Abstract:In the proper clinical situation such as pure anticholinergic overdose with severe symptoms, physostigmine can be beneficial. The potential for side effects is not insignificant, and the antidote should be used with caution in any patient with unknown ingestions or those with cardiac conduction defects. More research is needed, especially involving children, before we will fully understand the indications and toxicities associated with physostigmine.
“…It led to controversies, despite the recent reports of its safe use [14]. Relative contraindication of physostigmine is cardiac conduction defects (AV block) [15].…”
Datura stramonium (DS) is a widespread annual plant, containing atropine, hyoscyamine, and scopolamine, which can produce poisoning with a severe anticholinergic syndrome. Teenagers ingest the roots, seeds or the entire plant to obtain its hallucinogenic and euphoric effects. We presented the case of a 22 year old male who was admitted to the Emergency Room in a coma after consuming Datura stramonium, 2 hours earlier. The patient presented with fever, tachycardia with right bundle branch block, and urinary retention. Rapid sequence induction and intubation was performed immediately, with sedation and assisted-control mechanical ventilation, after being transferred to the Intensive Care Unit. The patient received activated charcoal, in repeated doses, external and internal cooling was applied, and an infusion of neostigmine was started. The biological assessment revealed rhabdomyolysis and prevention of renal failure was initiated. After a proper neurological evaluation, 36 hours after using Datura stramonium, the patient was extubated and transferred to the Psychiatric ward for further assessment and care.
“…It led to controversies, despite the recent reports of its safe use [14]. Relative contraindication of physostigmine is cardiac conduction defects (AV block) [15].…”
Datura stramonium (DS) is a widespread annual plant, containing atropine, hyoscyamine, and scopolamine, which can produce poisoning with a severe anticholinergic syndrome. Teenagers ingest the roots, seeds or the entire plant to obtain its hallucinogenic and euphoric effects. We presented the case of a 22 year old male who was admitted to the Emergency Room in a coma after consuming Datura stramonium, 2 hours earlier. The patient presented with fever, tachycardia with right bundle branch block, and urinary retention. Rapid sequence induction and intubation was performed immediately, with sedation and assisted-control mechanical ventilation, after being transferred to the Intensive Care Unit. The patient received activated charcoal, in repeated doses, external and internal cooling was applied, and an infusion of neostigmine was started. The biological assessment revealed rhabdomyolysis and prevention of renal failure was initiated. After a proper neurological evaluation, 36 hours after using Datura stramonium, the patient was extubated and transferred to the Psychiatric ward for further assessment and care.
“…Physostigmine, an acetylcholinesterase inhibitor, has historically been an antidote for anticholinergic syndrome. However, the toxicities of physostigmine administration can be signifi cant including induction of a cholinergic syndrome, seizures, and cardiac toxicity [ 5 ]. The authors recommend avoiding physostigmine if possible, but especially in patients with TCA ingestions, seizures or abnormal electrocardiograms (ECGs).…”
IntroductionEven with public heightened awareness for potential home toxin exposures, poisonings continue to occur and pose a signifi cant challenge to the pediatric intensivist. In 2009, United States Poison Control centers reported 1,613,272 toxin exposures in children less than 20 years of age [ 1 ]. This represented 65 % of all reported human exposures. Children younger than 3 years were involved in 38.9 % of exposures and children younger than 6 years accounted for just over half of all human exposures (51.9 %). The three most common exposures in children age 5 years or younger were cosmetics/personal care products (13.0 %), analgesics (9.7 %), and household cleaning substances (9.3 %). Despite the majority of human exposures being in the pediatric age group, only 79 (6.8 %) of the 1,158 human deaths were in those less than 20 years of age. As expected, unintentional toxin exposures were more prevalent in children younger than 13 years of age (99.2 %) compared to teenagers (47 %) [ 1 ]. The intensivist must be prepared to care for the children who have serious and sometimes life-threatening exposures.
AbstractDespite the public's heightened awareness of potential toxin exposures in children, poisonings continue to occur and pose a signifi cant challenge to the pediatric intensivist. In 2009, the United States Poison Control centers reported 1,613,272 toxin exposures in children less than 20 years of age which represented 65 % of all reported human exposures. Children younger than 3 years were involved in 38.9 % and children younger than 6 years accounted for just over half of all human exposures (51.9 %). The three most common exposures in children age 5 years or younger were cosmetics/personal care products (13.0 %), analgesics (9.7 %), and household cleaning substances (9.3 %). Despite the majority of human exposures being in the pediatric age group, only 79 (6.8 %) of the 1,158 human deaths were in those less than 20 years of age. As expected, unintentional toxin exposures were more prevalent in children younger than 13 years of age (99.2 %) compared to teenagers (47 %). The intensivist must be prepared to care for children who have serious and sometimes life-threatening exposures. Supportive care is the mainstay of therapy because many poisons have no specifi c antidote. Much of the current clinical practices for treating the poisoned patient are based on anecdotal reports because there are limited evidenced-based clinical trials that provide guidance for treatment, safety, and outcome.
“…It was used prominently as an analeptic in the 1960s through the early 1980s. Case reports then described its adverse effects when used in severe tricyclic antidepressant (TCA) overdose including asystole and death [1,2]. One case in particular describes the association of physostigmine use with asystole and seizures in severe TCA poisoning [1].…”
Section: Introductionmentioning
confidence: 99%
“…It is still, however, underappreciated even in very pure anticholinergic drug overdose situations. There have been several excellent reviews with critical appraisal of the literature regarding the risk and benefits of physostigmine as an antidotal therapy, and these have essentially uniformly described overemphasis on toxicity and adverse effects related to its use in non-tricyclic antidepressant overdoses [2,6]. While there are many case reports and robust literature describing the efficacy of physostigmine administered as an intermittent bolus for the treatment of anticholinergic toxicity, there are only a few case reports describing its use as a continuous intravenous infusion [7][8][9][10].…”
Section: Introductionmentioning
confidence: 99%
“…There are predictable adverse effects when it is used inappropriately. Seizures tend to occur when physostigmine is administered too rapidly or in the setting of a pro-convulsant coingestant, and bradycardia and asystole are also associated with rapid administration and occur due to the potentiation of vagal effects on cardiac tissue [2]. Nausea, vomiting, bronchorrhea, hypersalivation, and incontinence of stool and urine can occur when excess cholinergic tone predominates [3,4].…”
Introduction Physostigmine was once a widely used antidote for the treatment of antimuscarinic toxicity. However, reports describing the association of physostigmine with asystole and seizures in severe tricyclic antidepressant poisoning resulted in a decrease in use. Recent literature has demonstrated that physostigmine is a safe and effective antidote for the treatment of antimuscarinic toxicity. There are only two previously published articles regarding the use of physostigmine administered as a continuous intravenous infusion for persistent antimuscarinic toxicity. We present a case of physostigmine continuous infusion for the treatment of antimuscarinic symptoms in a polydrug overdose due to the ingestion of diphenhydramine along with bupropion, citalopram, acetaminophen, and naproxen. Case Presentation A 13-year-old female presented with hyperthermia, myoclonus and rigidity, hallucinations, severe agitation, and antimuscarinic toxicity including inability to sweat after a polydrug overdose. Several doses of lorazepam were administered followed by physostigmine which produced resolution of hallucinations and attenuation of the antimuscarinic symptoms including perspiration, temperature improvement, and decreased agitation. After periods of improvement and recurrence of antimuscarinic effects, a continuous infusion of physostigmine was administered at 2 mg/h and continued for almost 8 h to maintain attenuation of symptoms. GABAergic agents including lorazepam and phenobarbital were used later in the hospital course for presumed symptoms of serotonergic and adrenergic toxicity after resolution of antimuscarinic effects. The patient did not experience any adverse effects of physostigmine administration. Discussion Physostigmine administered as a continuous infusion may be a reasonable treatment option for severe and recurrent symptoms related to antimuscarinic toxicity.
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