ON THE CAUSATION AND PREVENTION OF BONE NECROSIS IN THE COURSE OF CHRONIC PURULENT OTITIS.

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BY DR. A. SCHEIBE, MUNICH.

Translated by Dr. ARNOLD KNAPP.

N studying the proportion of cases of chronic purulent otitis which lead to necrosis of bone, we find that most authors, like Schwartze, Steinbruegge, Habermann, and others, confound the necrotic and the simple inflammatory processes in bone, and discuss them under the common title, "Caries and Necrosis." These are produced partly by general causes,-constitutional taint and acute infectious diseases, and partly by local conditions, such as retention and putrefaction of pus (Schwartze), and retention by polypi or cholesteatoma (Habermann). It is not possible to judge in what degree these causes are responsible for the osteitis on one hand and for the necrosis on the other. The question is also made difficult from the fact that most authors, with the exception of Politzer, do not separate bone diseases occurring in the course of acute from those occurring in the course of chronic purulent otitis, although they are entirely different, especially in regard to their etiology.

Bezold was the first to insist upon the separation of the simple inflammatory from the necrotic bone-process, and drew attention to the difference in the anatomical and clinical picture. Necrosis, according to him, was the reaction of the diseased and weakened general system as opposed to osteitis as a reaction of the healthy organism.

Necrosis can follow all general diseases which have depreciated the health of the organism, as well as follow a simple empyema. On the other hand, necrosis may be the result of exclusively local acting causes, such as processes of putrefaction, detachment of the external periosteum and of the dura, as well as the accumulation of epidermis in the middleear cavities.

Recently Koerner, in his book on The Purulent Diseases of the Temporal Bone, has sharply separated necrosis from the carious processes. He, however, only discusses necrosis in the course of acute purulent otitis. Agreeing with Bezold, he concludes that necrosis in the course of an acute suppuration generally occurs in constitutional diseases, though its appearance in the healthy organism cannot be entirely excluded. The necrosing process in the chronic cases is not discussed at all.

In 1892, I separated necrosis from osteitis, and discussed the etiology of necrosis in acute purulent otitis on a basis of 4 cases. In these 4 patients the bodily condition was a weakened one as opposed to the simple empyemata. I shall return to the bacteriological conditions found present in these cases.

The investigation of necrosis in the course of acute purulent otitis was continued, and I reported upon my results at the meeting of the German otologists in 1900. This new series consisted of 13 cases of necrosis occurring in the course of acute purulent otitis, which I had especially examined for the cause of necrosis in each case.

In all of these cases there were symptoms of severe general disturbance. These in order of frequency were: pulmonary tuberculosis, pyæmia, and sinus phlebitis, diabetes, influenza, and scarlet-fever. In the healthy organism, the acute suppurative otitis had not led to a destruction of bone in a single case.

The pus was examined bacteriologically. The streptococcus was generally found, and the diplococcus pneumoniæ was present in only one. If we compare this result with the bacteriological examination of all acute purulent otitides, where the streptococcus and the diplococcus, as is well

known, occur with equal frequency, we should be inclined to regard the preponderating presence of the streptococcus as the etiological factor in the production of necrosis. The streptococcus, however, cannot be given any essential etiological importance, as it does not produce necrosis in the healthy individual, as I was able to show by a number of examples in 1892. Its frequency in cases with necrosis is more likely due to the fact that it occurs more frequently than the diplococcus in weakened constitutions, especially in the otorrhoea after infectious diseases.

Retention of pus does not play an important rôle in the causation of necrosis in acute otitis, for in half of my cases the necrosis did not develop until after the opening of the mastoid process.

Putrefaction, on the other hand, is not entirely without influence. The discharge in 9 cases was without odor, but in 4 (30%) it was fetid.

My investigations show that the development of necrosis in acute purulent otitis depends exclusively, or almost exclusively, on the condition of the general system, which coincides with the experiences of Bezold and Koerner.

As a supplement to the above investigation, I have examined a large number of cases of necrosis in the course of chronic purulent otitis. In each case I endeavored to determine from what conditions the necrosis developed. The tuberculous middle-ear suppurations will be excluded, because necrosis is a constant condition, and its cause is well known. The necrosis in these cases occurs from the disintegration of the tubercle (Habermann); moreover, the severe general disturbance in nutrition following phthisis is of great importance in producing the decay of bone, as Bezold has shown. The necrosis in syphilis is similar. It develops from the disintegration of the gummata.

The non-specific chronic middle-ear suppurations remain for our investigation. There were 34 autopsy reports. In some cases the trouble had led to an endocranial complication, in others it was uncomplicated. In 25 of the 34 cases, the middle-ear suppuration was the cause of death. Of

these 25 cases, necrosis was present in 16 (64 %), a number which describes the great importance of necrosis for the transmission of chronic purulent otitis to the interior of the skull.

In 3 cases, the middle-ear suppuration was in no connection with death, and in these cases the inflammation was not of a necrotic character.

In 6 cases, it was uncertain whether the endocranial complication was due to the chronic middle-ear suppuration. In these 6 cases the bone was necrotic in I.

Of the remaining 17 cases suited for this investigation, 16 were taken from the dispensary and I from the private practice of Professor Bezold, a condition which is explained by the fact that disregard of the otorrhoea is an important factor in the production of necrosis.

I first want to specify what cases I regard as necrosis. As the bone substance, the periosteum, and the medulla are uniform structures, I have considered under necrosis not only the cases with the formation of sequestra, but those where the bone was exposed and discolored but still in connection with healthy bone. If this condition occurs in the interior of the middle-ear cavities, the periosteum is always necrotic, the medullary substance is decayed to a varying depth, and if the process continues a sequestrum is formed.

If we wish to describe this anatomical picture by a special name, then caries necrotica is the most suitable. Unfortunately the word "caries" is generally regarded as a simple inflammatory softening process of the bone in acute otitis which has nothing to do with necrosis, so in order to avoid being misunderstood I shall not make use of the word "caries" and consider the above cases as illustrating the first stage of necrosis, while the second stage is described by the formation of sequestra. These two stages are frequently found conjointly in the same case, and clinically we frequently observe how the exposed bone gradually becomes detached in the form of a sequestrum, unless under changed and improved conditions the exposed bone recovers and becomes covered with the soft parts.

In 17 cases, the bone was exposed in 10; sequestra were present in 7.

In 5 of the latter cases there was only I sequestrum; in the others there were several. Sequestration had exposed the cranial cavity in 3 and the labyrinth in 1. In the remaining 3 cases, superficial particles of bone had been cast off from the inner surface to the middle-ear cavities. As has been previously noted in several of the cases of sequestra, there was a simultaneous condition of necrosis without sequestration in other parts of the middle-ear cavities. The first stage of necrosis, in other words, was much more frequent than the second. In the cases of exposed bone, the surface in half of the cases was smooth and in the other half rough. The color was dark green or yellow. In one case, after irrigation of the canal, drops appeared on the apparently healthy tegmen, which speaks for necrosis extending into the medullary spaces.

The necrosis was found in the upper middle-ear cavities more frequently than in the tympanum or the tube. The aditus and antrum were generally both affected.

In frequency the antrum was affected 13 times

The question is, What led to the necrosis of the bone and of its soft coverings in these cases of middle-ear suppuration? Intercurrent infectious disease and severe disturbances of nutrition, which are so frequent in acute purulent otitis, were absent, with the exception of sinus phlebitis in I case. In 9 cases there was no other disease than the aural affection and its consecutive endocranial complication. In 6, the autopsy revealed diseases of other organs, but of a mild character. Sinus thrombosis, which is one of the causes for the decay of the bone in the acute processes, was present in 10, and in I there was an old obliteration of the sigmoid sinus. On the other hand, this is of secondary importance, as in most cases the necrosis was primary and the sinus thrombosis the secondary condition.