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Chapter 22-The Musculoskeletal System

Dottie Roberts, MSN, MACI, RN, CMSRN, OCNS-C

Objectives

Study of the information presented in this chapter will enable the learner to:

• Identify nursing assessment parameters for the musculoskeletal system.

• Discuss the pathophysiology, clinical manifestations, and treatment of osteoarthritis, rheumatoid arthritis, osteoporosis, and fibromyalgia.

• Describe the clinical manifestations and treatment of common injuries and disorders of the musculoskeletal system.

• Identify pharmacologic treatment options for disorders of the musculoskeletal system.

Key Points

• Osteoarthritis is the most common articular disease in adults and a frequent cause of progressive disability.

• Back pain affects 8 out of 10 people during their lives; more than 1 in 3 older adults experience low back pain, often due to biomechanical and soft tissue pathologies.

• Osteomyelitis is considered an orthopaedic emergency because delayed or inadequate treatment can lead to chronic infection.

• Although a specific cause for osteoporosis has not been identified, multiple factors are known to increase an individual’s risk of developing the disease.

• Fibromyalgia is a connective tissue disorder that may co-exist with other inflammatory diseases such as systemic lupus erythematosus and rheumatoid arthritis.

NURSING ASSESSMENT OF

THE MUSCULOSKELETAL SYSTEM

I. OVERVIEW

A. Components.

1. Skeleton of 206 bones provides body’s internal framework, protects vital organs, offers site for hematopoiesis (blood cell formation).

2. Soft tissues (muscles, cartilage, tendons, ligaments) maintain posture, stabilize joints, facilitate motion.

3. Bones, cartilage, tendons, fascia, and ligaments are connective tissues that vary in type and arrangement of fibers, cells, and “ground substance” or matrix.

a. Bone: 80% of bone tissue by weight is minerals, 20% water.

(1) Cancellous bone: spongy, porous-like bone usually found at distal and proximal ends (epiphyses) of long bones, in axial bones such as the skull.

(2) Cortical bone: dense, compact bone that forms shaft (diaphysis) of long bones.

(3) Bone marrow: found in medullary cavity of long bones, vertebrae, ribs, sternum, and flat bones of pelvis. Yellow marrow is primarily adipose cells; red marrow is site of hematopoiesis. At birth, nearly all marrow is red and hemapoietically active. As need decreases, red marrow is replaced gradually by yellow; only vertebrae, ribs, sternum, iliac bones have red marrow in adults

b. Cartilage: tough, semi-transparent, compressible, flexible connective tissue; about 75% water by weight; allows for diffusion of gases, nutrients, and waste

(1) Hyaline: most common type; covers articular surfaces to provide sliding area that reduces friction with movement.

(2) Fibrocartilage: extremely tough cartilage found in intervertebral discs, menisci of knee, other areas subjected to heavy pressure, stretching.

(3) Elastic (yellow cartilage): provides resiliency, allows repeated bending. Only found in two skeletal locations: supporting external ear and forming epiglottis.

c. Tendons and ligaments: dense, regular connective tissue with great tensile strength. Limited blood supply.

(1) Tendons attach muscle to bone, facilitate movement.

(2) Ligaments attach bone to bone, provide stability/limit undesirable movement.

d. Fascia: sheet or band of connective tissue that can withstand only limited stretching; minimizes friction by allowing one muscle to glide over another.

e. Skeletal muscle.

(1) Over 600 muscles under voluntary control, produce or prevent movements through contraction and relaxation of striated fibers.

(2) Fascia penetrates, subdivides muscle into muscle fiber bundles.

(3) Rich blood supply nourishes muscle tissue.

(4) Muscle action requires chemical energy in form of adenosine triphosphate (ATP). Creatinine phosphate produced and stored in muscle, serves as first source of ATP for burst of activity.

(5) Muscle metabolism produces heat essential for maintenance of body temperature.

II. Anatomy and Physiology

A. General anatomy and physiology.

1. Skeletal system.

a. Provides support for upright posture.

b. Facilitates movement through attachment to muscles.

c. Stores mineral salts, lipids and marrow.

(1) — about 99% of the body’s calcium is contained in bone (a calcium reserve); phosphorous also stored in bone.

d. Forms new red blood cells and other blood elements.

e.d. Protects vital organs.

2. Microscopic structure- External view of bone appears dense and solid, but microscopic structure is complex.

a. Cortical bone.

a(1) Cylindrical structural units (Haversian system) serve as tiny weight-bearing pillars; contain Haversian canals.

b. Haversian canals : contain blood vessels and lympatics. Responsible for maintaining and suppling nutrients to the bone tissue.

c(2) Surrounding Haversian canals in mature bone are concentric rings known as lamellae.

d(3) Smaller canals (canaliculi) extend from the Haversian canals to lacunae, where mature bone cells (osteocytes) are embedded.

3. bTypes of bone

a. Cortical bone.

(1) Compact bone.

(2) Hard layer of all bones

(3) Forms the shaft of long bones

(4) Poor blood supply

. b.Cancellous bone.

1) (1) light, porous , spongy bone

2) Absent of Haversian system

3) Web-like formations, irregular spaces are filled with red marrow (rich blood supply).

(2) Spaces are separated by bony projections called trabeculae.

c. Bone cells have distinct functions.

(1) Osteoblasts are basic bone-forming cells, participate in bone remodeling by synthesizing bone matrix and new cells.

(2) Osteoclasts participate in bone remodeling by breaking down bone tissue.

(3) Osteocytes are mature bone cells that function to keep the bone living tissue.

B. Classification of bones.

1. Long bones: found in the extremities.

a. Structure.

(1) Diaphysis: shaft.

(2) Metaphysis: flared portion between shaft and end of bones.

(3) Epiphysis: end of bone.

(4) Epiphyseal plate(growth plate): cartilage between epiphysis and diaphysis.

(5) Medullary cavity: inner hollow cavity containing yellow marrow.

(6) Endosteum: inner connective tissue layer.

(7) Periosteum: outer connective tissue layer covering bone surface.

b. Ends of long bones are covered with articular cartilage.

2. Short bones: spongy bones with a thin surface of compact bone; found mainly in hands (carpals) and feet (tarsals).

3. Flat bones: have thin layer of cancellous bone between two opposed layers of compact bone; provide extra protection for organs; ribs.

4. Irregular bones: odd-shaped; vertebrae, jaw.

C. Axial skeleton: 80 bones forming upright portion (axis) of body.

1. Skull: consists of cranium and facial bones.

a. Cranium: 8 bones. Occipital, parietal (pair), temporal (pair), frontal, sphenoid, ethmoid.

b. Facial: 14 bones.

2. Vertebral column: 33 vertebrae.

a. 7 cervical, 12 thoracic, 5 lumbar, 5 sacral (fused into one sacrum), 4 coccygeal (fused into one coccyx).

b. Vertebrae are separated by pads of fibrocartilage called intervertebral discs, which account for 20%-33% of spinal column weight.

3. Thorax: consists of sternum, ribs, 12 thoracic vertebrae.

a. Sternum: flat bone; xiphoid process often used as landmark for cardiovascular assessment.

b. 12 pairs of ribs form flaring sides of thorax: 7 pairs attached directly to sternum and 5 pairs of false ribs; 2 pairs of these are floating (no anterior attachment).

D. Appendicular skeleton: extremities and their girdles.

1. Pectoral girdle (shoulder): connects upper extremity to axial skeleton and provides attachment points for many muscles that move upper limbs.

a. Clavicle (collarbone): acts as brace to hold the arm away from thorax.

b. Scapula (shoulder blade): provides anchoring point for muscles of the back.

(1) Shoulder has maximal movement because there is only one connection to axial skeleton at the sternoclavicular joint.

(2) Scapulae are loosely attached by muscles.

(3) Joint is poorly reinforced with ligaments. These characteristics also make shoulder easy to dislocate.

2. Upper extremity.

a. Humerus: largest bone in upper extremity.

b. Forearm: articulates proximally with humerus and forms joints with bones of wrist distally.

(1) Radius: expands distally to articulate with carpal bones of wrist; major contributor to wrist joint (when radius moves, hand moves with it).

(2) Ulna: slightly longer than radius; ulna plays little or no role in hand movement.

c. Elbow: joint that allows flexion, extension, forearm rotation.

d. Hand.

(1) Wrist (carpus): allows flexion and extension, inversion and eversion; 8 carpals.

(2) Palm (metacarpus): 5 metacarpal bones radiate from wrist like spokes to form palm of hand

(a) Bones are not named, but numbered 1 to 5 from thumb to little finger.

(b) Metacarpal 1 associated with thumb is shortest, most mobile; allows opposition (touching thumb to tips of other fingers).

(3) Fingers (phalanges): 14 phalanges per hand..

(a) Numbered 1 to 5 beginning with the thumb.

(b) Except for thumb, each finger has 3 phalanges (distal, middle, proximal); thumb has no middle phalanx.

3. Pelvic girdle (hip): attaches lower extremities to axial skeleton, transmits weight of upper body to lower limbs, supports organs of pelvis.

a. Pelvic girdle formed by two large, irregularly shaped hip bones (os coxae). Each hip bone consists of:

(1) Iliuma connecting to the sacrum at the sacroiliac joint.

(2) Pubic bones connecting together at the symphysis pubis.

(3) Iliuma, ischiuma, and pubic fused to create the acetabulum.

b. The aAcetabulum on lateral surface of pelvis is the socket that receives femoral head to create hip joint.

4. Lower extremity.

a. Femur: single long bone of thigh; largest, longest, strongest bone in body.

b. Hip: weight-bearing ball-and-socket joint with femoral head and acetabulum as articulating surfaces.

(1) Forces across hip joint may be 3-6 times body weight during ambulation, 2.5-3 times body weight during standing.

(2) Stabilized by strong muscles, fibrous joint capsule.

c. Lower leg: composed of two parallel bones that form less flexible but stronger, more stable limb than bones of forearm.

(1) Tibia (shinbone): second only to femur in size and strength; receives body’s weight from femur and transmits it to foot.

(2) Fibula: stick-like bone with slightly expanded ends.

d. Knee (genu): structure composed of the articulation of the distal femur and the proximal tibia two joints; allows flexion, extension, pivot movements.

(1) Forces across knee may be 3-4 times body weight during ambulation.

(2) Medial and lateral menisci: specialized articular cartilage that distributes loading forces across tibial plateau.

(3) Knee joint is stabilized by two sets of ligaments, cushioned by menisci.

(a) Anterior and posterior cruciate ligaments (ACL, PCL): crisscrossed within knee to provide anterior and posterior stability.

(b) Medial and lateral collateral ligaments (MCL, LCL): on both sides of knee joint; give medial and lateral stability, help to prevent dislocation.

(c) Menisci: crescent-shaped fibrocartilage structures that transmit load forces across knee.

(4) Patella (knee cap): bone anterior to femur; secures anterior thigh muscles to tibia; connects to muscles of lower leg at patellar tendon; also protects knee anteriorly.

e. Foot: supports body weight and acts as lever to propel body forward during walking and running.

(1) Hindfoot (tarsus): made of 2 7 bones that form posterior half of foot.

(a) Body weight is carried primarily by two largest, most posterior tarsals.

(b) Calcaneal (Achilles) tendon of calf muscle attaches to posterior surface of calcaneus(largest bone of the foot/ heelbone).

(2) Midfoot (metatarsus): 5 tarsal bones small long bones called metatarsals.

(3) Forefoot (toes): 5 metatarsals and 14 phalanges.

(a) 3 phalanges in each digit (proximal, middle and distal) except great toe (hallux), which has only proximal and distal phalanges.

(4) Arches of the foot: segmented structure can bear weight only if it is arched.

E. Joints (articulations).

1. Sites where two or more bones meet. Prefix arthro- designates a joint.

2. Classification of joints by structure (based on material binding the bones together and presence of a joint cavity).

a. Fibrous: joined by fibrous tissue.

b. Cartilaginous: joined by cartilage.

c. Synovial: articulating bones separated by fluid-containing joint cavity.

3. Classification of joints by function (based on amount of movement allowed at joint).

a. Synarthrosis (fibrous): immovable joint in which bones come into direct contact with each other.

b. Amphiarthrosis (cartilaginous): slightly movable joint.

c. Diarthrosis (synovial): freely movable joint enclosed by joint capsule.

(1) External layer of joint capsule is tough, fibrous tissue that is continuous with periostea of articulating bones.

(2) Inner layer of joint capsule is synovial membrane of loose connective tissue.

(3) Synovial fluid occupies all free spaces within joint capsule.

(a) Provides slippery weight-bearing film that reduces friction between articulating cartilages.

(b) Contains phagocytic cells that rid joint cavity of microbes or microcellular debris.

(c) Normally clear or pale yellow, with viscous egg-white consistency due to hyaluronic acid secreted by cells of synovial membrane

(4) Ligaments: reinforce, strengthen and limit movement of a diarthrotic joint.

(5) Bursae: small, flattened fibrous sacs lined with synovial membrane, contain thin film of synovial fluid.

(a) Act as “ball bearings” to reduce friction between tendon and bone, or tendon and ligament, during joint activity.

(b) Can become injured or inflamed (bursitis), affecting joint movement.

(6) Types : gliding, hinge, condyloid, saddle, pivot, ball and socket.

III. Nursing Assessment

A. Assessment.

1. Patient history.

a. Biographic information: age, gender, ethnicity, occupation, site and type of residence (one floor vs. stairs required for access); source of information (patient, family, significant other, medical record).

b. Chief complaint: location, description of musculoskeletal problem with associated symptoms (pain, swelling, loss of function/range of motion); setting or circumstance in which problem occurs; prior occurrence; aggravating or relieving factors.

c. Past health: past illnesses (rheumatic fever, polio), injuries.

d. Present health: diet/exercise habits; exposure to environmental hazards.

e. Family history: presence of musculoskeletal disorders with familial link (rheumatoid arthritis).

f. Social history: patient’s role function in family, at work; activities that may predispose patient to injury (skateboard, tennis, golf, etc.).

2. Physical assessment: proceed systematically from head to toe.

a. Inspection.

(1) General appearance, body build, contours, alignment, symmetry.

(2) Posture: assessed unless patient cannot stand; observed from anterior, lateral, posterior perspectives while patient is standing, flexing forward at the waist, sitting.

(a) Scoliosis: lateral curvature of spine.

(b) Lordosis: posterior concavity of lumbar spine.

(c) Kyphosis: when normal curvature of thoracic spine greater than 45 degrees.

(3) Gait: pattern of achieving upright bipedal locomotion; assessed by having patient walk across room and back (10-20 feet).

(a) Stance (weight bearing).

(b) Swing (non-weight bearing).

(c) Abnormal gaits may indicate musculoskeletal or neurologic disorders.

(4) Local examination of affected area.

(a) Variations in skin color, nodules, masses, swelling (soft tissue or joint).

(b) Deformity possible following injury or disuse.

i. Dislocation: one or more bones of joint out of position.

ii. Subluxation: partial dislocation of joint.

iii. Contracture: lack of full passive range of motion due to shortening of muscle or ligaments.

iv. Ankylosis: stiffness or fixation of joint.

b. Palpation.

(1) Palpate affected area for tenderness, warmth, skin texture, bone continuity, abnormal mobility, bone or joint crepitus (audible crackling when the joint is moved), muscle weakness or hyperactivity.

(2) Joints not normally tender to palpation; determine specific location of any tenderness (e.g., at joint margin).

(3) Synovial membrane not normally palpable; when thickened, feels “doughy” or “boggy.”

(4) Palpable fluid (effusion) abnormal.

c. Range of motion (ROM): amount of motion available to a joint within anatomic limits of its structure.

(1) Active ROM: patient moves joint, either independently or with minimal assistance (active assisted ROM); typically assessed first.

(2) Passive ROM: examiner moves joint while patient’s muscles are relaxed.

(3) Assess for any stiffness, crepitus, limitation.

(4) Immediately cease passive manipulation if pain is encountered upon resistance.

(5) ROM measured in degrees.

(6) See Table 22-1 for types of joint movement.

d. Reflex testing.

(1) Reflex is an involuntary motor response by the nervous system to a specific stimulus.

(2) Tendon must be partly stretched then lightly tapped, usually with reflex hammer; repeat several times, alternate with other extremity to compare response.

(3) Reflex response is graded:

(a) Grade 4+: hyperactive, extremely brisk.

(b) Grade 3+: brisker than normal.

(c) Grade 2+: within normal limits.

(d) Grade 1+: hypoactive, diminished.

(e) Grade 0: no response, flaccid.

e. Muscle function testing provides information on strength, movement patterns. Entire ROM must be tested; movement must occur at steady speed throughout examination.

B. Diagnostic studies (see Table 22-2).

PHYSIOLOGIC ALTERATIONS OF

THE MUSCULOSKELETAL SYSTEM

I. DISEASES OF THE JOINTS

A. Rheumatoid arthritis (RA).

1. Definition: chronic, systemic autoimmune disease characterized by T-cell activation triggering inflammation of connective tissue as a response to cytokines and other mediators, leading to progressive deformity of joints, with unexplained periods of remission and exacerbation.

2. Pathophysiology.

a. Autoantibodies believed to develop in synovium against IgG.

(1) Formation of immune complexes, activation of complement cause inflammation.

(2) Synovial membrane of affected joints becomes swollen, congested, thickened.

b. Thickened tissue invades surrounding cartilage, ligaments, tendons.

(1) Granulation tissue eventually covers entire articular cartilage, leading to formation of highly vascularized fibrous scar tissue known as pannus.

(2) Pannus erodes, destroys articular cartilage; causes subchondral bone erosions, cysts, fissures, bone spurs, osteophytes.

(3) Pannus also can scar, shorten tendons and ligaments to cause laxity, subluxation, contracture.

c. Extra-articular features common, numerous, potentially fatal.

(1) Rheumatoid nodules develop around small blood vessels in up to 50% of patients with RA.

(2) Secondary Sjögren’s syndrome occurs in 10%-15% of patients with RA; characterized by hallmark symptoms of dry mouth and dry eye; however, the disorder is systemic in nature and affects the body’s moisture-producing organs.

(3) Felty syndrome (triad of RA, splenomegaly, and granulocytopenia) occurs in 1%-3% of RA patients with a long history of the disease.

(4) Inflammatory eye disorders, infection, pulmonary disease, vasculitis, cardiac abnormalities also possible.

3. Incidence.

a. Approximately 1% of population; estimates increase after age 55 for men and women to 2% and 5%, respectively.

b. Incidence increases with age, peaks between fourth and sixth decades.

4. Etiology.

a. Cause for autoimmune response essentially unknown.

(1) Infection suggested as cause of response, but no microorganism has been isolated from affected synovium with enough consistency to confirm this theory.

(2) Smoking increases the risk of developing RA.

b. Genetic predisposition.

(1) Genetic marker HLA-DR4 occurs in many people with RA, considered a predictor of genetic predisposition.

(2) RA is 2-3 times more likely to affect women than men.

5. Clinical manifestations.

a. May vary from one individual to another but also varies in an individual over course of disease.

b. Most common onset is insidious development of symptoms over several weeks, though acute polyarticular onset also can occur.

(1) Systemic symptoms, such as fatigue, anorexia, weight loss, fever.

(2) Joint pain and stiffness, swelling, redness usually affect multiple joints bilaterally; fingers, hands, wrists, knees, feet most commonly affected.

(a) Morning stiffness typically lasts more than 1 hour.

(b) Decreased ROM related to pain (early stage), fibrosis of joints (later).

c. Joint deformities are characteristic of progressive disease.

(1) Inflammation of proximal interphalangeal (PIP) joints contributes to spindle-shaped appearance of fingers (early disease).

(2) Swan-neck deformity of PIP joint results from contractures of muscles, tendons. (Clinical presentation: joint at base of finger bends in toward palm, middle joint remains straight, and most distal joint flexes in toward palm.)

(3) Boutonniere deformity of PIP joint results from rupture of extensor tendons over fingers. (Clinical presentation: second finger joint is flexed toward palm and most distal finger joint is extended away from palm).

(4) Ulnar deviation of metacarpophalangeal (MCP) joints of fingers and medial deviation of wrist result in typical ulnar drift.

6. Diagnosis.

a. Laboratory testing important, but no single set of tests can confirm diagnosis of RA.

(1) Mild normocytic anemia with thrombocytosis common.

(2) More than 75% of patients with RA have positive rheumatoid factor (RF), but presence of RF alone is not enough for diagnosis.

(a) Higher titers seen in active disease.

(b) Patients with seronegative (RF-) disease have better outcomes, rarely have extra-articular symptoms.

(3) Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) usually high due to active inflammatory process; serial results can be used to monitor effects of treatment.

b. Synovial fluid analysis shows change from normal, transparent yellow to milky, cloudy, or dark yellow.

(1) Normal synovial fluid has less than 200 white blood cells (WBCs)/mm3.

(2) In RA, synovial fluid has 15,000-20,000 WBCs/mm3.

c. Arthroscopic examination reveals pale, thick, edematous synovium, cartilage destruction.

d. Radiologic studies help to confirm disease, monitor effects of treatment.

(1) Soft tissue swelling in early disease indicated by shadowing around affected joint on x-ray.

(2) Subchondronal bone erosions evident as disease progresses.

(3) Subluxation also can be seen on x-ray.

e. 1987 revised criteria for classification of RA (see Table 22-3) serve as a framework for diagnosis but not intended to define criteria explicitly.

7. Common therapeutic modalities: goals are to maintain or restore joint function, prevent deformity, reduce inflammation and pain.

a. Patient/family involvement is basis of successful treatment (see Continued care and rehabilitation).

b. Physical therapy focuses on ROM, strengthening, endurance.

(1) ROM exercises improve joint motion (passive, assisted, active).

(2) Strengthening exercises preserve or improve muscle function.

(a) Isometric exercises allow muscle contraction without moving joint (quad sets).

(b) Isotonic exercises must be used carefully because they require repetitive joint motion, but low-resistance exercises (bike riding, swimming, golf, dance, tai chi) can increase muscle strength after pain, inflammation controlled.

c. Pharmacologic management (see Pharmacologic management of joint disease).

d. Surgical treatment (see Surgical treatment of joint disease).

8. Complications.

a. Musculoskeletal: contractures and deformity; joint destruction; loss of function.

b. Pulmonary: laryngeal pain, hoarseness, speaking difficulties; although patient may be asymptomatic, mortality from pulmonary disease in RA patients is twice that of general population.

c. Cardiac: effusion or abnormality of pericardium with no other symptom of heart disease.

d. Neurologic: cervical spine instability, peripheral nerve entrapment linked to synovial inflammation, mononeuritis multiplex (painful disease of peripheral nerves).

e. Optical: scleritis, with possible erosion through sclera.

f. Mortality: average life expectancy for a patient with RA may be shortened by 3 to 7 years. Those with severe forms of RA may die 10-15 years earlier than expected. However, as treatment for RA improves, severe disability and life-threatening complications appear to be decreasing.

9. Continued care and rehabilitation.

a. Education should be provided on multiple topics.

(1) Disease process, including cycle of remission, exacerbation.

(2) Management of pain, stiffness (paraffin baths, heat, ice).

(3) Fatigue, sleep/rest, energy conservation.

(4) Therapeutic exercise.

(5) Joint protection (splinting, bracing, traction).

(6) Medication use.

(7) Use of assistive devices.

(8) Complementary/alternative therapies.

b. Provide information on community resources and local support (Arthritis Foundation).

c. Work with patient/family to evaluate, modify home situation for improved patient mobility, safety.

B. Osteoarthritis (OA).

1. Definition: slowly progressive, non-inflammatory disease characterized by deterioration of articular cartilage; asymmetric joint involvement typical.

2. Pathophysiology.

a. Frequently unknown joint insult causes deterioration of cartilaginous matrix, triggering body’s ineffective attempts at repair.

(1) Damage to cartilage prompts metabolic response at level of chondrocytes.

(2) Cartilage becomes softer, loses its elasticity.

b. Chondrocyte activity cannot keep pace with progressive destruction by lysosomal enzymes.

(1) Cartilage becomes increasingly susceptible to friction.

(2) Collagen fibrils lose support; fibrous tissue replaces typical collagen.

(3) Cartilage loses its ability to resist wear, becomes yellow and dull in appearance.

c. New bone formation causes spur development, leads to incongruity in joint surfaces.

d. Small pieces of cartilage (osteophytes) may shear off joint surface and attract phagocytic cells, leading to secondary localized inflammatory response.

3. Incidence.

a. Most common articular disease in adults.

(1) More than 90% of people affected by age 6540.

(2) Symptoms in younger individuals most commonly due to trauma, repetitive occupational stress, joint hemorrhage, infection.

b. Affects twice as many women as men over age 50.

4. Etiology.

a. Search for single cause for OA has been unsuccessful, but multiple risk factors have been identified for idiopathic disease.

(1) Aging.

(2) Sex hormones and other hormonal factors: increased incidence of OA in aging women believed to result from estrogen reduction at menopause.

(3) Genetic factors.

(a) Mutations to type II collagen gene identified within families of affected individuals.

(b) Incidence of Heberden’s nodes (bony overgrowths at distal interphalangeal [DIP] joints) three times higher among sisters than in general population.

(4) Modifiable risk factors: excessive weight, level of activity.

b. Secondary OA can result from joint injury or disease, or systemic illness that may contribute to development of arthritis.

(1) Trauma.

(2) Long-term participation in repetitive physical activity (athletics).

(3) Joint instability following damage to supporting ligaments, tendons.

(4) Neurologic disorders (Charcot neuropathy) that contribute to abnormal positioning and weight-bearing.

(5) Congenital or acquired deformity (Legg-Calvé-Perthes disease, dislocated hip).

(6) Hematologic or endocrine disorders (hemophilia with chronic hemarthrosis, hyperparathyroidism).

(7) Medications (corticosteroids, colchicine).

(8) Infection.

c. Demonstrates site specificity; certain joints show high prevalence of disease: weight-bearing joints (hips, knees); cervical and lumbar spine; DIP, PIP, MCP joints in hands; metatarsophalangeal (MTP) joints in feet.

5. Clinical manifestations.

a. Joint pain often the primary symptom.

(1) Localized, asymmetrical mechanical pain (“aching”): differentiated from inflammatory arthritis.

(2) Increases with joint use, relieved by rest in early stages of disease.

(3) Night pain or pain at rest occurs with progressive disease.

(4) Pain also likely with joint palpation.

b. Stiffness may range from slow movement to pain with initial activity after rest.

(1) Often lasts less than 30 minutes, improves with ambulation or movement.

(2) Often accompanied by crepitus due to loose cartilage particles in joint capsule.

(3) Mild-to-moderate effusion resulting from over activity may exacerbate joint stiffness; large effusions uncommon with OA.

c. Joint deformity or instability.

(1) Heberden’s nodes.

(2) Bouchard’s nodes: bony overgrowths at PIP joints.

(3) Leg length discrepancy possible in advanced hip OA.

(4) About 50% of patients with knee OA have varus (bow-legged) deformity related to cartilage loss in medial compartment.

6. Diagnosis.

a. Diagnosis can almost always be made by history, physical examination.

b. X-rays findings do not always correlate with severity of patient’s symptoms.

c. Other radiologic studies.

(1) Bone scan especially sensitive to changes of early disease.

(2) MRI more sensitive than plain x-ray in identifying progressive joint destruction.

d. American College of Rheumatology criteria continue to guide disease diagnosis (see Table 22-4).

7. Common therapeutic modalities: goals are to maintain or improve joint function, manage pain and inflammation, limit disability.

a. Patient/family involvement is basis of successful treatment.

(1) Education should be provided on multiple topics.

(a) Disease process.

(b) Management of pain, stiffness (paraffin baths, heat, ice).

(c) Nutritional counseling, weight reduction and management.

(d) Therapeutic exercise.

(e) Joint protection (splinting, bracing, traction).

(f) Medication use.

(g) Use of assistive devices.

(h) Complementary and alternative therapies.

(2) Provide information on community resources and local support (Arthritis Foundation).

(3) Work with patient/family to evaluate, modify home situation for improved patient mobility, safety.

b. Physical therapy focuses on cardiovascular conditioning, improved strength and flexibility, increased joint mobility.

(1) Aerobic or resistance exercises can contribute to decreased pain, disability.

(2) Strength training, weight-bearing exercises improve gait, overall function.

(3) High impact activities (jogging) should be avoided unless adaptations can be made.

c. Pharmacologic management (see Pharmacologic management of joint disease).

d. Surgical treatment (see Surgical treatment of joint disease).

8. Complications: progressive disability.

9. Continued care and rehabilitation (see Rheumatoid arthritis).

C. Pharmacologic management of joint disease.

1. Rheumatoid arthritis.

a. Disease-modifying anti-rheumatic drugs (DMARDs) should be initiated early in RA treatment to modify or slow disease process.

(1) Methotrexate is frequently prescribed, available in oral or injectable forms (7.5-20 mg/week).

(2) Leflunomide (Arava®) prescribed at 10-20 mg/day in single dose.

(3) Other DMARDs may be prescribed, including gold salts, azathioprine (Imuran®), sulfasalazine (Azulfidine®), cyclophosphamide (Cytoxan®), cyclosporine (Neoral®), hydroxychloroquine (Plaquenil®).

b. Orencia® (abatacept), a first-in-class selective co-stimulation modulator, is a fully human receptor fusion protein that works early in the RA inflammatory process to reduce T-cell activation without completely blocking or depleting T-cells. May be used alone or concomitantly with DMARDs other than tumor necrosis factor (TNF) antagonists

c. Biologic response modifiers (BRMs) target molecules, cells (cytokines) involved in chronic inflammation. Previously used when DMARDs alone failed to control disease progression; now being prescribed early in treatment, often in conjunction with DMARDs.

(1) New agents block the action of TNF, the cytokine believed to be dominant in RA, or inhibit interleukin-1 (IL-1).

(2) Etanercept (Enbrel®)(50 mg weekly), anakinra (Kineret®) (100 mg qd; same dose qod for patients with severe kidney disease), adalimumab (Humira®) (40 mg every other week) given by subcutaneous injection.

(3) Infliximab (Remicade®) is dosed by body weight (3 mg/kg for RA, 5 mg/kg for psoriatic arthritis [PA], ankylosing spondylitis [AS] by IV injection); for RA and PA, initial dose repeated at 2 and 6 weeks, then once every 8 weeks thereafter; patient taking infliximab for RA also should be taking oral methotrexate.

d. Nonsteroidal anti-inflammatory drugs (NSAIDs) and salicylates help relieve pain, inflammation; should be used in conjunction with DMARD or BRM to manage symptoms but have no effect on disease progression.

(1) Salicylates: aspirin, choline magnesium salicylate (Trilisate®), choline salicylate (Arthropan®).

(2) Traditional NSAIDs: ibuprofen, naproxen.

(3) COX-2 inhibitor: celecoxib (Celebrex®) may be prescribed for patients with GI side effects from traditional NSAIDs.

e. Corticosteroids: used in varying doses to decrease damaging inflammation; should not be a mainstay of RA treatment.

2. Osteoarthritis.

a. Analgesics and NSAIDs.

(1) Acetaminophen recommended by American College of Rheumatology as the initial drug of choice for OA pain (up to 1000 mg four times daily).

(2) If acetaminophen is ineffective, treatment with low-dose OTC NSAID (ibuprofen up to 400 mg four times daily) recommended for patients with normal renal function, no history of GI disorder. Prescriptive doses may be indicated if pain persists.

(3) COX-2 inhibitors may be prescribed for patients at risk for GI complaint with traditional NSAIDs.

(4) Salicylates also may be prescribed for OA treatment.

b. Viscosupplementation.

(1) Two available products (sodium hyaluronate [Hyalgan®], hylan G-F 20 [Synvisc®]) for knee OA are believed to work as lubricants by supplementing hyaluronic acid, substance that gives synovial fluid its viscosity.

(2) Given by intra-articular injection (series of five shots for Hyalgan, three shots for Synvisc).

(3) May have anti-inflammatory effect but has not been shown to alter progression of OA or stimulate cartilage regrowth.

c. Corticosteroid therapy.

(1) Systemic corticosteroids not indicated in OA because of side effects.

(2) Intra-articular injections often used to treat inflamed joints; successive injections should be separated by 3-4 months because of possible damage to intra-articular structures by residual corticosteroid crystals.

d. Topical analgesics can provide some pain relief (capsaicin cream [Zostrix®]) but require several applications daily for effects.

D. Surgical treatment of joint disease (see Chapter 11).

1. Synovectomy: removal of synovial membrane in affected joints; palliative treatment for severe RA that decreases risk of joint flare-ups, tendon rupture.

2. Tenosynovectomy: removal of tendon sheath.

3. Autologous cartilage implantation: graft of cultured chondrocytes used to treat cartilage defects in knee OA.

4. Arthrodesis: fusion of joint to provide stability or relieve pain; sometimes performed after failed joint arthroplasty.

a. Bone ends fixed together by hardware (screws, pins, plates, nails).

b. Bone grafts used when fusing larger, more difficult joints, such as hips and ankles.

5. Osteotomy: removal of wedge of bone to correct deformity, relieve pain. High tibial osteotomy (wedge osteotomy) often performed on younger patients with unicompartmental knee OA; joint arthroplasty is recommended for treatment of advanced disease.

6. Arthroplasty: diseased joints are resected and replaced, either in part (hemiarthroplasty; unicompartmental knee arthroplasty) or in whole (total joint arthroplasty). Hips (THA), knees (TKA), ankles, elbows, and shoulders are common sites for arthroplasty.

a. Used when conservative treatment or previous surgery has failed to manage patient’s symptoms and allow adequate function.

b. Unicompartmental knee arthroplasty (UKA) indicated for patient age 60 or older, not obese, relatively sedentary with intact anterior cruciate ligament, no significant inflammation, no calcification or damage to other joint compartments,

c. Implants (prostheses) for total joint arthroplasty (TJA) may be cemented (using polymethylmethacrylate) or cementless (porous-coated surface).

(1) Cemented prosthesis indicated for patient whose activities place minimal demand on joint; allows early weight-bearing.

(2) Cementless prosthesis indicated for very active patient who places greater demand on joint; weight-bearing restricted while bone grows into porous surface of prosthesis.

d. Additional postoperative care following TJA.

(1) TJA carries a risk for neurologic or vascular impairment.

(a) Neurovascular assessment should be completed at least every 4 hours or in accordance with institution policy; operative leg should be compared to baseline assessment and to nonoperative leg.

i. Bilateral pedal pulses.

ii. Capillary refill of toes.

iii. Skin color and temperature.

iv. Sensation and movement of toes.

(b) Any changes that suggest com­partment syndrome (see below) or other neurovascular impairment should be reported immediately to surgeon.

(2) If wound drain placed by surgeon, output must be measured and monitored.

(a) Passive drainage (Hemovac®).

(b) Autotransfusion of salvaged wound drainage (Autovac™, OrthoPAT®) in accordance with institution policy.

(3) Blood transfusion may be ordered based on intraoperative blood loss, postoperative hemoglobin and hematocrit.

(4) Early mobility.

(a) Any limitation in weight-bearing determined by surgeon order based on type of implant.

i. Following cementless TJA, patient is probably non-weight-bearing (NWB) or toe-touch weight-bearing (TTWB).

ii. Following cemented TJA, order may stipulate weight-bearing as tolerated (WBAT) or full weight-bearing (FWB).

(b) Physical therapy often starts with bed exercises (straight leg raises, ankle pumps) on day of surgery, with transfers and ambulation beginning first postoperative day to decrease risk of complications associated with immobility (deep vein thrombosis, pulmonary embolism, constipation, respiratory compromise, pressure ulcer development)

(c) Patient receives instruction in safe use of crutches or walker.

(d) Over-the-bed trapeze helps patient with bed mobility, transfers.

(5) Continuous passive motion (CPM) device may be ordered following TKA to decrease risk of postoperative stiffness, improve knee ROM.

(a) CPM apparatus slowly moves knee through flexion and extension, with settings based on surgeon preference, patient tolerance.

(b) ROM gradually increased, with general goal of 90 110 degrees flexion and -10 degree extention.

(c) To encourage extention while resting in bed, there should be a towel roll placed beneath the ankle.

(dc) CPM should be used at least 6-8 hours daily to maximize benefit of therapy.

(ed) If CPM is not ordered, postoperative physical therapy will include regular exercise for muscle strengthening, ROM.

(6) Cryotherapy (ice)- frequency and duration will differ based on facility protocol or physician preference, however, it is important for the decrease in inflammation and pain.

7. Complications: occur in approximately 25% of TJA patients over age 65.

a. Venous thromboembolism (deep vein thrombosis [DVT], pulmonary embolism [PE]): most common medical problem encountered after TJA.

(1) Incidence of DVT may exceed 55% following THA, 80% following TKA among patients who have not received prophylactic treatment; incidence of PE 20%-40%.

(2) Risk increased following TJA because of venous stasis, vessel injury, hypercoagulability (Virchow’s triad).

(3) Prevention strategies.

(a) Early mobilization.

(b) Anticoagulant therapy typically initiated within 24 hours after surgery (see Chapter 11: Perioperative Care) and continued for approximately 4 weeks post operative.

(c) Intermittent pneumatic compression, antiembolic stockings (see Chapter 11: Perioperative Care).

(d) Ankle exercises (calf pumps): dorsiflexion, plantarflexion of ankle to contract calf muscle, increase venous blood return from the extremities; should be done every 1-2 hours when patient is in bed.

b. Compartment syndrome:is a medical emergency in which high pressure occurs in a muscle compartment in closed fascial space related to swelling; can occur within 6-8 hours after surgery, or may take up to 2 days to manifest. Result is decreased circulation.

(1) Primary symptom is increasing pain or pain out of proportion to injury.

(a) Occurs as early indicator of tissue compromise, should be recognized as “red flag.”

(b) Attention should be paid to patient who continues to complain of pain after receiving analgesics, or who states that pain is worsening.

(2) Patient also may report paresthesia (“pins and needles”).

(3) Later signs include diminished pulses, pallor, paresis (weakness).

(4) Treatment.

(a) Relieve pressure by removing tight stockings or loosening dressings.

(b) Keep affected extremity at heart level; elevation further compromises blood flow.

(c) Fasciotomy may be needed if symptoms persist due to unrelieved pressure.

c. Infection: occurs in 1% or less TJAs.

(1) Early infection can be either superficial or deep; early deep infection results from contamination at time of surgery.

(2) Late infection appears to occur from hematogenous seeding; presence of increasing joint pain may indicate delayed, deep infection.

(3) Prophylactic antibiotics routinely administered, with first dose given shortly before surgical incision is made; dosing continues for 24 hours postoperatively.

d. Dislocation.

(1) Joint remains unstable following THA until surrounding soft tissue heals.

(2) Patient must be reminded to observe activity precautions, which vary slightly based on the surgical approach.

(a) Posterior approach.

i. No hip flexion beyond 90 degrees.

ii. No internal rotation of operative hip.

iii. No crossing operative leg past body’s midline; maintain legs in abduction with wedge or pillow; assess peroneal nerve function of patient strapped into abductor wedge.

(b) Anterior approach.

i. Avoid active abduction, maintaining legs side-by-side without wedge or pillow between them.

ii. No external rotation of operative hip.

iii. No backward extension of operative hip.

e. Joint instability and loosening

(1) Prosthesis failure may lead to joint instability, increased tendency to dislocate.

(2) Loosening may occur at bone-cement interface, possibly related to mechanical stresses placed on joint.

(3) Progressive joint instability leads to patient complaints of increasing pain.

II. Spinal Disorders

A. Scoliosis.

1. Definition: lateral curvature of spine with vertebral rotation.

2. Pathophysiology.

a. Curve may occur in any area of spine: cervical, thoracic, thoracolumbar, lumbar.

b. Most common curvature is right thoracic pattern.

(1) As spine curves, vertebral column rotates around its long axis.

(2) Ribs become prominent on convex side.

c. Lumbar curve is usually a left curve. Curvature produces asymmetric waistline.

3. Etiology.

a. No known causes for idiopathic scoliosis.

b. Congenital scoliosis results from malformation of vertebral structures.

c. Spinal curvature of paralytic scoliosis results from various myopathies (polio, muscular dystrophy, cerebral palsy, spina bifida).

d. Scoliosis also can occur as result of neurofibromatosis, trauma/radiation, nerve root irritation (sciatic).

e. Leg length discrepancy can cause functional scoliosis.

4. Clinical manifestations.

a. Affected adult may complain of fatigue, back pain, shortness of breath depending on location of curvature.

(1) Cor pulmonale (right ventricle hypertrophy related to compromise of the lungs attributed to chest deformity) may result from severe thoracic scoliosis.

(2) Pain, numbness, tingling require further evaluation.

b. Patient notices difficulty in fitting clothes.

(1) Asymmetric waistline or prominent hip.

(2) Asymmetry in level of shoulders.

5. Diagnosis.

a. Use of scoliometer at apex of curvature will quantify prominence.

b. Initial x-rays should be taken of patient with positive assessment; follow-up x-rays when progression is suspected.

(1) X-rays taken posterior to anterior (PA) to minimize x-ray exposure to thyroid, breasts, and reproductive organs.

(2) Standing lateral view of spine also common; side bending view generally only required for preoperative planning.

c. While not used for diagnosis of scoliosis, pulmonary function tests (PFTs) are performed on patients with thoracic curves greater than 65 degrees.

6. Common therapeutic modalities.

a. Curves of 15-20 degrees are observed for progression; many curves never go beyond this point.

b. Postural exercises may be prescribed, but no data support theory that exercise can correct or prevent scoliosis.

c. Young adults (20-40 years of age).

(1) Curves < 40 degrees generally remain stable; patient is asymptomatic, no treatment required.

(2) Curves > 40 degrees may demonstrate progression but patient may remain asymptomatic; surgery may be required if progression is documented.

d. Adults (40 years or older).

(1) Curves < 40 degrees: same as young adults.

(2) Progressive curve in thoracic or lumbar spine may require surgery.

e. Surgery generally recommended for curves > 40 degrees.

(1) Anterior spinal fusion.

(2) Combined anterior and posterior surgery recommended for adults with severe curvature.

7. Complications: flatback syndrome related to poor spinal alignment after surgery (especially with placement of Harrington rods extending to lumbar spine); osteoporosis and degenenerative scoliosis; spinal cord/nerve damage or respiratory dysfunction from severe, uncorrected curve.

8. Continued care and rehabilitation: patient and family education.

a. Limitations, impact of treatments.

b. Value of participation in support group.

B. Low back pain (LBP).

1. Definition: pain in lumbar region of back; lumbar area is flexible, bears most of body’s weight, has nerve roots.

2. Pathophysiology.

a. Most common cause is mechanical strain of paravertebral muscles; pain may be related to single traumatic event but also can occur as result of excessive microtraumas.

b. Herniation often leads to LBP.

(1) Annulus fibrosis: fibrocartilaginous layer of disc weakens, cracks, becomes unable to contain disc material (nucleus pulposus).

(2) Bulging central disc material puts pressure on neural structures.

c. Spondylolysis: defect or break in pars interarticularis (arch between superior and inferior articulating surfaces of vertebrae); most often occurs at L4-L5 or L5-S1 vertebrae.

d. Spondylolisthesis: forward slippage of one vertebra over another; most often occurs at L4-L5 or L5-S1 but can occur at any level of spine.

e. Spinal stenosis: narrowing of spinal canal; can occur at any level in spine but most commonly seen in lower cervical or lumbar segments; gradual shift in spinal alignment (kyphosis, lordosis) also can exacerbate stenosis.

f. Degenerative disc disease: degeneration of intervertebral cartilage over time; thought to be normal variant of aging unless accompanied by back pain.

3. Etiology.

a. Trauma, repetitive stress, degenerative disorders can lead to LBP.

(1) Controversy exists with some complaints of LBP because diagnosis is often made when patient becomes symptomatic after motor vehicle accident or work-related accident.

(2) Symptoms, pain in these situations thought to be aggravation of pre-existing condition.

b. With spondylolysis, defect may be genetic; patient may remain asymptomatic until activity (such as involvement in wrestling or gymnastics) leads to hyperextension stress.

c. Incidence.

(1) Third most common disorder discussed with health care providers (after headache, fatigue).

(2) At any point in time, 10% of adults have experienced activity restrictions related to LBP in preceding 4 weeks.

(a) Approximately 50% of incidents of LBP resolve within 1 week, but recurrences are very common.

(b) Work loss related to LBP among employed adults is 20% annually.

4. Clinical manifestations.

a. Chief complaint is probably pain.

(1) Symptoms can occur following specific traumatic event, or patient may describe long history of progressively worsening pain.

(2) With lumbar herniation, pain often aggravated by activities that increase pressure in affected area (standing, walking, bending, coughing, sneezing).

(3) With spondylolysis and spondylolisthesis, pain may radiate to lower leg; patient also may develop slow or waddling gait.

(4) Patient with spinal stenosis likely to describe gradual onset of pain, increased with standing or walking and decreased with sitting.

b. Changes in affected dermatome may lead to diminished muscle strength, difficulty with heel or toe walking, sensory deficits in lower extremities.

c. Bowel or bladder dysfunction related to any lower back disorder requires emergent evaluation, treatment.

5. Diagnosis.

a. Most patients with LBP do not need radiographic evaluation: can be diagnosed with structured physical examination.

b. Reliable diagnostic tools should be used to evaluate any patient who describes trauma or strenuous lifting, bladder dysfunction, severe or progressive neurologic deficits in lower extremities.

c. Spine x-rays rule out any concomitant cause of LBP, reveal changes typical of each lower back disorder.

d. MRI is diagnostic tool of choice to demonstrate nerve root compromise related to disc herniation; myelograms have been largely replaced by MRI.

e. CT with contrast also can allow visualization of nerve roots and subarachnoid space, but invasiveness of exam has made it less popular than MRI.

6. Common therapeutic modalities.

a. Conservative treatment indicated if pain is not severe.

(1) Pharmacologic interventions.

(a) Analgesics are mainstay of treatment (acetaminophen, NSAIDs).

(b) Muscle relaxants effective in early stages of acute LBP.

(c) Use of epidural steroid injections common in treatment of LBP but remains controversial because of conflicting evidence about efficacy.

(2) Physical therapy.

(a) Stretching, strengthening, flexibility exercises.

(b) Ultrasound, heat, and/or ice as adjunct to exercise program.

(c) Transcutaneous electrical nerve stimulation (TENS).

(d) Corsets, spinal orthoses.

(e) Traction was once popular but has been shown to have little benefit.

(3) Alternative therapies (acupuncture) continue to be investigated as possible treatments for LBP.

b. Surgical interventions may be needed if conservative treatment becomes ineffective (see Chapter 11).

(1) Percutaneous disc excision: posterior vacuum removal of disk material via scope; not indicated for extruded discs.

(2) Interdiscal electrothermal annuloplasty: catheter and thermal coil are placed directly into disc, and heat introduced to shrink nucleus pulposus and seal outer layer of annulus; more research is needed to assure efficacy of this treatment.

(3) Decompression: posterior decompression recommended if neural contents compressed due to spinal stenosis; laminectomy alone may be adequate but further lateral decompression may be needed depending on location of defect.

(4) Laminectomy: most common procedure for lumbar disc disease; involves excision of part of posterior arch of vertebra with disc excision; removing only necessary bone is important to help maintain structural stability.

(5) Spinal fusion: performed if there is unstable bony mechanism present; spine is stabilized by fusion of vertebrae with bone graft from iliac crest, tibia, or resected rib; when anterior/posterior fusion may be performed, anterior fusion is usually performed first.

(a) Bone graft may be allograft (cadaver bone) but fuses slower.

(b) Hardware may be needed as an adjunct to help immobilize spine.

(c) Postoperative care.

i. Proper alignment of spine postoperatively (logroll, position with pillows); elevation of head may be contraindicated.

ii. Perform regular neurologic assessment to include muscle strength, mobility of all extremities (plantarflexion, dorsiflexion, inversion, eversion of lower extremities), response to painful stimuli.

(6) Postoperative complications: spinal cord injury, cauda equina, dural tear, thromboembolism, infection, failure to resolve complaint.

7. Continued care and rehabilitation: patient and family education.

a. Avoid low, overstuffed chairs.

b. Avoid standing for long periods of time; alternate weight between feet when standing.

c. No twisting, bending, lifting heavy objects.

d. Use firm mattress.

e. Use brace if indicated.

f. Modify home environment to meet restrictions.

C. Spinal fractures.

1. Pathophysiology.

a. Flexion: in minor injuries, posterior ligaments remain intact and cause wedge fracture of vertebra; severe injuries are considered unstable, associated with posterior ligamentous damage; spinous processes are separated and kyphotic angulation is noted.

b. Flexion/rotation: fracture/dislocation of spine with stretched or torn posterior ligament; separation of spinous processes occurs; unstable when located in thoracic and lumbar spine, usually associated with paraplegia.

c. Axial loading (burst): anterior and posterior ligaments usually intact; if fracture fragment impinges on spinal canal, it may cause quadriplegia (cervical spine) or paraplegia (lumbar spine).

d. Compression: most often due to disease process that leads to weakened vertebra; occurs with or without cord compression; most compression fractures are stable.

2. Incidence.

a. Affects all ages.

(1) Adults suffer more vertebral fractures than children.

(2) Child abuse, motor vehicle accidents, sports (diving, surfing, skiing) are common causes of paraplegia in children, adolescents, young adults.

b. Compression fractures usually in mid-lumbar region.

3. Etiology.

a. Trauma: diving accidents, automobile accidents, falls, blows to head.

b. Nontraumatic: osteoporosis, multiple myeloma, bone cancer (sarcomas, primary and metastatic lesions).

4. Diagnosis by x-ray, CT scan, MRI, myelogram, tomogram.

5. Common therapeutic modalities.

a. Nonsurgical.

(1) Cervical spine: skeletal traction.

(2) Thoracic spine: body cast.

(3) Lumbar spine: bed rest, corset, brace.

b. Surgical: unstable fractures require open reduction, internal fixation.

6. Complications.

a. Pain, progressive deformity related to displacement.

b. Impaired bowel, bladder function.

c. Paraplegia (injury below C8).

d. Quadriplegia (injury above C8).

e. Temporary symptoms may be related to cord contusions or concussion; may resolve in 24 hours or several days.

f. Long-term complications include chronic urinary tract infections, pressure ulcers, joint contractures, GI bleeding, sexual dysfunction (highly variable, depending on location, degree of injury).

7. Continued care and rehabilitation: assist patient and family to understand, have realistic expectations regarding prognosis, course of recovery.

III. Trauma

A. Overview.

1. A physical injury or wound caused by an external force or violence.

2. In the United States trauma is the principal cause of death of individuals ages 1-38.

3. Patients who sustain polytrauma are at increased risk to suffer a musculoskeletal injury.

4. Preventive measures.

a. Proper use of motor vehicle safety devices (seatbelts, motorcycle helmets, airbags) and education.

b. Proper use of sports and recreational safety devices (helmets, face guards).

c. Gun safety.

d. Home safety evaluation (especially for older adults) to reduce the risk of falls.

B. Fractures.

1. Definition: any disruption of continuity of bone, whether complete or incomplete. Multiple classification methods used to describe fractures (see Table 22-5).

a. Closed fracture has intact skin over site of injury; open fracture has break in skin over fracture site.

b. By fracture pattern or appearance.

c. By general description.

d. By anatomic location.

e. By eponym (named after first person to identify specific fracture).

2. Pathophysiology.

a. Fractures occur when bone is subject to more stress than it can absorb.

(1) Direct force: moving object directly contacts area over bone.

(2) Indirect force: powerful muscle contraction pulls on bone.

b. Amount of force required to cause fracture varies, depending on factors that predispose patient to injury.

(1) Osteopenia, osteoporosis.

(2) Cushing’s syndrome.

(3) Malnutrition, anorexia.

(4) Neoplasm.

(5) Osteogenesis imperfecta.

(6) Medication use (corticosteroids).

(7) Behavioral factors (curiosity, risk-taking).

(8) Violence (child or elder abuse).

3. Incidence: can occur at any age, including in utero.

4. Bone healing.

a. Fracture occurs and disrupts integrity of vascular system.

b. Hematoma formation at fracture site (stage I; occurs in first 3 days after injury).

c. Granular tissue (fibrocartilage) formation (stage II; occurs 3 days to 2 weeks after injury).

d. Callus formation as granulation tissue matures (stage III; occurs 2-6 weeks after injury).

e. Ossification results from union among fracture fragments (stage IV; occurs 3 weeks to 6 months after injury).

f. Consolidation and remodeling: bone is shaped to meet its mechanical demands (stage V; occurs 6 weeks to 1 year after injury).

5. Clinical manifestations.

a. Acute pain at time of injury followed by point tenderness, increased pain with movement.

b. Uncomfortable muscle spasms, sensations indicative of nerve involvement (paresthesia).

c. Swelling, ecchymosis at fracture site.

d. Change in length, shape, alignment, stability, or mobility of the affected bone.

e. Crepitus with inadvertent movement of fracture fragments.

6. Diagnosis by radiologic studies; arthroscopy in joint injuries. Additional studies to assess complications of injury (urine for occult blood following pelvic fracture).

7. Common therapeutic modalities.

a. Initial immobilization of injured area with splints, bandages, and/or supportive devices.

b. Realignment of fracture fragments.

(1) Closed reduction: alignment of bone fragments by manual manipulation or traction without surgical intervention.

(2) Open reduction: surgical alignment of fracture fragments.

(3) Internal fixation: immobilization of fracture fragments during surgery (open reduction) using pins, wires, screws, rods, nails, other types of hardware.

(4) External fixation: immobilization of fracture fragments with external frame; used to treat fracture with soft tissue damage, when use of a cast is precluded. Also used for limb length discrepancy, stabilization of arthrodesis.

c. Immobilization of realigned fragments with casts, traction (skin or skeletal), splint; more than one method may be used.

(1) Casts.

(a) Casting materials.

i. Plaster of Paris indicated for severely displaced fractures, or when multiple cast changes are expected; usually heavier than synthetic cast materials.

ii. Synthetic materials are lightweight, strong, durable; harden and dry rapidly; indicated for nondisplaced, closed fractures and long-term casting.

iii. Removable casts.

(b) Nursing care.

i. New cast is left open to air to dry (plaster may take 48-72 hours, synthetic cast often dries within 30 minutes); touched with palms of hands only while drying to avoid indentations that can create pressure points under the cast.

ii. Involved extremity should be elevated (“hands above the heart, toes above the nose”).

iii. Neurovascular assessment performed regularly for early detection of compromise (cast or compartment syndrome).

iv. Cast monitored for drainage, odor, warmth, soft spots.

v. Patient instructed not to place foreign objects inside the cast (coat hanger to scratch). For itching, the patient can try blowing cool air down cast or tapping over itching spot.

vi. Patient with body cast should be monitored for respiratory or cardiac distress.

(c) Bivalving or windowing a cast.

i. Cast may need to be cut to relieve pressure of swelling.

ii. Windowing: specific area cut out to permit inspection of skin or incision, remove sutures or staples, or relieve pressure.

(d) Complications.

i. Infection (see below).

ii. Compartment syndrome (see Complications of TJA).

(2) Traction: pulling force is applied to injured body part or extremity while a countertraction pulls in the opposite direction. Purposes are to reduce fracture, maintain alignment, decrease muscle spasm, relieve pain, correct or prevent deformities, promote rest.

(a) Manual traction: use of hands to exert pulling force.

(b) Skin traction: application of pulling force directly to skin through use of foam splints, boots, traction strips. Only appropriate for light weights (5-7 pounds) because of risk of skin breakdown. May help in relief of muscle spasms associated with fracture.

(c) Skeletal traction: pulling force applied directly to bone, allowing traction to be tolerated for longer periods of time. Stainless steel pins (Kirschner wires or Steinman pins) inserted through the bone under strict aseptic conditions. Weight may reach 10-40 pounds, depending on injury, pathology.

(d) Nursing care.

i. Countertraction must be provided, using patient’s body and bed positioning.

ii. Friction should be prevented by not tucking linens, not allowing foot-plate to rest against the bed.

iii. Weights should move freely through pulleys and line of pull should be maintained.

iv. Skin should be assessed regularly, kept clean and dry; no powder, lotion, or creams.

v. Pin care per facility policy for skeletal traction.

vi. Regular neurovascular assessment.

vii. Patient should be taught ROM exercises.

(e) Complications.

i. Neurovascular impairment.

ii. Inadequate alignment of fracture fragments.

iii. Skin traction: skin breakdown, post-treatment arthritis.

iv. Skeletal traction: pin tract infection, osteomyelitis, muscle or nerve weakness, pressure ulcers.

(3) Braces/splints.

(a) Used for maintenance of position, facilitation of movement, correction of deformities, control of involuntary muscle movement, and maintenance of surgical correction.

(b) An individualized treatment.

(c) Examples: knee immobilizers, thoracolumbosacral orthosis (TLSO) for scoliosis, short or long leg braces.

(d) Improperly applied or fitting braces may worsen deformity.

8. Complications.

a. Venous thromboembolism (VTE or DVT) (see complications of TJA).

b. Fat embolism syndrome (FES): presence of fat globules that deposit in bloodstream and move into pulmonary circulation.

(1) Associated with fractures of long bones, especially with multiple long bone fractures or concomitant pelvic fracture.

(2) Incidence is approximately 2% for single long bone fractures, 5%-10% in multiple fractures.

(3) Manifestations.

(a) Severe hypoxemia is hallmark sign; crackles and coarseness heard on auscultation of lungs.

i. First symptoms noted are restlessness, anxiety, disorientation secondary to poor gas exchange.

ii. Approximately 10% of patients develop respiratory failure requiring intubation, mechanical ventilation.

(b) Tachycardia, tachypnea, pyrexia consistently seen.

(c) Petechiae on upper chest, axilla, neck occur in 50%-60% of patients and occur within 24-48 hours.

(4) Diagnosis: arterial blood gases indicate respiratory alkalosis as early indicator of FES; sudden fall in hematocrit has been associated with hemorrhage into lungs.

(5) Treatment.

(a) Prevention is first aim of treatment — careful handling, avoidance of unnecessary manipulation of affected extremity; adequate splinting, early immobilization.

(b) Early aggressive resuscitation to prevent hypovolemic shock.

(c) Adequate analgesia.

(d) Administration of blood products.

(e) Use of corticosteroids to prevent FES remains controversial.

c. Post-traumatic arthritis: related to severity of trauma and effectiveness of reduction on weight-bearing joints.

d. Myositis ossificans: formation of abnormal bone as result of trauma.

e. Nonunion/malunion: failure of fracture to heal, or incomplete healing after 4-6 months.

(1) Most common in tibia and fibula.

(2) Treated by bone grafting, internal or external fixation, electrical bone stimulation.

f. Hemorrhage: related to pelvic fracture (can be life-threatening).

9. Continued care and rehabilitation.

a. Patient with cast.

(1) Signs and symptoms of complications: severe pain, burning, numbness, tingling, skin discoloration, swelling, paralysis, foul odor, elevated temperature, pallor/coolness of fingers or toes.

(2) Elevation of extremity.

(3) Skin care, activity level, sexual activity.

(4) General care: keep plaster cast dry; do not drop utensils down cast; keep clean.

(5) Pain management.

(6) Weight-bearing restrictions; use of ambulatory aids.

b. Patient in traction.

(1) Application/removal of skin traction if permitted.

(2) Signs/symptoms of complications.

(3) Skin and neurovascular assessment.

(4) Pin care.

(5) Pain management.

c. Patient in external fixator: percutaneous fixation of fracture via pins attached to a fixed external frame. Reduces the risks associated with immobilization and casting.

(1) Application and use of CPM machine if ordered.

(2) Signs and symptoms of complications: joint swelling, redness, tenderness; unusual pain.

(3) Pain management.

(4) Weight-bearing restrictions; use of ambulatory aids.

(5) Skin and neurovascular assessment.

(6) Pin care.

C. Sprains.

1. Definition: a traumatic joint injury in which fibers of surrounding ligament have been damaged by excessive stretching or exertion.

2. Pathophysiology.

a. Mechanism of injury for upper extremity sprain.

(1) Participation in sports activity.

(2) Overstressing joint while working or exercising.

(3) Trying to break a fall.

(4) Bracing self during impact in a motor vehicle accident.

b. Mechanism of injury for lower extremity sprain.

(1) Ankle: stepping on uneven surface, causing inversion or eversion of joint.

(2) Knee: sports injuries, motor vehicle accident, stepping on uneven surface.

c. Cervical: rear-end motor vehicle collisions.

3. Etiology: usually sudden, twisting injury or forcible hyperextension of the joint.

4. Clinical manifestations: depend on degree of injury.

a. classification : grades 1-3

(1) Grade 1: mild damage or over stretching results in mild pain and edema. No joint laxity.

(2) Grade 2: an increase in level of pain, tenderness and edema with noted ecchymosis. Some joint laxity is observed.

(3) Grade 3: severe pain, unale to bear weight, significant edema, complete laxity of the joint.

5. Diagnosis: x-ray important to rule out avulsion fracture, shows edema without bone injury or displacement.

6. Common therapeutic modalities.

a. RICE (rest, ice, compression, elevation).

b. Immediate treatment involves elevation, immobilization of affected joint, followed by application of ice; subsequent treatment depends on severity of injury.

D. Strains.

1. Definition: damage of muscle body or tendinous attachment from overstretching, misuse, or overexertion.

2. Pathophysiology.

a. Acute.

(1) First degree: mild stretching of muscle or tendon.

(2) Second degree: moderate stretching and/or tearing of muscle or tendon.

(3) Third degree: severe muscle or tendon stretching in which affected tissue is ruptured, torn completely through, or pulled away from bone.

b. Chronic.

(1) Mildly to moderately overstretched muscle or tendon that causes symptoms for prolonged period of time.

(2) Most often results from improper care of an acute strain, or repeated use of muscle beyond its normal capacity.

3. Etiology: overexertion or use beyond usual capacity.

4. Clinical manifestations.

a. First degree: no swelling or bruising; tenderness upon palpation, possible muscle spasm; no loss of ROM.

b. Second degree: swelling immediately after injury, bruising hours to days later; extreme muscle spasm likely; passive motion results in increased discomfort.

c. Third degree: muscle spasm with point tenderness; delayed bruising; edema noted; contracting muscle unable to produce motion; may note muscle bulge above palpable defect.

5. Diagnosis: x-ray to rule out avulsion fracture.

6. Common therapeutic modalities.

a. RICE.

b. Subsequent treatment depends on severity of injury.

E. Dislocations and subluxations.

1. Definition: displacement of bone from its normal position.

2. Pathophysiology.

a. Dislocation: articulating surfaces of joint completely lose contact.

b. Subluxation: articulating surfaces of joint partially lose contact.

3. Etiology: force applied to joint directly or indirectly.

a. Dislocations in upper extremity commonly due to direct blow or indirect force (fall on outstretched arm).

b. Dislocations of knee generally caused by severe twisting or blow to knee (result of motor vehicle accident).

(1) Anterior dislocation of knee is most common lower extremity dislocation; orthopaedic emergency because of associated vascular and neurologic injuries.

c. Posterior dislocation of hip frequently due to fall or dashboard injury.

4. Clinical manifestations: pain, deformity, loss of function.

5. Diagnosis by x-ray, with views of unaffected joint also taken; arteriogram or Doppler ultrasound for suspected vascular injuries with knee dislocation.

6. Collaborative treatment.

a. Closed reduction.

b. Subsequent immobilization depends on joint affected.

(1) Shoulder: commercial immobilizer or sling and swathe.

(2) Wrist: casting possible.

(3) Finger: dorsal splint in 30 degrees of flexion.

(4) Knee: posterior splint in 15 degrees of flexion to avoid tension on popliteal artery; external fixation if vascular repair is done.

(5) Hip: traction, abduction brace, or hip spica cast for posterior dislocation; hip brace or spica cast for anterior dislocation.

c. Regular neurovascular assessment.

IV. Infection – Osteomyelitis

A. Definition: pyrogenic infection of bone, surrounding tissue; considered an orthopaedic emergency because delayed or inadequate treatment can lead to chronic infection.

B. Pathophysiology.

1. Infecting organisms invade bone in one of three ways.

a. Through bloodstream from another site of infection (hematogenous).

b. By extension from adjacent soft tissue infection (contiguous focus).

c. By direct introduction to bone (trauma or surgery).

2. Bacteria generally become trapped in metaphyses of more vascular bones.

a. Staphylococcus aureus is most common causative organism in both acute and chronic infection.

b. S. epidermidis, Pseudomonas aeruginosa, Serratia marcescens, and Escherichia coli also can cause chronic infection.

3. Body’s inflammatory, immunologic responses lead to pus formation, edema, vascular congestion.

a. Without treatment, pus continues to collect and increasing pressure within bone leads to vascular occlusion, ischemia.

b. Pus spreads to other areas of bone via Volkman and Haversian canals, creating even more pressure and causing further vascular compromise.

4. If initial treatment is delayed or inadequate, necrotic bone separates from living bone to form segments (sequestra) that provide medium for additional bacterial growth.

a. During chronic infection, sequestra continue to enlarge, may extrude through bone into surrounding soft tissue.

b. Osteoblasts attempt to isolate necrotic fragments by forming new layer of bone (involucrum) around them; involucrum interferes with ability of antibiotics to reach area of infection.

c. If infection reaches outer layer of bone, soft tissue abscesses and cutaneous sinus tracts can develop.

5. Areas of severe cortical bone damage are prone to fracture.

C. Incidence.

1. Children under age 12 commonly affected.

2. Males have higher incidence than females because of higher incidence of blunt trauma.

3. Improved diagnosis, advanced antibiotics have decreased complication rate to 5%; mortality rate is negligible.

D. Etiology.

1. Even minor illness or trauma (a small cut) can allow bacteria to enter bloodstream.

a. In children, single organism usually enters blood from distant site of infection.

b. Urinary tract and upper respiratory infections are common sources of bacteria in adults.

2. Osteomyelitis secondary to soft tissue infection (pressure sore, burn) is primarily a disease of adults.

E. Clinical manifestations.

1. Symptoms may vary depending on site of involvement.

2. Localized acute pain and tenderness, swelling and warmth, restricted movement of affected bone.

3. Fever.

F. Diagnosis.

1. Preliminary diagnosis made based on patient history, initial physical examination; if osteomyelitis is suspected, antibiotic treatment should be initiated before definitive diagnosis is verified by laboratory studies.

2. Routine laboratory tests in diagnostic phase.

a. CBC (marked leukocytosis may be present in child but absent in adult; low hemoglobin, WBC count may result from bacterial toxins).

b. ESR (elevation indicates presence of inflammatory process).

3. Definitive diagnosis requires isolation of causative organism.

a. Gram stain provides initial information about organism’s identity.

b. Blood cultures, wound cultures (aerobic and anaerobic).

c. Superficial cultures of open wounds, skin ulcers, cutaneous tracts are usually polymicrobial and unreliable indicators of deep bone infection.

d. Needle aspiration or open bone biopsy provides specimen for culture and sensitivity testing.

4. Radiographic evidence lags behind symptoms and pathologic changes by 7-10 days.

a. Standard x-rays do not show evidence of infection for 3-4 weeks because 30%-50% of bone matrix must be lost to show lesion on films; initial x-rays serve to rule out fracture.

b. Bone scans are more efficient in early diagnosis of acute osteomyelitis, reveal increased uptake when symptoms begin.

G. Common therapeutic modalities.

1. Osteomyelitis may be more difficult to treat when occurring concomitantly with other diseases that reduce body’s ability to fight infection (malnutrition, alcoholism, AIDS, sickle cell anemia, renal or hepatic failure).

2. Antibiotics.

a. After cultures have been obtained, long course of parenterally administered semisynthetic penicillin or vancomycin is approach of choice; oral rifampicin in combination with quinolones may be effective for susceptible organisms to avoid extended hospitalization.

b. Antibiotic regimen may be revised when results of culture are known.

c. Antibiotic-impregnated implants may be used as an alternative to parenteral delivery; beads of polymethylmethacrylate (PMMA) or hydroxyapatite blocks are being used in treatment of chronic infection.

3. Surgical debridement often becomes necessary in chronic infection to remove all infected material, surrounding scar tissue, and to restore adequate blood flow to area; appropriate antibiotic therapy should continue concomitantly with surgical intervention.

4. Physical therapy provides ROM and other exercises to mobilize unaffected joints; if approved by physician, passive ROM on affected joints to decrease risk of contracture.

H. Complications: related to tenacity of organism, side effects of antibiotics, recurrence of infection.

1. Chronic or recurrent infection may affect patient’s role performance as family wage earner.

2. Resistant infection has led to need for amputation and additional treatment in long-term care facility.

I. Continued care and rehabilitation.

1. Patient and family education.

a. Importance of completing course of medications.

b. Handwashing to prevent spread of infection.

c. Wound and pin care.

2. Pain management.

V. Metabolic Bone Disease: Osteoporosis

A. Definition: common metabolic bone disease characterized by severe reduction of bone mass, subsequent susceptibility to fractures.

B. Pathophysiology.

1. Disturbance occurs in normal balance between osteoblastic (bone building) and osteoclastic (bone resorbing) activity.

2. Increased bone resorption leads to diminished mineral, protein components in bony matrix; decreased bone mineral density results.

C. Incidence.

1. 44 million men and women have osteoporosis or low bone mineral density.

2. As many as 70% of women over age 80 have osteoporosis.

3. Less is known about osteoporosis in men, who present unique challenges in screening, diagnosis, treatment (see Table 22-6 for significant risk factors).

D. Etiology.

1. Specific cause not known but multiple risk factors identified (see Table 22-6).

2. Bone mineral density (BMD).

a. Two factors contribute to bone mass: bone mass achieved during young adulthood and rate of bone loss during late childhood or after menopause.

b. Optimal bone mass achieved by about age 30 in both men and women.

c. Effects of menopause.

(1) Between age 30 and menopause in women, BMD may plateau or even decrease slightly.

(2) Perimenopausal women may experience up to 15% loss in BMD due to decreasing amount of natural estrogen.

(3) Bone loss accelerates in 2 years before last menstrual period; rapid loss continues for another 2 years after end of menses.

(4) Rapid loss of BMD also can occur after surgical menopause (result of removal of ovaries).

d. Secondary osteoporosis.

(1) Results from other medical conditions such as Cushing’s syndrome (see Table 22-6).

(2) Bariatric surgery for weight reduction causes calcium malabsorption, can contribute to osteoporosis.

(3) Medications such as glucocorticoids, anticonvulsants, thyroid hormone, furosemide, antipsychotic medications.

E. Clinical manifestations.

1. Fractures often first complaint to bring patient with osteoporosis to health care provider.

a. Hip, vertebrae, distal radius most often affected after fall; vertebral compression fractures also common with osteoporosis.

b. Patient with osteoporosis especially prone to fragility fractures from low-trauma events such as sneezing or stooping to pick up newspaper.

c. High incidence of fractures in women is due to fact that they live about 1/3 of their lives after menopause.

d. Annual cost of fracture treatment in United States and Europe is estimated at $18 billion.

2. Progressive spinal deformity.

a. Marked kyphosis of thoracic spine (“dowager’s hump”) causes lower ribs to rest on iliac crests.

(1) Downward pressure on internal organs leads to restricted breathing, abdominal distention, bloating.

(2) Patient often complains of difficulty in finding clothes that fit.

b. Loss of height, muscle atrophy occur.

F. Diagnosis.

1. Standard x-ray does not reveal osteoporotic changes until about 30% of BMD is lost.

2. BMD measurement (see Tables 22-2, 22-7).

a. Dual energy x-ray absorptiometry (DEXA) is gold standard for diagnosis of osteoporosis; results are reported as a T score, the difference between patient’s BMD and that of young adult of same gender.

b. Peripheral DEXAs and quantitative ultrasound (QUS) are less expensive than full table evaluation but not yet adopted by World Health Organization as preferred diagnostic.

3. Diagnosis may include serum and urine markers of bone remodeling.

a. Osteocalcin is synthesized by osteoblasts, increased in conditions of rapid bone turnover.

b. Urinary alkaline phosphatase is a marker of bone resorption.

c. Markers do not indicate BMD or fracture risk.

G. Common therapeutic modalities.

1. Medications can be used to prevent osteoporosis if started before BMD loss occurs, or to treat confirmed disease.

a. Findings of increased incidence of breast cancer from the Women’s Health Initiative led to suggestion that risks and benefits be fully evaluated before prescribing estrogen with progestin.

(1) Estrogen has been shown to exacerbate some pre-existing conditions (gallbladder and hepatic disease, coagulopathy, hypertension); adverse effects have been reduced through use of transdermal system for drug delivery.

(2) Debate continues on use of estrogen in women with family history of breast cancer.

b. Androgen replacement is important for hypogonadal men.

c. Bisphosphonates have been approved for both prevention and treatment of osteoporosis.

(1) Alendronate sodium (Fosamax®), risedronate (Actonel®), and ibandronate (Boniva®) inhibit osteoclast-mediated bone resorption.

(2) Bisphosphonates are absorbed poorly from GI tract so patient teaching must include requirements for effective drug administration.

(a) Take with 6-8 oz plain water at least 30 minutes before first food, drink, or medication of the day.

(b) Remain upright for 30-60 minutes after taking dose.

(3) Concomitant use of alendronate and estrogen is not recommended currently because of lack of clinical evidence about any interaction.

d. Calcitonin acts partly by blocking effects of parathyroid hormone on bone resorption.

(1) Has been used for many years to treat osteoporosis in women, but evidence of its efficacy in men is insufficient.

(2) Available in parenteral or nasal spray only; patient education must include appropriate administration.

e. Selective estrogen receptor modulators (SERMs) maximize estrogen’s effect on bone while minimizing its effects on the breast and endometrium.

(1) Raloxifene (Evista®), only drug from this class approved for treatment of osteoporosis, has been shown to increase BMD in spine and femoral neck, and to decrease fracture risk.

(2) Raloxifene is taken once a day at any time, with or without food.

f. Parathyroid hormone is primary anabolic (bone-forming) agent.

(1) Teriparatide (Forteo®) is administered as daily 20 mcg injection for up to 18 months.

(2) Individuals with moderate-to-severe osteoporosis may be good candidates for treatment, but long-term effects unknown.

g. Calcium is not treatment for osteoporosis, but adequate calcium is important to bone health; supplementation with vitamin D may be necessary to maximize absorption for patient who does not get enough sun exposure.

h. Analgesics/NSAIDs for back pain of vertebral compression fractures.

2. Surgical treatment recommended for vertebral compression fractures that do not respond to rest or bracing.

a. Percutaneous vertebroplasty involves injection of acrylic polymer into vertebral body to correct its collapse.

b. Kyphoplasty is minimally invasive alternative in which a catheter is introduced into vertebral body and balloon is inflated to help restore vertebral height; space is injected with PMMA under lower pressure than traditional vertebroplasty.

H. Continued care and rehabilitation.

1. Appropriate exercises to optimize bone quality, minimize risk for injury.

2. Assessment of home environment with initiation of fall prevention strategies.

3. Use of mobility aids, assistive devices.

4. Pain management.

5. Dietary choices to support bone health.

6. Comfortable clothing, footwear that promote safety and positive self-image.

VI. Connective Tissue Disorders

A. Fibromyalgia syndrome (FS).

1. Definition: syndrome of chronic nonarticular musculoskeletal pain that is nonprogressive and noninflammatory, of unknown cause.

2. Pathophysiology.

a. Believed to be either inflammatory or psychiatric condition, but no current evidence supports either theory.

b. Loss of stage 4 non-REM sleep is believed to cause ineffective tissue restoration, pain modulation.

c. Abnormality in serotonin metabolism can alter perception of pain in affected tissues.

d. Some preliminary work suggests possible role for autoimmunity.

3. Incidence.

a. Occurs in 3-6 million Americans; 80%-90% of affected individuals are women.

b. Peak age of onset is 30-50 years.

c. Prevalence reported to be increasing, with FS currently second most commonly diagnosed musculoskeletal disorder; diagnosis especially increasing in older adults.

4. Etiology.

a. Multifactorial features of FS contribute to its unknown etiology.

b. Abnormalities of musculature have been suggested, but none have been reproduced fully or confirmed.

c. May coexist with other inflammatory diseases such as RA or systemic lupus erythematosus (SLE), chronic fatigue syndrome, or may overlap with myofascial pain syndrome.

5. Clinical manifestations.

a. Skin and soft tissue tenderness, especially in skin folds.

b. Point tenderness at 11 or more points, existence of which is not generally known by patient.

c. Patient complains of diffuse, burning pain that comes and goes during day; reports difficulty in determining if pain is in joints, muscles, or soft tissues.

d. Sleep deprivation likely, with extreme fatigue.

e. Patient may describe frequent absence from work due to pain and fatigue.

f. Numerous conditions can coexist with FS: restless legs syndrome, irritable bowel syndrome, migraine headaches, temporomandibular joint dysfunction, sicca syndrome (Sjögren’s syndrome).

6. Diagnosis.

a. Routine diagnostic studies reveal little or nothing about course and symptoms of FS.

b. Diagnostic studies are chosen in most cases to rule out differential diagnoses considered from history, physical examination.

c. Low antinuclear antibody (ANA) titer may be seen occasionally but is not considered diagnostic.

d. American College of Rheumatology (ACR) criteria assist in diagnosis (see Table 22-8).

7. Common therapeutic modalities.

a. Pharmacologic management.

(1) Not generally responsive to corticosteroids, only minimally affected by NSAIDs.

(2) Pregabalin (Lyrica®) is first FDA-approved treatment for FS-related pain; administer 2-3 times daily with or without food.

(3) Adjunctive medications are often prescribed at bedtime to decrease pain, improve sleep.

(a) Low-dose tricylic antidepressants.

(b) Low-dose selective serotonin re-uptake inhibitors (SSRIs).

(c) Benzodiazepines.

(d) Muscle relaxants.

(4) Topical creams (capsaicin or EMLA) or injection of tender points.

(5) Dietary supplement S-adenosylme­thionine (SAM-e) may help symptoms.

(6) Exercise: encourage patient to start

low-impact aerobic exercise slowly and gradually increase.

b. Other interventions often attempted.

(1) Massage or reflexology.

(2) Local heat application.

(3) Meditation.

(4) Acupuncture.

8. Complications: progressive disability, depression.

9. Continued care and rehabilitation.

a. Sleep promotion

(1) Review sleep hygiene to try to maximize sleep behaviors.

(2) Encourage regular exercise to promote restorative sleep.

b. Possible nutritional triggers for symptoms.

(1) Wheat or corn cereal.

(2) Dairy products.

(3) Caffeine.

(4) Yeast.

(5) Citrus.

B. Systemic lupus erythematosus (see Chapter 24).

References

American College of Rheumatology Subcommittee on Osteoarthritis Guidelines. (1990). 1990 criteria for the classification of fibromyalgia. Arthritis and Rheumatism, 33(2), 160-172.

Arnett, F.C., Edworthy, S.M., Block, D.A., McShane, D.J., Fries, J.F., Cooper, N.S., et al. (1988). The American Rheumatism Association 1987 revised criteria for the classification of rheumatoid arthritis. Arthritis and Rheumatism, 31(3), 315-324.

Delbrouck, B. (2004). Introduction to the skeletal system. In An introduction to orthopaedic nursing (3rd ed., pp. 13). Chicago, IL: National Association of Orthopaedic Nurses.

Hochberg, M.C., Altman, R.D., Brandt, K.D., Clark, B.M., Dieppe, P.A., Griffin, M.R., et al. (1995a). Guidelines for the medical management of osteoarthritis: Part I. Osteoarthritis of the hip. Arthritis and Rheumatism, 38, 1535-1540.

Hochberg, M.C., Altman, R.D., Brandt, K.D., Clark, B.M., Dieppe, P.A., Griffin, M.R., et al. (1995b). Guidelines for the medical management of osteoarthritis: Part II. Osteo­arthritis of the knee. Arthritis and Rheumatism, 38, 1541-1546.

National Association of Orthopaedic Nurses (NAON). (2007). Core curriculum for orthopaedic nursing (6th ed.). Boston: Pearson Custom Publishing.

National Osteoporosis Foundation. (2007). Prevention: Who’s at risk? Retrieved November 11, 2007, from . org/prevention/risk.htm

World Health Organization. (1994). Assessment of fracture risk and its application to screening for postmenopausal osteoporosis. Technical Report Series, No. 843. Geneva, Switzerland: Author.

Additional Readings

Dell, D.D. (2007). Getting the point about fibromyalgia. Nursing 2007, 37(2), 61-64.

Gambrall, M.A. (2007). Anesthetic implications for surgical correction of scoliosis. AANA Journal, 75(4), 277-285.

Hall, V.L., Hardwick, M., Reden, L., Pulido, P., & Colwell, Jr., C. (2004). Unicompartmental knee arthroplasty (alias uni-knee): An overview with nursing implications. Orthopaedic Nursing, 23(3), 163-173.

Iaquinta, M.L., & Larrabee, J.H. (2004). Phenomenological lived experience of patients with rheumatoid arthritis. Journal of Nursing Care Quality, 19(3), 280-289.

Kent, M.E., Rapp, R.P., & Smith, K.M. (2006). Antibiotic beads and osteomyelitis: Here today, what’s coming tomorrow? Orthopedics, 29(7), 599-603.

Medline Plus® (a service of the U.S. National Library of Medicine and the National Institutes of Health). (2007). Back pain. Retrieved November 18, 2007, from [lus/print/backpain.html

Shaver, J.L., Wilbur, J., Robinson, F.P., Wang, E., & Buntin, M.S. (2006). Women’s health issues with fibromyalgia syndrome. Journal of Women’s Health, 15(9), 1035-1045.

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