Acute coronary syndrome and transient global amnesia with sumatriptan.

Triptans are potent serotoninergic vasoconstrictors. They are generally avoided in elderly patients age greater than 65 or in patients with a history of CAD. Although there are reported cases of Acute Coronary Syndrome (ACS) or Transient Global Amnesia (TGA) in patients after ingesting therapeutic doses of triptan or dihydroergotamine, this is the first case report, up to our knowledge, of a patient, who had no previous cardiac history, that was diagnosed with both ACS and TGA. A 59-year-old woman with a long-standing history of migraine, gastroesophageal reflux disease, and hypothyroidism, presented to the Emergency Department (ED) complaining of amnesia, chest pain, and left arm numbness after ingesting a single dose of oral sumatriptan approximately 1-2 h prior to arrival. She had no recollection of the events that occurred after taking sumatriptan. No acute laboratory abnormalities were found except for an elevated troponin, which continued to trend upwards. Her EKG had no ST-T wave abnormalities. She was diagnosed with Acute Coronary Syndrome (ACS), non-ST elevation MI. She had a negative noncontrast CT head. Neurology was consulted for her amnesia and diagnosed her with Transient Global Amnesia (TGA). They recommended discontinuing sumatriptan and beginning topiramate as a prophylactic therapy. There is an increasing number of reports delineating sumatriptan's adverse effects. Emergency medicine physicians should promptly recognize the toxic effects and adverse reactions from triptans. Sumatriptan-induced vasoconstriction may lead to cardiac and cerebral ischemic events.

A review of the existing literature on buprenorphine pharmacogenomics.

Buprenorphine is an effective treatment for opioid dependence; however, it demonstrates individual variability in efficacy. Pharmacogenomics may explain this drug response variability and could allow for tailored therapy on an individual basis. The Food and Drug Administration and the Clinical Pharmacogenomics Implementation Consortium have guidelines on pharmacogenomic testing for some opioids (e.g., codeine); however, no guidelines exist for the partial opioid agonist buprenorphine. Pharmacogenomic testing targets for buprenorphine include pharmacodynamic genes like the mu-opioid receptor (MOP receptor) and catechol-O-methyltransferase (COMT), as well as the pharmacokinetic genes like the CYP enzymes. In this review we identified genotypes in patients with opioid addiction receiving buprenorphine that may result in altered therapeutic dosing and increased rate of relapse. The OPRM1 A118G single nucleotide polymorphism (SNP rs1799971) gene variant encoding the N40D MOP receptor has been associated with variable efficacy and response to treatment in both adult and neonatal patients receiving buprenorphine for treatment of opioid withdrawal. An SNP associated with rs678849 of OPRD1, coding for the delta opioid receptor, was associated with opioid relapse as indicated by opioid positive urine drug screens; there was also sex specific SNP identified at rs581111 and rs529520 in the European American population. COMT variability, particularly in rs4680, has been associated with length of stay and need for opioid treatment in patients with neonatal abstinence syndrome. Variations of the pharmacokinetic gene for CYP3A4 showed that the ultrarapid metabolizer phenotype required higher doses of buprenorphine. Genotyping of patients may allow us to appropriately tailor buprenorphine therapy to individual patients and lead to improved patient outcomes; however, further research on the pharmacogenomics of buprenorphine is needed.

The Case of Flecainide Toxicity: What to Look for and How to Treat.

BACKGROUND: Flecainide is a class Ic antidysrhythmic agent used to prevent and treat both ventricular and supraventricular tachycardias, including atrial fibrillation, atrioventricular nodal re-entrant tachycardia, and Wolff-Parkinson-White syndrome. Flecainide can cause serious side effects, including cardiac arrest, dysrhythmias, and heart failure. Despite its growing use, the presenting signs and symptoms of flecainide toxicity are not familiar to most clinicians. In particular, our patient's particular presentation of acute kidney injury (AKI) resulting in flecainide accumulation is high risk for missed diagnosis in the emergency department. CASE REPORT: A 58-year-old woman presented with altered mental status and hypoxia that was later found to be secondary to sepsis. Medical history was notable for atrial fibrillation, for which she was on flecainide. Laboratory results were notable for hypokalemia and an AKI. Her wide complex tachycardia on admission was ultimately attributed to flecainide toxicity in the setting of AKI. Six days after presentation, it was found that her flecainide level was in the toxic range at 2.02 µg/mL (normal range 0.20-1.00 µg/mL, toxic >1.50 µg/mL). WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: Flecainide intoxication is rare but serious due to the potential for cardiogenic shock. Its diagnosis can be difficult, as the flecainide serum level may take days to result. This case demonstrates the necessity of keeping flecainide toxicity on the physician's differential for patients who are taking the drug, as well as what electrocardiogram findings suggest it as the etiology. Treatment can be lifesaving if initiated promptly.

Persistent effects after camphor ingestion: a case report and literature review.

BACKGROUND: Camphor is a well-known toxin responsible for thousands of poisonings per year. It can be found in many over-the-counter remedies and illegally imported substances. The toxidrome manifests within minutes and includes gastrointestinal, neurologic, pulmonary, and cardiac effects. Severe ingestions may progress to seizures, apnea, and coma. Most individuals are no longer symptomatic outside the 24-48 h window, but physiologic derangement may persist for far longer in some instances. CASE REPORT: This is a case report of a 25-year-old Guatemalan woman with no past medical history who ingested a cube of camphor for a facial rash. She presented to the Emergency Department with persistent delirium and headache 6 days after ingestion. She had a protracted recovery but returned to her baseline state of health 19 days after ingestion. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: Persistent toxic effects of camphor are not well described, and most sources state that the toxidrome resolves in 24-48 h. Given the frequency of camphor poisoning, it is crucial to increase public awareness of camphor toxicity, to understand the biological mechanism of the effects, and to develop more targeted treatments. From the emergency physician's perspective, it is important to realize that toxic effects of camphor poisoning may persist far beyond the 24-48 h window and require attention.

Which health care workers were most affected during the spring 2009 H1N1 pandemic?

OBJECTIVES: To identify health care workers most at risk for H1N1 infection before vaccination and compare health outcomes after vaccination. METHODS: The indices used to gauge employee health were laboratory-confirmed H1N1 data, laboratory-confirmed influenza A data, and employee sick hours records. In phase 1 of this 2-phase study, absenteeism records for 6,093 hospital employees before vaccine administration were analyzed according to department and employee position during the spring 2009 H1N1 pandemic. RESULTS: Records of 123 confirmed reports of laboratory-confirmed influenza A or novel H1N1 infections in hospital employees were also analyzed. Two thirds of the H1N1 cases occurred during June (infection rates in parentheses): 34 in physicians and medical personnel (6.7%), 36 in nurses and clinical technicians (2.2%), 39 in Administrative & Support Personnel (infection rate = 1.2%), 3 in Social Workers & Counselors (infection rate = 1.0%), 8 in Housekeeping & Food Services (infection rate = 2.7%), and 3 in Security & Transportation (infection rate=3.9%). When analyzed according to department, the adult emergency department (infection rate = 28.8%) and the pediatric emergency department (infection rate = 25.0%) had the highest infection rates per department. CONCLUSIONS: Of the reported cases of H1N1 in health care workers, 49% occurred in a population that constitutes less than 20% of the total population studied. Physicians and medical personnel had a higher infection rate than other employee positions, whereas ED personnel had the highest infection rate.