Septic arthritis is the one of the most serious medical emergency of a patient present with one or more hot and swollen joints.[1]
Bacterial arthritis is the most rapidly destructive joint disease.[2] Septic arthritis is most common in patients with longstanding rheumatoid arthritis. Septic arthritis is a an important consideration in adults presenting with monoarticular arthritis in 80 to 90% of patients. It can involve any joint, but most commonly involves knee > hip > shoulder > ankle.[3] Other joints such as sacroiliac joint, sternoclacicular or costoclavicular joints may be involved in patient with history of intravenous drug abuse (IVDA), penetrating trauma, animal or human bites and local steroid injections.
Septic arthritis is due to intra articular seeding of living microorganisms.[5] The most common etiological agent of all nongonococcal causes of septic arthritis in the United States is Staphylococcus aureus.[6]
Gram-negative bacilli account for 10 to 20% of septic arthritis causes.[6] ~10% of patients with nongonococcal septic arthritis are due to polymicrobial cause of infections. Anaerobes are also can cause septic arthritis in few cases.
Most common cause of septic arthritis in children age < 2 years are Haemophilus influenzae (in immunized children), Staph. aureus, group A Streptococcal infections and Kingella kingae.[7]
The source of infection in most of the cases (~50%) often from the skin, lungs or bladder.
Causes of infection include
Hematogenous dissemination
Post operative wound infection such as after arthroscopic procedures
Presence of extreme vasularity and absence of limiting of basement membrane, promotes the easy access of infections into the synovial space.[8]
Hematogenous spread: Septic arthritis most commonly develop as a result of hematogenous spreading bacteria into the vascular synovial membrane.[9] Hematogenous spread is commonly associate with injection drug use, presence of indwelling catheters, and an underlying immunocompromised state such as HIV infection.
Direct inoculation: Direct inoculation of microorganisms may occur during deep penetrating injuries, intra-articular steroid injection, arthroscopy or prosthetic joint surgery, particularly in association with knee and hip arthroplasties and contiguous osteomyelitis rupturing into the joint.[10][11]
Bone infection such as osteomyelitis can spread by breaking through its outer cortex and then into the intracapsular region that lead to joint infection. This kind of spread is more common in children as the small capillaries can cross the epiphyseal growth plate and permit extension of infection into the epiphysis and joint space.[3][12]
Pathogenesis of septic arthritis depends on multiple factors and it mainly depends on the balance between virulence of the microbial pathogen and the host immune response against the pathogen.
Staph. aureus is the most common pathogen non gonococcal pathogen that causes septic arthritis. The pathogenesis of septic arthritis by staphylococcus can be a better representation for pathogenesis of most non gonococcal arthritis.
Bacterial colonization and adherence into the synovium
Mechanism of infection transmission
Hematogenous spread: Septic arthritis most commonly develop as a result of hematogenous spreading bacteria into the vascular synovial membrane.[9] Hematogenous spread is commonly associate with injection drug use, presence of indwelling catheters, and an underlying immunocompromised state such as HIV infection.
Recent joint surgery, induces the production of host-derived extracellular matrix proteins( e.g. collagen) that aids in post surgical healing process, can assist bacterial attachment and progression to infection
Virulence of microorganism
Susceptibility of synovial membrane for microorganism
Direct inoculation: Direct inoculation of microorganisms may occur during deep penetrating injuries, intra-articular steroid injection, arthroscopy or prosthetic joint surgery, particularly in association with knee and hip arthroplasties.[10][11]
Contiguous spread: Bone infection such as osteomyelitis can spread by breaking through its outer cortex and then into the intracapsular region that lead to joint infection.
Role of bacterial products in pathogenesis
Bacterial colonization and adherence into the synovium π’
Mechanism of transmission
Hematogenous spread: Septic arthritis most commonly develop as a result of hematogenous spreading bacteria into the vascular synovial membrane.[9] Hematogenous spread is commonly associate with injection drug use, presence of indwelling catheters, and an underlying immunocompromised state such as HIV infection.
Recent joint surgery, induces the production of host-derived extracellular matrix proteins( e.g. collagen) that aids in post surgical healing process, can assist bacterial attachment and progression to infection
Virulence of microorganism
Susceptibility of synovial membrane for microorganism
Direct inoculation: Direct inoculation of microorganisms may occur during deep penetrating injuries, intra-articular steroid injection, arthroscopy or prosthetic joint surgery, particularly in association with knee and hip arthroplasties.[10][11]
Contiguous spread: Bone infection such as osteomyelitis can spread by breaking through its outer cortex and then into the intracapsular region that lead to joint infection.
Role of bacterial products in pathogenesis
Bacterial attachment proteins promote colonization and initiate the infectious process, a number of bacterial products activate the host immune response and increase tissue damage in cases of septic arthritis.
Most common risk factors that predisposes septic arthritis are rheumatoid arthritis, prosthetic joint or joint replacement and skin infections.[13][14][15][16]
Other common risk factors that predispose septic arthritis are as follows:[17][16][18][19][8]
Differentiating gonococcal arthritis from non-gonococcal arthritis
Characterestic
Gonococcal arthritis
Non gonococcal arthritis
Patient profile
Mostly sexually active young adult
Female > male
Patient with history of rheumatoid arthritis or other systemic arthritis
Immunocompromised patient
Common in extremes of age such as in newborn or elderly
Initial presentation
Migratory polyarthralgia is common
Tenosynovitis in majority of patients
Dermatitis in majority of patients
Single hot, swollen and painful joint
Polyarthralgia is very rare
Tenosynovitis and dermatitis are very rare.
Polyarticular involvement
Common (~40β70% of patients)
Usually involves 2-3 joints
Rare (~10β20% of patients).
Mostly monoarticular involvement (>85%)
Recovery of bacteria
Positive blood culture <10%
Positive synovial fluid culture <50%
Positive blood culture 50%
Positive synovial fluid culture >90%
Response to antibiotics
Within a few days outcome excellent
Takes weeks
Joint drainage must be adequate
Outcome often poor
Mycobacterial and fungal arthritis both present with the slow onset of a chronic monoarthritis and they are more prone to weight bearing joints and spine.
Incidence of septic arthritis approximately varies between 2 to 10 cases per 100,000 per year in the general population.[18]
Incidence of septic arthritis in patients with history of rheumatoid arthritis and patients with joint prostheses is ~ 30β70 cases per 100,000 per year.[16]
Incidence of septic arthritis in patients with joint prostheses is 40-68 cases per 100,000 per year.
The case-fatality rate of septic arthritis is estimated to be 10-25%.[8]
Even after survival from septic arthritis, 25-50% of the patients suffer from irreversible loss of joint function.[30][31]
Females are more at risk in getting gonorrheal arthritis and four fold risk compared to men, due to the asymptomatic nature of gonorrheal infection in women.
In children hip is most commonly involved.
PASA is more common in men when compared to women.[5]
Septic arthrtits can be affected by any age group, but most commonly affected are elderly and children <4 years.[32]
The first experimental model of septic arthritis mediated by staph. aureus is developed by Tarkowski and colleagues.[33]
Natural history, Complications and Prognosis[edit | edit source]
As the growth plate is in very close to the joint, direct extension of a joint infection to the growth plate can lead to reduced bone growth in children.[34][35]
Prognosis of septic arthritis depends on several factors.
Patients with history of chronic disease with concurrent septic arthritis can be misdiagnosed as acute flare of underlying chronic disease which often delays the treatment for septic arthritis. This diagnostic delay is an important prognostic factor contribute for the poor outcome of septic arthritis in rheumatoid arthritis, which carries a 30β50% case-fatality rate.[2] If septic arthritis involving multiple joints, case fatality rate will be >50%.[32]
Poor prognostic factors include age >50 years, history of rheumatoid arthritis as an underlying disease, staph. aureus is the causative agent.[5]
Patients with history of chronic disease with concurrent septic arthritis can be misdiagnosed as acute flareup of underlying chronic disease which often delays the treatment for septic arthritis. So, patients with acute flare of one or two new inflamed joints with underlying chronic joint diseases or with another connective tissue disease, it should be assumed that the joint is septic until proven otherwise, should always rule out concurrent septic arthritis with appropriate diagnostic studies.[2]
In patients with acute effusion of unknown etiology, might have concurrent crystal-induced arthritis and septic arthritis. So, the synovial fluid should always be cultured and examined for crystals in the evaluation of an acute effusion.[36]
Abrupt onset of a single hot, swollen, and painful joint indicate non gonococcal arthritis.[8] It can involve any joint, but most commonly knee is the site of infection in 50% of cases of adults and elderly patients. Hip infection is the most common site in children.[18]
Disseminated gonococcal infection(DGI) often present initially with migratory polyarthralgias, tenosynovitis, dermatitis, and fever and less commonly, <50% of patients with DGI will present with purulent joint effusion, most often of the knee or wrist..[37] Often present with inflamed and tender tendons of the wrist, ankles, and small joints.
Disseminated gonococcal infection often present with skin lesions, typically multiple, painless macules and papules, most often found on the arms or legs or on the trunk.[2]
Most commonly involves knee > hip > shoulder > ankle.[3] Other joints such as sacroiliac joint (~10%), sternoclacicular or costoclavicular joints may be involved in patient with history of intravenous drug abuse (IVDA), penetrating trauma, animal or human bites and local steroid injections.
Swelling of the joint that involved
Decreased range of motion
Patient hold the hip in flexed and externally rotated position if SA involving hip.
The definitive diagnosis of septic arthritis requires identification of bacteria in the synovial fluid by Gramβs stain or by culture.[2]
Clinical suspicion of joint sepsis should prompt for immediate synovial fluid aspiration. Septic arthritis should not be excluded even though the patient have low fever and normal WBC.
Diagnosis of septic arthritis depends maily on the arthrocentesis and isolation of the pathogen from aspirated joint fluid.[38]
If synovial fluid cannot be obtained with closed needle aspiration, the joint should be aspirated again with imaging guidance such as ultrasound guidance, computed tomography or fluoroscopic guidance.[2]
Prevention of septic arthritis is possible by intensive treatment of risk factors such as old age patients having rheumatoid arthritis, diabetes mellitus, joint prostheses or joint surgery and skin infection.[16]
Prognosis of septic arthritis depends on several factors.
Patients with history of chronic disease with concurrent septic arthritis can be misdiagnosed as acute flareup of underlying chronic disease which often delays the treatment for septic arthritis. This diagnostic delay is an important prognostic factor contribute for the poor outcome of septic arthritis in rheumatoid arthritis, which carries a 30β50% case-fatality rate.[2]
Poor prognostic factors include age >50 years, history of rheumatoid arthritis as an underlying disease, staph. aureus is the causative agent.[5]