Devastating Delayed Leukoencephalopathy Associated with Bath Salt Inhalation
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PRACTICAL PEARL
Devastating Delayed Leukoencephalopathy Associated with Bath Salt Inhalation C. L. Kramer1 • D. R. Wetzel2 • E. F. M. Wijdicks1
Ó Springer Science+Business Media New York 2015
Abstract Background ‘‘Bath salts’’ or synthetic cathinone toxicity remains a potentially deadly clinical condition. We report a delayed leukoencephalopathy with persistent minimally conscious state. Methods Case report. Results A 36-year-old man presents with delayed encephalopathy, dysautonomia, fulminant hepatic failure, and renal failure from severe rhabdomyolysis after consuming bath salts. MRI showed diffusion restriction in the splenium of the corpus callosum and subcortical white matter. Conclusions The combination of acute leukoencephalopathy, rhabdomyolysis and fulminant hepatic failure may point to bath salt inhalation and should be known to neurointensivists. Keywords Bath salts Bath salts toxicity Cathinone toxicity 3,4-Methylenedioxypyrovalerone (MDPV) Leukoencephalopathy Rhabdomyolysis Acute liver failure Fulminant hepatic failure Minimally conscious state Dysautonomia Neuroimaging Splenium of corpus callosum Subcortical white matter
& C. L. Kramer [email protected] 1
Division of Critical Care Neurology, Mayo Clinic Rochester, Rochester, MN, USA
2
Department of Anesthesiology, Division of Critical Care, Mayo Clinic Rochester, Rochester, MN, USA
Case Report A 36-year-old man with history of untreated bipolar disorder, post-traumatic stress disorder, and tobacco and alcohol abuse presented with nausea and vomiting that progressed to hematemesis. On admission, his liver function tests were mildly elevated [aspartate transaminase (AST) 75 U/L, alanine transaminase (ALT) 126 U/L and total bilirubin 1.2 mg/dL] and his INR was 1.2. Serum lactate was elevated at 5.4 mmol/L. Abdominal CT demonstrated mild hepatomegaly with diffuse fatty infiltration, but extensive laboratory testing, including toxicology screen, was unremarkable. Two days after admission, his transaminases abruptly spiked (AST 4022 U/L, ALT 5470 U/L) and his INR rose to 6.2. Liver ultrasound, including Doppler, was unrevealing for any portal or arterial thrombus. Ammonia was mildly elevated at 37 mmol/L and was not accompanied by encephalopathy. Lactate continued to rise, peaking at 9.5 mmol/L and he developed acute renal failure. Due to his clinical worsening, he was transferred to Mayo Clinic under the care of the Liver Transplant Service on the general care floor. On admission to our institution, he was tachycardic with a heart rate of 120 bpm and mildly hypertensive with a blood pressure of 135/96 mmHg. He was afebrile with a normal respiratory rate. Mild epigastric tenderness was noted, but the examination was otherwise normal. Initially his transaminases and lactate improved, but his renal function and hepatic synthetic function continued to worsen. His sodium was 127 mEq/L on admission to our institution, though this was gradually corrected over the course of the first couple days. By hospital day 3 he deteriorated
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