Asthma

Asthma: Excerpt from Professional Guide to Diseases (Eighth Edition)

Asthma is a reversible lung disease characterized by obstruction or narrowing of the airways, which are typically inflamed and hyperresponsive to a variety of stimuli. It may resolve spontaneously or with treatment. Its symptoms range from mild wheezing and dyspnea to life-threatening respiratory failure. (See Determining asthma’s severity.) Symptoms of bronchial airway obstruction may persist between acute episodes.

Causes and incidence

Asthma that results from sensitivity to specific external allergens is known as extrinsic. In cases in which the allergen isn’t obvious, asthma is referred to as intrinsic. Allergens that cause extrinsic asthma include pollen, animal dander, house dust or mold, kapok or feather pillows, food additives containing sulfites, and any other sensitizing substance. Extrinsic (atopic) asthma usually begins in childhood and is accompanied by other manifestations of atopy (type I, immunoglobulin [Ig] E-mediated allergy), such as eczema and allergic rhinitis. In intrinsic (nonatopic) asthma, no extrinsic allergen can be identified. Most cases are preceded by a severe respiratory infection. Irritants, emotional stress, fatigue, exposure to noxious fumes as well as changes in endocrine, temperature, and humidity may aggravate intrinsic asthma attacks. In many asthmatics, intrinsic and extrinsic asthma coexist.

Several drugs and chemicals may provoke an asthma attack without using the IgE pathway. Apparently, they trigger release of mast-cell mediators by way of prostaglandin inhibition. Examples of these substances include aspirin, various nonsteroidal anti-inflammatory drugs (such as indomethacin and mefenamic acid), and tartrazine, a yellow food dye. Exercise may also provoke an asthma attack. In exercise-induced asthma, bronchospasm may follow heat and moisture loss in the upper airways.

The allergic response has two phases. When the patient inhales an allergenic substance, sensitized IgE antibodies trigger mast-cell degranulation in the lung interstitium, releasing histamine, cytokines, prostaglandins, thromboxanes, leukotrienes, and eosinophil chemotaxic factors. Histamine then attaches to receptor sites in the larger bronchi, causing irritation, inflammation, and edema. In the late phase, inflammatory cells flow in. The influx of eosinophils provides additional inflammatory mediators and contributes to local injury.

Although this common condition can strike at any age, half of all cases first occur in children younger than age 10; in this age-group, asthma affects twice as many males as females. Nearly 1 in 13 children have asthma, which is increasing worldwide. Emergency department visits, hospitalizations, and mortality from asthma have been increasing for more than 20 years, especially among children and blacks.

Signs and symptoms

An asthma attack may begin dramatically, with simultaneous onset of many severe symptoms, or insidiously, with gradually increasing respiratory distress. It typically includes progressively worsening shortness of breath, cough, wheezing, and chest tightness or some combination of these signs or symptoms.

During an acute attack, the cough sounds tight and dry. As the attack subsides, tenacious mucoid sputum is produced (except in young children, who don’t expectorate). Characteristic wheezing may be accompanied by coarse rhonchi, but fine crackles aren’t heard unless associated with a related complication. Between acute attacks, breath sounds may be normal.

The intensity of breath sounds in symptomatic asthma is typically reduced. A prolonged phase of forced expiration is typical of airflow obstruction. Evidence of lung hyperinflation (use of accessory muscles, for example) is particularly common in children. Acute attacks may be accompanied by tachycardia, tachypnea, and diaphoresis. In severe attacks, the patient may be unable to speak more than a few words without pausing for breath. Cyanosis, confusion, and lethargy indicate the onset of respiratory failure.

Diagnosis

Laboratory studies in patients with asthma commonly show these abnormalities:

❑ Pulmonary function studies reveal signs of airway obstruction (decreased peak expiratory flow rates and forced expiratory volume in 1 second), low-normal or decreased vital capacity, and increased total lung and residual capacity. However, pulmonary function studies may be normal between attacks.

❑ Pulse oximetry may reveal decreased arterial oxygen saturation (Sao₂).

❑ Arterial blood gas (ABG) analysis provides the best indications of an attack’s severity. In acutely severe asthma, the partial pressure of arterial oxygen is less than 60 mm Hg, the partial pressure of arterial carbon dioxide (Paco₂) is 40 mm Hg or more, and pH is usually decreased.

❑ Complete blood count with differential reveals increased eosinophil count.

❑ Chest X-rays may show hyperinflation with areas of focal atelectasis.

Before initiating tests for asthma, rule out other causes of airway obstruction and wheezing. In children, such causes include cystic fibrosis, tumors of the bronchi or mediastinum, and acute viral bronchitis; in adults, other causes include obstructive pulmonary disease, heart failure, and epiglottitis.

Treatment

Treatment of acute asthma aims to decrease bronchoconstriction, reduce bronchial airway edema, and increase pulmonary ventilation. After an acute episode, treatment focuses on avoiding or removing precipitating factors, such as environmental allergens or irritants.

If asthma is known to be caused by a particular antigen, it may be treated by desensitizing the patient through a series of injections of limited amounts of the antigen. The aim is to curb the patient’s immune response to the antigen.

If asthma results from an infection, antibiotics are prescribed. Drug therapy is most effective when begun soon after the onset of signs and symptoms. For relief of symptoms in adults and children older than age 5, short-acting inhaled beta₂-adrenergic agonists for bronchodilation may be used, and a course of systemic corticosteroids may be needed. The goal of therapy is asthma control with minimal or no adverse effects from medication.

Acute attacks that don’t respond to self-treatment may require hospital care, beta₂-adrenergic agonists by inhalation or subcutaneous (S.C.) injection (in three doses over 60 to 90 minutes) and, possibly, oxygen for hypoxemia. If the patient responds poorly, systemic corticosteroids and, possibly, S.C. epinephrine may help. Beta₂-adrenergic agonist inhalation continues hourly. I.V. aminophylline may be added to the regimen and I.V. fluid therapy is started. Patients who don’t respond to this treatment, whose airways remain obstructed, and who have increasing respiratory difficulty are at risk for status asthmaticus and may require mechanical ventilation.

Treatment of status asthmaticus consists of aggressive drug therapy with a beta₂-adrenergic agonist by nebulizer every 30 to 60 minutes, possibly supplemented with S.C. epinephrine, I.V. corticosteroids, I.V. aminophylline, oxygen administration, I.V. fluid therapy, and intubation and mechanical ventilation for hypercapnic respiratory failure (Paco₂ of 40 mm Hg or more). (See How status asthmaticus progresses, pages 354 and 355.)

Special considerations

During an acute attack, proceed as follows:

❑ First, assess the severity of asthma.

❑ Administer the prescribed treatments and assess the patient’s response.

❑ Place the patient in high Fowler’s position. Encourage pursed-lip and diaphragmatic breathing. Help him to relax.

❑ Monitor the patient’s vital signs. Keep in mind that developing or increasing tachypnea may indicate worsening asthma or drug toxicity. Blood pressure readings may reveal pulsus paradoxus, indicating severe asthma. Hypertension may indicate asthma-related hypoxemia.

❑ Administer prescribed humidified oxygen by nasal cannula at 2 L/minute to ease breathing and to increase Sao₂. Later, adjust oxygen according to the patient’s vital signs and ABG levels.

❑ Anticipate intubation and mechanical ventilation if the patient fails to maintain adequate oxygenation.

❑ Monitor serum theophylline levels to ensure they’re in the therapeutic range. Observe your patient for signs and symptoms of theophylline toxicity (vomiting, diarrhea, and headache), as well as for signs of subtherapeutic dosage (respiratory distress and increased wheezing).

❑ Observe the frequency and severity of your patient’s cough, and note whether it’s productive. Then auscultate his lungs, noting adventitious or absent breath sounds. If his cough isn’t productive and rhonchi are present, teach him effective coughing techniques. If the patient can tolerate postural drainage and chest percussion, perform these procedures to clear secretions. Suction an intubated patient as needed.

❑ Treat dehydration with I.V. fluids until the patient can tolerate oral fluids, which will help loosen secretions.

❑ If conservative treatment fails to improve the airway obstruction, anticipate bronchoscopy or bronchial lavage when a lobe or larger area collapses.

During long-term care, proceed as follows:

❑ Monitor the patient’s respiratory status to detect baseline changes, to assess response to treatment, and to prevent or detect complications.

❑ Auscultate the lungs frequently, noting the degree of wheezing and quality of air movement.

❑ Review ABG levels, pulmonary function test results, and Sao₂ readings.

❑ If the patient is taking systemic corticosteroids, observe for complications, such as elevated blood glucose levels and friable skin and bruising.

❑ Cushingoid effects resulting from long-term use of corticosteroids may be minimized by alternate-day dosage or use of prescribed inhaled corticosteroids.

❑ If the patient is taking corticosteroids by inhaler, watch for signs of candidal infection in the mouth and pharynx. Using an extender device and rinsing the mouth afterward may prevent this.

❑ Observe the patient’s anxiety level. Keep in mind that measures that reduce hypoxemia and breathlessness should help relieve anxiety.

❑ Keep the room temperature comfortable and use an air conditioner or a fan in hot, humid weather.

❑ Control exercise-induced asthma by instructing the patient to use a bronchodilator or cromolyn 30 minutes before exercise. Also instruct him to use pursed-lip breathing while exercising.

All patients should know the following:

❑ Teach the patient and his family to avoid known allergens and irritants.

❑ Describe to the patient prescribed drugs, including their names, dosages, actions, adverse effects, and special instructions.

❑ Teach the patient how to use a metered-dose inhaler. If he has difficulty using an inhaler, he may need an extender device to optimize drug delivery and lower the risk of candidal infection with orally inhaled corticosteroids.

❑ If the patient has moderate to severe asthma, explain how to use a peak flow meter to measure the degree of airway obstruction. Tell him to keep a record of peak flow readings and to bring it to medical appointments. Explain the importance of calling the physician at once if the peak flow drops suddenly (may signal severe respiratory problems).

❑ Tell the patient to notify the physician if he develops a fever above 100° F (37.8° C), chest pain, shortness of breath without coughing or exercising, or uncontrollable coughing. An uncontrollable asthma attack requires immediate attention.

❑ Teach the patient diaphragmatic and pursed-lip breathing as well as effective coughing techniques.

❑ Urge him to drink at least 3 qt (3 L) of fluids daily to help loosen secretions and maintain hydration.

Pictures

Book Source Details

• Book Title: Professional Guide to Diseases (Eighth Edition)
• Author(s): Springhouse
• Year of Publication: 2005
• Copyright Details: Professional Guide to Diseases (Eighth Edition), Copyright © 2005 Lippincott Williams & Wilkins.

More About Asthma

• Back to disease: Asthma: Introduction
• Next Book Extract About Asthma: Stridor (Professional Guide to Signs & Symptoms (Fifth Edition))
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.

More About This Book: Title: Professional Guide to Diseases (Eighth Edition) Authors: Springhouse Publisher: Lippincott Williams & Wilkins Copyright: 2005 ISBN: 1-58255-370-X

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