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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 lakh
persons/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& morbidityin
relation 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,T
inversion,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, &adq
of 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 til
term
• Caeserean / vaginal delivery has no influence on
meternal or fetal outcome
Grading system for AVM
Spetzler &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