Eye structures and visual disturbances that occur when they are affected
Cornea is the main refractive surface of the eye. Due to the peculiarities of its structure and location, the surface of the cornea is very sensitive to impact. In this regard, the following pathological conditions are possible:
- environmental damage to the cornea - direct trauma, drying out, radiation and ionizing radiation
- corneal damage by infectious agents - bacteria, viruses, especially herpes simplex and herpes zoster viruses, fungi, parasites
- corneal damage by inflammatory processes, sometimes in combination with general skin diseases - atopic dermatitis, scarring pemphigoid and erythema multiforme (Stevens-Johnson syndrome)
Inflammation and infection of the cornea are called keratitis. Keratitis is often accompanied by inflammation of the iris (iritis) or the uveal tract of the iris, the ciliary body, and the choroid itself (uveitis).
Keratitis (inflammation of the cornea) combined with uveitis (inflammation of the choroid) or iritis (inflammation of the iris) is commonly seen in Reiter's disease (a consequence of chlamydial infection) and, in some cases, Behcet's disease. Keratitis (inflammation of the cornea) and uveitis (inflammation of the choroid of the eye) can also occur with herpes simplex, sarcoidosis, collagenosis.
Metabolic disorders in humans can also lead to clouding of the cornea since substances that are in excess in the patient's body are deposited in it:
- with secondary hypercalcemia against the background of sarcoidosis, hyperparathyroidism, vitamin D poisoning, calcium phosphate, and carbonate is deposited under the corneal epithelium in the projection of the palpebral fissure - the so-called ribbon keratopathy
- cystine crystals are deposited in the cornea during cystinosis
- cholesterol esters are deposited in the cornea with hypercholesterolemia (senile arch)
- chloroquine crystals are deposited in the cornea when treating discoid lupus
- polysaccharides are deposited in the cornea in Harler's disease
- copper is deposited in the cornea during hepatolenticular degeneration - Kaiser-Fleischer ring
In case of severe scarring and/or clouding of the cornea, the patient may be indicated for keratoplasty (corneal transplant) to restore vision.
Pupil size is determined by the intensity of light entering the eye. The size of the pupil is used to judge the presence or absence of difficulty in the innervation of the eye in a particular pathological condition in the patient.
Normally, moderate asymmetry of the pupils (anisocoria) of both eyes may occur, while their reactions to light and accommodation are preserved. Pathological anisocoria (asymmetry of the pupils) occurs with lesions of the sympathetic (Horner's syndrome) or parasympathetic (internal ophthalmoplegia) innervation of the eye. Horner's syndrome is characterized by a persistent reaction of the constricted pupil to light on the affected side, partial ptosis, and, in some cases, increased perspiration on the face.
Internal ophthalmoplegia (III pair of cranial nerves) is manifested by dilatation of the pupil (mydriasis) with no or weak reaction to light; when a 1% solution of pilocarpine is instilled, the pupil narrows. Local application of pilocarpine in various concentrations allows the doctor to distinguish cranial nerve palsy from mydriasis (dilated pupil) caused by the administration of drugs (atropine) or from Edie's mystical pupil.
Intraocular fluid and glaucoma
A glaucoma is a condition in which intraocular pressure (IOP) rises. An increase in intraocular pressure in glaucoma leads to damage to the optic nerve that enters the eyeball from the fundus. The intraocular fluid is secreted by the epithelium of the ciliated body. Intraocular fluid provides metabolism in the lens and cornea, which lack their blood vessels. The level of intraocular pressure (IOP) is the ratio between the rate of production of intraocular fluid and the resistance to its outflow through the trabecular network into the Schlemm canal and venous collectors. In most cases, the cause of glaucoma is not increased production of intraocular fluid, but an impaired outflow from the anterior chamber of the eye.
Glaucoma is the second leading cause of blindness in the world. Glaucoma develops in about 1 in 50 people over the age of 35. The majority of the population already has glaucoma, unaware of its existence. Therefore, the detection of glaucoma, as well as the measurement of blood pressure, is one of the necessary components when examining adult patients during routine medical examinations. Measurement of intraocular pressure must be included in the ophthalmological examination. Intraocular pressure (IOP) is considered elevated above 22 mm Hg. Art. (Shetz tonometry).
Patients with glaucoma may have significant daily fluctuations in intraocular pressure (IOP), including within the normal range, so it is very important to examine the optic discs to confirm glaucoma. The loss of the visual field follows the progressive depression of the optic nipple. This asymmetry of the optic nerve nipples can serve as an early diagnostic sign of glaucoma. With the progression of damage to the optic nerve, the death of the nerve tissue occurs as a result of its compression ischemia. This is followed by the development of optic nerve atrophy with a change in its contour (depression) and disc color (blanching).
Types of glaucoma
The main types of glaucoma that affect the human eye include:
Open angle glaucoma
Open-angle glaucoma arises as a complication of chronic difficulty in reabsorption (absorption) of intraocular fluid in the trabecular network. Open-angle glaucoma is usually asymptomatic, only in rare cases pain in the eyeball and corneal edema develops. Initially, the peripheral visual fields fall out, visual acuity remains normal until the later stages of the disease.
The diagnosis of open-angle glaucoma is based on the detection of increased intraocular pressure (IOP) and direct examination (gonioscopy) of the formations of the anterior chamber angle. The tactics of managing a patient with open-angle glaucoma in the early stages consist of detailed re-examinations with repeated measurements of intraocular pressure (IOP), the examination of the visual fields, thorough examinations of the fundus to detect the retraction of the optic nerve disk.
Treatment of open-angle glaucoma begins with conservative methods. To reduce intraocular pressure (IOP), cholinergic drugs (pilocarpine or carbacholine) and beta-blockers (timolol) are used topically. Diuretics - carbonic anhydrase inhibitors (diacarb) - can have a positive effect in the treatment of open-angle glaucoma.
In rare cases, there is a need for surgical treatment of open-angle glaucoma. This prevents the patient from developing permanent visual impairment. For this, the following operations are used:
- лазерную трабекулопластику
- формируют соустье из передней камеры глаза в подконъюнктивальное пространство
Angle-closure glaucoma develops when fluid outflow is obstructed by narrowing of the anterior chamber of the eye. The tissues at the periphery of the iris overlap the trabecular meshwork, preventing the exit of intraocular fluid. The obstruction to the flow of fluid occurs suddenly, usually on one side. At the same time, the patient's vision deteriorates. Chronic angle-closure glaucoma can lead to the dilated pupil (mydriasis), pain, and loss of vision in the patient. In the chronic and subacute course of angle-closure glaucoma, it is necessary to conduct a direct examination of the formations of the anterior chamber angle of the eye (gonioscopy) to determine the type of glaucoma.
The use of drugs that cause dilatation of the pupil can lead to the progression of angle-closure glaucoma. Since the narrowing of the angle of the anterior chamber of the eye contributes to the development of angle-closure glaucoma, in patients over the age of 50, it should be examined (gonioscopy) before prescribing drugs that dilate the pupil.
Treatment of acute angle-closure glaucoma in a patient requires urgent measures. To combat a sharp increase in intraocular pressure (IOP), drugs are used:
- intravenous mannitol
- parenteral - diacarb
- pilocarpine or timolol used topically
After urgent measures, surgical treatment of acute angle-closure glaucoma may be required, aimed at creating a message between the anterior and posterior chambers of the eye.
Congenital glaucoma is a rare type of open-angle glaucoma. Congenital glaucoma develops as a result of underdevelopment (dysplasia) of the formations of the angle of the anterior chamber of the eye. Congenital glaucoma can cause loss of vision, enlargement of the eyeball, and corneal damage. Early diagnosis of congenital glaucoma is important for conservative and surgical treatment of this disease.
Secondary glaucoma develops as a complication of a general disease already existing in the patient or as a local lesion of the eye. Among the common diseases and complications from taking medications that can lead to the development of secondary glaucoma, there are:
- blood diseases (leukemia, sickle cell anemia, Waldenstrom macroglobulinemia)
- collagen diseases (ankylosing spondylitis, rheumatoid arthritis, sarcoidosis)
- skin diseases (allergic reactions to taking corticosteroids, Ota's nevus)
- infectious diseases (congenital rubella, onchocerciasis)
- metabolic disorders (amyloidosis, Markezani syndrome)
- skeletal muscle lesions (Conradi's disease, osteogenesis imperfecta)
- neoplasms (metastases in the trabecular network)
- phakomatosis (neurofibromatosis, Sturge-Weber disease)
- lung diseases (asthma, emphysema as a result of taking corticosteroids)
- kidney damage (Lowe's syndrome - aminoaciduria), Wilms tumor, kidney transplant (as a result of taking corticosteroids)
- medicines (phenamine, corticosteroids, benzohexonium, reserpine, anticholinergics)
Local eye lesions that cause the development of secondary glaucoma in a patient include trauma to the eyeball. The development of secondary glaucoma is also possible with dislocation of the lens that occurs in a patient with homocystinuria or Marfan syndrome.
Lens and cataracts
A cataract is a clouding of the lens that is localized in its center (nuclear), in the superficial cortical region, or the posterior subcapsular region of the lens. A cataract develops in response to changes in the physical and chemical properties of the environment inside its semi-permeable capsule. By its origin, cataracts can be congenital and acquired.
Congenital cataracts occur in the following diseases of the patient:
- herpes simplex
Acquired cataracts result from:
- drug use
- metabolic disorders as well as in the elderly (senile cataract)
Two types of cataracts are described in diabetic patients:
- metabolic (like snow flakes)
Snowflake cataracts are common in insulin-dependent diabetes. The development of a snowflake-type cataract begins in the subcapsular region. Senile cataracts develop at an earlier age in diabetics than in non-diabetic people and mature faster.
Other metabolic disorders that often lead to the development of cataracts include:
Cataracts located in the back of the lens develop in more than one-third of patients with myotonic dystrophy. The formation of cataracts in the posterior subcapsular region is facilitated by the systematic intake of corticosteroids. Also, the following diseases can lead to the development of cataracts:
- chromosomal abnormalities (Alport syndrome, screaming cat syndrome, Conradi's disease, Cruson's syndrome, Turner syndrome)
- metabolic diseases or alimentary disorders (aminoaciduria (Lowe's syndrome), Fabry's disease, hypervitaminosis D, hypoparathyroidism, hypothyroidism, mucopolysaccharidosis, Wilson's disease)
- infectious diseases (acquired cysticercosis, leprosy, onchocerciasis, and toxoplasmosis)
- taking medications (corticosteroids, haloperidol, and miotics)
Visual disturbances in cataracts are manifested by blurred vision with preserved light perception, duplication of the image (monocular diplopia), a change in color perception, and a decrease in visual acuity. Surgical removal of the cataract can lead to complete restoration of the patient's vision.
Dislocation or subluxation (ectopia) of the lens occurs with homocystinuria and Marfan syndrome. In such conditions, dislocation of the lens can accelerate the development of glaucoma.
As a person ages, the vitreous body undergoes significant physical and biochemical changes, like the rest of the body's connective tissue.
Among the opacities of the vitreous body, benign "floating opacities" are most often found. Benign "floating opacities" are described by patients as gray or white spots or elongated irregular objects that move when the eyeballs move.
Hemorrhage in the vitreous body usually occurs from the retinal vessels and can spread diffusely throughout the vitreous cavity. In the case of massive hemorrhages, vision can deteriorate significantly. Bleeding in the vitreous body and membrane formation are observed in the following diseases:
- with diabetic retinopathy
- in case of retinal vein occlusions
- with sickle cell retinopathy
- with congenital anomalies of retinal vessels
- as a result of injury
- with discal macular degeneration
- with malignant melanoma of the choroid itself
- with subarachnoid hemorrhage in case of traumatic brain injury or ruptured cerebral artery aneurysm
Asteroid hyalite (Benson's disease) is characterized by the formation of minute yellow opacities in the vitreous body. These opacities are composed of calcium soaps (palmitate and stearate). A similar condition, reflecting vitreous dystrophy, can occur in patients with diabetes mellitus, and also often occurs in patients without signs of obvious eye disease. Vitreous opacity can occur with primary amyloidosis. With reticulosarcoma and retinoblastoma, tumor cells can be found floating freely in the liquid part of the vitreous.
Vitrectomy, the most important advance in the treatment of vitreous lesions, is used to cleanse the vitreous from opacities and reduce or prevent vitreoretinal traction. If amyloidosis or reticulosarcoma is suspected, a routine vitreous biopsy can provide valuable information.
The choroid itself
Lesions of the choroid itself are rare in clinical practice.
- Anatomy of the nervous system
- Spinal disc herniation
- Pain in the arm and neck (trauma, cervical radiculopathy)
- The eyeball and the visual pathway:
- Optic nerve and retina:
- Compression neuropathy of the optic nerve
- Edema of the optic disc (papilledema)
- Ischemic neuropathy of the optic nerve
- Meningioma of the optic nerve sheath
- Optic nerve atrophy
- Optic neuritis in adults
- Optic neuritis in children
- Opto-chiasmal arachnoiditis
- Pseudo-edema of the optic disc (pseudopapilledema)
- Toxic and nutritional optic neuropathy
- Neuropathies and neuralgia:
- Diabetic, alcoholic, toxic and small fiber sensory neuropathy (SFSN)
- Facial nerve neuritis (Bell's palsy, post-traumatic neuropathy)
- Fibular (peroneal) nerve neuropathy
- Median nerve neuropathy
- Neuralgia (intercostal, occipital, facial, glossopharyngeal, trigeminal, metatarsal)
- Post-traumatic neuropathies
- Post-traumatic trigeminal neuropathy
- Post-traumatic sciatic nerve neuropathy
- Radial nerve neuropathy
- Tibial nerve neuropathy
- Ulnar nerve neuropathy
- Tumors (neoplasms) of the peripheral nerves and autonomic nervous system (neuroma, sarcomatosis, melanoma, neurofibromatosis, Recklinghausen's disease)
- Carpal tunnel syndrome
- Ulnar nerve compression in the cubital canal