Upgrade to remove ads
Only $2.99/month

CM: Portal Hypertension

Terms in this set (34)

3 categories of portal hypertension, and e.g. of each
PRE-hepatic (thrombosis in splenic or portal vein), INTRA-hepatic (post-sinusoidal = veno-occlusive disease, sinusoidal = cirrhosis, pre-sinusoidal = schistomiasis), POST-hepatic (heart failure, constrictive pericarditis, cor pulmonale aka RV enlargement from pulmonary disease)
pre-hepatic portal hypertension: pathophysiology
pre-hepatic thrombosis > blood from splanchnic circulation can't go forward to liver, so goes backward through collaterals to systemic venous circulation > now high afterload to liver > portal HTN
pre-hepatic portal hypertension: complications
varices (dilated portal-systemic collaterals) at gastro-esophageal junction (hemorrhage common), anus (hemorrhoids), recanalization of umbilical vein > caput medusae (visible varicose veins around umbilicus); no ascites
intra-hepatic, pre-sinusoidal portal hypertension: pathophysiology
ie schistomiasis > granuloma formation, portal fibrosis, and obstruction of the intrahepatic branches of portal vein
intra-hepatic portal hypertension: complications
ascites (if sinusoidal - ie cirrhosis) AND varices (dilated portal-systemic collaterals) at gastro-esophageal junction (hemorrhage common), anus (hemorrhoids), recanalization of umbilical vein > caput medusae
post-hepatic portal hypertension: pathophysiology
any condition causing increased right atrial pressure (e.g. CHF, constrictive pericarditis) > blood P increases in portal circulation relative to systemic circulation
post-hepatic portal hypertension: complications
ascites (no varices because post-hepatic obstruction > blood backs up in pre-hepatic AND systemic circulations > no gradient to generate varices)
portal hypertension: clinical features
splenomegaly (also associated with "plain" cirrhosis) +/- thrombocytopenia; if esophageal varices form and rupture > melena, hematemesis
GI bleeding from portal HTN: how to Dx cause of bleeding
direct endoscopic inspection, by colonoscopy or EGD (into other end); collaterals can also be visualized on XRAY
GI bleeding from portal HTN: short-term management
beta-blockers, ADH, somatostatin, and IV octreotide (for hemorrhage) are splanchnic vascoconstrictors (ADH is systemic too > side effect of ischemia) > decrease portal blood flow and thus portal HTN
GI bleeding from portal HTN: long-term management
surgically or radiologically (TIPS) introduce shunt between portal and systemic venous circulations to decrease portal P (provides alternative outflow pathways > less P in varices > controls bleeding)
GI bleeding from portal HTN: mangagement based on urgency/severity
acute bleeding: if volume can be controlled by hydration + tranfusions, use IV somatostatin (splanchnic vasoconstrictor); then prescribe beta-blockers on discharge; if uncontrollable bleeding: emergent TIPS
ascites: clinical presentation, exam
abdominal swelling (if tense, can impair respiration and food intake), early satiety, enlargement of inguinal/periumbilical hernias; shifting dullness on abdominal percussion when patient rolls back and forth (pocket of air in ascites fluid rises to highest point upon position change)
pathophysiology of portal hypertension (and which forms?) > ascites
if post-hepatic or intra-hepatic SINUSOIDAL portal hypertension: increased extra-hepatic NO production > splanchnic vasodilation > decreases EABV > renal retention of sodium > expansion of plasma V along with portal HTN increases hydrostatic P in splanchnic capillaries > eventual ascites
pathophysiology of NON-portal hypertensive ascites
inflammatory processes (e.g. TB infection of peritoneum) causing increased vessel permeability, or hypoalbuminemia from nephrotic syndrome > secondary ascites from fluid/water retention
examples of non-portal hypertensive ascites
secondary to peritoneal TB, carcinomatosis, nephrotic syndrome
ascites from uncomplicated cirrhosis: results of peritoneal fluid/serum analysis
high serum-ascitic fluid [albumin] gradient > 1.1 g/dL because portal HTN ascites, with low [protein] < 2.5 g/dL (resistance to intrahepatic flow > buildup in pre-hepatic veins, which don't allow protein leakage); WBCs < 500 (mostly macrophages)
ascites from uncomplicated cirrhosis: management
reduce portal HTN by sodium restriction + diuretics; TIPS/liver transplantation if recurrent ascites
ascites from heart failure: results of peritoneal fluid/serum analysis
high serum-ascitic fluid [albumin] gradient > 1.1 g/dL because portal HTN ascites, with high total [protein] > 2.5 g/dL because post-sinusoidal obstruction: fluid buildup in hepatic sinusoids > fenestrations leak protein (unlike normal veins)
ascites from heart failure: management
manage portal HTN by sodium restriction + diuretics (also need HF drugs)
ascites from nephrotic syndrome: results of peritoneal fluid/serum analysis
low serum - ascites [albumin] gradient < 1.1 because systemic hypoalbuminemia (renal protein loss), with low total [protein] < 2.5 g/dL
ascites from spontaneous bacterial peritonitis: results of peritoneal fluid/serum analysis
FLUID: > 250 NTs and > 500 WBCs/mL, very low [protein] (reflecting low level of opsonins > can't control bacterial seeding); SERUM: bacteremia
Dx: ascites with [protein] < 1 g/dL
spontaneous bacterial peritonitis
abdominal swelling + fever, abdominal pain: Dx
spontaneous bacterial peritonitis
ascites from TB: results of peritoneal fluid/serum analysis
low serum - ascites [albumin] gradient because non-portal HTN ascites, with high total [protein] > 2.5 g/dL from exudative process (pyogenic NT response to TB); many T-cells and RBCs
ascites fluid Dx: Serum-ascites [albumin] = 2, total [protein] = 1.4
cirrhosis (high gradient, low total protein)
ascites fluid Dx: Serum-ascites [albumin] = 2, total [protein] = 3
CHF (high gradient, high total protein)
ascites fluid Dx: Serum-ascites [albumin] = .5, total [protein] = 3
TB (low gradient because non-portal HTN, high total protein from NT exudative process)
ascites fluid Dx: Serum-ascites [albumin] = .5, total [protein] = 1.4
nephrotic syndrome (low gradient because systemic hypoalbuminemia, low total protein)
numerical limits for assessing ascitic fluid
Serum-ascites [albumin] gradient: 1.1 g/dL; total [protein] = 2.5 g/dL
hepatic encephalopathy: clinical presentation
patient with cirrhosis, acute liver failure, or post-TIPS (most common) presents with impaired consciousness, asterixis (hand flapping tremor), constructional apraxia
hepatic encephalopathy: lab tests
elevated serum [ammonia] (but level doesn't correlate with severity); EEG disturbances, CT shows cerebral edema if acute hepatic failure (but used more to rule out other causes of encephalopathy)
hepatic encephalopathy: pathophysiology
liver dysfunction > ; if post-TIPS, patient will develop spontaneous encephalopathy (not due to bleeding, infection, or electrolyte abnormalities) because of direct connection between portal and systemic circulation without liver filtratoin
precipitants of hepatic encephalopathy
TIPS, infection (SBP manifests as fever + abdominal pain); GI bleeding, excess dietary protein (metabolized into more ammonia), other fluid/electrolyte abnormalities (e.g. hypokalemic alkalosis)
YOU MIGHT ALSO LIKE...