TOPIC:

EVALUATION OF BRACHIAL PLEXUS INJURY

Moderator: Presenter:Dr. J.K.REDDY Dr.Jaipalsinh MahidaProfessor & HOD Jr. Resident M.S OrthoDept. of Orthopaedics. Dept. of Orthopaedics.

SRI SIDDHARTHA MEDICAL COLLEGE, TUMKURDepartment Of Orthopaedics

Brachial plexus - Anatomy:

• is a complex network of nerves, which is responsible for innervation of upper extremity.• Formed in posterior cervical triangle by union of ventral rami of 5th ,6th , 7th ,

& 8th cervical nerve roots & 1st thorasic nerve root.• Occasionally contribution from C4 & T2.• Prefixed – with contribution of C4 (more common)• Postfixed – with contribution of T2

• This composite nerve network can be divided into:1. Roots:As each spinal nerve exists intervertebral foramen they divide into

anterior primary division(roots of brachial plexus) & posterior primary division(innervates paraspinal muscles).

2. Trunks:Roots runs in cleft between anterior & medial scalene muscle where they form trunk• Upper trunk – C5 & C6

• Middle trunk – C7

• Lower trunk – C8 & T1

3. Division:Each trunk behind clavicle divides into• Anterior division• Posterior division

4. Cords:Divisions combines to form the cords, which are named according to its relation to axillary artery• Lateral cord – anterior division of upper & middle trunks• Medial cord – anterior division of lower trunk• Posterior cord – posterior division of all 3 trunks.• Cords then divides and recombines to form major nerves of upper

limb.5. Branches:• supraclavicular region – from Roots & Trunks• Infraclavicular region – from cords

Branches from Roots:

• Nerve to Scalene & long colli – C5,6,7,8 – scalene , longus colli• Branch to phrenic Nerve – C5 - Supplies ipsilateral diaphragm• Dorsal scapular nerve - C5 – Rhomboids• Long thorasic nerve of bell - C5,6 – serratus anterior

• Branches from Trunks:• Nerve to subclavius - C5,6 – Subclavius• Suprascapular nerve - C5,6 – Supraspinatus, Infraspinatus

Branches from Cords:• Lateral cord

• Lateral pectoral - C5,6,7 – pectoralis major, pectoralis minor• Musculocutaneous - C5,6 ,7 – corachobrachialis, both head of biceps, most of brachialis, it continues as

lateral cutaneous nerve of forearm• Lateral root of median nerve - C5,6,7

•  Medial cord• Medial pectoral - C8, T1 – pectoralis major• Medial cutaneous nerve of arm - C8, T1 – supplies skin over front & medial side of arm• Medial cutaneous nerve of forearm - C8, T1 – supplies skin over lower part of arm & medial side of

forearm• Medial root of median nerve• Ulnar nerve :-

• Forearm – flexor carpi ulnaris, medial ½ of FDP• Palm – Interossei, 3rd & 4th lumbricals• Hypothenar – palmaris brevis, abductor digiti minimi, flexor digiti minimi, Opponens digiti minimi.• Thenar - adductor pollicis , Flexor Pollicis brevis

• Sensation medial 1½ finger

• Posterior cord• Upper Subscapular – partly supplies subscapular • Lower subscapular – subscapular , teres major• Thoracodorsal – lattismus dorsi• Axillary nerve – Deltoid, teres minor, Supplies skin over lower part of deltoid &

upper part of triceps• Radial nerve – Supplies triceps, anconies, brachioradialis, brachialis, extensor

muscle of forarm• Median Nerve: • Forearm – all flexor muscle of forearm except flexor carpi ulnaris & medial ½ of

FDP• Thenar – flexor pollicis brevis, abductor pollicis brevis, Opponens Pollicis Brevis• 1st & 2nd lumbricals• Sensory – supplies thenar palmar skin , lateral 3½ digits

ETIOLOGY:

• Road traffic injuries• Various other accidents – in factories, building sites, sports, sever falls• Iatrogenic (ligatures, drills, mastectomies, resection of 1st rib, etc)• Obstetric palsy• Gunshot wounds• Tumors• Secondary compression from trauma (callus , fibrous band, scar)• Electrocution

Machanism Of Injury:• Tractions / Over Stretching : the mechanism is violent traction of upper limb against the

body(RTA, other accident, etc)• Increased angle between head & neck Results in C5 C6 & C7 root or upper trunk disruption.• when upper limb is abducted above level of head with considerable force, can result in

avulsion of C8, T1 roots or lower trunk• Compression:

• Fracture of clavicle and callus formation may lead to compression of lower trunk• Tumors• Haemorrhage• Direct blow to side of neack

• Penetrating wounds / direct trauma: • this includes stab/ gunshot wound • direct blow to supraclavicular fossa over Erb’s Point

Classification of Peripheral Nerves Injuries: • Seddon’s Classification:• NEURAPRAXIA: Is a physiological block of electrical conduction without

anatomical axonal interruption. Recovery is complete in few days or weeks. E.g: Torniquet palsy, Saturday night plasy, skin traction palsy, crutch palsy.

•AXONOTMESIS: Is a physiological block of electric

conduction with anatomical interruption but without disruption of connective tissue framework created by endoneurium, perinuerium & epineurium. Spontaneous recovery is possible but takes longer than neurapraxia because of distal wallerian degeneration.

•NEUROTMESIS: : Is a physiological block of electric conduction due to anatomical axonal interruption & accompanying disruption of entire connective tissue framework created by endoneurium, perinuerium & epineurium. Spontaneous recovery is not expected unless surgery is intervened.

• SUNDERLAND’S CLASSIFICATION:According to sunderland, peripheral nerve injuries are arranged in ascending order of severity from 1st to 5th degree. Anatomically each degree represents injury to• Myelin• Axon• Endoneurial tube & its Contents• Perineurium• Entire nerve trunk

I. FIRST DEGREE INJURY: conduction along axon is physiologically

interrupted at site of injury but axon is not disrupted. No wallerian degeneration occurs. Recovery is spontaneous and coincides with neurapraxia of Seddon. Tinnel’s sing is negative.

II. SECOND DEGREE INJURY: Disruption of axon is evident.Wallerian

degeneration takes place distal to point of injury and primary degeneration takes place proximally for one/two nodal segments.integrity of endoneurial tube is maintained. Clinically neurological deficit is complete with loss of motor, sensory & sympathetic function. Tinnel’s sign is present and is progressive.

III. THIRD DEGREE INJURY: axons & endoneurial tubes are disrupted, but perineurium is preserved. The result

then is disorganization resulting from disruption of endoneurial tubes. Clinically neurological loss is complete in most instances, & because of additional time required for regenerating axon tips to penetrate the fibrous barrier, the duration of loss os more prolonged than in SECOND degree. Returning motor function is evident from proximal to distal but with varying degrees of permanent motor or sensory deficit. Advancing Tinel’s sign is present, however complete return of neural function doesn’t occur

IV. FOURTH DEGREE INJURY: Axons & endoneurial tubes are disrupted with disruption of perineurium,

but some epineurium and perineurium is preserved, so complete severance of the entire trunk doesn’t occur. Retrograde degeneration is more severe. Essentially, nerve continuity is maintained only by scar tissue preventing proximal axons from entering distal endoneurial tubes. Axonal sprouts exit through defects in the perineurium & epineurium & wander about in surrounding tissues. There will be no advancing tinel’s sign. Prognosis for significant return of sueful function is uniformly poor without surgery

V. FIFTH DEGREE INJURY: Nerve is completely transected,

resulting in variable distance between neural stumps. Occurs in open wounds & usually are identified at the time of early surgical exploration. Likelihood of any significant bridging by axonal sprouts is remote, & possibility of any significant functional return without appropriate surgery is equally remote.

VI. SIXTH DEGREE INJURY(described by Mac Kinnon) or Mixed injuries: In this type of injury nerve is partially severed & remaining part of the trunk

sustain forth, third, second or rarely even first degree injury. A neuroma in continuity will be present, & recovery pattern will be mixed depending on degree of injury to each portion of nerve. Surgical intervention to correct fourth & fifth degree component may sacrifice the function of lesser injured fascicles.

Classification of brachial plexus lesions:

• leffert classification is commonly used system to describe brachial plexus lesions• Power modification of leffert classification is more comprehensive & provides

useful prognostic information regarding injury.• Types defines mechanism of injury• Sub-types define severity of injury • Sub-type “C” injuries are severe & most likely to have associated vascular involvement.

Leffert Classification of brachial plexus injuries:I. Open (usually from stabbing)II. Closed (usually from motorcycle accident)

II-a: supraclavicular- preganglionic• Avulsion of nerve root usually from high speed injury• No proximal stump, no neuroma formation• Pseudomeningocele, denervation of neck muscles are common• Hornor’s sign (ptosis, miosis, anhydrosis)- postganglionic• Roots remains intact• Usually from traction injuries• There are proximal stump & neuroma formation• Deep dorsal neck muscles are intact & pseudomeningocele will not develop.

II-b: infraclavicularusually involves branches from trunkFunction is affected based on trunk involvement

upper- biceps, shouldermiddle- wrist, finger extensionlower- wrist, finger flexion

III. Radiation indusedIV. Obstetric

IV-a: Erb’s (Upper root) – waiter’s tip handIV-b: Klumke (lower root)

Power modification of leffert classification

CLINICAL FEATURES:• History regarding mechanism of injury

• Birth injury – rupture occurs most frequently in that portion of plexus subjected to greatest stretch namely 5th & 6th roots & upper trunk.

• Axillary & infraclavicular wounds – individual nerves & large blood vessels are more likely injured

• Stab & bullet wounds – most exposed portion are injured C5 ,C6 C7

• High velocity m• Patients may present with symptoms like – pain especially of neck & shoulder,

paresthesia, weakness or heaviness in the extremity

GENERAL EXAMINATION:• Especially important in case of RTA to rule out conditions which may require

emergency treatment like head injury, chest injury, abdominal injury, injuries to other limbs.• Associated injuries – like cervical vertebral fracture, clavicular fracture,

fracture proximal humerus, rupture of subclavian vessels should be ruled out.

• NEUROLOGICAL EXAMINATION:• Detailed motor & sensory chart should be documented to determine nature of

lesion & to act as a baseline for further examination.• Neurological examination should be given an idea about

• Location of brachial plexus injury• Severity of brachial plexus injury

• LOCATION OF BRACHIAL PLEXUS INJURY:• Injury to roots results in:

• C5 – Affects the shoulder abduction, extension, external rotation & elbow flexion.• C6 – affects sternal head of pectoral major & triceps• C7 – Affects extensors of wrist & fingers• C8 – Affects flexors of wrist & fingers• T1 – Affects intrinsic muscles of hand.

• These roots may be involved in different combination, when all roots are involved – complete plexus syndrome.

• Clinical signs indicating more proximal injury & hence a preganglionic injury of plexus:• Involvement of long thorasic nerve – paralysis of serratus anterior – winging of scapula• Involvement of dorsal scapular nerve – rhomboid & levator scapulae • Involvement of sympathetic fibers of 1st thorasic ganglion – Horner’s syndrome : ptosis,

miosis, anhydrosis

• Injury to TRUNKS:• Upper arm syndrome(Erb – Duchenne type ) : this syndrome is probably most

common brachial plexus palsy that is now seen particularly following motorcycle accident.• Site – Erb’s point – upper two cervical nerves (C5 & C6) or upper trunk• Casuse – any force that increase the angle between neck and shoulder – producing traction

force on upper trunk.  Muscle paralyzed Deformity

Shoulder Deltoid, teres minor, supraspinatus, clavicular head of pectoralis major

Arm is therefore rotated internally & adducted

Elbow Biceps, coracobrachialis, brachialis (weakened) Elbow extended

Forearm Supinators are affected Forearm is pronated

Wrist Radial extensors of wrist & brachioradialis are paralyzed

Ulnar deviation of hand

• The deformity is called police man’s tip / porter’s tip deformity.• Sensory sign : this minimal if lesion is confined to anterior primary ramus of C5,

but if C6 is affected, there is loss of sensation of lateral aspect of arm, forarm & thumb.• Lower arm syndrome (Klumpke’s Paralysis): • Site of injury : usually affects 1st thorasic nerve but may involve whole lower

trunk – mainly T1 partly C8 • Cause – undue abduction of arm as clutching something with the hand during

fall from height, birth injuries, crushing between clavicle & 1st rib.

• Sensory sign: Zone of anaesthesia over ulnar side of hand & forearm and narrow strip of upper arm.• Associated with HORNER’s Syndrome : this occurs when 1st thorasic nerve is

injured proximal to its original injury – injury to sympathetic fibers – cause Horner’s syndrome.

Muscle paralyzed Deformity

Intrinsic muscles in han d – T1

Ulnar flexors of wrist & fingers – C8

Claw hand deformity - IP joints being flexed, MCP joints Hyperextended

• INJURY TO CORDS: • Injury to lateral cord:

• Nerve involved – Musculocutaneous, lateral root of median nerve.• Muscle paralyzed – biceps & coracobrachialis, all muscles supplied by median nerve except those to

hand• Deformity & disability – midprone of forearm, loss of flexion of forearm, loss of flexion of wrist,

sensory loss on radial side of forearm.• Injury to medial cord:

• Nerve involved – Ulnar nerve, ,edial root of median nerve• Muscle paralyzed – miscle supplied by ulnar nerve , 5 muscles of hand supplied by median nerve• Deformity – claw hand , sensory loss on ulnar side of forearm

• Injury to posterior cord:• Nerve involved – radial, axillary, subscapularis , thoracodorsi• Muscles paralyzed – extensors of forearm & wrist, deltoid, teres, lattismus dorsi

INVESTIGATIONS:

• Tests for peripheral nerve lesion – EMG, nerve conduction velocity(NCV), somatosensory evoked potential (SEP), intraoperative nerve action potential (NAP)• EMG(electromyography):

• It studies extracellular recording of propogating muscle action potential• Electrode used – bipolar fine wire,or Teflon coated simple amplifier• Recording device – it is an amplifier, it photographic or electromagnetic frequency modulation tape recording.• Importance of EMG studies:

• Defibrillation potential: when a nerve is cut & muscle is denervated , for initial 3-4 weeks no muscle contraction occurs. After 4 weeks – muscle fibers starts contracting independently & in rhythmical manner – Fibrillation of muscle. These contraction can’t be seen but can be noted in EMG – known as defibrillation potential (high amplitude waves)

• Reinnervation potential : Now if nerve regeneration & conduction of action potential to muscle starts, the denervated potential changes to prolonged polyphasic low amplitude waves. These waves are called Reinnervation potential.

• So to detect renervation , EMG studies should be started 4 weeks onwards after injury & should be reported at lest for 3 times. If after 12 weeks of EMG studies, no reinnervation potential develops – it indicates no nerve regeneration occurs on its own & surgical intervention in needed.

• So important use of EMG studies in Serial evaluation of injury is• For first 3-4 weeks after injury – no response• Roughly 3 weeks after deinnervationm EMG shows

• If Defibrillation potential & positive sharp waves typical of denervated muscle – axonotmesis or neurotmesis

• If defibrillation potential not seen, early EMG detects minimal residual innervation – neuropraxia• A decrease in number of fibrillation potential & positive sharp waves

apparence of prolonged polyphasic low amplitude potential verifies reinnervation – seen several weeks before onset of detectable voluntary muscle power – signifies further period of observation.• EMG examination of cervical paraspinal muscle spasm which are innervated

by primary division of spinal nerve signifies atleast some roots sustained preganglionic injury, although this specific nerves cannot be identified because of overlap of segmental innervation of paraspinal muscles.

• Nerve conduction velocity:• It tests only peripheral or postganglionic fibers i.e if postganglionic fibers are damaged – it

will be absent & if preganglionic fibers are damaged – it will be present• Loss of sensation in area supplied by spinal nerve

• If normal sensory nerve conduction (no wallerian degeneration) – pregsnglionic, (radial / median C6,C7, ulnar – C8, T1)

• If sensory nerve conduction is absent (wallerian degeneration) – postganglionic

• The severed motor axons continue to conduct action potential for several days, this ability is lost in 2 weeks as wallerian degeneration proceeds. If distal motor conduction is preserved beyond this period, the nerve injury must be a conduction block (neuropaxia) even though involved muscle may be still paralyzed

• SEP(Somatosensory Evoked Potential):• It tests the entire sensory pathway from stimulus to cerebral cortex• So in any case, if preganglionic or postganglionic Fibers are damaged – evoked potential will

be absent.• SEP is elicited by stimulation of distal median, ulnar, radial nerve & recorded over spinous

process of C2, & Contralateral somatosensory cortex.• Factors limiting values of SEP in early evaluation of plexus injury

• Peripheral nerve is made up of fibers from more than one spinal nerve so since unless multiple roots are avulsed some EP’s transmitted to CNS

• Only small No. of functional axons between stimulus sites & CNS are required to transmit EP. thus nearly completely disrupted dorsal root may appear intact in study.so a negative SEP examination is more important than positive.

• No adequate peripheral stimulating site for important C5 root.

• Intraoperative NAP:• Is extraordinary value in evaluation of injury in continuity. This technique establish whether

axonal regrowth across area of injury. Several thousand functioning axons are required to transmit NAP.• If NAP can be elicited across the area of injury, many viable conduction axons have

transverse the injury and progressing distally down the nerve.• The lack of NAP indicates complete neurotemetic injury requiring resection of damaged

area and grafting.• NAP testing should be delayed 3-4 months post injury to allow time for sufficient axonal

regrowth, if NAP can be transmitted across the area of injury the patient has 93% chances that useful motor function will develop in the muscle supplied by the nerve.

• Imaging studies:• X-ray of cervical spine: fracture of lateral masses of cervical vertebrae strongly associated

with pre-ganglionic injury• Chest X-ray: fracture of 1st & 2nd rib indicates severity of trauma, elevated hemi diaphragm –

phrenic palsy – hence a proximal injury to upper plexus. Fracture of scapula, clavicle may suggest infra clavicular brachial plexus injury

• Cervical myelography with CT scan: should be obtained 2-3 months after injury if possible injury is strongly suspected • Absence of demonstrable rootlets in the sub arachnoid space at the level of myelogram or CT

suggest that avulsion has occurred • Presence of meningocele is evidence only that arachnoid was torn at a given root level and it is

not proved that root has avulsed

• CT scanning: In conjugation with cervical myelography is helpful however by itself. It is of little value in plexus injury. CT scan obtained for cervical spine injury can show evidence of fracture lateral masses

• MRI: Usefulness of MRI evaluation of plexus injury is still unclear, however MRI can demonstrate distal plexus better than compared to CT.

THANK YOU