Acute Iridocyclitis

Acute iridocyclitis begins suddenly. The first subjective symptoms of acute iridocyclitis are sharp pain in the eye, irradiating into the corresponding half of the head, and pain that occurs when touching the eyeball in the projection zone of the ciliary body. An excruciating painful syndrome is caused by profuse sensory innervation. At night, pains increase due to stagnation of blood and compression of nerve endings, in addition, at night, the influence of the parasympathetic nervous system increases. If acute iridocyclitis begins with iritis, the pain is determined only by touching the eyeball. After the addition of the cyclite, the pain is greatly enhanced. The patient also complains of photophobia, lacrimation, difficulty opening the eyes. This corneal triad of symptoms (photophobia, lacrimation, blepharospasm) appears due to the fact that the fullness of the vessels in the basin of the large arterial circle of the iris is transmitted to the vessels of the marginal loop network around the cornea, since they have anastomoses.

With an objective examination, attention is drawn to the easy swelling of the eyelids. It increases because of photophobia and blepharospasm. One of the main and very characteristic signs of inflammation of the iris and ciliary body (as well as the cornea) is pericorneal injection of vessels. It can be seen already with an external examination in the form of a ring of pink-cyanotic color around the limb: hyperemic vessels of the marginal loop network of the cornea gleam through the thin layer of the sclera. With prolonged inflammatory processes, this corolla acquires a purple hue. The iris is edematous, thickened, because of the increased blood filling of radially extending vessels, they become more straight and long, so the pupil narrows, becomes inactive. When compared with a healthy eye, you can notice a change in the color of the full-blooded iris. Inflamed, dilated walls of blood vessels flow through the blood elements, the destruction of which iris acquires shades of green.

In the inflamed processes of the ciliary body, the thinness of the thin-walled capillaries increases. The composition of the produced liquid changes: in it appear the protein, the uniform elements of the blood, the obliterated epithelial cells. With a mild violation of the permeability of blood vessels, albumin predominates in the exudate, while large protein molecules, globulin and fibrin, pass through the walls of the capillaries through abrupt changes. In the light section of the slit lamp, the moisture of the anterior chamber opalesces due to the reflection of light by the suspension of floating protein flakes. With serous inflammation, they are very small, hardly noticeable, with exudative suspension is thick. The fibrinous process is characterized by a less acute current and the production of an adhesive protein substance. It is easy to form a fusion of the iris with the anterior surface of the lens. This is facilitated by the limited mobility of the narrow pupil and the tight contact of the thickened iris with the lens. A complete fusion of the pupil can be formed in a circle, and after this fibrinous exudate closes the pupil lumen. In this case, the intraocular fluid produced in the posterior chamber of the eye has no outlet to the anterior chamber, resulting in a bombardment of the iris - bulging it anteriorly and a sharp increase in intraocular pressure. Spikes of the pupillary margin of the iris with the lens are called posterior synechiae. They are formed not only with fibrinous-plastic iridocyclitis, but in other forms of inflammation they are rarely circular. If a local epithelial fusion is formed, it will come off when the pupil is dilated. Old, gross stromal synechia no longer detaches and changes the shape of the pupil. The pupil reaction in unchanged areas can be normal.

With purulent inflammation, the exudate has a yellowish-green hue. It can exfoliate as a result of sedimentation of leukocytes and protein fractions, forming a sediment at the bottom of the anterior chamber with a horizontal level - hypopion. If blood enters the moisture of the anterior chamber, the blood cells also settle on the bottom of the anterior chamber, forming a hyphema.

With any form of inflammatory reaction, the protein suspension from the intraocular fluid settles on all tissues of the eye, "signifying" the symptoms of iridocyclitis. If the cellular elements and minute pigment crumbs, glued together with fibrin, settle on the back surface of the cornea, they are called precipitates. This is one of the characteristic symptoms of iridocyclitis. Precipitates can be colorless, but sometimes they have a yellowish or gray hue. In the initial phase of the disease, they have a rounded shape and clear boundaries, in the period of resorption - they acquire uneven, as it were, swollen edges. Precipitates are usually located in the lower half of the cornea, with larger ones settling lower than small ones. Exudative overlays on the surface of the iris fade its pattern, the gaps become less deep. The protein suspension settles both on the surface of the lens and on vitreous body fibers, as a result of which visual acuity can be significantly reduced. The number of overlays depends on the etiology and severity of the inflammatory process. Any, even small, suspension in the vitreous is difficult to resolve. With fibrinous-plastic iridocyclitis, small flakes of exudate glue the vitreous fibers into coarse moorings, which reduce visual acuity if they are located in the central section. Peripherally located moorings sometimes lead to the formation of retinal detachment.

Intraocular pressure in the initial stage of acute iridocyclitis may increase due to hyperproduction of the intraocular fluid in conditions of increased blood filling of the vessels of the ciliary processes and a decrease in the rate of outflow of the more viscous liquid. After a prolonged inflammatory process, hypertension is often replaced by hypotension due to partial adhesion and atrophy of the ciliary processes. This is a terrible symptom, as in hypotension the metabolic processes in the eye tissues slow down, the functions of the eye decrease, resulting in a threat of subatrophy of the eyeball.

With the timely start of proper treatment, acute iridocyclitis can be stopped within 10-15 days, however, in case of persistent cases, treatment lasts longer - up to 6 weeks. In most cases, there are no traces of the disease in the eye: precipitates resolve, intraocular pressure normalizes, visual acuity is restored.

[1], [2], [3], [4], [5], [6], [7], [8], [9], [10], [11], [12], [13], [14]