MUSCULOSKELETAL DISEASES AND DISORDERS

MUSCULOSKELETAL DISEASES AND DISORDERS
Suggestions for Lecturer -1-hour lecture -Use GRS slides alone or to supplement own teaching materials. -Refer to the GRS chapter on musculoskeletal diseases and disorders for further content, including strength of evidence (SOE) levels. -Supplement the lecture with handouts. -See GRS8 questions 16, 42, 66, 233, 258, 259, and 307 for case vignettes. Topic

OBJECTIVES Know and understand:
The factors unique to the management of older adults with musculoskeletal symptoms Recognition and treatment of specific rheumatologic diseases and symptoms Differential diagnosis and management of pain in the shoulder, elbow, wrist, hip, and knee Topic

Special Considerations in Older Adults Diagnosis
TOPICS COVERED Special Considerations in Older Adults Diagnosis Specific Rheumatologic Diseases Regional Musculoskeletal Complaints General Management Strategies Topic

Specific diseases in combination are of clinical importance
COMORBIDITIES Thorough assessment of comorbid illnesses is a necessary part of caring for older adults with musculoskeletal disorders Diseases and their treatments often compete, complicating medical management and increasing risk of functional limitations Specific diseases in combination are of clinical importance An example of a significant clinical challenge is comorbid arthritis and heart disease. Patients with rheumatoid arthritis appear to be predisposed to premature cardiovascular events. Additionally, anti- inflammatory therapies commonly prescribed to manage painful symptoms must be used cautiously in patients with underlying heart disease. Finally, patients with severe heart disease may not be able to undergo surgery for joint reconstruction or replacement despite the severity of symptoms and disability. Topic

FUNCTIONAL LIMITATIONS
Arthritis and pain contribute to functional limitations in late life The accompanying muscle weakness increases the risk of further functional limitations and disability Being overweight or obese contributes to mobility limitations that are compounded by arthritis of weight-bearing joints Topic

Do the symptoms arise from the joint or elsewhere?
DIAGNOSIS Information that is critical to the diagnosis of musculoskeletal complaints: Do the symptoms arise from the joint or elsewhere? Is the process inflammatory? How many joints are involved? Topic

SYMPTOMS INDICATING ARTHRITIS
Reproducible on active and passive joint range of motion Joint line is painful or tender on palpation Range of motion may/may not be limited Inflammatory signs may be present: Warmth Erythema Swelling Effusion The most useful indication that pain is coming from the joint rather than from supporting structures is the presence of pain with both active and passive movement, particularly if combined with tenderness along the joint line. Restriction of range of motion and inflammatory signs may or may not be present, particularly early on, and could support both articular and non-articular diagnoses. Topic

SYMPTOMS INDICATING TENDINITIS
Reproducible on active but not passive range of motion Range of motion is preserved unless limited because of contracture Maneuvers specific to the region are helpful when pain is elicited For example, forced supination against resistance results in anterior shoulder pain due to bicipital tendinitis Inflammatory signs may be present Topic

SYMPTOMS INDICATING BURSITIS
Tenderness on palpation over the bursa Range of motion Active range of motion may be painful Passive range of motion is neither painful nor limited unless there is an underlying arthritis Inflammatory findings may be present Topic

SYMPTOMS ARISING FROM BONE PROBLEMS
Pain that is not reproducible with range of movement Localized tenderness may be present The source may be distinct from the joint Topic

SIGNS OF INFLAMMATORY ARTHRITIS
Stiffness that is present on awakening and persists for hours Features of systemic illness (sometimes) Joints that are palpably warmer than surrounding tissues, visibly red, or swollen Occasionally effusions may be palpated Noninflammatory stiffness generally resolves within an hour after awakening or recurs after periods of inactivity. Unintentional weight loss, fever, loss of appetite, or a general feeling of poor health are features of a systemic illness and may accompany an inflammatory arthritis. The presence of rash, fever, stomatitis, dysphagia, Raynaud phenomenon, or true muscle weakness suggests an autoimmune rheumatologic disorder. Topic

ARTHRITIS DIFFERENTIAL DIAGNOSIS
Monoarthritis (1 joint) Pauci-arthritis (2 or 3 joints) Polyarthritis (≥4 joints) Trauma Infection-related (eg, bacterial, fungal, TB, Lyme disease) Crystal-mediated Hemarthrosis Osteoarthritis Psoriatic arthritis Reactive (Reiter syndrome) Enteropathic (eg, IBS) Sarcoidosis (knees, ankles) Ankylosing spondylitis Amyloid (shoulder) Infection-related (eg, Lyme disease, rheumatic fever, endocarditis) Rheumatoid arthritis Immune complex (eg, lupus, serum sickness, hypersensitivity drug reaction) Infection-related (eg, Lyme disease, viral arthritis, rheumatic fever, endocarditis) IBS = inflammatory bowel disease Identifying the number of involved joints can often be helpful in guiding diagnosis. Arthrocentesis should be performed to evaluate the etiology of an undiagnosed monoarthritis to exclude an infection and to evaluate for crystals. Topic

LABORATORY TESTS (1 of 2) Westergren erythrocyte sedimentation rate (ESR) is useful in patients with headache, fever of unknown origin, or unintentional weight loss if vasculitis (eg, giant cell arteritis) or other systemic inflammatory disease is suspected Rheumatoid factor may be useful in supporting the diagnosis of rheumatoid arthritis (RA) in patients with the symmetric inflammatory polyarthritis The ESR can be increased in older adults even in the absence of identifiable illness; it increases normally with aging according to the following formula: men: (age); women: (age). The ESR is useful in evaluating patients with headache, fever of unknown origin, or unintentional weight loss if temporal or giant cell arteritis is suspected; however, diagnosis requires biopsy of the temporal artery. ESR increases can also accompany nonrheumatic systemic illness and therefore cannot distinguish, based on the laboratory result alone, giant cell arteritis from systemic infection, myeloma, or other advanced malignancy. Rheumatoid factor is an antibody (usually IgM) that reacts with the Fc portion of IgG. It can be detected in 70%–80% of patients with RA but is not specific to this disease. It can also be detected in up to 30% of apparently healthy older adults, but when present it is usually at a titer of 1:80 or less. This test may be most useful in evaluation of older adults with symmetric inflammatory polyarthritis that is characteristic of RA. More recent studies suggest that using anti-cyclic citrullinated peptide antibodies (anti-CCP) together with the rheumatoid factor latex assay enhances specificity in the diagnosis of RA. Neither test should be used to evaluate older adults with diffuse and vague musculoskeletal complaints in the absence of symmetric inflammatory small-joint findings on examination. Topic

LABORATORY TESTS (2 of 2) Antinuclear antibodies (ANA) in high titers may signal systemic lupus erythematous or drug-induced lupus, inflammatory muscle disease (myositis), or scleroderma Arthrocentesis should be performed when joint infection is suspected, or to confirm crystal-mediated arthritis Antinuclear antibodies (ANAs) are immunoglobulins directed against DNA, RNA, and other nuclear or cytoplasmic proteins. Both the pattern of immunofluorescence (rim, speckled, nucleolar, or diffuse) and titer provide useful clinical information. ANAs can be found in healthy older adults but usually are in a diffuse pattern, and at a low titer, in the absence of rheumatic disease. The ANA test is highly sensitive for systemic lupus erythematosus in that a negative test essentially excludes a diagnosis of lupus. ANAs can be present in high titers in older adults with systemic or medication-induced lupus, inflammatory muscle disease, or scleroderma. Arthrocentesis should be performed when infection or crystalline- mediated inflammatory joint disease is suspected. Fluid should be sent for cell count, Gram stain, culture, and crystal analysis. Bloody effusions may be due to joint trauma and may signal a coagulopathy or periarticular fracture. Topic

IMAGING Radiographs are used to confirm a diagnosis of arthritis, distinguish inflammatory or destructive arthritis from noninflammatory forms, and to assess severity of joint damage MRI is preferred to visualize peri-articular and articular structures, when internal derangement of a joint is suspected (eg, meniscal disease), and to assess spinal cord integrity in patients with back pain CT is preferred to evaluate cortical abnormalities of axial bone (eg, spine, sacroiliac joint) and of intermediate to large joints Joint findings in inflammatory arthritis (eg, RA) are symmetric joint space narrowing, juxta-articular or generalized osteopenia, and erosions at or next to the joint. In contrast, degenerative arthritis or noninflammatory arthritis is characterized by asymmetric joint space narrowing, osteophytes, sclerosis, and cysts. Presence of radiographic osteoarthritis does not exclude the possibility that a periarticular or inflammatory condition coexists. Radiographs can also help distinguish arthritis from a periarticular or bony process (eg, osteomyelitis, periostitis, fracture). MRI provides high-resolution imaging of articular structures (cartilage, synovium, meniscus, ligaments) and periarticular structures. It can detect intraosseous processes, including infection, occult fracture, and avascular necrosis. It is significantly more expensive than plain radiographs and not superior for imaging the wrist, hand, and foot. Topic

RHEUMATOLOGIC DISEASES
Osteoarthritis (OA) Rheumatoid Arthritis (RA) Gout Calcium Pyrophosphate Dihydrate Deposition Disease (CPPD) Polymyalgia Rheumatica (PMR) Giant Cell Arteritis (Temporal Arteritis) Systemic Lupus Erythematosus Polymyositis and Dermatomyositis Sjögren Syndrome (Sjögren Disease) Topic

OSTEOARTHRITIS Present in 50%–90% of older adults
The major cause of knee, hip, and back pain in older adults Can develop in any joint that has suffered injury or other types of arthritis The hallmark is cartilage degeneration Fibrillation and ulceration begins superficially Eventually extends into deeper layers Recent evidence indicates that OA is not a purely degenerative disease restricted to the cartilage; subchondral bone abnormalities and focal synovial inflammation have also been seen in pathologic specimens. These pathologic characteristics are thought to arise as a result of repetitive cycles of degradation and repair responses that eventually become inadequate to maintain joint health. Inflammatory cytokines, matrix-degrading metalloproteinase enzymes, and chondrocyte apoptosis are likely contributors to this process. Topic

RADIOGRAPHIC FINDINGS IN OA
Bony enlargement and crepitus suggest OA. In the fingers, this enlargement is called Heberden nodes when it occurs in the distal interphalangeal joints and Bouchard nodes in the proximal interphalangeal joints. Joint tenderness and warmth may appear, but intense inflammation suggests an alternative or concomitant diagnosis. Osteophytes are the radiographic counterpart of this enlargement, and asymmetric joint space narrowing is also common. MRI can help evaluate back and neck symptoms that may require surgical intervention. Left half of slide: Radiographic OA of the knee with medial compartment osteophytes, joint space narrowing, and sclerosis. Right half of slide: Radiographic OA of the hand with osteophytes, asymmetric joint space narrowing, and sclerosis of varying degrees of the thumb base (carpometacarpal joint) and interphalangeal joints. Topic

NONSURGICAL OA THERAPIES
Weight reduction to help reduce pain and improve function in OA of the knee, hip, or spine Exercise for OA of the knee Orthotics for OA of the hip or knee Acetaminophen is the initial medication Low-dose narcotics Low-dose NSAID in cases of narcotic intolerance Topical therapies for hand or knee Glucocorticoid injections In knee OA, neoprene braces can alleviate patellofemoral symptoms by improving patellar tracking, and they can improve joint proprioception. Specific orthoses designed to reduce medial knee pain by unloading the medial compartment of the knee include a valgus unloader brace and a lateral wedge insole. A well-designed running shoe can also lessen pain and damage by decreasing the impact transmitted during ambulation. Finally, a properly fitted and used cane can provide stability and unload the symptomatic knee or hip. Topical therapies (eg, analgesic balms, capsaicin, topical NSAIDs) can be useful in hand or knee OA. Studies evaluating glucosamine and chondroitin sulfate for pain have had conflicting results Glucocorticoid injections can be used for knee pain, although whether they are more effective than placebo injection is unclear. Hyaluronic acid and hyaluronan polymers given in a series of weekly injections in the knee are approved as viscosupplementation therapy. The benefits of these preparations vary substantially, but they last longer than the benefits of corticosteroid injections in those who respond. Topic

Arthroscopic debridement for knee OA High tibial osteotomy
SURGICAL OA THERAPIES Arthroscopic debridement for knee OA High tibial osteotomy Unicompartment joint replacement Total joint arthroplasty Arthroscopic debridement for knee OA is usually reserved for patients who report mechanical symptoms (eg, locking, “giveway” weakness), but effectiveness has not been proved. Joint-“sparing” high tibial osteotomy can realign the knee but requires considerable rehabilitation. Unicompartment joint replacement can be done in patients whose disease is limited to one compartment (eg, isolated medial, lateral, or patellofemoral knee OA). Total joint arthroplasty can be considered in patients with more extensive, disabling disease of the knee or hip. Although surgery remains the definitive intervention, it should be performed at a point when the patient is likely to be able to withstand both the surgery and the ensuing rehabilitation and is debilitated enough from the OA that the benefits of surgery outweigh the risks. Topic

RHEUMATOID ARTHRITIS Up to 40% of patients with RA are older than 60 years Some of these individuals have aged with the disease, while 20%–55% develop RA late in life Older adults with late-onset RA may present similarly to young adults with acute inflammatory polyarthritis that involves the small joints of the hands and feet and that is accompanied by a positive rheumatoid factor. Seronegative presentations that are unique to older adults include the “RS3PE” syndrome of remitting seronegative symmetrical synovitis with pitting edema, and an inflammatory arthritis of the shoulder and hips similar to polymyalgia rheumatica (PMR). In fact, descriptive studies suggest that late-onset RA should be considered in the differential diagnosis of PMR and vice versa. Other diseases that mimic RA include CPPD and carcinoma polyarthritis. As with young adults, the diagnosis of RA relies on clinical, radiologic, and laboratory criteria. In contrast to young adults with RA, older adults with RA are more likely to have a higher initial ESR. Topic

MANAGEMENT OF RA (1 of 2) Seropositive RA, even late-onset disease, should be managed aggressively, including use of disease-modifying anti-inflammatory drugs (DMARDs): Methotrexate Hydroxychloroquine Leflunomide Topic

MANAGEMENT OF RA (2 of 2) Several biologic agents for RA are available, but experience with these agents in older adults is limited, so their use is generally limited to those in whom conventional DMARD therapy has not been effective Low-dose prednisone (10–20 mg/day) may be used as the primary treatment for seronegative PMR-like disease and the “RS3PE” syndrome Several biologic agents for RA are available, but experience with these agents in older adults is limited, so their use is generally limited to those in whom conventional DMARD therapy has not been effective. These agents work by inhibiting tumor necrosis factor α (etanercept, infliximab, adalimumab, golimumab, and certolizumab), antagonizing the interleukin-1 receptor (anakinra), serving as a fusion protein co- stimulation modulator via inhibition of CD28 (abatacept), or binding the CD20 antigen on B lymphocytes (rituximab); they are given via injection or infusion. Infliximab, adalimumab, and rituximab all increase the risk of granulomatous infections with organisms such as Mycobacterium tuberculosis, atypical mycobacteria, yeast, Listeria, and Nocardia. Infliximab can also cause post-infusion fever, chills, headache, chest pain, and dyspnea. Anakinra is associated with bacterial respiratory tract infections. In contrast to classic PMR, late-onset RA may not respond promptly to low-dose prednisone. Prednisone alone is often not sufficient in managing seropositive RA but may be useful as an adjunctive agent. Its use is associated with increased risk of infectious complications, fluid retention, and osteoporosis. Topic

GOUT Clinical characteristics in older patients can differ appreciably from those in younger adults Diuretic use is an important predisposing factor After menopause, women are affected at the same rate as men Diagnosis requires sodium urate crystals from synovial fluid or an aspirate of a tophus Radiographs show juxta-articular erosions of the involved joints In older adults, gout can present as a subacute smoldering oligoarthritis rather than as an acute, monarticular, and incapacitating attack, as in classic podagra. Tophaceous deposits in the DIP and PIP joints can be mistaken for or coexist with OA. Similarly, tophi at the extensor surfaces can be confused with rheumatoid nodules. Acute attacks of gout can be precipitated by trauma, acute nonarticular illness requiring hospitalization, dehydration (acute gout is particularly common after surgery), and abrupt changes in uric acid concentration. On radiographs, an overhanging edge (ie, Martel sign) is helpful in distinguishing gout from RA. With rare exceptions, asymptomatic hyperuricemia precedes the development of gouty arthritis. However, hyperuricemia is not uniformly present at the time of an acute gout attack, nor does the presence of hyperuricemia confirm a diagnosis of gout. Topic

MANAGEMENT OF GOUT For acute gout attack:
Short-acting NSAID, if tolerated, is best option Narcotic medication or oral, IM, or intraarticular glucocorticoids IM or short-term oral glucocorticoids (prednisone 30 mg/day  5 days) preferred for managing a polyarticular gouty flare For recurrent episodes, colchicine can be added to reduce the frequency of gouty attacks The approved dose of colchicine for an acute attack is 1.2 mg orally at the onset of the attack and then 0.6 mg 1 hour later (total dose 1.8 mg). For patients who have recurrent episodes of gout, colchicine can be added prophylactically to reduce the frequency of recurrent gouty attacks. Conventional dosing is 0.6 mg orally q12h; the dosage should be reduced to 0.6 mg/day to 3 times weekly in patients with renal insufficiency; colchicine dosage adjustment is warranted among patients with hepatic insufficiency. Medications such as allopurinol, febuxostat, or probenecid, which can acutely lower uric acid levels, should not be used in the management of acute gout, because premature lowering of uric acid level paradoxically intensifies and prolongs an acute gout attack. Probenecid works as a uricosuric agent but is ineffective if creatinine clearance is <30 to 40 mL/minute. Allopurinol and febuxostat lower serum uric acid via inhibition of xanthine oxidase and are beneficial in management of chronic gout, particularly for those with tophi, renal stones, or for whom colchicine is ineffective; the dosage should be adjusted in patients with renal or hepatic impairment. Topic

CALCIUM PYROPHOSPHATE DIHYDRATE DEPOSITION DISEASE
Also known as “pseudogout”; can mimic RA, inflammatory OA, acute gout attack, or septic arthritis When fever is present, it is imperative to distinguish CPPD from septic arthritis Associated with disorders of calcium metabolism, hypothyroidism, and hemochromatosis CPPD of the wrist can be distinguished from RA by prominent synovitis and chondrocalcinosis of the wrist and MCP joints. CPPD can mimic inflammatory OA with rapid joint destruction of the wrist, patellofemoral knee compartment, and hip joint. CPPD can mimic an acute gout attack with sudden onset of pain and swelling that coincide with or immediately follow an acute illness or traumatic event such as surgery. Arthrocentesis with crystal analysis is diagnostic and useful to distinguish CPPD from gout and infection. CPPD crystals are weakly positive birefringent rhomboids or squares. Tests for rheumatoid factor and anti-CCP antibodies are negative in CPPD. Topic

RADIOGRAPHIC FINDINGS IN CPPD
CPPD is most commonly diagnosed by finding chondrocalcinosis on plain radiographs. Chondrocalcinosis appears as a stippled or linear calcification of the articular cartilage of the knee, wrist, hip, shoulder, and pubic symphysis. Left half of slide: Chondrocalcinosis of the meniscus. Right half of slide: Chondrocalcinosis of the triangular cartilage of the wrist. Topic

MANAGEMENT OF CPPD Arthrocentesis can result in significant relief of painful symptoms Short-acting NSAIDs and steroidal agents are useful if tolerated; otherwise, try intraarticular or parenteral corticosteroids Use of colchicine to prevent future acute episodes of CPPD has not been substantiated in clinical trials Given once and possibly repeated in 1–2 days, triamcinolone acetonide (60 mg IM), betamethasone (7 mg IM), or methylprednisolone (125 mg IV) are all safe and effective. Topic

POLYMYALGIA RHEUMATICA
Unique to older adults Should be suspected in patients who: Are ≥50 years old Have persistent pain or stiffness of the upper arms, shoulders, hips, or thighs Have constitutional symptoms of fatigue, low-grade fever, and weight loss Ischemic symptoms (eg, headache, claudication): evaluate patient for giant cell arteritis Poor or non-sustained response to glucocorticoid therapy: consider RA or concomitant giant cell arthritis Approximately 53 new cases of PMR develop per 100,000 persons per year, with an estimated prevalence of 600 cases per 100,000 and higher prevalence in older adults. Patients lack physical evidence of an inflammatory arthritis of the small hand joints, distinguishing PMR from RA, and they also have normal muscle bulk and strength. Diagnostic criteria include limb-girdle stiffness, a ESR often >50 mm/h, and normal levels of muscle enzymes. Recent studies of PMR have confirmed the presence of synovitis identical to that seen in RA, with synovial thickening, effusions, and lymphocytic synovial infiltration. Topic

Mild symptoms can respond to NSAIDs Most patients require prednisone
MANAGEMENT OF PMR Mild symptoms can respond to NSAIDs Most patients require prednisone Maintain starting dosage for 4–6 weeks before attempting gradual tapering Short-acting NSAID can be added during the taper Consider concomitant giant cell arteritis or alternative diagnosis of RA if response is incomplete or not sustained The prednisone dosage for PMR is 10 to 20 mg/day, given as a single dose in the early morning. Dosage reduction should be gradual with monitoring for symptom recurrence and laboratory studies suggesting reactivation (C-reactive protein, ESR). The duration of treatment required varies considerably, from 3 months to several years. Osteoporosis prophylaxis is recommended for all patients on systemic steroids for >2 months. Topic

GIANT CELL ARTERITIS (TEMPORAL ARTERITIS)
Granulomatous vasculitis that involves large and medium-sized arteries Notable overlap with PMR Presentation varies; head and neck symptoms are headache, jaw and tongue claudication with tenderness, erythema, and (occasionally) palpable nodules along the temporal artery Incidence of aneurysm is about 10% Temporal artery biopsy = gold standard for diagnosis Optic nerve pallor or swelling portends ischemia with impending blindness that warrants immediate glucocorticoid therapy. GCA can also appear as sudden blindness with no prior systemic illness or with claudication in the arms. Other manifestations can include stroke, ischemic necrosis of tongue or scalp, or rarely myocardial infarction. Aortic aneurysm, predominantly thoracic, is a late manifestation of GCA even when previously appropriately treated. The incidence of aneurysm in GCA is about 10%, with discovery of thoracic and abdominal aneurysm occurring at a median of 5.8 and 2.5 years, respectively, after GCA diagnosis. Constitutional symptoms of weight loss, malaise, fever, and depression may be the only manifestations of GCA. Temporal artery biopsy is the gold standard for diagnosis; a specimen several centimeters in length should be obtained from the symptomatic side and immediately processed by frozen-section staining of multiple cross- and longitudinal sections. A section of the contralateral side can be obtained if the initial specimens are negative. Evidence of vasculitis without giant cells suggests other diagnoses (eg, polyarteritis nodosa) that may require cytotoxic therapy. Ultrasound, angiography, MRI with gadolinium, and positron emission tomography have been investigated as diagnostic modalities for demonstrating vascular inflammation; however, none has replaced biopsy as the gold standard diagnostic test. Topic

MANAGEMENT OF GCA Patients suspected of having GCA should begin prednisone while awaiting biopsy, to reduce the risk of sudden blindness IV glucocorticoids are occasionally recommended for patients at high risk of blindness or other ischemic events Methotrexate not proven as a steroid-sparing agent Monitoring should be lifelong Pathologic evidence of GCA persists for up to 2 weeks of prednisone therapy. Prednisone is given at a dosage of 40–60 mg/day and should be maintained for at least 1 month before considering dosage reduction. Intravenous glucocorticoids (prednisolone or methylprednisolone 80–100 mg) are occasionally recommended for patients at high risk of blindness or impending ischemic events of other organs. Treatment should continue for approximately 1–2 years. Long- term glucocorticoid therapy warrants prophylaxis for osteoporosis. Published studies of methotrexate as a steroid-sparing agent have not consistently demonstrated a benefit. In addition, concomitant administration of low-dose aspirin may decrease the risk of cranial ischemic complications. Monitoring for return of symptoms of PMR or temporal arteritis, increase of inflammatory markers, and radiographic screening for aortic aneurysms should continue lifelong after ceasing immunosuppressive therapy. Topic

SYSTEMIC LUPUS ERYTHEMATOSUS
Autoimmune multisystemic disease Up to 20% of cases affect older adults “Elderly-onset lupus” (after age 50) often difficult to distinguish clinically from drug- induced lupus The diagnosis of lupus rests on a constellation of clinical criteria along with serologic evidence of autoimmunity (positive antinuclear antibody, anti–double-stranded DNA, anti–SM, or false-positive test for syphilis). Rheumatoid factor, anti-Ro/Sjögren syndrome (SS)A, and anti-La/SSB are more often positive in patients with elderly-onset lupus than in younger adults. Anti–double-stranded DNA and hypocomplementemia, both useful in monitoring disease activity in younger patients, are less frequently found in older adults. Both elderly-onset lupus and drug-induced lupus erythematosus (DILE) have a positive antinuclear antibody test, although DILE is associated with a speckled pattern with antihistone antibodies. Topic

CONSIDER ELDERLY-ONSET LUPUS IN THE DIFFERENTIAL DIAGNOSIS OF:
Rash Nonerosive arthritis Serositis (pleuritis, pericarditis) Cytopenias (leukopenia, hemolytic anemia, or thrombocytopenia) Neuropsychiatric symptoms (cognitive, seizures) Symptoms of sicca (in the absence of medication- induced dry mouth) Raynaud phenomenon Additional physical findings in lupus can include periungual or palmar erythema, asymptomatic oral or nasal ulcers, and livedo reticularis. When present, these should raise suspicion of anti-cardiolipin antibody syndrome (venous or arterial thromboembolic phenomena). Lupus should be considered in someone with persistent fever or thromboembolic phenomena, including stroke. Serologic evaluation for thromboembolic phenomena includes IgG and IgM anti-cardiolipin antibody levels and lupus anticoagulant testing, with mixing studies for a circulating anticoagulant to explain prolonged partial thromboplastin times. Renal involvement is less common in older lupus patients than in younger adults. Renal biopsy should be pursued to evaluate patients with proteinuria or an active urine sediment to determine the underlying pathophysiology before initiating treatment. Topic

MANAGEMENT OF LUPUS Short-acting NSAIDs, if tolerated, to treat arthritis and serositis Hydroxychloroquine for skin and joint manifestations Preventive anticoagulant therapy for patients who are cardiolipin and lupus anticoagulant positive IV methylprednisolone and monthly IV pulse cyclophosphamide for severe, renal (with an active urine sediment), or CNS disease Mycophenolate mofetil, taken orally on a daily basis, is an effective treatment option for lupus nephritis Treatment recommendations are based entirely on extrapolation from younger adults; no studies of these therapies have been done in older adults with lupus. Hydroxychloroquine is effective in managing skin and joint manifestations (begun at 200 mg/day for a week, then increased to mg/day). However, older adults should be evaluated for age-associated macular degeneration and monitored for visual field deficits possibly related to drug-induced retinopathy while receiving hydroxychloroquine treatment. Patients who are cardiolipin and lupus anticoagulant positive should receive preventive anticoagulant therapy. Intravenous methylprednisolone and monthly intravenous pulse cyclophosphamide is reserved for severe or renal (with an active urine sediment) or CNS disease. Methotrexate, azathioprine, mycophenolate mofetil, or cyclosporine (all off-label) can be of benefit as corticosteroid-sparing agents. Topic

POLYMYOSITIS & DERMATOMYOSITIS (1 of 2)
Heterogeneous and uncommon Incidence peaks in adults in their 50s Muscle weakness is the central feature of myositis: most prominent in the proximal muscle groups Serum creatine kinase is often markedly elevated Exclude conditions that can result in muscle weakness, including medications and metabolic derangements Patients with myositis report difficulty with tasks such as standing from a chair, ascending stairs, or lifting a light package above the head. Muscle tenderness is usually not a manifestation and should raise suspicion of other conditions. Arthritis, when present, is inflammatory and occasionally erosive, suggesting overlap with RA. Esophageal dysmotility can cause dysphagia, hoarseness, and aspiration. Arrhythmia, symptoms of congestive heart disease, dyspnea on exertion, or persistent cough suggest cardiac or interstitial lung disease. Raynaud phenomenon or Sjögren syndrome can also be present. The facial rash in dermatomyositis can involve the eyelids or the nose and malar areas, or it can be more generalized. Rash can also be apparent over the neck and upper torso in sun-exposed areas. Gottron papules (skin thickening over the interphalangeal joints) can also be observed. . Topic

POLYMYOSITIS & DERMATOMYOSITIS (2 of 2)
Muscle biopsy is the gold standard for diagnosis, but exclude other causes of muscle weakness first Diagnosis of polymyositis warrants an exam for cardiac and pulmonary disease; polymyositis or dermatomyositis warrants a search for underlying malignancy Electromyographic testing is used to exclude neuropathy. MRI using fat suppression sequences can help to select which muscle to biopsy. Associations with colon, lung, breast, prostate, ovarian, and uterine tumors have been reported, as have remission of polymyositis and dermatomyositis after treatment of the underlying malignancy. Topic

MANAGEMENT OF MYOSITIS
Glucocorticoids are the initial therapy Try tapering by 10%–20% per month Parenteral methotrexate in a weekly pulse regimen can be combined with corticosteroids and may have a steroid-sparing effect in long-term therapy Weekly oral methotrexate for refractory dermatomyositis Supervised exercise Prednisone at 1 mg/kg/day is a typical starting dosage for myositis, or an initial IV dose of methylprednisolone 1000 mg for severe disease. Prolonged glucocorticoid use at high dosages can result in a myopathy with resultant proximal muscle weakness. Prednisone can be tapered after an initial phase of improved muscle strength and normalized muscle enzyme levels. Tapering the total dose by 10% to 20% per month should be attempted. Supervised exercise over 6-week and 6-month study periods has proved beneficial in polymyositis, improving function without aggravating underlying disease. Topic

SJÖGREN SYNDROME (SJÖGREN DISEASE)
Systemic, multiorgan chronic disease with lymphocytic infiltration of exocrine glands Consider in patients with rash, interstitial lung disease, malabsorption, CNS disease that mimics MS, or unexplained renal, liver, or thyroid disease Management: symptomatic treatment of xerostomia and xerophthalmia; treat underlying inflammatory disease Sicca symptoms (dry mouth and dry eyes) are common but are frequently caused by medications and other connective tissue syndromes. An ophthalmologic examination that includes a Schirmer test and slit- lamp examination (to assess corneal damage) can confirm the presence of keratoconjunctivitis in Sjögren syndrome. Antinuclear, anti-SSA, and anti-SSB antibodies are usually present. Rheumatoid factor and a variety of autoantibodies are often seen. Biopsy of a skin rash can verify the presence of cutaneous vasculitis. Biopsies of a salivary or lacrimal gland can confirm the presence of characteristic lymphocytic infiltration. Sugar-free candies and artificial saliva can alleviate symptoms of xerostomia. Symptomatic treatment of xerophthalmia consists of lubricating ointments and artificial tears. Punctal plugs can be tried to retain tears. Ophthalmic cyclosporine can be used to treat inflammatory eye disease. Treatment of an underlying inflammatory disease (RA, lupus, myositis, scleroderma) can improve symptoms as well. Topic

REGIONAL RHEUMATIC PROBLEMS
The Painful Shoulder The Painful Elbow The Painful Wrist The Painful Hip The Painful Knee The Patient with Diffuse Pain Fibromyalgia Topic

Pain can occur as a local manifestation of a systemic process
THE PAINFUL SHOULDER Pain can be referred From cervical spine, heart, or subdiaphragm Pain can occur as a local manifestation of a systemic process RA, PMR, or amyloidosis Pain can arise from the shoulder itself Bursitis, tendinitis, capsulitis, or arthritis Subacromial bursitis causes a dull ache that precludes sleeping on the affected side, with tenderness to palpation diffusely along the shoulder. Bicipital tendinitis causes pain in the anterior-lateral aspect of the humeral head. Forced supination of the forearm against resistance with the elbow flexed at 90 reproduces the pain (Yergason sign). In contrast, rotator cuff tendinitis results in shoulder pain that is worse between 60 and 120 of abduction. Patients may have mild to no symptoms on passive abduction but often “drop” their arm when asked to abduct against gravity. This is difficult to distinguish clinically from an incomplete tear of the rotator cuff. However, patients with a complete rotator cuff tear are unable to sustain the weight of their arm against gravity at all. Adhesive capsulitis (ie, “frozen” shoulder) is a painful loss of range of motion in all directions. It can result from stroke, trauma, untreated arthritis, or relatively minor injury. Osteoarthritis, RA, and CPPD can all contribute to shoulder pain. Plain radiographs are most useful in assessing the shoulder for evidence of joint degeneration and can demonstrate calcification of the tendons or superior migration of the humeral head in the case of a complete rotator cuff tear. Shoulder pain often responds to local steroid injections administered in conjunction with the beginning of physical therapy. Surgical intervention is rarely pursued for these conditions in older adults. Topic

THE PAINFUL ELBOW Most common causes: bursitis and arthritis
Can be part of an inflammatory arthritis Evaluate monoarthritis for infectious etiology Tendinitis can cause elbow pain in overuse syndromes Olecranon bursitis, with swelling of the bursa and pain only at the extremes of range of movement, is commonly associated with RA and gout, both of which also result in palpable nodules or tophi Olecranon bursitis can be managed conservatively by using padding and avoiding pressure on the elbow. Excessive redness, warmth, or exquisite tenderness prompts evaluation for infection. Unlike bursitis, arthritis results in painful passive motion (supination or flexion) and tenderness on palpation over the joint line. Overlying cellulitis does not preclude joint aspiration for culture and cell count, but empiric antibiotic coverage is warranted. Topic

THE PAINFUL WRIST Can be a manifestation of: Arthritis
Inflammatory arthritis (RA, CPPD, gout) results in other joint involvement; evaluate monoarthritis for possible septic arthritis or gout Periostitis (occasionally) Carpal tunnel syndrome This in turn can be a manifestation of systemic disease (eg, diabetes, hypothyroidism, amyloidosis) Arthritis of the wrist results in painful passive motion that is usually accompanied by fullness and tenderness on palpation, which can be due to either synovial tissue inflammation or joint effusion. Radiographs are useful in distinguishing between the different types of arthritis. MRI should be pursued in patients with tenderness over the ulnar styloid process, to detect impending extension tendon rupture that requires tendon transfer surgery. Occasionally, wrist pain can be a manifestation of periostitis. Examination reveals tenderness on compression of the distal radius or ulna that can be confirmed on radiograph or bone scan. In carpal tunnel syndrome, the impingement of the median nerve causes pain and paresthesia of the hand that are prominent at night. Paresthesia can be reproduced by tapping over the flexor retinaculum (Tinel sign) or by forced flexion of the wrist (Phalen sign). The diagnosis is confirmed by demonstrating nerve conduction delay at the wrist. Older adults with cervical spine arthritis can manifest a “double crush” phenomenon that can be detected on electrodiagnostic testing. Management options include the consistent use of neutral wrist splints and judicious glucocorticoid injections into the carpal tunnel, taking care not to inject the median nerve. Surgical decompression should be pursued if conservative measures fail or if thumb apposition weakness or thenar muscle atrophy is apparent. Topic

THE PAINFUL HIP Pain can be referred from the spine, retro-peritoneal area, or knee, or arise in the joint/surrounding area Pain can be a manifestation of: Trochanteric bursitis Iliotibial band syndrome OA or RA PMR Fractures Paget disease of the bone, avascular necrosis, osteomyelitis, bone metastasis Trochanteric bursitis results in pain that is localized over the lateral proximal thigh and can be reproduced on palpation over the trochanter. Patients often complain of difficulty sleeping on the affected side. Response is good to glucocorticoid injection. Iliotibial band syndrome causes lateral thigh pain that is worse with walking and can be reproduced by having the patient bend forward at the waist while crossing the legs. Although also responsive to a steroid injection, iliotibial band syndrome should also be managed with stretching exercises and massage. Hip pain that is reproduced on passive motion of the hip suggests arthritis. Hip range of motion may be limited (especially internal rotation). Weakness of the hip muscles may be notable with a Trendelenburg sign or lurch during walking. Pain that is diffuse, bilateral, and accompanied by prolonged morning stiffness should raise suspicion of PMR. Plain radiographs are useful to evaluate for OA, RA, Paget disease of the bone, and fractures, while avascular necrosis is best demonstrated by MRI. Patients with hemoglobinopathy, traumatic injury to the hip, or malignancy who are receiving chronic steroid therapy and who report hip pain that is not reproduced on passive motion should be evaluated with a radiograph or MRI for avascular necrosis, osteomyelitis, or bone metastasis. Therapies usually include devices to reduce weightbearing on the affected hip (eg, cane, orthotics), weight loss and exercise, medications, and surgery. Topic

THE PAINFUL KNEE Knee pain affects >20% of adults ≥60 years, including close to 30% of those ≥80 years Pain can be a manifestation of: Inflammation of the anserine bursa Suprapatellar bursitis OA Popliteal cyst Meniscal disease Gout, CPPD, RA, psoriatic arthritis, reactive arthritis, avascular necrosis of the tibia, referred pain from hip disease, septic joint The anserine bursa is located inferior-medial to the knee joint, and when inflamed it causes knee pain that is most notable at night. There is exquisite tenderness to palpation over the area, with occasional swelling and erythema. Injection with a small amount of glucocorticoid mixed with anesthetic can be both diagnostic and therapeutic. Knee pain with visible fluid or swelling at the superior aspect of the knee is more consistent with suprapatellar bursitis. This is commonly exacerbated by frequent kneeling. Because mechanical irritation aggravates the suprapatellar bursa, avoidance of kneeling is recommended rather than injections or NSAIDs. Adequate padding between the knees while sleeping (for anserine bursitis) and thick padding while kneeling (for suprapatellar bursitis) can alleviate symptoms as well as prevent recurrence. Arthritis should be suspected with a history of knee pain that is aggravated by activity (eg, bending, stooping, walking) and alleviated with rest. The skin may or may not be warm. Passive motion and palpation of the joint line reproduces the pain. Occasionally there may be a small joint effusion. Patients with posterior knee pain should be examined for a popliteal cyst. Inspection of both popliteal fossae with the patient standing can reveal asymmetric fullness on one side and can be confirmed by ultrasound. The knee should be assessed for ligamentous instability (medial and lateral collateral and cruciate) by gently stressing the joint in all directions. Patients should be asked about locking or instability. Rotational extension can elicit pain localized to the site of meniscal disease, and MRI is needed to assess the extent of damage. Topic

THE PATIENT WITH DIFFUSE PAIN
Persistent pain with diffuse tenderness of periarticular regions warrants evaluation for metabolic disturbances that affect bone, eg: Vitamin D deficiency Hyperparathyroidism Hypothyroidism Systemic infection of any source can manifest with diffuse pain Topic

FIBROMYALGIA Chronic disorder characterized by pain, nonrestorative sleep, soft-tissue tenderness Becomes more prevalent in late life Frequently accompanied by fatigue, insomnia, depression, and anxiety Research suggests it is related to a problem with CNS processing of pain No diagnostic tests are available Commonly requested laboratory studies (eg, thyroid, vitamin D, antinuclear antibody, ESR, C-reactive protein) and imaging studies are usually negative or normal in patients with fibromyalgia. Aerobic exercise and stretching, as well as Tai Chi, are recommended for all but should be started slowly, and progressed patiently, to avoid overuse and strain injuries. Tricyclic antidepressants (off-label) can be helpful but should be started at low dosages and increased slowly with caution because of anticholinergic adverse events. Duloxetine, pregabalin, and gabapentin (off-label) have been studied in treatment of fibromyalgia and may have modest benefit for some patients. Topic

GENERAL MANAGEMENT STRATEGIES: NONPHARMACOLOGIC
Patient and family education is the first step Exercise has proven value for RA, OA, polymyositis, and lupus Therapeutic ultrasound is helpful for OA Cold/heat can decrease pain/muscle spasms Massage, acupuncture, TENS, neuromuscular electrical stimulation, and consultation with OT and PT are additional options TENS=transcutaneous electrical stimulation, OT=occupational therapist, PT=physical therapist. Patients should be provided with an exercise “prescription” that details warm- up activities, followed by instructions for the type of exercise (eg, strengthening, flexibility, and endurance), intensity, duration, and frequency during a given week. Patients should be advised to watch for signs of excessive joint strain, including pain during activity, or pain that lasts >1–2 h after exercise, swelling, fatigue, and weakness. Ultrasound uses high-frequency sound waves by pulsed delivery for acute pain and inflammation, or by continuous delivery for patients with chronic symptoms that have resulted in joint limitations. Use of ice or cold packs should be limited to 20 minutes or until the area becomes numb. Cautious use of heat can reduce pain and muscle spasm but should be limited to 20-minute intervals using a heating modality that is unlikely to cause skin scalding. Contrast therapy, which alternates between hot and cold treatment modalities, can provide additional therapeutic benefits compared with either alone. Neuromuscular electrical stimulation (NMES) delivers low-voltage electrical impulses through surface electrodes placed over motor points of the targeted muscle, inducing muscle contraction. NMES may be an alternative for patients who are unable to participate in exercise because of severe pain or contraindications. Topic

GENERAL MANAGEMENT STRATEGIES: PHARMACOLOGIC (1 of 2)
Generally reserved for severe symptoms or failure of nonpharmacological approaches Topical balms and creams, applied 2 or 3 times daily, can help control arthritis symptoms in small and intermediate joints Acetaminophen (500–1000 mg q8h) remains the preferred simple analgesic for older adults NSAIDs are often used only in good candidates for short terms Capsaicin cream is effective for OA of the hand(s) but must be used carefully to avoid contact with mucous membranes, particularly to the eyes. The risk of nephropathy from acetaminophen remains low when it is used in modest dosages in patients without preexisting kidney disease and with cautious supervision in patients with renal insufficiency. Excessive dosages can result in hepatotoxicity. NSAIDs can be prescribed at either analgesic (lower) or anti-inflammatory dosages, but because of their toxicity in older adults, they are recommended only in suitable candidates for short periods. Analgesic medications include choline magnesium trisalicylate (750 mg q8h) and ibuprofen (200–800 mg q8h). Nonacetylated salicylates such as salsalate or magnesium choline salicylate and COX-2 agents are thought to have lower GI toxicity when used short term, but equivalent GI toxicity may result when used long term. All agents in this class are equally effective at their recommended dosages. Patients with a high risk of GI bleeding and ulceration should either avoid NSAIDs or be given prophylaxis concurrent with NSAID use (ie, prostaglandin analogs or proton-pump inhibitors). Patients prescribed NSAIDs should be monitored for renal insufficiency and fluid retention, which can be particularly severe in patients who have heart failure or are taking ACE inhibitors. Delirium is common in older adults with NSAID use. COX-2 inhibitors have been associated with higher rates of stroke and myocardial infarction, but some relatively selective COX-2 inhibitors remain available (ie, celecoxib, nabumetone, and meloxicam). Topic

GENERAL MANAGEMENT STRATEGIES: PHARMACOLOGIC (2 of 2)
Because of their adverse effects, prednisone and other glucocorticoids should not be used indiscriminately Consultation with a rheumatologist can be helpful Narcotic medications, started in low dosages and titrated slowly, are often useful when pain is unresponsive to nonpharmacologic therapy or acetaminophen Dosages of glucocorticoids depend on the particular disease being treated, with benefits usually realized within 5 to 10 days. Toxicities include cataracts, poor wound healing, gastric ulcers, mental status change, hyperglycemia, hypertension, osteoporosis, and immunosuppression. Full recovery of the hypothalamic-pituitary axis can require up to a year after chronic steroid use. Individuals on chronic steroid therapy should receive therapy to prevent osteoporosis, usually with calcium, vitamin D, and bisphosphonates. Topic

SUMMARY (1 of 2) Musculoskeletal symptoms in older adults can be caused not only by true arthritis but also by derangement of tendons, bursae, muscles, connective tissue, or nerves Because older adults often exhibit incidental abnormalities on imaging and laboratory testing, these should be used to confirm clinical impressions rather than to search for a diagnosis Topic

SUMMARY (2 of 2) Comorbid medical conditions and treatments should be considered, and potential toxicities should be weighed against potential treatment benefits Exercise and other nondrug treatments should be considered in management of all articular and regional musculoskeletal problems Topic

CASE 1 (1 of 3) An 82-year-old woman is admitted to the hospital with delirium secondary to a UTI and dehydration. She is treated with IV hydration and antibiotics, and her mental status improves within 48 hours. On day 3 she has a temperature of 38.5°C (101.3°F) and severe swelling and erythema on her left wrist and hand. She has pain in her wrist with palpation and with passive dorsi- and palmar flexion. She reports no falls, and none have been documented in the nursing notes. She has no history of similar symptoms. Topic

CASE 1 (2 of 3) Which of the following is the most likely cause of the patient’s acute symptoms? Monosodium urate monohydrate crystal–associated arthritis Calcium pyrophosphate crystal–associated arthritis Group A streptococcal septic arthritis Occult fracture of the distal radius Topic

CASE 1 (3 of 3) Which of the following is the most likely cause of the patient’s acute symptoms? Monosodium urate monohydrate crystal–associated arthritis Calcium pyrophosphate crystal–associated arthritis Group A streptococcal septic arthritis Occult fracture of the distal radius ANSWER: B The most likely cause of this patient’s acute wrist monoarthritis is crystal-induced synovitis caused by calcium pyrophosphate dihydrate (pseudogout). Calcium pyrophosphate dihydrate is a common cause of acute monoarthritis in older adults and is especially common in the setting of acute illness or surgery. The most frequent sites are the knee and wrist. Fever is common with acute crystalline arthritis. Although gout should be considered in the differential diagnosis, it occurs more commonly in men and is more common in the lower extremities. Older women with gout are more likely to take diuretics and have arthritic symptoms in the proximal and distal interphalangeal joints of the hand. Septic arthritis must be considered and excluded with arthrocentesis, even though the absence of a history of joint disease or trauma lowers its likelihood. This patient most likely has pseudogout, but because septic and crystalline arthritides can coexist, septic arthritis should be excluded with evaluation of joint fluid. Septic arthritis involving the wrist is most effectively treated with open irrigation and debridement. An occult fracture of the distal radius is possible, but neither the patient nor the nursing staff reports a history of trauma. It is possible that the patient, who had delirium on admission, does not recall falling, but her symptoms did not appear until >48 hours into her hospitalization. A fracture is possible in older adults with osteoporosis and no overt trauma, but this is less likely than pseudogout with this presentation. Topic

CASE 2 (1 of 4) A 70-year-old man comes to the office for a comprehensive assessment. He describes 5 years of slowly progressive fatigue, decreased muscle strength, and difficulty swallowing. He has had un-intentional weight loss of 4.5 kg (10 lb). He is unable to rise from a chair without pushing himself up with his arms. His wife says his handwriting has become illegible and that he sometimes chokes on food. History includes hyperlipidemia, hypertension, and benign prostatic hyperplasia. Medications are simvastatin 40 mg/day and diltiazem 180 mg/day for the past 8 years. Topic

CASE 2 (2 of 4) Physical examination is remarkable for atrophy of the forearm musculature on the left side only and bi-lateral quadriceps femoris atrophy with associated diminished strength of these muscles (4–/5). He has 4/5 hand grip strength on the right, and normal strength on the left. Reflexes are normal throughout. Creatine kinase and aldolase levels are ordered, and the patient is referred for muscle biopsy. He recognizes that he must await test results, but because he is anxious about his condition, he wants to know possible management strategies. Topic

CASE 2 (3 of 4) Which of the following will most likely be indicated by the test results? Evaluation for underlying malignancy Discontinuation of or decrease in the dosage of simvastatin Referral to physical therapy Initiation of prednisone 1 mg/kg/day in divided doses Topic

CASE 2 (4 of 4) Which of the following will most likely be indicated by the test results? Evaluation for underlying malignancy Discontinuation of or decrease in the dosage of simvastatin Referral to physical therapy Initiation of prednisone 1 mg/kg/day in divided doses ANSWER: C This patient’s slowly progressive proximal and distal muscle weakness and asymmetric muscle atrophy represent the classic presentation for inclusion body myositis. Preliminary evidence indicates that an exercise program consisting of an aerobic component and resistance training results in improvement. In clinical trials, inclusion body myositis has not responded to corticosteroids or other immuno-modulatory agents. A search for an underlying malignancy would be indicated if the patient had symmetric proximal muscle weakness and a skin rash indicative of dermatomyositis. Both dermatomyositis and, less commonly, polymyositis have been associated with an increased risk of underlying malignancy; inclusion body myositis has not. The patient’s clinical presentation is not consistent with statin myopathy, which is characterized by muscle symptoms, most commonly myalgia, fatigue, weakness, generalized aching, low back pain, and proximal muscle pain. Rhabdomyolysis is much less common. Prednisone 1 mg/kg/day is appropriate initial therapy for treatment of the other idiopathic inflammatory myopathies (polymyositis, dermatomyositis) but not for inclusion body myositis. Topic

CASE 3 (1 of 4) A 68-year-old woman comes to the office because she has shoulder and hip girdle stiffness that is present on awakening and lasts for 90 minutes. The stiffness began suddenly 2 months ago. She reports intermittent fevers to 38.9°C (102°F) and unintentional weight loss of 3.2 kg (7 lb). History includes hypertension treated with lisinopril and hydrochlorothiazide. Physical examination is normal, except that strength testing demonstrates impaired effort and strength in her deltoids and hip flexors secondary to pain. Topic

CASE 3 (2 of 4) Laboratory results: Hemoglobin 11.2 g/dL
Hematocrit % Aspartate aminotransferase 54 U/L Alanine aminotransferase 58 U/L Alkaline phosphatase U/L Erythrocyte sedimentation rate 15 mm/h Treatment is initiated with prednisone 15 mg/day. She returns 1 week later for follow-up and reports no change in her symptoms. Topic

CASE 3 (3 of 4) Which of the following is the most appropriate next step? Obtain autoimmune serology panel, including antihistone antibodies. Increase prednisone to 1 mg/kg/day and refer for biopsy of the temporal artery. Evaluate for occult malignancy, including CT of the abdomen. Measure creatine kinase and aldolase levels and refer for electromyography of hip flexors. Topic

CASE 3 (4 of 4) Which of the following is the most appropriate next step? Obtain autoimmune serology panel, including antihistone antibodies. Increase prednisone to 1 mg/kg/day and refer for biopsy of the temporal artery. Evaluate for occult malignancy, including CT of the abdomen. Measure creatine kinase and aldolase levels and refer for electromyography of hip flexors. ANSWER: B The sudden onset of prolonged morning stiffness of shoulders and hip girdle is typical of polymyalgia rheumatica (PMR), yet the patient’s symptoms did not respond to a corticosteroid dosage that typically results in rapid, dramatic improvement. The presence of constitutional symptoms in patients with PMR increases the likelihood of giant cell arteritis, even in the absence of increased ESR, abnormal CRP levels, or classic giant cell arteritis symptoms, such as headache and jaw claudication. Patients who do not respond to low- dose corticosteroid therapy and have constitutional symptoms should undergo biopsy of the temporal artery. To avoid the risk of sudden, irreversible blindness, patients should be treated with prednisone 1 mg/kg/day while awaiting biopsy. Histopathologic changes supportive of giant cell arteritis remain for weeks to months after initiation of prednisone. Antihistone antibodies are helpful in diagnosing drug-induced systemic lupus erythematosus, which can be precipitated by hydralazine. However, this patient’s symptoms, are not consistent with systemic lupus erythematosus. Occult malignancy is part of the differential diagnosis for an older adult who has fever and weight loss. CT of the abdomen is unnecessary, however, because the increased ALT and AST levels suggest PMR and giant cell arteritis. Although uncommon, PMR may occur as a paraneoplastic syndrome; this possibility should be considered if the patient does not respond to high-dose corticosteroid therapy or if her symptoms quickly recur with attempted corticosteroid taper. Measurement of creatine kinase and aldolase levels and electromyography are indicated for the evaluation of an inflammatory myopathy, such as polymyositis. Patients with polymyositis have proximal muscle weakness, not morning stiffness. This patient’s weakness is related to suboptimal effort because of pain. Topic

Copyright © 2013 American Geriatrics Society
GRS Slides Editor: Annette Medina-Walpole, MD, AGSF GRS8 Chapter Author: Allan C. Gelber, MD, MPH, PhD GRS8 Question Writer: Debra K. Weiner, MD Medical Writers: Beverly A. Caley Faith Reidenbach Managing Editor: Andrea N. Sherman, MS Copyright © 2013 American Geriatrics Society Slide 64

MUSCULOSKELETAL DISEASES AND DISORDERS

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