colsedangleglaucoma 150905111947 lva1 app6891
TRANSCRIPT
COLSED ANGLE GLAUCOMA
ANIL REGMIMedical student
NGMC9/4/2015
April 22, 2023
It is the chronic, progressive optic neuropathy caused by a group of ocular condition, which lead to damage of optic nerve with loss of visual function. Most common risk factor is raised IOP.
Glaucoma:
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1. mechanical change due to raised IOP: Raised IOP
↓Mechanical pressure to lamina cribrosa
↓Backward displacement and compaction of laminar
plates↓
Narrows the opening through which axon passes↓
Damage the nerve fibre bundle
pathogenesis:
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2. Vascular perfusion:Raised IOP
↓Mechanical pressure on lamina cribrosa
↓Decrease capillary blood flow
↓Decrease perfusion to the optic nerve head
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It includes the spectrum of condition in which peripheral iris moves forward to block the openings of the trabecular meshwork in an occludable angle causing rise in intra ocular pressure.
CLOSE ANGLE GLAUCOMA
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Common in Asians and Eskimos Uncommon in African and Caucasians Age: 4th to 5th decade Sex: female: male = 4: 1 First degree relative are at increased risk
Epidemiology:
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1. Anatomical: Short eye Smaller corneal diameter Shallow anterior chamber Relative anterior positioning of lens-iris and
diaphragm.2. Physiological: Dim illumination Emotional stress3. Pharmacological : Use of mydriatic drug like atropine, tropicamide
Predisposing factors:
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Generally bilateral though the involvement of two eye is often asymmetrical.
Number of clinical subtypes have been described.
Clinical features:
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Shallow anterior chamber with occludable angle (angle recess < 20’ )
No other gonioscopic abnormalities are present.
Provocative test: dark room test : IOP rise by 8mm Hg. mydriatic provocative test : 2%
pilocarpine No any clinical symptoms.
1. Primary angle closure glaucoma suspect
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Shallow anterior chamber with occludable angle (angle recess < 20’ )
IOP rise suddenly while reading in dim light, watching the film in darkened room for short period followed by spontaneous resolution of pupillary block, which is possible due to physiological myosis, which occur during sleep.
2. Subacute or intermittent primary angle closure glaucoma
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Patient complains: Unilateral headache or brow ache. Blurring of vision Unbroken colored halos around light during
episodes. Between the recurrent attacks, eyes are
free of symptoms and only sign of narrow angle recess, clumping of pigment in angle, or occasional peripheral anterior synechiae.
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It is caused by sudden occlusion of entire angle with resultant acute rise in IOP to extremely high level.
Patient complains: Severe unilateral headache. Diminution of vision in red eye. Nausea may be frequently associated.
3. Acute Primary angle closure glaucoma
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On examination: Corneal edema Shallow anterior chamber Iris bombe with vertically oval. Mid dilated pupil. After resolution of corneal edema,
gonioscopically closed angle can be seen i.e. extensive irido-corneal synechiae and optic disc may be found to be either hyperemic or normal.
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It is said if IOP is chronically raised in eyes if synechial closure over at least 180 degree.
Change in optic nerve head or visual field may or may not be present.
Causes: a. repeated subacute attacks of primary angle-
closure glaucoma↓
Extensive synechial closure↓
Chronoically elevated IOP
4. Chronic primary angle closure glaucoma:
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b. acute primary angle closure glaucoma, which persists more than few hours
↓Irreversible synechial closure of angle and permanent damage to trabecular meshwork.
c. asymptomatic or ‘creeping’ angle closure↓
Synechial closure occurs within depth of angle.↓
Progressively involves the entire angle.
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Acute congestive glaucoma is the emergency condition and need to be controlled immediately.
Management is essentially surgical. Medical therapy is given as an emergency
and temporary measure in order to decrease IOP before ready for operation.
Treatment:
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1. systemic hyperosmotics to decrease IOP given as soon as diagnosed.
i.v. Mannitol (1gm/kg body wt) Oral glycerol (1.5gm/kg)2. tab. Acetazolmide3. Analgesics and antiemetics4. Pilocarpine eyedrops – started after IOP is bit
lowered by hyperosmolar agents.5. Beta-blocker – 0.5% Timolol BD 6. Corticosteroid eyedrop. E.g. dexamethasone 3-
4times/day to reduce inflammation.
Medical therapy:
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1. Peripheral laser iridotomy:Indications: Peripheral anterior synechiae: <50% of
angle Prophylactic Bypass pupillary block A hole is made in peripheral iris allowing
the aqueous to drain directly from posterior chamber to region of trabecular meshwork.
Laser iridotomy : non invasive method
Surgical treatment:
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2. Trabeculectomy (filtration surgery)Indication: IOP not controlled within 12 hours of
vigorous medical therapy Peripheral anterior synechiae: >50% of
angle It provides an alternative to angle of
drainage of aqueous from anterior chamber into subconjunctival space.
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1. All of following anatomical change predispose to primary angle closure glaucoma expect?
a. Small corneab. Flat corneac. Shallow anterior chamberd. Short axial length of eyeball
MCQs
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2. All are the feature of acute attack of primary narrow angle glaucoma expect?
a. IOP raised up to 40-70mm Hgb. Eye red, painful, and tenderc. Disc shows glaucomatous cuppingd. Fellow eye also shows shallow anterior
chamber
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3. The most common provocative test for angle closure glaucoma is:
a. Water drink testb. Dark room testc. Mydriatic-miotic testd. Homatropine mydriatic test
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1. A 55 years old patient with moderate hypermetropia in both eyes presented in emergency department with sudden painful diminution of vision. O/E, her right eye was red with high IOP and shallow anterior chamber and her left eye also had shallow anterior chamber.
a) What is your most likely diagnosis?b) Write about the treatment?c) Write briefly about the aqueous secretion and
drainage?
PBQs
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THANK YOU