Comparison of Intravenous Ibuprofen and Dexamethasone Preemptive Analgesia on Postoperative NLR after Gynecological Laparotomy

Background: Postoperative pain management in gynecological surgery remains a clinical challenge, particularly after gynecological laparotomy, which triggers inflammatory responses reflected by changes in the Neutrophil-to-Lymphocyte Ratio (NLR). Preemptive analgesia using NSAIDs (ibuprofen) and corticosteroids (dexamethasone) are widely used; however, their comparative effects on postoperative inflammatory markers remain unclear. This study aimed to compare the effects of preemptive intravenous ibuprofen and intravenous dexamethasone on postoperative NLR levels in gynecological laparotomy patients. Methods: This quasi-experimental study employed a pretest–posttest non-randomized controlled design. Thirty patients undergoing gynecological laparotomy were recruited through consecutive sampling and assigned alternately into two groups: intravenous ibuprofen (n = 15) and intravenous dexamethasone (n = 15). Levels of NLR were measured preoperatively and 24 hours postoperatively. Within-group comparisons were analyzed using the Wilcoxon signed-rank test, while between-group differences in ΔNLR were analyzed using the Mann–Whitney U test. Results: The dexamethasone group showed a significant increase in postoperative NLR compared with baseline values (median: 2.20 vs. 14.20; p = 0.002), consistent with steroid-induced neutrophil demargination. In contrast, the ibuprofen group demonstrated no significant change in NLR (median: 2.10 vs. 4.50; p = 0.62). Comparison of ΔNLR between groups revealed a highly significant difference (p < 0.001), with a greater median increase observed in the dexamethasone group (11.00) than in the ibuprofen group (1.10). Conclusion: Preemptive dexamethasone significantly increases postoperative NLR, whereas ibuprofen does not. Elevated postoperative NLR following dexamethasone administration should therefore be interpreted cautiously, as it may reflect pharmacologically induced leukocyte redistribution rather than excessive inflammation.