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EYE CHANGES IN VASCULAR PATHOLOGY

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).


Date: 2015-02-03; view: 1258


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