Drug-Induced Extrapyramidal Symptoms at the Pediatric Emergency Department.

OBJECTIVES: Extrapyramidal symptoms (EPS) induced by pharmacologic agents can cause patient discomfort and lead to emergency department visits. Analyzing these cases at a pediatric emergency department may help to elucidate the characteristic features of extrapyramidal syndrome in children. METHODS: This retrospective study was conducted at Chang Gung Memorial Hospital in Taiwan. Pediatric patients with drug-induced extrapyramidal syndrome seeking treatment at our emergency department from January 2001 to December 2010 were enrolled. The patients' clinical features, drug history, demographic data, and treatment data were collected and analyzed. RESULTS: One hundred nineteen patients (61 females, 58 males) were enrolled. Ninety-six patients could provide their drug history; all of whom took dopamine antagonists and 90% of whom took dopamine antagonists as antiemetic agents, with only 9 patients taking them for antipsychotic purposes. Metoclopramide syrup overdose was the main cause of extrapyramidal syndrome in patients under 2 years old. The average emergency room stay of the patients who could provide their drug history was shorter than that of those who could not. CONCLUSIONS: It is not uncommon for patients with drug-induced EPS to present to a pediatric emergency room owing to the use of dopamine antagonists as antiemetic agents. Clinical symptoms with a clear drug history are helpful for the diagnosis and management. Emphasizing the correct usage of liquid medications will reduce the risk of EPS.

Acute encephalopathy with concurrent respiratory and metabolic disturbances in first known parenteral human administration of flunixin meglumine and acepromazine maleate.

BACKGROUND: Flunexin is a nonsteroidal anti-inflammatory drug approved for veterinary use in horses and cattle. Acepromazine is a phenothiazine derivative used in horses, dogs, and cats. Human exposure to these substances is rare. CASE REPORT: We report a case of a human injection of two equine medications, flunixin and acepromazine, which resulted in altered mental status, respiratory alkalosis, gastrointestinal bleeding, and elevation of liver transaminases in a 43-year-old woman who worked as a horse trainer. The patient intentionally self-injected these medications and subsequently presented to the Emergency Department with altered mental status and lethargy. The patient required hospitalization for metabolic abnormalities, including respiratory alkalosis, and suffered a gastrointestinal bleed requiring blood transfusion. The patient ultimately recovered with supportive measures. We believe this to be the first case of concomitant injection of flunixin and acepromazine in a human. CONCLUSIONS: This report explains a case of parenteral administration of two equine medications and the subsequent complications in a patient that presented to the Emergency Department. Human exposure to veterinary medications cannot be predicted by their effect in animals due to variations in absorption, distribution, and metabolism. Physicians should be aware that individuals who work with animals may have access to large quantities of veterinary medicine. This case also exemplifies the challenges that Emergency Physicians face on a daily basis, and generates additional consideration for overdoses and intoxications from medications that are not considered commonplace in humans.

Long QT syndrome and torsades de pointes induced by acute sulpiride poisoning.

Sulpiride, a selective dopamine D2 antagonist and a substituted benzamide derivative, is considered a safe antipsychotic and antidepressant agent with few adverse effects on the cardiovascular system. Sulpiride-induced torsades de pointes is rare. We report a case of long QT syndrome and torsades de pointes induced by ingestion of 1.5 g of sulpiride. Ventricular arrhythmia was initially treated with amiodarone, without success. Eventually, lidocaine and magnesium sulfate successfully terminated the ventricular arrhythmia. The patient was discharged uneventfully after 3 days of hospitalization. This case illustrates the fact that acute sulpiride poisoning may lead to life-threatening ventricular arrhythmia. Early recognition followed by effective therapy is crucial. Intensive cardiac monitoring is recommended for sulpiride poisoning.

Delayed dystonia following pimozide overdose in a child.

BACKGROUND: Pimozide overdose has rarely been reported in children. In adults, pimozide intoxication may cause seizures, extrapyramidal and anticholinergic effects, hypotension, QTc prolongation and torsades de pointes. We report dystonia, hypotension and drowsiness following pimozide ingestion in a child. CASE REPORT: An alert 18-month-old presented to hospital 40 minutes after ingesting up to 6 mg (0.5 mg/kg) of pimozide. Vital signs: BP 91/62 mmHg, HR 130/min, RR 26/min, temperature 97.2 degrees F (36.2 degrees C). She received gastric lavage and activated charcoal. One hour later, her QTc interval was 420 msec, HR 150. She remained asymptomatic until 12 hours post-ingestion, when she developed drooling, tongue thrusting and drowsiness. BP was 75/40, HR 150, QTc 440 msec. BP increased to 95/50 after a bolus of normal saline. Her dystonia subsided over the next 12 hours without treatment. Drowsiness and tachycardia persisted until 40 hours post-ingestion. QTc interval at this time was 370 msec. Patient recovered without sequelae. CONCLUSION: Pimozide overdose in children may be associated with delayed onset of symptoms, including dystonia.

[Acute dystonia from metoclopramide in children]. / Dystonies aiguës au métoclopramide chez l'enfant.

A retrospective study (1995-2000) of reports of cases of metoclopramide poisoning collected at the Lille poison control centre (184 phone calls) shows the frequent occurrence of acute dystonia in children (81 cases). These spectacular extrapyramidal symptoms consist of abnormal movements (31 cases), local hypertonia (30 cases), acute dyskinesia (17 cases), general hypertonia (16 cases) and oculogyric crisis (13 cases). There is no dose-effect correlation and sex has no influence on the occurrence of neurological symptoms. Medical management is simple surveillance or symptomatic therapy (a sedative drug and/or anti-parkinsonian therapy and/or a gastrointestinal adsorbent). Hospitalisation was needed in only 9.1% of cases. Providing better information to physicians about metoclopramide adverse effects and their medical management should allow a reduction in the number of unnecessary hospitalizations.

Human exposure to pet prescription medications.

Veterinarians commonly prescribe medications to treat a variety of companion animal clinical conditions. Many pet medications are pharmacologically the same product prescribed for human use. We report 2 cases in which pet medications were used for self poisoning. Obtaining a pet history may provide critical information in the assessment of a patient with a suspected overdose.

Restraint as a stressor in mice: against the dopaminergic neurotoxicity of D-MDMA, low body weight mitigates restraint-induced hypothermia and consequent neuroprotection.

In experimental studies of stress, restraint of laboratory rodents, perceived as easy to apply and believed to be reproducible, is a commonly used manipulation. The restraint manipulation is utilized as a technique to characterize the physiological, cellular and molecular consequences of stress as well as a tool to understand the ways in which stress may interact with toxic substances. In previous work, we utilized restraint in an examination of the effect of stress on the striatal dopaminergic neurotoxicity engendered by a series of substituted amphetamines. Contrary to our expectations, and most likely due to its body temperature-reducing properties in the mouse, restraint provided total or near total protection against the neurotoxicity of these agents. During subsequent studies utilizing C57Bl6/J female mice of varying weights and ages the degree of temperature reduction and the associated ability to block (20-100%) the dopamine depletion associated with the neurotoxic amphetamine 3,4-methylendioxyamphetamine (D-MDMA, 20 mg/kg of mouse body weight, every 2 h, s.c., total of four doses) were found to vary considerably more than had been previously observed. An in-depth analysis of the role mouse weight plays in the temperature reduction induced by restraint indicates mouse weight is a primary determinant of hypothermia and subsequent neuroprotection. It suggests the induction of stress in rodents by restraint is a complex effect that may lead to unanticipated results. The restraint manipulation is not as straight-forward a procedure as is commonly believed. Our data indicate that consistent application of restraint may require an adjustment of the restrainer device to mouse body weight.

Acute risperidone overdose.

Risperidone (Risperdal) is a recently released novel antipsychotic medication. It is different from the conventional neuroleptics, such as haloperidol, as it has both serotinergic and dopaminergic activity. It has a more tolerable side-effect profile compared with other antipsychotic medications. We review the literature regarding the side effects of risperidone use, describe a case of overdose with risperidone, and discuss the clinical sequelae and management of such an overdose.

Chemical exposures and Parkinson's disease in residents of three Negev kibbutzim.

We consider whether chemical pollutants in drinking water (including aromatic hydrocarbons, alkanes, halogenated aliphatic hydrocarbons, and phthalic acid) or used occupationally in agriculture that have shown no parkinsonism-inducing effect may be responsible for excess cases of Parkinson's disease (PD) in three adjacent kibbutzim in southern Israel (Negev). Literature data on PD pathogenesis have been compared with common pathogenetic pathways to xenobiotics effects; the following neurotoxic mechanisms, besides individual sensitivity, have been suggested: (1) impairment of the protective role of the substantia nigra against toxicants by binding of chemicals to melanin; (2) oxidative stress induction, including glutathione reduction, impaired calcium metabolism, and alteration of cytochrome P-450 activity; (3) blockade of iron chelators because of structural similarities to them or their precursors; (4) mediation of the production of endogenous dopaminergic neurotoxins, such as trichloroharmanes or isoquinolines; (5) blockade of dopamine receptors because of their resemblance to chemicals with affinity to these receptors; (6) stimulation of prostaglandin-H synthase and monooxygenase activity; and (7) stimulation of autoimmune processes and creation of autoimmunity to structures of the dopaminergic system caused by chemical similarity.

[Acute poisoning with thioridazine]. / Akute Intoxikationen mit Thioridazin.

OBJECTIVE: As previous single case reports have indicated that acute poisoning with thioridazine can be potentially dangerous, an investigation was undertaken to find out whether the risk of severe poisoning in adults and children can be judged from the amount of the drug that has been taken. PATIENTS AND METHODS: In a case-control study 202 medical notes of 202 patients were analysed (141 adults, aged 16-82 years; 61 children, aged 0.3-15 years) in which thioridazine was the only potentially harmful substance taken, the precise amount swallowed was known and the drug was the certain or probable cause of the signs. 30 children were excluded from the study, because their body weight was not known. RESULTS: Mild thioridazine poisoning was characterized by somnolence, tremor, ataxia and dysarthria. The severity of the poisoning and the degree of disorder of consciousness correlated significantly with the amount of thioridazine taken. Severe intoxication with coma and ventricular arrhythmias was observed at a dose of 2 g and more. While the disorder of consciousness completely regressed in the first 24 hours, in a few of the patients the cardiac arrhythmias persisted for up to 28 hours after the drug intake. Charcoal administration seemed to influence the course favourably. CONCLUSION: Prolonged, intensive care supervision and treatment are essential if more than 2 g thioridazine have been swallowed. In addition to standard treatment with gastric lavage charcoal should be given as early as possible to limit absorption.