Monthly Archives: April 2018

The Neurovascular Bundle

Depiction of neurovascular unit displaying relationships between neurons and their supply capillaries. (From del Zoppo GJ: Stroke and neurovascular protection. N Eng! J Med 354:553-555, 2006.)

Post-capillary venule from rat cortex. “10 \im diameter. (Courtesy of J. H. Heo.) Key to the to EM imag, indfcating the endothelium (endo), basal lamina matrix (arrowheads), astrocyte and astrocyte end-feet (/^, and pericytes (*)

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Blood Pressure Augmentation in DCI

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%.

Indications:

  1. decrease in GCS >=1
  2. new focal deficits
  3. other etiologies excluded:
    1. worsening HCP
    2. recurrent bleeding
    3. epilepsy
    4. infectious disease
    5. hypoglycemia
    6. hyponatremia
    7. 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)

End points:

  1. improvement of neurologic deficits
  2. occurrence of complication
  3. MAP 130 mm Hg
  4. SBP 230 mm Hg

 

Risks of Induced HTN:

  1.  line placement risks
  2. vasopressor risks
  3. 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?

Critique:

  1. 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).
  2. 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.

References:

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.