trabecular meshwork

**Anatomy/location:** Lies in the iridocorneal (anterior chamber) angle, between the peripheral cornea (Schwalbe's line) and the scleral spur/ciliary body. Has three regions from anterior chamber outward: uveal meshwork, corneoscleral meshwork, and juxtacanalicular (cribriform) meshwork, the latter providing the greatest resistance to outflow. Drains into Schlemm's canal.

**Aqueous humor pathway:** Ciliary body epithelium (non-pigmented; produced via carbonic anhydrase and beta-2 receptor-stimulated secretion) → posterior chamber → through pupil → anterior chamber → trabecular meshwork → Schlemm's canal → episcleral veins. About 90% drains by this conventional (pressure-dependent) pathway; ~10% drains via the uveoscleral pathway (through ciliary muscle into suprachoroidal space; pressure-independent).

**Clinical significance:** - **Primary open-angle glaucoma (POAG):** Angle is anatomically open, but increased resistance in the meshwork (especially juxtacanalicular region) reduces outflow. Gradual, painless, bilateral peripheral vision loss, with increased cup-to-disc ratio (optic nerve cupping). Most common type in the US; risk factors include age, African American race, family history, and myopia. - **Angle-closure glaucoma:** Iris bulges forward and physically blocks the meshwork. Presents as an ophthalmologic emergency with severe eye pain, halos around lights, a fixed mid-dilated pupil, a red eye, headache, and nausea/vomiting. Treatment: acetazolamide, topical beta-blockers, pilocarpine, and definitive laser peripheral iridotomy. Avoid mydriatics (anticholinergics, sympathomimetics). - **Secondary open-angle glaucoma:** Pigment dispersion syndrome (pigment clogs the meshwork), pseudoexfoliation syndrome (flaky material clogs the meshwork), and trauma/hyphema/inflammation (e.g., uveitis, red blood cells or debris clog the meshwork). - **Congenital glaucoma:** Trabeculodysgenesis (maldevelopment of the angle), presenting with buphthalmos, epiphora, photophobia, and corneal clouding.

**Pharmacology (drugs acting on the outflow pathways):** - **Cholinergic agonists (pilocarpine, carbachol):** Ciliary muscle contraction pulls on the scleral spur and opens the meshwork, increasing conventional outflow. Also cause miosis. - **Rho kinase inhibitors (netarsudil):** Relax the meshwork cells and increase conventional outflow. - **Prostaglandin analogs (latanoprost, bimatoprost):** Increase uveoscleral outflow (first-line for POAG). Side effects: eyelash growth, iris hyperpigmentation, periorbital fat atrophy. - **Alpha agonists (brimonidine):** Decrease aqueous production and increase uveoscleral outflow. Apraclonidine is a related alpha-2 agonist. - **Beta-blockers (timolol), carbonic anhydrase inhibitors (dorzolamide, acetazolamide):** Decrease aqueous production. - **Procedures:** Laser trabeculoplasty (selective or argon) improves meshwork outflow. MIGS (minimally invasive glaucoma surgery) devices (e.g., iStent) bypass the meshwork. Trabeculectomy creates a new drainage route.

**High-yield pearls:** Normal IOP is ~10–21 mmHg. IOP is determined by aqueous production and outflow resistance. Glaucoma is optic neuropathy; IOP elevation is a risk factor, not required for diagnosis (normal-tension glaucoma exists). Gonioscopy is used to visualize the angle and the meshwork.