An introduction to anaesthesia for neurosurgery

Barbara Stanley, Norfolk and Norwich University Hospital, UK

Email: [email protected]

Introduction • Intracranial hypertension

Anaesthesia for neurosurgical procedures requires • Associated conditions or trauma
understanding of the normal anatomy and physiology
of the central nervous system and the likely changes The procedure
that occur in response to the presence of space • Short procedure time
occupying lesions, trauma or infection.
• Great surgical stimulation whilst shunt is
In addition to balanced anaesthesia with smooth tunnelled
induction and emergence, particular attention should
The practicalities
be paid to the maintenance of an adequate cerebral
perfusion pressure (CPP), avoidance of intracranial • Supine position
hypertension and the provision of optimal surgical • Invasive monitoring for burr hole
conditions to avoid further progression of the pre-
existing neurological insult. Postoperative care

Aims of neuroanaesthesia • Rapid recovery and neurological assessment

• To maintain an adequate cerebral perfusion Physiological Principals

pressure (CPP) Cerebral perfusion pressure and the intracranial
pressure/volume relationship
• To maintain a stable intracranial pressure (ICP)
Maintenance of adequate blood flow to the brain is
• To create optimal surgical conditions of fundamental importance in neuroanaesthesia.
• To ensure an adequately anaesthetised patient Cerebral blood flow (CBF) accounts for approximately
who is not coughing or straining 15% of cardiac output, or 700ml/min. This equates to
• To enable rapid return to consciousness to allow approximately 50ml/100g of brain tissue per minute
neurological assessment postoperatively under normal conditions. The brain is contained
within the cranial vault which is non distensible and
General considerations for craniotomy has a fixed volume. Cerebral blood flow is therefore
The patients affected by the pressure within the cranial vault and
• Acute neurological condition or injury possibly a useful measure of this is the cerebral perfusion
with intracranial hypertension pressure, the effective pressure which results in blood
flow to the brain. Cerebral perfusion pressure (CPP)
• Medical therapy – anticonvulsants
is the difference between the mean arterial pressure
• Pre-existing medical problems (MAP) and the sum of the intracranial pressure and
The procedure the central venous pressure (CVP):
• Long operation time CPP = MAP - (ICP + CVP)
• Blood loss Under normal conditions, the ICP remains at 5-12
• Surgical stimulation / brain stem manipulation mmHg, the venous pressure at the base of skull is
zero, and CPP varies with the individual’s MAP. CPP
The practicalities is reduced in the presence of raised ICP, raised
• Position venous pressure or low MAP. Therapeutic measures
• Access (intravenous and access to the airway) to maintain optimal CPP are therefore aimed at
maintaining MAP whilst lowering ICP and avoiding
• Invasive monitoring
venous obstruction or hypertension.
Postoperative care
Autoregulation is the ability of the brain to maintain
• Rapid recovery and neurological assessment stable CBF in the face of a changing MAP/CPP. As
• Balanced analgesia to avoid sedation shown in figure 1, this is achieved by alterations in
cerebrovascular resistance. The calibre of intracranial
General considerations for other procedures vessels alters automatically – vessels dilate if perfusion
e.g. burr holes and shunts pressure is low (or if metabolic activity in one region
The patients is high). Under normal conditions, cerebral blood
• Often extremes of age flow is kept at a stable level over a range of cerebral
perfusion pressures between 50 and 150mmHg.

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 Figure 1: The relationship
between cerebral blood
flow and cerebral perfusion
pressure. CBF is maintained
at a constant value over
a range of CPP (between
50 and 150mmHg) by
alterations in cerebral
vascular resistance.
Decreased CPP causes
vasodilation, increased CPP
results in vasoconstriction.
Conditions such as head
injury disrupt autoregulation
and the relationship
becomes ‘pressure-passive’.

In the presence of a space-occupying lesion (e.g. Flow-metabolism coupling

blood, tumour or oedema), the brain has limited Under normal circumstances, the brain is able to
compensatory ability before ICP increases. To alter the supply of oxygen (by changing blood flow)
avoid a rise in ICP, an increase in the volume of one to specific areas of the brain which have increased
component of the contents of the rigid cranial vault metabolic activity.
must be compensated by a reduction in the volume
Arterial oxygen and carbon dioxide tensions
of another. As the volume increases in the vault (figure
Carbon dioxide tension in the blood has a marked
2), the pressure is initially controlled by a reduction
effect on the cerebral vasculature. A rise in arterial
in CSF and cerebral venous blood volume. Once
carbon dioxide (PaCO2) causes cerebral vasodilation,
this mechanism is exhausted, then small increases
an effect magnified in the presence of a reduced
in volume of the lesion lead to steep increases in
arterial oxygen tension. Cerebrovascular vasodilation
intracranial pressure and eventually may cause
causes an increase in intracranial volume that can
displacement of brain tissue and cerebellar tonsillar
cause coning under circumstances of raised ICP.
herniation through the foramen magnum (coning).

In patients with raised intracranial pressure it is

vital to control the PaCO2 to normal and to ensure
provision of adequate oxygen to avoid hypoxia.

Pathophysiological consequences of injury or

disease
The pathophysiological consequences of injury
depend upon the speed of onset and whether the
compensatory mechanisms are overwhelmed. For
example, a sudden catastrophic increase in ICP due
to intracerebral haemorrhage can cause otherwise
normal tissue to infarct, whereas slow increases due
to hydrocephalus allow compensation, but may give
rise to the symptoms of headache and nausea.
Once CBF falls below 18ml/100g/min, alterations
in cellular activity occur, with intracellular acidosis
Figure 2: As the volume of a space occupying lesion within and cessation of protein metabolism. At less than
the intracranial vault rises, compensatory mechanisms 12ml/100g/min electrical activity ceases and at 8ml/
allow intracranial pressure to remain stable (1). Once these 100g/min cell death occurs.
mechanisms are exhausted, intracranial pressure rises very
sharply (2). Autoregulation in injured parts of the brain is impaired

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 Ketamine
• This NMDA antagonist has traditionally been
avoided because it increases ICP and CBF,
although these effects are less marked if PaCO2 is
controlled to normal levels.
• It is not routinely used for elective neurosurgical
anaesthesia at present, but has gained acceptance
as an appropriate agent for emergency induction
of anaesthesia and maintenance of sedation in
head injured patients, particularly those with
multiple injuries and haemodynamic compromise.
Inhalational agents
• Sevoflurane has less cerebral vasodilatory effects
than other inhalational agents and preserves CO2
reactivity. Also it allows a rapid recovery due to its
lower blood:gas solubility coefficient.
Figure 3: The effects of changes in PaCO2 and PaO2 on
cerebral blood flow. A rise in PaCO2 causes a marked rise
• Desflurane at 1 MAC has been shown to increase
in CBF. Fall in oxygen tension has a little effect on CBF until ICP in patients with supra-tentorial space
PaO2 reaches a value of less than 8kPa. occupying lesions, in contrast to isoflurane.
• Most of the inhalational agents are deemed safe at
concentrations of less than 1 MAC.
and the threshold at which the vasculature can
maintain CBF is elevated, from CPP of 50mmHg • Nitrous oxide increases ICP, CBF and CMRO2.
to 60–70mmHg. Hypoxia and hypercapnia These effects, together with its adverse effect on
cause secondary brain injury through ischaemic closed gas spaces preclude its use, especially in
mechanisms. Hypercapnia causes vasodilation, an trauma patients who may also have undetected
increase intracranial volume, subsequent reduction in chest injury.
CPP, further increase in PaCO2 and a downward spiral Opioids
in blood flow and worsening ischaemia.
• Remifentanil – has a rapid onset and offset which
The effects of anaesthetic agents on cerebral allows titration to counter stimulating events such
blood flow as the application of the Mayfield clamp (see
Most anaesthetic agents reduce neuronal activity and below). A dose dependent fall in MAP and rapid
so reduce the brain’s cerebral metabolic requirement offset mean that a longer acting analgesic agent is
for oxygen (CMR02). They provide a protective required prior to cessation of surgery.
mechanism when oxygen demand may outweigh
supply. Unfortunately, many anaesthetic agents also • Fentanyl and morphine – these agents have little
reduce the mean arterial blood pressure by causing effect on intracranial pressure or blood flow which
arterial vasodilatation with a potentially adverse effect makes them suitable for titration to provide post-
on CPP. operative analgesia.

Thiopentone Neuromuscular blocking drugs

• Causes a dose-dependent fall in CMR02, also a • The non-depolarizing agents do not have an effect
fall in CBF. These effects are useful during on ICP.
craniotomy in the presence of elevated ICP. • Suxamethonium causes a transient rise in ICP, in
• Anticonvulsant properties are advantageous. part due to muscle fasciculation and increased
venous pressure. There may also be a slight
Propofol increase in CMR02 and cerebral blood flow. These
• Similar effects to thiopentone but may preserve considerations must be weighed against the need
autoregulation more effectively. for rapid airway control. Suxamethonium is usually
reserved for emergency anaesthesia rather than
• It is useful for maintenance of anaesthesia elective cases.
and its amnesic and antiemetic properties make it
advantageous for a smooth recovery. Other drugs
Diuretics
• It does cause a fall in MAP which may have
disadvantageous effects on CPP. • Mannitol is a large molecule that will not cross the
intact blood brain barrier. It is useful in the

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 prevention and treatment of cerebral oedema and anticonvulsants, steroids and cardiac drugs, should
it causes a reduction in ICP. It can cause a transient be continued until and including the day of surgery if
rise in cerebral blood volume and this effect can possible. Antiplatelet drugs should be discontinued if
last for up to 20 minutes. It also causes a transient possible, although the risks of stopping these drugs
rise in CVP. The usual dose is 0.5 – 1g/kg. It has the must be considered.
additional effect of haemodilution which is thought
Airway assessment is important because prolonged
to improve blood flow characteristics. If the blood
attempts at laryngoscopy are extremely stimulating
brain barrier is damaged it may worsen raised
and increase cerebral oxygen demand and ICP.
ICP.
Patients are often anxious and a sedative premedication
• Furosemide 1mg/kg produces a reduction in
such as a benzodiazepine can be offered.
ICP to the same extent as mannitol at 1g/kg. It is
advantageous as it also reduces CVP. Conduct of anaesthesia
Induction needs to be smooth and blood pressure
Steroids
maintained near preoperative values to maintain
• Dexamethasone 8-16mg is useful to reduce cerebral blood flow. A bolus of either propofol
cerebral oedema associated with tumours. It is (0.5-1mg/kg) or opiate should be given immediately
less effective for reduction in global oedema. prior to laryngoscopy as this is very stimulating.
Adequate time should be allowed for non depolarising
Anticonvulsants
muscle relaxant to work before intubation is
• For frontal and temporal surgery phenytoin can be attempted.
given as a loading dose, 15mg/kg intravenously,
Once the patient is draped and surgery underway
but should be given slowly as it causes hypotension
access to the airway is very limited, so it is absolutely
and can cause arrhythmias.
vital that the airway is secured reliably, preferably
Drugs to manipulate the cardiovascular system with waterproof tapes. An armoured cuffed tracheal
tube prevents the tube kinking when the patient’s
• a-agonists such as phenylephrine and
head is manipulated, particularly if the patient is to
noradrenaline are used to increase blood pressure
be positioned prone. Meticulous attention to securing
as there are fewer alpha receptors in the cerebral
the tube is vital. A prone patient whose skull is pinned
vasculature. These agents have a selective effect
is very difficult to manage should the tube fall out.
on systemic vascular resistance and cerebral
vascular resistance is relatively unaffected. Intravenous access must be of large bore and reliable
as sudden massive haemorrhage can occur. Invasive
• Clonidine, an α2-antagonist, can be used to treat
arterial monitoring is very useful for reliable minute
hypertension at the start of surgery. It has analgesic
to minute blood pressure assessment and also for
and sedative properties which are a useful adjunct
evaluating arterial blood gasses and haemoglobin
to anaesthesia but these effects must be weighed
levels. Consideration should be given to site the
against the need for rapid emergence at the end of
IV access and arterial pressure monitoring before
surgery.
induction of anaesthesia (although not in children).
Anaesthesia for craniotomy for tumour or
Central venous access is appropriate as a guide to
intracranial bleed
venous pressure and to administer drug infusions.
General considerations
The sitting position is used much less frequently now,
History and examination is important to detect signs
but placement of the tip of a central line in the right
and symptoms such as convulsions, nerve palsies
atrium should be considered for these patients and
and reduced levels of consciousness (assess GCS).
others at risk of air embolus, to allow aspiration of air
Posterior fossa tumours occasionally cause bulbar from the heart should this occur.
palsies and lower cranial nerve lesions which increase
Anaesthesia can be maintained using a volatile
the risk of laryngeal incompetence and thus chronic
agent in air and oxygen or propofol infusion. The
or acute aspiration of gastric contents and hypoxia.
patent’s lungs are ventilated to achieve normocapnia
Subarachnoid haemorrhage can cause massive - normal areas of the brain vasoconstrict secondary
release of catecholamines which can cause acute to hypocapnia and total cerebral blood flow will be
heart failure and malignant arrhythmias. Non-specific reduced inappropriately. Hypocapnia is reserved for
T-wave and ST segment abnormalities may be seen situations where ICP is very high; it may be life saving
on the ECG. in this situation but there can be rebound vasodilation
The patient’s general medical condition must be when normal CO2 levels are achieved subsequently.
stabilised, especially any respiratory or cardiovascular Surgical procedures are often very lengthy and so
disease, as hypoxia, hypercarbia or failure to maintain attention must be paid to patient position, protection
blood pressure will be detrimental, as will uncontrolled of pressure areas, including the eyes, and to ensuring
hypertension. Preoperative medications, especially unrestricted venous drainage from the head.

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The patient must have a urinary catheter for lengthy During surgery, especially posterior fossa surgery,
craniotomy or if diuretics are used. Calf compressors the brainstem may be manipulated, which can cause
help to reduce thromboembolic risk. Core body profound bradycardias. If this occurs, communicate
temperature should be measured, preferably with an with the surgeon to release traction or pressure
oesophageal probe. and treat with glycopyrrolate 200–400 micrograms
(atropine crosses the blood-brain barrier) and allow
During patient positioning in theatre the skull is often
surgery to resume when the heart rate is normal.
pinned into a clamp (a Mayfield clamp) to maintain
optimal surgical positioning. This is stimulating and so Once surgery is drawing to a close the surgeon closes
a pre-emptive bolus of propofol or an opioid should the dura, cranium and scalp, which can take up to 30
be given to prevent a sudden rise in blood pressure. minutes. If anaesthesia is too light the patient may
cough as the head is moved to apply the dressings
Once the skull is open a bolus of diuretic optimises
at the end of surgery. Good communication between
operating conditions if intracranial pressure is
surgeon and anaesthetist will help with timing of
elevated and the surgeon comments that the dura is
paralysis and cessation of anaesthesia. Remifentanil
bulging. Mannitol 0.5mg/kg or furosemide 1mg/kg are
infusion, if available, helps to smooth out the waking
appropriate. Mannitol increases the central venous
and extubation process, but remember to give a
pressure so should be given slowly - especially if the
bolus of longer acting opioid to avoid postoperative
patient’s myocardial function is impaired.
agitation. Whichever agent has been used, aim for a
During the procedure, maintain low normal end tidal smooth extubation with a minimum of straining and
CO2 (around 4.0 kPa), normotension and normal coughing.
oxygen levels. Mild hypotension can help improve
Pain from craniotomy is described as ‘mild to
the surgical field if necessary. Normothermia should
moderate’ and paracetamol and codeine are popular
be maintained, especially if the procedure is long.
analgesics. Non-steroidal anti-inflammatory drugs
Temperature should be allowed to passively drift to
have an anti-platelet effect and should be used
about 35 degrees centigrade if the patient’s cerebral
with caution. Small (1-2mg) boluses of intravenous
blood supply is at risk – for instance during aneurysm
morphine are appropriate for patients in severe
surgery. Allowing the patient to become hypothermic
discomfort. The aim at the end of surgery is to have
has consequences of poor clotting function, impaired
a comfortable, co-operative and lucid patient whose
cardiac contractility and postoperative shivering
neurology can be assessed.
which increases oxygen demand.
Anaesthesia for other neurosurgical procedures
Fluid replacement with glucose-free crystalloid, such
Burr holes
as normal saline or lactated Ringers, is appropriate.
Burr holes are usually performed as an emergency
Hyperglycaemia is associated with worse neurological
procedure in those who have had an extradural
outcome and tight glycaemic control may help improve
haemorrhage (arterial, usually associated with a skull
outcome and avoids lactate accumulation. Hypotonic
fracture) or subdural haemorrhage (venous, may be
intravenous solutions must never be used as they will
chronic especially in the elderly). Patients will usually
exacerbate cerebral oedema.
have:

If the ICP is high during surgery • Altered level of consciousness (measure GCS).
• Raised ICP.
• Place the patient in a slightly head up
position. • Focal neurology, such as a dilating pupil.

• Check there is no neck vein kinking or Other injuries may be present that need consideration.
compression and the abdomen can move Protection of the patient’s cervical spine must be
freely with no diaphragmatic compression. considered.

• Ensure the patient is paralysed. Preoperative interventions include:

• Ventilate without PEEP. • Secure the airway with cervical spine control
if GCS is <9/15 or ventilation is inadequate for
• Ensure the blood pressure is adequate. normal oxygenation and carbon dioxide elimination
• Ensure the PaCO2 is not raised and consider (rapid sequence induction with thiopentone and
reducing it to 4-4.5kPa. suxamethonium is appropriate).
• Ensure the PaO2 is normal. • Maintain normal blood pressure with fluids and
inotropes, using non-glucose containing crystalloid
• Reduce the brain’s metabolic activity – bolus and a-agonists if necessary. Aim for a MAP of
thiopentone 3mg/kg or propofol 1mg/kg, or 90mmHg in adults.
lidocaine 1.5mg/kg if cardiovascularly
unstable . • Nurse the patient 15-30 degrees head up with no
tube tie.

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 • Ventilate the patient to achieve normocapnia and In treatment of hydrocephalus a fine bore tube with a
normoxia. valve is inserted to drain CSF from the dilated ventricle
into the peritoneal cavity.
• Sedate, for example using a propofol infusion
1-3mg/kg/hr. • Patients may be children.
• Insert invasive arterial pressure monitoring • The commonest shunt is from the lateral ventricle
to the peritoneum.
• Monitor the CVP.
• The commonest complication of VP shunts are
Extracranial injuries must be assessed and their infection and blockage.
management incorporated into the definitive treatment • Patients can have an intracranial haemorrhage if
plan. CSF is drained too quickly.
Communication between the trauma team and The procedure is shorter than full craniotomy and
neurosurgical/ICU team is of paramount importance. invasive monitoring is not usually required unless
Other life threatening injuries must be dealt with and the patient is medically unwell. The airway should
stabilised and may occasionally take priority over be secured and attention paid to good oxygenation,
evacuation of an intracranial haematoma. In this normalising PaCO2 and preventing coughing
situation, intracranial pressure must be assumed to and straining – especially during the stimulating
be raised and diuretics and low CO2 may delay brain part of surgery when the shunt is being tunnelled
herniation. Patients are often transferred to regional subcutaneously. As with craniotomy, arrhythmias or
neurosurgical centres, making management of raised bradycardia can occur as the catheter is placed.
ICP even more important. Make sure cross-matched
blood is available Post-operatively the aim is to have an awake and
comfortable patient in recovery that can co-operate
Patients who have a low GCS preoperatively or who with neurological assessment. Paracetamol and
have high ICP intraoperatively should be managed codeine phosphate are the mainstay of analgesia and
in an intensive care unit postoperatively and kept intravenous morphine titrated to effect may also be
sedated and ventilated for 24 hours after surgery. required.
Ventriculoperitoneal (VP) shunt for hydrocephalus Further reading
Hydrocephalus can present acutely with a low GCS,
or chronically with headaches, neurological symptoms • Matta B, Menon DK, Turner JM et al. Textbook
and vomiting. It can result from the overproduction of of Neuroanaesthesia and Critical Care. Published by
CSF (non-obstructive and very rare), blockage of CSF Cambridge University Press, Cambridge, UK
absorption (obstructive, communicating resulting • Clayton T and Manara A. Neurosurgery in the
from arachnoiditis) or obstruction to normal CSF flow Oxford Handbook of Anaesthesia (second edition).
(obstructive, non-communicating). Published by Oxford University Press, Oxford, UK
The author would like to acknowledge the help of Dr Jurgens
Nortje in preparing this article.

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