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Acad Emerg Med 2002 Sep;9(9):962
The Poison Control Center, Philadelphia, PA.
[Medline record in process]
PMID: 12208689, UI: 22196594
Other Formats:
Am J Emerg Med 2002 Sep;20(5):391-452
Centers participating in this report include Regional Poison Control Center, Birmingham, AL; Alabama Poison Center, Tuscaloosa, AL; Arizona Poison and Drug Information Center, Tucson, AZ; Samaritan Regional Poison Center, Phoenix, AZ; Arkansas Poison and Drug Information Center, Little Rock, AR; California Poison Control System-Fresno/Madera Division, CA; California Poison Control System-Sacramento Division, CA; California Poison Control System-San Diego Division, CA; California Poison Control System-San Francisco Division, CA; Rocky Mountain Poison and Drug Center, Denver, CO; Connecticut Poison Control Center, Farmington, CT; National Capital Poison Center, Washington, DC; Florida Poison Information Center, Tampa, FL; Florida Poison Information Center, Jacksonville, FL; Florida Poison Information Center, Miami, FL; Georgia Poison Center, Atlanta, GA; Illinois Poison Center, Chicago, IL; Indiana Poison Center, Indianapolis, IN; Iowa Statewide Poison Control Center, Sioux City, IA; Mid-America Poison Control Center, Kansas City, KS; Kentucky Regional Poison Center, Louisville, KY; Louisiana Drug and Poison Information Center, Monroe, LA; Northern New England Poison Center, Portland, ME; Maryland Poison Center, Baltimore, MD; Regional Center for Poison Control and Prevention Serving Massachusetts and Rhode Island, Boston, MA; Children's Hospital of Michigan Regional Poison Control Center, Detroit, MI; DeVos Children's Hospital Regional Poison Center, Grand Rapids, MI; Hennepin Regional Poison Center, Minneapolis, MN; Missouri Regional Poison Center, St. Louis, MO; The Poison Center, Omaha, NE; New Hampshire Poison Information Center, Lebanon, NH; New Jersey Poison Information and Education System, Newark, NJ; New Mexico Poison and Drug Information Center, Albuquerque, NM; New York City Poison Control Center, New York, NY; Hudson Valley Regional Poison Center, Sleepy Hollow, NY; Long Island Regional Poison and Drug Information Center, Mineola, NY; Finger Lakes Regional Poison and Drug Information Center, Rochester, NY; Central New York Poison Control Center, Syracuse, NY; Western New York Regional Poison Control Center, Buffalo, NY; Carolinas Poison Center, Charlotte, NC; Cincinnati Drug and Poison Information Center, Cincinnati, OH; Central Ohio Poison Center, Columbus, OH; Greater Cleveland Poison Control Center, Cleveland, OH; Oklahoma Poison Control Center, Oklahoma City, OK; Oregon Poison Center, Portland, OR; Pittsburgh Poison Center, Pittsburgh, PA; The Poison Control Center, Philadelphia, PA; Penn State Poison Center, Hershey, PA; Palmetto Poison Center, Columbia, SC; Middle Tennessee Poison Center, Nashville, TN; Southern Poison Center, Memphis, TN; Central Texas Poison Center, Temple, TX; North Texas Poison Center, Dallas, TX; Southeast Texas Poison Center, Galveston, TX; Texas Panhandle Poison Center, Amarillo, TX; West Texas Regional Poison Center, El Paso, TX; South Texas Poison Center, San Antonio, TX; Utah Poison Control Center, Salt Lake City, UT; Virginia Poison Center, Richmond, VA; Blue Ridge Poison Center, Charlottesville, VA; Washington Poison Center, Seattle, WA; West Virginia Poison Center, Charleston, WV; University of Wisconsin Hospital Clinics Poison Control Center, Madison, WI; Children's Hospital of Wisconsin Poison Center, Milwaukee, WI.
[Record supplied by publisher]
PMID: 12216043
Forensic Sci Int 2002 Aug 14;128(1-2):50
Department of Toxicology, Institute of Forensic Medicine and Toxicology, 1st Faculty of Medicine and Teaching Hospital, Charles University in Prague, Na Bojisti 3, 121 08 2, Prague, Czech Republic
An incident wherein more than 30 people were poisoned with a herbal infusion during a meditation session is described. The clinical features observed were hallucinations, agression, agitation, amnesia, mydriasis, dry skin, tachycardia, hyperthermia, hypotension, collapse, coma and respiratory depression. All patients recovered, although mechanical ventilation was required in some instances. A portion of the herbal infusion was found to contain atropine (hyoscyamine), scopolamine (hyoscine), harmine, and other alkaloids. The estimated ingested doses (free bases) were atropine 4mg, harmine 27mg, and scopolamine 78mg. The mean concentrations in 21 serum samples obtained approximately 6h after ingestion of the infusion were atropine 5ng/ml, harmine 8ng/ml, and scopolamine 13ng/ml.
PMID: 12208022
Forensic Sci Int 2002 Aug 14;128(1-2):41
Toxicology Laboratory, Leiden University Medical Center L1-P, P.O. Box 9600, NL-2300 RC, Leiden, The Netherlands
The population of Curacao, Netherlands Antilles (133,000) shows a very high prevalence of end-stage renal disease (approximately 1 per 1000). These patients are often treated chronically with haemodialysis. As the drinking water on the island is prepared by distillation of sea water, the haemodialysis fluid used to be prepared with tap water without further treatment.In 1996, the 27 patients of one of the dialysis centers on the island presented with nausea, vomiting, and hypercalcaemia in a short time span, which was initially diagnosed as 'hard water syndrome'. In spite of treatment with low-calcium dialysate, microcytic anaemia and neurological symptoms developed. Ten patients died of convulsions, sepsis, and coma. As aluminum (Al) intoxication was suspected, Al in serum (AlS) was measured. Ante mortem AlS was 808&mgr;g/l (n=7; range 359-1189); in the survivors AlS was 255&mgr;g/l (n=17; range 113-490). Normal AlS is <10&mgr;g/l, and <50&mgr;g/l in asymptomatic dialyzed patients.The court requested post-mortem toxicological analysis of four patients. Al concentrations in liver, bone, and cerebral cortex were significantly increased as compared with background levels. Al intoxication was, therefore, considered to be the most likely cause of death in these patients.Investigations of the tap water supply revealed that a few weeks before the onset of the symptoms, a water conduit pipe to the dialysis unit had been replaced, which was lined with Al- and Ca-rich cement mortar. These ions leached into the distilled water and caused both Ca- and Al-intoxication through uptake from the dialysate into the patients' circulation. The symptoms of the latter were initially not recognized as they were masked by the symptoms of hypercalcaemia.
PMID: 12208020
Forensic Sci Int 2002 Aug 14;128(1-2):3
Medical Toxicology Unit, Guy's and St. Thomas' Hospital Trust, Avonley Road, SE14 5ER, London, UK
Recording deaths from acute poisoning/substance abuse is not straightforward. The International Classification of Diseases (ICD), used to code mortality statistics, is aimed towards recording the underlying cause of death such as suicide or drug dependence rather than gathering data on poisoning per se. Despite the inherent difficulties clear trends can be observed from the data available for England and Wales. There have been marked changes in the compounds featuring in suicidal poisoning in the last 35 years reflecting changes in the availability of poisons, notably carbon monoxide and prescription barbiturates. However, although the number of poisoning suicides has decreased in the recent years, suicides from other means have increased in males (suicides in 1999, 75% male), hence there has been little change in the annual total of suicides. There are also striking differences in drug abuse- and volatile substance abuse (VSA)-related deaths between males and females. Drug abuse-related fatal poisoning (83% male, 1979-1999, European Monitoring Centre for Drugs and Drug Addiction (EMCDDA) definition which does not include suicide), largely attributable to heroin and methadone, increased markedly during the 1990s, with a sharp rise in deaths attributed to accidental poisoning, although deaths involving methadone are now declining. VSA-related deaths (90% male, 1971-1999, almost entirely accidental deaths), nowadays predominantly from abuse of fuel gases (liquefied petroleum gas, LPG) from, for example, cigarette lighter refills, have declined from a peak in the early 1990s and are now becoming manifest in an older age group. These two latter instances especially provide examples where ICD-derived fatal poisoning data are inadequate and a 'poisons oriented' approach to data collection and analysis is necessary.
PMID: 12208016, UI: 22198033
Int J Dermatol 2002 May;41(5):279-81
Di.S.E.M., Section of Dermatology, University of Genoa, Italy. rebdermo@unige.it
Solitary dermatofibromas are a common occurrence, especially on the lower limbs of young women, while multiple dermatofibromas (MDF) are rare, accounting for less than 0.3% of all dermatofibromas and may suddenly develop in immunosuppressed patients. We report a patient with systemic lupus erythematosus (SLE) who developed MDF while she was taking oral prednisone. A 46-year-old woman presented in 1989 complaining of photosensitivity, arthralgias, fatigue, malaise and dyspepsia. The patient denied fever, Raynaud's phenomenon, oral ulcer and hair loss. On examination she presented a typical SLE malar rash. Erythrocyte sedimentation rate (ESR) was elevated (54 mm/h). Speckle patterned IgG/IgM antinuclear antibodies were present at 1/1280 titer. Antibodies anti Ro/SSA were detected by counterimmunelectrophoresis up to 1/8 titer. Other laboratory findings were negative or within normal limits. Systemic lupus erythematosus was diagnosed and the patient given 50 mg/day prednisone. After a few months, both clinical symptoms and immunologic parameters improved. Eighteen months later, prednisone was replaced by 500 mg/day hydroxychloroquine. In 1994, she presented again with malar rash, arthralgias and facial hyperpigmentation. Prednisone 15 mg/day was reintroduced and hydroxychloroquine stopped being a possible cause of the facial hyperpigmented macules. In 1996, while she was taking 5 mg/day prednisone, several nodules developed on her limbs within a few months. On examination we observed 16 firm, slightly elevated 3-15-mm wide brown nodules on her arms, legs and trunk. A biopsy specimen of a lesion of the trunk revealed an epidermal seborrheic-keratosis-like hyperplasia with dermal fibrosis and fibroblastic proliferation (Fig. 1). Dermatofibroma was diagnosed.
PMID: 12100703, UI: 22095396
J Toxicol Clin Toxicol 2002;40(5):567-9
NPIS Edinburgh Centre, Scottish Poisons Information Bureau, Royal Infirmary of Edinburgh, UK. spib@luht.scot.nhs.uk
PMID: 12215052, UI: 22203397
J Toxicol Clin Toxicol 2002;40(5):551-5
Faculty of Medicine, National Poisons Information Centre, National Hospital of Sri Lanka, Colombo. ravindrafernando@hotmail.com
INTRODUCTION: Poisoning is a major health concern in Sri Lanka, which has a very high morbidity and mortality from pesticide poisoning. Poisoning, which continues to be in the first five leading causes of death, accounts for about 80,000 hospitalizations and over 3,000 deaths per year. The National Poisons Information Centre in Sri Lanka, thefirst such centre to be established in South Asia, completed 10 years service in 1997. The 4,070 calls received in thefirst 10 years are analyzed and compared with the national hospitalization pattern. METHODS: The recorded data sheets of all enquiries received from 1988 to 1997 were analyzed retrospectively to study (1) purpose of enquiry, (2) category of enquirer, (3) circumstances of poisoning, (4) gender of victim, (5) age of victim, (6) type of poison, and (7) outcome. Items (6) and (7) were compared with the national hospital statistics for 1998. RESULTS: Of the 4,070 enquiries, 92% concerned specific patients and 6% were for information on poisons. Almost 90% of the enquiries were from medical or paramedical personnel, 5% from relatives or friends, and 3% from the victims. Nearly 38% of enquiries concerned pesticides compared to 27% of poisoning hospitalizations. Medicinal agents were the subject of 20% of enquiries compared to 13% of hospitalizations. The major discrepancy was for snake bites, accounting for only 6% of enquiries but 42% of hospitalizations. Sex distribution of enquiries showed more males than females. Thirty-seven percent of the victims were young adults-15-29years age group. Nearly 49% of the enquiries were for suicidal attempts. Seventy-one percent of the victims recovered. CONCLUSIONS: Although enquiries to the NPIC averaged only 0.5% of poisoning hospitalizations, they were sufficiently representative of the national pattern to predict that increasing utilization of the NPIC would offer a much needed service, both for
PMID: 12215049, UI: 22203394
J Toxicol Clin Toxicol 2002;40(5):547-9
Maimonides Medical Center, Brooklyn, New York, USA. rjhoffman@pol.net
OBJECTIVE: Ferric chloride (FeCl3) is used to qualitatively test the urine of patients with presumed salicylate exposure. FeCl3 testing of an unidentified poison might provide evidence of salicylate exposure in situations where FeCl3 urine testing cannot be used. Such situations include the absence of a urine sample, immediately after ingestion before urine contains a detectable quantity of salicylate, or for patients chronically using salicylatesfor which FeCl3 testing is unhelpful. This study seeks to determine if FeCl3 can be used to identify salicylate-containing products. METHODS: We assessed the reactivity of FeCl3 with commercially available salicylate-containing products. We applied 0.1 mL of 10% FeCl3 solution to each of 15 various salicylate-containing products including: regular and buffered acetylsalicylic acid, bismuth subsalicylate, methylsalicylate, physostigmine salicylate, salicylic acid, trolamine salicylate, and herbal tablets with salicin-containing white willow bark (Salix sp.). These products tested were: regular and enteric-coatedpills (n = 4), powder (n = 1), topical creams (n = 5), topical liquids (n = 4), and intravenous solution (n = 1). FeCl3 was applied to crushed tablets and added directly to liquids and creams. Fifteen salicylate-free controls including liquids, pills, and creams similar in appearance to experimental samples were also tested. Three blinded physiciansfamiliar with FeCl3 testing independently observed the addition of FeCl3 to each sample and rated a positive or negative result. RESULTS: All salicylate-containing products were interpreted to be clearly FeCl3 positive and all control samples were interpreted to be clearly FeCl3 negative. CONCLUSION: Salicylate-containing products may be identified using FeCl33. When using FeCl3
PMID: 12215048, UI: 22203393
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