Indian Journal of Ophthalmology

EDITORIAL
Year
: 2001  |  Volume : 49  |  Issue : 2  |  Page : 79--80

Glaucoma therapy: "Above all do no harm"


G Chandra Sekhar 
 VST Center for Glaucoma Care, LV Prasad Eye Institute, LV Prasad Marg, Banjara Hills, Hyderabad - 500 034, India

Correspondence Address:
G Chandra Sekhar
VST Center for Glaucoma Care, LV Prasad Eye Institute, LV Prasad Marg, Banjara Hills, Hyderabad - 500 034, India




How to cite this article:
Sekhar G C. Glaucoma therapy: "Above all do no harm".Indian J Ophthalmol 2001;49:79-80


How to cite this URL:
Sekhar G C. Glaucoma therapy: "Above all do no harm". Indian J Ophthalmol [serial online] 2001 [cited 2020 Apr 1 ];49:79-80
Available from: http://www.ijo.in/text.asp?2001/49/2/79/22653


Full Text

Primary open-angle glaucoma (POAG) is an asymptomatic disease. Because of this the compliance to therapy is suboptimal. Since this is a potentially blinding disease and evidence suggests that surgical therapy is better than medical therapy, there is an argument in favour of surgical intervention once the diagnosis is established. With the advances in psychophysical tests, imaging of the optic nerve head and nerve fibre layer analysis, we feel equipped to diagnose the disease even before the visual field defect is detected on "white-on-white perimetry" (WWP). This is reassuring since 20-40% of the retinal ganglion cells could be lost before a visual field defect develops.[1] The WWP is considered the gold standard. Then one can argue that if there is an abnormality on Heidelberg Retina Tomogram or Nerve Fiber Analyzer, or if there is a defect on "blue on yellow perimetry" (Short Wavelength Automated Perimetry - SWAP) or "frequency doubling perimetry" (FDP), despite the WWP being normal, there is significant retinal ganglion cell loss and therapy is required. The intraocular pressure (IOP) then needs to be reduced by at least 30% as shown by the normal tension group (NTG) study,[2] to prevent further loss. The best way to achieve this would be by a pharmacologically modulated trabeculectomy. The logic seems reasonable, doesn't it? However, science is often counterintuitive and before we succumb to this logic we need to re-examine the goals of glaucoma therapy, and examine the risk of treatment as opposed to its benefits.

The goal of glaucoma therapy is not treat the IOP nor the disc, not even the visual field. The goal is to ensure that the patient has good functional vision for the duration of his/her lifetime while maintaining the quality of life. The quality of life in glaucoma is affected not just by the loss of vision but also by the fear of potential blindness before the disease produces any visual disability. It is essential to note that a false diagnosis, or even a diagnosis of "glaucoma suspect" can lead to "labeling" and psychological problems, which translate into functional problems and a lack of well being. Early diagnosis in a nonprogressive disease or a slowly progressive disease, especially one for which safe and effective treatment is not available, only increases the "duration" of the disease (lead-time bias) and the duration of this psychological worry for the patient. Our treatment is aimed at preventing the visual disability but could also affect the quality of life. This is affected by the need for multiple medications, the side effects of the medications or surgical complications that may reduce vision. While the risks of many of the therapeutic regimens are reported in literature, the benefit from therapy is not always unequivocal.

The natural course of the disease is not known. The rate of ganglion cell loss and functional decay varies across individuals. To preserve the quality of life, patients must remain above the threshold of significant functional impairment throughout their life. While the natural course of the disease in some individuals allows them to remain above this line with or without treatment, in others the disease has a steep downhill course and unless appropriately treated such patients could be visually disabled during a significant part of their lifetime. It is our responsibility to differentiate these two groups of patients to the best of our ability. The amount of damage at the time of diagnosis, the rate of disease progression and the life expectancy of the patient are variables that need to be considered in deciding the aggressiveness of therapy in a given glaucoma patient. For example, there is no need to be aggressive with therapy in a 75-year-old patient with multiple systemic diseases and bilateral POAG with early arcuate scotoma; on the other hand, a healthy 45-year-old patient with high IOP, suspicious discs, repeatable abnormality on SWAP and a family history of glaucoma may be a strong candidate for therapy at least in one eye.

Evaluating progression of visual damage by clinical assessment of the optic nerve head and visual fields continues to be a difficult task despite the advances in these areas.[3] Currently close follow-up using these methods is the only way of measuring of the rate of visual function decay in a given patient. One needs to be cautious about interpreting the changes in numbers generated by new technologies as true disease (or progression) unless they are confirmed by comparison to the gold standard. As of now this validation for earlier diagnosis has been done for SWAP only. Small changes in the early stages of the disease with no significant damage may be innocuous but similar changes among patients with advanced damage would warrant aggressive therapy.

Medical and surgical lowering of IOP is a common, time honoured practice. But it is not unquestioned. While there are reports linking IOP to glaucomatous damage,[4] there are also others that do not find a correlation between the level of IOP and the amount of visual field damage.[5]

There have been two major multicentre trials that have assessed the benefit of IOP reduction in the natural course of POAG - the Collaborative NTG study and the Advanced Glaucoma Intervention Study (AGIS).[2,6] Both studies have shown a protective effect of IOP reduction on stability of the visual field. Attempts to reduce the IOP surgically in the NTG study were associated with increased cataract formation and reduced vision. The benefit of IOP reduction on the visual field was evident only after the eyes that developed cataract were excluded from the analysis. An analysis of the natural course of NTG by the study group showed that only half the cases showed a confirmed localized visual field deterioration by seven years. The changes were typically small and slow; they were often insufficient to measurably affect the mean defect index.[7] This observation is important in deciding on therapy in these patients.

In both the AGIS and the NTG studies the benefit of the therapy was not seen in hundred percent of the subjects. In clinical practice we come across patients who fail to achieve the desired IOP despite multiple surgeries or medications. There are also patients who achieve the desired response in IOP control, but the field damage is not arrested. This observation supports Van Buskirk's comment that the sensitivity of the optic nerve head to IOP-induced damage varies widely from none to maximal.[8] Currently there is no definitive means of either assessing the sensitivity of the optic nerve head to the IOP induced damage or of differentiating the subgroup of glaucoma patients where IOP is not a contributing factor for the disc damage. Hence all glaucoma patients are subjected to the available means of reducing IOP. In patients whose optic nerves are insensitive to IOP- induced damage some therapeutic interventions such as the mitomicin-C augmented filtering surgery to lower the IOP could actually be worse than the natural course of the disease.

In conclusion, the physician should consider the amount of visual damage and the rate of progression of the disease along with the patient's age and life expectancy in deciding the appropriate therapy for arresting the disease in a patient with POAG. One must also remember that in some patients IOP is not a risk factor and the disease will progress despite achieving the target IOP. If clinical trials demonstrate their efficacy, neuro-protective agents may in future help to arrest the disease.

References

1Quigley HA, Durkelseya GR, Green WR. Retinal ganglion cell atrophy correlated with automated perimetry in human eyes with glaucoma. Am J Ophthalmo 1989;107:453-64.
2Collaborative Normal Tension Glaucoma Study Group. The effectiveness of intraocular pressure reduction in the treatment of normal tension glaucoma. Am J Ophthalmol 1998;126:498-505.
3Schulzer M. The normal-tension glaucoma study group. Errors in the diagnosis of visual field progression in normal tension glaucoma. Ophthalmology 1994;101:1589-95.
4Cartiwright MJ, Anderson DR. Correlation of asymmetric damage with asymmetric intraocular pressure in normal tension glaucoma. Arch. Ophthalmol 1988;106:898-900.
5Schulzer M, Drance SM. Biostatistical evidence for two distinct COAG populations. Br.J.Ophthalmol 1990;74:196-200.
6The AGIS Investigators. The advanced glaucoma intervention study (AGIS): 7. The relationship between control of intraocular pressure and visual field deterioration. Am J Ophthalmol 2000;130:423-434.
7Collaborative normal tension glaucoma study group. Natural history of normal-tension glaucoma. Ophthalmology 2001;108:247-253.
8Van Burskirk ME, Cioffi GE. Predicted outcome from hypotensive therapy for glaucomatous optic neuropathy. Am J Ophthalmol 1993;116:636-640.