Pathologies of fundus of the eye have immense diagnosis and prognostic value in hypertonic disease. The changes of retinal vessels are a model of vascular changes developing in the less accessible organism's regions. Branches of the central artery of the retina are arterioles and precapillaries by their own structure and calibre. Thus, the ophthalmologist can immediately observe intimate vascular processes occurring in the retina and which are inaccessible to clinician's eye in other organs. Owing to this, he can in the life time determine functional condition of arterioles — the most important organ of blood pressure regulation.
Hypertensive changes of the retina become apparent in so early period and they are so typical that the ophthalmologist can primary diagnose hypertonic disease in patients which are unaware of their disease.
There are distinguished the following forms of changes of fundus of the eye in hypertonic disease: hypertonic angiopathy; hypertonic angiosclerosis; hypertonic retinopathy; hypertonic neuroreti-nopathy.
In hypertonic angiopathy, dilatation and sinuation of veins, constriction of arteries are observed. The ratio of artery calibre to vein decreases to 1:2, 1:3. Puller-shaped sinuation of macular veins (Ovist's symptom) which is the index of stasis in capillary-vein piece of vascular net of the retina. Conic constriction of the vein on either side of the artery in the point of their cross (1st symptom of Saluse — Hunne) is possible.
Hypertonic angiosclerosis of the retina becomes apparent in inequality of arteries calibre, hardening of vascular paries (as a result of this the artery shapes of white, silvery band (silver wire symptom). Reflex line with goldish color (copper wire symptom) arises in the artery by plasmatic impregnation with separate lipid sediments. The vein arciformly bends and is pushed back deep into the retina (2nd symptom of Saluse — Hunne), sometimes it grows indistinct or is interrupted in the center of the arch (3rd symptom of Saluse — Hunne).
In hypertensive retinopathy, blur of the retina, its oedema in per-ipapilar, perivascular and macular regions predominantly arise. With retinoscopy oedematic parts of the retina reflect light, bright highlights arise. Sometimes blur in macular region is enclosed by haemorrhages.
Hypertensive neuroretinopathy develops on both eyes. The visual functions are sharply reduced. Oedema of the optic disc and retina, haemorrhages and white foci are observed with ophthalmoscopy. Haemorrhages are small, pointed. They arise by diapedesis way. Aside from this, haemorrhages have place by the way of large vessels in inner layers of the retina.
It was considered before that the patient's life expectancy in hypertensive retinopathy makes out 2-3 years. But now, it is possible to achieve a considerable improvement of general state of patients being accompanied with total or partial reverse process of hypertensive changes in fundus of the eye in many cases owing to timely carried out effective treatment.
In late stages of hypertonic disease, the picture of papillary stasis can arise because of increase of intracranial pressure; atrophy of the optic nerve evolutes later.
In all stages of hypertonic disease development, but oftener in II and III stages of its development, evolution of central vein thrombosis and acute occlusion of the central artery of the retina are possible. Both the basic trunk of the artery or the vein and their branches can be affected.
It is necessary to remember about possibility of basic retrobulbar neuritis because of circulatory disorders in the optic nerve in patients with hypertonic disease of II or III stages.
Besides secondary atrophy of optic nerves (after retinopathies, papillary stasis), primary atrophy may develop because of disorders of blood circulation and trophies processes in patients with III stage of hypertonic disease.
In late stages of disease affection of optic tracts and centers, development of different forms of hemianopsies (next to always with macular region preservation), central and peripheral hemian-optic scotomae evolute as the result of appearance of malacia and haemorrhages foci in the brain.
Sometimes, changes of vessels of anterior part of the eye, which are determined with biomicroscopy, arise with absence of changes in fundus of the eye. Dilatation and puller-shaped sinuation of conjunctiva vessels, microaneurysms, dilatation of perilimbusic net noose have place in early stages of hypertonic diseases.
Spastic changes of vessels being accompanied with small haemorrhages and perivasal oedema prevail in later stages of disease.
With biomicroscopy, filamentous or granular destruction of the vitreous is observed in patients with hypertonic disease. Haemorrhages and fibrinose effusion in the form of float flakes, diffuse blur are often revealed. This changes usually have place in neuroretin-opathies, thromboses of retina vessels.
Thus, it is possible to differentiate functional stage of hypertonic disease from organic, to reveal changes in brain vessels by the state of fundus of the eye and bulbar conjunctiva. But strict division of fundus of the eye picture in accordance of stages of hypertonic diseases is impossible.
In renal hypertension, transsudative syndrome occurs as a result of sharp spasm of the artery. Constriction of arteries, dilatation of veins without marked sclerotic changes with a large number of exsudative foci, plasmorrhages and haemorrhages are detected in fundus of the eye. Star figure in macular region is typical. Retinal detachment can arise.
Fundus of the eye pathology is less marked in children and adolescents suffering from hypertonic disease. It arises in constriction of retinal arteries and dilatation of veins. In case of secondary renal hypertension ophthalmoscopic picture is similar to that one in adults.
Treatment for hypertonic changes in fundus of the eye consists of compensation of hypertension previously. Local treatment is symptomatic.
Atherosclerosis manifests itself in sclerosis of small vessels of the anterior part and fundus of the eye, subconjunctival haemorrhages, haemorrhages in the retina and the vitreous.
Examinations of the fundus of the eye have a vital importance in toxemia of pregnancy. Ophthalmoscopic changes are the same as in renal retinopathy. In marked oedema transsudative retinal detachment can develope in one or both eyes. Thrombosis of the central vein of the retina or its branches is possible.
In some cases, fundus of the eye changes are the only indication for therapeutic abortion. Absolute indications are: retinal detachment being caused with toxemia of pregnancy, retinopathy and neurorethinopathy, thrombosis of the central vein of the retina.
CHANGES OF FUNDUS OCULI IN BLOOD DISEASES
Ophthalmoscopic changes are typical for some diseases and give assistance in diagnosis.
Leukosis. General painless and yellowish tint of fundus of the eye, dilatation and sinuation of vessels, arising of white wadded like foci and haemorrhages, white membranes along vessels are observed. This membranes are leukocytar infiltration of paravascular areas and vascular walls.
Pappilary stasis of the optic nerve and exophthalmos arise due to affection of eye-socket bones and with arising of leukemic infiltration in the skull cavity, retrobulbar area. Diplopia, limitation of eye mobility can develope.
General treatment (cytostatics, corticosteroids) can result in resorption of infiltrates and haemorrhages, recovery of optic functions in a period of remission.
Anemia. The fundus of the eye is pale with different tints (from yellowish to cyanotic). Vein pulse can be observed. Peripapillar oedema of the retina is most often determined. Plasmorrhages, pre-retinal, subretinal and retinal haemorrhages arise in severe cases, they usually localize alongside large vessels and don't involve macular region.
Genera! treatment results in reverse changes in the fundus of the eye.
OCULAR MANIFESTATIONS IN ENDOCRINE DISEASES
AND METABOLISM DISORDERS
Exophthalmic goiter. Typical changes of the optic system are observed in exophthalmic goiter: bilateral exophthalmos, but first it can develop in one eye. Reduction (eye comes in eye-socket with pressure), retraction of upper eyelid, eye slit dilatation imparting frightened look to a patient (Dalrimple's symptom), lag of the eyelid when looking down (Grefe's symptom), infrequent nictitation (Shtelfag's symptom), convergence insufficiency (Mebius' symptom) are typical for exophthalmos with diffuse toxic goitre. Exophthalmos can result sometimes in dryness of the cornea or keratitis development.
For prophylaxis of the complications mentioned above, vitamin eye drops, ointments, sometimes temporary suture of eyelids is carried out.
Oedematic or malignant exophthlmia develops against a background of superfluous secretion of thyrotropic hormone by anterior lobe of the pituitary gland, sometimes after thyreoidectomia. Persons older than 40 suffer from this disease. Exophthlmia may be unilateral or bilateral, it is so marked sometimes that spontaneous dislocation of the eyeball can arise. Sharp pain, diplopia and limitation of eye mobility, more often up-side and out-side, presence of inflammation and chemosis of the conjunctive, oedema of orbital and periorbital tissues are typical. The disease is quite often complicated by keratitis with inclination to erosions and corneal distruction.
Besides of symptomatic and hormonal agents, roentgenotherapy of pituitary body and orbital region is prescribed, decompressive trepanation of the eye-socket is carried out in some cases.
Parathyreoid gland function disorders cause cataract (more often zonular one), as well as tetany, spasmophilia, rachitis, renal insufficiency are observed at the same time. Cataract development can be suspended by timely treatment (thyroid glands agents, intravenous injection of 5-10% solution of calcium chloride).
Diabetes mellitus. Ocular lesions reflect pathogenesis of the disease and they are one of main causes of irreversible blindness now. Changes in the fundus of the eye are especially typical, such as diabetic retinopathy, simple and proliferating diabetic retinopathy.
Angiopathy. Unevenness of vascular calibre, microaneurysms formation are registered.
Simple diabetic retinopathy. Formation of simple diabetic retinopathy occurs at the background of marked disorders of lipid metabolism. During its development proper vascular changes take place (sclerosing of arteriolar vascular net of the eye with next neglect of capillaries and dystrophic changes in the retina).
Proliferating diabetic retinopathy occurs at the background of decreased immunological status of the organism and it is accompanied with autoimmune disorders, increase of quantity of immune complexes being circulated in blood and their sedimentation in vascular walls of the eye. This causes progressive character of proliferative process tendency. In the period of its evolution, intravascular thromboembolic changes occupying arterioles, capillaries and veinules result in marked anemization of the eye, affection of vascular walls with following neovascularization.
Vascular aneurysms, haemorrhages and foci of opacity of the retina, phenomena of thrombosis of vessels, exudates in yellow spot region, proliferation of connective tissue and new-formed vessels, retinal detachment are determined in the fundus of the eye, hemo-phthalmia often develops.
Biomicroscopic examination of the anterior part of the eye is of great importance now in diagnosis of vascular pathology in diabetes mellitus. Disorders of blood circulation in conjunctival vessels are diagnosed earlier than changes in the fundus of the eye. Newly formed vessels — rubeosis, growing into the corner of the anterior chamber are often revealed in the iris. Fibrinous-plastic iridocyclitis develops in some patients. It is necessary to remark a big frequency of cataracts and glaucomas (primary, secondary, neovascular).
Treatment of diabetic retinopathy includes pathogenetic, medi-camentous, immunocorrecting therapy. Fotolasercoagulants, cri-opexia are used too. Treatment for cataract, glaucoma, hemoph-thalmia is surgical.
Now many eye changes with different forms of genetically-determined disorders of the metabolism are known and in most cases only optic symptoms are the earliest signs of organism's metabolism pathology with complete diagnosis at early stages.
Application of great doses of retinol (vitamin A) can detain development of the process.
Pathology of aminoacid metabolism is accompanied by appearance of albinism. Photophobia, failing of visual acuity, nystagmus, ametropia are noted. Irides are bright-grey or blue, fundus of the eye is pale-pink or orange; vessels of choroid are seen well on it. It is recommended wearing of defensive spectacles, early correction of ametropia.
Niemann — Pick's disease (reticuloendothelial sphingomyelinosis). The main eye's symptom is degeneration of macula lutea. In the central area of the retina it is found out white-grey oval focus with dark red spot in the centre (symptom of a "cherry seed"). The optic disc is pale. There may be exophthalmos, nystagmus.
Tay — Sachs' disease (sphingophospholipoidosis). Similar changes in the area of macula lutea are found. The optic nerve atrophy develops in the late terms of the disease. There are no effective methods of treatment.
Eosinophilic granuloma in the bones of orbit can develop due to disturbances of lipoproteid metabolism. By X-ray examination it's found out bones' destruction, shaped like a geographical map. Exophthalmos appears. The upper lid is oedematous cyanotic, dense, palpebral fissura is narrowed. The eyeball is dislocated, its mobility is failed. It is engorged pupilla, and then the optic nerve atrophy occurs.
It is necessary to differentiate the disease with orbit sarcoma. The treatment is X-ray and hormonal therapy. Prognosis is favourable.
Hypovitaminosis belong to metabolism disturbances in which injuries of eyes are observed.
Hypovitaminosis A is one of the main reasons of blindness in the developing countries as a result of xerophthalmia development. First of all in the disease the function of pigmentary epithelium and bacillary devices fail, hemeralopia appears (night blindness). There happens a decreasing of photosensitivity, failing of darkness adaptation process, changing of electroretinogramme, narrowing of the visual field (before all on the colours), fundus of the eye is not changed when hemeralopia.
Then xerosis joins hemeralopia. In the area of opened eye-slit appear triangular-shaped plots of rough, dim, dry dull-white conjunctiva (granulomae of Iskersky — Bito). Xerosis of the cornea begins with punctate keratopathy, oedema, decreasing of its sensitivity. Then destruction of the corneal stroma occurs, ulcers appear, more often on periphery, when severe form of the process, keratomalacia occurs — melting of the cornea with coming out of internal membranes of the eye and lens. Inflammatory phenomena are absent in this case. When secondary infection joins purulent panophthalmitis appears with following wrinkling of the eyeball.
Treatment consists of administration of vitamin A preparations orally or intramuscularly, local instillations of desinfecting drops and ointments of broad-spectrum antibiotics for prophylaxis of secondary infection.
Avitaminosis Bl. Injuries of eyes are caused by failing of sensitive and sympathetic innervation. It is determined eye's irritation, failing of visual acuity. Central opacities in superficial and middle layers are appearing in the cornea. Then the corneal injuries can develop in different forms: disciform keratites with disintegration and insignificant vascularisation of the cornea; circular abscess of the cornea with perforation and coming out of membranes, herpetic keratites, reminding a metaherpetic form. It is also characteristic development of optic nerve neuritis. Choroid is involved in process rarely.
Treatment consists of bringing in vitamin Bl (thiamin) intravenously (1-2% solution) or intramuscularly (6% solution), local application of 0,5% ointment. In case of timely treatment full recovery occurs.
Avitaminosis B2 is characterized by epithelial vascularisation of the cornea, interstitial and ulceral keratitis, which have a slow and comparatively benign course. Treatment consists of prescription of vitamin B2 in a dose of 5-20 mg per day orally and locally as 0.02% solution or subconjunctival injections. Prognosis is favourable.
Avitaminosis E. Narrowing of the cornea and its deformation in a form of keratotonus foundation occurs. It is indicated the use of vitamin E orally, intramuscularly, in a number of cases — surgical treatment (keratoplasty).