glaucoma review by dr. allen

Glaucoma Review

Fritz Allen, MD Visionary Ophthalmology

April 22th 2012

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Overview of Content• Diagnostic Tests• Open-Angle Glaucomas• Angle-Closure Glaucomas• Medical Management of

Glaucoma

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Diagnostic Tests• Gonioscopy• Examination of the Optic Nerve• Standard Automated Static

Perimetry• Corneal Pachymetry

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Gonioscopy• Indications

– Overcomes problem of total internal reflectivity to see angle structures

– Indirect gonioscopy (e.g., Goldmann or four mirror lens)

• Essential diagnostic tool in glaucoma (viewing the iridocorneal angle)

– Most common cause of incorrect diagnosis is omission of gonioscopy

– Omission causes overlooking secondary glaucomas and other glaucomas

– Periodically performed can detect secondary emergence of mixed mechanism

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Gonioscopy• Identification of angle recession, foreign

bodies, abnormal pigmentation, tumors, angle neovascularization, angle synechiae

• Glaucoma treatment in the angle – Laser trabeculoplasty– Goniosynechialysis– Treatment and evaluation of internal ostium

of trabeculectomy site– Gonioplasty/iridoplasty

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Gonioscopy• Contraindications

– Inability of patient to cooperate– Corneal abrasion or disease precluding

application of corneal lens• Pre-procedure evaluation• Indirect gonioscopy

– View angle with slit-lamp using a gonioscopic lens

• Technique– Indirect gonioscopy

• Produces inverted image 180 away from origination

• Two types of lenses are in common use

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Gonioscopy– Goldmann type

• Goldmann lens requires clear fluid to fill space between cornea and goniolens

• Lens is brought toward patient’s eye and tipped forward quickly enough to trap the clear fluid

– 4 mirror type• Rests solely on cornea / tear film• Requires only drop of anesthetic• Indentation gonioscopy can be performed • Technique to differentiate appositional and

synechial angle-closure

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Gonioscopy• Complications

– Corneal abrasion• Prevention: moist cornea, topical

anesthesia, minimize movement of lens on cornea

• Considerations in interpretation

– Normal angle landmarks (best viewed with parallelepiped method)

• Anterior to posterior: cornea, Schwalbe’s line, non-pigmented trabecular meshwork, pigmented trabecular meshwork, scleral spur, ciliary band, iris root

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Gonioscopy

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Examination of Optic Nerve

• Indications– To examine the optic nerve head for

clinical signs of glaucoma or other optic neuropathy

– To examine the macula and posterior pole

• Contraindications – No absolute contraindications– Difficult to use in cases of very small

pupils and dense media opacities– Poor patient cooperation

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• Pre-procedure evaluation– Evaluate pupil function– Evaluate anterior segment– Evaluate angle by gonioscopy if glaucoma

suspected– Dilate pupil

• Techniques– Handheld– Contact lens (center of a gonio lens)– Indirect ophthalmoscopy– Direct ophthalmoscopy– Hruby lens

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• Technique– Slit-lamp biomicroscope and indirect and

direct ophthalmoscopy – used to provide illumination and magnification, enabling a sense of contour of the optic nerve

– Binocular viewing is easier through a dilated pupil, but with experience one can see optic nerve through an undilated pupil though usually monoscopically

– A fixation target helps to stabilize and to manipulate the position of the eye

• Complications – Corneal abrasion (complication of contact

lens use)– Complications of dilation

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• Considerations in interpretation – Look for signs of glaucoma

• Generalized– Large optic cup– Asymmetry of the cups– Progressive enlargement of the cup

• Focal– Narrowing (notching) of the rim– Vertical elongation of the cup– Cupping to the rim margin– Regional pallor– Splinter hemorrhage– Nerve fiber layer loss

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© 2005 G.A. Cioffi, MD. Used by permission.

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Standard Automated Static Perimetry

• Indications– Diagnosis of disease

• Suspected diagnosis of glaucoma (suspicious disc, ocular hypertension)

• Neurologic vision loss• Subjective VF loss• Macular/retinal disease

– Monitoring of disease process• Interval follow-up of suspected or

established VF loss

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• Pre-procedure evaluation– Ensure patient can understand and

follow instructions– Assess for refractive error– Ensure there are no physical limitations

to performing test• Seat patient comfortably• Check head and eyelid position

• Alternatives– Goldmann perimetry– Confrontation visual fields– Amsler grid (to test central VF)

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• Considerations in interpretation – Assess patient reliability – Review threshold values, global

indices, total and pattern deviation plots

– Correlate test results with anatomy• Optic disc and retina appearance should

correspond to VF• Be aware of neurological defects

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– Rule-out artifactual field loss• Lens rim artifact• Incorrect refractive correction used for test

– Compare to prior tests• Establish good baseline

– Repeat testing takes into account learning effect

– Establishes presence of scotomas and fluctuation level of patient’s responses

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Automated Static Perimetry

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Corneal Pachymetry

• Indications– Measurement of central corneal thickness

(CCT)– Known diagnosis of glaucoma, including

normal-tension glaucoma– Glaucoma suspect and/or ocular

hypertension

• Considerations in interpretation – Thinner corneas underestimate IOP while

thicker corneas overestimate IOP

• Patient instructions– Explanation of how CCT could alter course

of glaucoma treatment

21Photo courtesy of Jeff Henderer, MD

Corneal Pachymetry

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Corneal pachymetry is important in the evaluation of which of the following

diseases?A. Anterior basement membrane

dystrophyB. Normal tension glaucomaC. Anterior uveitisD. Senile cataracts

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Open-Angle Glaucomas• Primary open-angle glaucoma• Primary open-angle glaucoma

suspect• Normal tension glaucoma• Secondary open-angle

glaucomas• Post-traumatic or angle

recession glauocma• Hyphema• Corticosteroid-induced

glaucoma

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Primary Open-Angle Glaucoma

• Etiology– Elevated IOP is acknowledged as the

principal etiologic risk factor

• Epidemiology– Significant public health problem

• Prevalence in African-Americans higher• Prevalence increases with age• Most frequent cause of blindness in

Hispanic and African-Americans

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• History– Age– Race– Symptoms

• Usually asymptomatic until late in disease

– Family history– Cardiovascular disease, diabetes– Refractive state– Medications– Rule out secondary causes (i.e.,

corticosteroids)– Previous eye injury and surgery

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Primary Open-Angle Glaucoma• Features

– Usually insidious onset– Slowly progressive visual loss without

symptoms– Painless– Usually bilateral, can be asymmetric– Central acuity unaffected until late in the

disease– Elevated IOP

• Can be intermittent (diurnal fluctuation)• Subset who never have high IOP (normal-

tension glaucoma)– Consider corneal pachymetry measurement

when assessing the accuracy of applanation tonometry

– Open angle by gonioscopy

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– Optic disc appearance• Asymmetry of the neuroretinal rim area or

cupping• Focal thinning or notching of the neuroretinal

rim• Optic disc hemorrhage• Any acquired change in the disc rim area or the

surrounding retinal nerve fiber layer• Large optic disc, large cup/disc ratio,

peripapillary atrophy

– Visual fields• Defects can precede visible optic nerve damage• VF defects may not be detectable by standard

perimetry

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Primary Open-Angle Glaucoma– Typical glaucoma defects

• Paracentral scotoma• Arcuate or Bjerrum scotoma• Nasal step• Altitudinal defect• Temporal wedge• Central island in far advanced cases

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Primary Open-Angle Glaucoma• Testing

– Visual fields• Automated static perimetry (most useful

for glaucoma diagnosis)

– Optic nerve photography or detailed drawing and description

• Stereo photography particularly useful

– Optic nerve head image analysis systems

– Central corneal thickness measurement

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• Risk factors– Strongest evidence

• Older age• Race (higher prevalence in African-Americans)• Elevated IOP• Positive family history

• Differential diagnosis– Disc abnormalities– Other glaucomas

• Secondary open-angle types• Angle-closure types • Normal tension glaucoma

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• Medical therapy – Beta-adrenergic antagonists– CAIs– Adrenergic agonists (sympathomimetics)– Prostaglandin analogues– Parasympathomimetic agents

• Surgical therapy– Laser trabeculoplasty– Trabeculectomy (with or without

antimetabolites)– Glaucoma drainage tube implants– Ciliary body ablation

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• Disease-related complications– Limitations due to VF loss– End stage glaucoma and blindness

• Patient instructions– Discussion of medications and surgical

treatments• Options, side effects, risk-benefit ratios• Instructions relating to compliance

– Appropriate drop timing– Nasolacrimal occlusion, passive lid closure– Prevention of washout effect by spacing drop

therapy– Discussion regarding quality of life issues

• Support groups, career issues, financial issues regarding treatment

– Importance of periodic follow-up

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Temporal pallor of the optic nerve

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Primary Open-Angle Glaucoma Suspect

• History– Previous history of elevated IOP– Family history of glaucoma– Age– Ethnicity of patient (e.g., African

descent)– Previous history of vision loss– Previous medication history

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• Features – Optic disc or nerve fiber layer

damage suggesting of glaucoma• Enlarged cup/disc ratio• Asymmetric cup/disc ratio• Notching or narrowing of the neural rim• Disc hemorrhage• Diffuse or local abnormality in the nerve

fiber layer– Visual fields suspicious for early

glaucomatous damage– IOP consistently above 21 mm Hg

(i.e., ocular hypertension)– Normal open angle on gonioscopy

with absence of secondary causes

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• Testing – Determination of central corneal

thickness – Evaluation of optic nerve head and

retinal nerve fiber layer– VF testing and analysis– Documentation of optic nerve head

appearance

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• Risk factors– Elevated IOP– History of glaucoma– Advancing age– Race and ethnicity (e.g., African

descent, Hispanics)– Associated disease states (systemic

hypertension, cardiovascular disease, diabetes mellitus)

– Vasospastic diseases (e.g. migraine, Raynauds)

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• Differential diagnosis– POAG (early)– Normal tension glaucoma (early)– Corticosteroid responder– Previous history of trauma (i.e., angle

recession glaucoma)– Previous or current uveitis– Nonglaucomatous causes (e.g.,

compressive lesions, ischemic episodes)

• Patient instructions– Need for periodic follow-up – Rationale for individualized therapy– Counseling / referral

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Primary Open-Angle Glaucoma Suspect - Case

Photos courtesy of Jeffrey Henderer, MD

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Primary Open-Angle Glaucoma Suspect - Case

Photos courtesy of Jeffrey Henderer, MD

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Normal Tension Glaucoma

• Definition– Characteristic features of POAG with

IOP in normal range without treatment; also known as low-tension glaucoma

• Features– No clear difference from optic nerve

cupping seen in POAG

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• Testing – Repetitive measurement of IOP– Automated VF– Gonioscopy– Stereoscopic optic disc evaluation– Measurement of corneal thickness

(pachymetry)

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Normal Tension Glaucoma• Differential diagnosis

– Undetected high-pressure glaucoma• POAG with large diurnal pressure

variation• Intermittent elevation of IOP caused by

another type of glaucoma• Previous episode of elevated IOP

– Decreased CCT– Nonglaucomatous optic nerve disease

resembling glaucoma• Congenital anomalies• Compressive lesions of the optic nerve

and chiasm• Arteritic ischemic optic neuropathy • Compromised ocular blood flow

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Secondary Open-Angle Glaucomas - Pseudoexfoliation

• Etiology– Systemic disorder with widespread

deposition of fibrillar material in many organs including the anterior segment of the eye

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• Features– Deposits of exfoliative material (XFM) on

anterior lens surface, pupillary margin, corneal endothelium, and zonules

– Transillumination defects at pupillary margin– Pigment deposition on iris surface,

endothelium– Patchy increased pigmentation of trabecular

meshwork– Poor pupillary dilation– Higher incidence of narrow angles– +/- IOP elevation– Zonular weakness, phacodonesis

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Secondary Open-Angle Glaucomas – Pigmentary

• Etiology– Concave peripheral iris configuration,

usually in myopic eye with deep AC• Posterior iris surface comes into contact

with lens zonule and with physiologic dilation/constriction of pupil, packets of pigment rubbed free from iris and become dispersed in aqueous

• Collection of pigment within angle/trabecular meshwork occurs during normal aqueous circulation and causes obstruction to outflow and chronic IOP elevation

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• Features– Classic triad of pigmentary glaucoma:

Krukenberg spindle, heavy 360 degree pigmentation of the trabecular meshwork, and mid-peripheral iris transillumination defects.

– Gonioscopy• Angle recess very wide, usually approx. 45

degrees• Heavy dark pigmentation of TM fairly well

distributed throughout entire circumference• May have pigmentation on or anterior to

Schwalbe’s line, heaviest inferiorly

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Krukenberg spindle

Photo courtesy of Jeffrey Henderer, MDPhoto courtesy of Eydie Miller, MD

Pigmentary Glaucoma

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Post-Traumatic or Angle Recession Glaucoma

• History– History of blunt ocular trauma usually

with hyphema– Traumatic event may occur months to

years prior to development of glaucoma

• Features– Elevated IOP– Optic nerve and VF findings consistent

with glaucoma

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– Gonioscopy reveals:• Angle recession (compare to opposite eye -

since some eyes have very wide angles that appear to be recessed but are normal)

• Broad angle recess-wide ciliary body face• Absent or torn iris processes• White glistening scleral spur• Depression in the overlying TM• Localized PAS at the border of the

recession - extensive PAS occasionally mask recession

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• Risk factors– History of blunt ocular trauma– Gonioscopic evidence of angle recession

of 180 degrees or more– Predisposition to, or family history of,

open angle glaucoma• Differential diagnosis

– Unilateral chronic open angle glaucoma– ICE syndromes (Chandler syndrome

particularly)– Contusion angle deformities (i.e.,

cyclodialysis cleft, which may look similar but has a different clinical course)

– Normal anomalous appearing angles

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Angle recession

Photo courtesy of Jane Durcan, MD

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Hyphema• Etiology

– Trauma – blunt or lacerating– Intraocular surgery– Spontaneous hyphemas

• Rubeosis iridis – diabetes, CRVO, carotid occlusive disease, chronic RD

• Anterior uveitis

• History– History of ocular trauma or surgery– History of ocular or systemic disorders

associated with spontaneous hyphemas– Medication history

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Hyphema• Features

– Decreased visual acuity– Elevated IOP

• Etiology of acute elevation– Occlusion of TM by clot, inflammatory cells,

erythrocytic debris– Pupillary block secondary to clot occluding

pupil• Late-onset glaucoma

– Days to years after injury– Etiology– Damage to TM– PAS leading to secondary angle closure

– Blood in AC: circulating RBCs, layered hyphema, total hyphema

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Hyphema• Testing

– Sickle cell hemoglobin screening in all African American patients

– Coagulation studies where indicated• Risk factors

– Risk of increased IOP is greater following rebleeding after a traumatic hyphema

– Rebleeding usually occurs during the first week after initial hyphema

– Larger hyphemas are associated with higher incidence of increased IOP

– Sickle cell hemoglobinopathy associated with higher incidence of glaucoma and vascular occlusions

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Hyphema

• Medical therapy – Cycloplegics– Topical and/or systemic

corticosteroids useful in treating inflammation

– Topical or systemic IOP-lowering medications as needed

– Cautious use of systemic CAIs in patients with sickle cell hemoglobinopathy

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Hyphema– Persistently elevated IOP, rebleeding

or persistent hyphema may necessitate consideration for surgical therapy

– Analgesics and antiemetic medications as needed

– Rigid shield– Elevate head of bed– Limit activity

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Hyphema• Complications

– Complications associated with use of topical and systemic IOP-lowering medications. Avoid use where contraindicated

– CAIs may increase sickling tendency in patients with sickle cell hemoglobinopathy

• Patient instructions– Comply with prescribed medical regimen– Use eye shield– Quiet activity and/or bedrest– Avoid bending over; elevate head of bed– Provide safe home environment– Reliable follow-up– No aspirin or NSAIDs

63Photo courtesy of Marlene Moster, MD

Hyphema

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Corticosteroid-induced Glaucoma

• Etiology – Caused by a reduction in facility of

outflow

• History– May develop at any time during long-

term corticosteroid administration, but IOP elevation typically occurs within a few weeks with potent corticosteroids, or in months with the weaker corticosteroids

– Routes of administration• Topical corticosteroid therapy is more often

associated with IOP rise than is the case with systemic administration

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Corticosteroid-Induced Glaucoma• Intraocular and periocular injections are the

most dangerous route of corticosteroid administration from the standpoint of corticosteroid-induced glaucoma

– IOP elevation may occur in response to subconjunctival, sub-Tenon’s, intravitreal or retrobulbar injections of corticosteroid

– Patient’s response to earlier topical corticosteroid therapy does not always predict how that individual will respond to periocular corticosteroids

• Systemic administration (oral or intravenous) of corticosteroids is least likely to induce glaucoma

– This response does not correlate with the dosage or duration of treatment, but is associated with the degree of pressure response to topical corticosteroids

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Corticosteroid-Induced Glaucoma

• Features– The clinical picture resembles that of

POAG with an open, normal-appearing AC angle and absence of symptoms

– Much less often, the condition may have an acute presentation, in which pressure rises have been observed within hours after corticosteroid administration

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• Risk factors– Individuals with POAG or a family

history of the disease are more likely to respond to chronic corticosteroid therapy with a significant rise in IOP

– High myopes, diabetics, and patients with connective tissue diseases have a similar predisposition to corticosteroid-induced glaucoma

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• Medical therapy options– Discontinuation of the corticosteroid – first

treatment option; often all that is required– The chronic form of this disease is said to

normalize in 1-4 weeks, while the acute form typically resolves within days of stopping the corticosteroid

– In rare cases, the glaucoma may persist despite stopping all corticosteroids

– Glaucoma medical therapy algorithm, as per treatment of POAG, although miotics and prostaglandin analogues should be avoided in cases of uveitis

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• Surgical therapy options– Laser trabeculoplasty– Filtration surgery

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Corticosteroid-Induced Glaucoma (steroid glaucoma)

Photo courtesy of Herbert Fechter, MD

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Angle-Closure Glaucomas• Acute Primary Angle-Closure

Glaucomas• Neovascular Glaucoma

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Acute Primary Angle-Closure Glaucoma

• Etiology– Physiologic pupillary block

• Excessive iris-lens apposition impedes flow of aqueous from PC to AC, elevating PC aqueous pressure

• Secondary forward bowing of peripheral iris results in occlusion of the TM

• Features– Symptoms

• Acute onset of brow ache, eye pain• Blurred vision• Colored haloes around lights• Nausea and vomiting

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Acute Primary-Angle Closure Glaucoma

• Signs– High IOP– Mid dilated, sluggish pupil– Corneal epithelial edema– Congested episcleral and conjunctival

vessels– Shallow AC– AC inflammation– Appositional angle-closure– Iris bombe– Glaukomflecken and sector iris atrophy –

indicators of previous bouts of acute-closure glaucoma

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Acute Primary Angle- Closure Glaucoma

• Risk factors– Hyperopia– Family history of angle-closure– Older age– Female gender– Age-related cataract (lens swelling)– Asian ethnicity

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• Medical therapy options– To lower the IOP and allow clearing of

corneal edema in preparation for laser iridotomy

• Beta-adrenergic antagonists• Alpha2-adrenergic agonists• CAIs – topical, oral, IV• Miotics – 1-2% pilocarpine after IOP starts

to normalize• Prostaglandin analogues• Hyperosmotic agents • Topical corticosteroids

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– Deformation of cornea with cotton tip applicator or Indentation gonioscopy occasionally opens the angle

– Topical glycerin or epithelial removal may be necessary to enable visualization of the chamber angle

• Surgical therapy – Laser peripheral iridotomy – Nd:YAG

and/or argon

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• Complications – Complications of laser iridotomy– Posterior synechiae– Miotics, especially strong miotics, may

increase pupillary block– Formation of PAS

• Perform laser iridotomy as soon as possible

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• Disease-related complications– Residual stage of angle-closure

glaucoma– Corneal decompensation– Sectoral iris atrophy– Posterior synechiae– Cataract formation– Optic nerve damage– Retinal vascular occlusion

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Glaukomflecken under the anterior lens capsule after an attack of acute angle closure. These lens changes are caused by necrosis of the lens epithelium.

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Neovascular Glaucoma• History

– Pain, photophobia (usual)– Markedly reduced vision (usual)– Diabetes– Hypertension, arteriosclerosis

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Neovascular Glaucoma• Epidemiology

– CRVO– PDR– Post cataract extraction, vitrectomy

• Particularly with breached posterior capsule

– Carotid occlusive disease• May have normal or low IOP

– CRAO

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Neovascular Glaucoma • Features: Early

– Tufts of new vessels at pupillary margin– Fine vessels crossing scleral spur

• Features: Late– Very high IOP– Conjunctival injection– Corneal edema– Florid iris neovascularization with ectropion

uveae– Fibrovascular membrane over iris and angle

structures– Variable synechial angle-closure– With total angle closure, there can be

minimal neovascularization of iris, and with pigmented Schwalbe's line, on gonioscopy can be mistaken for OAG

– AC cells and flare

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Neovascular Glaucoma• Risk factors

– Retinal hypoxia

• Disease-related complications– Absolute glaucoma with blindness– Intractable pain

• Patient instructions– Medication and surgical discussion– Referral for PRP, surgical intervention,

and/or cyclodestructive procedure

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Neovascularizationof the iris and angle

Photo courtesy of Teresa Chen, MD

Neovascular Glaucoma

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Glaucoma Medications – Side Effects and Contraindications

Beta Blockers Corneal toxicity

Allergic reactions

Congestive heart failure

Bronchospasm

Bradycardia

Depression

Impotence

COPD

Asthma

Emphysema

Congestive heart failure (relative)

Bradycardia

Hypotension

Greater than first degree heart block

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Alpha 2-adrenergic agonists

Burning on instillation

Conjunctival injection

Pupillary dilation

Allergic reactions

Increased blood pressure

Tachyarrhythmias

Tremor, headache

Monoamine oxidase inhibitor therapy

Infants and children younger than 2 years old due to apnea, bradycardia, and dyspnea

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Parasympatho-mimetics

Increased myopia

Eye or brow pain

Decreased vision

Cataract

Periocular contact dermatitis

Corneal toxicity

Paradoxical angle closure

Neovascular, uveitic, or malignant glaucoma

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CAIs Corneal toxicity

Stevens-Johnson syndrome

Malaise, anorexia, depression

Serum electrolyte abnormalities, renal calculi

Blood dyscrasias

Metallic taste

Sulfa allergy

Kidney stones

Aplastic anemia

Thrombocytopenia

Sickle cell disease

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Changes in iris pigmentation

glaucoma review by dr. allen

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