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CASE REPORT

TOTAL KNEE ARTHROPLASTY

ON OA KNEE JOINT

Diajukan untuk memenuhi tugas dan melengkapi salah satu syarat dalam

menempuh Program Pendidikan Profesi Dokter bagian Ilmu Bedah

di RSUD Dr. H. Soewondo Kendal

Disusunoleh:
Irfan Suryo Rakhmatto
01.211.6418

Pembimbing:

dr. Wisnu Murti, Sp.OT

FAKULTAS KEDOKTERAN

UNIVERSITAS ISLAM SULTAN AGUNG

SEMARANG

2016

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HALAMAN PENGESAHAN

Nama : Irfan Suryo Rakhmatto

NIM : 01.211.6418

Fakultas : Kedokteran

Universitas : Universitas Islam Sultan Agung ( UNISSULA )

Tingkat : Program Pendidikan Profesi Dokter

Bagian : Ilmu Bedah

Judul : TOTAL KNEE ARTHROPLASTY ON OA KNEE JOINT

Kendal, November 2016

Mengetahui dan Menyetujui

Pembimbing Kepaniteraan Klinik

Bagian Ilmu Bedah RSUD Dr. H.Soewondo Kendal

Pembimbing,

dr. Wisnu Murti Sp.OT

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CHAPTER I

INTRODUCTION

Osteoarthritis refers to a clinical syndrome of joint pain accompanied by


varying degrees of functional limitation and reduced quality of life. It is the most
common form of arthritis, and one of the leading causes of pain and disability
worldwide. The most commonly affected peripheral joints are the knees, hips and
small hand joints. Pain, reduced function and effects on a person's ability to carry
out their day-to-day activities can be important consequences of osteoarthritis.

Knee pain is one of the most common musculoskeletalcomplaints that


bring people to their physician. Withtoday’s increasingly active society, the
number of kneeproblems is increasing. Knee pain has a wide variety ofcauses and
treatments. Causes of knee pain include injury,degeneration, arthritis, infrequently
infection, and rarelybone tumours.

Knee osteoarthritis is a common degenerative joint condition which tends


to be progressive, debilitating and often recalcitrant to treatment. Given the rise in
the incidence of knee osteoarthritis in an increasingly younger patient population,
along with a more active lifestyle into later years, more effective conservative
treatment options are indicated.

Osteoarthritis (OA) of the knee, one of the mostcommon causes of


disability, continues to increasein prevalence as the older adult and obese
populationsgrow. Many other treatments are available for knee OA, including
education, bahavioural change, physical interventions and drugs. Several
management guidelines have been published over the last few years, most of
which recommend a sequential approach, using simple measures first, such us
education and advice about exercise, footwear and weight reduction, followed by
the use of analgesics and physical therapy, reserving non-steroidal anti-
inflammatory drugs, intra-articular interventions and surgery for the more severe

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cases. Often, the general practitioner is the firstto evaluate a patient with a painful
knee that hasarthritis. Evidence-based evaluation and treatmentguidelines
recommend the use of nonoperativetreatments before surgical treatment options
suchas total knee arthroplasty (TKA) are considered.Understanding available
nonoperative treatmentoptions is critical for physicians who first
encounterpatients with OA of the knee.

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CHAPTER II

CONTENTS REVIEW

1.ANATOMY

The knee joint is a synovial joint which connects the femur, our thigh bone
and longest bone in the body, to the tibia, our shinbone and second longest bone.
There are two joints in the knee—the tibiofemoral joint, which joins the tibia to
the femur and the patellofemoral joint which joins the kneecap to the femur.
These two joints work together to form a modified hinge joint that allows the knee
to bend and straighten, but also to rotate slightly and from side to side.

The main parts of the knee joint are bones, ligaments, tendons, cartilages
and a joint capsule, all of which are made of collagen. Collagen is a fibrous tissue
present throughout our body. As we age, collagen breaks down.

The adult skeleton is mainly made of bone and a little cartilage in places.
Bone and cartilage are both connective tissues, with specialized cells called
chondrocytes embedded in a gel-like matrix of collagen and elastin fibers.
Cartilage can be hyaline, fibrocartilage and elastic and differ based on the
proportions of collagen and elastin. Cartilage is a stiff but flexible tissue that is

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good with weight bearing which is why it is found in our joints. Cartilage has
almost no blood vessels and is very bad at repairing itself. Bone is full of blood
vessels and is very good at self repair. It is the high water content that makes
cartilage flexible.

Bones of the Knee

The bones give strength, stability and flexibility in the knee. Four bones
make up the knee (see above image):

 Tibia —commonly called the shin bone, runs from the knee to the
ankle. The top of the tibia is made of two plateaus and a knuckle-
like protuberance called the tibial tubercle. Attached to the top of
the tibia on each side of the tibial plateau are two crescent-shaped
shock-absorbing cartilages called menisci which help stabilize the
knee.
 Patella—the kneecap is a flat, triangular bone; the patella moves
when the leg moves. It’s function is to relieve friction between the
bones and muscles when the knee is bent or straightened and to
protect the knee joint. The kneecap glides along the bottom front
surface of the femur between two protuberances called femoral

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condyles. These condyles form a groove called the patellofemoral
groove.
 Femur—commonly called the thigh bone; it’s the largest, longest
and strongest bone in the body. The round knobs at the end of the
bone are called condyles.
 Fibula—long, thin bone in the lower leg on the lateral side, and
runs along side the tibia from the knee to the ankle.

Ligaments in the knee

The knee works similarly to a rounded surface sitting atop a flat surface.
The function of ligaments is to attach bones to bones and give strength and
stability to the knee as the knee has very little stability. Ligaments are strong,
tough bands that are not particularly flexible. Once stretched, they tend to stay
stretched and if stretched too far, they snap.

 Medial Collateral Ligament (tibial collateral ligament) – attaches


the medial side of the femur to the medial side of the tibia and
limits sideways motion of your knee.

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 Lateral Collateral Ligament (fibular collateral ligament) –
attaches the lateral side of the femur to the lateral side of the fibula
and limits sideways motion of your knee.
 Anterior cruciate ligament – attaches the tibia and the femur in
the center of your knee; it’s located deep inside the knee and in
front of the posterior cruciate ligament. It limits rotation and
forward motion of the tibia.
 Posterior cruciate ligament – is the strongest ligament and
attaches the tibia and the femur; it’s also deep inside the knee
behind the anterior cruciate ligament. It limits the backwards
motion of the knee.
 Patellar ligament – attaches the kneecap to the tibia

The pair of collateral ligaments keep the knee from moving too far side-to-
side. The cruciate ligaments crisscross each other in the center of the knee. They
allow the tibia to “swing” back and forth under the femur without the tibia sliding
too far forward or backward under the femur. Working together, the 4 ligaments
are the most important in structures in controlling stability of the knee. There is
also a patellar ligament that attaches the kneecap to the tibia and aids in stability.
A belt of fascia called the iliotibial band runs along the outside of the leg from the
hip down to the knee and helps limit the lateral movement of the knee.
Tendons in the Knee
Tendons are elastic tissues that technically part of the muscle and connect
muscles to bones. Many of the tendons serve to stabilize the knee. There are two
major tendons in the knee—the quadriceps and patellar. The quadriceps
tendon connects the quadriceps muscles of the thigh to the kneecap and provides
the power for straightening the knee. It also helps hold the patella in the
patellofemoral groove in the femur. The patellar tendon connects the kneecap to
the shinbone (tibia)—which means it’s really a ligament.

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Cartilage of the knee
The ends of bones that touch other bones—a joint—are covered with
articular cartilage. It’s gets its name “articular” because when bones move against
each other they are said to “articulate.” Articular cartilage is a white, smooth,
fibrous connective tissue that covers the ends of bones and protects the bones as
the joint moves. It also allows the bones to move more freely against each
other. The articular cartilages of the knee cover the ends of the femur, the top of
the tibia and the back of the patella. In the middle of the knee are menisci—disc
shaped cushions that act as shock absorbers.
 medial meniscus—made of fibrous, crescent shaped cartilage and
attached to the tibia, on the inside of the knee
 lateral meniscus—made of fibrous, crescent shaped cartilage and
attached to the tibia, on the outside of the knee
 articular cartilage is on the ends of all bones in any joint—in the
knee joint it covers the ends of the femur and tibia and the back of
the patella. The articular cartilage is kept slippery by synovial fluid
(which looks like egg white) made by the synovial membrane (joint
lining). Since the cartilage is smooth and slippery, the bones move
against each other easily and without pain.
In a healthy knee, the rubbery meniscus cartilage absorbs shock and the
side forces placed on the knee. Together, the menisci sit on top of the tibia and
help spread the weight bearing force over a larger area. Because the menisci are
shaped like a shallow socket to accommodate the end of the femur, they help the

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ligaments in making the knee stable. Because the menisci help spread out the
weight bearing across the joint, they keep the articular cartilage from wearing
away at friction points.

Muscles Around the Knee


The muscles in the leg keep the knee stable, well aligned and moving—the
quadriceps (thigh) and hamstrings. There are two main muscle groups—the
quadriceps and hamstrings. The quadriceps are a collection of 4 muscles on the
front of the thigh and are responsible for straightening the knee by bringing a bent
knee to a straight position. The hamstrings is a group of 3 muscles on the back of
the thigh and control the knee moving from a straight position to a bent position.
The Joint Capsule
The capsule is a thick, fibrous structure that wraps around the knee joint.
Inside the capsule is the synovial membrane which is lined by the synovium, a
soft tissue that secretes synovial fluid when it gets inflamed and provides
lubrication for the knee.
Bursae
There are up to 13 bursa of various sizes in and around the knee. These
fluid filled sacs cushion the joint and reduce friction between muscles, bones,
tendons and ligaments. There are bursa located underneath the tendons and
ligaments on both the lateral and medial sides of the knee. The prepatellar bursa is

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one of the most significant bursa and is located on the front of the knee just under
the skin. It protects the kneecap. In addition to bursae, there is a infra patellar fat
pad that helps cushion the kneecap.
Plicae
Plicae are folds in the synovium. Plicae rarely cause problems but
sometimes they can get caught between the femur and kneecap and cause pain.
Knee Function
So now we have all the parts, let’s see how the knee moves (articulates)—
which is how we walk, stoop, jump, etc. The knee has limited movement and is
designed to move like a hinge.
The Quadriceps Mechanism is made up of the patella (kneecap), patellar
tendon, and the quadriceps muscles (thigh) on the front of the upper leg. The
patella fits into the patellofemoral groove on the front of the femur and acts like a
fulcrum to give the leg its power. The patella slides up an down the groove as the
knee bends. When the quadriceps muscles contract they cause the knee to
straighten. When they relax, the knee bends.
In addition the hamstring and calf muscles help flex and support the knee.

2. OSTEOARTHRITIS

Osteoarthritis refers to a clinical syndrome of joint pain accompanied by


varying degrees of functional limitation and reduced quality of life. It is the most
common form of arthritis, and one of the leading causes of pain and disability
worldwide. The most commonly affected peripheral joints are the knees, hips and
small hand joints. Pain, reduced function and effects on a person's ability to carry
out their day-to-day activities can be important consequences of osteoarthritis.

Osteoarthritis (OA) is a chronic joint disorder in which there is


progressive softening and disintegration of articular cartilage accompained by
new growth of cartilage and bone at the joint margins (osteophytes) and capsular
fibrosis. It differs from simple wear and tear in several ways; it is asymmetrically
distributed and often localized to only one part of a joint; and it is related to

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abnormal loading rather than frictional wear. In its most common form, it is
unaccompanied by any systemic illness and, although there are sometimes local
signs of inflammation, it is not primarily an inflammatory disorder.

It is also not purely degenerative disorder, and the term ‘degenerative


arthritis’ – which is often used as a synonym for OA – is a misnomer. OA is a
dynamic phenomenon; it shows features of both destruction and repair. Cartilage
softening and disintegration are accompanied from the very outset by hyperactive
new bone formation, osteophytosis and remodelling. The final picture is
determined by the relative viour of these opposing processes. In addition, there are
various secondary factors which influence the progress of the disorder; the
appearance of calcium-containing crystals in the joint; ischaemic changes
(especially in elderly people) which result in areas of osteonecrosis in the
subchondral bone; the appearance of joint instability; and the effects of prolonged
anti-inflammatory medication

Etiology

The most obvious thing about OA is that it increases in frequency with


age. This does not mean that OA is simply an expression of senescence. Cartilage
does ‘age’, showing diminished cellularity, reduced proteoglycan concentration,
loss of elacticity and a decrease in breaking strength with advancing years. These
factors may well predispose to OA, but it is significant that the progressive
changes which are associated with clinical and radiological deterioration are
restricted to certain joint, and to specific areas of those joint, while other areas
show little oe no progression with age.

Primary change in cartillage matrix might (theoretically) weaken its


structure and thus predispose to cartilage breakdown; crystal deposition desease
and ochronosis are well-known examples, and genetic defects in type II collagen
have been demonstrated in some cases. However, it is unlikely that factors such as
these are the sole determinants of OA.

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Articular cartilage may be damaged by previous inflammatory disorder.
Enzyme release by synovial cells and leucocytes can cause leaching of
proteoglycans from matrix, and synovial-derived interleukin-1 (IL-1) may
suppress proteoglycan synthesis. This may explain the appearance of secondary
OA in patient with rheumatoid disease; whether similar process operate in
‘idiopathic’ OA is unkonown.

In the majority of cases the precipitating cause of OA is increase


mechanical stress in some part of the articular surface. This may be due to
increased load (e.g. in deformities that effect the lever system around a joint) or to
a reduction of the articular contact area (e.g. with joint incongruity or instability).
Both factor in varus deformity of the knee and in acetabular dysplasia – common
precusors of OA. Changes in the subchondral bone may also increase stress
concentration in the overlying cartilage, either by altering the shape of the
articular surface or by in an increase in bone density (e.g. following fracture
healing) which reduces the shockabsorbing effect if the supporting cancellous
bone.

From the foregoing outline it should be apparent that the division of OA


into ‘primary’ (when there is no obvious antecedent factor) and ‘secondary’ (when
ir follows a demonstrable abnormality) is somewhat artificial. This is borne out in
clinical practice: patient with secondary OA of the knee following meniscectomy
have been found also to have a higher than usual incidence of ‘primary’ OA in
other joint. Perhaps primary, generalized factors (genetic, metabolic or endocrine)
alter the physical properties of cartilage and thereby determine who is likely to
develop OA, while secondary factors such as anatomical defects or trauma specify
when and where it will occur. OA is, ultimately, more process than disease,
occuring in any condition which causes a disparity between the mechanical stress
to which articular cartilage is exposed and the ability of the cartilage to withstand
that stress.

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Pathogenesis

The initial stages of OA have been studied in animal models with induced
joint instability and may not be representative of all types of OA.

The earliest changes, when the cartilage is still morphologically intact, are
an increase in water content of the cartilage and easier extractability of the matrix
proteoglycans, similar findings in human cartilage have been ascribed to failure of
the internal collagen network that normally restrains the matrix gel. At a slightly
later stage there is loss of proteoglycans and defect appear in the cartilage. As the
cartilage becomes less stiff, secondary damage to chondrocytes may cause release
of cell enzymes and futher matrix breakdown. Cartilage deformation may also add
to the stress on the collagen network, thus amplifying the changes in a cylce that
leads to tissue breakdown.

Articular cartilage has an important role in distributing and dissipating the


forces associated with joint loading. When it loses its integrity these forces are
increasingly concentrated in the subchondral bone. The result: focal trabecular
degeneration and cyst formation, as well as increased vascularity and reactive
sclerosis in the zone of maximal loading.

What cartilage remains is still capable of regeneration, repair and


remodelling. As the articulare surfaces become increasingly malapposed and the
joint unstable, cartilage at the edges if the joint reverts to the more youthful
activities of growth and endochondral ossification, giving rise to the bony
excrescences, or osteophytes, that so clearly distinguish OA (once called
‘hypertrophic arthritis’) from ‘atrophic’ disorder such rheumatoid disease.

Pathology

The cardinal features are: (1) progressive cartilage destruction; (2)


subarticular cyst formation, with (3) sclerosis of the surrounding bone; (4)
osteophyte formation; and (5) capsular fibrosis.

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Initially the cartilaginous and bony change are confined to one part of the
joint – the mostly heavily loaded part. There is softening and friying, or
fibrillation, of the normally smooth and glistening cartilage. The term
‘chondromalacia’ (Gr = cartilage softening) seems apt for this stage of the disease,
but it is used only of the pattelar articular surface where it features as one of the
causes of anterior knee pain in young people.

With progressive disintegration of cartilage, the underlying bone becomes


exposed and some areas may be polished, or burnished, to ivory-like smoothness
(eburnation). Sometimes small tufts of fibrocartilage may be seen growing out of
the bony surface. At a distance from the damaged area the articular cartilage looks
relatively normal, but at the edges of the joint there is remodelling and growth of
ostephytes covered by thin, bluish cartilage.

Beneath the damage cartilage the bone is dense and sclerotic. Often within
this area of subchondral sclerosis, and immediately subjacent to the surface, are
one or more cysts containing thick, gelatinous material.

The joint capsule usually shows thickening and fibrosis, sometimes of


extraordinary degree. The synovial lining, as a rule, looks only mildly inflamed;
sometimes, however, it is thick and red and covered by villi.

The histological appearances vary considerably, according to the degree


of destruction. Early on, the cartilage shows small irregularities or splits in the
surface, while in the deeper layers there is patchy loss of metachromasia
(obviously corresponding to the depletion of matrix proteoglycans). Most striking,
however, is the increased cellularity, and the appearance of clusters, or clones, of
chondrocytes – 20 or more to a batch. In later stage, the clefts become more
extensive and in some areas cartilage is lost to the point where the underlying
bone is completely denuded. The biochemical abnormalities corresponding to
these changes were described by Mankinet al. (1971).

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The subchondral bone shows marked osteoblastic activity, especially on
the deep aspect of any cyst. The cyst itself contains amorphous material; its origin
is mysterious – it could arise from stress disintegration of small trabeculae, from
local areas of osteonecrosis or from the forceful pumping of synovial fluid trough
cracks in the subchondral bone plate. As in all types of arthritis, small areas of
osteonecrosis are quiet common.

The osteophytes appear to arise from cartilage hyperplasia and


ossofication at the edge of the articular surface.

The capsule and synovium are often thickened but cellular activity is
slight; however, sometimes there is marked inflammation or fibrosis of the
capsular tissues.

A feature of OA, which is difficult to appreciate from the morbid anatomy,


is the marked vascularity and venous congestion of the subchondral bone. This
can be shown by angiographic studies and the demonstration of increases
intraosseous pressure. It is also apparent from the intense activity around
osteoarthitic joints shown on radionuclide scanning.

Prevalence

OA is the commonest of all joint disease. It is truly universal disorder,


affecting both sexes all races; everyone who lives long enough will have it
somewhere, in some degree. However, there are significant differences in its rate
occurrence in different ethnic groups, in the different sexes within any group and
in the different joints.

Reports of prevalence rates vary, depending on the method of evaluation.


Autopsy studies show OA changes in everyone over the age of 65 years.
Radiographic surveys suggest that the prevalence rises from 1% below the age of
30 years to over 50% in people above the age of 60 years. OA of the finger joints

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is particularycmmon in elderly women, affecting more than 70% of those over 70
years.

Men and women are equally likely to develop OA, but more joints are
affected in women than in men.

OA is much more common in some joints (the fingers, hip, knee and
spine) than in others (the elbow, wrist and ankle). This may simply reflect the fact
that some joints are more prone to predisposing abnormalities than others.

A similar explanation may account for certain geographic and ethnic


differences in prevalence. For example, the female-to-male ratio for OA of the hip
is about 1:1 in northern Europe but it is nearer 2:1 in southern Europe where there
is a high incidence of acetabular dysplasia in girls. Even more striking is the
virtual absnce of hip OA in southern Chinese and African blacks; this mau simply
be because predisposing disorders such as developmental displacement of the hip,
Perthes’ disease and slipped femoral epiphysis are uncommon in these
populations. That they have no inherent resistance to OA is shown by the fact that
they often develop the condition in other joints, for example the knee.

Risk Factors

Joint dysplasia Disorders such as congenital acetabular dysplasia and


Perthes’ disease presage a greater than normal risk of OA in later life. However,
OA is by no means inevibakeadine should not be in any hurry to undertaje
‘prophylactic’ surgery in a child with asymptomatic dysplasia.

Traumafracture involving the articular surface are obvious precursors of


secondary OA. So, too, are lesser injuries which result in joint instability. What is
less certain is whether malunion of a long-bone fracture predisposes to OA by
causing segemental overload in a joint above or below the healed fracture (for
example, in the knee or ankle after a tibila fracture). Contrary to popular belief,
reasearch has shown that moderate angular deformities of the tibia (up to 150) are

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not associated with an incrased risk of OA. This applies to mid-shaft fractures;
malunion close to a joint may well predispose to secondary OA.

OccupationThere is good evidence of an association between OA and


certain occupation which cause repetitive stress; for example OA of the knees in
workers engaged in knee-bending activities, OA in the uooer limbs in people
working with heavy vibrating tools and OA of the gands in cotton mill workers.
More controversial is the relationship of OA to sporting activity. Boxers are
certainly prone to develomping OA of the hands but this may be due to trauma.
The same applies to footballers with OA of the knees and baseball pitchers with
OA of the shoulder. More convicing evidence og a causative relationship comes
from studies which have shown a significant increase in the risk of hip and knee
OA in athletes.

Bone densityIt has long been known that women with femoral neck
fractures seldom have OA of the hip. This negative assosiation between OA and
osteoporosis is reflected in studies which have demonstrated a significant increase
in bone mineral density in people with OA compared to those without. However,
this may not be simple cause and effect: bone density is determined by a variety
of genetic, hormonal and metabolic factors which may also influence cartilage
metabolism independently of any effect due to bone density.

Obesity The simple idea that obesity causes increased joint laoding and
therefore predisposes to OA may be correct, at least for OA of the knees.
However, the association is closer in women than in men and therefore (as with
bone density) it may reflect other endocrine or metabolic factors in the
pathogensis of OA.

Family history Women with generalized OA are likely to see the same
condition developing in their daughters. The particular trait which is responsible
for this is not known.

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Clinical features

Patients usually present after middle age. Joint involvement follows


several different patterns: symptoms centre either on one or two of the
wightbearing joints (hip or knee), on the interphalangeal joints (especially in
women) or on any joint that has suffered a previous affliction (e.g. congenital
dysplasia, osteonecrosis or intra-articular fracture). A family history is common
in patients with polyarticular OA.

Pain is the usual presenting symptom. It is often quite widespread, or it


may be referred to a distant site – for example, pain in the knee from OA of the
hip. It starts insidiously and increase slowly over months or years. It is aggravated
by exertion and relieved by rest, although with time relief is less and less
complete. In the late stage the patient may have pain in bed a night. There are
several possible causes of pain: capsular fibrosis, with pain on stretching the
shrunken capsule; muscular fatigue, and, perhaps most important of all, bone
pressure due to vascular congestion and intraosseous hypertension.

Stiffness is common; characteristically it occurs after periods of inactivity,


but with time it becomes constant and progressive.

Swelling may be intermittent (suggesting an effusion) or continuous (with


capsular thickening or large osteophytes).

Deformity may result from capsular contracture or joint disability; but


beware, it may have preceded and contributed to the onset of OA.

Loss of function, though not the most dramatic, is often the most
distressing symptom. A limp, difficulty in climbing stairs, restriction of walking
distance or progressive inability to perfirm everyday tasks or enjoy recreation may
eventually drive the patient to seek help.

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Typically, the symptoms of OA follow an intermittent course, with periods
of remission sometimes lasting for months.

Although the patient complains of only one or two joints, examination


may show that others are affected in varying degrees. Sweeling and deformity
may be obvious in peripheral joints; at the hip, deformity is usually masked by
postural adjustments of the pelvis and spine. In long-standing cases there is
muscle wasting. Tell-tale scars denote previous abnormalities. Local tenderness is
common, and in superficial joints fluid, synovial thickening or osteophytes may
be felt.

Movement is always restricted, but is often painless within the premitted


range; it may be accompanied by crepitus. Some movements are more curtailed
than others; thus, at the hip extension, abduction and intenal rotation are usually
the most severely limited.

In the late stages joint instability may occur for any of three reasons; loss
of cartilage and bone; asymmetrical capsular contracture; and muscle weakness.

Imaging

X-rays are so characteristic that other forms of imaging are seldom


necessary. The four cardinal signs are asymmetric loss of cartilago (narrowing of
the ‘joint space’), sceloris of the subchondral bone under the area of cartilage loss,
cyst close to the articular surface and osteophytes at the margins of the joint. In
addition there may be evidence of previous disorders (congenital defects, old
fractures, rheumatoid arthritis, chondrocalcinosis).

In the late stage, displacement if the joint is common and bone destruction
may be severe.

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99ar
Radionuclide scanning with Tc-HDP shows increased activity during
the bone phase in the subchondral regions of affected joints. This is due to
increased vascularity and new bone formation.

Typical radiographic by Kellgren& Lawrence 1957:

 Grade I : normal joint,minimal osteophyte


 Grade II : definite osteophyte on two places with
subchondral sclerosis, normal joint space, subchondral cyst
 Grade III : moderate osteophyte, deformity of bone margin,
narrowing of jointspace
 Grade IV : major osteophyte, narrowing of jointspace (+),
Cyst (+), Sclerosis ( + )

Arthroscopy

Arthroscopy may show cartilage damage long before x-ray change appear.
The problem is that it reveals too much, and the patient’s symptoms may be
ascribed to OA when they are, in fact, due to some other disorder.

Natural history

OA usually evolves as a slowly progressive disorder. However, symptoms


may wax and wane in intensity, sometimes disappearing for several months.

The x-rays show no such fluctuation. However, there is considerable


variation bertween cases in the relative degrees of destruction and repair. Most of
the men and half of the women gave hyoertropic reaction, with marked sclerosis
and large osteophytes. In about 20% of cases – most of them women – reactive
changes are more subdued, inviting descriptions such as atropic or osteopenic
OA. Occasionally OA takes the form of a rapidly progressive disorder.

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Complications

Capsular herniation OA of the knee is sometimes associated with a


marked effusion and herniation of the posterior capsule (Baker’s cyst).

Loose bodies Cartilage and bone fragments may give rise to loose bodies,
resulting in episodes of locking.

Rotator cuff dysfunction OA of the acromioclavicular joint may cause


rotator cuff impingement, tendinitis or cuff rupture.

Spinal stenosis Long-standing hypertrophic OA of the lumbar apophyseal


joints may give rise to acquired spinal stenosis. The abnormality is best
demonstrated by computed tomography (CT).

Spondylolisthesis In patient over 60 years if age, destructive OA of the


apophyseal joints may result in severe segmental instability and spondylolisthesis
(so called ‘degenerative’ spondylolisthesis, which almost always occours at L4/5).

Management

The management of OA depends on the joint (or joints) involved, the


stage of the disorder, the severity of the symptoms, the age of the patient and his
or her functional needs. Three observations should be borne in mind: (1)
symptoms characteristically wax and wane, and pain may subside spontaneously
for long periods; (2) some forms of OA actually become less painful with the
passage of time and the patient may need no more than reassurance and a
prescription for pain killers; (3) at the other extreme, the recognition (from serial
x-rays) that the patient has a rapidly progressive type of OA may warrant an early
move to reconstructive surgery before bone loss compromises the outcome of any
operation.

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EARLY TREATMENT

There is , as yet, no drug that can modify the effects of OA. Treatment is,
therefore, symptomatic. The principles are: (1) maintain movement and muscle
strength; (2) protect the joint from ‘overload’, (3) relieve pain; and (4) modify
daily activities.

Physiotherapy The mainstay of treatment in the early case is


physiotherapy, which should be directed at maintaining joint mobility and
improving muscle strength. The programme can include aerobic exercise, but care
should be taken to avoid activities which increase impact loading. Other
measures, such as massage and the application of warmth, may reduce pain but
improvement is short-lived and the treatment has to be repeated.

Lood reductionProtecting the joint from excessive load may slow down
the rate of cartillage loss. It is also effective in relieving pain. Common sense
measures such as weight reduction for obese patients, wearing shockabsorbing
shoes, avoiding activities like climbing stairs, and using a walking stick will pay
excellent dividends.

Analgesic medication Pain relief is important, but not all patients require
drug therapy and those who do may not need it all the time. If other measures do
not provide symptomatic improvement, patients may respond to a simple
anlagesic such as paracetamol. If this fails to control pain, a non-steroidal anti-
inflammatory preparation may be better.

23
INTERMEDIATE TREATMENT

Joint debridement (removal of interfering osteophytes, cartilage tags and


losse bodies) mau give some improvement. This technique, previously all but
abandoned, has gained acceptance again in the form of arthroscopic surgery for
OA of the knee.

Localized cartilage defects can be ‘grafted’ with autologous chondrocytes.


However, the use of cartilage transplants to obtain resurfacing of an osteoarthritic
joint is still in the realm of experimental surgery.

If symptoms and signs increase, then at some joints (chiefly the hip and
knee) realignment osteotomy should be considered. It must be done while the
joint is still stable and mobile and x-rays show that a major part of the articular
surface (the radiographic ‘joint space’) is preserved. Pain relief os often dramatic
and is ascribed to (1) vascular decompression of the subchondral bone, and (2)
redistribution of loading forces towards less damaged parts of the joint. After load
redistribution, fibrocartilage may grow to cover exposed bone.

24
LATE TREATMENT

Progressive joint destruction, with increasing pain, instability and


deformity (particularly of one of the weightbearing joints), usually requires
reconstructive surgery. Arthrodesis is indicated of the stiffness is acceptable and
neighbouring joints are not likely to be prejudiced. With arthroplasty, timing is
essential. Too early, and the odds against a durable result lengthen in proportion
to the demands of strenuous activity and time; too late, and bone destruction,
deformity, stiffness and muscle atrophy make the operation more difficult and the
result more unpredictable.

For OA of the hip and knee, total joint replacement has transformed the
lives of millions of patient. Similar operations for the shoulder, elbow and ankle
are less successful but techniques are improving year by year.

Operative Treatment

Non-TKA Surgical Options

When nonoperative treatment fails, less invasive surgicaloptions are


available before consideration of TKA. Mostsurgical options before TKA involve
the use of arthroscopyfor debridement of arthritic compartments of the knee
ormeniscectomy for meniscal tears. However, the treatmentof arthroscopic
debridement for primary OA is controversial.Approximately 50% to 75% of
patients will havesome type of relief after arthroscopic knee
debridement.However, 15% of these patients progress to TKA within 1year, and
only 44% have a statistically significant decreasein functional pain. Certain
factors have been identifiedin the literature that predict successful outcomes
witharthroscopic knee surgical procedures. These factorsinclude the presence of
mechanical symptoms such aslocking or catching of the knee that are associated
withunstable meniscal tear or unstable chondral flap.

25
In turn, some preoperative factors have been associatedwith a poorer
outcome after knee arthroscopy,including history of OA lasting longer than 24
months,obesity, medial tibial osteophytes, medial joint space lessthan 5 mm wide,
and smoking.30 A successful outcomeafter knee arthroscopy for primary OA
involves properpatient selection with the discussion of the limited goalsand
outcomes associated with the procedure. Otheroptions to consider before TKA
include unicompartmentalknee replacement and high tibial osteotomy.
Thesesurgical options are considered in patients who have unicompartmentalknee
arthritis or in patients who areyounger and active and who want to pursue other
optionsbefore TKA.

TKA

Orthopedic surgeons began performing TKA in the 1970s.Today it is a


commonly performed surgical procedurethat is beneficial to a majority of
recipients and is costeffective for quality of life assessments. It is indicated
fordisability, pain, limited function from osteoarthritis,rheumatoid arthritis, or any
type of arthritic deformityabout the knee. The goals of TKA include reducing
pain,returning to activities of daily living, restoring mechanicalalignment,
preserving the joint line, balancing the ligaments,and restoring a normal Q
angle.In 2008, 650,000 TKA procedures were performed inthe United
States.3More than 77,500 primary TKAs wereperformed in the United Kingdom
in 2009.30 The rates forTKA in the United States have risen from 31.2/100,000
person-years in the 1970s to more than 220/100,000 personyearsin 2008.Women
are more likely to undergo TKAsthan men with a ratio of 1.4/1, which was the
same ratio15 years ago. The main indication for TKA is OA, whichaccounts for
more than 94% to 97% of TKA operations.

End-stage degenerative knee joint disease, as evidencedby radiographs,


and persistent pain after all conservativetreatment measures have been exhausted
arethe key indications for total knee replacement (Figure 2).On the basis of our
experience, preoperative radiographicwork-up should include standing

26
anteroposterior radiographyof knees on large cassettes, standing extension
lateralradiography on large cassette, flexion lateral radiography,and a merchant
view. However, radiographicfindings alone are not enough. The patient history
isequally important.

The patient must have substantial knee pain limitinghis or her activities of
daily living, especially persistentpain occurring at night or with weight-bearing
activities.These symptoms must be refractory to conservative treatments.
Continued pain despite an attempt of a 6-monthcourse of nonoperative treatment
similar to that proposedby the Osteoarthritis Research Society International is
anindication for TKA. There is no standard regarding theseverity of symptoms in
the indication of TKA because thedecision to pursue TKA is partially subjective
on the basisof the patient’s response to nonoperative treatment.

Other factors such as age and weight need to be consideredprior to


proceeding with TKA. For instance, whilenot a contraindication, obesity or age
younger than 60years have resulted in more variable outcomes after TKA.Patients
must be medically capable of undergoing a surgicalprocedure and be able to
actively participate in therehabilitation process. Patients must be informed of all
the risks of, benefits of, and alternatives to surgery and provideinformed consent
for the procedure. Deciding whento proceed with TKA is a complex process for
both thephysician and the patient, a process that must take intoaccount factors
such as severity of symptoms, age, comorbidities,and socioeconomic variances.
Although physiciansmay offer the option of TKA when clinically indicated,the
ultimate decision to proceed with TKA is madewith the collaboration of surgeon
and patient.

A well-fixed, well-aligned TKA is considered successfulwhen performed


properly in the correct patients(Figure 3). The patient should have the correct
diagnosiswith substantial limitations in performing his or her
activities.Conservative treatments such as weight reduction,aerobic activity,

27
physical therapy, osteopathic manipulativetreatment, and analgesic and anti-
inflammatory medicationsshould be tried without relief before TKA.

28
CHAPTER III

PATIENT’S STATUS

I. IDENTITY

a. Name : Mrs. K

b. Age : 60 years old

c. Sex : Female

d. Job : Farmer

e. Address : Karangsari, Kendal

f. Room : Kenanga

g. Register Number : 449231

h. Date of in patient : October, 17th 2016

II. ANAMNESA

Chief complaint

Pain on the right knee.

Present status

The women came to the clinic orthopedic with complaints of pain and stiff

in the right knee since ± 4 months before entry hospital. Pain is felt like needles,

continuously and increasingly in ± 1 month before entry hospital, so that patients

complain of difficulties in the move and walk even in routine essential activities

(when she worked in the field). Complain about fever was denied. Patients

haven’t been treated for the disease in hospital or another clinic, so it was the first

time that she went to hospital.

29
Medical condition history

- History of trauma : denied

- History of asthma and allergies : denied

- History of heart disease : denied

- History of hypertension : denied

- History of diabetes : denied

Family history

- History of asthma and allergies : denied

- History of heart disease : denied

- History of hypertension : denied

- History of diabetes : denied

Socioeconomic status

The cost of treatment using BPJS Non-PBI

III. PHYSICAL EXAMINATION

GCS : 15

Vital sign

 BP : 130/90 mmHg

 HR : 82 x/m

 RR : 21 x/m

 to : 36,5 oC

Nutritional status

o Weight : 58 kg

30
o Height : 150 cm

58
o BMI : (1,5)2 = 25,78 kg/m2 (overweight)

Status Generalis

1. Skin : Turgor (N)

2. Head :Mesocephal, Wound (-)

3. Eyes : Anemis -/-, Icteric -/-

4. Ear : Discharge -/-

5. Nose : Deviation septum -/-, discharge -/-

6. Mouth : Bleeding (-)

7. Neck : Simetris, Trachea deviation (-)

8. Thorax : Normochest, simetris

COR

 Inspeksi : Ictus cordis (-)

 Palpasi : Ictus cordis palpable at SIC V, 2 cm medial to the

linea mid clavicularissinistra, pulsus sternal lift (-),

pulsusepigastric (-), pulsusparastrernal (-).

 Percussion : heart border

Bottom left: SIC V, 2 cm medial linea mid clavicularissinistra

Top left : SIC II lineasternalissinistra

Top right : SIC II lineasternalisdextra

Waist heart: SIC III lineaparasternalissinistra

Impression : configuration of the heart normal

31
 Auscultation : heart sound I-II regular, gallop (-), murmur (-)

Pulmo :

Anterior Posterior

I: Statis: normochest(+/+), simetris I: Statis: normochest(+/+), simetris

(+/+), retraction (-/-). Dinamis: (+/+), retraction (-/-).Dinamis: simetris

simetris Pa: statis: simetris (+), nothing

Pa: statis: simetris (+), nothing widening between the ribs, retraction (-

widening between the ribs, retraction /-), sterm fremitus dx=sin

(-/-), sterm fremitus dx=sin Pe: Sonor (+/+)

Pe: Sonor (+/+) Aus: vesicular (+/+), ronchi (-/-),

Aus: vesicular (+/+), ronchi (-/-), wheezing (-/-)

wheezing (-/-)

9. Abdomen

Inspection : normal, massa (-)

Palpation : Supel, pain (-), hepar and lien are not papble

Percussion : tympani (+)

Auscultation : bowel (+) Normal

10. Back : kifosis and lordosis (-)

11. Extremity:

Superior Inferior

Akral -/- -/-

Oedem -/- -/+

32
Capillary refill <2 “ <2”

Lession -/- -/-

Hematom -/- -/-

IV. LOCALIS STATUS

Right knee Left knee

Skin condition Eritema (-) Eritema (-)

Swelling (+) (-)

Quadriceps wasting (+) (-)

Local temperature Warm Normal

Tenderness (+) (-)

Crepitus (+) (-)

Fixed flexion deformity


(-) (-)
(FFD)

Hyperextension (-) (-)

Varus/Valgus deformity (-) (-)

Ligament laxity (-) (-)

Range of motion (ROM) Restricted Normal

True Length 82 cm 81 cm

Apperance Length 86 cm 85 cm

Anatomical Length 32 cm 32 cm

LLD ± 1 cm

33
Right knee

Look :swelling (+), deformity (-), eritema (-)

Feel :warm (+), pain (+), crepitus (+)

Auscultation :crepitus(+)

Move :

Active movement:

 Limitation (+) and pain (+) in flexion and extension of the knee.

 Clear (+) and pain (-) in plantar flexion and dorsoflexion of the

ankle joint.

 Clear (+) and pain (-) in inversion and eversion of the foot.

Passive Movement:

 Limitation (+) and pain (+) in flexion and extension of the knee.

 Clear (+) and pain (-) in plantar flexion and dorsoflexion of the

ankle joint.

 Clear (+) and pain (-) in inversion and eversion of the foot.

V. LABORATORY RESULT

October, 17th 2016

Hematology Result Reference value

Hemoglobin 13.8 gr/dL (L) 11.5 – 16.5

Leukosit 7.2 10^3/uL 4.0 – 10.0

Trombosit 278 10^3/uL 150 – 500

Hematokrit 41.9 % (L) 35.0 – 49.0

34
Reference
BLOOD CHEMISTRY Result
value

Glucose 109 (H) 75-115

Ureum 37 mg/dL 10 – 50

Creatinin 0.59 mg/dL (H) 0.50 – 1.10

VI. RADIOLOGY

Before:

X-Foto Rontgen Knee Dextra AP-Lat. (August, 24th 2016)

Major osteophytes (+)

Multiple scleroting (+)

Narrowing of jointspace (+)

After TKA:

X-Foto Rontgen Knee Dextra AP-Lat (October, 17th 2016)

35
VII. DIAGNOSE

Osteoarthritis of the Right Knee

VIII. INITIAL PLAN

a. IP Terapeutik

Medical treatment

- Infus Futrolit 20 tpm

- Inj. Cefazolin 2x1 g

- Inj. Dexketoprofen 3x50 mg

- Inj. Kalnex 2x500 mg (2 days)

- Inj. Ranitidine 3x50 mg

- Captopril tab 3x25 mg

b. IP. Operatif

Total Knee Arthroplasty Dextra

c. IP. Monitoring

36
General situation, Vital sign, drain, the result of supporting

examination, ROM exercise.

IX. PROGNOSIS

 Quo ad vitam : ad bonam

 Quo ad sanam : ad bonam

 Quo ad fungsionam : ad bonam

37
CHAPTER IV

DISCUSSION

Osteoarthritis refers to a clinical syndrome of joint pain accompanied by

varying degrees of functional limitation and reduced quality of life. It is the most

common form of arthritis, and one of the leading causes of pain and disability

worldwide. The most commonly affected peripheral joints are the knees, hips and

small hand joints. Pain, reduced function and effects on a person's ability to carry

out their day-to-day activities can be important consequences of osteoarthritis.

From the foregoing outline it should be apparent that the division of OA

into ‘primary’ (when there is no obvious antecedent factor) and ‘secondary’ (when

ir follows a demonstrable abnormality) is somewhat artificial. This is borne out in

clinical practice: patient with secondary OA of the knee following meniscectomy

have been found also to have a higher than usual incidence of ‘primary’ OA in

other joint. Perhaps primary, generalized factors (genetic, metabolic or endocrine)

alter the physical properties of cartilage and thereby determine who is likely to

develop OA, while secondary factors such as anatomical defects or trauma specify

when and where it will occur. OA is, ultimately, more process than disease,

occuring in any condition which causes a disparity between the mechanical stress

to which articular cartilage is exposed and the ability of the cartilage to withstand

that stress. These patients, based on history, the patient was a man aged 59 years

working as a farmer since 30 years ago so the patient a lot of activity using knee

joints, often run away and lifted yields. In addition, of the physical examination of

patients were overweight. This conditions is a risk factor for the occurrence of

38
secondary OA. So it can be concluded that the cause of OA in these patients is not

including the primary risk factor for OA.

The women came to the clinic orthopedic with complaints of pain and stiff

in the right knee since ± 4 months before entry hospital. Pain is felt like needles,

continuously and increasingly in ± 1 month before entry hospital, so that patients

complain of difficulties in the move and walk even in routine essential activities

(when she worked in the field). Fever (-). Patient have been treated for the disease

in internist and neurologist but no improvement. Such pain is usually found in

OA.

Patients also complained of stiff joints in the morning. This situation is

usually caused by an urge fluid is in arround inflamed tissue (joint capsule,

synovial, or exchange). Stiff joints especially in the morning or after the break.

Having moved about, the fluid will spread from network got inflamation so

people feel detached from the bonds and joints can move back in. Old stiff joints

in less than 30 minutes. It is appropriate to support the complaint OA.

Patients also experience swelling in both knees. swelling felt since 10

months. Swollen joints can be caused by herniated discs, synovitis, effusion and

osteophytes that may change due to the joint surfaces. In patients found

osteophytes on X-ray examination.

Physical examination localist on both knees obtained: the look is obtained

enlargement / swelling in the knee joint with no change in skin color. feel on both

knee joints obtained tenderness on palpation felt warm. Examination of motion

obtained flexion limitations that can only move the knee at 30. The resistance

39
movement is mainly caused by the presence of osteophytes remodeling,

thickening of the capsule and also effusion. On auscultation the knee joints of

patients found their voice crackles like krepitasi crushed. These symptoms may be

caused due to friction joint second irregular surfaces when the joint is moved or

passively manipulated.

Radiological examination in these patients got their picture in the form of

joint narrowing and osteophytes on the edges of the joint. On the other hand on

the bone will happen anyway subchondral bone changes and the formation of

marginal osteophytes, followed by changes in the molecular composition and

structure of the bone. Thinning of the joint cartilage as a result of a degenerative

process illustrates the narrowing gap joints are not symmetrical on plain

radiography radiology. Some subchondral can be observed on plain radiography

with formation of osteophytes, and subchondral sclerotic subchondral cyst

formation (OA grade IV).

The diagnosis of OA can already clinically established using criteria

Subcommitte OA made by the American College of Rheumatology (ACR). The

criteria for knee OA clinical, laboratory and radiological was their knee pain,

osteophytes, and one of the following signs, the age group over 50 years, stiff

joints less than 30 minutes or the presence of crepitus.

The management of patients with OA aims to eliminate complaints,

optimizing the function of motion, reduce dependency and improve quality of life.

The patient must have substantial knee pain limitinghis or her activities of

daily living, especially persistentpain occurring at night or with weight-bearing

40
activities.These symptoms must be refractory to conservative treatments.

Continued pain despite an attempt of a 6-monthcourse of nonoperative treatment

similar to that proposedby the Osteoarthritis Research Society International is

anindication for TKA. There is no standard regarding theseverity of symptoms in

the indication of TKA because thedecision to pursue TKA is partially subjective

on the basisof the patient’s response to nonoperative treatment.

Other factors such as age and weight need to be consideredprior to

proceeding with TKA. For instance, whilenot a contraindication, obesity or age

younger than 60years have resulted in more variable outcomes after TKA.Patients

must be medically capable of undergoing a surgicalprocedure and be able to

actively participate in therehabilitation process. Patients must be informed of all

the risks of, benefits of, and alternatives to surgery and provideinformed consent

for the procedure. Deciding whento proceed with TKA is a complex process for

both thephysician and the patient, a process that must take intoaccount factors

such as severity of symptoms, age, comorbidities,and socioeconomic variances.

Although physiciansmay offer the option of TKA when clinically indicated,the

ultimate decision to proceed with TKA is madewith the collaboration of surgeon

and patient.

41
BAB V

CONCLUSSION

Osteoarthritis (OA) of the knee, one of the mostcommon causes of


disability, continues to increasein prevalence as the older adult and obese
populationsgrow. Many other treatments are available for knee OA, including
education, bahavioural change, physical interventions and drugs. Evidence-based
evaluation and treatmentguidelines recommend the use of nonoperativetreatments
before surgical treatment options suchas total knee arthroplasty (TKA) are
considered.Understanding available nonoperative treatmentoptions is critical for
physicians who first encounterpatients with OA of the knee.

Pain is the usual presenting symptom. It is often quite widespread, or it


may be referred to a distant site – for example, pain in the knee from OA of the
hip. It starts insidiously and increase slowly over months or years. It is aggravated
by exertion and relieved by rest, although with time relief is less and less
complete. In the late stage the patient may have pain in bed a night. There are
several possible causes of pain: capsular fibrosis, with pain on stretching the
shrunken capsule; muscular fatigue, and, perhaps most important of all, bone
pressure due to vascular congestion and intraosseous hypertension.

End-stage degenerative knee joint disease, as evidencedby radiographs,


and persistent pain after all conservativetreatment measures have been exhausted
arethe key indications for total knee replacement.

The patient must have substantial knee pain limitinghis or her activities of
daily living, especially persistentpain occurring at night or with weight-bearing
activities.These symptoms must be refractory to conservative treatments.
Continued pain despite an attempt of a 6-monthcourse of nonoperative treatment
similar to that proposedby the Osteoarthritis Research Society International is
anindication for TKA.

42
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