Secondary glaucoma

Secondary glaucoma is a group of diseases that occur in the most diverse pathological processes in the eye.

Inflammatory diseases, injuries and even the use of certain drugs, surgical operations can lead to an increase in, or, less frequently, a decrease in intraocular pressure.

[1], [2], [3], [4]

Causes of secondary glaucoma

Most often the cause of secondary glaucoma is a violation of outflow of intraocular fluid (retention).

The distinction between primary and secondary glaucoma is arbitrary, any increase in intraocular pressure is secondary. The frequency of secondary glaucoma is 0.8-22% of all eye diseases (this is 1-2% of all inpatients). Glaucoma often leads to blindness (whose frequency is 28%). A high percentage of enucleation in secondary glaucoma is 20-45%.

[5], [6], [7]

What are the symptoms of secondary glaucoma?

Secondary glaucoma has the same stages and degrees of compensation as primary glaucoma, but there are some special features:

1. one-sided process;
2. can proceed either as an open-angle glaucoma, or as an angle-closure glaucoma (i.e., paroxysmal);
3. Invented type of the intraocular pressure increase curve (evening ascent);
4. very quickly reduced visual function, within 1 year;
5. with timely treatment, lowering of visual functions is reversible.

Classification of secondary glaucoma

There is no single classification of secondary glaucoma.

In 1982, Nesterov gave the most complete classification of secondary glaucoma.

• I - uveal after inflammatory.
• II - phacogenic (phakotopic, phakomorphic, phakometric).
• III - vascular (post-thrombotic, phlebocytotension).
• IV - traumatic (contusion, wound).
• V - degenerative (uveal, with retinal diseases, hemolytic, hypertensive).

[8], [9], [10], [11]

Uveal inflammatory secondary glaucoma

Uveal inflammatory secondary glaucoma occurs in 50% of cases. Increase in intraocular pressure is noted as a result of inflammatory processes of the vascular tract and the cornea or after their termination (with keratitis, recurrent episcleritis, scleritis and uveitis). The disease proceeds as a type of chronic open-angle glaucoma, when there is a widespread lesion of the drainage system of the eye, or an angle-closure glaucoma, if posterior synechiae, goniosinchia, fusion and infection of the pupil are formed.

Keratouveal secondary glaucoma is a purely uveal, corneal ulcer, keratitis (viral, syphilitic etiology) is accompanied by involvement of the vascular tract. The outcome of the inflammatory disease of the cornea (throat) can be complicated by secondary glaucoma, the formation of anterior synechia (on the pupillary margin). In addition to fur; HAI blockade of the anterior chamber anterior chamber and dissociation of the anterior and posterior chambers, has a significantly reflex increase in intraocular pressure due to the constant irritation of the cornea, which is soldered into the scar.

Purely uveal secondary glaucoma:

• with acute uveitis, there may be an increase in intraocular pressure as a result of hypersecretion (20% of cases);
• violation of vascular regulation due to venous inflammation (vascular permeability increases and intraocular pressure rises);
• mechanical blockade of the angle of the anterior chamber with exudate, edema of the trabeculae.

Secondary glaucoma may differ in the outcome of uveitis (as a result of the formation of goniosynexia, fusion and infection of the pupil occur, the organization of exudate on the trabeculae, development of neovascularization in the corner of the anterior chamber).

Features of uveal glaucoma - rapid decrease in visual functions.

Treatment of uveal glaucoma:

• treatment of the underlying disease - uveitis;
• mydriatica;
• paresis of the ciliary body (the disruption of the synechia lowers the production of the aqueous humor);
• hypotensive therapy with increased secretion;
• surgical treatment (often against the background of acute uveitis, transferred earlier) in combination with massive anti-inflammatory therapy;
• if there is a pupillary block, a corneal bombardment occurs, a small anterior chamber, in this case necessarily surgical treatment (previously used trepanation of the cornea).

Phacogenic secondary glaucoma

Phacotic glaucoma - when the lens is displaced (dislocated) in the anterior chamber and the vitreous. The reason is trauma, etc.

If the lens nodvivyhtnut in the vitreous body, the equator it presses from behind the cornea, presses it against the corner of the anterior chamber. In the anterior chamber, the equator of the crystalline lens presses on the trabeculae. When the lens is blended into the vitreous body, the hernia of the vitreous humor forms in the pupil, which can be trapped in the pupil, then a block will occur. There may be a liquid vitreous body, which clogs the intertubule cracks. The reflex increase in intraocular pressure also matters: the lens irritates the cornea and the vitreous, which leads to a reflex factor. The disease proceeds according to the type of closed-angle glaucoma, and the removal of the lens is mandatory.

Facomorphic glaucoma develops with immature age or traumatic cataract. Swelling of the lens fibers is noted, the lens is enlarged in volume, the pupillary block may come. At a narrow angle of the anterior chamber develops an acute or subacute attack of secondary closed-angle glaucoma. The extraction of the lens can completely cure the patient of glaucoma.

Facial glaucoma develops with senile overripe cataract in persons older than 70 years. Intraocular pressure rises to 60-70 mm Hg. Art. Clinically, the disease resembles an acute attack of glaucoma with severe pain syndrome, hyperemia of the eyeball and high intraocular pressure. The lens masses pass through the capsule and clog the trabecular gaps. There may be rupture of the lens capsule, the moisture in the anterior chamber is turbid, milky. The rupture can occur under the anterior and under the posterior capsule - the plastic iridocyclitis develops.

Vascular Glaucoma

Posttrombotic - with thrombosis of the retina veins. The mechanism of glaucoma development with this form is as follows. The thrombosis leads to ischemia, in response to this new vessels form in the retina, the cornea, they clog the angle of the anterior chamber, the intraocular pressure rises. The disease is accompanied by a hyphema. Vision falls sharply, blindness may occur.

Phlebohypertensive glaucoma occurs as a result of a persistent increase in pressure in the episcleral veins of the eye. The reason - the stasis of blood in the anterior ciliary arteries and vorticostasis. This occurs with thrombosis of the vortex veins when the upper vena cava is compressed, with malignant exophthalmos, and orbital tumors. Since the field of view is usually zero, all treatments are aimed at preserving the eye. Usually they resort to surgery. The effect is insignificant. In the early stages of thrombosis, total retinal laser-coagulation is effective.

Traumatic glaucoma

Traumatic glaucoma complicates the course of injuries in 20% of cases.

Features:

1. develops among young people;
2. is divided into wound, ionized, burn, chemical, surgical.

The causes of increased intraocular pressure are not the same in different cases; intraocular hemorrhage (hyphema, hemophthalmus), traumatic recession of the anterior chamber angle, blockage of the drainage system of the eye by a displaced lens or products of its decay. During chemical and radiation damage, epi- and intrascleral vessels are affected.

Glaucoma occurs at different times after the injury, sometimes in a few years.

Wound glaucoma

Traumatic cataract, traumatic iridocyclitis or epithelial ingrowth along the optic canal can develop. Prevention of secondary post-traumatic glaucoma is a thorough surgical treatment.

Contusional glaucoma

The position of the lens changes, and compression of the anterior chamber angle is observed. It can be caused by the appearance of hyphema and traumatic mydriasis. The neurovascular factor is expressed (the first three days after the concussion of mydriatica are not prescribed). Treatment of concomitant glaucoma - bed rest, analgesia, sedative, desensitizing drugs. When the lens is displaced, it is removed. With a stable mydriasis, a pouch is placed on the cornea,

[12], [13], [14], [15], [16]

Burn Glaucoma

Intraocular pressure may increase in the first hours due to hyperproduction of intraocular fluid. After-burn glaucoma appears after 1.5-3 months due to the scar process in the corner of the anterior chamber. In acute period, hypotensive treatment is carried out, gymnastics of the pupil are prescribed, leeches are placed on the affected side. Subsequent reconstructive operations are shown.

[17]

Postoperative glaucoma

It is regarded as a complication after surgery on the eyeball and orbit. There can be a temporary and constant increase in intraocular pressure. Most often postoperative glaucoma develops after cataract extraction (aphakic glaucoma), keratoplasty, operations performed with detachment of the retina. Postoperative glaucoma can be both open-ended and closed-angle. Sometimes secondary malignant glaucoma occurs with the vitreochrustal block.

Glaucoma of the aphakic eye

Glaucoma of the aphakic eye occurs in 24%. The cause is the loss of the vitreous body. The pupillary block (2-3 weeks after extraction) is caused by the infringement of the hernia of the vitreous body and the secondary membrane, soldered to the vitreous body. When the clinic of an acute attack of glaucoma can wait no more than 12 hours. If intraocular pressure does not decrease, ectomy is also done. If after this there is no success, therefore, goniosinechia (peripheral) has already formed. With a vitreochrustal block, vitrectomy is done. When the cornea is infringed in the wound, the wound is filtered at the time of extraction, the chambers are not restored; goniosinechia is formed, the ingrowth of the epithelium. The use of chymotrypsin is shown.

Degenerative glaucoma

Uveal glaucoma - with uveeopathies, iridocyclitis, Fuchs syndrome, etc. In diseases of the retina glaucoma develops, complicating the course of retinopathy (diabetic). Cause: a dystrophic process in the corner of the anterior chamber; scarring of the cornea and anterior chamber angle with hypertrophic retinopathy, retinal detachment, primary amyloidosis, retinal pigmentary degeneration, progressive myopathy.

Hemolytic glaucoma - with extensive intraocular hemorrhages, blood-dissolving products cause dystrophy in the trabeculae.

Hypertensive glaucoma - sympathetic hypertension with endocrine pathology leads to dystrophic changes and glaucoma.

Iridocorneal endothelial syndrome manifests in the inferiority of the corneal posterior epithelium, atrophy of the membrane on the structures of the anterior chamber angle and the anterior surface of the iris. These membranes consist of cells of the posterior epithelium of the cornea and descemet-like membrane. Scarring of the membrane leads to partial obliteration of the anterior chamber angle, deformation and pupil displacement, stretching of the iris and the formation of slits and openings in it. Violation of the outflow of intraocular moisture from the eye, and increased intraocular pressure. Usually only one eye is affected.

[18], [19], [20], [21], [22]

Neoplastic glaucoma

Neoplastic glaucoma occurs as a complication of intraocular or orbital formations. It appears with intraocular tumors: melanoblastoma of the cornea and ciliary body, tumors of the choroid, retinoblastoma. Intraocular pressure increases during stage II-III of the tumor, when blockade of the anterior chamber angle occurs, deposition of decay products of tumor tissue in the trabecular filter and formation of goniosinchia.

More often and faster glaucoma develops with tumors in the corner of the anterior chamber. If the tumor is at the posterior pole of the eye, there is a shift in the forward direction of the irradiation of the diaphragm and the development of secondary glaucoma (by the type of acute attack of glaucoma).

In tumors of the orbit glaucoma occurs as a result of increased pressure in the orbital, intraocular and episcleral veins or direct pressure of the orbit contents on the eyeball.

For the diagnosis of tumor eye processes, additional methods are used: echography, diaphacoscopy, radionuclide diagnostics.

If the diagnosis is still not clear, vision drops to zero, there is a suspicion of swelling, it is better to remove the eye.