Asthma, a chronic inflammatory disorder of the airways. It is characterized .by episodic airway narrowing, increased air-way reactivity to a variety of stimuli, and pharmacologic or spontaneous reversibility. The inflammatory response involves mast cells, T lymphocytes, and eosinophils, which produce multiple soluble mediators (e. g. , cytokines, leukotrienes, and bradykinins). An imbalance in proinflammatory versus in-hibitory cytokines may be a fundamental part of the pathogen-esis of asthma. The histologic findings in asthma are airway cellular infiltration, epithelial disruption, mucosal edema, and mucus plugging. The trigger or stimulus that provokes the in-flammatory response may be exposure to extrinsic allergens or intrinsic host factors with no identifiable external cause. Even in people with no history of asthma, viral respiratory infection is occasionally associated with increased airway reactivity for several weeks to months after resolution of the infection; some of these persons develop chronic asthma. When a clear envi-ronmental trigger for asthmatic attacks can be identified, it can be avoided, or, in some cases, irnmunotherapy can desensitize the patient to the allergen. Some nonallergic factors that can precipitate or exacerbate asthma include postnasal drip, gastroesophageal reflux disease, exposure to cold, exercise, exposure to gases or fumes, emotional stress, hormones, and respiratory infections.

The diagnosis of asthma is based on clinical and laboratory data. The classic triad of symptoms is persistent wheeze, chronic episodic dyspnea, and chronic cough. Other associated symptoms are sputum production and chest pain or tightness. If hemoptysis is present, Churg-Strauss vasculitis, allergic bronchopulmonary aspergillosis, or bronchiectasis should be suspected as underlying causes. Patients may present with only one or a combination of the foregoing symptoms. Symptoms may be worse or only present at night.

Diagnostic testing can aid in confirming the diagnosis of asthma and in assessing the severity of an acute exacerbation and the reversibility of air flow obstruction (Table 5). Migra-tory infiltrates on serial chest radiographs, coupled with bron-chospasm and expectoration, of mucus plugs suggest the diag-nosis of allergic bronchopulmonary aspergillosis. Provocation testing with methacholine or histamine may detect bronchial hyperreactivity and can establish the diagnosis of asthma when results of routine pulmonary function tests are normal. The management of asthma requires education and coop-eration on the part of the patient. Simple, inexpensive peak expiratory flow meters can be used by the patient at home to monitor air flow obstruction. A diary should be maintained. and a clear plan should be in place for using the information to intervene early in exacerbations and to alter long-term therapy for optimal control of symptoms. The cornerstone of mainte-nance therapy is scheduled administration of inhaled corticos-teroids. Long-acting and short-acting bronchodilators are added for additional symptomatic control as needed. Leukotriene inhibitors have been shown to be effective in maintenance therapy. Debate is ongoing about the relative effi-cacy of leukotriene antagonists versus inhaled corticosteroids may have additional beneficial effects in some patients, but the narrow therapeutic window and modest efficacy of these prepa-rations limit their value.

Acute severe asthma, or status asthmaticus, is an attack of severe bronchospasm that is unresponsive to routine thera-py. Such attacks may be sudden (hyperacute asthma) and may be rapidly fatal, often before medical care can be obtained. In most cases, however, patients have a history of progressive dyspnea over hours to days, with increasing bronchodilator use. Patients with severe exacerbations may 1. have difficulty in talking, 2. use accessory muscles of inspiration, 3. have a pulsus paradoxus, 4. have orthopnea, 5. be diaphoretic, or 6. have mental status changes ranging from agitation to somno-lence. In patients with these findings, treatment should be im-mediate and aggressive, with continuous monitoring of blood oxygen saturation by pulse oximetry, supplemented by arterial blood gas analysis to evaluate hypercarbia. Peak expiratory flow rates should be measured frequently to assess response to therapy. In patients who are unable to perform peak expirato-ry flow maneuvers and in those who have declining mental sta-tus or who appear to be worsening clinically, arterial blood gas analysis is essential. The arterial blood gas analysis in patients with mild attacks or early in the course of a severe attack shows hypoxemia (a widened alveolar--arterial oxygen gradi-ent) and hyperventilation (a decreased PaCO2). With increas-ing severity or respiratory muscle fatigue, the PaCO2 returns to normal and ultimately begins to rise. A rising PaCO2 in a pa-tient with asthma is an ominous sign and may portend a medical emergency. These patients require continuous direct observation and monitoring, and many require mechanical ventilation.

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