Ken Kulig

Cyanide and methemoglobin kinetics in smoke inhalation victims treated with the cyanide antidote kit

STUDY OBJECTIVEnTo evaluate serial cyanide, methemoglobin, and carbon monoxide levels in smoke inhalation patients.nnnSETTINGnRegional poison center and regional toxicology treatment center.nnnPARTICIPANTSnSeven critically ill smoke inhalation patients referred to the regional poison center.nnnINTERVENTIONSnPeak level and half-life were determined by obtaining serial carboxyhemoglobin, cyanide, and methemoglobin levels.nnnRESULTSnThe mean observed half-life of cyanide was 3.0 +/- 0.6 hours. Methemoglobinemia was evaluated in four patients after sodium nitrite administration. The peak measured methemoglobin levels (mean, 10.5% +/- 2%; range, 7.9% to 13.4%) did not occur until a mean of 50 minutes (range, 35 to 70 minutes) following administration of sodium nitrite. The total oxygen-carrying capacity reduced by the combination of carboxyhemoglobin and methemoglobin was never more than 21% (range, 10% to 21%) in this series.nnnCONCLUSIONnThe administration of sodium nitrite to smoke inhalation patients in the presence of concomitant carbon monoxide poisoning may be relatively safe.

Acute Zinc Chloride Ingestion in a Child: Local and Systemic Effects

A 16-month-old boy ingested liquid zinc chloride/ammonium chloride soldering flux. He developed severe local burns, metabolic acidosis, hepatic damage, hyperamylasemia, lethargy, and hypertension. Peak measured plasma zinc was 1,199 micrograms/dL. Because of persistent signs of systemic toxicity, he was chelated with dimercaprol (BAL) and EDTA. Although clinical improvement was noted coincident with the initiation of chelation, there was no apparent increase in urinary zinc excretion. Scarring in the gastric antrum necessitated an antrectomy. The child recovered without other apparent complications.

Predictors of Coronary Artery Disease in Patients With Cocaine-associated Myocardial Infarction

PURPOSEnTo identify clinical criteria predictive of underlying coronary artery disease in patients with cocaine-associated myocardial infarction.nnnPATIENTS AND METHODSnUsing a retrospective cross-sectional study design at 29 acute care hospitals, we identified 70 patients with cocaine-associated myocardial infarction who had a determination of the presence or absence of coronary artery disease. Clinical characteristics of patients with coronary artery disease (> 50% stenosis on cardiac catheterization or reversible ischemia on stress test) were compared with patients without coronary artery disease (< 50% stenosis on cardiac catheterization).nnnRESULTSnCompared with patients without coronary artery disease (n = 21), patients with coronary artery disease (n = 49) were older (42 versus 31 years; P < 0.001), had more traditional cardiac risk factors (2.3 versus 1.5; P < 0.001), more frequent history of hypertension (odds ratio [OR], 5.3; 95% confidence interval [CI], 1.4 to 20.4); more frequent family history of myocardial infarction (OR, 4.4; 95% CI, 1.3 to 15.1), more bradydysrhythmias (OR, 8.0; 95% CI, 1.0 to 65.5), and more likely to have an inferior infarct location (P = 0.04).nnnCONCLUSIONnAge, number of cardiac risk factors, location of myocardial infarction, and bradydysrhythmias predict underlying coronary artery disease in patients with cocaine-associated myocardial infarction. If validated, this knowledge may be used to develop a medically appropriate, cost-effective evaluation strategy for patients following cocaine-associated myocardial infarction.

Massive Ethylene Glycol Ingestion Treated with Fomepizole Alone—A Viable Therapeutic Option

Fomepizole is used to treat and prevent toxicity from ethylene glycol poisoning. Treatment with fomepizole without hemodialysis in massive ethylene glycol ingestion has been rarely reported in the literature; however, published literature and practice guidelines recommend considering dialysis for ethylene glycol levels >50xa0mg/dL. We report a case of massive ethylene glycol ingestion resulting in the highest serum ethylene glycol concentration in a patient without ethanol co-ingestion who was treated with fomepizole and was not hemodialyzed. A 48-year-old male presented to the emergency department after reportedly ingesting >1liter of antifreeze in an attempt at self-harm. He denied concomitant ethanol consumption. His initial presenting serum ethylene glycol level was 700xa0mg/dL, with normal renal function, and a metabolic acidosis with a high anion gap. One hour after presentation, he was started on intravenous fomepizole. Treatment with fomepizole continued until the patients plasma ethylene glycol concentration was 16xa0mg/dL. His metabolic acidosis quickly resolved, he had no adverse reactions to the treatment, and his renal function remained normal. Ultimately, he was discharged to a psychiatric unit without sequelae. Published literature and practice guidelines suggests considering hemodialysis initiation in patients with an ethylene glycol level >50xa0mg/dL. This recommendation is anecdotally, rather than evidence, based. With the potential risks inherent in hemodialysis, our case provides evidence that treatment with fomepizole without hemodialysis appears to be a viable alternative option in patients with even extremely high plasma ethylene glycol concentrations as long as their renal function is intact.

Methamphetamine toxicity prevented by activated charcoal in a mouse model.

STUDY OBJECTIVEnTo determine the effectiveness of activated charcoal in preventing toxicity from oral methamphetamine HCI.nnnDESIGNnRandomized, prospective, nonblinded, controlled animal study.nnnSETTINGnAnimal care facility.nnnPARTICIPANTSnCD-1 male mice.nnnINTERVENTIONSnMice were given 100 mg/kg methamphetamine HCI (lethal dose 60) in water by oral gavage. Within 1 minute of methamphetamine administration, mice received either 1 g/kg activated charcoal or an equivalent volume of water as control.nnnMEASUREMENTS AND MAIN RESULTSnMice were observed for time to onset of symptoms (piloerection, agitation, and tremor) and mortality at 1, 24, and 48 hours. Activated charcoal delayed onset of symptoms (5.53 +/- 1.25 minutes versus 4.27 +/- 1.22 minutes, P < .002) and decreased mortality compared to controls at 1 hour (1 of 20 versus 10 of 20, P < .003) and 24 hours (five of 20 versus 12 of 20, P < .05). There was no difference between groups in mortality at 48 hours.nnnCONCLUSIONnA single dose of activated charcoal given after oral methamphetamine delayed onset of toxicity and decreased early mortality in mice. There was no effect on overall mortality.

Amoxapine and neurologic deficits.

Excerpt To the editor: In the cases reported by Goldberg and Spector (1), the development of permanent neurologic deficits in two patients was attributed to the toxic effects of amoxapine. We quest...

The methodology in the paper by Chambers et al. raises serious questions about their conclusions

We read with great interest the recent article by Chambers et al. [1] comparing the prevalence of cognitive sequelae, depression and anxiety in patients with less severe vs. more severe carbon monoxide (CO) poisoning. However, due to serious methodological shortcomings, the authors’ conclusions are not fully supported by the data presented. The definition of ‘more severe CO poisoning’ in this study was a carboxyhemoglobin (COHb) level greater than 15% or loss of consciousness; 43% of the ‘more severely’ poisoned group was defined solely on the finding of a single COHb level >15%. A single COHb level has not been shown to be a valid determinant of CO poisoning severity. Given that many people are asymptomatic with a COHb level of >15% and that heavy cigarette smokers may achieve this level daily [2, 3] without developing the neurologic sequelae discussed in the paper, this definition is highly problematic. How can an asymptomatic cigarette smoker with a COHb level greater than 15% be considered to have ‘more severe CO poisoning’? This definition does not adequately define, nor differentiate between, ‘more’ and ‘less’ severe CO poisoned patients. Because CO poisoning is a frequent cause of litigation, it is likely that this publication will be cited in support of legal claims of neurological injuries from low-level CO exposures. The authors do not report how many of these patients were involved in or contemplating litigation as a result of their CO exposure. Involvement in litigation (not involving brain injury or toxic exposure) has been shown to result in many of the symptoms that the authors use as evidence of brain injury from CO exposure (e.g. depression, anxiety, memory problems) [4]. The possibility of secondary gain in patients who report purely subjective symptoms of depression, anxiety or cognitive difficulties while involved in litigation also exists. Contrary to the authors’ assertion, reports of such symptoms cannot be taken as ‘objective’ findings of brain injury. Likewise, we do not know how many of these patients, whether or not involved in litigation, developed depression or anxiety due to an adopted belief system that they were brain injured when they were not. A recent Google internet search using the term ‘carbon monoxide poisoning’ resulted in 828 000 hits, many of which discuss in great detail how even minimal exposure to carbon monoxide can result in permanent brain damage. Some websites encourage litigation (e.g. CarbonMonoxide Headquarter.com, Carbonmonoxidekills.com) and many present lists of symptoms that patients may subsequently develop purely as a result of suggestion and/or for litigation purposes. A patient who has been told (or who has seen on a website) information strongly suggesting that they are permanently brain-injured even from a trivial exposure is likely to become anxious and/or depressed, even when carbon monoxide did not cause actual physical harm. The suggestion of brain injury may also have been the inadvertent result of risk communication to study subjects by the investigators. The mere fact that these individuals were informed of being in a clinical trial to assess neurological injury from CO exposure could serve as a nidus for the development of patients’ perception of injury. Further, the testing protocol undoubtedly yielded many false positive diagnoses of brain injury, which would have been communicated to the patients. For example, brain injury was considered present if a patient had a single subjective complaint and any

Interpretation of Workplace Tests for Cannabinoids

Workplace urine drug testing for an inactive THC metabolite is common in both federally regulated and non-regulated drug testing. A positive result does not document impairment, or even recent use, when impairment is likely the most important parameter being searched for by the drug testing procedure. Most cannabinoid testing does not detect imported synthetics. Currently, urine is the most widely tested matrix, but blood, plasma, oral fluid, and hair may also be accepted in federally regulated testing in the future. This article will discuss the history, the status quo, and the possible near term future of workplace testing for marijuana in employees.

Clinical Neurotoxicology of Industrial and Agricultural Chemicals

Publisher Summary This chapter presents a brief overview of common neurotoxic substances, and briefly describes the prototypical chemicals that cause classic neurototoxic syndromes. Neurotoxic chemicals are commonly found in many workplaces, environment, and the homes. Thirty percent of the workplace chemicals for which the American Conference of Governmental Industrial Hygienists (ACGIH) has recommended maximum exposure concentrations have been so listed in part because of their neurotoxic potential. The incidence of human chemical neurotoxicity is difficult to determine with accuracy for many reasons. In many cases, symptoms and signs of neurotoxicity are insidious and not recognized. Concomitant ethanol, tobacco, street drug, prescription drug, family history of naturally occurring neurologic disease, normal aging, and other environmental factors may be offered as alternative explanations for a neurotoxic syndrome. A genetic predisposition to neurotoxicity may explain why one worker develops a neuropathy when similarly exposed coworkers do not. This chapter focuses on several prototypical neurotoxins, describing the classic neurotoxic syndrome associated with each and possible diagnostic strategies the clinician can take. This discussion emphasizes the initial history and physical examination and initial laboratory studies that assist in confirming the diagnosis.