Charles McKay

Ketamine abusers presenting to the emergency department: a case series

Ketamine hydrochloride, familiar to emergency physicians as a dissociative anesthetic, has been abused as a hallucinogen for almost 30 years. The drug produces effects similar to those of phencyclidine but with a much shorter duration of effect. Since 1996, an increasing number of patients have presented to Connecticut Emergency Departments (EDs) after the intentional abuse of ketamine. Because the medical literature contains almost no information on the consequences of ketamine abuse, we have compiled a series of ketamine abusers presenting to the ED. Among the 20 patients in this series, common presenting complaints included anxiety, chest pain, and palpitations. Tachycardia was the most common physical examination finding. Nystagmus, a common finding after phencyclidine use, was seen in only three cases. The most frequent complications after ketamine abuse were severe agitation and rhabdomyolysis. The symptoms of ketamine intoxication appear to be short-lived, with 18 of the 20 patients discharged from the ED within 5 h of presentation. Emergency physicians should include ketamine in the differential diagnosis of drug- or toxin-induced hallucinations. Methods for detecting this drug in biologic fluids are reviewed as are treatment recommendations for managing the patient who presents to the ED after abusing ketamine.

Definitive Identification of an Exceptionally High Methanol Concentration in an Intoxication of a Surviving Infant: Methanol Metabolism by First-Order Elimination Kinetics

Intoxication by methanol was identified in a five-week-old infant suffering from moderate metabolic acidosis. The initial serum methanol at admission was 1148 mg/dL as measured by gas chromatography. The osmolal gap and formic acid concentrations were consistent with methanol intoxication. The child was treated with folic acid and a continuous ethanol infusion and survived without any apparent permanent problems. Because expected toxic symptoms did not develop in this case, and the methanol concentrations were at levels that might be deemed to be incompatible with life, blood and urine samples were assayed by a specific enzymatic assay, and by gas chromatography/mass spectrometry (GC/MS). Positive results definitively confirmed the presence of methanol. In contrast to previous reports, the elimination of methanol in this case appeared to following first-order kinetics. If hepatic ADH activity is low in neonates and young infants, another enzyme system such as catalase may be involved to explain this data. The lack of formic acid accumulation may have been due to folic acid therapy.

Anticholinergic poisoning with adulterated intranasal cocaine

In recent years, emergency physicians have encountered a growing number of patients who present with anticholinergic toxicity after using adulterated heroin. Anticholinergic poisoning caused by adulterated cocaine is far less common. This report describes the case of a 39-year-old man who arrived in the emergency department several hours after the nasal insufflation of cocaine. Classic symptoms of anticholinergic toxicity were evident on examination, including dry, flushed skin, agitation, tachycardia, mydriasis, and absence of bowel sounds. Treatment included intravenous fluids and lorazepam, with resolution of symptoms over several hours. Urine samples revealed the presence of cocaine metabolites as well as the anticholinergic drug atropine, and infrequently encountered adulterant of cocaine. Anticholinergic poisoning is reviewed, and the physical examination findings that distinguish this syndrome from the closely related sympathomimetic syndrome typical of cocaine are detailed. Current treatment recommendations for anticholinergic poisoning are summarized.

ACMT and AACT position statement: preventing occupational fentanyl and fentanyl analog exposure to emergency responders

To cite this article: Michael J. Moss , Brandon J. Warrick, Lewis S. Nelson, Charles A. McKay, Pierre-André Dubé , Sophie Gosselin , Robert B. Palmer & Andrew I. Stolbach (2017): ACMT and AACT position statement: preventing occupational fentanyl and fentanyl analog exposure to emergency responders, Clinical Toxicology, DOI: 10.1080/15563650.2017.1373782 To link to this article: http://dx.doi.org/10.1080/15563650.2017.1373782

State-wide hospital clinical laboratory plan for measuring cholinesterase activity for individuals suspected of exposure to nerve agent chemical weapons.

Background. Hospital laboratories currently lack the capacity to provide emergency determination of cholinesterase activity. Methods. We have developed a hospital-based 3-tiered system to test plasma for butyrylcholinesterase (BChE) activity and whole blood for red cell acetylcholinesterase (AChE) activity using available technology and personnel. Interagency communications, toxidrome definition, and patient triage will be coordinated by the Connecticut Department of Public Health and the Poison Control Center. Data. Initial BChE data documents good precision between institutions (coefficient of variation < 8%). Summary. Laboratory testing of plasma or blood for cholinesterase activity is important in the management of nerve agent exposure and in ruling out disease in those with non-specific symptoms in the setting of a terrorist attack or accidental exposure. Rapid availability of strong hospital-based analytic support in a smoothly functioning network of clinical, public health, and laboratory services will facilitate overall regional response to chemical terrorism or large scale HazMat events.

Role of carnitine in valproic acid toxicity.

Dr. Sztajnkrycer provided an excellent review of valproic acid (VPA) toxicity (1), detailing the complex clinical spectrum of adverse effects and metabolic pathways seen with valproate therapy and overdose. Although he stated that hepatotoxicity has only been rarely reported with VPA overdose, it is rarer still that the definitive histology of microvesicular steatosis be documented. Given the typically prolonged coma, variable hyperammonemia, problems with VPA immunoassay reliability (2), and suggestive carnitine-modified metabolic pathways that may contribute in these abnormalities, we believe that carnitine therapy should play a more prominent role in treatment. Dr. Sztajnkrycer states that there is no evidence that L-carnitine supplementation changes the clinical outcome in VPA-induced hyperammonemia and acute overdose, but also notes that when assayed, this supplement has improved the pathways responsible for urea metabolism. Bohan et al. analyzed the association of L-carnitine treatment with hepatic survival in 92 patients with severe, symptomatic, VPA-induced hepatotoxicity (3). Isolated hyperammonia was not considered a laboratory sign of hepatic dysfunction, and the majority of these patients had histologic evaluation revealing microvesicular steatosis or mitochondrial abnormalities. The early intravenous administration of L-carnitine was associated with a survival rate of 50% compared with 10% in the untreated group, quite a significant difference. Furthermore, because early treatment in these chronic VPA cases was associated with improved outcome and L-carnitine itself is a safe therapy, all patients with significant VPA intoxication should be considered candidates for Lcarnitine therapy. We agree with the author that L-carnitine remains a reasonable intervention in acute VPA intoxication and hyperammonemia, given the potential for secondary cerebral edema. We recommend that intravenous Lcarnitine be used in any patient with coma, despite falling VPA concentration, and climbing ammonia levels and, pending further study, in all patients with VPA concentrations greater than 450 mg=L (4).