Neonates: Staphlycoccus aureus (80%), Group B Streptococci, E.coli
Children: Staphylococcus aureus, Group A Streptococci
Adults: Adults with compromised health: Chronically debilitated patients (gram+rods), peripheral vascular insufficiency (polymicrobic or anaerobic), Diabetes mellitus, Sickle Cell Disease (Salmonella), Drug addicts (Pseudomonas, Staph)
Uncommon in healthy adults. Mainly a condition seen in CHILDREN.
Sources of osteomyelitis:
Direct innoculation of bone (open fracture, trauma, puncture wounds)
Contiguous Spread (diabetic foot)
Hematogenous seeding (blood borne) most common via bacteremia, systemic or distant extraosseous infection
Location of primary infection dependent on age (because of difference in vascular circulation of bone)
: Metaphysis and Epiphysis metaphyseal vessels penetrate the growth plate communicating the two parts of the bone. Infection can cause destruction of the growth plate. Joint infection is most commonly seen at this age.
: Metaphysis metaphyseal vessels loop away from the growth plate forming capillary loops that act as dilated venous sinusoids. Capillary loops allow for areas of sluggish, turbulent blood flow which sets up the background for seeding of infection. Progression: Trauma Þ thrombus formation after trauma Þ bacteria collection Þ inflammatory response Þ damage to endothelial lining of blood vessels Þ necrosis.
: Metaphysis, epiphysis, subchondral bone after growth plate closure, the metaphyseal vessels reunite with epiphysis exposing all areas of bone to infection
: Abscess: initial focus of infection site - PMNs, fibrin, bacteria
Infection causes formation of SEQUESTRUM: necrotic bone resulting from destroyed blood vessels in the cortex that have thrombosed
Increased intraosseous tissue pressure within abscess allows infection to penetrate Haversian system (Volkmans canals)
Infection spreads along paths of least resistance going horizontally to subperiosteum
Periosteum reacts to infection by trying to replace necrotic bone with new bone (INVOLUCRUM: reactive viable bone) Þ periostieum elevates tearing the periosteal vessels causing thrombosis of these vessels and formation of more sequestrum (especially in neonates) endosteum will also react
Osteoclastic resorption of necrotic bone
Appositional new bone formation (involucrum- similar to a cast of pus) and creeping substitution (new bone replacing necrotic bone)
Dead vs. Necrotic bone: necrotic bone no nuclei in lacunar spaces. This takes 2 to 4 wks to be seen. Osteoclasts may be seen resorbing bone with nuclei. This bone is "dead" bone recognized by osteoclasts as necrotic bone (although microscopically not seen as necrotic because of present nuclei).
:Mycobacterium tuberculosis, M avium. 1% of TB patients develop musculoskeletal problems. Primary site usually lung or GI tract.
: typically involves lower thoracic spine. Mild, subtle presentation. Typically more destructive of bone/joints and more chronic debilitation because slow formation makes it more difficult to detect. Results in :
compression of spinal cord
vertebral collapse and angulatoin of vertebral column Potts disease