| OBJECTIVES
The learner will be better able to:
1) Explain the principles reflected in the history and discovery of
osteomyelitis
2) Generate a differential diagnosis given a patient case
3) Describe the distinct features of a radiological image of a patient
with osteomyelitis
4) Explain factors that influence the incidence of osteomyelitis in
a given population
5) Identify classic features of osteomyelitis given a patient case
INTRODUCTION
Osteomyelitis is defined as an inflammation or an infection in the bone
marrow and surrounding bone. The disease is classified as either acute
or chronic, depending on the length of time the infection or symptoms
persist. Symptoms include pain, warmth and/or swelling in the bone.
Chronic osteomyelitis may last for years , with slow death of bone tissue
from a reduced blood supply. Signs and symptoms may be absent, however,
causing difficulty in diagnosing the chronic infection. 
Pathogens infect bone in posttraumatic osteomyelitis after a recent
fracture. Bacteria, fungus and other microorganisms are typically the
causative agents. The more susceptible a bone is to fracturing, the
greater the chances of becoming infected and developing disease. Trauma
from recent injuries and diabetes are major risk factors for osteomyelitis.The
bone can be directly infected from the wound or indirectly via the blood
from another site of infection, called hematogenous osteomyelitis.
The vertebrae and pelvis are often affected in adults in this blood-borne
variety, while children are usually affected in long bones.
EPIDEMIOLOGY
The incidence of osteomyelitis after open fractures is reported to be
2% to 16%, depending significantly on the grade of trauma and the type
of treatment administered.
Prompt and thorough treatment help reduce the risk of infection, decreasing
the probability of developing osteomyelitis. This is particularly important
for patients with the following risk factors: diabetes, altered immune
states and recent trauma. The tibia is the most frequent site of posttraumatic
osteomyelitis ,
since it is the most vulnerable bone with the least vigorous blood supply
in the body.
The classification of osteomyelitis can
be broken down into the following categories: exogenous ostemyelitis
(47%), secondary to vascular insufficiency (34%) and hematogenous osteomyeltis
(19%).
The implantation of an orthopedic device (pins, plate, screws, artificial
joint) can also seed infection as a nidus for pathogens, and therefore
create post-operative osteomyelitis.
The growing skeleton is also at risk. Any bone can be affected but it
is usually the weight-bearing bones before the physis has closed. At
the physis on the metaphyseal side, end arteries form a capillar loop
which may rupture following minor trauma. This region of blood stasis
may attract circulating bacteria ("everybody has bacteria circulating,
periodically" -HH Jones) . Once escaped through the vascular system,
bacteria can set up shop in surrounding tissues.
ETIOLOGY
The presence of bacteria alone in an open fracture
is not sufficient to cause osteomyelitis. In most cases, the body's
immune system is capable of preventing the colonization of pathogens.
The micro-environment determines whether infection occurs. The timing
and extent of treatment are critical in determining whether infection
develops. The likelihood of developing ostemyelitis increases with impaired
immune function, extensive tissue damage, or reduced blood supply to
the affected area. Patients with diabetes, poor circulation or low white
blood cell count are at greater risk.
Bacterial or fungal infection cause most osteomyelitis. Infection induces
a large polymorphonuclear response from bone marrow, particularly staphylococcus
aureus, streptococcus and haemophilus influenza. Staphylococcus infection
predominates today and before the era of antiobiotics.
CLINICAL DIAGNOSIS AND MANIFESTATIONS
The diagnosis of osteomyelitis
is made from clinical, laboratory and imaging studies.
When the skeletal system is involved, pain, fever and leukocytosis (an
increase in white blood cell count due to infection or inflammation)
occur. The affected area is painful. Initial x-rays are typically normal.
As early as 4 days, an area of lucency may be seen on x-ray.
Usually, the changes are not recognized until 10 days or two weeks have
passed. Subperiosteal new bone formation in the affected area is present,
representing periosteal elevation from encroaching pus.
If
not successfully treated, pus enlarges the bone appearing as increased
lucency, which surrounds sclerotic, dead bone . This inner dead bone
is called the sequestrum (sequestered from blood supply), and
the outer periosteal reaction laminates to form the involucrum.
(See diagram at right.)
Draining sinuses develop when the pressure of pus exceeds the containment
of the soft tissue. This further deprives the bone of its blood supply.
This in turn harbors more bacteria, and the process cannot be reversed
until extensive debridement of the area occurs-until the environment
changes to one that promotes healing.
DIFFERENTIAL DIAGNOSIS
Ewing sarcoma
Osteosarcoma
Reactive bone marrow edema
Traumatic or stress fractures
Inflammatory arthritis
Gout
SUMMARY
Osteomyelitis is an infection involving the
bone. The bones usually affected are the weight-bearing bones, particularly
before the physis has closed. Exogenous osteomyelitis occurs from open
trauma, sometimes relatively minor in nature. Hematogenous osteomyelitis
occurs from bacteria circulating in the bloodstream. Acute and chronic
subtypes are classified according to the timing and duration of the
infection.
REFERENCES
1. Dirschl
DR, Almekinders LC. Osteomyelitis. Drugs. 1993; 45: 29-43.
2. Ehara
S. Complications of skeletal trauma. Radiol Clin North Am. 1997; 35:
767-781.
3. Sammak
B, Abd El Bagi M, Al Shahed M, et al. Osteomyelitis: a review of currently
used imaging techniques. Eur Radiol. 1999; 9: 894-900.
4. Waldvogel F, Medoff G, Swartz M. Osteomyelitis: a review of clinical
features, therapeutic considerations and unusual aspects (I). N Engl
J Med. 1970; 282: 198-206.
5. Widmer
AF. New developments in diagnosis and treatment of infection in orthopedic
implants. Clin Infect Dis. 2001; 33: S94-S106.
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