Joseph Mak
Saint Bernardine Medical Center
San Bernardino, California
Disclosure information not submitted.
Shivani Vora, MD
Fellow Physician
Saint Bernardine Medical Center, United States
Disclosure information not submitted.
Benjamin Tabibian, DO
Attending Physician
Saint Bernardine Medical Center, United States
Disclosure information not submitted.
Title: Methamphetamine-Induced Fulminant Liver Failure Exacerbated by Heat Stroke
Introduction: Though the neurotoxic effects of methamphetamine (meth) are known, its effects on the liver are not widely reported. Here, we describe a case of fulminant liver failure due to meth intoxication.
Description: A 43-year old male with no history of liver disease presented to the hospital after being found unconscious outside in 37.8 degrees Celsius weather. He was intubated for airway protection and admitted to the intensive care unit. Urine toxicology was positive for meth. His temperature was 42.2 degrees Celsius due to meth and heat stroke, so he was put on active cooling protocol. Laboratory studies showed aspartate aminotransferase 3611 IU/L, alanine aminotransferase 4113 IU/L, total serum bilirubin 10.9 mg/dL, and ammonia 207 u/dL. Prothrombin time 39.5 seconds, international normalized ratio 3.6, and fibrinogen 108 mg/dL was consistent with disseminated intravascular coagulation. Viral hepatitis panel, ethanol, acetaminophen, and salicylate levels were unremarkable. He was not a transplant candidate due to drug use. N-acetylcysteine (NAC) was given for 2 days with some improvement in liver function. Fluids were given for acute renal failure due to dehydration and rhabdomyolysis. Lactulose was also given for hepatic encephalopathy. However, he could not be extubated due to agitation. He was started on hemodialysis for uremic encephalopathy from acute tubular necrosis, with improvement in mentation. He was subsequently extubated and discharged with markedly improved liver function.
Discussion: Meth-induced hepatotoxicity may occur via several mechanisms. Liver ischemia can result from diffuse peripheral vasospasm, as well as myocardial injury with systemic hypoperfusion. Meth-induced hyperthermia can also cause hepatocellular damage through mitochondrial dysfunction, in addition to oxidative stress from reactive oxygen species production and glutathione depletion. Rhabdomyolysis from hyperthermia can also worsen liver injury. In our case, liver failure was likely exacerbated by heat stroke. Controlling elevated body temperatures may prevent hyperthermia-mediated hepatotoxicity from meth. NAC has also been shown to have benefit in liver failure not related to acetaminophen. Further studies are needed to evaluate the role of NAC and therapeutic hypothermia in meth-induced liver failure.