Secondary glaucoma

Secondary glaucoma is a group of diseases that occur with a wide variety of pathological processes in the eye.

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

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Causes of secondary glaucoma

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

The distinction between primary and secondary glaucoma is conditional, 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 hospitalized patients). Glaucoma often leads to blindness (the frequency of which is 28%). A high percentage of enucleation in secondary glaucoma is 20-45%.

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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-way process;
2. can occur either as open-angle glaucoma or as closed-angle glaucoma (i.e. in attacks);
3. inverted type of intraocular pressure increase curve (evening rise);
4. visual functions deteriorate very quickly, within 1 year;
5. With timely treatment, the decrease in 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 post-inflammatory.
• II - phacogenic (phacotopic, phacomorphic, phacometic).
• III - vascular (post-thrombotic, phlebohypertensive).
• IV - traumatic (contusion, wound).
• V - degenerative (uveal, in retinal diseases, hemolytic, hypertensive).

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Uveal post-inflammatory secondary glaucoma

Uveal post-inflammatory secondary glaucoma occurs in 50% of cases. Increased intraocular pressure is observed as a result of inflammatory processes of the vascular tract and cornea or after their termination (in keratitis, recurrent episcleritis, scleritis and uveitis). The disease proceeds as chronic open-angle glaucoma, when there is widespread damage to the drainage system of the eye, or closed-angle glaucoma, if posterior synechia, goniosynechia, adhesions and infections of the pupil are formed.

Kerato-uveal secondary glaucoma - purely uveal, corneal ulcer, keratitis (viral, syphilitic etiology) is accompanied by the involvement of the vascular tract. The outcome of an inflammatory disease of the cornea (leukoma) can be complicated by secondary glaucoma, the formation of anterior synechiae (along the pupillary margin). In addition to fur; gastric blockade of the anterior chamber angle and separation of the anterior and posterior chambers, there is a significant reflex increase in intraocular pressure due to constant irritation of the cornea, which is soldered into the scar.

Pure uveal secondary glaucoma:

• in acute uveitis, there may be an increase in intraocular pressure as a result of hypersecretion (20% of cases);
• disruption of vascular regulation due to inflammation of the veins (increased vascular permeability and increased intraocular pressure);
• mechanical blockade of the anterior chamber angle by exudate, trabecular edema.

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

The characteristics of uveal glaucoma are a rapid decline in visual function.

Treatment of uveal glaucoma:

• treatment of the underlying disease - uveitis;
• mydriatics;
• ciliary body paresis (rupture of the adhesions reduces the production of intraocular fluid);
• antihypertensive therapy in case of increased secretion;
• surgical treatment (often against the background of acute uveitis suffered earlier) in combination with massive anti-inflammatory therapy;
• if there is a pupillary block, corneal bombardment, shallow anterior chamber occurs, in this case surgical treatment is required (previously, corneal trepanation was used).

Phacogenic secondary glaucoma

Phacotic glaucoma - when the lens is displaced (dislocated) into the anterior chamber and vitreous body. Cause - trauma, etc.

If the lens is dislocated into the vitreous body, its equator presses on the cornea from behind, pressing it to the angle of the anterior chamber. In the anterior chamber, the equator of the lens presses on the trabecula. When the lens is displaced into the vitreous body, a vitreous hernia is formed in the pupil, which can be pinched in the pupil, then a block will occur. There may be liquid vitreous body, which clogs the intertrabecular gaps. Reflex increase in intraocular pressure is also important: the lens irritates the cornea and vitreous body, which leads to a reflex factor. The disease proceeds as a closed-angle glaucoma, and removal of the lens is mandatory.

Phacomorphic glaucoma develops with immature age-related or traumatic cataract. Swelling of the lens fibers is observed, the lens increases in volume, and pupillary block may occur. With a narrow angle of the anterior chamber, an acute or subacute attack of secondary closed-angle glaucoma develops. Extraction of the lens can completely cure the patient of glaucoma.

Phacolytic glaucoma develops with senile hypermature cataract in people over 70 years of age. Intraocular pressure increases to 60-70 mm Hg. Clinically, the disease resembles an acute attack of glaucoma with severe pain, hyperemia of the eyeball and high intraocular pressure. The lens masses pass through the capsule and clog the trabecular fissures. There may be a rupture of the lens capsule, the fluid in the anterior chamber is cloudy, milky. A rupture may occur under the anterior and posterior capsule - plastic iridocyclitis develops.

Vascular glaucoma

Post-thrombotic - with thrombosis of the retinal veins. The mechanism of glaucoma development in this form is as follows. Thrombosis leads to ischemia, in response to this new vessels are formed in the retina, cornea, they clog the angle of the anterior chamber, intraocular pressure increases. The disease is accompanied by hyphema. Vision drops sharply, blindness may occur.

Phlebohypertensive glaucoma occurs as a result of persistent pressure increase in the episcleral veins of the eye. The cause is blood stasis in the anterior ciliary arteries and vortex veins. This occurs with thrombosis of the vortex veins with compression of the superior vena cava, with malignant exophthalmos, and orbital tumors. Since the visual field is usually zero, all treatment is aimed at preserving the eye. Surgical intervention is usually used. The effect is insignificant. In the early stages of thrombosis, total laser coagulation of the retina is effective.

Traumatic glaucoma

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

Peculiarities:

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

The causes of increased intraocular pressure vary from case to case; intraocular hemorrhages (hyphema, hemophthalmos), traumatic recession of the anterior chamber angle, blockage of the eye drainage system by a displaced lens or its decay products. In case of chemical and radiation damage, epi- and intrascleral vessels are affected.

Glaucoma occurs at different times after injury, sometimes several years later.

Wound glaucoma

Traumatic cataract, traumatic iridocyclitis or epithelial ingrowth along the optic nerve canal may develop. Prevention of secondary posttraumatic glaucoma is thorough surgical treatment.

Contusion glaucoma

The position of the lens changes, compression of the anterior chamber angle is observed. It may be caused by the appearance of hyphema and traumatic mydriasis. The neurovascular factor is expressed (mydriatics are not prescribed for the first three days after contusion). Treatment of contusion glaucoma - bed rest, pain relief, sedatives, desensitizing drugs. If the lens is displaced, it is removed. In case of persistent mydriasis, a purse-string is applied to the cornea,

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Burn glaucoma

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

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Postoperative glaucoma

It is considered a complication after surgery on the eyeball and orbit. There may be a temporary and permanent increase in intraocular pressure. Most often, postoperative glaucoma develops after cataract extraction (aphakic glaucoma), keratoplasty, and surgeries performed for retinal detachment. Postoperative glaucoma can be either open-angle or closed-angle. Sometimes secondary malignant glaucoma occurs with a vitreoretinal block.

Glaucoma of the aphakic eye

Glaucoma of the aphakic eye occurs in 24%. The cause is prolapse of the vitreous body. Pupillary block (2-3 weeks after extraction) is caused by strangulation of the vitreous hernia and the secondary membrane fused with the vitreous body. In the case of an acute attack of glaucoma, one can wait no more than 12 hours. If the intraocular pressure does not decrease, an ectomy is performed. If this is still not successful, then goniosynechiae (peripheral) have already formed. In case of vitreocrystalline block, vitrectomy is performed. In case of strangulation of the cornea in the wound at the time of extraction, wound filtration occurs, the chambers are not restored; goniosynechiae and epithelial ingrowth are formed. The use of chymotrypsin is indicated.

Degenerative glaucoma

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

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

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

Iridocorneal endothelial syndrome is characterized by posterior corneal epithelium deficiency, membrane atrophy on the structures of the anterior chamber angle and the anterior surface of the iris. These membranes consist of posterior corneal epithelium cells and Descemet-like membrane. Cicatricial contraction of the membrane leads to partial obliteration of the anterior chamber angle, deformation and displacement of the pupil, stretching of the iris and formation of cracks and holes in it. The outflow of intraocular fluid from the eye is impaired, and intraocular pressure increases. Usually, only one eye is affected.

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Neoplastic glaucoma

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

Glaucoma develops more often and faster with tumors in the angle of the anterior chamber. If the tumor is located at the posterior pole of the eye, the iris-lens diaphragm shifts forward and secondary glaucoma develops (like an acute attack of glaucoma).

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

To diagnose tumor processes of the eye, additional methods are used: echography, diaphragmoscopy, radionuclide diagnostics.

If the diagnosis is still unclear, vision drops to zero, there is a suspicion of a tumor, then it is better to remove the eye.