8.1 Neurological Complications Flashcards
Regarding peripheral nerve injuries:
ga?
Most frequent nerve injured
Regarding peripheral nerve injuries:
Occur even with general anaesthesia
(without nerve block).
Ulnar nerve injury is the most frequent nerve injury
Regarding peripheral nerve injuries:
Is stretching safe?
Stretching the nerve during peripheral nerve
block can lead to pressure injury
(as the connective tissue may be poorly compliant).
Regarding peripheral nerve injuries:
needle bevel type
Shorter-bevel needles
push the nerve away
rather than cut it
(like long bevel needles),
but should an intraneural
injection occur, subsequent
nerve injury can be much worse.
Regarding peripheral nerve injuries:
fascicle size
Larger fascicle size makes the nerve more prone to damage, as it can accommodate the tip of the needle and an intraneural injection can occur.
Risk factors for the development of nerve damage are as follows
Patient-related factors
Patient-related factors
male sex, elderly, very thin or very obese, pre-existing diabetes or neurological damage.
Risk factors for the development of nerve damage are as follows
Surgical factors:
Surgical factors:
infection, inflammation, vascular compromise, tourniquet-induced ischaemia, stretch, positional and compression injury
Risk factors for the development of nerve damage are as follows
Anaesthetic factors:
Anaesthetic factors:
needle trauma
and local anaesthetic-
and
adrenaline- induced neurocytotoxicity
mechanisms involved in
nerve injury
Mechanically injuries
laceration due to needle trauma,
stretch injury due to exaggerated positioning,
and
intraneuronal injections can lead to nerve damage.
Lacerations sharp vs blunt
mechanisms involved in
nerve injury
Lacerations by sharp needles
(clear-cut wound) may be less injurious
than intrafascicular injections,
which may lead to extensive
disruption of fascicular architecture.
mechanisms involved in
nerve injury
pain
paraesthesia
Pain on injection is an
unreliable indicator of intraneural injections.
Paraesthesia may not be a
risk factor for nerve damage,
and stopping injection upon
paraesthesia may not reduce the chances
of ensuing nerve damage.
mechanisms involved in
nerve injury
Stim current 0.2mA
Stimulating currents less than 0.2 mA
are associated with a higher
chance of needle tip lying
within the nerve.
Hence injections should be made
within a range of 0.2–0.5 mA.
mechanisms involved in
nerve injury
Motor responses
stimulators?
Motor responses may not
always be seen with stimulation.
They may be absent even
when the needle tip is within the nerve itself!
Hence nerve stimulators may
not prevent nerve injuries.
Intraneural injection may be of two types
Interfascicular/extrafascicular:
Interfascicular:
Interfascicular/extrafascicular:
nerve injury common
when the injection is within the nerve,
but between the fascicles of the nerve.
This may be more common,
and
the developing block
may be faster than usual and
prolonged in duration.
Neural injury may not develop secondary to
interfascicular injections.
Interfascicular:
where
injury?
a/w
when the injection is made
within the nerve,
and
within a fascicle.
This disrupts the fascicular
architecture and leads to extensive injury.
This may be accompanied by pain, paraesthesia and difficulty in injecting (pressures exceeding 20 psi).
Classification of acute nerve injuries
Neuropraxia
Sunderland
class
Neuropraxia
Sunderland
damaged
intact
fxn
Neuropraxia
1
Myelin damage
Most
Conduction delay
prognosis is best in neuropraxia and worst in neurotmesis.
Axonotmesis
Sunderland
damaged
intact
fxn
Axonotmesis
2
Loss of axonal continuity
Endoneurium, perineurium
and epineurium intact
No conduction
3
Loss of axonal continuity
Endoneurium damaged
Perineurium and
epineurium intact
No conduction
4
Loss of axonal continuity
Endoneurium and
perineurium damaged
Only epineurium intact
No conduction
Neurotmesis
Sunderland
damaged
intact
fxn
Neurotmesis
5
Loss of axonal continuity
Endoneurium, perineurium
and epineurium damage
No layer intact
No conduction
Local anaesthetics may have neurocytotoxic effects mediated via:
Local anaesthetics may have
neurocytotoxic effects mediated via:
1 -
mitochondrial damage leading to loss of
adenosine triphosphate production,
accumulation of intracellular calcium,
activation of caspaces and
ensuing apoptosis
2
blockade of axonal transport
3
disruption of cell membranes.
The cytotoxic potential is greater with:
The cytotoxic potential is greater with:
1
lignocaine and tetracaine
than bupivacaine
2
addition of epinephrine
3
higher concentration of local anaesthetic
4
prolonged exposure
5
nerve stretching
6
pre-existing neurological condition
(‘double crush syndrome’)
7
intrathecal use rather than
epidural or peripheral use.
Systemic toxicity potential hights
(although systemic toxicity
is in the order
tetracaine >
bupivacaine >
lignocaine
Tourniquet-induced neuropathy
incidence
type
1
Incidence of 1 : 8000.
2
Varies in severity from neuropraxia
to permanent nerve damage.
Tourniquet-induced neuropathy
Pressure
duration
Associated with higher than recommended pressures.
Duration of application should
not exceed 90–120 minutes without a
10- to 15-minute deflation period.
Tourniquet-induced neuropathy
Bandages
Cuffs
Esmarch bandages may generate very high pressures immediately under the bandage (so should be avoided as sole method of tourniquet).
Wider cuffs generate lower
pressures than narrow cuffs
(so are preferred).
Optimal cuff inflation pressure in upper limb
Optimal cuff inflation pressure in upper limb is
‘LOP’ plus 50
Optimal cuff inflation pressure in Lower limb
While in the lower limb it is ‘LOP’ plus 75 mmHg
Limb occlusion pressure
Limb occlusion pressure (LOP) is the minimum pressure required to stop the flow of arterial blood into the limb distal to the cuff. It may be measured by a Doppler probe.
Nerve blocks under heavy premedication or general anaesthesia
Patients may not be able to report pain ?
Pain is an unreliable indicator of nerve injury
Stopping injection after pain does not
prevent the development of nerve damage
‘Pressure paraesthesia’ is normal
Nerve blocks under heavy premedication / GA
Premedication diminishes the patient’s
ability to report early indicators of local
anaesthetic toxicity?
Premedication has anticonvulsive actions which may
offer protection from local anaesthetic toxicity
With general anaesthesia, airway is already secured,
helping cardiopulmonary resuscitation should
cardiovascular problems develop
Nerve blocks under heavy premedication / GA
Paediatric population
Paediatric population
Are regularly anaesthetised for blocks
Do not show greater risk of nerve damage than adults
Recommendations to reduce the chance of nerve damage during a peripheral nerve block
(PNB)
Equipment:
Equipment:
Short-bevel/Tuohy needle less likely to
enter nerves than long-bevel
Use correct-length needles
Use pressure indicators (B-smart)
Accurate peripheral nervous system
Right probe for the given block (e.g.
high frequency for superficial blocks)
Ultrasound guidance vs peripheral
nervous system
Echogenic vs non-echogenic needles
Recommendations to reduce the chance of nerve damage during a peripheral nerve block
(PNB)
Technique
Technique:
Strict asepsis
Advance needle slowly
(peripheral nervous system),
and only after identifying needle tip (ultrasound guidance)
Fractionation of injections
Avoid rapid injections
Avoid injections when unusual high pressures are required
Avoid injection when patient complaint of pain (always ask where and what kind of pain)
Avoid heavy premedication
Adequately experienced operator
Avoid repeating block
Recommendations to reduce the chance of nerve damage during a peripheral nerve block
(PNB)
Drugs
Drugs: Avoid high concentration of adrenaline (1 : 400 000 than 1 : 200 000) Lower-toxicity drugs (ropivacaine than bupivacaine
Recommendations to reduce the chance of nerve damage during a peripheral nerve block
(PNB)
patient
Patient:
Keep patient awake when you can
Regarding nerve damage after a PNB:
duration afterblock
motor or sensory assesment
Regarding nerve damage after a PNB:
It usually presents after 48 hours
of recession of the block.
Motor loss is more informative than sensory loss in assessment of injury.
Regarding nerve damage after a PNB:
first step
if this proves negative what next
First thing to do is to exclude
any vascular compromise
(arterial/venous).
A Doppler may be used to do this.
If such a compromise is found, surgical exploration may be needed.
If there is no vascular compromise,
then the next thing to do is to
obtain an evaluation by a neurologist
Testing following a peripheral nerve injury
Test When and why
Nerve conduction study:
TABLE 8.4
Testing following a peripheral nerve injury
Test When and why
Nerve conduction study:
measures amplitude, time for signal
transmission and conduction velocity
Why? It helps to detect a nerve lesion
When? Within 1–2 days of nerve damage
Amplitude reduces in axonal injury
Velocity reduces in myelin damage
Electromyography:
Electromyography:
measures muscle depolarisation
Why? It helps to locate a nerve lesion
When? From 2 to 4 weeks after nerve injury
Muscle defibrillation occurs 2–4 weeks after denervation
High-frequency ultrasound
High-frequency ultrasound
Morphological changes in peripheral nerves
like nerve swelling, rupture, compression and so forth
Magnetic resonance imaging
Magnetic resonance imaging
(neurography)
Demonstrates nerve anatomy and can reveal nerve
swelling, rupture or compression
It is the earliest method to detect nerve injury (24 hours
What has the highest complication of the PNB
They noted
a higher complication rate with lumbar plexus block than other PNBs
Neuraxial complication highest with
Spinal anaesthetics were more commonly associated with complications than epidurals or PNBs
PNB block damage
Out of 12 patients with nerve damage subsequent to
PNB, blocks in nine were performed using a peripheral nerve stimulator.
