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William D. Townsend, OD, FAAO
Advanced Eye Care, Canyon, TX
Adjunct Professor, UHCO
During clinic, I initially note a few small
floaters that I had never noticed before
No flashes of light
No vision changes
I mentioned this to my extern, Juan
Menjivar, who wants to dilate me and
examine my peripheral retinas
I decline; it was a busy week
My mother was in the hospital- almost died
We had a bank stockholders meeting
I had to get ready to speak in Canada
I knew there wasn’t a problem: I am bullet proof
I am speaking to the New Brunswick
Association of Optometrists
Lectures are going great
The audience is very interactive
It is a perfect spring day in a beautiful,
historic Canadian city
I get to hang out with my friend, Dr. Diana
Shechtman who is speaking on retina
Things could not be better!
I start off the day in the gym with a 7 am
workout
Next, I work on today’s lecture to finalize
the content and add new information
As I work, I notice a small dark spot in my
OD lower temporal field
What the heck, I plunge on
Hit in the right eye with a tennis ball
Within a year, I noted my vision in that eye
was not as quite as bright
Over the years, the trend continued
Why? A progressive traumatic NS cataract
10 May 2007, successful cataract surgery
with implantation of Alcon Toric IOL
BVA without correction = 20/15
I tell Diana about my “spot” and express
concern; she calls me a hypochondriac
1:00 pm- I start my lecture, “Pain
Management”
As I speak, I note that the grey spot is
rapidly expanding upward reducing my
field in the inferior field. I run into things as I
deliver the lecture
Otherwise normal eyes- 5 in 100,000 per
year
Middle age & elderly eyes-20 in 100,000
per year
Highly myopic eyes- 5,000 in 100,000
Highly myopic eyes after cataract
surgery- 7%
The majority of retinal detachments are
rhegmatogenous (tear-induced).
Virtually all retinal tears are caused by
interaction between vitreous and retina.
Anatomical variations in the vitreous-retinal
relationship often lead to retinal tears
1.
2.
3.
4.
5.
Macula
Optic nerve
Ora serrata
Vitreous base
General vitreous-retina interface
Vitreous base
strongest
Optic nerve
Macula
Blood vessels
Vitreous-retinal interface
weakest
Peripheral senile pigment degeneration
Cystoid retinal degeneration
Oral pearls
Cobblestone (pavingstone)
degeneration
Non-cystic retinal tufts
Congenital RPE hyperplasia
Retinal white without pressure
Appearance- Peripheral areas of "'salt &
pepper" hyper-hypo pigmentation;
reticular form has net-like appearance
Histology- RPE degeneration w/
migration of pigment
Occurrence- 20% of population over 40
years of age
Risk- None
Differential- Retinitis pigmentosa
Management- None
Occurrence- 27% of adult autopsy
eyes, bilateral 38% of cases,
increases w/ age, inferior location
most common, high myopes
Risk- In retinal detachment, retina
may tear at border of lesion
Differential- Chorioretinal scars
Mgt- None
Degenerated glial tissue
Vitreous traction invariably present
Risk for tear depends on
Location
Size
Degree of traction present
Cystic: occur posterior to vitreous base
Non-cystic: occur within vitreous base
Appearance- small, thin projections of tissue
that appear as grey-white dots close to ora
Histology- composed of altered retinal tissue,
degenerated glial tissue; base diameter
usually less than .1 mm
Occurrence- 72% of adults and bilateral in
50% of cases; vast majority are intrabasal
Risk- low to none - small size and intrabasal
location
Differential- none
Management- none; rarely, small benign
holes are noted at their base
Appearance- flat, round pigmented lesions,
usually black or dark grey, distinct borders
Size- varies from small to several disc diameters.
May have a surrounding area of decreased
pigmentation (halo).
Histology- congenital hypertrophy of RPE; cells
have larger than normal melanin granules;.
Occurrence- unknown; unilateral in 85% of
cases
Risk- none
Differential- nevus, melanoma
Management- rule out traction as in cystic tufts,
otherwise none
Appearance- flat, round pigmented
lesions, usually black or dark grey,
distinct borders
Size- varies from small to several disc
diameters.
Histology- acquired (hyperplasia)
increased number of RPE cells
May occur at site of vitreoretinal traction
Unknown- unilateral in 85% of cases
Risk- none
Differential- nevus, melanoma, assess for
vitreoretinal traction
Enclosed ora bays
Meridional folds
Cystic retinal tufts
Zonular traction tufts
Acquired peripheral retinoschisis
Typical
Reticular
Atrophic retinal holes
Operculated retinal breaks
Lattice retinal degeneration
Appearance- grey nodules of varying size,
usually extrabasal
Histology- degenerated, proliferated cystic
tissue with some degree of vitreous traction
0.1 to 1 mm diam.
Occurrence- 6% of patients
Risk- varies depending on source
Byer: 10% of all retinal detachment caused by
CRT
Foos: CRT cause 82% of opercula, 97% of tears
Management: scleral indentation, patient
education, yearly DFE
Do not underestimate the potential damage!
Appearance- Usually round,
occasionally elongated red areas
in peripheral retina,
Often w/ cuff of subretinal fluid and
subclinical detachment (30%)
Opercula are almost universally seen
in adjacent vitreous
Pigment surround common
Histology- Full thickness break in
retina.
Caused by traction on CRT, or area
of abnormal vitreoretinal traction
Occurrence- 13.4% of retinal breaks, increased
in frequency w/ age, most common
extrabasal; 80% associated w/ PVD.
Large operculated breaks associated w/ lattice
degeneration & PVD are rare.
Reportedly associated w/ WWP & WWOP
Risk- Slight, increases w/ size
Differential- Atrophic hole, retinal hemorrhage,
flap tear
Management- If old, asymptomatic, patient
education, yearly DFE
If fresh, or symptomatic, patient education, 6 week
DFE.
If subclinical detachment > 2 dd, refer.
Occurs in two forms, typical and
reticular
Caused by splitting of sensory retina
Found in 4% of general population & 7%
of population over 40 years of age
Round or ovoid in shape,
Always associated w/ cystoid
degeneration; advanced stage of same
process
Bullous lesions more prone to progression
or detachment
Causes absolute scotoma
Appearance- Round or ovoid
shape w/ inner & outer layers
separated by fluid.
Details of choroidal vasculature are
obscured
White dots on inner surface (70%) of
lesions.
Inner layer smooth, has white dots on
inner surface (70% of lesions)
Outer layer has moth-eaten,
pockmarked appearance. Inner or
outer layer holes occasionally seen.
Histology- Splitting of neurosensory retina
in region of outer plexiform layer
Inner layer is relatively thick & smooth in
appearance. Supporting elements or pillars
between layers at margins of lesions.
Occurrence- found in .69% of eyes,
Bilateral in 33%-64% of cases, most common
inferior temporal quadrant (70%-82%),
some studies indicate more prevalent in
hyperopes.
Always associated w/ cystoid degeneration;
increases w/ age
Appearance- Round or ovoid
shape w/ inner & outer layers
separated by fluid.
Details of choroidal vasculature are
obscured; inner layer thinner than in
typical form.
White dots and an arborizing pattern
of white lines in inner layer; outer layer
has moth-eaten, pockmarked
appearance.
Inner or outer layer hole more
common.
Histology- Splitting of neurosensory retina
in region of internal limiting membrane;
inner layer is relatively thin & smooth in
appearance. Supporting elements or
pillars between layers at margins of
lesions.
Occurrence- 0.95% of eyes, bilateral in
15.8% of cases: found in 1.62% of
patients.
Most common in inferior temporal quadrant;
vast majority of lesions in temporal
quadrants.
Outer layer holes in 22.7% of eyes. ; increases
w/ age
Risk
More prone to progress past equator than
typical form
More prone to cause retinal detachment,
especially when outer layer holes are present
Greatest risk is when outer and inner layer
holes co-exist in same lesion
Appearance- small (<.5 dd) round red
areas in peripheral retina, often w/
surrounding cuff of fluid and subclinical
detachment
Histology- full thickness break in retina.
Occurrence- 76% of all retinal breaks,
occur in 2.4%of eyes, 4% of cases, 76%
found w/in lattice lesions, associated w/
meridional folds, ZTT, CRT; increased in
myopes, 80% have associated
subclinical detachment
Risk- minimal; 7% lead to clinical
detachment
Differential- tractional tear, retinal
hemorrhage; scleral depression
Management- document, yearly DFE,
refer if clinical detachment > 2 dd
noted
Appearance- red, U-shaped lesion w/
"horse running toward the posterior pole”
Cystic retinal tuft may be seen at end of flap;
25% < 1/4 dd in size
Histology- full thickness retinal break w/
attached flap of retina having traction from
vitreous on apex of the flap
Occurrence- 10% of all retinal breaks
Frequently symptomatic due to traction.
Often found at posterior border of lattice, scars,
CRT, enclosed ora bays, chorioretinal scars
81% occur in individuals over 40 years of age
50% in superior nasal quadrant.
Risk - moderate to high because of the continuing
presence of traction.
Differential- atrophic hole, operculated tear,
hemorrhage
Management- Small (< 1/4 dd) and asymptomatic:
patient education & 4 week DFE, Larger (> 1/4 dd)
or symptomatic, especially if superior, or Hx
detachment fellow eye: refer
Appearance
Varies widely; usually parallels the ora
White lines- 12%-15%
Atrophic holes- 18%-43%
Pigment- 83%
White spots- 80%
Histology- thinned area of peripheral
retina with overlying lacunae of
liquified vitreous, vitreous traction on
margins,especially posterior
Occurrence: 8%-11% of individuals
Increased in myopic eyes
Most common @ 12 o’clock & 6 o’clock
Risk
0.5% chance for detachment
30% of all detachments associated with
lattice
Greatest risk is large horseshoe tears
Differential: pavingstone, retinal dialysis,
scleral indentation is essential
Management:
Observe w/ annual DFE
Educate on signs & symptoms
Refer if breaks at margin are discovered
Examine parents, siblings
My macula is still on, but the detachment is
progressing quickly
In New Brunswick and neighboring Nova
Scotia - one surgical retinologist
He is out of the country on vacation
My options
Fly home- it will take too long
Get across the border to US health care
With Lil and Dwight at the helm, I head fo
the border
Our local retinal specialist back in Texas,
Dr. Eddie Ysasaga arranges for me to see
a retinal specialist in Portland, Maine the
next morning
Dr. Lil Linton and her husband Dwight drive
me 300 miles to Portland while I lie face
down in the back seat
Portland retinal surgeon Dr. Fred Miller has
made reservations for us at the La Quinta
across the street from his office
Sometimes ignorance is bliss
Macula on detachments have much better
prognosis- therefore an ocular emergency
I could tell from my vision that the detachment
was getting close to fixation
I knew exactly what was happening
Fear- what will I do if I lose my vision
Second guessing- I should have let Juan
dilate me
I am going to go through this without the
physical presence of family or friends
I pray a lot
7:00 am- Dr. Fred Miller is waiting at his
office- he has already contacted the
surgery center & has people in place
He confirms the diagnosis and we
discuss surgical options
We decide to go with a vitrectomy, cryo,
and air bubble- partly at my insistence
He personally drives me to the center
and we prep for surgery
9:00 am- I am ready for surgery and we
head for the OR
I get and IV and some Versed
I am awake, but “happy”
Dr. Miller inserts ports through my pars
plana, and performs a vitrectomy.
He fills my eye with air and cryos the area
around the flap tear
He then performs a retinotomy to allow
fluid under my retina to escape
They close. I can see nothing with my right
eye
Now the waiting begins- I go back to the
La Quinta and sleep
After a night of sleeping with my head
elevated, I awake, walk across the street to
Dr. Miller’s office
The initial findings; CF @ 2 feet, BUT if I hold a
near card close to my eye I can see 20/30
I celebrate with pizza!
My daughter Erin flies in- she will drive me
2300 miles back to Canyon, Texas
The pressure inside a commercial aircraft is
roughly equivalent to an altitude of 6000
feet
Rapid decline in air pressure causes the air
bubble to expand causing high IOP, pain,
vision loss
Even going over a mountain has the same
effects only more gradual
The air bubble usually lasts @ 1 week
Final check up with Dr. Miller looks good.
My retina is flat, no infection.
We hit the road
Along the way, I begin to watch the
bubble recede- I can read signs in my
upper field.
1 May 2008 we arrive in Canyon
The local retinal surgeon examines me the
following day and is concerned
He tells me to be still and limit activity
I am back at work on a limited schedule
2:00 pm- as I examine my patient, I note a
grey spot in my superior field and it makes
me nervous It is déjà vu from the opposite direction
2:30 pm- Dr. Janet Townsend informs me
that now my right inferior retina is
beginning to detach
The retinal specialist confirms her findings
and we schedule surgery for the next day
Pavingstone degeneration is common in
high myopes
It is innocuous unless the individual has a
retinal detachment
Pavingstone then becomes a potential site
for multiple tears to occur
I had seven tears
This time the bottom half of my retina is
detached
7:00 am- this time the procedure will be
much more invasive
Dr. Antonio Aragon inserts ports through
the pars plana
He fills my eye with air 83% air and 17%
C3F8, (octafluoropropane) the longest
residing gas used in retinal surgery.
Other options include air and SF6
Air- Cheap, only good in certain cases
Short residence time (@ 1 week)
May not be adequate for some cases
Require longer tamponade
SF 6 (sulfur hexafluoride)
Medium residence time (@ 2-3 weeks)
C3 F8 (octafluoropropane)
Long residence time (@ 6-8 weeks)
Longer duration reduces likelihood of
failure, redetachment
Dr. Aragon positions a silicone band
around my peripheral retina and tightens
it to bring it in contact with RPE
He then lasers the areas around the tears
and closes; we are finished!
I am now to lie face down for the next ten
days
This is no way to spend your birthday!
The initial post op report is good- I can see
some print if I hold it close
I wear a shield at all times, only removing it
to instill Vigamox, Omnipred, and Nevanac
Ten days later, I can only see hand motion
and my eye hurts, but I can discontinue
positioning face down
I am back at work, but can only see with one
eye.
Any procedure that requires binocular vision
goes to my associates
The bubble is regressing and I can see in my
superior field
Dr. Aragon is concerned; my eye is very
inflamed
The drops continue
The gas bubble is gone
I am now myopic, but with correction I am
20/20
But
My eye is still inflamed, with significant cells and
flare
My pressures are going up because I use
steroids every other hour.
I now know what it is like to need steroids,
but to be a steroid responder
My inflammation still persists, but is
beginning to decrease
I am on three meds for IOP, but my
pressure spikes as high as 51 mm Hg
I see halos around lights
I get discouraged
We increase the Nevanac and taper the
steroid
I am finally off all steroids
There is no flare, shaking my head results in
an amazing display of cells
Leukocytes still reside in my anterior
chamber blocking outflow.
I take my meds; the IOP is < 30 mm Hg
OCT of my nerve looks good
I continue Combigan Q 12 hours & Azopt Q
8 hours
Moderate NS OS
Pseudophakia OD with 20/20+ vision
No inflammation
No medications
I am blessed!
I appreciate vision more than ever before
I appreciate what we as optometrists do
more than ever
Know the risk factors for retinal tears &
detachment
Know how to recognize and manage
peripheral retinal conditions that pose a risk
of retinal tears, detachment
Take good care of your own eyes
THANK YOU