Improved prognosis of acute respiratory distress syndrome 15 years on
Objective: Evaluation of the impact of low-volume, pressure-limited ventilation on the recovery rate of acute respiratory distress syndrome (ARDS). Design: Prospective observational clinical study with historical control. Setting: University hospital intensive care unit (ICU). Patients: We studied two groups of, respectively, 33 and 37 ARDS patients separated by 15 years (“historical”, June 1978–April 1981, and “recent”, October 1993–June1996). Method: ARDS was defined as the presence of bilateral chest infiltrates and a PaO2/FIO2 ratio of less than 200 mmHg under controlled ventilation regardless of PEEP level. Any cardiac participation was excluded by right heart catheterization in the “historical” group and by echo-Doppler examination in the “recent” group. The origin of ARDS was principally pulmonary (ARDSp) in both groups (26/33 and 29/37, respectively), and secondarily extrapulmonary (ARDSexp) (7/33 and 8/37, respectively). In the “historical” group, normocapnia was the major goal for respiratory support and was achieved in all patients regardless of airway pressure levels. In contrast, end-inspiratory plateau pressure in the “recent” group was limited to 30 cmH2O under respiratory support, regardless of PaCO2 level. The “historical” and “recent” ARDS groups were compared with regard to therapeutic procedure and outcome. Results: Normalization of PaCO2 (36 ± 6 mmHg) in the “historical” group required high airway pressure (end-inspiratory plateau pressure at 39 ± 4 cmH2O) and high tidal volume (13 ml/kg). Respiratory support used in the “recent” group was less aggressive, with lower airway pressure (end-inspiratory plateau pressure 25 ± 4 cmH2O) and tidal volume (9 ml/kg) resulting in “permissive” hypercapnia (51 ± 10 mmHg).Mortality rates significantly decreased from 64 % in the “historical” group to 32 % in the “recent” group (p < 0.01). This decrease concerned only ARDSp, which was markedly predominant in both groups. Conclusion: Mortality due to ARDS of pulmonary origin has declined in our unit over the last 15 years. Low-volume, pressure-limited (protective) ventilation seems the most likely reason for improved survival, despite hypercapnia.