Tag Archives: ophthalmologic medications

Acute Angle Closure Glaucoma: ED-Relevant Management

Authors: Colton Langridge, MD (EM Resident Physician, UTSW / Parkland Memorial Hospital) and Dustin Williams, MD (EM Attending Physician / APD, UTSW / Parkland Memorial Hospital) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Brit Long, MD (@long_brit)


A 65-year-old female of Vietnamese descent with past medical history of hypertension and diabetes mellitus type 2 presents with acute onset right sided headache that began while reading in dim light 3 hours prior to arrival. The location of the pain is in the peri/retroorbital region on the right and radiates to the right temple. She is seeing halos around lights and has vomited twice on the way to the ED. She has never had a headache of this quality in the past. The remainder of her review of systems is negative, including trauma. She has a history of “sulfa allergy” 5 years ago while taking Bactrim in which she developed hives and shortness of breath.

She is hypertensive, while the remainder of her vital signs are unremarkable. On exam, she has scleral injection, a hazy cornea, and mid-dilated, fixed pupil. The globe itself feels rock hard on palpation. There is no proptosis or palpable cord in the R temporal region. Extraocular muscles are intact, and she has a normal neurological exam including no meningismus.

Visual acuity is performed, and she has 20/80 OS and 20/200 OD. Her baseline is 20/80 in each eye, and she does wear reading glasses. Her fluorescein stain reveals no abnormal uptake. Fundoscopic exam is difficult due to corneal haziness. Tonometry in the L eye shows a pressure of 28 mmHg. The pressure in her R eye is elevated to 72 mmHg.

Timolol and brimonidine eye drops are ordered and administered with repeat tonometry performed every 30 minutes, while awaiting ophthalmology’s arrival. Her OD pressure consistently drops until her IOP is under 35 mmHg. Ophthalmology recommends starting topical steroids and informs you that they plan to perform Laser Peripheral Iridotomy in the next 24 to 48 hours after the haziness in her cornea subsides.


Acute angle closure glaucoma (AACG) is the acute elevation of intraocular pressure due to diminished outflow of aqueous humor through the anterior chamber of the eye into the peripherally located canal of Schlemm. It occurs in 1 in 1000 whites and as frequently as 1 in 100 Asians. It occurs even more frequently in those of Inuit descent with estimates of 2-4 in 100 (1). The importance of this disease entity lies in its proclivity to cause optic nerve ischemia. As a result, AACG can lead to visual impairment or blindness if not treated early and appropriately.


Aqueous humor is produced by the ciliary epithelium covering the ciliary body in the posterior chamber of the eye. Production is under the control of sympathetic β receptors. After production, aqueous humor flows from the posterior chamber, then between the angle of the lens and iris, through the pupil into the anterior chamber, and finally into the trabecular meshwork located anterior to the ciliary body at the junction of the cornea and sclera. From the trabecular meshwork, aqueous humor flows through the canal of Schlemm where it is resorbed. Two types of acute angle closure glaucoma exist; primary and secondary. Primary AACG occurs in the absence of a precipitating event or insult. In Primary AACG aqueous humor is restricted from flowing through the more anteriorly located pupil due to the posterior iris becoming attached to the lens behind it causing diminished outflow. (6) As aqueous humor accumulates, the iris is pushed forward, especially at its peripheral margin, causing a bowing effect that then causes impingement on the trabecular network and canal of Schlemm.  This further restricts outflow. Patients who already have shallow anterior chambers are particularly at risk, as the angle between the peripheral iris and trabecular meshwork is already narrow and predisposed to sudden closure. Those of Asian (especially Inuit descent) and women tend to have a more narrow anterior chamber, which increases the risk of developing AACG.

There are many precipitants that can contribute to the development of AACG. A classic story is the acute onset of eye pain after walking into a movie theater (i.e. a dimly lit room). Reading in dim light can also precipitate AACG. Sympathomimetics and anticholinergics can both cause pupillary dilatation and thus AACG.


AACG, for the emergency physician, is a clinical entity that is diagnosed based on a combination of clinical suspicion and exam findings. IOP as detected by applanation tonometry will be elevated. Acute onset eye pain and a minimally reactive mid-dilated pupil with elevated intra-ocular pressure (usually greater than 30 mmHg) is highly suggestive of AACG.

In recent years, more formal criteria have been used to diagnose AACG. These criteria include at least 2 of the following complaints/symptoms: ocular pain, a history of intermittent visual blurring which may include the complaint of seeing halos, and nausea or vomiting. At least 3 of the following signs are required: IOP greater than 21 mm Hg, corneal edema, conjunctival injection, a mid-dilated minimally reactive pupil, and a shallow anterior chamber (11).

A narrow anterior chamber can be determined by oblique flashlight test. This test is performed by shining a flashlight tangentially in a lateral to medial direction across the patient’s eye in a dark room. If there is a shadow over the medial aspect of the iris then the anterior chamber is narrow (5).

Screen Shot 2017-02-05 at 10.28.20 AM

From: http://littlewhitecoats.blogspot.com/2010/12/what-is-oblique-flashlight-test.html


An immediate ophthalmology consultation should be made once the Emergency physician suspects this diagnosis. As more time elapses, more optic nerve atrophy will occur (10).


In the acute setting, the goal is to emergently reduce IOP, not to perform definitive therapy. This can be started before ophthalmology arrives. Several types of eye drops and a few intravenous medications are effective in rapidly reducing IOP. Most of these medications used for one of the following two mechanisms: increasing aqueous humor outflow or reducing production of aqueous humor altogether. The particular medication regimen that is chosen should be tailored based on a patients’ past medical history and previous drug allergies. The table below summarizes the various medication choices frequently chosen in the acute management of AACG.

Medication Class Medication Pharmacology Adverse Effects/Cautions
Beta Blockers Timolol 0.5% Decrease production of aqueous humor Systematically absorbed/caution in asthma/COPD
Alpha 2 Agonists Brimonidine 0.15% Decrease production of aqueous humor and increase outflow
Carbonic Anhydrase Inhibitors Acetazolamide (Diamox) 500 mg IV or PO Decrease production of aqueous humor Sulfa drug; Use caution in Sulfa allergic patients; Avoid in patients with Sickle cell disease (increased sickling)
Prostaglandin Analogs Latanoprost 0.005% Increase aqueous humor outflow Browning of the iris
Muscarinic Agonists Pilocarpine 1-2% Increase aqueous humor outflow


Ineffective at high IOP
Topical Steroids Prednisolone 1% Decrease inflammation and synechiae formation Use in conjunction with ophthalmology
Desiccating Agents/Hyperosmotic Agents Mannitol 1-2g/kg IV Draw fluid out of the vitreous humor by osmotic pressure Caution with use in patients with intravascular volume depletion

*Because aqueous humor production is stimulated by β receptors, β blockers are effective in decreasing further production of aqueous humor. Timolol functions in this way.

*Alpha 2 receptors in the eye (as elsewhere in the body) inhibit sympathetic stimulation. Alpha 2 agonism functions to decrease aqueous humor production by reducing sympathetic outflow and thereby decreasing the β mediated aqueous humor production. Alpha 2 agonism also decreases the mydriatic effect of sympathetic stimulation on the iris through alpha 1 receptors. Brimonidine functions in this manner.

*Carbonic anhydrase is an enzyme that is used in erythrocytes and in the renal tubule for bicarbonate/CO2 titration and/or buffering effects. In the eye it is used for aqueous humor production. Inhibition of this enzyme minimizes production through this pathway. Acetazolamide functions in this way.

*Prostaglandin analogs are thought to increase aqueous humor outflow without affecting its production. One proposed mechanism suggests that they work by altering the production of matrix metalloproteinases. These are thought to cause changes in the extracellular matrix of the iris and widening of connective tissue filled spaces. (4)

*Muscarinic agonists cause miosis. This may help pull the posterior iris from the lens, thereby helping to increases aqueous humor outflow through the pupil. Pilocarpine works by this mechanism. Unfortunately, under high intraocular pressure settings, pilocarpine is less effective. This is because during these conditions, pressure induced ischemic paralysis of the iris decreases its effectiveness. There is also concern that by constricting the ciliary muscles, pilocarpine may increase the axial thickness of the lens and cause anterior displacement, which may reduce the depth of the anterior chamber effectively worsening outflow of aqueous humor. Pilocarpine should be given after other eye drops.

*Topical steroids decrease the overall inflammatory response and scar tissue/synechiae formation.

*Mannitol works by drawing water out of the vitreous humor by osmotic means, thereby decreasing the overall fluid in the eye, dropping the pressure.

*It’s important to give adequate pain control with opioids such as morphine or fentanyl. Antiemetics should be given for nausea and vomiting.

Start with a topical β blocker and alpha 2 agonist +/- diamox. Diamox can be given by mouth if IOP is not excessively elevated (i.e. less than 40). If highly elevated, IV Diamox is preferred. Topical pilocarpine can be considered but should be used with caution 1-2 hours after IOP is reduced for the reasons stated earlier. If IOP is not significantly reduced by 25% at 30-60 minutes, an osmotic agent should be strongly considered. The goal IOP should be 35 or less (3).

If IOP is not effectively reduced in a timely manner, corneal indentation (CI) can be considered (9). This is performed by indenting the cornea with a soft instrument (i.e. cotton tipped applicator) after administration of a topical anesthetic. By indenting the cornea, aqueous humor is displaced peripherally, opening the angle and increasing aqueous outflow temporarily.

Definitive therapy is performed by ophthalmology by means of Laser Peripheral Iridotomy (LPI). Ideally, this is performed within 24 to 48 hours. However, LPI must be performed under circumstances in which visibility is optimal. In many cases of AACG, corneal haziness impairs visibility. Once IOP is reduced, water is drawn out of the cornea and visibility improves, thus allowing LPI to be performed. LPI may need to be performed on the consensual eye in order to prevent AACG in that eye as well.


Disposition should be made in conjunction with ophthalmology. There should be a low threshold for admission, especially for those who receive osmotic diuretics, as they may require further electrolyte monitoring. For those who will follow up as outpatients, patients must be able to reliably follow up in an ophthalmology clinic within the next 24-48 hours. In addition, they should be discharged with topical IOP lowering agents, as definitive therapy (LPI) will not have been performed yet.


  1. Consider AACG in all patients presenting with headache and visual changes, especially if associated with nausea and vomiting.
  2. AACG occurs more frequently in females and those of Asian descent.
  3. Early and effective therapy is vital in reducing optic nerve ischemia and vision loss. Time is optic nerve.
  4. Be aware of the patient’s comorbidities and allergies before treating (i.e. be aware of the risks of topical β blockers in COPD/asthma, sulfa allergy with acetazolamide use)
  5. Consider corneal indentation as a temporizing maneuver if IOP is not satisfactorily lowered in a reasonable amount of time.
  6. There is no emergent treatment that an ophthalmologist can offer that an emergency physician cannot. Definitive treatment is with LPI, however this is frequently delayed until corneal clearing occurs. Thus topical and IV agents are paramount in early treatment of AACG.


References / Further Reading

  1. He M, Foster PJ, Ge J, Huang W, Zheng Y, Friedman DS. Prevalence and clinical characteristics of glaucoma in adult Chinese: a population-based study in Liwan District, Guangzhou. Invest Ophthalmol Vis Sci. 2006 Jul. 47(7):2782-8.
  2. Ang LP, Ang LP. Current understanding of the treatment and outcome of acute primary angle-closure glaucoma: an Asian perspective. Ann Acad Med Singapore. 2008 Mar. 37(3):210-5.
  3. Singer MS, Salim S. Bilateral acute angle-closure glaucoma as a complication of facedown spine surgery. Spine J. 2010 Sep. 10(9):e7-9.
  4. Toris CB, Gabelt BT, Kaufman PL. Update on the mechanism of action of topical prostaglandins for intraocular pressure reduction. Surv Ophthalmol. 2008 Nov;53 Suppl1:S107-20.
  5. Coleman AL. Glaucoma. The Lancet; Nov 20, 1999; 354, 9192
  6. Tarongoy P, Lin C, Walton D. “Angle-closure Glaucoma: The Role of the Lens in the Pathogenesis, Prevention, and Treatment”. Survey of Ophthalmology, Volume 54   Number 2 2009.
  7. Choong YF, Irfan S, Menage M. Acute angle closure glaucoma: an evaluation of a protocol for acute treatment. Eye (1999) 13, 613-616.
  8. Emanuel ME et al. Evidence-based management of primary angle closure glaucoma. Curr Opin Ophthalmol 2014, 25:89–92.
  9. Masselos K, Bank A, Francis IC, Stapleton F. Corneal indentation in the early management of acute angle closure. Ophthalmology. 2009 Jan. 116(1):25-9.
  10. Weizer J. Angle-Closure Glaucoma. In: UpToDate, Post TW (Ed), UpToDate, Waltham, MA. (Accessed on August 5 2016.)
  11. Khondkaryan Ani, Francis Brian A. Angle Closure Glaucoma. American Academy of Ophthalmology. https://www.aao.org/munnerlyn-laser-surgery-center/angleclosure-glaucoma-19. Dec18, 2013.

Ophthalmologic Medications: Pearls & Pitfalls for the ED

Author: Brit Long, MD (@long_brit, SAUSHEC EM) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Stephen Alerhand, MD (@SAlerhand)

Emergency physicians manage ophthalmologic conditions daily, and we possess a vast array of medications to prescribe. This variety of medications and their indications can result in discomfort with ophthalmologic medications. This post examines the different classes of emergent ophthalmological medications, including dosing and indications.1-6

Your first patient of the day is an 18-year-old male who was playing baseball with his friends. He was sliding into second base, when he felt something fly into his right eye. He immediately began rubbing the eye, and he now has diffuse pain. Exam reveals diffuse redness of the right eye, with normal visual acuity. Your fluorescein exam reveals a small, peripheral corneal abrasion. What medication(s) can you provide?

Two types of anesthetics exist for use in ophthalmologic conditions: esters and amides. The most common esters are proparacaine (0.5%) and tetracaine (0.5%). Tetracaine lasts approximately 30 minutes once applied. In comparison, proparacaine lasts 15 minutes and is slightly more irritating and slower in onset.
Color Cap: WHITE
Mechanism of action: Anesthetics function as sodium channel blockers, which decrease depolarization and action potential propagation.
Indications: Used for topical anesthesia, assisting with examination and procedures. These medications can be used to help differentiate corneal causes of symptoms versus other causes. Use in an outpatient setting is controversial for pain control; however, diluting the solution is feasible and likely will not cause delayed healing or toxicity.1-3
Dosing: One to two drops in the ED.
Considerations: Recent literature supports increased patient satisfaction with local anesthetics within a 24 hour period and no evidence of difference in corneal healing. Literature and FOAM resources support the use of diluting the 0.5% concentration into 0.05%. This can be done using a 10cc flush, ejecting 1 cc of the saline, and replacing this with 1 cc of the anesthetic.7,8


A 7-year-old male presents with his mother for two days of diffuse, bilateral eye redness and “green” drainage. He recently recovered from an upper respiratory infection. His exam, including VS, visual acuity, and fluorescein staining, are normal. You are concerned about bacterial conjunctivitis. What are your choices for antibiotics?

Topical antibiotics are often over-prescribed. However, they are indicated for a number of ophthalmic diagnoses including bacterial conjunctivitis, corneal ulcers, and blepharitis. Antibiotics are administered as either solutions or ointments. Drops are rapidly absorbed and require frequent instillation. Ointments have longer duration and require less frequent administration. However, they cause blurred vision when applied.
Color Cap: TAN
Mechanism of Action: A variety of mechanisms exist for these medications. These are shown in Table 1.
Indications: As discussed previously, indications include bacterial conjunctivitis, corneal ulcers, and blepharitis.
Dosing: Usually dependent on specific agent, with one to two drops applied one to four times per day.
Considerations: Please see Table 1.

Table 1 – Specific Antibiotic Medications4

Class Medication Specifics
Macrolide Erythromycin 0.5% – Exists as ointment only, which is soothing

– Covers gram-positive agents

– Covers Chlamydia trachomatis

– Safe for newborns/infants

– Not for contact lens users

Fluoroquinolone Levofloxacin 1.5%


Ciprofloxacin 0.3%


Ofloxacin 0.3%


4th generation quinolones (moxifloxacin, gatifloxacin, besifloxacin)


– High resistance for early generation medications, but improved with 4th generation

– Expensive

– Can be used in monotherapy for contact lens wearers and ulcers

– 4th generation medications are expensive and have great gram-negative and Pseudomonas coverage

– 4th generation medications do not have good Streptococcal coverage

Aminoglycoside Tobramycin 0.3%


Gentamicin 0.3%

– Gram-negative and Streptococcal coverage

– Useful for contact lens wearers

Other options Bacitracin



Polymyxin B/trimethoprim




– Good gram-positive coverage, useful for blepharitis


– Broad coverage

– Useful in pediatric patients



– Inhibits production of folic acid, useful for blepharitis



Topical antivirals (idoxuridine, trifluridine, and ganciclovir) are used for treatment of herpes simplex keratitis but should not be given without consultation with an ophthalmologist. Dosing includes one drop every hour for idoxuridine, one drop every two hours for trifluridine, and one drop five times per day for ganciclovir.

Antibiotic-steroid combination medications exist, but should not be used in the ED. Leave these to the ophthalmologist.


Your next patient is a 32-year-old female with deep “boring” eye pain. Your exam reveals “cells and flare” on your slit lamp with normal visual acuity and no fluorescein uptake, consistent with iritis. What medication(s) can you use?

Mydriatics and Cycloplegics
Mydriatics and cycloplegics function to dilate the eye. Mydriatic medications accomplish this by paralyzing the iris sphincter, which causes dilation without affecting accommodation. On the other hand, cycloplegics paralyze both the iris sphincter and the ciliary muscles, causing dilation and affecting accommodation. Phenylephrine (2.5%) is a common dilating agent with onset 15 minutes, lasting for 3-4 hours. Cycloplegics are often used for conditions causing inflammation of the eye. Several cycloplegics include:

  • Cyclopentolate has an onset of 30-60 minutes with duration of approximately 24 hours.
  • Tropicamide has an onset of 15-20 minutes with duration of approximately 6 hours.
  • Homatropine and atropine have a duration of days to weeks and probably have little role in the ED due to this length of action.

Color Cap: RED
Mechanism of Action: Mydriatics are sympathomimetic agents that paralyze the iris sphincter. Cycloplegics are parasympatholytic agents that paralyze the iris sphincter and the ciliary muscles.
Indications: These medications are helpful for evaluating painless monocular vision complaints such as vision loss. They can be used to treat ciliary spasm, decreasing ocular pain, in iritis and deep corneal ulcers.
Dosing: One drop in the ED. These medications are usually required once per day if prescribed for home use.
Considerations: These medications are contraindicated in patients with suspicion for increased intraocular pressure, especially in acute angle closure glaucoma, as well as in the presence of shallow anterior chamber or concern for ruptured globe.


A 63-year-old female with near-sightedness presents with sudden, severe left-sided headache and eye pain after leaving a movie theater. Her vision is cloudy in the left eye. Visual acuity in the left eye is 20/400, with correction. Her intraocular pressure is 52 mm Hg in the left eye and 18 mm Hg in the right. Her left pupil is mid-dilated, and the cornea appears cloudy. What treatments are necessary?

Adrenergic Agents
Topical adrenergic agents include beta-antagonists (timolol, betaxolol) and alpha-2-agonists (apraclonidine, brimonidine).

Beta blockers
Color Cap:
Mechanism of Action: These medications reduce intraocular pressure through decreasing aqueous humor secretion by the ciliary body.
Indications: This class is only used in the setting of acute angle closure glaucoma.
Dosing: One drop two to three times per day (once in the ED).
Considerations: The provider must be wary of cardiopulmonary effects including hypotension, syncope, heart block, and worsening of asthma. Of note, combination beta blockers may have a dark blue cap.

Alpha agonists
Color Cap:
Mechanism of action: Similar to topical beta blockers, these medications decrease aqueous humor production, decreasing intraocular pressure.
Indications: Acute angle closure glaucoma.
Dosing: One drop three times per day (once in the ED).
Combigan Ophthalmic Solution® is a combination alpha-2-agonist and beta blocker used for acute angle closure glaucoma, with one drop provided every 12 hours.

Carbonic anhydrase inhibitors
Medications in this class include dorzolamide and brinzolamide (Trusopt and Azopt). They repress carbonic anhydrase, reducing pressure in the eye through reduction in aqueous humor production.
Color Cap: ORANGE
Mechanism of Action: These medications reduce intraocular pressure through decreasing aqueous humor secretion by the ciliary body.
Indications: This class is only used in the setting of acute angle closure glaucoma.
Dosing: One drop three times per day.
Considerations: This class should not be used in patients with sickle cell disease or trait, which may lead to acute angle closure glaucoma.

Prostaglandin analogues
This class consists of travoprost, latanoprost, bimatoprost, and tafluprost. These medications reduce intraocular pressure by increasing outflow of aqueous humor.
Color Cap: Turquoise
Mechanism of Action: These medications reduce intraocular pressure through increasing outflow of aqueous humor.
Indications: This class is used for acute angle closure glaucoma.
Dosing: One drop dosed one to four times per day, specific to the agent used.
Considerations: The provider must be wary of cardiopulmonary effects including hypotension, syncope, heart block and worsening of asthma.

Miotics (Cholinergic)
In emergency medicine, the most common use for miotic agents is acute angle closure glaucoma. The most common miotic is pilocarpine (2%), which facilitates drainage of the aqueous humor.
Mechanism of Action: Miotics cause pupillary constriction, pulling the iris back from an anterior position.
Indications: This class of medication is used in acute angle closure glaucoma.
Dosing: Two drops three to four times per day.
Considerations: In the ED, this medication will be used in acute angle closure glaucoma but is only efficacious once the intraocular pressure is less than 40 mm Hg. They should only be applied after initial measures are completed, and both eyes should be medicated with pilocarpine in the setting of acute angle closure glaucoma. In the setting of cataract surgery, it may be better to dilate the eye and avoid this agent.

Systemic Medications
Several systemic medications can be used in ophthalmologic conditions, specifically acute angle closure glaucoma.

– Hyperosmotic agents
Mannitol 1-2 g/kg IV – 20% solution reduces fluid volume in the eye, which decreases intraocular pressure. This medication is indicated in acute angle closure glaucoma.

– Carbonic anhydrase inhibitor
Acetazolamide 500 mg IV/PO decreases secretion of aqueous humor by the ciliary body, reducing intraocular pressure. The medication is indicated in acute angle closure glaucoma and refractory retinal artery occlusion. However, it is contraindicated in sickle cell disease. The change in intraocular pH can increase sickling of RBCs in anterior chamber, decreasing aqueous outflow and increasing IOP. Acetazolamide may also cause worsening renal function in those with preexisting renal disease.


You have a 43-year-old female who just moved into the area. She has a history of severe allergies to dust, pollen, ragweed, and oak, and she is presenting with bilateral eye redness and irritation, with nasal congestion and drainage. Her VS are normal, and her exam is consistent with allergic conjunctivitis. What medication(s) can you prescribe?

This medication class is useful for conjunctival congestion and pruritis. Medications include Naphazoline and pheniramine (Naphcon-A® and Visine A®).
Mechanism of Action: This class works as histamine receptor antagonists.
Indications: Medications are used for conjunctival congestion or pruritis.
Dosing: One drop two times per day.
Considerations: This class should not be used for over 72 hours. They should be avoided in narrow angle glaucoma, hypertension, and contact lens use.

Non-steroidal anti-inflammatory drugs
These medications provide another option for pain and inflammation control for ophthalmologic complaints. Medications include Ketorolac, Bromfenac, Nepafenac, Diclofenac sodium.
Color Cap: GRAY
Mechanism of Action: These agents reversibly inhibit cyclooxygenase-1 and 2 (COX-1 and 2 enzymes), which decrease formation of prostaglandin. They also decrease cytokine levels and immune cellular activation.
Indications: This class can be used in allergic conjunctivitis, corneal abrasions, and UV keratitis.
Dosing: Dependent on the specific agent. Ketorolac and diclofenac are given one drop three to four times per day, while bromfenac is given one drop per day.
Considerations: These agents may enhance topical glucocorticoid effects.

Mast cell stabilizers
These agents are primarily used in the setting of allergic conjunctivitis. Medications include Nedocromil sodium (Alocril Ophthalmic Solution®), Pemirolast potassium (Alamast Ophthalmic Solution®), Lodoxamide tromethamine (Alomide Ophthalmic Solution®), and Cromolyn sodium (Cromolyn Sodium Ophthalmic Solution®). These medications are not useful for acute symptoms, as full efficacy is not reached until at least 5 days of use.9
Mechanism of Action: This medication class functions to stabilize mast cell membranes, preventing the release of histamine and leukotrienes.
Indications: These are used for allergic conjunctivitis.
Dosing: One drop two times per day.
Considerations: Efficacy is not observed until 5-14 days of use.

Similar to mast cell stabilizers, these topical medications are used for allergic conjunctivitis. Medications include Bepotastine besilate (Bepreve Ophthalmic Solution®), Epinastine hydrochloride (Elestat Ophthalmic Solution®), Emedastine difumarate (Emadine Ophthalmic Solution®), Alcaftadine (Lastacraft Ophthalmic Solution®), and Azelastine hydrochloride (Optivar Ophthalmic Solution®)
Mechanism of Action: These medications are H1-receptor antagonists.
Indications: Used for allergic conjunctivitis.
Dosing: One drop two times per day.
Considerations: Combination agents consisting of H1 antagonist-mast cell stabilizer ophthalmologic medications include Olopatadine hydrochloride (Pataday Ophthalmic Solution®, Patanol Ophthalmic Solution®).


References/Further Reading:

  1. Nash, E.A. and C.E. Margo, Patterns of emergency department visits for disorders of the eye and ocular adnexa. Arch Ophthalmol, 1998. 116(9): p. 1222-6.
  2. Sklar, D.P., J.E. Lauth, and D.R. Johnson, Topical anesthesia of the eye as a diagnostic test. Annals of emergency medicine, 1989. 18(11): p. 1209-11.
  3. Waldman, N., I.K. Densie, and P. Herbison, Topical tetracaine used for 24 hours is safe and rated highly effective by patients for the treatment of pain caused by corneal abrasions: a double-blind, randomized clinical trial. Academic emergency medicine: official journal of the Society for Academic Emergency Medicine, 2014. 21(4): p. 374-82.
  4. Walker RA and Adhikaris. Eye Emergencies. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8e. Ch. 241.
  5. Sharma R and Brunette DD. Ophthalmology. Rosen’s Emergency Medicine, Chapter 71, 909-930.e2.
  6. http://www.aao.org/about/policies/color-codes-topical-ocular-medications.
  7. Swaminathan A et al. The Safety of Topical Anesthetics in the Treatment of Corneal Abrasions: A Review. J Emerg Med 2015 PMID: 26281814
  8. Puls HA et al. Safety and Effectiveness of Topical Anesthetics in Corneal Abrasions: Systematic Review and Meta-Analysis. J Emerg Med 2015 [epub ahead of print]
  9. Nizami RM. Treatment of ragweed allergic conjunctivitis with 2% cromolyn solution in unit doses. Ann Allergy 1981; 47:5.