Abstract
Background: Aneurysmal subarachnoid hemorrhage (aSAH) is associated with high early mortality and long-term disability. Prognostic assessment relies mainly on neurological grading scales, which may incompletely capture the systemic metabolic response to acute brain injury. Non-thyroidal illness syndrome (NTIS), particularly low triiodothyronine syndrome (LT3S), is common in critical illness, but its prognostic relevance in aSAH remains unclear. Objectives: To evaluate the prognostic impact of early thyroid hormone alterations on 30-day mortality and early clinical outcomes including delayed cerebral ischemia (DCI) in patients with aSAH, with particular emphasis on the magnitude of triiodothyronine (T3) deficiency. Methods: We conducted a retrospective single-center observational cohort study of 157 consecutive adult patients admitted with confirmed aSAH between 2014 and 2025. Serum free triiodothyronine (fT3), free thyroxine (fT4), and thyroid-stimulating hormone (TSH) were measured within 72 h of admission. Hormone values were normalized to contemporaneous reference intervals to generate continuous reference-adjusted metrics (FT3_level, TSH_level). Associations with 30-day in-hospital mortality were analyzed using logistic regression and Cox proportional hazards models adjusted for admission variables including age, sex, APACHE II score, World Federation of Neurosurgical Societies grade, Fisher grade, and treatment modality. Results: Binary LT3S classification was frequent but not independently associated with 30-day mortality. In contrast, lower FT3_level values were significantly associated with increased mortality and shorter survival time. In logistic regression analyses, each 0.1 increase in FT3_level was associated with an 18% lower odds of death (adjusted OR 0.82, 95% CI 0.69-0.97). This association persisted after adjustment for established clinical severity measures and was concordant with time-to-event analyses. FT3_level was not correlated with TSH_level, consistent with NTIS. Endovascular coiling was associated with more pronounced peripheral fT3 deficiency (p < 0.05) but was not independently associated with mortality. FT3_level was not independently associated with early neurological status or functional outcome at hospital discharge. Conclusions: Lower FT3_level values were independently associated with higher 30-day mortality, indicating that early peripheral T3 reduction reflects clinically relevant metabolic vulnerability in aSAH.