Neuroanaesthesia for the
final FRCAD Taylor, Anaesthetic ST5
Objectives
Help identify areas of learning
Teach a few areas
Predominantly clinically based lecture
Potential Question areas
Anatomy & Physiology
Elective work
Trauma & Acute
Critical care
Special environments
Anatomy & Physiology
Areas that you need to be familiar with: Many cross-link with basic sciences
areas
Anatomy Physiology
Skull & skull base ICP/CPP/CBF
Vertebral columnMonitoring systems
Paravertebral spaces Endocrine
Epidural spaceNerve conduction
Caudal canal
Spinal cord anatomy
Pituitary gland
Monitoring - ICP
Dynamic pressure system
Measured directly
LP
Lumbar drain
Intra-parenchymal sensor (bolt)
Normal variance with age
Adults 10-15mmHg
Neonates 3-5mmHg
When should we monitor it?
ICP waves
Example CRQ
Cerebral Oxygenation
Measuring SjvO2
Undertaken in severe TBI
Little use in focal injuries
High risk of thrombosis and misplacement
NIRS
Non-invasive
700-1000nm IR light – reflected, redirected, scattered & absorbed
Uses Beer-lambert law
Non-clinical – Brain tissue oxygenation – direct microcatheter
Cerebral blood flow
Autoregulation within MAP of 50-150mmHg
Factors affecting CBF autoregulation
Metabolism:
Increased by ?
Decreased by ?
CO2 Tension - @ normal baseline 1kPa variance results in 30% change in blood flow
O2 – little effect until PaO2 <7kPa
Temperature – 1 degree of hypothermia ~ 5% reduction in metabolism
Viscosity – Haematocrit of 30-50% has no effect
Cerebral blood flow
Transcranial Doppler
Non-invasive
Targets intracranial arteries
Utilising the doppler effect
Primary role in SAH
Secondary in detecting microemboli, during carotid surgery, estimating ICP though pulse variability
Elective Neuroanaesthesia
Pre-assessing the patient with neurological disease
Intra-op & post op
Positioning
Pos. fossa
Awake Craniotomy
Stereotactic Brain Surgery
Pre-assessment
Above the usual:
Presence of elevated ICP already
Documentation of neurological deficit
Consider checking gag reflex
Seizures + control
Airway examination – particular note to c-spine problems
Malignancy may be a met – where is the primary
Medication
Steroids, diuretics (deranging electrolytes), anti-epileptics (minimise the interruption to
established regimes)
Intra-op considerations
Which anaesthetic agent?
Volatile –various positive effects, dose dependant effect on autoregulation
IV agents
Ketamine – contraindicated
Propofol and Thio reduce CBF and ICP
Induce slowly to preserve BP
NMBD
Suxamethonium?
Opiates/Opiods
Little effect on CBF + ICP if CO2 is normal
Remi – good attenuation of HTN response to laryngoscopy
Intra-op considerations
Airway choice:
Armoured ET fairly standard due to risk of kinking and minimal access to the
airway
LMA may be used in awake craniotomy
Invasive monitoring
Arterial and CVP common place
Temp monitoring
Intra-op considerations
Goals of therapy
Preserve the norm
MAP
CO2
Temp
PaO2
Fluid status
Positioning
Head
Positioning – Patient as a whole
Supine – with head held in various devices
Reverse Trendelenburg
Lawn chair / Deck chair (more upright)
Sitting
Lateral
Park bench (almost exclusively used for pos. fossa)
Prone
Pos. fossa considerations
Surgery –
VAE
CVS instability
Bleeding
Respiratory anomalies
CSF leak
Brainstem damage
Infection
• Position –
• Airway loss
• Venous obstruction
• Hypotension
• Nerve damage
• Traction
• Pressure
• Musculocutaneous
• Pressure
• Compartment Sx
Prone
Patients may be turned from trolley onto table
May use a specialist table such as the Jackson
If asked to describe the process don’t forget the practicalities
Physiological effects of prone position
RS
FRC improves
Better V/Q matching
CVS
Decreasing SV and CO
Counteracted by rise in HR
• CBF
• Head rotation may impede venous drainage and arterial flow
• Renal
• Possible: studies show mildly reduced
Complications of prone position
Trauma & Acute
SAH & the IR suite
TBI / Transfer
Cardiac arrest during Neurosurgery
The IR suite
The IR suite
Special considerations:
Remote location
The C arm
Radiation – staff and patient
Contrast + flush
Anticoagulation
Patient position – distant, covered inaccessible
Environment – poor lighting, cold
SAH
SAH
5% of all strokes
Classic features
Sudden occipital headache
Associated feature
Nausea, neck stiffness, neurology, falling GCS
ECG changes
CT scan is >95% sensitive on D1
Typically becomes an anatomy question about the Circle of WIllis
SAH - complications
Early:
• Re-bleeding
• Seizure
• Hydrocephalus
Late:
Delayed cerebral ischaemia/vasospasm
Cognitive impairment
Neurocognitive symptoms such as fatigue, mood disturbance
Hypopituitarism
Traumatic Brain Injury
Primary Injury
Due to the insult
Secondary Injury
Due to the changes that occur in the hours and days following
Inflammatory
Neurogenic
Vasogenic
TBI
The chain:
Primary injury – raised ICP
Ischaemia and hypoxia
Inflammation – neuroexcitatory substances – calcium influx – oedema – death
Dying cells release inflammatory mediators
ICP raises more
Autoregulation fails
Cerebral perfusion lost
Management and Transfer
A - Indications to intubate
GCS <8, Airway threatened, Prevent 2ndry BI, C-spine protection, Imaging
B – PaO2>13kPa
Normal CO2
PEEP ( but minimise)
C – Access and monitoring (art line)
MAP >80
Ease venous drainage form the head (head up, no ties, paralyse)
D – Target CPP >60mmHg
Mannitol/Hypertonic saline
Seizure protection
Sedate adequately
Glucose 6-10mmol/l
Normothermia
CPR during
neuroanaesthesia
Questions?
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