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Ann Thorac Surg 1999;68:2387
© 1999 The Society of Thoracic Surgeons
a Department of Surgery, Heart & Chest Research Centre, Monash Medical Centre, Melbourne, 3168 Australia
To the Editor
Mathisen and colleagues are to be congratulated on demonstrating a substantial survival benefit in patients who develop post lung resection idiopathic pulmonary edema (ARDS) treated with nitric oxide (NO) [1].
Our experience with traditional methods of management for this condition was also poor, with no survivors. We clearly demonstrate, as others have, that fluid overload was not a causative factor in the etiology of this condition [2]. However, we discovered profound oliguria as the earliest sign to occur coincident with the development of pulmonary infiltrates on the chest roentgenogram. As all of our patients had low central filling pressures, we surmised that the oliguria was secondary to intravascular volume loss into a leaky lung [2].
Given the relentless and lethal nature of this syndrome we advocated an aggressive management protocol, in addition to traditional therapy, including early intubation and, like Mathisen’s group, the use of intravenous steroids [2, 3]. The clinical impact of this approach was profound in that we had survivors.
Unlike Mathisen, however, we found no additional benefit with the use of either intravenous prostacyclin or inhaled NO. This is not to suggest that NO therapy should not be com-menced however, as we did not use NO as early or as aggres-sively as the Massachusetts General group (MGH). As Slinger recently commented, "the use of specific pulmonary vasodilators, such as NO ... is an unproven but logical therapy guided by pulmonary artery pressures" [3].
It is of particular interest as to whether the MGH group can possibly add further to our knowledge of the specific clinical, hemodynamic details. Did they encounter profound oliguria (< 30 mL/hr) in the presence of clinically dry patients at the onset of the pulmonary infiltrates? Was there hemodynamic instability at the time of intubation of patients that did not receive the iv steroids? Was there evidence of a high cardiac output state in these patients at the time of the development of the pulmonary infiltrates? Unfortunately, there is a paucity of detailed clinical details in most reports dealing with this syndrome [3].
Although this syndrome is uncommon, when correctly diagnosed, we found it to be the leading cause of postlung resection death in our series. The series from MGH reports the best treatment results published to date. It therefore encourages the early and aggressive use of NO, in addition to early intubation and the use of iv steroids, to be scientifically trialed with meticulous detail given to clinical parameters.
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