1. Status asthmaticus is a medical emergency in which asthma
symptoms are resistant to initial bronchodilator therapy in the
emergency department. 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. It is a life-threatening episode of
airway obstruction considered a medical emergency. Complications
include cardiac and/or respiratory arrest.
Pathophysiology
Inflammation in asthma is characterized by an influx of eosinophils
during the early-phase reaction and a mixed cellular infiltrate
composed of eosinophils, mast cells, lymphocytes, and neutrophils
during the late-phase (or chronic) reaction. The simple explanation
for 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. Together, these
mediators cause bronchial smooth muscle constriction, vascular
leakage, inflammatory cell recruitment (with further mediator

2. release), and 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. The more severe the airway obstruction, the more likely
ventilation-perfusion mismatching will result in impaired gas
exchange and hypoxemia.
Clinical
History
- Patients with status asthmaticus have severe dyspnea that has
developed over hours to days.
- Frequently, patients have a prior history of endotracheal
intubation and mechanical ventilation, frequent emergency
department visits, and previous use of systemic corticosteroids.
- Patients usually present with audible wheezing.
Physical
- Patients are usually tachypneic upon examination and, in early
stages of status asthmaticus, may have significant wheezing.
Initially, wheezing is heard only during expiration, but, later,
wheezing occurs during both expiration and inspiration.
- The chest is hyperexpanded, and accessory muscles,
particularly the sternocleidomastoid, scalene, and intercostal
muscles, are used. Later, as bronchoconstriction worsens,
patients' wheezing may disappear, which may indicate severe
airflow obstruction.

3. - Normally, the pulsus paradoxus (ie, the difference in systolic
blood pressure between inspiration and expiration) does not
exceed 15 mm Hg. In patients with severe asthma, a pulsus
paradoxus of greater than 25 mm Hg usually indicates severe
airway obstruction.
Causes
- In persons with acute asthma, bronchospasms occur as a result
of one or more inciting factors that may include, but are not
limited to, a viral upper or lower respiratory tract infection,
significant allergic response to an allergen (eg, pollen, mold,
animal dander, house dust mites), exposure to an irritant, or
vigorous exercise in a cold environment.
- Precipitating factors can include infection, allergen or irritant
exposure, poor adherence to the medical regimen, strenuous
exercise, and a rapid decrease in long-term oral steroid
therapy.
- Inflammation can be the result of infection; lymphocyte, mast
cell, eosinophilic, and neutrophilic responses; and airway
epithelial damage. In addition, elevated plasma lactate levels
were noted in patients with this condition in the first hours of
inhaled beta-agonist treatment.
Differential diagnosis- Primary Pulmonary Hypertension
- Congestive heart failure
- Croup
- Stridor

4. - Upper airway obstruction
- Orthopnea
Diagnosis- Obtain a CBC count and differential to evaluate for infectious
causes (eg, pneumonia, viral infections such as croup), allergic
bronchopulmonary aspergillosis, and Churg-Strauss vasculitis.
As noted earlier, when elevated, serum lactate levels (when
obtained early at the onset of status asthmaticus) can correlate
with improved lung function.
- Obtain an arterial blood gas (ABG) value to assess the severity
of the asthma attack and to substantiate the need for more
intensive care. ABG determinations are indicated when the
peak expiratory flow (PEF) rate or forced expiratory volume in
one second (FEV1) is less than or equal to 30% of the predicted
value or when the patient shows evidence of fatigue or
progressive airway obstruction despite treatment.
- Obtain a chest radiograph to evaluate for pneumonia,
pneumothorax, congestive heart failure, and signs of chronic
obstructive pulmonary disease, which would complicate the
patient's response to treatment or reduce the patient's
baseline spirometry values.
- The most important and readily available test to evaluate the
severity of an asthma attack is the measurement of PEF (peak
expiratory flow)
- Hospitalization is generally indicated when the PEF or FEV1
after treatment is greater than 50% of the predicted value but
less than 70% of the predicted value. Hospitalization in the

5. ICU is indicated when the PEF value or FEV1 is less than 50%
of predicted.
Staging- The 4 stages of status asthmaticus are based on ABG
progressions in status asthma.
Patients in stage 1 or 2 may be admitted to the hospital, depending
on the severity of their dyspnea, their ability to use accessory
muscles, and their PEF values or FEV1 after treatment (>50% but
<70% of predicted values).
Patients with ABG determinations characteristic of stages 3 and 4
require admission to the ICU. The PEF value or FEV1 is less than 50%
of the predicted value after treatment.
Stage 1- Patients are not hypoxemic, but they are hyperventilating
and have a normal PO2.
- Data suggest that to possibly facilitate hospital discharge, these
patients may benefit from ipratropium treatment via a
handheld nebulizer in the emergency setting as an adjunct to
beta-agonists.
Stage 2- This stage is similar to stage 1, but patients are
hyperventilating and hypoxemic.
- Such patients may still be discharged from the emergency
department, depending on their response to bronchodilator
treatment, but will require systemic corticosteroids.
Stage 3- These patients are generally ill and have a normal PCO2 due
to respiratory muscle fatigue. Their PCO2 is considered a falsenormal value and is a very serious sign of fatigue that signals a need
for expanded care. This is generally an indication for elective

6. intubation and mechanical ventilation, and these patients require
admission to the ICU.
- Parenteral corticosteroids are indicated, as is continued
aggressive use of an inhaled beta2-adrenergic bronchodilator.
- These patients may benefit from theophylline.
Stage 4- This is a very serious stage in which the PO2 is low and the
PCO2 is high, signifying respiratory failure.
- These patients have less than 20% lung function or FEV1 and
require intubation and mechanical ventilation.
- Patients in stage 4 should be admitted to the ICU. Switching
from inhaled beta-2 agonists and anticholinergics to metereddose inhalers (MDIs) via mechanical ventilator tubing is
indicated.
- Parenteral steroids are essential, and theophylline may be
added, as with patients in stage 3.
TreatmentBronchodilator treatment with beta-2 agonists
- The first line of therapy is bronchodilator treatment with a
beta-2 agonist, typically albuterol.
- Handheld nebulizer treatments may be administered either
continuously (10-15 mg/h) or by frequent timing (eg, q520min), depending on the severity of the bronchospasm.
Nonselective beta-2 agonists
- Patients whose bronchoconstriction is resistant to continuous
handheld nebulizer treatments with traditional beta-2 agonists

7. may be candidates for nonselective beta-2 agonists (eg,
epinephrine [0.3-0.5 mg] or terbutaline [0.25 mg])
administered subcutaneously
Ipratropium treatment (anticholinergic, m-cholino blockers)
- Ipratropium, which comes in premixed vials at 0.2%, can be
synergistic with albuterol or other beta-2 agonists.
- Ipratropium is administered every 4-6 hours.
- Because children appear to have more cholinergic receptors,
they are more responsive to parasympathetic stimulation than
adults
Oxygen monitoring
- Monitoring the patient's oxygen saturation is essential during
the initial treatment.
- ABG values are usually used to assess hypercapnia during the
patient's initial assessment.
Oxygen therapy
- Oxygen therapy is essential. It can be administered via a nasal
canula or mask, although patients with dyspnea often do not
like masks.
- With the advent of pulse oximetry, oxygen therapy can be
easily titrated to maintain the patient's oxygen saturation
above 92% (>95% in pregnant patients or those with cardiac
disease).
Glucocorticosteroids

8. - Steroids are the most important treatment for status
asthmaticus.
- The usual dose is oral prednisone at 1-2 mg/kg/d.
Aminophylline
- Starting intravenous aminophylline may be reasonable in
patients who do not respond to medical treatment with
bronchodilators, oxygen, corticosteroids, and intravenous fluids
within 24 hours.
- The loading dose is usually 5-6 mg/kg, followed by a continuous
infusion of 0.5-0.9 mg/kg/h.
MedicationsBeta-adrenergic agonists- Relieve reversible bronchospasm by
relaxing smooth muscles of the bronchi.
Albuterol (Ventolin, Proventil)- Use for bronchospasms refractory to
epinephrine. Relaxes bronchial smooth muscles by action on beta-2
receptors, with little effect on cardiac muscle contractility.
PO: 2-4 mg PO tid/qid; not to exceed 32 mg/d
Inhaler: 1-2 puffs q4-6h; not to exceed 12 puffs/d
Nebulizer: Dilute 0.5 mL (2.5 mg) of 0.5% inhalation solution in 1-2.5
mL of NS; administer 2.5-5 mg q4-6h, diluted in 2-5 mL sterile saline
or water.
Levalbuterol (Xopenex)- Moderately selective beta2-receptor
agonist. Active enantiomer of racemic albuterol and more potent
than racemic mixture. Decreased occurrence of adverse effects may
allow use of more frequent nebulizer therapy in patients with acute

9. asthma with less concern over adverse effects of other
bronchodilators (eg, albuterol, metaproterenol).
Adult- 0.63-1.25 mg nebulized q6-8h; may be given more frequently
during emergent situations.
Mast cell stabilizers- These agents prevent histamine release from
mast cells following stimuli by specific antigens.
Cromolyn (Intal)- Inhibits degranulation of sensitized mast cells
following their exposure to specific antigens.
Adult dose-Powder in caps for use with Spinhaler: 20 mg inhaled qid
at regular intervals
- MDI: 2 puffs (800 mcg/puff) qid at regular intervals
- Nebulizer: 20 mg inhaled qid at regular intervals
- Once patient is stabilized, use lowest effective dose
Corticosteroids- Maintenance medications that decrease
inflammatory mediators to limit airway remodeling. Must be taken
regularly to be beneficial. Glucocorticoids do not relieve acute
bronchospasm, and short-acting bronchodilators must be available.
Multiple formulations are available that are not equivalent on a perdose or per-mcg basis. Inhaled corticosteroids are one of the most
important developments in asthma management because they
decrease inflammation.
Methylprednisolone (Solu-Medrol)- Loading dose: 125-250 mg IV
Maintenance dose: 4 mg/kg/d IV divided q4-6h.
Bronchodilators- Act to decrease muscle tone in both small and large
airways in lungs, thereby increasing ventilation.
Theophylline (Aminophyllin)- Potentiates exogenous catecholamines
and stimulates endogenous catecholamine release and

10. diaphragmatic muscular relaxation, which, in turn, stimulates
bronchodilation. For bronchodilation, near toxic (>20 mg/dL) levels
are usually required.
5.6 mg/kg loading dose (based on aminophylline) IV over 20 min,
followed by maintenance infusion of 0.1-1.1 mg/kg/h
Anticholinergics- Regarding magnesium sulfate, more studies have
not confirmed the effectiveness of intravenous administration of this
agent. Its use is still controversial. However, inhaled magnesium
sulfate has generated some interest in status asthmaticus when
combined with beta-agonist use.
Ipratropium bromide (Atrovent)- Synthetic ammonium compound
very structurally similar to atropine. May provide additive benefit to
inhaled beta-2 agonists when treating severe acute asthma
exacerbations. Also may be alternative bronchodilator for patients
unable to tolerate inhaled beta-2 agonists. Children may be more
responsive to parasympathetic inhibition than adults because
children appear to have more cholinergic receptors.
MDI: 2 puffs (18 mcg/puff) qid
500 mcg tid/qi
Nebulizer:
Magnesium sulphate- Magnesium sulfate intravenously has been
advocated in the past for the treatment of acute asthma. Usually 1 g
or a maximum of 2.5 g during the initiation of therapy may be
considered.
Adult- 1-2 g IV