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Glaucoma: The Perils of High Pressure

Gary M. Levin, M.D.

Dr. Levin is Clinical Assistant Professor, Department of Ophthalmology, Loma Linda University.

Within the past three years, Dr. Levin reports no commercial conflict of interest.


It's possible you may be going blind and don't even realize it. A leading cause of irreversible blindness, glaucoma, can happen without any noticeable warning signs or symptoms. Because doctors now have very effective technologies for early diagnosis, as well as new medicines and high-tech treatments (such as lasers), much can be done to slow down and control glaucoma in most patients before vision is permanently damaged. But early diagnosis is critical.

What Is Glaucoma?
The eyeball is bathed by fluid ("aqueous humor") that is produced by cells behind the colored part of the eye ("iris"). Not only does the fluid wash the eye but it helps the eye maintain its shape. When there is either over-production of aqueous humor or problems with the outflow drainage channels, the presence of too much fluid causes the pressure in the eye ("intraocular pressure") to rise. At the back of the eye sits the optic nerve, which connects to the brain and is the key component of sight. High intraocular pressure can permanently damage the optic nerve and result in vision loss. Glaucoma is the name given to the group of diseases that usually involve high intraocular pressure and produce optic nerve damage.

There are two main types of glaucoma -- open angle and closed angle. In typical open angle glaucoma,1 the outflow channels become blocked over time with aging or other disease processes. In closed angle glaucoma, the blockage occurs suddenly, raising the eye pressure rapidly. This is a true medical emergency requiring immediate treatment. Though eye pressure is not connected to blood pressure, the presence of high blood pressure can worsen the harmful effects of elevated intraocular pressure.

Glaucoma is frequently a complication of changes in the blood supply to the eye such as from a blocked central vein, diabetes and/or multiple surgical interventions. Tumors and some medicines (for example, antihistamines and H2 antagonists to reduce stomach acids) may worsen chronic open angle glaucoma. Severe acute angle closure glaucoma and acute myopia have been reported with topimarate, a drug used to treat epilepsy. The use of oral, injectable and inhaled corticosteroids causes an elevation of intraocular pressure in about 15% of the normal population. Medications prescribed for a variety of conditions (e.g., depression, allergies, Parkinson's Disease) can produce pupillary dilation and initiate an attack of acute angle-closure glaucoma in patients who have eyes with narrow angles.

Diagnosing Glaucoma
We know that certain populations are at higher risk of visual field loss from optic nerve damage. Hispanics, African Americans, patients with diabetes and patients who also have high blood pressure2 all are at greater risk of glaucomatous visual field loss. Ophthalmologists now define glaucomatous visual field loss as a loss of peripheral vision. While we are born with approximately one million optic nerve fibers, the classic early visual field loss occurs only after half of these fibers are lost.

To make the diagnosis of glaucoma, it is necessary to measure intraocular pressure. It is now also standard practice to measure corneal thickness in all glaucoma suspect patients. The cornea is the transparent covering of the front of the eye. The measurement takes about 30 seconds or less.3 The eye doctor will also shine a light in your eye with an ophthalmoscope and examine your retina, which is at the back of your eye, and specifically look at the optic disc (the head of the optic nerve) to see if any signs of damage are present. Damage to the optic nerve is called "cupping" and, if present, the doctor will measure and compare the optic nerve of the right eye and the left eye. The doctor will also plot your field of vision, carefully recording gaps in the field of vision for future comparison.

Signs and Symptoms of Angle Closure Glaucoma
The very sudden sudden and extreme rise in intraocular pressure is the significant event that defines angle closure glaucoma. Associated symptoms -- headache at the front of the head, halos around lights, nausea -- do not, however, always precede the attack. A small eye may be seen since the front of the eye, because of the increased pressure, is smaller, or crowded. A red eye with pain and a mid-sized fixed pupil are also very suspicious of this event. Intraocular pressures will often exceed 50 mm of mercury and this is a true medical emergency to be treated medically with a laser or surgically making a slit to allow drainage.

Medical Treatment
Doctors now prescribe prostaglandin agonists [bimataprost, latanaprost (Xalatan), travoprost (Travatan)] which lower eye pressure by increasing the fluid outflow.4,5 Beta-blocking agents, e.g., timolol (Timoptic) are also used as first- or second-line drugs.6 The beta-blockers act by decreasing aqueous production, increasing outflow and modifying blood flow to the eye.7 The selective beta-blocking agents, e.g., betaxolol (Betoptic), although less likely to cause bothersome side effects, still have some risk of causing problems in patients with bronchial disorders.

Topical carbonic acid anhydrase enzyme inhibitors such as dorzolamide hydrochloride (Trusopt) can be applied directly to the eye as a drop. Topical application of these agents has reduced side effects. (When administered systemically, these drugs can result in mood change and other side effects.) Combination drugs incorporating prostaglandin agonists, carbonic acid anhydrase inhibitors and/or beta-blockers are now commonly used as well.8,9 The efficacy and duration of these drugs have been enhanced so that once a day or twice a day dosage is often sufficient to maintain control.

It should be remembered that although these medications are given topically, there is some absorption into the bloodstream via the nasal passages, and a topically applied beta-blocker or carbonic acid anhydrase inhibitor have been known to create depression, behavioral changes or other reactions. The prostaglandin agonists are usually given only once a day at bedtime. One of their effects is vascular dilation, causing a red eye, and there have been reported cases of iris color darkening.10

Laser Treatments
Argon Laser Trabeculoplasty (ALT) is now being replaced by Selective Laser Trabeculoplasty (SLT).11,12 Both treatments focus laser energy on the delicate drainage meshwork of the eye, thereby increasing outflow of aqueous humor and thus lowering IOP. Because of its wavelength, Selective Laser Trabeculoplasty causes less injury to the meshwork.13

Surgical Treatment
If it is not possible to maintain a relatively normal IOP with multiple medications (or if patient compliance is poor) and when single or multiple laser treatments have also failed, filtering surgery may be needed. Filtering procedures can be divided into non-penetrating and penetrating. In the non-penetrating viscocanaliculostomy, a procedure used in Europe much more than the United States, surgeons place an opening into the front of the eye and insert a tube to help drainage. In the penetrating trabeculectomy, more extensive surgery is done to create a surgical "bleb" (blister) that functions as a drainage vehicle.

The long-term risks from the filtering surgery include leaking of the filtering bleb and/or blebitis, a potential infection that can evolve into blindness.14 All of these risks can be managed successfully with careful follow-up.

Patient Education
As with most diseases, patient education, a lifelong learning process, should be the main focus for patients with glaucoma. Unfortunately, there is little factual knowledge as to how to prevent glaucoma. Nevertheless, in the early stages, maintenance therapy can be expected to prevent further damage over a lifetime.

The key phrase is "early detection." A visual field that has been lost only very rarely returns. Once damage has occurred, it seems that the optic nerve becomes even more sensitive to changes in intraocular pressure. Emphasis on regular examination of the visual field and IOP checks, compliance with medication and proper training of use of eye drops [How to use eyedrops (streaming media will open in a new window.)] are very important. Proper diet and exercise in maintaining good health and elimination or reduction of tobacco use are also important. In addition, the patient should educate and inform their children and other family members about their condition as there is strong inheritance of glaucoma.

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References
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2. Denis P. Effect of intraocular pressure and arterial blood pressure variations on glaucoma progression. J Fr Ophtalmol. 2004 Sep;27 Spec No 2:2S27-2S32. Review. French. PMID: 15314572 [PubMed - indexed for MEDLINE]. return

3. Dave H, Kutschan A, Pauer A, Wiegand W. Measurement of corneal thickness in glaucoma patients. Ophthalmologe. 2004 Sep;101(9):919-24. German. PMID: 14999420 [PubMed - in process]. return

4. Katz LJ. Bimatoprost: establishing its role in glaucoma management. Surv Ophthalmol. 2004 Mar;49 Suppl 1:S1-4. Review. No abstract available. PMID: 15016555 [PubMed - indexed for MEDLINE]. return

5. Costagliola C, Parmeggiani F, Sebastiani A. Assessing the cost-effectiveness of switching from a beta-blocker to latanoprost in the treatment of ocular hypertension. Expert Opin Pharmacother. 2003 Oct;4(10):1775-88. Review. PMID: 14521487 [PubMed - indexed for MEDLINE]. return

6. Kosman ME. Timolol in the treatment of open angle glaucoma. JAMA. 1979 May 25;241(21):2301-3. PMID: 439303 [PubMed - indexed for MEDLINE]. 2003 Oct; 95(10): 986-90. return

7. Zimmerman TJ, Harbin R, Pett M, Kaufman HE. Timolol and facility of outflow. Invest Ophthalmol Vis Sci. 1977 Jul;16(7):623-4. No abstract available. PMID: 873723 [PubMed - indexed for MEDLINE]. return

8. Hamacher T, Schinzel M, Scholzel-Klatt A, Neff HM, Maier H, Schlaffer G, Beausencourt E, Jutte M, Scholz R, Lorger C, Stewart WC. Short term efficacy and safety in glaucoma patients changed to the latanoprost 0.005%/timolol maleate 0.5% fixed combination from monotherapies and adjunctive therapies. Br J Ophthalmol. 2004 Oct;88(10):1295-8. return

9. Fechtner RD, Realini T. Fixed combinations of topical glaucoma medications. Curr Opin Ophthalmol. 2004 Apr;15(2):132-5. Review. PMID: 15021225 [PubMed - indexed for MEDLINE]. return

10. Chou SY, Chou CK, Kuang TM, Hsu WM. Incidence and severity of iris pigmentation on latanoprost-treated glaucoma eyes. Eye. 2004 Sep 3; [Epub ahead of print] PMID: 15359238 [PubMed - as supplied by publisher]. return

11. Gierek-Lapinska A, Leszczynski R. [Laser therapy in the treatment of glaucoma] Klin Oczna. 2004;106(1-2 Suppl):269-72. Polish. PMID: 15510522 [PubMed - in process]. return

12. Gracner T, Pahor D, Gracner B. [Efficacy of selective laser trabeculoplasty in the treatment of primary open-angle glaucoma] Klin Monatsbl Augenheilkd. 2003 Dec;220(12):848-52. German. PMID: 14704942 [PubMed - indexed for MEDLINE]. return

13. Cvenkel B, Hvala A, Drnovsek-Olup B, Gale N. Acute ultrastructural changes of the trabecular meshwork after selective laser trabeculoplasty and low power argon laser trabeculoplasty. Lasers Surg Med. 2003;33(3):204-8. PMID: 12949951 [PubMed - indexed for MEDLINE]. return

14. Lehmann OJ, Bunce C, Matheson MM, Maurino V, Khaw PT, Wormald R, Barton K. Risk factors for development of post-trabeculectomy endophthalmitis. Br J Ophthalmol. 2000 Dec;84(12):1349-53. PMID: 11090471 [PubMed - indexed for MEDLINE]. return




  

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