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Acad Emerg Med 2002 Aug;9(8):824-8
Department of Emergency Medicine, Boston Medical Center, Boston, MA 02118, USA. ntathlev@bu.edu
OBJECTIVES: 1) To determine the prevalence of identifiable causes of alcohol-related seizures other than alcohol withdrawal. 2) To test the hypothesis that patients with alcohol-related seizures present with greater frequency following Sundays when alcohol is not commercially available. METHODS: This was a retrospective chart review of 140 consecutive patients presenting with alcohol-related seizures during a six-month period. Identifiable causes of seizures other than alcohol withdrawal and the day of the week of presentation were documented. RESULTS: One hundred forty individual patients were eligible for study. Identifiable causes of seizures other than alcohol withdrawal were found in 53.6% of patients, and they were distributed as follows: 1) current or past history of significant head trauma 25.7%, 2) idiopathic seizure disorder 15.7%, 3) cerebrovascular accident 5.7%, 4) nontraumatic intracranical lesion 3.6%, and 5) toxic/metabolic abnormalities 2.9%. Alcohol is not available for purchase on Sundays because of the "Blue Laws" in Massachusetts. A total of 34.5% of patients with alcohol withdrawal seizures presented on Mondays (p < 0.001). Of patients with identifiable causes of seizures other than alcohol withdrawal, only 16% presented on Mondays (p > 0.10). CONCLUSIONS: Approximately 50% of seizures in alcohol-dependent patients are potentially unrelated to alcohol withdrawal. Patients with alcohol withdrawal seizures presented with greater frequency on Mondays following the 24-hour period when alcohol was not commercially available in Boston. This suggests that patients with alcohol withdrawal seizures may present with greater frequency following periods of decreased availability of alcohol.
PMID: 12153888, UI: 22148180
Other Formats:
Ann Intern Med 2002 Sep 3;137(5 Part 1):374
Publication Types:
PMID: 12204041, UI: 22193509
Ann Intern Med 2002 Sep 3;137(5 Part 1):372-3; discussion 372-3
PMID: 12204038, UI: 22193506
Br J Dermatol 2002 Jun;146(6):1113-4
PMID: 12072100, UI: 22067128
Br J Dermatol 2002 Jun;146(6):1061-3
Department of Dermatology, Cumberland Infirmary, Carlisle CA2 7HY, UK. Neil.Cox@ncumbria-acute.nhs.uk
Severe drug eruptions may cause diagnostic and therapeutic difficulty when they mimic or provoke endogenous patterns of dermatosis. We report three patients with known psoriasis in whom use of bupropion (Zyban), prescribed to assist with cessation of smoking, led to severe pustular or erythrodermic exacerbation of psoriasis within 3-5 weeks. All patients were systemically unwell and required hospitalization to control the disease flare.
PMID: 12072078, UI: 22067106
Br J Dermatol 2002 Jun;146(6):1047-51
St John's Institute of Dermatology, St Thomas' Hospital, Lambeth Palace Road, London SE1 7EH, UK. drsm@doctorsnet.co.uk
BACKGROUND: Neomycin, clioquinol and fusidic acid are all topical antibiotics widely used in dermatological practice in the U.K., either as a single agent or in combination with topical corticosteroids. However, an adverse effect of topical antibiotics is contact sensitization. OBJECTIVES: To examine the frequency of positive patch test reactions to fusidic acid, clioquinol and neomycin. METHODS: To compare the frequency of allergic patch test reactions over 1 year, we patch tested all patients attending the St John's Institute of Dermatology contact dermatitis clinic for one calendar year with fusidic acid, neomycin and clioquinol. RESULTS: We patch tested 1119 patients. Positive patch test reactions to neomycin were noted in 40 patients (3.6%), compared with eight patients (0.7%) to clioquinol and three patients (0.3%) to fusidic acid. The frequency of medicament allergy to neomycin was thus five times more common than to clioquinol and ten times more common than to fusidic acid. Although fusidic acid is not part of our extended standard series, it is in our medicaments series. Therefore, in the second part of our study, we reviewed all cases of positive patch test reactions to fusidic acid over the last 20 years. We found that the frequency of hypersensitivity has decreased since the early 1980s despite increasing usage; the current average frequency being 1.62 patch-tested patients per year (1.45%) of those patch tested to the medicaments series). The most common diagnosis in such patients was stasis dermatitis (54.2%). CONCLUSIONS: The frequency of fusidic acid allergy in an eczema population is low and is comparable with published data from over 10 years ago.
PMID: 12072075, UI: 22067103
J Toxicol Clin Toxicol 2002;40(4):507-12
Intensive Care, Gosford Hospital, Gosford, New South Wales, Australia
BACKGROUND: Carbamazepine poisoning can be life threatening. The role and efficacy of extracorporeal drug clearance is not clearly defined. CASE REPORT: A 16-year-old male ingested 34g of slow-release carbamazepine. His course was complicated by seizures, recurrent cardiac arrests, and renalfailure. Intestinal ileus at the time of presentation prevented effective gastrointestinal decontamination. His carbamazepine concentration peaked at 93.8 mg/L (397micromol/L) 106 hours after ingestion. There was evidence suggesting ongoing absorption for 120 hours. He underwent seven episodes of charcoal hemoperfusion for a total of 109.25 hours. He subsequently made a full recovery. METHODS: The efficacy of charcoal hemoperfusion was evaluated by measuring the carbamazepine concentrations in the afferent and efferent loops of the hemoperfusion cartridge using 17 paired convenience samples. Extraction ratios were calculated and plotted against timefor each individual episode of charcoal hemoperfusion. CONCLUSION: The extraction ratio was linearly related to time, and ranged 0.46-0.02. The peak clearance was 69 mL/min. Cartridge saturation was defined as a clearance that was equal to an estimate of the patient's intrinsic clearance. In our patient, this was equivalent to an extraction ratio of 0.2 at a flow rate of 150 mL/min. By this definition, cartridge saturation appeared to occur at 7 hours. Charcoal hemoperfusion was associated with a significant reduction in the apparent half-life, which is most easily explained by clearance from the central vascular compartment, during a prolonged absorptive phase. The patient made full recovery without evidence of neurological deficit.
PMID: 12217004, UI: 22205161
J Toxicol Clin Toxicol 2002;40(4):499-505
Neurology Service, New Mexico VA Health Care System, Albuquerque, New Mexico 87108, USA. ledavis@unm.edu
OBJECTIVES: We investigated U.S. methanol-poisoning exposures since little recent information is available about the frequency, sources of methanol, or outcomes of individuals who consume methanol. METHODS: We reviewed human methanol exposures reported to the American Association of Poison Control Centers Toxic Exposure Surveillance System 1993-1998. RESULTS: The mean number of cases per year was 2254. Each year 167 cases had an outcome of moderate effect, major effect, or death. One death occurred in every 183 exposures to methanol. Symptomatic cases increased abruptly from 1.8 to 2.5% for infants and children, from 14.1 to 12.3% for adolescents and adults, while the intentional exposures increased from < 1 to 21% for adolescents, and 11% for adults. Cases occurred in every decade of life but toddlers had the highest number of exposures. In 68 methanol fatalities, confusion developedfollowed by coma, hypotension, respiratory depression, and cerebral edema. Blood methanol levels were above 100mg/dL (70%), metabolic acidoses (62%), and anion gaps > 25 (100%). Methanol products were recorded, showing windshield wiper fluids to be 60.8% of exposures. Other automotive sources were 23.7%. Commercial nonautomotive products were 12.2% and pure methanol products were 2.3%. Unintentional exposures were reported in 90.3% of all cases, while 8.3% were due to intentional exposures, and 1.4% wasfor unknown or mixed reasons. Intentional exposures resulted from suspected suicides (51.2%) and from abuse and misuse (38.8%). CONCLUSIONS: Methanol poisonings continue to occur in the United States with toddlers at the highest risk for exposure, but adolescents and adults at the highest risk for life-threatening intoxications. Over half of product-identified cases were due to consumption of windshield wiperfluid. Efforts should be undertaken to minimize methanol exposures.
PMID: 12217003, UI: 22205160
J Toxicol Clin Toxicol 2002;40(4):493-7
World Health Organization Task Force on the Protection of Children's Environmental Health, Geneva, Switzerland. pronczukj@who.ch
Growing concern exists about the threats posed by environmental pollutants and physical agents on children's health. A number offactors, including globalization, increased industrialization, and trade of chemicals and poverty have an impact on the quality of the environment and on children's health. Acute toxic exposures lead to poisoning, and chronic low-level exposures may cause functional and organ damage during periods of special vulnerability. The need to protect children's environmental health is urgent, in view of the magnitude of the problem and the fact that "children are not little adults." The effects suffered during special developmental periods-"windows of vulnerability"-can be permanent and irreversible. The main global environmental problems affecting children's health are lack of access to safe drinking water and sanitation and exposure to indoor air pollution. Furthermore, environmentally related accidents, injuries, and poisonings have a major impact on children and adolescent's morbidity and mortality. A number of examples that illustrate the complexity of assessing and dealing with children's environmental health issues are presented. A Task Force on the Protection of Children's Environmental Health that aims to prevent disease and disability in children associated with chemical and physical threats was set up in 1999 by the World Health Organization. The priorities for action include the consideration of accidents, injuries, and poisonings (accidental, intentional, and occupational), and children in the workplace (e.g., scavenging children, children in cottage industries). Poisons Centers and related toxicology centers are in a strategic position to play a "sentinel" role in the protection of children's environmental health. They record acute and chronic toxic exposures in children in a harmonized manner, using controlled vocabularies and definitions. This will allow collecting a large, highly valuable database on the main toxicological problems affecting children, including those of environmental origin. The analysis of observations entered in such a database will help assess the burden of disease and collect the evidence for planning prevention and promoting regulatory measures. Centers are called to play a proactive role in raising awareness about children's environmental health and contribute to research, information dissemination, training, and other activities required for the protection of children's health and development.
PMID: 12217002, UI: 22205159
J Toxicol Clin Toxicol 2002;40(4):483-91
Northern France Poison Center, Regional University Hospital, Lille, France. mmathieu@chru-lille.fr
Children represent the largest subpopulation of those susceptible to the adverse effects of air pollution. Compared to adults, children express a greater vulnerability, which can be explained by differences in: the circumstances of exposure related to age, their activities, their child status, differences in lung anatomy and physiology, differences in the clinical expression of disease, and their organ maturity. Many factors have to be assessed in order to evaluate the severity of toxic exposures: pollutant solubility, particle size, concentration, reactivity of pollutants, and pattern of ventilation. Within the numerous air pollutants, some are of special concern for children. For example, ozone has been shown to affect the lungs of healthy school children, especially asthmatics. Airborne particles, nitrogen oxides, sulfur oxides, and acid aerosols have also been shown to induce acute respiratory symptoms, asthma, and bronchitis. Of particular importance is carbon monoxide, which, under certain circumstances, may be found in highly toxic concentrations indoors where children spend most of their time. Special attention has to be given to children's unique differences in order to evaluate the clinical consequences of their toxic exposures. This circumstance emphasizes the key roles of poison centers, clinical toxicologists, and pediatricians, all of whom can collaborate on the identification, assessment, and surveillance of toxic risk for child health and development.
PMID: 12217001, UI: 22205158
J Toxicol Clin Toxicol 2002;40(4):415-46
American Academy of Clinical Toxicology, Harrisburg, Pennsylvania 17105-8820, USA.
EPIDEMIOLOGY: Almost all cases of acute methanol toxicity result from ingestion, though rarely cases of poisoning have followed inhalation or dermal absorption. The absorption of methanol following oral administration is rapid and peak methanol concentrations occur within 30-60minutes. MECHANISMS OF TOXICITY: Methanol has a relatively low toxicity and metabolism is responsible for the transformation of methanol to its toxic metabolites. Methanol is oxidized by alcohol dehydrogenase to formaldehyde. The oxidation of formaldehyde to formic acid is facilitated by formaldehyde dehydrogenase. Formic acid is converted by 10-formyl tetrahydrofolate synthetase to carbon dioxide and water. In cases of methanol poisoning, formic acid accumulates and there is a direct correlation between the formic acid concentration and increased morbidity and mortality. The acidosis observed in methanol poisoning appears to be caused directly or indirectly by formic acid production. Formic acid has also been shown to inhibit cytochrome oxidase and is the prime cause of ocular toxicity, though acidosis can increase toxicity further by enabling greater diffusion of formic acid into cells. FEATURES: Methanol poisoning typically induces nausea, vomiting, abdominal pain, and mild central nervous system depression. There is then a latent period lasting approximately 12-24 hours, depending, in part, on the methanol dose ingested, following which an uncompensated metabolic acidosis develops and visualfunction becomes impaired, ranging from blurred vision and altered visual fields to complete blindness. MANAGEMENT: For the patient presenting with ophthalmologic abnormalities or significant acidosis, the acidosis should be corrected with intravenous sodium bicarbonate, the further generation of toxic metabolite should be blocked by the administration of fomepizole or ethanol and formic acid metabolism should be enhanced by the administration of intravenous folinic acid. Hemodialysis may also be required to correct severe metabolic abnormalities and to enhance methanol and formate elimination. For the methanol poisoned patient without evidence of clinical toxicity, the first priority is to inhibit methanol metabolism with intravenous ethanol orfomepizole. Although there are no clinical outcome data confirming the superiority of either of these antidotes over the other, there are significant disadvantages associated with ethanol. These include complex dosing, difficulties with maintaining therapeutic concentrations, the need for more comprehensive clinical and laboratory monitoring, and more adverse effects. Thus fomepizole is very attractive, however, it has a relatively high acquisition cost. CONCLUSION: The management of methanol poisoning includes standard supportive care, the correction of metabolic acidosis, the administration of folinic acid, the provision of an antidote to inhibit the metabolism of methanol to formate, and selective hemodialysis to correct severe metabolic abnormalities and to enhance methanol and formate elimination. Although both ethanol and fomepizole are effective, fomepizole is the preferred antidote for methanol poisoning.
PMID: 12216995, UI: 22205152
JAMA 2002 Aug 28;288(8):1036
PMID: 12206155, UI: 22192500
JAMA 2002 Aug 28;288(8):951-3
Emerging Infections Program, New York State Department of Health, USA.
PMID: 12201274, UI: 22188098
JAMA 2002 Aug 28;288(8):988-95
Air Pollution and Respiratory Health Branch, National Center for Environmental Health, Centers for Disease Control and Prevention, 1600 Clifton Rd NE, MS E-17, Atlanta, GA 30333, USA. zud9@cdc.gov
CONTEXT: Carbon monoxide (CO) has been reported to contribute to more than 2000 poisoning deaths per year in the United States. OBJECTIVES: To evaluate the influence of national vehicle emissions policies and practices on CO-related mortality and to describe 31 years (1968-1998) of CO-related deaths in the United States. DESIGN AND SETTING: Longitudinal trend analysis using computerized death data from the Centers for Disease Control and Prevention, US Census Bureau population data, and annual CO emissions estimates for light-duty vehicles provided by the US Environmental Protection Agency. MAIN OUTCOME MEASURE: All deaths in the US for which non-fire-related CO poisoning was an underlying or contributing condition, classified by intent and mechanism of death. Negative binomial regression was used to incorporate every year of data into estimated percentage changes in CO emissions and mortality rates over time. RESULTS: During 1968-1998, CO-related mortality rates in the United States declined from 20.2 deaths to 8.8 deaths per 1 million person-years (an estimated decline of 57.8%; 95% confidence interval [CI], -62.4% to -52.6%). Following the introduction of the catalytic converter to automobiles in 1975, CO emissions from automobiles decreased by an estimated 76.3% of 1975 levels (95% CI, -82.0% to -70.4%) and unintentional motor vehicle-related CO death rates declined from 4.0 to 0.9 deaths per 1 million person-years (an estimated decline of 81.3%; 95% CI, -84.8% to -77.0%). Rates of motor vehicle-related CO suicides declined from 10.0 to 4.9 deaths per 1 million person-years (an estimated decline of 43.3%; 95% CI, -57.5% to -24.3%). During 1975-1996, an annual decrease of 10 g/mile of estimated CO emissions from automobiles was associated with a 21.3% decrease (95% CI, -24.2% to -18.4%) in the annual unintentional motor vehicle-related CO death rate and a 5.9% decrease (95%CI, -10.0% to -1.8%) in the annual rate of motor vehicle-related CO suicides. CONCLUSIONS: If rates of unintentional CO-related deaths had remained at pre-1975 levels, an estimated additional 11 700 motor vehicle-related CO poisoning deaths might have occurred by 1998. This decline in death rates appears to be a public health benefit associated with the enforcement of standards set by the 1970 Clean Air Act.
PMID: 12190369, UI: 22179606
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