6. More than 90% of cerebral aneurysm occur at the
following locations-
1-The origin of the posterior communicating artery
2- The region of the anterior communicating artery
3- Middle cerebral artery bifurcation
4- apex of basilar artery
5- internal carotid artery bifurcation.
7.
8. Acquired vascular lesions secondary to
degenerative changes in the muscular and elastic
components of the vessel wall.
Usually occuring at the branching points of the
major cerebral vessels.
A deficiency of type III collagen in arteries is
assosiated with SAH.
9. Congenital influences may play a role.
Disease processes associated with an increased
risk of IA
Polycystic kidney
Hypertension
Coarctation of the aorta
Ehler- Danlos syndrome
Fibromuscular disease
smoking
10. Small – less than 12 mm 78%
Large – 12-24 mm 20%
Giant - 24mm 2%
Majority of aneurysms that bleed are less than 1
cm of diameter.
Aneurysms that are less than .5 cm diameter
have less risk of bleeding.
12. Causes increase ICP
Increased ICP causes decrease CBF
Bleeding stops with decreased CBF
Decreased consciousness
2 clinical scenarios are seen typically
Return to normal ICP and CBF with return of function
High ICP continues with low CBF
13. Grade 0 - Aneurysm is not ruptured
Grade 1 - Asymptomatic, min. headache and sl. nuchal
rigidity
Grade 2 - Moderate to severe headache, nuchal rigidity, but
no neurologic deficit other than cranial nerve palsy
Grade 3 - Drowsiness, confusion, mild focal deficits
Grade 4 - Stupor, mild or severe hemiparesis, possible early
decerebrate rigidity, vegetative disturbances
Grade 5 - Deep coma, decerebrate rigidity, moribund
appearance
14. WFNS Grade GCS Score Motor Deficit
I 15 Absent
II 13-14 Absent
III 13-14 Present
IV 7-12 P or A
V 3-6 P or A
15. It is very important to assess the degree of SAH.
There are different grading scales for this
purpose.
Modified Hunt and Hess grading scale is most
commonly used because of ease of application.
Extent of vasospasm is related to the amount of
subarachnoid blood present.
CT scan is graded according to the Fisher grade
16. Grade 1 – No blood detected
Grade 2- Diffuse thin layer of subarachnoid
blood ( vertical layers less than 1 mm thick)
Grade 3 – Localised clot or thick layer of
suarachnoid blood( vertical layer = 1 mm thick)
Grade 4 – Intracerebral or intraventricular blood
with diffuse or no subarachnoid blood
17. The clinical management of cerebral aneurysms
centers on the reduction of risk of hemorrhage in
uruptured cases and of repeat hemarrhage in
SAH.
The major complications of SAH are –
1- Aneurysmal rebleeding
2- delayed cerebral ischemia secondary to
vasospasm
18. Incidence of rebleeding is 14-30 % .
Peak incidence at the end of the first week of
SAH.
High risk of rebleed during angiography
Assosiated with high rate of mortality and
morbidity.
19. Blood pressure control is of critical importance
in reduction of risk of rebleeding.
Antifibrinolytic agents have been used
successfully to control rebleeding
20. Vasospasm is the leading cause of morbidity and
mortality in patients who initially survive SAH
Radiological evidence of vasospasm is noted in upto
70% of patients .
Clinical vasospasm occur in almost 30% of patients
Clinical vasospasm occur after 4-9 days of SAH
It typically does not occur after 2 weeks of
aneurysmal rupture.
21. Pathological changes occur are contraction of
vascular smooth muscles and thickening of the
vessel wall
Prostaglandins , biological amines , peptides , cyclic
neucleotides , calcium , lipid peroxidation and free
redicals are implicated .
Conventional cerebral angiography , xenon-
enhanced CT and transcranial doppler is used to
confirm the presence of vasospasm
22. There is a correlation between the amount of
subarachnoid blood after aneurysmal rupture and
the occurrence and severity of vasospasm
Because of this , extensive removal of subarachnoid
blood by early surgery is attempted to decrease the
incidence of vasospasm.
Nimodipine , a calcium channel blocker is
successfully used .
23. Triple H therapy – hypertension , hypervolumia
and hemodilution is used in treatment of
vasospasm.
A new method for symptomatic vasospasm
includes use of cerebral angioplasty to dilate
constricted major cerebral vessels.
26. Assesment of patients neuroloical condition and
clinical grading of SAH
A review of patient,s intracranial pathological
conditions including CT scan and angiograms.
Monitoring of ICP and transcranial doppler
ultrasonography.
27. Evaluation of patients other systemic functions ,
premorbid as well as present
Systems known to affected by SAH
Communication with the neurosurgeon regarding
positioning and special monitoring
Optimisation of patient,s condition by correcting
any biochemical and physiological condition
28. To assess the CNS , as we have discussed before
there are grading scales-
1. Modified Hunt and Hess grading
2. WFNS grade scale
3. Fisher grading of CT scan
29. The greater the clinical grade , more likely
vasospasm , elevated ICP , impaired autoregulation
and disordered response to hypocapnia will occur
Worse clinical grade is also assosited with cardiac
arrythmia , myocardial dysfunction , hypovolumia
and hyponatremia.
30. ECG abnormalities
Very common
Many changes seen
cannon t wave, Q-T prolongation, ST changes
Autonomic surge may in fact cause some
subendocardial injury from increase myocardial wall
tension
31. Cardiac dysfunction does not appear to affect
morbidity or mortality (studies from Zaroff and
Browers)
Prolonged Q-T with increased incidence of
ventricular arrhythmias
PVC’s are seen in 80%
ECG changes occur during the first 48 hrs of SAH and
correlate with amount of intracranial bleed.
32. ECG changes reflect the severity of neurogenic
damage and have not shown to contribute
perioperative mortality and morbidity
The decision to operate should not be influenced
by these ECG changes.
33. Hydrocephalous
Seizures
13%
Vasospasm may be cause
Increased risk of rebleed
Treat and prophylaxis
Headache, visual field changes, motor
deficits
34. SIADH
Cerebral salt wasting syndrome
release of naturetic peptide
hypovolemia, increased urine NA and volume
contraction
Distinguish between the two and treat
accordingly
35. Neurogenic pulmonary edema
1-2% with SAH
Hyperactivity of the sympathetic nervous system
Pneumonia in 7-12% of hospitalized patients with
SAH
36. 0-3 days post bleed appears to be optimal
Improved outcome within 6 hours of rupture
despite high H/H grade
If delayed, should be done after 10 days post
bleed after fibrinolytic phase
The results are worst with surgery performed
between 7 to 10 days.
37. Avoid abrupt changes in BP
Maintain CBF with normal to high blood pressure
Avoid increase of ICP
Assess immobility & vital signs control
Achieve brain relaxation
Allow for swift emergence & neurologic assessment
Be prepared for disaster
38. Arterial blood pressure- beat to beat monitoring
of MAP
ECG- myocardial ischemia/ arrhythmia
Pulse oximetry- systemic hypoxia
EtCO2- trend monitor for Paco2/ detection of VAE
Temperature- via oesophageal lead; to allow
modest, passive hypothermia(~35o C)
Urine output- adequacy of renal function &
hydration
39. Blood glucose/ serum electrolytes/ osmolality
-particularly if mannitol is used
Hemoglobin & hematocrit- to estimate extent
of bleeding/ permissible blood loss
Jugular venous bulb monitoring- adequacy of
cerebral perfusion & oxygenation
EEG- CMR/ cerebral ischemia/ depth of
anaesthesia
40. Evoked potentials- intactness of specific CNS
pathways
Transcranial oximetry- noninvasive information
on regional cerebral oxygenation
TCD ultrasonorgaphy
41. TCD is a indirect measure CBF
It is unreliable as a measure of CBF in patients of
SAH because of changes in vessel diameter
But it has become valuable for diagnosing
vasospasm noninvasively before the onset of
clinical symptoms
TCD has been successfully used in the
perioperative management of patients with
cerebral aneurysm.
42. Continuous TCD monitoring may improve the safety
of induced hypotension by correlating the blood
velocity change to the decline in the blood
pressure.
It has been used perioperatively to confirm the
diagnosis of aneurysmal rupture.
43. Patients should receive their regular dose of
nimodipine and dexamethasone
Tab Loarazepam 1-2 mg and tab rantac 150
should be given in night before surgery
To relieve anxiety inj midazolam in incremental
dose of 1 mg is given in the morning of surgery.
44. There is risk of rupture of aneurysm at the time
of induction due to high blood pressure during
tracheal intubation
As a general principle , the patients blood
pressure should be reduced by 20-25% below the
baseline value and hypertensive response to the
tracheal intubation should be alleviated.
45. Another useful approach is to balance the risk of
ischemia from a decrease in CPP against the
benefit of a reduced chance of aneurysmal
rupture from a decrease TMP.
Conceptually induction phase is consisting of 2
parts
Induction to achieve loss of consciousness
Thiopental ( 3- 5 mg/kg ) or propofol (1-2.5
mg/kg ) in combination with fentanyl (3-7 ug/kg)
or sufentanil(.3-.7 ug/kg) is suitable
46. Other alternatives include etomidate (.3-.4 mg/kg)
and midazolam ( .1-.2mg/kg)
Prophylaxis against rise in BP during laryngoscopy
Many agents have been used successfully to
alleviate hypertensive response of intubation.
Fentanyl ( 5-10 ug/kg)
Sufentanil ( .5-1 ug/kg)
Esmolol (.5 mg/kg)
Labetolol (10-20 mg)
Intraveous or topical lidocaine (1.5-2 mg/kg)
Second dose of thiopental ( 1-2 mg/kg)
47. Intravenous adjuncts are preferred in patients
with poor SAH grades whereas deep inhalational
anesthetics are preferred in patients with good
SAH grades.
48. Choice of muscle relaxant
Vecuronium is most hemodyanamically stable
and suitable muscle relaxant.
Succinylcholine causes incease in ICP.
Atracurium may cause hypotension.
Pancuronium causes tachycardia and
hypertension
49. The location and size of aneurysm generally
determine the position of patient.
Anterior circulation aneurysm are usually
approached using fronto-temporal incision with the
patient in supine position
Basilar tip aneurysms are approached using
subtemporal incision with the patient in lareral
position
50. Vertebral and basilar trunk aneurysms approached using
suboccipital incision with the patient in sitting or park
bench position
Avoid extreme positioning (extreme rotation or flexion
of neck to avoid IJV compression)
Padding/ fixing of regions susceptible to injury by
pressure/ abrasion/ movement -groin, breasts, axillary
region
-falling extremities
-knees kept in mild flexion to prevent
backache postoperatively
Mild head-up position (to aid venous cerebral drainage)
51. Elevation of contralateral shoulder by wedge/ roll
(to prevent brachial plexus stretch injury if head is
turned laterally)
Meticulous attention to specific problems in prone/
lateral/ parkbench/ sitting positions
Care of ETT –easy intraoperative accessibility
-fixed & packed securely to
prevent accidental extubation, or abrasions
resulting from movement
52. Care of eyes- taped occlusively to prevent corneal
damage (from exposure/ irrigation with antiseptic
solutions)
APPLICATION OF SKULL PIN HOLDER FRAME
Pain- provides maximal nociceptive stimulus
- must be blocked adequately by
i. deepening of anaesthesia (i.v. bolus of
thiopentone 1mg/kg or propofol 0.5 mg/kg)
ii. analgesia (i.v. bolus of fentanyl 1-3
mcg/kg or alfentanil 10-20 mcg/kg or remifentanil 0.25-1
mcg/kg)
53. iii. local anaesthetic infiltration at pin site
iv. antihypertensive β-blockers e.g.
Esmolol 1 mg/kg or Labetalol 0.5-1 mg/kg
VAE- may occur with pin insertion
54. Positioning of Anaesthetist
-optimal patient monitoring
-access to airway/ intravenous & intraarterial
lines
55. The goals during maintainance of anesthesia are --
To provide a relaxed or ‘slack’ brain that will allow
minimum retraction pressure
To maintain perfusion to the brain
To reduce TMP if necessary during dissection of the
aneurysm and final clipping
Allow prompt awakening and assessment of
patients with good SAH grades
56. Maintenance
CHOICE OF TECHNIQUE
Volatile agents Intravenous agents
Advantages Controlability/ predictability/ early
awakening
Good control of CBF, ICP, & brain
bulk
-cerebrovasoconstriction
↓ in ICP
Disadvantages Poor control of CBF, ICP, & brain
bulk
-cerebrovasodilation
↑ in ICP
Prolonged/ unpredictable
awakening
May interfere with D/D of delayed
awakening
May require emergent CT scan
to rule out surgical complications
Type of
surgery
Simple, low risk of ↑ed ICP Complex, high risk of ↑ed ICP
57. Maintenance
CHOICE OF TECHNIQUE
Volatile agents Intravenous agents
Early institution of
moderate
hyperventilation
Mandatory Optional
Concurrent use with
N2O
Ideal agent
Usually avoided
-synergistic effects in ↑ing CBF &
CMR
-if used, ensure ↓in ICP by
i. hyperventilation
Ii. osmotic diuretics
Iii. BP control
Iv. adequate positioning/ cerebral
venous drainage
v. lumbar drainage
Vi. Use of < 1 MAC (e.g. < 1.15% of
isoflurane)
No
Can be used without
significant problems
Yes
58. Fluid Therapy
Fluid therapy should be guided by intraoperative blood
loss, urine output and CVP/PAWP
The aim is to maintain normovolumia before
aneurysmal clipping and slight hypervolumia and
hypertension after clipping.
Avoidance of hyperglycemia (worsens consequences of
cerebral ischemia)
59. Avoidance of hypoosmolality – can cause brain
oedema
i. Target osmolality: 290-320 mOsm/kg)
ii. Colloid oncotic pressure plays no significant role
in brain oedema
iii. Avoidance of glucose-containing & hypoosmolar
solutions (e.g. Ringer’s lactate, 254 mOsm/kg)
Preferred solutions – crystalloids: 0.9% NaCl
colloids: 6% HES (304 mOsm/kg)
60. Hematocrit- Target for >28%
Warming of I.V. solutions– may be avoided to
permit establishment of mild hypothermia (~350 C)
for neuroprotection
-must be essentially warmed at the end of
procedure to ensure normothermia for emergence
from anaesthesia
61. Hemodynamic control
-Undesirable CNS arousal & hemodynamic activation may
occur despite adequate depth of anaesthesia &
analgesia
-Consider use of i. Esmolol (1mg/kg: initial dose)
ii. Labetalol (0.5-1mg/kg: initial
dose)
iii. Clonidine (0.5-1mcg/kg: initial
dose)
Moderate hypothermia (~350C)
-may confer a degree of brain protection if ischemic
event occurs
62. Prevention
1. No over hydration
2. Sedation/ analgesia/ anxiolysis
3. Avoidance of application of any noxious stimulus with
sedation/ local anaesthesia
4. Head-up position
5. Osmotic agents (mannitol/ hypertonic saline)
6. β-blockers/ clonidine/ lignocaine
63. 7. Adequate hemodynamics: MAP, CVP, PCWP, HR
8. Adequate ventilation: PaO2>100mmHg;
PaCO2~35mmHg
9. Minimal possible intrathoracic pressure
10. Hyperventilation on demand (before induction)
11. Use of total I.V. anaesthestic agents for induction
& maintenance
12. Avoidance of cerebral vasodilators (e.g.
nitroglycerine)
64. Treatment
1.Hyperventilation
2.Osmotic agents
3.CSF drainage (if ventricular/ lumbar catheter in situ)
4.Augmentation of anaesthesia with I.V. anaesthetic
agents (e.g. propofol, thiopentone, etomidate)
5.Adequate muscle relaxation
6. Venous drainage (head-up/ avoidance of PEEP/
reduction of inspiratory time)
7.Mild controlled hypertension (if autoregulation is
present)
65. 5-7 minutes of occlusion with prompt reperfusion
are usually well tolerated but this duration is
insufficient for clipping difficult or giant aneurysms
A number of regimens have been used to extend
the occlusion duration
High dose Mannitol 2g/kg
SENDAI COCKTAIL - mannitol (500 ml of 20%
solution) + vitamin E (500 mg) + dexamethasone
(50 mg)
66. Pharmacological metabolic suppression by
thiopentone ( 5-6 mg/kg) or etomidate (.4-.5
mg/kg)
Etomidate is preferred over thiopental due to
greater hemodyanmic stability
Moderate hypothermia has also been to extend the
duration of tolerable occlusion
67. If the surgical procedure is uneventful , SAH grade I
and II patients should be extubated.
Because hypertensive therapy is useful in reversing
delated cerebral ischemia from vasospasm , modest
level of postoperative hypertension (<180mm hg )
should not be aggressively treated.
Depending on preoperative ventilatory status and
duration and difficulty of surgical procedure
68. SAH grade III patients may or may not be extubated.
Patients with preoperative SAH grade IV and V
usually require postoperative ventilatory support and
neurointensive care.
69. In the postoperative period blood pressure should be
maintained above 140-150 mm hg and less than 180
mm hg.
To distinguish residual anesthesia from surgical
cause following general guidelines are useful
1- Anesthesia causes global depression and any new
focal neurological deficit should alert to a surgical
cause
70. 2-The effect of potent inhaled anesthetics should
have larly dissipated after 30-60 minutes
3- patients whose pupils are midsized and having no
respiratoty depression are unlikly to experience a
narcotic overdose.
4- unequal pupils not present before surgery always
suggest a surgical cause.
Neurological assessment should be done every 15
minutes in the recovery room.