MEDizzy
MEDizzy
USMLE
Infectious Diseases
A 52-year-old woman with alcoholic cirrhosis, portal hypertension, esophageal varices, and history of hepatic encephalopathy presents to the hospital with confusion over several days. Her husband remarks that the patient has been adherent to her medicines.These medicines include labetalol, furosemide, aldactone, and lactulose.Physical examination is notable for temperature of 38.3°C, heart rate of 115 beats per minute, blood pressure of 105/62 mmHg, respiratory rate of 12 breaths per minute, and oxygen saturation of 96% on room air. The patient is extremely drowsy, only intermittently able to answer questions, and disoriented. She has slight asterixis. Lungs are clear. Cardiac examination is unremarkable. Her abdomen is distended and tense but non-tender. She has 3+ lower extremity edema extending to her thighs. She is guaiac negative.Her cranial nerves and extremity strength are symmetric and normal. Laboratory studies reveal a leukocyte count of 4830/µL, hematocrit = 33% (baseline = 30%), and platelet count of 94,000/µL. Basic metabolic panel is unremarkable. What is an essential component of the diagnostic workup?
Explanation
ExplanationPrimary bacterial peritonitis is a complication of ascites associated with cirrhosis. Clinical presentation can be misleading as only 80% of patients have fever, and abdominal symptoms are only variably present. Therefore, when patients with known cirrhosis develop worsening encephalopathy, fever, and/or malaise, the diagnosis should strongly be considered and ruled out. In this case, a peritoneal polymorphonuclear leukocyte count of >250/µL would be diagnostic of bacterial peritonitis even if Gram’s stain were negative.The paracentesis also might provide microbiologic confirmation. CT of the head would be useful for the diagnosis of cerebral edema associated with severe hepatic encephalopathy or in the presence of focal neurologic findings suggesting an epidural bleed. Cirrhotic patients are at great risk of gastrointestinal (GI) bleeding and it may worsen hepatic encephalopathy by increasing the protein load in the colon. Esophagastroduodenoscopy would be a reasonable course of action, particularly if stools were guaiac positive or there was gross evidence of hematemesis or melena. In this case, there is no evidence of GI bleeding and there is mild hemoconcentration, possibly from peritonitis. Lactulose, and possibly neomycin or rifaximin, is a logical therapeutic trial in this patient if peritonitis is not present. Serum ammonia level may suggest hepatic encephalopathy, if elevated, but does not have sufficient predictive value on its own to rule in or rule out this diagnosis.
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