Staphylococcus aureus is responsible for 80% to 90% of the cases of culture-positive pyogenic osteomyelitis. These organisms express cell wall proteins that bind to bone matrix components such as collagen and facilitate adherence to bone. Escherichia coli, Pseudomonas, and Klebsiella are more frequently isolated from individuals with genitourinary tract infections or who are intravenous drug abusers. Mixed bacterial infections are seen in the setting of direct spread, inoculation of organisms during surgery, or into open fractures. In the neonatal period, Haemophilus influenzae and group B streptococci are frequent pathogens, and individuals with sickle cell disease are predisposed to Salmonella infection. In almost 50% of suspected cases, no organisms can be isolated.
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The osseous vascular circulation, which varies with age, determines the location of infection in most long bones. In infants and adults, vascular communication allows the spread of infection between the metaphysis and the epiphysis. By contrast, the avascular growth plate in the child interrupts infection spread between the metaphysis and epiphysis.
MORPHOLOGYChangesassociatedwithosteomyelitisdependonthestage(acute,subacute,orchronic)andlocationoftheinfection.Intheacutephase,bacteriaproliferateandinduceaneutrophilicinflammatoryreaction.Necrosisofbonecellsandmarrowensueswithinthefirst48hours.ThebacteriaandinflammationspreadlongitudinallyandradiallythroughouttheHaversiansystemstoreachtheperiosteum.Inchildren,theperiosteumislooselyattachedtothecortex.Thus,sizablesubperiostealabscessmayformthatdissectforlongdistancesalongthebonesurface.Liftingoftheperiosteumfurtherimpairsthebloodsupplytotheaffectedregion,contributingtothenecrosis.Thedeadboneisknownasasequestrum. Ruptureoftheperiosteumleadstoasofttissueabscess,whichcanchanneltotheskin,creatingadrainingsinus.Sometimesthesequestrumcrumbles,releasingfragmentsthatpassthroughthesinustract.
Ininfants(anduncommonlyinadults),epiphysealinfectionmayspreadthroughthearticularsurfaceoralongcapsularandtendoligamentousinsertionsintoajoint,producingsepticorsuppurativearthritis,whichcancausedestructionofthearticularcartilageandpermanentdisability.
Afterthefirstweek,chronicinflammatorycellsreleasecytokinesthatstimulateosteoclasticboneresorption,ingrowthoffibroustissue,andthedepositionofreactiveboneattheperiphery.Thenewlydepositedbonecanformashelloflivingtissue,knownasaninvolucrum,aroundthesegmentofdevitalizedinfectedbone(
Fig.21.14 ).Thehistologicfindingsofchronicosteomyelitisaremoreproteanbuttypicallyinvolvemarrowfibrosis,sequestrum,andaninflammatoryinfiltrateoflymphocytesandplasmacells.
Hematogenous osteomyelitis sometimes manifests as an acute systemic illness with malaise, fever, chills, leukocytosis, and marked throbbing pain over the affected region. In other instances the presentation is subtle, with only unexplained fever (most often in infants) or localized pain (most often in adults). The diagnosis is strongly suggested by the characteristic radiographic findings of a lytic focus of bone destruction surrounded by a zone of sclerosis. Biopsy and bone cultures are required to identify the pathogen in most instances. The combination of antibiotics and surgical drainage is usually curative.