Kalani R Wells, APRN, MSN, ACNP-BC, CNRN - PowerPoint Presentation

Slide1

Kalani R Wells, APRN, MSN, ACNP-BC, CNRN Neurologic Associates, Ltd.AANN Neuroscience Nursing SymposiumMarch 14th 2015

Unique Cerebrovascular DisordersSlide2

Cerebrovascular Disease3rd leading cause of death behind heart disease and cancerPrevalence is 794 per 100,000>700,000 have a stroke every year in the U.S. One of the leading causes of disability, huge economical impact Slide3

Identify Associated Stroke disorders- Types, etiology, presentation, diagnostic workup, treatment TIA- transient ischemic attack Intracranial and extracranial stenosis Dissection- carotid and vertebral

Moya MoyaArteriovenous malformation

Arterio

-venous fistula and dural A-V fistula

Cavernous

Angioma

VasculitisHypercoaguable states Slide4

Cerebrovascular Disease Caused by one of 3 thingsSlide5

Cerebrovascular Disease Caused by one of 3 thingsBad blood vessels- atherosclerosis, inflammation, amyloid, dissection, AV malformation, aneurysm, venous thrombosis

Bad Heart- Afib , CHF, previous MI, cardiomyopathy, mural thrombus, PFO , vegetationBad Blood-

hypercoaguable

state, clotting disorder, malignancy, sickle cellSlide6

Transient Ischemic Attack-TIA Defined as transient episode of neurologic dysfunction caused by focal brain, spinal cord or retinal ischemia without evidence of tissue injury on imaging No longer a timeframe- used to be <24hrsSlide7

Transient Ischemic Attack-TIARisk of stroke in first 48 hrs is 4-10%

Esp if-DM,>60,BP >140/90, hemiplegia, speech changes during TIA, TIA >60 min

Diagnostic workup- CT brain, MRI/MRA brain, echo, CUS, labs (

inpt

vs

OP)

Identify modifiable risk factors- DM, HTN, HL, afib, cocaine, smoking cessation Treatment and interventions- ASA, statin, antihypertensive “triple therapyTreatment

is determined by findingsSlide8

Transient Ischemic Attack-TIA Things that can look like TIASeizures- partial or focal, Todd’s paralysisMigraine auras or complex migraineSyncope, convulsive syncope, vasovagal, Position related peripheral nerve root compression- “Saturday night palsy” wrist dropBPPV, vestibulopathies, Meniere’s

Metabolic-hypoglycemia, uremia, hyponatremia, hepatic, pulmonarySlide9

Extracranial StenosisSlide10

Carotid stenosisSlide11

Intracranial and Extracranial StenosisCarotid stenosis-In symptomatic good-risk patients with surgical morbidity and mortality (stroke and death) of less than 6%, proven indications for CEA include One or more transient ischemic attacks (TIAs) in the preceding 6 months and carotid artery stenosis exceeding 50%Acceptable but not proven indications include the following:Ipsilateral TIA and carotid artery stenosis exceeding 70%, combined with required coronary artery bypass grafting (CABG)

Progressive stroke and carotid artery stenosis exceeding 70%Asyptomatic

stenosis, rate of ipsilateral stroke increase with >70%Slide12

Carotid EndartarectomySlide13

Carotid Artery Stenting

Pre-Stenting

Post-StentingSlide14

Intracranial StenosisSAMPRISSIntracranial angioplasty or stentingTriple therapy- ASA, Plavix, statinClose follow up EC-IC bypassSlide15

Intracranial Stenosis - StentingSlide16

Dissection- Carotid and Vertebral Tear in the vessel wall Clinical presentation- stroke like symptoms, horners, neck painDiagnostic workup- CTA head and neck, MRI/MRA, tox screen, underlying collagen vascular disorder

Good history !!!! Trauma, strain, chiropractorTreatment- anticoagulation, antiplatelets

, stentingSlide17

Carotid dissectionSlide18

MOYAMOYASlide19

MoyAMoya Disease Moyamoya disease is a rare, progressive cerebrovascular disorder caused by blocked arteries at the base of the brain in the basal ganglia. “moyamoya” means “puff of smoke” in Japanese and describes the look of the tangle of tiny vessels formed to compensate for the blockage. 

Moyamoya disease was first described in Japan in the 1960’s and it has since been found in individuals in the United States , Europe, Australia , and Africa. 

Tends to be familial,

inherited genetic

abnormalities

The

disease primarily affects children, but it can also occur in

adults Slide20

Moya MoyaClinical Presentation-in children, the first symptom of Moyamoya disease is often stroke, or recurrent transient ischemic attacks (TIA, commonly referred to as “mini-strokes”), usually accompanied by muscular weakness or paralysis affecting one side of the body, or seizures. 

Adults most often experience a hemorrhagic stroke due to recurring blood clots in the affected brain vessels. May also have change in consciousness, speech deficits (usually aphasia), sensory and cognitive impairments, involuntary movements, and vision problems.

Diagnostic Workup- include images,

MR,angios

…Slide21

MoyaMOyaTreatment and Interventions-Encephaloduroarteriosynangiosis (EDAS)- Surgical transposition of the superficial temporal artery with attached galea to the underlying dura with hope for cerebral revascularization of collateral flowEC-IC bypass- extracranial to intracranial bypass

ASA , AED’S if seizures, symptom management Slide22

Arteriovenous MalformationAbnormal collection of blood vessels, tangle Arterial blood flows directly into draining veins, no capillary bedCongenital lesions

Lifelong risk of bleeding 2-4% per yr.Have a nidus, pedicle is small artery that feeds it ,can have one or many7% have aneurysms Slide23

AVMSlide24

Vascular MalformationsSlide25

Arteriovenous Malformation PresentationHemorrhage ≈ 50%(10% mortality,30-50% morbidity )Seizures Mass effect

Ischemia (steal)HeadacheIncreased ICP, bruit (dural based), hydrocephalus (

peds

)Slide26

SPETZLER-MARTIN AVM GRADING SYSTEM

Graded feature Score

Size

Venous drainage

Eloquence of adjacent brain

small ( < 3 cm) 1 medium(3-6 cm) 2 large (>6 cm) 3

non - eloquent 0

eloquent

1

superficial only 0

deep

1

Slide27

What is a DAVF? Intracranial dural arteriovenous fistulas (DAVFs), acquired lesions, an abnormal connection between intracranial arteries and veinsRare, pathology ranges from benign to deadlySlide28

Dural AV fistulas Actual incidence of DAVFs is unknown, thought to be one tenth that of brain arteriovenous malformations (AVMs

)The incidence of AVM’s is 3 per 100,000 annually (Nguyen, Raymond,

Norbash

, & Roy, 2011

) As

a result these lesions account for 10-15% of all intracranial arteriovenous

shunting Slide29

DAVF-Incidence, Natural History, PathophysiologyExact pathomechanism unknown Venous sinus

thrombosis, promotes venous hypertension, and hypoxia, the catalyst in opening up microscopic vascular dural

connections

Previous

surgery

Ear infection Head traumaSlide30

High pressure blood flow through the artery pumps directly into a vein which is normally accustom to a lower venous pressure, in turn can cause enlargement and rupture of cortical veins, resulting in intracranial hemorrhage (ICH

)

DAVFSlide31

Treatment GoalsUltimate goal to prevent ICH and complicationsTreatment tailored to the specific needs of the

patient, each patient’s clinical presentation and angioarchitecture is different

CVR(cortical venous reflux=aggressive, most likely present w/

ICH,neuro

deificts

Annual M&M~7.5% as high 15%

Benign stable over time 2% convert to aggressive>90% can be cured w/ Tx

.

Avg

risk of perm neuro deficit from

endo

tx

4-5%Slide32

DAVF Treatment ConsiderationsClinical presentationLocation and sizeAngioarchitecture Accessibility of pedicles

Venous drainageID of fistulous connectionSlide33
Slide34

Combined modality therapy for AVM/DAVF

Microsurgical removal

Neuroendovascular

therapy

Stereotactic radiosurgerySlide35

Controllable Material

Complete filling

Non-adhesive but Cohesive

Concurrent angiography

Time and Decision Making

ONYX

TM

- PerformanceSlide36

Contact with blood = “Precipitation”Solvent diffuses away

Forms a spongy polymeric castForms a skin - solidifies from the outside in

Liquid center continues to flow

ONYX

TM

Embolization ProcessSlide37

39 Y Male Gr 3 L frontal AVM

Pre

Post Slide38

Before After Embolization Slide39

Treatment Goals-TechnicalUnintentional embolization of these branches can occlude the arterial supply to the corresponding CN, causing infarct and subsequent CN palsy resulting in substantial morbiditySlide40

Always consider…Clinical presentationLocation and sizeAngioarchitecture

Accessibility of pediclesVenous drainageIdentification

of nidusSlide41

All Treatments may be necessary

Goal

Optimal treatment for each individual patientSlide42

Cerebral Venous ThrombosisLess common- obstruction of the venous structures - increased venous pressure, increase cerebral blood volume, disrupts blood brain barrier -> vasogenic edema, venous hemorrhage, venous infarct, impaired CSF absorptionFinding it more b/c of better imaging More common in women than men- associated with pregnancy, and oral contraceptives

Diagnostic workup- Testing for prothrombotic conditions (including protein C, protein S, or

antithrombin

deficiency),

antiphospholipid

syndrome,

prothrombin

G20210A mutation, and factor V Leiden can be beneficial for the management of patients with CVT. Testing for protein C, protein S, and antithrombin deficiency is generally indicated 2-4 weeks after completion of anticoagulation. There is a very limited value of testing in the acute setting or in patients taking warfarinSlide43

Cerebral Venous ThrombosisClinical Presentation- cerebral venous thrombosis present with a wide spectrum of signs and symptomsMost common are headaches (> 80%), seizures (approximately 40%), hemiparesis (approximately 40%), altered consciousness (15-20%), and papilledema (20-30%)

One study reports increasing headache without previous headaches history or headaches in combination with neurological deficits or seizures has been reported at approximately 10%, but has not yet been confirmed by other studies Slide44

Cerebral Venous ThrombosisTreatment and Interventions- angiogram, anticoagulation, thrombectomy, TPA infusionSlide45

Cavernous Angioma cavernomacavernous angiomacavernous hemangiomacerebral cavernous malformation (CCM)Cavernous malformations are dilated blood vessels that are characterized by multiple distended "caverns" of blood-filled vasculature through which the blood flows very

slowly Vessels of a cavernous malformation lesion have a tendency to leak because they lack the proper junctions between neighboring cells as well as the necessary structural support from smooth muscle and stretchable material (elastin

)

Leakage

(bleeding) from these vascular lesions is the underlying cause of clinical symptoms associated with the illness. Cavernous malformations are primarily located in the

brain

, but can also be found in the spinal

cordAngio occult Tx- surgical

vs

nothing, AED’sSlide46

Cavernous angiomaSlide47

CNS vascultitisVery rareInflammationStrokes, cognitive changes Workup- labs, angio,MRI/MRA, brain biopsy Treatment- steroids, cellcept,

Rituxan Slide48

VasculitisSlide49

CNS vasculitisSlide50

Hypercoaguable statesGood history- genetic disorders, factor 5 , anti-phospholipidLook for underlying malignancylabsAnticoagulation Look for this especially in young patients with stroke Slide51

Questions? Slide52

Thank You!

Kalaniwells1@gmail.comSlide53

ReferencesDe Keukeleire, K., Vanlangenhove, P.,

Kalala Okito, J., Hallaert

, G., Van Roost, D., &

Defreyne

, L. (2011). Transarterial embolization with ONYX for treatment of intracranial non-cavernous dural arteriovenous fistula with or without cortical venous reflux.

Journal of

NeuroInterventional

Surgery, 3(3), 224-228. doi:10.1136/jnis.2010.004119 Geibprasert S,

Pongpech

S, Armstrong D,

Krings

T. Dangerous extracranial-intracranial anastomoses and supply to the cranial nerves: vessels the neurointerventionalist needs to know.

AJNR Am J

Neuroradiol

. 2009;30(8):1459-

1468

Hu, Y. C., Newman, C. B.,

Dashti

, S. R., Albuquerque, F. C., & McDougall, C. G. (2011). Cranial dural arteriovenous fistula: Transarterial onyx embolization experience and technical nuances.

Journal of

NeuroInterventional

Surgery, 3

(1), 5-13. doi:10.1136/jnis.2010.003707 Slide54

ReferencesNorth American Symptomatic Carotid Endarterectomy Trial Collaborators. Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade carotid stenosis. N Engl J Med 1991; 325:445.MRC European Carotid Surgery Trial: interim results for symptomatic patients with severe (70-99%) or with mild (0-29%) carotid stenosis. European Carotid Surgery Trialists' Collaborative Group. Lancet 1991; 337:1235.Fukui M. Guidelines for the diagnosis and treatment of spontaneous occlusion of the circle of Willis ('moyamoya' disease). Research Committee on Spontaneous Occlusion of the Circle of Willis (Moyamoya Disease) of the Ministry of Health and Welfare, Japan. Clin Neurol Neurosurg 1997; 99 Suppl 2:S238.Slide55

ReferencesKiyosue, H., Hori, Y., Okahara, M., Tanoue, S.,

Sagara, Y., Matsumoto, S., . . . Mori, H. (2004). Treatment of intracranial dural arteriovenous fistulas: Current strategies based on location and hemodynamics, and alternative techniques of transcatheter Embolization1.

Radiographics

, 24

(6), 1637-1653. doi:10.1148/rg.246045026

Spiotta

, A. M., Hughes, G., Masaryk, T. J., &

Hui, F. K. (2011). Balloon-augmented onyx embolization of a dural arteriovenous fistula arising from the neuromeningeal trunk of the ascending pharyngeal artery: Technical report.

Journal of

NeuroInterventional

Surgery, 3

(3), 300-303. doi:10.1136/jnis.2010.003095