Journal of toxicology. Clinical toxicology最新文献

{"title":"Toxicity following unintentional DDT ingestion.","authors":"D Niyazi Ozucelik,&nbsp;Ozgur Karcioglu,&nbsp;Hakan Topacoglu,&nbsp;John R Fowler","doi":"10.1081/clt-120037432","DOIUrl":"https://doi.org/10.1081/clt-120037432","url":null,"abstract":"<p><strong>Introduction: </strong>Dichlorodiphenyltrichloroethane (DDT) ingestion is an uncommon cause of poisoning worldwide. To date, no cases of renal impairment after oral intake of DDT in humans have been reported. We describe the clinical course and management of two patients presenting after DDT ingestion, one of whom developed acute oliguric renal failure.</p><p><strong>Case report: </strong>A father and son mistook DDT powder for flour while preparing fish for a meal, and after eating they developed symptoms compatible with acute organochlorine insecticide poisoning. Both were intubated endotracheally due to recurrent convulsions and loss of consciousness followed by admission to the intensive care unit. Both cases developed severe metabolic acidosis. Acute oliguric renal failure (ARF) was diagnosed in the son in the second day, with a blood urea nitrogen level of 47 mg/dl and creatinine 6.4 mg/dl. Urinalysis disclosed abundant RBCs on the third day. Vigorous fluid resuscitation and strict monitoring helped reverse its clinical course by the tenth day. Both patients recovered within two weeks and were discharged without sequelae.</p><p><strong>Conclusion: </strong>Clinicians should not overlook the possibility of DDT poisoning in the differential diagnosis of acute renal failure and seizures. More strict measures should be taken to prohibit misidentification of DDT and similar products, particularly in the developing world.</p>","PeriodicalId":17447,"journal":{"name":"Journal of toxicology. Clinical toxicology","volume":"42 3","pages":"299-303"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1081/clt-120037432","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24678091","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Skin toxicity from glyphosate-surfactant formulation.","authors":"Paolo Amerio, Angela Motta, Paola Toto, Saman Mohammad Pour, Reza Pajand, Claudio Feliciani, Antonello Tulli","doi":"10.1081/clt-120038769","DOIUrl":"10.1081/clt-120038769","url":null,"abstract":"<p><p>Glyphosate (N-[phosphonomethyl]glycine) is a nonselective herbicide used in agriculture as a foliage spray for the control and the destruction of herbaceous plants. Adverse skin reactions due to contact with this compound have been rarely described. We report a case of a 78-year-old woman presenting with extensive chemical burns on her trunk and legs caused by accidental contact with a glyphosate-surfactant formulation. The lesions healed in four weeks without scarring.</p>","PeriodicalId":17447,"journal":{"name":"Journal of toxicology. Clinical toxicology","volume":"42 3","pages":"317-9"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1081/clt-120038769","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24678095","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Acute poisoning with emamectin benzoate.","authors":"Tzung-Hai Yen,&nbsp;Ja-Liang Lin","doi":"10.1081/clt-200026968","DOIUrl":"https://doi.org/10.1081/clt-200026968","url":null,"abstract":"<p><strong>Background: </strong>Emamectin benzoate is the 4'-deoxy-4'-epi-methyl-amino benzoate salt of avermectin B1 (abamectin), which is similar structurally to natural fermentation products of Streptomyces avermitilis. Emamectin benzoate is being developed as a newer broad-spectrum insecticide for vegetables and has a very low application rate. The mechanism of action involves stimulation of high-affinity GABA receptors and a consequent increase in membrane chloride ion permeability. Animal studies indicate a wide margin of safety because mammalian species are much less sensitive due to lower GABA receptor affinities and relative impermeability of the blood-brain barrier. Notably, the literature has not reported human exposure resulting in toxicity.</p><p><strong>Case report: </strong>This paper describes a case of acute poisoning with Proclaim insecticide (Syngenta, Taiwan), consisting of 2.15% w/w emamectin benzoate in 2, 6-bis (1, 1-dimethylethyl)-4-methyl-phenol and 1-hexanol. The clinical manifestation was transient gastrointestinal upset with endoscopy-proven gastric erosion and superficial gastritis, mild central nervous system depression, and aspiration pneumonia. No specific antidote exists for emamectin benzoate intoxication; this patient was treated successfully with gastric lavage, administration of activated charcoal, and empiric antibiotics. Drugs that enhance GABA activity such as barbiturates and benzodiazepines were avoided.</p>","PeriodicalId":17447,"journal":{"name":"Journal of toxicology. Clinical toxicology","volume":"42 5","pages":"657-61"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1081/clt-200026968","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40901026","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Near‐Fatal Overdose of Carisoprodol (SOMA): Case Report","authors":"M. Siddiqi, C. Jennings","doi":"10.1081/CLT-120030952","DOIUrl":"https://doi.org/10.1081/CLT-120030952","url":null,"abstract":"Carisoprodol is a centrally acting skeletal muscle relaxant, structurally and pharmacologically related to meprobamate (1). It was first introduced in the 1950s for the relief of back pain and muscle spasms. Carisoprodol is metabolized to meprobamate, a potent and addictive sedative. Carisoprodol also has weak anticholinergic, antipyretic, and analgesic properties (2,3). Poisoning with carisoprodol is reported infrequently. Following ingestion of a large dose, death is attributed to CNS depression with respiratory failure. Ingestion of 3.5 g of carisoprodol has resulted in the death of a 4-year-old (4). Seizures and coma persisting for 33h (5) followed ingestion of up to 14.7 g of carisoprodol in an adult, whereas ingestion of 9.45 g has resulted in milder CNS effects (2). We report a 40-year-old white male who ingested 21 g (60 tablets) of carisoprodol along with an unknown quantity of chlordiazepoxide and temazepam. This case is worth reporting because it illustrates one of the highest-reported blood levels of carisoprodol. The patient was found unresponsive by the paramedics at a video store, where he underwent emergent endotracheal intubation and received artificial ventilation. On arrival to the Emergency Department, he was unresponsive to painful stimuli. He had a HR of 130 bpm, BP 220/118 mm HG, a temperature of 100.5 F, and was manually ventilated. The patient also demonstrated anticholinergic signs. Pupils were symmetric, dilated, and sluggishly reactive to light. Breath sounds were coarse with rales on the right side. Abdominal exam revealed absent bowel sounds as often seen in an anticholinergic toxidrome. He was deeply comatose, with absent tendon and plantar reflexes. His skin was warm and dry. The patient had a past medical history significant for psychiatric illness, substance abuse, chronic back pain, and hypertension. Initial blood gas analysis revealed a mild respiratory acidosis with a ph of 7.31 and a pCO2 of 50.1 mmHg (partially compensated with artificial ventilation). Other baseline labs were normal. The toxicology urine immunoassay was positive for cocaine metabolites and benzodiazepines. Chest radiographs showed a right upper lobe infiltrate. EKG revealed sinus tachycardia with a prolonged QT interval (exact measurements no longer available) mimicking a possible tricyclic overdose. In view of the possibility of multiple-drug ingestion and since he presented to the ER within an hour after his ingestion, the treatment in the emergency department consisted of gastric lavage and activated charcoal with sorbitol. Naloxone was used as part of the coma cocktail, and sodium bicarbonate was used to reverse cardiac toxicity from a tricyclic antidepressant. The use of flumazenil to reverse the possible benzodiazepine component of his presentation was considered ill-advised as the patient was on chronic benzodiazepine therapy, thus increasing the risk of withdrawal seizures. Intravenous clindamycin was initiated for aspiration pneumo","PeriodicalId":17447,"journal":{"name":"Journal of toxicology. Clinical toxicology","volume":"101 1","pages":"239 - 240"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75858371","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Treatment of severe pediatric ethylene glycol intoxication without hemodialysis.","authors":"E Martin Caravati,&nbsp;Heather L Heileson,&nbsp;Michael Jones","doi":"10.1081/clt-120037424","DOIUrl":"https://doi.org/10.1081/clt-120037424","url":null,"abstract":"<p><strong>Background: </strong>There is limited experience treating severe ethylene glycol poisoning in children without hemodialysis. The objective of this study was to describe the clinical course and outcome of severe pediatric ethylene glycol poisoning treated without hemodialysis.</p><p><strong>Methods: </strong>Patient records were identified retrospectively by hospital discharge diagnosis (ICD-9 code) of ethylene glycol poisoning from 1999 through 2002 at a pediatric medial center. Patients with initial serum ethylene glycol concentrations less than 50 mg/dL or those who received hemodialysis were excluded.</p><p><strong>Results: </strong>Six patients with an age range of 22 months to 14 years were admitted for treatment of ethylene glycol poisoning over a four-year period. Initial serum ethylene glycol concentrations ranged from 62 to 304 mg/dL (mean 174.0 mg/dL). The lowest-measured individual serum bicarbonates ranged from 4 to 17 mEq/L. All patients were initially admitted to intensive care. One patient received ethanol only, two patients received fomepizole only, and three patients received a loading dose of ethanol and then were converted to fomepizole therapy. None of the patients received hemodialysis. Treatment was continued until the serum ethylene glycol was less than 10 mg/dL. Metabolic acidosis resolved with intravenous fluid and supplemental bicarbonate within 24h. All patients had a normal creatinine upon presentation and at discharge. The mean length of stay in intensive care was 21h and on the ward was 33.7h. One episode of hypoglycemia occurred in a 22-month-old. All patients recovered without evidence of renal insufficiency or other major complications at discharge.</p><p><strong>Conclusion: </strong>Six pediatric patients with severe ethylene glycol intoxication and normal renal function were successfully treated without hemodialysis.</p>","PeriodicalId":17447,"journal":{"name":"Journal of toxicology. Clinical toxicology","volume":"42 3","pages":"255-9"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1081/clt-120037424","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24677034","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oral sumatriptan-induced myocardial infarction.","authors":"Jason B Hack","doi":"10.1081/clt-120037434","DOIUrl":"https://doi.org/10.1081/clt-120037434","url":null,"abstract":"<p><strong>Background: </strong>Sumatriptan has been used in the treatment of migraine and other vascular headaches since 1993 in the United States. Its side effects include chest pains in 3% to 8% of patients who have known cardiac risk factors. This is a case report of a 45-year-old woman with no history of cardiac risk factors who had a myocardial infarction after her monthly dose of oral sumatriptan.</p><p><strong>Methods: </strong>The patient was examined in the emergency room, evaluated by electrocardiography, and serial evaluations of cardiac enzymes over the next 24 h. She was admitted to the cardiology ward. A cardiac catherization and additional laboratory studies were performed the following day.</p><p><strong>Results: </strong>The catherization revealed normal heart function, but a 60% to 70% non-flowing stenosis within the first septal perforator. Laboratory indices for cardiac risk were within normal ranges.</p><p><strong>Conclusions: </strong>Patients without cardiac risk factors may experience myocardial infarction following an oral dose of sumatriptan.</p>","PeriodicalId":17447,"journal":{"name":"Journal of toxicology. Clinical toxicology","volume":"42 3","pages":"309-11"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1081/clt-120037434","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24678093","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuroleptic malignant syndrome in a child treated with an atypical antipsychotic.","authors":"Ibrahim Abu-Kishk,&nbsp;Michal Toledano,&nbsp;Ahuva Reis,&nbsp;David Daniel,&nbsp;Matitiahu Berkovitch","doi":"10.1081/clt-200035214","DOIUrl":"https://doi.org/10.1081/clt-200035214","url":null,"abstract":"<p><p>Neuroleptic malignant syndrome (NMS) is an uncommon potentially fatal side effect of neuroleptic drugs, characterized by movement disorder, altered mental status and autonomic instability. A single dose of clotiapine was administered to an 11-year old male with acute psychosis. The previously healthy child had signs consistent with NMS including hyperthermia, hypertension, motor and mental changes. Repeat examination performed two weeks later, demonstrated that while his hyperthermia subsided, his mental status deteriorated. Olanzapine was administered, after which the child had hyperthermia, dystonia and more pronounced restlessness, once again consistent with NMS. He developed respiratory failure and was intubated and mechanically ventilated. Lorazepam, dantrolene and bromocriptine were administered as treatment of possible NMS. His mental condition, movement disorder and autonomic dysfunction improved significantly. Two weeks later, the patient was discharged in good general condition without the need for any ongoing medical treatment. There are only few case reports of NMS in children treated with olanzapine, an atypical antipsychotic. In children, caution must be exercised when prescribing antipsychotics, particularly atypical antipsychotics as these drugs may cause NMS. Because of the low incidence of NMS, a high index of suspicion is needed to identify cases so prompt treatment can be undertaken.</p>","PeriodicalId":17447,"journal":{"name":"Journal of toxicology. Clinical toxicology","volume":"42 6","pages":"921-5"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1081/clt-200035214","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24802901","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Speed of initial atropinisation in significant organophosphorus pesticide poisoning--a systematic comparison of recommended regimens.","authors":"Michael Eddleston,&nbsp;Nick A Buckley,&nbsp;Helaina Checketts,&nbsp;Lalith Senarathna,&nbsp;Fahim Mohamed,&nbsp;M H Rezvi Sheriff,&nbsp;Andrew Dawson","doi":"10.1081/clt-200035223","DOIUrl":"https://doi.org/10.1081/clt-200035223","url":null,"abstract":"<p><strong>Objective: </strong>Early deaths from organophosphorus (OP) pesticide self-poisoning result from respiratory failure and cardiovascular collapse. Therapy requires the urgent use of atropine to reverse cholinergic excess, thereby improving respiratory function, heart rate, and blood pressure. We aimed to assess variation in textbook recommendations for early atropinisation and to see whether this variation affected time to stabilisation using model data from 22 severely poisoned patients seen in a Sri Lankan clinical trial.</p><p><strong>Methods: </strong>We extracted prospectively recorded data on atropine requirements for 22 OP poisoned patients who required intubation but survived to discharge. We did a systematic search for textbook recommendations for initial atropinisation regimens. These regimens were then applied to data from the Sri Lankan patients.</p><p><strong>Results: </strong>The patients required a mean of 23.4 mg (standard deviation 22.0, range 1-75 mg) atropine to clear the lungs, raise the pulse above 80 bpm, and restore systolic blood pressure to more than 80 mmHg. Textbook recommendations varied markedly--atropinisation of an average patient, requiring the mean dose of 23.4 mg, would have taken 8 to 1380 mins; atropinisation of a very ill patient, requiring 75 mg, would have taken 25 to 4440 mins. Atropinisation was attained most rapidly with a regimen of increasing bolus doses after failure to respond to the previous bolus.</p><p><strong>Conclusions: </strong>There is great variation in recommendations for atropinisation, with some regimens taking hours and even days to stabilise a patient. The guidelines are very flexible--possibly appropriate for experienced emergency physicians or clinical toxicologists, but completely inappropriate for the inexperienced junior doctors who see most cases worldwide. We recommend that a consensus guideline be developed by appropriate organisations to bring order to this important part of OP therapy, while acknowledging the paucity of data to drive the guidelines.</p>","PeriodicalId":17447,"journal":{"name":"Journal of toxicology. Clinical toxicology","volume":"42 6","pages":"865-75"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1081/clt-200035223","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24802979","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comment on \"Treatment of hyperkalemia in a patient with unrecognized digitalis toxicity\".","authors":"Philip D Walson","doi":"10.1081/clt-120028758","DOIUrl":"https://doi.org/10.1081/clt-120028758","url":null,"abstract":"","PeriodicalId":17447,"journal":{"name":"Journal of toxicology. Clinical toxicology","volume":"42 1","pages":"119"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1081/clt-120028758","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24467194","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comment on \"The abrupt cessation of therapeutically administered sodium oxybate (GHB) may cause withdrawal symptoms\".","authors":"Deborah L Zvosec,&nbsp;Stephen W Smith","doi":"10.1081/clt-120028759","DOIUrl":"https://doi.org/10.1081/clt-120028759","url":null,"abstract":"","PeriodicalId":17447,"journal":{"name":"Journal of toxicology. Clinical toxicology","volume":"42 1","pages":"121-3; author reply 125-7"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1081/clt-120028759","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24467195","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}