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 (ARDS_p) in both groups (26/33 and 29/37, respectively), and secondarily extrapulmonary (ARDS_exp) (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 ARDS_p, 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. Received: 29 December 1998 Final revision received: 28 March 1999 Accepted: 8 June 1999