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Introduction

    Sternoclavicular septic arthritis is a rare infection that has been described in healthy adults and immunocompromised individuals. It accounts for 1% to 9% of septic arthritis.^1,2 Before the antibiotic era, the most common pathogenic species were within the genus Fusobacterium, described in 1936 by Lemierre as necrobacilliosis or postanginal septicemia, which affected otherwise healthy adults.^3,4 In the postantibiotic era, anaerobic organisms have been rarely reported.⁵ Instead, the isolated organisms are frequently related to bacteremic complications of intravenous access devices or intravenous drug abusers.

    We report a case of sternoclavicular joint (SCJ) infection, thought to be secondary to Fusobacterium, from a necrotic oral cavity infection or Pseudomonas aeruginosa catheter-associated bacteremia.

Case Report

    A 54-year-old man was admitted to the hospital due to left sternoclavicular area pain and swelling that had progressively worsened over two weeks. Non-Hodgkin’s lymphoma was diagnosed three months prior to admission. He underwent chemotherapy and an allogeneic bone marrow transplant. This was complicated by severe graft-vs-host disease (GVHD), renal insufficiency, and lower-extremity deep venous thrombosis that required maintenance on coumadin therapy. He also continued immunosuppressive therapy with 20 mg of oral prednisone daily and 200 mg of cyclosporin twice a day. A left subclavian central venous catheter had been removed six weeks prior to admission.

    Examination revealed a chronically ill man in no acute distress. His temperature was 102°F, and he had mild tachycardia. A nontender, slightly prominent soft-tissue swelling was noted over the left SCJ, with mild erythema but without limitation of range of shoulder motion. The white blood cell count was 7,380/mm³ with a normal differential and an erythrocyte sedimentation rate of 21. After cultures were obtained, 1 g of intravenous vancomycin every 12 hours and 2 g of ceftazidime every 8 hours were prescribed. A chest radiograph was unremarkable, and a computed tomogram showed soft-tissue thickening at the left clavicular head and SCJ (Fig 1). A four-phase bone scan showed increased uptake at the SCJ (Fig 2).

    The SCJ was not aspirated because of lack of sufficient fluid. Blood cultures remained negative during this admission. However, several weeks prior to presentation, peripheral blood cultures grew P. aeruginosa. The patient’s fever defervesced with the antibiotic treatment, and his SCJ infection clinically improved. He was discharged after one week and continued to receive intravenous ceftazadime and vancomycin as an outpatient. He was readmitted a week later with a low-grade fever of 100.1°F, increased SCJ pain and swelling, and diffuse necrotic oral ulcerations. The patient had noted mouth sores on and off over several weeks, and these had reappeared and worsened since being discharged. Oral culture of the ulcers revealed "normal mouth flora." To treat the presumed anaerobic stomatitis, 900 mg of intravenous clindamycin every 8 hours was given in place of vancomycin. He completed a six-week course of intravenous clindamycin and ceftazidime therapy with prompt resolution of his oral ulcers and gradual resolution of the SCJ arthritis.

Discussion

    The most likely source of this septic arthritis was thought to be Pseudomonas spp. from his prior central venous catheter or an anaerobic organism such as Fusobacterium from his recurrent oral ulcerations. Unfortunately, this could not be confirmed since a sternal aspiration or bone biopsy culture was not obtained. One year later, the patient has had no recurrence of the SCJ infection, despite recurrent anaerobic stomatitis, GVHD, and cytomegalovirus pneumonia.

    Septic arthritis of the SCJ is a rare condition that can occur in healthy adults and in individuals with several predisposing conditions (Table 1).^6,7 Our patient had several risk factors: immunosuppression from prednisone and cyclosporin use, prior chemotherapy treatment for non-Hodgkin’s lymphoma, central venous catheter access, and renal insufficiency.
 

Table 1. -- Predisposing Factors for Septic Arthritis of the Sternoclavicular Joint
Systemic diseases:	Diabetes mellitus
	Rheumatoid arthritis
	Renal failure/dialysis
	Liver disease
	Malignancy
	Gout
	Congestive heart failure
Infection:	Upper respiratory tract infections
	Pneumonia
	Sepsis/Bacteremia
	Tuberculosis
Trauma:	Closed chest trauma
	Heavy physical exercise
	Local trauma (eg, corticosteroid injection)
Other:	Intravenous drug abuse
	Central venous catheters
	Alcoholism
	Corticosteroids
Adapted from Bayer et al6 and Wohlgethan.7

    Prior to the antibiotic era, Bacteroides spp. and Fusobacterium spp. were the most common isolated organisms in sternoclavicular joint septic arthritis (SCJSA). SCJSA usually presented with an acute febrile illness in individuals without any obvious underlying illness. It usually followed postanginal septicemia or necrobacillosis.^3,5,8 In the postantibiotic era, various other organisms have been isolated (Table 2).^5,6,9,10 In our patient, the likely sources of infection were the oral ulcerations most likely due to anaerobic organisms or P. aeruginosa isolated from his blood.
 

Table 2. -- Organisms Isolated From Sternoclavicular Joint Septic Arthritis
Gram Positive	Gram Negative	Other
Staphylococcus aureus	Pseudomonas aeruginosa	Mycobacterium tuberculosis
Streptococcus group B	Serratia marcescens
Staphylococcus epidermidis	Acinetobacter spp.
Streptococcus anginosus	Citrobacter spp.
Streptococcus milleri	Klebsiella pneumoniae
Streptococcus pneumoniae	Escherichia coli
	Brucella melitensis
	Salmonella spp.
Adapted from Lau and Shuckett,5 Bayer et al,6 Pothula et al,9 and Carrascosa et al.10

    With nongonococcal septic arthritis, the SCJ is a common site for hematogenous dissemination because the subclavian vein lies just behind the SCJ. Organisms have to traverse only the vein wall to reach the SCJ. Seeding of the SCJ can readily occur if a central venous catheter or intravenous drug injection into the jugular vein produces a high concentration of bacteria in the subclavian vein.

    Clinical diagnosis requires a high index of suspicion since symptoms in the region of the SCJ can be confused with various rheumatic disorders, osteoarthrosis, hyperostosis, Tietze’s syndrome, abscess, or tumor.² Infection can present with localized swelling with or without tenderness or decreased range of motion. A concise diagnosis is important since management differs depending on the cause.

    Laboratory studies usually are not helpful since an elevated white blood cell count or sedimentation rate is nonspecific, and blood cultures are frequently negative. When possible, aspiration of the joint for Gram stain and culture can be helpful in confirming the diagnosis and direct antibiotic treatment. Unfortunately, the failure rate with this method is high due to technical difficulty in aspiration of the small joint space,^2,9 as was the case with our patient. Positive blood cultures and a subclavian central venous catheter on the same side may also be helpful in suggesting the diagnosis. Unusual organisms such as tuberculosis or fungi in an appropriate host also should be considered.^2,11,12

    Compared with routine radiographs, computed tomography (CT) and magnetic resonance imaging (MRI) provide superior anatomical images of the SCJ, as was seen in our patient. Extension of the infection to contigous or intrathoracic and extrathoracic extension can best be seen with CT scanning and MRI.

    The presence of an abscess warrants early surgical drainage, with arthrotomy and debridement with extensive bone involvement. Antibiotic therapy should be tailored to the sensitivity of the isolated organism or the most likely organism by clinical history if isolation is not possible. With early diagnosis, antibiotic therapy alone can be adequate for treating the disease,^11,12 as was seen in our patient, though therapeutic failures have been reported requiring more aggressive surgical management.

    This case emphasizes the importance of a high index of suspicion in SCJ septic arthritis. Though rare, early diagnosis and treatment promote a favorable clinical outcome.

References

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2. Yasuda T, Tamura K, Fujiwara M. Tuberculous arthritis of the sternoclavicular joint: a report of three cases. J Bone Joint Surg Am. 1995;77:136-139.

3. Lemierre A. On certain septicemia due to anaerobic organisms. Lancet. 1936; 1:701-703.

4. Gubler JG, Wuest J, Oneta C, et al. Sepsis caused by Fusobacterium necrophorum: the re-discovered postangina sepsis Lemierre syndrome and other manifestations [in German]. Schweiz Med Wochenschr. 1990;120:440-445.

5. Lau ES, Shuckett R. Fusobacterium septic arthritis of the sternoclavicular joint. J Rheumatol. 1993;20:1979-1981.

6. Bayer AS, Chow AW, Louie JS, et al. Sternoclavicular pyoarthrosis due to gram-negative bacilli. Arch Intern Med. 1977;137;1036-1040.

7. Wohlgethan JR, Newberg AH, Reed JI. The risk of abscess from sternoclavicular septic arthritis. J Rheumatol. 1988;15: 1302-1306.

8. Seidenfeld SM, Sutker WL, Luby JP. Fusobacterium necrophorum septicemia following oropharyngeal infection. JAMA. 1982;248:1348-1350.

9. Pothula V, Morrison NG, Martinez A, et al. Management of sternoclavicular joint septic arthritis. Infect Med. June 1991:16-18.

10. Carrascosa M, Pascual F, Corrales A, et al. Septic sternoclavicular arthritis caused by group B Streptococcus: case report and review. Clin Infect Dis. 1996;22:579-580.

11. Beutler SM, Bayer AS. Managing sternoclavicular septic arthritis. Drug Ther (Hosp Ed). 1982;7:101-109.

12. Enarson DA, Fugii M, Nakielna EM. Bone and joint tuberculosis: a continuing problem. Canadian Med Assn J. 1979;120: 130-145.