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Asymptomatic Hollenhorst Plaque and Microaneurysm


Lesley L. Walls, OD, MD


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A 67 year old Native American male presents for a routine eye examination with the following complaint, “my arms are too short.”  Other than having difficulty reading, he has no other ocular or systemic complaints.  He has been a “mild” diabetic, well-controlled for the past 10 years, and his only medication is an oral diabetic agent named Glyburide.  He also has had well-controlled hypertension for the past 25 years currently treated with Lisinopril.



2.0 Diopter Hyperope with no astigmatism OU and needs a 2.25 D add OU for near vision.  All other testing is within normal limits EXCEPT at ophthalmoscopy which revealed a totally asymptomatic Hollenhorst Plaque in the inferior temporal quadrant of the left eye.  Subsequent further examination revealed absence of a Carotid Bruit bilaterally and a normal Carotid Artery pulses bilaterally.  See Figure 1.

Hollenhorst Plaque

Figure 1: Hollenhorst Plaque


The patient is being seen in a multidisciplinary clinic and was immediately sent to the medical clinic to his primary care physician for evaluation.  He was examined by his primary care physician who is Board Certified in Internal Medicine.  His physician didn’t see anything “wrong” at ophthalmoscopy and since there were normal Carotid pulses and no bruits, sent the patient home on one baby aspirin per day and was told to return in 6 months for routine follow-up of his Diabetes and Hypertension.  His physician did verify that the patient’s Diabetes and Hypertension were under excellent control.  The Blood Pressure was 125/76, Random Blood Sugar of 110 and HbA1c of 6.9 at that time. 

The patient recalled how concerned the optometrists were about his eye so on his own returned to the Eye Clinic.  Repeat examination in the optometry clinic revealed TWO NEW HOLLENHORST PLAQUES and during the fundus examination another new one was observed as it “floated into” a retinal artery branch!




Recall the Anatomy of the blood flow to the eye and brain.  See Figures 2 and 3.

Carotid Anatomy Carotid and Vertebral Artery Anatomy

Figure 2: The flow is via the Common Carotid to the Internal Carotid to the Retina via the Central Retinal Artery

Circle of Willis Anatomy

Figure 3: The Circle of Willis allows for “retrograde” blood flow to the eye when obstruction occurs on one side only.



         In general, most vascular diseases cause problems due to progressive occlusion of the vessel lumen.  Additionally, there may be problems due to complications at the site of the vessel disease and this will be discussed in the lecture.

         These diseases account for the first and third most common causes of death in this country, namely, heart attacks and stroke.  Unfortunately, these diseases very commonly do not have signs or symptoms until very late in the course of the disease and then the manifestations may be dramatic, i.e., sudden and unexpected death!


         There are three main subjects within this category and we will spend virtually all of our time during this lecture on just one of them.  They are as follows:

         1.  Arteriolosclerosis - Here we see disease in the small arterial vessels named the arterioles.  The pathology is sclerosis which means thickening of the vessel wall and narrowing of the vessel lumen.  The eye is the only place these vessels can be directly visualized and is done so at ophthalmoscopy.  These changes account for the widening of the light reflex and narrowing of the blood column in affected vessels.  The primary underlying diseases leading to arteriolosclerosis are diabetes and hypertension.  It is also associated with the aging process.

         2.  Monckeberg's Medial Calcific Sclerosis - Here there is calcification of the tunica media (muscular coat) of the medium sized arteries.  This does not affect the lumen, but does decrease the elasticity of the vessel and can lead to systolic hypertension and factitious hypertension.  This is otherwise not important and is primarily a disease of the elderly.

         3.  Atherosclerosis is the main subject here and our topic for this lecture

This is the most prevalent disorder of humankind.  It affects both sexes and all ages above infancy.  It does not always cause disease and when it does it is usually very late in the course and after many, many years.

The basic pathologic lesion is the ATHEROMA that is an elevated, fibrous, fatty plaque (primarily cholesterol) that begins on the tunica intima of the artery.  It will progress to involve the tunica media and with time is at high risk to cause problems due to obstruction of the lumen or complications at the site of the atheroma. 

         What are these problems or complications at the site of an atheroma? See Figure 4.



Figure 4: The Stages of Atherosclerosis

(Open-source image from )

         a.  Occlusion: When the obstruction reaches about 70% it can begin to interfere with blood flow and lead to ischemia of the tissues it supplies.

         b.  Calcification: This is the "hardening" referred to in the lay term hardening of the arteries.

         c.  Ulceration: The surface tends to ulcerate and the necrotic and degenerating material to float on downstream which also may cause problems such as emboli.

         d.  Thrombosis on Site: This is especially true with ulceration as it is a focal point for clot formation due to the loss of endothelial covering.  Thrombosis can instantly lead to a 100% obstruction and an acute problem like heart attack or stroke.

         e.  Emboli Formation: Clotted blood, calcified tissue, cholesterol, etc. can embolize from the site of an atheroma.

         f.  Spasm: These lesions can somehow "irritate" the vessel and result in smooth muscle contraction.  Again, this can dramatically increase the obstruction.

         g.  Hemorrhage into the Plaque: With degeneration the vessels to the tissue of the plaque itself can rupture and bleed into the plaque dramatically increasing the size and increase the obstruction.

         h.  Aneurysm Formation: Due to weakening of the vessel wall so the pressure causes it to balloon out and it may even rupture.

         The patient in the optometrist’s office with severe atherosclerosis most commonly complains of symptoms of TIA (transient ischemic attack).  These include:  one or more episodes of ipsilateral visual obscuration (especially amaurosis fugax).  This is commonly combined with symptoms of paresis/paralysis and/or sensory changes on the contralateral side of the body.  By definition, no permanent damage occurs or it is a stroke, and not a TIA.


         While the pathogenesis is becoming clearer, exactly how several items are associated with the development of atherosclerosis is unclear.  However, endothelial cell injury is probably the basis of the process. This may occur due to elevated blood glucose over an extended period of time, even in absence of diabetes.

         Important risk factors for atherosclerosis that an optometrist may see and be concerned about include those shown in Figures 5-9:

Arcus Sen

Figure 5: Arcus Senilis

CRA Occlusion

Figure 6: Central Retinal Artery Occlusion

CRV Occlusion

Figure 7: Central Retinal Vein or Branch Retinal Vein Occlusion

Lipemia Retin

Figure 8: Lipemia Retinalis


Figure 9: Xanthalasma

Risk factors for atherosclerosis can be divided into non-controllable and controllable types:

         a.  Age: This is a major factor, since most patients develop atherosclerosis and prevalence definitely increases with age. 

         b.  Gender: All factors being equal, this is a male dominated disease.  This is thought to be somehow androgenically related as post menopausal females "catch up". Or could the female hormones be protective?

         c.  Genetics: There is no question that there can be strong familial predisposition to atherosclerosis. 


         The above are non-controllable and the following are at least somewhat controllable. While genetics may “load the gun”, environmental factors like obesity and poor nutrition are thought to be what “pulls the trigger”:

         d.  Hyperlipidemia: Especially with elevated LDL's.  The HDL's are protective.  This is somehow true for blood level and dietary intake as well.

         e.  Hypertension: Increased blood pressure somehow leads to atheromas

         f.  Smoking: This may be the biggest single reason the incidence has increased in premenopausal women.  Smoking may damage the endothelium, cause spasm of vasovasorum, etc. but leads to major increase in atheroma formation.

         g.  Diabetes Mellitus: Uncontrolled diabetes leads to a dramatic acceleration in atheroma development and arteriolosclerosis too.  We will discuss pathogenic mechanisms later in the course under this topic.

         h.  Other "softer" associated factors: Obesity, sedentary life style, abnormal handling of psychological stress, certain medications like oral contraceptives and male hormones.


         Control the controllable!  PCP’s typically rely on early testing to pick up disease like cardiac stress testing using a treadmill.  Good primary care by optometry should look for signs in the absence of symptoms.  Early and aggressive treatment when needed like proper nutrition and exercise can avoid later angioplasty, bypass surgery, and medications.


         The current thinking is that it is most likely the response to endothelial injury that leads to atheroma formation. Endothelial toxic substances such as high blood glucose levels, nicotine and tar from cigarettes, viruses, etc., may injure the endothelial cells  and lead to atherosclerosis.  This leads to macrophages adhering to the endothelial cells and migrating to the subendothelial area.  These macrophages engulf lipoproteins (mainly LDL's) to become foam cells.  Smooth muscle fibers multiply in the damaged endothelial area (recall they are stable cells) and also take up lipids.  This initially forms a "fatty streak" which later develops into an atheroma due to the ongoing process.  There are a number of chemical factors likely involved including platelet factors but we will not memorize the others.


         Clinically, stroke due to a complication at the site of an atheroma may be preceded by a TIA or series of TIA’s.  A TIA is defined as the temporary occlusion of a vessel to the brain tissue and commonly causes the following:  Transient ipsilateral monocular blindness (amaurosis fugax), and contralateral sensory or motor changes (paralysis to paresis, and numbness to total anesthesia).  The patient may manifest a Hollenhorst plaque in the retinal arterioles during these episodes or may have Hollenhorst plaques in the absence of symptoms, i.e. the asymptomatic Hollenhorst plaque we saw in Figure 1.


Always consider it to be an emergency situation.  If the patient has symptoms of TIA, strongly consider having the patient chew one adult (325 mg) aspirin as the anti-platelet effects begin in just minutes.  Keep the patient in the office and arrange an immediate consult by telephone with a Vascular Surgeon if possible and the patient’s Primary Care Physician if their insurance works that way.  The patient ultimately will need a series of Blood Tests to include a blood sugar, Complete Blood Count, Erythrocyte Sedimentation Rate, Lipid Profile, Thyroid Profile, etc.  The patient will also need the Carotid Artery Flow System evaluated. Options include Doppler Studies, Magnetic Resonance Imaging and very likely will require an Angiogram of the Carotid Flow System.  See Figures 10-11.

Carotid Dopler Normal 2 Carotid Dopler with Severe Disease

Figure 10: Carotid Doppler Study

MRA of entire Cerebral Circulation MRA Carotid 3

Figure 11: Carotid Angiography