Association Between Systolic Blood Pressure at Emergency Department Arrival and Time to Bleeding Cessation in Adult Non-Traumatic Epistaxis: A Retrospective Time-to-Event Analysis.

Objectives

Epistaxis is a common emergency department (ED) presentation, but the prognostic significance of triage blood pressure (BP) remains unclear. We evaluated whether elevated systolic BP (SBP) at ED arrival was associated with delayed bleeding cessation in adults with non-traumatic epistaxis.

Methods

We conducted a retrospective cohort study of adults (≥18 years) presenting with non-traumatic epistaxis to a tertiary ED in Northern Thailand between 2015 and 2025. Patients with documented triage SBP were included (n = 482). The exposure was SBP at ED arrival, categorized as ≥140 versus <140 mmHg. The primary outcome was time from ED arrival to first documented bleeding cessation. Adjusted hazard ratios (aHRs) were estimated using Cox proportional hazards regression, controlling for demographics, comorbidities, medication use, and ED interventions.

Results

Among 482 patients, 310 (64.3%) had SBP ≥ 140 mmHg. Median time to documented bleeding cessation was longer in patients with elevated SBP than in those with SBP < 140 mmHg (39 vs. 23 min). In adjusted analyses, SBP ≥ 140 mmHg was associated with delayed documented bleeding cessation (aHR, 0.71; 95% CI, 0.52-0.98). Mechanical nasal packing was also associated with slower bleeding control (aHR, 0.72; 95% CI, 0.54-0.95), whereas electrical cauterization was associated with faster cessation (aHR, 2.17; 95% CI, 1.19-3.96).

Conclusions

Elevated SBP at ED arrival was associated with prolonged time to documented bleeding cessation in non-traumatic epistaxis. Triage SBP may serve as a pragmatic early prognostic marker of prolonged ED management. However, important bleeding severity characteristics, including bleeding location and estimated blood loss, were unavailable, and residual confounding cannot be excluded. These findings should not be interpreted as evidence supporting acute antihypertensive therapy to accelerate hemostasis. Prospective studies are needed to validate these findings.