Transcript GLAUCOMA CME FOR GHs - General Hospital Lagos

GLAUCOMA- THE BASICS
DR. MOSURO ADEDAMOLA
LAMEED
CONSULTANT OPHTHALMOLOGIST
GENERAL HOSPITAL, LAGOS
Glaucoma
• The second most common cause of blindness
worldwide
• The leading cause of irreversible blindness
worldwide
• 70 million with the condition
• 7 million bilaterally blind (6/60 or worse
vision)
Definition of Glaucoma
• “Glaucoma is an optic neuropathy often, but
not always, associated with elevated intraocular pressure, having characteristic optic
nerve-head cupping and visual field loss on
conventional perimetry.”
Epidemiology
Affected
Blind
Developmental
300000
200000
Open angle
13.5M
3.0M
Angle closure
6.0M
2.0M
Total
Glaucoma suspects
5.2M
105M
Second leading cause of blindness
Leading cause of irreversible blindness
Ocular Hypertension
• “A disorder characterized by a statistically
elevated intra-ocular pressure”
• “≥ 21 mm Hg in patients with normal looking
optic discs and normal findings using
conventional perimetry.”
Glaucoma Suspect
• Includes those with “Ocular Hypertension”
• Suspicious, but no definite optic nerve damage
(e.g., large C/D or asymmetry)
• Suspicious, but no definite visual field loss
(e.g., suspicious Bjerrum scotomas)
• One or more major “Risk Factors”,
– eg., race, age, documented family history
Primary Open Angle Glaucoma
(POAG)
• A bilateral disease
• Usually appears after age 40 years
• No symptoms until the disease reaches an
advanced stage - thus, in the early and midstages it must be looked for by a doctor or
nurse
• There is treatment but no cure (usually for the
rest of a patient’s life)
Primary Open Angle Glaucoma (contd)
– A family of diseases
– Have progressive optic neuropathy
– Show as loss of optic nerve tissue and excavation
of the disc
– Over time, defects of retinal sensitivity
– Detected in decline of peripheral vision and
ultimate loss of central visual function
– Open angles on gonioscopy
POAG Risk Factors
(Classic and Strong)
• IOP
• Family history - glaucoma in a sibling or
parent
– must be a history of visual loss, not just
“glaucoma”
– increases risk of glaucoma by 5—10X
• Self-management ability (compliance)
– the most important single risk factor
• Race - African heritage (especially AfroCaribbean)
POAG Risk Factors
(Classic and Strong)
• Age - (causing a 2X prevalence of POAG in
year 2020)
• Pseudoexfoliation
• Pigment dispersion syndrome
• Age
– Risk for OAG increases 4-5 times between ages 40-70
– Prevalence is less than 0.1% below 30yrs but rises
above 10% or more in elderly
• Race
– Blacks 3-4 times more likely than whites to develop
glaucoma
– Prevalence of glaucoma in persons of African descent
up to more than 4 times other world populations
• Family history
– Previous family history imparts a 5 times risk of
developing glaucoma
– 10-15% first degree relatives of POAG patients
likely to develop glaucoma
– 40% risk in offspring of glaucoma patients
– AD and AR modes of inheritance with incomplete
penetrance and environmental influences have
been described
• Myopia
– An association has been established
– Possibly poor supporting structure for optic nerve
head in myopia
• Diabetes mellitus
– Higher prevalence of OAG among diabetics?
– Small vessel damage in diabetes may make optic
nerve head susceptible to damage from IOP rise
• Cardiovascular disease (hyper/hypotension)
– Microcirculatory changes in hypertension could make
optic nerve head susceptible to damage with longer
duration of raised BP and vascular changes making
damage poor likely
– Hypotension and reduced optic nerve head perfusion
has effects on ON head (low perfusion pressure)
– Migraine, peripheral vascular disease, stroke and
vasospasm with poor auto regulation to ON head may
predispose to damage
Other Risk Factors
• Sedentary life style (aerobic exercise is good
for glaucoma patients; it increases blood flow
to the optic nerve)
• Smoking
• Obesity
• Diet?
Combination of Risk Factors
• Risk factors are additive
• The appearance of a new risk factor in a
patient with stable glaucoma is suggested by
the loss of IOP control or a change in the optic
disc or visual field after a long period of
stability
• Examples: atrial fibrillation, nocturnal
hypotension, anemia
Risk Factors for Those With African
Heritage
• Much greater chance – to have glaucoma
– to have greater damage at presentation
– for medications not to work as well
– to have trabeculectomy not work as long
– to progress while receiving therapy
– not to be offered filtration surgery
– to have routine surgery fail
– to be blinded by the disease
Clinical features- Presentation
• Early
– Usually asymptomatic
– Incidental finding
• Late
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Poor vision
Bumping into objects
Heaviness in the eyes
Frequent change of
reading glasses
Clinical Signs
• Visual acuity is reduced but may be normal
• Pupillary reaction: normal, RAPD, amaurotic
• Disc
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Abnormal cupping
Asymmetry ≥ 0.2
Disc hemorrhage
Notching /thinning of neuro-retinal rim
• IOP is normal or raised
• Open angles on gonioscopy
• Visual field changes- characteristic
Medical Treatment
• Reduce aqueous humor production
– β-adrenergic blockers
• Non-selective: timolol, levobunolol 0.5% (betagan),
metipranolol 0.3%, cateolol hydrochloride 1.0%
• β 1- selective with less tendency for lung or CV problems:
betaxolol 0.5% (betoptic)
– Adrenergic agonists (cause vasoconstriction of ciliary
blood vessels thus reducing ultrafiltration)
• Non-selective: epinephrine, dipivefrin
• α selective: apraclonidine (iopidine)- also reduces episcleral
venous pressure; brimonidine (alphagan) increases
uveoscleral outflow
Medical Treatment (contd)
• Reduce aqueous humor production
– Carbonic anhydrase inhibitors (inhibit conversion
of carbondioxide to bicarbonate)
• Oral or IV: acetazolamide (diamox), dichlorphenamide,
methazolamide
• Topical: dorzolamide 2% (trusopt), brinzolamide 1%
Medical Treatment (contd)
• Increase outflow through trabecular
meshwork
– Adrenergic agonists:- mediated by α and β
stimulation
– Cholinergic agonists:- open up trabecular
meshwork by causing contraction of longitudinal
muscles
• Direct acting: acetylcholine (miochol)
• Cholinesterase inhibitors: echothiopate (phospholine
iodide), physostigmine (eserine)
Medical Treatment (contd)
• Increase uveoscleral outflow
– Hypotensive lipids
• Prostaglandin analogues: latanoprost 0.005%,
travoprost 0.004%
• Prostamide: bimatoprost 0.03%
• Decasanoid : unoprostone isopropyl 0.15%
– Hyperosmotic agents: increase blood osmolality
• Oral: glycerol, lsosorbide
• IV: 20% mannitol, urea
Medical Treatment (contd)
• Neuroprotection
– Prevent glutamate excitotoxicity: memantine
– Inhibition of apoptosis: caspase inhibitors
– Calcium homeostasis: calcium channel blockersbetaxolol, brimonidine (possible effects on blood
vessel stability or preventing vasoconstriction)
Surgical Treatment
– Primary surgical treatment gives better long term
results
– Better ways of handling conjunctiva and use of
releasable sutures give better results
– Use of antimetabolites (5FU, MMC, β-irradiation)
have also improved outcome
– Previous medical treatment with adrenaline and
pilocarpine reduce the prognosis for successful
medical treatment
Surgical Treatment (contd)
• Trabeculectomy
– Most common
– Creates alternative drainage channel (fistula)
• Laser trabeculoplasty
• Destruction of the ciliary body
– Cyclocryotherapy
– Cyclodiode treatment
• Shunts
Primary Angle Closure
Glaucoma (PACG)
• May be more common than POAG, prevalence
vary widely in different populations
• Main form of glaucoma in Mongolian races
(Mongols, Eskimos, Mainland China,
Vietnamese, 80-90% of glaucoma in Myanmar
• Has been recognized in various parts of Africa
(Somalia, Nigerians, south Africa)
• Need for gonioscopy in all patients
Risk factors
• Age
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Angle get more narrow with age and PAS increases
Steep and plateau iris profile increases with age
Rate of PAS increases as angle narrows
PAS is more common in eyes with steep iris
• Race
– More common in Inuit and Asians
– Acute forms seem to be more in whites while blacks
present with the chronic asymptomatic form
Risk Factors (contd)
• Gender
– More common in females
– Females may have smaller anterior segments and axial
lengths than men
• Refractive error
– May be more common in hyperopes
– May just be an indication of anterior segment dimensions
• Family history
– First degree relatives at greater risk
– Smaller dimensions of anterior segment may be inherited
Mechanism of angle closure
• Relative pupil block
– Maximum in mid-dilated position
– Iris hugs the lens over a greater surface area and
impedes the flow of aqueous from posterior to
anterior chamber
• Peripheral iris crowding
– Bulky peripheral roll
– Plateau iris
– Anteriorly rotated ciliary body
Clinical features
• Acute PAC
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Sudden onset
Severe ocular pain
Headache
Blurred vision
Haloes around light
Nausea
Vomitting
• Chronic
– Assymptomatic
– Similar to POAG
– Differentiated by
gonioscopy
Treatment
• Acute attack: reduce IOP immediately
– Topical anti-glaucoma medications: topical beta
blockers and alpha-2 adrenergic blockers.
Pilocarpine
– Acetazolamide
– Osmotic agents
Treatment (contd)
• Surgical treatment:- mainstay
– Surgical iridectomy
– Argon or YAG laser iridectomy
– Trabeculectomy
• Chronic phase
• Trabecular damage from previous acute or sub-acute
attacks
– Prophylactic iridotomy/iridectomy
Congenital Glaucoma
• Primary congenital
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Accounts for 50-70% of congenital glaucomas
Incidence vary from 1:2000- 1:20,000
Usually present at age of 6/12
75% bilateral involvement
Majority are sporadic with sibling risk of less than 2%
10% are hereditary with AR mode of inheritance
Immature drainage angle developmenttrabeculodysgenesis
Congenital Glaucoma Types
• Glaucoma associated with anterior segment
dysgenesis
– Axenfield Rieger syndrome
– Peter’s anomaly
– Aniridia
• Aphakic glaucoma
• Sturge-Weber syndrome
• Uveitic glaucoma
Presentation
• Symptoms
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Watery eyes
Blepharospasm
Photophobia
Eye rubbing
Reduced vision and
nystagmus
• Signs
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Reduced VA
Bupthalmos
Corneal edema
Haab’s striae
Asymmetric eye size
Rapidly increasing
myopia
– Strabismus
Assessment
• History
• General exam and examination of parents and
siblings
• Orthoptic assessment
• USS for biometry and posterior sement
anomalies
• EUA
– IOP
– Horizontal corneal diameter
– Optic disc assessment
Treatment
• Medical
– Usually temporising
• Surgical
– Goniotomy
– Trabeculotomy
– Trabeculectomy
– Tube drainage?
– Transcleral cyclophotocoagulation
Others
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Secondary glaucomas
Traumatic glaucomas
Irido-corneal syndromes
Epithelial in-growth
Pseudoexfoliation syndrome
Pigment dispersion
Post surgical (aphakic or psuedophakic)
Glaucomas resulting from Complicated cataracts