Heikki Nikkanen
Harvard University
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Annals of Emergency Medicine | 1998
Heikki Nikkanen; Claude Pouges; Lenworth M. Jacobs
The Essonne region of France is situated to the south of Paris. A population of more than 1 million, heavy commercial traffic, and industrial centers mandate first-rate prehospital and hospital emergency medicine. Medical education in France comprises 3 years of basic medical science, followed by 3 years of hospital rotations and a residency of variable length. Emergency medicine is struggling for recognition as a specialty. The ED at the hospital center in Corbeil-Essonnes, France, has 21,000 visits per year, accounting for 30% of hospital admissions. The physical plant is modern and well-organized, with 13 beds. Attention is paid to quality improvement. Prehospital emergency care also receives due attention. A two-tiered system of BLS ambulances run by the fire department and ALS ambulances run by hospitals provide 24-hour emergency coverage. Because of aggressive triage, only 65% of requests for service result in dispatch of an ambulance. Tasks for physicians involved in emergency medicine in France today include further development of firemens medical skills, development and use of telemedicine, and accreditation of emergency medicine as a recognized specialty.
Journal of Emergency Medicine | 2011
Michael Levine; Heikki Nikkanen; Daniel J. Pallin
BACKGROUND Digoxin is an inhibitor of the sodium-potassium ATPase. In overdose, hyperkalemia is common. Although hyperkalemia is often treated with intravenous calcium, it is traditionally contraindicated in digoxin toxicity. OBJECTIVES To analyze records from patients treated with intravenous calcium while digoxin-toxic. METHODS We reviewed the charts of all adult patients diagnosed with digoxin toxicity in a large teaching hospital over 17.5 years. The main outcome measures were frequency of life-threatening dysrhythmia within 1 h of calcium administration, and mortality rate in patients who did vs. patients who did not receive intravenous calcium. We use multivariate logistic regression to ensure that no relationship was overlooked due to negative confounders (controlling for age, creatinine, systolic blood pressure, peak serum potassium, time of development of digoxin toxicity, and digoxin concentration). RESULTS We identified 161 patients diagnosed with digoxin toxicity, and were able to retrieve 159 records. Of these, 23 patients received calcium. No life-threatening dysrhythmias occurred within 1 h of calcium administration. Mortality was similar among those who did not receive calcium (27/136, 20%) compared to those who did (5/23, 22%). In the multivariate analysis, calcium was non-significantly associated with decreased odds of death (odds ratio 0.76; 95% confidence interval [CI] 0.24-2.5). Each 1 mEq/L rise in serum potassium concentration was associated with an increased mortality odds ratio of 1.5 (95% CI 1.0-2.3). CONCLUSION Among digoxin-intoxicated humans, intravenous calcium does not seem to cause malignant dysrhythmias or increase mortality. We found no support for the historical belief that calcium administration is contraindicated in digoxin-toxic patients.
Journal of Emergency Medicine | 2002
Heikki Nikkanen; David F.M. Brown; Eric S. Nadel
A complete Works Cited list begins on page 63. Mention of commercial products does not indicate endorsement. Faculty Mark Rose, BS, MA, is a licensed psychologist and researcher in the field of alcoholism and drug addiction based in Minnesota. He has written or contributed to the authorship of numerous papers on addiction and other medical disorders and has written books on prescription opioids and alcoholism published by the Hazelden Foundation. He also serves as an Expert Advisor and Expert Witness to various law firms on matters related to substance abuse, is on the Board of Directors of the Minneapolis-based International Institute of Anti-Aging Medicine, and is a member of several professional organizations.
Pediatric Emergency Care | 2009
Mathew George; Nadeem Al-Duaij; Heikki Nikkanen; Michele Burns Ewald
To the Editors: The Mrvos and Krenzelok 1 article published in October 2007, which reviewed the impact of legislation on decreasing the frequency of adverse effects of mouthwash exposures in children, highlights an incredibly important poisoning prevention message. When analyzing the various public health initiatives undertaken for pharmaceutical agents, the 1970 Poison Prevention Packaging Act and, specifically, the 1995 Consumer Product Safety Commission legislation requiring child-resistant packaging for mouthwashes containing 3 g or more of ethanol, have certainly been significant in averting unintentional exposures in the pediatric population. The annual reports of the American Association of Poison Control Centers denote a reduction in the incidence of exposures between 2005 and 2006 as evidenced by 14,947 and 13,303 documented events, respectively. However, in light of recent aggressive advertising initiatives such as McNeil’s BHealthy Mouth, Healthy Body[ campaign and the American Dental Association’s increased focus on oral hygiene as well as the commercial product’s claim of the coveted BAmerican Dental Association seal of acceptance,[we foresee a persistent risk of exposures in the pediatric patient population given the continued availability of such products. Furthermore, many of the commercial mouthwash agents are marketed in bottles that have volumes as large as 2 L. Because of their small body mass and limited glycogen reserves, infants and toddlers are at a heightened risk of adverse effects from these ethanolbased mouthwash products. A recent case seen at the Children’s Hospital Boston readily illustrates this principle. A 3-year-oldmale, with an unremarkable medical history, was brought to our emergency department by his parents after they had noticed decreased responsiveness after he was thought to have ingested 200 to 300 mL of Listerine Antiseptic Mouthwash (21.6% ethyl alcohol). By report, the mother had found the child next to the halfempty 1-L bottle; no other coingestants were known. Although the patient had vomited several times and became lethargic immediately after the ingestion, the family believed that the product was safe and that these symptoms were only transient. He had otherwise been well that day, had no history of fevers, and no history of seizures, crampy abdominal pain, or head trauma. Approximately 6 to 8 hours later, the patient was found unresponsive in his crib and was immediately taken to our facility. In the emergency department, the bedside glucose was measured at 4 mg/dL, and the nadir serum bicarbonate concentration was 7 mEq/L. A medication history did not reveal any other medications in the home that could cause hypoglycemia (insulin, sulfonylureas,A-blockers, quinine, and/or salicylates). His Glasgow Coma Scale was 8 and his vital signs were within normal limits. The initial anion gap and osmolal gap were 28 mEq/L and 24mOsm/L, respectively. The phenolic component in Listerine may have contributed to this increased osmolal gap. His urine toxicology screen for drugs of abuse was negative. Both the patient’s mental status and blood glucose rapidly improved after a dextrose bolus; his repeat blood glucose rose to 285 mg/dL. However, shortly after the dextrose bolus was complete, the patient developed intermittent episodes of agitation and startle reaction. Another glucose was obtained and found to be 67 mg/dL, likely due to insulin release with subsequent hypoglycemia. The ethanol level 12 hours after the ingestion was 41 mg/dL. Thus, he was placed on a dextrose infusion and was admitted to the intensive care unit for serial examinations and close monitoring of his glucose and electrolyte parameters. A social work consult was obtained to review safety initiatives in the home, and the following day, the patient was medically cleared and discharged to home with no neurological sequelae. This case clearly illustrates the dangers of marketing large containers of ethanol-containing mouthwashes. The lethal dose of ethanol in a child is estimated at 3 g/kg. The approximate dose our patient ingested ranged from 2.8 g/kg to 4.3 g/kg. The implementation of effective injury prevention policies could help prevent numerous intoxications and reduce the financial burden on our health care system as the cost of each hospitalization due to a toxicologic cause is not insignificant. Such policies should not be restricted to limiting the volume of containers or adding exact dosage dispensers to bottles but, more importantly, should focus on removing ethanol from those products altogether. Indeed, ethanol is a nonessential component of mouthwash and has long been substituted by safer agents outside the United States. This more meaningful intervention would not only help alleviate the potential toxicological burden in the pediatric age groups, but would also reduce the risk of ethanol abuse in the substance abusing populations; both endeavors would be of great benefit to public health overall.
Pediatrics | 2004
Heikki Nikkanen; Michele M. Burns
Journal of Trauma-injury Infection and Critical Care | 1996
David L. Ciraulo; Heikki Nikkanen; Marc Palter; Stuart K. Markowitz; Sheryl G. A. Gabram; Vernon L. Cowell; Stephen Luk; Lenworth M. Jacobs
Emergency medicine practice | 2011
Heikki Nikkanen; Aaron Skolnik
Journal of Emergency Medicine | 2006
Michael Levine; Heikki Nikkanen; Eric S. Nadel; David F.M. Brown
Journal of Emergency Medicine | 2010
Amit Gupta; Mark Su; Howard A. Greller; Nima Majlesi; Robert S. Hoffman; Michael Levine; Heikki Nikkanen; Daniel J. Pallin
Journal of Emergency Medicine | 2010
Michael Levine; Heikki Nikkanen; Daniel J. Pallin