Chapter 120. Osteomyelitis (Part 1)

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Harrison's Internal Medicine Chapter 120. Osteomyelitis Osteomyelitis: Introduction Osteomyelitis, an infection of bone, is caused most commonly by pyogenic bacteria and mycobacteria. As a useful framework for evaluating a patient and planning treatment, cases are classified on the basis of the causative agent; the route by which organisms gain access to bone; the duration of infection; the anatomic location of infection; and the local and systemic host factors that have a bearing on pathogenesis and outcome. Pathogenesis and Pathology Microorganisms enter bone by hematogenous dissemination, by spread from a contiguous focus of infection, or by a penetrating wound. Trauma, ischemia, and foreign...

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Chapter 120. Osteomyelitis (Part 1) Harrison's Internal Medicine > Chapter 120. Osteomyelitis Osteomyelitis: Introduction Osteomyelitis, an infection of bone, is caused most commonly by pyogenic bacteria and mycobacteria. As a useful framework for evaluating a patient and planning treatment, cases are classified on the basis of the causative agent; the route by which organisms gain access to bone; the duration of infection; the anatomic location of infection; and the local and systemic host factors that have a bearing on pathogenesis and outcome. Pathogenesis and Pathology
Microorganisms enter bone by hematogenous dissemination, by spread from a contiguous focus of infection, or by a penetrating wound. Trauma, ischemia, and foreign bodies enhance the susceptibility of bone to microbial invasion by exposing sites to which bacteria can bind and by impeding host defenses. Phagocytes attempt to contain the infection and, in the process, release enzymes that lyse bone. Bacteria escape host defenses by adhering tightly to damaged bone, by entering and persisting within osteoblasts, and by coating themselves and underlying surfaces with a protective polysaccharide-rich biofilm. Pus spreads into vascular channels, raising intraosseous pressure and impairing the flow of blood; as the untreated infection becomes chronic, ischemic necrosis of bone results in the separation of large devascularized fragments (sequestra). When pus breaks through the cortex, subperiosteal or soft tissue abscesses form, and the elevated periosteum deposits new bone (an involucrum) around the sequestrum. Microorganisms, infiltrates of neutrophils, and congested or thrombosed blood vessels are the principal histologic findings of acute osteomyelitis. The distinguishing feature of chronic osteomyelitis is necrotic bone, which is characterized by the absence of living osteocytes. Mononuclear cells predominate in chronic infections, and granulation and fibrous tissues replace bone that has
been resorbed by osteoclasts. In the chronic stage, organisms may be too few to be seen on staining. Hematogenous Osteomyelitis Hematogenous infection accounts for ~20% of cases of osteomyelitis and primarily affects children, in whom the long bones are infected, and older adults and IV drug users, in whom the spine is the most common site of infection. Acute Hematogenous Osteomyelitis Infection usually involves a single bone, most commonly the tibia, femur, or humerus in children and vertebral bodies in injection drug users and older adults. Bacteria settle in the well-perfused metaphysis of growing bones, a network of venous sinusoids slows the flow of blood, and fenestrations in capillaries allow organisms to escape into the extravascular space. Because vascular anatomy changes with age, hematogenous infection of long bones is uncommon during adulthood and, when it occurs, usually involves the diaphysis.
On presentation, the child with osteomyelitis usually appears acutely ill, with fever, chills, localized pain and tenderness, and—in many cases—restriction of movement or difficulty bearing weight. Overlying erythema and swelling indicate extension of pus through the cortex. During infancy and after puberty, infection may spread through the epiphysis into the joint space. In children of other ages, extension of infection through the cortex results in involvement of joints if the metaphysis is intracapsular. Thus, septic arthritis of the elbow, shoulder, and hip may complicate osteomyelitis of the proximal radius, humerus, and femur, respectively. In children, the source of bacteremia is usually inapparent. A history is often obtained of recent blunt trauma to the area involved; presumably, this event results in a small intraosseous hematoma or vascular obstruction that predisposes to infection. Adults with hematogenous osteomyelitis may present either in the context of an infection elsewhere (e.g., the respiratory or urinary tract, a heart valve, or an intravascular catheter site) or without an obvious source of bacteremia. Plain radiographs obtained early in the course of infection may show soft tissue swelling, but the first change in bone—a periosteal reaction—is not evident until at least 10 days after the onset of infection. Lytic changes can be detected only after 2–6 weeks, when 50–75% of bone density has been lost. Rarely, a well- circumscribed lytic lesion, or Brodie's abscess, is seen in a child who has been in pain for several months but has had no fever.