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Biomedical subjects

Lewis S Nelson

Publications and source records attributed to Lewis S Nelson.

At least 55 records · Page 3Linked to original sources
PubMed2003

Efficacy of Crotalidae polyvalent antivenin for the treatment of hognosed viper (Porthidium nasutum) envenomation.

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.

Adult↗
PubMed2003

Cardioactive steroid poisoning from an herbal cleansing preparation.

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.

Adult↗
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

A fatal case of spongiform leukoencephalopathy linked to "chasing the dragon".

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.

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↗
PubMed2003

Status epilepticus from an illegally imported Chinese rodenticide: "tetramine".

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.

Bridged-Ring Compounds↗
PubMed2003

The resurgence and abuse of heroin by children in the United States.

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.

Child↗
PubMed2003

Amiodarone attenuates fluoride-induced hyperkalemia in vitro.

UNLABELLED: 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.

Amiodarone↗
PubMed2003

Fatality from administration of labetalol and crushed extended-release nifedipine.

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.

Administration, Intranasal↗
PubMed2003

Alpha-methyltryptamine revisited via easy Internet access.

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.

Adolescent↗
PubMed2002

Pediatric and young adult exposure to chemiluminescent glow sticks.

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.

Adolescent↗
PubMed2002

Use of ferric chloride to identify salicylate-containing poisons.

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

Chemistry, Pharmaceutical↗
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↗