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OPHTHALMOBYTES

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Elschnig’s Pearls


Posterior capsule opacification is the most common complication of cataract surgery.

Lens Epithelial Cells → Migration → Proliferation → Differentiation


Two types of PCO:


Fibrous Abnormal proliferation of LEC → presents as wrinkles and folds on the posterior capsule site at the fusion of anterior and posterior capsules


Proliferative → Elsching’s Pearls


  • Elsching’s Pearls result from aberrant attempts by lens cells attached to the capsule to form new lens fibres

  • Normally differentiated LEC that line the equatorial lens region migrate and proliferate between posterior capsule and the IOL

  • Clusters of residual LEC appear as round, clear pearls that shine on retro-illumination → Appearance of a bunch of grapes/ soap bubbles/ mass of fish eggs

  • Decreased visual acuity if they accumulate on visual axis





Histology:

Large clear lens cells (bladder cells) are seen behind iris, pupillary space or both areas


Treatment:

Nd:YAG Laser Capsulotomy


Image from Rajan Eye Care Hospital

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Cystoid Macular Edema


Accumulation of fluid intra-retinally in the outer plexiform layer and inner nuclear layer due to disruption of the normal blood retinal barrier which causes leakage from perifoveal retinal capillaries and accumulation of fluid with the formation of visible cystic spaces



Risk Factors

Mnemonic ‘DEPRIVENS’

D - Diabetes (Diabetic Macular Edema)

E - Epinephrine

P - Pars planitis/ Uveitis

R - Retinits Pigmentosa and other retinal dystrophies

I - Irvine Gass Syndrome (post cataract surgery)

V - Vein occlusions

E - E2 - Prostaglandins

N - Nicotinic acid and Niacin

S - Surgery/ Laser (PPV, Cryopexy, Laser photocoagulation, Glaucoma surgery)



Fundus:

Intraretinal cysts within the foveal region of macula in Henle’s layer in a honeycomb pattern

Loss of foveal reflex




OCT:

Intraretinal central cysts- hyporeflectivity at the level of the outer plexiform layer

Loss of foveal depression

Macular thickening


FFA:

Classic ‘petalloid pattern’ or expansile dot appearance in the late phase due to leakage of perifoveal capillaries into cystoid spaces distributed radially in Henle’s layer (OPL)

Leakage from disc and retinal vessels in late phases





Treatment depends on the cause of the CME


Image from Rajan Eye Care Hospital

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Macular Corneal Dystrophy


Autosomal Recessive, CHST6 gene, Chromosome 16q22 - abnormal keratan sulfate

Three types have been defined on the basis of immunoreactivity to specific markers of antigenic keratan sulfates


Type 1 : No AgKS reactivity in the cornea or serum

Type 1A : Keratocytes manifest the AgKS reactivity. Not the serum or corneal extracellular material

Type 2 : The abnormal deposits in the cornea and serum have positive AgKS reactivity.


Symptoms :

Decreased vision & Photophobia




Signs :

  • Anterior stromal white opacities seen in first decade

  • Opacities progress to form a grainy, ground-glass haze between them

  • Extend from limbus to limbus

  • Over time, the cornea thins, endothelium can develop guttae

  • Recurrent corneal erosions

  • Decreased corneal sensations


Histology


Glycosaminoglycan accumulation within and outside stromal keratocytes beneath the epithelium and within endothelial cells.

Stains with Alcian Blue, Colloidal Iron or PAS stain


Treatment :

Phototherapeutic keratectomy (high risk of recurrence)

Corneal transplantation


Mnemonic for main corneal dystrophies abnormal deposits and staining

"Marylin Monroe Always Gets Her Men in L. A. County"

Macular dystrophy - Mucopolysaccharide - Alcian blue

Granular dystrophy - Hyaline materials - Masson trichrome

Lattice dystrophy - Amyloid - Congo red


Image from Rajan Eye Care Hospital

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