L 71 Osteomyelitis Flashcards
What is osteomyelitis?
Progressive infection of bone
Results in inflammatory destruction, followed by new bone formation
3 Categories:
1) Secondary to a contiguous focus of infection
2) Secondary to a contiguous infection assoc with vascular insufficiency-diabetes
3) Hematogenous spread of infection, primarily long bones of kids, spine of adults, flat bones of adults often IV drug related
Gram (+) bac causing osteomyelitis
*S. aureus-all ages Coagulase-neg staph -Staph epidermidis Staph saprophyticus GBS Strep agalactiae-neonates Strep pneumonia-older infants, children, adults
Gram (-) bac causing osteomyelitis
Salmonella-sickle cell
Serratia marcescens-IV drugs
E coli-neonates
Pseudomonas aeruginosa-iv drug or punctures
Kingella kingae-aerobic, coccobacillus, usually in pairs, shown up because we are now able to culture it, normal microbiota, colonizes posterior pharynx, RTX toxin, Type IV pili adhesin responsible for twitching motility
Staph aureus virulence factors
MSCRAMMS: microbial surface components-clumping factor, FnBP A&B binds to fibronectin, binds natural and unnatural materials like metal implants in body
Staph can be taken up by cells such as osteoblasts and be hidden from the immune system and cause chronic osteomyelitis
Protein A: binds Fc portion of antibodies and prevents opsonization
Enterotoxins-SEA and SEB
TSST-1
Staph biofilm makeup and purpose
Made of eDNA, polysaccharides, proteins
Creates thick layer that antibodies and antimicrobials have hard time penetrating
Pathogenesis of hematogenous esteomyelitis
Blood origin of the bacteria
As the blood vessels enter the diaphysis of the bone they split and run to the metaphysis where they loop and the blood slows down. At this point, the bacteria escape the bone and establish abscesses.
Inflammatory exudates increase intramedullary pressure and eventually ruptures the periosteum, periosteal blood interrupted leading to necrosis.
Leads to dead bone fragments-sequestrum
New bone called involucrum
Acute osteomyelitis
Infection of bone prior to development of sequestra
Slow development with osteomyelitis, faster with fractures or prostheses
Gradual onset of symptoms over days
Dull pain over the site
HEET, fevers, rigors
May present as septic arthritis: spreading of infection from metaphysis into the joint capsule knee, hip, shoulder
Chronic osteomyelitis
After development of sequestra Formation of an involucrum Local bone loss Sinus tracts Pain, erythema, edema Sometimes assoc with draining sinus tract
Deep or extensive ulcers on feet that fail to heal after several weeks of appropriate care, especially over bony prominence, diabetic patients
Hematogenous vs contiguous osteomyelitis
Hematogenous is monomicrobic
Contiguous can be either poly or monomicrobic
How to differentiate between osteomyelitis and bone tumor on radiograph
Osteomyelitis has a penumbra sign=a distinct border around the abscess that is high in signal intensity on radiograph
Osteomyelitis diagnosis
Symptoms, bone biopsy
Radiographic abnormalities followed by biopsy taken from the bone and not the superficial lesions
Response to empiric therapy
Osteomyelitis treatment
Debridement of necrotic therapy
Antimicrobial therapy parentally
Continue until debrided bone is covered by vascularized soft tissue
Negative Pressure Wound Therapy
