Atlas fundus oculi / by William Holland Wilmer.

  • William Holland Wilmer
Date:
1934
Catalogue details

Licence: In copyright

Credit: Atlas fundus oculi / by William Holland Wilmer. Source: Wellcome Collection.

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    occupied the attention of many investigators, and in spite of the excellent investigations that have been devoted to it, there still remain questions for solution. The difficulty arises largely from the fact that our knowledge of Bright’s disease is incomplete. At the present time the tendency is to recognize at least three forms of the affection; namely, hemorrhagic Bright’s disease, or glomerular nephritis; degenerative Bright’s disease, or nephrosis; and arterio¬ sclerotic Bright’s disease, or nephrosclerosis. The acute forms of hemorrhagic, or diffuse glomerular nephritis, such as those which follow scarlatina or tonsillitis, are not often associated with extensive changes in the retina. Occasionally hemorrhages and small exudates are observed. The margins of the optic disks are sometimes blurred; the arteries and veins often appear tortuous, and edema of the retina is seen with remarkable regularity. The origin of the acute retinitis is not altogether clear. It usually occurs in those patients who have an infection due to hemolytic streptococci, who have a sudden and marked rise in both systolic and diastolic blood pressure, and who have subcutaneous edema generally ascribed to the effect of a toxin upon the blood vessels. Any of these factors acting alone or in combination might, therefore, be held responsible. In favourable cases the retinitis disappears as the patient recovers. The edema of the retina can be interpreted as a part of the generalized edema so characteristic of this condition. It subsides as the anasarca disappears, but either the edema of the retina recedes more slowly or it may be detected more readily in the retina than elsewhere, for distinct evidence of edema of the fundus may be seen long after all signs of edema of the subcutaneous tissues have vanished. The retrogression of edema of the retina, therefore, forms a delicate index of complete recovery from this symptom in acute glomerular nephritis. If the acute glomerular nephritis progresses to the active or nephrotic stage, the edema of the retina may increase. It is interesting to recall that uncom¬ plicated glomerular nephritis may reach the terminal stage without producing further damage to the retina or choroid than an occasional small exudate or hemorrhage; but it frequently happens, particularly in the patients who have persistent and marked hypertension, that varying degrees of choked disk are noted, and extensive hemorrhages and exudates are seen in the retina. When arteriolosclerosis complicates glomerular nephritis, the combination results in the most pronounced forms of hemorrhagic and exudative lesions in the retina with extreme grades of choked disk. In the nephrotic forms of Bright’s disease, the blood vessels are spared injury, and the blood pressure is not elevated. In the uncomplicated instances of this type of Bright’s disease, there are no hemorrhages, exudates, or vascular changes in the retina; edema sometimes involving the margins of the disks may be the only alteration in the fundus. The arteriosclerotic form of Bright’s disease, or nephrosclerosis, is often accompanied, early in its course, by the most astonishing changes in the fundus. Here one sees all the phases of arteriolar disease, from the early narrowing of the vessel with compression at the arterio-venous crossing to complete occlusion of branches of retinal and choroidal vessels. Hemorrhages and exudates of all types are common, and the most extreme grades of edema of the nerve head are observed. The grave nature of the malignant form of arteriolosclerotic Bright’s disease may