3. Important facts
• 15% died before reaching medical care
• 10% died within first few days
• > half died within 2 weeks of SAH
• Severity of clinical presentation is the strongest prognostic indicator
9. Pretruncal nonaneurysmal SAH (PNSAH)
• Aka “Dutch Disease”
• Good outcome: less rebleed and vasospasm
• Etiology: rupture of small perimesenphalic vein or capillary
• Similar sx of SAH, but usually WFNS grade ½
10. Pretruncal nonaneurysmal SAH (PNSAH)
• Diagnosis criteria
1. CT/MRI performed within 2 days of ictus meeting criteria below:
2. A negative high-quality-4-vessel cerebral angiogram
3. appropriate clinical picture: no loss of consciousness, no sentinel
H/A, SAH grade 1 or and absence of drug use.
13. Pretruncal nonaneurysmal SAH (PNSAH)
• Treatment:
- No need extreme measure
- Symptomatic treatment
- Electrolyte monitoring for hypoNa
- F/up clinically/imaging to w/o for 1% risk of hydrocephalus
14. SAH of unknown etiology
• Incidence: 10%
• Risk of rebleeding: 0.5%/yr
Management:
• Keep patient in hospital
• Repeat 2nd angiogram at Day 10 ( up to 10% can be +ve)
• If 2nd angiogram negative, but clinically suspicious, 3rd angiogram at
3-6mths (1% chance)
15. Cerebral Aneurysm
• A bulge or balloon like dilatation/swelling of wall of a blood vessel in
brain
• Develop as a result of weakness in wall of vessel, usually at branch
point
• 50% of aneurysm ruptured
• 2% of aneurysm present during childhood; if does, more common in
male and posterior circulation
16. Cerebral Aneurysm - Etiology
1. congenital predisposition
2. “atherosclerotic” or hypertensive
3. embolic: as in atrial myxoma
4. infectious—so called “mycotic aneurysms”
5. traumatic; see Traumatic aneurysms
6. associated with other conditions such as
ADPKD, FMD, AVM including MOYA-MOYA, Connective tissue disorder(Marfan,
Ehler-Danlos type IV), MEN type I, NF type I
19. Rhoton’s 4 rules of aneurysm
Aneurysms arise at branching sites on the
parent artery, which may be a side branch
or a bifurcation (rule 1)
Aneurysms arise at turns or curves in the
outer wall of the artery where
hemodynamic stress is greatest (rule 2)
aneurysms point in the direction that
blood would have gone if the curve at the
aneurysm site was not present (rule 3
each aneurysm is associated with a set of
perforating arteries that needs to be
preserved (rule 4).
20. Locations of cerebral aneurysms
Saccular aneurysms location:
1. 85–95% in carotid system, with the following 3 most common locations:
a) ACoA (single most common): 30%
b) b) p-comm: 25%
c) middle cerebral artery (MCA): 20%
2. 5–15% in posterior circulation (vertebro-basilar)
a) ≈ 10% on basilar artery: basilar bifurcation, AKA basilar tip, is the most common,
b) ≈ 5% on vertebral artery: VA-PICA junction is the most common
3. 20–30% of aneurysm patients have multiple aneurysms
21. Anterior communicating artery aneurysm (ACoA)
• Single most common site of aneurysm
• May present with DI and hypothalamic dysfunction
• CT scan: blood in anterior interhemispheric fissure ; intracerebral
hematoma 63%, IVH 79%, acute hydrocephalus 25%, frontal lobe
infarct 20%
28. Infundibulum
• A funnel shaped initial segment of an artery
• Bilateral in 25%
• Incidence up to 13%
• Common site P-COM
• Less risk of rupture( no bleed if < 3mm)
• Treatment: conservative; unless surgery for other reason,
consider wrapping or encircling clip
35. Mycotic aneurysm
• Referred to any infectious process
• 4 % of intracranial aneurysm
• Up to 15% with subacute endocarditis
• Most common location: distal MCA brances (80%)
• 20% developed multiple aneurysm
• Usually fusiform and friable
• Risk factors: immunocompromised patient and drug users
• Start from adventitia and spread inwards
• Most common pathogens: Strep, Staph
36. Mycotic aneurysm
• Treatment:
- Abx 4-6 weeks
- Serial angiography 1/52, 6/52, 3-, 6- and 12-month
- Indications of delayed clipping:
a) Patients with SAH
b) Increasing size while on abx
c) Failure to shrink after 4-6/52 of abx
37. Giant aneurysm
• Definition: > 2.5cm
• Up to 5% of intracranial aneurysm
• Drake’s series: bleeding rate is up to 50%/year
• Ix: Angiogram + CT / MRI
• Treatment:
a) Direct surgical clipping (only possible in 50% cases)
b) Vascular bypass with clipping
c) Trapping
d) Hunterian ligation
e) Wrapping
f) Endovascular treatment
Editor's Notes
Irritation of lumbar nerve root by dependent blood
OH: controversial, compression of retinal vein and retinochoroidal anastomoses by elevated CSF pressure, causing venous hypertension and disruption of retinal vein
Instead of perimesencephalic b/c neuroimaging proven mainly bleed in front of brainstem(truncus cerebri), pons rather than midbrain
Etiology has yet to be determined
Some show a/w venous abnormality like variants of basal vein of Rosenthal
Cerebral venous hypertension
Instead of perimesencephalic b/c neuroimaging proven mainly bleed in front of brainstem(truncus cerebri), pons rather than midbrain
Etiology has yet to be determined
Some show a/w venous abnormality like variants of basal vein of Rosenthal
Cerebral venous hypertension
≈ 3% of patients
with a ruptured basilar bifurcation aneurysm meet the criteria of ▶Table 78.5,106 and therefore
an initial arteriogram is mandatory
Instead of perimesencephalic b/c neuroimaging proven mainly bleed in front of brainstem(truncus cerebri), pons rather than midbrain
Etiology has yet to be determined
Some show a/w venous abnormality like variants of basal vein of Rosenthal
Cerebral venous hypertension
≈ 3% of patients
with a ruptured basilar bifurcation aneurysm meet the criteria of ▶Table 78.5,106 and therefore
an initial arteriogram is mandatory
Figure 2 Radiological anatomy. Sagittal (slightly paramedian) CISS image clearly demonstrating the LM and its three segments. Note the membrane insertion into the mammillary body, and its thickness much inferior to that of the third ventricle floor. The white arrow identifies the sellar segment; the black arrow, the diencephalic segment; and the arrow head, the mesencephalic segment.
Liliequist’s membrane (LM)101: Basically considered to separate the interpeduncular cistern
from the chiasmatic cistern102 (it forms a competent barrier in only 10–30% of the population). In
further detail, the superior leaflet of LM (diencephalic membrane) separates the interpeduncular
cistern from the chiasmatic cistern medially and from the carotid cisterns laterally.103,104 The inferior
leaflet (the mesencephalic membrane) separates the interpeduncular from the prepontine cistern.
The diencephalic membrane is thicker and is more often competent, effectively isolating the
chiasmatic cistern. However, the carotid cisterns often communicate with the crural cisterns and in
turn with the interpeduncular cistern.104
Thus, blood in the carotid or prepontine cistern is compatible with a low-pressure pretruncal
source of bleeding; however, blood in the chiasmatic cistern should raise concern about aneurysmal
rupture.
Optimal rx not known
No need extreme measure b/c low risk of rebleeding and delayed ischemia
Not recommened the standard SAH therapy
Day 10 allow vasospasm and clot to resolve; permit surgery at day 14; no-op window 3-12 days
1. congenital predisposition (e.g. defect in the muscular layer of the arterial wall, referred to as a
medial gap)
2. “atherosclerotic” or hypertensive: presumed etiology of most saccular aneurysms, probably
interacts with congenital predisposition described above
3. embolic: as in atrial myxoma
4. infectious—so called “mycotic aneurysms” (p.1288)
5. traumatic; see Traumatic aneurysms (p.1287)
6. associated with other conditions (see below)
Figure 5. This cartoon summarizes the main steps of the establishment of inflammation in intracranial aneurysms. Going counterclockwise: Increased mechanical stress in aneurysm-prone regions is believed to trigger events that culminate in vascular dysfunction, leaving the endothelium nude from antithrombotic protection. The inflammatory cascade then begins, with the expression of chemoattractants and proinflammatory cytokines and burgeoning of cell adhesion molecules at the surface of endothelial cells, which attract peripheral blood mononuclear cells, including monocytes and T cells. The complement is also activated through the classic pathway. Monocytes are able to adhere and transmigrate into the endothelium, which they would not do under normal conditions. They subsequently differentiate into macrophages, as observed in morphological studies of intracranial aneurysm wall. The level of proteases in aneurysmal wall is increased, and given the literature on macrophages, there is good evidence that macrophages are responsible for the imbalance of proteases. During remodeling, the medial layer is destroyed, and so is the internal elastic lamina, leading to lower mechanical properties and finally ballooning of the wall. IL indicates interleukin; MCP-1, monocyte chemoattractant protein-1; TNF-α, tumor necrosis factor-α; and VCAM-1, vascular cell adhesion molecule-1.
followed by
BA-SCA, BA-VA junction, AICA
False: rupture of all vessel wall layers with the wall of aneurysm being formed by surrounding cerebral structures
Closed head injury is due to traction to vessel wall or entrapment within #
peripherally:DACA(impact against falcine edge)
Distal cortical due to overlying skull fracture, sometimes growing skull #
Cavernous carotid aneurysm causing syndrome, CCF, if rupture
78.4.2 Presentation
1. delayed intracranial hemorrhage (subdural, subarachnoid, intraventricular, or intraparenchymal):
the most common presentation. TAs tend to have a high rate of rupture
2. recurrent epistaxis
3. progressive cranial nerve palsy
4. enlarging skull fracture
5. may be incidental finding on CT scan
6. severe headache
Mycotic originated from Osler
Pathogen same as SBE (Strep Viridan and Stap Aureus)
Mycotic originated from Osler
Pathogen same as SBE (Strep Viridan and Stap Aureus)
Why serial angiography even smaller b/c may subsequently increase and new ones might form
Serial MRA is viable alternative
Increasing size while on abx
- Controversial: morawetz evolution of mycotic aneurysm 1984
Angiogram underestimates the size of lesion due to thrombosed portion
Based on turbulence on T1W1, can differentiate aneurysm from cystic/solid lesion
