This document provides information on subarachnoid haemorrhage (SAH), including relevant anatomy, etiology, pathophysiology, risk factors, clinical presentation, grading scales, diagnostic workup and findings, and management. The key points are: - SAH is bleeding into the subarachnoid space between the arachnoid and pia mater layers, where blood vessels and CSF circulate. - The most common cause is aneurysm rupture (80-85%), followed by non-aneurysmal haemorrhage (10%) and other less common causes. - Clinical presentation includes thunderclap headache, reduced consciousness, meningism, seizures. Grading

1. SUBARACHNOID
HAEMORRHAGE
DR JIGAR R PADALIA

2.  Bleeding into the subarachnoid space
(space between pia & arachnoid layers)
where blood vessels lie & CSF flows

3. RELEVANT ANATOMY
 Arachnoid comes from the Greek "arachne" meaning spiderweb
+ "eidos" meaning resemblance = spider-web-like.
 Subarachnoid space is the interval between the arachnoid
membrane and pia mater.
 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 brainstem superiorly to S2 level inferiorly.
 Subarachnoid space is the location of the interface between the
vascular tissue and CSF.

5. SAH Etiology –Non Traumatic
 Aneurysmal Rupture : 80-85%
 Non aneurysmal perimesencephalic
haemorrhage : 10%
 AVM/ Fistula
 Intracranial vessel dissection
 Venous Sinus thrombosis
 Vasculitis
 Coagulopathy
 Drug & Toxins (cocaine abuse, amphetamine,
MAO inhibitor, alcohol, CO, nicotine, quinine, snake
venom)
 Hypertensive crisis

6. PATHOPHYSIOLOGY
 Blood extravasates under pressure into the subarachnoid
space and quickly spreads through the CSF around the
brain & spinal cord
 Blood released under high pressure – direct damage to
local tissues
 Blood extravasation - ↑ ICP
 Meningeal irritation occurs

7. Aneurysm
 Focal out pouching from the arterial wall

8. Incidence and
prevalence of aSAH
 12-15% die before hospital admission
 Incidence increases with age
 Typical average age of onset in adults ≥ 50 years
 Higher incidence of aSAH in women

9. Risk Factors for and Prevention of
aSAH
 Behavioral risk factors - hypertension, smoking, alcohol, and
use of sympathomimetic drugs (cocaine)
 Female sex
 Presence of an un-ruptured cerebral aneurysm
 H/o previous aSAH
 Familial aneurysms and family h/o aSAH
 Genetic syndromes - ADPKD & type IV Ehlers-Danlos
 Aneurysm size >7 mm - risk factor for rupture
 There does not appear to be an increased risk of aSAH in
pregnancy, delivery, and puerperium

10. Risk Factors for and Prevention of aSAH -
recommendations
 Treatment of high blood pressure with antihypertensive
medication is recommended to prevent ischemic stroke,
intracerebral hemorrhage, and cardiac, renal, and other
end-organ injury (Class I; Level of Evidence A).
 Hypertension should be treated, and such treatment may
reduce the risk of aSAH (Class I; Level of Evidence B).
 Tobacco use and alcohol misuse should be avoided to
reduce the risk of aSAH (Class I; Level of Evidence B).
 After any aneurysm repair, immediate cerebrovascular
imaging is generally recommended to identify remnants or
recurrence of the aneurysm that may require treatment
(Class I; Level of Evidence B) (New recommendation)

11. Natural History and Outcome
of aSAH
 Mortality rates - 8% to 67%
 The severity of clinical presentation is the strongest
prognostic indicator in aSAH (Hunt & Hess scale OR WFNS
Scale)
 Rebleeding is another major predictor of poor outcome
 Other factors predictive of poor prognosis include
 Older age
 Preexisting severe medical illness
 Global cerebral edema on CT scan
 IVH & ICH
 Symptomatic vasospasm, delayed cerebral infarction
 Hyperglycemia, fever, anemia
 Systemic complications - pneumonia and sepsis

12. Natural History and Outcome of aSAH:
Recommendations
 The initial clinical severity of aSAH should be determined
rapidly by use of simple validated scales (eg, Hunt and
Hess, World Federation of Neurological Surgeons),
because it is the most useful indicator of outcome after
aSAH (Class I; Level of Evidence B).
 The risk of early aneurysm rebleeding is high, and
rebleeding is associated with very poor outcomes.
Therefore, urgent evaluation and treatment of patients
with suspected aSAH is recommended (Class I; Level of
Evidence B).

13. CLINICAL PRESENTATION
 Headache
 97% of patients
 Thunderclap headache
 Warning/Sentinel headache - in 10-43% of aSAH
 Minor leaks are not a feature of AVM
 Reduced consciousness
 Meningism
 Vomiting/nausea
 Neck stiffness
 Photophobia/visual changes
 Seizures – 20%

14.  Meningeal irritation
 >75% of cases of aSAH
 May take several (6-24 hrs) hours to develop
 Coma - Raised ICP, ICH, HCP, seizures or low CBF
 Focal neurologic abnormalities - (25%)
 Ocular hemorrhages (20-40%)
 Temperature elevation
 Secondary to chemical meningitis from subarachnoid blood
products
 Common after the 4th day following bleeding

15.  Hypertension - 50% of patients.
 BP often becomes labile as ICP increases
 Tachycardia often is present for several days after SAH
 The most common diagnostic error - failure to obtain NCCT
Head

16. What causes symptoms &
signs?
 Blood leaking from the aneurysm
 Headache
 Meningism
 Local pressure effects of the aneurysm
 Associated ICH

17. Local pressure effects of the aneurysm
 ACom
 Visual symptoms due to optic chiasma compression
 Positive babinski
 Bilateral lower limb paresis
 MCA
 Contralateral hand & face paresis
 Contralateral visual neglect
 Aphasia (dominant side)
 ICA/PCom
 CN III signs

18. Associated ICH
 The aneurysm usually lies within the subarachnoid
cisterns
 It can become adherent to adjacent brain due
to adhesions (e.g. from a previous leak)
 The bleed therefore can also extend into the
brain
 MCA = hemiparesis & aphasia (if dominant)
 Acom = mutism
 AVM is more likely to cause ICH as they usually lie
somewhat in brain parenchyma

19. Findings Likely location of aneurysm
Mental status change Any
Meningismus
• Seen in 60% of pts of aSAH
• Takes 3-12hrs to develop
Any
Third nerve palsy
• 90% of pts with 3rd nerve palsy due
to aneurysm(compared to other
causes of 3rd nerve palsy) have
anisocoria >2mm
Posterior communicating artery
Sixth nerve palsy
• Presents 3-14 days after aSAH
• A/W higher clot burden
• Gradually resolves
Any (due to ↑ICP)
Bilateral weakness in legs or abulia Anterior communicating artery
Nystagmus, ataxia or dizziness Posterior circulation
Hemiparesis with aphasia or neglect Middle cerebral artery
Subhyaloid haemorrhage (Terson
syndrome)
• Seen in 10% of aSAH
• A/W worse clinical grades on
presentation and poorer outcome
Any

20. SAH GRADING
Hunt and Hess Scale
 Grade 1 - Asymptomatic or mild headache
 Grade 2 - Moderate-to-severe headache, nuchal
rigidity, and cranial nerve palsy
 Grade 3 - Mild alteration in mental status
(confusion, lethargy), mild focal
neurological deficit
 Grade 4 - Stupor and/or hemi paresis
 Grade 5 - Comatose and/or decerebrate rigidity

21. SAH GRADING
WFNS scale
 Grade 0 – Intact aneurysm
 Grade 1 - GCS of 15, major focal deficit absent
 Grade 2 - GCS of 13-14, major focal deficit absent
 Grade 3 - GCS of 13-14, major focal deficit present
 Grade 4 - GCS of 7-12, major focal deficit absent/present
 Grade 5 - GCS of 3-6, major focal deficit absent/present
* Major focal deficit – aphasia/hemiparesis/hemiplegia

22. SAH GRADING
Fischer scale (based on CT scan)
 Group 1 - No blood detected
 Group 2 - Diffuse deposition of subarachnoid blood
and no layers of blood greater than 1 mm
 Group 3 - Localized clots and/or vertical layers of blood
1 mm or greater in thickness
 Group 4 - Diffuse or no subarachnoid blood, but
intracerebral or intraventricular clots are
present

23. SAH GRADING
 The Hunt & Hess and the WFNS grade
 Correlate with patient outcome
 Fischer classification
 Predict the likelihood of symptomatic cerebral
vasospasm
 Admission H&H Gr 1 and 2 - 20% mortality
 Major cause is rebleed (international cooperative
aneurysm study)

24. WORK UP
 CBC
 PT INR & aPTT
 Serum Electrolytes
 BGRh
 Cardiac Enzymes
 ABG

25. CT SCAN
 NCCT – cornerstone of diagnosis
 Most sensitive imaging study in SAH
 The sensitivity of CT in the first 3 days after aSAH remains
very high (close to 100%)
 After 5 to 7 days, the rate of negative CT increases sharply
 CT scan head-positive in up to
- 95-100% in 12-24 hours
- 80% in 3 days
- 70% in 5 days
- 50% at1 week
- 30% at 2 weeks

26. CT SCAN
 The location of blood correlates with the location of the
aneurysm in 70% of cases
 In general, blood localized to the basal cisterns, the sylvian
fissure, or the intrahemispheric fissure indicates rupture of a
saccular aneurysm.
 Blood found lying over the convexities or within the
superficial parenchyma of the brain often is indicative of
AVM or mycotic aneurysm rupture.

27.  Anterior inter-hemispheric fissure bleed, frontal
lobe – ACom Rupture

28.  Sylvian fissure bleed – ICA/MCA/PCom aneurysm

29.  IVH (3 & 4th ventricular) - PICA/ VA aneurysm
rupture

30.  CT falsely negative
 Small hemorrhages
 Severe anemia
 CT also helpful to rule out HCP
 CECT head may reveal AVM

31. CT Scan
 Intraventricular Hemorrhage (IVH)
 Hydrocephalus
 Intracerebral hematoma (ICH)
 Brain edema
 Infarction caused by vasospasm

32. Lumbar puncture (LP)
Positive in
 100% in 12 hrs to 2 weeks
 >70% after 3 weeks
 40% after 4 weeks

33. LUMBAR PUNCTURE
 CT scan performed before LP to exclude
 Significant intracranial Mass effect
 Obstructive HCP or obvious
 Intracranial hematoma
 LP should not be performed if the CT scan demonstrates an
SAH
 because of the (small) risk of further intracranial bleeding
associated with a drop in ICP.
 Findings often are negative within 2 hours of the ictus & is most
sensitive 12 hours after the bleed.
 SAH can be distinguished from traumatic LP.

34.  Xanthochromia – because of bilirubin in CSF
 100% present 12 hours after the bleed
 Remains for approximately 2 weeks.
 3 weeks after the bleed in 70%
 4 weeks in 40% of patients
 Better appreciated by spectrophotometry.
 RBC count usually > 1,00000/cumm
 Higher protein level d/t blood break down product.

35.  When blood enters the CSF (e.g. from SAH or during LP)
the red cells are broken down & oxyhaemoglobin is
released
 Oxyhaemoglobin conversion to bilirubin
 Takes 12 hrs
 Enzyme found in the brain.
 Blood which entered the CSF during the LP would not
encounter the enzyme & could not produce bilirubin

36. Supernatant
xanthochromia

37. CEREBRAL ANGIOGRAPHY (DSA)
 Gold standard for evaluation of cerebral aneurysm (80-85%
sensitivity)
 Useful in cases of diagnostic uncertainty (after CT and LP)
 Can provide surgical information in the setting of SAH:
 Cerebrovascular anatomy
 Aneurysm location & source of bleeding
 Aneurysm size/shape/orientation of dome and neck
 Relation to the parent/perforating arteries
 Presence of multiple or mirror aneurysms
 If cerebral angiography findings are negative (10-20%) a
repeat test should be performed after 10-21 days
 May be useful to evaluate for possible cerebral vasospasm

38. DSA

39. DSA

40. CT ANGIOGRAPHY
 Non invasive
 Routinely performed
 Sensitivity and specificity comparable to DSA
 Beneficial in very unstable patients who cannot undergo
angiography
 Detect aneurysms larger than 3 mm
 sensitivity 95% and Specificity 83%
 Anatomic detail especially relation to near by bony structure.

41. CT Angiogram

42. MRI
 MRI is not sensitive for SAH within the first 48 hours.
 Useful tool to diagnose cerebral / spinal AVMs
causing SAH
 MRI can be used to evaluate the degree of
intramural thrombus in giant aneurysms.

43. MR Angiography
 The role of MRA in the detection of SAH currently is under
investigation.
 Risk/benefit ratio still favors conventional angiography
 Can detect aneurysms >3 mm with 86% sensitivity and is useful
for monitoring the status of small, unruptured aneurysms
 False +ve in approx. 16%
 Can be used to evaluate the degree of intramural thrombus in
giant aneurysms
 Useful as a screening test in high risk patients including 1st
degree relative of patients with IC aneurysm

44. MR Angiography
 Takes ½ to 1 hour
 Detects aneurysms >3 to
5 mm
 MRI detects thrombosed
aneurysms
 Screening modality

45. TCD :
 Detection and monitoring of arterial vasospasm
ECG :
 Changes attributed to ischemia/infarction
 ↑ catecholamines.
 Myocardial ischemia/infarction is present in 20% of SAH
cases
Chest radiograph:
 Baseline chest radiograph to serve as a reference point
Echocardiogram:
 Evaluation of ventricular wall motion may be necessary in
cases with suspected myocardial ischemia

46. Clinical Manifestations and Diagnosis of
aSAH -Recommendations
 aSAH is a medical emergency that is frequently
misdiagnosed. A high level of suspicion for aSAH should exist
in patients with acute onset of severe headache (Class I;
Level of Evidence B).
 Acute diagnostic workup should include noncontrast head
CT, which, if nondiagnostic, should be followed by lumbar
puncture (Class I; Level of Evidence B).
 DSA with 3D rotational angiography is indicated for detection
of aneurysm in patients with aSAH and for planning treatment
(to determine whether an aneurysm is amenable to coiling or
to expedite microsurgery) (Class I; Level of Evidence B). (New
recommendation)

47. Critical Care Management of Patients
Following aSAH
1. Medical measures to prevent rebleeding
2. Seizure and prophylactic anticonvulsant use
3. Cardiopulmonary complications
4. Management of hydrocephalus
5. Monitoring intravascular volume status
6. Managing intravascular volume status
7. Glucose management
8. Management of pyrexia
9. DVT prophylaxis
10. Statins
11. Magnesium
12. Delayed neurological deterioration(DND), Vasospasm and delayed cerebral
ischaemia(DCI)
13. Hemodynamic monitoring of DCI
14. Anemia and transfusion
15. Management of hyponatremia
16. Endocrine function

48. MANAGEMENT
 Initial management of patients with SAH is stabilization. Assess the
level of consciousness, airway, breathing and circulation (ABCs).
 Endotracheal intubation should be performed for patients
presenting with coma/depressed consciousness/inability to
protect airway/ increased ICP.
 Vascular access should be obtained, including central and
arterial lines.
 Monitoring
 Cardiac monitoring
 Pulse oximetry
 BP monitoring (arterial BP monitoring is indicated in high-grade SAH)
 End-tidal carbon dioxide.
 Urine output measurement via placement of a Foley’s catheter.

49. Patients with signs of increased ICP
 Intubated and hyperventilated to achieve a PCO2 of
30-35 mm Hg.
 Avoid excessive hyperventilation - may potentiate
vasospasm and ischemia.
 Osmotic agents (mannitol) - decrease ICP dramatically
(50% after 30 min post administration).
 Loop diuretics also can decrease ICP.
 IV steroids - controversial.

50. STANDARD ADMITTING ORDERS :
 Admission in ICU with monitored bed
 Vital parameter and neurological status check 1 hrly
 Bed rest with head end elevated by 30 degrees
 Nursing : strict I-O charting / daily weights / DVT pumps at LL
/ urinary catheterization/ NG tube
 IVF : Aggressive fluid therapy to head off cerebral salt
wasting.
 Oral Nimodipine 60mg q4h for 21 days
 Stool softeners

51.  Anti Convulsants - Phenytoin is the usual agent used.
 Mild sedation (propofol/midazolam/lorazepam)
 Analgesic : fentanyl ( lower ICP and doesn’t cause
histamine release unlike morphine )
 Steroid : effect on brain edema is controversial, usually
given prior to craniotomy

52.  Oxygenation :
 Non intubated - Oxygen support to maintain SPo2>92
 Intubated - Normocarbia & Po2 > 100 mm Hg
 Monitoring of CVP
 For unsecured aneurysm , gentle volume
expansion with slight hemodilution and mild
elevation of BP may help reducing effects of
vasospasm and cerebral salt wasting

53. REBLEEDING
 Most disastrous and disabling
 Mortality rate – up to 70%
 Incidence
 First 24 hrs- 4-6 %
 1-2 %/day for 2 weeks (cumulative 20%)
 30% rebleed by 30 days
 50% rebleed by 6 months
 There after 3% per year
 Risk increases with higher H/H grade

54. Measures to prevent
rebleeding
 Early aneurysm repair should be undertaken,
when possible and reasonable
 Blood pressure control
 Modest elevations of blood pressure (Mean
BP <110mmhg) does not require therapy

55. Seizures
 Early - 6% to 18%
 Delayed - 3% to 7%
 Risk factors
 MCA aneurysm
 Thickness of SAH
 ICH
 Re-bleeding
 Infarction
 Poor neurological grade
 History of hypertension
 Routine use of anticonvulsants is not recommended
 If prophylactic anticonvulsants are used – use for
shorter duration 3-7 days

56. CARDIAC PROBLEMS
 SAH may be a/w cardiac arrhythmias and ECG
changes in over 60% cases; may be
indistinguishable from acute MI
 Possible mechanism : hypothalamic ischemia
causes ↑sympathetic tone with resultant
catecholamine surge
 Stunned myocardium : reversible post ischemic
myocardial dysfunction
 Hypotension usually does not occur since
reduced CO is offset by increased SVR.

57. Cardiac Complications
 Hypertension (27%)
 Hypotension (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 changes (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%)

58. Neurogenic stunned
myocardium
 Most severe form of cardiac injury
 Transient lactic acidosis
 Cardiogenic shock
 Pulmonary edema
 Widespread T-wave inversions
 Prolonged QT interval
 Reversible left ventricular wall motion
abnormalities

59. Pulmonary complications
 Chest Infection
 Neurogenic pulmonary
edema

60. Neurogenic pulmonary
edema
 Symptomatic pulmonary edema occurs in
about 20% of SAH patients
 Detectable oxygenation abnormalities occur
in 80%
 Potential mechanisms:
 Hyper-sympathetic state
 Cardiogenic pulmonary edema
 Neurogenic pulmonary edema

61.  Radiographic pulmonary edema - 23% of SAH
patients
 A minority of cases are associated with
documented LV dysfunction or iatrogenic
volume overload
 Neurogenic pulmonary edema appears to
be a consequence of the constriction of
pulmonary venous sphincters

62. Conditions associated with
neurogenic pulmonary edema
 Common:
 SAH
 Status epilepticus
 Severe head trauma
 ICH
 Rare:
 Brainstem infections
 Medullary tumors
 Multiple sclerosis
 Spinal cord infarction
 ↑ICP from a variety
of causes

63. Mechanisms of neurogenic
pulmonary edema
 Hydrostatic:
 CNS disorder → hyper-sympathetic state →
↑ afterload → diastolic dysfunction → hydrostatic
pulmonary edema
 Neurogenic:
 Contraction of postcapillary venular sphincters raises
PCWP without raising left atrial pressure
 Structural:
 Fracture of pulmonary capillary endothelium

64. Managing neurogenic
pulmonary edema
 Supplemental oxygen and CPAP or PEEP
 Place pulmonary artery catheter and, if there
is coexisting cardiogenic edema, lower the
wedge pressure to ~ 18 mmHg
 Echocardiography may be useful to
determine whether cardiac dysfunction is
also present
 NPE usually resolves in a few days

65. Monitoring Intravascular
Volume Status
 Monitoring of volume status may be beneficial
 Vigilant fluid balance management should be the
foundation for monitoring intravascular volume status.
 Central venous lines should not be placed solely to obtain
CVP measures and fluid management based solely on CVP
measurements is not recommended.
 Routine use of PAC is not recommended

66. Managing Intravascular Volume
Status
 Target euvolemia
 Avoid prophylactic hypervolemia
 There is evidence for harm from aggressive administration of
fluid aimed at achieving hypervolemia (high quality evidence;
strong recommendation).
 Isotonic crystalloid is the preferred agent for volume
replacement (moderate quality evidence; weak
recommendation).
 In patients with a persistent negative fluid balance, use of
fludrocortisone or hydrocortisone may be considered
(moderate quality evidence; weak recommendation).

67. Glucose management
 Hypoglycemia (serum glucose <80 mg/dl) should be
avoided (High quality evidence-strong recommendation).
 Serum glucose should be maintained below 200 mg/dl
(Moderate quality evidence-strong recommendation).

68. Management of Pyrexia
 Temperature should be monitored frequently; infectious causes of
fever should always be sought and treated
(High quality evidence—strong recommendation).
 While the efficacy of most antipyretic agents (acetaminophen,
ibuprofen) is low, they should be used as the first line of therapy
(Moderate quality evidence—strong recommendation).
 Surface cooling or intravascular devices are more effective and
should be employed when antipyretics fail in cases where fever
control is highly desirable
(High quality evidence—strong recommendation).
 Patients should be monitored and treated for shivering
(High quality evidence-strong recommendation).

69. Deep Venous Thrombosis
Prophylaxis
 Measures to prevent DVT should be employed in all SAH
patients (high quality evidence - strong recommendation).
 Sequential compression devices, should be routinely used in all
patients (high quality evidence – strong recommendation).
 UFH for prophylaxis could be started 24 h after surgery
(moderate quality evidence - strong recommendation).
 UFH and LMWH should be withheld 24 h before and after
intracranial procedures (moderate quality evidence - strong
recommendation).

70. Magnesium
 Inducing hypermagnesemia is not recommended pending
the conclusion of current randomized trials (moderate
quality evidence, strong recommendation).
 Hypomagnesemia should be avoided (Moderate quality
evidence, strong recommendation).

71. VASOSPASM
 Delayed ischemic
neurologic deficit
 Onset on the 3rd day
 Peak 6_8 days
 Resolves by 3
weeks

72.  CLINICAL VASOSPASM
 Delayed ischemic neurological deficit (DIND) : a
delayed focal ischemic neurologic deficit following SAH,
clinically characterized by confusion/deceased level of
consciousness with FND (speech/motor)
 RADIOGRAPHIC VASOSPASM (angiographic
vasospasm)
 Arterial narrowing demonstrated on cerebral
angiography (Slow Contrast filling)
 SYMPTOMATIC VASOSPASM
 When DIND corresponds to a region of vasospasm seen
on angiogram

73.  Clinical finding of cerebral vasospasm – usually develop
gradually, may progress and fluctuate
 Non localizing findings
 New or increasing headache
 Alteration of level of consciousness
 Disorientation
 Meningismus
 Focal neurological sign
 Cranial nerve palsy
 Focal neurological deficit
 ACA syndrome (MC)
 MCA syndrome

74.  ACA syndrome
 Frontal lobe findings predominate ( abulia, grasp/suck
reflex, urinary incontinence, drowsiness, slowness,
delayed response, confusion ).
 B/L ACA infract are usually d/t vasospasm after AComA
aneurysm rupture
 MCA syndrome
 Hemiparesis, monoparesis, aphasia, ideomotor apraxia

75. SEVERITY :
 Cerebral vasospasm is the most significant cause of
morbidity and mortality in patients surviving SAH
 Ranges from mild reversible dysfunction to severe
permanent deficit secondary to ischemic infarction
(7%) and may be fatal (7%)
 Earlier onset Cerebral vasospasm is a/w greater deficit

76. TIME COURSE OF VASOSPASM
 Onset is almost never before day 3 post SAH.
 Max frequency on day 6-8 post SAH.
 Clinical Cerebral vasospasm usually resolves by day
12 post SAH but radiological Cerebral vasospasm is
demonstrated , it usually resolves slowly over 3-4
weeks time.
 Onset is usually insidious but in 10% may have abrupt
and severe deterioration.

77. Diagnosis of Cerebral vasospasm
 Clinical Criteria
 Delayed onset of persistent neuro deficit
 Onset 4-20 days post SAH
 Deficit appropriate to involved arteries
 R/O other causes of deterioration
 Rebleeding
 HCP
 Cerebral edema
 Seizure
 Metabolic disturbances
 Hypoxia
 Sepsis

78. Trans Cranial Doppler ( TCD )
 May precede clinical symptoms by 24-48 hrs
Mean MCA
velocity
MCA : ICA
(Lindegaard
Ratio)
Interpretation
< 120 cm/sec < 3 Normal
120- 200 cm/sec 3 -6 Mild vasospasm
> 200 cm/sec > 6 Severe vasospasm

79.  Cerebral IA-DSA : vasospasm appear as concentric narrowing
which can be focal/segmental/diffuse.
 Mild (<25%)
 Moderate (25-50%)
 Severe (>50%)
 MRA / CTA : may be useful, not a practical alternative to DSA
 EEG : decline in percent of Alpha activity - called relative
alpha
 predicted onset of vasospasm earlier then TCD
 MRI : DWI & PWI may detect early ischemia
 Xenon CT : insensitive to detect focal blood flow changes
 PET / SPECT : non-quantitative and takes longer time

80. STRATEGIES FOR VASOSPASM
PREVENTION
Strategies Mechanism
Avoidance of hypovolemia/
hypotension/ antihypertensive/
antifibrinolytics / raised ICP
Prevent ischemia
Subarachnoid clot removal or
lysis with fibrinolytic agents
Prevent vasospasm
CCB or other potential calcium
based neuro-protectant
Prevent ischemic
damage
21- aminosteroid & other
antioxidant, lipid peroxidation
inhibitor, free radical
scavenger
Prevent ischemic
damage (?)
Intra-thecal slow release
vasodilator
Prevent vasospasm
(experimental )
Endothelin inhibitor and
antagonist
Prevent vasospasm
(experimental )

81. STRATEGIES FOR VASOSPASM
REVERSAL
Strategies Mechanism
Hypervolemia,
hemodilution and
hypertension
Reverses ischemia
Intra-arterial papaverine
administration
Reverses vasospasm
Percutaneous
transluminal balloon
angioplasty (PTBA)
Reverses vasospasm
Intraventricular
nitroprusside
Reverses vasospasm
(experimental)
Intra aortic balloon
counterpulsation (for
concomitant
heart failure )
Reverses vasospasm
along With PTBA

82. VASOSPASM MANAGEMENT PROTOCOL –
POST INTERVENTION
Condition Management
No vasospasm
• Clinically intact
• Normal TCD
1. Hemodynamics : normotension,
SBP>120mmHg
2. IVF : NS 200 ml/hr
Subclinical vasospasm
• High TCD (> 200 cm/sec)
• Radiographic vasospasm
• Clinically intact
1. Monitors : PA/CVC catheter, Arterial line
2. ECG, cardiac echo, cardiac enzymes to
assess LVEF
3. Monitor for S/S of a/e of 3-H therapy (chest
pain , pulmonary rhonchi, ECG changes )
4. Hemodynamics : maintain SBP 160-220
mm Hg (may add DA/NorAd/Dobutamine),
maintain PCWP 12-14 mmHg
5. Hematocrit : to maintain < 33%
6. Fluid : - monitor I/O and ser. Na
IVF = NS + plasma 200-250 ml/hr,
0.45% NS if Na>150 meq/L
DDAVP if UO > 200 ml / hr X 4 hrs
Clinical vasospasm
• DIND
• High TCD (> 200 cm/sec)
• Radiographic vasospasm
1. Increase SBP 200-220 mm Hg
2. Increase PCWP to 18-21 mm Hg (CXR- to
r/o pulmonary edema) / CVP 8-12 cm H2O
3. Refractory case : angioplasty , IA verapamil

83. TRIPLE “H” THERAPY
HYPERTENSION 1. Dopamine : start at 2.5
mcg/kg/min and titrate up to
15-20 mcg/kg/min
2. Dobutamine : start at 5
mcg/min titrate to 20
mcg/kg/min
3. Phenylephrine : start at 5
mcg/min titrate up to 10
mcg/kg
4. Norepinephrine : start at 1-2
mcg/min & then increase by
10 mcg/min
HYPERVOLEMIA 1. IVF : NS @ 200 -250 ml / hr
2. Albumin / plasma
3. DDAVP : antidiuretic , 2-4 mcg
SQ q D in divided Doses
HEMODILUTION 1. Target hematocrit : < 33%
2. Blood transfusion for Hct < 25%

84. Complications of hyperdynamic
therapy
 Intra cranial
 Cerebral edema
 Raised ICP
 Hemorrhagic infarction in the area of ischemia
 Extra cranial
 Pulmonary edema (17%)
 Cardiac failure
 Dilutional hyponatremia (3%)
 MI (2%)
 Complication related to catheter
 Catheter related sepsis (13%)
 Subclavian vein thrombosis (1.3%)
 Pneumothorax (1%)
 Hemothorax

85.  Oral nimodipine (60 mg every 4 h) should be administered
after SAH for a period of 21 days
(High quality evidence – strong recommendation).
 TCD may be used for monitoring and detection of large
artery vasospasm with variable sensitivity.
(Moderate quality Evidence - strong recommendation).
 DSA is the gold standard for detection of large artery
vasospasm
(High quality evidence - strong recommendation).

86. ANTI-HYPERTENSIVE
 To maintain SBP 120-150 mm Hg for unclipped
aneurysm
 The current recommendations advocate the use of
antihypertensive agents when MAP > 130 mmHg
 Intravenous beta-blockers – Agents of choice
 Hydralazine and CCB’s - fast onset and lead to
relatively less increase in ICP
 ACE inhibitors - slow onset and are not first-line agents

87. Calcium channel blockers
 Nimodipine 60 mg PO/NG q4h, initiated within
96hrs of aSAH.
 BRANT : British aneurysm nimodipine trial shown
22% vs. 33% incidence of cerebral infarction in
compared to placebo.
 Side effects are – systemic hypotension / renal
failure / pulmonary edema.

88. Anemia and Transfusion
 Transfusion criteria for general medical patients should not
be applied to decisions in SAH patients.
 Patients should receive packed RBC transfusions to
maintain hemoglobin concentration above 8–10 g/dl
(moderate quality evidence, strong recommendation).

89. HYPONATREMIA
 10-30%
 Hypovolemia and hyponatremia as result of natriuresis /
diuresis.
 MC cause is SIADH & CSWS (↑ANP/BNP/C-peptide).
 Hyponatremia may mimic or a/w DIND.
 Risk factors : H/O DM, CHF, cirrhosis, adrenal insufficiency, use
of NSAID/narcotic/thiazide.
 Treatment : correction of hypovolemia & anemia / salt
replacement (oral/IV) fludrocortisone may be tried.

90. Cerebral salt
wasting syndrome
SIADH
ECF volume ↓ ↑
Hematocrit ↑ Normal
Albumin conc. ↑ Normal
BUN Normal / ↑ ↓
BUN/Creat ratio ↑ ↓
Potassium Normal / ↑ Normal
Uric acid Normal / ↓ ↓
Urine Na+ ↑↑ ↑
Treatment Normal saline Fluid restriction

91. HYDROCEPHALUS
ACUTE HCP
 Incidence 15-20% after initial CT
 30-60% has no impairment of consciousness.
 3% develop delayed HCP within 1 week.
 Possible mechanism : CSF outflow obstruction by blood at
aqueduct / 4th ventricular outlet / subarachnoid space
and/or at arachnoid granulation.

92. Treatment of acute HCP :
 Patients in poor grade SAH with large ventricles may be
symptomatic from HCP and considered for ventriculostomy,
which causes improvement in 80% cases.
 ICP recommended to keep in the range of 15-25 mm Hg.
After securing the aneurysm ICP should be maintained in
the range of 5-10 mm Hg.

93. Chronic HCP
 Reported range is 8-45%.
 Chronic HCP is due to pia-arachnoid adhesions or
permanent impairment of arachnoid granulations.
 Acute HCP does not inevitably lead to chronic HCP.
 50% need permanent CSF diversion.

94. Angiogram-negative SAH
 15 to 20%
 65 % are prepontine or perimesencephalic
 Causes
 Vasospasm
 Hypoperfusion
 Poor angiographic technique
 Thrombosis
 Repeat angiography
 Undetected aneurysms found in an additional 2–5% of cases
at 2–4 weeks

95. Perimesencephalic bleed
 Younger
 Non-hypertensive
 Better grade
 More in males
 Excellent prognosis
 Re-bleeding is rare
 Delayed ischemic
deficit very few

96. Perimesencephalic SAH
(pmSAH)
 10% of patients of SAH
 2/3rd patients of angiographic negative SAH
 Benign course
 Venous bleed
 Better clinical grade on presentation
 Excellent prognosis
 Blood confined to midbrain cisterns with no
evidence of ICH or IVH
 Rebleeding is rare
 Delayed ischaemic neurological deficit(DIND) in
very few cases

97. DEFINITIVE TREATMENT
 Microsurgical Clipping OR Endovascular
coiling - early as feasible
 Complete obliteration of the aneurysm
should be achieved whenever possible
 Multidisciplinary decision based on
characteristics of the patient and the
aneurysm

98. Coiling
 Endovascular technique
done in angiography by
interventional radiologists
under GA
 May be best if small
necked aneurysm
 Used in particularly
sensitive areas e.g. basilar
tip
 Must be able to access
the aneurysm (e.g. any
stenosis or tortuous vessels)
 Like dome:neck ratio to
be 2:1 or greater
Clipping
 Craniotomy & careful
dissection using
microscope to reach
aneurysm & clip usually
at neck
 May be performed
after failed clipping
 If aneurysm can’t be
reached by the
endovascular root

99. Coiling

100. DACA Aneurysm Coiling

102. Coiling or Clipping
 For patients with ruptured aneurysms judged to be
technically amenable to both endovascular
coiling and neurosurgical clipping, endovascular
coiling should be considered

103. Clipping preferred
 Patients presenting with large ICH and MCA
aneurysm
 Aneurysm characteristics
 Wide neck
 Blebs
 Geometrically complex with incorporation of branch
artery
 Partially thrombosed
 Giant
 Inability to navigate delivery system
 Patients preference

104. Coiling preferred
 In elderly
 In poor-grade
 Aneurysms of basilar artery

106. CTA Spot Sign

107. SAH: Differential Diagnosis
 Aneurysmal
 Non-aneurysmal
 Pseudo-SAH
 Reversible cerebral vasoconstriction syndrome
(RCVS)

108. Reversible Cerebral
Vasoconstriction Syndrome (RCVS)
 Reversible, multifocal cerebral vasoconstrictions
 Clinical thunderclap headache +/- neurodeficit
 NCCT often negative: 20% with small cortical SAH
 Vasculitic pattern on CTA, MRA and DSA
 Segmental arterial constriction
 Interval DSA may show rapid improvement with vasodilator Rx

109. Pseudo-SAH
Increased density in basal cisterns, frequently related to
cardiopulmonary arrest
• Hypodense brain (severe edema): cisternal effacement,
distension +/-thrombosis of vessels

110. Pseudo SAH
 Intrathecal contrast
 Meningitis
 Polycythemia
 Falx cerebri
 Tentorium cerebelli
 Streak artifact –
bone from skull base
 Motion artifact

112. Sudden onset severe
headache
ABCs
History – ask
about
anticoagulants
Routine bloods &
coag & group &
screen
IV access
Non-sedating
analgesia & hold
any
anticoagulants
ExaminationKeep fastingInvestigations
CT brain non-
contrast
Blood on CT =
SAH
Is there any other
pathology on
CT?
Where is the
aneurysm?
CT COW +/-
cerbral
angiogram
For angiogram &
coiling if suitable
For craniotomy &
clipping if not
suitable for
coiling
Meanwhile chart
nimodipne,
fluids, anti-
seizure
medication
Monitor GCS for
any changes
from admission
examination
Ensure pre-op
ready – consent,
G&S, check
bloods, fasting