otitis media makes its appearance, with rise of temperature and usually a small perforation, often with early involvement of the mastoid process. If the membrana tympani is promptly incised, recovery ensues; otherwise the condition is apt to go on to a chronic otitis. During the first days of typhoid fever, owing to disease of the eighth nerve and the central organs of hearing, there may be impaired hearing and tinnitus, though the drumhead is normal. The condition lasts a long time, but ends in recovery or very rarely in deafness.

Pneumonia. Perforative otitis media with rise of temperature may come on in the second or third week, the infectious material being propelled through the Eustachian tube during the paroxysms of cough (cerebral pneumonia).

Tuberculosis.-Tubercular infection of the middle ear is rarely primary or derived from the blood, the infection being most frequently carried by the sputum by way of the Eustachian tube, which is often dilated as a result of fatty atrophy. On the drumhead grayish-yellow nodules appear and rapidly break down (Schwartze), leaving multiple perforations (Plate 39, 13). A large defect in the membrane may be produced by the confluence of several perforations. The drumhead and mucous membrane are frequently covered with tenacious, whitish layers of fibrin (Scheibe). As a rule, there is no pain, but the hearing is markedly affected and grows rapidly worse. The aural discharge is fetid, thin, and cascous, and contains necrotic bone and tubercle bacilli. The tympanic mucous membrane is greatly swollen and contains caseous areas with and without giant-cells (Plate 31). The epithelium is destroyed, the bone often laid bare and eroded in places. Small sequestræ are seen lying in the granulating mucous membrane. Large portions of the temporal bone are often destroyed by caries (Plate 26). Palsy of the seventh nerve is common. The wall of the promontory feels rough to the probe, the tympanic ossicles are often carious, and the roof of the tympanum

is perforated like a sieve (Plate 24); there is often no tendency to external rupture. Death is usually due to the pulmonary disease, more rarely to intracranial complications or erosion of the carotid artery (Plate 26). The prognosis is bad, but a non-tubercular otitis may occur and be recovered from in tuberculosis (Schwabach). In rare cases tubercular bony tumors are formed in the temporal bone (Körner).

Treatment.-Constitutional. Locally, insufflation of iodoethyl, and instillation of glycerinated iodoform. Radical operative intervention is justifiable if the indications are urgent and the general condition is favorable. Syphilis.-Ulcerations in the nasopharynx in syphilis extend to the Eustachian tube and lead to middle-ear catarrh or inflammation. The interference with the hearing is usually great, particularly if disease of the labyrinth is also present. The functional test is important in establishing the prognosis. If there are symptoms of labyrinthine disease, such as positive Rinne, Weber in the healthy ear, shortening of Schwabach, and lowering of the upper tone limit, the prognosis is unfavorable. A purulent otitis media ends either in recovery or in chronic suppuration.

Treatment. Constitutional, inunctions, potassium iodid. Local, the same as in non-specific diseases.

Diabetes. Fulminating perforative otitis media with extensive destruction of the bone, but usually without involvement of the soft parts. Rapidly progressing destruction of bone is also occasionally observed in Bright's disease.

Actinomycosis. Rarely primary in the middle ear; usually secondary to actinomycosis of the lower jaw. It leads to grave disease of the middle ear and mastoid process. The diagnosis is confirmed by microscopic examination.

(c) Diseases of the Eustachian Tube.-Since the Eustachian tube is of the greatest importance to the middle ear as an organ of protection and ventilation,

disease of the tube is very frequently followed by disease of other portions of the middle ear, and it is rare that a morbid process is strictly confined to the tube alone.

1. Foreign bodies may enter the tube from the mouth during vomiting; a bougie, after being introduced, may break off; gunshot wounds have occasionally been reported. The foreign body is usually forced out of the tube during hawking and swallowing; if it is visible by postrhinoscopic examination, it may be removed with an instrument through the nasopharynx.

2. Salpingitis. (a) Acute.-Etiology and Pathology.Infection, especially of the cartilaginous portion, in catarrh of nasopharynx. The tube becomes occluded by swelling and increased secretion of mucus (Plate 23, 3 a).

Course and Symptoms. In the postrhinoscopic image the pharyngeal orifice of the tube appears reddened and often contains a plug of pus or a crust. During Politzerization air enters the tube with difficulty or not at all. The drumhead is retracted, and its luster normal. At first and so long as the disease is confined to the tube there is no exudate, but the patient complains of fulness in the ears and deafness (closing of a valve in the ear), pain on yawning and swallowing, and itching in the throat when the patient takes snuff. Sometimes the condition changes to chronic catarrh.

Treatment. Treat the disease of the nasopharynx ; inflation, if necessary, with the catheter.

(3) Chronic Salpingitis.-Etiology and Pathology.—An acute salpingitis may become chronic if the nasal obstruction persists. Stricture of the tube may result from hyperemia of the mucous membrane and the formation of connective tissue, or the lumen may become enlarged through atrophy.

Course and Symptoms.-Great auditory disturbance, with symptoms of catarrhal adhesions in the tympanic cavity. There is no pain. Auscultation reveals a murmur during inflation. If the tube is dilated, there is autophonia.

Treatment.-Inflation alternating with injections of zinc sulphate, ammonium muriate, and a glycerinated solution of iodin through the catheter. Introduction of bougies which may be tipped with a 10 per cent. solution of silver nitrate. Medicated vapors (turpentine, sal ammoniac, menthol). External massage of the neck and massage of the tube. Treat the nose.

3. Ulceration at the Pharyngeal Orifice of the Tube.Adenoid vegetations are sometimes accompanied by follicular abscesses that may invade the orifice of the tube (Trautmann). Ulceration occurs in diphtheria, tuberculosis, lupus, syphilis, scrofula, variola, and malignant tumors (carcinoma). They result in adhesions and scars at the tubal orifice or between the pharynx and the velum palati, thus occluding the tube.

Treatment.-Constitutional. Treat the disease of the nasopharynx. The ulcers at the tubal orifice may have to be cauterized with chromic acid. Irrigate the nasopharynx.

4. Alterations in the Lumen.-Stricture of the tube, especially in the neighborhood of the isthmus, occurs as a sequel of chronic middle-ear catarrh. Stricture at the pharyngeal opening may be caused by the pressure of a tumor in the nasopharynx, such as adenoid vegetations, hypertrophied tonsils, or polypi; by paralysis of the seventh nerve; and by congenital cleft palate, owing to collapse of the walls of the tube. Atresia results when denuded portions of the walls lying opposite one another become adherent, especially in the cartilaginous portion, and from hyperostosis in the bony portion (Plate 23). Stricture and atresia are recognized by the absence of an auscultation murmur during inflation. Sometimes catheterization meets with great resistance, and high-pitched whistling murmurs are heard, which become lower in pitch after the passage of a bougie. Politzerization and Valsalva's experiment cannot be carried out.

Treatment. Strictures are dilated by passing bougies of gradually increasing caliber, two or three times a

week for fifteen months. Massage of the tube may be useful. If the stricture consists of connective tissue, recovery is rare. In atresia an attempt may be made to divide the obstruction with a probe-pointed knife, introduced through a catheter or by means of electrolysis. If the atresia is incurable, some improvement is obtained by making a perforation in the drumhead with the galvanocautery, or, if the distress is great, by extirpating the malleus so as to allow air to be forced into the tympanum through the auditory canal. Insufficiency of the tubal muscles should be treated by galvanization.

C. Sequelæ of Suppurative Otitis Media. (a) Diseases of the Mastoid Process (after Körner).-Disease of the mastoid process is usually secondary. Primary infection of the mastoid process may occur by way of the blood, as in tuberculosis and osteomyelitis. The diseases of the mastoid process manifest themselves as periostitis and ostitis mastoidea. Mastoid disease may appear to be primary when it occurs after an otitis media has subsided; this is particularly common in pneumococcus and influenza infection. Periostitis must be distinguished from edema, broken-down lymph-glands, and soft tumors of the mastoid process. The symptomatology and treatment of primary mastoid disease, which is very rare, are the same as in the secondary form. Periostitis of the mastoid is usually secondary to ostitis. Primary periostitis practically occurs only after injuries in connection with abscess of the parotid gland and after otitis externa. It may in that case lead to secondary superficial caries of the cortical portion of the bone, which, however, usually runs a favorable course.

1. Acute Mastoiditis (Acute Necrosis of the Bone).— Etiology and Pathology.-Infection of the mastoid process occurs after an acute otitis media, particularly in patients suffering from syphilis, tuberculosis, diabetes, or weakened by influenza, scarlet fever, or diphtheria. One of the commonest causes is retention of pus owing to insufficient drainage, in spontaneous rupture of the drumhead,