- Email: [email protected]
Prediction of survival from cardiopulmonary resuscitation by CPR instructors
CORRESPONDENCE
She developed a sore throat and then noted a rash that appeared first on her back and then involved her extremities. She was then seen in an urgent care center and was diagnosed with strep throat and was treated with an unknown antibiotic. About 4 weeks after her symptoms started, the patient was seen in our Dermatology clinic. On exam, she was found to have multiple erythematous plaques and round papules with a dusky/ darker center (targetoid appearance) on her dorsal hands, palms, dorsal feet, and knees. Additionally, she had many discrete 1-2 mm pink papules on her abdomen, proximal thighs, and proximal arms. She was diagnosed with EM, which was thought to be secondary to her prior strep throat. Over the next 9 weeks, the patient was seen in our ED 3 times, in our Dermatology clinic twice, and by an outside physician 3 times. Her complaints included fatigue; malaise; the persistent rash, which was now pruritic; fever; night sweats; hair loss; weight loss; sinus pain; and increasing posterior cervical lymphadenopathy. On exam, findings included an erythematous oral mucosa with erosions of the buccal mucosa and soft palate, a white coating on her tongue, mild posterior cervical lymphadenopathy, and EM, which the Dermatology consultants felt was continuing secondary to an unknown persistent stimuli. The rash became confluent with some lichenification on her elbows and knees and desquamation of her palms. On her last visit prior to coming to our office, she was noted to have splenomegaly and enlarged and erythematous tonsils. Prior to her visit to our office, laboratory studies revealed that her white blood cell count was 5.1 x 109/L with 56% lymphocytes. After approximately 5 weeks of symptoms, HIV serology was negative. Heterophile antibody, antinuclear antibody, and cold agglutinin were negative. A throat culture revealed methicillinsensitive Staphylococcus aureus which was treated with dicloxacillin. In our office, her temperature was 99.3°F, pulse was 80 beats/ min, and blood pressure was 98/55 mm/Hg. Her tonsils were enlarged and erythematous. She had diffuse cervical and occipital lymphadenopathy, normal cardiac and pulmonary exams, left upper quadrant tenderness, and a fading macular rash on her hands, elbows, and feet. HIV serology was positive with a HIV RNA (viral load) of 348,000 copies/mL. Cytomegalovirus (CMV) IgM and IgG also returned as positive. She was started on nelfinavir, zidovudine, and lamivudine, and after 2 weeks of this regimen, her HIV RNA had dropped to 1,455 copies/mL. Her symptoms had markedly improved. Overall she felt less tired, her rash faded, and her lymphadenopathy decreased significantly. She continued to do well and 2 years after her diagnosis, her CD4 count was 646 cells per mm3 and her HIV RNA was undetectable at less than 50 copies/mL. Although the majority of people with acute HIV infection are ill enough to seek medical attention, the constitutional symptoms are seen in many other illnesses and, as was the case with our patient, most patients are not correctly diagnosed at presentation.6 When acute HIV infection is suspected, a HIV RNA or p24 antigen test is needed to make the diagnosis as antibodies are undetectable in the early stages.7 Our patient’s HIV antibody was negative early in the course of her illness. What made our case most interesting was the fact that, along with many of the usual symptoms of acute HIV infection, she also presented with EM, which is not a characteristic feature of this illness. The most common skin manifestation of acute HIV infection is an erythematous nonpruritic, maculopapular rash affecting the face or trunk.3 The rash can appear on the palms and soles and can be generalized.3 The rash can also manifest as a roseola-like eruption, a vesicular, pustular exanthem or enanthem, or diffuse urticaria.3 However, our patient did not have any of these types of rashes. Rather, her rash consisted of erythematous, pruritic papules with edematous, dusky centers consistent with EM according to several Dermatology consultants.
331
The cause of EM is varied, and it includes infectious agents such as herpes simplex and mycoplasma, drugs, connective tissue diseases, and malignancies, but in half of the cases no definitive cause is found.8 CMV possibly played a role in the EM seen in our patient. However, EM associated with acute CMV infection is also a rare and reportable occurrence.9 Although EM is an uncommon presentation of acute HIV infection, this illness should be considered in a patient presenting with EM and constitutional symptoms such as fever, arthralgia, lethargy, and headache. Early detection of HIV is important, and clinicians should be made more aware of the symptoms of acute HIV infection. From a public health standpoint, early identification is valuable since patients with acute HIV infection are highly infectious.10 With early treatment of HIV infection, there is a restoration of virus-specific cellular immune responses that appear to help control viremia.1 Early treatment may also restrict damage to the immune system and reduce the chance of disease progression.1 ADAM J. SCHECHNER, MD Department of Surgery Washington Hospital Center Washington, DC ANDY G. PINSON, MD Department of Internal Medicine Virginia Commonwealth University Richmond, VA
References 1. Kahn JO, Walker BD: Acute human immunodeficiency virus type 1 infection. N Engl J Med 1998;339:33-39 2. Ries K: HIV infection and AIDS: A diagnostic consideration in every patient. Consultant 1999;39:3027-3035 3. Vergis EN, Mellors JW: Natural history of HIV-1 infection. Infect Dis Clin North Am 2000;14:809-825 4. Lewis DA, Brook MG: Erythema multiforme as a presentation of human immunodeficiency virus seroconversion illness. Int J STD AIDS 1992;3:56-57 5. Mortier E: Primary infection with human immunodeficiency virus that presented as Stevens-Johnson Syndrome. Clin Infect Dis 1994;19:798 6. Schacker T, Collier AC, Hughes J, et al: Clinical and epidemiologic features of primary HIV infection. Ann Intern Med 1996;125: 257-264 7. Daar ES, Little S, Pitt J, et al: Diagnosis of primary HIV-1 infection. Ann Intern Med 2001;134:25-29 8. Habif TP: Clinical Dermatology. St. Louis, Mosby-Year Book, 3rd Ed., 1996, pp 566-570 9. Seishima M, Oyama Z, Yamamura M: Erythema multiforme associated with cytomegalovirus infection in nonimmunosuppressed patients. Dermatology 2001;203:299-302 10. Colson AE, Sax PE: Primary HIV-1 infection: Diagnosis and treatment, in Rose BD (ed): UpToDate, Wellesley, MA, UpToDate, 2002
PREDICTION OF SURVIVAL FROM CARDIOPULMONARY RESUSCITATION BY CPR INSTRUCTORS To the Editor:—Cardiopulmonary resuscitation (CPR) is highlighted frequently on television portraying unrealistically high success rates. Multiple surveys have also revealed unrealistically high expectations of success. A survey of the public found expected CPR survival to be 74%.1 A study of nurses and physicians predicted 50% and 40%, respectively2 whereas actual CPR sur-
Supported in part by Emergency Medical Associates Research Foundation. © 2004 Elsevier Inc. All rights reserved. 0735-6757/04/2204-0031$30.00/0 doi:10.1016/j.ajem.2004.04.027
332
AMERICAN JOURNAL OF EMERGENCY MEDICINE ■ Volume 22, Number 4 ■ July 2004
vival averages 16%. We found no studies of CPR Instructors (CPRIs) and sought to determine their expectations. This is important because CPRIs who convey overly optimistic success rates to trainees may result in futile prolonged resuscitations that may have adverse consequences. As a pilot study, we mailed surveys to CPRIs to learn whether they more accurately estimate survival to discharge from the hospital after CPR. Our hypothesis was, due to their additional education, they would more accurately predict survival than the public. Our survey asked demographics of the CPRI, medical training, instances of performing CPR, number of “CPR saves,” and expected survival to discharge in patients less than and greater or equal to 55 years old. Our American Heart Association Training Center (TC) approved and distributed the survey to a convenience sample of CPRIs. The Institutional Review Board approved the study. Of the 150 surveys, 76 (51%) were returned. Within the previous 2 years, 66% of the respondents reported performing CPR and 49% participated in at least one CPR save. Our respondents reported participating in 851 CPRs, with an estimated 209 initial saves, for a save rate of 25% for all patients undergoing CPR. Respondents predicted 31⫹27% of individuals ⬍55 and 24⫹25% of individuals ⬎55 would survive CPR to hospital discharge. Our results revealed a trend to lower expectations for older instructors. For patients ⬎55, each additional 10 years of age of the instructor was associated with a 5% (P ⫽ .07) lower predicted survival. Female CPRIs predicted 16% (P ⫽ .009) greater survival than males. Also there were lower expectations from prehospital providers. Instructors who were EMTs predicted 26% (P ⫽ .0007) lower survival than non-EMTs. Whereas, paramedics predicted 33% (P ⫽ .002) lower survival than nonparamedics. There have been numerous CPR survival studies. Schneider reviewed CPR survival over 30 years,3 identifying 98 studies, 19,995 patients, 15% overall survival to discharge. We reviewed the literature since Schneider’s paper, identifying an average survival of 16.2%.4-22 Expectations of survival studies, however, vary by population studied. Roberts surveyed laypersons, nurses, and physicians with survival estimates of 52%, 30%, and 24% respectively.23 In 1994, Godkin found most older adults had little accurate knowledge of CPR, with television the main information source, and most overestimated their chances of survival at 40%, average persons 49% and older adults 29%.24 We found that while more realistic than other groups studied, CPRIs’ perceptions were still higher than those reported. We found that instructors who were older, male and EMTs or paramedics had lower more realistic expectations of the success of CPR. Potential explanations for CPRIs’ high predictions include the philosophy of CPR, which minimizes the “negative,” yet likely, outcome of death. Performance-oriented instructors motivate and encourage students and emphasize survival. Additionally, our subset of CPRIs is medically sophisticated, and by self-report, average a high CPR survival rate. High survival expectations for CPRs may have a downside. Prolonged futile attempts may take resources away from other patients. In the prehospital setting, racing to the hospital may result in motor vehicle crashes. Also the high expectations of success may not allow for better preparation of patients, families, and health care providers for death as a natural and inevitable part of life. There were limitations to our study. Perhaps the most important one was the 51% response rate. We relied on one mailing as TC staff inadvertently lost the identity of the 150 survey recipients, prohibiting remailing to nonresponders. We may have had a more medically sophisticated group of CPRIs as 96% had medical
backgrounds. This is in contrast to our perception that most volunteer instructors are laypersons. This survey was also limited to one region. In conclusion we found that CPRIs had more realistic expectations of success of CPR than other groups previously surveyed. However the expectations were still high. We recommend that CPRIs convey to trainees the medically appropriate CPR recipient, to better equip providers to make their own end-of-life care decisions, and view death as a natural and inevitable part of life. DONALD ALVES, MD MICHELE WALLACE, BSc Department of Emergency Medicine University of Maryland Medical School Baltimore, MD JOHN ALLEGRA, MD, PhD GREG CABLE, PhD Department of Emergency Medicine Morristown Memorial Hospital Morristown, NJ
References 1. Jones GK, Brewer KL, Garrison HG: Public expectations of survival following cardiopulmonary resuscitation. Ann Emerg Med 2000;71:48-53 2. Wagg A, Kinirons M, Stewart K: Cardiopulmonary resuscitation: doctors and nurses expect too much. J Roy Coll Phys London 29(1) 1995;29:20-24 3. Schneider AP II, Nelson DJ, Brown DD: In-hospital cardiopulmonary resuscitation: a 30-year review. J Am Board Fam Pract 1993;6(2):91-101 4. de Leon AC Jr: The misuse of cardiopulmonary resuscitation. J OK State Med Assoc 1993;864:175-180 5. Dautzenberg PL, Broekman TC, Hooyer C, et al: ReviewPatient-related predictors of cardiopulmonary resuscitation of hospitalized patients. Age Aging 1993;22(6):464-475 6. Robinson GR 2nd, Hess D: Postdischarge survival and functional status following in-hospital cardiopulmonary resuscitation. Chest 1994;105(4):991-996 7. Diem SJ, Lantos JD, Tulsky JA: Cardiopulmonary resuscitation on television. miracles and misinformation. N Engl J Med 1996; 334(24):1578-1582 8. Schwenzer KJ, Smith WT, Durbin CG Jr: Selective application of cardiopulmonary resuscitation improves survival rates. Anesth Analg 1993;76(3):478-484 9. VonGunten CF: CPR in hospitalized patients: when is it futile? Am Fam Physician 1991;44(6):21304 10. Weil MH, Tang W, Sun S, et al: Cardiopulmonary resuscitation and survival. Arch Intern Med 1996;156(2):215-216 11. Miller DL, Gorbien MJ, Simbartl LA, et al: Factors influencing physicians in recommending in-hospital cardiopulmonary resuscitation. Arch Intern Med 1993;153(17):1999-2003 12. Ballew KA, Philbrick JT, Caven DE, et al: Predictors of survival following in-hospital cardiopulmonary resuscitation. a moving target. Arch Intern Med 1994;154(21):2426-2432 13. Thomas RD, Waites JH, Hubbard WN, et al: Cardiopulmonary resuscitation in a district general hospital: increased success over 7 years. Arch Em Med 1990;7(3):200-205 14. Ebell MH, Kruse JA, Smith M, et al: Failure of three decision rules to predict the outcome of in-hospital cardiopulmonary resuscitation. Med Decis Making 1997;17(2):171-177 15. Schoenenberger RA, von Planta M, von Planta I: Survival after failed out-of-hospital resuscitation. Are further therapeutic efforts in the emergency department futile? Arch Intern Med 1994;154(21): 2433-2437 16. Cohen EB, Leferve F, Yarnold PR, et al: Predicting survival from cpr: meta analysis and validation of a prediction model. J Gen Intern Med 1993;8(7):347-353 17. Thel MC, Armstrong AL, McNulty SE, et al: Randomised trial of magnesium in in-hospital cardiac arrest. Duke internal medicine house staff. Lancet 1997;350(9087):1272-1276 18. Murphy DJ, Burrows D, Santilli S, et al: The influence of the probability of survival on patients’ preferences regarding cardiopulmonary resuscitation. N Engl J Med 1994;330(8):545-549
CORRESPONDENCE
19. Tresch DD, Neahring JM, Duthie EH, et al: Outcomes of cardiopulmonary resuscitation in nursing homes: can we predict who will benefit? Am J Med Aug 1993;95(2):123-130 20. Hallstrom A, Cobb L, Johnson E, et al: Cardiopulmonary resuscitation by chest compression alone or with mouth-to mouth ventilation. N Engl J Med 2000;342(21):1546-1553 21. Skogvoll E, Wik L. Active compression-decompression cardiopulmonary resuscitation: a population-based, prospective randomized clinical trial in out-of-hospital cardiac arrest. Resuscitation 1999;42(3):163-172 22. Luiz T, Ellinger K, Denz C: Active compression-decompression cardiopulmonary resuscitation does not improve survival in patients with prehospital cardiac arrest in a physician-manned emergency medical system. J Cardiothoracic Vasc Anesth 1996; 10(2):178-186 23. Roberts D, Hirschman D, Scheltema K: Adult and pediatric cpr: attitudes and expectations of health professionals and lay persons. Am J Emerg Med 2000;18:465-468 24. Godkin MD, Toth EL: Cardiopulmonary Resuscitation and Older Adults’ Expectations. Gerontologist 1994;34(6):797-802
CORNEAL ABRASION FROM VICK’S VAPOR To the Editor:—The growing popularity of the street drug 3,4-methylenedioxymethamphetamine, known as MDMA or “ecstasy,” has been documented in the newspaper and television. This hallucinogenic amphetamine produces a hypersensory state that amplifies the mentholated sensation of Vick’s Vapor Rub placed on the body. I can report seeing multiple patients presenting to the emergency department (ED) with corneal abrasions, unilateral and bilateral, after having Vick’s Vapor “blown” into their eyes at close range through a nasal inhaler. An 18-year-old man presented to the ED complaining of pain in both of his eyes after partying the prior night with friends at a club. While under the influence of ecstasy, a friend blew through the fenestrated end of a Vick’s Vapor nasal inhaler into the patient’s eyes from a distance of inches. The goal was to feel the cool, mentholated sensation in his eyes. He denies any contact to his © 2004 Elsevier Inc. All rights reserved. 0735-6757/04/2204-0029$30.00/0 doi:10.1016/j.ajem.2004.05.002
333
eyes by the inhaler casing. He soon felt pain in his eyes and described a clouding of his corneas. In the ED, focal chemical injuries to the corneas were found. His visual acuity was 20/20 bilaterally. His extraocular movements were full. Visual fields were normal as tested. The fluorescein stain demonstrated confluent uptake, consistent with abrasion, on the inferior aspect of both corneas. The patient was seen by an ophthalmologist and discharged on Pred Forte drops and pain medication. As mentioned above, I have seen multiple cases of corneal injuries after contact with Vick’s vapor blown through inhalers. The painful keratitis appears as a corneal defect that is likely due to chemical injury. This is possibly the result of direct irritation from camphor (approximately 4.8% in Vick’s Vapor Rub). Also, Vick’s contains small amounts of spirit of Turpentine, the vapor of which has been reported as a corneal irritant. The subject of ecstasy abuse, with all night rave parties, and concurrent use of other drugs is well documented. This “designer drug” is synthesized in the laboratory and gives the user a feeling of enhanced pleasure, especially to sensory stimulation. Adolescents and young adults experimenting with ecstasy heighten their sensory stimulation by listening to “electronica” dance music, watching twirling glow sticks, and feeling the cool, mentholated sensation of Vick’s Vapor Rub on their bodies. This sensation is taken one step further by having someone blow the vapor directly onto their eyes via a Vick’s nasal inhaler. A review of the literature found no other reports of injury to the cornea sustained in this way. MICHAEL T. BRAZDA, MD Baptist Hospital of Miami Miami, FL
References 1. Grant WM: Toxicology of the Eye, ed 4, 1993. p. 306, 1480, 1497-98 2. Smith MB: Handbook of Ocular Toxicity, 1976, p. 253-54. 3. Microdex, Inc., 1974-1999, Volume 102 Expiration date: 11/ 30/99 4. Dahl AA, Grant WM: Unusual keratitis from a household remedy. Am J Ophthal 1969;685:858-862 5. Jaiwal AK: Vick’s Vaporub induced dermo keratoconjunctivitis-A case report. Ind J Ophthal 1989;37(3):154
She developed a sore throat and then noted a rash that appeared first on her back and then involved her extremities. She was then seen in an urgent care center and was diagnosed with strep throat and was treated with an unknown antibiotic. About 4 weeks after her symptoms started, the patient was seen in our Dermatology clinic. On exam, she was found to have multiple erythematous plaques and round papules with a dusky/ darker center (targetoid appearance) on her dorsal hands, palms, dorsal feet, and knees. Additionally, she had many discrete 1-2 mm pink papules on her abdomen, proximal thighs, and proximal arms. She was diagnosed with EM, which was thought to be secondary to her prior strep throat. Over the next 9 weeks, the patient was seen in our ED 3 times, in our Dermatology clinic twice, and by an outside physician 3 times. Her complaints included fatigue; malaise; the persistent rash, which was now pruritic; fever; night sweats; hair loss; weight loss; sinus pain; and increasing posterior cervical lymphadenopathy. On exam, findings included an erythematous oral mucosa with erosions of the buccal mucosa and soft palate, a white coating on her tongue, mild posterior cervical lymphadenopathy, and EM, which the Dermatology consultants felt was continuing secondary to an unknown persistent stimuli. The rash became confluent with some lichenification on her elbows and knees and desquamation of her palms. On her last visit prior to coming to our office, she was noted to have splenomegaly and enlarged and erythematous tonsils. Prior to her visit to our office, laboratory studies revealed that her white blood cell count was 5.1 x 109/L with 56% lymphocytes. After approximately 5 weeks of symptoms, HIV serology was negative. Heterophile antibody, antinuclear antibody, and cold agglutinin were negative. A throat culture revealed methicillinsensitive Staphylococcus aureus which was treated with dicloxacillin. In our office, her temperature was 99.3°F, pulse was 80 beats/ min, and blood pressure was 98/55 mm/Hg. Her tonsils were enlarged and erythematous. She had diffuse cervical and occipital lymphadenopathy, normal cardiac and pulmonary exams, left upper quadrant tenderness, and a fading macular rash on her hands, elbows, and feet. HIV serology was positive with a HIV RNA (viral load) of 348,000 copies/mL. Cytomegalovirus (CMV) IgM and IgG also returned as positive. She was started on nelfinavir, zidovudine, and lamivudine, and after 2 weeks of this regimen, her HIV RNA had dropped to 1,455 copies/mL. Her symptoms had markedly improved. Overall she felt less tired, her rash faded, and her lymphadenopathy decreased significantly. She continued to do well and 2 years after her diagnosis, her CD4 count was 646 cells per mm3 and her HIV RNA was undetectable at less than 50 copies/mL. Although the majority of people with acute HIV infection are ill enough to seek medical attention, the constitutional symptoms are seen in many other illnesses and, as was the case with our patient, most patients are not correctly diagnosed at presentation.6 When acute HIV infection is suspected, a HIV RNA or p24 antigen test is needed to make the diagnosis as antibodies are undetectable in the early stages.7 Our patient’s HIV antibody was negative early in the course of her illness. What made our case most interesting was the fact that, along with many of the usual symptoms of acute HIV infection, she also presented with EM, which is not a characteristic feature of this illness. The most common skin manifestation of acute HIV infection is an erythematous nonpruritic, maculopapular rash affecting the face or trunk.3 The rash can appear on the palms and soles and can be generalized.3 The rash can also manifest as a roseola-like eruption, a vesicular, pustular exanthem or enanthem, or diffuse urticaria.3 However, our patient did not have any of these types of rashes. Rather, her rash consisted of erythematous, pruritic papules with edematous, dusky centers consistent with EM according to several Dermatology consultants.
331
The cause of EM is varied, and it includes infectious agents such as herpes simplex and mycoplasma, drugs, connective tissue diseases, and malignancies, but in half of the cases no definitive cause is found.8 CMV possibly played a role in the EM seen in our patient. However, EM associated with acute CMV infection is also a rare and reportable occurrence.9 Although EM is an uncommon presentation of acute HIV infection, this illness should be considered in a patient presenting with EM and constitutional symptoms such as fever, arthralgia, lethargy, and headache. Early detection of HIV is important, and clinicians should be made more aware of the symptoms of acute HIV infection. From a public health standpoint, early identification is valuable since patients with acute HIV infection are highly infectious.10 With early treatment of HIV infection, there is a restoration of virus-specific cellular immune responses that appear to help control viremia.1 Early treatment may also restrict damage to the immune system and reduce the chance of disease progression.1 ADAM J. SCHECHNER, MD Department of Surgery Washington Hospital Center Washington, DC ANDY G. PINSON, MD Department of Internal Medicine Virginia Commonwealth University Richmond, VA
References 1. Kahn JO, Walker BD: Acute human immunodeficiency virus type 1 infection. N Engl J Med 1998;339:33-39 2. Ries K: HIV infection and AIDS: A diagnostic consideration in every patient. Consultant 1999;39:3027-3035 3. Vergis EN, Mellors JW: Natural history of HIV-1 infection. Infect Dis Clin North Am 2000;14:809-825 4. Lewis DA, Brook MG: Erythema multiforme as a presentation of human immunodeficiency virus seroconversion illness. Int J STD AIDS 1992;3:56-57 5. Mortier E: Primary infection with human immunodeficiency virus that presented as Stevens-Johnson Syndrome. Clin Infect Dis 1994;19:798 6. Schacker T, Collier AC, Hughes J, et al: Clinical and epidemiologic features of primary HIV infection. Ann Intern Med 1996;125: 257-264 7. Daar ES, Little S, Pitt J, et al: Diagnosis of primary HIV-1 infection. Ann Intern Med 2001;134:25-29 8. Habif TP: Clinical Dermatology. St. Louis, Mosby-Year Book, 3rd Ed., 1996, pp 566-570 9. Seishima M, Oyama Z, Yamamura M: Erythema multiforme associated with cytomegalovirus infection in nonimmunosuppressed patients. Dermatology 2001;203:299-302 10. Colson AE, Sax PE: Primary HIV-1 infection: Diagnosis and treatment, in Rose BD (ed): UpToDate, Wellesley, MA, UpToDate, 2002
PREDICTION OF SURVIVAL FROM CARDIOPULMONARY RESUSCITATION BY CPR INSTRUCTORS To the Editor:—Cardiopulmonary resuscitation (CPR) is highlighted frequently on television portraying unrealistically high success rates. Multiple surveys have also revealed unrealistically high expectations of success. A survey of the public found expected CPR survival to be 74%.1 A study of nurses and physicians predicted 50% and 40%, respectively2 whereas actual CPR sur-
Supported in part by Emergency Medical Associates Research Foundation. © 2004 Elsevier Inc. All rights reserved. 0735-6757/04/2204-0031$30.00/0 doi:10.1016/j.ajem.2004.04.027
332
AMERICAN JOURNAL OF EMERGENCY MEDICINE ■ Volume 22, Number 4 ■ July 2004
vival averages 16%. We found no studies of CPR Instructors (CPRIs) and sought to determine their expectations. This is important because CPRIs who convey overly optimistic success rates to trainees may result in futile prolonged resuscitations that may have adverse consequences. As a pilot study, we mailed surveys to CPRIs to learn whether they more accurately estimate survival to discharge from the hospital after CPR. Our hypothesis was, due to their additional education, they would more accurately predict survival than the public. Our survey asked demographics of the CPRI, medical training, instances of performing CPR, number of “CPR saves,” and expected survival to discharge in patients less than and greater or equal to 55 years old. Our American Heart Association Training Center (TC) approved and distributed the survey to a convenience sample of CPRIs. The Institutional Review Board approved the study. Of the 150 surveys, 76 (51%) were returned. Within the previous 2 years, 66% of the respondents reported performing CPR and 49% participated in at least one CPR save. Our respondents reported participating in 851 CPRs, with an estimated 209 initial saves, for a save rate of 25% for all patients undergoing CPR. Respondents predicted 31⫹27% of individuals ⬍55 and 24⫹25% of individuals ⬎55 would survive CPR to hospital discharge. Our results revealed a trend to lower expectations for older instructors. For patients ⬎55, each additional 10 years of age of the instructor was associated with a 5% (P ⫽ .07) lower predicted survival. Female CPRIs predicted 16% (P ⫽ .009) greater survival than males. Also there were lower expectations from prehospital providers. Instructors who were EMTs predicted 26% (P ⫽ .0007) lower survival than non-EMTs. Whereas, paramedics predicted 33% (P ⫽ .002) lower survival than nonparamedics. There have been numerous CPR survival studies. Schneider reviewed CPR survival over 30 years,3 identifying 98 studies, 19,995 patients, 15% overall survival to discharge. We reviewed the literature since Schneider’s paper, identifying an average survival of 16.2%.4-22 Expectations of survival studies, however, vary by population studied. Roberts surveyed laypersons, nurses, and physicians with survival estimates of 52%, 30%, and 24% respectively.23 In 1994, Godkin found most older adults had little accurate knowledge of CPR, with television the main information source, and most overestimated their chances of survival at 40%, average persons 49% and older adults 29%.24 We found that while more realistic than other groups studied, CPRIs’ perceptions were still higher than those reported. We found that instructors who were older, male and EMTs or paramedics had lower more realistic expectations of the success of CPR. Potential explanations for CPRIs’ high predictions include the philosophy of CPR, which minimizes the “negative,” yet likely, outcome of death. Performance-oriented instructors motivate and encourage students and emphasize survival. Additionally, our subset of CPRIs is medically sophisticated, and by self-report, average a high CPR survival rate. High survival expectations for CPRs may have a downside. Prolonged futile attempts may take resources away from other patients. In the prehospital setting, racing to the hospital may result in motor vehicle crashes. Also the high expectations of success may not allow for better preparation of patients, families, and health care providers for death as a natural and inevitable part of life. There were limitations to our study. Perhaps the most important one was the 51% response rate. We relied on one mailing as TC staff inadvertently lost the identity of the 150 survey recipients, prohibiting remailing to nonresponders. We may have had a more medically sophisticated group of CPRIs as 96% had medical
backgrounds. This is in contrast to our perception that most volunteer instructors are laypersons. This survey was also limited to one region. In conclusion we found that CPRIs had more realistic expectations of success of CPR than other groups previously surveyed. However the expectations were still high. We recommend that CPRIs convey to trainees the medically appropriate CPR recipient, to better equip providers to make their own end-of-life care decisions, and view death as a natural and inevitable part of life. DONALD ALVES, MD MICHELE WALLACE, BSc Department of Emergency Medicine University of Maryland Medical School Baltimore, MD JOHN ALLEGRA, MD, PhD GREG CABLE, PhD Department of Emergency Medicine Morristown Memorial Hospital Morristown, NJ
References 1. Jones GK, Brewer KL, Garrison HG: Public expectations of survival following cardiopulmonary resuscitation. Ann Emerg Med 2000;71:48-53 2. Wagg A, Kinirons M, Stewart K: Cardiopulmonary resuscitation: doctors and nurses expect too much. J Roy Coll Phys London 29(1) 1995;29:20-24 3. Schneider AP II, Nelson DJ, Brown DD: In-hospital cardiopulmonary resuscitation: a 30-year review. J Am Board Fam Pract 1993;6(2):91-101 4. de Leon AC Jr: The misuse of cardiopulmonary resuscitation. J OK State Med Assoc 1993;864:175-180 5. Dautzenberg PL, Broekman TC, Hooyer C, et al: ReviewPatient-related predictors of cardiopulmonary resuscitation of hospitalized patients. Age Aging 1993;22(6):464-475 6. Robinson GR 2nd, Hess D: Postdischarge survival and functional status following in-hospital cardiopulmonary resuscitation. Chest 1994;105(4):991-996 7. Diem SJ, Lantos JD, Tulsky JA: Cardiopulmonary resuscitation on television. miracles and misinformation. N Engl J Med 1996; 334(24):1578-1582 8. Schwenzer KJ, Smith WT, Durbin CG Jr: Selective application of cardiopulmonary resuscitation improves survival rates. Anesth Analg 1993;76(3):478-484 9. VonGunten CF: CPR in hospitalized patients: when is it futile? Am Fam Physician 1991;44(6):21304 10. Weil MH, Tang W, Sun S, et al: Cardiopulmonary resuscitation and survival. Arch Intern Med 1996;156(2):215-216 11. Miller DL, Gorbien MJ, Simbartl LA, et al: Factors influencing physicians in recommending in-hospital cardiopulmonary resuscitation. Arch Intern Med 1993;153(17):1999-2003 12. Ballew KA, Philbrick JT, Caven DE, et al: Predictors of survival following in-hospital cardiopulmonary resuscitation. a moving target. Arch Intern Med 1994;154(21):2426-2432 13. Thomas RD, Waites JH, Hubbard WN, et al: Cardiopulmonary resuscitation in a district general hospital: increased success over 7 years. Arch Em Med 1990;7(3):200-205 14. Ebell MH, Kruse JA, Smith M, et al: Failure of three decision rules to predict the outcome of in-hospital cardiopulmonary resuscitation. Med Decis Making 1997;17(2):171-177 15. Schoenenberger RA, von Planta M, von Planta I: Survival after failed out-of-hospital resuscitation. Are further therapeutic efforts in the emergency department futile? Arch Intern Med 1994;154(21): 2433-2437 16. Cohen EB, Leferve F, Yarnold PR, et al: Predicting survival from cpr: meta analysis and validation of a prediction model. J Gen Intern Med 1993;8(7):347-353 17. Thel MC, Armstrong AL, McNulty SE, et al: Randomised trial of magnesium in in-hospital cardiac arrest. Duke internal medicine house staff. Lancet 1997;350(9087):1272-1276 18. Murphy DJ, Burrows D, Santilli S, et al: The influence of the probability of survival on patients’ preferences regarding cardiopulmonary resuscitation. N Engl J Med 1994;330(8):545-549
CORRESPONDENCE
19. Tresch DD, Neahring JM, Duthie EH, et al: Outcomes of cardiopulmonary resuscitation in nursing homes: can we predict who will benefit? Am J Med Aug 1993;95(2):123-130 20. Hallstrom A, Cobb L, Johnson E, et al: Cardiopulmonary resuscitation by chest compression alone or with mouth-to mouth ventilation. N Engl J Med 2000;342(21):1546-1553 21. Skogvoll E, Wik L. Active compression-decompression cardiopulmonary resuscitation: a population-based, prospective randomized clinical trial in out-of-hospital cardiac arrest. Resuscitation 1999;42(3):163-172 22. Luiz T, Ellinger K, Denz C: Active compression-decompression cardiopulmonary resuscitation does not improve survival in patients with prehospital cardiac arrest in a physician-manned emergency medical system. J Cardiothoracic Vasc Anesth 1996; 10(2):178-186 23. Roberts D, Hirschman D, Scheltema K: Adult and pediatric cpr: attitudes and expectations of health professionals and lay persons. Am J Emerg Med 2000;18:465-468 24. Godkin MD, Toth EL: Cardiopulmonary Resuscitation and Older Adults’ Expectations. Gerontologist 1994;34(6):797-802
CORNEAL ABRASION FROM VICK’S VAPOR To the Editor:—The growing popularity of the street drug 3,4-methylenedioxymethamphetamine, known as MDMA or “ecstasy,” has been documented in the newspaper and television. This hallucinogenic amphetamine produces a hypersensory state that amplifies the mentholated sensation of Vick’s Vapor Rub placed on the body. I can report seeing multiple patients presenting to the emergency department (ED) with corneal abrasions, unilateral and bilateral, after having Vick’s Vapor “blown” into their eyes at close range through a nasal inhaler. An 18-year-old man presented to the ED complaining of pain in both of his eyes after partying the prior night with friends at a club. While under the influence of ecstasy, a friend blew through the fenestrated end of a Vick’s Vapor nasal inhaler into the patient’s eyes from a distance of inches. The goal was to feel the cool, mentholated sensation in his eyes. He denies any contact to his © 2004 Elsevier Inc. All rights reserved. 0735-6757/04/2204-0029$30.00/0 doi:10.1016/j.ajem.2004.05.002
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eyes by the inhaler casing. He soon felt pain in his eyes and described a clouding of his corneas. In the ED, focal chemical injuries to the corneas were found. His visual acuity was 20/20 bilaterally. His extraocular movements were full. Visual fields were normal as tested. The fluorescein stain demonstrated confluent uptake, consistent with abrasion, on the inferior aspect of both corneas. The patient was seen by an ophthalmologist and discharged on Pred Forte drops and pain medication. As mentioned above, I have seen multiple cases of corneal injuries after contact with Vick’s vapor blown through inhalers. The painful keratitis appears as a corneal defect that is likely due to chemical injury. This is possibly the result of direct irritation from camphor (approximately 4.8% in Vick’s Vapor Rub). Also, Vick’s contains small amounts of spirit of Turpentine, the vapor of which has been reported as a corneal irritant. The subject of ecstasy abuse, with all night rave parties, and concurrent use of other drugs is well documented. This “designer drug” is synthesized in the laboratory and gives the user a feeling of enhanced pleasure, especially to sensory stimulation. Adolescents and young adults experimenting with ecstasy heighten their sensory stimulation by listening to “electronica” dance music, watching twirling glow sticks, and feeling the cool, mentholated sensation of Vick’s Vapor Rub on their bodies. This sensation is taken one step further by having someone blow the vapor directly onto their eyes via a Vick’s nasal inhaler. A review of the literature found no other reports of injury to the cornea sustained in this way. MICHAEL T. BRAZDA, MD Baptist Hospital of Miami Miami, FL
References 1. Grant WM: Toxicology of the Eye, ed 4, 1993. p. 306, 1480, 1497-98 2. Smith MB: Handbook of Ocular Toxicity, 1976, p. 253-54. 3. Microdex, Inc., 1974-1999, Volume 102 Expiration date: 11/ 30/99 4. Dahl AA, Grant WM: Unusual keratitis from a household remedy. Am J Ophthal 1969;685:858-862 5. Jaiwal AK: Vick’s Vaporub induced dermo keratoconjunctivitis-A case report. Ind J Ophthal 1989;37(3):154