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ID 1382-1406



Most osteomyelitis is of hematogenous origin. The clinical picture varies with age. In children through the age of puberty the long bones of the extremities are most often involved with the metaphysis as the initial infected site. In adults hematogenous osteomyelitis most often affects the spine. This age-dependent preference for bone relates to the vasculature and blood flow to the site. In children, the metaphysis is very active metabolic tissue with a large blood flow and with vasculature predisposed to infection. Phagocytes lining the capillaries in this region are deficient in number and function. The nutrient arteries near the epiphyseal cartilage are nonanastomosing, thereby allowing any blockage to produce tissue necrosis and the sinusoids (venous side of capillary) have slow, turbulent flow predisposing to thrombosis. As aging occurs metaphysis metabolism slows down, blood flow decreases and phagocytic activity increases. Concomitant with these changes the vertebrae become more vascular with maturation (senile hyperemia) and bacteremias seed vertebral bodies preferentially at the more vascular anterior vertebral end plates. In addition, lumbar paracentral veins communicate freely with pelvic veins by valveless anastomoses. Theoretically, retrograde flow from pelvic tissues (urethra, prostate, bladder) to lumbar vertebrae explains the spread of pelvic infections preferentially to lumbar vertebrae.

In about 25% of patients with osteomyelitis, the predisposing factor is trauma to the bone at or near the site of infection. Infections of the mandible are often due to traumatic dental procedures while the installation of prosthetic devices, such as artificial joints, predisposes to long bone infection.


Osteomyelitis is a purulent inflammation of bone caused most often by bacteria and only occasionally by other microorganisms. In order of frequency of infection the bacterial species are:

Staphylococcus aureus )

Streptococcus spp. ) Long bone and spine infections

Members of the Enterobacteriaceae )

Bacteroides spp. - mandibular infections


The host responds to the presence of bacteria in the metaphysis with a local increase in vascular permeability, resulting in edema, increased vascularity and the influx of polymorphonuclear leukocytes. Pressure increases as pus collects and is confined within rigid bone. Exudation through Volkmann's canals and the haversian canal affords little relief, although the relatively inelastic periosteum may become elevated. The blood supply to the area of involvement is decreased secondary to the pressure; necrosis of the infected bone may result in the formation of a sequestrum. A protein-rich liquid containing inflammatory cells may collect in an adjacent joint but such effusions are sterile.

After the vascular supply to the involved area has been interrupted and necrosis has occurred, the chronic phase of osteomyelitis is established. The residual dead bone acts as a foreign body, making the eradication of bacteria impossible until the sequestrum is removed.

If the infected area becomes well demarcated and the infection is contained, the acute inflammatory process may subside, leaving a subperiosteal accumulation of pus which may be discovered by tenderness on palpation. This relatively quiescent form of subperiosteal infection is termed a Brodie's abscess. After some time, there is deposition of new bone, the involucrum, under the elevated periosteum.

In osteomyelitis of the spine, infection most often involves the vertebral body. It spreads readily through the anastomotic venous system to adjacent ligaments and vertebral bodies. It is common for more than one vertebral body to be involved. Pus may accumulate between the vertebral periosteum and dura mater, forming an extradural abscess. Compression of the spinal cord may result, yielding a paraplegia. If a subdural abscess ruptures into the subarachnoid space, meningitis results.


Hematogenous osteomyelitis is often preceded by the signs and symptoms of bacteremia:

Fever Inflammation

Malaise Cephalgia

Myalgia Anorexia

This phase of the illness may last for several days.

The second phase of the disease is the clinical onset of involvement of bone. This gives rise to:

Restricted motion


Soft tissue around the inflamed bone which is





Bone tenderness


Diagnosis is based upon:

Clinical symptoms of an infection

Laboratory evidence of an infection:

Isolation of an organism

Increase in antibody titer

Presence of bone pain

Soft tissue swelling

Limited motion of extremity

Roentgenographic changes occur late in disease and should not be waited for to make the diagnosis; this would allow the development of chronic osteomyelitis. A differential diagnosis should include:

Rheumatic fever - there is severe pain and limitation of joint motion in this disease but there is no bone tenderness.

Monoarthritic rheumatoid arthritis - the major swelling and tenderness is limited to the joint, without local tenderness on palpation over the adjacent metaphysis.

Poliomyelitis - tenderness of the bone in an apparently paralyzed extremity indicates osteomyelitis. There is no bone tenderness in polio.

Septic arthritis - joints are exquisitely tender and painful, whereas the swollen joint associated with osteomyelitis may be gently manipulated through a limited range of motion.

Bacterial cellulitis - there is warmth, erythema, pain and edema of the soft tissue but it is clearly demarcated whereas in osteomyelitis it is not clearly demarcated.


Acute osteomyelitis should be treated with a parenterally administered antibiotic based on the infecting organism:

Staphylococcus aureus - nafcillin

Streptococcus pyogenes - nafcillin

Gram-negative rods - ciprofloxacin

Bacteroides spp. - clindamycin

Chronic osteomyelitis requires surgical procedures as well as antibiotic therapy. This includes full debridement and excision of all dead bone and necrotic tissue (sequestrectomy).

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