Septic Arthritis Causes, Symptoms, and Treatment

Last updated by Peer reviewed by Dr Laurence Knott, MBBS
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Professional Reference articles are designed for health professionals to use. They are written by UK doctors and based on research evidence, UK and European Guidelines. You may find the Septic Arthritis article more useful, or one of our other health articles.

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Treatment of almost all medical conditions has been affected by the COVID-19 pandemic. NICE has issued rapid update guidelines in relation to many of these. This guidance is changing frequently. Please visit https://www.nice.org.uk/covid-19 to see if there is temporary guidance issued by NICE in relation to the management of this condition, which may vary from the information given below.

Septic arthritis is an infection producing inflammation in a native or prosthetic joint or more than one joint. It can be acute or chronic. Rapid diagnosis and treatment of an infected joint are essential in preserving orthopaedic function.[1] .

  • Staphylococcus aureus is the most frequent pathogen responsible for septic arthritis in any age group, mainly meticillin-sensitive strains.[2]
  • The incidence of disseminated gonococcal arthritis is 2.8 cases per 100,000 person-years. The disease is becoming increasingly common among the elderly with multiple morbidities and in the immunosuppressed.[3]
  • The incidence of prosthetic joint infection among all recipients ranges from 1.5-2.5% for primary interventions and up to 20% for revision procedures.[4]

Risk factors for septic arthritis

Risk factors for septic arthritis include:

  • Increasing age.
  • Diabetes mellitus.
  • Prior joint damage - eg, rheumatoid arthritis, gout, systemic connective tissue disorders.
  • Joint surgery.
  • Hip or knee prosthesis.
  • Skin infection in combination with joint prosthesis.
  • Immunodeficiency - eg, infection with HIV.

  • The classic picture is a single swollen joint with pain on active or passive movement.
  • Septic arthritis may present as polyarticular arthritis in a minority of patients.
  • Fevers and rigors are present in the majority of cases but their absence does not exclude the diagnosis. Bacteraemia is a common finding and, when present, may cause prostration, vomiting or hypotension.
  • Patients with septic arthritis of the sternoclavicular, acromioclavicular, sternocostal or manubrosternal joints may present with chest wall pain.
  • Infection of the sacroiliac joint may present as buttock, hip or anterior thigh pain.
  • Apart from pre-existing joint disease, associated conditions include immunosuppressive disease, recent steroid injection, sexually transmitted disease and intravenous drug use.

Children

Septic arthritis is easily missed in children, as localising signs may be absent, and may be confused with more common conditions - eg, transient synovitis and trauma. Septic arthritis can occur at any age but most commonly in preschool infants and toddlers. The hip and knee represent a third of cases each, with other joints making up the remainder. Patients usually present with fever, joint pain and/or unwillingness to move the affected joint (eg, a limp or refusal to weight bear if the hip joint is affected).

Signs of septic arthritis

The joint is usually swollen, warm, tender and exquisitely painful on movement. An effusion may be obvious. The knee is the most common joint involved with septic arthritis (about half of cases), followed by the hip, shoulder, ankle and wrists.

Signs may be less marked or poorly localised in the elderly, in the immunocompromised, in drug abusers and in infections of the spine, hip and shoulder joints.

Infection of a prosthetic joint may show few signs until a drainage sinus develops. Occasionally, an abscess around the joint, or loosening of the implant, is indicated by pain.

Septic arthritis should always be considered in patients presenting with one or a few acutely inflamed joints. The most important differential diagnosis is the crystal arthropathies. Gout and pseudogout can also present with pain, inflammation and, occasionally, spiky fevers and chills.

The triad of fever, pain and impaired range of motion is typical septic arthritis. Fevers are usually low-grade and rigors are only present in a minority of cases.

History and examination may not only yield clues as to the diagnosis of septic arthritis but also to the type of infection that is present. 85-90% of non-gonococcal suppurative arthritis affects one joint. S. aureus is the most common cause of polyarticular arthritis. Other causes include various viral infections, Lyme disease, gonococcal disease, reactive arthritis and various non-infective conditions.

  • Infection of the sternoclavicular and sacroiliac joints is commonly caused by Group B streptococcal infection.
  • Gonococcal disease usually presents with fever, arthralgia, multiple skin lesions (dermatitis-arthritis syndrome) and tenosynovitis of the hand joints, knees, wrists, ankles and elbows. However, it may also present as a monoarticular arthritis in which these other features are absent.
  • Lyme disease (caused by infection with Borrelia burgdorferi) may cause swelling disproportionate to the level of pain. It should be suspected in patients with a history of tick bite or who have travelled to endemic areas and present with transient polyarthralgia, typical erythema chronicum migrans and systemic symptoms. Joint inflammation may present many months after initial infection and occurs in 60% of untreated patients, mainly affecting the large joints - commonly the knee.
  • Hip joint infection may cause pain which does not localise directly and swelling which may not be obvious.
  • Sacroiliac joint infection often presents as buttock, anterior thigh or hip pain. Direct pressure may elicit tenderness.
  • Reactive arthritis, psoriatic arthritis, ankylosing spondylitis and arthritis associated with inflammatory bowel disease often present with inflammation in a few large joints, distributed asymmetrically. It may develop several weeks after the original infection has resolved and there may be few concurrent symptoms. Other symptoms of the disease process, such as gastrointestinal or genitourinary symptoms, skin lesions, or uveitis, may yield diagnostic clues.
  • Viral arthritis (eg, rubella, parvovirus, hepatitis C, HIV) often presents with symmetrical involvement of smaller joints such as the hands, accompanied by a rash.
  • Tuberculous arthritis may be associated with a joint which feels 'boggy' on palpation, due to granulomatous involvement. The symptoms may be quite indolent and the diagnosis may be delayed for many years.
  • Prosthetic joint infection may exhibit a prolonged low-grade course with gradually increasing pain. There is often no significant swelling or fever, although high-grade fever, focal swelling and redness occasionally occur. Cellulitis and sinus development are common presenting features.
  • Infective endocarditis may be complicated by septic arthritis or bone infection.

One study found the levels of blood C-reactive protein (CRP) and the synovial fluid white blood cell count, percentage of polymorphonuclear cells and lactate to be the best inflammatory markers in predicting a diagnosis of septic arthritis[7] .

The gold standard investigation is joint aspiration.

Laboratory tests

  • FBC. This may reveal an elevated white cell count. Inflammatory markers (ESR and CRP) are usually elevated in infection, and may be useful in following response to therapy.
  • Synovial fluid examination:
    • If synovial fluid can be aspirated, it should be sent for leukocyte count, Gram staining, polarising microscopy to exclude crystal arthropathy, and culture. Marked leukocytosis may be seen in mycobacterial infection.
    • Culture is the only reliable method of evaluating a potentially infected joint, as the white cell count is not itself diagnostic[8] .
    • Since time is of the essence, treatment should not be delayed for the results of culture but should be based on Gram stain and polarising microscopy results. An exception to this is where there is a signficant risk of infection elsewhere that could lead to bacteraemia (eg, pyelonephritis or pneumonia).
    • Fluid should always be sent for culture, irrespective of the screening result, as Gram staining is only 60% sensitive and a joint damaged by crystal arthropathy may well have co-existent infection. Culture is 80% sensitive for tuberculous infection.
    • Additional staining or cultures may be required as clinically indicated from the list of differential diagnoses. Fluid can be injected directly into aerobic/anaerobic 'blood' culture bottles to maximise the chance of growing organisms.
  • Synovial tissue culture. This is predominantly indicated where fungal or mycobacterial infection is suspected. Culture is 94% sensitive for tuberculous infection.
  • Blood cultures. At least two blood cultures should be taken to exclude bacteraemia.
  • Cultures for gonococcal infection. Rectal, cervical, urethral and pharyngeal swabs should be taken if this condition is suspected.
  • PCR:
    • This is a method of detecting bacterial DNA and has been used with some success in the diagnosis of reactive arthritis due to Yersinia spp., B. burgdorferi, Chlamydia spp., Neisseria gonorrhoeae and Ureaplasma spp.
    • The disadvantage of this test is that it cannot be used to distinguish between live and dead organisms and it is susceptible to contamination.
  • Tests for Lyme disease. See the separate Lyme Disease article.
  • Immunology. Serological tests for diagnosis of various rheumatological disorders and vasculitides should be arranged as clinically appropriate.

Imaging

  • Plain radiographs:
    • These are of limited value and may be normal in the first few days of the disease. However, they may show underlying osteomyelitis or periarticular osteomyelitis of the joint itself.
    • Fat pad displacement, swelling of capsule and soft tissue around the affected joint and, in some cases, joint space widening due to localised oedema and effusion, may be seen.
    • In later stages, diffuse joint space narrowing due to cartilage destruction may be evident. Plain radiographs may also be used to identify inadequately treated septic arthritis with generalised joint destruction, joint fusion and subchondral bone loss followed by reactive sclerosis, or calcification of periarticular tissue.
    • The linear deposition of calcium pyrophosphate can sometimes be detected on plain radiograph and is a pointer to the diagnosis of pseudogout.
  • Ultrasonography. This is not as sensitive as MRI or CT scan; however, it is an inexpensive non-invasive method that can be helpful in showing intra- and extra-articular abnormalities not obvious on plain X-ray, and it can detect early effusions, and guide joint aspiration and drainage procedures.
  • CT and MRI scanning. These are the most sensitive methods for diagnosing periarticular abscesses, joint effusions and osteomyelitis. They are usually reserved for cases of diagnostic difficulty and in specific clinical situations - eg, sacroiliac or sternoclavicular joint infection, to exclude extension into the mediastinum or pelvis.
  • Radionuclide scans. Technetium 99m Tc, gallium 67 Ga, and indium 111 In leukocyte scans are used to localise areas of inflammation and, although they cannot distinguish infections from sterile processes, they may be helpful in identifying septic arthritis in relatively sequestered areas such as the hip and sacroiliac joints.

Investigation of the prosthetic joint[9, 10]

  • A high index of suspicion should be maintained for any patient complaining of recurrent pain in a prosthetic joint. Fever and leukocytosis may be absent in elderly patients.
  • Plain radiographs may reveal transcortical sinus tracts and new subperiosteal bone growth. Contrast arthrography can demonstrate loosening of the prosthesis, synovial outpouchings and abscesses.
  • CT and MRI scans may also be helpful, as may scintigraphy. However, no single imaging technique is 100% sensitive and if the condition is suspected, joint aspiration or operative biopsy should be performed.
  • Aspiration of a prosthetic joint is normally only attempted by an orthopaedic specialist.

Management involves surgical drainage and lavage of the joint and high-dose intravenous antibiotics.[11]

Antibiotic therapy

  • Treatment should be started empirically before the results of cultures are known, as evidence suggests that a better functional result is obtained the sooner an antibiotic is commenced.
  • Gram staining, the clinical picture and the background of the patient should act as a guide. 40-50% of Gram stains fail to reveal any micro-organisms, in which case the individual's age and sexual activity become major determinants as to the likelihood of a gonococcal infection.
  • The antibiotic should at least cover S. aureus and Streptococcus spp. A microbiologist should also be consulted, as the choice of therapy should be based on resistance patterns in the local hospitals and community.
  • Antibiotics are given intravenously initially (usually for 2-3 weeks) before being switched to oral (often for at least a further 2-4 weeks).
  • Recommended antibiotic treatments include:[12]
    • Seek specialist advice if prostheses are present.
    • Flucloxacillin for 4-6 weeks (longer if infection complicated); if penicillin-allergic then use clindamycin instead.
    • If meticillin-resistant S. aureus (MRSA) is suspected, vancomycin (teicoplanin may also be used) for 4-6 weeks (longer if infection complicated)
    • If gonococcal arthritis or Gram-negative infection is suspected, cefotaxime (ceftriaxone may also be used). Treat Gram-negative infections for 4-6 weeks (longer if infection complicated). Treat gonococcal infection for two weeks.

MRSA is becoming an increasing problem, as is penicillin resistance in Group B streptococcal infection. Penicillin plus gentamicin, or later-generation cephalosporins, are often used. Treatment is generally administered intravenously for 3-4 weeks, except in the case of gonococcal infection, where a switch to oral antibiotics is often made after two weeks.

There is no benefit in injecting antibiotics intra-articularly. Most antibiotics have good penetration into bone and joint tissues, reaching concentrations exceeding the minimum inhibitory concentrations of common bone and joint infection pathogens. The few exceptions include penicillin and metronidazole, which show a lower than optimum penetration into bone, and metronidazole and flucloxacillin, which have poor profiles in terms of joint space penetration.[13] Intra-articular injection has the potential for causing a chemical synovitis.

Other medical therapy

If the septic arthritis fails to respond to five days of treatment with an appropriate antibiotic (as evidenced by persistent fever, positive cultures or synovial purulence), the therapeutic approach should be reassessed. Synovial fluid should be re-examined for crystals, and Lyme disease serology should be arranged. Consideration should be given to synovial biopsy (to exclude fungal or mycobacterial infection) and to the possibility of reactive arthritis requiring the use of non-steroidal anti-inflammatory drugs.

Chondral damage is one of the major sequelae of septic arthritis, occurring even after prompt treatment of a septic joint. Corticosteroids are known to have beneficial effects on the rate and extent of cartilage destruction in arthritis. Investigation into sepsis at other sites has suggested improved outcomes with corticosteroid use despite the theoretical risks. However, there is currently a lack of reliable data regarding the safety and efficacy of corticosteroids in septic arthritis.[14]

Joint drainage

  • Repeated percutaneous aspiration may be required if the infection does not respond to antibiotic treatment.
  • Joints difficult to access (eg, hip, shoulder and sacroiliac joints) may require ultrasound-guided needle aspiration or open arthrotomy.
  • Surgical drainage may be required in any infected joint which does not respond to medical treatment.

Splinting

The limb should be splinted in the position of function (knees in extension, elbows at 90°, wrists in neutral to slight extension, hips in balanced suspension in neutral rotation). Once the septic arthritis is under control, immediate joint mobilisation will promote healing of the articular cartilage and prevent contractures.

Treatment of septic arthritis-infected prosthetic joints[9, 10]

The prosthetic joints to get infected most commonly are the elbow, shoulder and ankle joints, followed by hips and knees. Early infection (less than 12 weeks after implantation) is usually caused by skin pathogens such as coagulase-negative Staphylococcus spp. It can often be cured medically, providing there is no evidence of periarticular soft tissue involvement or joint instability.

Late-onset septic arthritis infections (more than one year after implantation) are usually caused by haematogenous spread of common organisms such as Escherichia coli, Proteus mirabilis, Pseudomonas aeruginosa, Staphylococcus epidermis and S. aureus.

Prosthetic joint infections are often managed by surgical treatment of irrigation and debridement in acute infections, and 1-stage or 2-stage exchange arthroplasty in chronic infections.

  • Mortality rates of bacterial arthritis range from 10-20%, depending on the presence of comorbid conditions, such as older age, co-existing renal or cardiac disease and concurrent immunosuppression.
  • Factors associated with death include age 65 years or older, and infection in the shoulder, elbow, or at multiple sites.
  • After completing antimicrobial therapy, patients with S. aureus septic arthritis regain 45-50% of baseline joint function.
  • Adults with pneumococcal septic arthritis who survive infection (the mortality rate is approximately 20%) will return to 95% of baseline joint function after completing antimicrobial therapy.
  • Morbidity (eg, amputation, arthrodesis, prosthetic surgery, severe functional deterioration) occurs in one third of patients with bacterial arthritis, usually affecting older patients, those with pre-existing joint disease and those with synthetic intra-articular material.

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Further reading and references

  • Momodu II, Savaliya V; Septic Arthritis. StatPearls, July 2021.

  • Wang J, Wang L; Novel therapeutic interventions towards improved management of septic arthritis. BMC Musculoskelet Disord. 2021 Jun 922(1):530. doi: 10.1186/s12891-021-04383-6.

  1. Costales C, Butler-Wu SM; A Real Pain: Diagnostic Quandaries and Septic Arthritis. J Clin Microbiol. 2018 Jan 2456(2). pii: JCM.01358-17. doi: 10.1128/JCM.01358-17. Print 2018 Feb.

  2. Castellazzi L, Mantero M, Esposito S; Update on the Management of Pediatric Acute Osteomyelitis and Septic Arthritis. Int J Mol Sci. 2016 Jun 117(6). pii: E855. doi: 10.3390/ijms17060855.

  3. Mathews CJ, Weston VC, Jones A, et al; Bacterial septic arthritis in adults. Lancet. 2010 Mar 6375(9717):846-55.

  4. Cataldo MA, Petrosillo N, Cipriani M, et al; Prosthetic joint infection: recent developments in diagnosis and management. J Infect. 2010 Dec61(6):443-8. doi: 10.1016/j.jinf.2010.09.033. Epub 2010 Oct 7.

  5. Long B, Koyfman A, Gottlieb M; Evaluation and Management of Septic Arthritis and its Mimics in the Emergency Department. West J Emerg Med. 2019 Mar20(2):331-341. doi: 10.5811/westjem.2018.10.40974. Epub 2018 Dec 6.

  6. Gamalero L, Ferrara G, Giani T, et al; Acute Arthritis in Children: How to Discern between Septic and Non-Septic Arthritis? Children (Basel). 2021 Oct 138(10). pii: children8100912. doi: 10.3390/children8100912.

  7. Lenski M, Scherer MA; Diagnostic potential of inflammatory markers in septic arthritis and periprosthetic joint infections: a clinical study with 719 patients. Infect Dis (Lond). 2015 Jun47(6):399-409. doi: 10.3109/00365548.2015.1006674. Epub 2015 Mar 6.

  8. McGillicuddy DC, Shah KH, Friedberg RP, et al; How sensitive is the synovial fluid white blood cell count in diagnosing septic arthritis? Am J Emerg Med. 2007 Sep25(7):749-52.

  9. Lamagni T; Epidemiology and burden of prosthetic joint infections. J Antimicrob Chemother. 2014 Sep69 Suppl 1:i5-10. doi: 10.1093/jac/dku247.

  10. Chen AF, Heller S, Parvizi J; Prosthetic joint infections. Surg Clin North Am. 2014 Dec94(6):1265-81. doi: 10.1016/j.suc.2014.08.009. Epub 2014 Sep 30.

  11. Wall C, Donnan L; Septic arthritis in children. Aust Fam Physician. 2015 Apr44(4):213-5.

  12. British National Formulary (BNF); NICE Evidence Services (UK access only)

  13. Thabit AK, Fatani DF, Bamakhrama MS, et al; Antibiotic penetration into bone and joints: An updated review. Int J Infect Dis. 2019 Apr81:128-136. doi: 10.1016/j.ijid.2019.02.005. Epub 2019 Feb 14.

  14. Farrow L; A systematic review and meta-analysis regarding the use of corticosteroids in septic arthritis. BMC Musculoskelet Disord. 2015 Sep 516:241. doi: 10.1186/s12891-015-0702-3.

  15. Horowitz DL, Katzap E, Horowitz S, et al; Approach to septic arthritis. Am Fam Physician. 2011 Sep 1584(6):653-60.

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