CALIBRATION OF TONOMETER
Checking the calibration of a tonometer
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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.
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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.
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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.
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The animation shows a tonometer with an accurate calibration for 20 mmHg.
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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
Indentation
Applanation
Non-contact
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
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
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-
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-
Allignment system-
Optically aligns the patient’s cor in axial,vertical & lateral dimension
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 ]-
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
LAYDEN LENS-For premature infants
6.THORPE LENS-surgical & diagnostic lens for OT
ADVANTAGES-
Height of observer can be changed to look deeper into a narrow angle.
Less distortion of AC .
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
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-
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-
POLAR NOTCHING-Focal atrophy of the NRR begins at the inferotemporal quad leading to vertical enlargement of the cup.
SHARPENED POLAR NASAL EDGE-Focal defect enlarges & deepens & dev a sharp nasal margin adjacent to a major retinal V
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.
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-
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-
PREDISPOSING FACTORS-
PATHOGENESIS-
Mech of angle closure-
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
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.
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PACG
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PLATEAU IRIS SYN
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Mech of glauc
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Pupillary block
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Ant pos of peripheral iris→ TM block
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Age
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Old
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Young
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AC
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Shallow
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Deep centrally
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T/T
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Laser iridotomy
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Does not respond to iridotomy.Needs laser peripheral iridoplasty o
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-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
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-
Rise in IOP + creeping angle closure [synechial angle closure occurs within the depth of the angle i.e iridotrabecular synechiae & inv entire angle]
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
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-
CORNEA-
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-
MEDICAL-
OR –Brimonidine 0.2 % e/d BD
OR Travoprost 0.004 % e/d
OR Bimatoprost 0.003 % 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-
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-
CORNEA-Krukenberg spindle
AC-very deep
IRIS-
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
Ischaemic CRVO-Glaucoma dev 3mo after the occlusion-‘100 DAY GLAUCOMA’
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-
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-
Inflammatory glauc-
-AC cells & flare
-Dilated nml iris BVs
-open angle
-no nv
Prim acute angle closure glauc
Post sx dilatation of iris Vs
Fuch’s heterochromic iridocyclitis
essential iris atrophy
PXF
ROP
VIVA- Q.which drugs shud be avoided in uveitic glauc?
Prostaglandin analogue-enhance breakdown of BAB
-exacerbate CME
2. Pilocarpine-promotes post synechiae
POSNER SCHLOSSMAN SYND
OR HYPERTENSIVE IRIDOCYCLITIS
OR GLAUCOMATOCYCLITIC CRISIS
DEF-
EPID-
Young adults
M > F
HLA-Bw54
Recurrent attacks
PATHOGENESIS- Acute trabeculitis
C/F
-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
Secondary angle closure→ PHACOMORPHIC GLAUCOMA
→PHACOTOPIC GLAUCOMA
2. Secondary open angle → PHACOLYTIC GLAUCOMA
PHACOMORPHIC GLAUCOMA
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
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-
Removal of lens material
Anti-inflammatory therapy
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
Causes of hyphaema-
Trauma
Oper & PO
DM
Herpetic ant uveitis
Bld dyscrasias
Iris Nv
HT
IO tumours
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-
Small br of major arterial circle d/t tear in bet longitudinal & circular fib of CB
Capillaries of minor arterial circle wen there is a sphincteric tear
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-
Progressive iris atrophy
Iris naevus [Cogan Reese] syn
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-
COGAN REESE SYN-
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-
Cataract surg in the context of pre-existing VH
VH in an already aphakic / pseudophakic eye
Cataract surg complicated by VH & hyphaema
C/F-
T/T-
1.Med t/t
2.Irrigation of AC & washing out of ghost cells
3.PPV
BUPHTHALMOS
PATHOGENESIS-
Trabeculodysgenesis-Absence of angle recess with iris inserted directly into the surf of TM in one of the 2 configurations-
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-
True congenital glaucoma-Intrauterine life
Infantile glaucoma-prior to 3rd b’day
Juvenile glaucoma- 3-16 years
CAUSES-
Axenfeld’s anomaly
Reiger’s syn
Peter’s anomaly
Aniridia
Sturge weber syn
Neurofibromatosis
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-
Axial myopia
Lens subluxation
corneal decompensation
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
IOP –Perkin’s tono or tonopen
-nml IOP in an infant is 9-10mmHg. > than 20 is suspicious
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-
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-
-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-
AN-1- AD
-NO systemic implications
AN-2- [Miller syn]
-Will’s tum
AN-3-[Gillespie syn]
-AR
-Mental retard
-cerebellar ataxia
C/F-
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-
Cholinergic agonists- Pilocarpine
-Echothiophate iodide
-Carbachol
2. Prostaglandin derive- Latanoprost
3. alpha 2 agonists- Brimonidine
4.Adrenergic agonists-Epinephrine
DECREASE AQUEOUS HUMOUR PRODUCTION-
B- blockers
CAIs
Adrenergic agonists
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-
No mydriasis / miosis
Does not alter accommodation
No burning
No allergy
Only twice a day administrn d/t long DOA
IND-
1.POAG
2.Sec glauc
3.aphakic & pseudo glauc
4.Dev glauc
C/I-
B asthma
heart block
COPD
CCF
sinus bradycardia
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
-insomnia
-psychosis
B.ALPHA -2 AGONISTS-1. Brimonidine
-2. Apraclonidine
1] BRIMONIDINE- -0-2%--SN
MOA-
DOSE- 0.2 % BD
S/E-ocular-
Allergic conjunctivitis
ocular hyperaemia
Conj follicles
Corneal erosion
Stinging & burning
FB sensation
Systemic-
Dry mouth
Palpitation
Drowsiness
Depression
Insomnia
2] APRACLONIDINE- SN
MOA- * decrease aq prod
DOSE- 0.5 -1 % BD
IND-
1 Hour before & after trabeculoplasty, iridotomy & capsulotomy
Acute ACG
PO rise in IOP foll phaco, ecce,& trab ( Reduces blding in cat Sx & PO rise in IOP
S/E-ocular-
Follicular conj
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-
conj hyperaemia
Eyelash lengthening
Hyperpigmentation-eyelash,iris & periorbital skin
Ant uveitis [iritis]
CME
hypotony
Herpes simplex keratitis
Punctate KP
Dry eye
Pseudodendritic KP
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-
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-
Accomodative spasm
Myopia
Constriction of field
Cor endo toxicity
Cor edema
atypical band KP
Cataract
Cicatrial pemphigoid
Giant papillary c’vitis
Follicular rea
Iris cyst
RD
Brow ache d/t CB contraction
SYSTEMIC S/E-
bradycardia
arrhythmia
Hypersalivation
Bronchospasm
pulm edema
C/I-
Ant uveitis
Rubeosis iridis
DEV glau
Angle occlusion by membrane / synechiae
NVG
Malignant glauc
Aphakia
Retinal breaks & RD
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-
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-
Cardiovascular overload [ great caution in cardiac/ renal dis]
Urinary retention
HT
Acidosis
hyperglycaemia
C/I- oliguria/ anuria
CARBONIC ANHYDRASE INHIBITOR
TOPICAL CAI-
DORZOLAMIDE -2%
-inhibits CA→slow formn of bicarbonate ions→reduced sodium
& fld transport→decrease aq secn by ciliary processes
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-
Transient myopia
choroidal detachment
SYSTEMIC-
Paraesthesia
Malaise complex-Fatigue,depression,anorexia,wt loss, loss of libido
GI complex- Gastric irritation, cramps, diarrhea
Stevens Johnson syn
Bld dyscrasias
Renal stones
NEUROPROTECTIVE AGENTS-read from notes
Brimonidine
Memantine [N-methyl D-aspartate antagonist]
Nitric oxide synthetase [NOS] inhibitor
Calcium channel blockers
Neurotrophins
Endothelin receptor antagonist
.Betaxolol
LASERS IN GLAUCOMA- SPOT
ARGON LASER TRABECULOPLASTY-
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-
PAS-if burns are applied too post or energy level is too high
H’ages-if BVs on peripheral iris / CB are inadvertently t/ted
Ac elev of IOP
Ant uveitis
Encapsulated blebs
DIODE LASER TRABECULOPLASTY
Nd: YAG LASER IRIDOTOMY
IND-
PACG
Fellow eye in acute glauc
Narrow occludable angles
Sec angle closure with papillary blocks
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-
Bleeding
Iritis
cor burns
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-
-safe in aphakic eyes
Laser -5 pulses/ sec
COMPLICATIONS
Iris incarceration
cor edema
conj burn
conj buttonholing
hyphaema
DM detachment
cyclodialysis cleft
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-
Glauc ONH cupping
Glauc visual field progression
Intolerable S/e from med t/t
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-
FAILURE OF FILTRATION-
CAUSES-
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-
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-
POAG
Glaucoma with high myopia
Pigmentary glaucoma
Pseudoexf glauc
Aphakic & pseudophakic Glauc
Congenital & juvenile glauc
Sturge weber syn
Aniridia & ant seg dysgenesis syn
Glauc sec to uveitis
CONTRAINDICATIONS-
RELATIVE-
Narrow angle glauc
Post laser trabeculoplasty
Angle recession glauc
ABSOLUTE- NVG
COMPLICATIONS-
INTRAOPERATIVE-
Choroidal herniation during dissection of scleral flap
Trabeculodescemetic membrane perforation
POSTOPERATIVE-
Mod hypotony → transient CME
High IOP on 1st PO day [d/t insufficient dissection of TDM]
Rupture of TDM→ iris prolapse → Blockage of filtration site→Rise in IOP
PAS
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-
Gradual lowering of IOP
Flat AC-less chance
Bleb-less
Inf / endophthalmitis- less
Less cataractogenic
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-
Prim glauc filtering surg
Prev failed filtering surg
Aphakic & pseudophakic glauc
NVG
Uveitic glauc
C/I-
Active corneal dis
Recent penetrating KP
Hypersensitivity to the drug
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-
Corneal-
Cor epith def
Punctate keratopathy
Dellen
Filamentary keratitis
Conj wound leaks
Bleb related endophthalmitis
Hypotony related maculopathy [ much less in 5 FU]
Suprachoroidal detachment
Malignant glauc
RD
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-
Prim filtering surg
Prev failed filtering surg
NVG
Uveitic Glauc
Pre-existing cor dis in which 5 FU is C/I-
Aphakic/pseudophakic bullous KP
Keratoconjunctivitis
Penetrating KP
6.Combined procedure
COMPLICATIONS-
Corneal toxicity [less than 5FU]
Conj wound leak
MMC in contact with free conj margin→retards flap healing
Scleral necrosis
Hypotony related maculopathy [MMC> 5FU]
Choroidal effusion
Cataract [MMC > 5FU]
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-
Resistance to aq outflow-
Thicker the capsule→ higher the IOP
Total surface area of encapsulation-
Larger the surface→lower the IOP
IND- VIVA
Prev failed filtration surg
NVG
Silicone oil glauc
Aphakic /pseudophakic glauc
Complicated glauc-aniridia,ICE sy,uveitis
Traumatized eye with conj scarring
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-
Rise in IOP
Endo touch
Tube exposure / migration / extrusion
Cataract
Endophthalmitis
RD
Motility disturbance-diplopia
Epith downgrowth
