy is not uncommon.

AFP and other relevant markers may be useful. Serum iron, ∝1-antitrypsin, ceruloplasmin, autoantibodies, evaluation for hepatitis B, C, D are important.

Renal function test: blood urea, serum creatinine, serum potassium.

Ultrasound abdomen: easier, simple initial screening method to identify liver status, portal vein, ascites, splenomegaly. Doppler imaging will help to assess the vascular pattern, blood flow, size of the vein, thrombosis in the portal system.

Contrast CT and MRI are very useful to see nodules, collaterals, portal vein status/thrombosis, splenomegaly. CT angiogram is very useful.

MR venogram is very sensitive non-invasive method to study extrahepatic portal vein thrombosis. MR angiography/venography better delineates the portal and hepatic venous anatomy; it is very useful in Budd-Chiari syndrome.

Hepatic venous pressure gradient (HVPG): It is the gold standard to diagnose portal hypertension. Through transjugular or transfemoral (veins) route, balloon tip catheter passed under guidance into the hepatic vein via IVC; IVC pressure is assessed; free hepatic venous pressure (FHVP) is measured with catheter in the hepatic vein; catheter is further negotiated into the vein and balloon is inflated to wedge and pressure is measured. This wedge hepatic vein pressure (WHVP) is actually sinusoidal pressure and is equivalent to portal hypertension; 5-10 mmHg suggests subclinical type; >10 mmHg suggests significance shunting and varices; >12 mmHg suggests high risk for bleed. Often it may raise as high as 30 mmHg.

Oesophagogastroscopy to identify varices oesophageal and gastric or portal gastropathy; bleeding varices (spurt or ooze). Grading of the varices can be done. Other causes of bleed like gastric or duodenal ulcers or erosions will be relied out. Risk of bleeding increases with widened PT INR, thrombocytopenia, HPVG more than 12 mmHg, Portal vein diameter > 13 mm; presence of 'cherry red spots' or ' white nipple sign' suggest rebleed. Endosonography is also useful.

Liver biopsy to identify the aetiology once coagulation profile is corrected using FFP and vitamin K injection.

Ascitic tap is useful: fluid ie evaluated for cells, proteins. Serum ascitic albumin gradient if more than 1.1 suggests high gradient means portal hypertension.

• Transient elastography ultrasound based is non-invasive method to detect clinically significant portal hypertension.
• MELD scoring system is done using PT INR, creatinine and bilirubin. Child Turcotte Pugh scoring system also should be assessed.

Treatment of Portal Hypertension

General Measures

1. Anaemia to be corrected
2. Nutritional supplementation.
3. Inj vitamin K 10 mg for 5 days.
4. Blood and blood product transfusion as required.

Specific Measures

1. Treatment of oesophageal varices
2. Prevention of hepatic encephalopathy
3. Treatment of ascites
4. Measures to reducing portal pressure
• Surgeries-portosystemic shunt.
• TIPSS
• Drugs to reduce the portal pressure like propranolol, nadolol, isosorbide 5 mononitrate.

Liver transplantation.

Reference SRB Mnual surgery