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All patients with asthma are at risk of developing
exacerbations characterized by a progressive increase in
shortness of breath, cough, wheezing or chest tightness,
and by a decrease in expiratory airflow. The severity of
exacerbations may range from mild to near-fatal, and
deterioration usually progresses over hours, days, or
weeks; however, a few patients develop sudden (over
minutes) and unexpected increases in airway obstruction.
Progressive airway narrowing, due to airway inflammation
and/or increased bronchiolar smooth-muscle tone, is the
hallmark of an asthma attack and leads to (1) increased
flow resistance; (2) pulmonary hyperinflation; and (3)
ventilation/perfusion mismatching.
Without correction of the airway obstruction,
respiratory failure is a consequence of increased work
of breathing, gas exchange inefficiency, and respiratory
muscle exhaustion. The combination of acute hypercapnia
and high intrathoracic pressures can produce a
significant rise in intracranial pressure and neurologic
signs, such as unilateral or bilateral mydriasis,
quadriparesis, and subarachnoid and subconjunctival
hemorrhages during an acute episode (Fig 1). 
Figure 1.
A 35-year-old
white man with
severe
exacerbation of asthma. After 2 days of progressive
bronchospasm, he received medical treatment (high doses
of inhaled β-agonists) at his home by an emergency
medical service. After this treatment, his condition
showed an improvement, and he was admitted to an ICU to
continue treatment. A few hours after admission, he
presented bipalpebral hematomas (left), along
with subconjunctival hemorrhages (right).
When airway inflammation is predominant, patients show a
progressive (over many hours, days, or even weeks)
clinical and functional deterioration (type 1 or
slow-onset acute asthma) (Table 1).
In the less common asthma progression scenario,
bronchospasm is predominant and patients presented with
a sudden-onset asthma attack (type 2 or asphyxic
orhyperacuteasthma). Surprisingly, these patients show a
more rapid and complete response to treatment.
Table 1 — Main
Characteristics of Patients With Acute Asthma and Sudden
or Slow-Evolution*
|
Type 1.
Slow-progression |
Type
2. Sudden-progression |
|
Slow-onset acute asthma |
Sudden-onset, asphyxic, brittle or hyperacute asthma
|
|
Progressive deterioration: >6 h
(usually days or weeks) |
Rapid deterioration: <6 h |
|
80 to 90% of patients who presented to an ED
|
10 to 20% of patients who presented to an ED
|
|
Female predominance |
Male predominance |
|
More likely to be triggered by upper-respiratory
infections |
More likely to be triggered by respiratory
allergens, exercise, and psychosocial stress
|
|
Less severe obstruction at presentation |
More severe obstruction at presentation |
|
Slow response to treatment and higher hospital
admissions |
Rapid response to treatment and lower hospital
admissions |
|
Airflow inflammation mechanism |
Bronchospastic mechanism of deterioration
|
Fatal Asthma
Death
occurs typically in patients with a poorly controlled
disease, and the condition gradually deteriorates over a
period of days, or even weeks, before the fatal attack.
Infrequently, death occurs in a sudden fashion. Previous
ventilatory assistance, admission to an ICU, and a
history of recurrent hospitalizations are the most
specific markers associated with an increased risk of
dying from asthma. Nevertheless, <40% of fatal cases
have these risk factors. Data suggest that it is very
uncommon to die without substantial luminal obstruction.
Therefore, the most probable cause of death is asphyxia,
due to severe limitation of airflow and hypoxemia.
Smooth muscle contraction and production of inflammatory
mucus exudates are important mechanisms for fatal
attacks in young and old individuals with asthma.
Assessment
The
assessment of an episode of asthma exacerbation has two
different dimensions: (1) a static assessment
to determine the severity of attack; and (2) a
dynamic assessment to evaluate the response to
treatment (Table 2).
The
severity of airflow obstruction cannot be accurately
judged by means of symptoms and physical examination.
Only 15% of patients with acute severe asthma have
tachycardia (>120 beats/min), and <20% show tachypnea
(respiratory rate >30 breaths/min).
The
presence of wheeze and dyspnea correlated poorly with
the degree of airflow limitation, and pulsus paradoxus
has been abandoned as an indicator of severity, because
it is frequently difficult to measure.
On
the contrary, the presence of sternocleidomastoid or
suprasternal retractions correlate with impairment in
lung function and can be considered a useful sign of
severe airflow obstruction.
Table 2—
Main
Dimensions of the Assessment of the Adult Patient With
Acute Asthma in the ED*
|
Dimensions
|
Meaning |
|
Static assessment:
|
Severity of attack
(determines intensity of treatment)
Determination of hypoxemia level (goal of treatment
≥92%) |
|
Dynamic assessment
|
Response of treatment
(treatment guide and outcome prediction)
Achieving and keeping target Spo2 ≥92%
|
|
|
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