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Effect of deferoxamine on late deaths following CPR in rats
cent series in either emergency or general medicine literature have been reported on this topic. The purpose of this investigation was to review our experience with 12 patients presenting to the ED b e t w e e n 1978 and 1984 w i t h black w i d o w spider envenomation severe enough to warrant admission. We sought to establish the frequency of presenting signs and symptoms to the ED, to define the role of laboratory and radiographic studies in the ED, and to evaluate the effectiveness of drug therapies. We found no statistically significant relationship between site of envenomati0n and presenting symptom complex. Abdominal pain and bite site pain were present in 67% of patients; 50% had lower extremity pain. Lesions at the bite site were noted in 75% and abdominal tenderness noted in 67%. ED laboratory and radiographic Studies were performed in 8 of 12 patients with 5 patients having normal findings; 3 patients had nonspecific findings. A wide variety of drugs, including calcium gluconate (83%), muscle relaxants (42%), narcotics [42% ), steroids (17%), and antivenom (58%) were used with 2 complications noted: 1 episode of nausea and vomiting following excessive calcium gluconate administration, and 1 episode of serum sickness. There was uniformly excellent clinical outcome regardless of the therapies used, and statistical analysis (Fischer's exact test) showed no sig nificant association between any of the above therapies and complications. This review suggests 1) that there was no difference in presentation between upper and lower extremity envenomation with the majority of patients presenting with bite site pain, abdominal pain and tenderness, and lower extremity pain; 2) that laboratory and radiographic studies do not facilitate ED evaluation of black widow spider envenomation; and 3) that with uniformly excellent clinical outcome, only symptomatic therapy would seem justified. The use of antivenom in L a t r o d e c t u s m a c t a n s envenomation did not correlate with improved patient outcome, was associated with the complication Of serum sickness, and would appear unwarranted.
1
Nine-Year Evaluation of Emergency Department Personnel Exposure to ionizing Radiation
RE Grazer, HW Meislin, BR Westerman, EA Criss / Section of Emergency Medicine, University of Arizona Health Sciences Center, Tucson ED personnel experience potential OCCUpational hazards from exposure to ionizing radiation. This exposure occurs while working in the ED and/or while supervising patients in the x-ray and fluoroscopy suites. To assess the risk, a retrospective study was done analyzing ionizing radiation exposure over a 9-year period for 134 ED personnel. The group consisted of 21 physicians [(15.6%) for years 1982-1984], 92 nurses [(68.7%) for years 1975-1984], and 21 a n c i l l a r y p e r s o n n e l [(15.6%) for years 1975-1984]. Exposur e was measured for both penetrating and nonpenetrating radiation using standard film dosimeter badges. These badges were collected by the radiation safety department and read on a monthly basis; a m i n i m u m of 5 mrem dosage was required to effect a measurable reading. Compliance with film reading was 66.7% for phySicians, 86.2% for nurses, and 86.7% for ancillary personnel. Penetrating radiation exposure averaged 0.116 mrem per month for physicians, 0.703 mrem per month for nurses, and 0 mrem per month for ancillary personnel. Only 1 person had any measurable reading for nonpenetrating radiation, and that was believed to have been registered outside the ED. The average annual dose from exposure to natural, background radiation is on the order of 100-200 mrem. Thus it is concluded that 1) if standard radiation precautions are taken, the occupational risk from ionizing radiation exposure to personnel in the ED is minimal, and 2) that routine monitoring of radiation exposure of ED persovmel is unnecessary.
2
Cardiac Arrest and Resuscitation: Brain Iron Delocalization During Reperfusion
GS Krause, KM Joyce, NR Nayini, CL Zonia, AM Garritano, 14:5 May 1985
TJ Hoehner, AT Evans, RJ Indreri, SD Aust, BC White / Section of Emergency Medicine, Departments of Medicine and Biochemistry, College of Human Medicine, and College of Veterinary Medicine, Michigan State University, East Lansing; Department of Anesthesiology, Sinai Hospital of Detroit, Detroit It is our hypothesis that brain injury after resuscitation from cardiac arrest occurs during reperfusion and is in part mediated by iron-dependent lipid peroxidation. This study was undertaken to examine the time course of brain iron delocalization and lipid peroxidation in an animal model of cardiac arrest and resuscitation. Assays for brain tissue iron i n low molecular weight species (LMWS iron) utilized the o-phenanthroline test on an ultrafiltered tissue sample; malondialdehyde (MDA) in brain tissue was assayed by the thiobarbituric acid test. The data were examined statistically by the method of multivariance. Samples of the parietal cortex from 9 nonischemic control dogs (Group 1) had LMWS iron levels (in nm/100 mg tissue) of 9.6 + 3.8 and MDA levels (in nm/100 mg tissue) of 7.7 + 1.4. Samples of the parietal cortex taken from 5 dogs after 15 minutes of cardiac arrest without resuscitation (Group 2) had LMWS iron levels of 9.3 + 3.1 and MDA levels of 5.9 + 1.1. There is no significant difference in these values between Group 1 and Group 2. Five dogs were subjected to 15 minutes of cardiac arrest and definitive resuscitation by internal cardiac massage and defibrillation (Group 3). Following resuscitation, the chest was closed and the dogs were given intensive care for 2 hours. At two hours following resuscitation, samples of the parietal cortex had LMWS iron levels of 37.0 + 4.6 (P against both Group 1 and Group 2 < .01) and MDA levels of 12.2 _+ 1.9 (P against both Group 1 and Group 2 < .05). We conclude that brain lipid peroxidation does not occur during complete global brain ischemia, but it is evident after 2 hours of reperfusion. This is associated with concomitant increases in brain LMWS iron levels during reperfusion. Brain LMWS iron levels are not significantly elevated during complete global ischemia. Lipid peroxidation and LMWS iron delocalization in the brain is a reperfusion injury phenomenon that may be amenable to treatment with an iron chelator such as deferoxamine.
3
Effect of Deferoxamine on Late Deaths Following CPR in Rats
SD Kompala, CF Babbs / Biomedical Engineering Center, Purdue University, West Lafayette, Indiana Recent work by White et al indicates that free iron radicals, liberated intracellularly from bound sites, catalyze lipid peroxidation reactions that are responsible for continuing cell injury days after cardiac arrest and CPR, especially in the lipid-rich brain. If iron is the causative factor, an iron chelator given after cardiac resuscitation may reduce subsequent brain damage and improve outcome. We studied the effect of the iron chelator deferoxamine on survival in rats with experimentally induced cardiac arrest. The experimental model consisted of cold KC1 (1% 0.8 ml IC) induced cardiac arrest for 6 rain in healthy, ketamine-anesthetized rats, followed by 1 to 4 min of CPR. A single injection of deferoxamine (50 mg/kg IV) was given 5 min after successful resuscitation. In our study with 25 rats in the control group and 25 rats in the deferoxamine-treated group, survival was similar in both groups up to 48 h after arrest. At the end of 10 days, however, there was 64% survival in the deferoxamine-treated group vs 36% survival in the control group, a statistically significant difference (chi square = 3.92;df = 1;P < .05). Thus deferoxamine prevented late deaths. This model of complete circulatory arrest and resuscitation in intact animals demonstrates the potential usefulness of deferoxamine in brain resuscitation.
4
Effects of Carbon Dioxide, Lidoflazine, and Deferoxamine Administered After Cardiorespiratory Arrest and CPR in Rats
SF Badylak, CF Babbs / Biomedical Engineering Center, Purdue University, West Lafayette, Indiana
Annals of Emergency Medicine
509/189
1
Nine-Year Evaluation of Emergency Department Personnel Exposure to ionizing Radiation
RE Grazer, HW Meislin, BR Westerman, EA Criss / Section of Emergency Medicine, University of Arizona Health Sciences Center, Tucson ED personnel experience potential OCCUpational hazards from exposure to ionizing radiation. This exposure occurs while working in the ED and/or while supervising patients in the x-ray and fluoroscopy suites. To assess the risk, a retrospective study was done analyzing ionizing radiation exposure over a 9-year period for 134 ED personnel. The group consisted of 21 physicians [(15.6%) for years 1982-1984], 92 nurses [(68.7%) for years 1975-1984], and 21 a n c i l l a r y p e r s o n n e l [(15.6%) for years 1975-1984]. Exposur e was measured for both penetrating and nonpenetrating radiation using standard film dosimeter badges. These badges were collected by the radiation safety department and read on a monthly basis; a m i n i m u m of 5 mrem dosage was required to effect a measurable reading. Compliance with film reading was 66.7% for phySicians, 86.2% for nurses, and 86.7% for ancillary personnel. Penetrating radiation exposure averaged 0.116 mrem per month for physicians, 0.703 mrem per month for nurses, and 0 mrem per month for ancillary personnel. Only 1 person had any measurable reading for nonpenetrating radiation, and that was believed to have been registered outside the ED. The average annual dose from exposure to natural, background radiation is on the order of 100-200 mrem. Thus it is concluded that 1) if standard radiation precautions are taken, the occupational risk from ionizing radiation exposure to personnel in the ED is minimal, and 2) that routine monitoring of radiation exposure of ED persovmel is unnecessary.
2
Cardiac Arrest and Resuscitation: Brain Iron Delocalization During Reperfusion
GS Krause, KM Joyce, NR Nayini, CL Zonia, AM Garritano, 14:5 May 1985
TJ Hoehner, AT Evans, RJ Indreri, SD Aust, BC White / Section of Emergency Medicine, Departments of Medicine and Biochemistry, College of Human Medicine, and College of Veterinary Medicine, Michigan State University, East Lansing; Department of Anesthesiology, Sinai Hospital of Detroit, Detroit It is our hypothesis that brain injury after resuscitation from cardiac arrest occurs during reperfusion and is in part mediated by iron-dependent lipid peroxidation. This study was undertaken to examine the time course of brain iron delocalization and lipid peroxidation in an animal model of cardiac arrest and resuscitation. Assays for brain tissue iron i n low molecular weight species (LMWS iron) utilized the o-phenanthroline test on an ultrafiltered tissue sample; malondialdehyde (MDA) in brain tissue was assayed by the thiobarbituric acid test. The data were examined statistically by the method of multivariance. Samples of the parietal cortex from 9 nonischemic control dogs (Group 1) had LMWS iron levels (in nm/100 mg tissue) of 9.6 + 3.8 and MDA levels (in nm/100 mg tissue) of 7.7 + 1.4. Samples of the parietal cortex taken from 5 dogs after 15 minutes of cardiac arrest without resuscitation (Group 2) had LMWS iron levels of 9.3 + 3.1 and MDA levels of 5.9 + 1.1. There is no significant difference in these values between Group 1 and Group 2. Five dogs were subjected to 15 minutes of cardiac arrest and definitive resuscitation by internal cardiac massage and defibrillation (Group 3). Following resuscitation, the chest was closed and the dogs were given intensive care for 2 hours. At two hours following resuscitation, samples of the parietal cortex had LMWS iron levels of 37.0 + 4.6 (P against both Group 1 and Group 2 < .01) and MDA levels of 12.2 _+ 1.9 (P against both Group 1 and Group 2 < .05). We conclude that brain lipid peroxidation does not occur during complete global brain ischemia, but it is evident after 2 hours of reperfusion. This is associated with concomitant increases in brain LMWS iron levels during reperfusion. Brain LMWS iron levels are not significantly elevated during complete global ischemia. Lipid peroxidation and LMWS iron delocalization in the brain is a reperfusion injury phenomenon that may be amenable to treatment with an iron chelator such as deferoxamine.
3
Effect of Deferoxamine on Late Deaths Following CPR in Rats
SD Kompala, CF Babbs / Biomedical Engineering Center, Purdue University, West Lafayette, Indiana Recent work by White et al indicates that free iron radicals, liberated intracellularly from bound sites, catalyze lipid peroxidation reactions that are responsible for continuing cell injury days after cardiac arrest and CPR, especially in the lipid-rich brain. If iron is the causative factor, an iron chelator given after cardiac resuscitation may reduce subsequent brain damage and improve outcome. We studied the effect of the iron chelator deferoxamine on survival in rats with experimentally induced cardiac arrest. The experimental model consisted of cold KC1 (1% 0.8 ml IC) induced cardiac arrest for 6 rain in healthy, ketamine-anesthetized rats, followed by 1 to 4 min of CPR. A single injection of deferoxamine (50 mg/kg IV) was given 5 min after successful resuscitation. In our study with 25 rats in the control group and 25 rats in the deferoxamine-treated group, survival was similar in both groups up to 48 h after arrest. At the end of 10 days, however, there was 64% survival in the deferoxamine-treated group vs 36% survival in the control group, a statistically significant difference (chi square = 3.92;df = 1;P < .05). Thus deferoxamine prevented late deaths. This model of complete circulatory arrest and resuscitation in intact animals demonstrates the potential usefulness of deferoxamine in brain resuscitation.
4
Effects of Carbon Dioxide, Lidoflazine, and Deferoxamine Administered After Cardiorespiratory Arrest and CPR in Rats
SF Badylak, CF Babbs / Biomedical Engineering Center, Purdue University, West Lafayette, Indiana
Annals of Emergency Medicine
509/189