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Questions:

1. What signs and symptoms are consistent with acute bronchial obstruction?
 Symptoms include episodes of dyspnea, chest tightness, coughing (particularly at night),
wheezing, or a whistling sound when breathing. These often occur with exercise but
may occur spontaneously or in association with known allergens.
 Signs include expiratory wheezing on auscultation; dry, hacking cough; and atopy (eg,
allergic rhinitis or eczema)

2. What additional tests would be helpful in assessing the extent of pulmonary obstruction in this
patient?

CHRONIC ASTHMA

 Diagnosis is made primarily by history of recurrent episodes of coughing, wheezing, chest


tightness, or shortness of breath and confirmatory spirometry.
 Patients may have family history of allergy or asthma or symptoms of allergic rhinitis. History of
exercise or cold air precipitating dyspnea or increased symptoms during specific allergen
seasons suggests asthma.
 Spirometry demonstrates obstruction (forced expiratory volume in 1 second [FEV1]/ forced vital
capacity [FVC] <80%) with reversibility after inhaled β2-agonist administration (at least 12%
improvement in FEV1). If baseline spirometry is normal, challenge testing with exercise,
histamine, or methacholine can be used to elicit BHR.

ACUTE SEVERE ASTHMA

 Peak expiratory flow (PEF) and FEV1 are less than 40% of normal predicted values. Pulse
oximetry reveals decreased arterial oxygen and O2 saturations. The best predictor of outcome is
early response to treatment as measured by improvement in FEV1 at 30 minutes after inhaled
β2-agonists.
 Arterial blood gases may reveal metabolic acidosis and low partial pressure of oxygen (PaO2).
 History and physical examination should be obtained while initial therapy is provided. History of
previous asthma exacerbations (eg, hospitalizations, intubations) and complicating illnesses (eg,
cardiac disease, diabetes) should be documented. Patient should be examined to assess
hydration status; use of accessory muscles of respiration; and the presence of cyanosis,
pneumonia, pneumothorax, pneumomediastinum, and upper airway obstruction. Complete
blood count may be appropriate for patients with fever or purulent sputum.

3. Which clinical test is predictive of the need for admission or whether she will relapse if sent
home from the emergency department?
 Patients at high risk for a fatal attack require immediate medical attention after initial
treatment.
 Symptoms and signs suggestive of a more serious exacerbation such as marked
breathlessness, inability to speak more than short phrases, use of accessory muscles, or
drowsiness should result in initial treatment while immediately consulting with a
clinician.
 Less severe signs and symptoms can be treated initially with assessment of response to
therapy and further steps as listed below.
 •If available, measure PEF—values of 50%–79% predicted or personal best indicate the
need for quick-relief mediation. Depending on the response to treatment, contact with
a clinician may also be indicated. Values below 50% indicate the need for immediate
medical care.

4. Why was SABA selected as the bronchodilator of first choice in preference to other
bronchodilators such as aminophylline or ipratropium?
 Short-acting β2-agonists are the most effective bronchodilators. Aerosol administration
enhances broncho selectivity and provides more rapid response and greater protection
against provocations (eg, exercise, allergen challenges) than systemic administration.
 Albuterol and other inhaled short-acting selective β2-agonists are indicated for
intermittent episodes of bronchospasm and are the treatment of choice for acute
severe asthma and EIB. Regular treatment (four times daily) does not improve symptom
control over as-needed use.
 In acute severe asthma, continuous nebulization of short-acting β2-agonists (eg,
albuterol) is recommended for patients having unsatisfactory response after three
doses(every 20 min) of aerosolized β2-agonists and potentially for patients presenting
initially with PEF or FEV1 values less than 30% of predicted normal.
 Theophylline appears to produce bronchodilation through nonselective
phosphodiesterase inhibition. Methylxanthines are ineffective by aerosol and must be
taken systemically (orally or IV). Sustained-release theophylline is the preferred oral
preparation, whereas its complex with ethylenediamine (aminophylline) is the
preferred parenteral product due to increased solubility. IV theophylline is also
available.
 Ipratropium bromide and tiotropium bromide produce bronchodilation only in
cholinergic-mediated bronchoconstriction. Anticholinergics are effective
bronchodilators but are not as effective as β2-agonists. They attenuate but do not block
allergen or exercise-induced asthma in a dose-dependent fashion.

5. Should Q.C. receive corticosteroid therapy as part of her ED management?


• Inhaled corticosteroids are the preferred long-term control therapy for persistent
asthma because of potency and consistent effectiveness; they are the only therapy
shown to reduce risk of dying from asthma. Comparative doses are included in Table
77–3. Most patients with moderate disease can be controlled with twice-daily dosing;
some products have once-daily dosing indications. Patients with more severe disease
require multiple daily dosing. Because inflammation inhibits steroid receptor binding, patients
should be started on higher and more frequent doses and then tapered
down once control has been achieved. Response to inhaled corticosteroids is delayed;
symptoms improve in most patients within the first 1 to 2 weeks and reach maximum
improvement in 4 to 8 weeks. Maximum improvement in FEV1 and PEF rates may
require 3 to 6 weeks.
• Systemic toxicity of inhaled corticosteroids is minimal with low to moderate doses,
but risk of systemic effects increases with high doses. Local adverse effects include
dose-dependent oropharyngeal candidiasis and dysphonia, which can be reduced by
using a spacer device.
• Systemic corticosteroids (Table 77–4) are indicated in all patients with acute severe
asthma not responding completely to initial inhaled β2
-agonist administration
(every 20 min for 3 or 4 doses). Prednisone, 1 to 2 mg/kg/day (up to 40–60 mg/
day), is administered orally in two divided doses for 3 to 10 days. Because short-term
(1–2 week), high-dose systemic steroids do not produce serious toxicities, the ideal
method is to use a short burst and then maintain appropriate long-term control
therapy with inhaled corticosteroids.
• In patients who require chronic systemic corticosteroids for asthma control, the
lowest possible dose should be used. Toxicities may be decreased by alternate-day
therapy or high-dose inhaled corticosteroids

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