A 55-year-old man with known hepatic cirrhosis due to hepatitis C and alcohol abuse is brought to the emergency department with lethargy. His wife states that the patient has been confused for the past 2 days. He has not had any fevers, recent abdominal pain, or vomiting. He eats a regular diet and has no constipation or diarrhea. He was diagnosed with liver cirrhosis 2 years ago and quit drinking alcohol at that time. One year ago, he underwent upper GI endoscopy and was diagnosed with non-bleeding grade 2 esophageal varices. Since then, he has been maintained on propranolol. In addition, he had a large-volume paracentesis 5 months ago and has been taking spironolactone and furosemide. His wife states that he has been compliant with his medications.
His temperature is 36.7 C (98 F), blood pressure is 99/54 mm Hg, and pulse is 92/min and regular. Oxygen saturation is 97% on room air. Abdominal examination shows a distended but non-tender abdomen. There is shifting dullness and a fluid thrill is present. Rectal examination shows brown stool, which is negative for occult blood. There is 2+ pretibial edema. The patient is oriented to person only and has asterixis.
Laboratory results are as follows:

Urine toxicology screen is negative. Chest x-ray is unremarkable. Urinalysis is negative for infection. Blood and urine cultures are obtained. CT scan of the head shows mild cerebral atrophy, but no masses or bleeding.
Which of the following is the most appropriate next step in management?

Question

A 55-year-old man with known hepatic cirrhosis due to hepatitis C and alcohol abuse is brought to the emergency department with lethargy.  His wife states that the patient has been confused for the past 2 days.  He has not had any fevers, recent abdominal pain, or vomiting.  He eats a regular diet and has no constipation or diarrhea.  He was diagnosed with liver cirrhosis 2 years ago and quit drinking alcohol at that time.  One year ago, he underwent upper GI endoscopy and was diagnosed with non-bleeding grade 2 esophageal varices.  Since then, he has been maintained on propranolol.  In addition, he had a large-volume paracentesis 5 months ago and has been taking spironolactone and furosemide.  His wife states that he has been compliant with his medications.
His temperature is 36.7 C (98 F), blood pressure is 99/54 mm Hg, and pulse is 92/min and regular.  Oxygen saturation is 97% on room air.  Abdominal examination shows a distended but non-tender abdomen.  There is shifting dullness and a fluid thrill is present.  Rectal examination shows brown stool, which is negative for occult blood.  There is 2+ pretibial edema.  The patient is oriented to person only and has asterixis.
Laboratory results are as follows:

Urine toxicology screen is negative.  Chest x-ray is unremarkable.  Urinalysis is negative for infection.  Blood and urine cultures are obtained.  CT scan of the head shows mild cerebral atrophy, but no masses or bleeding.
Which of the following is the most appropriate next step in management?

Quizplus · Accepted Answer

11ec193a_96ca_233b_853d_af0ec9841845_MD0002_00 This patient with advanced cirrhosis has severe encephalopathy manifested by confusion and asterixis. Hepatic encephalopathy (HE) is a potentially reversible complication of cirrhosis that can manifest with subtle findings, such as reversal of the sleep-wake cycle, progressing to confusion and ultimately coma and death if left unrecognized and treated. The most important intervention in patients with HE is the identification and correction of precipitating causes; doing so will quickly resolve the HE. The majority of causes are identified by a thorough history, physical examination, laboratory tests (e.g., CBC, complete metabolic profile, toxicology screen, cultures), and basic imaging studies (e.g., chest x-ray). If no obvious cause is evident from this work-up, patients with ascites should have a diagnostic paracentesis to rule out spontaneous bacterial peritonitis (SBP). Diagnostic paracentesis should be performed even in the absence of signs of infection (i.e., leukocytosis, fever), as patients with end-stage liver disease may not be able to mount a typical inflammatory response. Diagnostic paracentesis can be performed in patients with coagulopathy (in some studies with an INR as high as 8 and platelet count as low as 19,000) without the need for prior transfusion of blood products. There are no cutoff values for coagulation parameters to avoid the procedure. However, there are few contraindications for paracentesis which include disseminated intravascular coagulation (oozing from needle sticks), primary fibrinolysis, and massive ileus with bowel distention (must use ultrasound guidance). This patient's mild hyponatremia is due to volume overload. Initial work-up showed no obvious precipitating cause for his HE. He requires a diagnostic paracentesis to rule out SBP. (Choice A) This patient's asterixis indicates hepatic or toxic-metabolic encephalopathy rather than meningitis. Lumbar puncture is not needed in this patient. Instead, blood ammonia levels can be helpful in monitoring the efficacy of ammonia lowering treatment. (Choice B) First line therapy for acute hepatic encephalopathy is lactulose (oral or rectal), and the dose should be titrated to achieve two to three bowel movements per day. For patients on lactulose therapy who do not improve within 48 hours, non-absorbed antibiotics such as rifaximin can be added. (Choices C & D) This patient's hemodynamic stability and negative stool occult blood makes a GI bleed unlikely. Therefore, upper endoscopy and nasogastric lavage is not indicated. Educational objective: History, physical examination, laboratory tests, and imaging studies should be aimed towards finding a precipitating cause in patients with hepatic encephalopathy. If no obvious cause is evident from this work-up, patients with ascites should undergo a diagnostic paracentesis to rule out spontaneous bacterial peritonitis. __________ References: Mechanisms, diagnosis and management of hepatic encephalopathy. (http://www.ncbi.nlm.nih.gov/pubmed/20703237)

A 55-Year-Old Man with Known Hepatic Cirrhosis Due to Hepatitis