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(NEJM Volume 355:281-287 July 20 @ 2006 Number 3
The "Gender Gap" in Authorship of Academic Medical Literature — A 35-Year Perspective
Reshma Jagsi, M.D., D.Phil., Elizabeth A. Guancial, M.D., Cynthia Cooper Worobey, M.D., Lori E. Henault, M.P.H., Yuchiao Chang, Ph.D., Rebecca Starr, M.B.A., M.S.W., Nancy J. Tarbell, M.D., and Elaine M. Hylek, M.D., M.P.H.)
ABSTRACTBackground Participation of women in the medical profession has increased during the past four decades, but issues of concern persist regarding disparities between the sexes in academic medicine. Advancement is largely driven by peer-reviewed original research, so we sought to determine the representation of female physician-investigators among the authors of selected publications during the past 35 years.
Methods Original articles from six prominent medical journals — the New England Journal of Medicine (NEJM), the Journal of the American Medical Association (JAMA), the Annals of Internal Medicine (Ann Intern Med), the Annals of Surgery (Ann Surg), Obstetrics & Gynecology (Obstet Gynecol), and the Journal of Pediatrics (J Pediatr) — were categorized according to the sex of both the first and the senior (last listed) author. Sex was also determined for the authors of guest editorials in NEJM and JAMA. Data were collected for the years 1970, 1980, 1990, 2000, and 2004. The analysis was restricted to authors from U.S. institutions holding M.D. degrees.
Results The sex was determined for 98.5 percent of the 7249 U.S. authors of original research with M.D. degrees. The proportion of first authors who were women increased from 5.9 percent in 1970 to 29.3 percent in 2004 (P<0.001), and the proportion of senior authors who were women increased from 3.7 percent to 19.3 percent (P<0.001) during the same period. The proportion of authors who were women increased most sharply in Obstet Gynecol (from 6.7 percent of first authors and 6.8 percent of senior authors in 1970 to 40.7 percent of first authors and 28.0 percent of senior authors in 2004) and J Pediatr (from 15.0 percent of first authors and 4.3 percent of senior authors in 1970 to 38.9 percent of first authors and 38.0 percent of senior authors in 2004) and remained low in Ann Surg (from 2.3 percent of first authors and 0.7 percent of senior authors in 1970 to 16.7 percent of first authors and 6.7 percent of senior authors in 2004). In 2004, 11.4 percent of the authors of guest editorials in NEJM and 18.8 percent of the authors of guest editorials in JAMA were women.
Conclusions Over the past four decades, the proportion of women among both first and senior physician-authors of original research in the United States has significantly increased. Nevertheless, women still compose a minority of the authors of original research and guest editorials in the journals studied.
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During the past four decades, the participation of women in medicine has increased dramatically. Women now represent 49 percent of all medical students,1 as compared with 6 percent in 1960.2 Overall, 25 percent of practicing physicians in the United States are women,3 and women now make up 32 percent of full-time medical faculty members.4 However, there is considerable evidence that women continue to be underrepresented in the top tiers of academic medicine.5,6,7 Women currently make up 10 percent of medical school deans, 11 percent of department chairs, and 14 percent of full professors among the clinical faculty in medical schools.4 Women last composed 14 percent of all medical students in 1972.8 In addition, only 10 percent of female clinical faculty members as compared with 28 percent of male clinical faculty members are full professors.4 Figure 1 depicts the number of female faculty members who served as professors and role models for both male and female residents in the main medical specialties in 2004. For example, in internal medicine, the ratio of residents to female professors was 31 to 1; this ratio was 44 to 1 with the inclusion of fellows.9,10
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Figure 1. Sex Distribution of Clinical Faculty Members and Resident Physicians in Medical Specialties, 2004.
Data from the Association of American Medical Colleges indicate that a relatively small absolute number of female faculty members serve as professors and role models for the large number of both male and female residents in the main medical specialties.
Publication in medical journals is an important measure of academic productivity. It is also highly emphasized in the academic promotion process and an important means by which the academic medical community communicates. Although several survey studies have suggested that female faculty members may be less likely to publish academic papers than their male colleagues,11,12 other studies have not found apparent differences.13,14,15 Few studies have attempted to quantify the sex distribution of authors of published research, and those that have done so have focused on the fields of otolaryngology16 and epidemiology17 or on authors of research published in journals outside the United States.18,19 In this study, we examined whether there was a "gender gap" in the authorship of six prestigious medical journals in the United States and we sought to quantify its magnitude. In addition, we examined the patterns of change in this gap over time and variations according to specialty area. We focused on published original research in these journals from 1970 to the present. We also assessed the sex composition of authors of guest editorials published during the same period.
Methods
Data Collection
We focused on the four medical specialties that have traditionally constituted the core clerkships in the education of medical students. These specialties, which together include the largest proportion of practicing physicians, include internal medicine, surgery, pediatrics, and obstetrics and gynecology. Journals were selected on the basis of "impact factors,"20,21 citation half-life,20 and comments solicited from faculty members regarding the long-term prestige and importance of the various journals in their fields. Six prominent medical journals published in the United States were included in this study: the New England Journal of Medicine (NEJM), the Journal of the American Medical Association (JAMA), the Annals of Internal Medicine (Ann Intern Med), the Annals of Surgery (Ann Surg), Obstetrics & Gynecology (Obstet Gynecol), and the Journal of Pediatrics (J Pediatr).
All original articles published in 1970, 1980, 1990, 2000, and 2004 were included in the data set. For each of these articles, we determined both the first and senior (last listed) authors' sex, graduate degrees, and institutional affiliation. An author's sex was determined by initial inspection of his or her first name. For cases in which an author's sex was not certain, attempts were made to discern the sex by visiting the institutional Web site and performing Internet searches with the use of the Google search engine.
Also included and separately identified in the study were guest editorials in the two nonspecialty journals, NEJM and JAMA. Only editorials authored by persons other than editorial-board members were considered for analysis. In the rare cases in which editorials were written by more than two authors, our analysis included just the first and last authors.
Statistical Analysis
Our analysis was restricted to investigators from U.S. institutions who held an M.D. degree. The tabulated data were stored in a Microsoft Access database and analyzed (with the use of SAS software, version 9.1) to determine the sex distributions of the first and senior (last listed) authors of original articles for each journal and the sex distributions of authors of guest editorials in NEJM and JAMA. The Cochran–Armitage trend test was used to test for the trend over time. Reported P values pertain to the significance of trends over time in these data.
Results
Authorship of Original Research
A total of 7249 authors of original articles who held M.D. degrees and were from U.S. institutions were identified in the six journals during the years studied; 3872 were first authors, and 3377 were senior authors. The sex of the author was determined for 98.5 percent. Overall, 15.9 percent of the first authors and 10.3 percent of the senior authors were women. An analysis of the data according to year demonstrated significant gains by female physician-investigators since 1970 (Figure 2). The proportion of women serving as first authors of published original research in these journals increased from 5.9 percent to 29.3 percent, and the proportion of women serving as senior authors increased from 3.7 percent to 19.3 percent. The data also suggested that this momentum may be reaching a plateau.
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Figure 2. Female Physician-Investigators Who Were First and Senior Authors of Published Original Research.
In the six journals studied, the representation of women among first and senior authors of published original research increased during the past four decades. The cumulative trends over time are depicted by curves showing female representation among students enrolled in medical school and among professors on medical school faculties (data on faculty rank according to sex were not available from the Association of American Medical Colleges for 1980, 1970, or 1960).
Significant trends of increased female representation were evident for each of the six journals during the 35-year period (Table 1). The proportions of first and senior authors who were women increased most sharply in the specialty journals of obstetrics and pediatrics and remained low in the journal having to do with surgery. In 2004, in the three general medical journals (Ann Intern Med, NEJM, and JAMA) collectively, female physicians made up 23.2 percent of the first authors and 12.7 percent of the senior authors of original research articles.
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Table 1. Representation of Female Physician-Investigators among First and Senior Authors of Published Original Research in Six U.S. Journals.
Of the U.S. authors in the years studied, 181 first authors held both M.D. and Ph.D. degrees and 236 senior authors held both M.D. and Ph.D. degrees. In this subgroup, the sex distribution over time was similar to that in the overall data set. Among the first authors holding both M.D. and Ph.D. degrees, 7.7 percent were female in 1970, 6.7 percent in 1980, 10.0 percent in 1990, 20.0 percent in 2000, and 17.9 percent in 2004 (P for trend=0.05). Of the senior authors holding both M.D and Ph.D. degrees, 3.7 percent were female in 1970, 0 percent in 1980, 12.5 percent in 1990, 22.9 percent in 2000, and 9.3 percent in 2004 (P for trend=0.02).
Sex of Authors of Guest Editorials
We determined the sex of 99.6 percent of the 808 U.S. investigators with an M.D. degree who served as first or senior (last listed) authors of guest editorials in NEJM and JAMA during the years studied. During this period, of the 514 authors of guest editorials in NEJM, women made up 8.8 percent overall and 1.5 percent in 1970, 2.4 percent in 1980, 9.7 percent in 1990, 20.4 percent in 2000, and 11.4 percent in 2004 (P for trend <0.001). Sex was determined for 291 of the 294 U.S. authors of guest editorials with M.D. degrees in JAMA during the years studied. Of these 291 authors, women made up 10 percent overall and 0 percent in 1970, 2.0 percent in 1980, 7.4 percent in 1990, 10.0 percent in 2000, and 18.8 percent in 2004 (P for trend <0.001).
Discussion
Advancement in academic medicine is largely contingent on productivity and the measured external influence of one's scholarly work. Objective measures of the effect of one's work include the publication of original research in prominent journals and invitations by editors to provide scientific opinions on the published research of others. In this study, we focused on six medical journals chosen specifically for their prominence and high visibility to medical students, residents, and fellows. We found that from 1970 to 2004, the proportion of women among the U.S. physician-authors of original research in these journals increased from 5.9 percent to 29.3 percent of first authors and from 3.7 percent to 19.3 percent of senior authors. The magnitude of change for both groups was highest for J Pediatr and Obstet Gynecol and lowest for Ann Surg; these findings may have reflected, at least in part, the numbers of women entering these fields.
Despite these positive overall findings, the results also raise potential areas of concern. Although the proportion of women among authors has increased over time, the data suggest a possible lack of continued momentum among both first authors and senior authors in 2004 as compared with 2000. The data also suggest that a gender gap in authorship remains, particularly among senior authors and editorial commentators.
Of the many possible explanations for our findings, one factor that probably explains at least some of the gender gap observed is that the pool of female faculty members who are eligible to serve as senior authors or editorial commentators remains limited. Nonnemaker examined the rates of academic advancement of men and women among different cohorts of U.S. medical school faculties from 1979 through 1997.7 The study revealed that the numbers of women advancing to the ranks of associate and full professor were significantly lower than expected. Longitudinal data from the American Association of Medical Colleges seem to reaffirm this finding (Table 2).4,8,22,23,24 In 2004, women made up only 19 percent of associate and full professors on the clinical faculties of medical schools.9 The low overall percentage of female senior authors in 2004 — 19 percent in the six journals studied — may reflect this smaller pool of senior faculty members who are women. Similarly, the low percentage of women among authors of guest editorials may indicate that there is a limited pool of women who have achieved sufficient international recognition and expertise to merit these invitations. Since the pool is limited, senior women may also be inundated with academic activities and may find it necessary to decline invitations more often, notwithstanding the potential for prestige and influence.
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Table 2. Academic Rank of Clinical Faculty in Main Specialties, According to Sex.
Several studies have explored the basis for the gender gap in academic medicine. In a study by Yedidia and Bickel,25 three important barriers to the academic advancement of women were identified from interviews of department chairs — the constraints of traditional sex roles, manifestations of sexism in the medical environment, and lack of effective mentors. Carr et al. reported that female faculty members who had children published less and had less institutional support than did male colleagues who had children.26 In addition, a study of female faculty members in the School of Science at the Massachusetts Institute of Technology found unanticipated patterns of inequity relative to the allocation of resources, space, salary, outside professional activities, and positions of influence.27
Some of the gap observed may also stem from career choices made by men and women. Studies have documented differences in career preferences between male and female medical students,28,29 and women may devote more of their working time to teaching and clinical activity than to research.30 Some have also speculated that women may have different priorities regarding the balance between work and other pursuits,31,32,33 although recent studies have suggested that a balance between work and other activities is as important to men as it is to women, at least among younger physicians.34,35,36 Ultimately, Nonnemaker found that fewer women were choosing academic career paths in the late 1990s.7
Finally, it has been suggested that the most productive period of women's careers is delayed, and this delay conflicts with traditional tenure clocks.37 Strategies like the National Institutes of Health supplements to promote reentry into biomedical and behavioral research careers are grounded in the assumption that measures that help women to address these issues of timing may promote their more equal participation in academic medicine. On the basis of a similar logic, it may also be appropriate to consider making awards for career development independent of the number of years since medical school or since one's first faculty appointment.
Given the design of our study, we were unable to assess the contribution of productivity, career choice, or other possible factors to the gender gap in authorship in the journals we studied. Future research should explore these questions, since it is only through analysis of the underlying forces that this gap in academic medicine may be understood. Faculty diversity is valuable in promoting new insights into and approaches to medical research, so efforts to increase the representation of women in academic medicine should be grounded in rigorous, evidence-based analysis.
Our findings validate the perception that although women have made substantial strides in the past four decades, a gender gap remains among the authors of original articles in prestigious academic medical journals. Further investigation is necessary to understand more fully the causes for this gap, including the possibility that certain barriers may impede women's participation as authors early in their careers and in turn may diminish the pool of female senior faculty members who may serve in prominent authorship positions.
Presented in part at the Society for General Internal Medicine Annual Meeting, New Orleans, May 13, 2005.
No potential conflict of interest relevant to this article was reported.
Source Information
From the Departments of Radiation Oncology (R.J., N.J.T.) and Nephrology (C.C.W.), the General Medicine Division (Y.C.), and the Office of Women's Careers (R.S., N.J.T.), Massachusetts General Hospital; Harvard Medical School (R.J., E.A.G., C.C.W., Y.C., N.J.T.); and the Section of General Internal Medicine–Research Unit, Boston Medical Center, Boston University School of Medicine (L.E.H., E.M.H.) — all in Boston.
Address reprint requests to Dr. Jagsi at the Office for Women's Careers, Bulfinch 370, Massachusetts General Hospital, 55 Fruit St., Boston, MA 02114, or at reshma_jagsi@post.harvard.edu.
References
Women in U.S. academic medicine: statistics and medical school benchmarking 2004-2005. Washington, D.C.: Association of American Medical Colleges, 2005:Table 1.
Women in U.S. academic medicine: statistics and medical school benchmarking 2003-2004. Washington, D.C.: Association of American Medical Colleges, 2004:Table 1.
Physician characteristics and distribution in the U.S. Chicago: American Medical Association, 2004:Table 1.
Women in U.S. academic medicine: statistics and medical school benchmarking 2004-2005. Washington, D.C.: Association of American Medical Colleges, 2005:Table 3.
Bickel J. 1989. Women in medical education: a status report. N Engl J Med 1989;319:1579-1584.
Bickel J, Wara D, Atkinson BF, et al. Increasing women's leadership in academic medicine: report of the AAMC Project Implementation Committee. Acad Med 2002;77:1043-1061. [Medline]
Nonnemaker L. Women physicians in academic medicine: new insights from cohort studies. N Engl J Med 2000;342:399-405. [Abstract/Full Text]
AAMC data book 2004. Washington, D.C.: Association of American Medical Colleges, 2004:Table B10.
Women in U.S. academic medicine: statistics and medical school benchmarking 2003-2004. Washington, D.C.: Association of American Medical Colleges, 2004:Table 3.
Women in U.S. academic medicine: statistics and medical school benchmarking 2004-2005. Washington, D.C.: Association of American Medical Colleges, 2005:Table 2.
Tesch BJ, Wood HM, Helwig AL, Nattinger AB. Promotion of women physicians in academic medicine: glass ceiling or sticky floor? JAMA 1995;273:1022-1025. [Abstract]
Barnett RC, Carr P, Boisnier AD, et al. Relationships of gender and career motivation to medical faculty members' production of academic publications. Acad Med 1998;73:180-186. [iSI][Medline]
Carr P, Friedman RH, Moskowitz MA, Kazis LE, Weed HG. Research, academic rank, and compensation of women and men faculty in academic general internal medicine. J Gen Intern Med 1992;7:418-423. [iSI][Medline]
Carr PL, Friedman RH, Moskowitz MA, Kazis LE. Comparing the status of women and men in academic medicine. Ann Intern Med 1993;119:908-913. [Abstract/Full Text]
Vydareny KH, Waldrop SM, Jackson VP, et al. Career advancement of men and women in academic radiology: is the playing field level? Acad Radiol 2000;7:493-501. [CrossRef][iSI][Medline]
Bhattacharyya N, Shapiro NL. Increased female authorship in otolargyngology over the past three decades. Laryngoscope 2000;110:358-361. [CrossRef][iSI][Medline]
Dickersin K, Fredman L, Flegal KM, Scott JD, Crawley B. Is there a sex bias in choosing editors? Epidemiology journals as an example. JAMA 1998;280:260-264. [Abstract/Full Text]
Schiaffino A, Garcia M, Fernandez E. Authorship and data reporting according to gender in four Spanish biomedical journals. Gac Sanit 2001;15:251-254. [Medline]
Bastuji-Garin S, Broquet E, Revuz J. Publications of French dermatology professors from 1996 to 1998. Ann Dermatol Venereol 2002;129:1354-1358. [iSI][Medline]
Thomson Institute for Scientific Information. Journal citation reports. Philadelphia: ISI Press, 2002.
Garfield E. The history and meaning of the journal impact factor. JAMA 2006;295:90-93. [Full Text]
AAMC data book 1990. Washington, D.C.: Association of American Medical Colleges, 1990:Table C4.
AAMC data book 1995. Washington, D.C.: Association of American Medical Colleges, 1995:Table C5.
AAMC data book 2000. Washington, D.C.: Association of American Medical Colleges, 2000:Table C5.
Yedidia MJ, Bickel J. Why aren't there more women leaders in academic medicine? The views of clinical department chairs. Acad Med 2001;76:453-465. [iSI][Medline]
Carr PL, Ash AS, Friedman RH, et al. Relation of family responsibilities and gender to the productivity and career satisfaction of medical faculty. Ann Intern Med 1998;129:532-538. [Abstract/Full Text]
A study on the status of women faculty in science at MIT. Cambridge, Mass.: The MIT Faculty Newsletter, March 1999. (Accessed June 23, 2006, at http://web.mit.edu/fnl/women/women.html.)
Cuca JM. The specialization and career preferences of women and men recently graduated from U.S. medical schools. J Am Med Womens Assoc 1979;34:425-435. [Medline]
Bickel J, Ruffin A. Gender-associated differences in matriculating and graduating medical students. Acad Med 1995;70:552-559. [iSI][Medline]
Buckley LM, Sanders K, Shih M, Hampton CL. Attitudes of clinical faculty about career progress, career success and recognition, and commitment to academic medicine: results of a survey. Arch Intern Med 2000;160:2625-2629. [Abstract/Full Text]
Dorsey ER, Jarjoura D, Rutecki GW. Influence of controllable lifestyle on recent trends in specialty choice by US medical students. JAMA 2003;290:1173-1178. [Erratum, JAMA 2003;290:2666.] [Abstract/Full Text]
Richtel M. Young doctors and wish lists: no weekend calls, no beepers. The New York Times. January 7, 2004:A1, A19.
Bland KI, Isaacs G. Contemporary trends in student selection of medical specialties: the potential impact on general surgery. Arch Surg 2002;137:259-267. [Abstract/Full Text]
Dorsey ER, Jarjoura D, Rutecki GW. The influence of controllable lifestyle and sex on the specialty choices of graduating U.S. medical students, 1996-2003. Acad Med 2005;80:791-796. [CrossRef][iSI][Medline]
Lambert EM, Holmboe ES. The relationship between specialty choice and gender of U.S. medical students, 1990-2003. Acad Med 2005;80:797-802. [CrossRef][iSI][Medline]
Wendel TM, Godellas CV, Prinz RA. Are there gender differences in choosing a surgical career? Surgery 2003;134:591-596. [CrossRef][iSI][Medline]
Grosz B, Dulac C, Dymecki S, et al. Report from the Task Force on Women in Science and Engineering. Cambridge, Mass.: Harvard University, May 2005. (Accessed June 23, 2006, at http://www.news.harvard.edu/gazette/daily/2005/05/wise.pdf.)
The Follow up::
(Women in Academic Medicine — Progress and ChallengesMary Beth Hamel @ M.D., M.P.H., Julie R. Ingelfinger, M.D., Elizabeth Phimister, Ph.D., and Caren G. Solomon, M.D., M.P.H.)
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PubMed Citation
In 1960, only about 5 percent of medical students in the United States were women; today, the numbers of women and men in medical school are approximately equal. This apparent success story, however, is tempered by observations that women who enter academic medicine have been less likely than men to be promoted or to serve in leadership positions.1 As of 2005, only 15 percent of full professors and 11 percent of department chairs were women.2
In this issue of the Journal, Jagsi et al.3 document similar trends for women as authors of articles in prominent medical journals. They report that nearly five times as many women authored original articles published in six major journals in 2004 than in 1970. Despite this progress, in 2004 small proportions of first and senior (last listed) authors were women (29.3 percent and 19.3 percent, respectively). Percentages of female authors were highest in those journals focused on pediatrics and obstetrics and gynecology — fields in which women compose a larger proportion of faculty members overall. In 2004, rates of female authorship were likewise low for guest editorials in two general medical journals (this journal and JAMA). As Jagsi and colleagues point out, invited editorialists and senior authors of original articles are typically more senior faculty members; the same may be true of first authors of articles in the high-impact journals included in this study. The authorship gap is likely to narrow substantially only when more women reach senior faculty positions.
What accounts for the apparent paradox of dramatic growth in the rate of women entering the field of medicine and the achievement of less success in academic medicine by women as compared with men, at least according to the conventional metrics of authorship and promotion? The answer remains unclear, but on the basis of available evidence and our own experiences in academic medicine, we believe that both institutional barriers to success and sex differences in career and life goals are important.
Published data during the past two to three decades, although limited, support real differences in the advancement and treatment of men and women in academic medicine. In a study of faculty members appointed to U.S. medical schools between 1979 and 1981, after a mean of 11 years as faculty members, only 5 percent of women, as compared with 23 percent of men, had achieved the rank of full professor; the difference was not fully explained by the number of hours worked or the number of articles published.4 This same study found that female faculty members were less likely than male faculty members to have laboratory space and grant support at the start of their academic careers.4 Studies have also documented that women receive lower salaries than men with similar experience and academic rank.5,6 In some surveys, female faculty members reported having fewer mentorship relationships or receiving less effective mentoring than that reported by male faculty members.7,8,9
Certain aspects of institutional culture and policy may pose challenges for women. Success in academic medicine has traditionally required working 60 to 70 hours per week, a time commitment that for many is incompatible with the responsibilities associated with raising children.10 In addition, tenure clocks at many institutions limit the number of years faculty members may remain at a given rank; this makes it difficult for someone to stay in academic medicine if he or she chooses to reduce work hours, even for a few years. Furthermore, meetings important to career advancement are frequently held outside of traditional working hours, when it is difficult for faculty members with children to attend. According to one study, as compared with male faculty members with children, female faculty members with children reported greater obstacles to career advancement and less institutional support. In contrast, such differences were not observed between male and female faculty members without children.11
While institutional barriers to the advancement of women must be addressed, we believe it is also important to consider the role of choice when comparing sex differences in faculty achievement. Each author of this editorial has experienced the challenges of raising children while working full-time in careers in medicine and science. Spending more time on scholarly activities necessarily means less time with family; women may be less likely than men to accept this trade-off. Indeed, surveys have documented that women in academic medicine work, on average, fewer hours than men work.4,12
Given that the roots of the "gender gap" in medicine are incompletely understood, what — if anything — should be done? Initiatives to support and promote women in academic medicine, which are already in place in some institutions and departments, should be encouraged and extended. Successful interventions should be emulated. For example, a program in a department of medicine that educated female faculty members about promotion criteria and provided a yearly assessment of each faculty member's appropriateness for promotion led to an increase from 4 to 20 female associate professors in just three years.7 National data also suggest that efforts may be paying off. Between 1999 and 2004, the Association of American Medical Colleges documented an increase in the promotion of women from assistant professor to associate professor.2 Mentorship is critical to academic success. Promotion of more women to senior faculty positions should provide more female mentors and role models for junior faculty members, but both men and women should be educated and encouraged to provide effective mentorship to women. Demonstrated success in providing equal opportunities and support for female faculty members should be included among our measures of job performance for leaders in academic medicine.
Finally, career paths in academic medicine should be more flexible and success less narrowly defined. Scholarly publications are important and are appropriately emphasized in promotion decisions, but achievements in medical education and clinical care also should be highly valued for both female and male faculty members. In many medical schools, promotion criteria and timelines require academic productivity that is unattainable without devotion of most waking hours to career activities, leaving little time for family and other priorities. This approach may prove untenable in the future, as women make up an increasing portion of the physician pool and as many male physicians take on more responsibility for child rearing and want more time for personal life.
Continued tracking of women's academic progress by the Association of American Medical Colleges and individual medical schools and attention to other measures of academic success, such as those reported by Jagsi and colleagues, are critical to the recognition of persistent inequities. Qualitative studies are also needed to assess the professional and personal aspirations of women and men in academic medicine. The future of academic medicine depends on its ability to attract and retain talented young men and women by offering opportunities that afford success and satisfaction in both their professional and personal lives.
References
Nonnemaker L. Women physicians in academic medicine -- new insights from cohort studies. N Engl J Med 2000;342:399-405. [Abstract/Full Text]
Magrane D, Lang J, Alexander H. Women in U.S. academic medicine: statistics and medical school benchmarking. Association of American Medical Colleges, 2005. (Accessed June 14, 2006, at http://www.aamc.org/members/wim/statistics...stats2005.pdf.)
Jagsi R, Guancial EA, Worobey CC, et al. The "gender gap" in authorship of academic medical literature -- a 35-year perspective. N Engl J Med 2006;355:281-287. [Abstract/Full Text]
Tesch BJ, Wood HM, Helwig AL, Nattinger AB. Promotion of women physicians in academic medicine: glass ceiling or sticky floor? JAMA 1995;273:1022-1025. [Abstract]
Ash AS, Carr PL, Goldstein R, Friedman RH. Compensation and advancement of women in academic medicine: is there equity? Ann Intern Med 2004;141:205-212. [Abstract/Full Text]
Carr P, Friedman RH, Moskowitz MA, Kazis LE, Weed HG. Research, academic rank, and compensation of women and men faculty in academic general internal medicine. J Gen Intern Med 1992;7:418-423. [iSI][Medline]
Fried LP, Francomano CA, MacDonald SM, et al. Career development for women in academic medicine: multiple interventions in a department of medicine. JAMA 1996;276:898-905. [Abstract]
Osborn EH, Ernster VL, Martin JB. Women's attitudes toward careers in academic medicine at the University of California, San Francisco. Acad Med 1992;67:59-62. [iSI][Medline]
Kaplan SH, Sullivan LM, Dukes KA, Phillips CF, Kelch RP, Schaller JG. Sex differences in academic advancement -- results of a national study of pediatricians. N Engl J Med 1996;335:1282-1289. [Abstract/Full Text]
Benz EJ, Clayton CP, Costa ST. Increasing academic internal medicine's investment in female faculty. Am J Med 1998;105:459-463. [CrossRef][iSI][Medline]
Carr PL, Ash AS, Friedman RH, et al. Relation of family responsibilities and gender to the productivity and career satisfaction of medical faculty. Ann Intern Med 1998;129:532-538. [Abstract/Full Text]
Carr PL, Friedman RH, Moskowitz MA, Kazis LE. Comparing the status of women and men in academic medicine. Ann Intern Med 1993;119:908-913. [Abstract/Full Text]
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Hello Everyone,
I saw this interesting case report and thought you all may be interested in reading it as it is about a situation which I think few of us consider as a possible etiology of this disorder...
HTH,
ACE844
(Characteristics of Meningitis Caused by Ibuprofen: Report of 2 Cases With Recurrent Episodes and Review of the LiteratureRodríguez @ Susana Casas MD; Olguín, Adriana Manzur MD; Miralles, Carmen Peña MD; Viladrich, Pedro Fernández MD
From Infectious Diseases Service (SCR, AMO, CPM, PFV), Hospital Universitari de Bellvitge, L'Hospitalet del Llobregat; and University of Barcelona (PFV), Barcelona, Spain.
Address reprint requests to: Dr. Pedro Fernández Viladrich, Hospital Universitari de Bellvitge, Feixa Llarga s/n 08907, L'Hospitalet del Llobregat, Barcelona, Spain. Fax: 0034-93-260-76-37; e-mail: pfviladrich@csub.scs.es.)
AbstractAbstract: Ibuprofen is a common nonsteroidal antiinflammatory drug that is the most frequent cause of aseptic meningitis induced by drugs. The incidence of this type of aseptic meningitis is increasing, mainly among patients with underlying autoimmune connective tissue disorder, but also among healthy people. We report 2 patients with recurrent meningitis caused by ibuprofen mimicking bacterial meningitis: the first patient a woman with dermatomyositis and the second patient a previously healthy woman who developed autoimmune thyroiditis a few months later.
We then review 71 episodes of ibuprofen-related meningitis in 36 patients reported in the literature. Twenty-two patients (61%) presented with an autoimmune connective tissue disorder, mainly systemic lupus erythematosus, and 22 (61%) had recurrent episodes. Most episodes consisted of an acute meningeal syndrome with a predominance of neutrophils in cerebrospinal fluid (CSF) in 72.2% of episodes and elevated protein in the CSF, so the clinical presentation of this type of aseptic meningitis may be quite similar to that of acute bacterial meningitis. CSF glucose levels are usually normal, which may help to differentiate between these 2 types of meningitis. In some cases the clinical presentation is that of meningoencephalitis with neurologic focal deficits.
Although based on the close relation between the administration of ibuprofen and the onset of symptoms, especially if previous episodes have occurred, the diagnosis of ibuprofen-induced aseptic meningitis is a diagnosis by exclusion. If the clinical picture is compatible with bacterial meningitis, empirical antibiotic therapy must be administered until negativity of cultures and other microbiologic tests is determined. Rechallenge to ibuprofen reproduces the symptoms and confirms the diagnosis, but is usually not advised.
Whatever the clinical presentation, physicians must consider the possibility of ibuprofen-related meningitis or meningoencephalitis in patients taking ibuprofen, especially if they are suffering from an autoimmune connective tissue disorder. On the other hand, we think it would be appropriate to screen for autoimmune disease in previously healthy patients diagnosed with ibuprofen-related meningitis or meningoencephalitis. Finally, we propose that meningitis due to ibuprofen be included in the list of causes of recurrent aseptic meningitis.
INTRODUCTION
Ibuprofen, a nonsteroidal antiinflammatory drug (NSAID) of the propionic acid group, is frequently used in patients with connective tissue disorders 16, and its use in patients without underlying diseases has progressively increased in the last years 25. Aseptic meningitis is a rare 31, albeit well-known, adverse effect of ibuprofen, and sporadic cases of patients with unique or recurrent episodes considered to be caused by this drug have been reported. In fact, it is the leading cause of aseptic meningitis induced by drugs 36. However, to our knowledge a comprehensive review of the characteristics of this type of meningitis has never been published.
We have recently seen 2 patients with recurrent episodes of meningitis induced by ibuprofen that mimicked bacterial meningitis, so they were hospitalized in an infectious disease ward. The diagnosis was reached by a rechallenge with the drug, thereby assuring accuracy. These cases have prompted us to review the literature to establish the clinical and biologic characteristics of this type of meningitis.
CASE REPORTS
Case 1
A 57-year-old woman with Sjögren syndrome and primary dermatomyositis presented in May 2003 with headache lasting 12 hours, nausea and vomiting, and without fever some hours after taking a tablet of ibuprofen. Physical findings, neurologic examination, computerized tomography (CT) of the brain, blood cell counts, and routine chemical serum determinations were all normal. Lumbar puncture revealed turbid cerebrospinal fluid (CSF) with opening pressure of 25 cm H2O. CSF cytochemical analysis showed 800 white blood cells (WBC)/mm3 (of which 85% were neutrophils and 15% lymphocytes), 372 mg/dL protein, and 57 mg/dL glucose. CSF Gram stain and culture were negative, and CSF pneumococcal antigen (Binax) was also negative. Empirical intravenous therapy with ceftriaxone and ampicillin was initiated and maintained for 10 days. The patient showed a rapid clinical response and was discharged without any apparent sequelae.
Three months later she was readmitted with similar symptoms beginning 12 hours after resumption of ibuprofen. This time neck stiffness was present. CSF was turbid with opening pressure of 24 cm H2O, WBC count of 1000/mm3 (90% neutrophils and 10% lymphocytes), 300 mg/dL protein, and 54 mg/dL glucose. CSF Gram stain was negative. Empirical intravenous antibiotic therapy was again administered but withdrawn 3 days later when blood and CSF cultures showed no microbial growth, and the patient was diagnosed with aseptic meningitis induced by ibuprofen. Her clinical symptoms improved shortly after admission, and the patient was discharged without symptoms.
Case 2
A previously healthy 49-year-old woman was admitted in October 2004 due to vertiginous syndrome lasting 5 days and headache, nausea, and vomiting a few hours before admission. On examination, positive findings included minimal pyrexia of 37.2 °C axillary temperature, confusion, horizontal nystagmus, and nuchal rigidity. WBC count was 27,120 cells/mm3 with neutrophilia. CSF was opalescent with opening pressure of 18 cm H2O and 2190 leukocytes/mm3 (76% neutrophils, 18% histiocytes, and 6% lymphocytes), 336 mg/dL protein, and 77.4 mg/dL glucose. CSF stains and cultures for bacteria, mycobacteria, and fungi were negative. CSF cryptococcal antigen and syphilis serology were also negative. She was treated empirically with intravenous ceftriaxone and ampicillin for 10 days. The patient recovered consciousness and meningeal signs disappeared but recovery from the vertiginous syndrome was slow. CSF obtained on day 8 was clear, with normal opening pressure and 315 leukocytes/mm3 (44% neutrophils, 2% histiocytes, and 54% lymphocytes), 178 mg/dL protein, and 63 mg/dL glucose. CSF bacterial cultures were negative. A CT of the brain was unremarkable.
On day 12 of hospitalization the patient was given a dose of ibuprofen for cervical pain, and 2 hours later, an abrupt onset of headache, fever of 39 °C, and vomiting occurred. On examination she was somnolent and confused, and neck stiffness and Kerning and Brudzinski signs were present. A lumbar puncture was not performed, and symptoms resolved promptly after ibuprofen was discontinued and corticosteroids were initiated. It was then that the patient reported that she had taken a dose of 400 mg ibuprofen 24 h before admission. She was discharged without sequelae, and a diagnosis of recurrent aseptic meningitis caused by ibuprofen. Four months later, she was diagnosed with autoimmune thyroiditis.
LITERATURE REVIEW METHODS
We conducted a MEDLINE (National Library of Medicine, Bethesda, MD) search with the subject headings "meningitis," "aseptic meningitis," "meningoencephalitis," "encephalitis," and "ibuprofen," to identify pertinent literature and case reports of aseptic meningitis or meningoencephalitis induced by ibuprofen published up to June 2005. We limited our search to the English and French literature available to us, with a few exceptions in other languages. All patient data we show were extracted from the reports we found, but sometimes not all clinical or laboratory data were detailed in the articles. We excluded all cases in which meningitis could not be related to ibuprofen 15,25,37,44,49. We have compiled the clinical and biologic characteristics of the 71 reported episodes of aseptic meningitis induced by ibuprofen.
RESULTS
We analyzed 71 episodes of aseptic meningitis induced by ibuprofen that occurred in 36 patients 1-3,5,8,9,11,12,14,16-21,23,24,27,29,30,32,33,35,37,39,41,42,44-46,49-53. There were 23 women (64%). The median age of the patients was 41 years (range, 21-74 yr). Twenty-two patients (61%) had recurrent episodes of aseptic meningitis after repeated ibuprofen ingestion. The number of recurrent episodes ranged from 2 to 4 (Table 1)1,3,8,12,14,18,19,23,24,29,32,35,37,39,42,44,46,51-53. Twenty-two patients (61%) suffered from an underlying autoimmune connective tissue disorder: 14 (39%) systemic lupus erythematosus (SLE)9,12,16,18-20,24,29,33,35,46,50,52,53; 6 (16.6%) undifferentiated or mixed connective tissue disease 1,3,17,21,41; 1 (2.8%) rheumatoid arthritis 23; and 1 (2.8%) Sjögren syndrome 2.
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[Email Jumpstart To Image] TABLE 1. CSF Characteristics in 54* of 71 Reported Episodes of Ibuprofen-Induced Aseptic Meningitis
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The latency period between intake of ibuprofen and onset of symptoms varied but it was less than 24 hours in 36 of the 46 episodes in which this information was reported 1,3,8,9,11,12,14,18-20,23,24,27,29,30,32,37,41,42,44-46,49,50,52,53. The doses of ibuprofen the patients had taken were also variable. Twenty-five episodes developed after only 1 dose of 200-600 mg of ibuprofen 1,3,9,12,14,16,17,20,24,29,30,32,35,37,42,44,49,51-53. But in 15 episodes, the symptoms appeared after taking more than 2 doses of ibuprofen 1,2,14,19,21,27,33,39,41,42,45,46. Time from exposure to ibuprofen before developing symptoms was very short except in 8 cases: 2 cases after taking ibuprofen for 1 week 2,39, 4 for 2 weeks 14,21,42,52, 1 for "several weeks"27, and 1 for 2 years 35. It is remarkable that 1 patient with ibuprofen-induced aseptic meningitis also developed 2 different episodes of aseptic meningitis in relation to naproxen and rofecoxib 2.
The frequency of symptoms and signs is described in Table 2. Many patients had typical meningeal syndrome with fever (69%), altered mental status (58%), headache (52%), neck stiffness (46.5%), and nausea and vomiting (42%). Some patients had meningoencephalitis 1,9,12,17,32,33,42 instead of meningitis. Of note is that 9 episodes (12.7%) presented with hypotension 1,12,35,52 and 10 (14%) with cutaneous rash 12,21,24,32,33,50,52, which was petechial in 2 of them 32. Other symptoms and signs were arthralgia/myalgia 11,14,21,24,30,35,42, photophobia 2,8,9,19,27,29,30,45, blurred vision 1,11,35, conjunctivitis 1,11,21,24,30,35, abdominal pain 11,50,53, and facial edema 11,21,32. Very infrequent symptoms such as iridocyclitis 27, syndrome of inappropriate antidiuretic hormone (SIADH)41, and acute renal failure 21 were also reported. One patient progressed to coma with bilateral Babinski 32 in his 2 episodes and had to be admitted to the intensive care unit (ICU) during 1 of them. Two more patients presented with bilateral Babinski 9,17. Another 2 patients with coma 24,33, 1 of them with papilledema 24, also required admission to the ICU. Five patients developed neurologic focal deficits: palsy of conjugate movement of the eyes to the right 1, tonic-clonic movements 9,12,33 (even status epilepticus 33), and paresthesia with left hemiparesis 1. But all patients had an excellent outcome after withdrawing the drug, and none had neurologic sequelae.
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[Email Jumpstart To Image] TABLE 2. Clinical Manifestations in 71 Episodes of Ibuprofen-Induced Aseptic Meningitis
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The characteristics of the CSF found in the literature, highlighting those cases similar to bacterial meningitis, are shown in Table 1. Some reports did not show the values of these determinations and only referred to them as "normal"1,27,33,39, "increased"5, or "low"5. In 17 episodes no CSF analysis was performed 3,11,12,18,19,23,24,35,53.
The CSF pressure varied from normal to elevated up to 22.4 cm H2O, but most of the articles did not refer to this value. The WBC count in CSF was also variable with a median of 280 cells/mm3 (range, 9-5,000/mm3). The WBC differential count in CSF was as follows: predominance of neutrophils in 39 cases (39/54; 72.2%)1,3,5,8,9,12,14,17-21,23,29,30,32,35,37,41,44,46,49-53, predominance of lymphocytes in 11 (20.4%)2,24,27,33,39,42,46,53, predominance of monocytes in 2 (3.7%)8,32, and eosinophils in only 1 case (1.8%)45. In 1 case, the CSF showed 50% neutrophils and 50% monocytes 16. The median value of protein was 132 mg/dL with a range of 32-857 mg/dL. The protein level was normal in 4 cases 1,14,27,35, moderately increased (50-100 mg/dL) in 17 cases 2,8,14,21,35,39,41,42,45,46,50,52, and more significantly increased (>100 mg/dL) in 30 cases 1,3,8,9,12,16-20,23,24,29,30,32,33,37,44,49,51,53. The median value of glucose in CSF was 62 mg/dL with a range of 27-109 mg/dL. CSF glucose was slightly down in 8 cases: 10-37 mg/dL in 5 1,8,37,46,53 and reported as "low" in the other 3 5.
DISCUSSION
Central nervous system (CNS) side effects have been reported to occur in 4%-10% of patients treated with NSAIDs. The most common are headache, tinnitus, and hearing loss. Infrequent CNS side effects are aseptic meningitis, psychosis, and cognitive dysfunction 10,22,40. Ibuprofen is the most frequent cause of aseptic meningitis induced by drugs 22,26,38. However, other NSAIDs have also been recognized as causes of aseptic meningitis: diclofenac, sulindac, naproxen, ketoprofen, tolmetin, piroxicam, and, more recently, rofecoxib and celecoxib 2,4,7,22,26,38,47. The exact incidence of meningitis as a side effect of these drugs is unknown. Clinical and biologic characteristics described in cases of aseptic meningitis due to NSAIDs other than ibuprofen are similar to those of ibuprofen-induced meningitis 23.
Aseptic meningitis is a rare adverse effect of ibuprofen. In 1 population study conducted in the United States from 1977 to 1981, there was no case of aseptic meningitis among 13,230 ibuprofen users 25. The first case of ibuprofen-related meningitis was reported in 1978 by Widener and Littman 53. They described a 26-year-old woman with SLE and recurrent aseptic meningitis that was not attributed to ibuprofen until she experienced her fourth episode of meningitis.
Since then, an increasing number of cases of aseptic meningitis or meningoencephalitis attributed to this drug have been reported 1-3,5,8,9,11,12,14,16-21,23,24,27,29,30,32,33,35,37,39,41,42,44-46,49-52. Most frequently they were patients with recurrent meningitis, which in part proves that this illness is not well known and that a high level of suspicion is required for diagnosis 6,34.
The first published cases occurred in patients with underlying autoimmune connective tissue disorders, mainly SLE 36,40, but also undifferentiated or mixed connective tissue, rheumatoid arthritis, and Sjögren syndrome. Our Case 1 constitutes the first report of aseptic meningitis attributed to ibuprofen in a patient with dermatomyositis that we know of, and our second patient was diagnosed with autoimmune thyroiditis 4 months after the episode. Autoimmune thyroiditis has not been previously related to this type of ibuprofen adverse effect, either, to our knowledge. Based on the relation between autoimmune problems and aseptic meningitis related to ibuprofen, we suggest that analytical screening for such disorders should be done on previously healthy subjects with a first episode 9,33.
In addition to those cases affecting patients with autoimmune disorders, several other cases have been reported in apparently healthy people 8,11,14,27,30,32,37,39,44,45,49,51. This might be related to the broad use of NSAIDs during the past years in the general population 5,14,17,18,22,25,45 (in Spain, they are purchased over-the-counter).
The pathogenesis of this reaction remains unclear. Ibuprofen does not achieve high concentrations in CSF 8. However, it does not seem to be mediated either by inhibition of prostaglandin synthesis 8,12,14,45,53 or by the accumulation of ibuprofen's metabolites within the CNS because the latency period after rechallenge is very short, as seen in the 2 cases in the current study. Since there is increased intrathecal synthesis of IgG and immune complex formation, a specific antigen-antibody response-a type III or IV hypersensitivity reaction-confined to CNS has been suggested 3,8,14,20,28,43. Thus, a preexisting autoantibody may be activated by ibuprofen 3,8.
The higher incidence of ibuprofen-induced aseptic meningitis in patients with autoimmune disorders could be explained by the widespread use of NSAIDs or by their tendency to autoreact 48. Experimental animal studies have shown that aseptic meningitis can be induced in NZB/NZW F1 mice 1,8,14,35 (mice that develop a lupus-like disease) after administration of ibuprofen. This supports the hypothesis that these types of patients develop this side effect more frequently.
Development of aseptic meningitis is independent of the dosage of ibuprofen 39, and it is likely to occur a few hours after intake, as in our cases. So the latency period is usually very short 44. Nevertheless, patients with previous exposure to the drug days 2,14,39,42, months, or even years 35 before can develop it.
Presenting clinical manifestations of ibuprofen-related meningitis may be indistinguishable from those of acute bacterial meningitis 13,41, because of the acute onset with fever, headache, nausea and vomiting, altered mental status, and neck stiffness as usual symptoms. It is even possible to observe a cutaneous rash mimicking meningococcal disease 32.
Moreover, in the majority of cases, CSF shows pleocytosis, often very intense, with neutrophilic predominance. CSF protein levels frequently exceed those usually seen in viral meningitis. So the initial diagnosis of bacterial meningitis is quite logical in such cases. In fact, our patients presented with turbid CSF containing intense neutrophilic pleocytosis and elevated protein, so bacterial meningitis was diagnosed and antimicrobial treatment was initiated.
Occasionally, CSF may contain a significant percentage of monocytes or histiocytes, as occurred in our second patient and in other reported episodes 8,14,16,32,42,52. To our knowledge, this finding has not been described in acute bacterial meningitis, and its presence would help physicians in the diagnosis of drug-related meningitis. Likewise, a significant percentage of eosinophils 45 in CSF suggests a nonbacterial cause of meningitis.
CSF glucose levels are usually normal in ibuprofen-related meningitis, although moderate hypoglycorrhachia may occur and add to the initial suspicion of bacterial meningitis. Nevertheless, the fact that we found no case with CSF glucose levels close to 0 mg/dL or undetectable leads us to believe that this is a helpful feature in making a differential diagnosis between acute bacterial meningitis and ibuprofen-related meningitis.
There are cases that simulate viral meningitis, especially if lymphocytes predominate in CSF. The occurrence of coma and focal neurologic deficits may suggest a viral meningoencephalitis syndrome 1,9,12,17,32,33,42.
The clinical course of ibuprofen meningitis or meningoencephalitis is relatively short and benign, with rapid resolution of symptoms after discontinuing the drug 2,3,11,12,16,17,20,22,32,35,53. However, CSF may return to normality quite slowly, as illustrated in our second case, in which CSF remained altered 14 days after the onset of symptoms, as well as in other reported cases 8,16,32,53. Cognitive or neurologic sequelae have not been reported 26.
In some cases, patients have been treated with corticoids to shorten the clinical course, but, obviously, there are no comparative studies done on this 3,16,35,36. It seems rational to administer those drugs for a short period of time, especially in the most severe cases. The courses of recurrent episodes of meningitis induced by ibuprofen in the same patient were not more severe than the initial episodes 11,39, although some authors have described increased severity of symptoms 14. In our patients, characteristics of the initial episodes and the recurrences were similar. However, if an episode of ibuprofen-related meningitis is suspected, rechallenging with the drug to obtain the diagnosis is not usually indicated. Patients must be informed to avoid re-exposure not only to ibuprofen 12,16,20 but also to all drugs from the same family (dexibuprofen, dexketoprofen, flurbiprofen, ketoprofen, and naproxen). It might even be advisable to avoid the other NSAIDs that have been related to aseptic meningitis 2,22, because there are a few reports of patients with recurrent episodes of aseptic meningitis due to different NSAIDs 2,11,47.
In conclusion, although aseptic meningitis is an uncommon side effect of ibuprofen, the widespread use of ibuprofen, as well as other NSAIDs, makes an increase in its incidence a possibility. Ibuprofen is the most frequently implicated drug in aseptic meningitis induced by drugs. The clinical course of this illness may be similar to that of acute bacterial meningitis, so physicians must consider it as a differential diagnosis, mainly in patients with underlying autoimmune connective tissue disorders and in patients with recurrent meningitis. In fact, meningitis due to ibuprofen must be added to the list of causes of recurrent aseptic meningitis, and it may be appropriate to screen for autoimmune diseases in healthy subjects who develop this adverse effect.
Ibuprofen-induced aseptic meningitis is a diagnosis by exclusion that depends on the chronology between drug administration and onset of symptoms, as well as on negativity of microbiologic tests. Re-exposure to ibuprofen, often by chance, reproduces the symptoms and confirms the diagnosis, as occurred in our 2 patients. However, when the illness is compatible with acute bacterial meningitis, empirical antibiotic therapy must be administered until negativity of cultures and other antigenic or molecular tests rule out that diagnosis. This is true even if the patient has a known condition of meningitis induced by drugs.
REFERENCES
1. Agus B, Nelson J, Kramer N, Mahal SS, Rosenstein ED. Acute central nervous system symptoms caused by ibuprofen in connective tissue disease. J Rheumatol. 1990;17:1094-1096. SFX Bibliographic Links Library Holdings [Context Link]
2. Ashwath ML, Katner HP. Recurrent aseptic meningitis due to different non-steroidal anti-inflammatory drugs including rofecoxib. Postgrad Med J. 2003;79:295-296. SFX Bibliographic Links Library Holdings [Context Link]
3. Bernstein RF. Ibuprofen-related meningitis in mixed connective tissue disease. Ann Intern Med. 1980;92:206-207. SFX Bibliographic Links Library Holdings [Context Link]
4. Bonnel RA, Villalba ML, Karwoski CB, Beitz J. Aseptic meningitis associated with rofecoxib. Arch Intern Med. 2002;162:713-715. Ovid Full Text Bibliographic Links Library Holdings [Context Link]
5. Bouland DL, Lennard N, Hegstad DR. Ibuprofen and aseptic meningitis [letter]. Ann Intern Med. 1986;104:731. SFX Bibliographic Links Library Holdings [Context Link]
6. Canoso JJ, Cohen A. Aseptic meningitis in systemic lupus erythematosus. Arthritis Rheum. 1975;18:369-374. SFX Bibliographic Links Library Holdings [Context Link]
7. Chazan B, Weiss A, Weiner Z, Rimbrot S, Raz R. Drug induced aseptic meningitis due to diclofenac [letter]. J Neurol. 2003;250:1503-1504. SFX Bibliographic Links Library Holdings [Context Link]
8. Chez M, Sila CA, Ransohoff RM, Longworth DL, Weida C. Ibuprofen-induced meningitis: detection of intrathecal IgG synthesis and immune complexes. Neurology. 1989;39:1578-1580. Ovid Full Text Bibliographic Links Library Holdings [Context Link]
9. Colamarino R, Soubrier M, Zenut-Leaud M, Prudat M, Tournilhac M, Bussiere JL. [Aseptic meningitis caused by ibuprofen (Nurofen) in connective tissue diseases.] Therapie. 1993;48:516-518. SFX Bibliographic Links Library Holdings [Context Link]
10. David A, Peter K, Neil G, Roy B. Cognitive decline with chronic meningitis secondary to a COX-2 inhibitor. Age Ageing. 2004;33:408-410. SFX Bibliographic Links Library Holdings [Context Link]
11. Davis BJ, Thompson J, Peimann A, Bendixen B. Drug-induced aseptic meningitis caused by two medications. Neurology. 1994;44:984-985. Ovid Full Text Bibliographic Links Library Holdings [Context Link]
12. Durback MA, Freeman J, Schumacher HR. Recurrent ibuprofen induced aseptic meningitis: third episode after only 200 mg of generic ibuprofen. Arthritis Rheum. 1988;31:813-815. SFX Bibliographic Links Library Holdings [Context Link]
13. Elmore JG, Horwitz RI, Quagliarello WJ. Acute meningitis with a negative Gram's stain: clinical and management outcomes in 171 episodes. Am J Med. 1996;100:78-84. SFX Bibliographic Links Library Holdings [Context Link]
14. Ewert BH. Ibuprofen-associated meningitis in a woman with only serologic evidence of rheumatologic disorder. Am J Med Sci. 1989;297:326-327. SFX Bibliographic Links Library Holdings [Context Link]
15. Finch WR, Strottman MP. Acute adverse reactions to ibuprofen in systemic lupus erythematosus. JAMA. 1979;241:2616-2618. SFX Bibliographic Links Library Holdings [Context Link]
16. Giansiracusa DF, Blumberg S, Kantrowitz FG. Aseptic meningitis associated with ibuprofen [letter]. Arch Intern Med. 1980;140:1553. SFX Bibliographic Links Library Holdings [Context Link]
17. Gilbert GJ, Eichenbaum HW. Ibuprofen-induced meningitis in an elderly patient with systemic lupus erythematosus. South Med J. 1989;82:514-515. SFX Bibliographic Links Library Holdings [Context Link]
18. Grimm AM, Wolf JE. Aseptic meningitis associated with nonprescription ibuprofen use [letter]. DICP. 1989;23:712. SFX Bibliographic Links Library Holdings [Context Link]
19. Hanson L. Ibuprofen-induced aseptic meningitis [case report]. J Tenn Med Assoc. 1994;87:58. SFX Bibliographic Links Library Holdings [Context Link]
20. Hidalgo A, Cardenas R, Najem N, Canto G. Meningitis aseptica probablemente inducida por Ibuprofeno en una paciente con lupus eritematoso sistemico. Med Clin (Barc). 2004;122:678-679. SFX Bibliographic Links Library Holdings [Context Link]
21. Hoffman M, Gray RG. Ibuprofen-induced meningitis in mixed connective tissue disease. Clin Rheumatol. 1982;1:128-130. SFX Bibliographic Links Library Holdings [Context Link]
22. Hoppmann RA, Peden JG, Obert SK. Central nervous system side effects of nonsteroidal anti-inflammatory drugs: aseptic meningitis, psychosis and cognitive dysfunction. Arch Intern Med. 1991;151:1309-1313. SFX Bibliographic Links Library Holdings [Context Link]
23. Horn AC, Jarrett SW. Ibuprofen-induced aseptic meningitis in rheumatoid arthritis. Ann Pharmacother. 1997;31:1009-1011. SFX Bibliographic Links Library Holdings [Context Link]
24. Jensen S, Glud TK, Bacher T, Ersgaard H. Ibuprofen-induced meningitis in a male with systemic lupus erythematosus. Acta Med Scand. 1987;221:509-511. SFX Bibliographic Links Library Holdings [Context Link]
25. Johnson JH, Jick H, Hunter JR, Dickson JF. A follow-up study of ibuprofen users. J Rheumatol. 1985;12:549-552. SFX Bibliographic Links Library Holdings [Context Link]
26. Jolles S, Sewell WA, Leighton C. Drug-induced aseptic meningitis: diagnosis and management. Drug Saf. 2000;22:215-226. SFX Bibliographic Links Library Holdings [Context Link]
27. Kaplan BH, Nevitt MP, Pach JM, Herman DC. Aseptic meningitis and iridocyclitis related to ibuprofen. Am J Ophthalmol. 1994;117:119-120. SFX Bibliographic Links Library Holdings [Context Link]
28. Kastenbauer S, Pfister H, Wick M. No evidence of type 1 or type 3 hypersensitivity mechanism in amoxicillin/clavulanic acid induced aseptic meningitis. J Neurol Neurosurg Psychiatry. 2003;74:690-691. Ovid Full Text Bibliographic Links Library Holdings [Context Link]
29. Katona B, Wigley F, Walters JK, Caspi M. Aseptic meningitis from over-the-counter ibuprofen [letter]. Lancet. 1988;1:59. SFX Bibliographic Links Library Holdings [Context Link]
30. Lawson JM, Grady MJ. Ibuprofen-induced aseptic meningitis in a previously healthy patient. West J Med. 1985;143:386-387. SFX Bibliographic Links Library Holdings [Context Link]
31. Lee RP, King EG, Russell AS. Ibuprofen: a severe systemic reaction. Can Med Assoc J. 1983;129:854-855. SFX Bibliographic Links Library Holdings [Context Link]
32. Lee RZ, Hardiman O, O'Connell PG. Ibuprofen-induced aseptic meningoencephalitis. Rheumatology. 2002;41:353-355. SFX Bibliographic Links Library Holdings [Context Link]
33. Lortholary A, Varache N, Bouachour G, Szapiro N, Bourrier P, Alquier P. [Generalized status epilepticus after ingestion of ibuprofen (Brufen), disclosing systemic lupus erythematosus.] Rev Med Interne. 1990;11:243-244. SFX Bibliographic Links Library Holdings [Context Link]
34. Maignen F, Castot A, Falcy M, Efthymiou ML. Les meningitis aseptiques d'origen medicamenteuse. Therapie. 1992;47:399-402. SFX Bibliographic Links Library Holdings [Context Link]
35. Mandell BF, Raps EC. Severe systemic hypersensitivity reaction to ibuprofen occurring after prolonged therapy. Am J Med. 1987;82:817-820. SFX Bibliographic Links Library Holdings [Context Link]
36. Marinac JS. Drug- and chemical-induced aseptic meningitis: a review of the literature. Ann Pharmacother. 1992;26:813-822. SFX Bibliographic Links Library Holdings [Context Link]
37. Mifsud AJ. Drug-related recurrent meningitis. J Infect. 1988;17:151-153. SFX Bibliographic Links Library Holdings [Context Link]
38. Moris G, Garcia-Monco JC. The challenge of drug-induced aseptic meningitis. Arch Intern Med. 1999;159:1185-1194. Ovid Full Text Bibliographic Links Library Holdings [Context Link]
39. Nguyen HTV, Juurlink DN. Recurrent ibuprofen-induced aseptic meningitis. Ann Pharmacother. 2004;38:408-410. SFX Bibliographic Links Library Holdings [Context Link]
40. Ostensen M, Villiger PM. Nonsteroidal anti-inflammatory drugs in systemic lupus erythematosus. Lupus. 2001;10:135-139. SFX Bibliographic Links Library Holdings [Context Link]
41. Peck MG, Joyner PU. Ibuprofen-associated aseptic meningitis. Clin Pharm. 1982;1:561-565. SFX Bibliographic Links Library Holdings [Context Link]
42. Perera DR, Kurt A, Greeley HM. Ibuprofen and meningoencephalitis [letter]. Ann Intern Med. 1984;100:619. SFX Bibliographic Links Library Holdings [Context Link]
43. Peter JB. Ibuprofen meningitis. Neurology. 1990;40:866-867. Ovid Full Text Bibliographic Links Library Holdings [Context Link]
44. Pisani E, Fattorello C, Leotta MR, Marcello O, Zuliani C. Recurrence of ibuprofen-induced aseptic meningitis in an otherwise healthy patient. Ital J Neurol Sci. 1999;20:59-62. SFX Bibliographic Links Library Holdings [Context Link]
45. Quinn JP, Weinstein RA, Caplan LR. Eosinophilic meningitis and ibuprofen therapy. Neurology. 1984;34:108-109. Ovid Full Text Bibliographic Links Library Holdings [Context Link]
46. Samuelson CO Jr, Williams HJ. Ibuprofen-associated aseptic meningitis in systemic lupus erythematosus. West J Med. 1979;131:57-59. SFX Bibliographic Links Library Holdings [Context Link]
47. Seaton RA, France AJ. Recurrent aseptic meningitis following non-steroidal anti-inflammatory drugs-a reminder. Postgrad Med J. 1999;75:771-772. SFX Bibliographic Links Library Holdings [Context Link]
48. Sonnenblick M, Abraham AS. Ibuprofen hypersensitivity in systemic lupus erythematosus. BMJ. 1978;1:619-620. SFX Bibliographic Links Library Holdings [Context Link]
49. Thilmann AF, Mobius E, Thilmann RR, Topper R. Recurrent aseptic meningitis (Mollaret meningitis)-spontaneous and drug-induced origin. Fortschr Neurol Psychiatr. 1991;59:493-497. SFX Bibliographic Links Library Holdings [Context Link]
50. Treves R, Gastine H, Richard A, Hugon J, Varnoux M, Gay R, Desproges-Gotteron R. [Aseptic meningitis and acute renal failure induced by ibuprofen during the treatment of systemic lupus erythematosus.] Rev Rhum Mal Osteoartic. 1983;50:75-76. SFX Bibliographic Links Library Holdings [Context Link]
51. van der Zwan A, van Dam JG. [ibuprofen meningitis.] Ned Tijdschr Geneeskd. 1992;136:1613-1614. SFX Bibliographic Links Library Holdings [Context Link]
52. Wasner CK. Ibuprofen, meningitis, and systemic lupus erythematosus. J Rheumatol. 1978;5:162-164. SFX Bibliographic Links Library Holdings [Context Link]
53. Widener HL, Littman BH. Ibuprofen-induced meningitis in systemic lupus erythematosus. JAMA. 1978;239:1062-1064. SFX Bibliographic Links Library Holdings [Context Link]
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Well the quote of ACEs that you list presumes that there isn't any option but to have nasty blades. I dont think that is the case. Sure if i am dying, i will take my chances with any germ that might be on your blade, but again I ask why cant i have the cleanest blade possible (I didnt even ask for sterile - just properly cleaned) ?
It sounds like that in your and ACE's service, I can expect to have a reasonably clean blade inserted into my mouth, but that is not the case country-wide. We have all reached into a jumpbag and grabbed a dirty blade at some point in our career, that couldve been used on a patient, had we not been so diligent in our morning inspection (and often times, it had been missed by 1 or 2 shifts).
Again your making statements for which you have no facts...prove this...
Also i find it interesting that you choose to continue your unsupported debate in this thread vs any of the others as well...But hey, keep trying...I can expect to have a reasonably clean blade inserted into my mouth, but that is not the case country-wide.out here,
ACE844
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We are fortunate that we have not had to deal with many of the third-world diseases that are currently killing thousands on other continents. But with the illegal exotic pet trade on our continent, and all of the intercontinental airline flights, our day is coming.
Are you kidding....what comes next... statements of THE END IS NEAR...YOUR ALL GOING TO DIE YOU SINNERS!!...[Ace shakes his head and waits in disbelief for whatever other drivel could possibly come next] If these statements aren't a trip to==>
then what is? -
Ace,
It seems that GAmedic lives rent free in your head, and others for that matter. Some of your replys to this thread are easier to read than others as your type face gets bigger and more colorful.........I almost feel as if you are shouting at us, the collective readers on this forum. You repeatedly ask GAmedic to answer your questions regarding documentation.............I dunno.....so
"What procedures do you use to insure your blades are clean ? "
If you answered all of his questions and I somehow missed it then please feel free to shout back at me!
"PT,"
I wasn't shouting at the forum in general. I was using caps and colors to highlight certain points in my posts..that's it. "GAmedic," has yet to post viable evidence to back up any of his statements which then takes the thread-posts to a place where he is preaching whatever propaganda he thinks you'll listen to, and then later contradicts his own statements. He has done this repeatedly.
I answered, although probably not enough to be satisfactory. We use disposable blades. The Hospitals that I spend alot of time in send the instruments off to be 'cleaned' chemically and then again via autoclave. Furthermore this thread was started by this individual as a rant about 'DIRTY-UNCLEAN LARYNGOSCOPE BLADES and infectious transmittal risk from them to patients'! He didn't make a general statement about how we need to be more cognizant of infection control and cleaning in EMS which i think we would all agree needs work. NO he repeatedly made this about the aforementioned issue and when asked to prevent facts to support those claims he couldn't produce them. That is the problem I have with this individual. He makes statements and purports them to be incontrovertiably true, then consistantly is unable to back them up with facts.
Out Here,
ACE844
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I would counter that misdirection is what you are using to ignore an obvious fact: Dirty laryngoscopes dont belong in patient's mouths, I dont care if you find 100 scientific studies that allow you to do it, my personal ethics will not allow it.
No one here advocated for the placement of grossly infectious or 'dirty non-cleaned and disinfected equipment' anywhere near a patient. Work on your reading comprehension.
There was a time in the US when the vast majority of people thought:That slavery was OK,
That women shouldnt vote,
That airplane flight was impossible,
That space exploration was impossible,
That curing Cancer and Polio was impossible,
That Paramedics shouldnt be allowed to intubate patients,
And they all had experts to back their "facts" -- it didnt make it right. Just because it is today's norm, doesnt mean that it will be heralded as a best practice in the future. There was a time when the best scientist of the day thought that leaches and lobotomies were good cures.
Actually in some areas PARAMEDICS were allowed to entubate from the beginning and thats what made them PARAMEDICS instead of funeralhome diesel fuel speed jockies who slapped o2 on and ran to the hospital...
Next, they still use leaches and maggots as medical therepy with grewat effect, educate yourself!!
Lastly, I am asking for evidenced based scientific information which supports your claim and now that you can't provide it you say
Seems to me you tried that arguement with no sucess in another thread...hmm...TRY AGAIN!!"Well... we used to....insert miscellaneous example here.."Out Here,
ACE844
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And for the record, Avian flu will be the most infectious pandemic we will ever see, if it occurs. And it is a solely respiratory based disease, spread through droplet form, that will kill 30-50% of people infected. This pandemic is expected to far exceed the death toll from the early 1900s that killed 600 million world wide. Since nothing can be stated in here without a scientific study, please go to www.pandemicflu.gov
But lets not worry about future boogey-men germs -- lets just deal with the ones we have now.
Again, there is nothing there to show that there has been or will be transmittal and spread of this disease via inproperly disinfected medical equipment or laryngoscope blades...WHICH IS WHAT YOU MADE THIS THREAD ABOUT... We're stil;l waiting for your viable response with evidence to support your claim which you have yet to post.
ACE
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This study on SARS showed no evidence of transmittable infection via laryngoscope blades... The nosocomial and pre-hospital infections were attributed to either inadequate or improrper use of PPE and lack of initial 'education' or knowledge of how SARS was transmitted...TRY AGAIN...THIS STUDY DOESN'T SUPPORT YOUR POINT!!
www.blackwell-synergy.com/doi/abs/10.1046/j.1365-2044.1999.01178.x -Most units autoclave laryngoscope blades at some time, but less than one-quarter ... Another study revealed that in two units in which only obviously dirty ...
www.blackwell-synergy.com/doi/full/10.1046/j.1365-2044.1999.00755.x -
LINKS DON'T WORK FOR ABOVE STUDIES, CAN'T COMMENT...
File Format: PDF/Adobe Acrobat - View as HTMLfailing to maintain separate clean and dirty work spaces; ... In one anesthesia equipment study, sixty-five laryngoscope blades and handles that were ...
www.dolphinmedical.com/brochures/Disinfection_Abstract1_Full.pdf - Similar pages
SPO[sub:d8a1e29d49]2[/sub:d8a1e29d49] SENSOR CLEANING HAS TO DO WITH LARYNGOSCOPE BLADES HOW?!?!?!?
Brindley M. Dirty ambulances endanger health. Western Mail. ... Disposable covers are provided for laryngoscope blades and single use bougies for intubation ...emj.bmjjournals.com/cgi/content/full/21/5/647-a - Similar pages
AGAIN, HAD NOTHING TO DO WITH LARYNGOSCOPE TRANSMITTAL OF INFECTIONS AND ...WENT ON FURTHER TO SAY
We fully accept that the methods used were not rigorous enough to accurately quantify numbers of bacteria for any given measured area. Most organisms identified in the study were unlikely to pose any threat of infection to patients or ambulance personnel. This was clearly stated in our article, but sadly was often ignored in the subsequent press reports, resulting in public concern.TRY AGAIN...
ACE844
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Its common sense ACE -- are you actually going to defend your right to put dirty equipment in your patient's mouth ?
ANSWER THE QUESTIONS.... MISDIRECTION IS WHAT POLITICIANS AND MAGICIANS DO TO DISTRACT YOU FROM EITHER INADEQUACY, LIES AND MISSTATEMENTS OR WHAT'S REALLY HAPPENING...BACK UP YOUR STATEMENTS AND ANSWER THE QUESTIONS POZED AND USE VERIFIABLE NON-ANECDOTAL INFORMATION TO DO SO..
Oh, and now that you've added AVIAN FLU to your mix of miscellaneous bugs, kindly include evidence of transmission of THAT via laryngoscope blades... Thank You,
ACE844
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Kindly respond to my previous requests in this thread for stats and verifiable information to back up your points and standards, as well as other information.
Thank You,
ACE844
Someone re-editied their post from the quote above... But still no adequate response or facts to back up the propagandists soapbox positions... :roll: Come GA... PROVE IT.. instead of diverting attention form your post with a mis-direction about potential MRSA and HEP. Miscellaneous letters...
Out Here,
ACE844
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hmmmmm.....got real quiet, real quick.... :roll: :shock:
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The question was would you put your current blades, as they sit in your bag, in your mouth. I didnt mention anything about intubation, but since everyone is hedging with "If I were dying - yes", I guess the answer is no. The restaurant industry has a saying that goes, "If you wouldn't eat it, dont serve it to your customers!". My question is that if it is so nasty that you wont put it in your mouth, why is it good enough for your patients. And no, I am not concerned over dust or sand, I am concerned about the germs from the last patient's vomit or blood. If you were about to have routine surgery, and the Anesthesiologist was using the same practice for his blades that you do for yours, would you allow it to be placed in your mouth ?
Kindly respond to my previous requests in this thread for stats and verifiable information to back up your points and standards, as well as other information.
Thank You,
ACE844
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Gee Ace, I think you made the pilot sick. :shock:
And strangely no responses from GA. Hmmm, maybe he wore himself out finding the next pet cause to espouse.
Just when things started getting interesting too. :?
Just so as not to offend any of the PC crowd i purposely made this a gender neutral statement, though that I am sure went unnoticed by card carrying ACLU value espousing GAmedic..... :roll: Still a bigger issue than a less than optimally clean laryngoscope blade...but I digress....Someone I know tried to augment the cleaning of an old school stainless blade with AJAX and a brillo in addition to cidefex, and well lets just say it left an interesting looking film on the blades...I wonder how that tastes? Any one up for a lick to let us know???
ACE
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So to get these kinds of results the facilities have to believe that we know what we are doing individually.
What would be the best way to get this message across? We all have worked with providers of all levels that we wouldn't let treat a sick cockroach, much less a human being, so how do we go about convincing the receiving physicians that, as a group, we can make this determination without them?
This is most definitely a serious question, because we are having this issue here locally. Perhaps I'm guilty of thinking locally and acting globally, but if anyone has suggestions, I'm willing to listen.
"AZCEP,"
Anecdotally I've found exposure and time together in a clinical environment makes the difference. This usually gets resisitance though from the EMS providers and soemtimes companies-municipalities as it requires them to debate issues like pay vs your own time and actually having to put forth effort above and beyond what time are we getting breakfast at the start of shift. Furthering this thought if you sit down with the docs and work out an outline whereby you all could spend time together clinically, them in the field on calls and you guys in the hospital I think that you'll find once they get to know the knowledge base, experience, etc... that they will be more comfortable with your local EMS clinicians. Food for thought and this is a potentially daunting migraine inducing task which will ultimately be decided by a combo of effort and politics.
ACE844
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:"EMSLT,"
We've had that discussion here a few times do a search and you will find a multitude of data and opinions on this...
ACE
: -
Alot of good posts everyone. This call did go BLS, my partners reasoning being a "normotensive" pressure (regardless of the change from baseline. He was wrong, and I knew it, but i've never made it a practice to kick calls back to the ALS provider. Simply stated, if you boot it to me, its your mistake. Thats why we do QA. He'll learn. I did the oxygen thing, treated for shock and got the bleeding stopped with a pressure dressing.
My point was simple. Theres alot of ways this could have gone, and sometimes we can disagree. Did this call go ok BLS? sure. Could she have crashed out? Certainly. Theres always a varied opinion, because ALs is an ART, not a science. If it was a defined science, would we really be here?
As long as we are doing the best we can with the clinical indicators we have, in the best interest of the patient, we've done our job, and we've done it well.
"PRPG,"
Don't you think that perhaps the call went as well as it did BLS was BECAUSE of who the BLS clinician was on this call? Do you think the outcome may have been alittle worse if it had been another BLS clinician?
Out here,
ACE844
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More and more it sounds like this lady need s to go back to the OR for further exploration...My $$"S are on my previous post..
OUT HERE,
ACE844
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Slightly
:BUT STILL AN ADDITIONAL CONCERN!!
I am also curious to know then if they allow their clinicians to wear nail polish or fake nails at work?...?
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ischemic and or septic bowel anyone???
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Not only is it degrading, but I think you missed the basic bashing I hid in there, as well. You're a smart guy, you'll find it.
In other words:
GUILTY AS CHARGED. :violent3:
What on earth could you possibly mean???
I'm stumped...
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Not safe for work:
New definition for 'Road Head', I guess.
OH... that's harrassment right there. I thought that maybe you thought that maybe this was funny...THAT'S DEGRADING...
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Shtttpuppoesooeosleoi, woveoiww Acaoerraioea, watehekwetio, a dsfsnafweo;i akfdjwefjwoejoio... Oh, sorry checking the cleanliness of my laryngoscope blade. Guess I have to go clean it now.
Shame on you Ace, wanting evidence to support a point made entirely on emotion.
Well now I am curious, he must have the information handy since he made this post, and is participating in the implementation of these policies at his service, I mean there is NO WAY THEY WOULD HAPPEN OR JUST DO IT JUST BECAUSE....RIGHT??? Either way, I'm sure he's got the information sitting there so we can all see. Why else would he stand up on a soap box and make proclimations or statements and not be able to back them up....I'm holding my breath and waiting to see what happens..He has to know by now the burden of proof is on him, and...if past performace is any indicator............................
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I can't decide whats worse...The fact he didn't 'correct' the problem, or that this was posted...JK :wink:
:shock: 8) 
ACE844
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I wonder if "GAmedic," could be so kind as to educate us about the incidence of primary infection as it directly relates to pre-hospital laryngoscopy with his 'dirty blades', and also please post your sources. Next I am further curious about which there is a higher incidence and occurance of; aspiration and or ET-vent pneumonia S/P pre-hopital ETI or the aforementioned dirty laryngoscopy. Lets also further contrast that wiht IN-hospital as well. Thanks,
ACE844
Teaching Points::::CHF
in Patient Care
Posted
Diastolic Heart Failure — A Common and Lethal Condition by Any Name
Gerard P. Aurigemma, M.D.)
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PubMed Citation
This issue of the Journal contains two provocative contributions to the literature on heart failure. Owan et al.1 describe the epidemiologic outcomes and survival rates among patients with heart failure who were admitted to the Mayo Clinic Hospitals for the disease from 1987 through 2001, extending results published in 19982; Bhatia et al.3 review the shorter-term outcomes among patients hospitalized for heart failure in the province of Ontario over a two-year period, beginning in April 1999. Both groups of investigators subdivided their patients according to the level of ejection fraction. They then compared the characteristics and clinical courses of the patients with a preserved ejection fraction of 50 percent or greater (Owan et al.) or more than 50 percent (Bhatia et al.) to those with a reduced ejection fraction.
Owan et al. and Bhatia et al. use the term "heart failure with preserved ejection fraction," as opposed to the term "diastolic heart failure." Strictly speaking, "heart failure with preserved (or normal) ejection fraction" is not incorrect and appears to be preferred by the American College of Cardiology and the American Heart Association.4 However, "diastolic heart failure" describes the dominant underlying pathophysiological features5,6 and has connotations familiar to the clinician. Furthermore, virtually all patients with heart failure and preserved ejection fraction who are studied carefully will show abnormalities in diastolic function and elevated left-ventricular filling pressures.7 The two current studies remind us that ejection fraction is not a good predictor of clinical disability and suggest that congestive symptoms are more closely related to the filling (diastolic) properties of the ventricle than to the ejection (systolic) properties. Accordingly, the terms "diastolic" and "systolic" heart failure are used here instead of heart failure with "preserved" or "reduced" ejection fractions, respectively.
A principal conclusion of these studies may come as a surprise: patients with diastolic heart failure have the same or only slightly better rates of survival than those with systolic heart failure at one year1,3 and at five years.1 These data challenge the widely held perception that the survival rate among patients with most forms of heart disease is inversely related to the ejection fraction, at least for ejection fractions below 45 percent.8,9,10 How do we reconcile the findings of Owan et al. and Bhatia et al. with the apparently contradictory results from previous studies, such as the Cardiovascular Health Study (a large, multicenter community-based study)9 or the Candesartan in Heart Failure: Assessment of Reduction in Mortality and Morbidity (CHARM) study (to our knowledge, the only large, randomized clinical trial of the treatment of diastolic heart failure published to date)?10
One may start by asking whether the patients in the two current studies could have been misclassified according to ejection fraction. Although there is not complete unanimity on what is the lower limit of normal, 50 percent is reasonable.5 In the study by Owan et al., the mean (±SD) ejection fraction was 29±10 percent among patients with systolic heart failure and 61±7 percent among patients with diastolic heart failure; this difference suggests that substantial overlap between the two subgroups was unlikely. (The data of Bhatia et al. are even more clear-cut on this point, since patients with an intermediate ejection fraction [40 to 50 percent] were a separate subgroup.) Furthermore, thanks to studies that involve serial echocardiography, we now know that the ejection fraction does not typically change appreciably between hospital admission and hospital discharge, despite dramatic changes in patients' clinical status.11 Therefore, the incorrect classification of patients according to their ejection fraction is unlikely.
In my judgment, the difference between the current results and those of previously published studies relates both to patient characteristics and to the growing recognition of diastolic heart failure. It may be important that Owan et al. studied only patients who survived long enough to be discharged from the hospital. As a result, a higher rate of in-hospital mortality among patients with systolic heart failure than among those with diastolic heart failure may have been overlooked in this study. Furthermore, in both studies, the mean age was higher among patients with diastolic heart failure than among those with systolic heart failure. An older population is more likely to have important coexisting medical conditions, such as cerebrovascular disease or renal insufficiency. Since the primary outcome was death from any cause rather than death from cardiac causes, it seems reasonable to postulate that older patients with diastolic heart failure would have been more likely to have complications from these coexisting medical conditions, despite the authors' attempts at statistical adjustment. Unfortunately, the comparison of these results with those of the CHARM study is bedeviled by what are undoubtedly significant differences in the mean age (which was likely to have been higher in the current studies) and the prevalence of severe coronary artery disease (which was likely to have been higher in the CHARM study).
Although the current analyses were carefully performed, one must be cautious in extrapolating the results. First, the population studied by Owan et al. is more than 97 percent white, and no data on ethnic background were given by Bhatia et al. Second, the authors studied the first or only hospitalization for heart failure. The study populations therefore may not reflect the patients who are hospitalized for heart failure in clinical practice, many of whom are admitted repeatedly for exacerbations of the disease or even for procedure-related heart failure. Finally, the study data may not be applicable to outpatients with heart failure.
Another principal conclusion of Owan et al. is that diastolic heart failure has increased in prevalence over time.1 The authors estimate that, in their study, more than half of the patients discharged with heart failure had diastolic heart failure, and they enumerate the probable explanations. One is the increasing percentage of older patients in the population, coupled with the fact that the prevalence of diastolic heart failure varies directly with the mean age of the population.6 I concur with the authors' observation that, owing to increasing awareness, clinicians were more likely to admit a patient to the hospital for diastolic heart failure in 2001 than previously. In fact, a systematic search of the literature for "diastolic heart failure" (and related terms) shows an increase in the number of publications by a factor of 20 between 1986 and 2002, which includes the study period of Owan et al. There was similar growth during that period in the number of publications with "diastolic dysfunction" in the title, a relative rarity in 1986. Although not mentioned by Owan et al., the growing availability of echocardiography, as well as point-of-care biomarkers such as brain natriuretic peptide, probably increases the likelihood that patients with dyspnea will be diagnosed as having diastolic heart failure, whether or not they are admitted to the hospital.
The nosology of heart failure has been the subject of much current debate, and some extreme positions have been taken. The observation that 22 to 29 percent of patients with diastolic heart failure die within one year of hospital discharge, and 65 percent die within five years, is a reminder that we are facing a lethal condition, regardless of its name. Owan et al. also show that, in recent years, there has been little improvement in survival rate among patients with diastolic heart failure, in contrast to the improvement in survival rate over time among patients with systolic heart failure.
The news is not all bad, however. The noted improvement in the survival rate of patients with systolic heart failure1 provides encouragement that emerging treatment strategies for diastolic heart failure, such as the use of angiotensin-receptor blockers,12,13 might eventually have a clinical effect. We should also not neglect preventive measures with proven efficacy (such as antihypertensive therapy),14 given that there is no effective cure for aging. The prevention of a first or recurrent myocardial infarction is likely to be the best means we have to keep the ejection fraction "preserved." However, the development of specific, effective management approaches for diastolic heart failure must also become a high priority.
Dr. Aurigemma reports having received grant support and consulting fees from Novartis and grant support from Biosite. No other potential conflict of interest relevant to this article was reported.
Source Information
From the Division of Cardiovascular Medicine, University of Massachusetts Medical School, Worcester.
References
Owan TE, Hodge DO, Herges RM, Jacobsen SJ, Roger VL, Redfield MM. Trends in prevalence and outcome of heart failure with preserved ejection fraction. N Engl J Med 2006;355:251-259. [Abstract/Full Text]
Senni M, Tribouilloy CM, Rodeheffer RJ, et al. Congestive heart failure in the community: a study of all incident cases in Olmsted County, Minnesota, in 1991. Circulation 1998;98:2282-2289. [Abstract/Full Text]
Bhatia RS, Tu JV, Lee DS, et al. Outcome of heart failure with preserved ejection fraction in a population-based study. N Engl J Med 2006;355:260-269. [Abstract/Full Text]
Hunt SA, Abraham WT, Chin MH, et al. ACC/AHA 2005 guideline update for the diagnosis and management of chronic heart failure in the adult: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure). J Am Coll Cardiol 2005;46:e1-e82. [Full Text]
Vasan RS, Levy D. Defining diastolic heart failure: a call for standardized diagnostic criteria. Circulation 2000;101:2118-2121. [Full Text]
Aurigemma GP, Gaasch WH. Diastolic heart failure. N Engl J Med 2004;351:1097-1105. [Full Text]
Zile MR, Gaasch WH, Carroll JD, et al. Heart failure with a normal ejection fraction: is measurement of diastolic function necessary to make the diagnosis of diastolic heart failure? Circulation 2001;104:779-782. [Abstract/Full Text]
Aurigemma GP, Gaasch WH, Villegas B, Meyer TE. Noninvasive assessment of left ventricular mass, chamber volume, and contractile function. Curr Probl Cardiol 1995;20:361-440. [Medline]
Gottdiener JS, McClelland RL, Marshall R, et al. Outcome of congestive heart failure in elderly persons: influence of left ventricular systolic function. Ann Intern Med 2002;137:631-639. [Abstract/Full Text]
Solomon SD, Anavekar N, Skali H, et al. Influence of ejection fraction on cardiovascular outcomes in a broad spectrum of heart failure patients. Circulation 2005;112:3738-3744. [Abstract/Full Text]
Gandhi SK, Powers JC, Nomeir AM, et al. The pathogenesis of acute pulmonary edema associated with hypertension. N Engl J Med 2001;344:17-22. [Abstract/Full Text]
Yusuf S, Pfeffer MA, Swedberg K, et al. Effects of candesartan in patients with chronic heart failure and preserved left-ventricular ejection fraction: the CHARM-Preserved Trial. Lancet 2003;362:777-781. [CrossRef][iSI][Medline]
Zile MR, Brutsaert DL. New concepts in diastolic dysfunction and diastolic heart failure. Part II: causal mechanisms and treatment. Circulation 2002;105:1503-1508. [Full Text]
Kostis JB, Davis BR, Cutler J, et al. Prevention of heart failure by antihypertensive drug treatment in older persons with isolated systolic hypertension. JAMA 1997;278:212-216. [Abstract]