Abstract Number ‐ 213: Single Center Experience of Intrathecal Nicardipine Use in The Treatment of Vasospasm‐ Lessons Learned

Abstract

Introduction Symptomatic cerebral vasospasm and delayed cerebral ischemia (DCI) following aneurysmal subarachnoid hemorrhage leads to significant morbidity and mortality. Intrathecal (IT) nicardipine has been shown to improve outcome and reduce DCIin retrospective cohort studies1. Ecological validity of such reported conclusions may be a real‐world test of the efficacy of the proposed treatment.We sought to study our limited experience with this treatment modality in our cohort, in order to potentially inform our practice in treating vasospasm. Methods Retrospective case series of all patients who received IT nicardipine for the treatment of cerebral vasospasm from 2016 to 2021 at our University Hospital. Demographics, risk factors, clinical course and outcomes were analyzed. Results In addition to standard of care treatments and interventions, 12 patients received intrathecal nicardipine during the study period. IT nicardipine was given at doses of 2 mg every 8 hrs. Linear regression was conducted and found that IT nicardipine was associated with a reduction of the mean cerebral blood flow velocity of 16% on average. Among 12 patients, 5 patients had in‐hospital mortality; 4 out of these 5 patients developed in‐hospital DCI. Age (p 0.017), history of hypertension(HTN) (p 0.0007) were significant predictors for in‐hospital mortality. 6 patients developed DCI: mFisher scale (p 0.03), admission GCS (p 0.000998), vasopressor requirement to maintain target pressure (p 0.04) were significant predictors for developing DCI. Only 1 patient was diagnosed with bacterial ventriculitis (positive CSF culture). 80% (n = 5) patients had a favorable functional outcome (mRS≤2) at 90 days. Conclusions Our experience does not conform to the reported outcomes in a much larger patient cohort1. Nonetheless, the choice of this treatment on a case‐by‐case basis somewhat has led to rendering it as a salvage treatment at our center. In our cohort we found significant mortality rate, with age and HTN as predictive factors for in‐hospital mortality, and mFisher scale, admission GCS and vasopressor usage as predictors for DCI development. These results can be difficult to interpret, especially that the use of IT nicardipine was in only few selected patients with initial comorbidities potentially confounding the high mortality and morbidity in our cohort. Intrathecal nicardipine treatment without a well‐vetted protocol with clear inclusion and exclusion criteria can potentially misinform the practice style and lead to early abandonment of this promising therapy as part of our armamentarium. Thus, it is important to develop a standardized protocol with participation of all stakeholders of neurosurgery, neurocritical care, vascular neurology, pharmacy, and patient/family input before deploying in clinical practice on institutional level. Such protocols allow for a pilot study and more contextual prospective assessment of outcomes.