Musculoskeletal System: Second Lecture Part Ii

Front 1

Osteonecrosis

Back 1

-Death of bone and morrow cellular components as a result of lost blood result of lost blood supply without presence of infection
-Avascular necrosis and aseptic necrosis are symptoms of this condition
-Avascular necrosis is the underlying cause of 10% of all total hip replacements
-Most commonly seen at femoral head but also seen at the scaphoid, talus, proximal humerus, tibial plateau and the small bones of the wrist and foot.

Front 2

What is Osteonecrosis?

Back 2

Death of bone and marrow as a result of lost blood supply, w/o the presence of infection. 10% all THR, most common head of femur

Front 3

Implications For PT intervention in osteonecrosis are:

Back 3

-osteonecrosis is difficult to diagnose early
-Differential diagnosis of lumbar, hip,thigh, groin or knee pain is essential as osteonecrosis may present as referred pain
-If sudden, worsening of pain is followed by a sudden loss of ROM; must consider fracture

Front 4

Legg-Calve-Perthes Disease I

Back 4

-Avascular or aseptic necrosis of the epiphysis at the proximal end of the femur
-Occurs in approximately 1 in 1200 children 3 to 12 yrs of age; more frequently seen in boys (5:1 ratio)
-Typically unilateral but may be bilateral
-Cause unknown although genetic coagulopathy that may possibly be triggered by exposure to cigarette smoke in utero and during early childhood

Front 5

Legg-Calve-Perthes Disease II

Back 5

-Condition may vary from a mild self-healing problem to a condition that will destroy the hip unless serious action is taken
-Disease consist of Four Stages lasting from 2 to 5 yrs
-Stage 1: Avascular: 1-2wks
-Stage 2: Revascularization: 6 to 12 months
-Stage 3: Reparative: 2-3 yrs
-Stage 4: Regenerative: Final Months

Front 6

Clinical Manifestations of Legg-Calve-Perthes Disease

Back 6

-Insidious onset- slow
-Intermittent limp on involved side
-Positive Trendelenburg from pain or hip abduction weakness
-Hip, groin or knee pain
-Pain with activity that eases with rest
-Decreased ROM especially in hip adduction and internal rotation
-Eventual weakness

Front 7

Treatment of Legg-Calve-Perthes Disease

Back 7

-Controlled weight bearing with femur abdcted and internally rotated will keep head of femur well seated in the acetabulum, decreasing focal areas of increased load: maintains ROM and prevents deformity
-Splints/bracing/surgery

Front 8

Implications for PT for Legg-Calve-Perthes Disease

Back 8

Goal of Physical Therapy Intervention is to preserve ROM and prevent premature degenerative joint disease

Front 9

Osgood-Schlatter Disease I

Back 9

-Patellar tendon pulls small bits of immature bone of the tibial tuberosity
-Considered to be a form of tendonitis
-Characterized by activity related pain and swelling at the insertion of the patellar tendon
-Associated with patellar alta: increased patellar height requires increased force from the quads for full extension which may result in this apophyseal lesion

Front 10

Osgood-Schlatter Disease II
Tibial Plateau

Back 10

-The tibial turberosity is often enlarged
-Three times more common in boys (10 to 15 yrs of age) but can occur in girls (8 to 13 yrs of age)
-Etiology: indirect trauma: repetitive stress before fusion of epiphysis
-Aggravated by the longitudinal traction associated with bone growth

Front 11

Treatment of Osgood-Schlatter Disease

Back 11

-Rest from aggravating activities (sports)
-Non-stressful (pain-free) quad excercises
-Avoid squatting and jumping activities
-ICE
-Neoprene sleeves/casting
-Typically the condition is self-limiting and resolves when the tubercle fuses to the main body of the tibia (typically around 15 yrs of age)

Front 12

Osteoarthritis (OA) I
Osteophytes

Back 12

-"Wear and Tear arthritis"
-Slow, progressive degeneration of joint surfaces
-Most commonly seen in hip, knee, lumbar spine, cervical spine and first MTP
-Primary OA: unknown cause (joint degeneration/defect incartilage)
-Secondary OA: known cause (trauma, infection, hemarthrosis)

Front 13

Osteoarthritis (OA) II
Osteophytes

Back 13

-60-85% of people over 60 yrs of age have some degree of OA
-Deep ache (can occur at rest at night if severe). Pain typically will gradually worsen
-Stiffness after periods of inactivity
-Loss of motion due to contractures, osteophytes, loss of join congruity

Front 14

Treatment of Osteoarthritis (OA) I

Back 14

-Decreased loading of the joint (splinting/assistive devices?
-Patient education (avoid excessive loading of joint)
-Exercise: ROM/strengthening/and endurance with joint protection
-Low load
-Aquatics
-Stationary Bike
-Beware of side affects of NSAIDS

Front 15

Treatment of Osteoarthritis (OA) II

Back 15

-Emphasize decreasing stress on joints:
-proper posture and body mechanics
-Avoid prolonged weight bearing
-Proper exercise form
-Pain may not necessarily correlate with X-ray findings
-Complete clinical exam necessary. Other conditions may be causing increased stress on the affected joints (pes planus for ex.)

Front 16

Degenerative Intervertebral Disk Disease

Back 16

-Intervertebral disk undergo "wear and tear" as well
-nucleus pulposis: lose water
-annulus fibrosis: fissuring, clefts, bulge
-Narrowing between the vertebrae due to decreased disk height results in:
-Pain
-decreased mobility
-Increased wight bearing on the facet joints
-Narrowing of intravertebral foramen and vertebral canal (bulging/stenosis)
-Radiculopathy

Front 17

Clinical Manifestations of Degenerative Intervertebral Disk Disease

Back 17

-Disk degeneration is most often asymptomatic
-Spinal stenosis
-Lytic spondylolisthesis
-anterior slippage of one vertebrae over another with defective posterior neural arch
-most commonly seen at the L5-S1 spinal segment
-Degenerative Spondylolisthesis
-Anterior slippage of one vertebra over another with intact posterior neural arch
-Most commonly seen at the L4-L5 spinal segment

Front 18

Rheumatoid Arthritis (RA) I

Back 18

-Chronic, systemic inflammatory disease
-1-2 % of adults have RA
-JRA
-Onset may be at any age
-more common in the 3rd & 4th decade of life
-Two to three times more common in females
-Women who have had children or who take oral contraceptives have a decreased incidence/severity of RA
-Etiology Unknown

Front 19

Rheumatoid Arthritis (RA) II

Back 19

-80% of patients with RA are rheumatoid factor (RF) positive
-RF: antibodies that react with immuniglobulin antibodies found in the blood. This triggers a systemic inflammatory reaction. Destructive enzymes are released that destroy articular cartilage and cause synovial hyperplasia

Front 20

Rheumatoid Arthritis (RA) III

Back 20

-Pannus develops
-An abnormal synovial granulation which proliferates
-Contains inflammatory cells which are destructive to cartilage, bone, the joint capsule, and ligaments

Front 21

Clinical Manifestations of RA

Back 21

-Refer to Box 27-9, p 1266
-Multiple joints: symmetrical and bilateral presentation
-Most frequently occurs in the wrists, knees, fingers, hands,feet, cervical spine (instabiltiy)
-Signs of inflammation
-Rheumatoid nodules
-Occur in areas of repeated mechanical pressure (extensor surface of elbow/achilles tendon/extensor surface of the fingers)
-Can also occur in the heart, lungs, GI tract
-Swan-neck Deformity
-Flexion of DIP/Extension of PIP
-Boutonniere
-Deformity
-Extension of DIP/Flexion of PIP
-C1-C2 joint
-Lhermitte sign: neck flexion leads to shock like sensation

Front 22

Treatment of RA

Back 22

-No Cure
-Control inflammation
-NSAIDS
-Coricosteroids
-Gold compounds
-Hand surgery to correct deformities
-rest
-splints

Front 23

Implications for PT intervention for RA

Back 23

-Goals:
-Decrease pain
-Maintain mobility
-Minimize stiffness/edema/joint destruction
-Patient education
-Joint Protection
-Be aware of possible instability (C1-C2)
-Be aware of fatigue

Front 24

Septic Arthritis

Back 24

-Infectious arthritis
-Bacteria, viruses or fungi can be responsible for septic arthritis
-Can affect people of any age but children and older adults are at greatest risk
-Microorganisms can be introduced into the joint by direct inoculation, direct extension, or by hematogenous spread (the most common route)

Front 25

Clinical Manifestations of Septic Arthritis I

Back 25

-Acute Joint pain
-Fever, chills and other systemic symptoms
-Examination of the joint may reveal classic signs of inflammation
-Increased Temps
-Swelling
-Redness
-Loss of Function

Front 26

Clinical Manifestations of Septic Arthritis II

Back 26

-Pus may drain through a sinus formed from the joint to the outside
-A child may refuse to weight bear through the affected extremity
-Destruction of the joint can proceed rapidly and have long-lasting effects
-In addition to the infection, the WBC's that enter the joint to fight the infection release enzymes that have a negative effect on articular cartilage

Front 27

Treatment of Septic Arthritis I

Back 27

-Any joint infection is considered to be a medical emergency
-IV antibiotics with follow up oral antibiotics
-Aspiration or surgical drainage of the joint may be indicated
-If a prosthetic joint is infected, the hardware and cement may be removed

Front 28

Treatment of Septic Arthritis II

Back 28

-Early in the course of treatment, the joint typically rested (splinting, traction or casting)
-Care in application of the splint and removal of the splint for periodic ROM exercise can help prevent joint contractures.

Front 29

Myositis

Back 29

-Inflammatory muscle disease caused by viral, bacterial or parasitic agents
-most frequently caused by S.aureus or by parasites such as trichinella and the tapeworm larva Taenia solium
-The most common forms of myositis are polymyositis and dermatomyositis

Front 30

Clinical Manifestations of Myositis

Back 30

-Malaise, fever, and lethargy
-Muscle swelling
-Pain
-Tenderness
-Muscle weakness
-Increased levels of creatine kinase
-Electromyography demonstrates muscle irritability and myopathic changes

Front 31

Treatment of Myositis

Back 31

-Often includes the use of immunosuppressive therapy and corticosteroids
-Resulting muscle weakness typically means that aggressive and potentially prolonged physical and occupational therapy intervention my be indicated

Front 32

Ankylosing Spondylitis (AS) I

Back 32

-Inflammatory arthropathy of the axial skeleton including the sacroiliac joints, apophyseal joints, costovertebral joints and intervertebral disk articulations
-One-third of patients with AS have asymmetric involvement of the peripheral joints (knee, hip, shoulder)
-Typically affects young people (15 -30 yrs of age) Rare after 40 yrs
-Men are affected two to three times more often than women

Front 33

Ankylosing Spondylitis (AS) II

Back 33

-AS is marked by chronic nongranulomatous inflammation at the area where ligaments attach to the vertebrae
-The replacement of inflamed cartilaginous structures by bone contributes to progressive ossification with bony growth between the vertebrae. This leads to a fused, rigid or "bamboo" spine that is characteristic of end-stage disease

Front 34

Clinical Manifestations of Ankylosing Spondylits (AS)

Back 34

-Limitations in spinal mobility (especially in forward flexion)
-early loss of typical lumbar lordosis
-hip flexor contractures often present bilaterally
-loss of chest wall excursion
-osteoporosis
-may have subluxations at C1-C2

Front 35

Treatment of Ankylosing Spondylitis (AS)

Back 35

Primary focus is to reduce inflammation in the joints, maintain mobility and proper postural alignment at the spine
-Relieve pain
-NSAIDS

Front 36

Implications of PT Intervention of Ankylosing Spondylits (AS)

Back 36

-Avoid high impact and flexion activities
-Emphasize low impact aerobic exercise with extension and rotation components
-Avoid contact sports
-Over-exercising can be potentially harmful
-Firm, supportive mattress recommended to maintain spinal alignment. Soft mattresses or water beds should be avoided as these can contribute to excessive flexion and the development of stooped postures

Front 37

GOUT

Back 37

-Heterogeneous group of metabolic disorders marked by an elevated level of serum uric acid and the deposits of urate crystals in the joints, soft tissues and kidneys
-Uric acid is normally formed when the body breaks down cellular waste products. Typically dissolves in the blood and is excreted throught urine. If the body produces more uric acid than the kidneys can handle, the blood levels of uric acid rise. It may then precipitate out and accumulate in body tissues including joints.
Typically monoarticular

Front 38

Clinical Manifestations of Gout

Back 38

-Acute, inflamed joint manifested by exquisite pain that occurs suddenly at night
-Gout is common in the first MTP but also seen in the ankle, instep, knee, wrist, elbow and fingers
-Chills and fever may accompany joint pain
-After recovering from initial episode of gout, the patient enters an asymptomatic period which can last for months or yrs
-Gout attacks return suddenly with increasing severity and frequency and often different joints
-"attacks" may be precipitated by trauma, surgery, alcohol, consumption, or eating certain foods

Front 39

Treatment of Gout

Back 39

-NSAIDS
-Corticosteroids may be used
-Treatment of hyperuricemia
-Diet
-Weight loss
-Moderation of alcohol consumption

Front 40

Myofascial Pain Dysfunction I

Back 40

-Regional pain disorder marked by the presense of myofasical trigger points with in taut band of muscle
-"Hyper-irritable"foci in skeletal muscle or its fascial components
-Trigger points may be active or latent
-A latent trigger point may become active in the presense of an acute overload of the muscle or with chronic strain

Front 41

Myofacial Pain Dysfunction II

Back 41

-Trigger points are different from the tender points associated with fibromylagia
-Trigger points have been described as a rope-like, nodular, or crepitant area within a muscle
-Trigger points are self-sustained and self-perpetuating
-Local twitch response and "jump" sign

Front 42

Implications for PT intervention for Myofacial Pain Dsyfunction

Back 42

-Vapocoolant spray
-Low volt electrical stimulation
-Ultrasound (continuous mode appears to be more effective)
-HEP: sustained stretch