GLAUCOMA basics by 8Es2eL0

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									                VISION




       DR.K.SUDHAMATHI
         CONSULTANT
EYEQ SUPERSPECIALITY HOSPITALS
                          Magnitude
Second major cause of
blindness

Often asymptomatic in early
stage.

Damage is irreversible.

Effective treatment is
available
                   DEFINITION
  It is a heterogenous group of diseases in
  which damage to the optic nerve(optic
  neuropathy) is usually caused by raised
  ocular pressure

IOP: Depends on the
   balance between
   production and
   removal of
   aqueous humour
           Aqueous Humor Dynamics

• Produced by non-pigmented epithelia of pars
  plicata
  – Secretion
  – Ultrafiltration
  – Diffusion
• Aqueous production rate - 2µL/min
• Facility of outflow – 0.22µL/min/mm of Hg
           Aqueous outflow
     Anatomy                       Physiology




a - Uveal meshwork         a - Conventional outflow-90%
b - Corneoscleral meshwork b - Uveoscleral outflow
c - Schwalbe line
d - Schlemm canal
                           c - Iris outflow
e - Collector channels
f - Longitudinal muscle of
ciliary body
g - Scleral spur
                      Goldmann Equation

                             Po = (F/C) + Pv
Symb   Meaning                    Normal Value         Measured by
ol
Po     Intraocular pressure       Mean = 16 mm Hg      Tonometry
                                  Range = 10-21 mm
                                  Hg
F      Rate of aqueous            Mean = 2µl/min       Fluorophotometry
       production                 Range = 1.8-
                                  4.3µl/min
C      Facility of outflow        0.22-0.28µl/min/mm   Tonography
                                  Hg
Pv     Episcleral venous          8-12 mm Hg           Various devices
       pressure
                     NORMAL IOP

                Mean= 15.9mmHg ± 2 SD
                  IOP > 21.7 is abnormal.
                     Factor affect IOP
               *Age *Sex *Race *Heredity
              *Diurnal & Seasonal variation
            *Blood pressure *Obesity *Drugs
          *Posture *Exercise *Neural *Hormone
         *Refractive error *Eye movement *Eyelid
                          closure
                  *Inflammation *Surgery


Date Author Title         INTERNAL                 7
          STEPWISE DIAGNOSIS

   IOP with Applanation tonometry with Corneal Pachymetry

   Good S/L exam/. & Stereoscopic Dialated
    Ophtalmoscopic examination*AFTER AC DEPTH

   Gonioscopy

   Formal visual-field testing(WWP)

   Imaging
                             Tonometers




   Goldmann                        Perkins                        Schiotz
 Contact applanation     Portable contact applanation         Contact indentation




      Air-puff              Pulsair 2000 (Keeler)                Tono-Pen
Non-contact indentation Portable non-contact applanation portable contact applanation
 VON HERRICKS ANGLE
      GRADING-

SIMPLIFIED VAN HERRICKS


               IS IT >50% CORNEAL
                    THICKNESS




        YES                         NO


 ANGLE CLOSURE
                           GONIOSCOPY REQ.
    UNLIKELY
          Primary Glaucoma


               Is the iris:

   NOT covering the          Covering the
 Trabecular meshwork     Trabecular meshwork



OPEN angle glaucoma    CLOSED angle glaucoma
Indentation gonioscopy in iridocorneal contact

                During indentation          Before indentation




                                       •

•     Part of angle is forced open        Complete angle closure
      Part of angle remains closed by PAS Apex of corneal wedge
                                          not visible
                    Optic Nerve Head

•   Optic Disc 1.5 mm dia
•   1.2 million axons/1000 fascicles
•   Normal loss 5000 axons/year
•   Optic Nerve
    –   Surface nerve fibre layer
    –   Prelaminar
    –   Laminar
    –   Retrolaminar
          Anatomy of retinal nerve fibres
               Horizontal
               raphe




Papillo
macular
bundle



                            Normal         Slit Defect




                            Wedge defect     Total atrophy
                Theories of damage

1. Mechanical theory
  •   Compression of axons leads to axonal death
2. Vascular theory
  •   Ischemia causes axonal necrosis

         Direct damage due to Pr.   Capillary Occlusion




                                              Interference to
                                              Axoplasmic flow
               Glaucomatous Damage

• Axonal necrosis leading to cupping
• Loss of supporting glial tissue
• Normally leads to disc pallor

Histology of Normal and Glaucomatous Optic nerve
Glaucomatous Damage
          Types of physiological excavation




                           Larger and deeper         Cup with sloping temporal
Small dimple central cup   punched-out central cup   wall
            Pallor and cupping
    Pallor - maximal area of colour contrast
    Cupping - bending of small blood vessels crossing disc




Cupping and pallor correspond   Cupping is greater than pallor
                     GLAUCOMA
     Optic nerve signs of glaucoma progression
Increasing C:D ratio
 Development of disk pallor
 Disc hemorrhage (60% will show progression of VF damage)
 Vessel displacement
 Increased visibility of lamina cribosa
   STRUCTURE /FUNCTION EVALUATION




Date Author Title                   21
CLASSIFICATION
ACORDING TO AETIOLOGY
*Primary
*Secondary
*Congenital-present at birth.
           Infantile, present in first year of life.
           Juvenile, present in late childhood.

ACCORDING TO APPERANCE OF THE
ANGLE
*Open angle glaucoma.
*Closed angle glaucoma.
*Combined mechanism glaucoma


                                                       22
      GLAUCOMA CLASSIFICATION
PRIMARY VERSUS SECONDRY
*PRIMARY
No detectable ocular or systemic abnormality.
Often bilateral.
Often familial

*SECONDARY
Predisposing ocular or systemic abnormality.
Often unilateral.
Often sporadic

                                                23
   Primary OPEN angle glaucoma


• It is the most common type of
  glaucoma
• It is the 2nd cause of blindness in the
  India
• It is also called chronic open angle
  glaucoma.
• It causes SLOW damage to the optic
  nerve, causing gradual loss of vision.
      Primary OPEN angle glaucoma

 Pathogenesis:
 Resistance of drainage of aqueous
  through the Trabecular meshwok, due to:
1.Thickening of Trabecular lamellae
  (reduces pore size).
2.Reduction in number of lining Trabecular
  cells.
3.Increased extracellular material in the
  Trabecular meshwork spaces.
               Open Angle Glaucoma
Risk Factors
   Age
   Race
   Family History
   Diabetes
   Myopia
   Hypertension
   Smoking

Signs & symptoms
 1. “Silent thief of sight”
 2. Frequent change of
    presbyopic glasses
           Low-tension Glaucoma

• IOP<21
• Mostly elderly people
• Vasospastic disease – Migraine, Raynaud’s
  phenomena, Autoimmune disease
• Systemic hypotension
1.TRUE LTG
2.Non Progressive LTG
3.Pseudo LTG
   SECONDARY OPEN ANGLE GLAUCOMA
PreTrabecular-Membrane on T.M.
*Epithelial
                                  Trauma, Toxicity toTM
*Endothelial
                                  • Edema
*Fibrous
                                  • Tears
*Fibrovascular
                                  • Toxins
*Inflamatory
                                  • Laser
  TRABECULAR-Particle obstruct T.M.   Posttrabecular-Increased Episcleral VP
  *RBC-Haem                           SUPERIOR VENA CAVA OBSTRUCTION
  *WBC-Imflammation                   THYROID EYE DISEASE
  *NEOPLASTIC CELLS                   A/V FISTULA
  *PIGMENTS                           STURGE WEBER SYNDROME
  *PXF MATERIAL
  *VISCOUS MATERIAL-SILICONE OIL
  *HEALON
  *LENS PARTICLE
  *VITREOUS
  *FIBRIN

Date Author Title                                                      28
                 Pigmentary Glaucoma
•   Young, white, male myopes
•   Pigment dispersion due to zonular contact with iris
•   Krukenberg spindle
•   Radial transillumination defects
•   Trabecular meshwork pigmentation
         Pseudoexfoliation Glaucoma

• Elderly white women
• Fibrillar material deposited on trabecular
  meshwork
• Moth-eaten iris transillumination defects
• Pigment on trabecular meshwork
       STEROID INDUCED GLAUCOMA

• Risk Factors
    – POAG
    – Diabetes
    – Myopia
• Stronger the steroid more the elevation
•
                 Primary Angle Closure
                      Glaucomas
PRIMARY ANGLE-CLOSURE            PRIMARY ANGLE-CLOSURE
GLAUCOMA                         GLAUCOMA
ANATOMIC FEATURES:               A. INTERMITENT ANGLE-CLOSURE
• SMALL CORNEAL DIAMETER         GLAUCOMA
• SHALLOW ANTERIOR CHAMBER       B. SUBACUTE ANGLE-CLOSURE
• THICKER LENS                   GLAUCOMA
• SMALL RADIUS OF THE ANTERIOR   C. ACUTE ANGLE-CLOSURE
LENS CURVATURE                   GLAUCOMA
• ANTERIOR LENS POSITION         D. CHRONIC ANGLE-CLOSURE
• SHORT AXIAL LENGTH             GLAUCOMA
• HYPEROPIC EYES                 E. ABSOLUTE GLAUCOMA




                                                            32
 Classification of primary angle closure (PAC)

(1) Primary angle closure suspect
An eye in which appositional contact between the peripheral iris and
posterior trabecular meshwork is considered possible
(2) Primary angle closure (PAC)
An eye with an occludable drainage angle and features indicating that
trabecular obstruction by the peripheral iris has occurred, such as
peripheral anterior synechiae, elevated intraocular pressure, iris
whorling (distortion of the radially orientated iris fibres), “glaucomfleken”
lens opacities, or excessive pigment deposition on the trabecular
surface. The optic disc does not have glaucomatous damage.
(3) Primary angle closure glaucoma (PACG)
PAC together with evidence of glaucoma,
        Primary Angle Closure Glaucoma

•   Risk factors
    –   Elderly
    –   Hypermetropic
    –   Emotionally unstable women
Iris Atrophy   Glaucomflecken
    Primary Angle Closure Glaucoma-
 Acute congestive attack-EMERGENCY!!!
• Symptoms
  – Sudden pain
  – Loss of vision
  – Coloured halos

• Signs
  –   High IOP
  –   Shallow Ac
  –   Oedematous cornea
  –   Pupil mid-dilated & fixed
             Narrow Angle Glaucoma
Treatment: Peripheral Iridotomy
                      Secondary Angle Closure
• Anterior iris pulling mechanism
    – NVG                       1-Progressive iris atrophy
                                2-Chandler syndrome
    – ICE syndromes------------ 3-Cogan-reese syndrome
• Posterior pushing mechanism
    – Plateau iris
    – Malignant glaucoma

With pupil block - seclusio pupillae and   . Without pupil block - peripheral anterior
  iris bombé                                  synechiae
             Plateau Iris Syndrome
• Younger patients, uncommon
• Ac appears to be normal but gonioscopy demonstrates
  relatively flat iris
• Plateau iris syndrome – high IOP despite LI
• Plateau iris configuration – normal IOP after LI
• Laser Iridoplasty to shrink peripheral iris
              Neovascular Galucoma
• Causes
  –   Diabetes
  –   CRVO
  –   Carotid vascular disease
  –   CRAO
  –   Eales’ Disease
  –   Sickle cell anemia
  –   Coats disease
Signs & symptoms
  Rubeosis iridis
  Ectropion uveae
  NV of angle
             Malignant Glaucoma

• Aqueous misdirected posteriorly behind vitreous
• Vitreous moves forward, collapses iris & lens
  into AC
• Typically after intraocular surgery particularly
  cataract & glaucoma
      Lens related Glaucoma

Intumescence
Dislocation and Subluxation
Phacolytic
Lens particle
          Primary Congenital Glaucoma

•   From birth till 3 years of age
•   Autosomal recessive
•   Photophobia
•   Blephrospasm
•   Epiphora
•   Hazy cornea
•   Haab’s Striae
•   Deep AC
MANAGEMENT OF CONGENITAL
       GLAUCOMA

GONIOTOMY       TRABECULOTOMY




                           44
Medical Treatment of GLAUCOMA
      Beta-blockers
      Carbonic anhydrase inhibitors
      Prostaglandin analogues
      Miotics
      Alpha-2 agonists
      Surgical treatment of GLAUCOMA


Argon laser trabeculoplasty
 Trabeculectomy/Filtering Sx
 Cyclocryotherapy
 Cyclolaser ablation
 Iridotomy
Thank you

								
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