Salme Vannas

HLA-compatible donor cornea for prevention of allograft reaction

Our series comprises 80 penetrating grafts. Of the recipient corneas 36 were vascularized. Of the donor corneas 48 were fresh and 32 were cryopreserved. As prophylaxis, we gave topical and systemic prednisolone, combined, in heavily vascularized cases, with azathioprine. Corneal donor-recipient pairs were divided into three groups according to HLA histocompatibility. In Group I (0–1 mismatch) the rate of allograft reaction was 1 in 27, in Group II (2–4 mismatches) it was 4 in 19, and in the untyped Group III 9 in 34. Even when the prognosis was poor, a well-matched donor cornea (Group I) greatly improved the chances of success; when the corneal bed was vascularized, the well-matched donor corneas had a failure rate of 1 in 13, whereas in untyped pairs it was 7 in 18. The importance of possible presensitization is discussed. Das Untersuchungsmaterial umfaßt 80 Augen nach penetrierender Keratoplastik. In 36 Fällen fand sich die Empfängerhornhaut vaskularisiert und in 44 avaskulär. 48 der Spenderhornhäute waren frisch und 32 eingefroren. Prophylaktisch wurde Prednisolon lokal und systematisch kombiniert mit azathioprine in stark vaskularisierten Fällen verabreicht. Die Spender-Empfänger-Paare wurden gemäß ihrer Histokompatibilität in drei Gruppen eingeteilt. Bei bester Übereinstimmung war das Verhältnis der Allograftreaktion 1 zu 27, in Gruppe II mit 2–4 fremden Antigenen war sie 4 zu 19 und in Gruppe III ohne Bestimmung der HLA-Antigene war sie 9 zu 34. Spenderhornhaut mit guter Übereinstimmung, d.h. 0–1 fremdem Antigen scheint recht zuverlässig auch in Fällen mit schlechter Prognose. In vaskularisierter Empfänger-Hornhaut und Spender mit guter Übereinstimmung war das Verhältnis der mißlungenen Transplantationen 1 zu 13 und bei nicht typisierten Paaren 7 zu 18. Die Rolle einer Präsensibilisierung wird diskutiert.

OBSERVATIONS ON STRUCTURES AND AGE CHANGES IN THE HUMAN SCLERA

Of the local factors probably influencing intraocular pressure, the chamber angle and in particular the trabecular tissue still attract considerable attention (Goldmann 1951, Ashton 1956, Flocks, VrabeZ, Brini, Zimmermann, Grant, Unger, etc.). The outflow pathways outside Schlemm’s canal have also been carefully explored (Ascher 1942, 1954, Goldmann 1946, Thomassen & Bakken, Ashton 1952, 1953 and 1955, etc.). The role of the sclera as a possible regulator of intraocular pressure has not attracted as much attention. On the other hand, the structure of connective tissue and its chemistry in general have been a subject of lively interest for a decade now, and the importance of the ground substance and especially its mucopolysaccharide components have been emphasized (Meyer, Dorfman, Wassermann). Gersh and Catchpole reported the ground substance as an optically homogenous structure which, though normally gel-like in consistency, may become a fluid. Its consistency varies with age, its degree of activity or the pathologic condition of the tissue. The sclera too obviously undergoes changes with age. According to Friedenwald, the sclera of old persons is thinner and denser than that of the young, and shows a loss of water. The colour of the sclera changes with age from bluish to yellowish, most likely because of the accumulation of fat in scleral tissue (Wolf-Heidegger). I t has been assumed further that the thickening and sclerosis of collagenous fibres occurring with age result in the obstruction of outflow pathways (Sondermann, Schieck, Dvorak-Theobald & Kirk). A n unusual arrangement of connective tissue structures has been observed

Hemosiderosis in eyes with secondary glaucoma after delayed intraocular hemorrhages.

The present study was prompted by the question of the role of intraocular hemorrhages in the mechanism of secondary glaucoma. The mechanism seems clear when a dense organised mass of blood or a post-hemorrhagic anterior synechia closes the chamber angle. I t has been suggested, on he other hand, that the toxic breakdown products of hemorrhages of the retina and the vitreous e. g. due to central vein occlusion may also cause secondary glaucoma (Samuels, Sugar). Of the hemorrhagic breakdown products, hematogenic pigment can he demonstrated histologically. The occurrence of hematogenic pigment in the eye in connection with systemic heinosiderosis has been studied recently by Cibis & Brown SC Hong, and Duke. While the present work was in the manuscript stage Cibis SC Yamashita published an experimental study on the dispersion of saccharated iron oxide and heinosiderin in the different parts of the eye. While engaged in the sudy of eyes with secondary glaucoma, in some of which the disease had developed following intraocular hemorrhages, this question aroused my interest for two reasons. Firstly, there is the possibility that hemosiderin and other breakdown products of hemorrhages are deposited in the outflow channels and obstruct the outflow of intraocular fluid. Secondly, it is conceivable that hemosiderin, which is a biological substance, in the process of resorption and migration from inside the eye into the systemic circulation could perhaps serve as some kind of tracer in the examination of the outflow channels.

Uveitis resembling sympathetic ophthalmia induced by sensitization of intraperitoneally implanted eye.

There is an extensive literature dealing with the allergic characteristics of sympathetic ophthalmia. Elschnig (1910) first demonstrated organ specific antibodies in the serum by injecting uvea homogenate intraperitoneally; he suggested that the anaphylactic reaction resulted of the antigenic properties of the uveal pigment. Woods (1917, 1936) confirmed Elschnigs opinion and proved the allergenic properties of uveal pigment in animals by producing an experimental hypersensitivity to uveal tissue. This could be accomplished also by using the skin test. The cellular alterations resembling sympathetic ophthalmia are then seen in the biopsy-specimen (Friedenwald 1934). The ocular reactions produced by uveal tissue in the animals, however, were very slight and did not resemble sympathetic ophthalmia in man (Woods 1936). This has led to further studies and to the opinion that hypersensitivity to uveal antigen is not the cause of sympathetic ophthalmia; it merely sets the stage for infectious factor (Streiff & A. and P. Miescher, Woods 1956). Any specific cause for the disease, such as a bacteria or a virus has not been detected. Electronmicroscopic studies have recently revealed changes like inclusion bodies, similar to what have been found in viral diseases (Ikui et al.). However, attempts to transfer the disease from one animal to another have always failed. Sympathetic ophthalmia is generally included in the so called autoallergic diseases. Experimentally they can be induced by injecting the heterologous, homologous or autologous tissue homogenate in question with an additional adjuvant (Freund & McDermott, etc.). By using uveal tissue antigen plus

OCCURRENCE AND CAUSES OF BLINDNESS IN FINLAND

The incidence and causes of blindness vary, very considerably even, in the different countries of the world and even in the same country in different periods. Reliable statistics on the number of the blind constitute the basis of blind welfare as a whole. Another problem of obvious importance is encountered in the planning of the prevention of blindness. This is the causes of blindness. The number of the blind in Finland was counted for the first time in connection with the population census of 1864. A similar census of the blind has been conducted five times, most recently in 1900-1901 After that, the Ministry for Social Affairs in 1934, and most recently in 1961, conducted studies on the social conditions of the blind and carried out a census of the blind of working age. The number of the blind per 10,000 census-registered people was 21.4 in 1873, 8.7 in 1900 and 7.2 in 1934. The criterion of blindness was inability to move about unaided in an unfamiliar environment. The above figures are unfortunately not based on medical examinations, and this naturally influences the statistics essentially. The first actual study of the causes of blindness in Finland was made in 1899 by a Swede, Prof. J. Widmark, assisted by Finnish ophthalmologists. They examined 167 blind persons in different parts of Finland and 103 pupils at the Helsinki and Kuopio Schools for the Blind. The commonest reason of blindness in Finland at that time was trachoma (30.9 per cent). The second study of the causes of blindness was published by Prof. M. Vannas (1935). It was based on the material from 1922-1931 Qf the Eye Hospital, University of Helsinki. It showed that the causes of blindness had changed greatly during the approximately 30 years since the previous report. The role of trachoma had diminished appreciably.

MAST CELLS IN GLAUCOMATOUS EYES

Mast cells, discovered by P. Ehrlich in 1 8 7 7 , are characterised by cytoplasmic granules with a strong affinity for basic dyes and with metachromatic staining. Since that time they have been the subject of numerous investigations. Heparin, characterised by an anticoagulant property, was isolated first by MacLean in 1916. Jorpes, Holmgren and Wilander traced the heparin of the body to the metachromatic granular substance of the mast cells, whence the term heparinocytes. Besides its anticoagulative activity in circulating blood, many investigators have suggested that the metachromatic substance released by mast cells has a significance for connective tissue and its ground substance (Asboe-Hansen, Morrione). Recently, Riley, Adams, Fawcett etc. have shown that the evidence in support of histamine in tissue mast cells is at least as good as that in support of heparin. Both of these, histamine and heparin resp. mucopolysaccharides, have an interest from the standpoint of glaucoma. There are so far relatively few studies on the mast cells of the eye (Jorpes & Holmgren & Wilander, Hjelmman, Zollinger, Nover, Larsen); Gunther studied the occurrence of mast cells not only in normal bulb and adnexa but also in their pathologic conditions, for instance in conditions of inflammation, trauma and tumour, and also in absolute primary and secondary glaucoma. These investigation will be discussed later on. The intention of the present work was to study the occurrence of mast cells in the anterior part of the uvea and the sclera and their significance in the different forms and phases of glaucoma.

Experimental studies on iron compounds in the eye and their significance for the pathogenesis of hemorrhagic glaucoma.

When retinal and vitreal hemorrhages break down in the eye, products are formed which have been assumed to have a causal connection in some way with the onset of secondary glaucoma. It has been attributed to inflammatory changes induced by these toxic products and blocking the chamber angle (Coats, Samuels, Sugar), or to swelling of the vitreous due to absorption of disintegration products of hemorrhages (Wood, Weinstein). Of the disintegration products of the red blood cells the iron-containing, so-called hematogenic pigment (hemosiderin) can be demonstrated histologically. In working on my opening lecture *Glaucoma due to thrombosis of the central vein of the retinae for the 1st Congress of the European Ophthalmological Society in the spring, this problem cropped up in several connections among various etiological factors. The localisation of hemosiderin in these eyes lent support to the assumption that the disintegration products of the blood could well be concerned in the mechanism of secondary glaucoma after a central vein occlusion. After experimental intravitreal injections of iron compounds the migration of iron from the posterior part of the eye appeared along the central vessels in the optic nerve; Berens & Posner and Schreck suggested that this shows the outflow of the intraocular fluid via the optic nerve. Later, Cibis & Yamashita postulated the irreversible binding of iron to the perivascular

ELECTRORETINOGRAPHIC OBSERVATIONS IN CENTRAL VEIN OCCLUSION

In his monograph of 1945 and in 1949 Karpe studied the changes in the electroretinogram (ERG) of central vein occlusions. H e found that a normal or supernormal ERG indicated a fairly good prognosis, a negative or subnormal ERG a poor prognosis. Henkes later came to a similar conclusion. According to Karpe and Uchermann, nearly half of the cases of central vein occlusion show a normal ERG and the others generally a negative ERG in the initial phase. Thorough clinical examination of the etiological factors of central vein occlusion indicated that the prognosis was dependent on the pathogenetic mechanism of the occlusion (Klien &: Olwin, Vannas SC Orma). In addition to vascular sclerosis, hemodynamic disturbances and inflammatory factors, simple glaucoma obviously has a notable role in the development of total central vein occlusion. In tonography combined with suitable provocative tests simple glaucoma was established in 42 per cent of 71 central vein occlusions, closed-angle mechanism in 8 per cent. In persons over 65, primary glaucoma occurred in 76 per cent. Primary glaucoma also seemed to affect the prognosis adversely. Simple glaucoma was established in 9 out of I1 cases with hemorrhagic glaucoma (Vannas k Tarkkanen). The object of this study was to compare, principally in the light of follow-up study, the clinical findings of patients with central vein occlusion and simple glaucoma and patients with pure occlusion but no glaucoma. The electroretinogram records especially were taken into consideration.

The use of collagenous suture material in surgery of the cornea and sclera.

Cataract suture and corneal sutures in general are much-discussed problems in ophthalmology. The closing of a cataract incision with sutures was suggested ninety years ago by Williams. But it was not until the 1930s that corneal sutures had their penetration after the intracapsular cataract extraction method developed by Stanculeanu, Torok and Elschnig had gradually been adopted as common practice. There is considerable variation in the method of placing them and the number employed. The suture material is usually silk, less often surgical gut and cotton. Closure of the incision with appositional sutures promotes rapid healing and prevents complications, e. g. the occurrence of the dreaded epithelial invasion (Kirby etc.). However, appositional silk sutures have sometimes been found to cause epithelial invasion along the suture tracks (Berliner, Dunnington, Duke-Elder). I t is, moreover, common knowledge that complications may occur in connection with the removal of corneal and corneoscleral sutures as latest pointed out by Meacham and that they constitute an unpleasant surprise both for the patient awaiting discharge from hospital and for the surgeon. To provide against these dangers a new method was adopted in which a cataract incision is sewed with virgin silk and embedded under the conjunctival flap and left there (Barraquer Moner, Barraquer & Boberg-Ans). However, even such sutures may have to be removed, because of irritation (Editorial, Br. J. Ophth. 1959: 43: 253). Interest consequently seems which obviates the necessity

Ultrastructure of Bruch's membrane in senile macular degeneration.

In textbooks of ophthalmology the Bruchs membrane has usually been described as two-layered structure with one cuticular and one elastic layer. The cuticular layer is thought to be secreted by the pigment epithelium of the retina while the elastic layer would be of choroidal origin. With the aid of electron microscope, however, the structure has been found to be more complex consisting of five layers. The innermost layer is the basement membrane of the pigment epithelium of the retina. External to this layer is a loose collagenous zone and immediately external to this an elastic layer extending throughout the choroid. A second collagenous zone and a second basement membrane related to the endothelium of the choriocapillaris are located external to the elastic layer (Nakaizumi, 1964). Garron (1963) has pointed out the difference between the posterior portion and the equatorial and anterior portions of Bruchs membrane in the adult human eye. These findings have been confirmed by Nakaizumi et al. (1964). Posteriorly, the collagenous and elastic zones were found to be more dense due to short and broad banded fibers, 1.000 A, and due to meshwork of circular or oval vesicular structures as well as due to an increased density of the ground substance. Some sections showed a gap in the basement membrane of the capillary layer. Some areas showed also a gap in the basement membrane of the pigment epithelium containing herniated pigment epithelial cytoplasm and plasma membrane. The cause of ordinary senile macular degeneration is not known yet. So