Shoulder:Sepsis of the Shoulder

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Bullet Points

  • Periprosthetic shoulder infection is rare but potentially devastating. The rate of periprosthetic shoulder infection is increased in cases of revision procedures, reverse shoulder implants and comorbidities. One specific type of periprosthetic shoulder infection is the occurrence of low-grade infections caused by non-suppurative bacteria such as Cutibaterium acnes or Staphylococcus epidemermidis.
  • Success of treatment depends on micro-organism identification, appropriate surgical procedures and antibiotic administration efficiency. Post-operative early periprosthetic shoulder infection can be treated with simple debridement, while chronic periprosthetic shoulder infection requires a one- or two-stage revision procedure. Indication for one-time exchange is based on pre-operative identification of a causative agent. Resection arthroplasty remains an option for low-demand patients or recalcitrant infection.

Key Words

Infection; Arthroplasty; Shoulder; Cutibacterium acnes; Propionibacterium; Revision.



While more than 66 000 prosthetic shoulder procedures were performed in 2011 in the United States, the rate of post-operative infection seems to remain stable with 0.98% of cases.[2][3][4] However, when infection occurs, this complication is always devastating with significant clinical and socioeconomic consequences.2 The rate is higher after revision surgery than after a primary procedure and reaches close to 5% in cases of reverse shoulder arthroplasty.[5][6] Patients undergoing primary reverse shoulder arthroplasty are found to have a six times greater risk of infection compared with patients having primary unconstrained total shoulder arthroplasty.[6] Arthroplasties for trauma are more at risk of infection than those from other causes.[6] Comorbidities such as coagulopathy, renal failure, diabetes, lupus erythematosus, rheumatoid arthritis, intra-articular steroid injections and corticosteroid therapy increase the risk of periprosthetic shoulder infection.[7] Periprosthetic shoulder infection is the major cause for revision within the first two post-operative years after an arthroplasty.[8]



Antibiotic prophylaxis is not specific to shoulder arthroplasty compared with other arthroplasties. Intravenous cephalosporine (2 g) administration is mandatory, given 30 minutes before the skin incision in many countries. However, some authors recommend a single 160 mg of gentamicin by intra-articular injection at the end of the procedure to reduce the risk of periprosthetic shoulder infection.[9] Saltzman et al.[10] have shown that pre-operative preparation of the surgical site with chlorhexidine gluconate and 70% isopropyl alcohol was more effective than iodine povacrylex and 74% isopropyl alcohol and povidone-iodine at eliminating overall bacteria, and that the two first ones were more effective than povidone-iodine regarding coagulase-negative Staphylococcus.

Hair removal is commonly performed before orthopaedic procedures and the use of razors is classically discouraged because micro-abrasions are created by shaving. However, removal of axillary hairs for shoulder surgery did not prove to have any effect on the cell-count of Cutibacterium acnes before surgical preparation.[11]

Cutibacterium (Propionibacterium) acnes

Cutibacterium acnes (formerly Propionibacterium acnes) is a non-spore-forming, anaerobic, gram-positive bacillus. It is of low virulence and therefore can be a commensal in the lipid-rich sebaceous follicles and deep layers of the skin, conjunctiva, external auditory canal, respiratory tract and intestinal tract.[12][13] Cutibacterium acnes mostly colonises the pilosebaceous follicles in the skin of the upper-body, especially the head, neck, shoulders and axilla.[14][15] Pathogenic activity of the organism has, however, been shown in conditions such as meningitis, septic arthritis, osteomyelitis, chronic prostatitis and sarcoidosis. Cutibacterium acnes expresses proteins required for cell-adherence, which are also antigenic and therefore capable of initiating an inflammatory response of the host’s innate immune system within the joint.[12] Cutibacterium acnes also secretes cytotoxic chemicals and enzymes designed to degrade body tissues, which can be harmful within the shoulder capsule.[12] Furthermore, Cutibacterium acnes is also able to secrete and live within an extracellular polysaccharide biofilm aiding joint colonisation and micro-colony formation, as well as avoid phagocytosis and survive macrophage engulfment.[12] The combination of the bacterium’s upper-limb distribution and role in prosthetic joint infection is now forcing shoulder surgeons to consider Cutibacterium acnes as an ‘orthopaedic pathogen’.[13]

Drug resistance

Patient knowledge about Cutibacterium acnes is mostly limited to acne vulgaris, the skin infection present in the vast majority of young adults and teenagers.[12] Hormonal changes and genetics cause sebaceous gland inflammation, dysfunction and proliferation providing an environment for the opportunistic Cutibacterium acnes.[12] The treatment of this skin condition with experimental courses of broad-spectrum antibiotics, often combined with poor compliance, is thought to be a contributor to antibiotic resistance.[14] Gold standard antibiotics such as penicillins, vancomycin, tetracyclines and erythromycin often eradicate the bacterium, however, over half of Cutibacterium acnes cultures now carry resistance to more than one of the above antibiotics.[14]

Incidence and Prevalence

Over the past decade, Cutibacterium acnes has become increasingly recognised as a cause of infection in orthopaedic surgery, especially when prosthesis is involved.[16] With regards to shoulder replacement surgery, one study reported infection rates for primary shoulder replacement to be less than 4% but, following reverse replacement, to be as high as 18%. In this study the most common bacteria identified were Staphylococcus epidermis and Cutibacterium acnes.[17] However, in a retrospective review over 7 years carried out in Canada, 80 patients were identified who underwent joint cultures after primary shoulder arthoplasty and Cutibacterium acnes was found to be the only significant infectious agent in 25% of participants, making it the most common pathogenic organism.[18] A study of periprosthetic joint infections after total shoulder arthroplasty (in the last 33 years) found that Staphylococcus was the dominant organism in the vast majority of cases, whereas, from 2001 – 2008, the incidence of Cutibacterium acnes was found to be almost as high as Staphylococcus.[19] This increasing incidence could be the result of changes in the microbiology of shoulder infections, heightened awareness of the organism, better surveillance or improved laboratory diagnostic techniques[19] Cutibacterium acnes appears to be a prominent aggressor and is becoming more prevalent.

Risk Factors

Recorded risk factors for Cutibacterium acnes infection are male gender, surgery of the upper body (especially the shoulder), increased duration of surgery and, interestingly, being the first surgery of the day.[4][20] The predominance of Cutibacterium acnes in shoulder infections has been linked with the presence of the axillary lymph nodes.[21] A study that involved culturing the epidermis of wounds during revision surgery, found that 16 of the 18 males involved had Cutibacterium acnes infection whereas only 7 of the 12 female subjects tested positive.[22] Further studies have also found that male gender and prior prosthetic implants are significant risk factors for Cutibacterium acnes infection.[18][20] The male predisposition has been linked with the habitat of Cutibacterium acnes being in the hair follicles and therefore the upper body of males would harbour more of the bacterium.[20] Furthermore, males were found to have over 2.5 times higher risk than females after shoulder arthroplasty.[23] Interestingly, if shoulder arthroplasty was performed following trauma rather than elective surgery, the risk of infection was nearly 3 times higher. Reverse shoulder arthroplasty again was shown to increase the risk of infection with Cutibacterium acnes. Younger age was also identified as a risk factor, with each year of increasing age causing a risk reduction of 5%. Body Mass Index and diabetes mellitus, which are usually associated with increased risk of infection, were not found to be risk factors.[23] 

From the literature it is evident that patients most at risk of Cutibacterium acnes infection are young people, males, those who have undergone upper limb surgeries (especially reverse shoulder replacements) and those who have surgery following trauma.


Despite laboratory and investigative advances, the diagnosis of shoulder infections due to relatively low-virulence organisms, like Cutibacterium acnes, remains difficult. The non-specific clinical presentation, inadequate culture performance and the inability to accurately interpret positive cultures mean that diagnosis can be delayed.[18] Research has found that inflammatory markers usually indicative of infection may not be raised in Cutibacterium acnes infection.[24] In 2014, in a clinic in the US, C-reactive protein and erythrocyte sedimentation rate were both raised in only 10% of patients who were identified as having Cutibacterium acnes infections of the shoulder.[24] In a further study, the sensitivities of C-reactive protein and erythrocyte sedimentation rate in the shoulder were found to be 42% and 16% respectively, whereas in the lower limbs the sensitivities forC-reactive protein and erythrocyte sedimentation rate were 88% and 75% respectively.[25] Thus, although the sensitivity and specificity of these inflammatory markers are strong in the lower limbs, they are poor indicators of post-operative shoulder infections.[24] These data fit well with the distribution of Cutibacterium acnes and its indolent nature. It has been further suggested that, due to its slow growth, Cutibacterium acnes needs longer culture times (up to two weeks), making it harder to spot.[25] Furthermore, lowering the threshold for diagnosis (concentration of neutrophils in the tissues) would increase sensitivity because of the low inflammatory behavior of Cutibacterium acnes.[25]

Clinical Presentation

A common assumption is that the origin of Cutibacterium acnes infection is in the dermis of the patient’s skin and that it travels from the surface to contaminate the surgical site.[22] Surface sterilisation before surgery does not, however, eradicate the bacterium as the organism actually resides deep in the sebaceous glands. Scalpel incisions slice through these follicles, allowing for seeding and leakage of the bacteria.[22] Innovative methods of sterilization may therefore be required to penetrate the dermis and reduce Cutibacterium acnes spread. Further, the need for intraoperative screening of wounds and prolonged cultures to assess the risk of developing a postoperative shoulder infection has been emphasised.[22] For low-grade Cutibacterium acnes shoulder infections, pain may be the only symptom, followed by stiffness with all other signs of infection being absent.[26] Periprosthetic joint infections can be extremely serious and may result in loss of normal function of the joint or even progress to sepsis.[17]

A study which focussed on postoperative pain, found that patients felt pain for an average of 3 months before diagnosis of Cutibacterium acnes infection and that the mean time from surgery to diagnosis was almost 2 years.[14] It was also suggested that the variance in the clinical presentation of shoulder infections may not only be due to the non-specific clinical manifestation of Cutibacterium acnes, but also due to co-infection with other bacteria within the surgical site.[14]



Debridement, irrigation and multiple deep samples may be proposed in cases of acute infection in order to save the prosthesis.[27] treated eight cases of acute infection with debridement and succeeded when it was performed within eight days after the diagnosis. They concluded that the earlier the debridement is done, the more effective it is in eradicating the infection. This procedure can be repeated, based on the patient’s response.[28] Moreover, mobile parts of the prosthesis may be exchanged during the procedure especially in case of reverse shoulder arthroplasty (glenosphere, polyethylene liner) providing better access for debridement. Then, an appropriate antibiotics regime is required for a minimum of four weeks.[28][29][30] However, the rate of success reported in the literature is only in the range of 50% to 95%.[28][29][31]

Cement spacer

An antibiotic-loaded cement spacer can be used either permanently or as the first step of a two-stage revision procedure. In this case, it maintains the space and soft-tissue tension for re-implantation and theoretically releases antibiotics to decrease the growth of microorganisms. Antibiotic mean concentration peak is reached at day 1 and dramatically decreases during the following seven days.[32]7 Levy et al.[33] described a ‘functional cement spacer’ model, which is made of a hemi-arthroplasty coated with cement. In their series of 14 patients initially chosen for a two-stage procedure, nine did not undergo a prosthesis re-implantation because of satisfactory clinical outcomes. On the other hand, Verhelst et al.[34] did not prove any difference between patients with a cement spacer and resection arthroplasty regarding infection control and clinical outcomes. Complications of the cement-spacer such as breakage, glenoid erosion or dislocation have been reported.[34]

One-stage revision arthroplasty

Based on the experience of knee and hip infection management, a single-stage exchange is proposed as a reasonable option when the infecting micro-organism is satisfactorily identified. The advantages are a reduced hospital stay, costs, period of antibiotic administration and the best clinical outcomes (Table).[10][17][27][31][30][35][36][37][38] Klatte et al.33 reported the outcomes of the largest single-centre series of 35 patients with a mean follow-up of 4.7 years. The authors excised infected tissues, thoroughly irrigated the wound using pulsatile lavage with polyhexanide before re-implantation and delivered specific intravenous antibiotherapy for an average of two weeks post-operatively. The success rate was more than 90%. No recurrence was observed in the series of Coste et al.,[27] Ince et al.[35] and Cuff et al.[36] The presence of a productive fistula seems not to be a contra-indication for many authors.[17][37] Beekman et al.[37] performed a one-stage revision in 11 cases of reverse shoulder arthroplasties, among which eight had a fistula, and achieved a success rate of 90%.

Two-stage revision arthroplasty

In a medically stable patient with a high demand, a two stage revision procedure is generally accepted (Table).[17][27][31][30][39][40][41] It is highly recommended when the microorganism responsible for the infection is unknown. The first step consists of infection eradication after prosthetic removal: an antibiotic-loaded cement spacer is often implanted and general antibiotics are administrated, secondarily adapted to the micro-organism(s) identified. Antibiotics are generally continued for six to eight weeks. Markers such as C-reactive protein or interleukin-6 have been shown to be valuable to predict the eradication of infection and, so, the time of re-implantation.[42][43] However, interleukin-6 seems to be normalized faster than C-reactive protei and allows earlier revision for better outcomes.[42] An iterative irrigation and debridement could be proposed in case of persistent infection. For re-implantation, reverse shoulder arthroplasty has been gaining ground in recent years as the implant of choice. First, it allows a larger debridement at the first stage with less concern for soft-tissue preservation. Secondly, it offers the possibility of addressing the glenoid bone defect with or without bone graft. Shirwaiker et al.[44] reported that there is still uncertainty whether two-stage revision is superior to one-stage (Figure).

A) Radiograph of a 73-year-old man with a chronic periprosthetic shoulder infection of a reverse shoulder arthroplasty (RSA). B) A two-stage revision was decided with a cement spacer implantation for eight weeks. C) Propionibacterium acnes was identified on peri-operative samples taken from the back of the glenosphere. D) After four weeks free of antibiotics, a new RSA was implanted with a proximal humeral allograft. From Bonnevialle et al.,[1] with permission.

Resection arthroplasty

Shoulder resection should remain a salvage procedure for frail or low-demand patients, and recalcitrant infection. It offers the option of a single definitive procedure for infection eradication (Figure). It has been shown that functional results are poor, but pain relief is achieved in more than 50% of cases.[10][45] Rispoli et al.[45] reported a mean active elevation of 70 degrees at long-term follow-up after anatomical shoulder arthroplasty removal. Verhelst et al.[2] demonstrated that preservation of the tuberosities is a predictive factor for better results, because it can avoid antero-superior subluxation of the humerus. In cases of reverse shoulder arthroplasty, Jacquot et al.[29] did not improve functional outcomes after removal of the implant and identified a high rate of post-operative complications. Bone loss and soft-tissue impairment after such constrained prostheses could partly explain these findings. Despite Jacquot[29] and Coste’s[27] studies, the literature reports a high rate of infection eradication, reaching more than 90% of cases.[2][10][27][30] [46][47]

Radiographs (A and B) of an 86-year-old woman, with a loose implant secondary to chronic periprosthetic shoulder infection. C) Because of numbers of co-morbidities and huge bone loss on glenoid side, a simple resection arthroplasty was performed.From Bonnevialle et al.,[1] with permission.

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Show details Search term Sternoclavicular Joint Infection David C. Tapscott; Michael D. Benham.

Author Information Last Update: June 2, 2020.

Go to: Introduction

The sternoclavicular joint is a saddle-shaped diarthrodial joint that joins the upper extremity appendicular skeleton to the axial skeleton. The large medial clavicle articulates with the superomedial manubrium and costal cartilage of the first rib, forming a joint with very little bony stability.[1] Within the joint is an intra-articular disc ligament composed of dense fibrous cartilage that provides structural support and prevents medial displacement of the clavicle.[2] The surrounding robust costoclavicular ligament and capsule offers an added layer of support.[2] The primary restraints to anterior and posterior translation of the joint are the anterior and posterior sternoclavicular ligaments.[3] Despite these restrictions, the sternoclavicular joint is actually very mobile and moves more than 30 degrees in the axial and coronal planes while having more than 45 degrees of rotation.[4] Functionally, it is quite similar to other amphiarthroses, such as the sacroiliac joint or pubic symphysis.[5]

Blood supply to the joint comes from the articular branches of the suprascapular and internal thoracic arteries.[1] The nerve to the subclavius muscle and the medial suprascapular nerves provide innervation to the sternoclavicular joint.[1]

Septic arthritis of the sternoclavicular joint is rare and represents less than 1% of all bone and joint infections.[5][6] A sternoclavicular joint infection is, in the majority of cases, associated with other systemic illnesses and/or general poor health status. Common concurrent issues include diabetes, intravenous drug use, immunosuppression, and rheumatoid arthritis.[7] While rare, prompt diagnosis and treatment are essential to prevent spread into the posteriorly located great vessels, mediastinum, and pleural space.[7]

Go to: Etiology

Ross et al. reviewed 180 cases of sternoclavicular joint septic arthritis and found that the most common offending bacteria were Staphylococcus aureus (49%) followed by Pseudomonas aeruginosa (10%) and Brucella melitensis (7%).[5] In a similarly designed study, Brancos et al. reported on sternoclavicular joint infections in a population of heroin addicts. They confirmed S. aureus and P. aeruginosa as the most common isolates.[8] In 2015, Jain et al. described tuberculosis (TB) as an unusual cause of sternoclavicular septic arthritis. They reported a small series of 9 men and 4 women who eventually received a diagnosis of sternoclavicular septic arthritis secondary to TB.[9]

Go to: Epidemiology

In the general population, sternoclavicular septic arthritis accounts for less than 1% of bone and joint infections.[6] Interestingly, it accounts for 17% of septic arthritis cases amongst intravenous drug users.[5] The classic involved patient demographic consists of males in the fourth to fifth decade of life. In the previously mentioned case series by Ross et al., 73% of sternoclavicular joint infections involved males with a mean age of 45.[5] Interestingly, no risk factor for infection was identifiable in almost a quarter of the patients in the study.[5] Von Glinski et al. reported 13 cases of sternoclavicular joint infection involving eight men with a mean age of 37 years.[10]

Go to: Pathophysiology

Infection of the sternoclavicular joint can occur via direct inoculation of the joint or contiguous spread from a nearby area; however, the most common pathway is hematogenous spread via the blood-stream. This particular mechanism explains why the prevalence of this rare condition is so much more commonly seen in patients with a history of intravenous drug abuse.[11]

A healthy patient may be able to contract a spontaneous sternoclavicular joint infection. Sanelli et al. describe a case os staphylococcal septic arthritis that is associated with no known predisposing risk factor. That patient was able to be managed with medical therapy alone.[12]

There have been reports of patients contracting sternoclavicular joint infections in association with dialysis. Renoult et al. first reported on the association of hemodialysis and sternoclavicular joint infection. They reported on two patients who were able to be treated non-operatively after addressing the condition.[13] Renal failure may further immunosuppress and predispose such patients to a sternoclavicular joint infection.

Go to: History and Physical

An extensive history involving the assessment of systemic symptoms is vital as many of the conditions that affect the sternoclavicular joint are systemic. The clinician should question the patient regarding a family history of sternoclavicular arthritis, intravenous drug use, and systemic complaints such as subjective fevers, chills, night sweats, and malaise. Pain localized to the sternoclavicular joint or medial clavicle is a high-risk patient, or an individual with systemic symptoms should raise suspicion for infection.

On physical examination, an infected sternoclavicular joint is likely to be swollen, warm, tender, and erythematous. Patients are painful both with direct palpation of the joint as well as passive/active range of motion of the ipsilateral shoulder. Typically, sternoclavicular joint septic arthritis is a unilateral condition, while inflammatory arthritis such as rheumatoid arthritis affects both joints simultaneously. One should pay attention to any fluctuance, joint translation, joint asymmetry, and bony enlargement. Joint asymmetry should raise concern for a sternoclavicular joint dislocation, which may represent a surgical emergency if directed posteriorly with neurovascular changes.[14]

Go to: Evaluation

As in most cases of orthopedic infections, an elevated white blood cell count (WBC), erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP) present as elevated. These markers are relatively nonspecific and may increase in cases of gout, systemic illness, or infection of another joint. As previously stated, these patients may be immunosuppressed and may be unable to elicit a systemic response that produces impressive inflammatory labs. It is also reasonable to routinely obtain blood cultures on these patients at the time of presentation as estimates are that nearly two-thirds of patients with sternoclavicular joint infections are systemically septic.[5]

Imaging studies for these patients are, unfortunately, nonspecific and are most helpful in ruling out other painful etiologies. If deemed necessary, an MRI is an excellent tool to evaluate for joint effusion, nearby abscess, or early osteomyelitis.[5] Radiographs of the sternoclavicular joint may be helpful but likely only in the setting of osteomyelitis as isolated septic arthritis would lack bony involvement by definition. Von Glinski et al. obtained chest radiographs in all patients in their series of 13 to assess surrounding tissues.[10]

CT scan may hold some additional value as it may show earlier bony changes as well as demonstrate the presence of any peri-articular or retrosternal abscess. Von Glinski et al. described a series of 13 patients, of whom 10 had a periarticular abscess that was identifiable on a preoperative CT scan.[10]

The gold standard for diagnosing sternoclavicular joint septic arthritis remains arthrocentesis. Aspirated joint fluid should undergo evaluation for crystals, cell count, percentage of neutrophils, and the presence of bacteria using gram stain and culture. A total nucleated cell count greater than 50000 with over 90% neutrophils with no crystals is concerning for infection. A positive gram stain or culture is virtually diagnostic regardless of the other synovial fluid analyses.

Rochuae et al. reported on a group of sternoclavicular joint arthritis patients and found that only 53% had proven bacteremia at the time of evaluation.[15] Blood cultures are a reasonable adjunct to obtain during patient evaluation. However, this relatively low positivity rate means blood cultures cannot be solely relied upon to isolate the offending organism.

Go to: Treatment / Management

While there are reports of successful treatment with needle arthrocentesis and antibiotics, the mainstay of treatment for sternoclavicular joint infections is surgical irrigation and debridement with tailored intravenous antibiotic therapy.[9][16] Care should be taken to evaluate the surrounding chest wall for loculated abscesses that may be a source of continued infection at the time of operative irrigation and debridement. Particular aggressive organisms or recalcitrant infections may require resection of the medial clavicle with possible soft tissue coverage given the subcutaneous nature of the sternoclavicular joint. When resecting the medial clavicle, the vital retrosternal structures, as well as the surrounding ligamentous structures, must be protected.[1] If the supporting ligamentous structures are damaged, pain and instability can result.[17]

In a series of 10 patients who underwent resection arthroplasty for sternoclavicular joint septic arthritis, Chun et al. reported good functional results with intramedullary ligament reconstruction and 4 to 8 weeks of intravenous antibiotics.[18] There are multiple studies available in the literature detailing joint resection techniques as well as closure methods.[9][19][18] Whitlark et al. describe a single-stage washout with implantation of antibiotic laden beads and a good outcome in a single case.[20]

Less invasive management may be an option in less advanced disease or an immunocompetent host. Multiple authors have reported on cases or case series that were manageable with antibiotics alone.[13][12] However, due to a lack of larger studies with longer follow up, the success rate of this treatment technique is not well described. Isolated aspiration or needle lavage has also been suggested but lacks significant literature to prove its reliability.

If there becomes a significant soft tissue defect from adequate debridement, additional flap coverage may be required. Although uncommon, it is possible to need a soft tissue transfer. Opoku-Agyeman et al. reported on several surgical configurations for pectoralis major flaps in the reconstruction of sternoclavicular defects.[21] These techniques include a pectoralis split and advance, split and rotate, or entire pectoralis harvest and transfer. These techniques may be considered in surgical planning if significant debridement is required. Primary muscle flap closure has demonstrated excellent outcomes in a series of 40 patients, as described by Kachala et al.[19]

A multidisciplinary approach, including the involvement of infectious disease, may optimize the patient outcome. Postoperatively, or in the case of medical management, the mainstays of antibiotic therapy for any septic arthritis should be a post-operative course of antibiotics of at least two weeks depending on the offending agent and the recommendations of your infectious disease team.[22]

Go to: Differential Diagnosis

The differential diagnosis of sternoclavicular joint infection includes sternoclavicular joint arthritis, clavicular osteomyelitis, clavicular fracture, sternal fracture, pleuritis, gout, dislocation, condensing osteitis of the clavicle, mediastinitis, or rib fracture.

Go to: Prognosis

The prognosis for patients with sternoclavicular joint infections recognized promptly and treated appropriately is excellent. Burkhart et al. reported a case series of sternoclavicular joint infections treated with joint resection with no resulting limitations of the affected upper extremity.[23] Untreated infections can develop into extrapleural or intrathoracic abscesses and quickly become life-threatening if the retrosternal structures are involved.[1]

Initial post-operative care will revolve around clearing the infection and obtaining adequate soft tissue healing. After achieving source control, the function of the limb is the primary focus. In an excellent review of sternoclavicular joint instability, Sewell et al. describe physical therapy as being beneficial for patients with SC joint instability.[24] Being able to offer treatment as a postoperative adjunct for a patient experiencing slow recovery may increase patient rehabilitation and improve the overall outcome.

Go to: Complications

Complications include: the need for repeat surgery, osteomyelitis, skin loss over the affected area requiring flap coverage, instability of the joint, need for joint reconstruction, inability to clear the infection, and progression to the chest wall or mediastinal involvement. Patients may have chronic pain with shoulder range of motion or pain with heavy lifting in cases of chronic infections or delayed diagnoses.

Go to: Deterrence and Patient Education

Correcting modifiable risk factors and providing education regarding the dangers of intravenous drug use may lower the incidence of sternoclavicular joint infections.

Go to: Enhancing Healthcare Team Outcomes

The diagnosis and management of patients with sternoclavicular joint infection are complex and best done with an interprofessional team. The nurses may be the first to identify the pathology in in-patients, especially in those with central catheters. Outpatients usually present to the emergency room.

A combination of history, physical examination, and laboratory findings are necessary to make the diagnosis of sternoclavicular joint infection. Many of these patients likely present to primary care providers or emergency departments, so a basic knowledge of this condition is required to make a prompt diagnosis and avoid the spread of the infection or a poor outcome. The services of radiology are vital as imaging is often used to confirm the diagnosis. The infectious disease expert should be consulted for antibiotics and the duration of therapy. A surgeon is usually involved, as many patients require drainage and debridement. The board-certified infectious disease pharmacist should pay attention to culture results and ensure that the patient is on the appropriate antibiotics compared to antibiogram data. The pharmacist can also verify dosing and duration, and check for potential drug interaction, informing the team if there are any issues. Nursing can assist the clinician during the case, verifying patient compliance, acting as a bridge to the clinician for the patient and other providers (e.g., physical therapist), and providing patient counsel.

Prompt referral to an orthopedic or thoracic surgeon is vital if the infection has resulted in osteomyelitis of the sternum or clavicle. Orthopedic and thoracic surgeons must provide education on the ramifications of a missed diagnosis to other healthcare providers. Close communication between the team members is vital for improving outcomes. [Level 5]

Go to: Questions

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Sternoclavicular infection Figure

Sternoclavicular infection. Image courtesy S Bhimji MD Sternoclavicular joint anatomy Figure

Sternoclavicular joint anatomy. Image courtesy S Bhimji MD Sternoclavicular joint infection Figure

Sternoclavicular joint infection. Image courtesy S Bhimji MD Go to: References

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