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Glaucoma

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... Vessel displacement Increased visibility of lamina cribosa Mechanical theory Compression of axons leads to axonal death Vascular theory Ischemia causes ... – PowerPoint PPT presentation

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Title: Glaucoma


1
Glaucoma
  • Dr Mahmood FauziASSIST PROF OPHTHALMOLOGY AL
    MAAREFA COLLEGE

2
Objectives
  • Define glaucoma
  • Estimate magnitude of visual morbidity from
    glaucoma
  • Explain aqueous humor dynamics in glaucoma
    development
  • Outline features of open and close angle glaucoma
  • Contract case studies in open and close angle
    glaucoma
  • Review autonomic effects on the glaucomatous eye.
  • Treatment rationale
  • Reasoning through drug mechanism of action
    decrease aqueous production vs.. increase aqueous
    outflow

3
What is glaucoma?
  • Glaucoma is Optic neuropathy that is commonly
    associated with elevated intraocular pressure
    (IOP), but the disease can occur in normal IOP
  • Glaucomatous Optic neuropathy is the leading
    cause of irreversible blindness in the world
  • Major types are open angle and closed angle
  • Differences among various types of glaucoma
    complicate the nomenclature
  • Our understanding and treatment of the disease
    is very focused on IOP

4
Anatomy
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6
From www.ahaf.org
7
Basic physiology
  • Aqueous is produced by secretion and
    ultrafiltration from the ciliary processes into
    the posterior chamber.
  • It then passes through the pupil into the
    anterior chamber to leave the eye predominantly
    via the trabecular meshwork, Schlemms canal and
    the episcleral veins
  • (the conventional pathway).

8
  • A small proportion of the aqueous (4) drains
    across the ciliary body into the supra-choroidal
    space and into the venous circulation across the
    sclera (uveoscleral pathway)
  • The intraocular pressure level depends on the
    balance between production and removal of aqueous
    humour.

9
Classification of glaucoma
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11
Glaucoma Evaluation
  • Complete history
  • Complete examination
  • IOP
  • Gonioscopy
  • Optic disc
  • Visual Fields

12
Tonometers
Goldmann
Schiotz
Perkins
Contact applanation
Portable contact applanation
Contact indentation
Air-puff
Pulsair 2000 (Keeler)
Tono-Pen
Non-contact indentation
Portable non-contact applanation
portable contact applanation
13
  • The normal pressure is 15.5 mmHg.
  • The limits are defined as 2 standard deviations
    above and below the mean
  • (1121 mmHg).

14
STRUCTURE /FUNCTION EVALUATION
15
GLAUCOMA
Optic nerve signs of glaucoma progression
  • Increasing CD ratio
  • Development of disk pallor
  • Disc hemorrhage (60 will show progression of VF
    damage)
  • Vessel displacement
  • Increased visibility of lamina cribosa


16
Theories of damage
  • Mechanical theory
  • Compression of axons leads to axonal death
  • Vascular theory
  • Ischemia causes axonal necrosis

Direct damage due to Pr.
Capillary Occlusion
Interference to Axoplasmic flow
17
Glaucomatous Damage
  • Axonal necrosis leading to cupping
  • Loss of supporting glial tissue
  • Normally leads to disc pallor
  • Histology of Normal and Glaucomatous Optic nerve

18
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19
Glaucomatous Damage
20
Types of physiological excavation
Cup with sloping temporal wall
Larger and deeper punched-out central cup
Small dimple central cup
21
Pallor and cupping
Pallor - maximal area of color contrast
Cupping - bending of small blood vessels crossing
disc
Cupping and pallor correspond
Cupping is greater than pallor pallor pallor
22
Primary open angle glaucoma
  • Affects 1 in 200 subjects over the age of 40.
  • Affecting males and females equally.
  • There may be a family history.
  • The prevalence among blacks is 3 to 4 times
    higher than whites.
  • Symptomless unless the patient becomes aware of a
    severe visual deficit.

23
Open Angle Glaucoma
  • Obstruction at the level of the trabecular
    meshwork
  • Progressive loss of visual field over time from
    periphery to center
  • Presence of hollowed out optic disc (cupping)
    due to retinal ganglion cell death
  • Open anterior chamber angle
  • Majority of patients have IOP gt 21 mmHg,
    asymptomatic

24
Primary angle closure glaucoma
  • Affects 1 in 1000 subjects over 40 years.
  • Females more commonly affected than males.
  • Strong family history.
  • Prevalence is more common among Asians and
    Eskimos.
  • Patients are likely to be hyperopic.
  • In acute cases, patient may have sever pain,
    photophobia, vision loss and nausea.

25
  • On examination visual acuity is reduced,
  • Eye is red,
  • Cornea is cloudy
  • Pupil oval, fixed and dilated.

26
Closed Angle Glaucoma
  • Apposition of iris and trabecular meshwork
  • Parasympatholytics (pupillary dilation) can
    precipitate attack
  • Increase risk with age, increase in volume of
    lens
  • Acute onset, patient complains of nausea,
    headache (rather than eye ache), malaise, general
    distress
  • Requires immediate treatment

27
Secondary glaucoma
  • Open angle
  • Closed angle
  • Blood (hyphema), following blunt trauma.
  • Inflammatory cells (uveitis).
  • Pigment from the iris.
  • Deposition of material produced by the epithelium
    of the lens, iris and ciliary body in the
    trabecular meshwork (pseudoexfoliative glaucoma).
  • Steroid-induced glaucoma.
  • Raised episcleral venous pressure.
  • Abnormal iris blood vessels may obstruct the
    angle and cause the iris to adhere to the
    peripheral cornea, closing the angle (rubeosis
    iridis).
  • A large choroidal melanoma may push the iris
    forward.
  • A cataract may pushing the iris forward
    (phacomorphic).
  • Uveitis may cause the iris to adhere to the
    trabecular meshwork.

28
Neovascular Galucoma
  • Causes
  • Diabetes
  • CRVO
  • Carotid vascular disease
  • CRAO
  • Eales Disease
  • Sickle cell anemia
  • Coats disease

Signs symptoms Rubeosis iridis Ectropion
uveae NV of angle
29
Phacomorphic Glaucoma
30
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32
BOTTOM LINE ?IOP from ?Aqueous Flow, 3 Sites
1. Obstructed Trabecular Mesh Open Angle
Age-related, genetic Closed Angle Anatomic,
exacerbated by 2. Pupillary Block Dilation
of pupil? iris flattens, ? flow via
pupil, iris forward ?iris-cornea angle 3.
Swelling of Ciliary Body
Modified from Wood et al. NEJM 3391298 (1998)
33
REVIEW Autonomic NS Effect on the Eye
RECEPTOR ACTIVATION WILL TO LOWER IOP, AIM FOR
IRIS, Circular Fibers mAchR Constrict Pupil ? Activity
IRIS, Radial Fibers ?1 R Dilate Pupil ? Activity
CILIARY MUSCLES mAchR Contract for Accomodation ?2 R Relax for Far Vision Activity ?Activity
34
Management of glaucoma
  • Medical treatment.
  • Laser treatment.
  • Surgical treatment.

35
TREATMENT RATIONALE
  • LOWER IOP BY
  • Decreasing Production of Aqueous Humor
  • Increasing Outflow of Aqueous Humor

Focus on Pharmacologic Rx First-line
36
Medical treatment
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38
DRUGS THAT DECREASE AQUEOUS PRODUCTION
  • Beta-Blockers levobunolol, timolol, carteolol,
    betaxolol
  • -Mechanism Act on ciliary body to ? production
    of aqueous humor
  • -Administration Topical drops to avoid
    systemic effects
  • -Side Effects Cardiovascular (bradycardia,
    asystole, syncope), bronchoconstriction (avoid
    with b1-selective betaxolol), depression
  • Alpha-2 Adrenergic Agonists apraclonidine,
    brimonidine
  • -Mechanism ? production of aqueous humor
  • -Administration Topical drops
  • -Side Effects Lethargy, fatigue, dry mouth
    apraclonidine is a derivative of clonidine
    (antihypertensive) which cannot cross BBB to
    cause systemic hypotension
  • Carbonic Anhydrase Inhibitors acetazolamide,
    dorzolamide
  • -Mechanism Blocks CAII enzyme production of
    bicarbonate ions (transported to posterior
    chamber, carrying osmotic water flow),
    thus ? production of aqueous humor
  • -Administration Oral, topical
  • -Side Effects malaise, kidney stones,
    possible (rare) aplastic anemia

39
DRUGS THAT INCREASE AQUEOUS OUTFLOW
  • Nonspecific Adrenergic Agonists epinephrine,
    dipivefrin
  • -Mechanism ? uveoscleral outflow of aqueous
    humor
  • -Administration Topical drops
  • -Side Effects Can precipitate acute attack in
    patients with narrow iris-corneal angle,
    headaches, cardiovascular arrhythmia, tachycardia
  • Parasympathomimetics pilocarpine, carbachol,
    echothiophate
  • -Mechanism ? contractile force of ciliary body
    muscle, ? outflow via TM
  • -Administration Topical drops or gel,
    (slow-release plastic insert)
  • -Side Effects Headache, induced miopia. Few
    systemic SE for direct-acting agonists vs. AchE
    inhibitors (diarrhea, cramps, prolonged paralysis
    in setting of succinylcholine). Why isnt Ach
    used?
  • Prostaglandins latanoprost
  • -Mechanism May ? uveoscleral outflow by
    relaxing ciliary body muscle
  • -Administration Topical drops
  • -Side Effects Iris color change

40
Yag laser peripheral iridotomy(Yag PI)
41
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42
Surgical treatment
  • Drainage surgery (trabeculectomy) relies on the
    creation of a fistula between the anterior
    chamber and the subconjunctival space.
  • The operation is usually effective in
    substantially reducing intraocular pressure.
  • It is performed increasingly early in the
    treatment of glaucoma.

43
Trabeculectomy
44
Rx GLAUCOMA ADDITIONAL CONSIDERATIONS
  • No single medication can be used in all patients
  • Compliance
  • Critical Rx often requires several agents,
  • multiple times a day, everyday
  • - Role of slow-release drug delivery devices
    (Langer)
  • Non-pharmacologic ways to lower IOP
  • - Laser (argon laser trabeculoplasty)
  • - ? aqueous outflow, loses effectiveness over
    time
  • - Surgical (trabeculectomy)
  • Creates alternative path for aqueous outflow
  • Only definitive therapy for closed angle
  • Effectiveness of Rx measured by ability to lower
    IOP, but other factors may be (more) important
  • - Neuroprotection/increased blood flow to optic
    nerve

45
GLAUCOMA Key Points
Glaucoma -Visual loss from optic neuropathy
-Open angle chronic, Closed angle acute
-Final common pathway ? IOP (usually)
Drug Rx -All directed towards??IOP either
via - ? aqueous production Beta
blockers Alpha-2 agonists
Carbonic anhydrase inhibitors - ?
aqueous outflow (Adrenergic agonists,
nonspecific)
Parasympathomimetics
Prostaglandins Treatment slows progression
Understanding ANS effect on the eye is critical
for reasoning through drug mechanisms of
action Understanding ANS effect on the whole
body is critical for predicting and avoiding
dangerous side effects
46
Resources
  • http//www.webmd.com/eye-health/glaucoma-eyes
  • http//www.nhs.uk/conditions/glaucoma/pages/introd
    uction.aspx
  • http//www.aoa.org/patients-and-public/eye-and-vis
    ion-problems/glossary-of-eye-and-vision-conditions
    /glaucoma?ssoy

47
Test yourself
  • Glaucoma quiz
  • http//www.myeyes.com/glaucoma/glaucoma-quiz.shtml

48
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