INTRODUCTION Also k/a low tension glaucoma Characterized by:- Open angle of AC Typical glaucomatous cupping IOP (</= 21 mm of Hg) VF loss No obvious / apparent cause for these changes
Risk factors for NTG/LTG Age - > 50yrs Gender – F>M Race – Japan > Europe/ North America Family/H – POAG is more in families of NPG - mutation of OPTN gene at chr 10
Risk factors for NTG/LTG CCT Vascular diseases--Hemodynamic crisis Hypercoagulability High blood viscosity High cholesterol & lipids CAD Abnormal vasoregulation –Migraine & Raynauds phenomenon Syst. Hypotension –Nocturnal hypotension & pt. on oral anti-HTN Obs. Sleep apnoea syn.
PATHOGENESIS I. LOCAL & SYSTEMIC VASCULAR DYSFUNCTION
CONTD… AUTOIMMUNE MECHANISM anti-Ro/SS-A positivity and heat shock protein antibodies VASCULAR INFLAMMATION Elevated plasma C-reactive protein levels MUTATION & POLYMORPHISM located on chromosome 10 E50K mutation optineurin gene severe disease and progressive Polymorphisms OPA1 gene mutations dominant optic atrophy
CLINICAL FEATURES Usually asym . Symp . of decreased vision, fluctuating vision / VF loss Diag. by routine exam. / screening programme Borderline high IOP Wide DVT & postural fluctuation
Contd … FUNDUS FINDING :- OD is more cupped (pallor > cupping) Focal ischaemic Diffuse sclerotic Parapapillary atrophy is more Diffuse & focal hypoflourescence of OD & abnormal transit time on FFA Splinter haemorrhages are more VF CHANGES:- defects are denser, steeper, and closer to fixation Dense arcuate / dense hemifield scotoma
DIAGNOSIS PROPER HISTORY TAKING 1) Past ocular history Migraine headaches Previous eye disease, eye surgery /head trauma Short-sightedness (myopia) 2)Current medication history
Contd … 3) ANY ILLNESS Vasospasms such as Raynaud’s phenomenon Coagulopathies Previous blood loss or shock-like episodes Nocturnal hypotension Autoimmune disorders Vascular diseases including atherosclerosis Thyroid disease Sleep apnoea Alzheimer’s disease
OCULAR EXAMINATION & TESTS Slit lamp examination Tonometry Gonioscopy Optic nerve Different imaging studies Doppler USG- to monitor blood flow to the eye Fundus photographs Retinal exam. VF analysis
CONTD… SYSTEMIC EXAM. & TESTS Auscultation & palpation of carotid A. Neurologic exam. Blood for Hematocrit , ESR, Hb , ANA Serologic for Syphilis, Serum –ACE level, plasma electrophoresis, auto Ab Doppler of Carotid A. / Angiography CT MRI
Extensive systemic work up to be done in pt’s – < 60 yrs OD pallor> cupping IOP < 17 mm of Hg Rapid progression inspite of adequate t/t
D/D I. Glaucoma A. Elevated intraocular pressure (IOP) not detected 1. Undetected wide diurnal variation 2. Low scleral rigidity 3. Systemic medication 4. Past systemic medication that may have elevated IOP 5. Elevation of IOP in supine position only B. Glaucoma in remission 1. Past corticosteroid administration 2. Pigmentary glaucoma 3. Associated with past uveitis or trauma 4. Glaucomatocyclitic crisis 5. Burned-out primary open-angle glaucoma
Contd … II. Optic nerve damage A. Congenital optic nerve conditions – Pits, Colobomas , Tilted discs B. Ischemic optic neuropathy 1. Arteritic 2. Non- arteritic C. Compressed lesions 1. Tumors 2. Aneurysms 3. Cysts 4. Chiasmatic arachnoiditis D. Optic nerve drusen E. Demyelinating conditions F. Inflammatory diseases G. Hereditary optic atrophy H. Toxic drugs or chemicals
Contd … III Ocular disorders A. Myopia B. Retinal degeneration C. Myelinated nerve fibers D. Branch vascular occlusions E. Choroidal nevus or melanoma F. Choroidal rupture G. Retinoschisis H. Chorioretinal disease
Contd … IV . Systemic vascular conditions A. Anemia B. Carotid artery obstruction C. Acute blood loss D. Arrhythmia E. Hypotensive episodes V. Miscellanenous A. Hysteria B. Artifact of visual field testing
T/T MEDICAL Aim is to reduce the IOP upto 30% Control of systemic vascular disease Topical agents including b-blockers latanoprost brimonidine carbonic anhydrase inhibitor miotics
SURGICAL Laser trabeculoplasty (ALT / SLT) Trabeculectomy with anti-metabolite ( mitomycin C / 5-FU) Full-thickness filtering surgery
RECENT DRUGS- serotonin antagonist -- Naftidrofuryl a calcium channel blocker-- Nilvadipine a nimodipine -like agent -- brovincamines
CONCLUSION With early diagnosis and medical treatment, further optic nerve damage and/or vision loss may be prevented Follow up to be done every 3-6 mons Target IOP to be maintained for each pt. to prevent further progression of the disease