Picqué, in 1907, stated that infection occurs through the duct, and depends upon diminution of the saliva, and second upon disturbed mouth chemistry. He reported five cases, three associated with pneumonia, one with appendicectomy, and one with operation for ectopic gestation.

Hadda, in 1909, insists that the condition arises from staphylococcus infection from the mouth.

Soubeyran and Rives, in 1908, summarized the pathology as follows: The condition is dependent upon two factors, (1) the diminution of the salivary secretion, and (2) exaltation of the bacterial virulence of the buccal area. The reduction of the saliva is due to dehydration of the body incident to operations, such as purgation, hemorrhage, apprehension of the patient, the anesthesia, shock, and absence of mastication. The buccal flora flourish during abolition of salivary secretion. Parotitis is, therefore, due not to the operation, but to the coexisting conditions. Worms and Bertein, in 1908, mention as local causes, traumatism, inflammation of neighboring parts, obliteration of Stensen's duct; and as general causes, typhus, typhoid fever, other fevers, cancer of the stomach, pyemia, septicæmia, and operations.

Legueu and Morel add as a factor in etiology the influence of decubitus, stating that the inflammation usually occurs upon the side upon which the patient commonly lies.

Bucknall in 1904, and Billon in 1910, quote Claisse and Dupré, who state that to produce parotitis three factors are necessary: (1) numerous or virulent micro-organisms; (2) depression of the patient; (3) quantitative or qualitative changes in the saliva.

Billon thinks that the depression of the patient is most important, for this so seriously changes the character of the saliva. He believes that the saliva has no bacteriocidal action, but that it protects the parotid only by its mechanical action.

Orthner, in 1909, reported his conclusion that parotitis, after laparotomy, was not the result of an hemotogenous infection, but only through Stensen's duct.

Maggs has reported a case arising from infected roots of teeth following extraction.

In 1909 Rolleston and Oliver, and in the same year, Fenwick, comment upon a frequent occurrence of parotitis during the

medical treatment of gastric ulcer, and in both papers it is concluded that the cause is the dry mouth incident to the starvation method of treatment. In 1000 cases of gastric ulcer 23 developed the complication, with two deaths. Rolleston and Oliver believe that the use of mouth washes will not prevent its occurrence. Fenwick, after trying various expedients, now resorts to a rubber teat which the patient sucks hours at a time, stimulating the flow of saliva.

Ewing in 1898, and von Reuss in 1906, recorded one case each of chronic parotitis in otherwise healthy children. Both conclude that the cases were chronic infections of low grade.

Johnson, in 1896, reported five cases of chronic and recurring enlargement of the parotid gland, the essential feature of which he gives as obstruction of Stensen's duct by inflammation of its lining, and that the condition is relieved usually by probing and expression.

Talley, in 1900, reported four cases of parotitis secondary to croupous pneumonia. He found four cases reported in the ten years prior to his paper. Later in the same year, Coleman, Anders, Norris and Halliday brought the number to seventeen. In the Vienna statistics Stern found six cases in 5738 cases of pneumonia. Jurgenson gives the incidence of parotitis in pneumonia as I of 1 per cent., half that of typhoid fever.

Comby, in 1882, reported the first cases of parotitis in plumbism, and in 1897 discussed toxic parotitis, giving examples in lead, copper, iodine, mercury and uremic poisoning. He concluded that the parotid gland is susceptible to toxic agents which are excreted by it, making infection easy.

Secondary parotitis, as recorded, with few exceptions is an accident of adult life. In their text-books on diseases of children, Holt, Kerley, Koplik and Still do not consider it. Jacobi mentions its occurrence in stomatitis, diphtheria and anæmia.

The condition has occurred as a sequel to infectious fevers, including typhoid, typhus, pneumonia, cholera, plague, variola, measles, scarlet fever and dysentery; associated with puerperal fever and endocarditis, with injury and disease of the abdominal and pelvic organs and the peritoneum: following various opera

tions, with a great preponderance in surgery of the genital organs and finally in various conditions like uræmia, plumbism and the like.

The present series is fairly representative of the several types. Secondary parotitis is of wide distribution in disease states, although it is relatively less frequent than might be expected. We are chiefly interested in its cause and prevention, for as we have seen, its occurrence properly gives rise to grave apprehension on the part of the medical attendant, since it is so often a bad prognostic omen.

Considered from the anatomical and physiological standpoint, the parotid gland has some characteristics which render its infection easy. First in importance is its close connection with the mouth by a short duct lined only by simple columnar and squamous epithelium: and second, its rich nerve connection with the central and sympathetic systems. Stimulation of the sympathetic supply results in vasoconstriction and decreased formation of saliva. The varied conditions in which this decreased secretion occurs is a matter of common observation. That a perturbed mind frequently ends with a very dry mouth we all can testify. In other respects the anatomy presents no peculiarity. The blood and lymphatic supply are rich.

The salient points in the production of the complication seem to me to be, first, the ever present potential infection from the mouth, and second, those phenomena which induce decreased or abolished flow of saliva through the efferent duct. We have seen that infection of Stensen's duct is practically impossible when the gland is functionating normally, but that it is easy where there is no salivary stream to mechanically prevent migration of bacteria toward the gland.

In prevention it is theoretically clear that the nearest approach to a clean mouth is important. The essential point is to insure free discharge of saliva at all times. In the exhausting fevers and cachetic states we must have some substitute for mastication. The use of a rubber teat and gum chewing are good expedients. In operations of all kinds, but especially those involving the peritoneum and the generative organs, dehydration

of the body must be lessened by reducing to a minimum hemorrhage, shock, cathartics, vomiting, sweating, starvation and the use of morphine and atropin. Manipulations of the anesthetist should be guarded, and mouth swabbing gentle. apprehension of the patient should be minimized.

Fear and

In diagnosis the only difficulty is in eliminating epidemic parotitis or mumps. Mumps is usually bilateral and the flow of saliva but slightly affected, while in secondary parotitis it is greatly lessened or abolished. Secondary parotitis is usually easily traceable to the associated condition. Suppuration is common in secondary parotitis and does not occur in mumps.

Conclusions.

1. Secondary parotitis is usually an infection of the parotid gland via Stensen's duct.

2. Sympathetic or reflex influence from the generative organs, and others, is a factor in its production only as it produces, in common with other similar processes, vasoconstriction of the parotid blood vessels and inhibition of secretion.

3. Dehydration of the body, from any cause, is a predisposing factor.

Dyball, B. M. J. 1909, 1, 1012.

LITERATURE.

Atkinson, Bull. J. H. Hosp., Oct. 1897.
Bunts, Am. J. Med. So., May, 1904.

Tebbs, Med. Chir. Tr., London, 1905.

Picque, Bull. et Mem. de Soc. de Chir., 1907.

Hadda, Berl. Klin. Wchnschrft, 1909.

Soubeyran et Rives, Arch. Gen. de Chir., 1908.

Morley, Am. Gyn., Dec., 1902.

Dorland, Tr. Coll. Phys., Phila., 1908.

Worms et Bertein, La Med. Infant, 1908.

Legueu et Morel, La Gyn., 1908.

Billon, Marseille Med., 1910, 449.

Maggs, B. M. J., 1910, 1, 1051.

Fenwick, B. M. J., 1909, 1297.

Orthner, Wien. Klin. Wch., 1909.

Le Dentu, Arch. gen. de Par., 1903, 1, 721.
Comby, Med. Moderne. Par., 1897, 8, 401.

Ewing, Laryngoscope, 1898, 221.

von Reuss, Gesell. f. in. med. u. kinderheil, 1906.

Talley, Phila. Med. J., 1900, 691.

Coleman, ibid., 878.

Halliday, ibid., 1053.

Anders, ibid., 1157.
Sajous, Cyclopædia.

Jacobi, Theurapeutics.

Leube, Medical Diagnosis.

Osler, Practice of Medicine.

Strumpel, Text-book of Medicine.

Paget, Lancet, Lond., 1886 and 1887.
Norris, Phila. Med. J., 1901.

DISCUSSION.

DR. RUSH W. KIMBALL (Norwich): Mr. President and GentlemenAfter the complete review of the literature of the subject of secondary parotitis given by Dr. Hyde, it is not necessary to dwell further upon this point. The history of the cases that he has given is fairly representative, I think, of the different types of the disease in general. At the present time, in listening to the history of the literature of the subject, I find that different authorities give different views as to the cause of the condition and the means of infection. While it may not be definitely determined, it seems to me that whether the infection is through the blood or through Stensen's duct direct, the best working hypothesis is that in the majority of cases it is through Stensen's duct.

My own personal experience with secondary parotitis is limited to four cases. Case 1, a girl of six years, with acute dysentery of a severe type. On the sixteenth day, she developed suppuration of the right parotid, accompanied with marked cerebral symptoms. No fluctuation was made out; but incision and the evacuation of a small amount of pus, with drainage, were followed by a slow recovery. Case 2, a male, forty-five years old, with malignant typhoid fever, who had extensive purpuric eruption. During the fourth week, he developed double suppurative parotitis, accompanied with general sepsis and followed by death. Case 3, a male, twenty-five years old, a soldier in the Spanish-American War. He was treated at the Backus Hospital in Norwich. In the sixth week after the fever had subsided, he developed suppurative parotitis of the right parotid. The tumor was rather superficial, and was easily palpated, fluctuation being readily made out. Incision and drainage were followed by recovery. Case 4 was that of a female, twenty-four years of age, with carbuncle of the upper lip. In the beginning of the third week, the parotid became involved. Several incisions were made, a small amount of pus evacuated, and drainage established. The patient made an ultimate recovery. This is the only case that I could certainly say was caused by extension through Stensen's duct. These cases were all private cases.