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DR.K.S.N.CHENNA KESAVA RAO
(
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` Acute nerve injuries areeasily misssed,especially ifassociated with fractures ordislocations
` Clinical features includes
` Numbness` Paraesthesia or` Muscle weakness in the
related areas` Signs of abnormal postures` Weakness in specific
muscle groups` Areas of altered sensations
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` Chronic nerve injuries
` Anesthetic skin may besmooth and shiny, withevidence of diminishedsensations
` Muscle groups will bewasted
` Postural deformities maybecome fixed
` METEV SIGN-chronic
nerve entrapment inhealed callus can givethe appearance of a holein the bone
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` CLINICALLY
` Loss of pain perception in the tip of little fingerindicates ulnar nerve injury
` Loss of pain perception at the tip of index finger-
median nerve injury`hitchhikers sign-inability to extend the thumb
-indicates radial nerve injury
`in lower limb loss of pain perception at in the sole of the
foot - indicates sciatic or tibial nerve`Inability to extend great toe or foot indicates
-peroneal or sciatic nerve injury
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` Medical Research Council (MRC) Scale for
Muscle Strength
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` Nerve conduction velocity
` Electromyography` Tinel sign
` Sweat Test
` Skin Resistance Test
` Electrical Stimulation
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` Stimulation of a
peripheral nerve by an
electrode placed on the
skin overlying the nerve
readily evokes aresponse from the
muscle innervated by
that nerve. This
response can be seen,
palpated, and measured
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` The nerve is stimulated proximal to, distal to,
and across the level of injury with subsequent
distal evoked potential recording achieved
using a needle or surface pick-up electrode .` Immediately after injury, stimulation proximal
and distal to the insult elicits a normal
response, although stimulation across the
injured segment may vary, depending on thepresence of axonal or myelin injury.
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` Muscle activity observed with a needle pick-upelectrode (e.g., monopolar, concentric, singlefiber) placed in myotomes innervated by aninjured nerve provides crucial information.
` The basic monopolar needle electrode samplesapproximately eight muscle fibers, and byassessing different sites, fair representation ofmuscle groups is possible.
` The muscle initially is observed at rest (insertional
activity, approximately 200 ms) and subsequentlyduring volitional muscle recruitment
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` At approximately 10 to 14
days after neural injury,abnormal spontaneousrest potentials (positivesharp waves) appear ininnervated myotomeswhere axonal injury has
occurred` At 14 to 18 days,
fibrillations appear
` Denervation potentials(fibrillations or positive
sharp waves or both) lastindefinitely until themuscle has becomereinnervated or fibrotic.
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` The Tinel sign is elicited by gentle percussion by afinger or percussion hammer along the course ofan injured nerve.
` A transient tingling sensation should be felt by thepatient in the distribution of the injured nerverather than at the area percussed, and thesensation should persist for several seconds afterstimulation.
` It should be tested for in a distal-to-proximaldirection.
` A positive Tinel sign is presumptive evidence thatregenerating axonal sprouts that have notobtained complete myelinization are progressingalong the endoneurial tube
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` A Sunderland type 1 injury or neurapraxia
should not show an advancing Tinel sign
because wallerian degeneration and axonalregeneration do not occur
` A distally advancing Tinel sign should occur in
Sunderland types 2 and 3 nerve injuries.
` A Sunderland type 4 or type 5 injury would notshow an advancing Tinel sign unless repaired.
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` SWEAT TEST- Sympathetic fibers within aperipheral nerve are resistant to mechanical
trauma. The presence of sweating within theautonomous zone of an injured peripheral nervereassures the examiner to a degree, suggestingthat complete interruption of the nerve has notoccurred
` SKIN RESISTANCE TEST- In it a Richterdermometer is used. The autonomous zone withabsence of sweating shows an increasedresistance to the passage of electrical current.
` ELECTRICAL STIMULATION- Galvanic stimulationis useful in determining chronaxy and thestrength-duration curve
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` Treatment depends upon the type of fracture
whether closed or open
` Nerve injury associated with closed fracture ,the
type of damage generally is neuropraxia oraxonotmesis and nerve recovery is good with
conservative treatment
` When the nerve injury associated with an open
fracture, the type of nerve damage is oftenneurotmesis in such cases nerve should be
explored.
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` The classification of nerve injuries proposed by Seddon in 1943
1. Neurapraxia:-Transmission of impulses is physiologicallyinterrupted for a time, but recovery is complete in a few daysor weeks.
2. Axonotmesis:-breakdown of the axon and distal walleriandegeneration but with preservation of the Schwann cell andendoneurial tubes. Spontaneous regeneration with goodfunctional recovery can be expected.
3. Neurotmesis:-more severe injury with complete anatomical
severance of the nerve or extensive avulsing or crushinginjury. The axon and the Schwann cell and endoneurial tubesare completely disrupted. The perineurium and epineuriumalso are disrupted to varying degrees.
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Splints
Passive movements of joints to prevent contractures
Physiotherapy-exercises and nerve stimulation
splints Nerve injury
Aer l e li t Br i l lexus i jur
C k upspli t R di l erve i jur
S ulder bducti spli t Axill r erve i jur
F t dr pspli t C mm per eal erve
i jur
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` If fractures needs open reduction, nerve should beexplored
` Generally open fractures with neurotmesis need surgery
` 1.primary repair-done within 6-8 hours after injury ifwound is clean
` 2.delayed primary repairbetween 7-18days after injuryif wound contaminated
` 3.seconadary reapair-18 days after injury, if injury seen
late, failure of conservative treatment ,cases with signsof nerve irritation
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1) ENDONEUROLYSIS-freeing of trapped nerve
2) PARTIAL NEURORRHAPHY-done if one half of
large nerve disrupted
3)
NEURORRHAPHY ANDG
RAFTING
-if gap present(commonly graft taken from sural nerve)
4) TENDON TRANSFER-done after 18 months of
injury if indicated when nerve has not regenerated or
patients present late
5) ARTHRODESIS(FAIL JOINTS)-if no tendons
available for transfer and there is no hope for
recovery