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Dr. Christina
 Progressive disorder in which the cornea 
assumes a conical shape secondary to corneal 
thinning and protrusion 
 Onset is around puberty- progresses untill 3rd 
or 4th decades of life 
 Both eyes affected usually 
 Role of hereditary transmission is not clear.
PRESENTATION 
 Presents usually during puberty. 
 Impairment of vision due to progressive 
myopia and irregular astigmatism. 
 Asymmetrical nature. 
 Approximately 50% of normal fellow eyes will 
progress to keratoconus within16 years.
DIAGNOSIS 
 Central or paracentral stromal thinning, 
apical protrusion and irregular astigmatism 
SIGNS: 
 Direct ophthalmoscopy shows ‘oil droplet 
sign’. 
 Retinoscopy shows irregular’ scissor’ reflex’ 
 Slit lamp microscopy showsfine, vertical, 
deep stromal striae called vogts striae .
 Epithelial iron deposits may surround the 
base of cone –’fleischer ring’. 
 Marked irregular myopic astigmatism with 
steep keratometry reading. 
 Bulging of the lower lid in down gaze- 
‘munson sign’. 
 Corneal topography – sensitive method of 
detecting early keratoconus.
ACUTE HYDOPS 
 Caused by rupture of descemets membrane 
that allows influx of aqueous into the conea. 
 Causes sudden drop in visual acuity with 
discomfort and watering. 
 Usually the break heals within 6-10 weeks and 
edema clears but scarring results 
 Treatment is keratoplasty after edema 
resolves.
ASSOCIATIONS 
 SYSTEMIC DISORDERS LIKE Down, Turner, 
Ehler-Danlos and Marfan syndromes, atopy, 
oesteogenesis imperfecta, MVP, mental 
retardation. 
 OCULAR DISORDERS like vernal kerato 
conjunctivitis, blue sclera, aniridia, ectopia 
lentis, RP
TREATMENT 
 Spectacles in early stages. 
 Rigid contact lenses for higher degrees of 
irregular astigmatism..Piggy back lenses. 
 Keratoplasty : both lamellar and penetrating 
keratoplasty especially in cases of severe 
corneal scarring.
THANK YOU

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Keratoconus

  • 2.  Progressive disorder in which the cornea assumes a conical shape secondary to corneal thinning and protrusion  Onset is around puberty- progresses untill 3rd or 4th decades of life  Both eyes affected usually  Role of hereditary transmission is not clear.
  • 3. PRESENTATION  Presents usually during puberty.  Impairment of vision due to progressive myopia and irregular astigmatism.  Asymmetrical nature.  Approximately 50% of normal fellow eyes will progress to keratoconus within16 years.
  • 4.
  • 5. DIAGNOSIS  Central or paracentral stromal thinning, apical protrusion and irregular astigmatism SIGNS:  Direct ophthalmoscopy shows ‘oil droplet sign’.  Retinoscopy shows irregular’ scissor’ reflex’  Slit lamp microscopy showsfine, vertical, deep stromal striae called vogts striae .
  • 6.  Epithelial iron deposits may surround the base of cone –’fleischer ring’.  Marked irregular myopic astigmatism with steep keratometry reading.  Bulging of the lower lid in down gaze- ‘munson sign’.  Corneal topography – sensitive method of detecting early keratoconus.
  • 7. ACUTE HYDOPS  Caused by rupture of descemets membrane that allows influx of aqueous into the conea.  Causes sudden drop in visual acuity with discomfort and watering.  Usually the break heals within 6-10 weeks and edema clears but scarring results  Treatment is keratoplasty after edema resolves.
  • 8.
  • 9. ASSOCIATIONS  SYSTEMIC DISORDERS LIKE Down, Turner, Ehler-Danlos and Marfan syndromes, atopy, oesteogenesis imperfecta, MVP, mental retardation.  OCULAR DISORDERS like vernal kerato conjunctivitis, blue sclera, aniridia, ectopia lentis, RP
  • 10. TREATMENT  Spectacles in early stages.  Rigid contact lenses for higher degrees of irregular astigmatism..Piggy back lenses.  Keratoplasty : both lamellar and penetrating keratoplasty especially in cases of severe corneal scarring.