Secondary glaucoma is a disease in which an increase in intraocular pressure and damage to the optic nerve occurs against the background of the main pathology of the organ of vision. It is manifested by a progressive decrease in visual acuity, pain syndrome, spasm of accommodation. The diagnosis is based on the results of gonioscopy, tonometry, tonography, visometry, ophthalmoscopy, biomicroscopy and perimetry. Therapeutic tactics are determined by the etiology of the disease and may include hypotensive therapy, surgery, laser coagulation of the retina.
General information
Secondary glaucoma is one of the most dangerous diseases in ophthalmology. In the structure of all eye pathologies, this form of glaucoma occupies from 0.8 to 22%. On average, in one or two patients out of a hundred, it becomes the cause of hospitalization. The disease is among the disabling ones, because in 28% it leads to irreversible loss of visual functions. In 20-45%, a prolonged increase in intraocular pressure (IOP) leads to severe damage to the optic nerve and requires enucleation of the eyeball. In half of the cases, the uveal form of the disease is diagnosed. It occurs with the same frequency in males and females. Geographical features of epidemiology are not observed.
Causes
An increase in IOP in this form of glaucoma is associated with a number of pathogenetically heterogeneous factors. It is proved that the pathology is polyetiological. The main causes of development include:
- Inflammatory processes. The most common causes of the disease are recurrent episcleritis, scleritis and uveitis. In these pathological processes, the drainage system of the eye is affected, which entails an increase in IOP.
- Chronic keratitis. The increase in IOP is directly related to both the inflammation of the cornea and the secondary formation of the cataract, anterior synechiae and severe degenerative-dystrophic changes of the cornea. In addition to the organic prerequisites for the development of secondary glaucoma, constant irritation of the shell leads to reflex hypertension.
- Ectopia of the lens. Clinical manifestations develop with dislocation of the lens in the anterior chamber of the eye or the vitreous body, which is due to a violation of intraocular hydrodynamics.
- Cataract. Glaucomatous changes are characteristic only for an immature age-related, traumatic or senile overripe form of cataract. At the same time, IOP increases due to the accompanying lens block and narrowing of the anterior chamber.
- Thrombosis of the central retinal vein. Due to the fact that thrombosis of the central retinal vein leads to ischemia, neovascularization of the iris occurs, which further extends to the anterior chamber area.
- Traumatic injuries. The cause is a contusion of the eye or a wound, in which there is an ingrowth of the epithelium along the visual canal. With the burn nature of pathology, an increase in IOP is a consequence of the hyperproduction of watery moisture.
- Degenerative changes. The trigger is dystrophic changes in the area of the angle of the anterior chamber, in which the outflow of intraocular fluid becomes difficult.
- Pathological neoplasms of intraocular localization. IOP increases due to the presence of a bulky formation in the eyeball cavity. Of the malignant pathologies, retinoblastoma and melanoma of the eye are the most common.
Pathogenesis
The development of secondary glaucoma is based on a violation of the hydrodynamics of the intraocular fluid, in particular, its outflow. This is caused by mechanical blocking of the angle of the anterior chamber caused by edema of the trabecular network. In 20% of cases, pathological hypersecretion plays a key role in the mechanism of development, which leads to the accumulation of a large volume of exudate. An increase in the permeability of the vascular wall of the venous bed and spasm of arterioles additionally stimulate the development of ocular hypertension as one of the manifestations of the disease. With ectopia of the lens, compression of the cornea to the corner of the anterior chamber and trabecula occurs. In case of secondary damage to the vitreous body, in addition to the appearance of a pupillary block, its obturation by masses of intertrabecular slits is possible.
With a prolonged course of the disease in the drainage system of the eye, functional changes are replaced by the formation of organic barriers to the outflow path. The progressive formation of goniosynechiae, the organization of exudate in the trabecular zone and increased angiogenesis leads to an increase in clinical manifestations of visual dysfunction. With neoplastic origin of pathology, the degree of increase in clinical manifestations is determined by the growth rate of the neoplasm in the orbital cavity. When bleeding into the vitreous cavity or anterior chamber, an increase in IOP correlates with the volume of hemorrhage. The pressure decreases with the resorption of blood, however, due to the organization of clots and obturation of the trabecular network, it can quickly increase after a period of imaginary well-being.
Classification
The disease has an exclusively acquired origin. From a clinical point of view, there are single and double-sided forms. According to the etiology , secondary glaucoma is classified into:
- Uveal post-inflammatory. Occurs due to the prolonged course of inflammatory processes or the presence of post-inflammatory changes.
- Phacogenic. Develops due to traumatic damage to the lens or is a complication of cataracts.
- Vascular. The etiology of this form is directly related to thrombosis or persistent increase in pressure in the episcleral veins of the eyeball.
- Traumatic. The formation of glaucoma is based on damage to the visual organ caused by the action of thermal, chemical or ionizing factors.
- Degenerative. Degenerative-dystrophic changes lead to the development of the disease in patients with uveopathy, Fuchs anomaly and iridocorneal endothelial syndrome.
- Neoplastic. The appearance of this variant of pathology is preceded by the appearance of benign and malignant neoplasms of the eyeball, which lead to an increase in ophthalmotonus.
Symptoms
Clinical manifestations depend on the features of the course of the underlying pathology. In most cases, only one eye is affected. With a two-sided form, the changes develop asymmetrically. There are no symptoms of the disease for a long time, except in cases when the occurrence of pathology is caused by trauma or postoperative complications. With uveal form, patients often feel an increase in ophthalmotonus in the evening. There is a rapid, progressive decrease in visual acuity. Often, a complete loss of visual functions occurs within 1 year.
If the disease develops against the background of ectopia of the lens or cataracts, patients complain of sharp pain in the eye socket, decreased vision, redness of the anterior part of the eyeball. Pathology may be accompanied by nausea, vomiting, dizziness. A distinctive symptom is the trembling of the lens during the movements of the eyeballs (facodonaise). The peculiarity of glaucoma in patients with oncological neoplasms is a slow increase in clinical manifestations. Common symptoms for all forms are the appearance of iridescent circles in front of the eyes when looking at a light source, blurred vision, headache with irradiation into the brow arches. Accommodation capacity is often impaired, in which the spasm of accommodation prevails. Asthenopic complaints develop rapidly when performing visual work.
Complications
The most severe complication of secondary glaucoma is blindness. Patients with this pathology are at high risk of optic nerve atrophy. With the vascular form and wound genesis of the disease, hemorrhages in the vitreous body and hyphema are common. Possible iris rubeosis and corneal neovascularization. Uveal glaucoma is often complicated by inflammatory and infectious diseases (keratitis, conjunctivitis, blepharitis). Due to the rapid increase in ophthalmotonus with contusion of the eye, subconjunctival bleeding (hyposphagma) is widely found in practical ophthalmology. When the lens capsule ruptures, plastic iridocyclitis occurs in patients with a phacolytic form.
Diagnostics
To diagnose secondary glaucoma, it is necessary to carefully collect an anamnesis in order to identify the root cause of increased pressure inside the eyeball. External examination is uninformative, which often leads to untimely diagnosis. The specific complex of ophthalmological examination includes:
- Gonioscopy. The study makes it possible to study the condition of the anterior chamber of the eyeball, to identify morphological prerequisites for a violation of the outflow of intraocular fluid, namely, reduced chamber volume, closure of the anterior chamber angle, pathology of the structure of the corneal-scleral trabecula.
- Non-contact tonometry of the eye. The excess of the tolerance values by intraocular pressure (more than 20-22 mmHg) is detected. For more informative changes in intraocular pressure during the day, daily tonometry is used.
- Ultrasound of the eyes. The purpose of ultrasound examination is to identify organic changes that potentiate an increase in ophthalmotonus. It makes it possible to identify malignant neoplasms, signs of ectopia of the lens.
- Ophthalmoscopy. Examination of the fundus is informative for visualization of atrophic changes in the optic nerve disc, secondary damage to the inner shell, which occur with a prolonged increase in ophthalmotonus.
- Biomicroscopy of the eye. A detailed examination of the anterior surface of the eyeball is carried out to identify ulcers and a cornea cataract.
- Electronic tonography of the eye. Secondary glaucoma is characterized by an inverted type of pressure rise curve with a typical evening rise. Tonography of the eyeball allows you to measure the volume of intraocular fluid and calculate its outflow coefficient.
- Visometry. Patients are diagnosed with progressive visual dysfunction. With additional refractometry, the myopic type of clinical refraction is more often determined.
- Perimetry. The narrowing of the visual fields by the concentric type is determined.
Treatment
The aim of etiotropic therapy is to eliminate the underlying disease. With the concussion nature of the disease, therapeutic tactics are based on the appointment of analgesics, sedatives and desensitizing agents. In the complex treatment of pathology is used:
- Hypotensive therapy. It is used in the diagnosis of increased IOP caused by hypersecretion of watery moisture. To achieve tolerant values of intraocular pressure, drugs from the group of M-cholinomimetics, adrenoblockers, carbonic anhydrase inhibitors, alpha-2-agonists and prostaglandins are used.
- Surgical intervention. With the development of pathology due to the bombing of the cornea and a decrease in the volume of the anterior chamber, corneal trepanation is indicated. The appearance of a pupillary block due to ectopia requires the extraction of the lens. If the disease is accompanied by persistent pupil dilation, a pouch suture is applied to the cornea. When the corneal-scleral angle is narrowed, iridectomy is used.
- Laser coagulation of the retina. The method of treatment is used only with a persistent increase in pressure in the vessels of the episclera. The effectiveness of total laser coagulation of the retina at the first signs of blood stasis in the anterior ciliary arteries and whirlpool veins has been proven.
Prognosis and prevention
The prognosis for life and work capacity with timely diagnosis and treatment is favorable. The peculiarity of secondary glaucoma is that with adequate therapy, visual functions can be restored. There are no specific methods of prevention. The basis of non-specific preventive measures is the control of intraocular pressure indicators. It is recommended to regularly measure IOP for patients who have had surgical interventions on the eyeball for a year, who have traumatic injuries or a burdened ophthalmological history (ocular migraine, cataracts, hemorrhages in the anterior chamber).
