Acute iridocyclitis

Acute iridocyclitis begins suddenly. The first subjective symptoms of acute iridocyclitis are sharp pain in the eye, radiating to the corresponding half of the head, and pain that occurs when touching the eyeball in the projection zone of the ciliary body. The excruciating pain syndrome is caused by abundant sensory innervation. At night, the pain intensifies due to blood stagnation and compression of nerve endings; in addition, the influence of the parasympathetic nervous system increases at night. If acute iridocyclitis begins with iritis, then the pain is determined only when touching the eyeball. After cyclitis occurs, the pain intensifies significantly. The patient also complains of photophobia, lacrimation, and difficulty opening the eyes. This corneal triad of symptoms (photophobia, lacrimation, blepharospasm) appears because the vascular congestion in the basin of the large arterial circle of the iris is transmitted to the vessels of the marginal looped network around the cornea, since they have anastomoses.

During an objective examination, attention is drawn to a slight swelling of the eyelids. It increases due to 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 blood vessels. It is already visible during an external examination in the form of a pink-blue ring around the limbus: hyperemic vessels of the marginal looped network of the cornea shine through a thin layer of sclera. With prolonged inflammatory processes, this corolla acquires a purple hue. The iris is edematous, thickened, due to the increased blood filling of the radially running vessels, they become straighter and longer, so the pupil narrows and becomes less mobile. When compared with a healthy eye, a change in the color of the full-blooded iris can be seen. The inflamed stretched walls of the vessels pass formed elements of the blood, when they are destroyed, the iris acquires shades of green.

In the inflamed processes of the ciliary body, the porosity of the thin-walled capillaries increases. The composition of the produced fluid changes: protein, blood cells, and desquamated epithelial cells appear in it. With a mild violation of vascular permeability, albumin predominates in the exudate; with severe changes, large protein molecules - globulin and fibrin - pass through the capillary walls. In the light section of a slit lamp, the fluid of the anterior chamber opalescent due to the reflection of light by a suspension of floating protein flakes. With serous inflammation, they are very small, barely distinguishable; with exudative inflammation, the suspension is thick. The fibrinous process is characterized by a less acute course and the production of a sticky protein substance. Adhesions of the iris with the anterior surface of the lens easily form. This is facilitated by the limited mobility of the narrow pupil and the tight contact of the thickened iris with the lens. A complete adhesion of the pupil in a circle may form, and then the fibrinous exudate closes the lumen of the pupil. In this case, the intraocular fluid produced in the posterior chamber of the eye has no outlet into the anterior chamber, resulting in iris bombage - its bulging forward and a sharp increase in intraocular pressure. Adhesions of the pupillary edge of the iris with the lens are called posterior synechiae. They are formed not only in fibrinous-plastic iridocyclitis, but in other forms of inflammation they are rarely circular. If a local epithelial adhesion has formed, it breaks off when the pupil dilates. Old, coarse stromal synechiae no longer break off and change the shape of the pupil. The reaction of the pupil in unchanged areas may be normal.

In purulent inflammation, the exudate has a yellowish-green tint. It can stratify due to the sedimentation of leukocytes and protein fractions, forming a sediment with a horizontal level at the bottom of the anterior chamber - hypopyon. If blood gets into the moisture of the anterior chamber, then the formed elements of the blood also settle at the bottom of the anterior chamber, forming hyphema.

In any form of inflammatory reaction, protein suspension from the intraocular fluid settles on all tissues of the eye, "designating" the symptoms of iridocyclitis. If cellular elements and tiny 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 tint. In the initial phase of the disease, they have a rounded shape and clear boundaries, while during the period of resorption, they acquire uneven, as if melted edges. Precipitates are usually located in the lower half of the cornea, with larger ones settling lower than small ones. Exudative deposits on the surface of the iris blur its pattern, and the lacunae become less deep. Protein suspension settles on the surface of the lens and on the fibers of the vitreous body, as a result of which visual acuity can be significantly reduced. The number of superpositions depends on the etiology and severity of the inflammatory process. Any, even small, suspension in the vitreous body is difficult to dissolve. In fibrinous-plastic iridocyclitis, small flakes of exudate glue the fibers of the vitreous body into coarse adhesions, which reduce visual acuity if they are located in the central section. Peripherally located adhesions sometimes lead to the formation of retinal detachment.

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

With timely and correct treatment, acute iridocyclitis can be stopped in 10-15 days, but in persistent cases, treatment can be longer - up to 6 weeks. In most cases, no traces of the disease remain in the eye: precipitates are absorbed, intraocular pressure is normalized, and visual acuity is restored.

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