Content uploaded by Jonathan J Deeks
Author content
All content in this area was uploaded by Jonathan J Deeks on Feb 03, 2015
Content may be subject to copyright.
ORIGINAL CONTRIBUTION
The Accuracy of Patient History,
Wheezing, and Laryngeal Measurements
in Diagnosing Obstructive Airway Disease
Sharon E. Straus, MD
Finlay A. McAlister, MD
David L. Sackett, MD
Jonathan J. Deeks, MSc
for the CARE-COAD1 Group
DESPITE THE CENTRAL IMPOR-
tance of the initial clinical
examination in the care of
patients, its elements have
rarely been subjected to rigorous evalu-
ation. The evaluation of obstructive air-
way disease (OAD) is a typical ex-
ample: a systematic review of the
literature1identified 29 articles evalu-
ating a total of 32 clinical signs for the
detection of OAD (median of 1 sign, 2
clinicians, and 93 patients per study).
However, only 1 of these studies2ful-
filled standard criteria3for classifica-
tion as a methodologically rigorous
study (an independent, blind compari-
son with a reference standard among
an appropriate spectrum of consecu-
tive patients). In that study, 2 physi-
cians examined 164 consecutive pa-
tients in a preoperative evaluation clinic.
They reported likelihood ratios (LRs)
for several elements of the clinical ex-
amination, but none of the maneuvers
was sufficiently sensitive to allow their
absence to rule out OAD or suffi-
ciently specific for their presence to rule
in OAD.
The reported accuracies of com-
monly cited signs for OAD vary greatly
between studies. For example, the de-
Author Affiliations: The Centre for Evidence-Based
Medicine, Nuffield Department of Medicine, Ox-
ford, England (Drs Straus, McAlister, and Sackett); The
Division of General Internal Medicine, Mt Sinai Hos-
pital, University Health Network, Toronto, Ontario (Dr
Straus); The Division of General Internal Medicine, Uni-
versity of Alberta, Edmonton (Dr McAlister); and The
Imperial Cancer Research Fund/National Health
Service Centre for Statistics in Medicine, Institute
of Health Sciences, Oxford, England (Mr Deeks).
Members of the CARE-COAD1 Group are listed at the
end of this article.
Corresponding Author and Reprints: Finlay A.
McAlister, MD, Division of General Internal Medi-
cine, 2E3.24 Walter Mackenzie Centre, University
of Alberta Hospital, 8440 112 St, Edmonton,
Alberta, Canada T6G 2R7 (e-mail: Finlay.McAlister
@ualberta.ca).
Context The accuracy of the clinical examination in detecting obstructive airway
disease (OAD) is largely unknown because of a paucity of methodologically rigorous
studies.
Objective To determine the accuracy of patient history, wheezing, laryngeal height,
and laryngeal descent in the diagnosis of OAD.
Design Comparison study conducted from November 3, 1998, to December 4, 1998,
evaluating 4 clinical examination elements for diagnosis of OAD vs the gold standard
of forced expiratory volume in 1 second (FEV1) and FEV1–forced vital capacity (FVC)
ratio less than the fifth percentile (adjusted for patient height, age, and sex).
Setting Twenty-five sites, including primary care and referral practices, in 14 coun-
tries.
Participants A total of 309 consecutive patients were recruited (mean age, 56 years;
43% female), 76 (25%) with known chronic OAD, 114 (37%) with suspected chronic
OAD, and 119 (39%) with neither known nor suspected OAD.
Main Outcome Measures Sensitivity, specificity, and likelihood ratios (LRs) for each
of the 4 elements of the clinical examination compared with the gold standard.
Results Mean FEV1and FVC values were 2.1 L/s and 2.9 L; 52% had an FEV1and
FEV1-FVC ratio less than the fifth percentile. The LR for wheezing was 2.7 (95% con-
fidence interval [CI], 1.7-4.2) and was not statistically significant in the multivariate
model. The LR for laryngeal descent ranged from 0.9 (95% CI, 0.5-1.4) to 1.2 (95%
CI, 0.4-3.4), depending on the cut point chosen, and did not enter the multivariate
model. Only 4 of the history or physical examination elements we tested were sig-
nificantly associated with the diagnosis of OAD on multivariate analysis: smoking for
more than 40 pack-years (LR, 8.3), self-reported history of chronic OAD (LR, 7.3),
maximum laryngeal height of at least 4 cm (LR, 2.8), and age at least 45 years (LR,
1.3). Patients having all 4 findings had an LR of 220 (ruling in OAD); those with none
had an LR of 0.13 (ruling out OAD). The area under the receiver operating charac-
teristic curve for the model incorporating these 4 factors was 0.86.
Conclusions Further research is needed to validate our model, but in the mean-
time, our data suggest that less emphasis should be placed on the presence of indi-
vidual symptoms or signs (such as wheezing or laryngeal descent) in the diagnosis of
OAD.
JAMA. 2000;283:1853-1857 www.jama.com
See also Patient Page.
©2000 American Medical Association. All rights reserved. JAMA, April 12, 2000—Vol 283, No. 14 1853
Downloaded From: http://jama.jamanetwork.com/ on 02/25/2013
tection of wheezing on auscultation has
been evaluated in 7 studies: sensitivity
ranged from 9% to 100%, specificity
from 37% to 100%, and positive LRs
varied from 0.9 to infinity.1Even the
accuracy of the overall clinical impres-
sion (formed after obtaining complete
patient history and conducting physi-
cal examination) for the detection of
OAD is unclear, with sensitivity (50%-
64%), specificity (64%-93%), and posi-
tive (1.4-7.3) and negative (0.4-0.8) LRs
varying sharply between studies.1This
situation led to calls in THE JOURNAL4,5
for larger, better studies of the clinical
examination.
In an effort to obtain reliable infor-
mation on the accuracy of the history
and physical examination in diagnos-
ing OAD, a multinational study involv-
ing investigators at various levels (pri-
mary, secondary, and tertiary care) was
designed. In this study, the accuracy of
several elements of the clinical exami-
nation in predicting OAD were investi-
gated: patient self-reported history of
chronic OAD, smoking history (yes/
no, number of pack-years), wheezing on
auscultation, laryngeal height (maxi-
mum and minimum), and laryngeal de-
scent. A secondary objective was to as-
sess whether it was possible to do large,
fast, multicenter studies of the clinical
examination using the Internet for cli-
nician recruitment and data collection.
METHODS
Investigators were recruited from vari-
ous centers around the world via the
Internet using the study group Web site
(http://www.carestudy.com) and the
evidence-based health care e-mail dis-
cussion group. All investigators joined
the study in groups of 2 or more (at least
1 clinician and 1 spirometrist) and took
responsibility for obtaining local eth-
ics approval for the study. Investiga-
tor enrollment and data entry were done
via a secure Internet-based data entry
system, and data collation and analy-
sis were done at the Centre for Evi-
dence-Based Medicine at the Univer-
sity of Oxford in England.
Twenty investigator groups (46 in-
vestigators) enrolled consecutive pa-
tients (from November 3 to December
4, 1998) within 3 broad categories: pa-
tients who were known to have chronic
OAD, patients who were suspected of
having OAD, and patients who were nei-
ther known nor suspected of having
OAD. Investigators were asked to en-
roll a minimum of 4 consecutive pa-
tients from each category. Known
chronic OAD was defined as prior pul-
monary function test results demonstrat-
ing forced expiratory volume in 1 sec-
ond (FEV1) less than the fifth percentile,
FEV1–forced vital capacity (FVC) ratio
less than the fifth percentile, or FEV1-
FVC ratio less than 0.7; or patient self-
report of a prior diagnosis of chronic
OAD, emphysema, or chronic bronchi-
tis; or patient taking inhaled broncho-
dilators and/or inhaled steroids for long
periods. A case was defined as “sus-
pected OAD” if the patient did not ful-
fill any criteria for known chronic OAD
but was referred for suspected chronic
OAD, or if the participating clinician
thought that OAD was a diagnostic pos-
sibility before the structured examina-
tion. Patients with known or suspected
OAD were eligible for enrollment dur-
ing exacerbations of their disease if no
bronchodilator treatment was given be-
tween the clinical examination and spi-
rometry. Excluded were patients with
purely reversible airway obstruction (ie,
asthma); patients with a terminal ill-
ness whose goals of therapy were con-
fined to comfort and dignity; patients
younger than 18 years; patients with res-
piratory distress so severe that broncho-
dilators could not be withheld safely un-
til after spirometry; patients who were
medically unstable from other causes (eg,
acute myocardial infarction, drug over-
dose); and patients who were unable to
cooperate for the clinical examination or
spirometry (eg, impaired cognition, level
of consciousness, or language).
All patients underwent clinical exami-
nation and independent, blinded spi-
rometry. The items chosen for this study
were based on a review of the literature
and consensus among the investiga-
tors. The items assessed included self-
reported history of chronic OAD, smok-
ing history, laryngeal height (the distance
between the top of the thyroid cartilage
and the suprasternal notch), laryngeal de-
scent, and wheezing. Maximum laryn-
geal height was measured at the end of
expiration, minimum laryngeal height at
the end of inspiration.6,7 The difference
between the maximum and minimum la-
ryngeal heights is the laryngeal de-
scent. A videotape of the laryngeal ex-
amination was provided on the study
Web site for investigator training. Inves-
tigators listened for wheezes during res-
piration over 4 standardized areas (bi-
lateral upper and lower back).8Each
patient also underwent spirometry within
30 minutes of the clinical examination
(without intercurrent bronchodilator
use) to assess FEV1and FVC values. A
standard protocol for spirometry was
used and the better result of 2 attempts
was recorded. The spirometrists and cli-
nicians were blind to the results of the
others’ investigations.
Sensitivity, specificity, and LRs for each
element of the clinical examination were
calculated using spirometry as the gold
standard (OAD was defined as an FEV1
and FEV1-FVC ratio less than the fifth
percentile).9Percentile flow rates, ad-
justed for age, sex, and height, were cal-
culated using the regression equation
of Crapo et al.10 Continuous measure-
ments (age, pack-years of smoking, and
measurements of laryngeal position and
descent) were categorized, either accord-
ing to cut points previously published or
values derived from noting obvious
inflection points on receiver operating
characteristic (ROC) curves. Cut points
were chosen such that the slopes of the
ROC curve based on the selected cut
points mirrored those in the full ROC
curve. The relationships between each
diagnostic element and OAD were tested
using x2tests and the Fisher exact test
for dichotomous features, the x2test for
trend for categorical variables, and the t
test for continuous variables.
Multivariate analyses were carried
out using the method of Spiegelhalter
and Knill-Jones (which adjusts for con-
founding from related diagnostic ele-
ments),11,12 and a reduced multivari-
ate model was produced by grouping
categories with similar LRs within each
DIAGNOSING OBSTRUCTIVE AIRWAY DISEASE
1854 JAMA, April 12, 2000—Vol 283, No. 14 ©2000 American Medical Association. All rights reserved.
Downloaded From: http://jama.jamanetwork.com/ on 02/25/2013
element and only selecting diagnostic
elements with adjusted LRs greater than
2 or less than 0.5. All analyses were
done using statistical software.13
RESULTS
A total of 332 patients were recruited
by 25 investigator groups from 14 coun-
tries. Twenty-three patients were ex-
cluded from further analysis because
they had a primary diagnosis of asthma;
no other protocol violations were iden-
tified. Thus, the final sample size was
309. After the closing of the study, a
subset of investigators (chosen be-
cause of outlying results) were asked
to submit their original data collec-
tion sheets to be checked against the da-
tabase—11 of 680 data points were in-
correctly entered (error rate, 1.6%).
Patient demographics are outlined in
TABLE 1and the distribution of FEV1val-
ues are illustrated in the FIGURE.Onob-
jective testing, more than half (162
[52%]) of the patients had an FEV1and
FEV1-FVC ratio less than the fifth per-
centile. The accuracy of the various el-
ements of the clinical examination as-
sessed is outlined in TABLE 2. Whereas
we used FEV1and FEV1-FVC ratio less
than the fifth percentile as the reference
standard, given the controversy regard-
ing the spirometric definitions of OAD,5
the LRs for each element of the clinical
examination also were calculated using
other reference standards (FEV1-FVC ra-
tio ,0.7, FEV1-FVC ratio ,0.8, FEV1
value ,the fifth percentile, or FEV1-
FVC ratio ,the fifth percentile alone).
The accuracies reported in Table 2 did
not change appreciably: for example, the
positive LRs for wheezing were 1.9, 3.1,
2.6, and 2.1, respectively, using the al-
ternate reference standards. The mean
minimum and maximum laryngeal
Figure. Distribution of FEV1Values (n = 332)
40
30
20
10
0
0.25
0.75
1.25
1.75
2.25
2.75
3.25
3.75
4.25
4.75
5.25
FEV1, L
No. of Patients
Mean (SD)
=
2.1 (1.1) L
FEV1indicates forced expiratory volume in 1 second.
Table 1. Patient Demographics (N = 309)*
Variable Value
Age, mean (SD), y 56.2 (17.6)
Female sex, No. (%) 133 (43)
White, No. (%) 275 (89)
Smoking status, No. (%) [n = 292]†
Never smoked 119 (39)
Smoked ,20 pack-years 80 (26)
Smoked 20-40 pack-years 49 (16)
Smoked .40 pack-years 44 (14)
Chronic OAD status, No. (%)
Known 76 (25)
Suspected 114 (37)
Neither known nor suspected 119 (39)
Point of contact, No. (%)
Primary 156 (50)
Secondary/tertiary 153 (50)
Clinical findings, mean (SD)
Maximum laryngeal height, cm 5.8 (1.9)
Minimum laryngeal height, cm 4.1 (1.8)
Laryngeal descent, cm 1.7 (0.9)
FEV1, L/s 2.1 (1.1)
FVC, L 2.9 (1.2)
*OAD indicates obstructive airway disease; FEV1, forced
expiratory volume in 1 second; and FVC, forced vital ca-
pacity.
†Data on number of pack-years smoked unavailable for
17 smokers.
Table 2. Accuracy of Elements of the Clinical Examination in Diagnosing OAD (Univariate
Analysis)*
Diagnostic Element
All Patients
(N = 309)
Patients Without Known COPD
(n = 233)
No.
Crude
Likelihood Ratio
(95% CI)
P
Value No.
Crude
Likelihood Ratio
(95% CI)
P
Value
Chronic OAD history
Known 76 12.9 (5.4-31.0) ...
Not known but suspected 114 0.9 (0.6-1.1) ,.001 114 1.5 (1.1-1.9) .02
Not known or suspected 119 0.4 (0.3-0.5) 119 0.7 (0.5-0.9)
Smoking
Smoked .1 y 190 1.2 (1.0-1.5) .01 128 1.1 (0.8-1.4) .81
Never smoked, or
smoked ,1y
119 0.7 (0.5-0.9) 105 1.0 (0.8-1.2)
Amount smoked, pack-years
(n = 292)†
.40 44 19.1 (4.7-77.3) 17 11.7 (2.7-50.0)
20-40 49 0.9 (0.6-1.6) ,.001 30 0.8 (0.4-1.6) ,.001
,20 80 0.5 (04-0.8) 64 0.5 (0.3-0.9)
Age, y
$65 118 2.1 (1.5-2.9) 74 1.9 (1.3-2.8)
45-64 105 1.5 (1.1-2.0) ,.001 75 1.5 (1.1-2.2) ,.001
,45 86 0.2 (0.1-0.3) 84 0.3 (0.2-0.5)
Sex
Male 176 1.3 (1.1-1.6) .01 124 1.2 (1.0-1.5) .41
Female 133 0.7 (0.6-0.9) 109 0.8 (0.6-1.1)
Wheezing
Present 79 2.7 (1.7-4.2) ,.001 44 2.1 (1.2-3.5) .002
Absent 230 0.7 (0.6-0.8) 189 0.8 (0.7-1.0)
Maximum laryngeal height, cm
#4 74 3.6 (2.1-6.0) ,.001 45 4.2 (2.3-7.9) ,.001
.4 235 0.7 (0.6-0.8) 188 0.7 (0.5-0.9)
Minimum laryngeal height, cm
#4 168 1.5 (1.2-1.8) ,.001 116 1.3 (1.1-1.6) .008
.4 141 0.6 (0.5-0.8) 117 0.7 (0.5-0.9)
Laryngeal descent, cm
.3 57 0.9 (0.5-1.4) 22 0.9 (0.5-1.5)
2.01-3 137 1.0 (0.8-1.3) .50 108 1.0 (0.8-1.3) .21
1.01-2 99 1.1 (0.8-1.5) 91 1.1 (0.8-1.5)
#1 16 1.2 (0.4-3.4) 12 0.9 (0.3-3.2)
*OAD indicates obstructive airway disease; COPD, chronic obstructive pulmonary disease; and CI, confidence interval.
The reference standards were forced expiratory volume in 1 second (FEV1) and FEV1–forced vital capacity ratio less
than the fifth percentile.
†Data on number of pack-years smoked missing for 17 smokers.
DIAGNOSING OBSTRUCTIVE AIRWAY DISEASE
©2000 American Medical Association. All rights reserved. JAMA, April 12, 2000—Vol 283, No. 14 1855
Downloaded From: http://jama.jamanetwork.com/ on 02/25/2013
heights were significantly smaller in pa-
tients with FEV1values and FEV1-FVC
ratio less than the fifth percentile than
those with higher FEV1values (3.8 vs 4.6
cm, P,.001, and 5.4 vs 6.3 cm, P,.001).
Laryngeal descent was not significantly
associated with OAD diagnosis, even
when the analysis was restricted to sub-
groups of patients with more severe ob-
struction (data not shown). There was
no heterogeneity in accuracy across
countries, investigator groups, exam-
iner experience), or point of contact (pri-
mary or secondary/tertiary care). More-
over, the accuracy of the tested elements
was similar even after exclusion from
analysis of the 76 patients with known
chronic OAD (Table 2).
The ROC curve for smoking dem-
onstrated that the most appropriate cut
point was at 40 pack-years (data avail-
able on request).
The reduced multivariate model in-
cluded 4 items (TABLE 3). In patients with
all 4 items (self-reported history of chronic
OAD, smoked .40 pack-years, older than
45 years, and maximum laryngeal height
#4 cm), the LR for the diagnosis of OAD
is 220 (essentially ruling in the diagnosis).
In patients without any of these 4 char-
acteristics, the LR is 0.13 (essentially rul-
ing out the diagnosis). A multivariate
model derived from the 233 patients with-
out known chronic OAD included the
same 3 items (Table 3). In particular,
wheezing and laryngeal descent did not
enter the model even after exclusion of
known chronic OAD patients.
COMMENT
We evaluated the accuracy of several el-
ements of the clinical examination in di-
agnosing OAD. In terms of history, the
most useful points to rule in a diagnosis
of OAD are self-reported history of
chronic OAD and smoking in excess of
40 pack-years. Age younger than 45 years
virtually ruled out the diagnosis of OAD
(given that patients with asthma were
excluded). On physical examination,
auscultated wheezing and maximal la-
ryngeal height of 4 cm or less increased
the likelihood that OAD was present but
did not do so sufficiently to resolve the
diagnostic process. For example, in a pa-
tient with a prior likelihood of 10%—
the prevalence of chronic OAD among
smokers14—the presence of wheezing
raises the probability of OAD to only 23%
(similarly, a maximum laryngeal height
of #4 cm only increases the probability
to 28%). Laryngeal descent was not help-
ful in either ruling in or ruling out the
diagnosis of OAD. Although it may seem
tautologous to include “history of
chronic OAD” in a prediction rule for
OAD, it must be acknowledged that cli-
nicians usually collect history prior to
physical examination or further diag-
nostic testing, and thus it is important
to evaluate the accuracy of this element
of the clinical assessment. Further-
more, in testing the accuracy of a symp-
tom or sign, individuals representing a
full spectrum of disease should be in-
cluded. Finally, the accuracy of the tested
elements did not change even after ex-
clusion of patients with known chronic
OAD, and inclusion of this factor more
closely reflects actual practice.
Using multivariate analysis, we devel-
oped a 4-variable model for diagnosing
OAD. The LRs for each of these variables
can be multiplied (as they are adjusted
to account for their nonindependence)
to generate an LR for an individual pa-
tient.11,12 For example, in a 65-year-old
patient with self-reported chronic OAD,
a 45-pack-year smoking history, and a
maximum laryngeal height of 3 cm, the
LR is 220. Thus, even if the pretest prob-
ability was only 10%, the constellation
of symptoms and signs increases his/her
posttest probability to 96%. Although this
may obviate the need for spirometry for
diagnostic purposes, it does play a use-
ful role in identifying the severity of dis-
ease and the effects of therapy.
Our study adds substantially to the lit-
erature on the rigorous evaluation of the
clinical examination for OAD (it triples
the numbers of patients in such studies
and increases the numbers of clini-
cians 10-fold). Furthermore, our find-
ings are generally consistent with the lit-
erature. For example, Badgett and
colleagues14 found that the only useful
items on history were self-reported his-
tory of chronic OAD (positive LR, 3.1)
and smoking more than 70 pack-years
(positive LR, 8.0). Others5have re-
ported, as we did, that a history of never
smoking significantly decreases the like-
lihood of OAD, but the negative LR is
insufficient to allow the diagnosis to be
definitively ruled out. Although our
study contradicts previous studies that
suggested increased tracheal descent was
a useful sign in identifying OAD,7,15 these
were unblinded studies of nonconsecu-
tive patients and thus subject to poten-
tial selection and measurement bias. In
our study, the presence of wheezing was
not as useful in diagnosing OAD as other
investigators have reported it to be. In
Table 3. Multivariate Likelihood Ratios*
Diagnostic Element
Adjusted Likelihood Ratios
Factor Present Factor Absent
All Patients (N = 309)
Self-reported history of chronic OAD 7.3 0.5
Smoked .40 pack-years 8.3 0.8
Age $45 y 1.3 0.4
Maximum laryngeal height #4 cm 2.8 0.8
All 4 Factors 220.5 0.13
Patients Without Known Chronic OAD (n = 233)
Smoked .40 pack-years 11.6 0.9
Age $45 y 1.4 0.5
Maximum laryngeal height #4 cm 3.6 0.7
All 3 Factors 58.5 0.32
*Area under the receiver operating characteristic curve for full model = 0.86 and for model in those patients without
known chronic obstructive airway disease (OAD) = 0.77. The reported likelihood ratios (LRs) have been adjusted to
take into account the effect of other factors in the model. Thus, these LRs can be multiplied to determine patient-
specific LR in a patient with more than 1 factor. The other factors listed in Table 2 were not significant in either mul-
tivariate model. Confidence interval estimation for adjusted likelihood ratios requires evaluation of variance-
covariance matrix for each estimate and is not presented.
DIAGNOSING OBSTRUCTIVE AIRWAY DISEASE
1856 JAMA, April 12, 2000—Vol 283, No. 14 ©2000 American Medical Association. All rights reserved.
Downloaded From: http://jama.jamanetwork.com/ on 02/25/2013
their study of 164 patients, Holleman
and colleagues2reported a positive LR
of 12 for wheezing; however, the 95%
confidence interval ranged from 1.7 to
98. Our results are consistent with this
estimate and, given our larger sample
size, serve to refine the previously pub-
lished estimates. The ability of our model
to predict OAD is similar to previously
published models (one2incorporated
years of smoking exposure, patient-
reported wheezing, and auscultated
wheezing, and the other14 incorpo-
rated pack-year smoking history, self-
reported history of chronic OAD, and
decreased breath sounds); however, our
model is somewhat better at ruling out
OAD than were those models. For ex-
ample, in a 40-year-old nonsmoking pa-
tient without a prior diagnosis of chronic
OAD and with a maximum laryngeal
height of 7 cm, the LR of 0.13 virtually
rules out the diagnosis of OAD.
This study established the feasibil-
ity of using the Internet to recruit in-
vestigators and conduct studies of the
clinical examination. This approach al-
lowed the rapid accrual of patients to
this study (at a rate more than 20 times
faster than that of the only other meth-
odologically rigorous study2of the
clinical examination in OAD) and has
resulted in the development of a prac-
tice-based research network16,17 of cli-
nicians interested in performing other
studies of the clinical examination.
However, there were some limita-
tions to our study. First, we did not assess
interrater reliability. This was a deliber-
ate exclusion, as the primary focus of this
initial study was to evaluate the accu-
racy of elements of the clinical exami-
nation and prove the feasibility of the
study design. To achieve these objec-
tives, the study was designed such that
data collection would be brief. We
decided a priori to defer assessment of
interobserver variation for a future study
in which we will only evaluate those signs
that have been shown to be accurate. Sec-
ond, to participate, investigators had to
have access to the Internet. Critics might
be concerned that this may affect the
applicability of our results to patients or
clinicians in other settings. However, our
patients and results are similar to those
in other studies,5,14,15 suggesting that our
findings are generalizable. Third, the
applicability of our model for clinical
practice has yet to be determined,
although the preliminary observations
from our data set suggest it holds sig-
nificant promise. If it had been used to
assess the patients in our study, a diag-
nosis (ie, probability of OAD .90% or
,10%) could have been made and spi-
rometry for diagnosis avoided in 48% of
them. Furthermore, we derived LRs for
the tested elements of the clinical exami-
nation (rather than sensitivity or speci-
ficity) to permit the ready extrapolation
of our results to other settings with dif-
ferent prevalence of disease. Finally, our
model must be validated in an indepen-
dent sample of patients, and such a study
is being planned.18
In summary, our results suggest that
less emphasis should be placed on the
presence of wheezing or exaggerated la-
ryngeal descent in making a diagnosis
of OAD. We found that a combination
of 4 symptoms/signs (self-reported his-
tory of chronic OAD, pack-year smok-
ing history, age, and maximum laryn-
geal height) can be used to predict
airway obstruction. In those settings in
which spirometry is readily available, it
should be used because it takes only
slightly longer to do than the clinical ex-
amination, definitively establishes the di-
agnosis of airway obstruction, and pro-
vides prognostic information. However,
in those settings in which spirometry is
unavailable, our model provides useful
diagnostic support for the clinician. Fu-
ture studies are under way to evaluate
other signs and symptoms that have
been described for the diagnosis of OAD
and to test our model in an indepen-
dent sample of patients.
The CARE-COAD1 (Clinical Assessment of the Reli-
ability of the Examination–Chronic Obstructive Air-
ways Disease) Investigators are M. Bermudez-
Gomez, R. Dennis, Pontificia Universidad Javeriana,
Bogota´ , Colombia; S. Straus, F. McAlister, D. Sackett,
John Radcliffe Hospital, Oxford, England; C. Baicus, M.
Georgescu, N. Gh. Lupu Hospital, Bucharest, Roma-
nia; P. Sestini, R. Refini, R. Amerini, M. Vichi, Institute
of Respiratory Diseases, University of Siena, Siena, Italy;
D. Londono, A. Ruiz, Hospital San Ignacio, Universi-
dad Javeriana, Bogota´ ; A. Ramos, A. de Pablo, Clinica
Puerta de Hierro, Universidad Autonoma de Madrid,
Madrid, Spain; M. Urtasun, M. Molinari, Hospital Re-
gional Ushuaia, Ushuaia, Argentina; I. Scott, C. Mitchell,
T. Maddocks, K. Loff, Princess Alexandra Hospital, Bris-
bane, Australia; A. Jelani, King Fahd National Guard Hos-
pital, Riyadh, Saudi Arabia; O. Gajic, O. Yazdi, N. An-
andarao, M. Oloomi, New York Methodist Hospital,
Brooklyn, NY; E. M. Mutzig, M. Jelley, D. Bridges, Uni-
versity of Oklahoma College of Medicine, Tulsa; X. Cea,
A. Baeza, Universidad de la Fontera, Temuco, Chile; D.
Ross, Chorley, England; S. Salah, P. Badrinath, D. Obi-
nerche, O. Lloyd, Al Ain Hospital and Faculty of Medi-
cine and Health Sciences, Al Ain, United Arab Emir-
ates; E. Etchells, M. Schreiber, The Toronto Hospital,
Toronto, Ontario; K. Sharma, A. B. Fraser, Ottawa Hos-
pital, Ottawa, Ontario; D. Newberry, I. England, Ash-
ford Hospital, London, England; M. Kljakovic, S. Carr,
General Practice Department, Wellington School of
Medicine, Wellington, New Zealand; D. Teysseyre, St
Sulpice de Royan, France; and J. Ibarra, Vitoria, Spain.
Funding/Support: Drs Straus and Sackett and Mr
Deeks were supported by the National Health Ser-
vice Research and Development Programme, United
Kingdom. Dr McAlister is a population health inves-
tigator of the Alberta Heritage Foundation for Medi-
cal Research and was supported by the Medical Re-
search Council of Canada.
Acknowledgment: We thank Les Irwig, MD, for his
helpful comments on the data analysis.
REFERENCES
1. McAlister FA, Straus SE, Sackett DL, for the CARE-
COAD1 Group. Why we need large, simple studies of
the clinical examination. Lancet. 1999;354:1721-1724.
2. Holleman DR Jr, Simel DL, Goldberg JS. Diagnosis
of obstructive airways disease from the clinical exami-
nation. J Gen Intern Med. 1993;8:63-68.
3. Sackett DL, Richardson WS, Rosenberg W, Haynes
RB. Evidence-Based Medicine. London, England:
Churchill Livingstone; 1997.
4. Simel DL, Rennie D. The clinical examination. JAMA.
1997;277:572-574.
5. Holleman DR Jr, Simel DL. Does the clinical exami-
nation predict airflow limitation? JAMA. 1995;273:
313-319.
6. Campbell EJ. Physical signs of diffuse airways ob-
struction and lung distention. Thorax. 1969;24:1-3.
7. Stubbing DG, Mathur PN, Roberts RS, Campbell EJ.
Some physical signs in patients with chronic airflow ob-
struction. Am Rev Respir Dis. 1982;125:549-552.
8. Sapira JD. The Art and Science of Bedside Diagno-
sis. Munich, Germany: Urban & Schwarzenberg; 1990.
9. American Thoracic Society. Lung function testing.
Am Rev Respir Dis. 1991;144:1202-1218.
10. Crapo RO, Morris AH, Gardner RM. Reference
spirometric values using techniques and equipment that
meet ATS recommendations. Am Rev Respir Dis. 1981;
123:659-664.
11. Feinstein AR. Clinical biostatistics, XXXIX: the haze
of Bayes, the aerial palaces of decision analysis, and
the computerized Ouija board. Clin Pharmacol Ther.
1977;21:482-496.
12. Spiegelhalter DJ, Knill-Jones RP. Statistical and
knowledge-based approaches to clinical decision-
support systems, with an application in gastroenter-
ology. J R Stat Soc A. 1984;147:35-77.
13. StatCorp. STATA Statistical Software: Release 5.0.
College Station, Tex: Stata Corp; 1997.
14. Badgett RG, Tanaka DJ, Hunt DK, et al. Can mod-
erate chronic obstructive pulmonary disease be diag-
nosed by historical and physical findings alone? Am J
Med. 1993;94:188-196.
15. Godfrey S, Edwards RH, Campbell EJ, et al. Re-
peatability of physical signs in airways obstruction. Tho-
rax. 1969;24:4-9.
16. Green LA, Hames CG Sr, Nutting PA. Potential
of practice-based networks: experiences from ASPN.
J Fam Pract. 1994;38:400-406.
17. Nutting PA. Practice-based research networks.
J Fam Pract. 1996;42:199-203.
18. Laupacis A, Sekar N, Stiell IG. Clinical prediction
rules. JAMA. 1997;277:488-494.
DIAGNOSING OBSTRUCTIVE AIRWAY DISEASE
©2000 American Medical Association. All rights reserved. JAMA, April 12, 2000—Vol 283, No. 14 1857
Downloaded From: http://jama.jamanetwork.com/ on 02/25/2013
Supplemental Oxygen and Mountaineer
Death Rates on Everest and K2
To the Editor: The use of supplemental oxygen by Hima-
layan mountaineers has been debated for more than 8 de-
cades.1Although sometimes viewed as unsporting, supplemen-
tal-oxygen use may improve survival rates by increasing
performance and lowering hypoxic stress.1-3 Analyses of death
rates of mountaineers descending from high summits may re-
veal an impact of supplemental oxygen on survival because de-
scending mountaineers are often near exhaustion and vulner-
able to accident, storm, or illness during their descent.
Methods. We analyzed interview data4-6 and more recent data
(Elizabeth Hawley, oral communication, May 4, 2000) on all
mountaineers reaching the summit of the 2 highest peaks (Ever-
est and K2) from 1978 (year both summits first reached with-
out supplemental oxygen) through 1999. For “summit-team”
analyses on Everest, we excluded recent data (1993-1999) to
reduce the impact of guided expeditions, which may include
inexperienced climbers. We used exact logistic regression (con-
ditional maximum likelihood) with survival as the dependent
variable and supplemental oxygen (used and not used) as a fac-
tor, stratified by mountain (Everest and K2). In a preliminary
analysis, the year of summiting (covariate) was unrelated to
individual death rates on Everest (either directly or via an in-
teraction with supplemental oxygen, P..27) and hence ex-
cluded from final analyses.
Results. Individual mountaineers not using supplemental oxy-
gen had significantly higher death rates during descent than
did those using supplemental oxygen (TABLE,P,.001). This
pattern is especially evident on K2, where approximately 1 in
5 climbers not using supplemental oxygen died during de-
scent (Table).
To control for nonindependence of climbers in a team, we
used a “summit team” as a complementary unit of analysis and
determined (for each team reaching the summit on a given day
and route) whether supplemental oxygen was used and whether
any descending mountaineer died. Number of summiters was
a covariate because the probability of a death(s) may increase
with the number of climbers exposed to risk. Even by this con-
servative analysis, teams not using supplemental oxygen had
relatively high death incidences (P=.03).
Comment. Reaching the summit of Everest, and especially
of K2, is dangerous. Overall, 1 in 29 climbers died during de-
scent on Everest, and 1 in 7 died on K2 (Table). Reaching those
summits without supplemental oxygen is associated with an
even higher risk: 1 climber in 12 died on Everest, and approxi-
mately 1 in 5 died on K2 (Table). The survival impact of supple-
mental oxygen may be greater than suggested because moun-
taineers not using supplemental oxygen are probably relatively
more experienced and therefore might be expected to have lower
death rates. The association may be causal because supplemen-
tal oxygen decreases exposure time and reduces physical de-
terioration.1,3 Nevertheless, alternative explanations (eg, moun-
taineers using supplemental oxygen are more risk averse) cannot
be excluded. Moreover, a full risk assessment of supplemental
oxygen use awaits incorporation of data on death rates during
ascent, risk to porters ferrying oxygen canisters, actual causes
of death, and weather conditions. In any case, Himalayan moun-
taineering is a dangerous activity2that balances adventure against
risk. Mountaineers considering whether to use supplemental
oxygen should consider the risk of death during descent.
Raymond B. Huey, PhD
University of Washington
Seattle
Xavier Eguskitza
Worcester, England
Funding/Support: This study was funded by a fellowship to Dr Huey from the J.
S. Guggenheim Fellowship.
Acknowledgment: We thank T. Hornbein, MD, University of Washington, Se-
attle, and C. Houston, MD, University of Vermont, Burlington, for advice, and E.
Hawley, Consul for New Zealand, Kathmandu, Nepal, for sharing data.
1. West JB. High Life: A History of High-Altitude Physiology and Medicine.Ox-
ford, England: Oxford University Press; 1998:493.
2. Pollard A, Clarke C. Deaths during mountaineering at extreme altitude. Lan-
cet. 1988;1:1227.
3. Peacock AJ, Jones PL. Gas exchange at extreme altitude: results from the Brit-
ish 40th Anniversary Everest Expedition. Eur Respir J. 1997;10:1439-1444.
4. Eguskitza X. Everest—the first forty years. In: Gillman P, ed. Everest: The Best
Writing and Pictures from Seventy Years of Human Endeavour. Boston, Mass: Little
Brown & Co; 1993:191-201.
5. Hawley E, Eguskitza X. Everest—die ersten 45 Jahre. In: Gillman P, ed. Everest
8846m. Munich, Germany: J Berg bei Bruckmann; 1998:191-202.
6. Eguskitza X. Appendices I-III. In: Curran J, ed. K2: The Story of the Savage Moun-
tain. London, England: Hodder & Stoughton; 1996.
CORRECTION
Incorrect Wording: In the Original Contribution entitled “The Accuracy of Pa-
tient History, Wheezing, and Laryngeal Measurements in Diagnosing Obstructive
Airway Disease” published in the April 12, 2000, issue of THE JOURNAL (2000;283:
1853-1857), there was incorrect wording in the abstract. On page 1853, in the
“Results” section, the sentence that read “maximum laryngeal height of at least
4 cm” should have read “maximum laryngeal height of 4 cm or less.”
Table. Use of Supplemental Oxygen and Death Rates of Individual
Mountaineers and for Summit Teams*During Descent From
the Summits of Everest and K2 Between 1978 and 1999
Mountain
Individual
Mountaineers†
Summit Teams‡
Ascents,
No.
Deaths,
No. (%)
Teams
Summiting,
No.
Teams With
Death,
No. (%)
Everest
Used supplementary
oxygen
1077 32 (3.0) 93 8 (8.6)
No supplementary
oxygen
96 8 (8.3) 28 4 (14.3)
K2
Used supplementary
oxygen
47 0 (0) 12 0 (0)
No supplementary
oxygen
117 22 (18.8) 36 12 (33.3)
*Summit-team analyses for Everest restricted to 1978-1992, see “Methods” section.
†For comparison by exact logistic regression, stratified by mountain, P,.001.
‡For comparison by exact logistic regression, stratified by mountain and with number of
summiters per team as a covariate (included because the probability of a death should
increase with the number of climbers exposed to risk, all else being equal), P= .03.
LETTERS
©2000 American Medical Association. All rights reserved. (Reprinted) JAMA, July 12, 2000—Vol 284, No. 2 181
Downloaded From: http://jama.jamanetwork.com/ on 02/25/2013
