eMedicine Specialties > Radiology > Musculoskeletal
Osteomyelitis, Acute Pyogenic
Updated: Feb 10, 2009
Introduction
Background
Acute osteomyelitis is an inflammation of bone caused by an infecting organism. Staphylococcus aureus is the most common bacterium involved in the infection.1,2
On the basis of the route of infection, acute osteomyelitis can be classified as hematogenous or exogenous. Hematogenous osteomyelitis is predominantly seen in children and involves the highly vascular long bones, especially those of the lower limb. In adults, hematogenous spread is more common to the lumbar vertebral bodies than elsewhere.
Chest radiograph in an 8-year-old girl who presented with staphylococcal pneumonia.
Streptococcal osteomyelitis in a 3-year-old patient presenting with periosteal new-bone formation of the tibia.
Before puberty, infection starts in the metaphyseal sinusoidal veins. Because bones are relatively rigid structures, focal edema accumulates under pressure and leads to local tissue necrosis, breakdown of the trabecular bone structure, and removal of bone matrix and calcium. Infection spreads along the haversian canals, through the marrow cavity, and beneath the periosteal layer of the bone. Subsequent vascular damage causes the ischemic death of osteocytes, leading to the formation of a sequestrum. Periosteal new-bone formation on top of the sequestrum is known as involucrum.
Osteomyelitis may be acute, subacute, or chronic. With acute osteomyelitis, the presenting complaint is usually local pain, swelling, and warmth. These often occur in association with fever and malaise.
Osteomyelitis (from Orthopedic Surgery)
Osteomyelitis (from Emergency Medicine)
Pathophysiology
In summary, the pathophysiology depends on the degree of soft tissue damage and impairment of the blood supply; instability of the fracture fragments; inoculation of the bacterial flora; and the immune system of the host.3
Microbiology
Causative organisms may be summarized by patient group, as follows:
- Children younger than 1 year: Group B Streptococcus species, Staphylococcus aureus, Haemophilus influenza (5-50%), and Escherichia coli
- Children older than 1 year: S aureus, E coli, H influenza, Serratia marcescens, and Pseudomonas aeruginosa
- Adults: S aureus, E coli, S marcescens, and P aeruginosa
- Individuals with sickle cell anemia and trait: Salmonella species and S aureus
- Individuals with diabetes: Gram-positive cocci, such as Streptococcus, Staphylococcus, and Enterobacter species
- Individuals with an exogenous route of infection: Multiple organisms, including anaerobes and Pseudomonas species
S aureus is the causative agent in 70-90% of pediatric cases. Bacteria pass through nutrient vessels to the metaphyses, where they become lodged and proliferate. The physeal plate acts as a barrier to epiphyseal extension of infection because it is avascular. Infection commonly spreads from the primary intramedullary focus via the haversian canals of the cortex to the subperiosteal space, forming a subperiosteal abscess. If this ruptures, the infection extends into the overlying soft tissues. Metaphyseal inflammation leads to exudation, increased intraosseous pressure, vascular stasis, thrombosis, bone necrosis, and bone resorption. Sometimes, infection extends to the adjacent joint.
Tubular bones have the most rapid growth and the largest metaphyses; therefore, they are common sites of infection. As many as 75% of children have infections in sites such as distal and proximal femur and tibia, distal humerus, and fibula.
In older children, the infecting organism is usually S aureus, whereas in neonates and infants, group A beta-hemolytic Streptococcus organisms are common causative organisms. Mycobacterium species, Gram-negative bacteria, syphilis, and fungal and viral agents are less common causes of osteomyelitis. Salmonella osteomyelitis may occur, particularly in children with sickle cell disease. Local trauma may reduce host resistance and predispose an individual to osteomyelitis.
A Brodie abscess is a localized form of osteomyelitis that appears in a subacute stage without preceding acute symptoms. Histologic evaluation shows an intraosseous abscess cavity lined by granulation tissue. The infecting organism is usually S aureus. Patients typically present with relatively mild pain, which recurs over several months or sometimes years. The most common sites are the tibial or femoral metaphysis or diaphysis. The infection may cross the growth plate. Local soft tissue swelling is minimal, and no soft tissue mass is present.
Stages of disease
The disease process involves 5 stages:
- Inflammation: This stage represents initial inflammation with vascular congestion and increased intraosseous pressure. Obstruction to blood flow occurs with intravascular thrombosis.
- Suppuration: Pus within the bones forces its way through the haversian system and forms a subperiosteal abscess in 2-3 days.
- Sequestrum: Increased pressure, vascular obstruction, and infective thrombus compromise the periosteal and endosteal blood supply, causing bone necrosis and sequestrum formation in approximately 7 days.
- Involucrum: This is new bone formation from the stripped surface of periosteum.
- Resolution or progression to complications: With antibiotics and surgical treatment early in the course of disease, osteomyelitis resolves without any complications.
Hematogenous osteomyelitis
The spread of infection is usually hematogenous. Among children, the metaphysis of the long bones is the most common site; blood flow slows in the sinusoids, allowing bacteria to adhere to the vascular membranes. Local trauma with skin penetration and seeding of organisms is another pathway. Localized trauma to the bone, which causes hematoma and vascular obstruction in the metaphyseal region, and transient bacteremia around the same time result in infection.
Hematogenous disease involves the bones. In children and adults, the femur, humerus, and tibia are typically affected. In adults, the vertebral bodies may be affected as well.
Risk factors for hematogenous osteomyelitis in adults include the following:
- Indwelling vascular catheter
- Intravenous drug abuse
- Dialysis
- Immunocompromised state (eg, caused by HIV infection or use of immunosuppressive drugs)
- Indwelling urinary catheter
- Old age, debilitated state
- Recent history of pneumonia, urinary tract infection (UTI), or skin infection
Hematogenous spread mainly extends to the vertebral bodies from the Batson plexus. Pus spreads anteriorly along the vertebral body to form a paravertebral abscess, or it spreads posteriorly to form and extradural abscess. Weakening of the body results in collapse of the vertebra.
Exogenous osteomyelitis
With exogenous disease, the spread of infection may be the result of (1) direct trauma and the inoculation of infectious material in compound fractures; (2) iatrogenic causes, such as surgical procedures (eg, internal fixation of fractures, joint replacement); and (3) contiguous spread from soft tissue infections surrounding the bone, especially in individuals with diabetes.
Complications of osteomyelitis
Complications of osteomyelitis include sequestrum formation with recurrent relapses; skin sinus formation; and damage to the growth plate causing tethering, physeal bar, and subsequent growth deformity.
Frequency
United States
The prevalence in children younger than 1 year is 1 in 1000. The prevalence in older children is 1 in 5000.
The incidence of acute osteomyelitis in adults with diabetes is 30-40%, after puncture wounds to the feet. The incidence is 0.1-1.8% in the healthy adult population.
The incidence in sickle cell disease is 0.46%.
International
No figures are available to suggest that the incidence of acute osteomyelitis outside the US is different from that in the US. However, the incidence in young children may be higher in developing countries than elsewhere.
Mortality/Morbidity
In the preantibiotic era, the mortality rate was as high as 25-40%. Antibiotics have reduced the rate to almost 0%; the complication rate is about 5%.
Complications include the following: (1) chronic osteomyelitis resulting from the persistence of the infective organisms (5-25%), (2) metastatic infection, (3) septic arthritis in children younger than 2 years as a result of the transphyseal spread of the infection (in adults, it occurs in the joints where the epiphysis is enclosed in the joint capsule [eg, hip and elbow joints]), (4) angular deformity of bones as a result of arrest of bone growth, (5) pathologic fractures, (6) bacteremia and septicemia, (7) soft tissue infection and persistent sinuses, and (8) premature epiphyseal fusion.
O'Daly and associates retrospectively analyzed 23 cases of pyogenic spinal infections with the view of assessing long-term adverse functional outcome following pyogenic spinal infection using standardized outcome measures, the Oswestry disability index (ODI), and medical outcomes study short form-36 (SF-36).4 The patients were a mixed group; 23% were managed operatively, and 72% were managed with antibiotic therapy alone. Nineteen patients (66%) were found to have had an adverse outcome at a median follow-up of 61 months; only 5 patients (17%) had persistent neurologic deficit. In this study, high rates of adverse outcomes were detected using SF-36 and ODI, which suggests that poor outcomes are under-reported when the American Spinal Injury Association score alone is used to qualify outcome.
Race
The incidence of osteomyelitis associated with sickle cell disease is higher in people of African descent than in others.
Sex
Studies show a male preponderance, with a male-to-female ratio of 1.5:1 to 2:1.
Age
Persons of any age may develop osteomyelitis, but the disease is more common in neonates than in others.
Anatomy
The capillary ends of the nutrient artery are sharp, nonanastomosing loops, which enter the large venous sinusoids. This vasculature causes slowing of the circulation and a reduction in oxygen tension. The capillaries do not communicate because columns of calcified cartilage separate them from each other.
Children younger than 2 years of have transphyseal vessels, which cross from metaphysis to epiphysis. This causes the spread of infection into the joint. In children older than 2 years, the transphyseal vessels are absent; hence, the epiphyseal plate acts as a barrier to the spread of infection into the joint.
Presentation
Osteomyelitis may be acute, subacute, or chronic. With acute osteomyelitis, the presenting complaint is usually local pain, swelling, and warmth. These often occur with associated fever and malaise. Clinical examination reveals pyrexia, local erythema, and tenderness. Laboratory studies typically show leukocytosis and an elevated C-reactive protein (CRP) level and erythrocyte sedimentation rate (ESR).
Findings in infants include the following:
- Failure to thrive
- Drowsiness but irritability
- Minimal constitutional symptoms
- Effusions into neighboring joints (60%)
Findings in older children include the following:
- History of preceding minor trauma to the involved limb. recent infection (eg, upper respiratory tract infection or skin infection), or both
- Bone pain
- Malaise, irritability, and anorexia
- Fever
- Reluctance to use the limb
- Localized swelling, redness, and warmth
- Tenderness to finger pressure at a particular point
- Pain on moving an adjacent joint
- Regional lymphadenopathy
Findings in those with sickle cell disease include the following:
- Multiple areas of involvement in the diaphyses of long bones are more common than involvement of the metaphysis.
- Symptoms of fever, bone pain, swelling, and erythema are common for both osteomyelitis and acute bone crisis.
- Acute bone crisis is 50 times more common than acute osteomyelitis in patients with sickle cell disease.
- S aureus is commonly isolated in patients with sickle cell disease, though historically, Salmonella organisms are known to be the causative organisms.
Findings in adults include the following:
- With posttraumatic osteomyelitis, the disease may occur 1 week to 3 months after the injury.
- Severe systemic upset may be absent.
- Vertebral osteomyelitis may be present.
- Symptoms may include backache, reduced range of movement in the spine, and spasm of the paraspinal muscles.
- There may be tenderness of the spinous processes to palpation.
Involvement of the lumbar spine is more common than involvement of the thoracic or cervical spine. The incidence of paralysis is higher when thoracic or cervical spine is involved.
Preferred Examination
Imaging plays an important role in the diagnosis of osteomyelitis. It should always start with plain radiographs of the affected area. Current imaging recommendations include plain radiography followed by 3-phase bone scanning and/or MRI, if available.
Although osseous changes become apparent on conventional radiographs 5-7 days into the disease process, plain radiographs are useful in ruling out other causes of bone pain, such as stress fractures. Plain radiography and radionuclide bone scanning greatly aid early diagnosis in cases of acute osteomyelitis. Plain radiography is useful for excluding other conditions; radionuclide scanning reveals evidence of inflammation at the site of bone pain.
Nuclear medicine bone scans are a highly sensitive (>90%) modality in the diagnosis of osteomyelitis. This procedure is performed in 3 stages. Technetium-99m (99m Tc) is used to create images to determine areas of infection and bone remodeling dependent on local blood flow. The sensitivity of bone scans is often helpful when the exact site and extent of the infection is not known.
CT scanning allows for 3-dimensional (3D) examination of bone and surrounding soft tissue. CT scanning is an excellent modality for depicting periosteal new-bone formation and cortical bone destruction and for determining whether any sequestration or involucrum is present. Contrast-enhanced CT may show a ring-enhancing soft tissue abscess.
MRI, if available, is another useful modality for imaging acute osteomyelitis. Findings on MRI accurately demonstrate the extent and structure of the area involved in the pathologic process. The reported sensitivity is 88-100%; the specificity is 75-100%. Fat-suppression sequences allow for better detection of bone marrow edema; however, infection and inflammation cannot be differentiated. MRI may be the imaging modality of choice for infections involving the spine, pelvis, or limbs because of its ability to provide fine details of the osseous changes and soft tissue extension in these areas.
Additional imaging may be performed with indium-111–labeled leukocytes; gallium is used as needed. Gallium seems especially valuable in monitoring the efficacy of treatment. Urso and associates evaluated 40 pediatric patients (aged 2-16 y) with osteomyelitis to assess the roles of various imaging modalities, including conventional radiology, bone scanning with99m Tc methylene diphosphonate (MDP), scintigraphy with99m Tc hexamethylenepropyleneamineoxime (HMPAO)–labeled leukocytes, CT, and MRI.5
The modalities were used to detect lesions, to make a differential diagnosis, and to assess disease stages. As for acute osteomyelitis (6 patients), conventional radiography showed a lytic lesion and periosteal new-bone formation and soft tissue swelling (4 of 6 patients). (No abnormalities were demonstrated in the other 2 patients.) Bone scanning, CT, and MRI depicted bone involvement. CT and MRI also showed involvement and the spread of an inflammatory lesion to surrounding soft tissue.99m Tc-HMPAO scintigraphy was not performed to assess acute osteomyelitis, because of technical difficulties in performing the study promptly; thus, early analysis of the nature of the lesion was made with bone biopsy.
As for subacute osteomyelitis,99m Tc-HMPAO scintigraphy was performed in 8 of 23 patients; it proved to be highly sensitive, showing cell clusters and confirming the diagnosis of an inflammatory lesion. T1-weighted MRIs showed a focal area of intermediate to low signal intensity. These MRIs also showed small, focal, intralesional areas of low intensity; a low-signal perifocal rim; and diffusely low signal intensity of the surrounding bone marrow. T2-weighted images showed high signal intensity in both the abscess lesion and the bone marrow; the latter was probably the result of edema. For 5 patients, a paramagnetic contrast agent (gadopentetate dimeglumine) was administered during MRI and resulted in inhomogeneous enhancement of both the inflammatory lesion and the surrounding bone marrow.
Regarding chronic osteomyelitis (7 patients), MRI was performed in 5 patients. In 4 patients, the lesion appeared as a hypointense area on T1-weighted images; T2-weighted images showed an inhomogeneous hyperintense area. In the same patients,99m Tc-HMPAO scintigraphy was always positive. In the fifth patient, the lesion was represented by a hypointense area on both T1- and T2-weighted images;99m Tc-HMPAO scans were negative.
Therefore, in cases of chronic osteomyelitis, both MRI and99m Tc-HMPAO were useful in detecting spinal and peripheral bone involvement, which was asymptomatic at first observation in some cases. Conventional radiography, CT findings (3 of 4 patients), and MRI findings (4 of 4 patients) of extra-axial localizations were similar to those in the subacute-chronic forms.
Limitations of Techniques
Plain radiographs are often normal for at least 1 week following infection; the findings are nonspecific.
MRI is contraindicated in patients with certain implant devices and metallic clips, and it is not tolerated by all patients because of claustrophobia or morbid obesity. In addition, young children may require sedation. Use of MRI requires patient cooperation because patient motion may degrade the images.
CT is quick and inexpensive but exposes the patient to ionizing radiation. The risk of a reaction to radio-iodinated contrast material is low; the detection of bone destruction or a paraspinal mass does not require the use of contrast material.
Although radionuclide studies are sensitive, they can be time-consuming, and they have lower spatial resolution. The incidence of false-negative scans is low in neonates and in elderly patients with osteomyelitis.
Differential Diagnoses
Ewing Sarcoma
Osteomyelitis, Chronic
Septic Arthritis
Stress Fracture
Other Problems to Be Considered
Osteosarcoma
Juvenile arthritis
Other causes of periosteitis
Acute rheumatism
Sickle cell crisis
Gaucher disease
Eosinophilic granuloma
Chronic granulomatous disease of childhood
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References
Dirschl DR. Acute pyogenic osteomyelitis in children. Orthop Rev. Apr 1994;23(4):305-12. [Medline].
Kharbanda Y, Dhir RS. Natural course of hematogenous pyogenic osteomyelitis (a retrospective study of 110 cases). J Postgrad Med. Apr 1991;37(2):69-75. [Medline].
Dirschl DR, Almekinders LC. Osteomyelitis. Common causes and treatment recommendations. Drugs. Jan 1993;45(1):29-43. [Medline].
O'Daly BJ, Morris SF, O'Rourke SK. Long-term functional outcome in pyogenic spinal infection. Spine. Apr 15 2008;33(8):E246-53. [Medline].
Urso S, Pacciani E, Fariello G, et al. [Nonspecific osteomyelitis in childhood and adolescence. The contribution of imaging diagnosis]. Radiol Med (Torino). Sep 1995;90(3):212-8. [Medline].
Lipman BT, Collier BD, Carrera GF, et al. Detection of osteomyelitis in the neuropathic foot: nuclear medicine, MRI and conventional radiography. Clin Nucl Med. Feb 1998;23(2):77-82. [Medline].
Chandnani VP, Beltran J, Morris CS, et al. Acute experimental osteomyelitis and abscesses: detection with MR imaging versus CT. Radiology. Jan 1990;174(1):233-6. [Medline].
Piazza P, Comoretto M, Lutman M. [Computed tomography in acute inflammation of the orbit]. Radiol Med (Torino). Mar 1994;87(3):235-9. [Medline].
Azouz EM. Computed tomography in bone and joint infections. J Can Assoc Radiol. Jun 1981;32(2):102-6. [Medline].
Erdman WA, Tamburro F, Jayson HT, et al. Osteomyelitis: characteristics and pitfalls of diagnosis with MR imaging. Radiology. Aug 1991;180(2):533-9. [Medline].
Chao HC, Kong MS, Lin TY, et al. Sonographic and color Doppler sonographic diagnosis of acute osteomyelitis: report of one case. Acta Paediatr Taiwan. Jul-Aug 1999;40(4):268-70.
Cleveland TJ, Peck RJ. Case report: chronic osteomyelitis demonstrated by high resolution ultrasonography. Clin Radiol. Jun 1994;49(6):429-31. [Medline].
Taneja K, Mittal SK, Marya SK, et al. Acute osteomyelitis: early diagnosis by ultrasonography. Australas Radiol. Feb 1992;36(1):77-9. [Medline].
Abernethy LJ, Lee YC, Cole WG. Ultrasound localization of subperiosteal abscesses in children with late-acute osteomyelitis. J Pediatr Orthop. Nov-Dec 1993;13(6):766-8. [Medline].
Kang B, Zhu TB, Du JY, et al. Sonographic diagnosis of acute hematogenous osteomyelitis in the early stage. J Tongji Med Univ. 1994;14(1):61-4. [Medline].
Chao HC, Lin SJ, Huang YC, Lin TY. Color Doppler ultrasonographic evaluation of osteomyelitis in children. J Ultrasound Med. Nov 1999;18(11):729-34; quiz 735-6. [Medline].
Riebel TW, Nasir R, Nazarenko O. The value of sonography in the detection of osteomyelitis. Pediatr Radiol. 1996;26(4):291-7. [Medline].
Larcos G, Antico VF, Cormick W, et al. How useful is ultrasonography in suspected acute osteomyelitis?. J Ultrasound Med. Sep 1994;13(9):707-9. [Medline].
Peters AM. The utility of [99mTc]HMPAO-leukocytes for imaging infection. Semin Nucl Med. Apr 1994;24(2):110-27. [Medline].
Johnson JE, Kennedy EJ, Shereff MJ, et al. Prospective study of bone, indium-111-labeled white blood cell, and gallium-67 scanning for the evaluation of osteomyelitis in the diabetic foot. Foot Ankle Int. Jan 1996;17(1):10-6. [Medline].
Schauwecker DS, Park HM, Mock BH, et al. Evaluation of complicating osteomyelitis with Tc-99m MDP, In-111 granulocytes, and Ga-67 citrate. J Nucl Med. Aug 1984;25(8):849-53. [Medline].
Becker W. Imaging osteomyelitis and the diabetic foot. Q J Nucl Med. Mar 1999;43(1):9-20. [Medline].
Biviji AA, Paiement GD, Steinbach LS. Musculoskeletal manifestations of human immunodeficiency virus infection. J Am Acad Orthop Surg. Sep-Oct 2002;10(5):312-20. [Medline].
Carragee E, Iezza A. Does Acute placement of instrumentation in the treatment of vertebral osteomyelitis predispose to recurrent infection: long-term follow-up in immune-suppressed patients. Spine. Sep 1 2008;33(19):2089-93. [Medline].
Gold RH, Tong DJ, Crim JR, Seeger LL. Imaging the diabetic foot. Skeletal Radiol. Nov 1995;24(8):563-71. [Medline].
Isobe Z, Utsugi T, Ohyama Y, et al. Recurrent pyogenic vertebral osteomyelitis associated with type 2 diabetes mellitus. J Int Med Res. Sep-Oct 2001;29(5):445-50. [Medline].
Loredo R, Metter D. Imaging of the diabetic foot. Emphasis on nuclear medicine and magnetic resonance imaging. Clin Podiatr Med Surg. Apr 1997;14(2):235-64. [Medline].
Reid PJ, Holman PJ. Iatrogenic pyogenic osteomyelitis of C-1 and C-2 treated with transoral decompression and delayed posterior occipitocervical arthrodesis. Case report. J Neurosurg Spine. Dec 2007;7(6):664-8. [Medline].
Wong AL, Sakamoto KM, Johnson EE. Differentiating osteomyelitis from bone infarction in sickle cell disease. Pediatr Emerg Care. Feb 2001;17(1):60-3; quiz 64. [Medline].
Further Reading
Keywords
acute osteomyelitis, subacute osteomyelitis, chronic osteomyelitis, bone inflammation, hematogenous osteomyelitis, exogenous osteomyelitis
