Lewis S Nelson, M.D.

Solid-phase extraction and quantitative measurement of omega and omega-1 metabolites of JWH-018 and JWH-073 in human urine
Chimalakonda, Krishna C; Moran, Cindy L; Kennedy, Paul D; Endres, Gregory W; Uzieblo, Adam; Dobrowolski, Paul J; Fifer, E Kim; Lapoint, Jeff; Nelson, Lewis S; Hoffman, Robert S; James, Laura P; Radominska-Pandya, Anna; Moran, Jeffery H
2011 Aug 15;83(16):6381-6388, Analytical chemistry
The aminoalkylindole agonists JWH-018 and JWH-073 are contained in 'K2/SPICE' products sold as 'legal marijuana'. Previous human metabolic studies have identified (omega)-hydroxyl and (omega)-carboxyl metabolites as biomarkers that are indicative of product use. However, other primary metabolites exhibiting similar chromatographic properties and mass spectra are also excreted in human urine. Analytical standards were used in this study to identify new primary metabolites as (omega-1)-hydroxyl derivatives of JWH-018 and JWH-073. The liquid chromatography tandem mass spectrometry (LC-MS/MS) procedure, coupled with an automated solid-phase extraction procedure incorporating deuterium-labeled internal standards, provides rapid resolution of the (omega)- and (omega-1) metabolites with adequate sensitivity, precision, and accuracy for trace analysis in human urine. Results from four urine specimens collected after individuals reportedly self-administered either JWH-018 or a mixture of JWH-018 and JWH-073 showed the following: (1) all tested metabolites were excreted in high concentrations, (2) (omega)- and (omega-1)-hydroxyl metabolites were exclusively excreted as glucuronic acid conjugates, and (3) approximately 5%-80% of the (omega)-carboxyl metabolites was excreted as glucuronic acid conjugates. This is the first report to identify and quantify (omega-1)-hydroxyl metabolites of JWH-018 and JWH-073 and the first to incorporate automated extraction procedures using deuterium-labeled internal standards. Full clinical validation awaits further testing
— id: 137987, year: 2011, vol: 83, page: 6381, stat: Journal Article,

Conflicts of interest on pharmacy and therapeutics committees at academic medical centers
Farmer, Brenna M; Nelson, Lewis S
2011 Jun;7(2):175-176, Journal of medical toxicology
— id: 136482, year: 2011, vol: 7, page: 175, stat: Journal Article,

Hemodialysis Clearance of Glyphosate Following a Life-threatening Ingestion of Glyphosate-Containing Herbicide
Garlich, F. M.; Goldman, M.; Pepe, J.; Nelson, L. S.; Allan, M. J.; Goldstein, D. A.; Goldfarb, D. S.; Hoffman, R. S.
2011 MAR ;49(3):264-264, Clinical Toxicology (Philadelphia)
— id: 131941, year: 2011, vol: 49, page: 264, stat: Journal Article,

Delayed Respiratory Distress in an Infant Following Inhalation of Talc-Containing Baby Powder
Garlich, F. M.; Hoffman, R. S.; Nelson, L. S.
2011 MAR ;49(3):264-264, Clinical Toxicology (Philadelphia)
— id: 131940, year: 2011, vol: 49, page: 264, stat: Journal Article,

The Use of Extracorporeal Techniques in Acute Acetaminophen (Paracetamol) Poisoning
Holubek, W. J.; Kemp, B. O.; Goldfarb, D. S.; Nelson, L. S.; Hoffman, R. S.
2011 MAR ;49(3):248-248, Clinical Toxicology (Philadelphia)
— id: 131938, year: 2011, vol: 49, page: 248, stat: Journal Article,

Methylene Blue in the Treatment of Refractory Shock From an Amlodipine Overdose
Jang DH; Nelson LS; Hoffman RS
2011 Dec;58(6):565-567, Annals of emergency medicine
Amlodipine is a potent vasodilator with a long half-life and delayed onset of action that is particularly concerning after an overdose. Vasodilation occurs through stimulation of nitric oxide release with increased cyclic guanosine monophosphate (cGMP) production. Methylene blue inhibits guanylate cyclase. This enzyme is responsible for the production of cGMP. Methylene blue also has the ability to scavenge nitric oxide, as well as inhibit nitric oxide synthase. We report the use of methylene blue for refractory shock in a patient with amlodipine toxicity
— id: 134662, year: 2011, vol: 58, page: 565, stat: Journal Article,

Levamisole-induced Occlusive Necrotizing Vasculitis in a Pregnant Woman after Use of Cocaine Contaminated with Levamisole
Jang, D. H.; Hoffman, R. S.; Nelson, L. S.; Stajic, M.; Smith, S. W.
2011 MAR ;49(3):216-216, Clinical Toxicology (Philadelphia)
— id: 131937, year: 2011, vol: 49, page: 216, stat: Journal Article,

Fatal outcome of a propoxyphene/acetaminophen (Darvocet) overdose: should it still be used in the United States?
Jang, David H; Hoffman, Robert S; Nelson, Lewis S; Chu, Jason; Bhanot, Kavita; Bagley, William
2011 Apr;57(4):421-422, Annals of emergency medicine
— id: 133183, year: 2011, vol: 57, page: 421, stat: Journal Article,

Response to 'benefit effect of naloxone in benzodiazepines intoxication: findings of a preliminary study'
Jang, David H; Tolchin, Benjamin; Bruccoleri, Rebecca; Nelson, Lewis S
2011 Apr;30(4):343-343, Human & Experimental Toxicology
— id: 134664, year: 2011, vol: 30, page: 343, stat: Journal Article,

Severe toxicity following synthetic cannabinoid ingestion
Lapoint, J; James, L P; Moran, C L; Nelson, L S; Hoffman, R S; Moran, J H
2011 Oct;49(8):760-764, Clinical Toxicology (Philadelphia)
Objective. To report a case of seizures and supraventricular tachycardia (SVT) following confirmed synthetic cannabinoid ingestion. Background. Despite widespread use of legal synthetic cannabinoids, reports of serious toxicity following confirmed use of synthetic cannabinoids are rare. We report severe toxicity including seizures following intentional ingestion of the synthetic cannabinoid JWH-018 and detail confirmation by laboratory analysis. Case Report. A healthy 48 year old man had a generalized seizure within thirty minutes of ingesting an ethanol mixture containing a white powder he purchased from the Internet in an attempt to get high. Seizures recurred and abated with lorazepam. Initial vital signs were: pulse, 106/min; BP, 140/88 mmHg; respirations, 22/min; temperature, 37.7 degrees C. A noncontrast computed tomography of the brain and EEG were negative, and serum chemistry values were normal. The blood ethanol concentration was 3.8 mg/dL and the CPK 2,649 U/L. Urine drug screening by EMIT was negative for common drugs of abuse, including tetrahydrocannabinol. On hospital day 1, he developed medically refractory SVT. The patient had no further complications and was discharged in his normal state of health 10 days after admission. The original powder was confirmed by gas chromatography mass spectrometry to be JWH-018, and a primary JWH-018 metabolite was detected in the patient's urine (200 nM) using liquid chromatography tandem mass spectrometry. Discussion. Synthetic cannabinoids are legal in many parts of the world and easily obtained over the Internet. Data on human toxicity are limited and real-time confirmatory testing is unavailable to clinicians. The potential for toxicity exists for users mistakenly associating the dose and side effect profiles of synthetic cannabinoids to those of marijuana. Conclusion. Ingestion of JWH-018 can produce seizures and tachyarrhythmias. Clinicians, lawmakers, and the general public need to be aware of the potential for toxicity associated with synthetic cannabinoid use
— id: 139910, year: 2011, vol: 49, page: 760, stat: Journal Article,

Life-Threatening Bupropion Ingestion: Is There a Role for Intravenous Fat Emulsion?
Livshits Z; Feng Q; Chowdhury F; Amdo TD; Nelson LS; Hoffman RS
2011 Nov;109(5):418-22 L, Basic & Clinical Pharmacology & Toxicology
Intravenous fat emulsion (IFE) is emerging as a novel antidote in clinical toxicology. Its current usage is extending beyond local anaesthetic toxicity into management of severe toxicity from some lipophilic drugs. We present a 51-year-old woman with severe bupropion toxicity whose haemodynamic status transiently improved after IFE. Serum analysis demonstrated an increase in serum concentration of hydroxybupropion, an active metabolite of bupropion, after IFE administration, lending support to one of the proposed mechanisms of IFE. A 51-year-old woman presented to the emergency department with generalised tonic-clonic convulsions lasting approximately 30 sec., and a wide complex rhythm on her ECG that was suggestive of myocardial sodium channel blockade. Despite sodium bicarbonate therapy, the patient developed profound hypotension refractory to high-dose norepinephrine. IFE was administered with haemodynamic improvement over the course of 30 min., followed by a significant decrease in norepinephrine requirement. The patient had an episode of ventricular tachycardia 24 hr after presentation, and received a second infusion of IFE. Analysis of serum for a panel of myocardial sodium channel blocking drugs revealed that significant bupropion ingestion had occurred. Bupropion poisoning may produce life-threatening clinical effects, and IFE may be considered in cases of severe haemodynamic instability. Further studies would be instrumental in determining the optimal clinical situations for utilisation of IFE
— id: 137325, year: 2011, vol: 109, page: 418, stat: Journal Article,

Zidovudine (AZT) overdose in a healthy newborn receiving postnatal prophylaxis
Livshits Z; Lee S; Hoffman RS; Nelson LS; Esteban-Cruciani N
2011 Oct;49(8):747-749, Clinical Toxicology (Philadelphia)
Context. Pediatric medication dosing and administration, faced with inherent challenges of dose to body weight adjustment and variable delivery vehicles, may lead to inadvertent errors effectively resulting in overdose. Zidovudine (AZT), a nucleoside analog reverse transcriptase inhibitor (NRTI), is a commonly prescribed medication to treat HIV-exposed newborns, with limited overdose data in this patient population. Metabolic acidosis with elevated lactate is the most serious consequence of AZT toxicity in the adult population, associated with mortality. Other significant effects may include neutropenia and hepatic dysfunction. Case report. A 4-day-old male infant who received two inadvertent 10-fold overdoses of AZT while being treated for HIV postnatal prophylaxis. The newborn developed a transient metabolic acidosis with elevated lactate that resolved within 24 h, a small increase in AST, and persistent neutropenia for 5 weeks. The patient's mother cited several key factors leading to the dosing error. Discussion. The paucity of AZT overdose data in newborns and infants compels this case report, which reviews the published literature and provides insight into prevention and improvement of pediatric patient safety
— id: 137326, year: 2011, vol: 49, page: 747, stat: Journal Article,

Electroconvulsive Therapy for Severe Refractory Neuroleptic Malignant Syndrome
Livshits, Z.; Larocque, A.; Schwartz, D. R.; Papadopoulos, J.; Ying, P.; Nelson, L. S.; Hoffman, R. S.
2011 MAR ;49(3):209-210, Clinical Toxicology (Philadelphia)
— id: 131936, year: 2011, vol: 49, page: 209, stat: Journal Article,

Retained Drugs in the Deceased
Livshits, Z.; Sampson, B.; Howland, M. A.; Hoffman, R. S.; Garlich, F.; Nelson, L. S.
2011 MAR ;49(3):260-260, Clinical Toxicology (Philadelphia)
— id: 131939, year: 2011, vol: 49, page: 260, stat: Journal Article,

If vitamins could kill: massive hemolysis following naturopathic vitamin infusion
Livshits, Zhanna; Hoffman, Robert S; Hymes, Kenneth B; Nelson, Lewis S
2011 Sep;7(3):224-226, Journal of medical toxicology
INTRODUCTION: Hemolysis from naturopathic remedies remains poorly reported in the medical literature, although it is most commonly noted in the patients with glucose 6-phosphate dehydrogenase (G6PD) deficiency. We report a case of massive intravascular hemolysis following the infusion of a naturopathic preparation that contains vitamins. CASE REPORT: A 47-year-old African-American man presented to the hospital with 3 days of fever, dyspnea, emesis, dark urine, and progressive confusion. His symptoms began 1 day following an infusion of a vitamin complex. His physical examination was significant for lethargy and scleral icterus. Initial laboratory studies were notable for anemia (hemoglobin, 3.3 g/dL and hematocrit, 11%), brisk reticulocytosis (33%), acute renal insufficiency (creatinine, 2.8 mg/dL), and indirect hyperbilirubinemia (total bilirubin, 4.4 mg/dL). His peripheral smear demonstrated 'blister cells,' erythrocytes that have been left devoid of precipitated hemoglobin by the spleen, which are commonly seen in patients with G6PD deficiency. His physician revealed that the infusion contained vitamins B and D complex, free amino acids, magnesium, and taurine. The patient clinically improved and was discharged to home. G6PD concentration was significantly reduced to 4.7 U/g Hb upon recovery. DISCUSSION: Life-threatening intravascular hemolysis may occur following a naturopathic vitamin infusion and may identify previously unknown G6PD deficiency. Since most properly formulated naturopathic treatments have few toxic ingredients, the possibilities of improper formulation, toxic diluents, or contaminants should be considered. Inadequate regulatory oversight of naturopathic remedies has the potential to allow serious toxicity especially in genetically predisposed individuals
— id: 137324, year: 2011, vol: 7, page: 224, stat: Journal Article,

The authors' reply
Manini A.F.; Nelson L.S.; Hoffman R.S.
2011 ;11(6):419-420, American journal of cardiovascular drugs : drugs, devices, & other interventions
— id: 147757, year: 2011, vol: 11, page: 419, stat: Journal Article,

Prognostic utility of serum potassium in chronic digoxin toxicity: a case-control study
Manini, Alex F; Nelson, Lewis S; Hoffman, Robert S
2011 Jun 1;11(3):173-178, American journal of cardiovascular drugs : drugs, devices, & other interventions
OBJECTIVE: In contrast to patients with acute digoxin overdose, the prognostic utility of the serum potassium concentration for patients with chronic digoxin toxicity is unclear. In such patients, we aimed to evaluate the relationship between pre-treatment serum potassium and survival. METHODS: This was a case-control study at an urban Poison Control Center affiliated with a large urban medical center. We compared the serum potassium concentration between patients with chronic digoxin toxicity resulting in fatality (cases) over a 7-year period (2000-2006) versus survivors (controls) over a 1-year period (2007-2008). RESULTS: During the study period, there were 13 fatalities (cases) and 13 survivors (controls), of whom seven cases and five controls received appropriately dosed digoxin-specific antibody Fab fragments (Fab). There were no statistically significant differences between cases and controls with respect to serum digoxin concentration, creatinine, age, or sex. Serum potassium elevation pre-Fab was significantly associated with fatality both in mean difference (p < 0.03) and using a dichotomous cutoff of 5.0 mEq/L (p < 0.001), which performed with 92% sensitivity (95% CI 67, 99). In 86% of deaths despite appropriate Fab administration, the clinical presentation included the combination of bradycardia plus hyperkalemia. CONCLUSION: In these patients with chronic digoxin toxicity, elevated serum potassium was associated with fatality. The combination of bradycardia and hyperkalemia strongly predicted fatality even in cases with appropriate Fab administration
— id: 137997, year: 2011, vol: 11, page: 173, stat: Journal Article,

Medical examiner and medical toxicologist agreement on cause of death
Manini, Alex F; Nelson, Lewis S; Olsen, Dean; Vlahov, David; Hoffman, Robert S
2011 Mar 20;206(1-3):71-76, Forensic science international
Poisoning is a significant public health threat as the second leading cause of injury-related death in the US. Disagreements on cause of death determination may have widespread implications across several realms of public health including policy and prevention efforts, interpretation of the poisoning literature, epidemiologic data analysis, medical-legal case outcomes, and individualized autopsy interpretation. We aimed to test agreement between the cause of death determined by the medical examiner (ME) and a medical toxicologist (MT) adjudication panel (MTAP) in cases of poisoning. This retrospective 7-year study evaluated all deaths attributed to poisoning in one large urban catchment area. Cross-matched data were obtained from Department of Vital Statistics and the Poison Control Center (PCC). Out of >380,000 deaths in the catchment area over the study period, there were 7050 poisonings in the Vital Statistics database and 414 deaths reported to PCC. Cross-matching yielded 321 cases for analysis. The ME and MTAP concurred on cause of death in 66%, which was only fair agreement (kappa 0.25, CI 0.14-0.38). Factors associated with the likelihood of agreement were peri-mortem fire exposures, prehospital cardiac arrest, and timing of drug toxicity (chronic versus acute). In conclusion, agreement for poisoning cause of death between specialties was much lower than expected. We recommend an improved formal process of information sharing and consultation between specialties to assure that all existing information is analyzed thoroughly to enhance cause of death certainty
— id: 134209, year: 2011, vol: 206, page: 71, stat: Journal Article,

Bilateral loculated pleural effusion as a manifestation of acute parenteral organophosphate intoxication: A case report
Moin-Azad Tehrani M.-S.; Soltaninejad K.; Yazdani S.; Nelson L.S.; Shadnia S.
2011 ;41(6):630-634, Journal of emergency medicine
Acute organophosphate (OP) toxicity causes a wide range of clinical effects on the respiratory system, including pulmonary bronchoconstriction and bronchorrhea. Morbidity and mortality from acute OP toxicity correlate best with pulmonary secretions. In this article, we report bilateral loculated pleural effusion as a rare pulmonary effect in a patient with acute parenteral OP toxicity. A 25-year-old, previously healthy woman was transferred to our Poison Department 3 days after suicidal injection of malathion. At the time of presentation her vital signs were normal, except that her respiratory rate was 24 breaths/min. She complained of pleuritic chest pain and had a cough productive of yellow sputum. She had generalized chest wall tenderness, and breath sounds were decreased in the base of both lung fields. Standard therapy for OP toxicity, including atropine, pralidoxime, and diazepam, was initiated. Due to persistent pleuritic chest pain, a computed tomography (CT) scan was performed that showed bilateral loculated pleural effusions. Shortly after hospital admission, the patient developed respiratory distress, for which she was intubated and transferred to the Intensive Care Unit. She received continued medical therapy and was extubated on hospital day 3. A CT scan of the chest on hospital day 9, after completion of the treatment, documented resolution of the effusions. Parenteral OP toxicity occurs rarely, and in this case it was associated with bilateral loculated pleural effusions. In this regard, it should be considered in a patient with acute parenteral OP toxicity and persistent chest wall pain.
— id: 147738, year: 2011, vol: 41, page: 630, stat: Journal Article,

Abstracts from the joint american-israeli medical toxicology conference american college of medical toxicology and the Israel society of toxicology november 16-17, 2010 rambam medical center, haifa, Israel
Nelson, Lewis
2011 Mar;7(1):67-78, Journal of medical toxicology
— id: 127225, year: 2011, vol: 7, page: 67, stat: Journal Article,

Pharmacy and therapeutics committees: leadership opportunities in medication safety for medical toxicologists
Perrone, Jeanmarie; Nelson, Lewis S
2011 Jun;7(2):99-102, Journal of medical toxicology
— id: 136483, year: 2011, vol: 7, page: 99, stat: Journal Article,

Inaccuracy of ECG interpretations reported to the poison center
Prosser, Jane M; Smith, Silas W; Rhim, Eugene S; Olsen, Dean; Nelson, Lewis S; Hoffman, Robert S
2011 Feb;57(2):122-127, Annals of emergency medicine
STUDY OBJECTIVE: The ECG is an essential tool in the care of poisoned patients. This study is designed to investigate the accuracy of ECG interpretation reported to a poison center. METHODS: In this prospective study, all cases in which both an electronically faxed copy of the ECG and the caller's interpretation of the ECG were available were eligible for inclusion. ECG interpretation of callers was compared with that of a blinded electrophysiologist. In cases of disagreement, a Delphi panel of toxicologists decided whether the differences were clinically significant or would have changed recommendations. RESULTS: Two hundred cases were included, with complete agreement in 78. In 23 cases, the sole difference was nonspecific ST-T-wave changes, which were believed insignificant and classified as agreement for a total of 101. The Delphi panel reviewed the remaining 99. In 42 cases, the differences in ECG interpretations were thought to be clinically significant; 37 of these would have resulted in a change in management recommendations. Forty-five cases were thought not likely to be clinically significant and would not have resulted in a recommendation change. Twelve cases were thought not clinically significant but would still have resulted in a change in recommendations. CONCLUSION: Initial interpretation of the ECG reported by callers to the poison center is frequently inaccurate. In this study, the misinterpretation was clinically significant or would have resulted in a change in management recommendations in approximately one quarter of all calls
— id: 133208, year: 2011, vol: 57, page: 122, stat: Journal Article,

Emergency medicine residents' use of psychostimulants and sedatives to aid in shift work
Shy, Bradley D.; Portelli, Ian; Nelson, Lewis S.
2011 NOV ;29(9):1034-U342, American journal of emergency medicine
Objectives: We evaluated the frequency that emergency medicine house staff report use of stimulants and sedatives to aid in shift work and circadian transitions. Methods: We surveyed residents from 12 regional emergency medicine programs inviting them to complete a voluntary, anonymous electronic questionnaire regarding their use of stimulants and sedatives. Results: Out of 485 eligible residents invited to participate in the survey, 226 responded (47% response frequency). The reported use of prescription stimulants for shift work is uncommon (3.1% of respondents.) In contrast, 201 residents (89%) report use of caffeine during night shifts, including 118 residents (52%) who use this substance every night shift. Eighty-six residents (38%) reported using sedative agents to sleep following shift work with the most common agents being anti-histamines (31%), nonbenzodiazepine hypnotics such as zolpidem (14%), melatonin (10%), and benzodiazepines (9%). Conclusion: Emergency medicine residents report substantial use of several classes of hypnotics to aid in shift work. Despite anecdotal reports, use of prescription stimulants appears rare, and is notably less common than use of sedatives and non-prescription stimulants. (C) 2011 Elsevier Inc. All rights reserved
— id: 147015, year: 2011, vol: 29, page: 1034, stat: Journal Article,

Unusual complication of aluminum phosphide poisoning: Development of hemolysis and methemoglobinemia and its successful treatment
Soltaninejad, Kambiz; Nelson, Leiws S; Khodakarim, Nastaran; Dadvar, Zohreh; Shadnia, Shahin
2011 Apr;15(2):117-119, Indian Journal of Critical Care Medicine
Methemoglobinemia and hemolysis are rare findings following phosphine poisoning. In this paper, a case of aluminum phosphide (AlP) poisoning complicated by methemoglobinemia and hemolysis with a successful treatment is reported. A 28-year-old male patient presented following intentional ingestion of an AlP tablet. In this case, hematuria, hemolysis and methemoglobinemia were significant events. A methemoglobin level of 46% was detected by CO-oximetry. The patient was treated with ascorbic acid and methylene blue and he also received supportive care. Two weeks after admission, the patient was discharged from the hospital. Hemolysis and methemoglobinemia may complicate the course of phosphine poisoning
— id: 136487, year: 2011, vol: 15, page: 117, stat: Journal Article,

The Agent Profile: Sixteen Attributes as a Framework for Risk Determination and Response to Agents of Opportunity in Academic Medical Centers
Farmer, B. M.; Nelson, L. S.; Tunik, M. G.; Graham, M. E.; Bendzans, C.; McCrillis, A.; Portelli, I; Zhang, M.; Goldberg, J. D.; Goldfrank, L. R.
2010 MAR ;48(3):256-256, Clinical Toxicology (Philadelphia)
— id: 139127, year: 2010, vol: 48, page: 256, stat: Journal Article,

Developing a consensus framework and risk profile for agents of opportunity in academic medical centers: implications for public health preparedness
Farmer, Brenna M; Nelson, Lewis S; Graham, Margaret E; Bendzans, Carly; McCrillis, Aileen M; Portelli, Ian; Zhang, Meng; Goldberg, Judith; Rosenberg, Sheldon D; Goldfrank, Lewis R; Tunik, Michael
2010 Dec;4(4):318-325, Disaster medicine & public health preparedness
Agents of opportunity (AO) in academic medical centers (AMC) are defined as unregulated or lightly regulated substances used for medical research or patient care that can be used as 'dual purpose' substances by terrorists to inflict damage upon populations. Most of these agents are used routinely throughout AMC either during research or for general clinical practice. To date, the lack of careful regulations for AOs creates uncertain security conditions and increased malicious potential. Using a consensus-based approach, we collected information and opinions from staff working in an AMC and 4 AMC-affiliated hospitals concerning identification of AO, AO attributes, and AMC risk and preparedness, focusing on AO security and dissemination mechanisms and likely hospital response. The goal was to develop a risk profile and framework for AO in the institution. Agents of opportunity in 4 classes were identified and an AO profile was developed, comprising 16 attributes denoting information critical to preparedness for AO misuse. Agents of opportunity found in AMC present a unique and vital gap in public health preparedness. Findings of this project may provide a foundation for a discussion and consensus efforts to determine a nationally accepted risk profile framework for AO. This foundation may further lead to the implementation of appropriate regulatory policies to improve public health preparedness. Agents of opportunity modeling of dissemination properties should be developed to better predict AO risk
— id: 122674, year: 2010, vol: 4, page: 318, stat: Journal Article,

Extracorporeal Removal Techniques for the Poisoned Patient: A Review for the Intensivist
Fertel, Baruch S; Nelson, Lewis S; Goldfarb, David S
2010 May-Jun;25(3):139-148, Journal of intensive care medicine
The kidney is able to rapidly eliminate many water-soluble xenobiotics (exogenous chemicals). However, in the face of extraordinary serum concentrations of these xenobiotics or renal dysfunction, alternative elimination techniques often become necessary. Extracorporeal removal (ECR) techniques are used to increase the clearance of xenobiotics. These techniques include hemodialysis (HD), charcoal hemoperfusion (HP), and modalities grouped under the heading of continuous renal replacement therapy (CRRT): continuous venovenous hemofiltration (CVVH) and continuous venovenous hemodiafiltration (CVVHDF). Extracorporeal removal is limited to patients with significant or potentially significant clinical poisoning because the resources required to perform ECR are great. Therefore, most patients who are treated with these techniques are being cared for in intensive care units (ICUs). Our goal in this review is to discuss the properties that make xenobiotics amenable to removal by ECR and the advantages and disadvantages of the individual techniques. We discuss xenobiotics that constitute clear indications for ECR, including the toxic alcohols, salicylates, and lithium. We review the use of CRRT, a modality for which clear indications for treatment of poisonings are currently lacking
— id: 109553, year: 2010, vol: 25, page: 139, stat: Journal Article,

Agent of opportunity risk mitigation: people, engineering, and security efficacy
Graham, Margaret E; Tunik, Michael G; Farmer, Brenna M; Bendzans, Carly; McCrillis, Aileen M; Nelson, Lewis S; Portelli, Ian; Smith, Silas; Goldberg, Judith D; Zhang, Meng; Rosenberg, Sheldon D; Goldfrank, Lewis R
2010 Dec;4(4):291-299, Disaster medicine & public health preparedness
BACKGROUND: Agents of opportunity (AO) are potentially harmful biological, chemical, radiological, and pharmaceutical substances commonly used for health care delivery and research. AOs are present in all academic medical centers (AMC), creating vulnerability in the health care sector; AO attributes and dissemination methods likely predict risk; and AMCs are inadequately secured against a purposeful AO dissemination, with limited budgets and competing priorities. We explored health care workers' perceptions of AMC security and the impact of those perceptions on AO risk. METHODS: Qualitative methods (survey, interviews, and workshops) were used to collect opinions from staff working in a medical school and 4 AMC-affiliated hospitals concerning AOs and the risk to hospital infrastructure associated with their uncontrolled presence. Secondary to this goal, staff perception concerning security, or opinions about security behaviors of others, were extracted, analyzed, and grouped into themes. RESULTS: We provide a framework for depicting the interaction of staff behavior and access control engineering, including the tendency of staff to 'defeat' inconvenient access controls. In addition, 8 security themes emerged: staff security behavior is a significant source of AO risk; the wide range of opinions about 'open' front-door policies among AMC staff illustrates a disparity of perceptions about the need for security; interviewees expressed profound skepticism concerning the effectiveness of front-door access controls; an AO risk assessment requires reconsideration of the security levels historically assigned to areas such as the loading dock and central distribution sites, where many AOs are delivered and may remain unattended for substantial periods of time; researchers' view of AMC security is influenced by the ongoing debate within the scientific community about the wisdom of engaging in bioterrorism research; there was no agreement about which areas of the AMC should be subject to stronger access controls; security personnel play dual roles of security and customer service, creating the negative perception that neither role is done well; and budget was described as an important factor in explaining the state of security controls. CONCLUSIONS: We determined that AMCs seeking to reduce AO risk should assess their institutionally unique AO risks, understand staff security perceptions, and install access controls that are responsive to the staff's tendency to defeat them. The development of AO attribute fact sheets is desirable for AO risk assessment; new funding and administrative or legislative tools to improve AMC security are required; and security practices and methods that are convenient and effective should be engineered
— id: 116222, year: 2010, vol: 4, page: 291, stat: Journal Article,

Severe prolonged encephalopathy from an intentional lamotrigine overdose with significantly elevated and prolonged serum concentrations
Hernandez S.H.; Habib S.; Howland M.A.; Hoffman R.S.; Nelson L.S.
2010 ;48(6):645-645, Clinical Toxicology (Philadelphia)
Background: Lamotrigine (LTG) is well-tolerated in therapeutic doses, undergoes first order kinetics with a t1/2 of 22-36 h, and is hepatically metabolized mainly via UGT1A4. At 2.5 mg/kg/day, steady-state serum LTG concentrations are approximately 2.5 mug/mL. However, the toxicodynamics and toxicokinetics are poorly appreciated. We describe the toxicokinetics in massive extended-release (XR) LTG overdose with exceedingly high concentrations and prolonged encephalopathy. Case report: A 40-year-old woman ingested 6 g of XR-LTG. PMH included glioblastoma multiforme, seizures, and depression. She was recently admitted for a clonazepam and quetiapine overdose; both drugs were subsequently discontinued. On the afternoon of discharge a prescription was filled for 30 (200 mg) XR-LTG, 21 (2 mg) dexamethasone, and 30 (20 mg) famotidine. Within 24 h after discharge she presented to the ED, arousable to voice, answering questions appropriately, and admitting to ingesting 30 XR-LTG. Vitals signs were: BP, 109/67 mmHg; HR, 82/min; RR, 15/min; 100% SpO2 RA; T, 97.0degreeF orally. Physical exam and initial laboratory studies, including urine drug of abuse screen, and an ECG were unremarkable. A head CT was consistent with her previous surgery. Within 6 h of observation she developed agitated delirium, mutism and was unable to follow commands. Nystagmus and muscle rigidity were absent. Tremor was noted, lower extremity reflexes were hyperactive, and rectal temp was 99.1degreeF. Lorazepam controlled her agitation. Although all meds were discontinued except dexamethasone, she developed catatonia. Lab values and vital signs remained unchanged, and a video EEG was unremarkable. A serum LTG concentration collected 5 days post ingestion was 49.5, 40.5 mug/mL at 6 days, 29.3 mug/mL at 7 days, and 16.5 mug/mL at 9 days (apparent t1/2 of 60.6 h); she gradually improved returning to baseline by day 9. Discussion: In this patient with a solitary XR-LTG overdose the serial concentrations confirmed apparent first order elimination with a prolonged t1/2 that correlated with clinical toxicity. Conclusion: Significant prolonged encephalopathy can occur with XR-LTG overdose. The apparent t1/2 may be as long as 60 h
— id: 113827, year: 2010, vol: 48, page: 645, stat: Journal Article,

Prescription drug abuse: insight into the epidemic
Hernandez, S H; Nelson, L S
2010 Sep;88(3):307-317, Clinical pharmacology & therapeutics
The emergence of clinically efficacious prescription drugs to treat pain, anxiety, and learning disorders is accompanied by the potential for nonmedical use. Prescription drug abuse has become a modern-day epidemic in the United States and is now second only to marijuana use across all age groups. This article reviews the various data collection, analysis, and reporting systems that have been developed in response to the growing concern for nonmedical prescription drug use. The terminology used to categorize prescription drugs that are abused and the various definitions for abuse, misuse, and nonmedical use are discussed. The epidemiology of nonmedical prescription drug use and an overview of each class of prescription drug that is at risk for nonmedical use are presented along with details of specific drugs that are associated with significant morbidity or mortality
— id: 111966, year: 2010, vol: 88, page: 307, stat: Journal Article,

Paradichlorobenzene Induced Leukoencephalopathy
Hernandez, S; Wiener, SW; Hoffman, RS; Nelson, LS
2010 MAR ;48(3):255-255, Clinical Toxicology (Philadelphia)
— id: 111935, year: 2010, vol: 48, page: 255, stat: Journal Article,

Re-evaluating the Dose of N-Acetylcysteine in Massive Paracetamol Ingestion
Hernandez, SH; Morrissey, RP; Howland, MA; Nelson, LS; Hoffman, RS
2010 MAR ;48(3):277-277, Clinical Toxicology (Philadelphia)
— id: 111939, year: 2010, vol: 48, page: 277, stat: Journal Article,

Utility of Serum Aldicarb Concentrations in Cases of Tres Pasitos Poisoning
Hernandez, SH; Prosser, JM; Livshits, Z; Jang, DH; Stajic, M; Hoffman, RS; Nelson, LS
2010 MAR ;48(3):301-302, Clinical Toxicology (Philadelphia)
— id: 111941, year: 2010, vol: 48, page: 301, stat: Journal Article,

Fatal outcome of a propoxyphene/acetaminophen (darvocet) overdose: Should it still be legal in the United States?
Jang D.H.; Hoffman R.S.; Chu J.; Nelson L.S.
2010 ;48(6):658-659, Clinical Toxicology (Philadelphia)
Background: Propoxyphene, an opioid structurally similar to methadone is marketed in combination with acetaminophen or salicylates. Propoxyphene is also a sodiumchannel blocker. Death from propoxyphene overdose may result from respiratory depression or wide-complex dysrhythmias. We report a death from wide-complex dysrhythmia following an intentional propoxyphene/ acetaminophen overdose. Case report: A 37-year-old agitated woman was brought to the ED by EMS. Vital signs: BP, 150/106 mmHg; pulse, 120 beats/min; respirations, 30 breaths/min; room air O2 saturation, 99%. She rapidly became bradycardic with a HR of 40 beats/ min and unresponsive with no measurable blood pressure. CPR and endotracheal intubation were performed, and atropine and epinephrine were given with electrical defibrillation. The systolic BP returned to 40-65 mmHg with a pulse of 30 beats/min. The ECG showed a QRS interval of 180 ms. Sodium bicarbonate, calcium chloride, a glucagon infusion (5 mg/h) and high-dose insulin was administrated without improvement. A transcutaneous pacer was applied but could not capture. Despite high dose infusion of norepinephrine and vasopressin she expired about 4 h later. Tablets of propoxyphene/ acetaminophen were brought in by family and her serum propoxyphene concentration was subsequently reported as 615 ng/mL (200-400 ng/mL). Case discussion: Propoxyphene overdoses are characterized by respiratory depression and sodium channel blockade. Despite significant toxicity, several studies show that propoxyphene's analgesic effect is no better than acetaminophen alone. In 2005, British authorities initiated phased withdrawal of propoxyphene as a result of over 300 deaths/year. In the US since the 1980s, there have been over 2,000 deaths from propoxyphene. At an FDA meeting to determine if propoxyphene should be withdrawn, 14 members voted to withdraw the drug and 12 against withdrawal. Despite this vote, the FDA ultimately decided against withdrawal and recommended a boxed warning about the potential cardiotoxicity. Conclusion: Propoxyphene overdose and fatalities continues to occur in the US. This raises questions about the risk/benefit of this combination product
— id: 113829, year: 2010, vol: 48, page: 658, stat: Journal Article,

Methylene blue (MB) in the treatment of refractory shock from an amlodipine overdose
Jang D.H.; Nelson L.S.; Hoffman R.S.
2010 ;48(6):647-647, Clinical Toxicology (Philadelphia)
Background: Amlodipine is a potent vasodilator with a long half-life and delayed onset of action which is particularly concerning following an overdose. Vasodilation occurs through stimulation of nitric oxide (NO) release with increased cGMP production. MB inhibits guanylate cyclase (GC). This enzyme is responsible for the production cGMP. MB also has the ability to scavenge NO as well as inhibit NOS. We report the use of MB for refractory shock in amlodipine toxicity. Case report: A 25-year-old woman presented to the ED following ingestion of 30 tablets of amlodipine (10 mg). Vital signs were: BP, 120/86 mmHg; P, 110/min; R, 13/ min; T, 98degreeF; pulse oximetry, 98% on RA. Physical examination was unremarkable, and an ECG demonstrated sinus tachycardia with normal intervals. All laboratory studies were normal including negative acetaminophen and salicylate concentrations. Approximately 2-3 h after ingestion, her vital signs were: BP 75/40 mmHg; P, 120 beats/min. Three liters of NS, 40 mL of 10% calcium gluconate, and 10 mg of glucagon were given without improvement. Dopamine and norepinephrine were added, additional calcium, and highdose insulin-euglycemia therapy were initiated without benefit. Cardiac ultrasound demonstrated a hyperdynamic left ventricle, and a right heart catheterization showed a high pulmonary capillary wedge pressure (16 mmHg), high cardiac index (5.1 L/min/m2), and low systemic vascular resistance (400 dynes/s/cm⁵). Intravenous MB (2 mg/kg over 20 min followed by 1 mg/kg/h) was given. Vital signs: BP, 90/75 mmHg and HR, 90 beats/min within 1 h of administration. Patient was discharged in good condition 6 days later. Her amlodipine concentration later returned at 36 ng/mL (3-11 ng/mL). Case discussion: MB has been used for the treatment of refractory vasodilatory shock caused by sepsis and cardiac bypass. Inhibition of excessive production and activity of both NO and cGMP may be critical in the treatment of refractory vasodilatory shock. Despite many therapeutic options such as high-insulin euglycemic therapy, there are still reported deaths. Methylene blue may be a potential new antidotal treatment for refractory vasodilatory shock from an amlodipine overdose. Conclusion: Methylene blue appeared to have beneficial hemodynamic effects following amlodipine poisoning
— id: 113828, year: 2010, vol: 48, page: 647, stat: Journal Article,

Attempted suicide, by mail order: Abrus precatorius
Jang, David H; Hoffman, Robert S; Nelson, Lewis S
2010 Dec;6(4):427-430, Journal of medical toxicology
OBJECTIVE: Abrus precatorius is cultivated in many subtropical areas. The seeds exist in a variety of colors such as black, orange, and most commonly, glossy red. A black band is found at the end of the seed. The plant contains multiple pods which typically contain three to five Abrus seeds. The seeds contain abrin, which inhibits ribosomal function, halting protein synthesis and leading to cellular death. A unique aspect of this case is the use of the internet to order a potentially lethal poison as well as transmission of a picture to identify the seed. CASE REPORT: A 20-year-old man presented to the emergency department complaining of vomiting and watery diarrhea for 6-8 h prior to arrival. He denied any medication use, recent illness, travel, or changes in his diet. Initial vital signs were normal. The patient was diagnosed with viral gastroenteritis. During his evaluation, the patient admitted to feeling suicidal. While awaiting psychiatry evaluation, the patient's father arrived with a box of small hard red seeds, which he believed that his son ingested in a suicide attempt. The seeds could not be identified by the staff. A picture of the seeds was transmitted by e-mail to the New York City Poison Control Center, allowing their identification as A. precatorius. The patient was reinterviewed and admitted to chewing and swallowing 10 seeds. Given the potential toxicity of abrin, the patient was admitted to the intensive care unit. He continued to have frequent episodes of emesis as well as diarrhea. He gradually improved over 2 days. He admitted to ordering a box of Abrus seeds online from Asia after reading on the Internet about their use in suicide. He was eventually discharged for outpatient follow-up with no permanent sequelae. CONCLUSION: Abrin has an estimated human fatal dose of 0.1-1 mug/kg. Most cases of Abrus seed ingestions are unintentional and occur in children. Ingesting the intact seeds typically results in no clinical findings, as they pass through the gastrointestinal tract due to their hard shell. Abrin released during chewing is poorly absorbed systemically from the gastrointestinal tract. This causes the vomiting and diarrhea with resultant hypovolemia and electrolyte disturbances, which can be severe and life threatening, particularly in areas with less advanced health care systems. Management is primarily supportive
— id: 134666, year: 2010, vol: 6, page: 427, stat: Journal Article,

Status epilepticus and wide-complex tachycardia secondary to diphenhydramine overdose
Jang, David H; Manini, Alex F; Trueger, Nathan S; Duque, Danny; Nestor, Nestor B; Nelson, Lewis S; Hoffman, Robert S
2010 Nov;48(9):945-948, Clinical Toxicology (Philadelphia)
Objective. Diphenhydramine is an H1 histamine antagonist that is commonly used for allergic reactions, colds and cough, and as a sleep aid. In addition to anticholinergic and antihistaminergic effects, sodium channel blockade becomes evident following diphenhydramine overdose. While seizures may occur following overdose of a diphenhydramine, status epilepticus is distinctly uncommon. We report a case with both status epilepticus and wide-complex dysrhythmias following an intentional diphenhydramine overdose. Case report. A 36-year-old woman with a medical history of hypothyroidism on levothyroxine was brought to the emergency department with active seizures by emergency medical services after what was later determined to be a diphenhydramine overdose. One hour after an argument with her husband he found her lethargic in a locked room. Initial vital signs were: blood pressure, 90/55 mmHg; heart rate, 160 beats/min; respiratory rate 18 breaths/min; room air oxygen saturation, 99%; temperature, 99.8 degrees F; rapid point-of-care glucose, 130 mg/dL. The generalized seizures continued for duration of 30 min, despite the intravenous administration of 8 mg of lorazepam. The patient underwent endotracheal intubation and a propofol infusion terminated her seizures. An electrocardiogram after the status was terminated which revealed a wide-complex tachycardia with QRS duration of 127 ms. The QRS narrowed after 200 mEq of intravenous sodium bicarbonate was administrated. The patient was neurologically intact upon extubation on hospital day 2. The serum diphenhydramine concentration drawn on arrival to the ED was 1200 ng/mL (9-120 ng/mL); a tricyclic screen was negative. Discussion. While seizures and sodium channel blockade are recognized complications of diphenhydramine toxicity, reported cases of status epilepticus from diphenhydramine overdose are rare. Elements of the patient's presentation were similar to a tricyclic overdose and management required aggressive control of her seizures, sodium bicarbonate therapy, and recognizing that physostigmine was contraindicated due to wide complex tachycardia. Conclusions. Diphenhydramine overdose may cause status epilepticus and wide-complex tachycardia. Management should focus on antidotal therapy with sodium bicarbonate and supportive neurological management with appropriate anticonvulsants and airway protection if clinically indicated
— id: 116217, year: 2010, vol: 48, page: 945, stat: Journal Article,

Woman with unresponsiveness. Pesticide poisoning
Jang, David H; Nelson, Lewis S
2010 Aug;56(2):201, 207-, Annals of emergency medicine
— id: 111361, year: 2010, vol: 56, page: 201, 207, stat: Journal Article,

Hydroxocobalamin and sodium thiosulfate versus sodium nitrite and sodium thiosulfate in acute cyanide toxicity
Jang, David H; Nelson, Lewis S; Hoffman, Robert S
2010 Jun;55(6):582-582, Annals of emergency medicine
— id: 134669, year: 2010, vol: 55, page: 582, stat: Journal Article,

Images in toxicology: girl with constipation
Jang, David H; Nelson, Lewis S; Hoffman, Robert S
2010 Jun;48(5):468-468, Clinical Toxicology (Philadelphia)
— id: 111616, year: 2010, vol: 48, page: 468, stat: Journal Article,

Tryptase serum level as a possible indicator of scombroid syndrome
Jang, David H; Nelson, Lewis S; Hoffman, Robert S
2010 Jun;48(5):474-474, Clinical Toxicology (Philadelphia)
— id: 134670, year: 2010, vol: 48, page: 474, stat: Journal Article,

Severe opioid withdrawal due to misuse of new combined morphine and naltrexone product (Embeda)
Jang, David H; Rohe, John C; Hoffman, Robert S; Nelson, Lewis S
2010 Mar;55(3):303-304, Annals of emergency medicine
— id: 107792, year: 2010, vol: 55, page: 303, stat: Journal Article,

Metabolic and hepatobiliary side effects of antiretroviral therapy (ART)
Lugassy, Daniel M; Farmer, Brenna M; Nelson, Lewis S
2010 May;28(2):409-19, Table of Contents, Emergency medicine clinics of North America
Although antiretroviral therapy (ART) for human immunodeficiency virus (HIV) has been in use since 1987, the initiation of highly active ART has produced an increase in adverse drug reactions. This is a new challenge as many of the adverse drug reactions attributable to ART may be indistinguishable from non-drug-related illnesses. The emergency physician must be aware of the potential complications of ART as affected patients may present with nonspecific symptoms. The focus of this article is the metabolic and hepatobiliary adverse effects of ART
— id: 109516, year: 2010, vol: 28, page: 409, stat: Journal Article,

In response to Leppikangas H, et al, Levosimendan as a rescue drug in experimental propranolol-induced myocardial depression: a randomized study
Lugassy, Daniel M; Stefan, Alexandra; Dexeus, Daniel; Hoffman, Robert S; Nelson, Lewis S
2010 May;55(5):486-486, Annals of emergency medicine
— id: 112914, year: 2010, vol: 55, page: 486, stat: Journal Article,

Acute Strychnine-Belladonna Toxicity After Ingestion of Antique Pills Obtained from the Internet
Lugassy, DM; Chitu, C; Nelson, LS; Hoffman, RS; Howland, MA
2010 MAR ;48(3):254-254, Clinical Toxicology (Philadelphia)
— id: 111934, year: 2010, vol: 48, page: 254, stat: Journal Article,

Prolonged Hypertension after Empiric Treatment with Hydroxocobalamin for Presumed Cyanide Toxicity
Lugassy, DM; Weingart, SD; Ginsburg, BY; Howland, MA; Hoffman, RS; Nelson, LS
2010 MAR ;48(3):259-259, Clinical Toxicology (Philadelphia)
— id: 111936, year: 2010, vol: 48, page: 259, stat: Journal Article,

Chronic Digoxin Toxicity, Serum Potassium, and Fab Failure: A Case-control Study
Manini, AF; Nelson, LS; Hoffman, RS
2010 MAR ;48(3):295-295, Clinical Toxicology (Philadelphia)
— id: 111940, year: 2010, vol: 48, page: 295, stat: Journal Article,

Incidence of Adverse Cardiovascular Events Following Drug Overdose: A Pilot Study
Manini, AF; Nelson, LS; Stimmel, B; Vlahov, D; Hoffman, RS
2010 MAR ;48(3):242-242, Clinical Toxicology (Philadelphia)
— id: 111931, year: 2010, vol: 48, page: 242, stat: Journal Article,

Electrocardiographic predictors of adverse cardiovascular events in suspected poisoning
Manini, Alex F; Nelson, Lewis S; Skolnick, Adam H; Slater, William; Hoffman, Robert S
2010 Jun;6(2):106-115, Journal of medical toxicology
Poisoning is the second leading cause of injury-related fatality in the USA and the leading cause of cardiac arrest in victims under 40 years of age. The study objective was to define the electrocardiographic (ECG) predictors of adverse cardiovascular events (ACVE) complicating suspected acute poisoning (SAP). This was a case-control study in adults at three tertiary-care hospitals and one regional Poison Control Center. We compared 34 cases of SAP complicated by ACVE to 101 consecutive control patients with uncomplicated SAP. The initial ECG was analyzed for rhythm, intervals, QT dispersion, ischemia, and infarction. ECGs were interpreted by a cardiologist, blinded to study hypothesis and case data. Subjects were 48% male, with mean age 42 +/- 19 years. In addition to clinical suspicion of poisoning in 100% of patients, routine toxicology screens were positive in 77%, most commonly for benzodiazepines, opioids, and/or acetaminophen. Neither the ventricular rate, the QRS duration, nor the presence of infarction predicted the risk of ACVE. However, the rhythm, QTc, QT dispersion, and presence of ischemia correlated with the risk of ACVE. Independent predictors of ACVE based on multivariable logistic regression were prolonged QTc, any non-sinus rhythm, ventricular ectopy, and ischemia. Recursive partitioning analysis identified very low risk criteria (94.1% sensitivity, 96.2% NPV) and high risk criteria (95% specificity). Among patients with SAP, the presence of QTc prolongation, QT dispersion, ventricular ectopy, any non-sinus rhythm, and evidence of ischemia on the initial ECG are strongly associated with ACVE
— id: 138121, year: 2010, vol: 6, page: 106, stat: Journal Article,

'Scrotocaine': Toxicity from Scrotal Infusion of Lidocaine
Morrissey, RP; Fisher, W; Howland, MA; Hoffman, RS; Nelson, LS
2010 MAR ;48(3):252-252, Clinical Toxicology (Philadelphia)
— id: 111932, year: 2010, vol: 48, page: 252, stat: Journal Article,

'Popper' Retinopathy: Acute Isobutyl Nitrite Exposure Induces Red to Yellow Color Visual Disturbance
Morrissey, RP; Francis, JH; Howland, MA; Hoffman, RS; Nelson, LS
2010 MAR ;48(3):252-253, Clinical Toxicology (Philadelphia)
— id: 111933, year: 2010, vol: 48, page: 252, stat: Journal Article,

Complications of oral exposure to fentanyl transdermal delivery system patches
Prosser, Jane M; Jones, Brent E; Nelson, Lewis
2010 Dec;6(4):443-447, Journal of medical toxicology
PURPOSE: Fentanyl is a synthetic opioid available therapeutically as an intravenous, transbucal, or transdermal preparation. It is also used as a drug of abuse through a variety of different methods, including the oral abuse of transdermal fentanyl patches. This is a series of patients with oral fentanyl patch exposure reported to our center and represents the first series of oral fentanyl patch exposures collected outside of the postmortem setting. METHODS: In this series, we examined the New York Poison Control Center database for all cases of oral abuse of fentanyl reported between January 2000 and April 2008. RESULTS: Twenty cases were reported, nine were asymptomatic or had symptoms of opioid withdrawal; 11 had symptoms of opioid intoxication. Eight patients were administered naloxone and all showed improvement in clinical status. Only one case resulted in a confirmed fatality-this patient had an orally adherent patch discovered at intubation. CONCLUSIONS: Oral exposure may result in life-threatening toxicity. Patients should be closely assessed and monitored for the opioid toxidrome, and if symptomatic, should be managed with opioid antagonists and ventilatory support
— id: 133444, year: 2010, vol: 6, page: 443, stat: Journal Article,

Profiling the Risk to Academic Medical Centers by Agents of Opportunity
Smith, SW; Portelli, I; Farmer, BM; Nelson, LS; Rosenberg, S; Tunik, M; Bendzans, C; Graham, ME; Goldfrank, LR
2010 MAR ;48(3):259-260, Clinical Toxicology (Philadelphia)
— id: 111937, year: 2010, vol: 48, page: 259, stat: Journal Article,

Mandatory Carbon Monoxide Detectors Do not Appear to Reduce the Incidence of Death from Carbon Monoxide Poisoning
Soghoian, S; Prosser, JM; Manini, AF; Stajic, M; Marker, E; Prezant, D; Nelson, LS; Hoffman, RS
2010 MAR ;48(3):269-270, Clinical Toxicology (Philadelphia)
— id: 111938, year: 2010, vol: 48, page: 269, stat: Journal Article,

Unintentional i.v. injection of barium sulfate in a child
Soghoian, Samara; Hoffman, Robert S; Nelson, Lewis
2010 May 1;67(9):734-736, American journal of health-system pharmacy. AJHP
PURPOSE: A case of barium sulfate injection into the superior vena cava during an upper gastrointestinal series (UGIS) in which the patient's central venous line (CVL) was mistaken for her gastrostomy tube is reported. SUMMARY: A 17-month-old girl was brought to the fluoroscopy suite to undergo a UGIS with barium sulfate contrast. Her medical history included premature birth and short-gut syndrome after a bowel resection for necrotizing enterocolitis and gastroschisis. She had been treated for multiple bouts of sepsis and was currently receiving antibiotic therapy at home via a CVL. She was admitted to the hospital for replacement of her CVL. In the hospital, the patient developed a diarrheal illness with projectile vomiting, prompting the UGIS. In the fluoroscopy suite, approximately 3 mL of barium sulfate was injected into the patient's CVL, which was misidentified as her gastrostomy tube. The error was recognized when the first video fluoroscopic image revealed barium in the patient's right atrium, and 10 mL of blood containing a thick, chalky, whitish-pink suspension was immediately aspirated from the CVL. Peripheral venous access was established, and the CVL was removed. The patient vomited three times and developed rigors 30 minutes later. That evening, she developed a fever, which was treated with acetaminophen and a course of broad-spectrum antibiotics. Subsequent radiographs of the patient's chest failed to show any residual barium, and no respiratory distress developed. The patient was discharged in stable condition four days later. CONCLUSION: A 17-month-old girl inadvertently received barium sulfate by i.v. injection through a CVL that was mistaken for the patient's gastrostomy tube
— id: 133788, year: 2010, vol: 67, page: 734, stat: Journal Article,

Believing Is Seeing
Wears, Robert L; Nelson, Lewis S
2010 Jun;55(6):511-512, Annals of emergency medicine
— id: 107793, year: 2010, vol: 55, page: 511, stat: Journal Article,

Racial variations in the incidence of severe alcohol withdrawal
Chan, Gar Ming; Hoffman, Robert S; Gold, Jeffrey A; Whiteman, Paula J; Goldfrank, Lewis R; Nelson, Lewis S
2009 Mar;5(1):8-14, Journal of medical toxicology
The use of race as a risk assessment tool and pharmacologic target has garnered recent attention and debate. It is currently unclear if a relationship between race and the development of severe alcohol withdrawal exists. We explored this potential relationship using several study groups. Methods: A simultaneous prospective enrollment of patients and retrospective chart review of severe alcohol withdrawal in two separate settings was performed comparing both the incidence of withdrawal and alcoholism based on race. These two study groups were then compared to an 'at risk' group of alcoholics and the general ED population to determine differences in the distribution of race. Results: Individuals of white race in both study groups were at increased odds [OR 1.93 (CI 1.11-3.39) and 2.19 (CI 1.41-3.40)] of having severe alcohol withdrawal when compared to non-White 'at risk' alcoholics. Blacks in both study groups however, appear to have lower odds [OR 0.23 (CI 0.11-0.47) and 0.11 (CI 0.05-0.23)] of having severe alcohol withdrawal when compared to non-Black 'at risk' alcoholics. Conclusions: Despite the controversial use of race in medical research and targeting therapies, there appears to be a difference in the odds of severe alcohol withdrawal based on race. The reasons for this finding are currently unclear
— id: 96163, year: 2009, vol: 5, page: 8, stat: Journal Article,

Conflict of Interest (COI) Management among Pharmacy and Therapeutics (P&T) Committees
Farmer, BM; Lesar, T; Nelson, LS
2009 SEP-OCT ;47(7):758-758, Clinical Toxicology (Philadelphia)
— id: 102955, year: 2009, vol: 47, page: 758, stat: Journal Article,

Medication Error Resulting in Intravenous 1% Alum Administration
Farmer, BM; Mehta, RR; Nelson, LS; Howland, MA; Hoffman, RS; Rao, RB
2009 JUN ;47(5):509-509, Clinical Toxicology (Philadelphia)
— id: 101309, year: 2009, vol: 47, page: 509, stat: Journal Article,

Agents of Opportunity in the Healthcare Setting
Farmer, BM; Nelson, LS
2009 SEP-OCT ;47(7):746-746, Clinical Toxicology (Philadelphia)
— id: 102954, year: 2009, vol: 47, page: 746, stat: Journal Article,

A Systematic Evaluation of Medication Errors Reported to the Poison Center
Farmer, BM; Nelson, LS; Hoffman, RS
2009 JUN ;47(5):470-470, Clinical Toxicology (Philadelphia)
— id: 101303, year: 2009, vol: 47, page: 470, stat: Journal Article,

The underutilization of hemodialysis in patients with salicylate poisoning
Fertel, Baruch S; Nelson, Lewis S; Goldfarb, David S
2009 Jun;75(12):1349-1353, Kidney international
— id: 81363, year: 2009, vol: 75, page: 1349, stat: Journal Article,

Hypoglycemia Induced by Insulin Glargine Overdose
Hernandez, SH; Hoffman, RS; Howland, MA; Nelson, LS
2009 JUN ;47(5):509-509, Clinical Toxicology (Philadelphia)
— id: 101311, year: 2009, vol: 47, page: 509, stat: Journal Article,

Inadvertent Intravenous Infusion of Polyethylene Glycol and Electrolyte Solution in a 3 Year-Old Girl
Hernandez, SH; Hoffman, RS; Howland, MA; Nelson, LS; Bouchard, NC
2009 JUN ;47(5):509-509, Clinical Toxicology (Philadelphia)
— id: 101310, year: 2009, vol: 47, page: 509, stat: Journal Article,

Two Cases of Atropine Poisoning Suspected from Bottled Water
Hernandez, SH; Hoffman, RS; Olmedo, RE; Vashi, AA; Nelson, LS
2009 SEP-OCT ;47(7):719-719, Clinical Toxicology (Philadelphia)
— id: 102953, year: 2009, vol: 47, page: 719, stat: Journal Article,

Uvular Angioedema in a Non-Paracetamol Poisoned Patient Treated with N-Acetylcysteine and Physostigmine
Hernandez, SH; Nelson, LS; Borke, JA; Kim, J; Rao, R
2009 JUN ;47(5):498-498, Clinical Toxicology (Philadelphia)
— id: 101306, year: 2009, vol: 47, page: 498, stat: Journal Article,

Inconsistent approach to the treatment of chronic digoxin toxicity in the United States
Kirrane, B M; Olmedo, R E; Nelson, L S; Mercurio-Zappala, M; Howland, M A; Hoffman, R S
2009 May;28(5):285-292, Human & Experimental Toxicology
Evidence-based guidelines do not exist for the treatment of patients with chronic mild-moderate digoxin toxicity. We sought to evaluate differences among specialists in the use of digoxin-specific antibody fragments and the decision to admit these patients. A sample of cardiologists, emergency physicians, and medical toxicologists was surveyed. The survey detailed four hypothetical cases of chronic digoxin toxicity created by consensus among authors. All cases had the same digoxin concentration, but signs and symptoms varied in an attempt to explore four different thresholds. For each scenario, clinicians made decisions about admission and treatment. Survey response varied: cardiologists 17%, emergency physicians 6.7%, and toxicologists 39%. Statistically significant difference was found in the administration of Fab among cardiologists (67%), emergency physicians (82%), or toxicologists (91.5%) and admission rate (cardiologists 34%, emergency physicians 28%, and toxicologists 46%). Differences exist among clinicians of various specialties regarding treatment of chronic digoxin toxicity. These differences may reflect diverse perspectives or knowledge gaps and may translate into excess cost or less than ideal care. Exploring these differences may improve patient care, improve interactions among providers, and set the stage for development of consensus guidelines and research
— id: 107301, year: 2009, vol: 28, page: 285, stat: Journal Article,

Unrecognized hypoglycemia due to maltodextrin interference with bedside glucometry
Kirrane, Barbara M; Duthie, Elizabeth A; Nelson, Lewis S
2009 Mar;5(1):20-23, Journal of medical toxicology
INTRODUCTION: Glucometry is widely used to confirm or exclude hypoglycemia in patients with suggestive clinical findings. Nonglucose sugars may be detected by certain types of glucometers, causing false elevation of the glucometer analysis of the blood sugar. Since these other sugars are not functionally glucose and may even induce excess insulin release, clinical hypoglycemia may be missed. CASE REPORT: We report a 79-year-old man on enteral feeds containing maltodextrin, a glucose polymer, who had persistently high glucometer-measured blood glucose despite normal blood glucose measured by formal laboratory analysis. DISCUSSION: Excess insulin administration, based on the erroneous glucometer reading, may have caused unrecognized fatal clinical hypoglycemia. This has been reported following intravenous administration of related nonglucose sugars but not with enteral maltodextrin. Further study is required to confirm the effects of maltodextrin on glucometry. CONCLUSION: False elevation of blood glucose measured on certain point-of-care glucometers can occur following the oral administration of maltodextrin
— id: 107796, year: 2009, vol: 5, page: 20, stat: Journal Article,

Common toxidromes of plant poisonings in Taiwan
Lin, Tzeng Jih; Nelson, Lewis S; Tsai, Jin Lian; Hung, Dong Zong; Hu, Sheng Chuan; Chan, Hon Man; Deng, Jou-Fang
2009 Feb;47(2):161-168, Clinical Toxicology (Philadelphia)
OBJECTIVE: To describe the toxidromes associated with plant poisonings in Taiwan. METHODS: Retrospective review of acute single-plant exposures with clinical signs and symptoms reported between January 1987 and December 2006 by hospitals to the network of Taiwan Poison Control Centers. Recorded data included demographic data, intent of exposures, exposure routes, clinical findings, and therapeutic strategies. RESULTS: There were 389 cases that met the criteria. Each case was placed into one of the expected toxidromes: anticholinergic, mucosal inflammation, gastroenteritis, acute multisystem organ failure, delayed multisystem organ failure, cholinergic, cardiac dysrhythmia, hepatotoxicity, dermatitis, seizures, and dyspnea. Anticholinergic poisoning was the most common toxidrome. CONCLUSION: Plant poisonings can be classified into recognizable toxicologic syndromes. These toxidromes may guide a clinician's evaluation and management before a botanist can confirm the actual plant identity
— id: 135243, year: 2009, vol: 47, page: 161, stat: Journal Article,

Case files of the medical toxicology fellowship at the new york city poison control: bromism: forgotten, but not gone
Lugassy, Daniel; Nelson, Lewis
2009 Sep;5(3):151-157, Journal of medical toxicology
— id: 101335, year: 2009, vol: 5, page: 151, stat: Journal Article,

Torsade de Pointes Presenting as New-Onset Seizure in a Methadone Maintenance Patient
Lugassy, DM; Nelson, LS; Hoffman, RS; Howland, MA
2009 JUN ;47(5):501-501, Clinical Toxicology (Philadelphia)
— id: 101308, year: 2009, vol: 47, page: 501, stat: Journal Article,

Letters on "Predictors of mortality in patients with delerium tremens"
Majlesi, Nima; Hoffman, Robert S; Nelson, Lewis
2009 Jan;16(1):92-92, Academic emergency medicine
— id: 96656, year: 2009, vol: 16, page: 92, stat: Journal Article,

Hepatotoxicity despite early administration of intravenous N-acetylcysteine for acute acetaminophen overdose
Majlesi, Nima; Olsen, Andrew; Krishnan, Greeta P; Olsen, Dean; Nelson, Lewis
2009 Jun;16(6):574-574, Academic emergency medicine
— id: 106290, year: 2009, vol: 16, page: 574, stat: Journal Article,

What is the pertinent finding and an explanation for the cause?
Manini A.F.; Schwaner R.; Nelson L.S.; Hoffman R.S.
2009 ;5(3):149-150, Journal of medical toxicology
— id: 109692, year: 2009, vol: 5, page: 149, stat: Journal Article,

Ethylene Glycol Poisoning and Lactate Concentrations Reply
Manini, AF; Hoffman, RS; McMartin, KE; Nelson, LS
2009 SEP ;33(7):396-396, Journal of analytical toxicology
— id: 102144, year: 2009, vol: 33, page: 396, stat: Journal Article,

Do Medical Examiners and Medical Toxicologists Agree on the Cause of Death?
Manini, AF; Nelson, LS; Olsen, D; Vlahov, D; Hoffman, RS
2009 SEP-OCT ;47(7):705-705, Clinical Toxicology (Philadelphia)
— id: 102952, year: 2009, vol: 47, page: 705, stat: Journal Article,

Relationship between serum glycolate and falsely elevated lactate in severe ethylene glycol poisoning
Manini, Alex F; Hoffman, Robert S; McMartin, Kenneth E; Nelson, Lewis S
2009 Apr;33(3):174-176, Journal of analytical toxicology
In the setting of ethylene glycol (EG) poisoning, a falsely elevated serum lactate concentration is suggested to be an assay cross-reaction with glycolate, but a concentration-dependent relationship has never been identified. We correlate serum lactate and glycolate concentrations in a case of severe EG poisoning. Serial EG [by gas chromatography (GC)], glycolate (derivatized to methyl glycolate, analysis by GC), and lactate (both enzymatic spectrophotometry and GC) concentrations were correlated at five time points. False-positive lactate was confirmed by absence of lactate on GC analysis. The correlation coefficient (Pearson's r) between lactate (by enzymatic spectrophotometry) and glycolate was 0.984 and was statistically significant (p < 0.01). The mean lactate/glycolate conversion factor was 2.58 +/- 0.95. We demonstrate the linear correlation between falsely elevated serum lactate and glycolate concentrations in a case of severe EG poisoning. Our data provide further support to the belief that the lactate assay may cross-react with glycolate in EG poisoning
— id: 107795, year: 2009, vol: 33, page: 174, stat: Journal Article,

Sub-Acute High-Dose Nitrous Oxide (N2O) Exposure Produces Severe Peripheral Neuropathy
Morrissey, RP; Alt, RS; Howland, MA; Nelson, LS; Hoffman, RS
2009 JUN ;47(5):448-448, Clinical Toxicology (Philadelphia)
— id: 101301, year: 2009, vol: 47, page: 448, stat: Journal Article,

Premedication for Coronary Computed Tomographic Angiography Produces Symptomatic Atrio-Ventricular Dissociation
Morrissey, RP; Howland, MA; Hoffman, RS; Nelson, LS
2009 JUN ;47(5):496-496, Clinical Toxicology (Philadelphia)
— id: 101305, year: 2009, vol: 47, page: 496, stat: Journal Article,

Transdermal fentanyl: pharmacology and toxicology
Nelson, Lewis; Schwaner, Robert
2009 Dec;5(4):230-241, Journal of medical toxicology
OBJECTIVE: To evaluate the underlying pharmacology, safety, and misuse/abuse of transdermal fentanyl, one of the cornerstone pharmacotherapies for patients with chronic pain. METHODS: Literature was identified through searches of Medline (PubMed) and several textbooks in the areas of pharmacology, toxicology, and pain management. A bibliographical review of articles identified by these searches was also performed. Search terms included combinations of the following: fentanyl, transdermal, patch, pharmacology, kinetics, toxicity, and poisoning. All pertinent clinical trials, retrospective studies, and case reports relevant to fentanyl pharmacology and transdermal fentanyl administered by any route and published in English were identified. Each was reviewed for data regarding the clinical pharmacology, abuse, misuse, and safety of transdermal fentanyl. Data from these studies and information from review articles and pharmaceutical prescribing information were included in this review. RESULTS: Fentanyl is a high-potency opioid that has many uses in the treatment of both acute and chronic pain. Intentional or unintentional misuse, as well as abuse, may lead to significant clinical consequences, including death. Both the US Food and Drug Administration (FDA) and Health Canada have warned of potential pitfalls associated with transdermal fentanyl, although these have not been completely effective in preventing life-threatening adverse events and fatalities related to its inappropriate use. CONCLUSIONS: Clinically consequential adverse effects may occur unexpectedly with normal use of transdermal fentanyl, or if misused or abused. Misuse and therapeutic error may be largely preventable through better education at all levels for both the prescriber and patient. The prevention of intentional misuse or abuse may require regulatory intervention
— id: 111635, year: 2009, vol: 5, page: 230, stat: Journal Article,

Adverse effects associated with arginine {alpha}-ketoglutarate containing supplements
Prosser, J M; Majlesi, N; Chan, G M; Olsen, D; Hoffman, R S; Nelson, L S
2009 May;28(5):259-262, Human & Experimental Toxicology
The athletic performance supplement industry is a multibillion-dollar business and one popular category claims to increase nitric oxide (NO) production. We report three patients presenting to the emergency department with adverse effects. A 33-year-old man presented with palpitations, dizziness, vomiting, and syncope, after the use of NO(2) platinum. His examination and electrocardiogram (ECG) were normal. The dizziness persisted, requiring admission overnight. A 21-year-old man with palpitations and near syncope had used a 'nitric oxide' supplement. He was tachycardic to 115 bpm with otherwise normal examination. Laboratory values including methemoglobin, and ECG were unremarkable. He was treated with 1 L of saline with no change in heart rate. He was admitted for observation. A 24-year-old man presented after taking NO-Xplode with palpitations and a headache. His examination, laboratory values, and ECG were normal. He was discharged. The purported active ingredient in these products is arginine alpha-ketoglutarate (AAKG), which is claimed to increase NO production by supplying the precursor L-arginine. The symptoms could be due to vasodilation from increased levels of NO, though other etiologies cannot be excluded. AAKG containing supplements may be associated with adverse effects requiring hospital admission
— id: 102410, year: 2009, vol: 28, page: 259, stat: Journal Article,

Complications of Fentanyl Patch Ingestion
Prosser, JM; Howland, MA; Jones, BE; Hoffman, RS; Nelson, LS
2009 JUN ;47(5):449-449, Clinical Toxicology (Philadelphia)
— id: 101302, year: 2009, vol: 47, page: 449, stat: Journal Article,

Inaccuracy of Electrocardiogram Interpretations Reported to the Poison Center
Prosser, JM; Smith, SW; Olsen, D; Nelson, LS; Hoffman, RS
2009 JUN ;47(5):487-487, Clinical Toxicology (Philadelphia)
— id: 101304, year: 2009, vol: 47, page: 487, stat: Journal Article,

Slower infusion of metoclopramide decreases the rate of akathisia
Regan, Linda A; Hoffman, Robert S; Nelson, Lewis S
2009 May;27(4):475-480, American journal of emergency medicine
OBJECTIVE: We investigated the difference in incidence of acute akathisia related to the rate of infusion in patients receiving metoclopramide for acute nausea, vomiting, or migraine headache in the emergency department (ED). METHODS: Randomized, prospective, double-blind clinical trial of patients aged 18 years and older who were to receive intravenous metoclopramide for the treatment of nausea, vomiting, or headache were eligible. Patients were excluded if they were taking medications that might mimic or mask akathisia, had a movement disorder, renal insufficiency, or were unable or unwilling to consent. Pregnant women and prisoners were also excluded. Subjects were randomized to receive 1 of 2 accepted metoclopramide administration regimens. The regimens included 10 mg of metoclopramide administered either as a 2-minute bolus (BG) or as a slow infusion for 15 minutes (IG). All patients received a normal saline placebo at the opposite rate to maintain blinding. The main outcome was development of akathisia noted at 60 minutes after drug administration as measured either with The Prince Henry Hospital akathisia rating scale or by sudden unexplained departure from the ED during treatment. RESULTS: One hundred twenty-seven patients were eligible for the study. Fifty-nine patients met exclusion criteria. Of the remaining 68 patients, 36 were randomized to the BG and 32 were randomized to the IG. In the BG, 11.1% of patients developed akathisia compared with 0% in the IG (P = .026). Four patients developed akathisia based on the scale and 2 departed suddenly from the ED. CONCLUSIONS: Slower infusion of metoclopramide reduces the incidence of akathisia
— id: 107794, year: 2009, vol: 27, page: 475, stat: Journal Article,

Elemental mercury neurotoxicity from self-injection
Schaumburg, H H; Gellido, C; Smith, S W; Nelson, L S; Hoffman, R S
2009 Jan 27;72(4):377-378, Neurology
— id: 107797, year: 2009, vol: 72, page: 377, stat: Journal Article,

Multisystem organ failure after large volume injection of castor oil
Smith, Silas W; Graber, Nathan M; Johnson, Rudolph C; Barr, John R; Hoffman, Robert S; Nelson, Lewis S
2009 Jan;62(1):12-14, Annals of plastic surgery
We report a case of multisystem organ failure after large volume subcutaneous injection of castor oil for cosmetic enhancement. An unlicensed practitioner injected 500 mL of castor oil bilaterally to the hips and buttocks of a 28-year-old male to female transsexual. Immediate local pain and erythema were followed by abdominal and chest pain, emesis, headache, hematuria, jaundice, and tinnitus. She presented to an emergency department 12 hours postinjection. Persistently hemolyzed blood samples complicated preliminary laboratory analysis. She rapidly deteriorated despite treatment and developed fever, tachycardia, hemolysis, thrombocytopenia, hepatitis, respiratory distress, and anuric renal failure. An infectious diseases evaluation was negative. After intensive supportive care, including mechanical ventilation and hemodialysis, she was discharged 11 days later, requiring dialysis for an additional 1.5 months. Castor oil absorption was inferred from recovery of the Ricinus communis biomarker, ricinine, in the patient's urine (41 ng/mL). Clinicians should anticipate multiple complications after unapproved methods of cosmetic enhancement
— id: 96657, year: 2009, vol: 62, page: 12, stat: Journal Article,

A novel approach to multihazard modeling and simulation
Smith, Silas W; Portelli, Ian; Narzisi, Giuseppe; Nelson, Lewis S; Menges, Fabian; Rekow, E Dianne; Mincer, Joshua S; Mishra, Bhubaneswar; Goldfrank, Lewis R
2009 Jun;3(2):75-87, Disaster medicine & public health preparedness
OBJECTIVE: To develop and apply a novel modeling approach to support medical and public health disaster planning and response using a sarin release scenario in a metropolitan environment. METHODS: An agent-based disaster simulation model was developed incorporating the principles of dose response, surge response, and psychosocial characteristics superimposed on topographically accurate geographic information system architecture. The modeling scenarios involved passive and active releases of sarin in multiple transportation hubs in a metropolitan city. Parameters evaluated included emergency medical services, hospital surge capacity (including implementation of disaster plan), and behavioral and psychosocial characteristics of the victims. RESULTS: In passive sarin release scenarios of 5 to 15 L, mortality increased nonlinearly from 0.13% to 8.69%, reaching 55.4% with active dispersion, reflecting higher initial doses. Cumulative mortality rates from releases in 1 to 3 major transportation hubs similarly increased nonlinearly as a function of dose and systemic stress. The increase in mortality rate was most pronounced in the 80% to 100% emergency department occupancy range, analogous to the previously observed queuing phenomenon. Effective implementation of hospital disaster plans decreased mortality and injury severity. Decreasing ambulance response time and increasing available responding units reduced mortality among potentially salvageable patients. Adverse psychosocial characteristics (excess worry and low compliance) increased demands on health care resources. Transfer to alternative urban sites was possible. CONCLUSIONS: An agent-based modeling approach provides a mechanism to assess complex individual and systemwide effects in rare events
— id: 99323, year: 2009, vol: 3, page: 75, stat: Journal Article,

The dangers associated with fondaparinux (FDX) and reversal with recombinant factor VIIa
Farmer, BM; Duthie, E; Nelson, LS
2008 ;46(7):641-641 SUM, Clinical Toxicology (Philadelphia)
— id: 86835, year: 2008, vol: 46, page: 641, stat: Journal Article,

A case report of chronic bupivacaine toxicity
Farmer, BM; Hoffman, RS; Nelson, LS
2008 JUN ;46(5):367-367, Clinical Toxicology (Philadelphia)
— id: 86870, year: 2008, vol: 46, page: 367, stat: Journal Article,

Use of hemodialysis and hemoperfusion in poisoned patients
Holubek, William J; Hoffman, Robert S; Goldfarb, David S; Nelson, Lewis S
2008 Nov;74(10):1327-1334, Kidney international
Extracorporeal removal techniques such as hemodialysis, charcoal hemoperfusion, and peritoneal dialysis have been used to remove toxins from the body. To define trends in the use of these techniques for toxin removal, we analyzed the 19,351 cases requiring extracorporeal removal reported to U.S. poison centers from 1985-2005. The number of such patients who received hemodialysis, excluding those with other medical indications, (normalized per million calls) increased from 231 to 707 whereas hemoperfusion decreased from 53 to 12 in the years 1985-2005. Peritoneal dialysis decreased from 2.2 in 1985 to 1.6 in 1991. The most common toxins removed by hemodialysis were lithium and ethylene glycol. There were more dialysis treatments for poisonings with valproate and acetaminophen in 2001-2005 than for methanol and theophylline, although hemodialysis for acetaminophen removal is generally not recommended. Theophylline was the most common toxin removed by hemoperfusion from 1985-2000, but carbamazepine became the most frequent toxin for removal during 2001-2005. Our study shows that the profile of toxins and the type of extracorporeal technique used to remove the toxins have changed over the years.Kidney International advance online publication, 17 September 2008; doi:10.1038/ki.2008.462
— id: 83587, year: 2008, vol: 74, page: 1327, stat: Journal Article,

The toxic emergency. Working under pressure
Kwan A; Michaels J V; Nelson L
2008 ;40(5):21-4 May, Emergency medicine
— id: 80318, year: 2008, vol: 40, page: 21, stat: Journal Article,

A rapid qualitative test for suspected ethylene glycol poisoning
Long, Heather; Nelson, Lewis S; Hoffman, Robert S
2008 Jul;15(7):688-690, Academic emergency medicine
OBJECTIVES: Many hospitals must send out ethylene glycol (EG) samples to a reference laboratory, and delays in diagnosis and treatment may occur. A qualitative colorimetric test (ethylene glycol test [EGT] kit), already in use by veterinarians, gives results in 30 minutes with little expertise or cost. The EGT reliably detects the presence of EG in spiked human serum samples. The objective of this study was to prospectively assess the sensitivity and specificity of the EGT kit in actual clinical samples submitted for EG testing by the criterion standard gas chromatography (GC). METHODS: Blood samples from patients with suspected toxic alcohol poisoning submitted to a reference laboratory were tested by GC. An investigator blinded to the GC results tested the same sample with the EGT kit following the manufacturer's instructions and using the internal control. Three physicians also blinded to the GC results categorized the sample as positive for EG, negative, or inconclusive. Interrater reliability was assessed with a kappa statistic (kappa). Results of the EGT kit testing were then compared to those from GC testing. RESULTS: Data are reported on 24 samples submitted. By GC, 15 samples were confirmed for EG (range 27-281 mg/dL), 5 were confirmed for methanol (ME; range 64-101 mg/dL), and 4 were negative for both alcohols. The EGT was unanimously positive in all confirmed EG samples and negative in all ME samples. In one of the negative samples, an ambiguous result occurred and was counted as a false-positive. Interobserver agreement with the EGT was high (kappa = 0.909; 95% confidence interval [CI] = 0.735 to 1.0). Sensitivity and specificity were 100% (95% CI = 70% to 100%) and 88.8% (95% CI = 52% to 100%), respectively. CONCLUSIONS: The EGT appears to be a reliable qualitative test in cases of suspected human EG poisoning
— id: 96659, year: 2008, vol: 15, page: 688, stat: Journal Article,

Factors associated with poison related fatality: A case control study
Manini, AF; Nelson, LS; Olsen, D; Fulton, J; Hoffman, RS
2008 ;46(7):615-616 SUM, Clinical Toxicology (Philadelphia)
— id: 86833, year: 2008, vol: 46, page: 615, stat: Journal Article,

Factors associated with adverse cardiovascular events among patients with suspected acute poisoning
Manini, AF; Nelson, LS; Skolnick, A; Slater, W; Hoffman, RS
2008 ;46(7):631-632 SUM, Clinical Toxicology (Philadelphia)
— id: 86834, year: 2008, vol: 46, page: 631, stat: Journal Article,

Alcoholic ketoacidosis in an 11-year-old boy
Manini, Alex F; Hoffman, Robert S; Nelson, Lewis S
2008 Mar;24(3):170-171, Pediatric emergency care
A history of ethanol consumption combined with vomiting, anion gap metabolic acidosis, and altered mental status is consistent with a broad differential diagnosis, which requires a systematic approach. Alcoholic ketoacidosis is rare after binge drinking in the naive individual and typically occurs in patients with heavy, chronic use. We present the case of an 11-year-old boy with acute ethanol intoxication and a clinical course that is most consistent with alcoholic ketoacidosis. Alcoholic ketoacidosis should be considered in the differential diagnosis of children with unexplained ketoacidosis when there is history or evidence of ethanol consumption combined with the appropriate clinical presentation
— id: 76868, year: 2008, vol: 24, page: 170, stat: Journal Article,

A novel neuromuscular syndrome associated with clenbuterol-tainted heroin
Manini, Alex; Labinson, Robert M; Kirrane, Barbara; Hoffman, Robert S; Rao, Rama; Stajic, Marina; Nelson, Lewis S
2008 Dec;46(10):1088-1092, Clinical Toxicology (Philadelphia)
BACKGROUND: Clenbuterol is a potent, long-acting beta-adrenergic agonist that has been reported as an adulterant of heroin. We describe an atypical syndrome in five users of clenbuterol-tainted heroin. METHODS: All cases were referred to a regional Poison Control Center. Urine and blood were analyzed using gas and liquid chromatography as well as mass spectrometry. CASE SERIES: Five heroin users presented with a syndrome characterized by muscular spasm, tremor, hyperreflexia, and elevated serum creatine phosphokinase concentrations. All patients lacked findings of acute clenbuterol toxicity but tested positive for clenbuterol and negative for strychnine and a battery of common potential adulterants. CONCLUSIONS: We report five cases of a novel neuromuscular syndrome in users of clenbuterol-adulterated heroin. It is unclear whether these reactions represent an atypical response to clenbuterol or another unidentified contaminant
— id: 96660, year: 2008, vol: 46, page: 1088, stat: Journal Article,

Maternal toxicity following intra-amniotic digoxin administration
Odujebe, OA; Hoffinan, RS; Nelson, LS
2008 JUN ;46(5):361-361, Clinical Toxicology (Philadelphia)
— id: 86869, year: 2008, vol: 46, page: 361, stat: Journal Article,

High lead levels with minimal signs of encephalopathy
Odujebe, OA; Hoffman, RS; Nelson, LS
2008 JUN ;46(5):416-416, Clinical Toxicology (Philadelphia)
— id: 86872, year: 2008, vol: 46, page: 416, stat: Journal Article,

Phenibut withdrawal - A novel "Nutritional Supplement"
Odujebe, OA; Hoffman, RS; Nelson, LS
2008 ;46(7):605-605 SUM, Clinical Toxicology (Philadelphia)
— id: 86832, year: 2008, vol: 46, page: 605, stat: Journal Article,

Prolonged severe hypotension following combined amlodipine and valsartan ingestion
Smith, Silas W; Ferguson, Kathy L; Hoffman, Robert S; Nelson, Lewis S; Greller, Howard A
2008 Jun;46(5):470-474, Clinical Toxicology (Philadelphia)
INTRODUCTION: Compared to other calcium channel blockers (CCBs), overdose with dihydropyridine CCBs are considered relatively benign due to their vascular selectivity. Although not a sustained-release preparation, amlodipine's prolonged duration of effect is concerning following overdose. In addition, angiotensin II receptor blocker blunting of vasoconstrictive and sympathetic compensatory responses could exacerbate calcium channel blocker toxicity. We describe severe toxicity associated with an overdose of amlodipine and valsartan. CASE REPORT: A 75-year-old woman presented to the ED 45 minutes after a witnessed suicidal ingestion of a 'handful' of amlodipine and valsartan tablets. Hypotension, which appeared two hours after ingestion, was refractory to crystalloids and colloids, calcium gluconate, epinephrine, norepinephrine, phenylephrine, and vasopressin infusions. High-dose insulin euglycemia (HIE) therapy, and treatment with glucagon and naloxone were successful in improving her hemodynamic status. In this combined overdose, right heart catheterization demonstrated both negative inotropic effects and decreased systemic vascular resistance. CONCLUSION: Co-ingestion of amlodipine with valsartan produced profound toxicity. Early institution of HIE therapy may be beneficial to reverse these effects
— id: 80579, year: 2008, vol: 46, page: 470, stat: Journal Article,

Solanaceous steroidal glycoalkaloids and poisoning by Solanum torvum, the normally edible susumber berry
Smith, Silas W; Giesbrecht, Esther; Thompson, Margaret; Nelson, Lewis S; Hoffman, Robert S
2008 Nov;52(6):667-676, Toxicon
Ingestion of immature, environmentally stressed, or cultivar-specific Solanum species (particularly the potato) has been previously associated with gastrointestinal and neurological symptoms caused by solanaceous steroidal glycoalkaloids (SGAs). We report on two geographically, temporally disparate outbreaks of poisoning by susumber berries (Solanum torvum- Solanaceae) and on detection of alkaloids not present in non-toxic berries. Five family members in New York City participated in a traditional evening meal containing Jamaican susumber berries. All those consuming berries were symptomatic the following morning with varying degrees of gastrointestinal distress, dizziness, slurred speech, cranial nerve deficits, and ataxia. The most seriously afflicted patient developed hypertension, confusion, proximal upper extremity weakness, and hypercapnic respiratory failure requiring prolonged mechanical ventilation. A separate cohort of six patients in Toronto ate unripe Jamaican susumber berries. They presented 14h post-ingestion with varying degrees of diarrhea, weakness, facial paralysis, slurred speech, ataxia, early hypertension, and proximal weakness. Two patients had ventilatory decompensation; one required intubation. Poisonous berries appeared indistinguishable from non-toxic varieties. We isolated solasonine, larger amounts of solamargine, and other steroidal glycoalkaloids in the toxic berry strains. S. torvum poisoning can produce significant neurological and gastrointestinal effects which appear to be mediated by SGAs present in the berries
— id: 91970, year: 2008, vol: 52, page: 667, stat: Journal Article,

Altered Acetaminophen Pharmacokinetics and Hepatotoxicity Associated with Premature Cessation of Intravenous N-Acetylcysteine Therapy (September)
Smith, Silas W; Howland, Mary Ann; Hoffman, Robert S; Nelson, Lewis S
2008 Sep;42(9):1333-1339, Annals of pharmacotherapy
OBJECTIVE: To report a case of erratic absorption, double peak serum concentrations, and hepatotoxicity following premature cessation of intravenous Nacetylcysteine (NAC) treatment in the setting of a massive acetaminophen overdose. CASE SUMMARY: A 78-year-old man reportedly ingested approximately 96 immediate-release acetaminophen 500-mg tablets (48 g) over a one-hour period in an apparent suicide attempt. The acetaminophen concentration at 2.25 hours was 264 microg/mL. Intravenous NAC was initiated 5 hours postingestion. At 6.25 hours postingestion, the acetaminophen concentration was 281 microg/mL. Following administration of intravenous NAC for 21 hours, therapy was discontinued despite a residual acetaminophen concentration of 116 microg/mL. The patient experienced hepatotoxicity, coagulopathy, and renal injury. Pharmacokinetic analysis revealed significantly prolonged acetaminophen absorption and a second peak acetaminophen concentration of 228 microg/mL approximately 48 hours postingestion. Direct in-hospital monitoring of the patient made a second ingestion unlikely. DISCUSSION: Acetaminophen overdose is usually effectively managed with NAC. Patients with massive ingestions may have altered absorption kinetics due to acetaminophen's solubility being exceeded, physiologically or chemically altered gastrointestinal emptying or motility, or other factors. These patients may benefit from gastrointestinal decontamination and prolonged NAC therapy. CONCLUSIONS: In patients with massive acetaminophen ingestion, erratic absorption may occur, and toxic serum concentrations may persist beyond a standard 21-hour course of intravenous NAC therapy. Acetaminophen concentrations and aminotransferase levels should be evaluated at the completion of therapy intravenous NAC infusion to ensure complete elimination of acetaminophen and absence of hepatotoxicity and to exclude the need for prolonged treatment
— id: 80581, year: 2008, vol: 42, page: 1333, stat: Journal Article,

Case Files of the New York City Poison Control Center: Antidotal strategies for the Management of Methotrexate toxicity
Smith, Silas W; Nelson, Lewis S
2008 Jun;4(2):132-140, Journal of medical toxicology
A 10-year-old boy (37.5 kg; body surface area 1.26m2) with osteosarcoma of the right humerus received a planned 4-hour infusion of high-dose methotrexate (16 g, 12.7 g/m(2)). His previous medical history was notable for an implanted central venous catheter placement complicated by Horner's syndrome. Renal and hepatic functions were normal at baseline. A postinfusion methotrexate concentration was uninterpretable, but the significance of this result was not initially appreciated by the treating clinicians. Over the next 48 hours, the child developed blurry vision, painful mucositis, stomatitis, and facial blistering. Reported vital signs were: BP, 121/82 mm Hg; pulse, 111/minute; respirations, 16/minute. A physical examination was consistent with the reported symptoms. The 48-hour postinfusion serum methotrexate concentration at the time of poison control center (PCC) consultation was 171 micromol/L
— id: 80580, year: 2008, vol: 4, page: 132, stat: Journal Article,

Mechanical ventilation was associated with acidemia in a case series of salicylate-poisoned patients
Stolbach, Andrew I; Hoffman, Robert S; Nelson, Lewis S
2008 Sep;15(9):866-869, Academic emergency medicine
OBJECTIVES: Despite little empiric evidence, mechanical ventilation (MV) in the setting of salicylate poisoning is considered by many to be harmful. When salicylate-poisoned patients are ventilated at conventional settings, the respiratory alkalosis is abolished, more salicylate is able to pass into the central nervous system (CNS), and neurotoxicity worsens. The objective of this study was to identify a relationship between MV, acidosis, and outcome in salicylate-poisoned patients. METHODS: The authors electronically searched a poison control center (PCC) database (2001-2007) for patients with salicylate poisoning, defined as a serum concentration > 50 mg/dL, who had MV listed as a therapy. For the 7-year study period, a total of 3,144 salicylate-poisoning cases were identified. Eleven patients met the inclusion criteria of having both salicylate concentrations > 50 mg/dL and required MV; only 7 of them had post-MV data available. RESULTS: In all seven patients with post-MV blood gas data, the post-MV pH was < 7.4. In five of six patients with recorded PCO2, the post-MV PCO2 was > 50 mm Hg. Two of the seven patients in the study group died following intubation (two patients died within 3 hours [serum salicylate concentrations, 85 and 79 mg/dL, respectively]). Another patient sustained severe neurologic injury (serum salicylate concentration, 84 mg/dL). The other four patients were ultimately discharged home. In the three patients with the worst clinical outcome, deterioration was reported within hours of intubation. CONCLUSIONS: Inadequate MV of patients with salicylate poisoning is associated with respiratory acidosis, acidemia, and clinical deterioration in this series of cases. This supports warnings about the danger of improper MV in patients with salicylate poisoning. A prospective study should be performed
— id: 96661, year: 2008, vol: 15, page: 866, stat: Journal Article,

Adverse events associated with ketamine for procedural sedation in adults
Strayer, Reuben J; Nelson, Lewis S
2008 Nov;26(9):985-1028, American journal of emergency medicine
STUDY OBJECTIVES: Ketamine is widely used as a procedural sedation agent in pediatrics, where its safety and efficacy are supported by numerous studies. Emergency physicians use ketamine infrequently in adults, as it is believed to have a more significant side effect profile in this population. However, adult data on ketamine use in the emergency medicine literature are sparse. Our objective was to determine ketamine's adverse effect profile in adults when used for procedural sedation. METHODS: We performed a literature review based on adverse effect research methodology recommendations. PubMed, EMBASE, TOXNET, and a variety of specialized databases were queried without regard to publication date or language. Experts were contacted to locate additional data. Inclusion criteria included adult study; ketamine used to facilitate the performance of painful procedures; dose of at least 1 mg/kg intravenous or at least 2 mg/kg intramuscular; original data and adverse events reported; spontaneously breathing patient, and no continuous cotherapies. Studies that met inclusion criteria were abstracted onto structured forms and their results qualitatively summarized. RESULTS: Of the 5512 unique citations that were evaluated, 87 met criteria for inclusion. Most studies were performed in the 1970s and published in the anesthesia literature. Contexts, end points, and methodological quality varied widely across studies. Ketamine reliably produces conditions that facilitate the performance of painful procedures. Pharyngeal reflexes are generally preserved and cardiovascular tone stimulated, including a rise in blood pressure and myocardial oxygen demand. Laryngospasm and airway obstruction are reported, and though ketamine is a respiratory stimulant, a brief period of apnea around the time of injection is common. Reports of significant cardiorespiratory adverse events are rare, despite ketamine's frequent use in austere, poorly monitored settings. Dysphoric emergence phenomena occur in 10% to 20% of cases; sedating medications are effective in preventing and managing these reactions. CONCLUSION: When ketamine is used for procedural sedation in adults, emergence phenomena occur in 10% to 20% of patients. Although providers must be prepared to recognize and manage airway obstruction, cardiorespiratory adverse events are rare and typically do not affect outcomes
— id: 107798, year: 2008, vol: 26, page: 985, stat: Journal Article,

Citalopram overdose: late presentation of torsades de pointes (TdP) with cardiac arrest
Tarabar, Asim F; Hoffman, Robert S; Nelson, Lewis
2008 Jun;4(2):101-105, Journal of medical toxicology
INTRODUCTION: Citalopram overdose may produce bradycardia, QT prolongation, and torsades de pointes (TdP). A cardiotoxic metabolite may be responsible for the delayed onset of cardiotoxicity. Although some authorities recommend a minimum of 24 hours of observation following citalopram overdose, a recent analysis suggested that dysrhythmias rarely occur beyond 13 hours post-ingestion. We present a case of citalopram overdose with a substantially delayed onset of cardiac toxicity. CASE REPORT: A 36-year-old woman complained of shakiness, numbness in the arms, and palpitations that began approximately 32 hours after ingesting 50 (20-mg) tablets of citalopram. Her initial vital signs were: blood pressure, 84/44 mmHg; pulse, 102-150/minute; respirations, 17/min; temperature, 99.3 degrees F (37.3 degrees C). Her initial ECG showed sinus rhythm with a prolonged corrected QT interval (572 msec) with paroxysmal, self-limited runs of wide-complex tachycardia that appeared multifocal in nature. Approximately 20 minutes after presentation, she experienced self-terminating TdP, with transient hypotension and loss of consciousness. Her serum citalopram concentration (33 hours post-ingestion) was 477 ng/mL (therapeutic: 40-110 ng/mL); desmethylcitalopram concentration was 123.2 ng/mL (therapeutic: 14-40 ng/mL). She was treated with magnesium and lidocaine, and her corrected QT interval remained abnormal for 24 hours after presentation. DISCUSSION: Citalopram overdose can produce life-threatening cardiac toxicity with a clinical onset that may be delayed beyond a routine observation period of 6 hours. Once the QT interval is prolonged, it seems prudent to prolong the observation period
— id: 96665, year: 2008, vol: 4, page: 101, stat: Journal Article,

Comment on "Cytochrome-C oxidase inhibition in 26 aluminum phosphide poisoned patients"
Amores, E; Forde-Baker, J; Ginsburg, BY; Nelson, LS
2007 JUN-AUG ;45(5):461-461, Journal of toxicology. Clinical toxicology
— id: 73709, year: 2007, vol: 45, page: 461, stat: Journal Article,

Benzodiazepine administration and need for mechanical ventilation in delirium tremens - Reply
Gold, JA; Nolan, A; Rimal, B; Nelson, L
2007 JUL ;35(7):1811-1812, Critical care medicine
— id: 73415, year: 2007, vol: 35, page: 1811, stat: Journal Article,

A strategy of escalating doses of benzodiazepines and phenobarbital administration reduces the need for mechanical ventilation in delirium tremens
Gold, Jeffrey A; Rimal, Binaya; Nolan, Anna; Nelson, Lewis S
2007 Mar;35(3):724-730, Critical care medicine
OBJECTIVE: Patients with severe alcohol withdrawal and delirium tremens are frequently resistant to standard doses of benzodiazepines. Case reports suggest that these patients have a high incidence of requiring intensive care and many require mechanical ventilation. However, few data exist on treatment strategies and outcomes for these subjects in the medical intensive care unit (ICU). Our goal was a) to describe the outcomes of patients admitted to the medical ICU solely for treatment of severe alcohol withdrawal and b) to determine whether a strategy of escalating doses of benzodiazepines in combination with phenobarbital would improve outcomes. DESIGN: Retrospective cohort study. SETTING: Inner-city municipal hospital. PATIENTS: Subjects admitted to the medical ICU solely for the treatment of severe alcohol withdrawal. INTERVENTIONS: Institution of guidelines emphasizing escalating doses of diazepam in combination with phenobarbital. MEASUREMENTS AND MAIN RESULTS: Preguideline (n = 54) all subjects were treated with intermittent boluses of diazepam with an average total and maximal individual dose of 248 mg and 32 mg, respectively; 17% were treated with phenobarbital. Forty-seven percent required intubation due to inability to achieve adequate sedation and need for constant infusion of sedative-hypnotics. Intubated subjects had longer length of stay (5.6 vs. 3.4 days; p = .09) and higher incidence of nosocomial pneumonia (42 vs. 21% p = .08). Postguideline (n = 41) there were increases in maximum individual dose of diazepam (32 vs. 86 mg; p = .001), total amount of diazepam (248 vs. 562 mg; p = .001), and phenobarbital use (17 vs. 58%; p = .01). This was associated with a reduction in the need for mechanical ventilation (47 vs. 22%; p = .008), with trends toward reductions in ICU length of stay and nosocomial pneumonia. CONCLUSIONS: Patients admitted to a medical ICU solely for treatment of severe alcohol withdrawal have a high incidence of requiring mechanical ventilation. Guidelines emphasizing escalating bolus doses of diazepam, and barbiturates if necessary, significantly reduced the need for mechanical ventilation and showed trends toward reductions in ICU length of stay and nosocomial infections
— id: 71814, year: 2007, vol: 35, page: 724, stat: Journal Article,

In vitro-activated charcoal binding of staphylococcal enterotoxin B
Hoffman, Robert J; Hahn, In-Hei; Shen, James M; Protic, John; Nelson, Lewis S
2007 Oct-Nov;45(7):773-775, Clinical Toxicology (Philadelphia)
OBJECTIVE: Staphylococcal enterotoxin B (SEB) is a CDC category B bioterror agent that may cause significant morbidity. We assessed the in vitro binding of SEB by activated charcoal (AC). METHODS: Aqueous solutions of SEB at three concentrations (0.4, 2 and 10 mcg/mL) were combined in volume rations of 3:1, 6:1, and 12:1 with AC at three concentrations (62.5, 125, and 250 mg/mL) or left untreated as control samples. Subsequently, each sample was tested with a qualitative SEB immunoassay to detect the presence of SEB at concentrations of >12.5 ng/mL. RESULTS: SEB was detectable in each untreated control solution. SEB was undetectable in the 2 mcg/mL and 0.4 mcg/mL solutions after treatment with AC in all quantities. SEB was detected in the 10 mcg/mL solution after combination with all three concentrations of AC. The difference in assay results between charcoal treated and untreated pairs was statistically significant. CONCLUSION: At ratios of 3:1 and above, SEB was adsorbed by AC when combined in the manner described in concentrations of 2 mcg/mL and 0.4 mg/mL. In a quantity of 10 mcg/mL complete charcoal binding of SEB did not occur with any ratio of AC used. These results support a role for AC in treating patients exposed to SEB or purifying liquids or gases containing SEB
— id: 145502, year: 2007, vol: 45, page: 773, stat: Journal Article,

QT prolongation and Torsades de Pointes following overdose of ziprasidone and amantadine
Manini, Alex F; Raspberry, Dara; Hoffman, Robert S; Nelson, Lewis S
2007 Dec;3(4):178-181, Journal of medical toxicology
— id: 111672, year: 2007, vol: 3, page: 178, stat: Journal Article,

In response to Isbister et al.: Application of pharmacokinetic-pharmacodynamic modeling in management of QT abnormalities after citalopram overdose
Manini, Alex; Smith, Silas; Moskovitz, Joshua; Nelson, Lewis
2007 Apr;33(4):738-738, Intensive care medicine
— id: 80567, year: 2007, vol: 33, page: 738, stat: Journal Article,

Antimuscarinic agent attack
Barrueto F; Nelson LS
Disaster medicine Philadelphia : Elsevier/Mosby, 2006,
— id: 4134, year: 2006, vol: , page: ?, stat: Chapter,

Cardioactive steroid poisoning: a comparison of plant- and animal-derived compounds
Barrueto, Fermin Jr; Kirrane, Barbara M; Cotter, Brian W; Hoffman, Robert S; Nelson, Lewis S
2006 Dec;2(4):152-155, Journal of medical toxicology
INTRODUCTION: Cardioactive steroids (CASs) are found in plants, animals, and insects. Their affinity for Na+-K+ ATPase is attenuated by the type of lactone at carbon 17 (C17) of the steroid backbone: those with 5-membered lactone rings, or cardenolides, are derived mostly from plants with 6-membered rings or from animals with bufadienolides. A systematic review of CAS poisoning was performed to compare the mortality rate of cardenolides and bufadienolides. METHODS: MEDLINE was searched for articles using commonly reported names of CASs, and keywords were limited to human cases only. We searched cases from 1982 to 2003, so that supportive care was similar and digoxin-specific Fab was available. Identified reports of CAS poisoning were read to exclude cases involving licensed pharmaceuticals. Inclusion criteria included hyperkalemia, gastrointestinal symptoms, electrocardiographic evidence of CAS toxicity, digoxin serum concentration, or history of exposure to a substance containing a CAS. Clinical data was collected, including information about treatment with digoxin-specific Fab and treatment outcome. RESULTS: Fifty-nine articles, describing 924 patients, were identified. Eight hundred ninety-seven patients (97%) ingested a CAS with a 5-membered lactone ring, and mortality was 6% (n = 54). Twenty-seven patients (2.9%) ingested a CAS with a 6-membered lactone ring, and mortality was 29.6% (n = 8). The difference in mortality rates was statistically significant (p < 0.001, [X2]). CASs with 6-member rings accounted for the highest percentage of nonsuicidal exposures. CONCLUSION: Although cardenolides accounted for the majority of exposures, bufadienolides were five times more lethal than cardenolides
— id: 111610, year: 2006, vol: 2, page: 152, stat: Journal Article,

Lamotrigine and citalopram overdose: unmasking a brugada ECG pattern
Bouchard N; Halcomb SE; Hoffman RS; Nelson LS
2006 ;44:656-656, Clinical toxicology
— id: 70037, year: 2006, vol: 44, page: 656, stat: Journal Article,

Phentolamine therapy for cocaine-association acute coronary syndrome (CAACS)
Chan, Gar Ming; Sharma, Rahul; Price, Dennis; Hoffman, Robert S; Nelson, Lewis S
2006 Sep;2(3):108-111, Journal of medical toxicology
INTRODUCTION: The emergency department (ED) evaluation of cocaine-associated acute coronary syndrome (CAACS) is often a diagnostic and therapeutic challenge. CASE REPORT: We are reporting on the treatment of a patient with cocaine-associated acute coronary syndrome (CAACS) who did not benefit from standard therapy, but who eventually responded positively to phentolamine, an alpha-adrenergic receptor antagonist. DISCUSSION: This report should encourage physicians to add phentolamine to their pharmacotherapeutic armamentarium in the treatment of CAACS
— id: 75419, year: 2006, vol: 2, page: 108, stat: Journal Article,

Testing positive for methadone and either a tricyclic antidepressant or a benzodiazepine is associated with an accidental overdose death: analysis of medical examiner data
Chan, Gar Ming; Stajic, Marina; Marker, Elizabeth K; Hoffman, Robert S; Nelson, Lewis S
2006 May;13(5):543-547, Academic emergency medicine
OBJECTIVES: Patients in emergency departments who use methadone frequently use tricyclic antidepressants (TCAs) and/or benzodiazepines (BZDs). This is a potentially dangerous drug combination. The authors hypothesized that the presence of methadone and a TCA, a BZD, or both is associated with an 'accidental' overdose (AOD) death more often than a death from any other cause. METHODS: A retrospective chart review of New York City Office of Chief Medical Examiner data for 2003 was performed. Decedents who tested positive for methadone that were classified as an AOD death, as determined by the medical examiner, were compared with deaths from all other causes for the presence of a TCA, a BZD, or both. A logistical regression was performed to develop a multivariate model identifying additional variables associated with a methadone-positive AOD death. A p-value of <0.05 was considered significant, and 95% confidence intervals (CIs) were calculated. RESULTS: In 2003, there were 5,817 medical examiner cases, of which 500 (8.6%) were methadone positive. Of the methadone-positive cases, 493 were available for analysis; 95 (19.3%) were TCA positive and 158 (32.0%) were BZD positive. The odds of having an AOD death in methadone-positive decedents testing TCA positive, BZD positive, or both were 2.11 (95% CI = 1.32 to 3.37; p < 0.01) for TCAs, 1.66 (95% CI = 1.12 to 2.45; p < 0.02) for BZDs, and 4.34 (95% CI = 1.97 to 9.56; p < 0.001) for both. The multivariate logistic regression of analytes revealed the following covariates associated with an AOD death as well: amitriptyline, cocaine, morphine, or opiates. CONCLUSIONS: Among the methadone-positive cases, testing positive for a TCA, a BZD, or both was associated with an AOD death
— id: 65876, year: 2006, vol: 13, page: 543, stat: Journal Article,

Initial evaluation of the patient : vital signs and toxic syndromes
Flomenbaum NE; Goldfrank LR; Hoffman RS; Howland MA; Lewin NA; Nelson LS
Goldfrank's toxicologic emergencies New York : McGraw-Hill Medical, 2006,
— id: 4542, year: 2006, vol: , page: 37, stat: Chapter,

Principles of managing the poisoned or overdosed patient
Flomenbaum NE; Goldfrank LR; Hoffman RS; Howland MA; Lewin NA; Nelson LS
Goldfrank's toxicologic emergencies New York : McGraw-Hill Medical, 2006,
— id: 4541, year: 2006, vol: , page: 42, stat: Chapter,

Hypoglycemic agents
Fulton J; Nelson LS
Essentials of emergency medicine Sudbury Mass : Jones & Bartlett, 2006,
— id: 4153, year: 2006, vol: , page: ?, stat: Chapter,

Renal infarction during the use of rizatriptan and zolmitriptan: two case reports
Fulton, Jessica A; Kahn, Jason; Nelson, Lewis S; Hoffman, Robert S
2006 ;44(2):177-180, Clinical Toxicology (Philadelphia)
Rizatriptan and zolmitriptan are both used to relieve acute migraine and cluster headaches. The mechanism of action is similar to the other triptans, in that they reverse abnormal cerebral vasodilation through their activity as 5-HT1B receptor agonists. Triptan-induced vasoconstriction is attributed to its activity on peripheral 5-HT1B receptors and has rarely been reported to result in stroke, myocardial infarction and ischemic colitis. We present two cases of renal infarction associated with therapeutic triptan use. The first patient is a 57-year-old man with a history of hypertension that was well controlled on valsartan and hydrochlorothiazide. He was recently diagnosed with cluster headaches and was treated with indomethacin, prednisone, butalbital-acetaminophen-caffeine and hydrocodone without relief. He then received two therapeutic doses of rizatriptan on each of the two days prior to presentation. Subsequently, he presented to the emergency department complaining of nausea, vomiting and right-sided abdominal pain. A computerized tomography (CT) scan of the abdomen and pelvis with intravenous contrast revealed a very large wedge shaped infarction of the right kidney. The second patient is a 34-year-old man with a past medical history significant only for life-long migraine headaches successfully treated for the past six years with zolmitriptan. Shortly after taking one therapeutic dose of zolmitriptan, he presented to the emergency department complaining of nausea and left-sided abdominal pain. A CT scan of the abdomen and pelvis with intravenous contrast revealed multiple wedge-shaped infarctions of the left kidney. Renal infarction was confirmed in both patients by arteriogram of the renal arteries. Although both rizatriptan and zolmitriptan are effective in the treatment of migraine and cluster headaches, they may induce peripheral vasospasm leading to renal infarction
— id: 69759, year: 2006, vol: 44, page: 177, stat: Journal Article,

Is acidosis commonly seen in patients with elevated ethanol levels?
Ginsburg, Beth Y; Porter, Robert; Nelson, Lewis S
2006 ;44(2):193-193, Clinical Toxicology (Philadelphia)
— id: 69760, year: 2006, vol: 44, page: 193, stat: Journal Article,

Ethanol withdrawal
Gold J; Nelson LS
Goldfrank's toxicologic emergencies New York : McGraw-Hill, 2006,
— id: 4177, year: 2006, vol: , page: ?, stat: Chapter,

A strategy of escalating doses of benzodiazepines and phenobarbital administration reduces need for mechanical ventilation in delirium tremens
Gold JA; Rimal B; Nolan A; Nelson LN
2006 ;:A735-A735, American journal of respiratory & critical care medicine
— id: 101398, year: 2006, vol: , page: A735, stat: Journal Article,

Hydrocarbons
Greller HA; Nelson LS
Essentials of emergency medicine Sudbury Mass : Jones & Bartlett, 2006,
— id: 4154, year: 2006, vol: , page: ?, stat: Chapter,

Resistant alcohol withdrawal: does an unexpectedly large sedative requirement identify these patients early?
Hack, Jason B; Hoffmann, Robert S; Nelson, Lewis S
2006 Jun;2(2):55-60, Journal of medical toxicology
INTRODUCTION: While most patients with alcohol withdrawal (AW) respond to standard treatment that includes doses of benzodiazepines, nutrition and good supportive care (non resistant alcohol withdrawal-NRAW), a subgroup may resist therapy (resistant alcohol withdrawal-RAW). This study describes a distinct group of AW patients, their sedative requirements, and hospital courses. METHODS: Over a period of 6 months, AW patients requiring 50 mg diazepam IV in the first hour were followed. We recorded admission indices and diazepam doses with vital signs at 1, 2, 3, 6, 12, and 24 hours. Patients were considered to have RAW if they required additional sedatives for control of symptoms and/or were having persistent abnormal vital signs despite the physicians' choices of therapy. RESULTS: Nineteen patients were enrolled; all had similar admission indices. While the 4 NRAW had normal vital signs within 3 hours, all 15 RAW patients had abnormal vital signs; 15 RAW patients required escalating diazepam doses--14 required barbiturates, 7 were intubated, and 5 had hypotension. Comparing groups: interval and total diazepam doses were not different at 1,2, and 3 hours; interval doses at 6 and 12 hours, and total doses at 6, 12, and 24 hours were significantly different. CONCLUSIONS: RAW patients require large doses of benzodiazepine administration, additional sedatives, and undergo complicated hospitalizations
— id: 111611, year: 2006, vol: 2, page: 55, stat: Journal Article,

Massive yohimbine overdose associated with sodium channel blockage
Halcomb SE; Parab S; Ravikumar PR; Hoffman RS; Nelson LS
2006 ;44:731-731, Clinical toxicology
— id: 70042, year: 2006, vol: 44, page: 731, stat: Journal Article,

Case files of the medical toxicology fellowship training program at the New York city poison control center: hypotensive death--therapeutic complication or suicide?
Halcomb, S Eliza; Nelson, Lewis S
2006 Jun;2(2):75-80, Journal of medical toxicology
— id: 111677, year: 2006, vol: 2, page: 75, stat: Journal Article,

Delayed diagnosis of lead poisoning caused by an Indian ayurvedic
Holubek WJ; Howland MA; Hoffman RS; Nelson LS
2006 ;44:772-772, Clinical toxicology
— id: 70043, year: 2006, vol: 44, page: 772, stat: Journal Article,

Acetaminophen protein adducts: is acetaminophen to blame?
Holubek, William J; Nelson, Lewis S
2006 Oct;131(4):1360-1360, Gastroenterology
— id: 69763, year: 2006, vol: 131, page: 1360, stat: Journal Article,

Unrecognized, life-threatening hypoglycemia due to maltodextrin in enteral nutrition
Kirrane BM; Duthie B; Nelson LS
2006 ;44:731-731, Clinical toxicology
— id: 70041, year: 2006, vol: 44, page: 731, stat: Journal Article,

Massive strontium ferrite ingestion without acute toxicity
Kirrane, Barbara M; Nelson, Lewis S; Hoffman, Robert S
2006 Nov;99(5):358-359, Basic & Clinical Pharmacology & Toxicology
Ingestion of strontium ferrite is previously unreported. We document absorption of strontium without acute toxicity. A 22 year-old schizophrenic man was brought to hospital after he was witnessed to pulverize and ingest flexible adhesive magnets, which later were identified as strontium ferrite. Other than auditory hallucinations his vital signs, physical examination, ECG and routine laboratories were unremarkable. Abdominal radiographs revealed diffuse radiopaque material. He was treated with whole bowel irrigation with polyethylene glycol electrolyte lavage solution (PEG-ELS) until radiographically cleared. His initial blood and urine strontium levels were 2900 microg/l and 15,000 microg/l, respectively (reference range for urine: <240 microg/l, occupational threshold 800 microg/l). A repeat urine level one week later was 370 microg/l. His hospital course was complicated by bacteraemia secondary to a thrombophlebitis at the site of the intravenous catheter, and the patient was treated with intravenous and oral antibiotics. He remained otherwise asymptomatic and was discharged to a psychiatric unit approximately 3 weeks later. Although clearly absorbed, strontium ferrite does not appear to produce acute toxicity. Delayed, and or chronic toxicity cannot be excluded based on this report
— id: 69764, year: 2006, vol: 99, page: 358, stat: Journal Article,

Antidysrhythmic agents
Lewin N; Nelson LS
Goldfrank's toxicologic emergencies New York : McGraw-Hill, 2006,
— id: 4176, year: 2006, vol: , page: ?, stat: Chapter,

Antidysrhythmics
Lewin NA; Nelson LS
Goldfrank's toxicologic emergencies New York : McGraw-Hill Medical, 2006,
— id: 4545, year: 2006, vol: , page: 971, stat: Chapter,

Camphor Poisoning: an evidence-based practice guideline for out-of-hospital management
Manoguerra, Anthony S; Erdman, Andrew R; Wax, Paul M; Nelson, Lewis S; Caravati, E Martin; Cobaugh, Daniel J; Chyka, Peter A; Olson, Kent R; Booze, Lisa L; Woolf, Alan D; Keyes, Daniel C; Christianson, Gwenn; Scharman, Elizabeth J; Troutman, William G
2006 ;44(4):357-370, Clinical Toxicology (Philadelphia)
A review of national poison center data from 1990 through 2003 showed approximately 10,000 annual ingestion exposures to camphor-containing products. A guideline that determines the threshold dose for emergency department referral and need for pre-hospital decontamination could potentially avoid unnecessary emergency department visits, reduce health care costs, optimize patient outcome, and reduce life disruption for patients and caregivers. An evidence-based expert consensus process was used to create the guideline. Relevant articles were abstracted by a trained physician researcher. The first draft of the guideline was created by the primary author. The entire panel discussed and refined the guideline before distribution to secondary reviewers for comment. The panel then made changes based on the secondary review comments. The objective of this guideline is to assist poison center personnel in the appropriate out-of-hospital triage and initial management of patients with suspected exposures to camphor-containing products by 1) describing the manner in which an exposure to camphor might be managed, 2) identifying the key decision elements in managing cases of camphor exposure, 3) providing clear and practical recommendations that reflect the current state of knowledge, and 4) identifying needs for research. This guideline applies to camphor exposure alone. Co-ingestion of additional substances, such as in commercial products of camphor combined with other ingredients, could require different referral and management recommendations depending on the combined toxicities of the substances. This guideline is based on an assessment of current scientific and clinical information. The expert consensus panel recognizes that specific patient care decisions may be at variance with this guideline, and are the prerogative of the patient and the health professionals providing care, considering all of the circumstances involved. This guideline does not substitute for clinical judgment. Recommendations are in chronological order of likely clinical use. The grade of recommendation is in parentheses. 1) Patients with stated or suspected self-harm or who are the recipients of malicious administration of a camphor-containing product should be referred to an emergency department immediately, regardless of the amount ingested (Grade D). 2) Patients who have ingested more than 30 mg/kg of a camphor-containing product or who are exhibiting symptoms of moderate to severe toxicity (e.g., convulsions, lethargy, ataxia, severe nausea and vomiting) by any route of exposure should be referred to an emergency department for observation and treatment (Grade D). 3) Patients exhibiting convulsions following a camphor exposure should be transported to an emergency department by pre-hospital emergency medical care providers (Grade D). A benzodiazepine should be used to control convulsions (Grade C). 4) Patients who have been exposed to a camphor product and who remain asymptomatic after 4 hours can be safely observed at home (Grade C). 5) Induction of emesis with ipecac syrup should not be performed in patients who have ingested camphor products (Grade C). 6) Activated charcoal administration should not be used for the ingestion of camphor products. However, it could be considered if there are other ingredients in the product that are effectively adsorbed by activated charcoal or if other substances have been co-ingested. (Grade C). 7) For asymptomatic patients with topical exposures to camphor products, the skin should be thoroughly washed with soap and water and the patient can be observed at home for development of symptoms (Grade C). 8) For patients with topical splash exposures of camphor to the eye(s), the eye(s) should be irrigated in accordance with usual poison center procedures and that referral take place based on the presence and severity of symptoms (Grade D). 9) Patients with camphor inhalation exposures should be moved to a fresh air environment and referred for medical care based on the presence and severity of symptoms. It is unlikely that symptoms will progress once the patient is removed from the exposure environment (Grade D)
— id: 69762, year: 2006, vol: 44, page: 357, stat: Journal Article,

Copper poisoning
Nelson LS
Goldfrank's toxicologic emergencies New York : McGraw-Hill, 2006,
— id: 4174, year: 2006, vol: , page: ?, stat: Chapter,

Opioids
Nelson LS
Goldfrank's toxicologic emergencies New York : McGraw-Hill, 2006,
— id: 4172, year: 2006, vol: , page: ?, stat: Chapter,

Pulmonary irritants
Nelson LS
Goldfrank's toxicologic emergencies New York : McGraw-Hill, 2006,
— id: 4173, year: 2006, vol: , page: ?, stat: Chapter,

Inhaled toxins
Nelson LS; Hoffman RS
Rosen's emergency medicine : concepts and clinical practice Philadelphia : Mosby/Elseiver, 2006,
— id: 4168, year: 2006, vol: , page: ?, stat: Chapter,

Chemical principles
Nelson LS; Traub S
Goldfrank's toxicologic emergencies New York : McGraw-Hill, 2006,
— id: 4175, year: 2006, vol: , page: ?, stat: Chapter,

Acute cyanide toxicity: mechanisms and manifestations
Nelson, Lewis
2006 Aug;32(4 Suppl):S8-11, Journal of emergency nursing
— id: 68661, year: 2006, vol: 32, page: S8, stat: Journal Article,

Antidote worse than the poison? ["The Toxic Emergency"]
Nelson, Lewis S
2006 ;38:31-34 Junw, Emergency medicine
— id: 69802, year: 2006, vol: 38, page: 31, stat: Journal Article,

Rat poison equals human poison ["The Toxic Emergency"]
Nelson, Lewis S
2006 ;38:31-33 Dec, Emergency medicine
— id: 69801, year: 2006, vol: 38, page: 31, stat: Journal Article,

Handbook of poisonous and injurious plants
Nelson, Lewis; Shih, Richard D; Balick, Michael J; Lampe, Kenneth F
New York : New York Botanical Garden, 2006,
— id: 1198, year: 2006, vol: , page: , stat: ,

Diphenhydramine and dimenhydrinate poisoning: an evidence-based consensus guideline for out-of-hospital management
Scharman, Elizabeth J; Erdman, Andrew R; Wax, Paul M; Chyka, Peter A; Caravati, E Martin; Nelson, Lewis S; Manoguerra, Anthony S; Christianson, Gwenn; Olson, Kent R; Woolf, Alan D; Keyes, Daniel C; Booze, Lisa L; Troutman, William G
2006 ;44(3):205-223, Clinical Toxicology (Philadelphia)
In 2003, there were 28,092 human exposures to diphenhydramine reported to poison centers in the US. A related drug, dimenhydrinate, is a less frequent cause of poisonings. Between January 2000 and June 2004, there were 2,534 reported dimenhydrinate ingestions in children less than 6 years of age. An evidence-based expert consensus process was used to create this guideline. Relevant articles were abstracted by a trained physician researcher. The first draft was created by the primary author. The entire panel discussed and refined the guideline before distribution to secondary reviewers for comment. The panel then made changes based on the secondary review comments. The objective of this guideline is to assist poison center personnel in the appropriate out-of-hospital triage and initial management of patients with a suspected ingestion of diphenhydramine or dimenhydrinate, or a dermal exposure to diphenhydramine. This guideline is based on an assessment of current scientific and clinical information. The expert consensus panel recognizes that specific patient care decisions may be at variance with this guideline and are the prerogative of the patient and the health professionals providing care, considering all of the circumstances involved. This guideline does not substitute for clinical judgment. The panel's recommendations for dermal or oral exposures to diphenhydramine or oral exposures to dimenhydrinate follow. The grade of recommendation is in parentheses: 1) All patients with suicidal intent, intentional abuse, or in cases in which a malicious intent is suspected (e.g., child abuse or neglect) should be referred to an emergency department (Grade D). 2) In patients without evidence of self-harm, abuse, or malicious intent, poison center personnel should elicit additional information including the time of the ingestion or dermal exposure, determination of the precise dose ingested, and the presence of co-ingestants (Grade D). 3) Patients experiencing any changes in behavior other than mild drowsiness or mild stimulation should be referred to an emergency department. Examples of moderate to severe symptoms that warrant referral include agitation, staring spells, inconsolable crying, hallucinations, abnormal muscle movements, loss of consciousness, seizures, or respiratory depression (Grade D). 4) For patients referred to the emergency department, transportation via ambulance should be considered based on several factors including the condition of the patient and the length of time it will take the patient to arrive at the emergency department (Grade D). 5) If the patient has no symptoms, and more than 4 hours have elapsed between the time of diphenhydramine ingestion and the call to the poison center, referral to an emergency department is not recommended. For dermal exposures to diphenhydramine, if the patient has no symptoms and it has been more than 8 hours since the diphenhydramine was thoroughly removed from the skin, referral to an emergency department is not recommended (Grade D). 6) Patients with acute ingestions of less than a toxic dose of diphenhydramine, or chronic exposures to diphenhydramine and no or mild symptoms, can be observed at home with instructions to call the poison center back if symptoms develop or worsen. The poison center should consider making a follow-up call at approximately 4 hours after ingestion (Grade D). 7) Children less than 6 years of age who ingest at least 7.5 mg/kg of diphenhydramine should be referred to an emergency department (Grade D). 8) Patients 6 years of age and older who ingest at least 7.5 mg/kg or 300 mg of diphenhydramine (whichever is less), should be referred to an emergency department (Grade D). 9) If the patient has no symptoms, and more than 6 hours have elapsed between the time of dimenhydrinate ingestion and the call to the poison center, referral to an emergency department is not recommended (Grade D). 10) Patients with acute ingestions of less than a toxic dose of dimenhydrinate, or chronic exposures to dimenhydrinate and no or mild symptoms, can be observed at home with instructions to call the poison center back if symptoms develop or worsen. The poison center should consider making a follow-up call at approximately 6 hours after ingestion (Grade D). 11) Children less than 6 years of age ingesting at least 7.5 mg/kg of dimenhydrinate should be referred to an emergency department (Grade D). 12) Patients 6 years of age and older ingesting at least 7.5 mg/kg or 300 mg of dimenhydrinate (whichever is less), should be referred to an emergency department for evaluation (Grade D). 13) Following oral exposures of diphenhydramine or dimenhydrinate, do not induce emesis. Because of the potential for diphenhydramine or dimenhydrinate to cause loss of consciousness or seizures, activated charcoal should not be administered en route to an emergency department (Grade D). 14) For chronic dermal exposures of diphenhydramine, skin decontamination (with water or soap and water) should be attempted prior to transporting a patient to an emergency department unless moderate to severe symptoms are already present. In this circumstance, transportation should not be delayed, and EMS personnel should attempt skin decontamination en route to the emergency department (Grade D). 15) Intravenous sodium bicarbonate may be administered by EMS personnel if QRS widening (QRS >0.10 msec) is present and if authorized by EMS medical direction (Grade D). 16) Physostigmine should be reserved for administration in a hospital (Grade D). 17) Benzodiazepines may be administered by EMS personnel if agitation or seizures are present, and if authorized by EMS medical direction (Grade D)
— id: 69761, year: 2006, vol: 44, page: 205, stat: Journal Article,

Hypercalcemia in a 4-year-old child followin overdosage of vitamin D aupplementation: more is not better
Schwaner RA; Hoffman RS; Howland MA; Nelson LS
2006 ;44:654-654, Clinical toxicology
— id: 70036, year: 2006, vol: 44, page: 654, stat: Journal Article,

What roles does (should?) the PCC play regarding the medication safety of drugs administered off-label?
Schwaner RA; Hoffman RS; Howland MA; Nelson LS
2006 ;44:710-710, Clinical toxicology
— id: 70040, year: 2006, vol: 44, page: 710, stat: Journal Article,

The availability and use of charcoal hemoperfusion in the treatment of poisoned patients
Shalkham, Anna S; Kirrane, Barbara M; Hoffman, Robert S; Goldfarb, David S; Nelson, Lewis S
2006 Aug;48(2):239-241, American journal of kidney diseases
BACKGROUND: Charcoal hemoperfusion (CHP) has been one of the preferred methods to enhance the elimination of certain toxins in selected poisoned patients. However, the availability of CHP may be limited because of the expense of cartridges, their narrow indications, and their limited shelf life. Improvements in hemodialysis (HD) technology may contribute to making CHP obsolete. We investigated the availability of CHP in in-hospital HD units at hospitals receiving ambulances dispatched through New York City's emergency response system, hereafter referred to as 911-receiving hospitals, and their recent history of CHP use in poisoned patients. METHODS: The medical directors or managers of all in-hospital HD units in the 911-receiving hospitals of New York City were contacted by E-mail and/or telephone. Participants were administered a standard survey that included questions regarding the availability of CHP cartridges and the date and indication for last CHP use. Participants at institutions that did not stock CHP cartridges were questioned about their opinions on the utility of CHP. RESULTS: Forty-two in-hospital HD units were surveyed, of which 34 (81%) completed the survey. Ten units (29%) had CHP cartridges available for immediate use. Each of these 10 units stocked between 1 and 4 adult-size CHP cartridges, and 1 unit stocked 2 pediatric-size CHP cartridges. Nine units had in-date CHP cartridges, and 1 unit had only expired CHP cartridges. Only 3 units performed CHP in the past 5 years (2 units, theophylline poisonings; 1 unit, aluminum overload). In the 24 units without CHP cartridges, 21 directors believed that most common toxins could be removed effectively through HD and thus CHP rarely was indicated. Only 1 director cited expense as a factor in not stocking CHP cartridges. Two directors reported no specific reason for not stocking the cartridges. CONCLUSION: CHP cartridges are available in only approximately one third of 911-receiving hospitals in New York City. CHP is infrequently performed to enhance toxin elimination in poisoned patients
— id: 66409, year: 2006, vol: 48, page: 239, stat: Journal Article,

Publication of abstracts presented at 2001 NAACT
Smollin, Craig G; Nelson, Lewis S
2006 Sep;2(3):97-100, Journal of medical toxicology
INTRODUCTION: The timely and formal publication of material presented as abstracts at national meetings is critical to the dissemination of new information to the medical community. We designed a retrospective study to evaluate the publication rates of abstracts presented at a recent national toxicology conference. In addition, we attempted to determine whether readily identifiable characteristics could predict a greater likelihood of publication. METHODS: In June of 2004, we reviewed 237 abstracts from the 2001 North American Congress of Clinical Toxicology (NACCT). Abstracts were classified according to methodology and content. We then searched Medline, using PubMed, to determine the publication of each abstract. RESULTS: Fifty-seven of 237 abstracts (24.1%) were subsequently published in peer reviewed journals. There was no statistically significant difference in the rate of publication when abstracts were categorized with respect to methodology. When categorized with respect to content, abstracts related to natural toxins had a higher publication rate (41.2%; p < 0.05). CONCLUSIONS: Three years after presenting abstracts at the 2001 NACCT meeting, the majority of abstracts remain unpublished. This is a lower rate than noted by other specialty medical societies
— id: 111609, year: 2006, vol: 2, page: 97, stat: Journal Article,

Suicide with intravenous vecuronium
Stolbach AI; Catanese CA; Howland MA; Hoffman RS; Nelson LS
2006 ;44:709-709, Clinical toxicology
— id: 70039, year: 2006, vol: 44, page: 709, stat: Journal Article,

Esophageal perforation after "body packing" cigarette tobacco
Stolbach AI; Garra G; Howland MA; Hoffman RS; Nelson LS
2006 ;44:690-690, Clinical toxicology
— id: 70038, year: 2006, vol: 44, page: 690, stat: Journal Article,

Nicotinic agent attack
Wiener SW; Nelson LS
Disaster medicine Philadelphia : Elsevier/Mosby, 2006,
— id: 4133, year: 2006, vol: , page: ?, stat: Chapter,

Antiepileptic agents
Barrueto F; Nelson LS
Pediatric toxicology : diagnosis and management of the poisoned child New York : McGraw-Hill, 2005,
— id: 4180, year: 2005, vol: , page: ?, stat: Chapter,

Amiodarone fails to improve survival in amitriptyline-poisoned mice
Barrueto, Fermin Jr; Chuang, Amy; Cotter, Brian W; Hoffman, Robert S; Nelson, Lewis S
2005 ;43(3):147-149, Clinical Toxicology (Philadelphia)
OBJECTIVE: Amiodarone, a class III antidysrhythmic agent, blocks Na+, Ca2+, and K+ channels as well as the beta-adrenergic receptor. Despite increased use of amiodarone for wide-complex tachycardia, its efficacy in the treatment of dysrhythmias induced by tricyclic antidepressants has not been tested. We investigated the effect of amiodarone and amitriptyline in a mouse lethality model. METHODS: The LD50 of amitriptyline obtained from reference sources was confirmed by giving 100 mg/kg to 40 mice by intraperitoneal (IP) injection. The safety of the treatment dose of amiodarone was confirmed by giving 50 mg/kg by IP injection to 10 mice. One hundred and nine mice were randomized to receive pretreatment with 50 mg/kg amiodarone (n=55) or an equal volume of saline or water as a volume control (n=54). Thirty minutes after pretreatment or control injection, the mice received amitriptyline, 100 mg/kg. Outcome was defined as death or survival 3 h after amitriptyline injection. RESULTS: In our confirmation of the LD50 of amitriptyline, 25/40 mice died (62.5%). None of the 10 mice that received only amiodarone died. In the control + amitriptyline arm, 36/54 (66.7%) died, compared with 39/55 (70.9%) in the amiodarone+amitriptyline arm (X2, p=0.663). Power analysis demonstrated a 90% chance of finding a 28% difference. CONCLUSIONS: Pretreatment with amiodarone does not appear to significantly alter the lethality of amitriptyline poisoning in mice. Given the inability to monitor cardiac activity in this model, further investigation in a larger animal is required
— id: 69755, year: 2005, vol: 43, page: 147, stat: Journal Article,

Acute vitamin D intoxication in a child
Barrueto, Fermin Jr; Wang-Flores, Helena H; Howland, Mary Ann; Hoffman, Robert S; Nelson, Lewis S
2005 Sep;116(3):e453-e456, Pediatrics
We present the unique case of a previously healthy, 2-year-old boy with resistant hypercalcemia and hypertension resulting from an unintentional overdose with an imported vitamin D supplement. The patient presented initially to the emergency department with colic and constipation and was discharged after a benign physical examination. The symptoms persisted and, on the second visit, the patient was found to have a serum calcium level of 14.4 mg/dL. Despite therapy with intravenously administered 5% dextrose solution at one-half normal strength, furosemide, calcitonin, and hydrocortisone, the calcium concentration increased to 15.0 mg/dL on the second hospital day and did not decrease until the fourth hospital day, when it fell to 13.9 mg/dL. The vitamin D concentration peaked at 470 ng/mL on hospital day 3. With additional questioning, the mother revealed that she had been giving her son a daily dose of 1 ampule of Raquiferol, an imported vitamin D supplement, instead of the recommended 2 drops per day. Each ampule contained 600,000 IU of vitamin D; therefore, the boy received a total of 2,400,000 IU over 4 days. The patient's hypercalcemia persisted for 14 days and was complicated by persistent hypertension. No renal, cardiac, or neurologic complications were noted. At discharge, the vitamin D concentration was still elevated at 389 ng/mL and the total calcium level had decreased to 11 mg/dL. The boy made a complete clinical recovery. This case highlights the need for caution when using imported and/or unregulated medicines, as well as the dangers of parental dosing errors
— id: 69757, year: 2005, vol: 116, page: e453, stat: Journal Article,

Opioid poisoning
Bouchard NB; Nelson LS
Textbook of critical care Philadelphia : Elsevier Saunders, 2005,
— id: 4171, year: 2005, vol: , page: ?, stat: Chapter,

Severe lactic acidemia and systemic toxicity following oral propylene glycol ingestion : a role for fomepizole and hemodialysis
Bouchard NC; Abou Rjaili G; Choufani D; McGee MP; Stajic M; Hoffman RS; Nelson LS
2005 ;43:740-740, Clinical toxicology
— id: 70044, year: 2005, vol: 43, page: 740, stat: Journal Article,

Status epilepticus from intrathecal cefazolin : quantification of therapeutic CSF drainage
Bouchard NC; Etienne M; Marraffa JM; Liberate B; Edelstein E; Stork CM; Howlnad MA; Nelson LS; Hoffman RS
2005 ;43:646-646, Clinical toxicology
— id: 70045, year: 2005, vol: 43, page: 646, stat: Journal Article,

Acute aluminum encephalopathy from alum bladder irrigation : alumninum extraction with high flux hemodialysis is superior to charcoal hemoperfusion
Bouchard NC; Malostovker I; Harbord N; Nelson LS; Feinfeld DA; Dubrow A; Hoffman RS; Winchester JF
2005 ;43:677-678, Clinical toxicology
— id: 115908, year: 2005, vol: 43, page: 677, stat: Journal Article,

Recurrent torsades des pointes after abrupt self-escalation of dose in a chronic methadone patient
Bouchard NC; Nelson LS; Hoffman RS
2005 ;43:503-503, Clinical toxicology
— id: 70055, year: 2005, vol: 43, page: 503, stat: Journal Article,

Ischemic stroke associated with use of an ephedra-free dietary supplement containing synephrine
Bouchard, Nicole C; Howland, Mary Ann; Greller, Howard A; Hoffman, Robert S; Nelson, Lewis S
2005 Apr;80(4):541-545, Mayo Clinic proceedings
In response to concerns regarding the safety of ephedra-containing dietary supplements, manufacturers have marketed 'ephedra-free' products. Many of these contain synephrine, a sympathomimetic amine from the plant Citrus aurantium. Synephrine is structurally similar to ephedrine and has vasoconstrictor properties. We describe a 38-year-old patient with ischemic stroke associated with an ephedra-free dietary supplement containing synephrine and caffeine. The patient presented with memory loss and unsteady gait after taking 1 or 2 capsules per day of a dietary supplement (Stacker 2 Ephedra-Free) for 1 week. He had no notable medical history or major atherosclerotic risk factors and took no other medications. Physical examination showed a mildly ataxic gait and substantial Impairment of both concentration and memory. Computed tomography and magnetic resonance Imaging of the brain showed subacute infarctions in the left thalamus and left cerebellum in the distribution of the vertebrobasilar circulation. Other causes of ischemic stroke were evaluated, and findings were unremarkable; a vasospastic origin was considered most likely. The patient was discharged with nearly complete resolution of symptoms. Synephrine, a sympathomimetic amine related to ephedrine, may be associated with Ischemic stroke. Consumers and clinicians need to be Informed about the potential risks of ephedra-free products
— id: 64542, year: 2005, vol: 80, page: 541, stat: Journal Article,

Tiagabine overdose: a case of status epilepticus in a non-epileptic patient
Fulton, Jessica A; Hoffman, Robert S; Nelson, Lewis S
2005 ;43(7):869-871, Clinical Toxicology (Philadelphia)
Tiagabine is an antiepileptic drug used as adjunctive therapy for partial seizures that is believed to selectively inhibit the presynaptic reuptake of gamma aminobutyric acid (GABA). We describe a case of a tiagabine overdose that resulted in status epilepticus (SE) in a patient with no seizure history. A 14-year-old girl with a history of asthma presented with convulsive SE after ingestion of an unknown amount of her sister's tiagabine in a suicide attempt. Attempted anticonvulsant therapy included a total of diazepam 10 mg IV, lorazepam 6 mg IV, pyridoxine 5 g IV, and fosphenytoin 20 mg PE/kg. All were without effect. A computed tomography and electrocardiogram were normal. Continuous bedside EEG monitoring showed suppression of seizure activity following intravenous midazolam. A tiagabine level obtained on ED arrival was 420 ng/mL (therapeutic 20-103 ng/mL). The patient was discharged to psychiatry within 1 week with no neurologic sequelae
— id: 69758, year: 2005, vol: 43, page: 869, stat: Journal Article,

Medication labeling errors in non-English-speaking patients
Fulton, Jessica A; Nelson, Lewis S
2005 Feb;39(2):386-387, Annals of pharmacotherapy
— id: 69754, year: 2005, vol: 39, page: 386, stat: Journal Article,

Generalized, tonic-clonic seizure associated with a tiagabine overdose in a patient with no prior seizure history
Ginsburg BY; Chu J; Hoffman RS; Nelson LS
2005 ;43:481-481, Clinical toxicology
— id: 70056, year: 2005, vol: 43, page: 481, stat: Journal Article,

Mercury absorption following elemental mercury ingestion
Ginsburg BY; Greller HA; Freyberg C; Hoffman RS; Nelson LS
2005 ;43:749-750, Clinical toxicology
— id: 70046, year: 2005, vol: 43, page: 749, stat: Journal Article,

Symptomatic bilateral adrenal infarcation associated with cocaine use
Ginsburg BY; Weinberg HR; Hoffman RS; Nelson LS
2005 ;43:663-663, Clinical toxicology
— id: 70047, year: 2005, vol: 43, page: 663, stat: Journal Article,

QTc interval prolongation associated with escitalopram overdose
Ginsburg BY; Wiener SW; Henderson KJ; Hoffman RS; Nelson LS
2005 ;43:502-502, Clinical toxicology
— id: 70057, year: 2005, vol: 43, page: 502, stat: Journal Article,

Hallucinogens
Greller HA; Nelson LS
Harwood-Nus' clinical practice of emergency medicine Philadelphia : Lippincott Williams & Wilkins, 2005,
— id: 4130, year: 2005, vol: , page: ?, stat: Chapter,

Mothballs, camphor and deodorizers
Greller HA; Nelson LS
Pediatric toxicology : diagnosis and management of the poisoned child New York : McGraw-Hill, 2005,
— id: 4181, year: 2005, vol: , page: ?, stat: Chapter,

Use of ultrasound in the detection of intestinal drug smuggling
Greller, Howard A; McDonagh, John; Hoffman, Robert S; Nelson, Lewis S
2005 Jan;15(1):193-193, European radiology
— id: 69752, year: 2005, vol: 15, page: 193, stat: Journal Article,

Opioid poisoning
Hahn IH; Nelson LS
Critical care toxicology : diagnosis and management of the critically poisoned patient Philadelphia : Elsevier Mosby, 2005,
— id: 4132, year: 2005, vol: , page: ?, stat: Chapter,

Cellular phone interference as a cause of acute epinephrine poisoning
Hahn, In-Hei; Schnadower, David; Dakin, Richard J; Nelson, Lewis S
2005 Sep;46(3):298-299, Annals of emergency medicine
— id: 69756, year: 2005, vol: 46, page: 298, stat: Journal Article,

Telithromycin-induced cholinergic crisis in myasthenia gravis
Halcomb SE; Nelson LS; Shah C; Chaudry A; Hoffman RS
2005 ;43:632-632, Clinical toxicology
— id: 70051, year: 2005, vol: 43, page: 632, stat: Journal Article,

Poisoning by sympathomimetics
Hoffman RJ; Nelson LS
Critical care toxicology : diagnosis and management of the critically poisoned patient Philadelphia : Elsevier Mosby, 2005,
— id: 4131, year: 2005, vol: , page: ?, stat: Chapter,

Multistate outbreak of clenbuterol contaminated heroin and cocaine
Hoffman RS; Burkhart K; Chan G; Ford M; Ginsburg B; Hahn I; Halcomb S; Johnson-Arbor K; Kirrane B; McKay C; Nelson L; Poppenga R; Ruck B; Shechter E; Stajic M; Tarabar A; Marcus S
2005 ;43:?-?, Clinical toxicology
— id: 70050, year: 2005, vol: 43, page: ?, stat: Journal Article,

Acute coronary syndrome following subcutaneous sumatriptan administration in a child
Hoffman RS; Ginsburg RY; Nelson LS; Hahn I
2005 ;43:634-635, Clinical toxicology
— id: 70049, year: 2005, vol: 43, page: 634, stat: Journal Article,

In vitro charcoal binding of staphylococcal enterotoxin B
Hoffman RS; Hahn I; Shen JM; Sandoval M; Shu C; Nelson LS
2005 ;43:675-675, Clinical toxicology
— id: 70048, year: 2005, vol: 43, page: 675, stat: Journal Article,

Massive strontium ferrate ingestion does not produce acute toxicity
Kirrane BM; Hoffman RS; Nelson LS
2005 ;43:749-749, Clinical toxicology
— id: 70052, year: 2005, vol: 43, page: 749, stat: Journal Article,

Herbal medication use by patients presenting to the emergency department
Kwon, NS; Waxman, M; Moore, EC; Lewin, J; Mary, AH; Hoffman, RS; Nelson, LS; Chiang, WK; Goldfrank, LR
2005 SEP ;46(3):S77-S78, Annals of emergency medicine
— id: 58904, year: 2005, vol: 46, page: S77, stat: Journal Article,

Inhalants
Long H; Nelson LS
Pediatric toxicology : diagnosis and management of the poisoned child New York : McGraw-Hill, 2005,
— id: 4182, year: 2005, vol: , page: ?, stat: Chapter,

Pharmacology of ethanol dependence
Nelson LS
2005 ;43:393-393, Clinical toxicology
— id: 70058, year: 2005, vol: 43, page: 393, stat: Journal Article,

Sensory organs
Nelson LS
Encyclopedia of toxicology Oxford UK : Elsevier, 2005,
— id: 4151, year: 2005, vol: , page: ?, stat: Chapter,

Emergency potpurri
Nelson, Lewis; Schiavone, Frederick M; Jurkovich, Gregory J
Glendale CA : Audio-Digest Foundation, 2005,
— id: 1200, year: 2005, vol: , page: , stat: ,

Herbal products
Schier JG; Nelson LS
Pediatric toxicology : diagnosis and management of the poisoned child New York : McGraw-Hill, 2005,
— id: 4183, year: 2005, vol: , page: ?, stat: Chapter,

The availability and use of charcoal hemoperfusion in the treatment of poisoned patients
Shalkham AS; Kirrane BM; Goldfarb D; Hoffman RS; Nelson LS
2005 ;43:676-676, Clinical toxicology
— id: 70053, year: 2005, vol: 43, page: 676, stat: Journal Article,

A report of lupinus mutabilis anticholinergic toxicity
Smith SW; Halcomb SE; Hoffman RS; Nelson LS
2005 ;43:763-763, Clinical toxicology
— id: 70054, year: 2005, vol: 43, page: 763, stat: Journal Article,

Failed whole bowel irrigation in heroin body packer : late endoscopic removal of the packages
Tarabar AF; Greller H; Hoffman RS; Nelson LS; Vencantran R
2005 ;43:519-519, Clinical toxicology
— id: 70059, year: 2005, vol: 43, page: 519, stat: Journal Article,

Tetramethylenedisulfotetramine: old agent and new terror
Whitlow, K Scott; Belson, Martin; Barrueto, Fermin; Nelson, Lewis; Henderson, Alden K
2005 Jun;45(6):609-613, Annals of emergency medicine
Tetramethylenedisulfotetramine has accounted for numerous intentional and unintentional poisonings in China. In May 2002, the first known case of human illness in the United States caused by tetramethylenedisulfotetramine, a banned neurotoxic rodenticide from China, occurred in New York City. The clinical presentation after tetramethylenedisulfotetramine exposure is dose dependent, and the most recognized complication is status epilepticus. Poisonings may be fatal within hours. No known antidote exists, and treatment is mainly supportive. Anecdotal reports, case reports, and 2 animal studies suggest possible success with certain pharmacologic interventions, including pyridoxine and chelation therapy. Pesticide and rodenticide poisonings, whether intentional or unintentional, pose a serious threat to populations, and the availability of a banned rodenticide such as tetramethylenedisulfotetramine, with its associated morbidity and lethality, is a serious public health concern. Given the recent case report that confirms the presence of tetramethylenedisulfotetramine in the United States, the toxicity of the compound, its unique physical properties, the absence of an antidote, and the history of its use as an agent of intentional mass poisoning, public health entities have undertaken educational efforts to inform the public, health care providers, and emergency personnel of this potentially lethal rodenticide
— id: 69774, year: 2005, vol: 45, page: 609, stat: Journal Article,

Atypical reactions associated with heroin use : Five states
[Nelson LS; et al]
2005 ;54:793-796, MMWR
— id: 69788, year: 2005, vol: 54, page: 793, stat: Journal Article,

The fentanyl tea bag
Barrueto, Fermin Jr; Howland, Mary Ann; Hoffman, Robert S; Nelson, Lewis S
2004 Feb;46(1):30-31, Veternary & human toxicology
Fentanyl patches create unique opportunities for use and abuse. Each patch contains 100-fold more drug than is stated on the label in order to create the gradient required to deliver the stated amount (ie 25-100 microg/h). Several methods of abuse of this analgesic have been reported, ranging from ingestion to inhalation to application of multiple patches to the skin. We report the unique case of a 21-y-old woman who steeped a fentanyl patch in a cup of hot water and then drank the mixture. Coma and hypoventilation resulted. The woman was resuscitated with naloxone i.v. and recovered without sequelae
— id: 69747, year: 2004, vol: 46, page: 30, stat: Journal Article,

Ischemic stroke from "ephedra free" diatary supplement containing synephrine
Bouchard NC; Greller HA; Hoffman RS; Nelson LS
2004 ;42:555-555, Journal of toxicology. Clinical toxicology
— id: 70356, year: 2004, vol: 42, page: 555, stat: Journal Article,

Expired 2-PAM effectively reverses cholinergic crisis in humans
Bouchard NC; Mercurio-Zappala M; Abreu EM; Mendoza P; Nelson LS; Hoffman RS; Cabral-Baez JM
2004 ;42:742-742, Journal of toxicology. Clinical toxicology
— id: 70364, year: 2004, vol: 42, page: 742, stat: Journal Article,

Jewelry confusion : the importance of a site visits following toxin-induced injury in the workplace
Bouchard NC; Schmidt Jp; Goldfrank LS; Nelson LS
2004 ;42:809-809, Journal of toxicology. Clinical toxicology
— id: 70363, year: 2004, vol: 42, page: 809, stat: Journal Article,

Metformin clearance is poor with continuous veno-venous hemodiafiltration (CVVHDF)
Bouchard NC; Weisstuch JM; Hoffman RS; Nelson LS; Howland MA
2004 ;42:739-739, Journal of toxicology. Clinical toxicology
— id: 70365, year: 2004, vol: 42, page: 739, stat: Journal Article,

Cocaine induced myocardial ischemia treated with intravenous phentolamine
Chan GM; Hoffman RS; Nelson LS
2004 ;42:542-542, Journal of toxicology. Clinical toxicology
— id: 70355, year: 2004, vol: 42, page: 542, stat: Journal Article,

More on blue cohosh and perinatal stroke
Chan, Gar M; Nelson, Lewis S
2004 Nov 18;351(21):2239-2241, New England journal of medicine
— id: 69753, year: 2004, vol: 351, page: 2239, stat: Journal Article,

Get the lead out
Chan, Gar Ming; Hoffman, Robert S; Nelson, Lewis S
2004 Nov;44(5):551-552, Annals of emergency medicine
— id: 63373, year: 2004, vol: 44, page: 551, stat: Journal Article,

Holes in the article on whole bowel irrigation
Chan, Gar Ming; Johnson, Kirsten; Rodriguez, James E; Nelson, Lewis S
2004 Dec;44(6):669-669, Annals of emergency medicine
— id: 65879, year: 2004, vol: 44, page: 669, stat: Journal Article,

Delayed salicylate toxicity despite negative levels five hours post-ingestion
Chu J; Wiener SW; Tus S; Hahn I; Nelson LS; Hoffman RS
2004 ;42:553-553, Journal of toxicology. Clinical toxicology
— id: 70354, year: 2004, vol: 42, page: 553, stat: Journal Article,

Renal infarction associated with rizatriptan
Fulton JA; Nelson LS; Hoffman RS
2004 ;42:554-554, Journal of toxicology. Clinical toxicology
— id: 70353, year: 2004, vol: 42, page: 554, stat: Journal Article,

Fetal myocardial infarction from ephedra: an educational intervention
Greller HA; Flomenbaum M; Nelson LS; Hoffman RS
2004 ;42:528-528, Journal of toxicology. Clinical toxicology
— id: 70352, year: 2004, vol: 42, page: 528, stat: Journal Article,

Intestinal ischemia from an ephedra containing "smoothie"
Greller HA; Flomenbaum M; Nelson LS; Hoffman RS
2004 ;42:486-486, Journal of toxicology. Clinical toxicology
— id: 70351, year: 2004, vol: 42, page: 486, stat: Journal Article,

Chloral hydrate cardiotoxicity treated with amiodarone
Greller HA; Hoffman RS; Nelson LS
2004 ;42:548-548, Journal of toxicology. Clinical toxicology
— id: 70350, year: 2004, vol: 42, page: 548, stat: Journal Article,

Survival after intentional oral ingestion of an ammonium bifluoride containing commercial rust remover
Greller HA; Hoffman RS; Nelson LS
2004 ;42:485-485, Journal of toxicology. Clinical toxicology
— id: 70349, year: 2004, vol: 42, page: 485, stat: Journal Article,

Contrast CT scan fails to detect the last heroin packet
Hahn, In-Hei; Hoffman, Robert S; Nelson, Lewis S
2004 Oct;27(3):279-283, Journal of emergency medicine
We report on the comparative utility of the abdominal computed tomography (CT) scan and contrast-enhanced plain radiography in one case of a 'body packer' who claimed to have passed 50 out of 55 packets before being brought to the Emergency Department by the police for further gastrointestinal decontamination. The presence of retained packets was confirmed by plain radiography. The patient received whole bowel irrigation (WBI) with polyethylene glycol electrolyte solution (PEG-ELS) and passed four more packets. A helical abdominal CT scan with oral contrast was performed to identify any residual packets. A negative CT scan and a reliable patient prompted a subsequent upright abdominal radiograph that showed the last packet in the right lower quadrant. This packet ultimately passed with continued WBI. This case illustrates the failure of CT scan to identify the last packet and suggests that multiple modalities may be necessary to fully confirm a therapeutic endpoint
— id: 69751, year: 2004, vol: 27, page: 279, stat: Journal Article,

EMLA-induced methemoglobinemia and systemic topical anesthetic toxicity
Hahn, In-Hei; Hoffman, Robert S; Nelson, Lewis S
2004 Jan;26(1):85-88, Journal of emergency medicine
This case report illustrates an adult presenting with the simultaneous occurrence of both methemoglobinemia (MetHb) and systemic toxicity from the topical application of local anesthetics while undergoing laser epilation therapy of the legs. The concurrent development of both is considered uncommon in this setting and may have been related to several factors, including her recent previous treatment, increased absorption secondary to abraded skin with the addition of occlusive dressing, and possible alteration of protein binding and drug metabolism due to the use of medications. The clinical manifestations and mechanisms of MetHb and systemic local anesthetic toxicity are discussed
— id: 69748, year: 2004, vol: 26, page: 85, stat: Journal Article,

Extremely elevated relative risk of paraffin lamp oil exposures in Orthodox Jewish children
Hoffman, Robert J; Morgenstern, Solomon; Hoffman, Robert S; Nelson, Lewis S
2004 May;113(4):e377-e379, Pediatrics
BACKGROUND: In observance of the Sabbath and other religious holidays, many Orthodox Jews maintain a burning lamp that uses paraffin lamp oil as fuel. Unintentional pediatric exposure to paraffin lamp oil, a hydrocarbon, is typically by ingestion and carries a risk of aspiration with subsequent pneumonitis. This investigation was prompted by an apparent increase in paraffin lamp oil exposures during the Jewish Sabbath, from sunset Friday until sunset Saturday, noted by the staff of our regional poison control center. OBJECTIVE: In this investigation, we retrospectively reviewed all exposures to paraffin lamp oil occurring in our large city in children <18 years old reported to our regional poison control center between January 1, 2000, and February 1, 2003. Reports were investigated to ascertain the frequency of occurrence of paraffin lamp oil exposures on the Jewish Sabbath and Jewish religious holidays. Caregivers of involved children were surveyed by telephone to determine the exposed child's religion and circumstances of exposure. RESULTS: During these 25 months, 45 cases met inclusion criteria, and all were ingestions. Orthodox Jews accounted for 32 cases (71%), 4 cases (9%) occurred in children who were not Orthodox Jews, and demographic data were unavailable in 9 cases (20%). Twenty-four cases (53%) occurred within 10 hours before or during the Jewish Sabbath or Jewish religious holidays. The relative risk of Orthodox Jewish children to ingest paraffin lamp oil, calculated by using census data, is 374 times that of other children. CONCLUSIONS: Public health authorities and caregivers of Orthodox Jewish children should be cognizant of this phenomenon. Educational efforts directed toward both Orthodox Jews and the general public aimed at preventing paraffin lamp oil exposures are warranted
— id: 46219, year: 2004, vol: 113, page: e377, stat: Journal Article,

Acetominophen poisoning
Hung O; Nelson LS
Emergency medicine : a comprehensive study guide New York : McGraw-Hill, 2004,
— id: 4135, year: 2004, vol: , page: ?, stat: Chapter,

Metals
Long H; Nelson LS
Emergency medicine : a comprehensive study guide New York : McGraw-Hill, 2004,
— id: 4139, year: 2004, vol: , page: ?, stat: Chapter,

A rapid qualitative test for suspected ethyelen glycol poisoning
Long H; Nelson LS; Hoffman RS
2004 ;11:530-530, Academic emergency medicine
— id: 70060, year: 2004, vol: 11, page: 530, stat: Journal Article,

Medicinal use of cocaine: a shifting paradigm over 25 years
Long, Heather; Greller, Howard; Mercurio-Zappala, Maria; Nelson, Lewis S; Hoffman, Robert S
2004 Sep;114(9):1625-1629, Laryngoscope
OBJECTIVES/HYPOTHESIS: Human cocaine research is predicated on data from the clinical practice of otolaryngology that are more than 25 years old and predate both the cocaine epidemic and the first reported association between cocaine use and myocardial infarction. The authors' objective was to reassess the epidemiology and toxicity of medicinal cocaine use among otolaryngologists and to compare current trends in usage and safety data with previously reported data. STUDY DESIGN: An anonymous closed-question survey replicating the methodology of a previous study was used. METHODS: The survey was mailed to active members of the American Academy of Otolaryngology-Head and Neck Surgery. The survey used a closed-question format asking about the use of cocaine, safety measures taken, and adverse outcomes and included information about practice type and location. Results were compared with previously published data using a chi test with P < .05 considered significant. RESULTS: In all, 7815 surveys were mailed. Four thousand seventeen otolaryngologists returned the survey, representing a 54% response rate. Of the respondents, only 50% had used cocaine in their practice during the previous year. Physicians who had been in practice for less than 10 years were less likely to have used cocaine than those who had been in practice for more than 10 years (78% vs. 93% [P < .001]). Compared with the data reported in 1977, fewer physicians reported ever using cocaine in their practice (88% vs. 92% [P < .001]), fewer physicians had used cocaine in their practice at any time in the previous 10 years (68% vs. 92% [P < .001]), and a greater number of adverse reactions were reported by current respondents (26% vs. 22% [P < .001]). Tachycardia and hypertension were the most commonly reported adverse effects. Other important adverse events included 14 deaths, survivable cardiac arrest, ventricular tachycardia, and seizures. CONCLUSION: The clinical use of cocaine in otolaryngology has decreased significantly in the past 25 years as a result of discontinuation of use by physicians who had previously used cocaine and an increasing number of otolaryngologists who have never used it. This decline may reflect a better understanding of its potential toxicities, problems associated with storing and dispensing of a tightly controlled substance, increased availability of safer alternative medications, or a combination of these
— id: 65882, year: 2004, vol: 114, page: 1625, stat: Journal Article,

Patterns of heroin overdose-induced pulmonary edema
Mabry, Bob; Greller, Howard A; Nelson, Lewis S
2004 Jul;22(4):316-316, American journal of emergency medicine
— id: 45231, year: 2004, vol: 22, page: 316, stat: Journal Article,

Out of hospital naloxone : appopriate dose and route
Nelson LS
2004 ;42:404-404, Journal of toxicology. Clinical toxicology
— id: 70347, year: 2004, vol: 42, page: 404, stat: Journal Article,

Reporting hazardous products leads to changees in packaging
Nelson LS; Tarabar AF; Wiener SW; Marraffa JM; Stork CM; Hoffman RS
2004 ;42:532-532, Journal of toxicology. Clinical toxicology
— id: 70348, year: 2004, vol: 42, page: 532, stat: Journal Article,

Toxic hemoglobinopathies
Rees S; Nelson LS
Emergency medicine : a comprehensive study guide New York : McGraw-Hill, 2004,
— id: 4138, year: 2004, vol: , page: ?, stat: Chapter,

Hypoglycemic agents
Rella J; Nelson LS
Emergency medicine : a comprehensive study guide New York : McGraw-Hill, 2004,
— id: 4136, year: 2004, vol: , page: ?, stat: Chapter,

Iron poisoning
Rella J; Nelson LS
Emergency medicine : a comprehensive study guide New York : McGraw-Hill, 2004,
— id: 4137, year: 2004, vol: , page: ?, stat: Chapter,

Preparing for chemical terrorism: stability of injectable atropine sulfate
Schier, Joshua G; Ravikumar, Padinjarekuttu R; Nelson, Lewis S; Heller, Michael B; Howland, Mary Ann; Hoffman, Robert S
2004 Apr;11(4):329-334, Academic emergency medicine
OBJECTIVE: A massive nerve agent attack may rapidly deplete in-date supplies of atropine. The authors considered using atropine beyond its labeled shelf life. The objective was to determine the stability of premixed injectable atropine sulfate samples with different expiration dates. METHODS: This was an in-vitro study using gas chromatography and mass spectrometry (GC/MS). Four atropine solutions (labeled concentration of 400 microg/mL) ranging from in date to 12 years beyond expiration (exp) and an additional sample of atropine sulfate (labeled concentration of 2,000 microg/mL) obtained from a World War II era autoinjector were assayed for atropine stability. Standards of atropine sulfate and tropine were prepared and quantified by GC/MS. Study samples were prepared by adding a buffer solution to free the base, extracting with an isopropanol/methylene chloride mixture and followed by evaporating the organic layer to dryness. Pentafluoropropionic anhydride and pentafluoropropanol were then added as derivatization reagents. Study samples were heated, the derivitization reagents were evaporated, and the remaining compound was reconstituted in ethyl acetate for injection into the GC/MS. RESULTS: All solutions were clear and colorless. Atropine concentrations were as follows: in date, 252 microg/mL; 2001 exp, 290 microg/mL; 1999 exp, 314 microg/mL; 1990 exp, 398 microg/mL; and WW II specimen, 1,475 microg/mL. Tropine was found in concentrations of <10 microg/mL in all study samples. CONCLUSIONS: Significant amounts of atropine were found in all study samples. All samples remained clear and colorless, and no substantial amount of tropine was found in any study sample. Further testing is needed to determine clinical effect
— id: 69749, year: 2004, vol: 11, page: 329, stat: Journal Article,

Is regional ethnicity related to poison center utilization?
Schwartz L; Mercurio-Zappala M; Howland MA; Nelson LS; Hoffman RS
2004 ;42:778-778, Journal of toxicology. Clinical toxicology
— id: 70362, year: 2004, vol: 42, page: 778, stat: Journal Article,

Using GIS software for planning poison education programs
Schwartz L; Mercurio-Zappla M; Howland MA; Nelson LS; Resnick S; Hoffman RS
2004 ;42:778-778, Journal of toxicology. Clinical toxicology
— id: 70361, year: 2004, vol: 42, page: 778, stat: Journal Article,

Cerebrospinal fluid analysis in fatal thallium poisoning: evidence for delayed distribution into the central nervous system
Sharma, Adhi N; Nelson, Lewis S; Hoffman, Robert S
2004 Jul;25(2):156-158, American journal of forensic medicine & pathology
The neurologic manifestations of thallium poisoning include a severely painful ascending peripheral neuropathy, autonomic dysfunction, cranial nerve abnormalities, and a toxic encephalopathy. Although thallium has a short half-life, these neurologic manifestations commonly progress, even as the blood concentration of thallium decreases. This suggests either that thallium persists in neuronal tissues or that it initiates an injury cascade that takes time to fully manifest. As the latter mechanism is consistent with many toxin exposures, the concept of a central nervous system reservoir for thallium is often discounted. A recent case provided a unique opportunity to evaluate this possibility. A 48-year-old man was acutely and chronically thallium poisoned by his common-law wife. During his initial exposures, only gastrointestinal symptoms manifested. Following an acute ingestion, hospitalization was required. Over 3 days, his symptoms rapidly progressed from a severely painful neuropathy to slurred speech, ptosis, confusion, coma, respiratory insufficiency, and death. Because of considerations of alternative diagnoses, 2 lumbar punctures were performed, one on admission and another on the day of his death. Serum thallium concentrations obtained from stored blood samples were paired with spinal fluid concentrations from the same days. On day 1, serum and spinal fluid concentrations were 8700 mu/L and 1200 mu/L, respectively. On day 3, although the serum concentration had fallen to 7200 mu/L, the spinal fluid concentration had increased to 2100 mu/L. This case provides evidence to support the hypothesis that thallium distributes into the central nervous system more slowly than the blood compartment, and this may in part account for the progression of neurologic findings in the setting of decreasing serum concentrations
— id: 46038, year: 2004, vol: 25, page: 156, stat: Journal Article,

Publication of abstracts presented at NACCT
Smollin C; Nelson LS
2004 ;42:775-775, Journal of toxicology. Clinical toxicology
— id: 70360, year: 2004, vol: 42, page: 775, stat: Journal Article,

Infliximab induced critical thrombocytopenia
Tarabar AF; Allori; Hoffman RS; Nelson LS
2004 ;42:491-491, Journal of toxicology. Clinical toxicology
— id: 70346, year: 2004, vol: 42, page: 491, stat: Journal Article,

Phencyclidine (PCP) induced myocardial infarction
Tarabar AF; Jolin S; Trepp R; Nelson LS; Hoffman RS
2004 ;42:513-513, Journal of toxicology. Clinical toxicology
— id: 70345, year: 2004, vol: 42, page: 513, stat: Journal Article,

Antimony toxicity from the use of tartar emetic for the treatment of alcohol abuse
Tarabar, Asim F; Khan, Yasmin; Nelson, Lewis S; Hoffman, Robert S
2004 Dec;46(6):331-333, Veternary & human toxicology
Antimony is a poisonous element with toxic properties that mimic those of arsenic. Numerous reports describe gastrointestinal complications of vomiting, diarrhea and stomatitis associated with antimony exposure. However, antimony toxicity from the use of tartar emetic as a treatment for alcohol abuse has never been described previously. A 19-y-o man with a history of alcohol abuse ingested a 10 mL bottle of 'Soluto Vital' (tartar emetic, 50 mg/mL), produced in Guatemala for treatment of alcohol abuse. He presented 60 min after ingestion with severe vomiting, abdominal cramps, diarrhea, weakness and orthostasis. Initial laboratory evaluations were remarkable for creatinine of 2.5 mg/dL, potassium 6.1 mEq/L, and 60% hematocrit. He was given activated charcoal, iv saline and antiemetics. Over the next 48 h his creatinine normalized to 1.1 mg/dL and the hematocrit returned to 53%; urine had an antimony concentration of 1200 mcg/L (normal = < 10 mcg/L). It is important to recognize that foreign alcohol therapies aversive therapy other than disulfiram may be used, the contents of such a foreign product should be identified
— id: 48045, year: 2004, vol: 46, page: 331, stat: Journal Article,

The gamma-hydroxybutyrate withdrawal syndrome
Tarabar, Asim F; Nelson, Lewis S
2004 ;23(1):45-49, Toxicological reviews
gamma-Hydroxybutyrate (GHB) is endogenous inhibitory transmitter that, when administered in pharmacological doses, has sedative-hypnotic properties. It is used in anaesthesia for the treatment of narcolepsy/catalepsy and in alcohol/opioid detoxification treatment regimens. Based on its purported anabolic effects, GHB use became established among bodybuilders. As the euphorigenic effects of GHB became publicised, attendees at dance clubs and rave parties began to use it alone or in combination with other psychoactive drugs. Following the ban of GHB in 1990, several precursor products (e.g. gamma-butyrolactone, butanediol) became widely used as replacement drugs until their ultimate proscription from lawful use in 2000. GHB and its precursors, like most sedative-hypnotic agents, can induce tolerance and produce dependence. Although many GHB users will experience a mild withdrawal syndrome upon drug discontinuation, those with chronic heavy GHB use can experience severe withdrawal. This syndrome clinically resembles the withdrawal syndrome noted from alcohol and other sedative-hypnotic drugs (e.g. benzodiazepines). Distinct clinical features of GHB withdrawal are its relatively mild and brief autonomic instability with prolonged psychotic symptoms. Patients with fulminant GHB withdrawal require aggressive treatment with cross-tolerant sedative hypnotics, such as benzodiazepines
— id: 69750, year: 2004, vol: 23, page: 45, stat: Journal Article,

Body packing - Reply
Traub, SJ; Hoffman, RS; Nelson, LS
2004 MAR 18 ;350(12):1260-1261, New England journal of medicine
— id: 42468, year: 2004, vol: 350, page: 1260, stat: Journal Article,

The ACMT-ATSDR consultation network: first year's experience
Wax P; Nelson L; Seifert SA; Kirk M; McKay C; Clark R; White S; Cetaruk E; Liebelt E; Martin T; Boyer E; Snook CP; Keyes C; Haynes J; Burkhart K; Kosnett M
2004 ;42:777-777, Journal of toxicology. Clinical toxicology
— id: 70359, year: 2004, vol: 42, page: 777, stat: Journal Article,

"Booty bumping" : a novel route of methamphetamine abuse
Wiener SW; Hexdall A; McStay CM; Nelson LS; Hoffman RS
2004 ;42:553-553, Journal of toxicology. Clinical toxicology
— id: 70344, year: 2004, vol: 42, page: 553, stat: Journal Article,

Incapacitating agents
Wiener SW; Nelson LS
Physician's guide to terrorist attack Totowa NJ : Humana Press, 2004,
— id: 4170, year: 2004, vol: , page: ?, stat: Chapter,

Severe methemoglobinemia due to metoclopramide metabolite
Wiener SW; O'Shaughnessy P; Husk G; Howland MA; Nelson LS; Hoffman RS
2004 ;42:558-558, Journal of toxicology. Clinical toxicology
— id: 70343, year: 2004, vol: 42, page: 558, stat: Journal Article,

Variability in methanol content among solid fuel products
Wiener SW; Ravikumar PR; Cotter B; Nelson LS
2004 ;42:796-796, Journal of toxicology. Clinical toxicology
— id: 70358, year: 2004, vol: 42, page: 796, stat: Journal Article,

Cinnamoylecgonine in the urine of cocaine users
Wiener SW; Ravikumar PR; Hoffman RS; Nelson LS
2004 ;42:797-797, Journal of toxicology. Clinical toxicology
— id: 70357, year: 2004, vol: 42, page: 797, stat: Journal Article,

Nutropin or neupogen? A medication error resulting in leukocytosis
Wiener, Sage W; Liu, Steven; Nelson, Lewis S; Hoffman, Robert S
2004 Apr;38(4):721-721, Annals of pharmacotherapy
— id: 64550, year: 2004, vol: 38, page: 721, stat: Journal Article,

The effect of amiodarone on amitriptyline poisoned mice
Barrueto F Jr; Chuang A; Hoffman RS; Nelson LS
2003 ;41:695-695, Journal of toxicology. Clinical toxicology
— id: 136933, year: 2003, vol: 41, page: 695, stat: Journal Article,

Unintentional pediatric vitamin D intoxication
Barrueto F Jr; Howland MH; Hoffman RS; Nelson LS
2003 ;41:662-662, Journal of toxicology. Clinical toxicology
— id: 70366, year: 2003, vol: 41, page: 662, stat: Journal Article,

Poisoning by an illegally imported Chinese rodenticide containing tetramethylenedsulfotetramine
Barrueto F; Furdyna PM; Hller MB; Lajoie JM; Hoffman RJ; Nelson LS; Hoffman RS
2003 ;41:526-526, Journal of toxicology. Clinical toxicology
— id: 70380, year: 2003, vol: 41, page: 526, stat: Journal Article,

Poisoning by an illegally imported Chinese rodenticide containing tetramethylenedisulfotetramine -- New York City, 2002
Barrueto F; Nelson LS; Hoffman RS; et al
2003 ;52:199-201, MMWR
— id: 69785, year: 2003, vol: 52, page: 199, stat: Journal Article,

Phenazopyridine-induced sulfhemoglobinemia
Barrueto F; Ryon D; Howland MA; Hoffman RS; Nelson LS
2003 ;41:470-470, Journal of toxicology. Clinical toxicology
— id: 70381, year: 2003, vol: 41, page: 470, stat: Journal Article,

Status epilepticus from an illegally imported Chinese rodenticide: "tetramine"
Barrueto, Fermin Jr; Furdyna, Peter M; Hoffman, Robert S; Hoffman, Robert J; Nelson, Lewis S
2003 ;41(7):991-994, Journal of toxicology. Clinical toxicology
INTRODUCTION: The following case report demonstrates the severe consequences of refractory convulsive status epilepticus from an unfamiliar imported toxin, tetramethylenedisulfotetramine (TETS), and the difficulties of identifying the offending agent. CASE REPORT: A previously healthy 15-month-old girl was found by her parents playing with a white rodenticide powder brought from China. Fifteen minutes later, the child developed generalized seizures and was brought to an Emergency Department (ED). Her initial fingerstick blood glucose was 108 mg/dL. In the ED, the child was intubated for status epilepticus. Despite aggressive therapy with lorazepam, phenobarbital, and pyridoxine, she had 4 h of intermittent generalized seizure activity. She was extubated on the third hospital day, but appeared to have absence seizures and cortical blindness. Continuous electroencephalogram monitoring, performed weeks later, revealed severe diffuse cerebral dysfunction with multiple epileptogenic foci. The child remains developmentally delayed and is on valproic acid therapy for seizure control. Translation of the Chinese package labeling did not clarify its contents. Tetramethylenedisulfotetramine was finally confirmed by gas chromatography-mass spectrometry (GC-MS) in this rodenticide product and then quantified against a TETS standard that was synthesized in our laboratory. CONCLUSION: Tetramethylenedisulfotetramine is grouped with other 'cage convulsants,' such as picrotoxin, since they have a similar intercalating cyclical molecular structure and cause seizures through non-competitive gamma-aminobutyric acid (GABA) antagonism. The oral lethal dose 50% (LD50) in humans is estimated to be as low as 100 microg/kg. Our patient has severe diffuse cerebral dysfunction likely secondary to prolonged seizure activity after exposure to TETS
— id: 46059, year: 2003, vol: 41, page: 991, stat: Journal Article,

Cardioactive steroid poisoning from an herbal cleansing preparation
Barrueto, Fermin Jr; Jortani, Saeed A; Valdes, R Jr; Hoffman, Robert S; Nelson, Lewis S
2003 Mar;41(3):396-399, Annals of emergency medicine
We describe a case of unintentional poisoning from a cardioactive steroid and the subsequent analytic investigation. A 36-year-old woman with no past medical history and taking no conventional medications ingested an herbal preparation marketed for 'internal cleansing.' Its ingredients were neither known to the patient nor listed on the accompanying literature. The next morning, nausea, vomiting, and weakness developed. In the emergency department, her blood pressure was 110/60 mm Hg, and her pulse rate was 30 beats/min. Her ECG revealed a junctional rhythm at a rate of 30 beats/min and a digitalis effect on the ST segments. After empiric therapy with 10 vials of digoxin-specific Fab (Digibind), her symptoms resolved, and she reverted to a sinus rhythm at a rate of 68 beats/min. Her serum digoxin concentration measured by means of the fluorescence polarization immunoassay (Abbott TDx) was 1.7 ng/mL. Further serum analysis with the Tina Quant digoxin assay, a more digoxin-specific immunoassay, found a concentration of 0.34 ng/mL, and an enzyme immunoassay for digitoxin revealed a concentration of 20 ng/mL (therapeutic range 10 to 30 ng/mL). Serum analysis by means of high-performance liquid chromatography revealed the presence of active digitoxin metabolites; the parent compound was not present. When the diagnosis of cardioactive steroid poisoning is suspected clinically, laboratory analysis can confirm the presence of cardioactive steroids by using immunoassays of varying specificity. An empiric dose of 10 vials of digoxin-specific Fab might be beneficial in patients poisoned with an unknown cardioactive steroid
— id: 39291, year: 2003, vol: 41, page: 396, stat: Journal Article,

A 17-year-old with weakness
Barrueto, Fermin Jr; Long, Heather; Nelson, Lewis S; Osterhoudt, Kevin C
2003 Jan;3(1):55-59, Pediatric case reviews
— id: 61267, year: 2003, vol: 3, page: 55, stat: Journal Article,

Serum homocystgeine levels do not correlate with severity of alcohol withdrawal
Chan GM; Donnelly JG; Hoffman RS; Nelson LS
2003 ;41:745-745, Journal of toxicology. Clinical toxicology
— id: 70367, year: 2003, vol: 41, page: 745, stat: Journal Article,

Physician-patient miscommunication results in medication error
Greller H; Nelson LS
2003 ;6(1):3-3, Internet journal of medical toxicology
— id: 69779, year: 2003, vol: 6, page: 3, stat: Journal Article,

Intentional cardioactive steroid poisoning from Kyushin, a traditional Japanese medication
Greller HA; Ravikumar PR; Nelson LS; Hoffman RS
2003 ;41:666-666, Journal of toxicology. Clinical toxicology
— id: 70368, year: 2003, vol: 41, page: 666, stat: Journal Article,

High risk of paraffin exposure in orthodox Jewish children
Hoffman JJ; Morganstern SS; Hoffman RS; Nelson LS
2003 ;41:705-705, Journal of toxicology. Clinical toxicology
— id: 70369, year: 2003, vol: 41, page: 705, stat: Journal Article,

A retrospective analysis of cardioactive steroid poisoning
Kirrane BM; Barrueto F Jr; Hoffman RS; Nelson LS
2003 ;41:716-716, Journal of toxicology. Clinical toxicology
— id: 70370, year: 2003, vol: 41, page: 716, stat: Journal Article,

Methanol contamination of Romanian home-distilled alcohol
Levy, P; Hexdall, A; Gordon, P; Boeriu, C; Heller, M; Nelson, L
2003 ;41(1):23-28, Journal of toxicology. Clinical toxicology
— id: 42807, year: 2003, vol: 41, page: 23, stat: Journal Article,

Carbaryhl inhibition of plasma cholinesterase activity
Long H; Kirrane B; Nelson LS; Hoffman RS
2003 ;41:737-737, Journal of toxicology. Clinical toxicology
— id: 70371, year: 2003, vol: 41, page: 737, stat: Journal Article,

Alpha-methyltryptamine revisited due to easy internet access
Long H; Nelson LS
2003 ;41:541-541, Journal of toxicology. Clinical toxicology
— id: 70382, year: 2003, vol: 41, page: 541, stat: Journal Article,

Ketamine medication error resulting in death
Long H; Nelson LS
2003 ;6(1):2-2, Internet journal of medical toxicology
— id: 69778, year: 2003, vol: 6, page: 2, stat: Journal Article,

Medicinal use of cocaine: A shifting paradigm over 25 years
Long, H.; Greller, H.; Mercurio-Zappala, M.; Nelson, L. S.; Hoffman, R. S.
2003 ;41(5):717-717, Journal of toxicology. Clinical toxicology
— id: 107327, year: 2003, vol: 41, page: 717, stat: Journal Article,

A fatal case of spongiform leukoencephalopathy linked to "chasing the dragon"
Long, Heather; Deore, Kimberly; Hoffman, Robert S; Nelson, Lewis S
2003 ;41(6):887-891, Journal of toxicology. Clinical toxicology
BACKGROUND: 'Chasing the dragon' involves placing heroin on aluminum foil, heating it from below with a flame, and inhaling the pyrolysate through a straw. It has rarely been associated with the development of a progressive spongiform leukoencephalopathy. CASE REPORT: A 43-year-old woman presented with 2 weeks of bizarre behavior, forgetfulness, and slowed speech and movements. Serum, cerebrospinal fluid, and head computed tomography (CT) scan were normal. The patient progressed to coma and expired during week 4 of hospital admission. The family confirmed that she 'chased the dragon.' Cause of death at post mortem examination was spongiform leukoencephalopathy. CONCLUSION: The diagnosis of heroin pyrolysate-induced spongiform leukoencephalopathy should be considered in a patient with a history of 'chasing the dragon' and neurobehavioral changes, including confusion, apathy, cerebellar signs, and motor restlessness
— id: 65884, year: 2003, vol: 41, page: 887, stat: Journal Article,

Alpha-methyltryptamine revisited via easy Internet access
Long, Heather; Nelson, Lewis S; Hoffman, Robert S
2003 Jun;45(3):149-149, Veternary & human toxicology
Alpha-methyltryptamine (AMT) is a synthetic hallucinogenic indolealkylamine, that was initially studied as a monoamine oxidase inhibitor and used as an antidepressant. Although a popular hallucinogen in the 1960's, use of this drug is currently uncommon. We report a patient with sympathomimetic features who was found to have ingested AMT
— id: 39212, year: 2003, vol: 45, page: 149, stat: Journal Article,

A call to arms for medical toxicologists: the dose, not the detection, makes the poison
McKay CA; Holland MG; Nelson LS
2003 ;6:1-1, Internet journal of medical toxicology
— id: 69777, year: 2003, vol: 6, page: 1, stat: Journal Article,

Critical review of naloxone as an opoid antidote
Nelson LS
2003 ;41:413-413, Journal of toxicology. Clinical toxicology
— id: 70383, year: 2003, vol: 41, page: 413, stat: Journal Article,

Florists and groundskeepers
Nelson LS
Occupational, industrial, and environmental toxicology Philadelphia : Mosby, 2003,
— id: 4178, year: 2003, vol: , page: ?, stat: Chapter,

Adverse events associated with dietary supplements: an observational study
Palmer, Mary E; Haller, Christine; McKinney, Patrick E; Klein-Schwartz, Wendy; Tschirgi, Anne; Smolinske, Susan C; Woolf, Alan; Sprague, Bruce M; Ko, Richard; Everson, Gary; Nelson, Lewis S; Dodd-Butera, Teresa; Bartlett, W Dana; Landzberg, Brian R
2003 Jan 11;361(9352):101-106, Lancet
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
— id: 69738, year: 2003, vol: 361, page: 101, stat: Journal Article,

Ephedrine-induced cardiac ischemia :exposure confirmed with a serum level
Schier J; Nelson LS
2003 ;41:543-543, Journal of toxicology. Clinical toxicology
— id: 70384, year: 2003, vol: 41, page: 543, stat: Journal Article,

Lead-tainted herbal remedy used for developmental delay
Schier JG; Hoffman RS; Nelson LS
2003 ;41:740-740, Journal of toxicology. Clinical toxicology
— id: 70372, year: 2003, vol: 41, page: 740, stat: Journal Article,

Inappropriate laughter: an isoniazid adverse drug event
Schier JG; Nelson LS; Hoffman RS
2003 ;41:679-679, Journal of toxicology. Clinical toxicology
— id: 70373, year: 2003, vol: 41, page: 679, stat: Journal Article,

Role of continuous arteriovenous hemodialysis (CAVHD) in methanol poisoning
Schier JG; Shapiro WB; Howland MA; Hoffman RS; Nelson LS
2003 ;41:743-743, Journal of toxicology. Clinical toxicology
— id: 70375, year: 2003, vol: 41, page: 743, stat: Journal Article,

Fomepizole is not substantially eliminated by continuous arteriovenous hemodialysis (CAVHD)
Schier JG; Shapiro WB; Howland MA; Nelson LS; Hoffamn RS
2003 ;41:664-664, Journal of toxicology. Clinical toxicology
— id: 70374, year: 2003, vol: 41, page: 664, stat: Journal Article,

Metformin-induced acidosis due to a warfarin adverse drug event
Schier, Joshua G; Hoffman, Robert S; Nelson, Lewis S
2003 Jul-Aug;37(7-8):1145-1145, Annals of pharmacotherapy
— id: 69740, year: 2003, vol: 37, page: 1145, stat: Journal Article,

Fatality from administration of labetalol and crushed extended-release nifedipine
Schier, Joshua G; Howland, Mary Ann; Hoffman, Robert S; Nelson, Lewis S
2003 Oct;37(10):1420-1423, Annals of pharmacotherapy
OBJECTIVE: To report a case in which a crushed extended-release (XL) nifedipine tablet contributed to a patient fatality. CASE SUMMARY: A 38-year-old woman with multiple medical problems presented to the hospital in acute respiratory distress and was diagnosed with acute pulmonary edema and pneumonia. After initial stabilization, her medications were changed to oral hydralazine, labetalol, and nifedipine XL. These medications were crushed and administered through a nasogastric tube. The patient developed worsening bradycardia with hypotension and experienced asystolic cardiac arrest. She was resuscitated; however, the following morning, another dose of labetalol and nifedipine XL was crushed and administered through the nasogastric tube. She again developed worsening bradycardia with hypotension and ultimately died. DISCUSSION: The administration of a crushed nifedipine XL tablet resulted in the patient's severe hypotension. The concurrent administration of labetalol prevented a compensatory heart rate increase. The repeat administration of nifedipine XL in the same manner underscores a fundamental problem in healthcare worker communication and drug delivery system comprehension. Use of the Naranjo probability scale indicated a highly probable relationship between the patient's hypotension and the nifedipine and labetalol therapy. CONCLUSIONS: Simultaneous administration of a beta-blocker and a calcium-channel blocker may produce synergistic effects. The release characteristics of oral controlled-release medications are destroyed when crushed, resulting in the rapid bioavailability of the total drug amount. The importance of education and communication among nurses, physicians, and pharmacists regarding the mechanism of action of controlled-release medications and their administration needs to be emphasized
— id: 69742, year: 2003, vol: 37, page: 1420, stat: Journal Article,

Early exposure to marijuana and risk of later drug use
Schier, Joshua G; Nelson, Lewis S; Hoffman, Robert S
2003 Jul 16;290(3):329-329, JAMA
— id: 69741, year: 2003, vol: 290, page: 329, stat: Journal Article,

Ephedrine-induced cardiac ischemia: exposure confirmed with a serum level
Schier, Joshua G; Traub, Stephen J; Hoffman, Robert S; Nelson, Lewis S
2003 ;41(6):849-853, Journal of toxicology. Clinical toxicology
The temporal association of symptoms consistent with ephedrine toxicity after ingestion of ephedrine-containing dietary supplements is heavily relied upon to confirm exposure. Few reports in the literature attempt to associate toxicity with serum levels of these drugs. We report a case of ephedrine-induced cardiac ischemia confirmed by a plasma level. A 22-year-old woman ingesting an ephedrine- and caffeine-containing product for 2 days presented with multiple symptoms, including palpitations, nausea, tremulousness, abdominal pain, and vomiting. The initial electrocardiogram (ECG) revealed a normal sinus rhythm with 1 mm of ST segment depression in leads V3 and V4, along with inverted T waves in leads V1-V4. Her symptoms and ST segment depression resolved over several hours with medical management. The amplitude of her T wave inversions notably diminished with therapy; however, they did not completely resolve. Troponins at presentation and the following morning were negative, and an echocardiogram showed only trace tricuspid regurgitation. A serum ephedrine level, drawn approximately 6 to 7 hr after ingestion, was 150 ng/mL. She was discharged from the hospital after being instructed to avoid ephedrine-containing products
— id: 69745, year: 2003, vol: 41, page: 849, stat: Journal Article,

Efficacy of Crotalidae polyvalent antivenin for the treatment of hognosed viper (Porthidium nasutum) envenomation
Schier, Joshua G; Wiener, Sage W; Touger, Michael; Nelson, Lewis S; Hoffman, Robert S
2003 Mar;41(3):391-395, Annals of emergency medicine
Envenomation from pit vipers native to North America can be treated successfully with either of the 2 commercially available antivenoms licensed in the United States. However, envenomations from imported snakes held in zoos or private collections often pose unique challenges to management because of the lack of specific antivenom and the unclear efficacy of the available licensed products. We report the case of a 37-year-old man who was envenomated on his left hand by his pet hognosed viper (Porthidium nasutum ). He had swelling at the wound site that progressively worsened over 3 to 4 hours. His symptom progression included the structural motor impairment of his fingers and a sensory deficit. Treatment with 8 vials of Antivenin (Crotalidae) polyvalent was associated with a halt of extremity swelling and restoration of neurologic and motor function of his hand. Limited experimental evidence provides support for antigenic cross-reactivity between Antivenin (Crotalidae) polyvalent and P nasutum venom
— id: 64551, year: 2003, vol: 41, page: 391, stat: Journal Article,

Diphenhydramine-induced wide complex dysrhythmia responds to treatment with sodium bicarbonate
Sharma, Adhi N; Hexdall, Aaron H; Chang, Elbert K; Nelson, Lewis S; Hoffman, Robert S
2003 May;21(3):212-215, American journal of emergency medicine
Diphenhydramine, a common ingredient in over-the-counter medications, is often taken in overdose. Toxicity is usually limited to anticholinergic symptoms. However, because diphenhydramine also exhibits type IA sodium channel blockade, cardiac toxicity is also possible. Although it would be expected that, like other type IA toxicities, diphenhydramine-induced cardiotoxicity could be responsive to hypertonic sodium bicarbonate, this finding is largely unappreciated. We describe 3 cases of diphenhydramine-induced cardiac toxicity that were responsive to bicarbonate
— id: 42806, year: 2003, vol: 21, page: 212, stat: Journal Article,

Amiodarone attenuates fluoride-induced hyperkalemia in vitro
Su, Mark; Chu, Jason; Howland, Mary Ann; Nelson, Lewis S; Hoffman, Robert S
2003 Feb;10(2):105-109, Academic emergency medicine
Poisoning by hydrofluoric acid or fluoride salts results in hypocalcemia, hypomagnesemia, and hyperkalemia with subsequent cardiac dysrhythmias. In previous studies, quinidine attenuated fluoride-induced hyperkalemia in vitro, and enhanced survival in animals. Like quinidine, amiodarone is a potassium channel blocker, although amiodarone is more familiar to clinicians due to its recent inclusion in advanced cardiac life support (ACLS) protocols. OBJECTIVES: This in-vitro study of human erythrocytes was designed to determine whether amiodarone could attenuate fluoride-induced hyperkalemia. METHODS: Six healthy volunteers each donated 60 mL of blood on three occasions. Each specimen was divided into 12 tubes, incubated at 37 degrees C, and oxygenated with room air. An aqueous sodium fluoride (F(-)) solution was added to tubes 1-9. Incremental amounts of quinidine were added to tubes 1-4 (Q(1)-Q(4)) to attain calculated concentrations of 0.73 microg/mL, 1.45 microg/mL, 2.9 microg/mL, and 5.8 microg/mL, respectively. Incremental amounts of amiodarone were added to tubes 5-8 (A(1)-A(4)) to attain calculated concentrations of 0.38 microg/mL, 0.75 microg/mL, 1.5 microg/mL, and 3.0 microg/mL, respectively. Tubes 9-12 were controls for each of F(-), amiodarone, quinidine alone, and no additive, respectively. Extracellular potassium concentration ([K(+)]) was followed, and an objective endpoint was defined as the rise in potassium concentration at 6 hours. RESULTS: Fluoride produced a significant change in [K(+)] by 6 hours in all samples. Quinidine produced a J-shaped curve in its ability to attenuate the rise in [K(+)], with only one concentration, Q(3), demonstrating significance versus tube 9 (control). Amiodarone also demonstrated a J-shaped dose-response effect, with statistical significance at A(1), A(2), and A(3) versus tube 9 (control). There was no significant difference among the effective concentrations (Q(3), A(1), A(2), and A(3)) of both drugs. CONCLUSIONS: In this in-vitro model using human blood, amiodarone and quinidine both attenuated F(-)-induced hyperkalemia. Further study is indicated to determine whether amiodarone enhances survival in F(-)-poisoned animals
— id: 39311, year: 2003, vol: 10, page: 105, stat: Journal Article,

Antimony toxicity from the use of tartar emetic for the treatment of alcohol abuse
Tarabar A; Nelson LS
2003 ;41:469-469, Journal of toxicology. Clinical toxicology
— id: 70385, year: 2003, vol: 41, page: 469, stat: Journal Article,

Ephedrine-induced cardiomyopathy
Tarabar A; Nelson LS
2003 ;41:544-544, Journal of toxicology. Clinical toxicology
— id: 70386, year: 2003, vol: 41, page: 544, stat: Journal Article,

Citalopram overdose : late presentation of torades de pointes (TDP) with cardiac arrest
Tarabar AF; Hoffman RS; Nelson LS
2003 ;41:676-676, Journal of toxicology. Clinical toxicology
— id: 70376, year: 2003, vol: 41, page: 676, stat: Journal Article,

The resurgence and abuse of heroin by children in the United States
Tarabar, Asim F; Nelson, Lewis S
2003 Apr;15(2):210-215, Current opinion in pediatrics
Heroin, one of the most addictive and 'hardest' drugs of abuse, carries significant morbidity and mortality. Although its use is usually associated with the adult population in the United States, the last decade has witnessed a decrease in the median age of heroin users. An increase in the availability of inexpensive and pure heroin that could be snorted rather than injected made the drug accessible to adolescents and reduced the fear associated with the transmission of the human immunodeficiency virus (HIV). Because of the atypical demographics and the alternative drug use patterns, this young population of heroin users is not easily identified by parents or by healthcare providers. Lack of social support or access to healthcare prevents young heroin users from participation in detoxification programs, suggesting that changes may be needed in our healthcare and social systems to properly target and provide care to the youngest heroin abusers
— id: 39270, year: 2003, vol: 15, page: 210, stat: Journal Article,

Body packing--the internal concealment of illicit drugs
Traub, Stephen J; Hoffman, Robert S; Nelson, Lewis S
2003 ;349(26):2519-2526, New England journal of medicine
— id: 46074, year: 2003, vol: 349, page: 2519, stat: Journal Article,

False-positive abdominal radiography in a body packer resulting from intraabdominal calcifications
Traub, Stephen J; Hoffman, Robert S; Nelson, Lewis S
2003 Nov;21(7):607-608, American journal of emergency medicine
— id: 69744, year: 2003, vol: 21, page: 607, stat: Journal Article,

Acute topiramate toxicity
Traub, Stephen J; Howland, Mary Ann; Hoffman, Robert S; Nelson, Lewis S
2003 ;41(7):987-990, Journal of toxicology. Clinical toxicology
Topiramate (Topamax) is an anti-epileptic medication for which acute toxicity is infrequently reported. A 5-yr-old girl, not previously taking topiramate, developed neurological symptoms after acute ingestion of this medication. She was intermittently agitated, complained of 'not being able to feel anything,' demonstrated arching movements of the back, and perseverated upon questioning. Computerized tomography of the head and electroencephalography were both normal, and urine toxicology testing for drugs of abuse was negative. A serum topiramate level was 10.5 mcg/mL, confirming the ingestion. The patient was observed for 24 h, over which time her symptoms completely resolved
— id: 69746, year: 2003, vol: 41, page: 987, stat: Journal Article,

Pediatric "body packing"
Traub, Stephen J; Kohn, Gary L; Hoffman, Robert S; Nelson, Lewis S
2003 Feb;157(2):174-177, Archives of pediatrics & adolescent medicine
BACKGROUND: Recent events in the United States have led to increased security at national borders, resulting in an unexpected increase in drug seizures. In response, drug smugglers may begin using children as couriers, including using them as 'body packers.' OBJECTIVE: To look at the occurrence of body packing, the concealing of contraband within the human body, which is well documented in adults, in the pediatric literature. PATIENT REPORTS: Two cases of pediatric body packing, in boys aged 16 years and 12 years. Patient 1, a 16-year-old boy, presented with findings consistent with opioid intoxication after arriving in the United States on a transcontinental flight. His mental status improved after he received naloxone hydrochloride, and he subsequently confessed to body packing heroin. He was treated with a naloxone infusion and aggressive gastrointestinal decontamination. He ultimately passed 53 packets of heroin, one of which had ruptured. He recovered uneventfully. Patient 2, a 12-year-old boy, presented to the emergency department with rectal bleeding. He had recently arrived in the United States from Europe, and he confessed to body packing heroin. He was treated with whole-bowel irrigation and activated charcoal, and he subsequently passed 84 packets. He also recovered uneventfully. CONCLUSIONS: We report the first 2 cases of body packing in the pediatric literature and review the diagnosis and management of this clinical entity. Pediatricians should be aware that body packing, regrettably, is not confined to the adult population
— id: 69739, year: 2003, vol: 157, page: 174, stat: Journal Article,

Use of pharmaceutical promotility agents in the treatment of body packers
Traub, Stephen J; Su, Mark; Hoffman, Robert S; Nelson, Lewis S
2003 Oct;21(6):511-512, American journal of emergency medicine
— id: 69743, year: 2003, vol: 21, page: 511, stat: Journal Article,

A nation-wide consultative network between medical toxicology fellowship programs and ATSDR regional offices
Wax P; Nelson L; Kosnett M
2003 ;41:707-707, Journal of toxicology. Clinical toxicology
— id: 70377, year: 2003, vol: 41, page: 707, stat: Journal Article,

Ethanol elimination following massive ingestion in a child
Wiener S; Nelson LS
2003 ;41:476-476, Journal of toxicology. Clinical toxicology
— id: 70387, year: 2003, vol: 41, page: 476, stat: Journal Article,

Smoking : a novel route of olanzapine abuse
Wiener SW; Hoffman RS; Nelson LS
2003 ;41:742-742, Journal of toxicology. Clinical toxicology
— id: 70378, year: 2003, vol: 41, page: 742, stat: Journal Article,

Withdrawal symptoms after valerian cessation
Wiener SW; Hoffman RS; Nelson LS
2003 ;41:721-721, Journal of toxicology. Clinical toxicology
— id: 70379, year: 2003, vol: 41, page: 721, stat: Journal Article,

A possible molecular mechanism of action for the potential tumor suppressor gene INT6 provided by studies in fission yeast
Yen, HCS; Ren, G; Nelson, L; Sha, Z; Sap, J; Chang, E
2003 OCT 28 ;82(17):S172-S172, Breast cancer research & treatment
— id: 42532, year: 2003, vol: 82, page: S172, stat: Journal Article,

Gabapentin withdrawal presenting as status epilepticus
Barrueto F; Green J; Howland MA; Nelson LS
2002 ;40:326-326, Journal of toxicology. Clinical toxicology
— id: 70397, year: 2002, vol: 40, page: 326, stat: Journal Article,

Digitoxin poisoning from an herbal cleansing preparation
Barrueto F; Jortani SA; Valdes R; Hoffman RS; Nelson LS
2002 ;40:605-605, Journal of toxicology. Clinical toxicology
— id: 70388, year: 2002, vol: 40, page: 605, stat: Journal Article,

Levetiracetam poisoning induces coma: confirmed by laboratory analysis
Barrueto F; Williams K; Howland MA; Hoffman RS; Nelson LS
2002 ;40:605-605, Journal of toxicology. Clinical toxicology
— id: 70389, year: 2002, vol: 40, page: 605, stat: Journal Article,

A case of levetiracetam (Keppra) poisoning with clinical and toxicokinetic data
Barrueto, F Jr; Williams, K; Howland, M A; Hoffman, R S; Nelson, L S
2002 ;40(7):881-884, Journal of toxicology. Clinical toxicology
BACKGROUND: Levetiracetam (Keppra) is a new anticonvulsant used to treat partial complex seizures that is also being investigated for its mood-stabilizing properties. Although its precise mechanism of action is unknown, levetiracetam does not appear to directly interact with the GABA system. We report the first intentional overdose with levetiracetam including clinical effects and serial serum concentrations. CASE REPORT: A 38-year-old woman reportedly ingested 60 (500 mg) tablets of levetiracetam that she used as a mood-stabilizing medication for bipolar disorder. She had no other prescription medications available and no other medical history. She vomited 4 hours after ingestion and presented to the ED 2 hours later. In the ED, the patient was obtunded and was intubated secondary to respiratory depression. Her only other significant clinical finding was diminished deep tendon reflexes. Serum ethanol, lithium, carbamazepine, phenytoin, and valproic acid levels were all negative as was a subsequent urine screen for drugs of abuse. Her levetiracetam serum concentration was 400 microg/mL at 6 hours, 72 microg/mL at 18 hours, and 60 microg/mL at 20.5 hours (therapeutic serum concentration is 10-37 microg/mL). The elimination half-life was calculated to be 5.14 hours. She was extubated the next hospital day and recovered without sequelae. CONCLUSION: In overdose, levetiracetam is sedating and causes respiratory depression, however, recovery is rapid with supportive care. This is the first reported case of levetiracetam overdose; serial serum concentrations suggest first-order elimination even at concentrations 10-40 fold higher than therapeutic
— id: 39342, year: 2002, vol: 40, page: 881, stat: Journal Article,

Gabapentin withdrawal presenting as status epilepticus
Barrueto, Fermin Jr; Green, Jonah; Howland, Mary Ann; Hoffman, Robert S; Nelson, Lewis S
2002 ;40(7):925-928, Journal of toxicology. Clinical toxicology
A 34-year-old male with lumbar disc disease and surgery was placed on gabapentin daily for chronic back pain. He remained on a steady dose of 8000 mg/day for 9 months, almost doubled what is considered therapeutic. He ran out of medication, was unable to refill his prescription for 2 days and presented to the emergency department in status epilepticus. There was no previous history of seizure disorder and he was on no other medications. A medical evaluation for an alternative etiology of his seizures was negative. Although gabapentin withdrawal has been previously reported and usually consists of anxiety, diaphoresis, and palpitations, this is the first reported patient with generalized seizures and status epilepticus secondary to gabapentin withdrawal
— id: 39341, year: 2002, vol: 40, page: 925, stat: Journal Article,

Ethylene glycol causing mesenteric ischemia?
Barrueto, Fermin Jr; Nelson, Lewis S
2002 May;20(3):263-263, American journal of emergency medicine
— id: 69726, year: 2002, vol: 20, page: 263, stat: Journal Article,

Valproic acid is a structural analog of GABA that enters various metabolic pathways and has many clinical effects
Barrueto, Fermin Jr; Su, Mark; Nelson, Lewis S
2002 Oct;23(3):303-304, Journal of emergency medicine
— id: 69732, year: 2002, vol: 23, page: 303, stat: Journal Article,

Toxicity of rectally applied formalin/mercuric chloride solution
Hahn IH; Hoffman RJ; Hoffman RS; Nelson LS
2002 ;40:389-389, Journal of toxicology. Clinical toxicology
— id: 70398, year: 2002, vol: 40, page: 389, stat: Journal Article,

Complications of ultrarapid opioid detoxification with subcutaneous naltrexone pellets
Hamilton, Richard J; Olmedo, Ruben E; Shah, Sachin; Hung, Oliver L; Howland, Mary Ann; Perrone, Jeanmarie; Nelson, Lewis S; Lewin, Neal L; Hoffman, Robert S
2002 Jan;9(1):63-68, Academic emergency medicine
Rapid and ultrarapid opioid detoxification (ROD and UROD) centers promise quick, painless, same-day detoxification treatment for patients with opioid addiction. The goal of ROD and UROD is to provide a rapid transition from opioid dependency to oral naltrexone therapy. The patient is given general anesthesia and high-dose opioid antagonists. This induces a severe withdrawal but spares the patient the experience. In theory, the process is complete within four to five hours. The patient awakens without opioid dependency and is started on oral naltrexone. Any subsequent, persistent withdrawal symptoms are treated symptomatically. A novel, unapproved approach is to compound a pellet of naltrexone and implant it in the subcutaneous tissue. In theory, this should result in continuous therapeutic levels for this drug, and avoid issues with noncompliance. CASE SERIES: This article reports six cases of complications from the same detoxification center that performed UROD with naltrexone pellet implantation, including pulmonary edema, prolonged withdrawal, drug toxicity, withdrawal from cross-addiction to alcohol and benzodiazepines, variceal rupture, aspiration pneumonia, and death. CONCLUSIONS: The risks of this procedure are great and further studies should assess its safety and the novel use of naltrexone
— id: 69722, year: 2002, vol: 9, page: 63, stat: Journal Article,

Is medical toxicology becoming a pastime? Graduates of Medical Toxicology Fellowship Programs Will Not Primarily Practice The Specialty
Hoffman RJ; Kwok MY; Nelson LS
2002 ;5(1):4-4, Internet journal of medical toxicology
— id: 69780, year: 2002, vol: 5, page: 4, stat: Journal Article,

Use of ferric chloride to identify salicylate-containing poisons
Hoffman Rj; Nelson LS; Hoffman RS
2002 ;40:391-392, Journal of toxicology. Clinical toxicology
— id: 70399, year: 2002, vol: 40, page: 391, stat: Journal Article,

Effect of ketamine administration on phencyclidine immunoassys (PCPIa)
Hoffman RJ; Saddock V; Nelson LS; Hoffman RS
2002 ;19:A91-A91, Emergency Medicine Journal
— id: 70070, year: 2002, vol: 19, page: A91, stat: Journal Article,

Review of chemiluminscent glow stick exposures
Hoffman RJ; Winnik G; Nelson LS; Hoffman RS
2002 ;19:A91-A91, Emergency Medicine Journal
— id: 70071, year: 2002, vol: 19, page: A91, stat: Journal Article,

Pediatric and young adult exposure to chemiluminescent glow sticks
Hoffman, Robert J; Nelson, Lewis S; Hoffman, Robert S
2002 Sep;156(9):901-904, Archives of pediatrics & adolescent medicine
BACKGROUND: Although chemiluminescent plastic rods, commonly called 'glow sticks' or 'light sticks,' are typically considered to be minimally toxic or nontoxic, published data about exposure to these products are scarce. OBJECTIVES: To test our hypothesis that exposure to chemiluminescent products is unlikely to result in significant morbidity or mortality and to describe factors associated with exposure by reviewing reports to our urban poison control center of human exposure to chemiluminescent products. METHODS: Pediatric and young adult exposure to chemiluminescent products reported between January 1, 2000, and April 1, 2001, to our poison control center were evaluated with regard to demographic group, type of product involved, circumstances of exposure, symptoms, and management. RESULTS: Reported routes of exposure (n = 118) included ingestion (n = 108), ocular (n = 9), and dermal exposure (n = 1). Only patients exposed to chemiluminescent fluid from a leaking container reported symptoms (n = 27). Symptoms were limited to transient irritation of the exposure site, and no systemic toxicity occurred. All adults (n = 4) inadvertently ruptured or swallowed intact light sticks while at a dance club or dance party. Most exposure and all adult exposure occurred on holidays or weekends. CONCLUSIONS: Most incidences of exposure to chemiluminescent products involve asymptomatic ingestion of fluid that leaks from glow sticks or ingestion of an intact glow stick. Symptoms occur after exposure to chemiluminescent fluid and consist of transient irritation at the site of exposure. The clustering of reported exposure on weekends and in dance clubs and parties coupled with a lack of occupational or workplace exposure suggest that recreational use is a major contributory factor. Exposure to chemiluminescent products infrequently resulted in symptoms and the symptoms reported were minor. Exposure to chemiluminescent products as described is unlikely to cause significant morbidity or mortality
— id: 69730, year: 2002, vol: 156, page: 901, stat: Journal Article,

Use of ferric chloride to identify salicylate-containing poisons
Hoffman, Robert J; Nelson, Lewis S; Hoffman, Robert S
2002 ;40(5):547-549, Journal of toxicology. Clinical toxicology
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
— id: 69731, year: 2002, vol: 40, page: 547, stat: Journal Article,

Erythropoietin overdose treated with emergent erythropheresis
Hoffman, Robert S; Cobrin, Gina; Nelson, Lewis S; Howland, Mary Ann
2002 Jun;44(3):157-159, Veternary & human toxicology
Erythropoietin (EPO) is commonly used to treat anemias secondary to renal failure, malignancy, and AIDS. Although therapeutic complications are well described, overdose is rare. A 42-y-o man with AIDS confused his instructions for self-administration of interferon and EPO and began injecting himself daily with 10,000 units of EPO for several weeks. He presented with confusion, pain in his abdomen and feet, and a hemoglobin of 23.2 g/dLwith a hematocrit of 77.1%. The patient was treated with iv fluids, phlebotomy and 2 sessions of erythropheresis which removed 898 mL and 640 mL of red blood cells, respectively; his hemoglobin remained between 12-14 g/dL and symptoms resolved. His only sequelae involved skin loss over his toes, which did not require grafting. This rare case of EPO overdose highlights the complications of essential erythrocytosis, with central nervous system, peripheral, and presumed mesenteric ischemia
— id: 69727, year: 2002, vol: 44, page: 157, stat: Journal Article,

Methemoglobinemia following unintentional ingestion of sodium nitrite -- New York, 2002
Huang A; Terry W; Guido F; Nelson LS; et al
2002 ;51:639-642, MMWR
— id: 69789, year: 2002, vol: 51, page: 639, stat: Journal Article,

Antidysrhythmic agents
Lewin N; Nelson LS
Goldfrank's toxicologic emergencies New York : McGraw-Hill, 2002,
— id: 4159, year: 2002, vol: , page: ?, stat: Chapter,

Antidysrhythmic agents
Lewin NA; Nelson L
Goldfrank's toxicologic emergencies New York : McGraw-Hill Medical, 2002,
— id: 4535, year: 2002, vol: , page: 787, stat: Chapter,

Heroin-induced leukoencephalopathy due to chasing the dragon
Long H; Deore K; Hoffman RS; Nelson LS
2002 ;40:654-654, Journal of toxicology. Clinical toxicology
— id: 70390, year: 2002, vol: 40, page: 654, stat: Journal Article,

Smallpox : diagnosis, treatment, and prevention
Long H; Nelson LS
2002 ;48:58-63, Resident & staff physician
— id: 69813, year: 2002, vol: 48, page: 58, stat: Journal Article,

Ketamine medication error resulting in death
Long H; Nelson LS; Hoffman RS
2002 ;40:614-614, Journal of toxicology. Clinical toxicology
— id: 70391, year: 2002, vol: 40, page: 614, stat: Journal Article,

Potential utility of a rapid ethylene glycol (EG) bedside test
Long H; Nelson LS; Hoffman RS
2002 ;40:649-649, Journal of toxicology. Clinical toxicology
— id: 70392, year: 2002, vol: 40, page: 649, stat: Journal Article,

Characteristics of patients presenting to the ED following methadone overdose
Nath P; Kwon N; Nelson LS
2002 ;9:?-?, Academic emergency medicine
— id: 70061, year: 2002, vol: 9, page: ?, stat: Journal Article,

Copper poisoning
Nelson LS
Goldfrank's toxicologic emergencies New York : McGraw-Hill, 2002,
— id: 4157, year: 2002, vol: , page: ?, stat: Chapter,

Keynote lecture : Toxins affecting the neuromuscular junction
Nelson LS
2002 ;40:258-259, Journal of toxicology. Clinical toxicology
— id: 70400, year: 2002, vol: 40, page: 258, stat: Journal Article,

Opioids
Nelson LS
Goldfrank's toxicologic emergencies New York : McGraw-Hill, 2002,
— id: 4155, year: 2002, vol: , page: ?, stat: Chapter,

Pulmonary irritants
Nelson LS
Goldfrank's toxicologic emergencies New York : McGraw-Hill, 2002,
— id: 4156, year: 2002, vol: , page: ?, stat: Chapter,

Inhaled toxins
Nelson LS; Hoffman RS
Rosen's emergency medicine : concepts and clinical practice St. Louis : Mosby, 2002,
— id: 4169, year: 2002, vol: , page: ?, stat: Chapter,

Chemical principles
Nelson LS; Traub S
Goldfrank's toxicologic emergencies New York : McGraw-Hill, 2002,
— id: 4158, year: 2002, vol: , page: ?, stat: Chapter,

No cause for ecstasy
Nelson, L
2002 OCT ;34(10):49-50, Emergency medicine
— id: 55279, year: 2002, vol: 34, page: 49, stat: Journal Article,

All things fungal ["Toxwise - a guide to clinical toxicology resources available on the Internet"]
Nelson, Lewis
2002 ;40:207-208, Journal of toxicology. Clinical toxicology
— id: 69790, year: 2002, vol: 40, page: 207, stat: Journal Article,

Opioids : the good, the bad and the ugly
Nelson, Lewis S
[Danville PA] : GMC, 2002,
— id: 1201, year: 2002, vol: , page: , stat: ,

Herbicide poisoning ["The Toxic Emergency"]
Nelson, Lewis S
2002 ;34:48-49 May, Emergency medicine
— id: 69803, year: 2002, vol: 34, page: 48, stat: Journal Article,

Toxicologic myocardial sensitization
Nelson, Lewis S
2002 ;40(7):867-879, Journal of toxicology. Clinical toxicology
Drug-induced polymorphic ventricular tachycardia (torsades de pointes) may lead to syncope or sudden cardiac death. One mechanism by which drugs and toxins may predispose to the development of this malignant dysrhythmia is through their ability to produce myocardial sensitization. The concept of myocardial sensitization actually represents a series of events involving altered cellular repolarization produced by blockade of myocardial potassium channels. Altered potassium ion flow raises the likelihood that an ectopic beat will occur via an early afterdepolarization and simultaneously alters the myocardial tissue to make it favorable for reentrant dysrhythmias, such as torsades de pointes, to propagate. Alternatively, calcium overload of the myocyte produces ectopy by causing delayed afterdepolarizations, which if the substrate for reentry is present, will result in ventricular tachycardia. This paper discusses the mechanisms underlying the production of both the altered myocardial substrate and the afterdepolarizations
— id: 69737, year: 2002, vol: 40, page: 867, stat: Journal Article,

Cutaneous anthrax infection
Nelson, Lewis S; Hanner, Robert; Hoffman, Robert S
2002 Mar 21;346(12):945-946, New England journal of medicine
— id: 69725, year: 2002, vol: 346, page: 945, stat: Journal Article,

Body weight and response to vitamin K administration
Reinfried, Patrick; Su, Mark; Howland, Mary Ann; Nelson, Lewis
2002 Feb 1;112(2):158-160, American journal of medicine
— id: 112793, year: 2002, vol: 112, page: 158, stat: Journal Article,

Desiccant induced gastrointestinal burns
Schier JG; Hoffman RS; Nelson LS
2002 ;40:627-627, Journal of toxicology. Clinical toxicology
— id: 70393, year: 2002, vol: 40, page: 627, stat: Journal Article,

Preparing for chemical terrorism: Stability of expired atropine
Schier, J. G.; Mehta, R.; Mercurio-Zappala, M.; Nelson, L. S.; Howland, M. A.; Hoffman, R. S.
2002 ;40(5):625-626, Journal of toxicology. Clinical toxicology
— id: 107328, year: 2002, vol: 40, page: 625, stat: Journal Article,

Cocaine and body temperature regulation
Schier, Joshua G; Hoffman, Robert S; Nelson, Lewis S
2002 Nov 19;137(10):855-856, Annals of internal medicine
— id: 69733, year: 2002, vol: 137, page: 855, stat: Journal Article,

Desiccant-induced gastrointestinal burns in a child
Schier, Joshua G; Hoffman, Robert S; Nelson, Lewis S
2002 Dec;44(6):343-344, Veternary & human toxicology
Desiccants are commonly composed of non-toxic chemicals such as silica gel. A 2-y-old male unintentionally ingested the contents of a desiccant packet found in a container of imported Chinese cookies. He presented with vomiting, drooling and inability to drink. A caustic injury to his tongue and phaynx was noted. He improved over the next 12 h and was discharged a day later. The packet was found to contain caustic lime Although patients who ingest desiccant packets generally develop no clinical effects, ingestion of packets containing strong alkali may prove consequential. Providers should be aware of the potential for this toxicity before dismissing desiccant exposures as benign
— id: 69734, year: 2002, vol: 44, page: 343, stat: Journal Article,

Multiple-dose activated charcoal used to treat valproic acid overdose
Su M; Fong J; Howland MA; Nelson LS
2002 ;40:469-469, Journal of toxicology. Clinical toxicology
— id: 70401, year: 2002, vol: 40, page: 469, stat: Journal Article,

Amiodarone (Ami) attenuated fluoride-induced hyperkalemia in human erythrocytes
Su M; Nelson LS; Hoffman RS
2002 ;9:485-485, Academic emergency medicine
— id: 70063, year: 2002, vol: 9, page: 485, stat: Journal Article,

Acute tacrolimus overdose without significant toxicity
Su, Mark; Hoffman, Robert S; Nelson, Lewis S
2002 ;40(2):205-206, Journal of toxicology. Clinical toxicology
— id: 69728, year: 2002, vol: 40, page: 205, stat: Journal Article,

Error in an emergency medicine textbook: isopropyl alcohol toxicity
Su, Mark; Hoffman, Robert S; Nelson, Lewis S
2002 Feb;9(2):175-175, Academic emergency medicine
— id: 69724, year: 2002, vol: 9, page: 175, stat: Journal Article,

Tricyclic antidepresent-induced widening of the QRS complex refractory to hypertonic sodium bicarbonate
Traub SJ; Black J; Hoffman RS; Nelson LS
2002 ;9:?-?, Academic emergency medicine
— id: 70062, year: 2002, vol: 9, page: ?, stat: Journal Article,

Lead toxicity due to use of an ayurvedic compound
Traub SJ; Hoffman RS; Nelson LS
2002 ;40:322-322, Journal of toxicology. Clinical toxicology
— id: 70402, year: 2002, vol: 40, page: 322, stat: Journal Article,

Pediatric body-packing : a 12-year-old "mule"
Traub SJ; Hoffman RS; Nelson LS
2002 ;40:614-614, Journal of toxicology. Clinical toxicology
— id: 70394, year: 2002, vol: 40, page: 614, stat: Journal Article,

Neurological changes after ingestion of topiramate
Traub SJ; Howland MA; Hoffman RS; Nelson LS
2002 ;40:620-620, Journal of toxicology. Clinical toxicology
— id: 70395, year: 2002, vol: 40, page: 620, stat: Journal Article,

The use of promotility agents in the treatment of body packers
Traub SJ; Su M; Hoffman RS; Nelson LS
2002 ;40:619-619, Journal of toxicology. Clinical toxicology
— id: 70396, year: 2002, vol: 40, page: 619, stat: Journal Article,

QT prolongation associated with levo-alpha acetyl methadol
Traub SJ; Wani S; Hoffman RS; Nelson LS
2002 ;40:351-352, Journal of toxicology. Clinical toxicology
— id: 70403, year: 2002, vol: 40, page: 351, stat: Journal Article,

Case report and literature review of chlorine gas toxicity
Traub, Stephen J; Hoffman, Robert S; Nelson, Lewis S
2002 Aug;44(4):235-239, Veternary & human toxicology
Chlorine gas exposure is uncommon in children and when it occurs usually results in mild ocular, oropharyngeal, or respiratory symptoms. Occasionally, however, chlorine gas poisoning may cause severe pulmonay toxicity. We report the case of a 14-y-old boy with a history of asthma who was exposed to chlorine gas as a result of an ill-advised science experiment. His clinical condition deteriorated over the course of several hours, and he required intubation and ventilatory support. During his hospitalization, he developed the acute respiratory distress syndrome. He was treated with positive pressure ventilation, beta-adrenergic agonists, and corticosteroids. After 19 d, he was extubated and subsequently made an excellent recovery. We discuss his case and review the etiology, pathophysiology, clinical presentation, laboratory findings, treatment and possible long-term sequelae of chlorine gas toxicity
— id: 69729, year: 2002, vol: 44, page: 235, stat: Journal Article,

The "ecstasy" hangover: hyponatremia due to 3,4-methylenedioxymethamphetamine
Traub, Stephen J; Hoffman, Robert S; Nelson, Lewis S
2002 Dec;79(4):549-555, Journal of urban health
3,4-Methylenedioxymethamphetamine (MDMA, or 'ecstasy') has gained an undeserved reputation as a 'safe' drug among its users. However, hyperthermia, rhabdomyolysis, hepatotoxicity, disseminated intravascular coagulation, long-term serotonergic neurotoxicity, and death are all associated with MDMA use. Hyponatremia is also reported, and its manifestations are frequently delayed several hours after the drug is ingested. The etiology of this hyponatremia is unclear; both the syndrome of inappropriate antidiuretic hormone release (SIADH) and free-water intoxication are advanced as explanations. We describe a 19-year-old female who presented to the emergency department with altered mental status 1 day after using MDMA. Her initial serum sodium was 121 mmol/L, and computerized tomography (CT) of her head demonstrated cerebral edema. She was treated with hypertonic saline and fluid restriction, and her serum sodium increased to 132 mmol/L over the next 24 hours. She regained consciousness completely within 48 hours of presentation and recovered uneventfully. MDMA toxicity, particularly the pathophysiology and treatment of MDMA-induced hyponatremia, are discussed
— id: 69735, year: 2002, vol: 79, page: 549, stat: Journal Article,

Physostigmine as a treatment for gamma-hydroxybutyrate toxicity: a review
Traub, Stephen J; Nelson, Lewis S; Hoffman, Robert S
2002 ;40(6):781-787, Journal of toxicology. Clinical toxicology
INTRODUCTION: Gamma-hydroxybutyrate is a potent sedative-hypnotic agent and a popular drug of abuse. In the United States, gamma-hydroxybutyrate is a Schedule I controlled substance (sodium oxybate) with orphan drug status for the treatment of narcolepsy within approved clinical studies. Physostigmine is a carbamate inhibitor of acetylcholinesterase that is reported to attenuate the sedative effects of a number of drugs, including gamma-hydroxybutyrate. We reviewed the literature that pertains to the use of physostigmine to treat gamma-hydroxybutyrate-induced sedation. METHODS: A structured literature search was performed to identify articles in which physostigmine and gamma-hydroxybutyrate were mentioned. Keywords were used to identify relevant articles in the Medline database, and the reference sections of articles identified by this method were hand-checked to identify additional articles. Those articles that presented original evidence pertaining to the use of physostigmine to treat gamma-hydroxybutyrate-induced sedation were included in this review; those that did not were rejected. RESULTS: The literature search identified 22 articles, six of which did not pertain to the subject matter. Of the 16 articles which remained, 12 were rejected because they offered opinions without presenting original evidence. Of the four articles that presented original evidence, there were no in vitro studies and no animal studies. There were two small case series in which physostigmine was given to treat acute gamma-hydroxybutyrate toxicity in an emergency department setting, and two larger series in which physostigmine was given to attenuate the sedation induced by gamma-hydroxybutyrate in a more structured anesthesia setting. Although these references report that physostigmine attenuates gamma-hydroxybutyrate-induced sedation, there are methodological flaws and confounding factors that limit the scope of the conclusions that can be drawn from them. CONCLUSIONS: There is currently insufficient scientific evidence to support the routine use of physostigmine in the treatment of gamma-hydroxybutyrate toxicity. Further studies are needed to determine the role, if any, for physostigmine in this setting
— id: 69736, year: 2002, vol: 40, page: 781, stat: Journal Article,

Metformin-associated lactic acidosis vs. mesenteric ischemia
Chu J; Hoffman RS; Nelson LS
2001 ;39:511-511, Journal of toxicology. Clinical toxicology
— id: 70404, year: 2001, vol: 39, page: 511, stat: Journal Article,

Hypotension in an unintentional overdose of tizanidine
Chu J; Nelson LS; Hoffman RS
2001 ;39:283-283, Journal of toxicology. Clinical toxicology
— id: 70419, year: 2001, vol: 39, page: 283, stat: Journal Article,

Apnea in an infant after introcular administration of adult strength ophthalmic solutions for glaucoma
Chu J; Nelson LS; Howland MA; Hoffman RS
2001 ;39:304-304, Journal of toxicology. Clinical toxicology
— id: 70420, year: 2001, vol: 39, page: 304, stat: Journal Article,

Acetaminophen-induced fulminant hepatic failure treated with extracorporeal hemodiabsorption postpartum
Chu J; Regan LA; Nelson LS; Hoffman RS
2001 ;39:486-486, Journal of toxicology. Clinical toxicology
— id: 70405, year: 2001, vol: 39, page: 486, stat: Journal Article,

Survival after intentional hydrofluoric (HF) acid ingestion
Chu J; Ying R; Hoffman RS; Nelson LS
2001 ;39:509-509, Journal of toxicology. Clinical toxicology
— id: 70406, year: 2001, vol: 39, page: 509, stat: Journal Article,

Lithium poisoning causing severe bradycardia
Hahn I; Blancaflor G; Hoffman RS; Nelson LS
2001 ;39:317-318, Journal of toxicology. Clinical toxicology
— id: 70421, year: 2001, vol: 39, page: 317, stat: Journal Article,

Leucovorin rescue for malicious abortion attempt with methotrexate
Hahn I; Hoffman RS; Nelson LS
2001 ;39:507-507, Journal of toxicology. Clinical toxicology
— id: 70407, year: 2001, vol: 39, page: 507, stat: Journal Article,

Kinetics of methemoglobin degradation
Hahn IH; Park H; Weeks E; Nelson LS; Hoffman RS
2001 ;38:S38-S38, Annals of emergency medicine
— id: 70066, year: 2001, vol: 38, page: S38, stat: Journal Article,

Severe bradycardia in a pediatric lithium toxicity
Hanh I; Kwok M; Hoffman RS; Nelson LS
2001 ;39:303-303, Journal of toxicology. Clinical toxicology
— id: 70422, year: 2001, vol: 39, page: 303, stat: Journal Article,

Clenbuterol ingestion causing prolonged tachycardia, hypokalemia, and hypophosphatemia with confirmation by quantitative levels
Hoffman RJ; Hoffman RS; Freyberg CL; Poppenga RH; Nelson LS
2001 ;39(4):339-344, Journal of toxicology. Clinical toxicology
BACKGROUND: Clenbuterol is a long acting beta2-adrenergic agonist used in the treatment of pulmonary disorders. Acute clenbuterol toxicity resembles that of other beta2-adrenergic agonists. Most previously reported cases of clenbuterol toxicity describe patients who ate livestock illicitly treated with clenbuterol. CASE REPORT: We report a case of human clenbuterol toxicity confirmed and correlated with qualitative and quantitative serum clenbuterol assays. This poisoned patient, a 28-year-old woman, developed sustained sinus tachycardia at 140/min, hypokalemia (2.4 mEq/L, 2.4 mmol/L), hypophosphatemia (0.9 mg/dL, 0.29 mmol/L), and hypomagnesemia (1.52 mg/dL, 0.76 mmol/L) after ingesting a reportedly small quantity of clenbuterol. The patient received repeated doses of metoprolol to treat her cardiovascular stimulation and potassium chloride to treat her hypokalemia. She remained symptomatic for more than 20 hours after the ingestion. Analysis by enzyme-linked immunosorbent assay and liquid chromatography/mass spectrometry revealed a serum clenbuterol concentration of 2.93 mcg/L 3 hours after the ingestion and an undetectable serum concentration 20 hours after ingestion. It is noteworthy that at a serum concentration below the limit of detection by liquid chromatography/mass spectrometry, the patient remained symptomatic. Acute clenbuterol toxicity is rarely reported following illicit use in humans, and this is the first such case to provide confirmatory toxicological analysis
— id: 26679, year: 2001, vol: 39, page: 339, stat: Journal Article,

Ethylene glycol toxicity despite therapeutic ethanol level
Hoffman RJ; Hoffman RS; Nelson LS
2001 ;39:302-302, Journal of toxicology. Clinical toxicology
— id: 70423, year: 2001, vol: 39, page: 302, stat: Journal Article,

Review of chemoluminescent glow stick exposures
Hoffman RJ; Hoffman RS; Nelson LS
2001 ;39:273-273, Journal of toxicology. Clinical toxicology
— id: 70424, year: 2001, vol: 39, page: 273, stat: Journal Article,

Common methods of illicit preparation of ketamine : gas chromatography/mass spectroscopy (GC/MS) analysis of products
Hoffman RJ; Ravikumar PR; Nelson LS; Hoffman RS
2001 ;39:267-268, Journal of toxicology. Clinical toxicology
— id: 70425, year: 2001, vol: 39, page: 267, stat: Journal Article,

Effects of kemtamine administration of phencyclidine immunoassays
Hoffman RJ; Saddock V; Nelson LS; Hoffman RS
2001 ;38:S62-S62, Annals of emergency medicine
— id: 70067, year: 2001, vol: 38, page: S62, stat: Journal Article,

Review of chemiluminescent glow stick exposures
Hoffman RJ; Winnik G; Nelson LS; Hoffman RS
2001 ;38:S62-S62, Annals of emergency medicine
— id: 70068, year: 2001, vol: 38, page: S62, stat: Journal Article,

Prolonged QT segment and syncope with loratadine use
Hoffman RS; deSouza I; Stetz JE; Chu J; Nelson LS
2001 ;39:505-505, Journal of toxicology. Clinical toxicology
— id: 70408, year: 2001, vol: 39, page: 505, stat: Journal Article,

Performing orogastric lavage : training, experience necessary?
Hoffman RS; Kwok M; Winnik G; Nelson LS
2001 ;38:S62-S63, Annals of emergency medicine
— id: 70069, year: 2001, vol: 38, page: S62, stat: Journal Article,

Rational use of toxicology testing in children
Hoffman, R J; Nelson, L
2001 Apr;13(2):183-188, Current opinion in pediatrics
The majority of all patients with poison exposures in the United States are children. The evaluation and management of poisoned patients may be aided by the use of laboratory assays, ranging from basic assessments not uniquely indicated for the poisoned patient to highly sophisticated laboratory tests with very specific indications. Literature concerning poisoning in pregnant patients is evaluated and recommendations regarding the utility of pregnancy testing in poisoned females are discussed. Recent studies evaluating the use of toxicology testing in pediatrics have concluded that the use of comprehensive toxicology screening in pediatric patients is costly and does not affect the medical management of most poisoned patients. The utility of focused quantitative serum assays to determine serum levels of particular poisons is reviewed. Toxicology tests used for detection of drugs of abuse, with a particular focus on the capabilities and limitations of such tests, are discussed. The potential pitfalls that occur when toxicology tests are obtained indiscriminately, are misapplied, or are misunderstood are analyzed. Hair sampling as nonemergent toxicology testing for drugs of abuse is discussed
— id: 133553, year: 2001, vol: 13, page: 183, stat: Journal Article,

Methanol contamination of Romanian home-distilled alcohol
Levy P; Hexdall A; Heller M; Nelson L; Boeriu C; Gordon P
2001 ;39:478-479, Journal of toxicology. Clinical toxicology
— id: 70410, year: 2001, vol: 39, page: 478, stat: Journal Article,

Aldicarb poisoning by an illicit rodenticide imported into the United States: Tres Pasitos
Nelson LS; Perrone J; DeRoos F; Stork C; Hoffman RS
2001 ;39(5):447-452, Journal of toxicology. Clinical toxicology
OBJECTIVE: Although intentional and unintentional rodenticide poisoning is common, most readily available agents are of relatively low acute toxicity. A four-year long epidemic of severe toxicity from rodenticide exposure continues among patients predominantly of Dominican descent living in New York City. This study characterizes the ongoing epidemic of acute cholinesterase inhibitor poisoning due to an illicit rodenticide and identifies its etiology. METHODS: A prospectively collected case series of poisoned patients referred to the New York City Poison Control Center. The main outcome measures include the clinical characteristics upon presentation, antidotal and other therapeutic requirements, and patient outcome. Product analysis was performed with paper chromatography, gas chromatography/mass spectrometry, and high-performance liquid chromatography. A murine model assessing both clinical effect and cholinesterase activity was also performed. RESULTS: Thirty-five patients were referred following exposure to Tres Pasitos. Patients developed signs of cholinergic hyperactivity and many required high doses of atropine (>10 mg) to control these symptoms. The source was identified as a rodenticidal compound sold illicitly in local groceries primarily within the Dominican community. Murine cholinesterase activity fell significantly following exposure to the rodenticide. High-performance liquid chromatography identified aldicarb, an extremely potent carbamate-type cholinesterase inhibitor, not licensed for rodenticidal use in this country. CONCLUSION: Illicit sale of undocumented compounds poses a substantial public health threat. Despite several public health interventions, the epidemic continues
— id: 26672, year: 2001, vol: 39, page: 447, stat: Journal Article,

Forensics ["Toxwise - a guide to clinical toxicology resources available on the Internet"]
Nelson, Lewis
2001 ;39:745-746, Journal of toxicology. Clinical toxicology
— id: 69791, year: 2001, vol: 39, page: 745, stat: Journal Article,

Fun stuff ["Toxwise - a guide to clinical toxicology resources available on the Internet"]
Nelson, Lewis
2001 ;39:581-582, Journal of toxicology. Clinical toxicology
— id: 69792, year: 2001, vol: 39, page: 581, stat: Journal Article,

Metal poisoning ["Toxwise - a guide to clinical toxicology resources available on the Internet"]
Nelson, Lewis
2001 ;39:427-429, Journal of toxicology. Clinical toxicology
— id: 69793, year: 2001, vol: 39, page: 427, stat: Journal Article,

Crotalid snakebite ["The Toxic Emergency"]
Nelson, Lewis S
2001 ;33:87-88 May, Emergency medicine
— id: 69804, year: 2001, vol: 33, page: 87, stat: Journal Article,

Overdoses involving cardiovascular drugs ["The Toxic Emergency"]
Nelson, Lewis S
2001 ;33:68-72,78 Feb, Emergency medicine
— id: 69805, year: 2001, vol: 33, page: 68, stat: Journal Article,

Toxin-induced vision loss ["The Toxic Emergency"]
Nelson, Lewis S
2001 ;33:84-86 Jan, Emergency medicine
— id: 69806, year: 2001, vol: 33, page: 84, stat: Journal Article,

Is surgical decontamination definitive treatment of "body-packers"?
Olmedo, R; Nelson, L; Chu, J; Hoffman, R S
2001 Nov;19(7):593-596, American journal of emergency medicine
The current recommendations for body-packers are based on packet content, the presence of drug toxicity, or of bowel obstruction. Asymptomatic patients are usually treated with activated charcoal and whole bowel irrigation (WBI). Surgical removal of packets is advocated in symptomatic cocaine body-packers and in those with bowel obstruction. Currently, surgery is regarded as definitive. However, we report 2 body-packers who show the limitations of this technique. These cases show the importance of confirming the absence of drug packets in the gastrointestinal (GI) tract as the definitive end-point in the treatment of body-packers
— id: 145503, year: 2001, vol: 19, page: 593, stat: Journal Article,

High-efficiency dialysis is effective in removing valproic acid
Sharma AN; Ilamathi P; Nelson LS; Hoffman RS; Howland MA
2001 ;39:497-497, Journal of toxicology. Clinical toxicology
— id: 70411, year: 2001, vol: 39, page: 497, stat: Journal Article,

Cerebral spinal fluid (CSF) analysis in fatal thallium poisoning
Sharma AN; Nelson LS; Hoffman RS
2001 ;39:237-238, Journal of toxicology. Clinical toxicology
— id: 70426, year: 2001, vol: 39, page: 237, stat: Journal Article,

Ruta graveolens as an ethnic abortifacient
Sharma AN; Nelson LS; Hoffman RS
2001 ;39:312-313, Journal of toxicology. Clinical toxicology
— id: 70427, year: 2001, vol: 39, page: 312, stat: Journal Article,

Management of gamma-hydroxybutyrate withdrawal
Sharma, A N; Lombardi, M H; Illuzzi, F A; Nelson, L S
2001 Nov;38(5):605-607, Annals of emergency medicine
— id: 69721, year: 2001, vol: 38, page: 605, stat: Journal Article,

Elevated blood lead levels in urban moonshine drinkers
Silverberg, M; Chu, J; Nelson, L
2001 Oct;38(4):460-461, Annals of emergency medicine
— id: 69770, year: 2001, vol: 38, page: 460, stat: Journal Article,

Anoxic encephalopathy from carbon dioxide therapy (CDT) for the treatment of depression
Su M; Donnabella V; Hoffman RS; Nelson LS
2001 ;39:493-493, Journal of toxicology. Clinical toxicology
— id: 70412, year: 2001, vol: 39, page: 493, stat: Journal Article,

Actue tacrolimus overdose without significant toxicity
Su M; Hoffman RS; Nelson LS
2001 ;39:513-513, Journal of toxicology. Clinical toxicology
— id: 70413, year: 2001, vol: 39, page: 513, stat: Journal Article,

Severe methotrexate toxicity following elective termination of pregnancy
Su M; Rahman S; Howland MA; Nelson LS; Hoffman RS
2001 ;39:507-507, Journal of toxicology. Clinical toxicology
— id: 70414, year: 2001, vol: 39, page: 507, stat: Journal Article,

Sustained-release potassium chloride overdose
Su M; Stork C; Ravuri S; Lavoie T; Anguish D; Nelson LS; Hoffman RS
2001 Oct;39(6):641-648, Journal of toxicology. Clinical toxicology
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
— id: 26545, year: 2001, vol: 39, page: 641, stat: Journal Article,

1,4-Butanediol withdrawal complicated by urinary retention
Su M; Traub S; Hussain E; Nicolescu N; Majeed A; Nelson L
2001 ;39:542-542, Journal of toxicology. Clinical toxicology
— id: 70415, year: 2001, vol: 39, page: 542, stat: Journal Article,

Treatment of out-of-hospital epilepticus
Su, M; Chodosh, A; Nelson, L S
2001 Dec 27;345(26):1913-1914, New England journal of medicine
— id: 69723, year: 2001, vol: 345, page: 1913, stat: Journal Article,

Massive necrosis of the gastrointestinal tract after ingestion of hydrochloric acid
Su, M; Nelson, L
2001 Oct;167(10):798-798, European journal of surgery = Acta chirurgica
— id: 133547, year: 2001, vol: 167, page: 798, stat: Journal Article,

Histamine poisoning from seafood
Su, M; Nelson, L S
2001 Jun 20;285(23):2977-2978, JAMA
— id: 69720, year: 2001, vol: 285, page: 2977, stat: Journal Article,

Pharyngeal irritation after eating cooked tarantula
Traub SJ; Hoffman RS; Nelson LS
2001 ;39:562-562, Journal of toxicology. Clinical toxicology
— id: 70416, year: 2001, vol: 39, page: 562, stat: Journal Article,

Severe toxicity following 4-aminopyridine overdose : case report and pharmacokinetic data
Traub SJ; Howland M; Hoffman RS; Nelson LS
2001 ;39:503-503, Journal of toxicology. Clinical toxicology
— id: 70418, year: 2001, vol: 39, page: 503, stat: Journal Article,

In-vitro adsorption of copper and lead to activated charcoal
Traub SJ; Nelson LS; Hoffman RS
2001 ;39:520-521, Journal of toxicology. Clinical toxicology
— id: 70417, year: 2001, vol: 39, page: 520, stat: Journal Article,

Fluvoxamine overdose producing status epilepticus
Hahn I; Blancaflor G; Hoffman RS; Howland MA; Nelson LS
2000 ;38:573-573, Journal of toxicology. Clinical toxicology
— id: 112590, year: 2000, vol: 38, page: 573, stat: Journal Article,

Chronic pediatric arsenic poisoning from pressure-treated wood burned in fireplace
Hahn I; Kline SA; Howland MA; Hoffman RS; Nelson L
2000 ;38:550-550, Journal of toxicology. Clinical toxicology
— id: 70428, year: 2000, vol: 38, page: 550, stat: Journal Article,

Electromagnetic interference from a cellular phone as a cause of acute epinephrine poisoning
Hahn I; Schnadower D; Dakin RJ; Hoffman RS; Nelson LS
2000 ;38:524-524, Journal of toxicology. Clinical toxicology
— id: 70429, year: 2000, vol: 38, page: 524, stat: Journal Article,

Errors in reporting salicylate levels
Hahn, I H; Chu, J; Hoffman, R S; Nelson, L S
2000 Nov;7(11):1336-1337, Academic emergency medicine
— id: 69719, year: 2000, vol: 7, page: 1336, stat: Journal Article,

Cross-tolerance of gamma-butyrolactone (GBL) and benzodiazepine
Hoffman RJ; Hoffman RS; Nelson LS
2000 ;38:227-228, Journal of toxicology. Clinical toxicology
— id: 70439, year: 2000, vol: 38, page: 227, stat: Journal Article,

Prolonged tachycardia, hypokalemia, and hypophosphatemia after clenbuterol ingestion : confirmation by quantitative clenbuterol levels
Hoffman RJ; Hoffman RS; Nelson LS
2000 ;38:235-235, Journal of toxicology. Clinical toxicology
— id: 70440, year: 2000, vol: 38, page: 235, stat: Journal Article,

Is medical toxicology becoming a pastime: graduates of medical toxicology fellowship programs will not practice this specialty
Hoffman RJ; Kwok MY; Nelson LS; Hoffman RS
2000 ;38:567-567, Journal of toxicology. Clinical toxicology
— id: 70430, year: 2000, vol: 38, page: 567, stat: Journal Article,

Life threatening levo-alpha-acetylmethadol (LAAM) overdose (platform)
Hoffman RJ; Nelson LS; Hoffman RS
2000 ;38:188-189, Journal of toxicology. Clinical toxicology
— id: 70438, year: 2000, vol: 38, page: 188, stat: Journal Article,

Acetaminophen poisoning
Hung O; Nelson LS
Emergency medicine : a comprehensive study guide New York : McGraw-Hill, 2000,
— id: 4140, year: 2000, vol: , page: ?, stat: Chapter,

Butanediol and ethanol: a reverse Mickey Finn?
Nelson LS
2000 ;3(1):2-2, Internet journal of medical toxicology
— id: 69783, year: 2000, vol: 3, page: 2, stat: Journal Article,

Poisoning
Nelson LS; Goldfrank LR
Melmon and Morrelli's clinical pharmacology New York : McGraw-Hill, 2000,
— id: 3305, year: 2000, vol: , page: 1091, stat: Chapter,

Poisoning
Nelson LS; Goldfrank LR
Melmon and Morrelli's clinical pharmacology: basic principles in therapeutics New York : McGraw-Hill, 2000,
— id: 4129, year: 2000, vol: , page: ?, stat: Chapter,

The benefit of house officer education on the proper calculation of medication dosing
Nelson LS; Simmons MD; Gordon P; et al
2000 ;7:451-451, Academic emergency medicine
— id: 70064, year: 2000, vol: 7, page: 451, stat: Journal Article,

As if there weren't enough controversies in gastrointestinal decontamination..
Nelson, L
2000 ;38(5):483-484, Journal of toxicology. Clinical toxicology
— id: 69773, year: 2000, vol: 38, page: 483, stat: Journal Article,

Toxwise
Nelson, L S
2000 ;38(4):461-462, Journal of toxicology. Clinical toxicology
— id: 69717, year: 2000, vol: 38, page: 461, stat: Journal Article,

The benefit of houseofficer education on proper medication dose calculation and ordering
Nelson, L S; Gordon, P E; Simmons, M D; Goldberg, W L; Howland, M A; Hoffman, R S
2000 Nov;7(11):1311-1316, Academic emergency medicine
OBJECTIVES: Drug dosing errors commonly cause morbidity and mortality. This prospective controlled study was performed to determine: 1) residents' understanding of drug dose calculations and ordering; and 2) the short-term effect of a brief educational intervention on the skills required to properly calculate dosages and order medications. METHODS: The study was conducted at an urban public hospital with a four-year emergency medicine (EM) residency program. The EM residents served as the study group and were unaware of the study design. A written, eight-question test (T1) with clinical situations and factual questions was administered. Immediately following the test, correct answers were discussed for 30 minutes. Key concepts were emphasized. Six weeks later, a repeat test (T2a) with a similar format was administered to the study group. The same test (T2b) was simultaneously administered to a control group, residents of similar training who did not take T1, in order to determine test equivalency (T1 vs T2). Tests were graded using explicit criteria by a single investigator blinded to the order of administration. RESULTS: Twenty residents completed both tests T1 and T2a. Their mean scores were 48% and 70%, respectively (p < 0.001, paired t-test). The control group of ten residents had a mean score of 49% (T2b), similar to the study group's scores on T1 (T1 vs T2b, p = 0.40, unpaired t-test). CONCLUSION: Emergency medicine residents require specific training in calculating and executing drug ordering. A brief educational intervention significantly improved short-term performance when retested six weeks later. Long-term retention is unknown
— id: 69718, year: 2000, vol: 7, page: 1311, stat: Journal Article,

Herbal and alternative medicine
Nelson, L; Perrone, J
2000 NOV ;18(4):709-+, Emergency medicine clinics of North America
Although scientific and medical understanding of dietary supplements are in their infancy the acceptance of these unproven, sometimes beneficial, and occasionally harmful therapies is widespread. Patients may present with diseases induced, exacerbated, or concealed by their use of such alternative medical therapies, and the need for recognition and management of these events by emergency physicians is exceedingly important. Toxicities associated with alternative medicine use are reviewed, and commonly used herbal and dietary supplements are highlighted
— id: 54411, year: 2000, vol: 18, page: 709, stat: Journal Article,

Clinical concepts in clinical emergency medicine
Nelson, Lewis
[Cherry Hill NJ] : CMEinfo.com, 2000,
— id: 1199, year: 2000, vol: , page: , stat: ,

Clinical pharmacology and medication errors ["Toxwise - a guide to clinical toxicology resources available on the Internet"]
Nelson, Lewis
2000 ;38:271-272, Journal of toxicology. Clinical toxicology
— id: 69796, year: 2000, vol: 38, page: 271, stat: Journal Article,

Drugs of abuse ["Toxwise - a guide to clinical toxicology resources available on the Internet"]
Nelson, Lewis
2000 ;38:85-86, Journal of toxicology. Clinical toxicology
— id: 69797, year: 2000, vol: 38, page: 85, stat: Journal Article,

Occupational poisoning and hazardous occupations ["Toxwise - a guide to clinical toxicology resources available on the Internet"]
Nelson, Lewis
2000 ;38:461-462, Journal of toxicology. Clinical toxicology
— id: 69795, year: 2000, vol: 38, page: 461, stat: Journal Article,

Pesticides ["Toxwise - a guide to clinical toxicology resources available on the Internet"]
Nelson, Lewis
2000 ;38:811-812, Journal of toxicology. Clinical toxicology
— id: 69794, year: 2000, vol: 38, page: 811, stat: Journal Article,

Acute copper sulfate poisoning ["The Toxic Emergency"]
Nelson, Lewis S
2000 ;32:88-91 Feb, Emergency medicine
— id: 69809, year: 2000, vol: 32, page: 88, stat: Journal Article,

Carbon dioxide poisoning ["The Toxic Emergency"]
Nelson, Lewis S
2000 ;32:36-38 May, Emergency medicine
— id: 69808, year: 2000, vol: 32, page: 36, stat: Journal Article,

Nitroprusside toxicity ["The Toxic Emergency"]
Nelson, Lewis S
2000 ;32:36-38 Oct, Emergency medicine
— id: 69807, year: 2000, vol: 32, page: 36, stat: Journal Article,

Death as a complication of ultrarapid opioid detoxification (UROD)
Olmedo RE; Hoffman RS; Howland M; Nelson L
2000 ;38:536-536, Journal of toxicology. Clinical toxicology
— id: 70431, year: 2000, vol: 38, page: 536, stat: Journal Article,

Metabolic acidosis, hyperthermia, rhabdomyolysis and subsequent death after prolonged propofol infusion
Olmedo RE; Hoffman RS; Howland M; Nelson L
2000 ;38:538-538, Journal of toxicology. Clinical toxicology
— id: 70432, year: 2000, vol: 38, page: 538, stat: Journal Article,

Propofol safely controls delirium tremens
Olmedo RE; Nelson LS; Howland M; Hoffman RS
2000 ;38:537-537, Journal of toxicology. Clinical toxicology
— id: 70433, year: 2000, vol: 38, page: 537, stat: Journal Article,

Adverse events from botanicals and other dietary supplements : a multicenter poison control center study
Palmer ME; Haller C; McKinney P; Nelson LS; et al
2000 ;7:499-499, Academic emergency medicine
— id: 70065, year: 2000, vol: 7, page: 499, stat: Journal Article,

Hemoglobinopathies
Rees S; Nelson LS
Emergency medicine : a comprehensive study guide New York : McGraw-Hill, 2000,
— id: 4143, year: 2000, vol: , page: ?, stat: Chapter,

Hypoglycemic agents
Rella J; Nelson LS
Emergency medicine : a comprehensive study guide New York : McGraw-Hill, 2000,
— id: 4141, year: 2000, vol: , page: ?, stat: Chapter,

Iron poisoning
Rella J; Nelson LS
Emergency medicine : a comprehensive study guide New York : McGraw-Hill, 2000,
— id: 4142, year: 2000, vol: , page: ?, stat: Chapter,

7 Years of 3,4-Methylenedioxymethamphetamine (MDMA) Toxicity
Rella JG; Nelson LS; Hoffman RS
2000 ;3(5):28-28, Internet journal of medical toxicology
— id: 69781, year: 2000, vol: 3, page: 28, stat: Journal Article,

Methylene blue safely and effectively treats methemoglobinemia in a known G6PD deficient patient with hemolytic anemia
Sharma AN; Chawla S; Nelson L; Hoffman RS
2000 ;38:541-541, Journal of toxicology. Clinical toxicology
— id: 70434, year: 2000, vol: 38, page: 541, stat: Journal Article,

Diphenhydramine-induced wide-complex tachycardia responds to bicarbonate
Sharma AN; Hexdall AH; Nelson L; Hoffman RS
2000 ;38:572-572, Journal of toxicology. Clinical toxicology
— id: 70435, year: 2000, vol: 38, page: 572, stat: Journal Article,

Refractory sedative-hypnotic withdrawal treated with propofol
Sharma AN; Nelson L; Hoffman RS
2000 ;38:537-537, Journal of toxicology. Clinical toxicology
— id: 70436, year: 2000, vol: 38, page: 537, stat: Journal Article,

Severe gamma butyrolactone withdrawal
Sharma AN; Nelson LS; Hoffman RS
2000 ;38:535-535, Journal of toxicology. Clinical toxicology
— id: 70437, year: 2000, vol: 38, page: 535, stat: Journal Article,

Methylenedioxymethylamphetamine (MDMA) Induced Hyponatremia
Sharma R; Nelson LS
2000 ;3(5):29-29, Internet journal of medical toxicology
— id: 69782, year: 2000, vol: 3, page: 29, stat: Journal Article,

Akathisia and prochlorperazine
Sharma, A N; Steinberg, K; Nelson, L S
2000 Aug;36(2):169-170, Annals of emergency medicine
— id: 69716, year: 2000, vol: 36, page: 169, stat: Journal Article,

Asphyxiation by carbon dioxide due to sublimation of dry ice in a closed space
Ely S; Rao RB; Heller M; Nelson LS; Hoffman RS
1999 ;37:659-659, Journal of toxicology. Clinical toxicology
— id: 70441, year: 1999, vol: 37, page: 659, stat: Journal Article,

Early predictors of severity in resistant alcohol withdrawal (AW)
Hack JB; Buschmann D; Hoffman RS; Nelson LS
1999 ;37:651-651, Journal of toxicology. Clinical toxicology
— id: 70442, year: 1999, vol: 37, page: 651, stat: Journal Article,

Acido oxalico (Oxalic acid)
Hack JB; Nelson LS
Intoxicaciones agudas en medicina de urgencia y cuidados criticos Barcelona : Masson, 1999,
— id: 4163, year: 1999, vol: , page: ?, stat: Chapter,

Opiaceos (Opioids)
Hack JB; Nelson LS; Duenas A
Intoxicaciones agudas en medicina de urgencia y cuidados criticos Barcelona : Masson, 1999,
— id: 4166, year: 1999, vol: , page: ?, stat: Chapter,

Severe symptoms following a massive intentional L-thyroxine ingestion
Hack, J B; Leviss, J A; Nelson, L S; Hoffman, R S
1999 Oct;41(5):323-326, Veternary & human toxicology
L-Thyroxine (T4) is commonly prescribed medication for hypothyroidism in humans and animals. Overdose has generally resulted in limited symptomatology managed with sedatives and beta-adrenergic receptor antagonists. We describe the largest acute T4 ingestion ever reported, which resulted in a profound thyrotoxicosis, resistant to treatment. A 34-y-old man ingested 900 (0.8 mg) tablets of veterinary T4 (720 mg) and was given 60 g of activated charcoal. He became lethargic on post-ingestion days 2 and 3; had vomiting, diaphoresis and insomnia on day 4; on day 5 he 'looked like he had too much coffee', began 'using a lot of words' and became agitated, assaultive and stopped speaking intelligibly; and on day 6 returned to the hospital combative and confused. He was diaphoretic, mydriatic, hyperreflexic, tremulous, with clear lungs and active bowel sounds, and received activated charcoal, haloperidol, diazepam, and phenobarbital, and was tracheally intubated. During hospitalization he was rehydrated, treated with propranolol and diazepam, but remained continuously tachycardic. On day 12 he became afebrile and his tachycardia resolved. Free T4 levels ranged from > 13 mcg/dL on day 6 to 1.2 mcg/dL on day 12. By discharge (day 15) he had lost 20 kilograms of body weight, but was clinically euthyroid 2 w later. This case suggests that large intentional T4 ingestions should be managed differently than current T4 overdose protocol
— id: 69714, year: 1999, vol: 41, page: 323, stat: Journal Article,

Acute pediatric exposure to pramipexole dihydrochloride (Mirapex)
Hack, J B; Powell, G; Nelson, L S; Hoffman, R S; Howland, M A
1999 ;37(7):891-892, Journal of toxicology. Clinical toxicology
— id: 69715, year: 1999, vol: 37, page: 891, stat: Journal Article,

Contrast CT scan fails to detect the last heroin packet
Hahn I; Hoffman RS; Nelson LS
1999 ;37:644-645, Journal of toxicology. Clinical toxicology
— id: 70443, year: 1999, vol: 37, page: 644, stat: Journal Article,

EMLA-induced methemoglobinemia and lidocaine toxicity
Hahn I; Hoffman RS; Nelson LS
1999 ;37:621-621, Journal of toxicology. Clinical toxicology
— id: 70444, year: 1999, vol: 37, page: 621, stat: Journal Article,

Asthma/COPD
Nelson LS
Review and self-assessment to accompany Emergency medcine Philadelphia : Saunders, 1999,
— id: 4185, year: 1999, vol: , page: ?, stat: Chapter,

Etanol
Nelson LS
Intoxicaciones agudas en medicina de urgencia y cuidados criticos Barcelona : Masson, 1999,
— id: 4162, year: 1999, vol: , page: ?, stat: Chapter,

Pulmonary embolus
Nelson LS
Review and self-assessment to accompany Emergency medcine Philadelphia : Saunders, 1999,
— id: 4184, year: 1999, vol: , page: ?, stat: Chapter,

Dangerous form of marijuana
Nelson, L S; Holland, J A; Ravikumar, P R
1999 Jul;34(1):115-116, Annals of emergency medicine
— id: 69713, year: 1999, vol: 34, page: 115, stat: Journal Article,

Central nervous system depression after ingestion of RenewTrient
Nelson, L S; Howland, M A; Hoffman, R S
1999 Feb 18;340(7):570-570, New England journal of medicine
— id: 69711, year: 1999, vol: 340, page: 570, stat: Journal Article,

Dietary supplements ["Toxwise - a guide to clinical toxicology resources available on the Internet"]
Nelson, Lewis
1999 ;37:809-810, Journal of toxicology. Clinical toxicology
— id: 69798, year: 1999, vol: 37, page: 809, stat: Journal Article,

General toxicology I ["Toxwise - a guide to clinical toxicology resources available on the Internet"]
Nelson, Lewis
1999 ;37:677-679, Journal of toxicology. Clinical toxicology
— id: 69800, year: 1999, vol: 37, page: 677, stat: Journal Article,

General toxicology II ["Toxwise - a guide to clinical toxicology resources available on the Internet"]
Nelson, Lewis
1999 ;37:133-134, Journal of toxicology. Clinical toxicology
— id: 69799, year: 1999, vol: 37, page: 133, stat: Journal Article,

Herbal abortifacient ["The Toxic Emergency"]
Nelson, Lewis S
1999 ;31:102-103 Oct, Emergency medicine
— id: 69810, year: 1999, vol: 31, page: 102, stat: Journal Article,

Limitation of whole-bowel irrigation and laparotomy in cocaine "body-packer"
Olmedo RE; Hoffman RS; Nelson LS
1999 ;37:645-645, Journal of toxicology. Clinical toxicology
— id: 70445, year: 1999, vol: 37, page: 645, stat: Journal Article,

Ventricular dysrhythmia and subsequent death in a patient with acute promyelocytic leukemia treated with arsenic trioxide
Olmedo RE; Hoffman RS; Nelson LS
1999 ;37:622-622, Journal of toxicology. Clinical toxicology
— id: 70446, year: 1999, vol: 37, page: 622, stat: Journal Article,

Severe electrolyte abnormalities and tetany after inadvertant foscarnet infusion
Olmedo RE; Howland MA; Nelson L
1999 ;37:603-603, Journal of toxicology. Clinical toxicology
— id: 70447, year: 1999, vol: 37, page: 603, stat: Journal Article,

Lead poisoning in late pregnancy due to maternal pica
Olmedo RE; Rella RG; Hoffman RS; Nelson LS
1999 ;37:626-626, Journal of toxicology. Clinical toxicology
— id: 70448, year: 1999, vol: 37, page: 626, stat: Journal Article,

Botanicals and other dietary supplements: adverse events by age
Palmer M; Haller C; McKinney P; Tschirgi A; Klein-Schwartz W; Nelson L; Woolf A; Dodd-Butera T
1999 ;37:609-609, Journal of toxicology. Clinical toxicology
— id: 70449, year: 1999, vol: 37, page: 609, stat: Journal Article,

Paratonia (rapid rigor mortis) in salicylate (ASA) poisoning
Rao RB; Smiddy M; Nelson LS; Howland MA; Hoffman RS
1999 ;37:605-605, Journal of toxicology. Clinical toxicology
— id: 70450, year: 1999, vol: 37, page: 605, stat: Journal Article,

Nicotina
Rella JG; Nelson LS
Intoxicaciones agudas en medicina de urgencia y cuidados criticos Barcelona : Masson, 1999,
— id: 4165, year: 1999, vol: , page: ?, stat: Chapter,

5 years of 3,4-methylenedioxymethamphetamine (MDMA) toxicity
Rella JG; Nelson LS; Hoffman RS
1999 ;37:648-648, Journal of toxicology. Clinical toxicology
— id: 70451, year: 1999, vol: 37, page: 648, stat: Journal Article,

Cocaina
Rella JG; Nelson LS; Hoffman RS
Intoxicaciones agudas en medicina de urgencia y cuidados criticos Barcelona : Masson, 1999,
— id: 4164, year: 1999, vol: , page: ?, stat: Chapter,

Recovery after Ecstasy intoxication
Rella, J G; Nelson, L S
1999 ;37(3):341, 343-, Journal of toxicology. Clinical toxicology
— id: 69712, year: 1999, vol: 37, page: 341, 343, stat: Journal Article,

Erythropoietin overdose treated with emergent erythropheresis
Zelman, G; Howland, M A; Nelson, L S; Hoffman, R S
1999 Sep 28-Oct 4;37(5):602-603, Journal of toxicology. Clinical toxicology
— id: 15884, year: 1999, vol: 37, page: 602, stat: Journal Article,

Severe symptoms following a massive ingestion of veterinary lamba-thyroxine
Hack JB; Levis J; Hoffman RS; Nelson LS
1998 ;36:490-491, Journal of toxicology. Clinical toxicology
— id: 70452, year: 1998, vol: 36, page: 490, stat: Journal Article,

Acute pediatric exposure to pramipexole
Hack JB; Nelson LS; Hoffman RS; Powell G; Howland MA
1998 ;36:523-523, Journal of toxicology. Clinical toxicology
— id: 70453, year: 1998, vol: 36, page: 523, stat: Journal Article,

Embalming fluid-soaked marijuana: new high or new guise for PCP?
Holland JA; Nelson L; Ravikumar PR; Elwood WN
1998 Apr-Jun;30(2):215-219, Journal of psychoactive drugs
A growing trend of smoking marijuana soaked in what is purported to be embalming fluid has been reported in the literature since the mid-1980s. This article describes several cases of intoxication, gives regional epidemiological data on this phenomenon, and includes current nomenclature. The authors also analyze a sample of fluid said to be embalming fluid and discover PCP (phencyclidine) and multiple congeners and by-products of PCP manufacture. The implications of this finding are discussed, and the hypothesis that most embalming fluid-soaked marijuana likely contains PCP is considered
— id: 12086, year: 1998, vol: 30, page: 215, stat: Journal Article,

Organophosphates and carbamates
Hung O; Nelson LS
Emergency medicine : the core curriculum Philadelphia : Lippincott-Raven, 1998,
— id: 4147, year: 1998, vol: , page: ?, stat: Chapter,

Acute barium styphenate poisoning : a report of an unusual case
Hung O; Shih RD; Nelson L; et al
1998 ;36:498-498, Journal of toxicology. Clinical toxicology
— id: 70454, year: 1998, vol: 36, page: 498, stat: Journal Article,

Toxic baby formula: fleet enema confused for baby water bottle
Hung OL; Nelson LS; Howland MA; Hoffman RS
1998 ;36:436-436, Journal of toxicology. Clinical toxicology
— id: 70455, year: 1998, vol: 36, page: 436, stat: Journal Article,

Hallucinogens
Nelson LS
Emergency toxicology Philadelphia : Lippincott-Raven, 1998,
— id: 4149, year: 1998, vol: , page: ?, stat: Chapter,

Locally acting agents
Nelson LS
Emergency medicine : the core curriculum Philadelphia : Lippincott-Raven, 1998,
— id: 4145, year: 1998, vol: , page: ?, stat: Chapter,

Opioids
Nelson LS
Goldfrank's toxicologic emergencies New York : McGraw-Hill, 1998,
— id: 4160, year: 1998, vol: , page: ?, stat: Chapter,

Pulmonary irritants
Nelson LS
Goldfrank's toxicologic emergencies New York : McGraw-Hill, 1998,
— id: 4161, year: 1998, vol: , page: ?, stat: Chapter,

Toxicity of the non-steroidal antiinflammatory agents
Nelson LS
Emergency medicine : the core curriculum Philadelphia : Lippincott-Raven, 1998,
— id: 4144, year: 1998, vol: , page: ?, stat: Chapter,

Toxicology of the special sense organs
Nelson LS
Encyclopedia of toxicology San Diego CA : Academic Press, 1998,
— id: 4152, year: 1998, vol: , page: ?, stat: Chapter,

Intrathecal injection: unusual complication of trigger-point injection therapy
Nelson LS; Hoffman RS
1998 Oct;32(4):506-508, Annals of emergency medicine
Trigger-point injection therapy is a common procedure in primary care medicine and emergency medicine and is generally considered safe. A 28-year-old woman experienced respiratory depression and hemiplegia after the injection of a superficial trapezius trigger point. The patient required emergency tracheal intubation for ventilatory support. Computed tomography of her head revealed pneumocephalus. She recovered fully over the course of 24 hours. Intrathecal injection during a trigger-point injection is a previously unreported complication of trigger-point injection therapy
— id: 57218, year: 1998, vol: 32, page: 506, stat: Journal Article,

Physical and chemical irritants
Nelson LS; Hoffman RS
Emergency Medicine Philadelphia : Saunders, 1998,
— id: 4148, year: 1998, vol: , page: ?, stat: Chapter,

Toxic inhalations
Nelson LS; Hoffman RS
Emergency medicine : concepts and clinical practice St. Louis : Mosby, 1998,
— id: 4179, year: 1998, vol: , page: ?, stat: Chapter,

FMRFamide-related gene family in the nematode, Caenorhabditis elegans
Nelson, L S; Kim, K; Memmott, J E; Li, C
1998 Jul 15;58(1-2):103-111, Brain research. Molecular brain research
Many organisms, including mammals, use short peptides as neurotransmitters. The family of FMRFamide (Phe-Met-Arg-Phe-NH2)-like neuropeptides, which all share an -RFamide sequence at their C-termini, has been shown to have diverse functions, including neuromodulation and stimulation or inhibition of muscle contraction. In the nematode, Caenorhabditis elegans, FMRFamide-like peptides (FaRPs) are expressed in approximately 10% of the neurons, including motor, sensory, and interneurons that are involved in movement, feeding, defecation, and reproduction. At least 14 genes, designated flp-1 through flp-14, encode FaRPs in C. elegans. Here, we present data that all 14 flp genes are transcribed in C. elegans, and several of these genes are alternatively spliced. Each flp gene encodes a different set of FaRPs, yielding a predicted total of 44 distinct FaRPs. Using staged RNA for reverse-transcription/polymerase chain reactions (RT/PCR), we determined that most flp genes are expressed throughout development. These results suggest that a complex family of FaRPs have varied roles through all stages of development and in adulthood in C. elegans
— id: 69768, year: 1998, vol: 58, page: 103, stat: Journal Article,

Status epilepticus
Nelson, L S; Rella, J; Hoffman, R S
1998 Aug 6;339(6):409-410, New England journal of medicine
— id: 69769, year: 1998, vol: 339, page: 409, stat: Journal Article,

A gap in the safety net : a multi-center prospective study of herbals and other dietary supplements
Palmer M; Haller C; McKinney P; Nelson LS; et al
1998 ;36:454-454, Journal of toxicology. Clinical toxicology
— id: 70456, year: 1998, vol: 36, page: 454, stat: Journal Article,

Toxicology of herbal products
Pearl W; Nelson LS
Emergency toxicology Philadelphia : Lippincott-Raven, 1998,
— id: 4150, year: 1998, vol: , page: ?, stat: Chapter,

Opioids
Rao RB; Nelson LS
Emergency medicine : the core curriculum Philadelphia : Lippincott-Raven, 1998,
— id: 4146, year: 1998, vol: , page: ?, stat: Chapter,

Naloxone hazards overstated
Hsu, W; Rao, R B; Nelson, L S
1997 ;35(2):215-7, 219, Journal of toxicology. Clinical toxicology
— id: 69766, year: 1997, vol: 35, page: 215, stat: Journal Article,

Herbal preparation use among urban emergency department patients
Hung OL; Shih RD; Chiang WK; Nelson LS; Hoffman RS; Goldfrank LR
1997 Mar;4(3):209-213, Academic emergency medicine
OBJECTIVE: To determine the prevalence of herbal preparation use among patients presenting to an urban teaching hospital ED. METHODS: A prospective anonymous survey on herbal preparation use was performed. Consecutive, acutely ill or injured adult (> or = 18 years old) ED patients were offered the survey over a 1-month period. The survey also asked for information related to patient age, ethnicity, gender, employment, education, cigarette smoking history, ethanol consumption, use of illicit drugs, chief complaint, and HIV status. RESULTS: Of 2,473 eligible subjects, 623 (25%) participated. The overall reported prevalence of herbal preparation use among the participants was 21.7%. Women were more likely to use herbal preparations than men (28.5% vs 17.2%, p = 0.013). Prevalence rates in different ethnic populations were: whites, 18.2%; Hispanics, 13.9%; blacks, 26.4%; and Asians, 36.8%. Asians had a significantly higher use rate than the other ethnic groups (p = 0.039). Neither HIV positivity, educational level, employment status, nor age was significantly associated with herbal preparation use. The most commonly reported herbal preparations were goldenseal tea, garlic, and ginger. Several of the herbal preparations reported as used by patients in this study have been associated with severe systemic toxicity in the medical literature. CONCLUSION: Although the survey response rate was low, the prevalence of herbal preparation use among acutely ill or injured patients presenting to this urban ED remains significant. A directed history toward specific herbal preparation use may provide relevant pharmacologic information and uncover cases of herbal-preparation-induced toxicity
— id: 12373, year: 1997, vol: 4, page: 209, stat: Journal Article,

The use of analgesics in patients with acute abdominal pain
LoVecchio, F; Oster, N; Sturmann, K; Nelson, L S; Flashner, S; Finger, R
1997 Nov-Dec;15(6):775-779, Journal of emergency medicine
Analgesics in patients with acute abdominal pain are often withheld for fear that they may change physical examination findings and thus may be unsafe. We conducted a randomized, prospective, placebo-controlled trial to investigate changes in physical examination following the administration of placebo, 5 mg, or 10 mg of morphine to 49 patients with acute abdominal pain. One patient was withdrawn secondary to inadequate documentation. Of the 48 patients who completed the trial, a statistically significant change in physical examination was noted in both groups receiving analgesics, but not in the placebo group. No adverse events or delays in diagnosis were attributed to the administration of analgesics. We conclude that physical examination does change after the administration of analgesics in patients with acute abdominal pain and that a larger study is needed to evaluate analgesic safety in this subpopulation of emergency department patients
— id: 69767, year: 1997, vol: 15, page: 775, stat: Journal Article,

Florists and groundskeepers
Nelson LS
Occupational, industrial, and environmental toxicology St. Louis : Mosby, 1997,
— id: 4167, year: 1997, vol: , page: ?, stat: Chapter,

Poisonings associated with illegal use of aldicarb as a rodenticide -- New York City, 1994-1997
Nelson LS; Hoffman RS; Rao R; et al
1997 ;46:961-963, MMWR
— id: 69786, year: 1997, vol: 46, page: 961, stat: Journal Article,

Poppy tea and the baker's first seizure
Nelson LS; Hung OL
1997 Dec 20-27;350(9094):1859-1859, Lancet
— id: 57217, year: 1997, vol: 350, page: 1859, stat: Journal Article,

Opioids
Palmer M; Nelson LS
1997 ;19:17-22, Topics in emergency medicine
— id: 69784, year: 1997, vol: 19, page: 17, stat: Journal Article,

Digoxin, hyperkalemia, and kidney failure
Rees, S M; Nelson, L
1997 May;29(5):694-695, Annals of emergency medicine
— id: 69771, year: 1997, vol: 29, page: 694, stat: Journal Article,

Intraventricular bleeding after the use of thrombolytics in a cocaine user
LoVecchio, F; Nelson, L
1996 Nov;14(7):663-664, American journal of emergency medicine
Cocaine-induced myocardial infarct is a medical emergency with increasing prevalence. The efficacy of thrombolytics in patients with cocaine-induced infarcts has not been well studied. This report describes the case of a patient who presented with presumed cocaine-induced myocardial infarct. The patient was treated with intravenous thrombolysis and developed an intraventricular bleed with herniation and death. Physicians should be aware of this grave consequence in a generally young population
— id: 69772, year: 1996, vol: 14, page: 663, stat: Journal Article,

What to do when drug poisoning causes hypertension
Nelson LS
1996 ;11:88-92, Critical reviews in toxicology
— id: 69814, year: 1996, vol: 11, page: 88, stat: Journal Article,

Toxicologic cardiac arrest
Nelson LS; Hoffman RS
Cardiac arrest: the science and practice of resuscitation medicine Baltimore : Williams & Wilkins, 1996,
— id: 4128, year: 1996, vol: , page: xxii, 981, stat: Chapter,

Chloral hydrate and other sleep inducing agents ["The Toxic Emergency"]
Nelson, Lewis S
1996 ;28:82-83, Emergency medicine
— id: 69812, year: 1996, vol: 28, page: 82, stat: Journal Article,

Organophosphate poisoning ["The Toxic Emergency"]
Nelson, Lewis S
1996 ;28:110-111, Emergency medicine
— id: 69811, year: 1996, vol: 28, page: 110, stat: Journal Article,

Scopolamine poisoning among heroin users
Perrone J; Hamilton R; Nelson LS; et al
1996 ;45:457-460, MMWR
— id: 69787, year: 1996, vol: 45, page: 457, stat: Journal Article,

Cocaine-associated myocardial infarction. Clinical safety of thrombolytic therapy. Cocaine Associated Myocardial Infarction (CAMI) Study Group
Hollander, J E; Burstein, J L; Hoffman, R S; Shih, R D; Wilson, L D; Nelson, LS
1995 May;107(5):1237-1241, Chest
OBJECTIVE: To determine the safety of thrombolytic use in patients with cocaine-associated myocardial infarction. DESIGN: Retrospective cross-sectional survey. SETTING: Twenty-nine acute care institutions. PATIENTS: Patients who sustained cocaine-associated myocardial infarction from 1987 to 1993 were identified through medical record review. Those who received thrombolytic therapy (n = 25) were compared with those who met electrocardiographic TIMI criteria but did not receive thrombolytic therapy (n = 41). INTERVENTIONS: None. RESULTS: Both groups of patients were similar with respect to age, gender, race, cardiac risk factors, time from last cocaine use until presentation, and duration of chest pain at the time of presentation (p > 0.20). There were no major complications or deaths in patients who received thrombolytic therapy (95% confidence interval, 0 to 12%). Minor complications occurred in only two patients. The presence or absence of clinical criteria for reperfusion was noted in the charts of 21 patients who received thrombolytic therapy: 67% were believed to reperfuse. The patients who did and did not receive thrombolytic therapy had similar median peak creatine kinase-MB (CK-MB) levels (180 vs 154 mg/dL, p = NS) and time until peak CK-MB (11.3 vs 13.6 h; p = NS). CONCLUSION: Thrombolytic therapy for cocaine-associated myocardial infarction appears to be safe. It remains unclear whether thrombolytic therapy is an important therapeutic intervention for patients with cocaine-associated myocardial infarction. Further study on efficacy is recommended prior to routine use
— id: 69775, year: 1995, vol: 107, page: 1237, stat: Journal Article,

Cocaine-associated myocardial infarction. Mortality and complications. Cocaine-Associated Myocardial Infarction Study Group
Hollander, J E; Hoffman, R S; Burstein, J L; Shih, R D; Thode, H C Jr; Nelson, LS
1995 May 22;155(10):1081-1086, Archives of internal medicine
BACKGROUND: The frequency of complications in patients with cocaine-associated myocardial infarction is unknown. This study was performed to determine the short-term morbidity and mortality secondary to cocaine-associated myocardial infarction. METHODS: We performed a retrospective cohort study at 29 hospital centers throughout the United States. Patients with cocaine-associated myocardial infarction that occurred between 1987 and 1993 were identified through record review. The primary outcome measures were in-hospital mortality and the incidence and timing of major cardiovascular complications. RESULTS: Cocaine-associated myocardial infarction was identified 136 times in 130 patients. Patients were generally young (mean age, 38 years), nonwhite (72%), tobacco smokers (91%) with a history of cocaine use in the past 24 hours (88%). The initial electrocardiogram disclosed infarction in 44% and ischemia in an additional 18% of patients. Myocardial infarctions were evenly distributed between anterior (45%) and inferior (44%) and were most often non-Q-wave (61%). Complications occurred 64 times in 49 patients (36%; 95% confidence interval, 28% to 44%), including congestive heart failure in nine patients, ventricular tachycardia in 23 patients, supraventricular tachycardia in six patients, and brady-dysrhythmias in 26 patients. Most patients who had complications (90%) had them within 12 hours of presentation. Acute in-hospital mortality was 0% (95% confidence interval, 0% to 2%). CONCLUSIONS: The mortality of patients hospitalized with cocaine-associated myocardial infarction was low. The majority of complications occurred within 12 hours of presentation
— id: 69776, year: 1995, vol: 155, page: 1081, stat: Journal Article,

How to manage acute MI when cocaine is the cause
Nelson L; Hoffman RS
1995 ;10(1):39-43 Jan, Journal of critical illness
In patients with cocaine cardiotoxicity, adrenergic effects (such as vasoconstriction) and nervous system stimulation are amplified. The result is hypertension, tachycardia, and peripheral vasodilation; myocardial ischemia -- and even infarction -- is not uncommon. Following initial stabilization, beta-blockade (a recommended therapy for normal infarction) could potentiate cocaine induced changes. Early use of diazopam, which aims to control central excitation, is more appropriate. Beta-Blockers, vasodilators, and calcium channel blockers may also be useful. Bicarbonate is preferred to lidocaine for managing secondary tachycardia
— id: 75776, year: 1995, vol: 10, page: 39, stat: Journal Article,

Aplastic anemia induced by an adulterated herbal medication
Nelson L; Shih R; Hoffman R
1995 ;33(5):467-470, Journal of toxicology. Clinical toxicology
Herbal medication use is common in many cultural groups. Because these products are unregulated, the potential for significant toxicity exists. We report a case of aplastic anemia associated with the use of an herbal medication by a 12-year-old boy. On analysis, the herbal medication was found to contain phenylbutazone, which has been strongly associated with the production of similar hematologic abnormalities. The medication was not listed as an ingredient and no warning was present on the box
— id: 56781, year: 1995, vol: 33, page: 467, stat: Journal Article,

How to manage MI when cocaine is the cause?
Nelson LS; Hoffman RS
1995 ;10:39-43, Critical reviews in toxicology
— id: 69815, year: 1995, vol: 10, page: 39, stat: Journal Article,

Clinical safety of lidocaine in patients with cocaine-associated myocardial infarction
Shih RD; Hollander JE; Burstein JL; Nelson LS; Hoffman RS; Quick AM
1995 Dec;26(6):702-706, Annals of emergency medicine
STUDY OBJECTIVE: To evaluate the safety of lidocaine in the setting of cocaine-induced myocardial infarction (MI). DESIGN: A retrospective, multicenter study. SETTING: Twenty-nine university, university-affiliated, or community hospitals during a 6-year period (total of 117 cumulative hospital-years). PARTICIPANTS: Patients with cocaine-associated MI who received lidocaine in the emergency department. RESULTS: Of 29 patients who received lidocaine in the setting of cocaine-associated MI, no patient died; exhibited bradydysrhythmias, ventricular tachycardia, or ventricular fibrillation; or experienced seizures after administration of lidocaine (95% confidence interval, 0% to 11%). CONCLUSION: Despite theoretical concerns that lidocaine may enhance cocaine toxicity, the use of lidocaine in patients with cocaine-associated MI was not associated with significant cardiovascular or central nervous system toxicity
— id: 12711, year: 1995, vol: 26, page: 702, stat: Journal Article,

What to do when drug poisoning causes bradycardia
Nelson LS; Hoffman RS
1994 ;9:916-924, Critical reviews in toxicology
— id: 69816, year: 1994, vol: 9, page: 916, stat: Journal Article,

What to do when drug poisoning causes tachycardia
Nelson LS; Hoffman RS
1994 ;9:831-842, Critical reviews in toxicology
— id: 69817, year: 1994, vol: 9, page: 831, stat: Journal Article,

Mexiletine overdose producing status epilepticus without cardiovascular abnormalities
Nelson, L S; Hoffman, R S
1994 ;32(6):731-736, Journal of toxicology. Clinical toxicology
Few cases of mexiletine overdose have been reported in the literature. The available case reports have invariably noted significant hemodynamic or electrocardiographic abnormalities. A 41-year-old woman, on mexiletine for arrhythmia control, ingested up to 90 of her 200 mg mexiletine tablets in a suicide attempt. She presented to the emergency department awake with a normal blood pressure and pulse. Shortly afterwards, the patient had a generalized motor seizure, which responded after 40 minutes to intravenous diazepam 100 mg, phenobarbital 1 g and pyridoxine 5 g. Recurrent status epilepticus at one hour required an additional 40 mg of diazepam and a loading dose of pentobarbital. During the entire episode, her electrocardiogram remained normal. The patient's mexiletine level was 20 micrograms/mL (therapeutic 1-2 micrograms/mL) and the patient's urine screen was negative for cocaine. Mexiletine is a group Ib antidysrhythmic agent with electrophysiologic effects similar to lidocaine. Mexiletine has a little first pass hepatic metabolism and a large volume of distribution along with a high lipid solubility, and prolonged central nervous system toxicity may be expected. As with lidocaine, the toxic deaths from mexiletine have resulted from hypotension and bradycardia. The patient reported had a significant mexiletine overdose which resulted in convulsive status epilepticus, but was devoid of hemodynamic or electrocardiographic abnormalities
— id: 69765, year: 1994, vol: 32, page: 731, stat: Journal Article,

Accuracy and utility of differential white blood cell count in the neonatal intensive care unit
Charache, S; Nelson, L; Saw, D; Keyser, E; Wingfield, S
1992 Mar;97(3):338-344, American journal of clinical pathology
The clinical utility of the complete blood cell count (including the differential white blood cell count) as a means to follow the course of infants in a neonatal intensive care unit was assessed. Utility was judged for three purposes: (1) predicting the onset of clinically unrecognized disease, (2) assessing the severity of current disease, and (3) following a trend during treatment. Neither conventional nor automated differential counts were useful for surveillance (predicting the onset of clinically unrecognized disease). The white blood cell count, the platelet count, and the absolute immature neutrophil count and immature/total neutrophil ratio were useful to assess the severity of current clinical events. The white blood cell count was superior to the differential count for following trends in patients' conditions. Information regarding nuclear immaturity derived from automated counts and the cost and slowness of the manual differential count are good indications for decreased use of conventional counts, increased use of certain features of the automated differential, or both, in neonatal intensive care units
— id: 145501, year: 1992, vol: 97, page: 338, stat: Journal Article,