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Acute Affections Of The Larynx And Trachea

Acute Affections Of The Larynx And Trachea.

GUERSANT first clearly described the simple form of this disease. The disease process consists of a very mild non dangerous inflammation of the mucous membrane of the larynx, not absolutely confined to any age, but usually occurring in adults, and may run on to a chronic condition.

Etiology. It may be primary or secondary, idiopathic or the result of some direct and known irritation. Its principal causation is the process known as “catching cold," grafted upon an already slight and possibly chronic hyperemia or congestion of the lining membrane of the larynx. Occurring primarily in the larynx, this disease is extremely rare. Indeed, Bosworth considers it as invariably secondary to an inflammation in some other portion of the upper respiratory tract. The irritation caused by inhaling air not properly warmed and moistened or filled with particles of dust; irritating vapors, such as chlorin, bromin, sulphur, ammonia, tobacco smoke, etc., predispose to chronic change; and the stimulus of cold produces the acute condition. In early life, frequent attacks of tonsillitis, pharyngitis, and the hypertrophy of the pharyngeal tonsil predispose to attacks of this disease; while in later life some chronic process in the nose or naso pharynx is frequently found. On account of the greater exposure, it occurs most frequently in men.

Pathology. The changes in this disease are entirely similar to those occurring in acute catarrhal inflammations of all mucous membranes. There is at first dilatation with engorgement of the blood vessels and arrest of secretion from the muciparous glands; later there follows a serous and mucous hyper secretion. The greatest swelling is found where the membrane is most lax at the arytenoid commissure and subglottic region.

Symptoms. Changes in the voice are chiefly noted. It may be hoarse, dulled, or entirely lost; phonation may be slightly painful and labored; there may be slight dryness, roughness, or tenderness of the throat, accompanied by a tickling sensation. The cough, when present, is dry, harsh, and painful. Except in young children there is rarely any interference with respiration.

Diagnosis. Changes in the voice and the metallic cough will indicate the seat of disease. The laryngoscope will reveal in mild cases the enlarged blood vessels scattered over the mucous membrane, and especially noticeable on the cords, commissure, and ventricular bands; in severe cases the membrane may be pink or deep red in color, and there may be small localized hemorrhages. When swelling is noticeable the function of the cords may be interfered with, resulting in aphonia. Infiltration of the muscles interferes with proper adduction. The rise in temperature is very slight, rarely exceeding 100' F.

The disease runs a course lasting from five to ten days and ends in resolution. It is of importance chiefly to singers and public speakers.

Treatment. The whole upper air tract should be considered in treating this disease. In the, early stages direct local applications should, perhaps, be avoided. The inhalation of steam, medicated with the Oil Of Pine, compound tincture of benzoin or the oil of eucalyptus, with the wet pack locally, should be sufficient. The use of oil sprays is of unquestioned service. Later in the disease we may try the direct application of astringents, such as nitrate of silver (I to 2 per cent. solutions), menthol, or some preparation of tannin or iron. To relieve the cough a mild dose of codein may be prescribed. The exhibition of large doses of the muriate of ammonia (30 to 40 grains) will, at times, very rapidly control the disease.


It has been found that in childhood the mucous membrane of the larynx possesses a greater number of vessels and lymphatics than later in life, and that the tissues are less resistant and more relaxed. In consequence, there are some differences, from a clinical point of view, in the disease as occurring in childhood. When the disease develops in early life, certain characteristic features are noticeable in relation to the anatomical region attacked. According as the mucous membrane in the region above or below the vocal cords is the seat of the disease, it naturally follows that we may divide the disease for clinical 'study into supraglottic and subglottic laryngitis. We may meet either of these conditions up to about fourteen years, although a very large percentage of the cases will be encountered before the fourth year.

Acute Supraglottic Laryngitis. This runs a course very similar to that of the simple catarrhal laryngitis of adults, and may be considered as identical with it. There is, indeed, somewhat greater tenderness over the upper part of the larynx, and in very rare cases there may be very slight dyspnea. There is the usual morbid predisposing cause to be found in the naso pharyngeal region, and the common exciting cause of exposure and " taking cold." Its course is short, rarely lasting more than ten days. It is very mild in character and resolves naturally. It may be necessary to differentiate it from a slight croupous laryngitis. This may, be done by observing the suddenness of the onset of the latter disease and its steadily progressive course.

Subglottic Laryngitis; False Croup; Millar's Asthma; Laryngitis Stridulosa. The entire surface of the larynx is more or less involved in this form of inflammation, but the intensity of the process is much greater in the tissues below the vocal cords. The mucous and submucous connective tissue becomes infiltrated and swollen, leading to more or less dyspnea.

Etiology. There seems to be a constitutional tendency to this disease. Heredity seems to be associated with it. Several children in the same family or families closely related will 'stiffer from repeated attacks. Strumous children are predisposed to it, and those with an abnormally large and active lymphatic system. Gerhardt insists that the chief predisposing cause will be found above, in enlarged tonsils or other obstructions in the air passages. While this may undoubtedly influence any disease of the larynx, no close causative connection can be found associated with this particular form of laryngitis. The exciting cause is practically the same as in the previous class.

According to Sappey (Anatomie Descriptive, 1868, vol. ii. p. 869), the very abundant lymphatic supply found in this region in children explains the marked and at times extreme swelling found in the acute stage of the disease. The pathological condition is more or less stenosis from the crowding forward of the congested and inflamed mucous membrane by the engorged lymphatics.

Symptoms. There will be some prodromal symptoms sufficiently severe to indicate marked systemic disturbance the general feeling of malaise, severe or slight headache, the accelerated action of the heart, and the temperature increased to 100' or 10 1" F. The voice, at first hoarse, rapidly becomes shrill and metallic, and phonation may be very painful. A croupy cough sets in early, and is of a harsh, dry, barking nature. Even after phonation is entirely suspended this cough retains its characteristic sound, proving quite conclusively that it is produced by the dry, swollen tissues below the cords. This process is similar to inflammations of other mucous membranes, and after a period of variable length, usually two or three days, the mucous secre¬tion is resumed the cough becomes softer and less irritating, and there is some little frothy expectoration. During the day the symptoms are invariably less severe, while at night exacerbations occur that have a seemingly alarming import. The child, somewhat relieved by the restful day, falls into a calm and easy sleep. This may continue several hours, when he suddenly awakens in a violent and agonizing struggle for breath. The face is flushed, the lips purple, the nails blue, and every muscle tense and contracted all of the characteristic symptoms of marked dyspnea. These serious symptoms may continue for half an hour or longer; finally the child succeeds in coughing up a quantity of inspissated mucus and the attack subsides. A period of relief and rest will follow for a few hours;, when the child again wakens in a similar paroxysm. These exacerbations occur only at night and separated by periods of complete remission of dyspnea. Usually there will be from four to eight of these violent seizures during the progress of the disease. The question of muscular spasm is a mooted point. That true spasm of the laryngeal muscle is a prominent factor in these seizures is asserted by Rilliet and Benitez,' D'Espine and Picot, J. Lewis Smith,' and Gottstein;' while Bosworth,' Rauchfuss, and Dehio claim that muscular spasm plays no important part, and if it occur is purely incidental. Probably the principal cause is the swelling, which is greatly increased by the presence of the dried mucus acting a,, an irritant foreign body; it is also probable that the same irritation produces a certain amount of of the laryngeal muscles.

There is a persistence of more or less difficulty of breathing throughout the attack, but only at night do the paroxysms become sufficiently severe to occasion distress. During the remissions a slight inspiratory murmur, higher in pitch, will be heard. On succeeding nights the paroxysm will recur at about the same hour as the first, although, as a rule, with diminished severity.

Diagnosis. Though difficult and often impossible, an effort should be made to examine the parts with the laryngoscopic mirror. When a view is secured the mucous membrane appears inflamed and engorged, while protruding between the vocal cords will be seen the rounded swollen masses of the subglottic tissues. These are of a deeper red than the cords and the tissues above. Differentiation must be made between this condition and membranous croup, diphtheria, foreign bodies, and perichondritis. In both membranous croup and diphtheria there is much greater systemic disturbance ; the temperature ranges higher, the cough is less marked and not so severe, the disease is progressive, and is not characterized by nocturnal exacerbations with almost complete remissions; also the false membrane can generally be seen in situ or attached to surrounding tissues. A foreign body may give rise to many of the symptoms of acute subglottic laryngitis; but the history, together with an examination by means of either the mirror or the index finger, will generally clear up the diagnosis. Perichondritis of the cricoid cartilage is more difficult to exclude; but with the aid of the laryngoscope the irregular nodulated swellings, generally unilateral, can be seen and easily recognized.

The disease runs a course of from six to twelve days, and, as a rule, is not dangerous, a fatal termination being very rare.

Treatment. The general health of the patient should be considered. The strumous, lymphatic child, subject to attacks of croup, should be toned tip with syrup of the iodid of iron and cod liver oil. The passages above should be looked after with care and relieved if found in an unhealthy condition. During an attack the child should be confined in a warm and moisture saturated atmosphere; the bowels should be acted on by repeated small doses of calomel ; while internally the ammonias and small doses of an opiate should be administered to stimulate the secretion of mucus and to allay the irritating and exhausting cough. During the acute paroxysms at night every effort should be made to soften and expel the dried mucus and to moisten and soothe the dry, irritable, and inflamed mucous membrane. With this end in view we may use a hot bath, steam inhalations, or hot fomentations, and these failing, excite free emesis by tickling the fauces with the finger or a brush, or by administering an emetic, such as ipecac. If the attack is extremely severe or there is dangerous dyspnea, inhalations of ether or amyl nitrite may be given, the O'Dwyer tube introduced, or the trachea may be opened.


Much confusion in classification is encountered in the literature of this disease. Cohen 1 describes edema and acute, chronic, infraglottic, and hemorrhagic edematous laryngitis ; while the different forms of the disease are divided by Mackenzie' into typical, contiguous, and consecutive edematous laryngitis. Ziemssen 3 recognizes only One form, laryngitis phlegmonosa; while Gottstein' and Schrotter' describe acute and chronic submucous laryngitis and acute and chronic edematous laryngitis. Browne' acknowledges only acute and chronic inflammation of the submucous tissues.

The presence or absence of high temperature and other acute inflammatory symptoms renders this disease clearly divisible into two general formsacute phlegmonous laryngitis and simple edematous laryngitis. The occurrence of either form is rare, the latter especially so.

Acute Phlegmonous Laryngitis. This is an acute inflammation of the laryngeal mucous membrane, to which is added edema due to serous effusion. The edema here follows the characteristic course of inflammatory edema in other tissues and exhibits the different stages of serous, seropurulent, and purulent edema.

Etiology. In addition to cold, the usually assigned cause, there is undoubtedly exposure to some septic infection. Such an authority as Mackenzie states that he never encountered a case except of septic origin. Virchow considers it a true erysipelas of the larynx. It is indeed usually found among hospital physicians and nurses, undoubtedly the most exposed class of people. It is very rare as a primary condition, being found generally secondary to quinsy, abscess of the neck, follicular pharyngitis, and tonsillitis, or complicating an attack of typhoid, typhus, variola, or diphtheria. It may develop at any age, but is usually found between twenty and forty.

The same morbid changes are found as in inflammatory edema of mucous membranes elsewhere. There is first vascular engorgement followed by serous effusion, the swelling being most marked where the membrane is most relaxed that is, in the aryepiglottic folds, ventricular bands, and the epiglottis posteriorly. At first serous, the effusion gradually becomes purulent.

Symptoms. A slight chill accompanied by a corresponding rise of temperature is rapidly followed by decided impairment or loss of voice, with dyspnea and stridulous breathing. The condition is progressive, the dyspnea developing within twelve hours, growing steadily worse for twentyfour to thirty six hours, when it reaches its maximum. There is pain and soreness on pressure or swallowing, and cough is not often present.

Diagnosis. This disease can only be confounded with the presence of a foreign body or an attack of simple edema. The history of the case and the use of the mirror should prevent mistakes. You will see the red, tense, and glossy membrane with three rounded swollen masses of tissue above the small triangular opening of the glottis.

Prognosis. This is a disease of rapid development. It runs a short course of four or five days, the extent and severity of the symptoms varying largely. If at the end of thirty six hours the dyspnea has not become dangerous, the case will spontaneously resolve. Until this time, however, it should be closely watched, as symptoms sufficiently alarming to demand surgical interference may occur at any moment.

Treatment is at first the use of the ice bag or Leiter coil to the larnyx, with local depletion (leeches) externally, and free and frequent scarification of the swollen, inflamed mucous membrane within. The atmosphere should be warm and saturated with moisture, and only such drugs as will stimulate secretion should be administered. When serious symptoms develop so suddenly as to prevent tracheotomy, the introduction of a small laryngeal catheter is advised by Macewen.


Under this name is considered that morbid condition which presents a simple edema of the mucous membrane of the larynx, without inflammation, and which is certainly secondary to a more serious general condition.

Etiology. Some morbid' change in the kidneys, heart, or liver, an obstruction to the return circulation in the neck, a vaso motor paresis, or any general or local condition which tends to produce dropsical effusion may be the cause of this disease. There is an escape of normal healthy serum into the submucous tissues, producing general swelling of the parts and noticeable tumefaction in the relaxed portions of the mucous membrane, the aryepiglottic folds on each side, and the epiglottis in front and above.

Symptoms. The onset is sudden. There will be loss of voice, with great difficulty in breathing, inspiration being more difficult than expiration. There is little pain, soreness, or cough.

The diagnosis is easily made by the history of the case and laryngoscopic examination.

The prognosis is always grave. Death from the laryngeal stenosis is liable to occur and very quickly ; but even should this be controlled, the general condition is almost invariably of an organic nature and incurable.

Treatment. Efforts should be made to control, at least temporarily, the systemic cause. Free diaphoresis or catharsis is indicated, while local puncturing of the swollen tissues freely should be frequently done. This .not availing, resort should be bad to tracheotomy.


Synonyms. Croup; Membranous laryngitis.

It would hardly prove profitable to enter into the. active discussion that has been carried on for many years past regarding the unity or duality of croup and diphtheria. Perhaps the weight of modern, evidence tends to the belief that croupous laryngitis is a local affection with some general disturbance while diphtheria is a general systemic disease with local expression. It is not yet demonstrated, but largely a matter of opinion gained from personal observation and experience. The literature on the subject is most confusing. Statistics in general are Dot to be depended on, and even mortality statistics are unreliable owing to frequently varying opinion. While there are many points of similarity, there are also enough elements of distinction to warrant the consideration of croupous laryngitis as a disease distinct from diphtheria.

Etiology. That there is at least some similar or analogous causative element in this disease to diphtheria cannot be denied. In diphtheria proper its distinctive germ can generally be detected; while although the germ of non diphtheritic croup has not yet been separated, the possibility and probability of its future discovery had not been abandoned. It is likely that a germ finds lodgement in the pharynx, tonsils, or larynx, which excites an inflammatory process with certain well marked and peculiar characteristics. The disease may commence above in the pharynx or fauces, progress downward, and attack the laryngeal mucous membrane secondarily. It is selective, and age and susceptibility play important parts. True croupous laryngitis is practically unknown in adult life, while it is most common between the ages of one and nine years, rapidly diminishing in frequency from this time on.

Pathology. The membrane consists essentially of two layers a superficial, consisting of the epithelium that has proliferated and undergone mucoid degeneration, and a deeper, composed of fibrinous strata, with numerous leukocytes scattered throughout its layers.

Symptoms. At first there is generally slight catarrh, with some rise of temperature and a general feeling of languor; there may or may not have been a chill. Loss of appetite and persistent thirst accompany painful deglutition. The pulse is full and the skin hot and dry. After a few hours there is slight hoarseness and later a short, dry, shrill cough ; the voice becomes more impaired and assumes a whispering character. Then interference with respiration appears and there is some laryngeal stridor. The mucous membrane is bright red, and may show some patches of false membrane. These symptoms usually occupy the first twenty four to forty eight hours of the disease and are followed by attacks of dyspnea. The voice is lost, the face is red and anxious, and there is a hoarse, stifled cough, with little or no expectoration. The attacks at first last but a few moments and subside, although the stridor remains. The pulse increases in rapidity and is irregular. The attacks of dyspnea become more and more frequent until they are practically constant, with no remissions and occasional aggravation of the symptoms. From time to time pieces of the membrane are coughed up. The struggle for breath becomes each moment more painful and exhausting, and finally death supervenes from suffocation.

Diagnosis. True croup must be differentiated from acute catarrhal laryngitis of severe form and from diphtheria. In the former there is absence of the membrane, frequent cough, the attacks come on only at night, and there are absolute and prolonged periods of rest with complete absence of dyspnea.

For the differentiation from diphtheria, see the article on that disease.

Prognosis. This is a most serious disease; death may occur at any time from dyspnea.

Treatment. This should be both local and constitutional. Internally the preparations of mercury should be administered. They can be given in frequent and increased doses. The salts of iron, notably the tincture, are most valuable. Locally ice may be used in the form of the pack, and small lumps may be swallowed. Sprays of lactic acid and persulphate of iron are also valuable. The chief danger to be guarded against is suffocation; so everything should be in readiness for the performance of intubation or tracheotomy' and interference when demanded should not be delayed. An expert in both operations will generally select the former procedure as being simpler, more rapid and less dangerous in itself, knowing that should intubation fail, the trachea can then be opened.


This is an acute infectious disease having local manifestations in the upper air passages.

It has been known and studied from the earliest times, but no absolute evidence as to its causation was produced until 1868, when Oertel made the announcement of the presence of a micrococcus in the exudate that is characteristic of this disease alone. This view was confirmed by many other investigators, notably Recklinghausen, Prudden, and Wood and Formad, who carried on many elaborate culture experiments ; but until the announcement by Klebs and Loffler of the definite microscopic characters of the bacillus which is peculiar to this morbid process, the discussion was not set at rest.

Etiology. A. diphtheritic attack is undoubtedly precipitated by a deposit of the Klebs loffler bacillus upon the faucial or laryngeal mucosa. There, finding a favorable culture medium, it sets up its peculiar inflammatory process; and as the result of the life. functions of the bacilli there is generated a ptomain that, absorbed by the capillaries, enters the general circulation and produces the constitutional symptoms. This theory, first advanced by Cheyne, was subsequently confirmed by Brieger and Frankel, who injected in rabbits the filtrate of the diphtheritic membrane, entirely separated from the bacilli, and reproduced the general disease, but without the local laryngeal manifestations.

A very large majority of cases occur in childhood, and at least seventy-five per cent. prior to the age of ten years. Cold and damp climates and the periods of the year when these conditions prevail undoubtedly predispose to the, disease. All catarrhal processes, enlarged tonsils, the presence of' adenoid growths or diseased nasal fossae render one more liable to the infection. Absence of sanitary surroundings is an important element, the disease having undoubtedly a filth origin and the bacillus thriving best in the neighborhood of sewers, street cuttings, turned earth, and locations shut off from sunlight. Diphtheria is both contagious and infectious; it may attack individuals, it may develop only in a limited community from some special local origin, or it may be epidemic and spread over a very wide area; but wherever and whenever it makes its appearance, it is without doubt due to the presence of its own specific organism.

It may be carried in clothes, in letters, or in the furnishings of railwaycarriages; while drinking water and milk are favorable transportationmediums. It is a disease common to the lower animals, and a pet animal will often convey it to its Owner. There is no question as to the vitality of this germ, but its activity must be somewhat restricted. It will be found redeveloping in hospital wards years after their abandonment and thorough disinfection; but the area of its activity must be limited when you realize that. all cities and large towns are the best breeding places for the bacillus, and yet the number of cases occurring each year represents but about one to every thousand of population. The danger of breath transmission is small, the secretions retaining the bacilli ; yet small particles may be thrown out by coughing or sneezing, and these deposited on some mucous surface will serve to propagate the disease.

Pathology. The bacillus, finding lodgement on the mucous membrane, reproduces itself with great rapidity. It forces its way into and through the epithelial layers into the mucosa, causing inflammation of that membrane. There is dilatation of the blood vessels, exudation of serum, and escape of the leukocytes. The epithelial cells proliferate, and uniting with the fibrin, which coagulates on exposure to the air, form the false membrane. Thus will be seen a pathological process identical with croupous inflammation, except for the presence of a specific organism (Bosworth). The inflammatory process is so energetic, the fibrinous bands contract so rapidly, that necrosis of the false membrane, as well as of the superficial layers of the true mucosa, will take place, and sloughs will form and be thrown off, leaving the raw and bleeding surface exposed. The membrane quickly re forms on these spaces or resolution takes place. In mild cases the false membrane is very thin and superficial and penetrates to very little depth; while in malignant cases the entire mucous membrane may be infiltrated. As a rule, the exudate first appears on the tonsils or faucial arch. It may extend into the nasal spaces but, as a rule, it passes downward, involving the pharynx, larynx, trachea, and even extending into the bronchi. When in the lower air passages, the false membrane assumes more the croupous form, penetrating but slightly into the mucous tissue. Some of the organs show slight changes: the kidneys and liver may be somewhat enlarged and minute hemorrhages may be found; while in the brain and spinal cord minute extravasations of blood are found scattered throughout their tissue.

Symptoms. In direct contagion the period of incubation is very short, not more than thirty six hours ; where the infection is conveyed, it may be much longer, varying from three to ten days. Experimental inoculation may develop the disease in twelve hours. In a typical attack of the disease you will have the false membrane not only involving the tonsils and fauces, but penetrating the larynx, and in addition the serious constitutional disturbance caused by the toxic absorption. There may be the general prodromal symptoms of malaise, restlessness, and loss of appetite. Sometimes there is vomiting and great nervous excitement, even convulsions. The direct onset of the disease is marked by a chill or chilly sensation, followed by mild febrile disturbance, dry, flushed skin, headache, and scanty, highly colored urine. The mental processes are unusually dulled, and the patient often lies in a half stupid condition. The febrile reaction is not severe, the temperature rarely rising above 102' F. The heart's action is weak and rapid. Accompanying these symptoms there will be dryness of the throat, some pain and difficulty in swallowing, and soreness and tenderness in the tissues of the neck. At the end of twelve hours, if the throat is examined, thin circumscribed patches of whitish or pearl colored membrane will be seen on the tonsils or fauces; and at the end of twenty four hours these patches will have completely covered the tonsils and assumed the characteristic yellowish and velvety appearance. The mucous membrane is intensely injected and somewhat discolored. Within three days a purulent or muco purulent discharge sets in, the membrane continues to spread, the edges become ragged, and sloughing begins. If the membrane progresses upward, the soft palate swells, the uvula becomes edematous, and the nasal passages become occluded by a mass of membrane and muco purulent secretions; the tongue becomes dry and brown; the breath fetid from the necrotic membrane and decomposition of the secretions. About this time the serious symptoms of laryngeal involvement will appear. There will be another rise in temperature, the voice changes, and the development of dyspnea, as shown by increased inspiratory effort, the subclavicular depression, and the fixation of the chest muscles. The laryngeal obstruction is due to the narrowing of the passage by the exudation, and perhaps in part by muscular paresis. In the larynx the membrane is more characteristic of the croupous deposit, except in spots (Prudden) where it invades the mucous tissue.

If life be prolonged for two or three days the membrane may become separated, and at times a membranous cast of the trachea will be thrown off. Resolution may take place as in the upper part of the pharynx, or similarly there may be a fresh exudate. This may be considered as a description of a case of moderate severity. In the simpler forms there may be very slight systemic disturbances; and the false membrane, if any, thin, almost transparent, and consisting of a few scattered patches. In the malignant form the attack will be characterized by profound symptoms of toxic absorption. The usual features of blood poisoning will be noticed; and indeed, in a case of this class, the vital powers will apparently be overcome almost from the onset by the virulence of the poison. Convulsions or low, muttering delirium may be constant; there will be absence of tendon reflex; rapid, feeble, and irregular pulse, or a condition of semi coma.

Diagnosis. It is chiefly necessary to make the distinction between this disease and membranous croup. In the early stages this may be attended with some difficulty. The croupous membrane is thin, of a whitish color, with a glazed, shining surface, and can be easily wiped away without irritating the surface beneath; the diphtheritic membrane is thicker, has a soft, velvety appearance, a yellowish brown color, and is so adherent to the mucous tissue that its removal is not easy, and will leave a raw and bleeding surface beneath. Later in the diphtheritic process there will be fetor, a profuse muco purulent discharge, and the dirty bluish black, ragged, necrotic membrane. The croupous membrane undergoes no change until the end; it continues clean and white, and has no mucous or purulent discharge. In recent times the true scientific method for determining the presence of the diphtheritic process has been followed. Knowing with what rapidity the Klebs Lofller bacillus multiplies, a small portion of' the exudate is transferred from the throat to a properly prepared culture tube partly filled with peptone, bouillon, or blood serum. In twenty four hours colonies of the bacilli will form that can be recognized by the naked eve, and the bacilli can be demonstrated under the microscope. This plan, so simple, safe and certain, is being rapidly adopted by the entire profession ; and most of the large cities employ a competent bacteriologist, a large part of whose duty it is to make 'these investigations.

Prognosis. Diphtheria is rightly regarded as one of the most fatal of diseases. The mortality rate is large, and there are many complications and sequele. Until very recently the mortality rate varied from 40 to 60' per cent. Under the influence of the treatment by antitoxin this has fallen to from 12 to 20 per cent. Two causes are active in producing a fatal termination, the asphyxia secondary to laryngeal stenosis and the overwhelming of the nerve centers and organs by the blood poison. The toxic effects may be marked in the mildest form of the disease as well as in the most virulent. There may be much interference with the cardiac function, due to the action of the poison on the nervous centers controlling it, or there may be instant cessation of the heart's action, due to the overwhelming effect of the poison upon the heart muscle itself. Among the most important complications and sequelae may be noted albuminuria, bronchitis, changes in the abdominal viscera, purulent inflammation of the middle ear, and paralysis of the various muscles.

Treatment. The two points to be kept in mind in the treatment of diphtheria are to prevent the spread of the local process and to control the systemic effects of the ptomain poison. In consequence, there should be systematic local and constitutional treatment. Innumerable preparations have been used locally, and among them may be mentioned solutions of bichlorid of mercury, even as strong as I part to 500 (Sternberg), carbolic acid from 5 to 30 per cent. (Ranlin), lactic acid from 30 to 50 per cent. (Bosworth), the persulphate or perchlorid of iron (Bosworth), the nitrate of silver 5 to 10 per cent. (Trousseau), hydrochloric acid, nitrate of mercury, chlorid of zinc, bromin (15 per cent.), solution of pancreatin, trypsin, and other digestive ferments, the officinal aq. calcis, the peroxid of hydrogen by spray and inhalation all of these applications have their advantages, and each its special and ardent advocates. The application should be made only under good illumination and with the greatest care. The object of various local applications is to destroy the pathogenic organism by direct action; in consequence, they should be applied directly to and around the margins of the membranous deposits. Internal medication is indicated to combat the effects of the poison by sustaining the resisting powers of the system. The preparations of alcohol are undoubtedly best for this purpose, and whiskey and brandy should be freely and frequently administered. The tincture of iron in large doses is most important, while such drugs as digitalis, strophantbus, carbonate of ammonia, and musk, especially support the heart's action. The mercurial treatment is strongly advocated by eminent and experienced observers, the mild chlorid, the corrosive chloride and the cyanid each having its supporters. Various antiseptic sprays have been found extremely useful, and will come in contact with diseased tissues beyond the reach of direct applications. The constant use of steam, both in the atmosphere and by inhalation, prevents the dissemination of the germs, keeps the surface of the tissues moist, and enables the gangrenous membrane to separate more readily. The recent introduction of antitoxin in the treatment of diphtheria marks an important advance. It is too early as yet to decide upon the ultimate value of this method. It is claimed, however, that the mortality has been so greatly reduced by its use as to remove the fear heretofore felt for this dread disease.

After every effort has been made, every method tried, a very large proportion of cases will still show that the laryngeal stenosis is progressing, and without surgical interference there is imminent danger of suffocation. We may then choose between opening the air passages or introducing an intralaryngeal tube. The individual experience of the operator will decide which method to follow: either may be relied upon to give temporary relief; but the progressive advancement of the disease will overcome, at times, every. effort made (see page 1029).


Synonym. Spasm of the glottis.

This condition is more a symptom than a disease. It is a spasmodic closing of the glottis, purely neurotic in its character.

Etiology. It may occur at any age, but is most frequently found in children, especially if they are ill nourished or rachitic. The spasm is usually brought on by something that nervously imbalances the child loud talking, coughing, teasing, irritating, or perhaps a drop of water or milk finding its way into the larynx during feeding.

Symptoms. There are two or three labored efforts at inspiration, followed by total cessation of breathing. This may pass in a moment and respiration be resumed. The spasm may continue, the glottis never relax, and death at once supervene. There may be but one attack, or there may be several before the fatal issue; and there may be general systemic convulsions. There is no recognized pathological change whatever. The disease is instantly understood even by the inexperienced.

Treatment. Sudden shock, slapping the sides and back, dashing cold water on the naked body and face, the application of strong ammonia or amyl nitrite to the nose, or forcing a catheter or intubation tube past the obstruction in the larynx.


Acute inflammations of the perichondrium of the laryngeal cartilages are occasionally met with.

Etiology. The cause may be idiopathic, or the disease may follow typhoid, typhus, diphtheria, pneumonia, or any of the exanthemata. Syphilis is a very prevalent cause. The pathology is the same as that of a perichondritis in any location. Increased vascularity, followed by swelling, effusion and pus formation, separating the perichondrium from the cartilage.

Symptoms. There is usually some systemic disturbance, a feeling of malaise, chill, etc., followed by a slight rise of temperature, with a sense of fullness in the larynx, soreness, pain on swallowing, slight dyspnea, and more or less loss of phonation. The local symptoms depend largely upon the extent of inflammation and the particular cartilages involved.

When the cricoid cartilage is the seat of the trouble dyspnea and loss of phonation are the principal symptoms. There may be cough. In affection of the arytenoid there is some slight dyspnea and impairment of voice; but interference with deglutition is the principal symptom.

When the thyroid is involved it is usually unilateral, and interference with phonation is the principal symptom. The voice is never entirely lost, but becomes very hoarse. There may be a purulent discharge through a fistula in the neck.

Diagnosis. This is often made with very great difficulty. Careful and thoughtful consideration, with frequent examinations with the laryugoscope, will enable one to detect the diseased cartilage or exclude the diseases simulating it. These are croupous laryngitis and acute catarrhal laryngitis.

Prognosis. There may result necrosis of the cartilage, with fistulous passages to the surface. There is final resolution usually, with some permanent voice changes. There is little real danger to life.

Treatment should be the administration of mercury and iodid of' potassium, and surgical measures may be called for from time to time to curette or scarify the tissues internally or to open pus sacs or fistulous passages.


Hemorrhages into the larynx, or the so called hemorrhagic laryngitis, is an extremely rare condition, unless secondary to ulcerative processes such as are found in syphilitic or cancerous diseases. Turck cites a case as occurring from syphilitic ulceration and Mackenzie describes it as one of the symptoms of acute laryngitis. The only point of practical importance is to determine whether the bleeding is from the larynx or the bronchial tube.,,, ; as in the former case it is of little consequence, while in the latter it is an indication of probable tubercular changes.


The development of an acute inflammatory process localized solely in the trachea is indeed of very rare occurrence. That this structure takes part in every severe inflammation that involves the larynx and fauces above and the bronchial tubes below may be expected, both from its direct connection and similarity of structure. That, acute catarrhal tracheitis does occur, however, alone and idiopathically, is undoubtedly true; and it runs a course parallel to and of the same character and intensity as diseases of like nature in the tissues above and below. It is almost invariably of a catarrhal form, and is followed very rapidly by an extension of the disease to the larynx and bronchi.

Etiology. The causation when it develops independently is the same as in the neighboring structures. There is the usual predisposition dependent upon chronic changes in the mucous tissues above, and exposure serves to light up the process. It is in reality almost always an extension downward of a laryngeal catarrh that has it extended from above. In youth if is generally consequent upon an acute rhinitis; while in later life it is secondary to a bronchial catarrh. It may occur at any age; and, like other inflammations of the air tract, it is found most frequently in the male, dependent, no doubt, upon their greater exposure to the exciting causes i. e. sudden climatic changes, wet clothing, draughts, and dust.

Pathology. In the early stage there is the usual vascular injection and turgescence and some slight swelling from serous exudation. The surface will be dry and glazed. Later, when mucus secretion is resumed, the swelling subsides and resolution follows.

Symptoms. A dry irritating cough, caused by the air current passing over an inflamed surface and a constant tickling sensation causing a continuous effort at clearing the throat, but totally devoid of expectoration. Ordinarily there is no dyspnea, as the trachea will allow of great encroachment on the caliber of its lumen without interfering with the normal air current; but in very severe cases there may be slight dyspnea. As the disease runs its course the irritating cough gradually subsides and expectoration increases. This is greater in quantity than in catarrhal laryngitis and much less than in bronchitis. If the stethoscope is applied to the trachea there will be heard in the earl stage a harsh, dry, inspiratory sound, and later on an abundance of large moist rides.

Diagnosis. An acute respiratory disease with cough and expectoration, but without dyspnea or aphonia, must involve either the trachea or bronchi. The stethoscope will exclude the latter region, and if a tracheoscopic examination is made the mirror will quickly show the highly injected, dark red, inflamed mucous membrane.

Treatment. The local application of the wet compress or counter irritation with a tampon. The inhalation of vapors saturated with benzoin, eucalyptus, or some of the essential oils. A mild expectorant mixture containing ammonia may be given.

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