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REVIEW ARTICLE
Personalizing Intraocular Pressure: Target Intraocular Pressure
in the Setting of 24-Hour Intraocular Pressure Monitoring
Arthur J. Sit, MD, and Christopher M. Pruet, MD
Abstract: Determining target intraocular pressure (IOP) in glaucoma patients is multifaceted, requiring attention to many different factors such as
glaucoma type, severity of disease, age, race, family history, corneal thickness and hysteresis, and initial IOP. Even with all these variables accounted
for, there are still patients who have progression of the disease despite
achieving target IOP. Intraocular pressure variability has been identified
as a potential independent risk factor for glaucoma progression but is currently difficult to quantify in individual patients. New technologies enabling measurement of both diurnal and nocturnal IOP may necessitate
modifying our concept of target pressure.
Key Words: 24-hour intraocular pressure, target intraocular pressure
(Asia Pac J Ophthalmol 2016;5: 17–22)
G
laucoma is a characteristic optic neuropathy affected by multiple factors, but reduction of intraocular pressure (IOP) is
currently the only therapy demonstrated to be effective at reducing
the risk of disease progression. When evaluating a patient, a balance needs to be achieved between the benefits of lowering IOP
and the burdens of the therapy. Most practitioners determine a
target IOP after evaluating the risk factors of the individual patient, tailor their therapies toward achieving the target IOP, and
then modify their therapy or target IOP if the patient shows progression. Multiple variables contribute to the determination of
target IOP.
INITIAL FACTORS INFLUENCING TARGET IOP
Maximum IOP and Percentage Reduction
Large multicenter clinical trials have clearly demonstrated
that reduction of IOP decreases the risk of developing glaucoma
or disease progression. However, by design, clinical trials have
an IOP target based on a fixed percentage reduction. Reviewing
the various IOP targets used in clinical trials can provide some
guidance on optimal target IOP selection.
The Ocular Hypertension Treatment Study found that a 20%
reduction in IOP in patients with a baseline IOP of 24 to 31 mm Hg
in 1 eye and 21 to 31 mm Hg in the fellow eye reduced the rate of
developing glaucoma at 5 years from 9.5% to 4.5%.1 A follow-up
study from the same cohort of patients showed that those initially
randomized to observation had delayed treatment by a mean of
7.5 years before being placed on ocular antihypertensive therapy.
As a result, the 13-year rate of developing glaucoma after initial
randomization to observation was 22% in the observation group
From the Department of Ophthalmology, Mayo Clinic, Rochester, MN.
Received for publication September 20, 2015; accepted December 14, 2015.
A.J.S. is consultant to AcuMEMS Inc, Allergan Inc, and Sensimed AG and
received research support from Aerie Pharmaceuticals Inc and Glaukos
Corp. C.M.P. has no funding or conflicts of interest to declare.
All sources of support are processed through the Mayo Clinic and do not go
directly to either A.J.S. or C.M.P.
Reprints: Arthur J. Sit, MD, 200 1st St. SW, Rochester, MN 55905. E-mail: sit.
[email protected].
Copyright © 2016 by Asia Pacific Academy of Ophthalmology
ISSN: 2162-0989
DOI: 10.1097/APO.0000000000000178
compared with 16% in the initial treatment group. The IOP target
was set as a 20% reduction from baseline or an IOP less than
24 mm Hg, whichever was lower.2
The Early Manifest Glaucoma Trial (EMGT) compared treatment of patients with newly diagnosed glaucoma with a standardized protocol of argon laser trabeculoplasty and betaxolol (which
resulted in a 25% IOP reduction) with observation and no therapy.
The study found that the 25% reduction of IOP was associated
with a 45% rate of progression over 5 years as compared with a
62% rate of progression in patients who received no therapy.3
The Collaborative Initial Glaucoma Treatment Study (CIGTS)
randomized patients with newly diagnosed glaucoma to medical
treatment or trabeculectomy. After initiating treatment, the mean
IOP in the medical group was 17 to 18 mm Hg (roughly 35% reduction) and 14 to 15 mm Hg in the surgical group (roughly 40%
reduction). Overall, there was no significant difference in the progression rates between the medically and surgically treated groups.
This suggests that initial IOP reductions greater than 35% may have
a limited effect on progression in this patient population, but generalizability to other groups is uncertain, particularly in patients with
advanced disease.
Level of Disease
On subgroup analysis of the CIGTS study, 1 group in particular seemed to benefit from initial surgery. Patients who presented with advanced disease, defined as a mean deviation of
less than −10 dB on Humphrey Visual Field testing, had decreased
rates of progression (defined as a decrease in mean deviation of
≥3 dB) 7 years after randomization to surgery compared with medically treated patients.4 This suggests a benefit to having lower target IOP in the setting of advanced disease, although the decreased
progression in this group may also be related to a decrease in IOP
variability with trabeculectomy as compared with topical medications.5 A similar benefit of aggressive IOP reduction was reported
in the results of the Advanced Glaucoma Intervention Study. Patients with advanced disease (defined as glaucomatous visual field
defects and IOP > 18 mm Hg despite maximally tolerated medical
therapy) were less likely to progress if their average IOP was less
than 14 mm Hg over 6 to 18 months after argon laser trabeculoplasty or trabeculectomy.6 In contrast to the groups that had
higher average IOPs, this subgroup also consistently had IOP of
18 mm Hg or less during this time frame, suggesting more stable
IOP as well. It remains unclear whether the decreased rate of progression is due to lower IOP, lower IOP variability, or a combination of the two.
Glaucoma Type
Some types of glaucoma may have elevated risk of progression and warrant more aggressive target IOPs. When recruiting
for the EMGT trial, many patients with ocular hypertension and
without visual field deficits were enrolled. In a subgroup analysis,
ocular hypertensive patients (IOP 24–31 mm Hg) with pseudoexfoliation were age, sex, and IOP matched with patients without pseudoexfoliation. At a mean of 8.7 years, 28% of the control
subjects and 55% of the pseudoexfoliation patients had developed
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Asia-Pacific Journal of Ophthalmology • Volume 5, Number 1, January/February 2016
Sit and Pruet
glaucoma, indicating that pseudoexfoliation patents have a higher
risk of progression.7
Other Predictors of Progression
Numerous other risk factors for glaucoma have been identified in clinical trials.8 Decreased central corneal thickness is an
established risk factor for glaucomatous progression in both openangle and angle-closure glaucomas,9,10 as is older age, especially
in the setting of normal IOP.11 African ancestry is a risk factor for
both the development and progression of disease.12 Family history
also puts a patient at risk of developing glaucoma.13 Low corneal
hysteresis has also been associated with glaucomatous progression.14 Tissue biomechanical properties, such as scleral elasticity,
are likely risk factors for progression but cannot be easily measured at present.15 However, unlike IOP, these risk factors (as well
as others) currently cannot be, or are very difficult to, modify.
IOP VARIABILITY
With an impressively large number of factors contributing to
whether a patient will lose vision from glaucoma, setting the target
IOP is complex and must be individualized. Once a target IOP (or
range of IOPs) is set and therapy is initiated and stabilized, follow-up
visits are typically focused on determining if patients are at their
target pressure, if they are exhibiting progression of the disease,
and if their target IOP needs to be adjusted. As multiple IOP measurements are performed over extended periods, it may be possible to determine another potential risk factor for glaucomatous
progression: IOP variability.
Long-term Variability
The importance of long-term IOP variability over years is
difficult to study. However, post hoc analyses of clinical trial data
have suggested that at least some patient populations may be susceptible to IOP variations.
Nouri-Mahdavi et al16 performed a retrospective analysis of
the Advanced Glaucoma Intervention Study data and found that
IOP variation over years of follow-up was a significant risk factor
for progression. A problem with this particular study was that the
data included IOP measurements taken after therapy was modified
for visual field progression, resulting in a higher IOP variability in
patients with progression. Caprioli and Coleman17 performed an
analysis on the same cohort, this time analyzing data only before
visual field progression and excluding patients with multiple surgeries. They found that high variability in the lowest tertile of
mean IOP was linked to glaucomatous progression, whereas it
was not linked to progression in the highest tertile of mean IOP.17
In contrast, patients with early glaucoma were analyzed using
the EMGT data, which did not show a link between IOP variability and glaucomatous progression. Instead, only elevated mean
IOP was found to be related to disease progression.18
Retrospective analysis of the CIGTS data by Musch et al19
found no association between IOP variability and progression in
patients randomized to the trabeculectomy arm of the study. However, for patients randomized to medical therapy, maximum IOP,
IOP range, and IOP SD were all associated with visual field progression. The Ocular Hypertension Treatment Study data also indicated that IOP variability in the medically treated group was
linked to higher rates of developing glaucoma. However, this association was not seen in the ocular hypertensive patients randomized to observation.20
A possible reason why only certain groups seem to be affected
by IOP variability was suggested by Caprioli:21 mean IOP is the
predominant risk factor for patients with elevated IOP, whereas
when IOP is lower, its variability has a stronger influence on
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progression. Concerning the apparent susceptibility of medically
treated patients to IOP variations, treatments that suppress aqueous production do not stabilize IOP throughout a 24-hour period,
in contrast to treatments that improve outflow facility. This may
lead to an increase in IOP variability that is not easily captured
in single measurements recorded during the diurnal period.22
Diurnal Variability
Variation of IOP over the course of the day, instead of over
years, may also be a risk factor for glaucoma. Jonas et al23 obtained diurnal tension curves on control subjects and patients with
primary open-angle glaucoma (POAG) and secondary open-angle
glaucoma (pigmentary and pseudoexfoliation). They reported that
patients with secondary open-angle glaucoma had a diurnal IOP
peak in the afternoon, in contrast to both control subjects and
POAG patients who had a morning peak with a gradual decrease
in IOP throughout the day. This study also reported that patients
with secondary open-angle glaucoma tended to have greater IOP
variability compared with control subjects and POAG patients.
Bergeå et al24 obtained diurnal tension curves on patients every
2 months for 2 years in a group of patients with POAG and
pseudoexfoliation glaucoma. Their findings showed that POAG
patients tended to have lower pressures than pseudoexfoliation
glaucoma patients, and neither their mean IOP nor IOP variation
was clearly associated with progression. However, the number of
patients with POAG was small. In contrast, both mean IOP and
IOP variation were associated with visual field progression in pseudoexfoliation glaucoma patients.
Asrani et al studied a group of patients with open-angle glaucoma who measured their own IOP 5 times a day over 5 days using
a specially designed home applanation tonometer that required
topical anesthetic. In this group of patients, with a maximum inclinic IOP of 24 mm Hg and a maximum in-clinic variability of
8 mm Hg, self-measured IOP variability was found to be a risk
factor for progression after 1 year.25
Controversy exists regarding the repeatability of diurnal IOP
patterns. Realini et al26 found that, in treated POAG patients, the
agreement between serial diurnal curves was uniformly poor with
intraclass correlation coefficients ranging from −0.1 to 0.4. In
contrast, Mottet et al27 performed 6 diurnal curves on 6 healthy
patients and found that 80% of measurements demonstrated a
nyctohemeral rhythm. However, intrasubject and intersubject variability of rhythmic parameters and IOP values was relatively high.
Short-term Variability
There is currently a lack of evidence to conclude whether
short-term IOP variations, lasting seconds to minutes, may contribute to glaucoma.28 However, it is clear that there are a wide
range of normal behaviors that can influence IOP. McLaren et al29
demonstrated, by using a continuous pressure monitoring system
in rabbits, that IOP undergoes nearly constant change and is affected by breathing, lid position, eye position, pulse pressure, tonometer application, and physical activity. Downs et al30 similarly
used an implanted aqueous transducer (allowing for unrestricted
activity) in 3 female primates and documented IOP fluctuations
of up to 10 mm Hg on an hourly basis.
Other studies have demonstrated changes in IOP due to
blinking, head position, body position, eye position, blood pressure
(BP), and accommodation. Caffeine consumption, excessive water
intake, wearing a tight necktie, and playing a wind instrument affect
IOP as well.31 The mechanism of short-term IOP variations is unclear but does not appear to be related to systemic venous pressure.32
In addition to the intrinsic fluctuation of IOP, measurements can
vary because of operator error and patient factors.
© 2016 Asia Pacific Academy of Ophthalmology
Copyright © 2016 Asia Pacific Academy of Ophthalmology. Unauthorized reproduction of this article is prohibited.
Asia-Pacific Journal of Ophthalmology • Volume 5, Number 1, January/February 2016
One area of particular interest is the effect of body positioning
on IOP. Malihi and Sit33 found that in healthy patients, when sitting
with the neck in a neutral position, IOP is roughly 1.6 mm Hg
lower than in neck extension, 5.0 mm Hg less than in neck flexion,
and 2.5 mm Hg lower than in the supine position. Thus, IOP measurements in the clinic are typically performed with the body positioned to give the lowest possible readings. Further investigations
are required to decide if IOP variability in other body positions is
increased in glaucoma patients and to determine the role (if any)
of body position–induced IOP changes in glaucoma pathogenesis.
Circadian Variations
Intraocular pressure fluctuates with a circadian pattern, and
this pattern seems to be altered in glaucoma. In a series of studies,
Liu et al34 measured IOP every 2 hours in the sitting and supine
positions during the waking period and in the supine position during the sleeping period throughout a 24-hour period in patients
with newly diagnosed glaucoma and healthy control subjects.
They determined that, when in physiologic positions (sitting during the diurnal phase, supine in the nocturnal phase), IOP was
highest in the nocturnal period for most patients, including both
control and glaucomatous patients. However, when IOP was measured in the supine position, glaucomatous patients were found
to have a nocturnal decrease in supine IOP, in contrast to healthy
control subjects who had an increase in nocturnal supine IOP compared with diurnal supine IOP.
The potential clinical significance of the circadian IOP pattern is based on the circadian variation of ocular perfusion pressure (OPP), which is directly related to IOP and BP. Like IOP,
BP can vary significantly with a 24-hour cycle, but the magnitudes of the changes (in mm Hg) tend to be much larger than the
variations in IOP.35 In another study, Liu et al36 measured the diurnal (sitting) to nocturnal (supine) IOP change in healthy younger
and older adults. They found that nocturnal IOP increased by
5.1 mm Hg compared with diurnal IOP in young adults and
by 4.5 mm Hg in older adults. This nocturnal increase in IOP,
coupled with a decrease in mean arterial pressure from 95 to
83 mm Hg in young adults and 107 to 99 mm Hg in older adults,
suggests a decrease in OPP at night. However, this may be more
than compensated for by the local positional arterial BP changes
experienced by the eye in the supine position. Liu et al36 took
this into account and calculated that OPP may actually be increased during the nocturnal period, by 3.6 mm Hg in young
adults and 10.1 mm Hg in older adults without glaucoma. However, in glaucoma patients, these beneficial changes may be altered by vascular dysregulation and systemic hypotension.
Graham and Drance37 reported that patients with relative nocturnal systemic hypotension had significantly greater glaucoma
progression rates than did patients with higher nocturnal BP. Also
highlighting the importance of optic nerve perfusion, Sung et al35
found that, in patients with normal-tension glaucoma (NTG), circadian variation in OPP was the strongest prognostic factor for
progression, even more important than mean OPP.
Further complicating the issue of OPP in glaucoma is the
finding that circadian IOP patterns in glaucoma may be variable.
In a study by Renard et al of 22 NTG patients, a variety of IOP
patterns were detected, suggesting the loss of normal circadian
rhythms in this population.38 Fifty-eight percent of their patients
exhibited a diurnal acrophase (IOP highest during the day), which
was opposite to subjects without glaucoma described by Liu et al,
whereas only 42% exhibited a nocturnal acrophase (IOP highest
at night). Although there was no significant difference in OPP
between these 2 groups, the diurnal acrophase pattern was associated with capillopathy confirmed by nailed capillaroscopy, suggesting abnormal vascular regulation.
© 2016 Asia Pacific Academy of Ophthalmology
Personalizing Intraocular Pressure
Methods of Measuring IOP Over 24 Hours
Until recently, the only clinically available method for obtaining a 24-hour IOP curve was admission to the hospital where
a series of trained technicians or nurses would measure IOP at predetermined intervals using handheld or slit-lamp tonometry. Although this approach is reasonable for research purposes, it is not
a viable strategy for routine clinical use. It is inherently time consuming and disturbing for the patient to obtain IOP measurements
throughout the day and night, and the financial costs for hospital admission and staffing with trained personnel are prohibitive. Diurnal
curves can be performed during clinic hours, but these cannot
capture the nocturnal period where OPP may be at a minimum.
Self-tonometry has the potential to decrease the cost and increase the convenience of 24-hour IOP monitoring, as it would be
performed by the patients themselves outside the clinic or hospital. However, self-tonometry devices have met with limited success.
The Proview Eye Pressure Monitor (Bausch & Lomb Incorporated,
Bridgewater, NJ) functions by having the patient look inferotemporally and then press the instrument tip onto the closed eyelid in
the superonasal position with increasing force until a phosphene is
generated because of mechanical stimulation of the retina. The
force applied at the subjective phosphene initiation is then recorded. This method has been found to be less accurate and less
repeatable than Goldmann applanation tonometry.39 It detected
pressures of greater than 21 mm Hg in only 18% (4/22) of patients40 and had a discrepancy of 6.6 ± 3.6 mm Hg in patients with
pressures of more than 20 or less than 10 mm Hg.41 The Ocuton-S
(EPSa Elektronik & Praezisionsbau, Saalfeid, Germany) selfapplanator is similar to a Goldmann applanator, requiring corneal
anesthetic. In addition to its poor reproducibility compared with
the Goldmann, the additional risks of abrasion and infection have
limited its acceptance.42 The Icare (Icare Finland, Helsinki, Finland)
is a rebound contact tonometer that does not require corneal anesthesia. Its clinical use is already widespread. However, its use as a
self-tonometry device has met with limitations: nonperpendicular
and off-center measuring limit the reproducibility of its readings.43
In addition, any self-applied tonometer requires the patient to be
disturbed during sleep for measurements in the nocturnal period
if 24-hour pressures are desired.
In response to the need to measure ambulatory 24-hour IOP
in a patient-independent manner, multiple devices have been proposed and developed in the past decade. The first device that was
available for routine clinical use was the SENSIMED Triggerfish
(Sensimed AG, Lausanne, Switzerland), which is available in many
countries around the world but is not yet approved by the US Food
and Drug Administration. The Triggerfish is a disposable contact
lens sensor (CLS) that measures minute corneal curvature changes,
which occur with changes in IOP.44 These readings are wirelessly
transmitted to a sensor placed over the patient’s ocular rim. The
CLS records the voltage from an internal sensor 10 times a second
for 30 seconds, transmits its data, then repeats the process 5 minutes
later. One important limitation is that the output of the sensor is in
millivolts, not in actual IOP, highlighting that this device is designed
to monitor a profile of IOP, not IOP itself.
The validation of the relationship between millivolt and IOP
is difficult, given that Goldmann tonometry cannot be reliably performed on a patient wearing the CLS. In addition, controversy exists regarding the correlation of changes in CLS measurements
with IOP. Mottet et al45 studied 12 healthy volunteers over three
24-hour periods (performing noncontact tonometry during 2 sessions and CLS in 2 sessions) and found a significant correlation
between acrophase and bathyphase in all intrapatient sessions,
but the CLS data were not symmetric to noncontact tonometry
either individually or within the study population. In 1 report,
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Sit and Pruet
Asia-Pacific Journal of Ophthalmology • Volume 5, Number 1, January/February 2016
the millivolt profile for positional changes did not match the
IOP changes obtained from the fellow eyes in 5 subjects, and
a 5–mm Hg increase over 30 minutes in an enucleated human
eye was poorly reflected in the millivolt profile as well.46
Nevertheless, multiple studies have used data from the CLS
to infer IOP patterns. Lee et al47 recorded 24-hour Triggerfish data
in 18 NTG patients, half of whom were on prostaglandin therapy,
and found that the diurnal output voltage variability was higher than
nocturnal voltage variability, that there were more voltage spikes in
the diurnal period than in the nocturnal period, and that the voltage
changed more rapidly moving from the diurnal to nocturnal than
from the nocturnal to diurnal period.47 There was no significant difference between the prostaglandin- and non–prostaglandin-treated
groups. Lee et al48 also reported Triggerfish results in 18 NTG patients who underwent selective laser trabeculoplasty. Patients with
a 20% or greater reduction in IOP by Goldmann tonometry at
1 month had a 24.6% reduction of the amplitude of their 24-hour
cosine-wave-fitted Triggerfish output, whereas patients who did
not achieve a 20% decrease in IOP experienced a 19.2% increase
in the amplitude of their Triggerfish cosine-fit voltage profile
and had an increase in 24-hour millivolt variability. Mansouri
et al49 evaluated 21 healthy and 19 POAG patients with 2 Triggerfish sessions; correlation coefficients between the sessions
were 0.51 for patients not on glaucoma medication and 0.63
for those using glaucoma medication, but these correlations did
not reach statistical significance. Positive linear slopes from waking to 2 hours into sleep were detected in both sessions for the
no-glaucoma medication group but not for the glaucoma
medication group. This could mean that the diurnal pattern in
POAG is disrupted by either medication use or the pathology
of POAG itself.49
All of the aforementioned methods of measuring IOP are external and noninvasive and rely on the response of the cornea to
pressure. Because of the invasive nature of direct IOP measurement via manometry, this is typically performed only for research
purposes during unrelated surgery and in the laboratory setting
with animal models. However, attempts to develop an implantable
IOP monitoring device have continued for decades, and the first
devices appear to be nearing clinical availability. The Wireless IOP
Transducer (WIT; Implandata Ophthalmic Products GmbH) is
an implant designed to provide IOP measurements through direct
access to the posterior chamber. The WIT is a silicone-based sulcus implant with 8 individual pressure transducers that measure
IOP in the sulcus, then transmit the processed average measured
IOP to a radiofrequency receiver placed in front of the orbital rim.
Todani et al6 implanted 6 WITs in rabbits directly after either open
sky or manual extracapsular cataract extraction. These sensors were
noted to have good correlation with manometry in sedated rabbits
and were more precise than pneumotonometry or the Tono-Pen
(Reichert, Depew, NY). Two of the 6 implants exhibited a drift in
their readings necessitating recalibration to manometry: one at a rate
of 2 mm Hg per month that started after 1 year of implantation, and
the other was an abrupt drop at 1.5 years. Neither device showed
further drift after recalibration. No ocular toxicities or inflammation
were noted in the implanted rabbits over the 25-month study.6
The WIT has also been implanted in 1 human patient after
phacoemulsification through a 3-mm superior clear corneal incision. Corneal edema and iritis resolved within 1 month, and final
best corrected visual acuity was 20/25 after posterior YAG capsulotomy; the angle remained open except for peripheral anterior
synechiae at the surgery wound. The IOP measured by the WIT
differed by as much as 6.5 mm Hg and exhibited a drift to a lower
pressure after 36 weeks. The patient had an unexplained rise in IOP
to 25 mm Hg by Goldmann applanation tonometry at 31 weeks
after surgery, which resolved after a month’s course of latanoprost
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and did not recur after discontinuation of latanoprost.50 Although
these problems highlight the difficulties with long-term implantable pressure sensors, this approach shows promise as a tool to
enable 24-hour IOP monitoring and evaluation of IOP variation
in glaucoma patients.
MINIMIZING VARIATIONS
Appropriate selection of IOP-lowering therapy can help to
minimize IOP variations. The rationale for this comes from an understanding of the aqueous humor dynamics of normal IOP variations and the mechanisms of action of glaucoma therapies.
During the nocturnal period, the production of aqueous humor decreases roughly 50%, compensated by a small decrease
in outflow facility and a large decrease in uveoscleral outflow, to
produce a relatively stable IOP (when measured in the same body
position as in the diurnal period).51 Aqueous suppressants seem
to have minimal effect in the nocturnal phase, likely due to aqueous humor production being at a basal level during sleep. In contrast, prostaglandin analogs seem to maintain efficacy during the
nocturnal phase (albeit at a lower level than during the diurnal
phase), likely due to their effect on improving uveoscleral outflow,
which is reduced at night. In comparison, both aqueous suppressants and prostaglandin analogs have good efficacy during the diurnal phase.52 Prostaglandin analogs would be the medication
class of choice for patients who had nocturnal IOP rises thought
to be contributing to progression.
Typically, procedures that increase outflow facility tend to
lower IOP variations more than those that lower aqueous production.22 Laser trabeculoplasty has been shown to increase outflow
facility and also to decrease IOP rise in the nocturnal period.53
Awell-functioning trabeculectomy in patients with advanced glaucoma has also been shown to lower IOP in both the diurnal and
nocturnal periods and reduce pressure variations compared with
medical therapy.5
DETERMINING TARGET IOP IN THE SETTING
OF 24-HOUR MONITORING
In conclusion, some patients will continue to progress
despite an apparently adequate IOP when measured in a clinic
setting. In patients such as these, diurnal curve measurements
or 24-hour IOP monitoring may identify IOP variability as a potential cause of disease progression. As discussed in IOP VARIABILITY, this would be of particular importance in patients
with low mean IOPs (eg, in the range of 10–12 mm Hg) and
worsening glaucoma. In addition, detection of an IOP rise during
the nocturnal phase could indicate the need to advance therapy to
decrease IOP variability at night (as discussed in MINIMIZING
VARIATIONS).
Finally, the role of IOP variability in glaucoma cannot be
separated from variability in OPP. Blood pressure variations
are much larger than IOP variations, and the effect on mean arterial pressure at the optic nerve head is unclear. However, in
patients with disease progression despite seemingly wellcontrolled IOP, an assessment of 24-hour BP and vascular instability may be warranted. In particular, NTG patients may
benefit from these additional investigations, which could help
to stabilize their disease.
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© 2016 Asia Pacific Academy of Ophthalmology
Copyright © 2016 Asia Pacific Academy of Ophthalmology. Unauthorized reproduction of this article is prohibited.
Asia-Pacific Journal of Ophthalmology • Volume 5, Number 1, January/February 2016
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It is only with the heart that one can see rightly; what is essential is invisible to the eye.
— Antoine de Saint Exupéry
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