Osteomyelitis

Juliet Aizer

Barry D. Brause

KEY POINTS

The diagnosis of osteomyelitis is dependent upon understanding the pathogenetic mechanisms involved in the three routes of infection: hematogenous osteomyelitis, introduced infection, and contiguous infection.
The three routes of bone infection are associated with different and distinct clinical presentations.
X-ray is the most specific and least expensive imaging technique for diagnosing osteomyelitis (with the exception of childhood acute hematogenous infection).
Bone biopsies should be sought, percutaneously or by operative debridement, when there is no overlying skin ulcer and the microbiologic etiology has not been otherwise determined.
Sinus tract and sinus drainage cultures often reflect colonizing flora and cannot be relied upon to identify the actual cause of deep osseous infection.
Designing a therapeutic regimen for osteomyelitis depends substantially on the sensitivity of the isolated pathogen to specific antimicrobial agents, which underscores the essential importance of delineating the pathogen in these infections.
When acute osteomyelitis is complicated by abscess formation or extensive necrosis, surgical debridement is an important adjunct to antibiotics.
In chronic osteomyelitis microorganisms persist in foci of gross or microscopic necrotic bone (sequestra) and intermittently invade surrounding tissues, causing acute exacerbations.

Osteomyelitis represents the invasion of bone by microorganisms. A useful classification for bone infection, based on the pathogenetic route of infection, divides cases into three types: (a) hematogenous osteomyelitis; (b) introduced infection, which results from
contamination accompanying surgical and nonsurgical trauma; and (c) contiguous infection, which results from the spread of microorganisms from adjacent infected tissue and includes osteomyelitis associated with peripheral vascular disease.

ETIOPATHOGENESIS AND PREVALENCE

I. HEMATOGENOUS OSTEOMYELITIS

The etiologic pathogens in hematogenous osteomyelitis reflect the microorganisms associated with bacteremia in specific patient populations (Table 48-1). The osseous site of involvement in hematogenous infection is age-dependent.

Childhood hematogenous osteomyelitis. From birth through puberty, the metaphyseal regions in the long bones of the extremities (tibia, femur, humerus) are most frequently involved owing to their large blood flow during the developmental years.
Adult hematogenous osteomyelitis. In adults, blood-borne pathogens preferentially infect the spine (lumbosacral, thoracic) because vertebrae receive relatively more blood flow with maturation. In bacteremia, the more vascular anterior end plates are seeded, and osteomyelitis commonly involves two adjacent vertebral bodies and the intervertebral disc space. The septic process compromises the nutrient supply to the intervertebral disc, resulting in disc necrosis and disc space narrowing.

II. INTRODUCED OSTEOMYELITIS

Patients are at risk for the introduced form of osteomyelitis whenever the skin and soft tissues overlying and protecting bone are breached by trauma or surgery. Approximately 70% of compound fractures are contaminated by skin and soil microflora, but thanks to effective debridement and perioperative antibiotic therapy, infection develops in only 2% to 9%. Prophylactic antibiotics and extensive antiseptic operative techniques allow large foreign bodies to be inserted into bones during reparative and reconstructive orthopedic surgery with infection rates less than 2%. Indwelling foreign bodies decrease the magnitude of bacterial inoculum necessary to establish infection in bone, and they permit pathogens to persist on the surface of avascular material, often within host- or microbe-derived biofilms, sequestered from circulating immune factors and systemic antibiotics.

III. OSTEOMYELITIS BY CONTIGUOUS SPREAD (INCLUDING VASCULAR INSUFFICIENCY)

Osteomyelitis develops by contiguous spread in one-third to two-thirds of patients with diabetes who have longstanding foot ulcers. More hospital days are utilized to treat foot infection than any other complication of diabetes mellitus. Osseous involvement reflects unsuccessful reversal of or compensation for underlying severe neuropathy and vascular insufficiency. These neuropathic and vasculopathic processes prevent a skin ulcer from healing, so that progressively deeper microbial invasion culminates in spread to contiguous bone. This clinical scenario is also seen in patients with chronic skin ulcerations resulting from other conditions associated with severe sensory neuropathy (e.g., meningomyelocele) or vascular insufficiency (e.g., decubitus ulcers, vasculitis, atherosclerosis, and arteriosclerosis). The most common pathogens are staphylococci, streptococci, gram-negative bacilli, and anaerobes. Multiple organisms are isolated in more than 60% of cases.

IV. THE PATHOLOGIC PROCESS

In all three forms of osteomyelitis, the microorganisms induce local metabolic changes and inflammatory reactions that produce osseous edema. As infection spreads within the bone, local thrombophlebitis develops, increasing edema and intraosseous pressure, that can result in ischemic necrosis of large areas of bone, called sequestra. If the osseous cortex is breached, subperiosteal abscesses can develop, with periosteal inflammation and periosteal formation of new bone in adjacent soft tissue, called an involucrum.

V. MICROBIOLOGY

Virtually all microbes can infect bone. Bacteria are the usual pathogens, and staphylococci are the most common etiologic agents in all three types of osseous infection. Staphylococcus aureus causes approximately 60% of cases of hematogenous and introduced osteomyelitis and is the most prominent pathogen when osseous infection develops from sepsis in contiguous tissue. Staphylococcus epidermidis and the other coagulase-negative staphylococci have become the major
pathogens in bone infections associated with indwelling prosthetic materials and foreign bodies, such as joint replacement implants and fracture fixation devices, which are responsible for 30% of these cases. Streptococci, gram-negative bacilli, anaerobes, mycobacteria, and fungi are causative agents in a variety of clinical situations (see Table 48-1).

Table 48-1 Predispositions, Anatomic Sites, and Prominent Pathogens in Forms of Osteomyelitis

Form of osteomyelitis	Predisposing condition	Site	Prominent pathogens
I. Hematogenous
Childhood Adult	None Sickle cell hemoglobinopathy Urinary tract infection or instrumentation Skin infection Respiratory infection	Long bones Multiple Vertebrae Vertebrae Vertebrae	Staphylococcus aureus Streptococci Haemophilus Salmonella S. aureus GNB Streptococci S. aureus Streptococci Streptococci Mycobacterium tuberculosis
	Intravenous drug abuse or vascular catheters	Vertebrae	GNB Staphylococci Candida
	AIDS	Multiple Mycobacteria	Fungi
	Endocarditis	Vertebral	Streptococci Staphylococci
II. Introduced type	Fractures	Fracture site	S. aureus Staphylococcus epidermidis GNB
	Prosthetic joint	Prosthesis	S. epidermidis aureus
	Puncture wounds	Foot	Pseudomonas aeruginosa, S. aureus, anaerobes
III. Contiguous spread	Skin ulcer (e.g., diabetic, decubitus, stasis, and vasculitic)	Foot, leg	Polymicrobial –Staphylococci –Streptococci –GNB –Anaerobes
	Sinusitis	Skull	Streptococci Anaerobes
	Dental abscess	Mandible	Streptococci
	Dental abscess	Maxilla	Anaerobes
	Human or animal bites	Hand	Streptococci Anaerobes Pasteurella multocida
	Felon	Finger	S.aureus
	Gardening	Hand	Sporothrix
AIDS, acquired immunodeficiency syndrome; GNB, gram-negative bacilli. From Brause BD. Osteomyelitis. In: Bennett JC, Plum F. Cecil-Loeb Textbook of Medicine. 20th ed. Philadelphia, PA: WB Saunders; 1996:1625, with permission.