What is keratoconus Keratoconus ?
Keratoconus (KC) may be a progressive disorder during which central or paracentral corneal stromal thinning occurs, amid apical protrusion and irregular astigmatism.
Approximately 50% of normal fellow eyes will reach KC within 16 years. Both eyes are affected eventually, a minimum of on topographical imaging, in most cases. It are often graded by the very best axis of corneal power on keratometry as mild (54 D).
Most patients don't have a case history , with only about 10% of offspring developing KC; autosomal dominant transmission with incomplete penetrance has been proposed.
Presentation is usually during the teenagers or twenties, with features initially in just one eye. Systemic associations include Down, Ehlers–Danlos and Marfan syndromes and osteogenesis imperfecta; ocular associations include vernal keratoconjunctivitis, blue sclera, aniridia, Leber congenital amaurosis, retinitis pigmentosa, also as persistent eye rubbing from any cause.
Symptoms. Unilateral impairment of vision thanks to progressive myopia and astigmatism; occasionally, initial presentation is with acute hydrops.-
Approximately 50% of normal fellow eyes will reach KC within 16 years. Both eyes are affected eventually, a minimum of on topographical imaging, in most cases. It are often graded by the very best axis of corneal power on keratometry as mild (54 D).
Most patients don't have a case history , with only about 10% of offspring developing KC; autosomal dominant transmission with incomplete penetrance has been proposed.
Presentation is usually during the teenagers or twenties, with features initially in just one eye. Systemic associations include Down, Ehlers–Danlos and Marfan syndromes and osteogenesis imperfecta; ocular associations include vernal keratoconjunctivitis, blue sclera, aniridia, Leber congenital amaurosis, retinitis pigmentosa, also as persistent eye rubbing from any cause.
Diagnosis
Symptoms. Unilateral impairment of vision thanks to progressive myopia and astigmatism; occasionally, initial presentation is with acute hydrops.-
• Signs
○ Direct ophthalmoscopy from a distance of half a metre shows a reasonably well delineated ‘oil droplet’ reflex.
○ Retinoscopy shows an irregular ‘scissoring’ reflex.
○ Slit lamp biomicroscopy shows very fine, vertical, deep stromal stress lines, which disappear with pressure on the world .○ Epithelial iron deposits, best seen with a cobalt blue filter, may surround the bottom of the cone.
○ Progressive corneal protrusion during a cone configuration , with thinning maximal at the apex.
○ Bulging of the lower lid in downgaze (Munson sign).
○ Acute hydrops is caused by a rupture within the stretched Descemet membrane that permits a sudden influx of aqueous into the cornea, with accompanying pain, photophobia and decreased vision.
Although the break usually heals within 6–10 weeks and therefore the oedema clears, a variable amount of stromal scarring may develop; this sometimes gives improved vision by flattening the cornea.
Acute episodes are initially treated with cycloplegia, hypertonic (5%) saline ointment and patching or a soft bandage contact .
Accelerated resolution has been reported with intracameral gas injection within the acute stage.
• Keratometry readings are steep.
• Corneal topography (videokeratography) and various novel corneal profiling techniques are sensitive for detection and essential in monitoring. Characteristically, astigmatism progresses from a symmetrical bow-tie pattern, through an asymmetrical appearance to an inferotemporally displaced steep-sided cone. Sometimes a central (‘nipple’) cone may develop.
contact warpage can sometimes appear almost like a cone on topography, but is usually more arcuate-shaped.
○ Retinoscopy shows an irregular ‘scissoring’ reflex.
○ Slit lamp biomicroscopy shows very fine, vertical, deep stromal stress lines, which disappear with pressure on the world .○ Epithelial iron deposits, best seen with a cobalt blue filter, may surround the bottom of the cone.
○ Progressive corneal protrusion during a cone configuration , with thinning maximal at the apex.
○ Bulging of the lower lid in downgaze (Munson sign).
○ Acute hydrops is caused by a rupture within the stretched Descemet membrane that permits a sudden influx of aqueous into the cornea, with accompanying pain, photophobia and decreased vision.
Although the break usually heals within 6–10 weeks and therefore the oedema clears, a variable amount of stromal scarring may develop; this sometimes gives improved vision by flattening the cornea.
Acute episodes are initially treated with cycloplegia, hypertonic (5%) saline ointment and patching or a soft bandage contact .
Accelerated resolution has been reported with intracameral gas injection within the acute stage.
• Keratometry readings are steep.
• Corneal topography (videokeratography) and various novel corneal profiling techniques are sensitive for detection and essential in monitoring. Characteristically, astigmatism progresses from a symmetrical bow-tie pattern, through an asymmetrical appearance to an inferotemporally displaced steep-sided cone. Sometimes a central (‘nipple’) cone may develop.
contact warpage can sometimes appear almost like a cone on topography, but is usually more arcuate-shaped.
Treatment
LASIK is contraindicated; patients should be screened for KC before corneal refractive surgery.
• Eye rubbing should be avoided.
Spectacles or soft contact lenses are generally sufficient in early cases. If thinning is marked, it's going to be prudent to think about wearing safety spectacles over contact lenses.
• Rigid contact lenses, sometimes scleral, are required for higher degrees of astigmatism to supply a daily refracting
• Corneal collagen cross-linking (CXL), using riboflavin drops to photosensitize the attention followed by exposure to ultraviolet-A light, may stabilize or maybe reverse ectasia, but isn't without adverse effects.
It are often combined with ring segment insertion. CXL is usually used only after progression has been documented.
• Intracorneal ring segment implantation using laser or mechanical channel creation is comparatively safe, and typically provides a minimum of a moderate visual improvement, facilitating contact tolerance in advanced cases.
• Keratoplasty, either penetrating or deep anterior lamellar (DALK), could also be necessary in patients with severe disease.
A history of hydrops may be a contraindication to DALK thanks to the presence of a Descemet membrane discontinuity.
Outcomes could also be compromised by residual astigmatism and by anisometropia, necessitating contact correction for optimal acuity.-
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• Eye rubbing should be avoided.
Spectacles or soft contact lenses are generally sufficient in early cases. If thinning is marked, it's going to be prudent to think about wearing safety spectacles over contact lenses.
• Rigid contact lenses, sometimes scleral, are required for higher degrees of astigmatism to supply a daily refracting
• Corneal collagen cross-linking (CXL), using riboflavin drops to photosensitize the attention followed by exposure to ultraviolet-A light, may stabilize or maybe reverse ectasia, but isn't without adverse effects.
It are often combined with ring segment insertion. CXL is usually used only after progression has been documented.
• Intracorneal ring segment implantation using laser or mechanical channel creation is comparatively safe, and typically provides a minimum of a moderate visual improvement, facilitating contact tolerance in advanced cases.
• Keratoplasty, either penetrating or deep anterior lamellar (DALK), could also be necessary in patients with severe disease.
A history of hydrops may be a contraindication to DALK thanks to the presence of a Descemet membrane discontinuity.
Outcomes could also be compromised by residual astigmatism and by anisometropia, necessitating contact correction for optimal acuity.-
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