Peripheral Nerve Injury1

PERIPHERAL NERVE INJURY

DR. ASHISH GOHIYA Assistant Professor Dept. of Orthopaedics Gandhi Medical College Bhopal

ANATOMY  Peripheral

nerves are bundles of axons conducting afferenat & efferent impulses.  Each axon is elongated process of a nerve cell (Neuron).  Cell bodies of motor neuron – Ant horn cell  sensory neuron – dorsal root ganglia. 

 Single

neuron may supply 10 – 1000 fibres.

ANATOMY

ANATOMY

ANATOMY  Myelinated – All motor axons – Large sensory axons – (touch, pain

 Unmyelinated – Small diameter (crude

touch ) – Efferent sympathetic

proprioception)  Nodes

of Ranvier  Faster conduction

 No

nodes  Slower conduction

ANATOMY  Endoneurium

– covers

axon.  Perineurium

– covers

fascicles  Epineurium

nerve trunk

– covers

BLOOD SUPPLY OF NERVE  Blood

vessels run in the epineurium.  Become endoneurial capillaries after penetrating.  Sympathetic supply to vessels by same nerve. (cause for RSD)

MODE OF NERVE INJURY  Ischemia  Compression  Traction  Laceration  Burn.

NERVE INJURY HEALING

SEDDON CLASSIFICATION NEUROPRAXIA

AXONOTMESIS

NEUROTMESIS

•Axonal

•Division

interruption •Nerve in continuity block •Segmental demyelination •Axon disintegrate – phagocytosis – Wallerian •Crutch pasly degeneration Saturday nerve palsy •Regeneration at the rate Tourniquet palsy of 1 mm / day •Physiological

conduction

Transient Ischemia

of nerve trunnk •Endoneurial tube destroyed to variable length •Regenerating fibres+schwann cells+fibroblasts =Neuroma

SUNDERLAND CLASSIFICATION Sunder land

Seddon

Epineurium

Perineurium

Endoneurium

Axon

Outcome

1

Neuropraxia

+

+

+

Block

Good

2

Axonotmesis

+

+

+

_

G / fair

+

+

_

_

F /poor

+

_

_

_

Poor

_

_

_

_

Poor

3 4 5

Axonotmesis Axonotmesis

Neurotmesis

CLINICAL FEATURES High

index of suspicion. Symptoms – Numbness – Paraesthesia – Muscle weakness Signs – Abnormal posture – Weakness – Loss of sensation – Sudomotor changes (plastic pen test)

ASSESSMENT  Degree

of injury  Tinels sign (advancing at rate of 1 mm\day)  EMG – Denervation potential at

3 weeks – Does not distinguish between axonotmesis and neurontemesis.

ASSESSMENT Level

of function

– Sensory Two point discrimination (innervation density) Threshold test – Motor Medical Research Council Scale (0-5 grades)

TREATMENT Expectant – Dynamic splints – Passive manipulation – Drugs ?? Steroids  methylcobalamine 

TREATMENT Nerve Exploration  Indications – Type of injury suggest that nerve is divided. – If recovery is delayed

 Vascular

injury, unstable fracture contaminated soft tissue, tendon injury are dealt before nerve injury.

TREATMENT Primary Repair  Sooner

the better.  Ragged ends –pared.  Use microscope and 10\0 suture.  Suture epineurium.  Fascicular repair.  Avoid tension on suture line.  Splinting.

TREATMENT Delayed Repair  Indications – Closed injury not improving at expected time – Late presentation and missed diagnosis – Failed primary repair

 Nerve

Explored – scarred segment resected -nerve mobilized –transposition (if req.) graft (if req.).

TREATMENT Nerve Grafting  Used

to bridge gaps.  Sural nerve most commonly used. (single\cable).  Vascularised grafts also used.

TREATMENT Nerve Transfer  Indicated

forroot avulsions of brachial plexus.  Spinal accessory to suprascapular nerve.  Intercostal nerves to musculocutaneous nerve.

TREATMENT Tendon Transfer  Motor

end plate must have degenerated (i.e. 18 – 24 months after injury)  Assess – Muscles – lost – Muscles – available

 Donor Muscle – Expendable – Adequate power – Synergistic  Transferred tendon – Routed subcutaneously – Straight pull

PROGNOSIS DEPENDS ON  TYPE

OF LESION  LEVEL OF LESION  TYPE OF NERVE  SIZE OF GAP  AGE  DELAY IN SUTURE  ASSOCIATED LESION  SURGICAL SKILL