Portal hypertension Flashcards
Define portal hypertension.
Clinically significant portal hypertension is defined as a portal vein pressure >10 mm Hg, most commonly attributable to liver disease.
What is the normal venous pressure? What is the pressure in portal hypertension?
7-14mmHg
In portal hypertension: 20-50mmHg
How common is portal hypertension? Who is usually affected?
- Alcoholic and viral liver disease are the most common causes of cirrhosis → portal hypertension
- 90% of those with cirrhosis develop portal hypertension
- Schistosomiasis is the main cause of portal hypertension worldwide
When do oesophageal varices appear in portal hypertension?
When portal vein pressure rises to >10mmHg - variceal haemorrhage is the most serious complication of portal hypertension and aises when portal pressure is >12mmHg
What is the aetiology of portal hypertension?(PH)
1.Conditions resulting in an increased resistance to flow, can be:
- Prehepatic - e.g. portal vein thrombosis, splenic vein thrombosis, congenital stenosis
- Hepatic - e.g. cirrhosis, ALD, primary biliary cirrhosis, schistosomiasis
- Posthepatic - e.g. Budd-Chiari syndrome, constrictive pericarditis, IVC obstruction, cor pulmonale, tricuspid regurgitation
2.Conditions causing increased portal flow
- Splanchnic arterial vasodilation mediated by local release of NO in PH
- Arterial-portal venous fistulae
What is the pathophysiology of portal hypertension? Which site is most significant?
Raised pressure → expansion of collaterals between the portal and the systemic veins.
Varices at the gastro-oesophageal junction are most significant; they are superficial and drain into the azygos veins.
Under increased pressure, they may rupture causing haematemesis or melaena.
Rectal varices are found in 30% of cases. They may be differentiated from haemorrhoids which are lower in the anal canal.
How is portal hypertension diagnosed?
Clinical diagnosis
- history and physical examination
Invasive and non-invasive procedures confirm diagnosis and determine severity
- FBC and platelets
- LFTs and albumin
- Clotting studies
- Hep B and C
- Iron, TIBC, ferritin
- ANA, ASMA, AMA, ceruloplasmin, alpha-1 antitrypsin
- Ascitec fluid analysis
Imaging:
- OGD - assess oesophageal varices
- Duplex US
- CT/MRI/MRA - if results of US are unequivocal
What do ascitic fluid results suggest portal hypertension?
A serum to ascites albumin gradient (SAAG) ≥1.1 mg/dl = portal hypertension.
Polymorphonuclear cells ≥250 cells/ml or +ve Gram stain/culture = complicating spontaneous bacterial peritonitis (SBP)
What is the management of acute portal hypertension?
Dietary sodium restriction to 2000mg/day - limits fluid overload
Serial large-volume paracentesis (LVP) - if over 5L removed, it can be replaced with albumin infusion (8-10g/L of ascitic fluid removed) to prevent circulatory dysfunction
IV diuretics (furosemide and spironolactone) - monitor renal function and electrolytes frequently
IV antibiotics against enteric bacteria if SBP
Surgical:
TIPS (transjugular intrahepatic portosystemic shunt) - may be placed if unresponsive to above treatment or in presence of variceal bleeding
How is acute variceal haemorrhage managed?
- Crystalloids
- Blood product resuscitation
- IV octerotide
- Terlipressin/vasopressin or somatostatin
- Urgent UGI endoscopy with sclerotherapy/band ligation.
- Give empiric antibiotic therapy for SBP
What is the management of chronic ascites?
Conservative:
- Dietary sodium restriction
- Abstinenece from alcohol or treatment for HepB/C
- Vaccination for Hep A/B
Medical:
- Diuretics - 40mg furosemide and 100mg spironolactpne to retain normal sodium levels
- Non-selective beta-blocker (propanolol and nadolol) - to reduce resting HR by 25% (prevents variceal bleeding)
- long-acting nitrate (e.g. isosorbide-5-mononitrate) improves portal heamodynamics
- Antibiotic prophylaxis
Surgical:
- Intermittent LVP may be needed
- Hepatic transplantation for selected cases
What are the complications of portal hypertension?
Most common complication - variceal bleeding. Risk of bleeding is 15% at 1yr
Hepatorenal syndrome (high-near term mortality). HRS may complicate SBP so diagnosis and appropriate prophylaxis against SBP is necessary.
What is the prognosis with portal hypertension?
Any chronic liver disease will lead to cirrhosis.
Initially, cirrhosis will be compensated (median survival, >12 years), but once complications (ascites, variceal hemorrhage, encephalopathy, jaundice) develop, it becomes decompensated (median survival, 1.6 years). Hepatocellular carcinoma (HCC) can develop at any stage and precipitate decompensation and death.
Why do you get hypersplenism in early portal hypertension/
Spleen grows and sequesters platelets and other formed blood cells, leading to hypersplenism.
A 55-year-old man with chronic hepatitis C complains of fatigue. On physical examination, he has vascular spiders, palmar erythema, and a palpable left lobe of his liver. He has no ascites or asterixis. Laboratory analysis demonstrates aspartate aminotransferase 100, alanine aminotransferase 67, alkaline phosphatase 145, and platelet count of 120,000. CT scan shows a nodular liver contour, portosystemic collaterals, but no masses. Which of the following would you recommend as the next step?
- Liver biopsy
- Upper endoscopy
- Start nonselective β-blockers
- Start spironolactone
- Magnetic resonance imaging of the liver
2 - any patient with newly diagnosed cirrhosis should undergo upper endoscopy to investigate the presence and size of gastroesophageal varices.
NB: β-Blockers should be initiated in patients with medium or large varices or in patients with high-risk small varices (i.e., those present in a Child class C patient or with red wale marks). β-Blockers are not useful in patients without varices and are associated with significant adverse events.