Blunt Trauma

The type and extent of damage sustained by a traumatised eye depends on both the
mechanism and force of the injury. Penetrating injuries, whether due to large or small objects,
are known to carry a poorer prognosis than contusional injuries. However, considerable
disruption of the globe may occur with severe blunt trauma which causes tearing of intraocular structures and diffuse changes secondary to energy absorption by the tissues1.
Blunt Injuries
A direct blow to the eye and surrounding tissues causes a blunt, contusional injury.
This may result in a spectrum of injuries ranging from a simple black eye to severe intraocular disruption, including rupture of the globe. When the eye is struck, it is compressed
antero-posteriorly and correspond-ingly stretched in the equatorial plane which causes a
combination of contusional and tearing damage, resulting in a well-recognised pattern of
injuries (Figure 1). The increase in intra-orbital pressure may result in a blow-out fracture as
the floor of the orbit decompresses into the maxillary1.

Figure 1. Blunt trauma to the eye reault in a well recognised pattern of injury1

Blunt trauma of the Eye effect Retina, Choroid, and Optic Nerve
Retina
Commotio retinae describes graywhite opacification of the neuroretina after blunt
ocular trauma, which resolves over days to months. Visual loss (when the macula is affected)
may be transient or permanent. It has been induced using either a modified airgun or a
catapult in various species. A larger projectile gives a lower area-normalized impact energy,
which predicts injury better than total impact energy, explaining the high energy reported by
Hui et al2. Blunt injury may also cause part of the retina or the entire retina to tear or to
separate (detach) from its underlying surface at the back of the eyeball. Usually, only part of
the retina is detached (often the outside edge, or peripheral part, of the retina), but if
treatment does not occur soon, more of the retina can detach3.
Some studies used central corneal trauma, whereas others used lateral scleral injury.
Central corneal impact to enucleated pigs eyes reduces axial length by 40%, causing corneo
lenticular contact and leaving approximately 3.5 mm between the retina and posterior lens
surface. In a lateral scleral impact, the retina will contact the centrally positioned lens.
Despite this, ultrastructural findings are the same with both methods2.
Electron microscopy demonstrates traumatic disruption of the photoreceptor outer
segments, and intracellular edema of Muller cell processes and axons consistent with optical
coherence tomography findings in humans. The damaged outer segments are phagocytosed
by the RPE, which becomes multilayered2.
There is conflicting evidence about blood retinal barrier disruption from porcine,
feline, lapine, primate, and human studies. A normal fluorescein angiogram has been
reported, but indocyanine green angiography shows choroidal damage and horseradish
peroxidase and lanthanum detect leakage across the RPE( Regeneration of photoreceptor)
outer segments occurs from 1 week to 2 months2.
As for retinal detachment may create images of irregular dark floating shapes
(floaters) or flashes of light. Parts of vision may be blurred or lost, usually side (peripheral)
vision. If more of the retina detaches, more vision is blurred or lost3.
The diagnosis is made by an ophthalmologist, who examines the back of the eye with
a bright light (ophthalmoscopy) after the eye has been dilated. Sometimes an ultrasound
examination is done. An ophthalmologist can sometimes reattach a detached retina or prevent
the injury from worsening by using various treatments such as surgery, lasers, or freezing
therapy (cryopexy)3.

Choroid
Choroidal ruptures are breaks in the choroid, the Bruch membrane, and the retinal
pigment epithelium (RPE) that result from blunt ocular trauma (the most common eye
injury4.
Choroidal rupture can be secondary to indirect or direct trauma. Cases secondary to
direct trauma tend to be located more anteriorly and at the site of impact and parallel to the
ora, whereas those secondary to indirect trauma occur posteriorly. These ruptures have a
crescent shape and are concentric to the optic disc. Indirect choroidal ruptures are almost 4
times more common than direct ruptures. See the image below4.

A 23-year-old man was in a motor vehicle accident 2 months before his presentation. His
visual acuity is 20/400, and an afferent pupillary defect is present. Traumatic optic
neuropathy and choroidal rupture are observed. This is a red-free photograph. (Courtesy of

Jorge Gutierrez, MD.) 4.

Mid-phase fluorescein angiogram in a 23-year-old man whowas in a motor vehicle accident 2
months
before his presentation.Courtesy of Jorge Gutierrez, MD.)4.

Late-phase fluorescein angiogram in a 23-year-old who man was in a motor vehicle accident
2 months before his presentation. (Courtesy of Jorge Gutierrez, MD.)4.

Epidemiology
Blunt ocular trauma is the most common type of eye injury. Approximately 5-10% of
patients with such injury develop a choroidal rupture. Most eyes have a single rupture, but up
to 25% of eyes have multiple ruptures. About 80% of ruptures occur temporal to the disc, and
66% involve the macula4.
Mortality/Morbidity
Vision loss depends on whether the choroidal rupture involves the fovea and whether and
where CNV occurs4.
Sex
Men appear to be more prone to ocular trauma than women. A male-to-female ratio of 5:1 is
reported for choroidal ruptures4.
Symptoms

Retinal edema
Hemorrhagic detachment of the macula
Serous detachment of the macula
Subretinal haemorrhage
White curvilinear crescent-shaped streak concentric to the optic nerve

Pathogenesis
After blunt trauma, the ocular globe undergoes mechanical compression and then
sudden hyperextension. Because of its tensile strength, the sclera can resist this insult; the
retina is also protected because of its elasticity. The Bruch membrane does not have enough
elasticity or tensile strength; therefore, it breaks. Concurrently, the small capillaries in the
choriocapillaris are damaged, leading to subretinal or sub-RPE hemorrhage. Hemorrhage in
conjunction with retinal edema may obscure the choroidal rupture during the acute phases.
The deep choroidal vessels are usually spared. As the blood clears, a white, curvilinear,
crescent-shaped streak concentric to the optic nerve is seen. During the healing phase,
choroidal neovascularization (CNV) occurs. Vascular endothelial growth factor (VEGF) has
been shown to be a key molecular player in the pathogenesis of CNV. In most cases, it
involutes spontaneously. In 15-30% of patients, CNV may arise again and lead to a
hemorrhagic or serous macular detachment with concomitant visual loss. This usually occurs
during the first year but can also occur decades later. If the rupture does not involve the
fovea, good vision is expected. Older age and macular rupture, the length of the rupture, and
the distance of the rupture to the center of the fovea may be risk factors for CNV4.

Other Blunt Injuries to the Eyeball

Other injuries that can occur after a blunt force include bleeding in the back section of
the eye (vitreous hemorrhage), tearing of the iris, and displacement (dislocation) of the lens.
Usually, the force required to cause these injuries is high. Affected people tend to have
obvious, severe eye injuries with many abnormalities. All affected people have impaired
vision. Examination by an ophthalmologist and treatment should occur as soon as possible3.

Figure 2. Vitreous hemorrhage5.

Figure 3. Retinal hemorrhage6.

Optic Nerve
Traumatic optic neuropathy following blunt or penetrating injury occurs with an
incidence of 2% - 5% in facial trauma. The mechanism of the injury could be direct
mechanical compression of the optic nerve, this compression in combination with
compression of the central retinal artery and traction, or the compression effect on the small
nutrient vessels feeding the optic nerve. Compression forces transmitted to the orbital apex
cause a compartment syndrome whereby compression leads to a vicious cycle of swelling and
ischemia, release of free oxygen radicals, and damage to axons7.
Symptoms
Traumatic optic neuropathy causes vision loss in one eye that may worsen over
several days. Your ability to see color may be decreased and light may be dimmer in the
affected eye. You may notice that a part of your vision is missing. Depending on the type of
injury, you may also have pain, swelling, and double vision7.
Treatment
The treatment of traumatic optic neuropathy depends on the type of injury you have
had. If there is pressure on the nerve in the eye socket from blood, bone, or air, you may need
surgery to relieve the pressure. You may also need eyedrops to lower the eye pressure. You
may also be given steroid medicines through an IV. Your provider will explain which
treatments are best for you. The outcome of traumatic optic neuropathy depends on the type
of injury you have had and whether you have other injuries to the eye and/or brain. You may
regain good vision. Or, if your injuries are severe, you may have permanent changes in your
vision7.

Bibliography
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2. Lewis GP, Chapin EA, Luna G, Linberg KA, Fisher SK. The fate of Mullers glia
following experimental retinal detachment: nuclear migration, cell division, and
subretinal glial scar formation. Mol Vis 2010;16:13611372.
3. Can be accessed at:
http://www.merckmanuals.com/home/injuries_and_poisoning/injuries_to_the_eye/blu
nt_injuries_to_the_eye.html
4. Can be accessed at: http://emedicine.medscape.com/article/1190735-clinical
5. Can be accessed at: http://www.uniteforsight.org/eyesafety/image/blunttrauma3.jpg?
h=296&w=350
6. Can be accessed at:
http://www.kellogg.umich.edu/theeyeshaveit/acquired/images/child-abuse.jpg
7. Can be accessed at: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3194027/