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.

 

 

Stress Dose Steroids

WHEN IS STRESS DOSE STEROIDS INDICATED?

  • depends on history of steroid intake and likelihood of HPA supression + type and duration of surgery
  • NONSUPPRESSED HPA AXIS: 
    • < 3 weeks of steroids at any dose
    • prednisone <5mg/daily for any duration
    • prednisone <10mg every other day
    • PLAN:  continue same regimen perioperatively; no need for cosyntropin test or stress dose steroids
  • SUPPRESSED HPA AXIS
    • prednisone >20mg/day x 3 weeks or more OR Cushingoid appearance
    • PLAN:
      • give stress dose steroids based on type and duration of surgery (see below)
  • INTERMEDIATE HPA SUPPRESSION (Unknown HPA Axis suppression, previous 3 or more intraarticular or spinal steroid injections within 3 mos prior to suregery)
    • PLAN
      • evaluate HPA axis 
        • check AM cortisol (8a.m.) after 24h off steroids
        • if <5 ug/dL – likely suppressed axis; give stress dose steroids
        • if >10 ug/dL – likely no supression; continue current dose on day of surgery
        • if 5-10 ug/dL – ACTH stim test or empiric stress dose steroids
      • ACTH stim test (standard is 250 ug):
        • if serum cortisol <18 ug/dL 30 mins after ACTH – give stress dose steroids
        • if >serum cortisol >18 ug/dL 30 mins after ACTH – no stress dose steroids

 

STEROIDS BASED ON TYPE AND DURATION OF SURGERY

MINOR PROCEDURES / LOCAL ANESTHESIA – stress dose not necessary, take AM steroids

MODERATE SURGICAL STRESS: (eg. LE revascularization, total joint replacement)

  1. take AM steroids
  2. hydrocortisone 50mg IV prior to procedure, 25mg IV q8h x 24h
  3. resums usual dose after

MAJOR SURGICAL STRESS (e.g open heart surgery, proctocolectomy, esophagogastrectomy)

  1. take AM steroids
  2. hydrocortisone 100mg IV before induction of anesthesia
  3. hydrocortisone 50mg q8h x 24h
  4. taper by half per day to maintenance dose

 

 

 

Reference:

Uptodate.com. (2018). UpToDate. [online] Available at: http://www.uptodate.com/contents/the-management-of-the-surgical-patient-taking-glucocorticoids?search=stress+dose+steroids&source=search_result&selectedTitle=1~60#H6 [Accessed 25 Mar. 2018].

The PulseRider

Pulse Rider 02

 

PulseRider – stent frame opens to conform to vessel walls (see image below) designed to keep coil within aneurysmal sac, while preserving the patency of the parent vessels.  The stent is retrievable and may be repositioned.

Source: http://www.pulsarvascular.com/technology/the-pulserider/

 

Pulse Rider 01

Source: collection of author.

LHH Sepsis Bundle Cheat Sheet

LHH Contact Precaution Guidelines

Moyamoya Disease Suzuki Staging System

 

REFERENCE:

White, T. et al.  Moyamoya: An Update for the Practicing Neurologist.  Practical Neurology.  November / December, 2017.