Royal College of Ophthalmologists Guidelines (Focus)

Glaucoma Management 

This article will look at current management of open angle glaucoma, commenting on diagnosis and therapeutic options. 


Primary open angle glaucoma (POAG) is an optic neuropathy, associated with a characteristic deformity of the optic nerve head, recognised clinically as 'glaucomatous cupping'. This deformity s associated with loss of visual function, characterised by 'retinal nerve fibre' loss and visual field defects. Glaucomatous cupping can be identified before visual loss becomes detectable by white on white perimetry but other tests of visual function which may detect visual loss earlier are not yet universally accepted. 

Aetiological Risk Factors

There are a number of 'risk factors' predisposing to the development of glaucomatous cupping, the most important being elevated intraocular pressure (IOP). However, approximately 30% of newly diagnosed patients with open angle glaucoma will have IOP measurements within the 'normal range' (1) The relative risk for elevated IOP causing glaucoma increases significantly once the level exceeds 30mmHg (1) making prophylactic h hypotensive treatment advisable. 

Other risk factors implicated in the development of chronic glaucoma include age, optic disc morphology, black race (2), an abnormal blood pressure (hypertension in the young and hypotension in the elderly) (3), myopia, increased blood viscosity, vasospasm and a family history for glaucoma. With respect to the latter, the development of open angle glaucoma is likely to relate to the presence of one or more of the genes associated with primary open angle glaucoma (4-6, 7). These genes are also important in certain forms of secondary open angle glaucoma, such as pigment dispersion syndrome and pseudoexfoliation (8). 
ABSOLUTE:  Glaucomatous visual field defect 
Glaucomatous optic nerve head damage 
RELATIVE: Major: Elevated IOP 
Increasing age 
Genetic predisposition (includes race) 
Other: Myopia 
Cardiovascular/haematological factors 
Optic nerve head morphology 

Therapeutic Options 

The current options available to treat open angle glaucoma are limited to methods of lowering IOP which include medical, laser and surgical treatments. In the UK there have been three studies comparing medicine vs. surgery as first line treatment, the third of which also included primary laser treatment as an option (9-11). All three studies suggested, with varying degrees of certainty, that primary surgery was the most efficacious. However the advent of newer, more potent, topically applied hypotensive glaucoma drugs has maintained medical treatment as the first line treatment for POAG. 

Medical Therapy 

The options available in the UK include topically applied beta antagonists, various miotics, a carbonic anhydrase inhibitor, alpha receptor agonists and a prostaglandin analogue. The most extensively tested of all these is the non-selective beta antagonist timolol. Timolol will produce a long term IOP lowering of 4-5mmHg (1,2). If the hypotensive activity of this drug is taken as the benchmark, ranking of the hypotensive effect is as shown in Table 2. 

Individual patient responses may vary and overturn the generalisations outlined in Table 2. Drug combinations may produce an additive hypotensive effect with the probable exception of a beta-antagonist and an alpha-agonist. Somewhat surprisingly, miotics and latanoprost can have an additive effect (13). 

The required frequency of instillation varies. Any drug that needs to be instilled more than twice a day is liable to have the mid-day instillation missed or delayed. This apples to both miotic drops and dorzolamide. When combined with timolol, the same drugs seemingly have optotensive activity throughout the day as a twice a day preparation, although this needs to be confirmed for the individual patient. Latanoprost need only be given once a day, last thing at night. beta-antagonists can provide an 18 hour hypotensive effect. These drugs should be instilled first in the morning for when applied at night they (unlike carbonic anhydrase inhibitors) do not have much effect on aqueous secretion, and therefore on IOP (14). 

The number of medications that will be comfortably tolerated will vary from patient to patient, and as a general rule patient quality of life falls when more than two types are used. 

All the drugs produce side effects. The ocular side effects are usually recognised. Most topically applied drugs have been implicated in causing blurring of vision, although the mechanism is not always clear. Allergies are produced most frequently by the adrenergics, and next most commonly the miotics. All topically applied drugs use benzalonium as a preservative; for any patient allergic to this preservative there are only a limited number of preservative free preparations available. 
Betaxolol  Timolol  Latanoprost 
Dorzolamide  Brimonidine  Acetazolamide 
Certain miotics*  Adrenaline preparations  Certain miotics* 
All non-selective beta-blockers 
Certain miotics* 
*depending on type and concentration (Carbachol > Pilocarpine 4% > Pilocarpine 1%) 

The prostaglandin analogue, latanoprost will produce eye-lash growth in some, and iris hyper-pigmentation in the hazel-eyed. Neither effect has proved to be a bar to the use of the drug from most patients' viewpoint. Of more importance for the long term use of this drug is the development of macular oedema and uveitis. The former may develop in the aphakic and possibly the pseudophakic patient. Latanoprost will also produce uveitis in the eye with a poor blood aqueous barrier. 

Systemic side affects are most commonly seen with topical (-antagonist use with respiratory side effects being common in the elderly using non selective beta-antagonists. The same drugs may induce significant bradycardia in those with a naturally slow pulse rate. All the adrenergics, with the possible exception of dipivefrin, may produce a tachycardia. 

First line treatment will be to consider beta-antagonists (singly or in combination), although they should be avoided if the side effects noted above are likely. Latanoprost is approved for use as a second line drug. The majority of patients requiring hypotensive treatment are managed by medical treatment but laser or surgical approaches should be considered if the 'target IOP' is not met or side effects preclude continued use. Target pressures for high tension glaucoma are increasingly being set in the mid to low 'teens' following the recognition that for many patients progressive loss of visual field will continue at higher levels of IOP.

Laser Therapy 

Argon laser trabeculoplasty is of use as a supplement to medical treatment, and may produce a further IOP reduction with some if not all of the topically applied preparations. It is most effective in eyes with trabecular pigmentation, and the elderly, but only 50% of those initially responding will continue to do so at 5 years. Repeat laser treatment does not usually last and is rarely useful. The treatment is of most use in the elderly, the arthritic, and the amnesiac patient for whom a moderate IOP fall is needed. 

Surgical Therapy 

Fistulising surgery (trabeculectomy) should be considered for all patients when the 'target IOP' is not met with other therapeutic options, and the expected rate of visual loss will affect the patient during their lifetime. The younger the patient the more likely this will be, and surgery should probably be considered in all patients aged 50 or below. Scar tissue formation after surgery will prejudice the IOP reduction, therefore anti-proliferatives need be considered for all eyes with risk factors for failure. Peroperative 5-fluorouracil should be considered in patients considered at risk because of youth, and prior glaucoma treatment for more than 3 years, while peroperative 5-fluorouracil or mitomycin-C needs consideration in the eye with previous conjunctival surgery, aphakia, uveitis or in black races. 

Excess bulk outflow of aqueous immediately following filtration surgery is responsible for a large number of post operative complications. The more tightly the superficial scleral flap is sutured to its bed, the fewer these will be. If required post-operatively, aqueous flow around the cut edge of the flap can be promoted by displacement of the edge by massage (indenting the overlying eyelid with a cotton tip applicator), lessening suture tension (cutting one or more sutures with the argon laser or a needle) or by using releasable scleral flap sutures. 

Roger Hitchings


1. Wilson MR, Martone J. Epidemiology of chronic open angle glaucoma. In: Ritch, Shields MB, Krupin T, Eds. The Glaucomas. 1st Ed. St Louis, Mosby. 1996: 753-68. 

2. Tielsch JM, Sommer A, Katz J, Royall RM, Quigley HA, Javitt J. Racial variations in the prevalence of primary open angle glaucoma. JAMA. 1991: 266: 369-74. 

3. Tielsch JM, Katz J, Sommer A, Quigley HA, Javitt JC. Hypertension, perfusion pressure, and primary open angle glaucoma. A population-based assessment. Arch Ophthalmol. 1995; 113:216-21. 

4. Morissette J, Cote G, Anctil JL, et al. A common gene for juvenile and adult-onset primary open-angle glaucomas confined on chromosome lq. Am. J. Hum. Genet. 1995.56: 1431-42. 

5. Sarfarazi M, Akarsu AN, Hossain A, et al. Assignment of a locus (GLC3A) for primary congenital glaucoma (Buphthalmos) to 2p21 and evidence for genetic heterogeneity. Genomics. 1995; 30: 171-7. 

6. Ortego J, Escribano J, Coca-Prados M. Cloning and characterisation of subtracted cDNAs from a human ciliary body library encoding TIGR, a protein involved in juvenile open angle glaucoma with homology to myosin and olfactomedin. FEBS Lett. 1997; 413: 349-53. 

7. Bennett SR, Alward WL, Folberg R. An autosomal dominant form of low-tension glaucoma. Am. J. Ophthalmol. 1989; 108: 238-44. 

8. Anderson KL, Lewis RA, Bejjani BA, et al. A gene for primary congenital glaucoma is not linked to the locus on chromosome lq for autosomal dominant juvenile-onset open angle glaucoma. J. Glaucoma. 1996; 5: 416-21. 

9. Smith RJ. The Lang lecture 1986. The enigma of primary open-angle glaucoma. Trans. Ophthalmol. Soc. U.K. 1986; 105: 618-33. 

10. Jay JL, Murray SB. Early trabeculectomy versus conventional management in primary open angle glaucoma. Br. J. Ophthalmol. 1988; 72: 881-9. 

11. Migdal C, Gregory W, Hitchings R. Long-term functional outcome after early surgery compared with laser and medicine in open-angle glaucoma. Ophthalmology. 194; 101: 1651-6. 

12. Schulzer M, Drance SM, Douglas GR. A comparison of treated and untreated glaucoma suspects (see comments). Ophthalmology. 1991; 98: 3001-7. 

13. Linden C, Alm A. Latanoprost and physostigmine have mostly additive ocular hypotensive effects in human eyes (see comments). Arch. Ophthalmol. 1997; 115: 857-61. 

14. McCannel CA, Heinrich SR, Brubaker RF. Acetazolamide but not timolol lowers aqueous humor flow in sleeping humans. Graefes Arch. Clin. Exp. Ophthalmol. 1992; 230: 518-20. 

More Guidelines