Normal tension glaucoma
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This document discusses normal tension glaucoma, which is a type of open-angle glaucoma where the intraocular pressure is normal but the optic nerve is still damaged, leading to visual field loss. It is caused by chronic low blood flow to the optic nerve head, which makes the nerve susceptible to normal IOP levels. While elevated IOP is a major risk factor for glaucoma, normal tension glaucoma occurs without elevated pressure. The document covers classification of glaucoma, risk factors and clinical features of normal tension glaucoma such as optic nerve changes and visual field defects, as well as diagnostic evaluation and treatment options which aim to lower IOP as much as possible without complications.
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Normal Tension Glaucoma
Prevalence, Etiopathogenesis, differencial diagnosis, Basic work up, CNGTS and treatment of normal tension glaucoma.
Normal tension glaucoma
Normal tension glaucoma, also known as low tension glaucoma, is characterized by open angle glaucoma with typical optic nerve damage but intraocular pressure that is consistently normal or only slightly elevated. It has several risk factors such as older age, female sex, East Asian ethnicity, family history of glaucoma, and thin central corneal thickness. The pathogenesis involves vascular dysfunction, autoimmune mechanisms, vascular inflammation, and genetic mutations. Diagnosis involves a detailed medical history, eye examination, visual field testing, and sometimes additional imaging or blood work. Treatment aims to lower intraocular pressure by 30% using topical eye drops, laser trabeculoplasty, or filtering surgeries along with controlling any underlying vascular problems
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This document summarizes a presentation on normal tension glaucoma (NTG). It begins with an introduction defining NTG as open-angle glaucoma with characteristic optic nerve damage and visual field defects in patients with consistently low intraocular pressure (IOP) below 21 mmHg. It then describes a case presentation of a 47-year-old female patient. The remainder of the document discusses the history, examination, investigations, differential diagnosis, management, pathogenesis involving both IOP-dependent and independent factors, and epidemiology of NTG. Key points are that lowering IOP through medication or surgery can help prevent progression even in NTG, and that NTG may have an underlying vascular component involving low ocular perfusion pressure
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This document discusses the morphological changes that occur in the optic nerve head and retinal nerve fiber layer in glaucoma. It describes the various patterns of glaucomatous optic nerve damage including focal notching, concentric cupping, saucerization, and advanced cupping. Features that indicate glaucomatous damage include neuroretinal rim thinning, disc hemorrhages, and changes in the retinal vasculature around the optic disc. Evaluation of the optic nerve head is important for early detection of glaucoma before visual field loss occurs.
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This document discusses target intraocular pressure (IOP) for treating glaucoma. It defines target IOP as the upper limit of IOP that prevents further glaucoma damage. Establishing an individualized target IOP is important to slow retinal ganglion cell loss and glaucoma progression over a patient's lifetime with minimal effects on quality of life. The target IOP should be based on factors like the amount of existing eye damage, maximum past IOP levels, life expectancy, and risk factors. The target is dynamic and must be reevaluated periodically, lowering it if damage progresses or raising it if side effects occur from low IOP. Clinical studies show that greater IOP reductions correlate with less glaucoma progression
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Normal Tension Glaucoma
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Normal tension glaucoma
Normal tension glaucoma, also known as low tension glaucoma, is characterized by open angle glaucoma with typical optic nerve damage but intraocular pressure that is consistently normal or only slightly elevated. It has several risk factors such as older age, female sex, East Asian ethnicity, family history of glaucoma, and thin central corneal thickness. The pathogenesis involves vascular dysfunction, autoimmune mechanisms, vascular inflammation, and genetic mutations. Diagnosis involves a detailed medical history, eye examination, visual field testing, and sometimes additional imaging or blood work. Treatment aims to lower intraocular pressure by 30% using topical eye drops, laser trabeculoplasty, or filtering surgeries along with controlling any underlying vascular problems
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- Accuracy of A-scan ultrasound is ±0.1mm. Differences between eyes should be ≤0.3mm.
- Potential sources of error include corneal compression, fluid excess, misalignment, inappropriate eye type settings.
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- Accuracy of A-scan ultrasound is ±0.1mm. Differences between eyes should be ≤0.3mm.
- Potential sources of error include corneal compression, fluid excess, misalignment, inappropriate eye type settings.
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The most common aetiological factor is compression by adjacent atherosclerotic retinal arteries.
Other possible causes are external compression or disease of the vein wall e.g. vasculitis.
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Glaucoma is always a chronic, long term disease.
Glaucoma is always associated with some damage to the optic nerve and often a related change in the visual field.
Glucoma.pptx
This document provides an overview of glaucoma, including its definition, types, risk factors, diagnosis, management, and nursing considerations. Glaucoma is a group of eye diseases characterized by optic nerve damage that results from fluid buildup in the eye that increases intraocular pressure. The main types are open-angle glaucoma, which is the most common; closed-angle glaucoma; normal tension glaucoma; and congenital glaucoma. Risk factors include age, family history, diabetes, and high blood pressure. Diagnosis involves eye pressure tests, optic nerve exams, and visual field tests. Treatment includes eye drop medications, laser treatments, surgery, and lifestyle changes to control pressure and prevent further vision loss
Glaucoma diska
Glaucoma is an optic neuropathy characterized by cupping of the optic disc and loss of visual field. It is usually associated with increased intraocular pressure (IOP). If left untreated, glaucoma can lead to irreversible blindness. There are several types of glaucoma including open-angle glaucoma, angle-closure glaucoma, congenital glaucoma, and secondary glaucoma caused by injuries, infections, tumors or inflammation. Treatment options include medications, laser treatment, or surgery to lower IOP and prevent further vision loss. The goal is early detection and treatment to preserve sight.
Glaucoma ppt kiran oli
This ppt can be useful for students. It is simple and covers most information on glaucoma examination.
Lecture 9 ON &R.pptx
Optic nerve and retinal diseases are described including optic neuritis, anterior ischemic optic neuropathy, central retinal vein occlusion, central retinal artery occlusion, and age-related macular degeneration. Optic neuritis causes eye pain, vision loss, and color vision changes. Central retinal vein occlusion blocks the main vein draining the retina causing hemorrhages and macular edema. Central retinal artery occlusion involves sudden vision loss from blockage of the artery supplying the retina. Age-related macular degeneration is the leading cause of vision loss in older adults and involves the degeneration of the macula.
aion.pptx
This document discusses various types of ischemic optic neuropathies including anterior ischemic optic neuropathy (AION) and posterior ischemic optic neuropathy (PION). It describes the differences between arteritic AION (caused by giant cell arteritis) and non-arteritic AION, with the former affecting older patients and often causing bilateral simultaneous vision loss. Risk factors for NAION include hypertension, diabetes, and sleep apnea. The document provides details on clinical evaluation, imaging, and management of these vision-threatening conditions.
case report.This is a 60 years old female patient, a known Glaucoma patient:pptx
The document discusses various causes of unilateral acute granulomatous anterior uvitis with high intraocular pressure (IOP). It describes conditions like glaucomatocyclitic crisis, Fuchs heterochromic iridocyclitis, herpes zoster or simplex-associated uveitis, phacolytic and phacoantigenic glaucoma, and ciliary body inflammation and rotation with angle closure glaucoma that can lead to these symptoms. It also discusses evaluating and managing patients with uveitis and elevated pressure, including recognizing underlying syndromes, controlling IOP and inflammation, and addressing specific conditions like Fuchs heterochromic iridocyclitis and herpetic uveitis.
Optic neuritis
By Dr Piyush Ojha , DM Resident, GMC Kota
under guidance of Prof. Dr Vijay Sardana (HOD,Neurology)
POAG.pptx
This document provides information about primary open-angle glaucoma (POAG):
- It defines POAG as a chronic, progressive optic neuropathy characterized by an open anterior chamber angle and elevated intraocular pressure.
- Risk factors, clinical presentation, diagnosis, differential diagnosis, evaluation, and treatment options are discussed. Treatment may involve medications, laser trabeculoplasty, or glaucoma surgery with the goal of reducing intraocular pressure to halt optic nerve damage.
- Two case studies are presented to exemplify the evaluation and treatment of patients with POAG.
POAG by junaid afsar.pptx
This document discusses primary open-angle glaucoma (POAG), including its definition, risk factors, prevalence, characteristics, symptoms, signs, progression, evaluations methods, and treatment options. POAG is the most common type of glaucoma, has no known cause but may be genetic or due to poor circulation. Treatments include pharmaceutical options like beta-blockers, prostaglandins, and surgery. The goal of treatment is to lower intraocular pressure to prevent further optic nerve damage and vision loss.
Glaucoma 2nd class
Congenital or infantile glaucoma occurs in babies and young children, usually within the first year of life. It is a rare condition caused by incorrect development of the eye's drainage system before birth. The mainstay treatment is surgical, through procedures like goniotomy or trabeculotomy to create an opening in the trabecular meshwork and improve aqueous outflow. These surgeries may need to be repeated if the first procedure fails to sufficiently lower intraocular pressure.
Transient visual loss
Transient loss of vision is common clinical problem that ophthalmologists and neurologists can face. This presentation will highlight clinical approach and important causes with management.
Gradual vision loss
Gradual vision loss is caused by many conditions that develop over weeks to years. The most common causes are age-related macular degeneration, cataracts, glaucoma, diabetic retinopathy, and refractive errors. A thorough history and eye exam can help identify the cause by examining symptoms, visual acuity, the retina, and optic nerve. Treatment depends on the specific condition but may include eye drops, laser therapy, surgery, or lifestyle changes.
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Glaucoma 3 primary open angle glaucoma,dr.k.n.jha, 03.11.16
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NORMAL TENSION GLAUCOMA "An exception in the glaucoma family"
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case report.This is a 60 years old female patient, a known Glaucoma patient:pptx
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Glaucoma drainage devices (GDDs) provide an alternative pathway for aqueous humor outflow and are used to treat refractory glaucoma. The document discusses the history, design, and types of various GDDs including non-valved devices like Baerveldt and Molteno implants as well as valved devices like the Ahmed Glaucoma Valve. The key components, materials, and surgical techniques for GDD implantation are also summarized.
Prism
1. Prism is a portion of a refractive medium bounded by two plane surfaces inclined at an angle. It deviates light passing through it towards its base due to refraction.
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Intravitreal antibiotics new
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Gonioscopy
Gonioscopy is an examination of the anterior chamber angle using a gonioscopy lens and slit lamp microscope. It allows visualization of key angle structures including the trabecular meshwork, Schwalbe's line, scleral spur, and ciliary body band. The examination is used to diagnose glaucoma and angle closure risk. There are two main techniques - direct gonioscopy using a contact lens and indirect gonioscopy using a single or multiple mirror lens. Angle structures may be difficult to see, requiring manipulations like indentation and corneal wedge to improve visualization. Gonioscopy is essential for glaucoma evaluation and management.
Corneal blindness in a southern indian population [autosaved]
This document summarizes a study on corneal blindness in southern India. The study assessed the prevalence and causes of corneal blindness by examining over 10,000 people across both rural and urban areas. The prevalence of corneal blindness was found to be 0.66% (1 in 150 people). The leading causes were childhood keratitis due to vitamin A deficiency, trauma from work or play, and corneal scarring. Most cases were preventable through improved nutrition, safety measures, and health promotion programs targeting at-risk groups. The document calls for strategies like keratoplasty and eye banking to help rehabilitate those already blinded and reduce the prevalence of preventable corneal blindness in India.
Cornea m.b
The cornea is the transparent front part of the eye that refracts light. It has five layers - epithelium, Bowman's layer, stroma, Descemet's membrane, and endothelium. The stroma comprises the majority of the cornea and contains collagen fibrils that maintain the cornea's shape and strength. The endothelium functions as a pump to remove fluid from the stroma and maintain corneal dehydration and transparency. Any disruption to this fluid regulation can lead to corneal swelling and loss of transparency.
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Normal tension glaucoma
- 2. • Glaucoma : Multifactorial optic neuropathy in where there is characteristic atrophy of optic nerve. • Although elevated IOP is clearly the most frequent causative risk factor • Normal IOP 10 – 21 mmHg
- 3. Classification Primary glaucoma Secondary glaucoma Open angle glaucoma Angle closure glaucoma Child-hood glaucoma Primary glaucoma : not ass. With known ocular (or) systemic diseases that cause an inc. resistance to aq. Flow (or) angle closure. Usually bilateral Secondary glaucoma : associated with ocular or systemic disorders responsible for dec. aq. Flow usually asymmetric and unilateral
- 4. Normal tension glaucoma • Type of open angle glaucoma without raise in IOP • Also called low tension glaucoma • Cause - Chronic low vascular perfusion, which makes optic nerve head susceptible to normal IOP • Stress markers –myocilin and aβ- crystalline in TMW • Inc. age, female, mutation of OPTN gene, sleep apnea, auto-antibodies, migraine and Raynaud's
- 5. • seen mostly with – Advancing age Myopes Monozygotics Type 2 D.M , systemic hypertension Atherosclosis, ischemic vascular dis GLClB and GLC1E genes Atypical – unilateral, dec central Vn, NRR pallor, VF loss not consistent with optic disc appearance, anemia , heart dis, syphilis, temporal arteritis, young age
- 6. • Clinical feat : higher prevalence of vasospastic disorders migraine, Raynaud phenomenon, ischemic vascular dis., coagulopathies Bilateral and progressive Normal but, asymmetric IOP Progressive visual field loss Peripapillary atrophy – senile sclerotic, focal ischemic Dense Para central scotoma
- 7. • Clinical features : • Optic nerve head – thin neuro-retinal rim, disc Hx, retinal nerve fiber defects • Visual fields – more deeper and localized scotoma with constant progression • IOP –normal asymmetric IOP, wide diurnal variation • Ocular vascular abr - vascular perfusion of optic head Non-progressive – transient vascular shock Progressive – Ch. Insufficiency • Sys vascular abr - alt BP (nocturnal dip) + elevated diastolic, Asymptomatic MI , frequent headache ± migraine,
- 8. • Differential diagnosis : Several contd. Mimic NTG causing arcuate-type of visual field defects , some are progressive IOP – raised IOP is noted with systemic β-blockers Tonometer – low readings due to Reduced scleral rigidity Corneal thickness Assessment of CCT – NTG (530 -545 μm) Refractive surgery Myopic disc with VF changes Previously elevated IOP Intermittent angle closure POAG with diurnal variation
- 9. • Diagnostic evaluation : Repeated testing Applanation tonometry at various times Gonioscopy Stereoscopic disc evaluation Complete medical history Provocation test Water drinking test Steroid provocation test Jugular vein compression test imaging – CT, MRI, OCT
- 10. • Prognosis and therapy : • According to Collaborative Normal-Tension Glaucoma Study (CNTGS) • Goal - to achieve an lOP that is as low as possible, without the development of complications. • Aggressive reduction in IOP by 30% to reduce progressive VF loss from base line • Criteria for initiation of thx Visual field loss threatening fixation Disc hemorrhage Documented VF or optic nerve progression • If independent of IOP check cvs, anemia, htn, CHF, TIH • Ensure maximum optic nerve head perfusion
- 11. • Systemic and tropical Calcium channel blockers – inc. capillary perfusion of optic nerve, dec. in progression Prostaglandin analogs – achieve target IOP , below episcleral venous pressure • Others – Tropical β-blockers, CAI, alpha agonist • Surgery – laser trabeculoplasty, glaucoma filtering Sx ±(anti-fibrotic agent)
- 12. Disc hemorrhage
- 13. Thank you
Editor's Notes
- factors determining IOP – rate of aq. Flow by C.Bresistance of aq. Out flow by TMW – schlemms canal sys ( juxtracanalicular meshwork )level of episcleral venous pressure Aq. Production – inner non-pig layer of ciliary process( rich in mito and vacuoles) then by active section (major) ultrafiltration(pressure dependent along ionic gradient) simple diffusion( passive)2 to 2.5 ≥μl/min, protien free for clarity
- Myocilin – 1st , post – dexmetha Rx, oxidative stress, streching, TGF- B aB – heat shock protein both found in COAG , exfoliative, NTGAuto-anti – higherApnea - perfusion
- GLClB and GLC1E genes appear to develop a type of glaucoma with lower pressure, these mutations cause optic nerve abnormally sensitive to lOP or otherwise facilitate optic nerve damage independent of lOP
- Visaul field los– slow , neuroretinal rim – inf and inf temp , scotoma encroching on fixaTION in not unsual
- Nrrm- inf & inf temp . Disc HX= vascuals dis, nfl= macula Scotoma = para central Oculo-vascular= focal arteriolar narrowing around the optic nerve,hemodynamic crisesSys = 24hr EKG shows asympt MI 45% in ntg with many ischemic episodes in night
- Past secondary glaucoma (eg, corticosteroid-induced glaucoma, uveiticglaucoma, pigmentary glaucoma, previous trauma)Nonglaucomatous optic nerve diseaseCongenital anomalies (coloboma, optic nerve pits)Compressive lesions of optic nerve and chiasmShock optic neuropathyAnterior ischemic optic neuropathyRetinal disorders (ie, retinal detachment, retinoschisis, vascular occlusions, chorioretinitis,syphilis)Optic nerve drusen
- Gonio- angle closure, recession, intraocular inflaSterio- disc and cup anamolies , nerve coloboma , drusensMedical- Cardio dis, low BP caused by Hx , M.I , shock VF is adviced after hypotensive crisesProvocation test – cause raise in IOP by obstructing aq flowwater – hospt – no food and water 10pm – IOP in morning then water 1liter quick – rept IOP for 15 min for 6 times and compare +ve if 7mm raise
- Anti- fibrotic – 5-florouracil and mitomycin C