Classification of severe asthma exacerbations: a proposal.
The intensity of asthma exacerbations may vary from mild to severe. Many studies have demonstrated that the speed at which severe asthma exacerbation (SAE) develops varies among patients. In some asthmatics, the exacerbation comes on very quickly, whereas in others there is a progressive deterioration of clinical, functional and blood gas parameters. Sudden SAE are characterised by their explosive presentation and quick recovery. This evolution contrasts with that of patients with a slow onset SAE, who often need prolonged hospitalization. Absence of secretions suctioned from the airways during mechanical ventilation has been reported in sudden SAE, whereas large amounts of viscid mucus are found in patients with the slow onset SAE. The lungs of patients who died during a sudden onset SAE often show empty airways and a predominant neutrophilic infiltration in the bronchial epithelium, in contrast to the presence of abundant eosinophils in patients who died during a slow onset SAE. Sudden onset SAE may occur as sporadic cases or in outbreaks. Sporadic cases may result from the ingestion of nonsteroidal anti-inflammatory drugs (NSAID) in patients with intolerance to these products, massive exposure to common allergens and ingestion of foods containing sulphites. Asthma outbreaks have been described in many cities. In contrast to sudden onset SAE, slow onset SAE is characterized by a progressive deterioration, accompanied by an increase in the use of bronchodilators. Lack of appropriate monitoring of function by peak expiratory flow (PEF) recording, failure of patients to recognize worsening symptoms and underusage of inhaled and oral steroid treatment have been repeatedly identified as factors which are likely to be associated with slow onset SAE. The contribution of psychosocial problems, depression, denial of asthma severity and nonadherence with the treatment should not be overlooked in patients with slow onset SAE. Classification of severe asthma exacerbations into two types (sudden onset and slow onset) could help to reveal the aetiology of the attack and may also be relevant to the management of the patient.
Picado
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Servei de Pneumologia, Hospital Clinic, Barcelona, Spain.
D000280:Administration, Inhalation; D000284:Administration, Oral; D000485:Allergens / Q000009:adverse effects; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects; D001980:Bronchi / Q000473:pathology; D001993:Bronchodilator Agents / Q000627:therapeutic use; D002245:Carbon Dioxide / Q000097:blood; D004196:Disease Outbreaks; D018450:Disease Progression; D004804:Eosinophils / Q000473:pathology; D004848:Epithelium / Q000473:pathology; D005512:Food Hypersensitivity / Q000150:complications; D006760:Hospitalization; D006801:Humans; D009093:Mucus / Q000502:physiology; D009504:Neutrophils / Q000473:pathology; D010100:Oxygen / Q000097:blood; D010349:Patient Compliance; D010366:Peak Expiratory Flow Rate; D012121:Respiration, Artificial; D013224:Status Asthmaticus / Q000097:blood / Q000145:classification* / Q000188:drug therapy / Q000473:pathology / Q000503:physiopathology; D013256:Steroids / Q000008:administration & dosage / Q000627:therapeutic use; D013396:Suction; D013447:Sulfites / Q000009:adverse effects
D000485:Allergens; D000894:Anti-Inflammatory Agents, Non-Steroidal; D001993:Bronchodilator Agents; D013256:Steroids; D013447:Sulfites; D002245:Carbon Dioxide; D010100:Oxygen