PRACTICAL PEARL Prolonged Hypothermia as a Bridge to Recovery for Cerebral Edema and Intracranial Hypertension Associated with Fulminant Hepatic Failure Shibin Jacob Æ Ahmed Khan Æ Elizabeth R. Jacobs Æ Prem Kandiah Æ Rahul Nanchal Published online: 1 September 2009 Ó Humana Press Inc. 2009 Abstract Background To review evidence-based treatment options in patients with cerebral edema complicating fulminant hepatic failure (FHF) and discuss the potential applications of hypothermia. Method Case-based observations from a medical inten- sive care unit (MICU) in a tertiary care facility in a 27-year-old female with FHF from acetaminophen and resultant cerebral edema. Results Our patient was admitted to the MICU after being found unresponsive with presumed toxicity from acetami- nophen which was ingested over a 2-day period. The patient had depressed of mental status lasting at least 24 h prior to admission. Initial evaluation confirmed FHF from acetami- nophen and cerebral edema. The patient was treated with hyperosmolar therapy, hyperventilation, sedation, and chemical paralysis. Her intracranial pressure remained ele- vated despite maximal medical therapy. We then initiated therapeutic hypothermia which was continued for 5 days. At re-warming, patient had resolution of her cerebral edema and intracranial hypertension. At discharge, she had com- plete recovery of neurological and hepatic functions. Conclusion In patients with FHF and cerebral edema from acetaminophen overdose, prolonged therapeutic hypothermia could potentially be used as a life saving therapy and a bridge to hepatic and neurological recovery. A clinical trial of hypothermia in patients with this con- dition is warranted. Keywords Acute liver failure Á Cerebral edema Á Hypothermia Á Fulminant hepatic failure Introduction A 27-year-old Caucasian female was admitted to the medical intensive care unit (MICU) from an outside hos- pital with fulminant hepatic failure (FHF) secondary to acetaminophen overdose. On initial presentation to the outside emergency room, the patient was noted to be lethargic, though still following simple commands. Her vitals at initial presentation were blood pressure of 128/ 77 mmHg, pulse rate of 130, respiratory rate of 20, tem- perature of 97°F, and Glasgow coma scale (GCS) of 12 (E3, V3, M6). The initial acetaminophen level was 99 mg/ dl and blood glucose was 66 mg/dl for which 25 g of iv dextrose was given (50 ml of 50% dextrose). Blood glu- cose improved to 186 mg/dl. The patient was started on intravenous N-acetyl cysteine (NAC), given vitamin K intravenously and was transferred to our MICU. There was no history of alcohol, illicit drugs, or other potentially hepatotoxic drug use. On admission to our ICU 7 h after initial presentation, the patient was found to have Grade 3 encephalopathy (West Haven Classification system [1] Grade 3 encepha- lopathy-Somnolent but can be aroused, unable to perform mental tasks, disorientation about time and place, marked confusion, amnesia, incomprehensible speech). She had a heart rate of 120, BP of 136/60 mmHg, temperature of 102°F, respiratory rate of 24, 6 mm bilateral pupils reacting briskly to light, and no meningeal signs. Her GCS declined to 6 (E1, V2, M3). Cardiac, respiratory, and abdominal exams were otherwise unremarkable. There were no clinical signs S. Jacob Á A. Khan Á E. R. Jacobs Á P. Kandiah Á R. Nanchal (&) Division of Pulmonary and Critical Care Medicine, The Medical College of Wisconsin, 9200 West Wisconsin Ave., Milwaukee, WI 53226, USA e-mail: rnanchal@mcw.edu Neurocrit Care (2009) 11:242–246 DOI 10.1007/s12028-009-9266-0