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| Figure:Glaucoma |
CONGENITAL/ DEVELOPMETAL GLAUCOMA
Types:
- Primary
dev/ cong.
- Developmental
Glaucoma with associated ocular anomalies.
Primary dev/ cong. Glaucoma:
High IOP due to dev anomaly of the angle of AC.
- True
cong. Glaucoma – 40%
- Infantile
glaucoma – 50% manifests within 3 yrs
- Juvenile
glaucoma – 10%, manifests b/w 3-16yrs of life.
WHEN THE DISEASE MANIFESTS PRIOR TP AGE 3YRS, THE EYEBALL
ENLARGES AND SO THE TERM ‘BUPHTHALMOS’ (HYDROPHTHALMOS)
IS USED.
Prevalence and genetic pattern: Mostly sporadic, 10% autosomal
recessive,
65% boys, 75% bilateral, may be asymmetric
Affects 1 child in 10,000 live births.
Pathogenesis:
Maldevelopment of trabeculum including the irido trabecular
junction (trabeculodysgenesis) is responsible for impaired aqueous outflow
resulting in raised IOP.
C/F:
- Photophobia,
blepharospasm, lacrimation. And eye rubbing.
- Corneal
signs:
i.
Corneal oedema
ii.
Corneal enlargement, normal infant
cornea measures 10.5 mm diameter > 13mm confirms enlargement.
iii.
Tears and breaks in Descemet’s membrane
(Haab’s sinae)
- Sclera:
thin and blue.
- AC:
deep.
- Iris:
iridodonesis, atrophic patches
- Lens:
flat, may subluxate.
- Optic
disc: variable cupping and atrophy, esp. after 3rd yr.
- IOP:
moderately high.
- Axial
myopia and anisometropic amblyopia may develop.
- Enlargement
of globe: Buphthalmos.
Examination:
- E
U A include:
1. Measurement
of IOP
2. Measurement
of corneal diameter.
3. Ophthalmoscopy
to evaluate optic disc.
4. Gonioscopic
examination of angle of AC to detect abnormality: Trabeculodysgenesis.
D/D:
- Keratitis.
- Megalocornea
- Lacrimation
due to cong. NLD obstruction.
- Retinoblastoma.
Treatment:
- Rx
is primarily surgical, after lowering of IOP by use of hyperosmotic
agents, Acetazolamide, beta blockers.
- Surgical
procedures:
i.
Goniotomy
ii.
Trabeculotomy
iii.
Combined Trabeculotomy and trabeculotectomy.
PRIMARY OPEN ANGLE GLAUCOMA (POAG)/ CHRONIC SIMPLE GLAUCOMA:
Definition:
Slowly progressive raised IOP associated with characteristic optic disc cupping
and specific field defect in eyes with open angle of AC. There is no obvious
systemic or ocular cause in rise in IOP.
Etiopathogenesis: Not known exactly.
- PDF
and risk factors:
- Heredity:
polygenic inheritance
- Age:
b/e 5th and 7th decade.
- Race:
common and severe in blacks.
- Myopes:
common.
- Diabetics:
higher prevalence.
- Smoking:
increased risk.
- More
prevalent in Hypertensive pts.
- Thyrotoxicosis:
more prevalence.
- Pathogenesis
of rise in IOP:
Decrease in aqueous outflow facility
due to increased resistance to aqueous outflow caused by age related thickening
and sclerosis of the trabeculae and absence of giant vacuoles in the cells
linning the canal
of Schlemm.
- Corticosteroid
responsiveness:
Pt. with POAG, offspring and siblings
are likely to respond to six wks topical steroid with a significant rise in
IOP.
Incidence of POAG: 1 in 100 of general population of either
sex above the age of 40 yrs. Forms about one third cases of all glaucoma.
C/F of POAG:
Symptoms:
- Insidious,
usually asymptomatic.
- Mild
headache and eye ache.
- Defect
in visual field.
- Increasing
difficulties in reading and close works.
- Frequent
changes in presbyopic glasses.
- Delayed
dark adaptation.
Signs:
- Anterior
segment signs: usually normal, in late stages, corneal haze and sluggish
pupil.
- IOP:
raised above 21 mm of Hg.
- Optic
disc changes:
- Vertically
oval cup.
- Asymmetry
of the cup, difference more than 0.2 b/w two eyes significant.
- Large
cup: Normal cup size, 0.3
- Splinter
hrgs on near disc margin.
- Pallor
areas on the disc.
- Atrophy
of the retinal nerve fibre layer.
- Thinning
of neuro retinal rim.
- Nasal
shifting of retinal vessels.
- Pulsation
of retinal arterioles. (pathognomic sign of raised IOP)
- Glaucomatous
optic atrophy, deeply excavated white disc.
- Lamellar
dot sign.
- Visual
field defects: Visual field defects initially observed in Bjerrum’s area
(10-25degree from fixation) and correlate with optic disc changes.
i.
Isopter contraction.
ii.
Baring of blind spots.
iii.
Small wing-shaped paracental scotoma.
iv.
Seidel’s scotoma.
v.
Arcuate or Bjerrum’s scotoma.
vi.
Ring or double arcuate scotoma.
vii.
Rönne’s central nasal step.
viii.
Peripheral field defects.
ix.
Advanced field defects:
- Tubular
or tunnel vision; small central island of vision.
- Temporal
island of vision.
Investigations:
- Tonometry
- Diurnal
variation of IOP
- Gonioscopy
- Documentation
of optic disc changes
- Slit-lamp
exam to rule out secondary causes of POAG.
- Perimetry
- Nerve
fiber layer analyzer.
- Provocation
test: water drinking test.
à 8 mm of Hg or more rises in IOP
diagnostic of POAG.
Diagnosis of POAG:
- POAG:
IOP>21 mm Hg.
à Glaucomatous optic disc cupping and or
visual field defects.
- Ocular
HTN or Glaucoma suspect:
à IOP>21mm Hg. No change in optic disc
or visual field.
- Normal
tension or Low tension Glaucoma (NTG, LTG):
à Typical glaucomatous disc cupping, with
or without visual field changes.
Mx of POAG:
General consideration:
Baseline evaluation and grading of severity of glaucoma.
Aim:
To lower IOP to a level where further visual loss does not occur.
Therapeutic choices:
- Medical
therapy: initial choice.
- Argon
or diode laser trabeculoplasty, and
- Filtration
surgery, last resort.
A. Basic principles of medical therapy of POAG:
- Identification
of target pressure below which glaucomatous damage is not likely to
progress.
Mild to moderate damage: target pressure 12-14mm Hg,
Severe damage: target pressure, 12-14 mm Hg, even lower in
NTG/ LTG.
- Single
drug therapy.
- Combination
therapy.
- Monitoring
of therapy.
Treatment regimens:
- Single
drug therapy:
i.
Topical beta blockers: these lower IOP
by reducing aqueous secretion due to their effect on beta receptors in the
ciliary processes.
Timolol maleate: 0.25, 0.5%: 1-2 times
a day.
C/I: BA or heart block.
ii.
Pilocarpine: 1, 2, 4%- 3-4 times daily.
M/A – contracts longitudinal muscle of
ciliary body and opens spaces in trabecular meshwork, thereby mechanically
increasing aqueous outflow.
iii.
Latanoprost: 0.005%; once daily
A PG analogue decreases IOP by
increasing uveo-scleral outflow of aqueous.
iv. Dorzolamide: 2%; 2-3
times a day.
Topical CA inhibitor lowers IOP by decreasing aqueous
secretion.
- Combination
topical therapy: If one drug is not effective; Add one drug which
decreases aqueous production, e.g.- Timolol, Brimonidine or dorzolamide,
and other drug which increases aqueous outflow. E.g.- Latanoprost,
Pilocarpine.
- Role
of oral CA inhibitor in POAG: Acetazolamide may be added for short term to
control IOP; long term use is not recommended because of their side
effects.
B. Argon or diod laser trabeculoplasty (ALT or DLT):
Indication:
- Uncontrolled
IOP despite maximal tolerated medical therapy.
- As
primary therapy where there is non compliance to medical therapy.
C. Surgical therapy:
Indications:
- Uncontrolled
glaucoma despite maximal medical therapy and laser trabeculoplasty.
- Non
compliance of medical therapy.
- Eyes
with advanced cupping and advanced field loss.
- As
a primary line of Rx by some workers.
Type of Surgery:
Fistulizing (Filtration) surgery makes a new channel for
aqueous outflow and successfully controls IOP.
TRABECULOTECTOMY IS THE MSOT EFFECTIVE FILTRATION SURGERY
FREQUENTLY PERFORMED.
PRIMARY ANGLE CLOSURE GLAUCOMA:
Definition:
Type of primary glaucoma wherein there is no obvious systemic or ocular cause,
in which rise in IOP occurs due to blockage of aqueous humour outflow by
closure of a narrower angle of the AC.
Etiology:
- PDF
risk factors-
i.
Anatomical factors. Anatomically
predisposed eyes to develop PACG:
- Hypermetropic
eyes with shallow AC
- Anteriorly
placed iris-lens diaphragm.
- Eyes
with narrow angle of AC may be due to small eyeball, smaller diameter of
cornea, relatively larger lens or bigger size of ciliary body.
- Plateau
iris contiguration
ii.
General factors:
- Age:
common in 5th decade.
- Sex:
F:M=4:1
- Type
of personality: Nervous individuals with unstable vasomotor system.
- Family
history: believed to be inherited.
- Race:
Common in Caucasians, South-East Asians, uncommon in blacks.
- Precipitating
factors:
- Dim
illumination.
- Emotional
stress.
- Use
of mydriatic drugs, atropine, cyclopentolate, Tropicamide, Phenylephrine etc.
Mechanism of rise in IOP:
- Anatomically
predisposed eye.
- Effect
of precipitating factors.
- Mild
dilatation of pupil
- Increases
amount of apposition b/w iris and lens.
- Relative
pupil block
- Aqueous
collects in PC
- Pushes
peripheral flaccid iris anteriorly, iris bombe.
- Appositional
angle closure due to iridocorneal contact,
- -Rise
in IOP begins, may be transient.
- Appositional
angle closure is converted into synechial angle closure: PAS
- Attack
of rise in IOP may last long.
Clinical presentation of PACG:
5 different clinical entities:
- Latent PACG (PACG suspect)
- Sub acute (Intermittent PACG)
- Acute PACG
- Post congestive ACG
- Chronic PACG
- Absolute glaucoma.
LATENT PACG (Suspect):
Symptoms: Absent
Signs:
- Anatomically
predisposed eye.
- Routine
slit lamp examination.
- Pt.
presenting with attack of PACG in one eye.
Diagnosis:
Clinical signs:
Provocative test:
- Prone-darkroom
tests
- Mydriatic
provocative tests: IOP rises > 8 mm Hg, positive.
Treatment: Prophylactic laser iridotomy in both eyes.
ACUTE PACG (ACUTE CONGESTIVE GLAUCOMA):
- Slight
threatening emergency
- Sudden
total angle closure
- Severe
rise in IOP
- Lasts
for many days unless treated.
- Profound
loss of vision.
C/F of acute PACG:
Symptoms:
- Pain:
sudden severe pain in the eye radiates along the branches of 5th
nerve.
- Nausea,
vomiting, and prostration.
- Rapidly
progressive impairment of vision.
- Redness,
photophobia, lacrimation.
- Past
history: about 5% pt, typical previous intermittent attacks of sub acute ACG,
coloured halos around light.
Signs:
- Lids:
oedematous
- Conjunctiva:
chemosed and congested. Ciliary and conjunctival congestion.
- Cornea:
Oedematous and insensitive.
- AC:
Shallow, Aqueous flare and cells may be seen.
- Angle
of AC: completely closed seen on Gonioscopy.
- Iris:
discoloured.
- Pupil:
Semi dilated, vertically oval and fixed.
- IOP:
Markedly elevated, b/w 40-70 mm Hg.
- Optic
disc: Oedematous and hyperemic
- Fellow
eye: Shallow AC with narrow angle. Features of latent ACG.
Dx of acute PACG: Obvious from clinical features.
D/D:
- From
other causes of red eye:
i.
Acute conjunctivitis
ii.
Acute iridocyclitis.
- From
secondary ACG:
i.
Phacomorphic glaucoma
ii.
Acute neovascular glaucoma
iii.
Glaucomatocyclitic crisis.
Mx of Acute PACG:
Essentially surgical
Emergency medical therapy to prepare the eye for surgery.
- Medical
therapy:
- Systemic
hyperosmotic agent: IV mannitol, 1gm/kg body wt. to lower IOP
- Acetazolamide:
500 mg IV followed by250 mg tab 3 times a day.
- Analgesics
and anti emetics
- Pilocarpine
eye drops 2% every 30 minutes for 1-2 hrs and then 6 hrly.
- Beta
blocker: 0..5% Timolol maleate BD
- Corticosteroid:
Betamethasone or dexamethasone 4 times a day to reduce inflammation.
- Surgical
Rx:
- Peripheral
iridotomy (PI) PAS if < 50%, LASER iridotomy is a good alternative.
- Filtration
surgery: IOP not controlled with best medical therapy, PAS is >50%,
Trabeculectomy, method of choice.
- Clear
lens extraction by phacoemulsification with IOL implantation has recently
been recommended by some workers.
SECONDARY GLAUCOMAS:
- Group of disorders
- Rise of IOP, associated with primary ocular or systemic
disease.
- C/F comprises that of primary disease and effects of
raised IOP.
PHACOLYTIC GLAUCOMA (LENS PROTEIN GLAUCOMA):
Pathogenesis:
Type of secondary open angle glaucoma in which trabecular
meshwork is clogged by the lens proteins and macrophages which have
phagocytosed the lens proteins.
Leakage of lens proteins occurs through an intact capsule of
hypermature or Morgagnian cataract.
C/F of phacolytic glaucoma:
- Features
of congestive glaucoma, acute rise of IOP, eye having a hypermature cataract.
- Deep
AC, aqueous may contain fine white protein particles.
Mx:
- Lower IOP by medical therapy.
- Extraction
of lens with PCIOL implantation.
STEROID INDUCED GLAUCOMA:
Secondary open angle glaucoma.
Develops following topical and rarely systemic steroid
therapy.
Etiopathogenesis:
- Steroid
responsiveness genetically determined.
- Rise
of IOP after 6wks topical steroid.
- 5%
general population, high responders.
Precise mechanism for rise in IOP not known.
Theories are:
- Glycosaminoglycans
(GAG): Accumulation of GAG in trabecular meshwork decreases aqueous outflow.
- Endothelial
cell theory: Suppression of phagocytic activity of living endothelial
cells of Schlemm’s cana;.
- Prostaglandin
theory: Steroid inhibits synthesis of PGE and PGF thereby decreases
aqueous outflow.
C/F: Resembles POAG, Develops following wks of topical
steroid..
Mx:
Treatment:
- Discontinuation
of steroid.
- Medical
therapy: 0.5% Timolol maleate.
- Trabeculectomy,
in intractable cases.
Prevention:
- Judicious
use of steroids.
- Regular
monitoring of IOP when on steroids.
