Subarachnoid Hemorrhage (SAH) and Aneurysm presentation.pptx

1. Subarachnoid Hemorrhage (SAH) and Aneurysm
2. SAH
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
4. Etiologies of SAH • Trauma (most common) • Spontaneous 1. Ruptured intracranial aneurysm (75-80%) 2. Rupture of an infundibulum 3. Pretruncal subarachnoid hemorrhage 4. Cerebral/Spinal AVM 5. Cerebral artery dissection 6. Tumour 7. Dural sinus thrombosis 8. Coagulation disorders 9. Vasculitides 10. Unknown causes ( 14-22%)
5. Clinical features of SAH • ‘Thunderclap’/Sentinel headache • Syncope • Vomiting • Meningismus: neck pain, photophobia, Kernig/Brudzinski sign • Coma • Low back pain • Ocular hemorrhage • Surgical 3rd nerve palsy
6. Non-aneurysmal SAH • Pretruncal nonaneurysmal SAH • SAH of unknown etiology
7. 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
8. 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.
9. Pretruncal nonaneurysmal SAH (PNSAH) • Diagnosis criteria 4. Negative angiogram +
10. PNSAH
11. 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
12. 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)
13. 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
14. 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
15. Cerebral Aneurysm - Etiology
16. 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).
17. 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
18. 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%
19. Anterior communicating artery aneurysm (ACoA)
20. P-Comm Aneurysm
21. P-Comm Aneurysm
22. P-Comm Aneurysm
23. 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
24. P-Comm Aneurysm
25. MCA aneurysm
26. MCA aneurysm
27. Special Aneurysm • Traumatic aneurysm • Mycotic Aneurysm • Giant Aneurysm • Familial Aneurysm
28. Traumatic aneurysm • < 1 % of intracranial aneurysm • Most’re false aneurysm/pseudoaneurysm • Subgroups: a. penetrating trauma e.g. gunshot b. closed head injury - peripherally:DACA, distal cortical artery aneurysm - Skull base: petrous portion, cavernous carotid artery c. iatrogenic
29. Traumatic aneurysm • Treatment usually recommended -skull base: trapping/embolization -peripherally:clipping/excision/ coiling/wrapping
30. 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
31. 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
32. 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


≈ 3% of patients
with a ruptured basilar bifurcation aneurysm meet the criteria of ▶Table 78.5,106 and therefore
an initial arteriogram is mandatory


≈ 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

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