Most pathological conditions can cause retinal vascular lesions. Retinal vascular involvement can lead to blindness.
The severity of changes in the retinal arteries in hypertensive retinopathy is associated with the level of total blood pressure:
- at stage I of hypertensive retinopathy, moderate narrowing of arterioles and a light reflex from the arteries of the "silver wire" type are noted
- stage II hypertensive retinopathy is characterized by the intersection of arteries and veins, solid exudates, and streak-like hemorrhages
- stage III of hypertensive retinopathy is characterized by retinal edema, hemorrhages, and foci in the form of cotton wool lumps, which are formed as a result of local ischemia of nerve fibers
- at stage IV of hypertensive retinopathy, the same signs are observed as at stage III of hypertensive retinopathy, and, in addition, edema of the optic nerve head, often with an accumulation of solid exudates in the macular region in the form of a star
Lesions in the form of lumps of cotton wool, when viewed from the retina, are the hallmarks of malignant hypertension. Foci in the form of cotton wool lumps can also be found in cases of anemia, leukemia, collagenosis, dysproteinemia, infective endocarditis, diabetes mellitus.
Cotton wool lesions are also common in acquired immunodeficiency syndrome (AIDS). Other ophthalmic manifestations of AIDS include cytomegalovirus retinitis and retinal vein periphlebitis.
Diabetic retinopathy is divided into two types:
- exudative retinopathy - characterized by the formation of microaneurysms, hemorrhages, foci in the form of cotton wool lumps, solid exudates, bypass microvessels inside the retina, and venous bleeding
- proliferative retinopathy - characterized by the presence of neovascularization and macular edema, which lead to a decrease in visual acuity to 20/200 or more; in such patients, panretinal photocoagulation is successfully used to slow the progression of blindness
With embolism (occlusion) of the central retinal artery, a retinal infarction (ischemic stroke) occurs. This leads to permanent blindness on the side of the ischemic retinal injury. When blockage (occlusion) of the central retinal artery in the fundus reveals:
- uneven narrowing of retinal veins
- the retina itself is milky white
- macula appears dark cherry as a result of visualization of the choroid itself
Occlusion (embolism) of the central retinal artery is a medical emergency. To enhance blood flow, paracentesis of the intraocular fluid is performed. Paracentesis lowers intraocular pressure. If atheromatous changes are detected in the internal carotid artery on the side of the affected eye, the aorta, or heart, embolism of the central retinal artery is suggested. Occlusion (embolism) of the central retinal artery can also develop when:
- giant cell (temporal) arteritis
- conditions accompanied by increased blood viscosity
Monocular, transient visual impairment (transient blindness) may portend central retinal artery occlusion and/or impending ischemic stroke. Patients with symptoms of transient visual impairment (transient blindness) need hospitalization and supervision by a neurologist and vascular neurosurgeon.
Venous retinopathies can also cause visual impairment in patients. Occlusion (blockage) of the central retinal vein and its branches (accompanied by arterial hypertension) and retinopathy with venostasis (obstruction of venous outflow of blood) can be caused by a decrease in pressure (due to a decrease in retinal perfusion). This pressure reduction is facilitated by:
- occlusive lesions (embolism) of the carotid artery on the side of the same name
- pulseless disease
Systemic coagulopathies (thrombocytopenia and disseminated intravascular coagulation) lead to retinal hemorrhages or clotting of blood in capillaries located in the macular region. Systemic coagulopathy is sometimes accompanied by hemorrhage into the choroid itself with retinal detachment. At the same time, patients complain of blurred images due to local loss of the visual field (scotoma).
Retinal vascular anomalies are rare. Retinal vascular anomalies include:
- telangiectasia (Coates disease)
- retinal angiomatosis (Hippel's disease)
- arteriovenous cavernous aneurysm (cavernous arteriovenous malformation with Wyburn-Mason syndrome)
In addition to vascular lesions (arteries and veins), other changes in the retina can also impair vision. The most significant of these is retinal detachment or rupture.
There are also several types of retinal degeneration. These include such changes in the retina as:
- Retinitis pigmentosa
- Degeneration of Bruch's membrane
- Extensive degeneration
- Degeneration of the outer retinal layers
- Degeneration of the inner retinal layers
With retinitis pigmentosa, the degeneration of the outer receptor layer and the adjacent pigment epithelium is hereditary. Retinal degeneration of the eye is accompanied by loss of night vision, followed by impairment of peripheral and, ultimately, central vision. Retinal degeneration can develop as a result of certain systemic diseases:
- abetalipoproteinemia (Bessen-Kornzweig syndrome)
- neuronal lipofuscinosis (Batten-Mayo disease)
- Refsum disease
- Kearns-Sayre syndrome
Degeneration of Bruch's membrane
Bruch's membrane protects the pigment epithelium adjacent to rods and cones. Degeneration of the Bruch's membrane leads to the formation of angioid stripes (tears) that run from the disc to the equator.
Angioid bands are often a sign of extensive degenerative changes occurring in the elastic connective tissue of any location. Extensive degeneration occurs when:
- elastic pseudoxanthoma
- Paget's disease
- lead poisoning
- familial hyperphosphatemia
Degeneration of the outer retinal layers
Degeneration of the outer retinal layers can occur as a complication while taking phenothiazine drugs. These drugs can bind melanin in the pigment layer and therefore should be used in minimal therapeutic doses. In patients who take such drugs for a long time, it is necessary to carry out color perimetry with red and white objects every three months to exclude the occurrence of degeneration of the outer layers of the retina.
Degeneration of the inner retinal layers
Degeneration of the inner retinal layers can be a side effect of hingamine and hydroxychloroquine.
Elevation or swelling of the optic disc is caused by the following factors:
- papillitis of the optic disc
- druses of the optic disc
- infiltration of the optic disc by malignant cells, etc.
True edema of the optic nerve head, caused by swelling of axons and stasis (congestion) of axoplasm, develops with an increase in intracranial pressure of the cerebrospinal fluid (CSF). Increased intracranial pressure is transmitted by CSF into the subarachnoid space, which surrounds the optic nerve (along its path from the cranial cavity to the orbit). Visual acuity at the beginning of the edema of the optic nerve head against the background of increased intracranial pressure decreases slightly. The patient has a transient sensation of darkness before the eyes, narrowing of the visual fields, and an increase in blind spots. Vascular changes in the form of hyperemia, venous stasis, and hemorrhage with edema of the optic nerve head are secondary. The presence of a spontaneous venous pulse on the disc indicates the absence of an increase in intracranial pressure.
Pseudo-edema of the optic discs is called congenital swelling of the discs due to the formation of vitreous tissue (drusen) or hyperopia.
Papillitis is a swelling of the disc associated with optic neuritis. Papillitis in patients leads to early loss of vision. Papillitis can develop in the following cases:
- in inflammatory processes of the optic disc
- if the optic nerve demyelination (multiple sclerosis, neuromyelitis optica,)
- with degeneration of the optic disc (Leber's optic neuropathy)
- with infiltration of the optic disc by malignant cells
- for vascular lesions of the optic disc
It is important to distinguish papillitis from retrobulbar neuritis. Retrobulbar neuritis is characterized by foci of demyelination in the nerve (visible on high-field MRI), which at the onset of the disease are not accompanied by changes in the fundus and the optic nerve head itself. Retrobulbar neuritis leads to loss of vision and loss of pupil response to light. Comparison of the direct reaction of the pupil to light with the indirect (involuntary reaction) is important for the localization of the lesion of the afferent link. The test to detect this reflex is sometimes called the flash test. The pupil of Markus Gunn is called the pupil, in which the indirect reaction to light is more pronounced than the direct one.
Retrobulbar neuritis must be distinguished from the loss of vision that occurs in some patients with hysteria. Binocular vision in such patients does not suffer, there is no defect in the afferent reaction of the pupil to light. A history of injury, drug abuse, exposure to toxic substances, or alcoholism is important for the diagnosis of optic neuritis. In young people with idiopathic optic neuritis (inflammatory or retrobulbar), the risk of developing multiple sclerosis is approximately 30–40%. In the elderly, the main cause of decreased visual acuity and loss of visual fields is optic nerve infarction (anterior ischemic optic neuropathy). Optic nerve infarction (anterior ischemic optic neuropathy) occurs in older people with giant cell (temporal) arteritis, non-arteritis arteriosclerosis, or posterior ciliary artery embolism.
Most optic nerve lesions are accompanied by discoloration of the optic nerve. There are three reasons for the blanching of his optic nerve head:
- hereditary familial optic nerve atrophy
- primary atrophy of the optic nerve, which develops as a result of the death of retinal ganglion cells and axons
- secondary atrophy of the optic nerve with papillitis and chronic edema of the optic nerve head