complications of cirrhosis
TRANSCRIPT
Complications of Cirrhosis
Table 302-1 Causes of Cirrhosis
Alcoholism Cardiac cirrhosis
Chronic viral hepatitis Inherited metabolic liver disease
Hepatitis B Hemochromatosis
Hepatitis C Wilson's disease
Autoimmune hepatitis 1 Antitrypsin deficiency
Nonalcoholic steatohepatitis Cystic fibrosis
Biliary cirrhosis Cryptogenic cirrhosis
Primary biliary cirrhosis
Primary sclerosing cholangitis
Autoimmune cholangiopathy
Table 302-2 Complications of Cirrhosis
Portal hypertension Coagulopathy
Gastroesophageal varices Factor deficiency
Portal hypertensive gastropathy Fibrinolysis
Splenomegaly, hypersplenism Thrombocytopenia
Ascites Bone disease
Spontaneous bacterial peritonitis Osteopenia
Hepatorenal syndrome Osteoporosis
Type 1 Osteomalacia
Type 2 Hematologic abnormalities
Hepatic encephalopathy Anemia
Hepatopulmonary syndrome Hemolysis
Portopulmonary hypertension Thrombocytopenia
Malnutrition Neutropenia
Portal hypertension
•Definition: Elevation of Hepatic venous pressure gradient (HVPG) to >5mmHg
•Causes: increased hepatic resistance to the passage of blood flow through the liver due to cirrhosis and regenerative nodules, and increased splanchnic blood flow secondary to vasodilation of the splanchnic vascular bed
Table 302-3 Classification of Portal HypertensionPre-hepatic
Portal vein thrombosis
Splenic vein thrombosis
Massive splenomegaly (Banti's syndrome)
Hepatic
Presinusoidal
Schistosomiasis
Congenital hepatic fibrosis
Sinusoidal
Cirrhosis—many causes
Alcoholic hepatitis
Postsinusoidal
Hepatic sinusoidal obstruction (venoocclusive syndrome)
Posthepatic
Budd-Chiari syndrome
Inferior vena caval webs
Cardiac causes
Restrictive cardiomyopathy
Constrictive pericarditis
Severe congestive heart failure
Clinical features
•Gastroesophageal varices•Ascites•Hypersplenism
Gastroesophageal Varices
•1/3 of cirrhotics will have varices on screening endoscopy
•1/3 will develop bleeding•5-15% will develop varices per year•Majority will develop varices in their
lifetime•Diagnosis: Endoscopy
Treatment
•Primary prophylaxis: Beta blocker, Endoscopic variceal ligation (EVL), sclerotherapy
•Prevention of rebleeding: EVL
Medical therapy Somatostatin, Octreotide
TIPS
•Transjugular Intrahepatic Portosystemic Shunt
•Alternative to surgery for acute decompression of portal hypertension
•Reserved for poor surgical risk, and those who fail endoscopic or medical therapies
•Encephalopathy in 20%
Table 302-2 Complications of Cirrhosis
Portal hypertension Coagulopathy
Gastroesophageal varices Factor deficiency
Portal hypertensive gastropathy Fibrinolysis
Splenomegaly, hypersplenism Thrombocytopenia
Ascites Bone disease
Spontaneous bacterial peritonitis Osteopenia
Hepatorenal syndrome Osteoporosis
Type 1 Osteomalacia
Type 2 Hematologic abnormalities
Hepatic encephalopathy Anemia
Hepatopulmonary syndrome Hemolysis
Portopulmonary hypertension Thrombocytopenia
Malnutrition Neutropenia
Ascites
Clinical History
•Progressive increase in abdominal girth•Increase in clothing size•Appearance of hernias•Maybe unnoticeable•Tense ascites causing increased
intraabdominal pressure, resulting to reflux symptoms
•Dyspnea, resulting from R sided pleural effusion
Physical Examination
•Distended abdomen•Bulging flanks•Everted umbilicus•Portal HPN: prominent venous collaterals•Fluid wave (1.5 L)
Ascites
•Often accompanied by edema•Insidious•Respiratory compromise•Excessive fatigue•Muscle wasting•Malnutrition•Weakness
Etiologies
•Cirrhosis•Congestive heart failure•Nephrosis•Malignancy•Infection (TB, pyogenic)•Pancreatitis
Table 44-1 Characteristics of Ascitic Fluid in Various Disease States
Condition Gross Appearance Protein, g/L
Serum-Ascites Albumin Gradient, g/dL
Cell Count Other Tests
Red Blood Cells, >10,000/ L
White Blood Cells, per L
Cirrhosis Straw-colored or bile-stained
<25 (95%)
>1.1 1% <250 (90%)a; predominantly mesothelial
Neoplasm Straw-colored, hemorrhagic, mucinous, or chylous
>25 (75%)
<1.1 20% >1000 (50%); variable cell types
Cytology, cell block, peritoneal biopsy
Tuberculous peritonitis
Clear, turbid, hemorrhagic, chylous
>25 (50%)
<1.1 7% >1000 (70%); usually >70% lymphocytes
Peritoneal biopsy, stain and culture for acid-fast bacilli
Pyogenic peritonitis Turbid or purulent If purulent, >25
<1.1 Unusual Predominantly polymorphonuclear leukocytes
Positive Gram's stain, culture
Congestive heart failure
Straw-colored Variable, 15–53
>1.1 10% <1000 (90%); usually mesothelial, mononuclear
Nephrosis Straw-colored or chylous
<25 (100%)
<1.1 Unusual <250; mesothelial, mononuclear
If chylous, ether extraction, Sudan staining
Pancreatic ascites (pancreatitis, pseudocyst)
Turbid, hemorrhagic, or chylous
Variable, often >25
<1.1 Variable, may be blood-stained
Variable Increased amylase in ascitic fluid and serum
Ascitic fluid analysis
•High SAAG gradient: cirrhosis, congestive heart failure, renal failure, Budd Chiari syndrome, hepatic metastases
•Low SAAG gradient: Malignancy, infection
Radiographic Exams
•Ultrasonography•CT scan
Table 44-1 Characteristics of Ascitic Fluid in Various Disease States
Condition Gross Appearance Protein, g/L
Serum-Ascites Albumin Gradient, g/dL
Cell Count Other Tests
Red Blood Cells, >10,000/ L
White Blood Cells, per L
Cirrhosis Straw-colored or bile-stained
<25 (95%)
>1.1 1% <250 (90%)a; predominantly mesothelial
Neoplasm Straw-colored, hemorrhagic, mucinous, or chylous
>25 (75%)
<1.1 20% >1000 (50%); variable cell types
Cytology, cell block, peritoneal biopsy
Tuberculous peritonitis
Clear, turbid, hemorrhagic, chylous
>25 (50%)
<1.1 7% >1000 (70%); usually >70% lymphocytes
Peritoneal biopsy, stain and culture for acid-fast bacilli
Pyogenic peritonitis Turbid or purulent If purulent, >25
<1.1 Unusual Predominantly polymorphonuclear leukocytes
Positive Gram's stain, culture
Congestive heart failure
Straw-colored Variable, 15–53
>1.1 10% <1000 (90%); usually mesothelial, mononuclear
Nephrosis Straw-colored or chylous
<25 (100%)
<1.1 Unusual <250; mesothelial, mononuclear
If chylous, ether extraction, Sudan staining
Pancreatic ascites (pancreatitis, pseudocyst)
Turbid, hemorrhagic, or chylous
Variable, often >25
<1.1 Variable, may be blood-stained
Variable Increased amylase in ascitic fluid and serum
Treatment
•Sodium restriction: 2 grams/day•Spironolactone 100-200 mg/day•Furosemide 40-80 mg/day
Spontaneous bacterial peritonitis•Spontaneous infection•30% of patients with ascites•25% mortality rate•Pathogens: E. coli, Streptococcus, Staph
aureus, Enterococcus sp•Frequency is high in + variceal bleed
Hepatorenal Syndrome
•Functional renal failure•10% in advanced cirrhosis or severe acute
hepatic failure•Increase vascular resistance renal
vasoconstriction•Diagnosis: large amount of ascites with
progressive rise in Creatinine
HRS
•HRS I: progressive impairment in renal function and a significant reduction of Creatinine clearance
•HRS II: reduction in GFR with elevation of serum creatinine (but stable)
•Treatment: Albumin, Somatostatin; Liver transplantation
Hepatic Encephalopathy
•Alteration in mental status and cognitive function in the presence of liver failure
•More common in chronic liver disease•Gut-derived neurotoxins•Elevated ammonia levels, but not a
reliable marker for diagnosis•False neurotransmitters: mercaptans
Precipitating factors
•Infection•Increased dietary protein load•Electrolyte imbalance, ie, hypokalemia•GI bleeding•Use of narcotic agents
Treatment•Multifactorial•Treat underlying precipitating factor•Hydration•Correction of electrolyte imbalance•Dietary restriction•Lactulose•Antibiotics: Neomycin, Metronidazole•Zinc supplementation
Malnutrition
•Factors: poor dietary intake, alteration in gut nutrient absorption, alterations in protein metabolism
•More catabolic muscle wasting•Treatment: dietary supplementation
Coagulation abnormalities
•Decreased synthesis of clotting factors; impaired clearance of anticoagulants
•Hypersplenism thrombocytopenia•Platelet function is abnormal•Vit K dependent factors: II, VII, IX, and X
levels are decreased
Hematologic Abnormalities
•Anemia: hypersplenism, hemolysis, Iron deficiency, Folate deficiency
•Macrocytosis•Neutropenia