Therapeutic Exercise: Foundations and Techniques, 6e

Chapter 11: Joint, Connective Tissue, and Bone Disorders and Management

Carolyn Kisner; Karen Holtgrefe

Introduction

General guidelines and principles for developing exercise interventions for patients with soft tissue lesions were presented in the previous chapter. The purpose of this chapter is to present principles of management of selected pathologies that affect joints, connective tissue, and bone. Characteristics of arthritis, fibromyalgia, myofascial pain syndrome, osteoporosis, and fractures are described in conjunction with the effects of therapeutic exercise on impairments associated with these pathological conditions.

Arthritis: Arthrosis

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Arthritis is inflammation of a joint. There are many types of arthritis, both inflammatory and noninflammatory, that affect joints and other connective tissues in the body. The most common types treated by therapists are rheumatoid arthritis and osteoarthritis. Arthrosis is limitation of a joint without inflammation. Unless the cause of the joint problems is known, such as recent trauma or immobility, medical intervention is necessary to diagnose and medically manage the pathology. Traumatic arthritis may require aspiration if there is bloody effusion. The therapist manages the impairments, activity limitations, and participation restrictions that result from the underlying pathology.

Clinical Signs and Symptoms

Signs and symptoms common to all types of arthritic conditions generally include the following.

Impaired Mobility

The patient usually presents with signs typical of joint involvement that include a characteristic pattern of limitation (called a capsular pattern), usually a firm end-feel (unless acute—then the end-feel may be guarded), decreased and possibly painful joint play, and joint swelling (effusion).⁴⁹ Additional signs and symptoms may be present depending on the specific disease process. Table 11.1 summarizes the characteristic signs and symptoms of osteoarthritis and rheumatoid arthritis.

TABLE 11.1Comparison of Osteoarthritis and Rheumatoid Arthritis^{5,18,44,84,91,92}

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TABLE 11.1 Comparison of Osteoarthritis and Rheumatoid Arthritis^{5,18,44,84,91,92}

Characteristics

Osteoarthritis

Rheumatoid Arthritis

Age of onset

Usually after age of 40

Usually begins between age 15 and 50

Progression

Usually develops slowly over many years in response to mechanical stress

May develop suddenly, within weeks or months

Manifestations

Cartilage degradation, altered joint architecture, osteophyte formation

Inflammatory synovitis and irreversible structural damage to cartilage and bone

Joint involvement

Affects a few joints (usually asymmetrical); typically:

—DIP, PIP, 1st CMC of hands

—Cervical and lumbar spine

—Hips, knees, 1st MTP of feet

Usually affects many joints, usually bilateral; typically:

—MCP and PIP of hands, wrists, elbows, shoulders

—Cervical spine

—MTP, talonavicular and ankle

Joint signs and symptoms

Morning stiffness (usually <30 min), increased joint pain with weight-bearing and strenuous activity; crepitus and loss of ROM

Redness, warmth, swelling, and prolonged morning stiffness; increased joint pain with activity

Systemic signs and symptoms

None

General feeling of sickness and fatigue, weight loss and fever; may develop rheumatoid nodules, may have ocular, respiratory, hematological, and cardiac symptoms

Arthrosis may be present if the individual is recovering from a fracture or other problem requiring immobilization. There is limited joint play along with other connective tissue and muscular contractures limiting ROM.

Impaired Muscle Performance

Weakness from disuse or reflex inhibition of stabilizing muscles occur when there is joint swelling or pain. Muscle weakness or inhibition leads to imbalances in strength and flexibility and poor support for the involved joints. Asymmetry in muscle pull may be a deforming force to the joints, and poor muscle support allows the joint to be more susceptible to trauma; conversely, good muscle support helps protect an arthritic joint.

Impaired Balance

Patients may develop balance deficits because of altered or decreased sensory input from joint mechanoreceptors and muscle spindle. This is particularly a problem with weight-bearing joints.⁹⁶

Activity Limitations and Participation Restrictions

The ability to carry out home, community, work-related, or social activities may be minimally to significantly restricted. Adaptive and assistive devices may be used by the patient to improve function or help prevent possible deforming forces. A variety of classification systems and functional instruments have been developed for use in clinical studies as well as routine practice to measure patient function and outcomes in response to interventions.⁴²

Rheumatoid Arthritis

Rheumatoid arthritis (RA) is an autoimmune, chronic, inflammatory, systemic disease primarily of unknown etiology affecting the synovial lining of joints as well as other connective tissue. It is characterized by a fluctuating course, with periods of active disease and remission. The onset and progression vary from mild joint symptoms with aching and stiffness to abrupt swelling, stiffness, and progressive deformity.^3,5,10,58,74 The criteria for classification of RA are summarized in Box 11.1.

BOX 11.1 Criteria for Diagnosis of Rheumatoid Arthritis⁶

Morning stiffness in and around the joints, lasting at least 1 hour before maximal improvement
At least three of the following joints simultaneously have soft tissue swelling or fluid observed by a physician: right or left proximal interphalangeal (PIP); metacarpophalangeal (MCP); wrist, elbow, knee, ankle, and metatarsophalangeal (MTP) joints).
Swelling in the wrist, MCP, or PIP joints
Symmetrical joint involvement (bilateral involvement of PIP, MCP, or MTP joints may occur without absolute symmetry)
Rheumatoid nodules
Positive serum rheumatoid factor
Radiographic changes including erosions or or boney decalcification localized in or adjacent to the involved joints

NOTE: RA is defined by the presence of at least four of these seven criteria. Numbers 1–4 must have been present for at least 6 weeks.

Characteristics of RA

Characterized by symmetric, errosive synovitis³ with periods of exacerbation (flare) and remission.^5,10,58 Joints are characteristically involved with early inflammatory changes in the synovial membrane, peripheral portions of the articular cartilage, and subchondral marrow spaces. In response, granulation tissue (pannus) forms, covers, and erodes the articular cartilage, bone, and ligaments in the joint capsule. Adhesions may form, restricting joint mobility. With progression of the disease, cancellous bone becomes exposed. Fibrosis, ossific ankylosis, or subluxation may eventually cause deformity and disability (Figs. 11.1, 11.2, 11.3).^5,74
Inflammatory changes also occur in tendon sheaths (tenosynovitis); if subjected to recurring friction, the tendons may fray or rupture.
Extra-articular pathological changes sometimes occur; they include rheumatoid nodules, atrophy and fibrosis of muscles with associated muscular weakness, fatigue, and mild cardiac changes.
Progressive deterioration and decline in the functional level of the individual attributed to the muscular changes and progressive muscle weakness is often seen,²⁴ leading to major economic loss and significant impact on families.³
The degree of involvement varies. Some individuals experience mild symptoms that require minor lifestyle changes and mild anti-inflammatory medications. Others experience significant pathological changes in the joints that require major adaptations in lifestyle. Loss of joint function is irreversible, and often surgery is needed to decrease pain and improve function. Early recognition is essential during the initial stages, with referral to a rheumatologist for diagnosis and medical management to control the inflammation and minimize joint damage.¹⁸

FIGURE 11.1

(A) Radiographic hallmarks and typical joint deformities with rheumatoid arthritis in small joints of the wrist and hand. (B) Radiographic hallmarks of rheumatoid arthritis in large joints.

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FIGURE 11.2

Advanced rheumatoid arthritis of the hip joints. Note that the destruction caused by rheumatoid arthritis involves the entire joint space and the boney regions on either side of the joint space. (From McKinnis,⁶² p 55, with permission.)

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FIGURE 11.3

Rheumatoid arthritis of the foot. First metatarsopha-langeal joint shows severe erosion of the joint surface with subluxation of the metatarsal (arrow). (From McKinnis,⁶² p 58, with permission.)

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Signs and Symptoms: Periods of Active Disease

With synovial inflammation, there is effusion and swelling of the joints, which cause aching and limited motion. Joint stiffness is prominent in the morning. Usually there is pain on motion, and a slight increase in skin temperature can be detected over the joints. Pain and stiffness worsen after strenuous activity.
Onset is usually in the smaller joints of the hands and feet, most commonly in the proximal interphalangeal joints. Usually symptoms are bilateral.
With progression, the joints become deformed and may ankylose or subluxate.
Pain is often felt in adjoining muscles, and eventually muscle atrophy and weakness occur. Asymmetry in muscle strength and alterations in the line of pull of muscles and tendons add to the deforming forces.
The person often experiences nonspecific symptoms such as low-grade fever, loss of appetite and weight, malaise, and fatigue.

Principles of Management: Active Inflammatory Period of RA

Management guidelines are summarized in Box 11.2.

BOX 11.2 MANAGEMENT GUIDELINES—Rheumatoid Arthritis/Active Disease Period Structural/Functional Impairments, Activity Limitations, and Participation Restrictions:

Tenderness and warmth over the involved joints with joint swelling

Muscle guarding and pain on motion

Joint stiffness and limited motion

Muscle weakness and atrophy

Potential deformity and ankylosis from the degenerative process and asymmetric muscle pull

Fatigue, malaise, sleep disorders

Restricted ADLs and IADLs

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Plan of Care

Interventions

1. Educate the patient.

1. Inform the patient on importance of rest, joint protection, energy conservation, and performance of ROM.

Teach home exercise program and activity modifications that conserve energy and minimize stress to vulnerable joints.

2. Relieve pain and muscle guarding and promote relaxation.

2. Modalities

Gentle massage

Immobilize in splint

Relaxation techniques

Medications as prescribed by physician

3. Minimize joint stiffness and maintain available motion.

3. Passive or active-assistive ROM within limits of pain, gradual progression as tolerated.

Gentle joint techniques using grade I or II oscillations.

4. Minimize muscle atrophy.

4. Gentle isometrics in pain-free positions, progression to ROM when tolerated.

5. Prevent deformity and protect the joint structures.

5. Use of supportive and assistive equipment for all pathologically active joints.

Good bed positioning while resting.

Avoidance of activities that stress the joints.

PRECAUTIONS: Respect fatigue and increased pain; do not overstress osteoporotic bone or lax ligaments.

CONTRAINDICATIONS: Do not stretch swollen joints or apply heavy resistance exercise that cause joint stress.

Patient Education. Because periods of active disease may last several months to more than a year, begin education in the overall treatment plan, safe activity, and joint protection (Box 11.3) as soon as possible.⁶⁰ It is imperative to involve the patient in the management, so he or she learns how to conserve energy and avoid potential deforming stresses during activities and when exercising.
Joint protection and energy conservation. It is important that the patient learns to respect fatigue and, when tired, rests to minimize undue stress to all the body systems. Because inflamed joints are easily damaged and rest is encouraged to protect the joints, teach the patient how to rest the joints in nondeforming positions and to intersperse rest with ROM.
Joint mobility. Use gentle grade I and II distraction and oscillation techniques to inhibit pain and minimize fluid stasis. Stretching techniques are not performed when joints are swollen.
Exercise. The type and intensity of exercise vary depending on the symptoms. Encourage the patient to do active exercises through as much ROM as possible (not stretching). If active exercises are not tolerated owing to pain and swelling, passive ROM is used. Once symptoms of pain and signs of swelling are controlled with medication, progress exercises as if subacute.
Functional training. Modify any activities of daily living (ADL) needed in order to protect the joints. If necessary, use splints and assistive devices to provide protection.

BOX 11.3 Principles of Joint Protection and Energy Conservation^53,73

Monitor activities and stop when discomfort or fatigue begins to develop.
Use frequent but short episodes of exercise (three to five sessions per day) rather than one long session.
Alternate activities to avoid fatigue.
Decrease level of activities or omit provoking activities if joint pain develops and persists for more than 1 hour after activity.
Maintain a functional level of joint ROM and muscular strength and endurance.
Balance work and rest to avoid muscular and total body fatigue.
Increase rest during flares of the disease.
Avoid deforming positions.
Avoid prolonged static positioning; change positions during the day every 20 to 30 minutes.
Use stronger and larger muscles and joints during activities whenever possible.
Use appropriate adaptive equipment.

CLINICAL TIP

Therapeutic exercises cannot positively alter the pathological process of RA, but if administered carefully, they can help prevent, retard, or correct the mechanical limitations and deforming forces that occur and therefore, help maintain function.

PRECAUTIONS: Secondary effects of steroidal medications may include osteoporosis and ligamentous laxity, so use exercises that do not cause excessive stress to bones or joints.

CONTRAINDICATIONS: Do not perform stretching techniques across swollen joints. When there is effusion, limited motion is the result of excessive fluid in the joint space. Forcing motion on the distended capsule overstretches it, leading to subsequent hypermobility (or subluxation) when the swelling abates. It may also increase the irritability of the joint and prolong the joint reaction.

Principles of Management: Subacute and Chronic Stages of RA

As the intensity of pain, joint swelling, morning stiffness, and systemic effects diminish, the disease is considered subacute. Often medications can decrease the acute symptoms, so the patient can function as if in the subacute stage. The chronic stage occurs between exacerbations. This may be very short in duration, or it may last many years.

Treatment approach. The treatment approach is the same as with any subacute and chronic musculoskeletal disorder, except appropriate precautions must be taken because the pathological changes from the disease process make the tissues more susceptible to damage.
Joint protection and activity modification. Continue to emphasize the importance of protecting the joints by modifying activity, using splints, asssistive devices, and environmental adaptations for safe function.
Flexibility and strength. To improve function, exercises should be aimed at improving flexibility, muscle strength, and muscle endurance within the tolerance of the joints.²⁴
Cardiopulmonary endurance. Nonimpact or low-impact conditioning exercises—such as aquatic exercise, cycling, aerobic dancing, and walking/running—performed within the tolerance of the individual with RA, improve aerobic capacity and physical activity and decrease depression and anxiety.^8,64,99 Group activities, such as water aerobics, also provide social support in conjunction with the activity. One randomized review suggested that aerobic training also has a positive impact on the cardiovascular status of patients with RA.⁶³

PRECAUTIONS: The joint capsule, ligaments, and tendons may be structurally weakened by the rheumatic process (also as a result of using steroids), so the dosage of stretching and joint mobilization techniques used to counter any contractures or adhesions must be carefully graded.

CONTRAINDICATIONS: Vigorous stretching or manipulative techniques.

FOCUS ON EVIDENCE

The results of a study⁹⁵ of patients with active but medically controlled RA demonstrated that subjects who participated in a carefully supervised intensive exercise program showed greater improvement in function and muscle strength, a greater decrease in the number of clinically active joints, and a faster rate of diminished disease activity compared to the control group of patients who participated in a program of ROM and isometric exercise. The intensive exercises included isokinetic resistance to the knees at 70% maximum voluntary contraction and angular velocity at 60°/sec, isometric exercises at 70% maximum voluntary contraction, bicycling at 60% of the age-predicted maximum for 15 minutes, and ROM exercises. All exercises were adjusted to the pain tolerance of the individual when needed. The primary conclusion of this study was that there is no evidence that patients with active disease should be prevented from vigorous exercise so long as fatigue and pain are respected. The study did not look at joint erosion or cartilage damage.

Several systematic reviews looking at best evidence for the use of therapeutic exercise in the treatment of RA have been published.^14,23,27,63 Although there are few randomized well-controlled studies looking at the outcome of exercise, studies of various strength do support that therapeutic exercise, including functional strengthening and aerobic exercise, are beneficial for patients with RA demonstrating relief of pain, improved muscle strength, and functional status. In one of the reviews,²⁷ investigators found that moderate- or high-intensity exercise in patients with RA has a minimal effect on disease activity and radiological evidence of damage in the hands and feet, but that there is insufficient radiological evidence to determine the effect in large joints. The reviewers also reported that long-term moderate- or high-intensity exercises (individualized to protect radiologically damaged joints) improve aerobic capacity, muscle strength, functional ability, and psychological well-being in patients with RA.²⁷

Osteoarthritis: Degenerative Joint Disease

Osteoarthritis (OA) is a chronic degenerative disorder primarily affecting the articular cartilage of synovial joints, with eventual boney remodeling and overgrowth at the margins of the joints (spurs and lipping) (Fig. 11.4). There is also progression of synovial and capsular thickening and joint effusion. The impairments from OA lead to activity limitations and participations restrictions in a substantial number of people with a significant social and financial impact as a result of surgical and medical interventions.¹⁵

FIGURE 11.4

Radiographic hallmarks of osteoarthritis. (From McKinnis,⁶² p 61, with permission.)

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Characteristics of OA

With degeneration, there may be capsular laxity as a result of bone remodeling and capsule distention, leading to hypermobility or instability in some ranges of joint motion. With pain and decreased willingness to move, contractures eventually develop in portions of the capsule and overlying muscle, so as the disease progresses, motion becomes more limited.^31,44
Although the etiology of OA is not known, mechanical injury to the joint due to a major stress or repeated minor stresses and poor movement of synovial fluid when the joint is immobilized are possible causes. Rapid destruction of articular cartilage occurs with immobilization, because the cartilage is not being bathed by moving synovial fluid and is thus deprived of its nutritional supply.¹⁰
OA is also genetically related, especially in the hands and hips and to some degree in the knees.³¹ Other risk factors that show a direct relationship to OA are obesity, weakness of the quadriceps muscles, joint impact, sports with repetitive impact and twisting (e.g., soccer, baseball pitching, football), and occupational activities such as jobs that require kneeling and squatting with heavy lifting.³¹
The cartilage splits and thins out, losing its ability to withstand stress. As a result, crepitation or loose bodies may occur in the joint. Eventually, subchondral bone becomes exposed. There is increased density of the bone along the joint line, with cystic bone loss and osteoporosis in the adjacent metaphysis. During the early stages, the joint is usually asymptomatic because the cartilage is avascular and aneural, but pain becomes constant in later stages.
Affected joints may become enlarged. Heberden's nodes (enlargement of the distal interphalangeal joints of the fingers) and Bouchard's nodes (enlargement of the proximal interphalangeal joints) are common.
Most commonly involved are weight-bearing joints (hips and knees), the cervical and lumbar spine, and the distal interphalangeal joints of the fingers and carpometacarpal joints of the thumbs (Figs. 11.5 and 11.6).

FIGURE 11.5

Osteoarthritis of the knees in a 66-year-old woman. This film was taken under weight-bearing conditions. At the patient's right knee, osteoarthritis is evidenced by narrowed joint space (white arrows), osteophyte formation at the joint margins (large white arrowhead), and sclerotic subchondral bone (small black arrowheads) of both the medial and lateral tibial plateaus. At the patient's left knee, it is interesting to note that in the area of minimal weight-bearing stress the subchondral bone has lost density, and rarefaction is present on the medial aspect of the joint. (From McKinnis,⁶² p 62, with permission.)

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FIGURE 11.6

Severe osteoarthritis of the hip with pseudocysts. The radiolucent cyst-like areas (arrows) are caused by intrusion of synovial fluid into areas of subchondral bone that have become weakened by microfractures. (From McKinnis,⁶² p 62, with permission.)

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Principles of Management: Osteoarthritis

Pain, joint stiffness, decreased muscle performance, and decreased aerobic capacity affect the quality of life and increase the risk for disability for the individual with OA.³² Therapeutic exercise and manual therapy interventions are important in the comprehensive management of OA. Management guidelines are summarized in Box 11.4.

BOX 11.4 MANAGEMENT GUIDELINES—Osteoarthritis Structural/Functional Impairments, Activity Limitations, and Participation Restrictions:

Pain with mechanical stress or excessive activity

Pain at rest in the advanced stages

Stiffness after inactivity

Limitation of motion

Muscle weakness

Decreased proprioception and balance

Functional limitations in ADLs and IADLs

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Plan of Care

Intervention

1. Educate the patient.

1. Teach about deforming forces and prevention.

Teach home exercise program to reinforce interventions and minimize symptoms.

2. Decrease effects of stiffness.

2. Active ROM

Joint-play mobilization techniques

3. Decrease pain from mechanical stress and prevent deforming forces.

3. Splinting and/or assistive equipment to minimize stress or to correct faulty biomechanics, strengthen supporting muscles.

Alternate activity with periods of rest.

4. Increase ROM.

4. Stretch muscle, joint, or soft tissue restrictions with specific techniques.

5. Improve neuromuscular control, strength, and muscle endurance.

5. Low-intensity resistance exercises and muscle repetitions.

6. Improve balance.

6. Balance training activities.

7. Improve physical conditioning.

7. Nonimpact or low-impact aerobic exercise.

PRECAUTIONS: When strengthening supporting muscles, increased pain in the joint during or following resistive exercises probably means that too great a weight is being used or stress is being placed at an inappropriate part of the ROM. Analyze the joint mechanics and at what point during the range the greatest compressive forces are occurring. Maximum resistance exercise should not be performed through that ROM.

Patient instruction. Education includes teaching the patient about the disease of OA, how to protect the joints while remaining active, and how to manage the symptoms. Instruct the patient in a home program of safe exercises to improve muscle performance, ROM, and endurance.
Pain management—Early stages. Pain and feelings of "stiffness" are common complaints during the early stages. Pain usually occurs because of excessive activity and stress on the involved joint and is relieved with rest. Brief periods of stiffness occur in the morning or after periods of inactivity. This is due to gelling of the involved joints after periods of inactivity.² Movement relieves the stasis and feelings of stiffness. Help the patient find a balance between activity and rest and correct biomechanical stresses in order to prevent, retard, or correct the mechanical limitations.
Pain management—Late stages. During the late stages of the disease, pain is often present at rest. The pain is probably from secondary involvement of subchondral bone, synovium, and the joint capsule. In the spine, if boney growth encroaches on the nerve root, there may be radicular pain (see chapter 15). Emphasize activity modification and use of assistive devices and/or splints to minimize joint stress. Pain that cannot be managed with activity modification (as described in the following bullet) and analgesics is usually an indication for surgical intervention.
Assistive and supportive devices and activity. With progression of the disease, the boney remodeling, swelling, and contractures alter the transmission of forces through the joint, which further perpetuates the deforming forces and creates joint deformity. Functional activities become more difficult. Adaptive or assistive devices, such as a raised toilet seat, cane, or walker, may be needed to decrease painful stresses and maintain function. Shock-absorbing footwear may decrease the stresses in OA of the knees.³¹ Aquatic therapy and group-based exercise in water decreases pain and improves physical function in patients with lower extremity OA.²⁵
Resistance exercise. Progressive weakening in the muscle occurs either from inactivity or from inhibition of the neuronal pools. Weak muscles may add to the joint dysfunction.² Strong muscles protect the joint. Use resistance exercises, within the tolerance of the joint, as part of the patient's exercise program. Avoid deforming forces and heavy weights that the patient cannot control or that cause joint pain. Adaptations include the use of multiple-angle isometrics in pain-free positions, applying resistance only through arcs of motion that are not painful, and use of a pool to decrease weight-bearing stresses and improve functional performance.³⁷
Stretching and joint mobilization. Use stretching and joint mobilization techniques to increase mobility. Teach the patient self-stretching/flexibility exercises and the importance of movement to counteract the developing restrictions.
Balance activities. Joint position sense may be impaired.⁹⁶ See Chapter 8 for principles and description of balance exercises. Nontraditional forms of exercise, such as Tai Chi, have been found to be effective for improving balance in patients with OA.⁸⁹
Aerobic conditioning. Instruct the patient in exercises designed to improve cardiopulmonary function.¹³ The choice of exercise should have low impact on the joints, such as walking, biking, or swimming. Avoid activities that cause repetitive intensive loading of the joints, such as jogging and jumping.

FOCUS ON EVIDENCE

In a single-blind, randomized clinical trial of 109 patients with OA of the hip, specific manipulations and mobilizations of the hip joint were reported to have a greater success rate than active exercise for improving muscle function and joint motion. Outcomes measured were perceived improvement after treatment (81% vs. 50%), pain, stiffness, hip function, and ROM.⁴⁵

FOCUS ON EVIDENCE

Recently published clinical practice guidelines based on a systematic review of randomized controlled and observational studies highlight the importance of therapeutic exercise and physical activity to increase strength, manage pain, and improve aerobic capacity and functional status in patients with OA.¹⁵

Two systematic reviews of studies designed to examine evidence of the effects of exercise in the management of hip and knee OA describe support for aerobic exercise and strengthening exercises to reduce pain and disability.^75,76 The consensus of expert opinion cited by Roddy⁷⁵ is that there are few contraindications and that exercise is relatively safe in patients with OA, but that exercise should be individualized and patient-centered with consideration for age, comorbidity, and general mobility.

In another study that followed 285 patients with knee OA for 3 years, investigators found that factors that protected the individuals from poor functional outcomes included strength and activity level, as well as factors such as mental health, self-efficacy, and social support.⁸²

Fibromyalgia and Myofascial Pain Syndrome

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Fibromyalgia (FM) and myofascial pain syndrome (MPS) are chronic pain syndromes that are often confused and interchanged. Each has a distinct proposed etiology. Individuals with FM process nociceptive signals differently from individuals without FM,^78,90 and individuals with MPS have localized changes in the muscle.^39,81,85,90 Although there are some similarities, the differences are significant and determine the method of treatment. They are summarized in Table 11.2.

TABLE 11.2Similarities and Differences Between Fibromyalgia and Myofascial Pain Syndrome

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TABLE 11.2 Similarities and Differences Between Fibromyalgia and Myofascial Pain Syndrome

Similarities

Pain in muscles

Decreased ROM

Postural stresses

Differences

Fibromyalgia

Myofascial Pain Syndrome

Tender points at specific cites

Trigger points in muscle

No referred patterns of pain

Referred patterns of pain

No tight band of muscle

Tight band of muscle

Fatigue and waking unrefreshed

No related fatigue complaints

Fibromyalgia

Fibromyalgia, as defined by the American College of Rheumatology in 1990,^1a,98 is a chronic condition characterized by widespread pain that covers half the body (right or left half, upper or lower half) plus the axial skeleton, and has lasted for more than 3 months. Additional symptoms include 11 of 18 tender points at specific sites throughout the body (Fig. 11.7), nonrestorative sleep, and morning stiffness. A final common problem is fatigue with subsequent diminished exercise tolerance.⁹⁸

FIGURE 11.7

Fibromyalgia tender points.

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FOCUS ON EVIDENCE

In 2010, Wolfe and associates⁹⁷ developed preliminary diagnostic criteria to complement the ACR-specific criteria, including the measurement of symptom severity. The authors recommend the following: widespread pain index (WPI) ≥7 and symptom severity (SS) scale ≥5, OR WPI 3 to 6 and SS ≥9. These criteria correctly classified 88.1% of individuals with FM determined from the ACR classification without tender point palpation. The SS scale includes items such as somatic symptoms, not feeling refreshed after sleeping, fatigue, and cognition.

Prevalence of FM

It is estimated that 2% of the population—nearly 5 million adults 18 years old or older—have FM, with women affected far more than men (3.4% to 0.5%). In addition, the prevalence increases with age, with 7.4% of women ages 70 to 79 affected.⁵²

Characteristics of FM

The characteristics of FM include the following.^1a,90

The first symptoms of FM can occur at any age but usually appear during early to middle adulthood.
For many of those diagnosed, the symptoms develop after physical trauma such as a motor vehicle accident or a viral infection.
Although the symptoms vary from individual to individual, there are several hallmark complaints. Pain is usually described as muscular in origin and is predominantly reported in the scapula, head, neck, chest, and low back.
Another common report is a significant fluctuation in symptoms. Some days an individual may be pain-free, whereas other days the pain is markedly increased. Most individuals report that, when they are in a cycle in which the symptoms are diminished, they try to do as much as possible. This is usually followed by several days of worsening symptoms and an inability to carry out their normal daily activities. This is often the response to exercise.
Individuals with FM have a higher incidence of tendonitis, headaches, irritable bowel, temporal mandibular joint dysfunction, restless leg syndrome, mitral valve prolapse, anxiety, depression, and memory problems.

Factors Contributing to a Flare

Although FM is a noninflammatory, nondegenerative, non-progressive disorder, several factors may affect the severity of symptoms. These factors include environmental stresses, physical stresses, and emotional stresses. FM is not caused by these various stresses, but it is aggravated by them.

Environmental stresses include weather changes, especially significant changes in barometric pressure, cold, dampness, fog, and rain. An additional environmental stress is fluorescent lights.
Physical stresses include repetitive activities, such as typing, playing piano, vacuuming; prolonged periods of sitting and/or standing; and working rotating shifts.
Emotional stresses are any normal life stresses.

Management: Fibromyalgia

Research supports the use of exercise,^{16,17,19,20,30,57} particularly aerobic exercise, to reduce the most common symptoms associated with FM.

FOCUS ON EVIDENCE

An evidence report from the Cochrane Collaborative¹⁹ summarized the findings of 34 randomized trials related to FM and exercise. The reviewers concluded that aerobic exercise was beneficial in reducing FM symptoms and improving exercise capacity, and resistance exercises might be beneficial in reducing symptoms.

The Ottawa Panel Evidence-Based Clinical Practice Guidelines^16,17 also support the use of aerobic and strengthening exercises.

In addition to exercise, interventions include:

Prescription medication
Over-the-counter medication
Instruction in pacing activities, in an attempt to avoid fluctuations in symptoms
Coginitive Behavior therapy
Avoidance of stress factors
Decreasing alcohol and caffeine consumption
Diet modification.

CLINICAL TIP

When beginning any type of exercise with individuals with FM,^16,17,19,46 it is best to begin at lower levels than recommended by the American College of Sports Medicine⁴ for aerobic and strengthening and to slowly increase the activity. If the exercise leads to an increase in FM symptoms, reduce the intensity, while encouraging continued participation in the exercise.

Myofascial Pain Syndrome

Myofascial pain syndrome (MPS) is defined as a chronic, regional pain syndrome.⁸⁵ The hallmark classification of MPS comprises the myofascial trigger points (MTrPs) in a muscle that have a specific referred pattern of pain (Fig. 11.8), along with sensory, motor, and autonomic symptoms.^29,86,87

FIGURE 11.8

Composite pattern of pain (dark red) referred from trigger points (TrPs) (Xs) in the right piriformis muscle (medium red). The lateral X (TrP₁) indicates the most common TrP location. The red stippling locates the spillover part of the pattern that may be felt as less intense pain than that of the essential pattern (solid red). The spillover pain may be absent. (From Travell, JG, Simmons, DG: Myofascial Pain and Dysfunction: The Trigger Point Manual: The Lower Extremities, Vol 2. Baltimore: Williams & Wilkins, 1992, p 188, with permission.)

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The trigger point is defined as a hyperirritable area in a tight band of muscle. The pain from these points is described as dull, aching, and deep. Additional impairments from the trigger points include decreased ROM when the muscle is being stretched, decreased strength in the muscle, and increased pain with muscle stretching. The trigger points may be active (producing a classic pain pattern) or latent (asymptomatic unless palpated).

Possible Causes of Trigger Points

Although the etiology of trigger points is not completely understood, some potential causes are:^85,86,87

Chronic overload of the muscle that occurs with repetitive activities or that maintain the muscle in a shortened position.
Acute overload of muscle, such as slipping and catching oneself, picking up an object that has an unexpected weight, or following trauma such as in a motor vehicle accident.
Poorly conditioned muscles compared to muscles that are exercised on a regular basis.
Postural stresses such as sitting for prolonged periods of time, especially if the workstation is not ergonomically correct, and leg length differences.
Poor body mechanics with lifting and other activities.

FOCUS ON EVIDENCE

Recently researchers have looked at the contribution of myofascial trigger points as a contributing factor in chronic headaches,⁸⁰ tension type headaches,^34,35 mechanical neck pain,³³ and shoulder disorders.^43,55,80 Lucas and associates⁵⁴ investigated the muscle activation pattern (MAP) of scapular muscles during arm elevation in pain-free individuals without trigger points and pain-free individuals with latent trigger points (LTrP). The LTrP group had a significant difference in MAP (p<0.05). These individuals were then treated with either a placebo or active intervention to deactivate the trigger point, and the MAP was reassessed. There was a significant difference (p<0.05) in MAP after deactivation of the LTrP.

Management: Myofascial Pain Syndrome

Treatment consists of three main components:^{1,56,85,86,87,93}

Correct contributing factors to chronic overload of the muscle.
Eliminate the trigger point. Several techniques are used to eliminate trigger points:

Contract-relax-passive stretch done repeatedly until the muscle lengthens

Contract-relax-active stretch also done in repetition Trigger point release

Spray and stretch

Modalities

Dry needling or injection
Strengthen the muscle.

CLINICAL TIP

If the cause of the trigger point in myofascial pain syndrome is a chronic overload of the muscle, eliminate the contributing factor prior to addressing the trigger point. Initiate muscle strengthening when ROM is restored and the trigger point has been addressed.

Osteoporosis

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Osteoporosis is a disease of bone that leads to decreased mineral content and weakening of the bone. This weakening may lead to fractures, especially of the spine, hip, and wrist. Approximately 10 million Americans have osteoporosis, 80% of them women, and an additional 34 million individuals are at increased risk due to decreased bone mass.⁶⁸ The diagnosis of osteoporosis is determined by the T-score of a bone mineral density (BMD) scan. The T- score is the number of standard deviations above or below a reference value (young, healthy Caucasian women). The World Health Organization (WHO) has established the following criteria.^67,94

Normal: –1.0 or higher
Osteopenia: –1.0 to –2.4
Osteoporosis: –2.5 or less

A decrease of 1 standard deviation represents a 10% to 12% loss of BMD.

Risk Factors

Primary osteoporosis. Risk factors for developing primary osteoporosis include being postmenopausal, Caucasian or Asian descent, family history, low body weight, little or no physical activity, diet low in calcium and vitamin D, and smoking.⁶⁸ Additional risk factors include prolonged bed rest and advanced age.

Secondary osteoporosis. Secondary osteoporosis develops owing to other medical conditions (i.e., gastrointestinal diseases, hyperthyroidism, chronic renal failure, excessive alcohol consumption) and the use of certain medications such as glucocorticoids.^67,94 Regardless of etiology, osteoporosis is detected radiographically by cortical thinning, osteopenia (increased bone radiolucency), trabecular changes, and fractures (Figs. 11.9 and 11.10).⁶²

FIGURE 11.9

Osteoporosis of the spine with multiple compression fractures. The arrow points to the T8-T9 disc space, which is deformed by the collapse of these two vertebrae from multiple compression fractures. This 94-year-old woman has severe kyphosis of the thoracic spine (also known as a gibbous deformity) accentuated by vertebral collapse at multiple levels. (From McKinnis,⁶² p 64, with permission.)

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FIGURE 11.10

Osteoporosis is evident in this knee by the accentuation of the remaining trabeculae. The trabeculae have diminished in number and thickness, and the remaining vertically oriented trabeculae stand out as thin, delicate line images. (From McKinnis,⁶² p 64, with permission.)

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Prevention of Osteoporosis

The National Osteoporosis Foundation (NOF) recommends five ways to prevent osteoporosis.⁶⁹

Diet rich in calcium and vitamin D
Weight-bearing exercise
Healthy lifestyle with moderate alcohol consumption and no smoking
Talking to a health care provider
Testing bone for its density and medication if needed

Bone is living tissue, continually replacing itself in response to the daily demands placed on it. Normally, this continual replacement keeps our bone at its optimum strength. Cells in bone called osteoclasts resorb bone, especially if calcium is needed for particular body functions and not enough is obtained in the diet. Another type of cell, the osteoblast, builds bone. This cycle is usually kept in balance with bone resorption equaling bone replacement until the third decade of life. At this point, peak bone mass should be reached. With increasing age, there is a shift to greater resorption. For women, resorption is accelerated during menopause owing to the decrease in estrogen.^67,70,94

Physical Activity

Physical activity has been shown to have a positive effect on bone remodeling. In children and adolescents, this activity may increase the peak bone mass. In adults, it has been shown to maintain or increase bone density; in the elderly, it has been shown to reduce the effects of age-related or disuse-related bone loss.⁶⁷ Maintenance of, or an increase in, bone density is important for preventing fractures associated with osteoporosis. Weak bones due to osteoporosis have been attributed to causing more than 1.5 million fractures per year at a cost of $19 billion dollars. Many of these individuals never return to their previous functional level.^68,94

Effects of Exercise

Muscle contraction (e.g., strengthening exercises, resistance training) and mechanical loading (weight bearing) deform bone. This deformation stimulates osteoblastic activity and improves BMD.⁸⁸

FOCUS ON EVIDENCE

Martyn-St James and Carroll⁵⁹ completed a meta-analysis of prescribed walking programs on BMD at the hip and spine in postmenopausal women. Results reported no increase in BMD at the spine, but a significant increase at the femoral neck.

Huntoon, Schmidt, and Sinaki⁴⁷ completed a retrospective analysis of medical records comparing the refracture rate following vertebral compression fractures (VCF) in patients instructed in a back extension program following percutaneous vertebroplasty (PVP) to those who did not perform the exercises. The nonexercise group refractured within an average of 4.5 months, whereas the exercise group average time to refracture was 20.4 months.

An evidence report from the Cochrane Collaborative¹¹ summarized the findings of 18 randomized trials related to exercise and osteoporosis in women. The reviewers concluded that exercise, particularly fast walking, was effective on the BMD of the spine and hip. Resistance and weight-bearing exercise were also beneficial on the BMD of the spine.

Recommendations for Exercise

The NOF recommends weight-bearing exercise in the prevention of osteoporosis but does not specify what type of exercise or how often it should be done. Based on current research, the following recommendations are made.^*

Weight-bearing exercise, such as walking, jogging, climbing stairs, jumping
Nonweight-bearing exercise, such as with a bicycle ergometer
Resistance (strength) training of 8 to 10 exercises that target major muscle groups

Mode: Aerobic

Frequency. Five or more days per week.

Intensity. Thirty minutes of moderate intensity (fast walking) or 20 minutes of vigorous intensity (running). Doing three short bouts per day of 10 minutes of activity is acceptable.

Mode: Resistance

Frequency. Two to three days per week with a day of rest in between each bout of exercise.

Intensity. Eight to 12 repetitions that lead to muscle fatigue.

CLINICAL TIP

The Borg rate of perceived exertion scale (RPE) is a good indicator of how difficult an exercise is for an individual.¹² A score of 16/20 is based on a 15-grade RPE scale (6 to 20). The individual rates how hard he or she is working (7 = very, very light; 13 = somewhat hard; 19 = very, very hard).

Precautions and Contraindications

Because osteoporosis changes the shape of the vertebral bodies (they become more wedge-shaped), leading to kyphosis, flexion activities and exercise, such as supine curl-ups and sit-ups, as well as the use of sitting abdominal machines should be avoided. Stress into spinal flexion increases the risk of a vertebral compression fracture.
Avoid combining flexion and rotation of the trunk to reduce stress on the vertebrae and the intervertebral discs.
When performing resistance exercise, it is important to increase the intensity progressively but within the structural capacity of the bone.

NOTE: Refer to Chapter 6 for a discussion of pathological fractures and precautions that should be taken during resistance exercise, identified in Box 6.12.

CLINICAL TIP

Utilizing a multimodal program of weight-bearing exercise, balance activities, and strengthening may help reduce the risk of falls and subsequent hip fractures in individuals with osteoporosis.^28,65

Fractures and Posttraumatic Immobilization

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A fracture is a structural break in the continuity of a bone, an epiphyseal plate, or a cartilaginous joint surface.⁷⁹ When there is a fracture, some degree of injury also occurs to the soft tissues surrounding the bone. Depending on the site of the fracture, the related soft tissue injury could be serious if a major artery or peripheral nerve is also involved. If the fracture is more central, the brain, spinal cord, or viscera could be involved. Causes and types of fractures are summarized in Table 11.3 and are illustrated in Figures 11.11, 11.12, and 11.13.

FIGURE 11.11

(A–F) The position of fracture fragments may be described by how the distal fragment displaces in relationship to the proximal fragment. (From McKinnis,⁶² p 84, with permission.)

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FIGURE 11.12

(A–D) Directions of fracture lines are described in reference to the longitudinal axis of the bone. (From McKinnis,⁶² p 85, with permission.)

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FIGURE 11.13

Comminuted fractures are fractures with more than two fragments. Some frequently occurring comminuted fracture patterns are (A) the wedge-shaped or butterfly pattern and (B) a two- or three-segmented level fracture. (C) Other fractures with multiple fragments, be it several or several hundred, are still described as comminuted. (From McKinnis,⁶² p 85, with permission.)

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TABLE 11.3Causes and Types of Fractures⁷⁹

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TABLE 11.3 Causes and Types of Fractures⁷⁹

Force

Effect on Bone

Type of Fracture

Bending (angulatory)

Long bone bends causing failure on convex side of bend

Transverse or oblique fracture

Greenstick fracture in children

Twisting (torsional)

Spiral tension failure in long bone

Spiral fracture

Straight pulling (traction)

Tension failure from pull of ligament or muscle

Avulsion fracture

Crushing (compression)

Usually in cancellous bone

Compression fracture

Torus (buckle) fracture in children

Repetitive microtrauma

Small crack in bone unaccustomed to the repetitive/rhythmic stress

Fatigue fracture or stress fracture

Normal force on abnormal bone

Such as with osteoporosis, boney tumor, or other diseased bone

Pathological fracture

A fracture is identified by⁷⁹:

Site: diaphyseal, metaphyseal, epiphyseal, intra-articular
Extent: complete, incomplete
Configuration: transverse, oblique or spiral, comminuted (two or more fragments)
Relationship of the fragments: undisplaced, displaced
Relationship to the environment: closed (skin in tact), open (fracture or object penetrated the skin)
Complications: local or systemic; related to the injury or to the treatment

The diagnosis, reduction, alignment, and immobilization for healing of a fracture are medical procedures and are not discussed in this text. There are times, though, when the therapist provides the initial screening following a traumatic event or examines a patient following repetitive microtrauma; moreover, a patient may sustain an injury while at a therapy session. Hence, the therapist must be aware of symptoms and signs of a potential fracture. If a fracture is suspected, refer the patient for radiographic examination, medical diagnosis, and management. Box 11.5 summarizes the typical symptoms and signs of a possible fracture.

BOX 11.5 Symptoms and Signs of a Possible Fracture

The following should alert the therapist to a possible fracture.

History of a fall, direct blow, twisting injury, accident
Localized pain aggravated by movement
Muscle guarding with passive movement
Decreased function of the part
Swelling, deformity, abnormal movement (may or may not be obvious)
Sharp, localized tenderness at the site

Risk Factors

Risk factors for fracture include¹⁰:

Sudden impact (e.g., accidents, abuse, assult)
Osteoporosis (women > men)
History of falls (expecially with increased age, low body mass index, and low levels of physical activity

Bone Healing Following a Fracture

Fracture healing has (1) an inflammatory phase in which there is hematoma formation and cellular proliferation; (2) a reparative phase in which there is callous formation uniting the breach and ossification; and (3) a remodeling phase in which there is consolidation and remodeling of the bone.^10,79

Cortical Bone Healing

Inflammatory Phase

When the dense cortical bone of the shaft of a long bone is fractured, the tiny blood vessels are torn at the site, resulting in internal bleeding followed by normal clotting. The amount of bleeding depends on the degree of fracture displacement and amount of soft tissue injury in the region.

Reparative Phase

The early stages of healing take place in the hematoma. Osteogenic cells proliferate from the periosteum and endosteum to form a thick callus, which envelopes the fracture site. At this stage, the callus does not contain bone and is, therefore, radiolucent.

As the callus starts to mature, the osteogenic cells differentiate into osteoblasts and chondroblasts. Initially, the chondroblasts form cartilage near the fracture site, and the osteoblasts form primary woven bone.

Remodeling Phase

Stage of clinical union. When the fracture site is firm enough that it no longer moves, it is clinically united. This occurs when the temporary callus consisting of the primary woven bone and cartilage surrounds the fracture site. The callus gradually hardens as the cartilage ossifies (endochondral ossification). On radiographic examination, the fracture line is still apparent, but there is evidence of bone in the callus. Usually at this stage, immobilization is no longer required. Movement of the related joints is allowed with the caution of avoiding deforming forces at the site of the healing fracture. When assessing the site, no movement of the fracture site or pain should be felt by the patient or therapist.
Stage of radiological union. The bone is considered radiographically healed, or consolidated, when the temporary callus has been replaced by mature lamellar bone. The callus is resorbed, and the bone returns to normal.

Rigid Internal Fixation

Sometimes it is necessary to surgically apply an internal fixation device, such as a rod or a plate with screws, to protect a healing bone. This allows the bone to be kept stable as it heals, but disuse osteoporosis of the bone under the device occurs because normal stresses are transmitted through the device and bypass the bone. Usually the fixation device is removed once the fracture is united in order to reverse the osteoporosis. Following removal of the rod or plate, the bone must be protected from excessive stress for several months until the osteoporosis is reversed.

Healing Time

Healing time varies with age of the patient, the location and type of fracture, whether it was displaced, and the blood supply to the fragments. Healing is assessed by the physician using radiological and clinical examinations. Generally, children heal within 4 to 6 weeks, adolescents within 6 to 8 weeks, and adults within 10 to 18 weeks.¹⁰ Several types of abnormal healing may occur. These are summarized in Box 11.6.

BOX 11.6 Types of Abnormal Healing of Fractures

Malunion: The fracture heals in an unsatisfactory position resulting in a boney deformity.
Delayed union: The fracture takes longer than normal to heal. Nonunion: The fracture fails to unite with a boney union. There may be a fibrous union or a pseudarthrosis.

Cancellous Bone Healing

When the sponge-like lattice of the trabeculae of cancellous bone fractures (in the metaphysis of long bones and bodies of short bones and flat bones), healing occurs primarily through formation of an internal callus (endosteal) callus. There is a rich blood supply and a large area of boney contact, so union is more rapid than in dense cortical bone.

Cancellous bone is more susceptible to compression forces, resulting in crush or compression fractures. If the surfaces of the fracture are pulled apart, which may occur during reduction of the fracture, healing is delayed.

Epiphyseal Plate Healing

If a fracture involves the epiphyseal plate, there may be growth disturbances and boney deformity as the skeleton continues to mature. The prognosis for growth disturbances depends on the type of injury, age of the child, blood supply to the epiphysis, method of reduction, and whether it is a closed or open injury.

Principles of Management: Period of Immobilization

Local Tissue Response

With immobilization, there is connective tissue weakening, articular cartilage degeneration, muscle atrophy, and contracture development as well as sluggish circulation.^10,26,61 In addition, there is soft tissue injury with bleeding and scar formation.⁷⁹ Because immobilization is necessary for bone healing, the soft tissue scar cannot become organized along lines of stress as it develops (described in Chapter 10). Early, nondestructive motion within the tolerance of the fracture site is ideal but usually not feasible unless there is some type of internal fixation to stabilize the fracture site. It is important to keep structures in the related area in a state as near normal as possible by using appropriate exercises without jeopardizing alignment of the fracture site while it is healing. The therapist must be alert to complications that can occur following a fracture (summarized in Box 11.7).

BOX 11.7 Complications of Fractures¹⁰

Swelling that is contained within a compartment (fascial compartment or tight cast) leading to nerve and circulatory compromise.
Fat embolism (may occur with fracture in bones with the most marrow, such as long bones and the pelvis) that migrates to the lungs and blocks pulmonary vessels. This is potentially life-threatening.
Problems with fixation devices such as displacement of screws and breakage of wires
Infection that occurs locally or systemically
Refracture
Delayed or malunion

Immobilization in Bed

If bed rest or immobilization in bed is required, as with skeletal traction, secondary physiological changes occur systematically throughout the body. General exercises for the uninvolved portions of the body are initiated to minimize these problems.

Functional Adaptations

If there is a lower extremity fracture, alternative modes of ambulation, such as the use of crutches or a walker, are taught to the patient who is allowed out of bed. The choice of device and gait pattern depends on the fracture site, the type of immobilization, and the functional capabilities of the patient. The patient's physician should be consulted to determine the amount of weight bearing allowed. Management guidelines are summarized in Box 11.8.

BOX 11.8 MANAGEMENT GUIDELINES—Postfracture/Period of Immobilization Impairments, Activity Limitations, and Participation Restrictions:

Initially, inflammation and swelling

Progressive muscle atrophy, contracture formation, cartilage degeneration, and decreased circulation in the immobilized area

Potential overall body weakening if confined to bed

Limited activity and restricted participation in ADLs, IADLs, and work imposed by the fracture site and method of immobilization used

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Plan of Care

Intervention

1. Educate the patient.

1. Teach functional adaptations.

Teach safe ambulation, bed mobility.

2. Decrease effects of inflammation during acute period.

2. Ice, elevation

3. Decrease effects of immobilization.

3. Intermittent muscle setting.

Active ROM to joints above and below immobilized region.

4. If patient is confined to bed, maintain strength and ROM in major muscle groups.

4. Resistive exercises to major muscle groups not immobilized, especially in preparation for future ambulation

Postimmobilization

Impairments

Decreased ROM, joint play, and muscle flexibility.
Muscle atrophy with weakness and poor muscle endurance.
Initially, the patient experiences pain as movement begins, but it should progressively decrease as joint movement, muscle strength, and ROM improve.
If there was soft tissue damage at the time of the fracture, an inelastic scar restricts tissue mobility in the region of the scar.

Management: Postimmobilization

Management guidelines are summarized in Box 11.9.

BOX 11.9 MANAGEMENT GUIDELINES—Postfracture/Postimmobilization Impairments:

Pain with movement, which progressively decreases

Decreased ROM

Decreased joint play

Scar tissue adhesions

Decreased strength and endurance

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Plan of Care

Interventions

1. Educate the patient.

1. Inform patient of limitations until fracture site is radiologically healed.

Teach home exercises that reinforce interventions.

2. Provide protection until radiologically healed.

2. Use partial weight bearing in lower extremity and nonstressful activities in the upper extremity.

3. Initiate active exercises.

3. Active ROM, gentle multiangle isometrics

4. Increase joint and soft tissue mobility.

4. Initiate joint play stretching techniques (using grades III and IV) with the force applied proximal to the healing fracture site.

For muscle stretching, apply the force proximal to the healing fracture site until radiologically healed.

5. Increase strength and muscle endurance.

5. As the ROM increases and the bone heals, initiate resistive and repetitive exercises.

6. Improve cardiorespiratory fitness.

6. Initiate safe aerobic exercises that do not stress the fracture site until it is healed.

PRECAUTIONS: No stretch or resistive forces distal to the fracture site until the bone is radiologically healed. No excessive joint compression or shear for several weeks after the period of immobilization. Use protected weight bearing until the site is radiologically healed.

Consultation with the referring physician is necessary to determine if there is clinical or radiological healing. Until the fracture site is radiologically healed, care should be used any time stress is placed across the fracture site, such as when applying resistance or a stretch force or during weight-bearing activities. Once radiologically healed, the bone has normal structural integrity and can withstand normal stress.

The patient is examined to identify impairments and determine the current functional status, activity level, and desired outcome. ROM, joint mobility, and muscle performance as well as any other impairments are measured and documented. Usually all of the joint and periarticular tissues are affected in the region that was immobilized.

Typical interventions include:

Joint mobilization. Joint mobilization techniques are effective for regaining lost joint play without traumatizing the articular cartilage or stressing the fracture site.⁴⁹ Intervention begins with gentle stretches and progresses in intensity as joint reaction becomes predictable.
PNF Stretching. Hold-relax and agonist-contraction techniques are used during the postimmobilization period because the intensity can be controlled by the patient. It is important to monitor the intensity of contraction and to not apply the resistive or stretch force beyond the fracture site until there is radiological healing of the bone in order to avoid a bending force across the fracture site. Once the bone is radiologically healed, the stretch force can be applied beyond the fracture site.
Functional activities. The patient can resume normal activities with caution. During the early postimmobilization period, it is important to not traumatize the weakened muscle, cartilage, bone, and connective tissue. Partial weight bearing must be continued for several weeks after a lower extremity fracture until the fracture site is completely healed and able to tolerate full weight bearing.
Muscle performance: Strengthening and muscle endurance. For 2 to 3 weeks following immobilization, because neither the bone nor cartilage can tolerate excessive compressive or bending forces, exercises are initiated with light isometrics. As joint play and ROM improve, progression is made to light resistance through the available range. The resistive force should be applied proximal to the fracture site until the bone is radiologically healed. Once healed, PRE and other more intense dynamic exercises can be initiated.
Scar tissue mobilization. If there is restricting scar tissue, manual techniques to mobilize the scar are used. The choice of technique depends on the tissue involved.

Independent Learning Activities

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Critical Thinking and Discussion

Your patient sustained a traumatic knee joint injury in an automobile accident. There is joint effusion, limited ROM, and decreased joint play 2 days after the accident. The patient guards against motion as you approach the end of the available range. Identify the principles of treatment, the goals, and plan of care for this patient. Describe and practice specific therapeutic techniques that you would use for intervention and describe how you would progress the techniques through the stages of healing.
Develop a program of interventions for a patient with osteoarthritis in the knees who has pain when ascending and descending steps and has difficulty standing up from a chair. What examination procedures do you want to do? What functional tests do you want to document? How would the program differ for an individual with symptoms of rheumatoid arthritis during a period of active disease (the acute phase)? During a period of remission (the chronic phase)?
Describe your plan of care and list specific interventions for a 55-year-old woman who is postmenopausal and has early signs of osteoporosis. What patient instructions would be important to include?
An individual sustained a fracture 6 weeks ago, and the limb was just removed from the cast. How does treatment differ from that of other traumatic conditions 6 weeks postinjury? Describe what precautions you will follow and why they are important.
Your patient was involved in a motor vehicle accident 6 months ago. You saw her 3 months ago, but now she has returned with a diagnosis of fibromyalgia (FM). Her physician recommends exercise. Describe your treatment program, taking into consideration the characteristics of FM and the benefits and problems of exercise in this population.
Your new patient is a secretary who presents with upper back and neck pain. She describes a gradual onset. She reports sitting at a computer for 6 to 8 hours each day and having to take phone calls on a regular basis as well. You examine the patient and find several active myofascial trigger points. Describe your course of treatment for this patient. How will you address the effect her work has on her problem?

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Clinical Signs and Symptoms

Impaired Mobility

Impaired Muscle Performance

Impaired Balance

Activity Limitations and Participation Restrictions

Rheumatoid Arthritis

Characteristics of RA

FIGURE 11.1

FIGURE 11.2

FIGURE 11.3

Signs and Symptoms: Periods of Active Disease

Principles of Management: Active Inflammatory Period of RA

Principles of Management: Subacute and Chronic Stages of RA

Osteoarthritis: Degenerative Joint Disease

FIGURE 11.4

Characteristics of OA

FIGURE 11.5

FIGURE 11.6

Principles of Management: Osteoarthritis

Fibromyalgia

FIGURE 11.7

Prevalence of FM

Characteristics of FM

Factors Contributing to a Flare

Management: Fibromyalgia

Myofascial Pain Syndrome

FIGURE 11.8

Possible Causes of Trigger Points

Management: Myofascial Pain Syndrome

Risk Factors

FIGURE 11.9

FIGURE 11.10

Prevention of Osteoporosis

Physical Activity

Effects of Exercise

Recommendations for Exercise

Mode: Aerobic

Mode: Resistance

Precautions and Contraindications

FIGURE 11.11

FIGURE 11.12

FIGURE 11.13

Risk Factors

Bone Healing Following a Fracture

Cortical Bone Healing

Inflammatory Phase

Reparative Phase

Remodeling Phase

Rigid Internal Fixation

Healing Time

Cancellous Bone Healing

Epiphyseal Plate Healing

Principles of Management: Period of Immobilization

Local Tissue Response

Immobilization in Bed

Functional Adaptations

Postimmobilization

Impairments

Management: Postimmobilization

Critical Thinking and Discussion

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