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Department of Anesthesiology Loyola University Medical Center , Maywood, Illinois 60153
We read with great interest the recent article by Sumida et al. (1) describing their work with methylprednisolone and the systemic inflammatory response syndrome. In their clinical model of intraperitoneal hyperthermic perfusion-induced systemic inflammatory response syndrome, they found that pretreatment with IV methylprednisolone (50 mg/kg, total) attenuated the increase in circulating tumor necrosis factor-
and prevented pulmonary dysfunction as assessed by lung injury scores (which incorporated a chest radiograph score, a hypoxemia score, and a positive end-expiratory pressure score) (1). They also found that the systemic vascular resistance was significantly decreased, and the cardiac index was significantly increased in the methylprednisolone-pretreated group, and they postulate that the drug may attenuate tumor necrosis factor--induced vasoconstriction or directly dilate resistance vessels (1).
We have recently studied the pulmonary and hemodynamic effects of methylprednisolone in patients undergoing cardiac surgery with cardiopulmonary bypass (which initiates the systemic inflammatory response syndrome) (2,3). Like Sumida et al., we found that pretreatment with IV methylprednisolone (60 mg/kg, total) significantly decreased systemic vascular resistance and significantly increased cardiac index in the immediate postoperative period (2,3). However, unlike Sumida et al., in our clinical model of the systemic inflammatory response syndrome, methylprednisolone induced pulmonary dysfunction in the immediate postoperative period (significantly larger increases in alveolar-arterial oxygen gradient and significantly prolonged extubation time) (2,3). We did not assess circulating tumor necrosis factor- levels in our study; yet we found that methylprednisolone was unable to attenuate complement activation associated with cardiopulmonary bypass (2,3).
It is apparent that methylprednisolone may benefit certain patients who experience the systemic inflammatory response syndrome. However, further study is required before specific indications are clear.
References
levels and lung injury associated with systemic inflammatory response syndrome due to intraperitoneal hyperthermia. Anesth Analg 1999;88:771–6.Department of Anesthesiology Tokyo Women’s Medical University Daini Hospital Tokyo 116, Japan
We appreciate Dr. Chaney’s interest in our article (1) and the opportunity to provide more details about our article. We reported that methylprednisolone (MPS) prevented lung injury in patients with systemic inflammatory response syndrome (SIRS) induced by intraperitoneal hyperthermic perfusion (IPHP). In contrast, Chaney et al. (2) reported that MPS worsened pulmonary function in patients undergoing coronary artery bypass grafting (CABG) in the immediate postoperative period. Although it is important to measure alveolar-arterial oxygen gradient, dynamic pulmonary compliance, static lung compliance, shunt, and dead space, these variables were not measured in our study. Instead, we determined the lung injury score postoperatively, including the chest radiograph score, hypoxemia score (PaO2/PAO2), and positive end-expiratory pressure score, as recommended by Marks et al. (3). Using this score, our results confirmed that pretreatment with MPS prevented lung injury. The discrepancy between the two studies might be caused by the following reasons.
Serum levels of tumor necrosis factor- were increased in patients with gastric cancer undergoing IPHP without pretreatment of MPS in our study. Denizot et al. (4) reported that no variation of tumor necrosis factor- levels were found in patients undergoing CABG in pre- and postoperative periods. These findings strongly suggest that differences in the severity of SIRS might contribute to the difference in MPS response between IPHP and CABG. In fact, all our patients with gastrointestinal cancer, in whom IPHP was performed, showed severe lung injury caused by SIRS compared with those undergoing CABG studied by Chaney et al. (2). In their study, 58 of 60 (97%) patients were tracheally extubated within 24 h of arrival in the intensive care unit, compared with only 2 of 17 (12%) patients in our study within the same period. Gott et al. (5) indicated that "ventilatory support for more than 48 h" is associated with high pulmonary morbidity after cardiopulmonary bypass. The time of extubation is determined clinically, based on several factors, such as lung function, level of consciousness, and cardiac function. In our study, intubation was prolonged in our MPS-treated and untreated patients compared with the other study (2).
Measurements of lung function were performed at different times in the two studies. We examined lung injury scores between 1 and 6 postoperative days, whereas Chaney et al. (2) measured alveolar-arterial gradient, dynamic pulmonary compliance, static lung compliance, shunt, and dead space at 10 min after intubation to 60 min after arrival in the intensive care unit. We did not analyze the lung injury score during operation or at the early postoperative period.
The dose of MPS used in the two studies was somewhat different. We used a dose of 50 mg/kg MPS compared with 60 mg/kg in the other study (2). This difference, though small, might produce a different response. The correct dose of MPS to prevent lung injury could not be determined at the present stage.
Further evidence for lung injury in our patients is demonstrated in preliminary studies showing recruitment of leukocytes into the lung. However, the discrepancy in the response to MPS between patients undergoing CABG (3) and those with IPHP (1) must not be ignored, and further work is needed.
References
levels and lung injury associated with systemic inflammatory response syndrome due to intraperitoneal hyperthermia. Anesth Analg 1999;88:771–6.
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