Reactive Arthritis

Definition/Description

Reactive arthritis (ReA) belongs to the family of the spondyloarthropathies and is a disease caused by an infection. [1][2][3][4][5] It is a systemic inflammatory disorder characterised by aseptic arthritis, which is triggered by an infection at a distant site, usually occurring in genetically susceptible people, marked by possession of the HLA-B27 gene, although the mechanism remains uncertain. The most frequent infectious triggers are those arising from the genitourinary, gastrointestinal, and possibly the respiratory tracts.[6] [7]

Clinically Relevant Anatomy

Reactive arthritis is not limited to inflamed joints, as it can also lead to symptoms in other body systems. For example in the ophthalmological, genitourinary, dermatological, musculoskeletal and gastrointestinal systems.[1][2] 

Epidemiology/Etiology

The true incidence of the condition is probably underestimated as milder forms of the condition go under recognised. This disease is spread worldwide, with an average prevalence of 30-40 cases per 100,000 adults. The risk of developing reactive arthritis is about 50 times greater in those people who are HLA B27 positive. Reactive arthritis occurs mostly in the age group 20-40, while (young) men are more affected than women.[1][2][3][4][6][7]

Characteristics/Clinical Presentation

Symptoms can be found in different parts of the body. [1] [4] 

Musculoskeletal

Arthritis occurs in 95% of cases and usually presents as an acute, asymmetrical, lower limb oligoarthritis (involving one to five joints), principally affecting the knees, metatarsophalangeal (MTP) joints, and ankles. Synovitis of the small joints particularly the MTP joints may be erosive. Involvement of the interphalangeal joints with digital tendonitis and probably multiple entheseal lesions give rise to dactylitis or “sausage digits”. It is highly unusual for upper limb joints to be involved.

Lower back and buttock pain is not unusual in the acute stage of the illness, attributable to sacroiliitis but the real origin of such symptoms is often difficult to establish. Some patients subsequently progress to develop ankylosing spondylitis.

Enthesitis, defined as inflammation of ligaments or tendons at their point of attachment to bone, is highly characteristic and is the defining lesion of the spondylarthropathies. Enthesitis gives rise to localised pain, swelling, and tenderness. The plantar aponeurosis (plantar fasciitis) and Achilles' tendon attachments to the calcaneum are most commonly affected, often giving rise to heel pain and difficulty walking. Enthesitis of the patella tendon and pelvic tendons may also give rise to knee and pelvic pain respectively. Enthesitis may be associated with adjacent osteitis detectable by magnetic resonance imaging[7].

Skin and mucous membrane


Keratoderma blenorrhagica[7] (pustular lesions) affects 5%–10% of patients and is highly characteristic of reactive arthritis. 

Other symptoms include skin rash; sterile urogenital inflammation, cystitis, and prostatitis, which may lead to infertility; patches on the tong, palate and mucosa of the cheeks and lips. [1]  

Ocular


Eye inflammations are common, such as conjunctivitis, keratitis and acute anterior uveitis.[1][4] These can be observed unilaterally or bilaterally and can also be the only manifestation of the disease.[1]

Prognosis


The prognosis for reactive arthritis is relatively positive depending on the trigger. Mostly, patients recover within a few months (2-6). However, recurrence is common, and some individuals will develop chronic reactive arthritis (>6months) or ankylosing spondylitis, with eventual cardiac or other complications.[1][2][3] 

Differential Diagnosis

It is important to examine other causes of acute mono- and oligoarthritis. Viruses such as hepatitis B and C as well as HIV often induce virally associated arthritis, although they look like Rheumatoid arthritis and develop symmetrically. Additionally, bacterial infections and trauma which can cause arthritis should be analysed. (ex. Disseminated gonococcal infection) [2]

Diagnostic Procedures

Microbiological and serological studies are needed. [1]

The following laboratory tests are completed: CBC (=complete blood count), ESR (= erythrocyte sedimentation rate), CRP (= C-reactive protein), RF (= rheumatoid factor), ANA (= antinuclear antibody), HLA-B27 (=Human leukocyte antigen B27). [2]

Usually, ESR and CRP are higher in the acute phase and become normal in the chronic stage. RF and ANA are analysed to rule out other causes of arthritis. HLA-B27 is tested as the presence of this antigen is associated with a higher risk of developing reactive arthritis. [2]

Evidence of the disease in the form of limited spinal movements or radiological syndesmophytes may already be evident. Radiographs may show syndesmophytes in the presence or absence of spinal symptoms.

Possible microorganisms causing reactive arthritis include:

  • Chlamydia trachomatis
  • Shigella flexneri
  • Salmonella enteritidis
  • Salmonella typhimurium
  • Yersinia enterocolitica
  • Yersinia pseudotuberculosis
  • Campylobacter Jejuni [1][2][4][5]

A few characteristics must be examined, to analyze the probability of reactive arthritis:

  1. Mono- or oligoarthritis of the lower extremities.
  2. Exclusion of other diagnoses including septic or traumatic arthritis and the other rarer conditions=> 1+2 = probability ReA 40%
  3. Previous infection = probability ReA 60% (most relevant criterion)
  4. History of symptomatic preceding infection with Chlamydia trachomatis = probability ReA 90%.[2]
     

Outcome Measures

Appropriate outcome measures are specific to the affected joint(s). Measurements of swelling (i.e. circumference of joint) and effusion tests may be used to document a reduction in joint swelling over time.

See Outcome Measures Database for joint-specific outcome measures.

Medical Management

Purpose and goals of management:

  • Decrease pain and inflammation [2]
  • Reduce disability [2]
  • Avoid a relapse [1][2]

Medical management may include:

  • NSAID’s to treat the inflammation (ex. Ibuprofen, naproxen) [1][2][4][5]
  • Biological agents blocking TNF-a or its receptor [1][6]
  • Anti-bacterial treatment (against original infection) [1]
  • Corticosteroids [3][4]

Physical Therapy Management

Provide information to the patient about the disease, the prognosis and the treatment to prevent superfluous anxiety and to improve compliance with therapy. [3] [6]

  • Further, for the acute joint inflammation, provide advice to avoid overuse.[2] [3]
  • If enthesitis is present, heel support and orthosis can be considered to decrease pain and thus improve mobility. [2] [3] [5] [8] You may choose to recommend a short period of non-weight bearing, to decrease the inflammation and limit the pressure of the body on the inflamed joints.
  • Stretching and ROM exercises should be completed to prevent muscle atrophy, especially if several joints are involved. [2] [3] The objective of physiotherapy is to avoid stiffness and deformities and to promote mobility and strength.[5][6]
  • When recovery takes place, patients must be advised not to overload their joints to soon, to avoid minor traumas which can cause a relapse. [1] [3]

References

  1. 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 1.14 Toivanen A, Toivanen P. Reactive arthritis. Best Practice & Research Clinical Rheumatology. 2004 Oct 1;18(5):689-703.
  2. 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 2.11 2.12 2.13 2.14 2.15 Kim PS, Klausmeier TL, Orr DP. Reactive arthritis: a review. J Adolesc Health 2009;44:309–315. (A1)
  3. 3.0 3.1 3.2 3.3 3.4 3.5 3.6 3.7 3.8 Toivanen A. Managing reactive arthritis. Rheumatol 2000;39:117-121. (D)
  4. 4.0 4.1 4.2 4.3 4.4 4.5 4.6 Leirisalo-Repo M. Reactive arthritis. Scand J Rheumatol 2005;34:251–259. (A1)
  5. 5.0 5.1 5.2 5.3 5.4 Koehler L, Kuipers JG, Zeidler H. Managing seronegative spondarthritides. Rheumatol 2000;39:360-368. (A1)
  6. 6.0 6.1 6.2 6.3 6.4 Rihl M, Klos A, Köhler L, Kuipers JG. Reactive arthritis. Best Pract Res Clin Rheumatol 2006;20(6):1119-1137. (D)
  7. 7.0 7.1 7.2 7.3 Hamdulay SS, Glynne SJ, Keat A. When is arthritis reactive?. Postgraduate medical journal. 2006 Jul 1;82(969):446-53.
  8. Olivieri I, Barozzi L, Padula A. Enthesiopathy: clinical manifestations, imaging and treatment. Baillieres Clin Rheumatol 1998;12(4). (A1)