Pathophysiology of Osteomyelitis

Pathophysiology of Osteomyelitis

Staphylococcus aureus is the cause of 70% to 80% of bone infection. Other pathogenic organisms often found in osteomyelitis include Proteus, Pseudomonas and Ecerichia coli. There is an increased incidence of penicillin-resistant infections, nosocomial gram-negative and anaerobic.

The onset of osteomyelitis after orthopedic surgery can occur within the first 3 months (acute fulminant stage I) and is often associated with the accumulation of superficial hematoma or infection. Late-onset infections (stage 2) occurs between 4 and 24 months after surgery. Osteomyelitis onset time (stage 3) is usually due to hematogenous spread and occurred 2 years or more after surgery.

Initial response to infection is one of the inflammation, increased vascularity and edema. After 2 or 3 days, in the vein thrombosis occurred in the area, resulting in ischemia with bone necrosis due to the increase and can spread to soft tissue or joints around it, unless the infection can be controlled early, then will form bone abscess.

In the natural journey, abscess can come out spontaneously; but more often incision and drainage should be performed by surgeons. Abscess formed in the walls formed area of dead tissue, but as the abscess cavity in general, the bone tissue dies (sequestrum) is not easy to melt and flow out. Cavities can not deflate and heal, as happens in the soft tissues. New bone growth occurs (involucrum) and surround the sequestrum. So even though there appeared to be healing, but a chronic infectious sequestrum remains vulnerable issuing recurrent abscesses throughout the life of the patient. Named types of chronic osteomyelitis.