- 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|
|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-
|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
- Less likelihood of rebleeding.
- Management of SAH after the episode requires volume loading and induced hypertension, early clipping eliminates risk of rebleeding associated with this therapy
- Blood in basal cistern due to aneurysm can be removed at the time of clipping with is associated with vasospasm.
- Direct instillation of tissue plasminogen activator into circle of willis is possible to aid clear the clot
- ↓ period of hospitalisation & hence the complications of DVT, atelactasis, pneumonia associated with lengthy period of bed rest.
→ Difficulties during early clipping
- Brain tissue in post –SAH period is more oedematous than after 2 wk delay.
- Mild degree of hydrocephalous, may require CSF shunting after contamination of blood with CSF
- 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
- Cerebral salt wasting syndrome.
Cerlbral salt wasting syndrome
Occurs as a result of release of natriuretic Peptide
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.
- 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
- Absolute avoidance of acute hypertension
- Provision of intra-op brain relaxation
- Maintenance of highnormal MAP to prevent critical reduction in CBF
- Prepared to perform precise manipulation of MAP during clipping of aneurysm or control bleeding from ruptured aneurysm.
- Intra arterial line must because of wide fluctuation during the procedure
- CVP line
- 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
- 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
- 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.
- 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
- 2nd dose of 1g/kg 15 min before temporary occlusion who believe in CBF enhancing effect of mannitol.
- 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 →
- maintain MAP to ensure collateral flow
- efficient brain relaxation
- limit duration of temporary occlusion
- induction of mild hypothermia 32-34°c –may cause delay in emergence
if rapidly rewarmed,coagulation dysfunction
Intra-op haemorrhage →
- aneurysm Surgery can result in exsanguinations due to rupture or rebleeding
- blood should be available prior to start of operation.
- 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