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.