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Biomedical subjects

Wendy Klein-Schwartz

Publications and source records attributed to Wendy Klein-Schwartz.

At least 19 recordsLinked to original sources
PubMed2006

Efficacy of activated charcoal administered more than four hours after acetaminophen overdose.

To evaluate whether administration of activated charcoal, in addition to standard N-acetylcysteine (NAC) therapy, after acetaminophen overdose provides additional patient benefit over NAC therapy alone, a 1-year non-randomized prospective, multi-center, observational case series was performed at three poison centers and one poison center system. Entrance criteria were all acute acetaminophen overdoses with: 1) an acetaminophen blood concentration determined to be in the toxic range by the Rumack-Matthew nomogram; and 2) all therapies, including NAC and activated charcoal, initiated between 4 and 16 h post-ingestion. There were 145 patients meeting entrance criteria, of whom 58 patients (40%) received NAC only and 87 patients (60%) received NAC and activated charcoal. Overall, 23 patients had elevations of AST or ALT greater than 1000 IU/L, of which 21 patients received NAC only (38% of total NAC only group) and 2 patients received NAC and activated charcoal (2% of total NAC+AC group). Administration of activated charcoal in this series of patients with toxic acetaminophen concentrations treated with NAC was associated with reduced incidence of liver injury, as measured by elevated serum transaminases and prothrombin times.

Acetaminophen↗
PubMed2006

2005 Annual Report of the American Association of Poison Control Centers' national poisoning and exposure database.

BACKGROUND: The American Association of Poison Control Centers (AAPCC; http://www.aapcc.org ) maintains the national database of information logged by the country's 61 Poison Control Centers (PCCs). Case records in this database are from self-reported calls: they reflect only information provided when the public or healthcare professionals report an actual or potential exposure to a substance (e.g., an ingestion, inhalation, or topical exposure.), or request information/educational materials. Exposures do not necessarily represent a poisoning or overdose. The AAPCC is not able to completely verify the accuracy of every report made to member centers. Additional exposures may go unreported to PCCs, and data referenced from the AAPCC should not be construed to represent the complete incidence of national exposures to any substance(s). U.S. Poison Centers make possible the compilation and reporting of this report through their staffs' meticulous documentation of each case using standardized definitions and compatible computer systems. The 61 participating poison centers in 2005 are: Regional Poison Control Center, Birmingham, AL; Alabama Poison Center, Tuscaloosa, AL; Arizona Poison and Drug Information Center, Tucson, AZ; Banner Poison Control Center, Phoenix, AZ; Arkansas Poison and Drug Information Center, Little Rock, AK; 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, KA; 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; Mississippi Regional Poison Control Center, Jackson, MS; Missouri Regional Poison Center, St Louis, MO; Nebraska Regional Poison Center, Omaha, NE; 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; Long Island Regional Poison and Drug Information Center, Mineola, NY; Ruth A. Lawrence Poison and Drug Information Center, Rochester, NY; Upstate (formerly Central) New York Poison Center, Syracuse, NY; Western New York Poison 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; Puerto Rico Poison Center, San Juan, PR; Palmetto Poison Center, Columbia, SC; Tennessee Poison Center, Nashville, 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; Wisconsin Poison Center, Milwaukee, WI.

Databases, Factual↗
PubMed2005

High-dose insulin therapy for calcium-channel blocker overdose.

OBJECTIVE: To evaluate the evidence for using high-dose insulin therapy with supplemental dextrose and potassium in calcium-channel blocker (CCB) overdose. DATA SOURCES: Evidence of efficacy for high-dose insulin therapy with supplemental dextrose and potassium was sought by performing a search of MEDLINE and Toxline between 1966 and July 2004 using combinations of the terms calcium-channel blocker, overdose, poisoning, antidote, and insulin. Abstracts from the North American Congress of Clinical Toxicology for the years 1996-2003 were also reviewed. STUDY SELECTION AND DATA EXTRACTION: Identified articles, including animal studies, case reports, and case series, were evaluated for this review. No clinical trials were available. DATA SYNTHESIS: Animal models of CCB overdose demonstrate that high-dose insulin with supplemental dextrose and potassium was a more effective therapy than calcium, glucagon, or catecholamines. High-dose insulin appears to enhance cardiac carbohydrate metabolism and has direct inotropic effects. Published clinical experience is limited to 13 case reports where insulin was used after other therapies were failing; 12 of these patients survived. High-dose insulin therapy was beneficial for CCB-induced hypotension, hyperglycemia, and metabolic acidosis. Bradycardia and heart block resolved in some patients, but persisted in others. CONCLUSIONS: Based on animal data and limited human experience, as well as the inadequacies of available alternatives for patients with significant poisoning, high-dose insulin therapy warrants further study and judicious use in patients with life-threatening CCB poisoning.

Adolescent↗
PubMed2005

Are 1-2 dangerous? Chloroquine and hydroxychloroquine exposure in toddlers.

Ingestion of 1-2 tablets of chloroquine or hydroxylchloroquine is thought to predispose children under 6 years of age to serious morbidity and mortality. The actual risk to the toddler and appropriate guidelines for care remain unclear at a time when both medications are therapeutically utilized as anti-inflammatory agents in addition to their main use as anti-parasitics. A review of the literature and data from the American Association of Poison Control Centers reveals instances where exposure to as little as 1-2 tablets of chloroquine resulted in serious consequences. Based on these findings, ingestions of greater than 10 mg/kg of chloroquine base or unknown amounts require triage to the nearest health care facility for 4-6 h of observation. There is very limited data on pediatric hydroxychloroquine overdoses and no reports of toxicity from 1-2 pills, but given its similarity to chloroquine, it also should be considered potentially toxic at small doses. Thus, similar recommendations should be followed for triage after accidental hydroxychloroquine overdose.

Animals↗
PubMed2005

Toxic clonidine ingestion in children.

OBJECTIVES: We performed a prospective case series to seek dosage or clinical parameters to better identify patients who need direct medical evaluation. STUDY DESIGN: All clonidine ingestions in children younger than 12 years of age reported to 6 poison centers were followed for a minimum of 24 hours. Exclusion criterion was polydrug ingestion. RESULTS: The study included 113 patients, of whom 63 were male. Mean age was 3.8 years (+/-2.4 SD). Clinical effects were common, but severe adverse effects occurred in <10% of patients. The dose ingested was reported for 90 patients (80%); 61 (68%) children ingested <0.3 mg and none had coma, respiratory depression, or hypotension. The lowest dose ingested by history with coma and respiratory depression was 0.3 mg (0.015 mg/kg). Prior clonidine therapy did not affect outcome. Onset of full clinical effects in all cases was complete within 4 hours of ingestion. CONCLUSIONS: We recommend direct medical evaluation for (1) all children 4 years of age and younger with unintentional clonidine ingestion of >or=0.1 mg, (2) ingestion of >0.2 mg in children 5 to 8 years of age, and (3) ingestion of >or=0.4 mg in children older than 8 years of age. Observation for 4 hours may be sufficient to detect patients who will develop severe effects.

Analgesics↗
PubMed2005

Evaluation of toxicity of topiramate exposures reported to poison centers.

Published literature on the toxicity of a topiramate overdose is limited to case reports. This retrospective study of poison center data was performed to examine the severity of topiramate overdoses. Data on single substance exposures to topiramate reported to the American Association of Poison Control Centers (AAPCC) Toxic Exposure Surveillance System (TESS) in 2000 and 2001 were retrospectively analysed. A total of 567 cases met the inclusion criteria, of which 39% occurred in adults over 19 years of age and 30.2% in children < or = 4 years old. The majority of patients (62.1%) experienced no toxicity. The most common clinical effects reported were drowsiness/lethargy (15.5%), dizziness/vertigo (4.9%), agitation (4.9%), confusion (3.9%), nausea (2.6%) and vomiting (2.5%). Symptomatic patients were older than asymptomatic patients and adults were more likely to be managed in a healthcare facility (P <0.0001). Patients who received gastrointestinal decontamination experienced less serious outcomes than those without decontamination (P <0.02). It is concluded that clinicians should expect relatively mild mental status changes in adults or children with toxicity from topiramate overdose. Serious toxic effects, such as CNS depression with respiratory depression or persistent non-anion gap metabolic acidosis, are infrequent.

Adolescent↗
PubMed2005

Atypical experience: a case series of pediatric aripiprazole exposures.

BACKGROUND: Aripiprazole is a new psychotropic agent that possesses a unique pharmacologic profile. The drug demonstrates mixed dopamine and serotonin agonist-antagonist activity and has been labeled a third-generation antipsychotic and dopamine-serotonin system stabilizer. Overdose experience is limited, especially in pediatrics. CASE SERIES: Of five pediatric cases identified, toxicity was mainly evident in younger patients. A 2-year-old who ingested 40 mg experienced vomiting and significant lethargy lasting approximately 30 h. A 6-year-old who received two doses of aripiprazole therapeutically experienced lethargy, drooling, and flaccid facial muscles which improved with diphenhydramine. Two adolescents remained asymptomatic despite doses of 120 mg and 300 mg while a third adolescent with an unknown dose experienced transient lethargy. CONCLUSION: Aripiprazole is capable of producing marked lethargy and gastrointestinal upset in pediatric patients. Adolescents in this series experienced only minor, if any, clinical effects. Major clinical effects, i.e., seizures, dysrhythmias, were not reported in this series.

Adolescent↗
PubMed2004

Evaluation of lamotrigine toxicity reported to poison centers.

BACKGROUND: Lamotrigine is an antiepileptic drug for the treatment of partial and generalized seizures as well as bipolar disorder. Limited published information exists describing the clinical effects of lamotrigine overdose. OBJECTIVE: To examine the toxicity of exposures to lamotrigine utilizing national poison center data. METHODS: Data on single-substance exposures to lamotrigine reported to the American Association of Poison Control Centers Toxic Exposure Surveillance System in 2000 and 2001 were retrospectively analyzed. RESULTS: There were 493 cases that met the inclusion criteria. The majority of exposures occurred within the age groups 20-59 years old (n = 198, 40.2%), followed by </=4 years old (n = 173, 35.1%). Overall, the majority of patients (52.1%) exposed to lamotrigine in overdose experienced no toxic clinical effects. The most common clinical effects reported in overdose were drowsiness/lethargy (20.9%), vomiting (11%), nausea (5.1%), ataxia (4.9%), dizziness/vertigo (4.5%), and tachycardia (4.3%). Major clinical effects included coma (n = 6), seizures (n = 8), and respiratory depression (n = 3). Medical outcome was reported as minor in 150 (30.4%), moderate in 73 (14.8%), and major in 13 (2.6%) cases. There were no deaths. CONCLUSIONS: These data demonstrate that the majority of patients exposed to lamotrigine in overdose experienced minor or no clinical effects. Although rare, serious effects can also occur.

Adolescent↗
PubMed2003

Adverse events associated with dietary supplements: an observational study.

BACKGROUND: Adverse events associated with dietary supplements are difficult to monitor in the USA, because such products are not registered before sale, and there is little information about their content and safety. METHODS: In 1998, 11 poison control centres in the USA recorded details of 2332 telephone calls about 1466 ingestions of dietary supplements, in 784 of which patients had symptoms. We used a multitiered review process (kappa 0.42) to select 489 cases for whom we were at least 50% certain that their negative events were associated with dietary supplements. We aimed to assess the effects of multiple ingredients and long-term use, and collated data for patterns of use and information resources. FINDINGS: A third of events were of greater than mild severity. We noted both new and previously reported associations that included myocardial infarction, liver failure, bleeding, seizures, and death. Increased symptom severity was associated with use of several ingredients, long-term use, and age. Paediatric exposures were more often unintentional than were adult ingestions, and treatment of disease was the reason for supplement use in at least 28% of reports. Most products and ingredients were not identified in the information database (Poisindex) used by poison control centres, and specific adverse events were reported variably among five additional sources. INTERPRETATION: Dietary supplements are associated with adverse events that include all levels of severity, organ systems, and age groups. Associations between adverse events and ingredients are difficult to verify if a product has more than one ingredient, and because of incomplete information systems. Research into hazards and risks of dietary supplements should be a priority.

Adolescent↗
PubMed2003

Characterization of gabapentin overdose using a poison center case series.

BACKGROUND: Gabapentin is an anticonvulsant that is being used for an increasing number of off-label indications. The purpose of this study is to document the clinical manifestations and outcomes of gabapentin exposures reported to poison centers. METHODS: A multicenter prospective observational study of all gabapentin exposures reported to three poisoncenters was conducted between 4/1/98 and 4/1/2000. Cases involving gabapentin only were evaluated. RESULTS: There were 20 cases with gabapentin as the sole substance in doses ranging from 50 mg to 35 g. Ten of the 20 cases involved children and adolescents. Clinical effects developed early and resolved within 10 hours in most patients. Seven cases were managed in the home with only observation. Four of these patients remained asymptomatic. Effects reported in the three symptomatic patients were drowsiness (3) and ataxia (1). Thirteen patients were managed in a health care facility. Nine were symptomatic with reported effects of drowsiness (6), dizziness (3), nausea/vomiting (2), tachycardia (2), and hypotension (2). None of the patients were admitted for medical care. CONCLUSION: In this cases series, gabapentin exposures caused no or minimal toxicity.

Acetates↗
PubMed2003

Poison centers' experience with methylphenidate abuse in pre-teens and adolescents.

OBJECTIVE: To evaluate trends and toxicity of methylphenidate abuse in pre-teens and adolescents reported to poison centers. METHOD: The 1993-1999 American Association of Poison Control Centers Toxic Exposure Surveillance System was queried for methylphenidate abuse cases in children aged 10 through 19 years that were followed to known outcome. Main outcome measures included number of cases annually, toxicity, management site, and coded medical outcome. RESULTS: Of 759 cases, 42.7% involved 10-through 14-year-olds. For the 530 (70.0%) cases involving methylphenidate only, the frequency increased sevenfold from 1993 to 1999. Of 570 patients (75.1%) managed in a health care facility, 398 were discharged from the emergency department and 172 were admitted. Symptoms occurred more commonly in exposures involving coingestants (84.3%) than in methylphenidate-only exposures (71.1%). The most common symptoms in adolescents with methylphenidate only were tachycardia (31.7%), agitation/irritability (25.7%), and hypertension (11.5%). Outcomes were no effect in 189 cases (24.9%) and mild, moderate, and severe in 318 (41.9%), 245 (32.3%), and 7 (0.9%) patients, respectively. CONCLUSIONS: Poison center data demonstrate increasing frequency of methylphenidate abuse. While the majority of adolescents experienced clinical effects and were managed in a health care facility, outcomes were good, especially in cases involving methylphenidate only.

Adolescent↗
PubMed2003

Pediatric methylphenidate exposures: 7-year experience of poison centers in the United States.

This study was undertaken to evaluate trends and toxicity of pediatric methylphenidate exposures; 1993 to 1999 national poison center data were analyzed. There were 12,917 exposures, increasing from 927 in 1993 to 2,445 in 1999. The majority of children during the entire study period experienced no effect (60.3%) or minor effects (28.7%), with no fatalities. Most common reasons were unintentional general or therapeutic errors in children under 13 years and suicide attempt in adolescents. Adolescents were more likely to experience clinical toxicity, hospitalizations and more serious outcomes. The trend of increasing frequency of methylphenidate exposures reported to poison centers exactly parallels increasing therapeutic use.

Adolescent↗
PubMed2002

Trends and toxic effects from pediatric clonidine exposures.

OBJECTIVE: To analyze the trends, demographics, and toxic effects associated with pediatric clonidine hydrochloride exposures reported to poison centers. DESIGN: Retrospective. SETTING AND PATIENTS: Clonidine-only exposures followed up to known outcome in children younger than 19 years reported to the American Association of Poison Control Center's database from January 1, 1993, through December 31, 1999. MAIN OUTCOME MEASURES: Frequency of exposures over time, acuity, reason, symptoms, management site, treatment, and outcome. RESULTS: There were 10 060 reported exposures with 57% reported for children younger than 6 years, 34% for children between 6 and 12 years old, and 9% for adolescents between 13 and 18 years old. In 1999 there were 2.5 times as many exposures as in 1993. In 6- through 12-year-olds, clonidine was the child's medication in 35% of the exposures, compared with 10% in children younger than 6 years and 26% in adolescents. The proportion of cases involving the child's medication increased over 7 years. While unintentional overdose was most common in children younger than 6 years, therapeutic errors and suicide attempts predominated in 6- through 12-year-olds and adolescents, respectively. In 6042 symptomatic children (60%), the most common symptoms were lethargy (80%), bradycardia (17%), hypotension (15%), and respiratory depression (5%). Most exposures resulted in no effect (40%) or minor effects (39%). Moderate effects occurred in 1907 children (19%), major effects in 230 children (2%); there was 1 fatality in a 23-month-old. CONCLUSIONS: While most of the clonidine exposures resulted in minimal toxic effects, serious toxic effects and death can occur. The trend toward increasing the number of exposures in children, especially with evidence of toxic effects in children receiving clonidine therapeutically, is cause for concern.

Adolescent↗