CLINICAL OPHTHALMOLOGY 2 COLOBOMA OF THE EYELID (FIG. 1.1) A notch or defect of the lid margin. Unilateral or bilateral; upper or lower. In upper lid: at the junction of middle and inner 1/3 and in lower lid at middle and outer 1/3 junction. Treatment: Urgent plastic repair at a very early age to prevent exposure keratitis. BLEPHAROPHIMOSIS SYNDROME (FIG. 1.2) Autosomal dominant. Consists of bilateral narrowing of palpe- bral apertures, telecanthus, inverse epicanthus folds, lateral ectropion and moderate to severe ptosis. Treatment: Plastic reconstruc- tion of the eyelids, along with bilateral brow suspension for ptosis. Fig. 1.1: Lid coloboma Fig. 1.

CLINICAL OPHTHALMOLOGY 22 Fig. 2.1A: Subconjunctival hemorrhage Fig. 2.1B: Bilateral subconjunctival hemorrhagewhooping cough SUBCONJUNCTIV A L HEMORRHAGE (FIGS 2.1A AND B) Rupture of a conjunctival blood vessel causes a bright red, shar- ply delineated area surrounded by the normal appearing con- junctiva. Usually unilateral, but it may be bilateral when precipitated by some straining factor. Treatment: Only assurance and astringents eyedrops.

CLINICAL OPHTHALMOLOGY 48 PIGMENT DEPOSITION IN THE CORNEA (FIGS 3.

CLINICAL OPHTHALMOLOGY 100 SHALLO W ANTERIOR CHAMBER (FIGS 4.1A T O D) Causes: Cornea plana; hyper- metropia; angle closure glau- coma; intumescent cataract ; Fig. 4.1A: Normal depth AC Fig. 4.1B: Mild shallow AC Fig. 4.1C: V e r y shallow A C Fig. 4.1D: Shallow ACmalignant glaucoma over filtration of filtering bleb; choroidal detachment; wound leak after intraocular surgery; penetrating injury; malignant glaucoma, etc.

CLINICAL OPHTHALMOLOGY 122 ANIRIDIA (FIGS 5.1A AND B) Whole of the iris is appeared to be missing on external exami- nation; Ciliary processes and suspensory ligaments of the lens are visible; Subluxation of lens and secondary glaucoma in 25% of the cases. Aniridia and Wilms tumor are associated with deletion of the short arm of chromosome-11 (Millers syndrome). Fig. 5.

CLINICAL OPHTHALMOLOGY 152 COLOBOMA OF THE LENS (FIGS 6.1A AND B) Rare unilateral or bilateral condition, may occur with typical coloboma of the uveal tract; or rarely in isolation. Notching of the lens at the inferior equator. Fig. 6.1A: Coloboma of the lens Fig. 6.

CLINICAL OPHTHALMOLOGY 178 CONGENIT AL GLA UCOMA (BUPHTHALMOS) Primary (Figs 7.1A to C) Congenital or infantile glau- coma is due to simple outflow obstruction; rare, unilateral or bilateral condition. Autosomal recessive; boys are more affec- ted than girls. Eyeball becomes enlarged, if the IOP becomes elevated prior to age of three years; cornea is enlarged, globular and steamy; horizontal curvilinear lines are seen on the back of the cornea, known as Haabs striae; blue discolouration of sclera; deep anterior chamber; cupping of the disc Treatment: Examination under anesthesia; goniotomy, trabe- culotomy or trabeculectomy and trabeculotomy, and visual rehabilitation. Fig. 7.1A: Primary congenital glaucoma Fig. 7.

CLINICAL OPHTHALMOLOGY 202 ASTEROID HYALOSIS (BENSONS DISEASE) (FIG. 8.1) Usually bilateral, that affects aged patients; appear as nume- rous, white, round or discoid bodies suspended throughout, or in a portion of the solid vitreous; represents calcium soap crystals from degeneration of vitreous fibrils. Asymptomatic and do not require treatment. SYNCHISIS SCINTILLANS (FIG. 8.2) Unilateral, with previous h/o vitreous hemorrhage or inflam- mation; crystals appear as gol- den glittering particles which settle at the bottom of vitreous cavity; can be thrown upwards by ocular movements, to form a golden shower. No effective treatment. Fig. 8.1: Asteroid hyalosis Fig. 8.

CLINICAL OPHTHALMOLOGY 278 MYELINA TED NER VE FIBERS (FIGS 9.1A AND B) Congenital1% of normal population; 20% cases bilateral. Appears as white patch with radial feathery striations at its peripheral edge; Usually peri- papillary, but sometimes peri- pheral and isolated; In optic atrophy, it disappears. No treatment is required. CONGENIT AL OPTIC DISK PIT (FIG. 9.2) Isolated unilateral condition; round or oval depression at the temporal margin. A central pit is less common. No treatment is required. Fig. 9.1A: Myelinated nerve fiberstypical Fig. 9.1B: Myelinated nerve fibersperipheral Fig. 9.

CLINICAL OPHTHALMOLOGY 300 CRANIOSYNOSTOSIS Follows premature closure of one/more cranial sutures. A complete arrest of bony growth perpendicular to the closed suture . Compensatory growth of the cranium in other diameters which causes the typical shape of the skull. Common features : B ilateral proptosis due to shallow orbit E sotropia or exotropia C hemosis of conjunctiva, corneal exposure P apilledema due to increased ICT O ptic atrophy. Treatment: by craniotomy or orbital compression to reduce CSF pressure and papilledema. CRANIOF A CIAL DYSOSTOSIS (CROUZON) (FIGS 10.1A AND B ) Brachycephaly: (clover leaf skull) premature closure of all sutures combined with hypo- plasia of the maxilla; often hereditary in nature. Figs 10.

CLINICAL OPHTHALMOLOGY 320 ACUTE DACRYOADENITIS (FIG. 11.1) Associated with systemic diseases like mumps, influenza or glandular fevers. Characterized by acute local pain, swelling and tenderness. Drooping of the outer part of upper lid with an S-shaped curve. Treatment: Usually self limiting, but systemic antibiotics and local hot compress are required in some cases. Fig. 11.

CLINICAL OPHTHALMOLOGY 328 APP ARENT SQUINT : PSEUDOSTRABISMUS (FIGS 12.1A AND B) Here, the visual axes are in fact parallel, but the eyes seem to have squint. Causes: Prominent epicanthic folds: May simulate a convergent squint Telecanthus: Also simulate a convergent squint Hypertelorism: May simulate a divergent squint Hypermetropia: An apparent divergent squint due to large angle kappa Myopia: An apparent conver- gent squint due to smaller or even negative angle kappa. Squint in these conditions may be easily excluded by checking the relative position of corneal light reflections and also by other means. Fig. 12.1A: Epicanthuspseudo- convergent squint Fig. 12.

CLINICAL OPHTHALMOLOGY 348 CONTUSIONS (BLUNT INJURIES) Ocular injuries by various blunt instruments vary in severity depending upon the nature of impact. It may be from simple sub- conjunctival hemorrhage to globe rupture; some effects are progressive or may be delayed. So during treatment, a guarded prognosis should be given to such injuries. VARIOUS EFFECTS RESULTING FROM CONTUSIONS Eyelids (Figs 13.1A to C) Lid lacerations; Swelling and ecchymosis (black eye) of the lids Panda bear sign; emphy- sema of the eyelids. Fig. 13.1A: Lid laceration Fig. 13.1B: Black eyePanda bear sign Fig. 13.

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