GLAUCOMA NOTES

GLAUCOMA

CALIBRATION OF TONOMETER

 

Checking the calibration of a tonometer

To ensure an accurate measurement of intraocular pressure, a tonometer needs accurate calibration. To check if the calibration is correct, a calibration bar is used.  Tonometer and a calibration bar. The following pictures and steps show how the calibration is checked: 1. Attach the calibration bar to the body of the tonometer as shown below. Attach the bar to the  tonometer. 2. The bar has five markings, the central one is used to check if the tonometer has been      calibrated accurately for 0 mmHg, the next markings on either side of the centre are      used to check for accurate calibration for 20 mmHg. The last markings nearest to the      end are used to check for 60 mmHg (see pictures below).  3. To check if the tonometer has been correctly calibrated for 60 mmHg, line up the      marking on the bar furthest from the centre with the marking on the knob that hold      up the bar (as shown in the picture below; to check for 0 and 20 mmHg line up the      bar as described in 2 and repeat steps 3 and 4).    4. Now move the knob on the tonometer and note the pressure at which the tonometer      tip tilt forward. If the tilt occurs when the pressure is at 60 the tonometer is calibrated      correctly. If the tilt occurs below or above 60, the tonometer should be sent for      re-calibration. Checking the calibration for 60 mm Hg. The end point occurs  when the  tip of the tonometer tilts forward and the bar moves to  horizontal position. If the reading is 60 at this point, the tonometer  is correctly calibrated. The animation shows a tonometer with an accurate calibration for 20 mmHg.

STIGMA OF ACUTE GLAUCOMA-

• iris atrophy
• sphincter paralysis
• pigment dispersion
• glaucomaflecken

HYPOTONY-[ < 6mmHg]

• cor edema
• disc edema
• macular edema
• uveal effusion
• choroidal folds
• choroidal detachment
• cataract
• Ruptured globe
• Phthisis bulbi
• RD

Q- How can hypotony be classified ?

A- 1. Decreased aq prod-

     *  Acetazolamide

     *  CB trauma

     * CB inflamn

     2. Increased aq prod

     *  Cyclodialysis cleft

     *   Excessive aq leakage

GLAUCOMA-[Parson]

Chronic , progressive optic neuropathy caused by a group of ocular conditions which lead to damage of the optic N with loss of visual function.

MC risk factor is raised IOP.      

   TONOMETRY-spot

DEF- Assessment of IOP

TECHNIQUES- 4 types

1. Indentation
2. Applanation
3. Non-contact
4. Digital

INDENTATION TYPE-

         A plunger is used to indent the cor which displaces a significant vol of IO fld at the time of cor deformation & results in a near doubling of IOP.

Shape of deformation-Truncated cone

Eg-Schiotz tonometer

Sources of error-

1.Errors inherent in the instrument-

-Diff in wt of diff parts of tono

-Diff in size,shape & curvature of footplate

-Friction arising in the working of footplate

-Diff in smoothness of gliding movt of pointer on scale

2.Reflex contraction of EO ms→ raises IOP

3.Error d/t accommodation-

When tono is brought close to the eye,accomdn comes into play→ciliary ms contract→pull on the TM→ increase the aq outflow→ reduce IOP

4.Error d/t ocular rigidity-

High ocular rigidity-

• high hyperopia
• high myopia
• longstanding glaucoma
• ARMD
• Vasoconstrictor

Low ocular rigidity-

• high myopia
• Raised IOP
• Osteogenesis imperfecta
• Miotic
• Vasodilator
• Cryopexy
• Scleral buckling
• V’tomy
• IV gas

5.Errors d/t variation in cor curvature-

Steep/thick cor→greater displacement of fld→ falsely high IOP

Eg-microphthalmos

    -buphthalmos

-high myopia

-cor scars

6.Blood vol alteration

7.Moses effect-

At low scale reading, cor may mould into the space bet the plunger & the hole→Pushes the plunger up→ falsely high IOP

APPLANATION TONO-

Shape of deformation-Simple flattening

2 types-

1.Variable force-Measures the force reqd to applanate a std area of cor surf

Eg- Goldmann AT

   -Perkin’s AT

   -Draeger’s AT

Mackay Marg tono-Pneumotonometer

                              -Tonopen

2.Variable area-Measures the area of the cor flattened by a known force.

Eg –Maklakov tono

Avg IOP by appln -15-17mmHg

               By indentn – 10-20mmHg

GOLDMANN TONO

• Based on Imbert Fick’s law-‘’Pressure within a sphere is equal to the force needed to flatten part of the sphere div by the area flattened.’’- P = F / A
• Instrument-

A spring balance is attached to a plastic biprism,which on contact with the cor creates two half semicircles.The prisms are so adjusted so that the inner margins of the semicircles overlap when 3.06 mm of cor is applanated.-→0.05 µl of aqueous vol is displaced

• Sources of error-1. Corneal thickness→d/t collagen fibrils→falsely high IOP

d/t edema→Falsely low IOP

2. Falsely low reading→ thin cor

3.Astigmatism > 3-4D→IOP error  of 1mmHg per 4D

With-the-rule ast→IOP Underestimated

Against –the –rule Ast→ IOP overestimated

4.Prolonged contact→ low IOP

5.Inaccurate caliberation of instrument

DISINFECTION-

Wipe the tono tip with 70% hydrogen peroxide or 70% isopropyl alcohol→ protects against HIV, hepatitis,adenovirus

PERKIN’S & DRAEGER’S AT-

• portable
• hand-held
• Goldman style
• Built-in-biprisms

     MACKAY-MARG TONO-

The force measured is that necessary to keep the plunger’s flat plate flush with its surrounding sleeve.The force reqd to bend the cor is transferred to the sleeve so the plate reads only the IOP

PNEUMOTONOMETER-

• Assesses IOP with a central sensing device controlled by air-pressure,while the force reqd to bend the cor is transferred to the sleeve.
• Not portable
• For irreg & scarred cor

TONOPEN-

• Hand-held
• As the footplate flattens the cor→The strain gauge creates an electric signal→A microprocessor chip senses approp force curves & calculates avg of 4-10 readings→final digital read-out
• Useful in irreg & scarred cor &CL wearers

MAKLAKOV AT-

IOP is estimated by measuring area of cor that is flattened by a known weight.

INSTRUMENT-

• A dumbbell shaped metal cylinder with flat end-plates of polished glass on either end with a dia of 10mm
• A set of 4 such instr weighing 5, 7.5, 10 & 15 gm
• A layer of dye [ argyrols,glycerol water suspension] is applied to either end-plate
• Cor anaesthetized & pt in supine pos.
• Rest the instr on cor for 1 sec
• White circular imprint on the end-plate which corresponds to the area of cor flattened.
• Dia of cor measured with a transparent plastic scale to 0.1mm
• IOP read from conversion table

NON-CONTACT TONO-

• Introd by grolman
• A jet of air is used to momentarily deform the cor & the time reqd to flatten the cor relates to the level of IOP
• Based on the principle of applanation but instead of biprism a jet of air is used.
• Time reqd for an avg measurement-1-3 millisec
• Advantages-1.No cor abrasion

                        2.No spread of inf

INSTRUMENT-

1. Allignment system-

Optically aligns the patient’s cor in axial,vertical & lateral dimension

2. optoelectronic applanation monitoring sys-

-Transmitter-Directs a collimated light beam at the cor vertex

-Reciever & detector-Accepts only parallel .coaxial rays reflected from the cor

3. pneumatic sys-Generates a puff of room air directed against the cor

New hand held NCT- Pulsair tono

Tech-

-Pt observes an internal target

-Collimated light is directed at the cor

-Trigger is depressed

-Puff of air deforms the cor

-Reflected light rays are received & recorded as the peak intensity of light detected

-Time interval from an internal reflex point to the moment of max light detection is converted to IOP & displayed digitally

Useful in mass screening

                     GONIOSCOPY-SPOT

DEF- Visualization of AC angle structures

PRINCIPLE-

    Total internal reflection is eliminated by placing a contact lens over cor which replaces cor – air interface,thus critical angle is not reached [ 46 deg] & we can visualize the angle struc  clearly.

Angle of Ac is k/as COCKPIT OF GLAUCOMA

TYPES-1. Direct Goniolenses

            2.Indirect Goniolenses

DIRECT GONIOLENSE [GONIOPRISM ]-

• direct view of angle struc
• does not req a slit lamp
• supine pos.

1. KOEPPE’S LENS-

-Prototype diagnostic lens

-Dome shaped

-Panaromic view [ie simultaneous comparison of one part of the angle can be done with another]

2. BARKAN’S LENS- Prototype  surgical lens

3. SWAN JACOB’S LENS-surg lens for childn

4.RICHARDSON SCHAFFER LENS-small koeppe lens for infants

5. LAYDEN LENS-For premature infants

    6.THORPE LENS-surgical & diagnostic lens for OT

ADVANTAGES-

1. Height of observer can be changed to look deeper into a narrow angle.
2. Less distortion of AC .
3. Useful in sedated pts & childn.

INDIRECT GONIOLENSES [GONIOMIRROR]-

• Provides a mirror image of opposite angle
• Image is inverted but not laterally reversed
• Used only with a slit lamp.
• Eg-

1.GOLDMANN SINGLE MIRROR-

- mirror inclined at 62 deg  

-Has to be rotated 3 times to examine the whole angle

                                                                                                                                                                                                                 

2.Goldmann 2 mirror-

-mirror inclined at 62deg

-Has to be rotated once

-Gives the best in situ view of the angle

                                                                                                                                                                                       

   3.GOLDMAN 3-MIRROR gonioprism or contact lens-

  - * Diam -12mm [so more stable]

* Disinfection-glutaraldehyde or sod hypochlorite for 25min

*Stabilizes the globe→useful for laser trabeculoplasty

*  Central-

 -30 deg of post pole

*  Equatorial-

73deg-

 30 deg to equator

[largest & oblong]

*  Peripheral –

67 deg  

[intermed & square shaped

] equator to ora serrata

*  Gonioscopic-

59deg   

[smallest & dome shaped]

 -Gonioscopy

 -pars plana & extreme retinal periphery

4. ZEISS 4 MIRROR-

-all 4 mirrors inclined at 64 deg

-Diam -9mm [so not stable & cannot be Used for argon laser t’plasty]

   -Indentation G’scopy→ To Differentiate appositional from    synechial angle closure.Goniolens is pressed against the cor→Forces the aq into the angle of AC & forces peripheral iris posteriorly.

→ If appositional→ angle will open

→If synechial     →angle remains closure

    

5.POSNER 4 MIRROR

6.SUSSMAN 4 MIRROR

7.THORPE 4 MIRROR

8.RITCH TRABECULOPLASTY LENS

ADVANTAGES-

1. Better optics & lighting of SL→ subtle details seen

2.fast

3.Zeiss can be used for indentation G’scopy

GRADES AC ANGLE-

SHAFFER SYSTEM-

GRADE 4→-35-45 deg

                  - Widest angle

                  -  Upto CB

                  - incapable of closure

GRADE 3→-25-35 deg

                   -open angle

                   -upto scleral spur

                   -incapable of closure

GRADE 2→20deg

                  -upto TM

                  -angle closure possible

GRADE 1→10 deg

                  -only schwalbe’s line visible

                  -very narrow angle

                 -high risk of angle closure

SLIT ANGLE→ No obvious iridocor contact,but no angle

                          Structures are visible.

                          -Greatest danger of imminent closure

GRADE 0→closed angle

                   -iridocor contact

                   -inability to visualize the cor wedge

SPAETH’S CLASS-Based on 3 variables-

1. ANGULAR WIDTH-10 deg

                                     -20 deg

                                     -30 deg

                                     -40 deg

2.CONFIGURATION OF PERIPHERAL IRIS-

   s- steep

   r- regular

   q- queer

3.APPARENT INSERTION OF IRIS-

* Ant to TM

* Behind the schwalbe’s line

* At the scleral spur

* Deeply with visible CB

* Extremely deeply

SCHEIE’S CLASS-

. Wide open- All structures visible

.Grade I- Hard to see over iris root into recess

.Grade II-CBB obscured

.Grade III-Posterior trabeculum obscured

GradeIV-Only Schwalbe’s line visible

VAN HERICK’S TECH-

GRADE IV or larger→PAC> CT

              III              →PAC= ½ - ¼  CT

              II               →PAC = ¼ CT

              I                →PAC < ¼ CT

RP CENTRE GRADING-

0-No dipping of beam

1-Dipping of beam

2-Schwalbe’s line & Ant 1/3rd of TM visualized

3-Middle 1/3rd of TM visualized

4-Post 1/3rd of TM visualized

5-Scleral spur visualized

6CBB visualized

MODIFIED GONIOSCOPIC GRADING-

N- No dipping

D- Dipping of the beam

SL-Schwalbe’s line & ant 1/3rd of TM seen

TM-Middle 1/3rd of TM seen

SC-Post 1/3rd of TM seen [location of schlemm’s canal]

SS- Scleral spur visualized

CB –CB seen

VIVA-

Q. What is a corneal wedge ?

A.The cor wedge is useful in locating an inconspiquous schwalbe’s line.

-Using a narrow slit beam, 2 linear reflections can be seen,one from the external surf of cor with its juncn with the sclera & the other from the internal surf of cor.

-The two reflections meet at the apex of the cor which coincides with the schwalbe’s line

Q.TM HYPERPIGMENTATION-

1. Pigment dispersion sy

2.Pseudoexfoliation sy

3.Blunt trauma

4.Ant uveitis

5.Foll acute angle closure glaucoma

6.Diabetes[ esp after cataract surg]

7.Naevus of ota

Q.Blood in schlemm’s canal-

* CCF & dural shunt

* Sturge Weber syn

* SVC obstrn

*Hypotony

Q. What is an angle recess?

A. Posterior dipping of iris as it inserts into the CB.

Q Blood Vs in the angle-

1. NV glauc

2.Fuch’s uveitis syn

3. Chr ant uveitis

OPTIC NERVE HEAD

* 1.2 million ganglion cell axons

* Arcuate fib – most vulnerable to glauc damage

* PM fib –most resistant

*OPTIC CUP-

-Pale depression in the centre of ON head , not occupied by neural tissue.

- Pallor results from exposure of lamina cribrosa & lack of glial tiss in the centre of disc

* LAYERS OF ONH-

1.Nerve fibre layer

2.Pre-laminar layer

3. laminar layer

4.Retro laminar layer

* CUP-DISC RATIO-

Diameter of the cup expressed as a fraction of diameter of the disc

* NEURORETINAL RIM-

-Tissue bet the outer edge of the cup & the disc margin

- Inferior rim is the broadest,foll by sup,nasal & temporal

  [ISNT]

Q-Diff bet physiological & pathological cup?

A-PHYSIOLOGICAL CUP-

D/t mismatch bet the scleral canal & the no of fibres traversing thru it which in health remains constant

PATHOLOGICAL CUP-

Irreversible decrease in the no N fib,glial cells, & BVs

GLAUCOMATOUS OPTIC DISC DAMAGE-

4 types-

1.Focal ischaemic

2.Myopic glaucomatous

3.Senile sclerotic

4.concentric enlargement

FOCAL ISCHAEMIC-

Focal tissue loss at sup/inf poles-POLAR NOTCHING

MYOPIC GLAUCOMATOUS-

Polar notching + Temporal crescent

SENILE SCLEROTIC-

-Shallow saucerized cup

-Sloping NR rim

-Parapapillary atrophy / choroidal sclerosis surrounding the ONH

CONCENTRIC GLAUCOMATOUS DAMAGE-

-Diffuse loss of NF inv the entire cross-section of ONH

-No localized thinning of NRR

PROGRESSION OF GLAUCOMATOUS OPTIC DISC DAMAGE-

EARLY SIGNS-

1. POLAR NOTCHING-Focal atrophy of the NRR begins at the inferotemporal quad leading to vertical enlargement of the cup.
2. SHARPENED POLAR NASAL EDGE-Focal defect enlarges & deepens & dev a sharp nasal margin adjacent to a major retinal V
3. BAYONETTING SIGN-When the local thinning of NRR reaches the disc margin [i.e no visible rim left] a sharpened rim is produced.If a retinal V crosses the rim, it will bend sharply at the edge of the disc.
4. PALLOR-CUP DISCREPANCY-DIFFUSE  

                                                          FOCAL

DIFFUSE SAUCERIZATION-diffuse shallow cupping extends to the disc margin with retention of the central cup.

FOCAL SAUCERIZATION-More localized shallow ,sloping cup usually  in the inferotemporal quad

5.TINTED HOLLOW-Retention of nml neural rim colour in the area of focal saucerization.

6 NASAL SHIFTING OF BV

7.BARING OF CIRCUMLINEAR Vs-Nmlly BVs curve along the cup margin,but with glauc enlargement of the cup,these circumlinear Vs get barred from the cup margin.

8.SPLINTER H’AGES- at the disc margin

                                    -may be the 1st sign of glauc damage

LATE SIGNS-

1.BEAN- POT CUPPING-

Total cupping appears as a white disc with loss of all neural rim & bending of all ret BVs at the disc margin

2.LAMINAR DOT SIGN-

Loss of neural tiss exposes the openings of lamina cribrosa

OCULAR HYPERTENSION-read from notes

IOP > 21mmHg on two consecutive occasions in the absence of detectable glaucomatous damage

TARGET PRESSURE-

DEF-It is the IOP at which deterioration of optic disc changes / visual field defects cease with min complications & S/E

Target press depends upon-

1. IOP level at which damage occurred.

Higher

Target IOP

                                 

                        

                          Early                   Short                       High

                         Damage               Life expectancy            IOP

                                                                                       When

                                                                                       Damage

                                                                                       occured

                        Advanced             long                    

                                                                                    Low

   Lower

   Target IOP

2.Severity of visual field damage-

Mild-Glaucomatous optic N damage + nml visual fields→ 20% of initial pretreatment press

Mod-Visual field abnmlity restricted to either of hemifields, but does not extend within 5 deg of fixation→30 %  of initial pretreatment press

Sev-Visual field defec in both hemifields or field loss within 5 deg        from fixation→ 35-40% of prêt/t press

3.Rate of progression of glauc damage-

Rapid damage-Lower target IOP should be set

Damage at a slower pace-Higher target IOP should be set

How to set target pressure?

Reduce the IOP by a % equal to the initial IOP & deduct a factor based on the visual field defects

For eg-1.Initial iop-30mmHg

            IOP after 30 % reduction-100-30

                                                      30- ?

                                                    = 9

                                    i.e 30-9=21

Target IOP in a pt with no field loss-21-0=21

                                     Mild  “         -21-1=20

                                     Mod   “        -21-2= 19

                                     Sev      “       -21-3=18

2.Initial IOP- 50mmHg

IOP after  50 % reduction = 50-25=25

Target iop in a pt with no field loss-25-0=25

                                   Mild              -25-1=24

                                   Mod              -25-2=23

                                   Sev               -25-3=22

RISK FACTORS FOR POAG [J-07]

A] Demographic risk factors-

1. Age-Increasing age is a major risk factor

2.Race-Caucasians & Africans

          -More severe in black

B] Ocular risk factors-

1. IOP

2.ONH Damage-

A] Mechanical theory-

The coats of the eye can withstand fairly high IOP except at the LC.Rise in IOP→ Backward displacement of LC→ compaction of the laminar plates→ narrows the openings thru which the axons pass→ mechanical damage to nerve fib bundle

B] Ischaemic theory-

Rise in IOP→Decrease ONH perfusion→ ischaemia→Dysfunctional axoplasmic transport→ Ganglion cell death→ apoptosis

3.Myopia

[HM- ACG]

C] Systemic risk factors-

1. DM

2. HT

D] Genetic risk factors-

-First degree relatives are at increased risk

-10 % risk to siblings & 4% risk to offsprings has been suggested

E]Retinal diseases-

-CRVO

RP

RD [rheg]

F]-Others-

Cigarette

Alcohol

                      NORMAL  TENSION  GLAUCOMA

Read from notes

• Variant of POAG
• MC in females
• IOP = / < 21mmHg
• Glaucomatous disc damage & visual field loss
• Open angle on G’scopy
• Absence of sec causes for glauc disc damage
• Splinter h’age
• Field defects- closer to fixation,deeper, steeper & more localized
• Other features- Peripheral vas spasm on cooling [Raynaud’s phen]

                         -Migraine

                         -Nocturnal sys hypotension

                         -Reduced bld flow velocity in oph A

                       -Paraproteinemia & serum autoantibodies

T/T-

1.Betaxolol-DOC

2.Trabeculectomy

3.CCB-Nifedipine

PRIMARY ANGLE CLOSURE GLAUCOMA case

DEF- Condition in which elev of IOP occurs as a result of aq flow obstrn by partial / complete closure of the angle by the peripheral iris.

EPID-

• Age> 60 yrs
• F : M-4:1
• Race-south east Asians,Chinese & Eskimos
• First deg relatives are at high risk

PREDISPOSING FACTORS-

• Small hypermetropic eye
• Shallow AC
• Narrow entrance to AC angle d/t-

• Lens continues to grow→Lens –iris diaphragm moves anteriorly → Shallow AC
• Small cor dia [0.25mm less than nml]
• Small axial length

PATHOGENESIS-

Mech of angle closure-

1. Pupillary block mech-

Contraction of dilator pupillae→ mydriasis → apposition of iris with ant lens surf→enhances physiological pupillary block→ aq unable to go into AC → collects in PC→ iris bombe → closure of Ac angle → rise in IOP

2. Plateau iris mech-

a.Peripheral iris tiss is thick [peripheral iris roll]→ when pupil dilates iris gets bunched up in the angle → blocks TM

b.Iris base inserts anteriorly & leaves only a narrow band of CB or inserts onto the scleral spur

c. Ciliary processes are displaced into the PC →pushes the iris base forwards into the angle recess.

	PACG	PLATEAU IRIS SYN
Mech of glauc	Pupillary block	Ant pos of peripheral iris→ TM block
Age	Old	Young
AC	Shallow	Deep centrally
T/T	Laser iridotomy	Does not respond to iridotomy.Needs laser peripheral iridoplasty o

                                                                     -y or miosis

STAGES-

1.PRODROMAL / LATENT /PACG SUSPECT-

- Asymptomatic

-Shallow AC

-G’scopy- ‘occludable angle’ i.e one in which pigmented TM is not visible without indentation or manipulation in atleast 3 of the 4 quad

-Dark room provocative test positive

-T/T-If one eye has acute / subacute PACG fellow eye shud undergo prophylactic peripheral laser iridotomy

2.SUBACUTE /INTERMITTENT PACG-

- Occurs in a predisposed eye with an occludable angle with pupillary block.

-Attack ppted by Physiological mydriasis-watching TV in a dark room.

Physiological shallowing of AC-Sewing / reading

-C/F-

* Headache / browache-UL

* Blurring of vision-same side

* coloured haloes- Red outermost & blue innermost

FINCHAM’S TEST-->

GLAUCOMATOUS HALO- Intact but diminished in intensity

LENTICULAR HALO- Broken up into segments

                            

-Recurrent attacks

-Broken after 1-2 hrs of miosis [bright sunlight or sleep]

-T/T- prophylactic peripheral iridotomy

3.ACUTE CONGESTIVE ACG-

-Sight threatening emergency

-C/F

Symptoms-Pain

                -UL

                -sudden LOV [HM]

                -Nausea & vomiting

Signs-

• Lid edema
• Tenderness
• Ciliary & conj congestion
• Cor-steamy,insensitive,epith vesicles,stromal thickening
• Ac-shallow,aq flare & cells
• Pupil-vertically oval,fixed in mid-dilated pos,unreactive to light & accomodn
• Iris –CP lost
• IOP-50-100mmHg
• G’scopy-schaffer gr-0-complete peripheral iridocor contact
• Fundus-Disc edema & hyperaemia

T/T-

1.Medical

* IV Mannitol 20 % 2gm/kg

* T. Diamox 250mg 6 hrly

* After 30 min, once IOP is reduced, 2 % pilocarpine every 5 min till pupil constricts & then qid.

Miotics are ineffective when IOP is high d/ t pressure induced ischaemia of iris which leads to paralysis of sphincter ms.

Therefore 1st line of defence –lower IOP with hyperosmotics & CA inhibitors

• Topical B –blockers-timolol 0.5 % bd
• Topical dexamethasone 0.1 % e/d qid
• Oral analgesics

2.Surgical- Nd – YAG iridotomy

               -Ind-less than 180 deg of angle closure

              - Aim-To reestablish communication bet AC & PC by making an opening in peripheral iris

              - 3 bursts of 3-6 mJ

              -Ideal hole size-150-200 µ

              -If no response→ trabeculectomy

4.CHRONIC /POSTCONGESTIVE ACG

Causes-

1. Rise in IOP + creeping angle closure [synechial angle closure occurs within the depth of the angle i.e iridotrabecular synechiae & inv entire angle]
2. Subacute attacks of PACG → synechial angle closure→ chronic rise in IOP

C/F-

• V/A –falls
• Congested & irritable eye
• Raised IOP
• Fine pigment granules on cor endothelium
• Aq flare & cells
• Stromal iris atrophy
• Fixed & semidilated pupil [d/t sphincter paralysis & post synechiae]
• Glaucomaflecken-Ant subcapsular / capsular lens opacities in the pupillary zone, diagnostic of a previous episode.Represents focal necrosis of lens epith
• Disc cupping
• Field defects

T/T-Creeping angle- PI

     -Secondary causes-med t/t

5. ABSOLUTE GLAUCOMA-case

• End stage
• C/F-
• Painful blind eye
• No PL
• Cor-cloudy,bullous & filamentary KP
• Sclera-porcelain white
• Ac-very shallow
• Iris-atrophic patches & ectropion
• Pupil- dilated & no reaction
• Optic disc-large,deep cup,atrophy
• IOP- raised [stony hard]

T/T-

1.Retrobulbar alcohol -70% - Destroys the ciliary ganglion & relieves  pain

2. Cyclocryotherapy

3. Enucleation

SEQUELAE-

Rise in IOP→ scleral thinning → staphyloma

Rise in IOP→ continued press on CB→ CB atrophy→ less aq → eyeball shrinks→ Atrophic bulbi [struc of eye can be identified]

[Phthisis bulbi- quadrilateral shape d/t pressure by recti]

PSEUDOEXFOLIATIVE  GLAUCOMA-case

• Also k/as Glaucoma capsulare
• Chronic open angle glaucoma
• 6-7 decade [ elderly]
• Females MC
• Gene- 2p16
• D/D- True exfoliation-Lamellar splitting of lens capsule sec to infra-red damage
• UL – 60 %

PATHOGENESIS-

• Grey-white fibrillogranular extracellular matrix is deposited onto ant lens capsule,zonules,Cb,iris,TM,ant vit face & conj.
• Material is produced by abnml BM from ageing epith cells
• Glaucoma d/t-Clogging of TM by Pseud material & trabecular endothelial dysfunction

C/F-

1. CORNEA-

• PEX on endo
• Pigment deposit-KRUKENBERG SPINDLE
• Endo cells reduced in no & morphologically abnml

2.AC-mild aqueous flare d/t breakdown  of iris-bld-aq-barrier [pseudouveitis]

3.IRIS-

* PEX on pupillary margin

* Sphincter atrophy-MOTH-EATEN transillumination defect[pupillary margin]

                              -poor pupillary dilatation

* Pigment dispersion

* Intrastromal h’age on mydriasis

* Post synechiae

4.LENS-

* PEX on ant lens surf→ constant rubbing of pupil scrapes the material off the mid-zone→ central disc & peripheral band of PEX with a clear zone in bet

* Zonular instability→ phacodonesis,lens subluxation or dislocation

* High risk of zonular dialysis & VL during cat Sx

T/T-

1. MEDICAL-

• β-blocker-Timolol 0.5 % e/d BD
• α-2 agonist-Apraclonidine 1 % e/d BD

                OR –Brimonidine 0.2 % e/d BD

• Prostaglandin- Latanoprost 0.005 % e/d OD

                 OR Travoprost 0.004 % e/d

                 OR Bimatoprost 0.003 %  e/d

• Topical CAI- Dorzolamide 2 % e/d

                     OR – Brinzolamide 1 % e/d

2 SURGICAL-

Laser trabeculoplasty  OR Trabeculectomy

     PIGMENTARY GLAUCOMA-case

DEF- Condition characterized by liberation of pigment granules from the iris pigment epith & their deposition thru out the ant seg.

EPID-

• BL
• Gene loci-chromosome 7 & 8
• Open angle glauc
• Common in myopes
• 3-4 decade

  PATHOGENESIS-

Excessive post bowing of the mid-peripheral iris→ mechanical rubbing of the post pigment layer of the iris against the packets of lens zonules→ Pigment shedding→ pig granules are dispersed by aq currents & deposited on all ant chamber struc→ TM obstrn → rise in IOP

Post bowing of iris & iridozonular touch→ Reverse pupil block→ increase in AC press

C/F-

1. CORNEA-Krukenberg spindle
2. AC-very deep
3. IRIS-

• Fine pigment granules within furrows→heterochromia iridis
• Iris atrophy→radial slit like transillumn defects-mid-peripheral

4.LENS-Pigment deposits

5.G’SCOPY-

* wide open angle

* Trab hyperpig

6.FUNDUS-retinal breaks

Lattice degeneration→RD

T/T-

1.medical- Miotics→ decrease iridozonular contact→increase aq outflow( ? pilocarpine causes RD.PDS patients are usually myopes & have LD)

2.laser trabeculoplasty

3.Laser iridotomy

4.Trabeculectomy + antimetabolites

NEOVASCULAR   GLAUCOMA-case

Def-Intractable glauc which results due to the formation of a NV memb across the AC angle

PATHOGENESIS-

Chronic retinal ischaemia → Hypoxia → Vasoproliferative growth factors →

1) Rubeosis iridis

2) Retinal NV

3)Angle NV-initially impairs aq outflow [open angle]

                   -later NV memb contracts [angle closure]            

                                                                                                CAUSES- VIVA

1. Ischaemic CRVO-Glaucoma dev 3mo after the occlusion-‘100 DAY GLAUCOMA’
2. Proliferative DR-Risk increased by cat extrn [particularly if PC is breached.Freq review is essential during the first 4 PO wks which represents the crucial period for dev of rubeosis iridis] &

- PPV

- Decreased by PRP

3.CRAO

4.Sickle cell RP

5.ROP

6.CCF

7.Carotid obstructive dis

f8.IO tumours

9.Longstanding RD

10.Chr. IO inflamn

STAGES-

1. RUBEOSIS IRIDIS-

• Tiny ,dilated capillary tufts dev at the pupillary margin first bcos of aq flow dynamics angiogenic factors prod in the post seg have the most contact with pupil
• The new Vs grow radially over the surface of iris towards the angle.At this stg IOP is nml
• T/T-suggests ischaemia
• 1. PRP-reduces stim for NV
• Retinal cryoablation
• Anti-VEGF –IV
• Triamcinolone acetonide -IV

2.SECONDARY OPEN ANGLE GLAUCOMA-

* The new Vs across the iris surf grow towards the iris root

* The NV then proliferates across the face of CB & scleral spur to invade the angle

*The NV arborize & form a fibrovascular memb→ Blocks TM→ sec open angle glauc

*  T/T-

1.Medical-Topical atropine 1 %

               -Topical steroids

              -miotics shud be avoided

2.Prophylactic PRP

3. SECONDARY ANGLE CLOSURE GLAUCOMA

• Contraction of fibrovascular tiss in the angle →Pulling of the peripheral iris over the TM→ Angle closes circumferentially like a zipper
• C/F-
• V/A –sev reduced
• Globe congestion & pain
• Very high IOP
• Cor edema
• Aq flare d/t leakage of proteins from iris new Vs.
• Sev rubeosis iridis
• Distortion of pupil
• Ectropion uveae
• G’scopy-Synechial angle closure & closed angle

b-wave amplitude ratio < 1 predicts dev of NVG in CRVO

T/T-V V IMP

1Medical-Atropine

                      -Steroids

                      -No miotics

2.Retinal ablation-Argon

                            -Diode

3.Surgery-Trabeculectomy + Mitomycin –C

               -Artificial filtering shunts ( Ahmed valve)

Role of filtering Sx is to prevent pressure induced injury to theON & to improve vascular perfusion

4.Cyclodestruction by trans-scleral diode

5.Retrobulbar alcohol

6.Enucleation

DDs-

1. Inflammatory glauc-

-AC cells & flare

    -Dilated nml iris BVs

    -open angle

    -no nv

2. Prim acute angle closure glauc
3. Post sx dilatation of iris Vs
4. Fuch’s heterochromic iridocyclitis
5. essential iris atrophy
6. PXF
7. ROP

                                     

VIVA- Q.which drugs shud be avoided in uveitic glauc?

1. Prostaglandin analogue-enhance breakdown of BAB

                                         -exacerbate CME

2. Pilocarpine-promotes post synechiae

POSNER SCHLOSSMAN SYND

OR   HYPERTENSIVE IRIDOCYCLITIS

OR   GLAUCOMATOCYCLITIC CRISIS

DEF-

• Sec open angle glaucoma + Mild ant uveitis

EPID-

• Young adults
• M > F
• HLA-Bw54
• Recurrent attacks

PATHOGENESIS- Acute trabeculitis

C/F

• Photophobia
• Haloes around light
• Blurring of vision
• SIGNS-
• Cor epith edema
• -ciliary flush
•  -Pupillary constriction
• -iris hypochromia
• -High IOP [40-80mmHg ]
• -Aq-few cells & mild flare

•  -fine white central KPs
• -G’scopy-open angle

                  -Absence of PAS

* T/T-

         1.Topical steroids-pred acetate 1% qid for 1 wk

         2.CAI-topical –dorzolamide 2%  bd

         3. Topical timolol 0.5% bd

         4. Cycloplegic- cyclopentolate 1% tds

         5. T.acetazolamide 250mg 6hrly

          6..Oral NSAIDs

Cycloplegics are C/I

LENS  INDUCED  GLAUCOMA-case

1. Secondary angle closure→ PHACOMORPHIC GLAUCOMA

                                           →PHACOTOPIC GLAUCOMA

2. Secondary open angle     → PHACOLYTIC GLAUCOMA

PHACOMORPHIC  GLAUCOMA

• Seen in Intumuscent cataract
• Intumuscent Cat lens → Forces iris root against the cor→ angle closure→ rise in IOP

s-

PHACOMORPHIC GLAUCOMA	ACUTE ANGLE CLOSURE GLAUC
Fellow eye- nml AC depth	Fellow eye-Shallow AC
Any ref error	Hyperopia
H/O-gradual LOV & myopia	No such history

T/T-

1.Reduce IOP

2. Laser iridotomy

3.Cataract extraction-definitive t/t

            PHACOLYTIC GLAUCOMA

• Also k/as Lens protein glaucoma
• Hypermature cataract wih an intact but permeable capsule→ lens protein leak out→ Macrophagic response [i.e. macrophages ingest the lens protein & plug the TM pores ]→ Aq outflow obstrn→rise in IOP
• C/F
• -Cor edema
• AC-deep

       -flare

       -pseudohypopyon

* Hypermat cat

* G’scopy-open angle

* No KPs [as cor endo is not disturbed ]

T/T-1. Control IOP

2. Lens extraction

D/D-Phacoanaphylactic uveitis-Capsule ruptured

                                                -Granulomatous reac

PHACOANAPHYLACTIC / PHACOANTIGENIC UVEITIS

Follows –

-Frank rupture of lens capsule d/t

*  ECCE

*  Trauma

* spontaneous rupture

results in --> lens protein initiate a type III immune reaction [antigen-antibody rec]→ granulomatous reaction

C/F-

-Prominent heavy KPs

-Lymphocytic & plasma cell infiltration of AC

Rx-

1. Removal of lens material
2. Anti-inflammatory therapy
3. Control of IOP

PHACOTOPIC GLAUCOMA-Subluxated /dislocated lens

         TRAUMATIC GLAUCOMA

     A}   RED    CELL   GLAUCOMA

PATHOGENESIS-

*Traumatic hyphaema   →  rise in IOP due to

                                   a) RBC s block TM

                                   B) pupillary occlusion by blood clot

• Rise in IOP→Damage the optic N & Bld staining of cornea

Causes of hyphaema-

1. Trauma
2. Oper & PO
3. DM
4. Herpetic ant uveitis
5. Bld dyscrasias
6. Iris Nv
7. HT
8. IO tumours
9. Juvenile xanthogranuloma [recurrent spontaneous hyphaema in children]

8 BALL OR BLACK BALL HYPHAEMA-

When the blood gets clotted the hyphaema appears as a small black ball like no 8 ball in billiards.This clotted bld causes sec glauc more frequently

Source of bleeding-

1. Small br of major arterial circle d/t tear in bet longitudinal & circular fib of CB
2. Capillaries of minor arterial circle wen there is a sphincteric tear
3. Radial Vs at the iris root asstd with iridodialysis

CLASSIFICATION-

A] According to type of h’age-

1. Primary

2. Sec

3. Continuous

B] According to volume-

I.  < 1/3 AC

II. 1/3 – ½ AC

III. > ½ AC

IV . Total

C] Duration-

1. Acute- 1-7 days

2. subacute- 7-14 days

3. Chronic- > 14 days

D] character-

1. Liquid- red

2.clotted- brown / black/ mixed

3. organized- tan grey white

T/T-

1.Head elev with propped up positn

2.sedation

3.Patching [BL] of eyes

4..Medical-

* Beta-blockers-timolol 0.5% BD

* CAI- T .acetazolamide 250 mg 6 hrly

*Topical steroids

* Mydriatics-atropine 1% e/o tds

* Miotics shud be avoided

* aspirin should not be used

5 .Surgical evacuation + / - trabeculectomy indicated in-

* IOP > 50 mmHg for 2 days or > 35mmHg for 7 days

* Early cor bld staining [as it can cause dense opacity]

* Total hyphaema for > 5 days to prevent PAS & chr sec glauc

B} ANGLE RECESSION GLAUCOMA

DEF-Rupture bet longitudinal & circular ms fib of CB

PATHOGENESIS-

Blunt trauma→ rupture bet longitudinal & circular ms fibres of CB→TM damage→ rise in IOP

C/F- UL rise in IOP

      -Hyphaema

      Other s/o trauma

G’SCOPY-irreg widening of CBB

                 -prominent scleral spur

                 -torn iris processes

           

T/T-

1.Med t/t –ineffective

2 Laser trabeculoplasty- ineffective

3.Trabeculectomy + antimetabolites- most effective

4.If above fails →Artificial filtering shunt

IRIDOCORNEAL ENDOTHELIAL SYN [ICE]

DEF-Grp of disorders with abnml cor endothelium responsible for iris atrophy,sec ACG with PAS & cor edema

• UL
• Young-mid aged women
• Herpes simplex virus DNA
• Includes 3 disorders-

1. Progressive iris atrophy
2. Iris naevus [Cogan Reese] syn
3. Chandler’s syn

PATHOGENESIS-

Abnml cor endothelial layer→ proliferates & migrates across the angle & onto the iris surf→ contraction of this membrane→synechial angle closure.

C/F-

• Pain
• DOV
• Abnml iris appearance
• Corectopia [malposition of pupil]
• Pseudopolycoria [supernumerary false pupils]
• Iris atrophy
• Cor endo- Hammered silver appear
• G’scopy-Broad based PAS extending anterior to schwalbe’s line
• Glaucoma

PROGRESSIVE IRIS ATROPHY-

• Stromal atrophy
• Hole formn
• Pupil displacement towards PAS

COGAN REESE SYN-

• Diffuse naevus & pigmented, pedunculated iris nodules
• Iris atrophy-Absent
• Corectopia- severe

CHANDLER’S SYN-

• sev corneal changes
• Stromal atrophy- absent
• Corectopia-mild-mod
• Glaucoma –less sev

T/T-

1.ARTIFICIAL FILTERING SHUNTS

2.Medical t/t –ineffective

3.Trab + antimetab- unsuccessful

         GHOST CELL GLAUCOMA

PATHOGENESIS-

Vitreous h’age → 2 wks → Haemoglobin leaks out from the RBCs→evolve into ghost cells→ Ghost cells pass thru a defect in ant hyaloid face→ AC.

Bcos their pliability is lost,the cells become entrapped within the TM pores & obstruct outflow

Ghost cells contain Heinz bodies which are oxidatively denatured Haemoglobin

AETIO-

1. Cataract surg in the context of pre-existing VH
2. VH in an already aphakic / pseudophakic eye
3. Cataract surg complicated by VH & hyphaema

C/F-

• Cor- edematous [d/t-raised IOP or surg trauma]
• AC- Ghost cells-Khaki / reddish brown particles

T/T-

1.Med t/t

2.Irrigation of AC & washing out of ghost cells

3.PPV

                         BUPHTHALMOS

• 1: 10,000 births
• Boys
• Most cases are sporadic. 10 % -auto recessive

PATHOGENESIS-

Trabeculodysgenesis-Absence of angle recess with iris inserted directly into the surf of TM in one of the 2 configurations-

1. Flat iris insertion-

Iris inserts flatly or abruptly into the thickened TM or ant to scleral spur

2.concave iris insertion-

The superficial iris tiss sweeps over the iridotrabecular junction & TM

CLASSIFICATION-

1. True congenital glaucoma-Intrauterine life
2. Infantile glaucoma-prior to 3rd b’day
3. Juvenile glaucoma- 3-16 years

    CAUSES-

1. Axenfeld’s anomaly
2. Reiger’s syn
3. Peter’s anomaly
4. Aniridia
5. Sturge weber syn
6. Neurofibromatosis
7. PHPV

    8. Rubella

C/F-

1.Corneal haze-D/t epith & stromal edema

                       -lacrimation

                       -photophobia

                       -blepharospasm--------triad

2.Buphthalmos-large eye→ sclera stretches→ underlying uvea appears blue.

3.AC deepens

4.Lens subluxation

5.Axial length increases-axial myopia→ anisometropic amblyopia

6.Breaks in DM d/t cor stretching

HAAB’S STRIAE-Healed double contoured breaks in DM

7.Optic disc cupping-

OCULAR ASSOCIATIONS-

1. Axial myopia
2. Lens subluxation
3. corneal decompensation
4. RD

DD-

1.Cloudy cor-Birth trauma

                    -rubella

                    -mucopolysaccharidoses & mucolipidoses

                    -CHED

2.Large cor-megalocor

                  -high myopia

3.Lacrimation-Delayed canalization of NLD

SECONDARY CONGENITAL GLAUCOMA-

Dev anomaly elsewhere

1.Aniridia

2.Peter’s anomaly

3.axenfeld’s anomaly

4.Reiger’s anomaly

5.Sturge Weber’s syn

6.Rubella

7. RB

8.Juvenile xanthogranuloma

9.PHPV

10.ROP

11.IO inflamn

12. trauma

13. Ectopia lentis

EVALUATION-

Exam under IV ketamine anaesthesia

1. IOP –Perkin’s tono or tonopen

-nml IOP in an infant is 9-10mmHg. > than 20 is suspicious

2. Cor diameter> 11mm prior to 1 year or > 13mm at any age-suspicious

> 14mm –adv buphthalmos

3.G’scopy-Koeppe lens

4. Fundus- OD cupping

5. Retinoscopy

T/T-

Prim infantile gl→ Goniotomy or trabeculotomy

Goniotomy req a clear cor whereas trabeculotomy can be done in a hazy cor

1.Goniotomy-

* surg goniolens→ Barkan’s G’tomy knife inserted thru limbus & passed across AC to the angle in the opp quad→angle tiss excised bet schwalbe’s line & scleral spur for 1/3rd of AC angle circumference.

Complications-

1.Bleeding from CB if too post incision

2.Cyclodialysis / iridodialysis

3 Hyphaema

2.Trabeculotomy-

Opening in TM→ direct communication bet Ac & schlemm’s canal.

Harm’s trabeculotome used.

Same complications

3.Trabeculectomy

IRIDOCORNEAL DYSGENESIS

DEF-

Abnml neural crest cell dev.

1.Axenfeld-Rieger syn

2.Peter’s anomaly

3.Aniridia

AXENFELD REIGER SYN

AXENFELD’S ANOMALY-

• G’scopy- Prominent & ant displaced Schwalbe’s line [post embryotoxon] onto which are attached strands of peripheral iris tiss
• Glaucoma-rare

     REIGER’S ANOMALY-

• AD
• BL
• Posterior embryotoxon
• Schwalbe’s line may become detached into the AC
• Iris stromal hypoplasia
• Corectopia
• Pseudopolycoria
• Ectropion uveae
• G’scopy-Broad leaves of iris stroma adhere to the cor ant to schwalbe’s line
• Glauc-50 %. D/t angle anomaly / sec synechial angle closure

   REIGER’S SYNDROME-

• Chromosome 4
• Rieger anomaly + extraocular malformn
• Dental anomalies--Hypodontia[few teeth]

                           -Microdontia [small teeth ]

* Facial anomalies-Maxillary hypoplasia

                            -Broad nasal bridge

                            -Telecanthus [increased intercanthal dist ]

                            -Hypertelorism [increased interorbital dist]

* Others-Redundant paraumbilical skin

            -Defects in pituitary gld

PETER’S ANOMALY-

• Defective neural crest cell migration in 6- 8wks of fetal dev
• Cor opacity[post stroma, DM & endo ]
• Iridocorneal adhesion
• Keratolenticular adhesion
• Glauc -50 %

   ANIRIDIA-

• BL
• Life-threatening
• Mutation in PAX6 gene linked to 11p13
• Glaucoma
• Class-

AN-1- AD

        -NO systemic implications

AN-2- [Miller syn]

        -Will’s tum

AN-3-[Gillespie syn]

        -AR

        -Mental retard

        -cerebellar ataxia

C/F-

• Nystagmus
• Photophobia
• Absent irides or dilated pupils

SIGNS-

• Aniridia- minimal ,partial or total
• On gonio-frill of iris  remnant may be seen
• Cornea-opacity, epibulbar dermoids, microcornea, sclerocornea, keratolenticular adhesions,limbal stem cell def
• Lens-cataract, subluxation, cong aphakia, persistent papillary memb
• Fundus- foveal hypoplasia, optic disc hypoplasia, choroidal coloboma

T/T-

1.Opaque CL-for photophobia

2.Topical lubricants

3.Cataract surg

4.G’tomy

5.Artificial filtering shunts

6.Diode laser cycloablation

         ANTIGLAUCOMA  DRUGS-spot

AQUEOUS OUTFLOW ENHANCERS-

1. Cholinergic agonists- Pilocarpine

                                         -Echothiophate iodide

                                         -Carbachol

2. Prostaglandin derive- Latanoprost

3. alpha 2 agonists- Brimonidine

4.Adrenergic agonists-Epinephrine

DECREASE AQUEOUS HUMOUR PRODUCTION-

1. B- blockers
2. CAIs
3. Adrenergic agonists
4. Alpha 2 agonists- Brimonidine

                               -Apraclonidine

ADRENERGIC RECEPTORS-

ADRENALINE-

*  α-1 receptors-Arterioles→ HT

                         -Dilator pupillae→mydriasis

                         -Muller’s ms→ Lid retraction

*  α-2 receptors-ciliary epithelium→ Reduce aqueous

*β-1 receptors-Heart→ Tachycardia

                                        Increased CO

* β-2 receptors-Bronchi → Bronchodilatation

                        - Ciliary epithelium→ increase aqueous prod.

                                                                       

                              A.  BETA- BLOCKERS

1] TIMOLOL-

MOA-Beta -2 blocker

        -Beta-2→ ciliary epith→ increase aqueous prod

Peak-2 hrs

Duration of action-24 hrs

DOSE- 0.25 % & 0.5 % BD.

Also avail as gel form-HS

ADVANTAGES-

1. No mydriasis / miosis
2. Does not alter accommodation
3. No burning
4. No allergy
5. Only twice a day administrn d/t long DOA

IND-

1.POAG

2.Sec glauc

3.aphakic & pseudo glauc

4.Dev glauc

C/I-

1. B asthma
2. heart block
3. COPD
4. CCF
5. sinus bradycardia
6. diab

SIDE-EFFECTS-

OCULAR-

1.Cor punctuate epith erosion

2.Damage to mucus layer of tear film

3.blepharitis

4.diplopia

5.ptosis

6. reduced cor sensation

SYSTEMIC-

1.bradycardia [C/I-ccf]

2.Hypotension

3.Bronchospasm [C/I-B.asthma]

- Can be given in HT patients

-Can be given even if pt is on sys b blocker

                                     2]     BETAXOLOL—[SN]

Beta-blockers→ Cardioselective→potent only on B1

                     →Non-cardioselective→B1 + B2

Betaxolol-Only cardioselective b. blocker

• Neuroprotective-Increases perfusion press→increases ret bld flow→preserves visual field.DOC in NTG
• Does not cause airflow obstrn→DOC in asthma & COPD
• DOSE- 0.5 % BD
• Onset –within 30 min
• Pek- 2 hrs
• S/E- Stinging & Burning

       -insomnia

        -psychosis

• MOA-Blocks B1-receptors which act on ciliary epith & increase aq prodn

B.ALPHA -2 AGONISTS-1. Brimonidine

                                     -2. Apraclonidine

                     1]  BRIMONIDINE- -0-2%--SN

• Alphagan
• Α-2 selectives

MOA-

• Increases uveoscleral outflow
• Decreases aq prodn
• Neuroprotective
• No significant vasoconstrictive effect

DOSE- 0.2 % BD

S/E-ocular-

1. Allergic conjunctivitis
2. ocular hyperaemia
3. Conj follicles
4. Corneal erosion
5. Stinging & burning
6. FB sensation

      Systemic-

1. Dry mouth
2. Palpitation
3. Drowsiness
4. Depression
5. Insomnia

• safe in asthma & HT
• Very useful in lowering IOP after ALT & fewer S/E than apraclonidine

                                       2]   APRACLONIDINE-  SN

MOA- * decrease aq prod

• increase aq outflow
• Decrease penetration of BBB→ less BP lowering effect

DOSE- 0.5 -1 % BD

IND-

1. 1 Hour before & after trabeculoplasty, iridotomy & capsulotomy
2. Acute ACG
3. PO rise in IOP foll phaco, ecce,& trab ( Reduces blding in cat Sx & PO rise in IOP

S/E-ocular-

1. Follicular conj
2. Allergic reac

    3. UL retraction

    4.conj blanching

   5. Mydriasis

   6. Subconj h’age

Systemic-

1. bradycardia

2. Vasovagal attack

3.Hypotension

4.Insomnia

5. Paraesthesia

6. Abdominal pain

C/I- 1. CV dis

       2. Preg /nursing mother

                          C. PROSTAGLANDIN ANALOGUES

1] LATANOPROST- [SN] ( Xalatan)

MOA-

• Prostaglandin F2α analogue
• Does not cause breakdown of BAB
• Latanoprost + PG receptors→ degradation of collagen in bet ciliary ms bundle
• Increases uveoscleral flow→reduces IOP
• During daytime, without drugs most of the aq flows out thru TM.At night US pathway plays a major role.So Latanoprost is given in evening.

DOSE-    0.005 %  OD [at night]

Onset-3 hrs

Peak-8 hrs

S/E-

1. conj hyperaemia
2. Eyelash lengthening
3. Hyperpigmentation-eyelash,iris & periorbital skin
4. Ant uveitis [iritis]
5. CME
6. hypotony
7. Herpes simplex keratitis
8. Punctate KP
9. Dry eye
10. Pseudodendritic KP
11. miosis

Systemic-

1. URI

2.,abnml LFT

3, hirsutism

4.bronchoconstriction

5. Increased coronary flow

    

CAUTION-

• Uveitic glaucoma
• CL wearers shud remove before instilling the drop & may reinsert it after 15 min
• Never use along with miotic
• Never use in pts at risk for CME

C/I- Childn & preg

IND-

• POAG
• OHT
• NTG

Stored at -2 to 8 deg cent when unopened.once opened can be stored at 25 deg C for 6weeks

                    CHOLINERGIC STIMULATERS

[DRUGS MIMICKING ACTION OF ACETYLCHOLINE]

CHOLINERGIC / PARASYMPATHETIC SYSTEM-

POSTGANGLIONIC NEURON

                        ↓

ACETYLCHOLINE

                  ↓

           MIOSIS

CHOLINESTERASE→ INHIBITS ACETYLCHOL

                                   PILOCARPINE- [SN]

*Parasympathomimetic [direct acting]

* Derived from the leaves of pilocarpus microphyllus

* peak -2-3 hrs

* lasts for 6-8 hrs

*MOA-

1.IN POAG-

  Contraction of ciliary ms→Increases aq outflow thru TM→     reduce IOP

2.In PACG-

  Contraction of sphincter pupillae→ miosis→pulls peripheral iris away from TM→ opens the angle

DOSE-1%, 2%, 3%, 4%  

IND-

1.POAG

2.Ac ACG

3.Preoper miosis for KP

4.Diff diag of dilated pupil→Neuroparalysis→mydriasis overcome

                                          →parasympathetic→poor response

S/E-

1. Accomodative spasm
2. Myopia
3. Constriction of field
4. Cor endo toxicity
5. Cor edema
6. atypical band KP
7. Cataract
8. Cicatrial pemphigoid
9. Giant papillary c’vitis
10. Follicular rea
11. Iris cyst
12. RD
13. Brow ache d/t CB contraction

SYSTEMIC S/E-

1. bradycardia
2. arrhythmia
3. Hypersalivation
4. Bronchospasm
5. pulm edema

C/I-

1. Ant uveitis
2. Rubeosis iridis
3. DEV glau
4. Angle occlusion by membrane / synechiae
5. NVG
6. Malignant glauc
7. Aphakia
8. Retinal breaks & RD
9. Concurrent use of Pg analogue

                HYPEROSMOTIC AGENTS

MOA-

• HA remain intravascular, thus increasing bld osmolality.
• They create an osmotic gradient bet bld & vitreous→water is drawn out of vitreous→IOP is lowered
• To be effective ,they must be unable to penetrate the BAB.They are of limited value in inflame glauc in which integrity of BAB is compromised

PREPARATIONS-

1. GLYCEROL-

DOSE- 1 gm/kg of 50 % sol

Peak- 1hour

Duration- 3 hrs

2.MANNITOL-

DOSE- 1 gm/kg of 20 % sol

Peak- 30 min

Duration- 6 hrs

S/E-

1. Cardiovascular overload [ great caution in cardiac/ renal dis]
2. Urinary retention
3. HT
4. Acidosis
5. hyperglycaemia

C/I- oliguria/ anuria

                 CARBONIC ANHYDRASE INHIBITOR

TOPICAL  CAI-

• Chemically related to sulphonamides
• Reduce aq sec→ lower IOP

                            DORZOLAMIDE  -2%

• MOA-

-inhibits CA→slow formn of bicarbonate ions→reduced sodium

& fld transport→decrease aq secn by ciliary processes

• 2 % tds

• IND-

1. OHT

2.POAG

     -S/E

   1 -Ocular burning & stinging

   2. Allergic c’vitis

   3. cor edema

    4  -endothelial dysfunctn

    5 -SPK

 6.   -Corneal epithelial defect

7.Hyperaemia

SYS S/E-

1.Aplastic anaemia

2. BM suppression

3. Renal calculi

*  BRINZOLAMIDE- 1 % tds

Abnml taste

Blurred vision

SYSTEMIC CAI-

ACETAZOLAMIDE TAB –

Neuroprotective

Dose- 250 mg Qid [5-10mg/kg]

Onset of action-1 hr

Peak- 4 hrs

Duration- 12 hrs

ACETAZOLAMIDE SUSTAINED RELEASE CAPSULES-

500mg 12 hourly

Duration- 24 hrs

S/E-

OCULAR-

1. Transient myopia
2. choroidal detachment

SYSTEMIC-

1. Paraesthesia
2. Malaise complex-Fatigue,depression,anorexia,wt loss, loss of libido
3. GI complex- Gastric irritation, cramps, diarrhea
4. Stevens Johnson syn
5. Bld dyscrasias
6. Renal stones

NEUROPROTECTIVE AGENTS-read from notes

1. Brimonidine
2. Memantine [N-methyl D-aspartate  antagonist]
3. Nitric oxide synthetase  [NOS] inhibitor
4. Calcium channel blockers
5. Neurotrophins
6. Endothelin receptor antagonist
7. .Betaxolol

                         LASERS IN GLAUCOMA- SPOT

ARGON LASER TRABECULOPLASTY-

• Application of discrete laser burns to TM→enhances aq outflow

IND-

• POAG
• Pseudoexfoliation glauc
• Pigmentary glauc

TECH-

• Apraclonidine 1% or Brimonidine 0.2 %
• Topical anaesth
• Goniolens inserted with mirror at 12 o’ clock to visualize the inferior angle
• Scleral spur, Schwalbe’s line & TM identified.
• Aiming beam focused at juncn of pigmented & non-pigmented TM
• Spot shud be round with a clear edge & not oval with blurred edge which means that the beam is not perpendicular
• Spot- 50 µm
• Duration- 0.1 s
• Power- 700 mW
• Ideal rea- transient blanching or minute gas bubble
• 25 burns over 90 deg.Goniolens rotated by 90 deg & another 25 burns applied making 50 burns over 180 deg
• Apraclonidine / brimonidine instilled

FOLL UP-After 6 wks, if IOP falls, gradually withdraw the drugs.

              -If IOP remains high,& only 180 deg has been t/ted ,then treat remaining 180 deg.

               -Foll 360 deg ALT retreatment is unlikely to benefit- consider Filtration surg

MOA-

ALT→ Shrinkage of TM→ opening up of aq channels

COMPLICATIONS-

1. PAS-if burns are applied too post or energy level is too high
2. H’ages-if BVs on peripheral iris / CB are inadvertently t/ted
3. Ac elev of IOP
4. Ant uveitis
5. Encapsulated blebs

    DIODE LASER TRABECULOPLASTY

• Less disruption of BAB
• Spot- 100µm
• Power800-1200mW
• Duration-0.1-0.2 sec
• Bubble form does not occur

                  Nd: YAG LASER IRIDOTOMY

IND-

1. PACG
2. Fellow eye in acute glauc
3. Narrow occludable angles
4. Sec angle closure with papillary blocks
5. Combined mech glauc

TECH-

• Apraclonidine 1% /Brimonidine 0.2%
• Pupil shud be miosed
• Topical anaesth
• Abraham iridotomy lens [has a +66D power peripheral button]
• Site- superior iris is selected, so that it is covered by the lid,to prevent diplopia.I’tomy Shud be as peripheral as possible to avoid damage to the crystalline lens
• Beam shud be non-perpendicular & aimed towards peripheral ret to avoid macular burn
• 3 BURSTS OF 3-6 mJ
• Successful penetration-Gush of pigment debris
• Apraclonidine / brim
• Topical steroid for 1 wk
• Ideal I’tomy size-150-200µm
• Incomplete t/t results in a thick cloud of dispersed iris pigment which impairs visualization.It is best to wait for the cloud to disperse & re-treat the same site or increase the energy level & try a diff site

COMPLICATIONS-

1. Bleeding
2. Iritis
3. cor burns
4. Glare & diplopia

SELECTIVE LASER TRABECULOPLASTY

• Nd:YAG double frequency
• Selectively targets only the pigment cells without any damage to the surrounding struc
• In contrast Argon Trab results in thermal coagn of angle str
• Spot-400µm
• Energy-0.8mJ
• Ideal reaction-blanching without bubble
• No of shots-25-50 over 180 deg

                    LASER SCLEROSTOMY

Laser energy delivered either internally [ab interno] or externally [ab externo] to produce a direct opening into the AC thru the limbal tiss to achieve filtration.

→ NON-CONTACT [Gonioscope]

→CONTACT  [probe]

→ AB-INTERNO [ Nd:YAG LASER]

→AB-EXTERNO [HOLMIUM]

                              { THULIUM-HOLMIUM-CHROMIUM:YAG}

Nd: YAG  AB-INTERNO  SCLEROSTOMY-

• Suitable for eyes with inferonasal blebs with excessive conj scarring
• Shud be avoided in chr blepharitis
• ADV-No conj dissection reqd
• DISADV- Only for aphakic /pseudophakic eye d/t risk of intraocular probe damaging the lens
• Laser setting- 3-5 pulses of 200mJ, 0.2 s

HOLMIUM AB-EXTERNO SCLEROSTOMY-

• suitable for eyes with heavy conj scarring
• Ideal site- prior surgical iridectomy to reduce the risk of PO iris incarceration
• ADV-No IO instrumentn

          -safe in aphakic eyes

Laser -5 pulses/ sec

COMPLICATIONS

1. Iris incarceration
2. cor edema
3. conj burn
4. conj buttonholing
5. hyphaema
6. DM detachment
7. cyclodialysis cleft
8. VH

                 TRABECULECTOMY-case-failed filtration,instrs

DEF-

Surgical process that lowers IOP by creating a fistula which allows aq outflow from AC to subtenon’s space.

IND-

1. Glauc ONH cupping
2. Glauc visual field progression
3. Intolerable S/e from med t/t
4. Procedure of choice-Uncontrollable POAG &PACG

                                  -Pseudoexfoliation sy

                                  -pigmentary glau

                                  - Pseudophakic glauc

STEPS-

• Conj flap [fornix /limbal based ]
• 3×4mm superficial scleral flap
• Superficial scleral flap dissected forwards until clear cor is visible
• Paracentesis
• AC entered along entire width of scleral flap.
• Deep scleral flap [1.5×2mm] excised with a knife or punch
• Peripheral iridectomy to prevent blockage of internal opening by peripheral iris
• Sup scleral flap sutured .[ Releasable sutures may be used to reduce the risk of PO scleral flap leakage & shallow AC]
• BSS injected thru paracentesis to test patency of the fistula & detect any holes / leak in the flap
• Conj flap sutured
• Atropine e/d 1 %
• G+W
• P&B

COMPLICATIONS-

1.SHALLOW AC

d/t-Pupillary block

   -overfiltration

  -malignant glauc

2. PUPILLARY BLOCK

D/t non-patent PI

Signs- rise in IOP

       -Flat bleb

       -Seidel’s test-ve

       -iris bombe

T/T- Argon laser to iridectomy site /new I’tomy

3.OVERFILTRATION-

D/t –scleral flap leak

     -Buttonholing→ Bleb leakage→flat bleb

T/T-Topical atropine

     -Aq suppressants

     -Cyanoacrylate glue

     -Soft bandage CL

     -AC reformed

     -Scleral & conj flap resutured

4.MALIGNANT GLAUCOMA-

D/T- Blockage of aq at pars plicata→ Aq forced back into vit

T/T-

• Topical mydriatics
• IV mannitol
• Aq suppressants
• Ant hyaloidectomy –Nd:YAG
• PPV

5. FAILURE OF FILTRATION-

CAUSES-

• Subconj & episcleral fibrosis
• Bleb encapsulation
• Overtight suturing
• Scarring of scleral bed
• Blockage of sclerostomy

     T/T-

• Ocular compression to force aq outflow
• Sutures released-releasable suture / argon laser suture lysis
• Needling an encapsulated cyst
• S/C 5FU 0.1ml of 50 mg/ml
• Nd:YAG laser –reopening of blocked ostium
• Repeat TRAB + antimetabolite

6.BLEB LEAKAGE-

D/T-Dissolution of conj by MMC

Signs-Low IOP

        -avascular bleb

T/T-

• Conj advancement to hood the bleb
• Conj autografts
• Scleral grafts

7.LATE ONSET BACTERIAL INFECTION

*  Seen in thin walled cystic bleb with H/O antimetab

*  Red & sticky eye

*  Blurring of vision

8.BLEBITIS-

*   Inf does not inv vitreous

*   White milky bleb surrounded by conj inj

*   T/T-Topical fluoroquinolones

9.BLEB ASSTD ENDOPHTHALMITIS-

*  White milky bleb

*   Sev ant uveitis + hypopyon

*   vitritis

*   Impaired red reflex

*   T/T-IV antibiotics

NON-PENETRATING GLAUCOMA SURG

IND-

1. POAG
2. Glaucoma with high myopia
3. Pigmentary glaucoma
4. Pseudoexf glauc
5. Aphakic & pseudophakic Glauc
6. Congenital & juvenile glauc
7. Sturge weber syn
8. Aniridia & ant seg dysgenesis syn
9. Glauc sec to uveitis

CONTRAINDICATIONS-

RELATIVE-

1. Narrow angle glauc
2. Post laser trabeculoplasty
3. Angle recession glauc

ABSOLUTE- NVG

COMPLICATIONS-

INTRAOPERATIVE-

1. Choroidal herniation during dissection of scleral flap
2. Trabeculodescemetic membrane perforation

POSTOPERATIVE-

1. Mod hypotony → transient CME
2. High IOP on 1st PO day [d/t insufficient dissection of TDM]
3. Rupture of TDM→ iris prolapse → Blockage of filtration site→Rise in IOP
4. PAS
5. DM detachment

DEEP SCLERECTOMY-

• 7mm Fornix / limbus based conj flap
• Superficial scleral flap 5×5mm, 40-50% depth dissected into clear cor
• Deep scleral flap 3×3mm, 90 % depth dissected
• Schlemm’s canal unroofed.Deep scleral flap excised at its base, ant to Schwalbe’s line to create a deep sclerectomy space
• Superficial scleral flap is resutured,thus creating a “scleral “ lake
• A collagen implant is often used to keep this lake patent.

VISCOCANALOSTOMY-

• Fornix based conj flap dissected
• Superficial partial thickness scleral flap dissected
• Deep scleral flap dissected to gain access to Schlemm’s canal
• High-viscosity viscoelastic subst is injected into Schlemm’s canal.
• A descemet’s window is created by dissecting the deep scleral flap ant to the schlemm’s canal & then excising it
• Superficial scleral flap is sutured
• Viscoelastic is injected into the area of sclerotomy
• Conj is closed.

ADVANTAGES OF NPGS-

1. Gradual lowering of IOP
2. Flat AC-less chance
3. Bleb-less
4. Inf / endophthalmitis- less
5. Less cataractogenic
6. H/P of TM can be studied

               ANTIMETABOLITES-spot

                             5-FLUOROURACIL

*   Inhibits DNA synthesis

*   Active on S-phase [synthesis phase] of cell cycle

*   Inhibits fibroblastic proliferation

*   No effect on fibroblast attachment & migration

IND-

1. Prim glauc filtering surg
2. Prev failed filtering surg
3. Aphakic & pseudophakic glauc
4. NVG
5. Uveitic glauc

C/I-

1. Active corneal dis
2. Recent penetrating KP
3. Hypersensitivity to the drug
4. Multiple filtering surg with sev scarring of conj

TECH-

• Conj is dissected
• Cellulose sponge [4.5×4.5mm] soaked in 50mg/ml of 5 FU
• Placed under the dissected flap of tenon’s capsule at the filtration site.Make sure that the edges of conj flap are not exposed to the drug.
• Remove the sponge after 5min
• Irrigate the conj & episclera with BSS
• Complete the trab

COMPLICATIONS-

1. Corneal-

• Cor  epith def
• Punctate keratopathy
• Dellen
• Filamentary keratitis

2. Conj wound leaks
3. Bleb related endophthalmitis
4. Hypotony related maculopathy [ much less in 5 FU]
5. Suprachoroidal detachment
6. Malignant glauc
7. RD
8. cataract

                            MITOMYCIN C

• Alkylating agent
• Inhibits-DNA replication

             -mitosis

             -Protein synthesis

             -Fibroblast proliferation

             -Vascular growth

Much more potent than 5-FU

DOSE-0.2-0.5mg/ml

TECH- same

IND-

1. Prim filtering surg
2. Prev failed filtering surg
3. NVG
4. Uveitic Glauc
5. Pre-existing cor dis  in which 5 FU is C/I-

Aphakic/pseudophakic bullous KP

Keratoconjunctivitis

Penetrating KP

6.Combined procedure

COMPLICATIONS-

1. Corneal toxicity [less than 5FU]
2. Conj wound leak
3. MMC in contact with free conj margin→retards flap healing
4. Scleral necrosis
5. Hypotony related maculopathy [MMC> 5FU]
6. Choroidal effusion
7. Cataract [MMC > 5FU]
8. Bleb related endo

            DRAINAGE IMPLANTS

DEF-

Plastic devices which create a communication bet AC & subtenon’s space.

Consists of → open tube-placed 2-3mm inside the AC

                  →explant / plate-Beneath the tenon’s capsule,10-12mm post to limbus

MATERIALS-

Plate- PMMA/polypropylene /silicone rubber

Tube-silicone rubber

ADV- Being biologically inert ,fibroblasts do not adhere to them→permanent conduit

IMPLANT FUNCTIONING-

• IOP reduction is d/t passive press dependant flow of aq across the capsular wall.
• Magnitude of press reduction depends upon-

1. Resistance to aq outflow-

Thicker the capsule→ higher the IOP

2. Total surface area of encapsulation-

Larger the surface→lower the IOP

IND- VIVA

1. Prev failed filtration surg
2. NVG
3. Silicone oil glauc
4. Aphakic /pseudophakic glauc
5. Complicated glauc-aniridia,ICE sy,uveitis
6. Traumatized eye with conj scarring
7. Dry eye

TYPES-

1.NON-VALVED- * Molteno

                               *Baerveldt

                               *schocket

2.VALVED-* Ahmed

                    * Krupin

                    *Joseph

                    *optimed

                    *white

COMPLICATIONS- Most imp → excessive drainage leading to HYPOTONY

EARLY-

1 Hypotony / choroidal detachment

2 Hyphaema

3 Cor endo touch

4 Rise in IOP

LATE-

1. Rise in IOP
2. Endo touch
3. Tube exposure / migration / extrusion
4. Cataract
5. Endophthalmitis
6. RD
7. Motility disturbance-diplopia
8. Epith downgrowth