Glaucoma

3,659 views 84 slides Nov 04, 2018
Slide 1
Slide 1 of 84
Slide 1
1
Slide 2
2
Slide 3
3
Slide 4
4
Slide 5
5
Slide 6
6
Slide 7
7
Slide 8
8
Slide 9
9
Slide 10
10
Slide 11
11
Slide 12
12
Slide 13
13
Slide 14
14
Slide 15
15
Slide 16
16
Slide 17
17
Slide 18
18
Slide 19
19
Slide 20
20
Slide 21
21
Slide 22
22
Slide 23
23
Slide 24
24
Slide 25
25
Slide 26
26
Slide 27
27
Slide 28
28
Slide 29
29
Slide 30
30
Slide 31
31
Slide 32
32
Slide 33
33
Slide 34
34
Slide 35
35
Slide 36
36
Slide 37
37
Slide 38
38
Slide 39
39
Slide 40
40
Slide 41
41
Slide 42
42
Slide 43
43
Slide 44
44
Slide 45
45
Slide 46
46
Slide 47
47
Slide 48
48
Slide 49
49
Slide 50
50
Slide 51
51
Slide 52
52
Slide 53
53
Slide 54
54
Slide 55
55
Slide 56
56
Slide 57
57
Slide 58
58
Slide 59
59
Slide 60
60
Slide 61
61
Slide 62
62
Slide 63
63
Slide 64
64
Slide 65
65
Slide 66
66
Slide 67
67
Slide 68
68
Slide 69
69
Slide 70
70
Slide 71
71
Slide 72
72
Slide 73
73
Slide 74
74
Slide 75
75
Slide 76
76
Slide 77
77
Slide 78
78
Slide 79
79
Slide 80
80
Slide 81
81
Slide 82
82
Slide 83
83
Slide 84
84

About This Presentation

topc for glaucoma


Slide Content

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%)

TRABECULAR OUTFLOW :- CILLIARY BODY POSTERIOR CHAMBER ANTERIOR CHAMBER TRABECULAR MESHWORK SCLEMNS CANEL COLLECTOR CHANELS EPISCLERAL VEIN

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 )

CLASSIFICATION of glaucoma ( A)Congenital/Developmental glaucoma 1)primary congenital glaucoma (without associated anomalies ) 2)developmental glaucoma (with associated anomalies )

( B)PRIMARY GLAUCOMA 1)POAG 2)PACG 3)Primary mixed mechanism glaucoma (C) SECONDARY GLAUCOMA P hacomorphic glaucoma Phacolytic glaucoma Pigmentary glaucoma Traumatic glaucoma Cilliary block glaucoma Neovascular glaucoma Glaucoma in aphakia

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

CLASSIFICATION Primary developmental/congenital glaucoma Developmental glaucoma with associated congenital ocular anomalies Developmental glaucoma with associated systemic anomalies ISOLATED CONGENITAL GLAUCOMA:- ISOLATED CONGENITAL GLAUCOMA

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

INVESTIGATION IOP measurement Corneal diameter measurement Slit lamp examination Ophthalmoscopy Gonioscopy

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

CD=0.5 CD=0.5 to 0.7 optic dics margine NRR CD=0.9 CD=1.0 0.9 CD=1.0

Cup-to-disk ratio

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

MANAGEMENT 1)Medicine:- - Acetazolamide -Topical steroids -Topical beta blockers 2)Surgical management:- -Peripheral laser iridotomy -Peripheral iridotomy INITIAL MANAGEMENT :- - Immediately on attack: - Pilocarpine -beta blockers -Topical corticosteroid

-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

LENS INDUCED ( phacogenic ) Pacomorphic –(due to swollen lens) Phacotopic -(anterior lens displacement) Phacolytic Lens partical glacucoma Phacoanaphylactic glaucoma

Figure 1: (a) Traumatic anterior dislocation of lens with pupillary block glaucoma; (b) lens particle glaucoma; (c) phacomorphic glaucoma; (d) phacolytic

PHACOMORPHIC GLAUCOMA Causes:- - Intumesent lens - ant.subluxation of lens & spherophakia Pathogenosis :- -swollen lens pushes iris forward Treatment:- -Medical:-control of IOP by- - iv mannitol - acetazolamide -topical beta blockers -LASER iridotomy

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

Clinical Profile:- - Pre- glaucomotous stage -Open angle glaucoma stage -Secondary angle closure glaucoma Treatment:- - Panretinal photocoagulation -Medical therapy not affective - Arteficial filtration shunt.

Neuvascular glaucoma

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 APLANATION TONOMETRY INDIRECT OPHTHALMOSCOPY REPORTS:-VFA:- RE- Trabeular vision LE-generalized depression A.T:- RE-55,LE-14 I.O:- RE-Total cupping,LE :-c/d=0:5 CONCLUSIONS:-

CASE:- 02 PT’S NAME :- Hiralal manjhi DATE:-12/10/2018 REG NO .:-1718-017579 AGE:-52y OCCUPATION:- bussinessman SEX:-male ADRESS :- P urulia,W.B C/O :-low vision,headache , FINDING :- Fundus -LE-cupping undialated V/A:-RE-NOPL ,LE:-6/18P CORNEA:-RE-Total corneal opacity

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:-

INVESTIGATION:- VFA OCT (DISC PROFILE) APLANATION TONOMETRY INDIRECT OPHTHALMOSCOPY REPORTS:- CONCLUSIONS:-

CASE:- 04 PT’S NAME :- DATE:- ID NO .:- AGE:- OCCUPATION:- SEX:- ADRESS :- C/O :- FINDING :- Fundus V/A:-RE- ,LE:-

INVESTIGATION:- VFA OCT (DISC PROFILE) APLANATION TONOMETRY INDIRECT OPHTHALMOSCOPY REPORTS:- CONCLUSIONS:-

CASE:-05 PT’S NAME :-REENA DEVI DATE:- 04/09/2018 REG NO.:- Reg1819-011281 AGE :-30 years SEX:- female OCCUPATION:- House wife ADRESS :-Ranchi C/O :- -painless loss of vision,-Mild headache -Changes in presbyopic glasses FINDING:- Fudus -Cupping V/A-RE-6/6P,LE-6/6P NCT-RE-22,LE-10

INVESTIGATION :- -VFA -OCT (DISC PROFILE) -INDIRECT OPHTHALMOSCOPY -APLANATION TONOMETRY REPORTS:- VFA :-Normal OCT :-Vertical C/D=RE-0.71,LE-0.72 I.O :-Cupping A.T:- RE-23,LE-13 (mm of Hg) CONCLUSIONS:-