•Congenital anomaly.
•Fine or thick strands of connective tissue bridging the pupillary area.
•Represents remnants of anterior tunica vasculosa lentis (supplies nutrition to the lens in the first six month of fetal life)
PATHOPHYSIOLOGY:
•The pupillary membrane undergoes regression aided by macrophage phagocytosis in the 6th month and disappears completely by the 8th month of gestation.
•A failure of resorption of pupillary membrane leads to PPM.
•Can be accelerated by intrauterine stress (maternal hypertension).
SIGNS:
•Lacy strands where one portion inserts into the iris collarette and the other portion can be attached to anterior lens capsule or free floating.
•Rarely, extensive sheet of iris membrane occludes the pupil.
ASSOCIATIONS:
•Amblyopia, coloboma, anterior polar cataract, strabismus, and anterior segment abnormalities like microcornea, microphthalmos and corneal opacity.
DIFFERENTIAL DIAGNOSIS:
•Posterior synechiae.
•Accessory Iris membrane (AIM).
•Axenfeld–Rieger syndrome.
•Peters anomaly.
•Iridocorneal endothelial syndrome (ICE).
MANAGEMENT:
•During the first year of life, most PPMs undergo atrophy and require no treatment.
•Membranes persisting after one year are less likely to regress spontaneously, increasing the risk of amblyopia.
•A 1.5-mm pupillary opening is necessary for adequate retinal stimulation and visual cortex development.
•Management of PPMs depends on the extent of the membrane, and size of the pupillary opening.
•Small PPMs: Mydriatics, refractive correction, and patching for amblyopia can be done.
•Thick, fibrotic membranes: Membranectomy with visco protection.
•Older patients with thin, sparse membranes: Nd:YAG laser membrane lysis.
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