Robert S. Hoffman

Citalopram overdose: late presentation of torsades de pointes (TdP) with cardiac arrest.

IntroductionCitalopram 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 ReportA 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° F (37.3° 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.DiscussionCitalopram 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.

Status epilepticus from an illegally imported Chinese rodenticide: Tetramine

Abstract Introduction:u2002The 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:u2002A 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:u2002 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 γ‐aminobutyric acid (GABA) antagonism. The oral lethal dose 50% (LD50) in humans is estimated to be as low as 100 µg/kg. Our patient has severe diffuse cerebral dysfunction likely secondary to prolonged seizure activity after exposure to TETS.

Medicinal use of cocaine: A shifting paradigm over 25 years

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.

Endogenous Digitalis-like factors in hypothermic patients

1Division of Medical Toxicology, Ronald O. Perelman Department of Emergency Medicine, NYU School of Medicine, USA 2Tufts University School of Medicine, Baystate Medical Center, USA 3Fredericksburg Emergency Medical Alliance, USA 4Norwalk Hospital, Western Connecticut Health system, USA 5Department of Emergency Medicine, University of British Columbia, Canada 6College of Pharmacy and Health Sciences, St. John’s University, USA

Chapter 57 – Cocaine and Other Sympathomimetics

Cocaine, a naturally occurring plant-derived alkaloid, has been used for centuries as a medicinal product. For thousands of years in South America, the leaves of the coca plant (Erythroxylon coca) have been chewed for treatment of various ailments. In 1860, the pure alkaloid form was isolated and became a popular constituent of various beverages, pharmaceuticals, and therapeutic tonics, but it was banned from these products in the United States in 1914. At the peak of the cocaine epidemic in the early 1990s, it was estimated that 5 million people used cocaine regularly in the United States. The drug is still popular, with up to 1.6 million current users of cocaine reported as of 2009. This is a decrease from 2.3 million users in 2003, but the consequences of recreational cocaine use are still profound. Cocaine is implicated in violent deaths and was detected in 25% of autopsies of fatal injuries in adults aged 15 to 44 years. In 2009, 39% of drug misuse deaths were due to cocaine. According to the Drug Abuse Warning Network, there were more than 423,000 cocaine-related emergency department (ED) visits representing 52% of drug abuse or misuse cases. As of 2009, cocaine ranked within the top three causes of illicit drug–related deaths at various cities across the United States. Amphetamines are stimulants originally designed for use as decongestants and dietary aids that became popular as recreational drugs in the mid-20th century. By modification of the amphetamine molecule, illicit “designer” amphetamines are inexpensively produced. The enhanced effects from these alterations add to the popularity of drugs such as 3,4-methylenedioxymethamphetamine (MDMA) and methamphetamines. Cocaine, amphetamines, and derivatives of amphetamines are called sympathomimetics (Box 154-1). These agents cause central nervous system (CNS) stimulation and a cascade of adrenergic physiologic effects. As of 2009, there were 502,000 methamphetamine current users in the United States.