TONOMETRY

The intraocular pressure (IOP) is measured with the
help of an instrument called tonometer. Two basic
types of tonometers available are: indentation and
applanation.
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
world.
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
footplate;
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
gm.
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
surgery.
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 =
W/A.
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
diameter.
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
position.
5. Tono-Pen is a computerised pocket tonometer. It
employs a microscopic transducer which applanates
the cornea and converts IOP into electric waves.
Tonography
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
Papilloedema
Giant cell arteritis
Migraine
Raynaud’s disease
Severe hypertension
Prodromal symptom of CRAO
Night blindness (Nyctalopia )
Vitamin A deficiency
Retinitis pigmentosa and other tapetoretinal
degenerations
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
Presbyopia
Cycloplegia
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
Retinitis
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
Keratoconus
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
glasses)
After squint correction in the presence of
abnormal retinal correspondence (paradoxical
diplopia).
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
abscess.
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
ulcer)

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
hordeolum
2. Conjunctiva. Telangiectasia, sludging of the blood
in conjunctival vessels and subcon-junctival
haemorrhage
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

XEROPHTHALMIA

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.
Etiology
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
pigmentation.
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
nasal.
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).
Treatment
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
simultaneously.
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

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.
Preparations
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
sulindac.
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.
19.9):
Multiple ‘cotton-wool spots’ occur in 50 percent
cases,
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
ulcers.
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
acyclovir.

Beta-adrenergic blockers

These are, presently, the most frequently used
antiglaucoma drugs. The commonly used
preparations are timolol and betaxolol. Other available
preparations include levobunolol, carteolol and
metipranolol.
Mechanism of action. Timolol and levobunolol are
non-selective beta-1 (Cardiac) and beta-2 (smooth
muscle, pulmonary) receptor blocking agents.
Betaxolol has 10 times more affinity for beta-1 than
beta-2 receptors.
The drugs timolol and levobunolol lower IOP by
blockade of beta-2 receptors in the ciliary processes,
resulting in decreased aqueous production. The exact
mechanism of action of betaxolol (cardioselective
beta-blocker) is unknown.
Indications. Beta adrenergic blockers are useful in
all types of glaucomas, viz., developmental, primary
and secondary; narrow as well as open angle. Unless
contraindicated due to systemic diseases, betablockers
are frequently used as the first choice drug
in POAG and all secondary glaucomas.
Contraindications. These drugs should be used with
caution or not at all, depending on the severity of the
systemic disease in patients with bronchial asthma,
emphysema, COPD, heart blocks, congestive heart
failure or cardiomyopathy. Betaxolol is the beta
blocker, of choice in patients at risk for pulmonary
diseases. The other contraindication includes known
drug allergies.
Additive effects. Beta-blockers have very good
synergistic effect when combined with miotics; and
are thus often used in combination in patients with
POAG, unresponsive to the single drug.
Side-effects
1. Ocular side-effects are not frequent. These include
burning and conjunctival hyperaemia, superficial
punctate keratopathy and corneal anaesthesia.
2. Systemic side-effects are also unusually low.
However, these are reported more often than ocular
side-effects. These include (i) Cardiovascular effects
which result from blockade of beta-1 receptors. These
are bradycardia, arrhythmias, heart failure and
syncope. (ii) Respiratory reactions: These include
bronchospasm and airway obstruction, especially in
asthmatics. These occur due to blockade of beta-2
receptors; and thus are not known with betaxolol.
(iii) Central nervous system effects. These include
depression, anxiety, confusion, drowsiness,
disorientation, hallucinations, emotional lability,
dysarthria and so on. (iv) Miscellaneous effects are
nausea, diarrhoea, decreased libido, skin rashes,
alopecia and exacerbation of myasthenia gravis.
Preparations
1. Timolol. It is a non-selective beta-1 and beta-2
blocker. It is available as 0.25 per cent and 0.5 percent
eye drops. The salt used is timolol maleate. Its action
starts within 30 minutes, peak reaches in 2 hours and
effects last up to 24 hours. Therefore, it is used once
or twice daily. The drug is very effective, however,
the phenomenon of ‘short-term escape’ and ‘longterm
drift’ are well known. ‘Short-term escape’ implies
marked initial fall in IOP, followed by a transient rise
with continued moderate fall in IOP. The ‘long-term
drift’ implies a slow rise in IOP in patients who were
well controlled with many months of therapy.
2. Betaxolol. It is a cardioselective beta-blocker and
thus can be used safely in patients prone to attack of
bronchial asthma; an advantage over timolol. It is
available as 0.5 percent suspension, and 0.25 percent
suspension, and is used twice daily. Its action starts
within 30 minutes, reaches peak in 2 hours and lasts
for 12 hours. It is slightly less effective than timolol
in lowering the IOP.
3. Levobunolol. It is available as 0.5 percent solution
and its salient features are almost similar to timolol.
4. Carteolol. It is available as 1 percent and 2 per
cent solution and is almost similar to timolol except
that it induces comparatively less bradycardia.
5. Metipranolol. It is available as 0.1 percent, 0.3
percent and 0.6 percent solution and is almost similar
to timolol in all aspects.
Carbonic anhydrase inhibitors (CAIs)
These are potent and most commonly used systemic
antiglaucoma drugs. These include acetazolamide
(most frequently used), methazolamide,
dichlorphenamide and ethoxzolamide.
Mechanism of action. As the name indicates CAIs
inhibit the enzyme carbonic anhydrase which is
related to the process of aqueous humour production.
Thus, CAIs lower the IOP by reducing the aqueous
humour formation.
Indications. These are used as additive therapy for
short term in the management of all types of acute
and chronic glaucomas. Their long-term use is
reserved for patients with high risk of visual loss,
where all other treatments fail.
Side-effects. Unfortunately, 40-50 percent of patients
are unable to tolerate CAIs for long term because of
various disabling side-effects. These include:
1. Paresthesias of the fingers, toes, hands, feet and
around the mouth are experienced by most of the
patients. However, these are transient and of no
consequence.
2. Urinary frequency may also be complained of by
most patients due to the diuretic effect.
3. Serum electrolyte imbalances may occur with
higher doses of CAIs. These may be in the form of (i)
Bicarbonate depletion leading to metabolic acidosis.
This is associated with ‘malaise symptom complex’,
which includes: malaise, fatigue, depression, loss of
libido, anorexia and weight loss. Treatment with
sodium bicarbonate or sodium acetate may help to
minimize this situation in many patients. (ii) Potassium
depletion. It may occur in some patients, especially
those simultaneously getting corticosteroids, aspirin
or thiazide diuretics. Potassium supplement is
indicated only when significant hypokalemia is
documented. (iii) Serum sodium and chloride may be
transiently reduced; more commonly with
dichlorphenamide.
4. Gastrointestinal symptom complex. It is also very
common. It is not related to the malaise symptom
complex caused by biochemical changes in the serum.
Its features include—vague abdominal discomfort,
gastric irritation, nausea, peculiar metallic taste and
diarrhoea.
5. Sulfonamide related side-effects of CAIs, seen
rarely, include renal calculi, blood dyscrasias,
Stevens-Johnson syndrome, transient myopia,
hypertensive nephropathy and teratogenic effects.
Preparations and doses
1. Acetazolamide (diamox). It is available as tablets,
capsules and injection for intravenous use. The
acetazolamide 250 mg tablet is used 6 hourly. Its action
starts within 1 hour, peak is reached in 4 hours and
the effect lasts for 6-8 hours.
2. Dichlorphenamide. It is available as 50 mg tablets.
Its recommended dose is 25 to 100 mg three times a
day. It causes less metabolic acidosis but has a
sustained diuretic effect.
3. Methazolamide. It is also available as 50 mg tablets.
It has a longer duration of action than acetazolamide.
Its dose is 50-100 mg, 2 or 3 times a day.
4. Ethoxzolamide. It is given in a dosage of 125 mg
every 6 hours and is similar to acetazolamide in all
aspects.
5. Dorzolamide (2%). It is a topical carbonic
anhydrase inhibitor. It is water soluble, stable in
solution and has excellent corneal penetration. It
decreases IOP by 22% and has got additive effect
with timolol. It is administered thrice daily. Its side
effects include burning sensation and local allergic
reaction.
6. Brinzolamide (1%). It is also a topical CAI which
decreases IOP by decreasing aqueous production. It
is administered twice daily (BD).

ANTI-GLAUCOMA DRUGS

Classification
A. Parasympathomimetic drugs (Miotics)
B. Sympathomimetic drugs (Adrenergic agonists)
C. β-blockers
D. Carbonic anhydrase inhibitors
E. Hyperosmotic agents
F. Prostaglandins
G. Calcium channel blockers

Sympathomimetic drugs

Sympathomimetics, also known as adrenergic
agonists, act by stimulation of alpha, beta or both
the receptors.
Classification
Depending upon the mode of action, these can be
classified as follows:
1. Both alpha and beta-receptor stimulators e.g.,
epinephrine.
2. Direct alpha-adrenergic stimulators e.g.,
norepinephrine and clonidine hydrochloride.
3. Indirect alpha-adrenergic stimulators e.g.,
pargyline.
4. Beta-adrenergic stimulator e.g., isoproterenol.
Mechanisms of action
1. Increased aqueous outflow results by virtue of
both alpha and beta-receptor stimulation.
2. Decreased aqueous humour production occurs
due to stimulation of alpha-receptors in the ciliary
body.
Side-effects
1. Systemic side-effects include hypertension,
tachycardia, headache, palpitation, tremors,
nervousness and anxiety.
2. Local side-effects are burning sensation, reactive
hyperaemia of conjunctiva, conjunctival
pigmentation, allergic blepharo conjunctivitis,
mydriasis and cystoid macular oedema (in
aphakics).
Preparations
1. Epinephrine. This direct-acting sympathomimetic
drug stimulates both alpha and beta- adrenergic
receptors. Indications: (i) It is one of the standard
drugs used for the management of POAG. (ii) It is also
useful in most of the secondary glaucomas.
Preparations: It is available as 0.5 percent, 1 percent
and 2 percent eyedrops. Dosage: The action starts
within 1 hour and lasts up to 12-24 hours. Therefore,
it is instilled twice daily.
2. Dipivefrine(Propine or dipivalylepinephrine). It is a
prodrug which is converted into epinephrine after its
absorption into the eye. It is more lipophilic than
epinephrine and thus its corneal penetration is
increased by 17 times. Preparations: It is available as
0.1 percent eyedrops. Dosage: Action and efficacy is
similar to 1 percent epinephrine. It is instilled twice daily.
3. Clonidine hydrochloride. It is a centrally-acting
systemic antihypertensive agent, which has been
shown to lower the IOP by decreasing aqueous
humour production by stimulation of alpha-receptors
in the ciliary body. Preparations and dosage. It is
used as 0.125 percent and 0.25 percent eye drops,
twice daily.
4. Brimonidine (0.2%). Mechanism of action. It is a
selective alpha-2 adrenergic agonist and lowers IOP
by decreasing aqueous production and enhancing
uveoscleral outflow. It has an additive effect to betablockers.
Dosage: It has a peak effect of 2 hours and
action lasts for 12 hours; so it is administered twice
daily.
5. Apraclonidine (0.5%, 1%). It is also alpha-2
adrenergic agonist like brimonidine. It is an extremely
potent ocular hypotensive drug and is commonly used
prophylactically for prevention of IOP elevation
following laser trabeculoplasty, YAG laser iridotomy
and posterior capsulotomy. It is of limited use for
long-term administration because of the high rate of
ocular side-effects.

Parasympathomimetic drugs (Miotics)

Parasympathomimetics, also called as cholinergic
drugs, either imitate or potentiate the effects of
acetylcholine.
Classification
Depending upon the mode of action, these can be
classified as follows:
1. Direct-acting or agonists e.g., pilocarpine.
2. Indirect-acting parasympathomimetics or
cholinesterase inhibitors: As the name indicates
these drugs act indirectly by destroying the
enzyme cholinesterase; thereby sparing the
naturallyacting acetylcholine for its actions. These
drugs have been divided into two subgroups,
designated as reversible (e.g., physostigmine)
and irreversible (e.g., echothiophate iodide,
demecarium and diisopropyl-fluoro-phosphate,
DFP3) antic-holinesterases.
3. Dual-action parasympathomimetics, i.e., which
act as both a muscarinic agonist as well as a
weak cholinesterase inhibitor e.g., carbachol.
Mechanism of action
1. In primary open-angle glaucoma the miotics
reduce the intraocular pressure (IOP) by
enhancing the aqueous outflow facility. This is
achieved by changes in the trabecular meshwork
produced by a pull exerted on the scleral spur by
contraction of the longitudinal fibres of ciliary
muscle.
2. In primary angle-closure glaucoma these reduce
the IOP due to their miotic effect by opening the
angle. The mechanical contraction of the pupil
moves the iris away from the trabecular meshwork.
Side-effects
1. Systemic side-effects noted are: bradycardia,
increased sweating, diarrhoea, excessive salivation
and anxiety. The only serious complication noted
with irreversible cholinesterase inhibitors is
‘scoline apnoea’, i.e., inability of the patient to
resume normal respiration after termination of
general anaesthesia.
2. Local side-effects are encountered more frequently
with long-acting miotics (i.e. irreversible
cholinesterase inhibitors). These include problems
due to miosis itself (e.g. reduced visual acuity in
the presence of polar cataracts, impairment of
night vision and generalized contraction of visual
fields), spasm of accommodation which may cause
myopia and frontal headache, retinal detachment,
lenticular opacities, iris cyst formation, mild iritis,
lacrimation and follicular conjunctivitis.
Preparations
1. Pilocarpine. It is a direct-acting parasympathomimetic
drug. It is the most commonly used and
the most extensively studied miotic. Indications: (i)
Primary open-angle glaucoma; (ii) Acute angle-closure
glaucoma; (iii) Chronic synechial angle-closure
glaucoma. Contraindications: inflammatory
glaucoma, malignant glaucoma and known allergy.
Available preparations and dosage are: (a) Eyedrops
are available in 1%, 2% and 4% strengths. Except in
very darkly pigmented irides maximum effect is
obtained with a 4 percent solution. In POAG, therapy
is usually initiated with 1 percent concentration. The
onset of action occurs in 20 minutes, peak in 2 hours
and duration of effect is 4-6 hours. Therefore, the
eyedrops are usually prescribed every 6 or 8 hourly.
(b) Ocuserts are available as pilo-20 and pilo-40. These
are changed once in a week. Pilo-20 is generally used
in patients controlled with 2 percent or less
concentration of eyedrops; and pilo-40 in those
requiring higher concentration of eyedrops.
(c) Pilocarpine gel (4%) is a bedtime adjunct to the
daytime medication.
2. Carbachol. It is a dual-action (agonist as well as
weak cholinesterase inhibitor) miotic. Indications. It
is a very good alternative to pilocarpine in resistant
or intolerant cases. Preparations. It is available as
0.75 percent and 3 percent eyedrops. Dosage: The
action ensues in 40 minutes and lasts for about 12
hours. Therefore, the drops are instilled 2 or 3 times a
day.
3. Echothiophate iodide (Phospholine iodide). It is
a long acting cholinesterase inhibitor. Indications: It
is very effective in POAG. Preparations: Available
as 0.03, 0.06 and 0.125 percent eye- drops. Dosage:
The onset of action occurs within 2 hours and lasts
up to 24 hours. Therefore, it is instilled once or twice
daily.
4. Demecarium bromide. It is similar to ecothiopate
iodide and is used as 0.125 percent or 0.25 per- cent
eyedrops.
5. Physostigmine (eserine). It is a reversible (weak)
cholinesterase inhibitor. It is used as 0.5 percent
ointment twice a day.

Acid burns

Acid burns are less serious than alkali burns. Common
acids responsible for burns are: sulphuric acid,
hydrochloric acid and nitric acid.
Chemical effects. The strong acids cause instant
coagulation of all the proteins which then act as a
barrier and prevent deeper penetration of the acids
into the tissues. Thus, the lesions become sharply
demarcated.
Ocular lesions
1. Conjunctiva. There occurs immediate necrosis
followed by sloughing. Later on symblepharon is
formed due to fibrosis.
2. Cornea. It is also necrosed and sloughed out.
The extent of damage depends upon the
concentration of acid and the duration of contact.
In severe cases, the whole cornea may slough
out followed by staphyloma formation.
Grading of chemical burns
Depending upon the severity of damage caused to
the conjunctiva and cornea, the extent of chemical
burns may be graded as follows (Table 17.1):
Treatment of chemical burns
1. Immediate and thorough wash with the available
clean water or saline.
2. Chemical neutralization. It should be carried out
when the nature of offending chemical is known.
For example, acid burns should be neutralized
with weak alkaline solutions (such as sodium
bicarbonate) and alkali burns with weak acidic
solutions (such as boric acid or mix)
Ethylenediamine tetra acetic acid (EDTA) 1%
solution can also be used as neutralizing agent.
3. Mechanical removal of contaminant. If any
particles are left behind, particularly in the case
of lime, these should be removed carefully with
a swab stick.
4. Removal of contaminated and necrotic tissue.
Necrosed conjunctiva should be excised.
Contaminated and necrosed corneal epithelium
should be removed with a cotton swab stick.
5. Maintenance of favourable conditions for rapid
and uncomplicated healing by frequent application
of topical atropine, corticosteroids and antibiotics.
6. Prevention of symblepharon can be done by
using a glass shell or sweeping a glass rod in the
fornices twice daily.
7. Treatment of complications
i. Secondary glaucoma should be treated by
topical 0.5 percent timolol instilled twice a day
along with oral acetazolamide 250 mg 3-4 times
a day.
ii. Corneal opacity may be treated by
keratoplasty.
iii. Treatment of symblepharon

Alkali burns

Alkali burns are among the most severe chemical
injuries known to the ophthalmologists. Common
alkalies responsible for burns are: lime, caustic potash
or caustic soda and liquid ammonia (most harmful).
Mechanisms of damage produced by alkalies
includes:
1. Alkalies dissociate and saponify fatty acids of
the cell membrane and, therefore, destroy the
structure of cell membrane of the tissues.
2. Being hygroscopic, they extract water from the
cells, a factor which contributes to the total
necrosis.
3. They combine with lipids of cells to form soluble
compounds, which produce a condition of
softening and gelatinisation.
The above effects result in an increased deep
penetration of the alkalies into the tissues. Alkali
burns, therefore, spread widely, their action continues
for some days and their effects are difficult to
circumscribe. Hence, prognosis in such cases must
always be guarded.
Clinical picture. It can be divided into three stages:
1. Stage of acute ischaemic necrosis. In this stage;
i. Conjunctiva shows marked oedema,
congestion, widespread necrosis and a copious
purulent discharge.
ii. Cornea develops widespread sloughing of the
epithelium, oedema and opalescence of the
stroma.
iii. Iris becomes violently inflamed and in severe
cases both iris and ciliary body are replaced
by granulation tissue.
2. Stage of reparation. In this stage conjunctival
and corneal epithelium regenerate, there occurs
corneal vascularization and inflammation of the
iris subsides.
3. Stage of complications. This is characterised by
development of symblepharon, recurrent corneal
ulceration and development of complicated
cataract and secondary glaucoma.

SYMPATHETIC OPHTHALMITIS

Sympathetic ophthalmitis is a serious bilateral
granulomatous panuveitis which follows a penetrating
ocular trauma. The injured eye is called exciting eye
and the fellow eye which also develops uveitis is
called sympathizing eye. Very rarely, sympathetic
ophthalmitis can also occur following an intraocular
surgery.
Incidence
Incidence of sympathetic ophthalmitis has
tremendously decreased in the recent years due to
meticulous repair of the injured eye utilizing
microsurgical techniques and use of the potent
steroids.
Etiology
Etiology of sympathetic ophthalmitis is still not
known exactly. However, the facts related with its
occurrence are as follows:
A. Predisposing factors
1. It almost always follows a penetrating wound.
2. Wounds in the ciliary region (the so-called
dangerous zone) are more prone to it.
3. Wounds with incarceration of the iris, ciliary
body or lens capsule are more vulnerable.
4. It is more common in children than in adults.
5. It does not occur when actual suppuration
develops in the injured eye.
B. Pathogenesis. Various theories have been put
forward. Most accepted one is allergic theory, which
postulates that the uveal pigment acts as allergen
and excites plastic uveitis in the sound eye.
Pathology
It is characteristic of granulomatous uveitis, i.e., there
is nodular aggregation of lymphocytes, plasma cells,
epitheloid cells and giant cells scattered throughout
the uveal tract.
Dalen-Fuchs’ nodules are formed due to
proliferation of the pigment epithelium (of the iris,
ciliary body and choroid) associated with invasion
by the lymphocytes and epitheloid cells. Retina shows
perivascular cellular infiltration (sympathetic
perivasculitis).
Clinical picture
I. Exciting (injured) eye. It shows clinical features of
persistent low grade plastic uveitis, which include
ciliary congestion, lacrimation and tenderness.
Keratic precipitates may be present at the back of
cornea (dangerous sign).
II. Sympathizing (sound) eye. It is usually involved
after 4-8 weeks of injury in the other eye. Earliest
reported case is after 9 days of injury. Most of the
cases occur within the first year. However, delayed
and very late cases are also reported. Sympathetic
ophthalmitis, almost always, manifests as acute
plastic iridocyclitis. Rarely it may manifest as
neuroretinitis or choroiditis. Clinical picture of the
iridocyclitis in sympathizing eye can be divided into
two stages:
1. Prodromal stage. Symptoms. sensitivity to light
(photophobia) and transient indistinctness of near
objects (due to weakening of accommodation) are
the earliest symptoms.
Signs. In this stage the first sign may be presence of
retrolental flare and cells or the presence of a few
keratic precipitates (KPs) on back of cornea. Other
signs includes mild ciliary congestion, slight
tenderness of the globe, fine vitreous haze and disc
oedema which is seen occasionally.
2. Fully-developed stage. It is clinically characterised
by typical signs and symptoms consistent with acute
plastic iridocyclitis (see page 141).
Treatment
A. Prophylaxis
I. Early excision of the injured eye. It is the best
prophylaxis when there is no chance of saving useful
vision.
II. When there is hope of saving useful vision,
following steps should be taken:
1. A meticulous repair of the wound using
microsurgical technique should be carried out,
taking great care that uveal tissue is not
incarcerated in the wound.
2. Immediate expectant treatment with topical as
well as systemic steroids and antibiotics along
with topical atropine should be started.
3. When the uveitis is not controlled after 2 weeks
of expectant treatment, i.e., lacrimation,
photophobia and ciliary congestion persist and if
KPs appear, this eye should be excised
immediately.

Removal Of IntraOcular Foreign Body

IOFB should always be removed, except when it is
inert and probably sterile or when little damage has
been done to the vision and the process of removal
may be risky and destroy sight (e.g., minute FB in the
retina).
Removal of magnetic IOFB is easier than the removal
of non-magnetic FB. Usually a hand-held
electromagnet (Fig. 17.13) is used for the removal of
magnetic foreign body. Method of removal depends
upon the site (location) of the IOFB as follows:
1. Foreign body in the anterior chamber. It is
removed through a corresponding corneal incision
directed straight towards the foreign body. It should
be 3 mm internal to the limbus and in the quadrant of
the cornea lying over the foreign body (Fig. 17.14).
Magnetic foreign body is removed with a handheld
magnet. It may come out with a gush of
aqueous.
Non-magnetic foreign body is picked up with
toothless forceps.
2. Foreign body entangled in the iris tissue
(magnetic as well as non-magnetic) is removed by
performing sector iridectomy of the part containing
foreign body.
usually difficult for intralenticular foreign bodies.
Therefore, magnetic foreign body should also be
treated as non-magnetic foreign body. An
extracapsular cataract extraction (ECCE) with
intraocular lens implantation should be performed.
The foreign body may be evacuated itself along with
the lens matter or may be removed with the help of
forceps.
4. Foreign body in the vitreous and the retina is
removed by the posterior route as follows:
i. Magnetic removal. This technique is used to
remove a magnetic foreign body that can be well
localized and removed safely with a powerful magnet
without causing much damage to the intraocular
structures.
An intravitreal foreign body is preferably
removed through a pars plana sclerotomy (5 mm
from the limbus) (Fig 17.15A). At the site chosen
for incision, conjunctiva is reflected and the
incision is given in the sclera concentric to the
limbus. A preplaced suture is passed and lips of
the wound are retracted. A nick is given in the
underlying pars plana part of the ciliary body. And
the foreign body is removed with the help of a
powerful hand-held electromagnet. Preplaced
suture is tied to close the scleral wound.
Conjunctiva is stitched with one or two
interrupted sutures.
For an intraretinal foreign body, the site of
incision should be as close to the foreign body
as possible (Fig. 17.15 position ‘B’). A trapdoor
scleral flap is created, the choroidal bed is treated
with diathermy, choroid is incised and foreign
body is removed with either forceps or external
magnet.
ii. Forceps removal with pars plana vitrectomy. This
technique is used to remove all non-magnetic foreign
bodies and those magnetic foreign bodies that can
not be safely removed with a magnet. In this
technique, the foreign body is removed with vitreous
forceps after performing three-pore pars plana
vitrectomy under direct visualization using an
operating microscope

BLUNT TRAUMA

Modes of injury
Blunt trauma may occur following:
Direct blow to the eye ball by fist, ball or blunt
instruments like sticks, and big stones.
Accidental blunt trauma to eyeball may also
occur in roadside accidents, automobile accidents,
injuries by agricultural and industrial instruments/
machines and fall upon the projecting blunt
objects.
Mechanics of blunt trauma to eyeball
Blunt trauma of eyeball produces damage by different
forces as described below:
1. Direct impact on the globe. It produces maximum
damage at the point where the blow is received
(Fig. 17.2A).
2. Compression wave force. It is transmitted through
the fluid contents in all the directions and strikes
the angle of anterior chamber, pushes the irislens
diaphragm posteriorly, and also strikes the
retina and choroid (Fig. 17.2B). This may cause
considerable damage. Sometimes the compression
wave may be so explosive, that maximum damage
may be produced at a point distant from the
actual place of impact. This is called contre-coup
damage.
3. Reflected compression wave force. After striking
the outer coats the compression waves are
reflected towards the posterior pole and may
cause foveal damage (Fig. 17.2C).
4. Rebound compression wave force. After striking
the posterior wall of the globe, the compression
waves rebound back anteriorly. This force
damages the retina and choroid by forward pull
and lens-iris diaphragm by forward thrust from
the back (Fig. 17.2D).
5. Indirect force. Ocular damage may also be caused
by the indirect forces from the bony walls and
elastic contents of the orbit, when globe suddenly
strikes against these structures.
Modes of damage
The different forces of the blunt trauma described
above may cause damage to the structures of the
globe by one or more of the following modes:
1. Mechanical tearing of the tissues of eyeball.
2. Damage to the tissue cells sufficient to cause
disruption of their physiological activity.
3. Vascular damage leading to ischaemia, oedema
and haemorrhages.
4. Trophic changes due to disturbances of the
nerve supply.
5. Delayed complications of blunt trauma such as
secondary glaucoma, haemophthalmitis, late
rosette cataract and retinal detachment.
Traumatic lesions of blunt trauma
Traumatic lesions produced by blunt trauma can be
grouped as follows:
A. Closed globe injury
B. Globe rupture
C. Extraocular lesions
A. Closed-globe injury
Either there is no corneal or scleral wound at all
(contusion) or it is only of partial thickness (lamellar
laceration). Contusional injuries may vary in severity
from a simple corneal abrasion to an extensive
intraocular damage. Lesions seen in closed-globe
injury are briefly enumerated here structurewise.
I. Cornea
1. Simple abrasions. These are very painful and
diagnosed by fluorescein staining. These usually
heal up within 24 hours with ‘pad and bandage’
applied after instilling antibiotic ointment.
2. Recurrent corneal erosions (recurrent keractalgia).
These may sometimes follow simple abrasions,
especially those caused by fingernail trauma.
Patient usually gets recurrent attacks of acute
pain and lacrimation on opening the eye in the
morning. This occurs due to abnormally loose
attachment of epithelium to the underlying
Bowman’s membrane.
Treatment. Loosely attached epithelium should be
removed by debridement and ‘pad and bandage’
applied for 48 hours, so that firm healing is
established.
3. Partial corneal tears (lamellar corneal laceration).
These may also follow a blunt trauma.
4. Blood staining of cornea. It may occur
occasionally from the associated hyphaema and
raised intraocular pressure. Cornea becomes
reddish brown (Fig. 17.3) or greenish in colour
and in later stages simulates dislocation of the
clear lens into the anterior chamber. It clears very
slowly from the periphery towards the centre, the
whole process may take even more than two
years.
5. Deep corneal opacity. It may result from oedema
of corneal stroma or occasionally from folds in
the Descemet’s membrane.
II. Sclera
Partial thickness scleral wounds (lamellar scleral
lacerations) may occur alone or in association with
other lesions of closed-globe injury.
III. Anterior chamber
1. Traumatic hyphaema (blood in the anterior
chamber). It occurs due to injury to the iris or
ciliary body vessels (Fig. 17.4).
2. Exudates. These may collect in the anterior
chamber following traumatic uveitis.
IV. Iris, pupil and ciliary body
1. Traumatic miosis. It occurs initially due to
irritation of ciliary nerves. It may be associated
with spasm of accommodation.
2. Traumatic mydriasis (Iridoplegia). It is usually
permanent and may be associated with traumatic
cycloplegia.
3. Rupture of the pupillary margin is a common
occurrence in closed-globe injury.
4. Radiating tears in the iris stroma, sometimes
reaching up to ciliary body, may occur
occasionally.
5. Iridodialysis i.e., detachment of iris from its root
at the ciliary body occurs frequently. It results in
a D-shaped pupil and a black biconvex area seen
at the periphery (Fig. 17.5).
6. Antiflexion of the iris. It refers to rotation of the
detached portion of iris, in which its posterior
surface faces anteriorly. It occurs following
extensive iridodialysis.
7. Retroflexion of the iris. This term is used when
whole of the iris is doubled back into the ciliary
region and becomes invisible.
8. Traumatic aniridia or iridremia. In this
condition, the completely torn iris (from ciliary
body) sinks to the bottom of anterior chamber in
the form of a minute ball.
9. Angle recession refers to the tear between
longitudinal and circular muscle fibres of the
ciliary body. It is characterized by deepening of
the anterior chamber and widening of the ciliary
body band on gonioscopy. Later on it is
complicated by glaucoma.
10. Inflammatory changes. These include traumatic
iridocyclitis, haemophthalmitis, post-traumatic iris
atrophy and pigmentary changes.
Treatment. It consists of atropine, antibiotics and
steroids. In the presence of ruptures of pupillary
margins and subluxation of lens, atropine is
contraindicated.
V. Lens
It may show following changes:
1. Vossius ring. It is a circular ring of brown pigment
seen on the anterior capsule. It occurs due to
striking of the contracted pupillary margin against
the crystalline lens. It is always smaller than the
size of the pupil.
2. Concussion cataract. It occurs mainly due to
imbibition of aqueous and partly due to direct
mechanical effects of the injury on lens fibres. It
may assume any of the following shapes:
Discrete subepithelial opacities are of most
common occurrence.
Early rosette cataract (punctate). It is the
most typical form of concussion cataract. It
appears as feathery lines of opacities along
the star-shaped suture lines; usually in the
posterior cortex (Fig. 17.6).
Late rosette cataract. It develops in the
posterior cortex 1 to 2 years after the injury. Its
sutural extensions are shorter and more
compact than the early rosette cataract.
Traumatic zonular cataract. It may also occur
in some cases, though rarely.
Diffuse (total) concussion cataract. It is of
frequent occurrence.
Early maturation of senile cataract may follow
blunt truma.
Treatment of traumatic cataract is on general lines
(see pages 183-202).
3. Traumatic absorption of the lens. It may occur
sometimes in young children resulting in aphakia.
4. Subluxation of the lens (Fig. 8.31A). It may occur
due to partial tear of zonules. The subluxated
lens is slightly displaced but still present in the
pupillary area. On dilatation of the pupil its edge
may be seen. Depending upon the site of zonular
tear subluxation may be vertical (upward or
downward), or lateral (nasal or temporal).
5. Dislocation of the lens. It occurs when rupture of
the zonules is complete. It may be intraocular
(commonly) or extraocular (sometimes). Intraocular
dislocation may be anterior (into the anterior
chamber, Fig. 8.31B) or posterior (into the
vitreous, Fig. 8.31C). Extraocular dislocation may
be in the subconjunctival space (phakocele) or it
may fall outside the eye.
For treatment of the subluxated or dislocated lens
see page 204.
VI. Vitreous
1. Liquefaction and appearance of clouds of fine
pigmentary opacities (a most common change).
2. Detachment of the vitreous either anterior or
posterior.
3. Vitreous haemorrhage. It is of common
occurrence (see page 246).
4. Vitreous herniation in the anterior chamber may
occur with subluxation or dislocation of the lens.
VII. Choroid
1. Rupture of the choroid. The rupture of choroid
is concentric to the optic disc and situated
temporal to it. Rupture may be single or multiple.
On fundus examination, the choroidal rupture
looks like a whitish crescent (due to underlying
sclera) with fine pigmentation at its margins.
Retinal vessels pass over it (Fig. 17.7).
2. Choroidal haemorrhage may occur under the
retina (subretinal) or may even enter the vitreous
if retina is also torn.
3. Choroidal detachment is also known occur
following blunt trauma.
4. Traumatic choroiditis may be seen on fundus
examination as patches of pigmentation and
discoloration after the eye becomes silent.
VIII. Retina
1. Commotio retinae (Berlin’s oedema). It is of
common occurrence following a blow on the eye.
It manifests as milky white cloudiness involving
a considerable area of the posterior pole with a
‘cherry-red spot’ in the foveal region. It may
disappear after some days or may be followed by
pigmentary changes.
2. Retinal haemorrhages. These are quite common
following concussion trauma. Multiple
haemorrhages including flame-shaped and preretinal
(subhyaloid) D-shaped haemorrhage may
be associated with traumatic retinopathy.
3. Retinal tears. These may follow a contusion,
particularly in the peripheral region, especially in
eyes already suffering from myopia or senile
degenerations.
4. Traumatic proliferative retinopathy (Retinitis
proliferans). It may occur secondary to vitreous
haemorrhage, forming tractional bands.
5. Retinal detachment. It may follow retinal tears or
vitreo-retinal tractional bands.
6. Concussion changes at macula. Traumatic
macular oedema is usually followed by pigmentary
degeneration. Sometimes, a macular cyst is
formed, which on rupture may be converted into
a lamellar or full thickness macular hole.
IX. Intraocular pressure changes in closed-globe
injury
1. Traumatic glaucoma. It may occur due to multiple
factors, which are described in detail on page
235.
2. Traumatic hypotony. It may follow damage to the
ciliary body and may even result in phthisis
bulbi.
X. Traumatic changes in the refraction
1. Myopia may follow ciliary spasm or rupture of
zonules or anterior shift of the lens.
2. Hypermetropia and loss of accommodation may
result from damage to the ciliary body(cycloplegia).
B. Globe rupture
Globe rupture is a full-thickness wound of the eyewall
caused by a blunt object. Globe rupture may occur
in two ways:
1. Direct rupture may occur, though rarely, at the
site of injury.
2. Indirect rupture is more common and occurs
because of the compression force. The impact results
in momentary increase in the intraocular pressure and
an inside-out injury at the weakest part of eyewall,
i.e., in the vicinity of canal of Schlemm concentric to
the limbus. The superonasal limbus is the most
common site of globe rupture (contrecoup effect—
the lower temporal quadrant being most exposed to
trauma). Rupture of the globe may be associated with
prolapse of uveal tissue, vitreous loss, intraocular
haemorrhage and dislocation of the lens.
Treatment. A badly damaged globe should be
enucleated. In less severe cases, repair should be
done under general anaesthesia. Postoperatively
atropine, antibiotics and steroids should be used.
C. Extraocular lesions
Extraocular lesions caused by blunt trauma are as
follows:
1. Conjunctival lesions. Subconjunctival haemorrhage
occurs very commonly. It appears as a bright
red spot. Chemosis and lacerating wounds of
conjunctiva (tears) are also not uncommon.
2. Eyelid lesion. Ecchymosis of eyelids is of frequent
occurrence. Because of loose subcutaneous tissue,
blood collects easily into the lids and produces ‘blackeye’.
There may occur laceration and avulsion of the
lids. Traumatic ptosis may follow damage to the
levator muscle.
3. Lacrimal apparatus lesions. These include
dislocation of lacrimal gland and lacerations of
lacrimal passages especially the canaliculi.
4. Optic nerve injuries. These are commonly
associated with fractures of the base of skull. These
may be in the form of traumatic papillitis, lacerations
of optic nerve, optic nerve sheath haemorrhage and
avulsion of the optic nerve from back of the eye.
5. Orbital injury. There may occur fractures of the
orbital walls; commonest being the ‘blow-out fracture’
of the orbital floor. Orbital haemorrhage may produce
sudden proptosis. Orbital emphysema may occur
following ethmoidal sinus rupture.

EXTRAOCULAR FOREIGN BODIES: types, removal, prophylaxis

Extraocular foreign bodies are quite common in
industrial and agricultural workers. Even in day-today
life, these are not uncommon.
Common sites. A foreign body may be impacted in
the conjunctiva or cornea (Fig. 17.1).
On the conjunctiva, it may be lodged in the
sulcus subtarsalis, fornices or bulbar conjunctiva.
In the cornea, it is usually embedded in the
epithelium, or superficial stroma and rarely into
the deep stroma.

Common types. The usual foreign bodies:
In industrial workers are particles of iron
(especially in lathe and hammer-chisel workers),
emery and coal.
In agriculture workers, these are husk of paddy
and wings of insects.
Other common foreign bodies are particles of
dust, sand, steel, glass, wood and small insects
(mosquitoes).
Symptoms. A foreign body produces immediate:
Discomfort, profuse watering and redness in the
eye.
Pain and photophobia are more marked in corneal
foreign body than the conjunctival.
Defective vision occurs when it is lodged in the
centre of cornea.
Signs. Examination reveals marked blepharospasm
and conjunctival congestion. A foreign body can be
localized on the conjunctiva or cornea by oblique
illumination. Slit-lamp examination after fluorescein
staining is the best method to discover corneal foreign
body. Double eversion of the upper lid is required to
discover a foreign body in the superior fornix.
Complications. Acute bacterial conjunctivitis may
occur from infected foreign bodies or due to rubbing
with infected hands. A corneal foreign body may be
complicated by ulceration. Pigmentation and/or
opacity may be left behind by an iron or emery
particles embedded in the cornea.
Treatment. Extraocular foreign bodies should be
removed as early as possible.
1. Removal of conjunctival foreign body. A foreign
body lying loose in the lower fornix, sulcus
subtarsalis or in the canthi may be removed with
a swab stick or clean handkerchief even without
anaesthesia. Foreign bodies impacted in the
bulbar conjunctiva need to be removed with the
help of a hypodermic needle after topical
anaesthesia.
2. Removal of corneal foreign body. Eye is
anaesthetised with topical instillation of 2 to 4
percent xylocaine and the patient is made to lie
supine on an examination table. Lids are separated
with universal eye speculum, the patient is asked
to look straight upward and light is focused on
the cornea. First of all, an attempt is made to
remove the foreign body with the help of a wet
cotton swab stick. If it fails then foreign body
spud or hypodermic needle is used. Extra care is
taken while removing a deep corneal foreign
body, as it may enter the anterior chamber during
manoeuvring. If such a foreign body happens to
be magnetic, it is removed with a hand-held
magnet. After removal of foreign body, pad and
bandage with antibiotic eye ointment is applied
for 24 to 48 hours. Antibiotic eyedrops are
instilled 3-4 times a day for about a week.
Prophylaxis. Industrial and agricultural workers
should be advised to use special protective glasses.
Cyclists and scooterists should be advised to use
protective plain glasses or tinted goggles. Special
guards should be put on grinding machines and use
of tools with overhanging margins should be banned.
Eye health care education should be imparted,
especially to the industrial and agricultural workers.

Orbit Anatomy

BONY ORBIT
The bony orbits are quadrangular truncated pyramids
situated between the anterior cranial fossa above and
the maxillary sinuses below (Fig. 16.1). Each orbit is
about 40 mm in height, width and depth and is formed
by portions of seven bones : (1) frontal, (2) maxilla,
(3) zygomatic, (4) sphenoid, (5) palatine, (6) ethmoid
and (7) lacrimal. It has four walls (medial, lateral,
superior and inferior), base and an apex.
The medial walls of two orbits are parallel to each
other and, being thinnest, are frequently fractured
during injuries as well as during orbitotomy
operations and, it also accounts for ethmoiditis being
the commonest cause of orbital cellulitis.
The inferior orbital wall (floor) is triangular in shape
and being quite thin is commonly involved in blowout
fractures and is easily invaded by tumours of the
maxillary antrum.
The lateral wall of the orbit is triangular in shape. It
covers only posterior half of the eyeball. Therefore,
palpation of the retrobulbar tumours is easier from
this side. Because of its advantageous anatomical
position, a surgical approach to the orbit by lateral
orbitotomy is popular.
The roof is triangular in shape and is formed mainly
by the orbital plate of frontal bone.
Base of the orbit is the anterior open end of the
orbit. It is bounded by thick orbital margins.
The orbital apex (Fig. 16.2). It is the posterior end of
orbit. Here the four orbital walls converge. It has two
orifices, the optic canal which transmits optic nerve
and ophthalmic artery and the superior orbital fissure
which transmits a number of nerves, arteries and veins
(Fig. 13.2).
ORBITAL FASCIA
It is a thin connective tissue membrane lining various
intraorbital structures. Though, it is one continuous
tissue, but for the descriptive convenience it has been
divided into fascia bulbi, muscular sheaths,
intermuscular septa, membranous expansions of the
extraocular muscles and ligament of Lockwood.
Fascia bulbi (Tenon’s capsule) envelops the globe
from the margins of cornea to the optic nerve. Its
lower part is thickened to form a sling or hammock on
which the globe rests; this is called ‘suspensory
ligament of Lockwood’.
CONTENTS OF THE ORBIT
The volume of each orbit is about 30 cc.
Approximately one-fifth of it is occupied by the
eyeball. Other contents of the orbit include: part of
optic nerve, extraocular muscles, lacrimal gland,
lacrimal sac, ophthalmic artery and its branches, third,
fourth and sixth cranial nerves and ophthalmic and
maxillary divisions of the fifth cranial nerve,
sympathetic nerve, orbital fat and fascia.
SURGICAL SPACES IN THE ORBIT
These are of importance as most orbital pathologies
tend to remain in the space in which they are formed.
Therefore, their knowledge helps the surgeon in
choosing the most direct surgical approach. Each orbit
is divisible into four surgical spaces (Fig. 16.3).
1. The subperiosteal space. This is a potential space
between the bone and the periorbita (periosteum).
2. The peripheral space. It is bounded peripherally
by the periorbita and internally by the four recti
with thin intermuscular septa. Tumours present
here produce eccentric proptosis and can usually
be palpated. For peribulbar anaesthesia, injection
is made in this space.
3. The central space. It is also called muscular cone
or retrobulbar space. It is bounded anteriorly by
the Tenon’s capsule lining back of the eyeball
and peripherally by the four recti muscles and
their intermuscular septa in the anterior part. In
the posterior part, it becomes continuous with
the peripheral space. Tumours lying here usually
produce axial proptosis. Retrobulbar injections
are made in this space.
4. Tenon’s space. It is a potential space around
the eyeball between the sclera and Tenon’s
capsule.

DACRYOCYSTECTOMY (DCT)

1. Anaesthesia. General anaesthesia is preferred,
however, it may be performed with local infiltration
anaesthesia in adults.
2. Skin incision. Either a curved incision along the
anterior lacrimal crest or a straight incision 8 mm
medial to the medial canthus is made.
3. Exposure of medial palpebral ligament (MPL)
and Anterior lacrimal crest. MPL is exposed by
blunt dissection and cut with scissors to expose
the anterior lacrimal crest.
4. Dissection of lacrimal sac. Periosteum is separated
from the anterior lacrimal crest and along with the
lacrimal sac is reflected laterally with blunt
dissection exposing the lacrimal fossa.
5. Removal of lacrimal sac. After exposing the sac,
it is separated from the surrounding structures
by blunt dissection followed by cutting its
connections with the lacrimal canaliculi. It is then
held with artery forceps and twisted 3-4 times to
tear it away from the nasolacrimal duct (NLD).
6. Curettage of bony NLD. It is done with the help
of a lacrimal curette to remove the infected parts
of membranous NLD.
7. Closure. MPL is sutured to periosteum, orbicularis
muscle is sutured with 6-0 vicryl and skin is
closed with 6-0 silk sutures.

PROPTOSIS

It is defined as forward displacement of the eyeball
beyond the orbital margins. Though the word
exophthalmos (out eye) is synonymous with it; but
somehow it has become customary to use the term
exophthalmos for the displacement associated with
thyroid disease.
CLASSIFICATION
Proptosis can be divided into following clinical
groups:
Unilateral proptosis
Bilateral proptosis
Acute proptosis
Intermittent proptosis
Pulsating proptosis
ETIOLOGY
Important causes of proptosis in each clinical group
are listed here:
A. Causes of unilateral proptosis include:
1. Congenital conditions. These include: dermoid
cyst, congenital cystic eyeball, and orbital
teratoma.
2. Traumatic lesions. These are: orbital haemorrhage,
retained intraorbital foreign body, traumatic
aneurysm and emphysema of the orbit.
3. Inflammatory lesions. Acute inflammations are
orbital cellulitis, abscess, thrombophlebitis,
panophthalmitis, and cavernous sinus thrombosis
(proptosis is initially unilateral but ultimately
becomes bilateral). Chronic inflammatory lesions
include: pseudotumours, tuberculoma, gumma and
sarcoidosis.
4. Circulatory disturbances and vascular lesions.
These are: angioneurotic oedema, orbital varix
and aneurysms.
5. Cysts of orbit. These include: haematic cyst,
implantation cyst and parasitic cyst (hydatid cyst
and cysticercus cellulosae).
6. Tumours of the orbit. These can be primary,
secondary or metastatic.
7. Mucoceles of paranasal sinuses, especially frontal
(most common), ethmoidal and maxillary sinus are
common causes of unilateral proptosis.
B. Causes of bilateral proptosis include:
1. Developmental anomalies of the skull:
craniofacial dysostosis e.g., oxycephaly (tower
skull).
2. Osteopathies: Osteitis deformans, rickets and
acromegaly.
3. Inflammatory conditions: Mikulicz’s syndrome
and late stage of cavernous sinus thrombosis.
4. Endocrinal exophthalmos: It may be thyrotoxic
or thyrotropic.
5. Tumours: These include symmetrical lymphoma
or lymphosarcoma, secondaries from neuroblastoma,
nephroblastoma, Ewing’s sarcoma and
leukaemic infiltration.
6. Systemic diseases: Histiocytosis, systemic
amyloidosis, xanthomatosis and Wegener’s
granulomatosis.
C. Causes of acute proptosis. It develops with
extreme rapidity (sudden onset). Its common causes
are: orbital emphysema fracture of the medial orbital
wall, orbital haemorrhage and rupture of ethmoidal
mucocele.
D. Cause of intermittent proptosis. This type of
proptosis appears and disappears of its own. Its
common causes are: orbital varix, periodic orbital
oedema, recurrent orbital haemorrhage and highly
vascular tumours.
E. Causes of pulsating proptosis. It is caused by
pulsating vascular lesions such as caroticocavernous
fistula and saccular aneurysm of
ophthalmic artery. Pulsating proptosis also occurs
due to transmitted cerebral pulsations in conditions
associated with deficient orbital roof. These include
congenital meningocele or meningoencephalocele,
neurofibromatosis and traumatic or operative hiatus.
Investigation of a case of proptosis
I. Clinical evaluation
(A) History. It should include: age of onset, nature of
onset, duration, progression, chronology of orbital
signs and symptoms and associated symptoms.
(B) Local examination. It should be carried out as
follows:
1. Inspection. (i) To differentiate proptosis from
pseudoproptosis which is seen in patients with
buphthalmos, axial high myopia, retraction of
upper lid and enophthalmos of the opposite eye;
(ii) to ascertain whether the proptosis is unilateral
or bilateral; (iii) to note the shape of the skull;
and (iv) to observe whether proptosis is axial or
eccentric.
2. Palpation. It should be carried out for retrodisplacement
of globe to know compressibility of
the tumour, for orbital thrill, for any swelling
around the eyeball, regional lymph nodes and
orbital rim.
3. Auscultation. It is primarily of value in searching
for abnormal vascular communications that
generate a bruit, such as caroticocavernous fistula.
4. Transillumination. It is helpful in evaluating
anterior orbital lesions.
5. Visual acuity. Orbital lesions may reduce visual
acuity by three mechanisms: refractive changes
due to pressure on back of the eyeball, optic
nerve compression and exposure keratopathy.
6. Pupil reactions. The presence of Marcus Gunn
pupil is suggestive of optic nerve compression.
7. Fundoscopy. It may reveal venous engorgement,
haemorrhage, papilloedema and optic atrophy.
Choroidal folds and opticociliary shunts may be
seen in patients with meningiomas.
8. Ocular motility. It is restricted in thyroid
ophthalmopathy, extensive tumour growths and
neurological deficit.
9. Exophthalmometry. It measures protrusion of the
apex of cornea from the outer orbital margin (with
the eyes looking straight ahead). Normal values
vary between 10 and 21 mm and are symmetrical
in both eyes. A difference of more than 2 mm
between the two eyes is considered significant.
The simplest instrument to measure proptosis is
Luedde’s exophthalmometer (Fig. 16.4). However,
the Hertel’s exophthalmometer (Fig. 16.5) is the
most commonly used instrument. Its advantage
is that it measures the two eyes simultaneously.
(C) Systemic examination. A thorough examination
should be conducted to rule out systemic causes of
proptosis such as thyrotoxicosis, histiocytosis, and
primary tumours elsewhere in the body (secondaries
in orbits). Otorhinolaryngological examination is
necessary when the paranasal sinus or a
nasopharyngeal mass apears to be a possible
etiological factor.
II. Laboratory investigations
These should include:
Thyroid function tests,
Haematological studies (TLC, DLC, ESR, VDRL
test),
Casoni’s test (to rule out hydatid cyst),
Stool examination for cysts and ova, and
Urine analysis for Bence Jones proteins for
multiple myeloma.
III. Imaging Technique
(A) Non-invasive techniques
1. Plain X-rays. It is still the most frequently used
initial radiological examination. Commonly required
exposures are in the Caldwell view, the Water’s
view, a lateral view and the Rhese view (for optic
foramina). X-ray signs of orbital diseases include
enlargement of orbital cavity, enlargement of optic
foramina, calcification and hyperostosis.
2. Computed tomography scanning. It is very useful
for determining the location and size of an orbital
mass. A combination of axial (CAT) and coronal
(CCT) cuts enables a three-dimensional
visualisation. CT scan is capable of visualising
various structures like globe, extraocular muscles
and optic nerves. Further, this technique is also
useful in examining areas adjacent to the orbits
such as orbital walls, cranial cavity, paranasal
sinuses and nasal cavity. Its main disadvantage
is the inability to distinguish between
pathologically soft tissue masses which are
radiologically isodense.
3. Ultrasonography. It is a non-radiational noninvasive,
completely safe and extremely valuable
initial scanning procedure for orbital lesions. In
the diagnosis of orbital lesions, it is superior to
CT scanning in actual tissue diagnosis and can
usually differentiate between solid, cystic,
infiltrative and spongy masses.
4. Magnetic resonance imaging (MRI). It is a major
advance in the imaging techniques. It is very
sensitive for detecting differences between normal
and abnormal tissues and has excellent image
resolution. The technique produces tomographic
images which are superficially very similar to CT
scan but rely on entirely different physical
principles for their production.
(B) Invasive procedures
1. Orbital venography. It is required in patients
who are clinically suspected of having orbital
varix. It confirms the diagnosis and also outlines
the size and extent of the anomaly which facilitates
proper surgical planning.
2. Carotid angiography. It is now performed only
in cases of pulsating exophthalmos and in those
associated with a bruit or thrill. The principal role
of carotid angiography in orbital diagnosis is to
identify the location and extent of ophthalmic
artery aneurysms, and the pathologic circulation
associated with various arteriovenous
communications along the ophthalmic artery–
cavernous sinus complex. It is also useful to
identify the feeding vessels prior to undertaking
surgery in patients with vascular orbital tumours.
3. Radioisotope studies. These are, nowadays,
sparingly employed. Radioisotope arteriography
has been found useful in proptosis of vascular
lesions. In this technique, sodium pertechnetate
Tc 99 m is injected intravenously and its flow is
visualised by a gamma scintillation camera.
IV. Histopathological studies
The exact diagnosis of many orbital lesions cannot
be made without the help of histopathological studies
which can be accomplished by following techniques:
1. Fine-needle aspiration biopsy (FNAB). It is a
reliable, accurate (95%), quick and easy technique
for cytodiagnosis in orbital tumours. The biopsy
aspirate is obtained under direct vision in an
obvious mass and under CT scan or
ultrasonographic guidance in retrobulbar mass
using a 23-gauge needle.
2. Incisional biopsy. Undoubtedly, for accurate
tissue diagnosis a proper biopsy specimen at
least 5 to 10 mm in length is required. However,
the scope of incisional biopsy in the diagnosis of
orbital tumours is not clearly defined. It may be
undertaken along with frozen tissue study in
infiltrative lesions which remain undiagnosed.
3. Excisional biopsy. It should always be preferred
over incisional biopsy in orbital masses which
are well encapsulated or circumscribed. It is
performed by anterior orbitotomy for a mass in
the anterior part of orbit and by lateral orbitotomy
for a retrobulbar mass.

endonasal DCR vis-a-vis external DCR

Endoscopic DCR External DCR
Advantages Disadvantages
No external scar Cutaneous scar
Relatively blood less Relatively more
surgery bleeding during
surgery
Better visualisation of
nasal pathology
Less chances of injury to Potential injury to
ethmoidal vessels and adjacent medial
cribri form plate. canthus structures
Less time consuming More operating time
(15-30 mins) since nasal (45-60 minutes)
mucosal flaps and sac
wall flaps are not made.
No post operative Significant
morbidity postoperative
morbidity
Disadvantages Advantages
Less success rate More success rate
(70-90%) (95%)
Requires skilled ophthal- Easily performed by
mologist and/or rhinologist. ophthalmologists
Expensive equipment Cheap (expensive
equipment not
required)
Requires reasonable Does not require
access to middle familiarity with
meatus and familiarity endoscopic
with endoscopic anatomy. anatomy

CHRONIC DACRYOCYSTITIS

Chronic dacryocystitis is more common than the acute
dacryocystitis.
Etiology
The etiology of chronic dacryocystitis is
multifactorial. The well-established fact is a vicious
cycle of stasis and mild infection of long duration.The
etiological factors can be grouped as under:
A. Predisposing factors
1. Age. It is more common between 40 and 60 years
of age.
2. Sex. The disease is predominantly seen in females
(80%) probably due to comparatively narrow
lumen of the bony canal.
3. Race. It is rarer among Negroes than in Whites;
as in the former NLD is shorter, wider and less
sinuous.
4. Heredity. It plays an indirect role. It affects the
facial configuration and so also the length and
width of the bony canal.
5. Socio-economic status. It is more common in low
socio-economic group.
6. Poor personal hygiene. It is also an important
predisposing factor.
B. Factors responsible for stasis of tears in
lacrimal sac
1. Anatomical factors, which retard drainage of tears
include: comparatively narrow bony canal, partial
canalization of membranous NLD and excessive
membranous folds in NLD.
2. Foreign bodies in the sac may block opening of
NLD.
3. Excessive lacrimation, primary or reflex, causes
stagnation of tears in the sac.
4. Mild grade inflammation of lacrimal sac due to
associated recurrent conjunctivitis may block the
NLD by epithelial debris and mucus plugs.
5. Obstruction of lower end of the NLD by nasal
diseases such as polyps, hypertrophied inferior
concha, marked degree of deviated nasal septum,
tumours and atrophic rhinitis causing stenosis
may also cause stagnation of tears in the lacrimal
sac.
C. Source of infection. Lacrimal sac may get infected
from the conjunctiva, nasal cavity (retrograde
spread), or paranasal sinuses.
D. Causative organisms. These include: staphylococci,
pneumococci, streptococci and Pseudomonas
pyocyanea. Rarely chronic granulomatous
infections like tuberculosis, syphilis, leprosy and
occasionally rhinosporiodosis may also cause
dacryocystitis.
Clinical picture
Clinical picture of chronic dacryocystitis may be
divided into four stages:
1. Stage of chronic catarrhal dacryocystitis. It is
characterised by mild inflammation of the lacrimal sac
associated with blockage of NLD. In this stage the
only symptom is watering eye and sometimes mild
redness in the inner canthus. On syringing the lacrimal
sac, either clear fluid or few fibrinous mucoid flakes
regurgitate. Dacryocystography reveals block in NLD,
a normal-sized lacrimal sac with healthy mucosa.
2. Stage of lacrimal mucocoele. It follows chronic
stagnation causing distension of lacrimal sac. It is
characterised by constant epiphora associated with
a swelling just below the inner canthus (Fig. 15.8).
Milky or gelatinous mucoid fluid regurgitates from
the lower punctum on pressing the swelling.
Dacryocystography at this stage reveals a distended
sac with blockage somewhere in the NLD.
Sometimes due to continued chronic infection,
opening of both the canaliculi into the sac are blocked
and a large fluctuant swelling is seen at the inner
canthus with a negative regurgitation test. This is
called encysted mucocele.
3. Stage of chronic suppurative dacryocystitis. Due
to pyogenic infections, the mucoid discharge
becomes purulent, converting the mucocele into
‘pyocoele’. The condition is characterised by
epiphora, associated recurrent conjunctivitis and
swelling at the inner canthus with mild erythema of
the overlying skin. On regurgitation a frank purulent
discharge flows from the lower punctum. If openings
of canaliculi are blocked at this stage the so called
encysted pyocoele results.
4. Stage of chronic fibrotic sac. Low grade repeated
infections for a prolonged period ultimately result in
a small fibrotic sac due to thickening of mucosa, which
is often associated with persistent epiphora and
discharge. Dacryocystography at this stage reveals
a very small sac with irregular folds in the mucosa.
Complications
Chronic intractable conjunctivitis, acute on chronic
dacryocystitis.
Ectropion of lower lid, maceration and eczema of
lower lid skin due to prolonged watering.
Simple corneal abrasions may become infected
leading to hypopyon ulcer.
If an intraocular surgery is performed in the
presence of dacryocystitis, there is high risk of
developing endophthalmitis. Because of this,
syringing of lacrimal sac is always done before
attempting any intraocular surgery.
Treatment
1. Conservative treatment by repeated lacrimal
syringing. It may be useful in recent cases only. Longstanding
cases are almost always associated with
blockage of NLD which usually does not open up
with repeated lacrimal syringing or even probing.
2. Dacryocystorhinostomy (DCR). It should be the
operation of choice as it re-establishes the lacrimal
drainage. However, before performing surgery, the
infection especially in pyocoele should be controlled
by topical antibiotics and repeated lacrimal syringings.
3. Dacryocystectomy (DCT). It should be performed
only when DCR is contraindicated. Indications of
DCT include: (i) Too young (less than 4 years) or too
old (more than 60 years) patient. (ii) Markedly
shrunken and fibrosed sac. (iii) Tuberculosis, syphilis,
leprosy or mycotic infections of sac. (iv) Tumours of
sac. (v) Gross nasal diseases like atrophic rhinitis (vi)
An unskilled surgeon, because it is said that, a good
‘DCT’ is always better than a badly done ‘DCR’.
4. Conjunctivodacryocystorhinostomy (CDCR). It is
performed in the presence of blocked canaliculi.

DACRYOCYSTORHINOSTOMY

Dacryocystorhinostomy (DCR) operation can be
performed by two techniques:
Conventional external approach DCR, and
Endonasal DCR
Conventional external approach DCR (Fig. 15.11)
1. Anaesthesia. General anaesthesia is preferred,
however, it may be performed with local infiltration
anaesthesia in adults.
2. Skin incision. Either a curved incision along the
anterior lacrimal crest or a straight incision 8 mm
medial to the medial canthus is made.
3. Exposure of medial palpebral ligament (MPL)
and Anterior lacrimal crest. MPL is exposed by
blunt dissection and cut with scissors to expose
the anterior lacrimal crest 4. Dissection of lacrimal sac. Periosteum is separated
from the anterior lacrimal crest and along with the
lacrimal sac is reflected laterally with blunt
dissection exposing the lacrimal fossa.
5. Exposure of nasal mucosa. A 15 mm × 10 mm
bony osteum is made by removing the anterior
lacrimal crest and the bones forming lacrimal
fossa, exposing the thick pinkish white nasal
mucosa.
6. Preparation of flaps of sac. A probe is introduced
into the sac through lower canaliculus and the
sac is incised vertically. To prepare anterior and
posterior flaps, this incision is converted into H
shape.
7. Fashioning of nasal mucosal flaps. is also done
by vertical incision converted into H shape.
8. Suturing of flaps. Posterior flap of the nasal
mucosa is sutured with posterior flap of the sac
using 6-0 vicryl or chromic cat gut sutures. It is
followed by suturing of the anterior flaps.
9. Closure. MPL is sutured to periosteum, orbicularis
muscle is sutured with 6-0 vicryl and skin is
closed with 6-0 silk sutures.
Endonasal DCR
Presently many eye surgeons, alone or in
collaboration with the ENT surgeons, are pereferring
endonasal DCR over conventional external approach
DCR because of its advantages (described below).
surgical steps of endonasal DCR are (Fig. 15.12):
1. Preparation and anaesthesia. Nasal mucosa is
prepared for 15-30 minutes before operation with nasal
decongestant drops and local anaesthetic agent.
Conjunctival sac is anaesthetised with topically
instilled 2% lignocaine. Then 3 ml of lignocaine 2%
with 1 in 2 lac adrenaline is injected into the medial
parts of upper and lower eyelids and via subcaruncular
injection to the lacrimal fossa region.
2. Identification of sac area. A 20-gauge light pipe is
inserted via the upper canaliculi into the sac. With the
help of endoscope, the sac area which is
transilluminated by the light pipe is identified (Fig.
15.12A) and a further injection of lignocaine with
adrenaline is made below the nasal mucosa in this area.
3. Creation of opening in the nasal mucosa, bones
forming the lacrimal fossa and posteromedial wall
of sac can be accomplished by two techniques:
i By cutting the tissues with appropriate
instruments or
ii By ablating with Holmium YAG laser (endoscopic
laser assited DCR).
Note: The size of opening is about 12 mm × 10 mm
(Fig. 15.12B).
4. Stenting of rhinostomy opening. The outflow
system is then stented using fine silicone tubes
passed via the superior and inferior canaliculi into
the rhinostomy and secured with a process of knotting
(Fig. 15.12C). Nasal packing and dressing is done.
5. Postoperative care and removal of sialistic
lacrimal stents. After 24 hours of operation nasal
packs are removed and patient is advised to use
decongestent, antibiotic and steroid nasal drops for
3-4 weeks. The sialistic lacrimal stents are removed 8-
12 weeks after surgery and the nasal drops are
continued further for 2-3 weeks.