GLAUCOMA PRESENTED BY:- EMDADUL ISLAM B.OPTOM 7 TH SEM NHSHM KNOWLEDGE CAMPUS DURGAPUR
INTRODUCTION Usually with a charecteristics loss of visual function. Damage to a optic nerve is irreversible prosses Usually caused by raised IOP acting on the nerve head Normal IOP is - 15-21 mnn of hg It is a heterogenous group of diseases in whitch optic nerve is damage. IOP is the most common risk factor for development of glaucoma Vission loss is irreversible It is the secound leading causes of BLINDNESS. In its early stages it affects peripheral visual field only but as it advances it affects central vision and results in loss of visual acuity,
Intraocular pressure is not the only factor responsible for glaucoma! 95% of people with elevated IOP will never have the damage associated with glaucoma. One-third of patients with glaucoma do not have elevated IOP. Most of the ocular findings that occur in people with glaucoma also occur in people without glaucoma.
EPIDEMIOLOGY Globally estimated 8.4 million people who are blind on the result of glaucoma These number are set to increases to 11.2 million by 2020 It is the secound leading causes of BLINDNESS globally The highest prevelance of open angle glaucoma occures in AFRICA.( WWW.SCIENCEDIRECT.COM ) Global prevelance of glaucoma -2%of those over the age of 40 years and 10% of those over 80 years of age Glaucoma blindness- - global 8.0% - india 12.8%
Primary open-angle glaucoma (POAG) is the most common type of glaucoma, accounting for over 70% of cases. Ocular hypertension affects 3-5% of the population over 40 years of age .
from google
Population distribution of IOP
AQUEOUS PRODUCTION AND DRAINAGE SECRATION OF AQUEOUS HUMOR:- cilliary body ROUTE OF DRAINAGES- -TRABECULAR OUTFLOW(90%) -UVEAL-SCLERAL OUTFLOW(10%)
UVEOLSCLERAL OUTFLOW CILLIARY BODY POST. CHAMBER ANT. CHAMBER CILLIARY BODY SUPRA CHOROIDAL SPACE VENOUS CIRCULATION OF CILLIARY BODY ( The normal level of IOP is essentially maintained bye the formation and outflow of the aqueous humour )
Absolute glaucoma The end stage of glaucoma is referred to as absolute glaucoma. There is no functioning vision, the pupillary reflex is lost and the eye has a stony appearance. The condition is very painful and is treated by destructive processes.
CONGENITAL/DEVELOPMENTAL GLAUCOMA A rare condition Manifest without associated anomalies Bupthalmhos and cloudy cornea
Congenital Glaucoma Buphthalmos , glaucomatous cupping, and cloudy cornea OD Normal OS Haa’s bstriae
PATHOGENESIS Maldevelopmental of the angle structures Impaired aqueous outflow Raised IOP Damage optic nerve
V. INFANTILE CONGENITAL GLAUCOMA:- - synonymous with congenital glaucoma -1 months to 3 years JUVENILE GLAUCOMA :- -Primary glaucoma occuring latter in childhood -3years to 18years
EPIDEMIOLOGY -1 in 10,000 births -65% of patients are boys
CLINICAL FEATURES SYMPTOMS:- -Photophobia - Lacrimation - Blepharspasm -Irritation -Cloudy cornea -Red eye -Poor vission and pain
CLINICAL FEATURES SIGNS:- Corneal oedema Corneal enlargement Haab’s straie Sclera thin and blue A.chamber deep Iridodonesis Optic disc-variable cupping & atrophy
TREATMENT MEDICAL TREATMENT :- -Not very effective. -It is a surgical diseases . - Acetazolamide & beta-blockers use till surgery is taken
TREATMENT B .SURGICAL TRATMENT:- - Goniotomy - Trabeculectomy - Filteration surgery -Glaucoma drainage devices tr T T RABECULECTOMY
Images of surgical treatment GONIOTOMY
POAG ( PRIMARY OPEN ANGLE GLAUCOMA ) POAG is a commonly disease of a adult onset It is a charecterized by -IOP >21 mm of hg -open anterior chamber angle -optic dics cupping -optic dics damages -specific visual field damages
POAG is a bilateral disease IOP is the major risk factor Also known as chronic simple glaucoma Most prevalence of all glaucoma Most common glaucoma
PREDISPOSING & RISK FACTORS IOP –most common risk factors Age -most case >40 years BP -Diastolic pressure <55 mm of hg Retinal diseases -CRVO,RD,RP Diabetes melitus Central corneal thickness
PATHOGENESIS OF RISE IN IOP Certain rise of IOP that occures due to decrease of aqueous outflow . Aqueous outflow reduce due to -thickening of trabecular meshwork -sclerosis of trabecular meshwork -narrowing of intertrabecular spaces - trabecular meshwork stiffening
EPIDEMIOLOGY POAG affects about 1 in 100 of general population Forms about one third cases of all glaucoma
CLINICAL FEATURES - SYMPTOMS -Asymptomatic diseases -Gradual painless loss of vision -Mild headache -Visual field defect -Changes in presbyopic glasses -Delayed dark adaptation
SIGNS Ant.segment signs:- -normal -corneal haze -lazy pupil reflex Iop changes:- -Initial stages IOP normal -Doing DIURNAL variation test -In later stages,IOP is permanently raised -Range of IOP between 30 to 45 mm of hg
ONH evaluation:- Early glaucomatouas changes -Large cup - Asymetry of >0.2 between two eyes -Cup ratio 0.6 or more -pallor disc -vertical oval cup -splinter haemmorages Advavce glaucomatous chamges :- -Cup size 0.7 to 0.9 - Neuroretinal rim thinning -Nasal siftting of retinal vessels -Lamellar dot signs
Visual field deffects :- In glaucoma ,visual field defects observed in BJERRUM’S area .... -Retinal paracentral scotoma - Roenn’s nasal steep -Seidel scotoma - Arcuate scotoma
INVESTIGATION OF POAG 1)GONIOSCOPY:- -Wide open angle of ant.chamber -structure seen ROI,SS,SL,CBB,TM TONOMETRY :- - Tonometry shoul be preferred over Schitze tonometry -IOP <21 mm of hg PROGRESSIVE CUPPING:- CD= 0.3 to 0.4 normal fundus
MANAGEMENT Aim of treatment to prevent impairment of vision Require careful & regular periodic supervision by ophthalmologist Theraputic choices:- -Medical therapy:- - Parasympathomimetic drugs - Prostaglandine -Topical beta blockers -Carbonic anhydrase inhibitors Argon or diode laser trabeculoplasty :- Action:- outflow by causing shrinkage of TM Technique:-40-50 spots on the anterior half of TM over 180 using a Goniolens
SURGERY FOR POAG Fileration surgery Trabeculectomy Trabeculectomy
PACG PRIMARY ANGLE CLOSURE GLAUCOMA It refers to occlusion of the TM by the peripheral iris abstructing aqueous outflow Narrow angle/acute glaucoma Much more rare IOP is ries very queckly It is caused by a rapid or sudden increase in eye pressure
CLASSIFICATION ( 1)Primary angle closure suspect:- -Normal IOP,optic disc & visual field -No peripheral anterior synechiae ( 2)Primary angle closure:- -Optic nerve damage from an episode of severe IOP elevation -ITC in three or more quadrants ( 3)Primary angle closure glaucoma:- -Shows three or more quadrents of ITC with rised IOP. -Normal disc & field
RISK FACTORS Age:- -60 years- pupillary block -young non pupillary block Gender:- Female > Male Family history :-Genetic factors Race:- Asians Refraction:- Typically hypermetropic
CAUSES Angle beteween iris and cornea is closed Increase IOP suddenly Completely block the canals,which stops fluid flowing Some health condition can also cause ACG:- -Cataract -Ectopic lens -Diabetic retinopathy - Tumors
MECHANISM OF ACG 1)Relative pupil block:- 70% of case -Iris hase large arc of contact with anterior surface of lens 2)Iris bombe formation:- Responsible for few atypical case 3)Appositional angle closure:- mechanism along with pupillary block with iris bombe. Relative pupilary blok :-
IRIS BOMB
Iris bombe
CLINICAL FEATURES Symptoms:- -Rapidly progressive impairement of vision -Painful eye -Red eye -Nausea - Vomitting -photophobia -Haloes
Signs:- -Reduce visual acuity -Cornea cloudy,& oedemotous -Pupil oval,fixed,modaretly dilated -Eye feels hard on palpation -Elevated IOP 50-100 mm of Hg -Aqueous flare & cells -Optic disc oedema & hyperaema
-If patient in pain:- -Topical ketorolac -Systemic pain medication -If patient in vomitting :- - Intramascular metoclopromide -If patient in comfortable:- -Laser iridoctomy in fellow eye
SECONDARY GLAUCOA Group of disorder in which the raised IOP is assosiated with a primary ocular or systemic diseases.
CLASSIFICATION ( A)Depending on the mechanism of rise in IOP:- i )Secondary open angle glaucoma:- -In which aqueous outflow may be blocked by pretrabucular membrane or trabecular closing. ii)Secondary angle closure:- which may be or may not be assosiated with pupil block
( B)Depending on the cavsative primary diseases:- -Lens induced glaucoma - Inflamatory glaucoma - Neuvascular glaucoma - Cilliary block glaucoma -Traumatic glaucoma -Glaucoma in aphakia -glaucoma with assosiated with intra ocular haemorrhage
PHACOLYTIC GLAOCOMA Pathogenesis:- - T.M is clogged by the lens proteins,macrophages . -Deep anterior chamber and aqueous may contain fine white protein particles. Clinical features:- - Symptoms:- - pain,nausea,vomitting -rapidly progressive impairement of vision
Signs:- -Lid oedematous - Congunctiva-chemosed & congested - Cilliary vessel congested -A.C very shallow -Iris may be discolored -Optic disc oedematous & hyperaemic Management:- -Medical therapy to lower the IOP -Extraction of the hypermature catarctous lens with PCIOL implantation
Phacolytic glaucoma
NEUVASCULAR GLAUCOMA Result due to formation of neuvascular membrane involving the angle of anterior chamber Etiology:- Neuvascularization of iris following retina isvhaemia features of – -PDR -CRVO -Sickle-cell retinoparhy
TRAUMATIC GLAUCOMA Mechanism:- -Inflammatory glaucoma due to iridocyclitis -Due to intra ocular haemorrhage -Lens-induced glaucoma due to shollen lens -Epithelial grouth -Angle recession glaucoma -Angle-closure glaucoma due to anterior synechia
Management:- Medical therapy with topical 0.5% timolol and oral acetazolamide and surgical intervention according to situation. Image of traumatic glaucoma:-
GLAUCOMA INVESTIGATION Instrument which are use in glaucoma investigation are:- - OCT (Disc profile): -To measure the thickness of RNFL - VFA :- for visual field test - Perimetry :-visual field test - Tonometry :- measure the inner eye pressur - Opthalmoscopy :-for shape & color of optic nerve - Gonioscopy :-to see the iridocorneal angler - Pachymetry :- to measure thickness of cornea
Tonometry Applanation Schiotz Gonioscopy
THE VISUAL FIELD Humphrey automated perimetry
PATIENTS RECORDS
CASE:-01 PT’S NAME :- Vishwanath thakur DATE:- 09/10/2018 REG NO .:- 1819-011510 AGE:- 55 year OCCUPATION:- farmer SEX:- Male ADRESS :- west bengal C/O :- RE-Trauma by hand FINDING :- Fundus -RE- T otal cup ,LE -c/d=0:5 V/A:- RE-6/60p ,LE:-6/24p IOP:- RE-54,LE:-15
INVESTIGATION:- VFA OCT (DISC PROFILE) APLANATION TONOMETRY INDIRECT OPHTHALMOSCOPY REPORTS:-VFA:-LE- advanced field loss A.T:- RE-18,LE-27 OCT:-LE significant development seen of inferior quadrent (LE-vertical C/D=1.00) CONCLUSIONS :-
CASE:- 03 PT’S NAME :- DATE:- ID NO .:- AGE:- OCCUPATION:- SEX:- ADRESS :- C/O :- FINDING :- Fundus V/A:-RE- ,LE:-