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Title: GLAUCOMA (1)


1
GLAUCOMA
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  • Angle of anterior chamber
  • Angle of anterior chamber plays an important role
    in the process of aqueous drainage.
  • It is formed by root of iris,
  • anterior-most part of ciliary body,
  • scleral spur,
  • trabecular meshwork and
  • Schlemns canal .

3
  • Aqueous outflow system
  • It includes the trabecular meshwork, Schlemms
    canal, collector channels, aqueous veins and the
    episcleral veins

4
Production.
  • Aqueous humour is derived from plasma within the
    capillary network of ciliary processes.
  • The normal aqueous production rate is 2.3 µl/min.
  • The three mechanisms diffusion, ultrafiltration
    and secretion (active transport) play a part in
    its production at different levels.

5
  • Refractive index of aqueous humour is 1.336.
  • Composition. Constituents of normal aqueous
    humour are
  • Water, protein, amino acids, glucose, oxygen,
    urea nk

6
Aqueous humour and its production
  • Volume.
  • The aqueous humour is a clear watery fluid
    filling the anterior chamber (0.25 ml) and
    posterior chamber (0.06 ml) of the eyeball.

7
Applied physiology
  • The physiological processes concerned with the
    dynamics of aqueous humour are-
  • its production
  • drainage
  • and maintenance of intraocular pressure.

8
  • Drainage of aqueous humour
  • Aqueous humour flows from the posterior chamber
  • into the anterior chamber through the pupil
    against
  • slight physiologic resistance. From the anterior
  • chamber the aqueous is drained out by two routes
  • Trabecular (conventional) outflow.
  • Uveoscleral (unconventional) outlow

9
Function
  • Functions of aqueous humour are
  • It maintains a proper intraocular pressure.
  • It plays an important metabolic role by
    providing substrates and by removing metabolites
    from the avascular cornea and lens.
  • It maintains optical transparency.
  • It takes the place of lymph that is absent
    within the eyeball.

10
  • Drainage of aqueous humour
  • Aqueous humour flows from the posterior chamber
  • into the anterior chamber through the pupil
    against
  • slight physiologic resistance. From the anterior
  • chamber the aqueous is drained out by two routes
  • Trabecular (conventional) outflow.
  • Uveoscleral (unconventional) outlow

11
Intraocular pressure
  • The intraocular pressure (IOP) refers to the
    pressure exerted by intraocular fluids on the
    coats of the eyeball.
  • The normal IOP varies between 10 and 21 mm of Hg.
  • The normal level of IOP is essentially
    maintained by a dynamic equilibrium between the
    formation and outflow of the aqueous humour.

12
Factors affecting IOP
  • (A) Local factors
  • Rate of aqueous formation influences IOP levels.
    The aqueous formation in turn depends upon many
    factors such as permeability of ciliary
    capillaries and osmotic pressure of the blood.
  • 2. Resistance to aqueous outflow (drainage). From
    clinical point of view, this is the most
    important factor. Most of the resistance to
    aqueous outflow is at the level of trabecular
    meshwork.
  • 3. Increased episcleral venous pressure may
    result in rise of IOP. The Valsalva manoeuvre
    causes temporary increase in episcleral venous
    pressure and rise in IOP.
  • 4. Dilatation of pupil in patients with narrow
    anterior chamber angle may cause rise of IOP
    owing to a relative obstruction of the aqeuous
    drainage by the iris.

13
Factors affecting IOP cont..
  • (B) General factors
  • 1. Heredity. It influences IOP, possibly by
    multifactorial modes.
  • 2. Age. The mean IOP increases after the age of
    40 years.
  • 3. Sex. IOP is equal between the sexes in ages
    20- 40 years. In older age groups increase in
    mean IOP with age is greater in females.
  • 4. Diurnal variation of IOP. Usually, there is a
    tendency of higher IOP in the morning and lower
    in the evening This has been related to diurnal
    variation in the levels of plasma cortisol.
  • Normal eyes have a smaller fluctuation (lt 5 mm of
    Hg) than glaucomatous eyes (gt 8 mm of Hg).
  • 5. Postural variations. IOP increases when
    changing from the sitting to the supine position.

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  • 6. Blood pressure.
  • As such it does not have longterm effect on IOP.
    However, prevalence of glaucoma is marginally
    more in hypertensives than the normotensives.
  • 7. Osmotic pressure of blood.
  • An increase in plasma osmolarity (as occurs after
    intravenous mannitol, oral glycerol or in
    patients with uraemia) is associated with a fall
    in IOP, while a reduction in plasma osmolarity
    (as occurs with water drinking provocative tests)
    is associated with a rise in IOP.
  • 8. General anaesthetics and many other drugs also
    influence IOP
  • e.g., alcohol lowers IOP, tobacco smoking,
    caffeine and steroids may cause rise in IOP. In
    addition there are many antiglaucoma drugs which
    lower IOP.

15
Definition
  • Glaucoma is a group of disorders characterized
    by-
  • -A progressive optic neuropathy resulting in a
    characterstic appearance of the optic disc
  • -A specific pattern of irreversible visual field
    defects.
  • -HIGH IOP gt20mmgh

16
Classification
  • (A) Congenital and developmental glaucomas
  • 1. Primary congenital glaucoma (without
    associated anomalies).
  • 2. Developmental glaucoma (with associated).
  • (B) Primary adult glaucomas
  • 1. Primary open angle glaucomas (POAG)
  • 2. Primary angle closure glaucoma (PACG)
  • (C) Secondary glaucomas

17
PRIMARY OPEN ANGLE GLAUCOMA(POAG)
  • As the name implies, it is a type of primary
    glaucoma, where there is no obvious systemic or
    ocular cause of rise in the intraocular pressure.
  • It occurs in eyes with open angle of the
    anterior chamber.

18

19
ETIOPATHOGENESIS
  • Etiopathogenesis of POAG is not known exactly.
    Some of the known facts are as follows-
  • Predisposing and risk factors of POAG.
  • These include the following
  • Heredity. POAG has a polygenic inheritance. The
    approximate risk of getting disease is 10 in the
    siblings, and 4 in the offspring of patients
    with POAG.
  • 2. Age. The risk increases with increasing age.
  • 3. Race. POAG is significantly more common,
    develops earlier and is more severe in black
    people than in white.
  • 4. Myopes are more predisposed than the normals.

20
  • 5. Diabetics have a higher prevalence of POAG
    than non-diabetics.
  • 6. Cigarette smoking is also thought to increase
    its risk.
  • 7. High blood pressure is not the cause of rise
    in IOP, however the prevalence of POAG is more in
    hypertensives than the normotensives.
  • 8. Thyrotoxicosis is also not the cause of rise
    in IOP, but the prevalence of POAG is more in
    patients suffering from Graves ophthalmic
    disease than the normals.

21
CLINICAL FEATURES OF POAG
  • Symptoms
  • 1.The disease is insidious and usually
    asymptomatic.
  • 2. Patients may experience mild headache,
    eyeache, and tearing.
  • 3. Occasionally, an observant patient may notice
    a defect in the visual field.
  • 4. Reading and close work often present
    increasing difficulties owing to accommodative
    failure due to constant pressure on the ciliary
    muscle and its nerve supply. Therefore, patients
    usually complain of frequent changes in
    presbyopic glasses.
  • 5. Patients develop delayed dark adaptation, a
    disability which becomes increasingly disturbing
    in the later stages.

22
  • Signs
  • I. Anterior segment signs. may reveal normal
    anterior segment.
  • In late stages pupil reflex becomes sluggish and
    cornea may show slight haze.
  • Microcystic edema incase of very high IOP.
  • II. Intraocular pressure changes. gt 21mmhg

23
  • III. Optic disc changes.
  • Usually observed on routine fundus examination.
  • provide an important clue for suspecting POAG.
    These are typically progressive, asymmetric and
    present a variety of characteristic clinical
    patterns.
  • The C/D ratio indicates the diameter of the cup
    expressed as a fraction of the diameter of the
    disc.

24

25
Disc changes in glaucoma
26
  • IV. Visual field defects.
  • Visual field defects usually run parallel to the
    changes at the optic nerve head and continue to
    progress if IOP is not controlled. These can be
    described as early and late field defects.
  • end stage is TUNNEL VISION
  • Note patient can have normal VA even at end
    stage of glaucoma.

27

28
Tunnel vision
29

30
PRIMARY ANGLE-CLOSUREGLAUCOMA
  • It is a type of primary glaucoma (where in there
    is no obvious systemic or ocular cause) in which
    rise in intraocular pressure occurs due to
    blockage of the aqueous humour outflow by closure
    of a narrower angle of the anterior chamber.

31
ETIOLOGY
  • (A) Predisposing risk factors.
  • These can be divided into anatomical and general
    factors
  • I. Anatomical factors.
  • Eyes anatomically predisposed to develop primary
    angle-closure glaucoma (PACG) include
  • a)Hypermetropic eyes with shallow anterior
    chamber.
  • b) Eyes in which iris-lens diaphragm is placed
    anteriorly.
  • c) Eyes with narrow angle of anterior chamber,
    which may be due to small eyeball, relatively
    large size of the lens and smaller diameter of
    the cornea or bigger size of the ciliary body.
  • d) Plateau iris configuration.

32
  • II. General factors include
  • Age. more common in 5th decade of life.
  • Sex. Females more than males (14)
  • Type of personality -more common in nervous
    individuals
  • Family history- inherited.
  • Race. More in African

33
  • (B) Precipitating factors.
  • Dim illumination,
  • Emotional stress,
  • Use of mydriatic drugs like atropine,
    cyclopentolate, tropicamide and phenylephrine

34
Absolute primary angle-closure glaucoma
  • The chronic phase, if untreated, with or without
    the occurrence of intermittent subacute attacks,
    gradually passes into the final phase of absolute
    glaucoma.
  • Clinical features
  • Painful blind eye. The eye is painful, irritable
    and completely blind (no light perception).

35

36

37

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INVESTIGATIONS.
  • Regular glaucoma check-ups include two routine
    eye tests
  • 1.Tonometry eye pressure test IOP
  • 2.Ophthalmoscopy
  • Is a test that allows a health professional to
    see inside the back of the eye (called the
    fundus) and other structures using a magnifying
    instrument (ophthalmoscope) and a light source.
  • Additional tests
  • Perimetry
  • The perimetry test is also called a visual field
    test
  • Gonioscopy
  • is a painless eye test that checks if the angle
    where the iris meets the cornea is open or
    closed, showing if either open angle or closed
    angle glaucoma is present.

39
Types of Tonometers
  • The instruments are categorized into 2 groups
    based on the way they determine IOP
  • Indentation tonometers measure the amount of
    indentation of the cornea produced by a known
    weight.
  • 2. Applanation tonometers measure the force
    needed to applanate(or flatten) a small area of
    the central cornea.

40
1. Indentation Tonometer
  • Technique
  • Schiotz tonometer

41
2. Applanation tonometer
  • Goldmann tonometer

42
TONOMETRY
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Perimetry/visual field
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Visual field
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GONIOSCOPY
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Management
  • Medical therapy,
  • surgery
  • 1. Argon or diode laser trabeculoplasty
  • 2. filtration surgery

47
Medical treatment
  • ANTI-GLAUCOMA DRUGS
  • Classification
  • A. Parasympathomimetic drugs (Miotics)
  • Egpilocarpine,carbachol
  • B. Sympathomimetic drugs (Adrenergic agonists)
  • Eg epinephrine
  • C. ß-blockers
  • Eg atenolol,betaxolol

48
  • D. Carbonic anhydrase inhibitors
  • Eg acetazolamide
  • E. Hyperosmotic agents
  • Eg glycerol,mannitol,urea
  • F. Prostaglandins
  • Eg latanoprost
  • G. Calcium channel blockers
  • Eg nifedipine

49
C. Surgical therapy
  • Indications
  • 1. Uncontrolled glaucoma despite maximal medical
    therapy and laser trabeculoplasty.
  • 2. Non-compliance of medical therapy and non
    availability of ALT.
  • 3. Failure with medical therapy and unsuitable
    for ALT either due to lack of cooperation or
    inability to visualize the trabeculum.
  • 4. Eyes with advanced disease i.e., having very
    high IOP, advanced cupping and advanced field
    loss should be treated with filtration surgery as
    primary line of management.
  • 5. Recently, some workers are even recommending
    surgery as primary line of treatment in all cases.

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iridectomy
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Four Key Facts About Glaucoma
  • Glaucoma is a leading cause of blindness
  • Glaucoma can cause blindness if it is left
    untreated. And unfortunately approximately 10 of
    people with glaucoma who receive proper treatment
    still experience loss of vision.
  • There is no cure (yet) for glaucoma
  • Glaucoma is not curable, and vision lost cannot
    be regained. With medication and/or surgery, it
    is possible to halt further loss of vision. Since
    glaucoma is a chronic condition, it must be
    monitored for life. Screening, detection and
    prevention is the first step to preserving your
    vision.
  • Everyone is at risk for glaucoma
  • Everyone is at risk for glaucoma from babies to
    senior citizens. Yes, older people are at a
    higher risk for glaucoma but babies can be born
    with glaucoma. Young adults can get glaucoma,
    too. African-Americans in particular are
    susceptible at a younger age.
  • There may be no symptoms to warn you
  • With open angle glaucoma, the most common form,
    there are virtually no symptoms. Usually, no pain
    is associated with increased eye pressure. Vision
    loss begins with peripheral or side vision. You
    may compensate for this unconsciously by turning
    your head to the side, and may not notice
    anything until significant vision is lost. The
    best way to protect your sight from glaucoma is
    to get tested. If you have glaucoma, treatment
    can begin immediately.

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  • THE END.
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