DETERMINANTS OF NEAR FATALITY IN ACUTE SEVERE ASTHMA

PURPOSE: The data extrapolated from cases of acute severe asthma that narrowly miss being fatal may prove valuable in the identification of the factors implicated in mortality. The purpose of this study was, th erefore, to identify determinants of near fatality in patients with ac ute severe asthma. PATIENTS AND METHODS: We studied 81 patients with a cute severe asthma in whom mechanical ventilation was required. Near f atality was defined as the occurrence of respiratory arrest and/or com a necessitating emergency tracheal intubation and resuscitation. In th e cases that were not regarded as near fatal, tracheal intubation was performed electively because of deteriorating arterial blood gas value s and/or the anticipation of exhaustion. Various continuous and catego rical variables were compared in these two groups of patients. Patient s with a hyperacute attack (period from onset of attack to mechanical ventilation less than 3 hours) were specifically sought and studied to determine the impact of such a course on near fatality. RESULTS: The ''attack duration' (period from onset of attack to mechanical ventilat ion) was an important determinant of near fatality and of the subseque nt clinical course. It was shorter in the group with a near-fatal epis ode (p < 0.03), and hyperacute attacks were uniformly near fatal. The attack duration correlated positively with the duration of the require ment for mechanical ventilation (p < 0.01). A longer attack duration w as associated with an increased likelihood of the occurrence of major atelectasis (p < 0.01). There was no evidence of a relationship betwee n near fatality and the side effects of bronchodilators as regards hyp okalemia, arrhythmias, or cardiotoxicity. There was evidence of consid erable under-treatment in the patient population as a whole, particula rly in regard to the use of corticosteroids. CONCLUSIONS: A short atta ck duration is associated with an increased risk of near fatality in a cute severe asthma. This is particularly evident in hyperacute attacks . Hyperacute attacks resolve rapidly once bronchodilator therapy has b een instituted, suggesting that smooth muscle spasm is the predominant pathogenetic mechanism. The importance of routine anti-inflammatory t herapy in mild to moderate asthma requires re-emphasis but, in additio n, all patients should be provided with, and educated in the use of, b ronchodilator rescue therapy, which should be available at all times. Despite current trends, the use of regular, prophylactic bronchodilato r therapy in strict conjunction with anti-inflammatory agents may stil l be indicated. There is little evidence in the present data obtained from near-fatal cases to support the concept that cardiotoxicity relat ed to bronchodilators contributes significantly to mortality from asth ma.