Dr. Manoj Tripathi

75% of subarachnoid hemorrhages

27,000 American/year

6-49 per 100,00 year depending on location

Female predominance

Age 40-60

Ruptured intracranial aneurysm (IA)

20% morbidity

20% mortality

Unruptured IA

4% morbidity

0-2% mortality

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.

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.

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

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.

Hypertension

Pregnancy

Smoking

Heavy drinking

Strenuous activity

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

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

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

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

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

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

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.

Blood pressure control is of critical importance

in reduction of risk of rebleeding.

Antifibrinolytic agents have been used

successfully to control rebleeding

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.

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

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 .

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.

PREOPERATIVE ASSESSMENT

DETERMINATION OF

ANAESTHETIC STRATEGY

PREOPERATIVE

PREPARATION

INDUCTION

MAINTENANCE

EMERGENCE

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.

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

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

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.

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

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.

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.

Hydrocephalous

Seizures

13%

Vasospasm may be cause

Increased risk of rebleed

Treat and prophylaxis

Headache, visual field changes, motor

deficits

SIADH

Cerebral salt wasting syndrome

release of naturetic peptide

hypovolemia, increased urine NA and volume

contraction

Distinguish between the two and treat

accordingly

Neurogenic pulmonary edema

1-2% with SAH

Hyperactivity of the sympathetic nervous system

Pneumonia in 7-12% of hospitalized patients with

SAH

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.

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

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

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

Evoked potentials- intactness of specific CNS

pathways

Transcranial oximetry- noninvasive information

on regional cerebral oxygenation

TCD ultrasonorgaphy

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.

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.

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.

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.

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

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)

Intravenous adjuncts are preferred in patients

with poor SAH grades whereas deep inhalational

anesthetics are preferred in patients with good

SAH grades.

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

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

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)

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

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)

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

Positioning of Anaesthetist

-optimal patient monitoring

-access to airway/ intravenous & intraarterial

lines

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

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

Maintenance

CHOICE OF TECHNIQUEVolatile 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

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)

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)

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

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

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

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)

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)

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)

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

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

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.

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

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.

Thank you