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Evaluation of the Patient With Joint Disorders
Some musculoskeletal disorders affect primarily the joints, causing arthritis. Others affect primarily the bones (eg, fractures, Paget disease of bone, tumors), muscles or other extra-articular soft tissues (eg, fibromyalgia), or periarticular soft tissues (eg, bursitis, tendinitis, sprain). Arthritis has myriad possible causes, including infection, autoimmune disorders, crystal-induced inflammation, and minimally inflammatory cartilage and bone disorders (eg, osteoarthritis). Arthritis may affect single joints (monarthritis) or multiple joints (polyarthritis) in a symmetric or asymmetric manner. Joints may suffer fractures or sprains (see elsewhere in T he M anual ).
The clinician should focus on systemic and extra-articular symptoms as well as joint symptoms. Many symptoms, including fever, chills, malaise, weight loss, Raynaud phenomenon, mucocutaneous symptoms (eg, rash, eye redness or pain, photosensitivity), and GI or cardiopulmonary symptoms, can be associated with various joint disorders.
Pain is the most common symptom of joint disorders. The history should address the character, location, severity, factors that aggravate or relieve pain, and time frame (new-onset or recurrent). The clinician must determine whether pain is worse when first moving a joint or after prolonged use and whether it is present upon waking or develops during the day. Usually, pain originating from superficial structures is better localized than pain originating from deeper structures. Pain originating in small distal joints tends to be better localized than pain originating in large proximal joints. Joint pain can be referred from extra-articular structures or from other joints. Arthritis often causes aching pain, whereas neuropathies often cause burning pain.
Stiffness refers to difficulty in moving a joint, but to patients, stiffness also may mean weakness, fatigue, or fixed limitation of motion. The clinician must separate the inability to move a joint from reluctance to move a joint because of pain. Characteristics of stiffness may suggest a cause, as in the following:
Discomfort that occurs with motion when attempting to move a joint after a period of rest occurs in rheumatic disease.
Stiffness is more severe and prolonged with increasing severity of joint inflammation.
The theater sign (short-lived stiffness upon standing that necessitates walking slowly after sitting for several hours) is common in osteoarthritis.
Morning stiffness in peripheral joints that lasts > 1 h can be an important early symptom of joint inflammation, such as in RA, psoriatic arthritis, or chronic viral arthritis (see Distinguishing Inflammatory vs Noninflammatory Joint Disease by Features).
In the low back, morning stiffness that lasts > 1 h may reflect spondylitis.
Fatigue is a desire to rest that reflects exhaustion. It differs from weakness, inability to move, and reluctance to move because of pain with movement. Fatigue may reflect activity of a systemic inflammatory disorder.
Instability (buckling of a joint) suggests weakness of the ligaments or other structures that stabilize the joint, which are assessed by stress testing on physical examination. Buckling occurs most often in the knee and most often results from an internal joint derangement.
Distinguishing Inflammatory vs Noninflammatory Joint Disease by Features
Each involved joint should be inspected and palpated, and the range of motion should be estimated. With polyarticular disease, certain nonarticular signs (eg, fever, wasting, rash) may reflect systemic disorders.
The rest position of joints is noted, along with any erythema, swelling, deformity, and skin abrasions or punctures. Involved joints are compared with their uninvolved opposites or with those of the examiner.
Joints are gently palpated, noting the presence and location of tenderness, warmth, and swelling. Determining whether tenderness is present along the joint line or over tendon insertions or bursae is particularly important. Soft masses, bulges, or tissues that fill normal concavities or spaces (representing joint effusion or synovial proliferation) are noted. Palpation of swollen joints can sometimes differentiate among joint effusion, synovial thickening, and capsular or bony enlargement. Small joints (eg, acromioclavicular, tibiofibular, radioulnar) can be the source of pain that was initially believed to arise from a nearby major joint. Bony enlargement (often due to osteophytes) is noted.
Active range of motion (the maximum range through which the patient can move the joint) is assessed first; limitation may reflect weakness, pain, or stiffness as well as mechanical abnormalities. Then passive range of motion (the maximum range through which the examiner can move the joint) is assessed; passive limitation typically reflects mechanical abnormalities (eg, scarring, swelling, deformities) rather than weakness or pain. Active and passive movement of an inflamed joint (eg, due to infection or gout) may be very painful.
Inability to reproduce pain with motion or palpation of the joint suggests the possibility of referred pain.
Patterns of joint involvement should be noted. Symmetric involvement of multiple joints is common in systemic diseases (eg, RA); monarticular (involving one joint) or asymmetric oligoarticular (involving ≤ 4) joint involvement is more common in osteoarthritis and psoriatic arthritis. Small peripheral joints are commonly affected in RA, and the larger joints and spine are affected more in spondyloarthropathies. However, the full pattern of involvement may not be apparent in early disease.
Crepitus, a palpable or audible grinding produced by motion, is noted. It may be caused by roughened articular cartilage or by tendons; crepitus-causing motions should be determined and may suggest which structures are involved.
Specific features should be sought at each joint.
Synovial swelling and thickening caused by joint disease occur in the lateral aspect between the radial head and olecranon, causing a bulge. Full 180° extension of the joint should be attempted. Although full extension is possible with nonarthritic or extra-articular problems such as tendinitis, its loss is an early change in arthritis. The area around the joint is examined for swellings. Rheumatoid nodules are firm, occurring especially along the extensor surface of the forearm. Tophi are sometimes visible under the skin as cream-colored aggregates and indicate gout. Swelling of the olecranon bursa occurs over the tip of the olecranon, is cystic, and does not limit joint motion; infection, trauma, gout, and RA are possible causes. Epitrochlear nodes occur above the medial epicondyle; they can result from inflammation in the hand but can also suggest sarcoidosis or lymphoma.
Because pain can be referred to areas around the shoulder, shoulder palpation should include the glenohumeral, acromioclavicular, and sternoclavicular joints, the coracoid process, clavicle, acromion process, subacromial bursa, biceps tendon, and greater and lesser tuberosities of the humerus, as well as the neck. Glenohumeral joint effusions may cause a bulge between the coracoid process and the humeral head. Possible causes include RA, osteoarthritis, septic arthritis, Milwaukee shoulder (see Crystal-Induced Arthritides:Basic Ca phosphate crystal deposition disease), and other arthropathies.
Limited motion, weakness, pain, and other disturbances of mobility caused by rotator cuff impairment can be quickly identified by having the patient attempt to abduct and raise both arms above the head and then to slowly lower them. Specific maneuvers against resistance can help determine which tendons are affected. Muscle atrophy and neurologic abnormalities should be sought.
At the knee, gross deformities such as swelling (eg, joint effusion, popliteal cysts), quadriceps muscle atrophy, and joint instability may be obvious when the patient stands and walks. With the patient supine, the examiner should palpate the knee, identifying the patella, femoral condyles, tibial tuberosity, tibial plateau, fibular head, medial and lateral joint lines, popliteal fossa, and quadriceps and patellar tendons. The medial and lateral joint lines correspond to locations of the medial and lateral menisci and can be located by palpation while slowly flexing and extending the knee. Tender extra-articular bursae such as the anserine bursa below the medial joint line should be differentiated from true intra-articular disturbances.
Detection of small knee effusions is often difficult and is best accomplished using the bulge sign. The knee is fully extended and the leg slightly externally rotated while the patient is supine with muscles relaxed. The medial aspect of the knee is stroked to express any fluid away from this area. Placement of one hand on the suprapatellar pouch and gentle stroking or pressing on the lateral aspect of the knee can create a fluid wave or bulge, visible medially when an effusion is present. Larger effusions can be identified visually or by balloting the patella. Joint effusion can result from many joint diseases, including RA, osteoarthritis, gout, and trauma.
Full 180° extension of the knee is attempted to detect flexion contractures. The patella is tested for free, painless motion.
Examination begins with gait evaluation. A limp is common among patients with significant hip arthritis and may be caused by pain, leg shortening, flexion contracture, muscle weakness, or knee problems. Loss of internal rotation (an early change in hip osteoarthritis or any hip synovitis), flexion, extension, or abduction can usually be demonstrated. Placement of one hand on the patient’s iliac crest detects pelvic movement that might be mistaken for hip movement. Flexion contracture can be identified by attempting leg extension with the opposite hip maximally flexed to stabilize the pelvis. Tenderness over the femoral greater trochanter suggests bursitis (which is extra-articular) rather than an intra-articular disorder. Pain with passive range of motion (assessed by internal and external rotation with the patient supine and the hip and knee flexed to 90°) suggests intra-articular origin. However, patients may have simultaneous intra-articular and extra-articular disorders.
Laboratory testing and imaging studies often provide less information than do the history and physical examination. Although some testing may be warranted in some patients, extensive testing is often not. Blood tests should be selected based on history and examination findings.
Some tests, although not specific, can be helpful in supporting the possibility of certain systemic rheumatic diseases, as for the following:
Antinuclear antibodies (ANA) and anti–double-stranded DNA antibodies in SLE
Rheumatoid factor and anti-cyclic citrullinated peptide (anti-CCP) antibodies in RA
HLA-B27 in spondyloarthropathy (eg, with symptoms of inflammatory back pain and normal x-rays)
Antineutrophil cytoplasmic antibodies (ANCA) in certain vasculitides (sometimes useful when systemic involvement is suspected)
Tests such as WBC count, ESR, and C-reactive protein may help determine the likelihood that arthritis is inflammatory due to infectious or other systemic disorders, but these tests are not highly specific or sensitive. For example, an elevated ESR or C-reactive protein level suggests articular inflammation or may be due to a large number of nonarticular inflammatory conditions (eg, infection, cancer). Also, such markers may not be elevated in all inflammatory disorders.
Imaging studies are often unnecessary. Plain x-rays in particular reveal mainly bony abnormalities, and most joint disorders do not affect bone primarily. However, imaging may help in the initial evaluation of relatively localized, unexplained, persistent or severe joint and particularly spine abnormalities; it may reveal primary or metastatic tumors, osteomyelitis, bone infarctions, periarticular calcifications (as in calcific tendinitis), or other changes in deep structures that may escape physical examination. If chronic RA, gout, or osteoarthritis is suspected, erosions, cysts, and joint space narrowing with osteophytes may be visible. In pseudogout, Ca pyrophosphate deposition may be visible in intra-articular cartilage.
For musculoskeletal imaging, plain x-rays may be obtained first, but they are often less sensitive, particularly during early disease, than MRI, CT, or ultrasonography. MRI is the most accurate study for fractures not visible on plain x-rays, particularly in the hip and pelvis, and for soft tissues and internal derangements of the knee. CT is useful if MRI is contraindicated or unavailable. Ultrasonography, arthrography, and bone scanning may help in certain conditions, as can biopsy of bone, synovium, or other tissues.
Arthrocentesis is the process of puncturing the joint with a needle to withdraw fluid. If there is an effusion and arthrocentesis is done correctly, fluid can typically be withdrawn. Examination of synovial fluid is the most accurate way to exclude infection, diagnose crystal-induced arthritis, and otherwise determine the cause of joint effusions. This procedure is indicated for all patients with acute or unexplained monarticular joint effusions and for patients with unexplained polyarticular effusions.
Arthrocentesis of the shoulder.
Arthrocentesis is done using strictly sterile technique. Infection or other rash over the site used to enter the joint is a contraindication. Preparations for collecting samples should be made before doing the procedure. Local anesthesia, with lidocaine or difluoroethane spray, is often used. Many joints are punctured on the extensor surface to avoid nerves, arteries, and veins, which are usually on the joint’s flexor surface. A 20-gauge needle can be used for most larger joints. Smaller joints of the upper and lower extremities are probably easier to access using a 22- or 23-gauge needle. As much fluid as is possible should be removed. Specific anatomic landmarks are used (see see Figure: Arthrocentesis of the shoulder., Arthrocentesis of the elbow., and Arthrocentesis of the knee.).
Arthrocentesis of the knee.
Metacarpophalangeal joints, metatarsophalangeal joints, and interphalangeal joints of the hands and feet are punctured similarly to each other, using a 22- or 23-gauge needle. The needle is inserted dorsally, to either side of the extensor tendon. Distraction (pulling) of the joint is sometimes useful to open the joint space and allow easier access.
At the bedside, gross characteristics of the fluid are assessed, such as its color and clarity.
Gross characteristics allow many effusions to be tentatively classified as noninflammatory, inflammatory, or infectious (see Classification of Synovial Effusions). Effusions can also be hemorrhagic. Each type of effusion suggests certain joint diseases (see Differential Diagnosis Based on Synovial Fluid Classification*). So-called noninflammatory effusions are actually mildly inflammatory but tend to suggest diseases such as osteoarthritis, in which inflammation is not severe.
Classification of Synovial Effusions
Laboratory tests commonly done on joint fluid include cell count, leukocyte differential, Gram stain and culture (if infection is a concern—see Infections of Joints and Bones), and wet drop examination for cells and crystals. However, the exact tests often depend on which diagnoses are suspected.
Differential Diagnosis Based on Synovial Fluid Classification*
Type of Effusion
Neurogenic (neuropathic) arthropathy
Pigmented villonodular synovitis
Trauma with or without fracture
Various organisms depending on patient characteristics (see Organisms That Commonly Cause Acute Infectious Arthritis)
Acute crystal synovitis (gout and pseudogout)
Partially treated or less virulent bacterial infections
Reactive arthritis (including what was previously called Reiter syndrome)
SLE (mild inflammation)
Synovial infarction (eg, caused by sickle cell disease)
Hypertrophic pulmonary osteoarthropathy
Metabolic diseases causing osteoarthritis
Neurogenic (neuropathic) arthropathy
Osteonecrosis (including osteonecrosis caused by sickle cell disease)
Progressive systemic sclerosis
Subsiding or early inflammation
*See Classification of Synovial Effusions for classification. This differential diagnosis is only a partial listing.
Microscopic examination of a wet drop preparation of synovial fluid for crystals (only a single drop of fluid from a joint is needed) using polarized light is essential for definitive diagnosis of gout, pseudogout, and other crystal-induced arthritides (see Crystal-Induced Arthritides). A polarizer over the light source and another polarizer between the specimen and the examiner’s eye allow visualization of crystals with a shiny white birefringence. Compensated polarized light is provided by inserting a first-order red plate, as is found in commercially available microscopes. The effects of a compensator can be reproduced by placing 2 strips of clear adhesive tape on a glass slide and placing this slide over the lower polarizer. Such a homemade system should be tested against a commercial polarizing microscope. The most common crystals seen are those diagnostic of gout (monosodium urate, negatively birefringent needle-shaped crystals) and pseudogout (Ca pyrophosphate, rhomboid- or rod-shaped crystals that are positively birefringent or not birefringent). If crystals appear atypical in a wet drop, several less common crystals (cholesterol, liquid lipid crystals, oxalate, cryoglobulins) or artifacts (eg, depot corticosteroid crystals) should be considered.
Other synovial fluid findings that occasionally make or suggest a specific diagnosis include the following:
Specific organisms (identifiable by Gram or acid-fast stain)
Marrow spicules or fat globules (caused by fracture)
Reiter cells (monocytes on Wright-stained smears that have phagocytized PMNs), which appear most often in reactive arthritis
Amyloid fragments (identifiable by Congo red stain)
Sickled RBCs (caused by sickle cell hemoglobinopathies)
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