Eye symptoms and signs, Blindness, Basics of ophthalmology.

1. Causes of blindness and symptoms of eye
disorders
Dr Ashish Tripathi

2. WHO Definition of Blindness
WHO defines Blindness as a corrected visual
acuity in the better eye of less than 3/60, and
Severe visual impairment as a corrected acuity
in the better eye of less than 6/60.

3. Category of visual
impairment
Visual acuity
Cat I (Low vision) 6/18-6/60
Cat II (Low vision) <6/60-3/60
Cat III (Blind) <3/60-1/60
Cat IV (Blind) <1/60-PL
Cat V ( Blind) NPL

4. 0.4 - 0.6 0.6 - 1 > 1%< 0.4%Prevalences:© WHO

5. W Pacific
26%
Africa
17%
Middle East
10%
Americas
10%
Europe
10%
SE Asia
27%
Best corrected
visual acuity
< 6/18 (0.3)
© WHO

6. CATARACT
47%
TRACHOMA
4%
ONCHO
1%
AMD
9%
GLAUCOMA
12%
OTHERS
13%
CORNEAL OPACITY
5%
DIABETIC
RETINOPATHY
5%
CHILDHOOD
BLINDNESS.
4%
Best corrected
Visual Acuity
< 3/60 (0.05)
© WHO

7. Cataract
42 %
Trachoma
15 %
Glaucoma
14%
Oncho.
1 %
Other
28 %
Cataract
47 %
Trachoma
4 %
Glaucoma
12%
Oncho.
1 %
Other
13 %
ARMD
9%
Ch Bl
4%
DR
5%
CO
5%
1995 2002

8. Cataract
5%
Glaucoma
18%
Other
4%
ARMD
50%
Ch Bl
3%
DR
17%
CO
3%
Cataract
50 %
Trachoma
4 %
Glaucoma
12%
Oncho 0.8 %
Other
14 %
ARMD
6%
Ch Bl 4%
DR 4%
CO 5%
More Developed
Countries
Less Developed
Countries

9. Women
64%
Men
36%
Men
Women
© WHO

10. Defective vision
Sudden painless loss of vision
 Vitreous hemorrhage
 Retinal detachment
 Optic neuritis
 Central retinal vein occlusion
 Central retinal artery occlusion

11. Sudden painful loss of vision
 Acute congestive glaucoma
 Trauma
 Chemical injuries
 Foreign body in the eye
 Giant cell arteritis

12. Gradual painless diminution of vision
 Cataract
 Open angle glaucoma
 Refractive error
 Age related macular degeneration
 Diabetic retinopathy
 Corneal dystrophy and degeneration
 Optic atrophy

13. Gradual painful diminution of vision
 Corneal ulcer ( keratitis)
 Chronic iridocyclitis

14. Transient loss of vision (Amaurosis fugax)
 Carotid artery disease
 Papilloedema
 Migraine
 Prodormal symptom of CRAO

15. Night blindness
 Vitamin A deficiency
 Retinitis pigmentosa and other retinal dystrophies and
degenerations
 Congenital stationary night blindness
 Pathological myopia
 Peripheral cortical cataract

16. Day blindness (Hamarlopia)
 Central nuclear or polar cataract
 Central corneal opacity
 Central vitreous opacity
 Congenital deficiency of cones

17. Other visual symptoms
Floaters( Black spots in front of eyes)
 Vitreous degeneration: Myopia or senile degeneration
 Exudates in vitreous
 Intermediate uveitis
 Vitreous hemorrhage

18. Flashes of light in front of eyes (photopsia)
 Posterior vitreous detachment
 Prodromal symptoms of retinal detachment
 Traction bands in the retina

19. Distorted vision
 Micropsia (Small size of objects)
 Macropsia (Larger size of objects)
 Metamorphopsia (distorted shape of the image
In macular diseases ARMD, CSR

20. Colored haloes
 Acute congestive glaucoma
 Mucopurulent conjunctivitis
 Mature / Hypermature cataract

21. Diplopia (double vision)
Binocular diplopia:
 Paralytic and restrictive strabismus: Nerve palsies, Myasthenia
gravis, Thyroid diseases, blow out fracture of globe
Uniocular diplopia
 Subluxated lens
 Double pupil
 Decentered IOL
 High Astigmatism

22. Watering from the eye
 Lacrimation
 Epiphora: nld blockage

23. Discharge from the eyes
 Watery
 Purulent / mucopurulent
 Hemorrhagic
 Ropy discharge

24. Itching burning and foreign body sensation
 Chronic conjunctivitis , allergic or other
 Trachoma
 Dry eyes
 Trichiasis
 Foreign body

25.  Sub-conjunctival hemorrhage
 Conjunctivitis
 Episcleritis
 Kerato-conjunctivitis
 Scleritis
 Corneal ulcer
 Acute congestive glaucoma
 Anterior uveitis
Red eye

26. Ocular or periocular pain: @GITA
 Acute congestive glaucoma
 Iridocyclitis
 Trauma
 Giant cell arteritis

27. Headache
 ICSOL
 Pseudotumor cerebri
 Sinusitis
 Migraine
Asthenopic symptoms
 Convergence/ fusional insufficiency
 refractive error
 astigmatism

28. Impairment of vision
 Causes
• Defects in clear image formation on retina
 Eg. Cataract
• Defect in retinal processing of image
 Eg Retinal detachment
• Defect in impulse transmission to occipital cortex
 Eg. Optic neuritis

29.  Watering
 Photophobia
 Buphthalmos

30.  Clinical features
 Pain/headache, redness, DVA, Colored haloes
 Ciliary congestion
 Corneal edema
 High IOP
 Mid dilated pupil and shallow AC
 Glaukomflecken – anterior capsular or subcapsular lens
opacities

31.  Retinopathy
 Cotton-wool spots
 Hard exudates
 Extensive hemorrhage
 Retinal oedema
 Choroidopathy
 Exudative detachment
 Elschnig spots
 Seigrist streaks
 Optic neuropathy
 Disc oedema
 AION
 Optic atrophy

32.  Sudden onset of DVA preceded by
 Photopsia / flashes of light
 Floaters

33.  Clinical presentation
 Leucocoria
 Strabismus
 Endophthalmitis like feature
 Proptosis
 Feature of raised intraocular pressure

34. Confusion :
Superimposition of two images
Diplopia : Binocular

35. Strabismus
Classification of strabismus
Heterophoria (Latent) Heterotropia (Manifest)
Esophoria
Exophoria
Hyper / hypophoria
Nonparalytic ( Concomitant )
Paralytic ( Incomitant )
Vertical
Hypertropia Hypotropia
Exotropia
Intermittent
Alternate
Constant ( RDS / LDS)
Esotropia
Accommodative
Nonaccommodative
Infantile
3rd Nerve Palsy
4th Nerve Palsy
6th Nerve Palsy

36. Asymptomatic
Exophoria
Eye strain (asthenopia)-headache
Equal vision or blurring of vision
Amblyopia due to anisometropia
Diplopia (horizontal & crossed)
Photophobia
Micropsia( due to use of accommodative convergence)
Increase in temporal visual field called as panoramic viewing
-

37.  Rabies
 Hepatitis B
 Retinoblastoma
 Bacterial or fungal keratitis
 Corneal dystrophy
 HIV
 HSV

38.  Painful red eye
 Decrease in vision
 Corneal oedema
 Anterior chamber reaction
 Cells
 Flare
 KP’s/nodules
 Miotic pupil

39. Symptoms
 Redness
 Pain: Iritis, glaucoma
 Photophobia
 Diffuse blur :Inflammatory cells, debris
 Decrease vision : cataract, macular edema retinal
lesions
 floaters: vitreous cells, exudates
 Asymptomatic

40.  Eyelid and skin: Nodules, vitiligo
 Conjunctiva: nodules, congestion
 Cornea: Kps
Fresh, old, large mutton fat
 Anterior chamber: Cells, Flare

41.  Redness
 Self limiting
 Diffuse or localized
 Non tender/ no pain
 No discharge

42.  Pain
 Red eye
 Decrease vision
 Anterior chamber reaction
 Vitreous exudates
 Loss of red fundal glow

43.  Corneal causes
 Conjunctivitis
 Dry eye
 Acute angle closure glaucoma
 Sub-acute angle closure glaucoma
 Iritis
 optic neuritis
 Orbital infection, inflammation
 Paralysis of muscles
 Cavernous sinus thrombosis
 ICSOL
 Idiopathic intracranial
hypertension
 GCA
 Refractive errors
 Trigeminal neuralgia
 Focusing spasm (eyestrain)
 Tension type headache
 Cluster headache
 Migraine

44.  Eye trauma
 Intraocular inflammation
 Neovascularization
 Iris malformation eg coloboma, aniridia.
 Cataract surgery

45.  Old age
 Intraocular inflammation
 Sleep
 Pontine hemmorhage
 Pilocarpine /phospholine iodide use
 Horner syndrome

46.  Increased intraocular pressure.
 Drugs
1. Anticholinergics: Atropine, homatropine, tropicamide
2. Sympathomimetics: Phenylephrine,cocaine, amphetamine
 Eye trauma
 III Nerve palsy

47.  Argyll Robertson pupil
 Tonic pupil (Holmes-Adies syndrome)

48.  Light reflex absent but near reflex is preserved
 Usually bilateral but asymmetrical
 Small and irregular pupil
 The condition is pathognomonic of central nervous system
syphilis

49.  Caused by postganglionic parasympathetic pupillomotor
damage
 Pupils are dilated and poorly reacting
 Constrict to the near reflex but redilates very slowly
 Includes other features such as diminished deep tendon
reflexes, orthostatic hypotension. Common in females.
 Unilateral in 80% of cases.

50.  Characterized by:
1. Ptosis, miosis enophthalmous ,anhydrosis
2. Iris heterochromia in congenital type. Affected iris appear
lighter.
 Localization of lesion in Horner syndrome is important .
1. First order neuron lesions: central disorders of nervous system
2. Second order neuron lesion caused by apical lung tumors

51.  Enumerate the causes of blindness.
 List the symptoms of eye diseases. Give examples.

52.  promotion of public awareness about eye donation
 tissue harvesting,
 tissue evaluation,
 tissue preservation, and
 tissue distribution.

53.  Donor eye collected by 6 hours after death
 Moist chamber storage from the site of collection to the
hospital
 McCarey-Kaufman (MK) media – 4 days

54.  Chondroitin sulphate based media – 7 days
 K-sol, Opti-sol – 7 days
 Cryo preservation for one year

55.  Intracapsular cataract extraction ICCE
 Extracapsular cataract extraction: ECCE
Conventional extracapsular
Small inscision cataract extraction SICE
Phacoemulsifiation
 Lensectomy

56.  Papillae
 Follicles
 Congestion
 Chemosis
 Sub conjunctival Hemorrhages
 Discharge
 Membrane and Pseudomembrane

57.  These are dilated telangiectatic conjunctival blood vessels,
varying from dot like changes to enlarged tufts surrounded
by edema and inflammatory cells.
 Seen in : bacterial conjunctivitis, allergic conjunctivitis.

59.  Focal lymphoid nodules with accessory vascularization.
 Seen in: Benign lymphoid foliculosis
Adenoviral conjunctivitis
Herpes viral conjunctivitis
Molluscum contagiosum
conjunctivitis
Drug induced eg: dipeveprin

62.  True membrane:
Beta hemolytic streptococci
Diphtheria
 Pseudo membrane:
Severe adenoviral conjunctivitis
Gonococcal conjunctivitis
Stevens Johnson's syndromes.

63.  Chlamydia :Oral erythromycin 50 mg/kg/day in four divided
doses for 14 days
 Gram-negative, gonococcal :Intravenous or intramuscular
ceftriaxone 25–50 mg/kg/day once a day for 7 days
 Povidine Iodine for prophylaxis

64.  Follicular trachoma
 Intense inflammatory trachoma
 Trachomatous Scarring
 Trichiasis
 Corneal Opacity

65. The key to the treatment of trachoma is the SAFE strategy
developed by the WHO.
 Surgery
 Antibiotic therapy
 Facial cleanliness
 Environmental change

66.  Pathogenesis
 Conjunctival vasodilation
 Increased vascular
permeability
 Leucocyte chemotaxis
 Ocular surface destruction
 Subsequent repair

67.  Characteristic features
 Inflammation
 Recurrence
 Chronicity
 Itching – main complaint

68.  Bilateral, recurrent, during warm
months
 Itching, rubbing,
 Thin ropy discharge
 Papillary hyperplasia
 Tranta’s dots in limbus
 Eosinophils, plasma cells, mast
cells,
 Tears IgG and histamine

69.  Residence in a cool place –air conditioning or climate
 Acetylcystein gt 10% - mucolytic agent
 Steroid drops – careful use
 Antihistamine drops
 Mast cell stabilizer – Sodium chromoglycate
 NSAID

70.  Scarring of conjunctiva
 Thickening of tarsal plate
 Meibomian orifice occlusion
 Symblepharon
 Destruction of accessory lacrimal glands
 Dry eye
 Punctal and canalicular occlusion

73.  Symptoms
 Mimics bacterial keratitis
 Slow & torpid course, less pain
 Signs
 Filamentous keratitis
 A greyish stromal infiltrate with a dry texture and indistinct elevated rolled out margins
 A surrounding feathery ,finger like extensions into stroma
 Multiple, small Satellite lesions
 Big Hypopyon (may not be sterile, static)
 Corneal vascularisation is conspicuously absent
 Perforation in Mycotic ulcers are rare but can occur.
 Resembles bacterial keratitis, however usually there is a history of preexisting chronic
corneal disease
Fungal ulcer

74. STAGING CLINICAL FEATURES
XN Night Blindness
X1A Conjunctival Xerosis
X1B Bitot’s Spot
X2 Corneal Xerosis
X3A Corneal ulcer involving <1/3rd corneal surface
X3B Corneal ulcer involving >1/3rd corneal surface
XS Corneal Scar
XF Xerophthalmic Fundus

75.  Orbital cellulitis
 Pseudotumor
 Dermoid and epidermoid
 Capillary hemangioma
 Lymphangioma
 Rhabdomyosarcoma
 Optic nerve glioma
 Neurofibroma
 Leukemia
 Metastic neuroblastoma

76.  Thyroid related orbitopathy
 Pseudotumour
 Metastatic neoplasms
 Secondary spread
 Cavernous hemangioma
 Lymphangioma
 Lacrimal gland tumour
 Lymphoma
 Meningioma
 Dermoid / epidermpoid

77.  Orbital cellulitis
 Rhabdomyosarcoma
 Leukaemia
 Metastatic neuroblastoma
 Bleeding into lymphangioma
 Ruptured dermoid

78. 1. Pain
2. Proptosis
3. Progression
4. Palpation
5. Pulsation
6. Periorbital changes

80.  Congenital Cataract
 RB
 ROP
 Toxocariasis
 Coat’s disease
 HPPV
 Organised vitreous H’ge
 Incontinentia pigmenti

81.  MICROVASCULAR OCCLUSION
 Capillary changes: pericyte loss, thickening of basement
membrane and damage and proliferation of endothelial cells.
 Hematological changes: RBC deformation and increased
rouleaux formation. Increased platelet stickiness and aggregation.
 Consequence:
 Capillary non-perfusion and ischaemia, which leads to
 Arteriovenous shunts (IRMA’s)
 Neovascularisation (NVD and NVE)

82.  MICROVASCULAR LEAKAGE
 Break down of inner blood retinal barrier leading to
 Retinal oedema (diffuse and localized)
 Hard exudates
 Heamorrhage

83. # Leukocoria
# Strabismus
 Proptosis
 Glaucoma (Buphthalmos)
 Vitreous hemorrhage
 Hyphema
 Ocular and peri-ocular inflammation
 Hypopyon

84. Current treatment options
 Photocoagulation
 Chemotherapy
 External beam radiation therapy
 Enucleation/Exenteration

85.  Stage of progressive infiltration
 Stage of active ulceration
 Stage of regression
 Stage of cicatrisation

86.  Causes –
 Extreme proptosis
 Bell’s palsy
 Ectropion
 Symblepheron
 Lagopthalmus
 Pathogenesis –
 Due to exposure, corneal epithelium dries up followed
by dessication and after the epithelium is cast off,
invasion by infective organism occurs

87.  Toxic iridocyclitis
 Secondary glaucoma
 Desmatocele formation-sign of impending
perforation
 Perforation of corneal ulcer
 Sequalae of corneal perforation
 Corneal scarring

88.  May be caused by sneezing, coughing, etc.
 Acute rise of IOP
 Weak ulcer floor unable to support this pressure
 Perforation occurs
 Ones perforation occurs – leakage of aqueous – fall of
IOP – iris-lens diaphragm moves forward, leading to iris
prolapse, subluxation or ant. Disloction of lens,
anterior synachia, adherent leucoma, anterior
capsular cataract, corneal fistula, purulent uveitis,
endophthalmitis, panophthalmitis, intraocular hhg
etc.

89.  Clinical features
 Symptoms
 Similar to bacterial keratitis but less prominent than equal sized bacterial
ulcer
 Signs
 Dry looking, yellowish white, with indistinct margin
 Delicate, feathery, finger-like projections into adjacent stroma
 May be surrounded by greyish halo and multiple satellite lesions
 Overlying epithelium is elevated
 Hypopyon more common

90.  Acute pain, redness, lacrimation
 Photobhobia and blurring of vision
 Signs – CCC, initially numerous white plaques of epithelial cells
appear on cornea – superficial punctate keratitis (SPK’s)
 Erosions coalesce together, spread in all directions forming dendritic
figures (pathognomonic)
 Ulcer bed stains with fluorescein & rose bengal
 Corneal sensation diminished or absent
 Geographical keratitis – enlargement

91.  The diagnosis of corneal ulcer is made by-
[A] Clinical evaluation
• Thorough History taking
• General Physical examination
• Ocular Examination
[B] Laboratory investigations
• Routine Laboratory investigations
• Microbiological investigations

92. Routine lab investigations
 Hb, TLC, DLC, ESR,
 Blood Sugar
 LFT
Microbiological investigations
 These are done to identify causative organism, confirm the diagnosis
& guide the treatment to be instituted.
 Specimens used
Corneal scraping
Corneal Biopsy

94. • Can be performed with slit lamp under topical anaesthesia(0.5%propacaine hydrochloride)
• Heat-sterilized platinum (kimura) spatula blade, a No.15 BP blade or a large gauge hypodermic needle is used to
scrape corneal tissues from advancing borders of infected area
• Specimens obtained are usually small in quantity and should be inoculated directly onto appropriate culture media in
order to maximize culture yield
• While plating the culture medium, the specimen is inoculated in C streaks on fresh blood agar plate to differentiate
valid bacterial growth from plating contamination.
Corneal Scraping

95.  Primary staining of heat fixed smear with crystal violet for 1 min
 Pour off crystal violet and add grams iodine
 Keep for 1 min and wash with water
 Decolourise with an organic solvent (alcohol or acetone) for 10-30 sec
 Wash with water
 Counterstain with a dye of contrasting colour (safranin, carbol fuchsin)
for 20 sec

97.  Conventional route ( Trabecular) : 90%
 Unconventional ( Uveo-scleral) : 10%

98.  Visual acuity
 Young children
 Catford drum
 Acuity cards
 Preferential looking
Children > 3 years
Symbol matching games
Naming the pictures on a chart

99. Paralytic squint
 Onset- sudden
 Diplopia-present
 Ocular movements-limited
in direction of pralyzed
muscles
 False projection-positive
 Head posture-particular
 Nausea & vomiting-present
 2ry deviation > 1ry
deviation
 Pathologic sequelae of
muscles in old cases
 Slow
 Usually absent
 Full
 Negative
 Normal
 Absent
 2ry deviation = 1ry
deviation
 absent
Non-paralytic

100. Maturation of cortical cataract
 Lamellar seperation
 Stage of incipient cataract
Cuneiform
Cupuliform
 Immature senile cataract
 Mature cataract
 Hypermature cataract
Morgagnian, Sclerotic

101.  Anxiety
 Nausea & gastritis
 Irritative or allergic conjunctivitis
 Corneal abrasion
 d/t LA: retrobulbar hhg, oculocardiac reflex, perforation of
globe, subconj. Hhg

102.  Sup. Rectus ms laceration
 Excessive bleeding
 Injury to cornea, iris & lens
 Posterior capsule rupture
 Vitreous loss
 Expulsive choroidal hhg

103.  Hyphaema
 Iris prolapse
 Shallow ant. Chamber
 Post-op ant. Uveitis
 Bact. Endophthalmitis

104.  Cystoid macular edema
 Delayed post-op endophthalmitis
 Retinal detachment
 2ry cataract
 glaucoma

105.  Avascularity
 Tight packed nature of cells
 Arrangement of the lens protein
 Semipermeability of capsule
 Pumping mechanisms
 Auto oxidation and high concentration of reduced
glutathione

106. Symptoms
 Frequent change of glass
 Decreased visual acuity
 Myopic shift
 Loss of abilty to see in bright light
 Monocular diplopia
 Glare
 Coloured haloes around light

107.  Two light descrimination test
 Maddox rod test
 Entoptic phenomenon
 Laser interferometry
 Photo stress test
 ERG
 VER

108.  Suppression
 Amblyopia – continued monocular suppressions
 Anomalous retinal correspondence
 Abnormal Head Posture

109. Pupillary Light Reflex
Parasym. : 4 Neurons
1st order : Photoreceptors of Retina to Pretectal
Nucleus in Midbrain at level of Superior Colliculus
2nd order : Pretectal Nucleus to Both
Edinger – Westphal nuclei.
3rd order : Edinger – Westphal nuclei to Ciliary
Ganglion . Parasym fibres come by Inf div of 3rd nerve
via Nerve to Inf oblique muscle.
4th order : Ciliary Ganglion to Sphincter pupillae via
short ciliary nerves

110. Sympathetic Nerve Supply
3 Neurons
1st order : Posterior hypothalamus
to Ciliospinal centre of Budge
located between C8 and T2.
2nd order : CSC of Budge to
Superior Cervical Ganglion in
Neck
3rd order : Along ICA to enter skull
and joins Ophthalmic div of V
Nerve . Sym fibres reach Ciliary
body and Dilator pupillae via
Nasociliary and long ciliary
nerves.

111.  Insidious
 Asymptomatic
 Mild headache
 Eyeache
 Defect in visual field
 Frequent change in presbyopic glassse
 Delayed dark adoption

112.  Ant. Segment signs: sluggish pupillary reflex, hazy cornea
 IOP: falls during evening
 Optic disc changes: early
 vertically oval cup
 Asymmetry of cups
 Large cup ≥ 0.6mm
 Splinter hhg
 Pallor area on disc
 Atrophy of retinal nerve fibre layer

113.  Marked cupping 0.7-0.9
 Thinning of neuroretinal rim
 Nasal shifting of retinal vessels
 Pusation of retinal arterioles seen at disc margin
 Lamellar dot sign
 Optic disc changes: glaucomatous optic atrophy

114.  Isopter contraction
 Baring of blind spot
 Paracentral scotoma
 Seidel’s acotoma
 Arcuate or bjerrum’s scotoma
 Ring or double arcuate scotoma
 Roenne’s central nasal step
 Peripheral field defects
 Tubular vision

115. Complete
blindness
• Causes
Complete
blindness:
• Optic atrophy
• Traumatic avulsion of optic nerve
• Indirect optic neuropathy
• Acute optic neuritis

116. Ipsilateral blindness,
Contralateral
hemianopia

118. Distension of
3rd ventricle
Atheroma of
carotids

120. parietal lobe: inferior
quadrantic hemianopia
 Pie on the floor
Temporal lobe: superior
quadrantic hemianopia
Pie in the sky

121.  Mechanism of action
 They bind to β-adrenergic receptors and block sympathetic
transmission
 Lower IOP by reducing aqueous production by as much as 30% to
50%
 Most β-blockers are nonselective
 Betaxolol is β-1 selective, used to reduce pulmonary side effects.

122.  Side effects
 Ocular
 Stinging, burning, photophobia, blurred vision, dry eye, corneal
anesthesia & allergic conjunctivitis.
 Systemic
 Heart block, cardiac failure, asthma

123.  Contraindications
 Congestive heart failure
 Bradycardia
 Heart block
 Diabetic pts prone to hypoglycemia
 Asthma
 COPD

124. Drug receptor concentration Dose
Timolol nonselective 0.25%, 0.5% BD
betaxolol β-1 selective 0.5% OD
Levobunolol nonselective 0.25%, 0.5% BD
metipranolol nonselective 0.3% BD
Carteolol nonselective 1% BD

125.  Both topical and systemic carbonic anhydrase inhibitors
(CAIs) reduce IOP by reducing aqueous production.
 Topical CAIs dorzolamide & brinzolamide

126. Side effects
Ocular side effects
Irritation, stinging, superficial punctate keratitis and allergic
conjunctivitis.
 Anorexia, weight loss, paresthesia, fatigue, malaise and depression
 Potassium loss due to diuresis – hypokalemia
 Steven Johnson syndrome, blood dyscrasias, renal lithiasis.

127. Contraindications
 sulpha allergy
 Systemic not to be used in patients with renal lithiasis, renal
insufficiency, severe obstructive pulmonary disease and diabetic
ketoacidosis.

128.  Nonselective – epinephrine and dipivefrin
 Not used any more due to irritation & injection
 α-2 selective – apraclonidine and brimonidine

129.  Mechanism of action
 Apraclonidine – reduces IOP by increasing outflow
facility, decrease production, and decreasing episcleral
venous pressure
 Brimonidine – reduces IOP by decreasing aqueous production and
increasing uveoscleral outflow and may act as neuroprotective agent

130.  Side effects
 About 1/3rd of patients develop ocular allergy with apraclonidine
 Allergy to brimonidine is less common
 Newer formulation with purite preservative has even further reduced
incidence of allergy
 Life threatening hypotension and apnea have been reported in
infants treated with brimonidine

131.  Mechanism of action
 They reduce the IOP by increasing the osmolality
of the intravascular fluid
 As blood barrier prevents their entry into vitreous,
an osmotic gradient is established, causing fluid to
leave the vitreous to enter intravascular space

132.  Side effects
 Avoided in patients with compromised cardiac function
 Cerebral dehydration causes headache and disorientation
 Oral glycerol avoided in diabetics
 Contraindications
 Renal failure
 Cardiac failure
 Glycerol avoided in diabetics

133.  Preparation & administration
Drugs Concentration Dose
Latanoprost 0.005% OD
Bimatoprost 0.03% OD
Travoprost 0.004% OD
Isopropyl
unoprostone
0.15% BD

134. Mechanism of action
 Increase uveoscleral and also trabecular outflow
 Decrease production