2. Introduction
SAH : fourth most frequent cerebrovascular
disorder-following atherothrombosis,
embolism and primary intracerebral
hemorrhage.
CAUSE: Excluding head trauma, the most
common cause of SAH is rupture of
saccular aneurysm.
3. INCIDENCE
incidence of SAH increase with
age,occuring most commonly between 40
and 60 years of age,but it can occur from
childhood to old age
is ~1.6 times higher in women than in men.
5. Certain genetic syndromes
ADPKD
Type IV Ehlers-Danlos syndrome
Familial intracranial aneurysms
Increased incidence of fibromuscular
dysplasia of extracranial arteries,
moyamoya disease, AV malformation of
the brain , COA among persons with
saccular aneurysms
6. Saccular/berry aneurysm
About 2% of adults harbor intracranial
aneurysms.
Small thin walled blisters protruding from
arteries of circle of willis or its main
branches.
Rupture causes filling of the subarachnoid
space with blood under high pressure.
7. ~90-95% of saccular aneurysms lie on the
anterior part of circle of willis.
●4 most common sites are-
1)Proximal portions of the anterior
communicating arteries
2)At the origin of the posterior communicating
artery from the stem of the internal carotid
3)At the first major bifurcation of MCA
4)Bifurcation of the ICA into MCA and ACA
8.
9. Pathophysiology
results from development defects in the
media and elastica of the arteries.
Aneurysmal process initiation-> by focal
destruction of the internal elastic
membrane,which is produced by
hemodynamic forces at the apices of
bifurcation.
10. As a result of local weakness in the vessel
wall,the intima bulges outward, covered
only by adventitia, the sac then gradually
enlarges and finally ruptures.
At the site of rupture (mostly the dome), the
wall thins and the tear that allows bleeding
is often =<0.5mm long.
Those >7mm, at the top of the basilar
artery and at the origin of the posterior
communicating artery are at the greatest
risk of rupture.
The annual risk of rupture for aneurysms
<10mm is ~0.1% and for >10mm is 0.5 to
1%.
11. ➔GIANT CEREBRAL ANEURYSMS
➔Congenital anomalies
➔>2.5 cm in diameter
➔Located on carotid,basilar, anterior or middle
cerebral artery.
➔Compress adjacent structures eg those in the
cavernous sinus, optic nerve or lower
cranial nerves
12. There are several other type of aneurysms-
mycotic,
fusiform,
diffuse
and globular
Mycotic : caused by a septic embolus that
weakens the wall of the vesselin which it
lodges.
13. Clinical syndrome
One of the three
1) Excruciating generalized headache and
vomiting and falls unconscious almost
immediately.
2)Severe generalized headache but the
patients remain relatively lucid,
3)Consciousness is lost so quickly ,that there
is no preceding complaint.
Rupture usually occurs while the patient is
active.
14. Sentinel headache
Symptoms consistent with a minor
hemorrhage before a major rupture-
sentinel headache or warning leak.
Occur within 2-8weeks before overt SAH.
Headache often is unrelated to
hemorrhage and is attributable to migraine.
thunderclap headache: may be a variant of
migraine, pituatory apoplexy, hypertensive
encephalopathy, intracranial hypotension.
15. As the hemorrhage is localized to
subarachnoid space, there are few if any
local signs.
Convulsive seizure occur in 10 to 25 % of
cases.
16. Anatomic-clinical correlation
Third nerve palsy: indicates an aneurysm
at the junction of posterior communicating
artery and internal carotid artery.
Transient paresis of one or both of
lower limbs :suggests an anterior
communicating aneurysm that has
interfered with the circulation in the
anterior cerebral arteries.
Hemiparesis or aphasia :points to an
aneurysm at the first major bifurcation of
MCA.
17. U/L blindness : indicates an aneurysm lying
anteromedially in the circle of willis
20. Lab findings
CT scan- will detect blood locally or
diffusely in the subarachnoid space or
within the brain or ventricular system in
more than 90% of cases. first 24 hrs :
sensitivity of CT for SAH is 98%.
LP-when SAH is suspected but not
apparent on imaging studies.
The diagnosis of ruptured saccular
aneurysm is excluded if blood is not
present in the CSF, provided the spinal
fluid is examined more than 30 min after
21. RBC counts upto 1million/mm3
Xanthochromia
Bilirubin
4 vessel angiography- B/L external carotid
and vertebral arteries-to localize and define
the anatomic details of aneurysm. Selective
cerebral angiography is currently the
standard for diagnosing cerebral aneurysm
as the cause of SAH
MRA/CTA
22. Systemic changes associated with
SAH
ECG-symmetrical large peaked T waves-
cerebral T waves,prolonged ORS interval,
increased QT interval—suggesting
subendocardial or myocardial ischemia
Minor elevation in cardiac enzymes
Some cases -reversible cardiomyopathy
Leukocytosis -15,000-18,000cells/mm3
23. Treatment
Emergency evaluation and pre-op care
history
examination
clinical grading
CAB
24. Medical measures to prevent rebleeding
Blood pressure should be monitored and
controlled to balance the risk of
stroke,hypertension rebleeding and
maintainence of CPP.
to reduce BP nicardipine, labetalol and
esmolol used because of there safety
profile and short action
bed rest
Early treatment with short course of anti
fibrinolytic and prophylaxis against
hypovolemia and vasospasm may be
reasonable but further research is needed.
25. Surgical and endovascular
methods
Endovascular approach with electrolytically
detachable platinum coils
Aneurysm is packed with coils.
Coils induce thrombosis.
surgical clipping
26.
27.
28. Management of cerebral
vasospasm after SAH
It is the delayed narrowing of the large
capacitance arteries at the base of the
brain after SAH.
Angiographic vasospasm:seen in 30-70%
of patients with a typical onset 3-5days
after the hemorrhage,maximum narrowing
at 5-14 days and a gradual resolution over
2 to 4 weeks
29. The development of new focal deficit,
unexplained by hydrocephalus or
rebleeding is the first objective sign of
symptomatic vasospasm
The goal of management is to reduce the
threat of ischemic neuronal damage by
controlling ICP, decreasing the metabolic
rate of oxygen use, and improving CBF.
Volume expansion prevent hypotension,
augments cardiac output and reduces
blood viscosity by reducing the hematocrit.
30. This method is called triple H therapy
hypertension
hemodilution
hypervolemic
Nimodipine improves outcome py
preventing ischemic injury rather than
reducing the risk of vasospasm
Cerebral angioplasty and/or selective
intraarterial vasodilator therapy may be
reasonable after, together with or in place
of Triple H therapy.
31. Treatment of hyponatremia
CAUSE:
Due to natriursis and volume depletion.
Hypovolemic and hyponatremic
Clears over 1 to 2 weeks
Should not be treated with free water
clearance as it increases the risk of stroke
32. Management of hydrocephalus
Acute <72hrs of SAH:ventriculostomy
controversial.
Temporary or permanent CSF
diversion : recommended in symptomatic
patients with chronic hydrocephalus.
33. Management of seizures
Prophylactic antiepileptics -controversial
Risk factors for seizures post SAH-
MCA aneurysm,
intraparenchymal hematoma,
infarcts
and history of hypertension.
34. Prophylaxis for PE and DVT
Pneumatic compression stockings
UFH or LMWH-after surgical or
endovascular treatment.
Contraindicated inpatients with ruptured and
untreated aneurysm.
Use of IVC filters.
