of 2 /2
536 recommending intracardiac surgery. CAMPBELL suggests that the indications for operation include, in addition to the electrocardiographic pattern, a jugular " a " wave, severe symptoms, or much cardiac enlargement. Cyanosis with clubbing of the fingers always means severe stenosis, with rising pressure on the right side causing a shunt, usually through the foramen ovale or an atrial septal defect. It seems that patients with moderate or severe stenosis, but without any of these signs, should be seen regularly and, if there is any hint that their condition is deteriorating, should be examined by cardiac catheterisation. Angiocardiography is unlikely to help, for the experienced operator can detect with the catheter whether the stenosis is valvular or infundibular, besides recording pressures in each chamber. CAMPBELL believes that operation should not be be long delayed if the patient’s condi- tion is deteriorating and the right-ventricular pressure is 100 mm. Hg or more, while DIMOND and LiN suggest a figure of 75 mm. Certainly the risk of operation increases alarmingly as the patient becomes more severely disabled, 8 The results of pulmonary valvotomy to be published by CAMPBELL may give further information on these problems. 1. Lundbaek, K. Lancet, 1954, i, 377. 2. Ditzel, J. New Engl. J. Med. 1954, 250, 541. 3. Ditzel, J., Sagild, U. Ibid. p. 587. Diabetic Micro-angiopathy INCREASING success in the treatment of primary diabetic symptoms, and the consequent greater longevity of diabetics, accentuate the importance of work on the mechanism of diabetic complications. These involve mainly the vascular and nervous systems, eyes, and kidneys, and it would be satisfying to find explanations that were common to such varied manifestations. The most obvious common factor is the vascular supply, which might be particularly prone to involvement in certain organs because of special local conditions. In advanced vascular disease of diabetics all types of blood-vessel are involved, 1 but careful study indicates that capillary lesions may precede sclerosis in other parts of the vascular system.2 In this sense are the capillary changes primary ; and those tissues in which the capillary bed forms the only vascular component, such as the inner nuclear layer of the retina, the glomeruli of the kidney, and the pancreatic islets of Langerhans, are the very ones particularly prone to degenerative change in diabetes. Detailed study of the capillary changes in diabetics thus promises to increase our under- standing of the pathogenesis of the complications of diabetes. In two sites of the living body-the conjunctivas and the nail beds-capillaries can be examined with relative ease under normal conditions, using a corneal microscope which can give a magnification of from 16 to 150. It may be assumed that the conjunctival and nail-bed capillaries fairly represent all the capill- aries of the subcutaneous layer, but they may well be less affected by diabetes than those in the particular organs subject to the common complications. DITZEL and SAGILD 3 studied the conjunctival vessels of 150 diabetics and 90 normal controls. In the diabetics the capillaries were more numerous and elongated, par- ticularly in their venous parts, forming an irregular network. It was also noted that the blood within them was often in large aggregates which tended seriously to obstruct the rate of flow. The distension of the venules, sometimes to two or more times their normal diameter, contributed further to the sluggish flow. It is said that aggregation of red blood-cells or " sludging " does not occur to any significant degree in healthy people, although it is common in many diseases 4 ; and such gross distension of the venules was not seen in the 90 controls. Capillary micro-aneurysms, so characteristic of diabetic retino- pathy, were no more common in diabetic conjunctivae than in the normals. These studies of the living are reinforced by a formidable number of examinations of dead tissues. 5-8 Thus, the elongation and angular course of capillaries has been noted in diabetic retinze, 5 8 where in addition BALLANTYNE and LOWENSTEIN 9 described the micro-aneurysms in the venous segments of the capillaries. It is from these micro-aneurysms that red cells may escape to produce haemorrhages,1O and their subsequent hyalinisation and fusion produces the typical waxy exudates of diabetic retinopathy. In the glomeruli of the kidney, too, there is proliferation and hyalinisation of the capillary walls." Parts of the capillaries may be dilated,12 and, with the eye of faith, micro-aneurysms may be made out.13 Patients with these capillary changes in the fundi are extremely likely to have them in the kidneys as well, although they probably occur rather later there.l0 Hyalinisation of the islets of Langerhans, a common finding in older diabetics,14 may represent a similar process. There are conflicting accounts of the presence 15 16 or absence 7 10 of such changes in other tissues. Besides these morphological changes in the capill- aries there is also evidence for abnormal capillary function in diabetes. Some workers 17 18 have reported increased capillary fragility, measured usually by a tourniquet test; and FREHNER 15 noted increased capillary permeability using the method of fluorescein diffusion. The descriptive stage of study of these changes is well advanced, but there are many gaps in our understanding of how and why they occur. Is, for instance, the distension of the venules and capill. aries due to mechanical obstruction or to active dilatation ? GIBSON 19 believes that endothelial proliferation causes the venous distension and that the capillary micro-aneurysms develop later. In this he is supported by BECKER and POST,20 who found capillary changes, including micro-aneurysms, in the retinae of eyes with naturally occurring occlusion of 4. Knisely, M. H., Bloch, E. H., Eliot, T. S., Warner, L. Science, 1947, 106, 431. 5. Friedenwald, J. S. Amer. J. Ophthal. 1949, 32, 487. 6. Ashton, N. Brit. J. Ophthal. 1950, 34, 38. 7. Friedenwald, J. S. Amer. J. Ophthal. 1950, 33, 1187. 8. Ashton, N. Postgrad. med. J. 1950, 26, 391. 9. Ballantyne. A. J., Lowenstein, A. Trans. ophthal. Soc. U.K. 1944, 63, 95. 10. Ashton, N. Brit. J. Ophthal. 1949, 33, 407. 11. Kimmelstiel, P., Wilson, C. Amer. J. Path. 1936, 12, 83. 12. Allen, A. C. Arch. Path. 1941, 32, 33. 13. Friedenwald, J. S. Trans. Amer. Ass. Ophthal. 1948, 53, 73. 14. Opie, E. L. Special Cytology. New York, 1928. 15. Frehner, H. U. Thesis. University of Zürich, 1950. 16. McCulloch, J. C., Pashby, T. J. Brit. J. Ophthal. 1950, 34, 495 17. Hauum, S. Acta ophthal., Kbh. 1939, suppl. 16, p. 3. 18. Barnes, R. H. Amer. J. med. Sci. 1950, 219, 368. 19. Gibson, G. G. See Beetham, W. P. Trans. Amer. Ophthal. Soc. 1951, 48, 205. 20. Becker, B., Post, L. T. jun. Amer. J. Ophthal. 1951, 34, 677.