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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). 1 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 2 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 3 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 4