Management of Osteoarthritis



Management of Osteoarthritis





Osteoarthritis (OA), the most prevalent form of arthropathy, causes symptomatic discomfort in 10% to 20% of persons older than the age of 65 years and accounts for somewhat more than 30% of visits to primary care practitioners. OA is the most common cause of disability in the elderly. Most patients have primary or idiopathic disease that is strongly associated with aging. Others present with posttraumatic and hereditary forms of the disease (e.g., chondrodystrophy, hemochromatosis, inflammatory OA, chondrocalcinosis). Although many changes are irreversible, much can be done to relieve discomfort, prevent further articular damage, and keep the patient functioning independently.

Given the prevalence and disabling potential of OA and the wide range of treatments and remedies promoted to patients, the primary care physician and medical home team need to be knowledgeable about what works and what does not as well as understand the patient’s perspective and functional status in order to fashion a personalized, evidence-based program of care. This chapter focuses on basic principles of OA care and the specifics of hip and knee involvement. Specific treatment of disease in the back, neck, shoulders, and hands is discussed in chapters dealing with pain and dysfunction in those areas (see Chapters 147, 148, 149, 150, and 153).


PATHOPHYSIOLOGY AND CLINICAL PRESENTATION (1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12 and 13)


Pathogenesis and Pathophysiology

OA is characterized by (a) the degeneration of articular cartilage and (b) the reactive formation of new bone. What causes the demise of the articular cartilage and what causes the pain are incompletely understood.


Pathogenesis and Risk Factors

The simplistic “wear-and-tear” hypothesis has been superseded by an appreciation for the role of chondrocytes in actively remodeling cartilage. Articular damage appears to be the consequence of an interplay among systemic factors affecting the health of the cartilage and local biomechanical factors. Genetic determinants account for as much as 50% of the risk of developing OA of the hands and hips and somewhat less for the knees. Defective collagen synthesis has been identified in some familial forms. Bone density and vitamin D intake also contribute. Local biomechanical determinants of risk include poor joint alignment, obesity, joint laxity, prior injury, and muscle weakness. Excessive stress from obesity can be harmful, especially in the elderly. In the Framingham Study, women who lost an average of 11 lb experienced a 50% reduction in risk of knee OA. Running per se is neither protective nor destructive (unless the knee has been injured, in which case persistent running hastens degenerative change, as seen in competitive long-distance runners). The synovial inflammation that is characteristic of rheumatoid disease appears to play only a minor role, if any, in most cases of OA.



Mechanism(s) of Pain

Pain is the most disabling manifestation of OA, yet its mechanism(s) remains poorly understood, reflected in the modest efficacy of current methods of pain control. There are no pain fibers in cartilage; any pain that ensues as a result of articular damage must involve adjacent pain-sensitive structures, such as the joint capsule, ligaments, synovium, periosteal bone, and bone marrow. Capsular distention is one possible source, but the injection of anesthetic into painful osteoarthritic knees usually fails to relieve pain, suggesting that the principal source(s) of pain is extra-articular. Of interest is the observation that inhibition of nerve growth factor, which is overly expressed in the setting of tissue injury, reduces pain in patients with OA. However, the successful inhibition of such pain has also been associated with excessive wear and a hastening of joint failure.

Current research has concentrated on adjacent bone as an important source of pain. The periosteum and subchondral bone contain nociceptive nerve fibers capable of detecting injury to bone. A strong correlation has been noted between pain and marrow lesions (as identified by magnetic resonance imaging) in adjacent bone. Marrow edema has been found in bone with such lesions, suggesting an inflammatory response. If confirmed and proven causative, such a marrow response would help to explain why OA pain is often delayed until the evening and why some patients obtain better pain relief from anti-inflammatory agents than from pure analgesics (see later discussion). Although subchondral and periarticular bony changes are prominent, they do not respond to high-dose vitamin D supplementation in terms of pain reduction or cartilaginous loss despite 2 years of treatment.


Clinical Presentation

Radiologic evidence of OA can be found in more than 80% of adults by age 65 years. The subset who are symptomatic complain of deep, aching joint pain that is aggravated by motion and weight bearing; sometimes, it is worse at night after a day of vigorous activity. Those who come for medical attention often have a
concomitant psychosocial problem. OA patients characteristically report stiffness after periods of inactivity. The involved joint can be enlarged by the formation of osteophytes, but swelling is usually inconsequential because in most instances soft tissue involvement and effusions are minimal. In later stages, pain occurs on motion and at rest in conjunction with stiffness. Patients with advanced disease have pain on weight bearing and joint instability. Examination often reveals crepitus and discomfort on movement of the joint. Occasionally, slight warmth is noted in severely affected weight-bearing joints, but erythema and marked warmth are absent. Limitation of motion, malalignment, and bony protuberances from spurs are frequent findings. The joints most commonly affected include the knees, hips, distal interphalangeal (DIP) joints of the hands, carpometacarpal joint at the base of the thumb, and the joints of the cervical and lumbosacral spine.


Knees

Symptomatic knee involvement is estimated to affect as much as 10% of the population older than the age of 65 years. Obesity is a major risk factor. OA of the knee produces pain that is localized to the medial and/or lateral joint line and worsened by prolonged weight bearing and stair climbing. In later stages, crepitus is often marked and range of motion reduced. A very small effusion may be noted. The joint appears to be enlarged and feels bony. Patellofemoral joint involvement produces anterior knee pain that is exacerbated by going down stairs. On occasion, very few physical findings may be noted, although pain and radiographic changes are prominent. A skyline view of the flexed knee can reveal patellofemoral disease.


Hips

Degenerative hip disease arises in young patients with congenital dislocations or slipped femoral capital epiphyses. In the elderly, it results from wear and tear. A unilateral or asymmetric distribution is typical. The patient may describe pain that is deep in the hip and radiates into the anterior medial thigh, groin, buttock, or medial knee. The site of radiation (e.g., groin or buttock) may be the only area of reported pain. At first, pain occurs only on prolonged standing or walking, but as OA progresses, discomfort may become continuous and especially unbearable at night. The ability to engage in sexual intercourse is sometimes compromised. Loss of internal rotation during flexion is the earliest change and is as reliable as radiographic findings for diagnosis. The result of Trendelenburg test (see Chapter 151) is positive.


Hands

Characteristic sites include the DIP joints and base of the thumb (first carpometacarpal joint); sometimes, proximal interphalangeal (PIP) joint involvement is noted. Hand disease is most common in middle-aged and elderly women, many of whom have a strongly positive family history. In some, a low-grade inflammatory response may accompany early, rapid, mucinous degenerative changes, so that the joints take on a tender, cystic inflammatory appearance. Later, osteophytes form, giving rise to characteristic bony protuberances in the DIP joints (Heberden nodes) and occasionally PIP deformities (Bouchard nodes) that superficially resemble those of rheumatoid disease. Eventually, all inflammatory activity resolves, and the joints are left nontender with some limitation of motion.

The base of the thumb, a site of much physical stress, is vulnerable to degenerative change. Pain develops in the region of the thenar eminence and particularly over the carpometacarpal joint. Because the thumb is so important to manual dexterity, the development of arthritis at this site may be disabling. Grip becomes impaired, and fine movements of apposition are restricted. Osteophytes are palpable and, in rare instances, may encroach on the flexor tendon sheath, causing tenosynovitis.


Cervical Spine

Degenerative changes commonly involve the posterior diarthrodial joints of the lower cervical spine (see Chapter 148). Although radiographic changes are frequent, most persons are asymptomatic. Moreover, the correlation between symptoms and radiographic findings is often poor. The patient may have pain and stiffness in the neck, but sometimes, pain is reported only in the occiput, shoulder, arm, or hand. In a few instances, scapular or upper anterior chest pain is produced. Osteophytes can protrude into the foramina and impinge on nerve roots (most often C6 and C7), causing radicular pain that radiates to the shoulder, upper arms, hands, or fingers (see Chapter 167). At night, the patient may awaken with paresthesias and numbness in the arms that can be alleviated by getting up and shaking the arms. On examination, neck motion is restricted to some extent in all directions, especially lateral flexion and extension; movement reproduces or aggravates symptoms. Reactive muscle spasm and tenderness are often present, and decreased sensation, weakness, and diminished reflexes occur when root compression is marked. However, even when symptoms of root compression are reported, neurologic findings may be scant, and their absence does not rule out the complication.


Lumbosacral Spine

Degenerative changes in the lumbosacral spine involve the intervertebral disks and the apophyseal joints. With aging, the disk nucleus becomes brittle and less elastic. Herniation posteriorly or laterally through a defect in the disk annulus may occur. Intervertebral spaces narrow, and marginal osteophytes form. The apophyseal joints show typical secondary degenerative changes. Disk or osteophyte encroachment on the foramina can lead to nerve root compression. The L4, L5, and S1 roots are most commonly affected. The patient reports pain across the lower back with radiation into the buttock and posterior thigh or down into the lower leg if root compression has occurred. Forward flexion and extension are reduced, but lateral flexion is painless. Focal areas of tenderness are common and often caused by spasm of the paraspinous musculature. Disk or osteophyte encroachment into the spinal canal can lead to spinal stenosis, which affects the cauda equina and exiting nerve roots. Compression of nerve roots produces pseudoclaudication (pain in the buttocks or thighs during prolonged standing or walking that is relieved by sitting or bending). On examination, thigh symptoms may be brought on by 30 seconds of lumbar extension and then relieved by having the patient bend forward. In addition, the patient may have a wide-based gait and neurologic deficits in the lower extremities.


Other Sites

OA may involve the great toe at the metatarsophalangeal joint to cause bony enlargement and a valgus deformity. Crepitus and pain in the temporomandibular joint are sometimes seen secondary to bruxism (grinding of the teeth because of anxiety or anger). Pain is reproduced by opening the mouth widely. Because OA is not a systemic disease, no extra-articular manifestations and no serum abnormalities occur; the sedimentation rate is normal, as is the synovial fluid in early disease. Radiographic findings are limited to the joints and include irregular narrowing of the joint space, sclerosis of subchondral bone, bony cysts, marginal osteophytes, and buttressing of adjacent bone.


Natural History of Disease

In large, weight-bearing joints, OA tends to be a progressive condition causing chronic joint pain, restricted joint motion, and resultant muscle weakness that compromises mobility. Through a period of 10 to 20 years, pain at rest develops in the majority
of patients with untreated symptomatic OA of the knee, and they become unable to use public transportation; disability may ensue. An early onset of symptoms and varus deformity correlate with a poor prognosis. OA of the hip may follow a similar course. Obesity is a strong risk factor for progressive disease of the hips and knees (especially in women); heavy weight-bearing exercise is associated with an increased risk for knee disease in the elderly. Weight reduction reduces the risk. The progression of OA is typically limited to a few affected joints, and the disease does not become widespread. Clinical remissions do occur, especially in the hands, neck, and back.




PRINCIPLES OF MANAGEMENT (14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38, 39, 40, 41, 42, 43, 44, 45, 46, 47, 48 and 49)

The treatment of OA remains largely symptomatic. Except for total joint replacement, there are no disease-modifying therapies of proven effectiveness (though the search for them continues). Nonetheless, reduction in pain, improvement in joint function, and restoration of activity leading to a better quality of life can often be achieved with implementation of a comprehensive program. The immediate goals are to reduce pain and muscle spasm, alleviate abnormal stresses imposed on affected joints, restore joint alignment, and improve endurance. Nonopioid analgesics, exercise, and weight reduction (if overweight or obese) are core components of a comprehensive management program; joint replacement surgery is a viable option for many with end-stage disease. In addition, there are a large number of heavily promoted unproven remedies. The primary care physician has the important responsibilities of designing the basic treatment program, engaging a team of medical home and specialty colleagues in its implementation, and helping guide the patient through a daunting number of choices to ensure the care rendered is evidence based and personally meaningful.


Pharmacologic Therapy


Analgesics and Anti-inflammatory Agents

Pain relief is a top priority for most patients. Analgesics remain the predominant pharmacologic approach in the absence of disease-modifying therapy for OA. The basic approach to analgesic use in OA follows the standard paradigm of best practice for chronic nonmalignant pain (see Chapter 236). Because an individual patient’s response to analgesics is unpredictable, it may require some degree of a trial-and-error approach. Intermittent use of analgesics sometimes suffices, but continuous therapy is often needed in the absence of more definitive treatment. Whether to use a pure analgesic agent or a nonsteroidal anti-inflammatory drug (NSAID) with analgesic properties is a subject of debate. Of interest, there are few long-term study data on the efficacy of analgesic therapy, even though these drugs are often taken chronically. Chronic use has raised concerns about adverse effects, both for pure analgesics and for nonsteroidals taken for OA.


Acetaminophen.

Pure nonnarcotic analgesics, such as acetaminophen, should be tried first. Results from an often-cited, welldesigned study of OA patients with knee pain found acetaminophen comparable to nonsteroidal therapy (naproxen) in controlling pain and without the risk of adverse gastrointestinal effects. Other well-designed but small-scale, short-term studies failed to confirm these findings and suggested that acetaminophen is little better than placebo. Such variable findings parallel the experience of patients in everyday practice, some of whom find acetaminophen perfectly adequate, whereas others do not.

The cost of acetaminophen is low, and its long-term safety when used in moderate doses is well established, though use in the elderly, especially in doses in excess of 3 g/d, is associated with an increased risk of hepatic injury. The U.S. Food and Drug Administration (FDA) advised that individual tablet strength be no more than 325 mg and that total daily acetaminophen intake (including that contained in prescription and nonprescription medications) be noted and limited. Risk of liver injury is particularly substantial in the context of underlying alcoholic liver disease. Long-term therapy at high doses may increase the risk for renal tubular injury, but supporting data are sparse, and the risk appears to be no greater than that associated with prolonged NSAID use.


Nonsteroidal Anti-inflammatory Drugs.

Current consensus guidelines relegate NSAIDs to a second-line role in OA, but a large percentage of OA patients find them preferable for pain relief. Such observations from everyday practice suggest that there might be an underappreciated inflammatory component to the pain of OA (also supported by some research into the mechanisms of OA pain; see prior discussion). More clinical and fundamental research is needed to help guide analgesic therapy, but in the meantime, patients will continue to use whichever available analgesics provide them with the best pain relief over time. Those who fail acetaminophen can be started on a trial course of a generic nonselective NSAID (e.g., ibuprofen 400 mg thrice daily or naproxen 500 mg twice daily). Use of ibuprofen is not recommended in persons taking low-dose aspirin therapy for cardiovascular prophylaxis due to concern that ibuprofen may render aspirin ineffective by competing for binding sites on platelets.

Because analgesic therapy is often long term in OA, the adverse effects associated with chronic NSAID use become important considerations. Peptic ulceration and gastrointestinal bleeding are the predominant risks associated with nonselective NSAID use (see Chapter 68); these can be lessened to about 5% by a number of gastroprotective measures, including avoidance of concurrent aspirin intake, initiation of a proton pump inhibitor (e.g., omeprazole), and use of a more selective cyclooxygenase-2 (COX-2) NSAID (see Chapters 68 and 156). For this reason, COX-2 drugs were initially very popular among patients and physicians for use in OA, but after postmarketing data revealed an increased risk of adverse cardiovascular events (relative risk, 1.5 to 3.5 for myocardial infarction, stroke, and death, especially with extended use [>18 months]), their use has declined markedly, especially in the elderly and others at increased cardiovascular risk. These findings and concern about thromboembolic potentiation prompted the withdrawal of one COX-2 agent from the market and the issuance of warnings regarding the use of the others (see Chapter 156). Both their high cost and concerns about increased cardiovascular risk have relegated the COX-2 drugs to third-line status for the treatment of chronic OA pain.

Other adverse effects of NSAIDs include renal compromise that may develop in persons with underlying renal insufficiency or heart failure (see Chapters 32 and 142). Hypertension control may also be impeded (see Chapter 26). Some elderly patients experience mental confusion while taking NSAIDs that penetrate the central nervous system (e.g., indomethacin). There is some suggestive evidence that long-term use of nonspecific NSAIDs may have an adverse effect on articular cartilage, but this has yet to be confirmed.

Topical NSAID preparations (e.g., diclofenac gel) are recommended for use in elderly patients (>75 years of age) in lieu of oral NSAIDs because of the latter’s many serious adverse effects associated with chronic use. Topical NSAIDs provide a
modest but significant increase in pain relief in persons with OA of the knee or hands compared to placebo (the placebo benefit is considerable). Systemic toxicity is minimal; local skin irritation occurs in about 7%; cost is high. Animal data suggest an increased risk of UV-related skin tumors; exposure of the treated area to sunlight should be minimized.


Centrally Acting, Weak Opioid Analgesics: Tramadol.

This centrally acting analgesic with weak opioid effects might be considered if acetaminophen and NSAIDs fail to provide adequate pain relief. Comparative studies in patients with OA have shown it to be equivalent in analgesic effect to naproxen. It is rapidly absorbed, with a peak effect at 2 hours and a halflife of 6 hours in its short-acting formulation; a longer-acting extended-release formulation is also available. Benefits include a relative lack of potential for abuse and respiratory depression in comparison with pure mu-agonist opioids. But it still may have side effects typical of opioids including nausea, drowsiness, and constipation. It should be used with caution in patients with a history of seizures or those on other serotonergic medications.


Narcotic Analgesics.

Codeine, oxycodone, and other narcotic analgesics should be used sparingly, if at all, and only for acute disabling pain that interferes with essential activity. Increased appreciation for the risks associated with sustained use (e.g., abuse, dependence, falls, cognitive impairment) has led to calls for greatly limiting use for chronic pain, especially in the elderly (see Chapters 235 and 236). In cohort study of opioids for OA, opioids use was associated with a marked increase in all-cause mortality.

Results from intra-articular injection of a narcotic analgesic have been disappointing, with fewer than 10% of persons with knee pain responding.


New Approaches to Pain Control: Nerve Growth Factor Inhibition.

The expression of nerve growth factor (a neurotrophin that regulates sensory neurons) is increased in chronic pain syndromes from conditions such as OA that cause tissue injury. A new approach to pain control utilizing monoclonal antibodies directed against nerve growth factor has shown promise. Tanezumab, one such humanized monoclonal antibody, was found in an exploratory, randomized controlled trial to reduce joint pain and improve functioning; however, the subsequent finding of an increased rate of joint failure due to excessive wear and tear from increased activity in the absence of severe pain had given pause to this approach. Research has resumed.


Antidepressants and Antispasmodics

OA patients with unrecognized and untreated depression benefit from disease-specific treatment, be it pharmacologic and/or interpersonal. Pain control improves, as does functional state and overall quality of life. Starting a generic formulation of a selective serotonin reuptake inhibitor (SSRI) antidepressant (e.g., fluoxetine; see Chapter 227) to supplement the analgesic program can be particularly helpful in depressed OA patients, although it may take several weeks for benefits to be fully realized. Use of selective norepinephrine/serotonin reuptake inhibitors (SNRIs) (e.g., duloxetine) is under study.


Nonpharmacologic Measures


Exercise/Physical Therapy and Weight Reduction

Of the nonpharmacologic therapies, exercise/physical therapy and weight reduction show the most consistently beneficial results for patients with OA, especially in those who are overweight or obese and have disease of the major weight-bearing joints.


Exercise and Physical Therapy.

Restoration of favorable mechanics and reconditioning are essential to minimizing damage to diseased joints and maximizing function. Strengthening (anaerobic) and conditioning (aerobic) exercises are associated with the greatest and most sustained improvements in pain and overall functioning. Strengthening the supporting muscles helps maintain proper joint alignment; reconditioning enhances functional capacity and endurance. For patients with OA of weight-bearing joints, structured aerobic exercise programs with full or partial weight bearing can greatly improve walking distance and sense of well-being without aggravating the arthritis. Participation in a supervised conditioning program boosts morale and facilitates compliance.

Only gold members can continue reading. Log In or Register to continue

Stay updated, free articles. Join our Telegram channel

Aug 23, 2016 | Posted by in CRITICAL CARE | Comments Off on Management of Osteoarthritis

Full access? Get Clinical Tree

Get Clinical Tree app for offline access