Publication: Impact of acute alcohol intoxication and alcohol dependence on outcomes after subarachnoid hemorrhage
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2025-08-27
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Abstract
Background: Non-traumatic subarachnoid hemorrhage (SAH) is most commonly caused by a ruptured aneurysm. Risk factors for rupture include hypertension, smoking, and substance use, but the relationship between alcohol use and clinical outcomes after SAH is poorly understood. The objective of this population-based, longitudinal, study is to characterize the relationships between alcohol use, alcohol dependence, and adverse clinical outcomes following SAH.
Methods: Patients with alcohol use disorder (International Classification of Disease 10th Revision Diagnostic Code F10) in the TriNetX Research Network were compared to patients with no substance use disorders (None of F10-F19). Short-term (30-day) outcomes were assessed among patients with blood alcohol concentrations tested on the day of SAH. Outcome frequencies and Cox proportional hazard models used propensity score matching on demographics, comorbidities, blood counts, substance use, and SAH severity.
Results: We identified 216,894 patients with non-traumatic SAH. Of these, 11,648 were tested for alcohol and 27,079 patients had alcohol use disorder. Blood alcohol levels of 1-100 mg/dL and above at the time of SAH were associated with decreased 30-day mortality in acute alcohol use compared to 0 mg/dL, and alcohol concentrations of 201-300 mg/dL and higher were further protective relative to 1-100 mg/dL. Patients with alcohol use disorder exhibited an increased hazard of mortality (HR = 1.175 [95% CI: 1.129, 1.223]; p < 0.0001) compared to patients with no substance use disorders (n = 151,377). Patients with severe alcohol dependence had an even higher hazard of mortality compared to patients with mild/moderate use disorder (HR = 1.139 [1.128, 1.150] p < 0.0001).
Conclusions: In patients with non-traumatic SAH, alcohol in the blood at the time of SAH is protective against 30-day mortality, and increased alcohol concentration adds increased protection. Paradoxically, alcohol use disorder leads to a worsening of clinical outcomes, including mortality. There appears to be a significant dose-dependent effect of severity of alcohol dependence on mortality.
Methods: Patients with alcohol use disorder (International Classification of Disease 10th Revision Diagnostic Code F10) in the TriNetX Research Network were compared to patients with no substance use disorders (None of F10-F19). Short-term (30-day) outcomes were assessed among patients with blood alcohol concentrations tested on the day of SAH. Outcome frequencies and Cox proportional hazard models used propensity score matching on demographics, comorbidities, blood counts, substance use, and SAH severity.
Results: We identified 216,894 patients with non-traumatic SAH. Of these, 11,648 were tested for alcohol and 27,079 patients had alcohol use disorder. Blood alcohol levels of 1-100 mg/dL and above at the time of SAH were associated with decreased 30-day mortality in acute alcohol use compared to 0 mg/dL, and alcohol concentrations of 201-300 mg/dL and higher were further protective relative to 1-100 mg/dL. Patients with alcohol use disorder exhibited an increased hazard of mortality (HR = 1.175 [95% CI: 1.129, 1.223]; p < 0.0001) compared to patients with no substance use disorders (n = 151,377). Patients with severe alcohol dependence had an even higher hazard of mortality compared to patients with mild/moderate use disorder (HR = 1.139 [1.128, 1.150] p < 0.0001).
Conclusions: In patients with non-traumatic SAH, alcohol in the blood at the time of SAH is protective against 30-day mortality, and increased alcohol concentration adds increased protection. Paradoxically, alcohol use disorder leads to a worsening of clinical outcomes, including mortality. There appears to be a significant dose-dependent effect of severity of alcohol dependence on mortality.
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Critical care, Epidemiology, Neurology, Neurosurgery, Subarachnoid hemorrhage