Ophthalmology Notes @ OphthalNotes.blogspot.com

Ophthalmology Notes @ OphthalNotes.blogspot.com
A comprehensive collection of ophthalmology revision notes that cover a broad range of topics.
Showing posts with label INVESTIGATION. Show all posts
Showing posts with label INVESTIGATION. Show all posts

Common Drugs Used In Ophthalmology

 

Name of drug

Concentration used

(1% w/v = 10 mg/ml)

Volume of
vial/ample

Subconj.
injection

dexamethasone

4 mg/ml

2 ml

amikacin

500 mg/vial

2 ml

Sub tenon inj- hydrocortisone

40 mg/ml

1 ml

Intravitreal inj- vancomycin

500 mg

Powder form

Lignocain

Plain

2%

30 ml

With adrenalin

2% with adr 1 in 80,000

30 ml

Hyaluronic acid

1500 IU

Powder

Trypan blue

0.8 mg/ml

1 ml

Carbachol

0.01%

1 ml

Epitrate

1: 1000

1 ml

Atropine

0.6 mg/ml

2 ml

Neostigmine

0.5 mg/ample

 

Povidone
iodine

Hand wash

7.5%

 

Surgical wash

5%

Cidex (glutaraldehyde)

2.45% sharp inst sterilization

 

Topifrine

Tropicamide

0.8%

5 ml

Phenylephrine

5%

Carecain (proparacaine hydrochloride)

0.5% (5 mg/ml)

5 ml

Atropine & cyclopentolate

1% (10 mg/ml)

3 ml

Ciprofloxacin, ofloxacin, tobramycin

0.3% (3 mg/ml)

5 ml

Moxifloxacin

0.5% (5 mg/ml)

5 ml

Levofloxacin (preservative free)

1.5% (15 mg/ml)

 

Azithromycin

1%

 

Natamycin

5%

 

Antibiotic + prednisolon

Prednisolon= 1%

 

Antibiotic + dexamethasone

Dexamethasone= 0.1%

 

Flurbiprofen

0.03%

5 ml

MISC... NOTES

.                                             SPOTS

ULTRASOUND BIOMICROSCOPY
[ Dec-05 ]
      PRINCIPLES-
     It is an imaging process which involves  use of high frequency transducer to produce high resolution images of anterior segment structures.
  • Frequency- 50 MHz
  • Resolution- 60 microns
  • Depth perception- 4mm

TECHNIQUE-
  • Immersion tech
  • Topical anaes
  • Transducer is immersed in an eye-cup containing coupling soln-1% methyl cellulose

INDICATIONS-
  1. Anterior segment cysts & tumours
  2. Pars planitis.Uveitis with miotic pupils
  3. Cataract
  4. Assessment of zonular integrity
  5. Ant seg FB
  6. Plateau iris
  7. Post v’tomy VH
  8. Unexplained hypotony
  9. IOL malpositions
  10. Failed filtering surg
  11. Pigment dispersion syn
  12. Pre-penetrating KP angle assessment
  13. Malignant glaucoma

CONJUNCTIVAL PAPILLOMA-
  • Finger like processes on the conj
  • Lack of scleral inv
PLATEAU IRIS SYN-
  • Anteriorly placed ciliary processes

     IOL  COMPLICATIONS-
  • Malpositioned haptics
  • Zonular & capsular dehiscence
  • Haptic erosion into ocular tiss
  • IOL tilt

            DACRYOCYSTOGRAPHY

Helpful in documenting functional & morphological status of tear flow by visualizing the true dimensions of the passages.

TYPES-
1.Plain DCG
2.Distention DCG
3.Macro DCG
4.cinematography
5. Dacryosintography

DYES-
  1. Lipoidal in water / olive oil
  2. Iodized oil
  3. Neohydroil angiographin
  4. Dionosil aqueous
  5. Conray
  6. Diagonal viscous
    7. Ethiodized oil [0.5-1ml]
Viscous & water soluble contrast media stay well as well as spread well to give better contrast & do not hav globule formn

PLAIN DCG-
  • 0.5ml of dye is pushed into the sac thru the lower punctum & canaliculus.
  • X-ray- AP & lateral views taken


















DISTENTION DCG-
  • Named so, bcos the passage is kept distended throughout the procedure of taking x-ray by pushing the radioopaque dye till x-rays are taken.
  • Water’s & lateral view
  • Adv over plain DCG-exact idea of the size of sac
                                     -diverticula
                                     -false passage

MACRO DCG-
  • Film cassette is kept under the x-ray table on a wooden stool.
  • Head of the pt is midway bet the x-ray tube & the film.
  • AP & lateral views
  • A set of delayed films taken after 15-30 min to see for partial obstrn
  • Adv-
  1. Canalicular dis & obstrn are best seen by magnificatiom
  2. Details enhanced by very good contrast
  3. Small focus beam gives sharp image

CINEMATOGRAPHY-
  • Series of x-rays are taken after injecting the radioopaque dye
  • Partial obstrn visualized prominently.

DACRYOSINTIGRAPHY-
  • Non-invasive
  • Two drops of radiotracer Tc99m used in each eye
  • Series of images of both eyes taken at interval of 5 min for 35-40min by Gamma camera.
  • Appearance of tracer in nasal cavity noted.
  • Persistent pooling of radiotracer in lacrimal sac → obstrn at NLD-sac juncn
  • Also helps to diff epiphora d/t blockage from epiphora d/t lacrimal pump dysfunction

FLUORESCEIN   ANGIOGRAPHY
 
DEF-
Involves photographic surveillance of the passage of fluorescein thru the retinal & choroidal circulation.

HISTORY-
Earliest description-1958- Chao & Flocks
Clin use-1961- Novotny & Alvis

PRINCIPLES-
FLUORESCENCE- It is the property of certain molecules to  emit light energy of a longer wavelength wen stimulated by light of a shorter wavelength.

Excitation peak- 490 nm [ blue]
Represents the max absorption of light by fluorescein
Molecules stim by this wavelength will be excited to higher energy level & will emit light of a longer wavelength at 530nm [green]

FUNDUS CAMERA-
2 types of filters-
1. Blue excitation filter-
  Thru this passes white light from the camera flash. The emerging blue light enters the eye & excites the fluorescein molecules in retinal & choroidal cir→Light of a longer wavelength is emitted [ yellow-green]
2.Yellow –green barrier filter-
Blocks any reflected blue light from the eye,allowing only yellow-green light to pass thru unimpeded to be recorded on film.

CHEMICAL PROPERTIES-
  • Orange water soluble dye
  • Chem. Related to phenolphthalein
  • Results from interaction of phthalic acid anhydride & resorcinol which in an alkaline sodium salt sol form sodium fluorescein [ C20 H10 O5Na2]
  • Low mol wt-367.27
  • High water solubility→ rapid diffusion
  • Absorption peak- 420-490nm
  • Emission peak- 510-530nm
  • Fluorescein binding- 70-85% -fluo bound
  • Remainder –free
  • Diffuses freely thru-choriocapillaries
                                   -Bruch’s mem
                                   -ON
                                   -Sclera
                                   -Ciliary Vs
                                   -Ciliary body
*  Does not diffuse thru-Retinal BVs
                                    -RPE
                                    -Large choroidal Vs

TECHNIQUE-
  • Adequate pupillary dilatation [6-8mm]
  • Pt is seated in front of fundus camera
  • Fluorescein, 5ml of 10 % [ 3ml of 25% -opaque media]
  • Red free photo taken
  • Fluo is injected rapidly into antecubiatal vein
  • After 5-25 sec, photo taken at 1 sec interval
  • After transit phase has been photographed in one eye,Control pictures of other eye are taken.If leakage is anticipated, late photo may be taken after 10 min.

ADVERSE EFFECTS-
  1. Skin & urine discolouration
  2. Nausea & vomiting
  3. Flushing of skin, itching & hives
  4. Dyschromatopsia
  5. Phlebitis
  6. Syncope,laryngeal edema , bronchospasm & anaphylactic shock.

PRECAUTION-
Avoid extravasation of dye to prevent tiss infiltration & tiss necrosis

C/I- Relative- 1st trim of pregnancy

ENTRY OF FLUO →
Dye enters the eye thru the Ophthalmic A.
Flu→ Short PCA→ choroidal cir
Flu→Central retinal A→ Retinal cir
As the route to retinal cir is longer than the choroidal cir, ret BVs fill 1 sec later than the choroidal cir.

PHASES-
  1. Choroidal phase
  2. Arterial phase
  3. Arteriovenous phase
  4. Venous phase
  5. Late [Elimination phase]

1] CHOROIDAL PHASE-
*  Rapid phase
*   Dye reaches choroidal cir but not the ret As
*   Occurs 8-12 sec after inj
*    Patchy filling is d/t perfusion of choriocapillaries lobules sequentially rather than simultaneously.
*    Visualisation of the choroid is k/as-‘Choroidal flush’

2. ARTERIAL PHASE-
*  0.5-1 sec after choroidal phase.
*   Initially only the axial [midstream] segment of arterial bld fluoresces
*   Bld plasma adjacent to the vessel wall stains later.

3.ARTERIOVENOUS PHASE-
*  1-2 sec after arterial phase
*   Complete filling of arteries & capillaries & early laminar flow in the vein.
*    Laminar flow is d/t rapid flow of plasma along the wall & higher conc of RBCs in central V lumen

4. VENOUS PHASE-
3 phases-
a) Early phase-3 sec after arterial phase
                      -complete arterial & capillary filling & more marked
                       Laminar venous flow
b) Mid-phase-Almost complete venous filling
c)Late phase- 5-20 sec after arterial filling
                   -complete venous filling & reduced conc in arteries

5.LATE [ELIMINATION] PHASE-
* With each succeeding wave,intensity of fluo becomes weaker
*  Flu is absent from the angiogram after 5-10 min  & totally eliminated from the body in sev hrs.

RETINAL CIRCULATION TIME-
Duration of time bet the first appearance of dye in the arterial cir upto its appear in tributary venous sys.

ARM TO RETINA TIME-
Time bet fluo inj & appear of dye in the eye [ optic disc ]
8.5-11 sec

Clinically FA of the disc is of greatest value in diff pseudopapilloedema [ drusen- optic n head & hyperopic disc] from papillitis & papilledema [same appear]
Exposed drusens- Autofluorescence
Buried drusens- hyperfluorescence d/t staining .NO LEAKAGE
Papilloedema- Hyperfluorescence & leakage

ABNORMAL FLUORESCENCE-

HYPERFLUORESCENCE-
Increased fluor d/t visualization of a nml quantity of  fluo in the fundus or an absolute increase in the fluo content of the tissue.

  1. TRANSMISSION / WINDOW DEFECT-
  • Drusen
  • Atrophy
  • Hereditary maculopathy
  • Toxic maculopathy

2.POOLING OF DYE- d/t breakdown of outer BRB-
→ Subretinal space-  SRNVM
                              -CSR
→Sub-RPE Space- PED

3.STAINING OF TISSUE-
*  Drusen
*  Soft exud
*  Scar tiss
*  Vessel wall staining

4.LEAKAGE OF DYE-
- Abnormal choroidal vasculature→ Choroidal NV-Lacy pattern
- Abnormal disc / retinal vasculature→ PDR
-Breakdown of inner BRB→ CME-Petalloid appear

HYPOFLUORESCENCE-
Reduction / Absence of fluorescence
  1. BLOCKAGE OF RETINAL FLUORESCENCE-
  • Vitreous opacities & Pre-retinal lesions –bld
  • Deep retinal lesions- Intraretinal h’age & hard exud

  1. BLOCKAGE OF CHOROIDAL FLUORESCENCE-
-Sub-RPE / subretinal space- blood
-Choroidal lesions- neavi
-Increased density of RPE- Congenital hypertrophy of RPE

3.FILLING DEFECTS-
-Vascular occlusion- CRVO,
                               -  CRAO
                               -BRVO
                               -Capillary dropout
- Loss of vascular bed- sev myopic degeneration

RETROFLUORESCENCE
Occurs when a non-fluoresent structure is silhouted against a background fluorescence.

FLUORESCEIN LEAKAGE-
Passage of dye beyond the physiologic barrier of the retinal V or RPE & spread into spaces bet cells or tiss layers.

FLUORESCEIN POOLING-
Leakage into anatomic space.

FLUORESCEIN STAINING-
Dye transiently attaches to tissues thereby causing fluorescence.

PSEUDOFLUORESCENCE-
  • late fluorescence
  • Occurs when fluorescein molecules are activated within the aqueous / vitreous & the emitted fluor is reflected from the fundus structures.
  • Eg- Optic disc
  •    -medullated N fib
  •    -Chorioretinal scars

   AUTOFLUORESCENCE-
   It is the innate property of fluorescence of certain ocular tiss like lens, BM [ Descemet’s memb, Bruch’s memb] & CB.
D/t lipofuschin
Eg- optic disc drusen
   -Astrocytic hamartomas
   
VIVA-
  • RPE- 2 pigments-
  1. Melanin
  2. Lipofuschin

  • RPE cells at macula-
  • Longer
  • Thinner
  • Contain larger & more melanosomes

  • Dark appearance of Fovea-
  1. Avascularity of FAZ
  2. Blockage of choroidal  fluo by increased xanthophylls
  3. Blockage of choroidal fluo by longer & thinner melanin

  • Physiological fluid barriers
  1. Inner BRB-Tight endothelial cell juncn of ret capillaries
  2. Outer BRB- RPE cells [ zonula occludentes]

DARK CHOROID-
  • Due to deposition of abnml material at the RPE→ blocks choroidal transmission
  • Causes-
  1. Atypical Stargardt’s dis
[ Typical Stargardt’s –pisciform speckles are hyperfluor]
  1. Choroidal ischaemia
  2. Argyrosis

                  INDOCYANINE  GREEN

  • Particular value in studying choroidal cir
  • ICG BINDING-
-98 % albumin bound→Reduces passage of ICG thru the fenestrations of choriocapillaries which are impermeable to albumin.
*  Fluor is only 1/25th of fluorescein

Excitation peak- 805nm
Emission peak- 835nm [infrared spect]

  • Readily penetrates- melanin
                                 -xanthophyll
                                 -exud
                                 -thin layers of subret bld
TECH-
  • ICG powder -40mg in 2ml
  • Pt seated in front of fundus camera
  • Red-free photo
  • Bet 25-40mg dye injected
  • Photo taken at 3min, 10min & 30min
  • Late phase yields the most useful informn as dye remains in the NV tiss after leaving ret & choroidal cir.

ADVERSE EFFECTS-
  1. Staining of stools
  2. Nausea & vomiting
  3. Sneezing
  4. Pruritis

C/I-
  1. Pts allergic to iodine
  2. pregnancy

PHASES-
  1. EARLY PHASE-
  • 2-60 sec
  • Hypofluo of optic disc
  • Poor perfusion of watershed zone
  • Prominent filling of choroidal As & early filling of choroidal veins
  • Retinal As are visible but not veins

  1. EARLY MIDPHASE-
  • 1-3min
  • Fading of choroidal A filling & prominent filling of choroidal vein
  • Both ret A & V visible

  1. LATE MIDPHASE-
  • 3-15min
  • Fading of choroidal V filling
  • Retinal Vs are still visible
  • Diffuse hyperfluor d/t diffusion of dye from choriocapillaries

  1. LATE PHASE-
  • 15-30 min
  • Hypofluo of choroidal vasculature against background hyperfluor
  • Lack of visibility of ret Vs
  • Dye remains in NV tiss after it has left chor & ret cir.

ABNORMAL FLUORESCENCE-
HYPERFLUORESCENCE-
  1. RPE window defect
  2. leakage from ret / choroidal cir or ONH
  3. Abnml BVs

HYPOFLUORESCENCE-
  1. Blockage of fluor- by bld, pigment, exud
  2. Obstrn of cir
  3. Loss of vascular tiss
  4. RPE detachment [Hyperfluorescent on FA]


CORNEAL TOPOGRAPHY

For Cor topo images- my computer→ Anirban’s documents→my pictures
NORMAL CORNEA-
  • Centre of cor- 43D
  • Towards the periphery it declines
  • Nasal flattening is common [more bluish]
  • Upto 1.5d Cyl is nml
  • Above 1.5D is astigmatic

WITH-THE –RULE ASTIGMATISM-
  • Regular ast- steepest & flattest axes are at right angles to each other
  • With-the-rule Ast-Steepest axis is along the vertical meridian
  • Against-the-rule Ast-Steepest axis is along the horizontal meridian
  • Astigmatic pattern is k/as ‘’Bow-tie”

KERATOCONUS SUSPECT-
  • Inferior localized steepening

MILD KERATOCONUS-
  • Contour power less than 55D anywhere on the cor [usually inferiorly] [red]

MOD KERATOCONUS-
  • Contour powers at / above 55D [red-pink]
  • No mire disruption
  • No contour discontinuity

ADVANCED KERATOCONUS-
  • Contour powers at/ above 55D.
  • Mire disruption producing contour discontinuity at the cone apex.

PELLUCID’S MARGINAL DEGENERATION-
  • Localised inferior peripheral steepening
  • Inferior crescent shaped ectasia with its horns curved centrally .
  • Flattening of vertical axis in the central cor [blue]

PTERYGIUM-
  • With-the-rule Ast
  • However there is more flattening in the region of apex of the growth thereby producing irreg ast.

INTERPRETATION OF A COLOUR CODED MAP-
  • yellow & Green- Normal cornea
  • Hot colours- Red & its hues represent steep portions
  • Cool colours- Blue & its hues represents flat portions
  • SCALE-
  1. ABSOLUTE SCALE-
Each colour represents a 1.5 D interval between 35 & 50 D , whereas above & below this range ,colours represent 5D interval.This scale is used in preoperative screening.

  1. NORMALIZED SCALE-
Cornea is divided into 11 equal colours spanning the eye’s total diopteric power.
This scale gives more minute topographic details.

CLINICAL APPLICATIONS-
  1. Early diagnoses of corneal dis-
  • Keratoconus
  • Epith dystrophies & other epitheliopathies
  • Terrien’s marginal deg
  • Pellucid’s marginal deg

  1. Contact lens-
  • Routine CL [ rigid] fitting
  • Fitting in diff cases- post KP, keratoconus,postRK.
  • CL induced changes- central irreg astig, corneal warpage etc.

  1. Keratoconus-
Depicted as a localized area of increased surface power surrounded by concentric zones of of decreased power.
Initial inv is in inferotemporal quad
  • Useful in CL fitting
  • “Forme fruste” –videographic analysis  in family members of keratoconus pt without any overt clin signs.

                MICROBIOLOGY

  • CONJUNCTIVA-NORMAL FLORA
-Staph
-Strepto
-Moraxella
-Diphtheroids

STAINS-
  1. GRAM STAIN-
  • Stain with crystal violet [blue-black]
  • Then iodine
  • Decolorize with acetone
  • Counterstain with carbol fuschin [red]
  • Gm +ve→ Resist decolouration & stain blue
  • Gm –ve→ Decolourize to pink / red

     2.ZEIHL NEELSON STAIN-
     *   Stain with carbol fuschin
     *   Heat
     *   Decolourize with acid / alcohol
     *   Counterstain with Malachite green / methylene blue

     GRAM +VE COCCI-
  1. Staph aureus – coagulase +ve
                         _  aerobic
                         _  non-motile
                         _ non-sporing

  1. Staph epidermidis-Aerobic
                                 -non-motile
                                 -non-sporing

  1. Strepto pneum-encapsulated
                           -aerobic
                           -non-motile
                           -lyse RBC on agar ( alpha hemolysis)

Haemolysis- Partial- alpha- [ greenish]
                 -Complete- Beta- [colourless]

GRAM –VE  COCCI-
  1. Neisseria- diplococci
                   -aerobic
                   -non-motile
N. meningitides-Ferments glucose & maltose
N.gonorrhoea- Ferments only glucose
Growth- Thayer Martin med

GRAM +VE RODS-
  1. Bacillus
  2. Clostridium
  3. Corynebacterium
  4. Propionibacterium[ resides in meibomian glds]→ Endophthalmitis

    GRAM –VE RODS/ BACILLI-
  1. Pseudomonas-pyocin [green piment]
                         -aerobic
                         -non-motile
2. Haemophillus
3. Enterobactericiae- Grow on Mac conkey agar
                               -e.coli
                               -salmonella
                               -shigella
                               -proteus
                               -Klebsiella
                               -yersinia
4. Moraxella

FUNGUS-
  1. Yeasts
  2. Filamentous
  3. Dimorphic

YEAST-
  1. Candida
  2. Cryptococc

FILAMENTOUS-
  1. Aspergillus
  2. Mucormycosis rhizopus
       3.Fusarium
      DIMORPHIC-
  1. Blastomycosis
  2. Coccidiodomycosis
  3. Histoplasma

CULTURE MEDIA-
Staph aureus-

  1. NUTRIENT AGAR-
  • Colonies-large,circular,convex,smooth,shiny,opaque
  • Golden yellow pigment

    2.NUTRIENT AGAR SLOPE-
    *  Oil-paint appear

     3. MAC CONKEY’S MEDIUM-
     *  Smaller colonies
     *  Pink d/t lactose fermentation

 Streptococcus-
BLOOD AGAR-
  • Colonies- small,circular,semitransparent with clear hemolysis around them
  • Virulent strains- ‘matt’ colony
  • Avirulent strains- ‘glossy’ colony

Pneumococcus-
BLOOD AGAR-
  • colony- small, dome-shaped & glistening
  • area of greenish discolouration [haemolysis] around them,


      AUTOMATED PERIMETRY  [j-02]  

DEF-
Perimetry involves evaluation of the visual field.

VISUAL FIELD-
Island of vision surrounded by a sea of darkness.
Limits-Superiorly- 60 deg
         -Nasally- 60 deg
         -Inferiorly- 70 deg
         -Temporally- 90 deg
* Blind spot is located temporally bet 10 & 20deg.
-Represents the ONH.
ISOPTER-
Encloses an area within which a target of a given size is visible .

SCOTOMA-
An area of visual loss surrounded by vision.
ABSOLUTE SCOTOMA-
  • Total visual loss
  • Even the brightest & largest target cannot be perceived

RELATIVE SCOTOMA-
Area of partial visual loss within which brighter & larger targets can be seen but smaller & dimmer ones cannot be seen.

LUMINANCE-
Intensity or brightness of light stimulus, measured in apostilbs [asb]

DIFFERENTIAL LIGHT SENSITIVITY-
The degree by which luminance of a target requires to exceed background luminance so as to be perceived by the eye.

TYPES OF PERIMETRY-
  1. KINETIC PERIMETRY-
  • 2-dimensional assessment of boundary of hill of vision
  • Presentation of a moving stimulus of known intensity / luminance from a non-seeing to a seeing area until it is perceived.
  • Eg- Confrontation
        -Tangent screen
        -Lister perimeter
        -Goldman perimeter

  1. STATIC PERIMETER-
  • 3-dimensional assessment of the height of a pre-determined area of hill of vision
  • Presentation of a non-moving stimuli of varying luminance in the same pos to obtain a vertical boundary of the visual field.
  • Eg-Goldman’s peri
             -Friedman’s peri
    -Automated perimeter

    1. SUPRATHRESHOLD STATIC PERIMETRY-
  • Mainly for screening
  • Presentation of visual stim at luminance levels above expected nml threshold values

    1. THRESHOLD PERIMETRY-
  • Detailed assessment of hill of vision by plotting the threshold luminance values in various locations & comparing the results with age-matched normal values
In Humphery’s perimeter, intensity of stim is increased by 4 db steps until threshold is crossed.Threshold is then redetermined by decreasing the intensity by 2 db steps. This is k/as –Bracketing.

SOURCES OF ERROR-
  1. MIOSIS-Pupils less than 3mm shud be dilated
  2. LENS OPACITIES-
  3. UNCORRECTED REF ERROR-If a hyperopic person who usually wears contact lens is tested wearing spect→ magnify & enlarge the scotomas
  4. SPECTACLES- Rim scotomas
5.PTOSIS- Suppresion of superior field
    6.INADEQUATE RETINAL ADAPTATION- Leads to error if perimetry is performed soon after ophthalmoscopy.

HUMPHERY PERIMETRY-
  • Background luminance- 31.5 asb.This level was chosen bcos it  approximates the min brightness for photopic / daylight vision.
  • Programs- 30-1 & 24-2
The number before the dash (24- or 30-) indicates the area of the tested field in degrees from fixation
  • 24 deg tests 54 points & 30 deg tests 76 points
  • The no after the dash (-1 or-2) describes the  pattern of points tested.
-The -2 strategy inv a grid of test points spaced 6 deg apart, offset from the vertical & horizontal meridian whereas the -1 strategy includes points along the vertical & horizontal meridian.
*  RELIABILITY INDICES-
Reflect the extent to which patient’s results are reliable & shud be analysed first.
  1. FIXATION LOSSES-
  • Indicates steadiness of gaze during the test
  • Heijl- Krakau method-Physiological blind spot is detected by presenting stim in the phy blind spot.If the pt responds, a fixation loss is recorded.
  • Shud be less than 20 %.

   2.FALSE POSITIVES-
  • Stim is presented along with sound.
  • If sound alone is presented & pt responds→ False +ve→Trigger Happy pt
  • Shud not exceed 33%
  • Fields that show much larger defects in the pattern deviation plot than in the total deviation plot may be the result of high false positive errors.

   3.FALSE NEGATIVES-
*  Detected by presenting stim much brighter than threshold at a location where sensitivity has already been recorded.
*   If the pt fails to respond→ False Neg
*   Indicates- inattention
                  -Short term fluctuation
                 -disease severity
*  Shud not exceed 33 %.

DISPLAYS-
  1. GREYSCALE-
  • Decreasing sensitivity is represented by darker tones

  1. NUMERICAL DISPLAY-
  • Gives the threshold for all points checked
  • Figures in the bracket indicate threshold at the same point checked a second time,if on initial testing it was atleast 5 db less sensitive than expected.

  1. TOTAL DEVIATION-
  • Deviation of the pts result from that of age-matched controls

  1. PATTERN DEVIATION-
  • Similar to total deviation except that it is adjusted for any generalized depression in the overall field caused by lens opacities or miosis.

   PROBABILITY VALUES-
  • Indicate the significance of the defects
  • < 5%, < 2%, , 1% ,< 0.5%
  • Lower the P value the greater is its significance.

GLOBAL INDICES-

  • Summarize the results in a single number
  • Used to monitor progression of glaucomatous damage.

  1. MEAN DEVIATION [MD]-
Measures overall field loss i.e. elevation or depression

2.PATTERN STANDARD DEVIATION [PSD]-
*  Measure of focal loss or variability within the field taking into account any generalized depression in the hill of vision
*   More specific indicator than MD.

3. SHORT TERM FLUCTUATION [SF]-
    *   Indicator of consistency of responses
    *   Threshold is measured twice at ten pre-selected points & calculated on the basis of diff bet 1st & 2nd measurement
     * Shud nmlly be less than 2 db.
     * > 3dB suggests unreliable or damaged field

     4. CORRECTED PATTERN STANDARD DEVIATION [CPSD]-
*  Measure of variability within the field after correcting for short term fluctuation.

GLAUCOMATOUS FIELD DEFECTS-

ARCUATE / BJERRUM’S  AREA-
  • Arches above & below the fixation from the blindspot to the median raphe,corresponding to the arcuate retinal fib.
  • Early visual loss in glauc commonly occurs within this arcuate area, specially in the superior half which correlates with the predilection of the inferior & superior temporal poles of ONH for early glaucomatous damage.

DEFECTS-
  1. BARING OF BLIND SPOT
  2. PARACENTRAL SCOTOMA-
  • Appear within the arcuate area
  • More common nasally.

    3.SEIDEL SCOTOMA-
     -  The paracentral scotomas elongate circumferentially along the arcuate nerve fib & connect with blind spot to form Seidel  scotoma

    4. NASAL ROENNE’S STEP-
    Due to diff in sensitivity above & below the horizontal midline in the nasal field.

  1. ARCUATE / BJERRUM SCOTOMA-
  • The isolated scotomas enlarge & coalesce to form an arching scotoma which eventually fills the entire arcuate area from the blindspot to the median raphe.

    6.DOUBLE ARCUATE / RING SCOTOMA-
     -Seen with further progression.
   7. TEMPORAL & CENTRAL ISLAND OF VISION-
      Temporal island extinguishes before the central.

Few important points-
  • Glaucomatous defects start in the central 30 deg of visual field.
  • Neurological defects are hemianopic i.e they respect the vertical meridian.
  • The dimmest stimulus that can be seen by a young , well-trained observer is about- 38-40db.
  • 0db corresponds to the maximum brightness a perimeter can produce
  • Normal blind spot diameter- 6 degree
  • Normal testing distance of Humphery perimeter is 30 cm
  • If a large change is seen & part of field loss seems hemianopic or occurs in the other eye as well, neurological causes are generally the rule.

  • SHORT WAVELENGTH AUTOMATED PERIMETRY [SWAP]-
-Also k/as Blue-yellow perimetry
- Goldman size V stimuli of blue colour is presented on a bright yellow background
-The yellow background serves to reduce the responsiveness of the red & green cone systems so that the blue stimuli are primarily seen by the blue cone system only.
- SWAP is more sensitive than standard perimetry in detecting-
*  Neuro-ophthalmic dis
*   ARMD
*   Migraine
*   Diab macular edema
* OHT
-The defects are larger than those found with std perimetry
-Disadv- Lens absorbs blue light & so the field changes caused by absorption of light by the lens cannot be differentiated

GLAUCOMA HEMIFIELD TEST-
Gives information concerning differences bet the superior & inferior halves of the visual field by evaluating threshold at mirror image points above & below the horizontal meridian

NON-GLAUCOMATOUS FIELD DEFECTS-
  • Sec OA- Nasal field defect
  • Optic disc drusen- Arcuate defect
  • Chiasmal lesion- Bitemporal hemianopia
                                  -Respect the midline
 *   Postchiasmal lesion-Homonymous hemianopia [matching defects in the same hemifield of both eyes]
*    Occipital lobe lesions- more congruous
* Retinal lesions- Defects are deep & hav sharp borders
*  Diab r’pathy- Multifocal & mottled appear
*  RD- Relative defects
*  Retinoschisis- Absolute defect
*  RP- Ring scotoma in mid-periphery [d/t more rod population in mid-periphery]→ Tunnel vision
*  ARMD – Central scotoma
*  CSR- central scotoma
*  Retinochoroiditis- Arcuate defect
*  Arterial occlusion- Absolute field defect
*  Venous occlusion- Highly variable field loss.

CLOVERLEAF PATTERN-
  • Artifactual pattern
  • Threshold values are nml or near nml at & sometimes around the four primary points where the test begins, but are much reduced at other locations where the threshold is measured later in the test
  • This pattern occurs when the patient has responded more or less appropriately during the initial part of the test & then given up.


                                        LASERS [j-04,j-03]

LIGHT  AMPLIFICATION BY STIMULATED EMISSION OF RADIATION

Def-
Property to absorb light energy of one form & emit a new form of energy which is more useful.

LASER TISSUE INTERACTION-
2 variables-
1)  LASER VARIABLE-
*  Wavelength
*  Spotsize
*  Power
*  Duration    

2)  TISSUE VARIABLE-
*  Transparency
*  Pigmentation
*  Water content

-Only laser variables can be controlled.
-power is inversely proportional to spot size.Therefore if the spot size is decreased,the power must also be decreased to prevent a very intense burn

Laser tissue interaction-
  1. Photocoagulation
  2. Photovapourisation
  3. Photodisruption
  4. Photoablation
  5. Photodynamic therapy

  1. PHOTOCOAGULAION-
  • Photothermal phen
  • Pigment dependant
  1. Xanthophyll-Both plexiform layers of retina
                      -Absorbs blue light max

  1. Haemoglobin-BVs & H’ages
                         -Absorbs yellow light max
                             -Also blue & green

  1. Melanin-RPE & choroids            
                 -Absorbs entire visible spectrum

Pigment absorbs light energy→ Converted to heat energy → Temp elevation [10-20 deg C]→ protein denaturation→
  1. Tissue atrophy→ seen after PRP
  2. Thrombus formn
  3. Collagen contraction
2) & 3) cause occlusion of vascular lumen→Focal photo of new Vs on retina

Undesirable effects of collagen contraction→
Membrane shrinkage→ Retinal traction

Beneficial effects of collagen contraction→
Pulls the peripheral iris out & away from the angle in peripheral iridoplasty

Lasers- Argon, krypton, dye , diode, freq doubled YAG

Use- PRP
     -ALT

  1. PHOTOVAPOURISATION-
  • Thermal phen
  • Pigment dependant
  • Melanin- chief pigment
  • Pigment absorbs light → Temp elev [60-100 deg C]→ Vapourisation of tiss into CO2 & H2O
  • Eg- CO2 laser
  • USES-
  1. Kronlein’s proc
  2. Blepharoplasty
  3. Iridotomies
  4. Debulking of large conj tum

Undesirable effects-
  1. Break in Bruch’s memb→ CNV
  2. ` Rupture of BV wall→ IO h’age

3. PHOTODISRUPTION-
* Independent of pigment
*  Highly energized focal laser beam is delivered onto a tissue           over a period of nanosec / picosec→ Optical breakdown → i.e Tissue is converted into an amalgam of neutrons, ions & free electrons → All of them collide with each other→ This amalgam is k/as ‘ plasma’→ collisions→ Electromagnetic & acoustic waves.
*  These waves travel in all dir but rapidly dissipate resulting in a focal effect → Photodisruption

Eg- ND: YAG Capsulotomy

  • They do not photocoagulate a BV
  • Therefore when they strike a BV → rupture → h’age

  1. PHOTOABLATION-
  • Non-thermal
  • Non-pigment dependant
  • Highly localized→ very clean edged incisions
  • Cleavage of molecular bond→ therefore photochem process
  • USES- PRK
             -PTK
*  Risk- Mutagenecity
          -Alters structure of DNA & RNA

Read PDT & TTT from retina pg 83. folder.

                LASER
          WAVELENGTH
1. Ruby
                    694.3nm
2.Nd:YAG
                    1064nm
3. Double frequency Nd:YAG
                    532nm
4.  Argon
                    488-514nm
5.  Krypton
                    647nm
6.  Diode
                    780-840nm
7.  CO2
                    9000-11000nm

CLASSIFICATION-
  1. SOLID STATE-
  1. Ruby [694.3 nm]
  2. Nd:YAG [1064nm]
  3. Double frequency Nd: YAG [532nm]

  1. GAS LASER-
  1. Ion laser-  Argon laser [488-514nm]
                  -  Krypton laser [ 647nm]
b)  CO2 [9000-1100nm]

  1. METAL VAPOUR LASER-
  1. Copper
  2. Gold

  1. EXCIMER LASER-
  1. Argon fluoride-[ 193nm]
  2. Krypton chloride-[222nm]
  3. Krypton fluoride-[249nm]

  1. DYE LASER-

RUBY LASER-
  • First laser
  • Pulsed laser
  • Crystalline saphire + chromium
  • Pulsed with a xenon flash lamp.

DIODE LASER-
  • 780-840nm
  • Gallium-aluminium-arsenide
  • Monochromatic, coherent laser light in the near infra-red region
  • USES-
  1. TTT
  2. ICG guided t/t of CNV
  3. DME & PDR
  4. Trabeculoplasty
  5. Laser indirect O’scopy
  6. Cyclophotoablation

  • ADV-
  1. Small size
  2. Portable
  3. No special electrical / cooling system
  4. Little absorption of light in nuclear sclerosis
  5. effect thru surface h’age

  • DISADVANTAGE-Hb is not absorbed in the infra-red region→So bleeding stumps cannot be coagulated.
Better
Nd: YAG LASER-
  • MC used solid state  laser
  • Works on the principle of photodisruption
  • WORKING-
  • Active medium in Nd: YAG  is neodymium crystals which are embedded in Yttrium-aluminium-garnet.
  • These atoms are excited by optical pumping by-
  • Flash lamp
  • Continuous arc lamp
-There are 2 ways of pulsing Nd:YAG –
1) Q-switching
2) Mode-locking

Q-switching-
* A Shutter in front of one of the mirrors in the laser cavity blocks laser light emission until a large population inversion occurs→Shutter is opened quickly→ Stored energy bursts forward in the form of a brief pulse that lasts abt one-millionth of a second.
*  Inexpensive
* Cannot produce pulses as short or powerful as mode-locking
*  Most clinical Nd: YAG lasers today are Q-switched bcos mode-locked are more expensive & diff to maintain.

Mode-locking-
An optical element inside the cavity synchronises the mode.So all the light is emitted in brief pulses.

  • The light produced in Nd:YAG is infra-red [1064nm] which is invisible.
  • Delivery sys of Nd: YAG has 2 components-
  1. Binocular stereoscopic microscope
  2. Two Helium-Neon [He-Ne] laser aiming & focusing beams aligned in such a way that they outline the cone of the invisible infra-red Nd:YAG beam .

     APPLICATIONS-
1. Nd: YAG Capsulotomy-
IND- Posterior capsular opacification causing
-Decrease in V/A
-Diplopia
-Glare
-Invisible fundal glow

  • Abraham’s lens used
  • Power setting- 1mJ / pulse
  • Pattern- Cruciate
               -Christmas tree

Complications-
  1. Damage to IOL (pitting) d/t poor focusing
  2. CME
  3. Rheg RD
  4. Increase IOP
  5. Posterior IOL subluxation / dislocation
  6. Chr endophthalmitis [ d/t release of sequestered org in vit]

Post-laser-
  1. Topical Timolol 0.5 % e/d BD
  2. Topical steroids for 7 days

2. Nd: YAG Iridotomy-
IND-
  1. Prim angle closure glauc
  2. Fellow eye in acute glauc
  3. Narrow occludable angles
  4. Sec angle closure with papillary block

TECH-
  • Apraclonidine 1%  or Brimonidine 0.2%
  • Topical anaesthetic drop
  • Abraham’s lens
  • Site- Superior iris to avoid diplopia as it remains covered by lid
  • Beam shud be non-perpendicular
  • 3 Bursts of 3-6 mJ
  • Gush of pigment debris
  • Post-laser- Apraclonidine 1% or Brimonidine 0.2 %
  • Topical steroid for 7 days
  • Ideal opening- 150- 200micron

COMPLICATIONS-
  1. Bleeding
  2. Iritis [d/t over t/t & inadequate postlaser steroid]
  3. Cor burns
  4. glare & diplopia

Other indications-
  1. Nd: YAG vitreolysis
  2. Cyclophotocoagulation
  3. Iridolenticular synechiolysis
  4. Persistent hyperplastic papillary membrane
  5. Ant hyaloidotomy-For malignant glauc
  6. Rupture of conj cyst
  7. Radial iridotomy for rigid pupil
   10 Laser sclerotomies

ADV-
  1. High power density
  2. Small coagulation
  3. Cutting & lysing of small tiss
  4. Low maintenance
  5. Portable

DISADV-
  1. High absorption by media
  2. Potential for vascular rupture
  3. Non-thermal action on adjacent tissue.

DYE LASER-
2 Types-
1) Thermal – Photo of post pole lesion
                  _  PDT
2) Pulsed- Laser sclerostomy
             - Iridectomy
             - Periorbital portwine stain

EXCIMER LASER-
USES-
  1. PRK – For myopia
  2. Phototherapeutic keratectomy for corneal scars
  3. Sclerostomy
  4. Trabeculectomy

PHACOABLATION-
Sculpting & ablative decomposition of cataract.
2 methods-
1. Ant surf of lens & deeper layers are blasted & the products removed by AC lavage
2. Fibreoptic probe introduced into AC &Cataract decomposed

LASER ASEPSIS-
Organism + Topical drop on cor containing antibody to this org tagged with Fluorescein→ Subjected to argon laser→ Fluorescein absorbs argon → converts it into heat energy→ Death of org


        ELECTRORETINOGRAM

       There exists a potential difference of 1mV bet the cornea & post pole of the eye k/as corneoretinal potential.This potential is modified by the action of light on the retina.The resultant waveform from modification in the corneoretinal potential in response to a brief flash of light is k/as Electroretinogram.

Thus the ERG is a composite of electrical activity from the photoreceptors, muller cells & RPE.

COMPONENTS OF ERG-
1) a-wave-
-  Initial cornea negative wave
- Arises from photoreceptors [ rods & cones]

2)  b-wave-
-Large cornea –positive wave
-Arises from muller cells
-Represents activity of bipolar cell layer.
- Oscillatory potential- Ripple of 3 or 4 small wavelets on the b-wave.

3) c-wave-
-  prolonged positive wave with a lower amplitude
- Represents activity of RPE.

MEASUREMENT-
1. AMPLITUDE-
a)  a-wave amplitude-
Measured from the baseline to the trough of a-wave

b)  b-wave amplitude-
Measured from the trough of a-wave to the peak of b-wave

2. TIME SEQUENCES-
a) LATENCY-
    Time interval bet the onset of stimulus & beginning of a-wave
     Nml- 2msec
b) IMPLICIT TIME-
     Time from the onset of light stim until the max a-wave or b-wave response

ERG RECORDING-
Application of electrodes-
1. Active / main electrode-
-  Placed on the cornea, embedded in a contact lens
-  Or Wick electrodes in the conj sac
- Or  Skin electrodes of gold foil on eyelids
-This is the positive pole

2.  Referance electrode
 - Silver chloride electrode
 -Placed on pt’s forehead.
 - Serves as the negative pole.

3. Ground electrode
- Placed on the ear lobe.

RECORDING-
  • the contact lens electrode  picks up the electrical potential that exists bet the neg post pole & positive cor foll light stim of retina
  • after arising at the contact lens,the signal is channeled thru consecutive devices for preamplification , amplification & final display.

PHOTOPIC VERSUS SCOTOPIC ERG-
PHOTOPIC ERG-
  • D/t cone response [ 5-8 million cones]
  • Under light –adapted condition
  • Lower amplitude & shorter implicit time

SCOTOPIC ERG-
  • D/t rod & cone response
  • 6-8 million cones & 125 million rods
  • Recorded after 20 min of dark adaptation
  • Rod response can be isolated by stimulating the fully dark adapted eye with a flash of very dim light or blue light
  • Rod response gives reduced amplitude & longer implicit time

CLINICAL APPLICATIONS-
  • ERG can detect abnmlities upto bipolar cell layer.
  • It is nml in diseases inv ganglion cells & higher visual pathway such as optic atrophy
  • It measures diffuse responses of the retina, so isolated lesions cannot be detected like- localized macular h’age,macular holes,exudates,chorioretinitis & localized detachment

    1. Retinitis pigmentosa-Marked reduction in amplitude
    2. DR- Oscillatory potential is abolished. Disappearance of the wavelets suggests retinal ischaemia.Also seen in CRAO
    3. RD-Immediate reduction in size of b-wave co-incidental with loss of vision.
    4. ERG can be recorded even in the presence of dense opacities such as cor opacity, dense cataract & VH.

        ABNORMAL ERG RESPONSE-
       b-wave potential < 0.19 mV or > 0.54 mV→ abnml
        1. Supernml response-
           Potential above nml upper limit.
  • Subtotal circulatory disturbances of ret
  • Siderosis bulbi

2. Subnml response- < 0.08mV
- Indicates that a large area of retina is not functioning.
- Seen in-
*  Early RP
*  Chloroquine & quinine toxicity
*   RD
*  Vit A def
*  Hypothyroidism
*  Mucopolysachharidoses
*  anaemia

3. Extinguished response- Complete absence of response
*  Adv RP
*  Complete RD
*  Adv siderosis bulbi
*  Choroideremia
*   Leber’s cong amaurosis
*  Leutic chorioretinitis
4. Negative response-
 -Large a-wave
* Arteriosclerosis
*  Giant cell arteritis
*  CRVO
*  CRAO

              PATHOLOGY

STAINS-
1] HAEMATOXYLIN & EOSIN-
- Nuclei [ DNA] – Stains blue
-Ribosome & Rough ER [RNA] – blue
- Cyto stains pink with eosin which is an acidic dye

2] PERIODIC ACID SCHIFF [PAS]-
- Stains glycogen,mucin,mucoprotein, glycoprotein & fungi
-Outlines tiss struct- BM, capsule &BVs
- Red

3] GRAM STAIN-
-  + → blue / black
-   - → Red

4] ZEIHL NELSON STAIN
- Blue background with red stain
5] ALIZANIAN RED>
- For Ca ++
-Red / brown
-Band KP

6] CONGO RED-
- For amyloid
Lattice dyst

Marilyn Monroe Always Gets Her Men in LA City

Macular dystrophy→ mucopolysacch→Alcian blue
Granular dys→Hyaline→Masson trichome
Lattice dys→Amyloid→ Congo red

                  GIANT CELLS
3 types-
1]  Langerhan’s cells-
Peripheral horse-shoe shaped ring of nuclei
Eg-giant cell arteritis

2] FB cells-
Overlapped & centrally placed nuclei

3] TOUTON CELLS-
Ring of nuclei separate peripheral clear cyto from central eosinophilic cyto
-Eg – Juvenile xanthogranuloma

              CONJUNCTIVAL NAEVI
  • MC site- bulbar conj
  • Types-
  1. Junctional n- Between epith & substantia propria
  2. Subepithelial- Below the epith
  3. Compound n-Both epith & Subs propria

                  PTERYGIUM
DEF-Deg condition of the subconj tiss,which proliferates as a triangular fold to invade the cor, involving the BM & superficial stroma,the whole being covered by conj epith.

AETIO-
  • UV radiation
  • Hot,sandy & dusty climate

STAGES-
    1. PROGRESSIVE STG-
-Thick,fleshy & vascular
-Gradually increases in size & encroaches onto the cor
-Stocker’s line-iron deposited as aline in front of the apex in core pith
2.ATROPHIC / STATIONARY-
-Thin,attenuated & with poor vascularity
PARTS-
-Apex / head
-neck
-body
-cap-semilunar infiltrative opaque spot in front of the apex

SYMPTOMS-
-Masss on nasal or  temporal aspect
Read from basak-107
Diff from pinguecla-
    1. Pt- usually nasal
Pi- nasal & temp
            2.Pt- inv cor as well conj & destroys bowman’s memb
              Pi-Confined to conj

H/P-Stromal elastosis / basophilic degeneration
    - Normal conj shows eosinophilic stroma.
    -Sun-->Conj collagen stains blue resembling elastic tiss→So         elastotic /basophilic degn
   -Also seen in-Actinic keratosis
                    -BCC
                    -SCC
                    -melanoma

OCULAR  COHERENCE TOMOGRAPHY-
[j-07]

  • Non-invasive, non-contact imaging system
  • Prod micron-resolution retinal images in-vivo
  • Diode laser used
  • Analogous to B-scan ,instead of sound, it uses light

PRINCIPLE-
-A beam of near-infra-red light [830-850n] is directed into the tissue
-Using the principle of low-coherence interferometry time delay of reflected or backscattered light from the microstructures within the tiss is measured
-Optical –reflectivity is calculated by computerized image processing & images are displayed in false colour
-Bright colours [red to white]→High optical reflectivity [-50dB]
-Dark colours [blue to black]→low or no -  “  -[-100dB]
-Axial resolution-10-15 µm
-Interpretation-
*  The posterior red band corresponds to the RPE  & choriocapillaris
*  This layer terminates at the margin of the OD
* The anterior red band corresponds to the NFL.The NFL increases in thickness around the OD
* Bet these two red bands  are ares of low reflectivity – neurosensory retina
* Two bands of intermediate reflectivity correspond to  IPL & OPL within the neurosensory ret
-a light source is reflected onto a partially reflective mirror [optical beam splitter]
-One of the resulting beams is directed into the patient’s eye & reflected from IO structures
-This reflected beam consists of multiple echoes & provides information abt the distance & thickness of IO struc
- The second beam is reflected from a reference mirror at a known spatial location
-This beam travels back to the beam spilitter where it combines with the light reflected from the pt’s eye
-These two beams coincide & produce interference ,which is measured by a photodetector
Diag from notes

APPLICATIONS-
1] Macular holes-diag & staging
2] ERM-membrane thickness
            -cystic changes
            -focal vs global adherence to the ret surface
3]DME
4]CME
5] CSR
6]CNV
7] Postoper. Assessment of trabeculectomy site,AC angle & CB

DISADV-
1.High cost
2.Posterior subcap & cort cat impair performance
3.Pupillary dilatation is reqd for peripapillary measurement

             ANTIOXIDANTS [j-07]
DEF- Substances whose presence in relatively low conc significantly inhibits the rate of oxidation of the targets

How do they work?
They serve as natural protectors in the body, mopping up free radicals & reactive oxygen species,which are potentially damaging.
They work in 4 ways-
    1. Separate free radicals & reactive O2 species from the succeptible molecules  in the body
    2. Provide molecules which compete with O2
    3. Rapidly repair the damage caused by free rad / O2 species
    4. Lyse the free rad / reactive  O2 species & remove them

Free radicals are chemical species having single unpaired electron in outer orbit.So they are very unstable.Antioxid give up electrons to free radicals thus thwarting their deletrious effects

Antioxidants-
  1. Intracellular enzymes-
  1. Catalase –present in peroxisomes
  2. Superoxide dismutase-present in mito & cytosol
  3. Glutathione peroxidase-protects cell injury by catalyzing free radical breakdown
  1. Nutrients-
  1. Vit A-anticarcinogenic
             -Reduces susceptibility of LDL to oxidation
2. Vit E-      “
3.Vit C-ascorbic acid
          -scavenges oxygen radicals
          -increases ferritin conc in lens epith→ferritin sequesters iron which catalyzes free rad
4.Cu
5.Se-helps glutathione peroxidase in catalyzing breakdown of peroxidase which produces ocular damage.
6.Fluorides
7. Nuts
8. Friuts
9veg, cereals, pulses
10.Zn-integral part of superoxide dismutase & catalase
        -aids in capture of free rad release
        -retards ARMD progression

IND-
  1. ARMD
  2. DR
  3. ROP
  4. Ischaemic ophthalmopathy
  5. cor inflamn
  6. POAG
  7. Senile cataract

  C/I-Hypersensitivity to any of its constituents

DOSE- one capsule/day
Suitable for diab as they do not contain any sugar

MIXCAROTIN-contains essential carotenoids-alpha carotene,beta carotene,cryptoxanthin,lutein & zeaxanthin.Derived from sea algae