3 Infections of the Bones, Joints, and Soft tissues

3.1 Osteomyelitis and Osteitis

3.1.1 Terminology, Classification, and Infection Routes

Mycobacteria are—even in Europe and the United States—important pathogens for spondylitis (Chapter 3.1.5), osteomyelitis, and septic arthritis.

• The patient’s age: With osteomyelitis presenting an acute clinical course, a distinction is made between neonatal, pediatric, and (less common) adult forms.

3.1.2 Hematogenous Osteomyelitis

About 95% of cases of hematogenous osteomyelitis assume an acute course. It is divided according to age into neonatal, pediatric, and adult osteomyelitis, with the latter more frequently seen in patients over the age of 50 years (see spondylitis and spondylodiskitis in Chapter 3.1.5).

Brodie abscess is the predominant manifestation of the chronic hematogenous forms of osteomyelitis. If primarily acute hematogenous osteomyelitis assumes a chronic course, due to inadequate therapy, then this is also referred to as chronic hematogenous osteomyelitis. This applies, for example, to patients with a mixed spectrum of pathogens that has not been fully covered by antibiotics. Abscesses inadequately treated surgically are possible causes. It almost exclusively affects adults. The bacteria present in bone that has undergone reactive change and is commonly sclerotic are capable of triggering a renewed inflammatory episode at some future time. A reduced immune response, e.g., due to HIV infection or during chemotherapy and/or steroid therapy, is a possible contributory factor to reactivation.

Pathology. The medullary cavity is saturated with edema and filled with granulocytes. Osteocytes are hardly, or no longer, detectable. The associated ischemia can lead to sequestrum formation. Liquefaction of necrotic tissue results in the development of an abscess within the bone. Healing commences with the proliferation of connective tissue and capillary ingrowth.

Neonatal osteomyelitis. This is a highly acute disease with a predilection for the femoral metaphysis. Organisms are predominantly streptococci. If the infection spreads via the haversian canals into the subperiosteal space and/or via the still patent metaphyseal–epiphyseal vascular connections, the infection will involve the epiphysis.

Pediatric osteomyelitis. The metaphyseal–epiphyseal vessels occlude with increasing age. Dilated vascular loops are present in the metaphysis, favoring pathogen colonization. This is the reason why the focus of inflammation initially develops in the metaphysis. Rapid penetration of the thin cortical bone ensues, with subsequent subperiosteal spread of the infection. The periosteum is elevated. The infection can then spread to the adjacent joint, especially if the metaphysis is located within the joint capsule, as with the hip and knee joints.

Acute osteomyelitis of adulthood. Acute osteomyelitis at this age is being increasingly diagnosed, affecting primarily the vertebrae (Chapter 3.1.5).

Clinical presentation. Acute hematogenous osteomyelitis is a systemic disorder. Early symptoms include fever, chills and localized pain with focal swelling, erythema, and increased skin temperature. CRP and white blood cell count are elevated. In ~ 50% of cases it is possible to identify the pathogen in blood cultures.

Radiography. A number of findings should be looked for on the radiographs:

• The type and degree of bone destruction vary. A wide spectrum is possible, ranging from diffuse reduction of density, via solitary radiolucency, irregular multiple radiolucencies (moth-eaten or mottled pattern) to an extensive permeative pattern.

• The margins of the lesions are usually ill-defined and irregular ( Fig. 3.1) so that it is not possible to determine the exact extent of the infection.

• Uni- to multilaminated (onion skin) periosteal reactions are invariably found ( Fig. 3.2).

• The reparative phase during treatment and neglected chronic forms of osteomyelitis are characterized by endosteal and periosteal new bone formation, development of marginal sclerosis around the lesion and, in part, extensive areas of osteosclerosis.

• In neonatals and small children, radiographs already allow an early (within the first days after onset of symptoms) presumptive diagnosis of soft tissue swelling based on the obliteration of fat lines. The skeletal alterations require at least 7 to 10 days before they become radiographically evident. The laminated periosteal reactions are sometimes recognized before bone destruction. A late sign in this age group is swelling of the metaphysis, sometimes also involving the epiphysis. During the late phase of the disease, the extensive periosteal reaction can appear as periosteal ossification.

US. Imaging conditions are particularly favorable during the neonatal period. The first sign, evident even before any periosteal reaction, is the hypoechoic, or even hyperechoic, edematous soft tissue swelling. Then a thin, hypoechoic fluid layer develops, elevating the periosteum ( Fig. 3.3). This can go on to form a space-occupying abscess with an anechoic to hypoechoic intralesional structure and hyperechoic wall ( Fig. 3.4). With good imaging conditions, destruction of the cortex can be well visualized as disruption or distortion of the contour ( Fig. 3.5).

The diagnostic value of ultrasound decreases with increasing age of the patient. In osteomyelitis, its indication is essentially restricted to providing additional diagnostic soft tissue information. Abscesses, cysts, and hematomas are excellently visualized as anechoic or hypoechoic lesions and are therefore amenable to ultrasound-guided aspiration.

MRI. Examination technique. Fluid-sensitive fat saturated sequences (STIR, PDW or T2W) serve as sequences for screening; the T1W sequence demonstrates the anatomy and provides characteristic findings within the bone marrow, while the T1W sequence with fat saturation after administration of contrast agent is of help with reliably diagnosing abscesses and sequestrum formation, although it is not generally required for routine diagnostics.

Morphology and signal behavior. This usually involves circumscribed, very signal-intense areas on fluid-sensitive sequences. Intramedullary lesions are hypointense on T1W images ( Figs. 3.6a and 3.8b). An edematous halo forms around the focal lesion, extending as an irregular and ill-defined manifestation of normal bone marrow. Instead of small circumscribed lesions, large diffuse areas of increased signal intensity are also possible ( Fig. 3.8).

Differentiation between osteomyelitis and arthritis can be problematic. Septic arthritis may result in concomitant (completely unspecific) edematous involvement of the epiphysis and metaphysis, without any pathogen-induced osteomyelitis having to be present. On the other hand, juxta-articular osteomyelitis often results in a reactive joint effusion ( Figs. 3.9 and 3.10; cf. Chapter 3.3). The diagnosis of (concomitant) osteomyelitis in association with septic arthritis should only be made if the cortical bone is clearly disrupted (clarification is best obtained on T1W or T2W sequences without fat saturation).

Intraosseous abscesses tend to be small in size in acute osteomyelitis (0.5–3 cm); commonly they are relatively sharply delineated and occasionally display a hypointense cuff of normal tissue on fluid-sensitive sequences. Additional confirmation of an abscess is the marked marginal enhancement with no, or distinctly less, contrast enhancement in the center of the lesion corresponding to the abscess ( Fig. 3.10).

NUC MED. Bone-seeking tracers are used for acute osteomyelitis. Multiphase bone scintigraphy using technetium (99mTc)-labeled diphosphonates is primarily used. Here, fully developed osteomyelitis will display a marked focal accumulation of the radionuclide in all three phases. Increased uptake in the blood-pool phase, without accumulation in the bone phase, is regarded as being indicative of an inflammation of only the soft tissue. Because of its radiation exposure, the use of multiphase bone scintigraphy has been reduced in favor of ultrasound and MRI, especially in children. Nor have other nuclear medicine imaging procedures (leukocyte scintigraphy, PET, and hybrid procedures such as PET-CT) been able to assert themselves as diagnostic modalities of choice for acute osteomyelitis.

Signs of healing of acute osteomyelitis. The first sign of healing to appear on the radiograph is progressive sclerosis, beginning at the periphery. The bone scan displays a reduction in activity, the MRI scan a resolution of the edematous changes and the soft tissue swelling with the development of contrast-enhanced (fibrovascular) granulation tissue. Contrast agent uptake becomes less and less over the course of time (months). In the ideal case, complete resolution occurs ( Fig. 3.11). Many cases, however, end up with an incomplete recovery. Increased sclerosis or fibrosis with periosteal thickening or even fatty marrow conversion can remain on MRI as a “scar.”

Recommendations for an examination strategy

• Where there is clinical suspicion of acute osteomyelitis, radiography is the primary modality of choice, supplemented routinely by ultrasound in the neonatal period and early childhood. MRI should be used to confirm the diagnosis.

• When there is justified suspicion of multifocal involvement (particularly in the neonatal period), then a bone scan or whole-body MRI scan is useful. CT and nuclear medicine imaging modalities are reserved for special cases. Confirmation of the diagnosis “acute osteomyelitis” by biopsy is only rarely necessary, given that the combination of clinical presentation, laboratory results, and imagery is confirmation enough. Biopsy/aspiration is required for identification of the pathogen prior to commencement of appropriate antibiotic therapy.

DD. Primary and secondary bone tumors. Ewing’ s sarcoma and, less frequently, osteosarcoma, are important differential diagnoses in children and adolescents, given that their clinical presentation and laboratory findings often resemble an inflammatory process. Radiography and bone scan may not allow for differentiation. MRI is a great help here. The solid tumor has space-occupying character and has often already breached the cortex. The peritumoral edema is often well defined from the tumor. Osteoid osteoma may resemble a focal lesion of osteomyelitis on MRI. Characteristic for an osteoid osteoma, however, is the surrounding sclerotic margin, which is absent in acute osteomyelitis (a radiograph or CT image must be available when assessing the MRI findings; Fig. W3.1). In adults, the differential diagnosis “tumor versus inflammation” rarely arises as a clinical issue. The same criteria for differentiation apply as for children and adolescents.

Cysts and other lesions. Marginal enhancement around fluid-filled cavities is also found on MRI around cysts, necrotic tumors, and posttraumatic seromas (see also chronic osteomyelitis in Chapter 3.1.3). In these cases, differentiation is only possible from the thickness of the marginal enhancement and identification of an associated edema. An abscess typically displays the latter.

Brodie Abscess

Pathology. A pus-filled cavity measuring 1 to 5 cm is present within the cancellous bone. This is surrounded by marked sclerosis of the cancellous bone. Staphylococcus aureus can be grown from the abscess aspirate in one half of cases.

Clinical presentation. The clinical findings are relatively limited. Some patients do not consult a physician until late. The disorder has its peak incidence in the second decade of life. The findings are primarily located in the metaphyseal part of the distal femur or at the proximal tibia.

Radiography. Brodie abscesses cause osteolysis in the metaphysis or diametaphysis. Round, oval, and polymorphic forms are possible ( Fig. 3.12). The margin is characteristic, always being sharply delineated and demonstrating signs of surrounding sclerosis.

The osteosclerosis starts to fade toward the periphery so that the transition from sclerosis to normal bone is often ill-defined. Solid periosteal reactions are possible ( Fig. 3.13a). Brodie abscesses may be located in the cortex, where they are then associated with strong, solid periosteal reactions that cause the bone to appear “distended.”

MRI. The typical appearance of an abscess is a strongly contrast-enhanced margin around a fluid, nonenhancing center ( Fig. 3.14). However, weak contrast filling of the center can result from a rapid diffusion of contrast medium. A signal-intense edema is always recognizable around the abscess (on water-sensitive sequences and after contrast administration).

The “Penumbra sign” refers to the mildly hyperintense rim lining the abscess that is already evident on the unenhanced T1W image, especially in the case of a Brodie abscess ( Fig. 3.13b). This lining enhances readily.

DD. The radiological differential diagnosis includes osteoblastoma, chondroblastoma, nonossifying fibroma, giant cell tumor, eosinophilic granuloma, aneurysmal bone cyst, and fibrous dysplasia. It is possible to shorten this comprehensive list using MRI because tumors and tumorlike lesions usually enhance with contrast more clearly in their center when MRI is used. The differentiation between a simple cyst and a Brodie abscess is usually possible by a combined assessment of radiographs and MRI scans. A cyst displays only a narrow sclerotic margin on the radiograph and lacks perifocal edema on MRI—provided there are no fractures. Septations and fluid levels, as with an aneurysmal bone cyst, are not seen on MRI of a Brodie abscess.

3.1.3 Chronic Exogenous Osteomyelitis

Chronic exogenous osteomyelitis is an infection of the bone that is not induced hematogenously and demonstrates a chronic recurrent course (cf. Chapter 3.1.1).

Pathology. The disorder can be initiated by the migration of pathogens through natural barriers such as skin, teeth, or paranasal sinuses. Another route of spread results from injury to natural barriers, such as after cuts and lacerations, or secondarily to burns and bed sores.

The direct inoculation of pathogens into the bone due to trauma or iatrogenically is the most common form of exogenous osteomyelitis. The spread of the infection in posttraumatic osteomyelitis depends not only on the number and virulence of the pathogens and the resistance of the patient, but also, and above all, on local conditions such as the degree of soft tissue damage, disruption of vascularization of the bone, the stage of fracture healing, and the type of foreign material introduced. Poor vascularization and altered stability of the traumatized soft tissue and bone are cofactors, or even the cause, of the insidious development of chronic osteomyelitis.

Clinical presentation. The majority of cases of posttraumatic and postoperative forms of osteomyelitis begin acutely. As a rule, this is what is known as a “full-blown infection.” Cardinal symptoms are erythema, increased skin temperature and swelling of the surgical site, associated with abnormal wound healing. Fistula formation with purulent discharge or serous fluid is possible. Inflammatory parameters (white blood cell count, ESR and CRP) of laboratory tests are elevated. After these signs of early infection, the further course of such exogenous infections is chronic-recurrent. Even after several years of a clinically inapparent chronic infection, acute flares can recur (also known as the reactivation of chronic osteomyelitis).

Radiography. The radiological findings differ clearly depending on the route of infection. With posttraumatic, direct inoculation of the pathogen, the radiograph depends strongly on the presence of fractures and their healing and transformation processes. In some cases the infectious process is difficult to recognize. After surgery, especially after the introduction of fracture fixation hardware, screws, plates, and nails can superimpose and obscure the picture ( Fig. 3.16). If a soft tissue infection results in osteomyelitis, then the periosteum will react very early. Depending on the route of infection usually to be expected from the clinical presentation, the various imaging modalities will be accorded different degrees of importance.

In cases of pathogen migration or injury to the skin

• Consolidation of the soft tissue, disappearance of the fat lines.

• Periosteal reaction of varying degrees of expression and form.

• Mixed appearance combining destruction (small lytic areas) and consolidation.

• Lytic destruction of larger parts of the bone, particularly in the fingers and toes ( Fig. 3.15).

Posttraumatic, postoperative

• Mixed lytic and sclerotic appearance of the bone ( Figs. 3.17–3.19).

• Typically solid periosteal reaction with consecutive widening of the cortical bone (sclerosis of the internal table, even to the extent of eburnization of the entire bone marrow, can also result in increased thickness of the cortical bone [ Fig. 3.17]; caution—likelihood of confusion with cortical thickening secondary to callus formation!).

• Bony sequestrum formation (irregular, circumscribed zone of marked consolidation) or involucrum ( Fig. 3.18).

• Apparent “widening” of the fracture gap ( Fig. 3.18).

• Circumferential radiolucent lines without sclerotic margin around screws.

• Lucent zones with ill-defined margin around implants of more than 1.5 mm in size (cf. Fig. 2.368; caution—artifactual lucent zones at the high-contrast metal–bone interface on digital radiography).

US. Soft tissue abscesses around bones are well demarcated. Diffuse phlegmons may be seen as hypoechoic ill-defined areas. Cortical destruction and periosteal reaction can be detected ( Fig. 3.15).

CT. CT is ideally suited for the detection of a nonviable sequestrum, involucrum, and osseous fistulas. The sequestration is of high density and surrounded by a cuff of fluid and soft tissue.

MRI. The examination technique in cases of posttraumatic exogenous osteomyelitis is similar to that of the acute form (Chapter 3.1.1). Metal artifacts can restrict the diagnostic value of MRI due to local field inhomogeneities. The same also applies after removal of implants because troublesome metal debris remains. Even radiologically invisible abrasion artifacts can produce circumscribed signal distortions up to 1 cm in size: an area of complete signal loss is surrounded by a very hyperintense (semi-) circle. This ring is larger with fat-suppressed sequences than with normal SE sequences.

Findings

• Extensive bony remodeling, with hypointense sclerosis, fibrosis, and cortical thickening found on all sequences, determines the overall picture.

• Nevertheless, the principal rules applied for diagnosing inflammation, as described for acute osteomyelitis (Chapter 3.1.2), remain valid.

• On T1W sequences, bone marrow alterations are hypointense to fatty marrow ( Fig. 3.20a).

• The inflammed areas are hyperintense on fat-saturated fluid-sensitive sequences; abscesses are practically fluid-equivalent with a somewhat less signal-intense halo ( Fig. 3.19c).

• After injection of contrast, variable but increased signal intensity is seen in the abscess membrane and granulation tissue. The abscess cavity takes up no contrast, or takes it up only in a delayed manner ( Figs. 3.20b and 3.21). After contrast administration, at least a mild signal enhancement should be evident in the presence of an active process ( Fig. 3.21); otherwise, the diagnosis of an abscess should be challenged or only a very mildly active process should be assumed.

• Fistula tracts usually appear as contrast enhancements with a meandering pattern (see Fig. 3.25). They present as linear hyperintensities on fluid-sensitive sequences.

During the initial weeks after injury or a surgical intervention it is often not possible to diagnose an infection with any degree of confidence because edema, granulation tissue, fibrosis, and callus formation produce signal intensity changes that strongly resemble those of an infection. Only the positive identification of abscesses and fistulas should give cause for the unequivocal diagnosis of posttraumatic or postsurgical bacterial inflammation.

Related posts:

Interventions Involving the Bone, Soft Tissues, and Joints Congenital Disorders of Bone and Joint Development Osteochondroses Miscellaneous Bone, Joint, and Soft Tissue Disorders Acute Trauma and Overuse Injuries: Essentials Rheumatic Disorders

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