Prolonged Extubation Time Research Articles

Methylprednisolone and the Systemic Inflammatory Response Syndrome

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-α 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-α-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-α 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. Mark A. Chaney MD Mihail P. Nikolov MD

Methylprednisolone and the Systemic Inflammatory Response Syndrome

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-α 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-α-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-α 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. Mark A. Chaney MD Mihail P. Nikolov MD

Pulmonary Effects of Methylprednisolone in Patients Undergoing Coronary Artery Bypass Grafting and Early Tracheal Extubation

Numerous clinical studies suggest that methylprednisolone may facilitate early tracheal extubation after cardiac surgery, yet no investigation has rigorously examined the use of the drug in this setting.In this prospective, randomized, double-blind, placebo-controlled study, we examined the pulmonary effects of methylprednisolone in patients undergoing coronary artery bypass grafting (CABG) and early tracheal extubation. Sixty patients undergoing elective CABG and early tracheal extubation were randomized into two groups. Group MP patients received IV methylprednisolone (30 mg/kg during sternotomy and 30 mg/kg during initiation of cardiopulmonary bypass) and Group NS patients received IV placebo at the same two times. Perioperative management was standardized. Alveolar-arterial (A-a) oxygen gradient, lung compliance, shunt, and dead space were determined four times perioperatively. Postoperative tracheal extubation was accomplished at the earliest appropriate time. Both groups exhibited significant postoperative increases in A-a oxygen gradient and shunt (P < 0.000001 for each group) and significant postoperative decreases in dynamic lung compliance (P < 0.000001 for each group). Patients in Group MP exhibited significantly larger increases in postoperative A-a oxygen gradient (P = 0.001) and shunt (P = 0.001) compared with patients in Group NS. Postoperative alterations in dynamic lung compliance, static lung compliance, and dead space were not statistically significant between the groups. The time to postoperative tracheal extubation was prolonged in Group MP patients compared with Group NS patients (769 +/- 294 vs 604 +/- 315 min, respectively; P = 0.05). Methylprednisolone was associated with larger increases in postoperative A-a oxygen gradient and shunt, was unable to prevent postoperative decreases in lung compliance, and prolonged extubation time, which indicate that use of the drug may hinder early tracheal extubation in patients after cardiac surgery. Implications: Traditionally, methylprednisolone has been administered to patients undergoing cardiac surgery to decrease postoperative pulmonary dysfunction. This study revealed that the drug is associated with larger increases in postoperative alveolararterial oxygen gradient and shunt and prolonged tracheal extubation time in patients undergoing coronary artery bypass grafting, which indicate that use of the drug may hinder early tracheal extubation. (Anesth Analg 1998;87:27-33)