Chapter 48 The Assessment and Management of Septic Arthritis
Introduction
Septic arthritis is defined as a bacterial infection of the synovium and joint space. It is a relatively uncommon condition that may occur at any age being more common in children. In the pre-antibiotic era the mortality of all joint infections was 20% and morbidity in the region of 50%. Joint infection leads to rapid and irreversible damage to the articular cartilage. Any delay in the treatment of a septic joint will result in a poor outcome. While it is an infrequent presentation in the elbow, early recognition, diagnosis and treatment are essential to achieve a satisfactory outcome. This requires the clinician to have a high index of suspicion of sepsis in patients with predisposing conditions. In addition, infection can obviously follow any surgery to the elbow and is a particularly troublesome complication of elbow arthroplasty. This has been dealt with in Chapter 44 and will not be covered further in this chapter.
Epidemiology
In developed countries septic arthritis has shown no change in its incidence1 despite advances in antimicrobial therapy. Among children in Sweden the annual incidence is 10 per 100 000 children.2 In a separate study from the Mayo clinic over a 15-year period, the elbow accounted for 6% of all septic joints in the adult. To put this in context, however, the number of patients presenting to that unit with septic arthritis unrelated to previous surgery was only 10 new adult cases per year, thus emphasizing the uncommon nature of elbow sepsis. Most of these cases were over the age of 50 years with an equal sex ratio.3
The incidence in developing countries, particularly in Africa, is considerably higher.4,5 In contrast to the experience in Europe and North America, Goldschmidt and Hoffman5 reported a 100% increase in presentation of septic arthritis in Cape Town between 1983 and 1988, with a male to female ratio of 2:1. They also noted a seasonal variation with a 30% increase in incidence in the cooler months. This seasonal variation is the converse of their finding with other musculoskeletal infections which were 50% higher in the summer months. Other reports also suggest that musculoskeletal infections are commoner in warmer and more humid conditions.6
The presentation of septic arthritis may be monoarticular or polyarticular. The polyarticular form accounts for 10% of all presentations and, in adults, half of these are in rheumatoid arthritis patients.1
Aetiology and pathogenesis
There are four routes by which bacteria can spread to the elbow joint:
Haematogenous spread
Joint haemarthrosis may be due to direct trauma, a bleeding diathesis such as haemophilia or occur in patients on anticoagulant therapy. Neurological disorders resulting in a neuropathic (Charcot) joint may be more prone to haematogenous spread of infection, both due to the gross destructive change that may occur in the joint and due to any haemarthrosis.7 The presence of a haemarthrosis will create an inflammatory response within the joint with increased permeability of the basement membrane. In addition, the presence of blood within the joint will provide a rich culture medium for bacterial proliferation. These two factors make the joint susceptible to bacterial infection by a haematogenous route.
Systemic diseases may include those that affect joints directly and those that increase infection rates generally. The inflammatory arthropathies such as rheumatoid arthritis and the seronegative arthropathies have a significantly increased risk of developing septic joints, rheumatoid arthritis accounting for 50% of all adult polyarticular forms.1 This is likely to be multifactorial due to the joint damage, the nature of the condition and the disease-modifying drugs that these patients may be taking. Examples of such drugs used for treatment of rheumatoid arthritis include methotrexate, leflunomide and cytokine modulators such as the tumour necrosis factor (TNF) α inhibitors. These drugs are immunosuppressive and can significantly increase infection risk in their own right. Other medications that may predispose to infection include steroid therapy and the immunosuppressants used in the treatment of neoplasia and in transplant patients.
The rise in the incidence of human immunodeficiency virus (HIV) infection worldwide has been implicated in the increased incidence of septic arthritis, particular in Africa. Added to that, there is an increased incidence of haemophiliac people infected with the HIV virus.8 Other general conditions such as diabetes mellitus, malignancy, liver and renal disease have also been reported to increase the incidence of septic arthritis.9
Spread from a contiguous lesion
Spread from a contiguous lesion can occur from an overlying infected olecranon bursa, though any other local soft tissue infection such as cellulitis or an abscess can have the same effect. The olecranon bursa does not have a direct communication with the elbow joint thus bacterial spread in these local lesions must be by other routes. Contiguous needle aspiration of the bursa and aspiration of the elbow to exclude infection may be responsible for inoculation of the elbow joint with bacteria. Spread via the lymphatic system or local haematogenous spread accounts for the remainder. Olecranon bursitis is covered in Chapter 36 and will not be covered further in this chapter.
Spread from metaphyseal bone
Osseous infection principally affects the metaphysis due to the arrangement of the blood supply. The epiphyseal plate usually forms an effective barrier to the spread of bacteria from the metaphysis to the epiphysis. However, in children under the age of 18 months, blood vessels cross the epiphyseal plate allowing infection to spread from the metaphysis to the epiphysis, which is intracapsular. This allows spread of the infection into the joint.10
For transmission to occur from a metaphyseal infection directly to the joint after the age of 18 months, the metaphysis must be intracapsular. This arrangement of capsular attachment only occurs in few joints, one of which is the proximal radial metaphysis. As a consequence, the elbow is potentially susceptible to infection via this route. This again occurs more commonly in children. Accurate diagnosis in these cases may be difficult since the patient may have clear evidence of sepsis due to the metaphyseal infection masking the septic joint. Antibiotic treatment for the initial metaphyseal infection may also result in a negative culture from joint aspiration leading to the diagnosis of a reactive rather than a septic effusion.10,11
Pathology and microbiology
The commonest infective agent in joint sepsis in both the adult and child is Staphylococcus aureus (55%) with streptococcal infection accounting for 18% of infections, being commoner in patients over the age of 60.12,13 Meticillin-resistant S. aureus is increasing in frequency, causing a third of staphylococcal infections in one study. The affected patients were older and had more comorbidities and a higher 6-month mortality rate.14 N. gonorrhoeae infection is reducing in incidence but remains the commonest cause of septic arthritis in the young adult.15,16 A wide number of other infective agents have been described. There is, however, an association of different causative bacteria with age (Table 48.1).
| Age group | Organism | Comment |
|---|---|---|
| Neonates | Staphylococcus aureus | |
| Group B streptococci | ||
| Escherichia coli | ||
| Children and adolescents | Staphylococcus aureus | Less common with immunization |
| Haemophilus influenza | ||
| Streptococcus pyogenes | ||
| Adults | Staphylococcus aureus | Including meticillin-resistant |
| Neisseria gonorrhoeae | Young adults | |
| Staphylococcus epidermidis | Commonest with implants | |
| Proteus mirabilis | More common in debilitated patient | |
| Pseudomonas aeruginosa | More common in the immunocompromised | |
| Group B streptococci |
Natural history
The introduction of sulphonamides in the 1930s and the proliferation of antibiotic agents after 1940 led to a dramatic improvement in the outcomes of patients with septic arthritis. Before the antibiotic era there was 20% mortality and 50% morbidity from joint sepsis.17 However, even in the 1980s a 13% mortality rate was reported following disseminated joint infection in children.18 This therefore remains a serious condition particularly in the young, old and the immunocompromised.
The presence of active infection in the joint rapidly causes irreversible changes. In animal models, maximal arthritic symptoms occur 2 days following the inoculation of bacteria into a joint and at 7 days irreversible changes have taken place.19 The damage to the articular cartilage has historically been attributed solely to the effect of increased pressure within the joint resulting in the surgical drive to drain the joint as soon as possible. This has remained unquestioned until relatively recently. Other causes of high joint pressure are seen in effusions and haemarthrosis and yet the rapid destruction of the joint is not seen in these conditions. It is self-evident, therefore, that other factors which are not mechanical must have a part to play in the joint damage.
The effect of the inflammatory cascade releases proteolytic enzymes and cytokines into the joint. These have a rapid and devastating effect on the articular cartilage. Articular cartilage when exposed to fibronectin fragments undergoes proteoglycan depletion within 7 days.20 TNF-α, interleukin-1 and interleukin-6, which are released into the joint in sepsis, are inflammatory and cause rapid articular surface damage.21,22 These changes have been observed in the absence of mechanical factors. These studies demonstrating the rapid degradation of articular cartilage within a few days in animal models correlate with the clinical picture seen in humans and emphasize the need to diagnose and treat this condition early.
