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State of Illinois Trauma Nurse Specialist Program


Connie J. Mattera, M.S., R.N., TNS

Time allotment: 1 hour


Upon completion the participant will

1. identify the anatomical structures of the eye and describe the corresponding physiological functions.

2. explain the assessment maneuvers for evaluating the eye and adnexal areas.

3. describe and define cardinal signs and symptoms of ocular injury.

4. interpret assessment findings to formulate nursing diagnoses.

5. establish a nursing care plan based on the nursing diagnoses.

6. describe the correct method for removing contact lenses, irrigating eyes, applying eye shields or pressure patches.

7. discuss the etiology, pathophysiology, clinical presentation assessment findings, emergency management, and possible complications for specific ocular injuries including orbital fractures, lid lacerations, chemical and thermal burns, UV exposure, corneal/conjunctival foreign bodies, corneal abrasion/laceration, subconjunctival hemorrhage, globe penetration/perforation, hyphema, lens dislocation/subluxation, retinal detachment, optic nerve injury and enucleation.

CJM: 1/09

State of Illinois Trauma Nurse Specialist Program


Connie J. Mattera, M.S., R.N.

I. Incidence of ocular trauma

A. Approximately 1.2-2.5 million people suffer eye injuries each year in the U.S. of which 500,000 are serious (Broocker, Parke & Hamill, 1996; Mieler, 2001)). About 43% occur in the home (U.S. Eye Injury Registry).

B. Over 40,000 are associated with some visual loss and 25,000 result in total blindness (Shingleton, 1998).

C. Ocular trauma is the leading cause of visual loss in persons less than 25 years of age and the leading cause for eye-related hospital admissions.

D. The leading causes of eye injuries include household chemicals, workshop and yard debris, battery acid, sports accidents, consumer fireworks, over-exposure to UV radiation, and inappropriate toys and games used without supervision (Am Academy of Ophthalmology, 2002).

E. An estimated 40,000 sports-related eye injuries occur each year. About 90% are preventable by using appropriate sports-specific eyewear.

F. Workplace and MVC ocular injury rates have reduced significantly due to application of general safety measures, more effective safety glasses, mandatory seat belt legislation and use of airbags.

G. Specific ocular surveillance systems include the National Eye Trauma System (NETS) and the United States Eye Injury Registry (USEIR).

II. Immediate goals in ocular injuries

A. Protection of the intact portions of the visual system and avoidance of further injury to undamaged structures. A total loss of vision in one eye equals a 25% impairment of Visual System and a 24% impairment of Whole Man (Work Eye Injury Registry, 2002).

B. Accurate assessment of the extent of injury and referral of the patient for immediate repair of injured tissues to prevent further damage.

C. Institution of therapeutic measures that first achieve optimal function and secondarily achieve optimal cosmetic results.

III. Anatomy and physiology of the eye

The function of the eye depends on an exact maintenance of anatomical relationships between the eyelids, cornea, anterior chamber, lens, retina, extraocular muscles, and nerves. Permanent deficit in any of these components may result in altered visual function and potentially, loss of the eye.

A. The eye is composed of 3 types of tissues:

1. Surface ectoderm: Includes conjunctiva, lens, corneal epithelium, eyelid skin. Has the ability to regenerate.

2. Mesoderm: Includes bony orbit, extraocular muscles, sclera, corneal stroma, ocular and periocular connective tissues, blood vessels, and internal eyelid structures. Has some regenerating ability, depending on the extent of injury.

3. Neuroectoderm: Includes optic nerve, retina, portions of the iris and ciliary bodies and all central nervous system components. These all need continuous oxygen supply to survive and cannot regenerate.

B. Periocular and orbital structures (ocular adnexa)

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Damage to these bones can cause globe injury. Since the globe and orbit are in close approximation to many other important non- ocular structures, serious ocular injury is often seen in the context of serious non- ocular injury.

2. Eyelids or palpebrae: Continuation of the facial skin and serve as protective coverings to the eyes, distribute tear film evenly to lubricate the cornea and aid in the removal of excess tears and tear film debris. Eyelids close tightly to protect the eye. Both are lined with conjunctiva.

tightly to protect the eye. Both are lined with conjunctiva. a. Orbital portion b. Tarsal portion:

a. Orbital portion

b. Tarsal portion: dense, fibrous, connective tissue measuring 10 mm vertically in the upper eyelid and approx. 3.6 mm in the lower lid. The tarsus is the structural support for the lid.

c. Fornices: superior and inferior

support for the lid. c. Fornices: superior and inferior 3. Medial and lateral canthus (corners of

3. Medial and lateral canthus (corners of the eye): Points of attachment for upper and lower eyelids.

the eye): Points of attachment for upper and lower eyelids. 4. Eyelashes : Strong hairs that

4. Eyelashes: Strong hairs that help prevent foreign particles from reaching the surface of the eye.

5. Conjunctiva: Thin, vascular mucous membrane that lines the posterior surface of the eyelids and covers the anterior surface of the sclera. Contains many free nerve endings and is very

of the sclera. Contains many free nerve endings and is very sensitive. a. Bulbar: Outer surface


a. Bulbar: Outer surface of sclera – white

b. Palpebral: Lines inner surface of lids - reddish in color

6. Glands/drainage systems

a. Lacrimal gland: Located within a depression in the frontal bone, just inside the orbit and superior and lateral to the eyeball, the lacrimal gland has a dozen or more ducts that empty into the pocket between the eyelid and the eye. It continuously secretes tears, distributed across the eye through blinking, that reduce friction, remove debris, prevent bacterial infection, and provide nutrients and oxygen to the conjunctival epithelium (Martini, Bartholomew, & Bledsoe, 2002). Tears are watery, slightly alkaline, and contain lysozyme, an enzyme that attacks bacteria. Blinking the eye sweeps the tears to the medial canthus.

b. Puncta: Orifices leading to the lacrimal drainage system in the upper and lower eyelids located about 5 mm from the medial canthus.

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d. Sebaceous glands: Associated with the eyelashes as with other hair follicles. Secrete a lipid-rich substance that keeps lids from sticking together.

e. Lacrimal caruncle: Soft mass of tissue located at the medial canthus containing glands that produce thick secretions that contribute to the gritty deposits sometimes found after a night's sleep.

C. Extrinsic eye (oculomotor) muscles: Originate on the surface of the orbit and control the position of the eye.

1. Medial rectus:

Eye rotates toward the nose


2. Inferior rectus:

Eye looks downward


3. Inferior oblique:

Eye looks upward and to the side


4. Superior rectus:

Eye looks upward


5. Superior oblique:

Eye looks down and to the side


6. Lateral rectus:

Eye rotates laterally away from nose


rectus: Eye rotates laterally away from nose CN VI D. Eyeball (Globe) 1. Each eye is

D. Eyeball (Globe)

1. Each eye is roughly spherical with a diameter of about 2.5 cm (1 inch). The length from the apex of the cornea to the point at which the optic nerve exits the sclera is approximately 24.5 mm. The globe weighs 7.5-8.0 g and has a volume of 6.5 ml. It occupies 1/5th of the orbital volume. It shares space with the extrinsic eye muscles, the lacrimal gland, the various cranial nerves and blood vessels that service the eye and adjacent areas of the orbit and face, and orbital fat that provides padding and insulation (Martini, Bartholomew, & Bledsoe, 2002).

of the orbit and face, and orbital fat that provides padding and insulation (Martini, Bartholomew, &

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2. Wall of the eye has three distinct layers or tunics

a. Outer fibrous tunic: Outermost layer covering the eye; composed of the sclera and cornea


Provides mechanical support and some physical protection


Serves as an attachment site for extrinsic eye muscles


Assists in the focusing process

b. Intermediate vascular tunic: Contains numerous blood vessels, lymphatics, and all of the intrinsic eye muscles, iris, ciliary body, and the choroid.

c. Inner neural tunic or retina

3. Fibrous tunic structures

a. Sclera






b. Cornea





Dense, fibrous connective tissue that contains both collagen and elastic fibers. It forms the outer layer of the globe, and is composed of epithelial cells.

Thickest over the posterior and thinnest over the anterior surface

Extrinsic eye muscles insert on its surface

Its posterior surface contains nerves and small blood vessels that penetrate to reach internal structures. On the anterior surface, these vessels lie under the conjunctiva. Because the capillary network carries so little blood, there is no obvious color, so the white of the collagen fibers is visible (thus forming the white of the eye).


(a) Protect the internal ocular structures

(b) Act as the structural skeleton of the globe


concave dome continuous with the sclera that covers the iris (11.5 - 12.5 mm across).

It ranges in thickness from 0.7

mm peripherally to 0.5 mm


Collagen fibers are organized

into a series of layers that

permit the transmission of light through the cornea, pupil and lens to the retina. It is covered by a thin layer of epithelium overlying a basement membrane (Bowman's membrane).

Innervated by the sensory limb of CN V (trigeminal nerve). Because the cornea is so richly innervated beneath the corneal epithelium, the pain of corneal injury is often greater than that of iritis or conjunctivitis. Topical anesthesia freely penetrates the cornea, but not the inner aspect of the eye. Therefore it has little effect on pain caused by deeper problems.


little effect on pain caused by deeper problems. avascular, c. Limbus : Circular margin where the

c. Limbus: Circular margin where the conjunctiva meets the cornea

4. Vascular tunic includes the iris, ciliary body, and the choroid, also referred to as the uvea. It contains numerous blood vessels, lymphatics, and all of the intrinsic eye





Provides a route for blood vessels and lymphatics that supply tissues


of the eye Regulates the amount of light entering the eye

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Secretes and reabsorbs aqueous humor that circulates within the eye


Controls the shape of the lens (Martini et al, 2002)

b. Iris: Circular, contractile muscular disc that is an extension of the ciliary body that is located anterior to the lens. It contains pigment cells that produce the color of the eye and two layers of smooth muscle. The iris controls the amount of light reaching the retina by dilating and constricting its muscles to change pupillary size in response to impulses mediated by CNs II & III. When there are no pigment cells in the iris, light passes through it and bounces off its inner surface of pigmented epithelium. The eye then appears blue. In order, persons with gray, brown, or black eyes have increasing numbers of pigment cells in the body and surface of the iris (Martini, Bartholomew, & Bledsoe, 2002).

c. Pupil: Typically is a round central opening in the iris


Parasympathetic stimulation: Rapid reflex constriction of the pupil in response to bright light.


Sympathetic stimulation: Slower pupillary dilation in response to a reduction in light levels

dilation in response to a reduction in light levels d. Ciliary body : Along its outer

d. Ciliary body: Along its outer edge, the iris attaches to the anterior portion of the ciliary body which is composed primarily of a ring of ciliary muscle that projects into the interior of the eye. It begins at the junction between the cornea and sclera and extends to the anterior edge of the retina. Posterior to the iris, the suspensory ligaments of the lens attach to folds called the ciliary processes. These fibers position the lens so light passing through the pupil goes through the center of the lens. Responsible for producing aqueous humor and for changing the shape of the lens.

aqueous humor and for changing the shape of the lens. e. Lens : Disc-shaped structure approximately

e. Lens: Disc-shaped structure approximately 9 mm in diameter and 4 mm thick, containing transparent crystalline matter, suspended immediately behind the iris and anterior to the vitreous by suspensory ligaments that connect it to the wedge-shaped ciliary body. The lens is highly elastic and contraction or relaxation of the ciliary body changes its thickness and shape, thereby permitting images from varied distances to be focused on the retina.

Its shape changes for near and far vision, becoming flatter for far vision. The ability to change shape deteriorates with age explaining need for reading glasses after 40

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State of Illinois TNS Program Ocular Trauma page 6 f. Choroid: Layer of vascular channels that

f. Choroid: Layer of vascular channels that separates the fibrous and neural tunics posterior to the ciliary body. This layer delivers oxygen and nutrients to the retina.

5. Neural tunic or retina: Consists of a thin outer pigment layer and a thick inner layer of neural retina. The pigment layer absorbs light after it passes through the receptor layer. The neural retina contains photoreceptors that respond to light, supporting cells and neurons that perform preliminary processing and integration of visual information, and blood vessels supplying tissues that line the posterior cavity. The sensory network transforms light impulses into electrical impulses via rods and cones. Rods do not discriminate among colors. They enable us to see in poor lighting conditions. Cones provide color vision. They give sharper, clearer images but require more intense light.

a. Macula lutea (or yellow spot): Avascular region where the visual image arrives after passing through the cornea and lens. The area of greatest concentration of cones is located in the central portion, called the fovea (shallow depression). All color and sharpest vision better than 20:200 is located here.

b. Optic disc: A circular region just medial to the fovea. It measures 1.5 mm across and becomes the origin of the optic nerve, which is formed from the convergence of axons from 1 million retinal ganglion cells. The central depression or cup usually averages 1/3 of the disc diameter. Blood vessels that supply the retina (central retinal artery and vein) pass through the center of the optic nerve and emerge on the surface of the optic disc (Martini, Bartholomew, & Bledsoe, 2002). The disc has no photoreceptors or other retinal structures. Light striking this area is not perceived, so it is commonly called the blind spot.

c. Optic nerve - Sensory impulses are transmitted through the optic nerve (CN II) to the occipital lobe for conscious interpretation. Injury to the optic nerve and retina are most responsible for permanent visual loss in cases of trauma.

responsible for permanent visual loss in cases of trauma. 6. Chambers of the eye: The eye

6. Chambers of the eye: The eye is hollow. The ciliary body and lens divide the interior into two cavities:

a. Anterior cavity

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Divided into two chambers


Anterior chamber: Extends from the cornea to the iris


Posterior chamber: Extends from the iris to the ciliary body and lens.


Contents: Filled with aqueous humor produced by the ciliary processes and secreted into the posterior chamber. The fluid circulates within the anterior cavity, passing from the posterior to the anterior chamber through the pupil. It leaves the anterior chamber near the edge of the iris through the canal of Schlemm that returns the fluid to the venous system. The anterior cavity holds about 125 microliters of fluid. Interference with secretion, circulation, or absorption can change the pressure within the eye. Glaucoma is caused by an elevation in ocular pressure and can produce blindness by distorting the retina and the optic disc.

b. Posterior cavity or vitreous chamber contains the gelatinous vitreous body. Helps to maintain the shape of the eye and holds the retina against the choroid.

7. Vascular supply

a. Arterial: The ophthalmic (central retinal) artery is the main vessel that supplies blood to the globe and orbit and is the first branch off of the internal carotid after it enters the cranial cavity. Emboli from the internal carotid artery can enter the ophthalmic artery, producing visual problems. Facial and maxillary arteries feed the lower lid, medial canthus and inferior orbit.

b. Venous: Blood returns through the inferior and superior ophthalmic veins. Venous draining through the cavernous sinus is an important route for the intracranial spread of infection. There are no lymphatics in the orbit, but the eye lid has a rich lymphatic system.

IV. Assessment and management of ocular trauma

Many patients presenting with ocular trauma have other associated trauma to the head and neck with facial and skull injuries that may delay recognition of ocular damage. While understandable, an early consult with ophthalmology is desirable (Broocker et al, 1996).

A. Chief complaint/history of present illness: Because the nature of eye emergencies ranges from minor to severe, history taking may be done simultaneously with the eye exam. Whenever time permits, obtaining an accurate, detailed history can aid in the rapid treatment and evaluation of the patient. Important details to include:

1. Nature of complaint: traumatic vs. non-traumatic

a. Non-traumatic: Divided into c/o of vision, appearance or sensation

b. Traumatic: Mechanism of injury - blunt, penetrating, or explosive; thermal, UV, chemical materials involved. If chemical exposure was involved ask if it was toxic, acid or alkali.

2. HPI - Detailed description of chief complaint: Obtain OPQRST details about onset, provocation (what object or item caused the injury - magnetic?)/ palliation, quality, region/recurrence, severity, and date and time of injury.

a. Visual changes from baseline: Blurred, double, or deficits in acuity or visual fields

b. Is one or are both eyes affected?

c. Diplopia (double vision)


Diplopia may indicate trauma to the globe with muscle entrapment or nerve deficit, peripheral or central (Cuculino & DiMarco, 2002)


Monocular diplopia usually indicates a refractive error in the eye itself


Binocular diplopia, present only when both eyes are open, is the result of a deficiency in the movement of the eye

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d. Redness

e. Tearing, drainage

f. Pain

g. Note associated complaints/symptoms other than decreased vision

B. SAMPLE History

1. Allergies

2. Medications: Regular use of eye medications or over-the-counter remedies. Use of anticoagulants or aspirin. Include licit and illicit drug use, as they can affect pupillary size and reactivity.

3. Past ocular history

a. Any ocular or visual problems - past or present change in, or loss of, vision; ocular pain


Blurred vision that does not improve with blinking




Sectorial visual loss


Spots before eyes, curtain over the visual field?


Halos or rings around lights



b. Baseline visual acuity; ever worn glasses or contact lenses? How long? If contacts are worn: hard, soft, extended wear? For reading, driving, distance?

c. Eye injury or surgery? When?

d. Excessive tearing, crusting, discharge?

e. Burning (inflammation)

f. Relevant occupational hazards; dust, chemicals, metalwork


Use of protective devices


Use of safety glasses, if traumatic injury

4. Past medical history in self or family

a. Heart disease, hypertension

b. Diabetes

c. Sickle cell disease

d. Liver disease

e. Vascular disorders

f. Cataracts, glaucoma

5. Last oral intake; tetanus

6. Events surrounding the incident: Details regarding probable size, velocity, and

chemical constituency of pellets or projectiles; determine treatment rendered prior to


C. Physical exam

1. The physician may require the following for an adequate exam:

a. Near vision card, pinhole occluder (for vision < 20/30), loose +2.75 sphere spectacle lens for the presbyopic patient; occluder for assessing each eye separately.

b. Penlight with cobalt blue filter

c. Schiotz tonometer, tonopen

d. Ophthalmoscope

e. Topical anesthetic: Research by a group of New Mexico physicians suggests that a patient's response to local anesthesia may predict the complexity of a corneal lesion. Those that receive significant pain relief probably have an uncomplicated corneal lesion.

Patients with a diagnosis of conjunctivitis, iritis, corneal ulcer, hyphema, glaucoma, or subconjunctival hemorrhage typically had less pain initially and got little relief from proparacaine (Sklar et al, 1990).

f. Lid retractor or bent paper clip retractors

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g. Sodium fluorescein test strips to evaluate corneal epithelial loss

h. Short-acting dilating (mydriatic) drops; use with caution in patients with concomitant intracranial injury

i. Slit lamp: Aids in the evaluation of the conjunctiva, cornea, anterior chamber, iris, lens and anterior vitreous cavity. It can detect the presence of blood in the anterior chamber, inflammatory cells, and pus.

2. Remove and store contact lenses: Lenses should usually be removed as part of trauma assessment/management

a. Hard contact lenses: Remove with suction cup lens remover. Place in 0.9% NS and label containers left and right.

b. Soft contact lenses: Easily removed by pinching the lens together and pulling away from the eye. Place immediately in 0.9% NS and label containers left and right.

3. External structures - Inspect/palpate

Order: top to bottom; outside to inside (cornea to fundus); medial to lateral (inner canthus to outer canthus)

a. Orbit and periorbital structures: Often, one needs only to visually inspect the patient's face to suspect injury. However, bony palpation of the orbital rim can detect point tenderness, deformity or crepitus. Orbital rim should be smooth, without deformities or irregularities. Insect/palpate for the following:


Deformity, contusion, abrasion, punctures, laceration


Ecchymoses, bleeding, hemorrhage, hematoma, F/B


Periorbital edema, masses, asymmetry or missing tissue


Tenderness, instability, crepitus: may indicate a sinus fracture


Also examine for paresthesias possibly indicating injury to an infraorbital sensory nerve

b. Eyebrow size and extension

c. Lids: examine closed and open


Inspect integrity of the structure, symmetry; ecchymoses


Lacerations/lesions: Document whether the laceration involves the lid margins or loss of tissue. Lacerations to the medial 1/3 pose a risk for disrupting the lacrimal apparatus and require plastic surgery or ophthalmology for closure (Cuculino & DiMarco, 2002). While serious themselves, can also be associated with penetrating trauma to the globe. Look for prolapse of orbital fat.


Edema, inflammation


Ability to spontaneously lift and close lid to cover the superior limbus of the iris by 1 mm - 3 mm. Note the following:


Ptosis: If the lid cannot lift up and covers more of the iris than the other side or extends over the iris, suspect a congenital or acquired weakness of the levator (plus Muller's) muscle or paresis of the third cranial nerve.


If the lid cannot close, suspect dysfunction of CN VII which innervates the orbicularis muscle.


Surface growths/internal masses; never palpate an injured eye

d. Lashes, sebaceous glands, and drainage system


Presence or absence of discharge or matting


Scaling or lesions


Hair loss


Pus, blood, CSF from puncta

e. Position of globe within the orbit and in comparison with the ocular structures on the opposite side

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Proptosis or exophthalmos: Bulging or protrusion of the eye


Enophthalmos: Backward displacement of the eyeball causing it to recede within the orbit


Pupils should be on same horizontal plane. If one eye is lower than the other suspect orbital floor fracture. Eyes should be in line with top of ear. Is gaze focused on you?

4. Anterior segment: This examination includes the conjunctiva, cornea, anterior chamber, iris and lens and is done by the physician using a slit lamp or penlight with blue filter. The slit lamp allows for magnification of these structures to provide improved detail and visualization.

a. Conjunctiva: Penlight or light from ophthalmoscope is acceptable if no slit lamp is available. Evert eyelids to fully assess if necessary.

Inspect for







degree and depth of redness/injection; foreign body, embedded material, laceration; chemosis or hemorrhage; rust ring; black or brown defect (choroid prolapse); and pus.

b. Sclera




syndrome), injected.

Wounds, hemorrhage, ocular Battle sign?








c. Cornea: Should be smooth, round, clear, glistening and free of lesions. To assess for a corneal defect, instill sodium fluorescein. Wet the tip of a fluorescein strip with a commercial irrigating solution, touch to the conjunctiva in the inferior cul-de-sac. Blinking will disperse the fluorescein in the preocular tear film. Fluorescein adheres to and stains any exposed portion of the corneal basement membrane denuded of epithelium. Excess dye can be removed with an irrigating solution to provide contrast between the lesion and surrounding areas. Physicians will view under a cobalt blue light to inspect for:


foreign body;


clouding/opacity; could indicate acute glaucoma, edema from trauma, foreign body in the anterior chamber, or infection;


abnormal pigment;


irregular light reflection if irregular in size or shape;


abrasion/laceration: defects will appear bright green;


positive Seidel test: Positive if the fluorescein appears to be streaming away from the cornea, forming a pool in the cul-de-sac. The streaming is caused by the aqueous humor as it flows out of the defect (Cuculino & DiMarco, 2002). Indicates an open globe injury.


Anterior chamber: Should be clear and deep with the iris well separated from the posterior corneal surface. The depth of the anterior chamber is important to note, especially prior to instilling dilating drops (Cuculino & DiMarco, 2002). Shine a penlight across the cornea from the lateral to medial direction. With normal depth, the light will shine evenly across the iris. A shallow chamber will show a shadow on the medial aspect of the iris caused by the iris as it bulges outward into the anterior chamber. Patients with a shallow anterior chamber may be at risk for acute angle closure glaucoma if dilated. It may also indicate a globe rupture with loss of aqueous humor. If blood (hyphema) or white cells (hypopyon) are present, serious injury has occurred.

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d. Intraocular pressure: This should always be measured by a physician when there is suspicion of hyphema, or any other condition that would affect the intraocular pressure (IOP). It should be deferred if a penetrating globe injury is suspected (Cuculino & DiMarco, 2002). Normal IOP ranges from 8 to 21 mmHg (Varma, 1997). Low intraocular pressures may be found with inflammatory conditions (except iritis which may elevate pressures) and globe rupture. Instruments used to measure IOP are the Goldmann Application tonometer (attached to the slit lamp), the Schiotz tonometer, and the Tonopen. IOP can also be measured using puff bursts of air blown against the cornea. Two readings are obtained using this process.


Instill topical anesthetic in each eye if a sensor is placed on the cornea. If puffs of air are used, no anesthetic is necessary.


Have patient look forward with eyes open in a dimly lit room. If AMS, hold eyelids open, supporting upper lid against superior rim and the lower lid against inferior rim of the orbit. Do not push on eyeball!


The Tonopen is an automated, hand-held machine. After calibration, tap the covered tip gently against the anesthetized eye with the patient in a supine position. An average of three readings is taken.




Place 5.5 G wt on tonometer


Have pt. look up and rest foot-plate of the tonometer on the central portion of the cornea. Read the scale.


If the reading is less than 5 apply the 7.5 wt on top of the 5 G wt. Continue to add weights until the scale reads between 5 and 20.


The scale value is translated into an intraocular pressure using a special table. Normal pressure is 21. Dangerously high pressures are > 30 mmHg and indicate angle closure glaucoma, pupillary block glaucoma or a retrobulbar hemorrhage. This is an emergency and requires immediate treatment by an ophthalmologist.


Goldmann: Instill a drop of fluorescein, and at the slit lamp, a tonometer tip is laid against the cornea under a cobalt blue light. The dial is adjusted so that the inside borders of the split prism are aligned.

e. Iris: Should be flat and smooth with regular margins and a centrally located, round pupil. In trauma, may show tears, holes, or eccentric margins. If torn, suspect ruptured globe.

5. Lens: Should be transparent. Not uncommon to have post-traumatic cataracts develop which may be visible on penlight exam. In severe trauma, lens may subluxate or dislocate to float free in the vitreous or settle on the retina.

6. Cranial nerve assessment

a. II - Optic: Transmits sensory impulses from the retina to the occipital lobe for processing.

Assess visual acuity: Vital sign of the eye. Obtain on everyone presenting with an ocular complaint. Usually done as part of the initial assessment in the triage area, however, never delay ocular irrigation for chemical burns in order to obtain visual acuity. This is vital from both a medical and legal standpoint.


Test each eye separately; shield eye that is not being tested with an occluder. Assess with (cc) and without (sc) correction.


If patient normally wears corrective lenses and they are not available, use a pin hole occlusive device. If one is not available, use an index card with a small hole. The pinhole acts as a refractive device by aligning the beam of light as it enters the eye (Cuculino & DiMarco,


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Record results from both eyes using the following abbreviations:



Both eyes



Oculus dexter = R



Oculus sinister = L


Note their best vision using one or more of the following:



Snellen eye chart at 20 feet. Record best vision as a fraction. The numerator (20) always represents the distance in feet between the patient and the eye chart. The denominator depends on the smallest line of letters the patient is able to read without straining or squinting. The larger the denominator, the poorer the vision. Ex: Normal 20/20; very poor 20/200.


Rosenbaum "near" card held at 14 inches: Note smallest line of print that can be clearly read.


If patient cannot see largest print on eye chart, determine if they can count fingers or perceive hand motion. Document the distance at which they can see the stimulus.


If patient is unable to see hand motion, document if they can perceive light with or without the ability to determine the direction from which it is projecting.


If they cannot detect light, record the results as "No light perception" (NLP) or blind eye.


If pain is a significant factor in achieving patient cooperation for the exam, instill a topical ophthalmic anesthetic as prescribed.


For children who cannot read, use a picture card, such as an Allen chart, or cards with the letter "E" pointing in various directions.


Partial differential diagnosis of post-traumatic loss of vision


Lid swelling; blood or foreign material covering cornea; corneal damage


Hyphema; vitreous hemorrhage



Traumatic cataract; luxation of lens



Central retinal artery or vein occlusion (from markedly increased orbital pressure or embolus)


Traumatic retinal edema and hemorrhages of retina from direct or contrecoup blow to head


Retinal detachment



Avulsion of optic nerve by trauma of lateral orbital wall or contrecoup blow to head


Indirect trauma to optic nerves and/or chiasm (traumatic optic neuritis)








(hemorrhage/foreign body)



Cortical blindness from hematoma, ischemia, or anoxia (patient may be unaware of blindness)


Acute angle-closure glaucoma precipitated by emotional stress of recent trauma or from intumescent lens, etc.







Dislocation or loss of contact lens


Visual fields; peripheral vision

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b. CN III – Oculomotor

(1) Pupil size, shape, equality: Assess before installation of eye drops. Have the patient look at a distant object. This prevents distortion from accommodation (pupillary constriction that occurs when one looks at a near object). Compare one side to the other. Pupils should be round, symmetric, midpoint, and equal in size. The size, shape and reactivity of pupils can be affected by trauma, medications, previous ocular surgery, and central neurological events as well as by ocular processes. Obtaining an accurate history is essential.


MIOSIS: Possible etiologies of constricted or small pupils:


Drugs: Acetylcholine, Histamine, Picrotoxin, Mecholyl, Physostigmine, Morphine (narcotics), Pilocarpine, Neostigmine, Ergotamine, Diisopropyl & related drugs.


Physiological from: Sleep, forced closure of lid (Wesphal-Piltz), near reaction, old age; iris atrophy, direct light stimulation, congenital miosis with no dilator muscle, consensual light stimulation.


Pathological from: Areflexia of diabetes mellitus, meningitis, blind eye, alcoholism, Argyll-Robertson pupil, carbon dioxide poisoning, Horner's syndrome with ptosis, pontine lesions, encephalitis.


Mydriasis: Possible etiologies of enlarged pupils:


Drugs: Adrenalin, Paradrine, Atropine, Euphthalmine, Benzedrine, Homatropine, Canabis, Cocaine, Scopolamine, Ammonium chloride, Tetra- ethyl and related drugs.


Physiologically normal: Fright reaction, darkness, strong voluntary efforts to diverge, age - young myopes.





One eye: Apoplexy, tonic pupil (Adie), brain shift with pressure on 3rd nerve.


Both eyes: Diphtheria, ciliary gangliamitis (retrobulbar neuritis), juvenile paresis, pineal tumors, hysterical, botulism, generalized paresis, catatonia, herniation syndromes.


Causes of pupil asymmetry


Traumatic mydriasis or miosis from direct blow


Iridodialysis or rupture of iris sphincter


Unilateral use of topical drugs


Intraorbital trauma to ciliary nerves or ganglia


Acute intraocular inflammation with spasm or atony


Horner's syndrome; third-nerve palsy


Iritis; Adies pupil


Unilateral blindness


Stroke; Pontine lesions


Lues (Argyll-Robertson)

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c. CN II & III: Pupil reactivity to light; direct and consensual. Bring the light in from the side, observe the direct and consensual light reflex in each eye. The response should be brisk and symmetrical. (Assessing the sensory limb of CN II and the motor limb of CN III.)


Direct response: Each pupil should react by constricting briskly to a bright hand light.


Consensual response: The opposite eye's pupil should also constrict, even in the absence of direct illumination.


Afferent defect: Shine a bright light directly at the healthy eye for 30 seconds and quickly swing it to the other side. Note the first movement of the pupil. Repeat: swing the light to the other side. Both eyes should normally constrict or remain constricted in a consensual response. Any disease that blocks light from reaching the optic nerve or blocks transmission of the optic nerve will cause an afferent pupillary defect where the affected pupil dilates when light is shone into it. That eye is receiving less light than normal and dilates in an attempt to bring in more (Cuculino & DiMarco, 2002). This test can be performed even if only one pupil can be assessed.

In ambient light, even if the optic nerve of one eye has been completely transected, the pupils should be equal because the consensual response of the damaged eye to the good eye will result in equal pupils. Therefore, the swinging light test is essential.

d. Mobility of the globe (EOMs): CN III, IV, VI


Have the patient fixate on an object as it is moved up, down, left and right to evaluate nerve and muscle function. The eyes should move an equal amount in each gaze direction. Assess for range of each eye, symmetry, dysconjugate gaze, gaze palsies, or pain on movement. Defer this part of the assessment if a ruptured globe is suspected.


EOMs may be altered in cases of trauma, neurological events, infections, and tumors. Common causes include orbital edema, muscle entrapment and cranial nerve damage.


Inspect for nystagmus - vertical or horizontal

e. CN V: Trigeminal: Three branches (ophthalmic, maxillary, mandibular) supply sensation to the forehead, upper and lower eyelid, nose, cornea, cheek, upper lip and gums. Fractures of the orbit can cause loss of sensation to these areas.

7. Fundus/ophthalmoscopic examination: Includes inspection of the optic nerve, disc, macula, retina and blood vessels. Done through the use of an ophthalmoscope. Visualization is easier with dilation of the pupils (instillation of mydriatic drops), but is not necessary. The drop effects may last for hours to days and should be documented carefully, especially in trauma patients.

Examiner should note the following:

a. Red reflex: Present bilaterally; look for opacities

b. Optic nerve: Head should be somewhat yellow with sharply defined margins

c. Discs: Note shape and color. Should be well delineated; disc/cup ratio 1:3 (glaucoma increases size of cup); light yellow to pink; lighter than retinal background.

d. Retinal vessels: Central retinal artery and vein. Should have no A-V nicking; A-V ratio 4:5; no papilledema. Veins = no light reflex, arteries have a light reflex.

e. Background: Light red/orange, no hemorrhages, exudate, changes in pigmentation, or retinal detachment. Normal background color comes from the underlying retinal pigment epithelium and the vascular choroid. Retinal edema (Berlin's edema) is common after ocular trauma. Retina will appear milky white.

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f. Macula: No scarring. Inspect last, will cause tearing. In central retinal artery occlusion, the macula will present as a "Cherry Red Spot".

g. Vitreous abnormalities: Hemorrhages

D. Diagnostic studies

1. X-ray: Not used as often any more

2. CT scan: C-T scanning is essential to delineate completely the extent of orbital and optic canal fractures as well as intraocular and orbital foreign bodies.

3. Orbital and intraocular ultrasonography will aid in the evaluation of retinal and choroidal detachments, intraocular and intraorbital foreign bodies, vitreous hemorrhage, dislocation of the lens, and lacerations of the globe.

4. Optical Coherence Tomography (OCT): Noncontact, noninvasive imaging technique that uses light rather than sound waves to obtain a much higher longitudinal resolution of about 10 µm in the retina. Useful for imaging macular diseases and retinal inflammatory diseases. Has the capability of measuring the retinal nerve fiber layer thickness in glaucoma and other diseases of the optic nerve.

5. Evoked potentials: Helpful in the non-responsive or uncooperative patient for determining whether the visual pathways are intact.


V. Orbital (blow-out) fracture

A. Etiology: Pressures inside the bony orbit increase due to blunt trauma to the globe - often involve the orbital floor (maxillary bone), injury to the maxillary sinus, and entrapment of the inferior rectus muscle and inferior oblique muscles. May also involve the ethmoid sinus through the lamina papyracea with entrapment of the medial rectus muscle.

B. 32% of those with a medial blow out fracture will have a concomitant rupture of the globe.

C. Clinical presentation: Effects depend on the size and location within the orbital cavity

1. Periorbital pain, pain on upward gaze, point tenderness along orbital ridge, swelling, ecchymosis, crepitus if sinus cavity is involved

2. Abnormal EOMs: Paralysis of upward or vertical gaze indicates possible entrapment of the inferior

rectus muscle in the fracture of the orbital floor. If this is present, ophthalmology consult is


3. Diplopia: Due to muscle paresis, edema of the

3. Diplopia : Due to muscle paresis, edema of the orbital tissue, entrapment of muscle, fat,

orbital tissue, entrapment of muscle, fat, or orbital septa, and subsequent fibrosis and


4. Enophthalmos, hypophthalmos is often difficult to see in orbital blowout fractures as it is obscured by acute edema.

5. Subconjunctival air or hemorrhage; chemosis

6. Hyperesthesia or paresthesia over infraorbital nerve cutaneous distribution

7. Facial asymmetry

8. Rim fx. may be palpable; a fx. posterior to the rim may not be palpable

D. Radiological studies

1. CT of the orbits with thin 3 mm cuts with axial and coronal views. Will show fracture and associated sinus involvement or entrapped contents (preferred study).

2. X-ray - Water's view: shows maxillary clouding

3. Ultrasound may be a useful early diagnostic tool (Jenkins & Thuau, 1997).

E. Emergency management

1. No evidence of entrapment of orbital contents

a. Oral antibiotics to prevent cross contamination by the sinus

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b. Ice/cold pack if no globe rupture

c. Analgesics as prescribed

d. Decongestants as prescribed

e. Caution patients not to blow their nose or perform other Valsalva maneuvers. Precautions need to be taken to prevent vomiting. Potentially infectious material may be forced into the orbit from the sinuses leading to orbital cellulitis and loss of vision. Patients should be told to immediately see their physician if they notice any deterioration in vision, diplopia with the lid lifted an increase in pain or swelling or if they feel unwell (Shuttleworth et al, 1999).

f. Ophthalmology follow-up

2. Fractures involving muscle entrapment or evidence of enophthalmos

a. Analgesics as prescribed

b. Immediate ophthalmology consult

c. Repair is controversial. Some do immediate repair, others wait 10 to14 days and re-evaluate after edema resolves. Indications for surgery within the first two weeks include persistent symptomatic diplopia with a positive result on a forced duction test and evidence of herniated orbital contents on CT in the coronal plane.


A. Etiology: Blunt or sharp trauma to the orbital region may lead to significant functional and structural abnormalities including a possible penetrating globe injury. Before any attempt is made at lid repair, a thorough ocular exam must be performed and ocular injury excluded.

B. Types of lid injuries

and ocular injury excluded. B. Types of lid injuries 1. Simple partial thickness 2. Lid margins

1. Simple partial thickness

2. Lid margins

3. Canalicular system involvement

4. Lateral vs. medial to puncta involvement

5. Tissue loss

6. Violation of the orbital septum

C. Clinical significance: These may be associated with serious ocular injuries not apparent at first examination. Injuries to the lids can be serious because these structures protect the eyes and keep them moist, acting like windshield wipers to wash away foreign matter. An injured eyelid can lose its ability to cover the eye adequately, resulting in drying of the eye, infection or clouding of the normally clear cornea.

D. Clinical presentation/assessment

1. Note any abnormality of eyelid integrity, symmetry, contour. Avulsion injuries may result in loss of lid skin or deeper tissue. Measure and document the size and extent of the


2. Inspect for exposed eyeball

3. Describe the amount of edema, ecchymosis, erythema, and bleeding

4. Inspect for possible injury to the margin, canthal tendons, lacrimal drainage system, deeper lid structures or the globe

a. Medial: Damage to the lacrimal outflow system and medial canthal tendon

b. Lateral: Lacrimal gland or lateral canthal tendon

c. Fatty tissue within an eyelid laceration suggests violation of the orbital septum (Shingleton & Meade, 1998).

5. Measure the palpebral height (distance between the upper and lower lids), document ptosis

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E. Emergency management

1. Avoid vertical traction near the lid margin to prevent late ectropion (eversion or outward displacement of the margin of an eyelid)

2. Save and preserve all avulsed tissue, even if the viability is questioned

3. Cover wound with saline-moistened sterile dressing

4. Apply cold pack or ice compress to minimize swelling and decrease pain

5. Assist physician with irrigation and debridement

6. Do not shave the eye brow when it is lacerated. If shaved, the hair may not regrow or it may come back irregularly.

7. Tetanus immunization

8. May require surgical repair by experienced ophthalmologist. Prepare for OR if the patient sustained one or more of the following:

a. Wounds associated with ocular injury (ruptured globe)

b. Wounds involving the lacrimal drainage system (punctum, canaliculus, common duct, or lacrimal sac)

c. Involvement of the levator aponeurosis causing ptosis or if orbital fat is exposed

d. Lacerations with avulsion of the medial or lateral canthal tendon

e. Wounds with intraorbital F/B that may be removed

f. Those with loss of tissue (> 1/3 of the lid)

g. Lacerations of the eyelid margin. Some may be repaired in the ED by an ophthalmologist. Improper repair may lead to notching of the lid margin and severe cosmetic defects.

9. Delayed repair is usually indicated for

a. wounds at significant risk for infection;

b. human bites;

c. evaluations done 8-12 hours after injury; or

d. marked lid swelling or facial edema obscuring wound details.

10. All other injuries may be primarily repaired in the ED. If suspicion of ocular F/B or bony fracture send for US, CT, X-ray or MRI. Physician will do the following:

a. Clean area with Betadine

b. Inject local Sub-q anesthetic (2% Lidocaine with Epi)

c. Irrigate with saline

d. Search for and remove F/B

e. Apply sterile eye drape to isolate field

f. Instill topical anesthetic into the eye and apply a protective shell over the eye to avoid inadvertent ocular penetration

g. Repair the laceration. Suture materials to have available: 6-0 Vicryl; 6-0 or 7-0 nylon

h. Apply antibiotic ointment

i. Physician will likely prescribe systemic antibiotics if infection or contamination is suspected


VII. Chemical exposure: An ocular chemical burn is a true eye emergency. Apart from history, the

diagnosis of chemical burn is usually based on the presence of swollen eyelids with marked conjunctival


A. Incidence: 10% of all ocular complaints and 80% of all ocular burns (Cuculino & DiMarco, 2002)

B. Etiology: Degree of injury depends on the pH of the material, length of exposure, and permeability of the agent.

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Acid burns are generally less serious than alkali burns because they do not cause progressive destruction of ocular tissues or collagen swelling. However, hydrofluoric acid is extremely dangerous and can cause fatal systemic complications such as hypocalcemia and cardiac dysrhythmias (Cuculino & DiMarco, 2002). All hydrofluoric acid exposures need immediate ophthalmologic consult and irrigation with 1% calcium gluconate. Significant exposures require systemic treatment and decontamination.

2. Alkalis: Lipophilic and cause saponification of the fatty acids in the epithelial cell membranes. They bind to mucoproteins and collagen causing a liquefaction necrosis and collagen denaturation. They destroy the surface tissues, affecting the eyelid, conjunctiva and mucous secreting goblet cells. Once the epithelium is damaged, the chemical rapidly penetrates the cornea and anterior chamber. When the pH > 11.5 there is intraocular penetration. The higher the pH the worse the injury. They cause a severe inflammatory response



- Ammonia

- Sulfuric acid

- Sodium hydroxide

- Sulfurous acid

- Potassium hydroxide

- Hydrofluoric acid

- Calcium hydroxide

- Acetic acid

- Magnesium hydroxide

- Chromic acid

- Hydrochloric acid

Sources of alkali substances

Sources of acidic substances

- Fertilizers

- Battery acid (leading cause)

- Drain cleaners, lye

- Glass polish (hydrofluoric acid)

- Lime, mortar, cement, whitewash

- Bleach

- Fireworks, sparklers, flares

- Vinegar

C. Morbidity and prognosis for the affected eye

(Cuculino & DiMarco, 2002)

1. About 20% result in significant visual or cosmetic disability (Cuculino & DiMarco, 2002).

2. Even after apparent removal of the agent, lodgment of tiny particles within the cul-de- sac may continue and cause progressive damage to the eye.

3. It may take 48-72 hours to make an accurate assessment of burn damage. For alkali burns, the degree of corneal opacification and peri-limbal blanching correlate with


4. Corneal opacification occurs due to disruption of the regularly spaced collagen network by direct chemical damage, reactive edema, and damage from lysosomal enzymes released by the neutrophils. Burns at the limbal region are the most unfavorable, as they produce vascular damage with extensive thrombosis and eventually ischemic necrosis.

D. Clinical presentation: acute phase

ischemic necrosis. D. Clinical presentation: acute phase 1. Severe pain and diminished or blurred vision 2.

1. Severe pain and diminished or blurred vision

2. Conjunctival chemosis and injection; possible limbal blanching

3. Localized edema

4. Mild

a. Mild erosion of corneal epithelium

b. Faint haziness of cornea

c. No ischemic necrosis of conjunctiva or sclera

d. Prognosis: mild visual loss (usually 0-2 lines on Snellen chart)

mild visual loss (usually 0-2 lines on Snellen chart) 5. Moderately severe a. Corneal opacity blurs

5. Moderately severe

a. Corneal opacity blurs iris details

b. Limbal blanching < 1/3 of peri-limbal conjunctiva

c. Minimal ischemic necrosis of conjunctiva and sclera

d. Prognosis: visual preservation of 20/100 or less

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6. Very severe

a. Blurring of pupillary outline

b. Marbleized (opacified) cornea: corneal grafts may not take

c. Ischemia of 1/3-2/3 of peri-limbal conjunctiva

d. Blanching of conjunctiva and scleral vessels

e. Cataract formation

f. Glaucoma

g. Necrosis of intraocular contents

h. Prognosis: Poor with high incidence of corneal ulceration, perforation, vascularization and opacification. Vision - often count fingers or less.

E. Emergency management: Do not delay irrigation while trying to determine nature of the chemical.

1. Immediate decontamination with any neutral fluid available at injury site. Remove particulate matter immediately.

2. Rapid removal of contact lenses

3. Rapid visual acuity for light perception only while preparing to irrigate

4. Instill a topical anesthetic and/or cycloplegic/mydriatic if severe pain/ciliary spasm (will dilate pupil)

5. Immediate and profuse eye irrigation with 1 - 2 liters closest neutral solution. Aim stream from inner to outer canthus making sure that superior and inferior fornices are well flushed. Don't attempt to neutralize the chemical agent with a liquid of the opposite pH - will cause a heat reaction. Evert the eyelids, if necessary, to flush the cul-de-sacs. Normal tear pH ranges from 7.3 - 7.7. The eye must be allowed to equilibrate for 5-10 minutes after initial lavage before determining the pH. Check pH after each subsequent liter and discontinue lavage when pH of 7.4 to 7.6 is achieved.

6. Mild chemical burns can be treated as a corneal abrasion and followed as outpatients. Moderate to severe burns require immediate ophthalmologic consult. The ophthalmologist may prescribe treatment to reduce inflammation, promote epithelial healing, decrease intraocular pressure, or debride the injured area. Goal is to prevent scarring, cataract formation, perforation, and glaucoma (Cuculino & DiMarco, 2002).

7. Assess intraocular pressure in alkali burns after irrigation. If elevated, the physician may order any of the following:

a. Acetazolamide (Diamox) 500 mg IM/IV or 125-250 mg QID PO

b. IV Mannitol

c. Topical beta blockers: timolol maleate (Timoptic) drops

8. Ammonium titrate 5% dissolves lime

9. Narcotic analgesia and sedatives as prescribed

10. Topical antibiotic ointment as prescribed while epithelial defect exists

VIII. Thermal burn

A. Etiology: Flash burn, fiery explosion, cigarette ash, etc. Almost always associated with facial burns. Even severely burned patients may avoid direct injury to the cornea and conjunctiva due to protection by the eyelids. Burns due to toxic chemicals, hot liquids, and molten metal behave much like alkaline burns. Iron has a higher melting point (1200° C) and causes more damage than other metals (lead, tin, zinc, melting point below 1000° C). Arc welding injuries common without protective eyewear.

B. Clinical exam: May require local anesthetic, Desmarres lid retractors

1. Visual acuity; pupillary exam

2. External exam: Spastic entropion, lid edema, orbital cellulitis

3. Slit-lamp exam: Conjunctival chemosis, blanching, corneal clarity, anterior chamber inflammation, fluorescein testing

4. Intraocular pressure testing

5. In explosions: Must R/O perforating injuries, F/B

6. Cornea will slough and regenerate in 4-5 days in children; 3-4 weeks in adults

C. Treatment

1. Physician will debride devitalized lid epithelium and remove F/B

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2. Spastic entropion: Bandage with contact lens in place. Note: the contact lens will not remain moist if lids are not functioning properly, and frequent artificial tears and ointments are often necessary.

3. Antibiotic ointments/drops as prescribed

4. Cycloplegics as prescribed

5. Increased intraocular pressure: Diamox, Timoptic as prescribed

6. Eyelid burn: Cool burn and then apply sterile dressings

D. Complications: Infections such as Pseudomonas keratitis, endogenous enophthalmitis from septicemia, mucomycosis. Eyelid burns with skin loss can lead to scarring with cosmetic disfigurement, chronic tearing, exposure keratitis, and trichiasis.

IX. U.V. radiation burns

A. Etiology: Uncommon, yet may be seen in head and neck tumors treated with radiation or those who use tanning beds where the corneas were left unprotected, arc welders not using appropriate eye protection, mountain climbers, or skiers outdoors in the snow on a sunny day.

B. Clinical presentation

1. Superficial punctate keratitis on the exposed eye surface, corneal epithelium sloughs

2. Pain, 3-12 hours after exposure, is often delayed but severe

3. Increased tearing, burning, eyes feel full of sand

C. Emergency management

1. Treat like a corneal abrasion with pain control, antibiotic prophylaxis as prescribed, cold compresses, lubrication

2. 12-36 hour recovery period

3. Permanent scarring is rare

X. Corneal abrasion

period 3. Permanent scarring is rare X. Corneal abrasion A. Definition : Defect in the corneal

A. Definition: Defect in the corneal epithelium that does not penetrate Bowman's layer

B. Etiology: Very common. Results from a direct or tangential impact to the eye, contact lenses, and/or exposure to UV light. F/Bs can scratch the cornea at various depths. The sharp edges of hard contacts can cause small abrasions during normal use. Extended wear contacts cause epithelial hypoxia, which impairs the attachment of the epithelial cells to Bowman's membrane.

This weakened attachment makes the eye more susceptible to damage from minimal trauma, such as rubbing the eyes (Cuculino & DiMarco, 2002).

C. Clinical presentation: A corneal abrasion may be associated with serious ocular injury and therefore a complete ocular exam should be performed. Assess and record visual acuity. Topical anesthesia aids in exam.

1. Pain: Mild to severe, and foreign body sensation that is worsened by blinking

2. Copious tearing (epiphora)

3. Possible decrease in visual acuity if over the pupil

4. Irregular corneal light reflex

5. Diffuse conjunctival injection

6. Photophobia

7. Mild anterior chamber reaction

8. Lid spasm (blepharospasm)

D. Slit lamp examination

1. Remove contact lenses

2. Stain the cornea with fluorescein

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4. Note and diagram the size of the abrasion and its depth. Do not be fooled by a self- sealing full thickness laceration and treat it merely as an abrasion. A full thickness laceration often shows a positive Seidel's test.

5. Examine the anterior chamber for the presence of a hyphema which may result from blunt trauma and may require different treatment.

6. If the cornea has multiple vertical linear abrasions, a F/B adhered to the inner surface of the conjunctiva is likely. Evert the eyelids to examine for F/B.

E. Emergency management

1. Non-contact lens wearer

a. Pain control


Topical anesthetics: A topical anesthetic may make examination easier and alleviate pain, but DO NOT give the patient topical anesthetic to take home. They slow epithelial repair and may predispose the patient to further trauma as the protective reflexes of the eye are lost (Cuculino & DiMarco, 2002).


Cycloplegics (Cyclopentolate 2%) as prescribed to dilate pupil and decrease ciliary spasm and reduce photophobia


Topical NSAID drops or oral analgesics as needed

b. All objects that could cause an abrasion may be microbially contaminated and the possibility of infection should always be considered. Topical broad spectrum antibiotic ointment or drops per physician preference to help prevent infection. Instruct patients that ointments may blur vision for a short period of time. Instruct patients in the correct use of eye drops and ointments.

c. Eye patching decisions are made on a case by case basis (Cuculino & DiMarco, 2002). Patching may slow healing and may increase the rate of infection. It is rarely done today. Do not patch if an abrasion was caused by vegetable matter or artificial fingernails.

If prescribed, double-patch eye for 12-24 hours to help alleviate pain and limit eyelid movement. Use two pads with tape running from bone to bone in a diagonal fashion. A pressure patch is not usually indicated when microbial infection is suspected or a significant risk exists (contact lens wearers).

d. Tetanus prophylaxis as necessary

e. Follow-up with an ophthalmologist within 24-48 hours. The corneal epithelium heals rapidly and most small abrasions resolve during this time. Antibiotic drops may be continued for 5-7 days.

2. Contact lens wearer: Patients with contact lenses are at particular risk for gram

negative infections such as Pseudomonas and their treatment differs from a routine


a. Cycloplegics

b. Antibiotic drops with pseudomonas coverage (Gentamicin or Tobramycin 4-6 times/day and antibiotic ointment for H.S.


d. Abstain from lens wearing for at least one week

e. Oral analgesics

f. Follow-up in 24 hours in mandatory

3. Complications

a. Corneal ulcer: Can be viral, bacterial, fungal, or chlamydial. Should be considered a true emergency. Bacterial ulceration can rapidly progress to corneal perforation. Most bacterial cases result from trauma or contact lens use or abuse. They present with pain, photophobia, decreased visual acuity, a white corneal infiltrate

or contact lens use or abuse. They present with pain, photophobia, decreased visual acuity, a white

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(hypopyon) with ill-defined borders and/or an epithelial defect on fluorescein staining. They require culture, gram stain, and ophthalmology consultation. Fortified antibiotic drops are required for treatment. Steroids are not routinely indicated (Med-Challenger FM 06).

b. Decreased visual acuity if they involve the visual axis

c. Traumatic iritis may develop 24-72 hours after injury

d. Recurrent erosion syndrome: Recurrent abrasion days to years after a previous injury. Patient will present with sudden severe pain when they open their eyelids upon waking. At risk patients: large abrasions or those caused by fingernails or hard contact lenses.

XI. Cyanoacrylate (Krazy) Glue: Direct exposure can cause a chemical keratitis. Immediately irrigate with warm water for at least 15 minutes. Acetone or ethanol solutions should not be used in the eye. If eyelids are bonded together, gently rub with mineral oil or a petroleum-based ointment such as bacitracin or erythromycin. Forceful retraction should be avoided.

XII. Corneal laceration

retraction should be avoided. XII. Corneal laceration A. Definition: Full-thickness injury to the cornea B.

A. Definition: Full-thickness injury to the cornea

B. Patient presentation - much the same as globe rupture

1. Teardrop pupil

2. Flat anterior chamber

3. Hyphema

C. Emergency management

1. Cover eye with a protective shield

2. Instruct patient not to move the eye

3. Do not assess intraocular pressure

4. Position patient head up at a 30° to 45° angle

5. Immediate ophthalmology consult

6. Prophylactic antibiotics and tetanus as prescribed

7. Antiemetics as prescribed to prevent increase in intraocular pressure from vomiting

XIII. Corneal/conjunctival foreign bodies

from vomiting XIII. Corneal/conjunctival foreign bodies A. Etiology : Fragments fly into the eye from working

A. Etiology: Fragments fly into the eye from working without protective goggles. Industrial air pollution, BB pellets etc. also common.

B. History: Question patient about the use of safety goggles, the nature of the F/B, and if there was metal striking metal. If metal, identify the type of metal if possible; iron and copper are common. High-velocity mechanisms may cause corneal perforation.

C. Clinical assessment/presentation: Most F/Bs don't penetrate the globe. However, view them as a possible indicator of concurrent intraocular or intraorbital F/B. This is especially important in the setting of grinding or hammering metal upon metal in the absence of protective eyewear. Inspect conjunctiva, fornices, and evert the lids to search for additional F/B. If vertical linear abrasions are seen suspect occult F/B under the lid.

1. Chief complaint: Pain, foreign body sensation, photophobia, blurred vision

2. Obtain visual acuity before and after treatment

3. Observe unaffected eye first for comparison

4. Inspect for red eye, tearing

5. Always suspect corneal penetration if patient presents with a diffuse subconjunctival hemorrhage, diffuse corneal damage, abnormal pupillary shape, an hyphema, or a change in anterior chamber depth vs. the noninvolved eye (Cuculino & DiMarco, 2002).

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E. Emergency management

1. Topical anesthetic as prescribed

2. Evaluate the depth of the F/B with biomicroscopy. Those deeply imbedded or in the visual axis should be removed by ophthalmology.

3. Physician may dilate pupil with Cyclogyl 1% or Mydriacyl 1% or Homatropine 5% to relieve iritis unless history of glaucoma.

4. Antibiotic drops pre and post-removal as prescribed

5. Conjunctival F/B: Easily removed by physician using gentle irrigation with NS,

moistened cotton-tipped applicator, a foreign body spud or the bevel of a 25-27 gauge


6. Corneal F/B: Requires removal under the slit lamp

7. Iron-containing objects may leave a rust ring after removal of the F/B. The rust ring can be removed 24-48 hours later by a spud, a 25 g needle or an ophthalmic rust ring drill. It is sometimes safer to leave the rust ring, especially if it is central or deep. This will allow time for it to migrate to the surface and be easily removed at a later time. Debride as little tissue as possible.

8. Check for corneal abrasion and perforation. The physician should document a negative Seidel test to ensure that corneal perforation did not occur.

9. Once removed, treat the same as a corneal abrasion



Analgesics; may need narcotics if iritis is severe


Antibiotic ointments (erythromycin) as prescribed



1. Infection - disastrous; (pseudomonas in fluorescein)

2. Scarring - use slit lamp when available

XIV. Subconjunctival hemorrhage

A. Definition: Bleeding of the delicate conjunctival or episcleral vessels between conjunctiva and sclera into the subconjunctival space.

B. Etiology: Very common; can be initiated by Valsalva maneuvers such as sneezing, coughing, straining, or lifting heavy objects; trauma, hypertension, coagulopathy, febrile illness, or idiopathic causes.

C. Clinical presentation: Painless, blood-red eye; may be accompanied by some irritation. Looks terrible but is usually a non-emergency if non-traumatic origin. If trauma, physician must rule out globe rupture or retrobulbar hemorrhage.

D. Emergency management

1. Supportive and aimed to prevent further bleeding. Discontinue use of NSAIDS and aspirin for 24-48 hours.

2. Instruct patient to avoid Valsalva maneuvers

3. Instruct patient in use of artificial tears for irritation

4. Usually self-limiting, spontaneously resolves in 1 - 2 weeks. Instruct patient that the healing process will break the blood down and change color from red to green to yellow and then to brown.

5. Any globe tenderness should be evaluated for presence of infection

XV. Hyphema

A. Definition: Accumulation of blood within the anterior chamber due to rupture of a vessel in the iris.

B. Etiology/MOI: Usually caused by severe blunt, and less often perforating, trauma to the eye. In rare instances, hyphema may occur spontaneously as a complication of an ocular or systemic disorder or the use of anticoagulants.

C. Demographics

1. Incidence: 17-20/1000 population/yr

2. M:F 3:1

or systemic disorder or the use of anticoagulants. C. Demographics 1. Incidence: 17-20/1000 population/yr 2. M:F

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3. 70% < 20 years of age

4. 60% sports related

D. Pathophysiology

Bleeding occurs from the angle where the iris meets the cornea leading to hemorrhage from the circumferential iris-root vessels. The resulting pressure wave may cause bleeding from the ciliary body itself. Loss of blood is self-limited as vascular pressure and intraocular pressure equilibrates.

E. Severity: May range from cells visible only on biomicroscopy to large total ("eight-ball") hyphema where the iris is covered by gross blood.

1. Grade 1 (60%): small; 1/3 AC

2. Grade 2 (20%): moderate; 1/3 - ½ AC

3. Grade 3 (20%): severe; > ½ to near total AC

4. Grade 4: total or "eight-ball" hyphema

F. Clinical presentation

1. Chief complaint: Pain and decreased vision (25%); patient may report seeing red, moving spots that seem to drift in front of the eye.

2. Pain, nausea, vomiting: May be indicators of uncontrolled elevation of intraocular pressure.

3. Assess iris (may cause iridodialysis or iris root tear); active hemorrhage; R/O lens dislocation, cataract, posterior chamber blood.

4. Measure degree/height of hyphema. The size determines the visual outcome. Gravity and clotting mechanisms will eventually cause the blood to settle inferiorly under the pupil aperture, giving the hyphema a crescent shape, but allowing the patient to see.

5. Note the color of the blood: Red indicates a new bleed, brown is characteristic of older blood.

6. Measure intraocular pressure. Elevated intraocular pressure can cause angle recession and acute glaucoma.

7. Marcus Gunn Pupil: Detected by swinging light test. Paradoxical pupil dilation indicates the presence of an afferent pupillary defect and optic nerve damage.

G. Clinical significance: Suspicion of F/B, laceration, or concomitant globe rupture. All require immediate ophthalmology consult.

H. Labs - directed by history

1. CBC

2. Platelet count, PT, PTT helpful if suspected coagulopathy

3. Sickle cell prep

4. Hb electrophoresis (not sickle cell prep) mandatory in all blacks, Hispanics and those with Mediterranean origins.

I. Emergency management: Aimed at limiting acute and long term complications. Small hyphemas can be managed as outpatients. Larger ones need admission.

1. Total bed rest for 3-5 days. Sit up 30°-45° to facilitate settling of the hyphema into the inferior portion of the anterior chamber and away from the visual axis.

2. Place metal shield over involved eye to help prevent further injury

3. Strict eye rest; no reading permitted

4. Sedate the patient if overly anxious

5. Non-aspirin containing analgesics; avoid antiplatelet agents

6. Long acting cycloplegics such as Atropine 1% given to prevent movement of iris and clot dislodgement

J. Anticipated complications

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rebleed from 30% to 3%. Physicians may also prescribe oral prednisone to inhibit rebleeding through its stabilizing action on fragile vessels.



a. Beta blockers: Timolol to decrease production of aqueous humor

b. Adrenergics

c. Carbonic anhydrase inhibitors: Diamox

d. Avoid miotics

pressure: The physician may order topical and/or systemic


3. Chronic: Angle damage leading to glaucoma, corneal blood staining, optic atrophy

K. Associated injuries: Corneal laceration, occult scleral rupture, lens damage and/or dislocation, optic atrophy, angle recession, chronic glaucoma, vitreous hemorrhage, retial detachment and CN II damage.

XVI. Penetrating/perforating globe injuries: This is a major cause of traumatic visual loss due to damage of intraocular structures caused by the force required to rupture the globe. They require immediate careful assessment and prompt surgical repair to prevent loss of the eye.

A. Penetrating injuries are those that cause partial disruption of the outer coats of the eye without interrupting the anatomic continuity of the scleral or corneal layer, thus preventing prolapse of ocular contents.

B. Perforating injuries are those that result in complete anatomic disruption of the sclera or cornea. They may or may not be associated with prolapse of uveal structures.

C. Etiology

associated with prolapse of uveal structures. C. Etiology 1. Direct blunt or penetrating trauma to the

1. Direct blunt or penetrating trauma to the eye

2. As the intraocular pressure suddenly increases, the sclera ruptures where it is the thinnest, often at the limbus, the site of extraocular muscle insertion, and/or the site of optic nerve insertion.

D. Clinical assessment/presentation

1. Change in pupil shape (tear-drop pupil pulls to site of rupture)

2. Unequal pupils

3. Black or brown defect (choroid/uveal prolapse into defect)

4. Injected sclera, subconjunctival hemorrhage

5. Leakage of vitreous humor

6. Pain

7. Decreased visual acuity to hand movements or light perception

8. Enophthalmos

9. Lowered intraocular pressure; soft eye

10. Flat or shallow anterior chamber

11. Hyphema

12. Iris prolapse

13. Dislocated lens, traumatic cataract

14. If lids are swollen, use great caution in pulling them apart to prevent extrusion of the eye. If you cannot retract lids, get an ophthalmologist consult ASAP.

E. Radiological evaluation: for metal

F. Emergency management: Same as for an intraocular foreign body or corneal laceration

1. Never remove an impaled F/B

2. DO NOT manipulate the eye, instill eye drops, measure intraocular pressures, or apply antibiotic ointments

3. Shielding: A metal shield should rest on the bone of the brow and the cheek; it should not exert pressure on the eye. The patient must not be able to touch or rub the eye.

4. Do not remove any blood clots, foreign bodies or tissue from the eye

5. Tetanus prophylaxis

6. Analgesics and sedatives may be needed

7. Don't let patient bend, stoop, strain or move his or her head suddenly

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8. Keep patient NPO

9. IV antibiotics as prescribed

10. Surgical intervention by ophthalmologist

G. Prognosis

1. Related primarily to the location and extent of damage. The more posterior the penetration and the larger the laceration or rupture, the worse the prognosis. Through and through injuries (BBs or pellets) have a bad prognosis. Superficial injuries to the anterior segment structures can often be repaired by microsurgical closure, contact lens or intraocular lens optical correction, and corneal transplantation, if necessary. They have a high rate of visual rehabilitation (Broocker, Parke & Hamill, 1996). Posterior injuries involving the retina are more severe. Damage may cause proliferation of scar tissue throughout the vitreous that can result in retinal tears or detachment.

2. Also at risk for microbial endophthalmitis that can lead to blindness. This risk is increased with an intraocular foreign body.

3. Sympathetic ophthalmia: Bilateral inflammation of the uveal tract (iris, ciliary body, and choroid) associated with penetrating injury to one eye. Untreated, this often results in loss of the noninjured eye. This risk is reduced if the injured eye is enucleated within 10-14 days of the injury. However, the risk of this complication is very small and does not justify the primary removal of a severely traumatized eye unless the eye is completely blind and there is significant exposure or extrusion of posterior ocular contents (Broocker, Parke & Hamill, 1996).

XVII. Intraocular foreign body

A. Etiology: Metallic particles most common (80%)

B. History: Metal striking metal or mechanism indicating a high velocity projectile

C. Clinical presentation

1. Pain, irritation

2. Injection

3. Entry site may be visible on biomicroscopy as a disruption of the corneal surface with surrounding edema

4. Fluorescein stain may demonstrate a positive Seidel sign (streaking of the fluorescein as aqueous humor leaks out of the globe)

D. Diagnosis

1. No intraocular pressure measurements

2. Plain films of the orbits if suspected material is radio-opaque

3. CT of orbits is usually preferred

4. Ultrasound can also identify retinal detachments

5. MRI may visualize F/B not seen on CT but must be avoided if material is metallic

E. Emergency management

1. Cover eye with a protective shield

2. Apply no pressure to the globe

3. Tetanus prophylaxis as prescribed

4. Immediate ophthalmology consult for removal

5. IV antibiotics as prescribed - about 10% become infected. Beside usual gram positive coverage, add pseudomonas coverage if material is dirt or vegetable matter such as wood from tree branches.

6. Antiemetics as prescribed to prevent vomiting and increased intraocular pressure

XVIII. Lens dislocation/subluxation

A. Definition: Disruption of the zonular fibers that maintain the lens in its correct position. Partial disruption results in subluxation.

B. Etiology: Trauma to the eye. Minimal trauma can cause dislocation in patients with Marfan's syndrome, homocystinuria, or syphilis.

C. Clinical presentation

1. Pain

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2. Monocular diplopia

3. Edge of lens visible through the pupillary aperture. Total disruption may allow lens to displace into the posterior chamber leading to an acute rise in intraocular pressure.

D. Emergency management: Immediate ophthalmology consult

XIX. Iridodialysis

A. Definition: Iris is torn from the ciliary body

B. Patient presentation

1. Appears as if patient has a second pupil

2. May develop a secondary hyphema and monocular diplopia if the defect is large

C. Emergency management

1. Treat hyphema

2. Immediate ophthalmology consult

1. Treat hyphema 2. Immediate ophthalmology consult XX. Retinal detachment : Separation of the neurosensory

XX. Retinal detachment: Separation of the neurosensory layer of the retinal pigment epithelium from its source of blood supply via tear, fold or rent. Subretinal fluid accumulates under the neurosensory layer.

A. Etiology: Minimal to moderate trauma or proliferative retinopathy

B. Clinical presentation

1. Painless visual field deficit or decrease in vision. May be described as a darkening/haziness or a curtain or shadow being drawn over the visual field.

2. New onset of photopsia (flashes of light or sparks); spider webs; "Floaters" or black dots

3. If it involves the periphery, patient will have a visual field deficit

4. If it involves the macula, visual acuity will be diminished

5. Fundoscopic exam reveals billowing of the retina

6. A significant hyphema may obscure the fundus

C. Diagnosis: Beta scan ultrasound

D. Emergency management

1. Keep patient quiet and supine with both eyes patched

2. Immediate ophthalmologist intervention is required. Patients at increased risk include those with severe myopia, trauma, prior surgery and a significant family history.

3. Retinal attachment can only be accomplished by surgery which is successful in about 80% of the cases. The eye is filled with a perfluoropropane (C 3 F 8 ) and/or sulfur hexafluoride (SF 8 ) gas bubble to reattach the retina. Patients need to be warned that it takes six to eight weeks for these gasses to diffuse from the eye. If nitrous oxide is given to the patient while the C 3 F 8 or SF 8 are still present, it can diffuse rapidly into the gas bubble and raise intraocular pressure causing a central retinal artery occlusion and blindness. Patients should wear medic-alert bracelets postoperatively and warn healthcare providers that the gas bubbles may remain in their eye and they are at risk for a C 3 F 8 or SF 8 - nitrous oxide reaction. These patients should also be cautioned about avoiding high altitude travel until the surgeon gives them permission (Woo, 2002).

XXI. Optic nerve injury

A. Etiology: Transection or avulsion of optic nerve, hemorrhage, decreased blood flow to the optic nerve, or pressure from bony fracture.

B. Clinical significance: Resulting blindness is often irreversible

C. Clinical presentation: Visual deficit and afferent pupillary defect on affected side unrelated to any other associated eye injury. Physician should carefully rule out other causes of visual deficit such as hyphema or retinal tear. Initial fundoscopic exam may be normal.

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XXII. Retrobulbar hemorrhage (Orbital compartment syndrome)

A. Etiology: Post-trauma or post-operative; rare cases of spontaneous hemorrhages

B. Clinical presentation

1. Acute proptosis: accumulating blood puts pressure on the globe

2. Pain

3. Elevated intraocular pressures

4. Edema

5. Decreased range of motion due to blood within the bony orbital walls

6. Resistance to retropulsion of the globe

7. Irreversible vision loss in 60 minutes

C. Emergency management: Reduce intraocular pressure

1. Topical beta blockers: timolol 0.5% (1 drop every 30 minutes for 1 hour) decrease production of aqueous humor

2. Carbonic anhydrase inhibitors: acetazolamide 500 mg PO/IV/IM then 250 mg PO/IV/IM q. 6 hours also decrease production of aqueous humor

3. Hyperosmolar agents (mannitol 1-1.5 mg/kg) reduce vitreous volume

4. Severe cases: Lateral canthotomy allows the globe to protrude out of the orbit, thereby decreasing intraocular pressure

5. Immediate ophthalmology consult

XXIII. Globe luxation

A. Clinical presentation: One of the most dramatic traumatic eye presentations: entire globe is found outside of the bony orbit

B. Emergency management

1. Cover with a cone or cup

2. Early reduction to minimize traction on the optic nerve

3. Physician should apply gentle pressure as the eyelids are retracted. Edema and retrobulbar hemorrhage may make operative reduction mandatory.

XXIV. General nursing diagnoses/interventions

A. Pain

1. Application of cold packs: use with caution and never with severe eye injury or globe disruption

2. Instillation of local anesthetic agents as ordered: useful in minor corneal abrasions. Not to be used long term.

3. Administration of systemic analgesics as ordered: useful for severe eye injuries where local anesthetics are contraindicated.

4. Irrigation: copious irrigation with 1-2 liters saline essential for chemical injury, as well as any suspicion of foreign body.

B. Impaired tissue integrity

1. Removal of superficial foreign bodies

2. Stabilization of impaled object

C. Potential for infection

1. Wash hands first and use aseptic technique when touching eye

2. Monitor for signs of infection

3. Instill prescribed ointments/drops: never use ointment prior to eye exam

4. Use appropriate dressing techniques for specific problem to prevent further injury and complications

D. Knowledge deficit

1. Provide clear discharge instructions

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2. Instruct patient on administration technique of prescribed medication(s)

E. Potential for visual impairment

1. Caution patient regarding loss of depth perception. Instruct re: no driving, sports, and operating heavy machinery while patched.

2. If severely impaired, request social service assistance for help with activities of daily living (ADLs).

3. Instruct patient on maintaining a safe environment

F. Fear or anxiety related to potential or actual loss of vision

1. Maintain a quiet environment

2. Provide psychological and emotional support

3. Provide frequent orientation to date, time and place, situation

4. Describe self and the environment

5. Optimize use of other senses

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Selected Ophthalmic Medications





Sodium sulfacetamide solution

Instill 1-3 drops q. 2-3 hrs for 7 days


Sodium sulfacetamide ointment

Apply 1" ribbon to the eye QID for 7 days

This lacks pseudomonal coverage

Gentamicin ophthalmic solution

Instill 1-2 drops QID for 7 days



Gentamicin ophthalmic ointment

Apply 1" ribbon to eye QID for 7 days

This has anti-pseudomonal coverage


Erythromycin ophthalmic ointment

Apply 1" ribbon to eye QID for 7 days


Bacitracin ophthalmic ointment

Apply 1" ribbon to eye QID for 7 days

This has no pseudomonal coverage

Ciprofloxacin drops

Instill 1-2 drops QID for 7 days

This has pseudomonal activity, but there may be increasing strep pneumonia resistance. This may be used in children.

Trimethoprim/Polymyxin solution

Instill 1-2 drops QID for 7 days


Trimethoprim/Polymyxin ointment

Apply 1" ribbon to eye QID for 7 days

This has pseudomonal coverage

Tobramycin ophthalmic solution

Instill 1-2 drops QID for 7 days


Tobramycin ophthalmic ointment

Apply 1" ribbon to eye BID/QID for 7 days


Ofloxacin ophthalmic solution

Instill 1-2 drops QID for 7 days

This has anti-pseudomonal properties and may be used in children.

Beta blockers: Reduce production of aqueous humor. Indicated for glaucoma, ocular hypertension.

timolol maleate 0.25%, 0.5%, 2.5 mg/ml, 5 mg/ml (Timoptic, Timoptic- XE)

1 drop q. 30 minutes for 1 hour then 1 drop BID


Hypersensitivity to timolol Asthma Bradycardia; 2nd or 3rd degree AVB Overt cardiac failure Cardiogenic shock

levobunolol hydrochloride (Betagan)

1-2 drops 0.5% solution QD 1-2 drops 0.25% solution BID

Adverse effects:

Ocular stinging, burning Blepharitis; ocular irritation

Carbonic anhydrase inhibitors: Reduce production of aqueous humor. Indicated for chronic simple glaucoma, open-angle glaucoma, secondary glaucoma, and preoperatively for acute angle-closure glaucoma; and ocular hypertension

acetazolamide (Diamox)



500 mg PO/IV/IM then 250 mg q. 4-6 hrs Duration 14 hrs.

Hyponatremia/hypokalemia Severe hepatic, renal, or adrenal disease Hyperchloremic acidosis Chronic noncongestive angle-closure glaucoma Hypersensitivity to acetazolamide SE:

Taste disturbances Paresthesias Metabolic acidosis N/V; headache, malaise Depression Thrombocytopenia Risk of severe, potentially fatal skin reactions including Stevens-Johnson syndrome and Toxic Epidermal Necrosis, especially in those of Japanese or Korean descent.

dichlorphenamide (Daranide)

Loading dose of 100-200 mg followed by 100 mg q. 12 hr until desired response Onset: 1 hour


Same as above plus anorexia, N/V Drowsiness

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Selected Ophthalmic Medications





dorzolamide hydrochloride 2% sol. (Trusopt Ocumeter)


drop affected eye(s) TID

SE: same as above plus Bitter taste Superficial punctate keratitis Blurred vision Ocular burning Photophobia Conjunctivitis

methazolamide (Naptazane)

50-100 mg, BID or TID May be given in combination with miotic and osmotic agents Slower onset than acetazolamide, but duration is longer, lasting 10-18 hrs


Same as above

Osmotic agents: Given for the short-term reduction of vitreous volume and intraocular pressure as an adjunct in the management of acute glaucoma; may transiently reduce corneal edema.


1-1.5 mg/kg IVPB


Glycerin ophthalmic solution or oral solution 50% or 75% sol.

1-1.5 Gm/kg PO Onset: 1 - 1½ hours Duration: 5 hrs


Ocular pain if given topically, anesthetize eye prior to use

Parasympathomimetics: Constrict pupils (miotic), glaucoma - lowers ocular pressure by increasing aqueous outflow. Packaged with green tops



drop in affected eye of 1-2% solution Q


pilocarpine HCl (Ocusert Pilo, Pilocar, Pilopine HS, Salagen) 1%-


6-8 hr; or 0.5 inch ribbon of 4% gel in conjunctival sac HS or more often PRN; or 20-40 mcg/hr delivered via ocular system inserted Q 7 D

Hypersensitivity to pilocarpine products Acute iritis or glaucoma after cataract extraction Uncontrolled asthma Narrow-angle (angle-closure) glaucoma

Parasympatholytics: Dilate pupils (mydriasis), paralyze ciliary muscles to relieve photophobia (cycloplegia). Useful in conditions such as iritis where ciliary spasm is very painful, traumatic hyphema, also used as an aid in refraction, eye examinations, and other diagnostic purposes in children and adults. Packaged with red tops.

tropicamide (Mydriacyl, I-Picamide, Tropicacyl) 0.5%, 1.0%

1-2 drops 0.5% solution 15-20 minutes prior to eye exam, may repeat in 5 min Refractive procedures: 1-2 drops 1% solution; may repeat in 5 min Onset within 15 minutes; lasts about six hours


Narrow angle glaucoma Sensitivity to tropicamide SE:


Ocular burning Photophobia; blurred vision

cyclopentolate (Cyclogyl) 0.5%, 1%,

1-2 drops; repeat dose in 5-10 minutes if necessary in adults Onset 30-60 minutes with recovery of accommodation within 6-24 hours



Same as above plus Conjunctivitis, hyperemia Contraindications:


Can pressure in narrow angle glaucoma Myasthenia gravis Obstructive gastrointestinal disease Obstructive uropathy Paralytic ileus or intestinal atony Reflux esophagitis Ulcerative colitis or toxic megacolon Unstable cardiovascular status in acute hemorrhage

homatropine hydrobromide (Isopto Homatropine) 2%, 5% solution

Mydriasis: 1-2 drops, repeat 5-10 min PRN Uveitis: 1-2 drops Q 3-4 hr Lasts 1-3 days

Inferior compared to cyclopentolate. SE: Same as above plus Keratitis

Atropine 0.5%-1%


Rarely used as it lasts 5-10 days. Shorter acting cycloplegics are more desirable.

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Selected Ophthalmic Medications




Topical anesthetics: (white cap). Used for surface anesthesia in short ophthalmologic procedures such as tonometry, fitting of contact lenses, corneal abrasions, and minor eye surgery. These drops should not be used over a long period of time. Frequent or chronic use may result in acquired tolerance, severe corneal damage, and keratitis.

tetracaine hydrochloride 0.5%-1% sol. (pontocaine, Amethocaine)

1-2 drops


Hypersensitivity to ester-type anesthetics Inflamed or infected tissue Severe hypersensitivity to sulfite SE:


Local irritation and transient ocular burning Hypo or hypertension Systemic toxicity from CNS stimulation:

Hearing problems, visual disturbances Bradycardia, muscle twitching, seizures N/V

proparacaine hydrochloride 0.5% (Ak-taine, Alcaine, Fluoracaine, Kainair, Ocu-caine, Ophthaine, Ophthetic)

1-2 drops Onset: 30 seconds Duration: 15 minutes or longer


Same as above SE:


Above plus keratitis

benoxinate 0.4% sol (Fluress, Conjuncain, Novesine, Babesine, Flurecain, Fortasept, Novain, Oxbarukain, Prescaine, Univaine, Vesiform)

1-2 drops for tonometry 3-6 drops for removal of F/B from cornea Instill into the conjunctival sac at 30-90 second intervals. Onset within 1 minute; duration 20-30 minutes. Shorter duration of action than tetracaine. Anesthetic activity is 10 times that of cocaine and two times that of tetracaine


Same as above SE:

Same as above

diclofenac ophthalmic solution (Voltaren)

1 drop q. 6 hours while awake for 24 hours


Same as above SE:


Same as above

Micromedex Healthcare Series Vol. 113, 2002

General measures to avoid

- Anesthetic ointments. They have too prolonged an effect. The patient may inadvertently traumatize himself.

- Any anesthetic given to a patient for outpatient use. The patient may become addicted or may injure himself inadvertently. Prolonged use may cause sloughing of the cornea.

- Ointments of any kind when penetrating trauma is suspected or when fundoscopic examination will be required. They will blur vision, drops are preferred.

- Corticosteroids in any form. They may induce glaucoma, superimposed fungal infection or herpes. They will quiet down iritis.

- Never stain with Fluorescein until the presence of a soft lens is ruled out.

- Do not dilate a pupil in a patient with an intra-ocular lens implant.

- Do not use 10% Neo-Synephrine to dilate pupils in patients < 10 or > 60 years.

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Cuculino, G.P. & DiMarco, C.J. (2002). Common ophthalmologic emergencies: A systematic approach to evaluation and management. Emergency Medicine Reports, 23(13), 163-170.

Jenkins, C.N. & Thuau, H. (1997). Ultrasound imaging in assessment of fractures of the orbital floor. Clin Radiol, 52(9), 708-711.

Mieler, W.F. (2001). Ocular injuries: Is it possible to further limit the occurrence rate? Arch Ophthalmol 119, 1712-


Shingleton, B. & Meade, J. (1998). New England Eye Center Handbook of Eye Emergencies (pp. 45-49). Thorofare: Slack inc.

Shuttleworth, G.N., David, D.B., Potts, M.J., Bell, C.N., & Guest, P.G. (1999). Orbital trauma: do not blow your nose. BMJ 318, 1054-1055.

Woo, E. (2002). Retinal repair risks. Nursing Spectrum, 15(16)IL, 21.

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Bell's Phenomenon:

Reflex movement upward of eyes with eyelid closure.


Swelling of the conjunctiva around the cornea.


Pharmacologic paralysis of ciliary body musculature, reducing reactive spasm.


Inturning of eyelid and lid margin.




Inflammation of the cornea.


Incomplete lid closure.


Transition zone between clear cornea and white sclera.


Pupil dilation (opposite of miosis).

Phthisis bulbi:

End stage non-seeing eye, with associated shrinking and disorganization of intraocular contents.

Seidel test:

Use of fluorescein to detect perforating injury; leakage of aqueous humor will create green rivulets when observed with cobalt blue or Wood's light.


Inversion of hairs about an orifice, as eyelashes that turn in and cause irritation of the cornea.


The middle, pigmented, vascular layer of the eye consisting of the choroid, the ciliary body, and the iris. Also called the uveal tract.


Intraocular inflammation; may be anterior or posterior in location.

Eye Fun Facts:

You blink every 2-10 seconds. As you focus on each word in this sentence, your eyes swing back and forth 100 times a second; every second the retina performs 10 billion computer-like calculations.

The human eye can perceive more than 1 million simultaneous visual impressions and is able to discriminate among nearly 8 million gradations of color.

Having two eyes instead of just one provides us with stereo vision and depth perception. Each of our eyes views an object from a slightly different angle. Our brains put the different images together into one three- dimensional image.

The iris of the eye provides better identification than a fingerprint. A scan of the iris has 256 different unique characteristics. A fingerprint has only 40 (LWW.comInsider - December 2001).

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1. Matching



CN that closes the eyelid



CN that lifts the lid and pulls the eye to the nose



Structure that covers the pupil and iris forming a transparent, concave disc



Area of the retina responsible for all vision better than 20:200



Fluid contained in the anterior chamber



Tough, fibrous coat that serves as the structural skeleton of the globe



Region of the retina that becomes the origin of the optic nerve and is a

Acqueous humor H.

provides point of entry for the retinal vessels Gelatinous substance contained in the posterior cavity

Vitreous body I. Mucous membrane that lines the posterior surface of the eyelids and the anterior surface of the eye Optic disk J. Circular margin where the conjunctiva meets the cornea K. Disc-shaped structure changes its thickness and shape, thereby permitting images from varied distances to be focused on the retina

2. List four things you should ask about the patient's past ocular history.

4. List three things that can be detected by eye examination using a slit lamp.

5. List three things to observe when inspecting the orbit and periocular structures.

6. What color does a corneal defect stain after instillation of fluorescein?

What is a positive Seidel test?

7. What is the range for normal intraocular pressures?

8. Describe four methods used to assess visual acuity.

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10. What classic deficit in eye movement suggests a blow-out fracture?

A patient with a blow-out fracture is more likely to present with

A. exophthalmos.

B. enophthalmos.

Why is it important to instruct a patient with a blow-out fracture not to blow their nose or perform other Valsalva maneuvers?

11. What suture materials should you prepare if an eyelid will be primarily repaired in the ED?

12. What can be instilled into the eye prior to irrigating a chemical burn to relieve the severe pain?

13. What is the appropriate technique to irrigate an alkaline chemical burn to the eye?

What ocular pH should be achieved before irrigation is discontinued?

14. What is the appropriate management of a corneal abrasion?

Why should patients with corneal abrasions not be sent home with a bottle of a topical anesthetic?

15. What tools should you prepare for a physician to remove a superficial conjunctival foreign body?

What type of conjunctival foreign body may leave a rust ring?

16. What is the appropriate management of a patient with a hyphema?

17. What is the major complication of a hyphema?

What drug should the physician prescribe to reduce the risk of this complication?

18. What pupillary change suggests a ruptured globe?

True or false



Intraocular pressure must be measured in a patient with a suspected ruptured globe.



The nurse should remove blood clots, superficial foreign bodies, and avulsed tissue from the eye in the presence of a suspected perforated globe in order to facilitate an accurate eye exam.

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19. What should be placed over the eye if an intraocular foreign body is suspected?

If an intraocular F/B is dirt or vegetable material, what additional bacterial coverage must be present in the prescribed antibiotics?

20. What eye injury presents with painless visual field deficit where the patient complains of flashes of

light or sparks, floaters or black dots in his line of sight?