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normal: <120/ <80
pre-HTN: 120-139/ 80-89
HTN stage 1: 140-159/ 90-99
HTN stage 2: >160/ >100
systolic above 220!!!
diastolic may be above 125
diastolic above 130!!!
most likely have other end organ symptoms too
b/w ages of 25-55
no family history
ischemic CRVOHe also has papilledema (arrow in top left photo) OS. That tends to occur with a CRVO. There is vessel tortuosity in all 4 quadrants of the retina with engorged vessels, scattered dot blots, and scattered flame hemes throughout the posterior pole.
There are a lot of cotton wool spots present. A vein occlusion tends to be more ischemic so that’s why we have the cotton wool spots associated with it. You expect the visual outcome to not be as positive with more ischemia. There's also significant macular edema present.
Non-ischemic CRVOFavorable BCVA in the affected eye. A non-ischemic can change to ischemic, so you need to run an IVFA to tell for sure. This patient received multiple Lucentis injections over time. She went from BCVA 20/100 to BCVA 20/40. Also her HTN is under control now.
ONH OD arteries are attenuated (narrowed), cotton wool spots (microinfarct of superficial capillary bed), flames, and macular star. A macular start involves Henle’s layer with the “spokes on a wheel” appearance. The HTN changes are more significant in OS.
OD The arrows show straightened/narrowed vessels. A/V ratio haschanged instead of 2/3 it’s more like ¼. OS red line shows a vessel that has straightened out.
Everything in grade 1 and 2 (i.e. attenuation, crossing changes,straightening of vessels, etc.) Now with cotton wool spots, flame hemes, edema,exudate, etc.
ONH edema/papilledema, occurs in both eyes typically. Everythingelse from other grades (macular star, flame hemes, cotton wool spots, exudate,straightening vessels, crossing changes, etc.)
- Narrowing of arteries. True crossing changes in botheyes. HTN ret should be bilateral, butone eye can be more dramatic than the other. If the asymmetry is severe, youmight suspect something else going on like carotid blockage. This wouldindicate running tests for carotid blockage (ultrasounds, Bruit sounds, etc) Thereare crossing changes about 2DD from ONH (black arrows). The red line shows a straighteningof the blood vessels.
Hypertensive retinopathy grade 4The macula should be flat with an obvious foveal pit, but it’s elevated and lacking the pit. Macular cystic changes (edema) are located in the OPL (which is where it should be). The far right of the scan correlates with the elevated margin of the ONH (black double-headed arrow). Normally this should not be elevated, but the ONH swelling (papilledema) is causing this to show up on the OCT.
copper wire changes and sheathing
What do you do? Nothing, because he’s already well controlled with his HTN and DM. Just let his physician know what you’re finding on the retina.
Left: Focal constriction. Usually associated with malignant/poorly controlled HTN. This is more of a grade 2.
Right: Generalized constriction. The arteries are narrowed and straightened. This is a grade 1.
Top: Thickening ofblood vessel causing the lumen to narrow. Bottom: Artery is tortuous. Remember,we don’t normally expect arteries to be tortuous. This artery has significantcrossing change as it crosses over the vein (arrow) and then goes back under thevein (arrow). Notice the copper wire appearance and ALR broadening.
**A/V ratio gets (SMALLER/ LARGER) in HTN retinopathy and ALR gets (SMALLER/ LARGER)
Maturity onset diabetes of the young*
6 different types
genetic link and an ageonset of 25 years-old or less
MODY-3 is the mostcommon type, and is similar to Type 2 in terms of retinopathy
BP elevated on 3 differentoccasions for random in office checks
Fasting glucose blood work: fasting glucose needs to be elevated on 2 different occasions or the patientpresents with extreme symptoms. >126
OGTT (oral glucose tolerance test): it only needs to be elevated one time for a diagnosis. Do an initial reading, rechecks at 1 hr, 2 hrs, and 3 hrs. If level is >200, after 2 hours, then that is enough for a DM diagnosis
What are the 2 varieties of Type 1 diabetes? Which is most common?
Immune mediated - most common
100 million people
1/3 of the US population (out of 300 million)
· Developfrom post-arteriolar capillary or radial capillary networks
Intraretinalhemorrhages or “dot-blot”
· Developfrom the venous end of capillaries or the pre-venular deep capillary networks
---*thickening within 500 μm from the center of the fovea
---*Exudate within 500 μm from the center of the fovea with adjacentthickening of at least one disc diameter within one disc diameter of the center of thefovea
500 –3000μm from center or macula
Spot size = 50 –100μm with 0.1second exposure time and sufficient power
Spot size = 100um with 0.1 secondexposure time
EarlyTreatment Diabetic Retinopathy Study (ETDRS)
for macular edema!
stabilizes acuity but often does not improve it
Uses focal and grid laser photocoag using IVFA as a guide
Avoided if significant loss of perifoveal capillaries
o Intraretinal hemorrhages, Dot-blot, Flame-shaped, Microaneurysms, Saccular enlargement of retinalcapillaries, exudates, Hard yellow exudate (HYE), and Macular edema or CSME
*Pts can have ALL of these things above or just ONE of thesethings.*
"Vision is distorted OS.It’s hard to describeand a little bit blurred. It doesn’t seem clear and sharp like it usually does"
"Vision has been fluctuating"
BCVA OD 20/20 OS 20/25
Cotton wool spot (arrow). This bringsit to the next level of retinopathy. Exudate close to the macula, but still NOTCSME. There are scattered dot blot hemes as well. The main issue is the cottonwool spot, because this indicates ischemia.
tx: get back on target with his control.
start at the pupillary frill
workits way to the iris periphery
*Worsening exudation and capillaryocclusive changes
*Extensive IRH, venous beading,IRMA, and macular edema*Venous “sausaging” and “loops”
Topleft and right: NVD
Bottomleft: 4-2-1 with venous beading in at least 2 quadrants and hemes in all 4quadrants. Non-proliferative DR.
upper left: NVD and right:IVFA early fill of NVD.
Bottom left and right: late phase and later phasehyperfluorescence from NVD. Hypofluorescence at ischemic areas of retina,because there is a lack of functioning capillaries.
High risk characteristics (HRC)treated with PRP have a 50% decrease in severe vision loss
OD Severely ischemic retina. Vitreal heme superior to macular area.Fibrotic growth is occurring to support the neo that’s growing. OS has more of the same presentations.Fibrotic tissue is causing a tractional fibrotic retinal detachment
BCVA Hand MotionOD, OS
Pts will receive ananti-VEGF injection first and follow up in a week. If there is stillsignificant edema at 1 week, then the pt receives laser therapy (see below).
An IVFA is most likelydone and if there are “hot spots” (microaneurysms) away from the macula edemathey will probably laser those at the initial visit along with the injection.
“Light”, or low intensity andshort duration laser burns, for grid laser to areas of edema
go around the superior and inferior arcades (temporal) and drawa circle around those including the ONH
Patient’s BCVA may still be 20/20, but may have metamorphopsia/Amslerdefects. Some patients will notice that after cataract surgery, their visionwas great, but about a month later it’s not quite right. They have subtlecystic changes at the macula with an irregular FLR presentation and a smallyellow spot in the fovea.
Topical steroids (Durezol): Q2h
NSAIDs(Advil) 1800mg PO QD
Left OCT: Cystic areas in the macula present.
Right OCT: Multiple areas of cysts in the macula.
Fundus photos (not shown): Little yellow spot in the fovea andno FLR.
Left photo (at presentation): Hyaloid membrane intact with notraction.
Rx: Durazol Q2H x1 month.
Why don’t you get exudative changes from CME and you do withother types of edema?
Other conditions have a release of VEGF that is off-the-charts(occlusive disease, DM, etc.), because of that permeability of capillaries, wehave leakage of fluid causing cystic changes.
If VEGF is off-the-charts for awhile we get an accumulation of exudate.
There isn’t the same amount of VEGF inCME as compared to other disease processes.
Plan: Rx Durazol Q2H and Bromdayand he didn’t really improve. Then he was sent back to a retina specialist foran injection of Avastin. This CME is inflammatory in nature. The cataractsurgery OD was very complicated
Top left: Normal scan
Top right: Type 1B. Posterior hyaloid causing traction andcystic changes
Middle left: Stage 2. Posterior hyaloid (hyaloid condensation) stillattached with CME.
Middle right: Stage 3. PVD/hyaloid membrane.
Bottom left: Stage 4. Complete PVD, pseudo-operculum, cysticchanges at base.
Bottom right: Sx repair.
To look inside a macular hole·
Slit lamp technique: Shrink down to a narrow parallel beam. Usegonio lens to view the posterior pole. Tell the patient to look at the light.Ask patient if the beam is missing anything or if beam appears tapered. Pt willbe able to appreciate how beam changes. You will be able to see your beam dropdown into macular hole (Positive Watzke-Allen sign).
Stage 1A or 1B: Monitor. Usually spontaneously resolves on it's own. No sx required.
Stage 2 or 3: Pars plana vitrectomy to release the tractionalarea and stop progression. Outcome is 20/50-20/100 post treatment.
Stage4: No sx because complete PVD and no sx will help
Referred for a glaucoma eval.
Red arrow: ONH looks normal.
Left black arrow: EMM that developed from a PVD.
Right black arrow: Hole at macula.
It’s not 2, because we don’t have a through and through hole.Not a stage 3, because tissue is still in tact and not a stage 4 because wedon’t have a PVD.What do we do?
Top: Round area around macula. With stereo in the slit lamp vesselswill “come out at you” more due to the elevation of the macular area.
Top left: Early stage RPE defect starting to trickle through
Top right: Later phase it is leaking out like smoke out of achimney (smoke stack appearance).
Bottom left: Early stage RPE defect starting to trickle throughBottomright: Later phase it expands in size and begins to occupy that entire space(ink blot appearance).
It starts in the central area and then moves out from there andbegins to fill up the surrounding space.
No laser therapyis indicated, because the RPE defect is too close to macula.
Management: Rx +0.75to BCVA. Patient wore these for a couple of months and everything resolved onit’s own.
The edema is causing the macula to be pushed forward. This iscausing light to converge at a point behind the macula. Plus lenses will makelight converge at that point rather than behind the newly placed macula. It’slike the CSR is making the patient into an artificial hyperope (where lightfocuses behind the retina), and the low plus brings the image from “behind theretina” to focus on the macula.
Top left: Hard drusen, multiplenodules present
Top right: Soft (large) drusen has a“fluffy” appearance
Bottom left: Mixed with RPE changesBottomright: Calcific drusen
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