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The Eyes

Oct 03, 202461 min read

The eye is a sensitive, highly specialized sense organ subject to various disorders, many of which result in impaired vision. Impaired vision may affect individuals in many ways, including their independence in self-care, sense of self-esteem, safety, and overall quality of life. Many of the leading causes of visual impairment are associated with aging (e.g. cataracts, glaucoma. macular degeneration). Younger people are also at risk for eye disorders, particularly from traumatic injuries. All settings should assess visual acuity of those at risk (e.g. older adults, in hypertension, diabetics, and those with AIDS). Referral to eye care specialists aid in preventing further visual loss, and help patients adapt to impaired vision.

Anatomy of the Eye

Also read: Anatomy of the Eye The eye, unlike other organs, is available for external examination, and has simpler anatomy for assessment than other parts of the body.

  1. Orbit: the bony and protective region where the eyeball (or globe) is situated. It is lined with muscle, and connective and adipose tissues. It is shaped like a four-sided pyramid.
  2. Sinuses are air-filled spaces that surround the orbit on three sides: ethmoid (medial), frontal (superior), and maxillary (inferior).
  3. Optic Nerve and Ophthalmic Artery enter the orbit through its apex through the optic foramen.
  4. The Extraocular Muscles move the eyeball through all fields of gaze. There are four rectus (superior, inferior, medial, lateral) and two oblique (superior, inferior) muscles.
  5. Cranial Nerves III, IV, and VI (oculomotor, trochlear, abducens) (Also read: cranial nerve testing) innervate the extraocular muscles.
  6. Eyelids are composed of thin, elastic skin that covers striated and smooth muscles, and protects the anterior portion of the eye, as every blink allows it to “wash” the cornea and conjunctive with tears. It is innervated by the CN III They contain multiple glands (sebaceous, sweat, and lacrimal). Its margins contain meimbomian glands that, the inferior and superior puncta, and the eyelashes.
    • The triangular corners of the eye are called the inner and outer canthus.
  7. Tears are vital to eye health. They are formed by the lacrimal (crying) gland and the accessory lacrimal glands. They are secreted in response to reflex or emotional stimuli.
    • Tears are composed of three layers: lipoid, aqueous, and mucoid. These nourish the cornea and maintain a smooth optical surface of the cornea and conjunctival epithelium.
  8. Conjunctiva: a thin, transparent mucous membrane that provides a barrier to the external environment extending under the eyelids and over the sclera.
  9. The Eyeball is composed of three layers and is divided anatomically into two segments, and has three fluid-containing chambers.
    • Outer dense fibrous layer, including the sclera and transparent cornea
    • Middle vascular layer, containing the iris, ciliary body, and choroid
    • Inner neural layer, including the retina, optic nerve, and visual pathway
    • Anterior segment: between the anterior cornea and posterior iris, including the anterior and posterior chambers.
    • Posterior segment: between the posterior lens and the retina, including the vitreous chamber.
    • Anterior aqueous-filled chamber: between the posterior cornea and the anterior iris and pupil.
    • Posterior chamber: lies between the posterior iris and pupil and anterior lens.
    • Vitreous chamber: contains clear gelatinous vitreous fluid, and is the largest chamber in the ocular fundus between the lens and retina.
  10. Aqueous Humor: a transparent, nutrient-containing fluid that fills the anterior and posterior chambers and helps give the eye its shape. It is produced in the posterior chamber by the ciliary body, flowing through the pupil into the anterior chamber and draining through the trabecular meshwork into the canal of Schlemm. Production of aqueous humor is related to normal IOP, which is less than 21 mmHg.
  11. Vitreous Humor: composed of mostly water and is encapsulated by a hyaloid membrane. It helps maintain the shape of the eye. It is attached to the retina by scattered collagenous filaments.
    • This shrinks and shifts with age. With degeneration, its gel-like characteristics liquefy, causing stringy debris known as floaters.
  12. Sclera: a white, avascular, dense, and fibrous structure that helps maintain the shape of the eyeball and protects the intraocular contents. Scleral thinning and changes of the scleral collagen fibers can cause the underlying uveal pigment to be seen, resulting in a blue or gray sclera. The episclera is a vascularized, loose, elastic tissue that overlies the sclera, supplying nutritional support and reacting to inflammation.
  13. Cornea: a vulnerable transparent avascular dome-like structure, forming the most anterior portion of the eyeball, and is the main refracting surface of the eye. It is composed of five layers: epithelium (), Bowman’s membrane, stroma, Descemet’s membrane, and endothelium. It contains high concentrations of nerve fibers and is extremely sensitive to pain. (inc)

Ocular History

Questioning elicits necessary information for the diagnosis of an ophthalmic condition. Pertinent questions to ask when taking an ocular history include:

  • What does the patient perceive to be the problem?
  • Is visual acuity diminished?
  • Is the patient experiencing blurred, double, or distorted vision?
  • Is there pain? Is it sharp or dull? Does blinking make it worse?
  • Is the discomfort an itching sensation or more of a foreign-body sensation?
  • Are both eyes affected?
  • Is there a history of discharge? If so, inquire about the color, consistency, and odor.
  • What is the duration of the problem?
  • Is this a recurrence of a previous condition?
  • How has the patient self-treated?
  • What makes the symptoms improve or worsen?
  • Are there any systemic diseases? What medications are used in this treatment?
  • What other eye conditions does the patient have?
  • Is there a history of eye surgery?
  • Have other family members had the same symptoms or condition? Genetics may play a role in the causation and progression of eye and vision disorders.

Visual Acuity

Following health history, a patient’s visual acuity is assessed. This is a measure against which all therapeutic outcomes are based. It is tested for near (14 inches via a Rosenbaum pocket screener) and distance (20 feet via a Snellen chart) vision, performed separately for both eyes. Tumbling/Illiterate E Tests, Number Tests, or Picture Charts are used for illiterate patients or those who use other writing systems.

  1. Snellen Chart: a series of progressively smaller rows of letters. The patient is asked to read the lowest (smallest) line possible. Each line has its standardized score, with the smallest line being 20/20. The standard of vision (20/20) reflects normal vision, and indicates “able to see 20 feet away what a normal person can see 20 feet away”. As such, a reading of 20/100 would indicate that the patient is able to see only 20 feet away what a normal person can see 100 feet away.
  2. Counting Fingers (CF) Test: if the largest letter is unreadable, the nurse stands five feet from the person and holds up a random number of fingers, which the patient should state. If they are unable to, move one foot closer to the patient until they are able to. The result is recorded as CF/5, which indicates “can count fingers 5 feet away”.
  3. Hand Motion Test: if the patient is unable to count fingers, hand motions are used; moving the examiner’s hand up, down, or side-to-side, then asking the patient what direction the hand is moving in. This level of vision is known as hand motion.
  4. Light Perception: patients may only be able to see light, described as “having light perception”. If they are unable to perceive light, they have no light perception.

External Eye Examination

The nurse uses a systematic approach to perform an external eye examination. Assess for symmetry and placement of eyelids, pupils, and muscles. CNs III, IV, and VI (oculomotor, trochlear, abducens) control movement and pupil size.

  1. The eyelids should rest just above and below the corneal limbus without exposure of the sclera.
  2. Check for ptosis (drooping of the eyelid), ectropion (turning out of the lower eyelid), or entropion (turning in of the lower eyelid). Entropion may involve trichiasis (turning in of the eyelashes).
  3. Eyelids and lashes should be free of drainage and scaling.
  4. The room should be darkened so that the pupils can be examined. The pupillary response is checked with a penlight to determine if the pupils are equally reactive and regular. Pupils are normally black. Pupils may become abnormal due to trauma, previous surgery, or a disease process.
  5. Eyes are observed in primary or direct gaze, and any head tilt is noted. A head tilt may indicate CN palsy.
  6. Have the patient stare at a target; each eye is covered and uncovered quickly while the examiner looks for any shift in gaze.
  7. Nystagmus is noted when present.
  8. Extraocular movements are tested by having the patient follow the examiner’s finger, pencil, or a hand light through the six cardinal directions of gaze: up, down, right, left, and both diagonals.

Diagnostic Evaluation

Multiple diagnostic studies may be performed. Educate the patient about purpose, expectations, and any possible side effects related to the examinations prior to testing. Be aware of contraindications, complications, and trends in results (these provide information about disease progression and treatment response).

  1. Direct Ophthalmoscopy: the use of a handheld instrument with various plus and minus lenses that can be rotated into place, enabling the examiner to focus on different structures of the eye. The examiner should sketch the fundus and document and abnormalities.
    • Examine the fundus: vasculature comes into focus first. The veins are larger in diameter than the arteries. Focus on a large vessel and follow it towards the midline of the body, and it should lead to the optic nerve.
    • The optic disc is the central region of the eye where axons of the retinal ganglion cells pass. Document the disc margins as sharp or blurred. Silvery or coppery appearance suggests arteriolosclerosis.
    • The center of the optic disc has a depression known as the cup, normally a third of the disc’s diameter. Note its physiologic size.
    • Observe the periphery of the retina by having the patient shift their gaze.
    • The macula, the area most sensitive to light, is examined last. It is responsible for central vision.
    • The retina of a young person often has a glistening effect, sometimes referred to as a cellphone reflex.
    • Lesions, if any, are abnormal and should be noted. Look for any intraretinal hemorrhages (red smudges, or flame-shaped if hypertensive).
    • Lipids with a yellowish appearance may be present in patients with hypercholesterolemia or diabetes.
    • Soft exudates with a white, fuzzy appearance (i.e. “cotton -wool spots”) should be noted.
    • Microaneurysms should be noted. They appear as little red dots, and nevi.
    • Drusen (small, hyaline, globular deposits) appear as yellowish areas with indistinct edges (small ones have distinct edges). They are commonly found in macular degeneration.

Ophthalmoscopy

The examiner uses the same hand and eye side as the side being examined i.e. right hand and eye to examine the right eye of the patient, and vice versa. Encourage stable breathing, and have the patient stare at a target and keep both eyes open and steady.

  1. Indirect Ophthalmoscopy: an instrument used to see larger areas of the retina, although in an unmagnified state. It produces a bright, intense light. The light source is affixed with a pair of binocular lenses mounted on the examiner’s head. The ophthalmoscope is used with a handheld, 20-diopter lens.
  2. Slit-Lamp Examination: a table-mounted binocular microscope is used to examine the eye with a magnification of 10 to 40 times. Illumination can be varied for different parts of the eye, e.g. the anterior chamber can be examined for signs of inflammation, a different angle can evaluate cataracts, and a combination with a handheld contact lens allows for evaluation of the angle of the anterior chamber and ocular fundus.
  3. Tonometry: a common procedure for the measurement of IOP, which is normally below 21 mmHg. The device used is an accurately calibrated applanation tonometer, which measures how much pressure is required to flatten the cornea. This is used to screen for and monitor IOP in glaucoma.
    • Nursing Intervention: provide patient education prior to tonometry to help avoid possible errors in IOP measurement. Caution against squeezing the eyelids, holding their breath, or performing a Valsalva maneuver, as these may result in erroneously high IOP measurement.
  4. Color Vision Testing: color differentiation impacts ADL dramatically. Cones provide color vision (most concentrated in the macula). Basic tests such as asking the patient if an object looks redder in one eye than the other, can provide insight. Color vision deficits can be inherited (x-linked red-green color deficiency) or acquired (digitalis, cataracts).
    • The most common color vision test uses Ishihara Polychromatic Plates. A booklet contains plates with dots of primary colors in simple patterns integrated into a background of secondary colors. The patient is then tasked to determine the hidden pattern or figure.
    • Central vision conditions (e.g. macular degeneration) results in more difficult color identification compared to peripheral vision conditions (e.g. glaucoma)
  5. Amsler Grid: often used for macular problems, this consists of a geometric grid of identical squares with a central fixation point. The patient views the grid while wearing normal reading glasses. Each eye is tested separately. The patient is instructed to stare at the central fixation spot on the grid and report and distortion in the squares of the grid itself. For patients with macular problems, some squares may look faded, or some lines may appear wavy. Patients with age-related macular degeneration (AMD) can take home Amsler grids, and are encouraged to check the grids frequently to monitor macular function for early detection of changes requiring immediate attention.
  6. Ultrasonography: lesions in the globe or orbit may not be directly visible, or may be hidden by opaque media such as cataracts or hemorrhage. Brightness scan (B-scan) ultrasonography (USG) can identify pathologies such as orbital tumors, retinal detachment, and vitreous hemorrhage. Amplitude scan (A-scan) USG can measure the axial length for implants prior to cataract surgery.
  7. Optical Coherence Tomography: tomography involving low-coherence interferometry, where light is used to evaluate retinal and macular diseases as well as anterior segment conditions. This method is noninvasive and involves no physical contact with the eye.
  8. Fundus Photography: used to detect and document retinal lesions. The pupils are widely dilated before the procedure. Stereoscopic viewing of the photographs can show elevations such as macular edema.
  9. Laser Scanning: various techniques use laser light in evaluating eye disorders. Confocal laser scanning ophthalmoscopy provide a three-dimensional image of the optic nerve topography, and may be used along with fundus photography to provide comparative data for suspected optic nerve disease such as glaucoma and papilledema. Laser scanning polarimetry measures nerve fiber layer thickness and is an important indicator of glaucoma progression.
  10. Angiography: visualization and imaging of the retinal vessels.
    • Fluorescein angiography: used to evaluate clinically significant macular edema, document macular capillary nonperfusion, and identify retinal and choroidal neovascularization in AMD. The dye is injected often through the antecubital vein. Dye should appear in the retinal vessels within 10 to 15 seconds. Black and white photographs of the retinal vasculature are then taken over a 10-minute period.
    • Indocyanine green (IV) angiography: used to evaluate abnormalities in the choroidal vasculature, which are often seen in macular degeneration. Digital video angiography is used to capture multiple images.
  11. Perimetry Testing: evaluation of the field of vision. This helps identify which parts of the patient’s central and peripheral visual fields have useful vision. These are most helpful in detecting central scotomas (blind areas of vision) in macular degeneration, the peripheral field defects in glaucoma, and retinitis pigmentosa (night blindness). This is an especially useful monitoring tool for glaucoma progression.

Impaired Vision Disorders

Refractive Errors

Vision is impaired because a shortened or elongated eyeball prevents light rays from focusing sharply on the retina. This impairment may be corrected by eyeglasses or contact lenses.

  • Ophthalmic refraction determines refractive errors of the eye for vision correction, and consists of placing various types of lenses in front of the patient’s eyes to determine which lens best improves the patient’s vision.
  • LASER-assisted in situ keratomileusis (LASIK) procedures may be used to correct imperfections of the cornea or higher aberrations. Wavefront mapping technology is used to measure the unique refractive imperfections.
  • Emmetropia: the image is focused on the retina; normal refractive condition with no optical defects.
  • Myopia: the image is focused before it hits the retina (deep eyeball), resulting in nearsightedness.
  • Hyperopia: the image is not focused when it hits the retina (shallow eyeball), resulting in farsightedness.

Vision Impairment and Blindness

Vision impairment is defined as having central visual acuity of 20/40 or worse in the better eye with the best possible correction. Low vision describes visual impairment that requires the use of devices and strategies to perform visual tasks. Blindness is having a best corrected central visual acuity of 20/400 to no light perception (absolute blindness). Legal blindness only requires a best corrected central visual acuity of 20/200, or those whose widest visual field diameter is 20 degrees or less. This may range from inability to perceive light to having some vision remaining.

Diagnostic Examination

  1. Patient Interview: determine potential cause and duration of visual impairment. Customary ADLs, medication regimen, habits (e.g. smoking), acceptance of the physical limitations brought about by visual impairment, and realistic expectations of how low-vision aids are identified and included in the plan of care, as well as safety guidelines and referral to social services.
    • Retinitis pigmentosa is featured in genetic abnormality.
    • Diabetic macular edema typically feature fluctuating visual acuity.
    • Macular degeneration features central acuity problems that result in difficulties in activities requiring finer vision.
    • Peripheral field defects produce difficulty in mobility.
  2. Contrast-Sensitivity Testing measures visual acuity in different degrees of light and dark contrast to determine visual function. Glare testing measures visual acuity with glare, and also determines visual function.
    • Loss of contrast and glare sensitivity produce difficulty in low light environments, such as driving at night or in foggy conditions.

Medical Management

  1. Magnification and Image Enhancement through Low-vision Aids and Strategies: optimize the patient’s remaining vision and assist the patient to perform customary activities. These aids include hand magnifiers, bifocals, spectacles, and lightweight handheld monoscopes or telescopes.
  2. Medications may manage conditions that result in visual impairment, such as glaucoma.

Nursing Management

Sensitivity to challenges faced by patients with visual impairments is necessary. Emotional adjustment determines the success of the physical and social adjustments of the patient.

  1. Promote Coping: allow the patient to recognize the permanence of low vision or blindness. A newly visually impaired patient and family members can undergo various steps of grieving. Willingness to adapt to the changes influence successful rehabilitation of the patient with vision loss.
  2. Promote Spatial Orientation and Mobility: spatial concepts are required to perform some ADLs such as walking to a chair from a bed; their relative positions in the room should be known, and how to approach each area safely. Collaborative efforts between the patient and companions are required. Determine the degree of physical assistance required. Encourage independence and ensure safety.
  3. Promote Home, Community-Based, and Transitional Care: braille, service animals, print magnification technology, technology-assisted speech output, etc.

Ocular Medication Administration

The main goal of ocular medication delivery is to maximize the amount of medication that reaches the ocular site of action in sufficient concentration to produce a beneficial therapeutic effect, demonstrated by the dynamics of pharmacokinetics.

  • Absorption into the aqueous humor through the different routes of administration is determined by the characteristics of the medication. Natural barriers include: limited size of conjunctival sac (~50 mcL), worth ~2 drops of commercial topical ocular solutions (20 to 35 mcL); corneal membrane barriers; blood-ocular barriers; and tearing, blinking, drainage that dilute, wash out, or expel instilled eye drops.
  • Distribution vary by tissue type. Hydrophilic medications diffuse via intracellular diffusion, and lipophilic medications diffuse via intercellular diffusion. Topical administration usually does not reach the retina in adequate concentrations. If required, an intraocular injection is often chosen to bypass the natural barriers.
    • Aqueous solutions are the most affordable but have short corneal contact time as they become diluted from tears. Ophthalmic ointments improve concentration and retention, but blur vision. These are the best treatments used for the eyelids and their margins. Treatment for conjunctiva, limbus, cornea, and anterior chamber (this may also use subconjunctival injection) are effectively treated with instilled solutions or suspensions. High concentrations within the posterior chamber are delivered with intravitreal injections or systemically absorbed medications.
    • Contact lenses and collagen shields soaked in antibiotics may also be used for corneal infections.

Common Ocular Medications

These include topical anesthetics, mydriatic, and cycloplegic agents that reduce IOP; anti-infective medications; corticosteroids; NSAIDs; antiallergy medications; eye irrigants; and lubricants.

  1. Topical Anesthetic Agents: one or two drops of proparacaine hydrochloride and tetracaine hydrochloride are used prior to diagnostic procedures such as tonometry and minor ocular procedures such as removal of sutures or conjunctival or corneal scrapings. These may also be used for severe eye pain to allow the patient to open their eyes for examination or treatment (e.g. eye irrigation for chemical burns).
    • Onset occurs within 20 to 60 seconds, and lasts for 10 to 20 minutes.
    • Instruct the patient to not rub the eye while anesthetized, as this may result in damage to the cornea.
  2. Mydriatic and Cycloplegic Agents: “Mydriasis” or pupil dilation is the main objective of these medications. The two types function differently, and are used in combination to achieve maximal mydriasis that is needed during surgery and fundus examinations to give the ophthalmologist a better view of the internal eye structures.
    • Mydriatics potentiate alpha-adrenergic sympathetic effects that result in the relaxation of the ciliary muscle, causing dilation. This process, however, does not last long. The resultant light exposure stimulates miosis (pupillary constriction). Cycloplegic medications are given to paralyze the iris sphincter.
    • Effects of these drugs can last from 3 hours to several days. Difficulty reading, glare, and inability to focus the eyesight are common side effects. The patient is advised to wear sunglasses.
    • Other CNS manifestations may occur with patients, such as increased blood pressure, tachycardia, dizziness, ataxia, confusion, disorientation, incoherent speech, and hallucination.
    • Contraindications: patients with narrow angles or shallow anterior chambers, patients taking MAOIs, or patients taking TCAs.
  3. Glaucoma-Treating Medications are drugs that lower IOP either by decreasing aqueous production or increasing aqueous outflow. As these therapies are life-long, the patient must be educated with both ocular and systemic side effects of the medication. Read more: Glaucoma.
  4. Anti-Infective Medications: antibiotic (penicillin, cephalosporins, aminoglycosides, fluoroquinolones), antifungal (mainly amphotericin B), and antiviral agents (acyclovir, ganciclovir). Most are available as drops, ointments, or subconjunctival or intravitreal injections.
    • Side effects of Amphotericin, an antifungal, are serious. It includes severe pain, conjunctival necrosis, iritis, and retinal toxicity.
    • Antivirals are used for ocular infections associated with herpes virus or cytomegalovirus (CMV).
  5. Corticosteroids and NSAIDs are commonly used in inflammatory conditions of the eyelids, conjunctiva, cornea, anterior chamber, lens, and uvea. Other parts may be better treated with parenteral and oral routes.
    • Suspensions, when prescribed, require the patient to shake the bottle to promote mixture and maximize its therapeutic effect.
    • Common ocular side effects of long-term topical corticosteroid use are glaucoma, cataracts, susceptibility to infection, impaired wound healing, mydriasis, and ptosis. High IOP is reversible after discontinuation. NSAIDs are used as an alternative to avoid the side effects of corticosteroids.
  6. Antiallergy Medications: allergies (e.g. allergic conjunctivitis) are extremely common, primarily from environmental allergens. Corticosteroids are commonly used as anti-inflammatory and immunosuppressive agents to control ocular hypersensitivity reactions.
  7. Ocular Irrigants are mostly used to maintain lid hygiene, normalize pH (e.g. in chemical burns), eliminate debris, or to inflate the globe intraoperatively. Lubricants, like artificial tears, help alleviate corneal irritation, such as dry eye syndrome. These are preparations of carboxymethylcellulose or hydroxypropyl methylcellulose eye drop solutions, ointments, or ocular inserts (inserted at the lower conjunctival cul-de-sad once each day). Depending on the severity, eye drops can be instilled as often as every hour.
    • The corneal surface should not be irrigated in cases of threatened corneal perforation.
    • When chemical burns occur, NSS is commonly used to irrigate the corneal surface.

Instilling Eye Medications

  1. Patient Instructions:
    • Never use eye solutions that have changed colors.
    • Perform hand hygiene before and after instillation. Avoid touching the bottle to your eye or face, as this may contaminate it with bacteria.
    • Ensure adequate lighting.
    • Read the label of the eye medication to verify correct medication.
    • Remove contact lenses as needed.
    • Assume a comfortable position. Lying down is an easy method to ensure the drop enters the eye.
    • Hold the lower eyelid down, applying gentle pressure on the cheekbone (not the eye!) to anchor it down.
  2. Instillation:
    • Eye drops come before ointments.
    • Apply a 0.25 to 0.5 inch ribbon of ointment to the lower conjunctival sac.
  3. Absorption:
    • Keep the eyelids closed, applying gentle pressure on the inner canthus (for punctal occlusion) near the bridge on the nose for 1 to 2 minutes immediately after instillation.
    • Use a clean tissue to gently pat skin to absorb excess eye drops that run onto the cheeks.
    • Wait 5 minutes before another eye drop, and 10 minutes before another ointment.
    • Reinsert contact lenses (if applicable)

Nursing Management

  1. Ensure proper administration and maximize the therapeutic effects.
    • Inform the patient of the temporary side effects of instillation: blurred vision, stinging, and a burning sensation.
    • The patient may refrigerate their eye drops if they are unable to feel the drop when instilled. A cold drop is easier to detect.
  2. Ensure safety by monitoring for side effects (local and systemic).
    • Make sure to occlude the puncta to avoid systemic nasolacrimal duct absorption, especially for patients most vulnerable to medication overdose (older adults, pregnant or lactating women, and patients with cardiac/pulmonary/hepatic/kidney disease).
    • A five-minute interval between different types of ocular drops is recommended.
    • Prevent infection: maintain meticulous hand hygiene before and after instillation. Never touch any part of the eye with the tip of the eye drop bottle or ointment tube. Recap them immediately after use.

Glaucoma

Glaucoma is a term to denote any ocular condition characterized by elevated IOP, which, if left untreated, damages the optic nerve and nerve fiber layer to varying degrees. Damage from IOP is caused by congestion of aqueous humor in the eye. A range of IOP may be normal, but these may be associated with vision loss in some patients. Glaucoma is more prevalent in people order than 30 years old, and is the third most common age-related eye disease (in the U.S.). There is no cure for Glaucoma, but the disease can be controlled. Some risk factors include:

  • Black of Asian race
  • Cardiovascular disease
  • Diabetes
  • Family history
  • Migraine syndromes
  • Myopia
  • Obstructive sleep apnea
  • Older age
  • Previous eye trauma
  • Prolonged use of topical or systemic corticosteroids
  • Thin cornea

Physiology

Aqueous humor flows between the iris and the lens, nourishing the cornea and lens. Most (90%) of the fluid then flows out of the anterior chamber, draining through the spongy trabecular meshwork into the canal of Schlemm and the episcleral veins. About 10% of the aqueous fluid exits through the ciliary body into the suprachondrial space and then drains into the venous circulation of the ciliary body, choroid, and sclera.

  • Unimpeded outflow of aqueous fluid depends on intact drainage system and an open angle (~45°) between the iris and the cornea. A narrower angle places the iris closer to the trabecular meshwork, diminishing the angle.
  • Age, diabetes, and inflammatory ocular conditions tend to diminish the amount of aqueous humor produced.
  • IOP is determined by the rate of aqueous production, the resistance encountered by the aqueous humor as it flows out of the passages, and the venous pressure of the episcleral veins that drain into the anterior ciliary vein. When balanced, IOP is maintained around 10 to 21 mmHg.
  • Fluctuations in IOP occur with time of day, exertion, diet, and medications. It increases with blinking, tight lid squeezing, and upward gazing. Systemic conditions such as diabetes and intraocular conditions such as uveitis and retinal detachment have been associated with elevated IOP.
  • Thin corneas may result in false low IOP readings during tonometry.

Pathophysiology

Some glaucomas appear as exclusively mechanical, and some are exclusively ischemic types. Typically, most cases are a combination of both.

  1. Direct Mechanical Theory suggests that high IOP damages the retinal layer as it passes through the optic nerve head.
  2. Indirect Ischemic Theory suggests that high IOP compresses the microcirculation in the optic nerve head, resulting in cell injury and death.

Classifications

Glaucoma may be primary or secondary, depending on whether associated factors contribute to the rise of IOP. Two common clinical forms of glaucoma are wide-angle and narrow-angle forms, which produce different mechanisms that impair aqueous flow.

  1. Wide-angle Glaucoma: often bilateral, but may be asymmetrical in severity. The anterior chamber angle remains open and appears normal.
    • Normal-tension Glaucoma: IOP is 21 mmHg or below. Optic nerve damage occurs, with visual field defects.
      • If medical management is unsuccessful, laser trabeculoplasty (LT) can decrease IOP by 20%. If optic nerve damage continues, glaucoma filtering surgery may be used.
    • Ocular Hypertension: elevated IOP with possible ocular pain or headache. Ideal management is unestablished. The goal is to lower IOP by at least 30%.
  2. Narrow-angle Glaucoma: partial closure of the angle from the forward shift of the peripheral iris to the trabecula, resulting in increased IOP.
    • Acute Angle-closure Glaucoma: rapidly progressing visual impairment, periocular pain, reduced central visual acuity, severely elevated IOP, corneal edema, vertically oval appearance of the pupil fixed in a semidilated position, unreactive to light and accommodation. This is an ocular emergency.
      • Administration of hyperosmotics, acetazolamide, and topical ocular hypotensive agents is done.
      • Possible laser iridotomy to release blocked aqueous and reduce IOP.
      • The unaffected eye is treated with pilocarpine eye drops and/or surgical management to avoid a similar spontaneous attack.
    • Subacute Angle-closure Glaucoma: transient blurry vision, halos around light, temporal headaches and/or ocular pain, and potential semidilation of the pupil.
      • Prophylactic peripheral laser iridotomy, as this can lead to acute or chronic angle-closure glaucoma if untreated.
    • Chronic Angle-closure Glaucoma: progression of glaucomatous cupping and significant visual field loss; IOP may be normal or elevated; ocular pain and headache.
      • Laser iridotomy and medication.
  3. Congenital Glaucoma
  4. Glaucoma Associated with Other Conditions such as developmental anomalies or the use of corticosteroids.

Clinical Manifestations

Most patients are unaware that they have this disorder until visual changes and vision loss is experienced, granting it the name “silent thief of sight”. The patient may only seek health care when they experience blurred vision, halos around lights, difficulty focusing, difficulty adjusting eyes in low lighting, loss of peripheral vision, aching or discomfort around the eyes, and headache.

Diagnostic Examination

The purpose of a glaucoma workup is to establish the [[#Glaucoma#Classifications|diagnostic category]], assess optic nerve damage, and formulate a treatment plan.

  1. Ocular and medical history must be detailed to investigate the history of predisposing factors.
  2. Tonometry to measure IOP
  3. Ophthalmoscopy to inspect the optic nerve
    • Pallor (lack of blood supply) and cupping (exaggerated bending of blood vessels as they cross the optic disk, making a “basin-like” appearance) of the optic nerve disc. Cupping worsens with continued loss of retinal nerve fibers and blood supply.
  4. Central Visual Field Testing
    • Visual perception decreases as optic nerve damage increases. Localized areas of visual loss (scotomas) represent loss of retinal sensitivity and nerve fiber damage. These are measured and mapped on a graph, which forms a visual change map distinct to glaucoma.

Medical Management

The aim of all glaucoma treatment is to prevent optic nerve damage. Achieve the greatest benefit at the least risk, cost, and inconvenience to the patient. Maintain an IOP within a range unlikely to cause further damage. Initial goals for IOP reduction in patients with ocular hypertension and low-tension glaucoma associated with progressive visual field loss is 30% less than initial findings. With the lack of a cure, treatment is life-long. Pharmacologic therapy, laser procedures, surgery, or a combination of these approaches, all of which have potential complications, is used.

  1. Pharmacologic Therapy: systemic and topical ocular medications that lower IOP. Disease monitoring and treatment evaluation is essential. The patient is typically started on the lowest dose of topical medication and then advanced until desired IOP level is reached and maintained. If IOP elevation is unilateral, one eye is treated first, to allow the untreated eye to remain as a control variable. Treatment is started on the other eye once efficacy has been established (lowered IOP, stable optic nerve head, maintained visual field). If unsatisfactory, a new medication is used.
    • Beta-blockers (Timolol, Maleate) decrease aqueous humor production and are the preferred initial topical medication.
    • Alpha-adrenergic Agonists (Apraclonidine, Brimonidine) decrease aqueous humor production.
    • Cholinergics, functioning as miotics (Pilocarpine, Carbachol Intraocular), increase aqueous fluid outflow by contracting the ciliary muscle, and causing miosis and opening of trabecular meshwork.
    • Carbonic Anhydrate Inhibitors (Acetazolamide, Dorzolamide) decrease aqueous humor production.
    • Prostaglandin Analogues (Latanoprost, Bimatoprost) increase uveoscleral outflow.
  2. Surgical Management: reserved for patients in whom pharmacologic treatment has not been effective. Minimally invasive procedures have been specifically designed to improve drainage to balance IOP.
    • Trabeculectomy is performed through a small incision and does not require the creation of a permanent hole in the eye wall or an external filtering bleb or an implant.
    • Laser Trabeculoplasty (LT) applies a laser beam into the inner surface of the trabecular meshwork to open the intratrabecular spaces and widen the canal of Schlemm, promoting outflow of aqueous humor. This is contraindicated if a narrow angle obstructs full visualization of the trabecular meshwork.
    • Peripheral (Laser) Iridotomy is a procedure for pupillary block glaucoma. An opening in the iris is made to eliminate the blockage. This is contraindicated in patients with corneal edema, which interferes with laser targeting and intensity. Complications include burns on the cornea, lens, or retina; transient elevated IOP; closure of the iridotomy; uveitis; and blurring.
    • Filtering Procedures for glaucoma are used to create an opening or fistula in the trabecular meshwork to drain aqueous humor from the anterior chamber to the subconjunctival space into a bleb (fluid collection outside of the eye), bypassing the usual drainage structures. A common form of this is a trabeculectomy. Complications include hemorrhaging, extremely low (hypotonic) or extremely elevated IOP, uveitis, cataracts, bleb failure, bleb leakage, and endophthalmitis (an intraocular infection).
    • Drainage implants or shunts are tubes implanted in the anterior chamber to shunt aqueous humor to the episcleral plate in the conjunctival space. Implants are used when failure has occurs with one or more trabeculectomies in which antifibrotic agents were used.

Nursing Management

Education is required for adherence to lifelong therapy. Individualize the education plan. The use of a structured self-management program may increase adherence. Discussions about medication is crucial.

  • Ensure ability to instill eye medications by the patient or their caretakers.
  • Emphasize importance of follow-up appointments and monitoring.
  • Drug interactions should also be determined and explained e.g. the diuretic effects of acetazolamide with diuretic effects of some antihypertensive medications.

Cataracts

A cataract is a lens opacity or cloudiness that result in visual disability, being a leading cause of blindness in the world. By 80 years of age, over half of all Americans have cataracts. (Prevent Blindness America, 2020)

Pathophysiology

Cataracts may develop in one or both eyes at any age. The three most common types are traumatic, congenital, or senile cataracts. A variety of risk factors (associated ocular conditions, toxic factors, nutritional factors, physical factors, and systemic diseases or syndromes) exist, but aging is the most common one.

Clinical Manifestations

Painless, blurry vision is characteristic of cataracts. The person perceives that surroundings are dimmer, as if they glasses need cleaning. Light scattering is common, and the person experiences reduced contrast sensitivity, sensitivity to glare, and reduced visual acuity. Other effects include myopic shift (return of near vision), astigmatism (refractive error due to an irregularity in the curvature of the cornea), monocular diplopia, and color changes as lens become more brown in color.

Diagnostic Examination

  • Decreased visual acuity is directly proportionate to cataract density.
  • Snellen Visual Acuity Test, Ophthalmoscopy, and Slit-Lamp Biomicroscopic Examination are used to establish the degree of cataract formation.
  • The degree of opacity does not always correlate with status; some patients perform normal activities despite clinically significant cataracts. Visual acuity is an imperfect measure of visual impairment.

Medical Management

There are no nonsurgical measures that treat cataracts or prevent age-related cataracts. Optimal medical management is prevention. Patients should be educated about risk reduction strategies:

  • Smoking cessation, weight reduction, optimal blood glucose control (diabetics)
  • Wearing sunglasses outdoors to prevent early cataract formation.

Surgical management is not needed if reduced vision from cataracts do not interfere with normal activities. The patient’s functional and visual status are the primary considerations when deciding if cataract surgery should be performed. Restoration of visual function through a safe, minimally invasive procedure is the surgical goal, with advances in topical anesthesia, smaller wound incision, and lens design. Cataract removal is common, and is performed on an outpatient basis, usually taking less than 1 hour and patient discharge within 30 minutes after the procedure. Complications (hemorrhaging, infection, inflammation, malpositioned intraocular lens, opacification of the posterior capsule) are uncommon, but may still occur.

  • Injection-free Topical and Intraocular Anesthesia, such as 1% lidocaine gel is applied to the surface of the eye. IV Sedation may be used to minimize anxiety and discomfort.
  • If cataracts are bilateral, one eye is treated first to preclude whether the other eye should also be treated. The interval is several weeks, preferable months.
  1. Phacoemulsification: an extracapsular cataract surgery where a portion of the anterior capsule is removed, allowing extraction of the lens nucleus and cortex while the posterior capsule and zonular support are left intact.
    • The lens nucleus and cortex are liquefied with an ultrasonic device then suctioned out through a tube.
    • A small incision on the upper edge of the cornea and viscoelastic substance (clear gel) is injected into the space between the cornea and the lens, preventing the space from collapsing facilitating the insertion of the IOL.
    • Results in early stabilization of refractive error, and less astigmatism.
  2. Lens Replacement: after removal of the crystalline lens, the patient is referred to as aphakic (i.e. without lens). The lens that focuses light on the retina needs to be replaced. There are three options:
    • Aphakic Eyeglasses: are rarely used despite their effectivity, as objects become 25% magnified, causing distortion and limited peripheral vision.
    • Contact Lenses: corrects to almost normal vision; when removed as necessary, the patient uses aphakic eyeglasses. These are not advised for patients who have difficulty inserting, removing, and cleaning them. Frequent handling and improper disinfection increases risk of infection.
    • IOL Implants: the most common approach for lens replacement, like in cataract extraction or phacoemulsification. Complications (error, infection) are uncommon. This is contraindicated in patients with recurrent uveitis, proliferative diabetic retinopathy, neovascular glaucoma, or rubeosis iridis.

Nursing Management

  1. Provide Preoperative Care: receive the usual preoperative care for ambulatory surgical patients undergoing eye surgery. The standard battery of tests (CBC, ECG, Urinalysis) are only done when indicated by medical history.
    • Alpha-antagonists (particularly tamsulosin, used for prostate enlargement) are known to cause intraoperative floppy iris syndrome. Miosis and iris prolapse leads to complications. Ask the patient about history of its use, as it may occur even after cessation. Alert the team to this complications.
    • Dilating drops (mydriatics) is given prior to surgery. Patient education is begun about eye medications that will need to be self-administered to prevent postoperative infection and inflammation.
  2. Provide Postoperative Care: before discharge, written and verbal education about eye protection, administration of medications, recognition of complications, activities to avoid, and obtaining emergency care is done.
    • An eye shield is often used for the first week to avoid injury.
    • Mild analgesia (e.g. acetaminophen) may be taken as needed.
    • Antibiotic, anti-inflammatory, and corticosteroid eye drops or ointments are prescribed postoperatively. Anti-inflammatory and corticosteroid use should be monitored for increased IOP.
  3. Self-care: the patient wears a protective eye patch for the first ~24 hours, then eye glasses during the day and an eye shield at night. Educate the patient about applying and care of the eye shield, if recommended. Sunglasses should be worn outside due to light sensitivity.
    • Slight morning discharge, some redness, and a scratchy feeling may be expected for a few days. Clean, damn cloth can be used to remove discharge.
    • Inform the physician if floaters, flashing lights, decrease in vision, pain, or increase in redness occurs. The risk of retinal detachment increases after surgery.

Corneal Disorders

  1. Corneal Dystrophies
  2. Keratoconus
  3. Fuchs Endothelial Dystrophy

Corneal Surgeries

  1. Phototherapeutic Keratectomy (PTK): a laser removes corneal opacities and smooths the anterior corneal surface to improve functional vision. Contraindicated in patients with active hepatic keratitis as the latent virus may be reactivated by the ultraviolet rays.

  2. Penetrating Keratoplasty: corneal transplantation or grafting; replaces abnormal host tissue with healthy donor tissue. Sutures are used and remain in place for 12 to 18 months then removed. Early (poor quality, trauma, infection, increased IOP) and late (rejection) graft failure may occur.

  3. Keratoprosthesis: used in multiple graft failures or severe corneal disease; an (FDA approved) artificial cornea is used. Serious potential complications exist (glaucoma, endophthalmitis) and required close follow-up and monitoring.

  • Nursing Management: visual rehabilitation and visual improvement. Resulting vision may not be of great quality and takes months to return normal color vision. Correction of resultant refractive errors will determine final visual outcome.
    • Assess support systems and ability to comply with long-term follow-up (e.g. frequent clinic visits for tapering corticosteroid therapy, suture removal, ongoing evaluation).
    • Primary goal: educate patient to identify signs and symptoms of graft failure. Early signs include blurred vision, discomfort, tearing, or redness of the eye. Decreased vision results after graft destructions. Contact the ophthalmologist as soon as symptoms occur. Treatment of graft rejection usually involves prompt administration of hourly topical corticosteroids and periocular corticosteroid injections. Systemic immunosuppressive agents may be necessary for severe, resistant cases.

Refractive Surgeries

Elective procedures performed to correct refractive errors (myopia or hyperopia) and astigmatism by reshaping the cornea. Laser Vision Correction alters the major optical function of the eye and carries risks. Precise visual outcome cannot be guaranteed. Both the cornea and the error itself must be stable. Patients with conditions that are likely to adversely affect corneal wound healing are not good candidates for surgery. Any superficial eye disease must be diagnosed and treated before a refractive procedure.

  1. Laser Vision Correction Photorefractive Keratectomy: an excimer laser is applied directly to the cornea, which decreases relative curvature for myopia, or increases relative curvature with hyperopia. A bandage contact lens (like the one used in corneal abrasion) is used for promoting epithelial healing.
    • Laser-Assisted In Situ Keratomileusis (LASIK) flattens the anterior curvature of the cornea by removing a stromal lamella or layer. Corneal tissue is cut (not completely) to access the stromal bad, where the laser acts. There are few adverse outcomes of this procedure. Effectivity of myopic correction compared to PRK has not been determined.
    • Errors in LASIK may result in central islands and decentered ablations, resulting in monocular diplopia, halos, glare, and decreased visual acuity.
  2. Phakic Intraocular Lenses: increasingly being used for moderate to severe myopia. Phakic IOLs may be used in either the anterior or posterior chamber. Because it leaves the natural lens and anatomy in place, this surgery is reversible, and produce more predictable results. It is safer, and has higher patient satisfaction scores. Complications include cataract, iritis/uveitis, endothelial cell loss, and increased IOP.
  3. Conductive Keratoplasty: correction of low to mild hyperopia using thermal keratoplasty, applying a radiofrequency current to the peripheral cornea with a thin, handheld probe. This does not involve the removal of corneal tissue.

Retinal Disorders

The two most commonly implicated layers are the sensory retina and the retinal pigment epithelium.

Retinal Detachment

The separation of the retinal pigment epithelium (RPE) from the neurosensory layer. There are four types:

  1. Rhegmatogenous Retinal Detachment: the most common form, where a hole or tear develops in the sensory retina, allowing liquid vitreous to seep through and detach the RPE. People at risk for this form include those with high myopia or are aphakic. Trauma may also play a role. Between 5% to 10% of this form are from proliferative retinopathy, which is associated with diabetic neovascularization.
  2. Traction Retinal Detachment: a tension or pulling force physically detaches the RPE from the neurosensory layer. In general, patients with this type have developed fibrous scar tissue that exert a pulling force on the delicate retina. This tissue may form in diabetic retinopathy, vitreous hemorrhage, or retinopathy of prematurity. All the scars or bands of fibrous material providing traction are released.
  3. Combined form of Retinal Detachment
  4. Exudative Retinal Detachment

Clinical Manifestations

Patients feel no pain, but RD is an ocular emergency requiring immediate surgical intervention. Patients report a sensation of a “shade” or “curtain” coming across the vision of one eye, cobwebs, bright flashing lights, or the sudden onset of a great number of floaters.

Diagnostic Examination

All degenerative changes, retinal breaks, and fibrous bands that may be causing traction on the retina must be identified.

  • Determine visual acuity
  • Dilated fundus examination using an indirect ophthalmoscopy an d slit-lamp biomicroscopy
  • Stereo fundus photography and fluorescein angiography are commonly used.
  • Optical coherence tomography and ultrasound are used for complete retinal assessment, especially if the view is blocked by a dense cataract or vitreal hemorrhage.

Surgical Management

In rhegmatogenous retinal detachment, an attempt is made to surgically reattach the sensory retina to the RPE. In traction retinal detachment, an all sources of traction must be removed and the sensory retina reattached. The most common procedures include:

  1. Scleral Buckle: the globe is compressed with a scleral buckle or silicone band to indent the scleral wall from the outside of the eye, bringing the two retinal layers in contact with each other.
  2. Vitrectomy: a light source is introduced intraocularly through an incision, and a second incision allows for the vitrectomy. Traction may be relieved through vitrectomy, and may be combined with scleral buckling to repair retinal detachments. A gas bubble, silicone oil, or perfluorocarbon may be injected into the vitreous cavity to help push the sensory retina up against the RPE.

Nursing Management

Educate the patient and provide supportive care.

  • Postoperatively, if a gas bubble is used, the patient is positioned prone to ensure the gas functions as a tamponade, applying consistent pressure to reattach the sensory retina. Inform the patient and family prior to procedure to ensure maximal comfort.
  • Complications may include increased IOP, endophthalmitis, retinal detachment, and cataract development. Educate the patient about the signs and symptoms of these complications (esp. IOP and infection).

Retinal Vascular Disorders

Loss of vision can occur from occlusion of a retinal artery or vein. Such occlusions may result from atherosclerosis, valvular heart disease, venous stasis, hypertension, or increased blood viscosity. Associated risk factors include diabetes, glaucoma, and aging.

Central Retinal Vein Occlusion

Blood supply to and from the ocular fundus is provided by the central retinal artery and vein. CRVOs are found most often in people over 50 years old. They report variable decreased visual acuity ranging from mild blurring to severely limited.

  • Direct ophthalmoscopy show optic disc swelling, venous dilation, tortuousness, retinal hemorrhages, cotton-wool spots, and a bloody appearance of the retina.
  • Fluorescein angiograhy show extensive areas of capillary closure. Signs of neovascularization and neovascular glaucoma should be monitored for a several months.
  • Laser panretinal photocoagulation may be necessary to treat abnormal neovascularization.
  • Complications of CRVO are related to neovascularization: macular edema, macular nonperfusion, and vitreous hemorrhage
  • Better visual acuity is related to better prognosis.

Branch Retinal Vein Occlusion

BRVO may appear symptom-free, while others present with sudden loss of vision if the macular area is involved Gradual loss of vision may occur if macular edema in BRVO develops.

  • The ocular fundus appears similar to that in CRVO. Occlusions generally occur at the arteriovenous crossings. Diagnosis, follow-up assessments, and complications are the same as CRVO.
  • Associated conditions include glaucoma, systemic hypertension, diabetes, and hyperlipidemia.

Central Retinal Artery Occlusion

Relatively rare disorder that is a true ocular emergency. Visual loss associated with CRAO is severe and permanent. Presents with sudden vision loss. Visual acuity is reduced to CF level, or the field of vision is tremendously restricted.

  • A relative afferent pupillary defect is present. Examination of the fundus reveals a pale retina with a cherry-red-spot at the fovea.
  • Various treatments may include ocular massage, anterior chamber paracentesis, hyperbaric oxygen therapy, topical ocular hypotensive agents, anticoagulation, and intravenous mannitol and acetazolamide.

The leading cause of irreversible blindness and visual impairment in the world. AMD is characterized by drusen (clusters of debris or waste material) beneath the retina. A wide range of visual loss is experienced. Only a small portion experience total blindness. Most patients retain peripheral vision. There are two types of AMD:

  1. Dry Type AMD makes up 85% to 90% of people with AMD. The outer layers of the retina slowly break down, with the breakdown forming drusen. If this drusen forms outside of the macular area, no symptoms generally occur. If it does, however, there is a gradual blurring of vision that patients may notice when they try to read.
  2. Wet Type AMD: the neovascular or exudative type. These have abrupt onsets and are more damaging to vision. Patients report that straight lines appear crooked and distorted, or letters in words appear broken. This is a result of proliferation of abnormal blood vessels growing under the retina, within the choroid layer (choroidal neovascularization). The affected vessels can leak fluid and blood, elevating the retina.
    • Some patients may be treated with laser therapy to stop leakage from these vessels.

Medical Management

There is no known effective treatment or cure for dry advanced macular degeneration. An important component of treatment of wet AMD targets development and progression of angiogenesis. Vasoproliferation is believed to be caused by an underlying angiogenic stimulus (vascular endothelial growth factor; VEGF). Inhibitors for VEGF available by intravitreal injection include Ranibizumab and Brolucizumab.

Nursing Management

Amsler grids are given to patients to use in their homes to monitor for sudden onset or distortion of vision, potentially providing the earliest sign of progressing macular degeneration.

  • These should be used several times each week for each eye with glasses on if necessary. Any changes should prompt the client to inform the ophthalmologist. Digital forms of these grids are also available.

Orbital Trauma

  1. Orbital Trauma: often associated with a head injury; hence, the patient’s general medical condition must be stabilized before conducting an ocular examination. During inspection, the face is meticulously assessed for underlying fractures, which should always be suspected in blunt trauma.
    • Assess visual acuity as soon as possible, to determine the extent of ocular injury. Even a rough estimate is useful.
    • Soft tissue orbital injuries often result in optic nerve damage.
    • Major ocular injuries indicated by a soft/ruptured globe, prolapsing tissue, and hemorrhage require surgical attention.
  2. Soft Tissue Injury and Hemorrhage: signs and symptoms of blunt or penetrating trauma include tenderness, ecchymosis, lid swelling, exophthalmos, and hemorrhage.
    • Closed injuries result to contusions with subconjunctival hemorrhage, commonly referred to as a “black eye”. Blood accumulates in the tissues of the conjunctiva.
    • Hemorrhage may be caused by soft tissue injury to the eyelid or by an underlying fracture.
    • Management for soft tissue hemorrhage that does not threaten vision is often conservative, consisting of thorough inspection, cleansing, and repair of wounds. Cold compresses are used in the early phase, followed by warm compresses. Hematomas that appear as swollen, fluctuating areas may be surgically drained or aspirated; if significant orbital pressure occurs from hematoma, they may be surgically evacuated.
  3. Orbital Fractures: detected by facial x-rays. These may be classified as blowout, zygomatic or tripod, maxillary, midfacial, orbital apex, and orbital roof fractures depending on the structures involved.
    • Blowout fractures result from compression of soft tissue and the sudden increase in orbital pressure when the force is transmitted to the orbital floor, which is the area of least resistance. The inferior rectus and inferior oblique muscles, along with their fat, fascia, or the nerves that run across them, may become entrapped, resulting in enophthalmos. Computed tomography scanning can identify the muscle and its axillary structures that are entrapped. These fractures are often caused by blunt forces from a fist or baseball.
    • Orbital roof fractures are dangerous due to potential complications to the brain. Surgical management requires a neurosurgeon and an ophthalmologist. The most common indications for surgical intervention are displacement of bone fragments, disfiguring the normal facial contours; interference with normal binocular vision (extraocular muscle entrapment); interference with mastication (zygomatic fractures); and obstruction of the nasolacrimal duct.
  4. Foreign bodies that enter the orbit are often tolerated, except for steel, copper, iron, and vegetable materials that may cause purulent infection. A careful history is important, especially if the foreign body has been present for a long time and the incident forgotten. It is important to identify metallic foreign bodies, because they prohibit the use of MRI.
    • X-rays and CT scans are used to identify the foreign body.
    • Foreign bodies are removed if they are superficial and anterior in location, have sharp edges, or are composed of copper, iron, or vegetable material. Surgical interventions are directed at preventing further injury and maintaining the integrity of the affected areas. Cultures are usually obtained, and the patient is placed on prophylactic IV antibiotic medications that are later changed to an oral route.

Ocular Trauma

A leading cause of blindness among children and young adults, especially male trauma victims. These occur with occupational injuries, contact sports, weapons, assaults, motor vehicle crashes, and explosions. There are two types in which the first response is critical:

  1. Chemical Burns: the eye should be immediately irrigated with tap water or normal saline solution.
  2. Intraocular Foreign Object: no attempt to remove the foreign object shall be made. It object should be to protect from jarring or movement to prevent further damage. No pressure or patch should be applied to the affected eye.
  3. All other traumatic eye injuries should be protected using a patch or shield if available or a stiff paper cup until medical treatment can be obtained.

Diagnostic Examination

A thorough history is obtained, particularly in assessing the patient’s ocular history, such as pre-injury vision or past ocular surgery. Thorough relevant information regarding the injury should be obtained e.g. the nature of injury (blunt or penetrating), activity or nature of the force (assault, contact sports), onset of vision loss (sudden, slow, or progressive).

  • In eye burns, determine the chemical agent and test for pH if possible.
  • Examine the cornea for abrasion, foreign bodies, and wounds.
  • Pupil size, shape, and light reaction is compared with the unaffected eye. Ocular motility is also assessed.

Medical Management

  1. Splash Injuries: irrigation with NSS before evaluation. If ruptured, cycloplegic agents (ciliary paralysis) or topical antibiotics must be deferred due to potential toxicity to exposed tissues. Manipulation is deferred until the patient is under GA.
    • Parenteral broad-spectrum antibiotics are initiated
    • Tetanus antitoxin is given in indicated. Full thickness ocular and skin wounds indicate for Tetanus prophylaxis.
    • Analgesic agents
    • All topical medications should be sterile.
  2. Foreign Bodies and Corneal Abrasions: (1) removal of foreign body, (2) antibiotic ointment is applied, (3) eye is patched, (4) daily examination for infection and healing monitoring is done. Corneal abrasions are commonly caused by contact lenses. Severe pain and photophobia occur. Antibiotic ointment (and sometimes a pressure patch) is prescribed. Topical anesthetic eye drops are not given as they may mask effects, delay healing, and lead to corneal scarring.
  3. Penetrating Injuries and Contusions of the Globe: penetrating may rupture the eyeball. When the globe, cornea, and sclera rupture, rapid decompression or herniation of the orbital contents into adjacent sinuses can occur. Blunt traumatic injuries (with an increased incidence of Retinal Detachment, intraocular avulsion, and herniation) have a worse prognosis than penetrating injuries.
    • Most penetrating injuries result in marked vision loss, hemorrhagic chemosis, conjunctival laceration, shallow anterior chamber with or without an eccentrically placed pupil, hyphema (blood in the anterior chamber), or vitreous hemorrhage.
    • Hyphema is treated by preventing rebleeding and prolonged IOP elevation.
    • The patient may be hospitalized with moderate activity restriction. An eye shield is applied. Topical corticosteroids reduce inflammation, and an antifibrinolytic agent (aminocaproic acid) stabilizes clot formation at the site of hemorrhage. Aspirin is contraindicated.
    • Surgical intervention is required for a ruptured globe, and severe injuries with IOC hemorrhaging.
      • Vitrectomy is used for traumatic retinal detachment
      • Primary Enucleation (removal of the eyeball and part of the optic nerve) is done if the globe is irreparable and has no light perception. It is a general rule that this is performed within 2 weeks of the initial injury to prevent the risk of sympathetic ophthalmia (the unaffected eye becomes inflamed by the affected eye).
  4. Intraocular Foreign Bodies (IOFB): complaints of blurred vision and discomfort should be questioned about recent injuries and exposures. They may be injured in a number of different situations (construction, striking metal against metal, motor vehicle crashes with facial injury, GSW, grinding-wheel work, and explosions). IOFB is diagnosed and localized by slit-lamp biomicroscopy and indirect ophthalmoscopy, as well as CT or USG scanning. MRI is contraindicated because most foreign bodies are metallic and magnetic.
    • It is vital to determine the foreign body’s composition, size, location, and affected eye structures. Iron, steel, copper, and vegetable matter may result in inflammatory reactions.
    • Incidence of endophthalmitis is high.
    • Surgical excision of the foreign body depends on location, composition, and associated ocular injuries. Specially designed IOFB forceps and magnets are used to grasp and remove the foreign body. Any retinal injuries are treated to prevent rhegmatogenous retinal detachment.
  5. Ocular Burns: exposure to chemically active organic substances (mace, tear gas), acid, and alkali (lye, ammonia).
    • Alkali are the most severe, as they penetrate the ocular tissues rapidly and continue to cause long-term damage. Increased IOP also occurs.
    • Acids generally cause less damage because the precipitated necrotic tissue proteins from a form a barrier to further penetration and damage.
    • These burns may appear as superficial punctate keratopathy (spotty damage to cornea), subconjunctival hemorrhage, or complete marbleizing of the cornea.
    • Treatment: the primary goal is to prevent ulceration and promote re-epithelialization of the cornea. Immediate irrigation with tap water should be done on-site. In the ED, brief history and examination are performed. The most critical information includes the chemical agent involved.
      • The corneal surfaces and conjunctival fornices are immediately and copiously irrigated with normal saline or any neutral solution. This continues until conjunctival pH normalizes (between 7.3 and 7.6). Place a paper strip in the fornix to check corneal surface pH.
      • Local anesthetic is instilled.
      • A lid speculum is applied to prevent blepharospasm from closing the eyelids.
      • Moistened, cotton-tipped applicators remove particulate matter from the fornices. Apply minimal pressure on the globe.
      • Antibiotic agents are instilled, and the eye is usually patched. Intense lubrication with artificial tears is essential.
      • Long-term treatment consists of restoration of the ocular surface (grafting) and surgical restoration of corneal integrity and optical clarty.
    • Thermal injury or photochemical (UV, IR exposure) injury can cause a corneal epithelial defect, corneal opacity, conjunctival chemosis and injection (congestion of blood vessels), and burns of the eyelids and periocular region. Antibiotics and a patch for 24 hours constitute the treatment of mild injuries.

Infectious and Inflammatory Conditions

Dry Eyes

Dry eyes may be caused by decreased tear production/aqueous deficiency (systemic disease e.g. Sjogren, connective tissue disease; lacrimal gland obstruction; and systemic drugs e.g. diuretics, antihistamines, psychotropic drugs) or increased tear evaporation/evaporative dry eye (meimbomian gland deficiency, lid aperture disorder, vitamin A deficiency, reduced lid blinking rate, preservatives from topical drugs, ocular surface disease, contact lens wear), which can be episodic or chronic.

  • Risk Factors: increasing age, smoking, recent refractive surgery, postmenopausal status. Risk may be decreased by intake of omega-3 fatty acids.
  • Clinical Manifestations: most common complaints include photophobia, foreign body sensation, burning and stinging, redness, and decreased tearing.
  • Diagnostic Examination: chronic dry eyes may result in chronic conjunctival and corneal irritation that can lead to corneal erosion, scarring, ulceration, thinning, or perforation that can seriously threaten vision. Secondary bacterial infection can occur.
  • Management: long-term instillation of artificial tears during the day, and an ointment at night hydrates and lubricates the eye.
    • Cyclosporine ophthalmic emulsion is an effective agents that increases tear production, and is used once daily.
    • Anti-inflammatory Medications and Moisture Chambers can provide additional relief.
    • Concurrent treatment of infections or diseases (chronic blepharitis, acne rosacea, Sjogren syndrome)
    • Surgical Treatment: punctal occlusion (via silicone plugs), grafting, lateral tarsorrhaphy (uniting the edges of the lids).

Conjunctivitis

An inflammation of the conjunctiva. It is a common ocular disorder worldwide, characterized by a pink appearance (hence its name “pink eye”) because of subconjunctival blood vessel congestion.

Clinical Manifestations

General symptoms include foreign-body sensation, scratching or burning sensation, itching, and photophobia. It may be unilateral or bilateral, but the infection usually starts in one eye then spreads to the other eye through hand contact.

Diagnostic Examination

Diagnosis is based on the distinctive characteristics of ocular signs, acute or chronic presentation, and identification of any precipitating events. Positive results of swab smear preparations and cultures confirm the diagnosis. The four main clinical features important to evaluate are:

  1. Discharge: determine if the discharge is watery, mucoid, purulent, or mucopurulent.
  2. Conjunctival Reaction: determine if the reaction is follicular or papillary.
    • Follicles are multiple, slightly elevated lesions encircled by tiny blood vessels. They appear like grains of rice.
    • Papillae are hyperplastic conjunctival epithelium in numerous projections that are usually seen as a fine mosaic pattern under slit-lamp examination.
  3. Pseudomembranes or True Membranes: pseudomembranes consist of coagulated exudate that adheres to the surface of the inflamed conjunctiva. True membranes form when the exudate adhered to the superficial layer of the conjunctiva, and removal results in bleeding.
  4. Lymphadenopathy: enlargement of the periauricular and submandibular lymph nodes where the eyelids drain.

Types of Conjunctivitis

  1. Bacterial Conjunctivitis: acute or chronic; acute may become chronic.
    • Signs and symptoms vary from mild to severe: acute onset of redness, burning, and discharge. There is pupillary formation, conjunctival irritation, and injection in the fornices. Exudates are variable but are commonly present in the morning.
    • Exudates may cause adhesion, producing difficulty in opening the eyes. Mucopurulent discharge is seen in mild cases, while purulent discharge appear in severe acute bacterial infections.
    • Chronic form is often seen in patients with lacrimal duct obstruction, chronic dacryocystitis, and chronic blepharitis.
    • In gonococcal conjunctivitis, the symptoms appear more acute, exudate is profuse and purulent, and lymphadenopathy occurs. Pseudomembranes may be present.
    • Trachoma from Chlamydia trachomatis is the leading cause of preventable blindness, spread by direct contact or by carriers (insects).
    • Streptococcus pneumoniae, Haemophilus influenzae, Staphylococcus aureus
  2. Viral Conjunctivitis: acute or chronic.
    • Signs and symptoms vary from mild to severe: tearing, redness, foreign-body sensation, lid edema, ptosis, and conjunctival hyperemia (red eyes caused by dilation of blood vessels).
    • Symptoms of upper respiratory tract infection often precede the condition.
    • Discharge is watery, and follicles are prominent. Severe cases include pseudomembranes.
    • Corneal involvement produces photophobia
    • Adenovirus (highly contagious) and Herpes Simplex Virus (HSV).
    • Vital conjunctivitis is self-limiting but lasts longer than bacterial conjunctivitis.
    • Epidemic Keratoconjunctivitis is a seasonal outbreak of epidemics, especially during summer as people use swimming pools. This is often accompanied by periauricular lymphadenopathy and occasionally periorbital pain. There are marked follicular and papillary formations. This may lead to keratopathy.
  3. Allergic Conjunctivitis: a hypersensitvity reaction as a part of allergic rhinitis, or independent. A history is often present (pollens, other environmental allergens). Extreme pruritus, epiphora (excessive secretion of tears), injection, and usually severe photophobia. A string-like mucoid discharge is usually associated with rubbing the eyes because of severe pruritus.
    • Vernal conjunctivitis is also known as seasonal conjunctivities because it appears mostly during warm weather, and in children and young adults. Most affect people have a history of asthma or eczema. There may be large formations of papillae that have a cobblestone appearance.
  4. Toxic Conjunctivitis: potentially as a result of medications; chlorine from swimming pools; exposure to toxic fumes among industrial workers; or exposure to other irritants such as smoke, hair sprays, acids, and alkalis.

Medical Management

  1. Bacterial Conjunctivitis: acute forms are almost always self-limiting, lasting two weeks if left untreated. If treated with antibiotic agents, it may last a few days (except for gonococcal and staphylococcal conjunctivitis).
    • Trachoma is treated with broad-spectrum oral and systemic antibiotics. Surgical management includes correction of trichiasis to prevent conjunctival scarring.
    • Adult inclusion conjunctivitis requires 1 week of antibiotics. Prevention of reinfection is important. Affected people and their sexual partners should seek treatment for STIs if indicated.
  2. Viral Conjunctivitis: not responsive to any treatment. Patients should be made aware of the contagious nature of the disease (esp. for highly contagious forms like epidemic keratoconjunctivitis).
    • Cold compress may alleviate some symptoms.
    • Health care-associated infections should be prevented. Frequent hand hygiene and procedures for environmental cleaning and disinfection of equipment used for eye examination must be strictly followed at all times. Patients suspected of conjunctivitis caused by adenovirus should have their own specific areas for treatment during an adenovirus conjunctivitis outbreak.
    • Isolation for 3 to 7 days (until symptoms resolve) is prescribed for employees who are infection.
  3. Allergic Conjunctivitis: corticosteroids in ophthalmic preparations are given. Depending on severity, they may be oral. The use of vasoconstrictors, such as topical epinephrine solution, cold compresses, ice packs, and cool ventilation usually provide comfort by decreasing swelling.
  4. Toxic Conjunctivitis: profuse irrigation with saline or sterile water.

Uveitis

Inflammation of the uveal tract can affect the iris, the ciliary body, or the choroid. There are two types:

  1. Nongranulomatous Uveitis: more common form, manifesting as an acute condition with pain, photophobia, and a pattern of conjunctival infection, especially around the cornea. It may be unilateral, bilateral, and may be recurrent.
    • The pupil is small or irregular, and vision is blurred. There may be small, fine precipitates on the posterior corneal surface and cells in the aqueous humor (cell and flare).
    • In severe cases, a hypopyon (accumulation of inflammatory cells in the anterior chamber) may develop.
    • In recurrent cases, anterior and posterior synechiae (adhesion of peripheral iris and cornea/iris and lens respectively) may occur. Secondary glaucoma and cataracts may occur.
  2. Granulomatous Uveitis: potentially more insidious, this may involve any part of the uveal tract. It tends to be chronic. Symptoms such as photophobia and pain may be minimal. Vision is markedly and adversely affected. Conjunctival infection is diffuse, and there may be vitreous clouding. In severe posterior uveitis, such as chorioretinitis, there may be retinal and choroidal hemorrhages.

Medical Management

  • As photophobia is a common symptom, provide dark glasses for outdoor use.
  • Ciliary spasm and synechia are avoided with mydriasis. Cyclopentolate and atropine are commonly used.
  • Inflammation is decreased with four to six instillations of local corticosteroid drops a day.
  • Recurrent uveitis warrants a thorough assessment to determine an underlying cause (complete history, physical examination) and diagnostic testing including CBC, ESR, ANA, Venereal Disease Research Laboratory (VDRL) and Lyme disease titers). Underlying causes include autoimmune disorders (e.g. ankylosing spondylitis, sarcoidosis, toxoplasmosis, herpes zoster virus, ocular candidiasis, histoplasmosis, herpes simplex virus, tuberculosis, syphilis).

Orbital Cellulitis

Inflammation of the tissues surrounding the eye that may result from bacterial, fungal, or viral inflammatory conditions of the contiguous structures (face, oropharynx, dental structures, intracranial structures) or from foreign bodies and preexisting ocular infection (dacryocystitis, panophthalmitis, sepsis). Infection of the sinuses is the most common cause. Sinus infection can spread through the thin bony walls and foramina or by means of the interconnecting venous system of the orbit and sinuses.

  • Staphylococci and streptococci in adults.
  • Pain, eyelid swelling, conjunctival edema, proptosis, and decreased ocular motility. With edema, optic nerve compression can occur and IOP may increase.
  • Abscess formation producing severe intraorbital tension can impair the optic nerve function in orbital cellulitis, resulting in permanent visual loss. Because of its proximity to the brain, it can cause life-threatening complications such as intracranial abscess and cavernous sinus thrombosis.

Medical Management

  1. Immediate administration of high-dose, broad-spectrum, systemic antibiotics. Culture and Gram-stained smears are obtained.
  2. Monitor changes in visual acuity, degree of proptosis, CNS function (N&V, fever, cognitive changes), displacement of the globe, extraocular movements, pupillary signs, and the fundus.
  3. Sinusotomy (surgical drainage) and antibiotic irrigation is performed if abscess formation or progressive loss of vision occurs.

Ocular Surgeries

Ocular surgeries may be performed to repair fractures, remove foreign bodies, or to remove benign or malignant growths. Surgeries involving the orbit and lids affect cosmesis. The goals are to recover and preserve visual function and to maintain the anatomic relationship of the ocular structures to achieve cosmesis. During the repair of orbital fractures, they are realigned to preserve the anatomic positions of facial structures.

  • Complications of orbital surgical procedures (that work around delicate structures of the eyes) include blindness (damage to optic nerve and/or its blood supply), intraorbital hemorrhage or compression of the optic nerve (indicated by sudden pain and loss of vision), and ptosis and diplopia (damage to extraocular muscles). These typically resolve after a few weeks.
  • IV antibiotic prophylaxis is the usual postoperative regimen after orbital surgery.
  • IV corticosteroids may be used if there is concern for optic nerve swelling.
  • Topical ocular antibiotics are typically instilled, and antibiotic ointments applied externally to skin suture sites.
  • Ice compresses are used over the periocular area to decrease swelling and hematoma. Elevate the head of the bed to a comfortable position (30 to 45 degrees).
  • Provide discharge education about medications, and application of ice compresses.

Enucleation

The removal of the eyeball from the orbit, generally for injury resulting in total blindness, prolapse of uveal tissue, blind/painful/deformed/disfigured eye (glaucoma, retinal detachment, chronic inflammation), an eye producing sympathetic ophthalmia, and intraocular tumors.

  • Separation and cutting of each of the ocular muscles and surrounding soft tissue, and cutting of the optic nerve from the eyeball. An orbital implant typically follows, and the conjunctiva is closed. A large pressure dressing is applied over the area.
  • Evisceration is the removal of the intraocular contents through an incision or opening in the cornea or sclera. Used for severe ocular trauma with ruptured globe, severe ocular inflammation, severe ocular infection. This leaves some structures intact (sometimes even the cornea), enhancing cosmetic result and motility after fitting ocular prosthesis.
  • Exenteration is the surgical removal of all orbital contents, surrounding tissue, and most or all of the eyelids. This is indicated in malignancies of the orbit that are life-threatening or when conservative modalities have failed. In its most extensive form, this may involve the removal of all orbital tissues and resection of the orbital bones.

Ocular Prosthesis

Orbital implants (usually made of silicone rubber) and conformers maintain the shape of the eye after enucleation or evisceration to prevent a contracted, sunken appearance. The temporary conformer is placed over the conjunctival closure after the implantation of an orbital implant. The conformer protects the suture line, maintains the fornices, prevents contracture of the socket, and promotes the integrity of the eyelids.

  • All ocular prosthetics are limited in motility.
  • Anophthalmic ocular prosthesis (used in the absence of a globe) and scleral shells (look like the former, but are thinner and fit over a globe with intact corneal sensation).
  • Eye prosthesis often last about six years, depending on quality of fit, comfort, and cosmetic appearance. When the anophthalmic socket is completely healed (6 to 8 weeks), the conformer is replaced with prosthetic eyes made by an ocularist.

Medical Management

Removal of an eye has physical, social, and psychological ramifications for any person. The significance of eye loss and vision must be addressed in the plan of care. Include surgical procedure information, placement of orbital implants and conformers, and ocular prosthesis in patient preparation.

Nursing Management

Patients undergoing eye removal need to know that they will usually have a large ocular pressure dressing, typically removed after a week, and that an ophthalmic topical antibiotic ointment is applied in the socket three times daily.

  • Depth perception is lost. Patients must be advised to take extra caution in their ambulation and movement.
  • Conformers may fall out of the socket. If this happens, wash it, wipe it dry, then place it back in the socket.
  • Provide emotional support if eye removal was emergent and unexpected.

Ocular Consequences of Systemic Diseases

Diabetic Retinopathy

Long-term diabetes results in retinopathy. Patients with diabetes are also at higher risk of cataracts.

  • Atherosclerosis (retinal arteriolar changes), such as tortuousness, narrowing, and a change in light reflex.
  • Fundoscopic examination reveals a copper or silver coloration of the arterioles and venous compression (arteriovenous nicking) at the arteriolar and venous crossings.
  • Intraretinal hemorrhages from hypertension appear flame-shaped because they occur in the nerve fiber layer of the retina.
  • Hypertensive Crisis Retinopathy from acute consequences of conditions such as pheochromocytoma, acute kidney injury, and pregnancy-induced hypertension is extensive. Manifestations include cotton-wool spots, retinal hemorrhage, retinal edema, and retinal exudates, often clustered around the macula.
  • The choroid may also be affected. Ischemia may result in serious retinal detachments and infarction of the RPE. Ischemic optic neuropathy and papilledema may also result.
  • Blood pressure management should be gradual to avoid ischemia of the optic nerve and brain from a rapid fall in blood pressure.

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