Mastoiditis - Causes and Pathogenesis

Causes of Mastoiditis

In secondary mastoiditis, the infection penetrates the cellular structure of the mastoid process mainly through the otogenic route in acute or chronic otitis media. In primary mastoiditis, direct traumatic damage to the cellular structure of the mastoid process is significant due to blows, bruises, gunshot wounds, blast waves, fractures and cracks in the bones of the skull, including fractures of the base of the skull; hematogenous metastatic spread of pathogenic infection is possible in septicopyemia, the transition of the purulent process from the lymph nodes of the mastoid process to bone tissue; isolated damage to the mastoid process in specific infections (tuberculosis, infectious granulomas). The microflora in mastoiditis is quite diverse, but coccal flora predominates.

Pathogenesis of mastoiditis

The course of mastoiditis depends on the type and virulence of microflora, the state of immunity, changes in the ear as a result of previous diseases, the state of the nasal cavity and nasopharynx. Insufficient drainage of the purulent focus in the middle ear is important (in chronic epitympanitis due to the high location of the marginal perforation; with an insignificant size of the perforation of the eardrum or its closure by granulation, delayed drainage of the tympanic cavity associated with a delay in spontaneous perforation of the eardrum or paracentesis; difficulty in the outflow of secretion from the air system of the middle ear due to the closure of the communication between the cells, antrum and tympanic cavity by an inflamed and thickened mucous membrane). In traumatic mastoiditis, as a result of the formation of cracks and fractures, the relationships between the air cavity system are modified, multiple fractures of thin bone partitions occur, small bone fragments are formed and special conditions are created for the spread of the inflammatory process. The blood that spills out when the bones are damaged is a favorable environment for the development of infection with subsequent melting of bone fragments.

The following stages of development of the inflammatory process in the mastoid process in mastoiditis are distinguished.

• Exudative. It lasts for the first 7-10 days of the disease, during which inflammation of the mucous (endosteal) covering of the mastoid process cells develops - the so-called "internal periostitis of the mastoid process" (according to M.F. Tsytovich). As a result of the mucous membrane edema, the openings of the cells close, the cells are separated from the mastoid cave, and the communication of the mastoid cave with the tympanic cavity is also disrupted. The cessation of ventilation of the cave and the mastoid process cells leads to rarefaction of the air with expansion and blood filling of the vessels with subsequent transudation. The mastoid process cells are filled with inflammatory serous-purulent or purulent exudate. In this case, many closed empyemas are formed in the mastoid process. On the radiograph at this stage of inflammation, the septa between the veiled cells are still distinguishable.
• Proliferative-alterative (true mastoiditis). Usually formed on the 7-10th day of the disease (in children it develops much earlier). A combination of parallel productive (development of granulation) and destructive (melting of the bone with the formation of lacunae) changes occurs. These changes simultaneously occur not only in the bone walls, but also in the bone marrow spaces and in the vascular canals. Gradual resorption of bone tissue leads to the destruction of the bone septa between the cells of the mastoid process: separate destroyed groups of cells are formed, which, merging, form cavities of various sizes filled with pus and granulation, or one large cavity.

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