is an infection of medullary bone that results in the progressive inflammatory
destruction of bone and the apposition of new bone. Pus spreads in vascular
channels, increases intraosseus pressure and causes a decrease in blood
flow. Ischemic necrosis follows and the devascularized bone is known as
children Hematogenous spread of infection is common and presents as
a high fever, malaise, local pain and swelling. The plain radiographs
show a central lytic defect with surrounding sclerosis, termed a Brodie's
abcess. The clinical picture may be equivocal, and the concern
about the possibility of a tumor may arise. The most common organism
in patients over the age of three is coagulase positive staph aureus.
Hematogenous osteomyelitis occurs most commonly in the distal femur, proximal
tibia, proximal femur and proximal humerus, all areas of rapid growth
In adults hematogenous osteomyelitis is rare
except IV drug users and the elderly. The clinical presentation can be
quite deceptive, since fever, elevated white count, and history
of a possible source of infection are often lacking. In addition,
the relatively aggressive radiographic
appearance of the lesion may give rise to concern about a primary
or metastatic bone tumor. IV drug users often have unusual organisms such
as pseudomonas. Older patients may have gram negative bacteria in the
spine secondary to organisms that originate as a urinary tract infection
and travel through Batson's plexus. Spinal osteomyelitis may present as
back pain with negative blood cultures.
Osteomyelitis may be caused by direct innoculation
secondary to trauma or surgery. Osteomyelitis secondary to trauma is often
poly- microbial. Complete immobilization maybe necessary to protect the
vascular channels necessary to promote healing.
Osteomyelitis can also be the result of contiguous
spread from an abscess or sinus tract. Chronic osteomyelitis may occur
secondary to syphilis and can cause bony destruction known as a gumma.
Squamous cell carcinoma is a known complication of chronic long term draining
fistula sites due to osteomyelitis.
Suspected osteomyelitis may not be positive on plain
x-ray initially. Later, a mixed lytic
and sclerotic lesion is seen, which has a wide zone of transition
and a variable amount of periosteal reaction. The lesion may appear
quite aggressive by tumor criteria. Bone scan has poor specificity.
CT scan or MRI may show edema, medullary destruction, periosteal reaction,
soft tissue mass or damage
or articular involvement. On MRI scan, T1 weighted images demonstrate
infection as a low signal with ill defined margins. T2 images show infection
as a bright signal. MRI shows marrow replaced by edema and inflammatory
cells but is not useful if hardware is present.
Microscopic examination reveals micro-organisms, neutrophils,
congested or thrombosed blood vessels, and necrotic bone. Sequestra has
no living osteoblasts within lacunae.
Treatment for osteomyelitis is difficult. l Surgical
sampling or needle biopsy is necessary for diagnosis. Infected hardware
should be removed if the bone is healed and stable. Acute osteomyelitis
is treated with irrigation and debridement as necessary, followed
by four to six weeks of antibiotics. Chronic osteomyelitis is best treated
with thorough debridement, antibiotics, and local flap coverage
Lew, DP and FA Waldvogel, Osteomyelitis, New England Journal of Medicine,
336(14):999-1007, April 3, 1997.
Deely, DM and ME Schweitzer, MR Imaging of Bone Marrow Disorders,
Radiologic Clinics of North America, 35(1):193-211, January, 1997.
Bullough, Peter, Orthopedic Pathologv (third edition), Times Mirror International
Publishers Limited, London, 1997.
Huvos, Andrew. Bone Tumors: Diagnosis. Treatment and Prognosis, W.B.
Saunders, Co., 1991.