IntroductionCefepime, a broad spectrum antibiotic, is commonly prescribed in intensive care units (ICU) and may be an overlooked cause of neurologic symptoms such as encephalopathy, myoclonus, seizures, and coma. We aimed to characterize cefepime neurotoxicity in the ICU.MethodsWe performed a retrospective study of adult ICU patients treated with intravenous cefepime for at least 3 days between January 1, 2009 and December 31, 2011. The primary outcome was the development of cefepime neurotoxicity, with the likelihood of causality ascribed via a modified Delphi method.ResultsThis study included 100 patients. The mean age was 65.8 years (± 12.7 years). The median daily average dose of cefepime was 2.5 (IQR 2.0 to 3.5) grams. The median treatment duration was 6 (IQR 4 to 10) days. Renal failure in any form was present in 84 patients. Chronic kidney disease affected 40 patients, and 77 had acute kidney injury. Cefepime neurotoxicity occurred in 15 patients. Of these, seven were considered definite cases, three probable, and five possible. Neurotoxic symptoms included impaired consciousness (n = 13), myoclonus (n = 11), disorientation (n = 6), and nonconvulsive status epilepticus (n = 1). The dose of cefepime was appropriately adjusted for renal clearance in 64 patients (75.3%) without cefepime neurotoxicity and four patients (28.6%) with neurotoxicity (P = 0.001). Chronic kidney disease was present in 30 patients (35.3%) without neurotoxicity and in 10 (66.7%) of those with neurotoxicity (P = 0.04).ConclusionsCritically ill patients with chronic kidney disease are particularly susceptible to cefepime neurotoxicity. Myoclonus and impaired consciousness are the predominant clinical manifestations. Neurotoxic symptoms occur more often when the cefepime dose is not adjusted for renal function, but can still occur despite those modifications.

Orolingual angioedema can complicate rt-PA treatment of acute stroke and is often ipsilateral to the side of hemiparesis. Neurointensivists should be aware of this possibility, which is increased in patients taking ACE inhibitors. Epinephrine can be given safely in this scenario. Identification of high risk features may help guide decisions regarding early definitive airway management.

A 19-year-old woman was brought by ambulance to the emergency department (ED) from a police holding cell. Less than 3 hours earlier, the patient had been a passenger in a car stopped for a traffic violation. As the police officer approached the car, the patient was noted to hurriedly stuff 2 plastic bags containing a white powdery substance into her mouth. On questioning, it was reported that the packets contained cocaine. Less than an hour after being taken to the police station, the patient was witnessed to have a generalized seizure. Emergency medical services (EMS) were immediately summoned.Upon EMS arrival, the seizure activity had ceased. The patient was reportedly unresponsive and noted to have a narrow-complex supraventricular tachycardia. The paramedics provided oxygen by a non-rebreather mask, established intravenous (IV) access, and prepared the patient for rapid transport to the ED. En route to the ED, the patient's rhythm evolved into a wide-complex tachycardia. Due to suspected ventricular tachycardia (VT) and ongoing hemodynamic instability, the patient underwent synchronized cardioversion at 100 J with immediate conversion to sinus tachycardia just minutes prior to ED arrival. What is the pharmacological basis of acute cocaine intoxication?Cocaine intoxication typically produces a sympathomimetic toxidrome marked by tachycardia, hypertension, hyperthermia, diaphoresis, and increased psychomotor activity [1]. The pathophysiology of cocaine is driven by its sympathetic nervous system effects, central nervous system (CNS) stimulation, and local anesthetic effects. In addition to its effects on the vasomotor center, cocaine produces tachycardia and hypertension by inhibiting the reuptake of both norepinephrine and epinephrine. Catecholamine stimulation of peripheral postsynaptic ␣ 1 -adrenergic receptors helps mediate the hypertensive response, while binding at postsynaptic ␤ 1 -receptors is implicated in producing tachycardia. In the CNS, the enhanced release of excitatory amino acids plays a key role in mediating the seizures, agitation, and hyperthermia noted in severe cocaine poisoning. In addition, reuptake blockade of the biogenic amines norepinephrine, epinephrine, dopamine, and serotonin are also involved in producing the CNS and neuropsychiatric effects of cocaine [1][2][3].The dysrhythmogenic properties of cocaine, as well as its electrocardiographic manifestations, derive in part from cocaine's effects on cardiac sodium and potassium channels. Similar to other local anesthetics, cocaine blocks neuronal sodium channels, impeding sodium conductance during phase 0 of the cardiac action potential. This produces QRS widening in a manner analogous to Vaughn-Williams type IA and IC antidysrhythmic agents. Cocaine can also cause QTc prolongation via blockade of cardiac potassium efflux channels [1][2].