Osteomyelitis is defined as infection in bone. Osteomyelitis in long bones includes infections that differ from one another with regard to duration, etiology, pathogenesis, extent of bone involvement, and type of patient (which can be an infant, child, adult, or compromised or uncompromised host).
Etiology
In hematogenous osteomyelitis, a single pathogenic organism is almost always recovered from the bone. In infants, Staphylococcus aureus, Streptococcus agalactiae, and Escherichia coli are most frequently isolated from blood or bone.
However, in children over one year of age, Staphylococcus aureus, Streptococcus pyogenes, and Haemophilus influenzae are most commonly isolated. The incidence of Haemophilus influenza infection decreases after the age of four years.
In adults, Staphylococcus aureus is the most common organism isolated. Multiple organisms are usually isolated from bone infected as a result of direct inoculation or contiguous focus infection. Staphylococcus aureus remains the most commonly isolated pathogen. However, gram-negative bacilli and anaerobic organisms are also frequently isolated.
Pathogenesis
1. Source of Infection
Osteomyelitis can be caused by hematogenous spread, direct inoculation of microorganisms into bone, or a contiguous focus of infection. Hematogenous osteomyelitis usually involves the metaphysis of long bones in children because long bones of children have very active metabolic rates. The most common causes of direct-inoculation osteomyelitis are penetrating injuries and surgical contamination. Contiguous osteomyelitis commonly occurs in patients with severe vascular disease.
2. Host Factors
Host factors are primarily involved in the containment of the infection once it has been introduced adjacent to or into the bone. Host factors may predispose individuals to the development of osteomyelitis. Host deficiencies that lead to bacteremia favor the development of hematogenous osteomyelitis.
Host deficiencies that are involved in the direct inoculation of organisms and/or contiguous spread of infection from an adjacent area of soft-tissue infection are primarily involved in the lack of containment of the initial infection.
Some patients have an unusual susceptibility to acute skeletal infections when they have sickle cell anemia, chronic granulomatous disease, or diabetes mellitus. Many systemic and local factors influence the ability of the host to elicit an effective response to infection and treatment
Pathology
1. Acute Osteomyelitis
Acute osteomyelitis presents as inflammation accompanied by edema, vascular congestion, and small-vessel thrombosis. In early acute disease, the vascular supply to the bone is decreased by infection extending into the surrounding soft tissue. When both the medullary and the periosteal blood supplies are compromised, large areas of dead bone (sequestra) may be formed in chronic phase.
However, if treated promptly and aggressively with antibiotics and possibly with surgery, acute osteomyelitis can be arrested before dead bone presents.
2. Chronic Osteomyelitis
Pathologic features of chronic osteomyelitis are the presence of necrotic bone (sequestrum), the formation of new bone (involucrum), and the exudation of polymorphonuclear leukocytes joined by large numbers of lymphocytes, histiocytes, and occasionally plasma cells.
New bone forms from the surviving fragments of periosteum and endosteum in the region of the infection. It forms an encasing sheath of live bone, known as an involucrum, surrounding the dead bone under the periosteum.
The involucrum is irregular and is often perforated by openings through which pus may track into the surrounding soft tissues and eventually drain to the skin surfaces, forming a chronic sinus. The involucrum may gradually increase in density and thickness to form part or all of a new diaphysis.
New bone increases in amount and density for weeks or months, according to the size of the bone and the extent and duration of the infection. Endosteal new bone may proliferate and obstruct the medullary canal. After host defense or operative removal of the sequestrum, the remaining cavity may fill with new bone, especially in children. However, in adults, the cavity may persist or the space may be filled with fibrous tissue, which may connect with the skin surface by means of a sinus tract.
Signs and Symptoms
Children with hematogenous osteomyelitis may present with acute signs of infection including fever, irritability, lethargy, and local signs of inflammation. Children with hematogenous osteomyelitis usually have noninfected soft tissue enveloping the infected bone and are capable of mounting an effective response to the infection. The joint is usually spared from infection unless the metaphysis is intracapsular, as is found in the proximal part of the radius, humerus, or femur.
Adults with primary or recurrent hematogenous osteomyelitis usually present with vague symptoms consisting of nonspecific pain and low-grade fever of one to three months’ duration. However, acute clinical presentations with fever, chills, swelling, and erythema over the involved bone or bones are occasionally seen.
The source of bacteremia may be a trivial skin infection or a more serious infection such as acute or subacute bacterial endocarditis. Hematogenous osteomyelitis that involves either long bones or vertebrae is an important complication of injection drug abuse. Patients with contiguous osteomyelitis often present with localized bone and joint pain, erythema, swelling, and drainage around the area of trauma, surgery, or wound infection.
Signs of bacteremia such as fever, chills, and night sweats may be present in the acute phase of osteomyelitis but are not seen in the chronic phase. Both hematogenous and contiguous focus osteomyelitis can progress to a chronic condition. Local bone loss, sequestrum formation, and bone sclerosis are common. Persistent drainage and/or sinus tracts are often found adjacent to the area of infection. The patient usually presents with chronic pain and drainage. If fever is present, it is low grade.