be included in the therapeutic decision process because sometimes the major negative effect of glaucoma (especially early in the disease) may be from the treatment rather than the condition. Therapeutic goals and potential side effects and complications of each alternative of treatment should be discussed. Patient preferences should be sought.

Patients should be taught how to use eyedrops and about punctal occlusion and eyelid closure to minimize systemic side effects.The treating physician should encourage each patient to discuss possible side effects and effects on quality of life. Patients may not associate systemic side effects with eyedrop therapy or may be reluctant to mention such delicate issues as impotence or decreased libido with a busy eye doctor. An atmosphere of openness and partnership should be established from the beginning.

Patients with primary types of glaucoma also need to be reminded and re-reminded of the fact that their blood relatives, especially siblings, parents, and children are at increased risk of developing the disease and need to be screened at appropriate intervals to catch the onset at the earliest feasible point since progression is related to the degree of damage at onset.

Effective judgment

Society is demanding more of physicians than ever before. In these days of cost containment and spiraling utilization of newer and

better medical techniques, it is the physician’s responsibility to provide excellent and efficient care for each patient. The pressures of outside influences, such as managed care organizations, should not prevent the most effective care – cost and efficiency are important, but not the only considerations. By reducing the use of medical resources for those patients whose disease is well controlled and slowly (if at all) progressive, more resources can be directed toward patients whose conditions are uncontrolled or who face an imminent threat to their vision. It is a challenging but rewarding effort to tailor care to fit the patient’s needs.

The treating doctor also needs to be an advocate for the patient in several different arenas. Often, social circumstances prevent optimal care of glaucoma. A sick spouse at home, solitary living, multiple system diseases, and economic constraints are examples of situations that often impede glaucoma care. The physician should make him or herself aware of these and do his/her best to find accommodations for the patient such as social services and help with medication expenses, travel to and from medical offices, and physical disabilities. Written instructions regarding medicines are often very helpful especially if the patient has to juggle multiple medications for different diseases. The physician should be aware of bureaucratic and healthcare management hindrances to patient care and intervene with phone calls or letters as needed. Finally, physicians might consider the larger picture and become involved on the national or even international scene to help improve health care for all.

References

1.McNaught AI, et al:Accuracy and implications of a reported family history of glaucoma: experience from the Glaucoma Inheritance Study in Tasmania,Arch Ophthalmol 118:900, 2000.

2.Gordon MO, et al:The Ocular Hypertension Treatment Study: baseline factors that predict the onset of primary open-angle glaucoma,Arch Ophthalmol 120:714, 2002.

3.Tielsch JM, et al: Racial variations in the prevalence of primary open-angle glaucoma.The Baltimore Eye Survey, JAMA 266:369, 1991.

4.Sommer A, et al: Racial differences in the causespecific prevalence of blindness in east Baltimore, N Engl J Med 325:1412, 1991.

5.Rudnicka AR, et al: Variations in primary openangle glaucoma prevalence by age, gender, and race: a Bayesian meta-analysis, Invest OphthalmolVis Sci 47:4254, 2006.

6.Varma R, et al: Los Angeles Latino Eye Study Group: Prevalence of open-angle glaucoma and ocular hypertension in Latinos: the Los Angeles Latino Eye Study, Ophthalmology 111:1439, 2004.

 7. Nguyen N, et al:A high prevalence of occludable angles in aVietnamese population, Ophthalmology 103:1426, 1996.

 8. Seah SK, et al: Incidence of acute primary angleclosure glaucoma in Singapore.An island-wide survey,Arch Ophthalmol 115:1436, 1997.

 9. Hoskins HD Jr: Definition, classification and management of the glaucoma suspect. Proceedings from the New Orleans Academy of Ophthalmology

Glaucoma Symposium, St Louis, Mosby, 1980.

10.European Glaucoma Prevention Study (EGPS) Group; Miglior S, et al: Predictive factors for open-angle glaucoma among patients with ocular hypertension in the European Glaucoma Prevention Study, Ophthalmology 114:3, 2007. Epub Oct 27, 2006.

11.Mansberger SL:A risk calculator to determine the probability of glaucoma, J Glaucoma 13:345, 2004.

12.Ocular Hypertension Treatment Study Group; European Glaucoma Prevention Study Group; Gordon MO, et al: Validated prediction model for the development of primary open-angle glaucoma in individuals with ocular hypertension, Ophthalmology 114:10, 2007. Epub Nov 7, 2006.

13.Sommer A, et al: Relationship between intraocular pressure and primary open angle glaucoma among

white and black Americans.The Baltimore Eye Survey,Arch Ophthalmol 109:1090, 1991.

14.Kass MA: Compliance and prognosis in glaucoma (editorial),Arch Ophthalmol 103:504, 1985.

15.Kass MA, et al: Compliance with topical timolol treatment,Am J Ophthalmol 103:188, 1987.

16.Realini T, et al:The uniocular drug trial and second-eye response to glaucoma medications, Ophthalmology 111:421, 2004.

17.Richardson JT: Medical and surgical decisions in chronic glaucomas. In: Heilman K, editor: Glaucoma: conceptions of a disease, Stuttgart,Thieme, 1976.

18.Chandler PA: Long-term results in glaucoma therapy, Am J Ophthalmol 49:221, 1960.

19.Abedin S, Simmons RJ, Grant WM: Progressive lowtension glaucoma: treatment to stop glaucomatous cupping and field loss when these progress despite normal intraocular pressure, Ophthalmology 89:1, 1982.

20.Glaucoma Laser Trial Research Group:The Glaucoma Laser Trial (GLT) and Glaucoma Laser Trial Follow-up Study: 7. Results,Am J Ophthalmol 120:718, 1995.

21.The AGIS Investigators:The Advanced Glaucoma Intervention Study (AGIS): 7:The relationship between control of intraocular pressure and visual field deterioration,Am J Ophthalmol 130:429, 2000.

The ultimate goal of glaucoma treatment is to preserve enough vision during the patient’s lifetime to meet their functional needs; ideally, treatment should also delay, stop,1 and sometimes reverse2 the damage to the optic nerve and ganglion cell layer caused by the glaucomatous process. The only way currently proven to slow or stop damage from progressing is to reduce intraocular pressure (IOP) below the level that will cause continued damage to the optic nerve. Although a medication that would directly protect the optic nerve or reverse the damage from glaucoma would be most welcome, no such medication has yet been proven to be effective. Medications that have some promise in this regard are discussed in a later chapter.

Although the concept that lowering IOP truly helps prevent or reduce glaucomatous damage has been called into question,3 the overwhelming majority of studies produce evidence that lowering IOP is indeed beneficial.4,5 As has been noted in Chapters 17 and 21, animal studies and secondary glaucomas clearly point to IOP as an important risk factor, if not a causal factor. Other studies strongly suggest that the lower the IOP, the less likely optic nerve damage is to develop or progress.6–8 Some of these same data indicate that past efforts to lower IOP into the ‘normal’ range of 21 mmHg or lower may have been inadequate and that ‘control’ really means an IOP of less than 15 or 16 mmHg, especially in advanced glaucoma. One recent long-term study showed that lowering IOP in normal-pressure glaucoma by at least 30% protects at least some patients from progression.9 The issue has been put to rest by the publication of four long-term, controlled trials that conclusively show that lowering IOP will slow or delay the appearance or progression of glaucomatous damage; these include the Ocular Hypertension Treatment Study (OHTS),10 the Advanced Glaucoma Intervention Study (AGIS),11 the Collaborative Normal-Tension Glaucoma Study (CNTGS),9 and the Early Manifest Glaucoma Trial (EMGT).12 Many of these studies have helped to identify risk factors that auger progression within fully manifest glaucoma and from ocular hypertension to manifest glaucoma. These risk factors are outlined in Boxes 22-1 and 22-2. Fluctuation of IOP has also been identified as an important risk factor for progression.13,14

Box 22-1  Risk factors for progression from ocular hypertension to manifest glaucoma

Corneal thickness under 535 microns Elevated IOP

Increasing age

Enlarged vertical cup-to-disc ratio

Increased pattern standard deviation on static threshold perimetry

Box 22-2  Risk factors for progression of manifest glaucoma

Established

Elevated IOP

Over 18 mmHg any of the time

Increased fluctuation of IOP

Increasing age

Exfoliation of the lens capsule

Advanced cupping

Advanced visual field loss

Putative

Sleep apnea

Thin corneas

Nocturnal systemic hypotension

In approaching the treatment of someone who has glaucoma or who is at such high risk for its development that treatment is in order, many issues have to be considered. Among these are the level of IOP at which damage has occurred (or is likely to occur), the age of the patient, the degree of cupping and visual field loss, the presence of secondary features such as signs of exfoliative disease or pigmentary dispersion, systemic conditions or medications that might intereact with glaucoma progression or treatment, social issues such as presence or absence of support systems, and economic issues. Most physicians today try to tailor therapy to the individual patient and his or her situation. Many find it useful to estimate and then aim for a ‘target pressure.’

Target pressure

The concept of target pressure arose from the observation that progression in advanced glaucoma, and occasionally even in early glaucoma, often occurs at what are thought to be ‘physiologic’ pressures. An IOP of 21 mmHg or lower – the previously sought goal – may not be low enough for many glaucomatous eyes. This observation was supported by the findings of the AGIS study which showed that the risk of progression was greatly reduced if all IOPs were under 18 mmHg.11 The goal should be to lower the IOP to a level that is ‘safe’ for that particular eye. Because our current knowledge does not indicate with any certainty what a safe IOP level may be for any given patient, the target pressure is estimated for each patient based on initial IOP, degree of existing damage, how hard the patient has