Vascular Flashcards
Bow Hunter syndrome
Constellation of signs and symptoms of posterior circulation ischemia related to head movement/turning
Pathophysiology of Bow Hunter syndrome
Occlusion of one VA in the presence of a compromised contralateral one - because of chronic occlusion, hypoplasia, severe stenosis, or the VA ending in the PICA
Simultaneous dynamic compromise of both VAs during head turning
V1 segment of VA
Originates from the superior or posterior aspect of the subclavian artery and extends until its entrance into the transverse foramen of a cervical vertebra
V2 segment of VA
Ascends through the transverse foramina of the upper 6 cervical vertebrae, deviating laterally to reach the transverse foramen of the atlas
V3 segment of VA
Extends from the transverse foramen of the atlas to the site of passage through the dura mater and is closely related to the foramen magnum and the craniovertebral junction
V4 segment of VA
Intradural segment begins at the dural foramina and ascends anteromedially until it joins the contralateral VA at the pontomedullary sulcus to form the basilar artery
Most common site of compression in Bow Hunter syndrome
Level of the AA joint where the VA can be stretched between the C1 and C2 transverse foramina
Presentation of Bow Hunter syndrome
Vertigo, syncope, tinnitus, diplopia
Timeline of vasospasm after SAH
Typically occurs 3-14 days after SAH and generally peaks on days 6-10
Criteria for vasospasm using TCD
Flow velocity greater than 200 cm/s or less than 120 cm/s, significant increase in flow velocity from day to day (> 50 cm/s), and a Lindegaard ratio (MCA velocity/ICA velocity) higher than 3
Current standard for endovascular treatment of cerebral vasospasm
Mechanical dilation with a balloon and/or selective or superselective pharmacological vasorelaxation with IA agents (papaverine, verapamil, nicardipine, and milrinone)
Arteries that can be treated with endovascular treatment after vasospasm
Angioplasty can be used for larger vessels (2-3 mm in diameter) which includes the ICA segments M1, A1, intradural vertebral artery, basilar and P1
Mainstay of medical management for patients with carotid atherosclerosis
Risk factor modification and anti-platelet therapy (ASA)
Pathophysiology of moyamoya disease
Chronic, progressive occlusion of the ICA at and distal to the carotid siphon that may also involve the proximal segments of the MCA and ACA
Hallmark features of moyamoya on cerebral angiography
Narrowing of the C1 and C2 segments of the ICA and proximal involvement of the MCA and ACA bilaterally
Surgical intervention for moyamoya disease
Direct revascularization using an anastomosis between the ICA and ECA
Indirect revascularization involves placement of vascularized tissue on the surface of the ischemic brain, stimulation of angiogenesis, and formation of collateral networks between donor and recipient tissue
Conditions commonly associated with cerebral arterial dissection
Fibromuscular dysplasia, Marfan’s, polycystic kidney disease, and vasculitides
Grade 1 Hunt and Hess
Asymptomatic, mild HA, slight nuchal rigidity
Grade 2 Hunt and Hess
CN palsy, moderate to severe HA, severe nuchal rigidity
Grade 3 Hunt and Hess
Mild focal deficit, lethargy, confusion
Grade 4 Hunt and Hess
Stupor, moderate to severe hemiparesis, early decerebrate rigidity
Grade 5 Hunt and Hess
Deep coma, decerebrate rigidity, moribund appearance
Risk factors for rupture of AVMs
Previous rupture, high pressure over the malformation, small nidus, deep brain location, intranidal or feeding artery aneurysms, deep venous drainage, and venous occlusions
Definition of cavernous malformation
Vascular lesions with closely spaced sinusoidal vessels lacking a smooth muscle layer and without interspaced neural tissue
Two predictors of vasospasm after SAH
Thickness of SAH clot and the presence of IVH
Grade 0 on Modified Fisher scale
No SAH or IVH
Grade 1 on Modified Fisher scale
Thin SAH, no IVH
Grade 2 on Modified Fisher scale
Thin SAH with IVH
Grade 3 on Modified Fisher scale
Thick SAH, no IVH
Grade 4 on Modified Fisher scale
Thick SAH with IVH
Difference between thin and thick SAH on CT
About 1 mm vertical thickness is the cutoff between thin and thick SAH for Modified Fisher scale
Prevention of rebleeding after aneurysmal SAH
The only definitive method to prevent re-bleeding is securing the aneurysm via clipping or endovascular coiling
Medical prevention of re-bleeding after aneurysmal SAH
Antifibrinolytics (epsilon-aminocaproic acid) 4 mg IV load, then 1g/hour every 6 hours until aneurysm occlusion
BP parameters to maintain to prevent re-bleeding after aneurysmal SAH
BP lowering to a SBP of 140-160 is reasonable prior to securing the aneurysm and is usually done with a titratable drip of nicardipine or labetalol
Percentage of patients who get sentinel headaches before SAH?
Between 10-50% and they most commonly occur 2-8 weeks before overt SAH.
What are the three types of ocular hemorrhages that are associated with SAH?
- Subhyaloid (preretinal) hemorrhage.
- (intra) retinal hemorrhage.
- hemorrhage within the vitreous humor (Terson syndrome).
Percentage of rebleeding during SAH in the 2 weeks.
1.5% per day for the first 13 days, therefore overall rate is 15-20% within 14 days.
What percentage of aneurysms will rebleed within the first 6 months after SAH?
50%.
Risk factors for rebleeding after SAH.
Higher H/H scores, larger aneurysm size, poorly controlled BP, and pre-op ventriculostomy.
