Anesthesia For Intracranial Vascular

Lesions

BY DR: AHMED YEHIA,MD

LECTURE OF ANESTHESIOLOGYFACULTY OF MEDICINE-AIN SHAMES

UNIVERSITY

OBJECTIVES Epidemiology

Understand pathophysiology of aneurysms

Presentation of I.C aneurysms

complications of I.C aneurysms

Recognize the different treatment modalities of intracranial aneurysms

Understand the basic anesthetic management of intracranial aneurysm clipping

Select an anesthetic plan utilizing medications and or therapies designed to reduce brain injury during cerebral aneurysm repair.

EPIDEMIOLOGY

Incidence : 1 to 6% Incidence of ruptured aneurysm:

12/100,000 Age: any age, peaks 40 - 60 Sex: M/F 2:3 Sites : 30% ICA 40% ACA 20% MCA,10% Vertebro-basilar

systems

PATHOPHYSIOLOGYCausesRisk FactorsClassificationLocationsNeuronal injury and death

Causes Intracranial aneurysms are most likely

to develop over the course of an individual’s life, with only 10%accountable to a genetic/familial cause, it is primarily acquired 90%.

RISK FACTORS Inherited RF Others

Polycystic kidney disease Over 50 years of age

Type IV Ehler Danlos syndrome Female gender

Pseudoxanthoma elasticum Smoking

Neurofibromatosis type 1 Infection of vessel wall

Alpha 1 antitrypsin deficiency Head trauma

Coarctation of the aorta Septic emboli

Fibromuscular dysplasia Hypertension

Pheochromocytoma Alcohol abuse Klinfelter’s syndrome Oral

contraceptive pills Tuberous sclerosis hypercholesterolemia

CLASSIFICATION True or false By size: Small: ≤ 10mm Large: 11 to 25mm Giant: > 25mm

By shape: –Saccular

–berry aneurysm

–Fusiform

LOCATIONS

NEURONAL INJURY AND DEATH

Brain Ischemia Global Focal

Hypoperfusion contains tworegions

Vasospasm. 1st region receives no blood flow.

2nd receives collateral flow and is partially ischemic.

ISCHEMIA INDUCED NEURONAL CHANGES

Early is excitotoxicity.

Delayed Is death caused by apoptosis

PRESENTATION OF I.C ANEURYSMS

Ruptured Unruptured

(SAH) asymptomatic

ICP Hydrocephalus

Global,focal neurological deficitsMeningeal irritation (initially may be due

intracerebral bleeding, or from herniation).

NEUROLOGICAL COMPLICATIONS

Rebleeding

Vasospasm

Hydrocephalus

Seizure(seizure prone for 18 months after SAH)

Aneurysmal Rebleeding:Risk : 4% during the first 24 hrs and then 1.5%

per day Intraoperative 7%High mortality (78%)

IMPAIRED AUTOREGULATIONRisk of rebleeding proportional to

transmural pressure (MAP-ICP)MAP AVOID

CEREBRAL VASOSPASM

Peaks 5-7 days, resolves after 14 daysAngioplasty vasospasm 70%,symptoms

30%Transcranial droppler (TCD) blood

velocity changes

cerebral ischaemia & infarction

Presentation Reversability

Severity frequancy

Management:

Triple H therapy + Nimodipine

↑ perfusion pressure & ↓ blood viscosity → CBF ↑

SBP 120-150 mmhg in unclipped 160-200 mmHg in clipped

aneurysm. CVP 8-12mmHg HCT 30-35%

Nimodipine

V.D OF Collarerals Ca influx

60mg orally every 4 hours, continued for 21days.

I.V 1mg/h up to 2mg/h after 6 h

SBL.P NOT LESS THAN 150-130Balloon angioplastyIntraarterial papaverine

HYDROCEPHALUS

Early Late

IC H VASOSPASM BLOOD CSF

CO2 VS

Vasospasm CSF Drainage VS

ICP (Rebleed)

CoilingClipping VS

Poor HUNT&HESSCo morbidity

Basilar Artery

Surgical Treatment- Clipping

Aim: isolate the weakened vessel area from the blood supply

Direct Clipping

When the surgeon can visualize the surrounding structures, parent vessel and perforators and when the neck is soft

Temporary Clipping

SURGICAL PHARMACOLOGYtemporary clip is placed

on the parent vessel permanent clip is placed on the aneurysm neck temporary clip is removed from the parent vessel

Timing of surgery Late surgery

reduces the risk of a further bleed

provide excellent operating condition

30% of patients

did not survive

Early surgery

SYSTEMIC EVALUATION

CVS complications of SAH sympathetic cathecolamine release

posterior hypothalamus injury

systemic and pulmonary hypertension, cardiac arrhythmias,

myocardial infarction, and pulmonary oedema.

cardiogenic shock. Investigations may reveal an abnormal ECG and elevated cardiac troponin levels.

Management is mainly supportive (inotropes, ventilation), and cardiac dysfunction is reversible in most cases

ECG abnormalities25-100% of SAH patientshigher in poor grade patientsT wave inversion & ST depression (most common),

Prolong QT (arterial & ventricular dysrhytmias)Q waves

Preop echoserial cardiac enzymes

invasive haemodynamic monitoring & treatment

Respiratory systemMost common non-neurological cause of

death inSAHNeurogenic Pulmonary oedemaAtelectasis & pneumoniaAspiration risk (Loss of consciousness)Pulmonary embolism (immobility)

Fluid statusMore than one third of patients have decrease IVvolume

reduced fluid intake, vomitingdiuretic effect of IV contrast

vasodilatory effect of nimodipine

exacerbates vasospasm & cerebral ischaemiaCVP monitoring in poor grade patients

Electrolytes disturbancesHypopnatraemia

1. Cerebral salt wastingSecretion of brain and atrial natriuretic peptideIV volume depletionFluid replacement (normal or hypertonic saline)2. SIADHAccumulation of excess water with a high CVPFluid restriction

Hypokalaemia,Hypocalcaemia &Hypomagnesaemia

Radiological evaluationCerebral AngiogramSite of the aneurysmPrepare for intraop positioning, surgical exposure &monitoring

CT scan Increase ICP from IC haemorrhage, hydrocephalous or cerebral oedemaTCD facilitate vasospasm management.

MonitoringStandard monitoringIntra-arterial line preinduction under LACentral venous catheter for CVP monitoring

Fluid status & resuscitation, post op Triple H therapy

The use of neurophysiological monitoring, such as evoked potentials,EEG, has not been shown to improve outcome.

poor predictive valueaffected by the use of volatile anaesthetic

agents.

SSEPS ANT&POST ANEUYRISM

BAEPS POST ANEUYRISM

Guide safeTemporary Clipping

Detect burst supression

Jugular venous bulb monitoring has also not been established and may interfere with cerebral venous drainage.

CBF MONITOR

Transcranial droppler (TCD)

PremedicationContinue all usual medications

Pre op sedative medications are best

ICP

omitted(Paco2 &CBF) Sedate

Poor grade patients :intubated,ventilated & stable

haemodynamic

Avoid increases in transmural aneurysm pressure

Provide good conditions for the aneurysm surgery

a) "slack" brain b) reduce aneurysmal pressure during clipping

• Induced hypotension• Temporary clips

Brain protection

The principles

Transmural aneurysm pressure

Risk of rupture Risk of ischemia

Prevent changes in transmural pressure (TMP)TPMG= CPP = MAP-ICPMinimise TPMG to reduce risk of ruptureOptimise CPP to prevent ischemia

Maintain BP at pre op levels until the aneurysm is secured

↓ BP by 20-30% tolerable in good grade

patients but not in poor grade patients (with ICP ↑& CPP ↓)

HOW TO DEAL?Prophylaxis against increased BP

duringlaryngoscopy /intubation

IV narcotics, IV lignocaineAntihypertensives (e.g labetolol or

esmolol)Ensure full relaxation prior to intubation

Ensure optimal depth of anesthesiaMaintenance of anesthesia

IV technique (TIVA/TCI) Low

dose volatile agents< 1 MAC

+ Opoiod Infusion

Highly stimulating interventions:

placement of the pin head holder raising of the bone flap

dural incision, skin incision & closure

• bolus dose of anaesthetics (propofol, thiopentone)

• antihypertensives (esmolol, labetolol)

• IV narcotics

slack brain

TPMG= CPP = MAP-ICP

ICP AVOID

TILL DURA OPENED

sudden ↓ICP precipitates aneurysm rupture

HOW TO DEAL?Lumbar Subarachnoid Catheter(Amount accutely drained should not

exceed 20-30 ml)

Hyperventilation↓ CBF AVOID ISCHEMIA

(mild hypocapnia (PCO2 30-35mmHg) prior to dural opening & moderate hypocapnia (PaCO2 25-30mmHg) if needed after dural opening)

Mannitol(Osmotic diuresis & decrease CSF

production)IV infusion (1.5gm/kg), over 20 min

fluid overload & pulmonary oedema

Furosemide(0.3mg/kg) may be given with mannitol

Reduce aneurysmal pressure during clipping

•Induced hypotension•Temporary clips

Decrease TMP (wall stress) of the aneurysm

No longer used routinely

impair global perfusion risk of vasospasm Facilitate dissection &

clip placement

degree of hypotension…… MAP 50mmHgMonitor cerebral function

AgentsInhalational, SNP,GTN, Esmolol & Metaprolol

Temporary Surgical clipping

Of artery feeding the aneurysm

Risk of regional cerebral ischaemia

Duration should not exceed 20 min (monitor clamp time)

BP maintained at high normal or slightly above baseline to ensure adequate

collateral blood flow

Fluid therapy

Maintain normovolaemic until the aneurysm isclipped

Maintain adequate filling pressures & BP prevent postop vasospasm

Fluid therapy according to blood loss, urine output,CVP & PCWP

isotonic balance salt solutions (Normal saline)

Avoid IV solution containing glucose

Intraoperative aneurysms ruptureManagement

Volume resuscitation to maintain normovolaemia

Temporary occlusion of cerebral arteries proximal &distal to the aneurysm(preferred technique)

BP management↓ MAP to 40-50mmHg(risk profound cerebral ischaemia.when temporary occlusion is not possible)

Emergence

Rapid to allows neurologic assessment

Prevent post op hypertension (cough)

opioid infusion

IV lidocaine, or in ET tube PONV prophylaxis!

post op pain treatment BP 10-20% > baseline in patients at risk of cerebral vasospasm

Antihypertensive (labetolol & esmolol)

Postoperative intubation & ventilation:Higher grades

Intraoperative aneurysm rupturevertebrobasilar aneurysms

Post op problems are :

Vasospasm (delayed cerebral ischaemia)

Re bleeds

Infarction either due to the clip occluding avessels or to thrombosis

Pulmonary complications in high risk group ICU management & repeat angiography

Brain Protection

Glucose control

Corticosteroids

Barbiturates BURET SUPPRESSION

Hypothermia

Glucose> 150mg/dl Intracellular acidosis

decrease ICP, CBF and Metabolic rate

Etomidate or propofol alternatives, more hemodynamic stability

Moderate hypothermia determined to be protective in some animal studies (33-35 degrees)

Mild hypothermia (35.5) found to improve outcome but not statistically significant

Deep hypothermic arrest for giant aneurysms

PHARMACOLOGY OF CEREBRAL PROTECTION

Thiopental Propofol Fentanyl, Sufentanil, remifentanyl Etomidate Isoflurane, Desflurane Rocuronium, vecuronium, vs

atracurium, cisatracurium

ADJUNCTIVE PHARMACOLOGY OF CEREBRAL PROTECTION

Ma gnesium sulfate Methylene Blue Anti epileptic drugs Free radical scavengers Antioxidants (Tirilazad) Dexmedetomidine

Arteriovenous malformation

congenital vascular malformationDilated arteries and veins without communicating capillaries

AVMs are more common in males than femalesPresentation: hemorrhage

epilepsyFocal neurological deficit

Feeding arteries Draining veins

Peds: hydrocephalus, heart failure

AVM-Hemorrhage

Peak age: 15-20 y/o10 % mortality; 30-50% morbidityICH(80%)/IVH/SAH

Small AVMs are more lethal than larger ones

7% of pts with AVMs have aneurysms75% are located on major feeding artery

SurgeryStereotactic RadiosurgeryEmbolisation

Treatment

Anesthesia-related Considerations for Cerebral AVMs

Extensive blood lossPost-resection NPPB

Occlusive Hyperemia

RebleedingInduced Hypotension Safe

Normal Perfusion Pressure Breakthrough post-op swelling or hemorrhage loss of autoregulation CBF prevent post-op hypertension

BP control SBP< 120mmHgPre and intra op BB & good pain controlDiuritics

Occlusive Hyperemia immediate: obstruction of venous outflow delayed: venous or sinus thrombosis adequate post-op hydration