8

was entirely normal, the epiglottis was greatly swollen and œdematous. Three cases were reported by Sir Everard Home2 in 1808. These cases too came on suddenly. The epiglottis was greatly swollen while the tonsils and surrounding parts were practically normal. Burne's3 two cases were probably also of the same nature, one having a fatal ending. The pharynx was unaffected. Kesteven' reported two cases of epiglottitis (1849), and claimed that the disease was not met with except in connection with, or as a result of inflammation of the fauces, tonsils or larynx. One case has been reported by Windsor 11 and four by Larsen. Three of Larsen's cases were acute and one chronic. Two of the acute cases were primary and the chronic case was of syphilitic origin. This subject has also been alluded to by Wunderlich (1856). A case that had a sudden and fatal termination has been reported by Tompkins5 (1841). After death, the epiglottis was found to be greatly swollen. Other cases have been reported by Louis and Gibb.10 Another case that ended in death has been reported by Crisp.12 A boy eight years of age, after having been ill three or four days, died suddenly, apparently by suffocation. The autopsy revealed a swelling of the epiglottis which was also very red. No other lesion was discernible in any part. The peculiarities of this case were the sudden invasion of the symptoms and the circumscribed form of the inflammation, which was confined to the epiglottis. The author considered the death to be due to spasm of the glottis. No irritant had been taken. Fredet 16 has reported the case of a young man of twenty. He returned home one night after a debauch and suddenly developed great difficulty in breathing. The symptoms rapidly increased in severity and suffocation ensued in a short time. The autopsy showed great oedema of the epiglottis and ary-epiglottic folds. When the superior part of the epiglottis was incised a large amount of pus was evacuated. There was no fracture or necrosis of the cartilage. The suppurative epiglottitis was primary, followed by oedema, and the glottis ædema that caused death.

Now when we come to the more recently reported cases we find also a great similarity in nearly all, in the rapid development of the symptoms, and the almost constant presence of fever. This was particularly the case in the second case (that of a medical man, aged thirty-eight), reported by Milligan. 35 This case was considered to be of septic origin as the drains in his house were

in bad condition. The inflammation of the anterior surface of the epiglottis was probably not primary in Milligan's cases (two), as in both the faucial pillars were congested, which is not typical of acute anterior epiglottitis. In Meyje's case the anterior surface of the epiglottis was greatly swollen and there was some redness of the right palatine arch. This case is a very good example of the disease. Michel 14 did not find the pharynx particularly affected in the six cases reported by him. Two of his cases were associated with swelling of the ary-epiglottic folds, in one there was inflammation of a vocal cord, and two were complicated with Ludwig's angina. Moll19 has reported a characteristic case in which there were redness and swelling of the anterior surface of the epiglottis, dysphagia and fever. Pel13 has called attention to the condition, and also Wesseler. 17 Ruault 20 has recognized the existence of a primary circumscribed oedema of the epiglottis. In some cases observed by Gottstein22 no distinct cause could be ascertained. He questions whether oedema of the anterior surface of the epiglottis is ever primary. Schmidt 21 was and still is32 of the opinion that it is practically always secondary to injury or inflammation of the lingual tonsil. Kyle 36 states that "acute epiglottitis is not a separate condition." Störk18 on the other hand, twenty years ago recognized the fact that an "idiopathic epiglottitis" does occur under certain conditions. It is surprising that most of the prominent text books on the nose and throat either do not mention this at all or settle the entire question of the etiology of epiglottitis, with a few lines to the effect that it is very rarely, if ever, primary. Browne makes no mention of angina epiglottidea anterior as a separate condition, but believes that "acute cedematous laryngitis" is quite frequently primary. And as acute epiglottitis must be considered as perhaps a form of laryngeal oedema, and has some of the same etiologic factors, there is no reason why it may not very often occur as a primary condition. Moure15 too has mentioned the occurrence of primary œdema. Out of 6,062 autopsies held at the Charité, Berlin, thirty-three cases of oedema of the larynx were found, ten of which were primary. Bayliss 29 gives particular importance to malaria as an etiological factor in acute œdema. Kuttner, 26 Semon and Hajek have done much to clear up the vexed question of the etiology of laryngeal oedema in general, although both Kuttner and Semon are of the opinion that œdema should not be classified as a distinct condition. Semon27 claims

that many of these conditions that have been classified in the past as separate and distinct pathological conditions, have a pathological identity. I certainly believe that the whole chapter of laryngeal oedema will have to be rewritten some day. To dwell again briefly on my own three cases, we find that in each the attack came on very suddenly, with fairly high temperature, and symptoms of an acute infectious process. This is the evidenc we gather, too, from the other cases that have already been discussed.

While this is a most important point it still does not clear up the etiology, as in most of the later cases, no mention was made of bacteriological examinations. And while it is true that in a very careful search of the literature absolutely nothing was found about the bacteriology, I believe that the cultures taken in two of my cases will help to clear up the etiology. We found that the result of the culture examinations was a mixed infection in both cases. In the one a staphylococcus and pneumococcus, and in the other a streptococcus and pneumococcus infection. It will be said at once that this does not prove anything, that all these organisms, particularly the pneumococcus, are found in the mouth quite frequently, both under normal conditions (according to Park,24 who has often found the streptococcus), and also in cases of simple acute angina (Veillou25). This is of course well known, but one important fact must not be overlooked: the cultures taken in cases of simple acute angina, in which the streptococcus is nearly always found, are from surface swabbings. The swab is usually simply brushed over the surface of the mucous membrane. In my own cases, the cultures were taken immediately after scarification; after the infiltrated submucosa had been cut into, and some of the serous effusion obtained from the deeper tissues. Then too the colonies were very numerous, and there were large numbers of the organisms. This gives the question quite a different aspect, and so far as these cases are concerned, they must be regarded as examples of acute primary infectious epiglottitis. This is a reasonable deduction, and from a study of some of the other recorded cases, I believe we may come to the conclusion with a fair degree of certainty, that the majority of them were also cases of the same nature, i. e., acute infectious epiglottitis. It is of course a question, in the writer's cases, as to which organism was mainly responsible for the cedema. It

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is known that the pneumococcus, when some of the lower animals are inoculated with it, will sometimes produce local oedema. Welch, in his interesting article on the "micrococcus lanceolatus," has brought this out. He quotes Foa, who distinguished a special variety of this organism. His pneumococcus he called diplococcus lanceolatus of the oedematogenic variety. This oedematogenic variety of the pneumococcus often produces, after subcutaneous inoculation into the subcutaneous tissue of some of the lower animals, widely spreading or local oedema. Welch has also obtained cultures, which when injected subcutaneously produced uniformly extensive local subcutaneous œdema. So it is quite possible that in the two cases, the pneumococcus had something to do with the production of the œdema. At any rate it is quite clear that the oedema was an acute infectious one, and that it was primary. In a case of primary oedema of the epiglottis and larynx reported by Levi and Laurens, 28 the oedema was also considered to be of an infectious nature.

Diagnosis. The diagnosis has been sufficiently discussed in considering the etiology, so that it need only be said that the condition cannot well be mistaken for anything else. The uniform redness and swelling of the anterior surface of the epiglottis are quite characteristic. The author would enter a most earnest plea for the employment of the laryngoscope in all cases where patients complain of severe pain in the throat and inability to swallow, with a normal pharynx. It is of course not necessary to say this to a society of throat specialists, and it is only meant for the general practitioner. If the affection is not recognized early the patient's condition may become very grave and serious complications arise.

Treatment. The treatment has been largely considered in the report of my cases. I would emphasize however the vaiue of early scarifications. I thoroughly agree too with Meyje in regard to the value of an iced ichthyol spray. It certainly relieves the acute pain and reduces the inflammation very promptly. If for any reason ice, or iced sprays cannot be used, steam inhalations (medicated) would be of service.

Conclusions.

I. Angina epiglottidea anterior is very often primary and is an acute infectious process.