Status Asthmaticus

Rebanta K. Chakraborty; Sangita Basnet.

Author Information

Last Update: June 4, 2019.

Go to:

Introduction
All patients with bronchial asthma are at risk of developing an acute episode
with a progressive severity that is poorly responsive to standard therapeutic
measures, regardless of disease severity or phenotypic variant. This is also
known as status asthmaticus.
If not recognized and managed appropriately, asthmaticus portends risk of
acute ventilatory failure and even, death.
In spite of advances in pharmacotherapy and access to early diagnosis and
treatment of asthma itself, it remains one of the most common causes of visits
to the emergency department. No single clinical or diagnostic index has been
known to predict clinical outcome in status asthmaticus. Hence, a multi-
pronged and time-sensitive approach combining symptoms and signs,
assessment of airflow and blood gas, and a rapid escalation of treatment
based on initial treatment response are favored to diagnose and manage the
condition.
Go to:

Etiology
The time course of progression, as well as the severity of airway
obstruction, follows 2 distinct patterns.[1]
 One subgroup if appropriately documented, shows a slow subacute
worsening of peak expiratory flow rate (PEFR) over days, known as
"slow onset asthma exacerbation." This patient subgroup usually has
intrinsic patient induced factors of predisposition- including inadequate
inhaler regimen, suboptimal compliance, psychological stressor, among
others.
  The other phenotype, known as “sudden onset asthma exacerbation”
presents with severe deterioration within hours. They often correlate
with sudden massive exposure to external triggers like predisposed
allergens, food articles, sulfites, among others.
Eighty percent to 85% of asthma fatalities are in the subgroup of slow onset
asthma exacerbation, perhaps reflecting an inadequate disease control over
time. In contrast to the sudden onset exacerbation phenotype, which presents
mostly with clear airways, slow onset exacerbation patients have extensive
airway inflammation and mucus plugging.[2]
Go to:

Epidemiology
According to the Center for Disease Control and Prevention (CDC), about
10% of world population suffers from asthma, with a 15% increase in disease
burden in the United States over last 2 decades. Five percent of them are
classified as severe asthma.[1]
An estimated 3% to 16% of hospitalized adult asthmatic patients progress to
respiratory failure requiring ventilatory support, although the statistics might
be lower in children. Afessa et al. have reported mortality of around 10% in
intensive care unit (ICU) patients admitted with status asthmaticus.[3]
Increasing standardization of low tidal volume ventilation strategies,
avoidance of prolonged neuromuscular blockade, and assist control mode
ventilation hopefully helped reduce this trend even further over the past
decade. In a retrospective review of 280 hospitalizations over a period of 30
years in the University of Texas, Health Science Center, San Antonio, 61.2 %
patients required intubation and mechanical ventilation. Mortality rate was
about 0.35%.[4]
Multiple observational studies have reported a higher incidence in women,
among African Americans and in subjects with adult-onset asthma, which
developed after an age of 17 years.[5]
Go to:

Pathophysiology
At a physiological level, premature airway closure during exhalation causes
an increase in functional residual capacity and air trapping. Heterogeneous
distribution of air trapping results in ventilation-perfusion mismatch and
hypoxemia- triggering anaerobic metabolism and lactic acidosis. It is offset
initially by respiratory alkalosis and is compounded once respiratory fatigue
and respiratory acidosis ensue.
Go to:

Histopathology
Increasing understanding of the pathophysiology of asthma at the histological
level over last 2 decades has emphasized airway inflammation as the primary
player, over and above smooth muscle contraction and airway
hyperresponsiveness. An interplay of mast cells, T lymphocytes, and
epithelial cells result in a circulatory surge of inflammatory cells as well as
cytokines. Histamines, leukotrienes, and platelet-activating factors are found
in increased concentrations locally and systemically. Lymphocytic and
eosinophilic submucosal infiltrates in tracheal and bronchial biopsy
specimens have been reported to be associated with poorer outcomes in adult
asthmatics.[6]
Destruction of cilia and epithelial denudation render nerve endings irritable
resulting in hyperreactivity. Inflammation also causes hypertrophy and
hyperfunctioning of goblet cells and mucous glands resulting in mucus
plugging.
The scheming of the catastrophe in cellular level is orchestrated by a
dysregulated parasympathetic overdrive, mediated through pulmonary vagus
innervation in the parasympathetic ganglia of small bronchi. The release of
postganglionic acetylcholine causes bronchoconstriction and hypersecretion
through muscarinic receptors while the inhibitory M2 receptors are often
dysfunctional in individuals with atopy, sustained exposure to allergens, viral
infection and chronic inflammation.
Go to:

History and Physical

Risk Factors [7],[8]
  History of near fatal asthma in the past requiring endotracheal
intubation is the greatest single predictor of death from bronchial
asthma.
 Similarly, poor patient perception of dyspnea and hypercapnia due to a
blunted hypoxic ventilatory response rendered by the chronicity of
severe disease, or even psychiatric illness is also an ominous risk
factor.[9],[10]
 Recurrent hospitalizations or deteriorations in spite of chronic oral
steroid use, late presentation since the onset of symptoms, altered
mental status and sleep deprivation during an ongoing presentation can
also be bad prognostic markers of a favorable outcome to initial
treatment.
 History of coronary artery disease poses a risk of cardiological adverse
events with therapy itself. All these in medical history should alert the
evaluating clinical team for a level of preparedness towards risk of
imminent status asthmaticus.
Physical Examination [11]
Brenner and colleagues demonstrated certain hemodynamic traits in patients
who assumed an upright position than supine. They tend to have a
significantly higher heart and respiratory rate along with pulsus paradoxus, a
significantly lower PaO2 and lower peak expiratory flow rate (PEFR).
However, the progressive decline in clinical and mental status in late
presentation of status asthmaticus may also counter-intuitively lead patients
to assume a supine position. That alone should not be a decision maker. After
initial treatment, a diaphoretic patient, preferring to sit upright, unable to
speak complete sentences or using accessory muscles of respiration all point
toward status asthmaticus.
One of the circulatory consequences of status asthmaticus apart from
tachycardia and tachypnea is also a large respiratory phase variation in
pleural pressure. The increased inspiratory effort against obstructed airway
results in augmented negative intrathoracic pressure. This results in reduced
left ventricular filling and outflow due to a combination of (1) septal
deviation to the left due to an enlarged RV, (2) increased LV afterload, and
(3) increased RV afterload due to increase in pulmonary arterial pressure.
Systolic blood pressure, therefore, tends to fall at the height of inspiration.
Pulsus paradoxus is the difference between end-expiratory and end-
inspiratory systolic blood pressure. It is augmented to more than 12 mm Hg
in status asthmaticus, although it may paradoxically decline in late-stage with
increasing fatigability and loss of respiratory drive.[12]
Tachycardia greater than 120 can be an indicator of disease severity as well
as treatment response to beta agonists. Grossman et al. demonstrated that
successful treatment results in a 24-hour drop in heart rate from 120 per
minute to 105 per minute. Sinus tachycardia is the predominant rhythm,
although supraventricular and ventricular arrhythmias have also been
reported.[13]
Classic wheezing, as an indicator of bronchospasm, is poorly reliable, as the
extent of alveolar airflow is so significantly impaired in these subsets of
patients that it cannot generate a wheeze before bronchodilation.
Go to:

Evaluation
Measurement of airflow obstruction can be challenging to perform but is best
achieved at the bedside with an assessment of PEFR than FEV1.
[14] Reduction of both values by 50% from personal best of the patient is an
indicator of status. The absolute value of PEFR less than 120 L per minute
and FEV1 less than 1 L corresponds with the proportional reduction. These
absolute numbers should prompt an assessment of arterial blood gas (ABG)
immediately.[15] Initial blood gas results indicate respiratory alkalosis with
hypoxemia. Therefore, developing respiratory acidosis or elevated PCO2 is
indicators of status asthmaticus that is indicative of the need for ventilatory
support.[16],[9],[10]  However, it should not be the lone decision maker and
should be coupled with a serial physical examination, evidence of worsening
mentation, and fatigability or hemodynamic alterations.
Mountain and colleagues, in their study of 229 hospitalized patients with
acute asthma, detected a 28% incidence of anion gap metabolic acidosis,
caused by rising lactate.
ECG may also show transient and reversible signs of right heart strain
including peaked p wave or right axis deviation.
Chest radiography has little role to play in predicting the course of status
asthmaticus, other than ruling out alternate etiologies or associated
complicating diagnoses.
Go to:

Treatment / Management
Indication for Hospitalization and ICU
Serial measurement of PEFR is a practical and reliable predictor of severity
and need for hospitalization. Stein and Cole found that a significant
improvement in PEFR, 2 hours after treatment predicted the need for
hospitalization, even though initial PEFR on presentation did not
(improvement noted from a median of 250 L per minute to 330 L per
minute). Rodrigo and Rodrigo demonstrated a similar pattern with treatment
response in FEV1, although it may not be the most practical approach at the
bedside.[17],[18],[19]
 A favorable response to initial treatment of status asthmaticus should be a
visible improvement in symptoms which sustains 30 minutes or beyond the
last bronchodilator dose, and a PEFR greater than 70% of predicted.
On the other hand, patients with evidence of continuing clinical decline or
less than 10% improvement in PEFR or less than 40% of predicted, should be
considered for admission to the intensive care unit. Anyone with worsening
evidence of respiratory failure, alteration of mental status, arrhythmia,
cardiac or respiratory arrest, or complications like pneumothorax or
pneumomediastinum naturally requires ICU admission along with aggressive
resuscitation measures if consistent with their goals of care.
FEV1 or PEFR between 40% to 70% of predicted after initial treatment in the
emergency room is considered as “inadequate response." Duration of
management in the hospital does play a role in these subsets of patients.
Kelsen and colleagues showed a 50% relapse rate in patients treated for 2
hours or less in a facility as opposed to 4% in those treated and observed for
an additional 2 to 4 hours. The consensus, therefore, varies anywhere
between 4 to 6 hours of treatment in a facility in this group of patients before
deciding on admission versus discharge. A poor psychosocial makeup or a
hostile home environment with obvious exposure to triggers may tilt the
decision in favor of hospitalization.
Pharmacological Management [2]
Beta Agonists
Short-acting inhaled beta-agonists are the drug of first choice in acute
asthma.[20] Albuterol is preferred over metaproterenol in that class because
of its higher beta 2 selectivities and longer duration of action. The dose-
response curve and duration of action of these medications are adversely
affected by a combination of patient factors including preexisting
bronchoconstriction, airway inflammation, mucus plugging, poor patient
effort, and coordination. Therefore, larger and more frequent dosing than
conventional therapy is necessary. Initial treatment consists of 2.5 mg of
albuterol (0.5 mL of a 0.5% solution in 2.5 mL normal saline) by
nebulization every 20 minutes for 60 minutes (three doses) followed by
treatments hourly during the first several hours of therapy. Interestingly, Idris
and colleagues demonstrated that even in patients with severe disease, 4 puffs
of albuterol (0.36 mg) delivered with a metered dose inhaler (MDI) and
spacer was as effective as a 2.5-mg dose by nebulization. In an ER setting, a
nebulizer is still preferred because of less need for supervision, coordination
and continued instructions.
An area that needs clarity is the appropriate mode of delivery of these inhaled
medications in a ventilated patient. So far consensus prevails over a higher
dosage required to achieve physiologic benefits compared to non-intubated
patients. However, there is an ongoing debate about the use of MDI versus
nebulizers, the appropriate mode of ventilation, the exact site of the
connection of the delivery device on the ventilator circuit among others. The
optimal delivery device has been a point of polarizing opinion. Mcintyre and
colleagues demonstrated that only 2.9% of a radioactive aerosol was
deposited in the lungs when delivered by a small volume nebulizer. They,
therefore, advocated use of MDI via an adapter attached to the inspiratory
limb of the ventilator circuit. However, their findings were refuted by a
subsequent study by Manthous and colleagues demonstrating a poor effect on
inspiratory flow-resistive pressure by MDI as opposed to nebulized albuterol.
[21] Assessment of airway peak to pause pressure gradient can be a rational
indicator to use when either one of the delivery modes is used. A 15% or
greater decline in the gradient is[1] considered to be a favorable response to
be aimed for, with repetitive doses, monitoring for toxicity.
Subcutaneous epinephrine or terbutaline, used in the past, have fallen out of
favor due to their toxicity profile, as has direct endotracheal instillation of
epinephrine due to lack of demonstrated efficacy and evidence-based studies.
Intravenous beta agonists are not routinely recommended although there are
reports of center-specific use in younger patients with status asthmaticus,
nonresponsive to inhaled therapy demonstrating persistent severe
hyperinflation of airways.
There have been more recent concerns with several studies showing a
correlation between asthma mortality and use of inhaled beta-agonists. Suissa
and colleagues demonstrated that risk of asthma mortality increases
drastically with use of 1.4 canisters per month or more of inhaled beta-
agonists.
The Executive Committee of the American Academy of Allergy and
Immunology published a position statement on the use of inhaled beta-
agonists in asthma.[22]
Conclusions
 More than 1 canister per month use of beta-agonists is a marker for
severe asthma.
 Heavy or increased use of beta-agonists warrants additional therapy
such as the use of corticosteroids.
 Beta-agonists may make asthma worse, but the available data do not
allow for a definitive conclusion regarding this controversy.
 Patients currently using beta-agonists should slowly withdraw
nonessential doses and use them only for rescue purposes.
However significant the concerns are regarding their long-term use, the use
of short-acting inhaled beta agonists should not be withheld or underdosed
during acute attacks, and they remain the drug of first choice under those
circumstances. 
Corticosteroids
Most available data support a distinct benefit of corticosteroids in status
asthmaticus in an emergency setting.[23] Rowe et al. in their meta-analysis of
30 RCT concluded that use of steroids in emergency department significantly
reduces rates of admission and number of future relapses in subsequent 7 to
10 days. Route of administration did not make a difference, and McFadden
based on analysis of available data came up with a recommended dose of 150
to 225 mg per day of prednisone or its equivalent to reach maximum
therapeutic benefit. Littenberg and Gluck also demonstrated a significant
reduction in hospitalization with a methylprednisolone dose of 125 mg
intravenously on presentation in the emergency room. Currently available
data, therefore, support the approach of 60 to 125 mg methylprednisolone
intravenously every 6 hours for the initial 24 hours of treatment of status
asthmaticus. Oral steroids are usually required for the next 10 to 14 days.
In a physiologic level, steroids not only reduce airway inflammation and
mucus production but also potentiates beta-agonist activity in smooth
muscles and reduces beta agonists tachyphylaxis in patients with severe
asthma.
Anticholinergics
Anticholinergics have a variable response in acute exacerbation with a
somewhat underwhelming bronchodilatory role. However, they can be useful
in patients with bronchospasm induced by beta-blockade or severe underlying
obstructive disease with FEV1 less than 25% of predicted.
Bryant and Rogers demonstrated that 0.25 mg of ipratropium bromide with 5
mg of albuterol by nebulizer resulted in greater improvement in FEV1 than
albuterol alone. The response time was also much faster than corticosteroids
with a detectable change in FEV1 within 19 minutes. Nebulized
glycopyrrolate can also be an alternative although it is not as much in vogue
in the United States. Available data and practice still recommend
anticholinergics as second-line agents in status asthmaticus patients with
inadequate response to beta agonists or steroids. A 0.5-mg dose of
Ipratropium by nebulization in conjunction with albuterol is the consensus
choice.
Magnesium Sulfate
Magnesium inhibits calcium-mediated smooth muscle constriction, decreases
acetylcholine release in the neuromuscular junction, and affects respiratory
muscle force generation.
 Intravenous Magnesium sulfate has therefore been a useful adjunct in
patients with acute status asthmaticus refractory to beta agonists.[24] The
benefit does not seem to isolate patients with low serum magnesium levels
although 50% of patients with acute asthma tend to present with
hypomagnesemia. In spite of its widespread use in Emergency department
setting, 2 large prospective studies failed to demonstrate any statistically
significant improvement in lung function in severe asthma exacerbation.
However, it is relatively cheap and harmless and has been proposed to have a
trend towards female responsiveness, as estrogen potentiates bronchodilator
effects of magnesium. At the commonly used dose of 2 gm intravenously
(IV) in 2 separate doses over 20 minutes, side effects of hypotension or
hyporeflexia are fairly uncommon.
Heliox and Oxygen
True shunt in acute asthma averages only 1.5% of pulmonary blood flow.
Therefore, oxygen supplementation need in status asthmaticus is infrequent
and low dose. Refractory hypoxemia in status asthmaticus should trigger a
search for complications like pneumonia, atelectasis or barotrauma. Heliox as
a mixture of 70:30 or 60:40 helium:oxygen decreases airway resistance and
turbulence,  and therefore reduces work of breathing and inspiratory muscle
fatigue. There is a demonstrated reduction in pulsus paradoxus and
enhancement in peak flow. However, its routine use is hindered by the
prohibitive cost, infrequent indication and need for recalibration of gas
blenders and flow meters when used with mechanical ventilation.[25]
Antibiotics
Graham et al. conducted a randomized double-blinded trial and demonstrated
no difference in improvement in symptom score, spirometry or length of
hospitalization with routine use of antibiotics in status asthmaticus. That does
not mean that patients with clinical signs of infection should not be treated
with antimicrobials or due diligence should not be pursued in obtaining
respiratory culture specimens early on.[26],[27]
Mechanical Ventilation and Sedation[28]
The decision to intubate a patient presenting with status asthmaticus is a
clinical one and does not unequivocally require a blood gas assessment.
Immediate indications for intubation include:
 Acute cardiopulmonary arrest
 Severe obtundation or coma
 Frank evidence of respiratory fatigue with gasping or inability to speak
at all
If a patient continues to deteriorate in spite of initial pharmacologic
treatment, a bedside assessment around the time window of response needs to
be made.
Clinical findings that tilt a decision in favor include:
 Increasing lethargy
 Increasing use of accessory muscles
 Change in posture or speech
 Decreasing rate and depth of respiration
In patients who are not significantly encephalopathic,  and has no excessive
secretions, noninvasive ventilation with CPAP or BIPAP can be a useful
modality to support ventilation, and avoid the need for anesthesia and
sedation, as well as the risk of nosocomial infection with endotracheal
intubation. It is increasingly being used in the first 24 hours, at pressure
support titrated to reduce respiratory rate below 25 per minute and generate
tidal volume above 7 ml/kg body weight. Beyond that, there might be an
increased risk of aspiration, facial pressure necrosis and suboptimal
ventilation to reconsider invasive mechanical ventilation.[29],[30]
Once a decision to intubate is made, choice of sedation agent is of paramount
importance.
Ketamine
Ketamine has sedative, analgesic, anesthetic and bronchodilatory properties
and has been increasingly recommended for emergency intubation in status
asthmaticus along with succinylcholine. The usual dose is 1 to 2 mg/kg given
intravenously at a rate of 0.5 mg/kg per minute to provide 10 to 15 minutes of
general anesthesia without significant respiratory depression (as opposed to
bolus doses).
Potential risks to consider before deciding in favor of ketamine include:
 Ability to cause hypertension and tachycardia with sympathetic
stimulation. Thus it is to be avoided in patients with uncontrolled
hypertension, preeclampsia, raised intracranial pressure.
 Lowering of seizure threshold
 Increase in laryngeal secretion
 Metabolism through liver thus causing some accumulation with the
continuous infusion in liver failure
Propofol
Propofol is an equally preferred initial agent due to its rapid onset of action
and east titratability, ability to achieve deep sedation without paralytics and
mild bronchodilatory effects. However prolonged propofol administration in
this subset of patients raises the risk of increased carbon dioxide (CO2)
production, as it is constituted in a fat-based diluent.
Thus for ongoing sedation needs, lorazepam is preferred with caution to
minimize sedation to a level to maintain ventilator synchrony and allow
response to stimulation.
Paralytics
For patients who continue to remain desynchronized with the ventilator in
spite of sedation, and has a risk of generating auto-PEEP or barotrauma,
paralytics may need to be considered. Atracurium is the agent of choice
because of the lower risk of myopathy although it can cause
bronchoconstriction due to histamine release. Vecuronium is an alternative in
such circumstances.[31]
Go to:

Differential Diagnosis
Conditions that can mimic an asthma attack should always be considered in
physical examination, particularly, if the response to initial resuscitation is
not as expected.
Some of these conditions can also be a complication of an actual asthma
attack.
 Asymmetric breath sounds and tracheal deviation with hypoxia should
prompt evaluation for pneumothorax
 Mediastinal  crunch or crepitus on exam around neck or chest indicate
pneumomediastinum
 Inspiratory stridor should prompt evaluation for tracheal obstruction or
angioedema. Evaluation of the oral cavity and neck should consider
mass lesions in differentials as well in such a scenario. Prior history of
tracheostomy or recurrent intubation should prompt consideration of
tracheal stenosis.
 Localized wheezing on auscultation should lead to ruling out of foreign
body inhalation, mucus plugging, or focal atelectasis[32]
 Recurrent presentation with status asthmaticus resolved with positive
pressure ventilation, particularly in adults should raise suspicion for
excessive dynamic airway collapse (EDAC), confirmed by
bronchoscopy or laryngoscopy in a controlled setting. 
 Finally, the presence of other adventitious sounds like rhonchi or lobar
crackles brings pneumonia into the differential.
Go to:

Prognosis
Poor Prognostic Factors
 Leatherman et al. found an incidence of muscle weakness in asthmatic
patients treated with neuromuscular blockers and steroids of 29%.
 Adnet et al. evaluated complications and morbidities associated with a
prolonged neuromuscular blockade in status asthmaticus patients. The
incidence of post-intubation myopathy, ventilator-associated
 pneumonia, and duration of ICU stay was higher in the neuromuscular
blockade group in the population involving 5 centers. [10]
  A study by Afessa et al. also reported a higher incidence of acidemia
and carbon dioxide retention in nonsurvivors compared to survivors
with acute asthmaticus.
 Need for mechanical ventilation has also been reported as a poor
prognostic factor.[33]
Go to:

Complications
Acute Hypotension on Mechanical Ventilation
Acute hypotension beyond the initial period of sedation and paralytic effect
post-intubation needs immediate bedside intervention in status asthmaticus
patients.[34] The first and most time-sensitive pathology to be ruled out is
tension pneumothorax. If bedside clinical examination, ultrasound or chest x-
ray support so, it needs to be managed immediately with tube thoracostomy.
Apart from sedation and hypovolemia as other potential causes, a common
etiology of hypotension in mechanically ventilated asthma patients is
dynamic hyperinflation causing air trapping and auto-PEEP generation. It can
be detected by observing flow pattern in ventilator graphics and inability to
return airflow to baseline. It is confirmed by measuring total PEEP with
expiratory breath hold and then managed by increasing exhalation time,
either by reducing the tidal volume or respiratory rate. Sometimes deeper
sedation or paralysis may also be necessary.
Ventilator applied PEEP should be kept in moderation in status asthmaticus
patients because of the risk of barotrauma and hypotension as well.
In patients without raised intracranial pressure or severely depressed
myocardial function, purposeful hypoventilation and permissive hypercapnia
is, therefore, an often practiced strategy for above reasons. More importance
is paid to a ph target than a target PCO2, and ph greater than 7.25 is generally
well tolerated.
High peak pressure with stable plateau pressure on the ventilator should also
prompt effort at clearance of airway and endotracheal tube from secretion as
it tends to be thick and tenacious in this subgroup of patients. Larger lumen
endotracheal tube (7.5 or 8 Fr) is preferred due to higher airway resistance
and the need for airway clearance.
Other Complications
Apart from complications related to neuromuscular blockade and those that
are outcome of the pathophysiology of asthma itself, other commonly
reported complications are electrolyte abnormalities, hypotension, and
dysrhythmias.[35]
Severe hypotension and respiratory acidosis in refractory cases have resulted
in myocardial infarction, hypoxic and anoxic encephalopathy and death.
Go to:

Pearls and Other Issues

Incidence and prevalence of severe asthma are increasing in both adults and
children. Such episodes may progress to a status of progressive respiratory
failure refractory to standard therapeutic measures. Early recognition of such
severe episodes, based on clinical signs, lab data, and follow-up evaluations
at close intervals can be life-saving. An initial aggressive treatment trial of
beta-agonist, corticosteroids, and anticholinergics has to be tried followed by
adjunct measures which may not be based on robust guidelines but evidence.
Although initially avoided mechanical ventilation is indicated for certain
specific situations including alteration of consciousness, respiratory fatigue,
or cardiopulmonary arrest. There have been recent advances in ventilation
strategies to protect against barotrauma, alveolar trauma, and neuromyopathy.
Finally, once resolved, attention needs to be paid to measures for avoidance
of future severe episodes for which the patient carries an increased risk. 
Go to:

Enhancing Healthcare Team Outcomes

Preventing Future Attacks and an Interprofessional Team Approach
Beyond the period of recovery from an acute episode of status asthmaticus,
the management goal should shift to an interprofessional team approach to
help prevent future severe attacks. It should start with extensive patient
education from nurses, respiratory therapists, nurse practitioners, physician
assistants, and physicians about the pathophysiology of asthma, warning
signs and symptoms, elimination and avoidance of triggers, and early
identification and treatment of attacks. Inpatient education by respiratory
therapists or nursing team about an asthma action plan, tools of self-
assessment of severity with peak flowmetry, the appropriate technique of
inhaler use, and relevant numbers to call for specialist help. Maintenance
inhaler therapy should be appropriately addressed along with assessment for
the need for advanced immunotherapy based on asthma phenotype and
allergy profile.[36],[37]
Patients should be well-versed in detecting early warning signs at home and
be well equipped to detect and address, based on the asthma action plan.
A 20% drop in PEFR below predicted, or personal best is a good objective
indicator.
Finally, patients with a history of anaphylaxis or sudden asphyxic asthma
presentation should also be equipped with Epipen for immediate
subcutaneous use if needed.
Health systems across the United States are endorsing the role of outpatient
pharmacy in monitoring for patient compliance, as well as, an increase in
disease severity based on prescription refills. Bluetooth enabled monitors to
inhaler devices can be an answer to remote monitoring of rescue inhaler
needs and effective use for physicians. An example of a similar sensor-
enabled smart inhaler is the San Francisco based propeller health devices.[38]
Outcomes and Evidence-based Medicine
Over the years several protocols and guidelines have been developed to
manage patients with status asthmaticus. Overall, when the patient is brought
to the emergency room and quickly managed according to a streamlined
protocol, the outcomes are good.[39] (Level E) However, when the patient
does require mechanical ventilation, the outcomes vary from moderate to
severe.[40] (Level C) Mortality is not an uncommon event in these patients.
The reason for the high morbidity and mortality is due to nosocomial
pneumonia while on the ventilator. Thus, the importance of educating the
family on bringing the patient immediately to the ER at the first signs of
respiratory distress.
 Go to:

Questions
To access free multiple choice questions on this topic, click here.
Go to:

References
1.
Papiris S, Kotanidou A, Malagari K, Roussos C. Clinical review:
severe asthma. Crit Care. 2002 Feb;6(1):30-44. [PMC free article]
[PubMed]
2.
Siddiqui S, Gonem S, Wardlaw AJ. Advances in the management of
severe asthma. Semin Respir Crit Care Med. 2012 Dec;33(6):666-
84. [PubMed]
3.
McFadden ER. Acute severe asthma. Am. J. Respir. Crit. Care
Med. 2003 Oct 01;168(7):740-59. [PubMed]
4.
Afessa B, Morales I, Cury JD. Clinical course and outcome of patients
admitted to an ICU for status asthmaticus. Chest. 2001
Nov;120(5):1616-21. [PubMed]
5.
Peters JI, Stupka JE, Singh H, Rossrucker J, Angel LF, Melo J, Levine
SM. Status asthmaticus in the medical intensive care unit: a 30-year
experience. Respir Med. 2012 Mar;106(3):344-8. [PubMed]
6.
Braman SS, Kaemmerlen JT. Intensive care of status asthmaticus. A
10-year experience. JAMA. 1990 Jul 18;264(3):366-8. [PubMed]
7.
Corbridge TC, Hall JB. The assessment and management of adults with
status asthmaticus. Am. J. Respir. Crit. Care Med. 1995
May;151(5):1296-316. [PubMed]
8.
Rodriguez-Roisin R. Acute severe asthma: pathophysiology and
pathobiology of gas exchange abnormalities. Eur. Respir. J. 1997
Jun;10(6):1359-71. [PubMed]
9.
Meduri GU, Cook TR, Turner RE, Cohen M, Leeper KV. Noninvasive
positive pressure ventilation in status asthmaticus. Chest. 1996
Sep;110(3):767-74. [PubMed]
10.
Judson MA, Sperl PL. Status asthmaticus with acute decompensation
with therapy in a 27-year-old woman. Chest. 1995 Feb;107(2):563-
5. [PubMed]
11.
Tobias JD, Garrett JS. Therapeutic options for severe, refractory status
asthmaticus: inhalational anaesthetic agents, extracorporeal membrane
oxygenation and helium/oxygen ventilation. Paediatr
Anaesth. 1997;7(1):47-57. [PubMed]
12.
Williams TJ, Tuxen DV, Scheinkestel CD, Czarny D, Bowes G. Risk
factors for morbidity in mechanically ventilated patients with acute
severe asthma. Am. Rev. Respir. Dis. 1992 Sep;146(3):607-
15. [PubMed]
13.
Rebuck AS, Read J. Assessment and management of severe
asthma. Am. J. Med. 1971 Dec;51(6):788-98. [PubMed]
14.
Henke CA, Hertz M, Gustafson P. Combined bronchoscopy and
mucolytic therapy for patients with severe refractory status asthmaticus
on mechanical ventilation: a case report and review of the
literature. Crit. Care Med. 1994 Nov;22(11):1880-3. [PubMed]
15.
National Asthma Education and Prevention Program. Expert Panel
Report 3 (EPR-3): Guidelines for the Diagnosis and Management of
Asthma-Summary Report 2007. J. Allergy Clin. Immunol. 2007
Nov;120(5 Suppl):S94-138. [PubMed]
16.
Inhaled beta 2-adrenergic agonists in asthma. The Executive
Committee of the American Academy of Allergy and Immunology. J.
Allergy Clin. Immunol. 1993 Jun;91(6):1234-7. [PubMed]
17.
Frei SP. Cost comparison of bronchodilator delivery methods in
Emergency Department treatment of asthma. J Emerg Med. 2000
Nov;19(4):323-6. [PubMed]
18.
Griffiths B, Kew KM, Normansell R. Intravenous magnesium sulfate
for treating children with acute asthma in the emergency
department. Paediatr Respir Rev. 2016 Sep;20:45-47. [PubMed]
19.
Graham V, Lasserson T, Rowe BH. Antibiotics for acute
asthma. Cochrane Database Syst Rev. 2001;(3):CD002741. [PubMed]
20.
Johnston SL, Szigeti M, Cross M, Brightling C, Chaudhuri R, Harrison
T, Mansur A, Robison L, Sattar Z, Jackson D, Mallia P, Wong E,
Corrigan C, Higgins B, Ind P, Singh D, Thomson NC, Ashby D,
Chauhan A., AZALEA Trial Team. Azithromycin for Acute
Exacerbations of Asthma : The AZALEA Randomized Clinical
Trial. JAMA Intern Med. 2016 Nov 01;176(11):1630-1637. [PubMed]
21.
Hess DR. Noninvasive ventilation for acute respiratory failure. Respir
Care. 2013 Jun;58(6):950-72. [PubMed]
22.
Berg KT, O'Connor MG, Lescallette RD, Arnold DH, Stack LB.
AAIRS Score Overview: The Acute Asthma Intensity Research
Score. Acad Emerg Med. 2015 Oct;22(10):E25-6. [PMC free article]
[PubMed]
23.
Al-Muhsen S, Horanieh N, Dulgom S, Aseri ZA, Vazquez-Tello A,
Halwani R, Al-Jahdali H. Poor asthma education and medication
compliance are associated with increased emergency department visits
by asthmatic children. Ann Thorac Med. 2015 Apr-Jun;10(2):123-
31. [PMC free article] [PubMed]
24.
Pinnock H. Supported self-management for asthma. Breathe
(Sheff). 2015 Jun;11(2):98-109. [PMC free article] [PubMed]
25.
Tuxen DV. Detrimental effects of positive end-expiratory pressure
during controlled mechanical ventilation of patients with severe airflow
obstruction. Am. Rev. Respir. Dis. 1989 Jul;140(1):5-9. [PubMed]
26.
Goh AY, Chan PW. Acute myopathy after status asthmaticus: steroids,
myorelaxants or carbon dioxide? Respirology. 1999 Mar;4(1):97-
9. [PubMed]
27.
Nowak RM, Tomlanovich MC, Sarkar DD, Kvale PA, Anderson JA.
Arterial blood gases and pulmonary function testing in acute bronchial
asthma. Predicting patient outcomes. JAMA. 1983 Apr
15;249(15):2043-6. [PubMed]
28.
Mountain RD, Sahn SA. Clinical features and outcome in patients with
acute asthma presenting with hypercapnia. Am. Rev. Respir. Dis. 1988
Sep;138(3):535-9. [PubMed]
29.
Gunen H, Hacievliyagil SS, Kosar F, Gulbas G, Kizkin O, Sahin I. The
role of arterial blood gases, exercise testing, and cardiac examination in
asthma. Allergy Asthma Proc. 2006 Jan-Feb;27(1):45-52. [PubMed]
30.
Lamblin C, Gosset P, Tillie-Leblond I, Saulnier F, Marquette CH,
Wallaert B, Tonnel AB. Bronchial neutrophilia in patients with
noninfectious status asthmaticus. Am. J. Respir. Crit. Care Med. 1998
Feb;157(2):394-402. [PubMed]
31.
Sur S, Crotty TB, Kephart GM, Hyma BA, Colby TV, Reed CE, Hunt
LW, Gleich GJ. Sudden-onset fatal asthma. A distinct entity with few
eosinophils and relatively more neutrophils in the airway
submucosa? Am. Rev. Respir. Dis. 1993 Sep;148(3):713-9. [PubMed]
32.
Serrano-Pariente J, Rodrigo G, Fiz JA, Crespo A, Plaza V., High Risk
Asthma Research Group. Identification and characterization of near-
fatal asthma phenotypes by cluster analysis. Allergy. 2015
Sep;70(9):1139-47. [PubMed]
33.
Brenner BE, Abraham E, Simon RR. Position and diaphoresis in acute
asthma. Am. J. Med. 1983 Jun;74(6):1005-9. [PubMed]
34.
Paniagua N, Elosegi A, Duo I, Fernandez A, Mojica E, Martinez-Indart
L, Mintegi S, Benito J. Initial Asthma Severity Assessment Tools as
Predictors of Hospitalization. J Emerg Med. 2017 Jul;53(1):10-
17. [PubMed]
35.
Knowles GK, Clark TJ. Pulsus paradoxus as a valuable sign indicating
severity of asthma. Lancet. 1973 Dec 15;2(7842):1356-9. [PubMed]
36.
Grossman J. The occurrence of arrhythmias in hospitalized asthmatic
patients. J. Allergy Clin. Immunol. 1976 Apr;57(4):310-7. [PubMed]
37.
Edmonds ML, Milan SJ, Camargo CA, Pollack CV, Rowe BH. Early
use of inhaled corticosteroids in the emergency department treatment of
acute asthma. Cochrane Database Syst Rev. 2012 Dec
12;12:CD002308. [PMC free article] [PubMed]
3
8.
Su JG, Barrett MA, Henderson K, Humblet O, Smith T, Sublett JW,
Nesbitt L, Hogg C, Van Sickle D, Sublett JL. Feasibility of Deploying
Inhaler Sensors to Identify the Impacts of Environmental Triggers and
Built Environment Factors on Asthma Short-Acting Bronchodilator
Use. Environ. Health Perspect. 2017 Feb;125(2):254-261. [PMC free
article] [PubMed]
3
9
.
Miller AG, Breslin ME, Pineda LC, Fox JW. An Asthma Protocol
Improved Adherence to Evidence-Based Guidelines for Pediatric
Subjects With Status Asthmaticus in the Emergency
Department. Respir Care. 2015 Dec;60(12):1759-64. [PubMed]
 4
0
.
Rampa S, Allareddy V, Asad R, Nalliah RP, Allareddy V, Rotta AT.
Outcomes of invasive mechanical ventilation in children and
adolescents hospitalized due to status asthmaticus in United States: a
population based study. J Asthma. 2015 May;52(4):423-30. [PubMed]
Copyright © 2019, StatPearls Publishing LLC.

This book is distributed under the terms of the Creative Commons Attribution 4.0 International License

(http://creativecommons.org/licenses/by/4.0/), which permits use, duplication, adaptation, distribution, and reproduction in

any medium or format, as long as you give appropriate credit to the original author(s) and the source, a link is provided to

the Creative Commons license, and any changes made are indicated.

Bookshelf ID: NBK526070PMID: 30252326