1. SUBARRACHNOID
HAEMORRHAGE-AN UPDATE
DR. ARDAMAN SINGH
Professor
Dept. Of Medicine
1
Govt. Medical College Patiala

2. SUBARRACHNOID HAEMORRHAGE
• SAH is a neurological
emergency
• Hemorrhage in the
subarachnoid space
• Less common but an
important cause of stroke
2

3. CLASSIFICATION OF STROKE
Stroke
Primary Ischemic
(80% of Strokes)
Thrombotic
Embolic
50%
Primary Hemorrhagic
(20% of Strokes)
Intracerebral
Hemorrhage 15%
Subarachnoid
Hemorrhage 5%
30%
3

4. SAH- etiology
• Excluding head trauma, the most common cause of
SAH is rupture of a SACCULAR ANEURYSM.
• Other causes include bleeding from a vascular
malformation (arteriovenous malformation or dural
arterial-venous fistula) and
• Extension into the subarachnoid space from a primary
intracerebral hemorrhage.
• Mycotic aneurysms -Most result from infected emboli
due to bacterial endocarditis causing septic
degeneration of arteries and subsequent dilatation and
rupture
4

5. SACCULAR ("BERRY") ANEURYSM
• Autopsy and angiography studies have found that
about 2% of adults harbor intracranial aneurysms,
• Size- 2 mm. to 2-3 cm
• Average size- 7.5mm
• Those which rupture are usually 10mm or more but
smaller ones can also get ruptured
• Of different shapes and forms round connected to patrent artery by a narrow stalk
some others may be broad based without a stalk –
some may have cylindrical form
5

6. 6

7. Cerebral Aneurysms
7

8. Mechanism of formation of aneurysms
• One theory is – that they result from a developmental
defect in the media & elastica
• Other theory says that aneurysmal proscess is initiated
by the focal destruction of internal elastic membrane
caused by hemodynamic forces acting at bifurcations &
branching of arteries
As a result of local weakness in vessel wall intima
bulges out covered only by adventetia
• The sac gradually enlarges and subsequently rupture
8

9. • 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
Initial hemorrhage,
Cerebral vasospasm with infarction, or
Hydrocephalus.
9

10. SACCULAR ("BERRY") ANEURYSM- CONT
• If the patient survives but the aneurysm is not
obliterated, the rate of rebleeding is about
• 20% in the first 2 weeks,
• 30% in the first month, 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%;
• the surgical morbidity rate far exceeds these
percentages
10

11. SACCULAR ("BERRY") ANEURYSM- CONT
• GIANT ANEURYSMS, those >2.5 cm in diameter
account for 5% of cases.
The three most common locations are
-The terminal internal carotid artery,
-Middle cerebral artery (MCA) bifurcation, and
-Top of the basilar artery.
• Their risk of rupture is ~6% in the first year after
identification and may remain high indefinitely.
• They often cause symptoms by compressing the adjacent
brain or cranial nerves.
11

12. 12

13. PATHOPHYSIOLOGY
• Saccular aneurysms occur at the bifurcations of the large to
medium-sized intracranial arteries.
Rupture is into the
 subarachnoid space,
 in the basal cisterns and often into
 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

14. 14

15. PATHOPHYSIOLOGY- cont
• Aneurysms are seldom seen in childern on autopsy
and so SAH in childern is rare
• Beyond childhood they gradually increase in size & the
frequency of rupture increases between 35-65 yrs of age
• There is increased incidence of
 polycystic kidneys,
 fibromuscular dysplasia of extracranial arteries,
 moyamoya, AV malformations &
 coarctation of aorta
• Numerous studies have documented familial occurrence of
saccular aneurysms, lending support to the idea that
genetic factors may play a role in their development
15

16. PATHOPHYSIOLOGY- cont
• As an aneurysm develops, it typically forms a
neck with a dome.
• . At the site of rupture (most often the dome) the
wall thins, and the tear that allows bleeding is
often 0.5 mm long.
• Aneurysm size and site are important in
predicting risk of rupture.
 Those >7 mm in diameter and
 Those at the top of the basilar artery and
 At the origin of the posterior communicating
artery are at greater risk of rupture.
16

17. 17

18. CLINICAL MANIFESTATIONS-
18

19. CLINICAL MANIFESTATIONS• Most unruptured intracranial aneurysms are
completely asymptomatic.
• Aneurysms can undergo small ruptures and leaks of
blood into the subarachnoid space, so-called
SENTINEL BLEEDS.
• SYMPTOMS are usually due to rupture and resultant
SAH perse
• Although some present with mass effect on cranial
nerves or brain parenchyma.
19

20. CLINICAL MANIFESTATIONS-cont.
• With rupture , blood at high pressure gushes in the suarachnoid
space resulting in following three 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 stifness
 Rarely pt suddenly becomes unconsoius without any preceding
complaint.
If the bleed is massive pt may die in minute to hrs.
So ruptured aneurysm should be considered in the differential
diagnosis of sudden death
In these rapidly evolving cases the bleed is so massive that I/c
pressure approaches systemic BP, thus severly compromising the
20
cerebral perfusion

21. CLINICAL MANIFESTATIONS-cont.
• In less severe cases , consciousness if lost may
be regained in minutes to hrs
• Residual drowsiness, confusion and amnesia
accompanied by severe headache may persist
for several days
21

22. CLINICAL MANIFESTATIONS-cont.
• Aneurysmal rupture usually occurs while the
pt is active
• In some cases it may occur while straing on
stool, sexual intercourse, lifting a heavy weight
or some other sustained exertion
• In patients who survive initial rupture the most
feared complication is rerupture which may
occur at any time from minutes to 2-3 wks
22

23. HEADACHE
• In ~45% of cases, severe headache associated
with exertion is the presenting complaint.
• The patient often calls the headache "the
worst headache of my life";
• However, the most important characteristic
is sudden onset.
• Sudden unexplained headache at any location
should raise suspicion of SAH and must be
investigated,
23

24. The headache usually generalized,
often with neck stiffness, and vomiting
is common
24

25. Pain at other sites
• Occipital and posterior cervical pain may
signal a posterior inferior cerebellar artery
(PICA) or anterior inferior cerebellar artery
aneurysm.
• Pain in or behind the eye and in the low
temple can occur with an expanding MCA
aneurysm
25

26. Loss of consciousness
• At the moment of aneurysmal rupture with
major SAH, the ICP suddenly rises.
• This may account for the sudden transient
loss of consciousness that occurs in nearly
half of patients which may be preceded by
headache.
• In 10% of cases, aneurysmal bleeding is
severe enough to cause loss of consciousness
for several days.
26

27. CLINICAL MANIFESTATIONS- cont.
FOCAL NEUROLOGICAL DEFICITS
• Although sudden headache in the absence of focal
neurologic symptoms is the hallmark of aneurysmal
rupture, FOCAL NEUROLOGIC DEFICITS MAY OCCUR.
• Anterior communicating artery or MCA bifurcation
aneurysms may rupture into the adjacent brain or
subdural space and form a hematoma large enough
to produce mass effect.
The common deficits that result include
hemiparesis, aphasia, and abulia (progressive
drowsiness or slow mentation)
27

28. Anatomic – clinical corellation of focal
neurological Deficits
• Third nerve palsy (ptosis, diplopia,dilatation of
pupil & divergent squint) indicates an aneurysm
at the junction of post. Comunicating &post.
Cerebral arteries
• A sixth nerve palsy may indicate an aneurysm in
the cavernous sinus .but uni or bilateral palsy
could be because of raised ICP
• Unilateral blindness indicates aneurysm lying
anteromedially in the circle of willis usually at the
origin of opthalmic artery
28

29. Anatomic – clinical corellation of focal
neurological Deficits- cont
• Transient paresis of one or both lower limbs
indicates 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
29

30. The side of aneurysmal rupture may be
indicated by
• monocular pain
• unilateral preponderace of headache or
• unilateral preretinal(subhyaloid)
hemorrhage (Terson Syndrome)
30

31. D/D- SAH to be differentiated from
• THUNDERCLAP HEADACHE is a variant of
migraine that simulates a SAH.
• Headache of explosive onset may also be
caused be ingestion of sympathomimetic
drugs or ingestion of tyramine containg
foods in a pt. who is taking MAO inhibitors
• Sudden severe hadahe may also be a
symptom of phaeochromocytoma
31

32. D/D
• Other conditions which may present as severe
headache need to be differentiated, like: Cerebral venous thrombosis,
 Diffuse vasospasm (call-flemming syndrome),
 Pituatry apoplexy,
 Hypertensive encephalopathy,
 Intracranial or extracranial arterial dissection
• CSF examination assumes great importance in
differentiating these conditions from SAH
32

33. D/D
• Before concluding that a patient with
sudden, severe headache has thunderclap
migraine or any other type of severe
headache,
a definitive workup for aneurysm is always
required in the form of CT scan, Lumbar
puncture, and if the diagnosis still remains
doubtful, then cerebral angiography
33

34. DELAYED NEUROLOGIC DEFICITS
• There are four major causes of delayed
neurologic deficits:
1. RERUPTURE/REBLEED,
2.HYDROCEPHALUS
3.VASOSPASM
4.HYPONATREMIA.
34

35. 1.RERUPTURE/REBLEED.
• This is the 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.
• The cause of recurrence is not clearly understood but
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.
35

36. 2.HYDROCEPHALUS
• Acute hydrocephalus can cause stupor and
coma and can be mitigated by placement of
an external ventricular drain.
• More often, subacute hydrocephalus may
develop over a few days or weeks and causes
progressive drowsiness or slowed mentation
(abulia) with incontinence.. It may clear
spontaneously or require temporary
ventricular drainage.
36

37. Hydrocephalus-cont.
• Chronic hydrocephalus may develop
weeks to months after SAH and 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
37

38. 3.VASOSPASM
• Causes symptomatic ischemia and infarction in ~30%
of patients and is the 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.
• Vasospasm is believed to result from direct effects of
clotted blood and its breakdown products on the
arteries within the subarachnoid space.
38

39. VASOSPASM- cont.
• 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 hemiperisis or
aphasia
• Severe cerebral edema in patients with infarction
from vasospasm may increase the ICP enough to
reduce cerebral perfusion pressure.
39

40. 4.HYPONATREMIA
• Hyponatremia. Hyponatremia 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.
40

41. SYSTEMIC CHANGES ASSOCIATED WITH SAH
• 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
41

42. INVESTIGATIONS
42

43. NON CONTRAST CT SCAN.
• CT Scan is Initial investigative procedure
• The extent and location of subarachnoid blood on
noncontrast CT scan help
 locate the underlying aneurysm,
 identify the cause of any neurologic deficit, and
 predict delayed vasospasm.
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.
• CT scans less reliably predict vasospasm in the
vertebral, basilar, or posterior cerebral arteries.
43

44. More than 95% of cases have enough blood to be
visualized on a high-quality NONCONTRAST CT
SCAN obtained within 72 h.
44

45. IMAGING STUDIES-cont.
•
•
•
•
Exact site of offending aneurysm can be inferred
from the location of main clot in CT scan
Collection of blood in the anterior inter-hemispheric
fissure indicates rupture of an ant. Communicating
artery
Blood in sylvian fissure – middle cerebral artery
Blood in ant. Perimesencephalic cistern- post.
Communicating artery or distal basilar artery
aneurysm
MRI can also detect blood in the proton density
sequence
45

46. Lab investigations-cont
• If the scan fails to establish the diagnosis of SAH and no
mass lesion or obstructive hydrocephalus is found,
• Then a lumbar puncture should be performed to
establish the presence of subarachnoid blood.
• 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
within 6–12 h.
• This xanthochromic spinal fluid peaks in intensity at 48
h and lasts for 1–4 weeks, depending on the amount of
subarachnoid blood
46

47. Angiography
• Once the diagnosis of hemorrhage from a ruptured
saccular aneurysm is suspected, four-vessel
conventional x-ray angiography (both carotids and
both vertebrals) is generally performed
• to localize and define the anatomic details of the
offending aneurysm and
• to determine if other unruptured aneurysms exist).
• CT angiography is an alternative method for locating
the aneurysm and may be sufficient to plan definitive
therapy.
47

48. Angiography-cont.
• in 5-10% pts with aneurysmal bleed , there
may not be any evidence of aneurysmal
rupture on angiography.
It may be because
in some cases obliteration of lesion occurs
In some lesions were somewhat more benign
• Pts without evidence of an offending
aneurysm or an arteriovenous
malformationhave a better prognosis
48

49. Angiography-cont.
• Perimesencephalic hemorrhage also caries a
better prognosis
In this cisterns surrounding midbrain & upper
pons gets filled up with blood
Mild headache, no vasospasm
 Usually no aneurysm is found at the expected
site i.e. at the top of basillary artery
49

50. Lab Inv. – cont.
• Close monitoring (daily or twice daily) of
electrolytes is important because
hyponatremia can occur precipitously during
the first 2 weeks following SAH
• An asymptomatic troponin elevation is
common.
50

51. ECG Changes
• The electrocardiogram (ECG) frequently shows
ST-segment and T-wave changes similar to
those associated with cardiac ischemia.
• Prolonged QRS complex, increased QT
interval, and prominent "peaked" or deeply
inverted symmetric T waves are usually
secondary to the intracranial hemorrhage
( cerebral T waves).
• Serious ventricular dysrhythmias are unusual
51

52. 52

53. ECHO
• Echocardiography reveals a pattern of regional
wall motion abnormalities that follow the
distribution of sympathetic nerves rather than
the major coronary arteries
• The sympathetic nerves themselves appear to
be injured by direct toxicity from the excessive
catecholamine release.
53

54. TREATMENT
The medical management of SAH focuses on
•
•
•
•
•
•
•
Protecting the airway,
Managing blood pressure
Preventing rebleeding prior to treatment,
Managing vasospasm,
Treating hydrocephalus,
Treating hyponatremia, and
Preventing pulmonary embolus.
54

55. Treatment- cont
• Because rebleeding is common, all patients who are not
candidates for early aneurysm repair are put on bed rest in a
quiet room and are given stool softeners to prevent straining.
• If Headache or neck pain is severe, mild sedation and
analgesia are prescribed.
• Extreme sedation is avoided because it can obscure changes
in neurologic status.
• Adequate hydration is necessary to avoid a decrease in blood
volume predisposing to brain ischemia.
So adequate amount of fluid is administered so as to maintain
above normal circulating blood volume & central venous
pressure
55

56. Managing raised ICP
• Intracranial hypertension following aneurysmal
rupture occurs secondary to
subarachnoid blood,
parenchymal hematoma,
acute hydrocephalus, or
 loss of vascular autoregulation.
Perilesional edema if infarct occurs
56

57. Managing raised ICP- cont.
• Patients who are stuporous should undergo
emergent ventriculostomy to measure ICP and to
treat high ICP in order to prevent cerebral
ischemia.
• Medical therapies designed to combat raised ICP
e.g., mild hyperventilation, mannitol, and
sedation can also be used as needed.
(Mannitol dose-25-100gm q4h)
• High ICP refractory to treatment is a poor
prognostic sign
57

58. MANAGING BP
• Prior to definitive treatment of the ruptured
aneurysm, care is required to maintain adequate
cerebral perfusion pressure
while avoiding excessive elevation/fall of arterial
pressure.
• If the patient is alert, it is reasonable to lower the
blood pressure to <150 systolic using
nicardipine, labetolol, or esmolol.
• If the patient has a depressed level of
consciousness, then ICP(Intracranial pressure)
should be measured and the cerebral perfusion
pressure targeted to 60–70 mmHg.
58

59. Managing Seizure Activity
• Seizures are uncommon at the onset of
aneurysmal rupture.
• The quivering, jerking, and extensor posturing
that often accompany loss of consciousness with
SAH are probably related to
 the sharp rise in ICP or, perhaps,
 acute generalized vasospasm rather than seizure.
• Use of anti-seizure drugs is controvercial.
However, phenytoin is often given as prophylactic
therapy since a seizure may promote rebleeding.
59

60. MANAGING VASOSPASM
• Vasospasm remains the leading cause of
morbidity and mortality following aneurysmal
SAH.
• Treatment with the calcium channel
antagonist nimodipine (60 mg PO every 4 h)
improves outcome, perhaps by preventing
ischemic injury
• Nimodipine can cause significant hypotension
in some patients, which may worsen cerebral
ischemia in patients with vasospasm
60

61. Managing Hydrocephalus
• Acute hydrocephalus can cause stupor or
coma.
• It may clear spontaneously or require
temporary external ventricular drainage.
• When chronic hydrocephalus
develops, permanent ventricular shunting is
the treatment of choice.
61

62. Role of Steroids
• Glucocorticoids may help reduce the head and
neck ache caused by the irritative effect of the
subarachnoid blood.
• There is no good evidence that they reduce
cerebral edema, are neuroprotective, or
reduce vascular injury, and
• Their routine use therefore is not
recommended
62

63. 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" by a
neurosurgeon or "coiled" by an
endovascular surgeon.
63

64. Hunt - Hess scale
is helpful in assessing the patient before
deciding for intervntional management
64

65. HUNT-HESS SCALE
• GRADE1:
•
Mild headache, normal mental status, no cranial nerve
or motor findings –(GCS* score 15, no motor deficits)
• GRADE 2:
Severe headache, normal mental status, may have cranial
nerve deficit –(GCS score 13–14, no motor deficits)
• GRADE 3:
Somnolent, confused, may have cranial nerve or mild
motor DEFICIT- (GCS SCORE 13–14, WITH MOTOR DEFICITS)
• GRADE 4 :
Stupor, moderate to severe motor deficit, may have
intermittent reflex posturing- (GCS score 7–12, with or
without motor deficits)
• GRADE 5:
Coma, reflex posturing or flaccid (GCS score 3–6, with or
without motor deficits)
65

66. 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- the outcome is generally poor but some times by
putting a ventricular drain and improving the grade, pt are
66
sometimes taken for intervention

67. 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.
67

68. Endovascular techniques
involve placing platinum coils,
or other embolic material,
within the aneurysm via a
catheter that is passed from
the femoral artery.
68

69. . Endovascular techniques-CONT
• The aneurysm is packed tightly to enhance
thrombosis and over time is walled-off from the
circulation
• The benefit of endovascular therapy is durable.
• However, some aneurysms have a morphology
that is not amenable to endovascular treatment.
• Thus, surgery remains an important treatment
option
• But for aneurysms which are not approachable by
surgery, endovascular technique would become
the only choice
69

70. INTERNATIONAL SUBARACHNOID
ANEURYSM TRIAL (ISAT)
• The only prospective randomized trial of surgery
versus endovascular treatment for ruptured
aneurysm, the International Subarachnoid
Aneurysm Trial (ISAT), was terminated early when
24% of patients treated with endovascular
therapy were dead or dependent at 1 year
compared to 31% treated with surgery, a
significant 23% relative reduction.
• After 5 years, risk of death was lower in the
coiling group,
• Although the proportion of survivors who were
independent was the same in both groups
• Risk of rebleeding was low, but more common in
the coiling group
70

71. TO SUM-UP
• SAH is a neurolgical emergency
• It is less common but an important cause of stroke(5%)
• saccular/berry aneurysmal rupture is the commonest cause
of SAH
• Most common presenttion is an excruciating headache
which needs to be differentiated from other causes of
severe headache including thunderclap migrane
• CT scan is very helpful in making a dianosis and
differentiating it from other headaches of severe intensity
• If CT is negative but there s strong suspecion of SAH then
one should go for CSF examination
• If othe CT scan & CSF are inconclusive then cerebral
angiography is the last resort
• Complications include rerupture, hydrocephalus,
vasospasm and hyponatremia
71

72. • Management icludes – bed rest, maintaing a
clear airway, managing BP, giving adequate
amount of fluids, monitoring hyponatremia
preventing vasospasm and instituting
measures to lower ICP
• one third of patients are prone to develop
rebleed which can be effectively taken care
of by interventional modalities i.e. surgical
(clipping)/ endovascular technique (coiling)
• Randomzed trial (ISAT) has shown coiling to
superior to clipping
72

73. 73