Goldfrank's Toxicologic Emergencies

Arena, Jay M.

doi:10.1001/jama.1995.03520260092042

Cited by 48 publications

(145 citation statements)

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“…The mechanism of toxicity of amphetamines is primarily related to excessive extracellular dopamine, norepinephrine, and serotonin [22,23]. The most prominent clinical picture is alpha-and beta-adrenoreceptor-mediated sympathomimetic syndrome, with psychiatric symptoms and hyperthermia secondary to the dopamine and serotonin excess [23][24][25][26].…”

Section: Mechanism Of Toxicitymentioning

confidence: 99%

Overdose of Drugs for Attention-Deficit Hyperactivity Disorder: Clinical Presentation, Mechanisms of Toxicity, and Management

2013

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The prevalence of attention-deficit hyperactivity disorder (ADHD) in the USA is estimated at approximately 4-9% in children and 4% in adults. It is estimated that prescriptions for ADHD medications are written for more than 2.7 million children per year. In 2010, US poison centers reported 17,000 human exposures to ADHD medications, with 80% occurring in children <19 years old and 20% in adults. The drugs used for the treatment of ADHD are diverse but can be roughly separated into two groups: the stimulants such as amphetamine, methylphenidate, and modafinil; and the non-stimulants such as atomoxetine, guanfacine, and clonidine. This review focuses on mechanisms of toxicity after overdose with ADHD medications, clinical effects from overdose, and management. Amphetamine, dextroamphetamine, and methylphenidate act as substrates for the cellular monoamine transporter, especially the dopamine transporter (DAT) and less so the norepinephrine (NET) and serotonin transporter. The mechanism of toxicity is primarily related to excessive extracellular dopamine, norepinephrine, and serotonin. The primary clinical syndrome involves prominent neurological and cardiovascular effects, but secondary complications can involve renal, muscle, pulmonary, and gastrointestinal (GI) effects. In overdose, the patient may present with mydriasis, tremor, agitation, hyperreflexia, combative behavior, confusion, hallucinations, delirium, anxiety, paranoia, movement disorders, and seizures. The management of amphetamine, dextroamphetamine, and methylphenidate overdose is largely supportive, with a focus on interruption of the sympathomimetic syndrome with judicious use of benzodiazepines. In cases where agitation, delirium, and movement disorders are unresponsive to benzodiazepines, second-line therapies include antipsychotics such as ziprasidone or haloperidol, central alpha-adrenoreceptor agonists such as dexmedetomidine, or propofol. Modafinil is not US FDA approved for treatment of ADHD; however, it has been shown to improve ADHD signs and symptoms and has been used as an off-label pharmaceutical for this diagnosis in both adults and children. The mechanism of action of modafinil is complex and not fully understood. It is known to cause an increase in extracellular concentrations of dopamine, norepinephrine, and serotonin in the neocortex. Overdose with modafinil is generally of moderate severity, with reported ingestions of doses up to 8 g. The most common neurological effects include increased anxiety, agitation, headache, dizziness, insomnia, tremors, and dystonia. The management of modafinil overdose is largely supportive, with a focus on sedation, and control of dyskinesias and blood pressure. Atomoxetine is a selective presynaptic norepinephrine transporter inhibitor. The clinical presentation after overdose with atomoxetine has generally been mild. The primary effects have been drowsiness, agitation, hyperactivity, GI upset, tremor, hyperreflexia, tachycardia hypertension, and seizure. The management of atomoxetine overdose is la...

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Section: Mechanism Of Toxicitymentioning

confidence: 99%

Overdose of Drugs for Attention-Deficit Hyperactivity Disorder: Clinical Presentation, Mechanisms of Toxicity, and Management

2013

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“…All hydrocarbon toxicities can potentially cause ataxia, cognitive impairment, and arrhythmias to varying degrees based on their individual chemical properties [10,11]. A summary of more common inhalants of abuse can be found in Table 1.…”

Section: Discussionmentioning

confidence: 99%

Recognizing Ethyl Chloride Neurotoxicity: Inhalant Abuse Hidden in Plain Sight

Young¹,

Carter²,

Cardinali³

et al. 2023

Cureus

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Ethyl chloride is a common topical anesthetic. However, when abused as an inhalant, effects can range from headaches and dizziness to debilitating neurotoxicity requiring intubation. While previous case reports describe the short-term reversible neurotoxicity of ethyl chloride, ours show chronic morbidity and mortality outcome. During the initial evaluation, it is essential to consider the rising trend of commercially available inhalants being used as recreational drugs. We present a case of a middle-aged man presenting with subacute neurotoxicity due to repeated abuse of ethyl chloride.

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“…A 17-year-old male with type 1 diabetes presented to the emergency department (ED) with nausea, vomiting, abdominal pain, and hyperglycemia. His initial vital signs (VS) were as follows: blood pressure (BP), 121/73 mmHg; heart rate (HR), 115 beats per minute; temperature (T), 98.9 °F; respiratory rate (RR), 30 breaths per (3)(4)(5)(6)(7)(8)(9)(10)(11), and glucose 445 mg/dL (65-99). He also had significantly elevated transaminases with aspartate aminotransferase (AST) 2,819 U/L (<41) and alanine aminotransferase (ALT) 2,344 U/L (<56).…”

Section: Case Presentation Patientmentioning

confidence: 99%

“…three in the United States [4]. Exposures to hydrocarbons like CCl 4 continue to be a public health concern, specifically in populations such as unsupervised children with ingestions, workers prone to occupational exposures, and youth who abuse solvents by inhalation [5].…”

Section: Figure 1: An Antique Firebombmentioning

confidence: 99%

“…Metabolism of CCl 4 occurs via cytochrome CYP2E1 into its toxic metabolite, trichloromethyl radical. This radical covalently binds to hepatocyte macromolecules causing lipid peroxidation and oxidative damage [5]. The centrilobular region of the liver (zone 3) is most often damaged given the high concentration of CYP2E1 enzymes.…”

Section: Figure 1: An Antique Firebombmentioning

confidence: 99%

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You Dropped the Bomb on Me: A Case Series of Carbon Tetrachloride Toxicity

Stashin¹,

Fikse²,

Orta³

et al. 2023

Cureus

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Carbon tetrachloride (CCl 4 ) is a halogenated hydrocarbon that is a colorless, clear liquid with a sweetish, ether-like, nonirritant odor. It was previously used in dry cleaning agents, refrigerants, and fire extinguishers. CCl 4 toxicity is rarely observed. Two patients with acute hepatitis following exposure to a CCl 4 -containing antique fire extinguisher are presented. A son (patient 1) and father (patient 2) were admitted to the hospital with acute, unexplained elevated transaminases. After extensive questioning, they reported recent exposure to a large amount of CCl 4 when an antique firebomb shattered in their home. Both patients cleaned the debris without personal protective equipment and slept in the contaminated area. The patients presented to the emergency department (ED) at varying times between 24 and 72 hours after CCl 4 exposure. Both patients received intravenous N-acetylcysteine (NAC); patient 1 also received oral cimetidine. Both recovered uneventfully without sequelae. Extensive workup for other causes of elevated transaminases was unremarkable. Serum analyses for CCl 4 were also unremarkable due to the delay between exposure and hospital presentation. CCl 4 is a potent hepatotoxin. CCl 4 metabolism via cytochrome CYP2E1 produces its toxic metabolite, the trichloromethyl radical. This radical covalently binds to hepatocyte macromolecules and causes lipid peroxidation and oxidative damage with ensuing centrilobular necrosis. Treatment is not well established, but NAC is likely beneficial via glutathione repletion and antioxidant effects. Cimetidine blocks cytochrome P450 and, thus, metabolite formation. Cimetidine may also promote the stimulation of regenerative processes acting on DNA synthesis. CCl 4 toxicity is rare and infrequently reported in current literature but should be maintained in the differential of acute hepatitis. Two patients presenting nearly identically -at two different ages but from the same household -offered a clue to this enigmatic diagnosis.

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Goldfrank's Toxicologic Emergencies

Cited by 48 publications

References 0 publications

Overdose of Drugs for Attention-Deficit Hyperactivity Disorder: Clinical Presentation, Mechanisms of Toxicity, and Management

Overdose of Drugs for Attention-Deficit Hyperactivity Disorder: Clinical Presentation, Mechanisms of Toxicity, and Management

Recognizing Ethyl Chloride Neurotoxicity: Inhalant Abuse Hidden in Plain Sight

You Dropped the Bomb on Me: A Case Series of Carbon Tetrachloride Toxicity

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