brain aneurysms av malformations 12263

8/13/2019 Brain Aneurysms Av Malformations 12263

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Brain Aneurysms

and

AV Malformations


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Brain Circulation


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Brain Circulation


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Arterial Circulation in the Brain


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Circle of Willis


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Cerebral Arteries


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Cerebral Angiography


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Venous Drainage


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Cerebral Spinal Fluid Drainage


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Cerebral Spinal Fluid


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Cerebral Spinal Fluid


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The Human Brain


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Aneurysm

The word aneurysm comes from theLatin word aneurysma, which means

dilatation.


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Types of Aneurysms

Saccular aneurysm

Occurs at bifurcations

Fusiform aneurysm

Commonly in basilar artery

Dissecting aneurysm

Ruptured aneurysm


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Aneurysm Types

SaccularFusiform


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Large Aneurysm


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Cerebral Aneurysms

Cerebral aneurysms usually occur at thebifurcations and branches of the large arterieslocated at the Circle of Willis.

The most common sites include the:

Anterior Communicating artery (30 - 35%)

Bifurcation of the Internal Carotid andPosterior Communicating artery (30 - 35%)

Bifurcation of Middle cerebral (20%)

Basilar artery bifurcation (5%)

Remaining posterior circulation arteries (5%)


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Risk Factors for Aneurysms

Smoking

Hypertension

Polycystic kidney disease 15% have aneury

Coarctation of the aorta Anomalous vessels

FMD

Connective tissue disorders (eg, Marfan, Ehlers-Danlos)

High-flow states (eg, vascular malformations,fistulae)

Spontaneous dissections/Trauma


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Signs & Symptoms ofBrain Aneurysms

Usually asymptomatic until rupture

Cranial Nerve Palsy

Dilated Pupils

Double Vision

Pain Above and Behind Eye

Localized Headache


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Warning Signs ofBrain Aneurysms

Warning signs prior rupture

Localized Headache

Nausea & Vomiting

Stiff Neck

Blurred or Double Vision

Sensitivity to Light (photophobia)

Loss of Sensation


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Treatment of Brain Aneurysms

Surgery

craniotomy andclipping of aneurysm

Endovascularcoiling


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Aneurysm Post-Op Risks

Rebleeding Most frequently within the first 24 hours

Up to 20% of patients rebleed within 14 days

Main preventative measure is control of blood pressure

(preferably beta blockers)

Vasospasm Usually occurs before 3 days or after 10 days (post bleed)

May require hyper-volemic therapy

Hydrocephalus Hyponatremia

Fluids/Electrolytes


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Arterio-Venous Malformation

(AVM) Arteriovenous malformation (AVM) of the brain is a"short circuitbetween the arteries and veins.

Normally the connection between arteries and veins

is through a network of smaller vessels (capillaries)which slow the blood down and permit the exchangeof food, oxygen and nutrients into the tissues.

In arteriovenous malformations, the arteriesand veins have a direct connection,bypassing the capillary network.


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Arterio-Venous Malformation (AVM)


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AVM

Arteriovenous malformation of the brainpresents later in childhood or, more frequently,

in adults in the second to third decade of life.

AVMs present with seizures, hemorrhage,progressive neurological dysfunction or

headaches


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Complications of AVMs

Hemorrhage (into surrounding tissue)

Ischemia

Seizures

Brain Cell Death


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Signs & Symptoms of AVMs

Seizures

Headaches

Whooshing" Sound (bruit)

Other SignsSubtle behavioral changesCommunication or thinking disturbancesLoss of coordination and balance

Paralysis or weakness in one part of the bodyVisual disturbancesAbnormal sensations


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Diagnosing AVMs

MRI (including MR Angiography) as well as CTAngiography are among the initial neuro-imagingtests that help identify these problems.

Cerebral Angiography is a prerequisite to accuratelyand definitively identify the precise anatomy andconfiguration of both the lesion as well as

the feeding and draining vessels


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Treatment of AVMs

Surgery

usually delayed

open ligation and/or resection of the AVM

Radiosurgery

Embolization

usually as adjunct to surgery

Observation


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Radiosurgery

Believed to "work" by initiating an "inflammatory"response in the pathological blood vessels ultimatelyresulting in their progressive narrowing and ultimate

closure

The risk for hemorrhage is not reduced during thislag time

There is the added risk of radiation necrosis ofadjacent healthy brain tissue or brain cyst formation


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Radiosurgery

Advantages:

Noninvasive

Can access all anatomic locations of the Brain

Disadvantages:

Can only treat smaller lesions(


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AVM Post-Op Risks

Perfusion-breakthrough bleeding

Endovascular occlusion


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Intracranial Hemorrhage (ICH)

Epidural

Subdural

Subarachnoid

Intraparencymal

Intraventricular Cerebellar


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Subarachnoid Hemorrhage (SAH)

SAH may be spontaneous or traumatic

Spontaneous SAH are caused by

Cerebral aneurysms

AV malformations

Uncommon causesneoplasms,AVMs, venous angiomas, infectiousaneurysms


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SAH

Warning bleeds are relatively common

Sentinel headache 30-50%

Early diagnosis prior to rupture will improveoutcomes

Unusual headache

50% of patients die within 48 hoursirrespective of therapy


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SAH

Often accompanied by aperiod of unconsciousness(50% never wake up)

Common signs includeneck stiffness,photophobia, headache

20% have ECG evidenceof myocardial ischemia


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Complications of SAH

Hydrocephalusmay develop within the first 24hours because of obstruction of CSF outflow inthe ventricular system by clotted blood.

Rebleedingof SAH occurs in 20% of patients inthe first 2 weeks. Peak incidence of rebleedingoccurs the day after SAH. This may be from lysisof the aneurysmal clot.

Vasospasmfrom arterial smooth musclecontraction (symptomatic in 36% of patients).


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HydrocephalusAfter SAH

Caused by obstruction of CSF flow byclotted blood

Must be careful with drainageareduction in ICP can increase the riskof rebleeding


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RebleedingAfter SAH

Rebleeding occurs most frequently within the first24 hours

Up to 20% of patients rebleed within 14 days

The main preventative measure is to control theblood pressurepreferably beta blockers

Alternatively early clipping of the aneurysmallows hypertensive and hypervolemictherapy to prevent vasospasm


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VasospasmAfter SAH

Worst time is day 7 to day 10 (most frequenttime for vasospasms)

Diagnosed by neurologic exam, transcranial

doppler and angiography

May use calcium channel blockers

Reduce vasospasm, neurological deficit,

cerebral infarction and mortality

May use some antispasmodics


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VasospasmHHH Therapy

Hemodilution

Hct 30-35%

HypertensionPhenylephrine / Norepinephrine

BP titration to CPP/exam

Hypervolemia

Colloids/crystalloids


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Other VasospasmTherapy

Angioplasty

BP management during procedure

Reperfusion issues

Timing

Papaverine Infusion

Side effects

Repeated trips


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Other Complications of SAH

Neurologic deficitsfrom cerebral ischemia, peaks at days 4-12.

Hypothalamic dysfunctioncauses excessive sympatheticstimulation, which may lead to myocardial ischemia or labile

detrimental BP.

Hyponatremiamay result from cerebral salt wasting / SIADH

Nosocomial pneumoniaand other complications

of critical care may occur.

Pulmonary edemaneurogenic & nonneurogenic


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Treatment of SAHs

1) Identifying and treating the causativelesion, thus preventing re-bleeding

2) Treating hydrocephalus

3) Treating and preventing

vasospasm


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Treatment of SAHs

Maintain systolic BP >130mmHg

Use vasopressors if necessary to maintain

CPP and reduce ischemic complicationsfrom vasospasm

Generally avoid vasodilators (except

calcium channel blockers)


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The End

Thank You

brain aneurysms av malformations 12263

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