17.ophthalmology Final PDF

OPHTHALMOLOGY
INDEX
S. No. Topics Pg. Nos.
1 Glaucoma 3-13
2 Cataract 14-26
3 Uveitis 26-32
4 Conjunctivitis 32-34
5 Visual Field Defects 35-37
6 Diabetic Retinopathy 37-39
7 Retinoblastoma 40-41
8 Anatomy 42-50
9 Cranial Nerve Palsy 50-54
10 Myopia 54-55
11 Herpes 56-58
12 Papilledema 58-60
13 Strabismus 61-65
14 Corneal Ulcer 66-69
15 Ophthalmoscopy Direct & Indirect 69-71
16 Blunt Trauma Eye 71-72
17 Contact Lens 73-74
18 Trachoma 74-76
19 CRAO 76-78
20 Sympathetic Ophthalmitis 78-79
21 Proptosis 79-80
22 Blindness Control Programme 80-84
23 Amblyopia 84-86
24 Dacryocystitis 86-87
25 Hypermetropia 87-89
26 Mydriatics 89-93
27 Optic Neuritis 94-95
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OPHTHALMOLOGY
INDEX
S. No. Topics Pg. Nos.
28 Chalazion 95-96
29 Retinitis Pigmentosa 96-97
30 Colour Blindness 97-98
31 Keratomalacia 98-99
32 Lens Dislocation 100-101
33 Acanthamoeba 101-102
34 Central Serous Retinopathy 102-104
35 Corneal Dystrophy 104-105
36 Enucleation Evisceration 105
37 Foreign Body 105-106
38 Keratoconus 106-107
39 Melanoma 107-108
40 Orbit Fracture 108-109
41 Paras Planitis 109
42 Retinal Detatchment 109-111
43 Cavernous Sinus Thrombosis 111-112
44 CMV Retinitis 113
45 Eales Disease 113
46 Ophthalmia Neonatarum 113-114
47 Optic Nerve Glioma 114
48 Retrolental Fibroplasia 114-115
49 Aphakia 115-116
50 Band Keratopathy 116-117
51 Optic Atrophy 117-118
52 Ptosis 118-119
53 Rhabdomyosarcoma 119
54 Vitreous Hemorrhage 119-120
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TOPIC 1 - GLAUCOMA n abnormally high IOP which results due to
developmental anomaly of the angle of the anterior chamber,
n IOP is the most common risk for development of not associated with any other ocular or systemic
glaucoma. anomaly.
n ‘ocular hypertension’ is used for cases having constantly n True congenital glaucoma
raised IOP without any associated m labelled when IOP is raised during intrauterine
glaucomatous damage. life
n normal or low tension glaucoma (NTG/LTG) is suggested m child is born with ocular enlargement.
for the typical cupping of the disc and/or visual n Infantile glaucoma
field defects associated with a normal or low IOP. m labelled when the disease manifests prior to the
n Classification child’s third birthday.
m Congenital and developmental glaucomas m It occurs in about 50 percent of cases.(most
n Primary congenital glaucoma (without common type )
associated anomalies). m eyeball enlarges and so the term‘buphthalmos’
n Developmental glaucoma (with associated (bull-like eyes) is used.
anomalies).
OPHTHALMOLOGY
m results due to retention of aqueous humour – it is
m Primary adult glaucomas called ‘hydrophthalmos
n Primary open angle glaucomas (POAG) n Juvenile glaucoma
n Primary angle closure glaucoma (PACG) m develop pressure rise between 3-16 years of life.
n Primary mixed mechanism glaucoma n Prevalence and genetic pattern
m Secondary glaucomas m over 65 percent of the patients are boys.
n Pathogenesis of glaucomatous ocular damage m disease is bilateral in 75 percent cases
n all glaucomas are characterized by a n Pathogenesis
progressive optic neuropathy m Trabeculodysgenesis
n results from the death of retinal ganglion n Maldevelopment of trabeculum including the
cells (RGCs) iridotrabecular junction
n Retinal ganglion cell death is associated with n responsible for impaired aqueous outflow resulting
loss of retinal nerve fibres. in raised IOP.
n Etiological factors n Flat iris insertion is more common than the
GLAUCOMA
m Raised intraocular pressure (Mechanical theory). concave iris insertion.
n causes mechanical stretch on the lamina n Clinical features
cribrosa m Photophobia, blepharospasm, lacrimation and
n leads to axonal deformation and ischaemia eye rubbing often occur together (MCQ)
by altering capillary blood flow m Corneal signs
n neurotrophins (growth factors) are not able n Corneal oedema.
to reach the retinal ganglion cell bodies in l It is frequently the first sign which arouses
sufficient amount needed for their survival. suspicion.
m Pressure independent factors (Vascular insufficiency n Corneal enlargement.
theory). l Normal infant cornea measures 10.5 mm.
n Failure of autoregulatory mechanism of blood flow. l A diameter of more than 13 mm confirms
l NTG is vasospastic disorders (migranous enlargement. (MCQ)
headache and Raynaud’s phenomenon). l Prognosis is usually poor in infants with
n Systemic hypotension corneal diameter of more than 16 mm.
l nocturnal dips in patients with night time n Tears and breaks in Descemet’s membrane (Haab’s
administration of antihypertensive drugs striae). (MCQ)
cause low vascular perfusion of optic nerve head l Tears are usually peripheral and concentric
resulting in NTG. with the limbus.
m Secondary insults (Excitotoxicity theory) m Sclera becomes thin and appears blue due to
n glutamate (excitatory toxin), oxygen free underlying uveal tissue.
radicals, or nitric oxide which are released m Anterior chamber becomes deep.
when RGCs undergo death due to primary m Iris may show iridodonesis and atrophic
insults patches in late stage.
Primary developmental/congenital glaucoma
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m Lens becomes flat due to stretching of zonules n It forms about one- third cases of all glaucomas.
and may even subluxate. (MCQ) n Etiopathogenesis
m Optic disc may show variable cupping and m Predisposing and risk factors.
atrophy especially after third year. n POAG has a polygenic inheritance
m IOP is raised which is neither marked nor acute. n POAG is more commonly seen in elderly
m Axial myopia may occur because of increase in between 5th and 7th decades.
axial length which may give rise to n develops earlier and is more severe in black
anisometropic amblyopia. people than in white.
n Differential diagnosis n Myopes are more predisposed than the normal
m Raised IOP in infants may also be associated (MCQ)
with retinoblastoma, retinopathy of prematurity, persistent n Diabetics have a higher revalence of POAG
primary hyperplastic vitreous, traumatic glaucoma and (MCQ)
secondary congenital glaucoma seen in rubella, aniridia and n Cigarette smoking is also thought to increase
Sturge-Weber syndrome. its risk.
n Treatment n Systemic hypertension does not rise IOP
OPHTHALMOLOGY
m Treatment of congenital glaucoma is primarily n prevalence of POAG is more in hypertensives

surgical. than the normotensives.
m IOP must be lowered by use of hyperosmotic n Thyrotoxicosis is not a risk factor for POAG
agents, acetazolamide and beta- blockers till (MCQ)
surgery is taken up. n prevalence of POAG is more in patients
m Miotics are of no use in such cases. suffering from Graves’ ophthalmic disease
m Surgical procedures for congenital glaucoma m Corticosteroid responsiveness.
n Goniotomy n six weeks topical steroid therapy cause
n Trabeculotomy. (MCQ) significant rise of IOP.
l This is useful when corneal clouding n CLINICAL FEATURES
prevents visualization of the angle or in m Symptoms
cases where goniotomy has failed. n The disease is insidious
l The main difficulty in this operation is n usually asymptomatic, until it has caused a
GLAUCOMA
localization of the Schlemm’s canal. significant loss of visual field

n Combined trabeculotomy and l Therefore, periodic eye examination is
trabeculectomy is now-a-days the preferred required after middle age.
surgery with better results. (MCQ) n Patients may experience mild headache and
n Developmental glaucomas with associated eyeache.
anomalies n Rarely, patient may notice a defect in the visual
m Glaucoma associated with iridocorneal dysgenesis. field.
n posterior embryotoxon characterised by a n Reading and close work often present
prominent Schwalbe’s ring (Axenfeld anomaly) increasing difficulties
n Rieger anomaly l accommodative failure due to constant
n Peter’s anomaly pressure on the ciliary muscle and its nerve supply.
m Glaucoma associated with ectopia lentis syndromes l patients usually complain of frequent
n Marfan’ s syndrome, changes in presbyopic glasses (MCQ)
n Weil-Marchesani syndrome n Patients develop delayed dark adaptation
n homocystinuria. m Signs
m Glaucoma associated with phakomatosis n Anterior segment signs
n Sturge-Weber syndrome ( 50% cases) l slit-lamp biomicroscopy may reveal normal
n Von Recklinghausen’s neurofibromatosis (25% anterior segment
cases). l In late stages pupil reflex becomes sluggish
m Lowe’ s syndrome - oculo-cerebro-renal syndrome and cornea may show slight haze.
Primary open angle glaucoma n Intraocular pressure changes.
n also known as chronic simple glaucoma of adult l In the initial stages
onset „ the IOP may not be raised permanently
n typically characterised by slowly progressive raised
intraocular pressure (>21 mmHg)
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„ but there is an exaggeration of the „ Pallor areas on the disc.
normal diurnal variation. „ Atrophy of retinal nerve fibre layer (MCQ)
l Diurnal variation test ® may be seen with red free light.
„ repeated observations of IOP (every 3-4 l Advanced glaucomatous changes in the
hour), for 24 hours is required during this optic disc
stage). „ Marked cupping (cup size 0.7 to 0.9) (MCQ)
„ Patterns of diurnal variations of IOP ® Excavation may even reach the disc
® morning rise seen in 20% cases of margin
POAG ® the sides are steep and not shelving
® afternoon rise seen in 25% cases of (unlike deep physiological cup).
POAG; „ Thinning of neuroretinal rim
® biphasic variation seen in 55% cases of ® seen as a crescentric shadow adjacent
POAG. to the disc margin.
„ In most patients IOP falls during the „ Nasal shifting of retinal vessels
evening, contrary to what happens in closed angle ® Bayonetting sign (MCQ)
OPHTHALMOLOGY
glaucoma » have the appearance of being broken
„ A variation in IOP of over 5 mm Hg off at the margin
(Schiotz) is suspicious and over 8 mm of » When the edges overhang, the course
Hg is diagnostic of glaucoma. (MCQ) of the vessels as they climb the
l In later stages, IOP is permanently raised sides of the cup is hidden.
above 21 mm of Hg and ranges between 30 „ Pulsations of the retinal arterioles
and 45 mm of Hg. (MCQ) ® seen at the disc margin
n Optic disc changes ® a pathognomic sign of glaucoma
l provide an important clue for suspecting (MCQ)
POAG ® occur hen IOP is very high.
l These are typically progressive, asymmetric „ Lamellar dot sign (MCQ)
l present a variety of characteristic clinical ® pores in the lamina cribrosa are slit-
patterns. shaped and are visible up to the margin
l It is essential to record the appearance of of the disc.
GLAUCOMA
the nerve head n Glaucomatous optic atrophy.
l Record subtle glaucomatous changes over the „ optic nerve head appears white and deeply
course of follow-up evaluation. excavated
l Confocal scanning laser topography „ Cavernous optic atrophy
(CSLT) i.e., Heidelberg retinal ® ischaemic atrophy of the nerve fibres
tomograph (HRT) is an accurate and sensitive without corresponding increase of
method for this purpose. supporting glial tissue.
l advanced imaging techniques ® As a result, large caverns or lacunae are
„ optical coherence tomography (OCT) formed
„ scanning laser polarimetry i.e., Nerve fibre analyser n Visual field defects.
(NFA). „ Distribution of retinal nerve fibres
l Early glaucomatous changes ® Fibres from nasal half of the retina
„ Vertically oval cup (MCQ) » come directly to the optic disc
® due to selective loss of neural rim » as superior and inferior radiating
tissue in the inferior and superior poles. fibres (srf and irf).
„ Asymmetry of the cups ® Those from the macular area
® A difference of more than 0.2 between » come horizontally as papillomacular
two eyes is significant. bundle (pmb).
„ Large cup ® Fibres from the temporal retina
® 0.6 or more (normal cup size is 0.3 to » arch above and below the macula and
0.4) papillomacular bundle
® occur due to concentric expansion. » arch as superior and inferior arcuate
„ Splinter haemorrhages present on or near the fibres with a horizontal raphe in
optic disc margin. between (saf and iaf).
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„ Arrangement of nerve fibres within ® It may appear either below or above
optic nerve head the blind spot in Bjerrum’s area.
® fibres from the peripheral part of the „ Seidel’s scotoma. (MCQ)
retina ® With the passage of time paracental
» lie deep in the retina scotoma joins the blind spot to form
» occupy the most peripheral a sickle shaped scotoma known as Seidel’s
(superficial) part of the optic disc. scotoma
® fibres originating closer to the nerve „ Arcuate or Bjerrum’s scotoma. (MCQ)
head ® It is formed at a later stage
» lie superficially in the retina ® Formed by the extension of Seidel’s
» occupy a more central (deep) scotoma in an area either above or below
portion of the disc. the fixation point to reach the horizontal
„ Arcuate nerve fibres Versus Macular line
fibres (MCQ) ® Damage to the adjacent fibres causes a
® Arcuate nerve fibres occupy the superior peripheral breakthrough.
OPHTHALMOLOGY
and inferior temporal portions of „ Ring or double arcuate scotoma.

optic nerve head ® It develops when the two arcuate
» most sensitive to glaucomatous scotomas join together
damage (MCQ) „ Roenne’s central nasal step. (MCQ)
» account for the early loss in the ® It is created when the two arcuate
corresponding regions of the visual scotomas run in different arcs and meet
field. to form a sharp right-angled defect
® Macular fibres at the horizontal meridian
» most resistant to the glaucomatous „ The peripheral nasal step of Roenne’s
damage ® results from unequal contraction of
» explain the retention of the central the peripheral isopter.
vision till end „ Advanced glaucomatous field defects.
n Progression of field defects. ® eventually only a small island of central
GLAUCOMA
n Visual field defects in glaucoma are initially vision (tubular vision) and an
observed in Bjerrum’s area (MCQ) accompanying temporal island are left.
„ Bjerrum’s area is an arcuate area extending ® The temporal island of the vision is
above and below the blind spot to between more resistant and is lost in the end leaving
10o and 20o of fixation point the patient with no light perception.
n Sequence of changes in natural history of n POAG may sometimes be associated with
the progressive glaucomatous field loss „ high myopia
„ Isopter contraction (MCQ) „ Fuchs’ endothelial dystrophy
® mild generalised constriction of central „ retinitis pigmentosa
as well as peripheral field „ central retinal vein occlusion
® It is the earliest visual field defect „ primary retinal detachment.
occurring in glaucoma. n INVESTIGATIONS
® it is of limited diagnostic value, as it m Tonometry.
may also occur in many other conditions. n Applanation tonometry should be preferred
„ Baring of blind spot (MCQ) over Schiotz tonometry
® exclusion of the blind spot from the n Diurnal variation test is especially useful in
central field detection of early cases
® occur due to inward curve of the outer m Gonioscopy.
boundary of 30° central field n It reveals a wide open angle of anterior
® an early glaucomatous change chamber.
® very non-specific and thus of limited n Its primary importance in POAG is to rule out
diagnostic value. other forms of glaucoma.(MCQ)
„ Small wing-shaped paracentral scotoma m Documentation of optic disc changes is of utmost
® It is the earliest clinically significant importance
field defect.
6
Slit-lamp examination of anterior segment to rule
m n visual field charting.
out causes of secondary open angle glaucoma. n Medical therapy
m Perimetry to detect the visual field defects. m The initial therapy of POAG is still medical, with
m Nerve fibre layer analyzer (NFLA) surgery as the last resort.(MCQ)
n helps in detecting the glaucomatous damage to m Basic principles of medical therapy of POAG
the retinal nerve fibres before the appearance n Identification of target pressure.
of actual visual field changes and/or optic n progression is uncommon if IOP is
disc changes. maintained at less than 16 to 18 mm of Hg in
m Provocative tests are required in border-line cases. patients having mild to maderate damage.
n water drinking test - test commonly n Lower target pressures (12-14 mmHg) are
performed required in patients with severe damage.
l A rise of 8 mm of Hg or more is said to be m Treatment regimes.
diagnostic of POAG. n Single drug therapy
n combined water drinking and l Topical beta-blockers
tonography(MCQ) „ first drug of choice for medical therapy of
OPHTHALMOLOGY
n bulbar pressure test POAG in poor and average income
n prescoline test patients.
n caffeine test. „ Lower IOP by reducing the aqueous secretion
n DIAGNOSIS due to their effect on beta - receptors in
m 3 diagnostic entities the ciliary processes.
n Primary open angle glaucoma (POAG). l Timolol maleate
l raised IOP (>21 mm of Hg) is associated „ should not be used in patients having associated
with definite glaucomatous optic disc cupping and bronchial asthma and/or heart blocks.(MCQ)
visual field changes. l Betaxolol
n Ocular hypertension or glaucoma suspect. „ a selective beta-1 blocker
l when a patient has an IOP constantly more than „ it is preferred as initial therapy in patients
21 mm of Hg but no optic disc or visual with cardiopulmonary problems.
field changes l Levobunolol
n Normal tension glaucoma (NTG) or low „ Its action lasts the longest (MCQ)
GLAUCOMA
tension glaucoma (LTG) „ more reliable for once a day use than
l when typical glaucomatous disc cupping timolol.
with or without visual field changes is l Carteolol
associated with an intraocular pressure constantly „ It affect lipid profile the least.
below 21 mm of Hg „ Therefore, it is the best choice in patients
Severity of glaucoma damage with POAG having associated

hyperlipidemias or atherosclerotic
Degree Description
cardiovascular disease.
Mild Characteristic optic-nerve abnormalities l Pilocarpine
are consistent with glaucoma but with „ contracts longitudinal muscle of ciliary
normal visual field. body and opens spaces in trabecular
Moderate Visual-field abnormalities in one hemi-field meshwork
and not within 5 degrees of fixation. „ it mechanically increases aqueous outflow.
Severe Visual-field abnormalities in both „ It is sheet anchor in the medical management
hemifields and within 5 degrees of fixation. of POAG for a long time.(MCQ) presently
it is not being preferred as the first drug of
n MANAGEMENT choice or even as second choice.
m perform a good baseline examination with
„ presently pilocarpine is being considered
which future progress can be compared. visual acuity only as an adjunctive therapy
n slit-lamp examination of anterior segment
„ in younger patients it causes problems due to
n tonometry (preferably with applanation tonometer)
® spasm of accommodation
n optic disc evaluation (preferably with fundus
® miosis.
photography) „ Most, but not all, older patients tolerate
n gonioscopy
pilocarpine very well
7
® axial lenticular opacities when present m considered in patients where IOP is uncontrolled
precludes its use in many such patients. despite maximal tolerated medical therapy.
l Latanoprost (MCQ) m shown to lower IOP by
„ It is a prostaglandin n 8-10 mm of Hg in patients on medical therapy
„ decreases the IOP by increasing the uveo- n 12-16 mm in patients who are not receiving medical
scleral outflow of aqueous. treatment.
„ considered the drug of first choice for m Complications.
the treatment of POAG n transient acute rise of IOP
„ it is expensive to buy l can be prevented by pretreatment with
„ it is a very good adjunctive drug to beta- pilocarpine and/or acetazolamide
blockers, dorzolamide and even n inflammation
pilocarpine when additional therapy is l can be lessened by use of topical steroids
indicated. for 3-4 days.
l Dorzolamide n Haemorrhage
„ topical carbonic anhydrase inhibitor n Uveitis
OPHTHALMOLOGY
„ lowers IOP by decreasing aqueous n peripheral anterior synechiae

secretion. l reduced accommodation
„ It has replaced pilocarpine as the second n Surgical therapy
line of drug and even as an adjunct drug. m Eyes with advanced disease having very high IOP,
l Adrenergic drugs advanced cupping and advanced field loss should be treated
„ Epinephrine hydrochloride and dipivefrine with filtration surgery as primary line of
hydrochloride (MCQ) management.
„ lower the IOP by increasing aqueous m Trabeculectomy
outflow by stimulating beta recepters in the n most frequently performed filtration surgery now-a-
aqueous outflow system. days.
„ These are characterized by a high allergic n successfully controls the IOP (below 21 mm of
reaction rate. Hg)
„ long-term use is a risk factor for failure of n Ocular hypertension or glaucoma suspect
GLAUCOMA
filtration glaucoma surgery. m when a patient has an IOP constantly more than
„ epinephrine compounds are no longer 21 mm of Hg but no optic disc or visual field
being used as first line or second line changes.
drug. m should be treated as cases of POAG in the
l Brimonidine (MCQ) presence of high risk factors
„ It is a selective alpha-2-adrenergic agonist m High risk factors
„ lowers IOP by decreasing aqueous n Significant diurnal variation
production. l difference of more than 8 mm of Hg
„ increased allergic reactions and tachyphylaxis rates between the lowest and the highest values of
n Combination topical therapy IOP.
l a combination of two drugs n Significantly positive water drinking
„ one drug which decreases aqueous provocative test.
production n When associated with splinter haemorrhages
® timolol over or near the optic disc.
® other betablocker, n IOP constantly more than 28 mm of Hg.
® brimonidine n Retinal nerve fibre large defects.
® dorzolamide n Parapapillary changes.
„ other drug which increase aqueous n Central corneal thickness < 555 ìm.
outflow n Significant asymmetry in the cup size of the
® latanoprost two eyes, i.e., a difference of more than 0.2.
® brimonidine n Strong family history of glaucoma.
® pilocarpine n When associated with high myopia, diabetes
n Argon or diode laser trabeculoplasty (ALT or or pigmentary changes in the anterior
DLT) chamber.
n Normal tension glaucoma
8
m when typical glaucomatous disc changes with l Eyes with narrow angle of anterior chamber,
or without visual field defects are associated with an which may be due to:
intraocular pressure (IOP) constantly below „ small eyeball
21 mm of Hg. Characterstically the angle of „ relatively large size of the lens and smaller
anterior chamber is open on gonioscopy diameter of the cornea
m there is no secondary cause for glaucomatous „ bigger size of the ciliary body.
disc changes. l Plateau iris configuration.
m result from chronic low vascular perfusion, n General factors i
which makes the optic nerve head susceptible to normal l PACG is comparatively more common in
IOP. 5th decade of life.
m Associations of NTG l Females are more prone to get PACG than
n Raynauld phenomenon i.e., peripheral vascular males (male to female ratio is 1:4)
spasm on cooling, l It is more common in nervous individuals
n Migraine with unstable vasomotor system.
n Nocturnal systemic hypotension l Peak incidence is reported in rainy season.
OPHTHALMOLOGY
n Overtreated systemic hypertension. l Family history.
n Reduced blood flow velocity in the ophthalmic artery l It is more common in South-East Asians,
(as revealed on transcranial Doppler Chinese and Eskimos but uncommon in
ultrasonography). Blacks.
m Treatment l In Asians it presents in the 5th to 6th decade
n Betaxolol may be considered the drug of choice and accounts for 50% of primary adult
because in addition to lowering IOP it also increases glaucomas in this ethnic group.
optic nerve blood flow. n Precipitating factors (MCQ)
n Other beta blockers and adrenergic drugs l Dim illumination,
(such as dipiverafrine) should better be l Emotional stress,
avoided l Use of mydriatic drugs like atropine,
l these cause noctur nal systemic cyclopentolate, tropicamide and
hypotension phenylephrine.
l likely to affect adversely the optic nerve m Mechanism of rise in IOP – Sequence of
GLAUCOMA
perfusion events
n Drugs with neuroprotective effect like brimonidine n First of all there occurs mid dilatation of the
may be preferred. pupil which increases the amount of apposition
n Prostaglandin analogues, e.g., latanoprost between iris and anteriorly placed lens with a
tend to have a greater ocular hypotensive effect in considerable pressure resulting in relative pupil
eyes with normal IOP. block
n Trabeculectomy may be considered when n Consequently the aqueous collects in the posterior
progressive field loss occurs despite IOP in chamber and pushes the peripheral flaccid iris
lower teens. anteriorly (Iris bombe)
n Systemic calcium channel blockers (e.g., n results in appositional angle closure due to
nifedipine) iridocorneal contact
n Monitoring of systemic blood pressure n Eventually there occurs rise in IOP which is
should be done for 24 hours. transient to begin with.
l If nocturnal dip is detected, it may be n But slowly the appositional angle closure is
necessary to avoid night dose of anti-hypertensive converted into synechial angle closure (due
medication.PRIMARY ANGLE-CLOSURE to for mation of peripheral anterior
Primary angle-closure glaucoma (PACG) synechiae)
m Predisposing risk factors. l an attack of rise in IOP lasts long.
n Anatomical factors m CLINICAL PRESENTATION
l Hypermetropic eyes with shallow anterior n In clinical practice following clinical presentations
chamber.(MCQ) are seen:
l Eyes in which iris-lens diaphragm is placed l Latent primary angle-closure glaucoma
anteriorly. (primary angle-closure glaucoma suspect).
9
l Subacute (intermittent) primary angle-closure ® simultaneously a mydriatic and miotic
glaucoma. (10% phenylephrine and 2%
l Acute primary angle-closure glaucoma. pilocarpine)
l Postcongestive angle-closure glaucoma, „ A pressure rise of more than 8 mm Hg is
l Chronic primary angle-closure glaucoma, and considered positive.
l Absolute glaucoma l Inferences from provocative tests
m Latent primary angle-closure glaucoma „ A positive provocative test indicates that
n eyes have shallow anterior chamber associated angle is capable of spontaneous closure.
with an occludable angle. „ A negative provocative test in the
n Clinical features presence of a narrow angle of anterior
l Symptoms are absent in this stage. chamber does not rule out a possibility of
l Signs. spontaneous closure.
„ Eclipse sign. n Treatment
® Indicates decreased axial anterior l Prophylactic laser iridotomy should be
chamber depth performed in both eyes of all the patients
OPHTHALMOLOGY
® can be elicited by shining a penlight diagnosed as latent angle-closure glaucoma.

across the anterior chamber from the l If untreated, the risk of acute pressure rise
temporal side and noting a shadow on the during the next 5 years is about 50%.
nasal side n Subacute or intermittent primary angle-closure
„ Slit-lamp biomicroscopic signs include: glaucoma
® Decreased axial anterior chamber depth, m an attack of transient rise of IOP (40-50
® Convex shaped iris lens diaphragm mmHg) which may last for few minutes to 1-2 hours.
® Close proximity of the iris to cornea in m Such an attack in a patient with occludable angle is
the periphery. usually precipitated by :
„ Gonioscopic examination shows n Physiological mydriasis
® very narrow angle - Shaffer grade I l while reading in dim illumination
® pigmented trabecular meshwork is not l watching television or cinema in a darkened
visible without indentation or manipulation in room
GLAUCOMA
at least three of the four quadrants l during anxiety (sympathetic overactivity)

„ Van Herick slit-lamp grading of the angle n Physiological shallowing of anterior chamber
® peripheral anterior chamber depth l after lying in prone position.
(PACD) is compared to the adjacent m Clinical features
corneal thickness (CT) n The episode of subacute PACG
® Grade 4 (Wide open angle): PACD = l unilateral transient blurring of vision
3/4 to 1 CT l coloured halos around light (MCQ)
® Grade 3 (Mild narrow angle): PACD = l headache
1D 4 to 1D 2 CT l browache and eyeache on the affected side.
® Grade 2 (Moderate narrow angle): n Self-termination of the attack occurs possibly due
PACD = 1D 4 CT to physiological miosis induced by bright light,
® Grade 1 ( Extremely narrow angle): sleep or otherwise.
PACD <1D 4CT n Usually during examination the eye is white
® Grade 0 (closed angle): PACD = Nil and not congested.
n Diagnosis m Differential diagnosis of coloured halos in
l Prone-darkroom test PACG.
l Best and physiologic n Coloured halos in PACG
l An increase in IOP of more than 8 mm Hg l occur due to
is considered diagnostic of PACG. „ accumulation of fluid in the corneal
l Mydriatic provocative test epithelium
„ not physiological „ alteration in the refractive condition of
„ drugs used to produce a mid-dilated pupil the corneal lamellae.
® a weak mydriatic (e.g., 0.5% l Patient typically gives history of seeing
tropicamide) colours distributed as in the spectrum of
10
rainbow (red being outside and violet innermost) l Acetazolamide (a carbonic anhydrase inhibitor)
while watching on a lighted bulb or the moon. (MCQ)
n Coloured halos in acute purulent conjunctivitis l Analgesics and anti-emetics as required.
l the halos can be eliminated by irrigating the l Pilocarpine eyedrops
discharge. „ should be started after the IOP is bit lowered by
n Fincham’s test (MCQ) hyperosomtic agents.
l halos of glaucoma and immature cataract „ At higher pressure iris sphincter is
can be differentiated ischaemic and unresponsive to
l a stenopaeic slit is passed across the pupil pilocarpine.
l During this test glaucomatous halo remains l Beta blocker eyedrops like timolol maleate or
intact betaxolol
l a halo due to cataract is broken up into l Corticosteroid eyedrops
segments n Surgical treatment
n Acute primary angle-closure glaucoma l Peripheral iridotomy.
m occurs due to a sudden total angle closure „ Indications
OPHTHALMOLOGY
leading to severe rise in IOP ® peripheral anterior synechiae are
m It usually does not terminate of its own formed in less than 50 percent of the angle of
m This is sight threatening emergency. anterior chamber
m Clinical features ® as prophylaxis in the other eye.
n Pain. ® Peripheral iridotomy re-establishes
l sudden onset of very severe pain in the eye communication between posterior and
l radiates along the branches of 5th nerve. anterior chamber
n Nausea, vomiting and prostrations are frequently ® it bypasses the pupillary block and
associated with pain. thus helps in control of PACG
n Rapidly progressive impairment of vision, l Laser iridotomy
redness, photophobia and lacrimation „ a non-invasive procedure
develop in all cases. „ good alternative to surgical iridectomy.
n Past history. in 5 percent patients (MCQ)
n Lids may be oedematous, l Filtration surgery.
GLAUCOMA
n Conjunctiva is chemosed, and congested „ Indications
l Both conjunctival and ciliary vessels are ® IOP is not controlled with the best
congested medical therapy following an attack of
n Cornea becomes oedematous and insensitive, acute congestive glaucoma
n Anterior chamber is very shallow. ® when peripheral anterior synechiae are
l Aqueous flare or cells may be seen in formed in more than 50 percent of
anterior chamber the angle of the anterior chamber.
n Angle of anterior chamber is completely closed l Clear lens extraction by
as seen on gonioscopy (shaffer grade 0), phacoemulsification with intraocular lens
n Iris may be discoloured, implantation
n Pupil n Prophylactic treatment in the normal fellow
l semidilated, vertically oval and fixed. It eye
l is non-reactive to both light and l Prophylactic laser iridotomy (preferably) or
accommodation, (MCQ) surgical peripheral iridectomy should be
n IOP is markedly elevated, usually between 40 performed on the fellow asymptomatic eye.
and 70 mm of Hg, (MCQ)
n Optic disc is oedematous and hyperaemic, n Postcongestive angle-closure glaucoma
n Fellow eye shows shallow anterior chamber and m refers to the clinical status of the eye after an
a narrow angle (latent angle closure glaucoma). attack of acute PACG with or without treatment.
m Management m Ciliary body shut down
n It is essentially surgical n temporary cessation of aqueous humour
n Medical therapy secretion
l Systemic hyperosmotic agent intravenous mannitol n occurs due to ischaemic damage to the ciliary
epithelium after an attack of acute PACG.
11
n IOP is low and pain is markedly reduced. n Retrobulbar alcohol injection
n Subsequent recovery of ciliary function may l It destroys the ciliary ganglion.
lead to chronic elevation of IOP with cupping and n Destruction of secretory ciliary epithelium to lower
visual field defects. the IOP
m Vogt’s triad (MCQ l carried out by
n seen in patients with „ cyclo cryotherapy
l any type of postcongesive glaucoma „ cyclodiathermy
l treated cases of acute congestive „ cyclophotocoagulation.
glaucoma. n Enucleation of eyeball. (MCQ)
n It is characterized by: l It may be considered when pain is not
l Glaucomflecken (anterior subcapsular relieved by conservative methods.
lenticular opacity) m Complications.
l Patches of iris atrophy n Corneal ulceration.
l Slightly dilated non-reacting pupil (due to n Staphyloma formation.
sphincter atrophy) l sclera becomes very thin and atrophic
OPHTHALMOLOGY
n Chronic primary angle-closure glaucoma l sclera ultimately bulges out either in the
m Gonioscopy „ ciliary region (ciliary staphyloma) (MCQ)
n gonioscopic findings provide the only „ equatorial region (equatorial staphyloma).
differentiating feature between POAG and n Atrophic bulbi.
chronic PACG. l Ultimately the ciliary body degenerates
n reveals a variable degree of angle closure. l IOP falls and the eyeball shrinks.(MCQ)
n Permanent peripheral anterior synechiae do LENS-INDUCED (PHACOGENIC)
not usually develop until late. GLAUCOMAS
m Treatment n Phacomorphic glaucoma
n Laser iridotomy alone or along with medical m acute secondary angle-closure glaucoma
therapy should be tried first. m caused by :
n Trabeculectomy (filtration surgery) is n Intumescent lens - main cause of
needed when the above treatment fails to phacomorphic glaucoma.
GLAUCOMA
control IOP. l swollen cataractous lens due to

n Prophylactic laser iridotomy in fellow eye „ rapid maturation of cataract
must also be performed. „ following traumatic rupture of capsule
n Absolute primary angle-closure glaucoma n Anterior subluxation
m Painful blind eye. (MCQ) n dislocation of the lens and spherophakia (congenital
m Perilimbal reddish blue zone small spherical lens)
n a slight ciliary flush around the cornea due to dilated m Cataract extraction with implantation of
anterior ciliary veins. PCIOL
m Caput medusae n main treatment of phacomorphic glaucoma
n a few prominent and enlarged vessels are seen in long n should be performed once the eye becomes
standing cases. quite
m Cornea in early cases is clear but insensitive. n Phacolytic glaucoma (Lens protein glaucoma)
n Slowely it becomes hazy m a type of secondary open angle glaucoma
n develops epithelial bullae (bullous keratopathy) or m trabecular meshwork is clogged by the lens
filaments (filamentary keratitis). proteins and macrophages which have
m Anterior chamber is very shallow. phagocytosed the lens proteins.
m Iris becomes atrophic. m Leakage of the lens proteins occurs through an
m Pupil becomes fixed and dilated and gives a intact capsule in the hypermature (Morgagnian)
greenish hue. cataractous lens.(MCQ)
m Optic disc shows glaucomatous optic atrophy. m Management.
m Intraocular pressure is high n extraction of the hypermature cataractous lens
m eyeball becomes stony hard. with PCIOL implantation.
m Management of absolute glaucoma n Lens particle glaucoma
m a type of secondary open angle glaucoma
12
m trabecular meshwork is blocked by the lens n Treatment of all stages of primary angle-
particles floating in the aqueous humour. closure glaucoma.(MCQ)
m occur due to lens particles left after n Prophylaxis in the fellow eye.
n extracapsular cataract extraction (MCQ) m Laser iridotomy should always be perferred over
n following traumatic rupture of the lens. surgical iridectomy.
m Management n Trabeculectomy
n medical therapy to lower IOP m Trabeculectomyis the most frequently
n irrigation-aspiration of the lens particles performed partial thickness filtering surgery till date.
from the anterior chamber. m Indications
n Glaucoma associated with phacogenic uveitis n Primary angle-closure glaucoma with
m IOP is raised due to inflammatory reaction of peripheral anterior synechial involving more
the uveal tissue excited by the lens matter. than half of the angle.
m trabecular meshwork is clogged by both inflammatory n Primary open-angle glaucoma not controlled
cells and the lens particles. with medical treatment.
m Management n Congenital and developmental glaucomas
OPHTHALMOLOGY
n medical therapy to lower IOP where trabeculotomy and goniotomy fail.
n treatment of iridocyclitis with steroids and n Secondary glaucomas where medical therapy
cycloplegics is not effective.
n Irrigation-aspiration of the lens matter from m Mechanism
anterior chamber n A new channel (fistula) is created around the
n GLAUCOMAS-IN-APHAKIA/ margin of scleral flap, through which aqueous
PSEUDOPHAKIA flows from anterior chamber into the subconjunctival
m It includes following conditions: space.
n Raised IOP with deep anterior chamber in early n If the tissue is dissected posterior to the
postoperative period: scleral spur, a cyclodialysis may be produced leading
l It may be due to hyphaema, inflammation, to increased uveoscleral outflow.
retained cortical matter or vitreous filling n CYCLO-DESTRUCTIVE PROCEDURES
the anterior chamber. m Cyclo-destructive procedures lower IOP by
n Secondary angle-closure glaucoma due to flat anterior destroying part of the secretory ciliary
GLAUCOMA
chamber. epithelium thereby reducing aqueous secretion.
l It may occur following long- standing m Indications. These procedure are used mainly in
wound leak. absolute glaucomas.
n Secondary angle-closure glaucoma due to pupil block. m Cyclo-destructive procedures in current use are:
l It may occur following formation of n Cyclocryotherapy (most frequent),
annular synechiae or vitreous herniation. n Nd: Yag laser cyclodestruction, and
n Undiagnosed pre-existing primary open-angle glaucoma n Diode laser cyclophotocoagulation.
may be associated with aphakia/ pseudophakia.
n Steroid-induced glaucoma.
l develop in patients operated for cataract due
to postoperative treatment with steroids.
n Epithelial ingrowth
l may cause an intractable glaucoma in late
postoperative period by invading the
trabeculum and the anterior segment
structures.
n Aphakic/pseudophakic malignant glaucoma (MCQ)
n STEROID-INDUCED GLAUCOMA (MCQ)

m a type of secondary open-angle glaucoma
m develops following topical, and sometimes
systemic steroid therapy.
n PERIPHERAL IRIDECTOMY
m Indications
13
TOPIC 2 - CATARACT n Polar cataracts
l Anterior polar cataract.
n Congenital and developmental cataracts „ It involves the central part of the anterior
m occur due to some disturbance in the normal capsule and the adjoining superficial-most
growth of the lens. cortex.
m congenital cataract. „ It may arise in the following ways:
n disturbance occurs before birth ® Due to delayed development of anterior chamber.
n the opacity is limited to either embryonic or foetal » opacity is usually bilateral, stationary
nucleus. and visually insignificant.
m Developmental cataract ® Due to corneal perforation.
n occur from infancy to adolescence. » follow contact of the lens capsule with
n opacities may involve infantile or adult the back of cornea, usually after
nucleus, deeper parts of cortex or capsule. perforation due to ophthalmia
typically affects the particular zone which is neonatorum
being formed when this process is disturbed. „ Reduplicated cataract (double
m The fibres laid down previously and
OPHTHALMOLOGY
cataract).(MCQ)
subsequently are often normally formed and remain ® A morphologic type of anterior polar
clear. cataract
m minute opacities (without visual disturbance) ® along with thickening of central point
are very common in normal population. of anterior capsule, lens fibres lying
m These are detected with the beam of slit lamp immediately beneath it also become opaque
under full mydriasis. and are subsequently separated from
m About one-third of all congenital cataracts are the capsule by laying of transparent
hereditary. fibres in between.
m in acquired cataract, opacification occurs due to ® The burried opacity is called ‘imprint’
degeneration of the already formed normal ® the two together constitute
fibres reduplicated cataract.
m Clinical types l Posterior polar cataract.
n Congenital capsular cataracts „ It is a very common lens anomaly
CATARACT
„ Anterior capsular cataract „ consists of a small circular circumscribed

„ Posterior capsular cataract opacity involving the posterior pole.
n Polar cataracts „ Posterior polar cataract may be associated
„ Anterior polar cataract with :
„ Posterior polar cataract ® Persistent hyaloid artery remnants
n Nuclear cataract (Mittendorf dot)(MCQ)
n Lamellar cataract ® Posterior lenticonus
n Sutural and axial cataracts ® Persistent hyperplastic primary vitreous
„ Floriform cataract (PHPV).
„ Coralliform cataract m Nuclear cataracts
„ Spear-shaped cataract l Cataracta centralis pulverulenta
„ Anterior axial embryonic cataract (Embryonic nuclear cataract).
n Generalized cataracts „ It has dominant genetic trait
„ Coronary cataract „ occurs due to inhibition of the lens
„ Blue dot cataract development at a very early stage
„ Total congenital cataract „ involves the embryonic nucleus.
„ Congenital membranous cataract „ The condition is bilateral
m Congenital capsular cataracts „ characterised by a small rounded opacity
n Anterior capsular cataracts lying exactly in the centre of the lens.
l nonaxial, stationary (MCQ) „ The opacity has a powdery appearance
l visually insignificant. (pulverulenta)
n Posterior capsular cataracts „ usually does not affect the vision.
l associated with persistent hyaloid artery l Total nuclear cataract.
remnants.(MCQ)
14
„ usually involves the embryonic and fetal „ occur about puberty; thus involving either
nucleus the adolescent nucleus or deeper layer of
„ It is characterized by a dense chalky white the cortex.
central opacity „ opacities are often many hundreds in
„ seriously impair vision number
„ opacities are usually bilateral and non „ opacities have a regular radial
progressive. distribution in the periphery of lens
m Lamellar cataract or Zonular cataract (corona of club-shaped opacities) encircling
l opacity occupies a discrete zone in the lens. the central axis.
l It is the most common type of congenital „ Since the opacities are situated peripherally,
cataract presenting with visual vision is usually unaffected.
impairment. (MCQ) l Blue dot cataract. (MCQ)
l Etiology. „ It is also called cataracta- punctata-caerulea.
„ Genetic pattern is usually of dominant „ It usually forms in the first two decades
variety. of life.
OPHTHALMOLOGY
„ Environmental form is associated with „ Opacities are usually stationary and do
deficiency of vitamin D. (MCQ) not affect vision
„ Sometimes maternal rubella infection l Total congenital cataract.
contracted between 7th and 8th week of „ Its important cause is maternal rubella,
gestation may also cause lamellar cataract. occurring during the first trimester of pregnancy.
(MCQ) „ Typically, the child is born with a dense
l Characteristic features. white l nuclear cataract.
„ Typically, this cataract occurs in a zone of „ It is a progressive type of cataract.
foetal nucleus surrounding the „ The lens matter may remain soft or may
embryonic nucleus even liquefy (congenital Morgagnian
„ The main mass of the lens internal and cataract).
external to the zone of cataract is clear, l Congenital membranous cataract.
except for small linear opacities like „ occur due to total or partial absorption
spokes of a wheel (riders) which may of congenital cataract, leaving behind thin
CATARACT
be seen towards the equator. (MCQ) membranous cataract.
„ It is usually bilateral „ associated with Hallermann-Streiff-
„ frequently causes severe visual defects. Francois Synodrome.
m Sutural and axial cataracts m Management of congenital and
l Sutural cataracts are comparatively of developmental cataract
common occurrence l Indications and timing of paediatric
„ consist of a series of punctate opacities cataract surgery
„ scattered around the anterior and „ Partial cataracts and small central cataracts
posterior Y-sutures. ® are visually insignificant
„ usually static, bilateral ® can safely be ignored and observed
„ do not have much effect on the vision. ® may need non-surgical treatment with
l The individual opacities have different patterns pupillary dilatation.
„ Floriform cataract. - opacities are arranged like „ Bilateral dense cataracts
the petals of a flower. ® should be removed early (within 6 weeks
„ Coralliform cataract - opacities are arranged of birth) to prevent stimulus
in the form of a coral. deprivation amblyopia.
„ Spear-shaped cataract „ Unilateral dense cataract
„ Anterior axial embryonic cataract occurs as fine ® should preferably be removed as early
dots near the anterior Y-suture. as possible (within days) after birth.
m Generalized cataracts (MCQ) visual prognosis in most of
l Coronary cataract the unilateral cases is very poor even after
„ an extremely common for m of timely operation
developmental cataract l Surgical procedures.
15
„ Childhood cataracts, (congenital, n Morphologically, the senile cataract occurs in two
developmental as well as acquired) can be forms
dealt with m cortical (soft cataract)
® anterior capsulotomy and irrigation n may start as cuneiform (more commonly) or
aspiration of the lens matter (MCQ) cupuliform cataract.(MCQ)
® lensectomy. (MCQ) m nuclear (hard cataract).
® needling operation (which was performed n the predominant form can be given as
in the past) is now obsolete. m cuneiform 70 percent (MCQ)
l Correction of paediatric aphakia. m nuclear 25 percent
„ Children above the age of 2 years m cupuliform 5 percent.
® can be corrected by implantation of n Etiology
posterior chamber intraocular lens m Factors affecting age of onset, type and
during surgery. maturation of senile cataract.
„ Children below the age of 2 years n Heredity.
® Should preferably be treated by n Ultraviolet irradiations.
OPHTHALMOLOGY
extended wear contact lens. n Dietary factors.

„ Spectacles can be prescribed in bilateral n Diet deficient in vitamins (riboflavin, vitamin E,
cases. vitamin C),
„ Later on secondary IOL implantation n Dehydrational crisis.
may be considered. l An association with prior episode of severe
„ Present trend is to do primar y dehydrational crisis (due to diarrhoea, cholera
implantation at the earliest possible (2- etc.)
3 months) specially in unilateral cataract. n Smoking
„ Paediatric IOL: size, design and power. m Causes of presenile cataract.
® Size of IOL n The term presenile cataract is used when senile
» above the age of 2 years may be cataract occur before 50 years of age.
standard 12 to 12.75-mm diameter n Its common causes are:
for in the bag implantation. l Heredity
® Design of IOL l Diabetes mellitus.
CATARACT
» one-piece PMMA with modified C- „ Nuclear cataract is more common and

shaped haptics (preferably heparin tends to progress rapidly.
coated). l Myotonic dystrophy
® Power of IOL. l associated with posterior subcapsular type
» In children between 2-8 years of age of presenile cataract.(MCQ)
10% undercorrection from the l Atopic dermatitis
calculated biometric power is n Mechanism of loss of transparency
recommended to counter the m Cortical senile cataract.
myopic shift. n Its main biochemical features are
» Below 2 years on undercorrection n decreased levels of total proteins, amino
by 20% is recomended. acids and potassium
„ Correction of amblyopia. n increased concentration of sodium
® In spite of best efforts, amblyopia. n marked hydration of the lens, followed by
continues to be the main cause of coagulation of proteins.
ultimate low vision in these children m Nuclear senile cataract.
SENILE CATARACT m In it the usual degenerative changes
n also called as ‘age-related cataract’ m associated with dehydration and compaction of
n this is the commonest type of acquired cataract the nucleus
(MCQ) m result in a hard cataract.
n affecting equally persons of either sex m accompanied by a significant increase in water
n usually above the age of 50 years. insoluble proteins.
n By the age of 70 years, over 90% of the individuals m total protein content and distribution of
develop senile cataract. cations remain normal.
n The condition is usually bilateral
16
m associated with deposition of pigment l but clear cortex is still present and so iris shadow
urochrome and/or melanin derived from the is visible. (MCQ)
amino acids in the lens. l intumescent cataract (MCQ)
n Stages of maturation „ In some patients, at this stage, lens may
m Maturation of the cortical type of senile become swollen due to continued
cataract hydration. This condition is called
n Stage of lamellar separation. ‘intumescent cataract’.
l The earliest senile change is demarcation „ Due to swollen lens ,anterior chamber
of cortical fibres (MCQ) becomes shallow.
l Occur due to their separation by fluid. n Mature senile cataract (MSC).
l demonstrated by slit-lamp examination l In this stage, opacification becomes complete,
only. i.e., whole of the cortex is involved.
l changes are reversible. l Lens becomes pearly white in colour.
n Stage of incipient cataract. l Such a cataract is also labelled as ‘ripe
l early detectable opacities with clear areas cataract’
OPHTHALMOLOGY
between them are seen. n Hypermature senile cataract (HMSC).
l Two distinct types of senile cortical cataracts l The hypermature cataract may occur in any
can be recognised at this stage: of the two forms:
l Cuneiform senile cortical cataract.(MCQ) l Morgagnian hypermature cataract: (MCQ)
„ It is characterised by wedge-shaped „ In some patients, after maturity the whole
opacities with clear areas in between. cortex liquefies
„ These extend from equator towards „ the lens is converted into a bag of milky
centre fluid.
„ in early stages can only be demonstrated „ The small brownish nucleus settles at the
after dilatation of the pupil. bottom, altering its position with
„ They are first seen in the lower nasal change in the position of the head. Such
quadrant.(MCQ) a cataract is called Morgagnian cataract
„ These opacities are present both in „ Sometimes in this stage, calcium deposits
anterior and posterior cortex may also be seen on the lens capsule.
CATARACT
„ their apices slowly progress towards the „ Sclerotic type hypermature cataract:
pupil. ® Sometimes after the stage of maturity,
„ On oblique illumination these present a the cortex becomes disintegrated
typical radial spoke-like pattern of ® lens becomes shrunken due to leakage
greyish white opacities of water.
„ On distant direct ophthalmoscopy, these ® The anterior capsule is wrinkled and
opacities appear as dark lines against the thickened due to proliferation of anterior
red fundal glow. cells a dense white capsular cataract
„ Since the cuneiform cataract starts at may be formed in the pupillary area.
periphery and extends centrally, the visual ® Due to shrinkage of lens, anterior
disturbances are noted at a comparatively late chamber becomes deep and iris
stage. becomes tremulous
l Cupuliform senile cortical cataract. (iridodonesis).(MCQ)
„ Here a saucer- shaped opacity develops m Maturation of nuclear senile cataract
just below the capsule n In it, the sclerotic process renders the lens
„ usually in the central part of posterior inelastic and hard
cortex (posterior subcapsular cataract) n decreases its ability to accommodate and
„ it gradually extends outwards. obstructs the light rays.
„ Cupuliform cataract lies right in the n These changes begin centrally and slowly
pathway of the axial rays and thus causes spread peripherally almost up to the capsule
an early loss of visual acuity.(MCQ) when it becomes mature
n Immature senile cataract (ISC n a very thin layer of clear cortex may remain
l The lens appears greyish white unaffected.
17
n The nucleus may become diffusely cloudy n Visual acuity testing.
(greyish) or tinted (yellow to black) due to l the visual acuity may range from 6/9 to just
deposition of pigments. PL +
n In practice, the commonly observed pigmented n Oblique illumination examination.
nuclear cataracts are l It reveals colour of the lens in pupillary
l amber, brown (cataracta brunescens) (MCQ) area
l black (cataracta nigra) n Test for iris shadow.
l reddish (cataracta rubra) in colour l presence of iris shadow is a sign of
n Clinical features immature cataract.
m Glare. l When an oblique beam of light is thrown on
n One of the earliest visual disturbances with the pupil, a crescentric shadow of pupillary
the cataract is glare or intolerance of bright light; margin of the iris will be formed on the
such as direct sunlight or the headlights of greyish opacity of the lens
an oncoming motor vehicle. l iris shadow forms as long as clear cortex is
m Uniocular polyopia (i.e., doubling or trebling of present between the opacity and the
OPHTHALMOLOGY
objects): pupillary margin

n It is also one of the early symptoms. l When lens is completely transparent or
n It occurs due to irregular refraction by the completely opaque, no iris shadow is formed.
lens n Distant direct ophthalmoscopic examination
n occurs due to variable refractive index as a l in the absence of any opacity in the media.
result of cataractous process. „ a reddish yellow fundal glow is observed
m Coloured halos. (MCQ) l Partial cataractous lens
n Occur due to breaking of white light into „ shows black shadow against the red
coloured spectrum glow in the area of cataract.
n Occur due to presence of water droplets in l Complete cataractous lens
the lens. „ does not even reveal red glow
m Stationary Black spots in front of eyes
m Image blur, distortion of images and misty vision
n may occur in early stages of cataract.
CATARACT
m Loss of vision.
n It is painless and gradually progressive in
nature.
n Paitents with central opacities (e.g.,
cupuliform cataract)
l have early loss of vision.
l see better when pupil is dilated due to dim light in
the evening (day blindness).(MCQ)
n In patients with peripheral opacities (e.g.
cuneiform cataract)
l visual loss is delayed
l vision is improved in bright light when pupil
is contracted. (MCQ)
n In patients with sclerosis
l distant vision deteriorates due to
progressive index myopia. (MCQ)
l Such patients may be able to read without
presbyopic glasses. (MCQ)
l This improvement in near vision is referred
to as ‘second sight’. (MCQ)
n only perception of light and accurate
projection of rays remains in stage of mature
cataract.
m Examination of eye
18
Examination Nuclear Cataract ISC MSC HMSC (M) HMSC(S)
1. Visual acuity 6/9 to PL+ 6/9 to FC+ HM+to PL+ PL+ PL+
2. Colour of lens Grey, amber Greyish white Pearly white Milky white Dirty white with
brown, black with sinking hyper-white
or red brownish nucleus spots
3. Iris shadow seen seen not seen not seen not seen
4. Distant direct Central dark Multiple dark No red glow No red glow No red glow
opthalmoscopy area against red areas against but white pupil milky white
with dilated fundal glow red fundal glow due to complete Pupil
pupil cataract
5. Slit-lamp Nuclear opacity Areas of normal Complete cortex Milky white Shrunken
examination clear cortex with cataractous is cataractous sunken brown- cataractous lens
OPHTHALMOLOGY
cortex ish nucleus with thickened
anterior capsule
ISC: Immature senile cataract, MSC: Mature senile cataract, HMSC (M) Hypermature senile cataract (Morgagnian), HMSC (S) :
Hypermature senile cataract (Scleratic), PL : Preception of light, HM : Hand mvements, FC : Finger counting.
Immature senile cataract versus nuclear sclerosis

ISC Nuclear sclerosis
1. Painless progressive loss of vision 1. Painless progressive loss of vision

2. Greyish colour of lens 2. Greyish colour of lens
3. Irish shadow is present 3. Irish shadow is absent
CATARACT
4. Black spots against red glow are observed on 4. No black spots are seen red glow
distant direct ophthalmoscopy
5. Slit-lamp examination reveals area of 5. Slit-lamp examination
cataractour cortex reveals clear lens
6. Visual acuity doesnot 6. Visual acuity usually
improve on pin-hole testing improves on pin-hole testing
Differences between mature senile cataract and leukocoria

MSC Leukocoria
1. White reflex in pupillary area White reflex in pupillary area

2. Size of pupil usually normal Pupil usually semidilated
3. Fourth Purkinje image is absent Fourth Purkinje image is present
4. Slit-lamp examination shows cataractous lens Slit-lamp examination shows transperent lens
with white reflex behind the lens
5. Ultrasonography normal Ultrasonography reveals opacity in the Vitreous cavity
19
n Complications m Systemic features of this syndrome are mental
m Phacoanaphylactic uveitis.(MCQ) retardation, dwarfism, osteomalacia, muscular hypotonia and
n A hypermature cataract may leak lens proteins frontal prominence.
into anterior chamber. n COMPLICATED CATARACT
n these proteins may act as antigens m It refers to opacification of the lens secondary
n induce antigen- antibody reaction leading to to some other intraocular disease.
uveitis. m Etiology
m Lens-induced glaucoma. n Inflammatory conditions.
n It may occur by different mechanisms l uveal inflammations (like iridocyclitis,
l due to intumescent lens (phacomor phic parsplanitis, choroiditis),
glaucoma) (MCQ) l hypopyon corneal ulcer
l leakage of proteins into the anterior chamber l endophthalmitis.
from a hypermature cataract (phacolytic n Degenerative conditions
glaucoma). l retinitis pigmentosa
m Subluxation or dislocation of lens. (MCQ) l pigmentary retinal dystrophies
OPHTHALMOLOGY
n It may occur due to degeneration of zonules l myopic chorioretinal degeneration.

in hypermature stage n Retinal detachment.
n Diabetic cataract n Glaucoma (primary or secondary
m Diabetes is associated with two types of cataracts n Intraocular tumours such as retinoblastoma or
n Senile cataract in diabetics melanoma
„ appears at an early age and progresses rapidly. m Clinical features
n True diabetic cataract. n Typically the complicated cataract starts as
l It is also called ‘snow flake cataract’ or posterior cortical cataract. (MCQ
‘snow-storm cataract’.(MCQ n Lens changes appear typically in front of the
l usually occur in young adults posterior capsule.
l occur due to osmotic over-hydration of the n The opacity is irregular in outline and variable
lens. in density.
n Galactosaemic cataract (MCQ) n In the beam of slit- lamp the opacities have an
m bilateral cataract (oil droplet central lens appearance like ‘bread- crumb’.(MCQ)
CATARACT
opacities). (MCQ) n A very characteristic sign is the appearance of

m lens changes may be reversible iridescent coloured particles the so-called
m occurrence of cataract may be prevented, if ‘polychromatic lustre’ of reds, greens and
milk and milk products are eliminated from blues.(MCQ)
the diet when diagnosed at an early stage. n Corticosteroid-induced cataract (MCQ)
n Hypocalcaemic cataract (MCQ) m Posterior subcapsular opacities (MCQ)
m associated with parathyroid tetany m associated with the use of topical as well as
m Multicoloured crystals or small discrete white systemic steroids. (MCQ)
flecks of opacities m Children are more susceptible than adults.
m Opacities are formed in the cortex which seldom m it is recommended that all patients with diseases
mature. requiring prolonged corticosteroids therapy
n Cataract in Wilson’s disease (hepatolenticular should be regularly examined on slit-lamp by an
degeneration). ophthalmologist
m green ‘sunflower cataract’ (MCQ) n Miotics-induced cataract (MCQ)
m The more commonly observed ocular feature of m Anterior subcapsular granular type of cataract
Wilson’s disease is ‘Kayser-Fleischer ring’ (KF may be associated with long-term use of
ring) in the cornea. miotics,
n Cataract in Lowe’s syndrome m Occurs particularly with long acting
m Lowe’s (Oculo-cerebral-renal) syndrome cholinesterase inhibitors such as echothiophate,
m inborn error of amino acid metabolism. demecarium bromide, disopropyl
m Ocular features include congenital cataract and fluorophosphate (DFP).
glaucoma. n Drug induced toxic cataracts
m Other drugs associated with fine toxic cataracts
are
20
n Amiodarone (MCQ) m Extracapsular cataract extraction (ECCE).
n Chlorpromazine n major portion of anterior capsule with
n busulphan, gold and allopurinol epithelium, nucleus and cortex are removed
n RADIATIONAL CATARACT (MCQ)
m Infrared (heat) cataract n leaving behind intact posterior capsule.
n cause discoid posterior subcapsular n Indications.
opacities and true exfoliation of the anterior l Presently, extracapsular cataract extraction
capsule. technique is the surgery of choice for
n It is typically seen in persons working in glass almost all types of adulthood as well as
industries, so also called as ‘glass-blower’s or childhood cataracts unless contraindicated.
glass- worker’s cataract’(MCQ) n Contraindications.
m Irradiation cataract l The only absolute contraindication for
n Exposure to X-rays, ?-rays or neutrons ECCE is markedly subluxated or
n There is usually a latent period ranging from dislocated lens.(MCQ)
6 months to a few years between exposure and m Advantages of ECCE over ICCE (A very
OPHTHALMOLOGY
development of the cataract. important MCQ Zone)
m People prone to get such cataracts are n ECCE is a universal operation and can be
n inadequately protected technician performed at all ages, except when zonules
n patients treated for malignant tumours are not intact; whereas ICCE cannot be performed
n workers of atomic energy plants. below 40 years of age.
m Ultraviolet radiation cataract (MCQ) n Posterior chamber IOL can be implanted after
n ELECTRIC CATARACT ECCE, while it cannot be implanted after
m It is known to occur after passage of powerful ICCE.
electric current through the body. n Postoperative vitreous related problems (such
m The cataract usually starts as punctate subcapsular as herniation in anterior chamber, pupillary
opacities which mature rapidly.. block and vitreous touch syndrome) associated
n SYNDERMATOTIC CATARACT with ICCE are not seen after ECCE.
m Atopic der matitis is the most common n Incidence of postoperative complications such
cutaneous disease associated with cataract (Atopic as endophthalmitis, cystoid macular
CATARACT
cataract). oedema and retinal detachment are much less
m Other skin disorders associated with cataract after ECCE as compared to that after
include ICCE.(MCQ)
n poikiloderma, n Postoperative astigmatism is less, as the incision
n vasculare atrophicus is smaller. (MCQ)
n scleroderma m Advantages of ICCE over ECCE
n keratotis follicularis. n ECCE is a universal operation and can be
n MANAGEMENT OF CATARACT IN performed at all ages, except when zonules
ADULTS are not intact; whereas ICCE cannot be
m Intracapsular cataract extraction (ICCE) performed below 40 years of age.
n In this technique, the entire cataractous lens n Posterior chamber IOL can be implanted
along with the intact capsule is removed. (MCQ) after ECCE, while it cannot be implanted
n Therefore, weak and degenerated zonules after ICCE.
are a pre-requisite for this method. Because of n Postoperative vitreous related problems
this reason, this technique cannot be employed (such as herniation in anterior chamber,
in younger patients where zonules are strong (MCQ) pupillary block and vitreous touch syndrome)
n ICCE can be performed between 40-50 years associated with ICCE are not seen after
of age by use of the enzyme alpha- chymotrypsin ECCE.
(which will dissolve the zonules). n Incidence of postoperative complications
n Beyond 50 years of age usually there is no such as endophthalmitis, cystoid macular
need of this enzyme. oedema and retinal detachment are much
n Indications. less after ECCE as compared to that after
l At present the only indications of ICCE is ICCE.(MCQ
markedly subluxated and dislocated lens.
21
n Postoperative astigmatism is less, as the l The biggest advantage of manual SICS is that
incision is smaller. (MCQ) it is not machine dependent and thus can be
m Advantages of ICCE over ECCE practised anywhere.
n The technique of ICCE, as compared to n Less surgical complications.
ECCE, is simple, cheap, easy and does not need l Disastrous complication like nuclear drop
sophisticated microinstruments. into vitreous cavity is much less than

n Postoperative opacification of posterior phacoemulsification technique.
capsule is seen in a significant number of cases n Operating time in manual SICS is less than that
after ECCE. No such problem is known with of phocoemulsification, especially in hard

ICCE. cataract. Therefore, it is ideal for mass surgery.
n ICCE is less time consuming and hence more n Cost effective.
useful than ECCE for mass scale operations l No expenses in acquiring and maintaining
in eye camps. phaco machine.

m Types of extracapsular cataract extraction l in SICS always PMMA IOLs are used
n Conventional extracapsular cataract extraction which are much cheeper than foldable IOLs.
OPHTHALMOLOGY
(ECCE) m Demerits of manual SICS over

n Manual small incision cataract surgery (SICS) phacoemulsification
n Phacoemulsification n Conjunctival congestion persists for 5-7 days
m Merits of conventional ECCE over SICS. at the site of conjunctival flap.

n The only merit of conventional ECCE over n Mild tenderness sometime may be present
SICS is that it is a simple technique to master owing to scleral incision.

with short learning curve. n Postoperative hyphaema may be noted
m Dermerits of conventional ECCE over SICS sometimes.

include: n Surgical induced astigmatism is more as the
n Long incision (10 to 12 mm). incision in SICS is large (about 6 mm) as

n Multiple sutures are required. compared to phacoemulsification (about 3.2
n Open chamber surgery with high risk of mm)(MCQ)
l Vitreous prolapse m Merits of phacoemulsification over manual
l operative hard eye SICS
CATARACT
l expulsive choroidal haemorrhage. n Topical anaesthesia may be sufficient for
n High incidence of post-operative phacoemulsification in expert hands.

astigmatism. n Postoperative congestion is minimal after
n Postoperative suture-related problems like phacoemulsification, as phaco is usually performed

irritation and suture abscess etc. through a clear corneal incision.
n Postoperative wound-related problems such n Small incision. The chief advantage of
as phacoemulsification over manual SICS is that it

l wound leak can be performed through a smaller (3.2 mm)
l shallowing of anterior chamber incision. (MCQ)
l iris prolapse. n Less corneal complications.
n Needs suture removal, during which infection n Phacoemulsification can be performed in the
may occur. posterior chamber without prolapsing the nucleus

m Merits of manual SICS over into the anterior chamber, thereby minimising the
phacoemulsification risk of corneal complications.
n Universal applicability n Visual rehablitation is comparetively quicker in
l all types of cataracts including hard phacoemulsification as compared to manual

cataracts (grade IV and V) can be operated SICS.
by this technique. n Postoperative astigmatism is comparatively less when
n Learning curve. foldable IOLs are implanted through a smaller

l This procedure is much easier to learn as incision (3.2 mm).
compared to phacoemulsification. m Demerits of phacoemulsification vis-a-vis
n Not machine dependent. manual SICS
n Learning curve for phacoemulsification is more
painful both for the surgeons and patients.
22
n Complications encountered during m Corneoscleral incision required is very small (3
phacoemulsification like nuclear drop are mm).
unforgiving. m Therefore, sutureless surgery is possible with self-
n Machine dependent. sealing scleral tunnel or clear corneal incision made
l in the event of an unfortunate machine with a 3 mm keratome.(MCQ)
failure in the middle of surgery one has to m Laser phacoemulsification.
shift to conventional ECCE. n In it the lens nucleus is emulsified utilizing
n High cost laser energy.
n Limitations. n The advantage of this technique is that the laser
l It is very difficult to deal with hard cataracts energy used to emulsify cataractous lens is not
(grade IV and V) with this technique, there is exposed to other intraocular structures (c.f.
high risk of serious corneal complications ultrasonic energy).
due to more use of phaco energy in such n Intraocular lens implantation
cases. m Presently, intraocular lens (IOL) implantation is the
l Inspite of the demerits phacoemulsification method of choice for correcting aphakia.
OPHTHALMOLOGY
has become the preferred method of m Harold Ridley, a British ophthalmologist,
cataract extraction world performed his first case.
l However, for the masses, especially in m Types of intraocular lenses
developing countries, the manual SICS offers n The commonly used material for their
the advantages of sutureless cataract surgery as a manufacture is polymethylmethacrylate
low cost alternative to phacoemulsification with (PMMA).
the added advantages of having wider n The major classes of IOLs
applicability and an easier learning curve. l Anterior chamber IOL.
n Surgical steps of the ICCE technique „ These lenses lie entirely in front of the
m A peripheral iridectomy may be performed to iris
prevent postoperative pupil block glaucoma „ are supported in the angle of anterior
(MCQ) chamber
m Formation of anterior chamber. „ ACIOL can be inserted after ICCE or
n After the delivery of lens, iris is reposited into ECCE.
CATARACT
the anterior chamber with the help of iris „ These are not very popular due to
repositor and chamber is formed by injecting comparatively higher incidence of
sterile air or balanced salt solution.(MCQ) bullous keratopathy.
n Surgical steps of conventional ECCE l Iris-supported lenses.
m Injection of viscoelastic substance in anterior „ These lenses are fixed on the iris with the
chamber. help of sutures, loops or claws.
n A viscoelastic substance such as 2% „ These lenses are also not very popular due
methylcellulose or 1% sodium hyaluronate to a high incidence of postoperative
is injected into the anterior chamber. complications.
n This maintains the anterior chamber and protects l Posterior chamber lenses. (MCQ)
the endothelium. „ PCIOLs rest entirely behind the iris
m Implantation of IOL. (MCQ) „ They may be supported by the ciliary
n The PMMA posterior chamber IOL is sulcus or the capsular bag.
implanted in the capsular bag after inflating the „ Recent trend is towards ‘in-the-bag-
bag with viscoelastic substance fixation’. (MCQ)
n Closure of the incision is done by a total of „ Commonly used model of PCIOLs is
3 to 5 interrupted 10-0 nylon sutures or modified C-loop (MCQ)
continuous sutures l Depending on the material of
n Removal of viscoelastic substance. manufacturing, three types of PC-IOLs are
l Before tying the last suture the visco-elastic available :
material is aspirated out with 2 way „ Rigid IOLs.
cannula and anterior chamber is filled with ® The modern one piece rigid IOLs are
BSS. made entirely from PMMA.
n Phacoemulsification „ Foldable IOLs
23
® to be implanted through a small incision l manifests as bradycardia and/or cardiac
(3.2 mm) after phacoemulsification arrhythmia
® are made of silicone, acrylic, hydrogel l observed due to retrobulbar block.
and collamer.(MCQ) l An intravenous injection of atropine is
„ Rollable IOLs are ultra thin IOLs. helpful.
® These are implanted through micro n Perforation of globe
incision (1mm) after phakonit technique. l Subconjunctival haemorrhage
® These are made of hydrogel. l does not need much attention.
m Indications of IOL implantation n Spontaneous dislocation of lens in vitreous
n operation for unilateral cataract should always l Occur in patients with weak and
be followed by an IOL implantation. degenerated zonules especially with
m Calculation of IOL power (Biometry) hypermature cataract) during vigorous ocular
n The most common method of determining massage after retrobulbar block.
IOL power uses a regression formula called n Operative complications
‘SRK (Sanders, Retzlaff and Kraff) m Superior rectus muscle laceration and/or
OPHTHALMOLOGY
formula’. haematoma
n The formula is P = A – 2.5L – 0.9K, where: m Excessive bleeding
l P is the power of IOL, n may be encountered during the preparation of
l A is a constant which is specific for each lens conjunctival flap or during incision into the
type. anterior chamber.
l L is the axial length of the eyeball in mm m Incision related complications
„ determined by A-scan ultrasonography. m Injur y to the cor nea (Descemet’s
l K is average corneal curvature detachment), iris and lens
„ determined by keratometry.(MCQ) m Iris injury and iridodialysis (tear of iris from
n Postoperative management after cataract root)
operation m Complications related to anterior
m After 6-8 weeks of operation corneoscleral sutures capsulorhexis.
are removed (when applied). m Continuous curvilinear capsulorhexis (CCC)
m Now a days most surgeons are doing sutureless cataract is the preferred technique for opening the anterior capsule
CATARACT
surgery. for SICS and phacoemulsification.

m Final spectacles are prescribed after about 8 m Posterior capsular rupture (PCR).
weeks of operation. (MCQ) n It is a dreaded complication during
n Complications of cataract surgery and their extracapsular cataract extraction.
management n it can lead to nuclear drop into the vitreous
n Preoperative complications m Zonular dehiscence
m Anxiety. m may occur in all techniques of ECCE
m Nausea and gastritis m Vitreous loss
m Irritative or allergic conjunctivitis n It is the most serious complication
n occur in some patients due to preoperative n occur following accidental rupture of
topical antibiotic drops. posterior capsule during any technique of
n Postponing the operation for 2 days along ECCE.
with withdrawal of such drugs is required. m Nucleus drop into the vitreous cavity. I
m Corneal abrasion n it occurs more frequently with
n develop due to inadvertent injury during phacoemulsification,
Schiotz tonometry. m Posterior loss of lens fragments into the
m Complications due to local anaesthesia vitreous cavity
n Retrobulbar haemorrhage n It is potentially serious because it may result in
l may occur due to retrobulbar block. glaucoma, chronic uveitis, chronic CME
l Immediate pressure bandage after instilling and even retinal detachment.
one drop of 2% pilocarpine m Expulsive choroidal haemorrhage.
l postponement of operation for a week is advised. n It usually occurs in hypertensives and patients
n Oculocardiac reflex with arteriosclerotic changes.
24
n Its incidence was high in ICCE and n On fluorescein angiography it depicts typical
conventional ECCE but has decreased markedly flower petal pattern due to leakage of dye from
with valvular incision of manual SICS and phaco perifoveal capillaries.
emulsification technique. n In most cases it is associated with vitreous
n Early postoperative complications incarceration in the wound and mild iritis.
m Hyphaema. n immediate preoperative and postoperative
n Collection of blood in the anterior chamber use of antiprostaglandins (indomethacin or flurbiprofen
n may occur from conjunctival or scleral vessels due or ketorolac) eyedrops is recommended as
to minor ocular trauma or otherwise prophylaxis of CME.
n Most hyphaemas absorb spontaneously and n In cases of CME with vitreous incarceration,
thus need no treatment. anterior vitrectomy along with steroids and
m Iris prolapse. antiprostaglandins may improve visual acuity
n It is usually caused by inadequate suturing of m Delayed chronic postoperative
the incision after ICCE and conventional endophthalmitis
ECCE n caused when an organism of low virulence
OPHTHALMOLOGY
n occurs during first or second postoperative (Propionobacterium acne or staph epidermidis)
day. becomes trapped within the capsular bag.
m Striate keratopathy. n It has an onset ranging from 4 weeks to years
n Characterised by mild corneal oedema with (mean 9 months) postoperatively
Descemet’s folds n typically follows an uneventful cataract
n is a common complication observed during extraction with a PCIOL in the bag.
immediate postoperative period. m Pseudophakic bullous keratopathy (PBK)
n This occurs due to endothelial damage during n usually a continuation of postoperative
surgery. corneal oedema produced by surgical or
m Flat (shallow or nonformed) anterior chamber chemical insult to a healthy or compromised
n It may be due to wound leak, ciliochoroidal corneal endothelium.
detachment or pupil block. n PBK is becoming a common indication of
m Postoperative anterior uveitis penetrating keratoplasly (PK).
n can be induced by m Retinal detachment (RD).(MCQ)
CATARACT
l instrumental trauma, undue handling of uveal n Incidence of retinal detachment is higher in
tissue aphakic patients as compared to phakics.
l reaction to residual cortex n retinal detachment is more common after
l chemical reaction induced by viscoelastics, ICCE than after ECCE.
pilocarpine etc n Other risk factors for aphakic retinal detachment
m Bacterial endophthalmitis. (MCQ) include
n This is one of the most dreaded l vitreous loss during operation
complications l associated myopia
n Symptoms and signs of bacterial endophthalmitis l lattice degeneration of the retina.
are generally present between 48 and 72 m Epithelial ingrowth.
hours after surgery m Fibrous downgrowth into the anterior chamber
n Late postoperative complications (MCQ) n It may cause secondary glaucoma,
m Cystoid macular oedema (CME).(MCQ) m After cataract.
n Collection of fluid in the form of cystic loculi n It is also known as ‘secondary cataract’.
in the Henle’s layer of macula n It is the opacity which persists or develops
n a frequent complication of cataract surgery. after extracapsular lens extraction.
n However, in most cases it is clinically n Clinical types.
insignificant, does not produce any visual l After cataract may present as
problem and undergoes spontaneous regression. „ thickened posterior capsule
n clinically significant CME typically produces „ dense membranous after cataract
visual diminution one to three months after „ Soemmering’s ring
cataract extraction. (MCQ) ® refers to a thick ring of after cataract
n On funduscopy it gives honeycomb formed behind the iris, enclosed between
appearance. the two layers of capsule
25
„ Elschnig’s pearls TOPIC 3 - UVEITIS
® vacuolated subcapsular epithelial cells
are clustered like soap bubbles along the n Anatomic Classification
m Anterior uveitis.
posterior capsule
n It is inflammation of the uveal tissue from iris
n Treatment is as follows :
l Thin membranous after cataract and thickened
up to pars plicata of ciliary body.
n It may be subdivided into
posterior capsule
l Iritis, in which inflammation predominantly
„ best treated by YAG-laser capsulotomy
or discission with cystitome or Zeigler’s affects the iris.
l Iridocyctitis in which iris and pars plicata
knife.(MCQ)
l Dense membranous after cataract needs
part of ciliary body are equally involved
l Cyclitis, in which pars plicata part of
surgical membranectomy.
l Soemmering’s ring after cataract with
ciliary body is predominantly affected.
m Intermediate uveitis.
clean central posterior capsule needs no
n It includes inflammation of the pars plana and
treatment.
peripheral part of the retina and underlying
OPHTHALMOLOGY
l Elschnig’s pearls involving the central

part of the posterior capsule can be treated ‘choroid’.
n It is also called ‘pars planitis’.
by YAG- laser capsulotomy or discission with
m Posterior uveitis.
cystitome.
n It refers to inflammation of the choroid
m Glaucoma-in-aphakia and pseudophakia
(choroiditis).
n IOL-related complications n Always there is associated inflammation of retina
m UGH syndrome (MCQ) and hence the term ‘chorioretinitis’ is used.
n refers to concurrent occurrence of uveitis, n Panuveitis. It is inflammation of the whole uvea.
glaucoma and hyphaema. n Clinical classification
n It used to occur with rigid anterior chamber m Acute uveitis.
IOLs, which are not used now. n It has got a sudden symptomatic onset
m Malpositions of IOL n the disease lasts for about six weeks to 3
n Sun-set syndrome (Inferior subluxation of IOL). months.
n Sun-rise syndrome (Superior subluxation of IOL). m Chronic uveitis.
UVEITIS
n Lost lens syndrome refers to complete dislocation n It frequently has an insiduous and
of an IOL into the vitreous cavity. asymptomatic onset.
n Windshield wiper syndrome. n It persists longer than 3 months to even years
l It results when a very small IOL is placed n usually diagnosed when it causes defective
vertically in the sulcus. vision.
l In it the superior loop moves to the left and n Pathological classification - Wood’s classification
right, with movements of the head. m Suppurative or purulent uveitis.
m Pupillary capture of the IOL m Non-suppurative uveitis.
n occur following postoperative iritis or proliferation n Non-granulomatous uveitis, and
of the remains of lens fibres. n Granulomatous uveitis
m Toxic lens syndrome. n Etiology of uveitis
n It is the uveal inflammation m Types of infectious uveitis. (MCQ)
n excited by either the ethylene gas used for n Bacterial infections
sterilising IOLs (in early cases) or by the lens l granulomatous
material (in late cases). „ tubercular, leprotic, syphilitic, brucellosis
l pyogenic
„ streptococci, staphylococci, pneumococci
and gonococcus
n Viral infections associated with uveitis are
l herpes simplex, herpes zoster and cytomegalo
inclusionvirus (CMV).
n Fungal uveitis
l systemic aspergillosis
26
l candidiasis n sarocoidosis
l blastomycosis. n collagen related diseases (polyarteritis nodosa
n Parasitic uveitis (PAN), disseminated lupus erythematosus (DLE),
l toxoplasmosis, toxocariasis, onchocerciasis rheumatic and rheumatoid arthritis)
and amoebiasis. n metabolic diseases (diabetes mellitus and gout),
n Rickettsial uveitis n disease of the central nervous system
l scrub typhus and epidemic typhus. (disseminated sclerosis)
m Allergic (hypersensitivity linked) uveitis. n diseases of skin (psoriasis, lichen planus,
n Allergic uveitis is of the commonest erythema nodosum, pemphigus)
occurrence in clinical practice. m Idiopathic uveitis.
n It may be caused by the following ways n Idiopathic specific uveitis entities
l Microbial allergy l pars planitis,
„ In India tubercular infections still play an l sympathetic ophthalmitis
important role. l Fuchs’ hetero-chromic iridocyclitis.
l Anaphylactic uveitis n Nonspecific idiopathic uveitis entities
OPHTHALMOLOGY
l Atopic uveitis. l About more than 25 percent cases of
l Autoimmune uveitis. uveitis fall in this group.
„ It is found in association with autoimmune n Pathology of uveitis
disorders such as m Pathology of non-granulomatous uveitis.
® Still’s disease, rheumatoid arthritis, Wegener’ s n iris
granulomatosis l becomes waterlogged, oedematous,
® systemic lupus erythematosus, Reiter’s disease muddy with blurring of crypts and furrows.
„ In phacoanaphytic endophthalmitis l its mobility is reduced
® lens proteins play role of autoantigens n pupil
„ sympathetic ophthalmitis l becomes small in size due to
® autoimmune reaction to uveal „ sphincter irritation
pigments „ engorgement of radial vessels of iris.
l HLA-associated uveitis n aqueous flare and fine KPs
„ HLA-B27.-ankylosing spondylitis and l Exudates and lymphocytes poured into the
Reiter’ s syndrome. anterior chamber result in
UVEITIS
„ HLA-B5: Uveitis in Behcet’s disease.) „ aqueous flare (MCQ)
„ HLA-DR4 and DW15: Vogt Koyanagi „ deposition of fine KPs at the back of
Harada’s disease (MCQ) cornea (MCQ)
l Toxic uveitis. n posterior synechiae (MCQ)
„ Endotoxins, l Due to exudates in the posterior chamber,
„ seen in patients with the posterior surface of iris adheres to the
® acute pneumococcal or gonococcal anterior capsule of lens leading to posterior
conjunctivitis synechiae formation.
® fungal corneal ulcer n cyclitic membrane (MCQ)
„ Endocular toxins l In severe inflammation, due to pouring of
„ Uveitis seen in patients with exudate from ciliary processes, behind the
® blind eyes le7ns, an exudative membrane called cyclitic
® long-standing retinal detachment membrane may be formed.
® intraocular haemorrhages n After healing, pin-point areas of necrosis or
® intraocular tumours atrophy are evident.
® phacotoxic uveitis. n Subsequent attacks lead to structural changes
„ Exogenous toxins like atrophy, gliosis and fibrosis which cause
„ miotics and cytotoxic drugs are exogenous adhesions, scarring and eventually destruction of
toxins. eye.
m Traumatic uveitis. m Pathology of granulomatous uveitis.
n Sympathetic ophthalmia in the other eye. n Iris nodules (MCQ)
m Uveitis associated with non-infective systemic l Iris nodules are usually formed near pupillary
diseases. border (Koeppe’s nodules)( MCQ)
27
l characterised by infiltration with lymphocytes, „ associated macular oedema, papillitis or
plasma cells, with mobilization and secondary glaucoma
proliferation of large mononuclear cells m Signs
which eventually become epithelioid and giant n Slit lamp biomicroscopic examination is
cells and aggregate into nodules. essential to elicit most of the signs of uveitis
n mutton fat keratic precipitates (MCQ) n Lid oedema
l Similar nodular collection of the cells is n Circumcorneal congestion
deposited at the back of cornea l marked in acute iridocyclitis and minimal
n aqueous flare is minimal. in chronic iridocyclitis.
n Anterior uveitis (iridocyclitis) l differentiated from superficial congestion
m Clinical features occurring in acute conjunctivitis.
n Main symptoms of acute anterior uveitis are pain, n Corneal signs
photophobia, redness, lacrimation and l Corneal oedema
decreased vision. „ due to
n In chronic uveitis, however the eye may be white ® toxic endothelitis
OPHTHALMOLOGY
with minimal symptoms even in the presence ® raised intraocular pressure when
of signs of severe inflammation. present.
m Symptoms l Keratic precipitates (KPs) (MCQ)
n Pain. „ proteinaceous- cellular deposits
l It is dominating symptom of acute anterior occurring at the back of cornea.
uveitis. „ Mostly, these are arranged in a triangular
l dull aching throbbing sensation which is fashion occupying the centre and inferior part
typically worse at night. of cornea due to convection currents in
l The ocular pain is usually referred along the the aqueous humour
distribution of branches of fifth nerve, l Mutton fat KPs. (MCQ)
especially towards forehead and scalp. „ typically occur in granulomatous
n Redness. iridocyclitis
l It is due to circumcorneal congestion „ composed of epithelioid cells and
l occurs as a result of active hyperaemia of macrophages.
UVEITIS
anterior ciliary vessels „ They are large, thick, fluffy, lardaceous

l due to the effect of toxins, histamine and KPs
histamine-like substances and axon „ have a greasy or waxy appearance.
reflex. „ Mutton fat KPs are usually a few (10 to
n Photophobia and blepharospasm 15) in number
l due to a reflex between sensory fibres of l Small and medium KPs (granular KPs). (MCQ)
fifth nerve (which are irritated) and motor „ pathognomic of non-granulomatous uveitis
fibres of the seventh nerve, supplying the „ composed of lymphocytes.
orbicularis oculi muscle. „ small, discrete, dirty white KPs
n Lacrimation „ arranged irregularly at the back of cornea.
l occurs as a result of lacrimatory reflex „ Small KPs may be hundreds in number
mediated by fifth nerve (afferent) and and form the so called endothelial dusting.
secretomotor fibres of the seventh nerve l Red KPs.
(efferent). „ RBCs also take part in composition.
n Defective vision „ seen in haemorrhagic uveitis.
l Factors responsible for visual disturbance l Old KPs.
include „ These are sign of healed uveitis
„ induced myopia due to ciliary spasm „ with healing process KPs shrink, fade,
„ corneal haze (due to oedema and KPs) become pigmented and irregular in shape
„ aqueous turbidity (crenated margins).
„ pupillary block due to exudates „ Old mutton fat KPs usually have a ground
„ complicated cataract glass appearance due to hyalinization.
„ vitreous haze l Posterior corneal opacity
„ cyclitic membrane,
28
„ formed in long- standing cases of „ Iris atrophy is typically observed in Fuchs’
iridocyclitis. heterochromic iridocyclitis. (MCQ)
n Anterior chamber signs l Changes in iris colour.
l Aqueous cells. „ muddy in colour during active phase
„ It is an early feature of iridocyclitis. „ show hyperpigmented and depigmented
„ The cells should be counted in an oblique areas in healed stage.
slit-lamp beam, l Iris nodules
„ graded as : „ These occur typically in granulomatous
® = 0cells, uveitis
® ± = 1–5 cells, „ Koeppe’s nodules
® +1 = 6–10 cells, ® situated at the pupillary border
® +2 = 11-20 cells, ® may initiate posterior synechia.
® +3 = 21–50 cells, and „ Busacca’s nodules (MCQ)
® +4 = over 50 cells ® situated near the collarette
l Aqueous flare. (MCQ) ® are large but less common than the
OPHTHALMOLOGY
„ It is due to leakage of protein particles Koeppe’s nodules.
into the aqueous humour from damaged blood l Posterior synechiae.
vessels „ formed due to organisation of the fibrin-
„ It is demonstrated on the slit lamp rich exudates.
examination by a point beam of light passed „ These are adhesions between the posterior
obliquely to the plane of iris surface of iris and
„ In the beam of light, protein particles are ® anterior capsule of crystalline lens
seen as suspended and moving dust or
particles. ® any other structure which may be
„ This is based on the ‘Brownian » artificial lens
movements’ or ‘Tyndal phenomenon’. » after cataract
„ Aqueous flare is usually (MCQ) » posterior capsule (left after extracapsular
® marked in nongranulomatous uveitis cataract extraction)
® minimal in granulomatous uveitis. ® anterior hyaloid face.
„ The flare is graded from ‘0’ to +4. Grade : „ Morphologically, posterior synechiae may
UVEITIS
® 0= no aqueous flare be segmental, annular or total.
® +1= just detectable ® Segmental posterior synechiae refers
® +2= moderate flare with clear iris details to adhesions of iris to the lens at some
® +3= marked flare (iris details not clear); points
® +4= intense flare (fixed coagulated ® Annular posterior synechiae
aqueous with considerable fibrin). » ring synechiae are 360 adhesions of
o
l Hypopyon. (MCQ) pupillar y margin to anterior

„ When exudates are heavy and thick, they capsule of lens.
settle down in lower part of the anterior chamber » seclusio pupillae (MCQ)
as hypopyon (sterile pus in the anterior ö These prevent the circulation of
chamber) aqueous humour from posterior
l Hyphaema (blood in the anterior chamber): chamber to anterior chamber
„ seen in haemorrhagic type of uveitis. » ‘iris-bombe’ (MCQ)
l Changes in depth and shape of anterior ö Thus, the aqueous collects behind
chamber the iris and pushes it anteriorly leading
„ occur due to synechiae formation. to ‘iris-bombe’ formation
l Changes in the angle of anterior chamber ö This is usually followed by a rise
n Iris signs in intraocular pressure.
l Loss of normal pattern. ® Total posterior synechiae
„ It occurs due to » Occur due to plastering of total
® oedema and waterlogging of iris in posterior surface of iris with the
active phase anterior capsule of lens
® atrophic changes in chronic phase.
29
» formed in acute plastic type of n Early glaucoma (hypertensive uveitis)
uveitis. (MCQ)
» These result in deepening of l In active phase of the disease, presence of
anterior chamber exudates and inflammatory cells in the anterior
l Neovascularsation of iris (rubeosis iridis) chamber may cause clogging of trabecular
(MCQ) meshwork
„ develops in some eyes with chronic l result in the decreased aqueous drainage
iridocyclitis. l cause a rise in intraocular pressure
n Pupillary signs (MCQ) (hypertensive uveitis).
l Narrow pupil. n Late glaucoma in iridocyclitis (post-
„ It occurs in acute attack of iridocyclitis inflammatory glaucoma)
„ occurs due to l result of pupil block not allowing the
® irritation of sphincter pupillae by aqueous to flow from posterior to anterior
toxins chamber.
® Iris oedema and engorged radial „ seclusio pupillae due to ring synechiae
OPHTHALMOLOGY
vessels of iris formation

l Irregular pupil shape. (MCQ) „ occlusio pupillae due to organised
„ It results from segmental posterior exudates
synechiae formation. n Cyclitic membrane.
„ Dilatation of pupil with atropine at this stage l late complication of acute plastic type of
results in festooned (MCQ) iridocyclitis.
l Ectropion pupillae (evertion of pupillary n Choroiditis.
margin). (MCQ) n Retinal complications.
„ develop due to contraction of fibrinous l cystoid macular oedema, macular
exudate on the anterior surface of the iris. degeneration
l Pupillary reaction (MCQ) l exudative retinal detachment and secondary
„ becomes sluggish or absent periphlebitis retinae.
„ occurs due to oedema and hyperaemia n Papillitis (inflammation of the optic disc).
of iris which hamper its movements. n Band-shaped keratopathy (MCQ)
UVEITIS
l Occlusio pupillae (MCQ) l Occurs especially in children having Still’s

„ results when the pupil is completely disease.
occluded n Phthisis bulbi.
„ occur due to organisation of the
exudates across the entire pupillary area.
n Changes in the lens
l Pigment dispersal on the anterior capsule
of lens
„ almost of universal occurrence in a case
of anterior uveitis.
l Exudates may be deposited on the lens
„ Occur in cases with acute plastic
iridocyclitis.
l Complicated cataract
„ develop as a complication of persistent
iridocyclitis.
n Change in the vitreous
l Anterior vitreous may show exudates and
inflammatory cells after an attack of acute
iridocyclitis.
m Complications and sequelae (mcq)
n Complicated cataract.
n Secondary glaucoma.
30
Feature Acute `Acute Acute
Conjunctivitis Iridocyclitis glaucoma
1. Onset Gradual Usually gradual Sudden
2. Pain Mild discomfort Moderate in eye and along Severe in eye and the entire
the first division of trigeminal area
trigeminal nerve
3. Discharge Mucopurulent Watery Watery
4. Coloured halos May be present Absent Present
5. Vision Good Slightly impaired Markedly impaired
6. Congestion Superficial Deep ciliary Deep ciliary
Conjunctival
7. Tenderness Absent Marked Marked
8. Pupil Normal Small and Irregular Large and verticall oval
9. Media Clear Hazy due to KPs, aqueous Hazy due to edematous
flare and pupillary exudates. cornea
OPHTHALMOLOGY
10. Anterior chamber Normal May be deep Very shallow
11. Iris Normal Muddy oedematous
12. Intraocular Pressure Normal Usually normal Raised
13. Constitutional Absent Litttle Prostration and vomitting
stmptoms
Feature Granulomatous Non-granulomatous

1. Onset Insidious Acute
2. Pain Minimal Marked
3. Photophobia Slight Marked
4. Ciliary congestion Minimal Marked
5. Keratic precipitates (KPs) Mutton fat Small
UVEITIS
6. Aqueous flare Mild Marked
7. Iris nodules Usually present Absent
8. Posterior synechiae Thick and broad based Thin and tenuous
9. Fundus Nodular lesions Diffuse involvement
n Treatment of iridocyclitis (A Very High yield „ cycloplegics should be continued for at

MCQ Zone ) least 2-3 weeks after the eye becomes
m Non-specific treatment quiet, otherwise relapse may occur.
n Local therapy „ Mode of action (MCQ frequently
l Mydriatic-cycloplegic drugs. (MCQ) asked
„ very useful and most effective during „ In iridocyclitis, atropine
acute phase of iridocyclitis. ® gives comfort and rest to the eye by
„ Commonly used drugs relieving spasm of iris sphincter and
® 1 percent atropine sulfate eye ointment or ciliary muscle
drops ® prevents the formation of synechiae
® In case of atropine allergy, and may break the already formed
» 2 percent homatropine synechiae, reduces exudation by
» 1 percent cyclopentolate eyedrops decreasing hyperaemia and vascular
® a subconjunctival injection of 0.25 ml permeability
mydricain ® increases the blood supply to anterior
» a mixture of atropine, adrenaline uvea by relieving pressure on the anterior
and procaine ciliary arteries. As a result more antibodies
» provides more powerful cycloplegic
effect
31
reach the target tissues and more toxins are TOPIC 4 - CONJUNCTIVITIS
absorbed. n Bacterial conjunctivitis
l Corticosteroids, (MCQ) administered locally
m Staphylococcus aureus is the most common cause
n Systemic therapy
(MCQ)
l Corticosteroids
m Haemophilus influenzae (aegyptius, Koch- Weeks
l Non-steroidalanti-inflammatorydrugs
bacillus).
(NSAIDS) (MCQ) n classically causes epidemics of mucopurulent
l Immunosuppressive drugs
conjunctivitis, known as ‘red-eye’.
n Physical measures
m Moraxella lacunate (Moraxella Axenfeld bacillus)
l Hot fomentation
(MCQ)
l Dark goggles
n most common cause of angular conjunctivitis
n Treatment of complications and angular blepharoconjunctivitis.
m Inflammatory glaucoma (hypertensive uveitis)
m Neisseria gonorrhoeae
(MCQ commonly asked in exam) n typically produces
n drugs to lower intraocular pressure
l acute purulent conjunctivitis in adults
OPHTHALMOLOGY
l 0.5 percent timolol maleate eyedrops

l ophthalmia neonatorum in new born.
l tablet acetazolamide (250 mg thrice a day)
n It is capable of invading intact corneal
n Pilocarpine and latanoprost eye drops are
epithelium.(MCQ)
contraindicated in inflammatory glaucoma. (MCQ) n Angular conjunctivitis (MCQ)
m Post-inflammatory glaucoma due to ring
m It is a type of chronic conjunctivitis
synechiae m characterised by mild grade inflammation
n treated by laser iridotomy
confined to the conjunctiva and lid margins
n Surgical iridectomy may be done when laser
near the angles (hence the name) associated with
is not available. maceration of the surrounding skin.
n Surgery should be performed in a quiet eye
m Etiology
under high doses of corticosteroids. n Moraxella Axenfeld is the commonest
m Complicated cataract
causative organism.
CONJUNCTIVITIS
n requires lens extraction with guarded

n MA bacilli are placed end to end, so the disease
prognosis in spite of all precautions. is also called ‘diplobacillary conjunctivitis’
n The presence of fresh KPs is considered a
m Curative treatment consists of :
contraindication for intraocular surgery.(MCQ) n Oxytetracycline (1%) eye ointment
m Retinal detachment
n Zinc lotion
n of exudative type usually settles itself if uveitis
n Viral conjunctivitis
is treated aggressively. m Most of the viral infections tend to affect the
n A tractional detachment
epithelium, both of the conjunctiva and
l requires vitrectomy
cornea,
l poor visual prognosis.
m typical viral lesion is a ‘keratoconjunctivitis’.
m Phthisis bulbi especially when painful,
m conjunctival involvement is more prominent (e.g.,
n requires removal by enucleation operation.
pharyngo-conjunctival fever)
m corneal involvement is more prominent (e.g.,
herpes simplex).
n Acute haemorrhagic conjunctivitis (mcq)
m It is an acute inflammation of conjunctiva charac-
terised by multiple conjunctival haemorrhages,
conjunctival hyperaemia and mild follicular
hyperplasia.
m The disease is caused by picor naviruses
(enterovirus type 70) which are RNA viruses
of small (pico) size. (MCQ)
m The disease is very contagious
m transmitted by direct hand-to-eye contact.
m The disease is also called
32
n epidemic haemorrhagic conjunctivitis l More common in summer; hence the name
(EHC) (MCQ) spring catarrh looks a misnomer.
n Apollo conjunctivitis l Recently it is being labelled as ‘Warm weather
m Incubation period of EHC is very short (1-2 days). conjunctivitis’.
m Usually the disease has a self-limiting course of n Climate. More prevalent in tropics
5-7 days. m Pathology
n Follicular conjunctivitis n Conjunctival epithelium
m Follicles are formed due to localised aggregation of l undergoes hyperplasia
lymphocytes in the adenoid layer of conjunctiva. l sends downward projections into the
m Their appearance resembles boiled sago- subepithelial tissue.
grains. n Adenoid layer
n Epidemic Keratoconjunctivitis (EKC) (MCQ) l shows marked cellular infiltration by
m It is a type of acute follicular conjunctivitis eosinophils, plasma cells, lymphocytes
m mostly associated with superficial punctate and histiocytes.
keratitis n Fibrous layer
OPHTHALMOLOGY
n a distinctive feature of EKC l shows proliferation which later on
m usually occurs in epidemics, hence the name undergoes hyaline changes.
EKC. n Conjunctival vessels
m EKC is mostly caused by adenoviruses type 8 n show proliferation, increased permeability
and 19 (MCQ) and vasodilation.
m The condition is markedly contagious m Clinical picture
m spreads through contact with contaminated n Symptoms.
fingers, solutions and tonometers. l marked burning and itching sensation
m Incubation period after infection is about 8 days which is usually intolerable
m virus is shed from the inflamed eye for 2-3 weeks. „ accentuated when patient comes in a warm
m Preauricular lymphadenopathy is associated in humid atmosphere.
almost all cases (MCQ) l Itching is more marked with palpebral form
m Treatment. of disease.
CONJUNCTIVITIS
n results are reported with adenine arabinoside l Other associated symptoms include:
(Ara-A). „ mild photophobia
n Corticosteroids should not be used during „ lacrimation
active stage. „ stringy (ropy) discharge (MCQ)
n Vernal keratoconjunctivitis (vkc) or spring „ heaviness of lids.
catarrh n Signs
m It is a recurrent, bilateral, interstitial, self- l Palpebral form.
limiting, allergic inf lammation of the „ Usually upper tarsal conjunctiva of both
conjunctiva having a periodic seasonal eyes is involved. (MCQ)
incidence. „ ‘cobble-stone’ apprearence (MCQ)
m It is considered a hypersensitivity reaction to ® The typical lesion is characterized by
some exogenous allergen, such as grass pollens. the presence of hard, flat topped,
m It is atopic allergic disorder in many cases papillae arranged in a ‘cobble-stone’
m IgE-mediated mechanisms play an important or ‘pavement stone’, fashion
role. „ ‘giant papillae’
m Such patients may give personal or family history ® In severe cases, papillae may hypertrophy
of other atopic diseases such as hay fever, to produce cauliflower like
asthma, or eczema excrescences of ‘giant papillae’.
m peripheral blood shows eosinophilia and „ Conjunctival changes are associated with
inceased serum IgE levels. white ropy discharge. (MCQ)
m Predisposing factors l Bulbar form is characterised by
n Age and sex. „ dusky red triangular congestion of
l 4-20 years bulbar conjunctiva in palpebral area;
l more common in boys than girls (MCQ) „ gelatinous thickened accumulation of
n Season. tissue around the limbus;
33
„ presence of discrete whitish raised dots m occur as an allergic response of the conjunctival
along the limbus (Tranta’s spots) (MCQ) and corneal epithelium to some endogenous
l Mixed form shows combined features of both allergens to which they have become sensitized.
palpebral and bulbar forms m It is believed to be a delayed hypersensitivity
l Vernal keratopathy. (Type IV-cell mediated) response to
„ Corneal involvement in VKC shows 5 endogenous microbial proteins.(MCQ)
types of lesions: m Causative allergens
„ Punctate epithelial keratitis n Tuberculous proteins
® involves upper cornea n Staphylococcus proteins are now most
® usually associated with palpebral form common cause.(MCQ)
of disease. n Other allergens may be
® The lesions always stain with rose l proteins of Moraxella Axenfeld bacillius
bengal and invariably with fluorescein l certain parasites (worm infestation).
dye. m Predisposing factors
„ Ulcerative vernal keratitis (shield ulceration) n Age. Peak age group is 3-15 years.
OPHTHALMOLOGY
(MCQ) n Sex. Incidence is higher in girls than boys.

® presents as a shallow transverse ulcer in upper n Undernourishment. Disease is more common in
part of cornea. undernourished children.
„ Vernal corneal plaques n Living conditions. Overcrowded and
„ Subepithelial scarring occurs in the form of a unhygienic.
ring scar. n Season.
„ Pseudogerontoxon (MCQ) l It occurs in all climates
® characterised by a classical ‘cupid’s l incidence is high in spring and summer
bow’ outline. seasons.
m Clinical course of disease m Presence of one or more whitish raised nodules
n often self-limiting on the bulbar conjunctiva near the limbus,
n usually burns out spontaneously after 5-10 with hyperaemia usually of the surrounding
CONJUNCTIVITIS
years. conjunctiva, in a child living in bad hygienic

m Differential diagnosis. conditions (most of the times) are the diagnostic
n Palpebral form of VKC needs to be features of the phlyctenular conjunctivitis.
differentiated from trachoma with pre- m Clinical course
dominant papillary hypertrophy n usually self-limiting
m Treatment n phlycten disappears in 8-10 days leaving no
n Local therapy trace.
l Topical steroids n However, recurrences are very common.
„ Medrysone and fluorometholone are m Management
safest of all these. n Local therapy.
l Mast cell stabilizers such as sodium l Topical steroids
cromoglycate (2%) drops (MCQ) l Antibiotic drops and ointment
l Topical antihistaminics are also effective. l Atropine (1%) eye when cornea is involved.
l Acetyl cysteine (0.5%) used topically has
mucolytic properties
l Topical cyclosporine (1%) drops
n Systemic therapy
l Oral antihistaminics
l Oral steroids
n Treatment of large papillae.
l Supratarsal injection of long acting steroid
l Cryo application
l Surgical excision
n Phlyctenular keratoconjunctivitis (MCQ)
m a characteristic nodular affection
34
TOPIC 5 - VISUAL FIELD DEFECTS m Common causes of optic tract lesions
n syphilitic meningitis or gumma
n tuberculosis and tumours of optic thalamus
n Lesions of the optic nerve.
n aneurysms of superior cerebellar or posterior
m characterised by marked loss of vision or
complete blindness on the affected side cerebral arteries.
m associated with abolition of the
n Lesions of lateral geniculate body.
m These produce homonymous hemianopia with
n direct light reflex on the ipsilateral side and
n consensual on the contralateral side.
sparing of pupillary reflexes
m end in partial optic atrophy.
m Near (accommodation) reflex is present.
m Common causes of optic nerve lesions are:
n Lesions of optic radiations.
m Involvement of total optic radiations
n optic atrophy
m produce complete homonymous hemianopia
n acute optic neuritis
n Lesions through proximal part of the optic (sometimes sparing the macula).
m in lesions of parietal lobe (containing superior
nerve.
m Ipsilateral blindness
fibres of optic radiations) (MCQ)
OPHTHALMOLOGY
n Inferior quadrantic hemianopia (pie on the floor)
m contralateral hemianopia
m abolition of
occurs
m In lesions of the temporal lobe (containing inferior
l direct light reflex on the affected side
l consensual on the contralateral side.
fibres of optic radiations) (MCQ)
n Superior quadrantic hemianopia (pie in the sky)
m Near reflex is intact.
n Sagittal (central) lesions of the chiasma. occurs
m Pupillary reactions are normal as the fibres of the
m bitemporal hemianopia (MCQ)
m bitemporal hemianopic paralysis of pupillary
light reflex leave the optic tracts to synapse in the
reflexes. superior colliculi.
m Lesions of optic radiations do not produce optic
m These usually lead to partial descending optic
atrophy. atrophy, as the second order neurons (optic nerve fibres)
synapse in the lateral geniculate body.
VISUAL FIELD DEFECTS

m Common causes of central chiasmal lesion are:
m Common lesions of the optic radiations include
n suprasellar aneurysms
n tumours of pituitary gland
vascular occlusions, primary and secondary
n craniopharyngioma
tumours, and trauma.
n suprasellar meningioma and glioma of third n Lesions of the visual cortex.
ventricle m occlusion of posterior cerebral artery supplying
n third ventricular dilatation due to obstructive the anterior part of occipital cortex
hydrocephalus m Congruous homonymous hemianopia (usually
n chronic chiasmal arachnoiditis. sparing the macula)
n Lateral chiasmal lesions n lesions of the tip of the occipital cortex
m binasal hemianopia
following head injury or gun shot injuries.
m Congruous homonymous macular defect
m binasal hemianopic paralysis of the pupillary
n Pupillary light reflexes are normal
reflexes.
m optic atrophy does not occur following visual
m usually lead to partial descending optic atrophy
m Common causes of such lesions
cortex lesions
n distension of third ventricle causing pressure on each
n Pupillary reflexes
m Light reflex
side of the chiasma
n When light is shone in one eye, both the pupils
n atheroma of the carotids or posterior
communicating arteries. constrict.
l Constriction of the pupil to which light is
n Lesions of optic tract.
m incongruous homonymous hemianopia (MCQ)
shone is called direct light reflex and that of the
m contralateral hemianopic pupillary reaction (Wernicke’s
other pupil is called consensual (indirect) light reflex
n Light reflex is initiated by rods and cones.
reaction) MCQ)
n Pathway of light reflex
m usually lead to partial descending optic atrophy
l Afferent pathway
m associated with contralateral third nerve
„ The afferent fibres extend from retina to the
paralysis and ipsilateral hemiplegia.
pretectal nucleus in the midbrain. 35
„ These travel along the optic nerve to the „ The efferent fibres relay in the accessory
optic chiasma ganglion before reaching the sphincter
® where fibres from the nasal retina pupillae.
decussate n Pathway of accommodation reflex
» travel along the opposite optic tract l The afferent impulses extend from the retina
» terminate in the contralateral to the parastriate cortex via
pretectal nucleus. „ the optic nerve, chiasma, optic tract, lateral
® While the fibres from the temporal geniculate body, optic radiations, and striate
retina cortex.
» remain uncrossed and travel along the l From the parastriate cortex the impulses are
optic tract of the same side relayed to the Edinger- Westphal nucleus
» terminate in the ipsilateral pretectal of both sides via the occipito-
nucleus. mesencephalic tract and the pontine
„ Internuncial fibres centre.
® connect each pretectal nucleus with l From the Edinger-Westphal nucleus the
OPHTHALMOLOGY
Edinger-Westphal nuclei of both efferent impulses travel along the 3rd nerve
sides. and reach the sphincter pupillae and
® This connection forms the basis of ciliary muscle after relaying in the accessory
consensual light reflex. and ciliary ganglions.
l Efferent pathway n Abnormalities of pupillary reactions
„ consists of the parasympathetic fibres n Amaurotic light reflex.
which arise from the Edinger-Westphal m It refers to the
nucleus in the mid-brain and travel along n absence of direct light reflex on the affected
the Efferent pathway side (say right eye) and
„ Preganglionic fibres n absence of consensual light reflex on the
® enter the inferior division of the third normal side (i.e., left eye).
VISUAL FIELD DEFECTS
nerve and via the nerve to the inferior m This indicates lesions of the optic nerve or
oblique reach the ciliary ganglion to retina on the affected side (i.e., right eye), leading
relay. to complete blindness.
„ Post-ganglionic fibres m In diffuse illumination both pupils are of equal
® travel along the short ciliary nerves size.
® innervate the sphincter pupillae. n Wernicke’s hemianopic pupil.
m Near reflex m It indicates lesion of the optic tract.
n Near reflex occurs on looking at a near m In this condition light reflex (ipsilateral direct and
object. contralateral consensual)
n It consists of two components: m is absent when light is thrown on the
l convergence reflex, i.e., contraction of pupil n temporal half of the retina of the affected
on convergence; side and
l accommodation reflex, i.e., contraction of n nasal half of the opposite side
pupil associated with accommodation. m is present when the light is thrown on the
n Pathway of convergence reflex n nasal half of the affected side and
l Afferent pathway n temporal half of the opposite side.
„ afferents from the medial recti travel n Marcus Gunn pupil.
centrally via the third nerve to the m It is the paradoxical response of a pupil of light
mesencephalic nucleus of the fifth m Occurs in the presence of a relative afferent
nerve, to a presumptive convergence pathway defect (RAPD).
centre in the tectal or pretectal region. m It is tested by swinging flash light test.
l Efferent pathway n Argyll Robertson pupil (ARP) .
„ From this the impulse is relayed to the m Here the pupil is slightly small in size
Edinger-Westphal nucleus m reaction to near reflex is present but light reflex
„ subsequent efferent pathway of near reflex is absent, i.e., there is light near dissociation (
is along the 3rd nerve. m ARP may stand for ‘accommodation reflex
present’
36
m Prostitute pupil ( it accommodates but does not react ) TOPIC 6 - DIABETIC RETINOPATHY
m Both pupils are involved and dilate poorly with
n Risk factors associated with occurence of DR are:
mydriatics.
m Duration of diabetes is the most important
m It is caused by a lesion (usually neurosyphilis) in
determining factor (MCQ)
the region of tectum.
n 50 percent of patients develop DR after 10 years
n The Adie’s tonic pupil
n 70 percent after 20 years
m reaction to light is absent and to near reflex is
n 90 percent after 30 years of onset of the disease.
very slow and tonic.
m More in females than males (4:3)
m The affected pupil is larger (anisocoria).
m Poor metabolic control is less important than duration
m It is usually unilateral
m Heredity.
m associated with absent knee jerk
n It is transmitted as a recessive trait without
m occurs more often in young women.
sex linkage.
m Adie’s pupil constricts with weak pilocarpine
n The effect of heredity is more on the
(0.125%) drops, while normal pupil does not.
proliferative retinopathy.
n Cortical blindness
m Pregnancy
OPHTHALMOLOGY
m produced by bilateral occipital lobe lesions.
m Hypertension
m Unilateral occipital lobe lesions typically
m Other risk factors include smoking, obesity and
produce contralateral macular sparing congruous
hyperlipidemia.
homonymous hemianopia.
n Pathogenesis.
m Causes of cortical blindness include:
m Essentially, it is a microangiopathy affecting retinal
n Vascular lesions are the commonest cause of
precapillary arterioles, capillaries and venules.
cortical blindness (e.g., embolisation of
posterior cerebral arteries).
Vascular changes seen in diabetes mellitus
n Head injury
n Tumours,
l Thickening of capillary basement membrane
n Other rare causes of cortical blindness are l Capillary endothelial cell damage
DIABETIC RETINOPATHY
migraine, hypoxic encephalopathy, l Changes in RBCs
Schilder’s disease and other l Incresed stickiness of platelets
leukodystrophies. l Loss of capillary pericytes
m Cortical blindness is characterized by:
n Bilateral loss of vision, Microvascular occlusion
n Normal pupillary light reflexes,
Retinal ischaemia
n Visual imagination and visual imagery in
dream are preserved
Capillary leakage
n Anton syndrome (MCQ)
Microaneurysms
l denial of blindness by the patients who obviously Haemorrhage
cannot see. Retinal oedema
n Riddoch phenomenon (MCQ) Hard exudates
l ability to perceive kinetic but not static Arteriovenous shunts
targets. (Intraretinal microvascular
abnormalities - IRMA)
Neovascularisation
n Classification
m Non-proliferative diabetic retinopathy (NPDR)
n Mild NPDR
n Moderate NPDR
n Severe NPDR
n Very severe NPDR
m Proliferative diabetic retinopathy (PDR)
m Diabetic maculopathy
m Advanced diabetic eye disease (ADED)
n Non-proliferative diabetic retinopathy (NPDR)
37
m Ophthalmoscopic features of NPDR include: n NVE > 1/2 disc area with VH or PRH
n Microaneurysms in the macular area n Diabetic maculopathy (MCQ)
l the earliest detectable lesion (MCQ) m diabetic macular edema
n Retinal haemorrhages n Have effect on vision.
l deep (dot and blot haemorrhages) n These changes may be associated with
l superficial haemorrhages (flame-shaped). l non-proliferative diabetic retinopathy (NPDR) or
n Hard exudates l proliferative diabetic retinopathy (PDR).
l yellowish-white waxy-looking patches n occurs due to increased permeability of the
l arranged in clumps or in circinate pattern. retinal capillaries.
l These are commonly seen in the macular n It is termed as clinically significant macular
area. edema (CSME) if one of the following three
n Retinal oedema characterized by retinal thickening. criteria are present on slit-lamp examination with
n Cotton-wool spots (MCQ) 90D lens:
l if > 8, there is high risk of developing PDR l Thickening of the retina at or within 500
n Venous abnormalities micron of the centre of the fovea.
OPHTHALMOLOGY
l beading, looping and dilatation. l Hard exudate at or within 500 micron of

n Intraretinal microvascular abnormalities (IRMA). the centre of fovea associated with adjacent
n Dark-blot haemorrhages retinal thickening.
l representing haemorrhagic retinal infarcts. l Development of a zone of retinal
n Proliferative diabetic retinopathy (PDR thickening
m develops in more than 50 percent of cases after „ one disc diameter or larger in size
about 25 years of the onset of disease. „ at least a part of which is within one disc
m it is more common in patients with juvenile onset diameter of the foveal centre.
diabetes. n Advanced diabetic eye disease
m neovascularisation m It is marked by complications such as:
n hallmark of PDR n Persistent vitreous haemorrhage,
n characterised by proliferation of new vessels n Tractional retinal detachment and

from the capillaries n Neovascular glaucoma.
l neovascularisation at the optic disc (NVD) n Management
l neovascularisation elsewhere (NVE) in the m Screening for diabetic retinopathy (MCQ)
fundus n Every year, till there is no diabetic retinopathy or
n occurs usually along the course of the major there is mild NPDR.
temporal retinal vessels. n Every 6 months, in moderate NPDR.
n new vessels may proliferate in the plane of n Every 3 months, in severe NPDR.
retina or spread into the vitreous as vascular n Every 2 months, in PDR with no high risk
fronds. characteristic.
m Later on condensation of connective tissue around n Medical treatment.
the new vessels results in formation of m Role of pharmacological modulation.(MCQ)
fibrovascular epiretinal membrane. n Protein kinase C (PKC) inhbitors,
m Vitreous detachment and vitreous n Vascular endothelial growth factors
haemorrhage may occur in this stage. (VEGF) inhibitors (MCQ)
m Types. n Aldose reductase and ACE inhibitors
m On the basis of high risk characteristics (HRCs) n Antioxidants such as vitamin E
described by diabetic retinopathy study (DRS) m Role of intravitreal steroids in reducing diabetic
group, the PDR can be further classified as below: macular oedema
n PDR without HRCs (Early PDR) n Flucinolone acetonide intravitreal implant and
n PDR with HRCs (Advanced PDR) n Intravitreal injection of triamcinolone
m High risk characteristics (HRC) of PDR are as n Photocoagulation. (MCQ)
follows m It remains the mainstay in the treatment of
n NVD 1/4 to 1/3 of disc area with or without diabetic retinopathy and maculopathy.
vitreous haemorrhage (VH) or pre-retinal m Either argon or diode laser can be used.
haemorrhage (PRH) m Macular photocoagulation.
n NVD < 1/4 disc area with VH or PRH
38
n Macula is treated by laser only if there is l Grade I
clinically significant macular oedema (CSME). „ mild generalized arteriolar attenuation,
n Laser treatment is contraindicated in ischaemic particularly of small branches
diabetic maculopathy. „ broadening of the arteriolar light reflex
n In patients with PDR associated with CSME, „ vein concealment.
macular photo-coagulation should be considered first i.e., l Grade II
before PRP since the PRP may worsen „ marked generalized narrowing and focal
macular oedema. (MCQ) attenuation of arterioles
n Macular photocoagulation includes two „ associated with deflection of veins at
techniques: arteriovenous crossings (Salus’ sign).
l Focal treatment l Grade III
„ done with argon laser (MCQ) „ This consists of Grade II changes plus
„ carried out for all lesions ® copper-wiring of arterioles
(microaneur ysms, IRMA or short ® banking of veins distal to arteriovenous
capillary segments) 500-3000 microns crossings (Bonnet sign)
OPHTHALMOLOGY
from the centre of the macula ® tapering of veins on either side of the
„ Spot size of 100-200 ìm of 0.1 second crossings (Gunn sign)
duration is used. ® right-angle deflection of veins (Salu’ s
l Grid treatment. sign).
„ Grid pattern laser burns are applied in ® Flame-shaped haemorrhages
the macular area for diffuse diabetic macular ® cotton-wool spots
oedema ® hard exudates
m Panretinal photocoagulation (PRP) or scatter laser l Grade IV
n consists of 1200-1600 spots „ This consists of all changes of Grade III
n each 500 ìm in size and 0.1 sec. duration. plus
n Laser burns are applied 2-3 disc areas from ® silver-wiring of arterioles
the centre of the macula extending peripherally ® papilloedema.
to the equator m Arteriosclerotic changes
n In PRP, temporal quadrant of retina is first n manifest as changes in arteriolar reflex and
coagulated. (MCQ) A-V nipping
n PRP produces destruction of ischaemic n result from thickening of the vessel wall
retina which is responsible for the production n are a reflection of the duration of
of vasoformative factors. hypertension.
n Indications for PRP are: m Increased vascular permeability
l PDR with HRCs n results from hypoxia
l Neovascularization of iris (NVI), n responsible for haemorrhages, exudates and
l Severe NPDR associated with: focal retinal oedema.
„ Poor compliance for follow up,
„ Before cataract surgery/YAG capsulotomy,
„ Renal failure,
„ ne-eyed patient
„ Pregnancy
n Surgical treatment.
m It is required in advanced cases of PDR.
m Pars plana vitrectomy is indicated for
n dense persistent vitreous haemorrhage
n tractional retinal detachment
n epiretinal membranes.
n HYPERTENSIVE RETINOPATHY
m Grading of hypertensive retinopathy
n Keith and Wegner (1939) have classified
hypertensive retinopathy changes into following
four grades:
39
TOPIC 7 - RETINOBLASTOMA l Some facts about non-hereditar y (somatic)
retinoblastoma are:
n Retinoblastoma
l Accounts for 60% of all cases.
m It is the most common intraocular tumour of
l All non-hereditary cases are unilateral and
childhood (MCQ)
unifocal
m usually seen between 1 and 2 years of age.
l accounts for 85% of the all unilateral cases
m There is no sex predisposition.
of retinoblastoma.
m In 25-30 percent cases, there is bilateral
l Patient is not predisposed to get second non-
involvement,
ocular cancer.
m Genetics and heredity
l Tumour is not transmissible.
n Retinoblastoma (RB) gene
m Pathology
l identified as 14 band on the long-arm of
n It arises as malignant proliferation of the
chromosome 13 (13q 14) (MCQ)
immature retinal neural cells called,
l is a ‘cancer suppressor’ or ‘antioncogenic’
retinoblasts, which have lost both
gene.
antioncogenic genes.
l Deletion or inactivation of this protective
n Growth chiefly consists of small round cells
gene by two mutations (Knudson’s two hit
OPHTHALMOLOGY
with large nuclei, resembling the cells of the

hypothesis) results in occurrence of
nuclear layer of retina.
retinoblastoma. (MCQ)
n Microscopic features of a well differentiated
n Retinoblastoma may arise as hereditary and
tumour include
non- herditary forms.
l Flexner-Wintersteiner rosettes, (highly
n Hereditary or familial cases.
specific of retinoblastoma)
l first hit (mutation)
l Homer-Wright rosettes
® occurs in one of the parental germ cells
l pseudorosettes and fleurettes formation
before fertilization.
l presence of areas of necrosis and
® This means mutation will occur in all
calcification
somatic cells (predisposing to develop even
m Clinical picture
non- ocular tumour).
n Quiescent stage.
RETINOBLASTOMA
l Second hit (mutation)

l It lasts for about 6 months to one year.
„ occurs late in postzygote phase
l Leukocoria or yellowish-white pupillary reflex
„ affects the second allele, resulting in
„ also called as amaurotic cat’s eye appearance
development of retinoblastoma.
„ commonest feature noticed in this stage
l Some facts about hereditary retinoblastoma are:
l Squint - usually convergen
® Accounts for 40% of all cases.
l Nystagmus is noticed in bilateral cases.
® All bilateral cases and about 15% of
l Defective vision.
the unilateral cases are hereditary.
„ when the tumour arises late (3-5 years of
® Most hereditary cases are multifocal.
age), the child may complain of defective
® Some hereditary cases have trilateral
vision.
retinoblastoma
l Ophthalmoscopic features of tumour
® have associated pinealoblastoma
l Endophytic retinoblastoma
(MCQ)
„ In the presence of calcification, it gives the
® Inheritance is autosomal dominant and
typical ‘cottage cheese’ appearance.
the risk of transmitting the gene
l Exophytic retinoblastoma
mutation is 50%.
„ On fundus examination it gives appearance
® Because of high peneterance 40% of
of exudative retinal detachment
offspring of a surviver of heraditar y
n Glaucomatous stage.
retinoblastoma will develop the tumour.
n Stage of extraocular extension.
® There are 40% chances of developing
n Stage of distant metastasis
tumour in a sibling of a child with bilateral
l Lymphatic spread first occurs in the
retinoblastoma (with unaffected parents).
preauricular and neighbouring lymph nodes.
n Non-hereditary or sporadic cases.
l Direct extension by continuity to the optic
l both hits (mutations) occur in the embryo
nerve and brain is common.
l after fertilization and in the same retinal cell.
m Differential diagnosis of leukocoria. (MCQ)
40
n congenital cataract l The eyeball should be enucleated along with
n inflammatory deposits in vitreous following a maximum length of the optic nerve taking
plastic cyclitis or choroiditis special care not to perforate the eyeball.
n coloboma of the choroid l If optic ner ve shows invasion,
n retrolental fibroplasia (retinopathy of postoperative treatment should include:
prematurity) „ Radiotherapy (5000 rads) should be applied
n persistent hyperplastic primary vitreous to the orbital apex.
n toxocara endophthalmitis „ Chemotherapy, consisting of vincristine,
n exudative retinopathy of Coats. carboplatin, and etoposide which may
m Diagnosis be combined with cyclosporin should be
n Plain X-rays of orbit may show calcification supplemented.
n Lactic dehydrogenase (LDH) level is raised in m Palliative therapy is given in following cases where
aqueous humour. prognosis for life is dismal in spite of aggressive
m Treatment treatment:
n Tumour destructive therapy n Retinoblastoma with orbital extension,
l Indication n Retinoblastoma with intracranial extension
OPHTHALMOLOGY
„ When tumour is diagnosed at an early stage n Retinoblastoma with distant metastasis.
„ when tumour is involving less than half m Palliative therapy should include combination of :
of retina n Chemotherapy
„ optic nerve is not involved (usually in the n Surgical debulking of the orbit or orbital
second eye of bilateral cases) exentration
l sequential aggressive local therapy l now not preferred by many surgeons.
(SALT) n External beam radiotherapy (EBRT)
„ Chemoreduction followed by local n Prognosis
therapy n Rarely spontaneous regression with resultant
® (Cryotherapy, thermochemotherapy or cure and shrinkage of the eyeball may occur
brachytherapy) due to necrosis followed by calcification;
® recommended for large tumours (>12 suggesting role of some immunological phenomenon.
RETINOBLASTOMA
mm in diameter) n Poor prognostic factors are:
„ Radiotherapy (exter nal beam l Optic nerve involvement
radiotherapy i.e., EBRT or l undifferentiated tumour cells
brachytherapy) combined with l massive choroidal invasion.
chemotherapy
® recommended for medium size tumour
<12 mm in diameter and <8mm in
thickness).
„ Cryotherapy
® indicated for a small tumour (<4.5 mm
indiameter and <2.5 mm in thickness)
located anterior to equator.
„ Laser photocoagulation
® used for a small tumour located posterior
to equator <3 mm from fovea.
„ Thermotherapy with diode laser
® used for a small tumour located posterior
to equator away from macula.
n Enucleation
l is the treatment of choice when:
„ Tumour involves more than half of the
retina.
„ Optic nerve is involved.
„ Glaucoma is present and anterior
chamber is involved.
41
TOPIC 8 - ANATOMY m Tarsal conjunctiva has 2-layered epithelium:
superficial layer of cylindrical cells and a deep layer
n The eyeball
of flat cells.
m Fibrous coat.
m Fornix and bulbar conjunctiva have 3-layered
l Anterior 1/6th of this fibrous coat is
epithelium: a superficial layer of cylindrical cells,
transparent and is called cornea.
middle layer of polyhedral cells and a deep layer
l Posterior 5/6th opaque part is called sclera.
of cuboidal cells.
Dimensions of an adult eye ball m Limbal conjunctiva has again many layered (5
Anteroposterior diameter 24 mm to 6) stratified squamous epithelium.
Horizontal diameter 23.5 mm n Adenoid layer.
Vertical diameter 23 mm m It is also called lymphoid layer
Circumference 75 mm m This layer is most developed in the fornices
Volume 6.5 ml m It is not present since birth but develops after
Weight 7 gm 3-4 months of life.
m For this reason, conjunctival inflammation in an infant
n Segments and chambers of the eyeball
does not produce follicular reaction.
m The eyeball can be divided into two segments:
OPHTHALMOLOGY
n Glands of conjunctiva
anterior and posterior.
m Mucin secretory glands.
m Anterior segment includes
n goblet cells (the unicellular glands located within
n crystalline lens (which is suspended from the
the epithelium)
ciliary body by zonules),
n crypts of Henle (present in the tarsal conjunctiva)
n structures anterior to it
n glands of Manz (found in limbal conjunctiva).
n iris
n These glands secrete mucus which is essential
n cornea
for wetting the cornea and conjunctiva.
n two aqueous humour-filled spaces : anterior and
m Accessory lacrimal glands.
posterior chambers.
n Glands of Krause
m Posterior segment includes the structures
l present in subconjunctival connective tissue of
posterior to lens fornix
n vitreous humour
l about 42 in upper fornix and 8 in lower fornix
n retina
n Glands of Wolfring
ANATOMY
n choroid
l present along the upper border of superior
n optic disc.
tarsus and along the lower border of
m I Anterior chamber.
inferior tarsus
n It is bounded anteriorly by the back of cornea,
n Plicasemilunaris
and posteriorly by the iris and part of ciliary body. m It is a pinkish crescentric fold of conjunctiva
n The anterior chamber is about 2.5 mm deep in
m present in the medial canthus.
the centre in normal adults. m It is a vestigeal structure in human beings
n It is shallower in hypermetropes and deeper in
m represents the nictitating membrane (or third
myopes, eyelid) of lower animals.
n It contains about 0.25 ml of the aqueous
n Caruncle
humour. m small, ovoid, pinkish mass
m I Posterior chamber.
m situated in the inner canthus, just medial to the
n It is a triangular space
plica semilunaris.
n contains 0.06 ml of aqueous humour.
m covered with stratified squamous epithelium
n It is bounded anteriorly by the posterior surface
m contains sweat glands, sebaceous glands and
of iris and part of ciliary body, posteriorly by the hair follicles.
crystalline lens and its zonules, and laterally by the n Lymphatics of conjunctiva
ciliary body. m from the lateral side drain into preauricular
The conjunctiva lymph nodes
n Epithelium.
m those from the medial side into the
m Marginal conjunctiva has 5-layered stratified
submandibular lymph nodes.
squamous type of epithelium. n Nerve supply of conjunctiva
42
m A circumcorneal zone of conjunctiva is supplied n In each layer they are not only parallel to each
by the branches from long ciliary nerves which supply the other but also to the corneal plane
cornea. n Among the lamellae are present keratocytes,
m Rest of the conjunctiva is supplied by the branches wandering macrophages, histiocytes and a few leucocytes.
from lacrimal, infratrochlear, supratrochlear, supraorbital m Descemet’s membrane (posterior elastic
and frontal nerves. lamina).
The cornea n It is a strong homogenous layer
n The cornea is a transparent, avascular, watch-glass n It is very resistant to chemical agents, trauma
like structure. and pathological processes. Therefore,
n Dimensions ‘Descemetocele’ can maintain the integrity of eyeball
m The anterior surface of cornea is elliptical for long.
n average horizontal diameter of 11.7 mm and n Descemet’s membrane consists of collagen and
vertical diameter of 11 mm. glycoproteins.
n The posterior surface of cornea is circular n Unlike Bowman’s membrane it can
n average diameter of 11.5 mm. regenerate.
m Thickness of cornea n Normally it remains in a state of tension and
OPHTHALMOLOGY
n in the centre is about 0.52 mm when torn it curls inwards on itself.
n at the periphery it is 0.7 mm. n In the periphery it appears to end at the anterior
m Radius of curvature. limit of trabecular meshwork as Schwalbe’s
n The central 5 mm area of the cornea forms line (ring).
the powerful refracting surface of the eye. m Endothelium.
n The anterior and posterior radii of curvature n It consists of a single layer of flat polygonal
of this central part of cornea are 7.8 mm and 6.5 (mainly hexagonal) cells
mm, respectively. n on slit lamp biomicroscopy appear as a
n Refractive power of the cornea is about 45 dioptres, mosaic.
which is roughly three-fourth of the total n The cell density of endothelium is around 3000
refractive power of the eye (60 dioptres) (MCQ) cells/mm2 in young adults, which decreases
n Histology with the advancing age.
m Histologically, the cornea consists of five distinct n There is a considerable functional reserve for
layers. the endothelium. Therefore, corneal decompensation
ANATOMY
n From anterior to posterior these are: occurs only after more than 75 percent of
l Epithelium the cells are lost.
l Bowman’s membrane n The endothelial cells contain ‘active-pump’
l substantia propria (corneal stroma) mechanism.
l Descemet’s membrane n Blood supply
l endothelium m Cornea is an avascular structure.
m Epithelium. n Nerve supply
n It is of stratified squamous type (MCQ) m Cornea is supplied by anterior ciliary nerves
m Bowman’s membrane. which are branches of ophthalmic division of the 5th
n This layer consists of acellular mass of cranial nerve.
condensed collagen fibrils. n Corneal transparency
n It is not a true elastic membrane but simply m The transparency is the result of :
a condensed superficial part of the stroma. n Peculiar arrangement of corneal lamellae
n It shows considerable resistance to infection. (lattice theory of Maurice),
n But once destroyed, it does not regenerate.(MCQ) n Avascularity
m Stroma (substantia propria). n Relative state of dehydration, which is
n This layer is about 0.5 mm in thickness maintained by
n constitutes most of the cornea (90% of total l barrier effects of epithelium and endothelium
thickness). l active bicarbonate pump of the endothelium.
n It consists of collagen fibrils (lamellae) l For these processes, cornea needs some energy.
embedded in hydrated matrix of proteoglycans. n Source of nutrients
n The lamellae are arranged in many layers. m Solutes (glucose and others) enter the cornea by
either
43
n simple diffusion n It constricts the pupil.
n active transport through aqueous humour m The dilator pupillae muscle
n diffusion from the perilimbal capillaries. n It is supplied by cervical sympathetic nerves
m Oxygen and dilates the pupil.
n derived directly from air through the tear film. n Ciliary body
n This is an active process undertaken by the m Ciliary body is forward continuation of the choroid at
epithelium. ora serrata.
n Metabolism of cornea m In cut-section, it is triangular in shape.
m The most actively metabolising layers of the cornea n The anterior part (about 2 mm) having finger-
are epithelium and endothelium, under like ciliary processes is called pars plicata
anaerobic conditions lactic acid accumulates in the n the posterior smooth part (about 4 mm) is
cornea. called pars plana
The Sclera m Ciliary muscle
n Sclera forms the posterior five-sixth opaque part n occupies most of the outer part of ciliary
of the external fibrous tunic of the eyeball. body
n Its whole outer surface is covered by Tenon’s n In cut section it is triangular in shape.
OPHTHALMOLOGY
capsule. m It is a non-striated muscle having three parts:

n Its inner surface lies in contact with choroid with n the longitudinal or meridional fibres which help in
a potential suprachoroidal space in between. aqueous outflow
n In its anterior most part near the limbus there is a n the circular fibres which help in accommodation
furrow which encloses the canal of Schlemm. n the radial or oblique fibres act in the same way as
n Thickness of sclera the longitudinal fibres.
m It is generally thinner in children than the adults m Ciliary muscle is supplied by parasympathetic
and in females than the males. Sclera is thickest fibres through the short ciliary nerves.
posteriorly (1mm) and gradually becomes thin m Ciliary processes.
when traced anteriorly. n These are finger-like projections from the
m It is thinnest at the insertion of extraocular pars plicata part of the ciliary body.
muscles (0.3 mm). n These are about 70-80 in number.
n Lamina cribrosa is a sieve-like sclera from which fibres of n These processes are the site of aqueous
optic nerve pass. production.
ANATOMY
n Nerve supply. n Choroid

n Sclera is supplied by branches from the long ciliary m Choroid is the posterior most part of the
nerves which pierce it 2-4 mm from the limbus to vascular coat of the eyeball.
form a plexus. m It extends from the optic disc to ora serrata.
The Uveal tract m Its inner surface is smooth, brown and lies in
n From anterior to posterior it can be divided into three contact with pigment epithelium of the retina.
parts, namely, iris, ciliary body and choroid. m From without inwards choroid consists of
n The iris following three layers:
m Iris is the anterior most part of the uveal tract. n Suprachoroidal lamina
m It is a thin circular disc corresponding to the l The potential space between this membrane
diaphragm of a camera. and sclera is called suprachoroidal space which
m In its centre is an aperture of about 4-mm contains long and short posterior ciliary arteries and
diameter called pupil nerves.
m At the periphery, the iris is attached to the middle n Stroma of the choroid.
of anterior surface of the ciliary body. l It consists of
m It divides the space between the cornea and lens into „ loose collagenous tissue with some elastic
anterior and posterior chambers. and reticulum fibres.
m Anterior surface of the iris can be divided into a „ pigment cells
ciliary zone and a pupillary zone by a zigzag „ plasma cells.
line called collarette l Its main bulk is formed by vessels which are
m The sphincter pupillae muscle arranged in three layers.
n supplied by parasympathetic fibres through l From without inwards these are
third nerve. „ layer of large vessels (Haller’s layer),
44
„ layer of medium vessels (Sattler’s layer) n placed between iris and the vitreous in a saucer
„ layer of choriocapillaris which nourishes shaped depression the patellar fossa.
the outer layers of the retina. n Its diameter is 9-10 mm and thickness varies with
n Basal lamina. age from 3.5 mm (at birth) to 5 mm (at extreme
l It is also called Bruch’ s membrane of age).
l lines the layer of choriocapillaris. n Its weight varies from 135 mg (0-9 years) to 255
l It lies in approximation with pigment mg (40-80 years of age).
epithelium of the retina. n It has got two surfaces:
n Blood supply of the uveal tract (MCQ) n the anterior surface is less convex (radius of curvature
m Arterial supply. 10 mm) than the posterior (radius of curvature 6 mm).
n The uveal tract is supplied by three sets of arteries n Its refractive index is 1.39 (MCQ)
n Short posterior ciliary arteries. n total power is 15-16 D.
l These arise as two trunks from the n The accommodative power of lens varies with age,
ophthalmic artery being
l each trunk divides into 10-20 branches m 14-16 D (at birth);
l supply the choroid in a segmental manner. m 7-8 D (at 25 years of age)
OPHTHALMOLOGY
n Long posterior ciliary arteries. m 1-2 D (at 50 years of age).
l These are two in number, nasal and temporal. n Lens capsule
l gives branches which supply the ciliary m It is a thin, transparent, hyaline membrane
body. surrounding the lens
n Anterior ciliary arteries. m thicker over the anterior than the posterior
l These are derived from the muscular surface.
branches of ophthalmic artery. m Lens capsule is
l These are 7 in number; 2 each from arteries n thickest at pre-equator regions (14 ì)
of superior rectus, inferior rectus, and medial n thinnest at the posterior pole (3 ì).
rectus muscle and one from that of lateral m Anterior epithelium.
rectus muscle. n It is a single layer of cuboidal cells which
l These arteries give branches to sclera, limbus lies deep to the anterior capsule.
and conjunctiva; n In the equatorial region these cells become
l they anastomose with the two long columnar
ANATOMY
posterior ciliary arteries to form the circulus n Cells are actively dividing and elongating to
arteriosus major, near the root of iris. form new lens fibres throughout the life.
l Several branches arise from the circulus n There is no posterior epithelium, as these cells
arteriosus major and supply the ciliary are used up in filling the central cavity of lens vesicle
processes (one branch for each process). during development of the lens.
l Similarly, many branches from this major n Lens fibres.
arterial circle run radially through the iris m The epithelial cells elongate to form lens fibres
towards pupillary margin, where they m Mature lens fibres are cells which have lost their nuclei
anastomose with each other to form circulus m Nucleus.
arteriosus minor. n It is the central part containing the oldest fibres.
m Venous drainage. n Depending upon the period of development,
n A series of small veins which drain blood from the different zones of the lens nucleus
the iris, ciliary body and choroid join to form include:
the vortex veins. n Embryonic nucleus.
n The vortex veins are four in number–superior l It is the innermost part of nucleus
temporal, inferior temporal, superior nasal l corresponds to the lens upto the first 3
and inferior nasal. months of gestation.
n They drain into superior and inferior l It consists of the primary lens fibres which are
ophthalmic veins which in turn drain into the formed by elongation of the cells of posterior
cavernous sinus. wall of lens vesicle.
Lens n Fetal nucleus.
n The lens is a transparent, biconvex, crystalline l It lies around the embryonic nucleus
structure
45
l corresponds to the lens from 3 months of l 15 percent by pentose hexose
gestation till birth. monophosphate (HMP) shunt
l Its fibres meet around sutures which are l a small proportion via oxidative Kreb’s citric
anteriorly Y-shaped and posteriorly acid cycle.
inverted Y-shaped n Sorbitol pathway
n Infantile nucleus corresponds to the lens from birth l is relatively inconsequential in the normal lens
to puberty l it is extremely important in the production
n Adult nucleus corresponds to the lens fibres of cataract in diabetic and galactosemic
formed after puberty to rest of the life. patients.
m Cortex. It is the peripheral part which comprises Aqueous humour
the youngest lens fibres. n Ciliary body is the seat of aqueous production.
n Suspensory ligaments of lens (Zonules of Zinn). n Angle of anterior chamber
m these consist essentially of a series of fibres m Angle of anterior chamber plays an important
passing from ciliary body to the lens. These role in the process of aqueous drainage.
hold the lens in position and enable the ciliary m It is formed by
muscle to act on it. n root of iris
OPHTHALMOLOGY
n Lens transparency n anterior-most part of ciliary body

m Factors that play significant role in maintaining n scleral spur
outstanding clarity and transparency of lens are: n trabecular meshwork and Schwalbe’s line
n Avascularity (prominent end of Descemet’s membrane of
n Tightly-packed nature of lens cells, cornea)
n The arrangement of lens proteins, n Clinically the angle structures can be visualised by
n Semipermeable character of lens capsule, gonioscopic examination
n Pump mechanism of lens fibre membranes n Shaffer’s system of grading the angle is most
that regulate the electrolyte and water balance commonly used
in the lens, maintaining relative dehydration n Volume. The aqueous humour is a clear watery fluid
n Auto-oxidation and high concentration of filling the anterior chamber (0.25 ml) and posterior
reduced glutathione in the lens chamber (0.06 ml) of the eyeball.
l maintains the lens proteins in a reduced state n Functions of aqueous humour are:
l ensures the integrity of the cell membrane pump. m It maintains a proper intraocular pressure.
ANATOMY
n Metabolism m It plays an important metabolic role by providing

m Lens requires a continuous supply of energy substrates and by removing metabolites from the
(ATP) for avascular cornea and lens.
n active transport of ions and aminoacids m It maintains optical transparency.
n maintenance of lens dehydration, m It takes the place of lymph that is absent within
n for a continuous protein and GSH synthesis. the eyeball.
m Most of the energy produced is utilized in the n Refractive index of aqueous humour is 1.336.
epithelium which is the major site of all active n Composition.
transport processes. n Proteins (colloid content).
m Source of nutrient supply. m Because of blood aqueous barrier the protein
n The crystalline lens, being an avascular structure content of aqueous humour (5-16 mg%) is much
is dependent for its metabolism less than that of plasma (6-7 gm%).
n on chemical exchanges with the aqueous m However, in inflammation of uvea (iridocyclitis) the
humour. blood-aqueous barrier is broken and the protein
m Pathways of glucose metabolism. content of aqueous is increased (plasmoid
n Glucose is very essential for the normal aqueous)
working of the lens. n Oxygen is present in aqueous in dissolved state.
n Metabolic activity of the lens is largely limited n Composition of aqueous is similar to plasma except
to epithelium, and cortex that it has:
n the nucleus is relatively inert. m High concentrations of ascorbate, pyruvate and
n In the lens, lactate (MCQ)
l 80% glucose is metabolised anaerobically by m Low concentration of protein, urea and glucose
the glycolytic pathway
46
n Aqueous humour: anterior chamber versus DRAINAGE OF AQUEOUS HUMOUR
posterior chamber.
m HCO3— in posterior chamber aqueous is higher Ciliary process
than in the anterior chamber. $
m Cl— concentration in posterior chamber is lower Aqueous in the posterior chamber
than in the anterior chamber. (through pupil)
m Ascorbate concentration of posterior aqueous
$
is slightly higher than that of anterior chamber
Anterior chamber
aqueous.
n Production. $ $
m Aqueous humour is derived from plasma within
Trabecular
the capillary network of ciliary processes. Meshwork Ciliary body
m The normal aqueous production rate is 2.3 ìl/ $ $
min. Schlemm’s Suprachoroidal
m The three mechanisms diffusion, ultrafiltration canal space
and secretion (active transport) $ $
OPHTHALMOLOGY
n Ultrafiltration. Venous circulation
l plasma filtrate accumulates behind the non-
Collector of ciliary body.
pigment epithelium of ciliary processes.
channels choroid and sclera
n Secretion.
l The tight junctions between the cells of
the non-pigment epithelium create part of Trabecular Uveascleral
blood aqueous barrier. (conventional) (Unconventional)
l Substances that are actively transported
outflow=90% outflow=10%
include sodium, chlorides, potassium, ascorbic acid,
amino acids and bicarbonates.
n Diffusion.
Vitreous
l Active transport of these substances across
n Vitreous humour is an inert, transparent, jelly-like
the non-pigmented ciliary epithelium structure
results in an osmotic gradient leading to the
ANATOMY
n fills the posterior four-fifth of the cavity of eyeball
movement of other plasma constituents into n about 4 ml in volume.
the posterior chamber by ultrafiltration and n It is a hydrophilic gel that mainly serves the optical
diffusion. functions.
m Sodium is primarily responsible for the
n it mechanically stabilizes the volume of the globe
movement of water into the posterior chamber. n it is a pathway for nutrients to reach the lens and
m Control of aqueous formation.
retina.
n Vasopressin and adenyl-cyclase affect
n Structure.
aqueous formation by influencing active transport m Cortical vitreous.
of sodium. n The density of collagen fibrils is greater in this
peripheral part.
n The condensation of these fibrils form a false
anatomic membrane which is called as
anterior hyaloid membrane anterior to ora
serrata and posterior hyaloid membrane
posterior to ora
n The attachment of the anterior hyaloid
membrane to the posterior lens surface is
firm in the young and weak in the elderly
n posterior hyaloid membrane remains loosely
attached to the internal limiting membrane
of the retina throughout life
m The main vitreous body (nucleus).
47
m It has a less dense fibrillar structure and is a n central depressed part of the macula.
true biological gel. n It is about 1.5 mm in diameter
m It is here where liquefactions of the vitreous gel start first. n most sensitive part of the retina.
m Microscopically the vitreous body is homogenous, n In this area there are no rods
but exhibits wavy lines as of watered silk in the slit-lamp n cones are tightly packed
beams. n other layers of retina are very thin.
m Running down the centre of the vitreous body n In its centre is a shining pit called foveola (0.35-mm
from the optic disc to the posterior pole of the diameter)
lens is the hyaloid canal (Cloquet’s canal) of l It is situated about 2 disc diameters (3 mm)
doubtful existence in adults. away from the temporal margin of the disc and
n Attachments of Vitreous about 1 mm below the horizontal meridian.
m vitreous base n An area about 0.8 mm in diameter (including
n The part of the vitreous about 4 mm across foveola and some surrounding area) does not
the ora serrata is called as vitreous base contain any retinal capillaries and is called foveal
n attachment of the vitreous is strongest. avascular zone (FAZ).
m around the margins of the optic disc n Peripheral retina
OPHTHALMOLOGY
m foveal region m refers to the area bounded posteriorly by the retinal equator
m back of the crystalline lens by hyloidocapsular and anteriorly by the ora serrata.
ligament of Wieger. m best examined with indirect ophthalmoscopy and
Retina by the use of Goldman three mirror contact
n It appears purplish-red due to the visual purple of lens.
the rods and underlying vascular choroid. n Ora serrata.
n Retina extends from the optic disc to the ora serrata. m It is the serrated peripheral margin where the
n Grossly it is divided into two distinct regions: retina ends.
posterior pole and peripheral retina separated by m Here the retina is firmly attached both to the vitreous
the so called retinal equator. and the choroid.
n Retinal equator is an imaginary line which is m The pars plana extends anteriorly from the ora
considered to lie in line with the exit of the four vena serrata.
verticose. n Microscopic structure
n Posterior pole m Retina consists of 3 types of cells and their
ANATOMY
m includes two distinct areas: the optic disc and synapses arranged (from without inward) in the
macula lutea following ten layers
m Posterior pole of the retina is best examined by n Pigment epithelium.
m slit-lamp indirect biomicroscopy using +78D l It is f irmly adherent to the underlying basal
and +90D lens lamina (Bruch’s membrane) of the choroid.
m direct ophthalmoscopy. n Layer of rods and cones.
n Optic disc l Layer of rods and cones contains only the
m It is a pink coloured, well-defined circular area outer segments of photoreceptor cells
of 1.5-mm diameter. arranged in a palisade manner.
m At the optic disc all the retinal layers terminate except l There are about 120 millions rods and 6.5
the nerve fibres, which pass through the lamina millions cones.
cribrosa to run into the optic nerve. l Rods
m A depression seen in the disc is called the physiological „ contain a photosensitive substance visual
cup. purple (rhodopsin)
m The central retinal artery and vein emerge „ subserve the peripheral vision and vision of
through the centre of this cup. low illumination (scotopic vision).
n Macula lutea. l Cones
m It is also called the yellow spot. „ contain a photosensitive substance
m It is comparatively deeper red than the „ are primarily responsible for
surrounding fundus r situated at the ® highly discriminatory central vision
posterior pole temporal to the optic disc. (photopic vision)
m It is about 5.5 mm in diameter. ® colour vision.
m Fovea centralis n External limiting membrane.
48
n Outer nuclear layer. n These are end arteries i.e., they do not
n Outer plexiform layer. anastomose with each other.
n Inner nuclear layer. m The retinal veins.
l It mainly consists of cell bodies of bipolar n The central retinal vein drains into the cavernous
cells. sinus directly or through the superior
l It also contains cell bodies of horizontal ophthalmic vein.
amacrine and Muller’s cells and capillaries n The only place where the retinal system
of central artery of retina. anastomosis with ciliary system is in the
l The bipolar cells constitute the first order region of lamina cribrosa.
neurons. Anatomy of the visual pathway
n Inner plexiform layer n Optic nerve
n Ganglion cell layer. m It is the backward continuation of the nerve fibre
l It mainly contains the cell bodies of layer of the retina
ganglion cells (the second order neurons of visual m consists of the axons originating from the
pathway). ganglion cells.
l There are two types of ganglion cells. m It also contains the afferent fibres of the
OPHTHALMOLOGY
„ The midget ganglion cells pupillary light reflex.
® present in the macular region and the m Morphologically and embryologically, the optic
dendrite of each such cell synapses with nerve is comparable to a sensory tract.
the axon of single bipolar cell. m Unlike peripheral nerves it is not covered by neurilemma
„ Polysynaptic ganglion cells (so it does not regenerate when cut).
® lie predominantly in peripheral retina m The fibres of optic nerve, numbering about a
® each such cell may synapse with upto a million, are very fine (2-10 ìm in diameter as
hundred bipolar cells. compared to 20 ìm of sensory nerves).
n Nerve fibre layer (stratum opticum) consists of m Parts of optic nerve.
axons of the ganglion cells n The optic nerve is about 47-50 mm in length,
n Internal limiting membrane. n can be divided into 4 parts:
l It is the innermost layer n intraocular (1 mm), intraorbital (30 mm), intra-
l It is formed by the union of terminal canalicular (6-9 mm) and intracranial (10 mm).
expansions of the Muller’s fibres, n Intraorbital part
ANATOMY
l It is essentially a basement membrane. l Posteriorly, near the optic foramina, it is
n Functional divisions of retina closely surrounded by the annulus of Zinn and the
m Functionally retina can be divided into temporal retina origin of the four rectus muscles.
and nasal retina l Some fibres of superior rectus muscle are
m Divided by a line drawn vertically through the adherent to its sheath here, and accounts
centre of fovea. for the painful ocular movements seen in retrobulbar
n Nerve fibres arising from temporal retina pass neuritis.
through the optic nerve and optic tract of the same side n Intracanalicular part is closely related to the
to terminate in the ipsilateral geniculate body ophthalmic artery which lies inferolateral to
n Nerve fibres originating from the nasal retina it and crosses obliquely over it, as it enters the
after passing through the optic nerve cross in the orbit, to lie on its medial side.
optic chiasma and travel through the contralateral n Sphenoid and posterior ethmoidal sinuses
optic tract to terminate in the contralateral geniculate lie medial to it and are separated by a thin bony
body. lamina. This relation accounts for retrobulbar
n Blood supply neuritis following infection of the sinuses.
m Outer four layers of the retina, viz, pigment n Optic chiasma
epithelium, layer of rods and cones, external m Fibres originating from the nasal halves of the retina
limiting membrane and outer nuclear layer get decussate at the chiasma.
their nutrition from the choroidal vessels. n Optic tracts
m Inner six layers get their supply from the central m Each optic tract consists of fibres from the
retinal artery, which is a branch of the ophthalmic temporal half of the retina of the same eye and
artery. the nasal half of the opposite eye.
m Central retinal artery divides into four branches,
49
m Posteriorly each optic tract ends in the lateral nThese are modified sweat glands situated near
geniculate body. the hair follicle.
m The pupillary reflex fibres pass on to pretectal n They open into the hair follicles or into the
nucleus in the midbrain through the superior ducts of Zeis glands.
brachium. some fibres terminate in the superior n They do not open directly onto the skin surface
colliculus. as elsewhere.
n Lateral geniculate bodies m Accessory lacrimal glands of Wolfring.
m Each geniculate body consists of six layers of n Nerves of lids
neurons (grey matter) alternating with white m Motor nerves are
matter (formed by optic fibres). n facial (which supplies orbicularis muscle)
n Optic radiations n oculomotor (which supplies LPS muscle)
m These extend from the lateral geniculate bodies n sympathetic fibres (which supply the Muller’s
to the visual cortex and consist of the axons of muscle).
third- order neurons of visual pathway. m Sensory nerve supply is derived from branches of
n Visual cortex the trigeminal nerve.
CRANIAL NERVE PALSY
m It is located on the medial aspect of the occipital

lobe, above and below the calcarine fissure. TOPIC 9 - CRANIAL NERVE PALSY
m It is subdivided into the visuosensory area
(striate area 17) that receives the fibres of the n Extraocular muscles
m Origin and insertion
radiations, and the surrounding visuopsychic area
n The annulus of Zinn
(peristriate area 18 and parastriate area 19).
l The rectus muscles originate from a
n Blood supply of the visual pathway
n The visual pathway is mainly supplied by pial network common tendinous ring (the annulus of
of vessels except the orbital part of optic nerve Zinn) it is attached at the apex of the orbit
which is also supplied by an axial system derived from the (MCQ)
l It encircles the optic foramina and medial
central artery of retina.
n Blood supply of the optic nerve head needs part of the superior orbital fissure
n All the four recti run forward around the
special mention.
m The surface layer of the optic disc is supplied by
eyeball and are inserted into the sclera, by flat
capillaries derived from the retinal arterioles. tendons (about 10-mm broad) at different
ANATOMY
m The prelaminar region is mainly supplied by

distances from the limbus
n The superior oblique muscle
centripetal branches of the peripapillary choroid with some
l arises from the bone above and medial to
contribution from the vessels of lamina cribrosa.
m The lamina cribrosa is supplied by branches from
the optic foramina.
l It runs forward and turns around a pulley -
the posterior ciliary arteries and arterial circle of Zinn.
m The retrolaminar part of the optic nerve is
‘the trochlea’ (MCQ)
l It is inserted in the upper and outer part of
supplied by
n centrifugal branches from central retinal artery and
the sclera behind the equator
n The inferior oblique muscle
n centripetal branches from pial plexus formed by
l inserted into the lower and outer part of
branches from the choroidal arteries, circle of
Zinn, central retinal artery and ophthalmic artery. the sclera behind the equator
m Nerve supply
n Glands of eyelids
n third cranial nerve (oculomotor) supplies the
m Meibomian glands.
n These are also known as tarsal glands
superior, medial and inferior recti and inferior oblique
n They are modified sebaceous glands.
muscles.
n fourth cranial nerve (trochlear) supplies the
n Their ducts open at the lid margin.
n Their secretion constitutes the oily layer of
superior oblique
n sixth nerve (abducent) supplies the lateral
tear film.
m Glands of Zeis.
rectus muscle.
m Actions
n These are also sebaceous glands
n The extraocular muscles rotate the eyeball
n They open into the follicles of eyelashes.
m Glands of Moll.
around vertical, horizontal and antero-posterior axes.
50
n Medial and lateral rectus muscles are almost „ It results due to simultaneous contraction
parallel to the optical axis of the eyeball; so they of right lateral rectus and left medial
have got only the main action. rectus.
n While superior and inferior rectus muscles l Levoversion.
make an angle of 23o and reflected tendons „ It refers to movement of both eyes to the
of the superior and inferior oblique muscles left.
of 51o with the optical axis in the primary „ It is produced by simultaneous contraction
position; so they have subsidiary actions in of left lateral rectus and right medial
addition to the main action. rectus.
l Supraversion.
Actions of extraocular muscles „ It is upward movement of both eyes in
Muscle Primary Secondary Tertiary primary position.

action action action „ It results due to simultaneous contraction
MR Adduction - - of bilateral superior recti and inferior

LR Abduction - - obliques.
SR Elevation Intorsion Adduction l Infraversion.
OPHTHALMOLOGY
IR Depression Extorsion Adduction „ It is downward movement of both eyes
SO Intorsion Depression Abduction in primary position.

IO Extorsion Elevation Abduction „ It results due to simultaneous contraction
of bilateral inferior recti and superior
n Types of ocular movements obliques.
m Uniocular movements are called ‘ductions’ l Dextrocycloversion.
n Adduction „ It is rotational movement around the
l It is inward movement (medialrotation) along the anteroposterior axis

vertical axis. „ superior pole of cornea of both the eyes
n Abduction. tilts towards the right.

l It is outward movement (lateral rotation) along the l Levocycloversion.
CRANIAL NERVE PALSY

vertical axis. „ It is just the reverse of dextrocycloversion.
n Supraduction. „ In it superior pole of cornea of both the
l It is upward movement (elevation) along the eyes tilts towards the left.
horizontal axis. n Vergences, also called disjugate movements, are
n Infraduction. synchronous and symmetric movements of

l It is downward movement (depression) along the both eyes in opposite directions
horizontal axis. l Convergence
n Incycloduction (intorsion). „ It is simultaneous inward movement of both eyes
l It is a rotatory movement along the anteroposterior „ results from contraction of the medial
axis in which superior pole of the cornea recti.

(12 O’clock point) moves medially. l Divergence.
n Excycloduction (extorsion). „ It is simultaneous outward movementof both
l It is a rotatory movement along the anteroposterior eyes

axis in which superior pole of the cornea „ produced by contraction of the lateral
(12 O’clock point) moves laterally. recti.

m Binocular movements. These are of two types: n Synergists, antagonists and yoke muscles
versions and vergences. m Synergists.
n Versions n It refers to the muscles having the same
l also known as conjugate movements primary action in the same eye
l are synchronous (simultaneous) symmetric n superior rectus and inferior oblique of the
movements of both eyes in the same same eye act as synergistic elevators.
direction. m Antagonists.
l Dextroversion. n These are the muscles having opposite actions
„ It is the movement of both eyes to the in the same eye.
right. n antagonists to each other in the same eye
l medial and lateral recti
51
l superior and inferior recti m Secondary positions of gaze.
l superior and inferior obliques n These are the positions assumed by the eyes while
m Yoke muscles (contralateral synergists) looking straight up, straight down, to the right and to
n It refers to the pair of muscles (one from the left
each eye) which contract simultaneously m Tertiary positions of gaze.
during version movements. n These describe the positions assumed by the eyes
n right lateral rectus and left medial rectus when combination of vertical and horizontal movements
act as yoke muscles for dextroversion movements. occur.
n Other pairs of yoke muscles are: n These include position of eyes in
l right MR and left LR l Dextroelevation
l right LR and left MR l Dextrodepression
l right SR and left IO l Levoelevation
l right IR and left SO l levodepression
l right SO and left IR m Cardinal positions of gaze.
l right IO and left SR. n These are the positions which allow
m Contralateral antagonists. examination of each of the 12 extraocular
OPHTHALMOLOGY
n These are a pair of muscles (one from each muscles in their main field of action.
eye) having opposite action n There are six cardinal positions of gaze,
n for example, l Dextroversion
l right LR and left LR l Levoversion
l right MR and left MR l Dextroelevation
n Laws governing ocular movements l Levoelevation
m Hering’s law of equal innervation (MCQ) l dextrodepression
n an equal and simultaneous innervation flows l levodepression
from the brain to a pair of muscles which n PARALYTIC STRABISMUS
contract simultaneously (yoke muscles) in m It refers to ocular deviation resulting from complete
different binocular movements or incomplete paralysis of one or more
CRANIAL NERVE PALSY
n During dextroversion extraocular muscles.

l right lateral rectus and left medial rectus muscles receive m Symptoms
an equal and simultaneous f low of n Diplopia.
innervation. l It is the main symptom of paralytic squint.
n During convergence l It is more marked towards the action of
l both medial recti get equal innervation. paralysed muscle.
n During dextroelevation l It may be crossed (in divergent squint) or
l right superior rectus and left inferior uncrossed (in convergent squint).
oblique receive equal and simultaneous innervation. l It may be horizontal, vertical or oblique
m Sherrington’s law of reciprocal innervation. depending on the muscle paralysed. Diplopia
n during ocular motility, increased flow of occurs due to formation of image on dissimilar points
innervation to the contracting muscle is of the two retinae
accompanied by decreased flow of innervation to the n Confusion.
relaxing antagonist muscle. n Nausea and vertigo.
n For example, during dextroversion, n Ocular deviation.: It is of sudden onset.
l an increased innervation flow to the right LR m Signs
and left MR is accompanied by decreased flow n Primary deviation. (MCQ)
to the right MR and left LR muscles. l It is deviation of the affected eye
n Diagnostic positions of gaze l It is away from the action of paralysed
m There are nine diagnostic positions of gaze muscle, e.g., if lateral rectus is paralysed the eye is
m These include one primary, four secondary and converged.
four tertiary positions. n Secondary deviation (MCQ)
m Primary position of gaze. l It is deviation of the normal eye seen
n It is the position assumed by the eyes when fixating under cover, when the patient is made to fix with
a distant object (straight ahead) with the erect the squinting eye.
position of head l It is greater than the primary deviation.
52
l This is based on Hering’s law of equal „ Occurs due to paralysis of the LPS
innervation of yoke muscles. muscle.
l This is due to the fact that the strong impulse l Deviation.
of innervation required to enable the eye with „ Eyeball is turned down, out and slightly
paralysed muscle to fix is also transmitted to intorted due to actions of the lateral rectus
the yoke muscle of the sound eye resulting and superior oblique muscles.
in a greater amount of deviation. l Ocular movements are restricted
n Restriction of ocular movement. „ occurs in all the directions except
l It occurs in the direction of the action of outward.
paralysed muscles l Pupil is fixed and dilated
n Compensatory head posture. „ occurs due to paralysis of the sphincter
l It is adopted to avoid diplopia and pupillae muscle.
confusion. l Accommodation is completely lost
l Head is turned towards the direction of action of „ occurs due to paralysis of the ciliary
the paralysed muscle, muscle.
l if the right lateral rectus is paralysed, l Crossed diplopia is elicited on raising the eyelid.
OPHTHALMOLOGY
patient will keep the head turned towards right l Head posture may be changed if pupillary
n False projection or orientation. area remains uncovered.
l It is due to increased innervational impulse m Total ophthalmoplegia.
conveyed to the paralysed muscle. n In this condition all extraocular muscles
l It can be demonstrated by asking the including LPS and intraocular muscles, viz.,
patient to close the sound eye and then sphincter pupillae, and ciliary muscle are
to fix an object placed on the side of paralysed.
paralysed muscle. n It results from combined paralysis of third,
l Patient will locate it further away in the fourth and sixth cranial nerves.
same direction. n It is a common feature of orbital apex
l For example, a patient with paralysis of syndrome and cavernous sinus thrombosis.
right lateral rectus will point towards right m External ophthalmoplegia.
CRANIAL NERVE PALSY

more than the object actually is. n In this condition, all extraocular muscles are
m Pathological sequelae of an extraocular paralysed, sparing the intraocular muscles.
muscle palsy n It results from lesions at the level of motor
n These occur more in paralysis due to lesions nuclei sparing the Edinger-Westphal nucleus.
of the nerves than the lesions of muscles. m Internuclear ophthalmoplegia.
n These include: n In this condition there is lesion of the medial
l Overaction of the contralateral synergistic longitudinal bundle.
muscle. n it is characterised by:
l Contracture of the direct antagonist muscle. l defective action of medial rectus on the
l Secondary inhibitional palsy of the side of lesion
contralateral antagonist muscle. l horizontal nystagmus of the opposite eye
n For example, in paralysis of the right lateral l normal convergence.
rectus muscle there occurs n Investigations of a case of paralytic squint
l Overaction of the left medial rectus, m Diplopia charting
l Contracture of the right medial rectus and n In it patient is asked to wear red and green
l Inhibitional palsy of the left lateral rectus muscle. diplopia charting glasses.
n Clinical varieties of ocular palsies n Red glass being in front of the right eye and
m Isolated muscle paralysis. green in front of the left.
n Lateral rectus and superior oblique are the n Then in a semi-dark room, he is shown a fine
most common muscles to be paralysed singly, as they linear light from a distance of 4 ft. and asked
have separate nerve supply to comment on the images in primary
m Paralysis of the third cranial nerve (MCQ) position and in other positions of gaze.
n Clinical features of third nerve palsy include: n Patient tells about the position and the separation
l Ptosis of the two images in different fields.
53
m Hess screen test. Hess screen/Lees screen test as anisometropia.
tells about the paralysed muscles and the n Usually the error is of about 8 to 10 which mostly
pathological sequelae of the paralysis, viz., remains constant.
overaction, contracture and secondar y n The child may develop convergent squint in order
inhibitional palsy. to preferentially see clear at its far point (which is
m Field of binocular fixation. about 10-12 cms).
m Forced duction test (FDT). n Congenital myopia may sometimes be associated with
n It is performed to differentiate between the other congenital anomalies such as cataract,
incomitant squint due to paralysis of extraocular muscle microphthalmos, aniridia, megalocornea, and
and that due to mechanical restriction of the ocular congenital separation of retina.
movements. FDT is positive (resistance Simple myopia
encountered during passive rotation) in cases n Simple or developmental myopia is the commonest
of incomitant squint due to mechanical restriction variety.
n FDT is negative in cases of extraocular muscle n It is considered as a physiological error not
palsy. associated with any disease of the eye. Its
n Management prevalence increases from 2% at 5 years to 14% at
OPHTHALMOLOGY
m Surgical treatment. It should be carried out in case 15 years of age.

the recovery does not occur in 6 months. n Why is Simple myopia is called school myopia.
m Since the fastest rise occurs at school going age
TOPIC 10 - MYOPIA i.e., between 8 year to 12 years so, it is also called

school myopia.
n Myopia or short-sightedness is a type of refractive n prevelance of myopia is more in children with both
error in which parallel rays of light coming from parents myopic (20%) than the children with one
infinity are focused in front of the retina when parent myopic (10%) and children with no parent
accommodation is at rest myopic (5%).
Etiology n Symptoms
n Axial myopia results from increase in m Poor vision for distance (short-sightedness) is the main
anteroposterior length of the eyeball. It is the symptom
commonest form. m Asthenopic symptoms may occur in patients with small
n Curvatural myopia occurs due to increased curvature
degree of myopia.
of the cornea, lens or both. m Half shutting of the eyes to achieve the greater
MYOPIA
n Positional myopia is produced by anterior placement

clarity of stenopaeic vision.
of crystalline lens in the eye. n Signs
n Index myopia results from increase in the refractive
m Prominent eyeballs.
index of crystalline lens associated with nuclear m Anterior chamber is slightly deeper than normal.
sclerosis. m Pupils are somewhat large and a bit sluggishly
n Myopia due to excessive accommodation occurs in
reacting.
patients with spasm of accommodation. m Fundus is normal
Clinical varieties of myopia m Magnitude of refractive errror.
n Congenital myopia
n Simple myopia usually occur between 5 and
n Simple or developmental myopia
10 year of age and it keeps on increasing till
n Pathological or degenerative myopia
about 18-20 years of age at a rate of about –
n Acquired myopia which may be:
0.5 ± 0.30 every year.
m post-traumatic;
n In simple myopia, usually the error does not
m post-keratitic;
exceed 6 to 8.
m drug-induced,
n Diagnosis is confirmed by performing retinoscopy
m pseudomyopia;
Pathological myopia
m space myopia;
n a rapidly progressive error which starts in childhood
m night myopia;
at 5-10 years of age and results in high myopia
m consecutive myopia.
during early adult life which is usually associated
Congenital myopia with degenerative changes in the eye.
n usually diagnosed by the age of 2-3 years.
n Most of the time the error is unilateral and manifests
54
n pathological myopia results from a rapid axial growth n ERG reveals subnormal electroretinogram due to
of the eyeball which is outside the normal biological chorioretinal atrophy.
variations of development. n Complications
n Symptoms m Retinal detachment
m Defective vision. due to progressive degenerative m complicated cataract
changes, an uncorrectable loss of vision may occur. m vitreous haemorrhage
m Muscae volitantes i.e., floating black opacities in m choroidal haemorrhage
front of the eyes are also complained of by many m Strabismus fixus convergence.
patients. These occur due to degenerated liquified Treatment of myopia
vitreous. n Optical treatment of myopia constitutes prescription of
m Night blindness may be complained by very high appropriate concave lenses, so that clear image is
myopes having marked degenerative changes. formed on the retina
n Signs n The basic rule of correcting myopia is converse of that in
m Prominent eye balls. hypermetropia, i.e., the minimum acceptance
m The elongation of the eyeball mainly affects the providing maximum vision should be prescribed.
posterior pole and surrounding area; the part of n In very high myopia , undercorrection is always
OPHTHALMOLOGY
the eye anterior to the equator may be normal better to avoid the problem of near vision and that
m Cornea is large. of minification of images.
m Anterior chamber is deep. n Contact lenses are particularly justified in cases of
m Pupils are slightly large and react sluggishly to ( high myopia as they avoid peripheral distortion and
light. minification produced by strong concave spectacle
m Fundus examination reveals following characteristic lens.
signs : n Surgical treatment of myopia
n Optic disc appears large and pale and at its n Low vision aids (LVA) are indicated in patients of
temporal edge a characteristic myopic progressive myopia with advanced degenerative
crescent is present changes, where useful vision cannot be obtained with
n Sometimes peripapillary crescent encircling spectacles and contact lenses.
the disc may be present, where the choroid and n Genetic counselling. Chances of pathological myopia may
retina is distracted away from the disc margin. be decreased by advising against marriage
n A super-traction crescent (where the retina between two individuals with progressive
MYOPIA
is pulled over the disc margin) may be present myopia.
on the nasal side.
m Degenerative changes in retina and choroid are common
in progressive myopia
n These are characterised by white atrophic
patches at the macula with a little heaping up
of pigment around them.
n Foster-Fuchs’ spot (dark red circular patch due
to sub-retinal neovas-cularization and
choroidal haemorrhage) may be present at the
macula.
n Cystoid degeneration may be seen at the periphery.
n In an advanced case there occurs total retinal
atrophy, particularly in the central area.
m Posterior staphyloma due to ectasia of sclera at posterior
pole may be apparent as an excavation with the vessels
bending backward over its margins.
m Degenerative changes in vitreous include: liquefaction,
vitreous opacities, and posterior vitreous
detachment (PVD) appearing as Weiss’ reflex.
n Visual fields show contraction and in some cases ring
scotoma may be seen.
55
TOPIC 11 - HERPES n exposure to ultraviolet rays
n general ill- health,
n emotional or physical exhaustion,
Herpes simplex keratitis
n mild trauma,
n Herpes simplex virus (HSV).
n menstrual stress,
m It is a DNA virus.
n following administration of topical or
m Its only natural host is man
m HSV is epitheliotropic but may become
systemic steroids and immunosuppressive
neurotropic. agents.
m HSV type I typically causes infection above the
n Dendritic ulcer (MCQ)
m typical lesion of recurrent epithelial keratitis.
waist
m The ulcer is of an irregular, zigzag linear
m HSV type II below the waist (herpes genitalis)
n Mode of Infection
branching shape.
m The branches are generally knobbed at the ends.
m HSV-1 infection
m Floor of the ulcer stains with fluorescein
n It is acquired by kissing or coming in close contact
m virus-laden cells at the margin take up rose bengal.
with a patient suffering from herpes labialis.
m There is an associated marked diminution of
m HSV-II infection.
OPHTHALMOLOGY
n It is transmitted to eyes of neonates through

corneal sensations
infected genitalia of the mother(MCQ) n Geographical ulcer (MCQ)
m branches of dendritic ulcer enlarge and coalesce
n Ocular lesions of herpes simplex
m Primary herpes
to form a large epithelial ulcer with a ‘geographical’
n Skin lesions
or ‘amoeboid’ configuration
m The use of steroids in dendritic ulcer hastens
n Conjunctiva-acute follicular conjunctivitis
n Cornea
the formation of geographical ulcer. (MCQ)
l Fine epithelial punctate keratitis
n Symptoms of epithelial keratitis are: photophobia
l Coarse epithelial punctate keratitis
lacrimation, pain.
l Dendritic ulcer
n Treatment of epithelial keratitis
m Antiviral drugs are the first choice presently.
m Recurrent herpes
n Acycloguanosine (Aciclovir) 3 percent
n Active epithelial keratitis
l Punctate epthelial keratitis
ointment:(MCQ)
l It is least toxic and most commonly used
l Dendritic ulcer
antiviral drug.
HERPES
l Geographical ulcer
l It penetrates intact corneal epithelium and
n Stromal keratitis
l Disciform keratitis
stroma
l achieves therapeutic levels in aqueous humour
l Diffuse stromal necrotic keratitis
l used to treat herpetic keratitis.
n Trophic keratitis (meta-herpetic)
n Ganciclovir (0.15% gel)
n Herpetic iridocyclitis
n Triflurothymidine 1 percent
n Primary ocular herpes
n Adenine arabinoside (Vidarabine) 3 percent
m Primary infection (first attack) involves a
nonimmune person. ointment
m Mechanical debridement of the involved area along
m It typically occurs in children between 6 months
and 5 years of age and in teenagers. with a rim of surrounding healthy epithelium
n helps by removing the virus-laden cells.
m Primary infection is usually self-limiting but the
n it is reserved for: resistant cases
virus travels up to the trigeminal ganglion and establishes
the latent infection n Disciform keratitis (MCQ)
m It is due to delayed hypersensitivity reaction
n Recurrent ocular herpes
m The virus which lies dormant in the trigeminal
to the HSV antigen (MCQ)
m There occurs low grade stromal inflammation
ganglion
m periodically reactivates and causes recurrent
and damage to the underlying endothelium.
m Endothelial damage results in corneal oedema
infection.
m Predisposing stress stimuli which trigger an
due to imbibation of aqueous humour.
m Disciform keratitis is characterized by
attack of herpetic keratitis include
n Focal disc-shaped patch of stromal oedema
n fever such as malaria, flu
without necrosis
56
n Folds in Descemet’s membrane, n In due course of time vesicles are converted
n Keratic precipitates, into pustules, which subsequently burst to
n Ring of stromal infilterate (Wessley immune become crusting ulcers.
ring) (MCQ) n When crusts are shed, permanent pitted scars
l may be present surrounding the stromal are left.
oedema n The active eruptive phase lasts for about 3
l It signifies the junction between viral antigen weeks.
and host antibody. n Main symptom is severe neuralgic pain
n Corneal sensations are diminished. n anaesthesia dolorosa
n Intraocular pressure (IOP) may be raised l There occurs some anaesthesia of the
despite only mild anterior uveitis. affected skin associated with continued
m During active stage diminished corneal sensations and post-herpetic neuralgia
keratic precipitates are the differentiating points m Ocular lesions.
from other causes of stromal oedema. n usually appear at the subsidence of skin
m Treatment eruptions
n consists of diluted steroid eye drops instilled n Conjunctivitis
OPHTHALMOLOGY
4-5 times a day with an antiviral cover l one of the most common complication of
(aciclovir 3%) twice a day. herpes zoster.
n When disciform keratitis is present with an n Zoster keratitis
infected epithelial ulcer, antiviral drugs should l Fine or coarse punctate epithelial keratitis.
be started 5-7 days before the steroids. l 4 Microdendritic epithelial ulcers.
HERPES ZOSTER OPHTHALMICUS „ These unlike dendritic ulcers of herpes
n an acute infection of Gasserian ganglion of the simplex are usually peripheral and stellate
fifth cranial nerve by the varicella-zoster virus (VZV) rather than exactly dendritic in shape.
n Varicella -zoster virus. „ It contrast to Herpes simplex dendrites, they
m It is a DNA virus have tapered ends which lack bulbs.
m produces acidophilic intranuclear inclusion bodies. l 4 Nummular keratitis
m It is neurotropic in nature. „ is seen in about one-third number of total
n Mode of infection. cases.
m The infection is contracted in childhood, which „ It typically occurs as multiple tiny granular
HERPES
manifests as chickenpox deposits surrounded by a halo of stromal
m virus then remains dormant in the sensory haze.
ganglion of trigeminal nerve. l 4 Disciform keratitis
m in elderly people with depressed cellular „ occurs in about 50 percent of cases
immunity, the virus reactivates, replicates and travels „ is always preceded by nummular keratitis.
down along one or more of the branches of the n Neuroparalytic ulceration may occur as a sequelae
ophthalmic division of the fifth nerve. of acute infection and Gasserian ganglion
n Clinical features destruction.
m 3 In herpes zoster ophthalmicus, frontal nerve is n Exposure keratitis due to associated facial palsy.
more frequently affected than the lacrimal and n Mucous plaque keratitis develops
nasociliary nerves.(MCQ) l Occurs between 3rd and 5th months
m 3 The Hutchinson’s rule l characterised by sudden development of
n ocular involvement is frequent if the side or elevated mucous plaque with stain brilliantly
tip of nose presents vesicles (cutaneous with rose Bengal
involvement of nasociliary nerve) n Episcleritis and scleritis.
n 3 Lesions of herpes zoster are strictly limited n Iridocyclitis
to one side of the midline of head. n Acute retinal necrosis
m Cutaneous lesions. n Anterior segment necrosis and phthisis bulbi
n appear usually after 3-4 days of onset of the n Secondary glaucoma.
disease. n Treatment
n To begin with, the skin of lids and other affected m Oral antiviral drugs.
areas become red and oedematous (mimicking n These significantly decrease pain, curtail
erysipelas), followed by vesicle formation. vesiculation, stop viral progression and
57
reduce the incidence as well as severity of keratitis TOPIC 12 - PAPILLEDEMA
and iritis.
n In order to be effective, the treatment should
n passive disc swelling associated with increased
be started immediately after the onset of intracranial pressure
rash. n almost always bilateral although it may be
n It has no effect on post herpetic
asymmetrical.
neuralgia(MCQ) n The ICSOLs in any position excepting medulla
n Acyclovir , Valaciclovir are used
oblongata may induce papilloedema.
m Systemic steroids. n Papilloedema is most frequently associated with
n They appear to inhibit development of post-
tumours arising in posterior fossa, which obstruct
herpetic neuralgia when given in high doses. aqueduct of Sylvius and least with pituitary tumours.
n Steroids are commonly recommended in cases
n ICSOLs of cerebellum, midbrain and parieto-
developing neurological complications such as occipital region produce papilloedema more rapidly than
third nerve palsy and optic neuritis. the mass lesions of other areas.
m Amitriptyline should be used to relieve the n Idiopathic intracranial hypertension (IIH)(MCQ)
m Also known as pseudotumour cerebri
accompanying depression in acute phase.
m an important cause of raised intracranial
OPHTHALMOLOGY
m No calamine lotion.
n Cool zinc calamine application, as advocated
pressure.
m usually found in young obese women.
earlier, is better avoided
m It is characterised by chronic headache and bilateral
n it promotes crust formation.
papilloedema without any ICSOLs or
enlargement of the ventricles due to
hydrocephalus.
n Unilateral versus bilateral papilloedema.
m Disc swelling due to ocular and orbital lesions
is usually unilateral.
m with raised intracranial pressure, papilloedema
is bilateral.
m Foster-Kennedy syndrome.(MCQ)
n It is associated with olfactory or sphenoidal
PAPILLEDEMA
meningiomata and frontal lobe tumours.

n pressure optic atrophy occurs on the side of
lesion
n papilloedema occurs on the other side (due to
raised intracranial pressure).
m Pseudo-Foster-Kennedy syndrome.
n occurrence of unilateral papilloedema
associated with raised intracranial pressure (due
to any cause) and a pre-existing optic atrophy
(due to any cause) on the other side.
n Pathogenesis.
m Hayreh’s theory (MCQ)
n papilloedema develops as a result of stasis of
axoplasm in the prelaminar region of optic disc
n occurs due to an alteration in the pressure gradient
across the lamina cribrosa
n Increased intracranial pressure, malignant
hypertension and orbital lesions produce
disturbance in the pressure gradient by increasing
the tissue pressure within the retrolaminar region.
n ocular hypotony cause papilledema by lowering
the tissue pressure within the prelaminar area.
n Thus the axonal swelling in prelaminar
58 region is the initial structural alteration, which
in turn produces venous congestion and ultimately ® hard exudates may radiate from the
the extracellular oedema. fovea in the form of an incomplete star.
n Clinical features l Visual fields show enlargement of blind
m Visual acuity and pupillary reactions usually spot
remain fairly normal until the late stages of diseases n Chronic or long standing (vintage)
when optic atrophy sets in. papilloedema
m Clinical features of papilloedema can be described l Visual acuity is variably reduced depending
under four stages: early, fully developed, chronic upon the duration of the papilloedema.
and atrophic. l Pupillary reactions are usually normal
n Early (incipient) papilloedema l Ophthalmoscopic features
l Symptoms are usually absent and visual acuity „ acute haemorrhages and exudates resolve
is normal. „ peripapillary oedema is resorbed
l Pupillary reactions are normal. „ optic disc gives appearance of the dome
l Ophthalmoscopic features of early papilloedema of a champagne cork.
are (MCQ) „ The central cup remains obliterated.
„ Obscuration of the disc margins „ Small drusen like crystalline deposits
OPHTHALMOLOGY
® nasal margins are involved first followed (corpora amylacea) may appear on the disc
by the superior, inferior and temporal surface.
(MCQ) l Visual fields.
„ Blurring of peripapillary nerve fibre layer „ Blind spot is enlarged
„ Absence of spontaneous venous „ visual fields begin to constrict.
pulsation at the disc n Atrophic papilloedema
® appreciated in 80% of the normal l develops after 6-9 months of chronic
individuals papilloedema
„ Mild hyperaemia of the disc l characterized by severely impaired visual
„ Splinter haemorrhages in the peripapillary acuity.
region may be present. l Pupillary reaction. Light reflex is impaired.
l Visual fields are fairly normal. l Ophthalmoscopic features
n Established (fully developed) papilloedema „ greyish white discoloration and pallor of
PAPILLEDEMA
l Patient may give history of transient visual the disc due to atrophy of the neurons and
obscurations in one or both eyes, lasting a few associated gliosis.
seconds, after standing. „ Prominence of the disc decreases in
l Visual acuity is usually normal, spite of persistent raised intracranial
l Pupillary reaction remain fairly normal, pressure.
l Ophthalmoscopic features (MCQ) „ Retinal arterioles are narrowed
„ Apparent optic disc oedema is seen as its „ Retinal veins become less congested.
forward elevation above the plane of retina; „ Whitish sheathing develops around the
usually up to 1-2 mm vessels.
® 1 mm elevation is equivalent to +3 l Visual fields.
dioptres „ Concentric contraction of peripheral
„ Physiological cup of the optic disc is fields becomes apparent as atrophy sets in.
obliterated. n Differential diagnosis
„ Disc becomes markedly hyperaemic m Papilloedema should be differentiated from
„ blurring of the margin is present all-around. pseudopapilloedema and papillitis.
„ Multiple soft exudates and superficial m Pseudopapilloedema (MCQ)
haemorrhages may be seen near the disc. n non-specific term used to describe elevation
„ Veins becomes tortuous and engorged. of the disc similar to papilloedema
„ In advanced cases n Seen in
® disc appears to be enlarged l optic disc drusen
® circumferential greyish white folds l hypermetropia
may develop due to separation of nerve l persistent hyaloid tissue.
fibres by the oedema.
59
Differentiating features of papilloedima, papillitis and pseudopapillitis
Feature Papilloedema Papillitis Pseudopapillitis

1. Laterality Usually bilateral Usually unilateral May be unilateral
or bilateral
2. Symptoms
(i) Visual acuity Transient attacks of Marked loss of Defective vision
blurred vision vision of depending upon
OPHTHALMOLOGY
Later vision decreases sudden onset the degree of

due to optic atrophy refractive error
(ii) Pain and tenderness Absent May be present Absent
with ocular movements
3. Fundas examination
(i) Media Clear Posterior vitreous haze Clear
is common
(ii) Disc colour Red and juicy Marked Reddish
appearance hyperaemia
Disc margins Blurred Blurred Not well defined
Disc swelling 2-6 dioptres Usually not morethan Depending upon the
PAPILLEDEMA
3 dioptress degree of hypermetropia

(iii) Peripapillary oedema Present Present Absent
(iv) Venous engorgement More marked Less marked Not present
(v) Retinal haemorrhages Marked Usually not present Not present
(vi) Retinal exudates More marked Less marked Absent
(vii) Macula Macular star may be Macular fan may be Absent
present present
4. Fields Enlarged blind spot Central scotoma No defect
more for colours
5. Flurescein angiography Vertical oval pool of Minimal No leakage of dye
dye due of leakage leakage of dye
60
TOPIC 13 - STRABISMUS l Exophoria.
„ It is a tendency to diverge
n Definition
„ It may be:
n Normally visual axis of the two eyes are
® Convergence weakness type
parallel to each other in the ‘primary position of
» exophoria greater for near than
gaze’ and this alignment is maintained in all
positions of gaze. distance).
® Divergence excess type
n A misalignment of the visual axes of the
» exophoria greater on distant fixation
two eyes is called squint or strabismus.
n Classification of strabismus than the near
® Non-specific type
m Apparent squint or pseudostrabismus.
» exophoria which does not vary
m Latent squint (Heterophoria) (MCQ)
m Manifest squint (Heterotropia) (MCQ)
significantly in degree for any distance
l Hyperphoria.
n Concomitant squint
„ It is a tendency to deviate upwards,
n Incomitant squint.
l Hypophoria
n Pseudostrabismus
„ it is a tendency to deviate downwards
n In pseudostrabismus (apparent squint), the visual
OPHTHALMOLOGY
l Cyclophoria.
axes are in fact parallel, but the eyes seem to have
„ It is a tendency to rotate around the
a squin
n Pseudoesotropia or apparent convergent squint is
anteroposterior axis.
„ When the 12 O’clock meridian of cornea
associated with
l a prominent epicanthal fold (which covers
rotates nasally, it is called incyclophoria
„ when the 12 O’clock meridian of cornea
the normally visible nasal aspect of the
globe and gives a false impression of rotates temporally it is called excyclophoria.
esotropia) n Etiology
l Anatomical factors responsible for
l negative angle kappa.
n Pseudoexotropia or apparent divergent squint may
development of heterophoria include:
„ Orbital asymmetry.
be associated with
„ Abnormal interpupillary distance (IPD)
l hypertelorism, a condition of wide
® A wide IPD is associated with exophoria
separation of the two eyes
STRABISMUS
l positive angle kappa.
and small with esophoria.
„ Faulty insertion of extraocular muscle.
n Heterophoria
„ A mild degree of extraocular muscle
n Heterophoria also known as ‘latent strabismus’,
n the tendency of the eyes to deviate is kept
weakness.
„ Anomalous central distribution of the
latent by fusion.
n Therefore, when the influence of fusion is
tonic innervation of the two eyes.
„ Anatomical variation in the position of the
removed the visual axis of one eye deviates away.
n Practically a small amount of heterophoria
macula in relation to the optical axis of
is of universal occurrence and is known as the eye.
l Physiological factors
‘physiological heterophoria’.
„ Age
n Types of heterophoria
® Esophoria is more common in younger age
l Esophoria.
„ It is a tendency to converge.
group
® Exophoria which is more often seen in elderly.
„ It may be:
„ Role of accommodation.
® Convergence excess type
® Increased accommodation is
» esophoria greater for near than
distance associated with esophoria (as seen in
® Divergence weakness type
hypermetropes and individuals doing
» esophoria greater for distance than
excessive near work)
® Decreased accommodation is
near
® Non-specific type
associated with exophoria (as seen in
» esophoria which does not var y
simple myopes).
„ Role of convergence.
significantly in degree for any distance
61
® Excessive use of convergence may n Testing for vision and refractive error.
cause esophoria (as occurs in bilateral l It is most important, because a refractive
congenital myopes) error may be responsible for the symptoms
® Decreased use of convergence is often of the patient or for the deviation itself.
associated with exophoria (as seen in n Cover-uncover test. (MCQ)
presbyopes). l It tells about the presence and type of
„ Dissociation factor such as prolonged heterophoria.
constant use of one eye may result in l To perform it, one eye is covered with an
exophoria as occurs in occluder and the other is made to fix an object.
® individuals using uniocular microscope l In the presence of heterophoria, the eye
® watch makers using uniocular under cover will deviate.
magnifying glass l After a few seconds the cover is quickly
n Depending upon the symptoms ,heterophoria can be removed and the movement of the eye
divided into compensated and (which was under cover) is observed.
decompensated. l Direction of movement of the eyeball tells the type
l Compensated heterophoria. of heterophoria (e.g., the eye will move
OPHTHALMOLOGY
„ It is associated with no subjective outward in the presence of esophoria)

symptoms. l speed of movement tells whether recovery is
„ Compensation of heterophoria depends slow or rapid.
upon the n Prism cover test.
® reserve neuro-muscular power to n Maddox rod test.
overcome the muscular imbalance l A Maddox rod consists of many glass rods
® individual’s desire for maintenance of of red colour set together in a metallic disc
binocular vision. l The Maddox rod converts the point light
l Decompensated heterophoria. image into a line
„ Symptoms of muscular fatigue l Patient is asked to fix on a point light in the
® Headache and eyeache after prolonged use centre of Maddox tangent scale at a distance
of eyes, which is relieved when the of 6 metres.
eyes are closed. l A Maddox rod is placed in front of one
® Difficulty in changing the focus from near to eye with axis of the rod parallel to the axis of
STRABISMUS
distant objects of fixation or vice-versa. deviation

® Photophobia due to muscular fatigue is not l The Maddox rod converts the point light
relieved by using dark glasses, but image into a line. Thus, the patient will see
relieved by closing one eye. a point light with one eye and a red line
„ Symptoms of failure to maintain with the other.
binocular single vision l Due to dissimilar images of the two eyes,
® Blurring or crowding of words while fusion is broken and heterophoria
reading; becomes manifest.
® Inter mittent diplopia due to n Maddox wing test.
temporary manifest deviation under l Maddox wing is an instrument by which the
conditions of fatigue amount of phoria for near (at a distance of 33 cm)
® Inter mittent squint (without can be measured.
diplopia) which is usually noticed by the l It is also based on the basic principle of
patient’s close relations or friends. dissociation of fusion by dissimilar
„ Symptoms of defective postural objects.
sensations n Treatment
® Cause problems in judging distances l It is indicated in decompensated heterophoria
and positions especially of the moving (i.e., symptomatic cases).
objects. „ Correction of refractive error when
® This difficulty may be experienced by detected is most important.
cricketers, tennis players and pilots „ Orthoptic treatment.
during landing. l It is indicated in
n Examination of a case of heterophoria „ patients with heterophoria without refractive error
62
„ those where heterophoria and/or symptoms „ Abnormalities of extraocular muscles
are not corrected by glasses. such as faulty insertion, faulty innervation and
l Aim of orthoptic treatment is to improve mild paresis,
convergence insufficiency and the „ Abnormalities of accommodation,
fusional reserve. convergence and AC/A ratio.
l Orthoptic exercises can be done with n Central obstacles.
synoptophore. m Clinical features of concomitant strabismus
l Prescription of prism in glasses (in general)
l Surgical treatment. n Ocular deviation can be
„ Aim of the surgical management is to l Unilateral (monocular squint)
strengthen the weak muscle or weaken l alternating (alternate squint).
the strong muscle. l Inward deviation (esotropia)
n Concomitant strabismus l outward deviation (exotropia)
m It is a type of manifest squint l vertical deviation (hypertropia).
m amount of deviation in the squinting eye n Primary deviation is equal to secondary
remains constant (unaltered) in all the directions of gaze deviation
OPHTHALMOLOGY
m there is no associated limitation of ocular n Ocular deviation is equal in all the directions
movements. of gaze.
m Etiology n Ocular movements are not limited in any
n Binocular vision and coordination of ocular direction
movements n Refractive error may or may not be associated
l not present since birth n Suppression and amblyopia may develop as
l starts by the age of 3-6 months sensory adaptation to strabismus..
l completed up to 5-6 years. n A-V patterns may be observed in horizontal
l Therefore, any obstacle to the strabismus.
development of these processes may result n Types of concomitant squint
in concomitant squint. m Convergent squint (esotropia)
l These obstacles can be arranged into three m Divergent squint (exotropia)
groups, namely: sensory, motor and central. m Vertical squint (hypertropia)
STRABISMUS
n Sensory obstacles. n Convergent squint
l These are the factors which hinder the m denotes inward deviation of one eye
formation of a clear image in one eye. m It can be
l These include: n unilateral (the same eye always deviates inwards and
„ Refractive errors the second normal eye takes fixation) or
„ Prolonged use of incorrect spectacles n alternating (either of the eyes deviates inwards and
„ Anisometropia the other eye takes up fixation, alternately).
„ Corneal opacities, m Clinico-etiological types
„ Lenticular opacities n Accommodative esotropia.
„ Diseases of macula (e.g., central l It occurs due to overaction of convergence
chorioretinitis), associated with accommodation reflex.
„ Optic atrophy l It is of three types: refractive, non-refractive
„ Obstruction in the pupillary area due to and mixed.
congenital ptosis. l Refractive accommodative esotropia:
n Motor obstacles. „ It usually develops at the age of 2 to 3
l These factors hinder the maintenance of years
the two eyes in the correct positional „ associated with high hypermetropia (+4
relationship in primary gaze and/or during to +7 D).
different ocular movements. „ Mostly it is for near and distance
l A few such factors are: „ It is fully correctable by use of spectacles.
„ Congenital abnormalities of the shape and l Non-refractive accommodative esotropia:
size of the orbit, „ It is caused by abnormally AC/A
(accommodative convergence/
accommodation) ratio.
63
„ This may occur even in patients with no l It differentiates concomitant squint from
refractive error. paralytic squint (where secondary deviation is
„ Esotropia is greater for near than that for greater than primary).
distance m Estimation of angle of deviation
„ It is fully corrected by adding +3 DS for n Hirschberg corneal reflex test. (MCQ)
near vision. l It is a rough but handy method to estimate the
l Mixed accommodative esotropia angle of manifest squint.
n Non-accommodative esotropias. l In it the patient is asked to fixate at point
l Essential infantile esotropia. light held at a distance of 33 cm
„ It usually presents at 1-2 months of age. l deviation of the corneal light reflex from
„ It is characterised by fairly large angle of the centre of pupil is noted in the squinting
squint (> 30 ) o
eye.
l Essential acquired or late onset esotropia. l Roughly, the angle of squint is 15 and 45
o o
n Secondary esotropia. when the corneal light reflex falls on the border of
l Sensory deprivation esotropia. pupil and limbus, respectively
l It results from monocular lesions (in n The prism and cover test
OPHTHALMOLOGY
childhood) which either prevent the development n Krimsky corneal reflex test.
of normal binocular vision or interfere with its n Measurement of deviation with
maintenance. synoptophore.
l Examples of such lesions are: cataract, m Tests for grade of binocular vision and
severe congenital ptosis, aphakia, sensory functions.
anisometropia, optic atrophy, n Worth’ s four-dot test.
retinoblastoma, central chorioretinitis n Test for fixation.
n Consecutive esotropia. n After-image test.
l It results from surgical overcorrection of n Sensory
exotropia. n Synoptophore (major amblyoscope) tests for
n Divergent squint sensory functions
m Concomitant divergent squint (exotropia) is m Treatment of concomitant strabismus
characterised by outward deviation of one eye while the n Spectacles with full correction of refractive
other eye fixates. error
STRABISMUS
n Evaluation of a case of concomitant strabismus l correct the squint in accommodative squint.

m Testing of vision and refractive error. (MCQ)
n It is most important, because a refractive error n Occlusion therapy.
may be responsible for the symptoms of the l It is indicated in the presence of amblyopia.
patient or for the deviation itself. l Occlusion helps to improve the vision in
m Cover tests children below the age of 10 years.
n Direct cover test n Preoperative orthoptic exercises.
l It confirms the presence of manifest n Squint surgery.
squint. l Basic principles of squint surgery.
l To perform it, the patient is asked to fixate l These are to
on a point light. „ weaken the strong muscle by recession
l Then, the normal looking eye is covered (shifting the insertion posteriorly)
while observing the movement of the „ to strengthen the weak muscle by
uncovered eye. resection (shortening the muscle).
l In the presence of squint the uncovered eye l Type and amount of muscle surgery
will move in opposite direction to take fixation, while „ 1 mm resection of medial rectus (MR) will
in apparent squint there will be no movement. correct about 1°-1.5°
l This test should be performed for near „ 1 mm recession will correct about 2°-2.5°.
texation (i.e., at 33 cm) distance tixation(i.e., „ 1 mm resection and recession of lateral
at 6 metres). rectus (LR) muscle will correct 1°-2°.
n Alternate cover test. l The maximum limit allowed for
l It reveals whether the squint is unilateral or „ MR resection is 8 mm
alternate „ MR recession is 5.5 mm.
64
„ LR muscle resection is 10 mm
„ LR recession 8 mm
n Postoperative orthoptic exercises
Differences between paralytic and non-paralytic squint

Features Paralytic squint Non-paralytic squint
1. Onset Usually sudden Usually slow
2. Diplopia Usually present Usually absent
3. Ocular movements Limited in the direction Full
of action of paralysed muscle.
OPHTHALMOLOGY
4. False projection It is positive i.e., patient cannot correctly False projection is negative.
locate the object in space when asked to
see in the directon of paralysed muscle
in early stages.
5. Head posture A particular head posture depending Normal
upon the muscle paralysed may be present.
6. Nausea and Vertigo Present Absent
7. Secondary deviation Morethan the primary deviation Equal to primary deviation.
8. In old cases pathological Present Absent
sequelae in the muscles
STRABISMUS
65
TOPIC - 14 CORNEAL ULCER bulges forward along with the plastered iris
tissue.
n Bacterial corneal ulcer l This ectatic cicatrix is called anterior staphyloma
m Normal defence mechanisms are present in
which, depending upon its extent, may be
tears in the form of lysozyme, betalysin, and either partial or total.
other protective proteins. l The bands of scar tissue on the staphyloma
m three pathogens can invade the intact corneal
has a lobulated surface often blackened
epithelium and produce ulceration (MCQ) with iris tissue which resembles a bunch of
n Neisseria gonorrhoeae
black grapes -hence the name staphyloma)
n Corynebacterium diphtheria
m Clinical picture
n Neisseria meningitidis.
n Bacterial corneal ulcers may manifest as:
m When ulcer involves Bowman’s membrane and
l Purulent corneal ulcer without hypopyon
few superficial stromal lamellae, the resultant l Hypopyon corneal ulcer.
scar is called a ‘nebula’. n Symptoms (MCQ)
m Macula and leucoma result after healing of ulcers
l Pain and foreign body sensation
involving up to one-third and more than one- „ occurs due to mechanical effects of lids and
third of corneal stroma, respectively.
OPHTHALMOLOGY
chemical effects of toxins on the exposed

m Pathology of perforated corneal ulcer
nerve endings.
n Perforation of corneal ulcer occurs when the
l Watering from the eye
ulcerative process deepens and reaches up to „ occurs due to reflex hyperlacrimation.
Descemet’s membrane. l Photophobia
n Descemet’s membrane. is tough and bulges
l Blurred vision
out as Descemetocele l Redness of eyes
n At this stage, any exertion on the part of patient,
„ occurs due to congestion of circumcorneal
such as coughing, sneezing, straining for vessels.
stool etc. will perforate the corneal ulcer. n Signs
n Immediately after perforation, the aqueous
l Lids are swollen.
escapes, intraocular pressure falls and the iris- l Marked blepharospasm may be there.
lens diaphragm moves forward. l Conjunctiva
CORNEAL ULCER
n When the perforation is small and opposite

„ chemosed
to iris tissue, it is usually plugged and healing by „ shows conjunctival hyperaemia and
cicatrization proceeds rapidly ciliary congestion.
n Adherent leucoma is the commonest end result
l A well established bacterial ulcer is
after such a catastrophe. characterized by
m Pathology of sloughing corneal ulcer and
„ Yellowish-white area of ulcer which may
formation of anterior staphyloma be oval or irregular in shape.
n false cornea
„ Margins of the ulcer are swollen and over
l occurs when the infecting agent is highly virulent
hanging.
and/or body resistance is very low „ Floor of the ulcer is covered by necrotic
l the whole cornea sloughs with the exception
material.
of a narrow rim at the margin „ Stromal oedema is present surrounding
l total prolapse of iris occurs.
the ulcer area.
l The iris becomes inflamed and exudates block
l Anterior chamber
the pupil and cover the iris surface; thus a false „ may or may not show pus (hypopyon).
cornea is formed. „ In bacterial corneal ulcers the hypopyon
n pseudocornea
remains sterile so long as the Descemet’s
l Ultimately these exudates organize and form
membrane is intact.
a thin fibrous layer over which the conjunctival l Iris may be slightly muddy in colour.
or corneal epithelium rapidly grows and thus a l Pupil may be small due to associated toxin–
pseudocornea is formed. induced iritis.
n anterior staphyloma
l Intraocular pressure may some times be
l Since the pseudocornea is thin and cannot
raised (inflammatory glaucoma).
withstand the intraocular pressure, so it usually
66
m Characteristic features produced by some of „ As a result the treatment is often undully
the causative bacteria delayed.
n Staphylococal aureus and streptococcus pneumonia l Signs.
l usually produce an oval, yellowish white „ Typical features of ulcus serpens are :
densely opaque ulcer which is surrounded ® Ulcus serpens is a greyish white or
by relatively clear cornea. yellowish disc shaped ulcer
n Pseudomonas species ® occur near the centre of cornea
l irregular sharp ulcer with thick greenish ® The ulcer has a tendency to creep over
mucopurulent exudate the cornea in a serpiginous fashion.
l diffuse liquefactive necrosis ® One edge of the ulcer, along which
l semiopaque (ground glass) surrounding cornea. the ulcer spreads, shows more infiltration.
l Such ulcers spread very rapidly and may ® The other side of the ulcer may be
even perforate within 48 to 72 hours. undergoing simultaneous cicatrization and
n Enterobacteriae (E. coli, Proteus sp., and Klebsiella the edges may be covered with fresh
sp.) epithelium.
l shallow ulcer with greyish white pleomorphic ® Violent iridocyclitis is commonly
OPHTHALMOLOGY
suppuration and diffuse stromal opalescence. associated with a definite hypopyon.
l The endotoxins produced by these Gram –ve ® Hypopyon increases in size very rapidly
bacilli may produce ring-shaped corneal and often results in secondar y
infilterate glaucoma.
m Hypopyon corneal ulcer ® Ulcer spreads rapidly and has a great
n most dangerous organisms causing hypopyon tendency for early perforation.
are pseudomonas pyocyanea and m Complications of corneal ulcer
pneumococcus. n Toxic iridocyclitis.
n ‘hypopyon corneal ulcer’ is the characteristic l It is due to absorption of toxins in the anterior
ulcer caused by pneumococcus chamber.
n ‘corneal ulcer with hypopyon’ are the ulcers n Secondary glaucoma.
associated with hypopyon due to other causes. l It occurs due to fibrinous exudates blocking
n The characteristic hypopyon corneal ulcer caused the angle of anterior chamber (inflammatory
CORNEAL ULCER
by pneumococcus is called ulcus glaucoma).
serpens.(MCQ) n Descemetocele.
n Source of infection for pneumococcal infection is l This is a sign of impending perforation
usually the chronic dacryocystitis. l it is usually associated with severe pain.
n hypopyon ulcers are much more common in n Perforation of corneal ulcer.
old debilitated or alcoholic subjects. l Sudden strain due to cough, sneeze or spasm
n Mechanism of development of hypopyon. of orbicularis muscle may convert
l Corneal ulcer is often associated with some impending perforation into actual perforation
iritis owing to diffusion of bacterial l Following perforation, immediately pain is
toxins. decreased
l When the iritis is severe the outpouring of l patient feels some hot fluid (aqueous)
leucocytes from the vessels is so great these coming out of eyes.
cells gravitate to the bottom of the anterior chamber m Sequelae of corneal perforation include :
to form a hypopyon. n Prolapse of iris.
l hypopyon is sterile since the outpouring of l It occurs immediately following perforation
polymorphonuclear cells is due to the toxins and in a bid to plug it.
not due to actual invasion by bacteria. n Subluxation or anterior dislocation of lens
Once the ulcerative process is controlled, the l occur due to sudden stretching and rupture
hypopyon is absorbed. of zonules.
n Clinical features n Anterior capsular cataract.
l Symptoms l It is formed when the lens comes in contact
„ during initial stage of ulcus serpens there with the ulcer
is remarkably little pain. l Occur following a perforation in the
pupillary area.
67
n Corneal fistula „ The patient should be advised to avoid
l It is formed when the perforation in the sneezing, coughing and straining during stool etc.
pupillary area is not plugged by iris and is He should be advised strict bed rest
lined by epithelium which gives way l Pressure bandage should be applied to give some
repeatedly. external support.
l There occurs continuous leak of aqueous l Lowering of intraocular pressure by
through the fistula. „ acetazolamide
n Purulent uveitis „ intravenous mannitol
n endophthalmitis „ oral glycerol
n panophthalmitis „ 0.5% timolol eyedrops
n Intraocular haemorrhage in the form of „ paracentesis
either vitreous haemorrhage or expulsive l Tissue adhesive glue such as cynoacrylate is
choroidal haemorrhage helpful in preventing perforation.
l occur due to sudden lowering of intraocular l Conjunctival flap.
pressure. l Bandage soft contact lens
n Corneal scarring. l Penetrating therapeutic keratoplasty
OPHTHALMOLOGY
m Management of a case of corneal ulcer (tectonic graft)

n Treatment of uncomplicated corneal ulcer l Treatment of perforated corneal ulcer
n Topical antibiotics. „ urgent therapeutic keratoplasty.
l fortified gentamycin n Marginal catarrhal ulcer
l fortified tobramycin m superificial ulcers situated near the limbus
l fortified cephazoline m frequently seen especially in old people.
l Ciprofloxacin m thought to be caused by a hypersensitivity
l Ofloxacin reaction to staphylococcal toxins
l Gatifloxacin m occurs in association with chronic
n Cycloplegic drugs.(MCQ) staphylococcal blepharoconjunctivitis
l Preferably 1 percent atropine eye ointment m Moraxella and Haemophilus are also known
or drops should be used to cause such ulcers.
l 2 per cent homatropine eye drops can also Mycotic corneal ulcer (Very High yield topic
CORNEAL ULCER
n
be used for MD Entrance)
l Mechanism of action m Causative fungi
„ reduce pain from ciliary spasm n Filamentous fungi (MCQ)
„ prevent the formation of posterior l Aspergillus, Fusarium, Alternaria,
synechiae from secondary iridocyclitis. Cephalosporium, Curvularia and Penicillium.
„ Atropine also increases the blood supply n Yeasts e.g., Candida and Cryptococcus.
to anterior uvea by relieving pressure m The fungi more commonly responsible for
on the anterior ciliary arteries and so mycotic corneal ulcers are
brings more antibodies in the aqueous humour. n Aspergillus (most common) (MCQ)
„ It also reduces exudation by decreasing n Candida
hyperaemia and vascular permeability n Fusarium
n Treatment of non-healing corneal ulcer m Modes of infection (MCQ)
l Cauterisation of the ulcer n Injury by vegetative material such as crop
„ performed with pure carbolic acid or 10- leaf, branch of a tree, straw, hay or
20 per cent trichloracetic acid. decaying vegetable matter. (Many times asked
l Bandage soft contact lens may also help in healing. in MD Entrance as a clinical vignette)
l Peritomy n Common sufferers are field workers
„ severing of perilimbal conjunctival especially during harvesting season.
vessels may be performed when excessive n Injur y by animal tail is another mode
corneal vascularization is hindering healing. ofinfection.
n Treatment of impending perforation m Secondary fungal ulcers are common in patients who
l No strain. are immunosuppressed systemically or locally such
as patients suffering from dry eye, herpetic
68
keratitis, bullous keratopathy or postoperative TOPIC 15 - OPHTHALMOSCOPY
cases of keratoplasty. DIRECT& INDIRECT
m Role of antibiotics and steroids.
n Antibiotics disturb the symbiosis between n The ophthalmoscope was invented by Babbage in 1848,
bacteria and fungi n it was re-invented by von Helmholtz in 1850.
n steroids make the fungi facultative pathogens n Three methods of examination
which are otherwise symbiotic saprophytes. m distant direct ophthalmoscopy
n Therefore, excessive use of these drugs predisposes m direct ophthalmoscopy
the patients to fungal infections. m indirect ophthalmoscopy.
m Clinical features n Distant direct ophthalmoscopy
n A typical fungal corneal ulcer has following m It should be performed routinely before the
salient features( MCQ) direct ophthalmoscopy
n Corneal ulcer is dry-looking, greyish white, m It can be performed with the help of a
with elevated rolled out margins. (MCQ) n self-illuminated ophthalmoscope
n Delicate feathery finger-like extensions are n simple plain mirror with a hole at the centre.
present into the surrounding stroma under the m The light is thrown into patient’s eye sitting in a
OPHTHALMOLOGY
intact epithelium. semi-darkroom, from a distance of 20-25 cm
n A sterile immune ring (yellow line of and the features of the red glow in the pupillary
demarcation) may be present where fungal area are noted. (MCQ)
antigen and host antibodies meet. m Applications of distant direct
n Multiple, small satellite lesions may be present ophthalmoscopy
around the ulcer. (MCQ) n To diagnose opacities in the refractive media.
n Usually a big hypopyon is present even if the n Any opacity in the refractive media is seen
ulcer is very small. (MCQ) as a black shadow in the red glow.
n Unlike bacterial ulcer, the hypopyon may not be n The exact location of the opacity can be
sterile as the fungi can penetrate into the anterior determined by obser ving the parallactic
chamber without perforation(MCQ) displacement. (MCQ)
n Perforation in mycotic ulcer is rare but can occur.
OPHTHALMOSCOPY DIRECT & INDIRECT

l For this, the patient is asked to move the
n Corneal vascularization is conspicuously absent. eye up and down while the examiner is
(MCQ) observing the pupillary glow.
m Diagnosis „ The opacities in the pupillary plane remain
m Typical clinical manifestations associated with history stationary
of injury by vegetative material are diagnostic „ those in front of the pupillary plane
of a mycotic corneal ulcer. move in the direction of the movement of the eye
m Chronic ulcer worsening in spite of most efficient „ those behind the pupillary plane will
treatment should arouse suspicion of mycotic move in opposite direction
involvement. n To differentiate between a mole and a hole of the iris.
m Treatment (MCQ) (MCQ)
n Topical antifungal eye drops should be used l A small hole and a mole on the iris appear
for a long period (6 to 8 weeks as a black spot on oblique illumination. On
l Natamycin (5%) eye drops (MCQ) distant direct ophthalmoscopy
l Fluconazol (0.2%) eye drops l the mole looks black (as earlier)
l Nystatin (3.5%) eye ointment. l a red reflex is seen through the hole in the iris.
n Systemic antifungal n To recognize detached retina or a tumour arising from
l fluconazole or ketoconazole. the fundus. (MCQ)
l A grayish reflex seen on distant direct
ophthalmoscopy indicates either a detached
retina or a tumour arising from the fundus.
n Direct ophthalmoscopy
m It is the most commonly practised method for
routine fundus examination.
m A convergent beam of light is reflected into the
patient’s pupil
69
m The emergent rays from any point on the to focus as a real, inverted image between
patient’s fundus reach the observer’s retina through the lens and the observer’s eye
the viewing hole in the ophthalmoscope m The image formed in indirect ophthalmoscopy
m if the patient or/and the observer is/are (MCQ)
ametropic, a correcting lens (equivalent to the sum of n real, inverted and magnified.
the patient’s and observer’s refractive error) must be n About 5 times magnification is obtained with
interposed (from the system of plus and minus a +13 D lens.
lenses, inbuilt in the modern ophthalmoscopes). n With a stronger lens, image will be smaller, but
m Characteristics of image formed. brighter and field of vision will be more.
n In direct ophthalmoscopy, the image m Prerequisites.
l is erect, virtual (MCQ) n convex lens (now-a-days commonly employed
l about 15 times magnified in emmetropes lens is of +20 D)
(more in myopes and less in hypermetropes). (MCQ) n pupils of the patient should be dilated.
m Once the red reflex is seen the observer should n By asking the patient to look in extreme gaze,
move as close to the patient’s eye as possible and using of scleral indenter, the whole
(theoretically at the anterior focal plane of the patient’s peripheral retina up to ora serrata can be examined.
OPHTHALMOLOGY
eye, i.e., 15.4 mm from the cornea) m Advantages of the binocular indirect
n Indirect ophthalmoscopy ophthalmoscope
m Indirect ophthalmoscopy introduced by Nagel n The inbuilt illumination is strong and its
in 1864 intensity can be changed.
m now a very popular method for examination n It allows stereoscopic view of the image
of the posterior segment.
m Optical principle.
n make the eye highly myopic by placing a strong
convex lens in front of patient’s eye emergent
rays from an area of the fundus are brought
OPHTHALMOSCOPY DIRECT & INDIRECT
Sr. Feature Direct Indirect

no. ophthalmoscopy ophthalmoscopy
1. Condensing lens Not required Required
2. Examination distance As close to patient’s eye as possible At an arm’s length
3. Image Virtual, Erect Real, inverted
4. Magnification About 15 times 4-5 times
5. Illumination Not so bright; so not useful in hazy media Bright; so, useful for hazy media
6. Area of field in focus About 2 disc dioptres diopter About 8 disc diopter
7. Stereopsis Absent Present
8. Accessible fundus view Slightly beyond equator Up to ora serrata
9. Examination Not possible Possible
through hazy media
70
n Slit-lamp biomicroscopic examination of the l It may be associated with spasm of
fundus accommodation.
m Biomicroscopic examination of the fundus can n Traumatic mydriasis (Iridoplegia).
be performed after full mydriasis using a slit-lamp l It is usually permanent
and any one of the following lenses: l may be associated with traumatic cycloplegia.
n Indirect slit-lamp biomicroscopy. n Rupture of the pupillary margin
l +78 D, +90 D small diameter lenses is presently n Radiating tears in the iris stroma
the most commonly employed technique for n Iridodialysis
biomicroscopic examination of the fundus. l detachment of iris from its root at the ciliary
n Hruby lens biomicroscopy. body occurs frequently.

l Hruby lens is a planoconcave lens with dioptric l It results in a D-shaped pupil and a black
power 58.6D biconvex area seen at the periphery

l This lens provides a small field with low n Antiflexion of the iris.
magnification l It refers to rotation of the detached portion
l cannot visualize the fundus beyond equator. of iris, in which its posterior surface faces anteriorly.
m Contant lens biomicroscopy can be performed l It occurs following extensive iridodialysis.
OPHTHALMOLOGY
by following lenses: n Retroflexion of the iris
n Posterior fundus contact lens is a modified n Traumatic aniridia or iridremia
Koeppe’s lens n Angle recession
l The image produced by it is virtual and l refers to the tear between longitudinal and
erect. circular muscle fibres of the ciliary body.

n Goldmann’ s three-mirror contact lens l It is characterized by deepening of the
(MCQ) anterior chamber and widening of the

l With this the central as well as peripheral ciliary body band on gonioscopy.
parts of the fundus can be visualized. l Later on it is complicated by glaucoma
(MCQ)
m Lens
n Vossius ring(MCQ)
BLUNT TRAUMA EYE

TOPIC 16 - BLUNT TRAUMA EYE
l It is a circular ring of brownpigment
l seen on the anterior capsule.
n Blunt trauma
l It occurs due to striking of the contracted
n Traumatic lesions produced by blunt trauma can be
grouped as follows: pupillary margin against the crystalline lens.
l It is always smaller than the size of the pupil.
m Closed globe injury
n Concussion cataract.
m Globe rupture
l It occurs mainly due to
m Extraocular lesions
„ imbibition of aqueous
n Closed-globe injury
„ direct mechanical effects of the injury
m Cornea
n Simple abrasions.
on lens fibres.
l It may assume any of the following shapes:
l These are very painful
„ Discrete subepithelial opacities are of most
l diagnosed by fluorescein staining.
l These usually heal up within 24 hours with
common occurrence.
„ Early rosette cataract (punctate).
‘pad and bandage’ applied after instilling
® It is the most typical for m of
antibiotic ointment.
m Anterior chamber
concussion cataract.
® It appears as feather y lines of
n Traumatic hyphaema (blood in the anterior
chamber).(MCQ) opacities along the star-shaped suture
l It occurs due to injury to the iris or ciliary
lines
® Occurs usually in the posterior cortex
body vessels
„ Late rosette cataract.
m Iris, pupil and ciliary body
® It develops in the posterior cortex 1 to 2
n Traumatic miosis.
l It occurs initially due to irritation of ciliary
years after the injury
„ Traumatic zonular cataract.
nerves.
„ Diffuse (total) concussion cataract
71
n Early maturation of senile cataract may follow blunt l Traumatic macular oedema is usually
truma. followed by pigmentary degeneration. Sometimes,
n Traumatic absorption of the lens. a macular cyst is formed, which on rupture
l It may occur sometimes in young children may be converted into a lamellar or full
resulting in aphakia thickness macular hole. (MCQ)
n Subluxation of the lens m Intraocular pressure changes in closed-globe
l It may occur due to partial tear of zonules. injury
n Dislocation of the lens.(MCQ) n Traumatic glaucoma.
l It occurs when rupture of the zonules is n Traumatic hypotony.
complete. l It may follow damage to the ciliary body
l It may be intraocular (commonly) or l It may even result in phthisis bulbi.
extraocular (sometimes n Traumatic changes in the refraction
l Extraocular dislocation may be in the l Myopia may follow
subconjunctival space (phakocele) „ ciliary spasm
m Vitreous „ rupture of zonules or anterior shift of the
n Liquefaction and appearance of clouds of fine lens.
OPHTHALMOLOGY
pigmentary opacities (a most common change). l Hypermetropia and loss of accommodation may
n Detachment of the vitreous either anterior or result from damage to the ciliary body
posterior. (cycloplegia).
n Vitreous haemorrhage. n Globe rupture
n Vitreous herniation in the anterior chamber m Globe rupture is a full-thickness wound of the
m Choroid eyewall caused by a blunt object.
n Rupture of the choroid. m Globe rupture may occur in two ways:
l The rupture of choroid is concentric to the n Direct rupture may occur, though rarely, at
optic disc and situated temporal to it. the site of injury.
n Choroidal haemorrhage n Indirect rupture
n Choroidal detachment m Indirect rupture
n Traumatic choroiditis n more common
BLUNT TRAUMA EYE
m Retina n occurs because of the compression force.

n Commotio retinae (Berlin’s oedema).(MCQ) n Results in inside-out injury at the weakest part
l It is of common occurrence following a blow of eyewall, i.e., in the vicinity of canal of Schlemm
on the eye. concentric to the limbus.
l It manifests as milky white cloudiness n The superonasal limbus is the most common site
l Involves a considerable area of the posterior of globe rupture (MCQ)
pole with a ‘cherry-red spot’ in the foveal n contrecoup effect— the lower temporal
region. (MCQ) quadrant being most exposed to trauma.
l It may disappear after some days or may be m Treatment.
followed by pigmentary changes. n A badly damaged globe should be enucleated.
n Retinal haemorrhages. (MCQ)
l These are quite common following
concussion trauma.
n Retinal tears.
l These may follow a contusion
l Occur particularly in the peripheral region
l Occur especially in eyes already suffering from
myopia or senile degenerations.
n Traumatic proliferative retinopathy (Retinitis
proliferans).
l It may occur secondary to vitreous
haemorrhage, forming tractional bands.
n Retinal detachment
n Concussion changes at macula.
72
TOPIC 17 - CONTACT LENS l more chances of corneal infections
l cannot correct astigmatism of more than 2
n Contact lens is an artificial device whose front surface
dioptres.
substitutes the anterior surface of the cornea.
n Indications of contact lens use (MCQ)
n Used for correction of refractive error
m Optical indications
n irregularities of the front surface of cornea can
n Anisometropia
also be corrected
n unilateral aphakia
n Types of contact lenses
n high myopia
m contact lenses can be divided into following three
n keratoconus
types:
n irregular astigmatism.
n Hard lenses,
n Optically they can be used by every patient
n Rigid gas permeable lenses, and
having refractive error for cosmetic purposes.
n Soft lenses.
m Advantages of contact lenses over spectacles (MCQ)
m Hard lenses
n Irregular corneal astigmatism which is not
n manufactured from PMMA
possible to correct with glasses can be corrected with
(polymethylmethacrylate). (MCQ)
contact lenses
n The PMMA has a high optical quality,
OPHTHALMOLOGY
n Contact lenses provide normal field of vision
stability and is light in weight, non- toxic,
n Aberrations associated with spectacles (such
durable and cheap.
as peripheral aberrations and prismatic distortions) are
n The hard corneal lenses have a diameter of
eliminated
8.5-10 mm.
n Binocular vision can be retained in high
n Presently these are not used commonly.
anisometropia (e.g., unilateral aphakia) owing to
n Disadvantages of PMMA hard contact lenses (MCQ)
less magnification of the retinal image.
l PMMA is practically impermeable to O2
n Rain and fog do not condense upon contact
thus restricting the tolerance.
lenses as they do on spectacles.
l Being hard, it can cause corneal abrasions.
n Cosmetically more acceptable especially by
l Being hydrophobic in nature, resists wetting
females and all patients with thick glasses in high
but a stable tear film can be formed over it.
refractive errors.
l PMMA contact lenses are sparingly used in
m Therapeutic indications are as follows : (MCQ)
CONTACT LENS
clinical practice because of poor patient
n Corneal diseases
acceptance.
l non-healing cor neal ulcers, bullous
m Rigid gas permeable (RGP) lenses
keratopathy, filamentary keratitis and
n made up of materials which are permeable to
l recurrent corneal erosion syndrome.
oxygen.
n Diseases of iris such as
n commonly manufactured from copolymer of
l aniridia, coloboma and albinism to avoid
PMMA and silicone containing vinyl
glare.
monomer.
n In glaucoma as vehicle for drug delivery.
m Soft lenses
n In amblyopia, opaque contact lenses are used for
n made up of HEMA (hydroxyme-
occlusion.
thymethacrylate). (MCQ)
n Bandage soft contact lenses are used following
n These are made about 1-2 mm larger than the
keratoplasty and in microcor neal
corneal diameter.
perforation.
n In clinical practice soft lenses are most
m Preventive indications include
frequently prescribed.
n prevention of symblepharon and restoration
n Advantages:
of fornices in chemical burns
l soft and oxygen permeable
n exposure keratitis
l most comfortable and so well tolerated.
n trichiasis.
n Disadvantages include
m Diagnostic indications include use during
l problem of wettability
n Gonioscopy
l proteinaceous deposits
n Electroretinography
l getting cracked
n examination of fundus in the presence of
l limited life
irregular corneal astigmatism
l inferior optical quality
n fundus photography
73
n Goldmann’s 3 mirror examination. TOPIC 18 - TRACHOMA
m Operative indications. Contact lenses are used
n Trachoma
during
m a chronic keratoconjunctivitis
n goniotomy operation for congenital glaucoma
m primarily affecting the superficial epithelium of
n vitrectomy;
conjunctiva and cornea simultaneously.
n endocular photocoagulation.
m It is characterised by a mixed follicular and
m Cosmetic indications include
papillary response of conjunctival tissue.
n unsightly corneal scars (colour contact lenses)
m one of the leading causes of preventable
n ptosis (haptic contact lens)
blindness in the world.
n cosmetic scleral lenses in phthisis bulbi.
m Etiology
m Occupational. indications include use by
n caused by a Bedsonian organism, the
n Sportsmen
Chlamydia trachomatis
n pilots
l belong to the Psittacosis-
n actors
lymphogranuloma- trachoma (PLT)
m Contraindications for contact lens use (MCQ)
group.
n Mental incompetence, and poor motivation;
l organism is epitheliotropic
OPHTHALMOLOGY
n chronic dacryocystitis;
l produces intracytoplasmic inclusion
n chronic blepharitis and recurrent styes
bodies called H.P. bodies (Halberstaedter
n chronic conjunctivitis
Prowazeke bodies) (MCQ)
n dry- eye syndromes
l Serotypes A, B, Ba and C are associated with
n corneal dystrophies and degenerations;
hyperendemic (blinding) trachoma
n recurrent diseases like episcleritis, scleritis and
l serotypes D-K are associated with
iridocyclitis.
paratrachoma (oculogenital chlamydial
m Complications due to contact lens wear
disease).
n Sleeping in lenses not designed or approved
n Predisposing factors
for extended wear is a common cause of
l infection is usually contracted during infancy
complications.
and early childhood
n Many people go too long before replacing
l preponderance exists in the females both in
their lenses, wearing lenses designed for 1, 14, or
number and in severity of disease.
TRACHOMA
30 days of wear for multiple months or years.

l more common in areas with dry and dusty
n People that suffer from dry eyes are particularly
weather.
vulnerable to mild discomfort and episodes of brief blurry
l More common in poor classes owing to
vision.
unhygienic living conditions
n Improper use of contact lenses may affect the
l outdoor workers are more affected in
eyelid, the conjunctiva, and the various layers of
comparison to office workers.
the cornea
n Source of infection
n Poor lens care can lead to infections by
l the main source of infection is the
Acanthamoeba. (MCQ)
conjunctival discharge of the affected
n Long-term (over 5 years) use of contact
person..
lenses may “decrease the entire corneal thickness and
l Modes of infection
increase the corneal curvature and surface irregularity.
„ Direct spread through contact by air-borne
n Long-term wear of rigid contact lens is
or water-borne modes.
associated with
„ Vector transmission is common through
l decreased corneal keratocyte density
flies.
l increased number of epithelial Langerhans cells
„ Material transfer through contaminated fingers
of doctors, nurses and contaminated tonometers ,
surma-rods
m Clinical profile of trachoma
n Incubation period 5-21 days.
n Natural history.
n development of acute disease occur in the first
decade of life
74
n sequelae occur at least after 20 years of the „ The vessels are superficial and lie between
disease. epithelium and Bowman’s membrane.
n peak incidence of blinding sequelae is seen „ Later on Bowman’s membrane is also
in the fourth and fifth decade of life. destroyed.
m Signs „ Pannus may be progressive or regressive.
n Conjunctival signs l Herbert pits
l Congestion of upper tarsal and forniceal „ oval or circular pitted scars, left after
conjunctiva. healing of Herbert follicles in the limbal area
l Conjunctival follicles. l Corneal opacity
„ Follicles look like boiled sagograins m Grading of trachoma
„ commonly seen on upper tarsal n McCallan’s classification (MCQ)
conjunctiva and fornix; l Stage I (Incipient trachoma or stage of
l follicles may be seen on the bulbar infiltration).
conjunctiva (pathognomic of trachoma). (MCQ) l Stage II (Established trachoma or stage of
l Structure of follicle. florid infiltration).
„ Follicles are formed due to scattered l Stage III (Cicatrising trachoma or stage of
OPHTHALMOLOGY
aggregation of lymphocytes and other scarring).
cells in the adenoid layer. l Stage IV (Healed trachoma or stage of
l Leber cells sequelae).
„ Central part of each follicle is made up of n WHO classification
mononuclear histiocytes, few l TF: Trachomatous inflammation-follicular
lymphocytes and large multinucleated l TI : Trachomatous inflammation intense.
cells l TS: Trachomatous scarring
l Presence of Leber cells and signs of l TT: Trachomatous trichiasis.
necrosis differentiate trachoma follicles from follicles l CO: Corneal opacity
of other forms of follicular conjunctivitis.(MCQ) m Sequelae of trachoma
l Papillary hyperplasia. n Sequelae in the lids may be trichiasis, entropion,
„ Papillae are reddish, flat topped raised tylosis (thickening of lid margin), ptosis,
areas madarosis and ankyloblepharon.
„ give red and velvety appearance to the m The clinical diagnosis of trachoma is made
TRACHOMA
tarsal conjunctiva from its typical signs; at least two sets of signs
„ Each papilla consists of central core of should be present out of the following:
numerous dilated blood vessels surrounded by n Conjunctival follicles and papillae
lymphocytes and covered by hypertrophic n Pannus progressive or regressive
epithelium. n Epithelial keratitis near superior limbus
l Conjunctival scarring n Signs of cicatrisation or its sequelae
„ irregular, star-shaped or linear. m Differential diagnosis
„ Linear scar present in the sulcus n Trachoma with follicular hypertrophy must
subtarsalis is called Arlt’s line (MCQ) be differentiated from acute adenoviral
l Concretions follicular conjunctivitis (epidemic
l formed due to accumulation of dead keratoconjunctivitis) as follows :
epithelial cells and inspissated mucus in l Distribution of follicles
the depressions called glands of Henle. „ in trachoma is mainly on upper palpebral
n Corneal signs conjunctiva and fornix
l Superficial keratitis may be present in the upper „ in EKC lower palpebral conjunctiva and fornix
part. is predominantly involved.
l Herbert follicles n Trachoma with predominant papillary
„ refer to typical follicles present in the hypertrophy needs to be differentiated from
limbal area palpebral form of spring catarrh as follows:
l Pannus l in spring catarrh.
„ infiltration of the cornea associated with „ Papillae are large in size
vascularization is seen in upper part „ usually there is typical cobble-stone
arrangement
75
l pH of tears TOPIC 19 - CRAO
„ usually alkaline in spring catarrh,
n RETINAL ARTERY OCCLUSION
„ while in trachoma it is acidic,
m Etiology
l Discharge is ropy in spring catarrh.
n Occlusive disorders of retinal vessels are more
l In trachoma, there may be associated
common in patients suffering from hypertension
follicles and pannus.
and other cardiovascular diseases.
m Management
n Common causes of retinal artery occlusion are:
n Treatment of active trachoma
l Atherosclerosis-related thrombosis at the
n Topical therapy regimes.
level of lamina cribrosa is the most common
l 1 percent tetracycline or 1 percent
cause (75%) of CRAO (MCQ)
erythromycin eye ointment for 6 weeks or
l Emboli from the carotid artery and those of
l 20 percent sulfacetamide eye drops along
cardiac origin
with 1 percent tetracycline eye ointment
l Retinal arteritis with obliteration associated
for 6 weeks.
with giant cell arteritis
n The continuous treatment for active trachoma
l Retinal periarteritis associated with
should be followed by an intermittent
„ polyarteritis nodosa
OPHTHALMOLOGY
treatment especially in endemic or

„ systemic lupus erythematosus
hyperendemic area.
„ Wegner’s granulomatosis and scleroderma
n Systemic therapy regimes.
l Angiospasm associated with amaurosis.
l Tetracycline
l Raised intraocular
l erythromycin
l Thrombophilic disorders is associated with
l doxycycline
CRAO in young individuals.
l azithromycin
m Clinical features
n Combined topical and systemic therapy regime
n more common in males than females.
m Prophylaxis
n It is usually unilateral
n Hygienic measures.
n Central retinal artery occlusion (CRAO).
l The use of common towel, handkerchief,
l It occurs due to obstruction at the level of
surma rods etc. should be discouraged.
lamina cribrosa
l A good environmental sanitation will reduce
l Symptoms
the flies.
„ Patient complains of sudden painless loss
l A good water supply would improve
CRAO
of vision. (MCQ)
washing habits.
l Signs
n Early treatment of conjunctivitis.
„ Direct pupillary light reflex is absent.
n Blanket antibiotic therapy (intermittent treatment
„ On ophthalmoscopic examination
l The regime is to apply 1 percent tetracycline
® retinal arteries are markedly narrowed
eye ointment twice daily for 5 days in a
but retinal veins look almost normal.
month for 6 months.
® Retina becomes milky white due to oedema.
® Central part of the macular area
shows cherry-red spot (MCQ)
» Occurs due to vascular choroid
shining through the thin retina of
this region.
» In eyes with a cilioretinal artery,
part of the macular will remain normal
® Blood column within the retinal veins is
segmented (cattle- trucking).
® After a few weeks the oedema subsides,
and atrophic changes occur which
include
» grossly attenuated thread-like arteries
» consecutive optic atrophy
m Management
76
n Retinal tissue cannot survive ischaemia for l a few superficial flame-shaped haemorrhages
more than a few hours. more in the peripheral than the posterior retina
n Immediate lowering of intraocular pressure l mild papilloedema
l intravenous mannitol l mild or no macular oedema.
l intermittent ocular massage. n In late stages (after 6-9 months),
„ It may aid the arterial perfusion and also l sheathing around the main veins
help in dislodging the embolus. l a few cilioretinal collaterals around the disc.
l Even paracentesis of anterior chamber has n Macula may show chronic cystoid oedema in
been recommended for this purpose. moderate
n Vasodilators m Treatment is usually not required.
n inhalation of a mixture of 5 percent carbon m The condition resolves with almost normal vision in
dioxide and 95 percent oxygen about 50 percent cases.
l help by relieving element of angiospasm. m Visual loss in rest of the cases is due to chronic
n Anticoagulants may be helpful in some cases. cystoid macular oedema, for which no treatment is
m Intravenous steroids are indicated in patients with effective
giant cell arteritis. m a course of oral steroids for 8-12 weeks may be
OPHTHALMOLOGY
n Complications effective.
m Rarely, ‘neovascular glaucoma’ may occur as a n Ischaemic CRVO
delayed complication m Ischaemic CRVO (Haemorrhagic retinopathy)
RETINAL VEIN OCCLUSION refers to acute (sudden) complete occlusion
n It is more common than the artery occlusion. of central retinal vein.
n It typically affects elderly patients in sixth or m It is characterised by marked sudden visual loss.
seventh decade of life. m Fundus examination
n Etiology n In early cases reveals
m Pressure on the vein by a sclerotic retinal artery l massive engorgement ,congestion and
where the two share a common adventitia (e.g., tortuousity of retinal veins
just behind the lamina cribrosa and at arteriovenous l massive retinal haemorrhages (almost whole
crossings). fundus is full of haemorrhages giving a
m Hyperviscosity of blood as in ‘splashed-tomato’ appearance)
n Polycythemia l numerous soft exudates
n hyperlipidemia l papilloedema.
CRAO
n macroglobulinemia. l Macular area is full of haemorrhages and is
m Periphlebitis retinae which can be central or peripheral. severely oedematous.
m Raised introcular pressure. n In late stages
n CRVO is more common in patients with l marked sheathing around veins and
primary open-angle glaucoma. collaterals is seen around the disc.
m Local causes are l Neovascularisation may be seen at the disc
n orbital cellulitis (NVD) or in the periphery (NVE).
n facial erysipelas l Macula shows marked pigmentary changes
n cavernous sinus thrombosis. and chronic cystoid oedema.
n Classification m The pathognomic features for differentiating
m Central retinal vein occlusion (CRVO) ischaemic CRVO from non-ischaemic CRVO
n non-ischaemic CRVO (venous stasis retinopathy) are presence of (MCQ)
n ischaemic CRVO (haemorrhagic retinopathy). n relative afferent pupillary defect (RAPD)
m Branch retinal vein occlusion (BRVO) n visual field defects
n Non-ischaemic CRVO n reduced amplitude of b-wave of
m most common clinical variety (75%). electroretinogram (ERG).
m It is characterised by mild to moderate visual m Complications.
loss. n Rubeosis iridis and neovascular glaucoma
m Fundus examination (NVG) occur in more than 50 percent cases within 3
n early cases reveals months (so also called as 90 days
l mild venous congestion and tortuosity glaucoma),(MCQ)
n vitreous haemorrhage
77
n proliferative retinopathy. n It is characteristic of granulomatous uveitis,
m Treatment. n Dalen-Fuchs’ nodules (MCQ)
n Panretinal photocoagulation (PRP) l formed due to proliferation of the pigment
l prevents neovascular glaucoma in patients with epithelium (of the iris, ciliary body and
widespread capillary occlusion. choroid) associated with invasion by the
l Photocoagulation should be carried out when lymphocytes and epitheloid cells.
most of the intraretinal blood is absorbed, n Retina shows perivascular cellular infiltration
which usually takes about 3-4 months. (sympathetic perivasculitis)
n cryo-application,is done if the media is hazy m Clinical picture
n Branch retinal vein occlusion (BRVO) n Exciting (injured) eye.
m It is more common than the central retinal vein l It shows clinical features of persistent low
occlusion. grade plastic uveitis, which include ciliary
m It may occur at the following sites: congestion, lacrimation and tenderness.
n main branch at the disc margin causing l Keratic precipitates may be present at the
hemispheric occlusion back of cornea (dangerous sign).(MCQ)
n major branch vein away from the disc n Sympathizing (sound) eye
OPHTHALMOLOGY
n at A-V crossing causing quadrantic occlusion l It is usually involved after 4-8 weeks of
n small macular or peripheral branch occlusion. injury in the other eye. (MCQ)
m Vision is affected only when the macular area is l Sympathetic ophthalmitis, almost always,
involved. manifests as acute plastic iridocyclitis.
m Treatment. l Prodromal stage.
n Grid photocoagulation may be required in „ sensitivity to light (photophobia) and
patients with chronic macular oedema. transient indistinctness of near objects
n In patients with neovascularisation, scatter (due to weakening of accommodation) are
photocoagulation should be carried out. the earliest symptoms (MCQ)
„ In this stage the first sign may be presence
TOPIC 20 - SYMPATHETIC OPHTHALMITIS
of retrolental flare and cells or the
SYMPATHETIC OPHTHALMITIS
n Sympathetic ophthalmitis presence of a few keratic precipitates

m Sympathetic ophthalmitis is a serious bilateral
(KPs) on back of cornea.(MCQ)
granulomatous panuveitis which follows a l Fully-developed stage.
penetrating ocular trauma. (MCQ) „ typical signs and symptoms consistent with
m The injured eye is called exciting eye and the
acute plastic iridocyclitis
fellow eye which also develops uveitis is called m Treatment
sympathizing eye. n Prophylaxis
m can also occur following an intraocular surgery.
l Early excision of the injured eye.
m Etiology
n When there is hope of saving useful vision, following
n Predisposing factors
steps should be taken:
l It almost always follows a penetrating
l A meticulous repair of the wound using
wound. (MCQ) microsurgical technique should be carried
l Wounds in the ciliary region (the so-called
out
dangerous zone) are more prone to it. l Immediate expectant treatment with
(MCQ) topical as well as systemic steroids and
l Wounds with incarceration of the iris,
antibiotics along with topical atropine
ciliary body or lens capsule are more should be started.
vulnerable. l When the uveitis is not controlled after 2 weeks
l It is more common in children than in adults.
of expectant treatment, i.e., lacrimation,
l It does not occur when actual suppuration
photophobia and ciliary congestion persist and if
develops in the injured eye. (MCQ) KPs appear, this eye should be excised
n Pathogenesis
immediately.
l allergic theory, which postulates that the uveal
n Treatment when sympathetic ophthalmitis
pigment acts as allergen and excites plastic has already supervened
uveitis in the sound eye. l Useless injured eye should be excised at
m Pathology
once
78
„ If the case is seen shortly after the onset l Developmental anomalies of the skull
of inflammation (i.e., during prodromal „ craniofacial dysostosis e.g., oxycephaly
stage) in the sympathizing eye, and the (tower skull).
injured eye has no useful vision, this l Osteopathies
useless eye should be excised at once „ Osteitis deformans, rickets and acromegaly.
l Conservative treatment of sympathetic l Inflammatory conditions:
ophthalmitis on the lines of iridocyclitis for „ Mikulicz’s syndrome
sympathizing eye should be started „ late stage of cavernous sinus thrombosis.
immediately, as follows: l Endocrinal exophthalmos
„ Corticosteroids by all routes, i.e., systemic, „ Thyrotoxic (MCQ)
periocular injections and frequent instillation „ thyrotropic.
of topical drops. l Tumours
„ In severe cases, immunosuppressant „ symmetrical lymphoma
drugs should be started without delay. „ lymphosarcoma
„ Topical atropine. „ secondaries from neuroblastoma(MCQ),
nephroblastoma, Ewing’s sarcoma and
TOPIC 21 - PROPTOSIS
OPHTHALMOLOGY
leukaemic infiltration.
m It is defined as forward displacement of the l Systemic diseases:
eyeball beyond the orbital margins. „ Histiocytosis, systemic amyloidosis,
m Classification xanthomatosis and Wegener’ s
l Proptosis can be divided into following granulomatosis.
clinical groups: n Causes of acute proptosis.
„ Unilateral proptosis l orbital emphysema fracture of the medial
„ Bilateral proptosis orbital wall
„ Acute proptosis l orbital haemorrhage
„ Intermittent proptosis l rupture of ethmoidal mucocele.
„ Pulsating proptosis n Cause of intermittent proptosis.
m ETIOLOGY l This type of proptosis appears and
n Causes of unilateral proptosis include: disappears of its own.
l Congenital conditions l Its common causes are:
PROPTOSIS
„ dermoid cyst (MCQ), congenital cystic „ orbital varix (MCQ)
eyeball, and orbital teratoma. „ periodic orbital oedema
l Traumatic lesions. „ recurrent orbital haemorrhage
l Inflammatory lesions. „ highly vascular tumours.
„ orbital cellulitis, abscess, thrombophlebitis n Causes of pulsating proptosis.
„ panophthalmitis l It is caused by pulsating vascular lesions
„ cavernous sinus thrombosis (proptosis is such as caroticocavernous fistula and saccular
initially unilateral but ultimately becomes aneurysm of ophthalmic artery.
bilateral). l Pulsating proptosis also occurs due to
l Chronic inflammatory lesions transmitted cerebral pulsations in conditions
„ pseudotumours, tuberculoma, gumma and associated with deficient orbital roof.
sarcoidosis. „ congenital meningocele
„ Circulatory disturbances and vascular lesions. „ meningoencephalocele
® orbital varix (MCQ) „ neurofibromatosis
„ Cysts of orbit. m pseudoproptosis is seen in
® hydatid cyst l buphthalmos
® cysticercus cellulosae (MCQ) l axial high myopia
„ Tumours of the orbit. l retraction of upper lid
„ Mucoceles of paranasal sinuses l enophthalmos of the opposite eye
l Frontal (most common), ethmoidal and m Diagnostic findings in various causes of
maxillary sinus are common causes of unilateral Proptosis
proptosis. m abnormal vascular communications in
n Causes of bilateral proptosis include: Caroticocavernous fistula
79
generate a bruit n Task Force of International NGOs, which
m Transillumination is helpful in evaluating anterior has following members:
orbital lesions. n International Agency for Prevention of Blindness (IAPB)
m Orbital lesions may reduce visual acuity n Christopher Blindness Mission (CBM)
m The presence of Marcus Gunn pupil is suggestive n Helen Keller International
of optic nerve compression. n ORBIS International
m Fundoscopy. n Sight Savers International
l Choroidal folds and opticociliary shunts n Al Noor Foundation
may be seen in patients with meningiomas. n International Federation of Ophthalmological Societies
m Ocular motility. (MCQ) is restricted in n Lions Clubs International Foundation
l thyroid ophthalmopathy, n Operation Eye Sight Universal
l extensive tumour growths and neurological deficit. n The Carter Centre
n Exophthalmometry. m Objective of vision 2020.
m It measures protrusion of the apex of cornea n eliminate avoidable blindness by the year
from the outer orbital margin 2020
m A difference of more than 2 mm between the n to reduce the global burden of blindness
OPHTHALMOLOGY
two eyes is considered significant. which currently affects an estimated 45 million

people worldwide.
TOPIC 22 - m Implementation of vision 2020
BLINDNESS CONTROL PROGRAMME n implemented through four phases of five year

plans
n In developed countries n the first one started in 2000 and second in
m 50 percent of all blindness is because of age
2005.
related macular degeneration (ARMD) n The two subsequent phases of implementation
m another 10-20 percent each is because of
will commence from 2010 and 2015,
glaucoma, diabetic retinopathy and cataract. respectively.
n In developing countries m Strategic approaches of Vision 2020: Right to
m frequent causes are cataract, infectious diseases,
Sight (Global prospective) are: (MCQ)
BLINDNESS CONTROL PROGRAMME
xerophthalmia, injuries, glaucoma, and n Disease prevention and control,

onchocerciasis. n Training of eye health personnel
n The major global initiatives taken for prevention of n Strengthening of existing eye care infrastructure,
blindness are: n Use of appropriate and affordable technology
m Global programme for prevention of
n Mobilization of resources.
blindness. m Globally, WHO has identified five major blinding
m Vision 2020: The Right to Sight
eye conditions, for immediate attention to achieve
m Vision for the future (VFTF).
the goals of Vision 2020, which are: (MCQ)
n Global programme for control of blindness n Cataract
m The WHO launched a global programme for
n Childhood blindness
prevention of blindness in 1978. n Trachoma,
m Control strategies suggested by WHO include:
n Refractive errors and low vision,
n Assessment of common blinding disorders
n Onchocerciasis
at local, regional and national levels. n Cataract
n Establishment of national level programmes
m Cataract remains the single largest cause of
for control of blindness suited to the national blindness. (MCQ)
and local needs. m Aim under ‘Vision 2020’ is to eliminate avoidable
n Training of eye care providers.
blindness due to cataract, i.e., to decrease the number
n Operational research to improve and apply
of cataract blinds in the world from 19 million to
appropriate technology. zero by the year 2020.
n Vision 2020: the right to sight n Childhood blindness
m a global initiative launched by WHO in Geneva
m The main causes include: (MCQ)
on Feb. 18,1999 n Vitamin A deficiency
m Partners of Vision 2020: Right to Sight include:
n Measles
n World Health Organisation (WHO),
n Conjunctivitis
80
n ophthalmia neonatorum n Refraction services to be made available to
n congenital cataract individuals identified with significant refractive
n retinopathy of prematurity (ROP). errors.
m Aim is to eliminate avoidable causes of n Ensure optical services to provide affordable
childhood blindness by the year 2020. spectacles for individuals with significant
m Strategies and activities under the global refractive errors.
initiative vision 2020 include n Low vision services and low vision aids to
n Elimination of preventable blindness by: (MCQ) be provided for all those in need.
l Measles immunisation, n Onchocerciasis (river blindness)
l Vitamin A supplementation m Aim is to eliminate blindness due to
l Monitoring use of oxygen in the premature onchocerciasis by the year 2020.
new born, m Target is to develop ‘National Onchocerciasis
l Avoidance of harmful traditional practices, Control Programme’ with satisfactory coverage
l Promoting school screening programmes in all the 37 countries where disease is endemic.
for diagnosis and management of common m Strategy is to introduce community directed
conditions like refractive errors and treatment with annual doses of Mectizan
OPHTHALMOLOGY
trachoma in endemic areas (ivermectin).
l Promoting eye health education in schools. n VISION FOR THE FUTURE (VFTF)
n Management of surgically avoidable causes of m International Ophthalmology Strategic Plan
childhood blindness such as to Preserve and Restore Vision11
l Cataract m launched in Feb 2001
l Glaucoma m Implementation of this program isdone by
l retinopathy of prematurity (ROP) International Council of Ophthalmology
n Trachoma blindness (ICO) by working closely with other international,
m Trachoma is a leading cause of preventable supranational and national organizations.
blindness worldwide m It is parallel to and complementary of ‘Vision
m disease accounts for nearly one-sixth of the 2020’.

global burden of blindness m Care is being taken to avoid duplication.
m SAFE strategy: (MCQ) m Top priorties for action of this programme are:
n Surgery to correct lid deformity and prevent n Enhancement of ophthalmology residency
blindness, training around the world, particularly
n Antibiotics for acute infections and community through definition of principles, guidelines and
control, curricula.
n Facial hygiene, and n Development of model guidelines and
n Environmental change including recommendations for ophthalmic clinical
l Improved access to water and sanitation care in critical disease areas.
l health education. n Dissemination of sample curricula for
m Elimination of blindness due to trachoma is training of medical students and allied
considered feasible, eradication of trachoma is health personnel.
no n Advocacy and support for ‘Vision 2020: Right
m W.H.O. has organized an Alliance for Global to Sight’ , particularly by encouraging national
Elimination of Trachoma by the year 2020 ophthalmologic societies to support the
(GET 2020). initiative and become involved.
n Refractive errors and low vision n Helping national ophthalmologic societies
m Aim is to eliminate visual impairment (visual develop more effective organizations.
acuity less than 6/18)(MCQ) and blindness n National Programme for Control of Blindness
due to refractive errors or other causes of low (NPCB) , India
vision. m India was the first country in the world to launch
m Strategies recomended under ‘Vision 2020’ the ‘National Programme for Control of Blindness
initiative include: (NPCB)’ in the year 1976
n Screening to identify individuals with poor vision m 100 percent centrally sponsored programme
which can be improved by spectacles or other
optical devices.
81
m it incorporated the earlier trachoma control l Rehabilitation training of visually
programme started in the year 1963 and vitamin handicapped.
A prophylaxis programme launched in 1970. l General survey for prevalence of various
m Objectives eye diseases.
m In 1976, the NPCB was launched with following n Establishment of permanent infrastructure
goals: l The ultimate goal of NPCB is to establish
m To provide comprehensive eye care facilities for permanent infrastructure to provide eye
primary, secondary and tertiary levels of eye care services.
health care. l It is being done in three-tier system i.e.,
m To reduce the prevalence of blindness in peripheral, intermediate and central level.
population from 1.38% (ICMR 971-74) to 0.31 l Establishment of peripheral sector for
by 2000 AD. primary eye care.
m The programme got a major flip drug 1994-2001 „ A wide range of eye conditions can be
when World Bank assisted “Cataract Blindness treated/prevented at the grass- root
Control Project” was launched to reduce the level by locally-trained primary health workers
cataract back-log 7 States which were identified who are the first to make contact with the
OPHTHALMOLOGY
to have the highest prevalence of cataract community.

blindness by WHO- NPCB survey (1986-89). l Establishment of intermediate sector for
(MCQ) These, in descending order, are: Uttar ‘secondary eye care’.
Pradesh, Tamil Nadu, Madhya Pradesh, Maharashtra, „ Secondary eye care involves definitive
Andhra Pradesh, Rajasthan and Orissa. management of common blinding
m Plan of action and activities conditions such as cataract, glaucoma, trichiasis,
m The plan of action and activities of ‘National entropion and ocular trauma.
Programme for Control of Blindness (NPCB) in „ The intermediate sector for secondary eye care is
India can be described under three headings: being strengthened by development of
n Basic programme components, diagnostic and treatment facilities at
n Programme organization, and district and subdivisional levels under
n Strategic plan for ‘Vision 2020: Right to Sight’ the charge of an eye specialist.
in India. l Establishment of central level for ‘tertiary

m Basic programme components eye care’.
n Extension of eye care services. „ Tertiary eye care services include the
n Establishment of permanent infrastructure. sophisticated eye care such as retinal
n Intensification of eye health education. detachment surgery, laser treatment for
n Extension of eye care services various retinal and other ocular disorders,
l It is being done through the state and district corneal grafting and other complex
mobile units forms of management not available in
l by adopting an ‘eye camp approach’ secondary eye care centres.
l by enlisting the participation of voluntary „ The central level for tertiary eye care services
organisations. and development of manpower is being
l The following facilities are being provided in strengthened by upgradation of eye
remote areas: departments of state medical colleges
l Medical and surgical treatment for the and by establishment of regional institutes
prevention and control of common eye of ophthalmology (RIO).
diseases. l Establishment of an apex National
l Eye camp approach is of great help in Institute of Ophthalmology.
reducing the back- log of cataract by mass „ An apex National Institute of
surgeries. Ophthalmology has been established at Dr.
l Recent emphasis is on reach-in-approach. Rajendra Prasad Centre for Ophthalmic
l Detection and correction of refractive errors. Sciences, New Delhi.
l Thorough ocular examination including vision „ This institute has been converted into a centre
of school children for early detection of of excellence to provide overall leadership,
eye diseases and promoting ocular health. supervision and guidance in technical matters
82
to all services and technical institutions l Common causes of childhood blindness are
under the programme. vitamin A deficiency, measles,
n Intensification of eye health education conjunctivitis, ophthalmia neonatorum,
l Intensification of eye health education is being done injuries, congenital cataract, retinopathy
through mass communication media of prematurity (ROP), and childhood
(television talks, radio talks, films, seminars and glaucoma.(MCQ)
books), school teachers, social workers, community l Refractive errors are the commonest cause of
leaders, mobile ophthalmic units, and existing medical visual impairment in children. (MCQ)
and paramedical staff l Aim is to eliminate avoidable causes of
n Strategic plan for vision 2020 : the right to sight childhood blindness by the year 2020.
in india l Strategies and activities under Vision 2020:
m The Government of India has adopted ‘Vision Right to Sight initiative in India include:
2020: Right to Sight’ under ‘National Programme „ Detection of eye disorders.
for Control of Blindness’ at a meeting held in Goa „ Following schedule of ophthalmic
on October 10- 13, 2001 and constituted a examination of children is recommended
working group. to identify early childhood disorders,
OPHTHALMOLOGY
m The draft plan of action submitted by the refractive errors, squint, amblyopia and
‘Working Group’ to the Ministry of Health and corneal diseases:
Family Welfare Govt. of India in August, 2002 ® At the time of primary immunization,
includes following strategies: ® At school entry
n Strengthening advocacy ® Periodic check up every 3 years for
n Reduction of disease burden normal and every year for those with defects.
n Human resource development, „ Preventable childhood blindness to be
n Eye care infrastructure development taken care of through cost effective
n Reduction of disease burden (disease-specific measures:
approach) ® Prevention of xerophthalmia is of utmost
n Target diseases identified for intervention under value in preventing childhood blindness

‘Vision 2020’ initiative in India include:(MCQ) ® Prevention and early treatment of trachoma by
l Cataract, active intervention
l Childhood blindness, ® Refractive errors to be corrected at
l Refractive errors and low vision primary eye care centres.
l Corneal blindness, ® Childhood glaucomas to be treated promptly.
l Diabetic retinopathy, ® Harmful traditional practics need to be
l Glaucoma avoided.
l Trachoma (focal) ® Prevention of ROP by proper screening
n Cataract and monitoring use of oxygen in
l Cataract continues to be the single largest premature new borns.
cause of blindness. „ Curable childhood blindness due to
l Targets and strategies include: cataract, ROP, corneal opacity and other
„ To increase the cataract surgery rate to 4500 causes to be taken care of by the experts at
per million per year by 2005, 5000 by 2010, secondary and tertiary level eye care services.
5500 by 2015 and 6000 by 2020. n Refractive errors and low vision
„ To improve the visual outcome of l Refraction services to be available in all primary
surgery to conform to standards set by health centres by 2010. Availability of low-
WHO (i.e., 80% to have visual outcome 6/18 or cost, good quality spectacles for children
>6/18 after surgery). to be insured.
„ IOL surgery for >80% by the year 2005 l Low vision service centres
and for all by the year 2010. „ to be established at 150 tertiary level eye
„ YAG capsulotomy services at all district care institutions
hospitals by 2010. „ 50 such centres are to be developed by
„ Grant-in aid for cataract surgery may 2010, another 50 by 2015 and the final 50
continue to be released through DBCS. by 2020.
n Childhood blindness n Glaucoma
83
l opportunistic glaucoma screening (case „ Each advanced tertiary level center of
detection) is done by tonometry and fundus excellence will cater to a population of
examination: 50 millions.
l Opportunisitic screening at eye care institutions should
be done in TOPIC 23 - AMBLYOPIA
„ all persons above the age of 35 years
„ those with diabetes mellitus m Amblyopia, by definition, refers to a partial loss
„ those with family history of glaucoma. of vision in one or both eyes, in the absence of
l Community based referral by multi-purpose any organic disease of ocular media, retina and
workers of all persons with dimunition of vision, visual pathway.
coloured haloes, rapid change of glasses, ocular pain m Pathogenesis.
and family history of glaucoma. l critical period of visual development
l Opportunistic screening at eye camps in (birth to 6 years of age).
all patients above the age of 35 years. l The most sensitive period for development
m Human resource development of amblyopia is first six months of life
n Mid-Level Ophthalmic Personnel l it usually does not develop after the age of 6
(MLOP). years.
l Broadly two streams of such personnels are l Amblyogenic factors include :
AMBLYOPIA
envisaged: „ Visual (form sense) deprivation as occurs

l Hospital-based MLOP. in anisometropia,
„ These include ophthalmic nurses, „ Light deprivation e.g., due to congenital
ophthalmic technicians, optometrists, cataract
and orthoptists etc. „ Abnormal binocular interaction e.g., in
l Community-based MLOP strabismus.
„ These include those with out- reach/field m Types
functions such as primary eye care l Strabismic amblyopia
workers and ophthalmic assistants. „ results from prolonged uniocular
m Eye care infrastructure development
suppression in children with unilateral

n Based on the recommendations of WHO, there „ constant squint who fixate with normal
is need to develop the infrastructure pyramid eye.
which includes l Stimulus deprivation amblyopia (old term:
n Primary level Vision Centres. amblyopia ex anopsia)
„ There is a need to develop 20000 vision „ develops when one eye is totally
centres excluded from seeing early in life as, in
„ each with one Ophthalmic Assistant or equivalent ® congenital or traumatic cataract,
(Community based MLOP) covering a ® complete ptosis
population of 50000 ® dense central corneal opacity.
n Service centres at secondary level l Anisometropic amblyopia
„ each with two ophthalmologists and 8 „ occurs in an eye having higher degree of
paramedics (Hospital based MLOP) refractive error than the fellow eye.
„ covering a population of 500000 „ It is more common in aniso- hypermetropic
„ One eye care manager will be required than the anisomyopic children.
at each service centre. „ Even 1-2D hyper metropic
n Training Centres. anisometropia may cause amblyopia while
„ There is a need to develop 200 ‘Training upto 3D myopic anisometropia usually
Centres’ does not cause amblyopia.
„ for the training of Ophthalmologists. l Isoametropic amblyopia
„ Each tertiary level training centre will cater „ bilateral amblyopia occurring in children
to a population of 5 million. with bilateral uncorrected high
n Centre of Excellence (COE). refractive error.
„ There is need to develop 20 COE with l Meridional amblyopia
well developed all sub specialities of „ occurs in children with uncorrected
Ophthalmology. astigmatic refractive error.
84
„ It is a selective amblyopia for a specific in proteins and vitamin B complex; and thence
visual meridian. also labelled as ‘tobacco-alcohol-amblyopia.
m Clinical characteristics of an amblyopic eye are: n The toxic agent involved is cyanide found in
l Visual acuity is reduced. tobacco.
l Recognition acuity is more affected than resolution n usually occurs in men between 40 and 60 years
acuity. n characterised by bilateral gradually
l Effect of neutral density filter. progressive impairment in the central vision.
„ Visual acuity when tested through neutral Patients usually complain of fogginess and
density filter improves by one or two lines in difficulty in doing near work.
amblyopia and decreases in patients with organic n Visual field examination reveals bilateral
lesions. centrocaecal scotomas with diffuse margins
l Crowding phenomenon is present in amblyopics which are not easily defined.
„ visual acuity is less when tested with n The defect is greater for red than the white
multiple letter charts (e.g., Snellen’s colour.
chart) than when tested with single m Ethyl alcohol amblyopia
charts (optotype). n It usually occurs in association with tobacco
OPHTHALMOLOGY
l Fixation pattern may be central or eccentric. amblyopia.
„ Degree of amblyopia in eccentric fixation n However, it may also occur in non-smokers,
is proportionate to the distance of the who are heavy drinkers suffering from
eccentric point from the fovea. chronic gastritis.
l Colour vision is usually normal, may be affected n The optic neuritis occurs along with the
in deep amblyopia with vision below 6/ peripheral neuritis of chronic and debilitated
36. alcoholics.
m Treatment of amblyopia m Methyl alcohol amblyopia
l It should be started as early as possible n Unlike ethyl alcohol (which produces chronic
(younger the child, better the prognosis). Occlusion amblyopia), poisoning by methyl alcohol
therapy (methanol) is typically acute, usually resulting
l occlusion of the sound eye, to force use of in optic atrophy and permanent blindness.
amblyopic eye is the main stay in the treatment n Etiology.
of amblyopia. l It usually occurs due to intake of wood
AMBLYOPIA
l However, before the occlusion therapy is alcohol or methylated spirit in cheap
started, it should be ensured that: adulterated or fortified beverages.
„ Opacity in the media (e.g., cataract), if l Sometimes, it may also be absorbed by
any, should be removed first, and inhalation of fumes in industries, where
„ Refractive error, if any, should be fully methyl alcohol is used as a solvent.
corrected. n Methyl alcohol is metabolised very slowly and
l Simplified schedule for occlusion therapy depending up thus stays for a longer period in the body.
on the age is as below: n It is oxidised into formic acid and
„ the occlusion should be done in formaldehyde in the tissues. (MCQ)
® Upto 2 years, 2:1, i.e., 2 days in sound n These toxic agents cause oedema followed by
eye and one day in amblyopic eye. degeneration of the ganglion cells of the
® At the age of 3 years, 3:1, retina, resulting in complete blindness due to
® At the age of 4 years, 4:1, optic atrophy. (MCQ)
® At the age of 5 years, 5:1, and n Presence of a characteristic odour due to excretion
® After the age of 6 years, 6:1 of formaldehyde in the breath or sweat is a
l Duration of occlusion should be helpful diagnostic sign.
„ until the visual acuity develops fully, or m Quinine amblyopia
„ there is no further improvement of vision n It may occur even with small doses of the
for 3 months. drug in susceptible individuals.
Toxic amblyopias n Fundus examination reveals retinal oedema,
n Tobacco amblyopia marked pallor of the disc and extreme
m It typically occurs in men who are generally pipe attenuation of retinal vessels.
smokers, heavy drinkers and have a diet deficient n Visual fields are markedly contracted.
85
m Ethambutol amblyopia n It constitute the treatment of congenital NLD
n Sometimes, it may cause toxic optic block, up to 6-8 weeks of age. (MCQ)
neuropathy. n Massage increases the hydrostatic pressure
n usually occurs in patients who have associated in the sac and helps to open up the
alcoholism and diabetes. membranous occlusions.
n There may occur optic neuritis with typical n It should be carried out at least 4 times a day
central scotoma. to be followed by instillation of antibiotic drops.
n Involvement of optic chiasma may result in a n It cures obstruction in about 90 percent of
true bitemporal hemianopia. the infants.
n Patients usually complain of reduced vision m Lacrimal syringing (irrigation) with normal saline and
or impairment of colour vision during the antibiotic solution.
course of antitubercular treatment. n It should be added to the conservative treatment
n Fundus examination may reveal signs of papillitis. if the condition is not cured up to the age
n In most of the cases recovery occurs of 2 months.
following cessation of the intake of drug. n Syringing may be carried out once or twice a
week.
OPHTHALMOLOGY
TOPIC 24 - DACRYOCYSTITIS m Probing of NLD with Bowman’s probe.

n It should be performed, in case the condition is
CONGENITAL DACRYOCYSTITIS not cured by the age of 3-4 months. Some
n It is an inflammation of the lacrimal sac occurring surgeons prefer to wait till the age of 6
in newborn infants months.
n also known as dacryocystitis neonatorum. n It is usually performed under general
n Etiology anaesthesia.
m It follows stasis of secretions in the lacrimal n In case of failure, it may be repeated after an
sac due to congenital blockage in the nasolacrimal duct. interval of 3- 4 weeks.
m As many as 30 percent of newborn infants are m Intubations with silicone tube
believed to have closure of nasolacrimal duct at n performed if repeated probings are failure.
birth n The silicone tube should be kept in the NLD
m It occurs mostly due to ‘membranous occlusion’
DACRYOCYSTITIS
for about six months.

at its lower end, near the valve of Hasner. m Dacryocystorhinostomy(DCR)operations:
m Common bacteria associated are staphylococci, n When the child is brought very late or repeated
pneumococci and streptococci. probing is a failure, then conservative treatment
n Clinical picture by massaging, topical antibiotics and intermittent
m Epiphora lacrimal syringing should be continued till the
n usually develop after seven days of birth. age of 4 years.
(MCQ) n After this, DCR operation should be
n It is followed by copious mucopurulent performed.
discharge from the eyes. n Chronic dacryocystitis
m Regurgitation test is usually positive, m Etiology
n When pressure is applied over the lacrimal sac n Predisposing factors
area, purulent discharge regurgitates from the l Age. It is more common between 40 and 60
lower punctum. years of age.
m Swelling on the sac area l Sex. The disease is predominantly seen in
n Differential diagnosis females (80%) probably due to
m other causes of watering in early childhood comparatively narrow lumen of the bony
n ophthalmia neonatorum canal.
n congenital glaucoma. l Race.
n Complications „ It is rarer among Negroes than in Whites;
m complicated by recurrent conjunctivitis, acute on chronic as in the former NLD is shorter, wider and
dacryocystitis, lacrimal abscess and fistulae formation. less sinuous.
n Treatment l Heredity.
m Massage over the lacrimal sac area and topical antibiotics l more common in low socio-economic
group.
86
l Poor personal hygiene. TOPIC 25 - HYPERMETROPIA
n Factors responsible for stasis of tears in
n HYPERMETROPIA
lacrimal sac
m Hypermetropia (hyperopia) or long-sightedness
l Anatomical factors,which retard drainage of tears
is the refractive state of the eye wherein parallel
include: comparatively narrow bony canal,
rays of light coming from infinity are focused
partial canalization of membranous NLD and
behind the retina with accommodation being at rest
excessive membranous folds in NLD.
m Thus, the posterior focal point is behind the retina,
l Foreign bodies in the sac.
which therefore receives a blurred image.
l Excessive lacrimation
m Etiology
l Mild grade inflammation of lacrimal sac due to
n Axial hypermetropia
associated recurrent conjunctivitis
l Commonest form.
l Obstruction of lower end of the NLD by nasal
l In this condition the total refractive power
diseases such as polyps, hypertrophied inferior
of eye is normal but there is an axial
concha, marked degree of deviated nasal
shortening of eyeball.
septum, tumours and atrophic rhinitis causing
l About 1–mm shortening of the antero-
stenosis
posterior diameter of the eye results in 3
OPHTHALMOLOGY
m Dacryocystography reveals block in NLD.(MCQ)
dioptres of hypermetropia.
m Complications
n Curvatural hypermetropia
n Chronic intractable conjunctivitis
l condition in which the curvature of cornea,
n acute on chronic dacryocystitis.
lens or both is flatter than the normal results
n Ectropion of lower lid, maceration and
in a decrease in the refractive power of
eczema of lower lid skin due to prolonged
eye.
watering.
l About 1 mm increase in radius of curvature
n Simple corneal abrasions may become
results in 6 dioptres of hypermetropia.
infected leading to hypopyon ulcer.
n Index hypermetropia
n If an intraocular surgery is performed in the
l occurs due to decrease in refractive index
presence of dacryocystitis, there is high risk
of the lens in old age.
of developing endophthalmitis. Because of
l It may also occur in diabetics under
HYPERMETROPIA
this, syringing of lacrimal sac is always done before
treatment.
attempting any intraocular surgery. (MCQ)
n Positional hypermetropia results from posteriorly
m Treatment
placed crystalline lens.
n Conservative treatment by repeated lacrimal
n Absence of crystalline lens
syringing.
l either congenitally or acquired (following
n Dacryocystorhinostomy (DCR). (MCQ)
surgical removal or posterior dislocation)
l It is operation of choice as it re-establishes
leads to aphakia — a condition of high
the lacrimal drainage.
hypermetropia.
n Dacryocystectomy (DCT).
m Clinical types
l It should be performed only when DCR is
l Simple or developmental hypermetropia
contraindicated
„ commonest form
n Indications of DCT include:
„ results from normal biological variations
l Too young (less than 4 years) or too old
in the development of eyeball.
(more than 60 years) patient.
„ It includes axial and curvatural hypermetropia.
l Markedly shrunken and fibrosed sac
l Pathological hypermetropia
l Tuberculosis, syphilis, leprosy or mycotic
„ results due to either congenital or
infections of sac.
acquired conditions of the eyeball which
l Tumours of sac.
are outside the normal biological variations
l Gross nasal diseases like atrophic rhinitis
of the development.
l An unskilled surgeon, because it is said that, a
® Index hypermetropia (due to acquired
good ‘DCT’ is always better than a badly
cortical sclerosis),
done ‘DCR’.
® Positional hypermetropia (due to posterior
n Conjunctivodacr yocystorhinostomy
subluxation of lens),
(CDCR).
l It is performed in the presence of blocked
87
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® phakia (congenital or acquired absence of l Defective vision with asthenopic symptoms.
lens) „ Occur when the amount of hypermetropia
® Consecutive hypermetropia (due to surgically is such that it is not fully corrected by
over-corrected myopia). the voluntary accommodative efforts
l Functional hypermetropia l Defective vision only.
„ results from paralysis of accommodation „ When the amount of hypermetropia is very
„ seen in patients with third nerve paralysis high, the patients usually do not
and internal ophthalmoplegia. accommodate (especially adults) and
n Total hyper metropia = latent + manifest there occurs marked defective vision for near and
(facultative + absolute). distance.
m Total hypermetropia n Signs
n total amount of refractive error, which is l Size of eyeball may appear small as a whole.
estimated after complete cycloplegia with atropine l Cornea may be slightly smaller than the
n It consists of latent and manifest hypermetropia. normal.
m Latent hypermetropia l Anterior chamber is comparatively shallow.
n amount of hypermetropia (about 1D) which l Fundus examination reveals
OPHTHALMOLOGY
is normally corrected by the inherent tone of ciliary „ a small optic disc

muscle. ® which may look more vascular with
n The degree of latent hypermetropia is high in ill-defined margins
children and gradually decreases with age. ® simulate papillitis (though there is no
n The latent hypermetropia is disclosed when swelling of the disc, and so it is called
refraction is carried after abolishing the pseudopapillitis).
tone with atropine. „ The retina as a whole may shine due to
m Manifest hypermetropia i greater brilliance of light reflections
n remaining portion of total hypermetropia, (shot silk appearance).
which is not corrected by the ciliary tone. l A-scan ultrasonography (biometry) may reveal a
n It consists of two components, the facultative short antero-posterior length of the
and the absolute hypermetropia. eyeball.
HYPERMETROPIA
l Facultative hypermetropia constitutes that part m Complications

which can be corrected by the patient’s n Recurrent styes, blepharitis or chalazia
accommodative effort. l occur due to infection introduced by repeated rubbing
l Absolute hypermetropia is the residual part of of the eyes, which is often done to get relief
manifest hypermetropia which cannot be from fatigue and tiredness.
corrected by the patient’s n Accommodative convergent squint may develop in
accommodative efforts. children (usually by the age of 2-3 years) due to
m Clinical picture excessive use of accommodation.
n Symptoms n Amblyopia may develop in some cases.
l Asymptomatic. l anisometropic (in unilateral hypermetropia)
„ A small amount of refractive error in l strabismic (in children developing accommodative
young patients can be asymptomatic squint)
l Asthenopic symptoms. l ametropic (seen in children with uncorrected
„ Occur even when the amount of bilateral high hypermetropia).
hypermetropia is fully corrected n Predisposition to develop primary narrow angle glaucoma.
„ Occur due to sustained accommodative l The eye in hypermetropes is small with a
efforts patient develops asthenopic comparatively shallow anterior chamber.
symptoms. Due to regular increase in the size of the lens
„ These include with increasing age, these eyes become prone
® tiredness of eyes to an attack of narrow angle glaucoma.
® frontal or fronto-temporal headache l This point should be kept in mind while
® watering instilling mydriatics in elderly hypermetropes.
® mild photophobia. n Treatment
„ associated with near work m Optical treatment
„ increase towards evening.
88
n prescribe convex (plus) lenses, so that the light TOPIC 26 - MYDRIATICS
rays are brought to focus on the retina
n Fundamental rules for prescribing glasses in n Anti-glaucoma drugs
hypermetropia include: m Classification
l Total amount of hypermetropia should n Parasympathomimetic drugs (Miotics)
always be discovered by perfor ming n Sympathomimetic drugs (Adrenergic agonists)
refraction under complete cycloplegia. n B?t?-blockers
l The spherical correction given should be n Carbonic anhydrase inhibitors
comfortably acceptable to the patient. However, n Hyperosmotic agents
the astigmatism should be fully corrected. n Prostaglandins
l Gradually increase the spherical correction n Calcium channel blockers
at 6 months interval till the patient accepts m Antiglaucoma drugs: Mechanism of lowering
manifest hypermetropia. IOP -Summary
l In the presence of accommodative n Drugs which increase trabecular outflow
convergent squint, full correction should be l Miotics (e.g., pilocarpine)
given at the first sitting. l Epinephrine
OPHTHALMOLOGY
l If there is associated amblyopia, full correction l Dipivefrine
with occlusion therapy should be started. l Bimatoprost
m Modes of prescription of convex lenses n Drugs which increase uveoscleral outflow
l Spectacles are most comfortable, safe and l Prostaglandins (latanoprost)
easy method of correcting hypermetropia. l Epinephrine
l Contact lenses are indicated in unilateral l Dipivefrine
hypermetropia (anisometropia). l Brimonidine
m Refractive surgery for hyperopia l Apraclonidine
n It should be performed after 20 years of age. n Drugs which decrease aqueous production
n In general, refractive surgery for hyperopia is l Carbonic anhydrase inhibitors
not as effective or reliable as for myopia. „ acetazolamide, dorzolamide
n Holmium laser thermoplasty l Alpha receptor stimulators in ciliary process
l used for low degree of hyperopia. „ epinephrine, dipivefrine, clonidine, brimoni-
MYDRIATICS
l laser spots are applied in a ring at the dine, apraclonidine.
periphery to produce central steepening l Beta blockers (e.g., timolol, betaxolol,
l Regression effect and induced levobunolol)
astigmatism are the main problems. n Hyperosmotic agents
n Hyperopic PRK l glycerol, mannitol, urea
l Done using excimer laser m Parasympathomimetic drugs (Miotics)
l Regression effect and prolonged epithelial healing are n Depending upon the mode of action, these can
the main problems encountered. be classified as follows:
n Hyperopic LASIK l Direct-acting or agonists
l effective in correcting hypermetropia upto +4D. „ pilocarpine.
n Conductive keratoplasty (CK)
l Indirect-acting parasympathomimetics or cholinesterase
l nonablative and nonincisional procedure
inhibitors:
l cornea is steepened by collagen shrinkage
„ Reversible anticholinesterases.
through the radiofrequency energy
® physostigmine
l This technique is effective for correcting
„ irreversible anticholinesterases.
hyperopia of upto 3D.
® echothiophate iodide
® demecarium
® diisopropyl-fluoro-phosphate, DFP3
„ Dual-action parasympathomimetics
® act as both a muscarinic agonist as well

as a weak cholinesterase inhibitor
® carbachol.
89
n Mechanism of action – How miotics reduce ® Except in very darkly pigmented irides
the intraocular pressure (IOP) maximum effect is obtained with a 4
l In primary open-angle glaucoma percent solution.
„ enhance the aqueous outflow facility. ® In POAG, therapy is usually initiated with
„ cause changes in the trabecular 1 percent concentration.
meshwork produced by a pull exerted on ® The onset of action occurs in 20 minutes
the scleral spur by contraction of the longitudinal ® peak in 2 hours
fibres of ciliary muscle. ® duration of effect is 4-6 hours.
l In primary angle-closure glaucoma ® Therefore, the eyedrops are usually
„ these reduce the IOP due to their miotic prescribed every 6 or 8 hourly
effect by opening the angle. l Carbachol
„ The mechanical contraction of the pupil „ It is a dual-action (agonist as well as weak
moves the iris away from the trabecular meshwork. cholinesterase inhibitor) miotic.
n Side-effects „ It is a very good alter native to
l Systemic side-effects pilocarpine in resistant or intolerant cases.
„ bradycardia, increased sweating, diarrhoea, Echothiophate iodide (Phospholine
OPHTHALMOLOGY
excessive salivation and anxiety. iodide).

„ The only serious complication noted with „ It is a long acting cholinesterase
irreversible cholinesterase inhibitors is inhibitor.
‘scoline apnoea’, i.e., inability of the patient l Demecarium bromide
to resume normal respiration after termination of l Physostigmine (eserine).
general anaesthesia. m Sympathomimetic drugs
l Local side-effects n Classification
„ more frequently seen with long-acting l Both alpha and beta-receptor stimulators
miotics (i.e. irreversible cholinesterase „ epinephrine.
inhibitors). l Direct alpha-adrenergic stimulators
„ problems due to miosis itself „ norepinephrine
® reduced visual acuity in the presence of polar „ clonidine hydrochloride.
cataracts l Indirect alpha-adrenergic stimulators
MYDRIATICS
® impairment of night vision „ pargyline.

® generalized contraction of visual fields l Beta-adrenergic stimulator
„ spasm of accommodation may cause „ isoproterenol
® myopia and frontal headache n Mechanisms of action
® retinal detachment l Increased aqueous outflow results by virtue
® lenticular opacities of both alpha and beta-receptor stimulation.
® iris cyst formation l Decreased aqueous humour production
® mild iritis occurs due to stimulation of alpha-receptors in the
® lacrimation and follicular conjunctivitis. ciliary body.
n Preparations n Side-effects
l Pilocarpine l Systemic side-effects include hypertension,
„ It is a direct - acting para tachycardia, headache, palpitation, tremors,
sympathomimetic drug. nervousness and anxiety.
„ Indications l Local side-effects are burning sensation, reactive
® Primary open-angle glaucoma hyperaemia of conjunctiva, conjunctival
® Acute angle-closure glaucoma; pigmentation, allergic blepharo
® Chronic synechial angle-closure conjunctivitis, mydriasis and cystoid
glaucoma. macular oedema (in aphakics).
„ Contraindications: n Preparations
® inflammatory glaucoma, l Epinephrine.
® malignant glaucoma and known allergy. „ direct-acting sympathomimetic drug
„ Available preparations and dosage „ stimulates both alpha and beta- adrenergic
® Eyedrops are available in 1%, 2% and 4% receptors.
strengths. „ Indications
90
® management of POAG l Betaxolol is the beta blocker, of choice in
® useful in most of the secondar y patients at risk for pulmonary diseases (MCQ)
glaucomas. n Additive effects.
l Dipivefrine l Beta-blockers have very good synergistic
„ It is a prodrug effect when combined with miotics
„ converted into epinephrine after its n Preparations
absorption into the eye. l Timolol.
„ It is more lipophilic than epinephrine and „ It is a non-selective beta-1 and beta-2
thus its corneal penetration is increased by 17 times. blocker.
l Clonidine hydrochloride. „ ‘Short-term escape’
„ a centrally - acting systemic antihy- ® implies marked initial fall in IOP,
pertensive agent followed by a transient rise with
„ causes stimulation of alpha-receptors in continued moderate fall in IOP.
the ciliary body. „ ‘Long-term drift’
„ lower the IOP by decreasing aqueous ® implies a slow rise in IOP in patients
humour production who were well controlled with many months of
OPHTHALMOLOGY
l Brimonidine therapy.
„ a selective alpha-2 adrenergic agonist l Betaxolol.
„ lowers IOP by decreasing aqueous production and „ It is a cardioselective beta-blocker
enhancing uveoscleral outflow „ can be used safely in patients prone to
l Apraclonidine (0.5%, 1%). attack of bronchial asthma; an advantage
„ It is also alpha-2 adrenergic agonist like over timolol.
brimonidine. l Levobunolol
„ It is an extremely potent ocular l Carteolol.
hypotensive drug „ similar to timolol except that it induces
„ commonly used prophylactically for comparatively less bradycardia.
prevention of IOP elevation following l Metipranolol
laser trabeculoplasty, YAG laser m Carbonic anhydrase inhibitors (CAIs)
iridotomy and posterior capsulotomy. n These are potent and most commonly used
MYDRIATICS
m Beta-adrenergic blockers systemic antiglaucoma drugs.
n the most frequently used antiglaucoma drugs. n Mechanism of action.
n commonly used preparations are timolol and l lower the IOP by reducing the aqueous
betaxolol. humour formation.
n Mechanism of action. l Indications.
l Timolol and levobunolol are non-selective l These are used as additive therapy for short
beta-1 (Cardiac) and beta-2 (smooth term in the management of all types of acute
muscle, pulmonary) receptor blocking and chronic glaucomas.
agents. l Their long-term use is reserved for patients
l Betaxolol has 10 times more affinity for beta- with high risk of visual loss, where all other
1 than beta-2 receptors. treatments fail.
l The drugs timolol and levobunolol lower n Side-effects.
IOP by blockade of beta-2 receptors in the ciliary l Unfortunately, 40-50 percent of patients are
processes, resulting in decreased aqueous production. unable to tolerate CAIs for long term
n Indications. because of various disabling side-effects.
l Unless contraindicated due to systemic l Paresthesias of the fingers, toes, hands, feet
diseases, beta- blockers are frequently used as and around the mouth are experienced by
the first choice drug in POAG and all most of the patients. However, these are
secondary glaucomas. transient and of no consequence.
n Contraindications l Urinary frequency
l bronchial asthma, emphysema, COPD, heart „ complained of by most patients due to the
blocks, congestive heart diuretic effect.
l failure or cardiomyopathy l Serum electrolyte imbalances may occur
with higher doses of CAIs.
91
„ Bicarbonate depletion leading to metabolic l These are used as additive therapy for rapidly
acidosis. lowering the IOP in emergency situations, such as
® This is associated with ‘malaise acute angle-closure glaucoma or
symptom complex’, which includes: secondary glaucomas with very high IOP.
malaise, fatigue, depression, loss of (MCQ)
libido, anorexia and weight loss. l They are also used as a prophylactic measure
® Treatment with sodium bicarbonate or prior to intraocular surgery.
sodium acetate may help to minimize n Preparations
this situation in many patients l Glycerol.
„ Potassium depletion. „ It is metabolised to glucose in the body.
® occur in patients simultaneously getting Thus, its repeated use in diabetics is not
corticosteroids, aspirin or thiazide recommended.
diuretics. l Mannitol.
„ Serum sodium and chloride „ safe in diabetics
® may be transiently reduced „ it should be used cautiously in hypertensive
® more commonly with dichlorphenamide. patients.
OPHTHALMOLOGY
l Gastrointestinal symptom complex. l Urea.

„ ague abdominal discomfort, gastric „ more side-effects than mannitol, it is not
irritation, nausea, peculiar metallic taste recommended for routine use.
and diarrhoea. l Isosorbide
l Sulfonamide related side-effects of „ can be used repeatedly in diabetics.
„ renal calculi, blood dyscrasias, Stevens- m Prostaglandin derivatives
Johnson syndrome, transient myopia, n Latanoprost (0.005%).
hypertensive nephropathy and teratogenic l It is a synthetic drug
effects. l an ester analogue of prostaglandin F2-á.
n Preparations and doses l It acts by
l Acetazolamide (diamox). l increasing uveoscleral outflow
„ It is available as tablets, capsules and l causing reduction in episcleral venous
injection for intravenous use. pressure.
MYDRIATICS
l Dichlorphenamide l It is as effective as timolol.

„ causes less metabolic acidosis but has a l It has additive effect with pilocarpine and
sustained diuretic effect. timolol.
l Methazolamide l Its duration of action is 24 hours and is, thus,
l Ethoxzolamide administered once daily.
l Dorzolamide (2%). l Its side- effects include
„ It is a topical carbonic anhydrase „ conjunctival hyperaemia
inhibitor. (MCQ) „ foreign body sensation
l Brinzolamide (1%). „ increased pigmentation of the iris.
„ a topical CAI n Bimatoprost (0.03%).
m Hyperosmotic agents n Travoprost (0.004%)..
n These are the second class of compounds n Unoprostive isopropyl (0.12%).
n administered systemically to lower the IOP. m Calcium channel blockers
n These include: glycerol, mannitol, isosorbide n the IOP lowering effect of verapamil is not
and urea. superior than the standard topical antiglaucoma
n Mechanism of action. drugs
l Hyperosmotic agents increase the plasma n it has a place in the mangement of patients
tonicity. with POAG, where miotics, beta-blockers
l Thus, the osmotic pressure gradient created and sympathomimetics are all
between the blood and vitreous draws sufficient contraindicated
water out of the eyeball, thereby significantly n Used in patients suffering simultaneously from
lowering the IOP. axial cataract, bronchial asthma and raised
n Indications. blood pressure.
Mydriatics and Cycloplegic drugs
92
n Cycloplegics m It is used for most of the hypermetropic
m drugs which cause paralysis of accommodation individuals between 5 and 25 years of age.
and dilate the pupil. n Cyclopentolate
m These are used for retinoscopy, m a short acting cycloplegic.
m Used when the examiner suspects that accommodation m Its effect lasts for 6 to 18 hours.
is abnormally active and will hinder the exact retinoscopy. m It is used as 1 percent eyedrops in patients between
m Such a situation is encountered in young children 8 and 20 years of age.
and hypermetropes. m One drop of cyclopentolate is instilled after every
m When retinoscopy is performed after instilling 10-15 minutes for 3 times (Havener’ s
cycloplegic drugs it is termed as wet retinoscopy recommended dose)
in converse to dry retinoscopy (without m retinoscopy is performed 1 to 1/1D 2 hours or
cycloplegics 60 to 90 min. later, after estimating the residual
n Atropine accommodation which should not exceed one
m indicated in children below the age of 5 years. dioptre.
(MCQ) m Only mydriatic (10% phenylephrine) may be
m It is used as 1 percent ointment thrice daily for 3 needed in elderly patients when the pupil is narrow
OPHTHALMOLOGY
consecutive days before performing or media is slightly hazy.
m retinoscopy. n The mydriatics should be used with care in adults
m Its effect lasts for 10 to 20 days. with shallow anterior chamber, owing to the danger of
n Homatropine an attack of narrow-angle glaucoma.
m used as 2 percent drops. n In older people, mydriasis should be counteracted
m One drop is often instilled every 10 minutes by the use of miotic drug (2% pilocarpine).
for 6 times
m retinoscopy is performed after 1 to 2 hours.
m Its effect lasts for 48 to 72 hours.
Sl. Name of Age of the Dosage of Peak Time of Duration Period of Tonus
No. the drug patient when instillation effect performing of action postcyclo- allowance
MYDRIATICS
indicated restinoscopy plegic test
1. Atropine sulphate < 5 year TDS x 3 day 2-3 days 4th day 10-20 days After 3 weeks 1D
(1% ointment) of retinoscopy
2. Homatropine 5-8 years One drop every 60-90 min. After 90 min. 48-72 After 3 days of 0.5D
hydrobromide 10 min. for of instillation Hours retinoscopy
(2% drops) 6 times of first drop
3. Cyclopentolaet 8-20 years One drop every 80-90min. After 90 min. 6-18 hours After 3 days 0.75D
hydrochloride 15 min. for of instillation of retinoscopy
(1% drops) 3 times of first drop
4. Tropicamide Not used as One drop 20-40 min. -- 4-6 hours -- --
(0.5%, 1% drops) cycloplegic for every 15 min.
retinoscopy; used for 3-4 times
only as mydriatic
5. Phenyephrine Used only as One drop every 30-40 min -- 4-6 hours -- --
(5%, 10% drops) mydriatic alone 15 min. for
or in combination 3 to 4 times
with tropicamide
TOPIC 27 - OPTIC NEURITIS
93
n Optic neuritis includes inflammator y and (Uhthoff ’ s symptom) occurs in patient with
demyelinating disorders of the optic nerve. isolated optic neuritis.
n Etiology m Pulfrich’s phenomenon (MCQ)
m Idiopathic. n Depth perception, particularly for the moving
m Hereditary optic neuritis (Leber’s disease) object may be impaired (Pulfrich’s phenomenon).
m Demyelinating disorders are by far the most common m Pain.
cause of optic neuritis. (MCQ) n Patient may complain of mild dull eyeache.
n multiple sclerosis n It is more marked in patients with retrobulbar
n neuromyelitis optica (Devic’s disease) neuritis than with papillitis.
n diffuse periaxial encephalitis of Schilder. n Pain is usually aggravated by ocular
m Parainfectious optic neuritis is associated with various movements, especially in upward or downward
viral infections such as measles, mumps, directions due to attachment of some fibres
chickenpox, whooping cough and glandular of superior rectus to the dura mater.
fever. n Signs
m It may also occur following immunization. m Visual acuity is usually reduced markedly.
m Infectious optic neuritis m Colour vision is often severely impaired.
OPHTHALMOLOGY
n sinus related (with acute ethmoiditis) m Marcus Gunn pupil

n associated with cat scratch fever, syphilis n shows ill-sustained constriction to light.
(during primary or secondary stage), lyme n indicates relative afferent pupillary defect
disease and cryptococcal meningitis in (RAPD)
patients with AIDS. n it is a diagnostic sign.
m Toxic optic neuritis n It is detected by the swinging flash light test
n Anatomical types. m Ophthalmoscopic features.
m Papillitis. n Papillitis
n refers to involvement of the optic disc in l characterised by hyperaemia of the disc and
inflammatory and demyelinating disorders. This blurring of the margins.
condition is usually unilateral l Disc becomes oedematous
m Neuroretinitis l physiological cup is obliterated.
OPTIC NEURITIS
n refers to combined involvement of optic disc l Retinal veins are congested and tortuous.
and surrounding retina in the macular area. l Splinter haemorrhages and fine exudates
m Retrobulbar neuritis may be seen on the disc.
n characterized by involvement of optic nerve l Slit-lamp examination
behind the eyeball. „ reveal inflammatory cells in the vitreous.
n Symptoms „ Inflammatory signs may also be present in
m Visual loss the surrounding retina when papillitis is
n Sudden, progressive and profound visual loss associated with macular star formation
is the hallmark of acute optic neuritis. and the condition is labelled as ‘neuroretinitis’
m Dark adaptation may be lowered. n retrobulbar neuritis
m Visual obscuration in bright light is a typical symptom l fundus appears normal
of acute optic neuritis. l condition is typically defined as a disease where
m Impairment of colour vision is always present in optic neither the ophthalmologist nor the
neuritis. patient sees anything.
n Typically the patients obser ve reduced m Visual field changes.
vividness of saturated colours. n The most common field defect in optic neuritis
m Movement phosphenes and sound induced phosphenes is a relative central or centrocaecal scotoma.
n Phosphenes refer to glowing sensations (MCQ)
produced by nonphotic or the so called inadequate n The field defects are more marked to red colour
stimuli. than the white . (MCQ)
m Uhthoff ’ s symptom (MCQ) n Contrast sensitivity is impaired.
n Episodic transient obscuration of vision on n Visually evoked response (VER) shows
exertion and on exposure to heat, which recovers on l reduced amplitude
resting or moving away from the heat l delay in the transmission time.
n Evolution, recovery and complications
94
m In optic neuritis, typically, the visual acuity and colour n EXTERNAL HORDEOLUM (STYE)
vision is lost progressively over 2-5 days. m It is an acute suppurative inflammation of gland
m The rate of visual recovery is slower than the of the Zeis or Moll. (MCQ)
rate of visual loss and usually takes between 4 and m Etiology
6 weeks. n Predisposing factors.
m About 75 to 90 percent cases get good visual l children and young adults (though no age
recovery. is bar)
m Recurrent attacks of acute retrobulbar neuritis are l patients with eye strain due to muscle
followed by primary optic atrophy imbalance or refractive errors.
m Recurrent attack of papillitis are followed by l Habitual rubbing of the eyes or fingering of
postneuritic optic atrophy leading to complete the lids and nose, chronic blepharitis and diabetes
blindness. mellitus are usually associated with recurrent
n Treatment styes. (MCQ)
m Corticosteroid therapy l Metabolic factors, chronic debility, excessive intake of
n may shorten the period of visual loss carbohydrates and alcohol also act as predisposing
n will not influence the ultimate level of visual factors.
OPHTHALMOLOGY
recovery in patients with optic neuritis. n Causative organism commonly involved is
m Optic neuritis treatment trial (ONTT) Staphylococcus aureus. (MCQ)
recommendations for the use of corticosteroids: m Clinical picture
n Oral prednisolone therapy alone is contraindicated n usually present with a painless swelling in the
in the treatment of acute optic neuritis lid and a feeling of mild heaviness.
l it did not improve visual outcome Examination usually reveals small, firm to
l associated with a significant increase in the hard, non-tender swelling present slightly
risk of new attacks of optic neuritis. away from the lid margin
n A patient presenting with acute optic neuritis n It usually points on the conjunctival side, as
should have brain MRI scan. a red, purple or grey area, seen on everting the lid.
l If the brain shows lesions supportive of m Clinical course and complications
multiple sclerosis (MS), regardless of the n Complete spontaneous resolution may occur rarely.
severity of visual loss, each patient should receive n Often it slowly increases in size and becomes very
CHALAZION
immediate intravenous methylprednisolone (1 gm daily) large.
for 3 days followed by oral prednisolone (1 mg/ n A large chalazion of the upper lid may press
kg/day) for 11 days. on the cornea and cause blurred vision from induced
l This therapy will delay conversion to astigmatism.
clinical MS over the next 2 years. n A large chalazion of the lower lid may rarely
n Indications for intravenous cause eversion of the punctum or even ectropion and
methylprednisolone in acute optic neuritis epiphora.
patients with a normal brain MRI scan are: n Secondary infection leads to formation of
l Visual loss in both eyes simultaneously or hordeolum internum.
subsequently within hours or days of each n Calcification may occur.
other. n Malignant change into meibomian gland
l When the only good eye is affected. carcinoma in elderly people.
l When the slow progressive visual loss m Treatment
continues to occur. n Hot compresses 2-3 times a day are very useful
in cellulitis stage.
n When the pus point is formed it may be
evacuated by epilating the involved cilia. Surgical
incision is required rarely for a large abscess.
n Antibiotic eyedrops (3-4 times a day) and
eye ointment (at bed time) should be applied
to control infection.
n Anti-inflammatory and analgesics relieve
pain and reduce oedema.
TOPIC 28 - CHALAZION
95
n Systemic antibiotics may be used for early n RETINITIS PIGMENTOSA
control of infection. m primary pigmentary retinal dystrophy
n In recurrent styes, try to find out and treat m hereditary disorder predominantly affecting the
the associated predisposing condition. rods more than the cones.
n CHALAZION m Inheritance
m It is also called a tarsal or meibomian cyst. n Most common mode is autosomal recessive.
m It is a chronic non-infective granulomatous (MCQ)
inflammation of the meibomian gland. n Second common ,autosomal dominant
m Treatment n X-linked recessive is the least common.
n Conservative treatment.In a small,soft and recent m It appears in the childhood and progresses slowly
chalazion, self-resolution may be helped by m often result in blindness in advanced middle
conservative treatment in the form of hot age.
fomentation, topical antibiotic eyedrops and oral anti- m Males are more commonly affected than females
inflammatory drugs. in a ratio of 3:2.
n Intralesional injection of long-acting m Disease is almost invariably bilateral and both
steroid (triamcinolone the eyes are equally affected.
OPHTHALMOLOGY
n Incision and curettage is the conventional m Clinical features

and effective treatment for chalazion. n Visual symptoms
n Diathermy. A marginal chalazion is better l Night blindness .(MCQ)
treated by diathermy. „ It is the characteristic feature
n INTERNAL HORDEOLUM „ present several years before the visible
m It is a suppurative inflammation of the changes in the retina appear.
meibomian gland associated with blockage of „ It occurs due to degeneration of the rods.
the duct. l Dark adaptation.
m Etiology. „ Light threshold of the peripheral retina is
n It may occur as increased
l primary staphylococcal infection of the „ the process of dark adaptation itself is
RETINITIS PIGMENTOSA
meibomian gland not affected until very late.

l due to secondary infection in a chalazion l Tubular vision occurs in advanced cases.(MCQ)
(infected chalazion). m Fundus changes(A Frequently asked MCQ
m Clinical picture. in MD Entrance)
n Symptoms are similar to hordeolum externum, n Retinal pigmentary changes.
except that pain is more intense, due to the l These are typically perivascular
swelling being embedded deeply in the dense fibrous tissue. l resemble bone corpuscles in shape.
n How do we differentiate internal hordeolum l Initially, these changes are found in the
from hordeolum externum by the fact that equatorial region only and later spread
in internal hordeolum both anteriorly and posteriorly.
l the point of maximum tenderness and swelling is n Retinal arterioles are attenuated (narrowed) and
away from the lid margin may become thread-like in late stages.
l pus usually points on the tarsal conjunctiva (seen n Optic disc
as yellowish area on everting the lid) and not l becomes pale and waxy in later stages
on the root of cilia l ultimately consecutive optic atrophy occurs
m Treatment. n Other associated changes
n It is similar to hordeolum externum, except l colloid bodies
that, when the pus is formed, it should be l choroidal sclerosis
drained by a vertical incision from the tarsal l cystoid macular oedema
conjunctiva. l atrophic or cellophane maculopathy
(MCQ)
m Visual field changes
n Annular or ring-shaped scotoma
l a typical feature
TOPIC 29 - RETINITIS PIGMENTOSA l corresponds to the degenerated equatorial

zone of retina.
96
n As the disease progresses, scotoma increases n COLOUR BLINDNESS
anteriorly and posteriorly and ultimately m An individual with normal colour vision is known
only central vision is left (tubular vision). as trichromate.
n Eventually even this is also lost and the patient
m In colour blindness, faculty to appreciate one or
becomes blind.
more primary colours is either defective
m Electrophysiological changes
(anomalous) or absent (anopia).
n Typical electrophysiological changes
m It may be congenital or acquired.
appear early in the disease before the subjective
symptoms or the objective signs (fundus m Congenital Colour Blindness.
changes) appear. n It is an inherited condition affecting males more

l Electro-retinogram (ERG) is subnormal or (3-4%) than females (0.4%).
abolished. n It may be of the following types:
l Electro-oculogram (EOG) shows absence of light
l Dyschromatopsia
peak.
l Achromatopsia
m Associations of retinitis pigmentosa
n Ocular associations include n Dyschromatopsia
OPHTHALMOLOGY
l myopia, primary open angle glaucoma l means colour confusion due to deficiency
l microphthalmos, conical cornea of mechanism to perceive colours.
l posterior subcapsular cataract.
l It can be classified into:
n Systemic associations.
„ Anomalous trichromatism
l Laurence-Moon-Biedl syndrome is characterised by
„ retinitis pigmentosa „ Dichromatism
„ obesity l Anomalous trichromatic colour vision.

„ hypogenitalism, „ Here the mechanism to appreciate all the
„ polydactyly three primary colours is present but is
„ mental deficiency. defective for one or two of them.
l Cockayne’s syndrome comprises
„ Protanomalous. It refers to defective red
„ retinitis pigmentosa
COLOUR BLINDNESS
colour appreciation.
„ progressive infantile deafness
„ Deuteranomalous. It means defective green
„ dwarfism
„ mental retardation
colour appreciation.
„ nystagmus and ataxia. „ Tritanomalous. It implies defective blue
l Refsum’ssyndrome is characterized by colour appreciation.

„ retinitis pigmentosa l Dichromatic colour vision.
„ peripheral neuropathy
„ faculty to perceive one of the three
„ cerebellar ataxia.
primary colours is completely absent.
l Usher’ssyndrome includes
„ Such individuals are called dichromates
„ retinitispigmentosa
„ labyrinthine deafness. ® Protanopia, i.e., complete red colour
l Hallgren’ s syndrome comprises defect.

„ retinitis pigmentosa, vestibulo-cerebellar ® Deuteranopia, i.e., complete defect for
ataxia green colour.
„ congenital deafness and mental deficiency. ® Tritanopia, i.e., absence of blue colour
appreciation.
l Red-green deficiency (protanomalous,
protanopia, deuteranomalous and
deuteranopia)
„ more common.
„ Such a defect is a source of danger in certain

occupations such as drivers, sailors and
TOPIC 30 - COLOUR BLINDNESS traffic police.
97
l Blue deficiency (tritanomalous and l It is a quick method of screening colour
tritanopia) is comparatively rare. blinds from the normals.
n Achromatopsia n Hardy-Rand- Rittler plates (HRR).
l It is an extremely rare condition l test based on the same principle as Ishihara’s
l presents as cone monochromatism or rod plates

monochromatism. n The lantern test.
l Cone monochromatism is characterised by n Edridge-Green lantern is most popular.
„ presence of only one primary colour n Farnsworth-Munsell 100 hue test.
„ the person is truely colour blind. n City university colour vision test.
„ Such patients usually have a visual acuity n Nagel’s anomaloscope
of 6/12 or better. n Holmgren’s wools test
l Rod monochromatism may be complete or
incomplete. TOPIC 31- KERATOMALACIA
„ It is inherited as an autosomal recessive
n XEROPHTHALMIA
trait.
KERATOMALACIA
m WHO classification (1982)

„ It is characterized by:
n XN - Night blindness
® Total colour blindness, n X1A - Conjunctival xerosis
® Day blindness (visual acuity is about 6/ n X1B - Bitot’s spots
60), n X2 - Corneal xerosis
® Nystagmus,
n X3A- Corneal ulceration/keratomalacia
affecting less than one-third corneal surface
® Fundus is usually normal.
n X3B - Corneal ulceration/keratomalacia
m Acquired Colour Blindness. affecting more than one-third corneal surface.
n It may follow damage to macula or optic n XS - Corneal scar due to xerophthalmia
nerve, n XF - Xerophthalmic fundus.
COLOUR BLINDNESS
n Usually, it is associated with a central scotoma m Clinical features
or decreased visual acuity. n X N (night blindness).

l It is the earliest symptom of xerophthalmia
n Blue-yellow impairment is seen in retinal lesions
in children. (MCQ)
l CSR, macular oedema and shallow retinal
n X1A (conjunctival xerosis).
detachment. l It consists of one or more patches of dry,
n Red-green deficiency is seen in optic nerve lesions lustreless, nonwettable conjunctiva which
such as has been well described as ‘emerging like
l optic neuritis, Leber’s optic atrophy and sand banks at receding tide’ when the child
compression of the optic nerve. ceases to cry.
l These patches almost always involve the
n Acquired blue colour defect (blue blindness)
inter-palpebral area of the temporal quadrants and
l occur in old age due to increased sclerosis
often the nasal quadrants as well. (MCQ)
of the crystalline lens.
n X1B (Bitot’s spots
l It is owing to the physical absorption of
l The Bitot’s spot is a raised, silvery white,
the blue rays by the increased amber foamy, triangular patch of keratinised
coloured pigment in the nucleus. epithelium,
m Tests for Colour Vision l situated on the bulbar conjunctiva in the
n Pseudo-isochromatic charts. inter-palpebral area

l It is usually bilateral and temporal, and less
l It is the most commonly employed test
using Ishihara’s plates frequently nasal.(MCQ)
n X2 (corneal xerosis).
l In this there are patterns of coloured and
l The earliest change in the cornea is punctate
grey dots which reveal one pattern to the normal
keratopathy
individuals and another to the colour deficients.
l begins in the lower nasal quadrant
98
l followed by haziness and/or granular l Lactating ( mothers
pebbly dryness. „ 20,000 IU orally once at delivery or
l Involved cornea lacks lustre. during the next 2 months.
n X3A and X3B (cor neal ulceration/ „ This will raise the concentration of
eratomalacia) vitamin A in the breast milk and therefore,
l Stromal defects occur in the late stage help to protect the breastfed infant
l Occur due to colliquative necrosis l Infants less than 6 months old, not being breastfed.
n XS (corneal scars). „ 50,000 IU orally should be given before
l Healing of stromal defects results in corneal they attain the age of 6 months.
scars l A revised schedule of vitamin A supplements being
n XFC (Xerophthalmic fundus). followed in India since August 1992, under
l It is characterized by typical seed-like, the programme named as ‘Child Survival
raised, whitish lesions scattered uniformly and Safe Motherhood (CSSM)’ is as
over the part of the fundus at the level of follows:(MCQ)
optic disc „ First dose (1 lakh I.U.)—at 9 months of
m Treatment age along with measles vaccine.
OPHTHALMOLOGY
n Vitamin A therapy. „ Second dose (2 lakh I.U.)—at 18 months
l Oral administration is the recommended method of age along with booster dose of DPT/
of treatment. OPV.
n WHO recommended schedule is as given „ Third dose (2 lakh I.U.)—at 2 years of
below: age.
l All patients above the age of 1 year (except n Medium-term approach.
women of reproductive age): l It includes food fortification with vitamin A.
„ 200,000 IU of vitamin A orally or 100,000 n Long-term approach.
IU by intramuscular injection should be l It implies promotion of adequate intake of
given immediately on diagnosis and vitamin A rich foods such as green leafy
repeated the following day and 4 weeks vegetables, papaya and drum- sticks
later. l Nutritional health education should be
l Children under the age of 1 year and children of any included in the curriculum of school children.
KERATOMALACIA
age who weigh less than 8 kg treated with half
the doses for patients of more than 1 year
of age.
l Women of reproductive age, pregnant or not
„ Those having night blindness (XN), conjunctival
xerosis (X1A) and Bitot’s spots (X1B)
should be treated with a daily dose of
10,000 IU of vitamin A orally (1 sugar
coated tablet) for 2 weeks.
„ For corneal xerophthalmia, administration of
full dosage schedule (described for
patients above 1 year of age) is
recommended.
m Prophylaxis against xerophthalmia
n Short-term approach.
l It comprises periodic administration of
vitamin A supplements.
l WHO recommended, universal distribution
schedule of vitamin A for
l Infants 6-12 months old and ( any older children who
weigh less than 8 kg.
„ 100,000 IU orally every 3-6 months. TOPIC 32 - LENS DISLOCATION
l Children over 1 year and under 6 years of age
„ 200,000 IU orally every 6 months.
99
n Displacement of the lens from its normal position l Systemic features include lax ligaments, hypotonic
(in patellar fossa) results from partial or complete muscles, seizures and mental handicap.
rupture of the lens zonules. n Stickler syndrome
n Congenital displacements l Ectopia lentis is occasionally associated
m Simple ectopia lentis. n Sulphite oxidase deficiency.
n displacement is bilaterally symmetrical and l It is a very rare autosomal recessive
usually upwards. disorder of sulphur metabolism.
n It is transmitted by autosomal dominant n Ectopia lentis is a universal ocular feature.
inheritance. l The systemic features include progressive muscular
m Ectopia lentis et pupillae. rigidity, decerebrate posture, and mental handicap.
n It is characterised by displacement of the lens l It is a fatal disease, death usually occurs before 5 years
associated with slit-shaped pupil which is of age.
displaced in the opposite direction. r Traumatic displacement of the lens
n Other associations may be cataract, glaucoma m It is usually associated with concussion injuries.
and retinal detachment. r Consecutive or spontaneous displacement
m Ectopia lentis with systemic anomalies. m It results from intraocular diseases giving rise to
OPHTHALMOLOGY
n Marfan’s syndrome. mechanical stretching, inflammatory disintegration

l It is an autosomal dominant mesodermal or degeneration of the zonules.
dysplasia. m A few common conditions associated with
l In this condition lens is displaced upwards consecutive displacements are:
and temporally (bilaterally symmetrical). n hypermature cataract, buphthalmos
(MCQ) n high myopia, staphyloma
l Systemic anomalies include arachnodactyly (spider n intraocular tumours and uveitis.
fingers), long extremities, hyperextensibility of joints, TOPOGRAPHICAL TYPES
high arched palate and dissecting aortic aneurysm. n Subluxation
n Homocystinuria. m It is partial displacement in which lens is moved
l It is an autosomal recessive, inborn error of sideways (up, down, medially or laterally), but
metabolism. remains behind the pupil.
LENS DISLOCATION
l In it the lens is usually subluxated downwards m It results from partial rupture or unequal
and nasally.(MCQ) stretching of the zonules
l Systemic features are fair complexion, malar flush, n Clinical feautres are as follows
mental retardation, fits and poor motor control m Defective vision occurs due to marked astigmatism
n Weil-Marchesani syndrome. or lenticular myopia.
l It is condition of autosomal recessive m Uniocular diplopia may result from partial aphakia.
mesodermal dysplasia. m Anterior chamber becomes deep and irregular.
l Ocular features are m Iridodonesis is usually present.
„ Spherophakia m Dark edge of the subluxated lens is seen on
„ forward subluxation of lens which may distant direct ophthalmoscopy (mcq)
cause pupil block glaucoma. n Complications of subluxated lens include :
l Systemic features are short stature, stubby fingers and m Complete dislocation,
mental retardation. m Cataractous changes,
n Ehlers-Danlos syndrome. m Uveitis
l In it the ocular features are subluxation of lens m Secondary glaucoma.
and blue sclera. n Management.
l The systemic features include hyperextensibility of m Spectacles or contact lens correction for phakic or
joints and loose skin with folds. aphakic area (whichever is better) is helpful in
n Hyperlysinaemia. many cases.
l It is an autsomal recessive inborne error m Surgery is usually associated with high risk of
of metabolism retinal detachment.
l occurring due to deficiency of the enzyme n Lensectomy with anterior vitrectomy may
lysin alphaketoglutarate reductase. be performed in desperate cases.
l associated with ectopia lentis. n Dislocation or luxation of the lens
m In it all the zonules are severed from the lens.
100
m A dislocated lens may be ACANTHAMOEBA KERATITIS
n incarcerated into the pupil n Acanthamoeba is a free lying amoeba
n present in the anterior chamber n found in soil, fresh water, well water, sea water,
n present in the the vitreous sewage and air.
l where it may be floating – lens nutans n It exists in trophozoite and encysted forms.
l where it may be fixed to retina – lens fixate n Mode of infection.
n sub-retinal space m Contact lens wearers using home-made saline (from
n subscleral space contaminated tap water and saline tablets) is the
l extruded out of the globe, partially or commonest situation (MCQ)
completely. m Other situations include mild trauma associated with
m Clinical features of posterior dislocation. contaminated vegetable matter, salt water
n deep anterior chamber diving, wind blown contaminant and hot tub
n aphakia in pupillary area use. (MCQ)
n iridodonesis. m Trauma with organic matter and exposure to
n Ophthalmoscopic examination reveals lens in muddy water are the major predisposing factors
the vitreous cavity. in developing countries.
OPHTHALMOLOGY
m Clinical features of anterior dislocation m Opportunistic infection.
n deep anterior chamber n opportunistic infection in patients with herpetic
n presence of lens in the anterior chamber. keratitis, bacterial keratitis, bullous
n Clear lens looks like an oil drop in the aqueous. keratopathy and neuroparalytic keratitis.
m Complications associated with dislocated lens are n Clinical features
uveitis and secondary glaucoma. m Symptoms.
m Management. n very severe pain (out of proportion to the
n A lens dislocated in the anterior chamber and degree of inflammation)
that incarcerated in the pupil should be n watering, photophobia
removed as early as possible. n blepharospasm and blurred vision.
n A dislocated lens from the vitreous cavity m Signs
should be removed only if it is causing n Initial lesions of acanthamoeba keratitis are in the
uveitis or glaucoma. form of limbitis, coarse, opaque streaks, fine epithelial
ACANTHAMOEBA
l From the vitreous cavity lens can be removed and subepithelial opacities, and radial kerato-neuritis,
after total vitrectomy in the form of infiltrates along corneal nerves.
n Advanced cases show a central or paracentral
ring-shaped lesion with stromal infiltrates
and an overlying epithelial defect, ultimately
presenting as ring abscess (MCQ)
n Hypopyon may also be present.
n Laboratory diagnosis.
m Corneal scrapings may be helpful in some cases
as under:
m Potassium hydroxide(KOH) mount is reliable for
recognition of acanthamoeba cysts.
m Calcofluor white stain
n Fluorescent brightener
n stains the cysts of acanthamoeba bright apple
green under fluorescence microscope.
m Lactophenol cotton blue stained film
m Culture on non-nutrient agar (E. coli enriched)
n show trophozoites within 48 hours, which
gradually turn into cysts.
n Treatment
n Specific medical treatment includes:
m propamidine isethionate (Brolene) drops
TOPIC 33 - ACANTHAMEBA m Neomycin drops

101
m Polyhexamethylene biguanide n Reassurance is the only treatment required in
m Chlorhexidine majority of the cases (MCQ)
m paromomycin n CSR undergoes spontaneous resolution in
m oral imidazoles such as fluconazole, itraconazole 80 to 90 percent cases.
and miconazole. n Visual acuity returns to normal or near
n Duration of medical treatment is very large (6 normal within 4 to 12 weeks.
months to 1 year). n Laser photocoagulation is indicated in following
n Penetrating keratoplasty is frequently required in cases:
non-responsive cases. l Long-standing cases (more than 4
months) with marked loss of vision.
TOPIC 34 - l Patients having recurrent CSR with visual
CENTRAL SEROUS RETINOPATHY loss.
l Patients having permanent loss of vision
n Central serous retinopathy (CSR)
in the other eye due to this condition.
m characterised by spontaneous serous
n Cystoid macular edema (cme)
detachment of neurosensory retina in the
m It refers to collection of fluid in the outer
macular region, with or without retinal pigment
OPHTHALMOLOGY
plexiform (Henle’s layer) and inner nuclear

epithelium detachment.
layer of the retina, centred around the foveola.
m typically affects males between 20 and 40 years
m Common causes
of age.
n As postoperative complication following cataract
m an increase in choroidal hyperpermeability
extraction and penetrating keratoplasty.
causes a breach in the outer blood retinal barrier
n Retinal vascular disorders e.g., diabetic
(a small opening or blow out of RPE). (MCQ)
retinopathy and central retinal vein
m Leakage of fluid across this area results in
occlusion.
development of localized serous detachment
n Intraocular inflammations e.g., pars planitis,
of neurosensory retina.
posterior uveitis, Behcet disease.
m Factors reported to induce or aggravate CSR
n As a side-effect of drugs e.g., following use of
include: emotional stress, hypertension, and
CENTRAL SEROUS RETINOPATHY
adrenaline eyedrops, especially for aphakic

administration of systemic steroids. (MCQ)
glaucoma.
m Patient presents with a sudden onset of painless
n Retinal dystrophies e.g., retinitis pigmentosa.
loss of vision (6/9-6/24) associated with relative
m CME develops due to leakage of f luid
positive scotoma, micropsia and metamorphopsia.(MCQ)
following breakdown of inner blood-retinal barrier (i.e.,
m Ophthalmoscopic examination
leakage from the retinal capillaries).
n mild elevation of macular area, demarcated by
m If oedema persists, there may occur permanent
a circular ring-reflex.
decrease in vision.
n Foveal reflex is absent or distorted
m Ophthalmoscopy (MCQ)
m CSR is usually self-limiting but often recurrent.
n typical ‘Honey-comb appearance’ of macula
m Resolution may take three weeks to one year
(due to multiple cystoid oval spaces)
m Resolution often leaves behind small areas of
n CME is best examined with a fundus contact
atrophy and pigmentary disturbances.
lens on slit-lamp or +90D lens.
m Fundus fluorescein angiography helps in
m Fundus fluorescein angiography
confirming the diagnosis.
n demonstrates leakage and accumulation of dye
n Ink-blot pattern. (MCQ)
in the macular region
l It consists of small hyperfluorescent spot
n presents a ‘flower petal appearance’ (MCQ)
which gradually increases in size
n Long-standing CME may end in lamellar
n Smoke-stack pattern. (MCQ)
macular hole.
l It consists of a small hyperfluorescent spot
m Treatment
which ascends vertically like a smoke-
n Treatment of the causative factor
stack
l photocoagulation for diabetic CSME
l It gradually spreads laterally to take a
(MCQ)
mushroom or umbrella configuration
l cessation of causative topical 2%
m Treatment
adrenaline eye drops, so on. (MCQ)
102
l Topical antiprostaglandin drops like „ Stage of haemorrhagic detachment of neurosensory
indomethacin or flurbiprofen, used pre and retina, and
postoperatively, prevent the occurrence of „ Stage of disciform (scarring) macular degeneration.
CME associated with intraocular surgery. m Early versus late ARMD
(MCQ) n Eary ARMD includes
n Topical and systemic l Drusens
n Systemic carbonic anhydrase inhibitors (CAIs) e.g., oral l areas of RPE hyperpigmentation and/
acetazolamide or depigmentation.
n Age-related macular degeneration (ARMD) n Late ARMD includes
m also called senile macular degeneration l geographic atrophy of RPE with visible
m a bilateral disease of persons of 59 years of underlying choroidal vessels
age or older. l pigment epithelium detachment (PED)
m It is a leading cause of blindness in developed with or without neurosensory retinal
countries in population above the age of 65 detachment
years(MCQ) l subretinal or sub- RPE neovascularization
m It is of two types non-exudative and exudative. l haemorrhage and disciform scars.
OPHTHALMOLOGY
m risk factors which may affect the age of onset and/ m Treatment
or progression include n Role of dietar y supplements and
n heredity, nutrition antioxidants in prevention or treatment of
n smoking, hypertension ARMD. vitamin C and E ,beta carotene zinc
n exposure to sun light. and copper
m Clinical types n Treatment modalities available to treat
n Non-exudative or atrophic ARMD. exudative (neovascular) ARMD are:
l Also called dry or geographic ARMD l Argon green-laser photocoagulation
l responsible for 90 percent cases. „ treatment of choice for extrafoveal
l It typically causes mild to moderate, gradual choroidal neovascular membrane
loss of vision. (CNVM) (MCQ)
CENTRAL SEROUS RETINOPATHY

l Patients may complain of distorted vision, l Photodynamic therapy (PDT)
difficulty in reading due to central „ treatment of choice for subfoveal and
shadowing. juxtafoveal classic CNVM.
l Ophthalmoscopically, it is characterised by l Principles of PDT
occurrence of „ In PDT, vertiporfin, a photosensitizer or
„ drusens (colloid bodies) (MCQ) light activated dye is injected intravenously.
® appear as small discrete, yellowish- „ The area of CNVM is then exposed to light
white, slightly elevated spots from a diode laser source at a wavelength
„ pale areas of retinal pigment epithelium (689 nm) that corresponds to absorption
atrophy peak of the dye.
„ irregular or clustered pigmentation. „ The light-activated dye then causes
„ In later stages, there occurs enlargement disruption of cellular structures and
of the atrophic areas within which the occlusion of CNVM with minimum damage
larger choroidal vessels may become to adjacent RPE, photoreceptors and capillaries.
visible (geographic atrophy) (MCQ) l Transpupillary thermotherapy (TTT)
n Exudative ARMD. „ Done with a diode laser (810 nm)
l It is also called wet or neovascular ARMD. „ may be considered for subfoveal occult
l associated with comparatively rapidly CNVM.
progressive marked loss of vision. „ PDT is definitely better than TTT but is
l Typically, the course of exudative ARMD rapidly very costly.
passes through many stages. These include: l Surgical treatment
„ Stage of drusen formation, „ submacular surgery to remove CNVM
„ Stage of retinal pigment epithelium (RPE) and macular translocation surgery are being
detachment, evaluated.
„ Stage of choroidal neovascularisation (CNV) l Pharmacologic modulation with antiangiogenic
„ Stage of haemorrhagic detachment of RPE, agent
103
„ interferon alfa-29 n Most patients get frequent attacks of
„ inhibitor of vascular endothelial growth factor recurrent corneal erosions that usually result
(VEGF) in diffuse anterior scarring.
n most of the patients ultimately need lamellar
TOPIC 35 - CORNEAL DYSTROPHY or penetrating keratoplasty.

n Corneal dystrophies m Recurrent corneal erosion syndrome (MCQ)
n a type of dystrophy that typically follows
m inherited disorders in which the cells have some
inborn defects due to which pathological changes trauma to cornea by finger nail or any other
may occur with passage of time leading to sharp edge.
n It has been shown that a lack of basement
development of corneal haze in otherwise normal
eyes that are free from inflammation or vascularization. membrane and hemidesmosomes in the area
m There is no associated systemic disease.
of involvement, is the basic underlying cause.
n The condition is characterised by pain, photophobia,
m Dystrophies occur bilaterally
m manifesting more usually appear during first or
lacrimation and blurring of vision on awakening in the
second decade morning.
m Classification
m Macular dystrophy (Groenouw type-II)
OPHTHALMOLOGY
n It is an autosomal recessive dystrophy(MCQ)

n Anterior dystrophies (superficial dystrophies),
n characterised by appearance of dense grey
l Affect primarily affecting epithelium and
Bowman’s layer. opacity in the central cornea.
n The condition results due to accumulation of
„ Epithelial basement membrane dystrophy
„ Reis-Buckler’s dystrophy.
mucopolysaccharides owing to a local
„ Meesman’s dystrophy.
enzyme deficiency.
n It occurs in childhood (5 to 10 years) and
„ Recurrent corneal erosion syndrome.
„ Stocker-Holt dystrophy
leads to marked defective vision in early life
n usually requires penetrating keratoplasty.
n Stromal dystrophies
l Granular (Groenouw’s type I) dystrophy
m Lattice dystrophy
n Also known as ‘Biber-Haab-Dimmer dystrophy.
l Lattice dystrophy
CORNEAL DYSTROPHY
n autosomal dominant disease

l Macular (Groenouw’s type II) dystrophy
n characterised by branching spider-like
l Crystalline (Schnyder’s) dystrophy
n Posterior dystrophies
amyloid deposits forming an irregular lattice
l affect primarily the corneal endothelium
work in the corneal stroma, sparing the
and Descemet’s membrane. periphery.
n Usually penetrating keratoplasty is required
„ Cornea guttata
„ Fuchs’ epithelial-endothelial dystrophy
by the age of 30- 40 years.
(late hereditary endothelial dystrophy). m Cornea Guttata of vogt
n This condition is characterised by drop-like
„ Posterior polymorphous dystrophy (of
Schlichting). excrescences involving the entire posterior
„ Congenital hereditary endothelial dystrophy
surface of Descemet’s membrane.
n Hassal- Henle bodies
(CHED).
l represent the age change
m Epithelial basement membrane dystrophy
l mainly found in the peripheral part.
n Cogan’s microcystic dystrophy
n usually occurs in old age
n map-dot finger print dystrophy
n more common in females than males.
n it is the most common of all corneal
n It rarely affects the vision and hence treatment
dystrophies seen in working age adults. (MCQ)
n Most cases are asymptomatic.
is usually not required.
m Reis-Buckler dystrophy
m Fuch’s epithelial-endothelial dystrophy
n slowly progressive bilateral condition
n Also known as ring-shaped dystrophy (due
n affect females more than male
to the typical lesion)
n usually between fifth and seventh decade of
n primarily involve the Bowman’s layer
n a progressive corneal dystrophy occurring in
life.
n Primary open angle glaucoma is its common
childhood.
n It has got autosomal dominant inheritance.
association.
104
n Clinical features can be divided into following n Evisceration
four stages: m It is the removal of the contents of the eyeball
l Stage of cornea guttata. leaving behind the sclera.
„ Hassal-Henle type of excrescenses in m Frill evisceration
the central part of cornea. n preferred over simple evisceration
„ A gradual increase of central guttae n only about 3-mm frill of the sclera is left
with peripheral spread and confluence around the optic nerve.
gives rise to the so called ‘beaten-metal’ m Indications (MCQ)
appearance. This stage is asymptomatic. n Panophthalmitis
(MCQ) n expulsive choroidal haemorrhage
l Oedematous stage or stage of endothelial n bleeding anterior staphyloma.
ENUCLEATION EVISCERATION
l Stage of bullous keratopathy. m Surgical steps of frill evisceration
l Stage of scarring n Removal of cornea
n Treatment is as follows : n Removal of intraocular contents
l In early oedematous stage use 5 percent sodium n Separation of extraocular muscles
chloride (hypertonic saline) n Removal of sclera
l Bandage soft contact in bullous keratopathy n Closure of Tenon’s capsule and conjunctiva
stage.
l Penetrating keratoplasty is the treatment of choice TOPIC 37 - FOREIGN BODY
when the visual acuity is reduced markedly.
Intraocular foreign bodies
n Common foreign bodies
TOPIC 36 -
m chips of iron and steel (90%) (MCQ)
ENUCLEATION EVISCERATION m particles of glass, stone, lead pellets
n Enucleation m copper percussion caps
m It is excision of the eyeball m aluminium, plastic and wood.
m performed under local anaesthesia in adults n Specific reactions are produced by
and under general anaesthesia in children. m iron (Siderosis bulbi)
m Indications (MCQ) m copper alloys (Chalcosis)
FOREIGN BODY
n Absolute indications n CT scan is presently the best method of IOFB
l retinoblastoma localization. (MCQ)

l malignant melanoma n Siderosis bulbi (MCQ)
n Relative indications m refers to the degenerative changes produced by
l painful blind eye an iron foreign body.

l mutilating ocular injuries m usually occurs after 2 months to 2 years of the
l anterior staphyloma injury.

l phthisis bulbi. m the epithelial structures of the eye are most
m Surgical techniques affected.

n Separation of conjunctiva and Tenon’s capsule m The anterior epithelium and capsule of the lens are
n Separation of extraocular muscles involved first of all.

n Cutting of optic nerve n Here, the rusty deposits are arranged radially
n Removal of eyeball: in a ring.

n Haemostasis is achieved by packing the orbital n Eventually, the lens becomes cataractous.
cavity m Iris
n Inserting an orbital implant n It is first stained greenish and later on turns
l Preferably an orbital implant (made up of reddish brown.(MCQ)

PMMA Medpor or hydroxyapatite) of m Retina develops pigmentary degeneration which
appropriate size should be inserted into the resembles retinitis pigmentosa.

orbit and sutured with the rectus muscles. m Secondary open angle type of glaucoma occurs due to
n Closure of conjunctiva and T enon’ s capsule degenerative changes in the trabecular

n Dressing meshwork.
n A prosthesis can be fitted in the socket after three n Chalcosis (MCQ)
weeks of operation when the eye becomes

free of pain and inflammation. 105
m It refers to the specific changes produced by the „ folds in Descemet’s and Bowman’s
alloy of copper in the eye. membranes
m Unlike iron ions these do not enter into a chemical „ Very fine, vertical, deep stromal striae
combination with the proteins of the cells and thus (Vogt lines) which disappear with external
produce no degenerative changes. pressure on the globe are peculiar feature.
m Kayser-Fleischer ring. l On retinoscopy
n It is a golden brown ring „ yawning reflex (scissor reflex)
n occurs due to deposition of copper under „ high oblique or irregular astigmatism
peripheral parts of the Descemet’s l On distant direct ophthalmoscopy
membrane of the cornea. (MCQ) „ annular dark shadow (due to total internal
m Sunflower cataract. reflection of light) is seen which separates
n It is produced by deposition of copper under the central and peripheral areas of cornea (oil
the posterior capsule of the lens. droplet reflex).
n It is brilliant golden green in colour and l Munson’s sign
arranged like the petals of a sun flower. „ localised bulging of lower lid when patient
m Retina. looks down
OPHTHALMOLOGY
n It may show deposition of golden plaques at „ positive in late stages.

the posterior pole which reflect the light with m Morphological classification.
a metallic sheen. n Depending upon the size and shape of the cone.
n Ophthalmia nodosum (MCQ) the keratoconus is of three types:
m Caterpillar hair produces ophthalmia nodosum l Nipple cone has a small size (<5mm) and steep
m characterised by a severe granulomatous curvature.
iridocyclitis with nodule formation. l Oval cone is larger (5-6 mm) and ellipsoid in
shape.
TOPIC 38 - KERATOCONUS l Globus cone is very large (>6 mm) and globe
like.
n Keratoconus (conical cornea) m Complications.
m a non- inflammatory bilateral (85%) ectatic
n complicated by development of acute
condition of cornea in its axial part.
KERATOCONUS
hydrops due to rupture of Descemet’s membrane.

m It usually starts at puberty and progresses
l The condition is characterised by sudden
slowly.(MCQ) development of cor neal oedema
m Essential pathological changes
associated with marked defective vision,
n thinning and ectasia
pain, photophobia and lacrimation.
n occur as a result of defective synthesis of
m Associations.
mucopolysaccharide and collagen tissue. n Ocular conditions
m Clinical features.
l ectopia lentis
n Symptoms.
l congenital cataract
l Patient presents with a defective vision
l aniridia, retinitis pigmentosa,
„ due to progressive myopia and irregular
l vernal keratoconjunctivitis (VKC).
astigmatism n Systemic conditions
„ does not improve fully despite full
l Marfan’s sysndrome, atopy
correction with glasses. l Down’s syndrome
n Signs
l Ehlers-Danlos syndrome
l Window reflex is distorted.
l osteogenesis imperfecta and mitral valve
l Placido disc examination shows irregularity of
prolapse.
the circles m Treatment.
l Keratometry depicts extreme malalignment of
n Falling vision may not be corrected by glasses
mires. due to irregular astigmatism.
l Photokeratoscopy reveals distortion of circles
n Contact lenses (rigid gas permeable) usually
l Slit lamp examination
improve the vision in early cases.
„ thinning and ectasia of central cornea
n In later stages penetrating keratoplasty may
„ opacity at the apex
be required.
„ Fleischer’s ring at the base of cone
106
n Intacs, the intracorneal ring segments, - lThe earliest pathognomic sign at this stage
useful in early cases. is appearance of orange patches in the
Keratoglobus pigment epithelium due to
n It is a familial and hereditary bilateral congenital „ accumulation of the lipofuscin.
disorder „ intraretinal haemorrhage
n characterised by thinning and hemispherical „ choroidal folds
protrusion of the entire cornea. „ vitreous haemorrhage.
n It is non-progressive n Glaucomatous stage.
n inherited as an autosomal recessive trait. n Stage of extraocular extension
n It must be differentiated from congenital n Stage of distant metastasis.
buphthalmos, where increased corneal size is l Lymphatic spread is usually not known.
associated with l Blood-borne metastasis usually occurs in the
m raised intraocular pressure liver and is the commonest cause of death.

m angle anomaly, m Investigations
m cupping of optic disc.. n Indirect ophthalmoscopic examination. (MCQ)

l It allows three-dimensional stereoscopic
OPHTHALMOLOGY
TOPIC 39 - MELANOMA view of the lesion.
l It also depicts the presence of shifting fluid
n Malignant melanoma of choroid which is pathognomic of exudative retinal

m It is the most common primary intraocular detachment.
tumour of adults, n Transillumination test.
m usually seen between 40-70 years of age l It indicates a tumour mass and thus helps to
m arises from the neural crest derived pigment differentiate from choroidal detachment and simple
cells of the uvea retinal detachment.
m occur as a solitary tumour n Ultrasonography:
m usually unilateral. l Both A and B scan help to outline the
m Gross pathology. tumour mass in the presence of hazy media.

n Circumscribed (pedunculated) tumour. n Radioactive tracer:
l Initially it appears as flat, slate-grey area, l neoplastic tissue has an increased rate of
MELANOMA
which becomes raised and pigmented with phosphate (32p) uptake.
growth n MRI.
l It eventually ruptures through the Bruch’s l Choroidal melanomas are hyperintense in
membrane (Collar- Stud tumour). T1-weighted and hypointense in T2-

l Further, growth of the tumour produces weighted images.
exudative retinal detachment.(MCQ) m Treatment
n Diffuse (flat) malignant melanoma n Conservative treatment to salvage the eyeball
m Histopathology. l Brachytherapy
n Modified Callender’s classification „ usually the treatment of choice in
n Spindle cell melanomas. ® tumours less than 10mm in elevation
l make up 45% of all tumours. ® less than 20 mm in basal diameter.
l best prognosis „ Supplemental transpupillar y

n Epithelioid cell melanomas. ther motherapy may be required to
n Mixed cell melanomas - make up 45% of all enhance the results.
tumours. l External beam radiotherapy with protons or
n Necrotic melanomas helium ions

m Clinical picture „ Indicated for tumours unsuiatable for
n Quiescent stage. brachytherapy either because of size or

l Small tumour located in the periphery may posterior location to within 4mm of
not produce any symptom disc or fovea.
l tumours arising from the posterior pole l Transpupillary thermotherapy (TTT) with diode
present with early visual loss laser
107
„ indicated in selected small tumours, TOPIC 40 - ORBIT FRACTURE
particularly if pigmented and located
near the fovea or optic disc. n Blow-out orbital fracture
l Trans-scleral local resection m These are isolated comminuted fractures
„ indicated in tumours that are too thick m occur when the orbital walls are pressed
for radiotherapy and usually less than indirectly,

16mm in diameter. m mainly involve orbital floor and medial wall
„ It is a very difficult procedure which is (MCQ)

performed under systemic arterial m generally result from trauma to the orbit by a
hypotension. relatively large, often rounded object, such as

l Stereostatic radiosurgery with the help of Gamma tennis ball, cricket ball, human fist or part of
knife. an automobile.
„ new method indicated in large tumours. m The force of the blow causes a backward
It involves single- session delivery of displacement of the eye and an increase in

ionizing radiation intraorbital pressure
n Enucleation. m fracture occurs at weakest point of the orbital
OPHTHALMOLOGY
l It is indicated for for very larger tumours wall.

in which conservative methods to salvage the n Usually weakest point is the orbital floor, but
eyeball are not effective. this may be the medial wall also. (MCQ)
n Exenteration or debulking with m Clinical features
chemotherapy and radiotherapy is required in n Periorbital oedema and blood extravasation in and
the stage of extraocular spread. around the orbit (such as subconjunctival

n Palliative treatment with chemotherapy and ecchymosis)
immunotherapy in patients with distant n Emphysema of the eyelids
metastasis. l occurs more frequently with medial wall than
n Malignant melanoma in the ciliary body floor fractures.

m it is usually diagnosed very late, due to its hidden l It may be made worse by blowing of nose.
location. n Paraesthesia and anaesthesia in the distribution of

ORBIT FRACTURE
m Earliest features of a localised melonoma include infraorbital nerve (lower lid, cheek, side of
n slight hypotony nose, upper lip and upper teeth) are very
n unaccountable defective vision common.
n localised ‘sentinel’ dilated episcleral veins in n Ipsilateral epistaxis
the quadrant containing tumour. l as a result of bleeding from maxillary sinus
m Clinical presentation into the nose

n cause pressure on the lens resulting in anterior n Proptosis (MCQ)
displacement, subluxation and cataract n Enophthalmos and mechanical ptosis.
formation. l Three factors responsible for producing
n It may involve iris enophthalmos are:

n may involve the angle of anterior chamber „ escape of orbital fat into the maxillary
resulting in secondary glaucoma. sinus;

n epibulbar mass. „ backward traction on the globe by
n exudative retinal detachment. entrapped inferior rectus muscle

m Treatment „ enlargement of the orbital cavity from
n Enucleation displacement of fragments.

n Local resection. n Diplopia
l Cyclectomy or irido-cyclectomy if tumour is l typically occurs in both up and down gaze
detected in early stage. (double diplopia)

l occurs due to entrapment of soft tissue
structures in the area of the blowout
fracture.
l The presence of muscle restriction can be
confirmed by a positive ‘forced duction
test’ (MCQ)
108
n Severe ocular damage associated with „ These typical exudates are referred as snow
blowout fracture is rare. ball opacities.
l This is because a ‘blow-out fracture’ is l These may coalesce to form a grey white
nature’s way of protecting the globe from plaque called snow banking. (MCQ)
injury. m Complications of long-standing pars planitis
m Plain X-rays. include
n The most useful projection for detecting an n cystoid macular oedema
orbital floor fracture is a nose-chin (Water’s) n complicated cataract
view. (MCQ) n tractional retinal detachment.
n The common roentgen findings are : m Treatment
l fragmentation and irregularity of the orbital n Corticosteroids
floor n Immunosuppressive drugs
l depression of bony fragments n Peripheral cryotherapy
l ‘hanging drop’ opacity of the superior
maxillary antrum from orbital contents TOPIC 42 - RETINAL DETATCHMENT
herniating through the floor (MCQ) n Retinal detatchment
m Computerised tomography scanning and magnetic resonance m It is the separation of neurosensory retina
imaging (MRI).
PARAS PLANITIS
proper from the pigment epithelium. the term
n for detailed visualisation of soft tissues. retinal detachment is a misnomer and it should
m Management be retinal separation.
n The optimal time for surgery, when indicated, m Classification
is after 10-14 days of injury. l Primary
n Indications of surgical intervention include: „ Rhegmatogenous or primary retinal
l Diplopia not resolving significantly in the early detachment.
days after trauma. l Secondary retinal detachment
l A fracture with a large herniation of tissues „ Tractional retinal detachment
into the antrum. „ Exudative retinal detachment
RETINAL DETATCHMENT
l Incarceration of tissues in the fracture with n Rhegmatogenous or primary retinal detachment
resulting globe retraction and increased m It is usually associated with a retinal break (hole
applanation tension on attempted upward or tear) through which subretinal fluid (SRF)
gaze. seeps and separates the sensory retina from the
l Enophthalmos greater than 3 mm. pigmentary epithelium.
m Predisposing factors include:
TOPIC 41 - PARAS PLANITIS
l Age. The condition is most common in 40-
n Intermediate uveitis (pars planitis) 60 years
m It denotes inflammation of pars plana part of
l Sex. More common in males (M:F—3:2).
ciliary body and most peripheral part of the l Myopia. About 40 percent cases of
retina. rhegmatogenous retinal detachment are
m It is an idiopathic disease
myopic.
m usually affect both eyes (80 percent) of children
l Aphakia. (MCQ)
and young adults. l Retinal degenerations predisposed to retinal
m Symptoms.
detachment are as follows:
n Most of the patients present with history of
„ Lattice degeneration (MCQ)
floaters. „ Snail track degeneration.
n defective vision due to associated cystoid
„ White-with-pressure and white-without-or
macular oedema. occult pressure.
m Signs.
„ Acquired retinoschisis.
n Fundus examination
l Focal pigment clumps.
l Done with indirect ophthalmoscope
l Trauma
l snow ball opacities (MCQ)
l Senile posterior vitreous detachment
„ whitish exudates present near the ora serrata
(PVD).
in the inferior quadrant. m Clinical features
l Prodromal symptoms.
109
„ dark spots (floaters) in front of the eye „ Ultrasonography confirms the diagnosis.
(MCQ) ® It is of particular value in patients with
® occur due to rapid vitreous degeneration hazy media especially in the presence of
„ photopsia dense cataracts.
® sensation of flashes of light l Complications
® occur due to irritation of retina by „ proliferative vitreoretinopathy (PVR)
vitreous movements (MCQ) „ complicated cataract
l Symptoms of detached retina. „ uveitis
„ Localised relative loss in the field of vision (of „ phthisis bulbi. (MCQ)
detached retina) m Treatment
® noticed by the patient in early stage l Sealing of retinal breaks.
® it progresses to a total loss when „ sealed by producing aseptic
peripheral detachment proceeds gradually towards chorioretinitis, with cryocoagulation, or
the macular area. photocoagulation or diathermy.
„ Sudden painless loss of vision „ Cryocoagulation is more frequently
® occurs when the detachment is large and utilised
OPHTHALMOLOGY
central. l SRF drainage.

® Such patients usually complain of „ done very carefully by inserting a fine
sudden appearance of a dark cloud needle through the sclera and choroid
or veil in front of the eye. into the subretinal space
l Signs. l To maintain chorioretinal apposition for
„ Marcus Gunn pupil (relative afferent at least a couple of weeks.
pupillary defect) „ Scleral buckling
„ Plane mirror examination reveals ® inward indentation of sclera to
® an altered red reflex in pupillary area provide external
® greyish reflex in the quadrant of ® Scleral buckling is achieved by inserting
detached retina an explant (silicone sponge or solid
RETINAL DETATCHMENT
„ Ophthalmoscopy silicone band) with the help of mattress

® Retinal detachment is best examined by type sutures applied in the sclera
indirect ophthalmoscopy using scleral indentation „ Pneumatic retinopaxy is a simple outpatient
® It enhances visualization of the procedure
peripheral retina anterior to equator ® used to fix a fresh superior RD with
„ On examination one or two small holes extending over less
® freshly-detached retina gives grey reflex than two clock hours in upper two thirds
instead of normal pink reflex and is of the peripheral retina.
raised anteriorly (convex ® In this technique after sealing the
configuration). breaks with cryopaxy, an expanding gas
® It is thrown into folds which oscillate with bubble (SF6 or C3F8) is injected in the vitreous.
the movements of the eye. ® break is uppermost and the gas bubble
® retina becomes funnel-shaped, being remains in contact with the tear for
attached only at the disc and ora serrata. 5-7 days.
® Retinal vessels appear as dark tortuous „ Parsplana vitrectomy, endolaser photocoag lation and
cords oscillating with the movement of internal temponade.
detached retina. ² All complicated primary RDs
® Retinal breaks associated with ² All tractional RDs.
rhegmatogenous detachment ² Presently, even in uncomplicated primary
» most frequently found in the RDs (where scleral buckling is successful),
periphery m Prophylaxis
» commonest in the upper temporal l Occurrence of primary retinal detachment
quadrant (MCQ) can be prevented by timely application of
„ Visual field charting reveals scotomas laser photocoagulation or cryotherapy in
„ Electroretinography (ERG) is subnormal or the areas of retinal breaks and/or
absent.
110
predisposing lesions like lattice n Presence of intraocular tumours usually requires
degeneration. enucleation.
l Prophylactic measures -Indications m Tractional retinal detachment
„ myopia, n It occurs due to retina being mechanically
„ aphakia, pulled away from its bed by the contraction
„ retinal detachment in the fellow eye of fibrous tissue in the vitreous (vitreoretinal
„ history of retinal detachment in the family. tractional bands).
n Exudative or solid retinal detachment n Etiology
m It occurs due to the retina being pushed away l Post-traumatic retraction of scar tissue
by a neoplasm or accumulation of fluid beneath the retina especially following penetrating injury.
following inflammatory or vascular lesions. l Proliferative diabetic retinopathy.
m Common causes l Post-haemorrhagic retinitis proliferans.
l Systemic diseases. l Retinopathy of prematurity.
„ toxaemia of pregnancy l Plastic cyclitis.
„ renal hypertension l Sickle cell retinopathy.
„ blood dyscrasias l Proliferative retinopathy in Eales’ disease.
OPHTHALMOLOGY
„ polyarteritis nodosa. n Clinical features
l Ocular diseases. l charcterised by presence of vitreoretinal
„ Inflammations bands with lesions of the causative disease.
® Harada’ s disease l configuration of the detached area is
® sympathetic ophthalmia, concave.
® posterior scleritis, l The highest elevation of the retina occurs
® orbital cellulitis at sites of vitreoretinal traction.
„ Vascular diseases l Retinal mobility is severely reduced and
® central serous retinopathy shifting fluid is absent.
® exudative retinopathy of Coats n Treatment
„ Neoplasms l It is difficult and requires pars plana
® malignant melanoma of choroid vitrectomy to cut the vitreoretinal tractional
CAVERNOUS SINUS THROMBOSIS

® retinoblastoma (exophytic type bands and internal tamponade
„ Sudden hypotony due to perforation of n Prognosis in such cases is usually not so good.
globe and intraocular operations.
TOPIC 43 -
m Clinical features
l Exudative retinal detachment can be
differentiated from a simple primary Cavernous sinus thrombosis
detachment by: n Communications of caver nous sinus and
l Absence of photopsia, holes/tears, folds and sources of infection
undulations. m Anteriorly, (MCQ)
l The exudative detachment is smooth and convex n the superior and inferior ophthalmic veins
l At the summit of a tumour it is usually rounded drain in the sinus.
and fixed and may show pigmentary disturbances. n These veins receive blood from face, nose,
l Occasionally, pattern of retinal vessels may paranasal sinuses and orbits
be disturbed due to presence of n infection to cavernous sinus may spread from
neovascularisation on the tumour summit. infected facial wounds, eryseplas, squeezing
l Shifting fluid characterised by changing of stye, furuncles, orbital cellulitis and
position of the detached area with gravity is sinusitis.
the hallmark of exudative retinal m Posteriorly
detachment. (MCQ) n the superior and inferior petrosal sinuses
l On transillumination test a leave it to join the lateral sinus. Labyrinthine
„ simple detachment appears transparent veins opening into the inferior petrosal
„ solid detachment is opaque. sinuses bring infections from the middle ear.
m Treatment n Mastoid emissar y veins may spread
n the treatment should be for the causative disease. infection from the mastoid air cells.
m Superiorly
111
n the cavernous sinus communicates with veins n Conjunctiva is swollen and congested. (MCQ)
of the cerebrum n Proptosis develops rapidly. (MCQ)
n may be infected from meningitis and cerebral n Palsy of third, fourth and sixth cranial nerves
abscesses. occurs frequently.
m Inferiorly n Oedema in mastoid region is a pathognomonic sign.
n the sinus communicates with pterygoid (MCQ)
venous plexus. l It is due to back pressure in the mastoid
m Medially emissary vein.
n the two cavernous sinuses are connected with m Fundus
each other by transverse sinuses which account n normal with unimpaired vision in early cases.
for transfer of infection from one side to n In advanced cases
the other. l retinal veins show congestion
n Clinical picture l papilloedema
m starts initially as a unilateral condition n Complications
m soon becomes bilateral in more than 50 percent m hyperpyrexia
of cases due to intercavernous communication. m meningitis
OPHTHALMOLOGY
m General features. m pulmonary infarction

n Patient is seriously ill having high grade fever n Treatment
with rigors, vomiting and headache. m Antibiotics are the sheet anchor of treatment.
m Ocular features m Analgesics and anti-inflammatory drugs control
n Severe pain in the eye and forehead on the affected pain and fever.
side. m Anticoagulant
Clinical Cavernous sinus Orbital cellulitis Panophthalmitis

features thrombosis
1. Laterality Initially unilateral, Unilateral Unilateral
but soon
becomes bilateral
2. Degree of proptosis Moderate Marked Moderate
3. Vision Not affected in Not affected in Complete loss of
early stage early stage vision from the
beginning
4. Cornea and anterior Clear in early stages Clear in early stages Hazy due to corneal
oedema. Pus in the
anterior chamber
5. Ocular movements Complete limitation to Marked limitation Painful and limited
palsy
6. Oedema in mastoid region Present Absent Absent
7. General symptoms Marked Mild Mild
with fever, and prostrations
TOPIC 44 - CMV RE
112
TOPIC - 44 CMV RETINITIS l tractional retinal detachment (MCQ)
l rubeosis iridis
n Cytomegalic inclusion disease
l neovascular glaucoma.
m Congenital cytomegalic inclusion disease.
m Treatment
n Ocular involvement
n Medical treatment
l peripheral, central or total necrotizing
l Course of oral corticosteroids — main stay
chorioretinitis
of treatment during active inflammation.
l with associated vitreous haze
l A course of antitubercular therapy.
l Posterior pole is involved more commonly
n Laser photocoagulation of the retina is
m Acquired cytomegalic inclusion disease.
indicated in stage of neovascularizion.
n occurs only in the immunosuppressed
n Vitreoretinal surgery is required for
patients
l non-resolving vitreous haemorrhage
n CMV retinitis’ characterised by presence of
l tractional retinal detachment.
l yellow-white exudates (areas of retinal
necrosis)
l associated with areas of vasculitis and retinal
TOPIC 46 -
haemorrhages. OPHTHALMIA NEONATARUM
OPHTHALMOLOGY
l haemorrhagic retinal necrosis - sometimes n OPHTHALMIA NEONATORUM
described as ketchup (tomato sauce) on m bilateral inflammation of the conjunctiva
cottage cheese at the posterior pole (MCQ) m occur in an infant
n Some eyes may develop exudative retinal m any discharge or even watering from the eyes in the first
detachment. week of life should arouse suspicion of ophthalmia
n Ultimately, there occurs total retinal atrophy neonatorum, as tears are not formed till then.
m Treatment m During birth is most common mode of infection
n treatment with intravenous dihydroxy- from the infected birth canal especially when the
propylmethyl guanine has been shown to child is born with face presentation or with
cause regression in some cases. forceps.
n Causative agents
TOPIC 45 - EALES DISEASE m Chemical conjunctivitis caused by silver nitrate or
n Eales’ disease antibiotics used for prophylaxis.
TOPIC 44, 45, 46

m Gonococcal
m It is an idiopathic inf lammation of the
m Staphylococcus aureus, Streptococcus
peripheral retinal veins. (MCQ)
m It is characterised by recurrent vitreous
haemolyticus, and Streptococcus pneumoniae.
m Neonatal inclusion conjunctivitis caused by
haemorrhage (MCQ)
m a hypersensitivity reaction to tubercular
serotypes D to K of Chlamydia trachomatis
proteins. is the commonest cause of ophthalmia
m It is a bilateral disease
neonatorum in developed countries.(MCQ)
m Herpes simplex ophthalmia neonatorum caused by
m typically affecting young adult males. (MCQ)
m The common presenting symptoms
herpes simplex-II virus.
n sudden appearance of floaters (black spots)
n Symptoms and signs
m Pain and tenderness in the eyeball.
in front of the eye(MCQ)
m Conjunctival discharge.
n painless loss of vision due to vitreous
n It is purulent in gonococcal ophthalmia
haemorrhage. (MCQ)
l The haemorrhage clears up but recurrences
neonatorum
n mucoid or mucopurulent in other bacterial cases
are very common.
m Clinical course of the Eales’ disease
and neonatal inclusion conjunctivitis.
m Lids
n Stage of inflammation
n usually swollen in infants born to mothers with
n Stage of ischaemia
n Stage of retinal neovascularization leads to recurrent
untreated gonococcal infection.
vitreous haemorrhage. n Treatment
m Postnatal Prophylactic measures include :
n Stage of sequelae is characterized by development
n Use of either 1 percent tetracycline ointment
of complications
l proliferative vitreoretinopathy
or 0.5 percent erythromycin ointment or 1
113
percent silver nitrate solution (Crede’s method) cosmetically unacceptable proptosis is present in a blind
into the eyes of the babies immediately after eye (due to optic atrophy).
birth. n In unoperable cases, radiotherapy should be
m Curative treatment. given.
n Chemical ophthalmia neonatorum
TOPIC 48 - RETROLENTAL FIBROPLASIA
l a self-limiting condition, and does not
require any treatment. n Retinopathy of prematurity (ROP)
n Gonococcal ophthalmia m also known as retrolental fibroplasia.
l Topical therapy should include : m bilateral proliferative retinopathy
„ Saline lavage hourly till the discharge is m occur in premature infants with low birth
eliminated. weight who often have been exposed to high
concentration of oxygen.
RETROLENTAL FIBROPLASIA
„ Bacitracin eye ointment

„ penicillin drops m primary causative factors (MCQ)
„ If cornea is involved then atropine n Low birth weight
sulphate ointment should be applied. n decreased gestational age
l Systemic therapy for 7 days m Supplemental oxygen administration is now
„ Ceftriaxone considered only a risk factor.
„ Cefotaxime m Staging
„ Ciprofloxacin n Plus disease (MCQ)
„ crystalline benzyl penicillin l refers to presence of tortuous dilated
n Neonatal inclusion conjunctivitis vessels at posterior pole with any stage of
l topical ROP.
„ tetracycline 1 per cent l engorgment and dilatation of iris vessels,
„ erythromycin 0.5 per cent which result in poor pharmacological
l systemic erythromycin dilatation of pupil.
„ Both parents should also be treated with l Plus diseases signifies a tendency to
systemic erythromycin. progression.
n Prethreshold
OPTIC NERVE GLIOMA
TOPIC 47 - OPTIC NERVE GLIOMA n Threshold disease
n Optic nerve glioma. l This stage needs laser or cryotherapy in less
m It is a benign tumour arising from the astrocytes. than 72 hours.

m It usually occurs in first decade of life. m Screening and management
m Associated with von Recklinghausen’s n Prophylaxis to prevent ROP
neurofibromatosis (55%)(MCQ) l the premature newborns should not be
m Clinical features. placed in incubator with an O2

n early visual loss associated with a gradual, concentration of more than 30 percent
painless, unilateral axial proptosis l efforts should be made to avoid infection
n occurr in a child usually between 4 and 8 years and attacks of apnoea.

of age l a regular screening is very important.
n Fundus examination may show optic atrophy n Who should be screened for ROP (Important MCQ
(more common) or papilloedema and in exam )

venous engorgement. l All premature babies born at less than or
n Intracranial extension of the glioma equal to 32 weeks of gestational age

through optic canal is not uncommon. l those weighing 1500g or less
m Diagnosis. n The first examination by indirect

n X- rays show uniform regular rounded ophthalmosocpy should be done between 6
enlargement of optic and 7 weeks post-natal age or 34 weeks
n CT scan and ultrasonography depicting a post-conceptual age (whichever is earlier).
fusiform growth in relation to optic nerve (MCQ)
m Treatment. n Stages of Retinopathy of prematurity
n excision of the tumour mass with preservation l Mature retina
of the eyeball, by lateral orbitotomy when the

114
„ labelled when the vessels have reached l Normal antero-posterior length of eyeball
within one disc diameter of both nasal and is about 24 mm
temporal ora-serrata. n There occurs total loss of accommodation.
„ Infants with mature retina does not require m Clinical features
further follow-up. n Symptoms.
l Immature retina l Defective vision.
„ labelled when the vessels are short of one „ Main symptom in aphakia is marked
disc diameter of the nasal or temporal ora defective vision for both far and near due to
but ROP is not developed yet. ® high hypermetropia
„ Such infants require further follow-up ® absence of accommodation.
weekly. l Erythropsia and cynopsia i.e., seeing red and blue
l Retinopathy of prematurity images.
n When ROP is detected following measures should „ occurs due to excessive entr y of
be taken: ultraviolet and infrared rays in the
m Stage 1 and 2. absence of crystalline lens.
n Since spontaneous regression of disease occurs n Signs of aphakia include:
OPHTHALMOLOGY
in 80 to 90% of cases l Limbal scar may be seen in surgical aphakia
n only a weekly examination is recommended. l Anterior chamber is deeper than normal.
m Stage 3, threshold disease l Iridodonesis i.e., tremulousness of iris can be
n should be treated by cryo or laser to prevent demonstrated.
progression and to achieve regression. l Pupil is jet black in colour.
m Stage 4a. l Purkinje’s image test shows only two images
n Scleral buckling is recommended in addition (MCQ)
to cryo or laser therapy. „ (normally four images are seen).
m Stage 4b and 5. l Fundus examination shows hypermetropic
n Vitrectomy needs to be carried out in this stage. small disc.
n Prognosis is poor in stage 4b and 5. l Retinoscopy reveals high hypermetropia.
m Treatment
TOPIC 49 - APHAKIA n Optical principle is to correct the error by
convex lenses of appropriate power so that
n Aphakia
the image is formed on the retina
m a condition in which the lens is absent from the
APHAKIA
n Modalities for correcting aphakia include:
pupillary area.
l Spectacles
m Aphakia produces a high degree of
l contact lens
hypermetropia.
l intraocular lens
m Causes
l refractive corneal surgery.
n Congenital absence of lens.
n Spectacles prescription
n Surgical aphakia after removal of lens is the
l most commonly employed method of
commonest presentation. (MCQ)
correcting aphakia, especially in
n Aphakia due to absorption of lens matter is noticed
developing countries.
rarely after trauma in children.
l Roughly, about +10 D with cylindrical
n Traumatic extrusion of lens from the eye
lenses for surgically induced astigmatism
n Posterior dislocation of lens in vitreous
are required to correct aphakia in previously
m Following optical changes occur after removal
emmetropic patients
of crystalline lens:
l An addition of +3 to +4 D is required for
n Eye becomes highly hypermetropic.
near vision to compensate for loss of
n Total power of eye is reduced to about +44
accommodation.
D from +60 D. (MCQ)
l Advantages of spectacles. (MCQ)
n The anterior focal point becomes 23.2 mm in
„ It is a cheap, easy and safe method of
front of the cornea.
correcting aphakia.
n The posterior focal point is about 31 mm behind
l Disadvantages of spectacles (MCQ)
the cornea i.e., about 7 mm behind the eyeball.
„ Image is magnified by 30 percent
„ hence not useful in unilateral aphakia
115
„ it produce diplopia l Such patients require glasses to correct the
„ Problem of spherical and chromatic myopia for distance vision
aberrations of thick lenses l may or may not need glasses for near
„ Field of vision is limited. vision depending upon the degree of myopia.
„ Prismatic effect of thick glasses. n Consecutive hypermetropia
„ ‘Roving ring Scotoma’ (Jack in the box l develops when the under-power IOL is
phenomenon). (MCQ) implanted.
„ Cosmetic blemish especially in young l Such patients require plus glasses for
aphakes. distance vision and additional +2 to +3 D
n Contact lenses. for near vision.
l Advantages of contact lenses over l Varying degree of surgically-induced
spectacles include (MCQ) astigmatism is also present in pseudophakia
„ Less magnification of image m Signs of pseudophakia (with posterior chamber
„ Elimination of aberrations and prismatic IOL).
effect of thick glasses n Surgical scar may be seen near the limbus.
BAND KERATOPATHY
„ Wider and better field of vision n Anterior chamber is slightly deeper than normal
„ Cosmetically more acceptable. n Mild iridodonesis (tremulousness) of iris may be
„ Better suited for uniocular aphakia. demonstrated.
l Disadvantages of contact lenses are (MCQ) n Purkinje image test shows four images. (MCQ)
„ more cost n Pupil
„ cumbersome to wear, especially in old age l blackish in colour
and in childhood l but when light is thrown in pupillary area
„ corneal complications may be associated. shining reflexes are observed.
l Intraocular lens implantation
„ best available method of correcting aphakia. TOPIC 50- BAND KERATOPATHY
„ it is the commonest modality being
n Calcific degeneration (Band Shape keratopathy)
employed now a days
m a degenerative change associated with deposition
l Refractive corneal surgery
of calcium salts in
„ Keratophakia.
n Bowman’s membrane
® a lenticule prepared from the donor
n most superficial part of stroma
APHAKIA
cornea is placed between he lamellae of

n in deeper layers of epithelium.
patient’s cornea.
m Band keratopathy is seen in association with
„ Epikeratophakia.
n chronic uveitis in adults
® Lenticule prepared from the donor
n children with Still’s disease
cornea is stitched over the surface
n phthisis bulbi
of cor nea after removing the
n chronic glaucoma
epithelium.
n chronic keratitis
„ Hyperopic Lasik
n ocular trauma.
n Pseudophakia
m Age related BSK is common and affects otherwise
m condition of aphakia when corrected with an
healthy cornea.
intraocular lens implant (IOL) is referred to as
m Metabolic conditions rarely associated with BSK
pseudophakia or artephakia. (MCQ)
include
m Refractive status of a pseudophakic eye
n hypercalcaemia (MCQ)
depends upon the power of the IOL implanted:
n chronic renal failure.
n Emmetropia
m Clinical features.
l produced when the power of the IOL
n It typically presents as a band- shaped opacity
implanted is exact.
in the interpalpebral zone with a clear
l Such patients need plus glasses for near
interval between the ends of the band and
vision only
the limbus (MCQ)
n Consecutive myopia
n The condition begins at the periphery and
l occurs when the IOL implanted overcorrects
gradually progresses towards the centre.
the refraction of eye.
116
n The opacity is beneath the epithelium which l Post-neuritic optic atrophy
usually remains intact. l Vascular (ischaemic) optic atrophy.
n Surface of this opaque band is stippled due to m Pathological features
holes in the calcium plaques in the area of nerve n Degeneration of the nerve fibres may be associated with
canals of Bowman’s membrane excessive gliosis.
m Treatment l Seen in consecutive and postneuritic optic
n Chelation with EDTA (chelating agent) atrophy.
n Phototherapeutic keratectomy (PTK) with excimer n Degeneration and gliosis may be orderly
laser is very effective l proliferating astrocytes arrange themselves in
n Keratoplasty may be performed when the band longitudinal columns replacing the nerve
keratopathy is obscuring useful vision. fibres (columnar gliosis).
l seen in primary optic atrophy.
TOPIC 51 - OPTIC ATROPHY n Degeneration of the nerve fibres may be associated with
negligible gliosis.
n OPTIC ATROPHY l It occurs due to progressive decrease in
m It refers to degeneration of the optic nerve
blood supply.
m occurs as an end result of any pathologic process
OPHTHALMOLOGY
l Such pathological changes are labelled as
that damages axons in the anterior visual cavernous optic atrophy
system, i.e. from retinal ganglion cells to the l Seen in glaucomatous and ischaemic
lateral geniculate body.(MCQ) (vascular) optic atrophy.
m Classification
m Etiology
n Primary versus secondary optic atrophy.
n Primary (simple) optic atrophy
l Primary optic atrophy refers to the simple
l results from the lesions proximal to the optic disc
degeneration of the nerve fibres without without antecedent papilloedema.
any complicating process within the eye e.g., multiple sclerosis (MCQ)
syphilitic optic atrophy of tabes dorsalis. l Its common causes are:
l Secondary optic atrophy occurs following any
„ retrobulbar neuritis (idiopathic)
pathologic process which produces optic „ Leber’ s and other hereditary optic
neuritis or papilloedema. atrophies,
OPTIC ATROPHY
l Why Primary and Secondary classification is
„ intracranial tumours pressing directly on
obsolete (MCQ) the anterior visual pathway (e.g. pituitary
„ papillitis in multiple sclerosis produce
tumour)
secondary optic atrophy „ traumatic severance or avulsion of the
„ retrobulbar neuritis in multiple sclerosis
optic nerve
produce an apparently primary optic „ toxic amblyopias (chronic retrobulbar
atrophy. neuritis)
n Ascending versus descending optic atrophy.
„ tabes dorsalis.
l Ascending optic atrophy
n Consecutive optic atrophy
„ follows damage to ganglion cells or nerve
l It occurs following destruction of ganglion
fibre layer due to disease of the retina or cells
optic disc. l Occur secondary to degenerative or
„ In it the ner ve fibre degeneration
inflammatory lesions of the choroid and/
progresses (ascends) from the eyeball or retina.
towards the geniculate body. l Its common causes are:
l Descending or retrograde optic atrophy
„ diffuse chorioretinitis
„ proceeds from the region of the optic tract,
„ retinal pigmentary dystrophies such as
chiasma or posterior portion of the retinitis pigmentosa
optic nerve towards the optic disc. „ pathological myopia
n Ophthalmoscopic classification based on its
„ occlusion of central retinal artery.
ophthalmoscopic appearance. n Postneuritic optic atrophy.
l Primary (simple) optic atrophy
l It develops as a sequelae to long-standing
l Consecutive optic atrophy
papilloedema or papillitis.
l Glaucomatous optic atrophy
n Glaucomatous optic atrophy
117
n Vascular (ischaemic) optic atrophy. m Differential diagnosis
l giant cell arteritis n Non-pathological pallor of optic disc is seen in
l severe haemorrhage (MCQ)
l severe anaemia l axial myopia
l quinine poisoning. l infants
m Clinical features of optic atrophy l elderly people with sclerotic changes.
n Loss of vision n Temporal pallor is associated with large
l ophthalmoscopic signs cannot be correlated physiological cup.
with the amount of vision. n Pathological causes of pallor disc (other than optic
n Pupil atrophy) include
l Semidilated l hypoplasia,
l direct light reflex is very sluggish or absent l congenital pit
l Swinging flash light test depicts Marcus Gunn l coloboma.
pupil. (MCQ)
n Visual field loss TOPIC 52 - PTOSIS
l peripheral in systemic infections
n Types and etiology
OPHTHALMOLOGY
l central in focal optic neuritis

m Congenital ptosis
l eccentric when the nerve or tracts are
n congenital maldevelopment of the levator
compressed.
palpebrae superioris (LPS
m Ophthalmoscopic appearance of the disc
m Acquired ptosis
n pallor of the disc
n Neurogenic ptosis
n decrease in the number of small blood vessels
l third nerve palsy, Horner’s syndrome
(Kastenbaum index).
l ophthalmoplegic migraine and multiple
n The pallor is not due to atrophy of the nerve
sclerosis.
fibres but to loss of vasculature.
n Myogenic ptosis.
n Primary optic atrophy (MCQ)
l myasthenia gravis, dystrophia myotonica,
l Colour of the disc is chalky white or white
l ocular myopathy, oculo-pharyngeal muscular
with bluish hue.
dystrophy
l Its edges (margins) are sharply outlined.
l following trauma to the LPS muscle.
l Slight recession of the entire optic disc
n Aponeurotic ptosis.
occurs in total atrophy.
l defect of the levator aponeurosis in the
PTOSIS
l Lamina cribrosa is clearly seen at the

presence of a normal functioning muscle.
bottom of the physiological cup.
l It includes
l Major retinal vessels and surrounding retina
„ involutional (senile) ptosi
are normal.
„ postoperative ptosis (which is rarely
n Consecutive optic atrophy (MCQ)
observed after cataract and retinal
l Disc appears yellow waxy
detachment surgery)
l Its edges are not so sharply defined as in
n Mechanical ptosis
primary optic atrophy.
l lid tumours, multiple chalazia and lid oedema
l Retinal vessels are attenuated.
l cicatricial ptosisas seen in patients with ocular
n Post-neuritic optic atrophy (MCQ)
pemphigoid and trachoma.
l Optic disc looks dirty white in colour.
n Congenital synkinetic ptosis (Marcus Gunn jaw-
l Due to gliosis its edges are blurred,
winking ptosis). (MCQ)
l physiological cup is obliterated
n In this condition there occurs retraction of the
l lamina cribrosa is not visible
ptotic lid with jaw movements
l Retinal vessels are attenuated
n Occurs with stimulation of ipsilateral
l perivascular sheathing is often present.
pterygoid muscle.
n Glaucomatous optic at.rophy
n common causes of pseudoptosis (simulated ptosis)
l deep and wide cupping of the optic disc
are
l nasal shift of the blood vessels
n microphthalmos, anophthalmos
n Ischaemic optic atrophy
n enophthalmos and phthisis bulbi.
l pallor of the optic disc associated with marked
n Measurement of amount (degree) of ptosis.
attenuation of the vessels
118
n In unilateral cases, difference between the TOPIC 54 - VITREOUS HEMORRHAGE
vertical height of the palpebral fissures of
the two sides indicates the degree of ptosis n Vitreous haemorrhage
m usually occurs from the retinal vessels
n In bilateral cases it can be determined by
m may present as pre-retinal (sub-hyaloid) or an
measuring the amount of cornea covered
by the upper lid and then subtracting 2 mm. intragel haemorrhage.
m Causes
n Treatment
n Spontaneous vitreous haemorrhage from retinal
n Congenital ptosis.
m Fasanella-Servat operation. (MCQ)
breaks especially those associated with PVD.
n Trauma to eye, which may be blunt or perforating
n It is performed in cases having mild ptosis
n Inflammatory diseases
(1.5-2mm) and good levator function.
l occur due to erosion of the vessels
n In it, upper lid is everted and the upper tarsal
l Seen in acute chorioretinitis and
border along with its attached Muller’s
muscle and conjunctiva are resected periphlebitis retinae primary or secondary
m Levator resection. (MCQ)
to uveitis.
n Vascular disorders
n It is a very commonly performed operation
RHABDOMYOSARCOMA
l hypertensive retinopathy,
for moderate and severe grades of ptosis.
l central retinal vein occlusion.
l Conjunctival approach (Blaskowics’ operation)
n Metabolic diseases such as diabetic retinopathy.
(MCQ)
n Blood dyscrasias
l Skin approach (Everbusch’s operation
l retinopathy of anaemia,
l Frontalis sling operation (Brow suspension)
l leukaemias
l polycythemias
TOPIC 53 - RHABDOMYOSARCOMA
l sickle-cell retinopathy.
n Rhabdomyosarcoma. n Bleeding disorders
m It is a highly malignant tumour of the orbit l purpura,haemophilia and scurvy.
m arise from the extraocular muscles. .(MCQ) n Neoplasms.
m It is the most common primary orbital tumour l retinoblastoma.
VITREOUS HEMORRHAGE
among children (MCQ) n Idiopathic
m usually occurring below the age of 15 years n Clinical features
(90%)..(MCQ) m Symptoms
m Clinical features. n when the vitreous haemorrhage is small
n It classically presents as rapidly progressive l Sudden development of floaters occurs.
proptosis of sudden onset in a child of 7-8 n With massive vitreous haemorrhage
years l patient develops sudden painless loss of
n The tumour commonly involves the vision.
superionasal quadrant (MCQ) m Signs
m Diagnosis. n Distant direct ophthalmoscopy reveals
n X- rays showing bone destruction l black shadows against the red glow in
n CT scan demonstrating tumour in relation to small haemorrhages
an extraocular muscle. l no red glow in a large haemorrhage.
n Diagnosis is confirmed by biopsy. n Direct and indirect ophthalmoscopy show presence
m Treatment of blood in the vitreous cavity.
n High dose radiation therapy combined with n Ultrasonography with B-scan
systemic chemotherapy is very effective. m Fate of vitreous haemorrhage
n Chemotherapy regime consists of Vincristine and n Complete absorption within 4-8 weeks.
actinomycin-D , cyclophosphamide n Organization of haemorrhage
n Exenteration is required in a few unresponsive n Complications
patients.(MCQ) l vitreous liquefaction, degeneration
l khaki cell glaucoma (in aphakia)
n Retinitis proliferans complicated by tractional
retinal detachment.
119
n Treatment
m Conservative treatment
n consists of bed rest, elevation of patient’s
head and bilateral eye patches
m Treatment of the cause.
m Vitrectomy by pars plana route, if the
haemorrhage is not absorbed after 3 months.
OPTHOMOLOGY
VITREOUS HEMORRHAGE
120

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OPHTHALMOLOGY

m Treatment of congenital glaucoma is primarily n prevalence of POAG is more in hypertensives

localization of the Schlemm’s canal. significant loss of visual field

and inferior temporal portions of „ Ring or double arcuate scotoma.

Severity of glaucoma damage with POAG having associated

Severe Visual-field abnormalities in both „ It is sheet anchor in the medical management

„ lowers IOP by decreasing aqueous n peripheral anterior synechiae

® can be elicited by shining a penlight diagnosed as latent angle-closure glaucoma.

at least three of the four quadrants l during anxiety (sympathetic overactivity)

control IOP. l swollen cataractous lens due to

n STEROID-INDUCED GLAUCOMA (MCQ)

„ Anterior capsular cataract „ consists of a small circular circumscribed

extended wear contact lens. n Dietary factors.

» one-piece PMMA with modified C- „ Nuclear cataract is more common and

objects): pupillary margin

Immature senile cataract versus nuclear sclerosis

1. Painless progressive loss of vision 1. Painless progressive loss of vision

Differences between mature senile cataract and leukocoria

1. White reflex in pupillary area White reflex in pupillary area

n It may occur due to degeneration of zonules l myopic chorioretinal degeneration.

opacities). (MCQ) n A very characteristic sign is the appearance of

sophisticated microinstruments. into vitreous cavity is much less than

after ECCE. No such problem is known with of phocoemulsification, especially in hard

in eye camps. phaco machine.

(ECCE) m Demerits of manual SICS over

m Merits of conventional ECCE over SICS. at the site of conjunctival flap.

SICS is that it is a simple technique to master owing to scleral incision.

m Dermerits of conventional ECCE over SICS sometimes.

n Long incision (10 to 12 mm). incision in SICS is large (about 6 mm) as

l expulsive choroidal haemorrhage. n Topical anaesthesia may be sufficient for

n High incidence of post-operative phacoemulsification in expert hands.

n Postoperative suture-related problems like phacoemulsification, as phaco is usually performed

as phacoemulsification over manual SICS is that it

may occur. posterior chamber without prolapsing the nucleus

l all types of cataracts including hard phacoemulsification as compared to manual

n Learning curve. foldable IOLs are implanted through a smaller

surgery. for SICS and phacoemulsification.

l Elschnig’s pearls involving the central

anterior ciliary vessels „ They are large, thick, fluffy, lardaceous

l Hypopyon. (MCQ) pupillar y margin to anterior

vessels of iris formation

l Occlusio pupillae (MCQ) l Occurs especially in children having Still’s

Feature Granulomatous Non-granulomatous

n Treatment of iridocyclitis (A Very High yield „ cycloplegics should be continued for at

l 0.5 percent timolol maleate eyedrops

n requires lens extraction with guarded

(MCQ) n Sex. Incidence is higher in girls than boys.

years. conjunctiva, in a child living in bad hygienic

VISUAL FIELD DEFECTS

l beading, looping and dilatation. l Hard exudate at or within 500 micron of

n characterised by proliferation of new vessels n Tractional retinal detachment and

with large nuclei, resembling the cells of the

l Second hit (mutation)

capsule. m It is a non-striated muscle having three parts:

n Nerve supply. n Choroid

n Lens transparency n anterior-most part of ciliary body

n Metabolism m It plays an important metabolic role by providing

m It is located on the medial aspect of the occipital

m The prelaminar region is mainly supplied by

Actions of extraocular muscles „ It is upward movement of both eyes in

Muscle Primary Secondary Tertiary primary position.

MR Adduction - - of bilateral superior recti and inferior

SO Intorsion Depression Abduction in primary position.