Download Fordyce, S - American Academy of Optometry

Samantha Fordyce
ICO Pediatrics/Binocular Vision Resident
American Academy of Optometry Resident’s Day Submission
Neovascular Glaucoma with Prominent Iris Bombe Status-Post Funnel Retinal Detachment
Abstract – This case represents chronic iris neovascularization status-post funnel retinal
detachment in a 22-year-old male, resulting in angle closure secondary to posterior synchiae
and prominent iris bombe. Evisceration recommended preventing future phthisis bulbi.
I. Case History
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22yo African American Male
CC: red eye, discomfort, photophobia, and occasional headaches x 1-2 months OD
POHx: CRET since birth, EOM surgery as a child, degenerative myopia OD, retinal
detachment longstanding 4 years prior, (-) trauma
PMHx: No medical history, (-) Diabetes, (-) Hypertension, (-) automimmune disorders
Medications: None
Patient reports vision has been reduced OD for >1 year.
II. Pertinent findings
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Initial Exam (7/30/15):
o VA sc
 OD: Light Perception, NIPH
 OS: 20/40 PH:20/25
o EOMs: Restricted abduction OD, FROM OS
o Slit Lamp Findings:
 1+ injection OD
 Diffuse corneal edema with superficial punctate keratitis OD
 Angle: Grade 0, closed 360 degrees
 AC: possible cell/flare
 Iris: Significant NVI, Posterior synechiae 360 degrees, Prominent iris
bombe
 Lens: opacified nuclear sclerosis, no red reflex present
o IOP:
 OD: 26
 OS: 18
o DFE:
 OD: not visible, B-scan performed
 OS: within normal limits, (-) vitritis, (-) neovascularization, temporal ONH
pallor.
o B-scan, Anterior segment OCT, and slit lamp photos taken
Follow-up Exam (7/31/15):
o VA sc
 OD: Light Perception, NIPH
 OS: 20/40, PH: 20/25
o EOMs: restricted abduction OD, FROM OS
o Slit Lamp Findings:
 1+ injection OD
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Retinal
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Diffuse corneal edema with superficial punctate keratitis OD
Angle: Grade 0, closed 360 degrees
AC: 1+ cell/flare
Iris: Significant NVI, Posterior synechiae 360 degrees, Prominent iris
bombe
Lens: opacified nuclear sclerosis, no red reflex present
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IOP:
 OD: 17
 OS: 18
Specialist Appointment (Patient feeling discomfort again):
VA sc:
 OD: NLP
 OS: 20/40, PH: 20/25
EOMs: restricted abduction OD, FROM OS
Slit Lamp Findings:
 Mild chemosis, 1+ Injection OD
 Mild diffuse edema
 Angle: Grade 0, closed 360 degrees, iris bombe, fibroblastic membrane
in angle
 AC: possible flare
 Iris: Significant NVI, Posterior synechiae 360 degrees, Prominent iris
bombe
 Lens: yellowing
IOP:
 OD: 34
 OS: 17
No view of fundus
B-scan analysis: funnel retinal detachment with possible vitreous hemorrhage OD
III. Differential diagnosis
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Primary: Neovascular Glaucoma
Others: Chronic Angle Closure Glaucoma, Acute Angle Closure Glaucoma, Inflammatory
Glaucoma, Uveitis/Panuveitis
IV. Diagnosis and discussion
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Neovascular Glaucoma
o Retinal ischemia causes the release of VEGF, causing the growth of new, leaky
blood vessels. These leaky blood vessels travel from the retina forward through
the pupil, onto the iris and into the angle.
o Due to the neovascularization of the angle, fibroblastic membranes form and
block the trabecular meshwork.
o Most common causes: diabetic retinopathy, central retinal vein occlusion, and
branch retinal vein occlusion.
o Other possible causes: ocular ischemic syndrome, tumors, chronic inflammation,
chronic retinal detachment, and radiation therapy.
o Signs:
 Possible mild anterior chamber cells and flare due to leaky blood vessels
(neovascularization)
 Conjunctival Injection
 Corneal Edema with acute IOP increase
 Hyphema
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Unique
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 Eversion of pupillary margin
The most important is to identify the cause of neovascularization and start
treating immediately.
Even with IOP control, studies have shown 3-48% will still lose light perception.
Stages of Neovascular Glaucoma:
 Stage 1: NVI present, no angle closure, no elevated IOP
 Stage 2: NVA, elevated pressure, decreased vision
Treatment Options:
 Anti-VEGF injections, usually Lucentis or Avastin, or PRP to help blood
vessels retract and stop growing.
 IOP lowering drops or orals
 Trabeculectomy or glaucoma drainage implant
 Topical steroid to decrease inflammation
 In severe cases (vision is already lost) cyclodestructive procedure is an
option
 Evisceration/Enucleation
Features:
Dense cataract OD did not allow for a posterior pole view, therefore the
conclusion of the cause of NVI is unknown. Due to the patient’s eye history and
B-scan performed at initial exam, it is likely due to a chronic funnel retinal
detachment more than 4 years ago.
NVI can cause mild anterior chamber cells and flare. Due to longstanding and
prominent NVI, cell/flare eventually caused 360 posterior synechiae and resulted
in significant iris bombe and angle closure.
At initial exam, same-day Laser Peripheral Iridotomy (LPI) was considered, but
due to the amount of NVI and prominence of blood vessels, it could not be
performed due to risk of causing hyphema. The same was decided for breaking
the posterior synechiae, it likely would have resulted in a hemorrhage/hyphema.
Also, an LPI is contraindicated because it is uncertain what is going on behind
the iris, there could be a hemorrhage, the retinal detachment or choroid could be
pushing on the iris, etc.
To maintain patient comfort, IOP lowering drops were prescribed and the patient
was monitored until referral appointment to analyze the cause of NVI and
treatment plan could be devised.
 At retinal specialist appointment, IOP had increased to 34.
To ensure the patient did not have a systemic autoimmune disorder such as
sarcoidosis causing inflammation and NVI, OS was dilated and examined. No
signs were found.
Patient was not in significant pain or discomfort and vision had been decreased
to count fingers from retinal detachment 4 years prior, so the main treatment
plan was to maintain patient comfort until referral appointment.
 At retinal specialist appointment, patient was NLP. Retinal specialist
recommended evisceration to prevent phthisis bulbi.
 If patient had visual potential or was light perception, would consider
anti-VEGF injection, glaucoma shunt implant, and retinal surgery.
V. Treatment, management
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Most important in this case was patient comfort.
o IOP lowering drops: Combigan TID OD
o Refer to retinal specialist for evaluation of NVI
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Retinal
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Follow-up: 1 day for IOP check
 IOP decreased to 17, patient felt more comfortable and in less pain. Slit
lamp findings did not change.
 Continue Combigan BID OD until retinal specialist appointment in 1
week.
Specialist Appointment:
Combigan BID OD, Cyclopentolate BID OD, and Pred Forte BID OD to help
improve symptoms
Recommend evisceration OD, referral to oculoplastic surgeon to prevent further
progression of phthisis bulbi and improve cosmesis
Monitor OS annually
VI. Conclusion
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Pathogenesis: Retinal ischemia causes the release of vascular endothelial growth factor
(VEGF), causing the growth of new, leaky blood vessels. These leaky blood vessels travel
from the retina forward through the pupil, onto the iris and into the angle. The blood
vessels as well as the fibroblastic membranes form and block the trabecular meshwork.
Most importantly, identify the cause of neovascularization and start treating immediately,
such as anti-VEGF injections or PRP.
Even with IOP control, 3-48% will still lose light perception.
If no light perception or no visual potential of the eye, evisceration/enucleation
recommended preventing phthisis bulbi and improving cosmesis.
VII. References
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Every, S. Molteno A. Bevin, T. Herbison, P. “Long-term Results of Molteno Implant
Insertion in Cases of Neovascular Glaucoma.” Archives of Ophthalmology. 2006; 124 (3):
355-360.
Huang, A. “Preserving Vision in Neovascular Glaucoma: To effectively manage this
disease, be sure to address the underlying causes, not just the elevated pressure.”
Review of Ophthalmolgy. 2015 Jan; 56-58.
Gerstenblith, A. Rabinowitz, M. The Will’s Eye Manual: Office and Emergency Room
Diagnosis and Treatment of Eye Disease. Sixth Edition. City: Lippincott Williams &
Wilkins, 2012. 230-232. Print.
Mermoud, A. Salmon, JF. Alexander, P. Straker, C. Murray, AD. “Molteno tube
implantation for neovascular glaucoma. Long-term results and factors influencing the
outcome.” Ophthalmology. 1993 Jun;100(6)897-902.