ASTHMA



Asthma has been defined as a disease in which there is an increased responsiveness of the air­ways to various stimuli, causing widespread nar­rowing of the airways which varies over time. The stimulus may be immunologic in origin, as in classic extrinsic asthma, in which mast cells, sensi­tized by IgE antibodies, degranulate and release bronchoactive mediators following exposure to a specific antigen. The cause may also be unclear, as in adult-onset asthma, in which the patients frequently show no evidence of allergy. The air­way obstruction may be due to bronchoconstric-tion alone or may involve mucosal inflammation and excessive mucus production. Symptoms may be intermittent, or they may gradually become persistent. The recognized categories of asthma are listed in Table 19-2. Clinical differentiation is important only in situations in which there are clear-cut, easily identifiable, and avoidable ex­trinsic factors, such as drugs or industrial sub­stances.

The diagnosis of asthma is based on the pres­ence of episodic dyspnea associated with wheez­ing. Intermittent cough, probably due to stimu­lation of the irritant receptors, is the sole presenting symptom in some patients. Typically, symptoms are worse at night, following exercise, after going out in the cold, while exposed to ir­ritating gases, etc.

Laboratory studies may be required to deter­mine the presence of specific types of asthma (Table 19-3). The chest x-ray demonstrates hy­perinflation in the symptomatic patient, while in patients with allergic bronchopulmonary asper­gillosis, serial films may show infiltrates that change location or features suggestive of central bronchiectasis. Pulmonary function studies show the findings of obstruction, which improve sig­nificantly following the acute administration of bronchodilators. During the asymptomatic phase, the diagnosis can often be made by producing ob­struction by the inhalation of histamine, metha­choline, or cold air.
Acute severe asthma (status asthmaticus) refers to an attack of increased severity that is unres­ponsive to routine therapy. While the attack is sometimes prolonged, fatal episodes may occur unexpectedly with overwhelming suddenness. A history of increasing bronchodilator use with lit­tle benefit is expected, but clinical signs, includ­ing pulsus paradoxus, are extremely unreliable.in judging the severity. The degree of physiological disturbance can best be appreciated by a measure of expiratory flow rates. In the emergency room management of these patients such indices are very helpful in assessing the response to therapy, as they provide immediate quantitative informa­tion and can be obtained at frequent intervals without discomfort. Complementary information can be obtained by measurement of arterial blood gases, and this may be the only measurement pos­sible in the critically ill asthmatic. Hypoxemia is usually, but not invariably, present, and Paco2 is typically reduced early in an attack. With increas­ing severity, Pao2 falls and Paco2 returns to normal and then rises, accompanied by a mixed respi­ratory and metabolic acidosis, such that intuba­tion and mechanical ventilation may become nec­essary. Hypercapnia at presentation is not an indication for intubation, as most patients im­prove, but careful monitoring is essential. In gen­eral, arterial blood gas measurements are less sen­sitive and specific than assessment of airway obstruction in judging the response to therapy.