Anesthesia for cerebral aneurysm repair

Anesthetic
management of
Cerebral Aneurysm
By Dr. Veena Boswal
Under the guidance of
Dr. Poonam Kalra

Definitions
 A cerebral aneurysm is a
cerebrovascular disorder in which
weakness in the wall of a cerebral artery
or vein causes a localized dilatation or
ballooning of the blood vessel
 A common location of cerebral aneurysms
is on the arteries at the base of the brain,
known as the Circle of Willis

Anatomy
 The Circle of Willis is a circle of arteries that
supply blood to the brain
 Components
1. Anterior cerebral artery (left and right)
2. Anterior communicating artery
3. Internal carotid artery (left and right)
4. Posterior cerebral artery (left and right)
5. Posterior communicating artery (left and right)
The basilar artery and middle cerebral arteries,
though they supply the brain, are not
considered part of the circle

Epidemiology
 Exact incidence is unclear but probably about
4%.
 An annual incidence of rupture is about 15-20
per 100,000 population
 Age : At any age but peaks at 40-60 years
 Sex : Male to Female 2 : 3 but more males
below 40 and more females after 40years
 Sites : 30% ICA
40% ACA( Anterior Communicating)
20% MCA
10% Vertebro-basilar systems
 Rupture : 90% <12mm, 5% in 12-15mm, 5%
>15mm

Aetiology
 It had been thought to be a congenital disease but is now
thought to be primarily acquired (although there is a
congenital component in some cases)
 Most are of the saccular or berry aneurysms and
this type of aneurysm is unique to the cerebral circulation
 Rupture is thought to relate to the size of the lesion. This
clearly is due to Laplace's Law T = 2PR and the fact
that the wall also becomes thinner as the aneurysm
enlarges
 The lesions almost always occur at the bifurcation of
vessels . It is thought that the process starts with
degeneration of the internal elastic membrane at the
apex of a bifurcation. This is the site of the
maximum hemodynamic stress
 The pressure within the aneurysm is at systemic levels and
thus rupture is most likely to occur at moments of
raised BP. The larger the aneurysm the greater the
likelihood of rupture, however most rupture when they are
<12mm

Presentation
 The vast majority present with Sub Arachnoid
Haemorrhage
 Occasionally with pressure symptoms related to
direct pressure on nerves, eg. 3, 4, or 6 nerve palsies
 Many are now presenting with incidental findings on
MRI or CT scans
 Those patients who present with a SAH will in fact have
had some type of symptoms in the few days prior to the
major bleed
 Minor bleeds precede the major haemorrhage in 50%
of patients. The patients may have Hypertension
either as the cause or the result of the bleed.
Brainstem ischaemia is thought to be the cause of
the secondary form

Signs and Symptoms
 The Signs and Symptoms of SAH are due to

1. Raised ICP
2. Damage due to intra-cerebral bleeds
3. Regional vasospasm
4. Generalised vasospasm

Continued..
 The Signs and Symptoms are :

1) Result of Initial Rupture : There is an initial abrupt
rise in ICP that produces a severe headache ± loss of
consciousness. Blood in the CSF produces
meningism (photophobia, neck stiffness, and
headache)
2) Focal signs : The most commonly occurs 7 days later
from vasospasm, but if occurring initially may be due to
the direct effects of the jet of blood, intracerebral
bleeding, or from herniation
3) Hydrocephalus : Common, usually due to
impaired CSF passage through the basal cisterns.
Occasionally large basilar aneurysms may produce IV
ventricular obstruction and hydrocephalus

Classification Systems
 Botterell’s Clinical Grading
Grade Criteria
1) Conscious with or without Meningeal Signs
2) Drowsy without significant Neurological
3) Deficit
Drowsy with Neurological Deficit and
probable cerebral clot
4)
Major Neurological Deficit present.

5)
Moribund with Failing Vital Centers and
Extensor Rigidity.

 Modified Hunt and Hess’s Clinical
Grades
Grade Criteria
0) Unruptured Aneurysm
1) Asymptomatic or have mild headache or neck
stiffness
2) Headache and neck stiffness but no
neurological abnormalities other than cranial
nerve palsies

Drowsy, confused or have mild focal deficits
3)

Stuporosed and have moderate or severe
4)
hemiparesis

 World Federation of Neurological
Surgeons Grading

WNFS Grade GCS Score Motor Deficit
1) 15 Absent
2) 14 – 13 Absent
3) 14 – 13 Present
4) 12 – 7 Present or
5) 6 - 3 Absent
Present or
Absent

Diagnosis of SAH
 This is usually on
CT scan (SAH or
haematoma mainly but you may be able to
see the aneurysm on a plain CT
 MRI or CT angiography will have a
much better detection rate
 Ultimately Cerebral Angiography will
be done to determine whether there is an
aneurysm and how it should best be
treated

Management
 An angiogram is done as soon as possible to allow rational
management decisions to be made (aneurysms are not always
demonstrated in presumed subarachnoid bleeds and the absence of
an aneurysm obviously has a major impact on the patient’s
management)

 As the patients who have survived the initial bleed are at
risk of re-bleeding it would seem sensible to repair the aneurysm as
soon as possible. Almost all neurosurgeons will now operate as
soon as is practical except in Grade IV and V patients

 Those with severe vasospasm unresponsive to pharmacologic
treatment may also be clipped to allow the use of more
marked induced hypertension

 Obviously the patient who has a major intracranial bleed with
mass effects or obstructive hydrocephalus (blockage of the
arachnoid villi or the basal cisterns) will require urgent surgery. In
these cases the surgery may be restricted to relieving these
problems rather than the definitive repair

 In case Angiography (and thus definitive
diagnosis of Aneurysm) is delayed due to any
reasons, the intervening period is a dangerous
one with 20% suffering a re-bleed, with a >60%
mortality

 The goals of this period
1. Prevent re-bleeds
2. Prevent or treat vasospasm
3. Detect hydrocephalus
4. Avoid respiratory problems
5. Optimise the general medical state of the
patient

 The patient is confined to bed and they are to avoid
things that may increase their BP eg straining at stool
(given laxatives)
 Their BP control is difficult and depends on their
clinical status. As a rule hypertension should be
controlled however if they have vasospasm a
common treatment is to raise their BP
 If there is no obvious vasospasm then the BP is
controlled on empirical grounds to about 160 systolic and
100 diastolic
 Epsilon aminocaproic acid may be used to prevent
the clot around the aneurysm from being dissolved.
In general it has not proved useful
 Generally the patient’s fluid status needs to be very
carefully assessed and it may be necessary to measure
the CVP, of course the U/O and fluid balance
should be carefully measured
 The prolonged bed rest predisposes to respiratory
problems and these should be aggressively treated

Vasospasm
 It is one of the worst problems in this condition causing
ischaemia and subsequent cerebral oedema that further
compromises the cerebral circulation
 Radiological evidence of large vessel vasoconstriction is
present in about 60-80% of patients
 But is Clinically and hemodynamically significant in 33%
of patients
 The peak incidence is around 7th day from initial event.
 The exact mechanism for it is unclear but appears to be
due to the presence of blood breakdown products .
FFA derivatives such as the prostaglandins and
leukotrienes, oxyhaemoglobin and the oxygen
radicals.

 Clinical Manifestations – Are due to
Cerebral Ischemia:

1. Decrease in Level of Consciousness
2. New Onset of Focal Signs
3. Mutism

 Diagnosis :

1. Confirmed by Angiography
2. Non Invasive TCD USG may be used to
demonstrate increased cerebral artery Flow
Velocities

 Treatment :

1. Pharmacological : Calcium Channel Blockers –
Nimodipine is used. Beneficial effects occur either at
Distal Vessel Site or at a Cellular level

2. Surgical : Early Surgery (within 48 hrs of SAH) with
extensive irrigation of cisterns, removes the causative
agent (blood byproducts) of vasospasm.
Intraoperative cisternal injection of Papaverine may be
done to reduce vasospasm

3. Reduction of ICP : To improve Cerebral Perfusion
and alleviate the ischemic state, reduction of ICP may
be tried in patients with elevated ICP

4. Triple H Therapy : Hypervolaemia, Haemodilution, and
Hypertension
 Hypervolaemia – Increase CVP to 10 mm Hg or PAWP to
12 to 20 mm Hg. Colloids or Crystalloids may be used.
Hetastarch and Dextrans should be used sparingly due to
potential of coagulopathy
 Hypertension – To increase CPP, Vasopressors
(dopamine, dobutamine or phenylephrine) may be used to
titrate the blood pressure level till reversal of symptoms or
to a maximum of SBP of 160 -200 mm Hg in aneurysm
clipped patients and upto 120 – 150 mm Hg in patients with
non clipped aneurysms. The BP is maintained until
vasospasm resolves (usually in 3 to 7 days)
 Hemodilution – Based on correlation of hematocrit and
blood viscosity. The cerebral blood flow improves with
reduction of blood viscosity. Hematocrit of 33% provides
optimal balance between viscosity and oxygen carrying
capacity of blood

Intracranial Pressure
1. ICP rises rapidly after SAH. May also increase from
mass effect of clot, cerebral edema or hydrocephalus
due to blocked aqueduct or communicating
hydrocephalus due to arachnoidal adhesions from
extravasated blood that interferes with reabsorption of
CSF
2. Vasospasm can also exacerbate ICP increase
because the reduction in CBF is accompanied by
vasodilatation of distal vessels
3. ICP correlates well with clinical grade. Normal in Grade
1 or 2 and raised in grade 4 or 5 (Botterell’s grades)
4. Never normalize ICP too rapidly because it leads to a
rapid increase in Transmural Pressure across the
aneurysm wall, thus further increasing chances of
bleeding

 Impairment of Autoregulation : These patients
may have an impaired ability to autoregulate CBF and
the Degree of impairment correlates directly to Clinical
Grade. Thus it is advisable not to allow the Perfusion
pressure to decrease below the lower limit of
autoregulation perioperatively specially in Gradewise
poor patients. Thus it presents a relative contraindication
to Induced Hypotension in these patients

 Reactivity to CO 2 : Cerebrovascular response to
Hyperventilation is generally preserved after SAH . Thus
hyperventilation remains effective in reducing CBF
during perioperative management in these patients

Pre-operative Assessment
 These patients need very careful pre-op assessment

1. CVS : Baseline BP (to give some idea of the safe level of
hypotension)
Fluid Status (the fluid balance of these patients is very
important, they should not be overloaded otherwise they may
develop CCF but if they are dry, cerebral circulation maybe
compromised and vasospasm, if present, may be rendered
haemodynamically significant.
If hyponatremia is allowed to develop cerebral oedema may result

2. RESP : Prolonged bed rest runs the risk of atelectasis and
pneumonia if this is present, it should be cleared to the patient prior
to surgery. Patients with COPD may also need a higher FiO 2 intra-
op

3. CNS : A simple pre-op assessment will help in the rapid post-op
assessment of the patient. Pupil size, gross motor weakness,
presence of aphasia and any specific cranial nerve signs are
sufficient
4. GEN : As for any pre-op examination

Pre-op Tests
1. Blood Biochemistry : Electrolyte abnormalities are
common and should be corrected pre-op. Renal functions
should be assessed as this be a consideration in reducing the BP if
induced hypotension is used. Blood Sugar should be normalised
as hyperglycaemia has been shown to worsen neurological deficits
in the presence of cerebral ischaemia
2. CBC : Anaemia should be corrected pre-op
3. Coags : INR/APTT

4. ECG: This should be done on the day prior to surgery as these
patients have a high incidence of ECG abnormalities and these are
changeable over the time that surgery is delayed

5. CXR : As a general assessment of RESP and CVS pathology

6. Echo : Patients with questionable cardiac function should have a pre-
operative echocardiography

7. Other tests may be indicated in specific situations

Pre-Medication
 Adequate Explanation is the Best
Premedication.
 Aim of pre-med is to alleviate anxiety to prevent
shooting of blood pressure
 In general, pre-med is best omitted to allow
accurate assessment of patient’s pre-op
neurologic status
 In patients with Elevated ICP pre-medication
with barbiturates or narcotic should be used
judiciously to prevent respiratory depression and
hence hypercapnia induced increases in CBF
 In very anxious, grade 1 SAH patients, titrated
doses of sedatives might be used till anxiety is
relieved

Radiological Management of
Aneurysms
 Angiographic Coiling of an Aneurysm
 Usually done under GA
 Coiling works by placing extremely coiled material inside
the Aneurysm. The material coating the coils is
extremely thrombogenic and the aim is for the aneurysm
to thrombose and a new intima to grow over the inlet of
the aneurysm. A variable number of the coils are placed
until the aneurysm is full of them
 The usual anaesthesia is similar that for operative
neurosurgery with relaxation, intubation and ventilation
 The patients will develop a diuresis from all the contrast
material and should be catheterised after induction

 Risks of Angiographic Coiling:
1. The aneurysm may rupture with the angiographic
manipulation
2. Secondly part of the coil could embolise out of the
aneurysm into a more distal artery
3. The thrombus formation may extend out of the
aneurysm and cause thrombus formation in the
feeding vessels

Aneurysm rupture is uncommon and can vary from a
small leak to a full-blown rupture. Rupture can usually
be controlled angiographically but if this fails the
patient may need to go to theatre.
It is imperative however not to let the BP become elevated
and BP should be controlled with Propofol in the first
instance. DO NOT used vasodilators to control the
BP.

Intra-operative Anaesthesia
Principles
 The principles are :

1. Avoid increases in transmural aneurysm pressure

2. Provide good conditions for the aneurysm surgery
a) "slack" brain

b) Reduce aneurysmal pressure during clipping by
i) Induced hypotension
ii) Surgically by Temporary clips

3. Avoid damage to the brain

Monitoring
1. CVS : ECG, Arterial line (IBP), CVP (cubital fossa)
2. RESP : SpO2, End tidal CO2, oesophageal stethoscope
3. NEUROMUSCULAR : Train of 4 (by PNS) (it is
essential that these patients do not move)
4. CNS : Either BIS/EEG or EPs
5. RENAL : U/O, all these patients are catheterised the
U/O provides an indication that the diuretics are
working

Induction
 Principle of Induction is that rises in BP and falls
in ICP should be avoided at this stage as that
increases the transmural aneurysm pressure (the
pressure in the aneurysm is at arterial levels) and makes
rupture more likely; this is a disaster if it occurs
 Thiopentone (5-6 mg/kg) or carefully titrated Propofol
(1.5 – 2.5 mg/kg) may be used. These tend to reduce
CBF and hence ICP
 Narcotics ( sufentanyl, fentanyl, remifentanyl) tend to
increase ICP ( due to autoregulation mediated
compensatory cerebral vasodilation in response to
systemic hypotension)
Thus Normotension should be ensured before their
usage. Their Combination with Thiopentone is safe as
the opposing effects on ICP usually cancel each other.
Mild Hyperventilation may be instituted in patients with
elevated ICP.

Continued..
 Succinylcholine is often used for muscle relaxation for
intubation (found to be clinically safe although
theoretically it increases ICP)
 Atracurium (hypotension) and Pancuronium (tachycardia
and hypertension) are associated with Hemodynamic
disturbances and hence avoided
 Vecuronium might be used but long latency obviates its
use
 Rocuronium, due to short latency may be the NDMR of
choice in Neurosurgical Anaesthesia
 Complete muscle relaxation should be ensured using
PNS before attempting laryngoscopy

Laryngoscopy and Intubation
 Prophylaxis against BP rise during laryngoscopy may be
given in form of High dose Narcotics, Beta adrenergic
antagonists, IV or Topical Lignocaine, Second dose of
Thiopentone( 1-2 mg/kg), high MAC Isoflurane
 IV adjuncts best for poor SAH grades
 Deep Inhalational anaesthetics may be used in good
SAH grades but Avoided in those with increased ICP
 Laryngoscopy and Intubation should be smooth. If
unacceptable rises in BP are encountered, attempt is
aborted and resorted back to mask ventilation along with
deepening of anaesthesia until it is safe to try again

Maintainance
 Maintenance best with Nitrous, Remifentanil (due to
short duration of action), and a Propofol infusion.
 Avoidance of inhalational agents and the use of an
intravenous agent that causes cerebral
vasoconstriction helps to optimise cerebral conditions.
 BP should be kept within previously defined limits
according to the patient’s baseline BP. Target is usually
20 mm Hg below baseline
 Prior Beta blockade is preferable to reduce reflex
tachycardia due to hypotensive agents, to reduce the
total requirement of hypotensive agents and to reduce
rebound hypertension once the hypotensive agent is
discontinued
 Mannitol (1.5 gm/kg) combined with Frusemide
(0.3mg/kg) is given to shrink the brain and provide good
operating conditions. It takes about 1 hour for the
maximal effect so the mannitol should be started soon
after the BP has settled down from intubation

Critical Periods
 Securing of head with Mayfield pins
 Skin Incision
 Periosteal Flap elevation and Bone
cutting.
These stimuli might cause an increase in
BP and hence a preemptive bolus of
Narcotic or Propofol is advised before
these

Induced Hypotension
 As the pressure inside the aneurysm is at arterial levels
it is usual to induce hypotension during the time of
dissection and clipping
 It has been found that the aneurysm and it's
vascular tree are more mobile at MAPs of around 50
mmHg
 In general cerebral autoregulation preserves flow at
MAPs of 50 mmHg (providing that there is not raised
ICP) but in patients with pre-existing uncontrolled
hypertension this lower limit may be considerable raised
 It is important that the MAP is measured at the level of
the brain and not some point below this (due to very low
margin for error)

 The usual thing to do is to reduce the MAP to about 60
mmHg as they are approaching the aneurysm and only
go to 50mmHg with clipping
 Usual choice of agents is between Nitroglycerine and
Sodium Nitroprusside with a prior beta blockade

Hypothermia
 As the survival of tissues has been shown to
be prolonged by profound hypothermia (20-
25°C) it was felt that this might be beneficial in
this type of surgery
 Very rarely used these days
 Reasons:
1. For the average case it did not seem to cause
a decrease in the mortality ( because there
usually is no problem with adequate blood
supply as the degree and period of
hypotension is not usually great)
2. It increases the incidence of post-op
vasospasm

Post Clipping
 Once the aneurysm is clipped the BP is raised to
the pre-op level. This should be done slowly
over about 10 mins
 All the fluid loss including calculated insensible
losses should be replaced prior to the end of
surgery unless there was marked Cerebral
Oedema pre-op
 The maintenance of adequate filling pressures
and BP will help prevent vasospasm becoming
clinically significant

Reversal
 The patient is not extubated until they are awake
and breathing well
 BP should be controlled with Propofol or
Narcotics infusion
 Further agents to control BP (B blockers,
diazoxide) during extubation might be used if
infusions are found unsatisfactory
 If Remifentanyl has been used then Fentanyl
(50-100µg) should be given after the patient is
awake and appears neurologically normal

Post Operative Management
 The patients should be assessed in the recovery ward
prior to their return to ICU as there may be need to re-
operate if major new neurological signs have occured.
 The worries post-op are
1. Vasospasm
2. Re-bleeds
3. Infarction either due to the clip occluding a vessel or
to thrombosis
4. In the higher risk groups there may be continual
decreased level of consciousness and the usual
complications occur, eg pulmonary oedema
 Post op the Fluid status needs to be very
carefully looked at with enough fluids given to
maintain an adequate U/O but not to much as to
cause cerebral or pulmonary oedema
 Close eye kept on their Electrolyte status as
hyponatraemia (causes cerebral oedema)

 If new neurological deficits are
encountered some time after an
apparently successful surgery, CT scan is
done to rule out Hematoma

 If normal, Angiography needs to be done
to diagnose Vasospasm.Then the BP is
raised until the neurological deficit goes
or an arbitrary limit is reached

Conclusion
 Because of the systemic effects and surgical
requirements, patient with cerebral aneurysms
present a unique challenge to anaesthesiologist.
As an anaesthesiologist we should have a
thorough understanding of pathophysiology of
SAH, a communication with the neurosurgeon
regarding approach, a formulation of an
anaesthetic plan and its implementation. There
will always be patients who despite our best
efforts, fail to benefit from the surgical
procedure, however with proper planning optimal
results can be hoped for.

Anesthesia for cerebral aneurysm repair

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