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