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 Hypertension Pre-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%

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

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

Complications of cirrhosis

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Complications of cirrhosis