Status asthmaticus
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For patient information click here Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Lakshmi Gopalakrishnan, M.B.B.S. [2]
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Status Asthmaticus Microchapters |
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Diagnosis |
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Treatment |
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Case Studies |
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Status asthmaticus On the Web |
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American Roentgen Ray Society Images of Status asthmaticus |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [3]
==Overview
Overview
Status asthmaticus is an medical emergency caused by an acute exacerbation of asthma that does not respond to standard bronchodilator and corticosteroid therapy. Symptoms include chest tightness, rapidly progressive dyspnea, non-productive cough and wheezing. Status asthmaticus if left untreated may result in severe bronchospasm, mucus plugging and rapidly develops acidosis and respiratory failure as a consequent of carbon di oxide retention and hypoxemia.
References
Historical Perspective
Classification
Pathophysiology
Causes
Differentiating Status asthmaticus from other Diseases
Epidemiology and Demographics
Risk Factors
Screening
Natural History, Complications and Prognosis
Diagnosis
Diagnostic Criteria | History and Symptoms | Physical Examination | Laboratory Findings | Chest X ray | CT | MRI | Other Imaging Findings | Other Diagnostic Studies
Treatment
Medical Therapy | Surgery | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies
Case Studies
Epidemiology
Approximately 10% of the US population is affected by asthma and an increased prevalence of 60% is observed in all age groups, with status asthmaticus requiring the highest rates of hospitalization.[1]
Predisposing factors
- Increase use of bronchodilator despite resistance,
- Frequent exacerbations despite the use of corticosteroids,
- Despite adhering to therapy, a peak flow rate of less than 10% from baseline,
- Frequent hospitalization for acute attacks,
- History of syncope or seizure during an acute asthmatic attack,
- Oxygen saturation lower than 92% despite supplemental oxygen,
- Airway obstruction is significantly reduced, resulting in severe impairment of air motion that leads to a silent chest with the absence of wheeze suggestive of an imminent respiratory arrest.
Diagnosis
History and Symptoms
- Rapidly progressive dyspnea
- Non-productive cough
- Profuse sweating
- Central cyanosis
- Loss of consciousness and/or seizure secondary to severe hypoxia may be observed
- Inability to speak more than one or two words may be observed with severe airway obstruction
Physical Examination
Vital Signs
- Increased respiratory rate greater than 30 cycles per minute
- Increased heart rate
- Pulsus paradoxus (fall in SBP greater than 20-40 mmHg during inspiration)
General Physical Examination
- Sit upright with arms extended to support the upper chest (tripod position) that assists the use of accessory muscles of respiration
- Peak flow rate measurement is a simple bedside method to assess the severity of airway obstruction. A red zone indicates less than 50% of the usual or normal peak flow reading signifying a severe airway obstruction.
Respiratory Examination
Inspection
- Use of accessory muscles of respiration such as sternocleidomastoid, scalene and intercostal muscles, correlates with the disease severity
- Intercostal retractions
- Paradoxical thoraco-abdominal breathing
Auscultation
- High-pitch prolong polyphonic expiratory wheeze
- Bilateral crackles
- Air entry may or may not be reduced depending on the disease severity
- Absence of wheeze and breath sounds secondary to severe airway obstruction may represent a silent chest which is an ominous sign of imminent respiratory failure.
Cardiovascular Examination
Progressive untreated airway obstruction and increased work of breathing eventually leads to worsening hypoxemia, hypercarbia and increased air trapping with compromised stroke volume that results in bradycardia, hypotension, hypoventilation and subsequent cardiorespiratory arrest.
Neurological Examination
- Level of consciousness ranges from lethargy, agitation to even loss of consciousness or seizure, secondary to severe airway obstruction, hypoxia and carbon-di-oxide retention.
- Unable to speak in full sentences
Laboratory Tests
- Measurement of oxygen saturation by pulse oximetry may be useful to identify patients with acute severe asthma who may rapidly progress to respiratory failure and thereby require more intensive therapy.[2]
- Arterial blood gas may reveal respiratory alkalosis that is consistent with the hypoxemia and/or hypercarbia secondary to significant hypoventilation.
- CBC count may demonstrate an increase in peripheral WBCs secondary to the use of steroids and β-agonists.
Pulmonary Function Test
FEV1 lower than 60% predicted is strongly suggestive of severe airway obstruction.
ECG
The presence of supraventricular tachycardia on ECG should raise a suspicion of theophylline toxicity.
Imaging Modalities
High-resolution CT may reveal several structural changes related to small-airway disease including cylindrical bronchiectasis, bronchial wall thickening, and air trapping.[3]
Stating based on Arterial Blood Gas Analysis
Stage 1
- Hyperventilation with normal PO2
- No hypoxemia
- Patients may benefit from nebulized ipratropium used adjunctive to β2-agonist therapy
Stage 2
- Hyperventilation with hypoxemia (low PO2 and PCO2)
- Patients may require corticosteroids in addition to bronchodilator therapy
Stage 3
- CO2 retention due to respiratory muscle fatigue
- Markedly elevated PCO2 levels are an indicator for mechanical ventilation
- Aggressive β2-agonist therapy along with parenteral steroids and/or theophylline is indicated
Stage 4
- Severe hypoxia with markedly elevated PCO2
- FEV1 lower than 20% predicted is suggestive of an impending respiratory arrest that may require intubation and mechanical ventilation
- Metered-dose inhalation of β2-agonist and anticholinergics are recommended. Administration of parenteral steroids and/or theophylline has also shown to be beneficial.
Treatment
- Initial severity assessment is evaluated using arterial blood gas and pulmonary function test and aggressive therapy is initiated to prevent progression to respiratory failure
- Supplemental oxygen via nasal canula or face mask is recommended to alleviate severe hypoxia. Oxygen saturation is maintained above 92% and is monitored using pulse Oximetry
- Mainstay drugs for the management include nebulized β2-agonists such as albuterol, salbutamol or terbutaline, parenteral steroids such as hydrocortisone or prednisolone and theophylline
- Anti-cholinergics such as ipratropium bromide may be indicated in patients who are unable to tolerate inhaled β2-agonists.
- In patients non-responsive to nebulized bronchodilator, IV-aminophylline or oral-leukotriene inhibitor may be used.[4]
- Helium with oxygen mixture has shown to reduce airway resistance and thereby reduce the work of breathing and also improve bronchodilator efficacy.
- Use of magnesium sulphate administered either IV or nebulized in addition to β2-agonists remains controversial.[5][6][7][8]
- Non-invasive ventilation using C-PAP or tight-fitting face mask may be used to reduce the work of breathing without intubation.
- Endotracheal intubation and mechanical ventilation should be used with caution in asthmatics who are non-responsive to medical therapy or non-invasive methods of ventilation, due to the substantial risk of barotrauma. Common indications include impending respiratory arrest, severe hypoxia non-responsive to supplemental oxygen, CO2 retention with PaCO2 greater than 50 mmHg, acidosis and/or altered mental status.
Complications
- Pneumothorax as a complication of mechanical ventilation
- Intubation increases the risk of super-imposed infection
Prevention
- Compliant to medications
- Avoid triggering factors
References
- ↑ Gorelick M, Scribano PV, Stevens MW, Schultz T, Shults J (2008) Predicting need for hospitalization in acute pediatric asthma. Pediatr Emerg Care 24 (11):735-44. DOI:10.1097/PEC.0b013e31818c268f PMID: 18955910
- ↑ Overall JE (1975) Rating session. Video taped interviews and BPRS ratings. Psychopharmacol Bull 11 (1):15. PMID: 1121560
- ↑ Robards VL, Lubin EN, Medlock TR (1975) Renal transplantation and placement of ileal stoma. Urology 5 (6):787-9. PMID: 1094668
- ↑ Press S, Lipkind RS (1991) A treatment protocol of the acute asthma patient in a pediatric emergency department. Clin Pediatr (Phila) 30 (10):573-7. PMID: 1934839
- ↑ Scarfone RJ, Loiselle JM, Joffe MD, Mull CC, Stiller S, Thompson K et al. (2000) A randomized trial of magnesium in the emergency department treatment of children with asthma. Ann Emerg Med 36 (6):572-8. DOI:10.1067/mem.2000.111060 PMID: 11097697
- ↑ Bessmertny O, DiGregorio RV, Cohen H, Becker E, Looney D, Golden J et al. (2002) A randomized clinical trial of nebulized magnesium sulfate in addition to albuterol in the treatment of acute mild-to-moderate asthma exacerbations in adults. Ann Emerg Med 39 (6):585-91. PMID: 12023699
- ↑ Glover ML, Machado C, Totapally BR (2002) Magnesium sulfate administered via continuous intravenous infusion in pediatric patients with refractory wheezing. J Crit Care 17 (4):255-8. DOI:10.1053/jcrc.2002.36759 PMID: 12501154
- ↑ Blitz M, Blitz S, Beasely R, Diner BM, Hughes R, Knopp JA et al. (2005) Inhaled magnesium sulfate in the treatment of acute asthma. Cochrane Database Syst Rev (2):CD003898. DOI:10.1002/14651858.CD003898.pub2 PMID: 15846687