Neovascular Glaucoma

Neovascular Glaucoma
SYMPTOMS Typically vision will be decreased as neovascular glaucoma is associated with retinal ischemia, maculopathy, and severe retinopathy
In the later or more advanced stages of neovascular glaucoma, patients may report visual field loss such as scotomas or tunnel vision. If left untreated, complete blindness can occur
If IOP is too high (considered > 40mmHg), patient may experience Ocular pain, Pressure around the eye, Cloudy vision, Nausea, Vomiting, Headache, and Browache (these symptoms are exacerbated if patient develops a secondary angle closure)
SIGNS Secondary open angle glaucoma: Neovascularization of the iris (NVI) and/or Neovascularization of the angle (NVA) with open angles on Van Herick
Secondary angle closure glaucoma: Neovascularization of the iris (NVI) and/or Neovascularization of the angle (NVA) with Shallow anterior chamber, Bowed iris, Narrow angles on Van Herick, Fixed and mid-dilated pupil, Peripheral anterior synechiae, Circumlimbal injection, Corneal edema, Mild uveitis, Iris atrophy
Glaucomatous optic nerve damage (notching, rim tissue thinning, cupping, vessel shelving, vessel bearing, vessel bayonetting), RNFL thinning, Drance hemes, Peripapillary atrophy
With advanced glaucomatous optic nerve damage, Optic nerve pallor will be present
In the presence of NVI and/or NVA, there will also typically be extensive retinopathy, maculopathy, and retinal ischemia
WORK-UP Pupils (typically presents with a decrease in light response due to the presence of ischemia or an APD if glaucoma is asymmetric/ fixed, mid-dilated pupil in the presence of secondary angle closure), Color vision (typically abnormal due to associated retinal ischemia), Slit lamp examination, IOP with GAT or ORA (typically elevated especially in the presence of secondary angle closure where the IOP will typically be 40-80 mmHg), Dilated retinal exam (use caution in the presence of extensive NVI due to increased risk of a hyphema), Post-dilated IOP with GAT or ORA, Fundus photos, Visual field with Humphrey 24-2/30-2/24-2C threshold or 10-2 threshold in more advanced glaucoma (nasal step, arcuate defect, paracentral scotoma, tunnel vision with temporal crescent sparing), OCT analysis of the optic nerve/RNFL/GCL (RNFL and GCL thinning with GCL loss typically preceding RNFL loss), OCT-Angiography (decrease in density of the radial peripapillary capillary plexus and superficial capillary plexus/may also see a decrease in the intermediate and deep capillary plexus, enlargement of the foveal avascular zone, microaneurysms, and neovascularization secondary to associated retinal ischemia and retinopathy), Anterior segment OCT (open angles with fibrovascular proliferation in the presence of secondary open angle glaucoma/ narrow or occluded angles with a shallow anterior chamber, peripheral anterior synechiae, and fibrovascular proliferation in the presence of secondary angle closure glaucoma), Gonioscopy(open angles with associated NVI, NVA, and fibrovascular proliferation in the presence of secondary open angle glaucoma/ narrow or occluded angles with associated peripheral anterior synechiae, NVI, NVA, and fibrovascular proliferation in the presence of secondary angle closure glaucoma ), Pachymetry (thin corneas carry a higher risk of glaucoma), Corneal hysteresis (low hysteresis carries a higher risk of glaucoma), VEP/Pattern ERG (decrease in ganglion cell function), Ultrasound biomicroscopy (open angles with fibrovascular proliferation in the presence of secondary open angle glaucoma/ narrow or occluded angles with a shallow anterior chamber, peripheral anterior synechiae, and fibrovascular proliferation in the presence of secondary angle closure glaucoma)
TREATMENT NVI and/or NVA with normal IOP and no evidence of glaucomatous optic nerve damage: Refer to retinal specialist within 48 hours for anti-VEGF treatment and/or PRP
NVI and/or NVA with elevated IOPs but no evidence of glaucomatous optic nerve damage or with associated secondary open angle glaucoma: Begin treatment. Refer to retinal specialist within 48 hours for anti-VEGF treatment and/or PRP
First-line of treatment would typically be a combo drop which includes Cosopt 1 gtt BID, Combigan 1 gtt BID, or Simbrinza 1 gtt TID
If adjunct drop needed, consider Rhopressa which is to be used 1 gtt QHS
Topical carbonic anhydrase inhibitors to be used 1 gtt BID. alpha-2-agonists to be used 1 gtt BID, and/or topical beta blockers to be used 1 gtt once a day in the morning up to BID (the evening dose is thought to be minimally effective) can be considered as adjunct treatment (as long as class of medication is not currently being used in the first-line combo glaucoma drop)
Topical carbonic anhydrase inhibitors and alpha-2-agonists are to be used 1 gtt TID if utilized as stand-alone therapy
Topical apraclonidine and oral acetazolamide can be given in-office or on a short-term basis to quickly lower IOPs
Prostaglandins, pilocarpine, and Rocklatan (due to prostaglandin component) should be avoided
Always keep in mind the contraindications and side effects before prescribing any glaucoma medications
Patients will most likely need to be co-managed with a glaucoma specialist as further intervention such as blebs, MIGs, or shunts may be needed
NVI and/or NVA with secondary angle closure with or without glaucoma: The goal is to lower the IOP as quickly as possible in office and then refer to a retinal specialist ASAP for anti-VEGF treatment and/or PRP. A glaucoma specialist will most likely be involved as well as patient will need a trabeculectomy and/or shunt
Combigan (may use a separate topical beta blocker and topical alpha-2-agonist)
Cosopt (may use a separate topical beta blocker and topical carbonic anhydrase inhibitor)
Apraclonidine 1%
Pred Forte
Cyclopentolate 1%
Diamox 250mg (2 tablets given in one dose)
Prostaglandins and pilocarpine should be avoided with this type of secondary angle closure
Always keep in mind the contraindications and side effects before prescribing any glaucoma medications
FOLLOW-UP Patient will most likely continue care with a retinal specialist and/or glaucoma specialist
If condition is stable and patient is no longer seeing a retinal specialist and/or glaucoma specialist, the patient should be seen every 2-4 months
ADDITIONAL LAB | TESTS The patient needs to follow-up with their PCP for additional testing if not already done which includes the following: Blood pressure, Fasting blood sugar, HbA1c, Lipid panel, Erythrocyte sedimentation rate (ESR), CBC with differential, Renal function testing, Thrombophilia screening (PT, TT, BT, PTT, INR, Protein C, Protein S, Anticardiolipin antibodies, Factor V), Carotid duplex
ETIOLOGY Typically occurs due to presence of severe retinal ischemia. VEGF diffuses forward to the nearest ocular structure that has viable vasculature
Can also occur due to the presence of anterior segment ischemia
DIFFERENTIAL DX Uveitic glaucoma, Primary angle closure glaucoma
NOTES Neovascularization on the iris typically starts at the pupillary ruff (80% of the time)
The three most common associations with neovascular glaucoma is diabetes, CRVOs, and carotid disease
Neovascular Glaucoma: Secondary angle closure associated with iris/angle neovascularization https://sites.google.com/site/cameronswaby/rubreosisiridis.jpg
Posted in Glaucoma, Ocular Conditions