![]() Kembara Xtra - Medicine - Primary Open Angle Glaucoma The optic nerve margin and retinal nerve fiber layer (RNFL) are lost in primary open-angle glaucoma (POAG), a chronic, progressive optic neuropathy that is accompanied by visual field abnormalities. Increased intraocular pressure (IOP) is linked to POAG. IOP is typically 10 to 21 mm Hg. Pregnant women's issues When treating POAG during pregnancy, prostaglandins should be avoided. Prevention Incidence The majority of people are over 40 years old. Prevalence The prevalence among people over 40 is 1.8%. Pathophysiology and Etiology The ciliary epithelium of the ciliary body produces aqueous, which is then secreted into the eye's posterior chamber. The trabecular meshwork (TM) in the iridocorneal angle of the eye then drains the aqueous once it enters the anterior chamber through the pupil. Following that, it exits the Schlemm canal and enters the episcleral venous system. Impaired aqueous outflow through the TM results in higher resistance in the aqueous drainage system and raises IOP. 5–10% of the total aqueous outflow exits via the uveoscleral route. Genetics: Glaucoma is more likely to develop in people who have a family history of the disease. Non-Hispanic whites with the TMCO1 genotype have an increased chance of acquiring glaucoma. The first gene linked to POAG was the myocilin (MYOC) gene. Risk factors include: elevated intraocular pressure (IOP), myopia, diabetes mellitus (DM), aging, hypothyroidism, positive family history, prolonged use of topical, periocular, inhaled, or systemic corticosteroids, systemic calcium-channel blockers, previous pars plana vitrectomy, obstructive sleep apnea, hypertension, and corneal hysteresis (CH), a measure of the cornea' Prevention A decreased risk of POAG has been linked to dietary nitrate intake and consumption of green leafy vegetables. There is evidence that nitrate, which is a precursor to nitric oxide, is good for blood circulation. Nitric oxide is one of the vasoactive substances that the vascular endothelium uses to control the microcirculation. By inducing the TM and Schlemm canal to relax and promote aqueous outflow, nitric oxide lowers IOP. DIAGNOSIS HISTORY Patients typically do not become aware of their vision loss until the condition has advanced significantly. Until the condition is advanced, central vision is unaffected. clinical assessment Evaluation of visual acuity and visual field Ophthalmoscopy to check for glaucomatous damage to the optic nerve Using tonometry to calculate IOP. It's possible for the IOP to be normal or excessive. CDR > 0.5: Normal eyes display the distinctive configuration of inferior, superior, nasal, and temporal disc rim thickness (ISNT rule). The paracentral scotomas and peripheral nasal steps are the earliest visual field abnormalities. Differential, Normal-tension Glaucoma, Optic Nerve Pits, Anterior Ischemic Optic Neuropathy, Compressive Optic Nerve or Chiasmal Lesions, Posthemorrhagic (Shock Optic Neuropathy) Laboratory Results Initial examinations (lab, imaging) The early identification of glaucoma may be possible with optical coherence tomography (OCT). The retinal ganglion cells' (RGCs') axons make up the majority of the RNFL. In addition to the RGC axons, glaucoma also affects the bodies and dendrites. OCT assesses the peripapillary RNFL because RGC axonal thickness is greatest in the peripapillary retina. RGCs are concentrated in the macula, hence glaucoma progression can be determined by the thinning of the mGCIPL using OCT measurements of the macular ganglion cell-inner plexiform layer (mGCIPL). RNFL is thinner in glaucoma patients. In Caucasians, longer axial length, older age, and a smaller optic disc area are all associated with thinner RNFL. Before comparable visual field loss is noticed, there may be significant RGC loss at a particular site. In eyes with POAG, OCT angiography (OCTA) shows a reduction in macular vascular density. OCTA demonstrates that progressive RNFL thinning in POAG is related to parapapillary choroidal microvasculature dropout (mvD). Other/Diagnostic Procedures Perimetry is a visual field test, and tonometry is used to measure IOP: The distortion that is inherent in most tonometry techniques is resisted by thicker corneas, which could lead to an overestimation of IOP. Thinner corneas could result in an unnaturally low reading. IOP measurements following photorefractive keratectomy (PRK) and laser in situ keratomileusis (LASIK) may be unnaturally low because to the induced corneal thinning. Interpretation of the test RGC and axon loss causes faults and thinning in the RNFL. Atrophy and cupping of the optic nerve. OCT measurements of RNFL thickness can identify glaucomatous damage prior to the onset of visual field abnormalities on automated standard perimetry. The mGCIPL OCT thickness is effective for predicting glaucoma progression independent of the presence of high myopia. The RNFL OCT utility falls in advanced glaucoma, however the mGCIPL OCT remains a sensitive progression detector from early to advanced glaucoma. Highly myopic eyes typically have a thinner peripapillary RNFL than normal eyes. Management Early treatment delays progression, with the degree of initial IOP decrease influencing disease progression, according to the Early Manifest Glaucoma Trial, which compared observation to treatment with betaxolol combined with argon laser trabeculoplasty (ALT). Treatment for Ocular Hypertension IOP was treated with topical ocular hypotensive medicine in a study of patients with elevated IOP between 24 and 32 mm Hg, resulting in a 20% reduction in IOP. At 5 years, therapy decreased the incidence of POAG by more than 50%: 4.4% in the medication-treated group compared to 9.5% in the observation group. When medicinal treatment failed, individuals in the Advanced Glaucoma Intervention Study were randomly assigned to either laser trabeculoplasty or filtering surgery. If IOP remained consistently below 18 mm Hg over time, visual fields tended to stabilize. More than 50% of the time, patients tended to have poorer visual fields when IOP was >17 mm Hg. According to the Collaborative first Glaucoma Treatment Study, both first medicinal and surgical (trabeculectomy) treatment significantly lowered IOP and resulted in little long-term loss of visual field. Medication It may be necessary to take multiple medications with various methods of action. The following are some categories of ocular hypotensive agents: Prostaglandin analogues are frequently utilized as first therapy. Increase aqueous outflow and uveoscleral outflow through the TM: Latanoprost 0.005%, travoprost 0.004%, and bimatoprost 0.01% should all be taken one drop before bed. - Latanoprostene bunod, solution at 0.024%. The release of nitric oxide is one of the activities of this combination medication. Pour one drop before going to bed. - Warnings and contraindications The iris and periorbital tissue may become more pigmented as a result of prostaglandin analogues. An increase in pigmentation and eyelash growth Use caution if you have current intraocular inflammation (uveitis or iritis). Use caution if you have herpes simplex, iritis, or cystoid macular edema in your eyes. Macular edema may develop as a side effect of treatment. Avoid while expecting. Adrenergic antagonists (both nonselective and selective) reduce aqueous formation; they work best when used in conjunction with other treatments: Betaxolol 0.5% one drop affected eye; gel-forming solution (0.25% or 0.5%) one drop affected eye once daily (nonselective); timolol 0.25% (initial) to 0.5% one drop affected eye every 12 hours (Selective) BID Nonselective -adrenoceptor antagonists Avoid in cases of decompensated heart failure, 2nd and 3rd degree atrioventricular (AV) block, asthma, and chronic obstructive pulmonary disease (COPD). A selective beta-adrenergic antagonist, betaxolol is less dangerous for patients with pulmonary illness. - Caution should be used while administering adrenergic antagonists to patients on calcium antagonists due to the possibility of left ventricular failure, hypotension, or AV conduction issues. Brimonidine tartrate 0.2%, a selective 2-adrenergic agonist: One drop TID (2-adrenergic agonist) reduces aqueous formation and boosts uveoscleral outflow. Due to the possibility of CNS depression, apnea, bradycardia, and hypotension, brimonidine shouldn't be administered to newborns and young children. Tricyclic antidepressants and monoamine oxidase inhibitors may impair brimonidine metabolism and cause toxicity. Topical and oral carbonic anhydrase inhibitors: Reduce aqueous formation. - Dorzolamide 2%: one drop TID - Acetazolamide 250 mg PO 1 to 4 times daily - Brinzolamide 1%: one TID decrease - Inhibitors of carbonic anhydrase Avoid using if you have sulfa drug allergies. Use is contraindicated in cases of cirrhosis due to the possibility of hepatic encephalopathy. By reducing actomyosin-driven cellular contraction and the synthesis of fibrotic extracellular matrix proteins, Rho kinase (Rock) inhibitors enhance aqueous outflow via the trabecular outflow pathway. - One drop of netarsudil, 0.02%, taken once day in the evening. When used, it can lead to whorl keratopathy or corneal verticillata. Aqueous outflow is increased by parasympathomimetics (miotics), such as direct-acting cholinergic agonists. The Pilocarpine 1-4%: one drop of DAC (direct-acting cholinergic agonist) in the afflicted eye BID-QID - Miotics (parasympathomimetics): produce myopia or eye pain due to increased accommodation; cause pupillary constriction and perhaps reduce vision in patients with cataracts. The blood-aqueous barrier is broken by all miotics, which might result in chronic iridocyclitis. In order to increase blood osmolality and drain water from the vitreous cavity, hyperosmotic agents are used. Mannitol 20% solution is given intravenously (IV) at a rate of 0.5 to 2 g/kg of body weight over the course of 45 minutes. - Glycerin 50% solution is given orally; the dosage ranges from 1 to 1.5 g/kg, or around 4 to 7 oz. Pouring the solution over crushed ice can enhance the flavor by combining it with a tiny bit of orange juice. - Hyperosmotic agents should be used with caution in diabetics, dehydrated patients, and people who have heart, kidney, or liver illness. Wearers of contact lenses: Remove contact lenses before administering any benzalkonium chloride-containing glaucoma drops, and wait 15 minutes before re-putting them in. Surgical Techniques The Glaucoma Laser Trial Research Group demonstrated that ALT was equally beneficial as topical glaucoma medicine within the first two years of follow-up in newly diagnosed, previously untreated patients with POAG. Selective laser trabeculoplasty (SLT), which uses a 532-nm Nd:YAG laser, appears to be equally successful as ALT at lowering blood pressure. Trabeculectomy (glaucoma filtering surgery) is often only performed on patients who have had the maximum amount of medicinal therapy and who still require better IOP control. Shunt (tube) surgery, such as Molteno and Ahmed devices, is typically reserved for difficult glaucoma cases in which conventional filtering surgery has failed or is likely to fail. According to the Tube Versus Trabeculectomy (TVT) study, both procedures were linked to a similar reduction in IOP and the number of glaucoma medications required after 5 years of follow-up. Patients with limited visual potential or those who are poor candidates for filtering or shunt treatments should consider ciliary body ablation to decrease IOP. The Kahook Dual Blade performs an excisional goniotomy by removing a strip of TM. - Cataract extraction can lower IOP in patients with ocular hypertension. - Minimally invasive glaucoma surgery (MIGS) is frequently combined with cataract surgery. Currently targeted at patients with mild to moderate glaucoma. Patient Follow-Up Monitoring Depending on POAG control, evaluate the optic nerve and vision every 3 to 6 months. A worsening of the mean deviation by 2 dB on the Humphrey field analyzer and confirmed by a single test after 6 months had a 72% probability of progression. Visual field testing every 6 to 18 months. Patients may not understand the seriousness of their disease until a significant portion of their visual field has been gone because POAG steals eyesight silently. The rate of visual field loss in POAG is modest with normal glaucoma therapy, but patients may still lose their vision and go blind even with the proper care. Even when the IOPs were identical throughout follow-up in cases of advanced glaucoma, the structure of the mGCIPL was better retained in surgically treated eyes than in medically treated eyes. Consequences:Blindness
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