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Catarrhal Affections of theNasal Passages as a Causeof Pulmonary Phthisis,with Special Referenceto the Question of

Heredity.

BT

WILLIAM C. JAEVIS, M. D.,CLINICAL PROFESSOR OF LARYNGOLOGY AND DISEASES

OF THE NOSE AND THROAT IN THE NEW YORKUNIVERSITY MEDICAL COLLEGE.

REPRINTED PROM

Jibe ‘Meto ¥orft ifHeGtcal journal

for September 5 and 12, 1885.

CATARRHAL

AFFECTIONS OF THE NASAL PASSAGESAS A CAUSE OF

PULMONARY PHTHISIS

WITH SPECIAL REFERENCE TO THE QUESTION OFHEREDITY.

BY

WILLIAM CHAPMAN JARYIS, M. D.,CLINICAL PROFESSOR OP LARYNGOLOGY AND DISEASES OF THE NOSE AND

THROAT IN THE NEWYORK UNIVERSITY MEDICAL COLLEGE.

REPRINTED FROMTHE NEWYORK MEDICAL JOURNAL

FOll SEPTEMBER 5 AND 12, 1885.

NEWYORK:I). APPLETON AND COMPANY,

1, 3, and 5 BOND STREET.1885.

CATARRHAL AFFECTIONS OF THENASAL PASSAGES

AS A CAUSE OF

PULMONARY PHTHISIS,WITH SPECIAL REFERENCE TO THE QUESTION OF

HEREDITY*

The aetiology of pulmonary tuberculosis, a subjectalways replete with interest to the clinical investigatoi’, hasnaturally received a deeper significance since the discoveryof the Bacillus tuberculosis. Despite, however, the positivecharacter of Koch’s results, there remains, according to hisown admission, much yet to be learned concerning the prse-tubercular conditions which determine the development ofthe tubercle bacillus, f These conditions, variously and oft-times vaguely referred to by such terms as tubercular dispo-sition, predisposition, heredity, environment, etc., it wouldappear, are the principal avenues through which this mo-mentous question, affecting the lives of so many thousandsin our crowded city and elsewhere, is to be approached.

Several years ago, while studying the cause and compli-* Read before the American Climatological Association, May 27,

1885.■)■ “Mittheilungen aus dem kaiserlichen Gesundheitsamte.”

NASAL CATARRHAL AFFECTIONS

cations of nasal diseases, my attention was attracted to theco-existence of bronchial with nasal catarrh, and somewhatlater to the association of nasal disease with pulmonaryphthisis.

These earlier impressions did not assume the shape ofconvictions until the reliable evidence I am about to presentfor your serious consideration was forthcoming.

In view of the light already thrown upon the questionof the aetiology of tuberculosis through Koch’s bacillary in-vestigations, I have deemed it profitable to review some ofthe evidence he has offered us concerning the dispositionand predisposition to phthisis.

As regards the question of the physical conditions fa-vorable for the development of bacilli, we are informed byKoch that pent-up secretions, removal of the protectiveepithelia of the bronchi, abrasions, etc., are to be consideredthe proper soil—the “geeignete Baden”—for the lodgmentand growth of the deadly tubercular plant. Now, theseconditions will be recognized as the common results of ca-tarrhal inflammation of the upper and lower air-passages.One or more of them are frequently observed in nasal ca-tarrh, and may be also associated with catarrhal phthisiswhen taken in the popular sense of the term as taught tous by Dr. Alfred L. Loomis.

In certain cases we find pulmonary tuberculosis rapidlyfollowing in the train of a catarrhal bronchitis, while otherswill, apparently, resist the inroads of the bacillus for manyyears.

In treating my subject I shall begin with the nares andendeavor to distinctly trace the effects of nasal catarrh uponthe larynx, and then in turn explain the relation of theresultant laryngeal disease to bronchial catarrh, catarrhalphthisis, and, finally, pulmonary tuberculosis.

The relations of the nostrils to the lungs is so intimate

AS A CAUSE OE PULMONARY PHTHISIS. 5

that we are not surprised to find Koch involuntarily ad-dressing his attention to the nose for a partial solution atleast of the question of the setiological relations of the ba-cillus to pulmonary tuberculosis, with the remark, “Air in-haled through the nose is deprived of disease-germs, andnasal respiration, therefore, constitutes a positive protectionagainst infection by reason of the retention of the infec-tious material by the nasal mucous membrane.” Conspicu-ous among the complications traceable to nasal catarrh,and bearing upon the question of the causation of pulmo-nary phthisis, is chronic irritative hypercemia of the larynx.I can not at present enter into a description of this affec-tion, or fully explain how it is brought about by the entranceof nasal mucus into the larynx. I called especial attentionto this condition in a paper read before the American La-ryngological Association, session of 1881, to which I mustrefer you.*

This affection is usually observed as a peculiar red dis-colorationof the normally pearly white vocal cords, and, whenfound, constitutes an excellent guide for the determination ofthe amount of congestion of the general laryngeal mucousmembrane. Chronic hypersemia of the larynx frequently de-velops attacks of acute catarrhal laryngitis, and this affectionin turn often involves the tracheal and bronchial raucous

membrane by inflammatory extension. In other words,recognizing the larynx, with certain modifications, as the up-per portion of the lungs, catarrhal inflammationof this organclearly constitutes a menace to the integrity of the entirepulmonary tract. The laryngoscopic study of the patho-logical processes concerned in the production of laryngealhypersemia and its common sequela—laryngitis—is, there-fore, required to throw light upon the pulmonary diseasesfollowing in its wake.

* “ Archives of Laryngology,” vol. iii, p. 148,

6 NASAL CATARRHAL AFFECTIONS

Nasal stenosis and defective nasal drainage are the twomost important indirect agents concerned in the productionof this affection. The manner in which these intra-nasaldisturbances lead to laryngeal and lung complications isprincipally by habitual mouth-breathing, the irritating ac-tion of nasal mucus in the larynx, and inflammatory exten-sion from the posterior nares.

The part played by nasal mucus as an setiological fac-tor in the production of laryngeal and pulmonary diseaseis well pronounced and very important. The constancywith which chronic irritative hypersemia of the larynx oc-curs as a result of chronic nasal catarrh encouraged me tomake the statement that the simple discovery of this pecu-liar congestion was, as a rule, sufficient evidence of the ex-istence of a chronic nasal catarrh.

The manner in which chronic hypersemia of the larynxis induced through defective nasal drainage is exceedinglysimple, and is best understood by carefully studying thedirection of the several anatomical planes of the upper air-passages, I will refer you to a paper read by me before theNew York Academy of Medicine, in which is given a detaileddescription of this system of drainage.*

I may simply state in passing that the disturbances tonasal drainage originating from a nasal catarrh prevent thenatural disposition of nasal mucus, and, consequently, permitit to enter the larynx. Now, nasal mucus in the larynx is aforeign body, and as such invariably gives rise, by prolongedirritation, to a familiar train of signs and symptoms. Fore-most among the signs stands, as I have already pointed out,chronic irritative hyporsemia of the larynx. The larynxnaturally resents the invasion of its territory by irritatingnasal discharges, and we have, as one of a number of well-marked symptoms

, a constant inclination to “ clear the* “ Medical Record,” March 14, 1885.

AS A CAUSE OF PULMONARY PHTHISIS.

throat.” Tliis act in itself may constitute an additionalirritant by the rasping effect of the effort upon the vocalcords. The part played by habitual mouth-breathing as anexcitant of laryngeal disease is simply that resulting fromthe absence of those conditions so essential for the purifica-tion and preparation of the respired air, and attributable toprolonged nasal stenosis.

Having briefly presented the most conspicuous causeswhich serve to account for catarrhal disease in the larynx,the next step would naturally be to study the nasal compli-cations responsible for the existence of the laryngeal affec-tion.

Among these may be mentioned deviation of the nasalseptum, turbinated hypertrophies, polypi, adenomata of thevault of the pharynx, etc. The proper consideration ofeither one of these conditions, taken alone, would covermany pages. I shall, therefore, be compelled to entirelyomit the consideration of some, and only briefly accentuatethose most commonly concerned in the production of laryn-geal and pulmonary disease.

Hypertrophy of the turbinated tissues is an almost inva-riable concomitant of the moist forms of nasal catarrh. Itmay stand either alone or, as is commonly the case, existas the result of a deviated septum. The co-existing mouth-breathing, hypersecretion, and disturbed nasal drainage will,of course, be governed by the location and amount of theturbinatedhypertrophy. Passing promptly to the consider-ation of the second condition, the deviated septum, we areat once confronted by the most active and common agentconcerned in the production of pulmonary and laryngealdisease. This condition differs from turbinated hypertro-phy in being both a cause and result of catarrhal inflamma-tion. Its existence, furthermore, implies the co-existenceof a turbinated hypertrophy, barring, of course, recent trau-


matic deviations and extra-nasal distortions of the septum.*I have already had occasion to explain how a deviated sep-tum, through pressure irritation, excites catarrhal inflam-mation. j- Its action may he, to employ a homely example,compared to that of a shoe-button impacted in the nostril.The deviated cartilaginous spur, like this familiar foreignbody, presses against the exceedingly sensitive surfaces ofthe turbinated tissues, invariably exciting and keeping up acertain amount of inflammatory action.

Thus we have a system of reciprocal irritation provok-ing and prolonging a nasal catarrh. For want of a betterexpression, I have called this pressure irritation, and I trustthe terra may recall to your mind the pathological processit indicates when employed in this paper.

The role played by the turbinated tissues and septum inthe production of rhinitis hypertrophica was noted by mein a paper read before the American Laryngological Asso-ciation, session of 1880 ; and the setiological relation of thenasal septum to diseased turbinated bodies was also satis-factorily demonstrated by Dr. Harrison Allen, though in away differing from my own, in the same year.

Having determined the aetiological significance of thedeviated septum in nasal catarrh, for a more detailed de-scription of which I must refer you to my earlier paperson this subject. Another factor, which serves in turn toaccount for the deviated septum, requires a brief consid-eration—namely, heredity.

The term heredity, usually furnishing much materialfor uncertain speculation and little opportunity for satisfac-tory demonstration, has, in this connection, assumed a moredefinite meaning by reason of much corroborative testi-mony always at hand.

* See “Archives of Laryngology,” 1882, vol. iii, p. 300.f Ibid., vol. ii, p. 147.

AS A CAUSE OF PULMONARY PHTHISIS. 9

This evidence has convinced me that the deviated sep-tum is frequently transmitted from parent to child.

In 1882, while engaged relieving the sufferings of ayoung woman, brought on by a congenital occlusion of thenares, my attention was attracted to an abnormal contrac-tion of the superior maxillae. In reporting the case I laidgreat stress upon the possibility of the chronic coryza andturbinated hypertrophies being associated with this condi-tion as cause and effect.* Since that time, by careful in-vestigation and comparison, I have been enabled to supplythe necessary links in a chain of evidence which has demon-strated that one of the most common causes of catarrh isdiscoverable in the conformation of the hard palate. Thispeculiar malformation I find to be transmitted from parentto child withremarkable regularity, and its intelligent recog-nition and proper appreciation enables one to most satisfac-torily account for a large number of catarrhal disturbancesin the upper air-passages.

In these cases we find that the superior maxillary bonesare not only contracted, but are likewise elevated, abnor-mally increasing the depth and diminishing the diameter ofthe roof of the mouth. The vertical measurement of theosseous nares is naturally more or less affected by the en-croachment of the elevated hard palate, and the nasal sep-tum, as a consequence, is bent laterally, as exemplified inthe diagram, Fig. 1, A representing the normal septum andmaxillary arch, and B the abnormal.

These plaster impressions, kindly presented to me byDr. Eddy, nicely illustrate this peculiar palatine formation.They were selected from among thirty other plaster castsas the only two in which I could positively pronounce theexistence of a chronic nasal catarrh. The doctor, on refer-ring to the name of the subject, found thatboth belonged

* See “Archives of Laryngology,” 1882, vol. iii, p. 108,


to the same individual—a patient he had referred to meseveral years before for a severe chronic coryza, and the

Pig. 1.

only one out of the whole number of casts. On comparingthis plaster impression, Fig. 2, with the normal palatine arch,you will discern certain well-defined differences. The dis-

PIG. 2.

tance between the alveolar ridges is much greater in thenormal specimen. The transverse diameterof the abnormalspecimen is not only smaller, but its surface is markedly ir-regular. The maxillary arch may he considerably higher


than this normal specimen, and yet not constitute a patho-logical condition. No two maxillary arches are exactlyalike, and some exhibit an elevation easily mistaken for adeformity. The important distinction to bear in mind isthe abrupt elevation along the line of the median rhaphe.When such a condition is observed, we may at once lookfor, and, in my experience, invariably discover, a correspond-ing deviation of the septum. This condition, furthermore,is found associated with a chronic coryza. Indeed, I holdit to he possible in certain cases to diagnosticate the exist-ence of a chronic nasal catarrh by the simple examinationof the roof of the mouth, or, what amounts to the samething, by inspecting an impression in wax or plaster, fromany part of the world. After having ascertained the con-

genita] character of this nasal abnormality, the next stepwas an endeavor to account for its existence. In tracingthis peculiar formation to its hereditary origin, I was greatlyassisted by instituting a comparative study of the externalnose, and particularly the persistence of certain types in thesame family.* By employing a similar method of reason-ing to the internal configuration of the nares, I have beenable to trace the peculiar conformation back to a commonparental origin. This condition occurs as an hereditarymanifestation with great constancy. Once the peculiarnasal type of the parents is recognized, its modifications inthe children are easily determined.

It would appear that abnornal contraction of the naresis likely to be associated with intellectual enlargement ofthe skull in certain families, a fact which may serve toaccount for the tendency to phthisis attributed by someobservers to severely studious or sedentary habits,

* “ It is said by Ribot that, of all the features, the nose is the onewhich hereditypreserves best.”-—“ Hereditary Traits,” Richard A. Proc?tor.

NASAL CATARRHAL AFFECTIONS12

It is well known that a marked increase in the dimen-sions of the cranial dome is apt to be accompanied by acontraction of the osseous frame-work of the face. If itwere convenient I might cite a number of interesting exam-

ples, carefully collected by me, to prove the correctness ofthis view.

Through Dr. L. J. 8., referred to me by Dr. P, A. Mor-row, my interest in the elevated arch and the septum ofheredity received a fresh impulse.

Fig. 3 is a reproduction of the doctor’s palatine profile.He creditably appreciated the significance of the high-pitched arch, and directed my attention to the peculiar for-mation of his own. The co-existing deviation of the septumwas very well marked, and there were several other interest-ing features connected with this physician’s condition.

I might mention, for instance, the unique occurrence, asfar as I know, of a periodical perspiration over a circum-scribed area, above the left malar prominence, and aroundthe neighboring portion of the cheek.

There was an extensive general deviation of the septumto the left, and it was fair to presume that this peculiar per-spiratory anomaly was due to prolonged intra-nasal pressureexerted by the deflected structure.

The prompt disappearance of this annoying symptomafter removal of the offending tissues confirmed the correct-ness of this view. The doctor, although a life-long suffererwith nasal catarrh, was so much benefited by surgical treat-ment as to pronounce himself, in certain respects, a differ-ent man. Free nasal respiration through the left nostrilwas, for the first time in his life, made possible.

The following extract from his family history is of in-terest as regards the question of heredity: His father, aphysician now deceased, was all his life-time annoyed bya persistent coryza and throat trouble. On comparing the


Fig. 3,

doctor’s photograph with an oil-painting of his father, a re-semblance in respect to the shape of the nose and forehead


is sufficiently well marked to challenge the attention of evena casual observer. Furthermore, I ascertained, from amember of the family, that his grandfather, also a physician,looked like his father and was afflicted with a catarrhalaffection.

I have selected from my case-hook a few life-sketches,which will aid me in explaining what I mean by hereditary

Fig. 4.

deviation of the septum. This, Fig. 4, was copied from thelife-sketch of a boy, aged fourteen, referred to me by Dr.A. W. Berle, of New York, and the next drawing, Fig. 5,was taken from the father of the lad. The hard palates ofboth were markedly contracted and elevated. The fatherhad bilateral deviation of the septum with life-long nasalcatarrh, and the son was referred to me for relief from thesame trouble.

A cross-section of the elevated and contracted hardpalates is shown in Fig. 3, where No. 3 represents the fatherand No, 4 his son.

These tracings were obtained by taking a wax impressionof the roof of the mouth, then reproducing the deformityin plaster of Paris, and dividing the casts thus obtained


with a fine saw, in a transverse direction. The dividedfragments were then simply laid upon a piece of paper andoutlined.

You may be able to distinguish a slight resemblance intheir shape, when compared with each other, this similaritybeing rendered more distinct by their dissimilarity with theother arches.

An idea of their abnormal divergence from the truetype may be obtained by comparing the two arches withNo. I, taken from a plaster cast exhibiting an unusually flat-tened and expanded hard palate, and selected as an extremeillustration of the kind.

Eeturning to the sketches (Fig. 4) you observe the car-tilage of the son’s septum is deviated to the left as a local-ized nodular projection, almost on a level with the floor fthe nose

Fig. 5.

The father’s septum (Fig. 5) was also thrown to the left,but, in the form of general deviation, situated superiorly in


the nostril, the inferior-anterior edge of the septum beingdeflected into the right nostril in a manner similar to theson’s.

It may be worth noting that when the lad was firstbrought to me I sought the hereditary origin of his devi-ated septum in the mother’s nose, with a negative result;and yet, unwilling to be adjudged guilty of an erroneousconjecture, I persuaded the mother to induce her husbandto visit me, and proved the correctness of my inferences asjust described. The removal of the deviated cartilage fromthe boy’s nostril was followed by an excellent result. Thisdrawing (Fig. 6) shows the nose of a son aged twenty-two, and next to it (Fig. 7) that of the father. They arecopied from life-sketches. You observe that both septaare generally deviated in the same direction. Both wereseverely afflicted with a life-long coryza.

Fig. 0. Fig. 7.

Fig. 3, Nos. 5 and 6, exhibit transverse tracings of thefather’s and son’s hard palates in the order mentioned. Thepoint of highest elevation, it will be observed, is toward thenostrils into which the septa were deflected. The father,an old man, had become reconciled to his lot in life, although

AS A CAUSE OF PULMONARY PHTHISIS. 17the extremely harassing character of his complaint made memarvel at this decision.

His hitter experience had the happy effect of makinghim alive to his son’s life-interests. Directing our attentionagain to the sketches (Figs. 6 and 7), you observe the cartilageof the septum is conspicuously inclined to the left in bothfather and son. The father’s septum (Fig. 7) exhibits, how-ever, a greater degree of deflection, the respiratory spacebeing reduced to a useless slit.

You may be able to distinguish a similarity in the shapeof the external nose. The father, although a sufferer formany years with bronchitis and asthma, might be consid-ered, under the circumstances, tolerably well developed andpreserved. The son, on the contrary, also complaining oflung trouble, was stunted in stature, emaciated in appear-ance, with a haggard face and an unhealthy skin.

I operated upon the young man, removing two antero-inferior turbinated hypertrophies, and shaving off the sep-tum for the whole length of the triangular cartilage, ex-cising also a small portion of the anterior border of thevomer. Fig. 8, taken from a life-sketch, exhibits the left

Fig. 8.

nostril after excision of the deviated structures. I em-ployed my transfixion needles and ecraseur for the removal


of the redundant turbinated tissues, using my fenestratedcartilage forceps, tubular-spring forceps, and rongeur bonescissors for leveling the septum.

The subject of this illustration (Fig. 9) was afflictedwith, and cured by me of, an extensive osseo-cartilaginousdeviation of the septum. The drawing was taken from a

Fig. 9.

life-sketch, and the history of this individual throws muchlight upon the origin and growth of the septum of heredity.You may catch my meaning when I inform you that I wasenabled to correctly diagnosticate, or, more accurately speak-ing, infer, through this patient, the general condition of thenostrils and health of all his brothers, four in number, andhis father. In this family the nasal asymmetry was verywell marked, the septum in one instance being deviated tosuch an extent as to disturb the external symmetry of thenostril. All the young men seen by me, three in number,possessed the paternal nasal type and palatine arch in anexaggerated form. All have suffered with nasal catarrhdating far back in the memory of the family, and I am in-formed that the absent son, not yet examined by me, isseverely afflicted with the same complaint. The patient, an


engineer by profession and a very intelligent individual,referred to me by Dr. J. L. Corning, stated that a physi-cian informed him that his condition was due to a scrofuloustaint, probably inherited from his father. I failed to dis-cover the slightest trace of scrofula in any of these indi-viduals.

The cases I have just cited are not to be considered, as

regards their immediate condition, phthisical in character;they have simply been submitted as excellent examples ofthe influence of heredity as a determining factor in the pro-duction of nasal disease, and as such must assist us in inter-preting the same conditions when found in phthisis.

The testimony which I have just submitted, re-enforcedby much more which I could, but can not now conveniently,offer, affords, to my manner of thinking, excellent proof ofthe intimate association of a high-pitched hard palate witha deviated septum, and their transmission from parent tochild.

The relation of traumatic deviation of the septum tonasal catarrh and catarrhal phthisis is not so important as

that of the hereditary variety ; still it possesses many pointsof interest did time permit their consideration. Traumaticdeviations of the septum, especially in those not predis-posed to phthisis, are not likely to be followed by pulmo-nary tuberculosis. It shouldbe borne in mind that the twoconditions may be associated. The differentiation, however,as X shall have occasion to explain, is, as a rule, easily accom-plished.

Although the cases of induced coryza just cited by mewere of the hypertrophic variety, it should not be inferredthat rhinitis atrophica may not be developed by the devi-ated septum.

Deviations determining the existence of atrophic coryzaare general in character, and the dryness is evidently due to


the excessive drain upon the mucous follicles resulting fromthe prolonged passage of air through a single nostril.

As an example of pulmonary phthisis following in thetrain of a rhinitis atrophica, I may be permitted, in aneffort to make my meaning clearer, to precede my report ofcases with a brief reference to a patient, aged thirty, treatedby me at the University College Dispensary in the winterof 1882.* I found the nasal septum in this individual mostextensively deflected, the deviation being osseo-cartilaginousin character. An atrophic rhinitis existed as a result of thenasal disease, both nasal chambers being inordinately en-larged through long-standing atrophic processes. Large andfirm masses of muco-purulent matter clung to their smoothwalls. These dry crusts were constantly detached and pre-cipitated into the throat, irritating and inflaming the larynx.The patient was harassed and enfeebled by the unremit-ting efforts required to free his throat and larynx from thesesuffocating crusts. The atrophic processes had reached thepharynx, where, in the form of a pharyngitis sicca, it pre-sented a dry patch, which obstructed the downward flow ofthe scanty nasal mucus, collecting it in the shape of stickyincrustations just behind the velum.

A laryngoscopic examination showed the true cords tobe deeply injected and the contiguous structures inflamedby reason of the constant irritative action of the nasal in-crustations which had found lodgment there.

The patient was extremely emaciated, weak, and miser-able through the constant efforts required to free thethroat from inspissated irritating discharges. There werenight-sweats and the usual symptoms of advanced phthisis.An examination of his lungs, conducted by Dr. Moore,assistant to the Department of Medicine at the UniversityDispensary, and myself, revealed the existence of advanced

* See also No. I of illustrative cases.


destructive processes, as evidenced by the presence of cavi-ties, a profusion of fine crepitant rales, and otlier famil-iar signs of the last stage of a rapidly progressing pulmo-nary phthisis. It was clear that the patient had reached a

point where fatal prostration was imminent, and for an im-portant reason we considered it best to advise him of hishopeless condition. Hoping to delay the fatal issue asmuch as possible, the patient found it convenient to acceptthe invitation of relatives in Florida, and so passed fromunder my observation.

The points of interest to us as regards this case, brieflysummed up, are the history of a long-standing nasal ca-tarrh and the manner in which it developed a pulmonaryphthisis. That the nasal catarrh preceded the tuberculardisease is proved by two features of the affection—namely,a deviated septum, osseo-cartilaginous in character, notassociated with external nasal disfigurement, and thereforenon-traumatic but hereditary, and a rhinitis atrophica.

Either of these pathological conditions would indicatethe chronicity and persistency of the nasal catarrh, andtherefore prove that they must have preceded the pul-monary disease ; and in this, and in similar cases, we are

afforded excellent evidence of the occurrence of the pul-monary lesion as a secondary complication to the catarrhalprocesses.

I will now direct your attention to the color of the mu-

cous membrane of the upper air-passages as an indicationof incipient or developed pulmonary phthisis. The colorI refer to is a peculiar anaemic, pink hue, resembling thatsometimes observed in hypertrophy of the tonsils. Thispallor is by no means confined to the atrophic form ofrhinitis, Avhere, as far as the nostril is concerned, it invari-ably occurs, but exactly opposite to what we might expectis discoverable in rhinitis hypertrophica, where its presence

NASAL CATARRHAL AFFECTIONS

should naturally lead one to suspect and find the anmmia ofpulmonary phthisis. In two of the reported cases appendedto this paper the condition was found in connection witha rhinitis hypertrophica; and in another, likewise phthisic-ally inclined, it was associated with an hypertrophic andatrophic process in the same individual. I still favor theview advanced by me several years since, in an article onlaryngeal phthisis,* that anaemia of the upper respiratorymucous membranes influences the character of reparativechanges, as exhibited, for instance, in the conversion ofaccidental abrasions in the larynx into phthisical ulcerations.It would seem to indicate diminished vitality or a loweredpower of resistance. As an example, I might mention thatmy experience in operations upon the septum leads me toexpect an exceedingly slow reparative process, and oneusually requiring assistance in patients presenting markedanaemia of the septal mucous membrane.

In this class of cases, as we might naturally expect, theslight vascularity of the mucous membrane favors the ac-tion of the cocaine salts, and they are, in my experience,the only ones in which we can positively promise freedomfrom pain before operating.

I have selected a few histories from my case-book asgood illustrations of the aetiological relations of nasal ca-

tarrh to pulmonary phthisis.Case I.—Mr. , engineer, aged thirty, came to me

for treatment in October, 1884. His complaint was a long-standing catarrh. The right nostril (Fig. 9) for respira-tory purposes was practically useless, and had been so asfar back as he could remember. Nasal respiration was, andhad always been, carried on through the left nostril. De-spite, however, the ease with which air was inspired through

* “ Archives of Laryngology,” vol. iv, p. 187.


the free nostril, he had never been comfortable, on accountof the respiratory obstruction referred to the narrow nostril,and eagerly utilized the smallest amount of space affordedat intervals by the temporary subsidence of the congestedturbinated tissues. In addition to the respiratory discom-fort, he was annoyed by the accumulation of inspissatedmucus in the larger naris, and was wearied by the constantthough ineffectual efforts employed to remove the ropymuco-purulent matter and offensive crusts. He was alsotormented with the usual throat and laryngeal symptomswhich occur as a result of the disturbances to nasal respira-tion and drainage. The slightest exposure was likely to befollowed by obliteration of the insignificant respiratory aper-ture in the right naris, producing a disagreeable sense oftension in that nostril, evidently arising from the Turbinatedturgescence. The same exposure sometimes resulted inattacks of lung trouble, occasionally confining him to thehouse. In appearance he was thin and anaemic, his emacia-tion carrying with it more the impression of a peculiar buildthan an unusual or rapid loss of flesh. His appetite, thoughusually excellent, was capricious, and even at its best was

not followed by any noticeable increase in weight.Examination.—An examination of the nares anteriorly

with my nasal speculum revealed the presence of just thoseconditions which would serve to account for the symptomscomplained of. The vomer, ethmoid, and triangular carti-lage projected to the right in the form of a general and easyincline from above downward. Anteriorly, however, thecolumna was displaced laterally to the right as an irregularknuckle of cartilage (see Fig. 10). No evidence of disfig-urement of the external naris could be observed on ordinaryinspection (another indication of the hereditary characterof the complaint). An interesting feature observed uponthe septum in the left nostril was a vertical elevation near

[NASAL CATARRHAL AFFECTIONS

tlie ethmo-vomerine suture, caused by the abrupt interrup-tion of the perpendicular plate of the septum at this point.Behind this vertical ridge quantities of glairy or inspissatedmucus would collect, and, by reason of the excessive breadthof the inner naris at this point, they would effectually eludethe action of the respiratory pressure exerted by the pa-tient to remove them. The turbinated structures and peri-turbinated mucous membrane was markedly atrophic in thelarger or left nostril, but the inferior turbinated tissue in theright or narrow nostril was slightly hypertrophied. Justhere we note an instructive example of cause and effect, for,as we might have expected, the life-long inspiration of airthrough a single nostril—unable, through secretory disturb-ances, to furnish the necessary amount of moisture—is natu-rally followed by desiccation and atrophy of the pituitarymembrane. The right nostril, on the contrary, being almostcompletely stenosed, is always bathed in the nasal fluids.In other words, with certain modifications, it is a case ofunequal distribution of respiratory labor with the naturalconsequence, a rhinitis atrophica and hypertrophica occur-ring in the same individual. The pharynx, larynx, andtrachea presented the anaemia of phthisis. The patient’slungs were carefully examined by Dr. W. H. Katzenbach,of the Chest Department of Bellevue Hospital, and myself,and our suspicion was confirmed by the detection of thevery early signs of pulmonary phthisis.

An interesting point in the patient’s family history re-lated to his brother, a physician, who, several years since,was threatened with a pulmonary phthisis and only escapedwith his life by abandoning his labors and by careful treat-ment and systematic change of climate. It is easy to fore-see the probable fate of the subject of this history underunfavorable circumstances, for there is every reason to be-lieve that we have here an individual afflicted from child-


hood with a nasal disease due to a malformed septum,doubtless hereditary in character. I infer the hereditarycharacter of the complaint from the peculiar form of thedeviated septum already pointed out, from the fact that thebrother and several ancestors of the patient were afflictedwith -pulmonary phthisis, and for other reasons alreadygiven.

Treatment.—Measures were at once employed to relievethe patient of the discomfort occasioned by the accumula-tion of muco-purulent matter and crusts in the ample in-terior of the right nostril. This was readily accomplishedby thoroughly cleansing the nostril with warm detergentwashes, and by the assiduous employment of the cottonprobe. The naris, once renovated and relieved of alloffending substances, was kept constantly clean by thedaily employment of a convenient post-nasal douche, inthe use of which the patient acquired much manual dex-terity.

To prevent the adherence of nasal crusts to the sinuosi-ties of the nostrils, the membrane was bathed at convenientintervals in a fine spray of vaseline. The douche becamepart of the patient’s daily toilet, and he soon ceased to feelany discomfort except in the right nostril. A sense of op-pression from his inability to breathe through this side in-creased his desire to obtain any relief offered by a surgicalremedial measure, I therefore operated with this intent,leveling the deviated structure. This included a portion ofthe vomer as well as the deflected triangular cartilage. Iemployed my tubular forceps, fenestrated cartilage forceps,and rongeur or bone forceps. There were two sittings ofabout an hour each. The use of cocaine upon the patientwas particularly satisfactory. A ten-per-cent, solution was

applied in the form of a spray, and the parts in two or threeminutes were so completely benumbed that bone and carti-


lage were crushed at short intervals without the slightestmanifestation of pain. I have noticed a singular ohtusenessto pain in other cases in which cocaine has been applied toan anaemic mucous membrane.

Fig. 10.

Fig. 10, taken from a life-sketch, shows the deviated sep-tum anteriorly, and Fig. 11 the same after operating. Nasal

Fig. 11.

respiration was completely re-established through the ste-nosed nostril, and this and the relief from other catarrhal


complications left the patient in a most excellent condition—almost, in fact, unconscious of his trouble.

He embraced a good opportunity, and is now travelingabroad; on his return he will arrange to spend the winterfarther south than New York. Under the favorable condi-tions afforded by physical ease and a suitable climate thechances of this individual escaping the ravages of tubercu-lar phthisis appear most excellent.

Case II.—Mr. , merchant, aged thirty-one, fromOwego, N. Y., consulted me in January, 1884. The patientdistinctly recollects having suffered with a nasal catarrhseven years ago. Although the affection at that time provedtroublesome, still the excellent state of his general healthinduced him to consider the malady as trifling and transientin character. Small quantities of phlegm were constantlyhawked up from behind the palate. There was a disposi-tion to clear the windpipe of particles of viscid matter.At that time and for several years subsequently he plowedthe fields as a farmer.

The catarrhal symptoms, instead of disappearing, as hehad hoped and expected, became more pronounced andtroublesome, and, his stomach becoming incidentally in-volved, dyspepsia was added to his misery. The prolongedphysical and mental discomfort resulting from the persist-ent catarrhal disturbances ultimately sapped his energy andstrength, rendering him unfit to pursue his usual occupa-tions.

Clammy night-sweats commenced last summer, and havecontinued with varying frequency and severity since then.Becoming alarmed about himself, he was easily induced toseek medical advice.

Prominent among the symptoms given me at the firstinterview was a cough, which had, however, commencedonly about a year ago. Phlegm was expectorated with the


cough, particularly on rising in the morning. The cough,though annoying, was not painful. Six months ago onlya pellicle of mucus was raised in coughing. There is nowa disposition to draw flakes of mucus from behind the softpalate.

Examination. —General thickening of the nasal mucousmembrane, post-inferior turbinated hypertrophy (dextra).The usual inflammatory redness of chronic hypertrophiccoryza is replaced by the pale, ansemic hue peculiar toatrophic catarrh. The same pallor occurs upon the mu-

cous membrane of the throat, larynx, and trachea, A livid,circumscribed, inflammatory process is visible upon the edgeof the left true vocal cord.

Percussion furnished pronounced dullness over a largeextent of the chest. The resonance on the right side washigher pitched than on the left. Auscultation demonstrat-ed the presence of numerous fine crepitant rales diffusedthroughout the right lung and commencing in the left; alsocog-wheel respiration, etc.

The patient, though feeble, was able to exercise in theopen air and to visit ray office. This, however, was in ac-cordance with his own wish. Indeed, he seemed to dreadnothing so much as confinement to the house—a naturalfeeling for one who has largely led an out-of-door life. Theunusually cold and inclement February weather severelytried the patient’s feeble powers of endurance, and with thedecrease in his appetite and strength there was an increasein the copiousness and frequency of the night-sweats. Iforesaw the patient’s rapid decline under these unfavorablesurroundings. He followed ray advice and went South toescape the harsh wintry weather, and possibly to prolong hislife a little. On the advent of the warm weather he returned,passing through New York on his way home. I then ex-

amined his chest and found that the fine rales had become


generally diffused through out both lungs. The patientsafely reached home and died, near the middle of the sum-mer, surrounded by his family.

Remarks.—The important and instructive features ofthis case are, first, the history of a long-standing catarrhalaffection (of at least seven years’ duration) 'preceding anysymptom referable to the lungs. Although not holding my-self in abeyance to the history of patients as given by them-selves, still the exceptional intelligence displayed by this in-dividual in relating his symptoms, and their agreement withthe local findings, induces me to believe that the nasal catarrhpreceded the pulmonary disease. In other words, in the com-bined constitutional depression and pulmonary irritation,resulting from the mental and physical wear and tear, respi-ratory disturbances, dyspepsia, etc., following in the trainof a long-neglected nasal catarrh, we recognize the pre-cursors of a fatal pulmonary tuberculosis. The peculiarblanching of the intra-nasal mucous membrane, and alsoof the pharynx and larynx, afforded additional evidenceof the existence of a pulmonary phthisis secondary toa hypertrophic rhinitis. Such an appearance is justthe opposite to what we might expect to find in thisaffection, and therefore indicates the anaemia of phthisis,for, although the catarrhal hyperaemia had entirely disap-peared, its pre-existence is presumable from the presenceof the more persistent products, namely, the intra-nasalhypertrophies.

The circumscribed congested area upon the right vocalcord probably resulted from the rasping character of theefforts constantly employed to clear the larynx of irritatingmucus. Its very existence constituted an additional sourceof irritation, and, although not to be designated as an ulcer,it is highly probable that this abraded surface would haveeventually proved to be the starting-point of a phthisical


process, in accordance with a pathological process alreadydescribed by me.*

Case 111.—Mr. , aged fifty-three, from Ohio, cameto me, through the recommendation of his son, a patientreferred to me by Dr. M. J. Roberts, of New York, in questof relief from an annoying nasal catarrh. The malady hadexisted for many years. Much discomfort was caused bythe constant efforts required to remove a constant accumula-tion of thick, tenacious nasal mucus. Examination of thenostril revealed, among other signs of a rhinitis hypertro-phica, the presence of an irregularly shaped posterior tur-binated hypertrophy, occupying the right post-nasal fossa.The hypertrophy exhibited no signs of active congestion,but was dark-blue in color, evidently indicating much pas-sive engorgement of the turbinated venous sinuses. Thenasal mucous membrane, throughout almost its entire ex-tent, presented the pallid hue of phthisical anremia. Ex-ploration of the chest demonstrated the existence of ca-tarrhal phthisis, most markedly developed at the apex ofthe right lung.

Believing the posterior hypertrophy to be responsiblefor much of the patient’s discomfort, I concluded it best toremove this source of irritation. I employed my nasalecraseur, easily encircling the hypertrophied tissue with aloop of No. 5 piano-wire. As might naturally be anticipatedfrom the blanched appearance of the pituitary membrane,the operation was a bloodless one. The patient pronouncedhimself much benefited by the operation and after-treat-ment, and returned to his home well satisfied. This wasin January, 1881. In July, 1882, I was informed that hehad caught cold and was carried off by an attack of pneu-monia, thus confirming my suspicions that his pulmonaryphthisis would eventually lead to his death.

* “Archives of Laryngology,” vol. iv, p. 187,


The son of the deceased, a man about thirty years ofage, had, as I have already indicated, consulted me forrelief from a chronic coryza. The coryza, I discovered,was due to an hereditary malformation of the septum andnasal chamber. I succeeded in rendering him compara-tively free from his complaint by removing the offendingdeviation of the septum. He has enjoyed excellent healthever since. It was interesting and instructive to note theclose resemblance between the forehead and face of thefather and son. The frontal prominences of both pro-jected so far forward as to place the forehead almost ona vertical plane with the face. The face beneath the over-hanging forehead appeared unnaturally narrow, affordingan example of Blumenbach’s observation of the markedretrocession and contraction of the bones of the face inindividuals exhibiting great cranial development.

The father was an intelligent man, and his son, utiliz-ing excellent educational opportunities, developed unusualliterary ability as the editor of a journal. The young-est, and only other son of the family, about whom Iwas consulted but never saw, I am informed possessed a

rare degree of intelligence, and have a right to suspectthat he possessed the cranial conformation of his fatherand brother.

A few days ago I was informed that this son had justfallen a victim to consumption. Despite the discouragingfamily history of the surviving son, I feel confident thattimely treatment and care have sufficiently removed the im-press of his unfortunate inheritance to enable him to liveout his natural life.

Here, then, we have the mournful picture of a father,afflicted with a life-long catarrhal malady, eventually perish-ing with pulmonary tuberculosis, his eldest son harassedby a nasal catarrh traceable to a deviated septum, and an-


other son, a young man, dying two years after the fatherwith the same disease.

I might add other illustrations to the foregoing casesdid not the typical character of those just reported makethis unnecessary.

Treatment.—The treatment of these and similar cases isessentially one aimed at the direct cause of the disease—

namely, the deviated septum and co-existing turbinated hy-pertrophies. It largely consists in the restoration of nasalsymmetry by methods which facilitate the excision of honeand cartilage, and the removal of intra-nasal redundancies.A variety of instruments are therefore required, their char-acter being determined by the density and situation ofthe offending structures. My regular office operating-setconsists of my wire-snare nasal ecraseur, and transfixion-needles for removing soft redundancies; a fenestrated carti-lage forceps, tubular-spring forceps, beaked scissors, andtrimming scissors for excising cartilage ; and my rongeurforceps for cutting through bone. Nearly all the operationsindicated by these instruments are, through the benumb-ing influence of cocaine and rhigolene anaesthesia, renderedbloodless and painless. Most of you are acquainted withmy methods of operating, and, inasmuch as more thana mere reference to them would exceed the limits andnot accord with the purpose of this paper, I must referthose ignorant of these procedures to my earlier publi-cations.

Appropriate treatment should also be instituted to healand contract the raw surfaces, to remove and prevent thereformation of nasal crusts in the atrophic forms of thedisease, and to check excessive discharges of nasal mucus.In other words, to borrow an expression from Niemeyer,“Where there is the slightest suspicion of a predispositionto consumption, every catarrh, no matter how slight, is to


be treated with the utmost care, which is not to be relaxeduntil the catarrh is entirely well.”

Conclusions.—Briefly reviewing the subject-matter Ihave just presented, you will observe that, in determiningthe relations of nasal catarrh to pulmonary phthisis, I have,in the order of its origin and sequence, commenced by ob-serving and interpreting the catarrhal manifestations asthey occur in the nares, and have traced the gradual exten-sion of the nasal disease to the larynx.

Within the larynx we discovered the catarrhal impressin the form of a chronic irritative hypersemia of the larynx,brought about by the combined action of nasal discharges,habitual mouth-breathing, and inflammatory changes, chron-ic catarrhal hypersemia of the larynx; to go a step further,ofttimes merges into an acute laryngitis, and this in turnmay develop bronchitis. We recognize the deviated sep-tum as a most common cause of nasal catarrh, producingthis disease by pressure irritation, interference with nasaldrainage, and unequal distribution of the nasal respiratoryfunction. We have seen the importance of heredity as afactor responsible for the existence of certain forms of devi-ated septa, and noted the conditions indicating the heredi-tary character of these abnormalities.

Viewing the larynx as really the upper portion of thelung, although divorced from it on artificial anatomicalgrounds, we are often enabled to determine approximately,by the appearance of the laryngeal and tracheal mucousmembrane, what conditions may exist beyond the line oflaryngoscopic vision, and thus complete our pathologicalpicture, beginning in the nares and ending in the lungs.

It is hardly necessary for me to insist upon the value ofthe lessons to be derived from the early recognition of theclinical facts I have just presented. They at least offersomething tangible as regards prophylaxis against phthisis


or tuberculosis, for their successful treatment falls in thepositive domain of surgery. The results are for the mostpart favorable and speak for themselves, provided the meth-ods which I have proposed and published for removing re-dundancies or the remedying of defects are not commencedtoo late.

It is hardly necessary for me to add that great careshould be.exercised to properly discriminate between casesin which pulmonary phthisis or tuberculosis precedes orexists with nasal catarrh, and are, therefore, not related tothe last mentioned affection as cause and effect, and thosedeveloped by a catarrhal affection. Being mindful of this,I have felt the necessity of sometimes giving details whichwere indispensable but which may have been wearisome.It must also be borne in mind that errors are likely to creepin from difficulty or carelessness in differentiating distor-tions of the septum resulting from injury from those de-pendent upon heredity. My experience, however, encour-ages me to state that, different from what you might proba-bly imagine, in most instances, such a distinction, whenproperly made, constitutes a simple question of differentialdiagnosis. I have already referred to some of the ruleswhich facilitate the recognition of the septum of heredity ;

and, were it advisable just here, I could mention other cri-teria of equal value. It is obvious that, in treating a sub-ject of this kind, many questions present themselves, theproper interpretation of which must, for the present at least,baffle scientific investigation such, for instance, as theproneness of some families with malformedsepta to phthisisor tuberculosis, while others, on the contrary, are afflictedwith annoying sthenic but, as far as the life of the individ-ual is concerned, harmless pulmonary maladies. These,among similar speculations, though perhaps partly explain-able by ingenious hypothetical methods, must, nevertheless,


for want of sufficient demonstrative and experimental evi-dence, prove for the most part unintelligible. But even inthe contemplation of such obscure problems the earnestinvestigator may derive encouragement from Prof. Huxley’sremark, that “ whatever may he men’s speculative doctrines,it is quite certain that the order of nature is constant, andthat the chain of natural causation is never broken.”

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