Primary Open Angle Glaucoma (POAG)

Primary Open Angle Glaucoma (POAG)
SYMPTOMS Typically asymptomatic
In the later or more advanced stages, 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
SIGNS Typically bilateral but asymmetric
Open angles on Van Herick with no signs of secondary glaucomas
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
WORK-UP Pupils (typically normal but can present with a decrease in light response if glaucoma is advanced or an APD if glaucoma is asymmetric), Color vision (typically normal), Slit lamp examination, IOP with GAT or ORA (elevated unless if normal tension glaucoma), Dilated retinal exam, 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), Gonioscopy (angles should be open with no anomalies), 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)
TREATMENT First-line of treatment would be a topical prostaglandin to be used 1 gtt QHS
If adjunct drop needed, consider a topical carbonic anhydrase inhibitor to be used 1 gtt BID
Rhopressa should be considered as the next adjunct drop to be used 1 gtt QHS
Alpha-2-agonists should be considered as the next adjunct drop to be used 1 gtt BID
Topical beta blockers should be considered as the next adjunct drop to be used 1 gtt once a day in the morning up to BID (the evening dose is thought to be minimally effective)
Consider using combo drops in order further lower IOP and improve compliance especially if patient is on multiple drops: Cosopt 1 gtt BID, Combigan 1 gtt BID, Simbrinza 1 gtt TID, Rocklatan 1 gtt QHS
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
Always keep in mind the contraindications and side effects before prescribing any glaucoma medications
SLT may be used as a first-line of treatment in lieu of glaucoma drops or as an adjunct treatment along with glaucoma drops
If using more than 2 different types of glaucoma drops in order to manage patient, co-management with a glaucoma specialist should be considered
If using more than 3 different types of glaucoma drops, refer to glaucoma specialist for co-management
Patients with advanced, severe, or end stage glaucoma should be co-managed with a glaucoma specialist as further intervention such as blebs, MIGs, or shunts may be needed
FOLLOW-UP Patients should be seen back in 2-4 weeks after initiation of treatment in order to assess IOP (SLT and prostaglandins typically show maximal effectiveness at 4 weeks)
After the initial assessment of IOP with treatment, patients are typically seen back every 3-4 months for glaucoma testing in order to look for progression
ADDITIONAL LAB | TESTS Typically additional lab testing is not needed
If suspecting a neurologic condition (especially if glaucoma is rapidly progressing despite good IOP control or if amount of rim tissue pallor exceeds cupping), the following should be ordered: MRI of the brain and orbits with and without contrast
If suspecting ocular perfusion issues (especially with cases of normal tension glaucoma), the following should be ordered: CBC with differential, PT/TT/BT/PTT/INR, Fasting blood sugar, HbA1c, Blood pressure evaluation, Sleep study, Carotid duplex, Cardiac evaluation
ETIOLOGY Mulifactorial but essentially elevated IOP increases strain and pressure on the optic nerve which ultimately leads to damage on a cellular level. Perfusion to the optic nerve also plays a significant role
DIFFERENTIAL DX Ocular hypertension, Secondary open angle glaucoma, Angle closure glaucoma, Optic atrophy, Optic nerve drusen, Optic nerve pit, Optic nerve coloboma
NOTES A family history of glaucoma, especially on the maternal side, increases the risk of primary open angle glaucoma
Myopia is a risk factor for primary open angle glaucoma
A stage of pre-perimetric glaucoma indicates that the patient has evidence of glaucomatous optic nerve damage but no glaucomatous visual field loss
OCTs tend to be more valuable in pre-perimetric, early, or moderate glaucoma cases but become less valuable as the glaucoma becomes more severe or advanced
Normal tension glaucoma is now considered a subset of primary open angle glaucoma (by definition, IOP is 21 mmHg or less). Patients with normal tension glaucoma are more likely to have focal notching on the optic nerve, drance hemes, and paracentral scotomas
Primary Open Angle Glaucoma (POAG): OCT of a patient with primary open angle glaucoma showing ganglion cell and retinal nerve fiber thinning