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Complications Of Tympanic Inflammation

Complications Of Tympanic Inflammation

PATHOLOGICAL research, as well as clinical observation., demonstrates that inflammations of the tympanic cavity, as a rule, extend more or less to the mastoid process. This occurs in two ways, either through the Rivinian notch on the outside of the adjacent bone (mastoiditis sruperficialis), or through the aditus ad antrum into the interior of the mastoid (mastoiditis profunda). Both may be acute or chronic. They are infective diseases, produced by the various kinds of pyogenic micro organisms, in particular the staphylococcus aureus and albus, the streptococcus, and the pneumococcus, which find their way into the cavities of the middle ear by way of the Eustachian tube.

The superficial mastoiditis, also called mastoid periostitis, is in the great majority of cases only the burrowing of muco purulent secretion from the tympanic attic and neighboring cavities especially the pneumatic cells in the squamous portion of the temporal bone above, behind , and before the outer ear canal on and beneath the periosteum on the outer side of the temporal bone. This variety is frequently seen in children, and most often runs an acute course. The periosteal and cutaneous swelling around the upper part of the ear pushes the auricle forward and outward. If the purulent exudation finds an outlet, either by spontaneous perforation or by an incision of the skin, in the ear canal or behind the ear, there is often a rapid and permanent recovery.

This happy termination does not occur so frequently in the other variety, the mastoiditis profunda or interna, also called mastoid empyema, which of all diseases of the ear is, on account of its consequences, the most dangerous. We shall describe the acute and the chronic forms separately.


Etiology. The causes are those producing acute middle ear diseaseviz. acute rhino pharyngitis, as produced by various kinds of exposure, seabathing, rapid changes of temperature, and different general diseases, scarlet fever, measles, diphtheria, influenza, pneumonia, typhoid, etc. Some modes of treatment may produce mastoiditis viz. violent inflation, the nasal douche, forcible syringing, operation in the nose and naso pharynx e. g. for adenoid vegetations, especially if followed by douching.

A particular disposition for the propagation of the inflammation into the mastoid cavities depends
(a) On the anatomical structure of the mastoid: the pneumatic variety, it appears, being more disposed than the diploic and the compact; and when once invaded, this favors more than the two other varieties the extension of the suppuration into the cells remoter from the antrum and to the adjacent structures.

(b) On the kind of the pathogenic microbe. It seems that the pneumococcus and streptococcus are more prone to produce the severer and more extended forms of disease than the staphylococcus.

(c) On the nature of the primary disease scarlet fever, diphtheria, and influenza being the worst. Among the constitutional dispositions tuberculosis and diabetes should be mentioned as favoring the development of mastoiditis.

Pathology. In suppuration of the tympanum and attic the pus may by simple gravity or chemotaxis enter into the antrum and adjacent cells without producing an active suppuration in the mastoid, just as in corneal abscess pus accumulates at the bottom of the anterior chamber. To wake up an active inflammation infective microbe or their toxins must enter the mastoid; ripe pus, like hypopyon, is inert. Infective purulent matter may enter from the naso pharynx through the Eustachian tube and the tympanic cavity directly into the mastoid even without causing perforation of the drum membrane. In the mastoid it produces, according to its virulence, a catarrhal inflammation congestion, edematous swelling, sero mucous exudation or a destructive, purulent inflammation of the mucous membrane, the periosteum, and the bone. In the first the mucous membrane is swollen, presenting many folds and depressions and scant, ropy secretion; in the second there are larger and smaller cavities filled with thin or creamy pus (abscesses), usually communicating with one another by narrow passage ways (fistula); but not infrequently the abscesses in the course of the disease appear in different parts of the mastoid, first in the antrum, then either in the basal or apical, or in the anterior or posterior cells. In many cases these different foci develop successively, and when the suppuration is exhausted in the antrum, it appears in the upper, posterior, and anterior recesses or in the tip. In \ cry severe cases the suppuration invades with great rapidity the whole interior of the mastoid, destroys the mucous membrane, breaks down the bony partition walls, and converts the mastoid into one large cavity filled with pus, shreds of mucous membrane, granulation tissue, and decayed bone. The knowledge and diagnosis of these varieties of the morbid process are of great importance, for they indicate the direction in which the disease progresses.

Varieties of the Morbid Process. The catarrhal form may terminate by resolution the most frequent case or may only be a preliminary stage of the suppurative form. The latter in a multitude of cases ends by evacuation of the pus into the tympanum or by perforation of the outer table of the mastoid, most commonly in the region behind the car the long known post aural abscess or it may perforate the inner table, giving rise, according to the different regions it occupies, to the epidural abscess of the posterior or middle cranial fossa, or to the cervical abscesses, all of which we shall have to discuss later.

Symptoms. Pain is usual and occurs (a) spontaneously in all degrees; in some cases, particularly in tuberculous patients, insignificant and not at all in proportion with the gravity and extent of the morbid changes; in other cases it is so severe that the patients have no rest day and night, commonly worse at night. The pain extends over the head, especially in the parietal region, but also in the occipital and frontal regions, and not infrequently shoot down the neck to the shoulder.

(b) Pain on pressure (tenderness). This symptom is very important, as it demonstrates not only the presence but also the location of the suppurative foci. If the outer bony table of the mastoid is thick and not affected, only firm (deep) pressure may elicit the pain when moderate pressure and percussion have failed.

As a localizing symptom the tenderness is most valuable. In the beginning of the affection pain from pressure right behind the upper wall of the meatus (the fossula mastoidea or antrunt pit) will rarely be absent. It indicates suppuration in the antrum. Next in frequency is pain over the tip, the base, the posterior and anterior borders of the mastoid process.

Fever. The temperature rising from 99' F. to 102' F., sometimes higher, with moderate acceleration of pulse, thirst, general malaise.

Profuse discharge from the ear; creamy, thin, sanguinolent, the latter in the severer cases; often suddenly lessening.

Redness and prominence (bulging) of the posterior and tipper part of the tympanic membrane and the adjacent portion of the ear canal. This symptom is absent when the inflammation has left the antrum and continues in other parts.

Redness and swelling of the integument of the mastoid process, differing greatly in degree, in some cases being almost absent (see page 741), in others excessively developed, so that the knife enters I to 2 cm. before it touches the bone.

Course and Termination. Spontaneous recovery in many instances occurs in one or several weeks; but the cases are not rare where it takes months, particularly when the course of the inflammation is not continuous, but intermittent.

Perforation, spontaneous or by operation, behind the ear or in the ear canal. Even in these cases the intermittent character is frequently manifest. It means that the suppuration exhausts itself in the antrum and appears in mother place later on. Not rarely do we see cases in which the opening of the antrum is followed by an immediate improvement, but this does not lead to a permanent recovery ; the fever returns, the painfulness moves to another place, and on opening there we strike another abscess, macroscopically without any communication with the antrum. This is particularly exemplified by collections of pus in the tip.

Caries in greater or less extent. This is commonly a protracted process, but in some cases of unusual severity it mail develop over a large area in a few weeks.

Transition into the chronic state may lull us into false security.

Extension into the Neighboring Parts. This and the preceding condition will be considered presently.

The prognosis of acute mastoid empyema is good if the proper treatment (rest, antiphlogosis, operation) is not neglected. If, however, the disease becomes chronic, it is dangerous to life in a degree we shall point out in treating of the intracranial complications of ear disease. Mastoid disease proper has no direct influence on audition.


We distinguish the following varieties:

Condensing Mastoiditis; Eburnation. When muco purulent mastoiditis runs a chronic course without external perforation, or with recurrent otorrhea and outward perforation, as we notice so often after the scarlatinal. otitis, the mastoid process by plastic otitis is gradually converted into a mass of compact bone, perhaps of reduced dimensions (seepage 741). Before or after the condensation of the bone is completed or comes to a standstill, many patients complain of neuralgic pain, radiating from behind the ear over the adjacent side of the head mastoid neuralgia), incapacitating them for prolonged mental labor (aprosexia). Neither by palpation nor pressure can any focus of disease be detected, and the otorrhea has stopped for months or years. The distress of such patients is so great that they willingly consent to surgical treatment. If the operation is done, the supposed deep seated focus of pus is not found, even if, as I have done, the chiselling is pushed through the whole thickness of the bone, laying the [healthy] dura mater bare; yet these patients, according to the testimony of many aurists, lose their pain and aprosexia. It is not even necessary to go through the whole thickness of the bone to obtain this welcome effect.

Empyema of the Anterior Mastoid Cells, with Perforation into the External Meatus. The preliminary symptoms are those of acute suppurative otitis media with mastoid involvement, the swelling and pressure pain, however, being not so much over the mastoid as on the posterior wall of the ear canal. The swelling is diffuse and the painfulness rather dull when compared with the pointed swelling and the sharp pain of the furuncle. Any doubt in the diagnosis can be dispelled by a large and deep incision down to the bone in the whole length of the posterior wall of the meatus as it was (lone in a successful case of mine reported in a paper published in 1893.1 If' such an opening does Dot give permanent relief, the diagnosis should be verified by the usual opening of the mastoid, as was (lone by A. Broca .2

This variety is apt to complicate a more frequent and graver extension of mastoid suppuration viz:

Empyema of the Apex of the Mastoid with Perforation into the Digastric Fossa, the so called Bezold Variety. When the purulent tympano mastoiditis has lasted several weeks or months or longer, there is swelling and sharp painfulness over the tip of the mastoid, the head of the sterno cleido mastoid muscle, and in the grave cases along the muscle down the neck into the mediastinum (terminating fatally, case of Voltolini). In an ease of' Guye's pressure on the neck and on the mastoid brought forth Pus through a fistula in the posterior meatal wall. Guye opened the swelling at the head of the muscle and liberated a great deal of pus. Water injected into the abscess cavity escaped through a fistula in tile ear canal: recovery. The perforation of the bone shows usually only a small opening in the lower medial wall of the tip. When the mastoid is opened and tile tip laid bare by detaching the tendon of the muscle, pus occasionally will ooze through the upper end of the detached muscle when the latter is held between the fingers and stroked from below upward.

In some cases the pus escaping through a perforation at the media] surface of the tip of the mastoid into the digastric fossa does not travel down the neck along the sterno mastoid muscle, but backward toward the spinous processes of the cervical vertebra. Of this variety the writer has seen only two cases. The pus followed a deep and wide fistulous canal from tile mastoid underneath a thick layer of muscles which were laid bare by a long incision, with recovery. A good case is published by Dr. Henry F. Swain of New Haven, Conn. Under the name of splenius abscesses.

Caries and necrosis of the mastoid are in the majority of cases the results of a chronic destructive, usually suppurative, inflammation which breaks down the bone and forms smaller or larger cavities filled with cheesy masses debris of mucous membrane and bone mixed with putrescent or dried up products of secretion. They keep up a steady or intermittent offensive discharge.

A peculiar formation is the so called cholesteatoma of the ear. This formation has been found as a globular mass in the temporal bone, a genuine tumor independent of any inflammation of the ear; but by far the greater number of cases presents a scaly deposit which lines the cavities of the middle ear, especially those of the mastoid, and is always connected with chronic otorrhea. If the scaly masse's form only thin layers lining the cavities, they represent the initial stage of cholesteatoma which Wendt has termed desquainative otitis. The theory of Bezold and Habermann is that epidermis penetrates through a perforation of the tympanic membrane into the middle ear, proliferates, and gradually fills and expands the neighboring cavities, forming scaly masses of a pearly color in concentric layers like an onion.

Their course varies in three directions :

(1) They, produce purulent inflammation, destroy the structures of the auditory apparatus, creating on the one hand large sinuses by converting mastoid, tympanum, and meatus into one large cavity which communicates with the air through the meatus or through a permanent opening in the mastoid spontaneous recovery.

(2) They lead by proliferation of bone tissue to eburnation of the mastoid spontaneous recovery.

(3) They penetrate the cranial cavity and cause death by one of the otitic complications.

Another consequence of caries and necrosis is the separation of larger or smaller _portions of bone (sequestra). Their formation in the mastoid is common. They are eliminated through perforations of the skin (fistule) either spontaneously or artificially. Exfoliation of larger portions of the meatal wall and the petrous bone, including the whole inner ear, have been observed, and it is surprising bow people can live and how severe and fatal consequences are absent in so many cas'es and for so long a time.

In my collection there is a specimen of which the accompanying illustrations (Figs. 503, 504) give a true and life size illustration.

Fig. 503 presents the outer surface of the left temporal bone of an adult. On the posterior part the mastoid process is totally corroded from the posterior wall of the external auditory meatus (b) up to the base of the process (c). In the center a strip of the outer bone table (a) is preserved, the tip (x), however, and the whole lower (d) and medial (e) surface of the tip, as well as the adjacent bone substance, are totally corroded. The tip itself has a large hole (x) leading into the interior of the mastoid.

Fig. 504 shows the internal surface of the petrous bone evenly and deeply corroded from the base (.f) along the anterior surface to the hiatus Fallopii (g). The corroded part extends on the anterior surface to the medial side of the eminence of the superior semicircular canal (h), to the middle of the sigmoid groove (i), backward almost to the meatus audit. int. (n). 'Laterally the sigmoid groove is deeply and coarsely corroded (k), and fistulous passages lead through the decayed bone into the digastric fossa (Fig. 504). The tegmen tympani (t) et mastoidei (m) is corroded in its full extent. On the whole the mastoid process is totally decaved and the petrous bone in its entire lateral half.

It is a wonder that people can live when the caries has produced such ravages. A greater wonder it is that we can operate on such people in such a state, preserve their lives, and stamp out the destructive disease. In a child I operated on more than twenty years ago, the whole mastoid was destroyed; the place was occupied by crumbling pieces of bone and exuberant lardaceous granulations. I removed the whole decaying mass of morbid overgrowth. The dura lay extensively bare. The operation seemed to be an ante mortem autopsy, yet the child recovered. Ten months ago I removed carious and necrosed bone from the mastoid and petrous bone of a child, which in the living presented all the symptoms exhibited by the specimen depicted above; and, although tuberculosis was at the bottom of the affection, the child was perfectly cured. The tolerance by the organism of such deep and exten¬sive ravages cannot be depended on, however, and these destructive processes are the chief causes of the disastrous intracranial complications of ear disease which we shall now discuss.


Etiology. The intracranial complications of ear disease are almost exclusively produced by the propagation of purulent inflammation of the different parts of the middle ear.

Occurrence. They are met with in only a small percentage of ear diseases, but are most dangerous. According to Burkner,' who found 104 deaths in 33,107 ear cases, as well as according to Randall,' who found 15 in 5000, threetenths of one per cent. of all the ear patients die from otitic intracranial disease. Schwartze found in the Prussian army 30 deaths in 8425 diseases of the middle and inner ear i.e. e. 0.35 per cent.

The death rate from purulent ear disease, compared with the death rate from all diseases treated in a large general hospital, has been ascertained by N. Pitt,, who found among 9000 successive autopsies in Guy's Hospital (London) during the years 1869 1888, .57 deaths from purulent ear disease, which is I out of 1.58, or very nearly 2 of I per cent.

Prof. J. Gruber' examined the post mortem records of the Vienna Genoral Hospital and found 232 deaths from otitic intracranial disease among 40,073 autopsies i. e. 0.58 per cent.

Propagation. In the great majority of the ease, , ear disease extends into the brain through destructive inflammation of the bone (Fig. 505), by which infective material enter , the cranial cavity, accumulates between bone and dura, and causes pachymeningitis, leptomeningitis, sinus thrombosis, cerebral and cerebellar abscess. The infective material may, though rarely, be conveyed into the skull by offshoot , of the dura mater, the aqueducts (Fig. 506), and the canals through which blood vessels, lymphatics, and nerves pass from the tympanic into the cranial cavity.

The infective material consists of the different species of pyogenic microorganisms staphylococcus pyogenes, streptococcus, pneumococcus, and others, the same that cause the primary ear disease and their products, the toxins.

Causes. Generally only the severer forms of otitis media are complicated with brain disease, such forms as are caused either by certain acute general diseases scarlet fever, diphtheria, influenza, measles, variola, and typhoidor by some chronic, debilitating, constitutional affections tuberculosis, diabetes, syphilis. Sometimes grave cases of purulent otitis, terminating fatally by brain complications,. are caused by accidental atmospheric, chemical, and mechanical influences ; for instance, blizzards, sea bathing, foreign bodies in the ear, rough and unclean methods in removing foreign bodies and diseased deposits from the ear, forcible syringing in acute suppuration, all devices and remedies tending to pen up secretions, such as tampons and coagulating powders, morbid formations in the middle ear and auditory canal e. g. polypi, sequestra, exostoses, cutaneous membranes, cystic and other tumors.

Acute purulent otitis leads more rarely to intracranial complications than chronic; yet by no means so exceptionally as was formerly believed.

Passageways of Infection. The channel of invasion of the skull cavity most frequently passes through the medial and superior walls of the mastoid into the posterior cranial fossa ; next in frequency it passes through the tegmen tympani into the middle cranial fossa, then through the medial wall of. the drum by way of the labyrinth and the internal ear canal, or directly through the posterior wall of the petrous bone into the posterior cranial fossa ; rarely through the lower an(] anterior walls upward along the fossa for the bull) of the jugular vein or the carotid canal. Exceptionally the infective material travels through the tympanic ostium of the Eustachian tube or the semicanal for the tensor tympani muscle forward and inward, forms a retro pharyngeal abscess, and penetrates through one of the crevices at the base of the skull into the cranial cavity, as in a case of Troltsch' and another of the present writer!


Meningitis in general may result from a constitutional infective disease, such as tuberculosis or syphilis, or it may originate in a neighboring structure, from a wound of the skull, or, what concerns us here, a diseased i. e. suppurating ear. We may distinguish pachymeningitis from leptomeningitis.

Pachymeningitis may be external, the common kind, or internal.

Pachymeningitis Externa; Epidural or Extradural Abscess. The infection may be carried

(a) Through vascular and membranous canals from the inflamed tympanic cavity through healthy bone into the cranial cavity, which is very rare;

(b) through a fine, fistulous canal, not always macroscopically discoverable, through apparently healthy bone; or, the most frequent condition and

(C) through bone broken down by caries, necrosis, or erosion and atrophy from cholesteatonia and tumors. Jansen 3 describes a peculiar channel namely' through the labyrinth and the aqueductus vestibuli to the posterior surface of the petrous bone with formation of an empyema in the endolymphatic sac.

As pachymeningitis externa leads to thrombopblebitis and abscess, the reverse course may occur; thrombophlebitis and abscess may induce pachymeningitis and leptomeningitis, which then commonly prove fatal in a short time.

Pathology. W, hen we expose the dura in cases of acute purulent otitis media we usually find it either normal or slightly reddened and dull , in more advanced inflammation it is vascular, thickened, and beset with granulations. In chronic cases, with circumscribed caries or necrosis of the underlying bone, it is blackish like the bone, softened, gangrenous, and perforated, bathed in serum. In purulent destruction of the, bone it is separated from the latter by pus which has the characteristics of the pus in the middle ear, creamy and sweet in the acute, thin, greenish, and offensive in the chronic, cases. In a very chronic course the dura may be greatly thickened and fibrous or sarcomatous looking. Zaufal' describe , a case in which the dura was 1.5 cm. thick; and the writer has seen a similar case where chronic empyema of the sphenoidal and ethmoidal sinuses showed perforation of the optic groove at the sella turcica and the greatly thickened fleshy dura looked like a flat sarcoma, but gradually thinned down and was attached to the healthy neighboring bone. The pus between dura and bone does not collect in a circumscribed cavity, but spreads in different directions, following readily the sigmoid sulcus into the jugular foramen, and up along the transverse sulcus toward the torcular Herophili, also at the bend of the sinus into the middle cranial fossa.

Epidural abscess may be recovered front by a spontaneous opening into the ear through the medial wall of the mastoid, the roof of the tympanum, the squama temporalis, or through the occipital bone above and behind the ear canal. The writer has seen spontaneous perforation of the occipital bone 4 or 5 cm. behind and about I cm. above the ear canal in two cases. He opened the subperiosteal abscess, and could introduce a probe through the bone fistula into the posterior cranial fossa. One case made a spontaneous recovery,' and has been under observation these three years; the other died from sinus thrombosis and leptomeningitis fifteen years ago. The autopsy showed 3 that the bone fistula was about in the middle of the transverse sulcus. In the great majority of cases of epidural abscess the (lure perforates and the patient dies from consecutive cerebral abscess or purulent sinus thrombosis and leptomeningitis. All these grave affections may occur together in one case.'

Diagnosis. In most cases the presence of an epidural abscess is ascertained only during the operation, when the broken up medial wall of the mastoid or a fistula either in this wall, in the roof of the drum and mastoid or in some other part of the skull leads into the collection of pus. In many cases symptoms of meningeal irritation are present namely, headache, slight rise of temperature, pressure pain, somnolence, slowing of pulse, vomiting, stiffness of the neck, choked optic disk ; but these symptoms are too indefinite to make a diagnosis. If after the opening of a subperiosteal abscess a probe can be passed through a bone fistula into the cranium, we may be assured of the presence of an epidural collection of pus. In a number' of cases, however, doughy swelling and tenderness on pressure about one inch behind the car canal, the place of exit of the mastoid emissory vein, and the history and other symptoms make a cranial complication probable, and we may fairly suppose that we have to deal with an epidural abscess.

Prognosis. If we know that, with the few exceptions of a spontaneous perforation, epidural abscess is always fatal, the indication of operative interference is imperative. As in the majority of cases the diagnosis is uncertain, the operation should be begun in an exploratory way, and desisted from or continued and terminated according to the conditions revealed. When operated on, almost all cases recover.

Pachymeningitis interna (subdural, or intradural abscess) is not often met with. When in a circumscribed place the externally inflamed dura is corroded, softened, and perforated, exudation is deposited on its inner side in the subdural space. If during this process the araelmoid and pia are agglutinated to the dura, pus may accumulate in this place and form a subdural abscess, with softening and ulceration of the adjacent brain substance circumscribed encephalitis. W. Macewen, in his classical treatise on the 11 Infective Diseases of the Brain and Spinal Cord," described several cases of this variety, one of which (Case X., p. 75) was cured by an operation.' If, on the other hand, this agglutination does not occur, the infective exudation spreads in the subdural space and leads to

Purulent Leptomeningitis. The pathogenic substances may be carried into the arachnoid space in various ways (a) after perforation of the dura, as we have seen, or (b) without perceptible perforation. Leptomeningitis is developed chiefly in the neighborhood of the diseased dura, on the base of the brain, traveling thence to the convexity of the game side, and to the base and convexity of the other. In rare cases the convexity only shows macroscopic changes, whereas the base appears 'healthy, as it was in the case described and depicted by the writer in the Archives of Otology, 1895. p. 125. The pus is collected in the furrows between the convolutions and also in disseminates patches. The pia is hyperemic and edematous. In addition to the purulent meningitis we frequently find the tubercular kind; and lately attention has been called by Quincke, Levi, and others to serous meningitis.

Meningitis purulentq maybe general or partial (circumscribed). It has been found oftener on the right side than on the left (korner)

Etiology. Meningitis may be induced as well by acute as by chronic purulent otitis, with or without caries. It may be uncomplicated or accompanied and caused by sinus thrombosis and cerebral abscess. Otitis in tubercular and syphilitic subjects leads more readily to meningitis than otitis in healthy subjects. It rarely occurs in small children, which is remarkable. The author has operated on children between one and four years old where the greatest ravages caries and necrosis destroyed the mastoid and petrous and laid the dura bare to a very large extent; yet the children bad no symptom of Leptomeningitis and recovered.

Duration. Otitic meningitis may be acute in exceptional cases fulminating, setting in almost suddenly and terminating fatally in four or five hours or in several days or chronic, with mild symptoms and intermissions at first, then developing into the regular course, which usually lasts one week or less, more rarely two or three weeks.

Symptoms. Headache is, as a rule, the earliest and most pronounced symptom. At first it is parietal, occipital, or frontal, and on the same side, later general.

Dizziness, restlessness, irritability, auditory and visual hyperesthesia, mental weakness, loss of appetite, constipation, drowsiness without regular sleep, nausea, vomiting, optic neuritis (rare), more or less constant acceleration of pulse and elevation of temperature, delirium, convulsions, and coma are the chief symptoms of the regular course. They may be modified by complication with abscess (temperature high, pulse slow) and septic sinus thrombosis (rapid diurnal changes of temperature).

Prognosis. Purulent meningitis due to ear disease, like that due to other causes, terminates fatally in the great majority of eases. How numerous in well established diagnosis the exceptions are must be left to future observations in brain surgery to decide. The cases of diffuse purulent meningitis thus far reported as cured by operation do not stand criticism ; whereas .partial meningitis, epidural and subdural abscess, and the serous meningitis, which shows a majority of the symptoms of diffuse meningitis, have undoubtedly been cured by operation, and some have recovered spontaneously.

Sinus Thrombosis and Pyemia. Pathology, Course, and Termination. The destruction of mucous membrane and bone tissue in the middle ear and mastoid process by way of pachymeningitis, epidural abscess, and phlebitis frequently induces sinus thrombosis. If the thrombus is parietal and uninfected it causes no appreciable disturbance of the patient's health; if, however, it becomes contaminated with pyogenes matter through perviousness of the vessel wall by erosion, softening, and perforation, the thrombus becomes septic, decays, and causes pyemia. The lateral sinus is the one most exposed, but small bone veins may carry the infective material into the sinuses from different parts of the temporal bone. The thrombus may be partial or total (occlusive), uninfected or septic, single or multiple, limited to one sinus, or extending over almost all sinuses and veins of both cerebral and cerebellar hemispheres. The lateral sinus is more frequently thrombosed than any other, particularly its sigmoid segment; and then the inferior and superior petrosals, the cavernous sinus, the bulb and the whole length of the internal jugular.

Non infected thrombi may disappear by absorption, or may by a kind of “organization " obliterate the vessel and do no harm. Infected thrombi may in rare cases, by destruction of the sinus wall, be evacuated through a fistula, of the destroyed bone, without causing disastrous consequences. Not quite so they are carried by the blood current into distant organs, especially the lungs, and produce larger and smaller metastatic abscesses and pyemia. Even in such cases recovery by and even without surgical interference is possible. In the majority of cases, however, if the affected sinus is not operated on, septic sinus thrombosis proves fatal by metastatic abscesses, pyemia, cerebral or cerebellar abscess, and purulent meningitis.

Sinus thrombosis is more frequent in men than in women, and more frequent on the right than on the left side. It occurs more rarely in acute than in chronic cases, and the predisposition to it is greatest in the second and third decades of life.

Symptoms. Arranged according to their frequency and importance we note:

(1) Headache. It corresponds more or less to the situation of the thrombus, usually 2 or 3 cm. behind the upper edge of the external ear canal, over the knee of the lateral sinus where infective otitic thrombosis most often begins. It may, however, radiate over the parietal region of the head or be marked in the occiput, rarely in the forehead of the same side. The headache may be most intense, depriving the patient of all sleep during twenty four hours.

(2) Acceleration and weakness of the pulse, more or less constant.

(3) Rapid changes of temperature, running from near the normal up to 104' 106' F. in several hours, and falling again to the original level the same day the characteristic steep peaked temperature chart of pyemia. See the accompanying chart (Fig. .507), taken from a recent publication of Fred. Whiting of New York: “Three Successfully Operated Cases of Pyemic Sinus Thrombosis."

(4) Rigors._Quotidian or tertian chills lasting half an hour or longer, followed by profuse perspiration.

(5) Swelling and tenderness over awl behind the posterior edge of the mastoid (sigmoid sinus thrombosis); further back, half way between the ear and the occipital protuberance (transverse sinus); in the depth and around the orbit with protrusion of the eyeball (cavernous sinus); below the tip of the mastoid and down the anterior border of the sterno cleido mastoid muscle (bulb and internal jugular vein, which in its upper portion and sometimes in its whole extent is felt as a bard and tender cord.

(6) The tongue is dry and coated, and the appetite lost, in marked cases to the refusal of all food.

(7) Diarrhea in most cases, constipation in some.

(8) Comprehension slow.; stupor and optic neuritis only in complication with encephalic abscess and meningitis.

The diagnosis in uncomplicated infective sinus thrombosis is easy; in complicated cases (abscess and meningitis) the marked and characteristic symptoms (steep peaked temperature curve and rigors) of pyemia overshadow those. of abscess and meningitis, so that in complicated cases it is easier to recognize the presence or absence of thrombosis than that of abscess and meningitis.

The prognosis is bad it the disease is allowed to take its natural course only a few well established cases of spontaneous recovery are on record. The prognosis is much better since the advance of otology and surgery has led to the early recognition and the operative cure of this disease. The mortality even now is still considerable, and the records of well described cases at present at our disposal do not suffice reliably to express the percentage of mortality. The prognosis in any given case, short of deep coma, is not absolutely hopeless, since even patients with the severest cephalic symptoms and severe metastatic pneumonia have recovered.

Osteitic Pyemia with Sinus Phlebitis (Osteo phlebitis of the Temporal Bone).This disease is rare. It is caused by the entrance of pus from the primary focus in the ear or the temporal bone into the general circulation through small veins. The symptoms are like those of pyemia from sinus thrombosis. Its existence as distinct from the latter is doubted, but any one, who has ever seen, like the writer, a fatal case of pyemia from osteo myelitis of the thigh, will ask with Korner: Why should such a disease not originate in an acute inflammation of the mastoid? Rigors are not so frequent as in, sinus thrombosis; metastases are rare in the lungs, but occur in the joints, muscles, and the subcutaneous connective tissue, and the streptococcus has been found in them as the pathogenic germ. The prognosis is better than that of sinus phlebitis; and the treatment should be conducted according to general surgical principles; some cases in which the internal jugular was ligated have ended fatally (LaDe, Deansley, Langenbuch).

Septic Affections from Suppuration of the Ear and Temporal Bone. This variety is distinguished by a very rapid course (sometimes in a few days), severe cerebral symptoms, especially delirium, high continuous fever, septic endocarditis and nephritis, hemorrhages in the endocardium, the muscles the retina, etc. Korner describes two cases of his own practice in which he dwells on the rapidly increasing edema in the region of the diseased bone and the infected cervical glands, while the sinuses and emissary veins were entirely intact. In a case under Frankel's care, which ran its fatal course under the picture of a dermato myositis, the tissue juice and the muscles were filled with streptococci in pure culture. Korner says that this supports the supposition that these septic processes spread chiefly through the lymph channels, not like the pyemic through the blood vessels. The present writer cannot suppress his impression that the above observations might have been cases of primary otitis purulenta complicated with erysipelas.

Brain abscess (Cerebral and Cerebellar). This severe affection is induced in the great majority of the cases, not by disease of the mucous membrane, but “by disease of the bone which almost always extends to the dura, mater In 9 per cent. it has been caused by acute, in 91 per cent., By chronic otitis. The dura is almost always united to the surface of the brain at a point where the cerebral abscess is nearest to the diseased bone. The brain substance which separates the abscess cavity from the place of union between dura and bone is, as a rule, only a few millimeters broad, and has almost always in 84 out of 90 cases been found diseased “(Korner)..

The abscesses are found in the neighborhood of the diseased bone, about 66 per cent., in the temporo sphenoidal lobe, over the legman tympani et mas¬toidei, upon which the fusiform gyrus is situated ; 30 per cent. in the cerebellum, near the sigmoid groove, where the anterior surface of the cerebellar hemisphere is situated (Fig. 508) ; the remaining 4 per cent. are found in the crura cerebelli ad pontem, the pons, or very rarely in the occipital or frontal lobes. In children, statistics show that 82 per cent. are in the cerebrum, 18 per cent. in the cerebellum ; in advanced years we find 63 per cent. in the cerebrum, 37 per cent. in the cerebellum, all of which is explained by the development of the pneumatic spaces in the mastoid with advancing years.

In 15 per cent., more than one abscess has been found in the brain.

The size of the abscess varies from the smallest dimensions to the occupancy of almost the entire temporo sphenoidal lobe. Among the largest is the one described and depicted by the writer in 1895.1 It was 8 cm. long and 6 cm. high. They contain usually the same kind of pus as the otorrhea shows, thick and creamy or thin, frequently greenish and offensive. The majority being chronic are capsulated. The capsule has been found from 1 to 5 mm. in thickness. Those non capsulated are commonly surrounded by a zone of softened brain substance, which easily ruptures when the brain is removed. Not only abscesses that are free from ' but also most of those invested with, a capsule continue to grow nevertheless.

Abscesses may in their growth communicate with the mastoid or the middle ear and give off continuously, some of their contents; they may also erode and perforate the cranial capsule and discharge pus through a fistula, as in the case of Schede, one of the earliest to be successfully operated on. Spontaneous evacuation through the ear has been noticed by Randall' (Fig. 509) and many others, yet it did not cure the abscess. A notable fact is that a constant otorrhea from central abscess often suddenly stops during the course of an operation without any significance as to the result. The only case of spontaneous recovery of a cerebral abscess on record is by Sutphen, of Newark, N. J., who found at the autopsy of a patient dead from arrosion of the carotid an old abscess which had emptied itself previously by a carious perforation of the temporal bone. The almost unexceptional termination of an encephalic abscess, if not operated on, is death, caused either by cerebral pressure and edema, by perforation into the ventricles or the subarachnoid space, or through complicating sinus thrombosis and meningitis.

Symptoms, Course, and Termination. In manv cases we may distinguish four stages : the initial, with fever, headache, vomiting, etc. ; the latent, with milder discomfort; the manifest, with the full development of a severe brain disease; and the terminal, with exhaustion and coma, or sudden appearance of the fatal phenomena from perforation into the ventricular or arachnoid cavities.

According to v. Bergmann' three groups of symptoms may be distinguished viz. :

1. General Symptoms. WeakDess, loss of appetite, foul tongue, pale or yellow color as in all grave diseases ; fever moderate or absent.

2. Cerebral and pressure symptoms, generally more pronounced in cerebellar than in cerebral abscess.

Headache is the earliest, most conspicuous, and most constant symptom. It is usually in the neighborhood of the abscess, but not infrequently in other regions, particularly the occiput and forehead and all over the head.

Tenderness on percussion is frequently but by no means generally present. Macewen's symptom, that one ear applied to the vertex of the patient hears the percussion sound stronger from the diseased than from the healthy side, is ' as far as my experience goes, unreliable. Nausea and vomiting are almost always present,, but not characteristic. Dizziness and disturbance of equilibrium are frequent.

Disturbance of the functions of the brain is a frequent and marked symptom. Slow comprehension, apathy, incoherence of ideas, weakness of memory ; at night frequently great mental excitement, crying, restlessness, delirium, alternating with drowsiness, optic neuritis, earlier and more pronounced on the diseased side; convulsions; elevation of temperature, moderate, usually with evening exacerbations ; pulse slow; respiration regular.

3. Localizing Symptoms. Deafness in the non suppurating ear has been observed several times, and is explained by the fact that the auditory center of the right ear is situated in the temporal lobe of the left side, and vice versa. Word deafness mental or sensory deafness i. e. the patient hears the word but does not understand it. Amnesic aphasia, agraphia, anarythmia are rare, and motor aphasia has not yet been noticed in uncomplicated brain abscess. Word blindness, dyslexia (Berlin), letter blindness, and “word" without " letter " blindness,' conditions in which with normal vision the patients cannot understand written or printed language, are referred to the visual memory center situated in the angular and supramarginal gyri on the left side of the brain.

Crossed paresis, crossed atonic and tonic spasms, and convulsions, crossed facial paresis and crossed hermianesthesia, all due to a lesion of the internal capsule, are occasionally met with.

Homonymous hemianopsia has been recorded seven times. It would probably have been found oftener had it regularly been sought after. In a case of abscess of the temporo sphenoidal lobe operated on by the author, December 11, 1893, it was one of the determining SyMptOMS.3 The abscess was found at the first exploratory puncture and the patient is now perfectly well, but the homonymous hemianopsia is permanent. This symptom is produced by a destruction of the optic tract, somewhere along the optic radiation between the region around the calcarine fissure and the optic chiasm. In cerebral abscess it refers chiefly to the optic radiation in its subcortical passage through the temporo sphenoidal lobe.

Cerebellar ataxia and vertigo are due to lesions of the worm.

Opisthotonos, partial or total paralysis of the motor communis oculi and the abducens nerves, conjugated deviation of the eyes in some cases toward the affected, in others toward the unaffected, side, and. nystagmus, are rare and indefinite symptoms.

Differential Diagnosis of Purulent Mastoiditis and its Different Intracranial Complications. In children it is often difficult to ascertain whether the mastoid is diseased alone or together with the intracranial structures. Meningeal irritation caused by congestion and edema is not rare, but difficult to distinguish from infective intracranial inflammation. The course will show; and if on account of the persistence of alarming symptoms an operation is decided on, the conditions exposed by the chisel will lead to the diagnosis.

In children and adults the most important helps in the diagnosis are the kind and seat of the original (ear) affection. Here also an exploratory operation will frequently be the decisive step. The diseases in the middle cranial fossa are induced by disease of the tegmen tympani and tegmen tube. (The author has seen purulent meningitis of the anterior and middle lobes imitating a brain abscess from attic suppuration with extension to the pharynx by way of the semi canal of the tensor tympani muscle.) Disease of the cerebellum is produced chiefly by mastoid suppuration, rarely by disease of the petrous bone, in which case the infection is carried through the labyrinth and inner auditory meatus into the cerebellum. The latter variety can be recognized by the total deafness it produces in the affected car.

The diagnosis is difficult if tubercutosis, nephritis, diabetes, etc. are complicated with chronic otorrhea. The author, in a case of supposed brain abscess, decided to open the skull, but desisted when he found that the inner table of the mastoid was healthy. The patient died of tuberculous meningitis (autopsy).

If cerebral disease exists together with suppuration in both ears, it may be difficult to ascertain in which hemisphere the brain lesion is. Local pain, tenderness on percussion, and other local symptoms such as edema and redness over mastoid, etc., may help in making the diagnosis.

A cerebral tumor may coexist with purulent otitis media. The diagnosis will usually be possible. The tumor has a slow development, no fever, no rigors, almost always optic neuritis, and constant headache.

The diagnosis between abscess and meningitis is made by the high temperature and acceleration of the pulse, without remissions, and the irritability, general excitement, restlessness, and hyperesthesia of the organs of sense in meningitis, contrasted with the slow cerebration, apathy, and drowsiness in abscess. Slow pulse with meningitic temperature, etc., may indicate coexistent abscess (Randall)'

Infective sinus thrombosis is characterized by mental depression, rigors, constipation, anorexia, apathy, and the steep peaked pulse chart.

Two, three, or all the intracranial complications may be present in the same patient. The writer has had under observation a patient in whom the autopsy showed mastoid empyema, perforation of the lower mastoid wall and extension of the pus down the neck, epidural abscess in middle and posterior cranial fossa, septic thrombosis of all the sinuses of both internal jugular and most of the cerebral veins, an abscess in the temporo sphenoidal lobe, another in the cerebellum, and to render the morbid collection complete, diffuse purulent meningitis.'

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