OCULAR

BY
INJURIES
Dr. LUCKY NARAIN
(MS)
 OCULAR
TRAUMA
Damage or trauma inflicted to the eye by external means. The concept includes both surface injuries and
intraocular injuries. During trauma soft tissues and bony structures around the eye maybe involved.

CLOSED GLOBE INJURY OPEN GLOBE INJURY

Closed-globe injury is the one in which eyewall Open-globe injury is associated with a full-
(sclera and cornea) does not have a full thickness thickness
wound but there is intraocular damage. It includes wound of the sclera or cornea or both. It includes
contusion and lamellar laceration. rupture and laceration of eyewall.
 CLOSED GLOBE INJURY OPENED GLOBE INJURY
1. Contusion refers to the closed-globe injury 1. Rupture refers to a full-thickness wound of eyewall
resulting from blunt trauma. Damage may occur caused by the impact of blunt trauma.
at the site of impact or at a distant site. 2. Laceration refers to a full-thickness wound of
2. Lamellar laceration is a closed-globe injury eyewall caused by a sharp object.
characterized by a partial thickness wound of the a) Penetrating injury refers to a single laceration of
eyewall caused by a sharp object or blunt trauma eyewall caused by a sharp object which traverses
the coats only once.
b) Perforating injury refers to two full thickness
lacerations (one entry and one exit) of the eyewall
caused by a sharp object or missile. The two
wounds must have been caused by the same agent
(earlier known as double perforation).
c) lntraocular foreign body injury is technically
a penetrating injury associated with retained
intraocular foreign body. However, it is grouped
separately because of different clinical implications.
OPEN GLOBE
INJURY
 EXTRAOCULAR
INJURIES
Extraocular foreign bodies are quite common in industrial and agricultural workers. Even in day-to day life,
these are common.
Common sites and types
Common sites A foreign body may be impacted in the conjunctiva or cornea
• 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 common foreign bodies are particles of dust, sand, steel, glass, wood and small insects.
Clinical features
Symptoms • Discomfort, profuse watering and redness in the eye.
• Pain and photophobia are more marked in corneal foreign body than the conjunctiva.
• Defective vision occurs when it is lodged in the centre of cornea.
Signs • 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
1. Acute bacterial conjunctivitis
2. Corneal ulceration
3. Pigmentation and/or opacity may be left behind
Treatment
Extraocular foreign bodies should be removed as early as possible.
[Link] 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.
[Link] of corneal foreign body.
I. Eye is anaesthetised with topical instillation of 2 to 4% xylocaine and the patient is made to lie
supine on an examination table.
II. Lids are separated with universal eye speculum, the patient is asked to look straight upward and light
is focused on the cornea.
III. First of all, an attempt is made to remove the foreign body with the help of a wet cotton swap stick.
If it fails then foreign body spud or hypodermic needle is used.
IV. Extra care is taken while removing a deep corneal foreign body, as it may enter the anterior chamber
during manoeuvring.
V. If such a foreign body happens to be magnetic, it is removed with a hand-held magnet.
 VI. After removal of foreign body, patching with antibiotic eye ointment is applied for 24 to 48 hours.
VII. Antibiotic eyedrops are instilled 3-4 times a day for about a week.
 BLUNT
TRAUMA
CAUSES AND PATHOGENESIS OF DAMAGE
Modes of trauma
• Direct blow to the eyeball by fist, a tennis or cricket or another 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 forces of blunt trauma
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.
2. Compression wave force. It is transmitted through the fluid contents in all the directions and strikes the
angle of anterior chamber, pushes the iris-lens posteriorly, and also strikes the retina and Choroid.
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.
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.
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.
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.
I. Cornea
1. Simple abrasions. These are very painful and diagnosed by fluorescein staining. These usually heal up
within 24 hours with patching applied after instilling antibiotic ointment.
2. Partial corneal tears (lamellar corneal laceration). These may also follow a blunt trauma and are treated
by topical antibiotics and patching.
3. Acute corneal oedema may occur following traumatic dysfunction of endothelial cells. It may be
associated with Descemet’s folds and stromal thickening. It, usually, clears up spontaneously; rarely a
deep corneal opacity may be the sequelae.
4. Blood staining of cornea. It may occur occasionally from the associated hyphaema and raised
intraocular pressure. Cornea becomes reddish brown 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.
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.
■ Treatment includes:
• Conservative treatment is aimed at prevention of rise in IOP and occurrence of secondary haemorrhage
(re-bleed).
• Surgical treatment. A small hyphaema usually clears up with conservative treatment. A large non
resolving hyphaema causing raised IOP should be drained to avoid blood staining of the cornea.
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. 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.
5. 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.
6. Retroflexion of the iris. This term is used when whole of the iris is doubled back into the ciliary region
and becomes invisible.
7. Traumatic aniridia or iridemia. In this condition, the completely torn iris (from ciliary body) sinks to the
bottom of anterior chamber in the form of a minute ball.
8. 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.
9. 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
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.
• 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.
• 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.
• Diffuse (total) concussion cataract. It is of frequent occurrence.
3. Traumatic absorption of the lens. It may occur sometimes in young children resulting in aphakia.
4. Subluxation of the lens. It may occur due to partial tear of zonules. The subluxated lens is slightly
displaced but still present in the pupillary area. Subluxated lens may cause trembling of the iris
(iridodonesis) and/or trembling of lens (phacodonesis).
5. Dislocation of the lens. It occurs when rupture of the zonules is complete. It may be intraocular or
extraocular. Intraocular dislocation may be anterior or posterior. Extraocular dislocation may be in the
subconjunctival space.
VI. Vitreous
1. Liquefaction and appearance of clouds of fine pigmentary opacities (a most common change).
2. Detachment of the vitreous either anteriorly at the base or posterior (PVD) may occur.
3. Vitreous haemorrhage. It is of common occurrence
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. 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.
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 to occur following blunt trauma.
VIII. Retina
1. Commotio retinae. It is of common occurrence following a blow on the eye. It manifests as 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.
3. Retinal tears.
4. Retinal detachment.
5. 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.
B. Globe rupture
Globe rupture is a full-thickness wound of the eyeball (sclera, cornea or both) caused by a blunt object.
Types of globe rupture
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.
Clinical features
Rupture of the globe may be associated with: Prolapse of uveal tissue, vitreous loss, intraocular
haemorrhage and dislocation of the lens.
• Intraocular pressure may be raised initially, but ultimately it is decreased.
• Accompanying signs include irregular pupil, hyphaema, commotio retinae, choroidal rupture, and
retinal tears.
Treatment
• Repair of tear in the eyewall should be done under general anaesthesia to save the eyeball whenever
possible.
• Postoperative treatment should include antibiotics, steroids and atropine.
• Enucleation may be required in a badly damaged eye where salvation is not possible.
C. Extraocular lesions
1. Conjunctival lesions include:
• 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 include:
• Ecchymosis of eyelids is of frequent occurrence.
• Laceration and avulsion of the lids.
• Traumatic ptosis may follow damage to the levator muscle.
3. Lacrimal apparatus lesions
4. Optic nerve injuries
5. Orbital injury
 OPEN-GLOBE
Modes of injury INJURIES
1. Trauma by sharp and pointed instruments like needles, knives, nails, arrows, screw-drivers, pens,
pencils, compasses, glass pieces and so on.
2. Trauma by foreign bodies travelling at very high speed such as bullet injuries and iron foreign bodies
in lathe workers.
Mechanisms of damage
1. Mechanical effects of the trauma or physical changes.
2. Introduction of infection.
3. Post-traumatic iridocyclitis. It is of frequent occurrence and if not treated properly can cause
devastating damage, a rare but most dangerous complication of a perforating injury
Traumatic lesions with management
1. Wounds of the conjunctiva. These are common and usually associated with subconjunctival
haemorrhage. A wound of more than 3 mm should be sutured.
2. Wounds of the cornea. These can be divided into uncomplicated and complicated wounds.
[Link] corneal wounds. These are not associated with prolapse of intraocular contents.
Treatment. A small central wound does not need stitching. The only treatment required is pad and
bandage with atropine and antibiotic ointments. A large corneal wound (more than 2 mm) should
always be sutured.
[Link] corneal wounds. These are associated with prolapse of iris, sometimes lens
matter and even vitreous.
Treatment. Corneal wounds with iris prolapse should be sutured after abscising the iris. The
prolapsed iris should never be reposited; since it may cause infection. When associated with lens
injury and vitreous loss, lensectomy and anterior vitrectomy may be performed along with repair
of the corneal wound.
 3. Wounds of the sclera. These are usually associated with corneal wounds and should be managed as
above. In corneo-scleral tear, first suture should be applied at the limbus.
4. Wounds of the lens. Extensive lens ruptures with vitreous loss should be managed as above. Small
wounds in the anterior capsule may seal and lead on to traumatic cataract.
5. A badly (severely) wounded eye. It refers to extensive corneo-scleral tears associated with
prolapse of the uveal tissue, lens rupture, vitreous loss and injury to the retina and choroid. Usually
there seems to be no chance of getting useful vision in such cases. So, preferably such eyes should
be excised.
INTRAOCULAR FOREIGN BODIES
Penetrating injuries with foreign bodies are not infrequent. Seriousness of such injuries is compounded by
the retention of intraocular foreign bodies (IOFB).
Common foreign bodies chips of iron and steel (90%), particles of glass, stone, lead pellets, copper
percussion caps, aluminium, plastic and wood.
Modes of damage and lesions
A penetrating/perforating injury with retained foreign body may damage the ocular structures by the
following modes:
 A. Mechanical effects.
B. Introduction of infection.
C. Reaction of foreign bodies.
D. Post-traumatic iridocyclitis.
A. Mechanical effects
Mechanical effects depend upon the size, velocity and type of the foreign body. Foreign bodies
greater than 2 mm in size cause extensive damage. The lesions caused also depend upon the route of
entry and the site up to which a foreign body has travelled.
Traumatic lesions produced by intraocular foreign bodies include:
• Corneal or/and scleral perforation, hyphaema, iris hole,
• Rupture of the lens and traumatic cataract,
• Vitreous haemorrhage and/or degeneration,
• Choroidal perforation, haemorrhage and inflammation,
• Retinal hole, haemorrhages, oedema and detachment.
Locations of IOFB. Having entered the eye through the cornea or sclera a foreign body may be retained
at any of the following sites
1. Anterior chamber. In the anterior chamber, the IOFB usually sinks at the bottom. A tiny foreign body
may be concealed in the angle of anterior chamber, and visualised only on gonioscopy.
2. Iris. Here the foreign body is usually entangled in the stroma.
 3. Posterior chamber. Rarely, a foreign body may sink behind the iris after entering through pupil or
after making a hole in the iris.
4. Lens. Foreign body may be present on the anterior surface or inside the lens. Either an opaque
track may be seen in the lens or the lens may become completely cataractous.
5. Vitreous cavity. A foreign body may reach here through various routes.
6. Retina, choroid and sclera. A foreign body may obtain access to these structures through corneal
route or directly from scleral perforation.
7. Orbital cavity. A foreign body piercing the eyeball may occasionally cause double perforation and
come to rest in the orbital tissues.
Management of retained intraocular foreign bodies (IOFB)
Diagnosis. It is a matter of extreme importance particularly as the patient is often unaware that a
particle has entered the eye. To come to a correct diagnosis following steps should be taken:
[Link]
[Link] examination
[Link] X-rays
4.B scan
[Link]
[Link]
TREATMENT
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).
1. Foreign body in the anterior chamber. It is removed through a corresponding corneal incision directed
straight towards the foreign body.
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.
3. Foreign body in the [Link] extraction is 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.
[Link] body in the vitreous and the retina is removed as follow:
[Link] 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.
[Link] removal with pars plana vitrectomy. This technique is used to remove all non-magnetic foreign
bodies and those magnetic foreign bodies that cannot 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.
 CHEMICAL INJURIES
Chemical injuries are by no means uncommon. These vary in severity from a transient irritation of little
significance to complete and sudden loss of vision.
Modes of chemical injury
These usually occur due to external contact with chemicals under following circumstances:
1. Domestic accidents, e.g., with ammonia, solvents, detergents and cosmetics.
2. Agricultural accidents, e.g., due to fertilizers, insecticides, toxins of vegetable and animal origin.
3. Chemical laboratory accidents, with acids and alkalies.
4. Deliberate chemical attacks, especially with acids to disfigure the face.
5. Self-inflicted chemical injuries are seen in psychopaths.
Types of chemical injuries
In general, the serious chemical burns mainly comprise alkali and acid burns.
A. 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
B. 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. 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.
Treatment of chemical burns
1. Prevent further damage
Immediate and thorough irrigation with the available clean water or saline delivered through an IV
tubing. Deliver minimum of 2 L of water in 20-30 minutes or until pH is restored.
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.
• Removal of contaminated and necrotic tissue.
• Necrosed conjunctiva should be excised.
• Contaminated and necrosed corneal epithelium should be removed with a cotton swab stick.
2. Maintenance of favourable conditionsfor rapid and uncomplicated healing by following measures:
• Topical antibiotic dropse.g., moxifloxacin 4-6 times a day to prevent infection.
• Steroid eye drops
• Cycloplegics, e.g., atropine, may improve the comfort.
• Ascorbic acid, in the form of 10% sodium ascorbate eyedrops (4-5 times)
• Lubricant eyedrops (preservative free) should be used in abundance to promote the healing.
• Sodium citrate, used as 10% topical eyedrops stabilizes neutrophils and reduces collagenase release.
3. Prevention of symblepharon can be done by using a glass shell or sweeping a glass rod in the fornices
twice daily.
4. Treatment of complications, as below:
• Secondary glaucoma should be treated by topical 0.5% timolol, instilled twice a day along with oral
acetazolamide 250 mg 3-4 times a day.
• Pseudopterygium, when formed, should be excised together with conjunctival autograft
• Symblepharon needs surgical treatment.
• Corneal opacity may be treated by keratoplasty if adequate tear film and stem cell population available.
• Keratoprosthesis remains a surgical option in severely damaged eyes where keratoplasty is not
possible.
THANK
S