Chapter 31. Eye Emergencies

Evaluation of the Red or Painful Eye

See Figure 31–1 and Table 31–1.

History and Examination

Historical factors are important in determining the cause of ocular complaints. History, when correlated with characteristic ocular findings on focused physical examination, usually makes the diagnosis. History should include use of eye drops, previous episodes, onset of pain, contact lens use, systemic illnesses and findings, and associated symptoms.

The components of a complete eye examination include the following.

Visual Acuity

Visual acuity testing using a standard acuity chart (Snellen). An acute change in vision usually indicates disease of the eyeball globe or visual pathway. Pain and decreased acuity indicate corneal disease, acute angle-closure glaucoma, or iritis.

Inspection

Inspection of the eye to include conjunctiva, cornea, sclera, lens, and pupil, external lids, lashes, lacrimal ducts, orbits, and periorbital areas for sign of trauma, infection, exudate, or irritation.

Pupillary Function

Check pupillary function for shape, symmetry, and reactivity to light and accommodation.

Extraocular Muscle Function

Extraocular muscle function for any signs of entrapment or palsy.

Visual Fields

Check for abnormalities in the visual fields; this is generally done in the emergency department by confrontation.

Fundoscopy

Direct fundoscopy is generally used to check the retina, optic disc, and retinal vessels.

Slit-Lamp Examination

Slit-lamp examination should be done before and after fluorescein staining to check for corneal abnormalities and examine the anterior chamber.

Intraocular Pressure

Intraocular pressure (IOP) can be tested with a Tono-Pen or Schiotz tonometer (described later in this chapter). Abnormally high pressure may be grossly estimated by palpation, ie, tactile tonometry.

Other Studies

Further diagnostic studies including blood tests, cultures, plain X-rays, bedside ultrasound, computed tomography (CT) scan, or magnetic resonance imaging (MRI) of the orbits may be needed to definitively establish a diagnosis.

Disposition

Patients thought to have acute ocular conditions that may permanently decrease visual acuity (eg, acute angle-closure glaucoma) should have urgent ophthalmologic consultation. Patients with other conditions may receive treatment and be discharged with appropriate follow-up.

Evaluation of Acute Unilateral Visual Loss

See Figure 31–2.

Look for Trauma

Exclude trauma as a cause of visual loss. Both blunt and penetrating ocular injuries may result in blindness.

History and Examination

Obtain a history from the patient (rate of onset of visual loss; whether it is unilateral or bilateral, painful or painless, with or without redness). Ophthalmologic examination should emphasize visual acuity and visual field testing.

Inability to Visualize Retina

Cloudy media will may completely obscure the retina (red reflex blunted or absent) or will make it impossible to visualize retinal landmarks such as the optic disc. Chronic causes of hazy media are common (eg, cataracts) and may complicate the evaluation of acute visual loss.

Abnormal Visual Fields

Grossly abnormal visual fields are usually caused by central nervous system disease and thus generally affect both eyes (not always to the same degree). The retinas are usually normal on ophthalmoscopic examination.

Hemianopia

Hemianopia is usually due to postchiasmal neurologic disorders (eg, tumor, aneurysm, migraine, stroke), in which case other acute neurologic lesions are present as well. Rarely, it is psychogenic functional in origin.

Central Scotoma

A central scotoma indicates isolated macular involvement typical of retrobulbar neuritis and may or may not be associated with pain.

Tubular Vision

Tubular vision not in conformity with the laws of optics is characteristic of psychogenic functional visual loss.

Abnormal Retina

An abnormal retina, usually in the eye with visual loss, is characteristic of several rare but serious conditions.

Central Retinal Artery Occlusion

In central retinal artery occlusion, the fundus is usually pale with a cherry-red fovea. This is a medical emergency (see below).

Central Retinal Vein Occlusion

Central retinal vein occlusion is associated with multiple widespread retinal hemorrhages.

Retinal Hemorrhage

Retinal hemorrhage from other causes (eg, anticoagulation) may produce visual loss.

Retinal Detachment

Retinal detachment produces visual loss preceded by visual flashes. If visual acuity is affected, detachment is large and may be easily visible on direct ophthalmoscopy; however, small detachments may require indirect ophthalmoscopy for visualization. Flashes of light may also occur in patients with migraine or as a result of posterior vitreous detachment.

Differential Diagnosis

Causes of acute visual loss are listed and discussed below.

Acute Angle-Closure Glaucoma

Acute angle-closure glaucoma causes corneal edema, but the more striking findings are eye pain; pupils fixed in mid position or dilated, often with irregular margins; a shallow anterior chamber angle (Figure 31–3); hyperemic conjunctiva; and significantly increased IOP. Acute angle-closure glaucoma is a medical emergency (see below).

Corneal Edema

Severe corneal edema of diverse causes (eg, abrasion, keratitis, postoperative) may cause visual loss with eye pain.

Hyphema

Hyphema is the presence of blood in the anterior chamber. This is generally traumatic in nature, although spontaneous hyphema may occur especially in patients on anticoagulant medications.

Vitreous Hemorrhage

Vitreous hemorrhage causes painless visual loss due to accumulation of blood in the posterior chamber. The anterior chamber is clear. The red reflex is often absent.

Endophthalmitis

Endophthalmitis (intraocular infection) is a rare condition usually associated with eye pain and decreased visual acuity. Eye examination will disclose pus in the anterior chamber (hypopyon) or vitreous. Systemic illnesses associated with endophthalmitis include ankylosing spondylitis, ulcerative colitis, other seronegative arthropathies, sarcoidosis, toxoplasmosis, tuberculosis, syphilis, and herpes zoster.

Disposition

Patients with sudden visual loss due to ocular disease should have ophthalmologic consultation.

Acute Angle-Closure Glaucoma

Essentials of Diagnosis

• Acute onset of moderate to severe, unilateral eye pain with associated nausea and vomiting
• Perilimbal eye redness with a mid-dilated, unreactive, irregular pupil
• Increased IOP confirms diagnosis

General Considerations

Acute angle-closure glaucoma results from a sudden increase in IOP from blockage of the anterior chamber angle outflow channels by the iris root. This sudden rise in IOP causes intraocular vascular insufficiency that may lead to optic nerve or retinal ischemia and can cause permanent vision loss within hours. Prompt management is needed to minimize the likelihood of permanent vision loss.

Clinical Findings

Acute angle-closure glaucoma is characterized by sudden onset of blurry vision, followed by severe pain, halos around lights, photophobia, frontal headache and nausea and vomiting. Other findings include a red eye with fixed or sluggish mid-dilated pupil, shallow anterior chamber, and hazy cornea. IOP will be greater than 30 mm Hg. Risk factors include myopia, hyperopia, shallow anterior chamber, narrow angle, and anterior placement of lens.

Differential Diagnosis

(See Figure 31–2 and Table 31–1.) In iridocyclitis (iritis), IOP is normal and the pupil is small. In conjunctivitis, IOP is normal and the pupil is not affected. Corneal ulcer is diagnosed by fluorescein staining of the cornea.

Treatment

Acute angle-closure glaucoma is an emergency. Timely treatment is important. Obtain ophthalmologic consultation for emergency management and reduce the IOP by one or more of the following means:

• Timolol, 0.5%, one drop in the affected eye
• Pilocarpine, 2% eye drops, two drops every 15 minutes for 2–3 hours
• Mannitol, 20%, 250–500 mL intravenously over 2–3 hours
• Acetazolamide, 500 mg orally or 250 mg intravenously

Glycerin, 1g/kg orally in cold 50% solution mixed with chilled lemon juice. Give sedation, antiemetics, and analgesics as necessary to control pain nausea and agitation.

Disposition

Acute angle-closure glaucoma calls for urgent initiation of medical therapy and ophthalmologic consultation.

Central Retinal Artery Occlusion

Essentials of Diagnosis

• Sudden, painless complete loss of vision in one eye
• Ophthalmoscopy demonstrates pallor of disc, retinal edema, cherry-red fovea, and “boxcar” appearance of retinal veins
• Treatment should be initiated immediately

General Considerations

Central retinal artery occlusion is most commonly embolic in origin. Vision loss can occur in as little as 90 minutes from time of onset. Mitigating factors include occlusion time, cilioretinal artery patency, and cause of the occlusion.

Clinical Findings

There is typically a history of sudden, complete, painless loss of vision in one eye, usually in an older person or others at risk for thromboembolic disease. Ophthalmoscopic examination discloses pallor of the optic disc, edema of the retina, cherry-red fovea, bloodless constricted arterioles that may be difficult to detect, and “boxcar” segmentation of blood in the retinal veins.

Treatment

Central retinal artery occlusion is an emergency. Vision may be permanently lost in as short as 90 minutes, although visual recovery has occurred up to 3 days after occlusion. It is recommended that treatment be started if the patient is seen within 24 hours of symptom onset.

Treatment measures consist of ocular massage (moderate pressure for 10 seconds and release for 5 seconds), timolol ophthalmic, intravenous acetazolamide, or inhaled carbogen (oxygen–carbon dioxide mixture of 95% oxygen and 5% carbon dioxide). Other modalities to be considered by ophthalmology are direct infusion of thrombolytics in the ophthalmic artery or anterior chamber paracentesis. Hyperbaric treatment may be beneficial, if available.

Disposition

Ophthalmologic consultation should be obtained on an emergency basis.

Orbital Cellulitis

Essentials of Diagnosis

• Periorbital swelling and redness
• Painful, limited extraocular movement
• Intravenous antibiotics and admission

General Considerations

Acute infection of the orbital tissues is generally caused by Streptococcus pneumoniae, other streptococci, Staphylococcus aureus, and (previously, chiefly in children) Haemophilus influenzae. Less frequently, certain fungi of the Phycomycetes group may cause orbital infections (rhinoorbitocerebral mucormycosis) in diabetics. Most causative organisms enter the orbit by direct extension from the paranasal sinuses (primarily ethmoid) or through the vascular channels draining the periorbital tissues. Rarely, infection may spread to the cavernous sinus or meninges.

Clinical Findings

There may be a history of sinusitis or periorbital injury, pain in and around the eye, and possibly reduced visual acuity. Examination may demonstrate swelling and redness of the eyelids and periorbital tissues, chemosis of the conjunctiva, rapidly progressive exophthalmos, and ophthalmoplegia. Disc margins may be blurred, and fever is commonly present. Radiographic evaluation may demonstrate sinusitis with or without soft tissue orbital infiltration.

Patients with invasive infection due to the Phycomycetes group (Mucor, Rhizopus, and other genera) may present with rapidly progressive orbital cellulitis, often with cavernous sinus thrombosis. Diabetic and immunocompromised patients are at increased risk. Examination often reveals coexisting maxillary and/or ethmoid sinusitis and palatal or nasal mucosal ulceration.

Treatment and Disposition

Obtain cultures of blood and periorbital tissue fluid. Obtain CT scan of the orbit to rule out orbital abscess and intracranial involvement. Patients should be admitted and appropriate broad-spectrum intravenous antibiotics started (ceftriaxone 1–2 g IV plus vancomycin 1 g IV or piperacillin/tazobactam 3.375 g IV). Obtain immediate ophthalmologic and or otolaryngologic (ENT) consultation. Patients with orbital phycomycosis are given intravenous amphotericin B and require surgical intervention for debridement of infected tissue. Neurosurgical consultation may be needed for any intracranial involvement.

Cavernous Sinus Thrombosis

Essentials of Diagnosis

• Complication from facial or sinus infections
• Decreased vision associated with headache, nausea, fever, chills, and other signs of systemic infection
• Early administration of parenteral antibiotics

General Considerations

Cavernous sinus thrombosis is usually associated with orbital and ocular signs and symptoms. The infection results from hematogenous spread from a distant site or from local extension from the throat, face, paranasal sinuses, or orbits. Cavernous sinus thrombosis starts as a unilateral infection and commonly spreads to involve the other cavernous sinus.

Clinical Findings

The patient may complain of chills, headache, lethargy, nausea, pain, and decreased vision. Fever, vomiting, and other systemic signs of infection may be present. Ophthalmologic examination discloses unilateral or bilateral exophthalmos, absent pupillary reflexes, and papilledema. Involvement of the third, fourth, and sixth cranial nerves or of the ophthalmic branch of the fifth nerve leads to limitation of ocular movement and decrease in corneal sensation.

Treatment and Disposition

Obtain blood cultures and start appropriate antibiotics (nafcillin, plus a third-generation cephalosporin). Consider vancomycin if methicillin-resistant S. aureus is suspected or prevalent. Obtain CT scan of the head and orbits. Seek ophthalmologic, neurologic, and medical consultation early. Although controversial, anticoagulation with heparin can be safely considered for patients with a deteriorating clinical condition after excluding intracranial hemorrhage radiologically.

Endophthalmitis

Essentials of Diagnosis

• Pus in anterior chamber (hypopyon) is diagnostic
• Obtain emergency ophthalmology consultation for drainage and antibiotic treatment

General Considerations

Endophthalmitis is an acute microbial infection confined within the globe. Infection involving the sclera as well as other intraocular structures is called panophthalmitis. Infections of the globe can be exogenous or endogenous. Exogenous infection results from penetrating injury or may follow intraocular surgery or a ruptured corneal ulcer. Endogenous infection by the hematogenous route is less common and may be accompanied by fever and chills.

Clinical Findings

The patient complains of pain, blurred vision, and photophobia. Examination discloses redness and chemosis of the conjunctiva, swelling of the eyelid, hypopyon (pus in the anterior chamber), and cloudy media (fundus hazily seen, or absent red reflex).

Treatment and Disposition

Send blood culture, obtain emergency ophthalmologic consultation, and give sedation and analgesics. The patient may have to undergo anterior chamber tap and vitreous aspiration (by an ophthalmologist). Send specimens obtained for staining with Giemsa and Gram stains and for cultures on appropriate media.

Check stained smears of ocular fluid, and if no organisms are seen, give empiric subconjunctival and systemic antibiotics (vancomycin and an aminoglycoside or third-generation cephalosporin) while results of culture are pending.

Retinal Detachment

Essentials of Diagnosis

• Painless decrease in vision
• History of flashes of light, then “curtain” in visual field
• Urgent consultation for surgical repair

General Considerations

Detachment of the retina is actually separation of the neurosensory layer from the retinal pigment epithelium. Sub-retinal fluid accumulates under the neurosensory layer. Detachment may become bilateral in one-fourth of cases. Retinal detachment is more common in older people and in those who are highly myopic. Hereditary factors may also play a role. Three types of primary retinal detachment are recognized: (1) rhegmatogenous detachment (most common), from retinal holes or breaks; (2) exudative detachment, usually from inflammation; and (3) traction detachment, which occurs when vitreous bands pull on the retina.

Minimal to moderate trauma to the eye may cause retinal detachment, but in such cases predisposing factors such as changes in the vitreous, retina, and choroid play an important role in pathogenesis. Severe trauma may cause retinal tears and detachment even if there are no predisposing factors.

Clinical Findings

The patient complains of painless decrease in vision and may give a history of flashes of lights or sparks. Loss of vision may be described as a curtain in front of the eye or as cloudy or smoky. Central vision may not be affected if the macular area is not involved; this frequently causes a delay in seeking treatment. Patients in whom the macula is detached present to the emergency department with sudden deterioration of vision.

IOP is normal or low. The detached retina appears gray, with white folds and globular bullae. Round holes or horseshoe-shaped tears may be seen by indirect ophthalmoscopy in the rhegmatogenous detachment. Vitreous bands or other changes may be seen in the traction type of detachment.

Differential Diagnosis

Primary retinal detachment should be differentiated from detachment secondary to other causes, for example, from preeclampsia–eclampsia or tumors of the choroid.

Treatment and Disposition

Arrange for referral to an ophthalmologist. If the macula is attached and central visual acuity is normal, urgent surgery, which is successful in about 80% of cases, may be indicated. If the macula is detached or threatened, operation should be scheduled on an urgent basis, because prolonged detachment of the macula results in permanent loss of central vision.

Toxic Causes of Blindness

A wide variety of organic chemicals may lead to visual deterioration. Ingestion of chemicals that cause corneal or lenticular opacities usually leads to insidious onset of visual loss. Ingestion of compounds that cause damage to nervous tissue may lead to slow or rapid deterioration of vision. Exposure to toxic doses of methanol, halogenated hydrocarbons (eg, methyl chloride), arsenic, and lead may cause permanent visual damage. Acute or chronic administration of drugs such as ethambutol, chloramphenicol, quinine, and salicylates may also cause optic neuritis and loss of vision.

By far the most common toxic cause of blindness is methanol (methyl alcohol). Ingestion of only a few milliliters may cause permanent blindness. Acute methanol poisoning causes nausea, vomiting, and abdominal pain. Headache, dizziness, and delirium may occur. Loss of vision may be complete and sudden within a few hours after drinking methanol or may occasionally be noted about 3 days after exposure. Pupillary reflexes are sluggish. Ophthalmoscopic examination shows swelling and hyperemia of the optic nerve head, distention of the veins, and peripapillary edema of the retina.

Hospitalize the patient immediately. See Chapter 47 for details of evaluation and treatment.

Acute Dacryocystitis

Essentials of Diagnosis

• Swelling, redness, and tenderness over the lacrimal sac on the lateral, proximal aspect of the nose
• Warm compresses and systemic antibiotics for treatment

General Considerations

Acute infection of the lacrimal sac occurs in children and adults as a complication of nasolacrimal duct obstruction. The most frequently encountered causative organism is S pneumoniae.

Clinical Findings

The patient complains of pain. There may be a history of tearing and discharge. Examination discloses swelling, redness, and tenderness over the lacrimal sac (Figure 31–4).

Pus should be collected, for Gram-stained smear and culture, by applying pressure over the lacrimal sac.

Treatment

Begin systemic antibiotics with cephalexin or amoxicillin–clavulanate. Topical antibiotic drops may also be used, but not alone. Use warm compresses 3–4 times daily. Consider incision and drainage of a pointing abscess.

Disposition

The patient can be discharged to home care with a prescription for systemic antibiotics and instruction in how to apply warm local compresses. Consult an ophthalmologist for consideration of surgical correction. The patient should be seen again within 1–3 days.

Acute Dacryoadenitis

Essentials of Diagnosis

• Swelling, erythema, and pain at the lacrimal gland located at the temporal aspect of the upper eyelid

Clinical Findings

Infection and inflammation of the lacrimal gland is characterized by swelling, pain, tenderness, and redness over the upper temporal aspect of the upper eyelid.

Differential Diagnosis

Acute dacryoadenitis must be differentiated from viral infection (mumps), sarcoidosis, Sjögren's syndrome, tumors, leukemia, and lymphoma.

Treatment

Purulent bacterial infections should be treated by incision and drainage of localized pus collections, antibiotics, warm compresses, and systemic analgesics. Viral dacryoadenitis (mumps) is treated conservatively.

Disposition

The patient should be referred to an ophthalmologist for follow-up care in 2–3 days.

Acute Hordeolum (Stye)

Essentials of Diagnosis

• Pain and redness with swelling over the eyelid
• Warm compresses and topical antibiotic three times daily

General Considerations

Acute hordeolum is a common infection of the lid glands: the meibomian glands (internal hordeolum) and the glands of Zeis or Moll (external hordeolum). The most frequent causative organism is S. aureus.

Clinical Findings

A stye is characterized by pain and redness with variable swelling over the eyelid. A large hordeolum may rarely be associated with swelling of the preauricular lymph node on the affected side, fever, and leukocytosis.

Treatment

If pus is localized and pointing out to the skin or conjunctiva, a horizontal incision may be made through the skin or a vertical incision through the conjunctiva.

Disposition

The patient can be discharged to continue treatment with warm compresses three times daily and topical antibiotic ointment (erythromycin 0.5% or gentamicin 0.3%) twice daily at home.

Eyelid Infections (Preseptal Cellulitis)

Essentials of Diagnosis

• Pain, tenderness, edema, and erythema around the eye
• No pain with ocular movement
• Antibiotic treatment and daily follow-up to ensure that the infection does not progress to orbital cellulitis

General Considerations

Preseptal cellulitis is an infectious process of the eyelid. Common causative organisms are S. aureus, streptococci, and H. influenzae. Viral causes should be considered if associated with a skin rash (eg, herpes zoster).

Clinical Findings

There is tenderness, erythema, and edema of the eyelid. No proptosis, pain with ocular movement, or restriction of extraocular motility is present. If any of these are present, consider orbital cellulitis.

Treatment

Give amoxicillin-clavulanate or cephalexin for 10 days. Antivirals may be considered if herpes zoster is suspected. Incision and drainage may be needed in more severe cases.

Disposition

The patient can be discharged with daily follow-up. If the patient fails antibiotics or has worsening symptoms, administer intravenous antibiotics and obtain ophthalmology or ENT consultation.

Spontaneous Subconjunctival Hemorrhage

Essentials of Diagnosis

• Painless collection of blood in the subconjunctival tissue
• Vision is not affected

General Considerations

Rupture of small subconjunctival vessel that occurs spontaneously or preceded by a bout of coughing, sneezing, or vomiting.

Clinical Findings

Bright red to dark maroon blood underneath the conjunctiva. Painless with no visual loss. Check for hypertension or coagulopathies with recurrent or bilateral hemorrhage.

Treatment and Disposition

The best treatment is observation, although many patients are very concerned and require extensive reassurance before leaving the emergency department. Consider using artificial tear drops or ointment if needed for protruding chemotic tissue.

Conjunctivitis

Essentials of Diagnosis

• Most frequent cause of red eye
• Purulent drainage and conjunctival hyperemia help with diagnosis

General Considerations

Conjunctivitis is the most frequent cause of red eye. It should be dealt with as an urgent medical problem until it is certain that the process is under control.

Causes of Acute Conjunctivitis

Infection

Acute conjunctivitis may be caused by bacterial, viral, parasitic, fungal, or chlamydial infection.

Chemical Irritation

Chemical irritations causing acute conjunctivitis include chlorine gas and tear gas.

Allergy

Allergic causes of acute conjunctivitis include vernal keratoconjunctivitis, hay fever, and other common allergens.

Skin Disorders

Skin disorders such as Stevens–Johnson syndrome, acne rosacea, Lyell disease, Kawasaki disease, and psoriasis may cause acute conjunctivitis.

Systemic Disorders

Sjögren's syndrome and vitamin A deficiency may cause acute conjunctivitis.

Clinical Findings

(See Table 31–2.) The patient complains of a “scratchy” sensation or pain, with conjunctival discharge. One or both eyes may be affected. Adherence of the eyelids upon awakening is common in bacterial conjunctivitis.

Examination discloses conjunctival hyperemia, purulent or mucopurulent discharge, and variable degrees of lid swelling. In appropriate cases, material may be taken from the conjunctival sac for smear (Gram and Giemsa stains) and culture on blood and chocolate agar. Viral cultures may also be indicated.

Treatment

Prescribe topical sulfacetamide 10% eye drops, or ciprofloxacin 0.3% eye drops four times daily, and erythromycin or tetracycline ophthalmic ointment at bedtime for suspected bacterial conjunctivitis.

For suspected chlamydial infection (eg, history of urethritis), prescribe topical and systemic tetracycline or erythromycin. Give 0.5 g four times daily for 21 days (adult dose). Doxycycline, 100 mg twice daily, may be substituted for tetracycline. Consider treatment for gonorrhea.

Disposition

Discharge patients to home care with instructions to return for follow-up in 48–72 hours. Patients who do not respond to treatment should be referred to an ophthalmologist.

Bacterial Corneal Ulcer

Essentials of Diagnosis

• Examination with fluorescein aids in diagnosis
• Antibiotic treatment and close follow-up are mandatory
• Common in contact lens wearers

General Considerations

Corneal infections may be due to bacteria, viruses, chlamydia, or fungi. The conjunctiva may or may not be involved. Bacterial corneal ulcers are serious, because rapid perforation of the cornea and loss of aqueous humor may occur; bacterial endophthalmitis may occur if bacterial ulcers are not properly treated.

Clinical Findings

The patient complains of pain and photophobia, blurring of vision, and eye irritation. Examination discloses conjunctival hyperemia and chemosis, corneal ulceration, or whitish–yellowish infiltration. The examination is facilitated by fluorescein staining and inspection with ultraviolet light. Hypopyon may be present. Scrapings from the cornea should be taken for culture and staining with Gram and Giemsa stains.

Differential Diagnosis

See Table 31–1.

Treatment and Disposition

Management of bacterial corneal infections causing corneal ulcers must be instituted as early as possible. Ophthalmologic consultation should be obtained urgently.

Viral Keratoconjunctivitis

Essentials of Diagnosis

• Unilateral redness and pain with palpebral conjunctival follicles
• Adenovirus is most common; however, antibiotic eye drops are commonly used

Clinical Findings

Viral keratoconjunctivitis is an acute conjunctivitis and keratitis caused most frequently by adenovirus (types 8 and 19). The patient complains of eye redness associated with tearing and moderate pain. The onset is often unilateral, and this eye is more severely affected. Photophobia may be intense and noted 5–14 days after onset. Examination discloses swelling of the eyelids and bulbar conjunctival hyperemia, with follicles and possibly a pseudomembrane noted over the palpebral conjunctiva. A tender preauricular lymph node can often be palpated. Subconjunctival hemorrhage may occur within 48 hours. Corneal epithelial keratitis accompanies the conjunctivitis, but subepithelial opacities are not seen until 5–14 days after onset of symptoms.

In adults, the disease is confined to the external eye. Children may have fever, pharyngitis, and diarrhea (pharyngoconjunctival fever). Staining of conjunctival scrapings with Giemsa stain demonstrates a predominantly mononuclear inflammatory reaction. When pseudomembranes occur, polymorphonuclear neutrophils may be seen. Culture for adenovirus is usually positive in the first 2 weeks after onset. Chlamydial conjunctivitis should always be considered in the differential diagnosis.

Treatment

Treatment is symptomatic. Topical decongestants may be helpful. Dark glasses may relieve photophobia. If the diagnosis is uncertain, send material for bacterial culture, and start sulfacetamide, 10% eye drops four times daily, and tetracycline, 1% (10 mg/g) ointment twice daily, while awaiting laboratory results.

Since epidemics have been caused by iatrogenic spread of the viral agent, handwashing and other preventive measures are of utmost importance.

Disposition

The patient should be discharged with follow-up in 2–3 days. Patients should take care to avoid spread of virus from ocular secretions to other family members and coworkers. Ideally, they should be off work until symptoms resolve.

Acute Hydrops of the Cornea

Essentials of Diagnosis

• Sudden, painless decrease in vision
• Unaffected eye shows keratoconus

General Considerations

Acute hydrops of the cornea may occur in patients with keratoconus who develop rupture of Descemet's membrane, with resulting infiltration of the corneal stroma by aqueous humor. This may occur suddenly, resulting in corneal clouding.

Clinical Findings

The typical presentation is of sudden, painless, marked decrease in visual acuity in a patient with keratoconus. There may be mild eye irritation, and the cornea is cloudy as a result of corneal edema. Bacterial or viral keratitis must be ruled out.

Treatment

Hypertonic eye drops, for example, sodium chloride, 2% or 5% solution, should be instilled four times daily for 1 week. Apply a stream of hot air twice daily by hair dryer to speed dehydration of the cornea. Avoid rubbing the eye.

Disposition

Refer the patient to an ophthalmologist within 24–72 hours.

Hyphema

Essentials of Diagnosis

• Sudden decrease in visual acuity
• Sitting the patient up can aid in the diagnosis, because blood will accumulate inferiorly
• Must check IOP

General Considerations

Hyphema (blood in the anterior chamber) is usually caused by nonperforating trauma to the eye. In rare instances, hyphema may occur spontaneously as a complication of an ocular or systemic disorder or anticoagulation.

Clinical Findings

Hyphema is characterized by sudden decrease in visual acuity. If the IOP is elevated, there may be pain in the eye with or without headache. The whole anterior chamber may be filled with blood, or a blood level may be seen. The conjunctiva may be hyperemic with perilimbal injection.

Treatment

Elevate the patient's head 30°. Cover the affected eye with a shield. Ophthalmologic consultation is needed.

Recently, intracameral injection (performed by an ophthalmologist) of 25 μg of t-PA has been shown to expedite the resorption of blood clots in the anterior chamber. Aminocaproic acid can be used topically to stabilize the clot and decrease the rate of rebleeding.

Disposition

Acute care and evaluation by an ophthalmologist is essential. Operative evacuation of nonabsorbed blood clots may be required. Recurrence of bleeding on the third to fifth days following injury is not uncommon. Patients with hyphema should have daily follow-up for 5 days and then as directed by the ophthalmologist.

Uveitis (Iritis and Iridocyclitis)

Essentials of Diagnosis

• Photophobia, pain, and constricted pupil secondary to ciliary spasm
• Mydriatics are key to treatment

General Considerations

The uvea consists of the iris, ciliary body, and choroid. Anterior uveitis is inflammation of the iris and ciliary body, or iridocyclitis. Inflammation of all three structures is called panuveitis.

Clinical Findings

(See Table 31–1.) The patient complains of blurred vision, photophobia, and head or ocular pain. Ciliary injection may be present around the limbus, and conjunctival injection may be minimal. IOP may be elevated. There is no conjunctival discharge.

Treatment

Instill a cycloplegic mydriatic agent, such as tropicamide or cyclopentolate, 1% eye drops, one drop every 8 hours. If IOP is elevated, give acetazolamide, 250 mg orally every 6 hours. Prednisolone acetate, 1% eye drops, five times daily may be indicated after ophthalmologic consultation.

Disposition

Patients with uveitis should be seen the next day for follow-up care. Continuing care should be by an ophthalmologist. The cause of uveitis should be investigated.

Vitreous Hemorrhage

Essentials of Diagnosis

• Sudden, painless loss of vision
• Patient complains of seeing “floaters”
• Secondary to trauma, retinal detachment, or diabetic retinopathy
• Urgent ophthalmology consultation is needed

General Considerations

Spontaneous hemorrhage into the vitreous body may result from local factors in the eye (eg, retinal tears, tumors, inflammation, venous occlusion, retinal detachment) or from associated systemic disorders (eg, hematopoietic diseases, diabetes mellitus, hypertension) (Table 31–3). Blood in the vitreous body clots rapidly, and removal of red blood cells is retarded because of the network of collagen fibers and hyaluronic acid.

Clinical Findings

Vitreous hemorrhage is characterized by sudden, painless loss or deterioration of vision in the affected eye. The eye is not red. The red reflex of the fundus is hazy, faint, or becomes black. Details of the retina and optic nerve are obscured by the cloudy vitreous.

Treatment and Disposition

The patient should be evaluated urgently by an ophthalmologist. Partial or total vitrectomy may have to be considered later if absorption of blood does not occur or vitreous clouding occurs secondary to organization of the blood clot. Photocoagulation of the neovascular network (ie, new blood vessel formation, as occurs in diabetic or sickle cell retinopathy), when present, may be considered in some cases as a prophylactic measure.

Recent studies have shown that intravitreal injection of 25 μg of t-PA may be considered in selected patients with traumatic vitreous hemorrhage.

Retinal Hemorrhage

Essentials of Diagnosis

• Painless loss of vision occurs if the hemorrhage is in the macular area
• May be asymptomatic

General Considerations

Retinal hemorrhage may be due to trauma, local ocular disease, or systemic disorders (Table 31–4). Hemorrhages may occur in superficial or deep layers of the retina or in the preretinal or subhyaloid space.

Clinical Findings

The patient may complain of sudden decrease in vision when hemorrhage occurs in the macular or perimacular area. Small peripheral retinal hemorrhages cause no symptoms. Superficial retinal hemorrhages occurring in the nerve fiber layer are bright red and flame-shaped on ophthalmoscopic examination. Deep retinal hemorrhages are round and have a dark red color. Subhyaloid hemorrhage occurs in the space between the vitreous body and the internal limiting membrane and may have a boat-shaped appearance. A neovascular network may rupture and cause retinal or vitreous hemorrhage.

Treatment and Disposition

There is no specific treatment. The patient should be referred to an ophthalmologist for further care and to prevent recurrences.

Central Retinal Vein Occlusion

Essentials of Diagnosis

• Unilateral, painless loss of vision
• Often in elderly with glaucoma or hypertension

General Considerations

Central retinal vein occlusion occurs most frequently in elderly patients with glaucoma or hypertension. The incidence is also increased in diabetes mellitus, autoimmune diseases, Waldenström macroglobulinemia, cryoglobulinemia, sickle cell disease, polycythemia vera, and leukemia.

Clinical Findings

The patient complains of sudden painless unilateral loss of vision. Ophthalmoscopy reveals dilated and tortuous veins, retinal and macular edema, multiple or diffuse retinal hemorrhages, and attenuated arterioles.

Treatment and Disposition

There is no specific therapy. Refer the patient to an ophthalmologist for assessment of possible glaucoma or associated systemic disease. If local predisposing factors such as glaucoma are ruled out, patients with occlusion should have a complete medical evaluation.

Optic Neuritis

Essentials of Diagnosis

• Painful unilaterally, especially with movement
• Afferent pupillary defect
• Many causes: case should be discussed with ophthalmologist or neurologist

General Considerations

Optic neuritis may be due to a variety of causes, including demyelinating diseases; systemic infections; nutritional and metabolic disorders; exposure to toxic substances (eg, arsenic, methanol, lead, tobacco); vascular insufficiency; and local extension of infection from intraocular structures, sinuses, or meninges. Optic neuritis includes retrobulbar neuritis (inflammation of the optic nerve posterior to the globe), in which there are by definition no ophthalmoscopic findings.

Clinical Findings

Typical age of presentation is 25–40 years and females are represented twice as often as males. The patient complains of rapidly decreased vision in one (or rarely both) eyes and sometimes pain on moving the eye. Loss of central vision, tenderness in the eye, and perception of color as dull may also be present. Uhtoff phenomenon (decreased vision with heat or exercise) may be present. The pupillary reflex is sluggish. Ophthalmoscopic examination in optic neuritis shows hyperemia of the optic nerve head (may not be present in retrobulbar neuritis), congestion of the large veins, blurring of the disc margin, peripapillary retinal edema, and flame-shaped hemorrhages near the optic nerve head. Visual field testing discloses a central scotoma.

Treatment and Disposition

Treatment depends on the cause. Intravenous corticosteroids may be helpful in cases associated with demyelinating disease. The patient should be referred to an ophthalmologist or neurologist for further care within 1 or 2 days.

Ocular Burns

Essentials of Diagnosis

• History and physical examination
• Copious irrigation with normal saline, lactated Ringer's, or water after topical anesthetic is placed
• Check pH after irrigation; should be 6.8–7.4

General Considerations

Apart from the history, the diagnosis of burns is usually based on the presence of swollen eyelids with marked conjunctival hyperemia and chemosis. The limbus may show patchy balanced areas with conjunctival sloughing, especially in the interpalpebral area. There is usually corneal haze and diffuse edema, with wide areas of epithelial cell loss and corneal ulcerations. Corneal ulcerations can be better visualized with blue light following instillation of fluorescein.

Alkali Burns

Clinical Findings

Alkali burns (especially particulate alkali such as lime) are very serious, because even after apparent removal of the offending agent, tiny particles may remain lodged within the cul-de-sac and cause progressive damage to the eye.

Treatment

Instill a topical anesthetic immediately (proparacaine, 0.5%; or tetracaine, 0.5%), and then copiously irrigate the eye with 2–3 L isotonic saline solution, water, or lactated Ringer's solution. A lid retractor may be useful.

Double eversion of the eyelids should be performed to look for and remove material lodged in the cul-de-sac. Solid particles of alkali should be removed with forceps or a moist cotton swab. After particles have been removed, irrigate again. Do not attempt to neutralize the alkali with acid, because the exothermic reaction may cause further injury.

Instill topical mydriatic, cycloplegic eye drops, and antibiotic ointment. After irrigation, the pH of the eye should be checked and the range should be 6.8–7.4. If the pH is still high, continue with irrigation. Parenteral narcotic analgesia is often required for pain relief. If IOP is elevated, begin treatment with acetazolimide.

Disposition

Obtain ophthalmologic consultation.

Acid Burns

Clinical Findings

Acid burns as a rule cause damage more rapidly but are generally less serious than alkali burns, because they do not cause progressive destruction of ocular tissues (as do alkali burns).

Treatment

Immediately after exposure, irrigate the eyes copiously with sterile isotonic saline solution, lactated Ringer's, or tap water. Topical anesthetic (proparacaine, 0.5%) may be instilled to minimize pain during irrigation. Do not attempt to neutralize the acid with alkali.

Parenteral or oral narcotic analgesics may be necessary. Patch the eye if corneal defects are present.

Disposition

Obtain ophthalmologic consultation.

Thermal Burns

Clinical Findings

Injury due to thermal burns of the eyelids, cornea, and conjunctiva may range from minimal to extensive. Superficial corneal burns have a good prognosis, though corneal ulcers may occur as a result of loss of corneal epithelium.

Thermal burns of the skin of the eyelids may be first, second, or third degree. Conjunctival hyperemia is noted. The cornea may show diffuse necrosis of the exposed corneal epithelium in the interpalpebral area. Corneal haze due to corneal edema is frequently seen in thermal burns of the cornea and may lead to decrease in vision.

Treatment

The treatment of ocular burns is similar to the treatment of burns occurring elsewhere on the body (Chapter 45). Provide systemic analgesia. Instill proparacaine, 0.5%, or tetracaine, 0.5%, to minimize pain during manipulation. In cases of corneal burns, instill a mydriatic agent.

Disposition

Obtain ophthalmologic consultation.

Burns Due to Ultraviolet Radiation

Destruction of the corneal epithelium by ultraviolet light is known as actinic keratitis, snow blindness, and welder's arc burn (flash burn), depending on the source of ultraviolet radiation.

Clinical Findings

The patient complains of pain, extreme photophobia and gives a history of exposure to ultraviolet light 6–12 hours earlier (eg, skiing, welding, or tanning). Examination discloses tearing, conjunctival hyperemia, and corneal haziness. There may be a superficial punctate staining of the cornea seen with fluorescein and with magnification (eg, slit lamp).

Treatment

Topical anesthetic should be instilled during the eye examination only. Do not give the patient a topical anesthetic to use at home. Instill a mydriatic agent and an antibiotic ointment. Recovery occurs within 12–36 hours. Provide systemic analgesics for pain.

Disposition

Twenty-four hour follow-up should be arranged.

Mechanical Trauma to the Eye

Essentials of Diagnosis

• History is key to diagnosis
• Careful examination is needed
• Can be complicated by other injuries

General Considerations

Ocular trauma may be classified as penetrating or nonpenetrating. Trauma can lead to serious damage and loss of vision. Eye injuries are common in spite of the protection afforded by the bony orbit and the cushioning effect of orbital fat. Prevention and occupational safety measures should be stressed.

Evaluation

Obtain a history of the injury from the patient or witness. Measure and record visual acuity with and without correction. Inspect the eyelids, conjunctiva, cornea, anterior chamber, pupils, lens, vitreous, and fundus for breaks in tissue and hemorrhage. Search for corneal lesions (eg, abrasion) by instilling fluorescein dye and examining the eye using a light with a light-blue filter.

X-ray examination or CT scan may be indicated to rule out radiopaque foreign bodies and to look for fractures of orbital bones.

Treatment and Disposition

Consult an ophthalmologist immediately for patients with sight-threatening injuries. Avoid causing further damage by manipulation. For more detailed discussion of Treatment and Disposition, see under the specific type of injury.

For severe pain, photophobia, or foreign body sensation, instill a topical anesthetic (eg, proparacaine, 0.5%, one or two drops once or twice). Systemic analgesics may be required. Cover the eye with an eye shield.

Penetrating or Perforating Injuries

General Considerations

Penetrating or perforating ocular injuries require immediate careful attention and prompt surgical intervention to prevent possible loss of the eye and to preserve vision.

Many facial injuries, especially those occurring in automobile accidents, are associated with penetrating ocular trauma. Some injuries may be concealed and inapparent because of eyelid swelling or because the patient's other life-threatening injuries have (appropriately) dominated the attentions of the emergency department team. Such injuries, if not promptly attended to, may lead to loss of vision. Unfortunately, impaired or unconscious patients may have occult or untreated injuries as a cooperative patient is needed for an appropriate eye examination.

Evaluation

Obtain and record a description of how the injury occurred. Examine the eye and ocular adnexa, including vision testing if the patient's condition permits. Do not apply pressure on the globe. In the appropriate setting, CT scan is indicated to rule out intraocular radiopaque foreign body and to look for fractures of orbital bones.

Clinical Findings

Penetrating injuries are those that cause disruption of the outer coats of the eye (sclera, cornea) without interrupting the anatomic continuity of that layer, thus preventing prolapse or loss of ocular contents. Perforating injuries are those resulting in complete anatomic disruption (laceration) of the sclera or cornea. Such wounds may or may not be associated with prolapse of uveal structures. Wounds of the sclera or cornea are often associated with intraocular or intraorbital foreign bodies.

Treatment

The objectives of emergency management of ocular penetrating or perforating injuries are to relieve pain, preserve or restore vision, and achieve a good cosmetic result. Relieve pain with systemic analgesia, as needed. A sedative may be required. Cover the eye with an eye shield. Patch the uninjured eye also to minimize ocular movements. Do not manipulate the eye, instill eye drops, or apply antibiotic treatment.

Give tetanus prophylaxis, if needed (Chapter 30). Prohibit oral intake until the patient is examined by an ophthalmologist, since urgent surgery may be required. Provide hydration with intravenous fluids.

Give parenteral antibiotics directed against gram-negative and gram-positive organisms. Give antiemetic agents to prevent further injury from IOP increase.

Disposition

The patient should be seen on an emergency basis by an ophthalmologist for management of severe injuries, investigation of intraocular foreign bodies, and immediate surgical repair as required. Prompt repair of uveal prolapse decreases the risk of sympathetic ophthalmia in the uninjured eye. Delay in management of corneal lacerations may increase the risk of surgical and postoperative complications.

Blunt Trauma to the Eye, Adnexa, and Orbit

Contusions of the eyeball and ocular adnexa result from blunt trauma. The outcome of such an injury cannot always be determined, and the extent of damage may not be obvious upon superficial examination. Careful eye examination is needed, along with X-ray examination or CT scan when indicated.

Types of Injury

Eyelids

Check the eyelids for ecchymosis, swelling, laceration, and abrasions.

Conjunctiva

Check the conjunctiva for subconjunctival hemorrhages or laceration of the conjunctiva.

Cornea

Check the cornea for abrasion, edema, laceration, or rupture.

Anterior Chamber

Check the anterior chamber for hyphema, recession of angle, or secondary glaucoma.

Iris

Check the iris for iridodialysis, iridoplegia, rupture of iris sphincter, iris prolapse through corneal or scleral lacerations, or iris atrophy.

Ciliary Body

Check the ciliary body for hyposecretion of aqueous humor or for ciliary body prolapse through scleral lacerations.

Lens

Check the lens for dislocation or cataract.

Vitreous

Check the vitreous for hemorrhage or prolapse.

Ciliary Muscle

Check the ciliary muscle for paralysis or spasm.

Treatment and Disposition

Injury severe enough to cause intraocular hemorrhage (eg, vitreous hemorrhage or hyphema) involves the danger of delayed secondary hemorrhage from a damaged uveal vessel, which may cause intractable glaucoma and permanent damage to the globe. In such cases, ophthalmologic consultation is necessary to rule out other eye injuries.

Except for rupture of the globe itself, contusions do not usually require immediate definitive treatment. Apply an eye shield if the globe has been perforated and consult an ophthalmologist.

Ecchymosis of the Eyelids (Black Eye)

Clinical Findings

Blood in the periorbital tissues may occur from direct trauma or a blow to adjacent areas. The loose subcutaneous tissue around the eye permits blood to spread extensively. The diagnosis is usually obvious. Always rule out trauma to the eye itself (hyphema, blowout fracture, or retinal detachment).

Treatment

Apply cold compresses to decrease swelling and help stop bleeding. Exclude more serious ocular injury by careful examination.

Disposition

If the eye itself is uninjured, no follow-up contact is necessary.

Lacerations of the Eyelids

Clinical Findings

Lacerations or other wounds of the eyelids may be associated with serious ocular injuries not apparent at first examination. These could include injury to the lacrimal system, levator muscle, or optic nerve. A meticulous search for such injuries is indicated in every patient with eyelid lacerations.

Treatment and Disposition

Patients with lacerations of the eyelids require suturing and an extensive eye evaluation. Lacerations involving the tarsal plate, the upper eyelid levator mechanism, medial canthal area, and all through and through should be repaired by an ophthalmologist.

Orbital Hemorrhage

Clinical Findings

Exophthalmos and subconjunctival hemorrhage in a patient with a history of blunt trauma to the face suggest rupture of orbital blood vessels. There may be conjunctival chemosis or ecchymosis of the eyelids.

Treatment and Disposition

Apply cold compresses, and obtain urgent ophthalmologic consultation.

Fracture of the Ethmoid Bone

The ethmoid bone is part of the medial wall of the orbit. Fracture of the ethmoid bone most frequently occurs with blunt trauma to the orbit.

Clinical Findings

Fracture of the ethmoid bone is most commonly manifested by subcutaneous emphysema of the eyelids. There may or may not be ecchymosis of the eyelids. Imaging reveals air in the orbit. Fractures of other orbital bones should be ruled out by radiography.

Treatment

Fractures of the ethmoid bone usually do not require operative reduction. Provide analgesia as needed. Apply cold compresses. Give systemic antibiotic. Instruct the patient to avoid sneezing or blowing the nose.

Disposition

Refer the patient to an ophthalmologist or facial surgeon within 1 or 2 days.

Blowout Fractures of the Floor of the Orbit

Clinical Findings

Blowout fracture may be associated with enophthalmos and hypotropia (visual axis of the injured eye is displaced downward in comparison to that of the sound eye), diplopia in the primary position or in upward gaze, limitation of ocular movement in upward gaze, and decreased or absent sensation over the maxilla. CT scan of the orbit shows orbital floor displacement.

Treatment

Provide analgesia as needed. Apply a topical antibiotic ointment such as gentamicin, 0.3%. Apply cold compresses and a sterile eye patch.

Disposition

Seek early consultation with an ophthalmologist or other facial surgeon.

Corneal Abrasions

Essentials of Diagnosis

• Pain, photophobia, blurry vision
• Uptake of fluorescein stain is key to diagnosis
• Always rule out globe perforation

Clinical Findings

The patient complains of pain, photophobia, and blurring of vision. There is usually a history of trivial trauma. Patients with severe pain and blepharospasm may require proparacaine, 0.5%, instilled in the eye to facilitate eye examination. In severe cases, the eye is red and the corneal surface is irregular and loses its normal luster. Staining with fluorescein reveals a defect in the corneal epithelium. Rule out infection or perforation of the globe as necessary.

Treatment

Irrigate the eye gently with sterile saline solution if needed to remove debris and loose foreign bodies. In severe cases, instill tropicamide to relax the ciliary muscle and relieve pain. Instill ophthalmic antibiotic ointment. Caution: Do not use ointment containing corticosteroids. Consider nonsteroidal anti-inflammatory ophthalmic drops for pain control. Provide systemic analgesia as needed. Never give the patient topical anesthetics, which may lead to irreversible corneal damage.

Disposition

Refer patients for daily outpatient follow-up care. Ophthalmologic consultation should be obtained for corneal abrasions that fail to resolve in 48–72 hours.

Corneal and Conjunctival Foreign Bodies

Essentials of Diagnosis

• Pain, foreign body sensation
• Examine using fluorescein stain; make sure to look under lids
• May need to rule out intraocular foreign body

Clinical Findings

There may be a history of working with high-speed tempered steel tools (eg, drilling), or there may be no history of trauma to the eye and the patient may even be unaware of a foreign body in the eye. In most cases, however, the patient complains of a foreign body sensation in the eye or under the eyelid, or just irritation in the eye. A corneal foreign body can be seen with the aid of a loupe and well-focused diffuse light or slit lamp. Conjunctival foreign bodies often become embedded in the conjunctiva under the upper eyelid. The lid must be everted to facilitate inspection and removal.

Fluorescein should be instilled to visualize minute foreign bodies not readily visible with the naked eye, loupe, or slit lamp. Rule out intraocular foreign body with soft tissue X-ray or CT scan as indicated.

Treatment

Some loose foreign bodies can be removed with a moist cotton swab. Foreign bodies superficially embedded can be removed with the tip of a hypodermic needle or blunt spud. Anesthetize the cornea first with proparacaine or tetracaine solution, 0.5%. Instill ophthalmic antibiotic ointment (gentamicin, 0.3%; or sulfacetamide, 10%) or eye drops after the foreign body has been successfully removed.

Disposition

The patient should be seen again in 24 hours unless they have no symptoms or changes in vision. Referral to an ophthalmologist may be indicated for deep corneal foreign bodies or large foreign bodies within the visual axis.

Traumatic Lens Dislocation and Cataract Formation

Clinical Findings

Lens dislocation following blunt trauma to the eye may present with double vision in one eye (rarely both), blurred vision, and distortion. A tremor of the iris after rapid eye movements may also be present. The lens may be visualized by ophthalmoscopy or imaging with CT scan. History and physical are critical to diagnosis. Lens dislocation may also be associated with medical disorders, such as Marfan syndrome, homocystinuria, or spherophakia. Lens dislocation becomes an emergency if the subluxed lens (anterior subluxation) obstructs aqueous flow, leading to acute glaucoma. If the lens capsule is disrupted, the stroma of the lens may swell and become cloudy, also leading to acute glaucoma and development of cataracts. These may also be present after lightning strike or electrical injury.

Treatment

Patients with lens dislocation should be referred to an ophthalmologist for surgical repair, with emergent referral for increased IOP. There is no treatment for traumatic cataracts.

Disposition

Emergent ophthalmology referral for dislocation associated with increased IOP, otherwise timely referral to ophthalmologist is sufficient.

Basic Equipment

A great many specialized instruments have been devised for the investigation of eye disorders. Most emergency conditions can be diagnosed with the aid of a few relatively simple instruments. The following should be available in the emergency department:

• Hand held flashlight with fresh batteries
• Slit lamp
• Ophthalmoscope (preferably with a blue filter lens)
• Visual acuity chart (Snellen)
• Tonometer
• Pinhole and occluder
• Eye shield (plastic or metal) and tape

Basic Medications

See Table 31–5.

Local Anesthetics

Proparacaine, 0.5%, or tetracaine, 0.5%, may be used. These medications have white caps on the bottles.

Dyes

Fluorescein papers or drops should be available.

Mydriatics

These medications have red caps on the bottles. Tropicamide ophthalmic solution, 0.5% or 1%, is a satisfactory mydriatic when the examiner wishes to obtain a clear view of the lens, vitreous, or ocular fundus. It may also be used for short-term relief for ciliary spasm.

Miotics

Miotic drops have green caps. The miotic agent pilocarpine, 1% or 2%, should be on hand.

Antibacterial Agents

Antibacterial agents include tetracycline, 1% ophthalmic ointment; polymyxin B-bacitracin ophthalmic ointment; sulfacetamide, 10% ophthalmic solution or ointment; erythromycin, 0.5% ointment; ciprofloxacin, 0.3% drops; and polymyxin B trimethoprim solution or gentamicin, 0.3% ointment.

Eversion of the Upper Eyelid

The patient is instructed to look down. Grasp the eyelashes at the outer margin of the lid with the thumb and forefinger of one hand, and gently and slowly draw the lid downward and outward. Using a cotton swab, press against the upper edge of the tarsus over the center of the lid while turning the lid margin rapidly outward and upward over the applicator. With the lashes thus held against the upper orbital rim, the exposed palpebral conjunctiva can be inspected closely. After the examination is completed and the foreign body removed (if possible), when the patient looks up, the lid returns to its normal position.

Eye Drops

The patient should sit with both eyes open and looking up. Pull down slightly on the lower lid, and place two drops in the lower cul-de-sac. The patient is then asked to look down while finger contact on the lower lid is maintained. Do not let the patient squeeze the eye shut. Do not touch the eye or the eyelid with the applicator; likewise, do not instill eye drops with the dropper held far away from the eye.

Ointments

Ointments are instilled in the same way as liquids. While the patient is looking up, lift out the lower lid to trap the medication in the conjunctival sac.

Warm Compresses

Use a clean towel or washcloth soaked in warm tap water well below the temperature that will burn the thin skin covering the eyelids. Warm compresses are usually applied to the area for 15 minutes four times daily. The therapeutic rational is to increase blood flow to the affected area and decrease pain and inflammation.

Removal of Superficial Corneal Foreign Body

The main considerations are good illumination, magnification, anesthesia, proper positioning of the patient, and sterile technique. The patient's visual acuity should be recorded first.

The patient may be sitting or supine. A loupe should be used unless a slit lamp is available. An assistant should direct a strong flashlight into the eye at an oblique angle. The examiner may then see the corneal foreign body and remove it with a moist cotton swab. If this is not successful, the foreign body may be removed with a metal spud while the lids are held apart with the other hand to prevent blinking. An antibacterial ointment may be instilled after the foreign body has been removed.

Home Medication

At home, the same techniques should be used as described above except that drops should be instilled with the patient lying supine. Experienced patients (eg, those with glaucoma) are usually quite skillful in self-administration of eye drops.

Tonometry

Tonometry is the determination of IOP using a special instrument that measures the amount of corneal indentation produced by a given weight. Tonometry readings should be taken on any patient suspected of having increased IOP.

Precautions

Tonometry should be done with great caution on patients with corneal ulcers. It is extremely important to clean the tonometer before each use by carefully wiping the footplate with a cotton swab moistened with sterile solution (be sure it is dry before using) and to sterilize the instrument. Corneal abrasions are rarely caused by tonometry. Epidemic keratoconjunctivitis can be spread by tonometry, and this can be prevented if the tonometer is cleaned before each use and the principle of handwashing between patients is meticulously observed. Disposable covers are also available for some tonometers.

Technique

Anesthetic solution (tetracaine, 0.5%; or proparacaine, 0.5%) is instilled into each eye. The patient lies supine and is asked to stare at a spot on the ceiling with both eyes or at a finger held directly in the line of gaze overhead. The lids are held open without applying pressure on the globe. The tonometer is then placed on the corneal surface of each eye and the scale reading taken from the tonometer. The IOP is determined by referring to a chart that converts the scale reading to millimeters of mercury for a Schiotz tonometer or by digital readout on the electronic devices. Normal IOP is 12–20 mm Hg.

Interpretation of Abnormalities

If the IOP is 20 mm Hg or more, further investigation is indicated to determine whether glaucoma is present.

Corneal Staining

Corneal staining consists of instillation of fluorescein into the conjunctival sac to outline irregularities of the corneal surface. Staining is indicated in corneal trauma or other corneal disorders (eg, herpes simplex keratitis) when examination with a loupe or slit lamp in the absence of a stain has not been satisfactory.

Precautions

Because the corneal epithelium—the chief barrier to corneal infection—is usually interrupted when corneal staining is indicated, be certain that whatever dye is used (particularly fluorescein) is sterile.

Equipment and Materials

Note: Fluorescein must be sterile. Fluorescein papers or sterile individual dropper units are safest. Fluorescein solution from a dropper bottle may be used, but there is a substantial risk of contamination.

Technique

The individually wrapped fluorescein paper is wetted with sterile saline or touched to the wet conjunctiva so that a thin film of fluorescein spreads over the corneal surface. Any irregularity in the cornea is stained by the fluorescein and is thus more easily visualized using a light with a blue filter.

Normal and Abnormal Findings

If there is no superficial corneal irregularity, a uniform film of dye covers the cornea. If the corneal surface has been altered, the affected area absorbs more of the dye and will stain a deeper green.

Estimation of Anterior Chamber Depth

(See Figure 31–3.) Using a hand flashlight, shine the light obliquely and parallel to the plane of the iris across the cornea and anterior chamber. A normal anterior chamber will be fully illuminated. With a shallow anterior chamber (as in angle-closure glaucoma), the anteriorly displaced iris will cast a shadow.

Dangers in the Use of Local Anesthetics

Unsupervised self-administration of local anesthetics is dangerous, as the patient may further injure an anesthetized eye without knowing it. Furthermore, most anesthetics delay healing. This is particularly true of butacaine, which also elicits a high incidence of allergic responses. Therefore, patients should not be given local anesthetics to take home. Eye pain should be controlled by systemic analgesics.

Errors in Diagnosis

The most common mistaken ophthalmologic diagnosis is conjunctivitis when the correct diagnosis should be iritis (anterior uveitis), glaucoma, or corneal ulcer (especially herpes simplex ulcer). The differentiation between iritis and acute glaucoma may be difficult also.

Misuse of Atropine

Atropine must never be used in routine diagnosis. It causes cycloplegia (paralysis of the ciliary muscle) of about 14 days' duration and can precipitate an attack of glaucoma if the patient has a narrow anterior chamber angle.

Dangers of Local Corticosteroid Therapy

Local ophthalmologic corticosteroid preparations (eg, prednisolone) are often used for their anti-inflammatory effect on the conjunctiva, cornea, and iris. Although a patient with conjunctivitis, corneal inflammation, or iritis can be made more comfortable with topical corticosteroids, it must be stressed that the corticosteroids are associated with four very serious complications when used in the eye: herpes simplex keratitis, open-angle glaucoma, cataract formation, and fungal infection.

Corticosteroids should not be used unless specifically indicated (eg, in iritis, certain types of keratitis, and acute allergic disorders), and patients using prescribed topical corticosteroids should always see an ophthalmologist for follow-up examination.

Overtreatment

Some patients with chronic conjunctivitis or keratitis may be made worse by overtreatment with topical medications. These patients should be evaluated by an ophthalmologist.