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Rayos , K.- Rodas , F. Case 3. Case 3. 21 year old student CC:  Loss of vision OS and eye aches associated with movement.    PMH:  Similar episode in the OD three years ago with spontaneous resolution. Also, a history of right sided numbness made better with ‘ hilot ’. 

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case 3
Case 3
  • 21 year old student
  • CC: Loss of vision OS and eye aches associated with movement.   
  • PMH: Similar episode in the OD three years ago with spontaneous resolution. Also, a history of right sided numbness made better with ‘hilot’. 
  • Vision: Right 20/20-2Left 20/40-1   
  • IOP: OU 15mm Hg

(Normal IOP: 15.5 mmHg with fluctuations of 2.75)

what is your working diagnosis
What is your working diagnosis?
  • Hypertensive Retinopathy
hypertensive retinopathy
Hypertensive Retinopathy
  • Characterized by a variety of retinal vascular signs in individuals with elevated BP
  • Causes blurring of vision
  • Bilateral, symmetrical
  • End organ manifestation
hypertensive retinopathy1
Hypertensive Retinopathy
  • Funduscopic findings:
    • Focal attentuation of a major retinal arteriole
    • Broadening of the arteriolar light reflex
    • Arteriovenous crossing changes
    • Hemorrhages
    • Retinal infarcts (Cotton-wool spots)
    • Choroidal infarcts (Elschnig’s spots)
    • Serous dettachment of the retina
    • Severe disk edema
arteriosclerotic changes
Arteriosclerotic Changes
  • Arteriolar narrowing that is almost always bilateral
    • Grade I - 3/4 normal caliber
    • Grade II - 1/2 normal caliber
    • Grade III - 1/3 normal caliber
    • Grade IV - thread-like or invisible
  • Arterio-venous crossing changes (aka “AV nicking") with venous constriction and banking
  • Arteriolar color changes
    • Copper wire arterioles are those arterioles in which the central light reflex occupies most of the width of the arteriole.
    • Silver wire arterioles are those arterioles in which the central light reflex occupies all of the width of the arteriole.
stages of hypertensive retinopathy
Stages of Hypertensive Retinopathy
  • Grade 1 – general narrowing of arterioles
  • Grade 2- Narrowing of arterioles plus arteriolar spasm
  • Grade 3 – Grade 2 changes plus hemorrhage and exudates

- Flame-shaped (splinter hemorrhages)- seen in the nerve fiber layer

- Cotton wool spots – result of microinfarction of NFL which produces aggregates of Cytoid bodies

- Hard waxy exudates may be seen (lipophilic exudates located in Outer plexiform Inner Nuclear layer)

stages of hypertensive retinopathy1
Stages of Hypertensive Retinopathy
  • Grade 4- All grade 3 changes with optic disc edema, necrosis, thinning, clumping and proliferation of Retinal pigment epithelium
    • May also occur as a result of obliterative changes in the choriocapillary in malignant hypertension .
vascular changes
Vascular Changes
  • Arteriolar narrowing
    • A:V- 2:3
  • AV crossing changes
  • Grading
    • I- Leakage
    • II- Blood and hemorrhage
    • III- Cotton wool spots
    • IV- Optic disc swelling, subretinal exudates
what are your differentials
What are your differentials?

Other retinopathies that are known complications of high blood pressure are called:

  • Diabetic retinopathy
  • Ischemic optic neuropathy
  • Retinal artery occlusion
  • Retinal emboli
  • Retinal vein occlusion
diabetic retinopathy non proliferative type
Diabetic RetinopathyNon-proliferative Type
  • Capillaries develop:
    • Microaneurysms
    • Thickening of the BM
    • Dec # of pericytes
  • Classification based on severity:
    • Mild
      • Atleast 1 microaneurysm
    • Moderate
      • Extensive microaneurysm
      • Intraretinal hemorrhages
      • Venous beading
      • Cotton wool spots
    • Severe
      • Cotton wool spots
      • Venous beading
      • Intraretinalmicrovascular abnormalities (IRMA)
diabetic retinopathy proliferative type
Diabetic RetinopathyProliferative Type
  • Presence of neovascularization on optic disk
  • Bleeding of vessels
  • Massive vitreous hemorrhage
    • Sudden visual loss
ischemic optic neuropathy
Ischemic Optic Neuropathy
  • Age: older age groups
    • Nonarteritic: late 40s and older
    • Arteritic: >50 y/o
  • Gender predilection: F>M
  • History: painless visual loss upon awakening
    • Early: malaise, weight loss, fever, vague abdominal or GI pains, and anorexia
    • Late: abdominal aortic aneurysm
  • Clinical Findings:
    • Nonarteritic: visual loss and field loss, small cup disc ratio, sectorial disc edema, pale and swollen optic disc
    • Arteritic: chalky white, pale, and swollen optic disc; quite prominent, ropey, and tender temporal arteries; oral, tongue, or scalp ulcer
retinal artery occlusion
Retinal Artery Occlusion
  • Age: Mean: early in the 7th decade
  • Gender predilection: M>F
  • History: Acute persistent painless loss of vision, complete/sectional visual field defect, history of hypertension or diabetes mellitus, other medical problems (atrial fibrillation), prolonged direct pressure or drug-induced
  • Clinical Findings:
    • Fundoscopy: afferent pupillary defect, cherry red spot and a ground-glass retina, emboli, whitening of the retina and Boxcar segmentation (BRAO)
    • PE: can have murmurs, carotid bruits, or other signs of cardiovascular disease
retinal emboli
Retinal Emboli
  • Most commonly arise from carotid artery disease
  • In patients younger than 40, a cardiac origin such as atrial fibrillation, mitral valve prolapse or subacuteendocarditis is considered

Three types:

1. Cholesterol emboli

  • Also called Hollenhorst plaques
  • Usually arise from an atheromatous plaque in the carotid artery and consist of cholesterol and fibrin
  • Lodge at the bifurcation of the retinal arterioles, are refractile and appear larger than the vessel that contains them
retinal emboli1
Retinal Emboli

2. Calcific emboli

  • Originates from damaged cardiac valves producing complete occlusion and infarction of the distal retina
  • Solid and calcified and usually occur in younger patients

3. Platelet fibrin emboli

  • Account for most cases of amaurosisfugax
  • Due to the transit of platelet aggregates through the retinal and choroidal circulations
  • May be reduced by drugs that reduce platelet aggregation like aspirin
central retinal vein occlusion
Central Retinal Vein Occlusion
  • Increased incidence in smokers, hypertension, diabetes mellitus, hyperlipidemia,collagen-vascular disease, chronic renal failure and hyperviscosity syndromes
  • Fundoscopy shows
      • Dilated tortuous veins with retinal and macular edema
      • Hemorrhages all over the posterior pole
      • Cotton wool spots
diagnostic examinations
Diagnostic Examinations
  • Get patient’s Blood Pressure
  • Ophthalmoscopy
  • Flourescein angiography
  • Used to monitor the blood pressure of the patient

Source: Table 241-1. Harrison’s Principles of Internal Medicine 17thed.

  • Ophthalmoscope has long been regarded as part of the standard evaluation of persons with hypertension
  • Ophthalmoscope has been shown to have high rates of interobserver variability (20 to 42 percent)and intraobserver variability (10 to 33 percent) when used inpersons with mild hypertension
  • few studies have demonstrated associationsbetween hypertensive retinopathy and specific cardiovascularoutcomes (e.g., incident stroke and coronary heart disease)or have adequately controlled for relevant confounding factors(e.g., hyperlipidemia and cigarette smoking)


mild hypertensive retinopathy opthalmoscopy
Mild Hypertensive Retinopathy – Opthalmoscopy

Mild Hypertensive Retinopathy – Opthalmoscopy

Figure 1. Examples of Mild Hypertensive Retinopathy.

Panel A shows arteriovenous nicking (black arrow) and focal narrowing (white arrow).

Panel B shows arteriovenous nicking (black arrows) and widening or accentuation ("copper wiring") of the central light reflex of the arterioles (white arrows).

moderate hypertensive retinopathy opthalmoscopy
Moderate Hypertensive Retinopathy – Opthalmoscopy

Panel A shows retinal hemorrhages (black arrows) and a cotton-wool spot (white arrow).

Panel B shows cotton-wool spots (white arrows) and arteriovenous nicking (black arrows).

moderate hypertensive retinopathy opthalmoscopy1
Moderate Hypertensive Retinopathy – Opthalmoscopy

Multiple cotton-wool spots (white arrows), retinal hemorrhages (black arrows), and swelling of the optic disk are visible

fluorescein angiography
Fluorescein angiography
  • Technique for examining the circulation of the retina using the dye tracing method
  • Involves injection of sodium fluorescein into the systemic circulation, and then an angiogram is obtained by photographing the fluorescence emitted after illumination of the retina with blue light at a wavelength of 490 nanometers
  • Can detect diabetic retinopathy, vein occlusions, retinal artery occlusions, edema of the optic disc, and tumors.
Causes of hyperfluorescence:

Causes of hypofluorescence:

blocking defect (i.e. blood) filling defect (capillary blockage)

  • leaking defects (i.e. capillary leakage, aneurysm, neovascularization) pooling defects staining transmission (filling) defects abnormal vasculature
  • Control hypertension
  • Other vision- threatening conditions should also be controlled
  • Laser
  • Intravitreal injection of corticosteroids
  • Anti-vascular endothelial growth factor drugs
    • monoclonal antibodies such as bevacizumab (Avastin),
    • antibody derivatives such as ranibizumab (Lucentis), or
    • orally-available small molecules that inhibit the tyrosine kinases stimulated by VEGF:
      • lapatinib(Tykerb), sunitinib (Sutent), sorafenib (Nexavar), axitinib, and pazopanib

Merck manual online medical library