6. ο 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. ο Acquired vascular lesions secondary to
degenerative changes in the muscular and elastic
components of the vessel wall.
ο Usually occuring at the branching points of the
major cerebral vessels.
ο A deficiency of type III collagen in arteries is
assosiated with SAH.
9. ο Congenital influences may play a role.
ο Disease processes associated with an increased
risk of IA
ο‘ Polycystic kidney
ο‘ Hypertension
ο‘ Coarctation of the aorta
ο‘ Ehler- Danlos syndrome
ο‘ Fibromuscular disease
ο‘ smoking
10. ο Small β less than 12 mm 78%
ο Large β 12-24 mm 20%
ο Giant - 24mm 2%
ο Majority of aneurysms that bleed are less than 1
cm of diameter.
ο Aneurysms that are less than .5 cm diameter
have less risk of bleeding.
12. ο Causes increase ICP
ο Increased ICP causes decrease CBF
ο Bleeding stops with decreased CBF
ο Decreased consciousness
ο 2 clinical scenarios are seen typically
ο‘ Return to normal ICP and CBF with return of function
ο‘ High ICP continues with low CBF
13. ο Grade 0 - Aneurysm is not ruptured
ο Grade 1 - Asymptomatic, min. headache and sl. nuchal
rigidity
ο Grade 2 - Moderate to severe headache, nuchal rigidity, but
no neurologic deficit other than cranial nerve palsy
ο Grade 3 - Drowsiness, confusion, mild focal deficits
ο Grade 4 - Stupor, mild or severe hemiparesis, possible early
decerebrate rigidity, vegetative disturbances
ο 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. ο It is very important to assess the degree of SAH.
There are different grading scales for this
purpose.
ο Modified Hunt and Hess grading scale is most
commonly used because of ease of application.
ο Extent of vasospasm is related to the amount of
subarachnoid blood present.
ο CT scan is graded according to the Fisher grade
16. ο Grade 1 β No blood detected
ο Grade 2- Diffuse thin layer of subarachnoid
blood ( vertical layers less than 1 mm thick)
ο Grade 3 β Localised clot or thick layer of
suarachnoid blood( vertical layer = 1 mm thick)
ο Grade 4 β Intracerebral or intraventricular blood
with diffuse or no subarachnoid blood
17. ο The clinical management of cerebral aneurysms
centers on the reduction of risk of hemorrhage in
uruptured cases and of repeat hemarrhage in
SAH.
ο The major complications of SAH are β
1- Aneurysmal rebleeding
2- delayed cerebral ischemia secondary to
vasospasm
18. ο Incidence of rebleeding is 14-30 % .
ο Peak incidence at the end of the first week of
SAH.
ο High risk of rebleed during angiography
ο Assosiated with high rate of mortality and
morbidity.
19. ο Blood pressure control is of critical importance
in reduction of risk of rebleeding.
ο Antifibrinolytic agents have been used
successfully to control rebleeding
20. ο Vasospasm is the leading cause of morbidity and
mortality in patients who initially survive SAH
ο Radiological evidence of vasospasm is noted in upto
70% of patients .
ο Clinical vasospasm occur in almost 30% of patients
ο Clinical vasospasm occur after 4-9 days of SAH
ο It typically does not occur after 2 weeks of
aneurysmal rupture.
21. ο Pathological changes occur are contraction of
vascular smooth muscles and thickening of the
vessel wall
ο Prostaglandins , biological amines , peptides , cyclic
neucleotides , calcium , lipid peroxidation and free
redicals are implicated .
ο Conventional cerebral angiography , xenon-
enhanced CT and transcranial doppler is used to
confirm the presence of vasospasm
22. ο There is a correlation between the amount of
subarachnoid blood after aneurysmal rupture and
the occurrence and severity of vasospasm
ο Because of this , extensive removal of subarachnoid
blood by early surgery is attempted to decrease the
incidence of vasospasm.
ο Nimodipine , a calcium channel blocker is
successfully used .
23. ο Triple H therapy β hypertension , hypervolumia
and hemodilution is used in treatment of
vasospasm.
ο A new method for symptomatic vasospasm
includes use of cerebral angioplasty to dilate
constricted major cerebral vessels.
26. ο Assesment of patients neuroloical condition and
clinical grading of SAH
ο A review of patient,s intracranial pathological
conditions including CT scan and angiograms.
ο Monitoring of ICP and transcranial doppler
ultrasonography.
27. ο Evaluation of patients other systemic functions
, premorbid as well as present
ο Systems known to affected by SAH
ο Communication with the neurosurgeon regarding
positioning and special monitoring
ο Optimisation of patient,s condition by correcting
any biochemical and physiological condition
28. ο 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. ο The greater the clinical grade , more likely
vasospasm , elevated ICP , impaired autoregulation
and disordered response to hypocapnia will occur
ο Worse clinical grade is also assosited with cardiac
arrythmia , myocardial dysfunction , hypovolumia
and hyponatremia.
30. ο ECG abnormalities
ο‘ Very common
ο‘ Many changes seen
ο’ cannon t wave, Q-T prolongation, ST changes
ο‘ Autonomic surge may in fact cause some
subendocardial injury from increase myocardial wall
tension
31. ο Cardiac dysfunction does not appear to affect
morbidity or mortality (studies from Zaroff and
Browers)
ο Prolonged Q-T with increased incidence of
ventricular arrhythmias
ο PVCβs are seen in 80%
ο ECG changes occur during the first 48 hrs of SAH and
correlate with amount of intracranial bleed.
32. ο ECG changes reflect the severity of neurogenic
damage and have not shown to contribute
perioperative mortality and morbidity
ο The decision to operate should not be influenced
by these ECG changes.
33. ο Hydrocephalous
ο Seizures
ο‘ 13%
ο‘ Vasospasm may be cause
ο‘ Increased risk of rebleed
ο‘ Treat and prophylaxis
ο Headache, visual field changes, motor
deficits
34. ο SIADH
ο Cerebral salt wasting syndrome
ο‘ release of naturetic peptide
ο‘ hypovolemia, increased urine NA and volume
contraction
ο Distinguish between the two and treat
accordingly
35. ο Neurogenic pulmonary edema
ο 1-2% with SAH
ο Hyperactivity of the sympathetic nervous system
ο Pneumonia in 7-12% of hospitalized patients with
SAH
36. ο 0-3 days post bleed appears to be optimal
ο Improved outcome within 6 hours of rupture
despite high H/H grade
ο If delayed, should be done after 10 days post
bleed after fibrinolytic phase
ο The results are worst with surgery performed
between 7 to 10 days.
37. ο Avoid abrupt changes in BP
ο Maintain CBF with normal to high blood pressure
ο Avoid increase of ICP
ο Assess immobility & vital signs control
ο Achieve brain relaxation
ο Allow for swift emergence & neurologic assessment
ο Be prepared for disaster
38. ο Arterial blood pressure- beat to beat monitoring
of MAP
ο ECG- myocardial ischemia/ arrhythmia
ο Pulse oximetry- systemic hypoxia
ο EtCO2- trend monitor for Paco2/ detection of VAE
ο Temperature- via oesophageal lead; to allow
modest, passive hypothermia(~35o C)
ο Urine output- adequacy of renal function &
hydration
39. ο Blood glucose/ serum electrolytes/ osmolality
-particularly if mannitol is used
ο Hemoglobin & hematocrit- to estimate extent
of bleeding/ permissible blood loss
ο Jugular venous bulb monitoring- adequacy of
cerebral perfusion & oxygenation
ο EEG- CMR/ cerebral ischemia/ depth of
anaesthesia
40. ο Evoked potentials- intactness of specific CNS
pathways
ο Transcranial oximetry- noninvasive information
on regional cerebral oxygenation
ο TCD ultrasonorgaphy
41. ο TCD is a indirect measure CBF
ο It is unreliable as a measure of CBF in patients of
SAH because of changes in vessel diameter
ο But it has become valuable for diagnosing
vasospasm noninvasively before the onset of
clinical symptoms
ο TCD has been successfully used in the
perioperative management of patients with
cerebral aneurysm.
42. ο Continuous TCD monitoring may improve the safety
of induced hypotension by correlating the blood
velocity change to the decline in the blood
pressure.
ο It has been used perioperatively to confirm the
diagnosis of aneurysmal rupture.
43. ο Patients should receive their regular dose of
nimodipine and dexamethasone
ο Tab Loarazepam 1-2 mg and tab rantac 150
should be given in night before surgery
ο To relieve anxiety inj midazolam in incremental
dose of 1 mg is given in the morning of surgery.
44. ο There is risk of rupture of aneurysm at the time
of induction due to high blood pressure during
tracheal intubation
ο 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. ο 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.
ο Conceptually induction phase is consisting of 2
parts
Induction to achieve loss of consciousness
ο 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. ο Other alternatives include etomidate (.3-.4 mg/kg)
and midazolam ( .1-.2mg/kg)
Prophylaxis against rise in BP during laryngoscopy
ο 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. ο 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
ο Vecuronium is most hemodyanamically stable
and suitable muscle relaxant.
ο Succinylcholine causes incease in ICP.
ο Atracurium may cause hypotension.
ο Pancuronium causes tachycardia and
hypertension
49. ο The location and size of aneurysm generally
determine the position of patient.
ο Anterior circulation aneurysm are usually
approached using fronto-temporal incision with the
patient in supine position
ο Basilar tip aneurysms are approached using
subtemporal incision with the patient in lareral
position
50. ο Vertebral and basilar trunk aneurysms approached using
suboccipital incision with the patient in sitting or park
bench position
ο Avoid extreme positioning (extreme rotation or flexion
of neck to avoid IJV compression)
ο 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
ο Mild head-up position (to aid venous cerebral drainage)
51. ο Elevation of contralateral shoulder by wedge/ roll
(to prevent brachial plexus stretch injury if head is
turned laterally)
ο Meticulous attention to specific problems in prone/
lateral/ parkbench/ sitting positions
ο Care of ETT βeasy intraoperative accessibility
-fixed & packed securely to
prevent accidental extubation, or abrasions
resulting from movement
52. ο Care of eyes- taped occlusively to prevent corneal
damage (from exposure/ irrigation with antiseptic
solutions)
APPLICATION OF SKULL PIN HOLDER FRAME
ο 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 Ξ²-blockers e.g.
Esmolol 1 mg/kg or Labetalol 0.5-1 mg/kg
ο VAE- may occur with pin insertion
54. ο± Positioning of Anaesthetist
-optimal patient monitoring
-access to airway/ intravenous & intraarterial
lines
55. The goals during maintainance of anesthesia are --
ο To provide a relaxed or βslackβ brain that will allow
minimum retraction pressure
ο To maintain perfusion to the brain
ο To reduce TMP if necessary during dissection of the
aneurysm and final clipping
ο Allow prompt awakening and assessment of
patients with good SAH grades
56. ο Maintenance
CHOICE OF TECHNIQUE
Volatile agents Intravenous agents
Advantages Controlability/ predictability/ early
awakening
Good control of CBF, ICP, & brain
bulk
-cerebrovasoconstriction
β in ICP
Disadvantages Poor control of CBF, ICP, & brain
bulk
-cerebrovasodilation
β 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 βed ICP Complex, high risk of βed ICP
57. ο 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 βing CBF &
CMR
-if used, ensure βin 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
ο Fluid therapy should be guided by intraoperative blood
loss, urine output and CVP/PAWP
ο The aim is to maintain normovolumia before
aneurysmal clipping and slight hypervolumia and
hypertension after clipping.
ο Avoidance of hyperglycemia (worsens consequences of
cerebral ischemia)
59. ο Avoidance of hypoosmolality β 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. Ringerβs lactate, 254 mOsm/kg)
ο Preferred solutions β crystalloids: 0.9% NaCl
colloids: 6% HES (304 mOsm/kg)
60. ο Hematocrit- Target for >28%
ο Warming of I.V. solutionsβ 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. ο± 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)
ο± Moderate hypothermia (~350C)
-may confer a degree of brain protection if ischemic
event occurs
62. ο 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. Ξ²-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. ο 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. ο 5-7 minutes of occlusion with prompt reperfusion
are usually well tolerated but this duration is
insufficient for clipping difficult or giant aneurysms
ο A number of regimens have been used to extend
the occlusion duration
ο High dose Mannitol 2g/kg
ο SENDAI COCKTAIL - mannitol (500 ml of 20%
solution) + vitamin E (500 mg) + dexamethasone
(50 mg)
66. ο Pharmacological metabolic suppression by
thiopentone ( 5-6 mg/kg) or etomidate (.4-.5
mg/kg)
ο Etomidate is preferred over thiopental due to
greater hemodyanmic stability
ο Moderate hypothermia has also been to extend the
duration of tolerable occlusion
67. ο If the surgical procedure is uneventful , SAH grade I
and II patients should be extubated.
ο Because hypertensive therapy is useful in reversing
delated cerebral ischemia from vasospasm , modest
level of postoperative hypertension (<180mm hg )
should not be aggressively treated.
ο Depending on preoperative ventilatory status and
duration and difficulty of surgical procedure
68. ο SAH grade III patients may or may not be extubated.
ο Patients with preoperative SAH grade IV and V
usually require postoperative ventilatory support and
neurointensive care.
69. ο In the postoperative period blood pressure should be
maintained above 140-150 mm hg and less than 180
mm hg.
ο 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.
ο Neurological assessment should be done every 15
minutes in the recovery room.