People who ingest packets of illicit drugs or insert them into body cavities in an attempt to smuggle them are termed body packers. People who do this in an attempt to hide the drugs when encountered by law enforcement are called body stuffers. Severe toxicity and death occurs in body packers and body stuffers, and this is usually secondary to leaking of drug from packets in the gastrointestinal tract. This is well reported with cocaine and heroin and occurs less commonly with methamphetamine. We report an unusual case of intravaginal body stuffing that lead to severe methamphetamine toxicity in a young woman.A 20-year old female, who was in police custody, developed multiple seizures, altered mental status, tachycardia and hypertension shortly after admitting to having drugs enclosed in plastic bags in her vagina. She was hospitalized for 4 days with gradual improvement in her symptoms with the exception of a resting tachycardia. Gas chromatography and mass spectrometry of the urine at this time confirmed the presence of methamphetamine and the amphetamine metabolite, co-intoxicants were excluded based on comprehensive urine drug screening using GCMS. Quantitative serum levels of methamphetamine and amphetamine were 3100 ng/ml and 110 ng/ml, repectively.We report an unusual case of intravaginal body stuffing that lead to severe methamphetamine toxicity in a young woman. This case highlights the potential for severe methamphetamine poisoning secondary to intravaginal stuffing. If either body packing or stuffing is suspected, a vaginal exam may be warranted.

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.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.Pimozide overdose in children may be associated with delayed onset of symptoms, including dystonia.

Drugs and chemicals are almost easily available in Iran. Natural toxins as poisonous plants and animals also exist in most parts of the country. Therefore, acute poisonings, either intentional or accidental and also drug abuse/addiction are common in Iran. In spite of these difficulties there is no center for poison control and surveillance in this country to gather information and analyse data. The files of a systematic randomised ten percent of all hospital-referred poisoned patients from 21 March 1993 to 20 March 2000 in Imam Reza (p) University Hospital of Mashhad (71589 cases) were screened retrospectively. Young adults (40.3%) and school children (22.9%) were the most vulnerable group. Mean age was 22.3 (S.D. 14.38) years with a minimum of less than one and a maximum of 98 years old. A female predominance was found (53.4%). Intentional poisoning was more common (54.4%) than accidental exposures (45.2%). Fourteen cases were classified as criminal poisoning. 79.7% of exposures were via ingestion, followed by dermal exposures (14.1%), and inhalation (6.2%). The majority (83.7%) of patients were from urban areas. Most patients (68.6%) were treated in the Emergency Toxicology Clinic and discharged, 19.2% were temporarily hospitalized and 11.3% were hospitalized for 24 hr. Main groups of poisons were pharmaceuticals (61.4%), chemicals (22.8%), and natural toxins (16.6%). The overall number of poisoned patients was higher in spring and summer (62.8%). In conclusion, acute poisonings, particularly self-poisonings, are common in Iran. Since medical documentation is not routinely provided in this country the results of this retrospective study can be used for surveillance. Establishment of fluent data gathering and analysis within the local health system are challenges for the future.

Fipronil, a broad spectrum N-phenylpyrazole insecticide that inhibits GABAA-gated chloride channels, has been in use since the mid-1990s. A high affinity for insect compared to mammalian GABA receptors results in lower animal toxicity than other insecticides blocking this channel. To date, only two accidental cases of fipronil poisoning in humans have been published.We report seven patients with fipronil self-poisoning seen prospectively in Sri Lanka together with pharmacokinetics for four patients. Non-sustained generalized tonic-clonic seizures were seen in two patients (peak measured plasma fipronil concentrations 1600 and 3744 microg/L); both were managed with diazepam without complications. A patient with a peak measured plasma concentration of 1040 microg/L was asymptomatic throughout his stay. Plasma concentration was still high at discharge 3-4 days post-ingestion when the patients were well. Retrospective review of >1000 pesticide poisoning deaths since 1995 found only one death from fipronil-based products. In contrast to the good outcome of the above cases, this patient required intubation and ventilation and had continuous fits despite therapy with barbiturates and benzodiazepines.Our experience with prospectively observed patients suggests that fipronil poisoning is characterized by vomiting, agitation, and seizures, and normally has a favorable outcome. Management should concentrate on supportive care and early treatment of seizures. However, further experience is needed to determine whether increased susceptibility to fipronil or larger doses can produce status epilepticus.

The aim of the our study was to investigate the role of adenosine receptors on cardiovascular toxicity induced by amitriptyline, a tricyclic antidepressant agent. Therefore, the hypothesis of this study was that adenosine receptor antagonists would improve and/or prevent amitriptyline-induced hypotension and conduction abnormalities in an anesthetized rat model of amitriptyline intoxication.Two separate experimental protocols were performed. Amitriptyline intoxication was induced by the infusion of amitriptyline 0.94 mg/kg/min until 40-45% reduction of mean arterial pressure (MAP). Sodium cromoglycate (10 mg/kg) was injected i.v. to inhibit the A3 receptor-mediated activation of mast cells. In protocol 1, after amitriptyline infusion, while control animals (n=8) were given dextrose solution, treatment groups received a selective adenosine A1 antagonist DPCPX (8-cyclopentyl-1,3-Dipropylxanthine, 20 microg/kg/min, n=8) or a selective A2a antagonist CSC (8-(3-chlorostyryl) caffeine, 24 microg/kg/min, n=8) for 60 minutes. In protocol 2, after the sodium cromoglycate, while control group of rats (n=8) recevied a dextrose solution, treatment groups of rats were administered DPCPX (20 microg/kg/min, n=8) or CSC (24 microg/kg/min, n=8) infusion to block adenosine A1 and A2a receptors for 20 minutes before amitriptyline infusion. After pretreatment with adenosine antagonists, all rats were given a dose of 0.94 mg/kg/min of amitriptyline infusion during 60 minutes. Outcome measures were mean arterial pressure (MAP), heart rate (HR), QRS duration and survival rate.In protocol 1, amitriptyline infusion significantly reduced MAP and prolonged QRS within 15 minutes. HR was not changed significantly during the experiments. While dextrose did not improve MAP and QRS prolongation, DPCPX or CSC administration developed a significant improvement in MAP compared to the dextrose group within 10 min (88.5 +/- 2.8%, 75.6 +/- 4.7% and 50.1 +/- 14.7%, p<0.01, p<0.05, respectively). Both DPCPX and CSC decreased QRS prolongation (p<0.05) and increased median survival time significantly (log-rank test, p<0.00001). In protocol 2, pretreatment with DPCPX or CSC prevented the reduction in MAP due to amitriptyline toxicity compared to rats administered dextrose infusion (99.5 +/- 2.6%, 102.4 +/- 2.6%, 81.8 +/- 5.4, p<0.01 at 30 min; 98.0 +/- 2.9%, 93.5 +/- 6.0%, 64.9 +/- 4.7, p<0.001, p<0.01 at 40 min, respectively). Pretreatment with DPCPX or CSC also prevented the QRS prolongation (p<0.05) and increased median survival time significantly (log-rank test, p<0.0001).Adenosine antagonists were found to be effective in improving hypotension, QRS prolongation and survival time in our rat model of amitriptyline toxicity. Additionally, amitriptyline-induced cardiotoxicity was abolished by pretreatment with adenosine receptor antagonists. These results suggest that adenosine receptors may have a role in the pathophysiology of amitriptyline-induced cardiovascular toxicity. Adenosine A1 and A2a receptor antagonists may be promising agents for reversing amitriptyline-induced cardiovascular toxicity.

Gastric lavage should not be employed routinely, if ever, in the management of poisoned patients. In experimental studies, the amount of marker removed by gastric lavage was highly variable and diminished with time. The results of clinical outcome studies in overdose patients are weighed heavily on the side of showing a lack of beneficial effect. Serious risks of the procedure include hypoxia, dysrhythmias, laryngospasm, perforation of the GI tract or pharynx, fluid and electrolyte abnormalities, and aspiration pneumonitis. Contraindications include loss of protective airway reflexes (unless the patient is first intubated tracheally), ingestion of a strong acid or alkali, ingestion of a hydrocarbon with a high aspiration potential, or risk of GI hemorrhage due to an underlying medical or surgical condition. A review of the 1997 Gastric Lavage Position Statement revealed no new evidence that would require a revision of the conclusions of the Statement.

Organochlorine insecticides are highly toxic compounds that are responsible for a number of severe intoxications worldwide with several deaths. Despite their widespread use in agriculture during the 1940s to 1960s and the well-known signs and symptoms of intoxication, the clinical picture in case of poisoning varies. We report two cases of acute intentional endosulfan intoxication with cerebral edema and cardiac failure.Both cases developed life-threatening signs like epileptic state, respiratory insufficiency and hemodynamic instability soon after ingestion. The survivor developed severe myocardial insufficiency and pulmonary edema documented by echocardiography and x-ray of the chest. The deceased patient developed severe cerebral edema and multiorgan failure ten days after ingestion of Thiodan 35. The peak serum concentration of endosulfan in the survivor was 0.12 mg/L approximately 23 hours after ingestion, whereas the peak blood concentration in the fatal case was 0.86 mg/L approximately 25 hours post-ingestion. Post-mortem endosulfan levels in different organs were determined.Endosulfan is a highly toxic organochlorine insecticide that produces well-known neurological symptoms of tonic-clonic convulsions, headache, dizziness and ataxia but also can cause gastrointestinal symptoms and metabolic disturbances. Life-threatening cerebral edema and hemodynamic instability may occur. Treatment is symptomatic and supportive.