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ON OA KNEE JOINT
Diajukan untuk memenuhi tugas dan melengkapi salah satu syarat dalam
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.
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.
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.
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.
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.
2. OSTEOARTHRITIS
Etiology
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.
Pathology
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.
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 capsule and synovium are often thickened but cellular activity is
slight; however, sometimes there is marked inflammation or fibrosis of the
capsular tissues.
Prevalence
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.
Risk Factors
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
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.
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
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.
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
Complications
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.
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.
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
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
TKA
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.
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
routine essential activities. Patient also felt stiffness every morning on the
right knee. Patient never got same illness like this before. The same illness
Family history
History of asthma and allergies : denied
History of heart disease : denied
History of hypertension : denied
History of diabetes : denied
Socioeconomic status
Status Generalis
Anterior Posterior
I: Statis: normochest(+/+), simetris I: Statis: normochest(+/+), simetris (+/
Pa: statis: simetris (+), nothing widening between the ribs, retraction
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 -/- -/-
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
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
IX. PROGNOSIS
Quo ad vitam : ad bonam
Quo ad sanam : ad bonam
Quo ad fungsionam : ad bonam
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Fred Flandry, MD, FACS, Gabriel Hommel, MD. Review Article: Normal
Anatomy and Biomechanics of the Knee. Sports Med Arthrosc Rev 2011;19:82-92.
2011.
Hochberg, March C. et all. American College Of Rheumatology 2012
Recommendations For The Use OfKim RH, Springer BD, Douglas DA. Knee
reconstruction and replacement. In: Flynn F, ed. Orthopaedic Knowledge Update.
Rosemont, IL: American Academy of Orthopaedic Surgeons; 2011:469-475.
NonpharmacologicAnd Pharmacologic Therapies In Osteoarthritis Of The Hand,
Hip, And Knee. Arthritis Care & Research Vol. 64, No. 4, April 2012, pp 465-474