The document discusses the anatomy and pathophysiology of subarachnoid hemorrhage. It notes that the subarachnoid space lies between the arachnoid membrane and pia mater, and contains cerebrospinal fluid. Rupture of an intracranial aneurysm is the most common cause of subarachnoid hemorrhage, causing blood to enter the subarachnoid space. Presentation can range from sudden severe headache to loss of consciousness, depending on the severity of bleeding.

2. • Arachnoid comes from Greek “arachne” meaning spider web +
“eidos” meaning resemblance= spider web like
• Subarachnoid space is the interval between the arachnoid
membrane and piamater
• It is occupied by a spongy tissue consisting of trabeculae and
intercommunicating channels in which the CSF is contained
• The subarachnoid space extends from the basal cisterns
surrounding the brain stem superiorly to S2 level inferiorly
• Subarachnoid space is the is the location of the interface between
the vascular tissue and CSF

3. 3

4. • The annual incidence of aSAH varies across the world, ranging from 2 to 16 cases
per 100,000 in Finland and Japan and a low incidence in South and Central America
• Up to 15% of patients die before hospital admission, therefore, the true incidence of
aSAH might be even higher.
• The typical average age of adult patients with aSAH is ≥50 years.
• The incidence of aSAH is 1.2 times higher in women than in men.
• Prevalence of familial aneurysms, defined as ≥2 first-degree relatives affected,
ranges between 7% and 20%

5. • Subarachnoid hemorrhage includes the subset of ICH that lies in the space
between the thin arachnoid space and pia matter.
• Excluding head trauma, the most common cause of SAH is rupture of aneurysm
• Angiogram negative SAH(7-10%)
• Cerebral arteriovenous malformations(4-5%)
• Vasculitis
• Carotid or Vertebral artery dissection
• Cerebral venous sinus thrombosis
• Spinal AVM
• Cocaine Use
• SCD
• Tumour
• Cerebral amyloid angiopathy

6. • Hypertension
• Smoking/Alcohol/Cocaine
• Increasing Age
• ADPKD
• Fibromuscular Dysplasia
• Coarctation Of the Aorta
• Bacterial Endocarditis
• Connective tissue disease:Ehlers-Danlos type 4,Marfan's syndrome
• Osler weber Rendu syndrome

7. • Treatment of high blood pressure with antihypertensive medication is recommended to
prevent ICH,Ischemic stroke,Cardiac,Renal and other end organ injury( )
• Hypertension should be treated and such treatment may reduce the risk of aSAH( )
• Tobacco use and Alcohol misuse should be avoided to reduce the risk of aSAH( )
• Inaddition to the size and location of the aneurysm and the patient's age an health
status,it might be resonable to consider morphological and hemodynamic characteristics
of the aneurysm whendiscussing the risk of the aneurysm rupture( )
• Consumption of a diet rich in vegetables may lower the risk of aSAH( )
• After any aneurysm repair,immediate cerebrovascular imaging is generally
recommended to identify remants or recurrence of the aneurysm that may require
treatment( )

8. • An intracranial aneurysm is a cerebrovascular disorder in
which weakness in the wall of a brain artery causes
dilation or ballooning which can grow and rupture over
time.
• The term aneurysm originally comes from the Greek
aneurysma—ana meaning “across” and eurys meaning
“broad.”
• Rupture of an intracranial aneurysm causes aneurysmal
subarachnoid hemorrhage (aSAH), which accounts for 5%
to 10% of all strokes

9. BY MORPHOLOGY
• Saccular
• Fusiform
• Dissecting
BY PATHOGENESIS
• Genetic
• Hemodynamic (arteriovenous malformation, contralateral carotid
• ligation, etc.)
• Infection (bacterial, fungal)
• Trauma
• Atherosclerosis
• Neoplasm (primary or metastatic)
• Radiation
• Drug abuse
• Connective tissue disorders, Vasculopathy
• Miscellaneous conditions (moyamoya disease)

10. • <3 mm (very small)
• 3–6 mm (small)
• 7–12 mm (small–medium)
• 13–25 mm (large)
• >25 mm (giant)
Internal Carotid Artery:
• 1. Posterior communicating
• 2. Carotid cave
• 3. Paraclinoid
• 4. Ophthalmic
• 5. Superior hypophyseal
• 6. Anterior choroidal
• 7. Carotid bifurcation

11. :
• 1. A1
• 2. Anterior communicating
• 3. A1–2
• 4. A2 and distal
• 1. M1
• 2. Bifurcation
• 3. M2 and distal
• 1. PICA
• 1. Trunk
• 2. Fenestration
• 3. AICA
• 4. SCA
• 5. Basilar apex
• 1. P1

12. • The most common Intracranial aneurysms are saccular aneurysms, rounded,
berry-like outpouchings arising from first- and second-order branches in the
circle of Willis.
• They account for approximately 90% of intracranial aneurysms and are
responsible for most of the morbidity and mortality from aSAH
• Intracranial arteries are structurally unique since they lack external elastic
lamina, which disappears in the horizontal segment of the cavernous internal
carotid arteries.
• Significant reduction or disappearance of elastic fibers in the tunica media
and external elastic lamina also occurs in the vertebral arteries as they enter
the skull.

13. • These structural alterations weaken the arterial walls, making
them less resistant to constant hemodynamic forces such as
dynamic pressure, blood pressure, and shear stress.
• Although aneurysm formation involves multiple factors, the
most significant pathogenetic factor is considered to be the
degeneration of tunica media and internal elastic lamina at the
branching sites of intracranial arteries in regions of chronic
hemodynamic stress.
• In children, the abnormalities of tunica media and internal
elastic lamina may be congenital rather than degenerative as
in the adults

14.  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 14

15. • A fusiform aneurysm is defined as a circumferential dilatation in a
segment of an intracranial artery.
• Unlike a saccular aneurysm that has a single orifice (neck)
through which blood flow goes in and exits the aneurysm cavity
• A fusiform aneurysm does not have a defined orifice (neck).
• The inflow and outflow of fusiform aneurysms are longitudinally
separate, which often makes surgical or interventional treatment
of these aneurysms challenging.
• Fusiform aneurysms are generally associated with
atherosclerosis, which causes extensive damage to the tunica
media and results in arterial stretching to all sides or elongation.

16. • A dissecting aneurysm is formed as a result of splitting or
dissection of an arterial wall by blood entering through a tear.
• This may cause a ballooning out on one side of the artery, with
arterial narrowing an outpouching mimicking a saccular aneurysm
(pseudo aneurysm or false saccular aneurysm), or a fusiform
segmental dilatation
• It could obstruct blood flow through the dissecting segment of an
artery
• Intracranial dissecting aneurysms often present with hemorrhage

17. 17

18. • Subarachnoid hemorrhage (SAH) renders the brain
critically ill from both primary and secondary brain insults
• For patients of SAH who arrive alive at hospital, the
mortality rate over the next month is about 45%.
• Of those who survive, more than 50% are left with major
neurologic deficits as a result of the
1. Initial hemorrhage,
2. Cerebral vasospasm with infarction, or
3. Hydrocephalus.

19. • If the patient survives but the aneurysm is not obliterated, the
rate of rebleeding is about
1. 4-14% in first 24 hours
2. 20% in the first 2 weeks
3. 30% in the first month,
4. And about 3% per year afterwards
• The annual risk of rupture for aneurysms <10 mm in size is
0.1%, and for aneurysms >10 mm in size is 0.5–1%
• Their risk of rupture is ~6% in the first year after identification
and may remain high indefinitely

21. • GIANT ANEURYSMS, those >2.5 cm in diameter account for 5% of
cases.
• Aneurysms occur at the bifurcations of the large to medium-sized
intracranial arteries.
• Rupture is into the
1. subarachnoid space,
2. in the basal cisterns and often into
3. the parenchyma of the adjacent brain.
• Approximately 85% of aneurysms occur in the anterior circulation, mostly
on the circle of Willis.
• The three most common locations are
• -The terminal internal carotid artery,
• -Middle cerebral artery (MCA) bifurcation, and
• -Top of the basilar artery.

24. • Most aneurysms remain asymptomatic until the time of rupture.
• The typical symptom patients report with aneurysmal rupture is
sudden onset of severe (thunderclap) headache described as “the
worst headache of my life” in 80% of cases.
• This may be associated with other symptoms, such as nausea
and/or vomiting, stiff neck, photophobia, brief loss of
consciousness, or focal neurological deficits (including cranial
nerve palsies).
• Aneurysms do rupture during physical exertion or stress.
• However, the highest incidence of rupture occurs during regular
daily activity

25. • With rupture of the aneurysm, blood under high pressure is forced into the
subarachnoid space and the resulting clinical events assume one of three
patterns:
1) the patient is stricken with an excruciating
generalized headache and vomiting and falls unconscious
almost immediately;
2) severe generalized headache develops in the same
instantaneous manner but the patient remains relatively lucid
with varying degrees of stiff neck-the most common
syndrome
3) rarely, consciousness is lost so quickly that there is no
preceding complaint
• If hemorrhage is massive, death may ensue in a matter of minutes or hours,
so that ruptured aneurysm must be considered in the differential diagnosis of
sudden death

26. • In10-40 % of patients,this headache is preccedby a warning leak
or “sentinel” headache,which typically occours within 2-8 weeks
before overt SAH
• The degree of encephalopathy at presentation is the major
determinant(from mild lethargy to profound coma) of prognosis.
• Seizure activity may be present,but it is unclear that whether it
represents true epileptic seizures or reflex posturing due to
sudden rise in ICP
• Stiff neck indicates sterile meningial inflammation induced by the
presence of blood in the subarachnoid space.

28. • Cerebral Venous Thrombosis
• BIH
• ICH
• Arterial Dissection
• Posterior Reversible Leukoencephalopathy Syndrome
• Pitutary Apoplexy
• ICSOL
• Migraine Headache

30. Mild headache, normal mental status, no cranial nerve or
motor findings
Severe headache, normal mental status, may have
cranial nerve deficit
Somnolent, confused, may have cranial nerve or mild
motor deficit
Stupor, moderate to severe motor deficit, may have
intermittent reflex posturing
Coma, reflex posturing or flaccid

31. GCS score 15, no motor deficits
GCS score 13–14, no motor deficits
GCS score 13–14, with motor deficits
GCS score 7–12, with or without motor deficits
GCS score 3–6, with or without motor deficits

33. : No blood detected
: Diffuse deposition or thin layer of blood,
• with all vertical layers of blood
• (interhemispheric fissure, insular cistern,
• ambient cistern) <1 mm thick
: Localized clots or vertical layers of blood 1
• mm or greater in thickness
: Diffuse or no subarachnoid hemorrhage but
• with intraparenchymal or intraventricular
• clots

35. • The initial clinical severity of aSAH be determined rapidly
by use of simple validated scales(eg,HUNT and
HESS,WFNS)because it is most useful indicator of
outcomes after aSAH( )
• The risk of early aneurysm rebleeding is high,and
rebleeding is asscociated with very poor
outcomes.Therefore,urgent evaluation and treatment of
patients with suspected aSAH is recommended(
• After discharge it is resonble to refer patients with aSAH for
a comprehensive evaluation,including cognitive,behavioral
and psychosocial assessments( )

37. • Brain computed tomography (CT) remains the cornerstone
for diagnosis of SAH.Clot is demonstrated in 92% of cases if
performed within 24 hours.
• CT scan also provides other information such as the
presence of early hydrocephalus
• The distribution and pattern of hemorrhage on CT scan are
important in predicting the location of the rupture site, and it
is used to classify the appearance of SAH, predicting the
probability vasospasm / delayed cerebral ischemia .
• CT scan confirms SAH with very high sensitivity, close to
100%, in first 6-12 hours,decreasing to 58% on day 5
• The CT scan must be performed withh thin cuts through the
base of brain to increase the sensitivity .

38. Hydrocephalus IVH and ICH

41. • The sensitivity of lumbar puncture within 12 hours of hemorrhage is high when cases of
traumatic lumbar puncture are eliminated.
• The characteristics of cerebrospinal fluid (CSF) for patients with SAH include increased
red blood cell count (that doesn't diminish from tube 1 to tube 4)and xanthochromia.
• Approximately 2 hours after the hemorrhage, xanthochromia becomes detectable and
may last as long as several weeks.(100% till 2weeks and >70% till 3weeks)
• In a patient where there is clinical suspicion for SAH but CT scan is negative,lumbar
puncture is mandatory.
• Other conditions that can produce xanthochromia include increased CSF
concentrations of protein(150mg/dl),systemic hyperbilirubinemia(10-15mg/dl) and
traumatic lumber puncture with more than 1lakh redblood cells/microL

43. • Multimodal magnetic resonance imaging (MRI), including fluid-
attenuated inversion recovery (FLAIR), proton density, and
gradient echo (GRE) sequences, is becoming an important
diagnostic tool for detecting acute and chronic SAH.
• Recent data suggest that the FLAIR/T2 sequence have high
sensitivity in patients with subacute presentation(>4days from
bleed).
• GRE sequence overestimates the true volume of the hemorrhage
because of the blooming artifact, it is very useful in detecting
subacute or chronic SAH

45. • CT and MR anigiography are noninvasive tests that are
useful for screening,diagnosing and locating the aneurysm.
• Both CTA and MRA can identify aneurysm 3-5 mm or larger
with a high degree of sensitivity(92.7% and 95%) but they
donot achieve the resolution of conventional agiography
• A major advantage of CTA over conventional angiography is
the speed and eae by which it can be obtained and non-
invasive in nature.

47. • The gold standard for diagnosing and locating aSAH
• Once SAH has been diagnosed,cerebral angiogrphy should be
performed as soon as possible to identify the the responsible vascular
lesion.
• Multiple aneurysms are found in 20-30 % cases of patients with
aneurysmal SAH
• No angiographic cause of SAH was found in 14-22% cases
• Repeat angiography in one week time is recommended.
• Upto 24% of all SAH patients with initial negative angiogaphy(both
conventional and CTA)have an aneurysm found on repeat DSA
• Reasons for initial negative DSA include,obscuration of aneurysm due
to vasospasam,hematoma or thrombosis within aneurysm,or
inadequate views to detect subtle aneurysm in ACOM or Posterior

50. • aSAH is a medical emergency that is frequently misdiagnosed.Ahigh level of
suspicion for aSAH should exist in all patients with acute onset of severe
headache(
• Acute diagnostic workup should iclude noncontrast head CT,which if
nondiagnostic,should be followed by lumber puncture
• CTA may be Considered in the workup of aSAH,if an aneurysm is detected by
CTA,this study may help guide the decision for type of aeurysm repair,but if CTA
is inconclusive,DSA is still recommended(except possibly in the instance of
classic perimesencephalic aSAH) ( )
• Mgnetic resonance imaging(FLAIR,DWI,PROTON DENSITY AND GRE) may be
resonable for the diagnosis of aSAH in patients with a nondiagnostic CT
scan,although a negative result does not obviate the need for a CSF
analysis( )

51. • DSA with 3-dimensional angiography is indicated for
detection of aneurysm in patients with aSAH(except when
the aneurysm was previously diagnosed by a non-
invasive angiogram) and for planning treatment(to
determine whether an aneurysm is amenable to coiling or
to expedite microsurgery) ( )

53. • A patient presenting with aneurysmal SAH should be admitted to an ICU for
constant hemodynamic and neurologic monitoring.
A GCS<8 ,elevated ICP,poor
oxygenation,hypoventilation,hemodynamic instability and requirment of heavy
sedation.
-Under continuous monitoring
in ICU.Staff in this unit should have ample experience in assessing swallowing
function to prevent pneumonia,a frequent complication after SAH and
independent risk factor for poor outcome.ECG,GCS,focal
deficitis,temperature,cardiac rate and rhythm,BP should be monitored.ABP
monitoring is preffered in ICU setting.Headache can be managed with
paracetamol and opioid analgesics.Laxativies are used routinely,as straining to
defecate can potentially cause rebleeding.
-Hypoglycemia(<80MG/DL) should be avoided,to be
mantained below 200 mg/dl.Careful giucose management with strict avoidance
of hypoglycemia may be considered as part of the general critical care
management of patients with aSAH(2b,B)

54. -Temperature should be monitored frequently,infectious causes of fever
should always be sought and treated.In around 20% of patients no infection is found and fever is
attributed to inflammatory responses to extravasated blood in the subarachnoid space.Independent
risk factor for poor outcome.Antipyretic agents(paracetamol,ibuprofen) should be used as first line of
therapy.Surface cooling should be used when antipyretics fail,use of this devices should be
accompanied by monitoring for skin injury and venous thrombsis.Aggresive control of fever to a target
of normothermia by use of standard or advanced temperature modulating systems is resonable in the
acute phase of aSAH(2a,B)
-Patients with SAH may be given thromboProphylaxis with pneumatic devices
and/or stockings before occlusion of the aneurysm.In case deep vein thrombosis prevention is
indicated unfractiontaed/LMW heparin should be applied not earlier than 24 hours after surgical
occlusion of aneurysm and immediately after coiling.
-Patients with SAH usually devlop increased ICP that is usually due to acute
hydrocephalus and reactive hypermia after hemorrhageICP greater than 20mmhg is an independent
predictor of severe disability and death inaSAH.The initial approach is to keep head of bed
elevated(30*-45*) to optimise cerebral venous drainage,normoventilation(PaCO2-35-40 mmhg),use of
sedation and

55. analgesia to achieve a calm and quiet state(Richmond agitation sedation scale
score of -5 or Sedation-Agitation Scale score of 1) and mainatin normothermia.
is a mainstay ICP management in SAH patients.EVD should be
placed in appropriate patients(Obstructive hydrocephalus or WFNS>/= 3),it
allows not only CSF drainage but also ICP monitoring.Almost 30% patients with
poor-grade SAH(WFNS SCORE 4 AND 5) improve neurologically after EVD
insertion and CSF drainage.
is another possible stratregy for refractory ICP
managemnt in SAH patients.It has been associated with decreased
mortality,significant reduction of ICP,improved cerebral oxygenation and improved
cerebral metabolisim.However most patients undergoing decompressive
craniectomy due to refractory ICP have poor outcome due to severe
disability.Therefore the best time to obatin benefit is to perform it early(within 48
hours of bleeding) and in the absence of radiological signs of infarction.Finally in
poor-grade patients with large interparenchymal or Sylvian fissure hematomas
usually from MCA aneyrysms,prophylactic decompressive craniectomy should be
considered.

56. can
be considered in to control ICP.No study present on use of mannitol
in management of raised ICP in SAH patients and only one
small(16patients) placebo-controlled trial on use of hypertonic saline
avialable(may improve outcome).
as a temporary
measure.Avoid if no brain oxygen and cerebral metabolisim
monitoring is present.It may also precipitate or exacerbate
vasospasam
has been shown to
be effective to control ICP but has not been associated with
improved functional outcome and reduced mortality rates in poor-
grade SAH patients

57. • Administration of large volumes of hypotonic fluids and intravascular volume
contraction is not recommended after aSAH.(3,B)
• Monitoring volume status in certain patients with recent aSAH by some
combination of CVP,pulmonary wedge pressure,and fluid balance is resonable,as
it is treatment of volume contraction with crystalloid or colloid fluids(2a,B)
• Intravascular volume management should target euvolemia and avoid
prophylactic hypervolemic therapy.
• Hyponatremia is the most common electrolyte imbalance in patients with
aSAH,occuring in 30-50% of patients.Associated with the onset of sonographic
and clinical vasospasam.
• CSW is one of the major causes,more common in patients with poor-grade
aSAH,ruptured ACOM aneurysms and hydrocephalus.
• The use of fludricortisone acetate and hypertonic saline is resonable for
preventing and correcting hyponatremia(2a,B)
• SIADH may also be the cause of hyponatremia,excessive ADH secretion causing
dilutional hyponatremia

58. • It is important to distinguish between SIADH nad CSW.
• Electrolyte free water restriction forms the main stay of
SIADH treatment but this may increase the risk of cerebral
hypoperfusion(DCI)
• It is advised to maintain euvolemia and avoid fluid restriction
• Extreme caution to avoid hypovolemia is needed if
vasopressin-receptor antagonists are used for treatment of
hyponatremia

59. • Between the time of aSAH symptom onset and aneurysm obliteration,blood
pressure should be controlled with a tritrable agent to balance the risk of
stroke,hypertension related bleeding and maintenance of CPP.(1,B)
• The magnitude of blood pressure control to reduce the risk of rebleeding has not
been established,but a decrease in systolic blood pressure to <160 mm hg is
resonable(2a,C),MAP <110 mmhg in some guidelines.
• When blood pressure control is necessary,the use of vasodilators such as
nitroprusside or NTG should be avoided because of their propensity to increase
CBF and therefore ICP.Labetalol,nicardipine,enalpril are preferred.
• For patients with an unavoidable delay in obliteration of aneurysm,a significant risk
of rebleeding,and no compelling medical contraindications,short term(,72 hours)
therapy with tranexamic acid or aminocaproic acid is resonable to reduce the risk
of early aneurysm rebleeding(2a,B)

60. • Clinical experience and RCTs have shown that treatment for ruptured aneurysms
is safe and eliminates the immediate risk of aneurym rerupture.Treatment can be
achieved by means of open surgical clipping or edovascular aneurysm
obliteration;both treatments should be provided by specialized experienced
practitioners at high volume centres.
• Surgical clipping or endovascular coiling of the ruptured aneurysm should be
performed as early as possible in the majority of patients to reduce the rate of
rebleeding after aSAH.(1,B)
• Determination of aneurysm treatment,as judged by both experienced
cerebrovascular surgeons and endovascular specialists,should be multidisciplinary
decision based on characteristics of the patient and aneurysm(1,C)
• For patients with ruptured aneurysms judged to be technially amenable to both
endovascular coiling and neurosurgical clipping,endovascular coiling should be
considered(1,B)
• In the absence of a compellig contraindication,patients who undergo coiling or
clipping of a ruptured aneurysm should have delayed follow-up vascular imaging

61. • (timing and modality to be indivisualized) and strong
conideration should be given to retreatment,either by repeat
coiling or microsurgical clipping,if there is a clinically
significant(eg,gowing) remnant(1,B)
• Microsurgical clipping may receive increase consideration in
patients presenting with large(>50 ml),interparenchymal
hematomas and MCA aneurysms.Endovascular coiling may
receive increased consideration itn the elderly(>70 yrs), in
those presenting with poor-grade(WFNS 4/5)aSAH and in
those with aneurysms of basilar apex.(2b,C)
• Stenting of a ruptured aneurysm is associated with increased
morbidity and mortality,and should only be consisdered when
less risky options have been excluded.(3,C)

62. • In general,the decision on whether to clip or not depends on several factors related
to 3 major components:
• 1)Patient-age,comorbidity,presence of ICH,SAH,grade,aneurysm
size,location and configuration,as well as on status of collaterals.(3,B)
• 2)Procedure:competence,technical skills and variability(3,B)
• 3)Logistics:the grade of interdisciplinarity(3,B)
• Factors in favour of clipping are younger age,presence of space occupying ICH(3,B)
and aneurysm specific factors such as:
• -Location;MCA and pericallosal aneurysm(3,B)
• -Wide aneurysm neck(3,B)
• -Arterial branches exiting directly out of the aneurysmal sack
• -Other unfavourable vascular an aneurysmal configuration for coiling (4,C)

63. • Factors in favour of endovascular intervention(coiling) are:
• age above 70 years(2,B),SPACE OCCUPYING ICH
• not present(2,B) and aneurysm specific factors as:
• -Posterior location
• -Small aneurysm neck
• -Unilobar shape(3,B)
• Elderly patients should not per se be excluded from
treatment;decisions whether or not to treat depend on the
clinical and physical condition of the patients.

64. • Requires opening the skull(craniotomy).with the use of the
operating microscope,the subarachnoid spaces around the
cerebral arteries are opened at the base of the skull to mobilize
delicate brain tissue without injury.Once the aneurysm is exposed,a
titanium clip is placed across the neck of the aneurysm to
mechanically close the sac at its neck while preserving blood flow
through the adjacent normal arteries
• Risks associated with clipping include new or worsened neurologic
deficits caused by brain retraction,temporary arterial occlusion,and
intraoperative haemorrhage.Intraprocedural aneurysmal rupture
occured in 19%(5% with endovascular,coiling was done in 299
patients) of 711 patients treated with surgical clipping in the
CAART STUDY.The risk of intraprocedural rupture associated
death/disabilty was doubled in endovascular group(63% coiling vs

65. 65

66. 66

68.  But the incidence of late rebleeding,2.9% after endovascular repair
vs 0.9% after open surgery.
Also only 58% of coiled aneurysms are completely obliterated
compared to 81% of clipped aneurysms
• Although the complete obliteration rate can be increased by the
addition of a high porosity stent,this has been with an increased
risk of complications in SAH patients because of the need of
periprocedural dual antiplatlet therapy to prevent arterial
thromboembolisim.
• Thus,although the short term efficacy of endovascular coil
obliteration is well established compared with microsurgical
approaches,close long term surveillance ontinues to be warrented
becuse durability remains a significant concern.

69. 69

72. • Hydrocephalus may devlop soon after subarachnoid hemorrhage,owing to
presence of extravasated blood blocking normal cerebrospinal fluid
circulation through the subarachnoid cisterns that surround the major arteries
at the base of the brain.Estimates of the incidence of hydrocephalus range
from 15-85%,most of them being clinically not significant.
• In cases in which hydrocephalus causes encephalopathy,management of the
hydrocephalus typically involves placement of an EVD.
• Alternatively,lumbar drainage can be used to treat acute hydrocephalus and
is associatedwith reduced risk of vasospasam;however,obstructive
hydrocephalus and intraparenchymal hematoma which cause increased
ICP,are contraindications to lumbar drainage.
• Chronic smptomatic hydrocephalus occurs in upto one third of patients in
whom acute hydrocephalus devlopes and is treted with a VP shunt for
permanent diversion of CSF.

73. • aSAH associated acute symptomatic hydrocephalus should be
managed by cerbrospinal fluid diversion(EVD) or lumbar
drainage,depending on the clinical scenario( ).
• aSAH associated chronic symptomatic hydrocephalus should be
treated with permanent CSF diversion( )
• Weaning EVD over > 24 hours does not appear to be effective in
reducing the need for ventricular shunting( )
• Routine fenestration of the lamina terminalis is not useful for reducing
the rate of shunt-dependent hydrocephalus and therefore should not
be routinely performed( )
• Hydrocephalus may devlop days to weeks after subarachnoid
hemorrhage and should be suspected in patients who have a good
initial recovery followed by a plateau or decline in their

74. • An important distinction must be mde between angiographic vasospasm,which is
seen in 30-70% of angiograms performed at day 7 after aSAH,and clinical or
symptomatic(DCI) vasospasam which is seen in 20-30% of patients.
• DCI is a term applied to any neurological deterioration,including focal and
neurological deficits and altered consciousness,which persists for more than one
hour and cannot be explained by other abnormalities identified by
radiographic,electrophysiological and laboratory investigations.
• It occurs in around 30% patients,peaks between 4-14 days after the ictus and
persists for several days.It is 2nd only to the initial haemorrhage as a cause of
morbidity and mortality after SAH.
• Despite a general belief that vasospasm causes DCI,recent evidence suggest that
a variety of vascular and neural changes(vascular dysregulation,microthrombi,
direct neurotoxic effects and cortical spreading depolarization) that take place after
SAH are the other contributing factors.DCI devlopes in fewer than one half of
patients with angiographic vasospasam, and ischemia does not occur consistently
in the territory supplied by the vessel undergoing spasam

76. Changes commonly used to trigger intervention
-An increase in either (a) TCD mean flow velocity in the MCA(FVMCA) of more thn
50cm/sec over 24 hours or (b) mean FVMCA of at least 200cm/sec or MCA/ICA ratio of more
than 6 or both.TCD is resonable to monitor for devlopment of arterial vasospasam( )
-CBF of less than 25ml/100g/min or mean transient times of more than 6.5
seconds or both.Perfusion imaging with CT or magnetic resonance can be useful to identify
region of potential brain ischemia(
-Severe angiographic vasospasam (defined as a narrowing of at
least 70% from baseline) detected by DSA(gold standard) or CT angiography
-Reduced alpha varibability
-Abnormal levels of brain tissue oxygen(PtiO2 of less than 20mmhg) or
CMD (i.e,lactate/pyruvate ratio of more than 40 and glucose of less than 0.5mM and in second
line for glutamate of more than 40mM)

77. -Oral nimodipine should be administered to all patients
with aSAH( ).It should be noted that this agent has been shown to
improve neurological outcomes but not cerebral vasospasam.The
value of other calcium antagonists,whether administered orally or
IV,remains uncertain.The dose is 60mg 4th hourly via orally/NG
tube,continued for 21days.
-Maintenance of euvolemia and
normal circulating blood volume is recomended to prevent
DCI( ).Isotonic crystalloids are the fluids of choice,although
hypertonic saline solutions have a place in patients who are
hyponatremic.
• Induction of hypertension is recommended for patients with DCI
unless blood pressure is elevated at baseline ot cardiac status
precludes it.( ).

78. • Blood pressure is augmented in a step wise fashion by the use of a
vasopressor,typically noradrenalline(in the presence of adequate volume
status).The neurological exmination and clinical assesment done in each
step(180mmhg,190mmhg,200mmhg),and target should be based on clinical
improvement.
• Prophylactic hypervolemia or ballon angioplasty before the devlopment of
angiographic spasam is not recommended( )
• ENDOVASCULAR THERAPIES-Cerebral angioplasty and/or selective intra-
arterial vasodilator therapy is resonable in patient with symptomatic cerebral
vasospasam,particularly those who are not responding to hypertensive
therapy( )
• Intraarterial agents reported as effective for improving vasospasam include-
NICARDIPINE,MILRINONE,VERAPAMIL,NIMODIPINE and intrathecal

79. -Continue statins in patients with chronic therapy.NO
clinical benefit to add statin for vasospasam/DCI in aSAH(STASH
TRIAL)
-CONSCIOUS-1 and
CONSCIOUS-2 found that no improvment in clinical outcome in
CLAZOSENTAN group.
-Reverses cerebral arterial spasam in animal
models,but two completed phase-3 trials IMASH,MASH-2 did not
support any clinical benefit from magnesium infusionover placebo in
aSAH.Although hypomagnesemia shoild be avoided but induced
hypermagnesemia is not recommended.

80. -Seizures occur in approximately 20% patients after aSAH but
treatment remains controversial.
• The use of prophylactic anticonvulsants may be considered in the immediate
posthemorrhagic period( )
• The routine long-term use of anticonvulsants is not recommended( but may
be considered for patients with known risk factors for delayed seizure
disorder,such as prior seizure,intracerebral hematoma,intracable
hypertension,infarction,or aneuryam at the MCA( )
-Is very common as is associated with very poor outcome.
• The use of packed red blood cell transfusion to treat anemia might be resonable
in patients with aSAH who are at riskof cerebral ischemia.The optimal
hemoglobin level is still to br determined( .Current critical care practice is to
maintain hemoglobin concentration above 8-10g/dl.

81. • Cardiac complications following SAH can range from benign ECG
changes to overt cardiogenic shock requiring IABP.Most common in
1st 48 hours.
• In rare cases, STUNNED MYOCARDIUM may occur,due to
excessive noradrenaline release release from myocardial
sympathetic nerve terminals resulting in a physiological myocardial
denervation in the presence of normal coronary perfusion.
• This results in a characteristic pattern of LV regional wall motion
abnormalities involving the basal and middle portions of anteroseptal
and anterior ventricular walls with relative apical sparing.
• The treament is maainly supportive and most of the cases will
recover spontaneously within 2 weeks

82. • However aggressive ICU management may be required in the setting of severly
impaired LV dysfunction
• Thus the use of ionotropic agents such as DOBUTAMINE,LEVOSIMENDAN,
MILRINONE and even IABP counterpulsation can be considered to optimise the
cardiac function in order to improve CBF.
• Pulmonary complication,such as HAP,cardiogenic and /or neurogenic pulmonary
odema,aspiration pneumonia and PE our in approximately 30% of patients after
aSAH.
• ARDS can affect 27% of cases and is inependently associated with worse
outcomes.In this clinical scenario,extra caution should be taken to avoid fluid
overload,however diuretucs might be dangerous because of the risk of
hypovolemia induced cerebral ischemia.

83. Cardiac Complications
• Hypertension requiring IV
medication (27%)
• Hypotension requiring
pressors (18%)
• Life-threatening arrhythmia
(8%)
• Myocardial ischemia (6%)
• Successful resuscitation from
cardiac arrest (4%)
• Troponin I elevation (20%-
68%)
– Regional wall motion
abnormalities (26%)
ECG Changes
• ST segment alterations (15%–
67%)
• T-wave changes (12%–92%)
• Prominent U waves (4%–52%)
• QT prolongation (11%–66%)
• Conduction abnormalities
(7.5%)
• Sinus bradycardia (16%)
• Sinus tachycardia (8.5%)

84. Perimesencephalic bleed
• 10% of all SAH
• Venous hemorrhage
• Younger
• Non-hypertensive
• Better grade
• More in males
• Prognosis good
• Re-bleeding is rare
• Delayed ischemic deficit
very few

85. • SAH is a comon cause of stroke with high incidence
ofmorbidity and mortality
• Complex neuro vascular disease associated with multiple
neurological and systemic complications.
• Requires multidisciplinary specialized care best provided in
high volume centres.
• Patients who survive the inital bleed can deteriorate within
2weeks,especially because of DCI
• The major focus of treatment is to prevent rebeeding by
early seuring the aneurysm and prevention of secondary
braininjury by identification and treatment of complications

87. 87

88. 1