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?