vascular and retinal disorders Flashcards
progressive chronic retinal disease affecting aging eyes (central vision loss)
leading cause of vision loss globally, with adults > 50 years old
idiopathic
blurred central vision
distortion of images
scotomas (dark spots)
declining visual acuity (unable to read, distinguish faces)
macular degeneration (ARMD)
neovascular, exudative
more severe and faster progressing
10% of cases
wet macular degeneration
atrophic, geographic, non vascular, non exudative
yellow cellular debris (drusen)
90% of cases
dry macular degeneration
advancing age, female, white race, tobacco abuse, heavy alcohol use, increased sunlight exposure, cardiovascular disease, hypertension, hyperlipidemia, family history, farsightedness, light iris color
macular degeneration risk factors
new blood vessels grow up from the choroid (neovascularization) behind the retina which can leak exudate and fluid and cause hemorrhaging and fibrosis
onset more rapid and severe
“wet” ARMD
cellular debris (drusen) accumulates between retina and choroid leading to scarring and atrophy
atrophy in retina
gradual progressive bilateral visual loss of moderate severity due to atrophy and degeneration of outer retina and retinal pigment epithelium
“Dry” ARMD
macular degeneration diagnosis
snellen test (should see reduced visual acuity compared to previous tests)
amsler grid
opthalmolgy for definitive diagnosis
dry armd treatment
pegcetacoplan and avacincaptad pegol (inhibit complement pathway) injections
macular degeneration treatment
vitamins and STOP SMOKING
wet armd treatment
inhibitors of vascular endothelial growth factors (VEGF)
ranibizumab, bevacizumab, afilbercept injections
cause regression of choroidal neovascularization with resorption of sub retinal fluid and improvement or stabilization of vision
inhibitors of vascular endothelial growth factors (VEGF)
separation of neurosensory retina from underlying retinal pigment epithelium
considered medical emergency (vision loss)
can be primary or secondary
curtain vision loss
retinal detachment
most common predisposing causes for retinal detachment
age
nearsightedness
previous cataract extraction
also:
ocular trauma
smoking
diabetic retinopathy
caused by entry of liquid vitreous into subretinal space through retinal break
secondary to increasing age (>50 years old)
shrinking leads to pulling on retina (tear)
retinal detachment primary
rhegmatogenous detachment
accumulation of subretinal fluid
wet armd
choroidal tumor
fluid trapped behind retina –> detachment
exudative retinal detachment
preretinal fibrosis (scarring of retina)
proliferative retinopathy due to diabetic retinopathy
retinal vein occlusion
complication of rhegmatogenous retinal detachment
scars pull on retina –> detachment
traditional retinal detachment
acute onset
“tunnel vision” or loss of peripheral vision “curtain like”
recent onset or increase in floaters and photopsias (flashes of light)
central vision remains intact until macula becomes detached
retinal detachment
opthalmoscopic exam
retina may be seen elevated with irregular surface
retina appears gray or cloudy
superior temporal quadrant MC
retinal detachment diagnosis
when you have retinal detachment you do urgent referral to ophthalmologist. During transport how is patients head positioned?
patient head positioned so retinal tear is placed at lowest point of eye to minimize extension of detached retina. also try to minimize movement of eyes (patching)
retinal tear inferior
keep head upright
retinal tear temporal
keep temporal side of head down
retinal detachment treatment (primary)
closing retinal holes and tears
- laser photocoagulation
- cryopexy
- pneumatic retinopexy (gas injected into vitreous cavity)
retinal detachment treatment for more complicated detachments (traction)
vitrectomy
about 90% of uncomplicated primary detachments can be cured with ____ __________
one operation
retinal detachment worse prognosis
macula detaches
detachment of long duration
poorly controlled diabetes
diabetic retinopathy
damage to retina due to chronic systemic conditions (diabetes and hypertension)
can be acute or ongoing
leading cause of vision loss and blindness
early detection and management are crucial
retinopathy
leading cause of vision loss worldwide among adults aged 25-74 years
diabetic retinopathy
percentage of patients with retinopathy by 20 years after diagnosis. type 1:
99%
percentage of patients with retinopathy by 20 years after diagnosis. type 2:
60%
diabetic retinopathy present in about ____% of type 2 diabetic patients at diagnosis
20%
should be referred to ophthalmology for baseline exam with new diagnosis of type 2 diabetes
nonproliferative
microaneurysms, retinal hemorrhages, exudates*
no changes in vision - no immediate treatment required
background retinopathy- asymptomatic
two main categories of diabetic retinopathy
nonproliferative
proliferative
growth of new vessels and fibrous tissue on surface of retina (neovascularization)
extends into vitreous chamber
consequence of severe capillary occlusion –> retinal ischemia –> release of VEGF
stimulates the new vessel growth with vision loss from pre retinal hemorrhage, fibrosis, and retinal traction
vision usually normal until macular edema, vitreous hemorrhage, or retinal detachment occur
diabetic retinopathy classification
–> proliferative
diabetic retinopathy management
control of blood glucose, blood pressure, kidney function, and serum lipids
examine every 3-4 months*
proliferative
macular edema and exudates
blurry vision, decreased acuity, visual distortion, scotomas
most common cause of legal blindness in type 2 diabetes
maculopathy- symptomatic
diabetic retinopathy diagnosis
ophthalmology referral
- baseline fundoscopic exam at diagnosis of type 2
- type 1 diabetics should be screened 5 years after diagnosis
if visual symptoms and acuity not sufficient
- annual dilated* eye exam
nonproliferative retinopathy management: macular edema
intravitreal administration of VEGF inhibitor* (mainstay of treatment for macular edema)
(ranibizumab, bevacizumab)
laser photocoagualtion
intravitreal administration of corticosteroid
vitrectomy
nonproliferative retinopathy management: severe nonproliferative retinopathy
panretinal laser photocoagulation prophylactically
disease of vessels supplying the retina and choroid
secondary to severe acute or chronic uncontrolled systemic hypertension
usually not symptomatic
primarily seen in older patients
hypertensive retinopathy
can be encountered in any age group
sudden severe elevation in BP
major RF: degree of elevation of BP
acute malignant hypertensive retinopathy
older patients
secondary to long standing HTN+ atherosclerosis
major RF= duration of increased BP
chronic hypertension retinopathy
As BP increases, blood flow is maintained over wide range of pressures because blood vessels will constrict to maintain constant blood flow
autoregulation hypertensive retinopathy
with severe or sustained elevations in BP, the walls of the blood vessels must thicken to maintain blood flow
atherosclerosis
hypertensive retinopathy
typically seen in patients in hypertensive crisis (secondary HTN): BP > 200/110
damages vasculature of retina and choroid leading to ischemic necrosis
cotton wool spots
dot blot and flame hemorrhages
papilledema
acute hypertensive retinopathy
acute hypertensive retinopathy diagnosis
fundus abnormalities are hallmark of hypertensive crisis with retinopathy – requires emergency treatment
hypertensive retinopathy over time
loss of autoregulation
arteries/arterioles become ischemic
hemorrhages, exudates, cotton wool spots, copper wiring, etc
acute hypertensive retinopathy treatment
treat underlying cause
caution –> do not reduce BP too quickly or suddenly
acute hypertensive retinopathy common complications
retinal detachment
optic neuropathy
accelerates development of atherosclerosis –> if advances far enough, visual acuity decreases
focal/uniform narrowing or arterioles
AV nicking/crossing* (hallmark of chronic hypertensive retinopathy)
hemorrhage (flame, dot blot)
copper/silver wiring
macular star (advanced disease)- retinal exudates
chronic hypertensive retinopathy
chronic hypertensive retinopathy risk factors
high sodium diet
obesity
tobacco
alcohol
family history
occlusion of central retinal artery (eye stroke)
sudden monocular vision loss
no pain
no redness
central/branch retinal artery occlusion
in patients > 50 years with central retinal artery occlusion consider
giant cell arteritis
branch retinal artery occlusion presents in a similar way to central retinal artery occlusion but…
smaller portion of visual field
may be due to embolism or thrombosis
emboli may arise from:
- atherosclerotic plaques (carotid artery stenosis)
- atrial fibrillation
- endocarditis
thrombosis less common cause of retinal artery occlusion but can be seen with:
- various acquired/inherited thrombophilic disorders such as SLE and giant cell arteritis
retinal artery occlusion
etiologic factors for retinal artery occlusion
diabetes
hyperlipidemia
hypertension
young patients
- migraine
- oral contraceptives
fundus signs of retinal swelling
sometimes adjacent cotton wool spots limited to area of retina supplied by occluded artery
extent of arterial non perfusion is best seen with fluorescein angiography
branch retinal artery occlusion diagnosis
pale swelling of retina with cherry red spot at the fovea
retinal arteries are attenuated and “box car” segmentation of blood in arteries or veins (RBCs separate from serum when blood flow is slowed or arrested)
retinal swelling subsides over 4-6 weeks, leaving pale optic disk with thinning of inner retinal on optical coherence tomography scans
central retinal artery occlusion diagnosis
requires ophthalmology referral
color fundus photography and fluorescein angiography
retinal artery occlusion diagnosis
once retinal artery occlusion diagnosis is made
carotid doppler
echocardiogram
(similar work up as stroke)
giant cell arteritis diagnosis
ESR, CRP, platelet count
what do you worry about with younger patients and retinal artery occlusion
blood clotting disorders
retinal artery occlusion treatment
urgent referral to ER for imaging and clinical assessment to prevent subsequent stroke
lay patient flat, ocular massage, high concentrations of inhaled oxygen, IV acetazolamide, anterior chamber paracentesis
early thrombolysis
occlusion of central or branch retinal vein (branch 4x more common)
initial presentation:
no pain or redness
branch occlusion my present in variety of ways
- sudden loss of vision at time of occlusion of fovea is involved
- more gradual with development of macular edema
- retinal abnormalities confined to area drained by obstructed vein
retinal vein occlusion
RF of retinal vein occlusion
similar to artery occlusion
glaucoma major risk
retinal vein occlusion pathogenesis
virchow’s triad for thrombogenesis
- vessel damage
- stasis
- hypercoagulability
central retinal vein and artery share common sheath at AV crossing
retinal vein occlusion diagnosis
ophthalmology referral
widespread retinal hemorrhages
retinal venous dilation and tortuosity
retinal cotton wool spots
optic disk swelling
ophthalmoscopic signs for central
retinal abnormalities are confined to the area drained by obstructed vein
ophthalmoscopic signs for branch
retinal vein occlusion treatment: macular edema
intravitreal injection of VEGF inhibitors (branch or central)
and refer
retinal vein occlusion treatment: neovascularization
pan retinal laser photocoagulation for retinal or anterior segment neovascualrization
and refer
