Platelet Transfusion After Traumatic Intracranial Hemorrhage in Patients on Antiplatelet Agents.

BACKGROUND: With an aging population, the number of patients on antiplatelet medications and traumatic brain injury (TBI) is increasing. Our study aimed to evaluate the role of platelet transfusion on outcomes after traumatic intracranial bleeding (IB) in these patients. METHODS: We analyzed our prospectively maintained TBI database from 2014 to 2016. We included all isolated TBI patients with an IB, who were on preinjury antiplatelet agents and excluded patients taking anticoagulants. Outcome measures included the progression of IB, neurosurgical intervention, and mortality. Regression analysis was performed. RESULTS: A total of 343 patients met the inclusion criteria. Mean age was 58 ± 11 y, 58% were men, and median injury severity score was 15 (10-24). Distribution of antiplatelet agents was as follows: aspirin (60%) and clopidogrel (35%). Overall, 74% patients received platelet transfusion after admission with a median number of two platelet units. After controlling for confounders, patients who received one unit of pooled platelets had no difference in progression of IB (odds ratio [OR]: 0.98, [0.6-1.9], P = 0.41), need for neurosurgical intervention (OR: 1.09, [0.7-2.5], P = 0.53), and mortality (OR: 0.84, [0.6-1.8], P = 0.51). However, patients who received two units of pooled platelets had lower rate of progression of IB (OR: 0.69, [0.4-0.8], P = 0.02), the need for neurosurgical intervention (OR: 0.81, [0.3-0.9], P = 0.03), and mortality (OR: 0.84, [0.5-0.9], P = 0.04). Both groups were compared with those who did not receive platelet transfusion. CONCLUSIONS: The use of two units of platelet may decrease the risk of IB progression, neurosurgical intervention, and mortality in patients on preinjury antiplatelet agents and TBI. Further studies should focus on developing protocols for platelet transfusion to improve outcomes in these patients. LEVEL OF EVIDENCE: Level III prognostic.

The neuroprotective effect of quetiapine in critically ill traumatic brain injury patients.

INTRODUCTION: Quetiapine is an atypical antipsychotic commonly used in critical care. Cellular and animal models demonstrated its novel anti-inflammatory properties in traumatic brain injury (TBI). Our study aimed to assess the effect of quetiapine on outcomes in critically ill TBI patients. We hypothesize that quetiapine improves neurological outcomes. METHODS: The Multiparameter Intelligent Monitoring in Intensive Care database was queried, and all adult (age, ≥18 years) isolated TBI patients (extracranial Abbreviated Injury Scale, < 2) admitted to the intensive care unit for a period of >48 hours. Patients were stratified into quetiapine (+) and no-quetiapine (-) groups. Propensity score matching was performed (1:2 ratio). Outcome measures were intensive care unit length of stay, discharge Glasgow Coma Scale (GCS), and mortality. A subanalysis was performed for patients who underwent intracranial pressure (ICP) monitoring to ascertain the effect of quetiapine dose on ICP, and cerebral perfusion pressure (CPP). Survival curves and regression analyses were performed. RESULTS: A matched cohort of (quetiapine, 116 vs. no-quetiapine, 232) patients was obtained. Mean ± SD age was 65 ± 21 years, median head Abbreviated Injury Scale was 3 (3-4), and median GCS was 10 (9-16). The median quetiapine dose given was 50 (25-125) mg. Patients who received quetiapine had lower mortality (17.2% vs. 27.6%; p = 0.03) and a higher median GCS at discharge (12 [11-14] vs. 11 [10-13]; p < 0.04) but no difference in intensive care unit length of stay (4.1 days vs. 4.7 days; p = 0.75) or discharge to skilled nursing facility (34.5% vs. 31.9%; p = 0.63). On subanalysis of patients who received quetiapine, 40% had ICP monitoring. Higher doses of quetiapine were independently associated with progressively lower ICP (ß = -0.022 mm Hg/mg of quetiapine; p = 0.01) and higher CPP (ß = 0.031 mm Hg/mg quetiapine; p = 0.01). CONCLUSION: Quetiapine may decrease mortality and improve neurological outcomes in critically ill TBI patients. It has a dose-dependent effect to decrease ICP and increase CPP. Quetiapine may be a potential therapeutic modality in critically ill TBI patients, but further studies are required to explore these mechanisms. LEVEL OF EVIDENCE: Systematic Review, level III.

Preinjury Statins Are Associated With Improved Survival in Patients With Traumatic Brain Injury.

BACKGROUND: Statins have been shown to improve outcomes in traumatic brain injury (TBI) in animal models. The aim of our study was to determine the effect of preinjury statins on outcomes in TBI patients. METHODS: We performed a 4-y (2014-2017) review of our TBI database and included all patients aged ≥18 y with severe isolated TBI. Patients were stratified into those who were on statins and those who were not and were matched (1:2 ratio) using propensity score matching. The primary outcome was in-hospital mortality. The secondary outcomes were skilled nursing facility disposition, Glasgow Outcome Scale-extended score, and hospital and intensive care unit length of stay (LOS). RESULTS: We identified 1359 patients, of which 270 were matched (statin: 90, no-statin: 180). Mean age was 55 ± 8y, median Glasgow Coma Scale was 10 (8-12), and median head-abbreviated injury scale was 3 (3-5). Matched groups were similar in age, mechanism of injury, Glasgow Coma Scale, Injury Severity Score, neurosurgical intervention, type and size of intracranial hemorrhage, and preinjury anticoagulant or antiplatelet use. The overall in-hospital mortality rate was 18%. Patients who received statins had lower rates of in-hospital mortality (11% versus 21%, P = 0.01), skilled nursing facility disposition (19% versus 28%; P = 0.04), and a higher median Glasgow Outcome Scale-extended (11 [9-13] versus 9 [8-10]; P = 0.04). No differences were found between the two groups in terms of hospital LOS (6 [4-9] versus 5 [3-8]; P = 0.34) and intensive care unit LOS (3 [3-6] versus 4 [3-5]; P = 0.09). CONCLUSIONS: Preinjury statin use in isolated traumatic brain injury patients is associated with improved outcomes. This finding warrants further investigations to evaluate the potential beneficial role of statins as a therapeutic drug in a TBI. LEVEL OF EVIDENCE: Level III Therapeutic.

Transcatheter therapies for resistant hypertension: Clinical review.

Resistant hypertension (RHTN) is a commonly encountered clinical problem and its management remains a challenging task for healthcare providers. The prevalence of true RHTN has been difficult to assess due to pseudoresistance and secondary hypertension. Atherosclerotic renal artery stenosis (RAS) has been associated as a secondary cause of RHTN. Initial studies had shown that angioplasty and stenting for RAS were a promising therapeutic option when added to optimal medical management. However, recent randomized controlled trials in larger populations have failed to show any such benefit. Sympathetic autonomic nervous system dysfunction is commonly noted in individuals with resistant hypertension. Surgical sympathectomy was the treatment of choice for malignant hypertension and it significantly improved mortality. However, post-surgical complications and the advent of antihypertensive drugs made this approach less desirable and it was eventually abandoned. Increasing prevalence of RHTN in recent decades has led to the emergence of minimally invasive interventions such as transcatheter renal denervation for better control of blood pressure. It is a minimally invasive procedure which uses radiofrequency energy for selective ablation of renal sympathetic nerves located in the adventitia of the renal artery. It is a quick procedure and has a short recovery time. Early studies in small population showed significant reduction in blood pressure. The most recent Symplicity HTN-3 study, which is the largest randomized control trial and the only one to use a sham procedure in controls, failed to show significant BP reduction at 6 mo.

The role of vitamin supplementation in the prevention of cardiovascular disease events.

The production, sale, and consumption of multiple vitamins is a multibillion-dollar industry. Most Americans take some form of supplement ostensibly for prevention of cardiovascular disease. It has been claimed that vitamin A retards atherogenesis. Vitamin C is an antioxidant and is thought to possibly decrease free radical-induced endothelial injury, which can lead to atherosclerotic plaque formation. Vitamin E has been extensively studied for its possible effects on platelet function as well as inhibition of foam-cell formation. Low levels of vitamin D have been thought to negatively impact myocardial structure and increase the risk for cardiovascular events. Increased intake of vitamin B6, B12, and folate has been associated with reduction of homocysteine levels; elevated homocysteine blood levels have been associated with the occurrence of stroke, heart attack, and cardiovascular death. The purpose of this study was to review the currently available literature for vitamin supplementation with respect to prevention of cardiovascular disease. Unfortunately, the current evidence suggests no benefit exists with vitamin supplementation in the general US population. Further research is needed to evaluate whether there are specific populations that might benefit from vitamin supplementation.