Kolano bez ACL.pdf

ACL deficient knee

Kolano bez wiæzadÆa krzyºowego przedniego

Grzegorz Adamczyk

Carolina Medical Center, Warszawa

Summary

Anterior cruciate ligament (ACL) acts as a main re-

straint of anterior translation of the tibia. ACL is in-

trasynovial but extraarticular, because it reflects syno-

vium from posterior capsule of the knee joint and is

covered by a synovial fold that serves as a main sour-

ce of nutrition and vascularisation for ACL. Part of

ACL tear may spontaneously heal inside the synovial

coverage. Ligament is highly innervated, more than

1,5% of its volume is constituted by nerve endings,

4 types of receptors are detected inside the ACL,

mainly in approximity of bone attachments. ACL

serves as a main tract for proprioceptive reactions. In

the knee joint ACL is gradually loaded as the knee

extends. In the absence of sufficient coactivation from

the hamstrings, the posterior pull they apply to the

proximal tibia is not available, leaving the ACL as

the sole structure to stabilize the joint. Latency of

neuromuscular control of deformity in healthy indi-

viduals is 53 ms and among the ACL deficient in-

dividuals latency is about 200 ms. In the absence of

ACL patients tend to develop a quadriceps-avoidance

gait to reduce a quadriceps contraction during walk-

ing and finally loose about 10% of quadriceps muscle

strongth. Untreated ruptures lead to anterior laxity

and subsequent meniscal tears in a great majority of

cases, but about 1/3 patients in a long-term may be

asymptomatic, and 47% may for some time returned

to amateur sport. Meniscal tears are observed among

86% patients with an ACL lesion. The clinical inves-

tigation is highly unreliable among these patients

and arthroscopic assessment is necessary in such ca-

ses. Patients with an ACL tear and meniscal destruc-

tion develop degenerative joint disease (DJD) visible

on X-ray, theres no good evidence of DJD progres-

sion among patients with isolated ACL lesions. DJD

is visible in 65% of the ACL-deficient knees with me-

niscal lesions as early as 4,4 years post meniscectomy.

[Acta Clinica 2002 2:11-16]

Key words: ACL-deficient knee, ACL tear, knee ar-

throscopy, sensorimotor control of the knee joint

Streszczenie

Unaczynienie WKP pochodzi w wiækszo¥ci od tætnicy

¥rodkowej kolana, jak równieº z gaÆåzek koñcowych

tætnic dolnych kolana przy¥rodkowej i bocznej. Wiæk-

szo¥ì ukrwienia dociera z tylno-górnej okolicy przy-

czepu udowego. Naczynia krwiono¥ne rozgaÆæziajå siæ

w bÆonie maziowej formujåc oplatajåcå wiæzadÆo sieì,

która tworzy osÆonkæ odºywczå. Naczynia te komuni-

kujå siæ z sieciå naczyñ wewnåtrzwiæzadÆowych. PoÆå-

czenia wiæzadÆa z ko¥ciå nie uczestniczå w zaopatrze-

niu WKP w krew. Ponad 1,5% WKP stanowiå nerwy.

W wiæzadle stwierdza siæ 4 typy mechanoreceptorów,

pomiædzy nimi så np. wolne zakoñczenia nerwowe,

które inicjujå ochronne napiæcie miæ¥ni juº w 53 msek

po urazie, podczas gdy w kolanie pozbawionym WKP

ta reakcja jest opóªniona o koÆo 200 msek. WKP jest

wiæc bardzo waºnym ogniwem w szlakach czucia gÆæ-

bokiego, jego impulsacja peÆni podstawowå rolæ w re-

gulacji odruchowego napiæcia miæ¥ni zapewniajåcego

kontrolæ stabilno¥ci kolana w mechanizmach tzw. ko-

kontrakcji miæ¥niowej. Wiækszo¥ì pacjentów po uszko-

dzeniu WKP zmienia stereotyp chodu, by uniknåì

przedniego podwichniæcia piszczeli, które nasila siæ

przy skurczu miæ¥nia czworogÆowego (przy kåcie

15 25° podwichniæcie jest najwiæksze) i rozwija chód

z unikaniem jego aktywno¥ci. Nie leczone uszkodze-

nie WKP prowadzi do przedniej niestabilno¥ci stawu

kolanowego, a w konsekwencji do uszkodzenia Æåko-

tek, a nastæpnie degeneracji chrzåstki stawowej.

U mÆodych i aktywnych pacjentów postæp choroby jest

bardzo szybki, w grupie pacjentów starszych, o nie-

wielkich oczekiwaniach ruchowych okoÆo 1/3 nie od-

czuwa dolegliwo¥ci z powodu braku wiæzadÆa, A 47%

moºe na jaki¥ czas powróciì do amatorskiego uprawia-

nia sportu. Bardzo niekorzystne rokowniczo så: wystæ-

powanie objawów niestabilno¥ci rotacyjnej, np. testu

pivot-shift, uszkodzenie Æåkotek, nieprawidÆowa o¥

koñczyny, duºa aktywno¥ì fizyczna chorego czæsto

prowadzåca do ponownych urazów. Uszkodzenia Æå-

kotek towarzyszåce zerwaniu WKP zaobserwowano

u 86% pacjentów. Badanie kliniczne nie jest w peÆni

wiarygodne u tych pacjentów i wskazana jest artrosko-

pia, celem operacji naprawczych Æåkotek. Nie ma do-

wodów na to, ºe izolowane uszkodzenie WKP prowa-

dzi do zmian zwyrodnieniowych stawu kolanowego,

ale u pacjentów z rozlegÆymi uszkodzeniami Æåkotek

64% ma ewidentne cechy gonartrozy w badaniu rent-

genowskim juº w 4,4 lata po urazie. [Acta Clinica

2002 2:11-16]

SÆowa kluczowe: kolano bez wiæzadÆa krzyºowego

przedniego, uszkodzenie WKP, kontrola sensomoto-

ryczna stawu kolanowego

Tom 2, Numer 1 11

Acta Clinica

Vascularisation

Neuromuscular control

Anterior cruciate ligament (ACL) acts

as a main restraint of anterior translation of

the tibia. ACL originates from medial as-

pect of the lateral femoral condyle and pas-

ses anteriorly and medially to the posterior

cruciate ligament (PCL) to insertion on the

anterior aspect of the tibia in front of me-

dial tibial eminence. ACL is intracapsular

but extraarticular, because it reflects syno-

vium from posterior capsule of the knee jo-

int and is covered by a synovial fold that

serves as a main source of nutrition and

vascularisation for ACL. Vessels for ACL

originate from middle genicular artery and

5 types of mechanoreceptors appear in-

side the knee joint (Tab. 1), among them

4 types of receptors are detected inside the

ACL (27). So that ligament is highly inner-

vated, more than 1,5% of its volume is con-

stituted by nerve endings, mainly in appro-

ximity of bone attachments, and it serves as

a main tract for proprioceptive reactions.

Ligamento-muscular protective reflex

was proposed by Payr in 1900 as a part of

kinetic chain theory according to which

ligaments, bones, muscles and receptors

acts synergistically to provide safe, stable

motion of the joint. For example ACL is

subjected by large forces, when tibia is dis-

placed anteriorly beyond the physiologic

strain limits and then receptors of ACL re-

lease contraction of hamstrings, which will

protect against the anterior subluxation by

pulling the tibia posteriorly (4, 13, 17).

That observation was confirmed and docu-

mented in humans by Grüber in 1986 (11).

All experiments have confirmed the hypo-

thesis, that there is a direct neuromuscular

link in humans in between a ACL and all

the muscles surrounding the knee (9, 11,

27). Beard (4) defined a latency of neuro-

muscular control of deformity in healthy

individuals as 53 ms and among the ACL

deficient individuals latency was doubled.

The most primitive neuromuscular re-

flex is flexion reflex called withdrawal re-

flex, because it withdraw of the organism

away from noxious stimulus that may harm

it e.g. extreme heat, and invariably is as-

sociated with pain. The ligamento-muscu-

lar reflex may be considered as an example

of withdrawal reflex and is directly con-

nected to the ligament receptors. In the

knee its action consist of simultaneous hip

or knee flexion approximating the limb to

the trunk and away from stimulus. Parallel

flexion of two joints earned this reflex the

name flexion. This is a spinal reflex,

Figure 1. Partial lesion of anterior cruciate ligament

part of fibers outside the synovium, latero-poste-

rior bundle inside the synovial coverage

from terminal branches of medial and late-

ral inferion genicular circumflex artery.

Main part of that nutritional vessels penet-

rates from upper-posterior aspect of femo-

ral attachment and they form a rich net-

work of intraligamentary vessels. Bone at-

tachments do not participate in nutrition of

ACL, thats why part of ACL tear may

spontaneously heal inside the synovial cov-

erage (1, 2) (Fig. 1).

12 Wiosna 2002

ACL deficient knee

Tab. 1. Types of mechanoreceptors of the knee joint (acc. to Solomonow M., Krogsga-

ard M: Sensorimotor control of knee stability. A review. Scand J Med Sci Sports 2001

11:64 80)

Receptor

Type of stimulus

Localization

Projection

Bare nerve endings Extreme deformity, pain,

inflammation

Articular surface,

ligaments

Spinal cord (reflexes),

sensory cortex

Ruffian endings

Low-level deformation

(slow adapting)

Ligaments, menisci Spinal cord (reflexes),

sensory cortex

Pacinian corpuscles High forces

and pressure deformation

Ligaments, menisci Spinal cord (reflexes),

sensory cortex

Golgi receptors

Extreme forces

Tendons, ligaments,

menisci, capsule

Spinal cord (reflexes), sensory

cortex (capsule and menisci

Golgi tendons organs) to cere-

bellum only (Golgi tendons or-

gans)

Muscle spindles

Muscle elongation,

velocity and acceleration

Muscles crossing

the joint

Spinal cord (monosynaptic

reflexes), cerebellum

thats why it is fast, short neural pathway

eliminates the cooperation of brain and

perceived sensation of pain is delayed 2 sec

(4, 9, 22, 26).

Pope (22) identified an intentional vol-

untary contraction of the musculature for

protecting the knee joint from potentially

unstabilizing mechanical stimulus. He tes-

ted, whether an athlete could learn to con-

tract the muscles across the knee in respon-

se to force applied to the joint and prevent

subluxation. The patients were contracting

their muscles immediately after application

of a tap stimulus to the foot. Self-generated

acquired contraction required 220 ms and

was too long to protect the knee.

In 1909 Sherrington (7, quoted after 3)

published his classical work where he no-

ted that joint motion is always accompa-

nied by co-contraction, or co-activation of

the joint agonistic or antagonists muscles.

For the knee extension agonistic quadri-

ceps applies large forces and antagonistic

hamstrings and biceps are antagonists and

apply low-level forces. Sherrington thought

it was a central mechanisms, but Feneys

(9) demonstrated that it may also be a per-

ipheral reflex. Antagonistic activity com-

pensates the effect of gravity on the limb

mass, opposes torque of an acting joint and

maintains it despite changes in muscle

length and moment arm around the center

of rotation.

Sport, acquired skill has a significant

impact on coactivation pattern of the mus-

cles around the joint. Person as early as in

1957 was the first to show that as an athlete

acquires a skill by practicing the repetitive

joint motion, the antagonists coactivation

level is markedly decreased, increasing a jo-

int efficiency (4, 23).

In the knee joint ACL is gradually loa-

ded as the knee extends (23). In the absen-

ce of sufficient coactivation from the ham-

strings, the posterior pull they apply to the

proximal tibia is not available, leaving the

ACL as the sole structure to stabilize the

joint and it puts the ACL of highly skilled

athlete at a high risk of injury. Louie and

Mote measured (17) that contraction of the

Tom 2, Numer 1 13

Acta Clinica

hamstring reduces rotary laxity of the joint

by 76%, while contraction of quadriceps re-

duces laxity by 23%, the stiffness of the

knee joint increased by two- to threefold

when the muscles were active.

In the situation of absence of richly in-

nervated ACL, other structures capsule,

menisci may activate antagonists muscles

with significant delay (27).

Hirokawa (13, 27) showed, that isolated

loading of quadriceps in ACL deficient

patient at 15° of flexion leads to 4 mm an-

terior displacement of tibia under load of

only 12 kg. At 15° of flexion a 33% reduc-

tion is available by hamstrings, at 30° of fle-

xion a 70% reduction is evident. The exces-

sive anterior displacement of the tibia asso-

ciated with isolated quadriceps contraction

exhibits, why this muscle exhibits partial

atrophy post ACL rupture. Quadriceps

muscle atrophy was about 10% of its mass,

mainly of vastus medialis and hamstrings

about 4% (10). Patients tend to develop

a quadriceps-avoidance gait to reduce

a quadriceps contraction during walking.

other ligamentous lesions e.g. PCL,

lower limb alignment,

tibiofemoral crepitus,

patellofemoral problems,

patient compliance and expectations

(20).

Untreated ruptures lead to anterior lax-

ity and subsequent meniscal tears (15, 18)

in a great majority of cases, but about 1/3

patients in a long-term may be asymptoma-

tic, and 47% may for some time returned to

amateur sport (6, 15, 18, 20). In the group

of middle-aged, low expectation patients

(6) good results may be expected after

a conservative treatment, while the young,

active athletes will not do well. On the

other hand, the re-injury ratio is very high

among the other group and may occur in

50% of young patients over one year (20).

This observation is not confirmed by our

own data.

Partial ACL-tear

Among patients with an ACL tear in

about 30% of cases (in our material 21%)

(3) a partial tear is detected (21, 24). 38% of

these patients progressed to complete defi-

ciency one half of fibers in 50%, 3/4 th

tears in 86%. So theres a chance to treat it

conservatively in 2/3 of cases. Some of

them may develop a Wittek mechanism of

adhesions in between ACL and PCL thus

somehow decreasing a degree of instability

(16, 21, 24).

Meniscal tears are observed among 86%

patients with an ACL tear (15). The clini-

cal investigation is highly unreliable among

these patients and arthroscopic assessment

is necessary in such cases. Patients with an

ACL tear and meniscal destruction develop

degenerative joint disease (DJD) visible on

X-ray, theres no good evidence of DJD

progression among patients with isolated

ACL lesions (12, 25). DJD is visible in 65%

of the ACL-deficient knees as early as 4,4

years post meniscectomy. Secondary lesions

Natural history

of the ACL-deficient knee

In majority of cases with an evident

trauma and with a post-traumatic haemar-

throsis 72% to 84% presents lesion of ACL,

approximately 70% total rupture, 30% par-

tial (3, 8, 16, 19). In 86% ACL lesion was

accompanied by major meniscal tears.

There are many factors that should be

taken under the consideration, while plan-

ning the treatment of such a patients:

categories of activity level passive,

active, sportsmen,

type of athletic activity (jumping,

twisting activity versus light, recreational

pursuits),

age adolescents, middle aged, old,

level of instability in particular the

presence of pivot shift sign,

meniscal damage,

14 Wiosna 2002

ACL deficient knee

of menisci may develop in ACL deficient

knee (28).

In the conservatively treated patients

only 50% of results were graded as excellent

or good, in surgical group 94% (7).

The ACL deficient patients often deve-

lop an unicompartmental arthritis of the

knee, because the biomechanical effects of

ACL deficiency predispose the knee to

DJD, in particular among the patients with

often giving-way episodes. Probably also

o metabolic effect of inflammation caused

by ACL stump resorbtion may have a nega-

tive effect on viscoelastical properties of jo-

int fluid. Cameron reported elevated levels

of cytokines: Interleukin 1 and 6, TNF- a ;

and keratan sulphate (5) in an ACL-defi-

cient patient, that might be responsible for

a quick progression of DJD.

Our own clinical observations consider-

ing a natural course of degenerative knee

disease in ACL-deficient knee patients have

been already published in Acta Clinica No

2 (3).

Results after long-term follow-up. JBJS [Am] 1994

76 (9), 1315 21.

7. Clancy W.G., Ray J.M., Zoltan D.J.: Acute tears

of the anterior cruciate ligament. Surgical versus

conservative treatment. JBJS [Am] 1988 70 (10),

1483 8.

8. Dehaven K.: Diagnosis of acute knee injuries

with haemarthrosis Am J. Sports Med 1980 8 (1)

9 14.

9. Feneys I. Gergely C., Toth S.: Clinical and elec-

tromyological studies of spinal reflexes in premature

and full-term infants. J. Neuro Neurosurg Psych

1960 23: 63 68.

10. Gerber C., Hoppeler H., Claasen H., Robotti

G., Zehnder R., Jakob R.P.: The lower extremity

musculature in chronic symptomatic instability of

the anterior cruciate ligament, JBJS [Am] 1985 67

(7) 1034 43.

11. Grüber J., Wolter D., Lierse W.: Der vordere

Kreuzbandreflex (LCA-reflex), Unfallchirurgie 1986

89:551 554.

12. Hazel W.A., Rand J.A., Morrey B.F.: Results of

meniscectomy in the knee with anterior cruciate de-

ficiency. Clin Orthop& Rel Res 1993 292:232 8.

13. Hirokawa S., Solomonow M., Lu Y., Lou Z.P.,

Ambrosia L.: Muscular cocontraction and control of

knee stability J. EMG Kinesiol 1991 1:199 208.

14. Irvine G.B., Glasgow M.M.: The natural history

of the meniscus in anterior cruciate insufficiency

arthroscopic analysis. JBJS [B] 1992 74

(3):403 405.

15. Kannus P., Jarvinen M.: Conservatively treated

tears of the anterior cruciate ligament. Long-term

results. JBJS [Am] 1987 69 (7):1007 12.

16. Lo I., de Maat G., Valk J.W., Frank C.B.: The

Gross Morphology of Torn Human Anterior Cruci-

ate Ligaments in Unstable Knees. Arthroscopy 1999

15 (3): 301 306.

17. Louie J. Mote C.: Contribution of the muscula-

ture to rotatory laxity and torsional stiffness at the

knee. J. Biomech. 1987 20:281 300.

18. McDaniel W.J., Dameron T.B.: Untreated Rup-

tures of the Anterior Cruciate Ligament, J.B.J.S.

[Am] 1980; 62-A (5): 696 705.

19. Noyes F.R., Basset R.W., Grood E.S., et al. Ar-

throscopy in acute traumatic haemarthrosis of the

knee. J Bone Joint Surg 1980 62A:687 695.

20. Noyes F.R., McGinnis G.H.: Controversy about

treatment of the knee with anterior cruciate laxity,

Clin Orthop Rel Res 1985; 198: 61 76.

21. Noyes F., Mooar L.A., Moorman C.T., McGin-

nis G.H.: Partial tears of the anterior cruciate liga-

ment. JBJS [Br] 1989 71 (5):825 833.

References

1. Arnoczky S.P. Anatomy of the anterior cruciate

ligament. Clin Orthop 1983 172:19.

2. Arnoczky S.P. Blood supply to the anterior cruci-

ate ligament and supporting structures. Orthop Clin

North Am 1985 16:15 28.

3. Adamczyk G., Antolak £., Skrok T., ÿmigielski

R.: Chondral lesions accompanying to acute and

persistent tears of anterior cruciate ligament of the

knee joint, based on video data made during 144

operations, Acta Clinica 2001; Tom 1 (2), 138 144.

4. Beard D.J., Kyberd P.J., OConnor J.J., Fergusson

C.M., Dodd C.A.F.: Reflex hamstring contraction in

anterior cruciate deficiency. J. Orthop. Res. 1994

12:219 228.

5. Cameron J.C., Saha S.: Meniscal allograft trans-

plantation for unicompartmental arthritis of the

knee, Clin Orthop 1997 337:164 171.

6. Ciccotti M.G., Lombardo S.J., Nonweiler B.,

Pink M.: Non-operative treatment of ruptures of the

anterior cruciate ligament in middle-aged patients.

Tom 2, Numer 1 15

Plik z chomika:

Inne pliki z tego folderu:

Inne foldery tego chomika: