Asthma
Asthma: Excerpt from Handbook of Diseases
A reversible lung disease, asthma is characterized by obstruction or narrowing of the airways, which are typically inflamed and hyperresponsive to various stimuli. It may resolve spontaneously or with treatment.
Causes
AGE ALERT: 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 boys as girls. The sex ratio equalizes by age 30.
Extrinsic and intrinsic asthma
Asthma that results from sensitivity to specific external allergens is referred to as extrinsic (atopic). In those cases where the allergen isn’t obvious, asthma is referred to as intrinsic (nonatopic). 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 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.
With intrinsic asthma, no extrinsic allergen can be identified. Most cases are preceded by a severe respiratory tract infection. Irritants, emotional stress, fatigue, exposure to noxious fumes, and endocrine, temperature, and humidity changes may aggravate intrinsic asthma attacks.
For many asthmatics, intrinsic and extrinsic asthma coexist.
Other asthma triggers
Several drugs and chemicals may provoke an asthma attack without using the IgE pathway. Apparently, they trigger release of mast cell mediators via 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. With exercise-induced asthma, bronchospasm may follow heat and moisture loss in the upper airways.
Two-phase allergic response
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.
Signs and symptoms
An acute asthma attack begins dramatically, with simultaneous onset of severe multiple symptoms, or insidiously, with gradually increasing respiratory distress. Asthma that occurs with cyanosis, confusion, and lethargy indicates the onset of life-threatening status asthmaticus and respiratory failure. Symptoms of bronchial airway obstruction may persist between acute episodes.
Signs and symptoms of asthma include:
sudden dyspnea, wheezing, and tightness in the chest
coughing that produces thick, clear, or yellow sputum
tachypnea, along with use of accessory respiratory muscles
rapid pulse
profuse perspiration
hyperresonant lung fields
diminished breath sounds.
In 1997, the National Heart, Lung, and Blood Institute of the National Institutes of Health identified four levels of asthma severity based on the frequency of symptoms and exacerbations, effects on activity level, and lung function study results: mild intermittent, mild persistent, moderate persistent, and severe persistent.
Findings for mild intermittent asthma include the following:
Symptoms occur less than twice per week.
The patient is asymptomatic with normal peak expiratory flow (PEF) between exacerbations.
Brief exacerbations (from a few hours to a few days) vary in intensity.
Nighttime symptoms occur less than twice per month.
Lung function studies show forced expiratory volume in 1 second (FEV1) or PEF greater than 80% of normal values; PEF may vary by less than 20%.
Findings for mild persistent asthma include the following:
Symptoms occur more than twice per week, but less than once per day; exacerbations may affect activity.
Nighttime symptoms occur more than twice per month.
Lung function studies show FEV1 or PEF greater than 80% of normal values; PEF may vary by 20% to 30%.
Findings for moderate persistent asthma include the following:
Symptoms occur daily.
Exacerbations occur more than twice per week and may last for days; exacerbations affect activity.
A bronchodilator is used daily.
Nighttime symptoms occur more than once per week.
Lung function studies show FEV1 or PEF 60% to 80% of normal values; PEF may vary by greater than 30%.
Findings for severe persistent asthma include the following:
Symptoms occur on a continuous basis.
Exacerbations occur frequently and limit physical activity.
Nighttime symptoms occur frequently.
Lung function studies show FEV1 or PEF less than 60% of normal values; PEF may vary by greater than 30%.
Diagnosis
Laboratory tests in patients with asthma commonly show these abnormalities:
Pulmonary function studies reveal signs of airway obstruction (decreased PEF and FEV1), low-normal or decreased vital capacity, and increased total lung and residual capacity. However, pulmonary function studies may be normal between attacks. Reversitility of 15% or greater increase in FEV1 after two puffs of a beta2-adrenergic agonist confirms diagnosis.
Other supportive tests include:
Pulse oximetry may reveal decreased arterial oxygen saturation (Sao2).
Arterial blood gas (ABG) analysis provides the best indication of an attack’s severity. With acutely severe asthma, the partial pressure of arterial oxygen (Pao2) is less than 60 mm Hg, the partial pressure of arterial carbon dioxide (Paco2) is 40 mm Hg or more, and the pH is usually decreased.
Complete blood count with differential reveals an increased eosinophil count.
Chest X-rays may show hyperinflation with areas of focal atelectasis or may be normal.
Bronchial provocation studies, in which an attack is induced to a stimulus, may also be done; if a reaction is positive, the attack is reversed through drug administration.
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 epiglottiditis.
Treatment
Acute asthma is treated by decreasing bronchoconstriction, reducing bronchial airway edema, and increasing pulmonary ventilation. Treatment after an acute episode includes avoiding or removing precipitating factors, such as environmental allergens or irritants.
If asthma is 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, an antibiotic is prescribed. Drug therapy for asthma is typically based on the severity of the disease. Correcting asthma typically involves:
prevention, by identifying and avoiding precipitating factors such as environmental allergens or irritants, which is the best treatment
desensitization to specific antigens — helpful if the stimuli can’t be removed entirely — which decreases the severity of attacks of asthma with future exposure
bronchodilator therapy — including a methylxanthine (theophylline or aminophylline) and a beta2-adrenergic agonist (albuterol or terbutaline) — to decrease bronchoconstriction, reduce bronchial airway edema, and increase pulmonary ventilation
corticosteroid therapy (such as hydrocortisone sodium succinate, prednisone, methylprednisolone, and beclomethasone), which decreases inflammation and edema of the airways
mast cell stabilizer therapy (cromolyn sodium and nedocromil sodium), effective in patients with atopic asthma who have seasonal disease (When given prophylactically, they block the acute obstructive effects of antigen exposure by inhibiting the degranulation of mast cells, thereby preventing the release of chemical mediators responsible for anaphylaxis.)
anticholinergic bronchodilator therapy (such as ipratropium), which blocks acetylcholine, another chemical mediator
therapy with a leukotriene modifier, such as zileuton (Zyflo), or a leukotriene receptor antagonist, such as Montelukast (Singulair) and zafirlukast (Accolate), to inhibit the potent bronchoconstriction and inflammatory effects of the cysteinyl leukotrienes. Leukotriene receptor antagonists can be used as adjunctive therapy to avoid high-doses of inhaled corticosteroids. Although this class of drugs doesn’t replace inhaled corticosteroids as first-line anti-inflammatory treatment, they can be used successfully in a patient where poor compliance with inhaled corticosteroid therapy is suspected.
low-flow humidified oxygen, which may be needed to treat dyspnea, cyanosis, and hypoxemia (However, the amount delivered should maintain Pao2 between 65 and 85 mm Hg, as determined by ABG analysis.)
mechanical ventilation — necessary if the patient doesn’t respond to initial ventilatory support and drugs, or develops respiratory failure
relaxation exercises, such as yoga, to help increase circulation and to help a patient recover from an asthma attack.
Special considerations
During an acute attack, perform the following:
First assess the severity of the 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 and that tachycardia may indicate worsening asthma or drug toxicity. Blood pressure readings may reveal paradoxical pulse, 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 values.
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 the patient for signs and symptoms of theophylline toxicity (including vomiting, diarrhea, and headache) as well as for signs of subtherapeutic dosage (such as respiratory distress and increased wheezing).
Observe the frequency and severity of the patient’s cough, and note whether it’s productive. Then auscultate his lungs, noting adventitious or absent 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 the area of collapse is a lobe or larger.
During long-term care, perform the following:
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 a systemic corticosteroid, monitor him for complications, such as elevated blood glucose levels and friable skin and bruising. (Cushingoid effects resulting from long-term use of a corticosteroid may be minimized by alternate-day dosage or use of a prescribed inhaled corticosteroid.)
If the patient is taking an inhaled corticosteroid, watch for signs of candidal infection in the mouth and pharynx. Using an extender device and rinsing the mouth afterward may prevent this.
CLINICAL TIP: For patients with moderate to severe chronic disease, regular use of an extender device may facilitate better delivery of inhaled medications.
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 sodium 30 minutes before exercise. Also, instruct him to use pursed-lip breathing while exercising.
For all patients with asthma, perform the following:
Teach the patient and his family to avoid known allergens and irritants.
Describe prescribed drugs, including their names, dosages, actions, adverse effects, and special instructions.
Teach the patient how to use a metered-dose inhaler. (See Using a metered-dose inhaler, page 80.) If he has difficulty with it, he may need an extender device to optimize drug delivery and lower the risk of candidal infection that’s normally associated with orally inhaled corticosteroids.
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. (A drop can signal severe respiratory problems.)
Tell the patient to notify the physician if he develops a temperature higher than 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 the patient to drink at least 3 qt (3 L) of fluids daily to help loosen secretions and maintain hydration. Pictures
Book Source Details
- Book Title: Handbook of Diseases
- Author(s): Springhouse
- Year of Publication: 2003
- Copyright Details: Handbook of Diseases, Copyright © 2003 Lippincott Williams & Wilkins.
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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More About This Book:
Title: Handbook of Diseases
Authors: Springhouse
Publisher: Lippincott Williams & Wilkins
Copyright: 2003
ISBN: 1-58255-266-5
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» Next page: Stridor (Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)
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