peripheral nerve injury1
TRANSCRIPT
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