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.
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
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
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.
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
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
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.
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.
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).
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
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
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
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
111.
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
