Septic arthritis

I. What every physician needs to know.

While non-gonococcal arthritis is not the most common cause of a monoarticular arthritis, it is the most destructive. If not recognized early it can lead to rapid cartilage and joint destruction, and even carries a 7-15% in hospital mortality with antibiotics. It must be considered and evaluated for rapidly in those patients most at risk. Gonococcal arthritis will be discussed separately in another chapter.

The severity of the disease relates to its pathophysiology. Bacteria reach the synovial membrane most commonly by hematogenous spread or less commonly direct inoculation and quickly infect synovial fluid as well. This leads to synovial membrane hyperplasia and influx of inflammatory cells. The cytokines released by these cells lead to rapid cartilage and bone destruction which is compounded by the rapidly increasing pressure within the synovial fluid.

II. Diagnostic Confirmation: Are you sure your patient has septic arthritis?

A. History Part I: Pattern Recognition:

The most sensitive symptoms and signs for septic arthritis include acute joint pain, restricted motion, and a history of joint edema. Much less sensitive are fever, sweats and rigors. Classically, a patient with septic arthritis is thought to have greater pain and an even greater reported loss of range of motion than in other forms of monoarticular arthritis. No clear evidence supports this thinking and septic arthritis should be considered in any patient with new monoarticular joint pain with a history of edema. While septic arthritis can involve any joint, it is more commonly seen in larger, weight bearing joints in particular the knee.

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B. History Part 2: Prevalence:

Septic arthritis should be a particular concern in patients with prosthetic knee or hip replacement, particularly when there is evidence of cellulitis overlying the prosthetic joint. Outside of these patients, major risk factors for septic arthritis include age (greater than 80), a history of diabetes mellitus. intravenous drug abuse, underlying joint injury or damage, and a history of rheumatoid arthritis.

Joints already affected by other form of arthritis, particularly inflammatory arthritides like rheumatoid arthritis should be carefully evaluated.

C. History Part 3: Competing diagnoses that can mimic septic arthritis.

The differential for septic arthritis focuses on other major causes of a monoarticular arthritis as about 80% of cases of septic arthritis will present this way.

  • Gout and pseudogout – distinguished based on results of arthrocentesis as both can present as a monoarticular arthritis involving joints most susceptible to septic arthritis.

  • Rheumatoid arthritis – less commonly presents as a monoarticular arthritis.

  • Lupus – less commonly presents as a monoarticular arthritis in isolation of other clinical findings.

Other infectious causes
  • Lyme

Reactive arthritis

More commonly an oligoarthritis and very often involving smaller joints; seen after proceeding gastrointestinal or urethral infection.

Pigmented vilonodular synovitis

This very rare and slow growing, and potentially destructive, neoplasm of the synovium seen almost always in children and young adults will often cause recurrent episodes of pain and swelling though it can not be definitely eliminated without synovial biopsy.


While many of the same joints can be involved, hemarthrosis is most commonly seen post-trauma, surgery or injury or in those with bleeding disorders (particularly factor deficiencies). Aspiration will firmly distinguish.

Meniscus tear or bone fracture

Both usually present after a history of injury.

D. Physical Examination Findings.

No single physical exam finding is definitive. Redness, warmth and tenderness with swelling are the most commonly reported physical exam findings. The pain and limitation in range of movement are often described as more severe than in other forms of arthritis, but this is not clearly supported.

The knee is most commonly involved but the hips, wrists and ankles can also be involved.

Special mention should be made of patients with artificial joints who can often present with less warmth and erythema, and a less classical exam overall.

E. What diagnostic tests should be performed?

1. What laboratory studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

Whenever septic arthritis is considered as a possible diagnosis, examination of the synovial fluid is essential, prior to the initiation of antibiotics, if possible. Since cultures can take a day to several days to yield useful results, initial interpretation relies on analysis of cell counts.

While white blood cell counts from synovial fluid above 25,000 carry a reported likelihood ratio (LR) of around 3 for septic arthritis, using a single cut-off for white count to rule in or out the diagnosis is likely less helpful. More generally, instead, consider the presence of increasing numbers of white cells in the synovial fluids is suggestive of septic arthritis.

Classic teaching (differing though between sources) is that white counts in the single thousands suggest osteoarthritis. White counts from 9,000-20,000 uL suggest inflammatory arthritis and those above 20,000 uL suggest septic arthritis. In cases where the pre-test probability of septic arthritis is high, caution is usually advised to not rely strictly on the white count to rule out the diagnosis. In these cases, it is suggested to wait at least 48 hours to confirm no growth on culture.

Initial gram stain can also help to tailor antibiotic choice but is not sensitive enough to rule out the diagnosis.

When cultures do grow a bacteria, it will often be a single bug and sensitivities can help guide antibiotic choice. Examining the fluid for crystals is also helpful. While the presence of crystals does not rule out septic arthritis, in cases where clinical suspicion is low it can help further build an argument for an inflammatory rather than infectious source.

Blood cultures should routinely be drawn in any patient with the suspicion of septic arthritis as the blood culture may be positive even if the synovial fluid culture is not.

2. What imaging studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

Plain films of the joint will usually be ordered but this will more help to evaluate for other causes of acute monoarticular pain such as a bone fracture than to confirm a diagnosis of septic arthritis.

F. Over-utilized or “wasted” diagnostic tests associated with this diagnosis.

Serum white blood cell count, erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) have little effect on pretest probability, whether normal or abnormal. However, CRP and ESR are often used to monitor the response of treatment and are thus routinely ordered at the time of diagnosis.

III. Default Management.

Septic arthritis can be joint destructive if not recognized and then treated early and effectively. Management focuses on appropriate antibiotic administration and joint drainage.

A. Immediate management.

1) IV antibiotics should be given immediately in patients with exams consistent with septic arthritis and whose synovial fluids have white cell counts that support the presumed diagnosis, i.e. do not wait for culture confirmation of the diagnosis. Antibiotic choice is usually based off of gram stain.

  • Gram-positive cocci: Coverage including methicillin-resistant Staphylococcus aureus (MRSA) coverage should be given to all patients. The most common choice is vancomycin at -15-20 mg/kg every 8-12 hours.

  • Gram-negative cocci: Ceftriaxone 1gm IV daily.

  • Gram negative bacilli: Cefepime 2gm IV every 8-12 hours or Ceftazadime 2 gm IV every 8 hours

  • Gram stain negative: Antibiotic choice is usually vancomycin and cefepime

2) Joint drainage -. Joint drainage is considered standard of care although no randomized control trials have evaluated its efficacy. In most institutions this will involve consulting the orthopedic service. Drainage may be by aspiration (for smaller joints) or total wash out (for larger joints).

C. Laboratory Tests to Monitor Response To, and Adjustments in, Management.

There is no evidence to suggest re-taping the joint to confirm clearance, although re-tapping to further clear any remaining purulent material may be of value. Often, CRP and ESR are used to monitor response to treatment.

D. Long-term management.

The length of antibiotic course is unclear. Usually 14 days of IV antibiotics is recommended and then the patient can be switched to an oral regimen for a total of 3-4 weeks. Most prosthetic joint infections require extended antibiotic durations.

IV. Management with Co-Morbidities

A. Renal Insufficiency.

Vancomycin dosing and levels must be monitored closely.

G. Immunosuppression (HIV, chronic steroids, etc).

More concern should be given to the possibility of gram-negative rods as a source of infection. In cases where the gram stain and culture are unrevealing most would suggest continuing therapy for gram-negative rods in patients with immunosuppression.

V. Transitions of Care

A. Sign-out considerations While Hospitalized.

It is important to remind covering physicians to adjust antibiotic therapy based on any new culture data. For instance if both gram-positives and gram-negatives are empirically covered, antibiotics can be narrowed if only a single organism grows on culture.

B. Anticipated Length of Stay.

Patients will need to remain in house until joint drainage is completed and access for antibiotics is provided.

C. When is the Patient Ready for Discharge.

See above.

D. Arranging for Clinic Follow-up

1. When should clinic follow up be arranged and with whom?

Patients will typically need follow-up with an orthopedist, especially if joint drainage is performed. Follow-up with their primary care doctor is also usually helpful. Both should be within 1-2 weeks.

2. What tests should be conducted prior to discharge to enable best clinic first visit?

None in particular although some will request CRP and ESR (see discussion above).

3. What tests should be ordered as an outpatient prior to, or on the day of, the clinic visit?

None in particular although some will request CRP and ESR (see discussion above). For patients on longterm vancomycin or cephalosporins, consideration should be given to arranging follow-up drug levels, complete blood cells (CBCs) and panel 7’s for kidney function assessment.

E. Placement Considerations.

As discussed below, even with optimal management many patients will still suffer joint damage.

For those who are ambulatory without a problem, discharge to home with care for a peripherally-inserted central catheter and IV antibiotic administration, as well as lab draws.

For those with resulting issues with ambulation or difficulties with activities of daily living or an inability to receive IV antibiotic at home, sub-acute or acute rehabilitation will be needed depending on the patient’s baseline functional status.

F. Prognosis and Patient Counseling.

Even with proper therapy, many will suffer irreversible joint damage. Risk for this kind of damage is in part determined by age, co-morbid conditions and the destructiveness of the bacteria involved with some bugs like staphylococcus being more likely to cause extensive joint damage.

What's the evidence?

Mathews, CJ, Weston, VC, Jones, A, Field, M, Coakley, G. “Bacterial septic arthritis in adults”. Lancet. vol. 375. pp. 846-55.

Carpenter, CR, Schuur, JD, Everett, WW, Pines, JM. “Evidence-based diagnostics: adult septic arthritis”. Acad Emerg Med. vol. 18. 2011. pp. 781-96.

Sharff, KA, Richards, EP, Townes, JM. “Clinical management of septic arthritis”. Curr Rheumatol Rep. vol. 15. 2013. pp. 332

Diane Lewis, Horowitz, Elena, Katzap, Scott, Horowitz, Maria-Louise, Barilla-LaBarca. “Approach to Septic Arthritis”. Am Fam Physician. vol. 84. 2011. pp. 653-660.

Mary, E, Margaretten, MD, Jeffrey Kohlwes, MD, Dan, Moore, Stephen, Bent. “Does This Adult Patient Have Septic Arthritis”. . vol. 297. 2007. pp. 1478-1488.

Mathews, CJ, Coakley, G. “Septic arthritis: current diagnostic and therapeutic algorithm”. Curr Opin Rheumatol. vol. 20. 2008. pp. 457-62.