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Biomedical subjects

Stephen J Traub

Publications and source records attributed to Stephen J Traub.

9 recordsLinked to original sources
PubMed2003

Pediatric "body packing".

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.

Adolescent↗
PubMed2003

Ephedrine-induced cardiac ischemia: exposure confirmed with a serum level.

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.

Adult↗
PubMed2003

Acute topiramate toxicity.

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.

Acute Disease↗
PubMed2002

Physostigmine as a treatment for gamma-hydroxybutyrate toxicity: a review.

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.

Cholinesterase Inhibitors↗
PubMed2002

The "ecstasy" hangover: hyponatremia due to 3,4-methylenedioxymethamphetamine.

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.

Adult↗
PubMed2002

Case report and literature review of chlorine gas toxicity.

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.

Adolescent↗