Documenta Ophthalmologica 44,1 : 93-94, 1977 DIABETIC RET1NOPATHY AND LIGHT-COAGULATION M.C. COLENBRANDER
('s-Hertogen bosch) ABSTRACT In diabetic retinopathy, a low resistance of flow between choroid and retina is found which goes with an increased intake of tissue fluid into the retinal vessels and the appearance of retinal oedema. Light coagulation destroys the choriocapillaris which does not regenerate. As less fluid becomes available to be sucked up by the retinal vessels, the oedema will now disappear and consequently, the retinopathy subsides. Everyone agrees that light-coagulation has a favourable influence on diabetic retinopathy. But one question remains: why? The common opinion is that the destruction makes it easier for the capillaries to feed the remaining tissue. But which territories of the retina are destroyed? They are mainly the posterior layers, next to the pigment epithelium. But these layers have no retinal capillaries and are fed by the choroid. Thus photocoagulation of these layers does not reduce the territories that are dependent on the retinal capillaries. But perhaps it may be easier for the capillaries of the choroid to feed the reduced retina? No, this cannot be true, because the choriocapillaris is destroyed as well. If the hypothesis of the reduced retinal tissue to be fed cannot hold, what then may be the reason for the favourable influence of light-coagulation? I think that the following train of thought may be of some importance. Transparent tissues, like the cornea, the lens and the retina, are kept in a rather dessicated state. This means that they are eager to absorb water, but are held back by various provisions. The cornea keeps itself dry by pumping out water, mainly through the endothelium. It is, by the way, by means of this pumping mechanism that drugs are transported across the cornea and enter the anterior chamber so rapidly. If the pump is defective, the cornea swells up and becomes clouded. In the case of the lens, it is the tension of the lens capsule, that counteracts the tendency to swelling. The pressure within the lens is moreover responsible for the smooth surface of the lens. In the retina the blood-retina barrier restricts the outflow from the capillaries, while the inflow is n o t restricted. In consequence there is a low tissue pressure in the retina, which sucks the retina against its substratum and promotes a constant flow from the choriocapillaris, across Bruch's membrane
93
and the pigment epithelium into the retina, where the fluid is absorbed by the sucking retinal capillaries. If there is a tear in the retina, vitreous is sucked through the hole into the retro-retinal space. The retina, although it tries to absorb it, can no longer maintain its dried-up state, it swells and becomes opaque. Against this whitish background the retinal vessels look much darker. The detachment of the retina is maintained as long as the leak is not closed. After closure the remaining fluid is p r o m p t l y absorbed by the retina. In diabetic retinopathy one of the first signs is that the retinal veins become distended. This is tantamount to saying that more fluid is absorbed. And this means that somewhere between the ch0roid and the retina the resistance to the flow is diminished, so that more fluid is sucked in by the retina. Put in this way, the primary cause of the diabetic retinopathy is n o t situated in the retinal vessels, but somewhere between choriocapillaris and retinal tissue. As long as the retinal vessels are able to absorb the extra amount of fluid, the only signs are the enlarged veins. But if the amount of fluid surpasses the absorbing capacity of the retina, oedema develops. This means that the fibres of MiiUer come under tension, the tissue-pressure of the retina rises, m o s t capillaries are throttled, only a few are overstretched by the back-pressure in the arteries and survive as shunt-vessels. At the borders of the avascular areas the vessels try to bud forth Jinto. new capillanes, but these buds cannot grow out in the oedema and remain in the stage of microaneurysms. In short: the complete picture of diabetic retinopathy comes into being (Colenbrander, Klin. Mbl. Augenheilk. 1 6 7 : 9 4 (1975)). In this view of the mechanism of the successive events of d i a b e t i c retinopathy it is not difficult to explain the role of light-coagulation. In lightcoagulation the heat is generated in the pigment epithelium and the tissues on both sides are badly damaged. So, the choriocapiUary layer is destroyed. But why does it n o t regenerate? Everywhere in the body capillaries grow out if needed, but obviously the choroid feels no need to replace the destroyed choriocapillaris, because the greater vessels are still intact and there is no local asphyxia. In consequence the stream of fluid towards the retina is drastically diminished, the oedema subsides and the conditions within the retina are more or less normalized. So, in this view, oedema is the keyword to diabetic retinopathy. Without oedema: no retinopathy. Oedema explains all the signs of retinopathy. Retinopathy subsides if oedema is taken away by destroying the choriocapillaris. Author's address: Wagnerlaan 3 's-Hertogenbosch - The Netherlands
('s-Hertogen bosch) ABSTRACT In diabetic retinopathy, a low resistance of flow between choroid and retina is found which goes with an increased intake of tissue fluid into the retinal vessels and the appearance of retinal oedema. Light coagulation destroys the choriocapillaris which does not regenerate. As less fluid becomes available to be sucked up by the retinal vessels, the oedema will now disappear and consequently, the retinopathy subsides. Everyone agrees that light-coagulation has a favourable influence on diabetic retinopathy. But one question remains: why? The common opinion is that the destruction makes it easier for the capillaries to feed the remaining tissue. But which territories of the retina are destroyed? They are mainly the posterior layers, next to the pigment epithelium. But these layers have no retinal capillaries and are fed by the choroid. Thus photocoagulation of these layers does not reduce the territories that are dependent on the retinal capillaries. But perhaps it may be easier for the capillaries of the choroid to feed the reduced retina? No, this cannot be true, because the choriocapillaris is destroyed as well. If the hypothesis of the reduced retinal tissue to be fed cannot hold, what then may be the reason for the favourable influence of light-coagulation? I think that the following train of thought may be of some importance. Transparent tissues, like the cornea, the lens and the retina, are kept in a rather dessicated state. This means that they are eager to absorb water, but are held back by various provisions. The cornea keeps itself dry by pumping out water, mainly through the endothelium. It is, by the way, by means of this pumping mechanism that drugs are transported across the cornea and enter the anterior chamber so rapidly. If the pump is defective, the cornea swells up and becomes clouded. In the case of the lens, it is the tension of the lens capsule, that counteracts the tendency to swelling. The pressure within the lens is moreover responsible for the smooth surface of the lens. In the retina the blood-retina barrier restricts the outflow from the capillaries, while the inflow is n o t restricted. In consequence there is a low tissue pressure in the retina, which sucks the retina against its substratum and promotes a constant flow from the choriocapillaris, across Bruch's membrane
93
and the pigment epithelium into the retina, where the fluid is absorbed by the sucking retinal capillaries. If there is a tear in the retina, vitreous is sucked through the hole into the retro-retinal space. The retina, although it tries to absorb it, can no longer maintain its dried-up state, it swells and becomes opaque. Against this whitish background the retinal vessels look much darker. The detachment of the retina is maintained as long as the leak is not closed. After closure the remaining fluid is p r o m p t l y absorbed by the retina. In diabetic retinopathy one of the first signs is that the retinal veins become distended. This is tantamount to saying that more fluid is absorbed. And this means that somewhere between the ch0roid and the retina the resistance to the flow is diminished, so that more fluid is sucked in by the retina. Put in this way, the primary cause of the diabetic retinopathy is n o t situated in the retinal vessels, but somewhere between choriocapillaris and retinal tissue. As long as the retinal vessels are able to absorb the extra amount of fluid, the only signs are the enlarged veins. But if the amount of fluid surpasses the absorbing capacity of the retina, oedema develops. This means that the fibres of MiiUer come under tension, the tissue-pressure of the retina rises, m o s t capillaries are throttled, only a few are overstretched by the back-pressure in the arteries and survive as shunt-vessels. At the borders of the avascular areas the vessels try to bud forth Jinto. new capillanes, but these buds cannot grow out in the oedema and remain in the stage of microaneurysms. In short: the complete picture of diabetic retinopathy comes into being (Colenbrander, Klin. Mbl. Augenheilk. 1 6 7 : 9 4 (1975)). In this view of the mechanism of the successive events of d i a b e t i c retinopathy it is not difficult to explain the role of light-coagulation. In lightcoagulation the heat is generated in the pigment epithelium and the tissues on both sides are badly damaged. So, the choriocapiUary layer is destroyed. But why does it n o t regenerate? Everywhere in the body capillaries grow out if needed, but obviously the choroid feels no need to replace the destroyed choriocapillaris, because the greater vessels are still intact and there is no local asphyxia. In consequence the stream of fluid towards the retina is drastically diminished, the oedema subsides and the conditions within the retina are more or less normalized. So, in this view, oedema is the keyword to diabetic retinopathy. Without oedema: no retinopathy. Oedema explains all the signs of retinopathy. Retinopathy subsides if oedema is taken away by destroying the choriocapillaris. Author's address: Wagnerlaan 3 's-Hertogenbosch - The Netherlands
