Introduction
The eye is a delicate organ of the body, whose continuous normal function enables a better quality of life. While minor diseases that affect the eyes reduce the quality of life, other severe diseases may produce a more lethal condition. Here are some of the disorders of the eye:
Proptosis
This is the displacement of the eye, arising from increase in orbital contents from tumors of inflammation. Axial proptosis is due to tumor of the optic nerve- meningioma & glioma, which displace the eye directly forward.
Positional proptosis arises from an enlargement of the lacrimal gland in conditions such as sarcoidosis, lymphoma, pleomorphic adenoma, adenoid cystic carcinoma. It causes the displacement of the eye inferior medially.
Clinical manifestations: painful eye from corneal exposure; corneal ulceration & infection.
Thyroid ophthalmopathy
A disease of the eye that arises from hyperthyroidism in Graves’ disease. This leads to accumulation of extracellular matrix proteins with fibrosis development within the rectus muscles.
Clinical manifestations: Axial proptosis
Orbital cellulitis
This is the inflammation of the orbital tissues, arising from microbial infections or systemic conditions. The predisposing factors include: acute maxillary or ethmoidal infections; Wegener granulomatosis; diabetes.
Capillary hemangioma, Lymphangioma, & Cavernous hemangioma of the orbit
These are the most common tumor-like lesions of the orbit. Capillary hemangioma and lymphangioma occur during childhood and are unencapsulated. Cavernous hemangiomas affect adults and are encapsulated.
Blepharitis, Chalazion
Blepharitis is the acute or chronic inflammation of the eyelid margin, affecting sebaceous glands such as Meibomian glands.
Chalazion is a granulomatous lesion of the eyelid, that arises from the obstruction of sebaceous gland ducts by chronic blepharitis or tumors. Obstruction causes the rupture of sebaceous gland & leakage of lipids into the extracellular space, which initiates a granulomatous response.
Conjunctivitis, Conjunctival scaring
Conjunctivitis is the inflammation of the conjunctiva usually by allergy, viral & bacterial infections, resulting in redness & itching.
Conjunctival scarring is the chronic fibrosis of the conjunctiva that results in the reduction of goblet cells around the conjunctival fornix. The reduction in goblet cells causes decrease in mucin production important for adherence of the aqueous component of tears to the corneal epithelium.
Patient with conjunctival scarring may experience dry eye, painful eye, corneal opacity and ulceration. Causes include: chlamydia trachomatis; caustic alkalis; cicatricial pemphigoid.
Pterygium, Pinguecula
These are submucosal elevations on the conjunctival surface brought about by sunlight damage. Pterygium is a submucosal growth of fibrovascular tissue that originates in the conjunctiva around the limbus, that migrates onto the cornea. It doesn’t cross the axis of the pupil, & can cause mild astigmatism.
Pinguecula is a small yellowish submucosal elevation on the conjunctiva around the limbus, that doesn’t cross onto the cornea.
Myopia, Hyperopia
These disorders that affect the refractive power of the cornea, arising from changes in size of the eyeball. Myopia results from a longer eyeball, causing blurry images that appear before the retina.
hyperopia results from a shorter eyeball, that causes blurry images that appear after the retina.
Correctional procedure requires a laser-assisted in situ keratomileusis (LASIK) to reshape the cornea along with its refractive features.
Corneal opacification, Bullous keratopathy
Corneal opacification is the loss of corneal transparency, arising from trauma, non-immunological graft failure & inflammation. In this condition there is and edema & scarring within the corneal stroma.
Bullous keratopathy is a complication of corneal stroma edema, resulting in separation of corneal epithelium. It arises from malfunction or decreases in endothelial cells. The corneal endothelium originates from neural crest cells and it helps to drain fluid from stroma into the anterior chamber.
Keratitis, Corneal ulcers
These disorders are caused by viruses (herpes simplex, shingles); bacteria, fungi, protozoa (Acanthamoeba), which results in corneal inflammation.
Keratitis is an inflammation of the cornea, which causes cleavage of collagen by collagenases activated within corneal epithelium & keratocytes. Corneal ulcers result from shedding of necrotic tissues.
Investigation methods: slit-lamp & penlight examination. By these methods of investigation, hypopyon (collection of exudates and inflammatory cells from iris & ciliary body vessels) in the anterior chamber can be seen.
MECHANISM OF ACCOMODATION
Before we go further, it is important to understand the role of accommodation and the eye focal length in vision. Accommodation is the changes in the focal length of eye when we focus on far or near objects. The focal length of the eye is the distance between the lens and the retina.
During accommodation, the ciliary muscles contract & relax, which change the lens shape & eventually causes those changes in focal length. Ciliary muscles relax, pulling on suspensory ligaments (zonules), which stretches & flattens the lens for focusing far objects on the retina.
Ciliary muscles contract, relax the zonules, & eventually make the lens rounder and more curved for focusing near objects on the retina.
Cataract
This is the opacification of the eye lens following changes in the lens capsule, cortex & nucleus. The causes include: galactosemia; Wilson disease; trauma; diabetes mellitus; atopic dermatitis; corticosteroids; radiation; nuclear sclerosis (age-related).
Treatment: extracapsular cataract extraction & prosthetic intra-ocular lens placement.
Open- angle glaucoma, Closed- angle glaucoma
These are conditions that result from the interruption of the outflow of aqueous humor from anterior chamber through the trabecular meshwork. The trabecular meshwork is at an angle of intersection between the anterior surface of iris and periphery of cornea.
Open angle-glaucoma results from an increase in resistance to aqueous outflow in the open angle. Causes include: MYOC gene mutation which encodes myocilin present in trabecular meshwork; high molecular weight protein molecules from lens cortex liquefaction; senescent RBCs after trauma; iris epithelial pigment granules;
Other causes include episcleral venous pressure. This may be due to Sturge Werber syndrome & arterialization of episcleral veins following spontaneous or traumatic carotid cavernous fistula.
Closed- angle glaucoma results from an increase in resistance to aqueous outflow in a closed angle. It is caused by chronic retinal ischemia which induces formation of fibrovascular membrane on iris via VEGF upregulation. The myofibroblast component of this membrane contracts which occludes the trabecular meshwork.
Other causes include: pupillary block; retinoblastoma (induces iris neovascularization); pupillary block; hyperopia; ciliary body tumor.
Clinical manifestations: high intraocular pressure; visual field defects; optic nerve damage.
Uveitis, Sympathetic ophthalmia
This is the inflammation of one or more parts of the uvea including the choroid, iris and ciliary body.
Predisposing factors: blunt trauma; sarcoidosis; AIDs; mycobacterium tuberculosis; pneumocystis carini, rheumatoid arthritis; localized autoimmune disease (in sympathetic ophthalmia).
Sympathetic ophthalmia is a bilateral granulomatous inflammation affecting all parts of uvea, arising from a delayed hypersensitivity reaction. It may occur following a penetrating trauma to the eye.
Retinal detachment
This is the separation of the neurosensory retina from the retinal pigment epithelium (RPE). Two types include: rhegmatogenous & non-rhegmatogenous retinal detachment.
Rhegmatogenous retinal detachment arises from a break in the retina. Here, vitreous humor collapse causes the posterior hyaloid to pull apart weak points of attachment with retinal internal limiting membrane, resulting in a tear. Through this tear, liquid humor sips through the retina and in the space between the RPE and neurosensory epithelium.
Treatment: scleral buckling (requires indentation on the sclera with silicon strips) & vitrectomy.
Non-rhegmatogenous retinal detachment arises without a break within the retina. Causes are: RPE damage; exudates from the choroidal circulation; choroidal tumors; malignant hypertension.
Retinal arteriolosclerosis
This is the thickening of retinal arterioles, arising from chronic hypertension. This thickening narrows the arteriolar cavity & creates an ophthalmic view of the circulating blood under an ophthalmoscope.
The color perception may range vary from bright red to copper-silver wire & then to silver wire. In a significant retinal arteriolosclerosis, the arteriole may compress the vein at points where both cross, resulting in venous stasis & retinal vein occlusion.
Diabetic retinopathy
This disorder affects smaller retinal vessels of patients with diabetic mellitus. Two types include preproliferative & proliferative diabetic retinopathy.
In preproliferative diabetic retinopathy, there are structural and functional abnormalities of angiogenesis within retina, beneath the retinal internal limiting membrane.
There is basal membrane thickness of smaller retinal blood vessels, pericyte reduction, microaneurysm & microhemorrhages, which accompany blood-retinal barrier breakdown. Breakdown of blood-retina barrier results in macular edema & vision loss.
Proliferative diabetic retinopathy is the appearance of new blood vessels from existing vessels on optic nerve head or retinal surface. In this case, retinal neovascularization, applies to new blood vessels that cross into the retinal internal limiting membrane, underneath the vitreous humor.
Retinal neovascular membrane causes separation of vitreous humor from the retinal internal limiting membrane, vision loss and traction retinal detachment. Neovascular membrane on iris may follow retinal neovascularization secondary to VEGF in aqueous humor.
Age-related macular degeneration (ARMD)
This disorder arises from the abnormality in the structural & functional unit of the RPE- the Bruch membrane & choriocapillaris. This abnormality affects the condition of the overlying photoreceptors, eventually causing visual loss. Two types include: Non-neovascular & neovascular ARMD.
Non-neovascular ARMD arises from yellow deposits of fat within the Bruch membrane.
Neovascular ARMD is due to angiogenesis from choriocapillaris, which penetrates Bruch membrane or possibly RPE beneath the neurosensory retina. The neovascular membrane may rupture causing diffuse vitreous hemorrhage or be reorganized by RPE into macular scars.
Advancing age (≥75 years of age) is a risk factor for both types. Neovascular ARMD may also result from traumatic disruption of Bruch membrane & in individuals with CFH (complement factor H) CC genotype.
The observation of ARMD is done using an ophthalmoscope. Treatment includes the injection of VEGF antagonist into the vitreous chamber.
Retinitis pigmentosa
These are a group of inherited retinal disorders, that arise from mutation in genes which regulate the functions of either the photoreceptors or the RPE. In this disorder there is variable loss of rods and cones cells to apoptosis.
Clinical manifestations: night blindness; loss of central visual acuity; retinal atrophy; constriction of retinal vessels; atrophy of optic nerve head; accumulation of retinal pigments around blood vessels. Diagnosis requires the use of electroretinogram.