Category Archives: Uncategorized

Procedure for Securing Integra Lumbar Drain

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REFERENCE:

LHH Department of Neurosurgery Guideline. <pdf attached>

 

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Collateral Circulation Grading System

collateral circulation grading system from the American Society of Interventional and Therapeutic Neuroradiology/American Society of Interventional Radiology (ASITN/SIR)

Grade 0: No collaterals visible to the ischemic site

Grade 1: Slow collaterals to the periphery of the ischemic site with persistence of some of the defect

Grade 2: Rapid collaterals to the periphery of ischemic site with persistence of some of the defect and to only a portion of the ischemic territory

Grade, 3: Collaterals with slow but complete angiographic blood flow of the ischemic bed by the late venous phase

Grade 4: Complete and rapid collateral blood flow to the vascular bed in the entire ischemic territory by retrograde perfusion

Grade of 0-1 indicates poor collateral circulation

Grade 2 indicates moderate collateral circulation

Grades of 3-4 indicate good collateral circulation

References

Chen, W., Song, X., Tian, D., Sun, H., Zhang, L., Hui, X., Ip, B. and Wang, X. (2019). Clinical efficacy of collateral circulation in the evaluation of endovascular treatment for acute internal carotid artery occlusion. Heliyon, 5(4), p.e01476.

R.T. Higashida, A.J. Furlan, H. Roberts, T. Tomsick, B. Connors, J. Barr, W. Dillon, S. Warach, J. Broderick, B. Tilley, D. Sacks, I. Technology Assessment Committee of the American Society of, N. Therapeutic, R. Technology Assessment Committee of the Society of Interventional, Trial design and reporting standards for intra-arterial cerebral thrombolysis for acute ischemic stroke, Stroke 34 (8) (2003) e109ee137.

Arteriovenous Malformation Scores

Table.  Predictive grading systems for procedural risk in the endovascular treatment of brain AVMs.Capture

 

Buffalo score best predicts procedural risks, although predictive value is modest (AUC ~0.7).

 

Reference:

Pulli, B., Stapleton, C., Walcott, B., Koch, M., Raymond, S., & Leslie-Mazwi, T. et al. (2019). Comparison of predictive grading systems for procedural risk in endovascular treatment of brain arteriovenous malformations: analysis of 104 consecutive patients. Journal Of Neurosurgery, 1-9. doi: 10.3171/2019.4.jns19266

 

Indications for Screening Dopplers on Hospital Admission

  1. known hypercoagulable disorder
  2. admitted from another institution
  3. presents with significant leg immobility
  4. presents with signs and symptoms of VTE
  5. significant critical illness
  6. significant neurotraums (TBI, SCI / TLS spine fractures)
  7. comatose
  8. known malignancy (e.g. GBM, meningioma)
  9. CKD on hemodialysis
  10. received platelet transfusion or antithrombotic reversal
  11. recent major orthopedic surgery

Order screening dopplers as “urgent” and not routine.

 

Reference:

North Shore University Hospital VTE Prophylaxis Guidelines (Neurocritical Care)

Contrast-Induced Transient Cortical Blindness

 

  • Can occur with ionic or nonionic contrast media
  • MECHANISM: transient vasculopathy with disruption of BBB – a form of PRES
  • CLINICAL PRESENTATION
    • Onset within mins to hours after procedure
    • Begins with BOV –> complete blindness rapidly, associated with HA
    • Other symptoms: n/v, confusion, aphasia, memory impairment, weakness, ataxia
  • DIAGNOSTICS
    • CT head: enhancement from contrast during cardiac cath, affecting cortex (parieto-occipital lobes, deep gray structures, BS, cerebellum)
    • Symmetric white matter edema in posterior cerebral hemispheres
  • Neuro impairment and neuroimaging gradually resolve over days

 

Reference:

UpToDate. (2019). Retrieved from https://www.uptodate.com/contents/stroke-after-cardiac-catheterization?search=tpa%20cardiac%20cath&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1

Stroke After Cardiac Cath

MECHANISM

  • Catheter or wire manipulation dislodges debris (thrombus, calcified material, cholesterol particles) from plaques within aortic arch, prox carotid / vertebral arteries
  • Fresh thrombus may form at catheter and guidewire tips
  • Less common: air embolism, thromboembolism from LV clot, periprocedural hypotension, arterial dissection, fractured guidewire
  • Hemorrhagic stroke fromthrombolytics, anticoagulants and antiplatelets used periprocedurally

INCIDENCE

  • Cardiac cath (ALL) stroke within 36h occurs: 0.1-0.6%
  • PCI: 07-0.4%
  • Hemorrhagic stroke (mostly ICH): 8-45% of cardiac cath strokes
  • SAH after cardiac cath uncommon
  • Asymptomatic radiographic infarcts after diagnostic cardiac cath: 8%
    • clinically symptomatic events (stroke+TIA): 0.6%
  • TCD: higher prevalence (up to 100%) of microemboli during cardiac cath
    • Majority occur during contrast injection (mostly air bubbles)
    • Smallernumber with movement of catheter/guidewire (mostly particles – atheromatous debris)

RISK FACTORS

  • Clinical: >75-80y, HTN, DM, h/o stroke, renal failure, CHF, severity of CAD
  • Procedural: emergent, longer procedure, greater contrast, retrograde cath of LV in AS, interventions at bypass grafts, use of IABP, (+) coronary artery thrombus
  • Risks for ICH: (+) anticoagulation or thrombolytic therapy + any one of the ffg:  age >=75, femal, SBP >=160, black race, low body weight

TIMING

  • Mostly during procedure or within 24h after procedure
  • Maximal deficit at onset or fluctuating course = ischemic stroke
  • Gradual worsening over minutes to hours and signs of increased ICP= hemorrhage

SSX:

  • Ischemic stroke / ICH: Visual disturbance, aphasia, dysarthria, hemiparesis, AMS
  • SAH: HA, global neuro deficits, altered LOC
  • Diffuse embolization: nonfocal presentation, reduced alertness, encephalopathy

 

DIAGNOSTICS:

  • Activate stroke team, time of onset, last know normal (last time alert enough to be assessed, in sedated patient)
  • ABCs
  • Serum glucose
  • Platelets, coagulation studies (if suspected)
  • IMAGING
    • CT, CTA, CTP
    • Some experts advocate immediate angio + IA thrombolysis

 

DIFFERENTIALS:

  • TIA
  • Seizure
  • Migraine
  • Encephalopathy
  • Toxic-metabolic encephalopathy
    • Sedation from procedure
    • Co-morbid medical or neuro conditions
  • CONTRAST-INDUCED TRANSIENT CORTICAL BLINDNESS
    • Can occur with ionic or nonionic contrast media
    • MECHANISM: transient vasculopathy with disruption of BBB – a form of PRES
    • CLINICAL PRESENTATION
      • Onset within mins to hours after procedure
      • Begins with BOV à complete blindness rapidly, associated with HA
      • Other symptoms: n/v, confusion, aphasia, memory impairment, weakness, ataxia
    • DIAGNOSTICS
      • CT head: enhancement from contrast during cardiac cath, affecting cortex (parieto-occipital lobes, deep gray structures, BS, cerebellum)
      • Symmetric white matter edema in posterior cerebral hemispheres
    • Neuro impairment and neuroimaging gradually resolve over days

 

TREATMENT (Ischemic Stroke)

  • tPA for eligible patients (within 4.5h stroke onset)
    • safe and efficacious
    • evidence of benefit, but risk of bleeding high (recent use of antithrombotic therapy + procedural risks of bleeding)
    • studies show improved NIHSS, no difference inmortality or bleeding events
    • document normal PTT prior to IV tPA if heparin given within 48h
    • protamine can be used to reverse heparin
    • GP2B3A – unknown if may increase risk of bleed with tPA, but preliminary data suggests safety
    • Single or DAPT not contraindication
  • mechanical thrombectomy (within 6h)
  • IA alteplase in 4.5-6h time window if not eligible for tPA but eligible for thrombectomy

TREATMENT (Hemorrhagic Stroke)

  • Reversal of anticoagulation, stop all anticoagulants and antiplatelets
  • BP control
    • labetalol, nicardipine, esmolol, enalapril, hydralazine, nitroprusside, NTG
    • <=185/110 if tPA given
    • <=220/120 if no tPA given
  • Treatment of ICP
    • HOB 30 degrees, analgesia (morphine, alfentanil), sedation (propofol, etomidate, midazolam)
    • Mannitol, EVD, NM blockade, hyperventilation
    • ICP monitoring, goal CPP>70mm Hg
  • Surgery
    • Cerebellar bleed >3cm with BS compression / hydrocephalus – surgical evacuation
    • Supratentorial bleed: consider crani only for lobar clots within 1cm of surface

PROGNOSIS

  • Stroke after cardiac cath: high in-hospital and 30d mortality rate
  • 30d mortality rate after PCI
    • 19% (ischemic stroke)
    • 50% (hemorrhagic)
    • 2% (if no stroke)

 

Reference:

UpToDate. (2019). Retrieved from https://www.uptodate.com/contents/stroke-after-cardiac-catheterization?search=tpa%20cardiac%20cath&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1

How to Measure Transcalvarial Herniation

The volume of brain tissue herniated through the craniectomy (TCH) can be measured according to the model proposed by Liao et al. Based on trigonometry and the mathematical concepts of radius and diameter of a sphere (skull), a formula was created that uses simple measurements of the values and differences between height (h) of the apparently normal contralateral side of the brain and that of the side of herniation. Fig. 1 illustrates the method used to calculate the volume of TCH in millimeters.

REFERENCES:

Neto, A., et al. Clinical Neurology and Neurosurgery. Transcalvarial brain herniation volume as a predictor of posttraumatic hydrocephalus after decompressive craniectomy. https://doi.org/10.1016/j.clineuro.2019.05.003

C.C. Liao, Y.H. Tsai, Y.L. Chen, K.C. Huang, I.J. Chiang, J.M. Wong, F. Xiao, Transcalvarial brain herniation volume after decompressive craniectomy is the difference between two spherical caps, Med. Hypotheses 84 (3) (2015)(2015)