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Status Asthmaticus
Author: Constantine K Saadeh, MD; Chief Editor: Zab Mosenifar, MD more...

Updated: Mar 29, 2011
Overview
Status asthmaticus is a medical emergency in which asthma symptoms are refractory to initial bronchodilator
therapy in the emergency department. 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. Frequently,
patients have underused or have been underprescribed anti-inflammatory therapy. Illicit drug use may play a role
in poor adherence to anti-inflammatory therapy. Patients report chest tightness, rapidly progressive shortness of
breath, dry cough, and wheezing and may have increased their beta-agonist intake (either inhaled or nebulized) to
as often as every few minutes.
The prevalence and severity of asthma cases are on the rise, along with increasing occurrences of asthma
hospitalization and mortality resulting from status asthmaticus. Status asthmaticus is usually more common among
persons in low socioeconomic groups, regardless of race, as they have less access to regular specialist medical
care,
[1]
which leads to an increased risk of status asthmaticus. People who live alone are particularly affected.
A 2009 study suggested that one of the contributors to the increase in asthma severity in black children could be,
in addition to social and economic factors, a genetic factor as well.
[2]
An increase has been recognized in a single-
locus analysis with a genotype variation in glutathione dependent S-nitrosoglutathione (GSNOR). This single locus
is associated with a decreased response to asthma treatment and was present in approximately 70% of 107 black
children studied.
[2]
Patients who delay medical treatment, particularly treatment with systemic steroids, have a greater chance of
dying. Patients with other preexisting conditions (eg, restrictive lung disease, congestive heart failure, chest
deformities) are at particular risk of death from status asthmaticus. Patients who smoke regularly have chronic
inflammation of the small airways and are at particular risk of death from status asthmaticus.
A study conducted at the Columbia University Medical Center,
[3]
however, noted the number of patients with status
asthmaticus requiring intensive care admissions declined over the past 10 years. The trend was toward less
advanced presentations. This may reflect improvements in medication compliance, education, or access to
medical care. Nonetheless, concern has been raised about the recent increased severity of asthma symptoms and
the need for more intensive care management.
[4]
For patient education information, see eMedicine's Asthma Center, as well as Asthma, Asthma FAQs, and
Understanding Asthma Medications.
To see complete information on Asthma, please go to the main article by clicking here.
Evaluation
Patients with status asthmaticus have severe dyspnea that has developed over hours to days. Frequently, these
individuals have a previous history of endotracheal intubation and mechanical ventilation, frequent emergency
department visits, and previous use of systemic corticosteroids.
Patients are usually tachypneic upon examination and, in early stages of status asthmaticus, may have significant

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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, the wheezing may disappear, which may
indicate severe airflow obstruction.
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.
Staging
The 4 stages of status asthmaticus are based on arterial blood gas (ABG) progressions in status asthma (see
Laboratory Tests).
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 peak expiratory flow (PEF) values or forced expiratory volume in 1 second
(FEV
1
) after treatment (>50% but < 70% of predicted values).
Patients with ABG determinations characteristic of stages 3 and 4 require admission to an intensive care unit
(ICU). The PEF value or FEV
1
is less than 50% of the predicted value after treatment.
Stage 1
Patients are not hypoxemic, but they are hyperventilating and have a normal partial pressure of oxygen (PO
2
).
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 partial pressure of carbon dioxide (PCO
2
) due to respiratory
muscle fatigue. Their PCO
2
is considered a false-normal value and is a very serious sign of fatigue that signals a
need for expanded care. This is generally an indication for elective intubation and mechanical ventilation, and
these patients require admission to an 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 PO
2
is low and the PCO
2
is high, signifying respiratory failure. These
patients have less than 20% lung function or FEV
1
and require intubation and mechanical ventilation.
Patients in stage 4 should be admitted to an ICU. Switching from inhaled beta-2 agonists and anticholinergics to
metered-dose inhalers (MDIs) via mechanical ventilator tubing is indicated. Parenteral steroids are essential, and
theophylline may be added, as with patients in stage 3.
Differential Diagnosis
The differential diagnosis includes idiopathic pulmonary arterial hypertension. Other conditions to be considered
include congestive heart failure, croup, stridor, upper airway obstruction and orthopnea.
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Laboratory Tests
Complete blood cell count
Obtain a complete blood cell (CBC) count and differential to evaluate for infectious causes (eg, pneumonia, viral
infections such as croup), allergic bronchopulmonary aspergillosis, and Churg-Strauss vasculitis. When elevated,
serum lactate levels (when obtained early at the onset of status asthmaticus) can correlate with improved lung
function.
Arterial blood gas
Obtain an 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 PEF rate or FEV
1
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. ABG
values are important to help determine the severity of the asthma attack (see also Staging). The 4 stages of blood
gas progression in persons with status asthmaticus are as follows:
Stage 1 is characterized by hyperventilation with a normal PO
2
.
Stage 2 is characterized by hyperventilation accompanied by hypoxemia (ie, a low PCO
2
and low PO
2
).
Stage 3 is characterized by the presence of a false-normal PCO
2
; ventilation has decreased from the
hyperventilation present in the second stage. This is an extremely serious sign of respiratory muscle fatigue
that signals the need for more intensive medical care, such as admission to an ICU and, probably,
intubation with mechanical ventilation.
The last stage is characterized by a low PO
2
and a high PCO
2
, which occurs with respiratory muscle
insufficiency. This is an even more serious sign that mandates intubation and ventilatory support.
Chest Radiography
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.
Pulmonary Function Testing
The most important and readily available test to evaluate the severity of an asthma attack is the measurement of
PEF. PEF monitors are commonly available to patients for use at home, and they provide asthmatic patients with a
guideline for changes in lung function as they relate to changes in symptoms. In most patients with asthma, a
decrease in peak flow as a percentage of predicted value correlates with changes in spirometry values.
According to the guidelines of the National Heart, Lung, and Blood Institute/National Asthma Education and
Prevention Program,
[5]
severe asthma exacerbation is usually associated with a PEF rate or FEV
1
of less than
50% of the predicted value. Also, hospitalization is generally indicated when the PEF or FEV
1
after treatment is
greater than 50% of the predicted value but less than 70% of the predicted value. Hospitalization in an ICU is
indicated when the PEF value or FEV
1
is less than 50% of predicted.
A drop in the FEV
1
to less than 25% of the predicted value indicates a severe airway obstruction. A patient with an
FEV
1
of greater than 60% of the predicted value may be treated in an outpatient setting, depending on the clinical
situation. However, if the patient's FEV
1
or PEF rate drops to less than 50% of predicted, admission to the hospital
is recommended.
Pulse oximetry and spirometry values should be used to monitor the progression of asthma. As the results indicate
improvement, treatment may be adjusted accordingly.
If a portable spirometry unit is not available, a PEF rate of 20% or less of the predicted value (ie, usually < 100
L/min) suggests severe airflow obstruction and impending respiratory failure.
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Impulse Oscillometry Testing
Spahn et al demonstrated that the majority of children with asthma have normal spirometry results
[6]
; Goldman et
al
[7]
and Marotta et al
[8]
reported the assessment of children with asthma is enhanced by the use of forced
oscillation to measure respiratory resistance and reactance. Ducharme and Davis showed that forced oscillation
can be performed in the emergency department and that the results are reproducible.
[9, 10]
According to various articles, impulse oscillometry resistance and reactance magnitudes have been shown to be
more sensitive than FEV
1
to the daily variability in adolescents with asthma,
[7]
to the response to acute
bronchodilation,
[8, 11]
and to the response to exposure to toxic inhalants in persons with reactive airways.
[11]
In
patients with reactive airways, Saadeh et al reported that impulse oscillometry detects false-negative spirometry
values and provides a sensitive index of asthma control over the spectrum of mild to severe persistent asthma.
[12]
Patients can be shown the results of forced oscillation testing that occur with peripheral airway inflammation and
obstruction. Review the test results with patients and show them the improvement with inhaled corticosteroids and
the deterioration when they are not compliant with anti-inflammatory medications. This information may materially
enhance patients' awareness of the need for continuing treatment, despite an absence of wheezing.
Technique
With forced oscillation testing using the impulse oscillometry system (IOS), patients are tested for 30-40 seconds
during quiet breathing, without forced respiratory efforts. A small loudspeaker pushes "burps" of air into patients
and pulls them back from the mouthpiece 5 times each second.
The measurement of airflow resistance during normal breathing requires no maximal forced expiratory efforts and
does not subject patients to bronchoprovocation from forced expiration. Resistance is distributed between large
airways and smaller more peripheral airways, with distinct patterns attributable to each.
Bronchospasms and increased large airway resistance appear as increases in resistance at higher (25-35
cycles/s) components of oscillation frequency. Additionally, a pattern of increased resistance with increasing
airflow is typical of a large airway bronchospasm. In such patients, resistance at the beginning and end of both
inspiration and expiration is at its minimum, with increased levels during mid inspiration and mid expiration. In such
patients, a deep inspiration is often followed by reflex bronchoconstriction and increased resistance for 30 seconds
or more, signaling increased airway reactivity.
Peripheral airway inflammation and obstruction are signaled by increased resistance at low (5 cycles/s) oscillation
frequencies that are decreased at higher oscillation frequencies (15 or 20 cycles/s). In association with the fall in
resistance from 5 to 15 cycles per second, the magnitude of respiratory reactance in peripheral airway
inflammation and obstruction increases.
Careful attention must be paid to whether patients have their lips fully closed around the mouthpiece. Patients with
acute dyspnea may feel constrained breathing through a mouthpiece and may reflexively open their mouths to
increase airflow during late inspiration. This is analogous to flaring alae nasi with dyspnea and results in
characteristic airflow leak patterns. This causes underestimation of true airflow resistance. IOS tests with such
airflow leak patterns must be repeated after reassuring the patient and ensuring closure of the lips around the
mouthpiece.
Histologic Findings
Autopsy results from patients who died from status asthmaticus of brief duration (ie, developed within hours) show
neutrophilic infiltration of the airways. In contrast, results from patients who developed status asthmaticus over
days show eosinophilic infiltration. Autopsy results also show extensive mucus production and severe bronchial
smooth muscle hypertrophy. However, the predominant response, based on results from bronchoalveolar lavage
studies, is eosinophilic in nature. The eosinophil itself can lead to epithelial destruction through its own degrading
products (eg, cationic proteins). This destruction can result in inflammation and, later, a neutrophilic response.
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Medical Treatment
After confirming the diagnosis and assessing the severity of the asthma attack, direct treatment toward controlling
bronchoconstriction and inflammation. Beta-agonists, steroids, and theophylline are mainstays in the treatment of
status asthmaticus. Sevoflurane, a potent inhalation agent, was successful in a single case report in which it was
used when conventional treatment failed in a 26-year-old woman.
[13]
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, q5-20min), depending
on the severity of the bronchospasm.
The dose of albuterol for intermittent dosing is 0.3-0.5 mL of a 0.5% formulation mixed with 2.5 mL of normal
saline. Many of these preparations are available in a premixed form with a concentration of 0.083%.
Studies have also shown an excellent response to well-supervised use of albuterol via an MDI with a chamber.
The dose is 4 puffs, repeated at 15- to 30-minute intervals as needed. Most patients respond within 1 hour of
treatment.
The US Food and Drug Administration approved the use of the R isomer of albuterol, known as levalbuterol, for
treating patients with acute asthma. This isomer has fewer effects on the heart rhythm (ie, tachyarrhythmia) and is
associated with fewer occurrences of tremors, while having the same or greater clinical bronchodilator effects as
racemic albuterol.
However, a 2009 study by Andrews and colleagues from the Children's Hospital of Pennsylvania showed that
although q slight decrease may have occurred in the duration of continuous nebulizer treatment with levalbuterol
compared with albuterol, the difference was not statistically significant.
[14]
Endotracheal adrenaline in patients who are intubated has been associated with variable success in different
studies. However, based on the current literature, no specific advantage can be gained at this point by using
endotracheal adrenaline.
[15]
The decreased prevalence of adverse effects with this new medication may allow physicians to use nebulizer
therapy in patients with acute asthma more frequently with less concern over the adverse effects of other
bronchodilators (eg, albuterol, metaproterenol). The dose of levalbuterol is either a 0.63-mg vial for children or a
1.26-mg vial for adults.
These drugs, especially albuterol, are safe to use during pregnancy.
Nonselective beta-2 agonists
Patients whose bronchoconstriction is resistant to continuous handheld nebulizer treatments with traditional beta-2
agonists may be candidates for nonselective beta-2 agonists (eg, epinephrine [0.3-0.5 mg] or terbutaline [0.25
mg]) administered subcutaneously. However, systemic therapy has no proven advantage over aerosol therapy
with selective beta-2 agents.
Exercise caution in patients with other complicating factors (eg, congestive heart failure, history of cardiac
arrhythmia).
Intravenous isoproterenol is not recommended for the treatment of asthma because of the risk of myocardial
toxicity.
[16]
Anticholinergics
Anticholinergic agents s are believed to work centrally by suppressing conduction in vestibular cerebellar
pathways. They may have an inhibitory effect on parasympathetic nervous system.
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Ipratropium bromide is a synthetic ammonium compound very structurally similar to atropine. This agent comes in
premixed vials at 0.2%, is administered every 4-6 hours, and can be synergistic with albuterol or other beta-2
agonists when treating severe acute asthma exacerbations. Ipratropium may also be used as an alternative
bronchodilator in patients who are unable to tolerate inhaled beta-2 agonists. Because children appear to have
more cholinergic receptors, they are more responsive to parasympathetic stimulation than adults.
Intravenous magnesium sulfate 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. This therapy can be tried, especially in
pregnant women, as an adjunct to beta-2 bronchodilator therapy. However, more studies have not confirmed the
effectiveness of this treatment,
[17, 18]
and its use is still controversial. However, inhaled magnesium sulfate has
generated some interest in status asthmaticus when combined with beta-agonist use.
[19, 20]
Oxygen monitoring and therapy
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 saturation is then monitored via pulse oximetry
throughout the treatment protocol.
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
Steroids are the most important treatment for status asthmaticus. These agents can decrease mucus production,
improve oxygenation, reduce beta-agonist or theophylline requirements, and activate properties that may prevent
late bronchoconstrictive responses to allergies and provocation. In addition, corticosteroids can decrease bronchial
hypersensitivity, reduce the recovery of eosinophils and mast cells in bronchioalveolar lavage fluid, decrease the
number of activated lymphocytes, and help regenerate the bronchial epithelial cells.
Corticosteroid action usually requires at least 4-6 hours from administration because it requires protein synthesis
before it initiates anti-inflammatory effects. Because of this, patients with status asthmaticus must depend on other
supportive measures (eg, beta-2 agonists, oxygen, adequate ventilation) in their initial treatment while awaiting the
action of corticosteroids.
The usual dose is oral prednisone at 1-2 mg/kg/d.
Methylprednisolone is used to treat inflammatory and allergic reactions. By reversing increased capillary
permeability and suppressing PMN activity, it may decrease inflammation. Other corticosteroids may be used in
equivalent dosages. In some authors' experience, methylprednisolone provides excellent efficacy when given
intravenously at 1 mg/kg/dose every 6 hours.
[21]
Some authorities report that pulse therapy with steroids at a high dose (eg, 10-30 mg/kg/d as a single dose) is
associated with a more rapid response and shorter hospitalization and has similar adverse effects; however, this is
not standard therapy.
Adverse effects of pulse therapy, in some authors' experiences, are minimal and comparable to the traditional
doses of intravenous steroids. The adverse effects may include hyperglycemia, which is usually reversible once
steroid therapy is stopped; increased blood pressure; weight gain; increased striae formation; and hypokalemia.
Long-term adverse effects depend on the duration of steroid therapy after the patient leaves the hospital.
Steroid treatment for acute asthma is necessary but has potential adverse effects. The serum glucose value must
be monitored, and insulin can be administered on a sliding scale if needed. Monitoring a patient's electrolyte
levels, especially potassium, is essential. Hypokalemia can cause muscle weakness, which may worsen
respiratory distress and cause cardiac arrhythmias.
Nebulized steroids
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The use of nebulized steroids for treating status asthmaticus is controversial. Data comparing nebulized
budesonide with prednisone in children suggest that the latter therapy is more effective for treating status
asthmaticus.
No good scientific evidence supports using nebulized dexamethasone or triamcinolone via a handheld nebulizer.
In fact, in some authors' experiences, more adverse effects, including a cushingoid appearance and irritative
bronchospasms, have occurred with these nebulizers.
Fluid replacement
Hydration, such as normal saline at a reasonable rate (eg, 150 mL/h), is essential. Special attention to the patient's
electrolyte status is important.
Hypokalemia may result from either steroid use or beta-agonist use. Correcting hypokalemia helps wean an
intubated patient with asthma. Hypophosphatemia may result from poor oral intake and is also an important
consideration when weaning such patients.
Antibiotics
The routine administration of antibiotics is discouraged. Patients are administered antibiotics only when they show
evidence of infection (eg, pneumonia, sinusitis). In some situations, sinus imaging using computed tomography
(CT) scanning or plain radiography
[22, 23]
may be essential to help rule out chronic sinusitis.
[24]
Bronchodilators
Theophylline preparations are also used in patients with status asthmaticus. Usually, theophylline is given
parenterally, but it can also be given orally, depending on the severity of the attack and the patient's ability to take
medications. This class of drugs can induce tachycardia and decrease the seizure threshold (especially in
children); therefore, therapeutic monitoring is mandatory.
Typical theophylline levels range from 10-20 mcg/mL; however, adverse effects can occur even with therapeutic
levels. A safer range is 10-15 mcg/mL, although seizures have occurred even with levels below 10 mcg/mL.
Theophylline also has significant drug interactions with medications such as ciprofloxacin, digoxin, and warfarin
(Coumadin). These interactions may decrease the rate of theophylline clearance by interfering with P-450 site
metabolism. On the other hand, phenytoin (Dilantin) and cigarette smoking can increase the rate of metabolism of
theophylline and, therefore, can decrease the therapeutic level of the drug.
Manage the theophylline dose in persons who previously smoked but quit fewer than 6 months ago as if they are
still smoking. Patients who smoke or those on phenytoin require higher loading and maintenance doses of
theophylline. Other adverse effects can include nausea, vomiting, and palpitations.
The usual loading dose of theophylline is 6 mg/kg, followed by maintenance doses of 1 mg/kg/h in the emergent
setting. In patients who smoke, the maintenance dose may be higher and the loading dose may be slightly higher.
Patients on phenytoin should also receive increased maintenance doses of theophylline. Patients with liver
disease or elderly patients may require a maintenance dose as low as 0.25 mg/kg/h.
Conflicting reports on the efficacy of aminophylline therapy have made it controversial. 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.
[25]
Data suggest that aminophylline may have an anti-inflammatory effect in addition to its bronchodilator properties.
The loading dose is usually 5-6 mg/kg, followed by a continuous infusion of 0.5-0.9 mg/kg/h.
Sedatives
Patients may benefit from sedatives in very small doses and under controlled, monitored settings. Sedatives
should be used judiciously, if at all. For example, lorazepam (0.5 or 1 mg intravenously) could be used for patients
who are very anxious and are undergoing appropriate and aggressive bronchodilator therapy. More powerful
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agents (eg, oxybutynin) can be administered to intubated patients to achieve sedative, amnestic, and anxiolytic
effects.
Severe and Resistant Status Asthmaticus
In the past several years, new therapies have been developed in patients with severe and resistant status
asthmaticus despite mechanical ventilation.
Anesthetics
Ketamine has been used in the management of status asthmaticus in a prospective trial in patients with respiratory
failure who do not respond adequately to mechanical ventilation.
[26]
This agent has been shown to improve airway
resistance, particularly the lower airways, as well as improve lung compliance. Significant improvement in both
oxygenation and hypercarbia has been reported, even after 15 minutes of the administration of ketamine.
Other inhalational anesthetics that have been studied include propofol and sevoflurane. Prolonged propofol
administration, however, may be complicated by generalized seizure, increased carbon dioxide production, and
hypertriglyceridemia. Sevoflurane has been used more commonly than halothane and isoflurane. Care must be
used with this medication, even though it is relatively safe, because of the risk of hepatotoxicity and renal tubular
injury. In children, sevoflurane has been shown in some studies to be safe and effective. In adults, careful
monitoring of liver and kidney function, as well as serum fluoride concentration, is helpful for avoiding toxic levels
of sevoflurane.
[27]
Neuromuscular blockers may be used with caution in patients who are well sedated but exhibiting severe anxiety
and tachycardia, as well as in those intolerant of intubation.
[4, 15]
In patients with status asthmaticus, the use of deep anesthesia, such as with halothane or enflurane in
combination with propofol or ketamine, may also be effective treatment as potent bronchodilators and in
decreasing airway resistance, respectively.
[28, 29]
Nitric oxide has also been used in a similar fashion in the treatment of status asthmaticus in isolated case reports
and has also been effective when mechanical ventilation is not adequate.
[30, 31]
Additionally, the use of nebulized lidocaine in combination with albuterol or levalbuterol is effective in helping the
vocal cord dysfunction that may accompany status asthmaticus. This is an unpublished observation by an author
in clinical practice.
Extracorporeal life support
Mikkelsen and colleagues reported the successful use of extracorporeal life support in patients with status
asthmaticus and severe secondary asphyxia in any patient who otherwise was not responsive to aggressive
pulmonary support.
[32]
The role of extracorporeal life support has been studied and implemented in several
institutions and should be considered in patients at high risk of developing refractory status asthmaticus.
[33]
This
includes, but is not limited to, patients with a history of multiple incubations, respiratory failure requiring intubation
within 6 hours of admission, hemodynamic instability, neurologic impairment at the time of admission, and duration
of respiratory failure greater than 12 hours despite maximal medical therapy.
[34]
Noninvasive and mechanical ventilation
Noninvasive ventilation such as bilevel positive airway pressure can also be considered in patients who are in
impending respiratory failure in order to avoid intubation. In contrast to chronic obstructive respiratory disease
exacerbation and respiratory failure, however, asthma patients tend to require more invasive means of ventilation
with intubation when they are in status asthmaticus. The presence of severe bronchoconstriction with multiple
secretions and inflammatory processes are contributors to the need for more aggressive ventilation.
[34]
Ram et al demonstrated that the effectiveness of noninvasive positive pressure ventilation was affected by meta-
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analysis.
[35]
Ueda et al reported using noninvasive positive pressure ventilation to wean a patient with refractory
status asthmaticus who also had developed atelectasis.
[36]
Leatherman et al reported that prolongation of the
expiratory time can decrease dynamic inflation in patients with status asthmaticus and may have a minor positive
effect on weaning in these patients.
[37]
Consider mechanical ventilation as a last resort in patients with status asthmaticus. Mechanical ventilation in
patients with asthma requires careful monitoring, because these patients have high end-expiratory pressure and,
therefore, are at very high risk for pneumothorax.
Mechanical ventilation, when used in patients with asthma, is usually required for less than 72 hours; however, in
occasional patients with severe bronchospasm, mechanical ventilation can be prolonged. In these situations,
consultation with a pulmonologist or another expert in mechanical ventilatory techniques is likely useful.
Other treatments
Other treatments have been used in patients with severe acute asthma, but none is well proven. A combination of
helium and oxygen known as heliox (ie, 30/70 mixture) has been reported, but this treatment should only be
considered in patients who are able to take deep breaths, because the treatment is dependent on inspiratory
flow.
[38]
Nitrate oxide has been tried in a child with refractory asthma. The future role of this therapy remains to be
determined.
Leukotriene modifiers are useful for treating chronic asthma but not acute asthma. This treatment may be
beneficial if used via a nebulizer, but it remains experimental.
Complications
Pneumothorax may complicate acute asthma, either because of increased airway pressure or as a result of
mechanical ventilation. Superimposed infection can also occur in intubated patients. Patients may require a chest
tube for pneumothorax or aggressive antibiotic therapy for a superimposed infection.
Outpatient Monitoring
Instruct patients to use of inhalers appropriately, to be compliant with therapy, and to practice stress-avoidance
measures. Stress factors (ie, triggers of asthma attacks) include pet dander, house dust, and mold. Strongly
discourage patients from smoking; this practice should be avoided at all costs. Finally, appropriate follow-up is
important, as is checking the patient's peak flow meter and FEV
1
at home or in the office, respectively.
Children with asthma commonly present with normal FEV
1
, and, accordingly, more sensitive lung function testing
should be undertaken with regular IOS assessments. Medication titration may be usefully guided by IOS
resistance and reactance values.
Identify specific patients who are at risk for asthma exacerbation, such as younger children and adults older than
60 years. A retrospective analysis showed that the severity of asthma at baseline and the age of the patient are
the most important determining factors in the risk for recurrent status asthmaticus and for predicting the severity of
the attack.
[39]
In other words, patients older than 60 years who are also characterized as having either moderate
persistent asthma or severe persistent asthma are at higher risk of developing status asthmaticus. Therefore,
compliance with the National Institutes of Health (NIH) guidelines for the treatment and management of patients
with asthma should theoretically be an effective prophylaxis against the development of status asthmaticus.
In general, unless a complicating illness such as congestive heart failure or chronic obstructive pulmonary disease
is present, with appropriate therapy status asthmaticus has a good prognosis. A delay in initiating treatment is
probably the worst prognostic factor. Delays can result from poor access to health care on the part of the patient or
even delays in using steroids. Patients with acute asthma should use steroids early and aggressively.
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Prevention
Status asthmaticus can be prevented if patients are compliant with their medications and they avoid stress factors;
however, this condition can occur even when patients are compliant and doing well as outpatients. In such
situations, search for an occult infection (eg, respiratory syncytial virus [RSV] in children but rarely in adults; occult
sinus infection).
Prevention of status asthmaticus may be aided by monitoring forced oscillation test results rather than spirometry
findings. This is particularly true for children younger than 12 years; however, adults with reactive airways may be
undertreated if the criterion for stability and normality is a spirometric FEV
1
greater than 80% of the predicted
value.
Special Concerns
Note the following medicolegal pitfalls:
Failure to initiate steroid therapy or intubation with mechanical ventilation
Failure to obtain sinus imaging or to monitor the patient's electrolyte balance
Failure to admit a wheezing patient with a normal PCO
2
: Such patients typically have respiratory muscle
fatigue and require hospital admission.
Failure to treat expediently, especially with bronchodilators
Failure to educate patients upon discharge about the appropriate use of their inhalers, the importance of
therapy compliance, and the efficacy of stress-avoidance measures
Treat pregnant women with acute asthma in the same aggressive manner as nonpregnant women.
[40]
Respiratory
acidosis can be detrimental to both the fetus and the mother. Use special abdominal shielding during chest
radiography or sinus imaging.
Treat children with acute asthma in manner similar to that for adults, except when children are mechanically
ventilated, because their chests are more compliant and require special attention.

Contributor Information and Disclosures
Author
Constantine K Saadeh, MD President, Allergy ARTS, LLP; Principal Investigator, Amarillo Center for Clinical
Research, Ltd
Constantine K Saadeh, MD is a member of the following medical societies: American Academy of Allergy
Asthma and Immunology, American College of Rheumatology, American Medical Association, Southern
Medical Association, and Texas Medical Association
Disclosure: Nothing to disclose.
Specialty Editor Board
Helen M Hollingsworth, MD Director, Adult Asthma and Allergy Services, Associate Professor, Department of
Internal Medicine, Division of Pulmonary and Critical Care, Boston Medical Center
Helen M Hollingsworth, MD is a member of the following medical societies: American Academy of Allergy
Asthma and Immunology, American College of Chest Physicians, American Thoracic Society, and
Massachusetts Medical Society
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center
College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Medscape Salary Employment
11/1/11 5:54 PM Status Asthmaticus
Page 11 of 13 http://emedicine.medscape.com/article/302238-overview
Chief Editor
Zab Mosenifar, MD Director, Division of Pulmonary and Critical Care Medicine, Director, Women's Guild
Pulmonary Disease Institute, Professor and Executive Vice Chair, Department of Medicine, Cedars Sinai
Medical Center, University of California, Los Angeles, David Geffen School of Medicine
Zab Mosenifar, MD is a member of the following medical societies: American College of Chest Physicians,
American College of Physicians, American Federation for Medical Research, and American Thoracic Society
Disclosure: Nothing to disclose.
Acknowledgments
The authors and editors of eMedicine gratefully acknowledge the contributions of previous authors Michael
Goldman, MD, and Jan Malacara, PA-C, to the development and writing of the source article.
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