Figure 1
Anteroposterior radiograph of the left ankle
Septic monoarthritis in a patient with gout
SectionMusculoskeletal system
Case TypeClinical Cases
AuthorsJones TA, Filer A, Raza K
Connected authors
51 years, male
Clinical History
A 57-year-old male patient known to have gout presented with an erythematous, swollen and painful left ankle which he described as feeling like an attack of gout. Empirical treatment for 2 months with analgesics and corticosteroids was ineffective. Examination revealed tinea pedis of the left foot and low grade pyrexia.
Imaging Findings
Ultrasound of the left ankle (Fig. 1) confirmed synovitis, and 1 ml of purulent fluid was aspirated under ultrasound guidance (Fig. 2). Polarised light microscopy of the synovial fluid revealed urate crystals, while culture yielded Staphylococcus aureus. He had an elevated CRP of 244 mg/L (normal range <5), with a normal white cell count of 9.6 x 109/L (normal range 4.0-11.0). Serum uric acid was 345 umol/L (normal range <420).
Radiographs of the left ankle (Fig. 3a) demonstrated joint space narrowing, with erosion of the lateral malleolus which had markedly deteriorated within 3 months (Fig. 3b).
The patient underwent arthroscopy and lavage of the left ankle. He was treated with intravenous flucloxacillin 2g qds for two weeks and then oral flucloxacillin for a further five weeks.
Despite antibiotics symptoms were slow to resolve, and there was considerable residual pain and limitation of movement subsequently, therefore MRI and nuclear imaging were performed (Fig. 4-6).
Radiographs of the left ankle (Fig. 3a) demonstrated joint space narrowing, with erosion of the lateral malleolus which had markedly deteriorated within 3 months (Fig. 3b).
The patient underwent arthroscopy and lavage of the left ankle. He was treated with intravenous flucloxacillin 2g qds for two weeks and then oral flucloxacillin for a further five weeks.
Despite antibiotics symptoms were slow to resolve, and there was considerable residual pain and limitation of movement subsequently, therefore MRI and nuclear imaging were performed (Fig. 4-6).
Discussion
Gout is caused by deposition of urate crystals in joints, often when serum is saturated with urate (above 420 umol/L). Prevalence is approximately 1%, but varies between populations and is commoner in men [1]. Typical presentation is with a rapid onset of an acute monoarthritis of the great toe, ankle, knee, wrist, finger or elbow, though oligoarticular and polyarticular disease is described, particularly in the elderly. Without specific treatment gout usually resolves within 7-10 days [1]; progressive rather than resolving symptoms and in particular a lack of response to conventional therapies for gout as in the present case should always make one question the diagnosis. The definitive diagnostic test for gout is the identification of urate crystals in synovial fluid; however a normal serum urate level cannot be used to exclude a diagnosis of gout as serum urate levels may fall during an acute attack [1].
Other established rheumatological conditions, including rheumatoid arthritis, can present with an acute monoarticular flare, however the differential diagnoses in the acute situation must include septic arthritis. Importantly, rheumatoid arthritis is recognised as a risk factor for septic arthritis [1-4] particularly if anti-tumour necrosis factor alpha (TNF-alpha) agents are used, which increase the risk of infection at least two-fold [5-7].
Septic arthritis carries a substantial risk of morbidity and mortality. Bacterial septic polyarthritis carries a 30% mortality, while monoarticular disease carries a 4-8% risk [2], with a poor outcome of the infected joint in 45% of the surviving adults [3]. Prompt identification and treatment of septic arthritis can substantially reduce morbidity and mortality. Poor prognostic indicators include older age (>60 years), rheumatoid arthritis, Staphylococcal infection, and a delay in diagnosis.
However, septic arthritis can pose considerable diagnostic difficulty as it does not invariably present with a leucocytosis or pyrexia and the clinical features of gout and septic arthritis can be indistinguishable [8, 9]. Also, the presence of gout crystals in synovial fluid does not rule out septic arthritis [10] and the two conditions may, as in this case, co-exist [8, 11, 12]. The development of septic arthritis in individuals with pre-existing inflammatory joint disease is not uncommon but is frequently associated with diagnostic delay, therefore this case highlights that a high index of suspicion should be cultivated in patients who present with an acutely hot swollen joint [13] and careful consideration should be given to immediate joint aspiration.
Other established rheumatological conditions, including rheumatoid arthritis, can present with an acute monoarticular flare, however the differential diagnoses in the acute situation must include septic arthritis. Importantly, rheumatoid arthritis is recognised as a risk factor for septic arthritis [1-4] particularly if anti-tumour necrosis factor alpha (TNF-alpha) agents are used, which increase the risk of infection at least two-fold [5-7].
Septic arthritis carries a substantial risk of morbidity and mortality. Bacterial septic polyarthritis carries a 30% mortality, while monoarticular disease carries a 4-8% risk [2], with a poor outcome of the infected joint in 45% of the surviving adults [3]. Prompt identification and treatment of septic arthritis can substantially reduce morbidity and mortality. Poor prognostic indicators include older age (>60 years), rheumatoid arthritis, Staphylococcal infection, and a delay in diagnosis.
However, septic arthritis can pose considerable diagnostic difficulty as it does not invariably present with a leucocytosis or pyrexia and the clinical features of gout and septic arthritis can be indistinguishable [8, 9]. Also, the presence of gout crystals in synovial fluid does not rule out septic arthritis [10] and the two conditions may, as in this case, co-exist [8, 11, 12]. The development of septic arthritis in individuals with pre-existing inflammatory joint disease is not uncommon but is frequently associated with diagnostic delay, therefore this case highlights that a high index of suspicion should be cultivated in patients who present with an acutely hot swollen joint [13] and careful consideration should be given to immediate joint aspiration.
Differential Diagnosis List
Septic bacterial arthritis on a background of gout.
Gout
Septic arthritis
Final Diagnosis
Septic bacterial arthritis on a background of gout.
References
[1] Underwood M (2006) Diagnosis and management of gout. Br Med J 332:1315 - 1319 (PMID: 16740561)
[2] Dubost JJ, Soubrier M, Sauvezie B (2000) Pyogenic arthritis in adults. Joint Bone Spine 67:11-21 (PMID: 10773964)
[3] Kaandorp CJ, Krijnen P, Moens HJ, Habbema JD, van Schaardenburg D (1997) The outcome of bacterial arthritis: a prospective community-based study. Arthritis Rheum 40:884-92 (PMID: 9153550)
[4] Kaandorp CJ, Van Schaardenburg D, Krijnen P, Habbema JD, van de Laar MA (1995) Risk factors for septic arthritis in patients with joint disease. A prospective study. Arthritis Rheum 38:1819-25 (PMID: 8849354)
[5] Kroesen S, Widmer AF, Tyndall A, Hasler P (2003) Serious bacterial infections in patients with rheumatoid arthritis under anti-TNF-alpha therapy. Rheumatology (Oxford) 42:617-21 (PMID: 12709536)
[6] Dixon WG, Watson K, Lunt M, Hyrich KL, Silman AJ, Symmons DP, et al (2006) Rates of serious infection, including site-specific and bacterial intracellular infection, in rheumatoid arthritis patients receiving anti-tumor necrosis factor therapy: results from the British Society for Rheumatology Biologics Register. Arthritis Rheum 54:2368-76 (PMID: 16868999)
[7] Curtis JR, Patkar N, Xie A, Martin C, Allison JJ, Saag M, et al (2007) Risk of serious bacterial infections among rheumatoid arthritis patients exposed to tumor necrosis factor alpha antagonists. Arthritis Rheum 56:1125-33 (PMID: 17393394)
[8] Yu KH, Luo SF, Liou LB, Wu YJ, Tsai WP, Chen JY, et al (2003) Concomitant septic and gouty arthritis - an analysis of 30 cases. Rheumatology (Oxford) 42:1062-6 (PMID: 12730521)
[9] Margaretten ME, Kohlwes J, Moore D, Bent S (2007) Does this adult patient have septic arthritis?. JAMA 297:1478-88 (PMID: 17405973)
[10] Shah K, Spear J, Nathanson LA, McCauley J, Edlow JA (2007) Does the presence of crystal arthritis rule out septic arthritis?. J Emerg Med 32:23-6 (PMID: 17239729)
[11] Schuind FA, Remmelink M, Pasteels JL (2003) Co-existent gout and septic arthritis at the wrist: a case report. Hand Surg 8:107-9 (PMID: 12923944)
[12] Alappatt C, Clayburne G, Schumacher R (2006) Concomitant polyarticular septic and gouty arthritis. J Rheumatol 33:1707-8 (PMID: 16881130)
[13] Weston V, Coakley G; British Society for Rheumatology (BSR) Standards, Guidelines and Audit Working Group; British Society for Antimicrobial Chemotherapy; British Orthopaedic Association; Royal College of General Practitioners; British Health Profession (2006) Guideline for the management of the hot swollen joint in adults with a particular focus on septic arthritis. J Antimicrob Chemother 58:492-3 (PMID: 16857687)
Case information
| URL: | https://www.eurorad.org/case/9145 |
| DOI: | 10.1594/EURORAD/CASE.9145 |
| ISSN: | 1563-4086 |
Figure 2
Aspirate from the tibiotalar joint
1ml of purulent synovial fluid was drained under ultrasound guidance. Culture yielded Staphylococcus aureus. Polarised light microscopy revealed urate crystals.
Figure 3
Ultrasound examination of the left ankle
Anterior longitudinal view. Synovitis (S) appears as a hypoechoic area, the effusion (E) appears as an anechoic area and vascularity is demonstrated by power Doppler positivity.
Anterolateral/axial view. Synovitis (S) appears as a hypoechoic area, the effusion (E) appears as an anechoic area and vascularity is demonstrated by power Doppler positivity.
Figure 4
Technetium-99m dynamic isotope bone scan
Venous phase. There is intense uptake in both venous and delayed images in the left ankle, predominantly in the distal end of the tibia. This is consistent with infection or severe inflammation.
Intense uptake in the left ankle, and in particular the distal tibia on the delayed phase scan indicating infection, or any form of severe inflammation.
Figure 5
MRI left ankle
Sagittal T2 sequence showing joint effusion and rapidly progressive periarticular joint destruction involving the talus, distal tibia and fibula with oedema of the subarticular bone marrow supports a diagnosis of a septic or inflammatory arthropathy.
Figure 6
Tc99m-HMPAO white cell Fab leukoscan
Increased uptake of tracer in the left ankle, predominantly in the distal tibia is suggestive of infection or severe inflammation/arthritis.
Aspirate from the tibiotalar joint
1ml of purulent synovial fluid was drained under ultrasound guidance. Culture yielded Staphylococcus aureus. Polarised light microscopy revealed urate crystals.
Ultrasound examination of the left ankle
Anterior longitudinal view. Synovitis (S) appears as a hypoechoic area, the effusion (E) appears as an anechoic area and vascularity is demonstrated by power Doppler positivity.
Anterolateral/axial view. Synovitis (S) appears as a hypoechoic area, the effusion (E) appears as an anechoic area and vascularity is demonstrated by power Doppler positivity.
Technetium-99m dynamic isotope bone scan
Venous phase. There is intense uptake in both venous and delayed images in the left ankle, predominantly in the distal end of the tibia. This is consistent with infection or severe inflammation.
Intense uptake in the left ankle, and in particular the distal tibia on the delayed phase scan indicating infection, or any form of severe inflammation.
MRI left ankle
Sagittal T2 sequence showing joint effusion and rapidly progressive periarticular joint destruction involving the talus, distal tibia and fibula with oedema of the subarticular bone marrow supports a diagnosis of a septic or inflammatory arthropathy.
Tc99m-HMPAO white cell Fab leukoscan
Increased uptake of tracer in the left ankle, predominantly in the distal tibia is suggestive of infection or severe inflammation/arthritis.