peripheral nerve injury1

PERIPHERAL NERVE INJURYPERIPHERAL NERVE INJURY

DR. ASHISH GOHIYAAssistant Professor

Dept. of OrthopaedicsGandhi Medical College

Bhopal

ANATOMYANATOMYPeripheral 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.

ANATOMYANATOMY

ANATOMYANATOMY

ANATOMYANATOMY

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

proprioception)

Nodes of Ranvier Faster conduction

Unmyelinated – Small diameter (crude

touch )– Efferent sympathetic

No nodes Slower conduction

ANATOMYANATOMY

Endoneurium – covers

axon.

Perineurium – covers

fascicles

Epineurium – covers

nerve trunk

BLOOD SUPPLY OF NERVEBLOOD 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 INJURYMODE OF NERVE INJURY

Ischemia Compression Traction Laceration Burn.

NERVE INJURY HEALINGNERVE INJURY HEALING

SEDDON CLASSIFICATIONSEDDON CLASSIFICATION

NEUROPRAXIA AXONOTMESIS NEUROTMESIS

•Physiological conduction block•Segmental demyelination•Crutch pasly

Saturday nerve palsy

Tourniquet palsy

•Axonal interruption•Nerve in continuity•Axon disintegrate – phagocytosis – Wallerian degeneration•Regeneration at the rate of 1 mm / day

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

Transient Ischemia

SUNDERLAND CLASSIFICATIONSUNDERLAND CLASSIFICATION

Sunder

landSeddon Epineurium Perineurium Endoneurium Axon Outcome

1 Neuropraxia + + + Block Good

2 Axonotmesis + + + _ G / fair

3Axonotmesis

+ + _ _ F /poor

4Axonotmesis

+ _ _ _ Poor

5 Neurotmesis _ _ _ _ Poor

CLINICAL FEATURES CLINICAL FEATURES High index of suspicion.Symptoms

– Numbness– Paraesthesia– Muscle weakness

Signs– Abnormal posture– Weakness– Loss of sensation– Sudomotor changes (plastic pen test)

ASSESSMENTASSESSMENT

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.

ASSESSMENTASSESSMENT

Level of function– Sensory

Two point discrimination (innervation density)

Threshold test– Motor

Medical Research Council Scale (0-5 grades)

TREATMENTTREATMENT

Expectant– Dynamic splints– Passive manipulation– Drugs ??

Steroidsmethylcobalamine

TREATMENTTREATMENT

Nerve ExplorationIndications

– 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.

TREATMENTTREATMENT

Primary Repair Sooner the better. Ragged ends –pared. Use microscope and

10\0 suture. Suture epineurium. Fascicular repair. Avoid tension on suture

line. Splinting.

TREATMENTTREATMENT

Delayed RepairIndications

– 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.).

TREATMENTTREATMENT

Nerve GraftingUsed to bridge gaps.Sural nerve most commonly used. (single\

cable).Vascularised grafts also used.

TREATMENTTREATMENT

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

TREATMENTTREATMENTTendon 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

PROGNOSISPROGNOSISDEPENDS ONTYPE OF LESIONLEVEL OF LESIONTYPE OF NERVESIZE OF GAPAGE DELAY IN SUTUREASSOCIATED LESIONSURGICAL SKILL