Circulatory Support with Venoarterial ECMO Unsuccessful in Aiding Endogenous Diltiazem Clearance after Overdose.

Introduction. In cardiovascular collapse from diltiazem poisoning, extracorporeal membrane oxygenation (ECMO) may offer circulatory support sufficient to preserve endogenous hepatic drug clearance. Little is known about patient outcomes and diltiazem toxicokinetics in this setting. Case Report. A 36-year-old woman with a history of myocardial bridging syndrome presented with chest pain for which she self-medicated with 2.4 g of sustained release diltiazem over the course of 8 hours. Hemodynamics and mentation were satisfactory on presentation, but precipitously deteriorated after ICU transfer. She was given fluids, calcium, vasopressors, glucagon, high-dose insulin, and lipid emulsion. Due to circulatory collapse and multiorgan failure including ischemic hepatopathy, she underwent transvenous pacing and emergent initiation of venoarterial ECMO. The peak diltiazem level was 13150 ng/mL (normal 100-200 ng/mL) and it remained elevated at 6340 ng/mL at hour 90. Unfortunately, the patient developed multiple complications which resulted in her death on ICU day 9. Conclusion. This case describes the unsuccessful use of ECMO for diltiazem intoxication. Although past reports suggest that support with ECMO may facilitate endogenous diltiazem clearance, it may be dependent on preserved hepatic function at the time of cannulation, a factor not present in this case.

Cefepime neurotoxicity in the intensive care unit: a cause of severe, underappreciated encephalopathy.

INTRODUCTION: Cefepime, 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. METHODS: We 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. RESULTS: This 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). CONCLUSIONS: Critically 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.

Angioedema after tPA: what neurointensivists should know.

BACKGROUND: Angioedema is an underappreciated and potentially life-threatening complication of intravenous (IV) recombinant tissue plasminogen activator (rt-PA). Patients taking angiotensin converting enzyme (ACE) inhibitors are at increased risk of this rare complication. METHODS: Case report. RESULTS: A 74 year-old woman taking lisinopril for hypertension was treated with IV rt-PA for right hemispheric acute ischemic stroke. Shortly after completion of the rt-PA infusion, she developed asymmetric angioedema involving the tongue and left lower lip. No emergent airway intervention was needed. Following treatment with epinephrine, antihistamines, and corticosteroids, the edema resolved within 24 h. The patient made an excellent recovery from the ischemic stroke. CONCLUSIONS: 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.

Etomidate as an induction agent in septic patients: red flags or false alarms?

Despite its widespread use in North America and many other parts of the world, the safety of etomidate as an induction agent for rapid sequence intubation in septic patients is still debated. In this article, we evaluate the current literature on etomidate, review its clinical history, and discuss the controversy regarding its use, especially in sepsis. We address eight questions: (i) When did concern over the safety of etomidate first arise? (ii) What is the mechanism by which etomidate is thought to affect the adrenal axis? (iii) How has adrenal insufficiency in relation to etomidate use been defined or identified in the literature? (iv) What is the evidence that single dose etomidate is associated with subsequent adrenal-cortisol dysfunction? (v) What is the clinical significance of adrenal insufficiency or dysfunction associated with single dose etomidate, and where are the data that support or refute the contention that single-dose etomidate is associated with increased mortality or important post emergency department (ED) clinical outcomes? (vi) How should etomidate's effects in septic patients best be measured? (vii) What are alternative induction agents and what are the advantages and disadvantages of these agents relative to etomidate? (viii) What future work is needed to further clarify the characteristics of etomidate as it is currently used in patients with sepsis? We conclude that the observational nature of almost all available data suggesting adverse outcomes from etomidate does not support abandoning its use for rapid sequence induction. However, because we see a need to balance theoretical harms and benefits in the presence of data supporting the non-inferiority of alternative agents without similar theoretical risks associated with them, we suggest that the burden of proof to support continued widespread use may rest with the proponents of etomidate. We further suggest that practitioners become familiar with the use of more than one agent while awaiting further definitive data.

Case files of the medical toxicology fellowship at the toxikon consortium in Chicago: cocaine-associated wide-complex dysrhythmias and cardiac arrest - treatment nuances and controversies.

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. What is the pharmacological basis of acute cocaine intoxication? What are the cardiovascular manifestations of acute cocaine intoxication? What is the basis for using sodium bicarbonate in cocaine-induced wide-complex dysrhythmias? What is the basis for the use of lidocaine in cocaine-induced wide-complex dysrhythmias? Is there any evidence for the use of amiodarone to treat cocaine-induced wide-complex dysrhythmias?