Signs and Symptoms

The word embolus comes from the Greek word emballein, meaning “wedge-shaped stopper.” Today, the term is used to describe an abnormal particle within the circulatory system.1-10 Patients observed to have retinal emboli are typically elderly and often have a concurrent history of hypertension, diabetes, carotid artery disease, peripheral vascular disease, blood dyscrasia, hypercholesterolemia, hyperlipidemia, smoking and atherosclerosis.2-20 The three most common retinal emboli are cholesterol (Hollenhorst plaque), fibrinogen platelet aggregate (fibroemboli, or Fisher plug) and calcium (calcific valvular debris).11-13 Other exogenous and endogenous sources of embolic material include air, infectious/inflammatory debris, talc and amniotic fluid.14-20

Emboli are markers of local or systemic processes, not a disease per se.2-17 Patients with retinal emboli are often asymptomatic, with plaque found during routine dilated eye examination. Since they represent intravascular matter capable of interrupting blood flow, similar to the way corrosive material can block the flow of fluid thorough a pipe, patients who form emboli often present having experienced transient episodes of interrupted function.5,8,12,20 This might manifest as tingling or weakness of limbs or a momentary loss of dexterity or altered mentation.18,19 In the eye, these particles can produce varying degrees of monocular vision loss and visual field disturbance.7,8,20-27

Today, these episodes of transient monocular vision loss (TMVL), historically termed amaurosis fugax (from the Latin and Greek meaning “fleeting darkness”), constitute a transient ischemic attack (TIA). TIAs are focal ischemic events lasting less than 24 hours (most resolving within minutes) with no subsequent neuroimaging abnormalities.20,21 Symptoms that arise are consistent with the extent and portions of the affected vascular stream.20 Patients experiencing TVML/TIA secondary to retinal embolization have described episodes of visual blur, visual fuzziness (sometimes referred to as transient visual obscurations or TVO), altitudinal and sector field loss, “blotchy/patchy” field loss, visual dimming and the experience of “a curtain coming down over their eyes.”20

Embolic TIA may often include more complicated and integrated presentations with additional neuro-systemic findings such as hemiparesis, paraesthesia, dysphagia and/or altered mentation.18,19,21 In the absence of complete retinal artery occlusion, emboli-associated TIA/TMVL, whether lasting seconds or hours, permits full restoration of function as the plaque dissipates, flows downstream, or shifts position.20,21,27 TIA/TMVL may be non-embolic and can also serve as a clue for hemodynamic (blood dyscrasias), vascular (giant cell arteritis), cardiac (myopathy), vasospastic (migraine) and inflammatory (optic neuropathy) events.2,13-21 This is another reason why no retinal emboli are seen upon examination in patients with TIA/TMVL.7,20 Ophthalmoscopic clues persist, allowing the clinician to observe related clinical manifestations, including Roth spots, cotton wool spots, flame-shaped hemorrhages, arteriolar narrowing, venous nicking, increased arterial light reflex or venous sheathing.7,13-21

Ophthalmoscopically, intra-arteriolar or intracapillary plaques are seen as one or more small, round to oval, white/yellow masses.20-25 Emboli trapped in capillaries may appear suspended as the vessel walls are too small to be appreciated. Larger obstructions typically lodge in retinal vessels near the optic disc or at a vessel bifurcation.7,9 Simultaneous bilateral involvement is possible but uncommon. There may be multiple emboli within the same eye.

The incidence and epidemiology of retinal emboli depend on the disease influencing their production.9-23 Incidence is approximately 1.5% in the general population with an increasing prevalence associated with Caucasian race, increased age (>70 years) and male gender.3,9,10,22,23 There is increased risk of stroke, with decreased survivorship with the appearance of retinal emboli.9,26


The mechanism by which an embolus creates compromise—whether in the eye, an organ or the central nervous system—is through mechanical obstruction of blood flow.13-28 The formation of cholesterol and fibrinogen platelet emboli is related to progressing arteriolar and atherosclerotic disease.5,12,13,20,26,28 Here, the end process creates an atheroma, which leads to atheromatous plaques that cause vascular endothelial rupture, casting participating cholesterol crystals, clotting elements and immune system cells into the lumen.12,13,20,28 Lipid retention, inflammation, phosphate signaling and osteogenic transition play roles in the development of cardiovascular calcific valve disease.29,30 When the friction of cardiac output pries them loose, they become calcific emboli.20,29-31

Once an embolus has entered the circulatory system, it will travel until it lodges in a vessel whose caliber will impede further flow. If blood flow is significantly impaired distal to the blockage, ischemia to that tissue will ensue. In the eye, if the embolus completely obstructs blood flow, retinal ischemia with corresponding vision loss occurs secondary to retinal artery occlusion. In the case of cholesterol emboli, most blockages quickly dislodge without permanent vision impairment, and the patient may experience TMVL.7,20,27 Multiple bouts of TMVL may indicate multiple emboli or secondary partial interruptions outside the boundaries of the eye.

The physical appearance of the embolus is determined by its makeup. Hollenhorst plaques are composed mainly of cholesterol. They present with a reflective or retractile appearance.24,25 Calcific plaques such as those generated by the dislodged debris from the valves of the heart have a white, dull and bulky presentation.10 Fibrinogen-platelet plaques have an elongated, white, chalky presentation, resembling caulking within the vessel.1,4,7,9,10,22-25 Cholesterol emboli are the most commonly encountered, representing 80% of emboli.10 Fibrin-platelet emboli represent 14% of emboli and calcific emboli account for just 6% of visible retinal emboli.10


There is no direct treatment for asymptomatic visible retinal emboli. In fact, when blood flow is uninterrupted, ocular intervention is contraindicated.20,27 The proper approach to patients manifesting TIA/TMVL or visible asymptomatic retinal emboli is to find the underlying cause. Patients should be referred to their internist with appropriate correspondence explaining the findings and recommending a course of action.20 Reasonable first round testing should rule out hypertension, atherosclerosis, diabetes, coagulopathy, hyperviscosity, carotid artery disease and cardiac sources. The first wave of laboratory testing should include a complete blood count with differential and platelets (CBC c Diff and PL), a lipid panel, an echocardiogram with ultrasound of the heart valves (ECG c 2D echo), sphygmomanometry, fasting blood sugar (FBS), prothrombin time (PT), and partial thromboplastin time (PTT).3-27

The key to visual recovery in any persisting embolic retinal arterial occlusion is timely intervention. The potential for recovering any vision is greatest when the blockage is dislodged within 100 minutes of the onset of the first symptoms.32,33-37 While frequently unsuccessful, all treatments are designed to increase retinal perfusion by re-establishing retinal blood flow.33-37 The traditional acute intervention for new onset artery occlusion is intraocular pressure lowering and digital ocular massage. Fast-acting topical pharmaceuticals such as timolol 0.5%, apraclonidine 1% or brimonidine 0.1% and oral carbonic anhydrase inhibitors (such as two acetazolamide 250mg tablets PO or neptazane 50mg PO) lower intraocular pressure for the purpose of lowering the resistance to ocular perfusion. Simultaneously, aggressive digital palpation with sudden release will stimulate retinal autoregulatory mechanisms so that arterioles and capillaries vasodilate, allowing the embolus pass downstream. This also creates vascular back-pressure, which when released might force embolus dislodgement.32-34 If these actions fail, emergent paracentesis will rapidly drop the IOP to zero, fostering minimal resistance to in-flow.36 An alternate strategy involves stimulating retinal vascular dilation by increasing blood carbon dioxide levels, either by breathing into a paper bag or by inhaling a carbogen mixture (95% oxygen, 5% carbon dioxide), or with sublingual nitroglycerine.32,36

The oral agent pentoxifylline has been used to increase red blood cell (RBC) deformability, with the hope of allowing easier RBC passage through the capillaries. New strategies include attempting to vaporize retinal emboli via Nd:YAG laser; however, this procedure is still being refined.24,31 Selective intra-arterial ophthalmic or meningo-ophthalmic artery thrombolysis using thrombolytic agents such as urokinase or tissue plasminogen activating factor (tPA) has also been attempted with mixed success.35 Hyperbaric oxygen (HBO2) has demonstrated promise for incomplete central artery occlusions when instituted within eight to 24 hours of the onset of the event.37 If the patient responds to HBO2, follow-up treatment with supplemental oxygen can be customized to maintain retinal viability until the obstructed retinal artery recanalizes, typically within 72 hours.37 Unfortunately, even given these innovations, heroic measures rarely impact the final outcome.32-37

For all cases of retinal embolization, the concern must be subsequent occurrences with permanent retinal infarct, cerebrovascular accident or myocardial infarction. A preventative approach dictates that all modifiable risk factors, such as diet, obesity, sedentary lifestyle and smoking, be altered. Magnetic resonance angiography, transthoracic and transesophageal echocardiography may be indicated.7 There is poor consensus on the need for carotid ultrasonography in patients with asymptomatic retinal emboli, as the majority of these patients do not have high grade carotid stenosis.5,9,24,25,38 Thus, carotid imaging is not necessarily mandated in patients with visible retinal emboli.

A large population study, collecting data over a 10- to 12-year period, found a 30% rate of mortality for those who presented with retinal emboli, with 4% dying from stroke-related complications and 16% from cardiovascular causes.26 These death rates were greater than those for age-matched people not having retinal emboli. There is no clear indication for carotid endarterectomy in patients with asymptomatic retinal emboli, even in the setting of concurrent high grade carotid stenosis.5,9,38-40 There does seem to be a benefit to carotid endarterectomy in patients with TIA/TMVL and high-grade carotid stenosis.41

Clinical Pearls

Retinal emboli can be difficult to detect ophthalmoscopically.

Older males with a history of hypertension and smoking are at greatest risk for retinal emboli. The retinal arterial tree should be examined most closely in these patients.

Asymptomatic retinal emboli are not highly associated with severe carotid stenosis. Carotid ultrasonography may be suggested, but is not required.

Retinal artery occlusion is rarely reversible; however, treatment should be attempted out of compassion and the possibility, however slight, of a positive outcome.

Patients with asymptomatic retinal emboli are typically not endarterectomy surgical candidates, especially if they are older than age 70.

The most significant modifiable risk factor for retinal emboli is smoking. Smoking cessation is crucial in reducing the risk of future embolic phenomenon in patients with asymptomatic retinal emboli.

Rather than automatically ordering carotid studies, it may be preferable to refer the patient to a primary care physician and recommend an atherosclerotic evaluation.

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