glaucoma-before

Without Glaucoma

glaucoma-after

With Glaucoma

Glaucoma is a group of diseases of the optic nerve involving loss of retinal ganglion cells in a characteristic pattern of optic neuropathy.  Although raised intraocular pressure is a significant risk factor for developing glaucoma, there is no set threshold for intraocular pressure that causes glaucoma.  One person may develop nerve damage at a relatively low pressure, while another person may have high eye pressure for years and yet never develop damage.  Untreated glaucoma leads to permanent damage of the optic nerve and resultant visual field loss, which can progress to blindness.

Glaucoma has been nicknamed “the silent sight thief”.  Worldwide, it is the second leading cause of blindness.  Glaucoma affects one in two hundred people aged fifty and younger and one in ten over the age of eighty.

 

  1. Risk Factors

    People with a family history of glaucoma have about a six percent chance of developing glaucoma.  Diabetics and African Americans are three times more likely to develop primary open angle glaucoma.  Asians are susceptible to angle-closure glaucoma, and Inuit have a twenty to forty times higher risk than caucasians of developing primary angle closure glaucoma.  Women are three times more likely than men to develop acute angle-closure glaucoma due to their shallower anterior chambers.  Use of steroids can also cause glaucoma.

    There is increasing evidence of ocular blood flow to be involved in the pathogenesis of glaucoma.  Current data indicate that fluctuations in blood flow are more harmful in glaucomatous optic neuropathy than steady reductions.  Unstable blood pressure and dips are linked to optic nerve head damage and correlate with visual field deterioration.

    A number of studies also suggest that there is a correlation, not necessarily causal, between glaucoma and systemic hypertension (i.e. high blood pressure).  In normal tension glaucoma, nocturnal hypotension may play a significant role.  On the other hand there is no clear evidence that vitamin deficiencies cause glaucoma in humans, nor that oral vitamin supplementation is useful in glaucoma treatment.

    Those at risk for glaucoma are advised to have a dilated eye examination at least once a year.

  2. Diagnosis

    Screening for glaucoma is usually performed as part of a standard eye examination performed by your optometrist.  Testing for glaucoma should include measurements of the intraocular pressure via tonometry, changes in size or shape of the eye, and an examination of the optic nerve to look for any visible damage to it, or change in the cup-to-disc ratio.  If there is any suspicion of damage to the optic nerve, a formal visual field test should be performed.  Scanning laser ophthalmoscopy may also be performed.
  3. Treatment

    Although intraocular pressure is only one major risk factors of glaucoma, lowering it via pharmaceuticals or surgery is currently the mainstay of glaucoma treatment.  In Europe, Japan and Canada laser treatment is often the first line of therapy. In the U.S., adoption of early laser has lagged, even though prospective, multi-centered, peer-reviewed studies, since the early '90s, have shown laser to be at least as effective as topical medications in controlling intraocular pressure and preserving visual field.
  4. Drugs

    Intraocular pressure can be lowered with medication, usually eye drops.  There are several different classes of medications to treat glaucoma with several different medications in each class.

    Each of these medicines may have local and systemic side effects.  Adherence to medication protocol can be confusing and expensive; if side effects occur, the patient must be willing either to tolerate these, or to communicate with the treating physician to improve the drug regimen.

    Poor compliance with medications and follow-up visits is a major reason for vision loss in glaucoma patients. Patient education and communication must be ongoing to sustain successful treatment plans for this lifelong disease with no early symptoms.

    The possible neuroprotective effects of various topical and systemic medications are also being investigCommonly used medications

    • Prostaglandin analogs like latanoprost (Xalatan), bimatoprost (Lumigan) and travoprost (Travatan) increase uveoscleral outflow of aqueous humor.
    • Topical beta-adrenergic receptor antagonists such as timolol, levobunolol (Betagan), and betaxolol decrease aqueous humor production by the ciliary body.
    • Alpha2-adrenergic agonists such as brimonidine (Alphagan) work by a dual mechanism, decreasing aqueous production and increasing uveo-scleral outflow.
    • Less-selective sympathomimetics like epinephrine and dipivefrin (Propine) increase outflow of aqueous humor through trabecular meshwork and possibly through uveoscleral outflow pathway, probably by a beta2-agonist action.
    • Miotic agents (parasympathomimetics) like pilocarpine work by contraction of the ciliary muscle, tightening the trabecular meshwork and allowing increased outflow of the aqueous humour.
    • Carbonic anhydrase inhibitors like dorzolamide (Trusopt), brinzolamide (Azopt), acetazolamide (Diamox) lower secretion of aqueous humor by inhibiting carbonic anhydrase in the ciliary body.


  5. Surgery

    Conventional surgery to treat glaucoma makes a new opening in the meshwork.  This new opening helps fluid to leave the eye and lowers intraocular pressure.

    Surgery is the primary therapy for those with congenital glaucoma.  Both laser and conventional surgeries are performed.  Generally, these operations are a temporary solution, as there is no cure for glaucoma as of yet.

  6. Canaloplasty

    Canaloplasty is an advanced, nonpenetrating procedure designed to enhance and restore the eye's natural drainage system to provide sustained reduction of IOP.  Canaloplasty utilizes breakthrough microcatheter technology in a simple and minimally invasive procedure.  To perform a canaloplasty, a doctor will create a tiny incision to gain access to a canal in the eye.  A microcatheter will circumnavigate the canal around the iris, enlarging the main drainage channel and its smaller collector channels through the injection of a sterile, gel-like material called viscoelastic.  The catheter is then removed and a suture is placed within the canal and tightened. By opening the canal, the pressure inside the eye will be relieved.
  7. Laser Surgery

    Laser trabeculoplasty may be used to treat open angle glaucoma.  It is a temporary solution, not a cure.  A 50 μm argon laser spot is aimed at the trabecular meshwork to stimulate opening of the mesh to allow more outflow of aqueous fluid.  Usually, half of the angle is treated at a time.  Traditional laser trabeculoplasty utilizes a thermal argon laser.  The procedure is called argon laser trabeculoplasty or ALT.  A newer type of laser trabeculoplasty uses a "cold" (non-thermal) laser to stimulate drainage in the trabecular meshwork.  This newer procedure is call selective laser trabeculoplasty or SLT.  Studies show that SLT is as effective as ALT at lowering eye pressure.  In addition, SLT may be repeated three to four times, whereas ALT can usually be repeated only once.

    Laser peripheral iridotomy may be used in patients susceptible to or affected by angle closure glaucoma.  During laser iridotomy, laser energy is used to make a small full-thickness opening in the iris.  This opening equalizes the pressure between the front and back of the iris, causing the iris to move backward.  This uncovers the trabecular meshwork. In some cases of intermittent or short-term angle closure this may lower the eye pressure.  Laser iridotomy reduces the risk of developing an attack of acute angle closure.  In most cases it also reduces the risk of developing chronic angle closure or gradual adhesion of the iris to the trabecular meshwork.

  8. Risk Factors

    The most common conventional surgery performed for glaucoma is the trabeculectomy.  Here, a partial thickness flap is made in the scleral wall of the eye, and a window opening made under the flap to remove a portion of the trabecular meshwork.  The scleral flap is then sutured loosely back in place.  This allows fluid to flow out of the eye through this opening, resulting in lowered intraocular pressure and the formation of a bleb or fluid bubble on the surface of the eye.  Scarring can occur around or over the flap opening, causing it to become less effective or lose effectiveness altogether.  One person can have multiple surgical procedures of the same or different types.
  9. Glaucoma Drainage Implants

    There are also several different glaucoma drainage implants.  These include the original Molteno implant (1966), the Baerveldt tube shunt, or the valved implants, such as the Ahmed glaucoma valve implant or the ExPress Mini Shunt and the later generation pressure ridge Molteno implants.  These are indicated for glaucoma patients not responding to maximal medical therapy, with previous failed guarded filtering surgery (trabeculectomy).  The flow tube is inserted into the anterior chamber of the eye and the plate is implanted underneath the conjunctiva to allow flow of aqueous fluid out of the eye into a chamber called a bleb.
  10. Primary Glaucoma and its Variants

    Primary Glaucoma

    • Primary open-angle glaucoma, also known as chronic open-angle glaucoma, chronic simple glaucoma, glaucoma simplex
    • Low-tension glaucoma
    • Primary angle-closure glaucoma, also known as primary closed-angle glaucoma, narrow-angle glaucoma, iris-block glaucoma, acute congestive glaucoma
    • Acute angle-closure glaucoma
    • Chronic angle-closure glaucoma
    • Intermittent angle-closure glaucoma
    • Superimposed on chronic open-angle closure glaucoma (combined mechanism)


    Variants of Primary Glaucoma

    • Pigmentary glaucoma
    • Exfoliation glaucoma, also known as pseudoexfoliative glaucoma or glaucoma capsulare


    Developmental Glaucoma

    • Primary congenital glaucoma
    • Infantile glaucoma
    • Glaucoma associated with hereditary of familial diseases


    Secondary Glaucoma

    • Inflammatory glaucoma
    • Uveitis of all types
    • Fuchs heterochromic iridocyclitis
    • Phacogenic glaucoma
    • Angle-closure glaucoma with mature cataract
    • Phacoanaphylactic glaucoma secondary to rupture of lens capsule
    • Phacolytic glaucoma due to phacotoxic meshwork blockage
    • Subluxation of lens
    • Glaucoma secondary to intraocular hemorrhage
    • Hyphema
    • Hemolytic glaucoma, also known as erythroclastic glaucoma
    • Traumatic glaucoma
    • Angle recession glaucoma: Traumatic recession on anterior chamber angle
    • Postsurgical glaucoma
    • Aphakic pupillary block
    • Ciliary block glaucoma
    • Neovascular glaucoma
    • Drug-induced glaucoma
    • Corticosteroid induced glaucoma
    • Alpha-chymotrypsin glaucoma.  Postoperative ocular hypertension from use of alpha chymotrypsin.
    • Glaucoma of miscellaneous origin
    • Associated with intraocular tumors
    • Associated with retinal deatchments
    • Secondary to severe chemical burns of the eye
    • Associated with essential iris atrophy