this presentation will be very useful for the candidates of neuroanesthesia....

1. Dr. Manoj Tripathi

2.  75% of subarachnoid hemorrhages
 27,000 American/year
 6-49 per 100,00 year depending on location
 Female predominance
 Age 40-60

3.  Ruptured intracranial aneurysm (IA)
 20% morbidity
 20% mortality
 Unruptured IA
 4% morbidity
 0-2% mortality

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.

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.

11.  Hypertension
 Pregnancy
 Smoking
 Heavy drinking
 Strenuous activity

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.

24. 

25. PREOPERATIVE ASSESSMENT
DETERMINATION OF
ANAESTHETIC STRATEGY
PREOPERATIVE
PREPARATION
INDUCTION
MAINTENANCE
EMERGENCE

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.

71. Thank you