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

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
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.
 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
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
 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.
 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.
 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
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
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
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.

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.

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.

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 very 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).

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
is particulary common 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
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.

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.

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.

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.

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.

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 reduction Protecting 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 shock absorbing
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.

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.

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 surgical options are

available before consideration of TKA. Most surgical options before TKA involve
the use of arthroscopy for debridement of arthritic compartments of the knee or
meniscectomy for meniscal tears. However, the treatment of arthroscopic
debridement for primary OA is controversial.Approximately 50% to 75% of
patients will have some 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 with
arthroscopic knee surgical procedures. These factors include the presence of
mechanical symptoms such as locking or catching of the knee that are associated
with unstable meniscal tear or unstable chondral flap.

In turn, some preoperative factors have been associated with a poorer

outcome after knee arthroscopy, including history of OA lasting longer than 24
months, obesity, medial tibial osteophytes, medial joint space less than 5 mm
wide. A successful outcome after knee arthroscopy for primary OA involves
proper patient selection with the discussion of the limited goals and outcomes
associated with the procedure. Other options to consider before TKA include
unicompartmental knee replacement and high tibial osteotomy. These surgical
options are considered in patients who have unicompartmental knee arthritis or in
patients who are younger and active and who want to pursue other options before
TKA.

TKA

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

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

End-stage degenerative knee joint disease, as evidenced by radiographs,

and persistent pain after all conservative treatment measures have been exhausted
are the key indications for total knee replacement (Figure 2).On the basis of our
experience, preoperative radiographic work-up should include standing
anteroposterior radiography of knees on large cassettes, standing extension lateral
radiography on large cassette, flexion lateral radiography, and a merchant view.
However, radiographic findings alone are not enough. The patient history is
equally important.

The patient must have substantial knee pain limiting his or her activities of
daily living, especially persistent pain 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 non operative treatment
similar to that proposed by the Osteoarthritis Research Society International is an
indication for TKA. There is no standard regarding the severity of symptoms in
the indication of TKA because the decision to pursue TKA is partially subjective
on the basis of the patient’s response to non operative treatment.

Other factors such as age and weight need to be considered prior to

proceeding with TKA. For instance, while not a contraindication, obesity or age
younger than 60years have resulted in more variable outcomes after TKA.
Patients must be medically capable of undergoing a surgical procedure and be able
to actively participate in the rehabilitation process. Patients must be informed of
all the risks of, benefits of, and alternatives to surgery and provide informed
consent for the procedure. Deciding when to proceed with TKA is a complex
process for both the physician and the patient, a process that must take into
account factors such as severity of symptoms, age, comorbidities, and
socioeconomic variances. Although physicians may offer the option of TKA when
clinically indicated, the ultimate decision to proceed with TKA is made with the
collaboration of surgeon and patient.

A well-fixed, well-aligned TKA is considered successful when performed

properly in the correct patients(Figure 3). The patient should have the correct
diagnosis with substantial limitations in performing his or her activities.
Conservative treatments such as weight reduction, aerobic activity, physical
therapy, osteopathic manipulative treatment, and analgesic and anti-inflammatory
medications should be tried without relief before TKA.
 CHAPTER III

PATIENT’S STATUS

I. IDENTITY
 Name : Mr. S
 Age : 67 years old
 Sex : MALE
 Address : Pegandon, Kendal
 Room : Anggrek
 Register Number : 499491
 Date of entry : 17/07/2018
II. ANAMNESA
Chief complaint
Pain on the right knee.
Present status
A man came to the orthopedic clinic complaining of pain and stiff

in the right knee since ± 1 years 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. Patient also felt stiffness every morning on the

right knee. Patient never got same illness like this before. The same illness

on his family has been denied. This patient covered by BPJS.

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
· HR : 97 x/m
· RR : 23 x/m
· to : 36,7o
· BP : 190/110

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
 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 -/- -/-

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

Right knee
Look :swelling (-), deformity (-), eritema (-)
Feel :warm (+), pain (+), 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
July 17 2018

Hematology Result Reference value

Hemoglobin 14.7 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 44.9 % (L) 35.0 – 49.0

PT 12,5 detik 11,3 – 14,7

APTT 31,0 detik 27,4 – 39,3

VI. RADIOLOGY
Before:
 Major osteophytes (+)
Narrowing of jointspace (+)

After TKA:

VII. DIAGNOSE
 Osteoarthritis of the Right Knee
VIII. INITIAL PLAN
a. IP Terapeutik
Medical treatment
• Inf. RL 20 tpm
• Inf. Cefazolin 2x1 gr
• Inj. Dexketoprofen 2x50mg
• Inj, Ranitidine 3x50mg
• Amlodipin 10mg 0-0-1
• Irbesartan 300mg 1-0-0
• Levfloxacin 1x500 (post op)
• Dex ketoprofen tab 2x25mg(post op)

b. IP. Operatif
Total Knee Arthroplasty Dextra
c. IP. Monitoring
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
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