Traumatic cataract. Penetrating wounds of the anterior part of the eyes are often complicated by traumatic cataract. It occurs in integrity impairment of the anterior lenticular capsule that results in passing of the anterior chamber humor into the lens causing swelling of the lenticular fibers and their opacity.
But there are cases when the lens is not clouded. It is observed in small injuries of the anterior capsule due to its fast regeneration.
Posttraumatic lenticular opacity develops gradually in most patients, such "stationary" cataracts are indicated for surgery at the most optimum time — 2-3 months after trauma when simultaneous implantation of the artificial lens is possible.
When there is fast swelling and prolapse of the lenticular masses into the anterior chamber, and intraocular pressure increases, then urgent surgery — extraction of the swollen cataract — is necessary.
Traumatic iridocyclitis. The penetrating wounds of the eye-ball may be accompanied by inflammatory reaction of the vascular membrane. There are serous, purulent and fibrinous-plastic iridocyclitis.
Serous iridocyclitis occurs on the 2nd-3rd day after the wound. It should be considered as eye tissue response to the trauma: pain in the eye, pericorneal injection, iris hyperemia, tenderness of the ciliary body area on palpation, precipitates. The degree of mark-edness depends on the character of the trauma. The course of acute serous iridocyclitis is favourable: all signs of iridocyclitis subside under the influence of treatment and the eye is all right.
Purulent iridocyclitis manifests on the 2nd-3rd day after trauma by increased irritation of the eye. There is intensive mixed injection and hypopion in the anterior chamber. The colour and pattern of the iris change due to hyperemia of its vessels. Not infrequently yellow-grayish film of exudates appears in the pupil area. The eye is tender even to slight touch.
Treatment includes massive antiinflammatory therapy with broad spectrum antibiotics subconjunctively twice a day as well as intramuscularly or intravenously, hemodesis autohemoosmothe-rapy, dehydratation and desensitizing therapy.
Now antibiotics are used as antibacterial eye therapeutical films (ETF) into the conjunctival sac twice a day instead of painful subconjunctival injections. If there is no decrease of symptoms during a few days, we administer paracentesis with washing out of the anterior chamber and introduction of gentamycinum sulfate.
Endophthalmitis is a more severe form of purulent infection. Besides marked mixed injection there is conjunctival chemosis. On investigation in the transmitted light we observe green-yellowish or green-gray reflex from the eye fundus instead of red one. It is evidence of infection in the vitreous. Abscess of the vitreous is formed, vision drops to photoperception or to the zero. As a rule the prognosis is unfavourable.
Treatment is also a complex one including antibiotics, sulfanilamides, corticosteroids as well as nonspecific, dissolving disintoxication and generally strengthening therapy: autohemo- and lacto-therapy, fibrinolysine, pyrogenalum, glucose, urotropinum, sodium chloride, vitamins. We use antistaphylococcus plantal gammaglobulin which is immunologic remedy of the direct action. It brings about passive but quickly occurring immunity. To provide necessary therapeutic effect antibiotics (gentamycine) are introduced directly into the place of infection — intravitreally. It is possible to introduce antibiotics intraarterially into the system of the ocular artery in retrograde way via supraorbital artery, continuous perfusion of the vitreous with the corresponding solution of antibiotics.
Lately radical surgical method of endoophthalmitis treatment has been widely used, i.e. closed vitrectomy with intravitreal introduction of gentamycine and hordox. If the treatment proved unsuccessful, the blind eye is removed by evisceration. The operation consists of the cornea dissection with linear knife and scissors with further curretage of suppurative inflamed inner membranes and eye content with a special spoon. Prosthesis of the conjunctival cavity is performed in 2-3 weeks.
Panophthalmia. In severe infection the inflammatory process may involve all membranes of the eye. There are severe pains in the eye, oedema and hyperemia of the eyelids, chemosis of the conjunctiva. Inflammation of the orbit tissue develops and as a consequence exophthalmia and limited mobility of the eye-ball. The cornea becomes purulent infiltrated up to complete dissolution. The disease is accompanied by general malaise, headache, rise of temperature.
As a rule in panophthalmia the eye can't be saved. The aim of the treatment is not to save the eye but prophylaxis of meningitis. Therefore it is recommended to perform evisceration of the eyeball.
Fibrinous-plastic iridocyclitis after the penetrating wound has, as a rule, a chronic character. In spite of intensive anti-inflammatory treatment the damaged eye continues disturbing the patient. There are pericorneal injection, precipitates on the posterior cornea surface, posterior synechia, sometimes adhesion or closing of the pupil. Nevertheless the intraocular pressure subsides, the eye is moderately tender on palpation which is indicative of chronic slow inflammation of the ciliary body. Object vision disappears, there is only photoperception, more often with wrong light projection. Such an eye becomes dangerous for another undamaged eye where similar inflammation may develop. It is called sympathic inflammation. In such cases iridocyclitis on the damaged eye is called sympathetic.
Sympathic inflammation. Sympathic inflammation is a specific form of chronic malignant inflammation of the choroid of the undamaged eye. It develops in slow posttraumatic (sympathetic) iridocyclitis on the second eye, having had trauma.
Etiology and pathogenesis. Under the name "sympathic opth-talmia" it was described by Mackenzie in 1835 but till now its etiology and pathogenesis remain obscure. At first many scientists considered microbe infection to be the cause of sympathic inflammation, thinking it is very specific and passing into another eye via blood (theory of Leber).
At present most of ophthalmologists are for autoimmune mechanism of sympathic inflammation. The idea was first suggested by S. S. Golovin in 1904, later on it was supported by Elshing (1910) and only now it was confirmed thanks to achievements of the modern clinical immunology. Autoimmune theory runs as follows: there is dysfunction of hematoophthalmic barrier in penetrating wounds of the eye especially with prolapse of the choroid. Due to auto-sensitization tissue and humoral antibodies are produced to uveo-retinal antigens affecting the cells of both damaged and healthy eye resulting in development of sympathic inflammation.
Sympathic inflammation occurs rarely. Untill 1910 its rate among penetrating wounds didn't exceed 3%, then it decreased and last 30-40 years it is on the same level making about 0.2%. In spite of this fact the severe outcomes attract constant attention of ophthalmologists to this disease.
Sympathic inflammation occurs more often after penetrating wounds connected with trauma, rarely after intraocular operations. The disease may develop at any time after eye trauma but not earlier than in two weeks.
Clinical course. The disease may be manifested in three forms of inflammation of the vascular membrane (serous, fibrinous-plas-tic iridocyclitis) and not infrequently in combination with neu-roretinitis (a mixed form).
Sympathic serous iridocyclitis is characterized by mixed injection of the eye-ball, whitish precipitations on the posterior surface of the cornea, oedema and hyperemia of the iris, opacity of the vitreous. In a mixed form there are hyperemia, blurred optic disc borders, vein dilatation on the eye expansion of the blind spot in campimetry and narrowing of the visual field to colours.
The fibrinous-plastic form of iridocyclitis is characterized by marked mixed injection of the eye-ball, quick formation of anterior and posterior synechia, exudates in the anterior chamber and pupil area with its further closing. It results in disturbance of in-troocular humor outflow from the posterior chamber into the anterior one — secondary glaucoma occurs, which leads the eye to destruction.
Sometimes in sympathic inflammation we observe atrophy of the ciliary body promoting reduction of intraocular humor secretion. Hypotonia occurs, the eye diminishes in size and then wrinkles till complete atrophy of the eye-ball.
Chorioditis has a clinical course of typical exudative chorioiditis: large white-eyellowish foci covered by oedematous retina are formed on the eye fundus. This form is often combined with neu-roretinitis.
Diagnosis of sympathic inflammation is not difficult if during first weeks and months after severe penetrating wound complicated by slow uveitis, the second eye develop characteristic picture of serous, fibrinous-plastic iridocyclitis or chorioneuroretinitis. Difficulties may arise in unclear symptoms or at later terms after injury (several years).
Differentiated diagnosis. Sympathic inflammation should be differentiated from sympathic irritation. The latter is connected with paraocular response and manifested by lacrimation, photophobia, conjunctival or pericorneal injection of the eye-ball. However, there are no objective signs of inflammation in the anterior and posterior parts of the uveal tract characteristic of sympathic ophthalmia.
Prophylaxis of sympathic inflammation consists of thorough surgical treatment of the penetrating eye wounds on the microsurgical level (in order to reduce severe posttraumatic complications) and intensive anti-inflammatory therapy at early terms after trauma. If the treatment is ineffective and inflammation of the injured eye persists and it loses its functions completely, the injured eye should be enucleated.
In sympathic inflammation the damaged eye should be removed only if it is blind. If there is object vision in it, enucleation should be avoided as further this eye may see better.
Treatment of sympathic inflammation is difficult. Sympathic inflammation may be sometimes stopped because of application of new medical preparations, especially corticosteroids and immuno-correctors. It speaks for autoimmune origin of this disease.
Corticosteroids are administered as subconjunctival or para-bulbar injections, instillations and per os according to the scheme. Besides, antibiotics are administered under the conjunctiva and intramuscularly; sulfonamides, desensitizing remedies, indometaci-num, voltaren per os; midriatics are administered locally (atropi-num, skopolamin) or under the conjunctiva (adrenalinum, mesaton).
In the period between recurrences surgical treatment is indicated — antiglaucomatous operation, removal of the supracrystalline film, extraction of the complicated cataract, vitrectomy.
Intensive anti-inflammatory therapy should be given in the postoperative period to prevent exacerbation of the disease.