Thursday, December 30, 2010


The intraocular pressure (IOP) is measured with the
help of an instrument called tonometer. Two basic
types of tonometers available are: indentation and
Indentation tonometery
Indentation (impression) tonometry is based on the
fundamental fact that a plunger will indent a soft eye
more than a hard eye. The indentation tonometer in
current use is that of Schiotz, who devised it in 1905
and continued to refine it through 1927. Because of
its simplicity, reliability, low price and relative
accuracy, it is the most widely used tonometer in the
Schiotz tonometer. It consists of (Fig. 21.12):
Handle for holding the instrument in vertical
position on the cornea;
Footplate which rests on the cornea;
Plunger which moves freely within a shaft in the
Bent lever whose short arm rests on the upper
end of the plunger and a long arm which acts as
a pointer needle. The degree to which the plunger
indents the cornea is indicated by the movement
of this needle on a scale; and
Weights: a 5.5 g weight is permanently fixed to
the plunger, which can be increased to 7.5 and 10
Technique of Schiotz tonometry. Before tonometry,
the footplate and lower end of plunger should be
sterilized. For repeated use in multiple patients it can
be sterilized by dipping the footplate in ether, absolute
alcohol, acetone or by heating the footplate in the
flame of spirit.
After anaesthetising the cornea with 2-4 per cent
topical xylocaine, patient is made to lie supine on a
couch and instructed to fix at a target on the ceiling.
Then the examiner separates the lids with left hand
and gently rests the footplate of the tonometer
vertically on the centre of cornea. The reading on
scale is recorded as soon as the needle becomes
steady It is customary to start with 5.5 gm weight.
However, if the scale reading is less than 3, additional
weight should be added to the plunger to make it 7.5
gm or 10 gm, as indicated; since with Schiotz
tonometer the greatest accuracy is attained if the
deflection of lever is between 3 and 4. In the end,
tonometer is lifted and a drop of antibiotic is instilled.
A conversion table is then used to derive the
intraocular pressure in mm of mercury (mmHg) from
the scale reading and the plunger weight.
The main advantages of Schiotz tonometer are that
it is cheap, handy and easy to use. Its main
disadvantage is that it gives a false reading when
used in eyes with abnormal scleral rigidity. False low
levels of IOP are obtained in eyes with low scleral
rigidity seen in high myopes and following ocular
Applanation tonometry
The concept of applanation tonometry was
introduced by Goldmann is 1954. It is based on Imbert-
Fick law which states that the pressure inside a sphere
(P) is equal to the force (W) required to flatten its
surface divided by the area of flattening (A); i.e., P =
The commonly used applanation tonometers are:
1. Goldmann tonometer. Currently, it is the most
popular and accurate tonometer. It consists of a
double prism mounted on a standard slit-lamp. The
prism applanates the cornea in an area of 3.06 mm
Technique (Fig. 21.14). After anaesthetising the
cornea with a drop of 2 per cent xylocaine and staining
the tear film with fluorescein patient is made to sit in
front of slit-lamp. The cornea and biprisms are
illuminated with cobalt blue light from the slit-lamp.
Biprism is then advanced until it just touches the
apex of cornea. At this point two fluorescent
semicircles are viewed through the prism. Then, the
applanation force against cornea is adjusted until the
inner edges of the two semicircles just touch (Fig.
21.15). This is the end point. The intraocular pressure
is determined by multiplying the dial reading with
ten. 2. Perkin’s applanation tonometer (Fig. 21.16). This
is a hand-held tonometer utilizing the same biprism
as in the Goldmann applanation tonometer. It is small,
easy to carry and does not require slit lamp. However,
it requires considerable practice before, reliable
readings can be obtained.
3. Pneumatic tonometer. In this, the cornea is
applanated by touching its apex by a silastic
diaphragm covering the sensing nozzle (which is
connected to a central chamber containing
pressurised air). In this tonometer, there is a
pneumatic-to-electronic transducer, which converts
the air pressure to a recording on a paper-strip, from
where IOP is read.
4. Pulse air tonometer is a hand-held, non-contact
tonometer that can be used with the patient in any
5. Tono-Pen is a computerised pocket tonometer. It
employs a microscopic transducer which applanates
the cornea and converts IOP into electric waves.
Tonography is a non-invasive technique for
determining the facility of aqueous outflow (C-value).
The C-value is expressed as aqueous outflow in
microlitres per minute per millimetre of mercury. It is
estimated by placing Schiotz tonometer on the eye
for 4 minutes. For a graphic record the electronic
Schiotz tonometer is used. C-value is calculated from
special tonographic tables taking into consideration
the initial IOP (P0) and the change in scale reading
over the 4 minutes.
Clinically, C-value does not play much role in the
management of a glaucoma patient. Although, in
general, C-values more than 0.20 are considered
normal, between 0.2 and 0.11 border line, and those
below 0.11 abnormal.

Common ocular symptoms and their causes

1. Defective vision. It is the commonest ocular
symptom. Enquiry should reveal its onset (sudden or
gradual), duration, whether it is painless or painful,
whether it is more during the day, night or constant,
and so on. Important causes of defective vision can
be grouped as under:
Sudden painless loss of vision
Central retinal artery occlusion
Massive vitreous haemorrhage
Retinal detachment involving macular area
Ischacmic central retinal vein occlusion
Sudden painless onset of defective vision
Central serous retinopathy
Optic neuritis
Methyl alcohol amblyopia
Non-ischacmic central retinal vein occlusion
Sudden painful loss of vision
Acute congestive glaucoma
Acute iridocyclitis
Chemical injuries to the eyeball
Mechanical injuries to the eyeball
Gradual painless defective vision
Progressive pterygium involving pupillary area
Corneal degenerations
Corneal dystrophies
Developmental cataract
Senile cataract
Optic atrophy
Chorioretinal degenerations
Age-related macular degeneration
Diabetic retinopathy
Refractive errors
Gradual painful defective vision
Chronic iridocyclitis
Corneal ulceration
Chronic simple glaucoma
Transient loss of vision (Amaurosis fugax)
Carotid artery disease
Giant cell arteritis
Raynaud’s disease
Severe hypertension
Prodromal symptom of CRAO
Night blindness (Nyctalopia )
Vitamin A deficiency
Retinitis pigmentosa and other tapetoretinal
Congenital night blindness
Pathological myopia
Peripheral cortical cataract
Day blindness (Hamarlopia)
Central nuclear or polar cataracts
Central corneal opacity
Central vitreous opacity
Congenital deficiency of cones (rarely)
Diminution of vision for near only
Internal or total ophthalmoplegia
Insufficiency of accommodation
2. Other visual symptoms. Visual symptoms other
than the defective vision are as follows:
Black spots or floaters in front of the eyes may appear
singly or in clusters. They move with the movement
of the eyes and become more apparent when viewed
against a clear surface e.g., the sky. Common causes
of black floaters are:
Vitreous haemorrhage
Vitreous degeneration. e.g.,
– senile vitreous degeneration
– vitreous degeneration in pathological myopia
Exudates in vitreous
Lenticular opacity
Flashes of light in front of the eyes (photopsia). Occur
due to traction on retina in following conditions:
Posterior vitreous detachment
Prodromal symptom of retinal detachment
Vitreous traction bands
Sudden appearance of flashes with floaters is a
sign of a retinal tear
Distorted vision. Distorted vision is a feature of
macular lesions e.g., central chorioretinitis. It may be
in the form of:
Micropsia (small size of objects),
Macropsia (large size of objects),
Metamorphopsia (distorted shape of objects).
Coloured halos. Patient may perceive coloured halos
around the light. It is a feature of:
Acute congestive glaucoma
Early stages of cataract
Mucopurulent conjunctivitis
Diplopia, i.e., perceiving double images of an object
is a very annoying symptom. It should be ascertained
whether it occurs even when the normal eye is closed
(uniocular diplopia) or only when both eyes are open
(binocular diplopia). Common causes of diplopia are:
Uniocular diplopia
Subluxated lens
Double pupil
Incipient cataract
Eccentric IOL
Binocular diplopia
Paralytic squint
Myasthenia gravis
Diabetes mellitus
Thyroid disorders
Blow-out fracture of floor of the orbit
Anisometropic glasses (e.g., uniocular aphakic
After squint correction in the presence of
abnormal retinal correspondence (paradoxical
3. Watering from the eyes. Watering from the eyes is
another common ocular symptom. Its causes can be
grouped as follows:
Excessive lacrimation, i.e., excessive formation of
tears occurs in multiple conditions (see page 367).
Epiphora, i.e., watering from the eyes due to blockage
in the flow of normally formed tears somewhere in the
lacrimal drainage system (see page 367).
4. Discharge from the eyes. When a patient complains
of a discharge from the eyes, it should be ascertained
whether it is mucoid, mucopurulent, purulent,
serosanguinous or ropy. Discharge from the eyes is a
feature of conjunctivitis, corneal ulcer, stye, burst
orbital abscess, and dacryocystitis.
5. Itching, burning and foreign body sensation in
the eyes. These are very common ocular symptoms.
Their causes are:
Chronic simple conjunctivitis
Dry eye
Trachoma and other conjunctival inflammations
Trichiasis and entropion
6. Redness of the eyes. It is a common presenting
symptom in many conditions such as conjunctivitis,
keratitis, iridocyclitis and acute glaucomas.
7. Ocular pain. Pain in and around the eyes should
be probed for its onset, severity, and associated
symptoms. It is a feature of ocular inflammations and
acute glaucoma. Ocular pain may also occur as
referred pain from the inflammation of surrounding
structures such as sinusitis, dental caries and
8. Asthenopic symptoms. Asthenopia refers to mild
eyeache, headache and tiredness of the eyes which
are aggravated by near work. Asthenopia is a feature
of extraocular muscle imbalance and uncorrected mild
refractive errors especially astigmatism.
9. Other ocular symptoms are as follows:
Deviation of the eyeball (squint)
Protrusion of the eyeball (proptosis)
Drooping of the upper lid (ptosis)
Retraction of the upper lid
Sagging down of the lower lids (ectropion)
Swelling on the lids (e.g., chalazion and tumours)

Differences between conjunctival and ciliary congestion

S. no. Feature Conjunctival congestion Ciliary congestion
1. Site More marked in the fornices More marked around the limbus
2. Colour Bright red Purple or dull red
3. Arrangement of vessels Superficial and branching Deep and radiating from limbus
4. On moving conjunctiva Congested vessels also move Congested vessels do not move
5. On mechanically squeezing out Vessels fill slowly from Vessels fill rapidly from
the blood vessels fornix towards limbus limbus towards fornices
6. Blanching, i.e., on putting one Vessels immediately blanch Do not blanch
drop of 1 in 10000 adrenaline
7. Common causes Acute conjunctivitis Acute iridocyclitis, keratitis (corneal

Ocular Manifestations Of Diabetes mellitus

Ocular involvement in diabetes is very common.
Structure-wise ocular lesions are as follows:
1. Lids. Xanthelasma and recurrent stye or internal
2. Conjunctiva. Telangiectasia, sludging of the blood
in conjunctival vessels and subcon-junctival
3. Cornea. Pigment dispersal at back of cornea,
decreased corneal sensations (due to trigeminal
neuropathy), punctate kerotapathy, Descemet’s
folds, higher incidence of infective corneal ulcers
and delayed epithelial healing due to abnormality
in epithelial basement membrane
4. Iris. Rubeosis iridis (neovascularization)
5. Lens. Snow-flake cataract in patients with IDDM,
posterior subcapsular cataract, early onset and
early maturation of senile cataract
6. Vitreous. Vitreous haemorrhage and fibre- vascular
proliferation secondary to diabetic retinopathy
7. Retina. Diabetic retinopathy and lipaemia retinalis
(see page 259).
8. Intraocular pressure. Increased incidence of
POAG, neovascular glaucoma and hypotony in
diabetic ketoacidosis (due to increased plasma
bicarbonate levels)
9. Optic nerve. Optic neuritis
10. Extraocular muscles. Ophthalmoplegia due to
diabetic neuropathy
11. Changes in refraction. Hypermetropic shift in
hypoglycemia, myopic shift in hyperglycemia and
decreased accommodation


They term xerophthalmia is now reserved (by a joint
WHO and USAID Committee, 1976) to cover all the
ocular manifestations of vitamin A deficiency,
including not only the structural changes affecting
the conjunctiva, cornea and occasionally retina, but
also the biophysical disorders of retinal rods and
cones functions.
It occurs either due to dietary deficiency of vitamin
A or its defective absorption from the gut. It has long
been recognised that vitamin A deficiency does not
occur as an isolated problem but is almost invariably
accompanied by protein-energy malnutrition (PEM)
and infections.
WHO classification (1982)
The new xerophthalmia classification (modification
of original 1976 classification) is as follows:
XN Night blindness
X1A Conjunctival xerosis
X1B Bitot’s spots
X2 Corneal xerosis
X3A Corneal ulceration/keratomalacia affecting
less than one-third corneal surface
X3B Corneal ulceration/keratomalacia affecting
more than one-third corneal surface.
XS Corneal scar due to xerophthalmia
XF Xerophthalmic fundus.
Clinical features
1. X N (night blindness). It is the earliest symptom of
xerophthalmia in children. It has to be elicited by
taking detailed history from the guardian or relative.
2. X1A (conjunctival xerosis). It consists of one or
more patches of dry, lustreless, nonwettable
conjunctiva (Fig. 19.1), which has been well described
as ‘emerging like sand banks at receding tide’ when
the child ceases to cry. These patches almost always
involve the inter-palpebral area of the temporal
quadrants and often the nasal quadrants as well. In
more advanced cases, the entire bulbar conjunctiva
may be affected. Typical xerosis may be associated
with conjunctival thickening, wrinkling and
3. X1B (Bitot’s spots). It is an extension of the xerotic
process seen in stage X1A. The Bitot’s spot is a
raised, silvery white, foamy, triangular patch of
keratinised epithelium, situated on the bulbar
conjunctiva in the inter-palpebral area (Fig. 19.2). It is
usually bilateral and temporal, and less frequently
4. X2 (corneal xerosis). The earliest change in the
cornea is punctate keratopathy which begins in the
lower nasal quadrant, followed by haziness and/or
granular pebbly dryness (Fig. 19.3). Involved cornea
lacks lustre.
5. X3A and X3B (corneal ulceration/keratomalacia),
Stromal defects occur in the late stage due to
colliquative necrosis and take several forms. Small
ulcers (1-3 mm) occur peripherally; they are
characteristically circular, with steep margins and are
sharply demarcated (Fig. 19.4). Large ulcers and areas
of necrosis may extend centrally or involve the entire
cornea. If appropriate therapy is instituted immediately,
stromal defects involving less than one-third of
corneal surface (X3A) usually heal, leaving some
useful vision. However, larger stromal defects (X3B)
(Fig. 19.5) commonly result in blindness.
6. XS (corneal scars). Healing of stromal defects
results in corneal scars of different densities and sizes
which may or may not cover the pupillary area (Fig.
19.6). A detailed history is required to ascertain the
cause of corneal opacity.
7. XFC (Xerophthalmic fundus). It is characterized
by typical seed-like, raised, whitish lesions scattered
uniformly over the part of the fundus at the level of
optic disc (Fig. 19.7).
It includes local ocular therapy, vitamin A therapy
and treatment of underlying general disease.
1. Local ocular therapy. For conjunctival xerosis
artificial tears (0.7 percent hydroxypropyl methyl
cellulose or 0.3 percent hypromellose) should be
instilled every 3-4 hours. In the stage of keratomalacia,
full-fledged treatment of bacterial corneal ulcer
should be instituted (see pages 120-123).
2. Vitamin A therapy. Treatment schedules apply to
all stages of active xerophthalmia viz. XN, X1A, X1B,
X2, X3A and X3B. Oral administration is the
recommended method of treatment. However, in the
presence of repeated vomiting and severe diarrhoea,
intramuscular injections of water-miscible preparation
should be preferred. The WHO recommended
schedule is as given below:
i. All patients above the age of 1 year (except
women of reproductive age): 200,000 IU of vitamin
A orally or 100,000 IU by intramuscular injection
should be given immediately on diagnosis and
repeated the following day and 4 weeks later.
ii. Children under the age of 1 year and children
of any age who weigh less than 8 kg should be
treated with half the doses for patients of more
than 1 year of age.
iii. Women of reproductive age, pregnant or not: (a)
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.
(b) For corneal xerophthalmia, administration of
full dosage schedule (described for patients above
1 year of age) is recommended.
3. Treatment of underlying conditions such as PEM
and other nutritional disorders, diarrhoea,
dehydration and electrolyte imbalance, infections and
parasitic conditions should be considered
Prophylaxis against xerophthalmia
The three major known intervention strategies for the
prevention and control of vitamin A deficiency are:
1. Short-term approach. It comprises periodic
administration of vitamin A supplements. WHO
recommended, universal distribution schedule of
vitamin A for prevention is as follows:
i. Infants 6-12 100,000 IU orally every
months old and 3-6 months.
any older children
who weigh less
than 8 kg.
ii. Children over 200,000 IU orally every
1 year and under 6 months.
6 years of age
iii. Lactating 20,000 IU orally once at
mothers delivery or during the next
2 months. This will raise
the concentration of vitamin
A in the breast milk and
therefore, help to protect
the breastfed infant.
iv. Infants less 50,000 IU orally should
than 6 months be given before they
old, not being attain the age of 6
breastfed. months.
A revised schedule of vitamin A supplements being
followed in India since August 1992, under the
programme named as ‘Child Survival and Safe
Motherhood (CSSM)’ is as follows:
First dose (1 lakh I.U.)—at 9 months of age along
with measles vaccine.
Second dose (2 lakh I.U.)—at 18 months of age
along with booster dose of DPT/OPV.
Third dose (2 lakh I.U.)—at 2 years of age.
2. Medium-term approach. It includes food
fortification with vitamin A.
3. Long-term approach. It should be the ultimate
aim. It implies promotion of adequate intake of vitamin
A rich foods such as green leafy vegetables, papaya
and drum- sticks (Fig. 19.8). Nutritional health
education should be included in the curriculum of
school children.


Nonsteroidal anti-inflammatory drugs (NSAIDs),
often referred to as ‘aspirin-like drugs’, are a
heterogeneous group of anti-inflammatory, analgesic
and antipyretic compounds. These are often
chemically unrelated (although most of them are
organic acids), but share certain therapeutic actions
and side-effects.
Mechanisms of action
The NSAIDs largely act by irreversibly blocking the
enzyme cyclo-oxygenase, thus inhibiting the
prostaglandin biosynthesis. They also appear to block
other local mediators of the inflammatory response
such as polypeptides of the kinin system, lysosomal
enzymes, lymphokinase and thromboxane A2; but not
the leukotrienes.
A. NSAIDs available for systemic use can be
grouped as follows:
1. Salicylates e.g., aspirin.
2. Pyrazolone derivatives e.g., phenylbutazone,
oxyphenbutazone, aminopyrine and apazone.
3. Para-aminophenol derivatives e.g., phenacetin
and acetaminophen.
4. Indole derivatives e.g., indomethacin and
5. Propionic acid derivatives e.g., ibuprofen,
naproxen and flurbiprofen.
6. Anthranilic acid derivatives e.g., mefenamic
acid and flufenamic acid.
7. Other newer NSAIDs e.g., ketorolac tromethamine,
carprofen and diclofenac.
B. Topical ophthalmic NSAIDs preparations
available include:
1. Indomethacin suspension (0.1%)
2. Flurbiprofen, 0.3% eyedrops
3. Ketorolac tromethamine, 0.5% eyedrops
4. Diclofenac sodium, 0.1% eyedrops
Ophthalmic indications of NSAIDs
1. Episcleritis and scleritis. Recalcitrant cases of
episcleritis may be treated with systemic NSAIDs
such as oxyphenbutazone 100 mg TDS or
indomethacin 25 mg BD.
NSAIDs may also suppress the inflammation in
diffuse and nodular varieties of scleritis, but are
not likely to control the necrotizing form.
2. Uveitis. NSAIDs are usually not used as the
primary agents in therapy of uveitis. They are,
however, useful in the long-term therapy of
recurrent anterior uveitis, initially controlled by
steroid therapy. Phenylbutazone is of use in
uveitis associated with ankylosing spondylitis.
3. Cystoid macular oedema (CME). Topical and/or
systemic antiprostaglandin drugs are effective in
preventing the postoperative CME occurring after
cataract operation. The drug (e.g., 0.03%
flurbiprofen eyedrops) is started 2 days
preoperatively and continued for 6-8 weeks postoperatively.
4. Pre-operatively to maintain dilatation of the
pupil. Flurbiprofen drops used every 5 minutes
for 2 hours preoperatively are very effective in
maintaining the pupillary dilatation during the
operation of extracapsular cataract extraction with
or without intraocular lens implantation.
5. Spring catarrh. Sodium cromoglycate 2 percent
inhibits degranulation of the mast cells and thus
is more useful when used prophylactically in
patients with spring catarrh. Topical
antiprostaglandins are effective in the treatment
of spring catarrh.
6. Topical antihistaminics are helpful in cases of
mild allergic conjunctivitis.

Ocular Manifestations of AIDS

These occur in about 75
percent of patients and sometimes may be the
presenting features of AIDS in an otherwise healthy
person or the patient may be a known case of AIDS
when his eye problems occur. Ocular lesions of AIDS
may be classified as follows:
1. Retinal microvasculopathy. It develops from
vaso-occlusive process which may be either due to
direct toxic effects of virus on the vascular
endothelium or immune complex deposits in the
precapillary arterioles.
It is characterised by non-specific lesions (Fig.
Multiple ‘cotton-wool spots’ occur in 50 percent
Superficial and deep retinal hemorrhages occur in
15-40 percent cases.
Microaneurysms and telangiectasia may also be
seen rarely.
2. Usual ocular infections. These are also seen in
healthy people, but occur with greater frequency and
produce more severe infections in patients with AIDS.
These include:
Herpes zoster ophthalmicus,
Herpes simplex infections,
Toxoplasmosis (chorioretinitis),
Ocular tuberculosis, syphilis and fungal corneal
3. Opportunistic infections of the eye. These are
caused by microorganisms which do not affect normal
patients. They can infect someone whose cellular
immunity is suppressed by HIV infection or by other
causes such as leukaemia. These include:
cytomegalovirus (CMV) retinitis (see page 253 Fig
11.5), candida endophthalmitis, cryptococcal
infections and pneumocystis carini, choroiditis.
4. Unusual neoplasms. Kaposi’s sarcoma is a
malignant vascular tumour which may appear on the
eyelid or conjunctiva as multiple nodules. It is seen
in about 3 percent cases of AIDS. Burkitt’s lymphoma
of the orbit is also seen in a few patients.
5. Neuro-ophthalmic lesions. These are thought to
be due to CMV or other infections of the brain. These
include isolated or multiple cranial nerve palsies
resulting in paralysis of eyelids, extraocular muscles,
loss of sensory supply to the eye and optic nerve
involvement causing loss of vision.
Management. It consists of the measures directed
against the associated infection/lesions. For example:
CMV infections can be treated by zidovudine,
gancyclovir and foscarnet (see page 422).
Kaposi’s sarcoma responds to radiotherapy.
Horpes zoster ophthalmicus, is treated by