14. Primary glaucoma.pptx
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Primary glaucoma refers to a group of eye diseases characterized by optic nerve damage and vision loss caused by increased intraocular pressure (IOP). The two main types are primary open-angle glaucoma (POAG) and primary angle-closure glaucoma (PACG). POAG is chronic, progressive, and characterized by an open iridocorneal angle and loss of retinal ganglion cells leading to visual field defects. PACG occurs when the iris blocks the drainage angle, increasing IOP and potentially causing severe eye pain and vision loss if not treated quickly. Both can lead to permanent vision loss if left untreated.
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14. Primary glaucoma.pptx
- 1. PRIMARY GLAUCOMA By: Qurat-ul-ain Ophthalmic Medical Technologist/ MBA Health & Hospital management
- 2. D E F I N I T I O N • Optic disc cupping • VF loss Refers to collection of diseases with chronic optic-neuropathy showing distinctive changes. Mostly associated with IOP, NTG is also possible Ocular HTN: constantly IOP w/o any associated glaucomatous damage. NTG: with cupping of the disc or visual field defects with a normal or IOP
- 3. Primary glaucoma Open-angle glaucoma Chronic NTG Angle-closure glaucoma Acute Sub-acute Chronic Plateau Iris Classificati on
- 4. PRIMARY OPEN ANGLE GLAUCOMA A chronic , progressive optic neuropathy of adult onset. It is characterized by: • RNFL thinning • Glaucomatous optic nerve damage • VF loss as damage progresses • An open ACA • Absence of signs of secondary glaucoma or a non-glaucomatous cause for the optic neuropathy. • IOP is a key modifiable risk factor
- 5. Predisposing and risk factors: Heredity polygenic inheritance, 4% risk in the offspring of patients. Age risk increases with increase in age Race more severe in black Myopes near-sighted person Diabetics higher prevalence Smoking higher risk High B.P Anti-VEGF after recurrent injections Trabecular meshwork Thickening & sclerosis Absence of giant vacuoles canal of shlemm Resistance to aqueous flow Decrease aqueous outflow IOP Mechanical effect Vascular effect Forces Lamina cribrosa backward & squeezes the nerve fibers Ischemic atrophy resulting in cavernous optic atrophy Damaging cascade Death of retinal ganglion cells Visual Field Defects
- 6. CLINICAL MANIFESTATIONS Symptoms: Insidious & usually asymptomatic. Mild headache & eye pain. Frequent changes in presbyopia glasses. Delayed dark adaptation. Signs: Anterior segment Pupil reflex becomes sluggish & cornea may show slight haze (late stages) IOP changes Falls during evening in Diurnal variation test. Visual Field Defects Usually run parallel to the changes at optic nerve head & progresses if IOP is not controlled.
- 7. OPTIC DISC CHANGES: Early glaucomatous changes: o Vertically oval cup o Asymmetry of the cups o Large cup o Splinter hemorrhages o Pallor areas o Atrophy of RNFL Advanced glaucomatous changes: o Marked cupping o Thinning of neuro-retinal rim o Nasal shifting of retinal vessels o Appearance of Bayonetting sign o Pulsation of retinal arterioles o Lamellar dot sign Glaucomatous optic atrophy o All the neural tissue of disc destroyed and optic nerve head appears white & excavated. o VF defects
- 8. DIAGNOSIS History Visual symptoms Pre-ophthalmic history Family history Past-medical history Current medication Examination VA Pupil Color vision assessment Slit-lamp examination Tonometry Perimetry Gonioscopy
- 9. NORMAL TENSION GLAUCOMA A.K.A low tension glaucoma Typical glaucomatous disc changes With/ without visual field defects Associated with IOP constantly <21mmHg
- 10. Predisposing and risk factors: Raynauld phenomena Migraine Nocturnal systemic hypertension Overtreated systemic hypertension Decreased blood flow (ophthalmic artery Chronic low vascular perfusion Optic-nerve susceptible PATHOPHYSIOLO GY
- 11. CLINICAL MANIFESTATIONS • Disc changes and visual field defects similar to POAG • Normal IOP DIFFERENTIAL DIAGNOSIS • POAG early stages POAG may present with normal IOP • Congenital optic disc anomalies • Approximately 60% have progressive VF loss.
- 12. PRIMARY ANGLE CLOSURE GLAUCOMA Increased IOP Blockage of the aqueous humor outflow Closure of the narrower angle of the anterior chamber. Epidemiology: Age more common in 5th decade Gender F>M (4:1) Race South east- Asian, Chinese Season higher in rainy season Family history inherited Type of personality unstable vasomotors
- 13. Etiology & Pathophysiology Anatomical factors Hypermetropia with shallow anterior chamber Iris-lens diaphragm placed anteriorly Narrow angle of anterior chamber, may be due to: Small eyeball Relatively large size of the lens & smaller diameter of the cornea. Bigger size of the ciliary body. Pre-disposing risk factors: Age Gender Race Family history Type of personality Precipitating factors: Dim illumination Emotional stress Mydriatic drugs Anteriorly placed lens with considerable pressure Relative pupil block Aqueous humor collect in the posterior chamber Pushes the peripheral flaccid iris anteriorly Appositional angle closure Synechial angle closure Chronic PACG Attack of IOP
- 14. CLINICAL MANIFESTATIONS Latent primary angle closure • Shallow AC • Occludable angle • No symptoms • Eclipse sign • Decreased ACD • Narrow angle (Shaffer grade-1) • Convex shaped lens diaphragm • Close proximity of Sub-acute or intermittent • Attack of transient IOP (40-50 mmHg) • Physiological mydriasis • Physiological shallowing of AC after lying in prone position • Unilateral transient Sub-acute or intermittent • Eye is white and non-congested • All the signs of latent PACG. • Attack of acute PACG • Chronic PACG without passing to acute stage.
- 15. Acute Angle Closure • Due to sudden total angle closure leading to sever rise in IOP. • Pain (radiates along the CN V), nausea, vomiting, prostrations, rapid onset of vision loss, redness, photophobia, lacrimation, edematous lids & cornea, congested conjunctiva, AC completely closed, iris discolored • Elevated IOP 40-70mmHg, pupil semi-dilated & usually non- Post-congestive AC glaucoma • Vogt’S Triad • Glaucoma lecken • Patches of iris atrophy • Slightly dilated non-reacting pupil
- 16. Chronic PACG • Similar to POAG except angle is narrower • IOP constantly raised • Eyeball remains white & without congestion and pain • Optic disc shows cupping Absolute PACG • Painful blind eye • Perilimbal reddish blue zone • Cornea clear but insensitive • Shallow AC • Atrophic iris • Fixed, dilated pupil • Atrophy of optic disc • High IOP • Eyeball becomes stony hard
- 17. COMPLICATIONS If untreated causes: • Corneal ulceration • Staphyloma formation • Atrophic bulbi
- 18. THANK YOU