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Primary Glaucoma

POAG and PACG are inlcluded.

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Primary Glaucoma

  1. 1. GLAUC MA JOHN PAUL A. TADAY, RN, MD-MPA LEVEL 2
  2. 2. GLAUCOMA: CLASSIFICATION CONGENITAL & DEVELOPMENTAL GLAUCOMAS1 PRIMARY ADULT GLAUCOMAS1 SECONDARY GLAUCOMAS1 ABSOLUTE GLAUCOMA2
  3. 3. GLAUCOMA: CLASSIFICATION
  4. 4. PRIMARY GLAUCOMA GENERAL INFORMATION
  5. 5. PRIMARY GLAUCOMA: DEFINITION OPTIC DISK CUPPING VISUAL FIELD LOSS OCULAR HYPERTENSION  cases with constantly IOP w/o any assoc. glaucomatous damage NORMAL or LOW TENSION GLAUCOMA  cases with cupping of the disc and/or visual field defects with a normal or IOP, NTG/LTG PRIMARY OPEN-ANGLE GLAUCOMA & PRIMARY ANGLE-CLOSURE GLAUCOMA • Refers to collection of diseases with chronic optic neuropathy showing DISTINCTIVE CHANGES • Mostly associated with IOP • Normal or low-tension glaucoma also possible1
  6. 6. PRIMARY GLAUCOMA: EPIDEMIOLOGY INCIDENCE  ~60M people affected (Worldwide) • Expected to  from 64M (2015) to 76M (2020), and 111M (2040)3 • 3M people (US) & 50% undiagnosed RACE  African Countries (highest prevalence)3 • Blacks & Whites (POAG > PCAG) • China & Asians (PCAG – 90% of cases) • Japan (Normal-tension glaucoma most common) • Philippines (POAG = PCAG)4 AGE  the mean IOP  after 40 y/o possibly d/t  facility of aqueous outflow2 GENDER  in older age groups IOP with age greater in females2
  7. 7. PRIMARY GLAUCOMA: PHYSIOLOGY • Pathophysiology revolves around the AQUEOUS HUMOUR DYNAMICS • CILIARY BODY  aqueous production • ANGLE OF ANTERIOR CHAMBER  formed by root of iris, anterior-most part of ciliary body, scleral spur, trabecular meshwork and Schwalbe’s linePRINCIPAL OCULAR STRUCTURES:
  8. 8. PRIMARY GLAUCOMA: PHYSIOLOGY • AQUEOUS OUTFLOW SYSTEM TRABECULAR MESHWORK (CONVENTIONAL)
  9. 9. PRIMARY GLAUCOMA: PHYSIOLOGY • AQUEOUS OUTFLOW SYSTEM UVEOSCLERAL OUTLOW (UNCONVEN- TIONAL)
  10. 10. PRIMARY GLAUCOMA: PHYSIOLOGY • AQUEOUS OUTFLOW SYSTEM UVEAL MESHWORK CORNEOSCLERAL MESHWORK JUXTACANALICULAR (ENDOTHELIAL) MESHWORK • TRABECULAR MESHWORK  sieve- like structure through which aqueous humour leaves the eye
  11. 11. • SCHLEMM’S CANAL  endothelial lined oval channel to the aqueous vein and intrascleral plexus PRIMARY GLAUCOMA: PHYSIOLOGY • AQUEOUS OUTFLOW SYSTEM • COLLECTOR CHANNELS  called “Intrascleral Aqueous Vessels”, about 25-35 in number, terminate into episcleral veins AQUEOUS HUMOUR PRODUCTION: • ULTRAFILTRATION • SECRETION (ACTIVE TRANSPORT) • DIFFUSION (PASSIVE TRANSPORT)
  12. 12. PRIMARY GLAUCOMA: PHYSIOLOGY VACUOLATION THEORY 1 – Non-vacuolated stage 2 – Stage of early infolding of basal surface of the endothelial cell 3 – Stage of macrovacuolar structure formation 4 – Stage of vacuolar transcellular channel formation 5 – Stage of occlusion of the basal infolding • “Most Accepted View” in aqueous humor flow • Transcellular spaces exist in the endothelial cells  OPEN AS A SYSTEM OF VACUOLES AND PORES, primarily in response to pressure
  13. 13. PRIMARY GLAUCOMA: MAJOR TYPES OPEN ANGLE CLOSED ANGLE
  14. 14. PRIMARY OPEN ANGLE GLAUCOMA
  15. 15. PRIMARY OPEN ANGLE GLAUCOMA DEFINITION • A type of primary glaucoma • (–) obvious systemic or ocular cause • IOP OPEN ANGLE of anterior chamber • A.k.a. “CHRONIC SIMPLE GLAUCOMA OF ADULT ONSET” EPIDEMIOLOGY • Varies in different populations & 1/3 of all cases of glaucoma • RACE  4X more common & 6X more likely to cause blindness in BLACKS • AGE  5th & 7th decades • INCIDENCE  affects ~ 1/100 of the population (of either sex) >40 y/o
  16. 16. PRIMARY OPEN ANGLE GLAUCOMA ETIOLOGY & PATHOPHYSIOLOGY PREDISPOSING AND RISK FACTORS • HEREDITY  polygenic inheritance, 4% risk in the offspring of patients • AGE  risk  with  age • RACE  more severe in black • MYOPES  nearsighted person • DIABETICS  higher prevalence • SMOKING  higher risk • HIGH BLOOD PRESSURE • THYROTOXICOSIS  does not cause IOP, but prevalence more in Graves’ ophthalmic patients than the normals IOP  AQUEOUS OUTFLOW FACILITY  RESISTANCE TO AQUEOUS OUTFLOW TRABECULAR MESHWORK THICKENING & SCLEROSIS ABSENCE OF GIANT VACUOLES (CANAL OF SCHLEMM) CAUSE UNCERTAIN UNCONTROLLED
  17. 17. PRIMARY OPEN ANGLE GLAUCOMA VISUAL FIELD DEFECTS FORCES THE LAMINA CRIBROSA BACKWARDS MECHANICAL EFFECTS VASCULAR EFFECTS DAMAGING CASCADE ISCHAEMIC ATROPHY SQUEEZES THE NERVE FIBRES VISUAL FIELD LOSS DEATH OF RETINAL GANGLION CELLS (RGC’s) LARGE CAVERNS OR LACUNAE ARE FORMED (CAVERNOUS OPTIC ATROPHY)
  18. 18. PRIMARY OPEN ANGLE GLAUCOMA CLINICAL MANIFESTATIONS SYMPTOMS • Insidious & usually ASYMPTOMATIC • Mild headache & eyeache • Frequent changes in presbyopic glasses • Delayed dark adaptation SIGNS • ANTERIOR SEGMENT SIGNS  pupil reflex becomes sluggish & cornea may show slight haze (LATE STAGES) SIGNS • IOP CHANGES  IOP falls during the evening (most patients) in Diurnal Variation Test
  19. 19. PRIMARY OPEN ANGLE GLAUCOMA SIGNS • OPTIC DISC CHANGES  seen on fundoscopic exam • VERTICALLY OVAL CUP  d/t selective loss of neural rim tissue in the inferior and superior poles • ASYMMETRY OF THE CUPS  difference of > 0.2 b/w two eyes OPTIC DISK CUPPING 1. EARLY GLAUCOMATOUS CHANGES Reveals one or more of the following signs: NORMAL
  20. 20. PRIMARY OPEN ANGLE GLAUCOMA • LARGE CUP  0.6 or more (Normal cup size – 0.3 to 0.4) may occur d/t concentric expansion • SPLINTER HAEMORRHAGES  present on/near optic disc margin • PALLOR AREAS  present on disc • ATROPHY OF RETINAL NERVE FIBRE LAYER  seen with red free light 1. EARLY GLAUCOMATOUS CHANGES Reveals one or more of the following signs: NORMAL EARLY CHANGE
  21. 21. PRIMARY OPEN ANGLE GLAUCOMA • MARKED CUPPING  cup size 0.7 to 0.9, excavation may even reach the disc margin • THINNING OF NEURORETINAL RIM  seen as a crescentric shadow adjacent to the disc margin • NASAL SHIFTING OF RETINAL VESSELS  appearance of being broken off at the margin – BAYONETTING SIGN 2. ADVANCED GLAUCOMATOUS CHANGES Reveals one or more of the following signs: NORMAL LATE CHANGE
  22. 22. PRIMARY OPEN ANGLE GLAUCOMA • PULSATIONS OF THE RETINAL ARTERIOLES  may be seen at the disc margin (a PATHOGNOMIC SIGN of glaucoma), when IOP is very high • LAMELLAR DOT SIGN  pores in the lamina cribrosa are slit-shaped and are visible up to the margin of the disc 2. ADVANCED GLAUCOMATOUS CHANGES Reveals one or more of the following signs: NORMAL LATE CHANGE
  23. 23. PRIMARY OPEN ANGLE GLAUCOMA • As the damage progresses, all the NEURAL TISSUE of the disc is destroyed and the OPTIC NERVE HEAD appears white & excavated 3. GLAUCOMATOUS OPTIC ATROPHY Reveals one or more of the following signs: NORMAL OPTIC ATROPHY
  24. 24. PRIMARY OPEN ANGLE GLAUCOMA • VISUAL FIELD DEFECTS  usually run parallel to the changes at optic nerve head & progresses if IOP is not controlled • SRF & IRF  superior and inferior radiating fibres from nasal half • PMB  PAPILLOMACULAR BUNDLE from macular area • SAF & IAF  superior & inferior arcuate fibres from the temporal half ANATOMICAL BASIS OF FIELD DEFECTS • DISTRIBUTION OF RETINAL NERVE FIBRES
  25. 25. PRIMARY OPEN ANGLE GLAUCOMA • VISUAL FIELD DEFECTS  usually run parallel to the changes at optic nerve head & progresses if IOP is not controlled • From peripheral part – lie deep in the retina but occupy the most peripheral (superficial) part of the optic disc • Fibres originating closer to the nerve head – lie superficially and occupy a more central (deep) portion of the disc. EARLY LOSS IN THE VISUAL FIELD REGIONS RETENTION OF CENTRAL VISION TILL END ANATOMICAL BASIS OF FIELD DEFECTS • ARRANGEMENT OF NERVE FIBRES WITHIN OPTIC NERVE HEAD • ARCUATE FIBERS (SAF & IAF)  occupy the superior & inferior temporal half of optic nerve head – most sensitive to damage • MACULAR FIBRES  most resistant to the glaucomatous damage
  26. 26. PRIMARY OPEN ANGLE GLAUCOMA • VISUAL FIELD DEFECTS  usually run parallel to the changes at optic nerve head & progresses if IOP is not controlled PROGRESSION OF FIELD DEFECTS • ISOPTER CONTRACTION  mild generalized constriction of central as well as peripheral field EARLIEST VISUAL FIELD DEFECT • BARING OF BLIND SPOT  exclusion of the blind spot from the central field d/t inward curve of the outer boundary of 30° central field • SMALL WING-SHAPED PARACENTRAL SCOTOMA  appear below or above the blind spot in BJERRUM'S AREA EARLIEST CLINICALLY SIGNIFICANT FIELD DEFECT • SEIDEL’S SCOTOMA  “Sickle-shaped” in time, paracental scotoma joins the blind spot
  27. 27. PRIMARY OPEN ANGLE GLAUCOMA • ARCUATE OR BJERRUM’S SCOTOMA  formed by extension of Seidel’s scotoma in an area either above or below the fixation point to reach the horizontal line • RING / DOUBLE ARCUATE SCOTOMA  develops when the two arcuate scotomas join together • ROENNE'S CENTRAL NASAL STEP  two arcuate scotomas run in different arcs and meet to form a sharp right-angled defect at the horizontal meridian • PERIPHERAL FIELD DEFECTS  can appear in early and late stages • ADVANCED FIELD DEFECTS  eventually only a small island of central vision (TUBULAR VISION) are left
  28. 28. PRIMARY OPEN ANGLE GLAUCOMA
  29. 29. PRIMARY OPEN ANGLE GLAUCOMA DIAGNOSTIC FACTORS • CRITERIA to diagnose EARLY, MODERATE and SEVERE glaucomatous field defects
  30. 30. PRIMARY OPEN ANGLE GLAUCOMA • TONOMETRY  measures the IOP TWO BASIC TYPES OF TONOMETERS: INDENTATION (IMPRESSION) 2. Schiotz Tonometer APPLANATION 1. Goldmann Tonometer
  31. 31. PRIMARY OPEN ANGLE GLAUCOMA • DIURNAL VARIATION TEST  useful in detection of early cases A – Normal slight morning rise B – Morning rise seen in 20% cases C – Afternoon rise seen in 25% D – Biphasic variation seen in 55% • SLIT-LAMP EXAMINATION  to R/O causes of 2° Open Angle Glaucoma • WATER DRINKING TEST  eyes with glaucoma with greater response to water drinking a. 8 hours fasting, then baseline IOP b. Patient drinks 1L of water, then IOP noted q 15min for 1 hour c. Rise of 8 mmHg or more (DIAGNOSTIC) • NERVE FIBRE LAYER ANALYZER  to detect damage in retinal nerve fibres
  32. 32. PRIMARY OPEN ANGLE GLAUCOMA • PERIMETRY  detect visual field defects TWO CLASSIFICATIONS OF PERIMETERS: GOLDMANN’S PERIMETER 1. Manual PerimeterLISTER’S PERIMETER 2. Automated Perimeter HUMPHREY FIELD ANALYSER • ADVANTAGES OF AUTOMATED: 1. Level of precision & consistency 2. data storage capability & ease 3. Statistical comparison
  33. 33. PRIMARY OPEN ANGLE GLAUCOMA • GONIOSCOPY  primary importance in POAG is to rule out other forms of glaucoma GOLDMANN’S GONIOLENS & TECHNIQUE OF GONIOSCOPY • APPLICATIONS OF GONIOSCOPY: 1. Classification of glaucoma into open angle and closed angle based on configuration of the angle 2. Localization of foreign bodies, abnormal blood vessels or tumors in the angle. 3. Demonstration of extent of peripheral anterior synechiae and hence planning of glaucoma surgery 4. Direct goniolens is used during goniotomy
  34. 34. PRIMARY OPEN ANGLE GLAUCOMA SHAFFER’S SYSTEM OF GRADING THE ANGLE WIDTH MOST COMMONLY USED
  35. 35. OCULAR HYPERTENSION
  36. 36. OCULAR HYPERTENSION DEFINITION • “Glaucoma Suspect” • IOP constantly >21mmHg but NO OPTIC DISC or VISUAL FIELD CHANGES ETIOLOGIC FACTORS HIGH RISK FACTORS • IOP CONSTANTLY >28 mmHg • SIGNIFICANT DIURNAL VARIATION  difference of > 8mmHg • Significantly positive WATER DRINKING TEST • Association with SPLINTER HEMORRHAGES • RETINAL NERVE FIBER LARGE DEFECTS • PARAPAPILLARY CHANGES • CENTRAL CORNEAL THICKNESS < 555 μm Should be CAREFULLY MONITORED by an ophthalmologist, should be treated as cases of POAG in the presence of HIGH RISK FACTORS
  37. 37. OCULAR HYPERTENSION OTHER RISK FACTORS • SIGNIFICANT ASYMMETRY in the cup size of the two eyes  difference of more than 0.2 • Strong FAMILY HISTORY of glaucoma • When associated with HIGH MYOPIA, DIABETES or PIGMENTARY CHANGES in the anterior chamber MANAGEMENT • WITH HIGH RISK FACTORS  treated on the lines of POAG (aim is to reduce IOP by 20%) • NO HIGH RISK FACTORS  annually followed by examination of optic disc, perimetry and record of IOP, treatment not required till glaucomatous damage is documented
  38. 38. NORMAL TENSION GLAUCOMA
  39. 39. NORMAL TENSION GLAUCOMA DEFINITION • (NTG), A.k.a LOW TENSION GLAUCOMA, typical glaucomatous DISC CHANGES, but WITH / WITHOUT VISUAL FIELD DEFECTS • Associated with IOP constantly <21 mmHg EPIDEMIOLOGY • Variant of POAG (16% of all cases of POAG) • AGE  prevalence >40 y/o is 0.2% ETIOLOGY & PATHOPHYSIOLOGY OPTIC NERVE SUSCEPTIBLE CHRONIC LOW VASCULAR PERFUSION PREDISPOSING AND RISK FACTORS • Raynauld phenomenon • Migraine • Nocturnal systemic hypotension • Overtreated systemic hypertension • blood flow velocity (ophthalmic artery) VASCULAR EFFECT ONLY!
  40. 40. NORMAL TENSION GLAUCOMA CLINICAL MANIFESTATIONS • Disc changes & visual field defects (Similar to POAG) • NORMAL IOP • Other features of NTG are some ASSOCIATIONS mentioned DIFFERENTIAL DIAGNOSIS • POAG  early stages POAG may present with normal IOP • Congenital optic disc anomalies • APPROXIMATELY 60% HAVE PROGRESSIVE VISUAL FIELD LOSS
  41. 41. NORMAL TENSION GLAUCOMA MANAGEMENT • MEDICAL TREATMENT to IOP  IOP by 30% (about 12-14 mmHg) a. BETAXOLOL  DOC d/t in addition to IOP, also optic nerve blood flow b. Other Beta Blockers and Adrenergic drugs (DIPIVERAFRINE)  be avoided (causes nocturnal systemic hypotension & are likely to affect adversely the optic nerve perfusion) c. NEUROPROTECTIVE DRUGS  may be preferred like “Brimonidine” d. PROSTAGLANDIN ANALOGUES  greater ocular hypotensive effect • TRABECULECTOMY  considered when progressive field loss occurs despite IOP in lower teens • SYSTEMIC Ca2+ BLOCKERS  for confirmed peripheral vasospasm • SYSTEMIC BP MONITORING
  42. 42. PRIMARY ANGLE-CLOSURE GLAUCOMA
  43. 43. PRIMARY ANGLE-CLOSURE GLAUCOMA DEFINITION • A type of primary glaucoma, (–) obvious systemic or ocular cause •  IOP occurs d/t BLOCKAGE of the aqueous humour outflow • Closure of a NARROWER ANGLE of the anterior chamber EPIDEMIOLOGY • AGE  more common in 5th decade of life • GENDER  F>M (Ratio 4:1) • RACE  South-East Asian, Chinese (50% of all primary glaucoma) or Inuit/ Eskimos2 • SEASON  higher in rainy season • FAMILY HISTORY  inherited • TYPE OF PERSONALITY  common in individuals with unstable vasomotors
  44. 44. PRIMARY ANGLE-CLOSURE GLAUCOMA ETIOLOGY & PATHOPHYSIOLOGY I. ANATOMICAL FACTORS • HYPERMETROPIA with shallow anterior chamber • Iris-lens DIAPHRAGM placed anteriorly • NARROW ANGLE of anterior chamber, which may be d/t: a. Small eyeball b. Relatively large size of the lens & smaller diameter of the cornea c. Bigger size of the ciliary body II. GENERAL FACTORS • AGE • GENDER • RACESEASON • FAMILY HISTORY • TYPE OF PERSO- NALITY PREDISPOSING RISK FACTORS The following factors may PRECIPITATE an attack: • DIM ILLUMINATION • EMOTIONAL STRESS • MYDRIATIC DRUGS like Atropine, Tropicamide PRECIPITATING FACTORS INCREASED AMOUNT OF APPOSITION B/W IRIS ANTERIORLY PLACED LENS WITH CONSIDERABLE PRESSURE NORMAL PUPIL MILD PUPIL DILATATION
  45. 45. PRIMARY ANGLE-CLOSURE GLAUCOMA RELATIVE PUPIL BLOCK AQUEOUS HUMOR COLLECTS IN THE POSTERIOR CHAMBER PUSHES THE PERIPHERAL FLACCID IRIS ANTERIORLY IRIS BOMBE APPOSITIONAL ANGLE CLOSURE SYNECHIAL ANGLE CLOSURE ATTACK OF  IOP MAY LAST LONGER ACUTE PACG CHRONIC PACG Results from the following CIRCUMSTANCES: • CREEPING SYNECHIAE • SUBACUTE PACG ATTACKS • MIXED MECHANISM
  46. 46. PRIMARY ANGLE-CLOSURE GLAUCOMA CLINICAL MANIFESTATIONS: LATENT PRIMARY ANGLE-CLOSURE GLAUCOMA  “Glaucoma suspect” SUBACUTE OR INTERMITTENT PACG ACUTE ANGLE-CLOSURE GLAUCOMA POSTCONGESTIVE ANGLE-CLOSURE GLAUCOMA CHRONIC PACG FIVE DIFFERENT CLINICAL ENTITIES
  47. 47. PRIMARY ANGLE-CLOSURE GLAUCOMA CLINICAL MANIFESTATIONS: LATENT PRIMARY ANGLE-CLOSURE GLAUCOMA  “Glaucoma suspect” INDICATES DECREASED AXIAL ANTERIOR CHAMBER DEPTH • Eyes with shallow anterior chamber with an OCCLUDABLE ANGLE • SYMPTOMS  absent • ECLIPSE SIGN  elicited by shining a penlight across the anterior chamber from temporal side, noting a shadow on the nasal side FIVE DIFFERENT CLINICAL ENTITIES
  48. 48. PRIMARY ANGLE-CLOSURE GLAUCOMA CLINICAL MANIFESTATIONS: • GONIOSCOPIC EXAMINATION  it shows very narrow angle (SHAFFER GRADE 1) • SLIT-LAMP BIOMICROSCOPIC SIGNS: a.axial anterior chamber depth b.Convex shaped iris lens diaphragm c. Close proximity of the iris to cornea in the periphery LATENT PRIMARY ANGLE-CLOSURE GLAUCOMA  “Glaucoma suspect” FIVE DIFFERENT CLINICAL ENTITIES
  49. 49. PRIMARY ANGLE-CLOSURE GLAUCOMA CLINICAL MANIFESTATIONS: LATENT PRIMARY ANGLE-CLOSURE GLAUCOMA  “Glaucoma suspect” • VAN HERICK SLIT-LAMP GRADING  used when gonioscope is not available (FAIR ACCURACY) • Peripheral Anterior Chamber Depth (PACD) compared to the adjacent corneal thickness (CT) and the presumed angle width • CLINICAL COURSE  if without Tx, may follow any of the following: a. IOP may remain NORMAL b. SUBACUTE or ACUTE angle-closure glaucoma may occur subsequently c. CHRONIC angle-closure glaucoma may develop without passing through subacute or acute stage FIVE DIFFERENT CLINICAL ENTITIES
  50. 50. PRIMARY ANGLE-CLOSURE GLAUCOMA VAN HERICK METHOD OF SLIT-LAMP GRADING A – Grade IV B – Grade III C – Grade II D – Grade I E – Grade 0 GRADES: Grade 4 (WIDE OPEN ANGLE) • PACD = 3/4 to 1 CT Grade 3 (MILD NARROW) • PACD = ¼ to ½ CT Grade 2 (MODERATE NARROW) • PACD = ¼ CT Grade 1 (EXTREMELY NARROW) • PACD < ¼ CT Grade 0 (CLOSED ANGLE) • PACD Nil
  51. 51. PRIMARY ANGLE-CLOSURE GLAUCOMA CLINICAL MANIFESTATIONS: FIVE DIFFERENT CLINICAL ENTITIES • Attack of TRANSIENT IOP (40-50 mmHg) (last for minutes to 1-2 hours) • Usually PRECIPITATED by: a. PHYSIOLOGICAL MYDRIASIS  reading in dim light, watching TV or cinema in darkened room, or during anxiety (Sympathetic Overactivity) b. PHYSIOLOGICAL SHALLOWING OF ANTERIOR CHAMBER  after lying in prone position SUBACUTE OR INTERMITTENT PACG • SYMPTOMS  unilateral transient blurring of vision, coloured halos around light, headache, browache and eyeache on the affected side COLOURED HALOS AROUND LIGHT
  52. 52. PRIMARY ANGLE-CLOSURE GLAUCOMA CLINICAL MANIFESTATIONS: FIVE DIFFERENT CLINICAL ENTITIES • During PE, eye is white & not congested • All the signs described in LATENT PACG can be elicited in this phase ALSO • CLINICAL COURSE  if without Tx, may follow any of the following: a. Attack of ACUTE PACG b. CHRONIC PACG without passing through acute stage SUBACUTE OR INTERMITTENT PACG
  53. 53. PRIMARY ANGLE-CLOSURE GLAUCOMA CLINICAL MANIFESTATIONS: FIVE DIFFERENT CLINICAL ENTITIES • Attack of Acute PACG occurs d/t a sudden total angle closure leading to SEVERE RISE in IOP ACUTE ANGLE-CLOSURE GLAUCOMA SIGHT THREATENING EMERGENCY! SYMPTOMS • PAIN  sudden onset of very severe pain that radiates along the CN-V branches • NAUSEA, VOMITING, PROSTRATIONS • Rapid progress of VISION LOSS  also with redness, photophobia & lacrimation (PRESENT IN ALL CASES) • PAST HISTORY  ~5% (+)Hx of typical previous transient attacks of subacute angle-closure glaucoma
  54. 54. SIGNS • LIDS  may be edematous • CONJUNCTIVA  congested • CORNEA  edematous & insensitive • ANTERIOR CHAMBER  very shallow • ANGLE OF ANTERIOR CHAMBER  closed completely (SHAFFER GRADE0) • IRIS  may be discoloured PRIMARY ANGLE-CLOSURE GLAUCOMA CLINICAL MANIFESTATIONS: FIVE DIFFERENT CLINICAL ENTITIES ACUTE ANGLE-CLOSURE GLAUCOMA •NOTE CILIARY CONGESTION, •CORNEAL EDEMA & MIDDILATED PUPIL DISCOLOURED IRIS VERY SHALLOW – ANTERIOR CHAMBER
  55. 55. SIGNS • IOP  it is usually markedly elevated, b/w 40-70 mmHg (NV:10-21mmHg) • PUPIL  semi-dilated, vertically oval and fixed, usually non-reactive to both light & accommodation • OPTIC DISC  edematous, hyperemic • FELLOW EYE  shows shallow anterior chamber and a narrow angle PRIMARY ANGLE-CLOSURE GLAUCOMA CLINICAL MANIFESTATIONS: FIVE DIFFERENT CLINICAL ENTITIES ACUTE ANGLE-CLOSURE GLAUCOMA PUPIL NON-REACTIVE TO BOTH LIGHT & ACCOMMODATION EDEMATOUS & HYPEREMIC OPTIC DISC
  56. 56. PRIMARY ANGLE-CLOSURE GLAUCOMA CLINICAL MANIFESTATIONS: FIVE DIFFERENT CLINICAL ENTITIES POSTCONGESTIVE ANGLE-CLOSURE GLAUCOMA • VOGT’S TRIAD  seen with any type of post-congesive glaucoma & in treated acute congestive glaucoma: a. GLAUCOMFLECKEN  an anterior sub-capsular lenticular opacity b. PATCHES OF IRIS ATROPHY c. SLIGHTLY DILATED NON-REACTING PUPIL  due to sphincter atrophy PATCHES OF IRIS ATROPHY SLIGHTLY DILATED NON- REACTING PUPIL GLAUCOMFLECKEN VOGT’S TRIAD
  57. 57. PRIMARY ANGLE-CLOSURE GLAUCOMA CLINICAL MANIFESTATIONS: FIVE DIFFERENT CLINICAL ENTITIES POSTCONGESTIVE ANGLE-CLOSURE GLAUCOMA 1.POSTSURGICAL POSTCONGESTIVE PACG  after laser peripheral iridotomy (PI) treatment for an attack of acute PACG FOUR CLINICAL SETTINGS • Clinical status of eye after an attack of acute PACG with or without treatment • With normalized IOP post-laser Tx, the eye usually “QUITENS” after some time with/without s/s of acute attack • With raised IOP after unsuccessful Tx, there occurs a STATE OF CHRONIC CONGESTIVE GLAUCOMA
  58. 58. PRIMARY ANGLE-CLOSURE GLAUCOMA CLINICAL MANIFESTATIONS: FIVE DIFFERENT CLINICAL ENTITIES POSTCONGESTIVE ANGLE-CLOSURE GLAUCOMA 2.SPONTANEOUS ANGLE OPENING  may very rarely occur in some cases and the attack of acute PACG may subside itself without treatment FOUR CLINICAL SETTINGS • Clinical status of eye after an attack of acute PACG with or without treatment 3. CHRONIC CONGESTIVE PACG  continuation of acute congestive angle- closure glaucoma when no Tx or when is unsuccessful a. EYE  permanently congested, pain reduced d/t “ACCLAMATIZATION” b. IOP  remains constantly raised c.  LID & CONJUCTIVAL EDEMA d. OPTIC DISC  may show cupping e. Other features are similar to acute congestive angle-closure glaucoma 4. CILIARY BODY SHUT DOWN  temporary cessation of aqueous humor secretion due to ischemic damage a. IOP is low, PAIN is “MARKEDLY”
  59. 59. • Similar to POAG, EXCEPT that the angle in Chronic PACG is narrow • IOP  constantly raised • EYEBALL  it is usually remains white (without congestion) & PAINLESS • OPTIC DISC  may show cupping • VISUAL FIELD DEFECTS  like POAG • GONIOSCOPY  variable degree of angle closure PRIMARY ANGLE-CLOSURE GLAUCOMA CLINICAL MANIFESTATIONS: FIVE DIFFERENT CLINICAL ENTITIES CHRONIC PACG PAINLESS EYEBALL
  60. 60. PRIMARY ANGLE-CLOSURE GLAUCOMA ABSOLUTE PACG  if no Tx for chronic phase, with/without sub-acute attacks, gradually passes into “FINAL PHASE” a. PAINFUL BLIND EYE  irritability & now completely blind (NO LIGHT PERCEPTION) b. PERILIMBAL REDDISH BLUE ZONE  slight ciliary flush around the cornea d/t dilated anterior veins c. CORNEA  clear but insensitive d. ANTERIOR CHAMBER  very shallow e. IRIS  becomes atrophic f. PUPIL  fixed, dilated, greenish hue g. OPTIC DISC  shows atrophy h. INTRAOCULAR PRESSURE  high i. EYEBALL  becomes stony hard PERILIMBAL REDDISH BLUE ZONE PAINFUL BLIND EYE INSENSITIVE CORNEA
  61. 61. PRIMARY ANGLE-CLOSURE GLAUCOMA DIAGNOSTIC FACTORS: CLINICAL ENTITY DIAGNOSIS LATENT PRIMARY ANGLE- CLOSURE GLAUCOMA DIAGNOSIS MADE BY: • CLINICAL SIGNS  described beforehand • PROVOCATIVE TESTS  designed to precipitate closure of the angle in the ophthalmologist’s office, where it can be treated promptly a. PRONE-DARKROOM TEST  it is the most popular & best physiological provocative test for PACG b. MYDRIATIC PROVOCATIVE TEST  not preferred now SUBACUTE PRIMARY ANGLE- CLOSURE GLAUCOMA ACUTE, POSTCONGESTIVE, CHRONIC, ABSOLUTE PACG *DIAGNOSIS USUALLY OBVIOUS FROM THE CLINICAL SIGNS1
  62. 62. PRIMARY ANGLE-CLOSURE GLAUCOMA PRONE-DARKROOM TEST MYDRIATIC PROVOCATIVE TEST DIAGNOSTIC FACTORS:
  63. 63. PRIMARY ANGLE-CLOSURE GLAUCOMA CORNEAL ULCERATION STAPHYLOMA FORMATION ATROPHIC BULBI D/T prolonged epithelial edema & insensitivity Sclera becomes very thin and atrophic, ultimately bulges out (CILIARY staphyloma & EQUATORIAL staphyloma) Ciliary body degenerates,  IOP and the eyeball shrinks COMPLICATIONS If untreated, d/t prolonged IOP the following may occur: CORNEAL ULCERATION STAPHYLOMA FORMATION ATROPHIC BULBI
  64. 64. REFERENCES 1 – Khurana's Ophthalmology - 4th Edition 2007 2 – Vaughan and Asbury's Ophthalmology - 17th Edition 2007 3 – http://eyewiki.aao.org/Glaucoma_in_the_Developing_World 4 – http://roqueeyeclinic.com/eye-conditions/glaucoma/80-glaucoma-classification-epidemiology
  65. 65. -- DR. JOSE RIZAL Philippine National Hero Ophthalmologist
  66. 66. END

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