Week 4: complications of portal hypertension

Question 1

normal portal pressure and pressure with portal hypertension

Answer 1

• normal less than 5mmHG

- portal HTN> 8mm Hg

Question 2

Classification/causes of portal HTN

Answer 2

1. Pre hepatic
   - Portal vein thrombosis, splenic vein thrombosis, AVM
2. Hepatic
   - Pre-sinusoidal: congenital hepatic fibrosis, idiopathic
   - Sinusoidal: cirrhosis, infiltrating diseases, granulomatous disease
   - post sinusoidal: acute alcoholic hepatitis, vent-occlusive disease
3. Post hepatic
   - Budd chiari syndrome (hepatic vein occlusion), IVC obstruction, cardiopulmonary disease

Question 3

Cirrhosis-definition

Answer 3

-advanced fibrosis due to insults to the liver, leads to distortion of hepatic architecture and the formation of regenerative nodes

Question 4

Portal pressure = ?

Answer 4

portal pressure= portal inflow x outflow resistance

• and increase in outflow resistance leads to portal HTN, and an increase in portal inflow makes it worse
  1. causes of increase resistance
• structural: fibrosis
• increase in vascular tone:
• decrease endothelial relaxing factors: NO, others
• decrease response to NO
• endogenous vasoconstrictors
  2. increased blood flow
• increase cardiac index, increase Na retention

Question 5

Pressure gradient across the liver

Answer 5

hepatic venous pressure gradient (HVPG)= portal vein pressure-hepatic vein pressure

• normally < 5mmHg
• greater than 10mmHg; assoc. with esophageal varices and ascites
• greater than 12mmHg assoc. with variceal bleeding

Question 6

Varices

Answer 6

• portal HTN leads to re-establishment of portosystemic shunts to relieve pressure
• the most clinically relevant are Esophageal veins to Azygos vein shunt
• esophageal, gastroesophageal, gastric varices, and portal gastropathy (gastric mucosal vessels, not true varices)

Question 7

Management of esophageal varices

Answer 7

• will have hematemesis and melena, hemodynamic instability
• admit to ICU, protect airways, blood transfuse but not too much because can increase portal pressure and perpetuate bleeding
• prophylactic antibiotics
  1. Pharmacology
• splanchnic vasoconstrictor to reduce portal flow: octreotide, vasopressin
• if haven’t bleed: beta blockers
  2. Endoscopic treatment w/ band ligation or sclerotherapy

Question 8

Salvage therapy for esophageal variceal bleeding

Answer 8

1. balloon tamponade: up to 24 hrs only
2. Transjugar intrahepatic portal systemic shunt (TIPS): shunt between hepatic vein and portal vein. Can decompensated liver if very sick liver.
3. Liver transplantation

Question 9

Ascites

Answer 9

• most common complication of cirrhosis, which is the most common cause
• findings: ab distension, bulgin flanks, hernias, scrotal edema, fluid wave, shifting dullness

Question 10

Pathophysiology of ascites

Answer 10

• portal hypertension leads to systemic vasodilation
• causes activation of baroreceptors detecting drop in bp
• activates RAAS leading to renal vasoconstriction and Na retention
• also activates ADH for free water retention

Question 11

Management of ascites

Answer 11

• treat underlying inflammation
• avoid nephrotoxic drugs that can promote Na retention: NSAIDs, and ACEI
• low Na diet
• Diuretics: Aldosterone antagonist and/or loop diuretic

Question 12

Refractory ascites

Answer 12

• being unresponsive to Na restricted diet and high dose diuretics
• or inability to tolerate high dose diuretics secondary to side effects: electrolyte abnormalities, renal failure, worsening encephalopathy
• therapeutic paracenteses with albumin replacement
• or shunt to relieve portal pressure
• liver transplant

Question 13

Hepatorenal syndrome

Answer 13

• severe renal vasoconstriction leading to renal failure, Cr increases
• presence of cirrhosis and ascites
• poor prognosis
• liver transplant only real treatment. can use splanchnic and peripheral vasoconstrictors to improve renal perfusion

Question 14

Hepatic encephalopathy

Answer 14

• neuro disorder due to failure of liver to metabolize toxins absorbed in the GI tract
• ammonia and false neurotransmitters from GI tract implicated in pathogenesis
• TIPs may worsen it
• splenorenal shunt is a risk factor for development of overt hepatic encephalopathy
• presentation will vary from mild confusion to coma. Asterixis to myoclonus can be present.

Question 15

Treatment of hepatic encephalopathy

Answer 15

1. pharmacologic
   - lactulose: broken down by gut bacteria, acidifies and decreases ammonia absorption
   - antibiotics: decrease bacteria in GI tract
   - Osmolar laxative: decrease gut transit time
   - L ornithine L aspartate: enhances metabolism of ammonia to gleaming
2. eliminate precipitating factors: infection, bleeding, dehydration, electrolyte imbalance, use of sedatives, constipation
3. liver transplant