4. Epidemiology
9.7-14.5 per 100,000 population
• peak age for aneurismal SAH is 55–60 years, ≈
20% of cases occur between ages 15–45 yrs
• higher in women (1.24 times higher than men)
• higher in African Americans(2.1 times higher
than whites)
4
6. SAH- etiology
• CLASSIFIED AS: TRAUMATIC
NON TRAUMATIC
• Excluding head trauma, the most common cause of
SAH is rupture of a SACCULAR ANEURYSM.
• Other causes :
bleeding from a vascular malformation (AV malformation
or dural AV fistula )
Extension into the subarachnoid space from a primary
intracerebral haemorrhage.
Mycotic aneurysms
Associated with genetic disorders 6
7. Mechanism of formation of aneurysms
developmental defect in the media & elastica
focal destruction of internal elastic membrane
caused by hemodynamic forces acting at
bifurcations & branching of arteries
local weakness in vessel wall, intima bulges out
covered only by adventitia
The sac gradually enlarges and subsequently rupture
7
9. SACCULAR ("BERRY") ANEURYSM
• Autopsy and angiography studies have found that
about 2% of adults harbor intracranial aneurysms,
• Size- 2 mm. to 2-3 cm
9
13. PATHOPHYSIOLOGY
• Saccular aneurysms occur at the bifurcations of the large to
medium-sized intracranial arteries.
Rupture is into the
subarachnoid space,
basal cisterns
the parenchyma of the adjacent brain.
• Approximately 85% of aneurysms occur in the
anterior circulation, mostly on the circle of Willis.
• About 20% of patients have multiple aneurysms,
- - many at mirror sites bilaterally.
13
16. • Aneurysms can undergo small ruptures and blood leaks into the
subarachnoid space, so-called SENTINEL BLEED.
SYMPTOMS are usually due to rupture of aneurysm and resultant SAH
• some present with mass effect on cranial nerves or brain
parenchyma.
• Aneurysmal rupture usually occurs while the pt is active
• may occur while straining on stool, sexual intercourse, lifting a heavy
weight or some other sustained exertion
• 30% of aneurysmal SAHs occurs during sleep
16
17. Four patterns of presentations:
Pt. is stricken with severe headache & vomiting , and falls
unconscious immediately
Severe generalized headache occurs suddenly but pt remains
lucid with varying degrees of neck stiffness
Rarely pt suddenly becomes unconscious without any preceding
complaint.
patient may die within min to hours
17
18. • In patients who survive initial rupture the most
feared complication is rerupture which may
occur at any time from minutes to 2-3 wks
18
19. HEADACHE
In ~45% of cases,sudden onset severe headache
associated with exertion is the presenting
complaint.
"the worst headache of life";
usually generalized,
often with neck stiffness,
vomiting is common
19
20. Pain at other sites
• Occipital and posterior cervical pain may
signal a posterior /anterior inferior cerebellar
artery (PICA/AICA) aneurysm.
• Pain in or behind the eye and in the low
temple can occur with an expanding MCA
aneurysm
20
21. Loss of consciousness
• sudden transient loss of consciousness in
nearly half of patients
• 6-16% patients develop seizures
• In 10% of cases, aneurysmal bleeding is severe
enough to cause loss of consciousness for
several days.
21
22. Ocular hemorrhage
• Due to compression of central retinal vein and
retrochoroidal anastomoses by elevated CSF
pressure causing venous hypertension and
disruption of retinal veins
• Occurs in 20-40% of patients
• Types: subhyaloid/preretinal hemorrhage
intraretinal hemorrhage
Viterous hemorrhage(Terson syndrome)
22
23. FOCAL NEUROLOGICAL DEFICITS
• ACA or MCA bifurcation aneurysms may rupture
into the adjacent brain or subdural space and form
a hematoma large enough to produce mass effect.
hemiparesis,
aphasia,
progressive drowsiness or slow mentation
23
24. • Third nerve palsy : aneurysm at the junction
of post. Communicating & post. Cerebral
arteries
• A sixth nerve palsy: an aneurysm in the
cavernous sinus
uni or bilateral palsy could be because of raised
ICP
• Unilateral blindness : aneurysm lying
anteromedially in the circle of willis usually at
the origin of opthalmic artery
24
25. Transient paresis of one or both lower limbs :
ant comunicating A. aneurysm that has interfered
with circulation in ant. Cerebral arteries.
Hemiperesis or aphasia suggests aneurysm at the first
bifurcation of middle cerebral artery
25
26. D/D severe headache
Migraine headache
ingestion of sympathomimetic drugs
ingestion of tyramine containg foods in a pt. who is taking
MAO inhibitors
phaeochromocytoma
Cerebral venous thrombosis,
Diffuse vasospasm (call-flemming syndrome),
Hypertensive encephalopathy,
Intracranial or extracranial arterial dissection
26
31. NON CONTRAST CT SCAN.
• CT Scan is Initial investigative procedure
More than 95% of cases have enough blood to be
visualized on a high-quality NONCONTRAST CT
SCAN obtained within 48 h.
locate the underlying aneurysm,
identify the cause of any neurologic deficit, and
predict delayed vasospasm
31
36. lumbar puncture
• Usually CSF becomes grossly bloody within 30 minutes of bleed with
RBC counts upto 1 million/c mm or more
• Lysis of the red blood cells and subsequent conversion of
hemoglobin to bilirubin stains the spinal fluid yellow( xanthochromia)
within 2-4 h max by 12 hrs
• lasts for 1–4 weeks, depending on the amount of subarachnoid
blood
• Protein: high due to blood breakdown products
• Glucose: normal or reduced
36
37. Angiography
CT angiography
• for locating the aneurysm and its relation with nearby
bony structures
• Evaluation of vasospasm
MR angiography
87% sensitive 92% specific
Catheter angiogram
GOLD STANDARD
Demonstrates source in 80-85% cases
37
42. OTHER INVESTIGATIONS
Close monitoring (daily or twice daily) of
electrolytes : hyponatremia occur
precipitously during the first 2 weeks following
SAH
An asymptomatic troponin elevation is
common.
ECG
ECHO
42
43. TREATMENT
The medical management of SAH focuses on
• Managing blood pressure and maintaining
euvolemia
• Maintaining ICP
• Preventing rebleeding prior to treatment,
• Managing vasospasm, delayed neurological deficits
• managing seizures
• Treating hydrocephalus,
• Treating hyponatremia,
43
44. • bed rest in a quiet room
• stool softeners to prevent straining.
• If Headache or neck pain is severe, mild sedation
and analgesia
• Extreme sedation is avoided because it can obscure
changes in neurologic status.
• Adequate hydration
44
45. Prevention of vasospasm
• Calcium channel blockers: oral nimodipine
should be administered in all patients with
aSAH
• Maintainance of euvolemia and normal
circulating volume
• Induction of hypertension is recommended for
patients with DCI unless BP is elevated at
baseline
45
46. POST SAH SEIZURES
46
• Prophylactic anticonvulsant may be considered in
immediate post hemorrhagic state
• Routine long term use of anticonvulsant is not
recommended
• long term use of anticonvulsant may be
considered in patients with risk factors for deayed
seizure disorder (prior seizure, intracerebral
hematoma, intractable hypertension,infarction,or
MCA aneurysm)
47. Antifibrinolytic therapy
• For patients with aneurismal SAH where:
1. unavoidable delay in t/t of aneurysm
2.pt with significant risk of re bleeding
3. no compelling medical contraindications
Upto 72 hrs of therapy with tranexemic acid or
aminocaproic acid is reasonable
47
48. Acute hydrocephalus
• CSF diversion or lumbar drain
Chronic hydrocephalus
Permanent CSF diversion for symptomatic
patients
48
49. INTERVENTIONAL MANAGEMENT
• Early aneurysm repair prevents
rerupture/rebleeding and
allows the safe application of techniques to
improve blood flow (e.g., induced hypertension
and hypervolemia) should symptomatic vasospasm
develop.
• An aneurysm can be "clipped" or "coiled”
49
50. Angiographic findings: general features to take note
when analysing anuerysm
1.size of aneurysm dome
2.neck size
3.dome neck ratio
Large aneurysms > 15 mm diameter are a/w lower rates
of complete occlusion by endovascular coiling
Narrow neck <5 mm are ideal for coiling
Broad neck > 5mm a/w increased risk of incomplete
occlusion and recanalization by coiling
Stent or balloon assisted coiling may be needed for wide
necked aneurysm
Dome neck ratio : > or equal to 2 are a/w higher rate of
successful coil occlusion 6
50
51. 51
SURGICAL REPAIR
•Involves placing a metal clip across the aneurysm
neck, thereby immediately eliminating the risk of
rebleeding.
•This approach requires craniotomy and brain
retraction, which is associated with neurologic
morbidity.
58. Management based on HH scale
Grades 1 & 2
• Current approach is to go for intervention within 24 hrs
This will prevent rebleed and will allow measures to be taken to
improve cerebral circulation
• Grade 3 patients- if their condition allows , they too would be
benefitted by the procedure
• Grade4/5- the outcome is generally poor but by putting a ventricular
drain and improving the grade, pt are sometimes taken for
intervention
58
68. References
• Bailey and love’s Short Practice of Surgery,26th
edition
• AHA/ASA guideline for management of
aneurysmal suarachnoid hemorrhage, june
2012
• Giovanni Grasso, et al authors, Management
of aneurysmal SAH : state of the art and
future perspectives, surgical neurology
international ,2017
68
sentinel bleeds: patient may have a unusual headach
esentinel headaches that precede the SAH-associated ictus have been reported by 10-50% of patients and most commonly occur within 2-8 weeks before overt SAH
With ruptue , blood at high pressure gushes in the suarachnoid space resulting in following three patterns of presentations: In rapidly evolving cases the bleed is so massive that I/c pressure approaches systemic BP, thus severely compromising the cerebral perfusion
Sudden unexplained headache at any location should raise suspicion of SAH and must be investigated,
COMA is d/t increased ICP, damage to the brain tissue from intraparenchymal hemorrhage
Hydrocephalus , diffuse ischaemia, seizures,, low blood flow d/t reduced cardiac output
4-27% common with anterior circulation aneurysms. d/t raised iop----retinal membrane formation ---.retinal detachment
tendency for the hemorrhage to recur from the same site in more than one third of patients, often catastrophically
The incidence of rerupture of an untreated aneurysm in the first month following SAH is ~30%, with the peak in the first 7 days.
appears to be related to naturally ocuring mechanisms of clot lysis at the initial site of rupture
Rerupture is associated with a 60% mortality and poor outcome.
cause stupor and coma
subacute hydrocephalus may develop over a few days or weeks
causes progressive drowsiness or slowed mentation (abulia) with incontinence.
Chronic hydrocephalus may develop weeks to months after SAH
present as normal pressure hydrocephalus (NPH) manifested by gait difficulty, incontinence, or impaired mentation.
Subtle signs may be a lack of initiative in conversation or a failure to recover independence
Vasospasm is believed to result from direct effects of clotted blood and its breakdown products on the arteries within the subarachnoid space.
Causes symptomatic ischemia and infarction in ~30% of patients
major cause of delayed morbidity and death.
Signs of ischemia appear 4–14 days after the hemorrhage, most often at 7 days.
The severity and distribution of vasospasm determine whether infarction will occur.
Spasm of major arteries produces focal symptoms referable to the appropriate vascular territory.
All of these focal symptoms may present abruptly, fluctuate, or develop over a few days.
In most cases, focal spasm is preceded by a decline in mental status.
Patient may develop fluctuating hemiparesis or aphasia
Severe cerebral edema in patients with infarction from vasospasm may increase the ICP enough to reduce cerebral perfusion pressure.
may be profound and can develop quickly in the first 2 weeks following SAH. There is both natriuresis and volume depletion with SAH, so that patients become both hyponatremic and hypovolemic.
Both atrial natriuretic peptide (ANP)and brain natriuretic peptide (BNP) have a role in producing this "cerebral salt-wasting syndrome.“
There may some role of antidiuretic hormone also, causing water retention
Typically it clears over the course of 1–2 weeks and, in the setting of SAH, should not be treated with free-water restriction as this may increase the risk of stroke.
A high incidence of symptomatic vasospasm in the MCA and ACA has been found when early CT scans show subarachnoid clots >5 x 3 mm in the basal cisterns or layers of blood >1 mm thick in the cerebral fissures.
Collection of blood in the anterior inter-hemispheric fissure,blood in lateral ventricles,gyrus rectus: rupture of an ant. Communicating artery
Blood in sylvian fissure – middle cerebral artery or post comm a
4th and third ventricle:lower posterior fossa source PICA or VA dissetion
Third ventricle : basilar apex aneurysm
False positive in increased protein in csf or jaundice
DYE KEPT IN FEMORAL ARTERY. TAKING SERIAL X-RAYS.DEMON
ECG changes suggestive of subendicardial or myocardial ischemia
Elevation of troponis/CPK (MB) levels
In some patients cardiac dysfunction may be severe enough to cause fall in EF % and heart failure
There is evidence that structural myocardial lesions produced by
circulating catecholamines and
excessive discharge of sympathetic neurons
may occur after SAH, causing these ECG changes and a reversible cardiomyopathy sufficient to cause shock or congestive heart failure.
Hyponatremia
D. Insipidus
Albuminuria,
Glycosuria
leukocytosis
avoid decrease in blood volume predisposing to brain ischemia