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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
sphygmomanometry
Sphygmomanometry
  • Used to monitor the blood pressure of the patient

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

ophthalmoscopy
Ophthalmoscopy
  • 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)

http://content.nejm.org/cgi/content/full/351/22/2310

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.
slide26
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
treatment
Treatment
  • 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

slide28

http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=cardio&part=A379&rendertype=table&id=A433http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=cardio&part=A379&rendertype=table&id=A433