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Etiology And Pathology

Etiology And Pathology
By C. R. HOLMES, M. D.,

Age. Infancy and childhood, the latter of which we shall consider as ending at fifteen years, furnish relatively a much larger percentage of ear affections than youth and adult life. In childhood there is greater tendency to purulent inflammation, while later the chronic catarrhal form predominates. The percentage of ear affections in childhood, as given by different authors, varies considerably: Bezold found it to be 23 per cent., while Hesse puts it at 43 per cent. Difference in locality, climate, altitude, etc. must naturally produce diverse results in affections so readily influenced by external surroundings,

Heredity plays an important part in ear affections: especially is one impressed with this when examining the reports of our deaf mute institutes, where 25 per cent. or more are so attributed. From extensive observations, however, I am satisfied that quite a number of these cases are not congenital, but acquire deafness during the first and second years of life as a result of adenoids, which cause inflammation and hyperplasia, with extension to the middle and internal ear.

Predisposition. The transmission from parent to child of a predisposition to catarrhal or purulent inflammations of the mucous membranes in general, and of those lining the cavities of the middle ear, nose, and pharynx in particular, while first recognized and most ably described by v. Troltsch, has not as yet received the attention due its importance; for by an early recognition of this the physician may by prophylactics, such as early treatment, removal of adenoids and hypertrophied tonsils , favorable climatic influences, etc., limit or entirely prevent the development of ear affections.

Anatomical development is an important factor in predisposition to ear affections: deep niches in which are set the round and oval windows, unusual development of the promontory, extra thickness of the tegmen tympani, and general reduction in the size of the attic necessarily favor adhesions and deafness after inflammation.

Sex. Up to the twelfth year the percentage of aural diseases is about equally divided between the sexes, but in youth and adult life men are more frequently affected than women, which may readily be accounted for by intemperance, excessive use of tobacco, and greater amount of exposure to wet and cold.

Burkner found, from statistics of nearly 100,000 ear patients of various observers, that in 24.44 per cent. the disease involved the external ear, in 68.52 per cent., the middle ear and tympanic membrane, in 7.04 per cent., the internal ear.

Seasons. Winter and spring, the seasons when pneumonia is most prevalent, furnish about 66 per cent. of acute middle car affections. While bacteriology has proven that "catching cold " is not so frequent a cause as formerly supposed, yet the fact still remains that it predisposes through vasomotor disturbances, paralyzing the action of the ciliated epithelium, etc., and causing secretions favorable to the development of bacteria. Violent and rapidly developing middle ear inflammations are frequently due to imprudent exposure when overheated, to drafts, standing with thin soled shoes on damp and cold earth or stones, etc. Chronic catarrh involving the ear is perhaps always associated with a similar condition of the naso pharynx.

Injuries. Injuries are either followed directly by ear affections or predispose to them. Those of the external ear are least dangerous, rarely leading to permanent defect. Bruises of the auricle, as from a blow, may cause hematoma and resulting deformity; injuries supplemented by infection directly to the external meatus lead to localized or diffused inflammation, which may extend to the membrana tympani and middle ear, with extensive destruction. Rupture of the tympanic membrane may result from direct injury, such as clumsy efforts at the removal of foreign bodies from the meatus; also from violent explosions, or a blow upon the ear with the open hand, causing sudden condensation of the air in the external meatus.

Injuries involving the base of the skull generally extend to the inner and middle ear, with rupture of the tympanic membrane although the latter may not rupture, and may prevent the escape of blood and cerebrospinal fluid. The line of fracture runs usually either transversely or parallel to the long axis of the petrous portion. In a specimen in my collection, taken from a man fifty years of age who fell from a high scaffold, there are extensive fractures at the base, involving both temporal bones, with hemorrhage into both tympanic cavities. The right temporal bone has a fracture extending from the orifice of the internal carotid between the foramen spinosum and hiatus Fallopii, passing outward through the Eustachian tube and anterior portion of the tympanic cavity. Another irregular fracture runs at right angles to the first, passing through the apex of the petrous bone and through the canal of the internal carotid, immediately internal to the internal auditory meatus, down to, but not opening, the .jugular bulb; and yet both tympanic membranes are intact and normal. Where death does not result from the primary injury, inflammation and suppuration have frequently followed, which I believe to be largely due to subsequent infection in examining or treating the parts with non aseptic instruments.

Occupations involving much noise, such as those of boiler makers, coppersmiths, machinists, locomotive engineers and firemen, etc., often cause deafness. Aeronauts and divers at times suffer from tinnitus, dizziness, and deafness due to hemorrhages into the labyrinth, tympanum, or meatus.


Nervous System. Hemorrhagic pachymeningitis may cause sudden loss of hearing through extensive hemorrhage into the internal ear; or repeated small hemorrhages may take place, with resulting nerve degeneration and progressive loss of hearing, until total deafness results, associated with various noises, hallucinations and dizziness. According to Moos, the disturbance of hearing in multiple cerebral sclerosis in all probability results from sclerotic degeneration of the nucleus and trunk of the eighth nerve.

Cerebral tumors may indirectly cause disturbance of hearing. The interesting experiments of Gelle, Berthold, and Baratoux demonstrated that cutting of' the trunk of the trigeminus led to inflammatory symptoms, hyperemia, and exudation of pus in the middle ear. Kirschner also demonstrated that irritation of the fifth caused increased secretion of mucus in the middle ear. Gradenigo has proven that with increased intracranial pressure we may have changes of the acusticus similar to those observed in choked disk. Ladame and Bernhardt found that disturbance of hearing as a result of tumors of the pons occurs in about 27 per cent., and, as a rule, on one side only. Tumors of the cerebellum may cause disturbance of bearing on the side affected, opposite, or both sides. Ladame found disturbance of hearing in 9 per cent. In cases whore tumors of the corpora quadrigemina existed Bernhardt found the ears involved 4 times in 11 cases, or 36:36+ per cent. ; in 2 total deafness, in 1 subjective noises, and in I case noises and partial deafness. In tumors of the base the disturbance is seldom limited to any individual nerve, because of the close proximity of the origin of all the cranial nerves; the eighth is involved in about one third of the cases, while the optic nerve is more frequently affected than any of the others. Tumors involving the eighth nerve are sarcoma, neuroma, glioma, gummata, tubercular nodules, psammoma, and fibroma (see p. 769).

General Symptoms It is difficult to make a diagnosis of brain tumors from aural symptoms alone I especially if we find disease existing in the middle or internal ear; but subjective noises, dizziness, unsteady gait, partial or total deafness affecting one or' both sides or crossed, are important aids.

Tischkow has demonstrated that in progressive paralysis there is a formation of new blood vessels in the cartilage of the ear, growing into it from the perichondrium : it is from these easily ruptured vessels that the hemorrbages take place in hematoma.

Epilepsy and hysteria have each some influence upon the ear, but as yet the results and conclusions are too much at variance to follow up the finelyspun theories in the brief space of this article.

Respiratory Organs and their Relation to Ear affections. The respiratory organs are by far the most important causative factors in inflammations of the ear. Biirkner found 22.6 per cent., of acute middle ear catarrh and 26 per cent. of the chronic variety ascribed to cold in the head. Nasal and pharyngeal catarrh is responsible, according to various authors, for from 33 per cent., to 60 per cent., of ear affections. My belief, based upon a careful investigation of this point, is that the higher percentages are more nearly correct. We are daily more forcibly impressed with the great importance of the above named disease as a cause of ear affections. Pertussis, bay fever, measles, etc. have their influence on account of the extension of catarrhal inflammation to the middle ear. Hemorrhages into the car can occur as a result of whooping cough.

Vascular System. Atheromatous changes not infrequently cause subjective noises in the ears, which are constant and increased by circulatory disturbances. Where there is no other middle ear affection, hearing is, as a rule, normal in this class of cases.

Many aural inflammations are ascribed to dentition with as much probability as the concurrent intestinal involvement; and others are doubtless influenced by dental irritation.

Nephritis, whether interstitia ' I or parenchymatous, frequently leads to disturbances of hearing. Doumergue found it in 35 per cent. The symp¬toms vary from subjective noises to partial and total deafness, either one or both sides becoming affected, the causes being hemorrhages, inflammatory changes of the mucous membrane, or pressure from edema, while the purely nervous manifestations can be caused by the uremic poisons. The subjective symptoms and the hearing often improve temporarily after the elimination of poisonous products and the reduction of arterial tension and edema by medication.

Sexual Organs. Disturbance of menstruation, especially its cessation, influences the ears. Levy reports a typical case of complete deafness on both sides after cessation of the menses, without any other symptoms. Upon return of menstruation, three months later, hearing was completely restored.

Hemorrhage from the ear (vicarious menstruation) can also occur with or without perforation of the membrana tympani and without existing inflammatory symptoms. In the unperforated cases the hemorrhage comes from the surface of the membrana tympani and external meatus (probably out of ceruminous glands) (Gradenigo).

General Conditions. Rachitic children are frequently affected with cardisease, which is probably due to malnutrition and catarrhal predisposition. Eitelberg examined both ears of 250 children belonging to this class, and of the 500 tympanic membranes only 39 were normal.'

Gouty deposits are, according to Garrod, more frequently found in the ear than in any other organ. These deposits vary in size from a pinhead to half a pea, of pear like appearance, generally located in the folds of the auricle, hard or soft, and contain a milky or creamy fluid. Victims of this disease generally suffer lancinating pains in the ear before and during a gouty attack. Gout predisposes to the formation of exostoses of the external meatus, and these are found more frequently among the English than any other nationality.

Eczema, hemorrhage, purulent inflammation, and rapid necrosis of the temporal bones are encountered as a result of diabetes: the rapid destruction is accounted for by the lowered resisting power of the tissues, combined with extensive arterial sclerosis. This explains why in these cases violent mastoiditis can rapidly develop from a simple naso pharyngeal catarrh. The arterial changes favor excessive hemorrhages a fact to be remembered when operating. The diplococcus of pneumonia is often found in the acute purulent secretion of these cases, and is generally associated with the streptococcus pyogenes and staphylococcus pyogenes albus: Habermann demonstrated the staphylococcus pyogenes aureus in the walls of the blood vessels; the resulting toxin may lead to necrosis of the vesselwall and hemorrhage.

Caries of the teeth not infrequently causes otalgia, either constant or intermittent. The pain may radiate to the ear, shoulder, and from there to the fingers of the affected side (Urbantschitsch).

Acute and Chronic Infectious Diseases. Bacteriological studies of the effect of acute and chronic infectious diseases upon the ear have during recent years been pursued with much energy by many able investigators. The principal bacteria which so far have been studied as causative factors of inflammation of the ear are

a. The diplococcus of pneumonia;

b. Staphylococcus pyogenes albus and aureus c. Streptococcus pyogenes;

d. Bacillus pyocyaneus.

Each may be found alone or two or more varieties (mixed forms) may be found at the same time, making it impossible to state which is the primary causative agent.

Pathogenic Germs. The various streptococci are divided into two main groups streptococcus brevis and longus: the first is non pathogenetic (saprophyte); the second is virulent, and may be found in the different inflammatory processes. Furuncles of the external meatus can be caused by any of the staphylococci, although the staphylococcus aureus is the most frequent cause, gaining an entrance by the hair shafts. The middle ear may, according to the cause and character of the inflammation, harbor any of the above named varieties. In inflammation of the internal ear we find principally the streptococcus.

Avenues of Infection. There are several paths by which the microorganisms may enter the ear:

1. Through the Eustachian tube;

2. Through the external meatus and perforated membrana tympani;

3. Through the dural process in the petro squamous fissure;

4. Through the lymph and blood vessels.

While the Eustachian tube is the most frequent avenue for the bacteria to enter, nature has provided an important barrier against invasion from the nose and pharynx in the ciliated epithelium, whose motion is from the tympanic cavity toward the pharynx; it is when this epithelium is rendered defective by pathological changes that the exciting cause may enter. The main defence against bacterial invasion i's a perfectly healthy organism. Infection of the internal ear occurs most frequently through the lymphatics, especially those of the periosteum.

The character of the inflammation, whether catarrhal or purulent, active or passive, depends largely upon the virulence and number of the invading bacteria and the resisting power of the invaded mucous membrane. If the bacteria enter in small numbers and slowly, they may cause only an irritation with lymph exudation, division of the lymph nuclei, but not of the protoplasm (Moos), formation of giant cells, blood vessels, connective and even osseous tissue. If, however, they enter suddenly in large numbers, then the resulting disturbance of nutrition causes a rapid breaking down of the parts; reaction may begin and new tissue develop, resulting in hyperplasia and partial or total obliteration of the original anatomical relations.

Whether the disease shall promptly run its course or change into the chronic form depends upon the continued activity of the germs present or upon the gradual dying out of the first culture, and implantation of new varieties upon the now affected membrane. The general health is often impaired by previous disease and permits only slow restoration. We also find, especially in measles and diphtheria, that there are extensive changes in the endothelium of the blood vessels fatty degeneration and thrombosis, with necrosis of the vessel walls, resulting hemorrhages, and extensive or total loss of hearing. Minute capillary hemorrhages may also result, causing the death of a limited area only of the nerve tissues, with temporary or permanent partial deafness.

Diphtheria and Scarlet Fever. Burkner found acute otitis media purulenta resulting in 1.5 per cent., of all cases of primary diphtheria of the pharynx, and nerve deafness in 7 per cent. The ear is, however, more frequently involved in diphtheria than would appear from statistics, because in fatal cases of diphtheria (average duration six days) death results before the ear affection has become fully developed. The authorities nearly all agree that purulent otitis media results in about 5 per cent., of all scarlet fever cases. Bezold found in 185 cases of purulent otitis media from scarlet fever 30 times total destruction of the tympanic membrane I with loss of one or more ossieles, and 59 times destruction of at least two thirds of the membrane.

The author found, in an examination of 500 children at the Institute for Deaf mutes in Jacksonville, Ill., that their deafness was ascribed to scarlet fever in 7.2 per cent. and to diphtheria in 0.8 per cent.

The rapidity with which destruction may result to the ear from diphtheria is almost incomprehensible. Where death has occurred sixty to seventy two hours after the beginning of the disease the microscopic examination of the middle and internal ear has revealed numerous micrococci, not alone in the blood vessels, but also in the deeper layers of the mucous membrane and in the lacuna of the adjoining bone, often leading to extensive or circumscribed necrosis.

In measles we find that while the cars are frequently involved, there is much less tendency to extensive destruction than in diphtheria or scarlet fever, the disease rarely going beyond an acute catarrh. Solomonson found deaf mutism caused by measles in 5.6 per cent., Hartmann, 3.6 per cent. Tobeitz found otitis media in 21.9 per cent. in convalescent children. Of 22 children dying from measles, the ears of 17 were examined post mortem, and in every one the mucous membrane of the middle ear was fouud to be .diseased, although in only 7 of them had there been any clinical manifestation Of ear complication.

Typhoid fever is at times accompanied by aural inflammation varying from a slight catarrhal to a violent purulent form. This is, however, often overshadowed by the severity of other symptoms, and not noticed until convalescence has begun. The severe deafness at times present may be due to weakness of the nerve centers, and in a few cases to changes in the labyrinth: mastoiditis may also occur; while with parotid suppuration discharge of pus into the external meatus is not an infrequent occurrence.

Cerebral Origin. Disturbance of hearing of cerebral origin is frequent, and includes a wide range of manifestations, which may be caused by morbid processes of the brain or its membranes, but most frequently by involvement of the internal ear. By far the largest numbers are found as sequele to cerebro spinal meningitis: according to Knapp and Moos, the deafness develops in most cases in the first or second week.

The percentage of cases where the ears are involved in cerebro spinal meningitis varies greatly in different epidemics. Competent observers have reported on epidemics where disturbance of hearing seldom occurred, while in others nearly all who recovered were deaf. In Ziemssen's Handbuch Dr. Roth reported that from the district of Oberfrank, with 55,000 inhabitants, there were during a period of two year , 58 cases sent to the Bamberg Deaf and Dumb Institute as a result of cerebro spinal meningitis, and Moos reports that in his own practice 59.3 per cent., became deaf mute

In the Jacksonville Institute for Deaf mutes 11 found cerebro spinal meningitis given as the cause of deafness in 14 per cent., of the cases.

Larsen reports the following carefully examined case: “A girl aged seven years became hard of hearing on the tenth day of an attack of cerebrospinal meningitis, totally deaf on the sixteenth day, and died on the thirtyfirst day. Section showed the tympanic membrane normal; fine and intense injection in the entire middle ear, with muco purulent contents. In the internal auditory canal the nerves were imbedded in pus. The membranous labyrinth could not be recognized; the semicircular canals were filled with a soft reddish tissue (connective tissue with fatty degenerated round cells and blood corpuscles); the same condition was found in the vestibule and in the cochlea; and in the vestibule of the left ear also a small quantity of pus; extensive purulent meningitis of the convexity and base; the medulla was also surrounded by purulent exudations. The microscopical examination of the acoustic, the facial, cochlear, and vestibular nerves revealed no pathological changes. The otitis was evidently caused by direct infection from the meningitis."

Micrococei. The diplococcus of pneumonia is frequently found in middle ear secretions, often in pure cultures, even in cases where there is no evidence of involvement of the lungs.

Since the appearance of influenza otologists have had abundant opportunity to study its influence upon the sound conducting apparatus, and the resulting inflammations of the ears have been classified into four varieties (Moos):

1. Swelling and hyperemia of the lining of the middle ear, with little or no interference with hearing.

2. Pain, fever, diffuse redness of the tympanic membrane, and exudation into the middle ear, at first sero mucoid, later muco purulent.

3. 11 The hemorrhagic " (myringitis hemorrhagica bullosa), the most typical of the four varieties; bulle varying from bright red to a dull venous color are usually situated on the tympanic membrane, but at times found in the osseous portion of the canal ; there are much pain, fever, and deafness.

4. The form characterized by violent purulent inflammation of all parts of the middle ear, generally involving the mastoid, with fever, pain, and great prostration.

The author has bad occasion to study all of these forms, and, while the first two varieties have nothing very distinctive by which to differentiate them from similar affections due to other causes, those of the third and fourth classes are characteristic when taken in connection with the general symptoms. The hemorrhages which are so frequent in this affection, not alone in the ear ' but in other parts of the body, are perhaps to be attributed to necrosis of the vessel walls by the toxin of the influenza bacillus, which seems to have been positively identified by Pfeiffer, Kitasato, Canon, and others. This bacterium is not easy of isolation, and appears always to be found in connection with one or more pathogenic germs, or, as Ribbert states it, "the exciting germ of influenza is everywhere the quartermaster for the various pathogenic organisms."

Mumps is probably due to a bacterium which A. Ollivier claims to have isolated. In recent years quite a number of cases have been reported with severe involvement of the ears. Complete deafness of both ears has been reported, even where the parotitis was limited to one side.

Tuberculosis. Suppuration of the middle ear is a frequent affection in the later stages of lung tuberculosis. The ear affection usually develops painlessly the first symptom noticed is more or less marked deafness, followed by a slight discharge of a watery consistency; the disease in the severe form may, however, be accompanied by the usual symptoms of acute otitis. In case the chronic form becomes painful, we have to deal with a mixed infection of tubercle bacilli and streptococcus, with resulting increase of offensive purulent secretion, often leading to total destruction of the ossicles and necrosis of the mucous membrane, the bony walls becoming denuded, especially the promontory. There is nearly always extensive breaking down of osseous tissue, which may cause facial paralysis and even erosion of the carotid. (Seven deaths have been reported from carotid hemorrhage.)

Microscopically, we may find it a very difficult task to demonstrate the tubercular nature of the affection by examination of the secretions from the car alone, the tubercle bacilli often being absent, while the sputum contains them in great abundance. In many cases this is due to the development of the streptococci upon the soil first occupied by the tubercle bacilli, the new arrivals flourishing, while the others become few or are not at all present in the discharge. But we must also remember that a non tubercular suppuration of the middle ear may occur in a patient suffering from phthisis pulmonalis.

Syphilis. Strange as it may seem, considering the prevalence of acquired syphilis, there are no reliable data as to the frequency of this factor being a causative agent in ear affections. That it is one of importance is well understood; but so long as the statistics of authorities vary from 20 per cent. to less than I per cent., we must consider them of little value. The following changes have been observed: Condylomata of the external meatus; while inflammation of the middle ear often results from syphilitic infection of the nose and pharynx. In the internal ear we may find hyperemia, small cell infiltration, connective tissue formation, chalk deposits, ossifying periostitis, stapes ankylosis, and primary suppurative inflammation of the labyrinth. In inherited syphilis the disease chiefly attacks the labyrinth, developing most frequently between the ages of eight and twenty years. Hutchinson teeth and other stigmata are generally present.

Toxicants. The abuse of certain drugs has a marked influence upon the ears, quinin, salicylic acid, and tobacco being the most important. Every one is familiar with the effect of large doses of quinin. The tinnitus and deafness have in some cases proven permanent. The subjective noises are caused by labyrinthine hyperemia in the first instance, but may later be due to ischemia. The action of salicylic acid is similar, but less marked than quinin. The direct action of tobacco upon the nerve of hearing has, so far, not been clearly established, but is perhaps similar to the action upon the optic nerve. Its deleterious effect upon the mucous membrane, causing dryness, brings about or greatly aggravates existing catarrhal troubles, involving the Eustachian tube and middle car, causing tinnitus and the usual labyrinthine complications in advanced cases.


Auricle. Transitory hyperemia of the auricle occurs not infrequently in patients suffering from c9ronic tympanic catarrh or from a healed purulent middle ear inflammation associated with naso pharyngeal catarrh, and is referable to the sympathetic nerve.

Intertrigo is an excoriation of the skin behind the ears, accompanied by secretion of serum and formation of crusts. It is often caused by keeping the ears pressed firmly against the head by infant caps, and is favored by a lack of cleanliness and a tender skin in a strumous subject.

Eczema. The various classifications of eczema mark, after all, only different stages of the same disease, and here we need only recognize the affection as acute and chronic. Every exciting cause giving rise to hyperemia is capable of producing eczema by favoring development of bacteria. Gout, rheumatism, etc, predispose to this disease, in adults generally limited to the external meatus.

Herpes auricularis is a rare affection, distinguished by the formation of vesicles, generally located upon the anterior surface, and caused by irritation of the trophic nerves supplying the affected area.

Phlegmonous inflammation may result from infected wounds or infectious diseases, as typhoid (suppuration of the parotid), erysipelas, measles, scarlet fever, and diphtheria, and may develop primarily or by extension from the throat and middle ear.

Diphtheria may involve the aural region through the infection of open surfaces. In two patients, males, eighteen and thirty years of age, upon whom the author had performed the radical mastoid operation, there was diphtheritic infection of the wounds; in the younger, preceded by tonsillar and pharyngeal involvement; in the other the wound only was affected: both cases, however, experienced but slight constitutional disturbances. Cultures and microscopic examinations gave the typical Klebs Lofler bacilli.

Perichondritis of the auricle is not often encountered. The cause is frequently obscure, sometimes resulting from injury or metastatic infection, as from furuncles or otitis externa diflusa. A swelling similar to othematoma develops, and a synovial like fluid, which later becomes purulent, separates the perichondrium from the cartilage. Deformity usually results through chondromalacia. Othematoma, or blood tumor of the auricle, is formed by an exudation of blood between the pericliondrium and cartilage,' but may occur between the perichondrium and skin. The affection is either traumatic or idiopathic, the former result ing from direct injury, causing rupture of the blood vessels. The idiopathic variety is generally encountered in the insane, in whom the intracranial lesion, with degeneration and softening of the vessel walls and formation of calcareous deposits, favors spontaneous rupture under increased blood pressure during maniacal excitement or from slight self inflicted bruises when violent. The theory of intracranial disease as a cause of the idiopathic variety has found strong support in the experiments of Brown Sequard, who caused hemorrhage in the ears of animals in from twelve to twenty four hours after section of the restiform bodies. The lobule is rarely affected, but may suffer. It is more frequently the seat of abscess from infection after piercing for ear rings.

Keloids (fibromata) occur now and then as a result of wearing heavy earrings of impure metal; the growths may vary in size from a pea to a chicken's egg (Knapp), and are more common in the negro.

Atheromatous cysts are also found upon the auricle, generally upon the posterior surface (see Fig. 461). The serous variety also develops, although less frequently.

There are a number of affections which so rarely involve the external ear that it would be out of place to describe them at length in this article, and I shall merely name them to wit: syphilis, lupus, hypertrophy of a part or all of the auricle, necrosis, chalk deposits, ossification, and injuries.

The External Meatus. Hyperemia is often found in connection with inflammation of the auricle or middle ear, and may be quickly evoked by the speculum; and hemorrhage of the external meatus may result from injuries, careless removal of inspissated cerumen, or foreign bodies.

Furuncles are circumscribed glandular inflammations; hence they are most frequently situated in the cartilaginous portion of the meatus, but may also be found in the osseous canal. The central mass breaks down, forming a necrotic slough surrounded by pus; left to itself, it usually evacuates spontaneously. It is now generally accepted that the cause is in most, if not all, cases due to a bacterial infection, the staphylococcus aureus being found much more frequently than any of the other bacteria. The point of entrance is along the hair shafts and by the mouths of the sebaceous or sweat glands. Abrasion of the skin by finger nails, ear curettes, hair pins, etc. is a frequent cause of infection. Transmission by failure to disinfect the syringenozzle was observed in the Cincinnati Hospital in 1892. A typical case of furuncular inflammation of the external meatus was admitted, and within a short time eight cases developed among ear patients in different parts of the house, who up to this time had Dot suffered from the affection. In searching for a cause I found that the same syringe had been used for all of these cases without disinfecting the nozzle ; after correcting this no more cases of furuncles developed in the service.

Reflex tropho neurosis is also cited as a cause. The inflammation may in severe cases extend deeply, giving rise to perichondritis of the canal and auricle : even in the less severe cases we at times find extension to the tympanic membrane and middle ear. The author recently observed a case where two furuncles of the cartilaginous portion, accompanied by only slight swelling and pain, caused marked deafness, tinnitus, and the loss of a calcareous plaque in the anterior half of the tympanic membrane, with resulting perforation. When located on the posterior wall and near the orifice of the external canal, they may lead to great edematous swelling behind the auricle, even causing the latter to stand out at right angles closely resembling, and being mistaken for, acute mastoiditis.

Otitis externa diffusa is a general inflammation of the external ear which may result from the causes given under “Furuncles." The whole lining of the canal becomes a deep red, swollen, and covered with more or less seropurulent secretion. In severe cases there is swelling and inflammation of the auricle, even extending over the mastoid and parotid, with enlargement of the glands about the ear. The middle car is seldom involved, yet perforation of the tympanic membrane and purulent otitis media and mastoid complications may result; but the inflammation in the external meatus is not infrequently secondary to involvement of the tympanic cavity, attic, and mastoid cells.

From the latter there may be a direct opening through the posterior wall of the canal, with protrusion of granulations and discharge of pus.

Cholesteatoma (or pearl tumor) of the external canal is rare. The growth results from prolonged inflammation of the epithelium, causing excessive proliferation of the rete mucosum and exfoliation of the epidermal layer, forming laminated mother of pearl colored masses, in which are found numerous ebolesterin crystals. Fig. 462 clearly shows the laminated structure of the growth. The ear from which this specimen was taken showed extensive changes secondary to an arrested otitis media purulenta. The external meatus was almost filled with the epithelial mass, imbedded in which were three firm globular pearl tumors from 3 to 6 mm. in diameter. Removal of these left three corresponding depressions in the floor of the meatus, equal in depth to about one half the diameter of the round masses, and lined with a pearly membrane.

Neaplasm. Exostoses, and hyperostoses, or bony growths of the external canal, are most frequently situated on the posterior wall, at the junction of the cartilaginous and bony canals (Figs. 463, 494). In structure they are generally of ivory hardness, but may be cance Bons. They are ascribed to the irritation of discharge in some cases, and in the British upper classes, among whom they are not uncommon, to gout or inordinate bathing.

Lupus, syphilis, cysts, angioma, osteosarcoma, and epithelioma have been reported.

Otomycosis. A number of vegetable parasites develop in the external meatus, especially the aspergillus niger, flavus, and fumigants. Macroscopically, they appear in the deeper part of the meatus and on the tympanic membrane as brownish black, grayish white, or yellowish punctated masses. The germs cannot develop in the normal ear, but maceration of the epithelium from any inflammatory cause favors their growth. Examination of a fragment placed under the microscope reveals irregularly interlaced threads or hyphe (mycelium (a), Fig. 464), covered more. or less densely by globular masses of fallen spores (6) ; here and there a flowerlike mass is found, supported upon hyphe i. a. the sporangium or fruit capsule (c), consisting of the central receptaculum. (d), upon which are seated the long radiating cells (sterigmata), (e) ; bearing the round conidia or spores.

Ceruminous masses consist of secretion from the ceruminal and fat glands, exfoliated epithelium, hairs, and dust: their formation primarily depends upon hypersecretion, due to an excitation of the glands secondary to middle ear congestion or inflammation. It is also claimed that subnormal secretion, comparable to the dry pharyngitis often present, is responsible for the unnatural consistence and faulty exit. When large they may lead to p athological changes by pressure, erosion of the external meatus, atrophy, ulceration, and even perforation of the tympanic membrane.

The Tympanic Membrane. Vascular engorgement, especially along the hammer handle and Shrapnell's membrane, results readily from undue pressure of a speculum while making an examination or after syringing and forcible inflation.

Primary inflammation is rare. In mild cases the dermal or mucous layers only are affected, according as the inflammation originates from the meatus or tympanic cavity; while in the severer form , the fibrous layer is also affected with round cell infiltration and softening, favoring perforation. Chronic inflammations lead to hypertrophic changes in the cuticular and mucous layers, with increased growth of the rete Malpighii and exfoliation of the epithelial layers. Granulations may also form.

Practically, the same changes occur in the mucous layers, but here the granulations become larger, even polypoid. The changes in the membrana propria or middle layer are of an atrophic character: the infiltration and softening, aided by pressure of the pent up exudation, soon lead to perforation, the size of which depends much upon the virulence of the bacterial infection. The seat of perforation is most frequently in the anterior lower quadrant. When the attic and mastoid cells are involved the opening is often in the upper and posterior portion. The healing of perforations is participated in only by the epidermic and mucous layers, hence the secondary membranes are always flaccid, unless, as frequently occurs, infiltration and formation of calcareous plates have resulted. When the openings are very large or repeated ruptures have taken place, the perforations become permanent, especially if the patient is past thirty

Atrophic changes of a part or all of the drumhead are found in chronic middle ear catarrh. The membrane is thin and drawn in sometimes in scarlike areas, strongly suggesting past perforation.

Chalky deposits are generally located in the middle portion of the anterior or posterior half of the tympanic membrane; they are most often halfmoon or horseshoe shaped, and rarely reach to the hammer handle or tympanic ring. The deposits may be found only in the membrana propria, but in severe cases all lavers are involved. The pathological changes found in the tympanic membrane are of themselves of little value as an index of bearing (Fig. 465), as witness the right and left drumheads of a man twenty four years of age who suffered for many years from chronic purulent otitis media.

Hearing distance, watch, right ear, whispered voice, at 20 feet, 28/40;

Hearing distance, watch, left ear, A; only low voice spoken into the external canal.

Tympanic Cavity. From a pathological point of view we find the most important factor in middle ear inflammation to be its mucous membrane. It is in this that the inflammation must begin, and because of its peculiarly intimate relation with its underlying periosteum do we so frequently find that the pathological changes extend to the bone, resulting in hyperostosis or necrosis. There is great tendency to thickening of the mucous membrane, favored by the many irregularities slit like passages and depressions due to the chain of ossicles, ligaments, and numerous bony projections within this small space. Various classifications have been attempted; the most practical is a clinical basis, where we divide the inflammations into

a. Sero mucous middle ear catarrh.
b. Proliferous inflammation of the middle ear.
c. Muco purulent inflammation of the middle ear.
d. Acute purulent inflammation of the middle ear.
e. Chronic purulent inflammation of the middle ear.

(a) Sero mucous Middle ear Catarrh. Synonyms. Acute middleear catarrh; Secreting form of middle ear catarrh; Otitis media serosa; Catarrh of the cavum tympani and Eustachian tube.

This form most frequently results as an extension from the nose and pharynx through the Eustachian tube. There is congestion of the mucous membrane and exudation of serum, which may be mixed with mucus, the latter resulting from the beaker cells of the epithelium, as mucous glands are rare or entirely absent in the middle ear. A few pyogenic organisms may also be found, having entered through the tube, and may in most cases be regarded as the exciting cause. The exudation may fill a part or all of the cavity. The picture frequently presented is shown in Fig. 466. The drumhead seldom ruptures in this affection. Resorption, aided by paracentesis or spontaneously, with complete restoration of the parts, is the usual result if properly treated and the exciting cause corrected. The affection, having once developed, is liable to recurrence and may pass into the chronic form.

(b) Proliferous Inflammation of the Middle Ear. Synonyms. Otitis media catarrbalis chronica Otitis media sclerotica; Otitis media catarrbalis sicca.

This form, as stated above, may also develop from the acute variety, but very often it begins without any active inflammatory symptoms. There is a general or circumscribed involvement of the mucous membrane, the former most often after the exudative variety; localized forms frequently involve the oval and round windows or their immediate surroundings. The mucous membrane becomes swollen by round cell infiltration and proliferation of all its structures, which is later followed by connective tissue formation, sclerosis, atrophy, or calcareous changes. The ossicles may be completely imbedded and the niches filled with the swollen membrane; even the space between the stapes crura and the niche wall may be obliterated. The opposing surfaces of the membrane press upon each other, the inflamed epithelium becomes eroded by pressure, and adhesions form which may completely fill the round window niche. Adhesive fibrous bands may form between any or all of the ossicles and their surrounding walls. Even calcareous changes take place in the mucous membrane, generally limited to the promontory.

Ankylosis of the foot plate of the stapes with the oval window is unfortunately a condition frequently encountered in this form of middle ear inflammation caused by calcification and ossification of the ligamentous ring of the foot plate or by the formation of bony masses involving the footplate, niche, oval window, or in the vestibule (Politzer).

In most cases progressing toward stirrup ankylosis there is intense hyperemia of the wall of the ppornontory (Schwartze); and Hartmann found in this class of cases purulent naso pbaryngeal catarrh, with intense hyperemia and swelling of the mucous membranes of these parts.

(c) Muco purulent Inflammation of the Middle Ear. Synonyms.Acute catarrhal inflammation of the middle ear; Otitis media acuta.

(d) Acute Purulent Inflammation of the Middle Ear. Synonyms-Acute suppuration of the middle ear; Otitis media acuta suppurativa seu perforativa.

The pathological changes are very similar to otitis media acuta, described above, but much more intense, the purulent exudation much more copious, with breaking down of the mucous membrane in circumscribed areas and early perforation of the tympanic membrane. The inflammatory changes are not limited to the lower tympanum, but the attic, antrum, and even the mastoid cells, are affected. The internal ear is generally not involved; but the free anastomosis between the vessels of the middle and inner ear may lead to great hyperemia in the labyrinth and serous effusion, seldom to purulent inflammation (Politzer). On account of the intimate relation between the mucous membrane and the periosteum we frequently see subperiosteal abscesses and bone necrosis. This condition may run its course and end in resolution, with scarcely any visible changes of the tympanic membrane and middle ear, and with or without marked changes of hearing power; or the disease may continue and pass into the chronic stage.

(e) Chronic Purulent Inflammation of the Middle Ear. Synonyms. Otitis media suppurativa seu perforativa chronica; chronic otorrhea.

For convenience of study we may divide the pathological changes occurring in this disease into five headings:

1. We encounter formation of connective tissue bands, membranes, and masses filling the round window, partially imbedding the ossicles, and in rare cases even filling all of the tympanic cavity.

2. Cystoid spaces are nearly always found in the enormously hypertrophied mucous membranes (see a, Fig. 467). The formation of numerous bands and membranes within the middle ear results in the formation of spaces between them, either entirely closed off or as irregular ea I nals which become lined with cubical or cylindrical epithelium (b c). These spaces are often filled with mucus and degenerated epithelial masses (df).

3. Aural Polypi. These tumors originate from the mucous membrane or periosteum of the middle ear, or in rare instances from the dermoid laver of the tympanic membrane. Practically, we need only recognize two varieties: (a) The round celled polypus (synonyms, Mucous polypus, Cellular polypus, Granulation tumor) ; and (b) Fibroma.

The former variety is by far the more frequent, and consists of a hyaline, homogeneous, myxomatous stroma, sustained by a delicate fibrous structure enclosing numerous round cells. They are very vascular, the vessel walls being of the embryonal type. The epithelial covering may occur in single or multiple layers of columnar or squamous cells, and varies according to the location from which the growth has its origin (see Fig. 467).

The fibroma, as its name indicates, contains a denser fibrous framework and is less rich in blood vessels. Its surface is covered with several layers of pavement epithelium, which penetrate into the stroma with finger like projections.

4. Cholesteatoma. There is still no unanimity among authors as to the origin of cholesteatoma, but the best theory is that advanced by Haberman, Politzer, and Bezold, that it is due to an extension of the epithelium from the external canal or outer surface of the tympanic membrane through an opening in the latter into the tympanic cavity, attic, and mastoid cells.

In cholesteatoma of the middle ear we find the rete Malpighii in most intimate anatomical relation with the periosteal layer (see Fig. 468), the blood vessels in the former being in direct connection with those of the latter. Continued irritation from existing otitis causes rapid proliferation of epidermic cells, resulting in the “throwing off “of pearl colored layers from the stratum corneum, which explains the laminated structure of the cholesteatomatous mass.

Complete epidermization of the middle ear (including the mastoid cells) can, according to Schwartze and Politzer, occur without leading to the formation of cholesteatoma if the inflammatory process is arrested early. This is also proven in those cases where the radical mastoid operation has been performed on patients suffering from extensive cholesteatoma formation in the middle ear. Here we aim to “paper " the whole of the bony cavity with an epithelial lining, taking its origin from the transplanted flaps formed from the external meatus: notwithstanding these conditions we are now enabled to cure most of this class of cases. I have operated upon several cases from three to five years ago, which can now be classified as cured, since there is no sign of any return up to date.

The epithelial invasion may also take place through a fistulous opening of the mastoid cortex or posterior bony meatus (Politzer).

The size of the cholesteatomata may vary from a pinhead to a pigeon's egg. When large they cause absorption of the bony walls in any direction. In two of my cases the cortical plate of the mastoid had been entirely absorbed, so that when making the incision the knife cut directly through the skin and into the cholesteatomatous mass.

5. Bone involvement. Because of the intimate relation of the mucous membrane of the middle car and its periosteum we frequently encounter superficial or deep bone involvement in purulent inflammations. The hammer and anvil (rarely the stirrup) are often eroded or even totally destroyed (Fig. 469).

Suppurative Middle ear Inflammation with Tuberculosis. Middle ear suppuration is frequently associated with lung tuberculosis, and is characterized by the formation of one large or several small perforations in the tympanic membrane, with extensive tissue changes, without the usual pain and inflammatory symptoms. But we must bear in mind that we may find non tubercular purulent otitis media in a patient suffering from tuberculosis in other parts of the body. Neither must we conclude that the aural affection is non tubercular when we fail to find the tubercle bacilli in the secretion: their presence or absence in the ear may depend upon the period of the infection and upon the number and activity of the streptococci (Moos). The mucous membrane first becomes infiltrated by cellular proliferation, followed by ulceration, tubercle formation, and caseous degeneration. This may extend deeper, involving the bone, which becomes denuded or carious; the ossicles are also generally involved, even the foot plate of the stirrup may be eroded and the disease extend to the internal ear and cranial cavity.

Eustachian Tube. The mucous membrane of the Eustachian tube is subject to the same changes that we find in the naso pharynx, and disease may extend to the middle ear by continuity of tissue or by the entrance of infected secretion through its lumen during violent acts of coughing and sneezing, by Valsalva's method, or by the use of unclean catheters and bougies.

To guard against infection the movement of the ciliated epithelium is directed from the tympanic cavity toward the pharynx; while the isthmus, or narrowest portion of the tube at the junction of the bony and cartilaginous, portions, forms another barrier. If the disease has once passed beyond these, and especially the chronic catarrh then we cannot hope for a cure in the middle ear until the inflammation of the nose and pharynx has been relieved (see pp. 727 and 747).

Where the inflammation becomes chronic, there is thickening of the mucous membrane, with increased prominence of the normally existing folds in the tube, which, with increased secretion from the glands, causes occlusion of the lumen, preventing free ventilation of the middle ear. This condition may continue for years, but sooner or later the atrophic changes begin, with partial destruction of the glands, and reduction or obliteration of the folds; the mucous membrane becomes thin and the tube patulous. Occlusion of the tube is observed as a result of ulceration from syphilis, diphtheria, and tuberculosis.

The Mastoid. The intimate communication between the tympanic cavity and mastoid cells, and direct continuation of the mucous membrane from one to the other, explain why in severe inflammation pathological changes are found both in the antrum and adjoining cavities. There is great tendency to periosteal involvement and necrosis of the bone (see Fig. 504), with formation of abscesses subperiosteal or extradural as well as truly empyemic: especially is this likely to occur if through swelling of the mucous membrane the passage is closed between the antrum and the rest of the tympanic cavity.

Where the inflammation is chronic we may have hyperplasia of the osseous tissue, which gradually obliterates all of the pneumatic spaces, resulting in sclerosis or even in eburnation of the bone. At the same time, periosteal irritation may lead to hyperostosis of the exterior of the mastoid (see p. 751).

Labyrinth. In general anemia we observe disturbance of the internal car. The symptoms are at times especially marked where there has been great and sudden loss of blood. Diminution of the caliber of the labyrinthine vessels, due to endarteritis, is also a factor. Hyperemia may result from a number of causes, such as general congestion, 'inflammation of the middle ear, meningitis, and the various infectious diseases.

Hemorrhage into the labyrinth may result from injury, infectious disease, meningitis, pernicious anemia, and abuse of various drugs. The hemorrhages may be small and quickly absorbed, with restoration of function, or more extensive, with partial or total loss of bearing. The apoplectic forms of Meniere's disease are regarded as due to hemorrhage or acute exudation.

Secondary inflammation of the internal ear is frequent and may result from

a. Inflammation of the middle ear, the avenue of infection being generally through the windows, external semicircular canal, lymph and blood vessels.

b. Meningitis, often resulting in total deafness and, if in early childhood, deaf-mutism. In this disease we often find thrombosis of the smaller vessels and erosion of their walls, due to bacterial toxin, while the acoustic nerve is often infiltrated with small hemorrhages and bacterial colonies. If the patient survives the meningeal attack, the inflammation in the labyrinth may run a chronic course, granulation tissue forms, which again changes to connective tissue associated with development of new bone, partially obliterating the spaces within the labyrinth (see Fig. 514, p. 768).

Acquired Syphilis. Considering the frequency of this disease, we, must regard labyrinth complication as rare, and in cases where it does occur we nearly always find that the patient has previously suffered from catarrhal or purulent otitis, which caused congestion of the internal ear, acting as a predisposing factor.

The syphilitic inflammation of the labyrinth may develop in one or both ears at almost any period after the infection, but most frequently during the first two years. The chief pathological changes found consist of endarteritis, with partial or total obliteration of the vessel lumen. The inflammation may lead to necrosis or the formation of new osseous deposits, causing synostosis ,of the stapedio vestibular articulation : strangulation of the auditory nerve by periostitis and bony deposits in the internal auditory canal are also encountered.

Hereditary syphilis generally attacks the internal ear between the eighth and twentieth years, and is found from three to five times more frequently in the female than in the male. It is generally associated with interstitial keratitis, but the latter often exists without affection of the labyrinth. Hutchinson found deafness only 15 times in 102 patients suffering from syphilitic keratitis. The pathological changes found in the internal ear as a result of inherited syphilis are very similar to those resulting from the acquired infection.

Internal Auditory Canal. Inflammation of the acoustic nerve is encountered as a result of extension from the labyrinth to the brain, or the process maybe reversed. In 14 cases of mixed forms of meningitis examined by Gradenigo be found that the inflammation involved the nerve in the internal meatus 13 times, the one exception being in a case where the meningitis had existed only a few hours.

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