REFERAT

BLUNT TRAUMA

Tutor :

Dr. Gilbert W.S. Simanjuntak SpM

Arranged by:

Indriyanti Natasya Ayu Utami Kotten (0961050038)

Virginia Cynthiara Maharani Aritonang (0961050039)

Friska Karolina (0961050041)

Andhika Djajadi (0961050043)

DEPARTMENT OF OPHTHALMOLOGIC

MEDICAL FACULTY

CHRISTIAN UNIVERSITY OF INDONESIA

JAKARTA

2013

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PREFACE

A. Anatomy and Physiology of the Eye

The eye is the organ that allows us to see. The eyeball itself is a sphere spanning approximately

24 mm in diameter. It is suspended in the bony socket by muscles controlling its movements, and

is partially cushioned by a thick layer of fatty tissue within the skull that protects it during

movement.

The eyes move symmetrically (in the same direction at the same time). These

symmetrical movements are made possible through the coordination of the extraocular

muscles (muscles outside the eye).

Since the eyes are paired structures, the brain receives two slightly different images that

overlap with one another. Interpretation of the different images is possible via coordinated eye

movements achieved by complex neural mechanisms. Humans are also able to perceive three-

dimensional images because they possess binocular vision, which enables the perception of

depth and distance.

The eyeball consists of three main components:

1. The tunics, which are three layers that make up the wall of the eyeball

2. The optical components, also known as the refractile media components, which

admit and focus light

3. The neural components, which consist of the retina and the optic nerve. The retina

is also part of the inner tunic

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Image 1. Anatomy of the eye (Courtesy of virtualmedicalcentre.com)

1. Layers (tunics) of the eye

The tunics of the eye consist of the following three layers:

a. Tunica fibrosa

Tunica fibrosa refers to the outer fibrous layer of the eye. This includes the sclera and the cornea,

which are continuous with one another.

- Sclera: The sclera is the white part of the eye, and covers most of the eye surface. It is

made up of a dense tissue which has a rich supply of blood vessels and nerves, and

provides attachment for the external muscles of the eye. The sclera tends to have a slight

blue tinge during childhood because of its thinness. It also can appear yellow in the

elderly due to the accumulation of a pigment associated with age-related wear and tear in

the tissue.

- Cornea: The cornea allows light to enter to the eye, and can be thought of as being part

of the modified sclera

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b. Tunica vasculosa

Tunica vasculosa refers to the middle vascular layer. This is also called the uvea. The uvea is

made up of the choroid, ciliary body, and iris.

- Ciliary body: The ciliary body forms a muscular ring around the lens. It secrets a fluid

called the aqueous humour, and supports the iris and lens. The ciliary muscle, which is a

smooth muscle responsible for lens accommodation, is contained within the ciliary body.

Contraction of the ciliary muscle enables the lens to focus light onto the retina by

changing its shape.

- Iris: The iris is an adjustable thin muscle controlling pupil diameter. It consists of two

layers - one that blocks stray light from reaching the retina, and another containing cells

called chromatophores which contain a substance called melanin. The concentrations of

melanin within these chromatophores give rise to eye colour. High concentrations of

melanin give the iris a black or brown colour. When there is scarce melanin, light reflects

from the epithelium of the posterior pigment, giving the iris a blue, green, or grey color.

c. Tunica interna

Tunica interna refers to the innermost layer. This layer is made up of the neural components - the

retina and optic nerve.

Image 2. Sclera (Courtesy of Wikipedia.org)

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Chambers of the eye

The three layers of the eye, along with the lens, act as boundaries for the three chambers within

the eye:

1. Anterior chamber: The space between the cornea and the iris.

2. Posterior chamber: The space between the iris and the lens.

3. Vitreous chamber: The space between the lens and the retina.

The eye can also be divided into its anterior (front) and posterior (back) segments. The former

consists of the cornea, as well as the anterior and posterior chambers and their contents. The

posterior segment contains the vitreous chamber, the visual retina, retinal pigment epithelium

(RPE), posterior sclera, and the uvea.

2. Optical components of the eye

The optical components are transparent elements that admit, bend, and focus light onto the cells

of the retina to form images. This occurs through the process of refraction, so the optical

components are also known as refractile media components. These components are:

a. The cornea: Acts as the main window of the eye. This is the major refractive element of

the eye.

b. Aqueous humour: Aqueous humour is a watery fluid in the anterior and posterior

chamber that is secreted by the ciliary body. Its role in refraction is relatively minor, but

it is important in providing nutrients to the lens and cornea, which do not have the means

to support themselves, and are the two critical refractile elements.

c. The lens: The lens is second most in importance to the cornea in the refraction of light

rays. It is elastic, so that the shape of the lens can undergo minor changes in response to

tension of the ciliary muscle. Tension on the muscle flattens the lens, whereas it relaxes

into a more spheroid shape when it is not under tension. These changes allow for

accommodation to allow proper focusing on near objects.

d. Vitreous body: The vitreous body contains a fluid component called the vitreous humour.

The vitreous body acts as a shock absorber that protects the retina during rapid eye

movements and helps to maintain the shape of the eye. In addition to refracting light, it

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also helps maintain the position of the lens and to keep the neural retina in contact with

the retinal pigment epithelium.

3. Neural components of the eye

As previously mentioned, the neural components of the eye are the retina and the optic nerve.

a. Retina

The retina is a cup-shaped outgrowth of the brain. It is a thin transparent membrane attached at

two points - the optic disc, where the optic nerve leaves the rear of the eye, and the ora serrata,

which is the junction between the retina and the ciliary body. It is smoothly pressed against the

rear of the eyeball due to pressure coming from the vitreous body.

A detached retina can result from blows to the head or inadequate pressure from the

vitreous body, and can cause blurry areas in the field of vision. Since the retina normally attaches

to and depends on the choroid for oxygen, nutrition and waste removal, prolonged detachment of

the retina from the choroid can lead to blindness.

b. Macula lutea

A patch of cells about 3mm in diameter can be found in the retina, known as the macula lutea. In

the centre of this patch is a small pit called the fovea centralis, which produces finely detailed

images.

The optic disc is found close to the macula lutea, and is the point on which nerve fibres

from all regions of the retina converge on. These nerve fibres then exit the eye to form the optic

nerve, so that the neural retina is continuous with the central nervous system through the optic

nerve.

c. Neural retina

The neural retina contains light-sensitive receptors and complex neural networks, and the retinal

pigment epithelium (RPE). It consists largely of photoreceptor cells called retinal rods and cones.

Visual information encoded by the rod and cones is sent to the brain via impulses conveyed

along the optic nerve.

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d. Pupil

The pupil, which looks black because of the heavily pigmented back of the eye; changes size to

control and regulate the amount of light passing through the lens to reach the retina.

Image 3. The eye (Courtesy of virtualmedicalcentre.com)

4. Accessory structures

- Conjunctiva: The conjunctiva refers to the lining of the eye. It helps lubricate the eye by

secreting mucous and tears, and serves as a protective barrier again microbes. It contains

many goblet cells which secrete a component of the tears that bathe the eye.

- Eyelid: The main function of the eyelid is to provide the eye with protection. The skin of

the eyelids is loose and elastic, allowing for movement. There are several types of glands

in the eyelids, including tarsal glands that produce a sebaceous secretion that results in an

oily surface of the tear film to prevent the evaporation of the normal tear layer.

- Eyelashes: Eyelashes are short stiff curved hairs that may occur in double or triple rows.

They function to protect the eye from debris. Lashes may also have different lengths and

diameters to one another.

- Lacrimal gland: The lacrimal glands are the sites of tear production. Tears function to

keep the conjunctiva and corneal epithelium moist, and wash away foreign material from

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the eye. The film of tears covering the corneal surface is a mixture of proteins, enzymes,

lipids, metabolites, electrolytes, and drugs (secreted during therapy).

- Extraocular muscles: Extraocular muscles (muscles outside the eye) allow the eye to

move within its orbit. Six of these eyeball muscles attach to each eye. The actions of

these muscles of both eyes are coordinated to enable the eyes to move in parallel, a

phenomenon known as conjugate gaze.

B. Blunt Eye Trauma

Even though the eyes have good protective systems such as orbital cavity, eyelids, and

retrobulbar fat tissue in addition to the blink reflex, the eyes still often gets traumatized from the

outside world. Trauma can result in damage to the eyeball and eyelid, optic nerve and orbital

cavity. Eye damage can interfere with the function of vision. Trauma to the eye can occur in the

following forms:

- Blunt trauma

- Penetrating trauma to the eyeball

- Chemical trauma

- Radiation injury

Blunt trauma can caused by hard or soft objects, where the objects can hit the eyes slowly or

quickly. In this writing, we will discuss about many kinds of blunt eye trauma.

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a. BLUNT TRAUMA OF THE CONJUNCTIVA

CHEMOSIS

Chemosis is the swelling (or edema) of the conjunctiva. It is due to exudation from abnormally permeable capillaries.

In general, chemosis is a nonspecific sign of eye irritation. The outer surface covering appears to have fluid in it. The conjunctiva becomes swollen and gelatinous in appearance.

Often, the eye area swells so much that the eyes become difficult or impossible to close fully. Sometimes, it may also appear as if the eye ball has moved slightly backwards from the white part of the eye due to the fluid filled in the Conjunctiva all over the eyes except the eye ball.

The eye ball is not covered by this fluid and so it appears to be moved slightly inwards. It is usually caused by allergies or viral infections, often inciting excessive eye rubbing.

Chemosis is also included in the Chandler Classification system of orbital infections. If chemosis has occurred due to excessive rubbing of the eye, the first aid to be given is a cold water wash for eyes and use of FluoroMetholone Ophthalmic Suspension USP, commonly known as FML which is an eye drop available in medical stores. Other cases of severe chemosis must be referred to a medical practitioner.

Image 4. Chemosis on the eye

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SUBCONJUNCTIVAL HEMORRHAGE

Subconjunctival hemorrhage is a bright red patch appearing in the white of the eye. This condition is also called red eye.

A subconjunctival hemorrhage occurs when a small blood vessel breaks open and bleeds near the surface of the white of the eye (bulbar conjunctiva). It may happen without injury, and is often first noticed when you wake up and look in a mirror. Sudden increases in pressure such as violent sneezing or coughing can cause a subconjunctival hemorrhage. The hemorrhage may also occur in persons with high blood pressure or who take blood thinners.

A subconjunctival hemorrhage is common in newborn infants. In this case, the condition is thought to be caused by the pressure changes across the infant's body during childbirth. A subconjunctival hemorrhage also known as hyposphagma, is bleeding underneath the conjunctiva. The conjunctiva contains many small, fragile blood vessels that are easily ruptured or broken. When this happens, blood leaks into the space between the conjunctiva and sclera.

Such a hemorrhage may be caused by a sudden or severe sneeze or cough, or due to hypertension or as a side effect of blood thinners. It may also be caused by heavy lifting, vomiting, or even rubbing one's eyes too roughly. In other cases, it may be due to, from being choked, or from straining due to constipation. Also, it can result as a minor post-operative complication in eye surgeries such as LASIK.

Whereas a bruise typically appears black or blue underneath the skin, a subconjunctival hemorrhage initially appears bright-red underneath the transparent conjunctiva. Later, the hemorrhage may spread and become green or yellow, like a bruise. Usually this disappears within 2 weeks.

Although its appearance may be alarming, in general a subconjunctival hemorrhage is a painless and harmless condition however, it may be associated with high blood pressure, trauma to the eye, or a base of skull fracture if there is no posterior border of the hemorrhage visible.

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Image 5. Subconjunctival hemorrhage

b. BLUNT TRAUMA OF THE CORNEA

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CORNEAL EDEMA

Fuchs Corneal Endothelial Dystrophy and Corneal Edema

Situated at the front of the eye, the cornea is the transparent dome overlying the colored iris of the eye. The cornea is composed of thin layers of tissue that allow light into the eye and focus the rays of light entering the eye. The cornea and the lens of the eye, a separate structure located just behind the iris, are responsible for creating a sharply focused image on the back of the eye so that we can see clearly. The cornea is responsible for roughly two-thirds of the focusing power of the eye, with the lens responsible for the remainder.

Clarity of the cornea is essential for sharp vision. Clarity of the cornea is largely dependent upon two factors: regular arrangement of protein fibers of the cornea, and the constant removal of fluid from the cornea. The endothelium of the cornea is a single layer of cells along the inner surface of the cornea that continuously pumps fluid from the cornea, keeping the cornea clear. When these cells are injured, they cannot regenerate, and fluid will accumulate in the cornea, resulting in swelling (edema) of the cornea and progressive clouding of vision.

Corneal edema can sometimes develop after eye surgery, especially after cataract surgery. Some terms for corneal edema after cataract surgery include “pseudophakic corneal edema”, “pseudophakic bullous keratopathy”, and “aphakic bullous keratopathy.” Also notable among the causes of corneal edema is Fuchs corneal endothelial dystrophy, sometimes also termed “Fuchs dystrophy”.

Abnormal swelling of the cornea is more likely to occur in people 50 years of age and older. Early symptoms of corneal edema might include blurred vision or haloes, often in the early morning. Very mild corneal edema may not require any treatment. In some cases, a physician may recommend use of a concentrated saline eye drops to draw fluid from the affected eye, thereby reducing the corneal swelling. Ultimately, if swelling of the cornea progresses to a level that a person’s vision is substantially impaired, a corneal surgeon can transplant either the entire cornea or just the abnormal endothelial (inner) layer of the cornea from an organ donor. Surgeons have performed cornea transplants for more than 100 years, and more than 40,000 are currently performed in the United States each year.

Corneal transplantation procedures vary slightly, depending on underlying eye diseases, presence of corneal scarring, or history of eye surgery. The procedures, when paired with glasses or contact lenses, can often restore vision to a significant degree. In contrast to cataract surgery, corneal transplant procedures tend to be performed for more significant impairment of vision, as corneal transplant procedures and their recovery are much more involved.

Corneal edema is the swelling of the cornea following ocular surgery, trauma, infection, inflammation as well as a secondary result of various ocular diseases. Corneal edema can also

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occur following over-wear of certain types of contact lenses.  The cornea is part of the eye's focusing system that transmits and focuses light into the eye. When the cornea swells, it may impair transmission of light possibly decreasing vision. Bausch + Lomb creates products for temporary daytime and nighttime relief from corneal edema.

A corneal erosion or abrasion can occur when the cornea is scraped or injured. In these cases, there may be a loss of the corneal epithelium, the cornea's outer layer. These painful conditions quite commonly arise after a poke from a baby's fingernail or tree limbs and bushes, or vigorous rubbing of the eye. Sometimes they are caused by contact lenses. Corneal disease can also be a contributing factor.

Detecting an erosion or abrasion requires the use of fluorescein dye, which highlights the injured tissue by causing it to fluoresce. Symptoms:

- Blurred vision

- Light sensitivity

The symptoms described above may not necessarily mean that you have a corneal erosion or abrasion. However, if you experience one or more of these symptoms, contact your eye doctor for a complete exam.

Corneal erosion affects the cornea, the clear dome covering the front of the eye. The cornea is composed of five layers. The outermost layer is the epithelium. When the epithelium does not stay attached correctly to the corneal tissue below, including the layer called the Bowman's layer or the basement membrane, this can cause a condition called corneal erosion. If the problem occurs repeatedly, it is called recurrent corneal erosion.

The most common symptom of corneal erosion is mild to severe pain. The pain may be particularly uncomfortable in the morning upon awakening because the eyes naturally get dry at night, and the eyelid can stick slightly to the epithelium. If the epithelium is not firmly attached, sometimes opening the lids can cause the epithelium to tear off. Without treatment, your eyes may continue to experience this erosion. Other symptoms include:

- Feeling of something in the eye

- Light sensitivity

- Blurred vision

- Watery eyes (particularly on awakening)

- Dryness.

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RECURRENT CORNEAL EROSION

Recurrent corneal erosion is a disorder of the eyes characterized by the failure of the cornea's outermost layer of epithelial cells to attach to the underlying basement membrane (Bowman's layer). The condition is excruciatingly painful because the loss of these cells results in the exposure of sensitive corneal nerves.

There is often a history of previous corneal injury (corneal abrasion or ulcer), but also may be due to corneal dystrophy or corneal disease. In other words, one may suffer from corneal erosions as a result of another disorder, such as map dot fingerprint disease.

Symptoms include recurring attacks of severe acute ocular pain, foreign-body sensation, photophobia, and tearing often at the time of awakening or during sleep when the eyelids are rubbed or opened. Signs of the condition include corneal abrasion or localized roughening of the corneal epithelium, sometimes with map-like lines, epithelial dots or microcyts, or fingerprint patterns. An epithelial defect may be present, usually in the inferior interpalpebral zone.

Recurrent corneal erosion (RCE) syndrome is a condition that is characterized by a disturbance at the level of the corneal epithelial basement membrane, resulting in defective adhesions and recurrent breakdowns of the epithelium.

RCE syndrome may occur secondary to corneal injury or spontaneously. In the latter case, some predisposing factor, such as diabetes or a corneal dystrophy, may be the underlying cause. Management of RCE syndrome is usually aimed at regenerating or repairing the epithelial basement membrane to restore the adhesion between the epithelium and the anterior stroma.

Corneal erosions are perhaps one of the most common and neglected ocular disorders. Some of these cases occur after ocular trauma, but most of them occur spontaneously. Painful RCE syndrome, whether due to trauma or to anterior basement membrane dystrophy (Cogan dystrophy or map-dot-fingerprint dystrophy), results from abnormalities in the epithelial basement membrane.

Recurrent corneal erosions and epithelial basement membrane dystrophy are usually bilateral and are characterized by various patterns of dots, parallel lines that mimic fingerprints, and patterns that resemble maps, which appear in the epithelium. Individual microcysts may be oval, oblong, or comma-shaped and rarely appear alone but usually are associated with map and fingerprint patterns. On the other hand, the map and fingerprint patterns appear without dots or individual microcysts.

Map and fingerprint alterations of the corneal epithelium are not rare and can be found in asymptomatic individuals without prior history of trauma or ocular disease. Literature suggests that these epithelial changes are more common than previously recognized. They frequently are

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seen in conditions involving corneal edema, such as near a healing cataract surgery incision, or in the center of the cornea associated with Fuchs corneal dystrophy.

Three stages of Fuchs endothelial dystrophy are recognized. The 3 stages usually evolve gradually over a period of 25 years, and, like other corneal dystrophies, they usually are bilateral but asymmetric.

The first stage is the onset of cornea guttata, usually in the fourth decade of life. Subjective symptoms rarely occur until the fifth or sixth decade. During the asymptomatic phase, endothelial guttata and pigment dusting can be seen by slit lamp examination of the central corneal endothelium and by specular reflection. The guttate excrescences can become more numerous and confluent so that individual guttata are lost completely in the beaten-metal appearance of the endothelial surface. The central cornea is involved first, and, as the disease progresses, it spreads toward the periphery.

In the second phase of the disease, blurred vision, glare, and halos around lights develop because of incipient corneal edema in the stroma and epithelium. Epithelial edema can be seen as small droplets (bedewing) on retroillumination with the slit lamp. Epithelial microcysts coalesce to form bullae, which produce varying amounts of pain when they burst; hence, the name bullous keratopathy. Striae form in the Descemet membrane as the cornea thickens posteriorly due to stromal swelling. The arc of the Descemet membrane from limbus to limbus is shortened, causing wrinkles in the Descemet membrane called striae. The microcystic epithelial vesicles may break, causing foreign body sensations and severe pain with more extensive corneal epithelial disruption.

In the third stage, recurrent corneal erosions, microbial ulceration, and persistent pain may occur. Corneal sensitivity usually is reduced.

Image 6. Corneal erosion

c. BLUNT TRAUMA OF THE UVEA

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HYPHEMA

Traumatic hyphema is encountered in children and adults. Hyphema is usually the result of a projectile or deliberate punch that hits the exposed portion of the eye despite the protection of the bony orbital rim. Various missiles and objects have been incriminated, including balls, rocks, projectile toys, air gun pellets, BB gun pellets, hockey pucks, bungee cords, paint balls, and the human fist. More recently, air gun pellets and BB gun pellets have been made of plastic polymers. There have even been cases involving objects larger than the orbit, such as soccer balls. Slow motion photography has demonstrated deformation of the soccer balls as impact occurs with the orbital rim, thereby causing the hyphema. With the increase of child abuse, fists and belts have started to play a prominent role. Males are involved in three fourths of cases.

Hyphema can also occur intraoperatively or postoperatively. Surgical hyphema is a known complication of intraocular surgery and should be managed in a similar manner as traumatic hyphema.

Rarely, spontaneous hyphemas may occur and be confused with traumatic hyphemas. Spontaneous hyphemas are secondary to neovascularization (eg, diabetes mellitus, ischemia, cicatrix formation), ocular neoplasms (eg, retinoblastoma), uveitis, and vascular anomalies (eg, juvenile xanthogranuloma). Vascular tufts that exist at the pupillary border have been implicated in spontaneous hyphemas.

The angular vessels first described by Arlt, as seen in Fuchs uveitis syndrome, produce a filiform angular hemorrhage and subsequent microhyphema when a diagnostic 30-gauge needle is placed through the limbus. This is known as Arlt’s sign.

Finally, an idiopathic hyphema may occur with spontaneous resolution and no known cause or recurrence. This is extremely rare.

The following clinical grading system for traumatic hyphemas is preferred:

Grade 1 - Layered blood occupying less than one third of the anterior chamber

Grade 2 - Blood filling one third to one half of the anterior chamber

Grade 3 - Layered blood filling one half to less than total of the anterior chamber

Grade 4 - Total clotted blood, often referred to as blackball or 8-ball hyphema

Most hyphemas fill less than one third of the anterior chamber. When hyphemas are divided into 4 groups according to the amount of filling of the anterior chamber, 58% involve less than one third of the anterior chamber, 20% involve one third to one half of the anterior chamber, 14% involve one half to less than total of the anterior chamber, and 8% are total hyphemas. Slightly fewer than one half of all hyphemas settle inferiorly to form a level; approximately 40% form a definite clot, usually adherent to the iris stroma; and 10% have a dark

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clot in contact with the endothelium. This last form may portend a poor outcome and corneal staining.

An alternative method of grading hyphemas involves measuring (in millimeters) the hyphema from the inferior 6-o'clock limbus. This method may help in monitoring the progress of resolution or the occurrence of rebleeding. Digital imaging analysis is also useful and objective but is available in only a few research or academic facilities.

The cause of an anterior chamber hemorrhage in contusion injuries is thought to be related to the posterior displacement of tissue or to the resultant fluid wave in the aqueous humor and the vitreous. This sudden dynamic shift stretches the limbal vessels and displaces the iris and the lens. This displacement may result in a tear at the iris or the ciliary body, usually at the angle structures. A tear at the anterior aspect of the ciliary body is the most common site of bleeding and occurs in about 71% of cases. The blood exits from the anterior chamber via the trabecular meshwork and the Schlemm canal or the juxtacanalicular tissue. The usual duration of an uncomplicated hyphema is 5-6 days. The mean duration of elevated intraocular pressure is 6 days.

Hyphema describes the condition of the aqueous humor when red blood cells form a suspension in it.

The choroid and the iris contain a rich complex of vessels. The pupil is outlined and controlled by a complex set of iridial muscles, sphincters, and dilators. These muscles can be ruptured by sharp and/or blunt trauma. This is a frequent source of intraocular hemorrhage (hyphema). In addition, the iris root and/or the ciliary spur is a common location of bleeding from blunt trauma.

Surgical intervention into the eye for anterior segment procedures is accomplished routinely through various approaches. The most commonly used approaches in modern small incision surgery are via the limbus and/or the clear cornea. Clear cornea surgery markedly reduces the risk of bleeding from limbal vessels since the cornea in its healthy state is avascular. Scleral tunnel incision is subject to unpredictable hemorrhage, and the incision must be closed carefully with sutures.

Hyphema can occur as a result of intraocular surgery, as follows:

Intraoperative bleeding - Ciliary body or iris injury seen during a peripheral iridectomy,

cataract extraction, cyclodialysis, and filtration procedure (laser peripheral iridectomy,

especially with YAG laser than with argon laser; argon laser trabeculoplasty [ALT] not very

common)

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Early postoperative bleeding (a traumatized uveal vessel that was in spasm and suddenly

dilates; conjunctival bleeding that makes its way into the anterior chamber via a corneoscleral

wound or sclerostomy)

Late postoperative bleeding (new vessels growing across the corneoscleral wound that bleed

when manipulated; a uveal wound that is reopened; an intraocular lens [IOL] that causes

chronic iris erosion)

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d. BLUNT TRAUMA OF THE LENS

TRAUMATIC CATARACT

Traumatic cataracts occurred secondary to blunt or penetrating ocular trauma. Infrared energy

(glass-blower's cataract), electric shock, and ionizing radiation are other rare causes of traumatic

cataracts.

Cataracts caused by blunt trauma classically form stellate- or rosette-shaped posterior

axial opacities that may be stable or progressive, whereas penetrating trauma with disruption of

the lens capsule forms cortical changes that may remain focal if small or may progress rapidly to

total cortical opacification.

Lens dislocation and subluxation are commonly found in conjunction with traumatic

cataract. Other associated complications include phacolytic, phacomorphic, pupillary block, and

angle-recession glaucoma; phacoanaphylactic uveitis; retinal detachment; choroidal rupture;

hyphema; retrobulbar hemorrhage; traumatic optic neuropathy; and globe rupture.

Traumatic cataract can present many medical and surgical challenges to the

ophthalmologist. Careful examination and a management plan can simplify these difficult cases

and provide the best possible outcome.

Blunt trauma is responsible for coup and contrecoup ocular injury. Coup is the

mechanism of direct impact. It is responsible for Vossius ring (imprinted iris pigment)

sometimes found on the anterior lens capsule following blunt injury. Contrecoup refers to distant

injury caused by shockwaves traveling along the line of concussion.

When the anterior surface of the eye is struck bluntly, there is a rapid anterior-posterior

shortening accompanied by equatorial expansion. This equatorial stretching can disrupt the lens

capsule, zonules, or both. Combination of coup, contrecoup, and equatorial expansion is

responsible for formation of traumatic cataract following blunt ocular injury.

Penetrating trauma that directly compromises the lens capsule leads to cortical

opacification at the site of injury. If the rent is sufficiently large, the entire lens rapidly opacifies,

but when small, cortical cataract can seal itself off and remain localized.

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INTRAOCULAR LENS DISLOCATION 

Cataract surgery is the most common operation performed by ophthalmologists. Although it has

a very high success rate, certain complications may occur. Intraocular lens (IOL) malpositions

range from simple IOL decentration to luxation into the posterior segment. Subluxated IOLs

involve such extreme decentration that the IOL optic covers only a small fraction of the pupillary

space. Luxation involves total dislocation of the IOL into the posterior segment. Decentration of

an IOL may be the result of the original surgical placement of the lens, or it may develop in the

postoperative period because of external (eg, trauma, eye rubbing) or internal forces (eg,

scarring, peripheral anterior synechiae [PAS], capsular contraction, size disparity). Posterior

dislocation of an intraocular lens (IOL) is an uncommon complication of cataract surgery and

Nd:YAG posterior capsulotomy.

IOL dislocation can be subdivided into early and late dislocation. Early dislocation refers

to dislocation occurring within 3 months of cataract surgery, whereas late dislocation occurs

more than 3 months after cataract extraction.

Posterior dislocation of an IOL may occur during or shortly after cataract surgery. In

these cases, posterior capsular rupture or zonular dialysis usually is present. It occurs because of

improper fixation within the capsular bag and instability of the IOL–capsular bag complex. The

implementation of a continuous curvilinear capsulorrhexis (CCC) during phacoemulsification

has decreased the rate of early IOL dislocation.  CCC gives support to the IOL optic for 360

degrees and permits excellent IOL fixation. Prior to CCC, most IOL dislocation occurred

secondary to asymmetric IOL fixation or IOL malposition within the capsular bag. Rarely, it may

occur following Nd:YAG capsulotomy or beyond the immediate postoperative period. Trauma

may be a precipitant in these cases.

Late IOL dislocation has been noted to occur more frequently than previously thought.

Late IOL dislocation results from zonular weakness since the IOL is adequately fixed within the

capsular bag. Several risk factors, including pseudoexfoliation syndrome, trauma, prior

vitreoretinal surgery, and connective tissue disorders, have been associated with zonular

weakness. In a retrospective case series of 86 late IOL dislocations, the IOL dislocated on

average 8.5 years after phacoemulsification and IOL implantation.[1] These same authors reported

that patients with any type of IOL were at risk for late in-the-bag IOL dislocation. A population-

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based study of patients by Pueringer et al found that after cataract extraction, the long-term risk

of late IOL dislocation was low and had no significant change over the almost 30-year study

period.[4]

The IOL rarely dislocates completely onto the retinal surface. It usually lies meshed into

the anterior vitreous with one haptic still adherent to the capsule or iris. It may cause a vitreous

hemorrhage by mechanical contact with ciliary body vessels. The IOL may be related to retinal

detachment or cystoid macular edema secondary to vitreous changes and may cause pupillary

block or corneal contact with secondary corneal edema. On many occasions, it does not cause

any complications and may be left alone if the patient is able to use aphakic spectacles or contact

lenses.

LENS LUXATION / SUBLUXATION

Originally known as “Ectopia Lentis”, the term may still be found in literature but lens luxation/subluxation is the most current usage.

Therefore, ectopia lentis means displacement or malposition of the eye’s lens from its

normal location. It is no longer centered. This condition usually applies to bilateral lens

displacement. When the lens is off center or partially dislocated, but still held within the lens

space, it is termed subluxated or subluxation. When the lens is completely dislocated out of its

normal position altogether, and no longer behind the iris, it is termed luxated or luxation.

The occurrence of/or sudden change in the appearance of the eye. In the event both eyes

are involved the appearance of luxation or subluxation may seem to occur more gradually in one

eye than the other. This is more likely to be seen in cases where the condition was due to

genetics.

Anterior Luxation

Pain

Tearing (excessive Porphyrin [rust-colored tears] in the rat)

Floating lens

20

Prolapse of lens

Abnormal pupil

If corneal involvement cloudiness in the eye may be seen

Posterior Luxation

May not be apparent initially

Pupillary abnormality (pupillary abnormality, a generic term, meaning an abnormality

due to either the iris sphincter or iris dilator muscles not functioning properly, or any

change in size or shape of the pupil)

Subluxation

Trembling (vibration) of the iris or lens

Mild redness of the conjunctiva

Eye may appear to be cloudy/ white

Change in pupillary shape or contour (Distortion of pupil shape and/or size with lens

movement)

Aphakic (“a” meaning absent, “phak” meaning lens) crescent (pupillary aperture appears

shaped like a crescent where the lens is no longer in place)

The lens, a focusing device of the eye located behind the iris, is held in place by zonular fibers that extend from the ciliary body to the lens equator, but is not within the ciliary body. It can be visualized through the pupil.

The vitreous body (a gelatinous substance) is behind the lens (between the lens and the retina), and gives the eye its shape. The suspensory ligaments composed of straight fibers called zonules keep the lens centered in its normal position.

A displacement of the lens can be due to either a primary or secondary condition. When

the fibers (zonules) that suspend the lens and hold it in place are weak due to a congenital defect,

the condition is said to be primary. When the fibers (zonules) become stretched, weakened, or

break due to disease or conditions such as inflammation, cataracts, glaucoma, cancer, or as a

result of trauma (e.g. injuries to the cornea or iris), the condition is said to be of a secondary

nature.

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Note: while lens dislocation can occur in only one eye, it is more common for primary lens

luxations to be bilateral, although they may not necessarily develop at the same time.

When luxation of the lens occurs, the lens floats freely in the eye. This can result in the

lens either drifting or being pushed into the anterior chamber of the eye (anterior luxation), or to

fall toward the back of the eye (posterior luxation).

With anterior lens luxation, conditions such as glaucoma and uveitis, as well as corneal

damage can develop. As the luxated lens rubs on the iris, poking through the pupil opening, it

can apply pressure to the cells that line the inner surface of the cornea, thereby damaging the

cornea. With uveitis, and inflammatory eye conditions, it can cause the pupil of the eye to

constrict. This results in the lens of the eye becoming trapped in the anterior chamber of the eye

which then leads to the obstruction of flow of aqueous humour and results in the development of

glaucoma (increased intraocular pressure).

When posterior lens luxation occurs there is less of an issue. The lens falls backward into

the vitreous humour lying flat so there is a lesser chance of the development of inflammation and

glaucoma, although glaucoma can occur.

In subluxation of the lens, there is only a partial displacement initially, just shifting the

lens slightly from its normal location. This can eventually cause prolapse of the vitreous humour

into the anterior chamber of the eye leading to glaucoma.

Lens luxation or subluxation can also be associated with other developmental eye

anomalies such as microphakia (an abnormally small lens), spherophakia (abnormally round

lens), and colobomas (equatorial lens defects).

Diagnostics:

- External examination of the eye.

- Use of ophthalmoscope to view eye surface, anterior chamber, vitreous, and retina

- Use of slit lamp to visualize

- Measurement of intraocular pressure.

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Lens surgery is challenging at best, even in larger animals. In very small animals, such as rats, surgical intervention of the type needed to do a repair may not be considered prudent or in the rat’s best interest. In humans as well, the condition depending upon severity, may just be closely observed, and medically rather than surgically managed. Rats can do well with observation and medical treatment for any secondary involvement arising from complete or partial lens displacement.

The treatment of lens luxation varies depending on the location of the lens, the presence

of secondary eye conditions, and any associated pain. The main goals of treatment include

reducing intraocular pressure (IOP) if possible, treating underlying causes, and surgical

enucleation where pain cannot be controlled.

Treatment may include the following:

Treating, and/or control of glaucoma by reducing intraocular pressure (IOP) with an

osmotic agent, topical miotic, topical or oral antiglaucoma medication, or a topical anti-

inflammatory agent, or may include a combination of medications.

Treating, and/or control of anterior uveitis. Treatment may include the use of topical

ophthalmic anti-inflammatory agents, or an oral anti-inflammatory agent along with a

topical ophthalmic or oral antibiotic.

Treating corneal abrasions with a topical ophthalmic antibiotic.

Enucleation of the eye may be necessary when pain is not able to be controlled.

Nursing Care

Monitor lens position if the lens is loose, but still in place.

If a primary lens luxation is diagnosed in one eye, the other eye must be closely

monitored for degeneration of the zonules and loosening of the lens.

INTRAOCULAR LENS DISLOCATION

A study by Tappin et al examined some of the intraoperative and postoperative factors

leading to IOL decentration in patients requiring IOL exchange in an attempt to identify

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avoidable causes of IOL decentration. They concluded that significant postoperative

subluxation of injected silicone IOLs may be minimized by implanting only into a lens

capsule bag with an intact capsulorrhexis. The risk of decentration of a small optic (5.5

mm) PMMA IOL may be minimized by positioning the haptics at 90° to any

capsulorrhexis tear. After cataract surgery complicated by posterior capsular rupture or

zonular dehiscence, it is important to assess the remaining capsular support and, if

sufficient, implant a large optic diameter (7 mm) PCL in the ciliary sulcus.

The anterior segment surgeon should be advised to avoid implantation of a flexible

silicone plate IOL if there is a break in the posterior capsule, radial notch, or tear in the

anterior capsular rim or zonular dialysis.

Small capsulorrhexis openings should be avoided.

Current models of ACIOLs often do not result in the same types of complications as

older models. These lenses should be considered if adequate capsular support is lacking

rather than risking a posterior dislocation of an IOL.

Selection of treatment in the case of a decentered IOL should be based on the patient's

symptoms, needs, and expectations.

Observation: In the absence of symptoms and no evidence of inflammatory sequelae,

observation is an option. In the case of an ACIOL associated with a peaked or oval pupil,

careful observation is warranted if there are no signs or symptoms of intraocular

inflammation.

Miotics: If symptoms from a decentered PCIOL are infrequent and limited to evening,

due to a dilated pupil, these patients may be treated conservatively by using a topical

miotic such as pilocarpine 0.5-1% qhs. A trial of miotic agents may be warranted prior to

removing or repositioning an implant.

Observation may be recommended in dislocated IOLs if the following conditions are met:

The IOL is not mobile.

There are no retinal complications.

The patient is satisfied with aphakic spectacle correction or contact lenses.

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When more severe and disabling symptoms or if inflammation is present with the

potential for further complications in the future, treatment should include either repositioning,

explanting, or exchanging the decentered IOL. Selection of treatment is based on the patient's

symptoms, visual needs, and expectations, and an assessment of which option is likely to provide

the best long-term benefit with the least risk.

IOL reposition: An IOL may become decentered due to either insufficient zonular

support or to irregular fibrosis of the posterior capsule. In the case of inadequate support,

early in the postoperative period the surgeon may attempt to rotate the IOL surgically

where there is clinical evidence of sufficient capsule and zonules to support the implant.

A helpful maneuver is the bounce test where the optic is pushed gently toward each

haptic to ensure spontaneous recentration.

IOL reposition with McCannel sutures: In some cases, repositioning may be

supplemented by the use of trans-iris IOL fixation (McCannel) suture.

IOL explantation: Certain circumstances warrant removal of an IOL without secondary

IOL implantation. This is determined on an individual basis and taking into account the

patient's expectation.

IOL exchange: The most common indications for removal or exchange of a modern PCL

are wrong IOL power and malposition. Deformation of the implant due to irregular

capsular fibrosis may make simple rotation insufficient to properly center the IOL. The

IOL may be exchanged for an ACIOL, a sulcus-fixated IOL with or without McCannel

sutures, or a transsclerally sutured PCIOL.

To determine whether the risk-to-benefit ratio favors IOL exchange over observation, the

surgeon should consider the following:

o Severity, duration, and chronology of the problem

o Response to nonsurgical treatment

o Natural history of a specific IOL

o Likelihood that surgical removal would provide substantial relief or benefits

o Ease of surgical removal and potential for aggravating or creating additional

complications

o Status of the other eye

25

o Patient and family expectations and visual needs

o Life expectancy and overall health of the patient

Several indications for surgical intervention exist for a dislocated IOL. If the patient is

not satisfied or cannot tolerate aphakic spectacle correction or contact lenses or if there is

concomitant retinal pathology, such as a retinal detachment, surgery must be considered.

Several surgical options are available. These options include removal, exchange, or

repositioning of the IOL. A multitude of techniques has been described on how to grasp, suture,

and place the IOL. Repositioning of the IOL into the ciliary sulcus or over capsular remnants

with less than a total of 6 clock hours of inferior capsular support is not a stable situation, as

many of those repositioned IOLs will end up dislocating again. Transscleral suturing or IOL

exchange (removal of the dislocated IOL and placement of a flexible open loop ACIOL) is

recommended in these cases.

In 1996, Kelman proposed a technique called posterior-assisted levitation, in which

nuclear fragments or dislocated IOLs into the anterior vitreous are retrieved through a

pars plana sclerotomy and the insertion of a cyclodialysis spatula, a needle, or a

viscosurgical device. However, this maneuver can be complicated with retinal

detachment or cystoid macular edema and should not be performed at all.

If transscleral suturing of the IOL is planned, modifications to the usual placement of the

sclerotomies are made. Two triangular scleral flaps are made 180 degrees apart in the

horizontal meridian. Then, two sclerotomies are made 1-1.5 mm posterior to the limbus

under the flaps. The infusion cannula is sutured to the usual position. A complete

vitrectomy is performed, paying close attention to removing all vitreous and capsular

attachments to the IOL, making it freely mobile. The posterior hyaloid, if still attached, is

peeled. This allows the IOL to gently fall over the posterior pole of the eye.

If the IOL does not have positioning holes, the edge of the IOL is elevated with a lighted

vitreoretinal pick or hook. If positioning holes are present, the IOL may be engaged

through them by the pick or hook. The IOL is elevated into the midvitreous cavity, and

the optic is grasped with serrated jaw foreign body forceps or diamond-coated forceps.

The haptics should not be grasped, or they will be bent.

26

Aspiration through the silicone soft tipped cannula also has been used in the retrieval and

manipulation of the IOL, but this technique may result in inadvertent vitreoretinal

traction.

Silicone plate lenses are difficult to manipulate, and, in certain cases, standard techniques

will not suffice. The endocryoprobe has been used to engage the IOL, but diamond-

coated forceps are much safer. It is recommended that the gas pressure be lowered to 525

psi to avoid freezing the entire shaft. Another problem is that transscleral suturing is not

an option because cheese wiring through the silicone will occur.

Liquid perfluorocarbons, such as Perflubron, can be used to float the IOL to the pupillary

plane.

Once the IOL is engaged and elevated, it is brought to the posterior chamber. One haptic

may be brought in front of the iris. The other haptic may be positioned in the sulcus.

Using a Sinskey hook either through a limbal stab incision or through the sclerotomy, the

IOL is rotated into place. If more than a total of 6 clock hours of capsular support are

present inferiorly, one may elect to reposition the IOL into the sulcus without suturing it.

If there is not enough capsular support, either transscleral sutures or iris sutures are

necessary. Several techniques have been described.

o If the IOL has positioning holes, the haptics are rotated until they are in the

vertical meridian. Single armed 9-0 Prolene sutures are grasped with intraocular

forceps and introduced through the sclerotomies. They are passed through the

positioning holes from posterior to anterior. The sutures are tied to the

sclerotomies under the scleral flaps.

o With the intraocular snare, one of the haptics may be looped, and, at the same

time, a 7-0 Prolene suture can be tied to it.

o Another option is to temporarily externalize the haptics through the sclerotomies

so that they can be tied with 10-0 Prolene sutures. This technique may cause

peripheral retina breaks or bleeding. The IOL is repositioned into the sulcus, and

the sutures are secured to the sclerotomy.

o Needle-guided techniques also have been described where a 9-0 or 10-0 Prolene

suture may be threaded retrograde up the bore of a five-eighths-inch 25-gauge

needle. The end of the suture that is not threaded is retrieved through the hub of

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the needle. This results in a suture loop. The needle with the suture is inserted

through the base of the scleral flap. As the IOL is being grasped by forceps, the

haptic is manipulated into the loop; then, the suture is tied under the scleral flaps.

Under certain situations, an IOL must be exchanged. For instance, if the dislocated IOL is

damaged (ie, broken haptic), it must be removed. The damaged IOL may be removed

through the pars plana or through a limbal incision at the surgeon's discretion. Pars plana

removal increases the risk of retinal detachment and severe choroidal bleeding.

o The surgeon has the choice of suturing a posterior IOL or inserting an ACIOL.

Modern flexible open loop ACIOLs do not appear to result in the complications

seen with older types (ie, corneal decompensation, uveitis-glaucoma-hyphema

syndrome).

o Another option is to manipulate the dislocated IOL into the anterior chamber and

leave it there. Potential drawbacks of this option are endothelial cell and

trabecular meshwork damage. This technique works well with 3-piece polymethyl

methacrylate (PMMA) IOLS but requires a peripheral iridectomy to prevent

pupillary block.

Perfluorocarbon liquids are very useful if a retinal detachment is also present. The

perfluorocarbon liquid bubble displaces the subretinal fluid through the retinal breaks

reattaching the retina and, at the same time, serves as a cushion between the IOL and the

retina. Thus, the retina is protected from potential damage from IOL impact during

surgical manipulation. If a silicone plate lens is dislocated, special care with the use of

perfluorocarbon liquids is necessary. It has been reported that these lenses often "skate or

glide" on the bubble across the retina. In addition, perfluorocarbon liquids make the

grasping of the IOL somewhat more difficult by making the IOL more slippery. If the

retina is not detached, the use of perfluorocarbon liquids probably is not necessary.

On certain cases, an ACIOL is present in addition to the dislocated IOL. Surgical

management of these cases is made more difficult by the presence of the ACIOL,

especially if a concomitant retinal detachment is present. The vitreoretinal surgeon has

several options.

o The surgeon may opt to remove the ACIOL, reposition the dislocated IOL, or

suture the dislocated IOL.

28

o Another option is to leave the ACIOL and remove the dislocated IOL. The

dislocated IOL may be removed via the pars plana or through a limbal incision. If

pars plana removal is entertained, a 7-mm partial-thickness scleral groove is

created 3 mm posterior and parallel to the superior limbus. This groove should be

contiguous with one of the superior sclerotomies. 8-0 silk sutures should be

preplaced through the lips of the scleral groove. Once the IOL is ready to be

extracted, the microvitreoretinal (MVR) blade is used to extend the sclerotomy

into the scleral groove to make it full thickness. After the IOL is removed, the

preplaced sutures are tied. This area is inspected by indirect ophthalmoscopy. If

needed, retinopexy is applied.

o If extraction through a limbal incision is planned, the ACIOL must be removed

first. Then, the dislocated IOL is brought to the anterior chamber and removed

through the limbal wound. The ACIOL is reinserted. The limbal wound is closed

with 10-0 nylon sutures. The sclerotomies are closed in the usual fashion.

Although dislocated foldable IOLs were traditionally treated with removal of the lens and

exchange to a PMMA IOL, one report demonstrates the feasibility of using existing

surgical techniques to reposition the dislocated foldable IOLs.

A vitreoretinal specialist should be consulted whenever this complication occurs, such as:

Complications from a decentered IOL

o Complications associated with ACIOL, iris-fixated IOLs, and older PCIOLs are

much more severe than those encountered with modern PCIOL decentration.

Corneal edema and inflammatory consequences such as uveitis-glaucoma-

hyphema syndrome and chronic CME were common reasons for explanation in

the above cases.

Complications from a dislocated IOL

o Vitreous hemorrhage

o Retinal detachment has been estimated to occur in at least 2% of cases. It

frequently is caused by attempts at relocation by the cataract surgeon or as a

complication of vitreoretinal surgery.

o Cystoid macular edema

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o Uncorrected aphakia, glare, or distortion

Complications from transscleral suture fixation

o Late endophthalmitis through the suture track has been reported.

o IOL torque may occur. In addition, to place the IOL truly in the sulcus, the suture

must be placed 0.8 mm posterior to the limbus in the vertical meridian and 0.46

mm in the horizontal meridian. The effective lens power is probably less than the

desired one.

o Vitreous hemorrhage may occur if the major arterial circle of the iris is pierced

inadvertently during the maneuvers required to suture the IOL. In addition, these

maneuvers also may raise the risk of a postoperative retinal detachment.

o Erosion of the suture through the conjunctiva also has been reported in cases

where scleral flaps were used. An attempt to melt the eroded sutures with the

argon laser has been recommended. The sutures cannot be removed because the

IOL haptics do not scar into place if placed in the ciliary sulcus. Once the sutures

are removed, the IOL will redislocate.

With proper vitreoretinal techniques, excellent visual results and a low complication rate

is possible. Long-term prognosis is highly dependent on the prevention of retinal detachment and

choroidal hemorrhage secondary to surgical manipulation.

30

e. BLUNT TRAUMA OF THE RETINA

Commotio retinae describes gray–white 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 al. 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 detach.

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 methods.

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 multilayered.

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 months.

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 lost.

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).

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f. BLUNT TRAUMA OF THE 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.

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 macula.

Vision loss depends on whether the choroidal rupture involves the fovea and whether and where CNV occurs.

Men appear to be more prone to ocular trauma than women. A male-to-female ratio of 5:1 is reported for choroidal ruptures.

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

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

32

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 CNV.

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 possible.

Image 7. Vitreous hemorrhage.

Image 8. Retinal hemorrhage.

33

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 axons.

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 vision.

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 vision.

34

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