• Contemporary management of intracranial aneurysm after Sub arachnoid haemorrhage (SAH) calls for early intervention
• Early – within 72 hrs of SAH
• Ultra early → within 18 hrs of SAH
• Intervention applied to I to IV grades of “world federation of neurosurgeons SAH scale”( WFNS) or I to III of “hunt –Hess classification”

WFNS classification →

WFNS grade	GCS score	Motor deficit
I	15	Absent
II	14-13	Absent
III	14-13	present
IV	12-7	Present or Absent
V	6-3	Present or Absent

Delayed intervention > 2 WHS of SAH when vasospasm will re relived (day 4 to 12 after SAH)

Hunt – Hess classification-

Category grade	Criteria
I	Asymptomatic/minimal headache slight nuchal rigidity
II	Mod to severe headache, nuchal rigidity, no deficit other than cranial N palsy
III	Drowsiness, confusion or mild focal deficit.
IV	stupor, Mod to server hemiperesis, early decerebrate rigidity & vegetative Disturbances
V	Deep coma, decerebrate rigidty,moribund appearance

→Rationale for early clipping

1. Less likelihood of rebleeding.
2. Management of SAH after the episode requires volume loading and induced hypertension, early clipping eliminates risk of rebleeding associated with this therapy
3. Blood in basal cistern due to aneurysm can be removed at the time of clipping with is associated with vasospasm.
4. Direct instillation of tissue plasminogen activator into circle of willis is possible to aid clear the clot
5. ↓ period of hospitalisation & hence the complications of DVT, atelactasis, pneumonia associated with lengthy period of bed rest.

→ Difficulties during early clipping

1. Brain tissue in post –SAH period is more oedematous than after 2 wk delay.
2. Mild degree of hydrocephalous, may require CSF shunting after contamination of blood with CSF
3. Intra operative aneurysm rupture because of lesser time for clot to reorganise over the site of bleeding

Pre-op evaluation →

• Many patients of intracranial aneurysm will come directly from ICU.
• Elements of their management may influence pre-op status.
• Pre-op evaluation should include fluid status, neurologic status, management of SAH, ECG abnormalities

1) Fluid management →

After SAH 2 syndromes can develop

1. Cerebral salt wasting syndrome.
2. SIADH

Cerlbral salt wasting syndrome

Occurs as a result of release of natriuretic Peptide

Hyponatremia

Volume contraction           urine NA > 50 mmol/L

treatment is isotonic fluid & maintain intravascular volume

SIADH → Hypervolumia or Normovolumia, treated with volume restriction.

• Clinical distinction between two may be difficult.
• Administration of isotonic fluid to maintain intravascular volume used as end point.

2) Neurological status →

• deterioration in neurological status is frequently due to vasospasm.
• Drowsiness– common initial sign.
• Surgery usually deferred if vasospasm is suspected or angiographically demonstrated.
• Maintenance of CPP is crucial if surgery is to proceed by maintaining MAP in high normal range
• Induced hypotension can cause further cerebral ischemia
• Vasospasm -> due to breakdown products of Hb from blood that accumulates around circle of willis after SAH.
• Regimes to treat vasospasm is “triple H” therapy.

➤ Hypervolumia
➤ Hemodilution
➤ Hypertension

• Efficacy of this therapy is not proved.
• Dopamine & phenylephrine rise are most common used vasprossors
• Objective -> ↑ in MAP 20-30mm Hg above baseline.

3) Management of SAH →

• Ca channel blockers : Nimodipine ↓ incidence of morbidity from cerebral ischemia after SAH. Oral nimodipine & I.V. nicardipine can be administered.
• Antifibrinolytics : Were administered in the past, Role of antifibrinolytics is yet to be proved

4) ECG Abnormalities ->

• ECG abnormalities who have sustained SAH
• Coynon ‘T’ Waves
• Non specific ‘T’ wave changes, QT Prolongation
• ST Depression
• U waves

→ Episode of Extreme Hypertension and autonomic discharge with high catecholamine’s levels with initial event of SAH can come reversible stunning like myocardial activity

→ Cardiac dysfunction associated with SAH doesn’t contribute to morbidity & mortality

• QT interval > 550 msec has been associated with malignant ventricular rhythm
• Cardiac dysfunction is proportional to neurological condition rather than ECG Changes

Anaesthetic principle→

1. Absolute avoidance of acute hypertension
2. Provision of intra-op brain relaxation
3. Maintenance of highnormal MAP to prevent critical reduction in CBF
4. Prepared to perform precise manipulation of MAP during clipping of aneurysm or control bleeding from ruptured aneurysm.

Monitoring →

• Intra arterial line must because of wide fluctuation during the procedure
• CVP line
• Etco2
• Temp
• ECG
• Pulse oximetry
• ICP Monitoring
• Neurophysiologic monitoring – EEG to detect any episode of cerebral ischemia
• Intra-op angiography
• Urine output

Selection of anaesthetic agent→

• Any technique that controls MAP
• Volatile anaesthetics less preferable
• Present paroxysmal hypertension is absolute requirement.
• Rebleeding kills
• Early clipping makes aneurysm more prone for bleeding because of poorly organised clot.
• Rebleeding at induction is fatal event. Escaping arterial blood is more likely to penetrate brain substance because canot dissect through CSF space.
• ↑ in ICP is extreme because of poor compliance of intracranial space.
• Technique of induced hypotension →
• Technique is diminishing.
• Should be prepared to lower immediately & precisely when required
• Nitroprurside 0.5 – 1µg/kg/min
• Deep isoflurane & nitroprusside regime may require to ↓ MAP to 30-50 mmhg in case of rupture of aneurysm

Induce Hypertension →

• May be requested during periods of temporary arterial occlusion to augment collateral CBF.
• phenylephrine can be used (dopamine)
• After clipping to check the adequacy of clipping surgeon may request to ↑ systolic BP to 150mmHg.

Technique of brain relaxation

1. Hypocapnia →

– Used as an adjunct to brain relaxation technique

• Excessive hypocapnia avoided due to risk of vasoconstriction → ischemia
• 25-30 mm Hg paco₂ is adequate.
• ↓ in paco2 comes ↓ in CBF for limited period of time & thereafter slowly CBF comes to over a period of 8-12 HRS

1. Lumbar CSF drainage →

• Electively done
• Extremely effective
• Other application of brain volume reducing techniques almost unnecessary
• Sudden reduction on pressure gradient across dome of aneurysm avoided.
• Can lead to bleeding
• Common practice to close drain till dura is opened
• Discontinued promptly after final withdrawal of retractors to allow CSF to reaccumalate & reduce the size of pneumocephalus the drain usually removed post operatively.

1. Mannitol →

• Used to shrink brain
• Facilitate exposure & reduce retractor pressure
• Administered in dose of 1gm/kg just before dural opening
• Mannitol may have CBF enhancing effect in regions of moderate CBF reduction
• 2^nd dose of 1g/kg 15 min before temporary occlusion who believe in CBF enhancing effect of mannitol.

Trapping →

• Temporary occluding the vessel on either side of aneurysm to complete dissection of neck & apply clip.
• Technique more common with large aneurysm
• Occlusion time < 14 min is tolerated
• threshold for ischemia injury is 20 min
• maintain MAP High during this period to facilitate collateral CBF

 Brain protection →

1. maintain MAP to ensure collateral flow
2. efficient brain relaxation
3. limit duration of temporary occlusion
4. induction of mild hypothermia 32-34°c –may cause delay in emergence

if rapidly rewarmed,coagulation dysfunction
↓
Hypertension
↓
Rebleeding
↓
Ischaemia

Intra-op haemorrhage →

• aneurysm Surgery can result in exsanguinations due to rupture or rebleeding
• blood should be available prior to start of operation.

Extubation →

• should be smooth.
• Avoid intracranial HIN
• Extubation depends on Neurological condition.
• Immediate post-Op extubation allows neurological assessment prior to transfer to intensive care unit.
• Drugs used for smooth emergence inj. lidocoine 1.5mg/kg
• Esmolol
• Netoprolol
• Nitroprusside