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(Chest. 2004;125:473-481.)
© 2004 American College of Chest Physicians

Prospective Multicenter Study of Relapse Following Emergency Department Treatment of COPD Exacerbation*

Sunghye Kim, MD; Charles L. Emerman, MD; Rita K. Cydulka, MD, MS; Brian H. Rowe, MD, MSc, FCCP; Sunday Clark, MPH and Carlos A. Camargo, MD, DrPH, FCCP; on behalf of the MARC Investigators{dagger}

* From the Department of Emergency Medicine (Drs. Kim and Camargo, and Ms. Clark), Massachusetts General Hospital, Boston, MA; the Department of Emergency Medicine (Drs. Emerman and Cydulka), MetroHealth Medical Center, Cleveland, OH; and the Department of Emergency Medicine (Dr. Rowe), University of Alberta, Edmonton, AB, Canada. {dagger} A list of MARC site investigators is located in the Appendix.

Correspondence to: Carlos Camargo MD, DrPH, FCCP, Director, EMNet Coordinating Center, Massachusetts General Hospital, 55 Fruit St, Clinics Building 397, Boston, MA 02114; e-mail: ccamargo{at}partners.org


   Abstract
TOP
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 Appendix
 References
 
Study objectives: To determine the incidence and risk factors of relapse after an emergency department (ED) visit for COPD exacerbation.

Design: Prospective cohort study as part of the Multicenter Airway Research Collaboration.

Setting: Twenty-nine North American EDs.

Patients: ED patients with COPD exacerbations, age >= 55 years. For the present analysis of post-ED relapse, the cohort was restricted to COPD patients who had been discharged from the ED directly to home.

Measurements and results: Eligible patients underwent a structured interview to assess their demographic characteristics, COPD history, and details of the current COPD exacerbation. Data on ED medical management and disposition were obtained by chart review. Patients were contacted by telephone 2 weeks later regarding incident relapse events (ie, urgent clinic or ED visit for worsening COPD). The cohort consisted of 140 COPD patients. Over the next 2 weeks, patients demonstrated a consistent daily relapse rate that summed to 21% (95% confidence interval, 15 to 28%) at day 14. In a multivariate model, the significant risk factors for relapse were the number of urgent clinic or ED visits for COPD exacerbation in the past year (odds ratio [OR], 1.49 [per five visits]), self-reported activity limitation during the past 24 h (OR, 2.93 [per unit on scale of 1 [none] to 4 [severe]), and respiratory rate at ED presentation (OR, 1.76 [per 5 breaths/min]).

Conclusions: Among patients discharged to home after ED treatment of a COPD exacerbation, one in five patients will experience an urgent/emergent relapse event during the next 2 weeks. Both chronic factors (ie, a history of urgent clinic or ED visits) and acute factors (ie, activity limitations and initial respiratory rate) are associated with increased risk. Further research should focus on ways to decrease the relapse rate among these high-risk patients. The clinicians may wish to consider these historical factors when making ED decisions.

Key Words: acute exacerbation • COPD • emergency medicine • relapse


   Introduction
TOP
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 Appendix
 References
 
Acute exacerbation of COPD is defined as a sustained worsening of the patient’s condition, from the stable state and beyond normal day-to-day variations, that is acute in onset and necessitates a change in regular medication in a patient with underlying COPD.1 2 While many of the mild COPD exacerbations are never brought to a physician’s attention,3 moderate-to-severe exacerbations, by definition requiring increased medication or hospitalization,1 involve formal medical evaluation and treatment. In the United States, the emergency department (ED) is an important setting for this care, with > 1 million ED visits for COPD exacerbations every year.4

ED management focuses on the relief of respiratory symptoms and on disposition decisions, not only concerning the need for inpatient vs outpatient management, but increasingly the need for close outpatient follow-up (eg, primary care visits and nursing visits to the home). For a variety of reasons, there is a drive to manage a greater number of acutely ill individuals in the outpatient setting.5 6 While the recognition of impending death is possible,7 there are sparse data on the incidence and risk factors for urgent/emergent relapse events after treatment for a COPD exacerbation. Previous studies have reported a range of relapse rates over the several weeks following acute COPD exacerbations of 12 to 32%,8 9 10 11 12 13 14 15 16 with increased risk among those with home oxygen use,14 older age and female sex,9 comorbidity,13 17 spirometry performance,9 12 14 frequent COPD exacerbations during the previous year,8 14 15 and the presence or absence of specific short-term treatment.8 9 10 12 Unfortunately, most of the epidemiologic studies to date have employed a retrospective single-center design, so generalizability is problematic. The purpose of this multicenter, prospective study was to determine the incidence and risk factors of relapse after an ED visit for COPD exacerbation.


   Materials and Methods
TOP
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 Appendix
 References
 
Subjects
This study combines data from two prospective cohort studies performed from November 1999 to June 2000, and from December 2000 to May 2001 as part of the Multicenter Airway Research Collaboration (MARC). MARC is part of the Emergency Medicine Network (EMNet), a large collaboration with > 130 participating EDs across North America (http://www.emnet-usa.org). Using a standardized protocol, investigators at 29 EDs in 15 US states and 3 Canadian provinces provided 24 h/d coverage for a median duration of 2 weeks each year. Repeat visits by individual subjects were excluded. All patients were managed at the discretion of the treating physician. To capture all COPD patients, every patient who might have COPD (eg, patients with COPD or asthma exacerbation) was approached. Inclusion criteria were physician diagnosis of asthma/COPD exacerbation, age >= 55 years, and the ability to give informed consent.

The present analysis is restricted to subjects who reported physician diagnosis of COPD exacerbation and were discharged directly to home from the ED (151 patients). Of those patients, 140 (93%) underwent the 2-week telephone interview and have relapse data. The institutional review board at each of the 29 participating hospitals approved the study, and informed consent was obtained from all participants.

Data Collection
The ED interview assessed patients’ demographic characteristics, COPD history, and details of their COPD exacerbation. Data on ED management and disposition were obtained by chart review. Follow-up data were collected by telephone interview 2 weeks later using a structured interview and included details of any urgent COPD visits, including changes in medical management. Data collection forms are based on the MARC interview forms used in several prior studies.18 19 All forms were reviewed by site investigators before submission to the EMNet Coordinating Center in Boston, MA, where they underwent further review by trained personnel and then double data entry.

The preferred term used for a patient’s diagnosis (ie, COPD, emphysema, or chronic bronchitis) was determined based on the following question: "Has a doctor ever said that you have asthma ... COPD ... emphysema... or chronic bronchitis?" Patients were assigned to the COPD group if they reported COPD, emphysema, or chronic bronchitis. To address possible diagnostic misclassification, we performed a validation study involving all patients presenting with asthma and/or COPD during the study period at 3 of the 29 sites: MetroHealth Medical Center; University of Alberta Hospital; and Massachusetts General Hospital. Patients were confirmed to have COPD (regardless of asthma status) if they met both of the following criteria: (1) they stated that a physician had given them a diagnosis of COPD, emphysema, or chronic bronchitis; and (2), if on review of their medical records, they had either a baseline FEV1 of < 80% predicted or an FEV1/FVC ratio of < 70%, or evidence of obvious bullous disease or hyperinflation with flattening of the diaphragm seen on a baseline chest radiograph or CT scan. Among the 66 cases, no patient who reported doctor-diagnosed COPD had spirometric results that contradicted their self-reported diagnosis. Spirometry, chest radiograph, and chest CT scan were not performed (or at least were not available) for all patients, yet we confirmed 82% of self-reported cases as having COPD.20

For all patients, primary care provider (PCP) status was based on the following question: "Do you have a primary care provider (such as a family doctor, internist, or nurse practitioner)?" If the answer was yes, patients were asked to provide the name and address of their PCP. Median family income was estimated using the patient’s home ZIP or postal codes.21 22 Inflation rate was reflected using the consumer price index,23 24 and Canadian dollars were converted to US dollars using the conversion rate as of January 1, 2001.23 24 25 Patients also were asked a series of standardized questions, which included those about smoking history, age at diagnosis, and history of cough with sputum production. The severity of underlying COPD and its control were assessed by the use of medications (eg, inhaled ß-agonists, anticholinergic, inhaled corticosteroids, and systemic corticosteroids) and the frequency of moderate-to-severe COPD exacerbations, as measured by the number of urgent clinic or ED visits for COPD during the previous 12 months.

Subjective symptom severity and activity limitation during the exacerbation were ascertained by the answers to the following questions: "Over the past 24 h, how often did you experience COPD symptoms?"; "Over the past 24 h, how much discomfort or distress have you felt because of these COPD symptoms?"; and "Among all of the activities that you have done over the past 24 h, how much has your COPD limited you?" The three questions used a 4-point scale (1, none; and 4, severe). Quality of life during the exacerbation was measured by the short version of the chronic respiratory disease questionnaire (CRQ). The CRQ is a well-validated, repeatable, and responsive disease-specific instrument with four domains (ie, dyspnea, emotional function, fatigue, and mastery).26 27 For current analysis, we used the average of each domain. We used the short version CRQ to make the interview more feasible in the ED.28 Each question has scale of 1 (ie, extremely short of breath, having difficulty all of the time, and no energy at all) to 7 (ie, not at all short of breath, having difficulty none of the time, and full of energy).

A relapse was defined as any urgent or unscheduled visit to any physician (ED or clinic) for worsening COPD within 2 weeks of the ED visits. Other definitions of relapse also were examined, as follows: (1) any urgent or unscheduled clinic or ED visit within 2 weeks of the ED visits with worsening COPD, which led to the prescription of rescue medication (eg, systemic steroid, parenteral ß-agonist, or inhaled ß-agonist administered by health provider), or hospital admission; and (2) any ED visit for COPD within 2 weeks of the ED visits. Results from analyses using these alternative relapse definitions were not materially different from the primary definition (data not shown).

Statistical Analysis
All analyses were performed using a statistical software package (STATA, version 7.0; StataCorp; College Station, TX). Data are presented as proportions (with 95% confidence intervals [CIs]), means (SDs), and median (with interquartile range [IQR]). The association between relapse and other factors was examined using the {chi}2 test, the Student t test, the rank-sum test, and the Kruskal-Wallis rank test, as appropriate. Age and sex were included in multivariate logistic regression models because of their potential clinical significance. Other variables associated with relapse at p < 0.10 in univariate analysis were evaluated for inclusion in multivariate logistic regression models. All odds ratios are presented with 95% CIs. The area under the receiver operating characteristic curve was calculated for the final multivariate logistic regression models. The final model was further evaluated using the Hosmer-Lemeshow statistic.29 30 All p values are two-tailed, with p < 0.05 considered to be statistically significant.


   Results
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 Appendix
 References
 
Of 853 potentially eligible patients, 222 patients (26%) who reported only asthma and 47 patients (6%) for whom a diagnosis was missing were excluded from current analysis. We also excluded 385 patients (66%) who were not discharged to home (ie, admitted to observation unit, 5 patients [1%]; admitted to a regular ward, 300 patients [51%]; admitted to the ICU, 63 patients [11%]; or transferred to another hospital or received other disposition, 17 patients [3%]). Among the 199 patients with COPD exacerbations who were discharged to home, we enrolled 151 patients (76%). The enrolled patients did not differ from the nonenrolled patients across multiple sociodemographic factors. A total of 140 patients had complete follow-up data (follow-up rate, 93%). Of the original 29 sites, 28 contributed patients to this analysis (range, 2 to 13 patients per site). These 140 patients, compared to those not contacted by telephone (11 patients), did not differ by age, sex, race, reported diagnosis (ie, mixed asthma-COPD or COPD only), number of COPD exacerbations during the past year, home oxygen use, and COPD medications used before/during/after the ED visit.

Among the 140 patients, 30 patients (21%; 95% CI, 15 to 29) reported COPD exacerbation relapse within 14 days of their original ED visit. Relapse events occurred over the entire follow-up period, with an average daily relapse rate of 1.4% (Fig 1 ).



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  		Figure 1. Daily relapse rate (bars) and cumulative relapse rate (line) after ED treatment of COPD exacerbations.

 
The cohort consisted of almost the same number of men and women, and 60% of patients were white. Most of the patients had a PCP and some type of medical insurance. None of these demographic factors were different in the relapse and nonrelapse groups (Table 1 ). A total of 32% of patients were current smokers, 57% were past smokers, and 11% were never-smokers. Among the 15 never-smokers, 8 reported symptoms compatible with chronic bronchitis (ie, mucus-producing cough most days of the month, 3 months of the year for two successive years) and/or they received diagnoses of asthma/COPD after age 35 years. When we excluded the seven never-smokers, who did not report chronic bronchitis symptoms and whose age of diagnosis was < 35 years, the results did not vary materially (data not shown).


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  		Table 1. Demographic and Baseline Clinical Characteristics of Patients Presenting to the ED With Acute Exacerbation of COPD by Relapse Status

 
Half of the patients reported an asthmatic component to their COPD, but this physician diagnosis was unrelated to relapse risk (Table 1) . On univariate analysis, chronic severity and management of COPD were not different in the relapse and nonrelapse groups, except for the number of urgent clinic or ED visits for COPD exacerbation during the past year, and receiving systemic corticosteroids over the past 4 weeks.

Peak expiratory flow (PEF) was obtained in only 51 patients (36%). Although infrequently performed, the PEF data indicated severe obstruction (median PEF, 40% of predicted; IQR, 31 to 52). While a higher initial respiratory rate at ED presentation was associated with relapse at 2 weeks, the initial oxygen saturation level breathing room air or PEF was not related to relapse risk (Table 2 ).


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  		Table 2. ED Presentation, Management, and Discharge Medications of Patients Presenting to the ED With Acute Exacerbation of COPD by Relapse Status*

 
All three questions on subjective symptom severity and activity limitation during the past 24 h were rated as moderate to severe by patients. While two questions on the frequency and severity of symptoms during exacerbation were unrelated to relapse status, self-perceived activity limitation was associated with relapse risk. The quality of life measured by short-version CRQ was uniformly poor across four domains (ie, dyspnea, emotional function, fatigue, and mastery). None of the four domains was related to relapse (Table 2) .

There also was no difference in ED treatment between the two groups (Table 2) . The only factor of potential significance was discharge from the hospital while receiving inhaled anticholinergic agents, which, paradoxically, appeared to increase relapse risk. Given numerous randomized blinded trials that have demonstrated the benefit of anticholinergic agents in COPD patients31 32 and the likelihood of confounding by indication in this observational study,33 we further examined this issue. Controlling for any one of the available measures of exacerbation severity (eg, respiratory rate) rendered this result nonsignificant (all p > 0.05; data not shown).

Finally, Table 3 shows a multivariate model for COPD exacerbation relapse after ED treatments. Statistically (and clinically) significant factors were the number of urgent clinic or ED visits in the past year, self-reported activity limitation during the past 24 h, and respiratory rate at ED presentation. While self-reported activity limitation was a significant independent risk factor, none of the four domains in CRQ was significant (data not shown). The area under receiver operating characteristic curve was calculated as 0.77, and the Hosmer-Lemeshow test demonstrated a good fit (p = 0.14).


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  		Table 3. Multivariate Model of Relapse 2 Weeks After ED Visit for COPD Exacerbation

 

   Discussion
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
Appendix
 References
 
This study confirms previous findings that a substantial proportion of patients treated for COPD exacerbation experience significant relapse events in the days and weeks after ED treatment. A wide range of relapse rates following COPD exacerbation have been reported, as follows: 12%8 and 17%9 within 48 h; 22 to 32% within 2 weeks10 11 12 ; and 13 to 21% in 1 month.13 14 15 Despite significant improvements in the prognosis of other diseases such as coronary artery disease during the past decade,34 it is disturbing that the relapse rate in this study (21%) does not differ greatly from the 28% reported in the late 1980s.11 In this study, we have confirmed that easily ascertainable chronic factors (ie, the number of urgent clinic or ED visits for COPD during the past year) and short-term factors (ie, self-reported activity limitation and respiratory rate at ED presentation) can define patients who are at the highest risk of relapse.

The frequency of COPD exacerbations during the past year has been suggested as a risk factor for relapse after COPD exacerbation.8 13 14 15 However, until recently, there had been no plausible biological explanation for this relationship, except vague explanations that "host factors" affect relapse risk. Bhowmik et al35 showed that stable sputum interleukin (IL)-6 and IL-8 levels were increased in patients who experienced three or more exacerbations per year, suggesting that patients who experience more frequent exacerbations have a greater degree of underlying airway inflammation during their apparently stable periods. Another study by Gompertz et al,36 which sought the relationship between airway inflammation and frequency of exacerbation in COPD patients, found that the frequent exacerbation group (ie, three or more per year) had lower sputum concentrations of an antiprotease named secretory leukoproteinase inhibitor, which also has antibacterial and antiviral activity. A study37 examining the sputum of COPD patients found that the patients in whom viruses were detected during a stable state had a history of more frequent exacerbations than those in whom no virus was detected, while another study by Patel et al38 reported a relationship between bacterial colonization and the frequency of exacerbation, symptom severity at exacerbation, and sputum IL-6 level. Taking these findings together, one might hypothesize that there are various degrees of inflammation in COPD patients, induced either by the imbalance of inflammatory/anti-inflammatory factors or by viral and/or bacterial colonization, and that the degree of inflammation determines the frequency and also the outcome of exacerbations. This hypothesis is supported by the finding by Donaldson et al39 that exacerbation frequency is a consistent feature within a patient.

One might further argue that our study used an arbitrary definition for frequency of COPD exacerbation, which was determined as the number of urgent clinic or ED visits for COPD during the past year. Using the number of urgent clinic or ED visits for COPD exacerbation might not be an accurate way of assessing the frequency of COPD exacerbations, considering that only half of the patients with COPD exacerbations seek medical care.3 In the clinical setting, however, the number of urgent clinic or ED visits for COPD is easier to recall than the total number of COPD exacerbations. Our study suggests a simple and practical assessment of exacerbation frequency that can be used for relapse prediction.

Self-perceived activity limitation also was associated with relapse after ED treatment. Several studies have examined the relationship between quality of life and clinical outcomes among COPD patients. Fan et al40 used a baseline-measured, COPD-specific quality-of-life measure, the Seattle obstructive lung disease questionnaire, and found that among the three scales (ie, physical function, emotional function, and coping skills), the physical function scale was the best predictor of hospitalization for COPD. Domingo-Salvany et al41 studied 303 male COPD patients and found that baseline disease-specific (using the St. George respiratory questionnaire42 ) and general health-related (ie, the 36-item short form43 ) quality-of-life questionnaires were independently associated with total and respiratory mortality in multivariate modeling. Another study by Osman et al44 measured quality of life during exacerbation using the St. George respiratory questionnaire.42 They reported44 that all three subscales (ie, symptom, impact, and activity) measured during an exacerbation were related to hospital readmission within 12 months using multivariate analysis. Finally, a study by Aaron et al45 measured baseline dyspnea index and CRQ during acute COPD exacerbation. Although they found significant improvement in both of the measurements 10 days later, there was no difference by relapse group in baseline dyspnea index or CRQ measured during exacerbation.45

In the present study, we found that among questions regarding acute symptom severity and CRQ, only activity limitations were associated with relapse. Activity limitations were ascertained by asking the question "How much has your COPD limited you over the past 24 h?" Moreover, other questions on the frequency and severity of COPD symptoms in the past 24 h or answers to the CRQ in four domains (ie, dyspnea, emotion, fatigue, and mastery) were not associated with relapse. To our knowledge, this is the first study that shows the validity of self-perceived activity limitation as a predictor of relapse after COPD exacerbation. In asthma, there was one study46 that reported a relationship between activity limitation due to asthma within 4 weeks and relapse after ED treatment. Functional status or its impairment during COPD exacerbation may reflect exacerbation severity and may predict the short-term outcome of an exacerbation. However, future research might develop a rating system with more discriminating power than the 4-point test system that we employed.

The ED respiratory rate at presentation was also significantly associated with later relapse. Respiratory rate is relatively simple to measure and directly reflects respiratory difficulty. We are not aware of a published study that examined the association of triage respiratory rate with relapse following COPD exacerbation. Although clinical research studies have shown that performance in spirometry or peak flowmeter was related to relapse,8 12 14 in actual clinical practice it is not always performed,47 and the quality of the test is questionable.48 In this observational study, PEF was measured in only 36% of patients, and FEV1 in < 5%.

It is interesting that respiratory rate was related to COPD exacerbation relapse, while none of the objective measurements of acute severity (eg, respiratory rate, FEV1, and PEF) was related to relapse in our prior work on asthma.49 This difference could represent a pathophysiologic difference between asthma and COPD. However, we should take into account two facts in interpreting these results. First, in both studies we restricted the data set to patients discharged from the hospital in whom the discharge decision was made by the treating ED physician. Second, in the asthma study,49 objective measures were more commonly recorded, (eg, in our prior asthma study, PEF was measured in 80% of patients). Taken together, the observations suggest that ED physicians had more information (eg, PEF) when they made the hospital discharge decision for asthma patients compared to when they made it for COPD patients. In other words, in the asthma study, we probably eliminated the variance in respiratory function by restricting the data set to patients discharged from the hospital (eg, patients with severe respiratory dysfunction would have been admitted to the hospital at the treating physician’s discretion). In the current study, however, since PEF was performed in only one third of the patients, ED physicians might have discharged patients from the hospital who had poorer lung function, who might not have been discharged had the physician known their lung function level. These differences might explain the discrepancy between the asthma and COPD studies in terms of the role of acute respiratory function measurement and its association with relapse.

This study has a few potential limitations. First, ED management was not standardized. It is possible that some differences in patient management may have masked factors associated with relapse. To counter this concern, it is reassuring that patients in both the relapse and nonrelapse groups appeared to receive similar therapies (apart from receiving anticholinergic agents) and that pharmacotherapy did not factor into the final model. Second, the definition of relapse is somewhat arbitrary. We have used an end point of urgent or unscheduled visit (to the clinic or ED) at 2 weeks, while some authors have used other end points at different follow-up intervals. As previously discussed, using other end point definitions (eg, ED relapse, inpatient relapse, or outpatient relapse that led to the prescription of rescue medication) did not materially change the results. Third, this study is not population-based since it examines the exacerbations of patients who presented to the ED. The results may not be generalizable to all exacerbations among individuals with COPD, however, we think that they are useful for the ED setting. Likewise, while the cohort is composed predominantly of low-income and minority patients, these demographic characteristics identify a high-risk group for COPD morbidity and mortality.50 Another possible limitation is the rarity of objective measures of lung function such as FEV1. Considering the hectic environment and the potential risk of performing spirometry in COPD patients during exacerbation, we believe that it is not realistic or desirable to expect to obtain spirometry measurements in most COPD patients. Also, the ability of patients to perform spirometry at American Thoracic Society-recommended standards51 during an exacerbation is questionable. Consequently, even though our study did not include PEF or FEV1 data, we believe that this accurately reflects current emergency medicine practice.

In conclusion, the results of our study suggest that both chronic COPD severity (measured by exacerbation frequency during the past 12 months) and acute COPD exacerbation severity (assessed by self-reported activity limitation and respiratory rate at ED presentation) can predict the relapse of a COPD exacerbation within 14 days of an ED visit. Future studies might focus on developing simpler ways of assessing chronic COPD severity, COPD exacerbation severity, along with biomarker profiles to explore the underlying pathophysiology. In addition, larger ED-based cohort studies are required to confirm these findings, especially with more standardized treatment following hospital discharge. This future work may provide greater insight into this complex clinical presentation and may help to identify more useful indicators of post-ED relapse.


   Appendix
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 Appendix
References
 
EMNet Steering Committee
Edwin D. Boudreaux, PhD; Barry E. Brenner, MD, PhD; Carlos A. Camargo, Jr., MD (Chair); Rita K. Cydulka, MD; Theodore J. Gaeta, DO, MPH; and Michael S. Radeos, MD, MPH.

EMNet Coordinating Center
Carlos A. Camargo, Jr., MD, FCCP (Director); Sunday Clark, MPH; Jennifer A. Emond, MS; Jessica L. Hohrmann, MPH; Gabrielle C. Hunter; and Sunghye Kim, MD (all at Massachusetts General Hospital, Boston, MA).

Principal Investigators at the 29 Participating Sites
F.C. Baker III (Maine Medical Center, Portland, ME); M.P. Blanda (Summa Health System, Akron, OH); E.D. Boudreaux (Earl K. Long Memorial Hospital, Baton Rouge, LA); B.E. Brenner (The Brooklyn Hospital Center, Brooklyn, NY); C.A. Camargo, Jr. (Massachusetts General Hospital, Boston, MA); R.K. Cydulka (MetroHealth Medical Center, Cleveland, OH); T.J. Gaeta (New York Methodist Hospital, Brooklyn, NY); B. Goldfeder (Shands Hospital at the Univeristy of Florida, Gainesville, FL); R.J. Grant (Hartford Hospital, Hartford, CT); R.O. Gray (Hennepin County Medical Center, Minneapolis, MN); A. Guttman (Sir Mortimer B. Davis-Jewish General Hospital, Montreal, QC, Canada); L.W. Kreplick (Christ Hospital & Medical Center, Oak Lawn, IL); D.S. Mackey (Lethbridge Regional Hospital, Lethbridge, AB, Canada); A. Mangione (Albert Einstein Medical Center, Philadelphia, PA); J. Peters (University of Texas Health Sciences Center at San Antonio, San Antonio, TX); M.S. Radeos (Lincoln Medical Center, Bronx, NY); P.L. Rice (Brigham and Women’s Hospital, Boston, MA); B.H. Rowe (University of Alberta Hospital, Edmonton, AB, Canada); M. Sama (St. Joseph Mercy Hospital, Ann Arbor, MI); D. Schreiber (Stanford University Medical Center, Stanford, CA); N.I. Shapiro (Beth Israel Deaconess Medical Center, Boston, MA); P.C. Shukla (University of Texas Southwestern Medical Center, Dallas, TX); D. Sinclair (Queen Elizabeth II Health Science Centre (Halifax, NS, Canada); H. Smithline (Baystate Medical Center, Springfield, MA); P.E. Sokolove (University of California Davis Medical Center, Sacramento, CA); M. Steffens (Palmetto Richland Memorial Hospital, Columbia, SC); C.A. Terregino (Cooper Hospital/University Medical Center, Camden, NJ); A. Travers (Royal Alexandria Hospital, Edmonton, AB, Canada); and E.J. Weber (University of California San Francisco Medical Center, San Francisco, CA).


   Acknowledgements
 
ACKOWLEDGMENT: We thank the MARC investigators for their ongoing dedication to emergency airway research.


   Footnotes
 
Abbreviations: CI = confidence interval; CRQ = chronic respiratory disease questionnaire; ED = emergency department; EMNet = Emergency Medicine Network; IQR = interquartile range; MARC = Multicenter Airway Research Collaboration; PCP = primary care provider; PEF = peak expiratory flow

Dr. Kim was supported by grant K30 HL04095, Ms. Clark by grant T32 ES07069, and Dr. Camargo by grant R01 HL63841 from the National Institutes of Health (Bethesda, MD). Dr. Rowe is supported by the Canadian Institutes of Health Research as a Canada Research Chair (Ottawa, ON, Canada). The project was supported by an unrestricted grant from Boehringer Ingelheim (Ridgefield, CT, and Burlington, ON, Canada).

Received for publication May 22, 2003. Accepted for publication September 5, 2003.


   References
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 Appendix
 References
 

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S. D. Ramsey and F. D. R. Hobbs
Chronic Obstructive Pulmonary Disease, Risk Factors, and Outcome Trials: Comparisons with Cardiovascular Disease
Proceedings of the ATS, September 1, 2006; 3(7): 635 - 640.
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