GLAUCOMA (1)

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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 .

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

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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.

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

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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.

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Applied physiology

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

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• 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

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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.

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• 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

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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.

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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.

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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.

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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

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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

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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.

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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.

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• 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.

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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.

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• 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

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• 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.

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Disc changes in glaucoma
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• 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.

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Tunnel vision
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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.

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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.

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• 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

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

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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).

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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.

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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.

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1. Indentation Tonometer

• Technique

• Schiotz tonometer

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2. Applanation tonometer

• Goldmann tonometer

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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

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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

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

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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.