EVALUATION OF A GLAUCOMA PATIENT

Presented byDr. (Maj.) Rashed

F.C.P.S Part-II TraineeCMH Dhaka

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

ClassificationCongenital & AcquiredPrimary & Secondary Open angle & Angle-closure

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.

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

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

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

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

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 **

Iris◦Heterochromia, iris atrophy,

transillumination defects, ectropion uveae. corectopia, nevi, nodules, exfoliative material & NVI

◦Trauma Lens

◦Size, shape, clarity & stability of the lensFundus

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

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

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

Gonioscopy

CLASSIFICATION

INDIRECT GONIOSCOPYNon-Indentation Indentatioin

DIRECT GONIOSCOPY

GonioscopyAngle Blood vesslesPASPigmentation Sign of trauma

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

 

Shaffer system

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.

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

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

I>S>N>T I<S<N>T

The visual field An island hill of vision in a sea of darkness

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

Glaucomatous visual field defects

Generalized depressionParacentral scotomaArcuate scotomaNasal stepAltitudinal defectTemporal wedge

Paracentral scotoma

Arcuate scotoma

Nasal step

Gross cupping with ring scotoma Tubular field

Progression of glaucomatous damage

OCT

Normal Glaucoma patient

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

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)

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

Open angle glaucoma mechanism:

Post trabecular: • Obstruction of Schlemm’s canal• Elevated intra ocular pressure

(e.g. sturge weber syndromethyroid ophthalmopathyretrobulbar tumours)

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)

Developmental anomaliesCongenital glaucomaAniridia Axenfeld - Rieger syndrome

In-direct gonioscopy

Non-Indentation◦ Goldmann three

mirrors Indentatioin

◦ Zeiss◦ Posner◦ Sussman

Direct gonioscopyDiagnostic – KoeppeSurgical –

Medical workshop

Barken Swan- Jacob