neuroanesthesia

DR ALAA HUSSEIN ALTAEI

CONSULTANT ANESTHETIST
 Cerebral Blood Flow (CBF)
The normal cerebral blood flow is
approximately 50ml/100g/min or 700
ml/min, which is roughly 14 % of the
cardiac output.
This ranges from 20ml/100g/min in
white matter to 70ml/100g/min in
grey matter.
 CBF = CPP / CVR

• Cerebral Blood Flow = Cerebral Perfusion

Pressure / Cerebrovascular resistance
•
 Cerebral Perfusion Pressure
CPP = CBF X CVR (Compare BP = CO X SVR)
•
Cerebral perfusion pressure (CPP) is defined as
the difference between mean arterial pressure
(MAP) and intracranial (ICP) or central venous
pressures (CVP), whichever is the highest. MAP
is the diastolic pressure plus one third of the
pulse pressure (difference between the systolic
and diastolic).
CPP = MAP – ICP (or CVP, whichever is the
highest)
 Cerebral Perfusion Pressure

– CPP is effective pressure that drives blood flow

to the brain
– CPP = MAP - ICP or CVP (whichever is greater)
– normal CPP = 80-100 mmHg
– normal ICP = 5-12mmHg
– Moderate to severe increases in ICP
(>30mmHg) can significantly compromise
CPP and CBF even in the presence of normal
MAP
•
Cerebral Perfusion Pressure
 Effects of chemical factors on CBP
• Carbon dioxide can have a significant influence on CBF. As
the arterial pCO2 rises, vasodilatation increases CBF and
when CO2 is reduced vasoconstriction occurs. When
PaCO2 is less than 3.3kPa (25 mmHg) there is no further
reduction in CBF. Therefore there is no advantage in
inducing further hypocapnia as this will only shift the
oxygen dissociation curve further to the left, making
oxygen less available to the tissues.

Arterial pO2 has a minimal effect until pO2 drops below

6.7 kPa (50 mmHg), when CBF increases significantly.
,
 Cerebral metabolic rate for oxygen
(CMRO2)
• This is the volume of O2 metabolised by the
brain and is normally around 3.5
ml/100g/min or roughly 50 ml/min (20% of
total basal requirements).
It can be calculated using the Fick principal
and equals CBF X arteriovenous O2 content
difference.
ICP depends on the volume of the intracranial contents: normally 1.4 kg brain, 50-70 ml blood
and 50-120 ml CSF.

Normal ICP is 7-17 mmHg (1-2kPa)

 Management of raised intracranial pressure

• Airway
Intubate, if not already done so.
Cervical spine protection (trauma patients) with in-
line immobilization.
Avoid tight ETT ties as this will hamper venous
drainage
Breathing
IPPV with hyperventilation to arterial PaCO2 4 - 4.5
kPa.
Maintain SpO2 > 96% and PaO2 > 12 kPa
Avoid coughing with sufficient sedation and muscle
relaxation
 Management of raised intracranial
pressure
• Circulation
Hypotension is the biggest cause of secondary brain
injury and should be treated aggressively.
Maintain CPP > 70 mmHg (MAP > 90), with fluid
initially and commence vasopressors if necessary.
Invasive arterial blood pressure and central venous
pressure monitoring.
Urinary catheter to monitor urine output and
especially if mannitol is used.
 Management of raised intracranial
pressure
• Drugs
Adequate sedation, propofol infusion
Muscle relaxation
Mannitol 0.25 – 0.5 g/kg
Hypertonic saline (NaCl 3%) 1 – 2 ml/kg
Thiopentone may be considered in severe cases
Paracetamol for raised temperature
Exposure
Maintain normothermia and especially avoid
hyperthermia as this will increase the CMRO2. Mild
hypothermia may be protective, but extreme levels will
exacerbate a coagulopathy and bleeding. A 30o head-up
position will improve venous drainage.
 Management of raised intracranial
pressure
• Fluids
Maintenance fluids should be given judiciously, so as not to
exacerbate cerebral oedema. Isotonic saline is preferred to
glucose containing solutions, aiming to keep the serum sodium
above 135 mmol/l.
Glucose
Maintain normoglycaemia with insulin if necessary.
Haematology
Ensure that haemoglobin is adequate to optimize the
oxygen content of blood. Correct any coagulopathy in event of
intracranial bleeding.
 Management of raised intracranial
pressure
• Investigations
Urgent CT scan for neurosurgical review.
Routine blood tests including, FBC, clotting
studies, U&Es, arterial blood gas and cross-
match blood for theatre.

•
-Effects of anesthetic agents Methods to acutely
decrease intracranial pressure (ICP) include:
• -head up position -deliberate hyperventilation -
barbiturates/sedatives -osmotic and/or renal tubular
diuretics/ hypertonic saline* -CSF drainage.
• Anesthetic Agents Propofol Propofol was originally
recommended with caution because of its potential
to decrease mean arterial pressure (MAP) and thus,
cerebral perfusion pressure (CPP). It is now
recognized as a useful agent in neuroanesthesia,
particularly for induction, sedation or as a
component of total intravenous anesthesia (TIVA). It
produces a decrease in CBF, cerebral metabolic rate
(CMRO2), and ICP.
 Intracranial Hypertension
•  Defined as a sustained increase in ICP above
15mmHg.
•  Uncompensated increases in tissue or fluid
within the rigid cranial vault produce sustained
ICP elevations.
•  If ICP exceeds 30 mmHg, CBF progressively
decreases and vicious circle is established:
ischaemia causes brain oedema, which
increases ICP hence more ischaemia
• . Cycle continues – pt dies of progressive
neurological damage or catastrophic herniation
 Cerebral Oedema
•  Increase in brain water content- produced by
several mechanisms:1)Vasogenic  Disruption
of BBB. Most common & allows entry of
plasma-like fluid into the brain.
•  Causes Mechanical trauma, inflammatory
lesion, tumours, hypertension &infarction.
2)Cytotoxic  Following metabolic insults-
hypoxaemia or ischaemia, results from failure
of brain cells to actively extrude sodium &
progressive cellular swelling.
•
 Treatment
•  Directed at underlying cause.
•  Metabolic disturbances are corrected &
operative intervention undertaken whenever
possible.
•  Vasogenic oedema (tumours) responds to
steroids (dexamethasone). A single 10 mg dose
can significantly increase blood glucose
concentrations in non-diabetic patients.
•  There is evidence to support tight glycaemic
control in critically ill, neurologically impaired
patients
•
 Treatment
• Fluid restriction, osmotic agents & loop
diuretics usually effective in temporarily
decreasing oedema.
•  Moderate hyperventilation (PaCo2 30-33) –
may aggravate ischaemia in patients with
focal ischaemia
• . Mannitol 0.5-1gm/kg effective in rapid
reduction in ICP
 drugs
• Concentrations of 1.5 MAC or higher may
increase CBF and thus, cerebral blood
volume. Emergence from anesthesia with
desflurane is more rapid than with
isoflurane it may be preferred in patients
undergoing prolonged procedures.
 drugs
• Desflurane This volatile anesthetic agent has
effects similar to isoflurane on CBF and ICP.
Sevoflurane This agent also has similar effects
on CBF and ICP yet onset and emergence from
anesthesia is more rapid. Sevoflurane has a
"less noxious" smell and can be used more
efficiently for mask inductions in children and
adults.
• . Remifentanil The profound hemodynamic
control and ultra-short half-life of remifentanil
have made it an attractive agent for
neuroanesthesia.
 Monitoring
• Monitoring in neuroanesthesia now includes cerebral
oximetry as well as neurophysiologic techniques
such as EEG and evoked potentials.
• Monitoring of motor-evoked potentials allows for
accurate mapping of the motor cortex and brain-
stem if needed.
• A new EEG parameter, the bispectral index (BIS) is now
gaining acceptance as a guide to monitoring
anesthetic depth and the hypnotic effect of
anesthetic agents. Intraoperative titration using BIS
may allow for more rapid recovery from anesthetics
and may be used for monitoring of burst supression.
 Cerebral Oximetry Is…..
• A non-invasive method to measure the brains cerebral
oxygen status at a specific region
• Real time and continuous
• Co-related to vastly improved patient outcomes
• Cost-effective
• Clinically relevant in all critical patient conditions.
NIRS
Non-invasive technology
for monitoring venous–
weighted hemoglobin
saturation
Transparency of tissue to
light in the near infrared
spectral region
 1st Wavelength 730 [nm]

• Visible Light
•
• Absorption depends on hemoglobin
concentration
•
• Absorption depends on hemoglobin oxygen
saturation – local svO2 & saO2 (!)
 2nd Wavelength 810 [nm]

• Near Infrared Light A

•
• Absorption depends on hemoglobin
concentration
•
• Absorption depends NOT on hemoglobin
oxygen saturation – local svO2 & saO2 (!)
 Aims of anaesthesia
• Optimal operating conditions
• Maintenance of stable ICP
• Stable haemodynamics, oxygenation and
ventilation parameters
• Appropriate CPP and oxygenation while
minimising CMRO2 to protect against
ischaemia
• Early detection & prompt management of
intra-op complications-, intracranial bleed
ANAESTHESIA & CRANIOTOMY FOR
PATIENTS WITH MASS LESIONS
•
Confirm diagnosis,indication and consent •
Routine pre-op assessment
Airway, CVS and respiratory system •
Details of concomitant medical •
illnesses,nature of treatment and
compliance to therapy
Investigations appropriate for age, general •
status of patient and type of surgery
 Detailed CNS assessment
• . Level of consciousness, presence and extent of
neurological deficit(clear documentation)
•  Observe respiratory effort in terms of tachypnoea,
laboured breathing or Cheyne-Stokes pattern of
breathing Assess the presence of cough/gag reflex if
bulbar involvement is suspected.
•  Look for clinical manifestation of raised ICP:
headache,vomiting,focal neurological signs and
papilloedema
•  Late signs: deteriorating GCS, Cushings reflex,dilated
pupils,decorticate then decerebrate posturing and
coma
•
 Review CT scan or MRI
• : Size and location mass, size of ventricles, presence of
midline shift and evidence of generalised/peri-tumour
cerebral
•  Assess the fluid status: possibility of dehydration and
electrolyte imbalance in patient who has been
vomiting, fluid restricted/receiving diuretic therapy
•  Assess glycaemic status: rule out hyperglycemia in
diabetic patient/patient treated with dexamethasone
•  Rule out endocrine dysfunction esp in pituitary
tumours: hypo/hyperthyroidism, acromegaly,
hypo/hyperadrenalism
•
 Based on overall assessment
• ., identify patients who would requires post-
op ventilation in ICU
•  GCS</=6
•  Evidence of raised ICP
•  Large or deep seated tumour
•  Presence of midline shift and/or significant
cerebral oedema
•
 Premedication
•  Opiod premedication often avoided:
hypercarbia increasedCBF and ICP and
possibility of disrupting early postop
neurological assessment
•  For patient who is going for spine surgery who
is alert, conscious and anxious: Small dose of
benzodiazepine may be prescribed
•  Alternatively a small IV dose of benzodiazepine
can be administered in OT prior to induction
•  Effect of benzodiazepines are not detrimental
as long as hypotension is avoided
 Anaesthetic Management
• .Reassess the patients neurological status before
induction
•  Confirm availability of ICU or HDU
•  Establish venous access w large bore IV
cannulae.
•  Monitors: ECG, non-invasive BP, pulse oximetry,
and capnography for minor cases (VP shunt,
EVD, Burrhole, cranioplasty)
•  Additional monitors: u/o, temperature,
neuromascular blockade, invasive BP and CVP
(Major)
•
•  PreoxygenationCommon drugs at induction
• .
: Fentanyl, Thiopentone or Propofol
•  Atracurium, Vecuronium or Rocuronium
•  Lignocaine or Esmolol may be used to obtund
sympathetic reflex during airway manipulation
•  Propofol has many theoretical advantages by
reducing CBV and ICP and preserving both
autoregulation and vascular reactivity. In
healthy subjects, propofol reduced CBF, as
measured by positron emission tomography
(PET), more than sevoflurane at equipotent
concentrations. Correlation of EEG spectral
entropy with regional cerebral blood flow
during sevoflurane and propofol anaesthesia.)
 .
•  Suxamethonium transiently increases ICP
and best avoided in elective cases (except in
difficult intubation)-should not be withheld
in emergency cases
•  Monitor the degree of neuromuscular
blockade with peripheral nerve stimulator
•  Allow non-depolarising NMB take effect
•  Laryngoscopy and intubation should be
attempted when patient is adequately
paralysed
•  Maintain head-up tilt of 15-20 deg and avoid
extreme neck flexion or.rotation
•  Re-check placement of ETT after positioning
•  Head is often secured in place using Mayfield3-point
fixator
•  An additional dose of Fentanyl before the pins
inserted helps to prevent marked hypertension and
tachycardia
•  In cases of intracranial HTN lower ICP by
administering mannitol 0.5-1g/kg and/or frusemide
0.5mg/kg Maintain PaO2>100mmHg and PaCO2
between 30-35 mmHg.
•  Avoid overventilation since hypocarbia may result in
cerebral vasoconstriction and reduce cerebral
perfusion
 Maintenance of anesthesia
• . TIVA with propofol
•  Inhalation technique with volatile agent
•  NMB administered by continuous infusion or
intermittent boluses
•  Analgesia maintained with intermittent boluses
of Fentanyl or infusion of Remifentanyl
•  Isoflurane and Sevoflurane are preferred
• : Maintenance of cerebral auto-regulation up to
MAC 1.5
•
•
 . induction, rapid
•  Sevoflurane gives smooth
onset and offset of action
•  In a study comparing desflurane, isoflurane,
and sevoflurane in a porcine model of
intracranial hypertension, at equipotent doses
and normocapnia, CBF and ICP were greatest
with desflurane and least with sevoflurane. ()
•  Nitrous oxide causes cerebral vasodilatation,
increased CBV and ICP. Also contribute to
development of pneumoencephalocele.
•  Should be avoided:-in patient with cerebral
ischaemia/reduced intracranial compliance-
Surgery with significant risk of (posterior fossa
surgery)
 Fluid management
•  IV fluid used judiciously and be sufficient to maintain
IV volume and hemodynamic stability
•  Dextrose-containing solutions should be avoided
unless indicated-Hypo-osmolar causing fluid shift-
Hyperglycemia can cause impaired neurological
recovery
•  Ringers lactate is also hypo-osmolar and can cause
increase plasma glucose via lactate metabolism
•  0.9% saline is the preferred crystalloid but may cause
hyperchloraemic acidosis when large doses are infused
•  Blood loss may be torrential.
•
 Temperature control
• . Permissive hypothermia 33-35 deg celcius
decreases CMRO2 and may increase the period of
ischaemia tolerated intra-op
•  Normothermia should be achieved before patient
awakens to avoid shivering which markedly
increases O2 demand
• Thromboembolic prophylaxis
•  Neurosurgical patients are at risk for DVT and PE
•  Heparin should not be used because of risk of
bleeding in confined cavity
•  Mechanical means  graduated compression
stockings and intermittent pneumatic leg
•
 .Emergence
•  The patient should not be allowed to cough through
ETT(tachycardia, hypertension and increased ICP)
•  Systemic hypertension is common and may
contribute to the development of post-op
haematomas.
•  The increased use of remifentanil may be associated
with more postoperative hypertension  avoided
with effective transitional analgesia
•  The a-2 agonist dexmedetomidine has been shown
to provide good haemodynamic stability during
intracranial tumour surgery, attenuating the
response to intubation and emergence.)
•
 .
• Post-op ventilatory support
•  Patientss pre-op neurological status
•  Intra-op events (duration and complexity of
surgery, hemodynamic stability,
complications, hypovolemia, massive
transfusion)
•  Evidence of raised ICP(tense dura/tight
brain)
•
 Post-op
•  Regular neurological observations
•  Any neurological deterioration should raise suspicion
of ICB/ oedema. Urgent CT should be
considered.Other aspects
• : Hemodynamic should be closely monitored to
maintain adequate CPP.
•  Post-op pain often not severe and can be managed
by intermittent bolus doses or morphine infusion
•  Electrolyte imbalance(esp sodium)
•  U/o should be monitored(diabetes insipidus)
•
Thanks