Clinical Toxicology

Although the ingestion of a dose of colchicine lower than 0.5 mg/kg is usually complicated by a mortality rate less than 5%, severe complications may be associated with drug-drug interactions in case of overdose combining other drugs.  A 33-year-old previously healthy woman was admitted after a drug overdose combining colchicine, atorvastatin, ibuprofen, diclofenac, and furosemide. The amount of colchicine ingested was exactly 20 mg, corresponding to 0.33 mg/kg. Despite this relatively low dose, she presented the clinical course that is usually seen with much larger colchicine ingestions. She developed acute renal and liver failure, acute lung injury, pancytopenia with sepsis, rhabdomyolysis, hypertriglyceridemia, and ultimately died on Day 14 from hyperammonemic encephalopathy, refractory hypoxemia, and cardiac arrhythmias.  Serious drug-drug interactions may have complicated colchicine poisoning. In particular, atorvastatin, an inhibitor of P-glycoprotein and cytochrome P450 3A4, was likely responsible for an increased severity of rhabdomyolysis. In addition, propofol used for sedation during mechanical ventilation may have induced symptoms consistent with "propofol infusion syndrome," with further muscular injury and hypertriglyceridemia. The mechanism of death was unusual and similar to Reye's syndrome.

Acute poisoning is a significant health problem all over the world. In Malaysia, nationwide data on poisoning pattern is scarce and incomplete. The objectives of our study were to determine the pattern of acute drug and chemical poisoning at Penang General Hospital (PGH), in the northern region of Malaysia, and to compare poisoning characteristics between different ethnic groups. The study was a retrospective case review of all poisoned patients admitted to PGH during the years 2000-2002. We collected data concerning demographic parameters of patients, information about the agent(s) implicated, and circumstances surrounding the event. There were 493 poisoning incidents. Nearly two-thirds of the poisoned cases involved female patients. The predominant mode of poisoning was intentional (51.5%). The age group 15.1-30 years ranked at the top, constituting 55.2% of all cases. Drugs were the predominant agents implicated. Among cases associated with drugs, paracetamol was the main causative agent (44.7%). Chinese patients constituted 37.7% of all poisoning cases, followed by the Indians (31.6%) and Malays (26.6%). Between ethnic groups, Indian patients were found to have the highest rate of poisoning admission of 75.2 per 100,000 persons.

Gamma-hydroxybutyrate (GHB) and its precursors, gamma-butyrolactone (GBL) and 1,4-butanediol (1,4-BD), are drugs of abuse which act primarily as central nervous system (CNS) depressants. In recent years, the rising recreational use of these drugs has led to an increasing burden upon health care providers. Understanding their toxicity is therefore essential for the successful management of intoxicated patients. We review the epidemiology, mechanisms of toxicity, toxicokinetics, clinical features, diagnosis, and management of poisoning due to GHB and its analogs and discuss the features and management of GHB withdrawal. OVID MEDLINE and ISI Web of Science databases were searched using the terms "GHB," "gamma-hydroxybutyrate," "gamma-hydroxybutyric acid," "4-hydroxybutanoic acid," "sodium oxybate," "gamma-butyrolactone," "GBL," "1,4-butanediol," and "1,4-BD" alone and in combination with the keywords "pharmacokinetics," "kinetics," "poisoning," "poison," "toxicity," "ingestion," "adverse effects," "overdose," and "intoxication." In addition, bibliographies of identified articles were screened for additional relevant studies including nonindexed reports. Non-peer-reviewed sources were also included: books, relevant newspaper reports, and applicable Internet resources. These searches produced 2059 nonduplicate citations of which 219 were considered relevant. There is limited information regarding statistical trends on world-wide use of GHB and its analogs. European data suggests that the use of GHB is generally low; however, there is some evidence of higher use among some sub-populations, settings, and geographical areas. In the United States of America, poison control center data have shown that enquiries regarding GHB have decreased between 2002 and 2010 suggesting a decline in use over this timeframe. MECHANISMS OF ACTION: GHB is an endogenous neurotransmitter synthesized from glutamate with a high affinity for GHB-receptors, present on both on pre- and postsynaptic neurons, thereby inhibiting GABA release. In overdose, GHB acts both directly as a partial GABA(b) receptor agonist and indirectly through its metabolism to form GABA. TOXICOKINETICS: GHB is rapidly absorbed by the oral route with peak blood concentrations typically occurring within 1 hour. It has a relatively small volume of distribution and is rapidly distributed across the blood-brain barrier. GHB is metabolized primarily in the liver and is eliminated rapidly with a reported 20-60 minute half-life. The majority of a dose is eliminated completely within 4-8 hours. The related chemicals, 1,4-butanediol and gamma butyrolactone, are metabolized endogenously to GHB. CLINICAL FEATURES OF POISONING: GHB produces CNS and respiratory depression of relatively short duration. Other commonly reported features include gastrointestinal upset, bradycardia, myoclonus, and hypothermia. Fatalities have been reported. MANAGEMENT OF POISONING: Supportive care is the mainstay of management with primary emphasis on respiratory and cardiovascular support. Airway protection, intubation, and/or assisted ventilation may be indicated for severe respiratory depression. Gastrointestinal decontamination is unlikely to be beneficial. Pharmacological intervention is rarely required for bradycardia; however, atropine administration may occasionally be warranted. WITHDRAWAL SYNDROME: Abstinence after chronic use may result in a withdrawal syndrome, which may persist for days in severe cases. Features include auditory and visual hallucinations, tremors, tachycardia, hypertension, sweating, anxiety, agitation, paranoia, insomnia, disorientation, confusion, and aggression/combativeness. Benzodiazepine administration appears to be the treatment of choice, with barbiturates, baclofen, or propofol as second line management options. GHB poisoning can cause potentially life-threatening CNS and respiratory depression, requiring appropriate, symptom-directed supportive care to ensure complete recovery. Withdrawal from GHB may continue for up to 21 days and can be life-threatening, though treatment with benzodiazepines is usually effective.

Fructose-1,6-diphosphate (FDP) is a metabolite in the glycolytic pathway created from glucose. Exogenously administered FDP increases the yield of ATP from anaerobic glycolysis. FDP reduces ischaemic tissue area in experimentally-induced cerebral and myocardial infarction and improves haemodynamics post-cardiac bypass. We hypothesised that FDP improves haemodynamics in propranolol and verapamil poisoning. Anesthetized Wistar rats were instrumented to record BP, heart rate (HR), cardiac output (CO) and QRS-duration. Propranolol or verapamil were infused continually. When BP dropped by 50%, propranolol-poisoned rats received one of 10% FDP125 mg/kg or 10% FDP250 mg/kg loading dose over 20 minutes followed by infusion 20 mg/kg/h. Verapamil-poisoned rats received the higher dosing regimen of FDP250. Controls received comparable volumes of 10% glucose. Haemodynamic time-points were compared for FDP to control by unpaired t-test or Mann-Whitney test as appropriate (p <  0.05). Survival was assessed using Kaplan-Meier survival analysis. FDP-treated animals survived significantly longer than glucose-treated controls at both doses in propranolol poisoning and in verapamil-poisoning. In propranolol poisoning, FDP250-treated animals showed a statistically significant increase in BP. However, there was no significant difference in cardiac output at this dose. There were also no significant differences in any haemodynamic parameters compared to control at the lower FDP dose in propranolol poisoning or in verapamil poisoning. FDP improved survival for both toxicants with an improvement in haemodynamics at the higher dose in propranolol poisoning. Future research could examine the efficacy of FDP in other beta-blocker and calcium channel-blocker poisoning as well as in concert with established inotropic therapies in drug-induced cardiovascular collapse.

In our study, we did not consider to give the control group ’ s laboratory results as short-term air monitoring results of the workplaces that were found to be below recommended exposure limits of National Institute for Occupational Safety and Health (NIOSH). 1 Supporting this, the control group ’ s toxicology test results were signifi cantly lower (mostly undetectable) compared to those of the exposed group. On the other hand, request for demographic characteristics of exposed group is justifi able. But we can easily say that, when the exposed and control groups were compared for alcohol consumption and cigarette smoking, there was no difference between groups and in the exposed group, alcohol consumption was very low and cigarette smoking did not exceed 10 patients, not more than 5 pack years. In the literature, we have found no study which emphasizes a relationship between NSE/S 100B and these levels of cigarette smoking and alcohol consumption. Carpal tunnel syndrome (CTS) is a complex of symptoms and signs such as paresthesia and pain in the median nerve innervation area. 2 In the evaluation of a peripheral neuropathy of a toxic exposure, (our) neurologists determined timing measures, distal latency, conduction velocity, and F-wave latency of median, ulnar, radial (in upper extremities), peroneal, and suralis nerves (in lower extremities). 3 For this reason, in daily practice of a neurologist, it is not hard to fi nd that a neuropathy is a consequence of CTS or other causes. A biomarker is accepted as a measurable and supportive indicator of a disease and can be divided into three groups as biomarkers of exposure, effect, and susceptibility. In clinical practice, it is very hard to fi nd a thorough relation between an ongoing or past exposure of a toxic substance and peripheral or central neurological disorder. Especially in chronic and low-dose solvent exposure, it is very diffi cult to detect it in biological samples because of rapid elimination from the body. 4 In this case, any probable correlation should be taken into account. 5 So, in our opinion, from the neurological point of view, any parameter which is weakly or strongly related to these disorders should be accepted, as a valuable tool for clinical evaluation or diagnosis of a toxic exposure.

Problems associated with the increasing abuse of plant-derived psychoactive substances have recently attracted attention. This study involved bioanalytical and clinical examinations of intoxication cases suspected to be linked to such plant materials. Urine samples were collected at emergency wards in Sweden from patients who either admitted or were suspected of ingestion of psychoactive plant materials. The bioanalytical investigation employed a liquid chromatography-tandem mass spectrometry multicomponent method covering 10 plant-derived substances (atropine, dimethyltryptamine, ephedrine, harmaline, harmine, ibogaine, lysergic acid amide, psilocin, scopolamine, and yohimbine) and a gas chromatography-mass spectrometry method for asarone. Routine testing for illicit drugs was also performed. Over a 4-year period, 103 urine samples collected from mainly young people (age range 13-52 years, median 19) were studied. Among 53 cases where ingestion of any of the 11 plant-derived substances covered in this study was admitted or suspected, 41 (77%) could be confirmed bioanalytically. Nine of the 11 substances tested for were detected, the exceptions being ibogaine and yohimbine. Psilocin, originating from ingestion of hallucinogenic mushrooms, was the most frequent drug accounting for 54% of the cases. The most common means of drug acquisition (56%) was purchase over the Internet. The patients using psychoactive plant materials were mainly young and commonly used the Internet for drug acquisition. Having access to bioanalytical methods for detection of plant-derived psychoactives is therefore considered important, when providing clinical toxicology service.

Fatalities due to mushroom poisonings are increasing worldwide, with more than 90% of deaths resulting from ingestion of amatoxin-containing species. A retrospective evaluation of the history and clinical outcome of each patient treated from 1988 to 2002 in the Toxicological Unit of Careggi General Hospital (University of Florence, Italy) for amatoxin poisoning. Data included the biological parameters monitored, the treatment protocols used (intensive fluid and supportive therapy, restitution of the altered coagulation factors, multiple-dose activated charcoal, mannitol, dexamethasone, glutathione, and penicillin G), and outpatient follow-up evaluations. The clinical data of 111 patients were evaluated; their biological parameters were monitored every 12-24 hours until discharge. Two patients died; both were admitted to the hospital more than 60 hours after mushroom ingestion. Of all the laboratory parameters evaluated, the evolution of hepatic transaminases and prothrombin activity over four days were the most predictive indicators of recovery or death. Our follow-up evaluation of 105 patients demonstrated that our survivors recovered completely. Our experience indicates that the protocol used in our Toxicologicy Unit is effective for amatoxin poisoning, and that all patients treated within 36 hours after mushroom ingestion were cured without sequelae.

Fipronil is a broad-spectrum phenylpyrazole insecticide widely used to control residential pests and is also commonly used for flea and tick treatment on pets. It is a relatively new insecticide and few human toxicity data exist on fipronil. This paper describes the magnitude and characteristics of acute illnesses associated with fipronil exposure. Illness cases associated with exposure to fipronil-containing products from 2001 to 2007 were identified from the Sentinel Event Notification System for Occupational Risks (SENSOR)-Pesticides Program and the California Department of Pesticide Regulation. A total of 103 cases were identified in 11 states. Annual case counts increased from 5 in 2001 to 30 in 2007. Of the cases, 55% were female, the median age was 37 years, and 11% were <15 years old. The majority (76%) had exposure in a private residence, 37% involved the use of pet-care products, and 26% had work-related exposures. Most cases (89%) had mild, temporary health effects. Neurological symptoms (50%) such as headache, dizziness, and paresthesia were the most common, followed by ocular (44%), gastrointestinal (28%), respiratory (27%), and dermal (21%) symptoms/signs. Exposures usually occurred from inadvertent spray/splash/spill of products or inadequate ventilation of the treated area before re-entry. Our findings indicate that exposure to fipronil can pose a risk for mild, temporary health effects in various body systems. Precautionary actions should be reinforced to prevent fipronil exposure to product users.

Introduction: Datura stramonium (DS) (jimsonweed) is well known for its abuse potential for hallucinogenic effects and Datura inoxia (DI) (moonflower) has been abused for similar effects. To our knowledge, only one case report describes rhabdomyolysis in association with DS or DI ingestion. Case identification and details: Patient hospital charts were retrospectively screened from January 1, 2002 to December 31, 2007 to identify patients with qualifying ICD-9 codes for toxic plant ingestions. We report on 11 patient cases of DS/DI ingestions in which serum creatine kinase (CK) concentrations were monitored. These admissions occurred at our hospital over a 6-year period. Serum CK concentrations ranged from 72 to 70,230 U/L. Only three patients had serum CK concentrations greater than 1,000 U/L. One patient with a peak concentration of 70,230 U/L and a positive myoglobinuria was diagnosed with rhabdomyolysis. Discussion: Based on our review of the literature and these cases, it is possible that serum CK concentrations may be elevated more frequently than previously realized. The clinical significance of this abnormal laboratory value is uncertain with the majority of patients remaining asymptomatic without any clinical evidence of rhabdomyolysis.

The presence of exotic, and sometimes venomous, pets in European homes is becoming more common. This phenomenon is the basis of a French-German cooperative evaluation of the species causing the injuries and the circumstances, severity, and treatment of the envenomations A retrospective, descriptive, cross-sectional, case series of data from 1996 to 2006. The study sample consists of all cases of bites and stings by exotic pets that were registered at four poisons European poisons centers. The inclusion criteria were bites and stings of human beings. From 1996 to 2006 four poisons centers in Europe were consulted on 404 bites and stings by exotic pets. The average age of the patients was 36 (2 to 75) years and 73% of the patients were male. The severity of the envenomations, according to the Poisoning Severity Score, was as follows: 29 severe (7.1%), 55 moderate (14.2%) and 320 minor (78.7%). There were no fatalities in this case series. Exotic snakebites from rattlesnakes, cobras, mambas, and other venomous snakes caused 39% of envenomations, aquatic animals (mostly lionfish of the Pterois genus and stingrays) caused 30% of envenomations and arthropods (tarantulas and scorpions) caused 27% of envenomations. All severe envenomations were caused by venomous snakes. European healthcare professionals may encounter patients bitten or stung by exotic pets. Poisons center consultation can help manage these unusual presentations and help obtain rarely used antivenoms.

Background: Lisinopril is an angiotensin converting enzyme inhibitor used for treatment of hypertension, congestive heart failure, and acute myocardial infarction. Reports of clinical experience with pediatric ingestions are minimal. Method: A 13-year retrospective study of lisinopril ingestions in children reported to the California Poison Control System was analyzed and case notes were reviewed. Institutional Review Board approval was obtained and cases were blinded. Inclusion criteria were lisinopril as a single ingestant, age less than 6 years, treatment in a health care facility, case followed to a known outcome. Results: Inclusion criteria were met in 296 cases. Demographics include 51% of male patients and the mean age was 1.97 years (range: 9 months-5 years). Of the 296 patients, 8 patients (2.7%) developed hypotension (ranges: 55-74 mm Hg systolic and 22-48 mm Hg diastolic). The lowest blood pressure of 55/22 mm Hg was recorded in a 22-month old male who ingested an estimated 120-mg lisinopril (13.3 mg/kg). The lowest dose of lisinopril causing hypotension was with an estimated dose of approximately 50 mg or 3.9 mg/kg in a 2-year old. Two hundred and eighty-two patients (95.3%) were treated and released from the emergency department and 14 patients (4.7%) were admitted. The dose ingested was reported in 189 cases and an exact-dose of lisinopril was reported in 61 patients (20.6%); mean amount ingested was 3.0 mg/kg, median amount ingested was 2.1 mg/kg (range: 0.1-10.9 mg/kg, N = 38); and mean total dose was 33.4 mg, median total dose was 20 mg (range: 2.5-160 mg, N = 61). None of the patients with exact-dose lisinopril ingestions developed hypotension, received intravenous fluids, or were admitted. Conclusion: The lowest estimated dose of lisinopril to cause hypotension was 50 mg or 3.9 mg/kg. Although continued evaluation of pediatric lisinopril ingestions is essential to determine more specific thresholds of toxicity, the lack of effect on blood pressure in children with exact-dose ingestions indicate that pediatric lisinopril ingestions (for ages > 9 months) ≤ 4 mg/kg up to 40 mg total may be safely managed at home.

Purpose: To analyze clinical feature and evaluate long-term outcome of patients with thallium poisoning. Materials and methods: An observational series of cases with acute thallium poisoning was analyzed retrospectively in West China Hospital of Sichuan University between 2000 and 2010. The clinical data including symptom, determination of thallium level, treatment, neurophysiological examination, and neuropsychological evaluation were analyzed. The patients were followed up until December 2012. Results: Seven men and six women were enrolled in the study. The median patient age was 37 years (range: 15-53 years). The median duration of hospitalization was 44 days (range: 7-72). All the patients were misdiagnosed initially. One patient died in the hospital. The other 12 patients were followed for a median of 7 years (range: 1-12 years) after discharge from hospital. One patient died from leukemia in the first year of follow-up. Long-term outcome results showed peripheral neuropathy improved substantially. However, many patients have mild or moderate sequelae in sensory nerve fibers of distal lower extremity. A sural nerve biopsy in one patient revealed shrunken axons, distorted myelin sheath, and myelinated fibers loss. During follow-up period, problem of intelligence (4/12 patients, 33%), memory impairment (4/12, 33%), anxiety (6/12, 50%), and depression (5/12, 42%) were demonstrated. Conclusions: Neurological symptoms may lead to misdiagnosis of thallium poisoning. Mild or moderate neurological sequelae may last for a long time after thallium poisoning.

A 14-month-old child was brought to the pediatric emergency unit in the morning, after his parents discovered inflammatory lesion on his left thigh. Three hours later, he was admitted to our unit, his vital signs were normal and his physical examination revealed a round swollen lesion of 7-8 cm in diameter with blisters on the surface and an additional inflammatory reaction of his left thigh ( Figs. 1 and 2 ). The parental interview provides the cause. The child was discharged after the lesion was dressed and a follow-up scheduled.

Fomepizole is the antidote of choice in toxic alcohol poisonings. Potential side effects from frequent use of fomepizole were studied in a patient admitted 154 times with ethylene glycol (EG) poisoning. The intra-individual correlation between the serum-ethylene glycol (serum-EG) and the osmolal gap (OG) EG-kinetics, and other laboratory parameters were also studied. Combined pro- and retrospective collection of material from three different hospitals, and results from autopsy. A 26-year-old female with a dissociative disorder was admitted with EG poisoning a total of 154 times. Her admission data revealed a median pH of 7.31 (range 6.87-7.49), pCO(2): 4.2 kPa (1.2-6.7) (32 mmHg [9-50]), HCO-3: 15 mmol/L (4-26) (15 mEq/L [4-26]), base deficit (BD): 10 mmol/L (- 4 to 27) (10 mEq/L [-4 to 27]), serum-creatinine 65 μmol/L (40-133) (0.74 mg/dL [0.45-1.51]), OG 81 mOsm/kgH(2)O (25-132), and serum-EG 44 mmol/L (4-112) (250 mg/dL [25-700]). She was treated with fomepizole 99 times, ethanol 60 times (with a combination of both six times), and dialysis 73 times. The correlation between serum-EG and OG was good (r(2) = 0.76). She was finally found dead outside hospital with an EG blood concentration of 81 mmol/L (506 mg/dL). An autopsy revealed calcium oxalate crystals in the kidneys, slight liver steatosis, and slight edema of the lungs. The frequent use of fomepizole in this young patient was not associated with any detectable side effects; neither on clinical examination and lab screening, nor on the later autopsy. Regarding the sequelae from the repetitive EG-poisoning episodes, her kidney function seemed to normalize after each overdose. She was treated with buffer and antidote without hemodialysis 81 times without complications, supporting the safety of this approach in selected cases.

Knowledge of methanol toxicity is based on human data from case series and larger outbreaks. In many of these cases, however, diagnosis was not verified by methanol determinations. We present epidemiological and clinical data from one of the largest methanol outbreaks in which all patients had detectable serum methanol levels. Retrospective case series study of hospital and forensic charts from the five hospitals where patients were treated. Of the 147 patients admitted with suspected methanol poisoning, the diagnosis was confirmed in 111, of whom 25 (23 %) died. In addition, 43 patients died outside the hospital, giving a total of 154 patients and a death toll of 68 (44 %). Outcome was related to the degree of metabolic acidosis, serum methanol concentration, coma upon admission, and the patient's ability to hyperventilate. Patients were treated with bicarbonate (85 %), ethanol (87 %), hemodialysis (71 %), and mechanical ventilation (61%) according to clinical features and blood gases, since serum methanol concentrations were analyzed retrospectively. Twenty patients (18 %) survived with permanent sequelae, 18 suffered from impaired vision, and 3 developed permanent brain damage. Given limited resources, triage and use age of tertiary care centers allowed a small community hospital to treat a high number of methanol-poisoned patients. Critical resources were ventilators and dialyzing machines, whereas stores of antidote (ethanol) and bicarbonate were sufficient. Many patients were mechanically ventilated by hand and treated with bicarbonate and ethanol during transport to tertiary care centers for hemodialysis.

Methanol poisoning continues to be a public health problem in Tunisia in spite of the different legislative measures. We report a series of 16 cases of methanol poisoning admitted to our Intensive Care Unit between December 2003 and April 2004. The patients' median age was 21.5 years (range 16 to 53 years) with a median SAPS II of 14 (range 12 to 84) and an APACHE II of 8 (range 6 to 36). The median latent period was 9.5 hours (range 4 to 24 hours) with a delay to medical consultation of 36 hours (range 6 to 48 hours), and a median serum methanol concentration of 1.4 g/L (range 0.19 to 3.62 g/L). Clinical signs included central nervous system symptoms (69%), gastrointestinal complaints (87%), visual disturbances (69%) and metabolic acidosis (94%). Three patients (19%) required mechanical ventilation because of deep coma or shock and died within 6 hours. Hemodialysis was performed in eleven patients (69%) because of visual disturbances and/or metabolic acidosis. One patient developed irreversible bilateral blindness and another unilateral blindness secondary to optic neuropathy. Statistical significant risk factors for the developing of visual disturbances were found to be the ingested quantity of methanol, the latent period, acidosis and serum methanol concentration on admission.

Renal insufficiency is less common than liver failure in acetaminophen overdose but renal tubular damage occurs even in the absence of hepatotoxicity. Data published on this topic are rare consisting mostly of case reports or reports in a small number of patients. Presently, a larger number of patients with renal insufficiency associated with acetaminophen overdose should be analyzed using a multicenter approach. Retrospective analysis of patients with acetaminophen-related nephrotoxicity reported to a poison center network from 1995 to 2003. Renal insufficiency was defined as elevated serum creatinine of more than double of the normal range (>2.4 mg/dL [212 micromol/L]). Patients were classified into 4 groups (A: creatinine 2.4-5.0 mg/dL, B: creatinine>5.0 mg/dL requiring no dialysis, C: creatinine>5.0 mg/dL requiring dialysis, D: creatinine>5.0 mg/dL with fatal outcome). Seventeen patients were included (8 female, 9 male, average age 31.7 +/- 21.1 yrs) with 6 patients in group A (B: 7, C: 2, D: 2). In 5 patients renal insufficiency occurred without elevation of liver enzymes. Regarding possible risk factors 5 patients concomitantly ingested nephrotoxic substances, 4 presented with dehydration due to vomiting, 4 with chronic excessive dosing (overdose) of acetaminophen, 3 showed pre-existing renal insufficiency, 2 pre-existing liver disease and 2 died with multiple organ failure. Renal insufficiency in acetaminophen overdose mostly resolved without dialysis and occurred isolated without hepatotoxicity in less than one-third of the investigated patients. Conditions which might play a role as influencing factors for renal complications included concomitant ingestion of nephrotoxic drugs, dehydration, chronic excessive dosing (overdose) of acetaminophen, pre-existing renal or liver disease and multiple organ failure. Renal function should be monitored in acetaminophen overdose particularly in patients showing the latter comorbidity.

The Twin-Barred Tree Snake, Chrysopelea pelias, is a colubrine that, like other members of the genus Chrysopelea, is able to glide in the arboreal strata. Little is known about the effects of its bite. This report is the first clinically documented bite by this relatively uncommon rear-fanged species. The patient was a 19-year-old female who arrived at the Emergency Department (ED) of an urban teaching hospital 6 h after being bitten by a snake that was later provisionally identified as a C. pelias. Noted on presentation were bite marks on the right middle toe with minimal inflammation and tenderness. There was slight numbness over the dorsum of the right foot and discomforting sensation radiating up the thigh that persisted for several days. There was mild pyrexia, but no evidence of any systemic effects. The full blood count did show neutrophil leucocytosis, and transient hemoglobinuria was noted in an initial urine analysis. The properties of Duvernoy's secretion of C. pelias remain uncharacterized. In this case, the clinical course featured only the local effects noted above. However, the significant local pain reported by the patient suggests that bites by C. pelias are not necessarily trivial and do require full evaluation and observation in a medical facility. Discussed also is the importance of the establishment of a national registry for animal bites and stings in Malaysia. Such a facility could expedite safe and appropriate management of envenomed patients.

An 18-month-old boy ingested a small amount of homemade lavandin extract. The child developed a central nervous system depression and a confused state three hours after ingestion. The electroencephalogram showed fast rhythm disorders consistent with a toxic etiology. The outcome was favorable. Poisoning was confirmed by headspace-gas chromatography-mass spectrometry. Linalyl acetate, linalyl formate, and acetone were identified in pure lavandin extract and in the child's blood and urine. We report the only case of lavandin extract poisoning confirmed by toxicological analysis.

Objective: Thallium toxicity induces cellular injury through impaired Na-K-ATPase activity. The aim of this study was to investigate functional imaging and the long-term clinical-imaging correlations of thallium toxicity. Materials and methods: We measured thallium concentrations in blood, urine, stools, and hair of a 48-year-old woman and a 52-year-old man (patients 1 and 2) in the first 3 months after exposure to thallium containing water, and studied their neuropsychological functions. Using fluorodeoxyglucose positron emission tomography ((18)FDG PET) scans, we examined the brain involvement and correlated the image findings with the clinical presentations. Results: On the 1st, 30th, and 61st days after exposure, the thallium concentrations in patient 1 were 2056, 311, and 7.5 μg/L in the blood, and 11400, 4570, and 36.4 μg/L in the urine. The concentrations in patient 2 were 956, 235, and 15.6 μg/L in the blood, and 11900, 2670, and 101 μg/L in the urine. On the 40th, 50th and 89th days after exposure, the thallium concentration in the stools were 21.6, 3.6, and 0.35 μg/g in patient 1, and 22.2, 3.2, and 0.37 μg/g in patient 2. Executive function, perceptual motor speed, and learning memory were initially abnormal but recovered particularly within the first year. The first (18)FDG PET studies of both patients disclosed a decreased uptake of glucose metabolism in the cingulate gyrus, bilateral frontal, and parietal lobes 2-5 months after exposure. The follow-up (18)FDG PET scan of patient 2 revealed a partial recovery. Conclusion: This study indicates that damage to the central nervous system after acute thallium poisoning may be reversible after a long-term follow-up. Brain (18)FDG PET demonstrated the brain involvement and was correlated with cognitive impairment.

Alcohol intolerance after consumption of wild mushrooms is a recognized phenomenon. This is best understood with Coprinus atramentarius. Its active component Coprine blocks enzymatic ethanol degradation at the stage of acetaldehyde, which is responsible for the well-recognized symptoms. Here, we report three events in five patients experiencing the same symptoms after consumption of self-collected Lepiota aspera. All had mistaken L. aspera for edible mushrooms as Amanita rubescens or Macrolepiota procera. In all events, L. aspera was identified by mycologists and no other mushrooms were involved. The mushrooms were well sautéed and tolerated well until an alcoholic beverage was consumed. Then within few minutes facial flushing, throbbing headache, tachycardia, and shortness of breath all occurred. The symptoms abated within a few hours with no sequelae but could be re-provoked by further alcohol consumption up to 48 h later. This syndrome appears to be identical with the one known from C. atramentarius. However, the toxin in L. aspera or its mechanism is not yet known.

Context: Mulga snakes (Pseudechis australis) are venomous snakes with a wide distribution in Australia. Objective. The objective of this study was to describe mulga snake envenoming and the response of envenoming to antivenom therapy. Materials and methods: Definite mulga bites, based on expert identification or venom-specific enzyme immunoassay, were recruited from the Australian Snakebite Project. Demographics, information about the bite, clinical effects, laboratory investigations and antivenom treatment are recorded for all patients. Blood samples are collected to measure the serum venom concentrations pre- and post-antivenom therapy using enzyme immunoassay. Results: There were 17 patients with definite mulga snake bites. The median age was 37 years (6-70 years); 16 were male and six were snake handlers. Thirteen patients had systemic envenoming with non-specific systemic symptoms (11), anticoagulant coagulopathy (10), myotoxicity (7) and haemolysis (6). Antivenom was given to ten patients; the median dose was one vial (range, one-three vials). Three patients had systemic hypersensitivity reactions post-antivenom. Antivenom reversed the coagulopathy in all cases. Antivenom appeared to prevent myotoxicity in three patients with high venom concentrations, given antivenom within 2 h of the bite. Median peak venom concentration in 12 envenomed patients with samples was 29 ng/mL (range, 0.6-624 ng/mL). There was a good correlation between venom concentrations and the area under the curve of the creatine kinase for patients receiving antivenom after 2 h. Higher venom concentrations were also associated with coagulopathy and haemolysis. Venom was not detected after antivenom administration except in one patient who had a venom concentration of 8.3 ng/ml after one vial of antivenom, but immediate reversal of the coagulopathy. Discussion: Mulga snake envenoming is characterised by myotoxicity, anticoagulant coagulopathy and haemolysis, and has a spectrum of toxicity that is venom dose dependant. This study supports a dose of one vial of antivenom, given as soon as a systemic envenoming is identified, rather than waiting for the development of myotoxicity.

Context: Pyrethroids are synthetic pyrethrin analogues that induce sodium-channel depolarization and hyperexcitation. Severe pyrethroid poisoning is manifested by a "Tremor Syndrome" (Type I cyano-agents) or a "Choreoathetosis/Salivation Syndrome" (Type II non cyano-agents). Very few reports of neurotoxic effects caused by Type I pyrethroids ingestion are available, and no human data concerning Type I pyrethroid blood levels in pediatric poisoning are reported in the medical literature. Case details: A 19-month-old female patient presented with irritability and inconsolable crying that rapidly worsened to tonic-clonic seizures and coma (GCS 6). On admission vital signs including BP 110/70 mmHg, HR 110 beats/min, and SpO2 98% on room air were normal. Orotracheal intubation, oxygen administration, and midazolam infusion (4 μg/kg/min) were performed. Intravenous thiopental sodium, up to 18 mg/kg/hour, was administered to control convulsions. An inquiry revealed that 9 h before presentation the patient had ingested an unknown amount of an insecticide containing 7% piperonyl-butoxide and a mixture of the Type I pyrethroids bifenthrin (5%) and esbiothrin (3%). Consequently, gastric lavage was performed, followed by administration of activated charcoal and cathartics. On the subsequent 48 h, the patient returned progressively alert; she was extubated on day 4 and discharged asymptomatically 12 days after hospitalization. After 9, 48, and 72 h of ingestion, the plasma levels were 500, 95, and 40 ng/mL for bifenthrin and 1,640, 640, and 165 ng/mL for piperonyl-butoxide respectively. Discussion: This pediatric case showed severe pyrethroid neurotoxicity associated with measurable plasma levels of bifenthrin and piperonyl-butoxide. In pediatric pyrethroid poisoning, coma and seizures may represent the main life-threatening features. First-aid therapy including airway maintenance and control of muscle fasciculation and seizures is of major importance. Benzodiazepines and high-dose thiopental sodium were effective treatments for convulsion.

Botulism was believed to be a rare disease in both the US and UK in the 1920's, until two deadly outbreaks altered that view and launched public health measures to control it. In the United States, the ripe olive scare of 1920 found glass-packaged olives linked to multiple deaths. In the United Kingdom, eight deaths from glass-potted duck paste, in the summer of 1922 at Loch Maree, Scotland will always be associated with botulism.

Although steroids are usually withheld in grades I and III esophageal burns, controversy continues regarding their use in grade II burns. Two analyses, including data from 1956-1991 and 1991-2003, respectively, disagreed in their therapeutic recommendations. Our objective is to re-evaluate the usefulness of steroids in grade II burns. The two previous analyses and their references were reviewed. Medline was searched for additional recent human reports. Inclusion criteria were endoscopically documented grade II burns and at least ten days of steroids or no steroids. Pooled data were evaluated by X(2) test with alpha set at 0.05. Prior analyses identified 12 studies, and one additional study was found during the literature search for a total of 328 patients. 30/244 patients receiving steroids and 16/84 patients who did not receive steroids developed strictures, respectively. This difference was not statistically significant. Heterogeneity of the data prevented formal metanalysis. Although methodologically limited, the existing data fail to support the use of steroids in patients with caustic-induced grade II esophageal burns.

Context: Unintentional carbon monoxide poisoning remains a significant cause of morbidity and mortality in England and Wales. METHODS. Study design: observational case series. Data on fatal carbon monoxide poisoning in England and Wales from 1979 to 2012 were obtained from coroner reports. Data on unintentional non-fire-related carbon monoxide poisoning were extracted and were analysed by year of registration of death, sex, age group, and whether death occurred at a private house, flat, associated garage, or residential caravan ('home'), or elsewhere. Results and discussion: There were 28,944 carbon monoxide-related deaths, of which 82% were male. Deaths increased from 965 (1979) to 1700 (1987), and then fell to 182 (2012). Of these 2208 (64% male) were recorded as unintentional non-fire-related deaths. Annual numbers of these latter deaths fell from 166 in 1979 to 25 in 2012 (i.e. from 3.37 to 0.44 per million population). Some 81 and 92% of such deaths in males and in females, respectively, occurred at 'home'. A clear preponderance of male versus female deaths was seen in the 10-19, 20-39 and 40-64 years age groups, with similar numbers of deaths in males and in females in the younger (< 1 and 1-9 year) and higher (65-79 and 80 + years) age groups. A higher proportion of these excess deaths in males occurred outside the deceased's 'home' in those aged 10-19, 20-39 and 40-64 years. Conclusion: Deaths from unintentional non-fire-related carbon monoxide poisoning are now much less common in England and Wales than in earlier years, but remain a cause for concern. Installation and proper maintenance of carbon monoxide alarms in dwellings and outhouses, for example, and education not only of the public, but also of health and other professionals as to the danger posed by carbon monoxide could help prevent such deaths.

Bites from reptiles cause thousands of injuries but fortunately few deaths in the U.S. each year. This article reviews deaths from reptile bites over the last 25 years. Mortality data was obtained using CDC WONDER to evaluate deaths that occurred from 1979 to 2004 due to reptile bites. Information on race, gender, ages, and state where death occurred is reported. There were 134 deaths reported over this 25-year time period. Whites were 93.3% of the victims, and males were 79.1% of the victims. The age group reporting the most deaths was the 25 to 34 year old category. There were 17 (12.7%) victims less than 15 years of age, and 25 (18.7%) victims older than 65 years of age. Seventy-five of the fatalities (55.9%) occurred in five states. An average of five deaths occurs from reptile bites each year in the U.S. White males living in the Southern part of the United States are more likely to be the victim of a fatal reptile envenomation.

Poisonings with rodenticides containing hydrogen phosphide-releasing compounds may lead to deleterious organ dysfunction and death. Since data of hydrogen phosphide poisonings is limited to case reports/series, this study was intended to elucidate hydrogen phosphide poisonings based on a 20-year data collection. Explorative data analysis of the Poison Center Mainz database looking for route of exposure, symptoms, and severity using the Poisoning Severity Score. From 1983-2003, 188 hydrogen phosphide poisonings were reported. Sixty-five percent of these were unintentional residential, 28% attempts to commit suicide (intentional), 5% occupational, and 2% undetermined. In the majority of intentional poisonings the poison was ingested, whereas in unintentional poisoning of adults inhalation exposure dominated, caused by inappropriate self-protection from the released hydrogen phosphide gas during usage. Frequently observed symptoms in unintentional poisonings were nausea, vomiting, pain, coughing, and dizziness with no further worsening of symptoms. In intentional poisonings frequent symptoms were vomiting, somnolence, seizures, coma, and shock with two initially fatal poisonings. Follow-up on these cases showed a significant worsening of symptoms and a two-fold increase in fatal poisonings. Route of exposure, severity of symptoms, and the necessary treatment differs substantially between unintentional and intentional poisonings. In this study, two initially symptomatic intentional poisonings were later reported fatal. Careful monitoring is recommended in symptomatic intentional poisonings.

The only U.S. Food and Drug Administration-approved coral snake antivenom was officially discontinued in 2007, causing ever-diminishing supplies. This study describes the severity of U.S. coral snakebites during the last 25 years to determine trends in annual rates of these bites' medical outcomes. This study retrospectively analyzed all human coral snakebites voluntarily reported by the public and/or health care professionals to poison centers that were subsequently published in the Annual Reports of the American Association of Poison Control Centers (AAPCC) from 1983 through 2007. Annual rates of medical outcomes from coral snakebites were calculated by dividing the annual number of people bitten by coral snakes who developed fatal, major, moderate, minor, or no effect outcomes by the total annual number of people bitten by coral snakes. Negative binomial regression was used to examine trends in annual rates. From 1983 through 2007, the incidence rate of coral snakebites producing no effects significantly decreased by 4.7% per year [incidence rate ratio (IRR) = 0.953; 95% confidence interval (CI) = 0.920-0.987]. From 1985 through 2007, the incidence rates of minor and major outcomes did not significantly change; however, moderate outcomes significantly increased by 3.4% per year (IRR = 1.034; 95% CI = 1.004-1.064). No fatalities were reported from 1983 through 2007. Annual rates of coral snakebites producing no effects significantly decreased and those producing moderate outcomes significantly increased in our analyses of data from the last 25 years of published AAPCC Annual Reports. This study has important limitations that must be considered when interpreting these conclusions.

Glyphosate-surfactant herbicide (GlySH) is widely used in agriculture and has been associated with numerous toxicities following oral ingestion. However, there are many controversies with regard to the exact causes and determinants of developing severe/death outcome after exposure to GlySH. We conducted an analysis of all GlySH exposures reported to the Taiwan National Poison Control Center between 1986 and 2007. Patients' baseline characteristics and clinical data were reviewed and analyzed. A total of 2,186 patients were eligible for analysis. Most of the exposures were related to oral ingestion (n = 2,023, 92.5%) and attempted suicide (n = 1,631, 74.6%). The mean age of exposure was 42.8 +/- 18.6 years. One hundred patients developed severe effects and 146 patients died following oral GlySH exposure, resulting in a case fatality rate of 7.2%. Shock (n = 85, 58.2%) and respiratory failure (n = 34, 23.3%) accounted for most fatalities. Four out of eight patients with injection exposure manifested severe (n = 3) or fatal outcome (n = 1). In a multivariate logistic regression analysis, increasing age, larger amount of exposure, longer elapsed time to presentation, attempted suicide, receipt of atropine therapy, and being exposed in certain calendar years were positively associated with the severity of poisoning following oral GlySH exposure. Age, ingested amount, delayed presentation, and reason for exposure were likely to be determinants of the severity of GlySH exposure. Because shock is the major cause of death and usually develops early after GlySH exposure, prompt fluid replacement therapy seems critical in the initial management of such exposures. Patients' airway should also be secured to avoid aspiration and subsequent respiratory failure.

Context: Gathering information on the circumstances that give rise to unintentional domestic non-fire related carbon monoxide poisoning and the associated morbidity and mortality is not straightforward because the diagnosis is so often missed in life. Methods: We searched Newsbank and related databases (at least 332 sources, UK and Republic of Ireland) for reports of domestic carbon monoxide poisoning, 1986-end 2011 inclusive. The search terms were 'carbon monoxide AND (house* OR home* OR caravan* OR tent*) NOT (work OR fire OR suicide*)'. Newsbank includes full-text articles from 19 UK national newspapers and over 140 UK & Irish regional and local newspapers and periodicals. Results and discussion: There were reports of 348 incidents (880 victims: 334 male, 352 female, 194 sex not stated). Reports of incidents increased from 1986 (1) to 2011 (28). There were 298 deaths (169 male, 124 female, 5 sex not reported). The likelihood of a fatal outcome increased with age for both males and females (28%, 1-9 years; 71%, 80 + years). The source of carbon monoxide was often a central heating or water boiler (48% of 244 incidents). Many incidents (49%) occurred in private dwellings. However, incidents in caravans, tents, sheds and outhouses had a much higher death rate. If a victim was discovered alive chances of survival were relatively good (87%), even if found unconscious. The estimated duration of carbon monoxide exposure ranged from minutes to years in both fatal and non-fatal incidents. Pets were recorded in 31 incidents (17 died). In 5 cases, carbon monoxide poisoning was identified through illness or death of a pet. Prosecutions were recorded in 49 incidents and at least 7 custodial (prison) sentences resulted, with 34 further convictions resulting in a fine. Charges were preferred against either an installer/maintenance engineer (42%), or the landlord (31%). Conclusion: Deaths and permanent injuries from unintentional domestic non-fire related carbon monoxide poisoning continue. Survival rates are relatively high if poisoning is diagnosed in life, but warning signs are often missed and inappropriate behavior such as placing barbecues in tents and failure to perform proper safety checks by gas appliance fitters still kills.

Pesticide self-poisoning accounts for one-third of suicides worldwide, but few studies have investigated the national epidemiology of pesticide suicide in countries where it is a commonly used method. We investigated trends in pesticide suicide, and factors associated with such trends, in Taiwan, a rapidly developing East Asian country. We conducted an ecological study using graphical approaches and Spearman's correlation coefficients to examine trends in pesticide suicide (1987-2010) in Taiwan in relation to pesticide sales, bans on selected pesticides, the proportion of the workforce involved in agriculture and unemployment. We compared pesticide products banned by the Taiwanese government with products that remained on the market and pesticides that accounted for the most poisoning deaths in Taiwan. Age-standardised rates of pesticide suicide showed a 67% reduction from 7.7 per 100,000 (42% of all suicides) in 1987 to 2.5 per 100,000 (12% of all suicides) in 2010, in contrast to a 69% increase in suicide rates by other methods. Pesticide poisoning was the most commonly used method of suicide in 1987 but had become the third most common method by 2010. The reduction was paralleled by a 66% fall in the workforce involved in agriculture but there was no strong evidence for its association with trends in pesticide sales, bans on selected pesticide products or unemployment. The bans mostly post-dated the decline in pesticide suicides; furthermore, they did not include products (e.g. paraquat) that accounted for most deaths and were mainly restricted to selected high-strength formulated products whilst their equivalent low-strength products were not banned. Access to pesticides, indicated by the size of agricultural workforce, appears to influence trends in pesticide suicide in Taiwan. Targeted bans on pesticides should focus on those products that account for most deaths.

Ephedra is a botanical product widely used to enhance alertness, as a weight loss aide, and as a decongestant. Its reported adverse effects led the Food and Drug Administration (FDA) to ban ephedra-containing products in the United States in 2004. This study's purpose was to compare toxicity from botanical products containing ephedra to nonephedra products. The Toxic Exposure Surveillance System (TESS), a national poison center database, was utilized to determine the number and outcomes of cases involving botanical products reported from 1993-2002. Cases listing both a botanical product and any other drugs or chemicals were excluded a priori. Ten-year hazard rates (moderate outcomes + major outcomes + deaths per 1000 exposures) were used to compare botanical product categories. There were 21,533 toxic exposures with definitive medical outcomes reported over the 10 yrs where a botanical product was the only substance involved. Of these, 4306 (19.9%) had moderate or major medical outcomes and there were two deaths, for an overall hazard score of 200 per 1000 exposures. The number of ephedra reports to poison centers increased 150-fold over the 10-yr period. The hazard rate for products that contained only ephedra was 250 per 1000 exposures and 267 per 1000 exposures for products that contained ephedra and additional ingredients; whereas the hazard score for only nonephedra botanical products was 96 per 1000 exposures. The rate ratios for multibotanical products with ephedra (RR 1.33; 95% C.I. 1.27-1.40) and for single-ingredient ephedra products (RR 1.25; 95% C.I. 1.11-1.40) were both two to six times higher than those of other common botanical products. Yohimbe-containing products had the highest hazard score (417) and rate ratio (2.08; 95% C.I. 1.59-2.80). Ephedra-containing botanical products accounted for a significant number of toxic exposures with severe medical outcomes reported to poison centers. Hazard rate analysis suggests poison center-reported events involving ephedra-containing botanical products were much more likely to result in severe medical outcomes than those involving nonephedra-containing botanical products. These data support recommendations by policymakers that the sale of ephedra should be prohibited to protect consumers. Our data suggest that the botanical product, yohimbe, may also be associated with unacceptably high risks of toxicity and should receive close scrutiny from health policymakers.

To determine current trends in the use of gastric decontamination for the emergency department (ED) treatment of overdose patients. In the National Health Ambulatory Medical Care Survey (NHAMCS), a weighted sampling of U.S. EDs, overdose-related visits were examined using ICD-9 CM E codes and NHAMCS' "reason-for-visit" classification. From 1993 to 2003 there were an estimated 11.68 million ED-treated poisoning events. Some 13.7% of those treated were lavaged. Rates fell significantly, from an annual average of 18.7% of cases during 1993-97 to 10.3% during 1998-2003 (p < 0.001). Controlling for year, urgency, and admission status in multivariate logistic modeling, lavage was significantly and positively associated with private insurance payor status, younger age (<30), female gender, white race, 8 PM-8 AM presentation, and intentional rather than unintentional overdose. ED use of gastric lavage in poisoned patients has decreased significantly over the past decade but varies by demographic and non-clinical factors.

Trends in rates of unintentional pesticide illnesses and injuries by type were estimated for the United States from 1995 to 2004. Poison Control Center data were examined for the years 1995 through 2004. Rates were calculated for pesticide type and selected pesticide classes based on estimated total United States population and proportion of population served. Pesticides as a proportion of poisonings to all substances over the years and vital statistics on deaths were examined to validate trends. Incidence rates of serious pesticide poisonings and injuries have declined 42% from 1995 to 2004 and death rates declined 62% over the same period. Selected, more toxic pesticides such as organophosphate and carbamate insecticides, strychnine rodenticides, and paraquat herbicides have shown greater declines, ranging 63% to 79%. Pesticide poisonings and injuries appear to have declined in the past decade.

Non-native (exotic) snake exposures in the United States have not been systematically characterized. The Toxic Exposure Surveillance System (TESS) database of the American Association of Poison Control Centers was analyzed to quantify the number and types, demographic associations, clinical presentations, managements and outcomes, and the health resource utilization of non-native snake exposures. From 1995 through 2004, there were 399 non-native exposures in the TESS database. Of these, 350 snakes (87%) were identified by genus and species, comprising at least 77 different varieties. Roughly equal percentages of snakes originated in Asia, Africa and Latin America, with a smaller number from the Middle-East, Australia, and Europe. Nearly half were viperids and a little more than a third were elapids. The vast majority of exposed individuals were adults. However, almost 15% were aged 17 years or less, and almost 7% were children aged 5 years or younger. Eighty-four percent were males. The vast majority of exposures occurred at the victim's own residence. Over 50% were evaluated at a healthcare facility, with 28.7% admitted to an ICU. Overall, 26% of patients were coded as receiving antivenom treatment. Coded outcomes were similar between viperid and elapid envenomations. There were three deaths, two involving viperid snakes and one elapid. Enhancements to the TESS database are required for better precision in and more complete characterization of non-native snake envenomations.

Acute poisonings are frequent causes of admission to emergency departments and these cases may have hazardous outcomes. In the present study, medical records of 1818 poisoned patients admitted to Uludag University Medical School's Emergency Department between January 1996 and December 2001 were investigated. The age, sex, outcomes of the patients, and type of poisoning are described. . The mean age for females (63% of the patients) was 27 years, whilst the mean age of male patients was 31 years. The major types of poisonings were ingestions of medications (59.6%), mushrooms (3.3%), corrosives (2.5%), organophosphates (3.2%), and methyl alcohol (0.4%). Carbon monoxide accounted for 6.9% of intoxications. Approximately 65% of the patients survived, while the methyl alcohol and corrosive ingestions led to the highest fatality averages (100% and 14.8%, respectively). The demographic and diagnostic features of acute poisoning cases treated in our hospital are similar to those reported in the literature. Adults and women are in a high-risk group for acute poisonings and medicine poisoning, which is the most common type of poisoning.

Context: The risk of toxicity from exposure to ergot alkaloid-containing medications in children is uncertain. Due to the alarming historical experience with severe toxicity and the syndrome of ergotism from natural and synthetic ergot alkaloids, triage recommendations for pediatric exposures to medicinal agents containing ergot alkaloids may be inappropriate and inconsistent. Objectives: The goal of this study was to describe the clinical effects of unintentional ergot alkaloid exposures in children and to identify the need for hospitalization in these cases. Methods: This was a retrospective cohort study of all pediatric (< 7 years old) ergot alkaloid exposures reported to the California Poison Control System (CPCS) from 1997 to 2008. Case narratives were reviewed and assessed for patient demographics, ergot alkaloid agent and dose, route of and reason for exposure, symptoms, therapy, hospitalization period, and final outcome. Results: Of the 374 cases, 353 met the inclusion criteria. The median age was 24 months (Range: 7-72 months) with more than 99% oral route of exposure. The most frequent clinical effect was gastrointestinal distress (16%), followed by lethargy (5%). Two cases with significant vascular and CNS symptoms were identified, both with complete recovery. For symptomatic patients, all symptoms were there at time of initial presentation. The majority, 62%, of all patients were treated in the hospital setting. The median length of hospital stay was 4 h (Range: 1-36 h). Ergot exposures had a similar number of serious outcomes (moderate or worse effects) compared to all other pediatric poisonings reported to the CPCS during the study period (odds ratio [OR], 0.98; 95% confidence interval [CI], 0.25-3.95), but were associated with a disproportionately higher number of hospitalizations (OR, 13.8; 95% CI, 11.1-17.1). Conclusions: Pediatric ergot exposures were associated with few transient adverse effects but multiple hospitalizations. Rare cases of significant toxicity associated with methylergonovine exposures were found. Current poison control send-in protocols and emergency department (ED) guidelines should consider home management and short ED stays as opposed to lengthy critical care bed admissions.

Each year, 80,000 to 100,000 calls to the Poison Information Centres (PIC) concern pediatric exposures in Germany. Plant exposures are the fourth most common category, accounting for 22% of pediatric exposures. Information on plant exposures in children (0-14 years) was collected from annual reports of German PIC. The severity of pediatric plant exposures was classified using the number of ingestions and a calculated hazard factor. A total of 58,641 cases involving 248 different plant genera were reported from 1998 to 2004. Most plant exposures were not associated with clinical effects at time of call, but 9.6% of cases had noticeable effects, including 0.4% classified as moderate and major effect. The majority of plant genera have low hazard factors. Most severe poisoning (highest hazard factors and exposures) in children involved Brugmansia, Laburnum, Phaseolus, and Thuja.

Information on the management of potentially adverse exposures to clopidogrel is limited. This study examined the distribution of 582 clopidogrel exposures reported to Texas poison control centers during 1998-2004. Eighty-four percent of cases with a reported dose having a dose < or = 150 mg. Management of 65% of the exposures occurred on site. Of those exposures with a final medical outcome, 73% were classified as no effect. Of those exposures to clopidogrel alone, the most frequent adverse clinical effects were vomiting (2.4%) and dizziness (2.4%). The most frequent treatments were decontamination by dilution (30%), food (12%), and activated charcoal (7%). In the majority of potentially adverse clopidogrel exposures reported to poison control centers the doses are twice the recommended dosage or less. The outcome of such exposures are generally favorable, with few adverse clinical effects occurring.

To explore the circumstances associated with hospital admission of adults of working age for accidental pesticide poisoning in England. From Hospital Episode Statistics we identified all adults aged 16-69 years who completed hospital admissions nationally for accidental pesticide poisoning during April 1998 to March 2003. Further information was obtained through a postal questionnaire completed by the treating consultant. Questionnaires were returned for 62% of 237 identified admissions, including 89 in which definite or possible accidental pesticide poisoning was confirmed. Fifty-four percent of episodes arose from an identifiable mishap, and 26% from unsatisfactory storage or transport of pesticides. Only two incidents resulted from exposure to spray drift. Three patients needed intensive care, but none died. Serious accidental pesticide poisoning is rare among adults in England. There is an important contribution from poor storage of pesticides. Non-occupational acute poisoning by spray drift is seldom if ever a cause of hospital admission.

The use of complementary and alternative medicine (CAM), particularly herbal medicine and their derived products, have been increasing. However, sporadic reports of serious adverse effects associated with the use of these products have become a source of concern. Spontaneous adverse event reporting may be used to monitor the safety of these products. The objectives of this study is to analyze and describe the patterns of adverse events associated with the use of Chinese Proprietary Medicine, other complementary medicine and health supplements (termed CAM products) in the Singapore Pharmacovigilance database from 1998 to 2009 and to highlight areas of safety concerns. Adverse events associated with CAM products reviewed by the Vigilance Branch of the Health Sciences Authority for the period 1998-2009 were collated and analyzed. The following information was extracted and collated: patient demographics, type and indication of CAM products, system-organ class affected, seriousness of the adverse event, route of administration, hospitalization status, outcome of adverse event, concomitant use of conventional medicine, adulterant testing and profession of the reporter. In the period 1998-2009, 627 cases of adverse events due to CAM products were reported. Most of these 627 cases (80.2%) were found to be serious and most of the patients used CAM products for sexual performance enhancement (291, 46.4%), to relieve pain such as joint and neck pain (36, 5.9%) and for slimming purposes (27, 4.3%). Of the 627 cases, endocrine disorders constituted 22.5% and central nervous system disorders constituted 20.6%. Liver was the main organ involved in the serious cases. Twenty-two fatalities were reported and hepatotoxicity was responsible for the deaths of 10 patients during the study period. In conclusion, 627 adverse event reports associated with CAM products had been successfully analyzed and described. They constituted ~3.8% of the total number of adverse events reported from 1998 to 2009. Outbreaks of severe hypoglycemia in 2008 and 2009 were associated with the use of adulterated and illegal sexual performance enhancement products. Further work to confirm the hepatotoxicity of implicated CAM products is warranted. Reporting of suspected adverse events is strongly encouraged even if the causality is not confirmed because any signs of clustering will allow rapid regulatory actions to be taken. The analysis of spontaneously reported adverse events is important in monitoring the safety of CAM products and helps in the understanding of the benefits and risks associated with the use of such products.

Homicidal poisoning is an intriguing but poorly described phenomenon. This study describes homicidal poisoning deaths in the United States during 1999-2005. A trend analysis of homicidal poisoning death was performed using Vital Statistics data. The National Mortality Statistics database was queried using "homicide" as injury intent and "poisoning" as mechanism for the years 1999-2005. Counts and rates were obtained for subgrouping by using demographic data and ICD-10 codes. Chi-square analysis calculated subgroup odds ratios (OR) and 95% confidence intervals (CI). A total of 523 homicidal poisoning deaths were identified. The overall rate for the period was 0.26/million/year. Males were significantly (OR 1.34, CI 1.13-1.59) more likely to victims than females. Death was more likely at extremes of age. Rates were 2.05/million (OR 8.72, CI 6.63-11.49) in children <1 year and 0.56/million (OR 2.20, CI 1.38-3.52) at ages >or=85 years. Rates also varied by race and were more common among Blacks (0.43/million; OR 1.83, CI 1.47-2.26). The greatest rate was observed in Black infants (5.3/million; OR 21.34, CI 14.17-32.15). ICD-10 codes indicated that medications were the most common poison. Rates were significantly higher in the West and lower in the Northeast. The overall homicidal poisoning death rate was low between 1999 and 2005. The most common type of poison used was medications. Substantially higher rates were observed in vulnerable populations at extremes of age, particularly infants, and among Blacks. This challenges common notions of the victims of homicidal poisoning and the underlying motivation of their poisoners.