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Upper-extremity nerve-traction palsies related to positioning have been reported with a higher incidence of ulnar nerve damage in arthroplasty pa-tients with inflammatory arthritis.1 Obt

Nerve injury after total hip

arthro-plasty (THA) can be a devastating

complication Upper-extremity

nerve-traction palsies related to

positioning have been reported

with a higher incidence of ulnar

nerve damage in arthroplasty

pa-tients with inflammatory arthritis.1

Obturator nerve injuries are

ex-ceedingly uncommon but have

been the subject of case reports

Superior gluteal nerve and femoral

nerve injury are relatively rare and

in general have a better prognosis

than sciatic nerve injuries Most of

the literature focuses on the

per-oneal division of the sciatic nerve

The physiologic demands as well

as the structural anatomy of the

nerves about the hip predispose

these structures to injury during

surgical procedures In this article,

we will review clinical studies on

the diagnosis, treatment, and

prog-nosis of this infrequent

complica-tion and focus attencomplica-tion on the

importance of prevention

Peripheral Nerve Anatomy and Physiology

Nerves are uniquely designed to quickly transmit electrical impulses,

or action potentials, over long dis-tances Each nerve cell is composed

of four regions (Fig 1) Dendrites are the thin processes that collect signals from other nerve cells The cell body contains the nucleus and organelles, which tend to the meta-bolic needs of the neuron A single axon branches off each cell body and acts as a transport tube for pro-teins and a conduit for transmission

of action potentials

Sensory nerves are afferent fibers that transmit action poten-tials from nociceptors or mechano-receptors toward the dorsal root ganglia of the central nervous sys-tem Motor nerves are efferent fibers that carry action potentials to special motor end-plates on muscle spindles Presynaptic terminals are the specialized nerve endings that

transmit information to dendrites

of other nerves or to a neuromus-cular junction The model hypoth-esized for transmission of proteins and transport of neurotransmitter vesicles from cell body to axon involves carrier proteins, micro-tubules, and an adenosine triphos-phate (ATP)Ðdependent protein called kinesin Retrograde axoplas-mic transport serves to recycle empty vesicles and has been linked

to the transmission of herpes sim-plex, rabies, and polio viruses and tetanus toxin

A number of other cell types are associated with the primary nerve cells Glial cells surround nerve cell bodies and their axons Microglia are the phagocytes that mobilize after injury Oligodendrocytes and Schwann cells are macroglia cells that produce the myelin sheath, which enhances the speed of signal transmission Oligodendrocytes are found only in the central ner-vous system; each one myelinates many different axons Schwann

Dr DeHart is Attending Orthopaedic Surgeon, Huebner Medical Center, San Antonio, Tex; and Clinical Assistant Professor, Department

of Orthopaedic Surgery, University of Texas Health Science Center at San Antonio Dr Riley is Professor of Orthopaedic Surgery, Johns Hopkins University, Baltimore Reprint requests: Dr DeHart, Suite 390, 9150 Huebner Road, San Antonio, TX 78240 Copyright 1999 by the American Academy of Orthopaedic Surgeons.

Abstract

Nerve injury occurs in 1% to 2% of patients who undergo total hip

arthroplas-ty and is more frequent in patients who need acetabular reconstruction for

dys-plasia and those undergoing revision arthroplasty Injury to the peroneal

divi-sion of the sciatic nerve is most common, but the superior gluteal, obturator,

and femoral nerves can also be injured Nerve injury can be classified as

neu-rapraxia, axonotmesis, or neurotmesis The worst prognosis is seen in patients

with complete motor and sensory deficits and in patients with causalgic pain.

Prevention is of overriding importance, but use of ankle-foot orthoses and

prompt management of pain syndromes can be useful in the treatment of

patients with nerve injury Electrodiagnostic studies hold promise in complex

cases; however, their intraoperative role requires objective, prospective,

con-trolled scientific study before routine use can be recommended.

J Am Acad Orthop Surg 1999;7:101-111

Marc M DeHart, MD, and Lee H Riley, Jr, MD

Nerve Injury

Seddon classified nerve injuries into three types (Fig 5) Neura-praxia is a conduction block of anatomically intact nerves caused

by minor injury A period of loss

of sensation may occur, but recov-ery is likely to be complete Axon-otmesis is a more severe injury in which axons are disrupted but the investing connective tissue sur-vives Wallerian degeneration is the process of disintegration of the axon and myelin sheath over the entire axon distal to the site of injury Preservation of the endo-neurial supporting structures can

cells are found in the peripheral

nervous system; each provides

myelination for only a 0.1- to

1.0-mm segment of the axon of one

neuron (Fig 2)

The spaces between Schwann

cells, or nodes of Ranvier, are the

sites of action potential initiation

The internal milieu of a resting

nerve cell is electronegative

com-pared with the extracellular fluid

This electrical difference is

main-tained by energy from ATP and a

sodium-potassium pump that

con-stantly pumps sodium out of the

cell Chemical, mechanical, or

volt-age changes can cause sodium

gates to open, allowing an influx of

positive sodium ions, a process known as depolarization (Fig 3)

The result is an action potential Ñ

a brief explosive change in the nerve cell to a very positive value

Nodes of Ranvier have high con-centrations of voltage-gated

sodi-um channels that ease initiation of action potentials The insulating myelin allows action potential cur-rent to flow quickly with little attenuation to the next node of Ranvier This jumping of the ac-tion potential down the neuron from node to node is very effective

in increasing the conduction speed

of the signal down the axon De-myelinating diseases, such as mul-tiple sclerosis and Guillain-BarrŽ syndrome, interfere with the prop-agation of the signal, slowing or completely stopping conduction

As many as several thousand axons and their accompanying Schwann cells are bundled together

by a loose endoneurial connective tissue into fascicles (Fig 4) Edema

of this endoneurium is the hallmark

of irreversible nerve damage Peri-neurium is the expansion of dense connective tissue that surrounds each fascicle It has high tensile strength and serves as the major barrier for endoneurial edema

Fascicles are bundled together into nerves by epineurium, which is a loose meshwork composed of colla-gen and elastin that protects the nerve from compressive forces

Spinal nerves do not have peri-neurium or epiperi-neurium and are more vulnerable to tensile and com-pressive forces.2

Because of the high metabolic demands of the nerve tissue, blood supply is crucial for effective signal transmission The vascular supply

to the nerves is derived from both a segmental extrinsic system of superficial vessels, which give off perforating branches, and an intrin-sic system of epineurial, perineu-rial, and endoneurial plexuses with their communicating branches

Fig 1 A typical neuron (Adapted with

permission from Bodine SC, Lieber RL:

Peripheral nerve physiology, anatomy, and

pathology, in Simon SR (ed): Orthopaedic

Basic Science Rosemont, Ill: American

Academy of Orthopaedic Surgeons, 1993,

p 327.)

Cell body

Nucleus

Myelin sheath

Dendrites

Axon hillock Axon Node of Ranvier Terminal branches Presynaptic

terminal

Postsynaptic neuron

Nodes of Ranvier

Nucleus

Inner tongue

Axon

Layers of myelin

Fig 2 The Schwann cell wraps lipid-rich myelin around the axon to enhance con-duction of electrical impulses (Adapted with permission from Bodine SC, Lieber RL: Peripheral nerve physiology, anatomy,

and pathology, in Simon SR (ed): Ortho-paedic Basic Science Rosemont, Ill:

Amer-ican Academy of Orthopaedic Surgeons,

1993, p 328.)

sis The effect of ischemia with compression in the tissue under a tourniquet was compared with ischemia alone in more distal tissue Evidence of endoneurial edema was found after 2 to 4 hours of com-pression

The amount of stretch a nerve will tolerate depends on whether the nerve is freely mobile in supple soft tissue or whether it is bound down by osseous prominences, fascia, or scar Rabbit sciatic nerve showed conduc-tion failure with 25% lengthening Histologic changes were found after lengthening of nerves by 4% to 11% Nerve microcirculation was found to

be impaired after 8% stretch and stopped after 15% stretch.5 The rup-ture of axon fibers precedes the fail-ure of fascicles and may occur with stretch of as little as 4% to 6%.2 Four major factors that increase the probability of mechanical dis-ruption include increased load due

to compression or stretch, increased rate of loading, increased duration

of loading, and uneven application

of load to tissues Clinical experi-ence and LaplaceÕs law (tension is proportional to the pressure and radius of a cylindrical structure) demonstrate that large-diameter axons are more susceptible to

dam-guide the slow (1 mm per day)

regeneration of sprouts to their

original end-organ Atrophy and

scarring of muscle can prevent

effective function if axons fail to

reach motor end-plates within 2

years of the time of injury.3 This

accounts for the variability in

de-gree of recovery Complete

disrup-tion of the nerve, or neurotmesis,

carries the worst prognosis for

recovery and may lead to abortive

efforts at regeneration, which can

result in painful neuromas

Damage to nerves and their

blood supply can be caused by

var-ious combinations of compression,

stretch, ischemia, and transection

Compressive trauma affects both

the structure of the nerve and the

neural vascular supply Large,

closely packed fasciculi have less

cushioning epineurium and are

more vulnerable than nerves with

smaller fasciculi and a greater

amount of epineurial tissue.2

LundborgÕs classic experiments

involving tourniquet application4

demonstrated that normal

circula-tion returned within seconds when inflation time was 2 hours or less

For tourniquet times between 4 and

6 hours, it took 2 to 3 minutes for the circulation to return, and a

peri-od of hyperemia was observed

After 8 to 10 hours, blood flow took

5 to 20 minutes to return, and there was evidence of microvascular

sta-Fig 3 A,When the cell is at rest, the passive fluxes of Na+and K+into and out of the cell

are balanced by the energy-dependent sodium-potassium pump (Adapted with

permis-sion from Bodine SC, Lieber RL: Peripheral nerve physiology, anatomy, and pathology, in

Simon SR [ed]: Orthopaedic Basic Science Rosemont, Ill: American Academy of

Orthopaedic Surgeons, 1993, p 332.) B, An action potential can be the result of voltage

(top) , chemical (center), or mechanical (bottom) changes that open axon sodium channels.

The resulting sodium influx causes an explosive positive change in the nerve cell.

(Adapted with permission from Kandel ER, Schwartz JH, Jessell TM: Principles of Neural

Science, 3rd ed Norwalk, Conn: Appleton & Lange, 1991, pp 75-76.)

Perineurium Endoneurium

Fascicle Nerve fiber

Epineurium Perineurium Endoneurium

Fig 4 Cross-sectional anatomy of a nerve (Adapted with permission from Wilgis EFS,

Brushart TM: Nerve repair and grafting, in Green DP (ed): Operative Hand Surgery New

York: Churchill Livingstone, 1993.)

Closed

Ligand binding

Stretch

Open

Pi

∆ Vm

age than smaller fibers Clinical

factors, which will be discussed

later, also play a role in nerve injury

and repair

Anatomy of the Peripheral

Nerves About the Hip

The superior gluteal nerve arises

from the L4, L5, and S1 nerve roots

and exits at the sciatic notch to

sup-ply the gluteus medius, gluteus

minimus, and tensor fascia lata It

travels with the superior gluteal

artery deep to the gluteus maximus

and medius but superficial to the

gluteus minimus In one study,6

subclinical superior gluteal nerve

injury was found in 77% of cases in

which a transtrochanteric lateral or

posterior hip approach was used

Anterior branches supplying the

distal tensor fascia lata may be

sac-rificed during the anterolateral

approach when dissecting the

inter-val between the gluteus medius and the tensor It is also at risk if the 3- to 5-cm Òsafe areaÓ proximal

to the greater trochanter is violated during direct lateral approaches to the hip.7 When this safe area is respected, clinical deficits are rare.8

A positive Trendelenburg sign or Trendelenburg gait and weak ab-duction can indicate damage to this nerve

The obturator nerve arises from the L2, L3, and L4 nerve roots within the posterior psoas and then emerges medially at the sacral ala to travel along the ilio-pectineal line (Fig 6) It is rarely injured,9 but case reports docu-ment a risk of injury when cedocu-ment, screws, or reamers penetrate the anterior quadrants of the acetabu-lum (Fig 7) The obturator nerve exits the pelvis at the superior aspect of the obturator foramen, where it supplies the adductor muscles and a medial patch of thigh skin Persistent pain in the groin or thigh, adductor weakness after placement of intrapelvic screws, or allograft or cement visi-ble on radiographs after hip arthro-plasty suggests obturator nerve

in-jury.10 Hip disease can cause re-ferred pain to the knee through the obturator distribution

The femoral nerve arises from the L2, L3, and L4 nerve roots; passes through the psoas major muscle; and then travels between the psoas and the iliacus to enter the thigh as the lateralmost structure of the femoral triangle The femoral nerve supplies motor impulses to the mus-cles of knee extension (the quadri-ceps) and sensation to most of the medial thigh and calf Prolonged hyperextension of the thigh can cause femoral-nerve traction in-juries Iliacus hematomas in patients who have bleeding disorders or are taking anticoagulants are well-known causes of femoral nerve palsy The femoral nerve is rarely injured after hip arthroplasty (0.04%

to 0.4% of cases)1,9,11; it is most at risk during placement of anterior acetabular retractors when anterior

or anterolateral approaches are used (Fig 8) Simmons et al12 reported the highest rate of femoral nerve palsy after hip arthroplasty (2%); however, all patients had full func-tional recovery by 12 months The presence of thigh pain, anteromedial

Fig 5 Spectrum of injury to a nerve as it

is stretched (Only one axon in its

connec-tive tissue layers is shown.) A =

Neura-praxia, with all anatomic structures intact.

B = Axonotmesis, with disruption of the

axon but intact connective tissues C =

Neurotmesis, with complete disruption of

all layers (Adapted with permission from

Sunderland S: Nerve Injuries and Their

Repair: A Critical Appraisal New York:

Churchill Livingstone, 1991, p 148.)

A

B

C

Fig 6 Cross section of the pelvis at the level of the hip joint shows location of the obtura-tor, femoral, and sciatic nerves (Adapted with permission from Weber ER: Peripheral

neuropathies associated with total hip arthroplasty J Bone Joint Surg Am 1976;58:66-69.)

Obturator nerve

Femoral nerve

Sciatic nerve Femoral artery

Femoral vein

thigh and medial leg numbness,

quadriceps weakness, and difficulty

climbing stairs suggests femoral

nerve injury

The sciatic nerve arises from the

L4, L5, S1, S2, and S3 nerve roots

and is composed of the preaxial

anterior tibial and postaxial

poste-rior peroneal divisions These

divi-sions usually travel together in a

single sheath, but in 10% to 30% of

cases they are separate as high as

the greater sciatic notch The nerve

is located deep to the piriformis

inside the pelvis and then travels

distally deep to the gluteus muscles

and superficial to the external

rota-tors at the level of the hip joint It

is the nerve most frequently in-jured during hip arthroplasty and

is at risk for injury either from placement of posterior acetabular retractors or from anterior or lateral traction on the femur

Distal to the level of the lesser trochanter and the ischial

tuberosi-ty, the sciatic nerve passes between the adductor magnus and the long head of the biceps femoris, just medial to the insertion of the gluteal sling All medial branches

of the sciatic nerve arise from the tibial division and supply the ham-strings The short head of the biceps

is the only thigh muscle supplied

by the peroneal division of the sci-atic nerve At the superior aspect

of the popliteal fossa, the two divi-sions split into the tibial nerve and the common peroneal nerve The peroneal nerve innervates the dor-siflexors and evertors of the foot and ankle The tibial nerve inner-vates the plantar flexors and inver-tors The sural nerve provides sen-sation to most of the lateral aspect

of the calf and arises from both the medial sural cutaneous branch of the tibial nerve and the lateral sural cutaneous branch of the common peroneal nerve

Sciatic Nerve Injury in THA

As mentioned previously, the

sciat-ic nerve is the nerve most

common-ly injured during THA It was in-volved in over 90% of the 53 nerve injuries reported by Schmalzried et

al11 in their series of more than 3,000 cases The incidence of sciatic nerve injury in primary THA has been reported to be between 0.6%

and 3.7%, with most large series citing a rate of about 1.5%.9,11 Overall rates are elevated by the relatively higher incidence in revi-sions (3% to 8%) and in patients with developmental dysplasia of the hip (DDH) (5.8%).11 In

uncom-plicated primary THA, sciatic nerve injury occurs in fewer than 1% of cases Weber et al9 noted that since only severe injury pre-sents as a clinical problem, the con-dition may be more common than

is generally appreciated They reported that in a study utilizing preoperative and postoperative electromyography, 70% of THA patients had subclinical sciatic nerve injury

The etiology of nerve injury

is protean Direct trauma from scalpel, electrocautery, retractors, wires, reamers, Gigli saw, bone fragments, or cement protrusion; constriction by suture, wire, or cable; heat from the polymeriza-tion of cement; compression from dislocation; excessive lengthening; and subfascial hematoma have all been reported However, the cause

of 50% of all sciatic nerve palsies is unknown.11,13

Fig 7 The acetabular-quadrant system

(ASIS = anterosuperior iliac spine) Screws

originating in the anterosuperior quadrant

threaten the external iliac artery and vein.

Screws from the anteroinferior quadrant

threaten the iliac vessels and the obturator

nerve There is less risk of neurovascular

injury with placement of short (<25 mm)

screws in the posterosuperior quadrant.

(Adapted with permission from

Wasielew-ski RC, Cooperstein LA, Kruger MP,

Rubash HE: Acetabular anatomy and the

transacetabular fixation of screws in total

hip arthroplasty J Bone Joint Surg Am 1990;

72:501-508.)

ASIS

Postero-superior

Postero-inferior

Antero-superior

Antero-inferior

Fig 8 The close proximity of the femoral nerve and vessels to an anteriorly placed acetabular retractor (Adapted with permis-sion from Shaw JA, Greer RB: Compli-cations of total hip replacement, in Epps CH

[ed]: Complications in Orthopaedic Surgery.

Philadelphia: JB Lippincott, 1994, p 1035.)

The peroneal division of the

sci-atic nerve is more susceptible to

injury than the tibial division

Schmalzried et al11found that 94%

of the sciatic nerve injuries in their

study involved the peroneal

divi-sion The tibial division was only

rarely involved by itself (2% of

cases) The superficial position of

the common peroneal nerve as it

wraps around the neck of the fibula

makes it vulnerable to

compres-sion The peroneal division may be

more susceptible to stretch injuries

because it is relatively more fixed

between the sciatic notch and the

fibular head Another explanation

is based on morphologic differences

between the tightly packed fascicles

of the peroneal division and those

of the tibial division, which has

relatively more connective tissue

(Fig 9) The fact that the peroneal

division is more lateral may also

increase its vulnerability to trauma

Generally accepted risk factors

for sciatic nerve injuries include

THA in patients with DDH and

revision THA Johanson et al13

noted increased blood loss and time

of surgery in their patients with

nerve injury and considered all

fac-tors to be related to the level of

diffi-culty of the case Whether the risk

is higher in women and to what

degree leg lengthening increases

risk remain controversial Some

hypothesize that the increased risk

in women is due to less soft-tissue

mass,9while others believe that the

increased risk is related to the

prevalence of DDH.3 Pritchett14

suggests that a Òdouble crushÓ

phe-nomenon, as described in carpal

tunnel syndrome, may play a role in

hip arthroplasty patients who also

have spinal stenosis Of 16 spinal

stenosis patients with footdrop of

unknown cause diagnosed after hip

arthroplasty, 12 had improvement

of the nerve palsy after spinal

decompression with laminectomy

The role of leg lengthening in

cases of nerve injury is unclear

Nerves will tolerate only a finite amount of acute stretch A soft-tissue bed that is scarred and has compromised vascularity should in-crease the potential for injury with lengthening Both the presence of scar from previous operations and the desire to increase leg length must

be considered in revisions and DDH cases Edwards et al15noted that 6 of

10 patients with nerve palsy had leg lengthening of more than 3 cm

Lengthening of less than 3.8 cm was associated with only peroneal-division palsies; lengthening by more than 3.8 cm was associated with both peroneal- and tibial-division palsies

A Mayo Clinic review of DDH pa-tients who underwent THA demon-strated a 13% incidence of sciatic nerve palsy.16 Of those patients with lengthening of 4 cm or more, 28%

had palsy No nerve injuries oc-curred in those with lengthening of less than 4 cm Kennedy et al17

de-monstrated acute progressive wors-ening of somatosensory evoked potential (SSEP) changes when reduction of the femoral head was achieved after increasing the neck length All four patients in whom causalgia developed postoperatively had SSEP reductions in amplitude greater than 75% after component reduction Nercessian et al18

report-ed on 66 patients with lengthening between 2.0 and 5.8 cm without neu-rologic deficit They calculated the amount of lengthening as a percent-age of the length of the femur and concluded that lengthening of up to 10% was safe

Diagnosis

Clinical assessment alone underesti-mates the true incidence of nerve injury after hip arthroplasty.6,9,19 The diagnosis of significant nerve

Transection

Fig 9 Multifascicular nerves with abundant connective tissue (as seen in the tibial divi-sion) are less vulnerable to transection or compression than nerves with tightly packed fas-cicles (as seen in the peroneal division) (Adapted with permission from Bodine SC, Lieber

RL: Peripheral nerve physiology, anatomy, and pathology, in Simon SR (ed): Orthopaedic Basic Science Rosemont, Ill: American Academy of Orthopaedic Surgeons, 1993, p 361.)

Tibial Division Peroneal Division

injuries is usually not challenging

and should begin with adequate

pre-operative documentation of motor

strength and sensation Thorough

evaluation of patients before revision

procedures may help demonstrate

minor nerve damage caused by prior

procedures Complaints of

weak-ness, numbweak-ness, or paresthesias may

indicate a compromised nerve that is

at increased risk during the next

operation Electrodiagnostic tests

can indicate nerve impairment and

the presence of preexisting

neu-ropathies of diabetes, chronic alcohol

abuse, or hypothyroidism

Weakness of the muscles of ankle

dorsiflexion can indicate damage to

the peroneal division of the sciatic

nerve Its sensory distribution

in-cludes the dorsum of the foot, with

the deep peroneal nerve supplying

the web space between the first and

second toes The short head of the

biceps is the only muscle above the

knee that is supplied by the peroneal

division Electromyographic (EMG)

recordings of this muscle can show

whether peroneal division injury is

at the level of the hip or at another

site of vulnerability, the fibular head

Damage to only the tibial division is

rare and results in weakness of all

knee flexors except the short head of

the biceps Weakness of the

posteri-or muscles of ankle and toe plantar

flexion should also be seen

Prognosis

The prognosis of a nerve injury is

related to factors specific to the

injury and clinical factors related to

the patient (Table 1) In the case of

nerve injuries related to THA, the

patient is often elderly, with

multi-ple concurrent medical problems

The damaged nerve is large, and the

distance from the end-organ is great

In revision surgery, the previous

operation may leave binding scar

tissue and an altered vascular

sup-ply to the nerve All these factors

decrease the likelihood of successful nerve regeneration In a large series

of primary THA procedures, as many as 2% of patients had tran-sient neurologic problems, and 0.5%

had permanent nerve damage.20 Although 80% of patients with nerve injuries have some persistent neurologic dysfunction,11,13 causal-gic pain most highly predicts major disability.13 Edwards et al15found that patients who had palsy of only the peroneal division did well, but that patients with injury to both the tibial and the peroneal divisions had less optimal recovery of func-tion In a review of over 3,100 hip arthroplasty operations, Schmalz-ried et al11 found that patients who recovered neurologic function usu-ally did so by 7 months All pa-tients who had evidence of some motor function immediately after the operation or who recovered some motor function during their hospital stay had a good recovery

No patient with dysesthesias had satisfactory recovery of function

Treatment

If no specific cause is identified, often no immediate treatment to decrease compression or stretch of the nerve is indicated Serial exam-inations may demonstrate nerve recovery An advancing Tinel sign distal to the site of injury signifies regeneration of axons and at least partial nerve continuity Electro-myograms and nerve conduction velocity measurements may pro-vide a more objective measure of the level of injury, the degree of injury, and evidence of recovery of motor function

When transection of the nerve is discovered intraoperatively, an attempt at nerve repair seems war-ranted Sunderland et al21reported

a single case of a sharply transected sciatic nerve in a young patient that was repaired early with a good result The results of nerve repair in elderly patients are not promising

In the rare case in which a mechani-cal source of compression can be identified, it should be removed Removal of long-skirted femoral heads or more superior placement

of the acetabular component can relieve tension on the nerve; how-ever, this may require trochanteric advancement to restore soft-tissue tension Delayed onset of progres-sive neurologic symptoms after a normal postoperative check should alert the physician to consider evac-uation of a subfascial hematoma In patients who have received anti-coagulation therapy, motor and sen-sory deterioration with increasing thigh circumference demands cor-rection of coagulation status and surgical decompression

Motor deficits can often be man-aged with physical therapy to strengthen ankle dorsiflexors and stretch antagonist muscles so as to prevent joint contractures Ankle-foot orthoses can be used to treat footdrop, allowing clearance dur-ing the swdur-ing phase and

prevent-Table 1 Clinical Factors in Nerve Injury and Repair

Injury factors Nerve injured Degree of injury Size of zone of injury Distance of zone of injury from

an end-organ Local tissue condition at injury site (tension, vascularity, presence of scar and infection) Patient factors

Age Preexisting neuropathies (e.g., those due to diabetes, alco-holism, hypothyroidism, spinal stenosis)

General medical condition (e.g., history of smoking or cortico-steroid use)

ing the steppage gait indicative of

weak dorsiflexors Orthoses may

also help prevent equinus

defor-mity

The presence of sensory deficits

requires diligence from the patient

in preventing inadvertent trauma

to the extremity, as may occur in

patients with diabetic neuropathy

Dysesthesia and causalgic pain

postoperatively are best treated

with antidepressants as well as

with early and repeated

sympa-thetic nerve blocks as needed.13

Surgical correction of late

equino-varus deformities may be necessary

in rare cases to provide stability of

the ankle joint, to release

contrac-tures, or to provide active

dorsi-flexion

Prevention

The best treatment of any

complica-tion is prevencomplica-tion The first step in

prevention is to identify the

pa-tients who are most at risk Papa-tients

with hip dysplasia and those who

will undergo revisions are clearly at

increased risk Minimizing the

amount of leg lengthening during

preoperative planning and using

leg-length measurement techniques

may decrease the risk to the nerve

There is no strong evidence

favor-ing any one approach for

prevent-ing nerve injury

Whether it is prudent to expose

the nerve in high-risk cases is still

debated Stillwell22 performed

neurolysis to free the sciatic nerve

from binding scar and to allow

mobilization during revision cases

Simon et al23recommend exposure,

macroneurolysis, and protection

routinely in every posterior

ap-proach and noted only one instance

of sensory loss in 400 cases

In-creased intraoperative attention

with palpation of the nerve before

and after arthroplasty and limited

sciatic neurolysis of nerves that are

tethered or difficult to locate may

help to decrease the prevalence of nerve injury.24 However, direct exposure of the nerve may damage the anastomotic blood supply and can lead to increased scarring

Technical factors that may help decrease the incidence of nerve damage include wide exposure and meticulous hemostasis to ensure visualization of the anatomy, con-stant attention to nerve position, and careful placement and replace-ment of retractors Deliberate con-trol of scalpels and reamers is essential to avoid unwanted injury

to soft tissue Careful placement of fixation screws and attention to drill-bit depth are essential Use of anterior-quadrant screws predis-poses to nerve injury (Fig 7)

Internal rotation of the femur dur-ing placement of cerclage wires and cables is recommended to help visualize the soft tissue of the pos-terior femur.25

Proper placement of compo-nents helps minimize dislocations

and the need for revisions that put the nerve at increased risk Black et

al26recommend extreme care when revising only the acetabular com-ponent in patients with monolithic stems, which can rest directly on the sciatic nerve When cementing the cup in acetabular revision cases, the use of bone graft may help prevent intrapelvic extravasa-tion of cement

Electrodiagnostic Studies

Several studies have reported the use of electrodiagnostic tools, such

as evoked potentials (Fig 10) and electromyography (Fig 11), to warn surgeons of impending damage to peripheral nerves during surgery Evoked potentials, first described in

1875 by Caton, are voltage changes

in sensory fibers after stimulation

of peripheral nerves Damage or irritation of nerves can alter electri-cal signals by decreasing the size

Fig 10 Examples of SSEP recordings A, Baseline B, Increased latency and decreased amplitude associated with retractor compression of the sciatic nerve C, Recovery of

trac-ing when the retractor is removed (Reproduced with permission from Stone RG, Weeks

LE, et al: Evaluation of sciatic nerve compromise during total hip arthroplasty Clin Orthop 1985;201:26-31.)

Postincision P1 = 39.2 msec N1 = 46.4 msec P1 − N1 = 1.5 µ V

Retractor on sciatic nerve P1 = 46.4 msec N1 = 54.4 msec P1 − N1 = 0.7 µ V

Retractor removed P1 = 40.8 msec N1 = 52.0 msec P1 − N1 = 1.2 µ V

A

B

C

1.5 µ V

10 msec +

−

(amplitude) or increasing the

trans-mission time (latency) of the evoked

potential Somatosensory evoked

potentials (SSEPs) are recorded

over the somatosensory cortex and

are monitored by an

electroen-cephalographlike device to give

feedback to the operating surgeon

Somatosensory potentials are used

commonly in spine surgery The

American Electroencephalographic

Society guidelines recommend

using a decrease of 50% or more in

amplitude or an increase of 10% or

more in latency to identify

neuro-logic compromise In an animal

study,27 statistically significant

SSEP changes were seen prior to

damage that caused postoperative

motor changes However,

com-plete motor palsy in one division

can be caused while normal SSEP

tracings are seen in the other

divi-sion

Amplitude changes can be

influ-enced by changes in patient

tem-perature, blood pressure, PCO2,

level of anesthesia, and the

electri-cal noise in the operating room

Cortical SSEPs cannot be recorded

during spinal anesthesia For these

reasons, Kennedy et al17

recom-mend placing the monitoring

elec-trode directly on the most proximal

extent of the sciatic nerve

Stone et al28 first used SSEP

monitoring of the peroneal nerve

during total hip arthroplasty and

found a 20% incidence of

intraoper-ative signal changes Changes in SSEPs have been noted with retrac-tor placement, leg positioning for femoral reaming and cement re-moval, anterior or lateral retraction

of the femur, and hip reduction.29,30

In a nonrandomized, unmonitored control group,31 2 of 35 patients (6%) had postoperative incomplete sciatic nerve palsy, while none of the 25 patients in the monitored group had neurologic compromise

Intraoperative monitoring was con-sidered to be a valuable method for use in revisions and reoperations

Black et al26found no reduction

in sciatic nerve palsy in monitored patients compared with an unmon-itored historical control group from the same institution They felt that monitoring may be more appropri-ate in selected high-risk groups In

a follow-up study, Rasmussen et

al29found no difference in the inci-dence of sciatic nerve injury be-tween 290 monitored patients and

a historical control group of 450 unmonitored patients (2.8% vs 2.7%) When they compared only revision cases, no statistically sig-nificant difference between groups was found (6.7% vs 5.3%) They concluded that SSEP monitoring was not effective in predicting or preventing nerve injuries They also reported that 2 patients who were found to have postoperative palsies had no SSEP changes dur-ing the procedure

Another method for monitoring nerve function is to record EMG responses Intraoperative electro-myography has been used to moni-tor nerve function during opera-tions that place the recurrent laryn-geal nerve, facial nerve, spinal nerves, and sciatic nerves at risk Electromyographic responses can

be recorded either as an averaged motor evoked potential or as the individual contraction of a muscle

If an averaged motor evoked poten-tial is recorded, either the spinal cord or the nerve must be

stimulat-ed proximal to the site of surgery After changes through the site of surgery, the elicited neurologic activity is recorded as an EMG trac-ing from a peripheral muscle Multiple stimulations are made, and the muscle responses are aver-aged by a computer

Yet another technique is the mechanically elicited, or sponta-neous, electromyogram Mechan-ical irritation of the nerve results in

an action potential that produces a muscle contraction measured by an EMG response The EMG response elicited by mechanical irritation provides the surgeon immediate real-time feedback of exploration Muscle relaxation must be kept to a minimum of two twitches of a train-of-four stimulation for EMG recording to be possible

Because the site of hip surgery and the site of calf muscle recording

Fig 11 Example of EMG tracings during hip arthroplasty Baseline is on the left Repetitive firing of anterior tibialis muscle is

represent-ed during compression of the peroneal division of the sciatic nerve.

LT ANT TIB

LT GASTROC

are both peripheral, anesthetic

effects on the brain and spinal cord

do not interfere with the

perfor-mance of mechanically elicited

elec-tromyography This allows use of

spinal or epidural anesthesia

with-out signal interference Sutherland

et al32 used spontaneous

electro-myography in 44 consecutive

revi-sion and complex hip arthroplasty

procedures In 5, intraoperative

EMG activity resolved with

retrac-tor or limb adjustments None of

the patients in that study had

post-operative nerve deficits

Intraoperative electromyography

may be a helpful adjunct in the

pre-vention of nerve palsy in high-risk

patients However, larger

prospec-tive trials are necessary to

demon-strate a reduction in the overall rate

of sciatic nerve palsy between

mon-itored and unmonmon-itored patients

Summary

Preservation of neurologic struc-tures is important to maintain high levels of limb function and patient satisfaction after hip arthroplasty

Fortunately, nerve injury in THA is

an uncommon complication, occur-ring in only 1% to 2% of patients who undergo primary hip arthro-plasty

The peroneal division of the sci-atic nerve is the nerve most fre-quently injured during revision cases and in the treatment of demanding cases of hip dysplasia

There is a trend in the literature that supports an increase in sciatic nerve injuries when the leg is lengthened

by more than 4 cm or by more than 10% of the length of the femur

Postoperative footdrop or weakness

of ankle dorsiflexors results from

peroneal division palsy and causes

a steppage gait Often, an ankle-foot orthosis is all that a patient requires to manage the deficit Complete loss of neurologic function or severe causalgic pain carries the worst prognosis The role of electrodiagnostic studies intraoperatively requires further study before recommendations for routine use can be made The importance of prevention is best summarized by Schmalzried et al,11 who stated, ÒNo amount of preop-erative discussion or postoppreop-erative consultation decreased the high degree of dissatisfaction that was expressed by these patients.Ó

Acknowledgments: The authors would like to thank Taryn Tuinstra, Kym Palatto, PAC, and Jeffery H Owen, PhD, for their valuable assistance in preparing this manu-script.

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