Anterior Chamber and Glaucoma

• Dr. Cliff Muturi discusses the anterior chamber and glaucoma.

Anterior Segment

• The iris and ciliary body are key structures in the anterior segment of the eye.

Aqueous Outflow

• Aqueous humor flows from the posterior chamber through the pupil into the anterior chamber.
• From the anterior chamber, aqueous humor exits the eye via three routes.
• Around 90% of aqueous humor exits through the trabecular outflow.
• The outflow courses through the trabeculum, into the Schlemm canal, and then into the episcleral veins.
• Trabecular outflow is pressure-sensitive, so increasing intraocular pressure (IOP) will increase outflow.
• Uveoscleral drainage accounts for 10% of the outflow.
• Aqueous passes across the face of the ciliary body into the suprachoroidal space.
• It is drained by venous circulation in the ciliary body, choroid, and sclera.
• Some aqueous drains via the iris.

Anterior Chamber Angle

• The anterior chamber angle includes the trabecular meshwork, which facilitates aqueous outflow.

Intraocular Pressure

• IOP is the intrinsic pressure within the eye.
• It is determined by the balance between aqueous production and outflow rates, measured through tonometry.
• Normal IOP ranges from 10 to 21 mmHg.
• Factors like diurnal variation, blood pressure, astigmatism, pressure on the globe, and breath-holding can influence IOP.

Optic Nerve Head

• The neuroretinal rim is the orange-pink tissue between the edge of the cup and the optic disc margin.
• The cup-disc ratio (CDR) is the diameter of the cup divided by the diameter of the disc.
• The vertical CDR is used.
• Normal CDR is up to 0.7, depending on disc size.

Perimetry - Visual Field Assessment

• Visual field is the total area in which objects can be seen while focusing on a central point.
• Assessment of optic nerve functions includes visual acuity (VA), pupillary reactions, color vision, and fundoscopy.

Glaucoma

• Glaucoma is a potentially progressive optic neuropathy associated with visual field loss.
• A key modifiable factor in glaucoma is intraocular pressure (IOP).
• Glaucoma is classified as primary versus secondary, open-angle versus angle-closure, and congenital versus acquired.
• Epidemiology: 2-3% of people over the age of 40 are affected and 50% may be undiagnosed.

Open Angle vs Angle Closure Glaucoma

• Open-angle and angle-closure glaucoma are distinguished by the accessibility of the trabecular meshwork.

Assessment of a Glaucoma Patient

• Assessing the history of a glaucoma patient includes visual symptoms (open angle vs. angle closure), past ophthalmic history (myopia, steroid use, trauma), family history and past medical history.

Investigations for Glaucoma

• Examination includes visual acuity, pupil assessment, slit lamp examination, tonometry, fundoscopy and gonioscopy.
• Investigations include perimetry, OCT and Pachymetry (CCT).

Perimetry - Glaucomatous Defects

• Glaucomatous defects in perimetry include nasal step, paracentral defects, temporal wedge defects, altitudinal defects, arcuate defects, and advanced defects.

Ocular Hypertension

• Ocular hypertension is raised IOP without optic nerve damage.
• Risk factors include higher IOP, older age, lower central corneal thickness (CCT), greater cup/disc ratio, African-American race, male gender, and heart disease.

Primary Open Angle Glaucoma(POAG)

• POAG is commonly a bilateral disease of adult onset, criteria includes having IOP>21mmHg, glaucomatous optic nerve damage, open anterior chamber angle, characteristic visual field loss as damage progresses, and absence of signs of secondary glaucoma or a non-glaucomatous cause for the optic neuropathy.
• Risk factors for POAG include IOP, age, race, family history, diabetes mellitus, vascular disease, myopia, and contraceptive pill use.

Normotensive Glaucoma (NTG)

• NTG is a variant of POAG.
• Criteria include IOP consistently equal to or less than 21 mmHg, signs of optic nerve damage in a characteristic glaucomatous pattern, an open anterior chamber angle, visual field loss as damage progresses, consistent pattern with nerve appearance and no features of secondary glaucoma or a non-glaucomatous cause for the neuropathy.

Primary Angle Closure Glaucoma (PACG)

• PACG involves occlusion of the trabecular meshwork by the peripheral iris (iridotrabecular contact), obstructing aqueous outflow.
• It can be primary, occurring in an anatomically predisposed eye, or secondary to another ocular or systemic factor.
• Sequelae includes PAC suspect, PAC and PAC Glaucoma.
• Mechanisms leading to primary angle closure glaucoma include pupillary block, non-pupillary block, lens-induced, retrolenticular mechanisms, and combined mechanisms.

Secondary Glaucoma (Open Angle)

• Secondary open-angle glaucomas include pre-trabecular, trabecular, and post-trabecular mechanisms.
• Pre-trabecular causes include neovascular glaucoma (NVG), iridocorneal endothelial syndrome, and epithelial ingrowth.
• Trabecular causes include pigmentary glaucoma, hyphema, scarring, and uveitis.
• Post-trabecular causes include carotid cavernous fistula and superior vena cava (SVC) obstruction.

Secondary Glaucoma (Angle Closure)

• Secondary angle-closure glaucoma can occur with or without pupillary block.
• With pupillary block, conditions include seclusio pupillae (360° posterior synechiae due to chronic uveitis), subluxated lens, and phacomorphic glaucoma.
• Without pupillary block, conditions include advanced NVG and uveitis.

Neovascular Glaucoma

• Neovascular glaucoma is a result of aggressive iris neovascularization (rubeosis iridis).
• A common etiological factor is severe, diffuse, and chronic retinal ischemia.
• Risk factors include central retinal vein occlusion (CRVO), central retinal artery occlusion (CRAO), diabetes mellitus, chronic uveitis, longstanding retinal detachment (RD), and intraocular tumors.

Congenital Glaucoma

• Primary congenital glaucoma involves trabeculodysgenesis.
• Blindness results in at least 50% of eyes, and it is rare (1:10,000).
• It is more common in boys than girls and is frequently asymmetrical.
• True congenital glaucoma (40%) occurs in intrauterine life.
• Infantile glaucoma (55%) occurs before age 3.
• Juvenile glaucoma (5%) occurs between ages 3 and 16.
• Secondary congenital glaucoma can be caused by tumors (e.g., retinoblastoma), persistent fetal vasculature, and uveitis.
• Symptoms include watering, photophobia, and blepharospasms.
• Signs include corneal haze, buphthalmos, corneal scarring and vascularization, and optic disc cupping.

Syndromes Associated with Glaucoma (Iridocorneal Dysgenesis)

• Syndromes linked to glaucoma include posterior embryotoxon, Axenfeld-Rieger syndrome, aniridia, Peters anomaly, and phacomatoses.

Treatment of Glaucoma

• The medical management includes beta blockers, prostaglandin analogues, alpha agonists and CAIs.
• Laser treatments include laser iridotomy for angle closure, ALT, SLT, MLT, and CPC.
• Surgical options include trabeculectomy and Ahmed glaucoma valve implantation.