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