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.