Edema and Related Medical Conditions

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Sunday, November 13, 2005

Joint Edema

Joint Swelling

Alternative names

Swelling of a joint; Knee swelling; Toe swelling; Finger swelling; Hip swelling

Definition

Swelling occurs in the joints when fluid accumulates in the soft tissue, such as "water on the knee."

Considerations

Joint swelling may occur along with joint pain.

Common Causes

Osteoarthritis
Trauma
Acute gouty arthritis (gout)
Chronic gouty arthritis
Rheumatoid arthritis
Ankylosing spondylitis
Enteropathic arthropathy
Infection
Ludwig's angina
Pseudogout
Psoriatic arthritis
Reiter's syndrome
Systemic lupus erythematosus
Hemarthrosis

Home Care

For unexplained soft tissue joint swelling, contact your health care provider. Follow prescribed therapy to treat the underlying cause.

Call your health care provider if

Call your health care provider if any of the following occurs:

Severe, unexplained joint pain
Severe, unexplained stiffness or swelling, especially if accompanied by other unexplained symptoms

What to expect at your health care provider's office

Your health care provider will obtain your medical history and will perform a physical examination.

Medical history questions documenting joint swelling may include the following:

Location

Which joint is swollen?
Is it the big toe?
Is the jaw or neck swollen?
Are multiple joints swollen?

Time pattern

When did the joint swelling develop?
Is it always present or off and on?
Is this the first time you have had swollen joints?

Quality

How swollen is the area?
If you press over the swollen area with a finger, does it leave a dent after you take the finger away?

Aggravating factors

What makes the swelling worse?
Is it any worse in the morning or at night?
Does exercise make it worse?

Relieving factors

What make the swelling better?
Does elevating the affected body part make the swelling go down?
Is it better if you use an elastic wrap?
What home treatment have you tried? How effective was it?

Other

What other symptoms are also present?
Is there joint pain?
Is there fever?
Is there a rash?

The physical examination will include a detailed examination of the affected joint(s).

Diagnostic tests that may be performed include the following:

Blood studies (such as a CBC or blood differential)
Joint X-rays Physical therapy for muscle and joint rehabilitation may be recommended.

Update Date: 7/4/2004
Updated by: Andrew L. Chen, M.D., M.S., Steadman-Hawkins Sports Medicine Foundation, Vail, CO. Review provided by VeriMed Healthcare Network.

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Joint Symptoms - Joint Swelling

A complete history and physical examination are important in a patient with joint symptoms, which may be part of localized or systemic disease. Laboratory and x-ray data are usually of only supplementary help.

Physical Examination

Each involved joint should be inspected and palpated, and the range of motion measured. This usually determines the presence of joint disease and establishes whether the joint, the adjacent structures, or both are involved. Involved joints should be compared with their uninvolved opposites or with those of the examiner. Information is recorded objectively and quantitatively (eg, using a numbered grading system, measuring the range of motion in degrees).

Joint motion, generally painful in joint disease, may not be painful in periarticular, bone, or soft tissue disease. Swelling is an important finding. Palpation of swollen joints helps to (1) elicit the presence of fluid; (2) differentiate among simple effusion, synovial thickening, and capsule or bony enlargement; and (3) determine whether the swelling is confined to the joint or is periarticular. Tenderness or swelling at only one side of a joint may actually arise in adjacent ligaments, tendons, or bursae; findings from several approaches to the joint substantiate articular involvement. Monarthritis always suggests infection, crystal-induced arthritis, trauma, or rarely, tumor.

Increased heat over the joint should be carefully localized. Many normal joints are actually cooler than adjacent skin. Crepitus may arise from intra-articular structures or from tendons; the crepitus-producing motions should be determined (eg, knee crepitus may arise from patellofemoral grinding or from femorotibial motion).

Small joints (eg, the acromioclavicular near the shoulder, the tibiofibular at the lateral aspect of the knee, the radioulnar at the elbow) can be the source of pain that was initially believed to arise from the major joint.

Hand: The main differential features of the hand in osteoarthritis and RA are outlined in Table 49-1. Subluxations producing swan-neck or boutonnière deformities (see Ch. 61) occur in chronic RA. In psoriatic arthritis, the distal interphalangeal (DIP) joints are commonly affected, psoriasis often is evident around the adjacent nail, and other joint involvement is more asymmetric than in RA. In Reiter's syndrome, synovial, periarticular, and periosteal changes can be present in a few DIP, proximal interphalangeal, or metacarpophalangeal joints, and there is asymmetric finger joint involvement. Asymmetric DIP joint involvement also occurs in chronic gout, in which irregular joint or extra-articular tophaceous deposits occur, some of which can be seen under the skin as cream-colored aggregates.

Changes in the hand are generalized in the shoulder-hand syndrome (reflex sympathetic dystrophy), with diffuse edema and mottled, mildly cyanotic skin. In progressive systemic sclerosis, there may be initial diffuse puffiness, but with time the skin thickens, and flexion contractures often develop; Raynaud's phenomenon may be noted. Findings in hypertrophic pulmonary osteoarthropathy include clubbing of the fingertips and bony tenderness of the distal radius and ulna caused by underlying periostitis. Joint synovitis similar to that in RA occurs in SLE and, less often, in dermatomyositis, although arthralgias and sore, painful hands lacking objective joint swelling are more typical of both these disorders. Finger deformities resembling RA can occur in SLE but are caused by soft tissue disease, not advanced erosive arthritis. Raynaud's phenomenon can be present in SLE, and scaling erythema may be found over the extensor joint surfaces in dermatomyositis.

Elbow: Synovial swelling and thickening caused by joint disease occur in the lateral area between the radial head and olecranon, producing a bulge. Fluid or thickening in the olecranon bursa, rheumatoid nodules, and epitrochlear nodes should also be sought. Full 180° extension of the joint should be attempted. Although full extension is possible with nonarthritic or extra-articular lesions, its loss is an early change in arthritis. In tennis elbow, sharply localized pain is elicited by placing firm pressure over the lateral epicondyle.

Shoulder: Limited motion, weakness, pain, and disturbed mobility can be tested by having the patient attempt to raise both arms above the head. Muscle atrophy and neurologic changes should be sought. Although swelling is not common, a bulge in the anterior area of the shoulder is occasionally present in RA as a result of forward dissection of glenohumeral synovitis. Careful palpation of the relaxed shoulder may identify tenderness caused by inflammation of bursae or tendons, with common conditions occurring primarily in the subacromial area or in the long head of the biceps tendon. Localization may permit aspiration and injection of a corticosteroid-lidocaine solution to relieve acute tendinitis and to confirm the diagnosis.

Foot and ankle: Because weight bearing may elucidate certain abnormalities, the patient should stand for part of the examination. In the normal ankle joint, 15° dorsiflexion and 40° plantar flexion are possible. Swelling just below and in front of the malleoli is characteristic of synovial or intra-articular disease. Palpation of such tender soft swelling, with pain elicited on extension and flexion of the foot, demonstrates synovitis of the ankle joint. Pain on inversion or eversion suggests subtalar or ligament disease. Ankle edema, which is associated with normal ankle joint motion, can be differentiated from true joint swelling by its diffuse, superficial, pitting, nontender character. Metatarsophalangeal joints are commonly swollen and tender in RA. Interphalangeal synovitis, not as common in the feet in RA, may indicate Reiter's syndrome, other reactive arthritis, psoriatic arthritis, or gout. In gout, the first metatarsophalangeal (MTP) or bunion joint is most commonly affected, but the midtarsal or ankle areas can also be involved. Diffuse erythema is striking in an acute attack of gout. First metatarsophalangeal pain on motion with crepitus suggests osteoarthritis.

Knee: Gross deformities such as swelling (eg, popliteal cysts), quadriceps muscle atrophy, and joint instability may be more obvious when the patient stands and walks. Careful palpation of the knee in a supine patient, especially noting the presence of joint fluid, synovial thickening, and local tenderness, helps detect arthritis. Tender extra-articular bursae and true intra-articular disturbances should be differentiated.

Detection of small knee effusions is commonly problematic and is best accomplished using the "bulge sign." The knee is extended and the leg is 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.

Full 180° extension of the knee should be attempted to detect knee flexion contractures. With meniscus tears or collateral ligament injuries, forceful lateral or medial bending on leg extension produces pain by compressing the meniscus and simultaneously stretching the opposite collateral ligament. The joint line can be located by medial and lateral palpation while slowly flexing and extending the knee. A displaced meniscus is painful on firm pressure; a collateral ligament injury is tender longitudinally. The intactness of the cruciate ligaments can be determined by grasping the leg with the knee flexed at 90° (best performed with the patient sitting on a table with legs dangling) and estimating the amount of posterior-anterior movement (which should be minimal). The patella should be tested for free, painless motion. To gauge excess knee mobility, especially lateral instability, the thigh is firmly fixed and an attempt is made to rock the relaxed, almost extended knee from side to side.

Hip: A limp is common in patients with significant hip arthritis or disease in other joints of the leg. It may be caused by pain, shortening of the leg, flexion contracture, or muscle weakness. Loss of internal rotation (often the earliest change), 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 indicates local bursitis rather than arthritis.

Vertebral column: Cervical and lumbar motion should be measured. Inability to reverse the normal lumbar lordosis on flexion occurs in degenerative arthritis; limited lumbar flexion is also characteristic of ankylosing spondylitis. Degenerative arthritis or ankylosing spondylitis also limits neck motion. Either soft tissue disease or arthritis may cause pain and limited movement. The effect of movement on pain should be noted. Palpation and firm percussion over each vertebra and sacroiliac joint may elicit superficial or deep bone tenderness that should be distinguished from muscle spasm lateral to the spine. Localized bone pain suggests osteomyelitis, leukemia, primary or metastatic cancer, compression fracture, or herniated disk. Psychogenic ("touch-me-not") reactions should be noted, as should muscular tender points typical of fibromyalgia. Chest expansion should be measured because it is typically impaired in ankylosing spondylitis.

Diagnosis

Conditions easily misinterpreted as arthritis by the patient include phlebitis, arteriosclerosis obliterans, cellulitis, edema, neuropathy, vascular compression syndromes, the stiffness of Parkinson's disease, periarticular stress fractures, spinal stenosis, myositis, polymyalgia rheumatica, and fibromyositis. These can each be distinguished by their typical features (described elsewhere in The Manual) and by the absence or paucity of joint findings. Popliteal cysts resulting from knee arthritis can cause local popliteal pain, venous compression, or rupture into the calf and can be confused with phlebitis.

Extra-articular findings can be significant in helping to identify the type of arthritis (eg, tophi in gout, nodules in RA, pustular rash in gonococcemia). Coexisting periarticular disease also may facilitate diagnosis. For example, tendinitis commonly coexists with gonococcal arthritis, RA, and other systemic diseases; prominent tenderness of bones adjacent to joints and joint effusions occur in sickle cell disease and hypertrophic pulmonary osteoarthropathy; and enthesitis with tenderness and swelling at tendon insertions suggests reactive arthritis.

Often, arthritis is transient and resolves without diagnosis. Arthritis also may not fulfill the criteria for any defined rheumatic disease (see Table 49-2). A tentative diagnosis is made for treatment, with other possibilities kept in mind. Systemic disease should be considered in all atypical and undiagnosed conditions. Lyme disease and other infections should always be considered early because they may respond to specific treatment.

Certain problems require immediate attention and prompt treatment. Acute monarthritis is one example, and joint fluid examination is essential (see below). Hemorrhagic joint fluid suggests fracture, bleeding diathesis, or malignancy. Intensely inflammatory effusions suggest pyogenic infection, requiring immediate antibiotic therapy and aspiration or other drainage to establish the diagnosis and to prevent joint destruction.

Blood tests are useful in diagnosing some specific types of arthritis (for specific tests, see the chapters for each disease). Elevated ESR or C-reactive protein suggests inflammatory disease. Serum uric acid levels are elevated by diuretics, low doses of aspirin, other drugs, diet, or alcohol and in gout. Latex fixation tests for rheumatoid factor are often highly positive in RA but may also be positive in hepatitis, cirrhosis, sarcoidosis, subacute bacterial endocarditis, TB, and other infections and collagen diseases. Antinuclear factors may be positive in RA, Sjögren's syndrome, progressive systemic sclerosis, SLE, hepatitis, and other diseases. If SLE is suspected, anti-double-stranded DNA, anti-Sm, and complement levels may also provide further support. Serum CK and AST are elevated in muscle disease, including certain forms of muscular dystrophy, crush injury, and polymyositis or dermatomyositis. CK can also be elevated in hypothyroidism.

X-rays are important in the initial evaluation of relatively localized, unexplained joint complaints to detect possible primary or metastatic tumors, osteomyelitis, bone infarctions, periarticular calcifications, or other changes in deep structures that may escape physical examination. Erosions, cysts, and joint space narrowing can occur in chronic RA, gout, and osteoarthritis. X-rays also are especially useful in examination of the spine but are usually not needed if the problem seems to be simple acute back strain. CT and MRI can help define puzzling persistent lesions.

Other useful studies may include needle or surgical synovial biopsy, ultrasound, arthroscopy, arthrography, bone scanning, electromyography, nerve conduction times, thermography, and muscle or bone biopsy. Evaluation of synovial fluid is discussed below.

Differentiating Inflammatory and Noninflammatory Joint Disease

Once joint involvement is established, inflammatory and noninflammatory processes must be differentiated. Among the typical local signs of inflammation, increased heat and erythema are most helpful in this differentiation. Erythema should not be expected over chronically inflamed joints in RA. ESR and C-reactive protein tend to elevate and fever often occurs with severe inflammatory arthritis, but these may also be caused by an inflammatory process elsewhere in the body. Soft-tissue swelling tends to favor an inflammatory process, but aspiration of an effusion is essential to determine its nature. Osteoarthritis of the knee, although primarily degenerative, often causes knee effusions. Preparation for handling the fluid obtained is critical. It is not necessary to perform all tests on each fluid.

Synovial fluid measurements allow most effusions to be classified as normal, noninflammatory, inflammatory, or septic (see Table 49-3). Effusions can also be hemorrhagic. Each type of effusion suggests certain joint diseases (see Table 49-4). So-called noninflammatory effusions are actually mildly inflammatory but tend to suggest diseases with less inflammatory mechanisms. If infection is suspected, a portion of the synovial fluid sample should be sent to the laboratory for bacteriologic assessment.

Microscopic examination of a wet synovial fluid smear for crystals (only a few drops of fluid or washings from a joint are needed), using polarized light, is essential for definitive diagnosis of gout, pseudogout, and other crystal-induced arthropathies (see Ch. 55). Use of an inexpensive polarizer over the light source and another between the specimen and the examiner's eye will visualize 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 two strips of clear adhesive tape on a glass slide and placing this slide over the lower polarizer. Any such homemade system should be tested against a commercial polarizing microscope before diagnostic use. If the crystals seen are not typical, several less common crystals (cholesterol, liquid lipid crystals, cryoglobulins) or artifacts (eg, depot corticosteroid crystals) should be considered.

Other synovial fluid findings that may occasionally make or suggest a specific diagnosis include specific organisms (identifiable by Gram or acid-fast stain); spontaneous in vivo-developed LE cells; marrow spicules (caused by fracture); Reiter's cells (monocytes that have phagocytized PMN), seen most often in reactive arthritis; amyloid fragments (identifiable by Congo red stain); sickled RBCs (caused by sickle cell hemoglobinopathies); and iron in large mononuclear synovial cells (identifiable by Prussian blue stain and present especially in hemochromatosis or pigmented villonodular synovitis).

Comparing synovial fluid and serum complement levels may only occasionally help evaluate inflammatory fluids. The synovial fluid complement level tends to be <>

Measurements of rheumatoid factor in synovial fluid can give false-positive or false-negative results and, thus, should not be performed. Extremely low synovial fluid glucose levels in carefully handled specimens in fluoride tubes may favor the presence of infection.

Merck Manual

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