Asthma
Chad A. Witt
Mario Castro
General Principles
Asthma is a disease of the airways characterized by airway inflammation and increased responsiveness (hyperreactivity) to a wide variety of stimuli (triggers).
Hyperreactivity leads to obstruction of the airways, the severity of which may be widely variable in the same individual.
As a consequence, patients have paroxysms of cough, dyspnea, chest tightness, and wheezing.
Other conditions may present with wheezing and must be considered, especially in patients who are unresponsive to therapy, see Table 9-1.
Asthma is an episodic disease, with acute exacerbations and attacks often interspersed with symptom-free periods.
Asthma exacerbations occur when airway reactivity is increased and lung function becomes unstable.
During an exacerbation, attacks occur more easily and are more severe and persistent.
Asthma attacks are episodes of shortness of breath or wheezing lasting minutes to hours.
Patients may be completely symptom-free between attacks.
Typically, attacks are triggered by acute exposure to irritants (e.g., smoke) or allergens.
Exacerbations are associated with factors that increase airway hyperreactivity, such as viral infections, allergens, and occupational exposures.
Diagnosis
Clinical Presentation
History
Acute asthma exacerbation
Patients with an acute asthma exacerbation present with worsening shortness of breath, wheezing, and/or cough.
Risk factors for severe exacerbations include
Previous history of mechanical ventilation
TABLE 9-1 CONDITIONS THAT MAY MIMIC ASTHMA
Upper Airway Obstruction
Adverse Drug Reaction
Other
Tumor
Epiglottitis
Vocal cord dysfunction
Obstructive sleep apnea
Aspirin
β-adrenergic antagonist
ACE inhibitors
Inhaled pentamidine
Tracheomalacia
Endobronchial lesion
Allergic bronchopulmonary aspergillosis
Sinusitis
Foreign body
Congestive heart failure
Gastroesophageal reflux
Hyperventilation with panic attacks
Recurrent need for oral corticosteroids
Hospitalization within the past year
Use of more than two canisters per month of inhaled short-acting bronchodilator
Seizures related to asthma attacks
Chronic asthma
Patients with chronic asthma present with episodic shortness of breath and/or cough, frequently accompanied by wheezing.
Patients often report worsening symptoms with specific exposures (e.g., smoke, volatile cleaning products, gasoline fumes, allergens, dust, etc.).
Physical Examination
Acute asthma exacerbation
Initial rapid assessment to identify patients who need immediate intervention is required.
Decreased breath sounds may be noted during severe exacerbations because there is not enough air flow to generate wheeze, thus wheezing is an unreliable indicator of severity of an attack.
Severe airflow obstruction is indicated by:
Pulsus paradoxus >25 mm Hg
Accessory respiratory muscle use
Nasal alar flaring
Inability to speak in full sentences
Tachycardia >110 beats/min
Tachypnea >28 breaths/min
Patients with decreased mental status require intubation.
SC emphysema should alert the examiner to the presence of a pneumothorax and/or pneumomediastinum.
Impending respiratory muscle fatigue may lead to depressed respiratory effort and paradoxical diaphragmatic movement.
Up to 50% of patients with severe airflow obstruction do not manifest any of the above findings.
Chronic asthma
Physical examination is frequently normal during symptom-free periods.
Auscultation of the lungs may reveal wheezing when asthma is symptomatic.
Diagnostic Testing
Acute asthma exacerbation
Peak expiratory flow (PEF) assessment:
Best method for assessment of severity of asthma attack
Normal values vary with size and age
PEF rate <200 L/min indicates severe obstruction for most adults
Serial PEF measurements are effective tools in assessment of patient’s response to therapy
Transcutaneous pulse oximetry:
PEF is a poor predictor of hypoxemia and thus transcutaneous pulse oximetry may be necessary
Supplemental oxygen is administered to maintain oxygen saturations >90%
Arterial blood gas (ABG):
PEF is a useful screening tool for the presence of hypercapnia
Hypercapnia typically develops when PEF <25% of normal
ABG is indicated with PEF remains <25% predicted after initial treatment
Most patients initially have a low PaCO2 secondary to hyperventilation
Normal or elevated PaCO2 indicates inability of the respiratory system to increase ventilation as needed because of severe airway obstruction, increased dead space ventilation, and/or respiratory muscle fatigue
Rising PaCO2 is concerning for impending respiratory failure
Imaging
CXR can be obtained and most frequently reveals hyperinflation.
Obtaining CXRs in the setting of asthma exacerbation should be limited to patients with suspected complications or significant comorbidities.1
Pneumothorax, pneumomediastinum, pneumonia, and atelectasis are sometimes found on CXRs obtained from patients presenting to ER with an asthma exacerbation.
Chronic asthma
Pulmonary function tests (PFTs) are essential for diagnosing asthma.
PFTs demonstrate an obstructive pattern, the hallmark of which is a decrease in expiratory flow rates.
Reduction in the forced expiratory volume over 1 second (FEV1) and a proportionally smaller reduction in the forced vital capacity (FVC), result in a decreased FEV1/FVC ratio (generally <0.70).
With mild obstructive disease that involves only the small airways, the FEV1/FVC ratio may be normal, and the only abnormality may be a decrease in airflow at midlung volumes (forced expiratory flow, 25–75%).
Lung hyperinflation causes an increased residual volume and increased residual volume–total lung capacity ratio.
The flow–volume loop demonstrates a decreased flow rate for any lung volume and is useful to rule out other causes of dyspnea, such as upper airway obstruction or restrictive lung disease.
The diagnosis of asthma is supported by an obstructive pattern that improves after bronchodilator therapy, defined as an increase in FEV1 of >12% and 200 mL after 2–4 puffs of a short-acting bronchodilator.
In patients with chronic, severe asthma with airway remodeling, the airflow obstruction may no longer be completely reversible.
An alternative method of establishing the maximal degree of airway reversibility is to repeat the spirometry after a course of oral corticosteroids (usually prednisone 40 mg/d PO in adults for 10 days).
Lack of demonstrable airway obstruction or bronchodilator reversibility does not rule out a diagnosis of asthma.
When the spirometry is normal, demonstrating heightened airway responsiveness to a methacholine or exercise bronchoprovocation challenge can substantiate the diagnosis of asthma.
Imaging: A CXR should be obtained to rule out other causes of dyspnea, cough, or wheezing in patients being evaluated for asthma.
Treatment
Acute Exacerbations
Indications for hospitalization and level of care:
Patient response to initial treatment (60–90 minutes after three treatments with short-acting bronchodilator) is a better predictor of need for hospitalization than initial severity of attack.
Prompt resolution of symptoms and PEF >70% of predicted can be discharged from the ER. Because bronchospasm can recur within 72 hours, education and an asthma action plan are essential.
Admission to the hospital is recommended when PEF <50% of predicted.
Recent hospitalization, failure of aggressive outpatient management (using oral corticosteroids), and history of life-threatening exacerbation should all prompt consideration for admission.
Admission to the ICU should be considered in patients with fatigue, drowsiness, confusion, use of accessory muscles of respiration, hypercapnia, marked hypoxemia, or PEF <150 L/min.
Medications
First Line
Inhaled short-acting β-adrenergic agonists (SABAs) are the mainstay of bronchodilator therapy. The primary agent is albuterol.
Albuterol is dosed as 2.5 mg by continuous flow (updraft) nebulization every 20 minutes until improvement or toxicity.
It can also be administered in a metered-dose inhaler (MDI) as 6–12 puffs at similar dosing intervals.
MDI plus spacer allows lower dose of β-adrenergic agonist to be used and is as effective as nebulized β-adrenergic agonist when performed under direct supervision.
Systemic corticosteroids speed resolution of asthma exacerbations and should be administered to all patients with moderate or severe exacerbations, though the ideal dose is poorly defined.
Methylprednisolone 40–60 mg IV every 6 hours is the drug of choice for IV therapy.
Oral corticosteroids are as effective if given in equivalent doses (e.g., prednisone 60 mg PO every 6–8 hours).
Tapering should not begin until there is objective evidence of clinical improvement, generally 36–48 hours.
Patients initially on IV therapy should be switched to PO.
7–14-day tapering dosage of prednisone is usually prescribed in combination with an inhaled corticosteroid (ICS) to be instituted at the beginning of the tapering schedule.
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