0071643192.pdf

■ Portal hypertension: Caput medusae, splenomegaly, ascites

■ Hepatic encephalopathy: Fetor hepaticus, asterixis, confusion

DIFFERENTIAL

CHF, nephrotic syndrome

DIAGNOSIS

■ Liver biopsy: The gold standard; also useful in assessing etiology

■ Physical exam

■ Labs: Thrombocytopenia (splenic sequestration); elevated INR and low

albumin (↓hepatic synthetic function); elevated alkaline phosphatase

COMPLICATIONS

Hepatic encephalopathy, varices, ascites/SBP, hepatorenal syndrome, hepatopul-

monary syndrome, hepatocellular carcinoma; portopulmonary syndrome

Ascites and Spontaneous Bacterial Peritonitis (SBP)

In the United States > 80% of ascites cases are due to chronic liver disease

(cirrhosis or alcoholic hepatitis). SBP is a spontaneous bacterial infection of

ascites. The most common organism implicated is E. coli. Other organisms

includeStreptococcussp. and Klebsiella.

SYMPTOMS/EXAM

■ Abdominal pain and tenderness, ranging from mild to severe

■ Other findings may include fever and altered mental status.

■ Characterized by shifting dullness, fluid wave, and bulging flanks (low

sensitivity, moderate specificity); imaging (ultrasound, CT) superior to

examination. SBP is often asymptomatic,but patients may have fever,

abdominal pain, and symptoms/signs of sepsis

DIAGNOSIS

■ Diagnostic paracentesis: Indicated in any patient with ascites and abdominal

pain, encephalopathy, or fever

■ Findings consistent with SBP include PMNs >250 cells/mm^3 and a

+Gram stain or culture

■ The presence of multiple organisms suggests secondary peritonitis from

bowel perforation.

TREATMENT

■ Third-generation cephalosporin (eg, cefotaxime or ceftriaxone)

■ Do not wait for culture results to begin treatment.

■ SBP prophylaxis: Fluoroquinolones or TMP-SMX

■ Indicated for cirrhotics hospitalized with GI bleed (3 days); ascites with

total protein <1.5 g/dL (while hospitalized); or prior SBP (if the patient

has ascites)

Hepatic Encephalopathy

Hepatic encephalopathy is caused by accumulation of nitrogenous waste prod-

ucts in liver failure. Neuropsychiatric changes in the setting of liver disease con-

stitute hepatic encephalopathy until proven otherwise. Look for precipitating

ABDOMINAL AND GASTROINTESTINAL

EMERGENCIES