Propylene Glycol Toxicity Complicating Use of Barbiturate Coma
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PRACTICAL PEARL
Propylene Glycol Toxicity Complicating Use of Barbiturate Coma Kathleen A. Bledsoe Æ Andreas H. Kramer
Published online: 13 February 2008 Ó Humana Press Inc. 2008
Abstract Introduction Barbiturate coma is a necessary medical therapy in certain instances, such as the treatment of refractory status epilepticus or severe intracranial hypertension, but its use is often wrought with serious complications. Potential complications include hemodynamic instability, respiratory depression, and immunosuppression with frequent nosocomial infections. High doses of barbiturates may also lead to the accumulation of propylene glycol, the vehicle used in the intravenous formulations of both pentobarbital and phenobarbital, thereby yielding another less-recognized complication of therapy. Results We present a case of propylene glycol toxicity associated with the use of high-dose intravenous pentobarbital and phenobarbital during the treatment of refractory status epilepticus.
treating refractory intracranial hypertension and status epilepticus [1–5]. Unfortunately, high-dose barbiturates have numerous, potentially life-threatening, adverse effects [6, 7]. Complications may include prolonged iatrogenic coma, even after cessation of the infusion; hypotension as a consequence of venous pooling, peripheral vasodilatation, and impaired myocardial contractility [8, 9]; respiratory depression [10]; severe electrolyte and endocrine disturbances [11, 12]; and immunosuppression with frequent nosocomial infections [13–15]. We present here a case demonstrating that an exacerbating factor may, in some cases, be the accumulation of propylene glycol, the vehicle used to administer intravenous pentobarbital and phenobarbital.
Case Report Keywords Propylene glycol Barbiturate coma Pentobarbital Phenobarbital Refractory status epilepticus
Introduction The induction of deep sedation with intravenous barbiturates (‘‘barbiturate coma’’) remains an accepted method of
K. A. Bledsoe (&) Department of Pharmacy, University of Virginia Health System, PO Box 800674, Charlottesville, VA 22908-0674, USA e-mail: [email protected] A. H. Kramer Departments of Critical Care Medicine & Clinical Neurosciences, Foothills Medical Center, University of Calgary, Room EG23J - 1403 29th St. N.W., Calgary, AB, Canada T2N 2T9
A 19-year-old man with an unremarkable past medical history was presented to an outside hospital with recurrent generalized convulsive seizures. Prior to presentation, he had experienced several weeks of fever, chills, sore throat, and headaches, for which he had received antibiotics without improvement. A brain computed tomography scan and lumbar puncture were unremarkable. His seizures did not abate with initial therapy, which included intravenous lorazepam and phenytoin, and he required endotracheal intubation for refractory status epilepticus. Several additional drugs, including midazolam, propofol, phenobarbital, levetiracetam, and valproic acid, were subsequently ineffective at consistently controlling his seizures. At
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