eMedicine Specialties > Radiology > Musculoskeletal

Septic Arthritis

Author: Larry Holder, MD, Residency Director, Department of Radiology, Virginia Mason Medical Center
Coauthor(s): Matthew Studley, MD, MPH, Consulting Staff, Department of Radiology, Virginia Mason Medical Center
Contributor Information and Disclosures

Updated: Mar 22, 2007

Introduction

Background

In general, infectious arthritis is classified as pyogenic (septic) or nonpyogenic. Pyogenic septic arthritis is most frequently caused by Staphylococcus aureus. It also may be caused multiple other organisms, including staphylococci, Streptococcus pneumoniae, group B streptococci, Gonococcus species, Escherichia coli, Haemophilus species, Klebsiella species, Pseudomonas species, and Candida species. Infection can lead to rapid and severe joint destruction.

Nonpyogenic infective arthritis tends to be less aggressive and have a more chronic course. Causative organisms include Mycobacterium tuberculosis, fungi, and spirochetes.

Septic arthritis can be acquired through several routes of transmission. The most common cause is hematogenous spread to a joint from a distant source such as pneumonia or a remote wound infection. Direct seeding from can occur through trauma, surgery, or spread from a contiguous infection such as osteomyelitis or cellulitis.

Pathophysiology

Infection of the synovial membrane precedes contamination of the synovial fluid in most cases. This lack of involvement of the synovial fluid is the proposed explanation for negative Gram stains and cultures that commonly occur in early infections. In response to the bacterial infection, the synovial membrane becomes edematous and hypertrophied. The synovium produces increased amounts of exudative fluid, and eventually, frank pus accumulates within the joint. Rarely, gas accumulates within the joint or adjacent soft tissues secondary to the presence of gas-forming organisms such as E coli.

The destruction of joint cartilage occurs secondary to the release of proteolytic enzymes in the synovial exudate. Abnormal fibrin deposition on the articular cartilage disrupts the nutrient supply, leading to further chondrolysis.

Rapid destruction of bone and cartilage is less characteristic of nonpyogenic mycobacterial and fungal infections probably because of lower concentrations of proteolytic enzymes in the joint exudate. However, tuberculous granulation tissue containing large numbers of leukocytes and macrophages can erode directly into cartilage or insinuate between the joint cartilage and subchondral bone, leading to detached cartilage and exposed subchondral bone.

Abnormalities appear at the joint margins or centrally due to overgrowth and hypertrophy of the synovial pannus and granulation tissue. Eventually, this process may extend into the underlying bone, leading to erosions and osteomyelitis.

Rupture of the synovium may lead to extracapsular infectious complications such as myositis and abscess formation in adjacent soft tissues.

In infants, septic arthritis is usually due to the hematogenous spread of disease, and it most commonly affects the hip. It may stem from perinatal infection of the umbilicus with hematogenous seeding of the femoral metaphysis. This leads to direct intra-articular extension due to the intracapsular location of the metaphysis. Increased intracapsular pressure reduces blood flow to the epiphysis, which can lead to ischemia compounding the damaging affects of the infection.

Frequency

United States

The incidence of septic arthritis varies dramatically among age groups and among groups with risk factors for the disease. A number of risk factors are associated with septic arthritis. These include chronic illness, rheumatoid arthritis, intravenous drug use, steroids, artificial joint prosthesis, recent joint trauma or surgery, and impaired cellular immunity. Approximately 50% of cases of septic arthritis are due to gonococcal infection in the United States.

International

Australian epidemiologists have reported an overall prevalence of 9.2 cases per 100,000 population. Nonpyogenic (granulomatous) joint infections occur less frequently in developed countries than in underdeveloped nations, where the prevalence of tuberculosis is higher.

Mortality/Morbidity

In the preantibiotic era, death was a common complication of septic arthritis. Those who survived the acute infection often had severe joint destruction with complete bony or fibrous ankylosis. Tuberculous infection is more likely to result in fibrous ankylosis than pyogenic infections.

  • Antibiotic therapy has greatly reduced the morbidity and mortality of the disease. Mortality rates are reported to be less than 10%. Approximately 60% of patients recover completely; the remainder have permanent damage to the joint.
  • Prompt treatment usually limits long-term damage. Patients who are symptomatic for more than 7 days before the disease is diagnosis tend to have more-severe joint damage. S aureus and gram-negative bacilli tend to be more destructive organisms. See also Intervention.
  • Infants with septic arthritis of the hip often have long-term disability. The prognosis for slightly older children is better. Long-term complications can arise from growth disturbances, bony or fibrous ankylosis, or osteonecrosis of the femoral head.

Sex

Reports about the sex predilection of septic arthritis have varied with the type of organism and with the geographic location of the study. Results have indicated either no difference or a slight male predominance.

Age

Septic arthritis can occur in those of any age, but it predominantly affects young children.

  • In children, septic arthritis most commonly occurs in those younger than 3 years. Septic arthritis is uncommon from age 3 years to adolescence.
  • The incidence increases during adolescence with the appearance of gonococcal infections.
  • Joint infection is more common in elderly persons than in others because of the increased number of associated risk factors, such as chronic illness and joint prostheses.
  • Persons who abuse intravenous drugs have a higher prevalence of septic arthritis characterized by unusual locations (eg, wrist, sacroiliac joint, sternoclavicular joint) and unusual organisms (Mycobacterium avium-intracellulare, Pseudomonas aeruginosa, Enterobacter species).

Anatomy

Simplistically, joints are composed of bone, articular cartilage, synovial lining, synovial fluid, and a fibrous capsule. Prosthetics or surgical hardware may also be present.

Hematogenous infection usually begins with seeding to the synovial lining. This process leads to increased synovial fluid production and pressure within the joint. Frank pus then accumulates in the joint fluid. Edema of the adjacent bones and soft tissues ensues. Erosion of cartilage and bone at the endplates can occur, as can direct extension of infection into the periarticular soft tissues, which leads to muscle or tendon-sheath abscesses.

In infant hips, the metaphysis is within the joint capsule, and hematogenous seeding of the metaphysis can lead to direct intra-articular extension.

Presentation

Sites of involvement

The site of involvement depends on the age of the patient, the organism, and the existence of underlying risk factors. In adults, the knee is the most commonly affected joint. In children, the knee and hip are the most common sites. Intravenous drug use may cause infections in unusual joints such as the sternoclavicular and sacroiliac joints.

Risk factors

A number of risk factors are associated with septic arthritis. These include chronic illness, rheumatoid arthritis, intravenous drug use, steroids, artificial joint prosthesis, recent joint trauma or surgery, and impaired cellular immunity.

General presentation

Patients usually present with generalized symptoms of an acute systemic infection such as fever, chills, and malaise. The affected joint is often painful, hot, and swollen. In 90% of cases, only 1 joint is involved.

Age-related findings

Gonococcal arthritis usually affects young sexually active adults, and it appears as an acute inflammatory arthritis of 1 or more joints. Two thirds of patients have an associated dermatitis, and 25% may present with coinciding genitourinary symptoms.

Infants can present with irritability, loss of appetite, and fever. Children of walking age may present with a limp. Thigh swelling or erythema may accompany hip infections. Infants and young children may hold the affected hip in flexion, abduction, and external rotation (obturator sign). However, localized clinical signs and symptoms are often absent; this possibility makes the identification of septic joints difficult in children.

Patients usually have and elevated erythrocyte sedimentation rate and an increased white blood cell count with a leftward shift. Blood culture results are positive in approximately 50% of patients with nongonococcal septic arthritis.

Tuberculous arthritis is usually monoarticular, affecting the hip or knee. Most patients are middle aged or elderly. In contrast to pyogenic arthritis, tuberculosis may result in chronic joint pain with only minimal signs of inflammation. This condition often leads to a delay in diagnosis. Cultures of synovial fluid and histologic evaluation of synovial tissue are best for establishing the diagnosis.

Preferred Examination

Imaging is not the primary means of diagnosing septic arthritis. Joint fluid aspiration and evaluation is the key to the diagnosis, and samples should be obtained in all suspected cases of septic arthritis. This sampling can usually be achieved with fine-needle aspiration performed either blindly or with fluoroscopic guidance, depending on the location. Surgical exploration may be necessary in unusual cases, such as those involving sacroiliac and sternoclavicular joint infections.

Fluid should be sent for Gram staining, culturing, glucose testing, and leukocyte count and differential determination. White blood cell counts are usually 50,000-60,000/µL, with more than 80% neutrophils. Synovial fluid glucose levels are decreased. Gram stain results are positive in 75% of patients with gram-positive cocci. Gram staining is less sensitive in cases of gonococcal infection. Only 25% of cultures of gonococcal synovial fluid are positive.

Multiple imaging modalities are available for assessing septic arthritis. Plain radiography should be used as the initial study. However, if further imaging is required, MRI is the most sensitive and specific technique. Scintigraphy, CT, and ultrasonography are also used, to a lesser extent.

Limitations of Techniques

Plain radiographs are not sensitive to early findings, such as joint effusion or soft tissue changes.

MRI is expensive and time consuming. It is usually unnecessary if clinical suspicion is high and if the joint is easily accessible for aspiration.

CT is similar to MRI, but it has the disadvantage of ionizing radiation. However, it can be useful for guiding the aspiration of certain joints.

Scintigraphy is extremely sensitive but extremely nonspecific.

Ultrasonographic findings can confirm a joint effusion, but it cannot be used to assess its cause. It cannot accurately depict bony or cartilaginous abnormalities. This modality also may be useful to guide joint aspiration, and it is generally less expensive than either CT or MRI.

Differential Diagnoses

Osteoporosis, Involutional

More on Septic Arthritis

Overview: Septic Arthritis
Imaging: Septic Arthritis
Follow-up: Septic Arthritis
Multimedia: Septic Arthritis
References

References

  1. Alazraki NP. Radionuclide imaging in the evaluation of infections and inflammatory disease. Radiol Clin North Am. Jul 1993;31(4):783-94. [Medline].

  2. Beltran J, Noto AM, McGhee RB. Infections of the musculoskeletal system: high-field-strength MR imaging. Radiology. Aug 1987;164(2):449-54. [Medline].

  3. Bennett OM, Namnyak SS. Acute septic arthritis of the hip joint in infancy and childhood. Clin Orthop. Aug 1992;(281):123-32. [Medline].

  4. Greenspan A, Tehranzadeh J. Imaging of infectious arthritis. Radiol Clin North Am. Mar 2001;39(2):267-76. [Medline].

  5. Hong S, Kim S, Ahn J. Tuberculous Versus Pyogenic Arthritis:MR Imaging Evaluation. Radiology. 2001;218:848-853. [Full Text].

  6. Jacobson AF, Harley JD, Lipsky BA, Pecoraro RE. Diagnosis of osteomyelitis in the presence of soft-tissue infection and radiologic evidence of osseous abnormalities: value of leukocyte scintigraphy. AJR Am J Roentgenol. Oct 1991;157(4):807-12. [Medline].

  7. Jaramillo D, Treves ST, Kasser JR, et al. Osteomyelitis and septic arthritis in children: appropriate use of imaging to guide treatment. AJR Am J Roentgenol. Aug 1995;165(2):399-403. [Medline].

  8. Karchevsky M, Schweitzer M, Morrison W. MRI FINDINGS OF SEPTIC ARTHRITIS AND ASSOCIATED OSTEOMYLEITIS IN ADULTS. AMERICAN JOURNAL OF ROENTGENOLOGY. 2004;182:119-122. [Full Text].

  9. Kirks DR. Practical Pediatric Imaging. 2nd ed. Lippincott-Raven;1998: 378-80.

  10. Lee SK, Suh KJ, Kim YW, et al. Septic arthritis versus transient synovitis at MR imaging: preliminary assessment with signal intensity alterations in bone marrow. Radiology. May 1999;211(2):459-65. [Medline].

  11. Miller TT, Randolph DA Jr, Staron RB, et al. Fat-suppressed MRI of musculoskeletal infection: fast T2-weighted techniques versus gadolinium-enhanced T1-weighted images. Skeletal Radiol. Nov 1997;26(11):654-8. [Medline].

  12. Morgan DS, Fisher D, Merianos A, Currie BJ. An 18 year clinical review of septic arthritis from tropical Australia. Epidemiol Infect. Dec 1996;117(3):423-8. [Medline].

  13. Resnik CS, Ammann AM, Walsh JW. Chronic septic arthritis of the adult hip: computed tomographic features. Skeletal Radiol. 1987;16(7):513-6. [Medline].

  14. Resnik D, Niwayaama G. Osteomyelitis, septic arthritis, and soft tissue infection. In: Diagnosis of Bone and Joint Disorders. Vol 4. Philadelphia: WB Saunders Co;1988: 2571-86.

  15. Schattner A, Vosti KL. Bacterial arthritis due to beta-hemolytic streptococci of serogroups A, B, C, F, and G. Analysis of 23 cases and a review of the literature. Medicine (Baltimore). Mar 1998;77(2):122-39. [Medline].

Further Reading

Keywords

infectious arthritis, pyogenic arthritis, pyogenic joint infections, nonpyogenic arthritis, non-pyogenic arthritis, nonpyogenic joint infections, granulomatous joint infections, bacterial arthritis, tuberculous arthritis

Contributor Information and Disclosures

Author

Larry Holder, MD, Residency Director, Department of Radiology, Virginia Mason Medical Center
Disclosure: Nothing to disclose.

Coauthor(s)

Matthew Studley, MD, MPH, Consulting Staff, Department of Radiology, Virginia Mason Medical Center
Matthew Studley, MD, MPH is a member of the following medical societies: American College of Radiology
Disclosure: Nothing to disclose.

Medical Editor

Giuseppe Guglielmi, MD, Associate Professor of Radiology, Department of Radiology, Scientific Institute Hospital
Disclosure: Nothing to disclose.

Pharmacy Editor

Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand
Disclosure: Nothing to disclose.

Managing Editor

William R Reinus, MD, MBA, FACR, Professor of Radiology, Temple University; Chief of Musculoskeletal and Trauma Radiology, Vice Chair, Department of Radiology, Temple University Hospital
William R Reinus, MD, MBA, FACR is a member of the following medical societies: American College of Physician Executives, American College of Radiology, American Roentgen Ray Society, Missouri State Medical Association, and Radiological Society of North America
Disclosure: Nothing to disclose.

CME Editor

Robert M Krasny, MD, Consulting Staff, Department of Radiology, The Angeles Clinic and Research Institute
Robert M Krasny, MD is a member of the following medical societies: American Roentgen Ray Society and Radiological Society of North America
Disclosure: Nothing to disclose.

Chief Editor

Felix S Chew, MD, EdM, MBA, Professor, Department of Radiology, Section Head of Musculoskeletal Radiology, Vice Chairman for Radiology Informatics, University of Washington
Felix S Chew, MD, EdM, MBA is a member of the following medical societies: American Roentgen Ray Society, Association of University Radiologists, and Radiological Society of North America
Disclosure: Nothing to disclose.

 
 
HONcode

We subscribe to the
HONcode principles of the
Health On the Net Foundation

All material on this website is protected by copyright, Copyright© 1994- by Medscape.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.