HIMALAIA Study – Netherlands. The only RCT looking at efficacy of BP augmentation in DCI in increasing cerebral blood flow (via CT perfusion). Small n, negative study.
Tey article – XeCt to measure regional CBF, at onset of DCI suspicion, 5 days of induced HTN, hypervolemia, hemodilution. Compared XeCT before and after treatment and showed increase in regional CBF in worst vascular territories from 19 to 227ml/100g/min, significant reduction of regions with CBF <20ml/100g/min from 26 to 10%.
- decrease in GCS >=1
- new focal deficits
- other etiologies excluded:
- worsening HCP
- recurrent bleeding
- infectious disease
- metabolic enceph from renal or liver failure
Baseline echo: cardiomyopathy is a contraindication
Drug of choice: Induce HTN with norepinephrine? based on reference below (we usually use phenylephrine)
- improvement of neurologic deficits
- occurrence of complication
- MAP 130 mm Hg
- SBP 230 mm Hg
Risks of Induced HTN:
- line placement risks
- vasopressor risks
- can induce PRES, neurologic deterioration
Literature does not support the use of induced HTN, but how can we ignore bedside observations of patients who clinically improve with induced HTN?
- Uses surrogate physiologic endpoints (CBF / cerebral o2 delivery). Are we looking at the right endpoint? CBF correlates with cerebral O2 delivery assuming that other factors are constant (cerebral metabolism, arterial O2 content, partial pressure of O2 and CO2).
- Different patients have varied responses to induced HTN. Induced HTN increases CBF only if cerebral autoregulation is distupted.
Dr. Diringer’s Advice: use induced HTN in a thoughtful and individualized manner. Trial of induced HTN at onset of DCI. If patient improves, continue. If no change, back off and explore alternative treatments. If patient exam is poor (no followable exam), answer less clear but prolonged extreme elevations should be avoided.
Another way of doing it (Continuum article on SAH)
Onset of DCI / symptomatic vasospasm – induced hypertension indicated. Standard treatment is now hypertensive and mild hpyervolemic therapy (HHT), and not Triple H therapy.
Initiate IV bolus, maintain fluids for euvolemia or mild hypervolemia.
Induce hypertension using Alpha 1 receptor agonists by infusion (norepinephrine or phenylephrine). Vasopressors of choice as brain vessels lack alpha 1 receptors. Stepwise progression of BP augmentation. Neuro assessment at each step.
Follow MAP. MAP about 20 mm Hg above baseline set as first goal, (often MAP>90).
Follow SBP: some institutions use SBP goals. No evidence exists which parameter is better to follow. Goal should be ~20-40mm Hg above baseline SBP. Commonly SBP goal >180 or >200 mm Hg.
If clinical exam returns to baseline – no further BP elevations. If exam deteriorates at this BP goal, attempt further increases. No optimal max BP goal known, but adverse effects (cardiopulmo, brain autoregulation, PRES) should be considered.
Inotropic agents (milrinone, dobutamine) reserved for patients with poor CO from acute or chronic CMP.
If neuro deficits persist despite induced HTN, perform CT/CTA ffd by DSA with endovascular therapy if VSP confirmed. NCCT prior to DSA to rule out HCP / determine pre-existing stroke prior to endovascular treatment.
Gathier, C., Dankbaar, J., van der Jagt, M., Verweij, B., Oldenbeuving, A., Rinkel, G., van den Bergh, W. and Slooter, A. (2015). Effects of Induced Hypertension on Cerebral Perfusion in Delayed Cerebral Ischemia After Aneurysmal Subarachnoid Hemorrhage. Stroke, 46(11), pp.3277-3281.
Diringer, M. Editorial. Hemodynamic Therapy for Delayed Cerebral Ischemia in SAH. Neurocritical Care Journal. Pre-print.
Muehlschlegel, S. (2018). Subarachnoid Hemorrhage. CONTINUUM: Lifelong Learning In Neurology, 24(6), 1623-1657. doi: 10.1212/con.0000000000000679