anatomi PBI

The anatomy, investigationsand management of adultbrachial plexus injuriesJonathan Gregory

Alex Cowey

Matthew Jones

Simon Pickard

David Ford

AbstractBrachial plexus injuries have increased in numbers since the turn of the

twentieth century in line with the increased use of motorcycles. Advances

in microsurgical and tissue transfer techniques have seen the management

of such injuries change dramatically during this time period. As a result,

surgery for plexus injuries is now considered a legitimate option. Such

injuries require extensive medical input in a multidisciplinary environment.

All patients should be thoroughly investigated to establish the exact extent

was confined to exploration in order to determine prognosis,

onic, as this significantly affects both management and prog-

PERIPHERAL NERVEof the injury andmanaged on an individual basis. The options available are

conservative or surgical. Conservative options include physiotherapy,

orthotics and pain control. Surgical reconstruction of the plexus may

involve neurolysis, nerve grafting, nerve transfer and late peripheral recon-

struction including arthrodesis, tendon transfers, free muscle transfers and

amputation. Despite many advances in the field, injuries still result in

considerable disability and loss of working days.

Keywords anatomy; brachial plexus; management; nerve injury;

neurophysiology

Jonathan Gregory BSc MB ChB FRCS (TO) Specialist Registrar Trauma andOrthopaedics, Robert Jones and Agnes Hunt Orthopaedic & District

General Hospital, Shropshire, UK.

Alex Cowey MB ChB FRCS (TO) Specialist Registrar Trauma andOrthopaedics, Robert Jones and Agnes Hunt Orthopaedic & District


Matthew Jones MB ChB MRCP Clinical Research Fellow and Specialist

Registrar in Neurology, University of Manchester, Wolfson Molecular

imaging Centre, Manchester, UK.

Simon Pickard MB ChB FRCS FRCS(Orth) Consultant Orthopaedic Surgeon

and Specialist in Hand, Upper limb and Nerve Injury Surgery, Nerve

Injury Unit, The Robert Jones and Agnes Hunt Orthopaedic & District


David Ford MB ChB FRCS FRCS(Orth) Consultant Orthopaedic Surgeon and

Specialist in Hand, Upper limb and Nerve Injury Surgery, Nerve Injury

Unit, The Robert Jones and Agnes Hunt Orthopaedic & District General

Hospital, Shropshire, UK.ORTHOPAEDICS AND TRAUMA 23:6 420nosis, and this may require supplementary tests such as

electrophysiological or radiological investigations. Concurrent

severe injuries occur in up to 80% of patients, and the attending

clinician must be alert to this. Commonly associated injuries

include dislocated shoulders, fractures of the proximal humerus,

clavicle, scapula and cervical spine, in addition to major upper

limb vascular injuries (subclavian or axillary artery). These

injuries require management in their own right but can also

provide vital clues to the extent and nature of the plexopathy.

A lesion can be classified using a variety of systems, which

often differentiate between upper plexus and lower plexus

injuries. Lefferts classification system6 based on aetiology and

level of the injury is commonly used (Table 1), but it must be

remembered that lesions may occur at more then one level.

Following a full evaluation the management plan should be

tailored to an individual patients needs and a time scale set out,

with consideration given to both conservative measures and

secondary reanimation of the limb.more complex interventions being associated with poor

results.1e4 The extent of this belief is highlighted by Seddons

comments in 1961 The results of reconstructive operations have

been so disappointing that we believe that this type of treatment

should be abandoned.5 Towards the end of the 20th century

advances in microsurgical techniques and tissue transfer proce-

dures have improved the functional outcome of these injuries.

However, many of these patients still require extensive medical

input and a multidisciplinary approach to their care.

Assessment

A full assessment to establish the aetiology, and clearly define

the level and severity of the injury must be performed. It is

important to ascertain whether the lesion is pre- or post gangli-Introduction

Brachial plexus injuries range from transient nerve dysfunction

to a completely flail upper limb associated with life-threatening

injuries. Significant injuries lead to physical disability in addition

to psychological and financial hardship. The management of

such cases is complicated by concurrent injuries that may delay

or cloud the neurological assessment. In addition to this,

anatomical variations within the brachial plexus make these

injuries a considerable challenge to clinicians responsible for

their care.

Traumatic lesions are most commonly the result of motor-

cycle accidents and typically affect young men.1e3 Lesions can

also occur following penetrating or sports related injuries, falls,

industrial accidents, radiation therapy and iatrogenic causes

(first rib resection, shoulder surgery, interventional radiology).

The most common mechanism is a traction injury to the nerves

secondary to forceful separation of the neck from the shoulder.1

History

Brachial plexus reconstruction began in earnest in the mid 20th

century with work by Barnes, Brooks, Bonney, Seddon and

Leffert and later Narakas. Despite their work the role of surgery 2009 Elsevier Ltd. All rights reserved.

Anatomy of the brachial plexus

The anatomy of the brachial plexus demonstrates a large

degree of variability, both between individuals and between

the left and right limbs of the same individual.7 Most

commonly the brachial plexus is formed by the confluence of

the ventral rami of the spinal nerve roots from C5 to T1.

Common variations include contributions to the plexus by

the C4 nerve root (described as a pre-fixed plexus) or the T2

nerve root (a post-fixed plexus). The 5 roots normally

contributing to the plexus merge into 3 trunks, each of which

Two anatomical triangles contain the proximal plexus. The

interscalene triangle is formed between the anterior and middle

scalene muscles superiorly and the first rib inferiorly and

contains the roots of the plexus. The posterior triangle of the

neck contains the trunks of the plexus and is formed by the

sternocleidomastoid muscle anteriorly, trapezius laterally and

the clavicle inferiorly.

Dorsal (sensory) and ventral (motor) rootlets arise from the

spinal cord and merge to form a root as they pass through

the vertebral foramen. Just prior to the formation of the root the

sensory rootlet enlarges in diameter forming the dorsal root

ganglia (DRG). The DRG contains the cell bodies of the sensory

nerves (motor nerve cell bodies are within the spinal cord). An

injury proximal to the DRG is described as pre-ganglionic. This

may be avulsion of the rootlets from the spinal cord or an injury,

which is still intradural, but just proximal to the DRG. The

rootlets have no connective tissue or meningeal covering as they

originate from the spinal cord; this contributes to their suscep-

tibility to avulsion from the cord. The roots have a protective

layer formed by the dura and are able to move freely within the

foramen. As the C4, C5, C6 and C7 roots emerge from the

foramen they are tethered to the transverse processes of their

respective vertebrae. C8 and T1 are not tethered in this way,

which leads to a higher incidence of root avulsion from the spinal

cord being seen at these levels compared to the upper plexus.

The roots enter the scalene triangle, being found between

anterior and middle scalene muscles. The first terminal nerves to

Leffert classification of brachial plexus injuries

I Open

II Closed IIa Supraclavicular

Preganglionic e nerve root avulsion

Postganglionic e traction injuries

IIb Infraclavicular

IIc Combined

III Radiotherapy induced

IV Obstetric IVa Upper root (Erbs palsy)

IVb Lower root (Klumpkes palsy)

IVc Mixed

Table 1

PERIPHERAL NERVEsplits into anterior and posterior divisions. The divisions

become 3 cords which give rise to the terminal branches

(Figure 1).Figure 1 Diagrammatic representation of the Brachial Plexus.

ORTHOPAEDICS AND TRAUMA 23:6 421arise from the plexus do so at this level. The C5 root has 3

branches at this point: contributions to the phrenic, long thoracic

and dorsal scapular nerves. The roots descend and move laterally

into the posterior triangle of the neck. 2009 Elsevier Ltd. All rights reserved.

Terminal branches of the roots, trunks and cords of the brachial plexus

Nerve Origin from plexus Root value Muscle/area innervated

Phrenic Root C345 Ipsilateral hemidiaphragm

Dorsal scapular Root C5 Rhomboids

Long thoracic Root C567 Serratus anterior

Subclavius Upper trunk C56 Subclavius

Suprascapular Upper trunk C56 Supraspinatus, infraspinatus

Lateral pectoral Lateral cord C56 Clavicular and sternocostal heads

Pectoralis major, Pectoralis minor

Medial pectoral Medial cord C678 Sternocostal head Pectoralis major,

Pectoralis minor

Medial brachial cutaneous Medial cord Medial arm above the elbow

Medial antebrachial cutaneous Medial cord Medial forearm

Upper subscapular Posterior cord C567 Subscapularis

Thoracodorsal Posterior cord C678 Latissimus dorsi

Lower subscapular Posterior cord C567 Subscapularis, Teres Major

Table 2

PERIPHERAL NERVEThe C5 and C6 roots combine to form the upper trunk of the

plexus. The point atwhich they become confluent is knownas Erbs

point.TheC7rootbecomes themiddle trunkand theC8andT1roots

merge into the lower trunk. If, on clinical examination, the rhom-

boids (dorsal scapular nerve) and serratus anterior (long thoracic

nerve) are functional the lesion must be distal to Erbs point.

The trunks divide to form anterior and posterior divisions,

which are located behind the clavicle. The upper trunk gives off

the nerve to subclavius and the suprascapular nerve, supplying

supraspinatus and infraspinatus, prior to forming its 2 divisions.

There are no branches given off by the divisions of the

brachial plexus. The posterior divisions all combine to form the

posterior cord located behind the axillary artery. The anterior

divisions of the upper and middle trunks form the lateral cord,

lateral to the axillary artery, and the anterior division of the lower

trunk forms the medial cord, medial to the axillary artery. Thereare terminal branches arising from all of the cords. The lateral

Dorsal rootganglion

A

C-spine

Posterior

B

Figure 2 Preganglionic and Postganglionic nerve lesions.

ORTHOPAEDICS AND TRAUMA 23:6 422cord gives off the lateral pectoral nerve to pectoralis major. The

posterior and medial cords each give rise to 3 terminal branches.

The posterior cord forms the upper subscapular, thoracodorsal

and lower subscapular nerves. The medial cord gives rise to the

medial pectoral nerve, the medial brachial cutaneous nerve and

the medial antebrachial cutaneous nerve.

The terminal branches of the plexus arise from the cords. The

posterior cord terminates as the axillary and radial nerves.

The lateral cord contributes to the median nerve and forms the

musculocutaneous nerve. The medial cord forms the ulnar nerve

and contributes to the median nerve (Table 2).

Clinical clues to the anatomical location of pathology

When considering the level of an injury to the brachial plexus

injury, the most important step is determining whether a lesion

affects the roots and is therefore pre-ganglionic (proximal to thedorsal root ganglion) or post ganglionic (Figure 2).

Stretch

RupturePOSTGANGLIONIC

Avulsion

PREGANGLIONIC

2009 Elsevier Ltd. All rights reserved.

nerve. This has finger-like projections called filopodia, which

explore the microenvironment. The axon grows and contracts by

the addition and removal of actin polypeptides. The filopodia

guide the growing axon towards the distal stump and its Bynger

bands. It responds to four classes of substances; neurotrophic

factors, neurite promoting factors, matrix forming precursors and

metabolic factors.

Pathological changes also occur in the target organs for the

nerve. When their motor supply is lost, muscle cells reduce in

volume leading to atrophy and interstitial fibrosis. Denervation

hypersensitivity is produced by an increase in the number of

motor endplates. The muscle then responds to smaller amounts

of acetylcholine than is normally effective, which is detected as

fibrillations on electromyography (EMG) and clinically may

produce fasciculation. Motor endplates start to be lost irretriev-

ably after 3 months. Sensory end organs such as Meissner

corpuscles also degenerate, although over a less clearly defined

time scale than muscle. These end organ changes are the factor

PERIPHERAL NERVEThere are clinical clues that indicate that an injury has

occurred in the vicinity of the DRG. If the rhomboids or serratus

anterior are weak then pre-ganglionic injury should be sus-

pected, as the dorsal scapular and long thoracic nerves arise at

the proximal ends of their roots. In a non-acute situation fasi-

culations may be seen in the paraspinal muscles. These are not

supplied by the plexus but from the dorsal rami, which arise from

the spinal nerves as they exit the intervertebral foramen.

The T1 root is in close proximity to the T1 sympathetic

ganglion. The inference is that if the T1 sympathetic ganglion is

injured then it is probable that the T1 root will also have been

injured. Injury to the T1 sympathetic ganglion will produce

a Horners syndrome of the ipsilateral eye. The 4 components of

Horners syndrome are; meiosis (unopposed parasympathetic

function), mild ptosis (weakness of Mullers muscle which

assists levator palpebrae superioris), enopthalmos and facial

anhydrosis.

Classification of peripheral nerve injury

Myelinated peripheral nerve fibres are surrounded by Schwann

cells. Each nerve fibre and its accompanying Schwann cell are

surrounded by loose vascular tissue called endoneurium.

Bundles of nerve fibers are grouped together into fascicles. Each

fascicle is covered in a layer of collagen called the perineurium.

Most nerves consist of numerous fascicles, which are held

together by loose collagenous tissue, which is condensed

peripherally into a strong outer layer; the epineurium.

Seddons classification of nerve injury is widely used and

describes nerve injuries as neurapraxia, axonotmesis and neu-

rotmesis.8 Neurapraxia is due to a physiological dysfunction

leading to a blockade of nerve conduction. The axon of the nerve

fibre remains in continuity, without any degeneration of the

nerve distal to the site of injury. There may be a local area of

myelin damage that is repaired by the Schwann cells9 and normal

conduction is restored. Axonotmesis describes loss of axonal

continuity of individual nerve fibres but the perineurium is

preserved. Neurotmesis is the most severe injury where all the

connective tissue elements and axons of the peripheral nerve are

disrupted.

The category of axonotmesis is very broad and contains

a variety of nerve injuries that have very different outcomes.

Therefore Seddonss classification was refined by Sunderland.10

Sunderlands classification is based upon 5 groups. The benefit of

Sunderlands classification is that it subdivides axonotmesis in to

injuries that recovery very well (type 2) from those that have

a poor outcome, (type 4) (Table 3).

The classification systems of Sunderland and Seddon can only

be applied retrospectively or at the time of surgical exploration.

Birch and Bonney developed a classification system based upon

neurophysiological testing.11 They defined injuries as those

producing a conduction block and those without a conduction

block with the hope of producing a more clinically useful clas-

sification system.

Pathophysiology of nerve regeneration

Axonotmesis and neurotmesis involve axonal damage, which

leads to pathological changes along the entire nerve, from the

nerve distal to the injury up to the cell body.12,13 There isORTHOPAEDICS AND TRAUMA 23:6 423swelling of the cell body and the nucleus moves to the periphery

of the cell body. Approximately 10% of the cell bodies may

undergo apoptosis. The rough endoplasmic reticulum changes,

with dispersal of the Nissl granules, which are usually involved

in neurotransmitter production, in a process called chromatol-

ysis. These changes occur as the cell switches its synthetic output

from neurotransmitters to the structural proteins required for

nerve repair. There is increased synthesis of mRNA, actin,

tubulin and growth factors. The axon proximal to the injury

undergoes retrograde degeneration to the node of Ranvier prox-

imal to the zone of injury. The nerve stump distal to the point of

injury undergoes Wallerian degeneration after 48 to 96 hours.

There is demyelination and axonal degeneration. Schwann cells

proliferate and act to phagocytose the degenerating nerve in

a calcium dependent process. Macrophages rapidly invade the

distal nerve stump removing debris14 and secreting neurotrophic

factors to commence repair. The neurobiology of nerve repair has

been discussed in a recent Current Orthopaedics article.15

Once Wallerian degeneration is complete the Schwann cells

begin to align themselves along their basal laminae. This leads to

the formation of columns of Schwann cells called Bynger bands.

These columns provide a structural framework for regeneration.

A growth cone emerges from the proximal end of the divided

Comparison of the Seddon and Sunderland classifi-cation of peripheral nerve injury

Sunderland

classification

Seddons

classification

Histology

1 Neurapraxia Physiological not

anatomical disruption

2 Axonotmesis Endoneurium and

perineurium intact

3 Axonotmesis Intact Perineurium

4 Axonotmesis Intact Epineurium

5 Neurotmesis All layers disrupted

Table 3 2009 Elsevier Ltd. All rights reserved.

that limits the time available for nerve repair. If the recovering

nerve does not reach the end effectors within approximately 18

months following injury then little functional improvement will

occur.

In addition to the type of nerve injury other factors determine

prognosis (Table 4).

Investigations

The aim of investigations is to localise the level of the brachial

plexus lesion and determine the prognosis for spontaneous

recovery. Knowledge of these two features determines the

subsequent patient management.

Radiological

During the initial assessment of the patient, plain films of the

clavicle and cervical spine may identify bony injuries and raise

the clinical suspicion for a brachial plexus injury e.g. displaced

fracture of the transverse process of the cervical spine, fracture of

the 1st and 2nd ribs. The complexity of the anatomical structure

of the plexus, combined with the number of air/fluid/fat inter-

Histamine test

Now rarely performed, it was of use in differentiating pre-

ganglionic from post ganglionic lesions. A drop of histamine is

placed on the skin and the skin is scratched through the hista-

mine. When the nerve is intact a triple response will occur

(vasodilatation, wheal formation and a flare response). The

histamine causes vasodilatation. The wheal is localised tissue

swelling due to increased capillary permeability secondary to

histamine and substance P. The flare is a mottled reddening

around the area of skin injury due to mechanical stimulation of

nociceptive nerve endings and C fibres. This leads to antidromic

conduction in axon branches, which then release substance P,

which causes vasodilatation and histamine release from mast

cells in the surrounding tissues. When there is nerve disruption

proximal to the DRG there will be a normal response in an area of

skin that is anaesthetic. If the nerve is injured distal to the DRG

there will be vasodilatation and wheal formation in an anaes-

thetic area of skin but no flare response will occur as this is an

axon-mediated response requiring a functioning axon in conti-

nuity with its cell body.

s are

o se

ion

Poorer outcome if arterial injury

reb

ette

lly

rog

m

eco

bro

s. E

PERIPHERAL NERVEAge of patient Better outcome in younger patients. Ce

changes in sensory input.

Type of nerve Purely motor or sensory nerves have b

reach an end organ that they can usefu

superficial radial nerve.

Level of injury Supraclavicular injuries have a poorer p

prognosis.

Pain Patients who have persistent pain for 6

prognosis with regard to neurological r

Time interval injury to surgery If surgery is delayed for months then fi

Patient factors Other medical co-morbidities, infection

Table 4Traction poorer than sharp divisfaces (due to its proximity to the lungs and vasculature struc-

tures) make interpretation of brachial plexus imaging difficult.

The main role of imaging in traumatic brachial plexus injuries

is to differentiate root avulsions from more distal injuries. Roots

are approximately 1 mm thick and, until recently, the conven-

tional slice thickness of CT and MR imaging was greater than

this. Improvements in hardware and scanning sequences mean

that useful information can now be obtained.

MR scanning is useful in the investigation of non-traumatic

lesions because of the wide variety of pathology that may be

responsible for non-traumatic brachial plexus dysfunction; infil-

trating tumours, compressive tumours, radiation injury, idio-

pathic brachial neuritis and vasculitic/granulomatous conditions

may all result in a brachial plexopathy. Oedema on a T2

weighted scan indicates the zone of injury and if it is within or

around the plexus it implies injury if the clinical situation

correlates with a plexus injury.

Factors affecting outcome of peripheral nerve injury

Factor Effect

Mechanism of injury High energy poorer prognosis related tORTHOPAEDICS AND TRAUMA 23:6 424verity of injury.

ral cortex plasticity allows adaption to new sizes of motor units and

r functional recovery than mixed nerves (growth cones more likely to

supply). Some pure nerves do poorly for unknown reasons eg

nosis than infraclavicular injuries. Upper trunk lesions have the best

onths after a brachial plexus injury have a poorer

very.

sis and degeneration of end organs make for a poorer outcome

ffect of smoking unknown but thought to be detrimental.stimulus arrive. The period during which the Na channelBasic electrophysiology

Action potentials (AP) are transient changes in axon membrane

potential, which are conducted over considerable distances

without any change in amplitude. Neurons have a negative

resting membrane potential - their internal charge is negative

relative to the surrounding environment. This is due to the rela-

tive levels of K, Na and Cl across the membrane. The restingmembrane potential for neurons is approximately70 mV.Whena neuron is stimulated above its threshold for activation there is

a rapid influx of Na, which causes depolarisation. Themembrane potential usually reaches approximately 30 mVbefore the Na channels are inactivated. Voltage sensitiveK channels open and release potassium into the surroundingenvironment and Cl channels allow chloride into the cell tore-establish the negative membrane potential of 70 mV. Thesodium channels are then capable of reactivation should another 2009 Elsevier Ltd. All rights reserved.

ed to

Changes in conduction velocity and amplitude can be used to help

differentiate between types of nerve injury andmay indicatewhether

demyelination or axonal damage or both has occurred (Figure 4).

5

10

15

20

mV

NormalVelocity

Reduced

ixed

Demylinat

ing

PERIPHERAL NERVEobtain greater reproducibility of results. The response of the

distal motor unit is usually recorded by a surface electrode

placed on the skin overlying the belly of the target muscle.

Needle electrodes are occasionally required if there has been

profound muscle wasting. The recording from the muscle is

called the motor action potential (MAP) or the compound

muscle AP (CMAP). The CMAP represents a summation of the

voltage responses from individual muscle fibre action potentials.

The time from the stimulus being applied and the appearance of

the MAP is called the distal motor latency. This period of time is

a composite of the time taken for nerve excitation, conduction of

the AP, Acetylcholine release at the NMJ and generation ofhave an effect on the amplitude of the motor potential. T

a supra-maximal stimulus. A supra-maximal stimulus is usclosed as the cell repolarises is called the refractory period, as the

cell is unable to respond in this period to standard stimuli.

At any time only a small area of the axon is depolarised as the

AP passes along it. The flow of the AP is unidirectional, as the

area the AP has passed through will enter a refractory period and

reversal of the direction of flow is thereby prevented.

AP velocity is increased by increasing nerve fibre size, as in

these circumstances there are more ions within the cell to carry

the current. Myelination means that depolarisation is limited to

the nodes of Ranvier. This reduces the number of depolarisations

required to travel the length of the nerve (salutatory conduction).

Nerve conduction studies (NCS)

Motor studies (Figure 3): An electrical stimulus is applied to the

skin directly over a nerve. The electrical stimulus intensity is

gradually increased until a further increase in stimulus does not

his is

5 10 15 20 25 30 35 40 45 50

m/s

Figure 3 CMAP recording - biphasic, large amplitude and long duration ofthe potential.a post synaptic muscle potential to trigger the muscle response.

To calculate conduction velocity the nerve must be stimulated at

2 points along its course with the MAP being measured by the

same muscle electrode. To remove the effect of the distal

apparatus the conduction velocity is then calculated.

The normal conduction velocity in the upper limbs is between

45 and 60 m/s, whilst in the lower limb it is between 40 and 55

Conduction Velocitym=s Distance bproxima

ORTHOPAEDICS AND TRAUMA 23:6 425m/s but absolute values vary between patients and with different

recording apparatus. Intra-examiner variability is low but there

can be considerable inter-observer variability of sensory and

motor amplitudes.16 For this reason serial studies should be

performed by the same neurophysiologist.

The amplitude of the CMAP relates to the number of working

muscle fibres in the muscle sampled. The conduction velocity is

proportional to the nerve diameter. Conduction velocity is lower

in unmyelinated axons and axons which have undergone

demylination. Motor and sensory conduction velocity decreases

with age; 0.4e1.7 m/s per decade after 20 years of age for motor

and 2e4 m/s for sensory.17

After the CMAP has been recorded there may be observed the

appearance of a small F wave. This is a rebound phenomenon. The

nerve has been stimulated somewhere along its length therefore

the AP can move proximally and distally (unlike under normal

circumstances where the AP begins either proximally or distally).

The AP therefore passes up the nerve to the motoneurone cell body

and then comes back down the nerve, eventually reaching the

recording electrode after the CMAP. F waves are a sensitive marker

of nerve pathology and are useful when the lesion is very proximal

and not therefore easily accessible by routine NCS techniques.

Reduced

Amplitu

de

M

Axonal

Figure 4 Differentiating types of nerve lesions using changes in conduc-tion velocity and amplitude.Sensory studies (Figure 5): A sensory nerve is stimulated distally

and the response is recorded proximally. The proximal response

is called the Sensory Nerve Action Potential (SNAP). In the upper

limb sensory nerves are often stimulated by the use of a ring

electrode placed on a digit served by the nerve of interest e.g.

middle finger for median nerve. SNAPs are much smaller than

CMAPs e in the micro-volt range. The conduction velocity and

etween the 2 sites of nerve stimulus

l latencyms distal latencyms


erve

denervation changes are localized to deltoid, triceps and extensor

digitorum communis a posterior cord lesion should suspected.

EMG is able to differentiate myopathic from neuropathic

causes of muscle weakness. EMG can also identify the first

signs of recovery after nerve injury. As the regenerating motor

axons start reforming motor units they initially conduct at

a slower velocity, leading to low amplitude complex poly-

phasic waveforms being recorded from the muscle. These are

called nascent potentials and are an early sign of reinnerva-

tion. Nascent potentials are the only way to differentiate

temporary from permanent denervation. As recovery

continues the waveforms become greater in amplitude and

have a simpler waveform. When reinnervation is complete the

EMG will still not be completely normal, as the size of the

1

10

20

30

40

2 3 4 5 6 7 8 9 10

uv

m/s

Figure 5 SNAP recording - triphasic, small amplitude and short duration of

potential.

PERIPHERAL NERVEroots or anterior horn cell diseases. They are caused by hyper-

sensitivity to acetylcholine as receptor numbers are up-regulated

to compensate for the reduced/lost innervation. The acetylcho-

line receptors are also found outside the confines of the previous

neuromuscular junction spreading across the whole muscle

surface. Fasciculations may be seen; these represent spontaneous

discharges. They develop approximately 7e14 days after dener-

vation. Muscles are sampled by EMG to map the distribution of

denervation changes. This information can then be interpreted to

allow localization of a brachial plexus lesion. For example ifproduce complex discharges. Spontaneous discharges are a

of partial or complete denervation, compression of spinal namplitude can be calculated. The amplitude of the SNAP gives an

indication of the number of functioning axons. It is also affected

by the synchrony of the AP arriving at the recording site e i.e. AP

arriving over a prolonged period will cause reduced peak SNAP

amplitude. Demylination will lead to a small SNAP as the AP will

have greater temporal spread. Axonal degeneration will lead to

an absent SNAP. Age does have an effect on the SNAP.

For further information regarding the technical aspects of

nerve conduction studies the following reference is suggested.17

Electromyography (EMG)

A needle is placed into a muscle to record the activity of motor

units at rest and on muscle contraction. The needle records from

a radius of approximately 1 mm around the needle. The number

of motor units in this field will vary between muscles.

A normal muscle will not have any spontaneous activity. A

sub-maximal contraction will allow individual motor unit

potentials to be identified and a maximal contraction will

signSummary of neurophysiological findings for the categoriNeurophysiological differentiation between axonotmesis and

Neurapraxia

Conduction velocity Normal in most cases

CMAP Amplitude Normal/Reduced

SNAP Amplitude Reduced

Spontaneous Activity on EMG Absent

Table 5

ORTHOPAEDICS AND TRAUMA 23:6 426motor units will be larger than prior to injury. To compensate

for this the firing pattern of each motor unit will be different,

usually with increased firing rates to try and maintain force

production.

For further information regarding the technical aspects of

electromyography the following reference is suggested.18

The neurophysiologic findings seen in nerve injuries are

shown in Table 5.

Neurophysiological assessment of the brachial plexus

Neurophysiology can confirm the diagnosis of a brachial plexus

injury. It can localise the site of the lesion, attempt to quantify the

degree of axonal loss and identify if recovery is occurring. Initial

NCS should be performed 3e4 weeks after injury, as Wallerian

degeneration will have been completed. Denervation changes

maybe seen in 10e14 days but can take up to 40 days to appear.

Proximal muscles are affected prior to distal muscles. When

denervation changes occur in the cervical paraspinal muscles,

rhomboids or serratus anterior it implies the lesion is proximal to

the brachial plexus. Motor responses are affected before sensory

responses when measured on NCS .16 The CMAP will be reduced

in amplitude, reflecting the loss of axons if an injury of greater

severity than neurapraxia/Sunderland 1 has been sustained.

The SNAP can indicate if a lesion is pre- or post-ganglionic. If

a SNAP is present the lesion is proximal to the sensory nerve

bodies in the DRG. If the SNAP is absent or reduced the lesion is

distal to the DRG. The number of intact axons dictates the

amplitude of the SNAP. One limitation is that a SNAP may be

absent due to a post-ganglionic injury but there may also be

a coexistent injury at the pre-ganglionic level.

es of peripheral nerve injury as defined by Seddon.neurotmesis can be challenging

Axonotmesis Neurotmesis

Normal/slight reduction Absent

Reduced Absent

Reduced Absent

Maybe present Present 2009 Elsevier Ltd. All rights reserved.

artefact when recording NAPs.

PERIPHERAL NERVEIf no NAP is recordable across a lesion then grafting is per-

formed if the proximal nerve root is in continuity. The presence

of a NAP across a lesion indicates either preserved axons or that

recovering axons have now traversed the lesion. If the nerves are

judged to be functional neurolysis rather than grafting may be

appropriate.

Somato-sensory evoked potentials (SSEP) and cortical evoked

potentials have also been used for intraoperative monitoring. If

an SSEP is present then there is contact between the peripheral

sensory nerve and the CNS suggesting that the DRG is intact.19

Management of open injuries

Open injuries are not common and range from minor penetrating

wounds to complex major blast injuries with near amputation of

the upper limb. These injuries are usually caused by sharp

penetrating implements or missiles, resulting in a neurotmesis. In

this situation, with sharp division of the nerve(s), primary

exploration and repair in the acute setting should be attempted if

the patients other injuries allow. It is not unusual however for

additional injuries to the major vessels or thoracic viscera to

preclude immediate exploration and in these cases repair must be

delayed. If a cursory plexus inspection and tagging of the injured

nerves is possible during the management of concurrent injuries

the opportunity should be taken.

If there is a delay between the initial injury and presentation

to the clinician responsible for the management of the brachial

plexus injury, then all wounds and other injuries should be left

to stabilise before considering any further surgical intervention.

The opportunity may be taken to perform EMG during this

period at 3e4 weeks, aiming for exploration and repair at 4e6

weeks. Due to the delay, in these cases primary nerve repair

may not be possible because of nerve retraction or following the

resection of neuromatous stumps, necessitating the need for

nerve grafting. Neurolysis of scarred nerve ends may also beThere is a lot of overlapping innervation of the paraspinal

muscles. One root injury may cause fibrillation potentials in

more than one paraspinal level. Therefore the number of para-

spinal fibrillations cannot tell you how many root injuries there

are, only that at least one root injury is present. However if no

paraspinal fibrillations are recorded then it is possible to say that

no root injuries have occurred.

Nascent potentials on EMG and reduced fibrillations can point

to nerve recovery long before clinical recovery is apparent.

Nascent potentials indicate that nerve fibres have reached the

muscles and established motor end-plate connections. However

EMG recovery does not always equate to useful clinical recovery.

Some centres use intra-operative nerve conduction studies.

The nerves of the plexus are stimulated across their damaged

areas to identify whether there are functional axons. These are

NAPs e nerve action potentials. They measure activity in sensory

and motor fibres in mixed nerves along the length of nerve tested

with no distal organ effect being measured. The nerve is stimu-

lated directly with an electrode and the recording is performed

with a hook or forceps type electrode at least 4 cm away from the

stimulating electrode. Four cm of separation between the stim-

ulating and recording electrodes is essential to produce reliable

recording of NAPs intra-operatively. There is a lot of stimulusORTHOPAEDICS AND TRAUMA 23:6 427Non-surgical management

The goals are to maintain passive motion, to strengthen those

muscles that remain functional, to protect anaesthetic skin areas

and to control pain. Physiotherapy plays an important role in

maintaining passive motion as well as strengthening muscles. A

home programme of physiotherapy should run alongside struc-

tured departmental sessions, to maximise the functional outcome

of the limb. Functional splinting will complement physiotherapy.

Chronic oedema can develop secondary to dependent posi-

tioning, loss of vascular tone due to sympathetic nerve dener-

vation and concurrent soft tissue injury to the limb. Elevation,

bracing and compression garments can all be used to reduce the

oedema that, if ignored, can lead to stiffness, particularly in the

hand.

The mainstay of the management of anaesthetic skin is

education, and the program is essentially the same as for diabetic

neuropathy with patients avoiding extreme temperatures and

inspecting the insensate area daily.

The management of pain can be difficult and significant pain

is more common with total plexus injuries than partial, particu-

larly with root avulsions. Pain, in addition to being very dis-

tressing, can also compromise rehabilitation, and its control is

paramount. Restoration of function, both of the limb and the

patient, including the return to employment, is often the most

effective form of pain control. The use of pharmacological agents

is vital, but dependency and side effects must be taken into

account. Non-steroidal anti-inflammatories and opioids insti-

gated at the time of injury may become ineffective with time,

particularly in relation to neuropathic pain. In these cases there isthese injuries.required in these cases. In one of the biggest series in the

literature of stab wounds to the plexus Dunkerton reported good

results with early exploration, with a better prognosis associated

with C5/C6 lesions.20

Open injuries secondary to low-velocity missiles (gunshot

wounds), do not warrant early exploration. This is because the

resultant injuries are mostly neurapraxic.21 It must be added,

though, that as technology advances more powerful weapons are

being produced leading to an increase in severe stretch injuries

(lesions in continuity) to the plexus. If there is no associated

vascular or thoracic injury, conservative management with local

wound care is advocated. If no recovery is seen by 3 months

exploration with repair/grafting is indicated. Kline reported on

a large series of civilian gunshot wounds in the era of low-

velocity weapons and found the best surgical outcomes were

associated with upper trunk and lateral and posterior cord

injuries.

Management of closed injuries

In the absence of any open wounds and life-threatening injuries

surgery is not traditionally the first line of treatment. The initial

management is observation, pain control and physiotherapy.

Electromyography is performed at 3e4 weeks and a myelogram

or magnetic resonance imaging at 6e8 weeks if a neurological

deficit persists. If function fails to return, or if initial neurological

recovery ceases, then surgical exploration is justified at 3 to 6

months, although there is no uniformly accepted algorithm for 2009 Elsevier Ltd. All rights reserved.

h the

in of

PERIPHERAL NERVEa role for carefully titrated doses of anti-epileptics (gabapentin

and carbamazipine) or tricyclic anti-depressant (amitriptyline). It

should be noted, though, that only one third of patients report

significant pain relief with these medications.22 Other modalities

including counseling, biofeedback, hypnosis, acupuncture and

transcutaneous nerve stimulation have all been used with mixed

results. Severe cases of intractable pain, which do not respond to

the above non-surgical measures, can be considered for dorsal

root entry zone (DREZ) ablation, described by Nashold23 or the

use of implantable dorsal root stimulators. Pain control should be

managed by a multi-disciplinary team and customised to the

character of the pain and to the patient. Access to a pain clinic is

an important adjunct.

Surgical management

Considerable advances have been made since the early 1900s,

when attempts at surgical repair and neurolysis proved almost

futile. Modern microsurgical techniques have led to improved

results, but as of yet no definitive management algorithm has

been constructed and uniformly accepted. There are several

general statements concerning surgical intervention of closed

injuries that can be made:

1. Patients who have complete loss of C5, C6 and C7 root

functions have the most to gain

2. Nerve grafting of the upper roots is often possible as rupture,

not avulsion, is the usual mechanism of injury.

3. Grafting C8 and T1 is often not an option, as at this level

avulsion injuries are likely to have occured. If grafting is

possible it is only likely to provide protective sensation and

no meaningful motor recovery. This is because muscle

atrophy occurs prior to reinnervation of the finger flexors

and intrinsics due to the considerable distance the regen-

erated nerves have to travel.

4. In a child any complete lesion regardless of level should be

repaired and grafted if possible.

5. Across the literature, timing of surgery most commonly

occurs between 3e6 months.

Surgical approach to the brachial plexus

The plexus can be exposed in its entirety or partially, depending

on the procedure being performed and the extent of the injury.

The patient is positioned for primary exposure allowing for intra-

operative adjustment. Any potential nerve grafts and transfer

sites and must also be readily accessible (intercostals or sural

nerve, for example).

Under general anaesthesia, with the use of a short acting

muscle relaxant for intubation to allow for intra-operative nerve

stimulation, the patient is placed in the semi-recumbent beach

chair position with the neck slightly extended and turned to the

contralateral shoulder. The arm is prepared so that it can be

moved intra-operatively to aid dissection.

The surface markings for exploration of the supraclavicular

plexus are the posterior border of sternocleidomastoid and a line

just superior and parallel to the clavicle. The skin and superficial

fascia are incised and subplatysmal flaps are raised to improve

exposure. Deep to the platysma are the external jugular vein,

which is retracted medially, and the cervical plexus, which

should be preserved where possible to prevent neuromaORTHOPAEDICS AND TRAUMA 23:6 428the vertebral artery lies close, as does the lung pleura.

Clavicular osteotomy can be performed to increase exposure,

facilitating closure by preparing a pre-contoured plate and pre-

drilling the lateral screws. The clavicle should be divided via

a low energy osteotomy at an oblique angle.

The infraclavicular plexus is exposed through the delto-

pectoral groove (Figure 6aef). To expose the entire plexus the

supraclavicular and infraclavicular approaches are linked over

the lateral clavicle. The cephalic vein is preserved and mobilised

laterally with the deltoid. The delto-pectoral interval is developed

and the clavicular attachments of pectoralis major and deltoid

may be partially released to optimise exposure. Distal exposure

requires the release of the humeral attachment of pectoralis

major. Pectoralis minor is divided close to its insertion onto the

coracoid (a stay suture is placed in the tendon) to expose a fat

pad which is swept aside bringing the cords of the brachial

plexus into view. The lateral cord is the most readily identifiable

and deep to this is the axillary artery which requires mobilisation

and protection. The medial and posterior cords are identified in

relation to the artery. The cords can be traced both distally, to

identify the branches, and proximally, to locate the divisions.

Surgical options

A variety of surgical strategies exist to improve function and the

choice used will depend on the extent and location of the injury.

A clear surgical plan with realistic expectations of the outcome

should be discussed with the patient. Surgical options available

include:

Neurolysis

Lesions in continuity, with external compression or scarring, can

be treated with neurolysis. For these procedures to be successful

the fascicular pattern and endoneural tissue must be preserved. If

there is concern or doubt over the integrity of the fascicle pattern,

resection of the segment and grafting is preferred.

Nerve grafting

This forms the basis of modern post-ganglionic plexus surgery.

Anatomical reconstruction, with connection of the proximal and

distal stumps is attempted. The limiting factors in reconstruction

tend to be the length of the gap that requires grafting and the

availability of a sufficient nerve graft. Therefore, priority is given

to 1, restoration of elbow flexion, 2, restoration of shoulder

abduction, and 3, restoration of sensation on the medial borderligated if necessary. To access the lower trunk the subcl

vasculature is mobilised and retracted with care as the origsubclavian vein anteriorly and the subclavian artery posteriorly.

For proximal foraminal exposure scalenius anterior is divided.

The upper trunk is located by tracing the C5 and C6 roots distally,

the middle trunk being found both deeper and medial to this.

Access may be limited by the transverse cervical artery, which is

avianthe lateral edge of the muscle. The lower roots can be visua

distally by retraction of scalenius anterior, taking care witformation. Omohyoid muscle, which signals the transition from

superficial to deep dissection, is divided and the supraclavicular

fat pad is swept away from the operative site. Below the fat pad is

the transverse cervical artery with Erbs point deep to this.

The phrenic nerve is identified, closely applied to scalenus

anterior, and is followed proximally to identify the root of C5 at

lised 2009 Elsevier Ltd. All rights reserved.

PERIPHERAL NERVEof the forearm. The commonly used donor sensory nerves for

grafting are, sural, saphenous, medial brachial and antebrachial

cutaneous and superficial radial nerves. Vascularised nerve

grafts24 have added another possibility and the most commonly

used is the ulnar nerve. In these cases the ulnar nerve should be

split into minor units roughly the size of the sural nerve before

grafting, in order to increase chances of success.25

Nerve transfer (Neurotization)

Neurotization is used more often in pre-ganglionic lesions. Nerve

fibres from one nerve are transferred to a denervated nerve, in

order to neurotize the nerve. Motor nerves have to be used as

donors to restore motor function and sensory nerves to restore

sensory function. Classically this technique involves sacrificing

Intra-operative photographs demonstrating exposure of the terminal bran

Figure 6

ORTHOPAEDICS AND TRAUMA 23:6 429the function of the axon donor, but new end-to-side26 techniques

mean this is not necessarily the case. From a surgical point of

view it must also be considered whether the donor nerve can be

transferred without tension. Table 6 shows the donor nerves

commonly used for transfers.

Some surgeons prefer to use intraplexus donors suggesting

they give better results, due to the greater number of axons

compared with extraplexus donors, therefore increasing the

chances of successful neurotization27. Despite this viewpoint,

some extraplexus donors give consistently good results in clinical

practice; the intercostals when used for shoulder and elbow

function are reported to give up to 70% good to excellent

results.27 The accessory nerve, according to published studies, is

also a reliable donor.27

ches of the brachial plexus.


work has emerged on human subjects. Despite this, to date,

this surgical option has not reached the stage where it warrants

re is

unlikely to be any substantial gain in function from shoulder

PERIPHERAL NERVEinclusion in the standard surgical armamentarium.

As with all peripheral nerve injuries, a considerable number

of factors influence the results of surgery to the brachial plexus.

As a result, firm statements regarding the prognosis of surgery

are difficult to justify. The literature indicates overall that

younger patients do better, as do upper plexus injuries. This

almost certainly reflects the fact that in upper lesions the target

organs are much closer to the plexus, making regeneration more

likely. Terzis27 in a series of over two hundred surgically

managed plexus injuries reported good to excellent results in

75% of suprascapular nerve reconstructions, 40% of biceps

reconstructions, 30% of triceps reconstructions, 35% finger

flexion reconstructions and 15% of finger extension reconstruc-

tions. Restoration of hand function secondary to a lower plexus

injury remains the most difficult area to address, but with

aggressive management, according to Terzis, it is not out of the

question.

Late reconstruction

In cases where spontaneous recovery has not occurred, or when

surgical intervention has failed to yield any functional benefit,

then late reconstructive options should be considered. In suchRepair of avulsed spinal nerve roots has been attempted by

many, with Bonney and Jamieson reporting on a case in 1979.

Both Jamieson and Carlstedt have published experimental work

on animal models with some functional success28,29 and early30,31

Donor nerves used for transfer

Donor nerve for transfer Described

Intercostal (to Musculocutaneous) Seddon 1961

Ipisilateral Cervical Plexus Brunelli 1980

Contralateral Lateral Pectoral Gibert 1992

Accessory Bonnel 1984

Hypoglossal Narakas 1984

Phrenic Zhen 1989

Contra lateral C7 Chen 1991

Ulnar nerve to Musculocutaneous Oberlin 1997

Table 6cases there needs to be conclusive evidence that neurological

recovery is unlikely, or sufficient time has elapsed without

functional improvement following the injury. Many of the tech-

niques used in reconstruction have been adapted from use in

poliomyelitis and peripheral nerve injuries. It must be acknowl-

edged, however, that in poliomyelitis there is no loss of sensation

and thus in plexus injuries the functional benefits from motor

improvement maybe less. The primary procedures in peripheral

reconstruction are arthrodesis and tendon transfers, with the

newer technique of free muscle transfers becoming an option.

There is also a limited place for amputation.

Numerous procedures have been described to improve the

function of the upper limb and, as previously stated, it is

important to assess each individual patient carefully and to

determine from which procedures they are likely to derive the

f the

ORTHOPAEDICS AND TRAUMA 23:6 430paralysis and donor muscles available. Thus, no precise

management algorithm can be constructed, although Alnot in

199633 outlined his surgical approach to shoulder muscle palsies

(Table 7).sion as to which is used will depend on the exact nature oarthrodesis.

Integrity of the acromioclavicular, sternoclavicular andscapulothoracic joints should be considered. Stiffness of these

joints may limit the success of arthrodesis and it is also

important to ensure the acromioclavicular joint is not incor-

porated into the arthrodesis

With advances in bone fixation, especially rigid compression

plating, the need for prolonged postoperative immobilisation is

no longer required. The most common position for arthrodesis is

20 of abduction, 30 of flexion and 30 internal rotation.Excessive abduction must be avoided, as it leads to chronic

fatigue around the shoulder girdle. This position should give

a strong and functional shoulder to feed and address personal

hygiene with an average movement of 60 of abduction andflexion32 being possible via the scapulothoracic articulation.

Shoulder arthrodesis gives predictable results and can improve

the function of the limb considerably. The strength and move-

ment is greater than is achieved with muscle transfers, but does

depend on the scapulothoracic muscles. It should be born in

mind when combining shoulder arthrodesis with other distal

procedures, that following the arthrodesis it can be difficult to

position the arm and thus the distal procedures may be more

easily performed first.

Tendon transfers to the shoulder

In cases where only partial paralysis of the shoulder has occurred

arthrodesismaynot be necessary and tendon transfers are sufficient

to restore function. Many transfers have been described including:

Trapezius to deltoid insertion on the humerus (Batemanprocedure)

Latissimus dorsi and teres major to the posterolateralhumerus (LEpiscopo) to improve external rotation

Anterior advancement of the posterior portion of deltoid toreplace non-functioning anterior segment.

Transfer of the long head of triceps to the acromionThere are many other described transfers and the final deci- Good distal function of the arm is needed for the procedube worthwhile. If the hand is completely paralysed themost benefit. In essence, peripheral reconstruction is aimed at

restoring shoulder stability, with or without movement, in

addition to restoring elbow flexion and hand function.

Shoulder arthrodesis

The role of shoulder arthrodesis is two-fold. Firstly, in total

plexus palsies, by stabilising the shoulder it enables the surgeon

to concentrate all available nerve grafts and transfers, which

maybe limited, on restoring elbow and hand function. Secondly,

in upper plexus palsies, it may be of benefit in unstable shoulders

(painful, subluxing or dislocating) where attempts to stabilise

have failed or where it is not appropriate to undertake such

procedures in the first place. Certain aspects are worth consid-

ering when planning shoulder arthrodesis:

Good scapulothoracic muscle function is vitalre to 2009 Elsevier Ltd. All rights reserved.

ce in

PERIPHERAL NERVE Sternocleidomastoid - rarely used due to web appearanTendon transfers to restore elbow flexion

Elbow flexion plays a vital role in upper limb function and its

restoration can significantly improve a patients functional

outcome. Depending on the level of the lesion and the degree of

successful reinnervation different reconstructive procedures are

available. Once again the final decision depends on the precise

functional deficit and on available donor muscles. When consid-

eringwhich transfer to use,muscle excursion, alignment, cosmesis

and pre-existing range of movement must be considered. The aim

of surgery is to restore good strength through a functional range of

30 to 130without excessive pronation. The commondonors usedin transfers to restore elbow flexion are:

Proximal advancement of the common origin of the forearmflexor-pronator muscles (Steindler) - historically most

popular, but can be weak and can lead to flexion contractures

and excessive pronation.

Latissimus dorsi - good power and excursion but frequentlydenervated along with elbow flexors and thus unavailable.

Pectoralis major (Clarke) - requires stable or arthrodesedshoulder to establish correct tension

Pectoralis minor - stable or arthrodesed shoulder Triceps - good strength, excursion and cosmesis but loss of

extension is a high price to pay.Table 7Alnots surgical approach to shoulder muscle palsies

Deltoid muscle palsy only Trapezius to deltoid (Bateman)

or

Long head triceps to Acromion

Deltoid & Infraspinatus palsy Derotation osteotomy of humeral

shaft for external rotation

Deltoid, Infraspinatus &

Supraspinatus

Stabilisation shoulder with long

head of biceps

Derotation osteotomy

Shoulder arthrodesis

Trapezius transferneck and the occasional need to preposition the head to

achieve elbow flexion.

Tendon transfers to restore hand function

This is a very difficult area to address and there are no simple

solutions. In essence the tendon transfers available are those

commonly used for isolated peripheral nerve injuries and to

cover them exhaustively is beyond the scope of this review. The

most notable difference is that often the donor muscles used in

isolated median, ulnar and radial nerve palsies are not neces-

sarily available or expendable in a brachial plexus lesion, due to

the more global effect they have on hand function. As with all

tendon transfers, consideration must be given to the potential

gains from the procedure and also the functional loses that will

occur. Ultimately the treating clinician must assess and discuss

with the patient the available options including risks and benefits

and come to a mutual conclusion as to what is the best

management plan. hilst

ORTHOPAEDICS AND TRAUMA 23:6 431Unfortunately brachial plexus injuries are becoming increas

common and they result in a very significant disability, wFree muscle transfers

Free muscle transfers are a feasible option in reconstruction of

elbow flexion and prehensile reconstruction of the hand.34,35 In

order for these transfers to function it is necessary for the prox-

imal joints to be stable. Thus in reconstruction of elbow flexion

function is compromised if the shoulder is not stable, and this

must be addressed either at the same time or before the free

muscle transfer. When addressing finger function, stability of the

elbow and wrist is mandatory. In addition to proximal joint

stability the presence of an antagonistic muscle greatly influences

functional outcome. The weight of the limb and the effects of

gravity to a certain extent act as antagonists, but this is often not

enough, and thus when addressing finger flexion in the absence

of active extension, splinting may be required. Double free

muscle transfers may deal with this potential problem.35 The

donor muscles commonly used are latissimus dorsi, gracilis and

rectus femoris. Consideration must be given to donor muscle

blood supply, length, volume and shape. Latissimus dorsi and

rectus femoris are mainly used for restoration of elbow flexion

whereas gracilis due to its shape and amplitude of contraction is

the preferred donor for wrist and finger function.

Orthotics

The role of orthotics should not be forgotten in brachial plexus

injuries, in both the non-surgically and surgically managed cases.

They can be used to immobilise, stabilise, and support a joint in

a desired position, protect weak muscles from overstretch,

prevent contractures and support structures following surgical

repair. They can be used instead of, or alongside, late recon-

struction to enhance the function of the limb. A static orthosis is

primarily intended to stabilise joints or place the limb in a posi-

tion of function. Dynamic orthoses are often more complex and

intended to more than simply stabilise a joint. Multiple dynamic

orthoses are available including shoulder, elbow, wrist and hand

orthotics. The exact orthoses used will depend on the functional

deficit and needs of the patient as assessed by a trained orthotist.

Consideration must be given to ease of use, wear and application

as well as the risks of skin problems, particularly with anaes-

thetic skin. Despite some patients finding orthotics undesirable,

they can be a very useful adjunct to management.

Amputation

With theadventof themodern techniques inbrachial plexus injuries

discussed above there has been a significant shift away from

amputation. This has occurred to the extent that Tervis in 1999

claimed Amputation has no place in the modern treatment of

traumatic plexopathies.With that considered, in some caseswhere

reconstruction has failed and the patient is left with a flail useless

arm, struggles with the weight of it and fails to properly care for the

anaesthetic skin, amputation is a viable option. The amputation can

be at any level, depending on the needs of the patient and maybe

combined with shoulder arthrodesis. Amputation is not an appro-

priate option for those who request it for neurological pain relief.

Summary

ingly 2009 Elsevier Ltd. All rights reserved.

occurring in young individuals, usually of working age. Conser-

vative management helps control pain and maintain movement

and function. Recent technical advances, however, have signifi-

cantly increased the role of early surgery employing neurolysis,

nerve grafting and nerve transfer. Functionmay also be helped by,

or in combinationwith, shoulder arthrodesis and a range of tendon

transfers to capitalise on any remaining functioning muscle units.

The care of patients with plexus injuries is complex and requires

a multiskilled, multidisciplinary approach for the best results. A

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21 Kline Dg. Civilian gunshot wounds to the brachial plexus. J Neurosurg

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22 Leffert RD. Brachial plexus injuries in the adult. In: Norris TR, ed.

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The anatomy, investigations and management of adult brachial plexus injuriesIntroductionHistoryAssessmentAnatomy of the brachial plexusClinical clues to the anatomical location of pathologyClassification of peripheral nerve injuryPathophysiology of nerve regenerationInvestigationsRadiologicalHistamine testBasic electrophysiologyNerve conduction studies (NCS)Electromyography (EMG)

Neurophysiological assessment of the brachial plexusManagement of open injuriesManagement of closed injuriesNon-surgical management

Surgical managementSurgical approach to the brachial plexusSurgical optionsNeurolysisNerve graftingNerve transfer (Neurotization)

Late reconstructionShoulder arthrodesisTendon transfers to the shoulderTendon transfers to restore elbow flexionTendon transfers to restore hand functionFree muscle transfers

OrthoticsAmputationSummaryReferences

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anatomi PBI