I thank Dr. Perel for his interest in my editorial.1He raises the question as to whether the presence of sepsis alters the effect of positive end-expiratory pressure (PEEP) on oxygenating capacity in patients with adult respiratory distress syndrome. Based on his own studies published in the late 1970s,2,3he gives a positive answer and argues that such a result supports the concept that the cause of adult respiratory distress syndrome influences the effectiveness of PEEP and contradicts Thille et al. ’s study.4Going all the way through his belief, he proposes to use the effect of PEEP on oxygenating capacity as a diagnostic test to determine whether adult respiratory distress syndrome is septic.
The body of evidence supporting Dr. Perel’s statement is small. The retrospective study he refers to2,3concerns a very heterogeneous population of 57 hypoxemic patients (23 with multiple trauma, 21 with sepsis, 6 who underwent cardiopulmonary bypass, 4 with left heart failure, 2 with acid aspiration, and 1 with cervical chord injury) and suggests that when severe hypoxemia is associated with or caused by sepsis, the increase in arterial oxygenation after the administration of a small PEEP (5.7 ± 1.2 mH2O) is less than that in the absence of sepsis. The heterogeneity of the patients studied (adult respiratory distress syndrome and cardiogenic pulmonary edema); the lack of any attempt made to optimize PEEP; and the absence of measurement of cardiac output, cardiac filling pressures, mixed venous oxygen saturation, pulmonary shunt, and alveolar recruitment preclude any analysis of the mechanisms involved in the observed difference. In addition, the second article,3which is similar to the first,2focuses on the 23 patients of the series, in whom lung injury was the result of traumatic lung contusion. It is well known that the initial phase of severe lung contusion can be characterized by severe hypoxemia, sometimes refractory to conventional means and requiring nonconventional mechanical ventilation.5If the patient survives the initial phase, however, there is a rapid and spectacular improvement in arterial oxygenation related to blood clearance from the alveolar space allowing early extubation and spontaneous breathing. If, for extrapulmonary reasons, the patient cannot be extubated, then a second direct insult to the lung rapidly occurs, ventilator-associated pneumonia. In fact, the late deterioration reported by Perel et al. 3has nothing to do with “the cause of adult respiratory distress syndrome” but is related to the impossibility of weaning the patient from mechanical ventilation for extrapulmonary reasons.
Among the most convincing data pleading against the hypothesis that the septic lung recruits less than the nonseptic lung are those recently published by Gattinoni himself, the initiator of the theory that patients with pulmonary adult respiratory distress syndrome caused by lung infection potentially have a much higher recruitable lung capacity than patients with extrapulmonary adult respiratory distress syndrome.6Because of the lack of evidence supporting Dr. Perel’s assertions, his clinical recommendations should be taken with caution. Unless new convincing data are provided, the non-response to PEEP should not be interpreted by clinicians in charge of patients with adult respiratory distress syndrome as an indirect sign of lung injury associated with or caused by sepsis.