You are in: eMedicine Specialties > Emergency Medicine > OPHTHALMOLOGY Retinal Vein OcclusionArticle Last Updated: Mar 30, 2006AUTHOR AND EDITOR INFORMATIONSection 1 of 10
  Author: Richard J Spitz, MD, Staff Physician, Assistant Professor of Emergency Medicine, Department of Surgery, Division of Emergency Medicine, University Of Texas Health Science Center Richard J Spitz is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine Coauthor(s): Loice Swisher, MD, Assistant Professor, Department of Emergency Medicine, Mercy Hospital of Philadelphia Editors: Joseph A Salomone, III, MD, Associate Professor, Department of Emergency Medicine, Truman Medical Center, University of Missouri at Kansas City School of Medicine; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Douglas Lavenburg, MD, Clinical Professor, Department of Emergency Medicine, Christiana Care Health Systems; John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center; Robert E O'Connor, MD, MPH, Professor and Chair, Department of Emergency Medicine, University of Virginia Health System Author and Editor Disclosure Synonyms and related keywords: RVO, ischemic retinal vein occlusion, nonischemic retinal vein occlusion, retinal apoplexy, venous stasis retinopathy, hemorrhagic retinopathy INTRODUCTIONSection 2 of 10
  BackgroundRetinal vein occlusion (RVO) has been recognized as a distinct entity for quite some time. In 1854, Leibreich described it as "retinal apoplexy," and Leber soon after in 1877 called it "haemorrhagic retinitis" based on its common retinal findings. Even today, the current understanding of the disease and its treatment is still evolving. From the perspective of emergency medicine, it is useful to conceptualize RVO as being composed of two distinct entities. The two entities have different etiologies, presentations, and ultimate outcomes. When a patient is referred for further evaluation and treatment by an ophthalmologist much of the ophthalmologist's initial work will be done to discern the two. Further separating RVO into a more elaborate framework depending on the vein affected is possible but that is more the realm of ophthalmology, and whether this detail is helpful to an emergency physician in the conceptualization, evaluation, treatment, and ultimate referral of RVO from the emergency department is debatable. Retinal vein occlusion (RVO) can be separated into the following categories:
PathophysiologyTendency for RVO can be remembered by recalling Virchow's triad.
Most researchers believe the pathogenesis is multifactorial. The most common associated diseases are hypertension, diabetes mellitus, and atherosclerotic heart disease. Patients with glaucoma have a 5 times more likely chance of developing RVO than patients without glaucoma. FrequencyUnited StatesRVO is the second most common retinal vascular disorder after diabetic retinopathy; however, exact frequencies are not known. InternationalInternational incidence is not known. Mortality/Morbidity
RaceLittle documentation exists regarding race and RVOs; however, they are thought to be rare in the Asian and West Indian populations. SexReportedly, all clinical categories are slightly more common in men than in women except major branch retinal vein occlusion (BRVO). AgeReported cases occur in those aged from 8 months to 92 years. More than one half of cases occur after the age of 65. CLINICALSection 3 of 10
History
Physical
Causes
DIFFERENTIALSSection 4 of 10
Retinal Artery Occlusion Retinal Detachment Temporal Arteritis Vitreous Hemorrhage
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| Drug Name | Prednisone (Deltasone) |
|---|---|
| Description | Useful in treatment of inflammatory and autoimmune reactions. By reversing increased capillary permeability and suppressing PMN activity, it may decrease inflammation. |
| Adult Dose | 5-60 mg/d qd or divided bid/qid; taper over 2 wk as symptoms resolve |
| Pediatric Dose | 4-5 mg/m2/d Alternative 1-2 mg/kg PO qd; taper over 2 wk as symptoms resolve |
| Contraindications | Documented hypersensitivity; viral, fungal, or tubercular skin infections |
| Interactions | Coadministration with estrogens may decrease prednisone clearance; concurrent use with digoxin, may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics |
| Pregnancy | B - Usually safe but benefits must outweigh the risks. |
| Precautions | Abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur with glucocorticoid use |
An enzyme found in many tissues of the body, including the eye, which catalyzes a reversible reaction that involves the hydration of carbon dioxide and the dehydration of carbonic acid.
Slowing the formation of bicarbonate ions with subsequent reduction in sodium and fluid transport may inhibit CA in the ciliary processes of the eye. This effect decreases aqueous humor secretion, reducing the intraocular pressure.
| Drug Name | Acetazolamide (Diamox) |
|---|---|
| Description | Inhibits enzyme carbonic anhydrase, reducing rate of aqueous humor formation, which, in turn, reduces intraocular pressure. Used for adjunctive treatment of chronic simple (open-angle) glaucoma and secondary glaucoma and preoperatively in acute angle-closure glaucoma when delay of surgery desired to lower IOP. |
| Adult Dose | 250-375 mg PO/IV/IM q4h or sustained release acetazolamide (Diamox Sequels) 500 mg bid |
| Pediatric Dose | 5 mg/kg/d or 150 mg/m2 PO/IV/IM qd |
| Contraindications | Documented hypersensitivity; hepatic disease; severe renal disease; adrenocortical insufficiency; severe pulmonary obstruction |
| Interactions | Can decrease therapeutic levels of lithium and alter excretion of drugs (amphetamines, quinidine, phenobarbital, salicylates) by alkalinizing urine |
| Pregnancy | C - Safety for use during pregnancy has not been established. |
| Precautions | Patients with impaired hepatic function may go into coma; may cause substantial increase in blood glucose in some diabetic patients |
| Drug Name | Dorzolamide (Trusopt) |
|---|---|
| Description | Use concomitantly with other topical ophthalmic drug products to lower intraocular pressure. If more than one ophthalmic drug is being used, administer the drugs at least 10 min apart. |
| Adult Dose | 1 gtt in affected eye or eyes tid |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity; hepatic disease; severe renal disease; adrenocortical insufficiency; severe pulmonary obstruction |
| Interactions | Can decrease therapeutic levels of lithium and alter excretion of drugs (amphetamines, quinidine, phenobarbital, salicylates) by alkalinizing urine |
| Pregnancy | C - Safety for use during pregnancy has not been established. |
| Precautions | Patients with impaired hepatic function may go into coma; may cause substantial increase in blood glucose in some diabetic patients |
Timolol, levobunolol, carteolol, betaxolol, and metipranolol are topical beta-blockers that reduce elevated and normal intraocular pressure, with or without glaucoma. The immediate objective in angle-closure glaucoma is to reopen the angle, requiring constriction of the pupil with a miotic. These agents have little or no effect on the pupil. When they are used to reduce elevated intraocular pressure in angle-closure glaucoma, they should be used concurrently with a miotic. The exact mechanism of ocular antihypertensive action is not established, but it appears to be a reduction of aqueous production. However, some studies show a slight increase in outflow facility with timolol and metipranolol.
| Drug Name | Timolol (Timoptic) |
|---|---|
| Description | Reduces elevated and normal intraocular pressure by reducing aqueous humor production or possibly the outflow. |
| Adult Dose | 1 gtt of 0.25% or 0.5% solution in affected eye or eyes bid; if intraocular pressure is maintained at satisfactory levels, reduce the dosage to 1 gtt qd in affected eye or eyes If intraocular pressure not at satisfactory level following regimen, consider concomitant therapy |
| Pediatric Dose | Administer as in adults |
| Contraindications | Documented hypersensitivity; bronchial asthma; sinus bradycardia; second- and third-degree AV block; severe chronic obstructive pulmonary disease; overt cardiac failure; cardiogenic shock |
| Interactions | May cause bradycardia and asystole when used in combination with systemic beta-blockers (may cause additive effects) |
| Pregnancy | C - Safety for use during pregnancy has not been established. |
| Precautions | Product may have sulfites, which may cause allergic-type reactions in susceptible patients; may exacerbate or precipitate heart block, asthma, chronic obstructive pulmonary disease, or mental changes (especially in elderly patients) |
| Drug Name | Levobunolol (Betagan, AKBeta) |
|---|---|
| Description | Nonselective beta-adrenergic blocking agent that lowers intraocular pressure by reducing aqueous humor production and may increase outflow of aqueous humor. Dosages of more than 1 gtt of 0.5% levobunolol twice daily have not been shown to be more effective. If intraocular pressure not at satisfactory level on this regimen, concomitant therapy can be instituted. However, do not administer 2 or more topical ophthalmic beta-adrenergic blocking agents simultaneously. |
| Adult Dose | 0.5% solution: 1-2 gtt in affected eye or eyes qd 0.25% solution: 1-2 gtt in affected eye or eyes bid Severe or uncontrolled glaucoma: 0.5% solution bid; closely monitor patient >1 gtt (0.5% levobunolol) bid not shown to be more effective; if intraocular pressure not at satisfactory level on this regimen, concomitant therapy can be instituted; do not administer 2 or more topical ophthalmic beta-adrenergic blocking agents simultaneously |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity; bronchial asthma; severe chronic obstructive pulmonary disease; sinus bradycardia; second- and third-degree AV block; overt cardiac failure; cardiogenic shock |
| Interactions | May cause bradycardia and asystole when used in combination with systemic beta-blockers (may cause additive effects) |
| Pregnancy | C - Safety for use during pregnancy has not been established. |
| Precautions | Beta-blockade may potentiate muscle weakness consistent with certain myasthenic symptoms (eg, diplopia, ptosis, generalized weakness); product may have sulfites, which may cause allergic-type reactions in certain susceptible persons |
| Drug Name | Betaxolol (Betoptic) |
|---|---|
| Description | Selectively blocks beta1-adrenergic receptors with little or no effect on beta2-receptors. Reduces intraocular pressure by reducing the production of aqueous humor. Consider concomitant therapy if intraocular pressure not satisfactory following this treatment. This beta-blocker tends to be less potent than the nonselective beta-blockers. |
| Adult Dose | 1-2 gtt in affected eye or eyes bid |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity; bronchial asthma; severe chronic obstructive pulmonary disease; sinus bradycardia; second- and third-degree AV block; overt cardiac failure; cardiogenic shock |
| Interactions | May have additive systemic effects if patient is already on systemic beta-blockers |
| Pregnancy | C - Safety for use during pregnancy has not been established. |
| Precautions | Beta-blockade may potentiate muscle weakness consistent with myasthenic symptoms; product may have sulfites, which may cause hypersensitivity reactions in susceptible persons |
Direct-acting miotics are parasympathomimetic (cholinergic) drugs, which duplicate the muscarinic effects of acetylcholine. These drugs produce pupillary constriction when applied topically and stimulate the ciliary muscles. These effects in turn result in an increase in aqueous humor outflow. In addition, contraction of the iris sphincter produces miosis causing increased tension on the scleral spur (reducing outflow resistance). This, in turn, opens the trabecular meshwork spaces, facilitating aqueous humor outflow. With the increase in outflow, a decrease in intraocular pressure results.
| Drug Name | Pilocarpine (Ocusert Pilo-20, Isopto, Pilocar, Piloptic, Pilostat) |
|---|---|
| Description | Patients may be maintained on pilocarpine as long as the intraocular pressure is controlled and no deterioration in the visual fields is present. May be used alone or in combination with other miotics, beta-adrenergic blocking agents, epinephrine, carbonic anhydrase inhibitors, or hyperosmotic agents to decrease intraocular pressure. Frequency of instillation and concentration are determined by the patient's response. Individuals with heavily pigmented irides may require higher strengths. |
| Adult Dose | Solution: 1-2 gtt tid/qid Gel: Apply a 0.5-inch ribbon in the lower conjunctival sac of affected eye or eyes hs If another glaucoma medication is being used hs, use gtt at least 5 min before the gel |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity; acute inflammatory disease of anterior chamber |
| Interactions | May be ineffective when used concomitantly with NSAIDs |
| Pregnancy | C - Safety for use during pregnancy has not been established. |
| Precautions | Caution in acute cardiac failure, peptic ulcer, hyperthyroidism, GI spasm, bronchial asthma, Parkinson disease, recent MI, urinary tract obstruction, hypertension, or hypotension |
Retinal Vein Occlusion excerpt
Article Last Updated: Mar 30, 2006
