Osteomyelitis

Osteomyelitis is a difficult-to-treat infection of bone and bone marrow. It is progressive and results in inflammatory destruction of the bone, bone necrosis, and new bone formation. Bacterial osteomyelitis causes substantial morbidity worldwide, despite continued progress toward understanding its pathophysiology and optimal management.

The approach to osteomyelitis depends upon the route by which bacteria gained access to bone, bacterial virulence, local and systemic host immune factors, and patient age. While imaging studies and nonspecific blood tests may suggest the diagnosis, an invasive technique is generally required to identify the causative pathogens. Antibacterial regimen selection has been largely guided by knowledge of the relative activities and pharmacokinetics of individual drugs, supported by data from animal models.

Definitive therapy often requires a combined medical and surgical approach. Newer microvascular and distraction osteogenesis techniques and the use of laser Doppler allow more complete surgical resection of infected material while maintaining function. Despite recent advances, aggressive medical and surgical therapy fails in many patients with osteomyelitis. More accurate diagnostic methods, better ways to assess and monitor the effectiveness of therapy, and novel approaches to eradicate sequestered bacteria are needed.

History : Osteomyelitis has been well known since antiquity.

Problem : Osteomyelitis results in inflammatory destruction of the bone, bone necrosis, and new bone formation. Three major categories of osteomyelitis exist, based upon pathogenic mechanisms of infection, as follows:

Osteomyelitis following hematogenous spread of infection

Osteomyelitis secondary to a contiguous focus of infection

Osteomyelitis associated with vascular insufficiency

Three different subtypes of osteomyelitis are known: acute osteomyelitis, subacute osteomyelitis, and chronic osteomyelitis.

Frequency : The overall prevalence of acute osteomyelitis is 2 cases per 10,000 children.

Neonatal prevalence is approximately 1 case per 1000 children. The annual incidence in patients with sickle cell anemia is approximately 0.36%.

The prevalence of osteomyelitis after foot puncture may be as high as 16% (30-40% in patients with diabetes).

Excluding the axial skeleton, lower extremity osteomyelitis accounts for 90% of osteomyelitis cases and is much more common than upper extremity osteomyelitis, which accounts for 10% of extremity cases.

The most common bones involved in osteomyelitis in descending order are as follows:

Tibia (50%)

Femur (30%)

Fibula (12%)

Humerus (3%)

Ulna (3%)

Radius (2%)

The prevalence of chronic osteomyelitis is 2 cases per 10,000 people.

Most studies support the idea that incidence is similar in developed countries. In developing countries, incidence is higher due to higher incidence of puncture wounds, contaminated injuries, and less wound care.

Epidemiology of vertebral osteomyelitis

It is primarily a disease of adults; most patients are older than 50 years. Generally, the incidence increases progressively with each successive decade of life. Men are affected approximately twice as often as women in most case series. The reason for this male predominance is not clearly understood.

Reliable information regarding the overall incidence of vertebral osteomyelitis is difficult to obtain. However, most authorities believe that the overall incidence of vertebral osteomyelitis has steadily increased in recent years for 3 primary reasons: increasing rates of nosocomial bacteremia due to intravascular devices and other forms of instrumentation, increasing age of the population, and increasing injection drug use.

Etiology : While normal bone is resistant to infection, a number of conditions can predispose one to development of osteomyelitis, including the following:

Large inoculation of an organism

Trauma leading to bone damage or infarction

Presence of a foreign body

Illnesses compromising host defense

A single pathogenic organism is almost always recovered from the bone. The most common bone isolates are Staphylococcus species, the most common gram-negative organism is Pseudomonas aeruginosa, and the most common anaerobes are Peptostreptococcus species. However, in immunocompromised patients, other organisms, including fungi and mycobacteria, also must be considered.

Commonly isolated organisms in osteomyelitis can be summarized as follows:

Hematogenous osteomyelitis (monomicrobial infection)

Infants (<1 y)

Group B Streptococcus

Staphylococcus aureus

Escherichia coli

Children (aged 1-16 y)

S aureus

Streptococcus pyogenes

Haemophilus influenzae

Adults (>16 y)

S aureus

Coagulase-negative Staphylococcus species

Gram-negative bacilli

P aeruginosa

Serratia marcescens

E coli

Contiguous focus osteomyelitis (polymicrobial infection)

S aureus

Coagulase-negative Staphylococcus species

S pyogenes

Enterococcus species

Gram-negative bacilli

Anaerobes

Diabetic foot osteomyelitis (polymicrobial Infection)

S aureus

Streptococcus species

Enterococcus species

Proteus mirabilis

P aeruginosa

Anaerobes

Pathophysiology : The pathogenesis of osteomyelitis is multifactorial and poorly understood. Some important factors include the following:

Virulence determinants of the organisms

Underlying disease and the immune status of the host

Type and location of the bone

It is clear that bacterial cells adhere to nucleated cells, platelets, and a variety of components of the extracellular bone matrix collagen and noncollagenous proteins.

Cellular and molecular pathogenesis

Cellular and molecular techniques provide new methods for determining the relative importance of the many potential virulence factors by facilitating study of the interaction between the host immune response and potential bacterial virulence factors. As an example, S aureus, which is an important cause of both hematogenous and contiguous focus osteomyelitis, produces a large number of extracellular and cell-associated factors that may contribute to virulence, including the following:

Bacterial adherence : Bacteria adhere to bone by expressing receptors for the components of bone matrix including fibronectin, laminin, collagen, and bone sialoglycoprotein. Adherence appears to play a central role in the early stages of S aureus-induced osteomyelitis or arthritis. Expression of adhesins permits attachment of the pathogen to cartilage and synovial membrane. Strains positive for collagen adhesin are also associated with the production of high levels of immunoglobulin G (IgG) and interleukin (IL)-6. Bone infection has been speculated to be possibly prevented by an adhesin-derived vaccine.

Proteolytic activity : Potential proteolytic activity present in normal joints is inhibited in the absence of infection. However, this protective effect may be lost with infection. In an in vitro model of adult chondrocytes inoculated with S aureus, for example, overall protein synthesis was reduced by 84%, with an increase in the release of collagenase and gelatinase.

Resistance to host defense mechanisms : The ability of microorganisms to resist host defense mechanisms at both the cellular and matrix levels presents difficulties in the treatment of osteomyelitis. S aureus can survive intracellularly in cultured osteoblasts. Furthermore, the presence of arachidonic acid metabolites such as prostaglandin E2, which is a strong osteoclast agonist, decreases the bacterial inoculum needed to produce infection. Once the microorganisms adhere to bone, they express phenotypic changes that make them resistant to antimicrobial treatment.

S aureus organisms express a 42-kd protein, protein A, which is bound covalently to the outer peptidoglycan layer of their cell walls. Protein A binds to the Fc portion of IgG on polymorphonuclear leukocytes, interfering with opsonization and phagocytosis of S aureus. This interference has been demonstrated in vitro and in animal models of subcutaneous abscess and peritonitis.

S aureus also secretes 2 toxins: exotoxin and toxic shock syndrome toxin (TSST)-1, which exert a profound effect on the immune system when administered parenterally. The toxins act as superantigens and suppress plasma cell differentiation. They also stimulate production of cytokines, such as IL-1, interferon-gamma, and tumor necrosis factor-alpha. Animals infected with strains of S aureus isogenic for TSST-1 developed frequent and severe arthritis. Staphylococcal enterotoxin and TSST-1 subvert the cellular and humoral immune system, which may determine whether a local infection is eliminated or develops into osteomyelitis or septic arthritis.

Nitric oxide : The increased turnover of bone in osteomyelitis suggests that the balance between bone formation and resorption is altered, an effect that may be mediated by nitric oxide. Greatly increased levels of nitric oxide and bone resorption have been recorded in the septic skeleton. This response may be driven by the increased levels of cytokines, enterotoxin, and TSST-1, which may stimulate nitric oxide production by endothelial, macrophage, and mesenchymal cells such as osteoblasts. Thus, while low concentrations of nitric oxide are typically thought to inhibit osteoclastic bone resorption, this response may be lost when cytokine and nitric oxide levels increase greatly in skeletal inflammatory disease. Adjunctive local treatment of osteomyelitis with nitric oxide synthetase inhibitors could be beneficial.

Routes of infection

As noted above, osteomyelitis develops via 3 major routes: hematogenous, contiguous focus spread, and vascular insufficiency.

Hematogenous osteomyelitis : Hematogenous osteomyelitis is predominantly encountered in children; 85% of patients with hematogenous osteomyelitis are younger than 17 years, accounting for 20% percent of the total cases of osteomyelitis. In one study of 659 cases of S aureus osteomyelitis occurring in Denmark from 1959-1988, the number of hematogenous osteomyelitis cases declined, especially in children, and cases of vertebral osteomyelitis, more common in adults, increased. In children, the bone infection usually affects the long bones, while in adults, the lesion is usually located in the thoracic or lumbar vertebrae.

Contiguous focus osteomyelitis without generalized vascular insufficiency : Osteomyelitis secondary to contiguous foci of infection accounts for at least one half of all cases and has increased in incidence. The organisms may be directly inoculated into the bone at the time of trauma, spread by nosocomial contamination during perioperative or intraoperative procedures, or extend from an adjacent soft tissue infection.

Contiguous focus osteomyelitis with generalized vascular insufficiency : The primary cause of vascular insufficiency in patients with osteomyelitis is diabetes mellitus. The small bones of the feet, talus, calcaneus and distal fibula, and tibia are commonly involved. The patients in this group are aged 35-70 years. The infection frequently is initiated by a portal of entry for organisms, such as infected nail beds, cellulitis, or atrophic skin ulceration.

Diminished arterial blood supply has traditionally been considered to be the major predisposing factor for contiguous focus osteomyelitis with generalized vascular insufficiency in patients with diabetic foot. However, neuropathy now appears to be an equally important factor. Identifiable neuropathy as a complication of diabetes mellitus is present in approximately 80% of patients with foot disease. Neuropathy can cause foot ulceration through 3 main mechanisms, as follows:

Decreased sensation leads to mechanical or thermal injuries in the unaware patient that can develop into skin ulcerations.

Motor neuropathy affecting the intrinsic muscles of the foot predisposes affected persons to gait disturbances and foot deformities, such as hammertoe, clawtoe deformity, and Charcot foot. These anatomic alterations can lead to a maldistribution of weight and elevated focal pressure over the bony prominences. Subsequently, the increase in pressure where the foot contacts the ground or rubs against shoes can lead to skin ulceration.

Autonomic neuropathy interferes with sweating; the resultant dry, cracked skin allows entry of microorganisms into the soft tissue.

A higher rate of nasal and skin colonization with S aureus, defects in host immunity, and impaired wound healing are all important factors in diabetic foot infection.

Superficial fungal skin infections, which are common in patients with diabetes, also can facilitate bacterial entry through macerated or broken skin.

Pathological differences based on age

Basic differences exist in the pathology of osteomyelitis in infants, children, and adults.

In infants, small capillaries cross the epiphyseal growth plate and permit extension of infection into the epiphysis and joint space. This is a newly well-understood condition referred to as septic osteomyelitis in infants. The cortical bone of neonates and infants is thin and loose, consisting predominantly of woven bone, which permits escape of the pressure caused by infection but promotes rapid spread of the infection directly into the subperiosteal region. A large sequestrum is not produced because extensive infarction of the cortex does not occur; however, a large subperiosteal abscess can form.

In children older than 1 year, infection presumably starts in the metaphyseal sinusoidal veins and is contained by the growth plate. The joint is spared unless the metaphysis is intracapsular. The infection spreads laterally where it breaks through the cortex and lifts the loose periosteum to form a subperiosteal abscess.

In adults, the growth plate has resorbed, and the infection may again extend to the joint spaces, as in infants. In addition, the periosteum is firmly attached to the underlying bone; as a result, subperiosteal abscess formation and intense periosteal proliferation are observed less frequently. The infection can erode through the periosteum, forming a draining sinus tract.

Clinical : The clinical presentation and location of osteomyelitis differ in infants, children, and adults. In infants, medullary infection may spread to the epiphysis and joint surfaces through capillaries that cross the growth plate. In contrast, in children older than 1 year, the growth plate is avascular and infection is confined to the metaphysis and diaphysis. The joint is spared unless the metaphysis is intracapsular. Thus, cortical perforation at the proximal radius, humerus, or femur enables the infection to migrate to the elbow, shoulder, or hip joint, respectively, regardless of the age of the patient.

Hematogenous osteomyelitis

In hematogenous osteomyelitis, local symptoms referable to bones are more frequently absent in neonates than in children. In adults, soft tissue findings may be more prominent than bony involvement.

In infants, local findings that may lead the clinician to suspect osteomyelitis are usually absent in neonates. When they develop, local findings can include decreased motion of a limb and edema (pseudoparalysis) and joint effusion adjacent to the bone infection (present in 60-70% of cases).

Systemic symptoms are frequently present in S aureus osteomyelitis but may be absent when other pathogens are involved.

Children with hematogenous osteomyelitis, in contrast with neonates, typically have the following systemic symptoms:

Abrupt fever

Irritability

Lethargy

Refusal to use the affected limb

Local signs of inflammation present for 3 weeks or less

While this is the classic presentation, signs of systemic toxicity other than minimal temperature elevation are absent in 50% of children with osteomyelitis.

In adults, acute clinical presentations of fever, chills, swelling, and erythema over the involved bones are usually seen in acute hematogenous osteomyelitis.

Vertebral osteomyelitis is usually hematogenous in origin but may be secondary to trauma. A preceding history of urinary tract infection or injection drug use often is present. Other sources of infection include skin and soft tissue, respiratory tract, infected intravascular device site, endocarditis, dental infection, or unknown sources.

The patient usually presents with vague symptoms and signs consisting of dull, constant back pain and spasm of the paravertebral muscles. Localized pain and tenderness of the involved bone segments is present in at least 90% of cases. The pain is usually insidious and slowly progresses over 3 weeks to 3 months.

Contiguous focus osteomyelitis without vascular compromise

Common predisposing factors for contiguous focus osteomyelitis include surgical reduction and internal fixation of a fracture, open fractures, and chronic soft tissue infections. This form of osteomyelitis is biphasic in its age distribution. The infection occurs in younger persons secondary to trauma and related surgery and in older adults from decubitus ulcers.

The infection usually manifests within 1 month after inoculation of the organisms from trauma, surgery, or a soft tissue infection. Affected patients typically present with low-grade fever, pain, and drainage. Loss of bone stability, bone necrosis, and soft tissue damage frequently occur, making this form of osteomyelitis difficult to treat.

Contiguous focus osteomyelitis with vascular compromise

Osteomyelitis in patients with vascular compromise, who are often diabetic, can be difficult to diagnose. Patients can present with an apparently localized process including an ingrown toenail, a perforating foot ulcer, cellulitis, or a deep space infection. Concurrent peripheral neuropathy often alters the patient's perception of pain. Fever and systemic toxicity are frequently absent.

Physical examination commonly reveals diminished dorsal pedis and posterior tibia pulses, poor capillary refill, and decreased sensation.

Chronic osteomyelitis

No exact criteria exist for defining when acute osteomyelitis becomes chronic. Clinically, the first bone infection is considered acute, and relapse of bone infection is labeled chronic. However, this simplistic classification is clearly inadequate. The hallmark of chronic osteomyelitis is the presence of dead bone (the sequestrum). Involucrum (reactive bony encasement of the sequestrum), local bone loss, persistent drainage, and/or sinus tracts are other common features of chronic disease.

The patient with chronic osteomyelitis commonly presents with chronic pain and sinus formation with purulent drainage. Fever is usually low grade or absent. The chronic infection usually does not progress or does so slowly. If a sinus tract becomes obstructed, the patient can present with a localized abscess, soft tissue infection, or both.

Prospects of halting the infection are reduced when the integrity of surrounding soft tissue is poor or the bone is unstable due to an infected nonunion or an adjacent septic joint. Squamous cell carcinoma at the site of tissue drainage and amyloidosis are rare complications of chronic osteomyelitis.

Host factors

Systemic host factors affecting immune surveillance, metabolism, and vascularity include the following:

Diabetes mellitus

Renal, hepatic failure

Malnutrition

Chronic hypoxia

Immunosuppression

Immunodeficiency

Malignancy

Immune disease

Extremes of age

Local host factors affecting immune surveillance, metabolism, and vascularity include the following:

Major vessel compromise

Small and medium vessel disease

Extensive scarring

Arteritis

Radiation fibrosis

Chronic lymphedema

Tobacco abuse (>2 packs per day)

Neuropathy

Venous stasis

Indications

Successful management of osteomyelitis requires aggressive pursuit of the diagnosis and early antimicrobial and surgical therapy. If acute osteomyelitis is not treated optimally, the risk is high of developing chronic osteomyelitis, which is significantly less amenable to treatment.

Staging and classification systems may be used in determining appropriate treatment for osteomyelitis.

Surgical intervention is indicated in the following situations:

The patient has not responded to specific antimicrobial therapy within 48 hours.

Evidence exists of a persistent soft tissue abscess.

Concomitant joint infection is suspected or diagnosed.

In adults with hematogenous osteomyelitis, a thorough intramedullary reaming and unroofing is usually performed with or without bone grafting. Soft tissues are reapproximated, and the limb is protected by external means (brace or cast) until the structural integrity of the bone is reestablished by normal remodeling.

Relevant Anatomy and Contraindications

Relevant Anatomy: In long bones such as the tibia and femur, the metaphysis is most frequently involved, probably due to the anatomy of this region. The organization of blood vessels feeding the metaphyseal region leads to a slowing of blood flow in this area, which presumably allows bacteria to settle and initiate an inflammatory response. The nutrient artery ends in the metaphyses as marrow capillaries that make sharp loops near the growth plate and enter a system of large venous sinusoids where the blood flow becomes slow and turbulent. These capillary loops are essentially the end-artery branches of the nutrient artery .The histology of the region may also contribute to the localization of infection. The metaphyseal capillaries lack phagocytic lining cells, and the sinusoidal veins contain functionally inactive phagocytic cells, both of which allow growth of microorganisms. In addition, any form of end-capillary obstruction could produce an area of avascular necrosis. Minor trauma probably predisposes the infant or child to infection by producing a small hematoma, vascular obstruction, and subsequent bone necrosis, which leaves the region susceptible to inoculation from a transient bacteremia.

Acute infection initially produces a local cellulitis, which results in a breakdown of leukocytes, increased bone pressure, reduced pH, and decreased oxygen tension. The cumulative effects of these physiologic factors further compromise the medullary circulation and enhance the spread of infection. Infection may proceed laterally through the haversian and Volkmann canal system, perforate the bony cortex, and lift the periosteum from the surface of the bone. When this occurs in the presence of medullary extension, the periosteal and endosteal circulations are compromised, capillaries are lost, and large segments of cortical and cancellous (trabecular) bone die.

In infants, medullary infection may spread to the epiphysis and joint surfaces through capillaries that cross the growth plate. In contrast, in children older than 1 year, the growth plate is avascular and infection is confined to the metaphysis and diaphysis.

The joint is spared unless the metaphysis is intracapsular. Thus, cortical perforation at the proximal radius, humerus, or femur enables the infection to migrate to the elbow, shoulder, or hip joint, respectively, regardless of the age of the patient.

Contraindications : Contraindications to debridement of infected bone are limited and include the following:

In acute osteomyelitis in infants, the infection usually responds well to medical therapy alone. Surgery should be reserved for nonresponsive cases.

Suspicion of malignancy or presence of secondary bone infection with malignancy should not be treated with debridement alone. Tumor workup and biopsy should be performed first. If infection cannot be eradicated or tumor is not resectable, amputation is indicated.

Massive debridement is not recommended in the presence of sickle cell disease; usually a mixture of infection and avascular necrosis is present that may improve after good reperfusion. Massive debridement may produce very large defects that may not be easily amenable to reconstruction surgeries.

The use of a tourniquet is not recommended by many authors due to the acute bacteremic phase after the tourniquet is released and toxemia.

Local anesthesia is generally ineffective and should be avoided due to the change in the local Ph of the tissue that prevents the metabolism of the local anesthetics to the active ingredients.

The general condition of the patient should not be considered a contraindication to urgent surgery. Delaying surgery may lead to further deterioration.

Workup

Lab Studies:

Routine laboratory test findings are usually nonspecific. These include CBC count, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), renal and hepatic profile, and bone profile.

Complete blood count: Leukocytosis is common in acute osteomyelitis but not in chronic osteomyelitis.

Erythrocyte sedimentation rate

The ESR is usually elevated but may be in the reference range. In a patient with a high ESR initially, monitoring the ESR may be useful in detecting a relapse. In patients with a foot ulcer and diabetes mellitus, an ESR greater than 100 mm/h is highly specific but insensitive for a diagnosis of osteomyelitis. n Although ESR is associated with low sensitivity and specificity, it is widely employed. In the patient without a prior history of osteomyelitis, the ESR is most helpful when infection is unlikely. For example, in patients with low-back pain but without historical clues to suggest vertebral osteomyelitis (eg, recent urinary tract infection), a normal ESR is a reassuring finding. Conversely, an elevated ESR suggests the need for further evaluation.

C-reactive protein

CRP, like ESR, is an acute-phase reactant. Although said to be more specific for infection than ESR, it is also relatively insensitive and nonspecific.

The primary difference between these tests is that the CRP has a shorter half-life than the ESR. Measuring in vitro clumping of venous leukocytes (leukergy) may more closely correlate with severity of infection than the ESR.

Renal and hepatic profile: Whether leukergy, which reflects altered surface expression of leukocyte adhesion molecules, will be useful for managing osteomyelitis is not known. This test is not routinely available.

Efforts have been made to develop serologic assays to diagnose osteomyelitis caused by S aureus. Patients with osteomyelitis mount a vigorous antibody response, but the utility of detecting antibodies to cell wall components such as peptidoglycan or teichoic acid has been limited by the presence of such antibodies in uninfected, healthy persons. In a preliminary study, serum antibodies to S aureus exoproteins differentiated 3 cases of S aureus osteomyelitis from 4 cases caused by other organisms. Another limitation of serology is that it is unlikely to be developed for nonstaphylococcal disease. However, highly specific assays for staphylococcal osteomyelitis would be very useful. At present, serology cannot be recommended clinically, and such tests are available only for research purposes.

Blood culture results are positive in 50% percent of cases of acute osteomyelitis. A positive blood culture result in a patient with radiological findings consistent with osteomyelitis obviates the need for biopsy to obtain the specific microbiologic diagnosis.

Imaging Studies:

Plain films : Plain radiographs are relatively inexpensive, may be used to make the diagnosis, help in interpreting and choosing other studies, and allow one to exclude other conditions (eg, gas in the soft tissues). In uncomplicated acute infection, the triad of soft tissue swelling, bone destruction, and periosteal reaction is fairly specific for osteomyelitis and is sufficient to warrant a course of therapy (empiric until the microbiologic diagnosis has been established).

Plain films are generally insensitive for the diagnosis of acute osteomyelitis. This is in part due to the 2-3 weeks required for bone changes to be evident on plain films, although changes may be seen at this time on the other imaging modalities. Furthermore, in complicated situations, bone changes may not be distinguishable from those due to another process, such as a Charcot joint, fractures, or cancer. Thus, the diagnosis of acute osteomyelitis cannot be excluded if the plain film findings are negative. Further testing should be performed because early therapy is essential to reduce the formation of necrotic bone and the development of chronic osteomyelitis.

The primary findings are different in chronic osteomyelitis, which is characterized by bone sclerosis, periosteal new bone formation, and sequestra. It is difficult to distinguish active from inactive infection.

CT scan : This modality is used to evaluate an area in which focal findings are present on examination and plain films findings are negative. The CT scan (with and without contrast) is very accurate for detecting cortical destruction, intraosseous gas, periosteal reaction, and soft tissue extension.

MRI : This study is an alternative to CT scan and is especially useful in evaluating a patient for osteomyelitis in the vertebrae and in the infected foot. In vertebral osteomyelitis, findings on T1-weighted images include decreased signal intensity in the disk and adjacent vertebral bodies and loss of endplate definition. Findings on T2-weighted images include increased signal intensity in the disk and adjacent vertebral bodies. With gadolinium, there is enhancement of the disk, adjacent vertebral bodies, and involved paraspinal and epidural soft tissue.

MRI provides useful anatomic detail in planning for surgical debridement, since it may show abscesses that need drainage, and can reduce the risk of operating on bland cellulitis. MRI can also be used to delineate soft tissue/epidural involvement and spinal cord impingement that cannot be seen on nuclear medicine images.

When evaluating the foot for osteomyelitis, MRI is as specific or more specific and more sensitive than technetium bone scan. In one series in which bone biopsy was used as the criterion standard, the sensitivity was 72% for MRI, 68% for bone scan, and 45% for indium white blood cell scan.

MRI cannot be used in patients with certain metal implants. In addition, false-positive results can occur with bone infarct or fracture or in healed osteomyelitis. Differentiating cancer from osteomyelitis may be difficult with MRI.

MRI for diabetic foot ulcers

The diagnosis of osteomyelitis in diabetic foot ulcers is often missed because of 2 major factors: most cases occur in ulcers not exposing bone and most have no evidence of inflammation on physical examination. In comparison, osteomyelitis was present in all patients in whom bone was exposed in one series.

MRI is the imaging procedure of choice for osteomyelitis in diabetic foot ulcers, being more accurate than the other modalities (95% vs 50-70% for plain films, bone scan, and indium scan in one series). Two clinical factors also may be useful in these patients, probing the ulcer and ulcer size.

Ultrasonography : Ultrasound findings consistent with osteomyelitis include fluid collection adjacent to the bone without intervening soft tissue, elevation of the periosteum by more than 2 mm, and thickening of the periosteum. Ultrasound may also improve the yield from fine-needle biopsies.

Scintigraphy : Multiple different nuclear medicine imaging procedures are available to evaluate for osteomyelitis, including bone scan, indium-labeled leukocyte scan, and bone marrow scan.

Histologic Findings : Acute osteomyelitis presents as a suppurative infection with acute inflammatory cells, accompanied by edema, vascular congestion, and small vessel thrombosis. In early acute disease, the vascular supply to the bone is compromised by infection extending into the surrounding soft tissue. When both the medullary and periosteal blood supplies are compromised, large areas of dead bone (sequestra) may be formed. Within this necrotic and ischemic tissue, the bacteria can be difficult to eradicate even after an intense host response, antibiotic therapy, or both.

Pathologic features of chronic osteomyelitis include necrotic bone, the formation of new bone, and polymorphonuclear leukocyte exudation joined by large numbers of lymphocytes, histiocytes, and occasional plasma cells.

Host defense and mesenchymal cells, mainly the polymorphonuclear leukocytes, macrophages, and the osteoclasts, release proteolytic enzymes that break down organic elements in the dead bone. Because of lost blood supply, dead bone appears whiter than living bone. Cancellous bone is absorbed rapidl

Submitted By:
AHMED BO-EISA, MD

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