broken bones and nerve injury Flashcards

1
Q

importance of broken bones and nerve injury

A
  • Impaired sensory and motor function
  • Impaired dexterity
  • Contracture of joints
  • Injury to insensate area - skin and
  • Destruction of joints – Charcot’s joint
  • Sensitivity to cold
  • Pain management issues
  • Drug dependency
  • Psychological problem
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2
Q

organisation of the nervous system

A

CNS, PNS and Autonomic
CNS – Brain, Brainstem & Spinal Cord
PNS -
• 12 paired cranial nerves
• 31 paired spinal nerves
- Spinal nerves divide very close to the cord
Sensory dorsal (afferent) rami
- Cell bodies reside in the dorsal root ganglion
Motor ventral (efferent) rami
- Cell bodies are within spinal cord in anterior horn
Autonomic Nervous System -
- Nerves arise from the spinal cord grey matter
T1 to L2 levels
- Exit via the ventral spinal roots (with the motor nerves)

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3
Q

modes of injury

A
  • Compression – Tourniquet injury, Neuropathies- Carpal tunnel syndrome, Cubital tunnel syndrome
    • Stretch – Sports injury, very susceptible to traction injury, will become ischaemic with 15% strain and can rupture at around 20% or more strain
    • Transection – knife injury
    • Avulsion – RTA (most common is Motor-bike incidents)
    • Crush / Laceration
    • Blast injury
    • Radiation therapy
    • Tumour invasion
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4
Q

what happens following nerve injury and Wallerian degeneration

A

The segment of the nerve distal to the site of a lesion undergoes the process that is known as Wallerian degeneration (named after Mr Waller), which starts immediately after an injury.
This process involves degeneration of the axons and breakdown of the myelin, with subsequent proliferation of the Schwann cells, recruitment of immune cells, such as macrophages (eliminating myelin and cell debris), as well as remodelling of the tissues.
Cell volume increases
Cell body nucleus migrates to the periphery of the cell
Chromatolysis occurs - dispersion of basophilic Nissl granules with relative eosinophilia of the cell body .
Cell body changes function - The nerve cell stops producing neurotransmitters and begins synthesizing proteins required for axonal regeneration.

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5
Q

classification

A

1) Seddon – Neuropraxia (Transient block), Axontmesis (Lesion in continuity), & Neurontomesis (Division of a nerve)
2) Sunderland – Numerical classification (I – V)
3) McKinnon & Dellon – added the 6th type (Mixed injury – all grades present)
4) Lundburg - proposed the concept of physiological conduction block, Type A & B
5) Birch & Bonney – Clinical classification

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6
Q

prognostic factors

A

The most important prognostic factor for recovery is patient age.
The prognosis for nerve recovery is more favourable in
- Children
- Stretch injuries or sharp transections that have been repaired less than 14 days after injury
- Clean, well-vascularized wound beds
- Early, direct surgical repair

Conversely, poor outcomes are expected in

- Elderly patients
- Crush or blast injuries
- Infected or poorly 	 	 	  vascularized wound beds
- Delayed surgical repair
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7
Q

basic neurological examination

A

Motor
Sensory
Proprioception
Jerks

- Accurate documentation
- Repeated clinical assessment

MRC- motor grading
MRC- sensory grading

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8
Q

neurophysiological test

A
Nerve Conduction Studies NCS
Motor
Sensory
Proprioception
Jerks
- Accurate documentation
- Repeated clinical assessment

Electromyography EMG

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9
Q

timings of the NCS

A

Ideal time for NCV after injury is 10 to 14 days after injury to discern between different types of nerve injury
Conduction failure is seen with stimulation proximal to a lesion in all three forms of nerve injury.
An evoked response is, however, present with distal stimulation in all three forms of injury acutely.
Once Wallerian degeneration has occurred, distal conduction can only occur in a neurapraxia.
Neuropraxia will improve (increased velocity and dcreased latency) with repeated test
The distinction between an axonotmesis and a neurotmesis is difficult both clinically and neuro-physiologically.
The presence of partial sensory or motor function may help differentiate them.
Evidence of nerve continuity – presence of sensory or motor response on nerve conduction test or the presence of any voluntarily recruited MAP on the EMG proves nerve continuity

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10
Q

what is EMG?

A

Electromyography is the study and graphical recording of the electrical activity (voluntary and spontaneous) of muscle.
Motor Unit
Motor Unit Potential (MUP)

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11
Q

motor unit potential morphology

A

Key parameters are,

- Amplitude, which is an indicator of muscle fibre density per axon near the tip of the needle electrode;
- Duration, which is an indicator of motor unit territory; and

		- Number of phases, which represents the positive and negative deflections of the 	  MUP from the baseline (normally triphasic  but 20% of MUP may have >5 phases in normal muscle)
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12
Q

how is an EMG carried out

A

A needle electrode is inserted in the muscle- the electrical activity is observed in 3 stages

- the insertional  activity
- the activity at rest
- the activity when muscle is contracted
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13
Q

EMG findings

A

Top, Normal motor unit action potential (MUAP), recorded using a needle electrode from muscle fibers within its recording area.
Middle, After denervation, single muscle fibers spontaneously discharge, producing fibrillations and positive sharp waves.
Bottom, When reinnervation by axon sprouting has occurred, the newly formed sprouts will conduct slowly, producing temporal dispersion (that is, prolonged MUAP duration) and MUAP polyphasicity.
MUP polyphasia -results from the desynchronization of nerve fibre conduction and muscle fibre discharges
The higher density of muscle fibers within the recording area of the needle belonging to the enlarging second motor unit results in an increased-amplitude MUAP

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14
Q

use of information from the tests

A

At between 15 and 30 days, spontaneous denervation fibrillation potentials are present
- Denervation fibrillation potentials

If denervation fibrillation potentials are not present by the end of the 2 nd week this is a good prognostic sign.
Evidence of reinnervation is when highly polyphasic motor unit potentials are detected at attempts at voluntary activity
Denervation fibrillations in a muscle only tell you that the muscle is not innervated. It does not determine whether the injury is 2 nd 3 rd or 4 th degree.
Reinnervation potentials by the same token can be restored after regeneration of only a few motor fibres and does not necessarily mean a good return to voluntary motor control
Evidence of nerve continuity – presence of sensory or motor response on nerve conduction test or the presence of any voluntarily recruited MUP on the EMG proves nerve continuity

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15
Q

management

A

Periodic examination
Considerable function may return
Indicated every 4 to 6 wk
Absence of recovery or any recovery that has halted – exploration is indicated
4 to 6 wk is reasonable period to expect some recovery

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16
Q

treatment options

A
Depends upon 
	- Location
	- Severity
Wait and Watch  – 
	- maintain the functionality
	- Maintain joint motion 
	- Use of Splint in functional 	  	  	  position to avoid contracture
	- Start Physio 
Surgical options
Primary reconstruction:
	- Neurolysis
	- Surgical repair – end to end
	- Use of nerve graft (Cable 	 	  	  grafting)
	- Use of Conduit
	- Neurotisation
Secondary reconstruction:
	- Tendon transfer
	- Free functioning muscle 	  	  	  transfer
	- Arthrodesis
	- Amputation (Controversial)
17
Q

timings of nerve exploration and repair

A

Low velocity injury – palsy associated with fractures; Wait and watch
Laceration – Early exploration
For high-velocity severe traction injuries and/or very proximal brachial plexus injuries, earlier exploration after several weeks is recommended
If recovery does not start to manifest after 3–4 months, nerve exploration is undertaken.

18
Q

Nerve Guidance Conduit NGC

A

As a basic concept, a NGC should act as a physical barrier from the external environment, concomitantly acting as physical guidance for the regenerative axons across the gap lesion.
NGCs should also be able to retain the naturally released nerve growth factors secreted by the damaged nerve stumps, as well as reducing the invasion of scar tissue-forming fibroblasts to the injury site.
Dealing with the several features that can be used to improve peripheral nerve regeneration (PNR), ranging from the simple use of hollow NGCs to tissue engineered intraluminal fillers.

19
Q

nerve transfers (Neurotisation)

A

Neurotisation: a functioning nerve of lesser importance is transferred to the more important denervated distal nerve
It is performed for pre-ganglionic lesion or to accelerate recovery by reducing the time for re innervation by reducing the distance between the site of nerve repair and the end organ.
Extra plexal sources : Spinal accessory nerve, Intercostal nerve , Contralateral C7
Intra plexal sources: Phrenic nerve, portion of working ulnar or median nerve, Intact pectoral nerve

20
Q

secondary reconstruction

A

Options

- Tendon transfer
- Free Muscle transfer
- Arthrodesis
- Amputation (Controversial
21
Q

clinical conditions

A

Trauma - predictable nerve injuries arise from certain fracture patterns and clinical scenarios
Brachial plexus injury - RTA
Axillary nerve palsy
- anterior shoulder dislocation
Radial nerve palsy
- distal 1/3 humeral shaft (Holstein- Lewis) fractures
- prolonged compression along the humerus while intoxicated (Saturday night palsy)

Sciatic nerve 
	- posterior hip dislocation
	- Itrogenic injury during Hip Replacement 	  surgery
Common peroneal nerve
	- Correction of severe valgus alignment 	   during a total knee arthroplasty
	- Knee dislocation
Compression Neuropathies – 
	- Carpal tunnel syndrome 
	- Cubital tunnel syndrome