Neurosurgery: Vascular Disease Flashcards by Hanna Algattas

What is the adult prevalence of aneurysms?

What is the annual incidence of aneurysmal SAH?

Adult prevalence: 2%

Annual incidence aSAH: 0.006-0.008%

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What are modifiable risk factors for aneurysmal SAH?

HTN, smoking, alcohol abuse

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What percent of patients with aSAH die before reaching the hospital? What percent die by one month?

Before hospital: 10-15%

One month: ~50%

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What are the major morbidities associated with aSAH?

Rebleeding, Vasospasm, Hydrocephalus, Seizures, Cardiac complications, Hyponatremia

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With aneurysms <7mm in size without a previous SAH what is the approximate 5 year risk of bleeding for each of the below categories:

Anterior circulation
Posterior circulation
Carotid Cavernous

Anterior circulation: 0%
Posterior circulation: 2.5%
Carotid cavernous: 0%

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After reaching approximately what size do carotid cavernous aneurysms start to have an appreciable risk of rupture over 5 years?

> 13mm

13-24mm: 3.0%
>24mm: 6.4%

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What is the 5 year risk of rupture of a posterior circulation aneurysm 7-12mm in size?

14.5%

much larger risk than anterior circularion, 2.6%, and carotid cavernous, 0%, risk

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What is the approximate risk of rupture of aneurysms > 24mm in size in the following locations:

Anterior circulation
Posterior circulation
Carotid Cavernous

Anterior: 40.0%
Posterior: 50.0%
Carotid cavernous: 6.4%

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Describe the categories of the Hunt-Hess Grading Score

I: Asymptomatic/minimal headache, nuchal rigidity
II: Moderate to severe headache, nuchal rigidity, +/- focal cranial nerve palsy
III: Drowsy, confused, mild focal deficit
IV: Stuporous, hemiparesis, +/- early decerebrate rigidity
V: Deep coma, decerebrate, moribund

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The grading schema designed by Hunt and Hess was designed for determining risk of what?

Risk for vasospasm after aSAH

I and II: 20-30% risk
III and IV: 50% risk
V: 75% risk

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Describe the WFNS systems for grading aSAH?

I: GCS 15 and no deficit
II: GCS 13-14 and no deficit
III: GCS 13-14 and deficit
IV: GCS 7-12 +/- deficit
V: GCS 3-6 +/- deficit

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Describe the Fisher radiographic grading scale for determining risk of vasospasm

I: No hemorrhage
II: Diffuse SAH with vertical laters <1mm thick
III: Localized clots and/or vertical layers >1mm thick
IV: With ICH or IVH

*Incidence of vasospasm is highest in grade III

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How are dissecting aneurysms managed depending on location?

If extracranial then antiplatelet/anticoagulation to reduce risk of ischemia

If intracranial then surgical or endovascular obliteration

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How do pseudoaneurysms typically form?

Often sequela of trauma (penetrating > blunt).

Hematoma from an arterial rupture forms in between outer walls of artery and can even lead to carotid cavernous fistula

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Relative to saccular or fusiform aneurysms, where are infectious/mycotic aneurysms more often located? What other condition are they associated with? What is first line treatment?

Distally located
Bacterial Endocarditis
Antibiotics (~ 6 weeks)

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What was the major finding of the International SAH Trial (ISAT)?

ISAT found that endovascular coiling is a good option compared to surgical clipping in aSAH.

At one year 31% of patients clipped were dead or dependent compared to 24% in the coiling arm

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What may be a good general rule of thumb for the type of surgical treatment most amenable to anterior, middle, and posterior circulation aneurysms respectively?

Anterior: Variable between clipping and coiling
Middle: Clipping
Posterior: Coiling

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What surgical approach is often most helpful for anterior, middle, and posterior circulation aneurysms?
What may need to be done for distal anterior cerebral aneurysms?

Pterional craniotomy

Anterior interhemispheric approach for distally located anterior circulation aneurysms

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What are the typical presentations for AVMs in order of most common symptoms?

Hemorrhage (50%)
Seizures (25%)
Headache, focal deficits from steal phenomenon

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What features of AVM are associated with increased risk of hemorrhage?

Hemorrhagic original presentation, large size, deep venous drainage, associated aneurysms

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What are the three categories involved in the Spetzler-Martin grading system for AVMs and the points involved?

Nidus size:
<3cm - 1
3-6cm - 2
>6cm - 3

Eloquence of adjacent brain:
No - 0
Yes - 1

Venous drainage pattern:
Superficial - 0
Deep - 1

What are the treatment options for AVMs?

Medical mgmt (e.g. antiepileptics)
Embolization
Radiosurgery
Surgical resection

If opting to use radiosurgery for an AVM is there still a hemorrhagic risk? What features of AVMs make them more amenable to radiosurgery?

Yes, in the 2-3 years post-radiosurgery before complete obliteration there is still risk of hemorrhage

Small nidus (<3cm) near eloquent brain or with deep venous drainage

What Borden grade for dural AVFs generally warrant treatment?

Borden II and III due to 15% annual event rate

What is the major goal in the treatment of dAVFs?

Elimination of cortical venous reflux (CVR)

Borden II dAVF

Dural venous drainage with no cortical venous reflux

Borden II dAVF

Dural venous drainage WITH cortical venous reflux

Borden III dAVF

Cortical Venous reflux only

How does the Cognard grading scale differ from the Borden scale for dAVFs?

Cognard scale separates dural venous drainage into anterograde and retrograde drainage. For Borden grade III, Cognard scale distinguishes between cortical venous reflux +/- venous ectasis

What if often preferred for dAVF treatment, transarterial embolization or transvenous coiling?

Transvenous coiling

What are the peaks for age of presentation with Moya-Moya disease?

Age 3 and 20-30s

What is the typical presentation of Moya-Moya disease and how does it differ with the age of presenation?

In pediatric cases more often presents with ischemia (80%) In adult cases more often presents with hemorrhage (60%)

CCM1-3 are autosomal dominant conditions placing patients at heightened risk for what vascular condition?

Cavernous malformations

How do cavernous malformations often present?

Seizures, focal deficits, headaches Hemorrhage may occur and is more common in deeper lesions and in the posterior fossa

What are appropriate treatments for cavernous malformations?

Medical mgmt/observance for seizure control Surgical removal is often very effective Radiosurgery usually doesn't alter their natural history

What are risk factors for ICH?

Age > 60, EtOH use, HTN, amyloid angiopathy, drugs (e.g. cocaine), coagulopathy

Above what ICH hematoma volume does prognosis steeply drop off?

> 30cc

What measures should be taken for initial medical mgmt of ICH?

Strict BP control (varies on center, at UPMC SBP goal <140 and can later be liberalized to <180) Correct coagulation Manage ICPs and frequent neuro exams

How does the mgmt of a cerebellar ICH differ from a lobar or even basal ganglia hemorrhage?

Need to be prudently watched because if there are signs of neurologic deterioration, brainstem compression, or obstructive HCP then urgent evacuation may be needed

What are the most common areas for hypertensive ICH to occur?

Basal Ganglia Thalamus Pons Cerebellum

What is the major concern for morbidity after a large stroke (e.g. MCA territory or cerebellar)?

Post-infarct edema which may cause obstructive HCP or malignant edema

In patients developing malignant edema after an infarct what is the appropriate management for: Cerebellar territory infarcts MCA territory infarcts

Cerebellar: craniectomy and possibly strokectomy MCA; Hemicraniectomy can be done but has severe morbidity; outcomes are better in younger patients and in nondominant hemisphere strokes

According to the NASCET trial, symptomatic stenosis greater than what percentage is associated with a 17% absolute risk reduction after two years if operated on with CEA compared to medical mgmt?

70-99% stenosis

Symptomatic carotid stenosis between 50 and 69% warrants what treatment?

NASCET shows very mild absolute risk reduction at 5 years with CEA (6% ARR)

Horner syndrome (miosis, anhidrosis, ptosis) in a young female may be due to what pathology?

Carotid dissection

What is the main treatment for patients with extracranial arterial dissection?

Antiplatelet/anticoagulate agents for 6-12 weeks

What is the main treatment for patients with intracranial arterial dissection?

Antiplatelet/anticoagulate for 6-12 weeks (unless SAH part of presentation) Surgical options: proximal clipping, vessel reconstruction, endovascular stenting

How are carotid-cavernous fistulas characterized?

High-flow (e.g. cavernous carotid aneurysm rupture) | Low-flow (e.g. dural carotid branch, ECA, etc.)

How do carotid-cavernous fistulas present?

Pulsatile proptosis, retro-orbital/orbital pain, chemosis, ocular bruit, visual deterioration, diplopia

Why is it that low-flow CCFs can be medically observed?

~50% thrombose on their own | (Medically managing is ok as long IOP < 25mmHg

What interventions serve as useful for the management of CCFs which failed medical management?

Endovascular transarterial embolization | Endovascular transvenous coiling