69
Arthritis and Connective
Tissue Diseases
Dottie Roberts
http://evolve.elsevier.com/Lewis/medsurg/
CONCEPTUAL FOCUS
Coping Mobility
Fatigue Pain
Functional Ability Self-Management
Inflammation
LEARNING OUTCOMES
1. Outline the sequence of events leading to joint destruction 5. Describe the pathophysiology, clinical manifestations,
in osteoarthritis and rheumatoid arthritis. and interprofessional and nursing management of
2. Detail the clinical manifestations and interprofessional systemic lupus erythematosus, scleroderma, polymyositis,
and nursing management of osteoarthritis and rheumatoid dermatomyositis, and Sjögren syndrome.
arthritis. 6. Explain the drug therapy and related nursing management
3. Describe the pathophysiology, clinical manifestations, and associated with arthritis and connective tissue diseases.
interprofessional care of gout, Lyme disease, and septic 7. Relate possible etiologies, clinical manifestations, and
arthritis. interprofessional and nursing management of fibromyalgia
4. Discuss the pathophysiology, clinical manifestations, and and systemic exertion tolerance disease.
interprofessional and nursing management of ankylosing
spondylitis, psoriatic arthritis, and reactive arthritis.
KEY TERMS
ankylosing spondylitis (AS) psoriatic arthritis (PsA)
arthritis Raynaud phenomenon
dermatomyositis (DM) rheumatoid arthritis (RA)
fibromyalgia (FMS) septic arthritis
gout scleroderma
Lyme disease Sjögren syndrome
osteoarthritis (OA) systemic exertion intolerance disease (SEID)
polymyositis (PM) systemic lupus erythematosus (SLE)
This chapter discusses rheumatic diseases, which mainly affect States have rheumatic conditions.2 By 2040, that number is
body joints, tendons, ligaments, muscles, and bones. These expected to exceed 78 million.
diseases are often marked by inflammation, pain, and loss of
function in 1 or more of the body’s connecting or supporting
structures. Limited function and fatigue, loss of self-esteem,
ARTHRITIS
altered body image, and fear of disability can challenge the Arthritis involves inflammation of a joint or joints. Most
patient’s ability to cope. We have found more than 100 kinds forms of arthritis affect women more often in every age group.2
of rheumatic diseases.1 At least 54 million adults in the United Osteoarthritis is the most common chronic condition of the
1696
, CHAPTER 69 Arthritis and Connective Tissue Diseases 1697
TABLE 69.1 Causes of OA BOX 69.1 BIOLOGIC SEX CONSIDERATIONS
Cause Effects on Joint Cartilage OA
Drugs Drugs, such as indomethacin and corticosteroids,
Men
may stimulate collagen-digesting enzymes in
• Except for traumatic arthritis, men do not have OA as often as women until
joint synovium.
age 70 or 80 years.
Hematologic or Chronic hemarthrosis (e.g., from hemophilia) may
• Hip OA is more common.
endocrine problems contribute to cartilage deterioration.
Inflammation Release of enzymes in response to local Women
inflammation may affect cartilage health. • Affects women more often.
Joint instability Damage to supporting structures causes instability, • More likely to have hand OA (interphalangeal joints and thumb base).
placing uneven stress on joint cartilage. • Knee OA is more common and likely to be more severe, especially after
Mechanical stress Repetitive physical activities (e.g., sports) can menopause.
cause cartilage deterioration.
Neurologic problems Pain and loss of reflexes from neurologic
disorders, such as diabetic neuropathy and smooth, white, translucent articular cartilage becomes dull, yel-
Charcot joint, cause abnormal movements that
low, and granular as OA progresses. Affected cartilage steadily
may contribute to cartilage deterioration.
Skeletal deformities Congenital or acquired conditions (e.g., dislocated
becomes softer and less elastic. It is less able to resist wear with
hip) may contribute to cartilage deterioration. heavy use.
Trauma Dislocations or fractures may lead to avascular The body’s attempts at cartilage repair cannot keep up with
necrosis or uneven stress on cartilage. the destruction of OA. As the collagen structure in the cartilage
changes, articular surfaces become cracked and worn. While
central cartilage becomes thinner, cartilage at the joint edges
becomes thicker and osteophytes form. Joint surfaces become
joints.3 Other forms include rheumatoid arthritis (RA), fibro- uneven, affecting the distribution of stress across the joint and
myalgia (FMS), systemic lupus erythematosus (SLE), and gout. causing reduced motion.
Although inflammation is not typical of OA, secondary syno-
OSTEOARTHRITIS vitis may occur when phagocytes try to rid the joint of small
pieces of cartilage torn from the joint surface. These changes
Osteoarthritis (OA) is a slowly progressive noninflammatory cause the early pain and stiffness of OA. Pain in later disease
disorder of the diarthrodial (synovial) joints. OA affects over 30 occurs when articular cartilage is lost, and bony joint surfaces
million adults in the United States.2 We expect this number to rub each other.
increase as the population ages.
Clinical Manifestations
Etiology and Pathophysiology Joints
OA involves the gradual loss of articular cartilage with forma- Manifestations range from mild discomfort to significant dis-
tion of bony outgrowths (spurs or osteophytes) at the joint mar- ability. Joint pain is the main symptom and the typical reason the
gins. OA is not a normal part of the aging process, but aging is patient seeks medical care. Pain typically worsens with activity.
one risk factor for disease development. Cartilage destruction In early stages of OA, rest relieves the joint pain. However, the
likely begins between ages 20 and 30. Most adults are affected patient with advanced OA may have pain at rest or have trouble
by age 40. Few patients have symptoms until after age 50. By age sleeping due to increased joint pain. Pain may worsen when the
65, almost 50% of adults report having arthritis.4 barometric pressure falls before the onset of severe weather.
OA may be caused by a known event or condition that As OA progresses, increasing pain can contribute to disabil-
directly damages cartilage or causes joint instability (Table ity and loss of function. Pain may be referred to the groin, but-
69.1). However, we cannot identify a single cause for many per- tock, or outside of the thigh or knee. It can be hard to sit down
sons with OA. In these situations, various genetic traits may or get up from a chair when the hips are lower than the knees.
contribute to the development of cartilage defects.5 As OA develops in the intervertebral (apophyseal) joints of the
Decreased estrogen at menopause may contribute to the spine, local pain and stiffness are common.
increased incidence of OA in aging women (Box 69.1). Obesity Joint stiffness occurs after periods of rest or an unchanged
contributes to hip and knee OA. It increases mechanical stress on position (gelling phenomenon). Early morning stiffness is com-
the joints. Regular moderate exercise, which helps with weight, mon. It often resolves within 30 minutes. This distinguishes OA
decreases the risk for OA development and progression. Anterior from inflammatory joint disorders, such as RA. Excess activity
cruciate ligament injury from quick stops and pivoting, as in foot- can cause a mild joint swelling that temporarily increases stiff-
ball and soccer, increase risk for knee OA.3 Work that requires fre- ness. Crepitation, a grating sensation caused by loose cartilage
quent kneeling and stooping also increases the risk for knee OA. particles in the joint cavity, can cause stiffness. Crepitation is
The development of OA is complex. Genetic, metabolic, and common in patients with knee OA.
local factors interact to cause cartilage deterioration from dam- OA usually affects joints on 1 side of the body (asymmetric)
age at the level of the chondrocytes (Fig. 69.1). The normally rather than in pairs. For example, the left knee may be affected
,1698 SECTION 12 Problems Related to Movement and Coordination
Synovium
inflamed
Wide space
Subchondral Joint space
between bone Joint capsule
bone plate narrowed
maintained inflamed and
Cartilage by loss of
by normal edematous
Synovium cartilage cartilage
Joint capsule thickness Cartilage splits
and is eroded
A B
Loss of cartilage,
Outgrowth
bone articulates
of bone
with bone
(osteophytes)
Hyperplasia
of synovium
with
inflammation
Development
Thickening of
of subarticular
subchondral
bone cysts
bone plate
C D
Fig. 69.1 Pathologic changes in OA. (A) Normal synovial joint. (B) Early change in OA is destruction of artic-
ular cartilage and narrowing of the joint space. There is inflammation and thickening of the joint capsule and
synovium. (C) With time, thickening of subarticular bone occurs, caused by constant friction of the 2 bone
surfaces. Osteophytes form around the periphery of the joint by irregular overgrowths of bone. (D) Heberden
nodes (red arrows) and Bouchard nodes (yellow areas) in a patient with OA. (From Forbes CD, Jackson WF:
Color atlas and text of clinical medicine, ed 3, London, 2003, Mosby.)
and the right knee unchanged. Weight-bearing joints (hips, Diagnostic Studies
knees), the metatarsophalangeal (MTP) joint of the foot, and X-rays help confirm disease and stage joint damage. As OA pro-
the cervical and lower lumbar vertebrae are often involved (Fig. gresses, x-rays often show joint space narrowing and increas-
69.2). Other affected joints include the distal interphalangeal ingly dense bone. Osteophytes may be visible. However, these
(DIP) and proximal interphalangeal (PIP) joints of the fingers, changes do not always reflect the degree of pain the patient has.
and the metacarpophalangeal (MCP) joint of the thumb. Despite strong x-ray evidence of disease, the patient may have
few symptoms. Another patient may have severe pain with only
Deformity slight x-ray changes. A bone scan, CT scan, or MRI can detect
Deformity or instability from OA is specific to the involved joint. early joint change. They are not typically used for diagnosis due
For example, Heberden nodes occur on the DIP joints due to osteo- to cost.
phyte formation and loss of joint space (Fig. 69.1D). They can Synovial fluid analysis helps distinguish OA from other types
appear as early as age 40. Bouchard nodes on the PIP joints indicate of inflammatory arthritis. In OA, the fluid is clear yellow with
similar disease involvement. Heberden and Bouchard nodes are little or no sign of inflammation. No laboratory tests or bio-
often red, swollen, and tender. They usually do not cause significant markers can be used to diagnose OA. The erythrocyte sedimen-
loss of function, but the visible deformity may bother the patient. tation rate (ESR) is normal except for slight increases during
Knee OA often leads to obvious joint deformity due to car- acute inflammation. Other routine blood tests (e.g., CBC, liver
tilage loss in 1 joint compartment. For example, the patient function tests) are useful only in screening for related condi-
becomes bowlegged (varus deformity) from medial joint arthri- tions or establishing baseline values before starting treatment.
tis. Lateral joint arthritis causes a knock-kneed appearance (val-
gus deformity). In advanced hip OA, 1 leg may become shorter Interprofessional Care
as the joint space narrows. OA has no cure. Care focuses on managing pain and inflam-
mation, preventing disability, and maintaining and improving
Systemic joint function (Table 69.2). A comprehensive treatment plan
Fatigue, fever, and organ involvement are not present in OA. may include education and behavioral, psychosocial, and phys-
This is an important distinction between OA and inflammatory ical interventions. Drug therapy can include topical, oral, and
joint disorders, such as RA. intraarticular agents.6
, CHAPTER 69 Arthritis and Connective Tissue Diseases 1699
TABLE 69.2 Interprofessional Care
OA
Diagnostic Assessment
• History and physical assessment
Cervical vertebrae • Radiologic studies of involved joints (e.g., x-ray, CT scan, MRI, bone scan)
• Possible synovial fluid analysis
Management
• Nutrition and weight management counseling
Lower lumbar vertebrae • Rest and joint protection, use of assistive devices
• Therapeutic exercise
• Heat and cold applications
Hip
• TENS
Metacarpophalangeal • Reconstructive joint surgery
(MCP)
Drug Therapy (Table 69.3)
• NSAIDs
• Intraarticular corticosteroids
Proximal
interphalangeal Distal interphalangeal
(PIP) (DIP)
Knee applications may be needed daily because topical agents have
short-acting effects.
Oral NSAID therapy typically is started in low-dose OTC
strengths (e.g., ibuprofen 200 mg up to 4 times daily). The dose
may be increased if needed. If the patient is at risk for or devel-
ops GI side effects with an NSAID, adding a protective agent,
Metatarsophalangeal
(MTP) such as misoprostol (Cytotec), may be needed. Arthrotec, a
combination of misoprostol and the NSAID diclofenac, is
available.
Fig. 69.2 Joints most often involved in OA.
Teach the patient who is taking an oral NSAID to avoid
use of a topical NSAID because of increased risk for adverse
Drugs thought to slow the progression of OA or support effects. Patients taking an anticoagulant (e.g., warfarin) and
joint healing are known as disease-modifying osteoarthritis drugs an oral NSAID are at high risk for bleeding. Long-term
(DMOADs). To date, no drugs have been approved to modify NSAID treatment may affect cartilage metabolism, especially
OA progression despite much research. in older patients who may have poor cartilage integrity. As
an alternative to traditional NSAIDs, the COX-2 selective
Drug Therapy inhibitor celecoxib (Celebrex) may be considered in selected
Drug therapy is based on the joint affected and symptom sever- patients.
ity (Table 69.3). Nonsteroidal antiinflammatory drugs (NSAID) Some patients still prefer aspirin, but it is no longer a com-
are first-line treatment for OA. NSAIDs inhibit the production mon treatment. It should be used cautiously with NSAIDs
of cyclooxygenase. When given in equivalent doses, all NSAIDs because both inhibit platelet function and prolong bleeding
are comparably effective. They vary widely in cost. Individual time.
responses to NSAIDs also vary. Most NSAIDs are nonspecific, Intraarticular corticosteroid injections may be needed for
affecting both COX-1 and COX-2.7 These 2 enzymes convert those with local inflammation and swelling. Four or more injec-
arachidonic acid into prostaglandins (see Fig. 9.5). COX-2 tions without relief suggest the need for more intervention.
plays a role in inflammation. COX-1 helps protect the stomach Systemic corticosteroids are not used as they may hasten the
lining. Inhibiting COX-1 causes many of the negative effects disease process. Hyaluronic acid injection (viscosupplementa-
of oral NSAIDs, including bleeding and gastrointestinal (GI) tion) has been a common treatment for knee OA. Neither the
irritation.7 American College of Rheumatology (ACR) nor the American
Some patients start with a topical agent, such as capsaicin Academy of Orthopaedic Surgeons (AAOS) recommends using
cream. It blocks pain by locally interfering with substance P. It hyaluronates.6
is responsible for the transmission of pain impulses. A concen-
trated product is available by prescription. Creams of 0.025% Surgical Therapy
to 0.075% capsaicin are available over the counter (OTC). Symptoms are often managed conservatively for many years.
Diclofenac gel is another option. OTC products that contain Loss of joint function, unmanaged pain, and increased
camphor, eucalyptus oil, and menthol (e.g., Bengay, Arthricare) dependence in self-care may lead to consideration of surgery.
may provide temporary pain relief. Topical salicylates (e.g., Reconstructive surgeries (e.g., hip and knee replacements) are
Aspercreme) may be an option for some patients. Several discussed in Chapter 67.
Arthritis and Connective
Tissue Diseases
Dottie Roberts
http://evolve.elsevier.com/Lewis/medsurg/
CONCEPTUAL FOCUS
Coping Mobility
Fatigue Pain
Functional Ability Self-Management
Inflammation
LEARNING OUTCOMES
1. Outline the sequence of events leading to joint destruction 5. Describe the pathophysiology, clinical manifestations,
in osteoarthritis and rheumatoid arthritis. and interprofessional and nursing management of
2. Detail the clinical manifestations and interprofessional systemic lupus erythematosus, scleroderma, polymyositis,
and nursing management of osteoarthritis and rheumatoid dermatomyositis, and Sjögren syndrome.
arthritis. 6. Explain the drug therapy and related nursing management
3. Describe the pathophysiology, clinical manifestations, and associated with arthritis and connective tissue diseases.
interprofessional care of gout, Lyme disease, and septic 7. Relate possible etiologies, clinical manifestations, and
arthritis. interprofessional and nursing management of fibromyalgia
4. Discuss the pathophysiology, clinical manifestations, and and systemic exertion tolerance disease.
interprofessional and nursing management of ankylosing
spondylitis, psoriatic arthritis, and reactive arthritis.
KEY TERMS
ankylosing spondylitis (AS) psoriatic arthritis (PsA)
arthritis Raynaud phenomenon
dermatomyositis (DM) rheumatoid arthritis (RA)
fibromyalgia (FMS) septic arthritis
gout scleroderma
Lyme disease Sjögren syndrome
osteoarthritis (OA) systemic exertion intolerance disease (SEID)
polymyositis (PM) systemic lupus erythematosus (SLE)
This chapter discusses rheumatic diseases, which mainly affect States have rheumatic conditions.2 By 2040, that number is
body joints, tendons, ligaments, muscles, and bones. These expected to exceed 78 million.
diseases are often marked by inflammation, pain, and loss of
function in 1 or more of the body’s connecting or supporting
structures. Limited function and fatigue, loss of self-esteem,
ARTHRITIS
altered body image, and fear of disability can challenge the Arthritis involves inflammation of a joint or joints. Most
patient’s ability to cope. We have found more than 100 kinds forms of arthritis affect women more often in every age group.2
of rheumatic diseases.1 At least 54 million adults in the United Osteoarthritis is the most common chronic condition of the
1696
, CHAPTER 69 Arthritis and Connective Tissue Diseases 1697
TABLE 69.1 Causes of OA BOX 69.1 BIOLOGIC SEX CONSIDERATIONS
Cause Effects on Joint Cartilage OA
Drugs Drugs, such as indomethacin and corticosteroids,
Men
may stimulate collagen-digesting enzymes in
• Except for traumatic arthritis, men do not have OA as often as women until
joint synovium.
age 70 or 80 years.
Hematologic or Chronic hemarthrosis (e.g., from hemophilia) may
• Hip OA is more common.
endocrine problems contribute to cartilage deterioration.
Inflammation Release of enzymes in response to local Women
inflammation may affect cartilage health. • Affects women more often.
Joint instability Damage to supporting structures causes instability, • More likely to have hand OA (interphalangeal joints and thumb base).
placing uneven stress on joint cartilage. • Knee OA is more common and likely to be more severe, especially after
Mechanical stress Repetitive physical activities (e.g., sports) can menopause.
cause cartilage deterioration.
Neurologic problems Pain and loss of reflexes from neurologic
disorders, such as diabetic neuropathy and smooth, white, translucent articular cartilage becomes dull, yel-
Charcot joint, cause abnormal movements that
low, and granular as OA progresses. Affected cartilage steadily
may contribute to cartilage deterioration.
Skeletal deformities Congenital or acquired conditions (e.g., dislocated
becomes softer and less elastic. It is less able to resist wear with
hip) may contribute to cartilage deterioration. heavy use.
Trauma Dislocations or fractures may lead to avascular The body’s attempts at cartilage repair cannot keep up with
necrosis or uneven stress on cartilage. the destruction of OA. As the collagen structure in the cartilage
changes, articular surfaces become cracked and worn. While
central cartilage becomes thinner, cartilage at the joint edges
becomes thicker and osteophytes form. Joint surfaces become
joints.3 Other forms include rheumatoid arthritis (RA), fibro- uneven, affecting the distribution of stress across the joint and
myalgia (FMS), systemic lupus erythematosus (SLE), and gout. causing reduced motion.
Although inflammation is not typical of OA, secondary syno-
OSTEOARTHRITIS vitis may occur when phagocytes try to rid the joint of small
pieces of cartilage torn from the joint surface. These changes
Osteoarthritis (OA) is a slowly progressive noninflammatory cause the early pain and stiffness of OA. Pain in later disease
disorder of the diarthrodial (synovial) joints. OA affects over 30 occurs when articular cartilage is lost, and bony joint surfaces
million adults in the United States.2 We expect this number to rub each other.
increase as the population ages.
Clinical Manifestations
Etiology and Pathophysiology Joints
OA involves the gradual loss of articular cartilage with forma- Manifestations range from mild discomfort to significant dis-
tion of bony outgrowths (spurs or osteophytes) at the joint mar- ability. Joint pain is the main symptom and the typical reason the
gins. OA is not a normal part of the aging process, but aging is patient seeks medical care. Pain typically worsens with activity.
one risk factor for disease development. Cartilage destruction In early stages of OA, rest relieves the joint pain. However, the
likely begins between ages 20 and 30. Most adults are affected patient with advanced OA may have pain at rest or have trouble
by age 40. Few patients have symptoms until after age 50. By age sleeping due to increased joint pain. Pain may worsen when the
65, almost 50% of adults report having arthritis.4 barometric pressure falls before the onset of severe weather.
OA may be caused by a known event or condition that As OA progresses, increasing pain can contribute to disabil-
directly damages cartilage or causes joint instability (Table ity and loss of function. Pain may be referred to the groin, but-
69.1). However, we cannot identify a single cause for many per- tock, or outside of the thigh or knee. It can be hard to sit down
sons with OA. In these situations, various genetic traits may or get up from a chair when the hips are lower than the knees.
contribute to the development of cartilage defects.5 As OA develops in the intervertebral (apophyseal) joints of the
Decreased estrogen at menopause may contribute to the spine, local pain and stiffness are common.
increased incidence of OA in aging women (Box 69.1). Obesity Joint stiffness occurs after periods of rest or an unchanged
contributes to hip and knee OA. It increases mechanical stress on position (gelling phenomenon). Early morning stiffness is com-
the joints. Regular moderate exercise, which helps with weight, mon. It often resolves within 30 minutes. This distinguishes OA
decreases the risk for OA development and progression. Anterior from inflammatory joint disorders, such as RA. Excess activity
cruciate ligament injury from quick stops and pivoting, as in foot- can cause a mild joint swelling that temporarily increases stiff-
ball and soccer, increase risk for knee OA.3 Work that requires fre- ness. Crepitation, a grating sensation caused by loose cartilage
quent kneeling and stooping also increases the risk for knee OA. particles in the joint cavity, can cause stiffness. Crepitation is
The development of OA is complex. Genetic, metabolic, and common in patients with knee OA.
local factors interact to cause cartilage deterioration from dam- OA usually affects joints on 1 side of the body (asymmetric)
age at the level of the chondrocytes (Fig. 69.1). The normally rather than in pairs. For example, the left knee may be affected
,1698 SECTION 12 Problems Related to Movement and Coordination
Synovium
inflamed
Wide space
Subchondral Joint space
between bone Joint capsule
bone plate narrowed
maintained inflamed and
Cartilage by loss of
by normal edematous
Synovium cartilage cartilage
Joint capsule thickness Cartilage splits
and is eroded
A B
Loss of cartilage,
Outgrowth
bone articulates
of bone
with bone
(osteophytes)
Hyperplasia
of synovium
with
inflammation
Development
Thickening of
of subarticular
subchondral
bone cysts
bone plate
C D
Fig. 69.1 Pathologic changes in OA. (A) Normal synovial joint. (B) Early change in OA is destruction of artic-
ular cartilage and narrowing of the joint space. There is inflammation and thickening of the joint capsule and
synovium. (C) With time, thickening of subarticular bone occurs, caused by constant friction of the 2 bone
surfaces. Osteophytes form around the periphery of the joint by irregular overgrowths of bone. (D) Heberden
nodes (red arrows) and Bouchard nodes (yellow areas) in a patient with OA. (From Forbes CD, Jackson WF:
Color atlas and text of clinical medicine, ed 3, London, 2003, Mosby.)
and the right knee unchanged. Weight-bearing joints (hips, Diagnostic Studies
knees), the metatarsophalangeal (MTP) joint of the foot, and X-rays help confirm disease and stage joint damage. As OA pro-
the cervical and lower lumbar vertebrae are often involved (Fig. gresses, x-rays often show joint space narrowing and increas-
69.2). Other affected joints include the distal interphalangeal ingly dense bone. Osteophytes may be visible. However, these
(DIP) and proximal interphalangeal (PIP) joints of the fingers, changes do not always reflect the degree of pain the patient has.
and the metacarpophalangeal (MCP) joint of the thumb. Despite strong x-ray evidence of disease, the patient may have
few symptoms. Another patient may have severe pain with only
Deformity slight x-ray changes. A bone scan, CT scan, or MRI can detect
Deformity or instability from OA is specific to the involved joint. early joint change. They are not typically used for diagnosis due
For example, Heberden nodes occur on the DIP joints due to osteo- to cost.
phyte formation and loss of joint space (Fig. 69.1D). They can Synovial fluid analysis helps distinguish OA from other types
appear as early as age 40. Bouchard nodes on the PIP joints indicate of inflammatory arthritis. In OA, the fluid is clear yellow with
similar disease involvement. Heberden and Bouchard nodes are little or no sign of inflammation. No laboratory tests or bio-
often red, swollen, and tender. They usually do not cause significant markers can be used to diagnose OA. The erythrocyte sedimen-
loss of function, but the visible deformity may bother the patient. tation rate (ESR) is normal except for slight increases during
Knee OA often leads to obvious joint deformity due to car- acute inflammation. Other routine blood tests (e.g., CBC, liver
tilage loss in 1 joint compartment. For example, the patient function tests) are useful only in screening for related condi-
becomes bowlegged (varus deformity) from medial joint arthri- tions or establishing baseline values before starting treatment.
tis. Lateral joint arthritis causes a knock-kneed appearance (val-
gus deformity). In advanced hip OA, 1 leg may become shorter Interprofessional Care
as the joint space narrows. OA has no cure. Care focuses on managing pain and inflam-
mation, preventing disability, and maintaining and improving
Systemic joint function (Table 69.2). A comprehensive treatment plan
Fatigue, fever, and organ involvement are not present in OA. may include education and behavioral, psychosocial, and phys-
This is an important distinction between OA and inflammatory ical interventions. Drug therapy can include topical, oral, and
joint disorders, such as RA. intraarticular agents.6
, CHAPTER 69 Arthritis and Connective Tissue Diseases 1699
TABLE 69.2 Interprofessional Care
OA
Diagnostic Assessment
• History and physical assessment
Cervical vertebrae • Radiologic studies of involved joints (e.g., x-ray, CT scan, MRI, bone scan)
• Possible synovial fluid analysis
Management
• Nutrition and weight management counseling
Lower lumbar vertebrae • Rest and joint protection, use of assistive devices
• Therapeutic exercise
• Heat and cold applications
Hip
• TENS
Metacarpophalangeal • Reconstructive joint surgery
(MCP)
Drug Therapy (Table 69.3)
• NSAIDs
• Intraarticular corticosteroids
Proximal
interphalangeal Distal interphalangeal
(PIP) (DIP)
Knee applications may be needed daily because topical agents have
short-acting effects.
Oral NSAID therapy typically is started in low-dose OTC
strengths (e.g., ibuprofen 200 mg up to 4 times daily). The dose
may be increased if needed. If the patient is at risk for or devel-
ops GI side effects with an NSAID, adding a protective agent,
Metatarsophalangeal
(MTP) such as misoprostol (Cytotec), may be needed. Arthrotec, a
combination of misoprostol and the NSAID diclofenac, is
available.
Fig. 69.2 Joints most often involved in OA.
Teach the patient who is taking an oral NSAID to avoid
use of a topical NSAID because of increased risk for adverse
Drugs thought to slow the progression of OA or support effects. Patients taking an anticoagulant (e.g., warfarin) and
joint healing are known as disease-modifying osteoarthritis drugs an oral NSAID are at high risk for bleeding. Long-term
(DMOADs). To date, no drugs have been approved to modify NSAID treatment may affect cartilage metabolism, especially
OA progression despite much research. in older patients who may have poor cartilage integrity. As
an alternative to traditional NSAIDs, the COX-2 selective
Drug Therapy inhibitor celecoxib (Celebrex) may be considered in selected
Drug therapy is based on the joint affected and symptom sever- patients.
ity (Table 69.3). Nonsteroidal antiinflammatory drugs (NSAID) Some patients still prefer aspirin, but it is no longer a com-
are first-line treatment for OA. NSAIDs inhibit the production mon treatment. It should be used cautiously with NSAIDs
of cyclooxygenase. When given in equivalent doses, all NSAIDs because both inhibit platelet function and prolong bleeding
are comparably effective. They vary widely in cost. Individual time.
responses to NSAIDs also vary. Most NSAIDs are nonspecific, Intraarticular corticosteroid injections may be needed for
affecting both COX-1 and COX-2.7 These 2 enzymes convert those with local inflammation and swelling. Four or more injec-
arachidonic acid into prostaglandins (see Fig. 9.5). COX-2 tions without relief suggest the need for more intervention.
plays a role in inflammation. COX-1 helps protect the stomach Systemic corticosteroids are not used as they may hasten the
lining. Inhibiting COX-1 causes many of the negative effects disease process. Hyaluronic acid injection (viscosupplementa-
of oral NSAIDs, including bleeding and gastrointestinal (GI) tion) has been a common treatment for knee OA. Neither the
irritation.7 American College of Rheumatology (ACR) nor the American
Some patients start with a topical agent, such as capsaicin Academy of Orthopaedic Surgeons (AAOS) recommends using
cream. It blocks pain by locally interfering with substance P. It hyaluronates.6
is responsible for the transmission of pain impulses. A concen-
trated product is available by prescription. Creams of 0.025% Surgical Therapy
to 0.075% capsaicin are available over the counter (OTC). Symptoms are often managed conservatively for many years.
Diclofenac gel is another option. OTC products that contain Loss of joint function, unmanaged pain, and increased
camphor, eucalyptus oil, and menthol (e.g., Bengay, Arthricare) dependence in self-care may lead to consideration of surgery.
may provide temporary pain relief. Topical salicylates (e.g., Reconstructive surgeries (e.g., hip and knee replacements) are
Aspercreme) may be an option for some patients. Several discussed in Chapter 67.
