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ajrccm-conference.2017.195.1 MeetingAbstracts.A3834

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B57 CRITICAL CARE CASE REPORTS: ACID-BASE, ELECTROLYTE, AND ENDOCRINE ABNORMALITIES / Thematic Poster Session / Monday, May 22/9:15 AM-4:15 PM / Area M, Hall B-C
(Middle Building, Lower Level) Walter E. Washington Convention Center
Emergent Hemodialysis For Severe Hyperammonemia Of Uncertain Etiology
B. Bixby1, S. Chaudhary1, Y. Raz2
1University of Arizona College of Medicine, Tucson, AZ, 2Massachusetts General Hospital, Boston, MA
Corresponding author's email: [email protected]
Introduction
Acute hyperammonemia with encephalopathy is common in the ICU. Severe hyperammonemia can be fatal and swift elimination must be
initiated to avoid intracerebral hypertension and death. While usually associated with severe liver disease, the etiology of
hyperammonemia is not always clear. Less common causes of hyperammonemia include infections, medication effects, starvation, or
inborn errors of metabolism (IEM). Empiric treatment for other etiologies of hyperammonemia must be initiated prior to results of
diagnostic testing.
Case Description
A 54 year old female presented to the emergency department with two days of altered mental status, anorexia and abdominal discomfort.
Her medical history was notable for type II diabetes, hypertension and depression. On presentation she was afebrile with stable vital signs
but was obtunded and intubated for airway protection. Initial labs were notable for mild metabolic acidosis with normal venous lactate, an
elevated creatinine of 4.6 mg/dL and normal transaminases, alkaline phosphatase and total bilirubin. Her platelet count was 83,000 and
INR was 1.3. An ammonia level was extremely elevated at 1716 mMol/L. No elevations were seen in acetaminophen, salicylate or valproic
acid levels. Brain imaging was normal. A chest radiograph revealed multifocal pneumonia versus pneumonitis. Abdominal imaging
revealed mild heptatosplenomegaly with decreased hepatic attenuation. Sequential Organ Failure Assessment (SOFA) score was 12. Given
her severe hyperammonemia, emergent hemodialysis was initiated upon arrival to the ICU. Lactulose and rifaximin was initiated. She was
empirically treated with broad-spectrum antibiotics. Nutritional support was provided and zinc, L-carnitine and arginine supplementation
was initiated. After three hours of hemodialysis, her ammonia level was less than 200 mMol/L and normalized in less than 24 hours. Her
mental status improved and she was extubated shortly after. Other than possible multifocal pneumonia, infectious work up was negative.
Quantitative plasma and urine amino acids were normal. Her INR and platelet count also normalized prior to discharge. Hepatitis C
antibody was positive.
Discussion
This patient had signs of chronic liver disease and ultimately was found to have hepatitis C, however, her hyperammonemia was
disproportionate to her liver disease. Severe elevations in ammonia can be seen in inborn errors of metabolism which were not found in
this patient. Hyperammonemia was likely related to starvation, critical illness and acute renal failure in the setting of chronic hepatitis C.
Severe hyperammonemia in these critically ill patients is a life-threatening disorder and emergent hemodialysis can be life-saving.
This abstract is funded by: None
Am J Respir Crit Care Med 2017;195:A3834
Internet address: www.atsjournals.org
Online Abstracts Issue
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