Septic arthritis – d/t bacterial or fungal contamination of the joint. SA may causes rapid joint destruction and requires prompt Dx and antibiotic administration
Joints affected: large joints with rich blood supply (knee 50%>hips>shoulders).
Routs of Infection:
1) Hematogenous is m/c
2) Spread from an adjacent site
3) Direct implantation (e.g. trauma, iatrogenically)
Patients at risk: children, diabetics, immunocompromised, pre-existing joint damage/inflammation e.g. RA etc.
I.V. drug users are particularly at risk and in addition may contaminate atypical joints “the S joints” SIJ, SCJ, Symphysis pubis, ACJ etc.
Clinically: may vary and depends on host immune response and bacterial virulence. May present with rapid onset or exacerbation of pre-existing joint pain, swelling, limitation of ROM. General signs of malaise, fever, fatigue and elevated ESR, CRP, Leucocytosis may be present.
N.B. Diabetics and immunocompromised may present with fewer manifistations and lack of fever d/t declining immune response
Dx: clinical, radiological and laboratory. Arthrocentesis may be necessary for culture, cell count and purulent synovial examination
Management: I.V. antibiotics
Imaging Dx: begins with radiography but in the early stage most likely will be unremarkable. MRI can be sensitive and help with early identification of joint effusion, bone edema etc. US may be helpful in the superficial joints and in children. US helps with needle guidance. Bone scintigraphy may be used occaisonally if MRI is contraindicated
Routes of Joint Contamination
1. Hematogenous (M/C)
2. Spread from the adjacent site
3. Direct inoculation
M/C organism-Staph aureus
N.B Gonococcal infection may be a top differential in some cases
IV drug users: pseudomonas, candida
Sickle cell: Salmonella
Animal (cats/dogs) bites: Pasteurella
Occaisonally fungal contamination may occur
Initially non-specific ST/joint effusion, obscuration/distortion of fat planes. Because it takes 30% of compact and 50-75% trabecula bone to be destroyed before seen on x-rays, radiography is insensitive to some of the early changes. MR imaging is the preferred modality
If MRI is not available or contraindicated. Bone scintigraphy with Tc-99 MDT can help
In children US preferred to avoid ionizing radiation. In children US can be more sensitive than in adults due to lack of bone maturation
Early findings are unrewarding. Early features may include: joint widening d/t effusion. Soft tissue swelling and obscuration/displacement of fat planes
1-2 weeks: periarticular and adjacent osseous changes manifesting as patchy demineralization, moth-eaten, permeating bone destruction, loss and indistinctness of the epiphyseal “white cortical line” with increase in soft tissue swelling. MRI may be helpful with early Dx.
Late features: complete joint destruction and ankyloses
N.B. Septic arthritis may progress rapidly within days and requires early I.V. antibiotic to prevent major joint destruction
T1 & T2 Knee MRI
T1 (above left) and T2 fat-sat sagittal knee MRI slices reveal loss of normal marrow signal on T1 and increase on T2 due to septic edema. Bone sequestrum d/t osteomyelitis progressing into septic arthritis is noted. Marked joint effusion with adjacent soft tissue edema are seen. Dx: OSM and septic arthritis
Imaging may help the Dx of septic joint. However, the final Dx is based on Hx, physical examination, blood tests and most importantly synovial aspiration (arthrosentisis)
Synovial fluid should be sent for Gram staining, culture, glucose testing, leukocyte count, and differential determination
ESR/CRP may be elevated
Synovial fluid: WBC can be 50,000-60,000/ul, with 80% neutrophils with depleted glucose levels Gram stain: in 75% gram-positive cocci. Gram staining is less sensitive in gonococcal infection with only 25% of cultures +
In 9% of cases, blood cultures are the only source of pathogen identification and should be obtained before antibiotic treatment
Gout: MSU deposition in and around joints and soft tissues. Elevated levels of seurm uric acid (UA) (>7mg/dL) causd by overproduction or under-excretion of uric acid
Once UA reached/exceeded 7mg/dL it will deposit in the peripheral tissues. Primary gout: disturbed metabolism of nucleic acids and purines breakdown. Secondary gout: increased cell turnover: Psoriasis, leukemia, multiple myeloma, hemolysis, chemotherapy etc.
Gout presents with 5-characteristic stages:
1)asymptomatic hyperuricemia (years/decades)
acute attacks of gouty arthritis (waxes and wanes and lasts for several years)
Interval phase between attacks
Chronic tophacious gout
Depends on stages
Acute attacks: acute joint pain “first and the worst” even painful to light touch
DDx: septic joint (both may co-exist) bursitis etc.
Gouty arthritis typically presents as monoarthropathy
Chronic tophacious stage: deposits in joints, ear pinna, ocular structures and other regions. Nephrolithiasis etc. Men>women. Obesity, diet, and age >50-60.
Radiography: early attacks are unremarkable and may present as non-specific joint effusion
Chronic tophacious gout radiography: punched out peri-articular, para-aticular and/or intraosseous erosions with overhanging edges. Characteristic rim of sclerosis and internal calcification, soft tissue tophi. Target sites: lower extremity m/c
Rx: allopurinol, colchicin (esp. preventing acute episodes and maintenance)
Synovial aspiration with polarized microscopy reveal negatively birefringent needle-shaped MSU crystals with large inflammatory PMN presence. DDx: positively birefringent rhomboid-shaped CPPD crystals (above bottom right) seen in Pseudogout and CPPD
Density and joint effusion puched out osseous erosion with overhanging margins, overall perservation of bone density, internal calcifications Dx: chronic tophacious gout
MRI Gout Features
Erosions with overhanging margins, low signal on T1 and high on T2 and fat suppressed images. Peripheral contrast enhancement of tophacious deposits d/t granulation tissue
Dx: final Dx; synovial aspiration and polarized microscopy