Acad Emerg Med 2002 Jan;9(1):1-8
Emergency Medicine Research, Carolinas Medical Center, Charlotte, NC (BG, JK, CT, JAW).
[Medline record in process]
Delayed neurologic sequelae occur in up to 40% of severe carbon monoxide (CO) poisonings. Conflicting clinical data support the efficacy of hyperbaric oxygen (HBO) therapy in the acute treatment of CO poisoning. OBJECTIVE: To determine whether oxygen therapy reduces neurologic sequelae after CO poisoning in mice. METHODS: Male Swiss-Webster mice were exposed to CO at 1,000 ppm for 40 minutes and then 50,000 ppm until loss of consciousness (LOC) (4-9 additional minutes). Total time of both phases of CO exposure was 40-49 minutes. Treatment included HBO with 3 atmospheres (ATA) 100% oxygen, normobaric oxygen (NBO) with 1 ATA 100% oxygen, or ambient air 15 minutes after LOC. All animals underwent passive avoidance training and memory was assessed by measuring step-down latency (SDL) and step-up latency (SUL) seven days following CO exposure. RESULTS: Carbon monoxide poisoning induced significant memory deficits (SDL(CO) = 156 sec; SUL(CO) = 75%) compared with nonpoisoned (NP) animals (SDL(NP) = 272 sec; SUL(NP) = 100%). Both HBO and NBO did not prevent these neurologic sequelae. Furthermore, no significant neurobehavioral differences were found between HBO and NBO. Histologic examination of the CA1 layer of the hippocampus for pyknotic cells showed significant damage from CO in the air-treated animals (9.6%) but not in the nonpoisoned animals (3.8%). No significant neuroprotection was seen histologically with NBO and HBO compared with ambient air. CONCLUSIONS: These results suggest that HBO is not effective in preventing neurologic sequelae in mice and that there is no benefit of HBO over NBO following severe CO neurotoxicity.
PMID: 11772662, UI: 21633499
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Ann Intern Med 2001 Dec 4;135(11):1011
Publication Types:
PMID: 11730416, UI: 21587486
Br J Dermatol 2001 Nov;145(5):856-7
PMID: 11736926, UI: 21599899
Br J Dermatol 2001 Nov;145(5):842-5
PMID: 11736916, UI: 21599889
Br J Dermatol 2001 Nov;145(5):821-2
Department of Dermatology, Karl-Franzens-University Graz, Auenbruggerplatz 8, A-8036 Graz, Austria. franz.legat@kfunigraz.ac.at
Photochemotherapy is very effective for the treatment of skin diseases such as psoriasis, as well as for the prophylactic 'hardening' therapy of patients suffering from polymorphic light eruption. The photosensitizers most widely used for oral photochemotherapy are the furocoumarins 8-methoxypsoralen and 5-methoxypsoralen. Beside light-induced phototoxic reactions due to the photosensitizing activity of psoralens, side-effects after the oral intake of psoralens are nausea and vomiting, headaches, anxiety and sleeplessness. We report a rare case of anaphylaxis to 5-methoxypsoralen that developed during prophylactic 'hardening' therapy in a 36-year-old woman suffering from polymorphic light eruption. Anaphylaxis to 5-methoxypsoralen was established by placebo-controlled oral provocation tests.
PMID: 11736909, UI: 21599882
Br J Dermatol 2001 Nov;145(5):816-20
Department of Dermatology, Royal South Hants Hospital, Southampton SO14 OYG, UK. roypalmer@totlise.co.uk
Linear IgA disease (LAD) is an acquired autoimmune subepidermal bullous disease characterized by the linear deposition of IgA at the basement membrane zone. A minority of cases are induced by drugs, of which the most frequently implicated is vancomycin. The target antigens in idiopathic LAD are heterogeneous, but have not previously been reported in vancomycin-induced LAD. We report three cases, and in two of these we investigated the target antigens. In both we identified IgA antibodies to LAD285 and IgA and IgG antibodies (dual response) to BP180.
PMID: 11736908, UI: 21599881
Br J Dermatol 2001 Nov;145(5):795-8
Department of Dermatology, Shiga University of Medical Science, Seta Tsukinowa-cho, 520-2192 Otsu, Japan. sugiurah@belle.shiga-med.ac.jp
BACKGROUND: We identified 19 patients with facial atopic eczema who failed to respond to tacrolimus (FK506) ointment, although tacrolimus ointment has shown excellent benefit for the treatment of recalcitrant facial erythema in most patients with atopic dermatitis. OBJECTIVES: We attempted to determine the efficacy of an original lotion formulation of tacrolimus for facial atopic dermatitis resistant to tacrolimus ointment. PATIENTS/METHODS: Recalcitrant facial erythema of these 19 patients was treated with an original tacrolimus lotion preparation for 6 months. Patch testing with white petrolatum was performed in both the 19 patients and in 30 other atopic dermatitis patients who had experienced excellent results with tacrolimus ointment. RESULTS: Of the 19 resistant patients, those whose symptoms were greatly or moderately improved by the lotion were 95%, 89% and 89% after 2 weeks, 3 months and 6 months of treatment, respectively. Further, patch testing to petrolatum showed positive reactions in several (six of 19) patients, compared with none of 30 controls with atopic eczema that had responded to topical tacrolimus ointment. CONCLUSIONS: The tacrolimus lotion had a significant effect on the recalcitrant facial erythema in adult patients with atopic dermatitis who were resistant to tacrolimus ointment. We suggest that one reason for the unresponsiveness to tacrolimus ointment may be because of contact sensitivity to white petrolatum.
PMID: 11736904, UI: 21599877
Hum Exp Toxicol 2001 Sep;20(9):491-5
Frenchay Hospital, Bristol, UK.
Aspirin (acetylsalicylic acid) is widely available without prescription. Although self-poisoning is rare, if severe it may be life threatening. Haemodialysis has been recommended in severe cases when salicylate levels exceed 7.3 mmol l(-1). We describe three cases of severe salicylate poisoning, which were treated with continuous veno-venous haemodiafiltration (CVVHDF). All patients survived. The first case had already undergone haemodialysis before transfer to the ICU, where CVVHDF was commenced because salicylism persisted at 3 mmol l(-1). A small reduction in serum salicylate was noted. In the second case, serum salicylate decreased from 8.5 to 3.5 mmol l(-1) after 3 h of CVVHDF even though only minimal urine was produced. Our third case is a chronic overdose in whom serum salicylate decreased from 6.2 to 4 mmol l(-1) after 4 h and to 1.4 mmol l(-1) after a further 7 h. No bicarbonate was administered to this patient and elimination can only be attributed to CVVHDF and urinary clearance, which is known to be slow. We discuss the pathogenesis of severe salicylate toxicity and postulate that CVVHDF, which is widely used in the intensive care setting, may be a useful therapy in severely poisoned patients who are unstable and cannot undergo haemodialysis or in situations where haemodialysis is unavailable.
PMID: 11776412, UI: 21632136
J Toxicol Clin Toxicol 2001 Oct;39(6):653-4
PMID: 11762678, UI: 21603853
J Toxicol Clin Toxicol 2001 Oct;39(6):641-8
New York City Poison Control Center, NYU/Bellevue Hospital Center, Department of Emergency Medicine, New York 10016, USA. MarkSMD@aol.com
BACKGROUND: Although ingestion of sustained-release potassium supplements can cause life-threatening hyperkalemia in patients with abnormal renal function, only a few previous reports suggest that this may occur in patients with normal renal function. We report 2 cases of hyperkalemia in patients with normal renal function who developed hyperkalemia after ingesting sustained-release potassium preparations and describe the use of radiography and whole-bowel irrigation in their care. CASE REPORTS: The first patient is a 50-year-old woman who ingested 100 K-Dur tablets (each tablet containing 750 mg KCl or 10 mEq potassium) in a suicide attempt 1 hour prior to presenting to the emergency department. She developed a peak serum potassium level of 9.7 mEq/L and had transient, potentially life-threatening electrocardiographic changes. The second patient was a 17-year-old man who ingested 20 to 30 Klor-Con tablets (each tablet containing 750 mg KCl or 10 mEq potassium) in a suicide attempt 10 hours prior to presentation. Although he developed a peak serum potassium level of 6.1 mEq/L, he had a persistently normal electrocardiogram. In both patients, the tablets were visualized on abdominal radiographs and the gastrointestinal tracts of both were successfully decontaminated using whole-bowel irrigation. DISCUSSION: Although the sensitivity and specificity are unknown, the abdominal radiograph appears to be useful in detecting sustained-release potassium tablets. Whole-bowel irrigation as a primary method of gastrointestinal decontamination also appears to be effective although its use is not previously reported for sustained-release potassium overdoses.
PMID: 11762675, UI: 21603850
J Toxicol Clin Toxicol 2001 Oct;39(6):633-6
Division of Emergency Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA. dribbenw@msnotes.wustl.edu
BACKGROUND: One of the major limitations to organ procurement and donation is the lack of suitable donors. As the demand for suitable organs exceeds the supply, identification of potential donors continues to evolve. Due to perceived risks of transmittable toxins and insufficient understanding of toxicological fate, poisoned patients are often overlooked as organ donors. CASE REPORT: A 17-year-old white male was found by his mother having a seizure in bed. A strong odor of pesticides was noted and an empty container of malathion was found. He was transported to an outlying hospital and underwent prolonged cardiopulmonary resuscitation. The patient exhibited symptoms consistent with cholinergic poisoning and received a total of 12 mg of atropine and a pralidoxime bolus of 1 g followed by an infusion at 500 mg/h. Initial plasma cholinesterase was 1433 IU/L (normal 7500-14,600). The patient developed aspiration pneumonia and remained comatose. No further treatment for cholinergic toxicity was needed 5 days after admission and a cerebral blood flow scan confirmed brain death. After review of the available literature on the disposition andfate of malathion in human tissues, the patient's liver and kidneys were harvested for transplantation. The recipients were all doing well 1 year posttransplantation. CONCLUSIONS: This case of successful transplantation after organophosphate exposure underscores the fact that poisoned patients should not be overlooked as transplant candidates. Decisions should be based on the clinical presentation and knowledge of the properties of the toxin.
PMID: 11762673, UI: 21603848
J Toxicol Clin Toxicol 2001 Oct;39(6):617-21
Chang Gun Memorial Hospital, Lin-Kuo Medical Center, Taipei, Taiwan, Republic of China.
BACKGROUND: Imidacloprid [1-(6-chloro-3-pyridylmethyl)-N-nitroimidazolidin-2-ylideneamine, CAS 138261-41-3] belongs to a relatively new class of insecticidal chemistry, the chloronicotinyl neonicotinoid compounds. Animal studies indicate relatively low toxicity to mammals because they have resistant nicotinic receptor subtypes compared to insects, as well as protection of the central nervous system by the blood brain barrier. Despite wide usage, human exposure experience resulting in toxicity is quite limited. CASE REPORT: Here, we report a case of acute ingestion of an insecticide formulation containing 9.7% imidacloprid, <2 % surfactant, and the balance as solvent, N-methyl pyrrolidone. Clinical manifestation included drowsiness, disorientation, dizziness, oral and gastroesophageal erosions, hemorrhagic gastritis, productive cough, fever, leukocytosis, and hyperglycemia. The patient recovered without complication with supportive treatment and was discharged 4 days after ingestion. Follow-up barium upper gastrointestinal examination 1 month later was normal. Because moderate to high dose imidacloprid in animals causes central nervous system activation similar to nicotine, including tremors, impaired pupillary function, and hypothermia, it is unclear whether imidacloprid had a causal role in the patient's initial drowsiness and dizziness. It is more likely that the formulation ingredients, particularly N-methyl pyrrolidone, caused most of the clinical symptoms including minor central nervous system depression, gastrointestinal irritation, and hyperglycemia.
PMID: 11762670, UI: 21603845
J Toxicol Clin Toxicol 2001 Oct;39(6):587-93
Department of Medicine, Veterans General Hospital-Taipei, Taiwan. jfdeng@vghtpe.gov.tw
BACKGROUND: Ethylene chlorohydrin (CAS 107-07-3), a chemical once used in hastening grape vine sprouting in Taiwan, has caused severe toxicity upon acute exposure. Although such use of ethylene chlorohydrin is now prohibited in Taiwan, poisoning still occurs following its illegal use. Since data concerning human ethylene chlorohydrin poisoning remain rare, we report our experience in treating acute ethylene chlorohydrin-poisoned patients. METHODS: A retrospective analysis was conducted to evaluate patients with ethylene chlorohydrin poisoning reported to Taiwan Poison Control Center during 1985-1998. RESULTS: Seventeen patients with ethylene chlorohydrin poisoning were identified. There were 11 male and 6 female patients, ranging in age from 2 to 70 years (median 53 years). The intent of exposure was suicide in 5, accident in 9, and occupational exposure in 3 patients. Oral ingestion was the most common route of exposure (14 patients). Seven out of the 17 patients died within 24 hours due to metabolic acidosis and respiratory failure. Ethanol therapy, used in 2 patients, had no apparent benefit. Moderate or mild poisoning was characterized by gastrointestinal effects only and an uneventful recovery. CONCLUSIONS: Ethylene chlorohydrin can result in severe metabolic acidosis, respiratory failure, coma, and death after acute exposure.
PMID: 11762666, UI: 21603841
JAMA 2001 Nov 7;286(17):2088-90
PMID: 11757497, UI: 21563184
JAMA 2001 Dec 5;286(21):2671
PMID: 11730441, UI: 21588585
Lancet 2001 Nov 24;358(9295):1814
PMID: 11734269, UI: 21592699
Med J Aust 2001 Nov 5;175(9):501
PMID: 11758085, UI: 21593607
Pediatr Emerg Care 2001 Dec;17(6):452-6
Kentucky Regional Poison Center, Louisville, Kentucky.
PMID: 11753195, UI: 21624968
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