Ophthalmology has evolved substantially over the past decade. Innovations in surgical techniques and tissue banking as well as developments in ophthalmic surgical devices and implants, allow an increasingly sophisticated approach to ophthalmic surgery. Advances in imaging the microanatomy of the eye facilitate diagnosis and guide treatment. Nonetheless, the majority of diagnoses in ophthalmology can be made after a targeted history and careful examination without the need for sophisticated equipment.
Evaluation of the eye and its adnexa requires a good history, assessment of visual function and physical examination of the eyes. Occasionally, special examinations may be required to identify specific ocular disorders or to establish the presence of associated systemic disease.
The basic equipment required for an eye examination by a nonophthalmologist includes the following: (1) a visual acuity chart, (2) a handheld flashlight, (3) an ophthalmoscope, and (4) a tonometer.
The basic medications required for an eye examination are (1) a local anesthetic such as proparacaine 0.5% or tetracaine 0.5%; (2) fluorescein strips; and (3) dilating drops, such as phenylephrine 2.5% or tropicamide 0.5%-1%.
In addition to eliciting a chief complaint, determining whether visual loss is monocular or binocular, central or peripheral, and painful or painless is important.
Prior ophthalmic history (including known ophthalmic conditions, prior eye surgery or trauma, history of contact lens use, and relevant family history) should be obtained.
A review of past medical history and all medications should be included as well.
Central visual acuity, using the patient’s glasses if available, should be determined in all patients. The Snellen chart is most commonly used. The patient faces the test chart at a distance of 6 m (20 ft). Each eye should be tested separately. Visual acuity corresponds to the smallest line the patient can read. The patient who is unable to read the largest letter on the chart (typically a 20/200 letter) should be moved progressively closer until that character can be read and that distance recorded in the chart. If no letters are recognizable, the patient should be tested for the ability to count fingers, see hand motion or perceive light. If a vision chart is not readily available, the ability to read small print or a name badge can provide useful information. Preschool children or illiterates can be tested with the E chart or Allen picture chart.
Confrontation visual fields can be used to detect gross visual field defects such as quadrantanopia, hemianopia, or severe visual field constriction. With one eye occluded, the patient is asked to fixate on the examiner’s face and detect finger count or hand motion in each quadrant. Formal visual field testing (perimetry) is used to more carefully examine the central and peripheral visual fields. The technique is performed separately for each eye and measures the function of the retina, the optic nerve and intracranial visual pathway. Perimetry relies on subjective patient responses so results will depend on the patient’s alertness and cooperation. Several methods are used to assess visual field functions, including the tangent screen, Goldmann perimetry, and computerized automated perimetry.
Ocular motility should be assessed in all positions of gaze. One should also observe the patient for random eye movement and assess the alignment of the eyes when the patient is looking straight ahead. The position of the light reflection from a penlight (“reflex”) on the cornea is at the same point in each eye when the eyes are properly aligned. The oculocephalic reflex (doll’s head) can be tested. The upward rotation of the cornea in response to resistance to forced eyelid closure (Bell phenomenon) should be noted when clinically appropriate.
Assessment of Pupillary Functions
Examination of the pupils should be performed before any dilating drops are instilled. Both the direct and consensual light reflex should be assessed. The pupils should constrict with accommodation. The size of the pupils should be noted in light and dark conditions and any difference in size (anisocoria) should be recorded. Irregular pupils may indicate traumatic, postsurgical, neurological, or congenital defects. In hospitalized patients and those with neurological disorders requiring monitoring of pupillary reaction to assess clinical status, pupils should be dilated with discretion and only with short-acting mydriatics.
Inspection of Anterior Segment & Adnexa
The eyelids, conjunctiva, cornea, sclera, and lacrimal apparatus should be evaluated. Unusual prominence of the globes (proptosis), abnormal eyelid position and the inability to fully close eyelids are important features that should be documented. Eversion of the upper eyelid to enable inspection of the hidden conjunctival surface should be performed when appropriate. The conjunctiva is inspected for anatomic defects, foreign bodies, lacerations, inflammation, discharge, tearing, dryness, or other abnormalities. In patients who are unconscious, the presence or absence of Bell phenomenon (upward rotation of the cornea during sleep) may be an important measure of neurological function. Corneal sensation should be tested before anesthetic drops are used.
A direct ophthalmoscope focused on the ocular surface can provide magnification for the examination. A magnifying glass and a handheld flashlight can also be used. Shining a light across the eye from the lateral to medial aspects and noting whether or not the nasal iris is shadowed can assess the depth of the anterior chamber. The presence of shadowing may indicate a narrow anterior chamber angle requiring special precautions if dilating drops are to be used.
Ophthalmoscopy is important for the diagnosis of both ocular and systemic conditions and can provide critical information in neurologic and neurosurgical contexts. In most instances, the optic nerve head can be clearly seen without dilating the pupils. When describing the optic nerve, it is important to note any nerve head edema and the cup-to-disc ratio. Vessel caliber, tortuosity, arteriovenous nicking, and the presence of retinal hemorrhages are additional findings that can aid in diagnosis. In hospitalized patients with neurologic and neurosurgical disorders, dilation of the pupils should be performed with discretion.
Tonometry measures intraocular pressure (IOP). The most common instruments used are the Tono-Pen and the Goldmann applanation tonometer. The normal intraocular pressure varies between 10 and 20 mm Hg. IOP measurements can vary slightly with corneal thickness.
SYMPTOMS & SIGNS OF OCULAR DISORDERS
Decrease in Visual Acuity
Efforts should be made to determine if the decrease in visual acuity is unilateral or bilateral, painful or painless, persistent or transient, recent or chronic, isolated or associated with other symptoms. Unilateral acute painful loss of vision may be due to angle-closure glaucoma, endophthalmitis, or uveitis. Painless unilateral loss of vision is often caused by ischemic optic neuropathy, optic neuritis, central retinal artery or vein occlusion, retinal detachment, vitreous hemorrhage or retinal hemorrhages. Transient painless unilateral loss may be due to retinal migraine or amaurosis fugax. Hemispheric strokes are often responsible for visual field loss with preservation of the central visual acuity.
Disturbances in vision include image distortion, light sensitivity (photophobia), color change, spots before the eyes, visual field defects, night blindness, momentary loss of vision, or halos around lights. Distortion of normal shape (metamorphopsia) is most commonly caused by macular lesions. Photophobia can be due to corneal inflammation, iritis, ocular albinism, or aniridia. Toxicity from systemic medications such as digoxin and certain retinal conditions can cause the patient to complain of abnormally colored vision (chromatopsia). Patients with vitreous opacities or intraocular inflammation may report floating spots in their vision, even if retinal tears and detachment have to be ruled out as a cause. Visual field defects may be due to lid edema, retinal and optic nerve lesions, visual pathway lesions, or cortical abnormalities. Night blindness may be genetic (as in patients with retinitis pigmentosa) or acquired. Important causes of acquired night blindness include vitamin A deficiency, glaucoma, optic atrophy, cataract, or retinal degeneration. Transient loss of vision may imply impending cerebrovascular accident or partial occlusion of the internal carotid artery. Colored halos around lights can be caused by elevated intraocular pressure, most commonly due to acute angle-closure glaucoma. Incipient cataract or incorrect refractive error can cause colorless halos around point light sources.
Diplopia can be constant or intermittent, sudden or gradual, painful or painless, horizontal or vertical. It may occur only in certain gaze positions. It is important to first determine if the diplopia is monocular or binocular. Binocular diplopia is only present when both eyes are open and disappears when either eye is closed. Binocular diplopia is most often due to misalignment of the eyes from extraocular muscle dysfunction or neurologic abnormalities. Monocular diplopia (multiple images in a single eye) occurs with refractive error, lenticular changes, macular lesions, malingering, or conversion reactions.
Ocular pain may result from corneal lesions, inflammation, rapid increase in intraocular pressure, anterior uveitis, cyclitis, scleritis, or optic neuritis. Other causes of pain include inflammation of the orbital contents, tumors in the orbit and dacryocystitis (lacrimal sac inflammation). Eyelid pain and irritation can also arise from infections of the meibomian glands and the glands of Zeis and Moll.
Acute redness (injection) of the eye not associated with trauma is caused by conjunctivitis, acute anterior uveitis, acute angle-closure glaucoma, corneal infection or corneal abrasion (Table 37–1). Subconjunctival hemorrhage may also present as a red eye but this is usually painless and otherwise asymptomatic. Conjunctivitis from bacterial, chlamydial, viral, or allergic causes is a frequent cause of red eye. Nonspecific irritation from exogenous agents or a foreign body can also cause redness. Chemical and thermal injuries cause similar findings. “Dry eye” or ocular surface anomalies can cause redness, a foreign-body sensation, and variable degrees of decreased vision.
Table 37–1.Differential diagnosis of common causes of inflamed eye. ||Download (.pdf) Table 37–1. Differential diagnosis of common causes of inflamed eye.
| ||Acute Conjunctivitis ||Acute Iritis1 ||Acute Glaucoma2 ||Corneal Trauma or Infection |
|Incidence ||Extremely common ||Common ||Uncommon ||Common |
|Discharge ||Moderate to copious ||None ||None ||Watery or purulent |
|Vision ||No effect on vision ||Slightly blurred ||Markedly blurred ||Usually blurred |
|Pain ||None ||Moderate ||Severe ||Moderate to severe |
|Conjunctival injection ||Diffuse; more toward fornices ||Mainly circumcorneal ||Diffuse ||Diffuse |
|Cornea ||Clear ||Usually clear ||Steamy ||Change in clarity related to cause |
|Pupil size ||Normal ||Small ||Moderately dilated and fixed ||Normal |
|Pupillary light response ||Normal ||Poor ||None ||Normal |
|Intraocular pressure ||Normal ||Normal ||Elevated ||Normal |
|Smear ||Causative organisms ||No organisms ||No organisms ||Organisms found only in corneal ulcers due to infection |
Ocular discharge may be described as watery, mucopurulent, purulent, or crusting of the lid margins. When watery discharge is not associated with redness or pain, it may be due to excessive tear production or obstruction of the lacrimal outflow passages. Watery discharge with photophobia, pain, or irritation indicates possible keratitis or keratoconjunctivitis. Purulent or mucopurulent discharge is a sign of bacterial infection, severe inflammation of the conjunctival surface, or bacterial infection of the lacrimal sac or canaliculus. Pseudomonas or Haemophilus species involvement is common. When the discharge forms mucoid strings, it is characteristic of allergic disorders involving the conjunctiva (vernal conjunctivitis) or dry eye syndrome.
For unilateral swelling, the cause is often a stye or chalazion. Bilateral swelling suggests blepharitis or allergic dermatitis. Systemic diseases associated with water retention, hyperthyroidism, or hypothyroidism can also cause swelling or puffiness of the eyelids.
The most common cause of both unilateral and bilateral exophthalmos (proptosis) is hyperthyroidism. Other etiologies include tumors of the orbit.
Strabismus results from misalignment of the eyes due to muscle imbalance. Ocular deviations may be lateral (exotropia), medial (esotropia), upward (hypertropia), or downward (hypotropia). Binocular diplopia is not a frequent complaint in congenital strabismus. Full ocular motility is intact in the majority of strabismus cases.
A white pupil in a child indicates a serious eye disorder. The most frequent cause of leukocoria is congenital cataract, which requires urgent management to prevent amblyopia. Other causes include retinoblastoma, retinopathy of prematurity, toxocariasis, persistent hyperplastic primary vitreous, vitreous hemorrhage, retinal detachment, retinal dysplasia, incontinentia pigmenti, Coats disease, and Norrie disease.
Patients may present with other symptoms such as burning, itching, gritty, and foreign-body sensations, or a “sandy” feeling. These symptoms in elderly patients are suggestive of dry eye syndrome. Itching is also frequently associated with allergic disorders.
DISEASES OF THE EYE & ADNEXA
DISEASES OF THE OCULAR ADNEXA
Acute hordeolum (stye) is a common infection of the glands of the eyelids. External hordeolum involve the glands of Zeis or Moll. Internal hordeolum is an infection of the meibomian glands. The usual causative agent is Staphylococcus aureus. Acute hordeolum is characterized by pain, localized swelling, and redness of the eyelid. A large hordeolum is infrequently associated with a preauricular lymph node.
If there is no abscess formation, treatment with warm compresses three times daily and topical broad-spectrum antibiotic drops such as tobramycin or sulfacetamide 10% three or four times daily for 5-7 days usually suffices. Ophthalmic ointments (erythromycin or bacitracin) twice daily for 5-7 days are also effective. Oral antibiotics, especially tetracycline derivatives, can be useful for patients with acne rosacea. If the infection does not resolve and is localized, treatment consists of making a local horizontal (skin) or vertical (conjunctiva) incision.
Herpes zoster virus (HZV) is caused by a reactivation of latent varicella virus (chickenpox) dormant in the dorsal root ganglion. Approximately 15% of herpes zoster cases arise from the ophthalmic division of the trigeminal nerve (herpes zoster ophthalmicus [HZO]). Hutchinson sign (involvement of the nasociliary nerve which supplies the tip of the nose) occurs in about one-third of patients with HZO. If present, it suggests intraocular involvement. Reactivation is associated with decreased cell-mediated immunity and patients with HIV, blood dyscrasias, neoplasms, or other forms of immunosuppression are at increased risk.
HZO can involve virtually any ocular and adnexal tissues. Reactivation often starts with headache, malaise, fever, and ocular pain without cutaneous findings. Within 24-48 hours, the classic vesicular lesions develop unilaterally in a dermatomal distribution. Corneal involvement presents with the acute event or may follow it by months or years. A corneal pseudodendritic pattern is common. Conjunctivitis, keratitis, episcleritis/scleritis, and uveitis can also occur. Dry eye and poor corneal sensation are common.
Treatments of skin lesions include warm compresses and topical antibiotic ointment. Aggressive lubrication is often needed for maintenance of the ocular surface. Oral antiviral medication is the standard of care. Oral acyclovir (800 mg five times a day) or valacyclovir (1000 mg three times a day) initiated within 72 hours of symptoms has been demonstrated to accelerate the resolution of skin rash and the healing of skin lesions, reduce lesion formation and viral shedding and reduce the incidence of episcleritis, keratitis, and iritis. Oral antivirals appear to reduce both acute zoster-associated pain and postherpetic neuralgia. Topical antiviral medication and steroids are used in certain situations to treat corneal lesions or uveitis. The Zostavax vaccine has been approved for the prevention of herpes zoster in the elderly. In patients without known risk factors for HZO (patients under age 50 without chronic immunosuppression) consider HIV testing.
et al.: Vaccination against herpes zoster and postherpetic neuralgia. J Infect Dis 2008;197(Suppl 2):S228–S236.
Dacryocystitis is a common infection of the lacrimal sac. Acute or chronic, it occurs most often in infants and in persons older than 40 years. It is usually unilateral and always secondary to obstruction of the nasolacrimal duct. In rare instances, the nasolacrimal duct may be obstructed by a tumor.
In children the nasolacrimal duct opens spontaneously during the first month of life. Failure of canalization leads to obstruction of the sac and secondary dacryocystitis. The cause of acquired nasolacrimal duct obstruction is often unclear, but trauma to the nose or infection may be responsible. In infants, dacryocystitis leading to obstruction may be due to Haemophilus influenzae, staphylococci, or streptococci. In patients with trachoma, nasolacrimal and canalicular obstruction is common. The cause of acute dacryocystitis in adults is usually S. aureus or β-hemolytic streptococci. In chronic dacryocystitis, Streptococcus pneumoniae is a common pathogen.
Acute dacryocystitis is characterized by pain, swelling, tenderness, and redness in the tear sac area. In chronic dacryocystitis, tearing and discharge are the principal signs. Purulent material can often be expressed through the puncta.
Culture and sensitivity of organisms obtained from cotton swab should be performed.
Acute dacryocystitis responds well to systemic antibiotic therapy, but recurrences are common if the obstruction is not surgically relieved.
When ductal obstruction is due to failure of canaliculization in the first month of life, daily vigorous massage of the tear sac is indicated. Topical antibiotics should be instilled in the conjunctival sac four or five times daily. If this is not successful, probing of the nasolacrimal duct is indicated. Most ophthalmologists postpone probing until age 6-9 months to allow sufficient time for the passage to open on its own. Both the upper and the lower canaliculi should be probed. In cases of previous failure or in children older than age 2, balloon dacryocystoplasty at the time of probing may increase chances of success. In recalcitrant cases, stenting of the nasolacrimal system or surgical creation of a new tear drain between the eye and nose (dacryocystorhinostomy) is required.
Orbital cellulitis is characterized by an abrupt onset of swelling and redness of the lids, accompanied by proptosis, decreased vision, diplopia, and fever. It is usually caused by staphylococci or streptococci. Immediate treatment with intravenous antibiotics is indicated to prevent abscess formation and rapid increase in the orbital pressure with compromise of the blood supply to the eye. The response to antibiotics is usually excellent, but surgical drainage may be required if an abscess forms. Computerized tomography (CT) is indicated to rule out abscess formation. Preseptal cellulitis is limited to the area anterior to the orbital septum and is treated with oral antibiotics while monitoring closely for progression to full-blown orbital infection.
DISEASES OF THE EYE SURFACE
Acute conjunctivitis is a common cause of red eye. Infectious causes include bacterial, viral, chlamydial, fungal, and parasitic agents. Noninfectious causes include chemical irritation, allergy, hypersensitivity to topical medications, vitamin A deficiency, dry eye syndrome, floppy eyelid syndrome associated with obstructive sleep apnea and injury.
Patients with conjunctivitis complain of redness, irritation, foreign-body sensation, and conjunctival discharge. One or both eyes may be affected. The eyelids are often stuck together in the morning. Bacterial conjunctivitis has conjunctival hyperemia with purulent or mucopurulent discharge and variable degrees of lid swelling. Gonococcal conjunctivitis is characterized by hyperacute onset of copious mucopurulent discharge and can be a vision-threatening infection. In viral conjunctivitis, follicles are present in the inferior conjunctival fornix and preauricular lymph nodes are often involved. The hallmark symptom of allergic conjunctivitis is itching.
If bacterial conjunctivitis is suspected, appropriate microbiologic testing should be performed, including blood and chocolate agar plates, Gram and Giemsa stains, and bacterial cultures.
For patients with suspected bacterial conjunctivitis, topical broad-spectrum antibacterial agents should be prescribed (eg, sulfacetamide 10% eye drops or ciprofloxacin 0.3% eye drops QID), with the addition of erythromycin or bacitracin ophthalmic ointment at bedtime if clinical indications warrant.
Viral conjunctivitis is usually self-limited and does not require treatment. If the diagnosis is unclear, topical antibiotics are often used. Contact precautions are necessary in all situations of suspected bacterial and viral conjunctivitis because spread of disease occurs through contact with contaminated tears.
Treatment of patients with allergic conjunctivitis consists of topical decongestants (naphazoline 0.1%) and H1 receptor blocker (levocabastine) or a mast cell stabilizer (cromolyn). Combination mast cell and antihistamine drops such as olopatadine are also available. In severe cases of allergic conjunctivitis, topical corticosteroids or cyclosporine might be required but should be initiated only with the assistance of an ophthalmologist.
Corneal infections leading to ulceration may be due to bacteria, viruses, fungi, or protozoa.
Patients with corneal ulcers complain of pain, photophobia, and blurring of vision. Patients develop conjunctival hyperemia and chemosis with ulceration of the cornea and whitish or yellowish infiltrate. Hypopyon (pus in the anterior chamber) may be present in cases caused by bacterial or fungal infections. Contact lens users and people with diminished corneal sensation or incomplete eyelid closure are at increased risk of developing corneal infections.
Laboratory studies include culture and cytologic inspection of corneal scrapings.
Corneal ulceration is a serious condition requiring careful management to avoid permanent visual loss. The most devastating infection of the cornea is caused by Pseudomonas aeruginosa. Topical antibiotics should be given on an empirical basis until the results of culture and sensitivity tests are available. Organism-specific antimicrobial treatment should then be started. Patients using topical corticosteroids should stop using them. Central corneal ulcers may leave corneal scars, causing loss of vision. Patients severely affected may require corneal transplantation.
Patients wearing contact lenses (especially extended-wear contacts) are at higher risk of corneal ulcers. Contact lens wear should be stopped if corneal infection is suspected.
Herpes simplex virus (HSV) is a DNA virus that can affect the eye either in a primary ocular reaction or a reactivated state when latent virus travels down the axon of the sensory nerve to its target tissue. HSV is extremely common, with about 90% of the population seropositive for HSV antibodies. HSV-1 usually causes infection above the waist (face, lips, and eyes); HSV-2 infections are usually below. Rarely, HSV-2 is transmitted during birth to the infant eye through infected genital secretions (Table 37-2).
Table 37–2.Herpes simplex virus (HSV) vs. herpes zoster virus (HZV). ||Download (.pdf) Table 37–2. Herpes simplex virus (HSV) vs. herpes zoster virus (HZV).
| ||HSV ||HZV |
|Rash ||Clear vesicles on erythematous base; crusting ||Vesicular rash along dermatomal distribution, not crossing midline; Hutchinson sign (nasociliary branch of V1) may be present |
|Epithelial lesion ||Dendritic epithelial lesions with heaped edges ||Pseudodendrites (mucous plaques without true terminal bulbs) |
|Staining ||Edges stain with rose bengal; central ulceration stains with fluorescein ||Minimal fluorescein staining |
|Patient population ||Young ||Older or immunocompromised |
Primary infections usually occur in children between ages 6 months and 5 years, accompanied by generalized symptoms of a viral illness. Ocular HSV is usually self-limited with the most common symptoms being blepharoconjunctivitis and a dendritic keratitis.
A clinical diagnosis can be made if there is a classic dendritic presentation. However, definitive diagnosis is made using viral culture or Giemsa-stained smears of corneal scrapings that reveal mononuclear cells, polymorphonuclear neutrophil leukocytes, multinucleated giant epithelial cells, and eosinophilic Lipschütz inclusion bodies in the cell nuclei. Enzyme-linked immunosorbent assay (ELISA) can be used to detect live viral particles.
The mainstays of treatment are topical and oral antiviral medications. Antibiotic ointment may be used at night to help prevent bacterial superinfection. Topical trifluorothymidine 1% (Viroptic) or ganciclovir ophthalmic gel 0.15% (Zirgan) is used to treat keratitis. Oral acyclovir (400 mg five times a day) or valacyclovir (500 mg three times a day) is usually added. Topical steroids can be used to treat corneal scarring or uveitis but only with concurrent topical or systemic antiviral therapy. Cost effectiveness of prophylaxis with valacyclovir or acyclovir has been analyzed but currently they are rarely used unless significant visual loss has occurred from previous herpetic episodes.
et al.: Ganciclovir
ophthalmic gel 0.15%: safety and efficacy of a new treatment for herpes simplex keratitis. Curr Eye Res
Dry eye is a disorder of the tear film due to either deficiency of production or excess tear evaporation. The tear film is composed of mucin, aqueous, and lipid components. Abnormalities of any layer lead to a wide variety of symptoms. Dry eye has become one of the most common reasons for visits to ophthalmologists. Symptoms are often exacerbated by weather, climate, reading, and computer use (decreased blink rate). Women have a much higher incidence of symptomatic dry eye. Primary lacrimal deficiency from disease such as Riley-Day syndrome and hypoplastic lacrimal glands is rare. Secondary lacrimal deficiency is more common and can be related to prior radiation therapy, lymphoma, sarcoidosis, graft-versus-host disease, HIV, hemochromatosis, and amyloidosis. Systemic medications such as anticholinergics (including antihistamines and antidepressants), antiadrenergics, and diuretics can cause decreased tear production. Dry eye has also been associated with menopause (presumably due to decreased androgens). Evaporative dry eye problems are usually associated with meibomian gland dysfunction. The protective lipid and mucin layers that normally keep the aqueous layer of tears stable are reduced, leading to a poor-quality tear film that breaks up easily. This problem is often associated with acne rosacea and treated conservatively with warm compresses and oral tetracycline if needed. Oral flax or fish oil supplements may help.
Symptoms of tear deficiency often include foreign-body sensation, redness, decreased vision, and even reflex tearing. Symptoms are usually worse at the end of the day or after prolonged visual tasks.
Symptoms of evaporative tear loss include a chronic “film” over the vision, redness, burning, and itching of the eyelid margin. These symptoms are often worse in the morning. The quick breakup time of the tear film can cause difficulty with reading.
Post-LASIK (laser-assisted in situ keratomileusis) patients have decreased corneal sensation, lower tear production, and diminished blink rate, which may cause dry eye symptoms for 6-18 months or more postoperatively.
Treatment for aqueous deficiency includes tear supplementation. Punctal occlusion may be used in eyes shown to have decreased tear production.
In meibomian gland disease, eyelid hygiene is extremely important. Hot compresses with eyelid scrubs can improve tear quality and prevent evaporative tear loss. Mild topical corticosteroids or systemic tetracycline may also be used, especially if the patient has associated signs of acne rosacea. Topical cyclosporine A, because of its anti-inflammatory action, has been found to dramatically improve dry eye symptoms, although it may take up to 6 weeks for improvement.
Pterygium is a fleshy, triangular conjunctival growth that is usually associated with excessive exposure to wind, sun, sand, and dust. Unilateral or bilateral, it is often on the nasal side of the cornea. There may be a genetic predisposition, but no hereditary pattern has been described.
Treatment is by superficial excision. Excision is indicated if the growth threatens vision by approaching the visual axis. After excising large or recurrent pterygia, autologous conjunctival tissue or amniotic membrane can be used to cover the defect. The conjunctiva is obtained from the upper bulbar conjunctiva and sutured to the denuded area. This leads to rapid restoration of integrity of the epithelial surface and may prevent recurrences. Patients should be advised to wear ultraviolet (UV) protection outdoors. Recurrences can occur. Topical mitomycin eye drops have been used to prevent recurrences of the disease, but serious complications such as scleral thinning and keratitis have been reported.
et al.: Comparison of pterygium recurrence rates after limbal conjunctival autograft transplantation and other techniques: meta-analysis. Cornea 2012 Dec;31(12):1422–1427.
Cataract is opacity of the lens and is the leading cause of curable blindness in the world. There are three types of cataracts: (1) congenital, (2) those associated with other disorders, and (3) age-related. Some cataracts are rapidly progressive, while others may develop more slowly. Surgical removal is indicated when patients have difficulty with daily activities or if visual development is at risk.
Congenital cataract may be genetically determined or may be caused by intrauterine factors that interfere with normal development of the lens. Intrauterine viral infections (most commonly rubella) can cause congenital cataracts. Congenital cataract can be unilateral or bilateral and complete or incomplete. Dense cataract present at birth is an indication for urgent surgical management to ensure proper development of visual function.
Phacoemulsification or simple aspiration with central posterior capsulotomy and limited anterior vitrectomy under general anesthesia is recommended for removal of congenital cataracts. Preservation of the peripheral posterior capsule and zonules is important for future implantation of intraocular lenses. If the cataract is aspirated, leaving the posterior capsule intact, the posterior capsule becomes opaque, requiring capsulotomy at a later stage. Correction with soft contact lenses can be started immediately after surgery. Posterior chamber intraocular lenses can be implanted when the child is older, although children as young as 2 years are being treated with primary intraocular lens implants. Restoration of true binocular vision is seldom achieved after removal of unilateral congenital cataracts.
2. Cataracts Associated With Other Disorders
Many systemic conditions are associated with cataracts, including diabetes mellitus, galactosemia, hypocalcemia, myotonic dystrophy, Down syndrome, and cutaneous disorders such as atopic dermatitis. Certain systemic medications and eye drops containing corticosteroids can also cause cataracts. Other disorders of the eye, such as retinal detachment or chronic uveitis, may also be associated with cataracts. Eyes that have undergone retinal surgical procedures, particularly vitrectomy, have increased risk of cataract development. Physical trauma to the lens as well as injury from thermal and ionizing radiation can cause cataract formation.
3. Age-Related (Senile) Cataract
This is the most common type of cataract. The rate of progression is variable. Diagnosis is by slit-lamp examination. Nuclear changes of the lens produce a brunescent color and often affect distance vision. In advanced cortical cataracts, a white opacity may be seen in the pupillary area upon gross inspection. Monocular diplopia can occur. Posterior subcapsular cataracts are often in younger patients, causing glare and affecting reading.
Once the cataract causes visual impairment, treatment is by surgical removal of the lens. Clinical trials of agents that might delay or prevent the formation of cataracts are under way, but no pharmacologic means of prevention is currently available.
Phacoemulsification of the cataract is the procedure of choice in most developed countries. Primary lens implant is preferred unless there is a contraindication to its use. In that situation, optical correction can be achieved with eyeglasses or contact lenses.
A. Intracapsular Lens Extraction
Intracapsular extraction, rarely used today, removes the lens entirely with its capsule either by forceps or a cryoprobe. This procedure cannot be performed on children or young adults because of the adhesion between the lens and the vitreous.
B. Extracapsular Extraction
For standard extracapsular cataract extraction, the anterior capsule of the lens is removed, the nucleus of the cataract is expressed, and the residual cortical material is aspirated from the eye through a 9-11 mm incision. Smaller incision techniques that involve manual fracturing the lens nucleus prior to expression are available. The posterior capsule is left intact and an intraocular lens is placed in the capsular bag. The incision is then sutured with 10-0 nylon. In 25%-35% of patients undergoing extracapsular cataract extraction, the posterior capsule will become opacified. This is treated by Nd:YAG laser capsulotomy. If such a laser is not available, surgical incision of the opaque posterior capsule is required.
See Figure 37–1. Phacoemulsification is the most common form of extracapsular cataract extraction and involves technology that fragments the nucleus of the lens using a high-frequency ultrasonic probe while simultaneously aspirating these fragments from the eye. The advantage of phacoemulsification is that incision size is reduced, less astigmatism is induced, and the patient can be more quickly rehabilitated. Remaining cortical material is removed by irrigation and aspiration, and an intraocular lens implanted. The insertion of foldable or injectable intraocular lenses through very small incisions is now possible, and often the wound is self-sealing. Local anesthesia (either by injection or topically) is used for most adult patients.
Phacoemulsification. A. Phacoemulsification probe removing lens nucleus through a clear corneal incision. B. Implantation of an injectable intraocular lens implant into the capsular bag through a small incision. (Photos, Courtesy of Alcon Laboratories, Inc.)
Recently, femtosecond lasers have been utilized to perform multiple steps of cataract surgery including wound creation, opening the anterior lens capsule (capsulotomy), and fragmenting the cataractous lens. Development of this technology for cataract surgery could have a significant impact in the future, but at the present time there is no evidence that this technique (which is more expensive) improves visual outcomes.
et al.: Femtosecond laser capsulotomy. J Cataract Refract Surg 2011 Jul;37(7):1189–1198.
et al.: Initial clinical evaluation of an intraocular femtosecond laser in cataract surgery. J Refract Surg 2009 Dec;25(12):1053–1060.
et al.: Phacoemulsification versus manual small-incision cataract surgery for white cataract. J Cataract Refract Surg 2010 Nov;36(11):1849–1854.
About 1% of people over age 35 have anatomically narrow anterior chamber angles. In such patients, if the pupil dilates spontaneously or is dilated with a mydriatic or cycloplegic agent, the angle may close and an attack of acute glaucoma precipitated. For this reason, it is wise to estimate the depth of the anterior chamber angle before instilling these drugs.
Acute angle-closure glaucoma is manifested by sudden onset of pain, headache, blurring of vision, and colored halos around lights. Some patients develop nausea and vomiting. The eye is red, the cornea is hazy, and the pupil is mid-dilated and does not react to light. Intraocular pressure is elevated.
The attack can be aborted by use of topical pilocarpine, beta-blockers, apraclonidine and latanoprost drops, systemic acetazolamide and, if necessary, an intravenous hyperosmotic agent such as Mannitol. Definitive treatment consists of peripheral iridotomy, which establishes a communication between the posterior and anterior chambers and reopens the angle. This is usually done with an argon or Nd:YAG laser. Rarely, surgical peripheral iridectomy is required.
In open-angle glaucoma, the intraocular pressure is elevated, causing gradual cupping (segmental atrophy) of the optic nerve. The damage to the nerve results in loss of vision, ranging in severity from slight constriction of the upper nasal peripheral visual field to complete blindness (absolute glaucoma). The cause of the decreased rate of aqueous outflow that characterizes open-angle glaucoma has not been fully determined. The disease is bilateral but can be asymmetric and is probably genetically influenced. African Americans are particularly at risk.
Open-angle glaucoma is painless, so patients are often unaware of damage until late in the course of the disease. On examination, there may be cupping of the optic disc. There is loss of peripheral visual field, but central vision acuity is usually preserved even when peripheral field loss is quite advanced. Tonometry, evaluation of the optic nerve and visual field testing are the three principal tests used for the diagnosis and continued clinical evaluation of glaucoma. Central corneal thickness should be assessed and included in risk calculations for glaucoma.
The normal intraocular pressure ranges from 10 to 20 mm Hg. Intraocular pressures higher than 21 is considered ocular hypertension, although this diagnosis should never be made on the basis of a single tonometric measurement. Transient elevations of intraocular pressure do not constitute glaucoma for the same reason that periodic or intermittent elevations of blood pressure do not constitute hypertensive disease. All persons over age 20 should have tonometric and ophthalmoscopic examinations every 3-5 years. If there is a family history of glaucoma or other risk factors, annual examination is indicated. Low-tension glaucoma is an uncommon condition characterized by visual field changes and optic nerve cupping in the presence of intraocular pressure that remains in the normal range.
See Table 37–3. Most patients can be controlled with topical medications including beta-blockers (eg, timolol maleate 0.25%-0.5%, one drop twice daily), α-adrenergic agonists (eg, brimonidine 0.2%, one drop twice daily), carbonic anhydrase inhibitors (eg, dorzolamide 2%, one drop twice daily), or prostaglandins (eg, latanoprost 0.005%, one drop once daily). Oral carbonic anhydrase inhibitors (eg, acetazolamide) can be used in patients with persistent elevation of intraocular pressures despite topical treatment. Miotics (eg, pilocarpine 1%-4%, one drop four times daily) and epinephrine eye drops (0.5%-2.0%, one drop twice daily) are less commonly used today.
Table 37–3.Types of glaucoma medications and side effects. ||Download (.pdf) Table 37–3. Types of glaucoma medications and side effects.
|Class ||Mechanism ||Side Effects ||PregnancyClass |
|Beta-blockers (eg, timolol) ||Decrease aqueous production ||Hypotension, bradycardia, asthma exacerbation ||C |
|α2-adrenergic agonist (eg, brimonidine, Propine) ||Decrease aqueous production ||Allergy, tachyphylaxis, CNS depression ||B |
|Cholinergics (eg, pilocarpine) ||Increase outflow ||Brow ache, cataract formation, retinal detachment ||C |
|Carbonic anhydrase inhibitors (eg, acetazolamide, dorzolamide) ||Decrease aqueous production ||Sulfa allergy, systemic metabolic acidosis, tingling, aplastic anemia, metallic taste ||C |
|Prostaglandin analogues (eg, latanoprost) ||Increase outflow ||Bitter taste, iris color change, red eye ||C |
In laser trabeculoplasty, laser energy is applied to the trabecular meshwork. This technique can lead to significant and sustained decreases in intraocular pressure. Argon laser trabeculoplasty (ALT) and selective laser trabeculoplasty (SLT) may be used in place or along with topical medications. SLT produces similar pressure responses to ALT, but studies suggest it can be repeated multiple times in each eye. In those with persistent pressure elevation, surgery is indicated to create an alternate drainage passage for fluid to exit the eye. The most common procedure is trabeculectomy. The success of this procedure has been improved by the use of intraoperative application of mitomycin or 5-fluorouracil to inhibit the fibrosis and closure of the newly created filtering channel.
Drainage devices are also used to facilitate fluid drainage from the eye to lower intraocular pressure. Currently, the most widely used is the Ex-Press glaucoma filtration device. In certain types of glaucoma (such as neovascular glaucoma, aphakic glaucoma or for those with who have failed previous surgery), insertion of a more complex drainage device is required, often referred to as a glaucoma valve or tube shunt. An alternative approach that aims to decrease aqueous production through destruction of ciliary body tissue (diode transscleral cyclophotocoagulation or endophotocoagulation) is also employed in some situations.
LA: The Ex-PRESS glaucoma shunt versus trabeculectomy in open-angle glaucoma: a prospective randomized study. Adv Ther 2009 Mar;26(3):336–345.
et al.: Five-year extension of a clinical trial comparing the EX-PRESS glaucoma filtration device and trabeculectomy in primary open-angle glaucoma. Clin Ophthalmol 2011;5:527–533.
Diabetes is the leading cause of new blindness in most industrialized countries. Diabetic retinopathy eventually develops in almost half of all diabetics and is a major cause of blindness. There are two clinical classifications: (1) nonproliferative or background diabetic retinopathy and (2) proliferative diabetic retinopathy. The prevalence of retinopathy increases with the duration of diabetes. Patients who have had type 1 diabetes for 5 years or less are at low risk of retinopathy. However, 27% of those with diabetes for 5-10 years and 71%-90% of those with diabetes for longer than 10 years have some form of diabetic retinopathy. After 20-30 years, the prevalence of retinopathy rises to 95%, with 30%-50% of those patients having proliferative changes. The risk for diabetic retinopathy also increases with duration for type 2 diabetes.
Diabetes can have other effects on the eye. Poor corneal healing and decreased corneal sensation have been noted. Neovascular glaucoma caused by iris neovascularization (which blocks the outflow passage in the anterior chamber angle) is seen in some patients with proliferative disease. Optic neuropathy and cranial neuropathies can also occur.
Microaneurysms, intraretinal hemorrhages, cotton wool spots, and lipid deposits due to vascular leakage are the retinal changes seen in early diabetic retinopathy. Later stages include retinal ischemia and neovascularization with subsequent vitreous hemorrhage often associated with traction or rhegmatogenous retinal detachment. Diabetic retinopathy may be asymptomatic until vision decreases, usually from macular edema or vitreous hemorrhage. The presence of renal microvascular disease correlates well with the presence of diabetic retinopathy.
Careful control of blood sugar and blood pressure appears to reduce the incidence and severity of diabetic retinopathy. Recent epidemiologic studies show that many diabetics fail to have recommended yearly eye examinations. If patients are followed closely and early retinopathy is detected and treated according to the guidelines of the early treatment diabetic retinopathy study (ETDRS), the risk of severe visual loss is less than 5%. Treatment consists of photocoagulation, either of the macula to reduce edema or of the retinal periphery to reduce ischemic neovascular changes. Adjunctive intravitreal injection of triamcinolone with laser treatment has been suggested for macular edema and proliferative retinopathy. Intravitreal injections of agents that neutralize vascular endothelial growth factor (VEGF) now play a central role in treatment of diabetic macular edema. These anti-VEGF agents may also be useful for the treatment of proliferative disease. Rare complications from these injections include endophthalmitis and steroid-induced glaucoma.
et al.: Long-term effect of intravitreal bevacizumab
(avastin) in patients with chronic diffuse diabetic macular edema. Retina
et al.: Ranibizumab
for diabetic macular edema: results from 2 phase III randomized trials: RISE and RIDE. Ophthalmology
AGE-RELATED MACULAR DEGENERATION
Age-related macular degeneration (AMD) is the leading cause of central visual loss among individuals 65 and older. The pathophysiology is not completely understood although there is a strong genetic component that interacts with aging and environmental influences such as tobacco use. Regardless of the mechanism, the disease appears to affect the retinal pigment epithelium at the level of Bruch membrane. Drusen (yellowish deposits in the retina caused by the thickening, hyalinization, and calcification of the retinal pigment epithelium) are characteristic of AMD.
1. Atrophic (“Dry”) Macular Degeneration
Atrophic (“dry”) macular degeneration is the most common form of AMD, occurring in approximately 80% of those with the disease. Drusen, pigment changes, and atrophy are present, but there is no leakage of fluid into the subretinal space. Usually, only minimal to moderate visual loss is present although patients may complain of distorted vision (metamorphopsia).
2. Exudative (“Wet”) Macular Degeneration
Exudative (“wet”) macular degeneration is characterized by the development of a choroidal neovascular membrane that leaks fluid and blood. This causes a serous detachment of the central fovea that can lead to profound vision loss.
Visual loss is caused by geographical atrophy, serous detachment of the retinal pigment epithelium, or choroidal neovascularization. Central visual acuity is primarily affected with the peripheral vision remaining intact. Metamorphopsia is a classic patient complaint. Patients can follow their own progression of disease with an Amsler grid.
The age-related eye disease study (AREDS) is the first large, prospective clinical trial to show the benefit of antioxidant and zinc supplementation on the progression of atrophic AMD and associated visual loss. In evaluating the rate of progression to advanced visual loss, nutritional supplements benefited only patients who had moderate to severe disease. Supplements were not found to prevent the development of AMD or to prevent progression in patients with mild disease. The AREDS2 study started in 2008 and is examining the use of alternate micronutrients including omega-3-fatty acids in preventing the progression of AMD.
Treatment of exudative AMD was revolutionized through the use of intravitreal injections of anti-VEGF agents. Previously established therapeutic strategies such as standard laser photocoagulation or photodynamic therapy (PDT) reduced the rate of vision loss when compared to controls but did not improve acuity. These treatments remain beneficial in certain specific situations. Intravitreal injection of anti-VEGF agents such as ranibizumab (Lucentis) and bevacizumab (Avastin) has led to actual improvements in visual acuity. Intravitreal injection carries a small risk of infection and treatment resistance can be seen.
Smoking cessation is extremely important in AMD patients and should be stressed. Exercise and control of other systemic diseases such as hypertension and hypercholesterolemia may also help.
Comparison of Age-related Macular Degeneration Treatments Trials (CATT) Research Group: Ranibizumab
for treatment of neovascular age-related macular degeneration: two-year results. Ophthalmology
et al.: Ranibizumab
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et al.: The relationship of dietary lipid intake and age-related macular degeneration in a case-control study: AREDS Report No. 20. Arch Ophthalmol[Archives of Ophthalmology Full Text]
et al.: Complement dysregulation in AMD: RPE-Bruch’s membrane-choroid. Mol Aspects Med 2012 Aug;33(4):436–445 [ Epub 2012 Apr 5].
Detachment of the retina is usually spontaneous but may be secondary to trauma. Spontaneous detachment occurs most frequently in persons over 50 years of age. Spontaneous detachments are ultimately bilateral in 20%-25% of cases.
Retinal tears or holes are the most important predisposing factor. Increased risk of retinal detachment is also associated with cataract surgery and high myopia. In the presence of a retinal tear or hole, fluid from the vitreous cavity enters the defect and transudation from choroidal vessels detaches the retina from the pigment epithelium (rhegmatogenous). These small retinal holes may be sealed prophylactically with laser or cryotherapy to prevent detachment.
The superior temporal retina is the most common site of detachment. The area of detachment can rapidly increase causing progressive visual loss. Central vision remains intact until the macula becomes detached. On ophthalmoscopic examination, the detached retina is seen as an elevated gray membrane.
All cases of retinal detachment should be referred immediately to an ophthalmologist. If the patient must be transported a long distance, the head should be positioned to try to minimize the progression of the detachment. If the upper retina is detached, the head should be kept flat. Patients with an inferior detachment should be kept upright.
Retinal detachment is a true ophthalmic emergency if the macula is threatened. If the macula is detached, permanent loss of central vision may occur even if the retina is successfully reattached by surgery. Treatment consists of drainage of subretinal fluid and closure of retinal tears by cryosurgery, laser, or scleral buckling. This produces an inflammatory reaction that causes the retina to adhere to the choroid. The creation of an inflammatory adhesion between the choroid and the retina helps to prevent future redetachment.
In uncomplicated retinal detachment with a superior retinal tear and healthy vitreous, pneumoretinopexy may be performed. The procedure consists of injection of air or certain gases into the vitreous cavity through the pars plana and positioning the patient to allow the gas bubble to seal the retinal hole and permit spontaneous reabsorption of the subretinal fluid.
About 85% of uncomplicated cases can be reattached with one operation. About 10% will need more than one procedure, and the remainder never reattach. The prognosis is worse if the macula is detached, if the vitreous is not healthy, or if the detachment is of long duration.
Without treatment, retinal detachment almost always becomes total in 1-6 months.
Any child under age 7 with obvious strabismus should be seen without delay to allow prompt treatment to prevent amblyopia. About 3% of children are born with or develop strabismus. In descending order of frequency, the eyes may deviate inward (esotropia), outward (exotropia), upward (hypertropia), or downward (hypotropia).
Children with manifest strabismus suppress the visual image from the deviating eye to avoid diplopia, and the vision in that eye fails to develop normally. This is the first stage of amblyopia. Most cases of strabismus are obvious, but if the angle of deviation is small or if the strabismus is intermittent, the diagnosis can be missed.
Fortunately, amblyopia due to strabismus can be detected by routine visual acuity testing of all preschool children. Those who cannot be tested with a standard eye chart can use visual acuity testing with an illiterate E card or Allen picture chart.
The objectives in the surgical treatment of strabismus in children (Figure 37–2) are to achieve good visual acuity in each eye and align the eyes so that normal binocular vision with fusion can occur. Surgery can be performed in infants, and the earlier the problem is detected and corrected, the better the chance of getting a good result. Correcting the problem in children above age 7-8 often fails to result in visual improvement.
A. Exposure of an extraocular muscle in surgery for strabismus. B. Recession of the muscle behind its original insertion followed by suturing to the sclera with absorbable suture.
If the child is under age 6 years and has an amblyopic eye and strabismus, patching of the better eye should be instituted to improve the vision before surgery for strabismus is performed. At age 1, patching may be successful within 1 week; at age 6, it may take a year to achieve the same result. Surgery to align the eye is usually performed after the visual acuity has been equalized.
Surgery for correction of strabismus consists of weakening or strengthening the extraocular muscles. To weaken the action of a muscle, it is recessed by detaching it from its insertion site and resuturing it to a more posterior location of the sclera. To strengthen a muscle’s action, it is separated at the insertion site from the globe, and a portion of it is resected and then resutured to its original insertion site. Muscles should not be recessed more than 8 mm or resected more than 6 mm.
For correction of exotropia, the lateral rectus muscles in both eyes can be recessed. Alternatively, the lateral rectus muscle can be recessed and the medial rectus muscle resected in the same eye. The amount of recession and resection and the number of extraocular muscles chosen is determined by the degree of ocular deviation. The decision to involve one or both eyes is influenced by the visual acuity and potential of each eye. In patients with esotropia, the options are to recess the medial recti of both eyes or to recess the medial rectus in combination with resecting the lateral rectus in the same eye.
For vertical deviation, the vertical muscles are recessed, resected, tucked, or weakened by myectomy.
In adults with mature visual systems, development of strabismus usually produces double vision. Strabismus can arise from head trauma, microvascular infarct as in diabetes, intracranial hemorrhage, elevated intracranial pressure, brain tumor, or orbital disease.
Surgical management of strabismus is the same as described for children. Since visual pathways have already been formed, the indications for surgery are for cosmetic reasons or because of diplopia. Care must be taken not to induce diplopia after surgery.
Migraine is a disorder with multiple clinical presentations. Recurrent headaches are classic, and ocular symptoms are often associated. The pathophysiology of migraine is uncertain and there may be a genetic component. The differential diagnosis for migraine headaches includes stress-tension headache, cluster headache, sinus congestion/pathology, elevated intracranial pressures, orbital inflammation, orbital neoplasia, and temporal arteritis. A thorough headache history and neurologic examination are important diagnostic tools.
Patients with ocular migraine present with visual symptoms; headache and nausea, if present at all, follow. The ocular symptoms can mimic retinal disease, and a dilated ocular examination is needed to rule out retinal pathology when the symptoms are atypical. The flashing lights from retinal disease are primarily unilateral, while migraine presents with bilateral visual distortion. Asking the patient to cover each eye and see if the symptoms are unilateral or bilateral may clarify the situation. Prophylaxis to prevent migraine with oral β-adrenergic blockers, calcium-channel blockers, and tricyclic antidepressants may be used. Triptans such as sumatriptan (Imitrex) are often used to treat the acute episodes. Onabotulinum toxin A (Botox) injections are an effective treatment option for debilitating migraine not controlled by other medications. Acephalgic migraine typically is not treated with systemic agents because of the self-limited nature of the disease.
Classical migraine is characterized by throbbing headaches preceded by visual auras lasting about 20 minutes. The aura may consist of bright or dark spots, zigzag lines (fortification scotoma), heat haze distortions, scintillating scotomas, and tunnel vision. Homonymous or altitudinal hemianopia may rarely occur. The headaches that follow may vary in intensity.
Retinal migraine is characterized by acute, transient unilateral loss of vision that can be identical to that seen in amaurosis fugax. Vascular etiologies must be ruled out with thorough ocular and medical examination before attributing symptoms to be migraine. Amaurosis is often shorter in duration and has a more “curtain-like” quality.
Ophthalmoplegic migraine is very rare and typically starts before the age of 10 years. It is characterized by a recurrent transient third nerve palsy that is associated with a typical migraine headache.
Complicated migraine is associated with neurologic deficits such as tingling in the extremities, hemisensory disturbance and partial visual loss. Rarely, the deficit persists after the headache has resolved. Antiplatelet therapy with aspirin is often recommended.
et al.: OnabotulinumtoxinA
for treatment of chronic migraine: results from the double-blind, randomized, placebo-controlled phase of the PREEMPT 2 trial. Cephalalgia
Apart from the history, the diagnosis of chemical eye burns is usually based on the presence of swelling of the eyelids and marked conjunctival hyperemia and chemosis. The limbal area may show blanched patchy areas and conjunctival sloughing, especially in the interpalpebral area. There is usually corneal stromal haze and diffuse edema, with wide areas of epithelial cell loss and corneal ulcerations. Defects in the corneal epithelium can be better visualized with the instillation of fluorescein dye.
Alkali burns of the eye are particularly serious because the agents tend to rapidly penetrate intraocularly. Retained particles in the conjunctival fornices may continue to release alkaline material and must be promptly removed. Patients are managed by instilling a topical anesthetic agent and then immediately irrigating copiously (at least several liters) with tap water or any other available solution until a neutral pH is reached. This may require hours of flushing. Double eversion of the upper eyelid should be performed to look for and remove material lodged in the superior fornix. This can be easily done by using a forceps or moist cotton applicator. Topical dilating drops such as atropine 1% or homatropine 5% are instilled, and a topical antibiotic ointment such as ophthalmic erythromycin and bacitracin should be applied. Severe injuries that result in eyelid destruction require hospitalization and specialized care.
Acid burns cause rapid damage but are in general less serious than alkali burns because of lack of intraocular penetration. Irrigation is carried out as described above, the patient is given an analgesic, and the eye is patched for a short time. Close follow-up is needed. Topical antibiotic ointment may also be used.
The treatment of thermal burns of the eyes is similar to the treatment of burns elsewhere on the body. Adequate systemic analgesia should be provided. A topical anesthetic agent such as proparacaine 0.5% or tetracaine 0.5% is used to minimize pain during manipulation. In cases of burns involving the cornea, topical dilating drops such as atropine 1% or homatropine 5% are instilled. Antibiotic drops are often prescribed for 3-5 days.
BURNS DUE TO ULTRAVIOLET RADIATION
Injuries to the corneal epithelium by UV rays vary in severity. They are described as actinic keratitis, snow blindness, welder’s arc burn or flash burn, depending on the source of ultraviolet radiation. Patients present with severe pain, tearing, and photophobia. The examination reveals diffuse punctate staining of the cornea, best seen with fluorescein staining, proper magnification, and a cobalt blue light.
A topical antibiotic such as ophthalmic erythromycin or bacitracin ointment is instilled. Topical nonsteroidal drops such as diclofenac or ketorolac tromethamine can be used for pain.
Eye injuries are common in spite of the protection afforded by the bony orbit. Blunt trauma is the most common injury, but penetrating injuries of the globe, although less frequent, are often more serious. The use of protective eyewear at work helps prevent most serious occupational injuries.
A careful history should be obtained from the patient or someone who knows what happened. Visual acuity should be checked. The eyelids, conjunctiva, cornea, anterior chamber, iris, lens, vitreous, and fundus should be evaluated. Corneal damage (such as abrasions) can be detected by instilling fluorescein dye and using a cobalt blue light to examine the anterior surface. CT scan or x-ray examination is helpful in looking for fractures of the orbital bones or foreign bodies. Patients with severe injuries should have immediate ophthalmic consultation.
PENETRATING OR PERFORATING INJURIES
Penetrating or perforating ocular injuries require immediate treatment and prompt surgical repair to maximize chances for preservation of vision.
Facial injuries—especially those occurring in automobile accidents can be associated with penetrating ocular trauma. Some injuries may be undetected because of eyelid swelling or because the patient’s other injuries have demanded the attention of the emergency room staff. Accurate records and a description of how the injury occurred should be obtained. The eye and ocular adnexa should be examined, including vision testing and testing of ocular motility. Do not apply pressure on the globe. X-ray examination and CT scan are performed to rule out fractures of orbital bones or the presence of intraocular foreign bodies. An eye with a penetrating injury should be protected from further injury with a Fox or similar shield and light dressing. Parenteral broad-spectrum antibiotics such as cefazolin or gentamicin should be given. Antiemetics (eg, ondansetron, 4 mg intravenously) should be given to the patient when needed to prevent vomiting, which can lead to extrusion of the intraocular contents.
Careful repair and approximation of corneal and scleral lacerations should be performed in the operating room. Magnetic metallic intraocular foreign bodies can be extracted with a magnet in the operating room. The major objectives in management of ocular penetrating or perforating injuries are to relieve pain, preserve or restore vision, and achieve good cosmetic results. Pain relief may be achieved by the administration of intravenous or subcutaneous morphine or meperidine. Sedatives such as diazepam 5 mg may be given orally as required.
LACERATIONS OF THE OCULAR ADNEXA
Lacerations of the eyelids and the periorbital skin should be carefully evaluated. Small linear skin lacerations can be easily repaired with 6-0 nylon sutures. The sutures can usually be removed in 3-5 days. In cases of deep eyelid lacerations, intraocular or orbital damage should be ruled out before the repair is performed. The skin of the eyelids has good elasticity and in adults is frequently present in surplus quantities. This facilitates the development of flaps and grafts. In deep lacerations of the eyelids, if the wound divides the orbicularis muscle parallel to its fibers, only skin sutures are generally required. When the muscle fibers are transversely divided, they should be approximated with 6-0 absorbable synthetic sutures. The skin can be approximated with nylon sutures. In patients with lacerations resulting in round or oval losses of skin, the skin is undermined and the laceration approximated. For larger defects, reconstruction with flaps may be required. Flaps used in reconstruction of the eyelids are advancement flaps, rotational flaps, transposition flaps, island flaps, and Z-plasty flaps.
When flaps cannot be used, free skin grafts may be obtained from behind the ear or from the skin of the inner upper arm. Special care should be taken with repair of lacerations of the lower lid to be certain that the lid is not closed under tension to prevent eversion and distortion of the lid margin.
BLUNT TRAUMA TO THE OCULAR ADNEXA & ORBIT
Contusions of the eyeball and ocular adnexa may result from blunt trauma (Table 37–4). The extent of damage to the vision may not be obvious upon initial examination. A careful dilated eye examination is needed for all patients with this type of injury.
Table 37–4.Types of ocular injury associated with blunt trauma. ||Download (.pdf) Table 37–4. Types of ocular injury associated with blunt trauma.
|Eyelids ||Ecchymosis, swelling, laceration, abrasions, conjunctival, or subconjunctival hemorrhages |
|Cornea ||Edema, lacerations |
|Anterior chamber ||Hyphema, recession of angle, secondary glaucoma |
|Iris ||Iridodialysis, iridoplegia, rupture of iris sphincter |
|Ciliary body ||Hyposecretion of aqueous humor |
|Lens ||Cataract, dislocation |
|Vitreous ||Vitreous hemorrhage |
|Ciliary muscle ||Paralysis |
|Retina ||Commotio retinae, retinal edema, choroidal breaks in Bruch membrane, choroidal hemorrhage |
BLOWOUT FRACTURE OF THE FLOOR OF THE ORBIT
Blowout fracture of the floor of the orbit can be associated with enophthalmos, double vision in primary position or upgaze, restriction of ocular movement, hypotropia, and decreased or absent sensation over the maxillary area in the distribution of the infraorbital nerve. CT scan of the orbit will document the extent of the orbital injury that can involve the medial wall as well as the floor. There may be air noted in the sinuses. Evaluation and management of patients with blowout fractures may involve both an ophthalmologist and an otolaryngologist because of potential associated fractures of the maxilla or zygoma. Patients are usually treated with a systemic antibiotic (cephalothin or amoxicillin/potassium clavulanate), told not to blow their nose and reassessed within 1 week by an ophthalmologist. Many blowout fractures do not require surgical correction. Operative management is recommended if there is significant enophthalmos, continued diplopia in primary gaze or significant instability of the orbital floor.
CORNEAL & CONJUNCTIVAL FOREIGN BODIES
Patients often give a history of working with high-speed tempered steel tools, drilling, or hammering against a hard object. There may be no history of trauma to the eye, and the patient may not be aware of a foreign body. In most cases, however, the patient complains of foreign-body sensation in the eye or under the eyelid with associated pain, tearing, and photophobia.
A corneal foreign body can be seen with the aid of a loupe and diffuse light. Conjunctival foreign bodies often become embedded in the inner surface of the upper lid, which must be everted to facilitate inspection and removal. A topical anesthetic such as proparacaine 0.5% or tetracaine 0.5% is applied. Sterile fluorescein should be instilled to assist in the visualization of small foreign bodies. Some loose foreign bodies can be removed with a moist cotton applicator; others require use of the tip of a hypodermic needle. Topical antibiotic ointment should be instilled (eg, erythromycin or bacitracin) and the eye patched for a few hours if necessary. Patients with continued foreign-body sensation, pain, or decreased vision need to be referred to an ophthalmologist for the possibility of corneal ulceration.
Use of the topical anesthetic by the patient will decrease healing and increase risk of corneal ulceration. Topical anesthetics should be used only for examination purposes, never for treatment. If there is any suspicion of penetrating trauma or history consistent with that type of injury, appropriate ultrasound and radiologic tests should be performed.