Modified Raymond–Roy Classification

  • Class I: complete obliteration12.jpg
  • Class II: residual neck
  • Class IIIa: residual aneurysm with contrast within coil interstices
  • Class IIIb: residual aneurysm with contrast along aneurysm wall





<click here to access MS ppt file>




Hospital, Massachusetts. “Endovascular Procedures To Prevent Ruptured Brain Aneurysms”. Massachusetts General Hospital. N.p., 2016. Web. 11 Dec. 2016.

Mascitelli, Justin R et al. “An Update To The Raymond–Roy Occlusion Classification Of Intracranial Aneurysms Treated With Coil Embolization”. Journal of NeuroInterventional Surgery 7.7 (2014): 496-502.


Antiplatelets for Stent-Coil Techniques

  • ASA (325 mg daily) and clopidogrel (75 mg daily) x 5 days prior to procedure
  • platelet aggregometry 1–2 days before procedure
  • further loading of aspirin and/or clopidogrel PRN
  • unanticipated stenting
    • load with IV or IA abciximab intraprocedurally
    • then load and maintain on ASA and clopidogrel
  • systemic heparinization prior to guide catheter introduction, target activated clotting time 2–2.5 greater than baseline



Spiotta, Alejandro M et al. “Comparison Of Techniques For Stent Assisted Coil Embolization Of Aneurysms”. Journal of NeuroInterventional Surgery 4.5 (2011): 339-344.


Stent-Assisted Coiling Techniques

  1. ‘jailing’ of microcatheter
    • stent deployed after the aneurysm is catheterized but before coil deployment
    • microcatheter pinned between intima and stent, coils are kept within the aneurysm and outside of vessel lumen
    • A.jpg
  2. ‘coil through’
    • stent fully deployed across aneurysm neck
    • aneurysm catheterized through the tines of the stent
    • b
  3. ‘coil stent’
    • unassisted coil embolization to completion followed by stent deployment
    • capitalizes on biologic benefit of vascular remodeling or to constrain a prolapsed coil loop
    • C.jpg
  4. ‘balloon stent’
    • stent placement after completion of balloon assisted embolization
    • D.jpg
  5. other techniques
    • coiling with ‘Y stent’ configuration for basilar tip aneurysms
    • depositing single or multiple stents for flow diversion for blister dorsal carotid wall aneurysms







Spiotta, Alejandro M et al. “Comparison Of Techniques For Stent Assisted Coil Embolization Of Aneurysms”. Journal of NeuroInterventional Surgery 4.5 (2011): 339-344.



Treatment of Aneurysms

  • Clipping Most aneurysms
  • Coiling Most aneurysms
  • Flow diversion Large proximal ICA aneurysms, blister aneurysms
  • Flow diversion with adjunctive coiling Large and giant aneurysms with wide necks
  • Intrasaccular flow diversion Bifurcation aneurysms with neck ≥4 mm
  • Coiling with assistive stenting Wide-neck aneurysms and aneurysms with branch vessels near/incorporating aneurysm neck
  • Parent vessel sacrifice or branch vessel sacrifice with bypass Dissecting aneurysms, giant aneurysms with branch vessels incorporating aneurysm neck
  • Parent vessel sacrifice without bypass Distal PICA aneurysms, distal PCA aneurysms, distal mycotic aneurysms



Walcott, Brian P. et al. “Blood Flow Diversion As A Primary Treatment Method For Ruptured Brain Aneurysms—Concerns, Controversy, And Future Directions”. Neurocritical Care (2016): pp 1-9.

FXa and “Universal” Reversal Agent Drug Targets

  • Andexanet alfa = recombinant modified FXa decoy molecule
    • see previous blog
  • Ciraparantag = reverse many anticoagulants including the FXa inhibitors
    • developed by Perosphere
    • formerly known as “aripazine” or “PER977”
    • di-arginine piperazine
    • small (512 Da) synthetic molecule
    • binds to UFH, LMWH, fondaparinux, DOACs
    • inactivates anticoagulants via noncovalent hydrogen binding, blocks binding to target sites of FIIa and FXa
FXa and “Universal” Reversal Agent Drug Targets:


Milling, Truman J. and Scott Kaatz. “Preclinical And Clinical Data For Factor Xa And “Universal” Reversal Agents”. The American Journal of Emergency Medicine 34.11 (2016): 39-45.

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

BEST TRIAL (2019) – BP after Endovacular Therapy for Ischemic Stroke [9]; study validates that a peak SBP of 158 mm Hg during 1st 24h post-EVT best dichotomies good versus bad outcomes in EVT-treated patients.

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


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.


[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.

[9] Mistry EA et al, Stroke. 2019 Oct 7:STROKEAHA119026889. doi: 10.1161/STROKEAHA.119.026889. [Epub ahead of print] Blood Pressure after Endovascular Therapy for Ischemic Stroke (BEST): A Multicenter Prospective Cohort Study.

SAH Management Algorithm



  • In our practice, we prefer to start seizure prophylaxis in the setting of an unsecured aneurysm to abate potential deleterious effects of seizures on an already dysregulated brain. (N.B. We prefer agents other than phenytoin.)
  • The 2012 American Stroke Association guidelines suggest that a decrease in systolic blood pressure to <160mm Hg is reasonable, but in our clinical practice,  we keep the systolic blood pressure <140mm hg to further lower the risk of aneurysmal rerupture, as long as the patient is alert and CPP is adequate.

pdf file: nrneurol.2013.246-pf1


Macdonald, R. Loch. “Delayed Neurological Deterioration After Subarachnoid Haemorrhage”. Nature Reviews Neurology 10.1 (2013): 44-58.


Checklist: Predictors of DCI

  • SAH Blood clot:  Volume, location, persistence over time and density
  • Poor clinical condition on admission and loss of consciousness at ictus
  • smoking (strong)
  • diabetes (mod)
  • systemic inflammatory response syndrome (mod)
  • hyperglycaemia (mod)
  • hydrocephalus (mod)
  • hex?
  • history of hypertension?
  • age (inconsistent)

CSF molecules that are possible markers of DCI

  • endothelin-1
  • IL-6
  • some markers of thrombin activation

Serum biomarkers (association, but not validated)

  • TNF
  • IL-6
  • S100β
  • ubiquitin C-terminal hydroxylase 1
  • phosphorylated axonal neurofilament heavy chain
  • matrix metalloproteinases
  • von Willebrand factor
  • endothelin-1
  • vascular endothelial growth factor
  • selectins
  • adhesion molecules



Macdonald, R. Loch. “Delayed Neurological Deterioration After Subarachnoid Haemorrhage”. Nature Reviews Neurology 10.1 (2013): 44-58.


How Cortical Spreading Ischemia leads to DCI



  • cortical neuronal swelling
  • dendrite spine distortion
  • slow changes in brain electrical potential (spreading depolarization)
  • decreased brain electric activity (spreading depression)

Normal Neurovascular Coupling:  Spreading depolarization –> arterioles vasodilate –> hyperemia –> no permanent damage

Abnormal Response:  Spreading depolarization –> inc astrocyte calcium and activation of calcium-activated potassium channels –> arterioles constrict –> waves of cortical hypoperfusion or cortical spreading ischemia

How does this happen?  sodium and calcium influx through multiple ion channels –> loss of electrically negative intraneuronal state –> spreading depolarizations –> prevents action potential formation –> propagates as a wave across cortex –> neurons lack adequate energy supplies to re-establish transmembrane ionic gradients –> cortical spreading ischemia

Subdural strip electrodes studies:

  • 70% of SAH aptients have repetitive cortical spreading depolarizations
  • some patients developed DCI that was spatially and temporally associated with angiographic vasospasm and cortical spreading depolarization
  • patients who had depolarization lasting >60minutes developed infarction on CT or MRI

Cortical spreading ischemia after SAH can be inhibited by nimodipine, NMDA receptor antagonists and prevention of systemic volume depletion


Macdonald, R. Loch. “Delayed Neurological Deterioration After Subarachnoid Haemorrhage”. Nature Reviews Neurology 10.1 (2013): 44-58.

CHESS (Chronic Hydrocephalus Ensuing from SAH Score)

The European Journal of Neurology recently published a risk score that allows early estimation of the probability for shunt dependency after subarachnoid hemorrhage. CHESS stands for Chronic Hydrocephalus Ensuing from SAH Score.  This score can be helpful in deciding whether a permanent CSF diversion is needed in post-hemorrhage hydrocephalus (PHH).

Inclusion criteria for the study:

  1. admission and treatment of ruptured aneurysm within 48 hours post-ictus
  2. patient survives up to the time of decision-making for shunt placement


Baseline Characteristics:


PHH was divided into 3 stages:

  1. acute (0-3 days post-SAH)
  2. subacute (4-13 days)
  3. chronic (>=14 days)


All patients with acute PHH underwent CSF diversion via EVD or lumbar drainage.  Continuous drianage was maintained for at least 7 days.  Patients who developed subacute PHH were treated with serial lumbar punctures.

The drain (EVD or lumbar drain) was challenged starting the second week of SAH in the absence of clinical contraindications (ICP issues or infection).  Drain was closed for 48 hours with CT scans performed before and after clamping.

Patients considered to fail EVD/LD challenge if:

  1. they deteriorate neurologically and/or they have increased headaches that improve with unclamping the drain
  2.  sustained ICP increase >20 cm H20
  3. radiographic evidence of increased ventricular size compared to baseline CT (CT prior to clamping)

Shunt placement was performed after two unsuccessful clamping trials.





The  following independent risk factors were identified and included in the CHESS:

  1. Hunt and Hess grade ≥IV (1 point, OR = 2.65)
  2. aneurysm in posterior circulation (1 point, OR = 2.37)
  3. (+) IVH on initial CT (1 point, OR = 2.41)
  4. (+) acute PHH (4 points, OR = 9.36)
  5. early cerebral infarction on follow-up CT scan (1 point, OR = 2.29)


The ROC curve between the CHESS and shunt rates showed a significant cutoff at 6 points.

  1. CHESS score ≥6 = 6.74-fold higher risk for shunt dependency (P < 0.0001)
  2. CHESS score <6 points showed NPV of 84.9%.
  3. CHESS <2 points showed NPV of 98.5%



  1. avoid unnecessary prolonged EVD/LD weaning (and reduce catheter-related meningitis)
  2. reduce readmission rates (for delayed shunt placement)

Based on this score, patients can be stratified into:

  1. high risk – score of 6-8
  2. moderate risk – 2-5
  3. low risk – 0-1

A shunt-restrictive policy as well as an early transfer to rehabilitation can be considered in SAH patients with low CHESS scores.



Jabbarli, R. et al. “The CHESS Score: A Simple Tool For Early Prediction Of Shunt Dependency After Aneurysmal Subarachnoid Hemorrhage”. Eur J Neurol (2016).