Imaging in infective arthritis: A comprehensive review

INTRODUCTION

Infective arthritis includes both pyogenic (septic) and non-pyogenic arthritis. Imaging is crucial in the workup of infective arthritis with a role in diagnosis, image guidance for arthrocentesis, and detection of complications. Septic arthritis is an orthopedic emergency warranting prompt diagnosis and treatment to prevent joint destruction. The incidence of septic arthritis is reported to be 2–20 cases/100000 people/year.^[1] The incidence of septic arthritis is rising consequent to an aging population and increasing immunosuppressed patients.^[2] The typical presentation of a patient with septic arthritis is with fever and a monoarticular joint involvement that is characterized by an acutely painful, swollen, and warm joint. However, polyarticular involvement can occur and joint pain can be minimal in the immunosuppressed patient. High-grade fever is seen in only 58% of patients while serum leukocytosis is seen in 50–60% of patients.^[3] Fungal and tuberculous arthritis have a more chronic and indolent course. Thus, the clinical diagnosis of infective arthritis can be challenging, necessitating further imaging and laboratory workup. Septic arthritis can also be confused with an acute flare of an inflammatory arthritis. Up to 47% of patients with septic arthritis have a pre-existing joint problem.^[3] The most common joint involved in adults is the knee joint, followed by the hip, ankle, wrist, shoulder, and elbow joints. In children, there is an equal affection of the knee and hip joints, followed by the ankle joint.^[4] Polyarticular involvement is usually asymmetric and at least one knee joint involvement is usual, with rheumatoid arthritis being a major risk factor for polyarticular involvement.^[3,5] Involvement in tuberculous arthritis is usually monoarticular.

RISK FACTORS FOR SEPTIC ARTHRITIS

Pre-existing joint diseases such as rheumatoid arthritis, osteoarthritis, gout, calcium pyrophosphate deposition disease, systemic lupus erythematosus, prosthetic joint, joint surgery, or trauma are predisposing factors for septic arthritis. Medical conditions such as diabetes, end-stage renal disease, cirrhosis, and immunosuppressed status also predispose to the development of septic arthritis. The other major risk factor includes skin diseases such as psoriasis, eczema, and skin ulcers as they are associated with skin breach, allowing bacteria to enter the bloodstream. Old age, low socioeconomic status, intravenous drug abuse, and medications such as immunosuppressive drugs, disease-modifying antirheumatic drugs, systemic and intra-articular steroids also make a patient vulnerable to developing infective arthritis.^[1] Predictors for mortality are older age (more than 65 years), delay in diagnosis, and polyarticular involvement while higher joint damage is associated with older age, diabetes, and β-hemolytic streptococcal infection.^[3]

PATHOPHYSIOLOGY

Infective arthritis is often hematogenous in origin [Figure 1]. The synovium’s rich vascularity and absence of a protective basement membrane render it particularly susceptible to such bacterial invasion during bacteremia. Skin and mucous membrane breach allows Staphylococci and Streptococci to cause bacteremia. Gram-negative septic arthritis may be consequent to bacteremia from breach of the gastrointestinal or urinary tracts. Infected indwelling medical devices such as central venous catheters, urinary catheters, endovascular, and biliary stents can be a source of hematogenous joint infection [Figure 2]. Intravenous drug abuse results in episodes of transient bacteremia. In this population, infections frequently involve the sternoclavicular joint, sacroiliac joint, and pubic symphysis. The involvement of the sternoclavicular joint is likely consequent to valvulitis or phlebitis of the subclavian vein. Organisms may also gain entry into the joint by direct inoculation either by a penetrating wound or after joint surgery or intra-articular injection. Human and animal bites, closed fist trauma, or thorn and nail injuries can result in penetrating joint injury. Infection may also be consequent to contiguous spread from adjacent soft tissues [Figure 3] or bones [Figure 4].^[2,3,6,7]

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Figure 1:

A 30-year-old lady with fever and right hip pain with erythrocyte sedimentation rate 35 mm/h and C-reactive protein 238.8 mg/L. (a) STIR and (b) post-contrast T1W coronal images reveal right hip joint effusion with bone marrow edema in the acetabulum (solid white arrow in a) and periarticular edema (dashed white arrows in a). Blood culture and synovial culture isolated methicillin-resistant Staphylococcus aureus. STIR: Short tau inversion recovery

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Figure 2:

Liver transplant recipient with graft rejection and anastomotic stricture, post-steroid pulse therapy and biliary stenting developed Klebsiella pneumoniae septic arthritis. (a) Post-contrast T1W sagittal image showing joint effusion (white star), synovial enhancement (solid white arrows), and bone infarcts (dashed white arrows). (b) Post-arthroscopic synovectomy and antibiotic bead placement radiograph. Septic arthritis could be treated only after the removal of the infected biliary stent.

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Figure 3:

A 64-year-old lady with uncontrolled diabetes, non-healing wound at the knee joint, and knee joint septic arthritis. Culture: Klebsiella pneumoniae. (a) Fat-saturated proton density sagittal and (b) post-contrast T1W sagittal image showing joint effusion, synovial enhancement (solid white arrow), patellar osteomyelitis (dashed white arrow in a and b), and ulcer in prepatellar tendon region (curved white arrow in b).

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Figure 4:

Schematic diagram showing routes of spread of infection to a joint.

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There is a three-pronged attack on the articular cartilage of joints in septic arthritis. Bacterial enzymes and toxins damage the articular cartilage directly. Increased joint pressure from the accumulation of purulent exudates in the joint cavity leads to anoxic damage of articular cartilage. This is the therapeutic basis for emergent joint aspiration in infective arthritis. Cytokines and proteolytic enzymes released from host neutrophils also damage the articular cartilage [Figure 5].^[2,3]

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Figure 5:

Schematic diagram showing the mechanism of articular cartilage damage in septic arthritis.

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CAUSATIVE ORGANISMS AND SPECIFIC CLINICAL SCENARIOS

The most common organism to cause septic arthritis in native joints is Staphylococcus aureus, accounting for over 50% of cases.^[3,8,9] The incidence of methicillin-resistant S. aureus (MRSA) septic arthritis is rising across the world. Gram-negative bacilli cause 10–15% of adult septic arthritis, especially in the elderly with comorbidities and in intravenous drug abusers. β-hemolytic Streptococci are also common organisms causing septic arthritis in the elderly with comorbidities. Tuberculous arthritis has an indolent presentation and is overdiagnosed in endemic areas and underdiagnosed in non-endemic areas.^[10] Drug resistance is increasing in endemic areas and every effort must be made to initiate antitubercular treatment only after a thorough culture and sensitivity workup for Mycobacterium tuberculosis (MTB) complex. Synovial biopsy for MTB culture and histology must be performed either as an image-guided or open surgical procedure. Brucellosis can also cause subacute or chronic arthritis, has a predilection for sacroiliac joint involvement, and is diagnosed by serological workup.^[3] Human and animal bites cause polymicrobial arthritis with both aerobic and anaerobic organisms. Staphylococci are the most common cause of prosthetic joint infection.^[11] Patients with multiple prosthetic joints who develop a prosthetic joint infection have a higher risk of a second prosthetic joint infection.^[1] Viral etiologies can cause arthritis such as mumps, rubella, alphavirus of the togaviridae family such as Chikungunya. Melioidosis caused by Burkholderia pseudomallei can be an important cause of septic arthritis in endemic areas with a high risk of musculoskeletal involvement in patients with diabetes mellitus.^[12] The causative organisms of infective arthritis seen commonly in specific clinical scenarios are listed in Table 1.

IMAGING FEATURES

In a patient with suspected infective arthritis, a multimodality approach is utilized to support the diagnosis, assess for disease extent, presence of complications and to guide joint fluid aspiration or synovial biopsy. Radiographs serve as an initial imaging tool, followed by tailored use of ultrasound or magnetic resonance imaging (MRI) or computed tomography (CT) and of image-guided aspiration.^[13] Table 2 lists the imaging features of septic arthritis.

Radiographs

Radiographs are often the first imaging performed for any patient with suspected bone and joint pathology. Early in the disease course, the radiographs may be normal. The characteristic radiographic feature of septic arthritis is rapid destruction of a joint [Figure 6]. The other features include joint effusion and soft tissue swelling [Figure 7], periarticular osteopenia, and erosions. Erosions in septic arthritis are marginal and characteristically occur at the bare areas of the joint. Early in the disease course, this may be seen as focal loss of the cortical line resulting in dot-dash sign.^[2] As the articular cartilage gets damaged, joint space narrowing ensues with subchondral bone destruction and eventual ankylosis of the joint. A specific sign on radiographs is the presence of air in the joint and adjacent soft tissues by gas-forming organisms [Figure 8] or consequent to a penetrating injury. If there is associated osteomyelitis, a periosteal reaction will be identified on radiographs. Tuberculous arthritis shows juxta-articular osteopenia, marginal erosions, and a gradual narrowing of the joint space, characterizing Phemister’s triad.^[7] Sclerosis and irregular bony destruction are seen in advanced tuberculous arthritis [Figure 9]. End-stage tuberculous arthritis shows fibrous ankylosis while bony ankylosis is more common in pyogenic arthritis.^[14]

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Figure 6:

A 77-year-old lady with total knee replacement, diabetic ketoacidosis, and Escherichia coli urosepsis. Radiographs at initial presentation and 10 days later show rapid joint destruction with lytic lesions along the tibial component (solid white arrows). Patient developed a discharging sinus in the infrapatellar region.

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Figure 7:

(a-b) Serial radiographs of a patient with Klebsiella pneumoniae septic arthritis showing increasing joint effusion, seen as soft tissue density in the suprapatellar recess (solid white arrows in a and b).

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Figure 8:

Radiograph of a patient with septic arthritis showing soft tissue air due to Escherichia coli infection (solid white arrow).

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Figure 9:

A 30-year-old lady with tuberculosis arthritis. Initial radiograph reveals juxta articular osteopenia (solid white arrow) with erosions (dashed white arrow) and preserved joint space that progresses to multiple erosions, sclerosis (solid white arrow) and reduced joint space (elbow white arrow) on a 2 year follow up radiograph.

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Ultrasound and CT

Ultrasound is an easy method to document joint effusion, periarticular collections, and synovial thickening [Figure 10]. It has the advantage of being a safe, non-radiating modality that can also be used at the bedside and for image-guided aspiration and biopsy. Joint effusion with echogenic debris and increased synovial vascularity on Doppler may be seen. Ultrasound is particularly useful in pediatric patients and for superficial joints.^[15] For deeper joints, CT becomes the imaging tool for guided aspiration and biopsy [Figure 11]. CT features of an infected joint include joint effusion and erosions that are better documented than radiographs for deep-seated joints such as the sacroiliac and sternoclavicular joints.^[7]

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Figure 10:

Ultrasound of the radio-capitellar joint in a patient with infective arthritis reveals joint effusion, marked synovial thickening, and erosion.

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Figure 11:

(a) Post-contrast T1W axial image showing bone marrow enhancement (solid white arrow) along the left SI joint with periarticular abscess (elbow white arrow). (b) Computed tomography guidance for abscess drainage revealed methicillin-resistant Staphylococcus aureus sacroiliitis.

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MRI

MRI is an excellent imaging modality for localizing the infection and documenting the extent of involvement in the joint and adjacent soft tissues. Abnormal MRI findings in septic arthritis can be seen as early as within 24 h of the onset of illness.^[16] Joint effusion, bone marrow edema, erosions, periarticular edema and collections, synovial thickening, outpouching and enhancement, and articular cartilage destruction can be seen on MRI in septic arthritis [Figure 12]. MRI helps assess the presence of concomitant osteomyelitis which is seen as confluent hypointensity on T1-weighted images in the medullary cavity of the affected bones with corresponding hyperintensity on fat-suppressed T2-weighted images.^[17-19] Periarticular abscess will show diffusion restriction. MRI can thus document complications such as osteomyelitis and adjacent soft tissue abscess in a patient with septic arthritis.^[17] Non-contrast MRI is sufficient for evaluation of septic arthritis, although post-contrast images document synovial thickening and hyperenhancement, features suggestive of synovitis. The use of contrast can help detect small abscesses, sinus tracts, ulcers, and devitalized tissue, thus assessing the adjacent soft tissues better.^[20]

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Figure 12:

(a) Fat-saturated proton density sagittal and (b) post-contrast T1W sagittal image showing joint effusion (white solid arrow in a), synovial enhancement (white solid arrow in b) consistent with septic arthritis of the elbow joint. (c) Post-contrast T1W axial image shows a peri-articular abscess in the brachialis muscle (white solid arrow in c).

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Graif et al. studied various imaging features to differentiate septic versus non-septic arthritis in 30 patients on MRI.^[21] They found an overlap in the imaging features of the two entities. The combination of bone erosions and bone marrow edema favored septic arthritis. Additional features of synovial thickening, synovial edema, soft tissue edema, or bone marrow enhancement favored septic arthritis. Karchevsky et al. found that synovial enhancement, peri-synovial edema, and joint effusion have a high correlation with septic arthritis.^[16] In their study, an abnormal marrow signal that is diffuse and seen on T1-weighted images favored concomitant osteomyelitis. However, 33% of their cases with diffuse pattern of marrow edema had no osteomyelitis while 29% of cases that had biopsy-proven osteomyelitis had normal marrow signal on T1-weighted images. Yun et al. compared MRI features of septic versus gouty arthritis and found the differentiation difficult.^[22] However, lamellated synovial thickening, bone marrow edema, and soft tissue abscess favored septic arthritis over acute gouty arthritis. Lamellated hyperintense synovitis [Figure 13] is also an indicator of prosthetic joint infection on MRI with other features being extracapsular soft tissue edema and collections, reactive lymphadenopathy, and sinus tract.^[23]

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Figure 13:

Proton density axial image in a patient with infected arthroplasty showing lamellated hyperintense synovitis (white solid arrow).

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Effusion, synovitis, peripheral and central erosions [Figure 14], pannus, hypointense synovium, bone chips, and abscess are features of tubercular arthritis.^[24] Cartilage damage in tuberculous arthritis occurs late in the course of the disease due to the absence of the release of proteolytic enzymes by mycobacteria.^[25] Thickened synovium in tuberculosis either appears intermediate to low in signal intensity [Figure 15] or high in signal intensity on T2-weighted images. The intermediate to low signal intensity is due to caseous necrosis.^[14,26] Hong et al. compared MRI features of tuberculous versus pyogenic arthritis and found that tuberculous arthritis had more erosions, smooth margins of extra-articular lesions, and thin smooth rim of abscesses while pyogenic arthritis had more subchondral marrow abnormality, irregular margins of extra-articular lesions, and thick irregular rim of abscesses. In their study, they found no significant difference in the signal intensity of synovial abnormalities between the two groups.^[27] Choi et al. compared MRI features of tuberculous arthritis versus rheumatoid arthritis and found that uniform synovial thickening, large bone erosions with rim enhancement, and extra-articular cystic mass were features favoring a tubercular etiology while pronounced non-uniform synovial thickening was seen in rheumatoid arthritis.^[28] The considerable overlap of MRI findings between infective and non-infective arthritis mandates that they should be interpreted along with the clinical details and laboratory workup.

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Figure 14:

(a-b) Proton density fat-saturated axial images in a patient with tuberculous arthritis showing erosions (short white arrows in a), joint effusion (solid white arrow in b), synovial thickening (dashed white arrow in b), and bone marrow edema.

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Figure 15:

(a) T2W and (b) post-contrast T1W sagittal images in a patient with tuberculous arthritis showing T2 hypointense synovium (solid white arrow in a), erosion (white arrowhead in b), joint effusion, and areas of marrow enhancement. Note also the popliteal fossa enhancing lymph nodes (white elbow arrows in b).

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LABORATORY WORKUP AND MANAGEMENT

A patient with septic arthritis usually has serum leukocytosis, raised erythrocyte sedimentation rate, and C-reactive protein. However, these serum inflammatory markers lack specificity and are often raised in crystalline arthropathies. Procalcitonin, tumor necrosis factor, and interleukin IL-6 and IL-β have higher specificity but low sensitivity.^[3,30] Blood cultures solely detect the organism in 9–14% of cases of septic arthritis.^[1] Synovial fluid analysis includes cell count and differential, Gram stain, and culture. The yield of culture is higher when synovial fluid is inoculated in a blood culture bottle. Septic arthritis should be suspected when the synovial leukocyte count exceeds 50,000 cells/mm³ with >75% polymorphonuclear leukocytes. Synovial biopsy should be performed in culture-negative synovial aspirate or when tubercular or fungal infection is suspected [Figure 16].^[1,3,31] Brucella serology by immunocapture agglutination test and using molecular diagnostics like GeneXpert for MTB, multiplex polymerase chain reaction (PCR), helps in early diagnosis of pathogens as well. Conventional synovial fluid culture is limited by delayed turnaround time and reduced sensitivity, particularly in patients who have already received antibiotics. Molecular diagnostic techniques, especially PCR-based assays performed directly on synovial fluid, have emerged as valuable adjuncts by enabling rapid detection of bacterial DNA within hours. Broad-range 16S rRNA gene PCR assays, with or without specific pathogen-specific probes, allow early confirmation of infection and basic organism classification.^[32,33]

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Figure 16:

Ultrasonography-guided synovial biopsy confirming tuberculous arthritis of the knee joint.

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Infective arthritis of native joints is managed with appropriate antibiotics and joint drainage.^[3] If concomitant osteomyelitis is seen, a longer course of antibiotics will be required.^[3] Prosthetic joint infection can be managed with medical therapy focused on appropriate antibiotics or in combination with surgery. The surgical options available include debridement, antibiotics, and implant retention (DAIR), one-stage exchange or two-stage arthroplasty exchange, resection without reimplantation and arthrodesis, and rarely, amputation.^[11]

CONCLUSION

Diagnosing infective arthritis can be clinically challenging and requires a comprehensive integration of clinical assessment, laboratory evaluation, and imaging. MRI is particularly valuable in the early detection of joint infection, providing detailed visualization of synovial inflammation, bone marrow edema, and adjacent soft tissue involvement. Ultrasound and CT are used for image guidance for arthrocentesis. Arthrocentesis remains pivotal for definitive diagnosis, enabling microbiological analysis to identify the causative organism and guide targeted antimicrobial therapy.