Date post: | 24-Dec-2015 |
Category: |
Documents |
Upload: | joseph-mckinney |
View: | 299 times |
Download: | 0 times |
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