GLAUCOMA

A SYMPOSIUM PRESENTED AT A MEETING OF THECHICAGO OPHTHALMOLOGICAL SOCIETY, NOVEMBER 17, 1913. 

EDITED BY

WILLIS O. NANCE, M. D. , PRESIDENT CHICAGO OPHTHALMOLOGICAL SOCIETY (1913); OPHTHALMICSURGEON, ILLINOIS CHARITABLE EYE AND EAR INFIRMARY; FORMEROCULIST AND AURIST, COOK COUNTY HOSPITAL; EDITORJOURNAL OF OPHTHALMOLOGY AND OTO-LARYNGOLOGY, AND

WESLEY HAMILTON PECK, M. D. , PRESIDENT CHICAGO OPHTHALMOLOGICAL SOCIETY (1914); FORMERPROFESSOR OPHTHALMOLOGY, CHICAGO EYE, EAR, NOSE ANDTHROAT COLLEGE; ASSISTANT SURGEON, ILLINOISCHARITABLE EYE AND EAR INFIRMARY;OPHTHALMIC SURGEON, OAKPARK HOSPITAL. 

1914CHICAGO MEDICAL BOOK COMPANYCHICAGO

COPYRIGHT 1914BYCHICAGO MEDICAL BOOK COMPANY

CONTRIBUTORS

EDWARD JACKSON, A. M. , M. D. Prof. Ophth. Univ. Colo. ; Emer. Prof. Ophth. Phila. Polyclinic; Ex-Ch. Sec. Ophth. A. M. A. ; Ex-Pres. Am. Acad. Med. And Am. Acad. Ophth. AndOto-Laryng. ; Mem. Am. Ophth. Soc. And Honorary Mem. Chicago Ophth. Society. 

JOHN ELMER WEEKS, M. D. , D. Sc. Prof. Ophth. Univ. And Bellevue Hosp. Med. Coll. , N. Y. ; Ophth. Surg. N. Y. Eye and Ear Inf. ; Mem. Am. Ophth. Soc. ; Hon. Mem. Chicago Ophth. Soc. And Royal Hungarian Med. Soc. Budapest. 

GEORGE EDMUND DE SCHWEINITZ, A. M. , LL. D. , M. D. Prof. Ophth. Univ. Penn. ; Ophth. Surg. Univ. Hosp. , Phila. Hosp. , Orthop. Hosp. And Inf. For Nerv. Dis. ; Consult. Ophth. Surg, Phila. Polyclinic; Honorary Member Chicago Ophth. Soc. 

ROBERT HENRY ELLIOT, M. D. , B. S. LOND. , Sc. D. EDIN. , F. R. C. S. ENG. , ETC. , LIEUT. -COLONEL, I. M. S. Supt. Gov. Ophth. Hosp. , Madras. India; Prof. Ophth. Med. Coll. , Madras;Fellow Univ. Of Madras; Honorary Member Chicago OphthalmologicalSociety, U. S. A. 

CASEY A. WOOD, M. D. , C. M. , D. C. L. Prof. Ophth. Univ. Ill. ; Late Prof. Ophth. N. W. Univ. ; Ex-Pres. Am. Acad. Of Med. ; Am. Acad. Ophth. And of the Chicago Ophth. Soc. ;Ophthalmic Surg. St. Luke's Hosp. ; Consulting Ophth. Surg. St. Luke'sand Cook County Hosp. ; Ex-Ch. Ophth. Sec. A. M. A. ; Editor System Ophth. Therapeutics. Sys. Ophth. Operations and American EncylopediaOphthalmology. 

FRANCIS LANE, A. B. , M. D. Pathologist and Asst. Ophthalmic Surgeon Ill. Char. Eye and Ear Inf. ;Instructor in Ophth. Rush Med. Coll. ; Asst, Ophth. Surg. PresbyterianHospital. 

E. V. L. BROWN, M. D. Asst. Prof. Pathology of the Eye, Univ. Chicago; Asst. Prof. Ophth. RushMed. College; Ophth. Surg. Ill. Eye and Ear Inf. And Cook County Hosp. ;Mem. Am. Ophth. Soc. 

NELSON M. BLACK, PH. G. , M. D. Author of The Development of the Fusion Center in the Treatment ofStrabismus; Examination of the Eyes of Transportation Employes;Artificial illumination a Factor in Ocular Discomfort, etc. 

FRANK C. TODD, M. D. Prof. Ophth. And Oto-Laryng. , Univ. Minn. ; Chairman Sec. Ophth. A. M. A. And second Vice-Pres. A. M. A. ; Ophth. Surg. Univ. And Hill CrestHospital. 

ALBERT EUGENE BULSON, JR. , B. S. , M. D. Prof. Ophth. Ind. School Med. ; Ex-Ch. Sec. Ophth. A. M. A. ; Ophth. Surg. St. Joseph's Hospital; Editor Jour. Ind, Slate Med. Assn. 

DEDICATED TODR. EDWARD JACKSONDR. JOHN E. WEEKSDR. GEORGE EDMUND DE SCHWEINITZLIEUTENANT COLONEL ROBERT HENRY ELLIOTHONORARY MEMBERSBY THE CHICAGO OPHTHALMOLOGICAL SOCIETYIN RECOGNITION OF THEIR SPLENDID ACHIEVEMENTSIN THE DOMAIN OF OPHTHALMOLOGY

ABSTRACTS. 

I. Etiology and Classification of Glaucoma. 

Abstract:--

Etiologic factors include: obstruction of lymph spaces, especially theangle of the anterior chamber; blood pressure, arterial, capillary andvenous; affinity of tissues for fluids; alterations of the intra-ocularfluids; inflammations in the eye ball; and failure of a nerve apparatusto control fluid in the globe. Classification: various types of glaucomaconstituting clinical entities must be recognised, as: simple glaucoma, recurring exacerbations, congestive, mechanical, and increased tensionarising during uveal inflammations. 

DR. EDWARD JACKSON, Denver. 

Discussion by DR. FRANCIS LANE, Chicago. 

II. Pathology of Glaucoma. 

Abstract:--

(a) Changes taking place in corneal tissue. 

(b) Iris angle with particular reference to the ligamentum pectinatum. 

(c) Variations in the condition of the ciliary body. 

(d) Consideration of the anatomical changes that take place in glaucomasecondary to retinal and chorioidal hemorrhage. 

DR. JOHN E. WEEKS, New York City. 

Discussion by DR. E. V. L. BROWN, Chicago. 

III. Concerning Non-surgical Measures for the Reduction of IncreasedIntra-ocular Tension. 

Abstract:--

(a) The use of myotics; their preparation, method of administration, andexplanation of their action. 

(b) Reduction of increased intra-ocular tension by means of variousmechanical measures, notably massage, vibration massage, suctionmassage, electricity and diathermy. 

(c) Indirect reduction of increased intra-ocular tension, brought aboutby lowering the general vascular pressure. 

(d) The relation of osmosis, lymphagogue activity, the absorption ofedema, the stimulation of capillary contractility, and the lowering ofthe affinity of ocular colloids for water in their relation to thereduction of increased intra-ocular tension. 

DR. GEORGE EDMUND DE SCHWEINITZ, Philadelphia. 

Discussion by DR. NELSON M. BLACK, Milwaukee. 

IV. Trephining for Glaucoma. 

Abstract:--

(a) The aim of the operation is the formation of a foreign-body-freefistula. 

(b) It is most important to leave uveal tissue untouched. 

(c) Method of doing this explained. 

(d) The area available for trephining. 

(e) Method of increasing that area. 

(f) Cornea splitting. 

(g) Placing of trephine. 

(h) Technique of using trephine. 

(i) The operation is not difficult. 

(j) The operation valuable as a prophylactic measure. 

DR. ROBERT H. ELLIOT, F. R. C. S. , Lieut. -Col. I. M. S. , Madras, India. 

Discussion by DR. FRANK C. TODD, Minneapolis. 

V. Operations Other than Scleral Trephining for the Relief of Glaucoma. 

Abstract:--

Most of the ordinary surgical procedures employed for loweringintra-ocular tension furnish a permanent cure of certain fairly welldefined varieties of glaucoma. They also relieve the symptoms and retardthe progress of other varieties of the disease, even if they do notperform a cure. In a third class of cases, they either have no effectwhatever in arresting the disease or they hasten its march towardsblindness. 

What operative procedure gives, on the whole, the best results? In otherwords, what operation is the easiest of performance, is the least likelyto be attended by serious complications and is available for the largestnumber of cases? Reasons for believing that of the better knownprocedures simple iridectomy is the least effective, while thoseinterventions producing a large, thin, scleral filtration-cicatrix arethe most valuable. 

DR. CASEY A. WOOD, Chicago. 

Discussion by DR. A. E. BULSON, JR. , Fort Wayne

Etiology and Classification of Glaucoma

BY

EDWARD JACKSON, M. D. , Denver. 

It is convenient to start with the conception that glaucoma is increasedtension of the eyeball, plus the causes and effects of such increase;although a broad survey of the facts may reveal a clinical entity to becalled glaucoma, without increased tension constantly or necessarilypresent, and cases of increased intra-ocular tension not to be classedas glaucoma. 

The physiologic tension of the eyeball is essential to ocularrefraction, and closely related to ocular nutrition. Fully to understandthe mechanism for its regulation would carry us far toward anunderstanding of the causes of glaucoma. Normal tension is maintainedwith a continuous flow of fluid into the eye and a correspondingoutflow. Complete interruption of the nutritional stream would be speedydeath; partial interruption may be held responsible for most of thevisual impairment and pain of glaucoma. 

The balance of intra-ocular pressure is not maintained by the slightdistensibility of the sclero-corneal coat. Increased pressure does notopen new channels for the escape of intra-ocular fluid; if, indeed, itdoes not tend to close the normal channels. 

The affinity of the tissues for water, or, as Fischer explains it, theaffinity of the tissue colloids for water, seems too little related tothe requirements of ocular function to furnish the needed regulation oftension. The lymph spaces and blood-channels of the eye are large, ascompared with the mass of its tissue colloids. In these spaces andchannels must be sought a means for rapid response to the need forregulation of intra-ocular tension. Fischer has shown, that when theenucleated eyeball is placed in a weak solution of hydrochloric acid, the swelling of the tissue colloids is sufficient in a few hours, toburst the sclero-corneal coat. But this is an eye in which allnutritional changes have ceased. He brings together many facts tosupport the view that in the living tissues impaired circulation, andespecially diminished oxidation, are the chief causes of increasedaffinity of the colloids for water. Such affinity increased by theimpairment of the intra-ocular circulation, may well constitute a factormaking for malignancy in glaucoma. But it can hardly explain theoriginal departure from a normal pressure balance. 

We must assume that intra-ocular pressure is kept down to the normallimit, by the prompt response of a regulative mechanism, whichdiminishes the flow of fluid into the eye, or permits its more rapidescape, whenever fluid tends to accumulate in the eye and increase itstension. 

Little has been done to show that increase of fluid entering into theeye is the cause of glaucoma. A normal, or even a low arterial bloodpressure is sufficiently above the normal intra-ocular pressure tofurnish a source of increased fluid in the eye. Increased arterialpressure has been found in a large proportion of cases of glaucoma; andmay be necessary to the production of the highest intra-ocular tension. A sudden relaxation of the arterial walls, that would permit thearterial blood pressure to make itself felt in the eye, might cause animportant rise of intra-ocular tension and may be a factor in theetiology of acute attacks. It affords a possible mechanism through whichmay be produced the recognized glaucomatous effects of certain nervedisturbances. But such attacks are not commonly associated withnoticeable flushing of the head and face generally; and paralysis of thecervical sympathetic is known to lower the intra-ocular tension. 

Capillary blood pressure must lie between the arterial blood pressureand the venous blood pressure. It must be closely associated with thenutritional processes like secretion or inflammation; beyond this weknow little about it. The association of increased blood pressure withglaucoma seems to be generally an indirect one through vascular lesionsand disturbances of nutrition. 

_Obstructed Outflow_

A reservoir with a free outlet can only fill during a flood; and thenquickly empties itself again. The outflow channels in the normal eyeprovide for carrying away of the waste products of such an activenutrition, that it is hard to think they will become inadequate inglaucoma until there has been a marked decrease from their normalcapacity. Priestley Smith has pointed out that the glaucomatous eyesoftens more slowly than the normal eye after enucleation, in spite ofthe fact that a greater force is operating to drive fluid out of theeye. In his recent tonometric studies Schoenberg noted that undermanipulation the glaucomatous eye softened more slowly than the normaleye; and suggests this diminished drainage as an important evidence ofglaucoma. 

Obstructed outflow might begin in an abnormal tendency of the tissues toretain fluid, a tendency that Fischer might locate in the colloids. Theincrease of intra-ocular pressure noted in cases of uveal inflammation, to be presently referred to, may be due to some such tendency. But it isrational to ascribe to obstruction of the filtration angle of theanterior chamber, the important part it has been supposed to play in thepathology of glaucoma. However this obstruction may be brought about, whether by thickening of the iris root during dilatation of the pupil, pushing forward of the iris root by the larger ciliary processes of age, or the enlarged crystalline lens pressing on the ciliary processes; orby inflammatory adhesion of the iris to the filtration area; ballooningof the iris, or its displacement by traumatic cataract; or adhesion tothe cornea after perforating ulcer in the secondary glaucomas; orwhether the obstruction is due to the accumulation of experimentalprecipitates, as shown by Schreiber and Wengler, or possibly of pigmentgranules into Fontana's space; or a process of sclerosis closing thespaces by contraction of new-formed connective tissue, or the coveringover with proliferating implanted epithelium following injury openingthe anterior chamber; glaucoma follows impairment of this drainagespace, and lessened outflow through it. This blocking of the angle ofthe anterior chamber must be regarded as an established fact in theetiology of glaucoma. But because it is so definitely established, andbecause so much work has been done with reference to it, we may attachto it an undue importance. 

The escape of the outflow of fluid from the eye is ultimately throughthe veins. The general venous blood pressure is so low (often negativein the great veins of the neck during inspiration) that no obstacle cancome from it to the ocular outflow. The venous blood pressure permitsthe eyeball to become perfectly soft. We have all seen tension of 5 mm. , or even less; and general venous pressure does not rise to the normalintra-ocular tension. Increased intra-ocular pressure requires thatthere must be some obstacle that keeps the intra-ocular fluid fromreaching the general venous system. This may be in the lymph drainagesystem of the eye; but it may also be in the ocular veins themselves. 

Experimentally the eyeball can be made to burst by tying all the venousoutlets from it. I have seen very high intra-ocular tension develop in afew hours after general thrombosis of the orbital veins. The absence ofthe canal of Schlemm is noted in congenital buphthalmos. The enlargementof the anterior perforating veins is an old symptom of chronic glaucoma. Obstruction to outflow of blood through the vorticose veins, by theincreased intra-ocular pressure, has long been a recognized explanationof the malignant tendency of glaucoma--a part of the vicious circleestablished in this disease. There is reason that we should give carefulattention to the views of Heerfordt and Zirm, that obstruction to thevenous outflow may be the effective cause of the disease. Zirm believesthe venous plexus of the choroid is an essential part of the mechanismfor the regulation of intra-ocular tension, the necessary vaso-motorcontrol depending on nerve centers situated in the iris. 

_Nerve Control_

The accurate control of normal intra-ocular pressure, by mutualadjustment of inflow and outflow of fluid, is scarcely conceivablewithout some highly specialized, extremely sensitive nerve mechanism topreside over it. This is suggested by analogy with the regulation ofsecretion in the lacrimal, salivary, or peptic glands, or themaintenance of blood pressure in the heart and arteries. Clinicalobservations point the same way. Many patients connect their attacks(especially their earlier ones of ocular discomfort, impaired vision, haloes around the light, and dilated pupil) with social excitement, anxiety, worry, anger or fatigue. A patient of mine gave up her cardparties, because an exciting game generally ended in blurred vision, arainbow around the light, and a dilated pupil, and sometimes an achingeye. Another woman watching beside her dying husband and exposed toextreme cold, had her first attack of glaucoma, so severe as to destroythe sight of one eye. The other eye, also affected at the time, recovered good vision, and has remained several years without a secondattack and without treatment. 

Laqueur's first attack occurred at the end of a long exhausting morningin the operating room, with luncheon delayed two hours. The connectionof his later attacks with anger, worry, embarrassment, even theexcitement of watching a play at the theatre, was noted again andagain. In Javal's case, the attack fatal to one eye came at theculmination of an exciting electoral campaign. The other eye wasstricken at the termination of the Dreyfus case, in which Javal wasintensely interested. There seems to be a special liability to glaucomaamong those residing at high altitudes, best explained by nerveinfluence. The frequency of glaucoma among Jews may be due to a smallcornea, as suggested by Priestley Smith; but it is quite as reasonableto connect it with a racial excitability or nervous instability. Moredefinite knowledge of the nervous mechanism concerned in the regulationof intra-ocular pressure and the production of glaucoma is much needed. 

_Alterations of Fluids and Tissues_

The influence of increased affinity of the tissues for fluid has alreadybeen referred to. That a similar obstacle to the escape of fluid fromthe eyeball might be due to a change of character in the fluid, is aconception that has been entertained as a working hypothesis, and muchexperimental and analytical work has been done to test its correctness. This work has been so slightly related to practical ophthalmology, andso contradictory in its results that alterations in the fluids can onlybe regarded as a possible etiologic factor. Glaucoma secondary tointra-ocular hemorrhage, operations on the lens or its capsule, orsevere nutritional disturbance may be capable of such explanation. 

_Different Kinds of Glaucoma_

A better grasp of the etiology of glaucoma may be attained byconsidering separately various types of cases; although perfectlytypical cases may be rare; and cases of mixed type and etiology muchmore frequent. 

Simple glaucoma has been recognized as closely related to atrophy of theoptic nerve with deep excavation. No line of demarcation can be drawnbetween them, except by reserving the term of glaucoma for cases thatdepart from the pure type, terminating in glaucoma of some other kind, which is no more significant than the passage of a conjunctivitis into akeratitis, or an iritis into a glaucoma. Cases of simple glaucoma do runtheir course of many years to complete blindness, or to death, withoutexacerbations, inflammation, or characteristic pain. In such cases theintra-ocular tension does not rise suddenly; and it may be little or notat all elevated above the usual normal limit. 

For nine years I have watched the progress of such a glaucoma in a mannow aged 87, with slow development of glaucomatous cupping of the opticdisc, now more than 3 D. Deep. The tension has never been noted at morethan Plus T (?), and when taken with the tonometer varied from 9 to 32mm. For the worse eye, and 13 to 24 mm. For the other. Similar cases inwhich the tension lay within the commonly accepted normal limits havebeen reported recently by Bietti and Stock. 

In the eye there is probably a normal equilibrium between bloodpressure, tissue activity, and intra-ocular tension. This may bedestroyed either by increasing the intra-ocular tension, or lowering thetissue activity, or the blood pressure. Lowered blood pressure has beensuggested by Paton as an explanation of symptoms usually ascribed tovascular obstruction. Rising blood pressure may be required in old ageto compensate for diminished tissue activity; and it is conceivable, under normal intra-ocular tension, that diminished nutritional activitymay result in the same symptoms as are produced in other eyes byincreased tension. Glaucoma is probably not so much an increase oftension as a loss of balance between intra-ocular tension andnutritional activity. 

In contrast with the above are the cases marked by sudden elevations ofocular tension recurring repeatedly over long periods without permanentvisual impairment. Laqueur's case continued of this character for sixyears, under the use of miotics, and then was cured by iridectomy, thecure remaining permanent with normal vision until his death after 30years. Millikin has reported the case of a patient who in five years had"many hundreds" of attacks, in which vision was impaired, haloesappeared about the light, the pupil dilated, the cornea became steamy, and tension rose to plus T. 1 or plus T. 2. After iridectomy the attacksceased, leaving no pathological cupping of the disc, full vision, and agood field. I have seen cases of this type in women under middle age, and of marked nervous instability. 

A third type which will come to be more generally recognized, as thetonometer comes to be more widely used, includes cases in which there islittle beside the increase of intra-ocular tension to justify theirmention in a discussion on glaucoma. A patient, then aged 21, sufferedthree years ago from a scotoma almost central; and was first seen sixmonths after that with a macular choroidal atrophy and abnormalpigmentation. She suffered, we afterwards concluded, from choroidaltuberculosis. A recurrence involving adjoining choroid occurred fourteenmonths ago. There was at the start pain, slight dilatation of the pupil, and slight general hyperemia of the globe. The tension of the eyeballrose to 60 mm. , that of the fellow eye being 20 mm. Under miotics thetension fell at first but slightly. It was 55 mm. At the end of a week;but after two weeks came down to normal, 20 mm. A month later thetension rose to 28 mm. , but for a year has continued normal; the eye didwell under tuberculin treatment, and without any local treatment. InSeptember of this year I had two cases of iritis in which theintra-ocular tension rose to 45 and 52 mm. , respectively, and graduallyreturned to normal, with the cure of the iritis under atropine. In oneof these cases, a lady of 70, I used atropine also in the other eye, but the tension of that eye remained normal, 22 to 24 mm. , throughout. After needling the lens in young people I have seen a rise ofintra-ocular tension to 50 and 60 mm. , maintained for many days, withconsiderable general deep hyperemia, and soreness of the globe, followedby gradual return to normal tension, and no permanent impairment ofvision or the visual field. 

One other type may be mentioned. That of an elderly patient with markedvascular disease, often renal involvement, and distinctly impairednutrition. There may be renal retinitis or retinal hemorrhages. The casemay easily become one of hemorrhagic glaucoma. It may run a very chroniccourse. But it may become suddenly worse, or go on to complete blindnesswith pain, demanding enucleation, after some temporary perturbation, asthe performance of a glaucoma operation. It is pre-eminently the kind ofa case you would prefer would go to some one else. 

Each of these types illustrate a distinct cause or group of causes. Thefirst type brings us near to what may be the essential nature ofglaucoma, impairment of ocular nutrition by the intra-ocular tension, which is generally elevated, but may not be above the usual normal. Aspecial weakness in the nutrition of nerve tissue may be assumed. Itwould help to explain the cavernous atrophy of the optic nerveassociated with simple glaucoma. The second type shows impairment of theregulative mechanism permitting rapid rise of the intra-ocular pressure. In persons of good nerve nutrition and strong recuperative power, it mayexist for years without doing permanent damage. But joined to causes ofthe first type, lowered nutritive activity, it causes rapid andpermanent loss of sight. The third group are cases associated withglaucoma only as causes. In eyes with low nutritive power, or subject toexacerbations of increased intra-ocular pressure, uveal inflammationsmay prove disastrous. The fourth type shows the results of thecombination of the causes of the other types; with the elements of acuteor slow malignancy added--the impaired circulation and lowered oxidationproducing some degree of edema of the tissues that insures a fatalresult. 

This is no complete presentation of my subject, but a selection of factsbearing on the etiology, to serve as a foundation for the discussion ofthose practical aspects of glaucoma which are to claim your attentionthrough the papers and remarks of subsequent speakers. 

Dr. Edward Jackson's Paper on Etiology and Classification of Glaucoma

Discussion, FRANCIS LANE, M. D. 

Chicago. 

Not one of the theories thus far propounded to explain the essentialcause of increased intra-ocular tension is satisfactory. Our present dayknowledge apparently ceases with a more or less incomplete understandingof the mere circumstance under which increase of tension in generaldepends. 

The question of the source of the normal intra-ocular pressure mustfirst be solved before any discussion of a pathological increase can beengaged in. This question primarily hinges on whether the corneo-sclerais to be regarded as an unelastic capsule with a fixed volume, or as ayielding envelope with an ever changing capacity. 

This brings us at once to the consideration of that theory whichprobably has held our attention for the longest period of time, _i. E. _, the volumetric theory. According to it, the normal intra-ocular tensiondepends on the volume of fluids within the eyeball. Any variation in thequantity of the contents gives rise to a change in the pressure, therefore, the globe has been regarded as "an elastic capsule, whosecapacity, form, and internal pressure depend on the balance struckbetween a constant inflow, or formation of aqueous, and a proportionateoutflow or resorption. " (Henderson. )

Hill has satisfactorily demonstrated that, under physiologicalconditions, the hydrostatic pressure within the eye and the skull isidentical; it rises and falls simultaneously; it is the same as thecerebral venous pressure; it is constantly varying, depending directlyon the general circulation. Upon these findings Henderson based hisopinion that the physiological properties of the tunica fibrosa and theskull are identical, realizing at the same time, that the rigidity ofthe corneo-sclera, because of its fibrous nature, is not as firm as thecranium. In accepting this belief the inference was that the cubiccapacity of both coverings is fixed. Applying these conclusions to theeye, it can be said that the pressure of the fixed intra-ocular volumevaries with the venous tension within the bulb, which in turn isinfluenced by the general circulation. Such a conception, while notstrictly in accord with recognized physiological teachings, proves thatthe normal intra-ocular pressure is not a question of volume content, but that it is purely a question of pressure of a fixed volume within anunyielding capsule. Dr. Jackson virtually puts aside the volumetrictheory with his statement, that "the balance of intra-ocular pressure isnot maintained by the slight distensibility of the sclero-corneal coat. "Further discussion on the inadequacy of the volumetric theory need notdetain us. 

It is well to recall a few anatomical features because of their bearingon the theories herein considered. 

1. The angle of the anterior chamber is a true angle and not an annularsinus. 

2. The meshwork of the iris angle (ligamentum pectinatum), a cellularstructure at birth, undergoes a progressive and physiological fibrosiswith early subsequent sclerosis, until finally it becomes a fibrousstructure. The individual strands of this meshwork are more than twotimes as large at advanced age as at birth, consequently the alveoli ofthe meshwork becomes markedly reduced in size. 

3. The spongy nature of this meshwork affords free access of aqueous tothe venous sinus of Schlemm, thence by tributaries into thesupra-choroidal space and anterior uveal venous system. 

4. Fuchs's iris cripts afford direct access of aqueous to the veins ofthe iris. 

Furthermore, two simple principles are taught by physics: Fluids areincompressible and they seek the lowest hydrostatic level. Theapplication of these perfectly obvious principles to the eyeball makesthe intra-ocular pressure the same as that within the elastic venouswalls, which is the lowest circulating pressure within the bulb. 

To summarize: The aqueous has direct access to the anterior uveal venoussystem; the physiological thickening of the strands of the meshwork ofthe iris angle supplies a mechanical obstruction between the anteriorchamber and the venous sinus of Schlemm; intra-ocular pressure stands atthe same level as the intra-venous, consequently, the hydrostaticpressure is the same on both sides of the iris angle meshwork, becausethe canal of Schlemm is a secondary venous system; lastly, the outflowof aqueous into the venous sinus is by diffusion, not by filtration, because the pressure is the same on both sides of the meshwork. 

These facts and deductions have given rise to the present daycirculatory theory of intra-ocular pressure, so we now can approach thepredisposing and exciting factors which determine glaucoma. 

The central fact to be borne in mind is, if the physiological pressureis vascular in origin and nature, the pathological pressure mustlikewise be derived from the same source. 

Sclerosis of the meshwork of the iris angle is the predisposing factorbecause it hinders free access of aqueous into the venous sinus ofSchlemm. Sclerosis alone, however, will not cause glaucoma so long asaccess to the iris veins can keep the intra-ocular pressure at theintra-venous level, and, too, as long as the exciting cause is absent. 

The exciting cause is vascular, maintained and influenced by the generalcirculatory pressure. A rise of the general vascular tension alone willnot cause glaucoma, because any alteration in intra-ocular pressureresulting would be purely a temporary change, easily taken care of bythe extensive access of aqueous to the intra-ocular venous system. Whenthese two factors coexist in their varying combinations, pathologicalincrease of pressure results--in short, glaucoma. 

Syphilis, rheumatism, gout, auto-intoxication and many otherconstitutional disorders are well recognized agencies which inducesclerosis in body tissues, so there can be little doubt that theseconditions produce pathological sclerosis of the meshwork of the irisangle. Psychic disturbances, congested portal or renal system, hardmental or muscular work, etc. , etc. , induce increased pressure of thegeneral circulation, and so simultaneously the intra-ocular pressure. 

According to the edema theory advanced by Fischer, glaucoma is"essentially an edema of the eyeball, and for its production we musthold responsible the same circumstances which are responsible for astate of edema in any other part of the body. " The magnificentexperimental work of this investigator has shown that edema is nothingmore or less than an increased capacity of the protein colloid tissuesfor water; that the most important factor leading to this increasedhydration capacity is an abnormal production or accumulation of acidcontent, effected by those agencies which are instrumental in causingsclerosis and an increase of blood pressure. 

It seems that both of these theories afford an explanation for many ofthe secondary pathological manifestations which characterize theintra-ocular tissues during a glaucomatous onset. 

Fischer criticizes the Henderson theory on the ground that increasedblood pressure alone does not lead to edema--edema is thwarted by highblood pressure. On the other hand, if Fischer believes that sclerosis ofthe meshwork of the iris angle is a result and not a cause of glaucoma, then it would seem that Henderson has the better of the argument. Thephysiological changes in this structure, which take place with advancingage, can rightfully be looked upon as a predisposing factor in glaucoma. 

Dr. Jackson has presented all other phases of this part of thesymposium in such a comprehensive manner that nothing further remains tobe said. 

Pathology of Glaucoma

BY

JOHN E. WEEKS, M. D. , New York City. 

In reviewing the pathology of glaucoma it seems proper to consider thevarious structures and tissues of the eye in logical order. 

_Lids and Conjunctiva. _ "The only change observed in these tissues is areflex edema, excited apparently by pressure on the ciliary nerves and, probably, irritation of the vaso-motor fibers of the sympathetic. "

_Lachrymal Gland. _ Hyper secretion due to reflex irritation. 

_Cornea. _ As has been shown by Priestley Smith, the cornea inglaucomatous eyes is, as a rule, smaller than in non-glaucomatous eyes, the mean of a series of measurements being 11. 1 mm. Horizontally and10. 3 mm. Vertically in glaucomatous and 11. 6 mm. Horizontally and 11mm. Vertically in non-glaucomatous eyes. In cases of considerableincrease of tension, particularly if the onset is sudden, thecirculation of lymph in the cornea is interfered with, the anteriorlayers of the cornea become edematous, the spaces between the lamellaefilled with albuminous fluid. Some of this fluid finds its way throughBowman's membrane, apparently by way of the minute channels which permitthe passage of small nerve twigs, and enters the epithelial cell layer. The fluid finds its way between the epithelial cells in the deeperlayers, apparently being taken into some of the superficial cells byimbibition. Some of the swollen surface cells open spontaneously anddischarge their contents, others drop off. The process causes aroughening of the surface of the cornea and produces a faint haziness. There is another form of haziness that develops on sudden rise intension and completely disappears on subsidence of the tension. This isdue, as has been shown by V. Fleischl (Sitzungsberichle d. Weiner Akad. D. Wissensch, 1880) and others, to increased tension on the fibrillae ofthe cornea, a double refraction being induced. In cases of longcontinued increase of tension minute permanent vesicles form in theepithelial layers, particularly in the superficial portion. Anaesthesiaof the cornea develops, due to pressure on the nerve fibers that aredistributed to the epithelium, the compression probably occurring alongthe course of the long ciliary nerves, from which the corneal nerves arederived, as they pass between the choroid and the unyielding sclera(Collins & Mayou). 

In advanced cases of glaucoma after the congestive period has subsidedthe cornea becomes somewhat condensed, the lymph spaces contracted; acondition of sclerosis obtains. Alteration in the shape of the corneaoccurs only rarely in adult life. When it does occur it takes place incorneĉ that have suffered from keratitis. The alteration is usually inthe form of ectasiĉ. In infancy and early youth (buphthalmia) the corneamay become uniformly enlarged and globular. Often, however, theenlargement of the cornea is irregular. Increase in tension may producefissures in Descemet's membrane. These occur more frequently in thecornea that have suffered a change in shape, as in buphthalmos. Gapsoccur in the elastic membrane which become covered by endothelium. Somecloudiness may be seen in the corneal lamellae adjacent to thesefissures, in some cases due evidently to the filtration of aqueous humorthrough defective endothelium. Prolonged high intra-ocular tension maybe accompanied, particularly in cases of secondary glaucoma, byvesicular and bullous keratitis. 

In acute glaucoma the sclera appears to be edematous and slightlythickened. As the disease progresses the sclera becomes denser thannormal. The oblique openings--passages for the venae vorticosae--aresaid to be narrowed. The openings for the passage of the anteriorciliary vessels are enlarged in many, particularly in advanced cases. Minute herniae at these openings are sometimes present. Dilatation andtortuosity of the anterior ciliary veins are due apparently to excessiveflow of blood through them on account of the abnormally small amountcarried off by the venae vorticosae. In the stage of degeneration, ectasae of the sclera occur most frequently near the equator of theglobe. Spontaneous rupture may take place. 

_Anterior Chamber. _ The anterior chamber is shallow, as a rule. This isalmost without exception in primary glaucoma in adults. In secondaryglaucoma in which occlusion of Fontana's spaces occurs as a result ofthe deposition of fibrin or other inflammatory products the anteriorchamber may be of normal depth, or deeper than normal. Very deepanterior chamber may occur in glaucoma, due to retraction of lens andiris following fibrinous or plastic exudation into the vitreous, orwhen it occurs in congenital glaucoma, due to enlargement of the globe. 

_Aqueous Humor. _ The aqueous humor, as has been pointed out byUribe-Troncoso (Pathoginie du Glaucome 1903) contains a greatlyincreased quantity of albuminoids and inorganic salts in glaucoma. Inacute glaucoma the increase of albuminoids (blood proteids) is greaterthan in chronic glaucoma. The aqueous humor becomes slightly turbid inacute attacks, coagulating more readily than the normal. The plasticprinciple contained in the aqueous is rarely sufficient to causeadhesion between the margin of the iris and the lens capsule, but thecolloid nature of the aqueous, according to Troncoso, lessens itsdiffusibility and prevents its free passage into the lymph channels. Theincrease in albuminoids is a consequence of congestion and venous stasisand does not precede the attack. 

_Filtration Angle. _ The changes that occur in the filtration anglebefore it is encroached upon by iris tissue are sclerosis of theligamentum pectinatum in adults to which Henderson (Trans. Ophth. Soc. U. K. Vol. Xxviii) has called our attention; the accompanying sclerosisof the other tissues to the inner side of Schlemm's canal; and, in somecases, the deposition of pigmented cells derived from the iris andciliary processes (Levinsohn) which serve to obstruct the lymph spaces. In many of the cases of acute glaucoma and almost all of the cases ofchronic glaucoma of long standing the filtration angle becomes blockedby the advance of the root of the iris. 

_Iris. _ In acute glaucoma the iris is congested and thickened. It ispushed forward and may lie against the cornea at its periphery. When theattack subsides, the iris falls away from the cornea. Aside from thecongestion, the primary changes that take place in the iris areindicative of paresis of the fibers of the motor oculi that supply thesphincter pupillae, and stimulation of the fibers from the sympatheticproducing vasomotor spasm. The long diameter of the pupil apparentlylies in the direction of the terminal vessels of the two principalbranches of each long ciliary artery which form the circulus iridismajor, where the vasomotor spasm would have the greatest effect inlessening the blood supply. The haziness of the cornea and slightturbidity of the aqueous contribute greatly to the apparent change inthe color of the iris. In cases of simple chronic glaucoma there is butlittle evidence of edema of the iris. If the iris lies in contact withthe sclera and cornea for some time, it becomes adherent (peripheralanterior synechia). As the disease progresses, the stroma of the irisatrophies and contracts. There is very little evidence of small-cellinfiltration or the formation of cicatrical tissue. Numerous slits maydevelop in the iris through which the fundus of the eye may be seen(polycoria). The pigment layer does not atrophy in proportion to thestroma of the iris; by the contraction of the stroma of the pigmentlayer is doubled upon itself at the pupillary margin, forming a blackring of greater or less width (ectropian uveae). The iris becomesattached to the pectinate ligament and to the endothelium of Descemet'smembrane. In a very few cases the closure of the angle is not completeat the apex, a small space remaining comparatively free for a long time. The adhesion of the iris to the pectinaform ligament and cornea is notuniform at all parts of the periphery; it varies in width. Portions ofthe iris angle may remain open while other parts are closed. Where theiris tissue lies in contact with the cornea, the stroma of the irisalmost totally disappears. In some cases the iris becomes totallyadherent to the cornea. 

_Ciliary Body and Chorioid. _ In acute glaucoma there is congestion ofthe entire uveal tract, the congestion partaking more of a venous stasisthan of an active or arterial congestion. The vessels of the ciliaryprocess, which are larger and more tortuous in adults of advanced yearsthan in the young, become enormously distended, causing almost completeobliteration of the perilental space. They press against the root of theiris and the equator of the lens, forcing them forward. There is edemaof the ureal tract, apparently from transudation of serum. Many small, and sometimes rather large hemorrhages may occur. There is but littlesmall cell infiltration, indicating almost total absence of what isordinarily recognized as true inflammation. It is probable that thesecretion from the glandular zone of the ciliary body is increased. 

On subsidence of the congestion, as after miotics or iridectomy, thetissues may return to very nearly a normal condition. The iris recedesfrom contact with the ligamentum pectinatum and cornea and thefiltration angle is again open. In some cases the iris becomes adherentto the head of the ciliary processes and, when atrophy of the ciliarybody occurs, is drawn backward at the base of the iris by the recedingtissues. If the hypertension persists or is repeated at varying periods, a slow atrophy of the uveal tract sets in. Eventually the ciliary bodybecomes very much reduced in thickness, is flattened out, the ciliaryprocesses reduced in size and the blood vessels disappear or are reducedmuch in caliber. Those that persist possess walls that are muchthickened. This is particularly true of hemorrhagic glaucoma. 

In advanced absolute glaucoma the chorioid may become reduced to a verythin membrane consisting of connective tissue and pigmented cells, scarcely distinguishable even by moderate powers of the microscope. Atrophy is marked in the vicinity of the venae vorticosae. Czermak andBirnbacher describe proliferation of the endothelium of the large veinswith contraction and obliteration of their lumen. 

_Optic Nerve and Retina. _ In the acute form the retina and optic nervepresent the same condition that is present in the vascular tunic;namely, that of venous stasis with the consequent edema. Frequentlyminute hemorrhages occur in the retina, particularly in violent acuteattacks. Cupping of the discs slowly develops, causing more or lessstretching of the nerve fibers over the edge of the cup. The gradualdiminution of the field of vision is due in greater part to death ofperipheral nervous elements of the retina, those parts of the fieldfarthest removed from the large arterial trunks suffering first. Thearrangement of the arteries at the disc, passing out as they do from thenasal side, of necessity make the vessels that pass to the temporal partof the retina longest and of less caliber. These vessels and theirterminals are first to suffer marked diminution in size; death of theperceptive elements supplied with nutrition by these vessels follows. For this reason the nasal part of the field of vision is more often thefirst to disappear. In congestive (inflammatory) glaucoma, the typicalfield of vision shows most marked contraction on the nasal side. Thedisturbance of the nutrition of the retina accounts in greater part forthe various forms of visual field met with. 

Death of all of the perceptive elements of the retina eventually occurs. The loss of nutrition is apparently not the whole cause of blindness. Atrophy of the nerve fibers follows death of retinal neurons, butatrophy of some of the nerve fibers may be, and probably is, due to thepressure and traction exerted upon them at the margin of the disc. It isprobable that too much importance has been given to this mode ofinterference with the nerve fibers. However, the change in the positionof the lamina cribrosa must exert a deleterious effect, particularly onthose fibers which pass through the peripheral meshes, the shape ofwhich must necessarily be much distorted. In glaucoma simplex, which islargely devoid of marked congestive periods (acute attacks), asurprisingly high degree of acuity of vision may exist with a deepexcavation and pale nerve. Careful studies of the retinal vessels inglaucoma (Verhoeff Arch. Of Ophth. XLII. P. 145; Opin. Soc. Françaised'Ophth. 1908) disclose the fact that an increase in the elastic tissueand connective tissue elements occurs in _some cases_, alsoproliferation of the endothelial cells, which serve to irregularlynarrow and, in some instances, obliterate the lumen of the vessel. Arteries and veins are both affected. Hyaline degeneration of the mediaalso occurs. The process is not uniform. 

_Glaucomatous Cup. _ The excavation of the disc progresses slowly and isdue in part to stretching the fibers of the lamina cribrosa pressingthis structure outward, and partly to atrophy and disappearance of thenerve tissue and much of the vascular tissues in the nerve head. Thedisplacement backward of the lamina cribrosa may cause that structureto lie behind the outer surface of the sclera. Atrophy and cysticdegeneration of the nerve trunk follows destruction of retinal neuronsand cupping of the disc. Neuroglia remains in part. Connective tissueelements increase in the optic nerve as the nerve fibers disappear. 

_Glaucomatous Ring. _ The development of the pale circle which surroundsthe disc, particularly in glaucomatous eyes, is due to a very slightrecession of the pigment layer of the retina and of the margin of thechorioid at this point with some atrophy, apparently consequent on thebeginning retraction of the lamina cribrosa and slightly increasedpressure of the nerve fiber layer on the underlying tissues at themargin of the disc. This permits the sclera to show through a verylittle at this part. In some eyes in which there is a beginningsclero-chorioiditis posterior, the condition is very similar to thatpresented by the glaucomatous ring. 

_Field of Vision. _ The two pathological processes that operate todestroy the function of the retina suffice to produce scotomata in thefield of vision of varying shapes. The typical glaucomatous field in theacute cases shows a defect most pronounced to the nasal side. As hasbeen shown by Bjeraum, the blind spot corresponding with the optic discis enlarged in glaucoma, a relative scotoma often connecting it with theblind nasal portion of the field either above or below the horizontalmeridian (Straub). The field in a simple glaucoma is apt to approachconcentric limitation; namely, more like the field in simple atrophy. This is consistent with the fact that simple glaucoma in many casespossesses the characteristics of glaucoma plus atrophy of the opticnerve. 

_Vitreous. _ During the acute attack, the vitreous may become slightlyturbid by transudation of serum from the vessel of the ciliary body andthe chorioid and may become filled with fibrin. In some chronic casesin which absolute glaucoma is reached the development of small bloodvessels in convoluted loops springing from the vessels of the discs hasbeen observed. Any process that increases the volume of the contents ofthe vitreous chamber, as hemorrhage, neoplasm, profuse serous or plasticexudation, may by pushing iris and lens forward produce an attack ofacute glaucoma. 

_Buphthalmos. _ Reis (Graefe's Arch. F. Ophth. V. LX. 1905) states thatthere is always obliteration of the anterior scleral venous channels(Schlemm's canal) in buphthalmos. Seefelder (Graefe's Arch. V. LXIII. 1906) mentions the abnormal position and abnormal narrowing of Schlemm'scanal and the imperfect and insufficient differentiation of thecornea-scleral junction. In all of the cases in which the eye has beenexamined microscopically obliteration of Schlemm's canal has beenreported. This is thought to be a defect in development. Magitot (Ann. D'Oculis CXLVII) suggests that injury to mesoderm which pushes itselfbetween the ectoderm and anterior surface of the lens would account forthe failure in development of Schlemm's canal. The changes that occur inthe tissues of the eye appear to be largely due to the stretchingconsequent on the more or less uniform distentions of the globe as aresult of hypertension. 

_Cornea. _ This portion of the fibrous membrane is enlarged, globous orflattened, irregularly thinned, particularly at the periphery, where itmay be as thin as tissue paper, nebulous because of the stretching ofits fibers principally, but in some degree (differing in differentcases) to edema of the epithelial layer. Fissures occur in Descemet'smembrane. 

_Anterior Chamber. _ This is very deep in the greater number of cases. However, this rule has many exceptions. 

The vascular tunic may be congested in young infants, but atrophy soondevelops and may reach an extreme degree. The sclera ordinarily becomesquite thin throughout, but may retain almost a normal thickness at theequator of the globe and posteriorly. Posterior sclera ectasae maydevelop. The iris, as a rule, hangs free from the cornea, oftentremulous because of retraction of the lens beyond the iris plane. Insome cases the iris is partly or totally adherent to the posteriorsurface of the cornea. 

The vascular membrane (iris, ciliary body and chorioid) and the retinabecome atrophic, the atrophy varying in degree in various parts. Detachment of the retina may occur, often preceded by or accompanied bysubretinal hemorrhage. The optic disc becomes deeply cupped and thetissues of the optic disc and optic nerve extremely atrophied. Thecrystalline lens may become cataractous and shrunken. Spontaneousrupture of the suspensory ligament with consequent subluxation of thelens may follow. 

_Secondary Glaucoma. _ The pathological conditions that precedesecondary glaucoma are many and differ widely. They may be brieflyclassified as:

1. Those that cause a partial or complete closure of the lymph spacesand Schlemm's canal by cicatrical contraction, as in sclero-keratitis. 

2. Those that cause obstruction to the lymph spaces at the filtrationangle by the deposition of fibrin or cellular elements, as in iritis, hemorrhage into the anterior chamber, etc. 

3. Those that cause obstruction of the filtration angle by advancementof the iris and lens, as occurs when the volume of the contents of thevitreous chamber is increased, as from retinal or chorioidal hemorrhageor neoplasm. 

The various changes are so numerous that they need not be describedfurther here. The ultimate changes due to high tension resemble thosealready described. 

Dr. John E. Weeks' Paper on Pathology of Glaucoma

Discussion, E. V. L. BROWN, M. D. , Chicago. 

I would like to emphasize one of the newer features of the pathologicanatomy of glaucoma, one which has received too little attention in thiscountry: the _lacunar_ or _cavernous atrophy_ of the _optic nerve_. 

The name accurately describes the condition. Tiny clear spaces form inthe lamina cribrosa and in front and behind it in the nerve tissue. Their exact nature is unknown. Usually they are entirely empty, oftenthey are traversed by fine glial fibers. They seem to be in no relationto the blood vessels. Adjoining lacunae are supposed to fuse to formlarger cavernae and these finally merge and constitute the finalglaucoma cup. The lamina may then bridge across the space like a cord, or lie back against the end of the nerve trunk. 

Schnabel considered all glaucoma cups to be formed in this way, independent of tension. His views were strongly supported by Elschnig, but as vigorously opposed by others. Axenfeld cites the fact that theglaucoma cup may disappear after operation. (I myself have seen a cup of7 D. Reduced to 1 D. In the course of a year after the tension had beenlowered from 62 to 12. ) Stock found the same lacunae in eight cases ofmyopia. The last extended study of the subject was made by E. V. Hippel, who found lacunae in 20 of 33 cases (60 per cent); enough certainly tomake one look for them carefully in every case. He publishes a largenumber of excellent photo-micrographs, but none more typical than one Ihave in my possession. 

I have been especially interested in this subject because I have metwith a complete and total glaucoma cup, with the typical (ampulliform)undermining of the scleral ring, in a pair of eyes without increasedtension. The (Schiotz) tonometer was used daily for 70 consecutive daysand never registered more than 12-14 mm. Hg. The man had been blinded bywood alcohol. At the time I could find no other report in theliterature, but overlooked a publication by Lewin and Guillery. Friedenberg has since reported cases of the same nature. 

If other conditions than increased tension can produce a typical(ampulliform) glaucomatous excavation of the disc, why may not thecavernous atrophy and cup in glaucoma be due in part at least to similarprocesses, possibly in the nature of a toxic oedema of the nerve, eitherin association with tension or independent of it, as contended for bySchnabel?

Concerning Non-Surgical Measures for the Reduction of IncreasedIntra-ocular Tension

BY

GEORGE EDMUND DE SCHWEINITZ, M. D. , Philadelphia. 

Only a few years ago the literature of glaucoma was big with discussionsof the comparative value of the surgical and non-surgical treatment ofglaucoma, and especially of the chronic types of this disease. Now, thanks to the achievements of Lagrange, Fergus, Herbert and Elliot, thevalue of a filtering cicatrix, although known for a long time, hasattained increased importance, due to the improvement and elaboration ofoperative technic, and the medical journals of the day are weighted withopinions and experiences from all over the world as to these surgicalmeasures. But true as this is, we are not yet in a position to discardnon-surgical procedures (1) because operation is not always possible, (2) because operation is not always permitted, and (3) because incertain circumstances operation is not advisable. Hence a glance at thenon-surgical methods of reducing increased intra-ocular tension is notout of place, and for convenience they may be catalogued as follows:

1. Myosis produced by means of solutions of various drugs, a myosisfollowed by reduction of intra-ocular tension. 

2. Reduction of tension by means of various mechanical measures, notablymassage, vibration massage and suction massage, and by means ofelectricity and diathermy. 

3. Indirect reduction of intra-ocular tension, accomplished by loweringgeneral vascular pressure. 

4. Reduction of ocular tension by stimulation of osmosis, of lymphagogactivity, of absorption of edema, and of capillary contractility, and bydecreasing affinity of ocular colloids for water. 

1. _The Myotics. _ Of these, eserin (physostigmin) and pilocarpin, withtheir respective salts, the sulphate and the salicylate in the firstinstance, and the hydrochlorid and the nitrate in the second, are wellestablished in favor and efficiency. Personally, it has always seemed tome that the salicylate of eserin is preferable to the sulphate, but Ihave not persuaded myself that the nitrate of pilocarpin possessesmaterial advantages over the hydrochlorid, although some authors preferit. With arecalin, the alkaloid of the Betel nut, I have no experience, nor have I used its mixture with eserin, recommended by Merck as morepotent than either of the drugs in separate solution. 

The substance isophysostigmin, found with eserin in Calabar bean, according to Ogiu, exceeds in its myotic activity the sulphate ofeserin, _i. E. _, 1/80 of a grain of the drug is equal to 1/60 of a grainof the sulphate of eserin, but it is certainly not less irritating thanphysostigmin, and according to Stephenson's researches, is more so, andin this sense has no superiority over the usual alkaloid. In generalterms, it may be said that the time has not arrived to make a preachment"on the passing of eserin and pilocarpin. "

_Physiologic Action. _ Concerning the ocular, physiologic action of thetwo chief alkaloids respectively of Calabar Bean and of Jaborandi, therestill exists difference of opinion. It has always been easy to attributethe myotic action of these drugs, or at least, of eserin, to theirstimulant action on the peripheral ends of the oculo-motor, thus causingsphincter contraction, and to a depressing action on the sympatheticfibers, thus causing removal of the action of the dilatator of the iris. But complete experimental proof of such action is wanting, and it isprobable that myosis follows a direct stimulation of the sphinctermuscle fibers, aided, perhaps, by contraction of the iris vessels, although the last named effect is denied by so competent an authority asHobart Hare. 

Exactly how the myotics reduce intra-ocular tension is not definitelyproven. Usually it is taught that because of the myosis the base of theiris wedged in the angle of the anterior chamber is loosened andwithdrawn, precisely as a fold in a coat is straightened by a tug on thefabric beneath it. Experiments, however, for example, by E. E. Henderson, have shown that the rate of filtration in an eye withartificially raised pressure is considerably larger when it is under theinfluence of eserin than it is when under the influence of atropin; thatis by the contraction of the pupil the iris-surface filtration isincreased and consequently the pressure is reduced. We all know thatThomas Henderson maintains that the results of iridectomy are beneficialbecause the raw edges of the coloboma, which do not cicatrize, permitaccess of the aqueous to the iris veins, and that myotics, inasmuch asthey contract the pupil, open the iris crypts and therefore act, lessefficiently, perhaps, but act none the less like an iridectomy. Thenormal intra-ocular pressure is uninfluenced by myotics because thispressure represents the lowest circulatory pressure in the eye, andfurther contact between aqueous and veins cannot reduce it below thislevel, another point which is made by Thomas Henderson in support of hiscontention. 

The clinical fact remains that either by mechanical means, as it were, in the liberation of a plugged filtering angle, or by the increasing ofiris-surface filtration, the myotics markedly reduce the abnormalintra-ocular pressure. 

_Methods of Administration and Indications. _ With the methods ofadministration of the myotics we are all so familiar that time need notbe wasted in their reiteration, except to refer to a few practicalpoints. In acute glaucoma, and every one knows that in this diseasetheir action is often prompt and sometimes curative, eserin in astrength of one to four grains to the ounce may be instilled withsufficient frequency to establish myosis, and its action in this respectis enhanced if the congestion of the eye is lowered by measures to whichI shall refer later. There is a good deal of clinical evidence toindicate that in this type of glaucoma, as well as in the so-calledsub-acute varieties, myotic activity is increased by a mixture ofpilocarpin and eserin in the same solution, exactly as a mixture ofarecalin and eserin is more potent than either of the drugs in separatesolution. 

Prior to the happy advent of technically correctly placed filteringcicatrices, a large number of surgeons depended almost exclusively onthe use of myotics in so-called simple, chronic or non-inflammatoryglaucoma. This is not the place to introduce a discussion of thecomparative value of iridectomy and myotic treatment in simple glaucomaas based upon statistical records. We must wait now for a sufficientperiod of time and then compare the value of myotic treatment with thatof operations by means of which satisfactory filtration is produced. Weare somewhat in the position that general surgeons occupied when asepticmethods first became prevalent. We do not usually compare the statisticsof early aseptic days with those of the pre-antiseptic period, and I donot think we ought to compare the statistics of myotic treatment withordinary iridectomy any longer, but that we should wait until we canmake a comparison between the results of prolonged myosis and those ofan improved modern technic which establishes a permanent filtration. Inthe meantime the patients who will not or cannot submit to operationmust be reckoned with. Doubtless many patients with chronic glaucoma canbe satisfactorily managed with myotic treatment, although personally Ihave always advocated operation when this could be performed, but itcannot always be performed. This rule should guide us, namely, to beginwith a comparatively weak solution of the selected drug, for example, asPosey has advocated a tenth of a grain of salicylate of eserin to theounce, and the strength gradually increased so that at the end of somemonths the patient is using a solution 1 grain to the ounce; or if thepilocarpin is preferred, solutions in double these strengths. It is myown belief, and that of many who have studied this subject, that if, without eserin irritation, a myosis can be maintained, and if thetreatment can be begun early enough, the chances of preserving visionand the field of vision are good. I believe that the two most importantinstillations during the twenty-four hours of the number necessary tomaintain this myosis are on retiring and if possible in the very earlymorning, some time between two and four o'clock. Most patients can betaught to wake themselves at the proper period of time, and are littleinconvenienced by this disturbance of their sleep. I believe that eserinirritation is most successfully avoided, not by preparations of themyotics in combination with the antiseptics, for example, tricresol, which has been so much advocated, but by ordering very small quantitiesof the solution, insisting that it shall be frequently renewed andsterilized at each preparation, and that a half an hour after itsinstillation, during the day time at least, the eye shall be thoroughlyflushed with some mild antiseptic solution, for example, boric acid andsodium chlorid. Whether the action of the eserin on the choroidalcirculation, which is maintained by Wahlfours, aids in this favorableaction of the myotics remains to be proved. It has been maintained bythis author and by others who have followed him. 

The great trouble with myotic treatment is not its lack of efficiency, but the difficulty of carrying it out successfully on ambulantpatients, even in the better walks of life. It is hard successfully tomaintain in a patient with chronic glaucoma what I may call an eserinlife, just as it is hard to maintain in a person with an enlargedprostate a catheter life and escape infection, resulting, if it occurs, in the one instance in a difficult and stubborn conjunctivitis, and inthe other in a cystitis. Still, we are obliged to use myotics, and theway to employ them to the patients' best advantage, I have ventured torepeat in spite of the universal familiarity with the methods. Perhapswe may reach that happy day when, especially with improved tonometricmethods, increased skill in measuring the rate of filtration and betterinstruments for determining the light sense, we can anticipate theadvent of glaucoma and get ahead of the ocular and visual deteriorationwhich increased tension produces, by performing preventive operationswhich shall aid nature's filtration channels in the establishment of anartificial one. But increased tension is not the whole story ofglaucoma, and a filtering cicatrix is not the last word in surgicaltherapeutics, and there is much to learn. 

2. _Reduction of tension by means of various mechanical measures, notably massage, and by means of electricity and diathermy. _ Massage isof ancient lineage. In general terms, in so far as ocular massage isconcerned, it may be applied to the eye with the finger tips (ordinarymassage), by means of various instruments (vibration massage), and withthe help of certain suction cups (suction massage, which is indeed aform of vibratory massage). Many authors are satisfied with theirresults without the employment of any instrument, and prefer simplemassage with the tip of the finger to any form of the instrumentalvariety, to quote the words of Casey Wood. At one time in my career Iexperimented very extensively with massage, not alone for the purposeof reducing intra-ocular tension, but in various diseases of the lid andcornea, and taught a trained nurse, who herself had a nebulous cornea, to make what I may call a specialty of this particular therapeuticprocedure. She became exceedingly skillful and was quite faithful. Webelieved that the best results were obtained in a seance of two or threeminutes, the finger tip being used over the lid, and the surface of thecornea lubricated with a drop of pure olive oil, although in glaucomathe addition of the oil is not necessary. Four movements were utilized, the first a stroking movement in lines radiating from the centralpressure, very much as the spokes of a wheel radiate from the hub, second a circular movement, third a pressure movement, a little dippingmotion, so that the cornea was slightly depressed, and finally, a gentletapping movement, precisely the same, except that it was a diminutiveone, as the tapping movement that the Swedish masseur makes. Usuallyeach movement occupied from a half to one minute, according to theresults desired. I agree with Casey Wood that such a technic furnishesjust as good results as any one with the aid of an instrument. 

Referring particularly to the reduction of intra-ocular tension, manysurgeons have been impressed with the value of various instruments. Thus, Ohm, who has worked particularly in the reduction of the increasedtension of secondary glaucoma, for example, after discussion of lamellarcataract, advocates the Piesbergen instrument, which makes 3, 000vibrations a minute, and is applied over the closed lids. I think theinstrument best known is the one introduced by Malakow. For this purposethe point of an Edison electric pen is armed with a small ivory ball, and the vibration rate varies from 200 to several thousand a minute, therapidly revolving ball being passed over the closed lids, in someinstances directly upon the cornea itself. I am frankly afraid of thesevibrating machines, and again make a plea for the finger tip, just as Iam afraid of a Von Hippel trephine, and prefer one which is rotated withthe fingers. 

A special investigation of pressure massage according to the method ofDomec has been made by Paul Knapp of Basel. This, as you know, consistsin applying the thumb to the cornea through the closed lids, and makingrepeated pressures upon it at the rate or 60 to 100 a minute. He checkedhis results with the tonometer after 200, 500 and 1, 000 pressures, andfound that even in normal eyeballs such massage was followed by a fallof intra-ocular tension, the average being nearly 9 mm. After a thousandpressures. Within three-quarters of an hour the tension returns to thenormal. In acute glaucoma such massage is not available, but it is ofassistance in encouraging a reduction of the intra-ocular tension andkeeping it at a normal grade after operative work, particularly after afiltering cicatrix has been made, as was well shown by Weeks in hisstudy of glaucomatous eyes operated upon by the Lagrange method. It isinteresting to remember that Paul Knapp, in the course of thisinvestigation, observed reduction of the tension after the use ofholocain. 

Another method of reducing the intra-ocular tension is by the suctionmethod, which consists in the use of certain cups from which the air isexhausted by means of a suction apparatus. Domec uses an elliptical eyecup, the concave margins of which fit closely about the globe. The airis exhausted with each respiration of the patient and from 50 to 200tractions are made at each sitting. Domec is of the opinion that thismethod succeeds in two ways, namely, in producing analgesia by tractionon the ciliary nerves, and in reducing intra-ocular tension. 

Unfortunately, it is difficult for regular physicians to make referenceto massage of the eyeball lest their words should be misquoted byirregular practitioners who employ this method, selling variousinstruments to trusting patients, and attributing to this simple andoften beneficial procedure all sorts of marvelous influences. Doubtlessall of us have seen eyes utterly ruined because the patient has trustedto the advertisements of these people, and has continued to use somefoolish little suction pump, when what his eye needed was operativeprocedure or skilled therapeutics. 

If I should sum up my opinion of massage in the reduction ofintra-ocular tension, I would say that it is useful in enhancing theaction of myotics, and particularly useful, as Domec, Knapp, Ohm, Weeksand many others have shown, after the filtering angle has been opened bya proper operative procedure. It seems to me that it is distinctly ourduty to inform patients that it is no panacea, and that they must nevertrust themselves in the hands of irregular practitioners who pretend tocure all ocular ills with massage. 

_Electricity. _ The credit of first using high frequency currents in thetreatment of glaucoma belongs to Truc, Imbert and Marques, and Roure'sexperiments indicate that this current suitably applied appears to havean influence not only in reducing the arterial tension, but also theocular tension. Thus, in an interesting series of experiments he hasbeen able to reduce an arterial pressure of 200 mm. To 140 mm. , and anocular tension of plus 2 to the normal after eighteen applications ofthe high frequency current. The current is applied for ten to fifteenminutes at a time twice a week. Some surgeons, for example, Würdemann, have suggested the use of electricity combined with massage, and haveapparently achieved satisfactory results. 

The constant current has also been much employed for the purpose ofreducing intra-ocular tension. Coleman quotes Le Prince's observations, who applies the negative pole to the eye and the positive pole to theneck, gradually passing a current of 30 to 40 ma. During a quarter of anhour, and who reports notable diminution of tension. Coleman points outthat in his own experience he has not found any patient who wouldwillingly tolerate more than 19 ma. Of current with an ordinary sizedelectrode, although he grants that it is possible that Le Prince used avery large electrode. Unfortunately he does not mention its size. Ziegler of my own city, who has studied most scientifically andintelligently the use of electricity in diseases of the eye, announcesthis rule: The positive pole should be used in all inflammatoryprocesses of the eye, glaucoma excepted, and with this rule Colemanagrees. Now, although the negative pole is a stimulant and therefore notgenerally indicated in inflammation, as Coleman points out, the objectin view is to diminish the density of the ocular capsule and itstension, hence the negative rather than the positive pole should beused, inasmuch as the former, according to him, while it is a sedative, hardens tissue and would tend to increase intra-ocular tension bydiminishing excretion. Moreover, in chronic glaucoma the ordinaryinflammatory processes are not present, indeed, primary acute glaucomaitself is not an inflammation. 

I have no personal experience in the use of the constant current withnegative pole application to the eye in the reduction of increasedintra-ocular tension, but quote for our general benefit the opinions ofthose who have employed it. I have always been very frankly pessimisticin regard to the therapeutic value of electricity in ocular disorders. Perhaps I am wrong; I am willing to be enlightened. There seems littledoubt that Truc and Imbert's observations that high frequency currentscan temporarily reduce intra-ocular tension is correct, that they areable to relieve the pain of primary and of secondary glaucoma wouldseem to be proved by many observations, some of which I have myselfmade, and other very accurate and excellent ones have been made byRisley in Philadelphia. 

A word might be said in regard to _diathermy_. According to Zahn, themethod of applying diathermy to the human eye is to take a layer ofcotton wool 1 cm. Thick soaked in a 2 per cent solution of sodiumchlorid, which is applied close to the outside of the lids. On this isput an electrode 15 cm. In size with a large indifferent electrodeapplied to the back of the neck. It is not germane to the subject toname the various ocular diseases which were treated in this manner, butClausnizer has made an investigation of the influence of diathermy onintra-ocular tension. In a number of diseases, for example, iridocyclitis, the method produced distinct rise of pressure. In one, apatient with secondary glaucoma, prior to the diathermic applicationthe tension was 37½ mm. , after the passage of the current it hadfallen to 28 mm. , but the next morning the tension rose to 45 mm. In apatient with chronic glaucoma no definite alteration of tension could befound. This observation is mentioned, not because it puts us inpossession of a valuable therapeutic measure, but largely because it isa good example of how in this disease it is wise to investigate anymethod which furnishes a hope of relief. 

In a few instances endeavor has been made to reduce the intra-oculartension, or at least to relieve glaucomatous symptoms, by galvanism ofthe cervical sympathetic, for example, by placing one electrode alongthe whole length of this nerve in the neck and one on the back of theneck on the opposite side, 15 to 20 ma. Of current being used. Goodresults have been reported by an observer named Allard. I confess that Iam entirely faithless in regard to any results that may be reached inthis manner. It is possible that as the positive pole is a sedative, ifthere were any influence, the influence of sedation would be present, but certainly it has over and over again been experimentally proved thatirritation of the cervical sympathetic quite rapidly produces elevationof intra-ocular tension of 2 to 4 mm. In some experimental work theprimary elevation of intra-ocular tension was followed by a secondarydrop. 

3. _Indirect reduction of increased intra-ocular tension brought aboutby lowering general vascular pressure. _ Much has been written in regardto the association between increased vascular pressure and increasedintra-ocular pressure. It is not my province to analyze observationsoften contradictory and not infrequently inaccurate. This much seems tobe established: First, that at corresponding ages there is usually ahigher average blood pressure in glaucomatous subjects than there is innon-glaucomatous subjects; second, that arteriosclerosis and thereforeusually increased blood pressure, with all its concomitant conditions, is correctly classified as an exciting cause of glaucoma; and third, that the regulation of this increased blood pressure is part of theadvantageous management of increased intra-ocular pressure, although itmay be too much to say, as Gilbert has, that blood pressure andintra-ocular pressure rise and fall together. It may be true, as ThomasHenderson says, that the intra-ocular pressure is influenced by changesin the general arterial or general venous pressures, whereby a rise ingeneral arterial pressure induces a proportionate rise in theintra-ocular pressure, but it would seem that future investigations mustconfirm this statement before it can be entirely accepted, as well ashis further statement that the effect of an increased general venouspressure is a direct one, producing millimeter for millimeter acorresponding increase in the intra-ocular pressure. 

Now, it goes without saying, if these data are correct, or even onlypartly correct, that part of the treatment of the increased intra-ocularpressure state must be constitutional in that the vascular pressuresshould be lowered in order that the beneficial effect of theirrelationship to the intra-ocular pressure shall be established. It isfurther a great mistake to drive down a high arterial pressure simplybecause that exists. In other words, it is often necessary from thegeneral standpoint that a certain amount of plus pressure shall remainif the patient's general well-being is to be maintained. There mustalways be a differential diagnosis between plus pressure and what may becalled over plus pressure. That is to say, a man may be perfectlycomfortable and properly need, for example, a pressure of 160 or 165mm. , which is above the physiologic limit, but which is a plus pressure, while some disturbance in his general life may add to that 10, 15 or 20mm. More of pressure, which is then the over plus amount. This overplus amount may be in association with a rise of intra-ocular pressure, and must be eliminated if the latter is to be controlled by anon-operative procedure, or, indeed, by an operative one. 

It is no easy matter to determine the presence of increased venouspressure, although there are tolerably accurate instrumental technics, and yet, as Henderson points out, it is just this increased generalvenous pressure which is often detrimental. Therefore the perfunctoryuse of such drugs as nitrite of amyl and the other nitrites may not bein the least indicated when, for example, the venous pressure dependsupon inability of the right heart to perform its functions, and the drugneeded may, for example, be digitalis. Far better than pressure-reducingdrugs like nitrite of amyl, urgently indicated in some instances and forsome purposes, is the regulation of life and the restoration to theirnormality of the metabolic processes, the elimination of the worrywhich is usually the exciting agent that brings about the over pluspressure, which may have as one of its expressions an acute rise ofintra-ocular tension. I believe that in the management of a case ofglaucoma, whether it be chronic or chronic with sub-acute exacerbations, the greatest care with the aid of an expert clinician must be exercisedto find out exactly what mean pressure of the arterial and venous systembest conforms with the patient's general welfare, and I am bitterlyopposed, and I think with right, to the sudden reduction of tensions, except in emergencies, without a perfect understanding of the facts Ihave ventured to indicate. This does not for a moment mean that prior, for example, to operative work it is not necessary to get rid by meansof drugs of an over plus tension, for surely the elimination of such anover plus tension may be the means of preventing, for example, anintra-ocular hemorrhage, and in this emergency we must not lose sightof Gilbert's recent investigation, who has found that blood withdrawn tothe extent of 8 grams to each kilogram of the body weight alwaysproduces lowering of the intra-ocular tension, appearing in six to eighthours and lasting to the next day in simple glaucoma, and ininflammatory glaucoma commencing the day after the venesection andlasting two to three days. It is not necessary for me to point out thevalue of free purgation and diaphoresis in this respect. 

In most instances the successful maintenance of a glaucomatous life, exclusive of operative interference, in addition to sustained myosis, demands the investigation of the patient's metabolism, which must bekept at the normal standard, the removal of the evil effects ofauto-infection, as we are wont to call it, and especially theelimination of the cause which is responsible for the over plus tensionof the arteries and of the veins. This is best secured by just suchregulation of life as has been referred to, aided when necessary by theordinary drugs which the patient's condition indicate, and the successof all treatments, be they operative or non-operative, is enhanced ifsuch a happy state of affairs can be brought about. 

I am firmly convinced that every glaucomatous patient, and I now referto those who are the subjects of chronic progressive glaucoma, should becarefully studied from the general standpoint by the oculist with theaid of an expert internist, just as I am convinced that the modernexpert internist should not study his cases of cardio-vascular diseasewithout the help of the oculist. Perhaps I am going a little far afield, but in justification of my statement I want to quote the opinion of Dr. Hobart Hare, one of America's most expert clinicians, on blood pressure, because it seems to me much harm has been done by the more or lessbrutal knocking down of blood pressure simply because blood pressureabove the normal existed. "Concerning the matter of high bloodpressure, " writes Hare, "independent of cerebral lesions, the longer Istudy the matter the more convinced I am that this blood pressure isdevised by nature to compensate for fibroid changes in peripheralvessels, in order that tissues which would otherwise be cut off fromadequate blood supply may receive plenty of blood, and I consider it oneof the most vital points to ascertain whether a pressure is what may becalled the patient's pathological norm, that is, the pressure which isrequired in the face of vascular changes, or whether this pressure is inexcess of his pathological norm. If it is in excess, measures directedto bring it to the pathological norm should be instituted, but if thepressure found proves to be the pathological norm it is a bitter mistaketo lower it, be the pressure what it may. If it is lowered below thepathological norm, all manner of disturbed cardiac action, etc. , mayresult. There is no more reason for reducing a blood pressure below hispathological norm than there is for reducing it below his physiologicalnorm. The adjustment of a man's blood pressure to his pathological normoften has to be as correctly done as the adjustment of a watch which islosing or gaining time. "

I shall not quote Hare's elaborate methods for determining these variouspoints because they do not belong to a paper of this character, but Iquote his admirable advice because it emphasizes what I believe to be anessential in the treatment of chronic glaucoma, exclusive of operativework, that is, the intelligent co-operation of the oculist and theinternist. 

Some such thought was in the mind of Ibershoff, who quotes Sterling andHenderson's views that the rate of secretion depends upon and varieswith the difference in the blood pressure and the tension of theeyeball, and that the specific gravity of the secretion increasesdirectly with the blood pressure and inversely with the ocular tension. Should the blood pressure be very high, paracentesis, for example, wouldapparently not be the proper procedure, and the resulting differenceproduced between the blood pressure and the eye tension would cause arapid reformation of fluid with higher specific gravity and higherosmotic coefficient. The proper procedure in these circumstances isfirst properly to reduce the blood pressure, or what I have, quotingHare, ventured to call the over plus pressure. 

4. _The relation of osmosis, lymphagogue activity, absorption of edema, capillary contractility and decreased affinity of ocular colloids forwater to the reduction of increased intra-ocular tension. _ We are allfamiliar with the attention which was directed some years ago to thestatements coming from French clinics that the treatment of glaucomashould include the administration of osmotic substances as adjuvants inthe reduction of increased intra-ocular tension. Particularly was thistreatment advocated by Cantonnet in the administration of daily doses of3 grams of chlorid of sodium, preceded, of course, by a careful urinaryexamination and the estimation of the amount of urine and its containedchlorids. Carefully this dose was increased in proper circumstances to15 grams per diem, and in Cantonnet's original paper good results wereachieved in 12 of the 17 patients so treated. I have myself experimentedsomewhat, not with the administration of sodium chlorid by the mouth, but with the introduction by the bowel of fairly large quantities ofphysiologic salt solution in patients with glaucoma whose quantity ofurinary secretion was markedly below the normal, and in one or twostartling instances, which have been reported, achieved success in therapid reduction of the intra-ocular tension when by this technic theurine secretion rose to the normal amount. To be sure, myotics werealso used, but these myotics were insufficient, totally so in the twoinstances noted prior to the enteroclysis. 

Very interesting are the observations on the subconjunctival injectionsof various substances, notably the citrate of sodium, because of itspower of decreasing the affinity of ocular colloids for water. Thismethod of treating increased intra-ocular tension, introduced, as youknow, by Thomas and Fischer, has met with confirmation from a number ofsources in spite of the fact that Happe's experimental study failed toconfirm Fischer's observations; indeed, he even reports in severalinstances a rise of tension. 

As you will remember, the strength of ordinary crystallized sodiumcitrate in water should be from 4. 05 to 5. 41 per cent. Of this five tofifteen minims are injected, the eye having been previously cocainizedand adrenalinized. With frequent injections the weaker of the twosolutions is mixed with 2 to 4 parts of physiologic salt solution. Theseauthors in no sense claim to cure glaucoma, but to ameloriate it andreduce the tension. Weekers has used the salts of calcium, 3 grams aday, with success in so far as lowering of tension is concerned, although it must be stated, as a reviewer of his work has said, that hisrecommendation of this drug in these respects is poorly supported. Onthe other hand, Tristiano seems to have proved that calcium chlorid iscapable of lowering ocular tension and clinically may be used as anadjuvant in the treatment of glaucoma for this purpose, largely becausehe believes that he has proven that it facilitates the absorption ofedema. Darier has reported that a single subconjunctival injection of amilligram of iodate of sodium has cleared the cornea and lessened theintra-ocular pain in glaucoma. 

What shall be said in regard to certain medicinal agents which stimulatethe lymphagogue activity of the eyeball in their relation to thereduction of intra-ocular tension, notably of dionin? Toczyski'sexperiments with this drug on the normal eye indicate that it producesfirst a rise of tension, which shortly falls to the normal and sometimesbelow it, the tension being high as long as the primary narrowing of thepupil is maintained, but more than one author, particularly A. Senn, holds an opposite view and reports acute glaucoma following itsinstillation into a chronic glaucomatous eye. He believes that dioninnot only does not reduce the tension but hinders the filtration throughthe anterior lymph channels by the pressure of the edema which isproduced on the veins and by the increased secretion of the ciliaryprocesses. In spite of this statement, most of us must agree with KarlGrossman's observations that certainly in acute and particularly inchronic secondary glaucoma, this is a most valuable agent, especially ifit is combined with holocain, which Paul Knapp in his well-knownresearch has proved can reduce the tension even of the normal eye. Icannot think that anybody who has systematically used dionin withholocain, the former in gradually increasing strength, beginning with 2per cent and going up to 8 per cent, in various types of acute glaucoma, particularly of the secondary variety, can fail to have noted afavorable influence. 

Many authors, for example, Darier, Grandclement and others, are strongin their recommendation of adrenalin, particularly if this drug is addedto the various myotic mixtures, and yet adrenalin is certainly notwithout danger in the treatment of glaucoma. McCallan has seen a numberof instances of striking increase of intra-ocular tension following thisinstillation in the conjunctival sac. Harmon has had a similarexperience, as also has Senn. It is possible that in these circumstancesthe solution was too strong. Should the rise of tension occur, and Ihave seen it myself, it is doubtless due to the fact that this drugdilates the pupil, which would be especially dangerous if the dilatationshould occur before contraction of the ciliary vessels; also thenarrowing of the ciliary veins by the adrenalin might by virtue of thisnarrowing obstruct the gate of outflow. I have never been able topersuade myself that, except as an adjuvant to operative work, there wasany real therapeutic value in the instillation of adrenalin. 

A word in regard to the effect of general narcosis on intra-oculartension. Thus, Neuschuler has observed that narcosis causes an elevationof the intra-ocular tension of from 2 to 6 degrees as measured withFick's tonometer. These observations were made while he wasexperimenting on irritation of the sympathetic as a method of producingincreased intra-ocular tension. This is not in accord with Axenfeld'srecent observations. It is well known, this observer points out, thatafter the period of excitation and muscular rigidity disappears, thereis a lowering of blood pressure in chloroform narcosis and coincidentlya sinking of the intra-ocular pressure. Not only this, the intra-oculartension of normal eyes during this narcosis drops several millimeters. Only such eyes as have high hypertony, for example, in absoluteglaucoma, are unaffected during chloroform narcosis. In the light ofthis observation it will be interesting to measure the tension both ofnormal and glaucomatous eyes during narcosis in a large series of cases, and if it is confirmed there will be an additional reason why in manycircumstances general narcosis is advantageous in glaucomatous patients. Formerly I thought it was essential, if iridectomy was to be performed, lest some sudden movement on the part of the patient might bring thepoint of the knife in contact with the lens. I have rarely employed itin corneo-scleral trephining, and yet if there is this temporaryreduction of intra-ocular pressure, it is not without a certaintherapeutic value, and the matter is mentioned as a suggestion thatadditional observations along this line shall be made. 

Dr. George Edmund de Schweinitz' Paper on Concerning Non-SurgicalMeasures for the Reduction of Increased Intra-ocular Tension

Discussion, NELSON MILES BLACK, M. D. , Milwaukee. 

It seems almost useless to attempt any discussion of Dr. De Schweinitz'most terse and comprehensive paper. However, Dr. De Schweinitz mentionedthe close relationship which should exist in the non-surgical treatmentof increased intra-ocular tension between the internist and theophthalmologist, but neglected to mention a corresponding relation whichshould exist between the rhinologist and the ophthalmologist, andpossibly between the dental surgeon and the ophthalmologist. 

I would like to refer to the _now_ recognized close relationship whichexists between disease of the nasal accessory sinuses and diseases ofthe eye. The definition of glaucoma found in Dr. Wood's system oftherapeutics gives rise to an hypothesis as to why disease of the nasalaccessory sinuses may be a factor in producing increased intra-oculartension and why treatment directed toward obtaining free drainage fromthe sinuses gives good results in so many cases, especially if therelationship is recognized sufficiently early. "Glaucoma proper isessentially a damming or blocking of the drainage from the interior ofthe eye. The chief lymph stream flows from the posterior chamber pastthe margin of the lens, through the zonula of Zinn, beneath the iris, through the pupil into the anterior chamber, thence through the tissueat the junction of the iris and sclera into the circular canal ofSchlemm and from this space into _the external lymph channels_. _Obstruction to the steady escape of the intra-ocular fluids at anypoint in this drainage system or any undue increase of the fluidsthemselves may produce glaucoma. _ Probably the most importantobstruction to the exosmosis is at the angle close to Schlemm's canal. "

The following hypothesis is based upon Fischer's edema theory ofglaucoma and the relation of the circulation of the eye and orbit andthat of the nose and the accessory sinuses, the minute anatomy of whichis not as yet thoroughly understood. However, sufficient work has beendone to make it appear that the lymph channels which drain the eyes andorbits empty into the same main channel as do those which drain thesinuses. Admitted for sake of argument that such is the case, thendisease either acute or chronic of one or more of the sinuses with theaccompanying inflammatory reaction, congestion and stasis, will cause anincreased amount of fluid to be taken care of by the lymph channelsdraining these sinuses. This will in turn cause flooding of the commonlymph channel, producing a stagnation in the flow of fluid from theorbits and eyes at the junction with the main channel, with backing upof the fluid within these channels and retention of the waste productswithin the orbits and eyes; thus will be brought about conditions mostfavorable (to quote from Fischer's theory of glaucoma) "to an abnormalproduction or accumulation of acid in the eye. In consequence of thisabnormal acid content the hydration capacity of the ocular colloids israised and glaucoma results, not because water is pushed into the ocularcolloids, but because these suffer changes which make them suck in waterfrom any available source. "

This hypothesis also might suggest why the subconjunctival injection ofsodium citrate in addition to alkalinizing the ocular contents, may beeffective in reducing tension, _i. E. _, the amount of fluid injectedbeneath conjunctiva may overcome the stagnation in the lymph passages, flush out these channels and improve ocular elimination. 

Fischer in a personal letter says:

"You have two possibilities for the production of glaucoma with sinusdisease: A toxic factor due to poisons being carried into the eye; andsecond, interference with a proper blood supply to the eye throughcompression of the efferent or afferent blood vessels supplying the eyefrom edema of the tissues about the eye consequent upon the sinusinfection. Either is associated with the production of substances whichincrease the hydration capacity of the ocular colloids. "

If such is the case why could not the existence of pyorrhea and blindabscesses about the roots of the teeth be the source of the toxicfactors mentioned by Fischer? Hence the suggested association of thedental surgeon with the ophthalmologist in these cases of apparentlyidiopathic increased intra-ocular tension. 

It would be well to state here a cursory examination of the mouth willnot discover root abscesses any more than such examination willdiscover non-suppurative sinus disease. A careful examination of eachtooth together with radiograms of the entire maxilla are absolutelyessential to determine their presence or absence. 

Trephining for Glaucoma

BY

ROBERT HENRY ELLIOT, M. D. , London, England. 

Mr. President and Members of The Chicago Ophthalmological Society:

As the hour is late I propose to take up only the principal points inconnection with my subject and to deal with each one shortly. 

First: The operation of trephining is suitable, not merely for chroniccases, but for sub-acute and acute cases of glaucoma as well. I wouldurge on your attention that, of all the operations dealing withglaucoma, this one involves the minimum of surgical violence, andshould, therefore, in acute cases be the operation of choice. It is, moreover, much safer than any other operation I know of, and is no lesscertain in its results. I do not advise trephining in the secondaryglaucoma following intumescent cataract, for in such cases thesemi-fluid lens bulges into and blocks the trephine hole. Nor forobvious reasons do I recommend it in cases where there is reason tobelieve that a communication exists between the aqueous and vitreouschambers. 

Second: The object of trephining is to tap and permanently drain theaqueous fluid from the anterior chamber of the eye into thesub-conjunctival space; in doing so it is essential to avoid as far aspossible all interference with the uveal tissue. The purpose of aniridectomy is to avoid the danger of the iris in the neighborhood of thewound being drawn and impacted in the trephined hole. We have found in alarge number of cases in which an iridectomy has been omitted, that theresults have been in no way inferior to those in which a piece of irishas been removed, provided always that no subsequent iris prolapsetakes place. In pursuance of our purpose to avoid uveal tissue, we splitthe cornea, and place the trephine as far forward as such splitting willallow, and we bear on the trephine in such a way that it cuts through onthe corneal edge of the wound first. This insures establishing ourfistula in the most anterior position possible, and, therefore, as faraway as possible from the ciliary body and the angle of the chamber. 

Third: The difficulties of the operation. Far too much stress has beenlaid on these. Trephining is an operation which can be performed by anysurgeon who is used to ophthalmic manipulations, and who has good sight. It is essential that he should work in a good light. The necessarytechnique can be acquired from a written description. It is not for amoment necessary that the surgeon who wishes to learn trephining shouldsee the originator of the operation at work. If, however, he feelsdiffident at undertaking the procedure until he has seen it done byanother, there are many centers in this country where the operation isnow being successfully performed. I would mention amongst those which Ihave visited New York, Minneapolis, St. Louis, Nashville, Louisville, Detroit and Chicago. I have seen results of trephining by Americansurgeons which could not be bettered anywhere. 

Fourth: I am sure that everybody will recognize the difficulties ofoperating during such a tour as I am now making. I have so far in thelast month performed over seventy trephinings in ten cities, and intwice as many clinics. To adapt one's self to different clinicalmethods, different assistants and different nurses is so difficult that, as you are aware, many distinguished surgeons refuse to work out oftheir own clinics. One cannot expect the results of such a tour to be ona par with those one obtains in one's own quiet daily surroundings. Iam, however, confident that you will make a generous allowance forthese difficulties, and I gladly welcome the suggestion that all thecases which I have operated on in America be collected together andreviewed as a whole. 

Fifth: In conclusion I would like to express the pleasure with which Ilistened to Dr. De Schweinitz' paper. I believed from the title thatthere might be a wide divergence of opinion between us. I find to mygreat relief that we are in absolute accord. I know, however, that thereare in America and elsewhere able men who consider that the medicaltreatment of glaucoma should be pushed as long as possible. I cannot butfeel that this is a survival of the dread that most surgeons have feltin recommending one of the older operations for glaucoma. We have now inour hands a method so safe, so easy and so certain that I feel sure thatthis dread will ere long pass away, and that the diagnosis of glaucomawill then be followed by a very early operation. In India I have gonefarther than this, and where one eye has shown high tension, I havefrequently trephined both. The prophylactic use of the operation is morethan justified in that land of long distances and scattered medical aid, and where the patient is not likely to return a second time for surgicalhelp. This prophylactic trephining is a proposition that I put beforeyou today for your consideration, reminding you at the same time thatglaucoma is practically invariably a bi-lateral condition. I have seeneven in America not a few people blind in both eyes who might haveretained the sight of the second eye had the surgeon advised a doublesclerectomy when he first saw the case, despite the fact that the secondeye was then to all appearances non-glaucomatous. 

Dr. Robert Henry Elliot's Paper on Trephining for Glaucoma

Discussion, FRANK C. TODD, M. D. , Minneapolis. 

It is very difficult for one of limited experience to discuss a subjectpresented so ably by Lieutenant Colonel Elliot to whom we are indebtedfor the sclero-corneal trephine operation. He has already over a periodof a little over four years performed over 900 trephinings, and has madea most careful subsequent study of the results of those operations on asmany cases as he had the opportunity to observe. 

Anyone who has read Colonel Elliot's book on the sclera-cornealtrephining operation will be struck with the fact that he has not onlyhad a tremendous experience in ophthalmic surgery, but that he has madethe best of that unusual opportunity, and that to a foundation of acareful training he has added the experience of twenty-two years of hardpainstaking work. 

I have recently had the privilege of entertaining Colonel Elliot in myown city, where I had the opportunity of assisting him and hence closelyobserving his technique in eighteen trephinings. It has since been myduty, and responsibility I may add, to care for those eighteen eyes. Fortwo years I have been doing the Herbert tongue flap, or a similaroperation. The results have been highly satisfactory thus far andsimilar to those following the trephining operation, which operation Ihave performed in a number of cases during the past ten months. Myconclusions as to these two operations are favorable to the trephiningoperation because the Herbert tongue flap operation is much moredifficult, and hence less certain than the Elliot trephining operation. 

The time for discussion does not permit a detailed statement of theresults nor experiences in the handling of these trephining cases. Ofthe entire number five totally blind eyes were trephined. Tension wasreduced in all but one. In that one hemorrhage occurred at the time ofthe operation. One of these blind eyes had not been totally blind longerthan a few weeks. Hand movement vision developed in this eye. Anothereye totally blind one year has thus far developed perception of light. Of the cases with varying degrees of vision from hand movements tosix-ninths all but one have either remained the same or shown someimprovement. The one exception was an eye having six-ninths vision. Asmall button hole iridectomy was made; prolapse of the iris into thewound occurred four days later requiring incision. Upon incision of theprolapse intra-ocular hemorrhage occurred, causing nearly totalblindness for two weeks. Vision is clearing fast and it remains yet tobe seen what the final results may be. One buphthalmic eye trephined bymyself gave good results. 

I have as yet seen no cases of remote infection, but the report ofAxenfeld and some others would indicate that this occurred following theLagrange as well as the trephining operation, the then bulgingconjunctiva having become eroded and infection having taken placethrough the eroded conjunctiva as shown when stained with flourescin. 

The opinion, not yet conclusive, that I have thus far formed as aconsequence of my experience and the information obtained from others ofgreater experience is as follows:

First: That in those cases of chronic glaucoma in which iridectomy hasbeen of benefit in preventing or retarding the oncoming of blindness, the result has apparently been secured by reason of the fact thatfiltration has been produced, and not merely because a piece of iris hasbeen removed. 

Second: That in chronic glaucoma (in acute glaucoma iridectomy hasproven a satisfactory operation) when the progress of the diseasecannot be arrested by non-surgical treatment (an even in some of these, where, for instance the patient cannot be kept under observation or willnot carry out the treatment) some form of operation intended to producefiltration should be performed. 

Third: The Elliot sclero-corneal trephining operation carefullyperformed in accordance with the author's technique in the light of ourpresent knowledge seems to be the best and safest operation to producethat result. 

Fourth: That to glaucoma may be added buphthalmos and staphyloma, asdiseases often capable of relief by trephining and indeed toward therelief of which trephining is the best form of operation yet presented. 

Fifth: That the results secured when the operation is well done and theafter care is properly followed out are satisfactory, in that theoperation in a large proportion of cases apparently permanently lowersthe tension to normal or below normal, relieves pain, prevents theoncoming blindness (otherwise inevitable) and in many cases causes animprovement in the acuity of vision, in the visual field. And inoccasional cases of blindness of not too long duration, it restores somevision, occasionally to a marked degree. 

Sixth: That it is not a simple nor easy operation and should, therefore, be performed only by an operator well trained in ophthalmic surgery. Thecareful and skillful technique of the originator of the operationperhaps accounts for his greater success in its results and those whoperform the operation should follow his technique and be capable ofhandling complications that may later arise. 

In conclusion, Mr. President, I wish to say that we ophthalmologists theworld over are indebted to Lieutenant Colonel Elliot not alone for hiscontributions to our knowledge, but for his persistence againstprecedent and criticism in establishing the facts upon which rest thefoundation for the success of his operation, and for so emphasizing thegreat importance of this epoch-making achievement. 

It is because we respect his wisdom gained by incessant study andexperience in a country where climatic conditions are such that a man ofordinary energy would have failed to do even average work that we soreadily welcome the teaching of this enthusiastic evangelist. 

His pilgrimage to our country will be the means of starting many in thisnew field, and we shall soon be able to draw more definite and finalconclusions from our own experiences. 

Operations Other than Scleral Trephining for the Relief of Glaucoma

BY

CASEY A. WOOD, M. D. , Chicago. 

In this paper I shall say a few words about the large number ofoperative procedures that, apart from trephining, or, preferably, _trepanation_, have been urged in the treatment of the various forms ofglaucoma. Their name is legion and among them we find peripheraliridectomy; anterior sclerotomy; irido-sclerotomy; scleriritomy; deWecker's dialysis of the iris; Hancock's division of the ciliary muscle;the incision of the iridian angle of de Vincentiis; sclero-cyclo-iridicpuncture; the Sterns-Semmereole _sclerotomia antero-posterior_; the_transfixio iridis_ of Fuchs; Antonelli's peripheral iritomy; Holth'sformation of a cystoid cicatrix; Hern's operation; Terson'ssclero-iridectomy; Abadie's ciliarotomy; Ballantyne's incarceration ofiris method; Masselon's small equatorial sclerotomy; Simi's equatorialsclerotomy; Galezowski's sclero-choriotomy; excision of the cervicalganglion; removal of the ciliary ganglion; Querenghi's operation ofsclero-choriotomy; Bettremieux's simple anterior sclerectomy; Heine'scyclodialysis; Herbert's wedge-isolation operation; Verhoeff's operationwith a special sclerotome; Holth's sclerectomy with a punch-forceps;Walker's hyposcleral cyclotomy; posterior sclerotomy; T-shapedsclerotomy; and last but not least the Lagrange form of sclerectomy withits various modifications by Brooksbank James, myself and others. 

In addition to the foregoing list--which is by no means complete--thereare several combinations of operations, as, for example, the Fergustrephining operation, which is really a combination of a sclero-cornealtrepanation and a cyclodialysis. 

So far as it is practicable there is a certain amount of wisdom incomparing the results of an operative procedure with others with whichit is brought in competition, and I believe we are even now in aposition to form at least some idea of the comparative value of thethree methods that comprise the great majority of interventions made useof by ophthalmic surgeons at the present time. I refer to _iridectomy_, the _Lagrange operation_, and the _Elliot operation_. So far as regardsthe last named procedure, I congratulate this Society that it has had anopportunity of seeing a demonstration and hearing a discussion by thefamous ophthalmic surgeon who perfected it. 

As regards the others let me recommend to you the complete descriptionof them given by Posey in _A System of Ophthalmic Operations_. 

Let us consider the first of the three procedures justmentioned--_iridectomy_--introduced by von Graefe. The mechanism of itsmode of cure is best studied in cases of acute primary glaucoma, whenthere is apposition of the periphery of the iris to the cornea. In theseacute cases there is probably only a mere _apposition_, and the blockingup of the sclero-iridian angle is largely mechanical. Here the root ofthe iris is readily removed in its entirety and a really peripheraliridectomy is easily done. When, however, a true _adhesion_ betweencorneal and iridic tissue takes place the filtration angle is not soeasily opened. True peripheral adhesions are not readily broken up orseparated, and the iridectomy is, for that reason at least, noteffective. Moreover, this form of anterior synechia (resulting from atrue union of iris and cornea) is so intimate that the iris root is, bythe iridectomy, torn away only at the sclero-iridian angle at theanterior border of the adhesion--and does not open up a channel intoSchlemm's canal. It is not, therefore, difficult to understand whyiridectomy alone in any of the forms of chronic glaucoma fails to openup the true filtration spaces and does not provide a drain that permitsof an escape of fluid from the posterior chamber through the loosetissue that surrounds it into the canal of Schlemm. Treacher Collinsfound, after a careful examination of eyes upon which iridectomy hadbeen performed for glaucoma, that it is extremely rare for the initialsection to pass through the pectinate ligament, while Schlemm's canalinvariably escapes. Moreover, since the sclero-corneal incision isuniformly oblique, the position and extent of the external wound doesnot always furnish evidence of the character of the internal wound. Inall likelihood many cases of relief or cure following iridectomy arethose due to the formation of cystoid scars or minute fistulae, ratherthan as a result of the removal of a portion of the iris periphery. 

The best brief tabulation of the results obtained by iridectomy, inglaucoma, is to be found in Weeks' textbook on _Diseases of the Eye_, page 417: "Sulzer reports as follows: Acute glaucoma, 149 cases;improved, 72. 5 per cent; serviceable vision preserved, 11. 3 per cent;vision impaired at once, 4. 08 per cent; very little vision, 12. 12 percent. 

"Zentmeyer and Posey: In simple glaucoma central vision increased in 60per cent; remained the same in 20 per cent; diminished in 20 per cent. 

"Wygodski: Inflammatory glaucoma, 37 cases; improvement, 76 per cent;unimproved, 5 per cent; deterioration, 19 per cent. Sub-acute (chronicinflammatory), 147 cases; improvement 10 per cent; unimproved (conditionthe same as before iridectomy), 40 per cent; deterioration, 30 per cent;blindness, 20 per cent. Cases operated on at an early stage gave 85 percent of good results. Simple glaucoma, 104 cases; improvement, O. 96 percent; condition as before, 10. 5 per cent; deterioration, 52 per cent;amaurosis, 36. 5 per cent. 

"Hahnloser and Sidler: One hundred seventy-two eyes observed not lessthan ten years after operation; acute inflammatory, 31 eyes; goodresults, 64 per cent; relatively good, 13 per cent; blind 23 per cent;chronic inflammatory, 37 eyes; good result, 29. 9 per cent; relativelygood, 27 per cent; blind, 43 per cent; simple glaucoma, 76 eyes; goodresults, 42 per cent; relatively good, 28. 9 per cent; blind, 28. 9 percent. "

As far as the _Lagrange procedure_ is concerned, you will remember thatafter eserinization an oblique incision is made through the sclera bymeans of a narrow Graefe knife and a large conjunctival flap secured. This is obtained by making a peripheral section of the sclero-cornealmargin with the knife and, as soon as the edge of the knife reaches theupper limit of the anterior chamber, it is turned backward and broughtout through the sclera obliquely. The conjunctival flap thus formed isturned back over the cornea, and the fragment of sclera that is leftattached to the cornea is removed by means of a fine pair of delicatecurved scissors. Following this an iridectomy is performed. Theconjunctival flap is now replaced and a bandage applied. 

This operation opens a large filtration passage for the intra-ocularfluids and the prompt healing of the wound with its mucous coveringprevents prolapse of the iris. 

Under no circumstances must iris be left between the lips of the wound. 

Although Lagrange advocated iridectomy in all cases in his firstcommunication, he no longer judges the procedure to be necessary in allinstances, reserving it for cases in which for any reason, such ashypertension, prolapse is to be feared. 

While Lagrange holds that it is necessary to open the anterior chamber, Bettremieux thinks that a removal of but a portion of the thickness ofthe sclera suffices. His procedure is as follows: After raising a flapof conjunctiva from the neighborhood of the limbus a medium sizedneedle, curved and flattened towards its point and firmly grasped in aneedle holder, is thrust superficially into the sclera tangentially tothe upper edge of the cornea, so as to become fixed in the capsule ofthe eyeball. A small shaving of the sclera, about ½ mm. Thick, 1½ to 2mm. Broad and from 2 to 3 mm. Long, is then excised by means of a narrowGraefe knife. The scleral slip is then freed from the conjunctiva ateach end and the mucous membrane brought together over the wound by finecatgut sutures. 

As you are well aware, numerous operators regard the Lagrange operationas superior to the iridectomy of von Graefe because they believe thereis filtration through the newly formed tissue between the lips of theoperative wound. Among those of many observers the conclusions ofBallantyne may be quoted: "The results of sclerectomy vary according tothe degree of hypertension of the eye operated on. Three varieties ofcicatrix are distinguishable according to the amount of sclera excised:(1) that in which there is mere thinning of the sclera owing to theexcised portion not reaching the posterior surface of the cornea(conjunctiva smoothly covers the cicatrix); (2) that represented by asubconjunctival fistulette, due to excision of the whole thickness ofthe sclera, in an eye with moderate tension (the conjunctiva liessmoothly over the cicatrix); (3) the fistulous cicatrix with anampulliform elevation of the overlying conjunctiva, resulting fromexcision of the whole thickness of the sclera in an eye the seat of hightension. In cases of high tension, even a simple sclerectomy will allowample filtration, owing to the gaping of the wound, while in caseswithout elevation of the tension, sclerectomy will be quite ineffectual. Lagrange therefore proposes the following rules of procedure: (a) Iftensions is normal to +1, do sclerectomy without iridectomy, the amountof sclera excised being inversely proportionate to the degree ofhypertension. (b) If tension is +1 to +3, do sclerotomy-iridectomy, theiridectomy being added to avoid entanglement of the iris. Lagrange doesnot recommend his operation for acute glaucoma. It is especially adaptedfor cases of chronic simple glaucoma. "

During the past ten years or more I have been doing a modification ofthe Lagrange operation, the details of which (The Operative Treatment ofGlaucoma with Special Reference to the Lagrange Method, _The CanadianMedical Association Journal_, November, 1911) I have elsewherepublished. 

As stated in this paper I have modified the procedure to the extent ofremoving _all_ the conjunctiva attached to the borders of the operativewound. I admit that this intervention exposes the root of the iris andthe ciliary body, but I have never yet had the slightest infection ofthe wound. I attribute this freedom from sepsis to careful cleansing ofthe conjunctival sac and to other pre-operative precautions, butespecially to the use, before and after the operation, of White'sointment--a preparation of 1-3000 mercuric chloride in sterile vaseline. One cannot use sublimate in such a strong _watery_ solution, but thevaseline seems to modify it and to allow of such slow absorption that itis not only a non-irritant but a most excellent antiseptic applicationin operations on the eye. 

In any event the result of the Lagrange operation proper, as well as mymodification of it, is to produce a drainage-oedema about the incisionalwound which persists almost indefinitely. In many cases this swellingamounts to a bleb which may be increased by massage of or pressure uponthe eyeball. The efficacy of the operation in lowering intra-oculartension is to some extent measured by the degree and the constancy ofthis epibulbar oedema; indeed, I suspect that the most successfulexamples are those in which sclera fistulae, minute or otherwise, formas a sequel of the operation. 

My object in excising the conjunctiva about the sclero-corneal flap, isto delay union of the wound edges, to widen the bridge of loosecicatricial tissue between them, to prevent such a complete growth ofthe endothelium as would cover the wound and block the exit of fluids, and to insure intra-ocular rest. 

In cases of _chronic_ increase of intra-ocular tension associated with aquiet uveitis or an iridokeratitis, when the patient exhibits traces ofold synechiae, or where there is danger of their re-formation, I do nothesitate to use atropia as long as the wound of operation has nothealed. 

To the present time I have done 72 operations of the sort and have seenno reason to alter the opinion of it expressed in the article mentioned. Whatever objection may in the future arise--and I freely confess thatit _seems_ to be fraught with the dangers that many of my colleagueshave pointed out as probable--I have so far not seen a single case ofinfection of the wound of operation. While I believe theanti-glaucomatous results to be excellent, I may also claim that theoperation is of the simplest character; and it is easy of performanceand the resulting filtration-scar is large and (perhaps) more permeableto the changed intra-ocular fluids than the quicker healing wounds ofthe usual Lagrange and Elliot procedures. 

It is regarded by most operators as desirable that there should not belong delayed healing of the operative wound, and the fact that theconjunctiva covers the incision is often spoken of as an advantage, partly because it shields the large open area produced by the Lagrangeincision from infection. 

My experience of this modified operation continues to be that it isnecessary to clear the neighborhood of the operation wound entirely ofconjunctiva. If the down-growth of epithelium into the operative woundis permitted the effects are by no means as pronounced, and the eventuallowering of tension is not as permanent as they otherwise would be. 

Another matter: I am satisfied that the delayed filling of the wound byconnective tissue is desirable in most cases of _chronic_ glaucoma. Acomplete drainage of the intra-ocular fluids that results from longdelayed union of the wound edges, allows the interior of the eye toregain, as far as possible, the _status quo ante_. On the other hand thecomparatively early closure of the wound (or the termination of _free_drainage and minus tension) tends to re-establish the _statusglaucamatosus_. Whether these desirable results are to be realized ornot will, of course, depend upon a future experience larger than I haveyet had. This modification of the Lagrange operation seems to be aradical one and I do not expect its adoption until the results of anextended trial are carefully recorded and reported. 

Quite recently several operators, who have been in a position to do so, have contrasted the results obtained by the Elliot method and thosefollowing the Lagrange procedure. Probably the most important of theseobservations is the experience of Meller (Die Sklerektomie nach Lagrangeund die Trepanation nach Elliot) set forth in a paper read by him at thelast meeting of the _Deutsche Naturforscher und Aertze_. In this reportMeller gives an account of 389 sclerectomies following the usualLagrange procedure. Twelve per cent of the cases were of acute glaucoma;61. 5 per cent of chronic inflammatory glaucoma, and 9 per cent of simpleglaucoma. The rest of the operations were done in other forms of thedisease. In more than half the cases the usual iridectomy was performed;in 30 per cent the procedure was peripheral; in 4 per cent there was noiridectomy. The patients were studied during a period of five years. Inmore than half the instances there was a pale, cystic, oedematouscicatrix; in 11 per cent the scar was ectatic, and in the remainder thefield of operation was quite flat. The form of the scar was described inmost instances, but it was not noticed that there was a definiterelation between the cicatrical formation and the intra-ocular tension. In 70 per cent of the cases a good result followed the operation, but in10 per cent the result was decidedly unsatisfactory. Cloudiness of thelens set in in 4 per cent of the cases, while posterior synechiaedeveloped in the great majority of them. In 2. 3 per cent the eye wasattacked by iridocyclitis and in 3. 4 per cent enucleation was found tobe necessary. Six eyes became atrophic but were not, for variousreasons, removed. One and three-tenths per cent of the eyes operated onwere lost from late infection. Vitreous was lost in 6. 2 per cent. Twoeyes became blind from expulsive hemorrhage. The large majority ofthese complications arose in the eyes operated on for chronic glaucoma. There were fewer eyes lost following the operation for glaucoma simplexthan in the other forms of the disease. Recurrences were noticed in 11. 3per cent of all the cases; in simple glaucoma 14. 3 per cent as againstthe acute and chronic forms with 6 per cent. A return of the glaucomawas noticed in 7 per cent of the pale, oedematous, post-operative scars, in 16 per cent of the flat cicatrices, and in 24 per cent of the ectaticvariety. Considerable stress is laid upon the fact of the markedsoftness of the eyes after each operation. There were histologicalexaminations made of the eyeballs in 11 cases, in which the position ofthe incision and excision, the development of the scar tissue, and theappearance of the complications were duly set forth. The operator thengave a history of over 178 trepanations after the Elliot method andcompares them with the procedure of Lagrange. He concludes that theElliot trephining operation is less dangerous, is more likely to befollowed by the development of a cystic scar, and leads to loss of theeye in only 2. 4 per cent of the eyes operated on. In Elliot's cases thepercentage of relapse was more noticeable than in the Lagrange caseswhere no iridectomy was done. This observer concludes that the method ofElliot is to be preferred to that of Lagrange, and that in the formercase iridectomy is an important factor in obtaining a favorable result. This being the case one cannot truthfully say that trephining alone cantake the place of the old Graefe iridectomy. On the other hand, trephining may with advantage be employed instead of iridectomy forcases difficult or dangerous under the latter method. 

Whatever difference of opinion was noticeable at the Vienna meeting, allof those present, especially Meller, the reader of the paper justquoted, were decidedly of the opinion that the Elliot operation is inevery respect the one best adapted to buphthalmia, or congenitalglaucoma. 

In conclusion let me say that the acceptance or rejection of ColonelElliot's procedure or any other operation is not to be decided by thepercentage of iritis, secondary cataract, relapses, lost eyes, etc. , butby deciding whether or not his procedure in the various forms ofglaucoma gives the best results, including the preservation ofcomfortable eyes. In other words, we are seeking not the operation thatwill cure _every_ case of glaucoma but the one which is capable, _in thehands of the average ophthalmic surgeon_, of relieving or curing _most_cases of that affection. 

Dr. Casey A. Wood's Paper on Operations Other than Scleral Trephiningfor the Relief of Glaucoma

Discussion, ALBERT E. BULSON, JR. , M. D. , Fort Wayne. 

Increasing belief in Colonel Elliot's view that trephining should be theoperation of choice in any form of glaucoma, makes it difficult toconsider operations other than trephining in anything but a spirit ofdisfavor. 

Until recently the decision as to the kind of operative procedure to beemployed for the relief of glaucoma has depended on the form and stageof the disease, and the amount and character of the vision of theaffected eye. Many operators still hold that an iridectomy is the mostvaluable of all operations for acute inflammatory glaucoma, and not afew hold that the operation has a decided place in the treatment ofsimple glaucoma. The operation is not without difficulties, and one isinclined to agree with Elliot who says that "The man who can make a'finished iridectomy' quietly and cleanly has graduated as an ophthalmicoperator. " The difficulties of an iridectomy are especially pronouncedin those cases in which the anterior chamber is extremely shallow andthe iris is pressed against the cornea. It is in such cases that thesuccess of the operation is increased by the addition of posteriorsclerotomy and the intelligent use of miotics prior to the performanceof the iridectomy. Even then the permanent results of the iridectomywill be modified in proportion to the success secured in freeing thefiltration angle and opening Schlemm's canal by thorough removal of theroot of the iris. 

The failure of many apparently well executed iridectomies may beattributed to the fact that the iris is not removed to the extremeroot, and the remaining stump is sufficient to block the drainage. Thisis especially apt to be the case in chronic glaucoma where the iris isadherent to the cornea, and in efforts to free the filtration angle byan iridectomy the iris is torn off in front of the adhesion and thefiltration angle is not opened. 

As Elliot has pointed out, iridectomy is most open to attack on theground of safety. We have to take into account the large scleral woundmade, and the fact that this lies close to the ciliary body. The suddenrelease of all tension and the simultaneous weakening of the supports ofthe lens and vitreous body create very unfavorable conditions underwhich to make the crucial step of the operation. 

The poor results following an iridectomy in chronic glaucoma have led tothe devising of many substitute operations, of which those tending tothe production of a filtering scar are now preferred, and, experienceshows, hold out the most hope of bringing about long continued relief. It even is considered probable that the effects of an iridectomy whichbrings about more or less permanent reduction in the intra-ocularpressure is due to the formation of a filtering scar which augmentswhatever results may have been secured in the attempt to open up thedrainage into the canal of Schlemm. 

Dr. Wood has referred to several of the many substitutes for iridectomythat have been proposed, and it is unnecessary to enumerate them againor to attempt to point out their good or bad features. It is sufficientto say that for the average operator and the larger per cent of cases, the operation which is easiest to perform, is attended with the leastrisk and offers the best hope of permanent results should be the one ofchoice. Sympathectomy has failed to secure a place in ophthalmicsurgery, sclerotomy has not been found adequate, and cyclodialysis isnot sufficiently simple of execution or permanently beneficial in itsresults to give it prominence. 

Of the operations proposed for the formation of a filtering cicatrix, those of Elliot and Lagrange are justifiably the most popular. Those ofus who have had the pleasure of seeing the trephining operation done byCol. Elliot are impressed with the fact that the operation, even in thehands of its originator, is not, when properly done, uniformly easy ofperformance. It does, however, offer the advantage of carrying with itthe minimum amount of risk, and the apparently permanent results securedjustify the ophthalmologist in acquainting himself with the technique ofthe operation, for, as pointed out by Sydney Stephenson and others, "thetechnique is responsible for success or failure. " Furthermore, there isno sufficient reason why the field of usefulness of the operation shouldbe confined to the chronic forms of glaucoma, and Col. Elliotunhesitatingly recommends trephining as safer and more efficient thanany other operative procedures at present employed for the relief ofacute glaucoma. 

The success of the Lagrange operation, which, like the Elliot operation, aims to produce a fistulous communication between the anterior chamberand the sub-conjunctival area, depends upon securing the removal of arelatively large section of all of the layers of the scleral and corneallip of the wound, so that a permanent opening, covered by the replacedconjunctival flap, is made. Unlike the trephine operation which wasevolved from it, the Lagrange operation requires the same kind of anopening of the eyeball as required for a well executed iridectomy, and aproperly placed section entirely in scleral tissue, with a good sizedconjunctival flap, are elements which enter into the ultimate success orfailure of the procedure. 

Aside from the dangers incident to a wide incision in the neighborhoodof the ciliary body and the possibility of accident to the lens orvitreous body, or of intra-ocular hemorrhage, there is for the averageoperator the added difficulty and danger in removing a piece of scleraof the exact size required. The technique of the operation is even moredifficult and exacting than in the performance of the trephineoperation, and it also compares unfavorably in safety. 

The advisability of removing the conjunctival flap, as advocated by Dr. Wood, as a modification of the Lagrange operation, may be seriouslyquestioned, for aside from the fact that apparently no advantages inaiding permanent filtration are added, there is, added to the objectionsto the Lagrange operation already mentioned, the very seriousdisadvantage of subjecting the area at the root of the iris to infectionfor a prolonged period of time. The advantages of the protectionafforded by a conjunctival flap far outweigh the disadvantages of aremotely possible interference of drainage by the blocking of the openwound with conjunctival tissue. The fortunate experience of Dr. Wood innot having infection in a wound which remains open and unprotected forvariable lengths of time is not likely to be the experience of anyconsiderable number of operators, and probably will not always be theexperience of Dr. Wood. Furthermore, the possibilities of damage byhemorrhage from the choroidal or retinal vessels, delayed formation ofthe anterior chamber and adhesion of the capsule of the lens to thewound, and the injurious effects of even slight trauma subsequent to theoperation, including loss of vitreous, are increased by omitting theconjunctival flap. 

The modern operation for the relief of glaucoma, by which a filteringscar is produced which permits escape of liquid from the anteriorchamber, is the one which apparently holds out the most hope ofpermanently relieving the condition. While success will depend always toa certain extent upon the personal equation, yet it seems now that fora large majority if not all of the cases we are justified in abandoningall other operations than trephining, notwithstanding the verdict ofElschnig and others that fistula forming operations eventually will bediscarded in favor of iridectomy and cyclodialysis. 

Late or secondary infection, not unknown following iridectomy, mayfollow the trephine operation, and already some fifteen or sixteen caseshave been reported. But while this possibility is a real danger, whichimproved technique may greatly minimize (Col. Elliot has not seen a caseof secondary infection in an experience of over 1200 trephining cases ofhis own and a large number of others performed by his assistants andpupils) the ultimate verdict must rest with results as compared withother measures. At present, as pointed out by Meller, whose statisticsDr. Wood has cited, trephining heads the list of remedial measures forthe relief of glaucoma, and it has the advantage of being applicable toany form of the disease, to be relatively free from danger, eitherimmediate or remote, and to produce the highest percentage of favorableresults. The addition of an iridectomy in every case of trephining doesnot unduly complicate the operation and has much to commend it inoffering the patient every possibility of relief. 

INDEX

 PAGEETIOLOGY AND CLASSIFICATION OF GLAUCOMA, _Edward Jackson, M. D. _ 9

ETIOLOGY AND CLASSIFICATION OF GLAUCOMA, Discussion, _Francis Lane, M. D. _ 28

PATHOLOGY OF GLAUCOMA, _John Elmer Weeks, M. D. _ 37

PATHOLOGY OF GLAUCOMA, Discussion, _E. V. L. Brown, M. D. _ 57

CONCERNING NON-SURGICAL MEASURES FOR THEREDUCTION OF INCREASED INTRA-OCULAR TENSION, _George Edmund de Schweinitz, M. D. _ 61

CONCERNING NON-SURGICAL MEASURES FOR THEREDUCTION OF INCREASED INTRA-OCULAR TENSION, Discussion, _Nelson Miles Black, M. D. _ 101

TREPHINING FOR GLAUCOMA, _Robert Henry Elliot, M. D. _ 107

TREPHINING FOR GLAUCOMA, Discussion, _Frank C. Todd, M. D. _ 113

OPERATIONS OTHER THAN SCLERAL TREPHININGFOR THE RELIEF OF GLAUCOMA, _Casey A. Wood, M. D. _ 121

OPERATIONS OTHER THAN SCLERAL TREPHININGFOR THE RELIEF OF GLAUCOMA, Discussion, _Albert E. Bulson, Jr. , M. D. _ 141