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Our objective was to compare the effectiveness of intravenous and enteral nimodipine in preventing poor outcome from delayed cerebral ischemia in patients with subarachnoid hemorrhage. We performed a systematic search and a network meta-analysis using the following databases: PubMed, Scopus, the Cochrane Central Register of Controlled Trials, and Google Scholar. Risk of Bias 2 tool was used to assess risk of bias of included studies. A ranking among methods was performed on the basis of the frequentist analog of the surface under the cumulative ranking curve. Published studies that met the following population, intervention, comparison, outcomes and study (PICOS) criteria were included: patients with subarachnoid hemorrhage aged 15 years or older (P); nimodipine, intravenous and oral formulation (I); placebo or no intervention (C); poor outcome measured at 3 months (defined as death, vegetative state, or severe disability), case fatality at 3 months, delayed cerebral ischemia, delayed ischaemic neurologic deficit, and vasospasm measured with transcranial Doppler or digital subtraction angiography (O); and randomized controlled trials (S). No language or publication date restrictions were applied. Ten studies were finally included, with a total of 1527 randomly assigned patients. Oral and intravenous nimodipine were both effective in preventing poor outcome, delayed cerebral ischemia, and delayed ischaemic neurological deficit. Neither treatment was effective in improving case fatality. Evolving clinical protocols over a 30-year period and the risk of bias of the included studies may limit the strength of our results. Enteral and intravenous nimodipine may have a similar effectiveness in terms of preventing poor outcome, delayed cerebral ischemia, and delayed ischaemic neurological deficit. More research may be needed to fully establish the role of intravenous nimodipine in current clinical practice., (© 2022. Springer Science+Business Media, LLC, part of Springer Nature and Neurocritical Care Society.)

Competing Interests: The authors have no funding or conflicts of interest to disclose.

Background: Subarachnoid hemorrhage is a severe subtype of hemorrhagic stroke, and deep-vein thrombosis is a frequent complication detected in these patients. In addition to other well-established risk factors, the early activation of coagulation systems present in patients with subarachnoid hemorrhage could potentially play a role in the incidence of deep-vein thrombosis. This study aims to identify possible predictors for deep-vein thrombosis related to subarachnoid hemorrhage., Methods: We conducted a retrospective cohort study on patients with a diagnosis of subarachnoid hemorrhage who presented to our institution between 1 January 2014 and 1 August 2018. We reviewed electronic medical records and analyzed several parameters such as Fisher scale, World Federation of Neurosurgical Surgeons scale, aneurysm site, surgical or endovascular treatment, decompressive craniectomy, vasospasm, infection (meningitis and pneumonia), presence of motor deficit, length of stay in the ICU, length of hospital stay, number of days under ventilator support, d-dimer at hospitalization, and the time to thromboprophylaxis (days)., Results: The univariate analysis showed that intraparenchymal cerebral hemorrhage, d-dimer at hospitalization, the time to thromboprophylaxis, motor deficit, and aneurysm located at the internal carotid artery were statistically significant factors. Intraparenchymal cerebral hemorrhage (OR 2,78 95%CI 1.07-7.12), motor deficit (OR 3.46; 95%CI 1.37-9.31), and d-dimer at hospitalization (OR 1.002 95% CI 1.001-1.003) were demonstrated as independent risk factors for deep-vein thrombosis. Length of hospital stay was also found to be significantly longer in patients who developed deep-vein thrombosis (p value 0.018)., Conclusion: Elevated d-dimer level at the time of hospitalization, motor deficit, and the presence of an intraparenchymal hemorrhage are independent risk factors for deep-vein thrombosis. Patients with DVT also had a significantly longer hospital stay. Even though further studies are needed, patients with elevated d-dimer at hospitalization and intraparenchymal cerebral hemorrhage may benefit from a more aggressive screening strategy for deep-vein thrombosis.

Traumatic brain injury (TBI) and subarachnoid hemorrhage (SAH) are critical neurological conditions that necessitate specialized care in the Intensive Care Unit (ICU). Managing cerebral perfusion pressure (CPP) and mean arterial pressure (MAP) is of primary importance in these patients. To maintain targeted MAP and CPP, vasopressors and/or inotropes are commonly used. However, their effects on cerebral oxygenation are not fully understood. The aim of this review is to provide an up-to date review regarding the current uses and pathophysiological issues related to the use of vasopressors and inotropes in TBI and SAH patients. According to our findings, despite achieving similar hemodynamic parameters and CPP, the effects of various vasopressors and inotropes on cerebral oxygenation, local CBF and metabolism are heterogeneous. Therefore, a more accurate understanding of the cerebral activity of these medications is crucial for optimizing patient management in the ICU setting. [ABSTRACT FROM AUTHOR]

As the authors state, meta-analyses are used to provide a "summary effect"; despite this, we disagree with their conclusions that this methodology should only be used to confirm "what we already know." Concerning nimodipine use in subarachnoid hemorrhage, current clinical practice is based on the studies performed between 30 and 40 years ago [[4]], and enteral nimodipine use especially was very similar in all the included studies [[2]]. This letter is a response to the Letter to the Editor available at https://link.springer.com/article/10.1007/s12028-022-01589-x. [Extracted from the article]