SURGERY FOR

INTRACRANIAL ANEURYSM

ALEX ZONSHAYN MD.

 QUESTION
35 y.o. female developed severe headache and
drowsiness while having sex. The pt. was taken
to the ER, and CT scan showed SAH. Most likely
cause is:
1.Rupture A-V malformation
2.Rupture of small vessel (of no major
importance)
3.Rupture of IA
4.Acute migraine
5.Stroke
 OBJECTIVES
Understanding the incidence and
pathophysiology of aneurysms
Considerations in management of
aneurysms.
Anesthetic management.
New consideration in management of
aneurysms.
 WHAT IS ANEURYSM?
AN ANEURYSM IS AN ABNORMAL
LOCALIZED DILATATION OF ANY
VESSEL.
 PREVALENCE
RECENT STUDY INVOLVING MORE THAN
56,000 PATIENTS FOUND THAT
UNRUPTURED INTRACRANIAL
ANEURYSM OCCURS IN 3.6 - 6% OF
GENERAL POPULATION.
 PREVALENCE
INCIDENTAL INTRACRANIAL ANEURYSM
DISCOVERY AMONG ADULTS
UNDERGOING CEREBRAL
ANGIOGRAPHY IS 0.5-1%.

BETWEEN 1MILLION AND 12 MILLION

AMERICANS HAVE INTRACRANIAL
ANEURYSM
 INCIDENCE
75% of subarachnoid hemorrhages
27,000 Americans/year have ruptured IA,which
is fatal in 14,000 cases.
Each year, new aneurysms develop in at least
2% of patients with previously ruptured
aneurysms.(In this group of patients, the
incidence of aneurysmal rupture is 6 per 10.000
per year.)
12% die before receiving medical help.
40% of hospitalized patients die within 1 month.
More than 1/3 live with major neurologic deficits.
 INCIDENCE
20-25% of all individuals have or will develop an IA during their
lifetime (autopsy series data)
- SAH lifetime incidence 11:100,000
-28,000 SAH cases/year in the US
-Mortality of SAH remains near 50%
-Two major causes of morbidity and
mortality are rebleeding and vasospasm
*Many never reach the hospital
*Of the initial survivors, 20% will rebleed
in the 1st 2 weeks and 50% of those will
die
*40% of pts. with SAH will develop vasospasm,
half of those will become symptomatic
 INCIDENCE

- RUPTURED IA
20% morbidity
20% mortality
-UNRUPTURED IA
4% morbidity
0.2% mortality
 INCIDENCE
Causes of early morbidity :
-cardiac arrhythmia/ hypoxia
-increased ICP
*intraparenchymal hemorrhage
*intraventricular hemorrhage
*hydrocephalus
 CAUSES OF
MORBIDITY/MORTALITY
in survivors of initial bleed
1.Rebleeding
2.Vasospasm
3.Hydrocephalus
 INTRACRANIAL ANEURYSM

IN SPITE OF DIAGNOSTIC,MEDICAL,AND
SURGICAL ADVANCES OVER THE PAST
SEVERAL DECADES,THE CASE
FATALITY RATE FOR ANEURYSMAL
SUBARACHNOID HEMORRHAGE HAS
NOT CHANGED.
 RISK FACTORS
GENETIC
Autosomal dominant polycystic kidney
disease.
Ehlers-Danlos syndrome.
Pseudoxanthoma elasticum.
Hemorrhagic telangectasia.
Neurofibromatosis type1.
Alpha1-antitrypsin deficiency.
Coarctation of the aorta.
Fibromuscular displasia.
Pheochromocytoma.
 RISK FACTORS
OTHER
Age over 50 years.
Female gender.
Cigarette smoking.
Cocaine use.
Infection of vessel wall.
Head trauma.
Intracranial neoplasm/neoplastic emboli.
HTN. (Significance is being studied.)
Alcohol. (Significance is being studied.)
 PATHOLOGY
Aneurysms arising from the intracranial
arteries are much more common then
those arising from extracranial arteries of
similar size.
- ICA have an attenuated tunica media.
-ICA lacking an external elastic lamina.
Thus, the wall of the aneurysm is composed
of only intima and adventitia with minimal
amount of fibrohyaline between.
 PATHOPHYSIOLOGY
CLASSIFICATION:
1.Saccular.
2.Fusiform.
3.Dissecting.
 PATHOPHYSIOLOGY
90% are SACCULAR ANEURYSMS
(berry).
Responsible for most morbidity and
mortality.
Develop at the sites of vessel bifurcation.
(BF is most turbulent and shear forces
against arterial wall are greatest.)
 PATHOPHYSIOLOGY
FUSIFORM ANEURYSMS develop from
tortuous cerebral arteries, most often in
the vertebrobasilar system. Can reach
several centimeters. Patients present with
symptoms of cranial nerve or brain stem
compression. Usually symptoms are not
associated with bleeding.
 PATHOPHYSIOLOGY
DISSECTING ANEURYSMS are the result
of traumatic tear of an artery. They form as
blood courses through a false lumen,
while the true lumen is collapsed upon
itself.
OTHER CLASSIFICATION

1.Small- less then 12mm 78%

2.Large-12-24mm. 20%
3.Giant- 24mm. 2%
CIRCLE OF WILLIS
CIRCLE OF WILLIS
CIRCLE OF WILLIS
 CIRCLE OF WILLIS

-90% occur in the anterior circulation.

-39% occur at the junction of the anterior
communicating artery and anterior
cerebral artery.
-30% located along the carotid artery.
-22% located along the middle cerebral
artery.
 CLINICAL PRESENTATION
Most IA are asymptomatic and undetected until
the time of rupture.
Symptoms of unruptured aneurysm(111 pts):
1.Acute
Severe headache 7
Transient ischemia 7
Seizures 3
Oculomotor nerve palsy/
vision loss 2
 CLINICAL PRESENTATION
Symptoms of unruptured aneurysms(111 pts)
2.Chronic
Noncatastrophic headache 18
Chronic loss of vision 10
Unilateral optic neuropathy 7
Motor weakness/cranial
neuropathy 4
Facial pain 3
ONLY 41% OF ANEURYSMS CAUSED
SYMPTOMS
 WHY DO UNRUPTERED IA
BECOME SYMPTOMATIC?
1.MASS EFFECT. (large or giant)
Symptoms depend on location (headache, cranial nerve
palsy, brainstem dysfunction, visual field defects,
trigeminal neuralgia,
cavernous sinus syndrome, seizures, hypothalamic-
pituitary dysfunction.
2.CEREBRAL ISCHEMIA.
Symptoms referable to vascular territory.
Can be result of embolization of intra- aneurysmal
thrombus.
 RISK OF IA RUPTURE
ISUIA-International study of unruptured IA
(1998).Examinaton of 2,621 pts. records.
Conclusion:
-Aneurysms less then 10mm had an
average annual rupture rate of 0.05%.
-The annual rupture rate for lager IA
approaches 1%.
-Rupture rate was 10 times higher for
IA of a similar size in pts with hx. of
subarachnoid hemorrhage.
 RISK OF IA RUPTURE
FACTORS ASSOCIATED WITH AN
INCREASED RISK OF RUPTURE:
- HTN
- Pregnancy
- Smoking
- Heavy drinking
- Strenuous activity
 IA RUPTURE
Increased ICP
ICP greater than MBP
Bleeding stops with decreased CBF
Decreased consciousness
2 clinical scenarios (typical)
1.Return to normal ICP and CBF with
return of function.
2.High ICP continues with low CBF.
 IA RUPTURE
Increase of intracranial volume due to the
accumulation of blood in the subarachnoid
space leads to increase in ICP
 IA RUPTURE
Increase in ICP produces a reduction of
CPP. The increase of ICP is the factor that
reduces or stops bleeding within the
intracranial space. The clinical
consequence is reduction in
consciousness due to global cerebral
ischemia.
 IA RUPTURE
The ICP rises toward the mean BP,
causing reduction of CBF, followed by
reduction of ICP and increase of CBF.
This leads to improvement of the cerebral
function.
 IA RUPTURE
Persistent increase of ICP with lack of
recovery may be due to:
Alteration in the dynamics of CSF,
caused by thrombi in the basal cisterns.
Cerebral swelling.
Vasospasm.
 IA RUPTURE
The reduction of CPP can produce
ischemia, alteration of auto regulation
and ICP increase due to rupture of the
brain-blood barrier.
 IA GRADING
- Grade 0. Perioperative mortality 0.5%
IA not ruptured
- Grade 1.Perioperative mortality 0-5%
asymptomatic, min. headache, sl. nuchal
rigidity
-Grade 2.Perioperative mortality 2-10%
mod.-severe headahe, nuchal rigidity,
cranial palsy.
- Grade 3.Perioperative mortality 10-15%
somnolence, confusion, medium focal deficits.
 IA GRADING
- Grade 4.Perioperative mortality 60-70%
Stupor, hemiparesis, early decerebrate
rigidity, vegetative disturbances.
- Grade 5.Perioperative mortality 70-100%
deep coma, decerebrate rigidity,
moribund appearance.
CAUSES of morbidity from SAH vs.
time after initial hemorrhage
 VASOSPASM
Abnormal narrowing of arteries
surrounded by blood (focal, segmental, or
diffuse)
 VASOSPASM

Angiographic vasospasm: 40-70% incidence

Clinical vasospasm: 20-30% incidence
Usually associated with aneurysmal SAH
4 11 days post bleed
Result of vasospasm: ischemia and infarction
 VASOSPASM
Vasospasm is the most important cause of
morbidity and mortality after SAH. The
clinical picture of vasospasm is completed
with : increase of headache,
meningismus,
fever, and
tachycardia.
 VASOSPASM

Free hemoglobin - activates cascade

Histamine, serotonin, catecholamines,
prostaglandins, angiotensin, and free radicals
Blood vessel walls abnormal
 VASOSPASM

Treatment
Triple H therapy (hypertensive hypervolemic
hemodilution)
Push blood into narrowed vessels
-Push CO
-Increase BP
Cerebral blood vessels dont have
many alpha/beta receptors
Calcium channel blocker - nimodipine
Early surgery with aggressive removal of
blood/angioplasty
 TRIPLE H THERAPY
Hct 30 35
SBP - 160
CVP 8-10
PAP 15-16
Most common complication is pulmonary
edema.
 TRIPLE H THERAPY
THE SCIENCE BEHINED THIS THERAPY
IS SOFT.
EMPIRICALLY, IT APPEARS TO WORK.
NEW IN VASOSPASM THERAPY

Tirilazad
Antioxidant
Appears to decrease need for HHH therapy in
men
No improved outcome
NEW IN VASOSPASM THERAPY
TAK-044 endothelin antagonist.
Endothelin is potent vasoconstrictor.
Demonstrates small, but statistically
significant reduction in delayed ischemic
deficits.
Hypotension is a side effect.
 NEW IN THERAPY OF
VASOSPASM
Magnesium sulfate therapy revealed a
nonsignificant trend toward improved
neurological outcome.
 NEW IN THERAPY OF
VASOSPASM
Anti fibrinolytics.
Recent results of brief administration of
tranexamic acid prior to early surgery
suggest a decreased rate of rebleeding
without any apparent increase in ischemic
complications.
NEW IN VASOSPASM THERAPY
Vasospasm
Intraventricular SNP used in severe refractory
cases, however effects are highly variable
 REBLEED

14-30 %
Peak incidence first few days post bleed
and second week post bleed
High risk of rebleed during angiography
 REBLEED
ONLY RELIABLE PREVENTION FOR
REBLEEDING IS THE EXPEDITIOUS
PLACEMENT OF A SURGICAL CLIP (OR
ENDOVASCULAR PROCEDURE)
IA WITH HYDROCEPHALUS
Indications for ventricular drainage:
-high clinical grade (grade 3 or higher)
-increased ICP
enlarged ventricles
tight ventricles with diffuse blood
over convexity
-thick subarachnoid clot
CARDIOVASCULAR EFFECTS

ECG abnormalities
Very common
Many changes seen
cannon t-wave, Q-T prolongation, ST changes
Autonomic surge may in fact cause some
subendocardial injury from increased
myocardial wall tension
CARDIOVASCULAR EFFECTS
-Significance of EKG changes associated
with SAH
Originally, EKG changes were thought
to be unrelated to cardiac disease.
Now multiple studies suggest otherwise.
-Normal EKG= No cardiac problems
-EKG changes may have clinical significance
Clinical significance much more likely
with postmenopausal women
CARDIOVASCULAR EFFECTS

Cardiac dysfunction does not appear to

affect morbidity or mortality (studies from
Zaroff and Browers)
CARDIOVASCULAR EFFECTS
SAH induced myocardial dysfunction
Similar to stunned myocardium
-may be caused by massive catecholamine
release
-associated with elevation in CPK-MB
-not associated with CAD but may
occur coincidentally
More common in post menopausal
women
Does not occur in the absence of EKG
changes
Resolves over several week time course
 ENDOCRINE EFFECT
SIADH ( fluid restriction is the mgmt.)
Cerebral salt wasting syndrome
release of naturetic peptide.
hypovolemia, volume contraction, high
urine sodium concentration.
While the clinical distinction may be difficult
mgmt is simple: ISOTONIC FLUID INFUSION
USING INTRAVASCULAR VOLUME AS THE
ENDPOINT.
 ENDOCRINE EFFECT
Dehydration along with hypotension
increases the risk of vasospasm.
 IA SURGERY
AN AREA OF CONTINUING
CONTROVERSY IN THE MANAGEMENT
OF RUPTURED IA IS THE TIMING OF
SURGERY.
 IA SURGERY
Early surgery ( within 48 to 72 hrs. of
hemorrhage )- contemporary mgmnt.
- decreased risk of rebleeding
- allows aggressive mgmt. of vasospasm
- reduces the incidence of medical
complications (DVT, pneumonia)
 IA SURGERY
Disadvantages of early clipping:
- more difficult surg. approach(edema).
- higher risk of intraop. aneurysmal
rupture.
ENDOVASCOLAR THERAPY
Insertion of metallic coils within the lumen
of IA, which are detached after placement.
Then, through the electrothrombosis, a
local thrombus forms around coils within
aneurysm,obliterating aneurysmal sac
Early experience suggests that procedural
risks are low, but the long term
effectiveness has not yet been proven
COILING
COILING
 PERIOPERATIVE ISSUES
- Transport to OR/ Premedication
- The patient with a ventriculostomy
1.CLOSE ventriculostomy prior to
transport
2.If ventriculostomy bag falls to the
floor with the system open to the
pt., fluid will drain rapidly causing
fall in CSF pressure
3.This fall may cause the IA rupture
TEMPERATURE MANAGEMENT
Previously thought that mild to moderate
hypothermia would be protective to the
brain.
- Much animal data to support this.
- Preliminary human data supported this
practice
- Large randomized trial FAILED to
support the use of mild to moderate
hypothermia ( T= 34 degrees ) for
improving outcome following IA clipping
 ANESTHETIC TECHNIQUE

NO DATA TO SUPPORT THE USE OF

ONE TECHNIQUE OVER ANOTHER.
 IA
(MAP ICP)/CVR =CBF

MAP, ICP, and CVR: all can be altered by

anesthesiologist!
 ANESTHETIC GOALS
Avoid abrupt changes in BP
Maint. CBF with normal to high blood
pressure
Be prepared for disaster
 MONITORING
Arterial line preinduction
CVP as indicated ( triple H therapy)
Neurologic monitoring (SSEP, BAER)
 INDUCTION
REBLEEDING IS LETHAL!!!
Careful blood pressure control
Weigh risk of full stomach vs. adequate
depth of anesthesia and relaxation
Titrate induction agent
Blunt response to intubation
 INDUCTION
Thiopental 3-6mg/kg reduces CBF and O2
consumption but does not blunt
hemodynamic response. Need
supplemental agents
Propofol and etomidate good alternates
Succinylcholine controversy .
Beta blockers and vasodilators on hand
 MAINTENENCE
Goals
Cerebral relaxation and protection
Hemodynamic stability
Normovolemia to hypervolemia
Control ICP
and wake up on a dime
 MAINTENENCE
Agents
Inhalational agents, narcotics, oxygen,
N2O controversial
Can increase CBF
Glucose management
Hyperventilation
 BRAIN RELAXATION
Ventriculostomy / spinal drain
Mannitol
Head up position
Mild hyperventilation ( not< 35 p a CO2 )
- Hyperventilation should NOT be used
any longer than absolutely needed.
 BRAIN RELAXATION
Lumbar CSF drainage.
Extremely effective ( to the point that other
techniques are unnecessary).
- avoid excess loss of CSF.
- discontinue drain after clipping
of IA.
 HYPERVENTILATION
pCO2 40 to 80 doubles CBF
pCO2 40 to 20 halves CBF
pCO2 < 20 changes autoregulation and
can lead to ischemia.
 CEREBRAL PROTECTION
Thiopental, 10-15 mg/kg loading dose
followed by infusion @ 15 mg/kg/hr
- Reduce dose with age
- Phenylephrine will likely be needed
- Hypertension may be needed during
temporary vessel occlusion
 FLUIDS
Isotonic or hypertonic solutions

Mannitol
Increase intravascular volume
Effect in 5-15 min. with peak at 30-45
Careful administration in those with reduced cardiac
function
Osmolality has more effect on cerebral edema
than oncotic pressure.
INTRAOP. HEMORRHAGE
Hypotension to control
Temporary clips
Pressure on ipsilateral carotid for anterior
circulation
 INDUCED HYPOTENSION
The choice of agent should be made
based on expertise. ( I prepare nipride drip
and bolus plus deepen anesthesia with
isoflurane).
 EMERGENCE
Anticipate stimulating events
Keep beta blockers and vasodilators on
hand
 EXTUBATION
Decision to extubate made by anesthesia
provider and surgeon
Higher grade bleeds may need to go to
ICU intubated
Depends on the grade of aneurysm
 CONCLUSIONS
Rapid advances in technology and
pharmacology have led to some
improvement in outcome following surgical
or endovascular mgmt. of a ruptured IA.
Much room for improvement remains.
Endovascular mgmt. provides treatment
options for high-risk patients previously
denied treatment.