Download Hypertensive Retinopathy

Hypertensive Retinopathy
Joseph Sowka, OD, FAAO, Diplomate
Systemic Manifestations of Hypertension
 Arteriolosclerosis: applies to arterioles
 Atherosclerosis: applies to medium and large muscular arteries
 Arteriosclerosis: broad term meaning thickening of vascular walls
 Thrombus: aggregation of fibrin, platelets, etc. on vessel walls (mural thrombi as found in
atrial fibrillation) or ulcerated artery plaque
 Emboli: A loose piece of thrombus flowing in vascular system
Hypertensive Retinopathy
 Arteriolosclerotic vessel changes
 Some classification schemes include vessel changes in hypertensive retinopathy and
others don’t
 Elschnig’s spots – subtle choroidal infarcts
 CWS
 Flame shaped hemorrhages
 Macular edema (rare)
 Macular star/ ring of exudates
 Disc edema
Clinical Pearl: A patient manifesting disc edema from hypertension has malignant
hypertension and this should be considered an emergency.
Clinical Pearl: In order for CWS to form from hypertension, autoregulatory
mechanisms must be overcome. For this to happen, the patient must have at least 110
mm hg diastolic readings.
Clinical Pearl: Patients who develop disc edema from hypertension typically have BP in
the 250/150 mm hg range.
Clinical Pearl:
retinopathy.
Fluorescein angiography is not indicated in cases of hypertensive
Clinical Pearl: Hypertensive retinopathy is frequently confused with diabetic retinopathy.
Remember: Hypertensive retinopathy is mostly a dry eye condition (multiple CWS, rare
hemorrhage, edema, and exudates) whereas diabetic retinopathy is a wet eye condition,
(rare CWS, extensive hemorrhages, edema, and exudates).
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Hypertensive Retinopathy: Clinical Course
 Arteriosclerotic changes persist
 Hypertensive changes can resolve after reduction of systemic blood pressure
Technically, that is the end of hypertensive retinopathy. The remainder involves other
manifestations of hypertension.
Stroke
 Sudden, acute, ischemic (below viability of brain tissue) neurological deficit.
Cerebrovascular accident (CVA) is synonymous with stroke. Infarct: cell death and
necrosis
 HTN - Rips vessel walls leading to lipid deposition
 Smoking - Increases CO and decreases O2. Leads to increases in norepinephrine which
causes increased platelet counts
Signs and symptoms of impending stroke
 Amaurosis fugax (AF)
 Transient ischemic attack (TIA)
 Visible retinal emboli
Clinical Pearl: TIA and AF are straws that tell which way the intracranial wind is
blowing.
Amaurosis Fugax
 Painless and isolated
 Total or sectorial
 Monocular
 Disease of the carotid artery (typically)
 Emboli are reaching the retinal arterial system and causing temporary occlusion
 Isolated or antecedent (long ago) without current symptoms are less dangerous than many
current episodes of AF
 No associated neurological baggage
 Ask about:
1) Contralateral weakness in the arm (most common), leg, face & arm, arm & leg.
2) Paresthesia or numbness in the hand, foot, face, ½ of tongue
3) Aphasia
 These findings do not occur with AF!
 Seconds to hours
 Typically 2-5 minutes
 Resolves completely
Uncomplicated Amaurosis Fugax
 85% recovery
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10-15% get central retinal artery occlusion (CRAO)
2% have CVA
2%-4% annual risk of mortality
Transient Ischemic Attack
 Painless
 Total vision loss or may have no ocular involvement whatsoever
 Contralateral hemiparesis; paresthesia
 Weakness and/or numbness of parts or all of the contralateral side with loss of motor
and/or sensory system. Typically arm (most common), leg, face & arm, arm & leg.
Numbness in the hand, foot, face, ½ of tongue
 Aphasia/ dysphasia
 Inability to understand spoken words or unable to speak, depending upon which part
of the brain is ischemic
 Typically lasts 15 minutes but may last for hours, though it will resolve
Transient Ischemic Attack (Hemispheric): Mortality
 25% in 1 month
 33% in 6 months
 60% within 7 years
Clinical Pearl: AF is an uncomplicated loss of vision in one eye with no other neurological
findings concurrent. TIA is a complicated neurological deficit, which may or may not involve
vision loss.
Pathophysiology of TIA and AF:
1. Atherosclerosis with subsequent emboli formation from hypertension
Cholesterol fatty streak atheroma ulceration thrombus plaques  emboli
2. Emboli-forming conditions (other than HTN)
 Rheumatic heart disease
 Prosthetic heart valves
 Bacterial endocarditis
 Indwelling catheters
 Rhythm disturbance - Mitral valve prolapse (Barlow’s syndrome).
 17% of females
 Blood regurgitates back into atrium and pools where platelets can aggregate and
clots can form
3. Giant Cell Arteritis (GCA)- Thrombus formation due to vessel wall and lumen
obliteration from inflammation
 In patients over the age of 60 years with transient visual loss (TVL), either TIA or AF,
you must get an erythrocyte sedimentation rate (ESR) and C-reactive protein to look
for GCA. AF in an elderly patient due to transient occlusion of the ophthalmic or
central retinal artery is a sign of impending, permanent, severe vision loss (often
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within several weeks).
4. Vasospastic
 Non-embolic arterial narrowing
 Vasospastic substance (Cocaine) use
 Migraine?
5. Hematological
 Polycythemia (Too much hemoglobin)
 Sickle cell (#1 hematological cause of transient vision loss)
 Anemia (Too little hemoglobin)
 Hypercoagulability states
 Anti-phospholipid antibody syndrome
Emboli: Just the Facts
 May be symptomatic (AF or TIA) or asymptomatic
 The main factor associated with retinal emboli is smoking
 Three types of plaques: Fischer, Hollenhorst, calcific
 Fischer- fibrin/platelet aggregate (carotid in origin, also walls of arteries and valves of
heart)
 Dull gray or white
 Readily migrate through vascular system producing symptoms (AF)
 Hollenhorst- cholesterol (carotid in origin)
 Refractile, glistening, yellow
 Most common (87%) of all emboli
 Typically do not occlude artery
 Malleable and allows for blood to pass though the artery may appear totally blocked
 Will readily break up and move distally, so will not be seen typically in patients
complaining of AF
 common cause of AF
 Calcific (cardiac)
 Dull white and non-refractile
 Usually from valvular calcification
 Most likely to cause artery occlusion and stroke
Clinical Pearl: The patient most likely to manifest a, asymptomatic retinal emboli is an
older hypertensive man that smokes. Smoking cessation is absolutely essential I these
patients.
Visible Retinal Emboli: Mortality
 15% within 1 yr.
 29% within 3 yrs
 54% within 7 yrs
 Cardiac death more prevalent than stroke
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