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Block 15 > Posterior Seg Disease > Flashcards

Posterior Seg Disease Flashcards

1
Q

Central serous chorioretinopathy (CSCR)

A 
Idiopathic
Local serous detachment of the macula
Common
Healthy individuals
Young men, Type A personality
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2
Q

Pathophysiology of CSCR

A

Due to retinal (RPE) and choroidal dysfunction

Fluid from leaky choriocapillaris filters up through defects in RPE

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3
Q

Where does the fluid accumulate in CSCR

A

Between neurosensory retina and RPE (retinal detachment), beneath RPE (PED), or both

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4
Q

Conditions associated with CSCR

A 
Male gender
Type A personality
Emotional stress
Steroid medications
Cushing’s disease
Systemic lupus erythematosus (SLE)
Pregnancy (later stages)
Sleep apnea
Increased level of glucocorticoids within the blood stream
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5
Q

Disease associated with increased levels of circulating glucocorticoids

A

CSCR

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6
Q

Chronically elevated glucocorticoid levels lead to:

A

Inc permeability of choroidal blood vessels

Defective RPE/outer blood-retinal barrier

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7
Q

Symptoms of CSCR

A

Subacute blurring or distortion of vision in one eye
Dark “smudge” in middle of vision
No discomfort or history of trauma
Well-circumscribed round or oval serous elevation of retina affecting the macula
Otherwise normal retina
Other eye normal

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8
Q

Diagnosis of CSCR

A

History alone
Fundoscopy
OCT
Angiographic studies

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9
Q

OCT appearance of CSCR

A

Serous fluid above the RPE with sometimes having a small leakage, forming another small detachment (like an RPE detachment)

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10
Q

Fluorescein angiography of CSCR appearance

A

Smoke-stack appearance

Pinpoint area of leakage that gradually enlarges

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11
Q

Management of Typical CSCR

A

Reassurance to pt
Consult with treating physician if using corticosteroid medications
Lifestyle modifications
Monitor periodically
Long-standing or recurrent cases may benefit from PDT (laser or anti-VEGF’s controversial)

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12
Q

Chronic CSCR

A

Atypical form of CSCR
Aka Diffuse retinal pigment epitheliopathy
More severe/much less common form of CSCR

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13
Q

Characteristics of Chronic CSCR

A

Widespread distribution of small PED’s
Extensive pigmentary changes
Chronic course with exacerbations and remissions
Visual prognosis is worse than with typical CSCR

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14
Q

Who usually gets chronic CSCR or diffuse retinal pigment epitheliopathy?

A

Patients older than 50 years

Asians and Hispanics

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15
Q

How do you manage chronic CSCR or diffuse retinal pigment epitheliopathy?

A

PDT with Verteporfin

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16
Q

Why is laser photocoagulation therapy controversial and inconclusive in chronic CSCR?

A

Area of RPE leakage in chronic CSCR is often so diffuse that laser is not a viable option

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17
Q

How can you improve vision in chronic CSCR?

A

With a weak plus lens

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18
Q

Why can a weak plus lens help a patient with chronic CSCR have better vision?

A

Fluid is making the eye seem shorter than it is, so you are effectively decreasing the axial length of the eye with this

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19
Q

How do you typically treat typical CSCR?

A

Let it run it’s course b/c it will typically heal on it’s own (laser is controversial b/c it can cause scotoma’s)

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20
Q

What are the two kinds of CSCR?

A

Classic

Atypical

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21
Q

PDT with Verteporfin helps treat what?

A

Chronic CSCR or diffuse retinal pigment epitheliopathy
-Causes closure of abnormally leaky vessels within the inner choroid = lower dose is necessary so you don’t cause choroidal ischemia, shutting down too many vessels

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22
Q

What is the key to diagnosing CSCR?

A

OCT

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23
Q

Prognosis for typical cases of CSCR?

A

Excellent

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24
Q

Prognosis for chronic CSCR

A

More guarded (PDT may be a beneficial treatment option, but is still new)

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25
Q

Polypoidal choroidal vasculopathy

A

Idiopathic vascular disease

Terminal aneurysmal “polyp-like” endings of inner choroidal vessels

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26
Q

What can polypoidal choroidal vasculopathy cause?

A

Exudation within the macula

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27
Q

What is polypoidal choroidal vasculopathy often mistaken with?

A

For exudative AMD (some consider it a subtype) or CSCR

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28
Q

Who is predominantly affected by Polyoidal choroidal vasculopathy

A

African or East Asian decent, typically older individuals (avg age = 60)

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29
Q

Pathophysiology of polypoidal choroidal vasculopathy

A

Defective clusters of choroidal vessels form terminal “polyps” beneath the RPE
Polyps leak or bleed, resulting in recurrent serous and/or hemorrhagic detachments of the retina and RPE

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30
Q

Symptoms for polypoidal choroidal vasculopathy

A

Often sudden visual impairment in one eye (condition usually bilateral, but asymmetric)

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31
Q

Signs of polypoidal choroidal vasculopathy

A

Reddish-orange nodules Near disc or macula

Multiple recurrent “serosanguinous” PED’s and RD’s

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32
Q

Diagnosis of polypoidal choroidal vasculopathy

A

Fundus appearance and demographics
OCT and FA
ICGA (indocyanine green angiography) to confirm diagnosis - binds to albumin, and most of it stays in the choroidal vasculature, helping you see deeper into the tissue

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33
Q

Management of polypoidal choroidal vasculopathy

A

Observation if symptoms tolerable (half spontaneously resolve)
PDT (photodynamic therapy) more successful than in AMD
Laser of persistent/progressive lesions or their feeder vessels if not beneath the fovea

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34
Q

Treatment for cystoid macular edema

A

Address underlying cause

Treat with NSAIDs/steroids or laser/surgery as indicated

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35
Q

Treatment for central serous chorioretinopathy (CSCR)

A

Monitor typical cases first 4-6 months

Coordinate PDT treatment for chronic/recurrent cases

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36
Q

Most common form of CME

A

After cataract surgery

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37
Q

Treatment for Polypoidal choroidal vasculopathy

A

Make proper diagnosis, to prevent inappropriate care
Monitor or direct to retinal specialst (based on symptoms)
Indocyanine green to help identify polyps in choroid

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38
Q

Cystoid macular edema (CME)

A

Accumulation of fluid in cyst-like intraretinal spaces within the perifoveal region
Nonspecific manifestation of macular edema from any cause
Fluid-filled microcystic spaces may coalesce into larger cavities, which may eventually form a lamellar macular hole

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39
Q

How does edema differ from serous detachment?

A

Edema - fluid collects within the retina

Serous - fluid collects between the retina

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40
Q

Causes of CME

A

Ocular surgery (Irvine-Gass syndrome) - cataract surgery
Retinal vascular disorders
Inflammation
Medications (glaucoma meds)
Retinal dystrophies (retinitis pigmentosa)
Any form of CNV (in patelloid pattern)
Ocular vascular tumors, systemic disease, etc.

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41
Q

How does CME occur in the eye?

A

Exact mechanisms by which fluid accumulates within the cystoid spaces in the retina is not fully understood
Breakdown of the blood-retina barrier
Muller cell abnormalities
Diffusion of mediators (prostaglandins, etc) released in the eye
Mechanical factors (tractional forces on the macula)

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42
Q

Outer blood-retina barrier

A

RPE and junction of RBC’s

-Kees fluid from choroid getting into retina

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43
Q

Inner blood-retina barrier

A

Inner retina

-keeping blood vessels themselves (leakiness) from getting into the retina

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44
Q

Presentations of CME

A

Gradually painless blurring or distortion of central vision in one eye
Pt may notice suddenly when good eye is covered
History of precipitating factors (recent cataract surgery, BRVO)
Presentation varies somewhat with cause

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45
Q

Clinical appearance of CME

A

Macula actually looks pretty normal

Fovea looks a little different (spoke pattern) = patellar pattern

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46
Q

Diagnosis of CME

A

Fundus appearance
FA
OCT

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47
Q

What does the fundus appear like with CME?

A

Initial changes subtle (loss of foveal depression)

Multiple cystoid areas best seen with red-free light

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48
Q

What does FA (fluorescein angiography) display on a CME patient?

A

Characteristic “petalloid” pattern around the macula

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49
Q

What does the OCT clearly show when diagnosing CME?

A

Cystic spaces and retinal thickening (also holds or traction if present)

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50
Q

OCT presentation of CME

A

Cystic spaces = optically empty areas within the retina right at the fovea
Air or serous fluid in these areas

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51
Q

Management of CME

A

Depends on cause (treating underlying cause may induce resolution)
Monitored
Post-op treatment is with anti-inflammatories (topical NSAIDs and/or steroids)
Oral CAI’s (Diamox)
Possible anti-VEGF’s (work fairly well, but use as 2ndary thought b/c don’t typically need entire shot in eye)
Laser or surgery in specific scenarios

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52
Q

What treatment option do you typically start off on a patient with CME?

A

NSAIDs (diclofenac) for awhile (several weeks or months); sometimes add steroids, but really depends on severity

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53
Q

Conditions in which mechanical forces distort the normal architecture of the macula

A

Tractional maculopathies

  • epiretinal membrane
  • vitreomacular traction syndrome
  • age-related macular holes
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54
Q

What is an ERM?

A

Membrane which forms on top of the retina (usually overlying the macula)
Fibrocellular membrane, composed of a sheet of cells (type varies) and fibrous tissue
May be idiopathic or secondary to a host of intraocular conditions (ex: retinal detachment surgery)

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55
Q

Appearance of epiretinal membranes (ERM)

A

Folds/wrinkles around macular region with puckering

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56
Q

Primary causes of epiretinal membranes

A

Idiopathic
Older individuals (age 50+)
Unilateral mostly
Mostly made up of glial cells derived from posterior hyaloid (often after Posterior vitreous detachment)
Relatively mild presentation (compared to those associated with intraocular pathology)

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57
Q

Secondary causes of epiretinal membranes

A

Associated with other intraocular conditions
May be binocular if pathology is
Composed of various cell types
Tend to be more problematic and severe than the idiopathic variety

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58
Q

Symptoms of epiretinal membrane

A

Mild cases may be asymptomatic

As membrane thickens/contracts, pt’s notice blurring or distortion of vision (metamorphosia)

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59
Q

What are some clinical signs for epiretinal membranes?

A

Glistening translucent membrane at or near the macula
As membrane thickens, it becomes opaque
Contraction will distort retinal blood vessels and cause wrinkling of the underlying retina

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60
Q

Diagnosis of epiretinal membrane

A

Direct observation

OCT

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61
Q

Appearance of OCT scan of ERM

A

Retina (thicker top green section) will look bunched up, with a thin green line most internal (toward the vitreous) looking like it’s pulled tighter and attaching at the fovea
The thin line is the epiretinal membrane

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62
Q

Management of ERM

A

Monitor pt’s who have minimal macular involvement (many remain stable for years; very rarely, symptoms may subside after spontaneous release from the retina)
Vitrectomy with membrane peeling for pt’s with intolerable distortion (generally favorable results; rarely ineffective or associate with complications)

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63
Q

What is guaranteed for a patient who has a vitrectomy?

A

Cataract formation

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64
Q

When do you perform surgical ERM peeling?

A

When it is bad enough for the pt, and the risks (like getting cataracts) outweighs the cost
It if is bothersome, with opacification

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65
Q

Vitreomacular traction syndrome

A

Occurs when the vitreous partially separates from the posterior pole, while remaining attached at the fovea
Observed in older individuals (+50)
Essentially, an incomplete PVD with “tugging” on the fovea

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66
Q

Symptoms of vitreomacular traction syndrome

A

Progressive “blurring” or “distortion” of vision in one eye
Flashes of light
(The tugging forward of the retina is more of a mechanical issue b/c it can cause a photoreceptor to fire when it shouldn’t)

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67
Q

Signs of vitreomacular traction syndrome

A

Macula may appear wrinkled/distorted

As associated ERM or CME may be present

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68
Q

Diagnosis of vitreomacular traction syndrome

A 
Macular appearance (mostly)
OCT is necessary to make a definitive diagnosis
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69
Q

Appearance of OCT for vitreomacular traction syndrome

A

Retina and everything looks normal, except there is a space between the surface of the retina and the gel, where another small green layer is (you can tell it’s a vitreous detachment)
However, it is still attached right at the fovea, which causes the fovea to sort of have a mountain peak appearance

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70
Q

Treatment for vitreomacular traction syndrome

A 
Spontaneous release may occur (observation of relatively mild cases)
Pars plana vitrectomy releases traction in more severe or progressive cases (usually with good results, but residual macular edema may preclude complete recovery)
Pharmacological vitreolysis (as adjunct or alternative to vitrectomy) - split or break the connection with medicine like aquaplasm; this method doesn’t work quite as well
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71
Q

Age-related macular hole

A

Round area of missing retina which occurs at the macula
Cause not entirely understood, but related to tractional forces exerted by the posterior hyaloid
Older population
Usually unilateral, but can be subsequent in other eye

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72
Q

What are some other things that can cause macular holes, besides age?

A

Degenerative myopia

Blunt trauma

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73
Q

Symptoms of age-related macular holes

A

Blurred central vision (variable)
Central distortion or scotoma, depending on stage of hole
Often not noticed until other eye is covered

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74
Q

Stage 1a of age-related macular hole

A

Impending macular hole (loss of foveal depression and split within retinal layers)

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75
Q

Stage 1b of age-related macular hole

A

Occult macular hole (gap in photoreceptors without full-thickness “hole”)

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76
Q

Stage 2 of age-related macular hole

A

Small full-thickness hole (often crescent shaped)

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77
Q

Stage 3 of age-related macular hole

A

Full-size macular hole (adjacent traction persists)

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78
Q

Stage 4 of age-related macular hole

A

Full-size macular hole (with complete PVD)

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79
Q

What is the appearance of an age-related macular hole?

A

Nice round borders, smaller than the optic nerve, right on the macula, sometimes with exudates
Looks just like a cigarette burn

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80
Q

OCT appearance of stage 1 age-related macular hole

A

Small gap in the retina right around the the fovea, with the vitreous still attached
Lamellar

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81
Q

OCT appearance of stage 2 age-related macular hole

A

Gap in retina, where they sides have completely come apart from each other at the fovea
Down to the bare RPE

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82
Q

OCT appearance of stage 3 age-related macular hole

A

Looks like a complete divet into the retina, right at the macula
You can notice that one side has some attachment still (posterior hyaloid is still partially attached)

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83
Q

OCT appearance of stage 4 age-related macular hole

A

Looks just like eyelids that are not completely closed onto the front of the eye (the two sides have completely detached from each other), with full detachment of the vitreous (you can see this as a thin green layer further into the eye than the retina layers

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84
Q

Diagnosis of age-related macular hole

A

Via slit-lamp biomicroscopy
Differentiate from pseudoholes (epiretinal membane with hole in it)
Watzke-Allen test
OCT (helps find out stage of macular hole)

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85
Q

Treatment of age-related macular hole

A

Stage 1: monitor it myself
Stage 2: send out and let retinal specialist decide

  • half stage 1 holes resolve after spontaneous release of traction, and 10% of full-thickness holes close on own
  • for stage 2, vitrectomy with peeling of internal limiting membane (provided VA <20/30) - use gas tamponade where pt has to look down and let gravity do it’s thing
  • most achieve final VA of better than 20/40
  • risks for cataract formation and endophthalmitis due to shot inside of eye
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86
Q

How does an epiretinal membrane affect the macula?

A

Contact inward toward the center of the membrane, causing distortion

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87
Q

How does vitreal macular traction affect the macula?

A

Pulls the surface of the retina forward, toward the front of the eye

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88
Q

How do macular holes affect the macula?

A

B/c of tangential forces pulling the retina apart laterally to the retina

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89
Q

Macular microhole

A

Small localized gap amongst photoreceptors, and/or a subtle RPE defect (uncommon)
Idiopathic
Easily overlooked

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90
Q

Symptoms of macular microhole

A

Minimal

  • subtle central scotoma
  • some notice faint central distortion or difficulty with reading
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91
Q

Diagnosis of macular microhole

A

OCT

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92
Q

Treatment of macular microhole

A

Safely watched as remains stable and patient’s minimally inconvenienced

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93
Q

OCT appearance of macular microhole

A

Very small missing circular bubble-like appearance in the foveal photoreceptor layer, just above the RPE (red line)

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94
Q

Degenerative myopia

A

Progressive elongation of the globe mechanically stretches the tissues of the eye, causing problems

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95
Q

High myopia

A

Refers to the length of the eye

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96
Q

Pathological myopia

A

When the amount of myopia is progressive
>6D myopia or >26 mm axial length
Legal blindness may result from 2 degrees of change
Damage to macula is usually cause of vision loss

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4
5
Perfectly
97
Q

In degenerative myopia, what is the usual cause of vision loss?

A

Damage to the macula

98
Q

Symptoms of degenerative myopia

A

Vision loss which may be slow or abrupt (depending on cause)

99
Q

Signs of degenerative myopia

A

Thinned retina (Tigroid)
Focal chorioretinal atrophy
Breaks in Bruch’s membrane (‘lacquer cracks)
Subretinal hemorrhages
Fuch’s spot
Distorted optic disc w/ temporal peripapillary atrophy
Posterior staphyloma

100
Q

When you see tigroid or tessellated retina associated with degenerative myopia, what is this a sign of?

A

Thinned retina

101
Q

Posterior staphyloma

A 
Posterior bulging of sclera
Weak spot (similar to bad/old basketball)
102
Q

Complications fo degenerative myopia

A

Rhegmatogenous RD
CNV
Foveal retinoschisis/macular hole

103
Q

Rhegmatogenous RD

A

Thinned, stretched retina prone to tearing

Associated with degenerative myopia

104
Q

CNV

A

Cracks in Bruch’s membrane - RPE complex (lacquer cracks) provide route for CNV to access subretinal space
Associated with degenerative myopia

105
Q

Foveal retinoschisis/macular hole

A

Posterior staphyloma increases vitreous traction (mechanical tear)
Associated with degenerative myopia

106
Q

Associated ocular condition with degenerative myopia

A

Cataract
Glaucoma (POAG, pigmentary, steroid-induced)
Amblyopia (at young age)

107
Q

Associated systemic conditions with degenerative myopia

A 
Various syndromes (Down, Marian, Ehlers-Danlos, etc.) - due to abnormal collagen being laid own
Premature birth
108
Q

Diagnosis of degenerative myopia

A

History of highly myopic refractive error
Measurement of increased axial length
Typical secondary changes at posterior pole
FA for CNV
OCT for foveal schisms and macular holes (splits in retina)

109
Q

Treatment of degenerative myopia

A

Consider refractive error

110
Q

Management of amblyopia associated with degenerative myopia

A

Occlusion therapy

111
Q

Management of CNV associated with degenerative myopia

A

Intravitreal anti-VEGF injections possibly

112
Q

Management of foveal schisms or hole formation associated with degenerative myopia

A

Vitrectomy may be indicate

113
Q

Management of RD associated with degenerative myopia

A

Surgical referral

114
Q

Angioid streaks represent what?

A

Breaks in an abnormally brittle Bruch’s membrane (encircling disc and radiating outward)

115
Q

Angioid steaks are associated with what?

A

Systemic disease about half the time; no known cause for the other half

116
Q

What can angioid streaks lead to?

A

Hemorrhages, either from CNV or trauma (which may be relatively minor)

117
Q

Represent breaks in an abnormally brittle Bruch’s membrane (arterial-like)

A

Angioid streaks

118
Q

What do you want to avoid in pt’s with angioid streaks?

A

Scleral depression

119
Q

Systemic associations with angioid streaks

A

Pseudoxanthoma elasticum (PXE)
Paget disease
Hemoglobinopathies (sickle cell disease)
Various connective tissue disorders, etc.

120
Q

Mottling of retinal pigment (“peau d’orange”) may be more noticeable than angioid streaks in what disease?

A

Pseudoxanthoma elasticum (PXE)

121
Q

Pseudoxanthoma elasticum (PXE) is associated with who and what disease?

A

Most patients’ eyes affected after teen years
Associated with systemic cardiovascular disease
Systemic association of angioid streaks

122
Q

Bone disorder associated with cardiovascular disease and angioid streaks

A

Paget disease

123
Q

Appearance of skin changes with PXE, associated with angioid streaks

A

‘Plucked chicken’ (looks like goose-bumps)

124
Q

Management of angioid streaks

A

Counsel on avoidance of contact sports and use of protective eyewear
If unknown systemic condition, communicate findings with pt’s PCP
Coordinate care with retinal specialist (CNV; choroidal rupture)

125
Q

Represent a wrinkling of the inner choroid, Bruch’s membrane, and RPE

A

Choroidal folds

126
Q

Choroidal folds are associated with compression of what?

A

Choroid

127
Q

Choroidal folds

A

Represent a wrinkling of the inner choroid, Bruch’s membrane, and RPE
Sometimes idiopathic

128
Q

What is it important to differentiate from choroidal folds?

A

From wrinkling of the retina alone (as seen with ERM = epiretinal membrane, etc.)

129
Q

Choroidal folds may be associated with what conditions?

A

Sight or life-threatening conditions

130
Q

Presentation of choroidal folds

A

Alternate parallel light and dark bands correspond to adjacent areas of thinner “stretched” RPE and thicker “compressed” RPE
Usually horizontal
May be asymptomatic (if long-standing)

131
Q

What systemic disease can be associated with choroidal folds?

A

Thyroid eye disease

Posterior scleritis

132
Q

Causes of choroidal folds

A 
Idiopathic (often hyperopic patients)
Pressure effects (inc or dec)
Mass effects (tumors, scleral buckles, thyroid ophthalmopathy, posterior scleritis)
133
Q

Evaluations of choroidal folds

A

Identification of underlying cause
OCT or FA
Ultrasound, MRI, or CT scans

134
Q

Management of choroidal folds

A

Depends on underlying cause

135
Q

Hypotony maculopathy

A

Denotes impaired macular function secondary to severely decreased IOP

136
Q

Cause of hypotony

A 
Glaucoma filtering surgery
Would leak
Penetrating trauma (grinder)
Inflammation (ciliary body slows production of aqueous fluid)
Cyclodialysis
RD
137
Q

Hypotony can allow what of the sclera?

A

Scleral collapse

138
Q

3 causes of hypotony that are associated with a loss of fluid through a hole in the eye

A

Glaucoma filtering surgery
Wound leak
Penetrating trauma

139
Q

3 causes of hypotony that are associate with decreased aqueous production

A

Inflammation
Cyclodialysis
RD

140
Q

Presentation of hypotony maculopathy

A

Reduced central vision

141
Q

Clinical findings of hypotony maculopathy

A

Chorioretinal folds (often affecting the macula)
Retinal folds
Low IOP

142
Q

Diagnosis of hypotony maculopathy

A

Tonometry defines the condition

143
Q

Management of hypotony maculopathy

A 
Restore normal IOP (seal “leak” if from penetrating surgery or trauma; treat inflammation or repair retinal/ciliary tear)
Prognosis variable (chronic cases can lead to phthisis bulbi and loss of eye; substantial improvement possible even after years)
144
Q

Solar maculopathy

A

Foveal damage caused by staring at the sun

145
Q

Presentation of solar maculopathy

A

Blurred central vision (or central scotoma) notice within hours of exposure
photochemical damage that occurs

146
Q

What do you see when you look at someone’s retina who has solar maculopathy?

A

Sharply demarcated yellow or reddish foveal spot, which fades over weeks leaving a foveal defect with pigmentary changes or lamellar hole

147
Q

OCT appearance of solar maculopathy

A

RPE complex (bright red) shows a gap right at the fovea

148
Q

Treatment for solar maculopathy

A

None (avoid looking at the sun!)

149
Q

Who do you usually see with solar maculopathy?

A

Major psychological disorders
History of psychotropic drug use
Religious or personal reasons for staring at the sun

150
Q

Prognosis for solar maculopathy

A

Surprisingly good (most recover normal or near-normal vision within months)

151
Q

Separation of the photoreceptors from the underlying RPE

A

Retinal detachment

152
Q

Different kinds of retinal detachment

A

Rhegmatogenous
Tractional
Exudative

153
Q

Full-thickness defect (tear/hole/split) in the sensory retina which may occur with or without detachment of the retina

A

Retinal break

154
Q

Rhegmatogenous retinal detachment

A

Specific type of RD which occurs when a retinal break allows liquefied vitreous to see into the potential space between the NSR and RPE

155
Q

Formation of a rhegmatogenous RD requires what?

A

Full-thickness retinal break
Traction holding the break open
Liquified vitreous

156
Q

Causes of retinal breaks

A

Mechanical tearing

Strophic hold formation

157
Q

What is happening when something can “tug” on the retina, ripping it, causing retinal breaks?

A

Mechanical tearing

158
Q

What is it called when the retina itself can degenerate (wither away), causing retinal breaks?

A

Atrophic hole formation

159
Q

Specific examples of retinal break causes

A

Posterior vitreous detachment (PVD)
Developmental or degenerative abnormalities
Trauma
Traction induced by fibrovascular proliferation (ex. DR)

160
Q

Vitreal synchysis

A

Normal age-related process, whereby vitreous gel liquifies over time
Will happen in all eyes eventually
Usually without causing RD

161
Q

What is vitreal synchysis due to?

A

Accumulated toxic effects of light irradiation and metabolic waste products

162
Q

Posterior vitreous detachment (PVD)

A

Normal age-related process, whereby the solid vitreous gel collapses/contracts forward while liquified fills retrohyaloid space
Will happen in all eyes eventually
Usually without causing RD

163
Q

PVD is accompanied by what?

A

Synchysis (liquificaiton of vitreous)

Syneresis (shrinkage or contraction of vitreous)

164
Q

Compilation of PVD

A

Usually none
Retinal tear at focal area of abnormally strong attachment to retina that does not “let go” as solid gel pulls away
Vitreous hemorrhage if vitreous gel strongly attached to retina vessel which is torn as it pulls away (with or without RD)

165
Q

Symptoms of PVD

A

Flashes (photopsia) when retina is tugged on as gel pulls away (subside when traction released)
Floaters when moving vitreous opacities case a shadow on the retina

166
Q

Examples of floaters pt’s with PVD can see

A

Single large floater (Weiss ring)
Cobwebs (condensation of collagen fibers)
Shower of small dark spots (RBC’s)

167
Q

Signs of PVD

A

Difficult (but not impossible) to observe detached/condensed vitreous gel at slit-lamp
Much easier to see Weiss ring
Vitreous hemorrhage (sparse)

168
Q

Management of PVD

A

Rule out RD in symptomatic pt’s
Monitor closely while “flashes” persist
Reassurance (no cure for any floaters; will become less noticeable over time)

169
Q

Symptoms of retinal detachments

A

Not all pt’s have symptoms
Spontaneous “flashes” and/or floaters with preceding PVD
“Curtain” or “shadow” in vision may be seen to progress centrally (initial location signals that of primary retinal break)

170
Q

What’s a pt’s biggest symptom that tells you they are having a retinal detachment?

A

Curtain or shadow in vision may be seen to progress centrally

171
Q

Signs associated with RD

A 
RAPD if RD is extensive
IOP slightly lower than fellow eye
Mild iritis
Pigment cells in anterior vitreous (Shafer’s sign or ‘tobacco’s dust”)
Retinal breaks
172
Q

Where are retinal breaks usually found with RD?

A

In superotemporal quadrant

173
Q

How may retinal breaks associated with RD appear?

A

Complete/incomplete flap tears, operculated tears, dialysis, holes

174
Q

Shafer’s sign

A

“Tobacco dust”

Brown looking pigmented cells/spots in the anterior vitreous

175
Q

A horseshoe tear is common in what disease?

A

RD

176
Q

Is a horseshoe tear important to treat immediately?

A

Yes! They are likely to progress.

Figure out if the macula is still on or if it is off.

177
Q

If horseshoe tear shows macula on, is this better or worse than macula off?

A

Need to treat immediately. If it was macula off, you can’t really do anything about it now.

178
Q

Operculated tear treatment

A

Sometimes don’t really even need to treat

179
Q

What is an operculated tear?

A

In RD, it’s just a chunk of the retina that is pulled off.
Hole/break in retina, with a piece now just free-floating into the vitreous.
Unlikely to predispose retinal detachment b/c no longer have the traction since it’s just floating in the vitreous..

180
Q

Clinical appearance of Fresh RD

A

Elevated retina has a translucent appearance
Appears “wrinkled”
Undulate with eye movements

181
Q

Clinical appearance of Long-standing RD

A

Detached retina becomes thinned and atrophied
Intraretinal cysts may form
Demarcation lines

182
Q

Appearance of fresh retinal detachment

A

Billowy (loose-sheet waving in the wind) detached retina

Long yellowy line in vitreous

183
Q

Appearance of old RD with demarcation line

A

Area above choroid is slightly translucent; relatively shallow; all of the line is detached. Everything above the line is still attached
Dark line across the retina (choroid)

184
Q

Diagnosis of rhegmatogenous RD

A

DFE with BIO (scleral indentation = pushing to check periphery)
Ultrasound (B scans)
Contact fundus lenses (gonioscopy)

185
Q

Treatment of rhegmatogenous RD

A

Successful reattachment by specialist depends on permanent closure of retinal beaks responsible in a timely fashion

186
Q

Most RD’s will progress to what VA’s?

A

Severe permanent vision loss without treatment

187
Q

Reattachment techniques for rhegmatogenous RD

A

Laser or cryotherapy (mostly prophylactic role)
Pneumatic retinopexy (gas bubble tamponade)
Scleral buckling (with or without fluid drainage)
Vitrectomy (often combined with a scleral buckle)

188
Q

What role does laser or cryotherapy have in rhegmatogenous RD?

A

Mostly prophylactic role
Reattachment technique to seal potential holes where there is a retinal detachment
Freeze-dried

189
Q

Gas bubble seal used in rhegmatogenous RD; how long does it take to work?

A

Pneumatic retinopexy
Smaller break/tear usually superior
3-4 days due to bubble and gravity
Take out all of the vitreous and insert gas bubble

190
Q

Gold standard for reattachment of rhegmatogenous RD

A

Scleral buckling (with or without fluid drainage)

191
Q

Scleral buckling..what is it?

A

Wherever the tear is, they will go on the outside of the eye, they will push the RPE back up against the retina and sew a spongy looking piece of stuff to maintain that connection between those structures
No chances of endophthalmitis

192
Q

Reattachment techniques for rhegmatogenous RD that we can do without referring

A

Laser or cryotherapy

193
Q

Reattachment techniques for rhegmatogenous RD that we must refer out to specials

A

Pneumatic retinopexy
Scleral buckling
Vitrectomy

194
Q

Vitrectomy treatment for rhegmatogenous RD

A

Relieves the traction; guarantee the pt will get cataracts; not quite as safe, as easy, or as cheap as scleral buckling, but it might be needed if the traction on the pt is too much and it needs to be done

195
Q

Proliferative vitreoretinopathy (PVR)

A

Membranes form on and under detached retina, which contract to cause fixed retinal folds

196
Q

In PVR, eventually, what happens to the detached retina?

A

Detached retina may be pulled together, as in a total RD, with a funnel-like appearance

197
Q

What is the most common cause of failure in RD surgery?

A

PVR (proliferative vitreoretinopathy)

198
Q

When can PVR occur?

A

In diabetic traction RD with retinal breaks.

Penetrating or blunt trauma may also result in PVR

199
Q

Complication that can occur in abut 3 weeks after retinal detachment surgery

A

PVR (proliferative vitreoretinopathy)

200
Q

Peripheral retinal degenerations may or may not lead to what?

A

RD

201
Q

Microcystoid degeneration is a formation of what?

A

An area of confluent tiny vesicles within the peripheral retina, such that it looks thickened or less transparent
Does not lead to RD by itself

202
Q

Microcystoid degeneration is also known as what?

A

Peripheral cystoid degeneration

203
Q

Microcystoid degeneration always extends from where?

A

Ora serrata posteriorly and circumferentially

204
Q

Management of microcystoid degeneration

A

Does not require Tx or referral
Benign
Document and monitor for progression to retinoschisis

205
Q

Pavingstone degeneration

A

Patches of chorioretinal atrophy aligned in a row parallel to the ora serrata
Occurs in roughly a quarter of normal eyes
Represents thinned intact retina and choroid overlying visible sclera
Does not lead to RD

206
Q

Management for pavingstone degeneration

A

Not due to other pathology
Understand there is no “break” in the thinned, ddegenerative retinal tissue
No need for Tx or referral
Document and educate pt

207
Q

Reticular pigmentary degeneration

A

Peripheral perivascular pigmentation which may extend posterior to the equator

208
Q

Who is reticular pigmentary degeneration common in?

A

Older patients

Not associated with pathology, decreased visual function or RD

209
Q

What is reticular pigmentary degeneration also known as?

A

Peripheral senile pigmentary degeneration
Tapetochoroidal degeneration
Honey comb dystrophy

210
Q

Management of reticular pigmentary degeneration

A

Benign age-related change and not pathological
Differentiate from similar appearing conditions with are pathological (retinitis pigmentosa for example)
Document, but probably no need to explain this relatively normal finding to the pt

211
Q

Peripheral drusen

A

Appearance of drusen outside the macular region

212
Q

Who is peripheral drusen typically found in?

A

Older patients
Not associated with AMD
Does not lead to RD or any other problems

213
Q

Management of peripheral drusen

A

Differentiate b/w this benign manifestation of drusen and that associated with progressive macular changes (AMD)
Clearly communicate findings to pt with reassurance they are not at increased risk for AMD
Monitor regularly

214
Q

Lattice degeneration

A

Elongated area of thinned (atrophic) retina beneath a pocket of liquefied vitreous which is surrounded by strong vitreal attacements at the margins of the lesion (runs parallel to ora serrata)

215
Q

What’s the most common retinal degeneration associated with retinal detachment?

A

Lattice degeneration

Up to nearly half of eyes with RD

216
Q

Who typically has lattice degeneration?

A

Myopes very common

217
Q

Pathogenesis of lattice degeneration

A

Uncertain

218
Q

Presentation of lattice degeneration

A

Bilateral
Superotemporal quadrant
Develops early (teens and 20’s)
White lines, “snowflakes,” pigmentation and/or small holes often found within lesion

219
Q

How many pt’s with lattice degeneration typically develop RD?

A

Many patients don’t develop RD

220
Q

RD may develop in patients with what degeneration and how?

A

Lattice degeneration
Following flap tear formation during PVD
From tears at posterior margin of lesion
From holes within lesion (rarely)

221
Q

Management of lattice degeneration

A

Without retinal breaks does not require Tx or referral
Prophylactic laser may be considered in specific limited circumstances
Monitor pt regularly
Advise pt of symptoms of RD and need for immediate care if such occurs

222
Q

Snailtrack degeneration

A

Peripheral retinal degeneration similar to lattice degeneration
Elongated patches of “frosted” looking retina in the periphery
May exhibit “holes” within the lesions

223
Q

How is snailtrack degeneration different than lattice degeneration?

A

Snailtrack is usually longer than those seen in lattice

Snailtrack has overlying vitreous liquification (like lattice), but without strong vitreoretinal attachments

224
Q

Management of snailtrack degeneration

A

Without retinal breaks does not require Tx or referral
Prophylactic laser may be considered in specific limited circumstances (rare)
Monitor pt’s regularly
Advise pt’s of symptoms of RD and need for immediate care if such occurs

225
Q

White With and Without Pressure

A

Describes the whitish opaque appearance of islands of peripheral retina that are attached more strongly to the cortical gel than normal

226
Q

When is white with pressure only observed?

A

In Scleral indentation

227
Q

White without pressure is ____.

A

Constant

228
Q

Management of white without pressure

A

Common ancillary finding during routine DFE of asymptomatic pt’s
Rarely causes problems, but giant retinal tears have been known to occur at posterior border
Document and educate pt about symptoms of RD

229
Q

Retinal tuft

A

Small area of retinal elevation occurring where focal vitreous traction “pulls up” the retina

230
Q

Who do you find has retinal tuft?

A

Very common (found in most adult eyes)

231
Q

Small, light-colored, raised area of retina (may be pigmented at base), usually an incidental finding with no symptoms, and does not require treatment

A

Retinal tuft

232
Q

Diffuse chorioretinal atrophy

A

Chorioretinal atrophy often seen in the equatorial region of highly myopic eyes (6 diopters or higher)

233
Q

What does diffuse chorioretinal atrophy represent?

A

Thinning of choroid/retina
Holes may form within the atrophied retina, leading to RD (holes often difficult to see due to lack of contrast b/w retinal and choroid)

234
Q

The following degenerations occur more frequently in myopia:

A

Lattice degeneration
Snailtrack degeneration
Diffuse chorioretinal atrophy
Macular holes

235
Q

The following processes also contribute to increased RD with myopia:

A

Vitreous degeneration with myopia
PVD earlier with myopia
Cataract treatment with RD in myopic pt’s (cataract surgery with vitreous loss and laser posterior capsulotomy)

236
Q

If a pt is a -6D or greater, what do you want to watch for?

A

Monitor closer b/c they are more prone to retinal detachment/posterior vitreous detachment

237
Q

Myopic pt’s should be informed of the risk and symptoms of what?

A

Retinal detachment

238
Q

Pt’s with high myopia should have periodic dilated fundus exams to check for what?

A

Periodic DFE’s to check for asymptomatic retinal breaks and detachments

239
Q

Peripheral retinal degeneration conditions which do not lead to RD

A

Microcystic degeneration
Pavingstone degeneration
Reticular pigmentary degeneration
Peripheral drusen

240
Q

Peripheral retinal degeneration conditions which may lead to retinal detachments

A

Lattice degeneration
Snailtrack degeneration
“White with and without pressure”
Diffuse chorioretinal atrophy

Block 15 (4 decks)

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