DEFINITION:  Other names includes: Degenerative joint disease (DJD), Hypertrophic arthritis, Degenerative disc disease (DDD in the

spine), Generalized osteoarthritis or Kellgren’s syndrome.  Marked by two localized, pathological features, the progressive destruction of articular cartilage and the formation of bone at the margins of the joint (Sullivan)  Most common type of arthritis is an asymmetrical non-inflammatory disease that has no systemic component. (De Lisa)  In OA, there are differences in the water content ratio of certain cartilage constituent. And an increase in degradative enzyme activity compared with in non – osteoarthritis joint. (Braddom)  Most common form of arthritis, is a primarily a disease of cartilage, not of the synovium. In the upper limb, it most commonly involves the CMC joint of the thumb. A thumb spica hand – based or forearm – based splint can be prescribed for CMC joint OA by limiting motion at the base of the thumb, the splint decrease pain, especially with pinching – type activity. (Braddom)  Characterized by degenerative changes in articular cartilage and bony overgrowth at the joint margin (Shunts)
 It is a group of diseases and mechanical abnormalities entailing degradation of

joints, including articular cartilage and the subchondral bone next to it.
 Osteoarthritis is a type of arthritis that is caused by the breakdown and eventual

loss of the cartilage of one or more joints. Classification of Osteoarthritis OA is often graded on radiographs according to the criteria of Kellgren and Lawrence using an ordinal scale of five levels: Grade 0 – normal radiograph Grade 1 – doubtful narrowing of the joint space and possible osteophytes Grade 2 – definite osteophytes and absent or questionable narrowing of the joint space Grade 3 – moderate osteophytes and joint space narrowing, some sclerosis and possible deformity

Grade 4 – large osteophytes, marked narrowing of joint space, severe sclerosis and definite deformity.

General Criteria of OA 1. Pain on motion relieve by rest. 2. Aching pain and stiffness in joint after prolonged rest especially in early morning hour relieve in less than 30 minutes with mild exercise. 3. Restraining of cartilage or loss of joint space seen X- ray examination. 4. Increase density of subchondral bone. 5. There is reactive bone overgrowth at margin of joint. Clinical classification criteria for knee and hip osteoarthritis Knee osteoarthritis 1. Knee pain 2. Joint stiffness < 30 minutes 3. Crepitus 4. Bony enlargement 5. Bony tenderness 6. No palpable warmth Hip osteoarthritis
1. Hip internal rotation > 15 degrees with pain, morning stiffness < 60 minutes, and

age > 50 years old, or 2. Hip internal rotation < 15 degrees and hip flexion < 155 degrees Two main types of arthritis I. Inflammatory arthritis fall into four groups: 1. Inflammatory connective tissue disease (RA, JRA, SLE, DM-PM, mixed connective tissue disease) 2. Inflammatory crystal induced disease (Gout , pseudogout)

3. Inflammation induced by infectious agent (Bacterial, viral, tuberculosis & fungal arthritis) 4. Seronegative spondyloarthropathies (AS, Psoriatic Arthritis[PSA],Reiter’s disease, Inflammatory bowel disease[BD]) II. Non – inflammatory arthritis
1. Degenerative (OA, Postraumatizing aseptic necrosis[AN])

2. Metabolic (Lipid storage disease, Hemochromatosis, Hypogammaglobulinemia, Hemoglobinopathies) RELATED ANATOMY:

Ochronosis,

JOINT Also called an articulation or arthrosis, is a point of contact between two bones, between the bone and cartilage. The structural classification of joints is based on two criteria. 1. Presence or absence of a space between the articulating bones, called synovial cavity. 2. Type of connective tissue that binds the bones together. Structurally
 Fibrous joints- bones re held together by fibrous connective tissue that is rich in

collagen fibers; they lack a synovial cavity.
 Cartilaginous joints- bones are held together by cartilage; they lack a synovial

cavity. The articulating bones are tightly connected by either Hyaline Cartilage (reduce friction, shock absorber).
 Synovial joints- bones forming the joint have a synovial cavity and are united by

the dense irregular connective tissue of an articular capsule, and often by accessory ligaments. Functionally
 Synarthrosis- immovable joint  Amphiarthrosis- slightly movable joint  Diarthrosis- a freely movable joint

Synovial Cavity - this allows a joint to be freely movable.

Synovial fluid -reduce friction by lubricating the joint and supplying nutrients to and removing metabolic wastes from the chondrocytes within the articular cartilage. Joint capsule - a tough membrane sac that encloses all the bones and other joint parts. Synovium - a thin membrane inside the joint capsule that secretes synovial fluid. Cartilage- covers the articulating surface of the bones with a smooth, slippery surface but does not bind them together. Subchondral bone - layer of bone in which is just below the cartilage. Osteophytes-typically develop as a reparative response by the remaining cartilage.

Back Anatomy The Spinal Column: The spinal column (also called the vertebral column) contains and protects the spinal cord and supports the body and head. The spinal column is flexible to allow movement of the body. The spinal column is comprised of a column of small bones called vertebrae. Shock absorbing discs separate the vertebrae. Vertebrae: The 24 vertebrae are named according to their location along the spine. We start out with 33 vertebrae but the lowest nine fuses together to form single bones- 5 fused vertebrae form the sacrum and 4 tiny fused vertebrae form the coccyx (tailbone).

 Articular processes meet and interlock at the facet joints to link one vertebra with the next.The 24 True or Movable Vertebrae:  Cervical spine (neck area) with 7 vertebrae (labeled C1 .  Transverse processes .projecting from the center of the vertebral arch. . Each vertebra arch has four (two superior and two inferior) articular processes. Main Parts of a Vertebra: The two main parts of the vertebra are the vertebral body and the vertebral arch.projecting from either side of the vertebral arch and serve as attachments for the muscles and ligaments.  Vertebral Arch: The posterior part of a vertebra. basically cylindrical in shape. Processes (bony projections) of the Vertebral Arch:  Spinous process . the vertebral arch has several processes (bony projections).C7)  Thoracic spine (chest area) with 12 vertebrae (labeled T1 . and serve as attachments for the muscles and ligaments.L5) Fused Vertebrae (Below the lumbar spine):  Sacrum: a triangular shaped solid base with 5 fused vertebrae .  Vertebral Body: The anterior segment and largest part of a vertebra.T12)  Lumbar spine (lower back) with 5 vertebrae (labeled L1 .connects with the pelvis  Coccyx: (the tailbone) with 4 very small fused vertebrae.

the spinal cord transmits messages from the brain to other parts of the body and vice versa. . Spinal Cord: A part of the central nervous system. The surfaces of the bones that make up the facet joints are coated with smooth cartilage that allows the bones to glide smoothly against each other. and dura mater. Discs: The vertebral bodies are separated by shock absorbing intervertebral discs. Theses discs have a tough outer coating with and contain a jelly-like substance.The spinal cord begins at the brain and runs down to the level of the second lumbar vertebrae.Intervertebral Foramen (plural: intervertebral foramina): The opening formed between adjacent vertebrae from which the spinal nerves exit. arachnoid. The dura mater is the outermost and toughest of the three meninges. There is an opening on each side. Muscles. Facet joints are hinge-like and allow adjacent vertebrae to move on one another to allow bending and twisting and also keep the spine within a normal range of motion. Three meninges (membranes) cover the spinal cord.the pia mater. Facet Joints: Facet joints (commonly called spinal joints) join adjacent vertebrae. Spinal nerves branch out form the spinal cord. ligaments and discs support the joints of the spine. Meninges: The three membranes enclosing the spinal cord and brain .

The wrist itself contains eight small bones. Muscles protect the spine by absorbing shock before it reaches the discs and facet joints. Muscles of the back. forming the wrist joint. Ligaments: Ligaments are tough bands of connective tissue that connect the vertebrae. Further into the palm. . Small bone shafts called phalanges line up to form each finger and thumb. the radius and ulna.Spinal Canal: Spinal Canal (also called vertebral canal) is the large canal in the center of the spinal column that contains the spinal cord and its membranes. called carpals. Hand Anatomy Bones and Joints There are 27 bones within the wrist and hand. Muscles: Muscles support the spine and allow movement. The carpals join with the two forearm bones. abdomen and buttocks stabilize the spine and maintain proper posture. One metacarpal connects to each finger and thumb. There are five metacarpals forming the palm of the hand. Facet joints and ligaments help protect the spine by limiting how far the spine can bend or twist. the carpals connect to the metacarpals.

This white. The thumb only has one IP joint between the two thumb phalanges. The three phalanges in each finger are separated by two joints. The joint near the end of the finger is called the distal IP joint (DIP joint). shiny material has a rubbery consistency. Ligaments and Tendons Ligaments are tough bands of tissue that connect bones together. called interphalangeal joints (IP joints).The main knuckle joints are formed by the connections of the phalanges to the metacarpals. and thumb are covered on the ends with articular cartilage. called collateral ligaments. Two important structures. There is articular cartilage essentially everywhere that two bony surfaces move against one another. The ligament tightens as the joint is . are found on either side of each finger and thumb joint. The one closest to the MCP joint (knuckle) is called the proximal IP joint (PIP joint). This ligament connects the proximal phalanx to the middle phalanx on the palm side of the joint. In the PIP joint (the middle joint between the main knuckle and the DIP joint). The function of articular cartilage is to absorb shock and provide an extremely smooth surface to facilitate motion. the strongest ligament is the volar plate. The MCP joints work like a hinge when you bend and straighten your fingers and thumb. fingers. The IP joints of the digits also work like hinges when you bend and straighten your fingers and thumb. or articulate. The function of the collateral ligaments is to prevent abnormal sideways bending of each joint. These joints are called the metacarpophalangeal joints (MCP joints). The joints of the hand.

. while the femoral neck is directed superiorly. and the ischial tuberosity ("sitting bone")  Proximally the femur is largely covered by muscles and. laterally and anteriorly. The tendons that allow each finger joint to straighten are called the extensor tendons. and ischium. pubis. It is a special type of spheroidal or ball and socket joint where the roughly spherical femoral head is largely contained within the acetabulum and has an average radius of curvature of 2. The hip joint is a synovial joint formed by the articulation of the rounded head of the femur and the cup-like acetabulum of the pelvis.] The head of the femur is attached to the shaft by a thin neck region The acetabulum is oriented inferiorly. It forms the primary connection between the bones of the lower limb and the axial skeleton of the trunk and pelvis.straightened and keeps the PIP joint from bending back too far (hyperextending). Finger deformities can occur when the volar plate loosens from disease or injury. the anterior superior (ASIS) and posterior superior iliac spines (PSIS). as can happen with a tear. as a consequence. where they eventually connect to the extensor tendons before crossing over the back of the wrist joint. Problems occur when the central slip is damaged. which extends the joint beyond the equator. a grip augmented by a ring-shaped fibrocartilaginous lip. the extensor tendons become the extensor hood.  Prominent palpable bony structures of the hip bone include the iliac crest. The cuplike acetabulum forms at the union of three pelvic bones — the ilium. Hip Anatomy The bones of the hip region are the hip bone and the femur (or thigh bone). Both joint surfaces are covered with a strong but lubricated layer called articular hyaline cartilage. When the extensor muscles contract. medially. The place where the extensor tendon attaches to the middle phalanx is called the central slip. As they travel into the fingers. they tug on the extensor tendon and straighten the finger. the acetabular labrum. and anteriorly. the posterior inferior iliac spine (PIIS).5 cm. The extensor hood flattens out to cover the top of the finger and sends out branches on each side that connect to the bones in the middle and end of the finger. The extensor tendons of the fingers begin as muscles that arise from the backside of the forearm bones. the greater trochanter is often the only palpable bony structure. the five or so tubercles and the lower lateral borders of the sacrum. These muscles travel towards the hand. The acetabulum grasps almost half the femoral ball.

The patella or what we call the knee cap. attaches by ligaments and a capsule to your tibia. and ischium respectively). flex and extend. Just below and next to the tibia is the fibula. The knee muscles which go across the knee joint are the quadriceps and the hamstrings. When the knee moves. The ligaments are equally important in the knee joint because they hold the joint together. which runs parallel to the tibia. or.Extends posteriorly and laterally from a point anterior to the intercondylar area of the tibia to the posterior part of the medial surface of the lateral condyle of the femur. Posterior Cruciate Ligament-Extends anteriorly and medially from a depression from the posterior intercondylar area of the tibia and lateral meniscus to the anterior part of the . The intracapsular ligament. The femur. This limits hyperextension of the knee and prevents the anterior sliding of the tibia in the femur. The bones support the knee and provide the rigid structure of the joint. rides on the knee joint as the knee bends. the ligamentum teres. the muscles move the joint. There is also a slight rotational component in this motion. pubis. All three strengthen the capsule and prevent an excessive range of movement in the joint. and pubofemoral ligaments attached to the bones of the pelvis (the ilium. and the ligaments stabilize the joint. as it is medically termed.The extracapsular ligaments are the iliofemoral. it does not just bend and straighten. ischiofemoral. is attached to a depression in the acetabulum (the acetabular notch) and a depression on the femoral head (the fovea of the head) Knee Anatomy The knee is essentially made up of four bones. which is the large bone in your thigh. Anterior Cruciate Ligament.

The talus is connected to the calcaneus at the subtalar joint. The subtalar joint allows the foot to rock from side to side. There are multiple joints between the tarsal bones. Just down the foot from the ankle is a set of five bones called tarsal bones that work together as a group. the large tibia and the smaller fibula.Prevents posteriorsliding of the tibia when the knee is flexed. When the foot is twisted in one direction by . These bones are unique in the way they fit together. A bursa is a little fluid sac that helps the muscles and tendons slide freely as the knee moves. that forms part of the ankle joint. The two bones that make up the back part of the foot (sometimes referred to as the hindfoot) are the talus and the calcaneus. or heelbone. or ankle bone. It helps to protect the joint and allows the bones to slide freely on each other. come together at the ankle joint to form a very stable structure known as a mortise and tenon joint. Feet Anatomy Bones and Joints The skeleton of the foot begins with the talus. The ankle joint allows the foot to bend up and down. There is also a bursa around the knee joint. The knee joint also has a structure made of cartilage.lateral surface of the medial condyle of femur. The arrangement is very stable. The mortise and tenon structure is well known to carpenters and craftsmen who use this joint in the construction of everything from furniture to large buildings. The two bones of the lower leg. The meniscus is a C-shaped piece of tissue which fits into the joint between the tibia and the femur. which is called the meniscus or meniscal cartilage.

The collagen fibers are bundled together to form a rope-like structure. without much movement at the joints. are made up of many smaller fibers. the phalanges. and movement in these joints is very important for a normal walking pattern. Not much motion occurs at the joints between the bones of the toes. This tendon helps support the arch and allows us to turn the foot inward. Both of these structures are made up of small fibers of a material called collagen. It attaches the calf muscles to the heel bone to allow us to raise up on our toes. Ligaments and Tendons Ligaments are the soft tissues that attach bones to bones. is the most important toe for walking. Finally. Ligaments are very similar to tendons. These joints form the ball of the foot. When they are twisted in the opposite direction. and jumping. The thicker the ligament (or tendon) the stronger the ligament (or tendon) is. The two groups of bones are fairly rigidly connected. The large Achilles tendon is the most important tendon for walking. The toes have tendons attached that bend the toes down (on the bottom of the toes) and straighten the toes (on the top of the toes). running. The joint between the metatarsals and the first phalanx is called the metatarsophalangeal joint (MTP). or hallux. The big toe. The anterior tibial tendon allows . The posterior tibial tendon attaches one of the smaller muscles of the calf to the underside of the foot. and the first MTP joint is a common area for problems in the foot.the muscles of the foot and leg. they become unlocked and allow the foot to conform to whatever surface the foot is contacting. The difference is that tendons attach muscles to bones. these bones lock together and form a very rigid structure. there are the bones of the toes. The tarsal bones are connected to the five long bones of the foot called the metatarsals. and like rope. Ligaments and tendons come in many different sizes.

changes in the synthesis of proteoglycan or its degradation. By 75 to 79 years of age all had evidence of OA. impairment and job loss among adults and limits everyday activities ETIOLOGY: Cartilage degeneration is the hallmark of the disease. makes arthritis the leading cause of disability.  Its prevalence increase with age 7% of men and 8% of women 18 – 24 years of age showed evidence of OA. Most of these ligaments form part of the joint capsule around each of the joints of the foot. 65 -74 years of age men more often have hip involvement than women. Two tendons run behind the outer bump of the ankle (called the lateral malleolus) and help turn the foot outward. CMC and MTP. but the possibilities include collagen framework damage secondary to fatigue or abrasion.us to raise the foot. A joint capsule is a watertight sac that forms around all joints. Many small ligaments hold the bones of the foot together.  Women experience greater severity of symptoms and report more problems with morning stiffness. Degenerative changes in articular cartilage are more common and more severe with advancing age.  Women more commonly have OA of the DIP.  The pervasiveness of osteoarthritis. and defects in synovial fluid and chondrocyte function. joint swelling and night pain. PIP. as well as its conditions. Knee involvement is seen in two genders from 55-64 years of age. The fact that osteoarthritic changes are . EPIDEMIOLOGY:  Most common form of arthritis  Extremely common condition after 40 years of age  It is estimated that 80% of the population will have radiographic evidence of OA by age 65  Widespread in adults older than 65 years old  Men > women before the age of 45 but reverses after age 45. The cause of the degeneration is unknown. in the weight bearing joints and in joints that have become incongruent or have been used abnormally. It is made up of the ligaments around the joint and the soft tissues between the ligaments that fill in the gaps and form the sac.

there is a greater succeptibility than in those who have no family history of arthritis. congenital subluxation of the hips and a host of others. These changes in cartilage and bone result in increase friction. however. In later stages of disease progression. proteoglycans are lost. which may consist of a single major trauma or repeated minor traumas. Mechanical injury. the kind found in skin and fibrous tissues. articular cartilage loses its compressive stiffness and elasticity. and the . Additionally there are changes in the composition of newly synthesized proteoglycan. although the mechanism by w/c this occurs is unknown. which in turn result in the transformation of compressive forces to underlying bone.  Primary osteoarthritis – used to designate cases in which no underlying cause for the joint disease is clearly apparent. The cartilage may degenerate to the point that subcondral bone is expose. current hypothesis have implicated increase vascularity in degenerated cartilage venous congestion from subchondral cyst and thickened subchondral trabeculae. malalignment as a result of fractures. It may be localized (confined to one or two joints) or generalized (present in three or more joints). Collagen synthesis is increased initially.often localized to only part of a single joint suggests that there are causative factors other than age and attrition. The traditional view of OA is that the disease process starts with an unpaired injury to articular cartilage.  Secondary osteoarthritis – in which an antecedent disease or injury is believed to be related to the arthritis. w/c has been confirmed in humans is an increase in water content. The process of osteophyte formation in OA is not well unerdstood. may cause intra-articular changes that act as a predisposing or aggravating cause. repeated trauma. although there is a shift from type II collagen fibers to a larger proportion of type I collagen. including burnt-out rheumatoid arthritis. Thus there may be genetically determined chemical differences in the cartilage of some individuals that predispose it to early degeneration. One of the first noticeable changes in cartilage is the mild “fraying” or “flaking” of superficial collagen fibers. It is frequently seen in the younger age range. Changes in cartilage proteoglycans will also negatively affect the ability of the cartilage to form a squeeze film over its surface during joint loading. As the articular cartilage is destroyed the joint space narrows. This increase suggests that the proteoglycan have been allowed to swell with water far beyond normal. Deeper fraying or fibrillation of the upper third of the cartilage follows and occurs in areas of greater weight bearing. may result from any condition that disturbs normal joint function. Subchondral bone in turn can then become sclerotic and stiffer than normal bone. decrease shock absorption and greater impact loading of the joint. there is also evidence that reduced compliance in bone and periarticular structure may initiate the degenerative process. In people over 45 years of age whose parents have suffered from arthritis late in life. PATHOPHYSIOLOGY: The first osteoarthritic change in articular cartilage.

In later stages the vertebral bodies becomes flattened and much new bone develops about their margin. Spur formation may occur about the articular facets. they may be represent a related but distinct degenerative process. this true of heavy individuals. Clinical features   Morning stiffness Radiating pain around toward the chest or abdomen or down the legs or arm. person over 40y/o Observed in lumbar and cervical levels Constant use of back are probably an important causative factor Pathology Pathological changes are take place in the spinal diarthrodial (apophyseal) and in the intervertebral joints. OSTEOARTHRITIS OF THE SPINE      Extremely common Seen often in stocky and obese Male > female. changes often termed spondylosis or spondylophytosis. . Ultimately there are frequently develops so much disk space narrowing and osteophyte formation that is stiffened but very stable and relatively painless articulation result. Thinning of the intervertebral disk and spur formation at the anterolateral margin of the of the vertebral bodies result from disk degeneration and reactive bone formation. Roentgenograms are present to some degree in a high percentage of old people who have never had significant backpain. Each of these hypotheses may explain how this bony growth contributes to the pain and loss of motion that accompany by OA.continued sloughing of articular cartilage. usually accompany OA of the facet joints. producing so called bridging and leaf formation.

Pain in the knee with OA may be due to:  Loss of cartilage  Mechanical compression of the medial knee compartment . Treatment      Rest and restriction of activity. Salicylates for relieving discomfort.   Attacks tend to occur less frequently when the spine becomes more stable.Radiating pain is particularly common in the lumboscaral joints and of the intervertebral foramina of the cervical spine  Deformity of the lumbar spine (lateral curvature and decrease normal lordosis may develop). Hot packs and the use of massage. bilateral or tricompartmental. Knee problems may be unilateral. Thomas collar may be very effective in the management of neck pain Surgical treatment when there are sign of nerve root or spinal cord compression by osteophytes. OSTEOARTHRITIS OF THE HANDS OSTEORTHRITIS OF THE KNEE Of the major joints the knee is the most frequently affected by OA.

often following a twisting injury or stressful use of the joint. is also characteristic of hip osteoarthritis. Arthroplasty. OSTEOARTHRITIS OF THE HIP Hip osteoarthritis is caused by deterioration of articular cartilage and wear-andtear of the hip joint. usually restriction of the last few degrees of flexion and extension. Arthrodesis for a younger. rest. and mild to moderate joint effusion. weight reduction in obese patients. Microfractures and subchondral fractures  Capsular distention by effusion Physical findings include slight limitation of the joint motion. Pain and swelling o the knee lead to restricted ROM and contractures of the joint capsule and hamstrings. Osteotomy can correct the deformity and shift the weight bearing load to the less involved side of the jt. but the durabiity of total knee arthroplasty in an active patient is yet to be established. Acute pain and swelling. Total joint replacement the treatment of choice in severe bilateral osteoarthritis of the knee. and an elastic knee support. there is . The treatment of early osteoarthritis of the knee consists of strengthening exercises for the quadriceps and hamstring muscles. active person with severe degenerative changes limited to one knee. A varus or valgus deformity may be associated with some mediolateral instability. Crutches may be needed until acute symptoms subside. Most significantly. by total joint replacement may result in a painless joint with satisfactory motion. are treated by hot compress. which changes hip alignment genetics congenital and developmental hip disease subchondral bone that is too soft or too hard avascular necrosis Patients who have hip osteoarthritis have pain localized to the groin area and the front or side of the thigh. There are several reasons this can develop:       previous hip injury previous fracture. though for less duration than occurs with rheumatoid arthritis. Morning stiffness.

Evidence from X-rays. CT scans. Symptoms of Foot Osteoarthritis .an arthroscope checks the condition of the articular cartilage osteotomy . Surgical procedures include:    arthroscopy . Medications are one way to treat hip osteoarthritis. bone spurs or other deformities.new acetabular and femoral components are implanted OSTEOARTHRITIS OF THE FEET Diagnosis of Foot Osteoarthritis Doctors will perform a physical examination. The symptoms can worsen to the point that pain is constantly present. Imaging studies of the bone structure of the affected foot will likely be performed.limited range of motion of the hip and pain during motion. joint protection) patient education Surgery is considered a last resort treatment option. acetaminophen is usually tried first. Foot will be examined for swelling. A gait analysis may be performed to evaluate stride while walking and the strength of the feet. limited range of motion. For mild cases.realigns angles of the hip joint total hip replacement . overweight have 25% risk. and obese have 39% risk) water exercise programs physical therapy (range of motion and strengthening exercises) occupational therapy (assistive devices. or MRI may be used to help diagnose foot osteoarthritis. There are also non-drug treatments that can help:      weight loss (normal weight people have a 20% risk of hip OA. Surgery is appropriate for patients with hip osteoarthritis who have failed other more conservative treatment options. NSAIDs (non-steroidal anti-inflammatory) and opioid analgesics are used for moderate to severe hip osteoarthritis. and pain which occurs with movement.

The usual symptoms associated with foot osteoarthritis include: • • • • pain and stiffness of the affected foot swelling near the affected joint limited range of motion and difficulty walking bony protrusions (spurs) There are 28 bones and more than 30 joints in the human foot. Depending on the joint involved. arthrodesis (fusion). calcaneocuboid joint) the midfoot (metatarsounieform joint) the great toe (first metatarsophalangeal joint) Treatment of Foot Osteoarthritis Treatment options for foot osteoarthritis are aimed at relieving symptoms. The foot joints that are most commonly affected by osteoarthritis include: • • • • the ankle (tibioltalar joint) the 3 joints of the hindfoot (talocalcaneal joint. or arthroplasty (joint replacement) may be considered. arthroscopy. Your doctor will likely recommend one or more nonsurgical options first. There are non-surgical and surgical options. Non-surgical options include: Non steroidal anti-inflammatory drugs or analgesics (to relieve pain and swelling) Shoe inserts (to add support or provide extra cushioning) Orthotics (custom-made shoes or suppports) Braces (to restrict motion or prevent more deformity)  Physical therapy or exercise (to improve range of motion and stability)  Steroid injections (to deliver anti-inflammatory medication to the joint directly)  Dietary supplements     If non-surgical options are ineffective. talonavicular joint. CLINICAL MANIFESTATIONS: . The goal of foot surgery is to relieve pain and restore function. your doctor may suggest surgery.

bony enlargement of the DIP joints (Heberden’s nodes) is one of the commonest sign. . associated with an aching pain in or about the affected joint  The involvement is more often monoarticular than polyarticular  Continued use of the joint increases discomfort which may be relieved by rest. wet weather  There is slight enlargement of the affected joints which may be slightly tender about margins (such changes are usually most noticeable in the fingers and knees)  In the hands. especially in the larger weightbearing joints  Pain may then be present even when the joint is at rest.Common Areas of Affection of Osteoarthritis Early Stage of Osteoarthritis  Usual complains of stiffness of one or more joints.  The patient tires easily on exertion  The symptoms are worse in cold. support and heat.  Less frequent is similar enlargement of the PIP joints (Bouchard’s nodes) Late Stage of Osteoarthritis  There is limitation of joint motion and disability.

unlike their usual course in rheumatoid arthritis. Aspiration of the joint may yield pus and a positive culture confirms the diagnosis. Culture of the joint exudates or biopsy of the synovial membrane may be necessary to establish the diagnosis. It may be possible to demonstrate urate crystals in the joint aspirate by means of polarized light microscopy. Serologic tests may aid in the differentiation. especially in the absence of an increase of the non-protein or urea nitrogen. The patient with acute rheumatic fever is more likely to have had a streptococcic throat infection and to have electrocardiographic changes and a high fever. it may be confused with rheumatoid arthritis. Malalignment of the joint is a frequent result of the irregular degeneration and loss of articular cartilage  Crepitation may be noticed frequently. more insidious its onset and is likely to show more bone destruction roentgenographically. After the acute phase of rheumatic fever the joints recover completely. Joint Tuberculosis  In its early stages. Gout  Its high blood uric acid level is characteristic. especially in the knee. In gout . however tuberculosis is more often monoarticular. High fever and leukocytosis may distinguish the early case from rheumatoid arthritis and destructive changes in the roentgenograms may distinguish the late case. may produce transient locking  Examination at this stage reveals moderate swelling and puffiness with loss of the normal joint contour  A tendency to early fatigue is more pronounced DIFFERENTIAL DIAGNOSIS: Rheumatic Fever  Acute inflammatory stage that may initially appear as migratory polyarthritis simulating early rheumatoid arthritis. Rheumatoid Arthritis  It is a connective tissue disease characterized by chronic inflammatory changes in the synovial membranes and other structures by migratory swelling and stiffness of the joints in its early stage and by a variable degree of deformity. ankylosis and invalidism in its late stage. Pyogenic Arthritis  A single large joint is involved.

nongonorrheal urethritis and conjunctivitis. sometimes associated with marked destruction of bone (arthritis mutilans) and the absence of subcutaneous nodules and of rheumatoid factor in the serum. Psoriatic Arthritis  A polyarthritis resembling but probably distinct which is associated with psoriasis. splenomegaly. Ankylosis Spondylitis  A chronic arthritis usually beginning in the sacroiliac joint and lumbar spine and extending proximally. Juvenile Rheumatoid Arthritis (Still’s Disease)  This is an uncommon crippling disease of childhood. This may be an atypical or prodromal form of rheumatoid arthritis or other connective tissue disease. The knee is most frequently affected. Distinguishing features include frequent involvement of the distal interphalangeal joints. Children s affected may develop morbilliform rash and severe systemic manifestations. the systemic form of which is associated with fever and enlargement of lymph nodes and spleen. Felty’s Syndrome  A severe arthritis associated with leucopenia. Intermittent Hydrarthrosis  A recurring joint effusion characterized by an absence of acute inflammatory signs and by a relatively constant periodicity. Reiter’s Syndrome  It is an ill-defined disease occurring chiefly in adult males and characterized by the triad of polyarthritis. Systemic Lupus Erythematous  The patient usually shows minimal joint changes. severe systemic symptoms and the characteristic lupus erythematosus cell phenomenon. Palindromic Rheumatism  Characterized by repeated brief episodes of acute arthritis with signs of local inflammation but without residual joint damage.the joint quickly loses its tenderness between attacks and the great toe is often the first part of the body to be affected. subcutaneous nodules and high titers of rheumatoid factor in the serum. Enteropathic Arthritis . There is also a postdysenteric form of the disease that may follow Shigella infections.

heart. then stabilization for a period). and those who are better able to perform aerobic exercise experience less disability than those with lesser amounts of these factors.  PROGNOSIS: Osteoarthritis generally worsens slowly over time. no trauma or disease is present. Eventually. impaired sensation.. An unstable joint. kidney and thyroid. the healthy part of the bone may collapse. Progressive Systemic Sclerosis (Scleroderma)  Generalized disorder of connective tissue characterized by fibrosis and degenerative changes in the skin.g. that affects the blood supply to the bone.  Aseptic necrosis can be caused by disease. which can increase the risk of joint instability). obesity. Sjorgren’s Syndrome  An immunologic disease characterized by deficient moisture production of the lacrimal.aseptic necrosis without any known cause. The course of the peripheral arthritis generally follows that of the bowel disorder.  Aseptic necrosis occurs when part of the bone does not get blood and dies. patients with better muscle strength. Patients with OA may be able to function normally despite pain or may have varying degrees of physical disability. bone damage gets worse. stronger social supports. synovium. or a severe trauma. and more severe joint pain can predict subsequent worsening in function in patients with OA of the knee. and shoulder. such as a break or dislocation. better mental health. It is most common in the hip. digital arteries or certain internal organs notably the esophagus. intestines. lungs. knee. After a while part of the bone breaks off. salivary and other glands. . rather than a slow decrease in function. This is called "idiopathic aseptic necrosis" -. If this condition is not treated. In contrast. Worsening disability may be correlated with coping styles (e. Many times. Exercise may help to prevent loss of strength and decrease disability. The course of those with progressive disease is usually one of intermittent worsening (worsening. although it stabilizes in some patients. Aseptic necrosis Bone death caused by poor blood supply to the area. A peripheral polyarthritis associated with chronic bowel disease such as ulcerative colitis or Crohn’s disease. those who avoid activity due to pain may develop muscle weakness.

mixed connective tissue disease or rheumatoid arthritis. MD. ANAs (abnormal antibodies directed against the cells’ nuclei) can also suggest the presence of polymyositis. according to Robert Lahita. Determining which joints is involved and how their function is impaired helps the physician to distinguish OA from other forms of arthritis. Sjogren’s syndrome. Lyme disease or one of a few other inflammatory forms of arthritis. redness and heat. and other bodily signs. The pattern of arthritis in the hands may be especially helpful in the diagnosis. tender points. lupus. checking for swelling.MEDICAL MANAGEMENT: Diagnostic Procedure Physical Examination A primary care physician or rheumatologist (specialist in rheumatic disorders of the joints and related structures) will ask about:       Joint symptoms Previous or current illnesses Traumatic injuries Operations you may have had Allergies Other medical conditions The physician will inspect the affected joint(s). chief of rheumatology at St. . OA tends to involve the base of the thumb and the middle and end joints of the digits. Laboratory Tests While lab tests aren’t needed for every form of arthritis. If your symptoms and physical examination suggest rheumatoid arthritis. the following tests can often confirm your doctor’s suspicions:  Antinuclear antibody (ANA) – Commonly found in the blood of people who have lupus. Sjogren’s syndrome. The muscles that surround painful. scleroderma. Luke’s/Roosevelt Hospital and associate professor of medicine at Columbia University. Tests to detect specific subsets of these antibodies can be used to confirm the diagnosis of a particular disease or form of arthritis. skin rashes. they are very important to verify and confirm the presence of some diseases. underused joints may show signs of weakness.

the surgeon can take a sample of muscle to be examined for signs of damage to the muscle fibers. this test helps doctors diagnose gout.  HLA tissue typing – This test.  Uric acid – By measuring the level of uric acid in the blood.  Joint fluid tests – In this procedure. which detects the presence of certain genetic markers in the blood.  Erythrocyte sedimentation rate – Also called ESR or “sed rate. vasculitis (inflammation of the blood vessels) and psoriatic arthritis. Monitoring Disease Severity and Medication Response To determine the progression of the disease or how it is responding to treatment. The genetic marker HLA-B27 is almost always present in people with either of these diseases. this test is often positive in people with rheumatoid arthritis.  Skin biopsy – Taking small samples of skin and examining them under a microscope can help doctors diagnose forms of arthritis that involve the skin. fall and settle (like sediment) in the bottom of a glass tube over the course of an hour. For example. causing inflammation and severe pain. Rheumatoid factor (RF) – Designed to detect and measure the level of an antibody that acts against the blood component gamma globulin.  Muscle biopsy – By going a little deeper into the tissue than with the skin biopsy. the greater the amount of inflammation. the doctor inserts a needle into a joint space and removes fluid. doctors sometimes use some of the same tests they use to diagnose arthritis. An examination of the fluid may reveal uric acid crystals. Findings can confirm a diagnosis of polymyositis or vasculitis. a condition that occurs when excess uric acid crystallizes and forms deposits in the joints and other tissues.  Lyme serology – This test detects an immune response to the infectious agent that causes Lyme disease and thus can be used to confirm a diagnosis of the disease. eyes and joints). confirming a diagnosis of gout or bacteria. suggesting that the joint inflammation is caused by infection. which is similar to drawing blood. The higher the rate. such as lupus. a joint fluid test may show that an infectious agent has been eradicated by . can often confirm a diagnosis of ankylosing spondylitis (a disease involving inflammation of the spine and sacroiliac joint) or Reiter’s syndrome (a disease involving inflammation of the urethra.” this test measures how fast red blood cells cling together.

The test can also determine if the level of salicylate is high enough to create dangerous side effects. and these enzymes can be detected through blood tests. SGPT. or “sticky” cells. in the blood.  Lab Tests’ Limitations . Such tests can measure the amount of muscle damaged as well as how effective medication has been in reducing the inflammation that caused the muscle damage. can help doctors determine if certain medications have caused damage to the liver. A test showing a high level of creatinine means that the kidneys are not working well enough to remove waste products from the body. The following tests are the most common: Liver enzyme tests (SGOT. the effects progress unnoticed – until a liver is damaged or a silent ulcer begins to bleed dangerously.   Checking for Drug Side Effects Often a drug side effect is obvious – you become nauseated. Low counts may suggest that your medications are causing gastrointestinal bleeding. a normal waste product of the muscles. aldolase) – Muscles that have been damaged by some rheumatic diseases release certain enzymes into the blood. Or a “sed rate” test may be conducted a number of times to determine if inflammation is subsiding. develop a rash or experience blurred vision or ringing in your ears.  White blood cell count – A blood test showing a low number of infection-fighting white blood cells may suggest that your medication is decreasing your supply of white blood cells and. Muscle Enzyme tests (CPK. doctors often use lab tests to check for side effects – before they become major problems. which measure levels of liver enzymes in the blood. thus. In other cases. Doctors may use this test to monitor kidney function in people with lupus or in those taking medications that could affect the kidneys. that help the blood to clot.  Hematocrit (HCT) and hemoglobin (Hgb) – These tests measure the number and quality of your red blood cells.  Salicylate level – This test measures the amount of salicylate (the main ingredient in aspirin and in some other NSAIDs) in the blood to determine if enough is being absorbed to effectively reduce inflammation. For that reason. A low number of platelets could suggest that your medication has put you at risk of bleeding heavily. your body’s chances of fighting infection. bilirubin.  Platelet count – This test measures the number of platelets.antibiotics. Creatinine test – This test is used to determine the extent of kidney function by measuring the level of creatinine. alkaline phosphatase) – These tests.

Some may show negative results even when a person has the disease being tested for. The right tests. lab tests have their limitations. Other tests. along with your doctor’s own observations and your participation in the process. PT Management . may be required to diagnose osteoarthritis. Not all forms of arthritis can be confirmed by lab tests. release c) Tendon transfers Three procedures for bone and joint: a) Osteotomy b) Arthroplasty c) Arthrodesis Drug Therapy Drug therapy on OA has no effect on disease progression and is ancillary to the more general measures of pain control. for instance. including X-rays and magnetic resonance imaging. and the careful selection of the patients and the timing of the procedure are critical. 15 to 20 percent of people without ankylosing spondylitis have the HLA-B27 genetic marker. determine the cause of chronic back pain or examine internal organs affected by some forms of arthritis. others may be positive in people who don’t have – or may never develop – a particular disease. The goals of drug therapy in patients with OA are to relieve pain and decrease inflammation when it is present. Surgery is not appropriate. Three procedures for soft tissue: a) Synovectomy b) Soft tse. can help you get the safest and most effective treatment for your disease. however. Surgical Intervention Surgery represents one of the greatest advances in the management of arthritis in the last 40 years.Despite their many benefits. Even so. lab tests are essential to the diagnostic and treatment process. and progression of deformity. for every individual with either RA or OA. In the early stages of rheumatoid arthritis. The primary indications for surgery are pain. loss of function. only one in five people tests positive for rheumatoid factor. although the last two are not always correlated.

Respect the pain.  With patellofemoral disorder. quadriceps isometrics with the knee extended are best to avoid patellafemoral compression. 3. x 10 reps. Prevent position of deformity. non-weight bearing quadriceps and hamstring isometric and should be performed 2x daily. 2. Joint conservation technique: 1. 4. Hot Packs  Cold Packs  PWB  TENS  orthoses alleviate pain through biomechanical support  Patellofemoral Taping  long shifting knee bones  Adequate quality and quantity of sleep at night and short rest during the day is advisable. ROM 5.  isotonic exercise  functional exercise  ROM  proprioceptive training  balance training  endurance training (walking. stationary bicycles)  progressive resistive isotonic exercise  For strengthening.  Maintain and regain adequate levels of physical activity. Use larger joint joint than smaller joint.  light intensity isometric contraction. Pacing . hold for 6 sec.

Manila Married ® Former teacher Philippine Orthopedic Center (OPD) Hospicio de San Jose Rehab Unit Dr.A 67 y/o ♀ 1928 Malvar St. Sta Ana. 2010 Feb. B. 2010 Feb. 7.A Dr. 2. 2010 Osteoarthritis of the ® knee HPI: .N Feb. 2. 1. Use devices to protect joint.D: Rehab M. M.6. INITIAL EVALUATION GEN INFO: Patient’s Initial: Age: Sex: Address: Civil Status: Handedness: Occupation: Referring Unit: Rehabilitation Unit: Referring M. 8.D: Date of Referral: Date of PT Consultation: Date of I. Use of adaptive device.E: Dx: O. Rest.

Pt. 2010 Feb. 1.1. These had made it difficult for the pt to do sit to stand activities (going to bathroom. 3months PTC. getting in and out of a car.A Dr. M. This prompted the pt to seek medical assistance and undergone diagnostic procedures (see ancillary procedures). was diagnosed to have OA of the ® knee. 2010 . 1 month PTC. M. A week after was referred to PT for further evaluation and tx. and was given medication (see present medications).2/10. 2010 Feb. This condition last for about 48 weeks. Pt. This lasted for about 47 weeks. the intermittent dull nagging pain on ® knee increased from 5/10 7/10 with marked stiffness. M.D Dr.1.A Dr.A Date Feb. 2010 Feb. experienced intermittent dull nagging pain on ® knee with a P/S of 3/10 upon walking from her house going to the park ~25 meters then pt decided to go home.A Dr. getting up and down from sitting) and using stairs. decided to take medication (Flanax 500 mg PRN) the pain decrease from 5/10 . ANCILLARY PROCEDURES: Diagnostic Procedure X-ray Findings Cartilage degeneration M. use eficascent oil and took a rest and the pain subsided. M. 2010 Laboratory Exams ESR RF ANA Synovial Fluid PRESENT MEDICATIONS: Findings (N) (-) RF (-) ANA Clear M. Pt also experienced ® knee joint stiffness upon awakening especially in the morning and relieve in less than 30 minutes with mild exercise. M. gardening. The pt lessened her daily activities (doing household chores. the intermittent dull nagging pain on ® knee increased from 3/10 -5 /10 upon walking from her house going to the sari – sari store ~12 meters.A Date Feb.1.D Dr.1. going to the park).Present condition started 6 months PTC when pt.

i. controlled (Metoprolol 50 mg) since 1986 Highest BP: 160/90 mmHg Baseline: 130/80 mmHg Lowest BP: 110/80 mmHg     (+) NIDDM. (-) fx FMHx: HTN DM Arthritis Cardiac Condition Pulmonary Condition PSEHx: Paternal (+) (+) (-) (-) (-) Maternal (+) (-) (+) (-) (-)        Type A personality. 50 mg P. meat and vegetables Hobbies include cross stitching.O.O. Analgesia Htn DM  (+) HTN.O. b. spends most of the time at home watching TV (-) alcohol beverage drinker (-) smoker Diet includes rice.i. cooking and gardening. (frequent walking) . Pt works as a teacher for 5yrs.d. controlled (Metformin 500 mg) since 1986 (-) hospitalization (-) Cardiopulmonary Problems (-) Trauma.Dosage Voltaren Metoprolol Metformin PMHx: 50mg P. Indication Osteoarthritis. b. b.i.d.d. jolly and happy person Sedentary Lifestyle. 500 mg P.

 Pt lives in a two-story house c her daughter’s family  Financially stable  Home set-up: ~ 10 steps from the garden to front door ~ 10 steps from the front door to living room ~ 10 steps from living room to bathroom ~ 15 steps from bathroom to dining room ~ 30 steps from dining room to master’s bedroom ~ 10 step-staircase S: c/o: “Sumasakit ang kanang tuhod ko lalo na kapag naglalakad ako” ~15 meters PT Translation: Pt complains of intermittent dull nagging pain (p/s 5/10-7/100 on ® knee and is aggravated upon walking approximately ~15 meter Pt Goal: To relieve the intermittent dull nagging pain on ® knee and eliminate the difficulty in ADL. O: VS: B.P a: p: 130/80 mmHg 130/70 mmHg 140/90 mmHg During: RR: a: p: 16 cpm 16 cpm .

1˚ C *(axillary) Findings: Normal VS Significance: For baseline purposes OI:          ambulatory c moderate difficulty s assistive device endomorph alert. cooperative (+) swelling ® knee (+)® genu varum (+) postural deviation (see postural analysis) (+) gait deviation (see gait analysis) (-) erythema on ® knee (-) skin discoloration PALPATION:  Normothermic on all exposed body parts on (B) UE/LE except Hyperthermic ® knee  Normotonic on all exposed body parts on (B) UE/LE  Senile skin turgor & consistency  (+) crepitus on ® knee  (+) grade 3 tenderness on ® knee  (+) joint effusion on ® knee  (+) moderate osteophyte formation SENSORY A: Superficial Somatic Sensation .PR: a: p: 80 bpm 79 bpm T: 37. coherent.

(STD Used)  Superfical pain-pinprick  Light touch-wisp of cotton  Thermal sensation-hot/cold using test tube Findings: (N) sensation of (B) UE/LE as to light touch. superficial pain and thermal sensation Significance: For baseline purposes DTR: Legend 0 + ++ +++ ++++ Areflexia Hyporeflexia Normoreflexia Hyperreflexia Clonus Findings: Normoreflexia on (B) UE/LE Findings: For baseline purposes ROM .

90 P 0 .135 P 0 .All joints of (B) UE and LE are WNL.105 35 30 boggy Findings: LOM on ® knee flexion and extension Significance: 2˚ to joint effusion MMT All ms of (B) UE and LE are grossly graded 5/5 except for: Note: Break Test was used on ® knee flexors at 90˚ and ® knee extensors at 100˚. Action ® Knee flexors ® Knee extensors Grade 3/5 3/5 Findings: muscle weakness on ® knee flexors and extensors Significance: 2˚ to pain .95 DIFFERENCE A 45 P 40 ENDFEEL boggy 135-0 135-0 0 . actively and passively done pain free c normal end feel except for the following: MOTION Knee flexion Knee extension (L) A 0 .135 ® A 0 .100 0 .

The wave of fluid may take up to 2 seconds to appear. Findings: Pain is evident all throughout the motion indicating of (-) osteochondritis dissecans Significance: for ruling out purposes FUNCTIONAL ANALYSIS: Legend Tolerance Balance . the examiner strokes down the lateral side of the patella. stroking proximally toward the patient’s hip as far as the suprapatellar pouch two or three times with the palm and fingers. At approximately 30° of flexion (0° being straight leg).SPECIAL TESTS Test: Bulge Test The examiner commences just below the joint line on the medial side of the patella. The knee is actively extended with the tibia medially rotated. Findings: (+) bulging of fluid just below the medial distal portion of the patella Significance: 2° to joint effusion Test: Wilson Test The patient sits with the knee flexed over the examining table. This finding indicates a positive test. A wave of fluid passes to the medial side of the joint and bulges out just below medial distal portion or border of the patella. With the opposite hand. and the patient is asked to stop the flexion movement. The patient is then asked to rotate the tibia laterally and the pain disappears. which is indicative of osteochondritis dissecans of the femoral condyle. the pain in the knee increases.

maintain and weight shift can assume and maintain can assume can neither assume nor maintain >45 31- 16-30 mins 1-15 mins 0 min Balance Sitting Standing N F Tolerance N F Findings: Pt has normal balance and tolerance as to sitting. maintain. (N) balance and fair tolerance as to standing Significance: 2˚ to pain on ® knee POSTURAL ANALYSIS: All bony landmarks are level except: Anterior ASIS are level ® Knee medial angulation Posterior PSIS are level ® Knee medial angulation Findings: (+) postural deviation manifested by genu varum on ® knee Significance: 2˚ to position of comfort . weight shift and challenged can assume.N (normal) mins G (good) 45 mins F (fair) P (poor) O (zero) can assume.

70 steps/min. 0 0 20 steps/min. 2-4 in. 2 in. 90-120 steps/min.GAIT ANALYSIS: Hip Stance phase Heel strike Foot Flat Mid Stance Heel Off Toe Off Swing phase Acceleration Mid Swing Deceleration ® Decrease Decrease Decrease Decrease Decrease (L) Increase Increase Increase Increase Increase ® Knee (L) Increase Increase Increase Increase Increase ® Ankle (L) Increase Increase Increase Increase Increase Decrease Decrease Decrease Decrease Decrease Decrease Decrease Decrease Decrease Decrease Increase Increase Increase Decrease Decrease Decrease Increase Increase Increase Decrease Decrease Decrease Increase Increase Increase Decrease Decrease Decrease Other Parameters Step length Stride length Base width Cadence Ave. speed Arm swing (N) 15 in. 30 in. 60 m (N) Difference 3 in. 20 m Findings: (+)antalgic gait Significance: 2˚ to OA of the ® knee ADL: Fully dependent Self-care: Bathing Toileting Eating Partially dependent Independent √ √ c minimal difficulty √ . walking 80 m Result 12 in. 30 in.

6. Intermittent dull nagging pain of 7/10 on ® knee LOM on ® knee flexion and extension ms. Rehab Precaution: monitor BP. 2. LE dressing and self-care as to . PROBLEM LIST: 1. Maintenance of physical therapy is advised to prevent aggravation of pain and deformity.Grooming UE dressing LE dressing Bed mobility: Supine to sidelying Supine to long sitting Rolling Transfers: Bed óchair Ambulation √ √ √ c minimal difficulty √ √ √ √ c minimal difficulty √ c moderate difficulty Findings: Pt can perform all ADL but with moderate difficulty at most as to ambulation. Avoid excessive knee motion. 3. 7. Pt have DM &Htn. transfer. 4. transfer lower extremity dressing and self-care as to toileting Significance: 2˚ to pain and deformity A: PT Impression: Pt presents with intermittent dull localized aching pain upon walking 2 0 to OA on ® knee Rehab Potential: Pt has only a fair potential 2˚ to old age. weakness on ® knee flexors and extensors Grade 3 tenderness on ® knee Joint effusion ® knee Impaired standing balance and tolerance Moderate difficulty as to ambulation. 5.

PRE’s on (L) side using ankle weights towards knee flexion and extension x 10 reps x 2 sets. LE dressing and self-care as to toileting) 1 1 To improve posture.5w/cm2 on ® knee. Gait training using cane. 1 1 To improve gait pattern. 2. 2. 5. LE dressing and self-care as to toileting) s pain s/c assistive device. To attain the highest functional level of the pt as to ADL (ambulation. STG: (6-8 sessions) 1 1 To decrease the intermittent dull nagging pain from 7/10 to 3/10 on ® knee.toileting 8. To increase ROM by 5-10 increments on ® knee flexion and extension To increase muscle strength on ® knee flexors and extensors To reduce swelling on ® knee To improve standing balance and tolerance. To maintain the normal integrity of unaffected limbs. To improve performance of ADL as to ambulation. 4. Bicycle ergometer x 10 minutes 6. US x 1. Postural deviation 9. Isometric exercise 4. 1 1 1 1 1 1 1 1 1 1 P: Mgt: 1. Pool Therapy x 1 a week. Patellar mobilization . 8. 3. 7. HMP with TENS x 20 min on ® knee.. transfer. 3. To prevent the progression of deformity. transfer. Gait deviation LTG: 1. To maintain the general body condition of the pt.

2. Put a hot towel over the ® knee every time the pain is felt. b. Avoid the use of pillow under the knee at night because this encourages knee and hip flexion contracture. 3. Perform the instructed exercises at home. . 5. plantar flexion at the ankle and venous obstruction in the popliteal area. 4. Always maintain an extended knee position during rest. Quadriceps isometrics x 6 secs hold x 10 reps x 2 sets. use a cane as an assist.HI: 1. a. Step exercises on the staircase as tolerated. Avoid walking far distances and if un-avoided.

ALAN TROY L. MANILA WRITTEN REPORT IN OSTEOARTHRITIS DE LEON.HOSPICIO DE SAN JOSE PHYSICAL THERAPY UNIT AYALA AVENUE. UDM PT-INTERN BATCH 2012 SUBMITTED TO: MS. MARY ROSE ROJO .

It is wonderful to think what music can do in their behavior that might help us understand & in order to treat them well as a whole individuals capable of connecting to the society through music.2011 It was my first time to attend & witness what a music therapy is. This music therapy is such a great opportunity for I witness the undisputed effect of music to those kids. ALAN TROY L.MUSIC THERAPY JUNE 13. There are no cryings or any unwanted behavior that manifest during that span of time. the children's behavior are the usual that they showed to us during treatments but when the music therapy started. Everything is in its right place. . acts in such a way that is in synchrony & some form of contact to the music. Music therapy is purely music being played in a room where the patients are gathered. It is composed of songs that is weel suited for pediatric patients. at first I thought that it would be just like any other treatments combined with background music but then I was mistaken. most of the children reacted positively to the music that is being played.DE LEON. Some of the children even dance and sing together with us. At first. It seems like they are in some form of state wherein everything is serene. UDM PT INTERN BATCH 2012 REACTION PAPER. Most of them. peaceful & calm.

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