Arthritides

6 Interesting Facts of Arthritides 

  1. A healthy articular joint such as the hip or knee is composed of two bony surfaces lined with hyaline cartilage that are surrounded by a joint capsule. The capsule is lined with a thin synovial membrane that is no more than a few cell layers thick.
  2. •Articular joints move freely and painlessly with a low coefficient of friction due to the smooth surfaces of articular cartilage and the lubricating properties of synovial fluid.
  3. •Joint pain due to arthritis arises from damage to articular surfaces and tension on the joint capsule from effusions. Joint damage can occur from several different processes including mechanical stresses over time, trauma, crystal deposition, primary joint inflammation, and primary joint infection.
  4. •The hallmarks of inflammatory joint pain include stiffness and pain that are most pronounced in the morning. These symptoms improve with activity and return after periods of rest. Prolonged stiffness is a key historical feature of inflammatory joint pain. Morning stiffness typically lasts more than 1 hour in individuals with inflammatory joint disease.
  5. •In contrast to inflammatory joint pain, mechanical joint pain is typically worse with activity and improves with rest. Morning stiffness may be present, though it tends to improve within 30 minutes of activity.
  6. •Additional features are important to consider as they may help narrow the differential diagnosis. Important features of arthritis include the duration of symptoms, the number of joint involved, the size of joints involved, symmetry of joint involvement, pattern of onset (episodic, additive, migratory, etc.), and axial involvement (SI joints and spine
  • Causes of Acute ArthritisAcute Monoarthritis
    • Septic arthritis
      • Gonococcal
      • Nongonococcal
    • Acute crystalline arthritis
      • Gout
      • Pseudogout (acute CPPD)
    • Trauma
    Acute Oligoarthritis
    • Septic arthritis
      • Gonococcal— often migratory
      • Nongonococcal— up to 25% of cases involve >1 joint
    Lyme Arthritis
    • Postinfectious arthritis
      • Rheumatic fever
      • Reactive arthritis
    • Acute sarcoid—Lofgren syndrome
    Acute Polyarthritis
    • Viral infections
      • Parvovirus B19
      • Acute hepatitis B
      • Hepatitis C
      • HIV
    • Acute sarcoid—Lofgren syndrome
    • Atypical manifestations of systemic autoimmune disease
      • Rheumatoid arthritis
      • Psoriatic arthritis
      • Systemic lupus
    BOX 15.2Causes of Chronic Noninflammatory Arthritis
    • Osteoarthritis
    • Internal and periarticular derangements
      • Meniscal
      • Ligament
      • Tendon
      • Labrum
    • Osteochondrosis dissecans
    • Osteonecrosis
    • Neuropathic arthritis (Charcot joint)
    BOX 15.3Causes of Chronic Inflammatory ArthritisChronic Monoarthritis
    • Infection
      • Gonococcal
      • Nongonococcal
      • Lyme arthritis
      • Fungal arthritis
      • Mycobacterial arthritis
      • Syphilis
    • Tophaceous gout
    Chronic Oligoarthritis
    • Tophaceous gout
    • Spondyloarthropathy
      • Psoriatic arthritis
      • Reactive arthritis
      • Ankylosing spondylitis
      • IBD related arthropathy
    • Rheumatoid arthritis
    • Systemic lupus erythematosus
    • Infection
      • Lyme
    Chronic Polyarthritis
    • Rheumatoid arthritis
    • Systemic lupus and related conditions
    • Spondyloarthropathy
    • Drug induced
      • Lupus (hydralazine and others)
      • Periostitis (voriconazole)
    • Tophaceous gout
    • Adult-onset Still’s
    • Systemic vasculitis
    • Paraneoplastic
  • •Acute (<2 weeks) joint pain and swelling requires a rapid workup and must include synovial fluid analysis including gram stain and cultures to evaluate for a bacterial infection suggestive of septic arthritis. Septic arthritis may lead to rapid joint damage and can be life threatening if left untreated.

Osteoarthritis

  • •Osteoarthritis (OA) arises due to degeneration of joint surfaces from mechanical stress over time or from prior trauma. Articular cartilage loss exposes underlying bone, ultimately resulting in the downstream activation of pain/sensory nerve endings in the subchondral bone.

History

  • •The hips, knees, and the first metatarsophalangeal joint (MTP) of the foot are the most common lower extremity joints affected. The first carpometacarpal joint (CMC), distal interphalangeal joints (DIPs), and proximal interphalangeal joints (PIPs) of the hands are the most commonly affected joints in the upper extremity. In the absence of trauma or other conditions, osteoarthritis is uncommon in the wrist, shoulder, and ankle.
  • •Pain related to osteoarthritis is worse with use of the involved joint and improves with rest.
  • •Stiffness typically resolves within 30 minutes of activity.

Physical Examination

  • •Vital signs
    • •Usually normal
  • •Gait
    • •Often antalgic with lower extremity joint involvement
  • •Joints
    • •Joint effusions may be present
    • •Bony swelling may be observed due to osteophyte formation.
    • •Joints affected by osteoarthritis are rarely warm to touch. Joint temperature should be assessed by comparing the temperature of the joint to a neighboring large muscle group. Normal joints are cooler than the area over normal muscle bellies.
    • •Joint range of motion may be limited, with pain at the endpoints of motion. On hip examination, internal rotation will often elicit pain when hip OA is present
    • •Joint lines may be tender to palpation
    • •Joint crepitations may be present.
    • •Ligament stability is usually unaffected in early disease but may occur in late disease.

Imaging

  • •Radiographic hallmarks of osteoarthritis include joint space narrowing (which may be asymmetric in weight bearing joints), osteophytes, joint line sclerosis, and subchondral cysts. Osteoarthritis of the medial compartment of the knee.Classic radiographic features seen here include asymmetric joint space narrowing, osteophyte formation, and joint line sclerosis.
  • •Magnetic resonance imaging is more sensitive than plain films at detecting osteoarthritis and may show chondral defects and subchondral bone edema.
  • •Bone scans have no utility in the workup of osteoarthritis

Additional Tests

  • •Synovial fluid analysis will demonstrate either normal or noninflammatory joint fluid with <2000 white blood cells

Synovial Fluid Characteristics

Type of FluidWBC Count (cells/mm3)Clarity and ViscosityExample
Normal<500Clear and viscousNormal
Noninflammatory500–2000Translucent and viscousOsteoarthritis
Inflammatory2000–50,000Opaque and wateryRheumatoid arthritis
Spondyloarthritis
Crystalline disease
“Septic”>50,000Opaque and viscousBacterial infection
Crystalline disease

Differential Diagnosis

  • •Joint sprain
  • •Periarticular injury (e.g., tendonitis or bursitis)
  • •Ligament injury
  • •Meniscal/labral injury
  • •Osteochondritis dissecans
  • •Osteonecrosis/avascular necrosis (AVN)

Treatment

  • •Nonpharmacologic Therapy
    • •Weight loss and activity modification can reduce stress across lower extremity joints.
    • •Physical therapy strengthens the musculature that supports the affected joint.
    • •Braces may assist in off-loading affected joints (e.g., unloader brace for knee OA).
  • •Pharmacologic Therapy
    • •Acetaminophen is the safest first-line agent.
    • •Nonsteroidal antiinflammatory drugs (NSAIDs) are often effective and can be combined with acetaminophen. Topical diclofenac is approved for hand and knee osteoarthritis and can be used in individuals with renal insufficiency or significant gastritis in whom NSAIDs are contraindicated.
    • •Oral corticosteroids should be avoided in osteoarthritis.
    • •Intra-articular injections often rapidly reduce pain but have been shown to lead to accelerated thinning of cartilage.
    • •Intra-articular viscosupplementation with hyaluronic acid derivatives has been shown to reduce symptoms in mild to moderate arthritis and does not appear to contribute to progression of cartilage loss.
  • •Surgery—advanced disease only
    • •Joint replacements are reasonably well tolerated and effective in the shoulder, hip, and knee.
    • •CMC arthritis in the hand often improves with resection of the trapezoid.

Acute Crystalline Arthropathies (Gout and Pseudogout)

  • •Gout and pseudogout arise in response to precipitation of crystals in and around joints. There are acute and chronic forms of each condition. The acute manifestations of these two conditions are similar and only differentiated by identification of the causative crystal on microscopic analysis of the synovial fluid.

History

  • •Acute flares of crystalline arthritis typically over the course of hours to days.
  • •Patients report warm, swollen, and exquisitely painful joints that are sensitive even to light touch.
  • •Involvement of the first metatarsophalangeal joint (called “podagra”) is highly characteristic of gout.

Physical Examination

  • •Vital signs
    • •May have increased heart rate due to pain and may have low-grade fevers
  • •Skin
    • •Affected joint is often warm to the touch and exquisitely tender
    • •Patients with chronic gout may have tophi (fingers, toes, olecranon bursae, and heels)
  • •Gait
    • •Antalgic with lower extremity joint involvement
  • •Joints
    • •Warm and very tender to touch; may mimic an infected joint.
    • •The range of motion is extremely limited due to pain and joint swelling.

Imaging

  • •Radiographs may be notable only for evidence of effusion in early disease.
  • •Chronic gout results in characteristic erosions. Erosions in chronic gout are often nonmarginal. They have an ovoid shape often with overhanging edges and sclerotic margins (so-called rat bite lesions). Chronic tophaceous gout.Gouty erosions are often nonmarginal with sclerotic margins and overhanging edges, as seen in the proximal phalanx of the great toe (horizontal arrow). There is a tophus over the fifth metatarsophalangeal joint, where there is erosive disease at the joint and focal areas of calcification in the soft tissue (diagonal arrow).
  • •Pseudogout is an acute manifestation of calcium pyrophosphate deposition disease (CPPD). This condition can lead to chondrocalcinosis, which is typically seen in the fibrocartilage structures of the knee and wrist. Chondrocalcinosis is a radiographic feature of calcium pyrophosphate deposition disease. It is commonly seen in the fibrocartilaginous menisci of the knee, appearing as thin radiopaque bands (white arrow).

Additional Tests

  • •There is no role for a uric acid level in diagnosing acute gout. It is helpful in managing chronic gout.
  • •Synovial fluid analysis with polarizing microscopy is essential to establish a diagnosis.
    • •Gout crystals are needle shaped with bright negative birefringence (yellow when plane of polarization is parallel to axis of crystal).
    • •CPPD crystals are rhomboid shaped with faint positive birefringence (blue when plane of polarization is parallel to axis of crystal).

Differential Diagnosis

  • •Septic arthritis
  • •Cellulitis/septic bursitis
  • •Acute trauma
  • •Atypical manifestation of rheumatoid arthritis (RA) and similar conditions

Treatment

  • •Acute treatment for both gout and pseudogout are the same. Medical comorbidities may guide choice of agent.
    • •Oral NSAIDs
    • •Oral corticosteroids (prednisone 20 to 60 mg daily for acute flares)
    • •Use caution with intraarticular steroids as septic arthritis can precipitate flares of crystalline disease.
    • •Colchicine (two 0.6 mg pills at first sign of flare and then one 0.6 mg pill 1 hour later followed by one 0.6 mg daily thereafter)
  • •Chronic gout is addressed with dietary changes and pharmacologic therapy that lowers the serum uric acid.

Rheumatoid Arthritis

  • •RA is a systemic autoimmune condition whose primary manifestation is an inflammatory arthritis. It affects approximately 1% of the US population and is more common in women than men (3: 1).

History

  • •Gradual onset of inflammatory joint symptoms over the course of weeks to months. Pain and stiffness tend to be worse in the morning and improve with activity only to return with rest.
  • •Symmetrical joint involvement with a predilection for the wrists, metocarpophalangeal joints (MCPs), and MTPs. It spares the DIPs in contrast to OA, psoriatic arthritis, and gout.
  • •General fatigue and malaise may be present though fever is uncommon.

Physical Examination

  • •Vital signs
    • •Usually normal
  • •Gait
    • •May be antalgic if lower extremity joints are affected
  • •Skin
    • •Skin nodules may present in RA
  • •Joints
    • •Involved joints are warm and swollen
    • •Progressive disease results in characteristic joint deformities such as ulnar deviation at the MCPs, and boutonniere and swan neck deformities in the fingers.

Imaging

  • •Bilateral hand and foot films are recommended at baseline. Hand views should include PA and Norgaard (“ball-catcher”) views.
  • •Early radiographic changes include soft-tissue swelling and periarticular osteopenia.
  • •With more advanced disease there may be uniform joint space narrowing , marginal erosions, and deformities. Rheumatoid arthritis.In contrast to osteoarthritis, inflammatory arthritis in the knee leads to uniform joint space narrowing throughout all compartments. Inflammatory arthritis is often associated with periarticular osteopenia.FIG 15.6Rheumatoid arthritis.The early erosions of rheumatoid arthritis (arrows) occur at the joint margins and have predilection for (A) the second and third MCPs in the hands, and (B) fourth and fifth metatarsophalangeal joints in the feet.
  • •RA involves the spine only at C1-C2, where it can lead to atlantoaxial instability. There is a risk of cord compression, especially with forceful neck extension, as occurs with intubation.

Additional Tests

  • •Auto-antibodies help define the disease and provide prognostic information.
    • •A rheumatoid factor (RF) is approximately 70% sensitive and 70% specific for RA.
    • •An anticyclic citrullinated peptide (CCP) is 70% sensitive but >90% specific for RA.
  • •Acute phase reactants: sedimentations rate (ESR) and C-reactive protein (CRP)

Differential Diagnosis

  • •Systemic lupus
  • •Psoriatic arthritis
  • •Reactive arthritis
  • •Acute parvovirus
  • •Chronic gout
  • •Chronic CPPD

Treatment

  • •At diagnosis, all RA patients should be referred to a rheumatologist and receive a trial of methotrexate, which is a disease-modifying antirheumatic drug (DMARD). An alternative DMARD to methotrexate is leflunomide.
  • •RA will often respond to modest doses of prednisone in the range of 5 to 10 mg daily.
  • •NSAIDs can help with pain but do not control the disease.

Other Conditions Associated With Inflammatory Arthritis

Lyme Arthritis

  • •Lyme disease is caused by the spirochete Borrelia burgdorferi, which is transmitted by a tick vector. Lyme is endemic to specific geographic regions of the United States, including New England, the Mid-Atlantic, and parts of the Midwest (notably Wisconsin).
  • •Lyme disease occurs in separate phases. Acute Lyme is characterized by the target-shaped rash of erythema migrans that occurs at the site of inoculation. The organism may spread, causing disseminated disease that can affect multiple organ systems including the heart, joints, and nervous system.
  • •An important manifestation of disseminated Lyme infection is an inflammatory arthritis. The weight-bearing joints, typically the knees, are involved. Lyme arthritis is often migratory, with pain moving between affected joints. Inflammation in the joint is caused by the presence of the spirochete in the joint.
  • •An initial diagnosis is often made with Lyme serologies in the right clinical context. Synovial fluid can be sent for a polymerase chain reaction analysis, which detects bacterial nucleic acid.
  • •Lyme arthritis should be suspected only in individuals who have lived or traveled in areas where the spirochete is endemic.
  • •First-line therapy for Lyme arthritis includes 28 days of doxycycline in adults and 28 days of Amoxicillin in children and pregnant women
  • •Reinfection can occur after treatment.

Systemic Lupus Erythematosus

  • •Systemic lupus erythematosus (SLE) is a multisystem autoimmune disease that commonly affects the skin, serosal surfaces of the heart and lung, joints, kidneys, and blood cell lines.
  • •It is more common in women, with a 9: 1 female predominance affecting women of childbearing age.
  • •Joint involvement can mimic RA, though erosions are not typically seen. With hand involvement, it is more likely to see the characteristic Jaccoud arthropathy characterized by reducible ulnar deviation and swan neck deformities. Systemic lupus is associated with a nonerosive inflammatory arthritis of the hands that leads to reducible ulnar deviation and swan neck deformities.
  • •Blood tests are critical in establishing a diagnosis of lupus. An antinuclear antibody (ANA) is a highly sensitive (>95%) but relatively nonspecific test for lupus.
  • •First-line therapy includes hydroxychloroquine and systemic steroids. Additional therapy is indicated if there is internal organ involvement.

Psoriatic Arthritis

  • •Psoriatic arthritis (PsA) belongs to a larger group of conditions known as the inflammatory spondyloarthropathies. These include ankylosing spondylitis, inflammatory bowel disease (IBD)–associated arthritis, and reactive arthritis. These conditions can affect the spine and sacroiliac joints, though peripheral arthritis is more common in PsA.
  • •PsA and the other spondyloarthropathies affect not only joints but also tendons and ligaments, leading to tenosynovitis and enthesitis. The entheses are special anatomical sites where tendons and ligaments insert onto bone.
  • •PsA develops most often in individuals with preexisting psoriasis. In a small minority of cases, the inflammatory arthritis predates the cutaneous manifestations.
  • •Men and women are equally affected.
  • •Joint involvement in the peripheral joints mirrors RA, with the notable exception that PsA often involves the DIPs in the hands and feet.
  • •Severe PsA can lead to dramatic deformities of the hands and feet. The classic radiographic deformity of PsA is the pencil-in-cup deformity.
  • •Therapy also mirrors that of RA OTE: Systemic steroids should be avoided in PsA if possible, as they are associated with severe rebound of skin and joint disease when tapered.

Reactive Arthritis

  • •In contrast to PsA, reactive arthritis (ReA) usually affects the larger joints, including knees and ankles.
  • •Reactive arthritis follows infections of various types, the most common of which include urethritis from chlamydia and enterocolitis due to campylobacter
  • •There is a variant of poststreptococcal reactive arthritis that must be differentiated from acute rheumatic fever.
  • •Reactive arthritis can be associated with conjunctivitis and a characteristic set of skin findings, including a psoriaform rash on the palms and soles known as keratoderma blennorrhagia.
  • •Reactive arthritis usually has a self-limited disease course and can be managed with NSAIDs alone. Persistent disease may require steroids and DMARDs. Sulfasalazine is the first-line agent if a DMARD is necessary.

Imaging

  • •Avascular necrosis of the knees, hips, and shoulders can be seen in lupus independent of steroid exposure.
  • •The spondyloarthropathies often have spine and sacroiliac involvement. A Ferguson view is recommended when assessing for sacroiliitis.

Troubleshooting

  • •Always perform arthrocentesis on an acutely warm and swollen joint in order to rule out septic arthritis. Synovial fluid analysis should include a cell count and differential, crystal analysis, and gram stain and culture

Considerations in Special Populations

  • •Monitor elderly patients closely for side effects of NSAIDs including gastrointestinal bleeding and renal function. Joint pain and disability have a negative effect on balance; canes and walkers—when used appropriately—lessen the chance of falling but require training.
  • •Any joint effusion in a child requires urgent attention.

Suggested Readings

  • Hochberg MC, Altman RD, April KT, et al.: American College of Rheumatology 2012 recommendations for the use of nonpharmacologic and pharmacologic therapies in osteoarthritis of the hand, hip, and knee. Arthritis Care Res (Hoboken) 2012; 64 (4): pp. 465-474.
  • Khanna D, Khanna PP, Fitzgerald JD, et al.: American College of Rheumatology guidelines for management of gout. Part 2: therapy and antiinflammatory prophylaxis of acute gouty arthritis. Arthritis Care Res (Hoboken) 2012; 64 (10): pp. 1447-1461.
  • Margaretten ME, Kohlwes J, Moore D, Bent S: Does this patient have septic arthritis? JAMA 2007; 297 (13): pp. 1478-1488.
  • Singh JA, Saag KG, Bridges SL, et al.: 2015 American College of Rheumatology guideline for the treatment of rheumatoid arthritis. Arthritis Care Res (Hoboken) 2016; 68 (1): pp. 1-25.
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