Tag Archives: CVA

ABCD2 Score

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Table: ABCD2 Score

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TIA Prognosis and Key Mx Considerations by National Stroke Association

ABCD2 Score:

  • Discharge low risk scores (ABCD 0-3)
    • outpatient work-up within 1-2 days (alternate option: admit for work-up)
    • DIAGNOSTICS:
      • carotid imaging (US, CTA, MRA)
      • Consider TTE; if high suspicion for cardioembolic source / bilateral infarcts, obtain TEE
      • Consider 30-d ambulatory cardiac monitor to detect cryptogenic Afib
    • smoking cessation
    • THERAPEUTICS:
      • Start antiplatelet therapy:
        • ASA 81mg/day or
        • Clopidogrel 75mg/day or
        • ASA 25mg/ER dipyridamole 200mg BID
      • start high-intensity statins
        • Atorvastatin 40-80mg/d or
        • Rosuvastatin 20-40mg/day
      • *consider moderate intensity statins if >75y/o
        • Atorvastatin 10-20mg/d or
        • Rosuvastatin 5-10mg/d or
        • Simvastatin 20-40mg/d or
        • Pravastatin 40-80mg/d
      • Consider OAC or LMWH if rhythm shows atrial fibrillation – calculate CHADSVASC and HAS BLED score to guide therapy

    Admit high risk TIAs (ABCD2 scores >3)

    • Admit to hospital
    • Permissive hypertension (up to 220/120mm Hg) and gradually lower over 24-48h

Reference:

Stroke.org. (2017). [online] Available at: http://www.stroke.org/sites/default/files/resources/tia-abcd2-tool.pdf?docID [Accessed 31 Jul. 2017].

Gross, Hartmut, and Noah Grose. 2017. “Emergency Neurological Life Support: Acute Ischemic Stroke”. Neurocritical Care 27 (S1): 102-115. doi:10.1007/s12028-017-0449-9.

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Watershed Infarcts

Patients presenting with severe hypertension are at risk for watershed infarcts if blood pressure is rapidly and dramatically reduced, even without frank hypotension.  Blood pressure should be lowered by no more than 25% to reduce the chance of cerebral, coronary or renal ischemia.

Watershed infarcts comprise ~10% of all ischemic strokes.  These infarcts are localized to borderzones between major vascular territories in the brain, and are classified as internal borderzone (IBZ) or cortical borderzone (CBZ) infarcts.

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*CBZ in red, IBZ in blue.

The CBZ are located at the junctions of the distal branches of the ACA, MCA and PCA territories.  CBZ infarcts are associated with small cortical infarcts that are more likely due to thromoembolism.

The IBZ are located at the junctions of the distal branches of the ACA/MCA/PCA with the deep perforating arteries (lenticulostriate, artery of Heubner, anterior choroidal artery).  IBZ infarcts are more often associated with severe stenosis or occlusion in the ICA or MCA.  The IBZ is more vulnerable to decreased perfusion due to the anatomic characteristics of cerebral arterioles within this area – being the most distal branches of the ICA, perfusion pressure is likely to be the lowest.  Also the lenticulostriate arteries have limited collateral blood supply.

Examples:

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Patient admitted for hypertensive emergency, started on nicardipine drip and blood pressure lowered from 200+ to 100 systolic.  Relative hypotension maintained for 2 hours.  Patient became comatose thereafter.  MRI showed IBZ infarcts.

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Patient with aortic dissection, BP lowered from 200s with nicardipine drip.  Patient became unarousable at SBP 114 where it remained for ~3 hours.   MRI showed IBZ and corpus callosum infarctions.  Patient never regained consciousness.

 

 

Reference:

Kurowski, Donna, Michael T. Mullen, and Steven R. Messé. “Pearls & Oy-Sters: Iatrogenic Relative Hypotension Leading To Diffuse Internal Borderzone Infarctions And Coma”. Neurology 86.24 (2016): e245-e247.

tPA Dosing for Acute Ischemic Stroke

Acute ischemic stroke:

  • Within 3 hours of the onset of symptom onset (labeled use)
  • Within 3 to 4.5 hours of symptom onset (off-label use)
  • Recommended total dose: 0.9 mg/Kg (max 90mg)
    • ≤100 kg:
      • Load 10% as IV bolus over 1 minute, then
      • 90% as continuous infusion over 1 hour
    • >100 kg:
      • Load 9 mg as IV bolus over 1 minute, then
      • 81 mg as continuous infusion over 1 hour
  • No heparin or aspirin within 24 hours after tPA, start 24-48 hours after stroke onset.
  • SQH (<10,000 units) or LMWH for DVT prophylaxis within 24 hours did not increase ICH

Low dose alteplase (0.6mg/kg) recently shown to be “not noninferior” in a recent trial published in NEJM (06/2017) by ENCHANTED group. Whether this lower dose (which resulted in less ICH) may benefit patients who are at higher risk of post-tPA hemorrhage remains to be investigated.  [2]

 

References

[1] Uptodate: “Alteplase: Drug information.” Accessed 07/08/2016.

[2] Anderson, Craig S. et al. “Low-Dose Versus Standard-Dose Intravenous Alteplase In Acute Ischemic Stroke”. New England Journal of Medicine 374.24 (2016): 2313-2323. Web.

 

Blood Pressure Goals in Neurocritical Care

Subarachnoid Hemorrhage (Take home:  target SBP <140mm Hg)

Optimal blood pressure target unknown.  2012 American Stroke Association guidelines suggests that a systolic BP goal <160mm Hg is reasonable.  Avoid nitroprusside or NTG (increases cerebral blood volume / ICP). Use labetalol, nicardipine, enalapril.

Lowering BP decreases risk of rebleeding in unsecured aneurysm, but may increase risk of infarction.  CPP = MAP – ICP.  Increased ICP necessitates an elevated MAP to keep CPP.  CPP threshold may be 70mm Hg.

In the absence of ICP measurement, clinical findings (i.e. alertness) may guide therapy, Uptodate recommends keep SBP <140mm Hg in these instances.

Traumatic Brain Injury (Take home:  target CPP 50-70mm Hg)

Cerebral autoregulation is disrupted in about a third of patients with severe TBI, these patients are described as “pressure-passive.”  In these patients, rise in MAP leads to elevated ICP due to increased cerebral blood volume, while drops in MAP may be associated with hypoperfusion and ischemia.

Bedside measurement of cerebral blood flow is not easily obtained.  CPP = MAP – ICP, is a surrogate measure.  Low MAP, high ICP or low CPP are associated with secondary brain injury and worse outcomes.

Old strategy to induce hypertension to CPP >70mm Hg (using saline boluses or vasopressors) does not improve outcome, and increases risks of other complications s.a. ARDS.  2007 Guidelines from BTF recommend CPP target of 60 mm Hg, avoid <50 and >70 mm Hg.  In children, lower thresholds are recommended (40-65 mm Hg).  Target ICP first before MAP.

Post-neurosurgical Procedure

[coming soon]  Our practice is to keep SBP within 100-150mm Hg during the immediate post-operative period.

Cerebrovascular Accident (Take home:  tPA <185/110 then <180/105; no tPA treat if >220/120)

After stroke, CPP distal to obstructed vessel is low and distal vessels are dilated.  Blood flow depends on systemic blood pressure.  Elevated BP is necessary to maintain perfusion in ischemic penumbra.  BP rises spontaneously after stroke, this is transient and BP falls by as much as 20/10 within 10 days.

Analysis from International Stroke Trial showed a U-shaped relationship between SBP and outcomes.  SBP >200mm Hg is associated with risk of recurrent stroke while SBP <120mm Hg was associated with excess number of deaths from coronary heart disease.

Lowering BP within 24 hours of acute stroke has been associated with clinical deterioration.  Some may even benefit from pharmacologic increases in BP (studies show improvement in aphasia or perfusion imaging). [Induced HTN currently not recommended except in the setting of a clinical trial.]  Severe increase in BP can also cause hypertensive encephalopathy.

No good RCTs to guide BP management in hyperacute phase (<12hours) of stroke.

Ultra-acute treatment: ongoing RIGHT-2 Trial is assessing safety and efficacy of transdermal NTG [8]

For patients eligible for tPA:  Blood pressure goal  ≤185/110 mmHg is recommended prior to starting lytic therapy.  Maintain BP ≤180/105 mmHg x 24 hours after tPA.

*Ongoing ENCHANTED trial is assessing effects of early intensive BP lowering post-tPA.  Results expected in early 2019.[8]

For patients not treated with tPA:  most guidelines recommend no treatment for BP unless hypertension is extreme (SBP >220mm Hg or diastolic >120m Hg) or patient has active ischemic coronary disease, heart failure, aortic dissection, hypertensive encephalopathy, acute renal failure, or pre-eclampsia / eclampsia.  If so, lower BP by ~15% during first 24 hours.

Restart antihypertensive medications ~24 hours after stroke in patients with pre-existing HTN who are neurologically stable.  Patients with large artery stenosis may require a slower reduction in BP (over 7-10 days after stroke)

Guidelines suggest IV labetalol and nicardipine as first-line antihypertensives.

*UK National Clinical Guidelines for stroke advocate only restarting preexisting antihypertensive therapy when patients are medically stable and can swallow their medication safely. [8]

Blood Pressure s/p thrombectomy:  optimal BP range not well defined; keep SBP 150-180mm Hg prior to reperfusion (to maintain adequate collateral flow while occluded);  keep SBP <140mm Hg once recanalized.

Blood Pressure s/p thrombectomy and s/p tPA:  keep SBP <=180/105 x 24h

Malignant MCA Infarction:  IV antihypertensive therapy recommended if SBP >220mm Hg or DBP >120mm Hg in trials demonstrating benefit with DHC (DECIMAL / HAMLET) [8]

 

Intracerebral Hemorrhage

Elevations in BP may cause hemorrhage to expand, but increased MAP may be necessary to maintain cerebral perfusion.  INTERACT2 trial compared intensive BP lowering (<140mm Hg within 1 hour) vs traditional management (<180mm Hg) in patients with acute ICH (within 6 hours).  Intensive BP lowering improved modified Rankin scores, with similar adverse events.  INTERACT study suggested that more aggressive BP lowering is associated iwth reduced hematoma growth.  ATACH II is in progress.

  • SBP >200 or MAP >150aggressively reduce BP   [aggressive lowering is safe based on INTERACT2]
  • SBP >180 or MAP >130 + high ICP – insert ICP bolt, keep CPP 61-80 mm Hg
  • SBP >180 or MAP >130 + no ICP issues – reduce BP modestly (MAP 110 or BP 160/90)

Useful IV antihypertensives include: labetalol, nicardipine, esmolol, enalapril, hydralazine, nitroprusside, and nitroglycerin.

The results of INTERACT2 trial was published in NEJM (June, 2013).  In this trial, early intensive lowering of BP compared with a more conservative BP control did not result in reduced rates of death or major disability.  However, there were significantly better functional outcomes among patients assigned to intensive treatment, as well as better physical and psychological well-being. [5]

(ENLS 2017) AHA/ASA Guidelines and European Stroke Organization recommend target BP of <140mm Hg

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INTERACT studies equivocal, but recent ATACH2 shows more definitely negative results. Aggressive control of BP does not result in improved functional outcome or decreased hematoma expansion. Consider SBP control to 140-160mm Hg instead of 120-140mm Hg. [7]

Spinal Surgery

[coming soon]  Some neurosurgeons routinely keep MAP goals >85 mm Hg in spinal surgeries where perfusion of the spinal cord is critical.  Evidence for this practice is lacking, whereas the harms from induced hypertension and prolonged ICU stay is real.

References

[1] Uptodate.  “Treatment of Aneurysmal Subarachnoid Hemorrhage.”  Accessed 07/07/2016.

[2] Uptodate.  “Initial assessment and management of acute stroke.”  Accessed 07/07/2016.

[3] Uptodate.  “Management of acute severe traumatic brain injury.”  Accessed 07/07/2016.

[4] Uptodate.  “Spontaneous intracerebral hemorrhage: Treatment and prognosis.”  Accessed 07/07/2016.

[5] Anderson, Craig S. et al. “Rapid Blood-Pressure Lowering In Patients With Acute Intracerebral Hemorrhage”. New England Journal of Medicine 368.25 (2013): 2355-2365.

[6] ENLS 2017 (ICH)

[7] Burns, J., Fisher, J. and Cervantes-Arslanian, A. (2018). Recent Advances in the Acute Management of Intracerebral Hemorrhage. Neurosurgery Clinics of North America, 29(2), pp.263-272.

[8] Appiah, K., Minhas, J. and Robinson, T. (2017). Managing high blood pressure during acute ischemic stroke and intracerebral hemorrhage. Current Opinion in Neurology, p.1.

Landmark Stroke Trials Summarized

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NIHSS for Comatose Patients

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HAT Score

HAT Score predicts the risk of ICH after giving tPA