OVERVIEW
Hypertensive retinopathy is a common cardiovascular disease. The central retinal artery is the only small artery in the body that can be directly observed in vivo. Therefore, observation of the fundus of hypertensive patients can often help to understand the degree of damage to the heart, kidney, brain and other organs of the patient’s organism, which is of great significance to the diagnosis and prognosis of hypertension.
About 70% of hypertensive patients have fundus changes. Fundus changes have nothing to do with gender, but are closely related to the patient’s age. In hypertensive patients with a chronic clinical course, fundus changes are directly proportional to the duration of the disease. The degree of increase in blood pressure was basically parallel to the fundus changes, and the effect of increased diastolic blood pressure on the fundus lesions was more significant. The refractive status of the eye has an effect on the fundus changes in hypertension, with hyperopia higher than orthopia and myopia lower than orthopia.
Etiology
Elevated arterial blood pressure is the main cause of hypertensive fundus pathophysiologic changes and clinical symptoms.
Symptoms
Hypertensive retinopathy is categorized into 4 stages according to the disease process: vasoconstriction, sclerosis, stenosis and exudation.
1. Vasoconstrictive phase
During the vasoconstrictive phase, the elevated blood pressure stimulates the soft and unhardened retinal arterioles and increases their tone through autoregulation. The younger and more elastic the retinal vessels are, the greater this response. Clinical examination reveals limited stenosis of the retinal arteries, or generalized stenosis if the disease is protracted.
2. Sclerosis
If the elevated blood pressure is rapidly controlled by medication or surgery during the vasoconstrictive phase, the retinal blood vessels may return to normal without permanent lesions. If hypertension persists for a period of time, sclerotic changes will occur. Clinically, sclerotic vessels are characterized by: (1) generalized narrowing of the arteries; (2) arteriovenous compression; (3) changes in the light reflection of the vessel wall due to wall sclerosis; (4) vessel tortuosity; and (5) increased angulation of the arterioles and arteriolar branches. Although these retinal vascular changes can be found in some “normal” individuals, they are certainly more common in hypertensive patients. These changes are associated with old age in both types of individuals. Clinical features such as “arterial straightening, arterial thinning, changes in arteriovenous crossings, and widening of arterial wall reflections” are not reliable indicators of hypertensive vascular disease.
3. Arterial stenosis
Generalized narrowing of the small arteries, with or without limited constriction, is a useful indicator of hypertension. Stenosis is extremely difficult to quantify. Some authors compare arterial diameter with venous, but venous dilatation is often not a good reference. Early stenosis is most commonly seen in the smaller branches of the retinal arteries from level 2 or 3 onwards. It is important to note that many ocular conditions such as high myopia, uveitis, and retinal dystrophy can lead to retinal stenosis. The examiner must use clinical judgment when estimating arterial stenosis.
Changes at the arteriovenous crossing are more objectively evaluated than arterial stenosis. Anterior to the arterial travel through the vein, a sign of arteriovenous compression is seen, but not vice versa. This feature can be categorized into 3 levels: (1) mild arteriovenous compression, (2) moderate arteriovenous compression, and (3) branch vein obstruction. In mild compression, the veins under the artery are deviated, and there is an early concealment phenomenon. In moderate compression, the veins behind the artery become pointed, narrowed, and shifted. The veins may be mildly distended a little beyond the crossing, which is called a venous “ramp”. In grade 3 damage, bleeding and oozing due to venous obstruction is seen at the distal end of the arteriovenous crossing.
The degree of arterial wall sclerosis is often estimated by the degree of light reflection in the vessel wall. Although this change is also seen in older individuals, it still provides a useful parameter for estimating the effect of chronic hypertension on the vessel wall.
Arterial tortuosity seen in chronic hypertension: increased pressure in the lumen and progressive hyalinization and fibrosis of the muscle fibers, resulting in increased arterial length. Retinal arteries travel in a tortuous fashion within the retina, but should be differentiated from a common benign retinal arterial tortuosity.
Another useful sign of hypertensive vascular disease is the angle of the arteries at the large branches, especially the second or third level branches. The higher the blood pressure, the greater the angle of the branches. In mild cases, the angle of the branching arteries is 45° to 60°, in moderate cases it is 60° to 90°, and in severe cases it is greater than 90°.
In the sclerotic phase of hypertensive retinopathy, there may be no active rupture of the blood-retinal barrier as measured by fluorescent angiography and vitreous fluorescence photometry. However, if there is a sudden or progressive increase in pressure, the patient may enter the exudative phase of hypertensive retinopathy.
4. Exudative phase
The exudative phase of hypertensive retinopathy may accompany or follow the vasoconstrictive or sclerotic phase of hypertensive choroidopathy or hypertensive retinopathy. The presence of this phase indicates that the retina’s perfusion pressure has exceeded its physiologic self-regulatory mechanisms, resulting in disruption of the blood-retinal barrier, leakage of fluid and blood cells from the circulatory system, vessel wall breakdown and abnormal blood flow, and often ischemia.
One of the early signs of exudative retinopathy is small linear or flame-shaped hemorrhages, mostly within the nerve fiber layer surrounding the optic disc. The linear pattern of the hemorrhages is due to (1) their occurrence in the nerve fiber layer of the retina, and (2) the fact that blood leaking from the vessels extends along the axons of the ganglion cells. The hemorrhage may also be patchy or punctate. If the hemorrhage occurs in the deeper layers of the retina, it has an oval outline because the spread of the leaking blood is limited by the Müller cell protrusions. Occasionally, blood may penetrate the inner border membrane and lie in the subvitreous, with a navicular hemorrhage at the posterior pole.
A hard, waxy exudate indicates vascular leakage of plasma lipoproteins, phospholipids, cholesterol, and triacylglycerols. This exudate is glossy yellow in color, most often located in the posterior pole, and may be stellate in the central area of the macula, radiating from the macula along the Henle fiber layer. In some patients, hard exudates may form a halo around a giant hemangioma or clusters of leaking microhemangiomas.
Absorbent cotton spots are gray or yellow spots with hairy edges, within the retinal nerve fiber layer, mostly located at the posterior pole, especially around the optic disc. Absorbent cotton spot is due to the pre-capillary small artery obstruction, the small arteries supplied by the retina occurs local ischemia, caused by the retinal nerve fibers of the tiny infarcts, so that the nerve fibers of the axial plasma transport is blocked, the axial plasma and the degeneration of the cellular organelles in the formation of the aggregation. The long axis of the cotton-padded spot is often at right angles to the direction of the nerve fiber layer, and is most often located on the superficial surface of the retinal blood vessels. After a period of time, the cotton-padded spot may develop a granular appearance and eventually disappear. The retina becomes thinner and the inner border membrane has a reflective, irregular appearance. These areas are referred to as “patchy depressions,” indicating localized loss of inner retinal structures due to infarction. Fluorescence angiography often shows areas of nonperfusion around the cotton-chip spots, as well as dilated capillaries and microangiomas, and side vessels with candidal vascular changes and fluorescein staining of the retinal tissue.
Examination
Fluorescein fundus angiography reveals dilated and tortuous optic disc capillaries with microangiomas and late fluorescein leakage, and large fluorescein leakage from retinal capillaries, which corresponds to the occlusion of capillaries in the area of the cotton-wool spots and the formation of a small area of nonperfusion, with dilated peripheral capillaries, microangiomas, and fluorescein leakage, which corresponds to the choroid at the Elschnig spot. Capillaries show hypoperfusion or no perfusion, with fluorescein leakage in advanced stages, with thin narrow arterioles and filling tortuous veins.
Diagnosis
Fundoscopy and fundus fluorescence angiography have important applications in understanding the progression of hypertensive fundus changes, and hypertensive retinopathy is categorized into four grades based on the findings:
Grade 1.1
Thinning of retinal arteries and widening of reflective bands.
Grade 2.2
Mainly atherosclerosis, with copper or silver wire-like changes in the retinal arteries and obvious dynamic and static cross-pressure traces.
Grade 3.3
The basis of the above vascular lesions is accompanied by fundus hemorrhage, absorbent cotton spots, and hard exudates.
Grade 4.4
Grade 3 changes plus optic nerve optic disc edema and various complications of atherosclerosis.
Treatment
After effective control of hypertension, optic disc edema and retinal edema, hemorrhage and exudation can be absorbed and subside, and the life prognosis is better than before. Retinopathy should be treated by a specialist.
Prognosis
In general, the more severe the fundus changes, the worse the prognosis. If the fundus changes are mainly atherosclerosis, congestive heart failure, coronary artery sclerosis heart disease, cerebrovascular accident will occur easily, and if retinopathy or optic nerve retinopathy is the main cause, uremia will occur easily.