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DOI: 10.1542/peds.2004-0294
2004;114;762Pediatrics
V. Connolly, William G. Harmon, John S. Sullivan and Jeffrey S. Rubenstein
Frank A. Maffei, Elise W. van der Jagt, Karen S. Powers, Stephen W. Standage, Heidi
Description of an Acute Asphyxial Subgroup
Duration of Mechanical Ventilation in Life-Threatening Pediatric Asthma:
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of Pediatrics. All rights reserved. Print ISSN: 0031-4005. Online ISSN: 1098-4275.
Boulevard, Elk Grove Village, Illinois, 60007. Copyright © 2004 by the American Academy
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Duration of Mechanical Ventilation in Life-Threatening Pediatric Asthma:
Description of an Acute Asphyxial Subgroup
Frank A. Maffei, MD; Elise W. van der Jagt, MD, MPH; Karen S. Powers, MD; Stephen W. Standage, BS;
Heidi V. Connolly, MD; William G. Harmon, MD; John S. Sullivan, MD; and
Jeffrey S. Rubenstein, MD, MBA
ABSTRACT. Objective. Acute asphyxial asthma
(AAA) is well described in adult patients and is charac-
terized by a sudden onset that may rapidly progress to a
near-arrest state. Despite the initial severity of AAA,
mechanical ventilation often restores gas exchange
promptly, resulting in shorter durations of ventilation.
We believe that AAA can occur in children and can lead
to respiratory failure that requires mechanical ventila-
tion. Furthermore, children with rapid-onset respiratory
failure that requires intubation in the emergency depart-
ment (ED) are more likely to have AAA and a shorter
duration of mechanical ventilation than those intubated
in the pediatric intensive care unit (PICU).
Methods. An 11-year retrospective chart review (1991-
2002) was conducted of all children who were aged 2
through 18 years and had the primary diagnosis of status
asthmaticus and required mechanical ventilation.
Results. During the study period, 33 (11.4%) of 290
PICU admissions for status asthmaticus required me-
chanical ventilation. Thirteen children presented with
rapid respiratory failure en route, on arrival, or within 30
minutes of arrival to the ED versus 20 children who
progressed to respiratory failure later in their ED course
or in the PICU. Mean duration of mechanical ventilation
was significantly shorter in the children who presented
with rapid respiratory failure versus those with progres-
sive respiratory failure (29 ⴞ 43 hours vs 88 ⴞ 72 hours).
Children with rapid respiratory failure had greater im-
provements in ventilation and oxygenation than those
with progressive respiratory failure as measured by pre-
and postintubation changes in arterial carbon dioxide
pressure, arterial oxygen pressure/fraction of inspired
oxygen ratio, and alveolar-arterial gradient. According to
site of intubation, 23 children required intubation in the
ED, whereas 10 were intubated later in the PICU. Mean
duration of mechanical ventilation was significantly
shorter in the ED group versus the PICU group (42 ⴞ 63
hours vs 118 ⴞ 46 hours). There were significantly greater
improvements in ventilation and oxygenation in the ED
group versus the PICU group as measured by pre- and
postintubation changes in arterial carbon dioxide pres-
sure and arterial oxygen pressure/fraction of inspired
oxygen ratio.
Conclusions. AAA occurs in children and shares char-
acteristics seen in adult counterparts. Need for early in-
tubation is a marker for AAA and may not represent a
failure to maximize preintubation therapies. AAA repre-
sents a distinct form of life-threatening asthma and re-
quires additional study in children. Pediatrics 2004;114:
762–767; acute asphyxial asthma, rapid onset near-fatal
asthma, respiratory failure, mechanical ventilation.
ABBREVIATIONS. AAA, acute asphyxial asthma; GCHaS, Gol-
isano Children’s Hospital at Strong; PICU, pediatric intensive care
unit; RRF, rapid respiratory failure; PRF, progressive respiratory
failure; ED, emergency department; Pao
2
, arterial oxygen pres
-
sure; Fio
2
, fraction of inspired oxygen; A-a, alveolar-arterial;
Paco
2
, partial pressure of carbon dioxide.
T
he prevalence of asthma continues to rise, with
5% to 10% of all children estimated to be af-
fected.
1
Five percent of these children will be
hospitalized during childhood
2
; of these, an even
smaller number require intensive care. Respiratory
failure is uncommon, occurring in only 8% to 24% of
children who have asthma and are admitted to in-
tensive care units.
3–9
Although few children have
life-threatening asthma episodes, these episodes are
associated with potential mortality, a high morbid-
ity, and a high cost of treatment. These life-threaten-
ing episodes can either present as a progressive ex-
acerbation refractory to escalating therapies or have
an abrupt onset with rapid deterioration to respira-
tory failure.
Acute asphyxial asthma (AAA), or rapid-onset
near-fatal asthma, is well described in adults. AAA
has a predilection for young male adults and is char-
acterized by a brief duration of symptoms (usually
⬍6 hours), few identifiable triggers, and a rapid pro-
gression to respiratory failure.
10,11
Often, the patient
will present in extremis, cyanotic, with little to no air
movement, and obtundation.
12
Despite the severity
of presentation, response to therapy is prompt. When
mechanical ventilation is warranted, its duration is
usually short, as a result of rapid improvements in
gas exchange.
12,13
Near-fatal asthma episodes are known to occur in
children.
14–17
There seems to be a subset of children
with near-fatal episodes whose presentation and
clinical course may be comparable to those seen in
AAA in adults.
18
We hypothesized that children who have rapidly
progressive asthma and require early mechanical
ventilation will have more rapid improvements in
gas exchange and require shorter durations of me-
From the Division of Pediatric Critical Care, Strong Children’s Research
Center of the University of Rochester, Rochester, New York.
Accepted for publication Apr 9, 2004.
DOI: 10.1542/peds.2004-0294
Reprint requests to (F.A.M.) Janet Weis Children’s Hospital, Geisinger
Medical Center, Division of Pediatric Critical Care, 100 N Academy St,
Danville, PA 17822. E-mail: famaffei@geisinger.edu
PEDIATRICS (ISSN 0031 4005). Copyright © 2004 by the American Acad-
emy of Pediatrics.
762 PEDIATRICS Vol. 114 No. 3 September 2004
by guest on June 6, 2013pediatrics.aappublications.orgDownloaded from
chanical ventilation than children who have asthma
and slowly progress to respiratory failure. The need
for early intubation and a shorter duration of me-
chanical ventilation may serve as markers of AAA in
these children.
METHODS
We identified and reviewed all charts of patients who were
between 2 through 18 years of age and had a primary discharge
diagnosis of asthma and required mechanical ventilation at Gol-
isano Children’s Hospital at Strong (GCHaS) during an 11-year
period (1991-2002). Children who were younger than 2 years were
excluded because of the significant overlap in the diagnoses of
asthma and bronchiolitis. The pediatric intensive care unit (PICU)
at GCHaS is a 12-bed medical-surgical unit with ⬃650 annual
admissions. It serves as the regional referral center in central
western New York State.
Before chart review, approval was obtained from the GCHaS
institutional review board. Two authors (F.M., S.S.) independently
reviewed all charts using a standardized approach. Children with
other preexisting respiratory diseases (eg, bronchopulmonary
dysplasia, interstitial lung disease) or significant comorbidities
(eg, congenital heart disease, malignancy, sickle cell disease) were
excluded from the review.
The following data were collected (when available): patient
demographics, asthma history, preexacerbation therapies, dura-
tion of symptoms before exacerbation, exacerbation therapies (in-
cluding mechanical ventilation), duration of mechanical ventila-
tion, and results from arterial blood gases drawn immediately
before and after intubation.
Patients were grouped and analyzed in 2 ways: 1) time of onset
of respiratory failure and 2) site of intubation. By time of onset of
respiratory failure, we compared children with rapid respiratory
failure (RRF) with those with progressive respiratory failure
(PRF). RRF was defined as respiratory failure diagnosed en route,
on arrival to the emergency department (ED), or within 30 min-
utes of arrival to the ED. We defined respiratory failure as the
need for assisted ventilation as a result of cardiopulmonary arrest,
apnea, central cyanosis despite high flow oxygen, or progressive
obtundation.
When grouping children by site of endotracheal intubation and
initiation of mechanical ventilation, we compared clinical charac-
teristics of children who were intubated in the ED with those who
were intubated in the PICU. We chose this secondary comparison
to attempt to detect a difference in the threshold for the initiation
of mechanical ventilation on the basis of alternative practice ap-
proaches in the ED versus the PICU.
For assessing differences between groups, [chi]
2
analyses were
applied to categorical data and unpaired t tests were applied to
interval data. P ⬍ .05 was used as the criterion for rejection of the
null hypothesis. A commercially available statistical program (Mi-
crosoft Excel 2000, Redmond, WA) was used for all calculations.
RESULTS
During the 11-year study period, there were 290
admissions to the PICU for severe asthma. Of these
admissions, 33 (11.4%) required mechanical ventila-
tion. The 33 episodes of mechanical ventilation oc-
curred among 32 children (12 girls, 20 boys); 1 girl
required mechanical ventilation on 2 occasions. The
mean age of the study group was 11.8 years with a
range of 2 to 18 years. There were no deaths among
the study group. No patient had a pneumothorax
before intubation or on the chest radiograph ob-
tained immediately after intubation.
Comparison by Time of Onset of Respiratory Failure
Thirteen children had RRF, and 20 children had
PRF. Of the 13 children who presented with RRF, 4
required bag mask ventilation or intubation en route
by emergency medical services as a result of pro-
found cyanosis, apnea, or cardiopulmonary arrest.
Two additional children were intubated immediately
on arrival for obvious respiratory failure, and 7 chil-
dren were intubated within 30 minutes of arrival
(mean: 8.5 minutes) as a result of respiratory failure
during initial treatment. All 7 of these children were
receiving a high-dose continuous inhalation of a

-agonist at the time of respiratory failure.
Of the 20 children with PRF, 10 developed respi-
ratory failure that required intubation late in their
ED course (34-120 minutes after arrival; mean: 72
minutes; median: 68 minutes) and 10 developed re-
spiratory failure that required intubation after trans-
fer to the PICU (2-24 hours after hospital arrival;
mean: 9 hours 6 minutes; median: 5 hours 35 min-
utes).
Children with RRF were older than those with PRF
(13.3 ⫾ 2.3 years vs 10.8 ⫾ 3.9 years; P ⫽ .03). There
were no significant differences in gender, race, pre-
vious PICU admissions or intubations, or mainte-
nance asthma medications in the RRF group versus
the PRF group. No trigger for the asthma attack was
identified in 8 (62%) of 13 children with RRF versus
9 (45%) of 20 children with PRF. This difference was
not statistically significant (P ⫽ .35)
Children with RRF had a significantly shorter
mean duration of mechanical ventilation than those
with PRF (29.2 ⫾ 43 hours vs 88.2 ⫾ 72 hours; P ⫽
.006; Fig 1). We also analyzed the data post hoc using
cutoffs of 5 (intubated on arrival or en route), 90, and
180 minutes; in all cases, the difference between
groups in duration of ventilation remained signifi-
cant, but the level of significance decreased (P ⫽ .004,
.01, and .02, respectively).
Paired preintubation (⬍30 minutes before intuba-
tion) and postintubation (⬍30 minutes after intuba-
tion) arterial blood gas data were available in 6 of
13 children with RRF and in 14 of 20 children with
PRF. Although there were no differences between
groups in immediate preintubation oxygen satura-
tion (RRF 71% vs PRF 88%; P ⫽ .12), preintubation
arterial oxygen pressure (Pao
2
)/fraction of inspired
oxygen (Fio
2
) ratio, preintubation alveolar-arterial
(A-a) gradient, or preintubation partial pressure of
carbon dioxide (Paco
2
), there were significant differ
-
ences between groups in improvements of gas ex-
change as measured by changes in Paco
2
,Pao
2
/Fio
2
ratio, and A-a gradients (Tables 1 and 2). The RRF
group had a mean reduction in Paco
2
of 46 mm Hg
versus a 1-mm Hg increase in the PRF group (P ⫽
.01). The RRF group had a mean improvement in
Pao
2
/Fio
2
ratio of 260 versus 88 in the PRF group
(P ⫽ .04). Similarly, the RRF group had a mean
decline of 327 in the A-a gradient versus a decline of
100 in the PRF group (P ⫽ .006).
Comparison by Site of Intubation
Twenty-three children were intubated the ED ver-
sus 10 children in the PICU. There were no signifi-
cant differences between groups in age (mean: 12.1
years vs 11.0 years), gender, race, previous PICU
admissions or intubations, or maintenance asthma
medications. Children who were intubated in the ED
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had a shorter mean duration of mechanical ventila-
tion (41.9 ⫾ 63 hours vs 118 ⫾ 46 hours in children
who were intubated in the PICU; P ⫽ .0008; Fig 2).
Paired pre- and postintubation arterial blood gas
data were available in 12 of 23 children who were
intubated in the ED and in 8 of 10 children who were
intubated in the PICU. Although there were no dif-
ferences between groups in immediate preintubation
oxygen saturations (ED 80.6% vs PICU 84.1%; P ⫽
.66), preintubation Pao
2
/Fio
2
ratio, preintubation
A-a gradient, or preintubation Paco
2
, there were sig
-
nificant differences in improvement in ventilation
and oxygenation between groups (Tables 3 and 4).
The ED group had a mean reduction in Paco
2
of 35
mm Hg versus a 21-mm Hg increase in the PICU
group (P ⫽ .004) and a mean improvement in Pao
2
/
Fio
2
ratio of 217 versus 43 in the PICU group (P ⫽
.02).
We found no differences in the duration of symp-
toms before presentation when comparing the RRF
and the PRF groups (35 hours vs 30 hours; P ⫽ .61).
Likewise, there were no differences in the duration of
symptoms when comparing the ED group and the
PICU group (ED 32.4 hours vs PICU 31.8 hours; P ⫽
.95). We did note, however, a trend toward shorter
lengths of ventilation among children with duration
of symptoms of 6 hours or less. Among children who
were intubated in the ED, 9 with short symptom
duration (⬍6 hours) had a mean length of ventilation
of 24 hours versus 54 hours in children with longer
symptom duration (P ⫽ .1).
DISCUSSION
Using early intubation and a brief duration of me-
chanical ventilation as clinical proxies, we have iden-
tified a population of children who are likely to have
a disease process similar to AAA seen in adults.
Although several authors have described adolescents
with fatal and near-fatal AAA events,
14–17
descrip
-
tions of AAA events in younger children are lacking.
An Australian study identified 30 near-fatal asthma
episodes that occurred in children who were
younger than 15 years. Most cases were marked by
progressive respiratory distress, but 5 (17%) had sud-
den onset with rapid respiratory collapse.
18
Al
-
though we found that children with RRF tended to
be older than those with PRF, a significant portion of
children in the present study who had RRF were
preadolescent; 4 (31%) of the 13 children with RRF
were 12 years or younger (age range: 10-18 years).
We chose to attempt to identify children with
AAA using the objective finding of respiratory fail-
ure evident on presentation or shortly thereafter
(during the ED course). Although prospective deter-
minants of respiratory failure could not be used,
evidence of true respiratory failure was clear in all
cases: requirement of assisted ventilation as a result
Fig 1. Duration of mechanical ventilation in
children with rapid respiratory failure versus
those who progress to respiratory failure.
TABLE 1. Mean Changes in Ventilation as Measured by ⌬
Paco
2
in Mechanically Ventilated Children With RRF Versus
Those With PRF (When Paired Blood Gas Data Available)
Respiratory
Failure
Preintubation
Paco
2
Postintubation
Paco
2
⌬ Paco
2
RRF (n ⫽ 6) 102 55 ⫺46
PRF (n ⫽ 14) 80 80 ⫹1
P ⫽ .2 P ⫽ .09 P ⫽ .02
TABLE 2. Mean Changes in Oxygenation as Measured by Changes in Pao
2
/Fio
2
Ratio and A-a Gradient in Mechanically Ventilated
Children With RRF Versus Those With PRF (When Paired Blood Gas Data Available)
Respiratory
Failure
Preintubation
Pao
2
/Fio
2
Postintubation
Pao
2
/Fio
2
⌬ Pao
2
/Fio
2
Preintubation
A-a Gradient
Postintubation
A-a Gradient
⌬ A-a Gradient
RRF (n ⫽ 6) 163 418 260 427 100 327
PRF (n ⫽ 14) 166 253 88 399 265 134
P ⫽ .96 P ⫽ .02 P ⫽ .04 P ⫽ .66 P ⫽ .002 P ⫽ .006
764 MECHANICAL VENTILATION IN PEDIATRIC ASTHMA
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of cardiopulmonary arrest, apnea, central cyanosis
despite high flow oxygen, or progressive obtunda-
tion. Arterial blood gas data were not obtained in
many of these overt cases because of the need to
initiate therapy promptly. In these cases, patients
necessarily received a diagnosis of respiratory failure
on clinical grounds; obtaining blood gases would
have been injudicious and posed needless risk to
these patients. When blood gas data were available,
we used these data to examine improvements in gas
exchange quantitatively.
We chose intubation within 30 minutes of ED
arrival as a cutoff time in delineating RRF from PRF.
Although arbitrary, 30 minutes is a rough estimate of
the time for initiation of urgent “rescue” therapy
(nebulized, subcutaneous, and/or intravenous

-agonists). Children who remained in respiratory
failure (or deteriorated further) during this brief trial
period without mechanical support did have clinical
findings and blood gas data (when available) sup-
porting a rapidly progressive disease process.
We found that children who had asthma with
respiratory failure on presentation or shortly there-
after often had prompt normalization of gas ex-
change and brief durations of mechanical ventilation.
This is consistent with adult descriptions of AAA.
Plaza et al
13
prospectively studied 220 adults with
near-fatal asthma attacks and identified 45 as rapid-
onset and rapidly progressive attacks. Patients in the
rapid-onset group often presented in arrest and had
very brief durations of ventilation when compared
with the slow-onset group. Likewise, Wasserfallen et
al
12
found rapid recovery and short durations of
ventilation (mean: 34 hours vs 91 hours) in adults
who were characterized as having sudden asphyxial
asthma compared with those having a more gradual
development of respiratory failure.
An expected shorter duration of symptoms before
intubation was not seen in our children with RRF as
compared with those who developed respiratory
failure later. This may be explained by several limi-
tations to our study. First, the retrospective nature of
the study does not allow for standardized documen-
tation of historical data. The recorded onset and du-
ration of symptoms before presentation may have
been inexact. Historical documentation of symptom
duration was often approximated, varied according
to clinician (eg, resident note vs attending note), and,
Fig 2. Duration of mechanical ventilation in chil-
dren who were intubated in the ED versus those
who were intubated in the PICU.
TABLE 3. Mean Changes in Ventilation as Measured by
Changes in Paco
2
in Mechanically Ventilated Children Intubated
in the ED Versus Those Intubated in the PICU (When Paired Blood
Gas Data Available)
Site of
Intubation
Preintubation
Paco
2
Postintubation
Paco
2
⌬ Paco
2
ED (n ⫽ 12) 96 60 ⫺35
PICU (n ⫽ 8) 72 92 21
P ⫽ .2 P ⫽ .09 P ⫽ .004
TABLE 4. Mean Changes in Oxygenation as Measured by Changes in Pao
2
/Fio
2
Ratio and A-a Gradient in Mechanically Ventilated
Children Intubated in the ED Versus Those Intubated in the PICU (When Paired Blood Gas Data Available)
Site of
Intubation
Preintubation
Pao
2
/Fio
2
Postintubation
Pao
2
/Fio
2
⌬ Pao
2
/Fio
2
Preintubation
A-a Gradient
Postintubation
A-a Gradient
⌬ A-a Gradient
ED (n ⫽ 12) 165 382 217 396 148 248
PICU (n ⫽ 8) 141 185 43 424 318 106
P ⫽ .6 P ⫽ .002 P ⫽ .02 P ⫽ .7 P ⫽ .02 P ⫽ .08
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at times, was lacking. Documentation of the onset
of symptoms was variable. Some historians docu-
mented the duration as beginning with any symp-
tom of an upper respiratory infection (eg, rhinorrhea,
cough), whereas others considered wheezing or
chest discomfort as the onset. Therefore, grouping
children according to duration of symptoms (rapid
onset vs slow onset) could lead to inaccurate conclu-
sions about differences between groups. Last, our
study may have lacked the number of patients nec-
essary to detect such a difference.
Another limitation of the study was lack of stan-
dardized preintubation treatment strategies. The lack
of a uniform treatment protocol may have had an
impact on the timing of the initiation of mechanical
ventilation. This would have a greater importance in
children who were intubated later in their hospital
course versus those who presented in respiratory
failure. Reviewing the treatment of the 20 children
who developed respiratory failure later in their hos-
pital course, we found that all children were receiv-
ing high-dose continuous inhalation

-agonist (albu-
terol 15-20 mg/hour) and intravenous steroids
(methylprednisolone 2-4 mg/kg/day) before intuba-
tion. Additional therapies before intubation were
used as follows: intravenous

-agonist (terbutaline
0.5-5.0
g/kg/min) in 18 (90%) of 20, inhaled ipra-
tropium bromide or atropine in 19 (95%) of 20, intra-
venous magnesium sulfate in 10 (50%) of 20, and
provision of a heliox gas mixture (70% helium:30%
oxygen) in 6 (30%) of 20. No child had a trial of
noninvasive ventilation attempted. Of note, the rate
of mechanical ventilation among children who had
asthma and were admitted to our PICU (11.4%) dur-
ing the study period was similar to or lower than that
reported previously.
3–6
AAA events may have a unique pathophysiology;
specifically, intense bronchospasm with a relative
absence of bronchial inflammation. The contribution
of mucus plugging to an AAA episode is unclear.
There have been clinical reports of a paucity of mu-
cus in adults with AAA during routine suction-
ing
12,16
; however, postmortem examination of adults
who have died of AAA has revealed an increased
mucus gland area.
19
Several authors have described
a characteristic submucosal cellular profile in adults
who have died during an AAA event. Surprising,
neutrophils are the predominate cell type in cases of
AAA, whereas eosinophils predominant in slow-on-
set cases.
19–21
Several theories have been postulated
to explain these cellular differences. Neutrophil pre-
dominance in AAA may simply be a function of
time. In animal models, the recruitment of neutro-
phils by a specific stimulus may precede and, in fact,
lead to later eosinophilic infiltration.
22,23
Second, the
nature of the stimulus itself may lead to a specific
initial cellular response. Bacterial endotoxin and
certain environmental agents such as ozone have
been shown to cause neutrophil-mediated bronchial
hyperresponsiveness.
24,25
Last, neutrophils may not
have been a primary component of the AAA event
and indeed were “innocent bystander” cells.
20
An
initial neurogenic event may have mediated intense
bronchospasm, independent of the submucosal cel-
lular profile. Alternatively, the predominance of
bronchial hyperresponsiveness with a relative lack
of bronchial inflammation may be a function of an
early therapeutic intervention (mechanical ventila-
tion) interrupting a pathophysiologic sequence of
events. This seems unlikely, as mechanical ventila-
tion has been known to induce proinflammatory
lung changes.
26,27
In conclusion, we believe that AAA can occur in
children and can lead to early respiratory failure.
Our patients with RRF caused by asthma share many
key characteristics seen in adults, namely, severity of
presentation, rapid improvements in gas exchange
after initiation of mechanical ventilation, and subse-
quent brief durations of mechanical ventilation. As in
adults, AAA in children may represent a pathologi-
cally distinct form of asthma. Therefore, the need for
early intubation and a short duration of mechanical
ventilation may serve as proxies for AAA and may
not represent a failure to maximize preintubation
therapies. Prospective study will be required to clar-
ify further these hypotheses.
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READ THIS, IT’S SHORT
”I recently gave 2 talks, both for quite decent fees, in which I was asked to speak
no longer than 25 or 30 minutes....Thefirst of my 2 talks was given to wealthy
country-club women. ‘If they’re bored, they walk out,’ the very nice woman who
had arranged for me to be the day’s speaker told me, ‘especially the younger
women.’ Henry James once called aristocracy ‘bad manners organized,’ and plu-
tocracy is apparently not much better. But I suspect something other than mere bad
manners is going on here. What is going on, I believe, is a shortened national
attention span. People have lost patience, endurance, tolerance for the lengthy,
possibly even the leisurely, presentation of culture, teaching, entertainment, and
much else. Some say television has helped bring this about. When on their nightly
news major networks promise an ‘in-depth report,’ they mean between 90 seconds
and 2 minutes....The half-hour lecture may soon be replaced by the 15-minute
one.”
Epstein J. Wall Street Journal. June 24, 2004
Noted by JFL, MD
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DOI: 10.1542/peds.2004-0294
2004;114;762Pediatrics
V. Connolly, William G. Harmon, John S. Sullivan and Jeffrey S. Rubenstein
Frank A. Maffei, Elise W. van der Jagt, Karen S. Powers, Stephen W. Standage, Heidi
Description of an Acute Asphyxial Subgroup
Duration of Mechanical Ventilation in Life-Threatening Pediatric Asthma:
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