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Glaucoma, Primary Open-Angle

BASICS

  • Chronic, progressive optic neuropathy with optic nerve rim and RNFL loss.
  • Associated with increased IOP, but can occur with normal IOP.
  • Normal IOP range: 10-21 mm Hg.
  • Early disease difficult to detect due to preserved central vision.

PREGNANCY CONSIDERATIONS

  • Avoid prostaglandin analogues during pregnancy.

EPIDEMIOLOGY

  • Prevalence in adults >40 years: ~3.5%.
  • Second leading cause of blindness in US.
  • Leading cause of blindness in African descent populations.

ETIOLOGY AND PATHOPHYSIOLOGY

  • Aqueous humor produced by ciliary epithelium in posterior chamber.
  • Flows through pupil to anterior chamber, drains via trabecular meshwork (TM) into Schlemm canal, then episcleral veins.
  • 5-10% drains via uveoscleral pathway.
  • IOP depends on balance between production and outflow; impaired TM outflow causes elevated IOP.
  • IOP fluctuates diurnally and with BP, respirations.
  • Elevated IOP damages optic nerve causing vision loss, starting peripherally.

GENETICS

  • TMCO1 genotype linked to glaucoma risk in non-Hispanic whites.
  • MYOC gene first associated with POAG.

RISK FACTORS

  • Myopia
  • Diabetes mellitus, hypothyroidism, hypertension
  • African descent
  • Family history of glaucoma
  • Prolonged corticosteroid use
  • Systemic calcium channel blockers
  • High coffee intake
  • Prior pars plana vitrectomy
  • Obstructive sleep apnea

GENERAL PREVENTION

  • Diet high in nitrates and green leafy vegetables linked to lower POAG risk, possibly via nitric oxide effects on circulation.

DIAGNOSIS

HISTORY

  • Painless, slowly progressive visual loss, usually unnoticed until late.
  • Central vision preserved until advanced.

PHYSICAL EXAM

  • Visual acuity and field testing essential.
  • Ophthalmoscopy shows optic nerve cupping.
  • Tonometry measures IOP, may be normal or elevated.
  • Cup-to-disc ratio (CDR) >0.5 suspicious (ISNT rule: inferior β‰₯ superior β‰₯ nasal β‰₯ temporal).
  • Early visual field defects: paracentral scotomas, nasal steps.

DIFFERENTIAL DIAGNOSIS

  • Normal-tension glaucoma
  • Optic nerve pits
  • Anterior ischemic optic neuropathy
  • Compressive optic neuropathy

DIAGNOSTIC TESTS

  • Optical coherence tomography (OCT): detects RNFL thinning.
  • OCT angiography (OCTA): shows decreased macular vessel density correlating with progression.
  • Visual field perimetry to assess functional loss.
  • Tonometry: assess IOP, consider corneal thickness influence.

TREATMENT

GENERAL MEASURES

  • Early treatment delays progression.
  • Target IOP reduction critical to slow damage.

MEDICATION

  • Multiple agents often required with different mechanisms.
  • Prostaglandin analogues (first line): latanoprost, travoprost, bimatoprost, latanoprostene bunod.
  • Ξ²-Adrenergic antagonists: timolol, betaxolol (selective safer in lung disease).
  • Ξ±2-Adrenergic agonists: brimonidine (avoid in young children).
  • Carbonic anhydrase inhibitors (oral and topical): acetazolamide, dorzolamide, brinzolamide (avoid in sulfa allergy and cirrhosis).
  • Rho kinase inhibitors: netarsudil (may cause corneal verticillata).
  • Parasympathomimetics (miotics): pilocarpine (can cause eye pain, myopia, iridocyclitis).
  • Hyperosmotic agents (acute): mannitol IV, glycerin oral (caution in diabetics and cardiac patients).

SURGERY/OTHER PROCEDURES

  • Argon laser trabeculoplasty (ALT).
  • Selective laser trabeculoplasty (SLT): as effective as ALT, repeatable.
  • Trabeculectomy: filtering surgery for advanced or refractory cases.
  • Tube shunts (Molteno, Ahmed): for difficult cases.
  • Ciliary body ablation: for poor visual potential or unfit patients.
  • Minimally invasive glaucoma surgery (MIGS): often combined with cataract surgery.
  • Cataract extraction can reduce IOP in ocular hypertension.

ONGOING CARE

FOLLOW-UP

  • Monitor vision and IOP every 3 to 6 months.
  • Optic nerve evaluation 3 to 18 months depending on control.
  • Visual field progression of 2 dB decline in 6 months indicates worsening.

PATIENT EDUCATION

  • POAG is a "silent thief of vision."
  • Emphasize medication compliance to preserve vision.

PROGNOSIS

  • Slow visual field loss with treatment.
  • Vision loss and blindness may still occur despite therapy.
  • Surgical treatment may better preserve macular ganglion cell layer structure.

COMPLICATIONS

  • Blindness

REFERENCES

  1. WuDunn D, Takusagawa HL, Sit AJ, et al. OCT angiography for the diagnosis of glaucoma: a report by the American Academy of Ophthalmology. Ophthalmology. 2021;128(8):1222-1235.
  2. Shin JW, Song MK, Sung KR. Longitudinal macular ganglion cell-inner plexiform layer measurements to detect glaucoma progression in high myopia. Am J Ophthalmol. 2021;223:9-20.

CODES

  • ICD10: H40.1190 Primary open-angle glaucoma, unspecified eye, stage unspecified

CLINICAL PEARLS

  • Painless, slowly progressive visual loss; central vision spared until late.
  • Patients may lose vision even when treated appropriately.
  • Topical/systemic steroids may increase IOP.