Bone Infection

Pyogenic Osteomyelitis – Inflammation of the bone and bone marrow

Etiology: infection due to bacteria, fungus, virus.

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

Pathology: Location of primary infection dependent on age (because of difference in vascular circulation of bone)

Neonates: 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.

Children: 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.

Adults: Metaphysis, epiphysis, subchondral bone – after growth plate closure, the metaphyseal vessels reunite with epiphysis exposing all areas of bone to infection

Histology: Abscess: initial focus of infection site - PMN’s, 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 (Volkman’s 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).

REVIEW: Bacaterial proliferation Þ inflammatory response Þ Ý intraosseous pressure Þ ß blood flow Þ abcess formation Þ haversian spread Þ subperiostal destruction (periosteum elevation) Þ involucrum formation Þ sequestrum

Suppurative arthritis: infection spreads to joint cavity Þ pus in the joint Þ surgical emergency

Histology: fibrin, granulation tissue

Diagnostic tests: culture site, culture blood, identify area of max tenderness, aspirate and exam subendochondral fluid

Classes:

Acute hematogenous: bacteria floating around in the blood set up in the bone (typically in the metaphysis)

Clinical Manifestations: pseudoparalysis, localized: tenderness, erythema, swelling, systemic: fever, malaise

can act like cellulitis (early stages) or abcess (late stages)

Treatment: antibiotics (broad spectrum, IV), surgery

Subacute: Long bones (metaphysis and diaphysis)

Clinical Manifestations: localized nagging pain

Treatment: surgery, antibiotics

Chronic (15-30%): symptoms of 3 wks or longer; can have diaphysis involvement

usually due to inadequate treatment with antibiotics or inadequate surgical debridement of necrotic bone

Histology: lymphocytes, fibrous cells (evidence of chronic inflammation)

Treatment: surgical debridement, Antibiotics (6wks IV, 6more P.O.)

Chronic recurrent multifocal:

Clinical Manifestations: multifocal, nonpyogenic, inflammatory osteomyelitis

Treatment: NO treatment helps

Tuberculosis Osteomyelitis – granulomatous arthritis

Etiology: Mycobacterium tuberculosis, M avium. 1% of TB patients develop musculoskeletal problems. Primary site usually lung or GI tract.

Clinical Manifestations: 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 :

meningitis
compression of spinal cord
vertebral collapse and angulatoin of vertebral column – Pott’s disease

Psoas muscle sheath fluctuant swelling – cold abcess

Histology: Granulomatous osteomyelitis with caseation necrosis. Nodular areas with surrounding histiocytes, Giant cells, chronic inflammatory cells.

in HIV patients – Mycobacterium avium – histiocytes containing acid-fast bacilli

Fungal Osteomyelitis – Rare

Etiology: Blastomycosis, Coccidioidomycosis, Cryptococcus neoformans

Clinical Manifestations: Occurs in chronically debilitated patients, narcotic addicts, and certain endemic areas.

Histology: Granulomas