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Rapid-Onset Asthma Attack*
A Prospective Cohort Study About Characteristics
and Response to Emergency Department
Treatment
Gustavo J. Rodrigo, MD; and Carlos Rodrigo, MD
Study objectives: (1) To determine the frequency of rapid-onset asthma attacks (ROAAs) and
slow-onset asthma attacks (SOAAs) in adult patients with acute, severe disease (18 to 50 years old),
who presented to an emergency department (ED); and (2) to establish whether ROAA patients
differ from SOAA patients in terms of clinical and spirometric characteristics; and (3) in terms of
the response of treatment.
Subjects and methods: Four hundred three patients (with peak expiratory flow [PEF] or FEV1 of
< 50% of predicted value) with acute exacerbations of asthma were enrolled in the trial using a
prospective cohort study. Asthma attacks were classified as an ROAA (< 6 h of symptoms) or an
SOAA (> 6 h). All patients were treated with albuterol, four puffs at 10-min intervals (100 ␮g per
actuation), delivered by metered-dose inhaler with a spacer device during 3 h.
Results: On the basis of previously determined criteria, 11.3% of patients were classified as having
a ROAA. Male patients comprised 53.6% of the ROAA group (p ⴝ 0.03). In ROAA patients, the
exacerbation was less likely to be attributed to respiratory tract infection (p ⴝ 0.001) and more
likely to have no identifiable cause (p ⴝ 0.0001). Also, ROAA patients had lower pulmonary
function (FEV1) at presentation (mean difference, ⴚ 0.13; 95% confidence interval [CI], ⴚ 0.22
to ⴚ 0.04 L; p ⴝ 0.04) than SOAA patients. At the end of treatment, ROAA patients had an overall
48.0 L/min (95% CI, 14.1 to 81.8 L/min) greater improvement in PEF and a 0.31 L (95% CI, 0.08
to 0.54 L) greater improvement in FEV1 than SOAA patients. Also, ROAA patients presented with
less accessory muscle use (p < 0.05) and higher oxygen saturation (p ⴝ 0.005). Finally, SOAA
patients showed an increased incidence of hospital admission (relative risk, 3.89; 95% CI, 1.01 to
15.0).
Conclusions: Data from this study support the notion that ROAAs constitute a distinct but
uncommon acute asthma ED presentation, with a predominance of male patients. Upper
respiratory tract infection was not believed to be a significant trigger factor in these patients, and
ROAA patients had rapid deterioration of their conditions followed by a more rapid response to
treatment and a lower hospital admission rate than SOAA patients. Thus, we have identified a
subgroup of patients who appear to have common characteristics with patients with sudden-onset
near-fatal/fatal asthma.
(CHEST 2000; 118:1547–1552)
Key words: acute severe asthma; near-fatal asthma; sudden-onset asthma
Abbreviations: ANOVA ⫽ analysis of variance; CI ⫽ confidence interval; ED ⫽ emergency department; PEF ⫽ peak
expiratory flow; ROAA ⫽ rapid-onset asthma attack; Sao2 ⫽ arterial oxygen saturation; SOAA ⫽ slow-onset asthma
attack
ince Roe drew attention to the distinction beS tween
death after a prolonged attack of asthma
1
and sudden unexpected death, it has been docu*From the Departamento de Emergencia (Dr. G. J. Rodrigo),
Hospital Central de las FF.AA.; and Unidad de Cuidado Intensivo (Dr. C. Rodrigo), Asociación Española 1a de Socorros
Mutuos, Montevideo, Uruguay.
Manuscript received December 30, 1999; revision accepted May
31, 2000.
Correspondence to: Gustavo J. Rodrigo, MD, Departamento de
Emergencia, Hospital Central de las FF.AA., Av. 8 de Octubre 3020,
Montevideo 11600, Uruguay; e-mail: [email protected]
mented2– 6 that acute severe asthma may have a rapid
or slow onset. Thus, rapid-onset asthma attacks
(ROAAs) are characterized by sudden development
of airway obstruction, sometimes with fatal consequences. This evolution contrasts with that of patients with slow-onset asthma attacks (SOAAs), who
are associated with a progressive clinical and functional deterioration. The prolonged duration of the
attack and the time frame over which symptoms
develop can give an indication of the development of
airflow inflammation, whereas a rapid deterioration
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1547
suggests predominant airway smooth muscle contraction. Several studies7–9 suggest that inhalation of
large doses of allergen by patients with asthma and
high levels of specific IgE to the allergen cause
ROAAs. At autopsy, the airways often lack secretions
and contain more neutrophils than eosinophils in the
submucosa.10,11
Most studies3,5,6,11–22 concerning the speed of
onset of acute severe asthma include retrospective
reports of patients free of asthma symptoms who
develop acute severe asthma and respiratory arrest
or failure (sudden-onset asthma attacks/sudden-asphyxic asthma/near-fatal asthma), sometimes with
fatal consequences (sudden-onset fatal asthma).
Since larger clinical trials that analyze the frequency
and main characteristics of this type of patient at
emergency department (ED) presentation are uncommon, we designed a prospective trial to study the
rapidity of onset in adults with acute severe asthma
attacks. The main objectives of this study were as
follows: (1) to determine the frequency of ROAAs and
SOAAs in adult patients with acute, severe asthma who
presented to an ED; (2) to establish whether ROAA
patients differ from SOAA patients in terms of clinical
and spirometric characteristics; and (3) to determine
whether ROAA patients differ from SOAA patients in
terms of response to treatment.
Materials and Methods
Subjects and Design
This study includes data from a prospective cohort study
performed at the ED of the Hospital Central de las FF.AA. in
Montevideo, Uruguay. This department sees ⬎ 60,000 patients
annually, with about 1,200 visits per year for adult patients with
acute asthma. We studied all adult subjects with acute asthma
who attended to the ED over a 1-year period. All patients met the
diagnosis criteria of asthma of the American Thoracic Society.23
The inclusion criteria were as follows: (1) age from 18 to 50 years;
(2) FEV1 and a peak expiratory flow (PEF) of ⬍ 50% of
predicted value; (3) absence of history of chronic cough, and
cardiac, hepatic, renal, or other medical disease, or pregnancy;
and (4) an expressed willingness to participate in the study, with
written informed consent obtained. The Hospital Ethics Committee approved the study.
Protocol
After initial assessment, all patients were treated with albuterol, four puffs at 10-min intervals (100 ␮g per actuation),
delivered by a metered-dose inhaler and a spacer device (Volumatic; Allen & Hansburys; Greenford, UK). Each dose was
followed by a deep inhalation from the spacer device. The
protocol involved 3 h of this treatment (1,200 ␮g of albuterol
every 30 min). After this time, all patients with a poor response
received hydrocortisone, 500 mg IV. The protocol included the
administration of O2 if arterial oxygen saturation (Sao2) decreased to ⬍ 92%. Aminophylline was excluded in all patients.
The patients were independently assessed and treated by physicians, all of whom were unaware of the previous duration of
attack and pulmonary function. All subjects completed the
protocol. The decision to discharge or admit a patient to the
hospital was made at the end of protocol by senior ED staff
without knowledge of previous patient group allocation. Patients
were discharged from the ED according to the following criteria:
if accessory muscle use had abated, if wheezing was judged to be
minimal or completely resolved, if dyspnea abated, and if FEV1
or PEF was ⬎ 60% of predicted. The physicians prescribed oral
prednisone, 60 mg for 7 days, for all discharged patients, or IV
steroids for those who were admitted.
Measurements
Patients or relatives were asked about relevant aspects of
asthma history and outpatient therapy. To determine the duration of onset of present attack, patients were asked to indicate the
onset of wheeze, cough, shortness of breath, or some combination of these symptoms; also, a decline in the PEF, if available,
was noted. When possible, the patient’s relatives were asked to
confirm information regarding the duration of symptoms before
ED presentation. Severe asthma attacks were classified in accord
with Kolbe et al5 as an ROAA (⬍ 6 h) or an SOAA (ⱖ 6 h). That
definition was selected to distinguish from previous definitions of
sudden-onset asthma attacks (respiratory arrest or failure within
11⁄2 h,8 or 3 h,3 after the onset of attack). The following variables
were measured in each patient immediately before starting
treatment, and at 30, 60, 90, 120, 150, and 180 min: FEV1, PEF,
respiratory rate, heart rate, accessory muscle use, dyspnea,
wheezing, and Sao2. PEF was measured with a mini-Wright peak
flowmeter (Clement Clarke; Harlow, UK). The highest of three
values was recorded. FEV1 was measured using a Vitalograph
Compact spirometer (Vitalograph; Maids Moreton House; Buckingham, UK). Three successive maximal expiratory curves were
recorded at each assessment, and the highest value was selected,
according to the criteria of the American Thoracic Society.24
Heart rate was measured from continuous ECG. Sao2 was
measured with a finger oximeter (N-180 Pulse Oximeter; Nellcor;
Hayward, CA). Accessory-muscle use was defined as visible
retraction of the sternocleidomastoid muscles.25 Dyspnea was
defined as the patient’s own assessment of breathlessness.
Wheezing was defined as musical or whistling breath sounds
heard with a stethoscope during expiration. These clinical factors
were graded in a scale from 0 to 3 in which 0 denoted absent, 1
denoted mild, 2 denoted moderate, and 3 denoted severe.
Finally, a score for severity was produced for each patient using
the National Asthma Education and Prevention Program (range
1 to 4; mild intermittent to severe persistent).26
Statistical Methods
All data were analyzed with an SPSS 10.0 for Windows
software package (SPSS; Chicago, IL). Changes in FEV1 and
PEF were evaluated using repeated-measures analysis of variance (ANOVA), with one between-subject factor (rapid-slow) and
one within-subject factor (time). One-way repeated-measures
ANOVA was used to compare baseline values for each variable,
after assessing both normality of distributions and homoscedasticity. When the F value indicated significant differences among
group means, post hoc pairwise multiple comparisons were
performed using the Newman-Keuls test. Baseline data of the
two treatments were compared by t test for normally distributed
independent samples or the Mann-Whitney U test for nonnormally distributed continuous variables. ␹2 with Yates correction
or Fisher’s Exact Test was used for categorical variables. Clinical
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Clinical Investigations
factors graded on a scale of 0 to 3 were reported as medians and
interquartile ranges. A p value of ⬍ 0.05 using a two-tailed test
was taken as being of significance for all statistical tests. Mean
values ⫾ SD were calculated for continuous variables. Ninetyfive percent confidence intervals (CIs) and relative risks were
calculated with standard formulas.27
Results
Four hundred three patients (mean age,
33.6 ⫾ 11.0 years) with acute exacerbations of
asthma were enrolled in the trial (Table 1). On the
basis of previously determined criteria, only 41 patients (11.3%) were classified as having a ROAA (⬍ 6
h). Rapid-onset asthma patients did not differ from
slow-onset asthma patients with respect to age,
weight, chronic asthma severity, season of presentation, heart and respiratory rates, wheezing, dyspnea,
PEF, Sao2, accessory muscle use, and previous use
of ␤-agonists, steroids, and theophylline. On the
contrary, the two groups differed with respect to sex:
male patients comprised 53.6% of the ROAA group,
but only 36.3% of the SOAA group (p ⫽ 0.03). The
two groups presented differences with regard to
trigger factor. In ROAA patients, the exacerbation
was less likely to be attributed to respiratory tract
infection (12.1% vs 38.1% for SOAA patients;
p ⫽ 0.001), and more likely to have no identifiable
cause (51.4% vs 19.1% for SOAA patients;
p ⫽ 0.0001). There were no differences among other
categories of triggers, including allergens (ingested
food or medications), medication noncompliance,
weather, and emotional or endocrine factors. Finally,
ROAA patients had lower pulmonary function at
presentation (FEV1, 0.7 L vs 0.9 L for SOAA
patients) (mean difference, ⫺ 0.13; 95% CI, ⫺ 0.22
L to ⫺ 0.04 L).
The relationship between the cumulative doses of
albuterol and the change in PEF and FEV1 were
analyzed (Fig 1, 2). Mean PEF improved significantly over baseline values for both groups
(p ⬍ 0.001). The magnitude of improvements in
PEFs over baseline values was significant at all times
Table 1—Characteristics of Patients With Rapid-Onset or Slow-Onset Acute Asthma at ED Presentation
Measures
Age, yr*
Sex, % male (No.)
Weight, kg*
Chronic asthma severity, % (No.)
Mild intermittent
Mild persistent
Moderate persistent
Severe persistent
Duration of attack prior to ED presentation, h*
Triggers, % (No.)
Upper respiratory tract infection
Other
No identifiable
Season of presentation, % (No.)
Summer (December–February)
Fall (March–May)
Winter (June–August)
Spring (September–November)
Heart rate, beats/min*
Respiratory rate, breaths/min*
Accessory muscle use†
Dyspnea†
Wheezing†
PEF, % predicted*
PEF, L/min*
FEV1, % predicted*
FEV1, L*
Sao2*
␤2-agonist used within 24 h, % (No.)
Steroids used within 24 h, % (No.)
Theophylline used within 24 h, % (No.)
Rapid Onset
(n ⫽ 41)
Slow Onset
(n ⫽ 362)
32.8 (10.7)
53.6 (22)
67.1 (12.9)
33.6 (11.1)
36.4 (132)
67.3 (11.9)
7.3 (3)
9.8 (4)
56.1 (23)
26.8 (11)
3.2 (1.1)
9.1 (33)
10.8 (39)
54.4 (197)
25.7 (93)
31.6 (25.4)
⫺ 1.8 (⫺ 10.8 to 7.2)
⫺ 1.0 (⫺ 10.0 to 8.0)
1.7 (⫺ 14.3 to 17.7)
1.1 (⫺ 12.9 to 15.1)
⫺ 28.4 (⫺ 31.3 to ⫺ 25.8)
0.8
0.9
0.8
0.8
0.0001
12.1 (5)
36.5 (15)
51.4 (21)
38.1 (138)
42.8 (155)
19.1 (69)
⫺ 26.0 (⫺ 41.6 to ⫺ 10.4)
⫺ 6.3 (⫺ 21.9 to 9.3)
32.3 (19.5 to 45.6)
0.001
0.4
0.0001
4.9 (2)
36.6 (15)
29.2 (12)
29.3 (12)
103.1 (18.7)
22.3 (4.8)
1.5 (1.0)
2.0 (1.0)
2.0 (1.0)
31.4 (8.8)
166.7 (49.5)
24.0 (10.1)
0.7 (0.3)
96.6 (1.0)
60.9 (25)
19.8 (8)
36.5 (15)
12.6 (46)
32.7 (119)
28.3 (103)
26.1 (95)
102.8 (18.5)
21.6 (4.4)
2.0 (1.0)
2.0 (1.0)
2.0 (1.0)
31.7 (9.5)
165.0 (55.2)
27.6 (10.9)
0.9 (0.3)
96.0 (1.7)
60.0 (216)
25.0 (90)
43.3 (167)
⫺ 7.7 (⫺ 17.8 to 2.4)
3.9 (⫺ 9.8 to 17.6)
0.9 (⫺ 12.8 to 14.6)
3.2 (⫺ 10.5 to 16.9)
1.4 (⫺ 4.4 to 7.2)
0.7 (⫺ 0.6 to 2.0)
Difference (95% CI)
⫺ 0.8 (⫺ 4.4 to 2.7)
17.2 (1.6 to 32.8)
⫺ 0.2 (⫺ 3.8 to 3.4)
0.3 (⫺ 3.3 to 2.8)
1.6 (⫺ 16.1 to 19.3)
⫺ 3.6 (⫺ 7.2 to ⫺ 0.4)
⫺ 0.1 (⫺ 0.2 to ⫺ 0.0)
0.6 (⫺ 0.2 to 1.4)
0.9 (⫺ 12.8 to 4.6)
⫺ 5.2 (⫺ 18.9 to 8.5)
⫺ 6.8 (⫺ 14.8 to 1.2)
p Value
0.6
0.03
0.7
0.2
0.6
0.8
0.6
0.6
0.6
0.6
0.1
0.6
0.8
0.8
0.04
0.04
0.2
0.8
0.4
0.4
*Mean values with ⫾ 1 SD shown in parentheses.
†Medians and interquartile ranges.
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1549
Figure 1. Mean PEF values (percent of predicted) in ROAA and
SOAA patients after the administration of high doses of albuterol.
Data points indicate mean values, and the brackets represent 1
SD. * ⫽ p ⬍ 0.05; Pre ⫽ before treatment.
of treatment (p ⬍ 0.01). The two-way repeatedmeasures ANOVA showed a significant difference
between groups (p ⫽ 0.03). At the end of treatment,
ROAA patients had an overall 48.0 L/min (95% CI,
14.1 to 81.8 L/min) greater improvement in PEF
than SOAA patients. The ANOVA suggested that the
difference between groups increased with time
(p ⫽ 0.0001). The mean percent of predicted PEF
values at 180 min was 64.5 ⫾ 19.3% (337.6 ⫾ 102.9
Figure 2. Mean FEV1 values (percent of predicted) in ROAA
and SOAA patients after the administration of high doses of
albuterol. Data points indicate mean values, and the brackets
represent 1 SD. * ⫽ p ⬍ 0.05; see Figure 1 legend for abbreviation.
L/min) in the ROAA group and 56.0 ⫾ 17.2%
(289.6 ⫾ 95.1 L/min) in the SOAA group. The same
pattern held for changes in FEV1. The improvement
over baseline was significant in both groups (p ⬍ 0.01).
There was a significant difference between both groups
(p ⫽ 0.02). Compared with the SOAA group, the
ROAA group had better FEV1 at 180 min (mean
difference, 0.31 L; 95% CI, 0.08 to 0.54 L). The mean
percent of predicted FEV1 values at 180 min was
53.3 ⫾ 19.2% (1.67 ⫾ 0.69 L) in the SOAA group and
61.0 ⫾ 22.0% (1.98 ⫾ 0.79 L) in the ROAA group.
Also, the difference between groups increased with
time (p ⫽ 0.001).
At the end of protocol (3 h), ROAA patients demonstrated less accessory muscle use (median ⫾ interquartile range, 0.0 ⫾ 1.0 vs 0.5 ⫾ 1.0 for SOAA
patients; p ⬍ 0.05) and a higher Sao2 (1.91%; 95%
CI, 0.61 to 3.22%). At the end of treatment, 4.9% of
patients (2 of 39) in the ROAA group and 19.1% of
patients (69 of 293) in the SOAA group were admitted to the hospital (p ⫽ 0.04). SOAA patients
showed an increased risk of hospital admission (relative risk, 3.89; 95% CI, 1.01 to 15.0). On the
contrary, there was no difference between groups in
heart rate (mean difference, 0.3 beats/min; 95% CI,
⫺ 5.7 to 6.3 beats/min). Despite continuous ECG
recording, there were no signs of arrhythmia in
either group.
Discussion
The purpose of this study was to determine the
frequency of ROAAs and SOAAs in adult patients
with acute, severe asthma who presented to an ED,
and to establish whether ROAA patients differ from
SOAA patients in terms of clinical and spirometric
characteristics. Data from this prospective cohort
study showed that the prevalence of ROAAs was
11.3%. Men comprised 53.6% of the ROAA patients
but only 36.4% of the SOAA patients. Upper respiratory tract infection was reported as the trigger
more commonly in SOAA patients, and ROAA patients were more likely to have an unidentifiable
trigger. We found no evidence that sensitivity to
specific aeroallergens or ingested substances or environmental factors predisposes patients to ROAAs.
Finally, at presentation, ROAA patients had lower
pulmonary function measurements.
These findings were in concurrence with Kolbe
and coworkers,5 who performed a cross-sectional
study on 316 patients aged 15 to 49 years who were
admitted to the hospital with acute, severe asthma
and found that only 8.5% were classified as having
rapid-onset asthma (⬍ 6-h duration), again with a
preponderance of male patients. Patients were interviewed within 24 to 48 h of hospital admission to
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Clinical Investigations
determine the duration of attack. Similarly, Woodruff et al,6 in a retrospective cohort study of 225
patients with severe (PEF of ⱕ 40% of predicted)
acute asthma (18 to 64 years old) who were seen in
an ED, reported 17% of patients as having “sudden
onset” asthma (ⱕ 3 h). These patients with suddenonset asthma were less likely to have reported an
upper respiratory tract infection and, as in our study,
were more likely to have no unidentifiable trigger.
No PEF baseline data were included. Recently, Barr
et al,28 in a large, multicenter, prospective study of
patients with severe, acute asthma (PEF ⬍ 50%),
found a rate of ROAA occurrence of 14%. ROAA
patients were more likely to be triggered by respiratory allergens, exercise, and psychosocial stress, and
less likely to be triggered by upper respiratory
infections. In addition, these patients demonstrate
greater improvement with therapy. Unlike our study,
treatment of patients was managed at the discretion
of treating physicians.
ROAA occurrence rates differ widely among studies. Arnold and colleagues,2 in a prospective study of
patients with acute asthma admitted to the hospital,
estimated that in 46% of cases the speed of onset was
⬍ 24 h and in 13% of cases it was ⬍ 1 h. The
duration of attack was determined from clinical
history. This study also reported an association between age and duration of attack: rapid-onset attacks
occurred more frequently in younger patients. Our
study did not find a similar association with age.
Our trial sample presented the typical features of
adult patients with severe asthma who presented for
care to an ED without life-threatening exacerbations. On the contrary, most studies3,5,6,11,12–22,29,30
regarding the speed of onset of acute severe asthma
include selected retrospective reports of patients
free of asthma symptoms who develop acute severe
asthma and respiratory arrest or failure (suddenonset asthma attacks/sudden-asphyxic asthma/nearfatal asthma), sometimes with fatal consequences
(sudden-onset fatal asthma). Wasserfallen et al3 studied 34 patients intubated for acute asthma and found
that 29.4% of patients had “rapid decompensation.”
However, the duration of attack was established by
“a history of extremely rapid deterioration, out of a
clear blue sky” leading to intubation and mechanical
ventilation within 3 h after the onset of the first
symptoms. These authors concluded that suddenonset asthma was more frequent in young men and
was characterized by more severe acidosis and hypercapnia.
Likewise, Kallenbach et al31 studied 81 patients
with acute severe asthma in whom mechanical ventilation was required, and concluded that a “hyperacute” attack duration (⬍ 3 h from onset of attack to
intubation) was associated with an increased risk of
near fatality. Martin and coworkers29 examined 30
cases of near-fatal asthma attacks in children ⬍ 15
years old and found a low prevalence of rapid-onset
attacks (17%). As in our study, the information was
obtained from a standardized interview and questionnaire that was completed with subjects/parents.
The third objective of our study was to determine
whether ROAA patients differ from SOAA patients
in terms of response to treatment. In accord with
previous work,30 our data suggest that 400 ␮g (four
puffs) of albuterol at 10-min intervals delivered with
a metered-dose inhaler and a spacer device is an
effective treatment that produces a dose-related
bronchodilator response in patients with acute severe asthma. However, we found two different therapeutic responses to treatment patterns: ROAA patients have rapid deterioration followed by a more
rapid response to treatment and a lower hospital
admission rate than SOAA patients. Similarly, other
studies have found a positive correlation between the
duration of attack and the duration of the required
mechanical ventilation3,4,8,31: SOAA patients required more-prolonged mechanical ventilation than
that observed in ROAA patients.
Conclusion
Data from this study support the notion that
ROAAs constitute a distinct but uncommon acute
asthma presentation, with predominance of male
patients. Upper respiratory tract infection was not
believed to be a trigger in these patients. The SOAA
group was more likely to have an upper respiratory
tract infection, to respond less to ED treatment, and
to require hospitalization. Thus, we have identified a
subgroup of patients who appear to have common
characteristics with sudden-onset near-fatal/fatal
asthma patients.
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