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Cases
Intraocular Worm
Intraocular Lymphoma
Malignant Hypertension and
the Retina
Chronic traumatic macular hole
Central Areolar Choroidal Dystrophy
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INTERESTING CLINICAL CASES
Intraocular Worm
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Figure 1: Upon presentation
VA: Count fingers 4 feet |
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Figure 2: Ultrasound of worm |
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Figure 3: Post-Op
VA: 20/25 |
This case has to be my all time favorite. A 25 year old
young man presented with 3 weeks of decreased vision. His
visual acuity was count fingers, and he complained of a
“worm coming across my vision”. In truth he was absolutely
correct! As illustrated in figure 1, there was a large 7mm
mobile cysticercosis cyst within the vitreous. An ultrasound
(figure 2) shows the circular cyst wall with the body of
the worm inside. I performed a vitrectomy surgery with a
scleral buckle, and removed the cyst whole. As shown in
the postoperative photo (figure 3), the worm left significant
areas of scarring superior to the macula which resulted
in some traction on the fovea. However, as his inflammation
subsided, his vision steadily improved to 20/25. More fortunate
still, he did not have any evidence of systemic disease
from this parasitic infection, and therefore has made a
full recovery.
Intraocular Lymphoma
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Figure 1 |
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Figure 2 |
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Figure 3 |
This is a fascinating case that presented to us with a previous
diagnosis of wet AMD. The patient was a 59 year old female
who had been receiving Avastin injections in her right eye
for wet AMD. (See Figure 1, and the OCT of the lesion in
Figure 2) However, on examination she was found to have
marked vitreous cell in both eyes, as well as subtle areas
of subretinal/choroidal infiltration in the mid-periphery.
We were unhappy with the previous diagnosis and decided
to perform a vitrectomy with vitreous biopsy based on the
exam. The pathology of the vitreous aspirate (Figure 3)
showed Large B Cell lymphoma. The patient was begun on intravitreal
methotrexate injections, and with the help of systemic treatment
from an oncologist, her vision improved from 20/200 to 20/25
in her left eye.
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Malignant Hypertension and the Retina
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Figure 1 |
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Figure 2 |
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Figure 3 |
Like most interesting cases, this patient was referred to
our office at 6PM on a Friday. The patient was a 37 year
old male visiting Los Angeles on vacation, who had noticed
decreasing vision, associated with changes in his color
perception, in both eyes over the last week. His vision
on examination was 20/200 OD and 20/150 OS. He denied any
known systemic medical conditions and was not taking any
medications. On dilated exam (Figures 1 and 3) he had optic
nerve edema, hard exudates tracking along Henle’s
layer, and flame hemorrhages. Cirrus OCT analysis revealed
a serous retinal detachment in his right eye (Figure 2)
As part of our routine workup of every new patient we check
blood pressure, and in his case it was 208/155! This very
quickly solved our diagnostic dilemma as this was clearly
Stage IV Hypertensive Retinopathy. He was immediately referred
to a local ED and from there admitted to the ICU where he
stayed for two days in order to safely bring down his blood
pressure.
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Chronic traumatic macular hole
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Figure 1 |
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Figure 2 |
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Figure 3 |
This patient was a 65 year old female with a history of
blunt trauma to her left eye over 40 years ago. Her vision
on examination was 20/20 OD and 20/400 OS. She reported
being punched in her left eye as a young woman with chronic
decreased vision in that eye ever since. On dilated exam
(Figure 1) she had a large macular hole with a cuff of subretinal
fluid. Temporal to this macular hole was a chorioretinal
scar running concentric to the optic nerve, and likely representing
an old choroidal rupture. Cirrus OCT analysis (Figures 2
and 3) illustrated wonderfully the macular hole and surrounding
detachment in this left eye. Fine crystals were visible
in the area of detached retina further indicating the chronic
nature of these changes. Unfortunately given the length
of time from the original injury, and the chorioretinal
scar underlying the fovea, this macular hole was not a good
candidate for surgical repair.
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Central Areolar Choroidal Dystrophy (CACD)
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Figure 1: OD Fundus Photo |
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Figure 2 |
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Figure 3: OS Fundus Photo |
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Figure A: Early CACD |
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Figure B: Mid CACD |
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Figure C: Late CACD |
This 50 year old white female has been losing vision in
both eyes over the last 10 years and gone undiagnosed. She
presented to our clinic with complaints of decreasing vision.
Her visual acuity was hand motions bilaterally. During the
history it was discovered that she had less than normal
vision (20/60 range) since early childhood. She had strabismus
surgery in the right eye in childhood. Throughout her early
to mid adult years, the patient was told that she had idiopathic
scar tissue on the retina. Color plate, amsler grid and
confrontation visual fields were unable to be performed.
She had sensory rotatory nystagmus and eccentric fixation.
Upon fundus examination, it was noted that the patient had
bilateral central macular atrophy (Figures 1 and 3). OCT
scans revealed bilateral thinning of both the retina and
choroid with non-existent retina where the fovea should
be (Figure 2). Central Areolar Choroidal Dystrophy (CACD)
is hard to diagnose in early stages since patients in this
stage usually have near normal visual acuity and non-specific
granular hyperpigmentation of the fovea, which has a myriad
of differential diagnoses (Figure A, from Ryan’s Retina,
4th edition, 2006). As CACD slowly progresses throughout
the fourth and fifth decade of life, visual acuity starts
to decrease and the area of hyperpigmentation becomes larger
(Figure B, from Ryan’s Retina, 4th edition, 2006).
In the later stages of CACD, the lesions that the patient
presented with are typical and at this stage, central visual
acuity is typically 20/200 or below (Figure C, from Ryan’s
Retina, 4th edition, 2006). Unfortunately, there is no known
cure for CACD at this time. The patient will undergo genotyping
for possible gene therapy and for genetic counseling.
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