2 out of 3:

Elevated intraocular pressure Optic Nerve Cupping Visual field defects

Optic nerve head cupping: Click  to enlarge

Most common is impaired outflow of aqueous.

• Aqueous is produced by the ciliary body, enters the posterior chamber between the iris and the lens and passes through the pupil into the anterior chamber then to the trabecular meshwork to the anterior chamber angle.
• The major resistance to aqueous outflow from the anterior chamber occurs at the trabecular meshwork and Schlem’s canal.
• Normal IOP is 16 +/- 5 mm Hg. It varies during the day with the highest readings in the early morning. Thus a single normal reading does not rule our glaucoma.
• Instruments to measure IOP include:

1. Goldmann applanation tonometer
2. Perkins tonometer
3. Tonopen
4. Schiotz indentation tonometer

• Characterized by loss of disc substance (enlargement of the optic cup). Normal is up to 0.4
• As cupping develops, the disc vessels are displaced nasally.
• Asymmetric cupping suggests glaucoma.

• Glaucomatous field loss mainly involves the central 30 degrees of vision.
• The earliest changes are enlargement of the blind spot, nasal scotomas (nasal step) followed by peripheral arcuate defects. With further loss, there is further constriction of the visual field that may end up in "tunnel vision", as can be seen below:
  
  

• An important step the assessment of glaucoma is to visualize the angle structures.
• Structures seen on gonioscopy of a normal angle include Schwalbe’s line, scleral spur and trabecular meshwork.
• The angle is graded according to the number of structures identified on gonioscopy.

Different classifications:

1. Congenital v/s acquired
2. Open angle v/s narrow-angle
3. Primary v/s Secondary.

Secondary Glaucoma:

1. Pigmentary
2. Exfoliation
3. Phacogenic
4. Phacomorphic
5. Traumatic
6. Neovascular
7. Steroid-induced

1. Age
2. Race : more common in blacks
3. Family history of glaucoma
4. Cardiovascular diseases
5. Myopia
6. Nutritional factors
7. Vasospastic disorders: migraine, Raynaud’s phenomenon.

1. Suppression of aqueous production:

1. Topical beta blockers:

• Timolol (TIMOPTOL) : contraindicated in asthma and cardiac diseases
• Betaxolol (BETOPTIC): more beta1 cardioselective.

  C. Epinephrine : decreases production of aqueous and facilitates outflow

  D. Carbonic Anhydrase Inhibitors:

• systemic: Acetazolamide (DIAMOX)
• topical : Dorzolamide (TRUSOPT)

1. Parasympathomimetics:

• Pilocarpine (SPERSACARPINE): acts through contraction of the ciliary muscle thus facilitating outflow.
• Carbachol

   C.  Dipivefrin: a prodrug of epinephrine

  3. Reduction of vitreous volume:

  4. Prostaglandin Analogs:

Latanoprost (XALATAN): facilitates aqueous outflow through the uveoscleral pathway (a secondary pathway for drainage of aqueous).

 

1. Peripheral Iridotomy or Iridectomy:

• Used in acute angle-closure glaucoma with pupillary block
• Creates an opening between the anterior and posterior chambers to relieve the pressure between the two compartments.
• Uses the Nd-YAG laser (iridotomy) or can be surgical (iridectomy).

• Argon laser application to the trabecular meshwork facilitates outflow of aqueous and enhances the function of the meshwork.
• Can be used in adjunction to medical therapy in order to postpone glaucoma surgery.

1. Trabeculectomy:

• Bypasses the normal drainage mechanisms of the eye by allowing direct access of aqueous from the anterior chamber tot he subconjunctival tissue (bleb), either by trabeculectomy or by insertion of a drainage tube.
• The major complication of trabeculectomy is bleb failure due to fibrosis of the episcleral tissue. Fibrosis more commonly occurs in young patients, blacks, and patients who have previously undergone glaucoma filtering surgery or other surgeries involving the episcleral tissues. In these cases, adjunctive treatment with an antimetabolite ex Mitomycin C or 5-FU is helpful to reduce the risk of bleb failure.
• Implantation of a silicone tube is an alternative to trabeculectomy if the latter cannot be performed successfully.

• These are reserved when both medical and surgical therapies are unsuccessful.
• They involve destruction of the ciliary body to control the IOP by cryotherapy, diathermy, or using the Nd-YAG laser applied just posterior to the limbus through a probe.
• They carry a high risk of phthisis thus they should be reserved only for intractable cases.

• Also called low-tension glaucoma
• Evidence of glaucomatous optic disc and/or visual field changes with a pressure consistently below 21 mm Hg.
• Pathology: Abnormal sensitivity of the disc to intraocular pressure because of vascular or mechanical abnormalities at the ONH.
• Disc hemorrhages are more commonly seen.
• Associated with other vasospastic disorders such as migraine, Raynaud’s phenomenon.
• More aggressive than primary open-angle glaucoma
• Treatment: Medications that increase blood flow to the ONH are favored ex: betaxolol , dorzolamide.

• Elevated IOP in the absence of visual field abnormalities or optic disc changes.
• Risk of developing glaucoma increases with rising IOP, increasing age, positive family history of glaucoma, myopia, diabetes, cardiovascular diseases, blacks, and the presence of disc hemorrhages.

• An ophthalmological emergency.
• Occurs when the iris occludes the angle (ex. In iris bombe or phacomorphic glaucoma) in eyes with narrow angles (ex. High hyperopes).
• Symptoms include sudden onset of severe eye pain and blurring of vision, halos around objects, headache, nausea and vomiting.
• Signs include:
• Increased IOP
• Shallow anterior chamber
• Edematous cornea
• Fixed mid-dilated pupil
• Ciliary injection
• Treatment: Acetazolamide

Topical beta blockers: timolol

IV mannitol

Cycloplegics: (if angle closure is secondary to anterior lens displacement ) to relax the ciliary muscle and tighten the zonular apparatus in order to draw the lens backwards.

Pilocarpine: in primary acute angle closure glaucoma

Peripheral iridotomy once the pressure is controlled, to prevent further attacks. It should be performed on the fellow eye as well.

Types: 1) Primary congenital glaucoma

1. Anterior Segment Developmental Anomalies (associated with congenital glaucoma ex. Axenfeld’s syndrome, Rieger’s syndrome)
2. Associated with other ocular or extraocular anomalies.

• Pathology: Arrest of development of the anterior chamber angle structures.
• Manifests at birth in 50% of patients but most patients present between the age of 3 and 9 months.
• Symptoms include:
• Epiphora (most common and earliest sign)
• Photophobia
• High IOP
• Corneal opacities
• Buphthalmos

• Differential includes nasolacrimal duct obstruction, corneal opacities secondary to other causes such as congenital dystrophies, mucopolysaccharidoses, and traumatic rupture of Descemet’s membrane (birth trauma) as well as megalocornea.

• Treatment: If early presentation à Goniotomy (may be repeated)

If late presentation à Trabeculectomy

• Both topical and periocular steroids can cause glaucoma in susceptible individuals (systemic steroids less likely)
• IOP decreases once the drug is discontinued
• The pressure rises because of an increased resistance to the outflow of aqueous due to deposition of glycosaminoglycans in the trabecular tissues that blocks outflow.
• Newer generations of topical steroids (ALREX, LOTEMAX) have a much lesser tendency to raise IOP.