The Changing Face of Organ Failure in ARDS: Conclusion

The Changing Face of Organ Failure in ARDS: ConclusionAPACHE II scores between the 1984-to-1990 and 1994-to-1999 patient groups were equivalent, so it is unlikely that group severity of illness was substantially different. The risk factors for the development of ARDS were not statistically different between the groups, but there was a nonstatistically greater percentage of pneumonia and sepsis (without significant changes in the contribution from trauma) in the earlier ARDS group. We recognize that the number of patients in this study may preclude finding a statistical difference in risk factors between the two groups that might be present, but this reinforces the necessity of reporting organ failure specifically in large future trials. itat on

Unidentified cointerventions may have altered organ failure distribution and therefore have affected mortality. Therapy for critically ill patients has evolved. Examples of cointerventions that may have impacted ARDS are numerous, and include permissive hypercapnea, lowered airway pressure, and reduced tidal volume during mechanical ventilation, All of these could have reduced intrathoracic pressure and led to higher cardiac output. CNS blood flow might have increased and thereby preserved neurologic function. We recognize that animal and human evidence indicate that ventilatory strategies can be important in the genesis of cytokines that cause lung damage. However, we do not have adequate ventilatory data available to assess whether more recent ventilatory strategies are responsible for the changes we observed in organ failure distributions.

Furthermore, our available data do not allow us to draw inferences regarding potential mechanisms of injury or repair. Until definitive data become available, any conclusions remain speculative.
We recognize that changes in care over time at our single center may not have reflected changes in care over time nationwide. However, many research centers have noted increased survival among ARDS patients, and the evidence suggests that mortality may have decreased since the 1970s. In addition, patients identified in the 1980s were identified using different criteria than those applied to patients in the 1990s. We accounted for this difference by comparing patients with similar oxygenation inefficiency criteria (ie, P/F).
Changes in organ failure distribution are a contributor in our environment to changes in mortality among ARDS patients. This observation may extend to the community at large. These observations of different organ failure distributions associated with different mortality rates among ARDS patients from 1987 to 1990 and from 1994 to 1999 emphasize the need for rigorous experimental design and reporting in future ARDS clinical investigations.