10 Glaucoma Now – Issue No 1, 2013. www.glaucomanow.com

Practical Tips:

iOP assessment with the water drinking testColin Clement BSc (Hon) MBBS PhD FRANZCO 1,2 & Shibal Bhartiya MBBS MS 3

1. Glaucoma unit, sydney eye Hospital, NsW, Australia, 2. Discipline of Ophthalmology, Central Clinical school, The university of sydney, NsW

Australia, 3. Fortis Memorial Research institute, sector 44, Gurgaon, Haryana, india

Core concepts• To identify both iOP-dependant and non iOP dependant factors is essen-tial to understand why progression takes place in patients.• We are currently unable to monitor 24 hour iOP continuously.• surrogate measures such as in-ter-visit iOP variation or diurnal iOP curves, although helpful, are some-times impractical.• An alternative to determine iOP fluctuation and peak iOP is the water-drinking test (WDT), which is simple to perform and evidence based. • Peak WDT-induced iOP correlates well with peak diurnal iOP and may help to identify patients with fluctuat-

ing iOP peaks outside or even within routine office hours.• The WDT requires the patient to drink a set volume of water within a short time period (usually 5 minutes).• Due the diuretic effect of the WDT, care should be taken in individuals with cardiovascular or renal co-mor-bidities.• Because of its poor sensitivity, the WDT is no longer acceptable as a pro-vocative test to diagnose glaucoma.• The WDT is a low cost, low tech practical alternative for cumbersome assessments of diurnal variations and peak iOPs and can highlight the need for further intervention or re-evalua-tion of current treatment plans.

Well-designed clinical trials provide strong evidence that elevated intraocular pressure (IOP) is a risk factor for the de-velopment of glaucoma and for progres-sion of established disease. For example, pooled data from the Ocular Hyper-tension Treatment Study (OHTS) and European Glaucoma Progression Study (EGPS) suggests that for every 1mmHg higher baseline IOP, there is a relative risk of 1.09 for glaucoma development.1

IOP reduction is a proven strategy to prevent progression from ocular hy-pertension (OHT) to glaucoma or to slow the rate of glaucoma progression. However, patients with glaucoma pro-gression despite IOP reduction remain a significant challenge. To identify both IOP-dependent and non IOP-depen-

and colleagues showed that CPAP nor-malized IOP and restored blood pres-sure to a normal rhythm.11 CPAP in patients with OSAS and glaucoma may have a beneficial effect for the glaucoma as well as the OSAS.

It is important when taking a patient history to inquire about snoring and daytime somnolence. Often a patient’s spouse or partner can elucidate if he or she snores or describe moments when he or she stops breathing for a few seconds then resumes snoring. These symptoms are possible indications for OSAS and these patients should consider a formal polysomnography. If diagnosed with OSAS, the patient should seriously con-sider CPAP treatment to aid glaucoma treatment as well as improve their sys-temic status.

References1. Faridi, O, Park, sC, Liebmann, JM, Ritch, R. Glaucoma and obstructive sleep apnoea syn-drome. Clinical and Experimental Ophthalmology. 2012; 40: 408–419.

2. Peppard, Pe, Young, T, Palta, M, skatrud, J. Prospective study of the association between sleep-disordered breathing and hypertension. N Engl J Med. 2000; 342: 1378–1384.

3. Chobanian, AV, Bakris, GL, Black, HR et al. Seventh report of the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure. Hypertension. 2003; 42: 1206–1252.

4. Waller, eW, Bendel, Re, Kaplan, J. Sleep disorders and the eye. Mayo Clin Proc. 2008; 83:1251–1261.

5. Gordon, MO, Beider, JA, Brandt, JD et al. The Ocular Hypertension Treatment Study: baseline factors that predict the onset of primary open-angle glaucoma. Atrch Ophthalmol. 2002; 120: 714–720.

6. sergi, M, salerno, De, Rizzi, M et al. Preva-lence of normal tension glaucoma in obstructive sleep apnea syndrome patients. J Glaucoma. 2007; 16: 42–46.

7. Mojon, Ds, Hess, CQ, Goldblum, D et al. High prevalence of glaucoma in patients with sleep ap-nea syndrome. Ophthalmology. 1999; 106: 1009–1012.

8. Lin PW, Friedman MW, Lin HC, et al. Normal tension glaucoma in patients with obstructive sleep apnea/hypopnea syndrome. J Glaucoma. 2010; Sep 16. [Epub ahead of print].

9. Bendel Re, Kaplan J, Heckman M, et al. Prevalence of glaucoma in patients with obstruc-tive sleep apnoea – a cross-sectional case-series. Eye. 2008;22:1105–9.

10. Karakucuk s, Goktas s, Aksu M, et al. Ocu-lar blood flow in patients with obstructive sleep apnea syndrome (OSAS). Graefes Arch Clin Exp Ophthalmol. 2008;246:129–34.

11. Pepin, JL, Chiquet, C, Tamisier, R, Levy, P, Almanjoumami, A, Romanet, JP. Frequent loss of nyctohemeral rhythm of intraocular pressure re-stored by nCPAP treatment in patients with severe apnea. Arch Ophthalmol. 2010; 128L 1257–1263.

12. Fletcher, eC. sympathetic overactivity in the etiology of hypertension of obstructive sleep ap-nea. Sleep. 2003; 26: 15–19.

13. Blumen Ohana e, Blumen MB, Bluwol e, et al. Primary open angle glaucoma and snoring: preva-lence of OSAS. Eur Ann Otorhinolaryngol Head Neck Dis. 2010;127:159–64.

14. Marcus DM, Costarides AP, Gokhale P, et al. Sleep disorders: A risk factor for normal-tension glaucoma? J Glaucoma. 2001;10:177–83.

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Baseline 15 mins 30 mins 45 mins 60 mins

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dant factors is essential to understand why progression occurs in these patients. IOP-dependant factors are likely to in-clude IOP fluctuation and peak IOP, both of which are associated with disease progression, both of which may be easily missed or underestimated with standard clinic based IOP measurements.2

We are currently unable to monitor 24 hour IOP continuously and surrogate measures such as inter-visit IOP varia-tion or diurnal /circadian IOP curves, although helpful, are sometimes imprac-tical. An alternative to determine IOP fluctuation and peak IOP, which is both evidence-based and simple to perform, is the water-drinking test (WDT).3 It is es-sentially a “stress-test” which may lead to elevated IOP in some eyes due to yet to be determined mechanisms, which may include increased episcleral venous pres-sure, choroidal thickening or sympathet-ic excitation. The peak WDT-induced IOP correlates well with peak diurnal IOP and may help to identify individu-als with fluctuating IOP peaks outside or even within routine office hours.4

The WDT requires the patient to drink a volume of water in a short pe-riod, usually 5 minutes. Our preferred protocol is 10ml/kg body weight such that a 70 kg patient would drink 700mls; others have used a fixed volume such as

1 litre. Very occasionally, patients are intolerant of this volume of water but we find the addition of a small volume of fruit juice can help. Patients should be warned of the diuretic effect and care taken in individuals with congestive cardiac failure, renal impairment, hypo-natraemia or significant cardiovascular disease. IOP is measured every 15 min-utes for 1 hour after the water is imbibed (figure 1). A modified WDT, where IOP is measured only 15 mins and 30 mins after consumption, may be adequate in the setting of significant time con-straints given peak IOP typically occurs within this time period. 5

Results of a WDT can aid patient management in a number of ways: • It facilitates discussion with the pa-

tient about reasons for progression• It helps assess efficacy of current treat-

ment• It potentially allows treatment to be

tailored if a high peak is identified. For example, prostaglandin analogues could be more suitable than beta-blockers for many patients or surgery more effective than medical treatment.

Because of poor sensitivity and specific-ity the WDT is no longer acceptable as a provocative test to diagnose glaucoma. However, it provides relevant informa-

tion about the homeostatic mechanisms of in vivo aqueous dynamics for an eye and a patient: the extent of IOP increase and the speed with which it recovers. It is, therefore, a low cost, low tech, prac-tical alternative for cumbersome assess-ments of diurnal variations and peak IOPs and can highlight the need for further interven tion or re-evaluation of treatment plans. This is especially so in those who progress despite having achieved previously determined “target” pressures, as well as those with advanced glaucomatous damage.

References:1. Coleman AL, Miglior s. Risk factors for glau-coma onset and progression. Surv Ophthalmol 2008;53: s3–s10.

2. Barkana Y, Anis s, Liebmann J, Tello C, Ritch R. Clinical utility of intraocular pressure monitor-ing outside of normal office hours in patients with glaucoma. Arch Ophthalmol. 2006;124:793–7.

3. Goldberg i, Clement Ci. The water drinking test. Am J Ophthalmol. 2010;150:447–9.

4. susanna, R. Jr, Vessani RM, sakata L, Zac-arias LC, Hatanaka M. The relation between in-traocular pressure peak in the water drinking test and visual field progression in glaucoma. Br J Ophthal mol 2005;89:1298–1301.

5. susanna R Jr, Hatanaka M, Vessani RM, Pinheiro A, Morita C.Correlation of asymmetric glaucomatous visual field damage and water-drinking test response. Invest Ophthalmol Vis Sci. 2006;47:641–4.