Transcript Slide 1

Anesthesia For
Intracranial Vascular
Lesions
BY
DR: AHMED YEHIA,MD
LECTURE OF ANESTHESIOLOGY
FACULTY 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

PATHOPHYSIOLOGY
Causes
Risk
Factors
Classification
Locations
Neuronal 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
Type IV Ehler Danlos syndrome
Over 50 years of age
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
Tuberous sclerosis
Oral contraceptive pills
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
(SAH)
ICP
Unruptured
asymptomatic
Hydrocephalus
Global,focal neurological deficits
Meningeal 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 AUTOREGULATION
Risk of rebleeding proportional to transmural
pressure (MAP-ICP)
MAP
AVOID
CEREBRAL VASOSPASM
Peaks 5-7 days, resolves after 14 days
Angioplasty 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 150-130
Balloon angioplasty
Intraarterial papaverine
HYDROCEPHALUS
Early
IC H
VASOSPASM
CO2
VS
CSF Drainage
VS
Late
BLOOD CSF
Vasospasm
ICP (Rebleed)
Clipping
VS
Coiling
Poor HUNT&HESS
Co 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
temporary clip is placed
on the parent vessel
permanent clip is placed
on the aneurysm neck
temporary clip is removed
from the parent vessel
PHARMACOLOGY
Timing of surgery
Early surgery
reduces the risk
of a further bleed
Late surgery
provide excellent
operating condition
30% of patients
did not survive
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 abnormalities
25-100% of SAH patients
higher in poor grade patients
T wave inversion & ST depression (most
common),
Prolong QT (arterial & ventricular dysrhytmias)
Q waves
Preop echo
serial cardiac enzymes
 invasive haemodynamic
monitoring & treatment
Respiratory system
Most common non-neurological cause of
death in
SAH
Neurogenic Pulmonary oedema
Atelectasis & pneumonia
Aspiration risk (Loss of consciousness)
Pulmonary embolism (immobility)
Fluid status
More than one third of patients have decrease IV
volume
reduced fluid intake, vomiting
diuretic effect of IV contrast
vasodilatory effect of nimodipine
exacerbates vasospasm & cerebral ischaemia
CVP monitoring in poor grade patients
Electrolytes disturbances
Hypopnatraemia
1. Cerebral salt wasting
Secretion of brain and atrial natriuretic peptide
IV volume depletion
Fluid replacement (normal or hypertonic saline)
2. SIADH
Accumulation of excess water with a high CVP
Fluid restriction
Hypokalaemia,Hypocalcaemia &
Hypomagnesaemia
Radiological evaluation
Cerebral Angiogram
Site of the aneurysm
Prepare for intraop positioning, surgical
exposure &monitoring
CT scan
Increase ICP from IC haemorrhage,
hydrocephalous or cerebral oedema
TCD
facilitate vasospasm management.
Monitoring
Standard monitoring
Intra-arterial line preinduction under LA
Central 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 value
affected by the use of volatile anaesthetic
agents.
SSEPS
ANT&POST ANEUYRISM
BAEPS
POST ANEUYRISM
Guide safeTemporary Clipping
Detect burst supression
CBF MONITOR
Jugular venous bulb monitoring has also
not been established and may interfere with
cerebral venous drainage.
Transcranial droppler (TCD)
Premedication
Continue all usual medications
Pre op sedative medications are best
ICP
omitted(Paco2 &CBF)
Sedate
Poor grade patients :
intubated,ventilated & stable
haemodynamic
The principles
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
Transmural aneurysm
pressure
Risk of rupture
Risk of ischemia
Prevent changes in transmural pressure (TMP)
TPMG= CPP = MAP-ICP
Minimise TPMG to reduce risk of rupture
Optimise 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 during
laryngoscopy /intubation
IV narcotics, IV lignocaine
Antihypertensives (e.g labetolol or esmolol)
Ensure full relaxation prior to intubation
Ensure optimal depth of anesthesia
Maintenance 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 2030 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 50mmHg
Monitor cerebral function
Agents
Inhalational, 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 rupture
Management
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)
Antihypertensive (labetolol & esmolol)
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
Postoperative intubation & ventilation:
Higher grades
Intraoperative aneurysm rupture
vertebrobasilar aneurysms
Post op problems are :
Vasospasm (delayed cerebral ischaemia)
Re bleeds
Infarction either due to the clip occluding a
vessels or to thrombosis
Pulmonary complications in high risk
group ICU management & repeat
angiography
Brain Protection
Glucose control
Glucose> 150mg/dl
Intracellular acidosis
Corticosteroids
Barbiturates
decrease ICP, CBF and
BURET SUPPRESSION
Metabolic rate
Hypothermia
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 malformation
Dilated arteries and veins without communicating
capillaries
Feeding arteries Draining veins
AVMs are more common in males than females
Presentation:
hemorrhage
epilepsy
Focal neurological deficit
Peds: hydrocephalus, heart failure
AVM-Hemorrhage
Peak age: 15-20 y/o
10 % mortality; 30-50% morbidity
ICH(80%)/IVH/SAH
Small AVMs are more lethal than larger ones
7% of pts with AVMs have aneurysms
75% are located on major feeding artery
Treatment
Surgery
Stereotactic Radiosurgery
Embolisation
Anesthesia-related Considerations
for Cerebral AVMs
Extensive blood loss
Post-resection NPPB
Occlusive Hyperemia
Rebleeding
Induced Hypotension Safe
Normal Perfusion Pressure
Breakthrough
post-op swelling or hemorrhage
loss of autoregulation CBF
prevent post-op hypertension
BP control SBP< 120mmHg
Pre and intra op BB & good pain control
Diuritics
Occlusive Hyperemia
immediate: obstruction of venous outflow
delayed: venous or sinus thrombosis
adequate post-op hydration