Evaluation of a glaucoma patient
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EVALUATION OF A GLAUCOMA PATIENT
Presented byDr. (Maj.) Rashed
F.C.P.S Part-II TraineeCMH Dhaka
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IntroductionGlaucoma refers to a group of diseases
having common characteristic of progressive optic neuropathy with associated visual field loss as progresses in which elevated intraocular pressure (IOP) is one of the key modifieable factors.
Normal IOP: 10-22 mmHg.Three risk factor determine the IOP:
◦ rate of aqueous humor production by ciliary body◦ resistance to aqueous outflow across the trabecular
meshwork-Schlemm’s canal system◦ The level of epischeral venous pressure
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ClassificationCongenital & AcquiredPrimary & Secondary Open angle & Angle-closure
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Clinical EvaluationAppropriate management of glaucoma
depends on the clinician's ability to diagnose the
◦specific form of glaucoma in a given patient,
◦severity of the condition,◦progression in that patient's disease
status.
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History Patient's current complaint History of present illness Past ocular, medical, and surgical
history Refraction history Past medications history Social history History of alcohol and tobacco use Occupation Family history
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Clinical examination and investigations
• BCVA distant & near• Pupillary reaction, relative afferent
pupillary defect• Slit lamp examination of lids, lid
margins, conjunctiva, cornea, anterior chamber & lens• IOP and time of measurement• CCT• Gonioscopy• Detailed examination of:
- Lens- Biomicroscopy of ONH and RNFL - Fundus
• Automated perimetry• OCT of ONH & RNFL
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Clinical examination
External Adnexa◦ Variety of conditions associated
with secondary glaucomas Neurofibromatosis type- I Oculodermal melanoeytosis (nevus of
Ota) Axenfeld-Rieger syndrome Orbital varices Thyroid associated orbitopathy
◦ External ocular manifestations of glaucoma therapy. Prostaglandin analogue
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Slit lamp biomicroscopy
Conjunctiva◦ Acute IOP ◦ Chronic IOP ◦ Long term use of
sympathomimetics and prostaglandin analogoues
◦ Long term use of epinephrine derivatives
◦ Filtering bleb +/-Episclera & Sclera
◦ Dilation of the episcleral vessels ◦ Sentinal vessels
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Cornea◦Developmental glaucoma◦Acute IOP◦Medication toxicity◦Corneal endothelial abnormality◦Scar ◦CCT
A/C◦Uniformity of depth of the anterior chamber◦Width of the chamber angle
** Before dilation of pupil; pupillary light reaction, iris & A/C should be examined **
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Iris◦Heterochromia, iris atrophy,
transillumination defects, ectropion uveae. corectopia, nevi, nodules, exfoliative material & NVI
◦Trauma Lens
◦Size, shape, clarity & stability of the lensFundus
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IOP Schiotz tonometry: indentation
procedure, now obsolete. Goldmann applanation tonometer :
most appropriate Noncontact tonometer (NCT): screening
purpose Tonopen: very small area, useful in corneal
scar or edema Digital pressure
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Possible source of error in TonometrySqueezing of the eyelidsBreath holding or Valsalva maneuverPressure on the globeExtra-ocular muscle force applied to a
restricted globeTight collar or tight necktieObesity or straining to sit on slit lampAn inaccurately calibrated tonometerExcessive or inadequate amount of
fluoresceinHigh corneal astigmatismCorneal thickness greater or less than
normalCorneal scarring or band keratopathyPhysician’s errors
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Dynamic contour tonometryThe tip of the device exactly matches the contour
of the cornea, the pressure measured by a transducer placed on its tip.
Measure true IOP irrespective of CCTCapable of measuring the ocular pulse amplitude
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Gonioscopy
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CLASSIFICATION
INDIRECT GONIOSCOPYNon-Indentation Indentatioin
DIRECT GONIOSCOPY
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GonioscopyAngle Blood vesslesPASPigmentation Sign of trauma
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VAN HERICK METHOD
Peripheral Chamber
DepthIn Corneal Thickness
Angle Grade Comment
≥ Cornea 4 Wide open1/4 to 1/2 3 Incapable of closure
1/4 2 Should be gonioscoped
<1/4 1 Dangerously narrowed angle
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Shaffer system
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Optic Disc Evaluation ..Slit lamp biomicroscopy : Ideal
◦Stereoscopic View –Cupping◦Measuring the optic disc size
Direct Ophthalmoscopy◦ Good Magnification
Indirect Ophthalmoscopy◦Overall View
Optic disc Photoghraphy.◦Documentation,Monitoring for
progression.
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The 7 parameters to look for…1)Disc size2)Neuroretinal Rim (NRR):
- ISNT rule 3)Cup: Disc ratio
- Vertical C/ D Ratio.4) Optic Disc Hemorrhage5) Nerve Fiber Layer Defect:
- focal & diffuse6) Para Papillary Atrophy:
- Size, location & Configuration7) Retinal Arterial Attenuation:
- focal & diffuse
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Ophthalmoscopic sign of glaucoma
Generalized Focal Less specifico Large optic cup o Asymetrical of
the cupo Progressive
enlargement of cup
o Notching of the rim
o Vertical elongation of the cup
o Region palloro Splinter
hemorrhageo Nerve fiber layer
loss
o Exposed lamina cribrosa
o Nasal displacement of the vessels
o Baring of circumlinear vessels
o Peripapillary crescent
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I>S>N>T I<S<N>T
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The visual field An island hill of vision in a sea of darkness
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Perimentry Kinetic
◦ Two dimensional ◦ Moving stimulus ◦ Known Luminance ◦ From non-seeing
area to seeing area until it is perceived.
◦ e.g. confrontation Tangent screen Lister perimeter Goldmann perimeter
Static◦ Three
dimensional ◦ Static stimulus ◦ varying
luminance in the same position
◦ e.g. Octopus Humphrey Hensen
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Glaucomatous visual field defects
Generalized depressionParacentral scotomaArcuate scotomaNasal stepAltitudinal defectTemporal wedge
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Paracentral scotoma
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Arcuate scotoma
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Nasal step
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Gross cupping with ring scotoma Tubular field
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Progression of glaucomatous damage
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OCT
Normal Glaucoma patient
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Classification based on mechanism of outflow obstruction
Open angle glaucoma mechanisms:
• Pretrabecular• Trabecular• Post trabecular Angle-closure glaucoma
mechanisms : • Anterior (pulling) mechanism• Postertior (pushing) mechanism Developmental anomalies
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Open angle glaucoma mechanism:
Pretrabecular: • fibrovascular membrane (e.g. neovascular membrane)• Endothelial layer (e.g. iridocorneal endothelial syndrome)• epithelial downgrowth• fibrous ingrowth• inflammatory (e.g. fuch’s iridocyclitis)
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Open angle glaucoma mechanism:
Trabecular: • Idiopathic (e.g. chronic & juvenile open
angle)• ‘Clogging’ of trabecular meshwork
(e.g. pigmentary, red cell, ghost cell glaucoma)
• Alteration of trabecular meshwork (e.g. steroid induced glaucoma)• Trauma (e.g. angle recession)• Intra ocular foreign bodies
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Open angle glaucoma mechanism:
Post trabecular: • Obstruction of Schlemm’s canal• Elevated intra ocular pressure
(e.g. sturge weber syndromethyroid ophthalmopathyretrobulbar tumours)
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Angle closure glaucoma mechanism:
Anterior (pulling) mechanism• Contracture of membrane (e.g. neovascular glaucoma)Postertior (pushing) mechanism• With pupillary block• Without pupillary block (e.g. malignant glaucoma)
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Developmental anomaliesCongenital glaucomaAniridia Axenfeld - Rieger syndrome
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In-direct gonioscopy
Non-Indentation◦ Goldmann three
mirrors Indentatioin
◦ Zeiss◦ Posner◦ Sussman
Direct gonioscopyDiagnostic – KoeppeSurgical –
Medical workshop
Barken Swan- Jacob