Anesthesia for intracranial aneurysm surgeries

Dr.R.Muthukumar

Anesthesia for intracranial aneurysm surgeries

• Epidemiology• World wide incidence of 10.5 per 1 lakh people /year

• In india 2 to 4 per 1 lakh persons /year

• Female : male is 1.3 :1

• Incidence of SAH due to rupture 6 to 8 per 1 lakhpersons/year.

• Peak incidence of SAH is in the 5th and 6th decade of life.

Etiology

• Inherant structural weekness of cerebral vessels

• Absence of external elastic lamina

• Unique branching &pulsatile bombardment

• Increased sheer stress at the bifurcation

• Common at branching

• Associated with collagen vascular diseases

Types and location

• Saccular (berry aneurysm) found usually on the major arteries at the apex of branch points( 85 to 95%)

• Acom- 30%• Pcom-25%• MCA- 20%• Fusiform aneurysm common in

vertibrobasillar system- 5 to 15 %

Presentation & clinical features

• Headache- sudden &severe. May be mild due to warning leaks (sentinal hemorrhage)

• LOC with headache(97%)• Meningismus(52%)• Confusion &coma due to rupture causing

hydrocephalus&ischemia• Focal neurological deficits –21%• Mass effect –gaint aneurysm(>24mm)

Potential risk factors for aneurysmal rupture

• Smoking

• Hypertension

• Alcohol consumption

• Hypercholestrolemia(250 mg/dl)

• Oral contraceptives

• 1st degree relatives

• Associated collagen vascular diseases

Predictors of outcome after rupture

Hunt &Hess grading• 0-unruptured aneurysm• 1-asymptomatic or minimal headache with slight

nuchial rigidity• 2-moderate to severe headache ,nuchial rigidity ,

no neurological deficits other than cranial palsies• 3-drowsiness,confusion,mild focal deficits• 4-stupor,mild/severe hemiperesis,early decerebrate

rigidity,veg disturbances• 5-deep coma,decerebrate rigidity,moribund

World federation of neurosurgeons’ grading

• WFNS GCS motor deficit

• 1 15 absent

• 11 14-13 absent

• 111 14-13 present

• 1V 12-7 present/abs

• V 6-3 present/abs

Surgical mortality& morbidityinrelation to grading

• H&H mortality morbidity

• 0 0-2% 0-2%

• 1 2-5% 2%

• 2 5-10% 7%

• 3 5-10% 25%

• 4 25-30% 25%

• 5 40 –50% 35-40%

Pathology of rupture of cerebral aneurysm

• Raised ICP-blood, csf obstruction,arteriolar dilation, vasoparalysis

• Reduction in CBF-hematoma,hydrocephalus,edema,vasospasm

• Reduction in CMRO2(25%)-• Increased CBV-vasodilation, microcirculation• Impaired autoregulation with rt shift• Impaired CO2 reactivity in reducing ICP• Increased sympathetic activity with activation of

coagulation & fibrinolytic system• Increased excitatory AA, cellular apoptsis, lactic acidosis

Medical complications following SAH

• BLOOD VOLUME & ELECTROLYTES

• Hyponatremia-ANP,SIADH• Hypernatremia-poor prognosis• Hypovolumia-bed rest, diuretics,-ve N2

balance,blood loss, raised catacholamines.• Trt-isotonic saline solution-normovolumia

delays incidence of ischemia

Medical complications following SAH

• CARDIOVASCULAR

• ECG changes.(50%)-Q waves,ST ele/depression,Tinversion,arrythmias.

• Hypokinetic LV,subendocardial damage

• Echo corelates clinical grading than ECG

• Hypertension-catacholmines,cushings reflex

• TMP=MAP-ICP/ CPP==TMP

• So MAP not decreased < 20%of baseline values.

Medical complications following SAH

• PULMONARY COMPLICATIONS• Aspiration

• Neurogenic pulmonary edema(13%,1st week

• Embolism

• Bronchospasm• Due to increased sympathetic outflow&

pulmonary capillary endothelium disruption

Medical complications following SAH

• DEEP VENOUS THROMBOSIS• 50% in patients not receiving prophylaxis

• Compression stockings

• LMWH(21%--14%)

• Intermittent calf compression

Surgical complication after SAH

• REBLEEDING• Most common cause of mortality(25%)• 4% on 1st day-1.5%daily for 13 days-• 7 to 20% rebleed by 1 month• 35% of them die• Early surgery is the choice. Adv:prevent

rebleed,vasospasm, hydrocephalus• Disadv:edema causing dificult exposure, rupture• Safe drugs,good monitors,microscopes– early

surgery fesible

Surgical complication after SAH

• HYDROCEPHALUS• Acute phase has negative impact onoutcome

• Chronic(6-67%)

• Shunt dependence due to:increase age,intraventricular hemorrmage,thick SAH

Surgical complication after SAH• VASOSPASM

• Focal or diffuse narrowing of large arteries• Hemiperesis,visual dis,alt consciousness• Onset 4-14 dayspeak at 7th day after bleed• Not before 72 hrs &resolves by 2 weeks• Oxyhemoglobin, endothelin,BNP• Diag by: TCD, EEG,angio, xenon study, PET or

SPECT scans• Trt:Nimodepin,balloon angioplasty,intraarterial

papavarine, tripple H therapy.(hemodilution,hypertension, hypervolumia)

Evaluation & investigation

• CT- Scan : detects SAH in 95% < 48 hrs.• : assess the amount of blood in

cisterns• : location in 70%• LP:most sensitive ,false positives.• csf flow under pressure,non-clotting blood

stained• RBCs > I lakh, high protiens &normal

glucose

Evaluation & investigation

• MRA(magnetic resonance angio)

• 86% sensitivity, only for screening.

• Cerebral 4 vessel angio

• demonstrates size, site, direction,presence of vasospasm, &adqof collateral

Anesthetic considerations

• GOALS

• Prevent intraop rupture

• Prevent cerebral ischemia

• Provide cerebral protection

• Provide lax brain

• Maintain CPP

Preoperative assessment

• Patients’ neurological status• Systemic dysfunction& medical disorders• Optimization &correction of physiological

disturbances• Review of CT& angio• Investigations:CBC, RBS, BUN. Creat, ECG,

CXR• Special investigation: LFT, Coagulation

profile,ECHO in high risk &poor grade patients

Premedication

• Anti convulsants, calcium channel blocker, & steroids to be continued.

• Heavy sedations avoided• Good grade &unruptured aneurysm may

require anxiolytic dose of BZD• Intubated patients are given muscle

relaxants to prevent coughing• Atropine or glycopyrrolate.

Monitoring for aneurysm clipping

• Before induction: ECG,SaO2, ETCO2, NIBP, invasive BP.

• After induction: CVP,/PCWP. Temperature; neuromuscular block monitor; urine output ;ABG; blood glucose;

• Special monitoring: SjVo2; TCD; EEG; Brain tissue oxygen tension ;SSEP;BAEP

Induction• Goal is to prevent rupture.(< 1%)• TMP=CPP=MAP-ICP• Pre-oxygenated• Induction with thio 3-5 mg/kg;propofol1.5-

2.5mg/kg;etomidate0.3-0.5 mg/kg.• Narcotics-morphine 0.1-0.2mg/kg; fentanyl 3-5mg/kg;

sufentanyl 0.3-0.7mg/kg;• Relaxants:scoline,NDMR• B blockers-esmolol-300 to 500mcg/kg• Lidocaine 1.5mg/kg +add thio or propofol• Isoflurane /sevoflurane.• No GTN /SNP.

Maintenance

• Goals: provide lax brain,maintain CPP,cerebral protection during temporary clipping,early recovery

• Inhalational:sevo/isoflurane(up to 2 mac)• Intravenous: propofol+ fentanyl / alfentanyl.

dose 5-8mg/kg/hr for maintenance, 500mcg/kg/min for burst suppression.

• MAP maintained with inotropes / IVF

Brain relaxation

• Mannitol 0.25 - 1gm/kg for 20 min ; onset within 10 min; peaks at 30 min;(rises TMP)

• CSF drainage by LP: excessive drainage causes rebleed &herniation.20 –30 ml before dural opening at 5 ml/min

• Optimal ETCO2 of 30 –35 mmhg is mandatory.

Deliberate hypo tension

• ADV:To prevent rupture,to make dissection easy &neck pliable for clipping.

• DISADV:worsen ischemia• Absolute Contandication in vasospasm.• Relatively in carotid artery stenosis , CAD

,Anaemia, hypovolumia, hypertension uncontrolled.

• BP reduced not more than 20% of baseline ,mostly during brief period of clipping.

Temporary clipping & cerebral protection

• Done to overcome the disadv of hypotension• Reduces TMP more effectively &reduces rupture of

aneurysm intraop.• Causes cerebral infarction & ischemia• Occlusion time <10 min.(< 1.5 % stroke)• Mild to mod hypertension +hemodilution (Hct –32%)-for

perfusion thro collaterals• Brain protection with thiopentone(5-10mg/kg) or propofol

to produce burst suppression.• Hypothermia: deep-15 to180c TCA up to 60 min under

CPB.• mild-32-330c CMRO2 falls by 15%;prevents

free radical & excitatory AA formation

Intraop rupture of aneurysm

• Incidence of leak- 6%, frank rupture –13%• Sudden &sustained hypertension with or without

bradycardia• Surgery postponed or rescue clipping done.• Outcome depends on timing of rupture (good in

later stages of surgery) & amount of blood.• Trt: Reduce MAP with NTG• Rapid craniotomy &clipping• blood loss replacement

Indication of DHCA

• Atherosclotic giant aneurysm

• Partially thrombosed giant aneurysm

• Giant aneurysm adherent to vital structures

• Basilar artery aneurysm

• Ophthalmic artery aneurysm

Emergence• Uneventful procedure for grade 1 &2–

extubation in OT

• Grade 3 ventilated based on post op neurological status.

• Grade 4 &5 ventilated electively , aggressive management in icu.

Complications

• Delayed recovery—due to anesthesia or surgery(global or focal deficits)

• Seizures due to brain retraction

• Pnemocephalus—repeat CT

• Hydrocephalus,ischemic neurological deficits, infections, hyponatremia.

Arterio-venous malformations

• Tangle of congenitally malformed blood vessels

• Arterial afferent to venous efferent—ischemic injury to the brain.

• Incidence: one tenth as aneurysm.

• Male :female 1:1

Development of AVM

• Congenital: during embryo genesis-high flow low resistance vessels shunting blood &increase in size.

• Trauma & occlusion of arteries or venous sinuses --- producing increase in perfusion pressure.

Pathogenesis

• Endothelial dysfunction and /or aberrant angiogenesis.

• Angiogenic growth factors.

Anatomic components of AVM

• Nidus

• Arterial feeders( MCA or dural)

• Arterial collaterals

• Venous outflow channels-superficial, deep

Location

• Supratentorial(70-90%)

• Posterior fossa(10%)

• Basal ganglia &internal capsule (7%)

• Dural (10%-15%)

• Neural elements of spine

Co-existence of Aneurysm

• 4 – 10% of AVM

• Occurs at Nidus (psedoaneurysm) hemorrhage

• Feeding arteries (flow related)37% -95%

• Theories: coincidence finding

• generalised vascular maldevlop

• flow causing degeneration

• Treatment: nidus & distal regress with AVM

• anesthetic precaution

Signs & symptoms

• Seizures & headache(20 –40 yrs of age)

• 20% asymptomatic.

• SAH followed by seizures and focal neurological deficits in young adults.

• Hydrocephalus &high output failure in infants with vein of galen AVM.

• Incidence declines > 50 yrs.

Clinical &angiographic factors for hemorrhage

• Deep venous drainage.

• Intranidal or multiple aneurysm.

• Samll AVM < 3 cm.

• High feeding artery or draining venous pressure.

• Diffuse morphological findings.

• Age> 40 yrs.

• Feeding by arterial perforators.

AVM in Obstetrics

• Meternal ICH 0.01 –0.05% of all pregnencies

• 23-50% of ICH results from AVM rupture

• Pregnancy is not a risk factor for hemorrhage.

• Unruptured or stable post hemorrhagic allowed tilterm

• Caeserean / vaginal delivery has no influence on meternal or fetal outcome

Grading system for AVMSpetzler &Martin

• Features points• Size:small <3cm 1• med 3-6cm 2• large >6cm 3• Eloquence of adj brain:• No-elo present 0• Elo present 1• Pattern of venous drainage:• Superficial 0• Deep 1

Management of AVM

• Surgical excision

• Embolization (single or multi staged).reduces the risk of intra op bleeding & post op hyperemic complications.

• Steriotactic radio surgery(small AVM in critical location)using Co 60.

• Conservative (grade 5 or 6).

Risk of unfavorable surgical outcome

• Age> 50 yrs

• Recruitment of perforating vessels

• Large size >5 cm

• Depressed total CBF

• H/o preop hemorrhage

• Co-existing aneurysm

• Hyperemic complication

Anesthetic consideration for Embolization

• General vs conscious sedation

• Propofol; midazolam;droperidol;fentanyl;

• intraop neurologic testing

• controlled ventilation(ICP)

• ability to still for long periods

• fluid &electrolytes &coagulation status

• contrast dye complications

• Radiation precautions

Anesthetic consideration for Embolization

• Complications

• new neurological deficits

• seizures

• pul embolism

• acute bleeding

• hyperemic complication

Anesthetic consideration for surgical resection

• Preop: preexisting med conditions • Neurological status• fluid &electrolyte & coagulation• Diagnostic studies• Monitors & induction:• Maintenance :• choice –neurological testing &stablity• brain protection• delibrate hypotension• Emergence:• BP control• evaluate neurological status

Anesthetic consideration for surgical resection

• complications• New neurological deficits

• Hyperemic complications(normal perfusion pressure breakthrough syndrome)

• Severe bleeding

Hyperemic complication

• Definition:cerebral hyper-perfusion with normal perfusion pressures.(spetzler 1978)

• Mechanism:• chronic hypoperfusion or ischemia in surrounding

brain tissue.(mech weekness &instablity)• vasomotor paralysis of vascular smooth muscle.• neuropeptides in perivascular area• left shift of autoregulatory curve.• complete venous &incomplete arterial

obstruction

Hyperemic complication• Prevention:• Staged removal via embolization• Carotid artery clamping• Barbiturate trt• Treatment:• control ICP- high dose thio• mannitol• hyperventilation• hypotension• hypothermia