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NEWS Review

By Currents Editor posted 06-26-2018 16:18

  
By Aimee Aysenne, MD, MPH, (left) and Kyle Hobbs, MD (right)
Aimee_Aysenne_Headshot_2.jpgKyle_Hobbs_Headshot.jpg

Antihypertensive medications are ubiquitous in ICUs. Still, complete understanding of the effect on the brain in neurologically patients is not well understood. In these reviews, we examine the cerebrovascular consequence of antihypertensives, namely the mortality benefit for patients who received beta blockers after TBI and the effect of nicardipine on transcranial Doppler in aneurysmal subarachnoid hemorrhage.

Beta blockers associated with improved survival after acute traumatic brain injury.

J Trauma Acute Care Surg 84(2):234-244, 2018.

Summary

This study is a multicenter, prospective, observational study of adults with TBI to evaluate the relationship between beta blocker use and mortality. Currently, no neuroprotective therapy exists to prevent secondary brain injury after TBI. After TBI, catecholamine levels surge resulting in inflammation and neuronal cell death. Beta blockers are a class of medication that inhibit this response. In this study, 2,252 adult patients with TBI presenting within 12 hours of injury at 15 trauma centers across the United States and Canada were analyzed. The use of beta blockers was at the discretion of the attending physician. The primary outcome was 30-day mortality. Patients who received beta blockers were significantly older, more likely to be on anticoagulants or preinjury beta blockers, and admitted more frequently after a fall compared with those who did not. Beta blocker patients were more often intubated in the ED and were more likely to have a higher head AIS. Mortality at 30 days was significantly lower in the group who received beta blockers. This association remained significant after adjusting for age, injury severity, neurosurgical intervention and other factors. However, patients who received beta blockers had a longer length of stay. In a subgroup analysis, mortality at 30 days was significantly lower in the propranolol cohort as compared to patients treated with other beta blockers

Comments

Early exposure to beta blockers, particularly propranolol, is associated with improved survival in adults with traumatic brain injury. This multicenter, prospective analysis adds to the growing body of restrospective data suggesting beta blockers reduce mortality in moderate-severe TBI. The mechanism for how beta blockers may be protective is undetermined. Propranolol is a nonspecific B-adrenergic receptor antagonist that crosses the blood brain barrier and may exert a neuroprotective response by reducing neuroinflammation. However, the primary indication for beta blocker use in this study was hypertension and not to treat the primary brain injury. The true benefit of beta blockers in TBI could be addressed with a randomized controlled trial in the future.

Nicardipine may increase arterial contractility in SAH as per TCD measurements.

J Neurosurg 128: 1015-1019, 2018.

Summary

Nicardipine is a commonly used intravenous dihydropyridine calcium channel blocker, which acts via smooth muscle relaxation, primarily of the systemic venous circulation. This is a single center retrospective observational study evaluating the affect of nicardipine on the cerebral vasculature evaluated by transcranial Doppler (TCD). Standard TCD measures velocities, including mean flow velocities (MFVs), which are proportional to vessel diameter. Additionally, pulsatility is a marker of distal vessel resistance; pulsatile index (PI) is calculated from peak systolic velocities (PSV), end diastolic velocities (EDV) and MFV using the formula (PSV-EVD)/ MFV. Nicardipine use was managed by the treating physician and was not started, stopped or adjusted for the purposes of the study. Retrospective chart review determined the timing of TCD in relationship to nicardipine use. The series describes the details of the TCD findings of nine patients, all with aneurysmal subarachnoid hemorrhage (aSAH). The use of nicardipine was associated with accelerated decelerations in late systolic phase, prominent dicrotic notch, and decreased EDV. PI was increased during the infusions, and MFV were decreased or unchanged, suggestive of distal vasoconstriction. In the first four cases, the nicardipine changes were in close temporal relationship to the TCD. In the latter five, the TCD findings were compared to before or after nicardipine use for each patient. For all cases, post nicardipine TCDs had significant increased PI compared to pre nicardipine use (p< 0.001), regardless of the temporal relationship.

Comments

This study raises interesting questions about the affect of a commonly used blood pressure medication, nicardipine, on intracranial vasculature for use in neurovascular patients. While, increased PI can be seen in other clinical settings including vasospasm, intravascular depletion, or increased intracranial pressures, and has been associated with worsened outcomes in the setting of aSAH, these causes were not found in any of these patients. Proposed mechanism of action for these findings has been suggested based on changes in venous return caused by the medication. As the venous resistance decreases, there may be an increase in central venous pressure, which can transfer to the intracranial venous system, impede drainage, and be transmitted to the arterial circulation. There are many limitations of this study including small sample size, single institution, and homogenous disease process of aneurysmal subarachnoid hemorrhage. Future studies should include additional disease processes and blood pressure medications to help select most appropriate treatment options.

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