MEDICAL DECISION MAKING

The first step is to determine the presence of pain

associated with the acute visual loss (Figure 76-4). In the

absence of pain, a history of complete sudden loss of

vision versus a gradual decrease in vision in conjunction

with the funduscopic examination should differentiate

CRAO from CRVO. Preceding symptoms of a shade drop ­

ping or scotoma often aid in the diagnosis of retinal

detachment. If retinal detachment is suspected, perform a

bedside ultrasound of the eye.

If pain is associated with visual loss, then an elevated

intra-ocular pressure suggests acute angle closure

glaucoma. Temporal arteritis is likely when an elderly

patient is complaining of headache and the ESR is

elevated. Optic neuritis is best diagnosed by the funduscopic examination.

TREATMENT

Treatment of CRAO must begin as soon as the diagnosis is

suspected because permanent visual loss typically occurs

after 90 minutes. The goal of treatment is to restore retinal

artery blood flow by dislodging the clot. This is

accomplished by dilating the artery and reducing

intraocular pressure through the following modalities:

intermittent digital massage of the globe (5 seconds on,

5 seconds off) for 5-15 minutes; hyperventilation into a

paper bag 10 minutes of every hour; acetawlamide 500 mg

intravenously (IV) and a beta-blocker (timolol 0.5% drops

intraocular). Immediate ophthalmology consultation is

paramount for paracentesis (aspiration of aqueous fluid)

of the anterior chamber.

ACUTE VISUAL LOSS

CRVO is not as emergent as CRAO because no immediate treatment is effective. Patients should be referred to

ophthalmology for confirmation of the diagnosis and

monitoring of disease progression.

Patients diagnosed with retinal detachment require

immediate ophthalmology consultation to evaluate for

retinal reattachment surgery. The patient should be

instructed to avoid activity and remain on bed rest until

seen by an ophthalmologist.

Optic neuritis is treated with a short course of highdose N methylprednisolone followed by a rapid oral taper

of prednisone. This provides a rapid recovery of symptoms

in the acute phase. This treatment may also delay the shortterm development of MS.

Temporal arteritis treatment begins with oral

prednisone (80 mg/day) initiated in the ED when the

diagnosis is suspected. Follow-up with an ophthalmologist

for evaluation and a temporal artery biopsy should be

arranged.

Treatment of acute angle-closure glaucoma consists of

the sequential administration of several agents to decrease

intraocular pressure: beta-blocker ( Timoptic 0.5%) 1 drop;

a agonist (Iopidine 0.1 %) 1 drop; acetazolamide 500 mg by

mouth or N; steroid (pred forte 1%) 1 drop; mannitol

1-2 g/kg rv. Pilocarpine 1-2% is administered to constrict the

pupil and pull the iris back, helping to prevent a recurrence.

The unaffected eye should be treated prophylactically. Consult

ophthalmology immediately because the definitive treatment

is bilateral laser iridectomy.

DISPOSITION

� Admission

Optic neuritis is frequently managed as an inpatient for

treatment and an expedited work-up, including magnetic

resonance imaging. CRAO, retinal detachment, and acute

angle-closure glaucoma require immediate ophthalmology

consultation. Admission is required when defmitive

treatment cannot be accomplished in the ED.

� Discharge

Temporal arteritis can be managed on an outpatient basis

after the initiation of steroids if the patient has appropriate

follow-up. CRVO is managed on an outpatient basis with

ophthalmology referral.

SUGGESTED READING

Graves JS, Galetta SL. Acute visual loss and other neuroopthalmologic emergencies: Management. Neural Clin.

201 2;30:75-99.

Vortmann, M, Schneider JI. Acute monocular visual loss. Emerg

Med Clin North Am. 2008;26:73-96.

Walker RA, Adhikari S. Eye emergencies. In: Tintinalli JE,

Stapczynski JS, Ma OJ, Cline DM, Cydulka RK, Meckler GD.

Tintinalli's Emergency Medicine: A Comprehensive Study

Guide. 7th ed. New York, NY: McGraw-Hill, 20 1 1 ,

pp. 1517- 1 549.

E pistaxis

Emily L. Senecal, MD

Key Points

• Anterior epistaxis is more common than posterior

epistaxis.

• Anterior epistaxis generally stops with pressu re, but

may require nasal packing.

INTRODUCTION

Epistaxis is common, occurring in 1 of every 7 persons in

the United States. The incidence is highest in persons aged

2-10 and 50-80 years. Epistaxis, like all hemorrhage, needs

prompt evaluation and treatment. The primary goal of diagnosis is to determine the location of bleeding: anterior versus posterior. Once the site of bleeding is identified, bleeding

is stopped using various techniques ranging from chemical

cautery (ie, silver nitrate) to nasal packing. Anterior epistaxis

accounts for 90% of nosebleeds. Most commonly, the bleeding is venous from Kiesselbach plexus, which is located

along the anteroinferior nasal septum. Posterior epistaxis

typically originates from the posteroinferior turbinate and is

more commonly arterial in origin, from the sphenopalatine

artery. Posterior epistaxis represents 10% of nosebleeds.

CLINICAL PRESENTATION

� History

Determine the onset and duration to assess severity of blood

loss. Inquire about comorbidities and medications, especially

blood thinners and antiplatelet drugs. Identify mechanisms

already used by the patient to attempt to stop the bleeding.

The most common etiologies of anterior epistaxis are

trauma, dehumidification of the nasal mucosa (typically

from dry air during winter months), and digital manipula ­

tion. Other common causes include allergies, nasal sprays,

• Posterior epistaxis requires emergent ear, nose, and

throat consu ltation and admission.

• Any patient who requires nasal packing should be given

antibiotics to prevent toxic shock syndrome or sinusitis.

illicit drugs, and nasal infections. Posterior epistaxis is

more common in elderly debilitated patients with comor ­

bid diseases such as a coagulopathy, atherosclerosis, neo ­

plasm, or hypertension.

PHYSICAL EXAMINATION

Inspect the nares to identify the site of bleeding. A nasal

speculum is useful to enhance visualization of the nares. If

the site of bleeding cannot be identified, have the patient

pinch the anterior soft portion of the nose, and examine

the patient's oropharynx. If blood is trickling down the

oropharynx while the patient is holding anterior pressure,

a posterior bleed may be present.

DIAGNOSTIC STUDIES

� Laboratory

Blood work is not indicated in the majority of patients

with epistaxis. Obtain a complete blood count in patients

at risk for thrombocytopenia or anemia. Obtain coagulation studies in patients taking the anticoagulant warfarin

and in patients with cirrhosis. Perform blood typing for

patients with severe bleeding who may require transfusion.

� Imaging

Imaging studies are rarely indicated in the work-up and

treatment of epistaxis. Angiography with interventional

324

radiology embolization can be utilized in rare cases of

refractory posterior bleeding from the sphenopalatine and

greater palatine arteries.

MEDI CAL DECISION MAKING

The mainstay of epistaxis evaluation and treatment is identification of the source of the bleed to facilitate prompt and

effective treatment. Bleeding that ceases with pressure over

the anterior soft portion of the nose is typically from an

anterior source. A posterior bleed is suspected when blood

continues to drain down the posterior pharynx while the

anterior portion of the nose is being squeezed (Figure 77 -1).

EPISTAXIS

TREATMENT

If bleeding is significant, insert an intravenous line and

place the patient on a cardiac monitor. Intubation is rarely

necessary, but indicated if bleeding is severe and is com ­

promising the airway. Consult ear, nose, and throat (ENT)

immediately in cases with severe bleeding.

If an anterior bleed is suspected, have the patient hold

continuous pressure over the soft cartilaginous portion of the

nose for 15 minutes. During this time, assemble equipment

including nasal speculum, headlight, suction, vasoconstric ­

tor, lubricant, and anterior packing or balloon (Figure 77-2).

If the bleeding has subsided after 15 minutes, gently apply

Apply pressure to anterior nose for 15 min

Bleeding persists after pressu re released

Admin ister topical vasoconstrictors and an<>cth<>tirc

or use chemical cautery for slow oozing

Bleeding resolved

Bleeding resolved

Bleeding resolved after pressure released

Apply topical bacitracin

and discharge home

1------ll>l Discharge on amoxicillin 500 mg TID

ENT or PCP follow-up in 48-72 hrs

Figure 77-1 . Epistaxis diagnostic algorithm. ENT, ear, nose and throat; PCP, primary care physician; TID, three times a day.

CHAPTER 77

Figure 77-2. Left, from top to bottom, anterior

packs include the Rhino Rocket, Merocel, and

petroleum gauze. Rig ht, nasa l speculum.

bacitracin to the anterior naris and discharge the patient. If

bleeding is ongoing after 15 minutes of direct pressure, initiate topical vasoconstriction with oxymetazoline (Afrin)

spray and topical anesthesia by inserting pledgets soaked in

2% lidocaine or 4% cocaine. Then hold pressure for

10-15 minutes and reassess. If slow bleeding persists, consider chemical cautery with silver nitrate sticks. Roll the stick

over the area until a gray eschar is formed. Never hold the

stick in one place for longer than 5 seconds, and never use

silver nitrate bilaterally due to risk for nasal septal perforation.

If topical vasoconstrictors and cautery fail to stop the

bleeding, pack the naris with petroleum gauze, a compressed sponge (Merocel or Rhino Rocket), or an anterior

epistaxis balloon. When using a compressed sponge, apply

lubricant to the sponge before inserting it into the nose,

and use approximately 10 mL of saline to expand the

sponge once it is in the nostril. Hemostatic material

(Surgicel, Gelfoam, topical thrombin) may also be useful in

controlling hemorrhage. Patients with nasal packing

should be treated with prophylactic antibiotics (amoxicillin 500 mg orally 3x a day) against staphylococci to prevent

toxic shock syndrome, sinusitis, and otitis media. Patients

with nasal packing should follow-up with ENT or with

their primary care physician in 2-3 days.

Posterior epistaxis is more challenging to treat because

it is difficult to tamponade the site of bleeding, because the

bleeding is often arterial, and because patients with

posterior bleeds frequently have significant comorbidities.

If a posterior bleed is suspected, consult ENT. In the

meantime, attempt tamponade using a balloon device or a

Foley catheter (Figure 77-3).

To tamponade using a balloon device, after applying

topical anesthesia and vasoconstriction to the naris, apply

lubricant to the catheter and insert the catheter into the nose

until the tip is seen in the oropharynx. Inflate the posterior

balloon with 4-8 mL of sterile saline; then pull the device

 

crusting

Conjunctivitis

and subconjunctival hemorrhage can be discharged to follow-up with their primary care physicians.

SUGGESTED READING

Cronau H, et al. Diagnosis and management of red eye in pri ­

mary care. Am Fam Physician. 20 1 0;81:1 37-144.

Jackson WB. Acute Red Eye: Diagnosis and Treatment Guidelines.

Ottawa, Ontario, Canada: University of Ottawa Eye Institute,

2004.

Kerns BL, Mason JD. Red eye: A guide through the differential

diagnosis. Emer Med. 2004;36:3 1-40.

Leibowitz HM. The red eye. N Engl J Med. 2000;343:345-35 1.

Walker RA, Adhikari S. Eye emergencies. In: Tintinalli JE,

Stapczynski JS, Ma OJ, Cline DM, Cydulka RK, Meckler GD.

Tintinalli's Emergency Medicine: A Comprehensive Study Guide.

7th ed. New York, NY: McGraw-Hill, 201 1, pp. 1517-1549.

Acute Visual Loss

jordan B. Moskoff, MD

Key Points

• History and physical examination alone wi ll lead to the

diagnosis in most patients presenting with acute visual loss.

• The most important first step in addressing the patient

with acute monocular visual loss is to determine

whether the loss of vision is associated with pain.

• In patients with acute visual loss without pa in, suspect

centra l retinal artery occlusion (CRAO), central reti nal

vein occlusion (CRVO), or retinal detachment.

INTRODUCTION

Central retinal artery occlusion ( CRAO) and central retinal

vein occlusion ( CRVO) occur most frequently in elderly

patients. About 90% of cases of CRVO occur in patients

older than 50 years. CRAO is a result of a thrombotic plaque

or more commonly an embolus of the central retinal artery,

whereas CRVO is caused by thrombosis of the retinal vein.

Optic neuritis is a painful rapid reduction of central

vision secondary to an inflammatory process of the optic

nerve. Optic neuritis occurs more commonly in women

aged 15 to 45 years. Retinal detachment results from

traction of the vitreous humor on the retina. This causes a

tear in the retina and a separation of the inner neuronal

retina from the outer pigment epithelial layer. Retinal

detachment may occur after ocular trauma, but in

atraumatic cases, this condition is more prevalent in men

>45 years old and in patients with significant myopia. The

prevalence in the United States is 0.3%.

Temporal (giant cell) arteritis is a vasculitis that results

in monocular loss of vision associated with a unilateral

temporal headache. Temporal arteritis occurs most

commonly in woman >50 years old. Whites are more

frequently affected than are other races. Temporal arteritis

319

• Patients with acute visual loss with associated pain may

have optic neu ritis, temporal (giant cel l) arteritis, acute

angle-closure glaucoma, or a large central cornea l abrasion or ulceration.

• An ophtha lmologist should be consulted immediately

when CRAO or acute angle-closure glaucoma are diagnosed in the emergency department.

is a vasculitis of medium and large arteries and can lead to

optic nerve infarction and blindness.

Acute angle-closure glaucoma is a sudden painful

monocular loss of vision secondary to increased pressure

in the anterior chamber. Acute angle-closure glaucoma

represents < 10% of all cases of glaucoma in the United

States. It is more common in women and is also more

common in African American and Asian populations.

Acute angle-closure glaucoma occurs in patients with

shallow (narrow) anterior chamber angles. As the pupil

dilates, the iris leaflet touches the lens. This impedes the

flow of aqueous humor from the posterior to the anterior

chamber with a subsequent increase in hydrostatic pressure.

CLINICAL PRESENTATION

..... History

Painless, acute loss of vision is characteristic of CRAO,

CRVO, and retinal detachment. In patients with CRAO, the

monocular vision loss is usually complete and quite

sudden. Risk factors include hypertension, carotid artery

disease, diabetes mellitus, cardiac disease (especially atrial

fibrillation and valvular disease), vasculitis, temporal

CHAPTER 76

artentls, and sickle cell disease. Central retinal artery

occlusion must be considered and treated early because

irreversible visual loss occurs after 90 minutes.

The presentation of CRVO is more insidious than retinal

artery occlusion. The patient will have a sudden painless

monocular decrease in vision that is most commonly noted

on awakening. Patients may also describe a sudden decrease,

acutely imposed on a chronic gradual worsening over a

longer period of time ( eg, 1 week). Risk relates to likelihood

of thrombosis. The physician should have increased suspicion in patients with diabetes mellitus, hypertension, arteriosclerosis, chronic glaucoma, and vasculitis.

Patients with retinal detachment present with painless

loss of vision often described as a sensation of a curtain

moving across the visual field or a shade being pulled

down over the eye. Flashing lights, "spider webs," or "coal

dust" in the visual field may precede visual loss. Risk is

related most closely to severe myopia. Other risk factors

include trauma, previous cataract surgery, family history,

Marfan syndrome (or other inherited connective tissue

disorders), and diabetes mellitus.

Painful loss of vision is seen in patients with optic

neuritis, temporal arteritis, and acute angle closure

glaucoma. Patients with optic neuritis will present with r apidly progressive reduction or blurring of their vision. Ocular

pain worsens with eye movement In patients without a

previous diagnosis, 25-65% will develop multiple sclerosis.

Temporal arteritis presents as a sudden monocular loss of

vision associated with a unilateral temporal headache. Eye

pain usually is not present. Risk factors include polymyalgia

rheumatica, female, Northern European descent, and

>50 years old.

Lastly, acute angle-closure glaucoma presents as cloudy

vision associated with halos around lights. In addition, the

patient will complain of eye pain or headache along with

nausea and vomiting and possibly abdominal pain. Often

patients will have no previous history of glaucoma.

Farsighted (hyperopic) persons are at r isk secondary to the

shape of their anterior chamber; female and elderly

patients are also at increased risk.

..... Physical Examination

For a full description of the physical examination of the

eye, see Chapter 75. In acute visual loss, fluorescein staining is essential to exclude corneal abrasions or ulcerations;

however, the funduscopic examination is usually most

diagnostic. To perform the funduscopic exam, allow the

patient to sit in a dark room for several minutes before

starting. When the pupil is sufficiently dilated, ask the

patient to focus on an object on the wall and ignore the

examiner. Focus the ophthalmoscope on the eye and

gradually approach the cornea from a lateral position. The

optic disc is noted medially. If only vessels are seen, the

optic disc can be located by knowing that the blood vessel's

branches "point" to the direction of the disc.

A

8

Figure 76-1 . A. Central retinal artery occlusion.

B. Central retinal vein occlusion.

CRAO

Visual acuity is markedly decreased, with the patient often

only able to perceive shadows or count fingers. Initial pupil

examination may be normal; however, after 1-2 hours, the

pupil may dilate. The pupil is poorly reactive to direct light

but has a greater consensual response to light (afferent

pupillary defect). On funduscopic examination, a pale

retina with a cherry-red spotin the macular area (fovea) is

the classic finding (Figure 76-1A).

CRVO

Visual acuity is variable but the deficit is usually less

severe than retinal artery occlusion. The patient may

retain the ability to see shadows or count fingers. The

pupil will react sluggishly to light. On funduscopic examination, there may be retinal hemorrhage, tortuous retinal

veins, and disc edema, referred to as "blood and thunder"

(Figure 76-1B).

ACUTE VISUAL LOSS

.6. Figure 76-2. Retinal detachment on bedside

u ltrasound.

Retinal detachment

The extent of the loss of vision is dependent on the degree

of detachment. Visual field defects will be noted on con ­

frontation. The pupil examination is unremarkable.

Funduscopic examination reveals an undulating, dull grey,

detached retina. Ocular ultrasound is a bedside procedure

that is very helpful to making the diagnosis of retinal

detachment (Figure 76-2).

Optic neuritis

Visual acuity varies from mildly reduced to no light

perception. Often the visual deficit will be limited to the

central visual field, and the patient will c omplain more of a

defect with color vision rather than sight. This can be evaluated using the red desaturation test.Have the patient look at

a dark red object with one eye and then test the other eye to

see if the object looks the same color. The affected eye will

often see the object as lighter or pink. An afferent pupillary

defect will often be present. If the fundus is normal, the

patient has retrobulbar optic neuritis. However, if the fundus is swollen or hyperemic, the patient has papillitis.

Temporal arteritis

Palpation may reveal tender, tortuous, and sometimes

pulseless temporal arteries. The degree of loss of vision

depends on when the diagnosis is made. If diagnosed late,

visual acuity will be markedly decreased. An afferent pupillary defect may be present. On funduscopic examination, a

pale, swollen optic disc will be present.

A

8

.6. Figure 76-3. A. Schititz tonometer B. Tono-Pen.

Acute angle-closure glaucoma

Visual acuity is markedly decreased. The patient's sclera

will be red due to ciliary injection. The cornea will be

cloudy. On gentle palpation, the eye may have a rock hard

consistency. The pupil is mid-dilated and nonreactive to

light. Funduscopic examination is difficult to perform in

the face of a cloudy cornea, but is otherwise unremarkable.

To diagnose acute angle-closure glaucoma, intraocular

pressure is measured with a Schiotz tonometer or TonoPen (Figure 76-3). Normal pressure is <20 mmHg. A pressure >40 mmHg is diagnostic.

DIAGNOSTIC FINDINGS

When temporal arteritis is suspected, an erythrocyte

sedimentation rate (ESR) should be obtained. An ESR

Retinal

detachment

CHAPTER 76

Increased

lOP

Glaucoma

Normal

lOP

Optic

neuritis

Headache

with

pain less

eye and

elevated

ESR

Temporal

arteritis

.A Figure 76-4. Acute visua l loss diagnostic algorithm. ESR, erythrocyte sedimentation rate;

lOP, intraocu lar pressure.

>50 mm/hr is almost universally present in patients with

temporal arteritis. Normal ESR for males is age/2; females

(age + 1 0)/2.

 

Acute anterior uveitis is defined as inflammation of

the iris and ciliary body. The most common cause is

trauma, with patients usually presenting 1-4 days after the

precipitating event. Systemic causes include ankylosing

spondylitis, Reiter syndrome, inflammatory bowel disease,

and chronic granulomatous conditions like tuberculosis or

sarcoidosis. Infectious ulcerations can also cause anterior

uveitis.

CLINICAL PRESENTATION

� History

The single most important historical feature that helps

determine the cause of red eye is the presence of eye pain.

Conjunctivitis is characterized by a gritty foreign body

sensation and tearing or discharge, but it is usually not

315

CHAPTER 75

particularly painful. Viral (ie, adenovirus) and allergic

sources tend to be pruritic with watery discharge, but suspect bacterial infection with mucopurulent discharge. An

infectious source often begins unilaterally and spreads

through autoinoculation. Constitutional symptoms such

as fever, rhinorrhea, and myalgias suggest a systemic viral

illness. Allergic conjunctivitis is associated with more

intense itching and seasonal history.

Similarly, subconjunctival hemorrhage is a painless

condition. Patients usually present to the ED merely

because the appearance of blood on the sclera of the eye is

concerning to the patient.

Eye pain is produced when the epithelium of the cornea

is injured or there is inflammation to deeper structures (ie,

iris). Corneal abrasions due to trauma or foreign body are

characterized by pain, foreign body sensation, tearing, and

photophobia. A history of working with power tools and

metal should raise the suspicion of a foreign body. If the

abrasion is large enough, patients may complain of

decreased vision. Contact lens use or exposure to ultraviolet light should be ascertained and raises the suspicion for

corneal inflammation/infection (ie, keratitis).

Acute anterior uveitis presents with a gradual onset of

a painful red eye with severe photophobia and diminished

vision. The patient will prefer to sit in a dark room with a

hand over the eye.

� Physical Examination

The exam should always follow the same pattern: visual acuity, lids and lashes, conjunctiva, sclera, cornea, pupil, ante ­

rior chamber, and fluorescein staining. The characteristic

findings in conjunctivitis, subconjunctival hemorrhage,

corneal abrasion, and acute anterior uveitis are listed in

Table 75-1. Additional characteristic features are listed here.

Patients with conjunctivitis will have diffuse injection of the

conjunctiva. With all causes of conjunctivitis, fluid can

accumulate behind the conjunctiva known as chemosis

(Figure 75-1). Allergic eyelids may be edematous and demonstrate bilateral cobblestone papillae.

Figure 75-1. Chemosis.

Subconjunctival hemorrhage has a characteristic

appearance with bright red blood on the sclera under the

thin conjunctival layer (Figure 75-2).

Corneal injury is signaled by uptake of fluorescein seen

with the cobalt blue light. Corneal abrasions will affect

.A. Figure 75-2. Subconjunctival hemorrhage.

Table 75-1. Physical examination findings in patients with red eye.

Examination Conjunctivitis Subconjunctival Hemorrhage Corneal Abrasion Acute Anterior Uveitis

Visual acuity Normal Normal Decreased when central Decreased due to pain, tearing

Lids Edema, erythema Normal Normal Normal

Conjunctiva Injection Normal Injection Normal

Sclera Normal Erythema Normal Ciliary flush

Cornea None, unless associated None Yes None

(fluorescein corneal ulcer

uptake)

Pupil Normal Normal Normal Constricted

Anterior chamber None None None Yes

(cell and flare)

visual acuity if large or there is central involvement. Lids

should always be everted to look for a foreign body. If

multiple lines of fluorescein uptake course together, this

is highly suggestive of a foreign body under the lid that

scratches the cornea with blinking. In herpes simplex

virus (HSV) infection, a branching dendritic ulcer is

characteristic, whereas involvement of the c ornea in herpes

zoster ophthalmicus causes a thin wavy lesion similar to

tangled spaghetti. In patients with herpes zoster ophthalmicus, a zoster-form rash is present on the forehead in the

Vl distribution of the trigeminal nerve. A bacterial cause

of a corneal ulceration will also demonstrate significant

uptake of fluorescein in the ulcer.

Acute anterior uveitis may affect visual acuity due to

pain and tearing. The sclera may have a ciliary flush

identified by redness at the limbus. No fluorescein uptake

is seen, and pain is not improved with topical anesthetic

application. The pupil is often constricted, and there is

consensual photophobia (pain produced by shining light

in the unaffected eye). On slit lamp exam, the anterior

chamber will show "cell and flare:' When cellular debris is

significant, it can layer at the bottom of the anterior

chamber between the cornea and iris. This collection is

known as a hypopyon (Figure 75-3). Cell and flare and a

hypopyon are also common with infectious causes of

corneal ulceration.

Figure 75-3. Hypopyon.

RED EYE

MEDICAL DECISION MAKING

The presence of pain, response to topical anesthetic application, and the findings on the fluorescein examination are

some of the most important features to determining the

cause of a red eye (Figure 75-4).

TREATMENT

Uncomplicated conjunctlVItls is treated with topical

antibiotic drops or ointment if a bacterial source is sus ­

pected. Options include sulfacetamide, quinolones,

arninoglycoside, trimethoprim, and polymyxin. The duration of treatment is 5-7 days. Remind patients of the

importance of handwashing for at least 2 weeks to limit

spread. Those who suffer from allergic conjunctivitis benefit from systemic antihistamines and histamine-blocking

eye drops. For symptomatic relief, patients can use cool

compresses and artificial tears. If Chlamydia trachomatis or

Neisseria gonorrhea are suspected, patients will require

systemic and topical antibiotics and must also have emergent ophthalmologic consult.

Patients with a subconjunctival hemorrhage need

only reassurance that the blood will resolve within a

couple weeks, similar to a bruise. If the patient has suffered recurrent subconjunctival hemorrhages, then consider coagulation studies and work-up for bleeding

disorders.

Treatment of corneal injury depends on the cause. A

patient with a corneal abrasion should be prescribed

pain relief and infection prophylaxis. Patients benefit

from a cycloplegic (cyclopentolate or homatropine) to

relieve ciliary spasm and reduce pain. They will often

need narcotic analgesia. To prevent secondary infec ­

tions, prescribe a topical antibiotic such as l Oo/o sulfa ­

cetamide.

Patients with herpes zoster ophthalmicus should receive

oral acyclovir if treatment can be instituted within 72 hours

of onset. Prompt treatment reduces the likelihood of eye

involvement from 50o/o to 25%. Intravenous (N) acyclovir is

indicatedforimmunocompromisedpatients. Ophthalmology

consultation is indicated. HSV is treated with topical antiviral drops, such as Viroptic, and consultation with an

ophthalmologist. Corneal ulcers require emergent ophthalmologic consultation. Contact lens wearers should

dispose of current lens and be given coverage for pseudomonas with a topical arninoglycoside or quinolone. The

patient should not resume use of new lens until symptoms

have resolved. Do not use an eye patch, as it is associated

with an increased rate of corneal ulceration and pseudo ­

monal infection. Tetanus prophylaxis should be updated.

Acute anterior uveitis treatment should be instituted

only in consultation with an ophthalmologist, as

continual monitoring and treatment is required. To

eliminate ciliary spasm, use a long-acting cycloplegic such

as 5o/o homatropine. To relieve inflammation, the

tetracaine

and upta ke of

fluorescein

Corneal

abrasion

CHAPTER 75

A. Figure 75-4. Red eye diag nostic algorithm.

ophthalmologist may also recommend a topical steroid

such as prednisolone.

DISPOSITION

� Admission

Patients with bacterial conjunctivitis secondary to N.

gonorrhea should be admitted for IV antibiotic therapy.

Consider admission of patients with corneal ulcers if the

patient is unable to self-administer antibiotics, there is a

high likelihood of noncompliance, or a large ulcer is present.

� Discharge

Patients with corneal abrasion, herpetic keratitis, and acute

anterior uveitis should be re-evaluated by an ophthalmologist within 24-48 hours. Patients with simple conjunctivitis

signs or

symptoms

Red conjunctiva

with chemosis,

discharge,

 

.A. Figure 74-2. Eva l uating the cornea l surface using a

narrow beam at a 45-degree angle. The curved beam

represents the reflection of l ight off the cornea . When

the cornea is in focus, protein deposits are freq uently

visual ized on its surface.

of fluorescein uptake (green fluorescence) that suggest corneal or conjunctival epithelial injury. Running or oozing of

the fluorescein (Seidel sign) is caused by aqueous humor

leaking from a full-thickness penetration of the cornea.

Evaluating the anterior chamber for cell and flare is the

third part of the examination. The slit height should be

decreased and the slit width increased to create a short,

wide beam of white light. Swing the light source temporally, aiming the beam of light nasally through the anterior

CHAPTER 74

.&. Figure 74-3. The appearance of the light when

eva l uating for cell and flare.

chamber at the height of the pupil (Figure 74-3 ). Push the

microscope forward until the patient's iris is in sharp

focus, then move back slightly until the iris is out of

focus-but not so far that the cornea comes into focus.

The focal plane is now between the iris and cornea, in the

anterior chamber. Using the pupil as a dark backdrop,

watch for any material reflecting the light. Flare is caused

by protein in the anterior chamber and creates a smoky

appearance in the beam of light (a common analogy is

"headlights in fog:') Cells will look like "dust particles in a

sunbeam." The presence of either signifies inflammation

of the anterior chamber. Use of dilating drops can cause

cells to be present and applanation tonometry can cause

flare, so slit lamp examination should be performed

before these other tests.

If a foreign body (FB) is identified during the examination, first attempt to wash it out using saline. If this is not

successful, it can be removed using a burr drill or a 25- or

27 -gauge needle. Anesthetize the patient's eye using proparacaine or tetracaine. Be sure the patient's head is stabilized by full contact with the forehead brace and chin rest.

Stabilize your hand on the patient's cheek or forehead so

the removal device will track any movements the patient

may make. Keep the removal device tangent to the surface

of the patient's cornea. Guide it to the cornea under direct

vision, switching to the eyepieces once the removal device

is in view. If using a burr drill, press the side of the burr

against the FB. When activated, the drill will "fling" the FB

out of the cornea. If using a needle, place it on a small

syringe (eg, insulin syringe) to provide better control.

Guide the needle to the FB and use a scooping or flicking

motion to pull the FB out of the cornea. Always move

tangential to the globe.

COMPLICATIONS

When using the slit lamp and syringe/needle to remove an

FB, careless attempts at removal or patient movement may

result in penetration through the cornea. Additionally, in

the setting of ocular trauma, avoid placing pressure on the

eye when the possibility of a globe rupture exists. Excessive

pressure may cause the intraocular contents to be extruded.

Suggested Reading

Knoop K, Dennis W, Hedges ]. Ophthalmologic procedures. In:

Roberts ]R, Hedges JR Roberts: Clinical Procedures in Emergency

Medicine. 5th ed. St. Louis, MO: Saunders, 2009, pp. l l4 1-l l 77.

Walker RA, Adhikari S. Eye emergencies. In: Tintinalli JE,

Stapczynski JS, Ma OJ, Cline DM, Cydulka RK, Meckler GD.

Tintinalli's Emergency Medicine: A Comprehensive Study Guide.

7th ed. New York, NY: McGraw-Hill, 201 1, pp. 1517-1 549.

Red Eye

Craig H uston, MD

Key Points

• Always begin with visual acuity, the vital sign of the eye.

• The patient should be instructed to remove contact lens and

not to put them back in until the symptoms have resolved.

• The presence of pain and the relief of pain with insti llation of anesthetic agents are helpful in determining the

cause of red eye.

INTRODUCTION

Eye complaints account for 3% of all emergency department (ED) visits. Red eye is a common complaint, and

although most cases are benign, self-limited conditions,

some may be vision-threatening. Conjunctivitis is the most

common cause of a red eye, but other frequent problems

include subconjunctival hemorrhage, corneal injuries

(abrasions, keratitis, and foreign bodies), and acute uveitis.

Conjunctivitis may be viral, bacterial, or allergic. Viruses

are the most frequent cause, especially adenovirus. The most

common bacterial pathogens are Staphylococcus aureus,

Streptococcus pneumoniae, and Haemophilus influenzae.

Chlamydia trachomatis or Neisseria gonorrhea are unusual,

butimportantcauses of conjunctivitis. Allergic conjunctivitis

is due to recurrent seasonal inflammation from allergen

exposure. About 15% of the population will experience

allergic conjunctivitis at one time in their life.

Subconjunctival hemorrhage is blood between the

conjunctiva and sclera that results from a ruptured con ­

junctival blood vessel. Subconjunctival hemorrhage is

caused by direct trauma or indirect injury. Although it may

be alarming to the patient, it is usually a benign process

that occurs with a sudden increase in pressure from sneez ­

ing, coughing, straining, or vomiting. If atraumatic, the

etiology is usually hypertension or spontaneous rupture.

• Follow a systematic approach to the physical examination:

visua l acuity, lids and lashes, conjunctiva, sclera, cornea,

pupil examination, and anterior chamber.

• Never prescribe topical steroids without consulting with

an ophthalmologist.

Corneal injury is common because the epithelium is

thin and easily damaged. Corneal abrasions are particularly

common, representing 10% of all ED visits for eye complaints. The cornea is resistant to infection, but when

injured, a potential portal to bacteria is created. Viral infections that cause injury to the cornea include herpes simplex

and varicella (ie, herpes zoster ophthalmicus). Contact lens

use may predispose the patient to keratitis or a corneal ulcer

due to gram-negative bacteria.