14 Otitis Media

Histopathologically, the term acute otitis refers to infiltration by polymorphonuclears and classic signs of acute inflammation. Chronic otitis implies infiltration of the mucoperiosteum by round cells or the cells of chronic inflammation. Clinically, the definitions are less demarcated and, for practical purposes, arbitrary. On the basis of duration, the disease is subdivided into three categories: acute (up to 3 weeks of duration), subacute (from 3 weeks to 3 months of duration), and chronic (more than 3 months of duration).1–8 The Task Force of the Fourth International Symposium of Otitis Media held in June 1987 in Bal Harbour, Florida, United States, classified otitis on clinical grounds as follows:

• Myringitis, which is an inflammation of the tympanic membrane that occurs alone or in association with external otitis or OM.

• Acute suppurative otitis media (acute purulent otitis media, acute otitis media), which refers to a clinically identifiable infection of the middle ear with sudden onset and short duration.

• Secretory otitis media (chronic otitis media with effusion, OM with effusion, nonsuppurative otitis media, catarrh, serous otitis media, serotympanum, mucoid otitis media, mucotympanum), which refers to the presence of middle ear effusion behind an intact tympanic membrane without acute signs or symptoms. This broad term includes nonsuppurative or clinically noninfectious forms of OM.

• Chronic suppurative otitis media (chronic otitis media), which refers to a chronic discharge from the middle ear through a perforation of the tympanic membrane. Suppurative refers to active clinical infection. A perforation without discharge can be an inactive stage of the infection.

For purposes of communication and uniform reporting, we should follow this classification, with the clear understanding, however, that it is a working classification subject to change. It is important to point out that more than a “final classification,” this description represents a “consensus or working agreement” between different clinicians and investigators who have different viewpoints and perspectives.

Because this is an agreed classification, there are some deficiencies. This classification leaves out “recurrent otitis.” Although patients who have repeated episodes of OM that alternate with periods of “apparent remission” can be fitted into the terms of the task force, the prevalence of these clinical manifestations is such that it deserves separate mention. At present, recurrent episodes of acute otitis media with in-between episodes of apparent remission (three episodes in 6 months or four episodes in 1 year) are termed as recurrent otitis and treated as such.

In addition, the chronic definition also can be applied to otitis with an intact tympanic membrane, as in the case of “silent otitis media.” The term silent otitis media was introduced by Paparella et al in 1980,^9,10 and it refers to middle ear inflammatory pathology that exists with the absence of perforation and otorrhea.

OM is associated with the presence of fluid (effusion). Basically, three types of effusions are found: serous,¹ mucoid,² and purulent.³ Two other types can be added: hemorrhagic and any combination of the previously mentioned fluids.⁵ In practice, it is unusual to see a pure effusion because most effusions occur in combination. These different fluids can be seen in acute and chronic cases. It is not clear whether these different effusions are independent of each other or if some are different forms or stages of the same process. There is increasing evidence to show that the effusion in secretory otitis is not necessarily noninfectious. On the contrary, cultures of effusions have yielded positive cultures in 22 to 52% of the cases, percentages that increase to 77.3% if polymerase chain reaction (PCR) is used.^11,12

In addition to the acute and chronic involvement of the mucoperiosteum by the OM process, there are potential complications and sequelae in this disease process. A complication occurs when the inflammatory process extends beyond the mucoperiosteum; the term sequela refers to a process that remains within the mucoperiosteum and has the capacity or potential of becoming a complication. For example, granulation tissue is an active sequela, but erosion of bone by granulation tissue is a complication. In addition, the overall consequences of a localized lesion (i.e., ossicular disruption causing conductive hearing loss) can have significant effects of communication, isolation, learning problems, and so forth on a person and on relationships with others.

In addition, the effusions (fluids) are not stagnant spillage but dynamic forms that evolve and change in response to and as part of the overall mucoperiosteal changes. The overall inflammatory changes are to be seen as a continuum, with some forms evolving or resolving to other forms and at times resulting in complications or sequelae, depending on the multiple factors involved. Moreover, this is a multifactorial disease that manifests primarily in a specific location and is influenced directly not only by the neighboring anatomical structures but also by the host and the relationship with the environment. When viewed in this perspective, it becomes obvious that OM certainly implies more than just fluid behind the tympanic membrane because the inflammatory process involves all structures, layers, and cavities in the middle ear mastoid and eustachian tube.

In other words, OM is a multifactorial, multifaceted disease that manifests as an inflammatory process that is the result of a prevailing aggression over the body’s defense system, the degree of which depends on the balance of these opposing forces—disease against the immunological defense system. It is a dynamic disease in which some forms lead to others (Table 14.1), resulting at times in complications and sequelae (Table 14.2). In addition to local factors, this process is influenced directly not only by the neighboring anatomic structures but also by the host’s relationship with the environment. This involves the concept that germs (which can be acquired or be part of the flora) require several favorable conditions to perpetuate the process and are not solely by themselves the factors of disease.

To select a rational therapy, it is essential to have an understanding of the anatomy, function, and pathology of the organs involved as well as of the mechanisms of disease. On the basis of the principles of pathogenesis, treatment is aimed at interfering in the pathologic process to stop the continuum of disease and to reestablish function.

Understanding the mechanisms of disease allows for the most important concept of timing. At the right time, insertion of a ventilating tube might be all that is needed, whereas at the wrong time, a tube will not suffice. The ultimate goal is to prevent OM (e.g., environment, vaccines, and immunity) and, if unsuccessful, to treat OM medically, reserving surgery for the restoration of function rather than for the eradication of disease. Eventually, with the full clinical incorporation of molecular biology and genetics, the approach to OM will be not only preventive but also predictive and individualized.

Substrate

The middle ear lining is of endodermal origin and is originated from the first pharyngeal pouch. The expansion of this pouch originates the eustachian tube, the middle ear and antrum, and mastoid air cells. This endoderm originates the epithelium of these structures that are surrounded by the mesoderm, which develops the connective tissue and muscles. The epithelium is continuous with that of the nasopharynx through the eustachian tube, and for practical purposes, in spite of being in a cavity it is exposed to the surface. The epithelium is uninterrupted; however, there are different types and the distribution of these different types of epithelia will depend on their location within the cavity.^13–17 The epithelium is respiratory (pseudostratified columnar with ciliated, goblet, intermediate, and basal cells) at the anterior wall and eustachian tube. The epithelium becomes ciliated cuboidal at the promontory, and toward the oval window it becomes shallower and at the mastoid it is flat.

Table 14.1 Practical Working Classification of Otitis Media

Table 14.2 Practical Working Classification of Complications and Sequelae of Otitis Media

The connective tissue is similar to other locatons.4,16,17 It brings together all elements and establishes a space. It is composed of fibers, cells, and amorphous substance. This tissue is continuous all over the body and allows the passage of blood and lymph vessels as well as nerve fibers. The main cells are the fibroblasts (that maintain the fibrillar system), but there are also ganglion cells, cells that are part of blood and lymph vessels, as well as defensive cells.

Once the aggression is established, the result is the nonspecific universal reaction of inflammation, which is the starting point of the sequential steps that will be described. Among the initial nonspecific cellular factors are the epithelial cells, the fibroblasts, and, with certain reserve, the endothelial cells. With the understanding that the reaction is simultaneous at all levels, for practical reasons the epithelial changes will be initially described.18–35

Changes in the Epithelium

The epithelial cells participate in the inflammatory reaction by themselves and also as part of the mucociliary system. The epithelial cells become taller and have an increased secretion. In early stages the secretory cells stain positively for periodic acid-Schiff. There is also some new gland formation. Cells become hyperplastic, and there is also an increase in goblet cells. Cells secrete different defensive substances such as lysozymes. The epithelial cells of middle ear also have the capacity of synthetizing the secretory piece of immunoglobulin A (IgA) (secretory IgA).

All these secretions plus the cellular elements that fall into the middle ear cavity contribute to develop the middle ear effusion (fluid ear). In some areas and depending on the degree of aggression, epithelial ruptures occur.

In some chronic cases, there are metaplastic changes of the epithelium toward squamous epithelium; however, these are only isolated occurrences without an apparent pathological significance. Cholesteatomas seem more likely to be the migration of the epithelium of the tympanic membrane (and/or ear canal) rather than the result of metaplastic changes of the middle ear mucosa. This statement is supported by histopathological findings described in temporal bones in which cholesteatomas do not seem to have any relationship with these isolated metaplastic islands.

Changes in the Connective Tissue and Periosteum

Changes in the connective tissue are characterized by thickening, edema, and increased vascularity.

Cellular changes are characterized by the following:

• Gradual cellular infiltration

• Changes in the type and number of cells

• Changes in the shape and number of fibers

• Inflammatory reaction of the periosteum

• Inflammatory reaction of the underlying bone

In early stages of the inflammatory process, the initial infiltration is based on polymorphonuclears that respond rapidly and traverse the capillaries toward the connective tissue. From there, some migrate through the epithelium toward the middle ear cavity. The majority are neutrophils, but there are occasional eosinophils. Their primary function is engulfment of particles and microorganisms.

The second cells to appear active are macrophages and fibroblasts. Macrophages, despite being nonspecific, marks the starting point toward the specific immunological reaction mediated by T and B lymphocytes. Macrophages play a role in processing antigens and interacting with B lymphocytes (humoral immunity) and T (cellular immunity) lymphocytes, which are the cells with capacity for specific recognition. B cells develop toward antibody-secreting cells.

The middle ear mucosa also has a local immunological system via secretory IgA, in which IgA is secreted by plasma cells (B cells) and the epithelial cells add the secretory piece. IgG and IgM could also be considered secretory because they are also synthesized by plasma cells and secreted toward the mucosal surface.

Fibroblasts become active at early stages of the inflammatory process. They become larger and start secreting fibers. This is also evident in chronic cases. The reaction of these cells at early stages is so prominent that these early stages could be described as a fibroblastic-macrophagic reaction with fiber and amorphous substance secretion. Over time, the collagen fibers become thicker and better organized.

Middle Ear Defense System

• An epithelium that is continuous and regenerative and constitutes a mechanical barrier

• Mucociliary transport system: mucus, lysozymes, and ciliated and secretory cells

• A patent and functional eustachian tube

• Inflammatory reaction of the connective tissue

• Edema

• Polymorphonuclears: macrophages, lymphocytes, plasma cells

• Lysozymes: small and large immunoglobulins (IgA, IgG, IgM, and IgE)

The main causes are bacteria, viruses, and the effusion itself. Eustachian tube dysfunction can be a primary factor, and it can be caused by bacteria, virus,36 as well as functional or anatomical alterations in the cartilaginous portion and/or its associated muscles.³⁷

OM usually coincides with respiratory viral infections.³⁸

The viral mechanisms are not clearly defined; however, experimental studies suggest that viruses can cause alterations of ciliary morphology, polymorphonuclear dysfunction, and morphological changes in the tubes with secondary bacterial infections.^36,39

Effusions are an important factor because these are rich in inflammatory agents that help perpetuate the histopathological process. This implies that effusions must be treated and eliminated.⁴⁰

Facilitating (Precipitating) Factors

Racial influences in OM are well documented. Studies that have been conducted in different groups have shown a higher prevalence in whites than in blacks and higher in American Indians and Eskimo than in whites.^38,41,42

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