Musculoskeletal Infection

Soft Tissue Infection

From penetrating injury, spread from adjacent osteomyelitis/septic arthritis or haematogenous. Mass with blurring/obliteration of fat planes. Central nonenhancing fluid density/signal with enhancing rim, nonspecific muscular and subcutaneous oedema. Nonenhancing areas may also represent devitalised tissue prone to abscess. In tight compartments (eg forearm, leg), a classic abscess cannot form hence instend develops oedema and compartment swelling. May have associated draining sinus tract, DVT, bone destruction. Fasciitis is a more serious infection with thickened enhancing setpa. Necrotizing fasciitis (usually Clostridium or aggresssive Gram-positive) is a surgical emergency, patient usually very unwell, may show soft tissue gas, tend to have thicker >3mm deep fascia, thick perifascial fluid/oedema, nonenhancing deep fascia. DDx necrotic tumours, myonecrosis (from severe trauma, extreme overuse, ischaemia eg diabetes or sickle cell).


Infection of bone marrow from penetrating injury/surgery (esp adults), adjacent soft tissue infection/septic arthritis or haematogenous (esp children). Contiguous spread begins with periosteum (periostitis) then cortex (osteitis) then marrow (osteomyelitis). 80-90% from Staphylococcus. Increased risk of fracture due to bone destruction. Infection from haematogenous spread depends on age:

  • <1yo – Metaphysis, epiphysis and joint as metaphyseal vessels penetrate physis anastomosing with epiphyseal vessels. May cause osteonecrosis, slipped epiphyses, growth deformity. Most commonly S.aureus, group B Strep, E.coli.
  • Toddlers and older children – Metaphysis as vessels don’t cross physis and metaphyseal vessels terminate in loops with sluggish flow, relative lack of phagocytes. Most commonly Staph, in children with sickle cell also Salmonella. Bacteraemia may be from trivial mucosal injury.
  • Adults – Spine and small bones. Metaphyseal vessels anastomose with epiphyseal, hence more likely involves joint as well. Most commonly Staph; IVDUs and UTI usually G neg (E.coli, Pseudomonas, Klebsiella).

Acute osteomyelitis XR/CT insensitive with blurring/obliteration of fat planes (1-2/52), serpiginous permeative lucency (subtle but specific), indistinct cortex, cortical destruction, endosteal scalloping, periostitis (initially aggressive) and occasionally endosteal new bone formation. Bone scan shows increased uptake on all phases, but may be cold on delayed images (esp children in acute phase). Gallium-67 almost 100% sensitive, but nonspecific. MRI highly sensitive and specific with marrow oedema and enhancement (esp if low T1, DDx trauma and tumour, neuropathic arthropathy in diabetic feet), bone or soft tissue abscess, ulcers extending to bone, sinus tracts between bone and ulcers. Oedema on T2 is more extensive than the area of active infection, reducing as the infection becomes more chronic. In children periosteum is loosely attached to the cortex allowing subperiosteal abscesses to commonly form, which may lift the periosteum and further impair blood supply.

  • Brodie’s abscess – Subacute/chronic osteomyelitis in child, usually metaphysis (occasionally epiphysis) abutting physis, typically cortical with significant periosteal reaction and sclerosis. Well-defined lytic lesion usually with broad sclerotic margin, usually oval with long axis parallel to bone. Channel extending to physis is pathognomonic.
  • Sclerosing osteomyelitis of Garré – Typically jaw, extensive new bone formation obscuring underlying osseous structure.

Chronic osteomyelitis is >6 weeks, occuring in 5-25% from failed resolution of acute osteomyelitis; from delayed diagnosis, extensive bone necrosis, inadequate antibiotic therapy or surgical debridement, weakend host defenses. Variable appereances, thickened cortex, variable lucency and sclerosis. Geographic/marginated from walling-off. Sequestrum – isolated devitalised necrotic bone, dense due to lack of blood supply (other bone is hyperaemic thus demineralised), may harbor bacteria. Involucrum – shell of bone surrounding sequestrum. Cloaca – cortical and periosteal defect/sinus. May be clinically silent for years before reactivation (usually from sequestrum acting as a nidus). If the draining sinus tract persists over years/decades there is an increased risk of SCC.

Diabetic feet – 90-95% is from direct spread of cutaneous infection (ulceration, cellulitis, sinus tract, abscess) esp plantar 1st/5th MT, midfoot (esp cuboid). Infection is not contained by fascial planes. High T2 with normal T1 is reactive oedema, from inflammation, surgery, fractures or neuroarthropathy. Nonenhacing regions suggest devitalised/gangrenous regions. DDx charcot arthropathy which tends to be periarticular, midfoot>forefoot, multiple joints.

Hand metacarpals and phalanges are commonly infected by human bite. Terminal tuft osteomyelitis commonly occurs after stubbed great toe or nail bed injury (periosteum immediately adjacent to nail bed). Infection may spread along tendon sheaths with osteomyelitis distant from site of injury.

Spinal osteomyelitis from surgery, haematogenous spread or UTI (via epidural venous plexus of Batson); starts at sub-endplate extending to adjacent vertebral body and disk. Endplate irregularity and loss of cortical density, loss of disk height, paravertebral mass, displaced psoas shadow; later sclerosis, may cause vertebral body fusion. Reduced T1, oedema and enhancement in disk and vertebral marrow. Epidural, paravertebral or disk space abscess. DDx dialysis-related amyloid deposition. Discitis in children is mostly from haematogenous seeding of the vascularised disk, usually less severe than adults.

Tuberculous osteomyelitis – 1-3% of those with TB have osseous infection. From haematogenous spread, direct extension (lung -> rib, nodes -> vertebrae) or from draining lymphatics. Usually solitary, but multifocal in AIDS. Esp spine, knees, hips. Tends to be more destructive than pyogenic osteomyelitis.

  • TB of the spine (40%, Pott’s disease) – Usually thoracolumbar. Preservation of disk height, lack of sclerosis, may spread under longitudinal ligaments involving several levels with paravertebral mass (highly suggestive); later acute angular kyphosis (gibbus deformity), calcified psoas abscess.
  • TB dactylitis – Esp children. Periosteal reaction then expansion of long bones in hands/feet. DDx JRA, sickle cell dactylitis, other infection.

Skeletal syphilis (Treponema pallidum) and yaws (Treponema pertenue) have similar apperances.

  • Congenital syphilitic osteomyelitis – Spirochetes tend to localise around active enchondral ossifications and periosteum. Metaphyseal irregularity and lucency, widened provisional calcification, slipped epiphyses. May invade diaphysis causing periosteal reaction.
  • Acquired syphylis – Usually early tertiary stage, 2-5 years after initial infection. Esp nose, palate, skull, long bones (eg tibia). Chronic osteomyelitis with periostitis, endosteal reaction, enlarged bowed bone (saber shin deformity, massive periosteal new bone on medial and anterior tibia causing anterior bowing), mixed sclerosis/lysis, may involve flat bones and cranium.

Chronic recurrent multifocal osteomyelitis (CRMO, plasma cell osteomyelitis) – Children and adolescents with episodic pain and swelling over bones showing signs of osteomyelitis. No infectious agent identified, ?viral ?related to SAPHO. Usually metaphyses of lower limbs and medial clavicle.

Bacillary angiomatosis – AIDS multifocal infection with Bartonella henselae (G neg), lytic lesions, variable sclerosis, periostitis, intramuscular high T2 masses.

Infectious Arthritis

(Septic arthritis). Joint effusion, synovial proliferation, capsulitis/synovitis with enhancement and debris within the joint fluid. Surrounding soft tissue oedema, bone marrow oedema (indicating osteomyelitis). Loss of subchondral bone plate in a haphazard manner (dot-dash). DDx toxic synovitis – noninfections joint inflammation, self-limited.

  • Bacterial arthritis – From bacteraemia or contiguous spread of epiphyseal osteomyelitis in neonates. Most commonly Staphylococcus, gonococcus (esp adolescents, young adults F>M), Streptococcus, Haemophilus influenzae (esp <2yo), gram-negative bacilli (E. coli, Salmonella esp sickle cell, Pseudomonas). Joint effusion, hyperaemia -> periarticular osteoporosis, cartilage destruction with reduced joint space, bone erosion and destruction (ill-defined cortex), osteomyelitis, later sclerosis, ankylosis. Knee > hip, shoulder, elbow, wrist, axial skeleton (esp sternoclavicular in IVDUs). Usually monoarticular, may involve more than one joint and more subacute if gonococcus. In children commonly hip with effusion (increased distance between teardrop and femoral metaphysis, bulging fat planes), excluded with vacuum phenomenon on traction.
  • Tuberculous arthritis – Chronic progressive monoarticular, usually from adjacent osteomyelitis or haematogenous spread. Synovial pannus, marginal erosions; later severe destruction with fibrous ankylosis. Usually weight bearing joints including hips, knees, ankles.
  • Lyme arthritis – Spirochete Borrelia burgdoferi, initial skin infection with dissemination esp to joints in 60-80% (may be late). Remitting, migratory, primarily large joints (knees, shoulders, elbows, ankles), attacks last for weeks-months. Similar changes to RA with synovial hyperplasia.
  • Viral arthritis – Alphavirus, parovirus, rubella, EBV, hepatitis B/C. ?Joint directly infected or generated autoimmune reaction.