INFECTIONS AND NONINFECTIOUS INFLAMMATORY DISORDERS: GENERAL MORPHOLOGY, CELLULITIS, ABSCESS, AND SUPPURATIVE ADENITIS
- The basis of the “inflammatory morphology” as seen on anatomic imaging studies is presented.
- The inflammatory morphology is nonspecific but useful in directing clinical thinking and imaging interpretation.
- The inflammatory morphology is best modeled by acute and subacute pyogenic infections but is shared by several other infections, noninfectious inflammatory diseases, and some neoplasms.
- The higher-grade patterns of disease seen here will be present in acute pyogenic infections and perhaps fungal infections, and the differential from a neoplasm is usually not difficult based on imaging and even less so when the clinical information is added.
- The lower-grade infections such as those that are partially treated or indolent fungal infections and noninfectious inflammatory diseases such as Wegener granulomatosis and Langerhans histiocytosis will more typically mimic malignancy (especially small round cell malignancies), and the differential may be more clear on the basis of imaging than it is based on the clinical situation.
- Pitfalls in the diagnosis of infectious and noninfectious inflammatory diseases versus neoplastic diseases exist and must be taken into account to produce the best possible interpretations.
- Pathophysiology of cellulitis, abscess, and suppurative adenitis is presented, and those entities are differentiated from one another.
- The effects of the pathophysiology of these conditions on their morphology as seen on computed tomography, magnetic resonance imaging, and ultrasound is presented.
- Relative value of imaging modalities in the evaluation of these conditions is considered.
Inflammation is a general response of the body to a variety of disease processes. The gross morphology of the response will vary with the inciting agent, status of the immune system, intercurrent therapy, and time course of the disorder. These and other factors will influence the appearance of the inflammatory process on anatomic and physiologic imaging studies. This discussion will focus in particular on computed tomography (CT) and secondarily on magnetic resonance imaging (MRI) as the anatomic imaging studies used to evaluate the vast majority of these conditions. Ultrasound has a relatively limited role as an anatomic imaging study. Radionuclide studies are used to more physiologically assess the likelihood of infection and to monitor therapeutic response in highly selected cases. Also, inflammatory conditions cause problems with false-positive fluorine-18 2-fluoro-2-deoxy-D-glucose positron emission tomography (FDG-PET) studies in patients being studied for cancer detection or surveillance. In this discussion, mainly acute and subacute infectious diseases are used as the primary model of the morphologic changes seen with inflammation. Of course, similar or identical changes may be present in response to trauma and radiation therapy or associated with malignant tumors; those situations and others wherein the inflammatory morphology is held in common are discussed elsewhere.
Hallmarks of most head and neck soft tissues infection or inflammation are the changes in fat surrounding the muscles and other structures in the head and neck region.1,2 The surrounding fat planes will often appear swollen, especially in the subcutaneous regions where there is no resistance to expansion. Reticulated and linear densities of varying thickness are often visible within the fat (Figs. 13.1–13.6). These may be due to enlargement of existing fibrous septae, perilymphatic thickening, distention of lymphatic channels, or any combination of the three. The overlying skin is frequently thick and indistinct. Deeper fibrofatty spaces, such as the parapharyngeal space or those within the masticator space, are less distensible and frequently become completely obliterated by the inflammatory process (Fig. 13.5), even when relatively low grade (Fig. 13.3). If extensive enough, the inflammatory reactions may completely obliterate the more superficial fat planes (Fig. 13.4). More frequently, one can observe a thickened, irregular superficial fascia (platysma) in the neck and its equivalent in the face called the superficial musculoaponeurotic system (SMAS) (Fig. 13.6). On CT, the edematous fat will be increased in density, with the actual appearance often depending on the relative amounts of fat, edema, and exudate present (Figs. 13.1–13.6).2–4 For example, in thin patients, the edema may not even be apparent, whereas in heavier patients even small amounts will produce obvious changes early in the disease process. On T1-weighted (T1W) magnetic resonance (MR), the signal intensity of involved fat will be diminished, but subtle changes are more easily seen on CT (Figs. 13.6J and 13.7). Edematous fat may appear bright on T2-weighted (T2W) images, but the signal increase is not nearly as conspicuous as that in edematous brain.3,4 Short T1 inversion recovery (STIR) and fat-suppression techniques improve the detection of edema in fat and muscle on MR (Figs. 13.5 and 13.7).
Most inflammatory lesions have indistinct margins at their interface with surrounding soft tissues, even when the inflammation is localized (Figs. 13.1 and 13.8). Lower-grade or partially treated infection may not appear so indistinct at their interface with adjacent tissue, but there may be other signs of inflammation present such as edema in adjacent spaces and/or reactive adenopathy (Fig. 13.3). This is in part due to edema and/or exudate and in part to the vascular reaction seen with inflammatory response. The indistinct margins are most easily perceived at the borders between the lesion and fat on CT and non–contrast-enhanced T1W and fat-suppressed MR images (Figs. 13.5 and 13.7). Diffuse swelling of involved and surrounding soft tissues is another sign of inflammation (Figs. 13.1–13.7)
On CT and T1W MR, an inflamed muscle will appear obviously larger than on the unaffected side, but little obvious density change is noticeable.3–5 On T2W, STIR, or fat-suppressed MR images, edematous muscle will appear brighter than normal because of the increased water content (Figs. 13.5 and 13.7). Typically, T1W images, whether spin echo or gradient echo sequences, are less sensitive to muscle edema.
Many inflammatory reactions include a phase of increased vascularity either because of loss of autoregulation, increased capillary permeability, new capillary in growth, or all three.2,6 This can be demonstrated on contrast-enhanced magnetic resonance (CEMR) and contrast-enhanced computed tomography (CECT). Contrast will leak into inflamed tissues at a higher rate than normal tissue because of the abnormal capillary permeability (Fig. 13.9). As a result, a combination of diffuse and peripheral enhancement may be present in an abscess and surrounding cellulitis/phlegmon (Figs. 13.1–13.7).
Injured and inflamed tissue may go on to a chronic state of increased vascularity as seen on enhanced CT and MR studies. One of the better examples of this chronic, relative hypervascularity outside of head and neck imaging is the granulation tissue seen in association with herniated and/or operated discs. On imaging studies, the amount of contrast enhancement in any inflamed area may range from florid to quite subtle. Peripheral enhancement is typically very easy to appreciate on CT at the lesion–fat interface (Figs. 13.1 and 13.6) and is also usually easily discernible at the border of the rim enhancement and muscle (Figs. 13.2 and 13.9). The enhancing lesion–fat border is often less obvious on CEMR because both the enhancing margin and fat tends to be bright on non–fat-suppressed T1W images (Figs. 13.5 and 13.6J). On the other hand, changes due to enhancement within muscle may be more apparent on CEMR than CECT. Fat-suppression techniques, used in conjunction with CEMR, improve overall performance of MRI helping to demonstrate enhancement within muscle as well as at lesion–fat interfaces.
Progression to healing may leave no visible evidence of prior disease, especially in acute infections (Fig. 13.9A,B). In those infections that go on to a healing by secondary intention or pass through some state resulting in the generation of granulation tissue, considerable scar will be left at the site of the infection (Figs. 13.10 and 13.11). Eventually, this will become nonenhancing muscle-equivalent tissue on CECT. Such residual end-stage fibrosis will also be nonenhancing and muscle equivalent or generally lower in signal intensity than muscle on all MRI sequences (13.11). With extensive scarring, there may be loss of surrounding fat planes and irreversible thickening of the skin, retraction of skin or deeper anatomic structures, and thickening of various fasciae and the fibrofatty “septae” within areas of previously normal fat.