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بســـم الله الرحمن الرحيم. Hazem Hantira,FRCSEd . Consultant Orth.Surgery Adan Hospital hhantira@hotmail.com. PERIPHERAL NERVE INJURY. Objectives. Anatomy of peripheral nerve Causes Types Pathological changes Clinical effect/ Diagnosis Principles of management The future???. ANATOMY.
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HazemHantira,FRCSEd.Consultant Orth.SurgeryAdan Hospitalhhantira@hotmail.com
Objectives Anatomy of peripheral nerve Causes Types Pathological changes Clinical effect/ Diagnosis Principles of management The future???
ANATOMY • Peripheral nerves are bundles of axons conducting afferent & efferent impulses. • Each group (bundle) of axons is called fascicle. • 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.
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 ANATOMY (Types of Nerve Fibers)
ANATOMY (Nerve Sheath) • Endoneurium – covers axon. • Perineurium – covers fascicles • Epineurium – covers nerve trunk
MODE OF NERVE INJURY • Ischemia • Compression • Traction • Laceration • Burn.
Sunderland.s classification Although Sunderland.s classification provides a concise and anatomic description of nerve injury, the clinical utility of this system is debatable. Many injuries cannot be classified into a single grade. Mixed nerve injuries, in which all fibers are affected but to varying degrees, are common among peripheral nerve injuries.
Sunderland’s clssification Furthermore, although Sunderland.s classification accurately describes the pathoanatomy of nerve injury, it is seldom possible to accurately subclassify an axonotmetic nerve injury on the basis of preoperative clinical and electromyographic data. The subtype is usually discernible only by histologic examination of the injured nerve
Wallerian degeneration Wallerian degeneration (i.e., breakdown of the axon distal to the site of injury) is initiated 48 to 96 hours after transection. breakdown of myelin begins, and the axon becomes disorganized. Schwann cells proliferate and phagocytose myelin and axonal debris .
CLINICAL FEATURES • High index of suspicion.(neuro.exam.of every Fx.) • Symptoms • Numbness • Paraesthesia,? loss of sensation • Muscle weakness, ?paralysis • Signs • Abnormal posture .eg.:wrist drop • Weakness • Loss of sensation • Sudomotor changes
ASSESSMENT • Degree of injury • Tinel’s 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) • Motor • Medical Research Council Scale (0-5 grades)
Clinical effects of nerve injury After injury (short of transection), function fails sequentially in the following order: motor, proprioception, touch, temperature, pain, and sympathetic. Recovery occurs sequentially in the reverse order
Clinical effects of denervation After denervation, distal structures undergo many changes. In major peripheral nerve injuries, such as brachial plexus palsy, bone develops disuse osteoporosis, and joints and soft tissues become fibrotic and stiff.
Clinical effects of denervation . Muscle: atrophies and undergoes interstitial fibrosis but remains viable for at least 2 years . Bones: disuse osteoporosis . Joints: fibrosis and stiffness
TREATMENT(preop.) • Expectant • Dynamic splints to avoid contracture • Passive manipulation to avoid stiffness • Direct galvanic stimulation(?) reduces muscle atrophy • Pool therapy can be helpful to improve joint contractures
TREATMENT (operation) Nerve Exploration • Indications • Type of injury suggest that nerve is divided. • If recovery is delayed • Vascular injury, unstable fracture, contaminated soft tissue, and tendon injury are treated before nerve injury.
TREATMENT Primary Repair • Sooner the better. • Ragged ends –pared. • Use microscope and 9\0 suture. Nylon, • Fibrin glue.?? • Suture epineurium. • Fascicular repair. ?? • Avoid tension on suture line. • Postop.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). • Other donors: lat.cut.n. of the thigh, superficial sensory br. of radial n. • Reverse direction? • Vascularised grafts also used.
TREATMENT Nerve Transfer • Indicated for root 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 • Expandable • Adequate power • Synergistic • Transferred tendon • Routed subcutaneously • Straight pull
PROGNOSIS DEPENDS ON • TYPE OF LESION • LEVEL OF LESION (proximal vs distal). • TYPE OF NERVE,( purely motor n.gives better result than mixed nerve.) • SIZE OF GAP • AGE (younger pts. give better results). • DELAY IN SUTURE • ASSOCIATED LESION • SURGICAL SKILL
The future? Use of neurotrphic and neuritogenic drugs to enhance survival and maintainance of n.fibres Use of immune system modulators to decrease fibrosis. Use of enhancing factors e.g. nerve growth factor . Entubulation chambers (silicon- Gore-tex.) to serve as conduit for loosely approximated nerve endings.
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