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Pathophysiology of Osteomyelitis

Pathophysiology of Osteomyelitis

Pathophysiology of Osteomyelitis

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

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

Initial response to infection is one of inflammation, increased Vascularization and edema. After 2 or 3 days, thrombosis in blood vessels occurs in the area, resulting in ischemia with bone necrosis associated with an increased and can spread to soft tissue or joints in the vicinity, unless the infection process can be controlled, then the bone will form an abscess.

Abscess formed in the walls forming the dead tissue, but as in the abscess cavity in general, the bone tissue dies (sequestrum) is not easy to melt and flow out. Cavity can not be deflated and healed, as occurs in soft tissues. New bone growth occurs (involukrum) and surrounds the sequestrum. Although there appeared to be healing, but the sequestrum remains vulnerable to infectious chronic recurrent abscesses issue.

Source : http://nanda-nursing-care-plan.blogspot.com/2012/07/pathophysiology-of-osteomyelitis.html