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Logo of procrsmedFormerly medchtJournal of the Royal Society of MedicineProceedings of the Royal Society of Medicine
 
Proc R Soc Med. 1928 August; 21(10): 1743–1758.
PMCID: PMC2101238

The Histopathology of Mastoiditis

Abstract

Mastoiditis, a broad term, with no strict anatomical basis, includes not only an inflammation of the pneumatic cells in the mastoid bone proper, but also all extensions into neighbouring bones (zygoma, occipitalis, etc.).

Thus the anatomical distribution of the pneumatic cells plays an important part in the course of the disease. This point is illustrated by Brock's case, in which a fatal meningitis ensued from a pneumatic cell in the wall of the internal auditory meatus. According to this author's investigations on pneumatized temporal bones of all ages, 11 per cent. had such an extension normally to this site. Even if diagnosed, the impossibility of opening up such a cell is evident.

In the present paper the various stages of acute mastoiditis are described and illustrated:—

The initial change in the directly infected zone is a local rise of blood-pressure, causing dilatation of the vessels in the Haversian systems and hyperæmia of the muco-endosteum. In the Haversian systems the rigid bony walls allow of no physiological expansion, and so, as early as the third day, osteoclasts are found actively eroding the bony walls. Meanwhile the vessels in the muco-endosteum endeavour to lessen their congestion by transuding fluid into the supporting endosteum, which consequently becomes swollen and œdematous.

The next stage is characterized by a more advanced degree of osteoclasis in the Haversian systems. The muco-endosteum is infiltrated by round mononucleated cells, the change being most marked under the epithelium; the infiltrating cells push forward the epithelium and escape into the cell lumen through the rents.

At the same time softening or halisteresis occurs in the bone and a few perforating vessels are seen.

In influenzal, but not in other types, hæmorrhages into the muco-endosteum occur.

The third stage is the period of active rarefaction of the bony wall of the pneumatic space by osteoclasts and perforating vessels. This takes place because of the new pressure conditions; in the former stages there has been no real increase of pressure in the cell space, but at this stage the epithelium has largely disappeared, and the pneumatic cell has become a cavity lined by granulations and full of unorganized exudate centrally.

The next change consists in the regeneration of the destroyed tissue by new bone formation. For this a reduction of the existing pressure is required, and may be explained by an equilibrium of pressure in the vascular system—a response by the organism to new conditions. The extra space obtained by the destruction of bone is also a factor.

The whole inflammatory condition is subject to phase-change, which can turn it from one of exudation, accompanied by increase of intravascular pressure, into a more proliferative one (Krainz). The latter phase is introduced by a transudation of œdema and tissue fluid back into the veins (Korner). This process is essential for the decrease of the local pressure, since the only outflow of the tissue fluid from the bones is by the veins (Recklinghausen). Thus is explained the occurrence of the proliferative process in those cases in which no eruption through the covering occurs.

In the regenerative stage the remnants of epithelium subserve the function of preserving portions of the original pneumatic cell lumen.

It thus becomes apparent, first, that a certain number of the pneumatic cells must be converted into spongy spaces and, secondly, that the process will be most pronounced in a very cellular mastoid, because such a mastoid contains outlying cells in which pus stagnates and in which organization will eventually take place. There is a distinct potentiality for the mastoid process to become converted into spongy bone. Granulations grow from one cell to another, from the actively diseased zone to the less diseased parts, until they are held up by a growth of epithelium barring their further progress. When it is remembered how quickly the “proud flesh” of some mastoid wounds sometimes grows, despite bluestone applications or instrumental removal, it will be readily realised how a similar condition inside the mastoid will eventually result in the bone being converted into the spongy type. It is not maintained that this change is a common occurrence; it may be exceedingly rare but such a possibility must be stressed.

What is removed at operation depends upon the time at which the operation is carried out. If this should be late, new-formed bone, organized tissue and diseased tissue are taken away, and macroscopally no differentiation can be made between them; hence a complete clearance is necessary.

The infecting micro-organism has some effect on the course of the disease, the most dangerous being Streptococcus hæmolyticus.

The disease is not influenced directly by age, provided that the patient is healthy, but its course is dependent on the acuteness and severity of the infection.

Briefly, then, the first stage of the disease consists in a destructive process beginning in the Haversian canals, and then involving the pneumatic cells. The disease extends from the interior to the exterior, and the same order of progress is observed in the subsequent regenerative processes.

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