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Chapter I - GENERAL: AETIOLOGY
- J. Ringland Anderson, John Herbert Parsons
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- Hydrophthalmia or Congenital Glaucoma
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- 31 October 2013, pp 1-18
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Summary
DEFINITION
The condition to be described is that of an eye which has become enlarged under the influence of increased intra-ocular pressure. As the ability of the ocular tissues to stretch is practically limited to the period of childhood, and as glaucoma in the first few years of life is almost always associated with ocular distension, the term “Congenital Glaucoma” appears suitable for this condition. By congenital glaucoma we mean a state of raised tension due to an intra-uterine defect and manifest during the first few years of life.
The definition excludes from the scope of this work true cases of infantile staphyloma, which show evidence of perforation, in which the iris is incorporated with the cornea. Of course, the hypertension that is the cause of enlargement in congenital glaucoma may not be in evidence at the time of examination. The state of raised tension may have passed, but before doing so it sets up a series of degenerative changes and interferes with the nutrition of the various tissues to such an extent that ultimate blindness is almost inevitable.
Glaucoma in children, as in adults, may be primary or secondary. The term primary is reserved for cases of obscure origin, and simply implies ignorance as to the cause. It is hoped that in time the term may become obsolete. This study is mainly concerned with primary infantile glaucoma.
Some cases of glaucoma in children are obviously due to certain malformations, of which the most common are aniridia and microphthalmia. In aniridia, glaucoma is undoubtedly often caused by the union of the iris root and the posterior surface of the cornea. In microphthalmia the narrowness of the circumlental space plays a part. As the finer changes which may hinder the function of the drainage channels are beyond our knowledge at present, our conceptions are largely hypothetical.
TITLE
Of the many different names given in the past to the condition under discussion, “Hydrophthalmia” and “Buphthalmia” have been most widely used. A. Fuchs (1924) reserved the term “buphthalmos” for the condition in which an anterior staphyloma arises in infancy and “hydrophthalmos” for “primary infantile (congenital) glaucoma”.
Hydrophthalmia or Congenital Glaucoma
- Its Causes, Treatment, and Outlook
- J. Ringland Anderson, John Herbert Parsons
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Originally published in 1939, this book presents a comprehensive study of hydrophthalmia, also known as buphthalmia, incorporating information on causes, treatment and outlook as they were understood at the time of publication. An approach based on comparative anatomy and pathology is used, with analysis of Australian fauna such as ornithorhyncus, echidna, pseudochirus and dasyurus incorporated into the study. The text also provides descriptions of all the different methods of operative treatment which had been tried, with a thorough analysis of the results obtained by various surgeons. Numerous illustrative figures are included throughout. This book will be of interest to anyone with an interest in the history of medicine and ophthalmology.
Illustrations
- J. Ringland Anderson, John Herbert Parsons
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- 31 October 2013, pp xiii-xvi
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Index
- J. Ringland Anderson, John Herbert Parsons
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- 31 October 2013, pp 371-377
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Frontmatter
- J. Ringland Anderson, John Herbert Parsons
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- 31 October 2013, pp i-iv
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Chapter IV - THE PATHOLOGY OF CONGENITAL GLAUCOMA 189 to 229
- J. Ringland Anderson, John Herbert Parsons
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Summary
A condition sometimes described as a “naevus of the choroid” must not be confused with the tumour formation being discussed. It is a melanoma, which appears uniformly grey in colour. It has either a definite or a feathery edge. It shows little or no elevation, but has a tendency to become malignant (Johnston, 1929).
Other ocular changes. The retinal vessels (Schirmer, Yamanaka, Beltmann, Aynsley) and the choroidal vessels (Salus, Steffens, Krause), as seen with the ophthalmoscope, have frequently been described as being dilated and tortuous. The fundi were dark red in colour in the patients of Perera, Padovani and Sturge. Several instances of large tortuous retinal vessels in hydrophthalmic eyes not accompanied by facial naevi have been reported. In Grimsdale's case (1917) the arteries were tortuous and much larger than the veins. Instances of tortuous retinal vessels, particularly in the neighbourhood of the disc on the same side as facial naevi in non-hydrophthalmic patients have been referred to by Collins (1917), Hartridge (1901), Voegele (1925), Yamanaka (1927), Work Dodd (1901) and others. It is not surprising that some of such patients have also a naevoid state of the nasal mucous membrane. The man reported by Collins had recurrent epistaxis. Such cases constitute a link with the syndrome of facial and intra-nasal naevi which is commonly hereditary and is known as Osier's disease. See Goldstein (1936) and McArthur (1937).
Bär (1925) described a case of glaucoma with naevus of the eyeball and numerous tortuous anastomosing retinal veins in the fundus. A clearly defined patch in the retina was found, and Bar considered it to be haemorrhagic in origin. O'Brien and Porter described an unusual pigmented patch near the temporal periphery of the affected eye in their patient. Enlarged choroidal vessels surrounded this area but the neighbouring retinal vessels were reduced in size. These patches, like other retinal anomalies, appear to be most commonly found in the inferior temporal quadrant. Compare anterior dialyses, falciform fold, cysts, and vascular tumours of the retina.
Chapter II - DIFFERENTIAL DIAGNOSIS
- J. Ringland Anderson, John Herbert Parsons
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Introduction
- J. Ringland Anderson, John Herbert Parsons
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- 31 October 2013, pp xix-xx
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Summary
CONSULTING ROOM, MELBOURNE, 1933.
Father of a 9-year-old boy blind from congenital glaucoma. Grahame had a trephine operation on each eye when he was a year old. Would he have had a better chance without such treatment?
Surgeon. I do not know.
Father. Do any untreated patients with this disease retain sufficient vision to enable them to earn their living for a few years?
Surgeon. I do not know.
Father. If he marries will his children be affected?
Surgeon. I do not know.
The following pages are the result of an attempt to answer these questions: Through the generosity of Messrs G. J. and E. B. Coles, it was possible to send out 874 Questionnaire forms to 346 oculists throughout the world. A summary of the data obtained will be found later in this book.
The author is grateful to the following surgeons for supplying valuable material: Humphrey Neame, London; E. O. Marks, Brisbane; W. R. Fairclough, Auckland, and J. M. Wheeler, New York. The author is indebted to Professor A. W. Mulock Houwer and Captain v. Blaauboer for the specimens from Tarsius. The following pathologists have most willingly aided in its investigation: Drs Rupert Willis, R. B. Maynard and Adelaide Gault. Dr Kevin O'Day kindly allowed the author to examine his sections of Dasyurus and Pseudochirus. The microphotographs are by Mr Lewis Booth of the Alfred Hospital and Mr H. Marriott of the Department of Anatomy, Melbourne University. The author would express his appreciation of the generosity of those who permitted the use of plates from older works. To Miss Jean McNab and Miss Elizabeth Agar the author would offer his warmest thanks for hours spent in typing and translation.
If it had not been for the enthusiasm and the outstanding ability of Miss Diana Mann, B.Sc, this book would not have been written. For three years her eagerness to understand some of the mysteries of congenital glaucoma has led her through many hundred pages of foreign works, through the examination of several hundred slides and through the almost endless arduous tasks that are known only by those who carry out a work of this kind. For these labours the author is deeply grateful.
Chapter V - PATHOGENESIS
- J. Ringland Anderson, John Herbert Parsons
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- 31 October 2013, pp 230-292
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Summary
THE THEORIES OF ORIGIN OF HYDROPHTHALMIA
A survey of the foregoing summary of the morbid anatomy of early specimens reveals two types of disorder in the ocular tissues. Firstly, one detects developmental defects due to an arrested or an otherwise faulty growth. Secondly, undoubted evidences of inflammatory changes are found.
It is difficult to divide with certainty all the changes into one or other of these types. The distension of the globe has led in most cases to so much distortion that it is not always possible to visualise the state of the affected tissues before they were stretched and affected by late or secondary degeneration and even inflammatory changes. One must be constantly asking whether the signs of inflammation in the iris, for example, are due to intra-uterine infection or to a relatively late postnatal process that developed with ease in an already over-stretched and disordered structure.
Even when one has decided that the main changes in a certain globe are such that one can label them as congenital anomalies, one has not definitely excluded them as ravages of intra-uterine infection.
One must remember that, even in such true examples of the developmental type as Seefelder specimens II and III, traces of an almost vanished intra-uterine iridocyclitis were found. This suggests that the initial cause was inflammation, and that the direct cause of hydrophthalmia was the developmental defect that resulted from the inflammatory state. Therefore, when we state that a certain specimen is of the developmental type we do not deny an initial role to an earlier inflammation. We simply mean the direct cause was an arrested or defective development of some structure. Possibly, however, in such an eye the nitration apparatus, though developmentally defective, was adequate until a mild attack of inflammation developed. Then the albuminous aqueous blocked the restricted means of escape and hydrophthalmia ensued.
The finding of such traces of iridocyclitis and the more obvious signs of secondary iridocyclitis tends to obscure the picture and make the recognition of the direct cause of hypertension very difficult.
Foreword
- J. Ringland Anderson, John Herbert Parsons
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- 31 October 2013, pp xvii-xviii
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In a foreword to Dr Ringland Anderson's book on Detachment of the Retina, I expressed the hope that others would follow his good example and provide other such monographs. It is a matter for congratulation that he himself has now written one on Hydrophthalmia, a disèase better known under the picturesque but otherwise unsatisfactory name Buphthalmia. The last monograph on this subject was published in 1897 by Dr Edmund L. Gros, under the title Étude sur l'Hydrophthalmie ou Glaucome infantile, and was an excellent résumé of our knowledge up to that date. The present is a much more extensive treatise and will long remain authoritative. In dealing with a disease of such obscure aetiology, in which, however, congenital malformations are a prominent factor, the scientific approach must be by way of pathology and comparative anatomy. In both of these respects the treatment here is exhaustive, and beautifully illustrated. Dr Anderson has taken advantage of his special opportunities to obtain specimens from Australian fauna—ornithorhyncus, echidna, pseudochirus, dasyurus— and to describe the condition of the angle of the anterior chamber in them and in tarsius. This is in itself a valuable contribution to comparative anatomy. The remarkable association of hydrophthalmia with neurofibromatosis, facial naevi and other angiomatous conditions is fully discussed.
To the practising ophthalmic surgeon the most important part of the book is the description of all the different methods of operative treatment which have been tried, with a thorough analysis of the results obtained by various surgeons. One cannot help regretting that the survey shows no signs of indicating in the treatment of hydrophthalmia any such hopeful improvements in operative technique as were beginning to bear fruit when Dr Anderson's book on Detachment of the Retina was published, and which have proved so successful.
Chapter VIII - GENERAL REFLECTIONS
- J. Ringland Anderson, John Herbert Parsons
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- 31 October 2013, pp 365-370
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Wisdom will repudiate thee, if thou think to enquire
WHY things are as they are or whence they came: thy task
is first to learn WHAT IS, and in pursuant knowledge
pure intellect will find pure pleasure and the only ground
for a philosophy conformable to truth.
ROBERT BRIDGES.Uncertainty regarding the ultimate cause of Congenital Glaucoma persists and will persist as long as so much concerning the influence of heredity and the forces in prenatal life that make for maldevelopment continues to be wrapped in mystery.
We have concentrated on an investigation of the earliest specimens with this disease and we have sought for traces of pre-existing inflammation, and we have found little. Either such a state is far from being universal or its manifestations in foetal life are not recognised because they can rapidly disappear or because they differ from those so well known in adult tissues. If an attack of inflammation had been initiated early, its influence would be great enough to lead to grave and obvious malformation. One may ask, can such an attack commence prior to the development of an efficient blood-vascular system? If not, its onset must be restricted to the second half of pregnancy. If this attack be of any but the mildest degree, surely histological evidence of inflammation would be revealed in an examination of specimens obtained during the first few weeks of life.
Though the abnormal findings in the earliest specimens are varied and diverse yet they as a whole resemble defects in development. They suggest that growth has been retarded or has become aberrant. A study of human embryology and of comparative anatomy throws light on these anomalous states. Collateral evidence is supplied by the presence of other developmental defects in patients with congenital glaucoma. Not only do we find ocular defects but facial naevi or neurofibromatous changes on the same side of the face and head as the affected eye.
We cannot, however, assume that congenital glaucoma is due, as a rule, to defective development and nothing else, for one does not know what factors underlie errors in development in general. It is conceivable that a deficiency in some vitamin or some endocrine substance may exist, or that some upset in the maternal nervous system may so lower resistance that inflammation or some other dystrophic influence may be permitted to disturb the smoothness that characterises normal growth.
Contents
- J. Ringland Anderson, John Herbert Parsons
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- 31 October 2013, pp vii-xii
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Chapter VI - TREATMENT
- J. Ringland Anderson, John Herbert Parsons
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- 31 October 2013, pp 293-346
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HISTORY OF TREATMENT
Soon after the first recognition of hydrophthalmia we find descriptions of the manner in which the early surgeons endeavoured to diminish the quantity of fluid in the eye. Boerhaave in 1749 advised, in addition to purgatives and mercurial hydragogues, a puncturing of the eye at the side of the lens from time to time until the eye recovered its normal size. Maitre-Jan (1740) proposed an anterior scleral incision in the external angle of the eye.
Pellier de Quengay (1789) wrote that if diuretics and hydrogogues failed one should not hesitate to puncture the eye. Amongst his good results one reads in his book of a certain “Ferrien of Cette, who after several punctures of the anterior chamber, the use of diuretics, and fondants and ophthalmic opiates, cured a buphthalmia so marked that the cornea was opaque and the globe of the eye so large that the lids could not cover it”.
Though Gleize (1786) preferred local medication, finding operation difficult and insufficient, he reported the facts that Guerin and Woolhouse advised scleral puncture and that Mr Toubervil, an English oculist, also performed this operation and considered it capable of lessening the size of the eye and preventing cataract.
A thesis by Grellois (1836) summarised the treatment in use at the time. He reviews the advantage of anti-herpetic, anti-syphilitic and anti-scrophulous methods, recommending blisters to the forehead “setons a la nuge”, compresses of lead acetate, and the application to the globe of hot sachets of dry aromatic plants. He recalled the fact that the surgeons who compressed the globe were using a procedure already employed by Rhazes.
In Annales d'oculistiques, March 1841, we read: “M. O'Beirne, the clever Irish surgeon, who has published a work on the treatment of hydrophthalmia, thinks that in the majority of cases this disease may be cured without operation. According to him, the trouble is usually connected with a rheumatic diathesis, and may fortunately be dissipated with the aid of calomel, repeated until there is salivation. He reports a serious case which he cured in this way, and refers to several others. Here is a new clinical history which supports this assertion.”
Dedication
- J. Ringland Anderson, John Herbert Parsons
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Chapter VII - PROGNOSIS
- J. Ringland Anderson, John Herbert Parsons
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Summary
THE FINAL PICTURE
Few diseases lead to such visual loss, discomfort and disfigurement. Lagrange referred to the final stage of a hydrophthalmic eye as completely “ désorganisé, disgracieux et douloureux ”.
A visit to a Blind Asylum and a search of its records afford ample evidence of this statement.
With head hung, watery eyes and every effort made to avoid light the victim seeks refuge in the dark. Relief may follow only bilateral enucleation.
One finds enormous eyes, infected and bleary, with lids that give very incomplete protection. The bluish sclera may be staphylomatous and the cornea so opaque that the iris is obscured. From the presence of retinal detachment and vitreous shrinkage there may be a greyish yellow reflex. The tension may be low from ciliary atrophy and phthisis bulbi or raised from an intra-ocular haemorrhage due to rupture of a branch of a long posterior ciliary artery.
A permanent cure. When one remembers the deep-seated cause of hypertension in the majority of cases of congenital glaucoma it is not surprising that complete and permanent cures are very rarely known. Even if the operation is performed in the earliest stages there is little chance of such a cure. However, since Seefelder's day the methods of treatment have improved so much that his views may be considered as unduly pessimistic. He wrote: “ I intentionally do not use the term ‘permanent cure ’, since I know of no case of operated hydrophthalmia where undiminished sight has been retained till later life. In my opinion there can be no definite point of time at which we can decide that a hydrophthalmia is permanently cured. Such observations as that of our case 20 must be highly disconcerting. Here, ten years after dismissal from the clinic, there was vision of 6/30 corrected with normal tension—definitely a gratifying result— while four years later the vision had inexplicably sunk to 6/100 and could not be improved by any correction.”
The oldest person with congenital glaucoma in Jaensch's own experience was a man aged forty-four years. He had been able to see until he was twelve when a detachment appeared in one eye. The other failed when he was thirty-six and both eyes developed phthisis bulbi. In his summary Jaensch wrote: “Thus hydrophthalmia is prognostically very unfavourable and therapeutically very difficult to influence”.
Chapter IV - THE PATHOLOGY OF CONGENITAL GLAUCOMA Pages 99 to 188
- J. Ringland Anderson, John Herbert Parsons
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Summary
The information for this chapter has been gleaned from previous writings and particularly the reports of specimens in the literature. The series of Seefelder, Takashima, Magitot and Lagrange have been most instructive. In addition five specimens have been described by the author for the first time. They are referred to in the following manner: unpublished specimen I, which may have been an example of infantile staphyloma; unpublished specimens II and V supplied by Dr W. A. Fairclough of Auckland—the former was described microscopically by Dr Eisdell Moore; unpublished specimens III and IV supplied by Mr Humphrey Neame, London; and unpublished specimen VI supplied by Dr E. 0. Marks of Brisbane. Dr J. M. Wheeler of New York very kindly sent the author slides of his specimen with neurofibromatosis described in the Transactions of the American Ophthalmological Society, 34, 151 (1936) (Figs. 88 to 94).
INTERFERENCE WITH FUNCTION
The child with hydrophthalmia when first brought to the doctor presents a characteristic picture. The enlarged and hazy cornea is usually obvious. As a rule the head is held down because of photophobia and therefore examination may be difficult. On closer inspection the widening and flattening of the sclero-corneal angle, the bluish sclera and the deep anterior chamber are noticed. Frequently a tremulousness of the iris and a yellowish pupillary reflex are observed in the late stages. The tension is usually raised, and the optic disc may be cupped. Some difficulty in fixation and later partial or complete blindness completes the clinical picture of advanced bilateral hydrophthalmia.
Refraction. Myopia is the most common refractive condition found. It is usually present in only a moderate degree, viz. from 1.7 dioptres, and is not as marked as the increased length of the eye would suggest. The relationship between the length of axis and the degree of ametropia which is nearly constant in myopia, does not hold in hydrophthalmia.
Parsons (1920) gave three reasons why the hydrophthalmic eye is not nearly so myopic as its axial elongation would suggest. They were:
(1) The flattening of the cornea. Its radius of curvature approximates that of the sclerotic and is not uncommonly 11.0 mm. instead of 7.8 mm.
Chapter III - THE STRUCTURE AND DEVELOPMENT OF THE INVOLVED TISSUES: THEIR EMBRYOLOGY AND THEIR COMPARATIVE ANATOMY
- J. Ringland Anderson, John Herbert Parsons
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THE DEVELOPMENT OF INVOLVED TISSUES
As an introduction to a study of congenital glaucoma, it is essential to consider the structural changes that occur during embryonic and early life in the anterior ocular tissues. There are two periods of relatively rapid ocular growth after birth, separated by a time when little change is found. The first period is during the first few years of life, and during this time it is the area in front of the muscle insertions that grows. This period and the tissues affected during it correspond with the time and site of the main development of hydrophthalmia.
The second period is from about puberty until the early twenties. During this time the tissues of the posterior segment are mainly affected, but the distance between the fovea and the optic disc remains the same as at birth. It is during this later period that the other common form of distension, viz. myopia, occurs, and the tissues growing then are those principally affected. If, later in life when growth is finished, hypertension occurs, the only part that can distend is the weakest part, viz. the lamina cribrosa. Medullation is complete during the first three weeks, and probably the lamina cribrosa is fully grown by then.
The sclera. In all species the anterior part of the sclera appears first and progresses farthest during embryonic life (Mann). The first sign of condensation of the outer sclera is found at the 48.0 mm. stage in that part which will later overlap the angle of the anterior chamber. At this stage condensation of the deep corneal layers is relatively advanced and a deep band runs towards the equator. Scleral condensation is more advanced by the 65.0 mm. stage, but the sclera is still thinner than the cornea.
The greater likelihood of scleral distension during the first two decades is suggested in the following paragraph. “At birth the sclera is immature and is lacking particularly in elastic fibres and until the beginning of the third decade it is particularly poor in this tissue. From then on, until the age of sixty years, this increases greatly” (Krekler, 1923).