E. R. Flotte MD, 2009
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Radiology
Blood
on MRI: (T1/T2) <24h (oxyhemoglobin):
iso/iso. 1-3d (DeoxyHgb): iso/hypo. 3-14d (intracellular metHgb):
hyper/hypo. >14d (extracellular metHgb): hyper/hyper. hemosiderin: hypo/hypo
Angiogram:
0.5%
risk of stroke, 7% w/atherosclerosis
·
Berry
aneurysms: Saccular.
·
Predispoition for braching points on
arteries (e.g. circle of Willis)
·
False aneurysms (lack media, defects in internal elastic lamina).
·
Other
types of aneurysms:
o
Oncotic aneurysms:
most common with left atrial myxoma, choriocarcinoma
o
Fusiform
(nonsaccular)
o
Mycotic
(infectious)
o
Pseudoaneurysms: encapsulated hematoma
from vessel injury. Often traumatic or
iatrogenic.
·
Prevalence 1-6%: 1% overall, 1% in
young, 4% in elderly. 20-30% multiple.
·
Locations: Pcom (35%) > Acom (30%)
> MCA (20%) > basilar tip (5%).
·
Risk factors:
age, smoking (3-10x), heavy alcohol use, HTN (3x), ?hormones
·
Predisposing
factors: Aortic coarctation, AD polycystic kidney
disease, fibromuscular dysplasia, Marfans, Ehlers-Danlos, homocystinuria, NF1,
AVMs
·
Aneurysm
growth rates: unclear if linear or episodic (Koffijberg H
JN8/08 – editorial Britz G)
·
Rupture risk:
o
International Study of Unruptured Intracranial Aneurysms
(ISUIA) (NEJM
12/10/1998): Retrospective.
§
Risk
for aneurysms <10mm = 0.05%/yr. (0.5%/yr in those with previous rupture from
another aneurysm). For >10mm = 1%/yr.
§
Other
studies refute this (rupture rate 1-2%/yr) (Juvela, Mocco, Rinkel). Some feel ISUIA selected for low-risk lesions
since high-risk lesions were treated and withdrawn.
o ISUIA Part 2 Wiebers DO Lancet 7/12/2003: Prospective: <7mm, 7–12mm, 13–24mm, and >25mm yearly rupture
rates were 0.15%, 1.2%, 3.1%, and 8.6%. (<7mm
with previous SAH was 0.4%)
§ 5-year rupture rates for anterior circulation: 0, 2.6, 14.5,
and 40%, posterior circulation: 2.5, 14, 18.4, and 50% (no history of SAH).
·
Rupture risk increased with: Large
size (no critical size), high dome/neck ratio, high aspect (aneurysm depth:neck
width), slow flow.
o Smaller aneurysms produce more extensive SAH (Russell SM JN8/03).
·
If two or more
family members have aneurysms, others should be screened by MRA or CTA (5-10%
positive). Frequency is debated (every 6mos to 5yrs) (Kim DH N8/03)
·
Presentation:
o
Incidental
unruptured
o
Symptomatic
unruptured: seizures, mass-effect (e.g. CN3 plasy from pcom)
o
Ruptured:
usually cause subarachnoid hemorrhage (SAH), occasionally ICH, IVH, SDH
Aneurysmal Subarachnoid Hemorrhage
(SAH)
·
Spontaneous
SAH Diagnosis:
o Presentation:
§ Sudden onset (“thunder-clap”) headache, back pain.
§ Loss of consciousness, new neurologic deficits.
§ Meningismus (nuchal rigidity; Kernig’s, Brudzinski’s
signs)
§ Subhyaloid, vitreous, or retinal hemorrhages on
fundoscopy
§ Mass-effect: CN3 palsy (pcom or basilar tip)
o CT
o
CT Angio:
Sensitivity/specificity >95% for aneurysms >7mm. Look for neck calcification or plaques. Especially
beneficial for emergent ICH evacuation.
§ With
SAH: If aneurysm seen it is reliable. Perform angio to confirm (-) CTA.
§ No
SAH: If (+) consider angio to confirm small aneurysms. If (-) then probably
reliable.
o
MRI/MR angio:
False-positive and false-negative rates 10%. Also consider MRI with gradient
echo sequence
§ Superficial siderosis (hemosiderin staining of
leptomeninges) may be seen with recurrent SAH on T2/GRE MRI (more often
non-aneurysmal)
o LP:
Performed if CT/CTA is negative – although efficacy with (-) combined CT/CTA
unclear.
§ CT negative in 5% of SAH.
§ LP
reported to cause neurologic worsening in 13% of SAH patients
§ Xanthochromia
becomes apparent after 4 hours.
§ “Bloody
Tap” – local hemorrhage during LP. May mimic SAH. Xanthochromia is absent.
Blood clots in tube (as opposed to SAH which won’t).
§ If
CT/CTA and LP negative but clinical suspicion high then some consider angio (LP
may be negative with loculated blood), but efficacy unclear
o Cerebral
angiogram: 4 vessel - gold standard.
§ Risk
of hemorrhage 3% with SAH.
§ Must
see both PICA origins to be adequate
§ May
need carotid compression to visualize flow through Acom from both ACAs
§ Alcock test: vertebral injection with carotid
compressions – test circle of Willis patency
§ Size: ICA 6mm, MCA 4mm (average)
§ 3D-angiography
·
“Angiogram-negative”
SAH (or “Occult” SAH)
o
10% of SAH.
Most common cause is non-visualized aneurysm due to aneurysm thrombosis or
inadequate study.
o
Other causes: Perimesencephalic SAH, spinal or cerebral AVM, sickle cell, pituitary
apoplexy, cocaine, arterial dissection, “SAH of truly unknown cause”
·
Spontaneous
thrombosis of aneurysms may occur (10% of autopsy series); however they may
reappear and rupture years later.
·
Cannot
diagnose “benign” SAH in presence of vasospasm
o
Acom is most
common location.
o
Hemorrhage rate is 0.5%/year (lower
than angiogram (+) SAH). Other SAH complications occur (vasospasm may be less
likely).
o
Consider repeat angiogram at 10-14
days. Overall 2-25% positive yield on repeat angiogram, but up to 70% with
interhemispheric SAH.
o
Surgical exploration has been
advocated by some, especially if re-bleeding occurs or if the SAH is in a
typical aneurysm location (interhemispheric, Sylvian fissure)
o
Isolated convexity SAH rarely due to
aneurysm – more commonly due to posterior reversible encephalopathy, venous
sinus thrombosis, vasculitis, etc (Refai D JN12/08)
·
SAH
Complications:
o
Rerupture:
4% 24hr, 20% 2wks, 50% 6mos, then 3%/yr.
o
Vasospasm:
See below.
o
Hydrocephalus: 10% require shunting.
§
If
placing EVD before securing aneurysm, drain at 15cmH2O to avoid detamponading
aneurysm
§
No difference in shunt placement between gradual and
rapid EVD weaning (Klopfenstein JD JN2/04)
§
Rammos S JN12/08 suggest EVD can be converted to VP shunt at the same
site, and CSF RBC and protein have no effect on shunt survival
o
Effect
of increased ICP on outcome unclear Heuer JC JN9/04
o
Seizures:
§ Seizure incidence after SAH is 5 to 8% Rosengart
AJ JN8/07
§
Based on meta-analysis of 4 RCTs, prophylactic
AED usage after SAH was significantly associated with worse outcome at 3
months, development of cerebral vasospasm, neurological deterioration, and
cerebral infarction as well as elevated temperature during hospitalization. Use
may be justified in high risk patients (cortical injury, unsecured aneurysms) Rosengart AJ JN8/07
o
Cardiac: elevated cardiac enzymes
and EKG changes common. MI.
Aneurysm
Treatment
·
Unruptured:
o
Reviews: Neurosurgical
Focus 11/04 (Spetzler, Dacey et al), Journal of Neurosurgery 1/02 Special
Section (Winn, Weir et. al.)
o
International Study of Unruptured Intracranial Aneurysms (ISUIA) (NEJM
12/10/1998): <10mm = 0.05%/yr
rupture rate does not justify surgery.
§
Advocated
by AHA Stroke Council (2000)
§
Other
studies refute this (rupture rate 1-2%/yr).
Most aneurysms with SAH are <10mm. Median size of rupture 7.5mm.
o
Komotar RJ N1/08: Symptomatic unruptured aneurysms generally should be
treated; incidental aneurysms < 5 mm should be managed conservatively;
aneurysms > 5 mm in patients younger than 60 years of age should be
seriously considered for treatment; incidental aneurysms > 10 mm should be
treated in nearly all patients younger than 70 years of age
o
Growth (>1mm), shape
(multilobulated, “tits”), genetic conditions, previous SAH from another
aneurysm may increase rupture rate and warrant treatment
·
With ICH:
Higher rebleed rates than pure SAH. Clot evacuation alone mortality 75-100%.
Must secure aneurysm. Consider coiling then evacuation.
·
E-ACA
(ε-aminocaproic acid, Amicar): Inhibits
plasminogen→plasmin (digests fibrin). Rebleeds decreased from 20% to 12%,
but vasospasm increased from 23%
to 32%, hydrocephalus increased, mortality unchanged. Consider in non-surgical
patients.
·
Poor Grade
(Hunt-Hess IV or V) controversial. Some favor early treatment because a subset (up
to 30%) will have good outcome (Laidlaw JD N12/03, Komotar RJ N2/09)
·
Seizures with unruptured aneurysm
usually treated with clipping and removal of aneurysm without extensive
cortical resection. Not clear if coiling improves seizures.
·
Ruptured:
Airway and hemodynamic stabilization, control BP, ventriculostomy/LD for
hydrocephalus, Nimodipine, analgesics, consider AEDs (until secured - see
above)
Aneurysm Surgery
o Timing: earlier (1 to 3 days
post-hemorrhage) generally favored in H/H I-III, but late has some advantages,
e.g. less brain swelling.
§
International
Cooperative Study on the Timing of Aneurysm Surgery (ICSTAS) concluded “early surgery was neither more
hazardous nor beneficial than delayed surgery” (Kassell NF JN7/90 – Part 1, Part 2)
§
Netherlands
observational study showed no difference in timing – Nieuwkamp DJ AN8/05
§
Reviews: deGans K N2/02 (meta-analysis)
o Consider: mannitol, CSF drainage, mild
hypothermia (33-36º), SBP <140 until clip placed.
o Hypothermia: IHAST study showed no
benefit, increase in bacteremia (Todd MM NEJM
1/13/05)
o Some routinely fenestrate the lamina
terminalis to prevent hydrocephalus, particularly for acoms (Komotar RJ N12/02, Andaluz N N11/04),
others show no benefit (Komotar RJ N1/08)
o
Some
achieve burst suppression on EEG on all aneurysm patients (Spetzler RF N10/01)
o Consider microdoppler, MEPs (more
sensitive than SSEPs).
o Previously coiled aneurysms: do not
remove coils if placed >3mos previously. <6mos removal is controversial.
o Obtain proximal control.
§ For ICA aneurysms, access carotid in
neck (or petrous) or have endovascular balloon in place
o Options for angiography include:
routine intraoperative, selective intraoperative, and routine postoperative.
§ Intraoperative angiogram: Estimated to
avert serious complications in 2-10% of patients. Complications 0.5-2.5%. (Chiang VL JN6/02, Tang G JN6/02 – editorial Heros RC, Klopfenstein JD JN2/04, Kivisarri RP N11/04)
§ Indocyanine green video angiography
also an option.
o Temporary occlusion:
§ Raise BP – normotension to mild
hypertension.
§ Etomidate (0.3mg/kg) or propofol to
burst suppression (Barbs cause hypotension, but pentobarb is used).
§ Less likely to be tolerated w/MCA
aneurysm (26% infarction, versus 9% with
§ Always clamp proximal first (clamping
distally first would increase transmural pressure and possible rupture)
§ Released every 10-15min.
§ Overall about 10% stroke rate.
o Aneurysmorraphy: opening of aneurysm
(after temporary clipping) to evacuate thrombus
o Complications: intraoperative rupture,
stroke
§ 
Intraop Rupture: Tamponade dome with
cottonoid, lower BP, consider burst suppression, temporary occlusion (remember
to occlude branching vessels – pcom, anterior choroidal, etc)
§ Neck avulsion: wrap with cotton then
apply clip (Lanzino G JN11/03)
o Remember to consider: nimodipine, BP
control, AEDs, lumbar drain, microdoppler, MEPs, EEG, intraop angio, ICA access
in neck
·
Audio: Advanced Strategies
for the Treatment of Intracranial Aneurysms – Giannotta SL, Cerebral Aneurysms: Effect of New Knowledge and Technology
on Current Practice – Heros RC
Aneurysm Endovascular Treatments (Coiling
& Stenting)
o
Cranial nerves deficits usually
improve post-coiling.
o
Timing of coiling does not affect
procedural morbidity or outcome.
o
Measure dome-to-neck ratio
o
Coil types: 3-D, complex
fill, biologically active.
§ Matrix
(bioactive coated): similar morbidity to bare platinum. Recanalization rate
25%. Pierot
L N11/08 (French Matrix Registry)
·
“Clearly, the Matrix coil is not better than bare platinum in the
current generation that was assessed. The cost differential between the bare
platinum and Matrix coils certainly indicates that the use of Matrix coils in
their current form is not cost-effective, and I would not recommend its use at
this time, as it has clearly shown no benefit.” - Rosenwasser RH,comment on Pierot
L N11/08
o
Adjuncts:
§ Balloon
remodeling: for wide-necked aneurysms.
§ Stent-assisted
coiling: for wide-neck & fusiform aneurysm.
§ Stenting
alone:
·
Most stents have 6-9% metal surface
coverage, except PED which has 30-35%
·
Wingspan (Yavuz K JN9/08)
·
Pipeline
Embolization Device: results in flow reduction and progressive occlusion over
months, requires dual antiplatelet therapy – not for acute SAH (Lylyk P N4/09)
o
Surgical remnants may be treated with
coiling (Bendok BR N9/02)
o
Follow-up angiography varies, commonly
done at 6 months, 3 years (safe time for end of follow-up is unknown)
§ Role
of CTA, MRA unclear.
·
3D TOF or contrast-enhanced MRA follow-up:
Gauvrit JY JN3/08
§
Risk of permanent major morbidity from surveillance angiography after coiling is
0.04% (other series 0.3-2.3%) (Ringer AJ N11/08)
o
Complications
§ 5-10%
morbidity, 2% mortality. Ischemia 9%, hemorrhage 3%.
§ Recurrence
10-15%.
§ Rupture
during coiling:
1.
Complete coiling
2.
Reverse heparin
3.
Consider EVD
4.
Stat CT
5.
Treat as for SAH
- Reviews:
Laterna LA N10/04, Bendok BR N5/03 (Operative Nuances)
- Videos: Bendok
BR N5/03
Coiling vs Clipping
o
Factors: aneurysm location, size,
shape, neck:dome
ratio, luminal thromus, calcification, collateral supply, parent vessel
morphology; patient age, clinical status, preference; vasospasm
o
International
Subarachnoid Aneurysm Trial (ISAT) (Molyneux
A Lancet 10/26/02):
§
1yr
neurologic outcome better with SAH (unruptured not studied) for CE. 7% risk
reduction CE vs SC. (Only 2 pts from US). For equivalent treatment.
§
Only
20% of eligible patients randomized – most of rest were clipped. Most centers
outside of US. Operator experience not reported. Patient characteristics
atypical (higher H/HI-II, anterior circulation, <10mm)
§
Mitchell P JN3/08: “Could late rebleeding overturn the
superiority of cranial aneurysm coil embolization over clip ligation seen in
the International Subarachnoid Aneurysm Trial”. “The advantage of coil
embolization over clip ligation cannot be assumed for patients < 40 years
old” Editorials: Mocco J, Heros RC
o
Others:
§ Johnston
SC Stroke 3/01:
California database. Mortality CE 0.5%, SC 3.5%. Poor outcome CE 9%,
SC 22%.
§ Raftopoulos C N6/03:
Unruptured. Occlusion rates: Total: CE 56%, SC 93%. Subtotal: CE 15%, SC 2%.
Fail: CE 29% (60% were MCA), SC 5%. Complications: temporary CE 10% SC 16%
permanent CE 8% SC 2%. Recommendation: coil only for DNR >2.5.
§ Barrow
Ruptured Aneurysm Trial
o
No
RCT for unruptured aneurysms
o
No difference in shunt-dependent
hydrocephalus between the two groups (except patients with IVH – higher with
coiling) (Dehdashti AR
JN9/04)
o
No difference in vasospasm (Hoh BL N10/04)
o
Clipping may have a better chance of
improving CN3 palsy (Chen PR N6/06)
Specific aneurysms
o
Cavernous
§ Unruptured
may cause ophthalmoplegia (usually without dilated pupil, cf. pcom), headache,
eye pain
§ Ruptured,
may cause:
·
SAH, if it expands through carotid
ring into subarachnoid space
·
Epistaxis, from rupture into sphenoid
sinus
·
Emboli
§ Treatment
·
Generally for symptoms (especially
visual problems), giant aneurysms (especially subarachnoid extension)
·
Incidentally usually followed – low
risk of CCF
·
Coiling or trapping. May reduce mass
effect. See CCF.
·
Cavernous aneurysm with carotid
stenosis requiring treatment is controversial, but each generally treated
separately on own merits
o
Proximal ICA/Paraclinoidal:
Aka carotidophthalmic / paraophthalmic. May cause blindness.
§ No
radiographic way to determine if they are intradural or extradural (Iihara K JN8/03).
§ Subtypes:
·
Carotid Cave (C3): usually point
medial. Mostly extradural but may be intradural. Coiling favored
·
Ophthalmic artery aneurysm: points
superiorly. May compress optic nerve/chiasm
·
Superior hypophyseal: points
inferiorly or medially
§ If
anterior wall (aka superior hypophyseal) or true ophthalmic (off C2) consider
surgery. If carotid cave (C3) or pointing inferiorly, consider coiling.
§
Endovascular
treatment generally favored if feasible
§
Surgical:
o Clipping if feasible – pterional approach. If not ICA occlusion ± EC-IC bypass
o
Proximal
control: Expose cervical ICA or have endovascular balloon in place
o
Usually
requires drilling anterior clinoid (possible removal of optic strut and
sectioning of falciform ligament)
o
Safe
to clip ophthalmic a. or superior hypophyseal a. if necessary
o
Bilateral
ophthalmic a. aneurysms may be approached from one side usually.
§
Case
Series: Fulkerson DH N2/09
§
Reviews: Giannotta SL N3/02 (Operative Nuances); Iihara K JN8/03 –
comment Heros RC
§ Videos: Giannotta SL N3/02
o
Posterior Communicating (Pcom):
§ Approach:
Pterional
§ Arise
distal to pcom. If no CN3 palsy more
likely to be adherent to temporal lobe – avoid retraction.
§ More
likely to cause subdural hematoma with SAH
§ Complete
CN3 palsy (or pupil only, often painful): pcom OR basilar apex aneurysms.
o
Versus Pupil sparing CN3 palsy (10-20%
involve pupil, may be painful): DM, HTN.
§ Look
for fetal PCA on angio.
§ Clipping:
o
Avoid temporal lobe retraction
o
Ensure patency of anterior choroidal
& thalamoperforators after clipping.
o
Pcom may be sacrificed if not fetal.
o
CN3 palsy: evacuate fundus, do not
dissect off CN3.
o
Small: clip perpendicular to
o
May need to temporarily clip proximal
and distal
o
Anterior Choroidal:
§
Approach:
Pterional.
§ Anterior choroidal
artery: 16% stroke rate with clipping. 25% arise from MCA or Pcom. Supplies
internal capsule, optic tract, lentiform nucleus, amygdala.
·
Anterior choroidal injury (pcom or
achor): Hemiplegia, hemihypesthesia, homonymous hemianopsia (cognition
unimpaired).
o
ICA bifurcation (Carotid Terminus):
§ May
cause ICH (resembling putaminal ICH).
§ Know
whether acom & A2s fill from contralateral A1 – if so can sacrifice ipsilateral
A1 if necessary.
§ Open
medial sylvian fissure distal to proximal after exposing
§ Watch
for anterior choroidal & lenticulostriates (off ACA & MCA). Must see
back side to avoid perforators. Clip parallel to M1.
o
MCA bifurcation:
§ Cause
ICH, SDH. Higher risk with temporary occlusion. More often multiple (up to
45%).
§ Treatment:
generally favors clipping.
§ Early
bifurcation may imply more lenticulostriates off M1/M2 – must be spared.
§ Approaches:
o
1) Pterional: Exposes ICA for proximal control, then follow
to MCA bifurcation.
o
2) Transsylvian: Splits Sylvian
fissure. Follow M2s to aneurysm. (Yasargil & Fox)
o
3) Superior Temporal Gyrus: Better if
ICH present. (Heros)
§ When
clip placement not possible consider STA-MCA bypass (spare STA in dissection)
or arterial reimplantation (threatened M2 grafted end-to-side to other M2)
§ Reviews:
Chyatte D N2/01 (Operative Nuances), Heros RC N4/01 (Operative Nuances)
§ Videos: Chyatte D N2/01, Heros RC N4/01
o
Anterior Communicating (Acom):
§ Look
for ACA and aneurysm filling from each side.
§ Approach:
Pterional.
o
Consider morphology, A1 dominance (for
proximal control), language dominance. Right generally favored.
§ Surgery:
Consider resecting gyrus rectus. Identify both A1s & A2s. Avoid perforators
from posterior Acom and recurrent artery of Heubner (86% off A2)
§ Reviews:
Solomon RA N1/01 (Operative Nuances), Riina HA N10/02 (Operative Nuances), Sekhar LN ON11/07 (Operative Nuances)
§ Videos: Solomon RN N1/01, Riina HA N10/02, Sekhar LN ON11/07
o
Distal ACA:
Note if aneurysm is supracallosal (above genu) or infracallosal (may require
anterior corpus callosotomy), azygous ACA (7-16%). Pterional/ subfrontal used
for low A2, interhemispheric for others
Posterior Circulation Aneurysms
o
General
§
Partially thrombosed giant posterior
circulation aneurysms (Iihara
K N11/08) – Figure 1 Management Algorithm
§ Books: Drake CG et al, Surgery
of Vertebrobasilar Aneurysms, Springer 1996
o
PCA:
o
P2: Pterional, subtemporal, or
occipital interhemispheric approach. See Terasaka S N8/00
o
Basilar apex:
§ Delayed
(non-emergent) surgery preferred, especially if complex
§ Must
preserve thalamoperforators – damage causes irreversible coma.
·
Use shortest possible clip
§ Approaches:
o
Pterional
(Yasargil) or Orbitozygomatic:
Consider COZ or zygomotomy for high bifurcation. Subtemporal craniectomy (for
temporal retraction). Wide dissection of Sylvian Fissure. Generally go between
ICA & CN3 – more perforators in opticocarotid window. Mobilize anterior
choroidal a. off temporal lobe. Resect uncus. Follow Pcom through Lillequist’s
membrane. Consider sharply ligating Pcom (if not fetal).
§ Advantages:
Less temporal retraction, less CN3 manipulation, better for high bifurcation.
Disadvantages: Deep field, poor proximal control.
§
Reviews:
Hsu FPK (Spetzler RF) ON1/05 (Operative Nuances)
o
Subtemporal
(Drake): Better for low bifurcation, posterior projection.
§ Advantages:
Short working distance, lateral view of aneurysms and perforators.
Disadvantages: Temporal retraction, CN3 & CN4 injury.
o
Combined
(Heros): Combined pterional/subtemporal craniotomy. Uncus mobilized
superolaterally out of incisura.
o
Temporopolar (Sano)
o
Extended Lateral Transsylvian (Batjer)
(Bendok
BR N7/04 – Video)
o
Vertebrobasilar junction:
Far
lateral, Transpetrosal.
o
AICA: Approaches:
Retrosigmoid,
Far
lateral, Transpetrosal
- see Gonzalez LF N11/04
o
PICA: May cause
4th ventricle IVH.
§ Retrosigmoid
or Far
lateral (less risk CN palsies). Can include CN12
fibers in clip. Spare brainstem perforators. (DAmbrosio
AL N7/04)
·
May
be approached via contralateral far-lateral (Bragg TF
NF12/08)
§ Proximal
PICA: Must spare perforators. See below as for fusiform
aneurysms.
§ Distal
PICA: Rare. Distal to perforators: May clip aneurysm, clip PICA proximal to
lesion, or trap
§ Case
Series: Al-khayat H (Samson D) N1/05
o
Giant aneurysms:
>25mm. Higher rate of rupture.
§ Most
common locations: cavernous/ophthalmic, MCA, basilar tip
§ Consider
clipping, trapping, bypass & clipping, hunterian ligation
§ Consider
using skull-base approaches – e.g. orbitozygomatic
§ Giant Serpentine aneurysm: > 25 mm in diameter that is partially thrombosed with a residual serpiginous vascular channel (Christano LD NF5/09)
§ Review:
Spetzler RF N10/01 (Operative Nuances)
§ Video: Spetzler RF N10/01
o
Infundibulum:
Triangular diverticulum <3mm at take-off of vessel (eg pcom). Bleeding
reported but felt to be extremely low.
Consider wrapping if doing surgery for another aneurysm.
o
Unclippable aneurysms:
Options include carotid ligation
o
Blood-blister aneurysms:
thin-walled, no neck, fragile, rupture during surgery. On nonbranching supraclinoid ICA (usually
dorsal wall). More common in young women? (Sim SY JN9/06)
§ Treatment
Options:
·
Surgical clipping/wrapping/ICA
sacrifice: Preop ICA Balloon Test Occlusion.
Prep for STA-MCA bypass. Consider wrapping (sliastic sling), bypass
·
Endovascular stenting (covered or
stent-within-stent advocated – Lee JH
JN3/09), coiling (stent-assisted), ICA sacrifice
·
Subarachoid
Hemorrhage grading
o
Hunt-Hess:
o
Grade 1-3 operated (some will manage
grade 3 until they improve to grade 2).
o
Grades
4&5: Clipping/Coiling may decrease rupture rate and enable aggressive
medical management– 35% favorable outcome (44% in Grade 4, 13% in Grade 5), 31%
death. (Suzuki S JN11/06)
§
Generally
4/5 previously managed non-operatively, but “recent
published data show that early or ultra-early aggressive surgical treatment
followed by NICU management may improve the risks of morbidity and mortality in
these patients.” Controversial. (Suzuki S JN11/06)
§
Patients with Grade 4/5 and an
intracerebral hematoma may benefit from surgical evacuation (with prior coiling
or concomitant clipping) (comment by
Heros RC JN11/06)
o
Over
90% or Grade 4/5 patients dead or disabled with no treatment
o
WFNS:
o
40%
of Grade 4/5 patients independent at 3mos – argues for aggressive treatment.
o
Glascow Coma Scale (GCS) may be more
predictive than Hunt-Hess or WFNS (St Julien J N8/08 – Table
1 comparison of systems)
o
Fisher:
CT grading. 1=none; 2 = <1mm thick; 3 = >1mm, clot; 4=ICH, IVH. (Table 1 Kramer JH JN8/08 – Fisher,
Modified Fisher, and Classen Scores comparison)
§ Grades
1, 2, 4 had minimal vasospasm. Grade 3 had 96% incidence of vasospasm.
Vasospasm
·
#1 cause of morbidity after SAH
·
Incidence: Angiographic 50-70%,
symptomatic 30%.
o Correlated
with Fisher grade on CT (Grade 3 is highest).
o Cigarette
smoking is a risk factor.
o Review
of risk factors – Harrod CG N4/05
·
Peak 7-10d. Range 3-14 days. If it develops, may last for weeks.
·
Symptoms: new focal deficits, worsened
headache, AMS
o ACA
spasm gives frontal lobe syndrome.
·
Detection:
o Transcranial
Doppler Ultrasound (TCDs): Mild: 120-200cm/s, MCA:
o Consider
DWI or perfusion MRI/CT
o Confirm
with Angiogram (possibly CTA/MRA)
o For
new deficits
Treatment:
·
Triple-H Therapy (HHH):
o IVF
+ colloid, vasopressors
o Targets:
CVP > 10, PCWP 14-18, HCT 30-35 prophylactically. SBP 160-220
o Unclipped
aneurysm: CVP & PCWP 6-10, SBP <160.
o For
deficit raise SBP >200.
o Can
use low-dose vasopressin/ddAVP to counteract diuresis.
o 75%
of deficits reversed, No RPT.
o Avoid
with cerebral edema or massive infarct
o Increasing
CO, MAP effective (not CVP) (Kim DH N11/03)
·
Nimodipine:
improves outcome by 40%, reduces stroke by 34% and clinical vasospasm from 30%
to 20%, no change in mortality or angiographic vasospasm. 60mg po q4hr for 21
days
·
Endovascular vasospasm treatment
o
Angioplasty:
Repeat CT first to rule out ICH.
o Papavarine: Intraarterial papavarine’s efficacy is inconclusive. Half-life is less than 24hrs, vasospasm recurs in 24-48hrs. Can increase ICP, cause transient deficits, blindness, seizures, thrombocytopenia and paradoxical exacerbation of vasospasm.
o Review: Eddleman CS NF3/09
·
Lumbar drainage reported in
retrospective trial to decrease vasospasm from 50% to 20% (Klimo P JN2/04)
·
Lovenox showed no benefit in prevention.
·
Cisternal thrombolytic therapy with
inflow/outflow catheters or “head shaking” have had mixed results. RCT showed
no overall difference in vasospasm with intraoperative cisternal injection of
rt-PA, but did show 56% decrease in patients with thick subarachnoid clot.
·
Audio: Scientific Basis of Cerebral Vasospasm – Dacey RG
·
aka Perimesencephalic Nonaneurysmal
SAH (PNSAH)
·
May be due to rupture of small perimesencephalic
vessels.
·
Young males, can occur during
exercise.
·
May have similar presentation to SAH
(headache, meningismus), but Hunt-Hess is 1-2.
·
All are angiogram-negative. CT/MRI
shows SAH only in interpeduncular/ ambient/ prepontine cisterns.
o 3%
of basilar tip aneurysms mimic BPS, so some feel angiogram is mandatory.
o Some
suggest CT-angiography alone may be sufficient (N10/06).
o Some
perform brain and spinal MRI to rule out dural fistula or spinal AVM.
o Cannot
diagnose PNSAH in presence of vasospasm – must repeat angio
·
Repeat angiography/CTA is
controversial. Most perform at 1-2 weeks
and some at 2-6 mos.
·
Rebleeding and vasospasm in true BPS
have not been reported.
o Nimodipine
is controversial.
·
“SAH of truly
unknown cause”: SAH outside perimesencephalic/prepontine cistern. May be occult
aneurysm. Higher complications.
Mycotic aneurysms
·
18% have SAH
·
10% of patients with endocarditis (SBE)
develop mycotic aneurysms.
o
SBE
Risk factors: IV drug use, immunosuppresion
o
SBE symptoms: fever, heart murmur,
Roth’s spots (retinal hemorrhages), Janeway’s lesions (macules on palms/soles),
Osler’s nodes (cutaneous nodules)
o
Check echocardiogram to r/o SBE
·
Most common in distal MCA. 20%
multiple.
·
Staph aureus, bhemolytic
Strep (viridans) most common organisms.
·
Treatment: Resolves w/in 6 wks
w/antibiotics. Follow with serial imaging (angiography).
o
Clipping controversial, consider for: SAH, growth on antibiotics, or failure to
decrease after 4-6 week of antibiotics.
§ Difficult
to find – use stereotaxy or have endovascularist place coil nearby.
o
Coiling is an option
o
Cardiac surgery (valve replacement)
with anticoagulation relatively safe (but risk must be discussed).
Bioprosthetic valve preferred over biomechanical valve to reduce need for
anticoagulation.
Traumatic
Aneurysms
·
Most are pseudoaneurysms from
ruptured/lacerated vessel wall
·
Most are peripheral (MCA, ACA
branches) or at skull base (petrous or cavernous
·
High rate of rupture
·
Suspect with delayed hemorrhage – SAH
or ICH
·
Diagnosis: MRA, CTA, angio
·
Treatment: endovascular coiling/trapping/stenting
(Cohen JE N9/08) or surgical
clipping usually recommended
o
Extracranial carotid pseudoaneurysms:
May expand. May be stented (covered or uncovered) or managed conservatively.
·
AKA dolichoectatic aneurysm,
nonsaccular intracranial aneurysm, giant serpentine aneurysm, dissecting
aneurysm
·
Terminology is not standardized &
may lead to confusion
·
Also defined as a spectrum:
dolichoectasia, fusiform, transitional, giant serpentine
·
Considered a different entity than
acute dissecting aneurysms (dissection)
·
Vertebrobasilar > carotid.
·
Most often due to atherosclerosis –
chronic, stable or variably progressive
·
May also occur with collagen vascular
disease, fibromuscular dysplasia
·
Presentation:
1.
Mass effect: on brainstem, cranial
nerves
2.
Ischemia: TIA, stroke
·
Due
to local perforating vessel thrombosis or distal thromboembolism
·
Cerebral
ischemia and BA thrombosis are the most common causes of death
·
New onset ischemic symptoms may herald
impending rupture (Flemming KD
JN7/04)
3.
Rupture/SAH: 1-2%/year risk. After SAH
30% rebleed rate, highest in first 24hrs. (Flemming KD
JN7/04)
·
56% 5-year mortality rate if aneurysm
is enlarging (4% if stable). About 50% will enlarge. (Mangrum WI
JN1/05)
Treatment:
·
Indications:
- Incidental:
Consider following with imaging at 6mos then yearly to look for growth;
MRA is adequate (Mangrum WI
JN1/05)
- Ischemic
symptoms: treated with
anticoagulation/antiplatelets, although increases risk with rupture
- Enlarging:
consider endovascular/surgical treatment. (Mangrum WI
JN1/05)
- Compression:
see below
- SAH:
early endovascular/surgical treatment is warranted because of high rebleed
rate
·
Surgical/endovascular Options:
1) Proximal
(Hunterian) ligation or trapping:
·
Endovascular is favored treatment.
Done with Balloon, GDC coils.
·
May also be done with surgical
ligation
·
Balloon test occlusion (BTO) necessary
first (20 minutes).
·
Based on location:
·
VA Involving PICA takeoff: coil
proximal to PICA/aneurysm
·
VA Proximal to PICA: trap (clip
proximal and distal)
·
VA Distal to PICA: clip/coil distal to
PICA, proximal to aneurysm
·
Basilar: staged bilateral vertebral
occlusion if pcoms adequate. (Axionnat
R N8/03)
·
If patient does not tolerate BTO
combine with bypass: contralateral PICA bypass, VA-PICA anastamosis (with
radial artery graft), occipital a. bypass.
·
Others feel that clipping proximally
only does not guarantee against re-bleeding and all VA aneurysms must be
trapped with PICA revascularization if patient doesn’t tolerate BTO or aneurysm
involves PICA (Hamada J JN12/03)
·
Risk of permanent deficits: 14%
basilar, higher with hypoplastic pcoms. Note if vert is dominant, or
contralateral vasospasm exists. May not cause resolution, occasional rebleed.
2) Endovascular
stenting ± coling (stent-assisted)
·
Case Series:
Greenberg E JN7/07,
Coert BA JN5/07
·
Reviews:
Hanel RA JN2/05
3) Wrapping:
Unproven efficacy.
4) Clipping/Reconstruction
·
Case Series:
Mangrum WI JN1/05, Flemming KD
JN7/04, Flemming
KD JN3/00, Vishteh
AC JN8/99, Drake CG JN 1997 (largest series)
Symptomatic
Vertebrobasilar Dolichoectasia
·
Vertebrobasilar ectasia may cause
brainstem or cranial nerve compression
·
Treatment: for significant, progressive symptoms
·
Pexy: Sling (e.g. Goretex) around
artery sutured to petrous/clival dura.
Usually via far
lateral approach.
·
Microvascular decompression: placement
of Teflon felt, usually for cranial nerves (e.g. CN6) (De Ridder D JN12/07)
·
Case Reports:
Ubogu EE JN1/02
MCA
fusiform aneurysms
·
Occur in children, young patients
(<40yo).
·
Lower bleed rate than VA & ICA
fusiform aneurysms.
·
Small aneurysms present with SAH,
large ones with ischemia or mass effect.
·
May be due to atherosclerosis or
dissection.
·
May be stenotic or dilated on angio,
but MRI/MRA shows external dilation.
·
Treatment:
·
Indications: SAH, very large aneurysms,
or symptomatic from chronic ischemia
or mass effect (acute ischemia treat as for stroke).
·
Proximal occlusion and distal bypass (saphenous or
arterial interposition if M1, otherwise can use STA).
·
Cannot trap and excise M1 due to lenticulostriates
(will thrombose with proximal occlusion).
·
Partial clipping is ineffective
·
Reviews:
Day AL JN8/03
·
Terminology varies: disruption between
intima & media or media &
adventitia (also called dissecting aneurysm)
· Pseudoaneurysm: encapsulated hematoma around
vessel, usually traumatic
·
Extracranial or intracranial
·
Spontaneous
or post-traumatic
o
Spontaneous:
Risks: OCPs, collagen vascular disease (RA, SLE), fibromuscular dysplasia
(“string of beads”), inherited (Marfan’s, Ehler-Danlos IV), migraines, HTN. Delivery, Pharyngeal
infections
o
Post-traumatic:
Suspect with evidence of blunt trauma to the neck
o
Iatrogenic:
during endovascular procedures
·
Causes TIA/CVA (occlusion, thrombosis,
or emboli) or SAH (if intracranial, less common)
o
Extracranial: sub-intimal, rupture
rare. Intracranial: lacks external elastic membrane, rupture (SAH) more common.
·
Angio, CTA, MRA patterns:
o
String sign (luminal stenosis)
o
Pearl and string sign (fusiform
dilation with adjacent stenosis - higher re-bleed rate?) (Figure 1 Chamoun RB JN:P8/08)
o
Intimal flap / Double lumen
o
Fusiform dilation.
o
T1 MRI: ↑T1 (mural hematoma)
around narrow flow void
o
CTA or MRA generally obtained first,
angiogram if CTA/MRA negative but high clinical suspicion
o
May also be diagnosed by ultrasound
Extracranial
Dissection
·
Hemorrhage is rare
·
Carotid:
Usually 2cm above bifurcation below skull base.
·
Symptoms:
Facial/eye pain, carotidynia (neck pain), pseudo-Horner’s (no
anhydrosis), cervical bruit
·
Vertebral:
Between skull base & C2 or C6. Occipital HA.
·
Symptoms:
occipital pain/headache (after trauma); brainstem signs (e.g. Wallenberg’s)
·
Treatment:
- Observation
for asymptomatic traumatic VA dissection (per cervical
trauma guidelines)
- Anticoagulation
6-12 wks (heparin 7-14d then coumadin) or until >50% re-canalized on
MRA/angio then antiplatelets.
- Serial
imaging until resolution.
- Do
not use if SAH present – surgical or endovascular
- No
randomized trials of effectiveness of anticoagulants or antiplatelets
- Consider
antiplatelets initially if high bleeding risk (large CVA).
- Consider
adding antiplatelets to anticoagulation for clinical progression.
- For
significant stenosis after healing of dissection, angioplasty ± stenting considered
(no randomized trials)
- Extracranial
carotid dissection in children: antiplatelet treatment recommended Chamoun RB JN:P8/08 – Management Flowchart
- For
persistent symptoms on anticoagulation and antiplatelets
- Endovascular
angioplasty ± stenting, or endovascular occlusion
- Surgery:
interposition graft repair, EC-IC
bypass or carotid
occlusion
Intracranial
Dissection
·
May occur on ACA (A2), MCA, PCA,
Vertebrobasilar
·
Treatment:
·
Endovascular angioplasty ± stenting
·
Endovascular proximal occlusion
(coils, balloons)
·
Vertebrobasilar: options as for fusiform aneurysm
above (trapping, proximal occlusion)
·
Case Series: Anxionnat R N8/03 (intracranial)
AVM – Arteriovenous
Malformations
·
Hemorrhage rate: 3-4%/yr.
Rehemorrhage: 6% @ 6-12mos then 3%/yr. (Ondra SL JN9/90,
Hernesniemi JA N11/08)
o
Risk of death from ruptured AVM:
1%/yr. Mortality from hemorrhage: 15%. Lifetime risk: 1-0.3life expectancy,
or 105-age.
o
For deep AVMs (basal ganglia,
thalamus, brainstem) risk is 10%/year.
o
Higher rupture rate: previous
hemorrhage, small size, deep drainage.
o
No increased risk if symptomatic (HA,
seizures, etc).
o
No known increase with pregnancy if
non-ruptured, but rehemorrhage rate may be higher (26%) if ruptured during
pregnancy - controversial. Generally managed expectantly until delivery.
C-section vs vaginal delivery is controversial.
·
15% have associated aneurysms (examine
imaging closely).
·
Vasospasm occurs in 1%.
·
Presentation: hemorrhage 50%, seizure
25%, deficit (2º to steal) 25%, headaches (migraine-like, more common
w/occipital AVM). Younger presentation than aneurysms.
·
Often wedge-shaped, apex at ventricle.
·
Audio: Cerebral AVMs: Changing Concepts in
Treatment Alternatives – Heros RC
Treatment
·
Based
on age, grade (location, size, drainage), symptoms.
·
Asymptomatic:
55yo used as general cutoff for treatment
o
New
York Islands AVM Study suggested conservative treatment if
asymptomatic, but study was problematic. (Stapf C Stroke 5/03)
o
“A randomized trial of unruptured brain arteriovenous
malformations (ARUBA)” is a currently ongoing RCT of observation
versus any treatment
·
Ruptured AVMs: usually treated
electively after 2-4weeks. Emergent ICH evacuation can be done with or without
AVM resection.
·
Spetzler-Martin Grade:
Spetzler RF JN86
o
Grade I-II: generally treated surgically
·
Some
feel embolization should not be performed for most Grade I or II AVMs, because they
can be resected with low risk of morbidity.
o
Grade III: treatment individualized
·
Lawton’s revisions to grade III: Grade III- (S1VD1E1; low grade - resectable), Grade III
(S2VD1E0; intermediate – ± resectable), Grade III+ (S2VD0E1; high-grade –
conservative management), and Grade III* (S3VD0E0; rare). Lawton MT N4/03
·
Medium-sized
Grade III AVMs in eloquent regions can be embolized to reduce surgical risk,
but lesions in noneloquent brain regions generally can be excised without
embolization
o
Grade IV-V: managed conservatively unless repeated
hemorrhages leads to deterioration
·
Barrow
Neurological Institute’s Grades IV and V AVMs showed a 1% annual bleeding rate
in patients treated conservatively compared with a 10.4% rate in patients whose
AVMs were treated partially or palliatively; they recommend conservative
treatment without embolization for most Grades IV and V AVMs. (Citation
pending)
o
Large-volume AVMs: embolization, embolization followed by
radiosurgery, radiosurgery with low radiation doses and planned repeat
radiosurgery for the expected residual, staged-volume radiosurgery, and
fractionated radiation therapy.
·
Surgery
o
Wait
3-30 days (e.g. 1 week) after embolization
o
Consider
pretreatment with propanolol to minimize NPPB
o
Wide
exposure. Circumferential dissection, preserving draining veins.
·
For
intraop bleeding: can use controlled hypotension. Check for venous compression
by retractors.
o
Postop/intraop
angio. Residual may have higher rupture risk – excise.
o
Complications: Postop ICH or severe edema in 3-12%.
o
Normal Perfusion Pressure Breakthrough (NPPB): Postop swelling or
hemorrhage. Hyperemia detected with Perfusion MRI. Control BP.
o
Reviews: Hashimoto N N6/01, Clatterbuck RE ON7/05 (Operative Nuances), Hashimoto N N7/07S, Natarajan SK N6/08
o
Videos:
Hashimoto N N6/01, Clatterbuck RE ON7/05, Hashimoto N N7/07S, Natarajan SK N6/08
·
Embolization:
o
NBCA
(N-butyl cyanoacrylate), polyvinyl alcohol particles, coils.
o
Almost
always adjunctive, not primary treatment (cure rates 5-40%).
o
Some
recommend 24-72 hrs ICU monitoring.
o
o
Risks:
ICH 1-4%. AVM may recanalize after successful embolization.
o
Staged
endovascular embolization may result in reduction of NPPB with very large
high-flow AVMs. Generally staged at days to weeks intervals, 20-30% per stage.
o
Valavanis
and Yasargil reported a 39% cure rate in 387 embolized AVMs. For AVMs that were
embolized with curative intent, they reported a 75% cure rate.
o
Large
AVMs in eloquent areas with progressive neurological deficit, palliative
embolization can improve or stabilize the neurological deficit in more than 90%
of cases
o
Adjunctive:
o
Wait
3-30 days before performing surgery
·
Embolization
can be used to obliterate deep arterial pedicles (such as the lenticulostriates
and thalamoperforators) that are inaccessible during the early surgical
exposure.
o
Previous
embolization is a negative predictor of successful AVM radiosurgery, and some
consider its use to be contraindicated prior to radiosurgery (Andrade-Souza YM N3/07)
·
Not
recommended before SRS, but if performed wait 30 days before SRS then repeat
angio.
·
Embolization
has been used pre-SRS in AVMs larger than 3 cm to reduce size and AVMs with
angioarchitectural abnormalities that predict a high risk of hemorrhage during
the latency period – i.e. intranidal and venous aneurysms or those associated
with a large arteriovenous fistula (AVF).
·
Radiosurgery:
o
Recommended
for AVMs smaller than 3 cm (volume <10cc) in diameter when surgery carries a
high risk of morbidity
o
The
3 cm size cut-off is supported by anecdotal case series and nonrandomized
cohort studies.
o
Radiosurgery
AVM score – Pollock/Flickinger (Pollock BE JN1/02) Modified System – Pollock BE N8/08
o
Bleeding
risk unchanged for 2-3yr latency (controversial – some studies report lower or
higher rates) (Marayuma K NEJM1/13/05)
o
Margin
doses: Small AVMs 23Gy (no benefit from higher doses). Large, risky location: 16-18Gy.
(<15Gy ineffective).
o
Use
MRI (Or CTA) with (or without) angio for targeting.
o
2yr
obliteration: >4cm3 = 40-60%, <4cm3
= 85-100%. Overall 75% (Pollock BE N6/03)
o
Factors reducing success: size,
location, age, prior embolization (Andrade-Souza YM N3/07)
o
Size: >15cm3 consider
staged SRS at 6mo intervals.
o
Hypofractionated Conformal
Stereotactic Radiotherapy has also been used (Lindvall
P N11/03)
o
Hematoma may compress vessels, may
targeting difficult. Perform SRS 2-3mos after hemorrhage.
o
Complications:
cyst formation (2%, may occur between 5 and 20 years post-treatment), edema
(10% symptomatic, 4% need surgery), necrosis 3-6%.
o
Follow-up:
Repeat angio not performed until 3yrs, then consider retreatment, repeat
SRS.
o
If early draining vein but no nidus,
consider it treated.
o
Follow-up MRI has 100% positive and
85% negative predictive values – some get only MRI only for follow-up.
o
Persistent
AVM may be treated with repeat SRS or surgery
·
Some
feel SRS make subsequent surgery easier in many cases (Sanchez-Mejia RO N2/09)
Deep
(Brainstem/Thalamic) AVMs
·
Rupture rate basal ganglia/thalamus
AVMs is 10%/year (Fleetwood IG JN4/03)
·
Basal
Ganglia/Thalamus: see Gross B N9/08
·
Radiosurgery:
66% success, 10% permanent deficits. Risk higher in tectum. Higher doses (20Gy)
preferred. (Pollock BE JN2/04, Maruyama K JN3/04, Andrade-Souza YM N1/05)
AVM-associated
aneurysms
·
10%
of aneurysms have associated by AVMs
·
Classifications:
terminology varies.
1.
Intranidal
aneurysms: increased risk of rebleeding (10%/year); can be targeted by
embolization.
2.
Pedicle
(flow-related distal) aneurysms: some report higher risk of bleeding
3.
(Flow-related)
Proximal aneurysms: on circle of Willis vessels feeding AVM.
§
Rupture
risk unclear but reported to be at least that of isolated aneurysm.
§
Obliteration
of AVM may reportedly increase risk of rupture.
4.
Incidental: unrelated circle of Willis
o
Drake Classification: see Chart (Cunha e Sa
MJ JN1992)
·
Treatment (flow-related):
Controversial
o
Some recommended treating the AVM suggesting
flow-related aneurysms will regress afterwards (Meisel
HJ N4/00)
o
Others recommend treating lesion that
probably bled 1st or both simultaneously. If its not clear which
bled, presume it’s the aneurysm. (Cunha e Sa
MJ JN1992)
§
“The
late Charles Drake taught that the aneurysm should be considered to have bled
whenever bleeding associated with an AVM and an aneurysm is observed” – Fox AJ, comment on Meisel HJ N4/00
o
Others
recommend always treating the aneurysm first (or both simultaneously), as
treatment of the AVM may increase the risk of rupture (Thompson
RC N8/98)
Dural Arteriovenous Fistulas (AVFs)
·
Acquired, due to venous sinus
thrombosis, fed from ECA (dural or transosseous) or less commonly ICA (dural –
tentorial, orbital or cavernous sinus).
·
May present with
local symptoms (e.g. tinnitus) or SAH/ICH
·
Cortical venous drainage
(CVD) (aka retrograde leptomeningeal venous drainage - RVLD) is #1 SAH risk –
10% mortality.
·
Locations:
o
Transverse/ sigmoid:
most common.
·
Symptoms: Pulsatile
tinnitus (also caused by aberrant ICA, glomus
tympanicum.), occipital bruit.
·
Less SAH risk.
·
Parallel venous channel may be the
recipient pouch near the transverse sinus (Caragine LP N12/03)
o
Cavernous sinus (CCF):
see below
o
Tentorial apex
(ICA/ECA to deep cortical veins): increased SAH risk
o
Orbital/ anterior fossa:
increased SAH risk. Can’t treat ophthalmic/ethmoidal feeders endovascularly
o
Others
·
Diagnosis:
o
MRI/MRA: multiple flow-voids in
enlarged, enhancing transverse sinus
·
Cortical drainage involvement may
mimic neoplasm
o
Angiogram: ECA or ICA feeders to
venous sinus
·
Borden and Cognard classifications
(see right – from Strom RG N2/09)
·
Treatment:
o
“Aggressive”: Cortical or retrograde venous drainage,
ICH/SAH, seizures, progressive neurologic deficit: requires urgent treatment.
o
“Benign”: Anterograde drainage: can
treat symptomatically.
o
Options for surgery or embolization
are disconnection of cortical venous drainage vs. complete obliteration
o Endovascular embolization: transarterial (higher recurrence) or
transvenous (riskier)
·
Anterior fossa lesions with feeders
via ethmoidals/ ophthalmic a. are treated surgically, not endovascularly
o
Surgery:
·
Single leptomeningeal draining vein
can be treated with vein ligation.
·
Alternative: excision and packing of
sinus. Potential for high blood loss early.
o SRS: 68% obliteration, 24% regression.
Considered for “benign” DAVFs (Soderman M JN6/06 – editorials by Heros RC, Sheehan J)
Carotid-cavernous fistula
·
Barrow Classification (A-D)