Status Asthmaticus


Article Author:
Rebanta Chakraborty


Article Editor:
Sangita Basnet


Editors In Chief:
Jason Nagle


Managing Editors:
Avais Raja
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Khalid Alsayouri
Trevor Nezwek
Radia Jamil
Patrick Le
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Hassam Zulfiqar
Steve Bhimji
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Sarosh Vaqar
Mark Pellegrini
James Hughes
Beata Beatty
Nazia Sadiq
Hajira Basit
Phillip Hynes
Tehmina Warsi


Updated:
6/4/2019 3:44:50 PM

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.

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]

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]

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.

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.

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.

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.

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]

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.

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]

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.

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. 

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.


Interested in Participating?

We are looking for contributors to author, edit, and peer review our vast library of review articles and multiple choice questions. In as little as 2-3 hours you can make a significant contribution to your specialty. In return for a small amount of your time, you will receive free access to all content and you will be published as an author or editor in eBooks, apps, online CME/CE activities, and an online Learning Management System for students, teachers, and program directors that allows access to review materials in over 500 specialties.

Improve Content - Become an Author or Editor

This is an academic project designed to provide inexpensive peer-reviewed Apps, eBooks, and very soon an online CME/CE system to help students identify weaknesses and improve knowledge. We would like you to consider being an author or editor. Please click here to learn more. Thank you for you for your interest, the StatPearls Publishing Editorial Team.

Status Asthmaticus - Questions

Take a quiz of the questions on this article.

Take Quiz
A young child with status asthmaticus is admitted to the emergency room. Despite all medical interventions, the child still continues to wheeze. It is decided to intubate the child and ventilate him. Which of the following is most likely to benefit this patient's respiratory status?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up
A 17-year-old female is admitted with status asthmaticus. She is treated with continuous albuterol nebulization, intravenous corticosteroids, and bilevel positive airway pressure mechanical respiration. The patient's respiratory status improves, but she develops generalized weakness, fatigue, and myalgias. The cardiac monitor shows prolonged QT interval, flattened T waves, and ST depression. What is the most likely etiology of these changes?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up
What may result from severe status asthmaticus?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up
A 30-year-old female dies suddenly when alone. The patient had been healthy earlier in the day. Autopsy shows lung hyperinflation, areas atelectasis, and thick mucus found in the bronchioles. Microscopic evaluation shows submucosal mucous gland hyperplasia, eosinophilic infiltration, bronchial smooth muscle hyperplasia, and bronchial epithelial basement membrane thickening. What is the most likely cause of death?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up
A 25-year-old female presents in status asthmaticus. She took 5 albuterol/ipratropium nebulizer treatments at home without relief. On EMS arrival, she is diaphoretic, in severe respiratory distress with significant accessory muscle use. Her vitals are HR 140, BP 105/50, RR 40, Sp02 80%, Temp 100.3 Fahrenheit. There is minimal air movement on physical exam. Which of the following treatments will be least likely to be helpful?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up
A 34-year-old male presents in extremis from status asthmaticus. EMS reports he is now unresponsive as his mental status was progressively worsening. The patient is intubated without issue. His weight is 75 kg. What are the most appropriate ventilator settings?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up
A patient is brought to the emergency department suffering from status asthmaticus, an acute exacerbation of asthma that is unresponsive to typical treatments. His workup reveals anoxia severe respiratory acidosis. A large parenteral dose of a beta-2 adrenergic agent is administered, but the response is very suboptimal. What medication can be administered in an effort to control symptomatology and potentiate the effect of adrenergic medication already given?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up
A 5-year-old was brought to the emergency department by his parents because of worsening shortness of breath and cough. He has a history of asthma, which further exacerbated since he started to have running nose, cough, and fever two days prior. The physical examination revealed a sick looking child with a temperature of 100.2 F, BP 80/50 mmHg, pulse 130/min, and respiratory rate of 30/min. He had difficulty talking. His chest exam revealed intercostal retraction and generalized wheezing. What is the clinical sign that indicated the most significant respiratory emergency?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up
A 28-year-old African American female is brought to the emergency department with acute onset shortness of breath that has progressively worsened over the past 12 hours. According to her boyfriend at the bedside, she has not slept all night and has been using her inhaler every hour without any benefit. Symptoms suddenly became much worse over the past 3 hours. On arrival she appears anxious, in visible respiratory distress, and unable to speak more than a couple of words at a time. She is using her accessory muscles to breathe. The calculated difference between systolic blood pressure at end inspiration and expiration is 14 mmHg. She is promptly started on nebulized albuterol and ipratropium for continuous hour-long treatment and administered a dose of 2 grams magnesium sulfate, 125 mg methylprednisolone, and 2 liters oxygen supplementation. Two hours later, she is finally lying in bed and sleeping without distress. Boyfriend feels reassured that she is finally able to catch some rest. Her wheeze is less than before. Difference between systolic blood pressure at inspiration and expiration is now 5 mmHg. Which of the following is the next best step in the management of this patient?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up
An African American female is brought to the emergency department with acute onset shortness of breath that has progressively worsened over the past 4 hours at home. She has a peak flow meter at home, and the number prior to arrival was 220 L, which is 51% of predicted. She has known bronchial asthma but hasn't had an exacerbation requiring an ED visit or hospitalization before. Her FEV1 in spirometry six months back was at 89%. After 2 hours of management in the emergency department, she feels significantly better and is able to speak in short sentences. Last breathing treatment was 15 minutes back. Repeat PEFR is 310 L/min, which is 68% of predicted. Her wheezing has improved, and she wants to go home. Which of the following is the next best step in the management of this patient?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up
A 16-year-old male presents to the emergency department with difficulty breathing. His symptoms and clinical presentation are consistent with status asthmaticus. WIthin 3 hours, he rapidly deteriorates with evidence fo fatigue, altered mental status and combined respiratory and metabolic acidosis. He was therefore intubated and placed on mechanical ventilation. Initial ventilator settings had to be adjusted due to asynchrony on ventilator and hypotension from intrinsic PEEP. He is still diffusely bronchospastic and is getting albuterol via a metered dose inhaler attached to the inspiratory limb of vent circuit. He is on assist-control volume-control mode ventilation. Which of the following is most accurate regarding his ongoing treatment strategy?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up
A 16-year-old Caucasian female presents to the emergency department with an acute exacerbation of shortness of breath, chest tightness, and wheezing that has not responded to her inhalers at home for over 4 hours. She is using accessory muscles to breathe and can only speak in one or two words. She mentions that she is tired. The difference in systolic blood pressure between inspiration and expiration is 10%. She needs 2 liters of oxygen to maintain saturation at 94%. She is diffusely wheezy but does not have any secretions. Which of the following treatment strategies is least likely to benefit her current disease process?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up
A 16-year-old Caucasian female presents to the emergency department with acute severe worsening of her asthma symptoms that would not respond to home inhalers over the past 6 hours. Medical history is significant for anxiety and bipolar disorder, irritable bowel syndrome, hypothyroidism, GERD and a recent diagnosis of bronchial asthma. This is her 4th episode of severe asthma exacerbation in the past 4 months. Each one of them required endotracheal intubation. She also gave birth to a healthy boy by a caesarian section last year. Symptoms escalate rapidly in requiring intubation again. Her bloodwork shows an absolute eosinophil count of 320/microL. Alarmed by these recurrent episodes of severe asthma, a CT angiogram of the chest is ordered as well. It does not show pulmonary embolism or chronic bronchiectasis. What further investigations may be most helpful in treating her condition?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up

Status Asthmaticus - References

References

Papiris S,Kotanidou A,Malagari K,Roussos C, Clinical review: severe asthma. Critical care (London, England). 2002 Feb     [PubMed]
Siddiqui S,Gonem S,Wardlaw AJ, Advances in the management of severe asthma. Seminars in respiratory and critical care medicine. 2012 Dec     [PubMed]
McFadden ER Jr, Acute severe asthma. American journal of respiratory and critical care medicine. 2003 Oct 1     [PubMed]
Afessa B,Morales I,Cury JD, Clinical course and outcome of patients admitted to an ICU for status asthmaticus. Chest. 2001 Nov     [PubMed]
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. Respiratory medicine. 2012 Mar     [PubMed]
Braman SS,Kaemmerlen JT, Intensive care of status asthmaticus. A 10-year experience. JAMA. 1990 Jul 18     [PubMed]
Corbridge TC,Hall JB, The assessment and management of adults with status asthmaticus. American journal of respiratory and critical care medicine. 1995 May     [PubMed]
Rodriguez-Roisin R, Acute severe asthma: pathophysiology and pathobiology of gas exchange abnormalities. The European respiratory journal. 1997 Jun     [PubMed]
Meduri GU,Cook TR,Turner RE,Cohen M,Leeper KV, Noninvasive positive pressure ventilation in status asthmaticus. Chest. 1996 Sep     [PubMed]
Judson MA,Sperl PL, Status asthmaticus with acute decompensation with therapy in a 27-year-old woman. Chest. 1995 Feb     [PubMed]
Tobias JD,Garrett JS, Therapeutic options for severe, refractory status asthmaticus: inhalational anaesthetic agents, extracorporeal membrane oxygenation and helium/oxygen ventilation. Paediatric anaesthesia. 1997     [PubMed]
Williams TJ,Tuxen DV,Scheinkestel CD,Czarny D,Bowes G, Risk factors for morbidity in mechanically ventilated patients with acute severe asthma. The American review of respiratory disease. 1992 Sep     [PubMed]
Rebuck AS,Read J, Assessment and management of severe asthma. The American journal of medicine. 1971 Dec     [PubMed]
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. Critical care medicine. 1994 Nov     [PubMed]
Expert Panel Report 3 (EPR-3): Guidelines for the Diagnosis and Management of Asthma-Summary Report 2007. The Journal of allergy and clinical immunology. 2007 Nov     [PubMed]
Inhaled beta 2-adrenergic agonists in asthma. The Executive Committee of the American Academy of Allergy and Immunology. The Journal of allergy and clinical immunology. 1993 Jun     [PubMed]
Frei SP, Cost comparison of bronchodilator delivery methods in Emergency Department treatment of asthma. The Journal of emergency medicine. 2000 Nov     [PubMed]
Griffiths B,Kew KM,Normansell R, Intravenous magnesium sulfate for treating children with acute asthma in the emergency department. Paediatric respiratory reviews. 2016 Sep     [PubMed]
Graham V,Lasserson T,Rowe BH, Antibiotics for acute asthma. The Cochrane database of systematic reviews. 2001     [PubMed]
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, Azithromycin for Acute Exacerbations of Asthma : The AZALEA Randomized Clinical Trial. JAMA internal medicine. 2016 Nov 1     [PubMed]
Hess DR, Noninvasive ventilation for acute respiratory failure. Respiratory care. 2013 Jun     [PubMed]
Berg KT,O'Connor MG,Lescallette RD,Arnold DH,Stack LB, AAIRS Score Overview: The Acute Asthma Intensity Research Score. Academic emergency medicine : official journal of the Society for Academic Emergency Medicine. 2015 Oct     [PubMed]
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. Annals of thoracic medicine. 2015 Apr-Jun     [PubMed]
Pinnock H, Supported self-management for asthma. Breathe (Sheffield, England). 2015 Jun     [PubMed]
Tuxen DV, Detrimental effects of positive end-expiratory pressure during controlled mechanical ventilation of patients with severe airflow obstruction. The American review of respiratory disease. 1989 Jul     [PubMed]
Goh AY,Chan PW, Acute myopathy after status asthmaticus: steroids, myorelaxants or carbon dioxide? Respirology (Carlton, Vic.). 1999 Mar     [PubMed]
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     [PubMed]
Mountain RD,Sahn SA, Clinical features and outcome in patients with acute asthma presenting with hypercapnia. The American review of respiratory disease. 1988 Sep     [PubMed]
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 and asthma proceedings. 2006 Jan-Feb     [PubMed]
Lamblin C,Gosset P,Tillie-Leblond I,Saulnier F,Marquette CH,Wallaert B,Tonnel AB, Bronchial neutrophilia in patients with noninfectious status asthmaticus. American journal of respiratory and critical care medicine. 1998 Feb     [PubMed]
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? The American review of respiratory disease. 1993 Sep     [PubMed]
Serrano-Pariente J,Rodrigo G,Fiz JA,Crespo A,Plaza V, Identification and characterization of near-fatal asthma phenotypes by cluster analysis. Allergy. 2015 Sep     [PubMed]
Brenner BE,Abraham E,Simon RR, Position and diaphoresis in acute asthma. The American journal of medicine. 1983 Jun     [PubMed]
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. The Journal of emergency medicine. 2017 Jul     [PubMed]
Knowles GK,Clark TJ, Pulsus paradoxus as a valuable sign indicating severity of asthma. Lancet (London, England). 1973 Dec 15     [PubMed]
Grossman J, The occurrence of arrhythmias in hospitalized asthmatic patients. The Journal of allergy and clinical immunology. 1976 Apr     [PubMed]
Edmonds ML,Milan SJ,Camargo CA Jr,Pollack CV,Rowe BH, Early use of inhaled corticosteroids in the emergency department treatment of acute asthma. The Cochrane database of systematic reviews. 2012 Dec 12     [PubMed]
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. Environmental health perspectives. 2017 Feb     [PubMed]
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. Respiratory care. 2015 Dec     [PubMed]
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. The Journal of asthma : official journal of the Association for the Care of Asthma. 2015 May     [PubMed]

Disclaimer

The intent of StatPearls is to provide practice questions and explanations to assist you in identifying and resolving knowledge deficits. These questions and explanations are not intended to be a source of the knowledge base of all of medicine, nor is it intended to be a board or certification review of PALS. The authors or editors do not warrant the information is complete or accurate. The reader is encouraged to verify each answer and explanation in several references. All drug indications and dosages should be verified before administration.

StatPearls offers the most comprehensive database of free multiple-choice questions with explanations and short review chapters ever developed. This system helps physicians, medical students, dentists, nurses, pharmacists, and allied health professionals identify education deficits and learn new concepts. StatPearls is not a board or certification review system for PALS, it is a learning system that you can use to help improve your knowledge base of medicine for life-long learning. StatPearls will help you identify your weaknesses so that when you are ready to study for a board or certification exam in PALS, you will already be prepared.

Our content is updated continuously through a multi-step peer review process that will help you be prepared and review for a thorough knowledge of PALS. When it is time for the PALS board and certification exam, you will already be ready. Besides online study quizzes, we also publish our peer-reviewed content in eBooks and mobile Apps. We also offer inexpensive CME/CE, so our content can be used to attain education credits while you study PALS.