Asthma
A chronic reactive airway disorder, asthma involves episodic, reversible airway obstruction resulting from bronchospasms, increased mucus secretions, and mucosal edema. Signs and symptoms range from mild wheezing and dyspnea to life-threatening respiratory failure. Signs and symptoms of bronchial airway obstruction may or may not persist between acute episodes.
Pediatric pointerAlthough this common respiratory condition can strike at any age, about half of all patients with asthma are younger than age 10. In this age-group, asthma affects twice as many boys as girls. About one-third of patients experience asthma’s onset between ages 10 and 30; in this group, incidence is the same in both sexes. Hereditary factors are also important: About one-third of all patients with asthma share the disease with at least one immediate family member.
Asthma may result from sensitivity to specific external allergens (extrinsic) or from internal, nonallergenic factors (intrinsic). Allergens that cause extrinsic asthma (atopic asthma) include pollen, animal dander, house dust or mold, kapok or feather pillows, food additives containing sulfites, and any other sensitizing substance. Extrinsic asthma begins in childhood and is commonly accompanied by other manifestations of atopy (Type I, immunoglobulin [Ig] E-mediated [IgE-mediated] allergy), such as eczema and allergic rhinitis.
In intrinsic asthma (nonatopic asthma), no extrinsic substance can be identified. Most episodes are preceded by a severe respiratory tract infection (especially in adults). Irritants, emotional stress, fatigue, endocrine changes, temperature and humidity variations, and exposure to noxious fumes may aggravate intrinsic asthma attacks. In many asthmatics, especially children, intrinsic and extrinsic asthma coexist.
Causes
In asthma, the tracheal and bronchial linings overreact to various stimuli, causing episodic smooth-muscle spasms that severely constrict the airways. Mucosal edema and thickened secretions further block the airways.
IgE antibodies, attached to histamine-containing mast cells and receptors on cell membranes, initiate intrinsic asthma attacks. When exposed to an antigen such as pollen, the IgE antibody combines with the antigen. On subsequent exposure to the antigen, mast cells degranulate and release mediators.
These mediators cause the bronchoconstriction and edema of an asthma attack. As a result, expiratory airflow decreases, trapping gas in the airways and causing alveolar hyperinflation. Atelectasis may develop in some lung regions. The increased airway resistance initiates labored breathing.
Several factors may contribute to bronchoconstriction. These include hereditary predisposition, sensitivity to allergens or irritants such as pollutants, viral infections, tartrazine (a yellow food dye), psychological stress, cold air, exercise, and aspirin, beta-adrenergic blockers,
nonsteroidal anti-inflammatory drugs, and other drugs.
nonsteroidal anti-inflammatory drugs, and other drugs.
Complications
Asthma can produce rib fractures, pneumonia, and atelectasis as well as status asthmaticus and respiratory failure, which are life-threatening complications. (See Responding to status asthmaticus.)
Pediatric pointerPay attention to children at high risk for asthma-related death. Risk factors include more than two hospitalizations or more than three emergency department visits in the month before the asthma attack. Current use of or recent withdrawal from corticosteroids is another risk factor.
Assessment
An asthma attack may begin dramatically, with simultaneous onset of severe, multiple symptoms, or insidiously, with gradually increasing respiratory distress. Typically, the patient reports exposure to a particular allergen followed by a sudden onset of dyspnea, wheezing, and tightness in the chest accompanied by a cough that produces thick, clear or yellow sputum.
The patient may complain of feeling suffocated. He may be visibly dyspneic and able to speak only a few words before pausing to catch his breath. You may also see him using accessory respiratory muscles to breathe. He may sweat profusely, and you may observe an increased anteroposterior thoracic diameter.
Percussion may produce hyperresonance. Palpation may reveal vocal fremitus. Auscultation may disclose tachycardia, tachypnea, mild systolic hypertension, harsh respirations with inspiratory and expiratory wheezes, prolonged expiratory phase of respiration, and diminished breath sounds.
Cyanosis, confusion, and lethargy indicate the onset of life-threatening status asthmaticus and respiratory failure.
Pediatric pointerA child with moderate or severe asthma is often unable to lie flat. Early symptoms of asthma exacerbation in a child include a scratchy throat, tightness in the throat, headache, earache, and a puffy face.
Diagnostic tests
Pulmonary function studies reveal signs of airway obstructive disease (decreased flow rates and forced expiratory volume in 1 second [FEV1]), low-normal or decreased vital capacity, and increased total lung and residual capacities. Despite abnormal findings during asthmatic episodes, pulmonary function may be normal between attacks.
Typically, the patient has decreased partial pressure of arterial oxygen (PaO2) and partial pressure of arterial carbon dioxide (PaCO2). However, in severe asthma, PaCO2 may be normal or increased, indicating severe bronchial obstruction. In fact, FEV1 will probably be less than 25% of the predicted value. Initiating treatment tends to improve the airflow. However, even when the asthma attack appears controlled, the spirometric values (FEV1 and forced expiratory flow) remain abnormal (between 25% and 75% of vital capacity), necessitating frequent arterial blood gas (ABG) analyses or pulse oximetry measurements. Residual volume remains abnormal for the longest period—up to 3 weeks after the attack.
