Impact of Elevated Blood Pressure Targets on Splanchnic Ischemia and Mortality in Septic Resuscitation: Systematic Review.

BACKGROUND: Sepsis causes deaths worldwide each day, with hemodynamic resuscitation being central to management. Guidelines recommend a 65-mm Hg mean arterial pressure (MAP) target, yet the evidence for elevated targets remains fragmented across mortality, renal, and splanchnic outcomes. OBJECTIVE: This review aims to comprehensively appraise the impact of elevated MAP targets on splanchnic ischemia, mortality, and organ-specific outcomes in septic resuscitation. METHODS: Following the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) 2020 guidelines, we systematically searched PubMed, the Cochrane Library, and Google Scholar for studies comparing MAP targets in septic shock. Risk of bias was assessed using the Cochrane Risk of Bias 2 (RoB 2; randomized controlled trials [RCTs]) and the Newcastle-Ottawa Scale (nonrandomized studies). The findings were synthesized narratively according to the Synthesis Without Meta-Analysis guidelines, with random-effects meta-analysis for mortality outcomes. Evidence certainty was graded using the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) framework. RESULTS: From 3254 records, 11 studies (2895 patients; 4 RCTs, 7 nonrandomized) met the inclusion criteria. Pooled 90-day mortality across 3 trials showed a nonsignificant trend toward higher mortality with elevated MAP targets (320/720, 44.4% vs 280/722, 38.8%; OR 1.31, 95% CI 0.97-1.77). Pooled 28- or 30-day mortality showed a similar nonsignificant trend (OR 1.25, 95% CI 0.98-1.61), which was robust to sensitivity analysis. Narratively, mortality findings across nonpooled observational studies were inconsistent; some linked low MAP to higher death risk, and others found no significant association. Renal outcomes were inconsistent, with some studies showing reduced renal replacement therapy or improved acute kidney injury recovery at higher targets, particularly in hypertensive or cirrhotic subgroups. Elevated MAP targets consistently increased vasopressor exposure and were associated with more arrhythmias and fewer organ support-free days. No study reported splanchnic ischemia as a discrete outcome; mesenteric ischemia rates were low and similar between arms. Overall certainty of evidence was very low. CONCLUSIONS: Higher MAP targets show no clear mortality or splanchnic perfusion benefit and may increase overall harm, though select subgroups, chronic hypertension, and cirrhosis, may benefit, supporting individualized, risk-stratified MAP targeting over uniformly elevated-target strategies.