Moinay Kim, Hyunchul Jung, Seung Bin Kim, Jun Ha Hwang, Hanwool Jeon, Yeongu Chung, Youngbo Shim, Jae Hyun Kim, Joonho Byun, Aiden Cousins, Wonhyoung Park, Jung Cheol Park, Jae Sung Ahn, Seungjoo Lee
Acute Crit Care. 2025;40(4):582-593. Published online November 28, 2025
Background Post-hemorrhagic hydrocephalus (PHH) is a frequent complication of aneurysmal subarachnoid hemorrhage (aSAH), yet the relationship between serum magnesium (Mg) level and PHH remains unclear. To our knowledge, this is the first prospective study to specifically examine the association between admission serum Mg level and PHH in aSAH patients.
Methods In this prospective, multicenter study (October 2019–October 2024), 131 patients with confirmed aSAH were enrolled from four neuro-intensive care units. Patients were stratified by admission serum Mg level as <2.2 mg/dL or ≥2.2 mg/dL. The primary outcome was PHH incidence; secondary outcomes were cerebral vasospasm (CV), delayed cerebral ischemia (DCI), and 30-day modified Rankin Scale (mRS) score.
Results Baseline characteristics were similar between groups. Serum Mg ≥2.2 mg/dL was not significantly associated with reduced vasospasm, DCI, or poor functional outcome. However, serum Mg >2.5 mg/dL correlated with lower PHH incidence in univariate analysis (odds ratio, 0.36; P=0.027) but not in multivariate analysis (P=0.136). Independent predictors of PHH were posterior circulation aneurysm, high Fisher grade, and high Hunt and Hess grade. Poor 30-day mRS was independently associated with high Fisher and Hunt and Hess grades.
Conclusions Admission serum Mg level was not independently associated with PHH, although a potential protective trend was noted at higher levels (>2.5 mg/dL). These findings suggest a possible role of Mg in PHH prevention. Further prospective trials are warranted to clarify the therapeutic potential of Mg and to establish optimal monitoring and correction strategies in aSAH management.
Background Inflammation is involved in the pathophysiology of postoperative acute kidney injury (AKI). We investigated whether preoperative platelet-to-white blood cell ratio (PWR), a novel serum biomarker of systemic inflammation, was associated with postoperative AKI following cerebral aneurysm treatment. We also compared the discrimination power of preoperative PWR with those of other preoperative systemic inflammatory indices in predicting postoperative AKI.
Methods Perioperative data including preoperative systemic inflammatory indices and cerebral aneurysm-related variables were retrospectively analyzed in 4,429 cerebral aneurysm patients undergoing surgical clipping or endovascular coiling. Based on the cutoff value of preoperative PWR, patients were divided into the high PWR (≥39.04, n=1,924) and low PWR (<39.04, n=2,505) groups. After propensity score matching (PSM), 1,168 patients in each group were included in the data analysis. AKI was defined according to the Kidney Disease Improving Global Outcomes guidelines.
Results Postoperative AKI occurred more frequently in the low PWR group than in the high PWR group before PSM (45 [1.8%] vs. 7 [0.4%], P<0.001) and after (17 [1.5%] vs. 5 [0.4%], P=0.016). A low preoperative PWR was predictive of postoperative AKI before PSM (odds ratio [95% CI], 3.93 [1.74–8.87]; P<0.001) and after (3.44 [1.26–9.34], P=0.016). Preoperative PWR showed the highest area under the curve for postoperative AKI (0.713 [0.644–0.782], P<0.001), followed by preoperative platelet-to-neutrophil ratio (0.694 [0.619–0.769], P<0.001), neutrophil percentage-to-albumin ratio (0.671 [0.592–0.750], P<0.001), white blood cell-to-hemoglobin ratio (0.665 [0.579–0.750], P<0.001), neutrophil-to-lymphocyte ratio (0.648 [0.569–0.728], P<0.001), and systemic inflammatory index (0.615 [0.532–0.698], P=0.004).
Conclusions A low preoperative PWR was associated with postoperative AKI following cerebral aneurysm treatment.
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In the first hours after initial hemorrhage, up to 15% of patients with subarachnoid hemorrhage (SAH) due to aneurysmal rupture may have a sudden episode of clinical deterioration resulting from rebleeding. In patients suffering from an aneurismal rebleeding, the prognosis becomes much poor. Early detection of rebleeding and preoperatively appropriate medical treatment for increased intracranial pressure (IICP) might be crucial to decrease the overall mortality and morbidity rate in a patient with aneurismal rebleeding. We report a case of a successful reversal of focal neurological deficit showed in a patient with abrupt rebleeding of ruptured aneurysm whose intracranial pressure was preoperatively reduced with hyperventilation, and thiopental and mannitol administration under general anesthesia in angiography suite, although the patient ended up in death due to postoperative IICP.