Steven Go
OCULAR INFECTIONS/ACUTE OCULAR INFLAMAITION
PRESEPTAL (PERIORBITAL) CELLUUTIS
Preseptal cellulitis occurs mostly in patients <10 years old, is commonly associated with upper respiratory infection (URI), eyelid problems, and trauma, and is usually caused by Staphylococcus aureus, Staphylococcus epidermidis, and Streptococcus species.
Preseptal cellulitis presents with warm, indurated, and erythematous eyelids, without decreased visual acuity, restriction of ocular motility, proptosis, painful eye movement, or impairment of pupillary function.
Emergency department (ED) care in patients >5 years old includes oral amoxicillin-clavulanate (22.5 milligrams/kg/dose up to 875 milligrams twice daily), warm packs, and close follow-up with an ophthalmologist.
For toxic-appearing patients, severe cases, patients with significant comorbidities, or children <5 years, hospital admission for parenteral broad-spectrum antibiotics (eg, ceftriaxone [50-75 milligrams/kg daily] and vancomycin [15 milligrams/kg every 12 hours]) may be required.
Young children also require an ophthalmology consultant and may require a septic workup because concurrent bacteremia and meningitis can be present.
POSTSEPTAL (ORBITAL) CELLULITIS
Postseptal cellulitis most frequently spreads from sinusitis (most commonly ethmoid), and predisposing factors also include preseptal cellulitis, trauma, foreign body, bacteremia, and ocular surgery. Infection is usually polymicrobial, with S. aureus, Streptococcus pneumoniae, and anaerobes being the most common. Atypical organisms can occur in the unimmunized (Haemophilus influenzae) and immunocompromised (mucormycosis in diabetics).
Postseptal cellulitis should be suspected whenever signs and symptoms of periorbital cellulitis presents with fever, painful ocular motility, proptosis, decreased visual acuity, limited extraocular movements (EOMs), chemosis, or pupillary abnormalities. Cranial nerve (CN) abnormalities indicate associated cavernous sinus thrombosis.
Emergent diagnosis with orbital and sinus thin-slice computed tomography (CT) scan without contrast is required. If this study is negative, a CT scan with contrast should be done, which may reveal a subperiosteal abscess.
Emergent ophthalmologic consultation and hospital admission for broad-spectrum intravenous antibiotics (with aerobic and anaerobic coverage) are required. In rare cases, emergent lateral canthotomy may be indicated for elevated intraocular pressure or optic neuropathy.
STYE (EXTERNAL HORDEOLUM)
A stye is an acute infection (usually S. aureus) of an oil gland at the lid margin.
ED care of a stye includes warm compresses and erythromycin ointment for 7 to 10 days. Lid hygiene with baby shampoo may also be helpful.
CHALAZION
A chalazion is an acute or chronic noninfectious inflammation of the meibomian gland. Acute cases tend to be painful and often cannot be differentiated from an internal hordeolum, while chronic cases are usually painless.
For an acute chalazion, ED care is the same as for a stye, plus a 14- to 21-day regimen of doxycycline (100 milligrams twice daily in adults, 2.2 milligrams/kg/dose twice daily in children) for refractory cases.
Persistent chalazia should be referred to an ophthalmologist for incision, curettage, and biopsy.
CONJUNCTIVITIS
Bacterial conjunctivitis presents with eyelash matting, mucopurulent discharge, and conjunctival inflammation without corneal lesions. Typical pathogens are Staphylococcus and Streptococcus species. A slit lamp examination with fluorescein should be done to exclude other important disease entities (eg, herpes keratitis).
Bacterial conjunctivitis is treated with topical antibiotic drops (Table 151-1).
TABLE 151-1 Common Ophthalmic Medications Used in the Emergency Department
Contact lens wears should receive ciprofloxacin, ofloxacin, or tobramycin topical antibiotic coverage for Pseudomonas. The worn contact lenses should be discarded and use of new contact lenses should not be resumed until the infection has completely cleared.
Childhood conjunctivitis pathogens may include H. influenzae and Moraxella catarrhalis, so if initial treatment is unsuccessful, a change in antibiotics is warranted.
A severe purulent discharge with a hyperacute onset (within 12-24 hours) should prompt an emergent consult with an ophthalmologist for an aggressive workup of possible gonococcal conjunctivitis. Initial ED treatment involves Neisseria gonorrhoeae culture, parenteral antibiotics, and saline irrigation to remove the discharge.
Viral conjunctivitis presents as a monocular or binocular watery discharge, chemosis, and conjunctival inflammation most commonly caused by adenovirus.
Viral conjunctivitis is often associated with viral respiratory symptoms and a palpable preauricular node. Conjunctival follicles are present.
Fluorescein staining may reveal occasional superficial punctate keratitis, but should otherwise be clear.
Treatment of viral conjunctivitis consists of cool compresses, naphazoline/pheniramine as needed for conjunctival congestion, and ophthalmology follow-up in 7 to 14 days.
Epidemic keratoconjunctivitis is a severe, epidemic, highly contagious type of adenovirus conjunctivitis. It is often preceded with flu-like symptoms (including nausea and vomiting), and often involves marked injection of the conjunctiva, sometimes with frank hemorrhage. Slit lamp examination reveals diffuse superficial keratitis without ulceration. Treatment is supportive as described above, but symptoms may persist for 2 or 3 weeks. The virus survives on inanimate objects for 5 weeks and is not killed by alcohol-based hand gels; therefore, proper anti-infective precautions should be taken.
Allergic conjunctivitis presents as a monocular or binocular pruritus, watery discharge, and chemosis with a history of allergies.
There should be no lesions with fluorescein staining, and preauricular nodes should be absent. Conjunctival papillae are seen on slit lamp examination.
Treatment of allergic conjunctivitis consists of elimination of the inciting agent, cool compresses, artificial tears, and naphazoline/pheniramine. Diphenhydramine and topical fluorometholone may be helpful in severe cases.
HERPES SIMPLEX VIRUS
Herpes simplex virus (HSV) infection can involve eyelids, conjunctiva, and cornea.
The classic dendrite of herpes keratitis appears as a linear branching, epithelial defect with terminal bulbs that stain brightly with fluorescein dye during slit lamp examination. However, variant presentations abound, including “geographic ulcer,” neurotrophic ulceration, and isolated uveitis. Decreased corneal sensation may be a clue to the diagnosis.
ED care depends on the site of infection: eyelid involvement may be treated with oral acyclovir, while conjunctival involvement requires topical antivirals (eg, trifluridine) five times daily with or without topical erythromycin ointment and warm soaks.
If the cornea is involved, the trifluorothymidine dosage is increased to nine times daily plus vidarabine ointment.
Steroids should not be prescribed, and telephone consult with an ophthalmologist to arrange 24- to 48-hour follow-up is probably prudent.
Neonatal HSV conjunctivitis requires an emergent ophthalmology consult, parenteral antivirals, and a septic workup.
HERPES ZOSTER OPHTHALMICUS
Herpes zoster ophthalmicus (HZO) is shingles with a trigeminal distribution, ocular involvement, and frequently, a concurrent iritis.
The presence or eventual development of HZO should be suspected in any patient whose shingles involve the tip of the nose (Hutchinson sign).
A “pseudo-dendrite” (a poorly staining mucous corneal plaque without epithelial erosion) may be seen. Iritis may also be seen.
ED care for cutaneous lesions includes oral acyclovir therapy (for lesions <1 week old), along with erythromycin ointment with cool compresses.
Conjunctivitis is treated with ophthalmic ointment, while iritis without corneal involvement may be treated with topical steroids and cycloplegics.
Ophthalmologic consultation is advised for iritis, corneal lesions, or involvement of the orbit, optic nerve, or CNs. Hospitalization and parenteral acyclovir may be required.
CORNEAL ULCER
These infections of the corneal stroma present with pain, redness, and photophobia. Etiologies include desiccation, trauma, direct invasion, and contact lens use, typically in association with Pseudomonas aeru-ginosa (see Fig. 151-1).
Additional organisms associated with corneal ulcer include the bacteria Strep. pneumoniae, Staphylococcus species, Moraxella species; the viruses herpes simplex and varicella zoster; and the fungi Candida, Aspergillus, Penicillium, and Cephalosporium.
Slit lamp examination reveals a staining corneal defect with a surrounding white hazy infiltrate, or heaped-up edges. If an associated iritis is present, a hypopyon may be seen.
ED care includes hourly topical ofloxacin or cipro-floxacin drops.
Topical cycloplegia helps relieve pain, but patching is contraindicated. An ophthalmologist should evaluate the patient within 12 to 24 hours.
FIG. 151-1. Corneal ulcer. An elliptical ulcer at 5 o’clock near the periphery is seen. This location is atypical for a bacterial ulcer. The patient presented with painful red eyes and normal uncorrected vision, but was a new wearer of soft contact lenses. Bilateral corneal ulcers were diagnosed, which cleared after treatment with topical ciprofloxacin. The impressive ciliary flush is pathognomonic for corneal (versus conjunctival) pathology. (Photo contributed by Kevin J. Knoop, MD, MS. Knoop KJ, Stack LB, Storrow AB, Thurman RJ: The Atlas of Emergency Medicine, 3rd ed: http://www.accessmedicine.com. © The McGraw Hill Companies, Inc. All rights reserved.)
UVEITIS/IRITIS
Iritis is inflammation of the anterior uveal tract (iris and ciliary body) that has many causes (Table 151-2). It presents with red eye, photophobia, and decreased vision.
Consensual photophobia, perilimbal flush, and a miotic poorly reactive pupil are characteristic of the diagnosis. Slit lamp examination reveals WBCs in the anterior chamber, usually with associated flare, and a hypopyon can eventually occur. Fluorescein examination should be done because possible etiologies may be detected (corneal abrasion, ulcer, or dendrite).
Once iritis is diagnosed, an appropriate ED workup for a systemic etiology should be undertaken (Table 151-2).
Treatment is directed toward the underlying cause if found, and symptomatic treatment with homatropine or tropicamide (Table 151-1) is helpful. Steroid drops can be of value, but should only be given if directed by the ophthalmologist.
Ophthalmology consultation is appropriate with follow up in 24 to 48 hours.
TABLE 151-2 Differential Diagnosis of Iritis
ENDOPHTHALMITIS
Endophthalmitis is inflammation involving the deep structures of the globe, most commonly postsurgical or from penetrating trauma, although hematologic spread is possible. Pathogens include Staphylococcus, Streptococcus, Haemophilus, and Bacillus.
Patients present with headache, eye pain, photophobia, ocular discharge, and vision loss. Examination reveals lid edema and erythema, conjunctival injection and chemosis, hypopyon, and evidence of uveitis.
Emergency ophthalmology consultation and admission are warranted. Treatment includes intraocular and systemic antibiotics. Steroids intravitreally or orally may be used by the ophthalmologist, and admission is warranted except for postoperative cases.
VITREOUS HEMORRHAGE
Traction to vitreous attachments from trauma or neo-vascularization can cause hemorrhage into or behind the vitreous.
Such bleeds are associated with diabetic retinopathy, sickle-cell disease, retinal detachment, central retinal vein occlusion, lupus, vitreous detachment in the elderly, and shaken baby syndrome. It is seen rarely in subarachnoid hemorrhage.
Patients present with sudden, painless vision loss with black spots, cobwebs, or hazy vision. Examination reveals a poor view of the posterior segment due to hemorrhage.
An emergent ophthalmology consult is warranted and ocular US may be used to rule out retinal detachment.
OCULAR TRAUMA
SUBCONJUNCTIVAL HEMORRHAGE
Disruption of conjunctival blood vessels may occur from trauma, sneezing, gagging, or the Valsalva maneuver, and will resolve spontaneously within 2 weeks.
When a dense, circumferential bloody chemosis is present, globe rupture must be excluded.
CONJUNCTIVAL ABRASION, LACERATION, AND FOREIGN BODY
These corneal lesions present primarily with a foreign body sensation without vision loss. They may be impossible to see without fluorescein slit lamp examination.
In the presence of abrasions or lacerations, an intraocular foreign body should be excluded. A Seidel’s test should be performed, but it can be falsely negative if a small laceration has spontaneously closed.
Foreign bodies can usually be removed with a moistened cotton applicator.
Superficial conjunctival lesions are treated with erythromycin ointment for 2 or 3 days.
CORNEAL ABRASION
Trauma may cause superficial or deep corneal abrasions that present with tearing, photophobia, blepharospasm, and severe pain, which are relieved by a topical anesthetic.
Instilled fluorescein will reveal dye uptake at the site of the defect. When multiple linear abrasions or punctate keratitis are present, an ocular foreign body underneath the upper lid must be excluded.
ED care includes administration of a cycloplegic (contraindicated in narrow anterior chamber angle patients) and topical antibiotics may be prescribed (Table 151-3).
Contact lens abrasions are treated with ciprofloxacin, ofloxacin, or tobramycin drops to cover Pseudomonas.
Tetanus status should probably be updated on all patients with corneal abrasions, especially when organic or soil-based materials are involved.
Recent studies suggest that patching does not facilitate abrasion healing and is also absolutely contraindicated in dirty abrasions and contact lens abrasions.
Once the diagnosis of a simple abrasion is made, NSAID ophthalmic drops should be considered for pain control. Opioid analgesia may also be necessary for severe pain.
Topical anesthetics for home use are strictly contraindicated.
Intraocular foreign bodies should be suspected if a history compatible with penetrating injury is present.
Ophthalmology follow-up is advised within 24 hours for all corneal abrasions.
TABLE 151-3 Suggested Ophthalmic Antibiotics for Corneal Abrasions
CORNEAL LACERATION
The presentation of corneal lacerations can vary from obvious (misshapen lens, shallow anterior chamber, and hyphema) to occult (spontaneous closure, negative Seidel’s test, and grossly normal anatomy).
Pain out of proportion to examination and decreased visual acuity associated with a high-risk mechanism (including the use of high-speed machinery) should raise suspicion of this injury.
CT of orbit should be obtained, but the sensitivity for this injury is only 56% to 68%.
ED consultation with an ophthalmologist should be obtained.
ULTRAVIOLET KERATITIS
Ultraviolet (UV) keratitis results from excess UV exposure, typically from tanning booths, welding flashes, or prolonged sun exposure.
Severe pain and photophobia develop 6 to 12 hours after exposure. Conjunctival hyperemia and superficial punctate keratitis are seen.
ED care is the same as for superficial corneal abrasions.
CORNEAL FOREIGN BODIES
Corneal foreign bodies can result from numerous mechanisms. They may present with associated iritis and presence of hyphema suggests the presence of globe perforation.
Superficial corneal foreign bodies may be removed with a fine needle tip, eye spud, or eye burr after applying a topical anesthetic. The resultant corneal defect should be treated as a corneal abrasion.
Deep corneal stoma foreign bodies or those in the central visual axis require ophthalmology consultation for removal.
Rust rings are associated with metallic foreign bodies and may be removed with an eye burr, although emergent removal is not required.
Residual rust, central visual axis lesions, or deep stro-mal involvement requires ophthalmologic follow-up within 24 hours.
LID LACERATIONS
Damage to the eye and nasolacrimal system must be excluded in all eyelid and adnexal lacerations.
Less than 1 mm lid edge lacerations do not require repair.
Visible orbital fat is a clue to a penetrated ocular septum.
Any full-thickness laceration raises the possibility of corneal laceration and globe rupture.
Fluorescein instilled into the tear layer that appears in an adjacent laceration confirms injury to the nasolacrimal system.
Suspected or proven nasolacrimal injuries, lid margin lacerations, levator mechanism lacerations, ptosis, and all through-and-through lid lacerations require ophthalmology consultation for repair.
BLUNT TRAUMA
In blunt trauma, the integrity of the globe must be immediately assessed, as well as the visual acuity.
Signs such as an abnormal anterior chamber depth, an irregular pupil, or blindness indicate a ruptured globe until proven otherwise. Therefore, if any of these signs are present, the examination should be terminated and the eye shielded, and an emergent ophthalmology referral is indicated.
If the globe appears intact, a complete examination (including a slit lamp examination with fluorescein) should be done and CT scan of facial bones be obtained.
Traumatic iritis in the absence of a corneal injury can be treated with topical prednisolone acetate and cyclopentolate in conjunction with an ophthalmologist.
The care of the blunt trauma eye patient should be discussed with an ophthalmologist, and the patient should follow up with them within 48 hours even if no significant injuries are initially found.
HYPHEMA
A hyphema is blood in the anterior chamber, and it can occur spontaneously (sickle-cell or coagulopathy patients) or following trauma (Fig. 151-2).
Rebleeding can occur 3 to 5 days following the initial injury and is associated with a high complication rate.
ED care includes placing the patient upright to allow the blood to settle inferiorly, and placement of a protective eye shield. Pupillary dilatation (to avoid stretching a presumed leaking iris vessel) may be indicated, but should be done in conjunction with an ophthalmologist.
After ruptured globe has been excluded, intraocular pressure should be measured and controlled (see the Acute Angle Closure Glaucoma section below).
Sickle-cell patients should not receive carbonic anhy-drase inhibitors, which can cause RBC sickling within the anterior chamber and thereby increase intraocular pressure.
In every hyphema, emergent evaluation at the bedside by an ophthalmologist is indicated.
FIG. 151-2. Hyphema. This hyphema is just beginning to layer out reflecting its acute nature. (Photo contributed by Lawrence B. Stack, MD. Knoop KJ, Stack LB, Storrow AB, Thurman RJ: The Atlas of Emergency Medicine, 3rded: http://www.accessmedicine.com. © The McGraw Hill Companies, Inc. All rights reserved.)
BLOWOUT FRACTURES
The inferior and medial wall (lamina papyracea) of the orbit may be fractured from blunt trauma.
One-third of blowout fractures are associated with ocular trauma.
Physical examination signs include evidence of inferior rectus entrapment (diplopia on upward gaze), paresthesia of the infraorbital nerve, and subcutaneous emphysema, especially when sneezing or blowing the nose.
CT of the orbit with thin cuts is the radiographie test of choice to define the lesion.
ED care includes excluding associated ocular traumatic lesions and oral antibiotics (typically cephalexin).
All blowout fractures (with or without entrapment) require referral to an appropriate specialist within the next 3 to 10 days. Even if the initial eye examination is normal, the patient should receive an outpatient fully dilated examination to rule out any associated retinal injuries.
RUPTURED GLOBE
Ruptured globe can result from both blunt and penetrating trauma. Any projectile injury can penetrate the eye and any puncture or laceration of the eyelid or periorbital area should raise suspicion of this injury.
High-risk mechanisms include hammering metal on metal, use of high-speed machinery, and explosion-related injuries.
Associated eye pain may range in severity, and visual acuity may or may not be affected.
Suggestive findings include a severe subconjunctival hemorrhage, irregular or teardrop-shaped pupil, afferent pupillary defect, shallow or deep anterior chamber compared with the other eye, hyphema, limitation of extraocular motility, extrusion of globe contents, lens dislocation, or a significant reduction in visual acuity. However, examination may be virtually normal as well with very small wounds.
Fluorescein streaming (Seidel’s test) is pathogno-monic, although it may be absent.
Once a globe injury is suspected, any further manipulation or examination of the eye must be avoided at all costs, including measurement of intraocular pressure.
ED care includes placing the patient upright and NPO (nothing by mouth), placing a protective metallic eye shield, administration of intravenous broad-spectrum antibiotics, analgesia, sedation, and antiemetic therapy. Tetanus status should be updated if necessary.
A CT of the orbit with thin cuts is the test of choice to screen for an intraocular foreign body. US may assist in the diagnosis, but care must be taken not to apply pressure to the eye. MR is contraindicated with metallic foreign bodies.
Whether or not ruptured globe is a contraindication to the use of succinylcholine remains a controversial topic.
An ophthalmologist should be called immediately if a globe rupture or a penetrating injury is strongly suspected.
RETROBULBAR HEMATOMA
Blunt trauma can cause blood to collect within the retrobulbar space, which can raise the intraocular pressure, causing decreased blood flow.
Patients present with pain, decreased vision, and proptosis.
Diagnosis is confirmed by CT scan of the orbit, and intraocular pressure should be measured if ruptured globe not present.
Intraocular pressure >40 mm Hg should prompt consideration of emergent lateral canthotomy.
Emergent ophthalmology consultation should be obtained, but should not delay canthotomy.
CHEMICAL OCULAR INJURY
Acid and alkali burns are managed similarly. The eye should be immediately flushed in the prehospital setting, and sterile normal saline or Ringer’s lactate Morgan Lens® irrigation should be continued in the ED immediately upon arrival (even before visual acuities or patient registration) until the pH is normal (7.0-7.4).
Once the pH is normal, the fornices should be swept to remove residual particles and any necrotic conjunctiva. The pH should be rechecked in 10 minutes to ensure that no additional corrosive is leaching out from the tissues.
After irrigation, a full slit lamp examination should be done to evaluate the cornea and detect iritis. Intraocular pressure should be measured.
An attempt to identify the substance should be made to research its pH.
A cycloplegic and narcotic pain medication should be prescribed. Tetanus status should be updated.
Chemosis indicates the existence of “chemical conjunctivitis” and requires the use of erythromycin ointment.
Ophthalmology consultation is appropriate for all but the most minor burns. An ophthalmologist should evaluate the patient in the ED if there are signs of a severe injury, such as a pronounced chemosis, conjunctival blanching, corneal edema, defect, or opacifi-cation, or increased intraocular pressure.
CYANOACRYLATE (SUPER GLUE/CRAZY GLUE) EXPOSURE
Cyanoacrylate glue easily adheres to the eyelids and corneal surface. Corneal injuries can occur from the hard particles that form.
Initial manual removal is facilitated by heavy application of erythromycin ointment, with special care taken not to damage underlying structures.
After the easily removable pieces are removed, the patient should be discharged with erythromycin ointment to be applied five times a day in order to soften the remaining glue.
Complete removal of the residual glue can be accomplished by the ophthalmologist at a follow-up visit within 24 hours.
ACUTE VISUAL REDUCTION OR LOSS
ACUTE ANGLE CLOSURE GLAUCOMA
Acute angle closure glaucoma presents with eye pain, headache, cloudy vision, colored halos around lights, cloudy or steamy appearance of the cornea (see Fig. 151-3), conjunctival injection, a fixed mid-dilated pupil, and increased intraocular pressure of 40 to 70 mm Hg (normal range: 10-20 mm Hg) (Fig. 151-3). Nausea and vomiting are also common.
Sudden attacks in patients with narrow anterior chamber angles can be precipitated by pupillary dilation in movie theaters, while reading, and after administration of dilatory agents or inhaled anticholinergics.
The diagnosis is confirmed by measuring the intraocular pressure as diagnosis by manual palpation is unreliable.
ED care is designed to decrease the intraocular pressure. Immediate medications to administer include timolol, apraclonidine, and prednisolone acetate (Table 151-4).
If intraocular pressure is greater than 50 mm Hg or if vision loss is severe, then acetazolamide 500 milligrams IV should be considered.
If intraocular pressure does not decrease and vision does not improve in 1 hour, IV mannitol should be given.
Pilocarpine 1% to 2% in the affected eye and pilocarpine 0.5% in the contralateral eye may be administered once intraocular pressure is less than 40 mm Hg as long as the patient has a natural lens in place.
Symptoms of pain and nausea should be treated, and the intraocular pressure monitored hourly. All cases require emergent in-person ophthalmologic consultation, but treatment should not be delayed for consultation. All subsequent treatment and disposition decisions should be made in conjunction with the ophthalmologist at the bedside.
FIG. 151-3. Acute angle-closure glaucoma: Note the cloudy/steamy appearance of the cornea and the midposition dilated pupil. Conjunctival injection is usually more prominent than in this case. (Reproduced with permission from Knoop K, Stack L, Storrow A: Atlas of Emergency Medicine, 2nd ed. © 2002, McGraw-Hill, New York.)
TABLE 151-4 Treatment of Acute Glaucoma
OPTIC NEURITIS
Inflammation of the optic nerve can be caused by infection, demyelination, and autoimmune disorders. It is famously associated with multiple sclerosis.
Optic neuritis may present with various degrees of vision loss (often with poor color perception), pain during extraocular movement, visual field cuts, and an afferent pupillary defect.
Swelling of the optic disc may be seen in anterior optic neuritis (30%).
Diagnosis can be made with the red desaturation test (after staring at a bright red object with the normal eye only, the object may subsequently appear pink or light red in the affected eye).
ED treatment with IV steroids is controversial and should be discussed with an ophthalmologist. A neurology consult may also be helpful.
CENTRAL RETINAL ARTERY OCCLUSION
Central retinal artery occlusion may be caused by embolus, thrombosis, giant-cell arteritis, vasculitis, sickle-cell disease, vasospasm (migraine) glaucoma, hypercoagulable states, low retinal blood flow, and trauma.
It is often preceded by amaurosis fugax.
The vision loss is painless, with complete or near-complete vision loss, unless only a single arterial branch is affected.
An afferent pupillary defect is often present and funduscopy classically reveals a pale fundus with narrowed arterioles with segmented flow (“boxcars”), with a bright red macula (“cherry red spot”).
Classic ED care includes ocular massage (digital pressure for 15 seconds, followed by sudden release) and topical timolol or IV acetazolamide; however, evidence-based treatment is lacking. Emergent ophthalmology consultation is indicated.
CENTRAL RETINAL VEIN OCCLUSION
Thrombosis of the central retinal vein causes painless, rapid monocular vision loss. It is associated with numerous medical conditions including diabetes, hypertension, CVD, CAD, dyslipidemia, hypercoagulable states, vasculitis, glaucoma, thyroid disease, and orbital tumors.
Funduscopy classically reveals diffuse retinal hemorrhages, cotton wool spots, and optic disc edema (“blood-and-thunder”). The contralateral optic nerve and fundus are usually normal.
Predisposing drugs (eg, oral contraceptives, diuretics) should be discontinued.
No specific treatment is available, and ophthalmology and neurology consultation should be obtained.
FLASHING LIGHTS (PHOTOPSIAS) AND FLOATERS/RETINAL DETACHMENT
Monocular symptoms indicate involvement of the symptomatic eye, whereas binocular symptoms suggest an intracranial etiology.
As the vitreous ages, it contracts and tugs on the retinal, causing flashes of light to be perceived. Floaters occur when the vitreous separates completely and are generally benign.
The separating vitreous can traumatize the retina as it separates, which can create a retinal hole and subsequent detachment (rhegmatogenous type).
Exudative retinal detachments occur when fluid accumulates behind the retina without a tear, while tractional detachments are caused when acquired fibrocellular bands in the vitreous detach the retina (associated with diabetic retinopathy, sickle-cell disease, and trauma).
Symptoms of retinal detachment include flashing lights, floaters, a dark curtain or veil in the field of vision, and diminished visual acuity.
Ultrasound may be useful in the diagnosis (Figure 151-4).
If retinal tear or detachment is suspected, a dilated indirect retinal examination by an ophthalmologist is mandatory within 24 hours because direct ophthal-moscopy can potentially miss most retinal injuries.
FIG. 151-4. Retinal detachment is seen as a hyperechoic membrane in the posterior aspect of the globe (arrow).
GIANT CELL ARTERITIS (TEMPORAL ARTERITIS)
Giant cell arteritis is a systemic vasculitis that can cause ischemic optic neuropathy. Patients are usually >50 years old, female, and often have polymyalgia rheumatica.
Symptoms and signs include headache, jaw claudication, myalgias, fatigue, fever, anorexia, temporal artery tenderness, and often neurologic findings (including transient ischemic attack [TIA] and stroke).
An afferent pupillary defect is often present.
C-reactive protein and erythrocyte sedimentation rate are usually elevated (70-110 seconds).
ED care includes IV steroids and ophthalmologic consultation.
Steroids should not be delayed for temporal artery biopsy, as they may be sight saving and biopsy results will still be positive for 7 days.
BELL’S PALSY
Bell’s palsy is a paralysis of peripheral nerve VII which can lead to exposure keratitis, which is treated with viscous topic wetting agents and eyelid taping.
It must not be confused with a Genu VII Bell’s palsy, which is a CVA. The differentiating feature is the presence of a CN VI paresis on the affected side, and that eye cannot abduct.
Treatment for Bell’s palsy is controversial, but current evidence suggests that antivirals with steroids provide benefit. A Genu VII Bell’s palsy should be treated as a CVA.
DIABETIC/HYPERTENSIVE CRANIAL NERVE PALSIES
Over time, diabetes and hypertension can cause a vascular-related CN III palsy.
Examination reveals ptosis with decreased EOMs (except for abduction). The pupillary reflex is normal.
Diplopia (especially with looking in the direction of the other eye) is a common finding.
CT scan is required in the ED to rule out an intracranial lesion.
Assuming glucose and blood pressure do not require acute treatment, the patient may be managed with follow-up with ophthalmology and/or neurology.
POSTERIOR COMMUNICATING ARTERY ANEURYSM
This presents as an acute CN III palsy with ipsilateral pupillary dilatation, commonly associated with headache.
ED care includes blood pressure management, emergent CT or MR angiogram, and neurosurgical consultation.
HORNER’S SYNDROME
The classic triad of ipsilateral ptosis, miosis (pupillary constriction), and anhydrosis (absence of sweating) is present.
It is associated with CVA, tumors (classically, Pancoast), internal carotid dissection, herpes zoster, and trauma. Childhood etiologies include neuroblastoma, lymphoma, and metastatic disease.
A CXR, CT scan of the brain and neck, as well as a CT or MR angiogram of the neck and cerebral arteries are indicated.
Specific treatment is determined by the etiology of the Homer’s syndrome.
PAPILLEDEMA
Papilledema is defined as bilateral edema of the head of the optic nerve due to increased intraocular pressure (ICP). It may be seen in any disease process that raises ICP.
Examination reveals a blurred disc margin with a diminished or absent cup, with an elevated nerve head (Fig. 151-5).
When the classic findings are unilateral, it is not from increased ICP and is referred to as optic nerve edema (noninflammatory) or papillitis (inflammatory).
Vision is generally preserved in true papilledema, whereas papillitis results in decreased visual acuity (eg, optic neuritis).
FIG. 151-5. Optic nerve head edema. Vascular congestion, elevation of the nerve head, and blurred disk margins are characteristically seen in papilledema, papillitis, and compressive lesions of the optic nerve. (Reproduced with permission from Knoop K, Stack L, Storrow A: Atlas of Emergency Medicine, 2nd ed. © 2002, McGraw-Hill, New York.)
BENIGN INTRACRANIAL HYPERTENSION (PSEUDOTUMOR CEREBRI)
Benign intracranial hypertension (BIH) consists of increased ICP and papilledema with normal mental status, CSF, and neuroimaging, and occurs most commonly in young women of childbearing age who are not necessarily obese.
BIH presents with headache, nausea, vomiting, visual field deficits, and blurred vision. It is sometimes associated with a CN VI deficit, with resultant horizontal diplopia on lateral gaze.
A CT of the head should be obtained to rule out intracranial pathology.
A lumbar puncture should be performed to measure ICP and to rule out CSF abnormalities.
A neurosurgery consult should be obtained for management recommendations, which typically include acetazolamide and visual field monitoring.
OCULAR ULTRASONOGRAPHY
Ocular ultrasonography may be helpful in the diagnosis of retinal detachment (Fig. 151-4), retrobulbar hematoma, globe preformation, lens dislocation, vitreous hemorrhage, and intraocular foreign body.
Caution must be used when a globe rupture is suspected, and copious gel must be applied to the closed eye to avoid touching the eyelid with the transducer.
The duration of ocular ultrasonography must be strictly limited due to concerns of mechanical energy (exposure limits that are roughly 50% for that of fetal ultrasonography).
Ocular ultrasonography is limited by patient cooperation, orbital emphysema, and various artifacts.
For further reading in Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7th ed., see Chapter 236, “Eye Emergencies,” by Richard A. Walker and Srikar Adhikari.