STATUS ASTHMATICUS
Introduction
-Status asthmaticus is an acute exacerbation of asthma
that remains unresponsive to initial treatment with
bronchodilators.
-Patients report chest tightness, rapidly progressive
shortness of breath, dry cough, and wheezing.
-Typically, patients present a few days after the onset of a
viral respiratory illness, following exposure to a potent
allergen or irritant, or after exercise in a cold
environment.
Pathophysiology
-Allergic inflammation in asthma begins with the
development of a predominantly helper T2 lymphocyte–
driven, as opposed to helper T1 lymphocyte–driven,
immune milieu, perhaps caused by certain types of
immune stimulation early in life.
-This is followed by allergen exposure in a genetically
susceptible individual. Specific allergen exposure (eg,
dust mites) under the influence of helper T2 lymphocytes
leads to B-lymphocyte elaboration of immunoglobulin E
(IgE) antibodies specific to that allergen.
-The IgE antibody attaches to surface receptors on airway
mucosal mast cells.
-Subsequent specific allergen exposure leads to cross-
bridging of IgE molecules and activation of mast cells,
with elaboration and release of a vast array of mediators.
-These mediators include histamine; leukotrienes C4, D4,
and E4; and a host of cytokines.
-These mediators cause:
 Bronchial smooth muscle constriction
 Vascular leakage
 Inflammatory cell recruitment (with further
mediator release)
 Mucous gland secretion
-These processes lead to airway obstruction by
constriction of the smooth muscles, edema of the
airways, influx of inflammatory cells, and formation of
intraluminal mucus.
-In addition, ongoing airway inflammation is thought to
cause the airway hyperreactivity characteristic of asthma.
-Physiologically, asthma has 2 components: an early
acute bronchospastic aspect marked by smooth muscle
bronchoconstriction and a later inflammatory component
resulting in airway swelling and edema.
Early bronchospastic response
Mediators, including histamine, prostaglandin D2, and
leukotriene C4. These substances cause airway smooth
muscle contraction, increased capillary permeability,
mucus secretion, and activation of neuronal reflexes.
Early asthmatic response is characterized by
bronchoconstriction that is generally responsive to
bronchodilators, such as beta2-agonist agents
Clinical presentation
History
-The symptoms of asthma consist of a triad of
 Dyspnea
 Cough
 wheezing
 Chest tightness
-Wheezing regarded as the sine qua non for asthma.
-Cough is non productive initially then thick sputum
later
- Personal or family history of allergic diseases such as
eczema, rhinitis, or urticaria is valuable contributory
evidence.
Late inflammatory response
Release of inflammatory mediators prime adhesion
molecules in the airway epithelium and capillary
endothelium, which then allows inflammatory cells, such
as eosinophils, neutrophils, and basophils, to attach to the
epithelium and endothelium and subsequently migrate
into the tissues of the airway.
Eosinophils release eosinophilic cationic protein (ECP)
and major basic protein (MBP). Both ECP and MBP
induce desquamation of the airway epithelium and
expose nerve endings. This interaction promotes further
airway hyperresponsiveness in asthma.
The 2 phases of asthma lead to:
 increased airway resistance and obstruction.
 Air trapping results in lung hyperinflation
 Ventilation/perfusion (V/Q) mismatch
 Increased dead space ventilation.
 Decreased compliance and increased work of
breathing.
-The increased pleural and intra-alveolar pressures that
result from obstruction and hyperinflation, together with
the mechanical forces of the distended alveoli, eventually
lead to a decrease in alveolar perfusion.
-The combination of atelectasis and decreased perfusion
leads to V/Q mismatch within lung units. The V/Q
mismatch and resultant hypoxemia trigger an increase in
minute ventilation.
The early stages of acute asthma, hyperventilation may
result in respiratory alkalosis but later respiratory acidosis
occurs V/Q mismatch.
Sex: In infants, males generally have more severe disease
than females.
In older children, males and females are equally affected.
Asthma has a higher incidence among adult females.
Age:
Asthma is well distributed among people of all age
groups.
Children who have asthma in the first year of life and
those aged 9-16 years tend to have much more severe
disease.
DDx
-Pulmonary Hypertension, Primary
-Congestive heart failure- Orthopnea, moist basilar rales,
gallop rhythms, blood-tinged sputum
-Croup
-Stridor
-Upper airway obstruction
-Foreign-body aspiration
-Neoplasm
-Bronchial stenosis.
-Recurrent episodes of bronchospasm can occur with
carcinoid tumors
-Recurrent pulmonary emboli
- Chronic bronchitis
- Eosinophilic pneumonias are often associated with
asthmatic symptoms, as are various chemical pneumonias
and exposures to insecticides and cholinergic drugs.
-Bronchospasm occasionally is a manifestation of
systemic vasculitis with pulmonary involvement.
INVESTIGATIONS
1-Spirometry
-The diagnosis of asthma is established by demonstrating
reversible airway obstruction.
-The evaluation for asthma should include spirometry
(FEV1, FVC, FEV1/FVC) before and after the
administration of a short-acting bronchodilator.
-Reversibility is traditionally defined as a 15% or
greater increase in FEV1 after two puffs of a b-
adrenergic agonist
-In severe airflow obstruction with significant air