Central Retinal Artery Occlusion (CRAO) 

Updated: Jun 11, 2019
Author: Robert H Graham, MD; Chief Editor: Andrew G Lee, MD 

Overview

Background

Central retinal artery occlusion (CRAO) was first described by Van Graefe in 1859 as an embolic event to the central retinal artery in a patient with endocarditis. In 1868, Mauthner suggested that “spasmodic contractions” could lead to retinal artery occlusion. CRAO has various causes, but patients typically present with sudden, severe, and painless loss of vision.

Pathophysiology

Visual loss due to CRAO occurs once the inner two-thirds of the retina has lost its blood supply. The ophthalmic artery is the first branch of the internal carotid artery and enters the orbit underneath the optic nerve through the optic canal. The central retinal artery, the first intraorbital branch of the ophthalmic artery, enters the optic nerve 8-15 mm behind the globe to supply the retina. The short posterior ciliary arteries branch distally from the ophthalmic artery and supply the choroid. Cilioretinal arteries, an anatomic variant present in 15%-30% of the population, branch from the short posterior ciliary artery. These arteries supply the macula in addition to the choroidal circulation. In CRAO in these patients, the central visual acuity may be preserved (>20/50), since the cilioretinal artery often supplies the papillomacular bundle and is a direct extension of the posterior ciliary artery.[1, 2, 3] In 10% of eyes, the cilioretinal artery supplies some or all of the foveola. Nevertheless, even with cilioretinal artery-sparing CRAO, peripheral vision remains poor.[2, 4]

Acute obstruction of the central retinal artery results in inner layer edema and death of the ganglion cell nuclei. The retina loses its transparency and becomes yellow-white in appearance owing to ischemic necrosis. The opacity is most dense in the posterior pole as a result of the increased thickness of the nerve fiber layer and ganglion cells in the macula. Furthermore, the foveola assumes a cherry-red spot because of a combination of 2 factors: (1) The foveolar retina remains transparent because it is nourished by the choriocapillaris and (2) the intact retinal pigment epithelium and choroid underlying the fovea are outlined by the opaque surrounding retina. The late stage of CRAO shows a homogenous scar replacing the inner layer of the retina. After a few weeks, the opacification resolves, and the retina remains thin and atrophic; although there may be arteriolar narrowing and optic atrophy, the retina may otherwise appear deceptively normal.[5]

Opacification of the retina in CRAO takes as little as 15 minutes to several hours before becoming evident and resolves in 4-6 weeks. The resulting pathology reflects a catastrophic insult to the inner retinal layers with attenuated retinal arterioles and optic nerve pallor. Pigmentary changes are typically absent since the retinal pigment epithelium remains unaffected; however, vesicular, pearly, and sometimes pigmented patches may appear in the retina, demonstrating remnants of hemorrhages and areas of severe degeneration.[5] A “boxcarring” appearance of the impaired blood column can be seen in both arteries and veins. This finding was previously seen by Wolf and Davies by experimentally occluding both ophthalmic arteries and veins with a clamp.[5] Hayreh et al have shown that irreversible cell injury occurs after 90-100 minutes of total CRAO in a healthy and young primate model[6] Additional studies on the hypertensive, elderly, or middle-aged atherosclerotic rhesus monkey showed the morphologic optic nerve damage starts after 105 minutes and is total after 240 minutes of occlusion.[7]

However, a 2018 meta-analysis by Tobalem et al suggests that retinal ischemia probably occurs within 12-15 minutes and that earlier experimental evidence suggesting a window of 90-120 minutes could be flawed and not applicable to the general population, since most of the experiments supporting this theory were performed in animals in a controlled environment of hypothermia and under barbiturate anesthesia, which have additional neuroprotective effects. This could explain why most rescue efforts in acute CRAO do not provide significant benefit.[8]

After some months, the optic disc becomes atrophic and pale.[5] Controversy exists regarding the optimal window of treatment in humans, but the conservative approach involves treatment up to 24 hours.

Epidemiology

Frequency

United States

CRAO is found in 1 per 10,000 outpatient visits. Of these patients, only 1%-2% present with bilateral involvement. The incidence of CRAO is slightly less than 2 per 100,000 among whites in the United States[9] and usually affects adult patients with cardiovascular risk factors[10] such as hypertension, hyperlipidemia, and diabetes.

Mortality/Morbidity

Patients with visualized retinal artery emboli, regardless of the presence of obstruction, have a 56% mortality rate over 9 years, compared to 27% in an age-matched population without retinal artery emboli. Life expectancy among patients with CRAO is 5.5 years, compared to 15.4 years in an age-matched population without CRAO.

Sex

CRAO is slightly more common in men than in women.

Age

The mean age of CRAO presentation is in the early seventh decade of life, although a few cases have been reported in patients younger than 30 years. The likely etiology of occlusion changes depending on the age at presentation.

Prognosis

Most patients with CRAO continue to experience severe vision loss, in the counting fingers to hand motion range.[11]

As many as 10% of patients retain central vision because of the presence of a cilioretinal artery. In this case, visual acuity improves to 20/50 or better in 80% of cases over a 2-week period.

The presence of a retinal embolus is associated with a 56% mortality rate over 9 years compared to 27% in patients without arterial emboli.

The life expectancy of patients with CRAO is 5.5 years compared to 15.4 years for an age-matched population without CRAO.

Patient Education

Patients with CRAO must understand that the prognosis for visual recovery is poor and that the visual changes usually result from a systemic process that needs treatment. The most important education is to control the cardiovascular risk factors that may lead to other complications such as cerebrovascular accident, among others. 

 

Presentation

History

The most common presenting complaint of central retinal artery occlusion (CRAO) is acute, unilateral, persistent, painless vision loss in the range of counting fingers to light perception in 90% of patients. The clinician should consider an ophthalmic artery occlusion if the visual acuity is worse or if the cherry red spot is absent (indicating possible choroidal as well as retinal artery occlusive disease).

Some patients with CRAO reveal a history of amaurosis fugax (transient vision loss lasting seconds to minutes but that may last up to 2 hours), which may result from transient CRAO. The vision usually returns to baseline after an episode of amaurosis fugax.

The clinician should inquire about the symptoms of temporal arteritis in older patients (eg, headache, jaw claudication, scalp tenderness, proximal muscle and joint aches, anorexia, weight loss, fever).

The past medical history should include any medical problems that could predispose to embolus formation (eg, atrial fibrillation, endocarditis, atherosclerotic disease, hypercoagulable state). Other predisposing factors include prolonged direct pressure to the globe during drug-induced stupor or improper positioning during face-down surgical procedures. The physician should also inquire about any illicit drug history.

Physical

Determine the degree of vision loss (eg, no light perception, hand movement, counting fingers).

Ocular examination includes the following:

  • Check for a relative afferent pupillary defect (rAPD).
  • Perform an optic nerve examination to look for signs of temporal arteritis (eg, concomitant ischemic optic neuropathy or cilioretinal artery occlusion). Critical signs include the rAPD and pale/swollen optic nerve (pallid edema) with splinter hemorrhages.
  • Cherry-red spot and a ground-glass retina may take hours to develop.
  • The funduscopic findings typically resolve within days to weeks of the acute event, sometimes leaving a pale optic disc as the only physical finding.
  • Emboli can be seen in about 20% of patients with CRAO.
  • Boxcar segmentation can be seen in both arteries and veins. This is a sign of severe obstruction.

Causes

Emboli dislodged from the carotid artery are the most common cause of CRAO, from either an unstable atherosclerotic plaque or a cardiac source.

The probable causes of CRAO vary depending on the age of the patient. A detailed analysis of comorbid disease is necessary to elucidate the cause of the acute visual loss. See the following:

  • Systemic hypertension, seen in two-thirds of patients
  • Diabetes mellitus
  • Cardiac valvular disease, seen in a quarter of patients
  • Cardiac anomalies, such as patent foramen ovale (PFO)
  • Embolism, as follows:
    • Cholesterol is the most common type, but it can also be from calcium, bacteria, or talc from intravenous drug use.
    • This is associated with poorer visual acuity and higher overall morbidity and mortality.
    • Emboli from the heart are the most common cause of CRAO in patients younger than 40 years.
  • Atherosclerotic changes, as follows:
    • Carotid atherosclerosis is seen in 45% of cases of CRAO, with 60% or greater stenosis in 20% of cases. Callizo et al found that ipsilateral carotid stenosis was the most significant risk factor for CRAO. [12]
    • Atherosclerotic disease is the leading cause of CRAO in patients aged 40-60 years.
    • Chang et al have found an increased risk of acute coronary syndrome (indicative of coronary atherosclerosis) in patients with retinal arterial occlusions. [13]
  • Amaurosis fugax preceding persistent vision loss suggests transient CRAO, branch retinal artery occlusion (BRAO), or temporal arteritis.
  • A hypercoagulable state, such as in patients with sickle cell anemia, polycythemia, or antiphospholipid syndrome or in those taking oral contraceptives, is a common etiology of CRAO in patients younger than 30 years.
  • Giant cell arteritis, as follows:
    • Giant cell arteritis should be considered in elderly patients
    • Giant cell arteritis may produce CRAO, cilioretinal artery occlusion, ischemic optic neuropathy, or a combination of these findings
  • Giant cell arteritis needs to be treated immediately with corticosteroids to preserve vision in the fellow eye.
  • Collagen vascular disease
  • Polyarteritis nodosa
  • Increased intraocular pressure due to glaucoma
  • Hydrostatic arterial occlusion
  • Iatrogenic: With the increasing popularity of cosmetic facial filler injections, Chen et al and Carle et al report that these injections are a cause of retinal artery occlusions. [14, 15] Other associations with CRAO, such as extracapsular cataract extraction with retrobulbar anesthesia, [16] strangulation, [17] or injection of stem cells for scalp baldness, [18] have been published.

Complications

Patients with CRAO may develop a cerebrovascular accident due to secondary emboli. Park et al found that patients with CRAO had a significantly increased risk for stroke and acute myocardial infarction, particularly during the first week following CRAO.[19] Further emboli could travel to the same or contralateral eye, resulting in further visual loss. Ocular neovascularization, including neovascular glaucoma, occurs in approximately 15% of patients with CRAO, especially in those with diabetes mellitus, type 2.[20]

 

DDx

 

Workup

Approach Considerations

The risk of stroke is higher in patients with central retinal artery occlusion (CRAO). Studies have indicated that the likelihood of stroke after CRAO is up to 10 times higher during the first 3.5 years than in the regular population. This risk may continue for the following 10 years after the CRAO event.[21, 22]

Laboratory Studies

Laboratory studies may be helpful in determining the etiology of CRAO, as follows:

  • Complete blood count (CBC) (eg, anemia, leukemia, polycythemia, platelet disorders)
  • Erythrocyte sedimentation rate (ESR) evaluation for giant cell arteritis in elderly patients
  • Hypercoagulable state evaluation (eg, factor V Leiden, prothrombin mutation, homocysteine levels, fibrinogen, antiphospholipid antibodies, prothrombin time/activated partial thromboplastin time [PT/aPTT], serum protein electrophoresis, among others)
  • Fasting blood sugar, cholesterol, triglycerides, and lipid panel to evaluate for atherosclerotic disease
  • Blood cultures to evaluate for suspected bacterial endocarditis and septic emboli

Imaging Studies

Imaging studies are helpful in determining the etiology of CRAO.

Carotid ultrasonography

Carotid ultrasonography may be used to evaluate for atherosclerotic plaque; this appears to be more sensitive than carotid ultrasonography with Doppler, which determines only the flow.

Magnetic resonance imaging

Approximately 20% of patients with a CRAO also have cerebral ischemia; therefore, magnetic resonance imaging (MRI) of the brain may reveal concurrent cerebral ischemia in patients without accompanying neurological symptoms.[23] Magnetic resonance angiography (MRA) of the head and neck may be more accurate in detecting vascular occlusive disease. Computerized tomography (CT) or computerized tomography angiography (CT/CTA) or MRI/MRA of the neck may be needed for carotid dissection.

Fundus autofluorescence

In the acute phase, fundus autofluorescence in ischemic areas is decreased because of retinal edema blocking the normal RPE. Eventually, this could return to normal baseline or may be associated with increased autofluorescence owing to a window defect created by the thinned-out inner retinal layers.[24]

Fluorescein angiography

Fluorescein angiography (see list of findings indicating CRAO below) may be a prognostic test.[25] Poor perfusion on fluorescein angiography has been associated with lower vision than exudative and mixed perfusion.[25] This finding does not influence therapy.

  • Normal choroidal filling begins 1-2 seconds before retinal filling and is complete within 5 seconds of dye appearance in healthy eyes. A delay of 5 or more seconds is seen in 10% of patients. Consider ophthalmic artery occlusion or carotid artery obstruction if choroidal filling is significantly delayed.
  • Delay in arteriovenous transit time (reference range, < 11 seconds)
  • Delay in retinal arterial filling
  • Arterial narrowing with normal fluorescein transit after recanalization

Spectral-domain optical coherent tomography

Spectral-domain optical coherent tomography (OCT) has been proposed as one modality that might be used to diagnose and monitor CRAO. 

In CRAO, there is an observed increase in intensity of inner retinal layers compared with age-matched controls, and it corresponds to the layers supplied by central retinal arteries. Chen et al showed that optical intensity on OCT can be correlated with visual prognosis.[26] Incomplete CRAO shows minimal  retinal architectural disruption and inner layer hyper-reflectivity without retinal edema. Subtotal CRAO demonstrated inner macular thickening and loss of organization of the inner retina, and total CRAO demonstrated marked inner retinal thickening and subfoveal choroidal thinning.[27, 28] In the chronic phase, there is a corresponding thinning of the inner retinal layers.

Optical coherent tomography angiography

Optical coherent tomography angiography (OCTA) is a novel noninvasive technique that eliminates the need for dye injection to evaluate the retinal microvasculature. It is based on the principle that static and nonstatic structures (ie, blood flowing through vessels) generate different signal amplitudes on repeated B scans from the same cross-sections. OCTA provides structural and functional (blood flow) information at a fixed point; however, it is not useful to appreciate leakage from vessels.[29]

OCTA shows decreased vascular perfusion in superficial and deep retinal plexus that corresponds to poor perfusion on fluorescein angiography. In patients with the cilioretinal artery–sparing variant, the deep capillary plexus retained perfusion. However, unlike fundus fluorescein angiography, OCTA cannot demonstrate a delay in transit time.[30]

Electroretinography

Electroretinography shows a diminished b-wave corresponding to Muller and/or bipolar cell ischemia.

Other Tests

Systemic tests are used to identify additional risks that may lead to cerebral ischemia, myocardial infarction, and cardiovascular death.

Electrocardiography 

Electrocardiography (ECG) is used to evaluate for possible atrial fibrillation.

Holter monitor

A 24-hour Holter monitor may be necessary if arrhythmia is suspected but not detected on ECG testing.

Echocardiography 

Echocardiography may reveal valvular disease, wall motion abnormalities, and/or mural thrombi.

 

Treatment

Approach Considerations

The most important tenet of treatment is rapid identification of central retinal artery occlusion (CRAO), which depends on logistic challenges specific to each care center.

Medical Care

There is no standard treatment for CRAO.[10]

Among the suggested treatments are noninvasive and more invasive treatments. Some of the noninvasive treatments include ocular massage, hyperbaric oxygen (HBO) therapy, carbogen inhalation therapy, intraocular pressure reduction (with systemic or local agents), anticoagulation therapy, sublingual isosorbide therapy, and systemic steroid therapy. The goal of each is to increase blood flow and blood oxygen content.

Invasive procedures include anterior chamber paracentesis, laser embolectomy, pars plana vitrectomy, and intraarterial thrombolysis. Most invasive procedures are aimed to reduce intraocular pressure and lyse/dislodge the obstructive embolus, although none of the treatments has enough supportive evidence to become the standard of care. Recent publications demonstrated that intraarterial thrombolysis may be an alternative to recover blood flow and vision after embolic CRAO.[31]

Ocular massage

Ocular massage can dislodge the embolus to a point further down the arterial circulation and improve retinal perfusion.

Anterior chamber paracentesis

This procedure involves letting out aqueous from the anterior chamber, which causes a decrease in intraocular pressure. This is believed to allow greater perfusion, pushing emboli further down the vascular tree. However, according to one study, anterior chamber paracentesis added no gain in visual acuity, regardless of the interval between onset of symptoms and time of treatment.[32]

Medical reduction of intraocular pressure

Acetazolamide 500 mg IV or 500 mg PO can be administered to immediately lower intraocular pressure.

Topical medications are also used to lower intraocular pressure.

Laser embolectomy

Lysis of the emboli can be achieved with Nd:YAG laser.[33, 34, 35] Retinal perfusion with gain of visual function can be achieved. However, complications such as creation of false aneurysms and vitreous hemorrhage may arise.

Pars plana vitrectomy with direct central retinal artery massage

A probe was designed to apply direct gentle pressure/massage over the CRA and the optic nerve head. Of 10 patients, circulation was restored in only 4.[36]

Intra-arterial fibrinolysis

CRAO is one of the few ophthalmology emergencies in which management depends on time of onset. Intraarterial thrombolysis has been used anywhere from 1 hour to up to 24 hours, although this procedure is very controversial.[37]

Thrombolytic agents that have been studied for CRAO treatment include intra-arterial tissue plasminogen activator (tPA) and urokinase.

According to Wang et al, digital subtraction angiography (DSA)–guided superselective ophthalmic artery or selective carotid thrombolysis remains the preferred treatment method for CRAO.[38] More recently, branch retrograde thrombolytic intervention of the ophthalmic artery (urokinase and papaverine) was shown to be effective for CRAO.[38] Mercier et al reported that fibrinolysis was more effective than conservative management in 16 patients with CRAO.[39] In 11 patients, Nedelmann et al found clinically relevant visual improvement with thrombolysis in patients with CRAO only in the absence of a “spot sign,” an ultrasonographic sign they hypothesize may indicate calcified intra-arterial emboli due to atherosclerotic plaques.[40]

Conversely, Pielen et al found no clear benefit from intra-arterial fibrinolysis, even in otherwise ideal candidates (ie, young age, without history of coronary heart disease, and early treatment).[41] Ahn et al showed that approximately 40% of patients undergoing intra-arterial thrombolysis showed a no-reflow phenomenon, and those with the no-reflow phenomenon suffered a worse visual outcome, with more retinal atrophy and disruption of photoreceptors.[42] However, in a separate study, Ahn et al concluded that intra-arterial thrombolysis may help patients with incomplete CRAO.[43]

McLeod and Beatty reported that, once CRAO exceeds 2 hours, emergency fibrinolytic therapy is inappropriate.[44]

Systemic complications of fibrinolytic therapy include transient ischemic attack (TIA), stroke, intra-cerebral hemorrhage, and hematoma.

In a meta-analysis, Schrag et al suggested that early systemic intravenous fibrinolytic therapy might be helpful in CRAO and called for a clinical trial.[45]

The European Assessment Group for Lysis in the Eye (EAGLE)[46] trial was a multicenter, randomized, controlled trial involving 82 patients with acute CRAO (< 20 hours). EAGLE compared the effect of intra-arterial tPA to “conservative” treatments (eg, IOP lowering medications, IV heparin, hemodilution, ocular massage, daily ASA therapy). In this trial, 42 patients (51.2%) received localized intra-arterial tPA in either the ophthalmic artery or external carotid artery collaterals feeding into the ophthalmic artery. There was no statistically significant improvement in visual acuity after intra-arterial tPA administration compared to conservative treatment. Interestingly, 60% of patients in the conservative treatment group and 57% of patients in the thrombolysis group experienced 3 or more lines of improvement in visual acuity. However, 37.1% of the thrombolysis group (versus only 4.3% of the conservative treatment group) experienced adverse reactions (eg, epistaxis, oral hemorrhage, dizziness, headaches, intracranial hemorrhages, hemiparesis, postprocedural hemorrhage). The study was terminated at the first interim analysis because of the increased incidence of adverse events in the tPA treatment group.

A second placebo-controlled randomized trial studying the effect of intravenous (IV) tPA on visual outcome in 8 patients with CRAO also did not show a significant improvement. One patient in the IV tPA cohort developed intracranial hemorrhage.

A meta-analysis of studies comparing standard therapy with intra-arterial thrombolysis included 5 retrospective studies and one randomized controlled trial (ie, EAGLE study). Pooled data from these studies favored use of intra-arterial thrombolysis over standard therapy, with 50.4% of those treated with intra-arterial thrombolysis demonstrating improved visual acuity versus 31.8% of those treated with standard therapy (P <  0.005). This was despite the fact that the EAGLE study did not show any statistical significance in improvement of best-corrected visual acuity (BCVA) among the two groups. However, the included studies showed dramatic variations in the efficacy of both intra-arterial thrombolysis (23.5%-80% in visual acuity improvement) and conservative therapies. The EAGLE study design has been questioned owing to its broad inclusion criteria, as it included patients with incomplete, subtotal, and complete occlusion. The treatment outcomes vary significantly depending on the type of presentation. Clinically significant visual outcomes can be expected in patients with incomplete or subtotal occlusion, as opposed to those with complete occlusion.

More randomized controlled studies, including limiting the study group to incomplete or subtotal CRAO, as opposed to including those with complete occlusion, which by itself has a poor prognostic outcome, would be a better design to analyze and compare the efficacy of standard therapy with intra-arterial thrombolysis.[47]

Hyperbaric Medicine

Early treatment (< 2 hours from onset of symptoms) with hyperbaric oxygen (HBO) therapy may be associated with increased visual recovery, but HBO therapy can be considered if the duration of visual loss is less than 12 hours.

Inhalation of 100% oxygen at 2 atmospheric absolute provides an arterial pO2 of 1000-1200 mm Hg, resulting in a 3-fold increase in oxygen diffusion distance through ischemic retinal tissues. Some studies show a 40% improvement of 2 or more levels of visual acuity.

Inpatient Care

Inpatient care is indicated only if comorbid disease is present. Acute cases may require in-hospital evaluation for stroke risk factors. In a 2009 survey of US ophthalmologists in Georgia, only 35% reported referring patients with CRAO to the hospital. Another US-based vitreoretinal specialist and neurologist survey revealed that, for a hypothetical patient with a CRAO (< 12 hours), only 18% of vitreoretinal specialists would pursue hospital admission to a stroke unit or ER referral. In contrast, 75% of neurologists would refer to the hospital. Only 46% of neurologists and 8% of vitreoretinal specialists would pursue hospital evaluation for CRAO onset between 24 and 48 hours.

Transfer

Transfer to a hyperbaric facility is necessary if HBOT is to be administered.

Prevention

Patients should control their blood pressure, lower their cholesterol, avoid intravenous drugs, and take their medication.

Long-Term Monitoring

A follow-up ophthalmic examination should be performed 1-4 weeks after the event to check for neovascularization of the disc or iris. Intravitreal injection of an anti-VEGF agent is first-line therapy for neovascularization of the iris, trabecular meshwork, or optic disc. Neovascularization of the iris occurs in 20% of patients at an average of 4-5 weeks after the event. Panretinal photocoagulation is effective in causing regression of iris neovascularization in 65% of patients. Neovascularization of the disc occurs in 2-3% of patients. Panretinal photocoagulation is effective for optic disc neovascularization.

A complete systemic workup should be performed by a primary care provider. Hospital admission, cranial MRI (including diffusion weighted imaging) and MRA, and consultation with the neurology stroke service may be useful, especially in acute cases.

If hyperbaric oxygen therapy (HBOT) is to be used, several treatments may be necessary, although this treatment is unproven.

 

Medication

Medication Summary

Medical therapy is directed toward lowering IOP, increasing retinal perfusion, and increasing oxygen delivery to hypoxic tissues. The first goal is accomplished by using the same drugs as those used in glaucoma. Retinal perfusion may be increased by administration of vasodilatory drugs although this is unproven, increasing arterial pCO2, or by giving intravascular thrombolytics to remove the offending embolus. Some physicians also advocate aspirin use in the acute phase. Oxygen delivery is improved by breathing higher concentrations of oxygen or with hyperbaric oxygen.

Carbonic anhydrase inhibitors

Class Summary

Carbonic anhydrase is an enzyme found in many tissues of the body, including the eye. The reversible reaction it catalyzes involves the hydration of carbon dioxide and the dehydration of carbonic acid.

Acetazolamide (Diamox)

Reduces rate of aqueous humor formation by inhibiting enzyme carbonic anhydrase, which results in decreased IOP. Used most frequently as single diuretic agent in acute management of CRAO. Other diuretics may be added if sufficient decrease in IOP is not attained.

Dorzolamide (Trusopt)

Used concomitantly with other topical ophthalmic drug products to lower IOP. If more than one ophthalmic drug is being used, administer the drugs at least 10 min apart. Reversibly inhibits carbonic anhydrase, reducing hydrogen ion secretion at renal tubule and increases renal excretion of sodium, potassium bicarbonate, and water to decrease production of aqueous humor.

Hyperosmotic diuretics

Class Summary

Lower IOP by creating an osmotic gradient between the ocular fluids and plasma (not for long-term use). Hemoconcentration is potentially an issue with this form of therapy.

Mannitol (Osmitrol)

Reduces elevated IOP when the pressure cannot be lowered by other means. First, assess for adequate renal function in adults by administering a test dose of 200 mg/kg, given IV over 3-5 min. It should produce a urine flow of at least 30-50 mL/h of urine over 2-3 h. In children, assess for adequate renal function by administering a test dose of 200 mg/kg, given IV over 3-5 min. It should produce a urine flow of at least 1 mL/h over 1-3 h.

Glycerin

Used in glaucoma to interrupt acute attacks. Oral osmotic agent for reducing IOP. Able to increase tonicity of blood until finally metabolized and eliminated by the kidneys. Maximum reduction of IOP usually occurs 1 h after glycerin administration. Effect usually lasts approximately 5 h.

Sympathomimetics

Class Summary

Lower IOP mainly by increasing outflow and reducing the production of aqueous humor. The combination of a miotic and a sympathomimetic has additive effects in lowering IOP. Each may be added in rotation after a 5-minute interval, until target IOP is reached.

Apraclonidine (Iopidine)

Reduces elevated, as well as normal, IOP whether or not accompanied by glaucoma. Apraclonidine is a relatively selective alpha-adrenergic agonist that does not have significant local anesthetic activity. Has minimal cardiovascular effects.

Dipivefrin (AKPro, Propine)

Converted to epinephrine in eye by enzymatic hydrolysis. Appears to act by decreasing aqueous production and enhancing outflow facility. Has same therapeutic effect as epinephrine with fewer local and systemic side effects. May be used as an initial therapy or as an adjunct with other antiglaucoma agents for the control of IOP.

Beta-adrenergic blocking agents

Class Summary

Lower IOP by decreasing the rate of aqueous humor production and possibly outflow. They may be more effective than either pilocarpine or epinephrine alone and have the advantage of not affecting pupil size or accommodation.

Timolol ophthalmic (Timoptic)

May reduce elevated and normal IOP, with or without glaucoma by reducing the production of aqueous humor or by outflow.

 

Questions & Answers

Overview

What is central retinal artery occlusion (CRAO)?

What is the pathophysiology of central retinal artery occlusion (CRAO)?

What is the incidence of central retinal artery occlusion (CRAO) in the US?

What is the mortality rate of central retinal artery occlusion (CRAO)?

Is central retinal artery occlusion (CRAO) more common in men or women?

At what age does central retinal artery occlusion (CRAO) typically present?

What is the prognosis of central retinal artery occlusion (CRAO)?

What educational information should be provided to patients with central retinal artery occlusion (CRAO)?

Presentation

What is the most common presenting complaint of central retinal artery occlusion (CRAO)?

What is the patient history associated with central retinal artery occlusion (CRAO)?

How is a physical exam performed in central retinal artery occlusion (CRAO)?

What causes central retinal artery occlusion (CRAO)?

What are the potential complications of central retinal artery occlusion (CRAO)?

DDX

What are the differential diagnoses for Central Retinal Artery Occlusion (CRAO)?

Workup

What are the approach considerations in the workup of central retinal artery occlusion (CRAO)?

Which lab studies are indicated in the workup of central retinal artery occlusion (CRAO)?

What is the role of imaging studies in the workup of central retinal artery occlusion (CRAO)?

What is the role of ultrasonography in the workup of central retinal artery occlusion (CRAO)?

What is the role of MRI and CT studies in the workup of central retinal artery occlusion (CRAO)?

What is the role of fluorescein angiography in the workup of central retinal artery occlusion (CRAO)?

What is the role of fundus autofluorescence (FA) in the workup of central retinal artery occlusion (CRAO)?

What is the role of spectral-domain OCT in the workup of central retinal artery occlusion (CRAO)?

What is the role of electroretinography in the workup of central retinal artery occlusion (CRAO)?

What is the role of optical coherent tomography angiography (OCTA) in the workup of central retinal artery occlusion (CRAO)?

What is the role of systemic tests in the workup of central retinal artery occlusion (CRAO)?

What is the role of ECG in the workup of central retinal artery occlusion (CRAO)?

When is Holter monitoring indicated in the workup of central retinal artery occlusion (CRAO)?

How is echocardiography used in the workup of central retinal artery occlusion (CRAO)?

Treatment

What are the approach considerations in the treatment of central retinal artery occlusion (CRAO)?

What is the standard treatment for central retinal artery occlusion (CRAO)?

How is ocular massage used to treat central retinal artery occlusion (CRAO)?

What is the role of anterior chamber paracentesis in the treatment of central retinal artery occlusion (CRAO)?

How is intraocular pressure lowered in the treatment of central retinal artery occlusion (CRAO)?

How is a laser embolectomy used in the treatment of central retinal artery occlusion (CRAO)?

How is pars plana vitrectomy used to treat central retinal artery occlusion (CRAO)?

What is the role of intra-arterial fibrinolysis in the treatment of central retinal artery occlusion (CRAO)?

How is hyperbaric oxygen therapy used to treat central retinal artery occlusion (CRAO)?

When is inpatient care indicated in the treatment of central retinal artery occlusion (CRAO)?

When is transfer indicated in the treatment of central retinal artery occlusion (CRAO)?

How is central retinal artery occlusion (CRAO) prevented?

What follow-up care is indicated in the treatment of central retinal artery occlusion (CRAO)?

Medications

Which medications are used to treat central retinal artery occlusion (CRAO)?

Which medications in the drug class Beta-adrenergic blocking agents are used in the treatment of Central Retinal Artery Occlusion (CRAO)?

Which medications in the drug class Sympathomimetics are used in the treatment of Central Retinal Artery Occlusion (CRAO)?

Which medications in the drug class Hyperosmotic diuretics are used in the treatment of Central Retinal Artery Occlusion (CRAO)?

Which medications in the drug class Carbonic anhydrase inhibitors are used in the treatment of Central Retinal Artery Occlusion (CRAO)?