Abstracts in this issue were prepared by residents in the Denver General/St Anthony's/St Joseph Hospitals Emergency Medicine Residency Program.

ABSTRACTS Harvey W Meislin, MD, FACEP Co-Editor Section of Emergency Medicine University of Arizona College of Medicine

Vincent J Markovchick, MD, FACEP Co-Editor Emergency Medical Services Denver General Hospital

ventricular fibrillation, resuscitation, dextrose

Dextrose containing intravenous fluid impairs outcome and increases death after eight minutes of card iac arrest and resusci tat ion in dogs D'Aiecy LG, Lundy EF, Barton K J, et al Surgery 100:505-511 Sep 1986

Ventricular fibrillation was induced in 12 anesthetized male mongrel dogs to determine the effect of physiologic quantities of 5% dextrose solution on the outcome of sur- vivable cardiac arrest. Following premedication with mor- phine, the dogs were anesthetized with halothane, instru- mented, intubated, and ventilated. Six dogs received 500 mL lactated Ringer's solution without dextrose (LR), and six dogs received 500 mL dextrose in lactated Ringer's solution (D5LR}. Blood glucose before cardiac arrest was 129 mg/dL in-LR dogs and 335 mg/dL in D5LR animals. After eight minutes of arrest, standard ACLS (modified for dogs) was undertaken until a stable cardiac rhythm was obtained. All six LR dogs survived, while five of the six D5LR dogs sur- vived the initial resuscitation. The resuscitation times and procedures did not differ. The dogs then were evaluated neurologically (scale: 0 = normal; 100 = dead) at one, two, six, and 24 hours post arrest. By two hours, the D5LR dogs had a significantly (P < .05) greater neurologic deficit than the LR dogs. By nine hours, four of six DSLR dogs displayed convulsive activity and died. It was concluded that the addi- tion of 5% dextrose to standard IV fluids greatly increased the mortality and morbidity associated with cardiac resusci- tation in this animal model. It is postulated that infusive glucose-containing IV fluids under conditions of hypoxia and ischemia may be deleterious due to increased lactic pro- duction, which may impede cellular metabolic processes.

Jeffrey Schaider, MD

nitrous oxide, concentrations

Environmenta l concentra t ions of nitrous oxide in amodular ambu lance Bristow A, Giesecke AH, Thai E, et al Crit Care Med 14:815-816 Sep 1986

Nitrous oxide (N20) has been used successfully as an an- algesic, but there has been no agreed upper limit of safe

environmental concentration. It has been suggested that N20 causes impaired coordina t ion , fetal wastage, teratogenesis, genetic abnormality, and various malignan- cies. A single study by Bruce and Bach, which had as its endpoint the minimum threshold for impaired coordina- tion, formed the basis of the recommendation by the Na- tional Institute for Occupational Safety and Health that no health care worker be exposed to time-weighed average N20 concentration of more than 25 ppm. The ambient N20 concentration in an ambulance was studied when the 50% mixture of N20 and oxygen gas was used as a self- administered analgesic. The patients were divided into two study groups. In the first group, both air conditioners in the ambulance were turned off, and the two back windows in the patient's compartment were opened. In the second group, the blower fans in the air conditioner were turned on to maximum. The window between the patient's compart- ment and the driver stayed open at all times. Use of the blower fan on the air conditioner reduced the N20 con- centrations from a range of 175 to 243 ppm to 39 to 56 ppm. It was concluded that the concentration of N20 can safely exceed the recommended maximum and that a blower fan on the air conditioner can significantly reduce the con- centration.

Nguyen Vo, MD

supraglottitis

Group A streptococcal supraglottitis Lacroix J, Ahronheim G, Arcand P, et al J Pediatr 109:20-24 Jul 1986

Four of 19 children admitted for epiglottitis secondary to Hemophilus influenzae were found to have a supraglottic infection secondary to group A [~-hemolytic streptococcus. The prodrome was longer than 24 hours, which is unusual in H influenzae-induced epiglottitis; the affected children were older, with a mean age of 6.2 years, as compared with a mean age of 3.8 years for H infhienzae-induced epiglot- titis. The primary site of inflammation was the supraglottic structures and not the epiglottis itself. Evidence of group A streptococcal infection was found in all four children, and none had evidence of H influenzae type b infection. The clinical course was much more protracted than that of epi- glottitis caused by H influenzae, and these children required intubation from 36 hours to 16 days. It is important to con- sider streptococcal supraglottitis in a child who presents with an "epiglottitis syndrome."

Pamela Downey, MD

16:1 January 1987 Annals of Emergency Medicine 129/175