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E P Krenzelok

Publications and source records attributed to E P Krenzelok.

At least 19 recordsLinked to original sources
PubMed2005

Position paper: Single-dose activated charcoal.

Single-dose activated charcoal therapy involves the oral administration or instillation by nasogastric tube of an aqueous preparation of activated charcoal after the ingestion of a poison. Volunteer studies demonstrate that the effectiveness of activated charcoal decreases with time. Data using at least 50 g of activated charcoal, showed a mean reduction in absorption of 47.3%, 40.07%, 16.5% and 21.13%, when activated charcoal was administered at 30 minutes, 60 minutes, 120 minutes and 180 minutes, respectively, after dosing. There are no satisfactorily designed clinical studies assessing benefit from single-dose activated charcoal to guide the use of this therapy. Single-dose activated charcoal should not be administered routinely in the management of poisoned patients. Based on volunteer studies, the administration of activated charcoal may be considered if a patient has ingested a potentially toxic amount of a poison (which is known to be adsorbed to charcoal) up to one hour previously. Although volunteer studies demonstrate that the reduction of drug absorption decreases to values of questionable clinical importance when charcoal is administered at times greater than one hour, the potential for benefit after one hour cannot be excluded. There is no evidence that the administration of activated charcoal improves clinical outcome. Unless a patient has an intact or protected airway, the administration of charcoal is contraindicated. A review of the literature since the preparation of the 1997 Single-dose Activated Charcoal Position Statement revealed no new evidence that would require a revision of the conclusions of the Statement.

Adsorption↗
PubMed2004

Position Paper on urine alkalinization.

This Position Paper was prepared using the methodology agreed by the American Academy of Clinical Toxicology (AACT) and the European Association of Poisons Centres and Clinical Toxicologists (EAPCCT). All relevant scientific literature was identified and reviewed critically by acknowledged experts using set criteria. Well-conducted clinical and experimental studies were given precedence over anecdotal case reports and abstracts were not considered. A draft Position Paper was then produced and presented at the North American Congress of Clinical Toxicology in October 2001 and at the EAPCCT Congress in May 2002 to allow participants to comment on the draft after which a revised draft was produced. The Position Paper was subjected to detailed peer review by an international group of clinical toxicologists chosen by the AACT and the EAPCCT, and a final draft was approved by the boards of the two societies. The Position Paper includes a summary statement (Position Statement) for ease of use, which will also be published separately, as well as the detailed scientific evidence on which the conclusions of the Position Paper are based. Urine alkalinization is a treatment regimen that increases poison elimination by the administration of intravenous sodium bicarbonate to produce urine with a pH > or = 7.5. The term urine alkalinization emphasizes that urine pH manipulation rather than a diuresis is the prime objective of treatment; the terms forced alkaline diuresis and alkaline diuresis should therefore be discontinued. Urine alkalinization increases the urine elimination of chlorpropamide, 2,4-dichlorophenoxyacetic acid, diflunisal, fluoride, mecoprop, methotrexate, phenobarbital, and salicylate. Based on volunteer and clinical studies, urine alkalinization should be considered as first line treatment for patients with moderately severe salicylate poisoning who do not meet the criteria for hemodialysis. Urine alkalinization cannot be recommended as first line treatment in cases of phenobarbital poisoning as multiple-dose activated charcoal is superior. Supportive care, including the infusion of dextrose, is invariably adequate in chlorpropamide poisoning. A substantial diuresis is required in addition to urine alkalinization in the chlorophenoxy herbicides, 2,4-dichlorophenoxyacetic acid, and mecoprop, if clinically important herbicide elimination is to be achieved. Volunteer studies strongly suggest that urine alkalinization increases fluoride elimination, but this is yet to be confirmed in clinical studies. Although urine alkalinization is employed clinically in methotrexate toxicity, currently there is only one study that supports its use. Urine alkalinization enhances diflunisal excretion, but this technique is unlikely to be of value in diflunisal poisoning. In conclusion, urine alkalinization should be considered first line treatment in patients with moderately severe salicylate poisoning who do not meet the criteria for hemodialysis. Urine alkalinization and high urine flow (approximately 600 mL/h) should also be considered in patients with severe 2,4-dichlorophenoxyacetic acid and mecoprop poisoning. Administration of bicarbonate to alkalinize the urine results in alkalemia (an increase in blood pH or reduction in its hydrogen ion concentration); pH values approaching 7.70 have been recorded. Hypokalemia is the most common complication but can be corrected by giving potassium supplements. Alkalotic tetany occurs occasionally, but hypocalcemia is rare. There is no evidence to suggest that relatively short-duration alkalemia (more than a few hours) poses a risk to life in normal individuals or in those with coronary and cerebral arterial disease.

Alkalies↗
PubMed2004

Mass sociogenic illness--real and imaginary.

Mass sociogenic illness is the occurrence of a group of nonspecific physical symptoms for which no organic cause can be determined and is often transmitted by 'line of sight'. The fear of bioterrorism can also lead to panic and produce cases of mass sociogenic illness, in which people develop symptoms in response to an imaginary threat. Poison centers are faced with resolving the dilemma of sociogenic vs poison related symptoms. We report 2 situations of mass sociogenic illnesses involving school age children where multiple victims exhibited similar symptoms prompted by the presence or suggestion of fumes. Symptoms resolved spontaneously. When clusters of unexplained illness occur, a sociogenic etiology should be considered in the differential diagnosis. As fears about bioterrorism increase, the frequency of such incidents and the anxiety generated may increase.

Child↗
PubMed2003

Acute hepatitis induced by kava kava.

BACKGROUND: Herbal preparations are available widely and regarded generally by the public as harmless remedies for a variety of medical ailments. We report a case of acute hepatitis associated with the use of kava kava, derived from the root of the pepper plant, Piper methysticum. It is used in the United States as an antianxiety and sedative agent. CASE REPORT: A previously healthy 14-year-old female was admitted to the hospital with hepatic failure. Initial therapy, including plasmapheresis, was unsuccessful and she deteriorated. She ultimately required a liver transplant and now remains well. The liver biopsy showed hepatocellular necrosis consistent with chemical hepatitis. A work-up for alternative causes of liver failure was negative. The patient gave a history of taking a kava kava-containing product for four months. The use of kava kava and liver failure, is supported by kava kava use, a negative work-up for alternative causes of liver failure, and histological changes in the liver. CONCLUSIONS: Health care professionals need to be aware of the possibility of kava kava-induced hepatotoxicity. The toxicity of these alternative remedies emphasizes the importance of surveillance programs and quality control in the manufacture of these products. Clinicians must remain aware of the toxic potential of herbal products and always inquire about their intake in cases of unexplained liver injury.

Adolescent↗
PubMed2001

Surveillance for carbon monoxide poisoning using a national media clipping service.

Using a novel method to review carbon monoxide (CO) exposures in the US, the role of CO detectors in prevention of CO-related deaths was studied. Using a national media clipping service, CO poisonings reported in the US were analyzed. The impact of CO detectors was investigated through nonfatal outcomes attributable to the presence of CO detectors and case fatality rate comparison among cities with and without CO detector ordinances. There were 4,564 CO exposures resulting in 406 (8.9%) fatalities. Of the exposures 2,617 (57.3%) occurred in the home, accounting for 374 (92.1%) deaths. Faulty heating systems constituted 2,540 (55.6%) exposures and 186 (45.8%) deaths, with alternate heating sources responsible for 389 (8.5%) exposures and 104 (25.6%) deaths. Cities with CO detector ordinances showed lower case fatality rates as reported in the media than those cities without ordinances (P <.001). There were 1,008 (24.2%) survivors who attributed their survival to the presence of a CO detector. A media clipping service provided insight into CO poisoning demographics. Despite its limitations, this tool may calibrate the positive impact of CO detectors on the prevention of CO-related deaths.

Carbon Monoxide Poisoning↗
PubMed2001

Human exposures to stinging caterpillar: Lophocampa caryae exposures.

The purpose of this project was to characterize the presentation and treatment associated with Lophocampa caryae caterpillar exposures. Three hundred sixty-five exposures to Lophocampa caryae managed by a certified regional poison information center over a 2-year period were analyzed. Pediatric exposures were responsible for 80% of the reports and 92.1% were dermal exposures, 7.5% oral, and 0.4% ocular. Dermal exposures with minimal symptoms were treated at home with the supportive measures of hair and spine removal, irrigation, antihistamine, and/or topical steroid administration. Symptom resolution occurred within 24 hours. Symptomatic patients with oral exposures and positive visualization of hairs or spines, were referred to an emergency department for medical evaluation and removal of the caterpillar hairs. Adult exposure and treatment patterns were similar to the pediatric exposures. Removal of the defensive guard hairs or spines is the primary treatment. Supportive care with irrigation, antihistamines, and/or corticosteroids can decrease the intensity of symptoms.

Adolescent↗
PubMed2001

Delayed life-threatening reaction to anthrax vaccine.

BACKGROUND: Anthrax is an acute infectious disease caused by the spore-forming bacterium Bacillus anthracis. Due to the current world threat of unpredictable biological terrorism, the Department of Defense has mandated the systematic vaccination of all US military personnel against this warfare agent. Many may experience al mild flu-like illness and soreness at the injection site, but systemic reactions are rare. CASE REPORT: We report a delayed and potentially serious life-threatening adverse reaction to anthrax vaccine. A previously healthy 34-year-old male was transported to the emergency department with dyspnea, diaphoresis, pallor, and urticarial wheals on his face, arms, and torso after the administration of the third dose of anthrax vaccine. All symptoms resolved after pharmacological intervention and the patient was discharged. Pharmaco-epidemiological data indicate that 30% of anthrax vaccine recipients experience mild local reactions. With large numbers of military personnel being vaccinated, emergency physicians may encounter more vaccine-related adverse reactions.

Adult↗
PubMed2001

Prolonged coma and loss of brainstem reflexes following amitriptyline overdose.

Severe tricyclic antidepressant (TCA) overdose is generally manifested by cardiovascular and/or central nervous system toxicity. Although the majority of patients who are comatose following these overdoses regain consciousness within 24 h, this case had 5-days of coma with associated loss of brainstem reflexes. Severe central nervous system depression can occur as a sole manifestation of TCA overdose without concomitant cardiovascular toxicity.

Adult↗
PubMed2001

Poison information centers save lives ... and money!

Poison information centers provide telephone advice on the treatment of poisonings to the lay public and medical professionals. In general, the services of a poison center are provided freely to the caller. However, poison center services are labor intensive and expensive since most poison centers utilize medical professionals to provide service and are available for consultation 24 hours/day. The failure of poison centers to produce revenue has made them vulnerable to closure. Poison centers provide a vital service to society by reducing morbidity and mortality. Often overlooked are the financial benefits of poison centers. By preventing unnecessary hospital admissions and by providing expert advice that may reduce the use of expensive antidotes and lengthy hospital admissions, poison centers save an estimated $6.50 for every dollar invested in their operation. The cost-effectiveness of poison centers is supported by a multitude of research. All entities that benefit from poison center services should assist in the financial support of poison centers.

Cost-Benefit Analysis↗
PubMed2001

The critical role of the Poison Center in the recognition, mitigation and management of biological and chemical terrorism.

Nuclear, biological and chemical (NBC) terrorism counter measures are a major priority with healthcare providers, municipalities, states and the federal government. Significant resources are being invested to enhance civilian domestic preparedness through training in anticipation of a NBC terroristic incident. The key to a successful response, in addition to education, is integration of efforts as well as thorough communication and understanding the role that each agency would play in an actual or impending NBC incident. In anticipation of a NBC event, a regional counter-terrorism task force was established in southwestern Pennsylvania to identify resources, establish responsibilities and coordinate the response to NBC terrorism. Members of the task force include first responders, hazmat, law enforcement (local, regional, national), government officials, health departments, the statewide emergency management agency and the regional poison information center. The poison center is one of several critical components of a regional counter-terrorism response force. It can conduct active and passive toxicosurveillance and identify sentinel events. To be responsive, the poison center staff must be knowledgeable about biological and chemical agents. The development of basic protocols and a standardized staff education program is essential. The use of the RaPID-T (R-recognition, P-protection, D-detection, T-triage/treatment) course can provide basic staff education for responding to this important but rare consultation to the poison center.

Bioterrorism↗
PubMed2001

Toxidromes associated with the most common plant ingestions.

Toxicology and botanical references describe a myriad of symptoms associated with the ingestion of plants. The symptoms are based largely on a limited number of case and anecdotal reports or the personal experience of authors: there is little consistency between and among the references. This project compiled a list of symptoms associated with common plant ingestions. Exposure data from the American Association of Poison Control Centers were queried to identify the 20 most commonly ingested plants and the most frequent symptoms associated with those ingestions; 768,284 plant exposures were analyzed and symptoms occurred in 53,081 patients. The 20 most frequently ingested plants accounted for 54.2% of the reported symptoms. Most plant ingestions were not associated with the development of symptoms.

Diagnosis, Differential↗
PubMed2000

Flumazenil reversal of carisoprodol (Soma) intoxication.

A 52-year-old woman presented with central nervous system depression and a Glasgow Coma Score of 9 secondary to ingestion of carisoprodol, a centrally acting muscle relaxant analgesic. After administration of i.v. flumazenil, the patient's neurologic status normalized and she required no further therapy. Carisoprodol and its active sedative-hypnotic metabolite, meprobamate, are gamma aminobutyric acid receptor indirect agonists with central nervous system chloride ion channel conduction effects similar to the benzodiazepines, thus making flumazenil a potentially useful antidote in toxic presentations.

Antidotes↗
PubMed2000

Transdermal drug delivery system exposure outcomes.

Transdermal drug delivery systems are increasingly popular, yet few data exist regarding medical outcomes after exposures. Using data collected through a Regional Poison Information System, this retrospective study identified 61 cases of transdermal drug delivery system exposures reported over a recent 5-year period. Exposure routes included dermal (48 patients), oral (10 patients), combined oral and dermal (one patient), parenteral use of gel residue (one patient), and combined oral and parenteral (one patient). Forty-four exposures (72%) were managed by home telephone consultation only. Eleven of 17 patients (18%) evaluated in health care facilities were admitted, including eight (13%) to intensive care units. Hospital admission correlated statistically with clonidine and fentanyl exposures, oral exposures, and drug abuse. Clonidine exposure also correlated statistically with intensive care admission. One fatality was recorded, and all other patients recovered uneventfully. Transdermal drug delivery system exposures are infrequently reported to our regional poison information center but are associated with a significant hospital use and admission rate.

Administration, Oral↗
PubMed2000

A profile of methylphenidate exposures.

INTRODUCTION: Methylphenidate is prescribed commonly for children with attention deficit hyperactivity disorder. An estimated 2.8% of US youths aged 5 to 18 years use it for the management of this disorder. Despite the widespread use of methylphenidate, the demographics and outcome of intentional and unintentional exposures to methylphenidate have not been described. METHODS: To profile human exposures to methylphenidate, a retrospective review of all reports to a certified regional poison information center during 1998 was conducted. Data analysis included patient demographics, reason for the exposure, dose ingested, clinical effects, and patient outcome. RESULTS: There were 113 methylphenidate human exposures. The following table summarizes the values for selected parameters that were investigated: [table in text] CONCLUSIONS: The majority of exposures in children < or = 12 years of age involved unintentional ingestion of a sibling's medication, self-administration of an excessive therapeutic dose, or the administration of an inadvertent dose given by a caregiver. Methylphenidate abuse was common among adolescents and adults. Regardless of the reason for the exposure, the amount ingested, or treatment, all exposures had a favorable outcome. Pediatric doses of less than 1 mg/kg were not associated with adverse events.

Adolescent↗
PubMed2000

Sildenafil: clinical toxicology profile.

BACKGROUND: Sildenafil is indicated for the treatment of male erectile dysfunction. It has been used successfully in males to remediate problems associated with impaired neural and/or hemodynamic response to sexual stimulation. Sildenafil is a cyclic guanosine-specific phosphodiesterase type 5 inhibitor that prevents the metabolism of cyclic guanosine which produces arterial smooth muscle relaxation within the corpora cavernosa of the penis and ultimately enhances penile tumescence. Inherent to its pharmacology, sildenafil produces mild decreases in systolic and diastolic blood pressure and an array of minimal side effects due to the inhibition of other types of phosphodiesterase. Drug interactions involving the concurrent use of sildenafil with nitrates and nitrites are well-documented and can produce profound hypotension leading to decreased coronary perfusion and myocardial infarction. Sildenafil is metabolized primarily by cytochrome P450 3A4, and inhibitors of this enzyme (e.g., macrolide antibiotics, antifungals, cimetidine) may increase sildenafil serum concentrations and lead to enhanced pharmacological and toxicological effects. The antiviral protease inhibitors have been demonstrated to inhibit first-pass metabolism and increase serum concentrations and half-life of sildenafil. DISCUSSION: Previously unpublished data from the American Association of Poison Control Centers Toxic Exposure Surveillance System indicate that unintentional pediatric exposures to sildenafil are unlikely to be associated with adverse effects. Adults may experience effects similar to those identified in the preclinical trials. This may be due to larger doses in this population, preexisting cardiovascular pathology, or the concomitant use of contraindicated medications.

Adolescent↗
PubMed2000

Multicenter case series of valproic acid ingestion: serum concentrations and toxicity.

BACKGROUND: Valproic acid exposures reported to poison centers have increased more than 4-fold over the last 5 years. There are no large case series published on valproic acid ingestion. METHODS: A prospective multicenter case series of all patients reporting an ingestion of valproic acid. Data collected included: age, gender, dose ingested, concomitant medications, symptoms and vital signs, laboratory values, length of hospital stay, and medical outcome. Entrance into the study required a serum valproic acid concentration above the therapeutic threshold of 100 microg/mL. Statistical analysis was by Fisher's exact test. RESULTS: A total of 335 patients were reported to participating centers of which 186 (55%) had serum valproic acid concentrations greater than 100 microg/mL. Of the 186 cases, 53 were multiple drug exposures leaving 133 cases of sole valproic acid ingestion for evaluation. Age ranged from 2 to 66 years with a mean of 30.1 years +/- 12. Peak serum valproic acid concentrations ranged from 110 microg/mL to 1840 microg/mL with a mean of 378.3 microg/mL +/- 310.2 microg/mL. Time from postingestion to the peak measured valproic acid concentration ranged from 1 to 18 hours, with a mean of 7.4 hours +/- 3.9. Symptoms included lethargy (n = 94), coma (n = 19), tachycardia (n = 24), aspiration (n = 8), metabolic acidosis (n = 8), and hypotension (n = 4). A peak concentration of > 450 microg/mL was more likely to be associated with a moderate or major adverse outcome (p < 0.005). A peak concentration > 850 microg/mL was more likely to be associated with coma (p < 0.005) and acidosis (p < 0.005). Eleven patients experienced transient thrombocytopenia (platelets < 150,000) and all had peak valproic acid concentrations >450 microg/mL. Four patients experienced transient leukopenia (WBC < 3,500). The mean hospital stay for all patients was 42 +/- 33.1 hours. A hospital stay > 48 hours was more likely to be associated with a peak valproic acid concentration > 450 microg/mL (p < 0.05). There were 2 fatalities. CONCLUSIONS: In this case series, patients with peak valproic acid concentrations above 450 microg/mL were more likely to develop significant clinical effects and have longer hospital stays. A peak valproic acid concentration above 850 microg/mL was more likely to be associated with coma, respiratory depression, aspiration, or metabolic acidosis.

Adolescent↗