CMO Oftalmología key terms

The single spherical lens power that best approximates a patient's refractive correction when astigmatism is averaged with sphere; calculated as sphere plus half the cylindrical power. Used to compare overall refractive error across eyes and over time.

A refractive condition in which the eye's optical power differs between meridians, so light does not focus at a single point. Regular forms arise from toroidal corneal or lens curvature; irregular forms follow scarring, ectasia, or surgery.

Sphere power plus half of the cylinder power, expressed as a single number. It estimates where the circle of least confusion falls and guides decisions when a full spherocylindrical correction cannot be used, such as in contact lens fitting.

A clinically meaningful difference in refractive error between the two eyes, commonly defined as at least one diopter of spherical or cylindrical difference. It can cause aniseikonia and, in children, dense amblyopia in the more ametropic eye.

A perceived difference in the size or shape of images formed by the two eyes, usually caused by unequal retinal image magnification from anisometropia or from dissimilar spectacle corrections. Symptoms include headache, asthenopia, and disturbed binocular vision.

A progressive noninflammatory corneal ectasia producing central or paracentral thinning and conical protrusion, with irregular myopic astigmatism and reduced best-corrected acuity. Corneal topography confirms the diagnosis; management ranges from spectacles and rigid lenses to cross-linking and keratoplasty.

A bilateral, noninflammatory peripheral corneal thinning located inferiorly, classically sparing the central cornea and producing against-the-rule astigmatism with a crab-claw topographic pattern. It is distinguished from keratoconus by the peripheral location of maximal thinning.

A procedure in which riboflavin is applied to the cornea and activated by ultraviolet-A light to create additional collagen cross-links, stiffening the tissue. It is used mainly to halt progression of keratoconus and other ectasias, and in some infectious melting states.

A superficial epithelial defect of the cornea caused by mechanical trauma, foreign bodies, or contact lens wear. It presents with pain, tearing, photophobia, and a positive fluorescein staining pattern; treatment is topical antibiotic prophylaxis and analgesia, with review for infection.

A defect of the corneal epithelium with underlying stromal inflammation and tissue loss, most often microbial. Bacterial ulcers are typically suppurative with hypopyon; fungal and acanthamoeba forms have distinct risk factors. It is a sight-threatening emergency requiring prompt scraping and fortified therapy.

A diagnostic technique using topical sodium fluorescein, viewed under cobalt-blue light with a yellow barrier filter, to highlight epithelial defects, assess tear film breakup time, and reveal aqueous leakage in perforation (Seidel test).

A slit-lamp maneuver in which concentrated fluorescein is applied over a suspected corneal or scleral wound; a positive result shows a dark aqueous stream diluting the dye, indicating full-thickness perforation with active leakage.

Small-incision cataract surgery in which a titanium needle vibrating at ultrasonic frequency fragments the lens nucleus and aspirates it through a self-sealing incision, followed by intraocular lens implantation. It is the dominant technique for age-related cataract worldwide.

Late clouding of the residual lens capsule after cataract surgery from proliferation and migration of lens epithelial cells, causing progressive visual decline months to years postoperatively. It is treated with neodymium:YAG laser capsulotomy.

Preoperative estimation of the intraocular lens power needed to reach a target refraction, using keratometry, axial length biometry, and formulas such as Barrett or SRK/T. Accuracy depends on effective lens position prediction, especially after corneal refractive surgery.

Severe intraocular inflammation involving the vitreous and aqueous, most often bacterial after surgery or trauma, presenting with pain, hypopyon, and profound vision loss. Acute postoperative cases require immediate vitreous tap and intravitreal antibiotic injection.

A layer of white blood cells settled in the anterior chamber, visible as a fluid level inferiorly. It signals severe intraocular inflammation such as endophthalmitis, severe uveitis, or a retained intraocular foreign body, and is an urgent finding.

A chronic optic neuropathy with characteristic retinal ganglion cell and nerve fiber layer loss, cupping, and field defects, in which the anterior chamber angle is open on gonioscopy. Elevated intraocular pressure is the main modifiable risk factor.

Slit-lamp examination using a mirrored or prismatic contact lens to visualize the anterior chamber angle, allowing classification as open, narrow, or closed and identification of peripheral anterior synechiae or neovascularization. It is essential before diagnosing or treating glaucoma.

Occlusion of the anterior chamber angle by iris tissue in an anatomically predisposed eye, which may be asymptomatic, intermittent, or present as acute angle-closure crisis with pain, halos, and mid-dilated pupil. Definitive treatment is laser peripheral iridotomy.

Creation of a small full-thickness opening in the peripheral iris with a laser to relieve pupillary block and open the angle in angle-closure disease. Patency is confirmed by seeing posterior capsule through the opening.

A guarded filtration procedure in which a partial-thickness scleral flap and ostium allow aqueous to drain into the subconjunctival space, forming a filtering bleb. It lowers intraocular pressure in glaucoma but carries risks of hypotony, bleb leak, and blebitis.

Enlargement of the central optic nerve head depression with loss of neuroretinal rim tissue, assessed by cup-to-disc ratio, rim thinning, and disc hemorrhages. Progressive cupping is a structural marker of glaucomatous damage.

Noninvasive cross-sectional imaging using low-coherence interferometry to quantify retinal layers, retinal nerve fiber layer thickness, and ganglion cell complexes. In glaucoma it detects structural loss before visual field defects appear; in retina it identifies edema, fluid, and holes.

Fluid accumulation within the macula from diabetes-induced breakdown of the blood-retinal barrier, causing central vision loss. It is the leading cause of vision loss in working-age adults with diabetes and is treated with intravitreal anti-VEGF agents.

Intravitreal injection of antibodies or fusion proteins that bind vascular endothelial growth factor, reducing neovascularization and vascular permeability. It is first-line treatment for neovascular age-related macular degeneration, diabetic macular edema, and retinal vein occlusion edema.

Advanced macular degeneration in which choroidal neovascular membranes grow beneath or through the retinal pigment epithelium, causing sudden metamorphopsia, hemorrhage, and rapid central vision loss. Anti-VEGF injections are the standard treatment.

Separation of the neurosensory retina from the retinal pigment epithelium caused by a full-thickness retinal break through which liquefied vitreous enters the subretinal space. It presents with flashes, floaters, and a progressive visual field curtain and requires urgent surgical repair.

Age-related separation of the vitreous cortex from the internal limiting membrane, producing sudden floaters and photopsias. It may be complicated by retinal tears or hemorrhage, so a dilated peripheral retinal examination is required.

Swelling of the macula from fluid accumulation within retinal tissue, most often from leakage of perifoveal capillaries. Causes include diabetes, uveitis, vein occlusion, and surgery; optical coherence tomography shows intraretinal cysts and subretinal fluid.

Inflammation of the iris and ciliary body, presenting with pain, photophobia, redness, cells and flare in the anterior chamber, and sometimes keratic precipitates or posterior synechiae. Treatment is topical corticosteroids with cycloplegia, plus investigation for underlying systemic disease.

An adhesion of the iris to adjacent structures. Posterior synechiae bind iris to lens and can cause iris bombé and angle closure; anterior synechiae bind iris to cornea and close the angle. Cycloplegia helps prevent posterior synechiae in uveitis.

A reduced pupillary constriction when light is swung from the healthy eye to the affected eye, indicating asymmetric or unilateral afferent pathway disease such as optic neuropathy or extensive retinal damage. It is elicited with the swinging flashlight test.

Inflammation of the optic nerve, typically presenting with subacute unilateral vision loss, pain on eye movement, color desaturation, and a relative afferent pupillary defect. It is strongly associated with multiple sclerosis and often treated with intravenous corticosteroids.

A bedside examination in which light is alternated between eyes to detect asymmetric afferent conduction. Paradoxical dilation of the pupil when light moves to the affected eye indicates a relative afferent pupillary defect.

A large-vessel vasculitis of older adults affecting cranial arteries, with headache, jaw claudication, scalp tenderness, and elevated inflammatory markers. It can cause irreversible anterior ischemic optic neuropathy; high-dose corticosteroids must start immediately on suspicion.

Infection of the lacrimal sac, usually from nasolacrimal duct obstruction, presenting with a painful, tender swelling below the medial canthus, tearing, and sometimes purulent reflux on pressure. Acute cases need antibiotics and later dacryocystorhinostomy.

Excessive tearing resulting from either overproduction or, more commonly, impaired drainage through the lacrimal system. Evaluation includes punctal examination, syringing, and probing to localize obstruction.

Reduced best-corrected visual acuity in one or both eyes caused by abnormal visual experience during the sensitive period, with no structural abnormality explaining it. Causes include strabismus, anisometropia, and deprivation; treatment is refractive correction plus occlusion or penalization.

Misalignment of the visual axes so the eyes are not simultaneously directed at the same target, classified as esotropia, exotropia, hypertropia, or hypotropia. Childhood-onset cases risk amblyopia and loss of binocularity.

An ocular hypotensive drug, such as timolol, that reduces aqueous production by blocking beta-adrenergic receptors on the ciliary epithelium. It is contraindicated in asthma and heart block and can cause bradycardia and bronchospasm.

A first-line ocular hypotensive agent, such as latanoprost, that increases uveoscleral outflow and is dosed once nightly. Adverse effects include iris darkening, eyelash lengthening, periorbital fat atrophy, and conjunctival hyperemia.

An anti-inflammatory eye drop used for uveitis, postoperative inflammation, and allergic disease. Prolonged use risks ocular hypertension, cataract, and infection; patients require intraocular pressure monitoring and slow tapering.

Exposure of the ocular surface to acid or, more damagingly, alkali, which causes liquefactive necrosis and penetrates deeply. It is a true emergency requiring immediate copious irrigation, pH testing, and urgent ophthalmologic assessment.

A retained object within the eye, typically from high-velocity injury such as hammering or grinding, which may be occult. Suspicion mandates imaging, and metallic or organic material requires urgent surgical removal with antibiotic cover to prevent endophthalmitis.

Determination of the eye's anteroposterior dimension by ultrasound or optical biometry, essential for intraocular lens power calculation and for identifying eyes at risk of refractive surprises.