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The urea-creatinine ratio (UCR) has been proposed as potential biomarker for critical illness-associated catabolism. Its role in the context of aneurysmal subarachnoid hemorrhage (aSAH) remains to be elucidated, which was the aim of the present study.We enrolled 66 patients with aSAH with normal renal function and 36 patients undergoing elective cardiac surgery as a control group for the effects of surgery. In patients with aSAH, the predictive or diagnostic value of early (day 0-2) and critical (day 5-7) UCRs was assessed with regard to delayed cerebral ischemia (DCI), DCI-related infarction, and clinical outcome after 12 months.Preoperatively, UCR was similar both groups. Within 2 days postoperatively, UCRs increased significantly in patients in the elective cardiac surgery group (P0.001) but decreased back to baseline on day 5-7 (P = 0.245), whereas UCRs in patients with aSAH increased to significantly greater levels on day 5-7 (P = 0.028). Greater early or critical UCRs were associated with poor clinical outcomes (P = 0.015) or DCI (P = 0.011), DCI-related infarction (P = 0.006), and poor clinical outcomes (P 0.001) respectively. In multivariate analysis, there was an independent association between greater early UCRs and poor clinical outcomes (P = 0.026).In this exploratory study of UCR in the context of aSAH, greater early values were predictive for a poor clinical outcome after 12 months, whereas greater critical values were associated with DCI, DCI-related infarctions, and poor clinical outcomes. The clinical implications as well as the pathophysiologic relevance of protein catabolism should be explored further in the context of aSAH.

Introduction Prediction of vasospasm after aneurysmal subarachnoid hemorrhage (aSAH) remains imperfect and currently relies on clinical and radiographic characteristics. Whether early hemodynamic changes may refine risk stratification for delayed vasospasm (DV) after aSAH was analyzed. Methods Patients with aSAH ( n = 53) and a control group with unruptured intracranial aneurysms (UIA) ( n = 12) with initial color-coding angiography at admission were included in this study ( n = 65). Clinical and radiologic data were collected, and uni- and multivariate analysis was used to correlate the occurrence of DV (manifesting clinically or detected with transcranial Doppler or angiography) with hemodynamic features of the initial angiography including Tmax and mean transit times (MTTs). Results In the aSAH patient cohort, 37 of 53 patients with aSAH (70%) developed DV. After we controlled for the effects of age, Hunt and Hess grade, and modified Fisher grade, patients with DV had a shorter mean region of interest peak time (Tmax) of the anterior cerebral artery A2 segment ( P = 0.036) and the middle cerebral artery M1 ( P = 0.045) and M3 ( P = 0.013) segments. Mean MTTs between internal carotid artery to middle cerebral artery M3 segment ( P = 0.026) was also significantly shorter in patients with DV when compared with controls. Conclusions Tmax and MTT on angiography within 48 hours of aneurysm rupture before treatment provide an early quantitative assessment in patients with aSAH and in this small study were predictive for the development of subsequent symptomatic DV. Early identification of patients with aSAH at greatest risk of DV may ameliorate clinical outcome through timely, selective implementation of aggressive prophylactic therapy to prevent the effects of DV.

Background Oral nimodipine is an established prophylactic agent for cerebral vasospasm after subarachnoid hemorrhage (SAH). In highly selected cases, intra-arterial (IA) or intravenous (IV) application of nimodipine may be considered; however, the optimum dosage and modality of application remain a matter of debate. The purpose of this investigation is analysis of nimodipine concentration in serum, cerebrospinal fluid, and cerebral microdialysate in the context of currently effective dose and route of application (oral, IA, IV). Methods We prospectively collected 156 samples from 37 patients treated for aneurysmal SAH from May 2014 to July 2015. Treatment groups were stratified according to modality of application and low-dose or high-dose treatment. At time of sampling, current dose and modality of application effectively sustained cerebral perfusion as documented by common diagnostics. Samples were analyzed for nimodipine concentration via high-performance liquid chromatography and tandem mass spectrometry. Results In most cases (94.3%), nimodipine remained below the limit of quantification (0.5 ng/mL) within the brain (microdialysis, cerebrospinal fluid), even during targeted, local application (IA nimodipine). The median serum concentration for all treatment groups was 17.3 ng/mL. Modality of application (oral, IA, IV) was not associated with significant differences in serum concentrations ( P = 0.712), even after stratification for dosage ( P = 0.371), implying a comparable systemic distribution, if not efficacy. Conclusions Nimodipine does not accumulate sufficiently within the target organ for treatment monitoring. Comparable systemic concentrations can be observed irrespective of application modality and dosing. Future studies will clarify the role of efficacy-driven treatment algorithms, in which lowest dose and least invasive mode of application still effective should be identified.