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Neurosurgery Boards - Citow > Neurosurgery: Vascular Disease > Flashcards

Neurosurgery: Vascular Disease Flashcards

1
Q

What is the adult prevalence of aneurysms?

What is the annual incidence of aneurysmal SAH?

A

Adult prevalence: 2%

Annual incidence aSAH: 0.006-0.008%

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2
Q

What are modifiable risk factors for aneurysmal SAH?

A

HTN, smoking, alcohol abuse

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3
Q

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

A

Before hospital: 10-15%

One month: ~50%

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4
Q

What are the major morbidities associated with aSAH?

A

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

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5
Q

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

A

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

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6
Q

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

A

> 13mm

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

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7
Q

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

A

14.5%

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

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8
Q

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

Anterior circulation
Posterior circulation
Carotid Cavernous

A

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

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9
Q

Describe the categories of the Hunt-Hess Grading Score

A

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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10
Q

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

A

Risk for vasospasm after aSAH

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

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11
Q

Describe the WFNS systems for grading aSAH?

A 
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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12
Q

Describe the Fisher radiographic grading scale for determining risk of vasospasm

A

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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13
Q

How are dissecting aneurysms managed depending on location?

A

If extracranial then antiplatelet/anticoagulation to reduce risk of ischemia

If intracranial then surgical or endovascular obliteration

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14
Q

How do pseudoaneurysms typically form?

A

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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15
Q

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?

A

Distally located
Bacterial Endocarditis
Antibiotics (~ 6 weeks)

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16
Q

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

A

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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17
Q

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?

A

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

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18
Q

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?

A

Pterional craniotomy

Anterior interhemispheric approach for distally located anterior circulation aneurysms

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19
Q

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

A

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

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20
Q

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

A

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

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21
Q

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

A

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

Eloquence of adjacent brain:
No - 0
Yes - 1

Venous drainage pattern:
Superficial - 0
Deep - 1

22
Q

What are the treatment options for AVMs?

A

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

23
Q

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

A

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

24
Q

What Borden grade for dural AVFs generally warrant treatment?

A

Borden II and III due to 15% annual event rate

25
Q

What is the major goal in the treatment of dAVFs?

A

Elimination of cortical venous reflux (CVR)

26
Q

Borden II dAVF

A

Dural venous drainage with no cortical venous reflux

27
Q

Borden II dAVF

A

Dural venous drainage WITH cortical venous reflux

28
Q

Borden III dAVF

A

Cortical Venous reflux only

29
Q

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

A

Cognard scale separates dural venous drainage into anterograde and retrograde drainage.

For Borden grade III, Cognard scale distinguishes between cortical venous reflux +/- venous ectasis

30
Q

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

A

Transvenous coiling

31
Q

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

A

Age 3 and 20-30s

32
Q

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

A

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

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

33
Q

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

A

Cavernous malformations

34
Q

How do cavernous malformations often present?

A

Seizures, focal deficits, headaches

Hemorrhage may occur and is more common in deeper lesions and in the posterior fossa

35
Q

What are appropriate treatments for cavernous malformations?

A

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

36
Q

What are risk factors for ICH?

A

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

37
Q

Above what ICH hematoma volume does prognosis steeply drop off?

A

> 30cc

38
Q

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

A

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

39
Q

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

A

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

40
Q

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

A

Basal Ganglia
Thalamus
Pons
Cerebellum

41
Q

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

A

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

42
Q

In patients developing malignant edema after an infarct what is the appropriate management for:

Cerebellar territory infarcts
MCA territory infarcts

A

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

43
Q

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?

A

70-99% stenosis

44
Q

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

A

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

45
Q

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

A

Carotid dissection

46
Q

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

A

Antiplatelet/anticoagulate agents for 6-12 weeks

47
Q

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

A

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

48
Q

How are carotid-cavernous fistulas characterized?

A

High-flow (e.g. cavernous carotid aneurysm rupture)

Low-flow (e.g. dural carotid branch, ECA, etc.)

49
Q

How do carotid-cavernous fistulas present?

A

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

50
Q

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

A

~50% thrombose on their own

(Medically managing is ok as long IOP < 25mmHg

51
Q

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

A

Endovascular transarterial embolization

Endovascular transvenous coiling

Neurosurgery Boards - Citow (9 decks)

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