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Aujla, Jaskirat, Lee, Graham, Vincent, Stephen, & Thomas, Ravi(2013)Incidence of hypotony and sympathetic ophthalmia following trans scleralcyclophotocoagulation for glaucoma and a report of risk factors.Clinical and Experimental Ophthalmology, 41(8), pp. 761-772.

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https://doi.org/10.1111/ceo.12088

https://eprints.qut.edu.au/view/person/Vincent,_Stephen.html

https://eprints.qut.edu.au/63705/

https://doi.org/10.1111/ceo.12088

© 2013 The Authors

Clinical and Experimental Ophthalmology © 2013 Royal Australian and New Zealand College of Ophthalmologists

Incidence of hypotony and sympathetic ophthalmia following trans scleral

cyclophotocoagulation for glaucoma and a report of risk factors1

Jaskirat S Aujla MBBS,1,2

Graham A Lee MD FRANZCO,1,2,3

Stephen J Vincent PhD4 and

Ravi Thomas MD FRANZCO2,5

1 City Eye Centre, Brisbane, Queensland, Australia

2 University of Queensland, Brisbane, Queensland, Australia

3 Royal Brisbane Hospital, Brisbane, Queensland, Australia

4 School of Optometry and Vision Science, Queensland University of Technology, Kelvin

Grove, Queensland, Australia

5 Queensland Eye Institute, Brisbane, Queensland, Australia

Correspondence: Associate Professor Graham A Lee, City Eye Centre, 10/135 Wickham Tce,

Brisbane, Queensland 4000, Australia

E-mail: [email protected]

Short running title: Hypotony, sympathetic ophthalmia and TSCPC

Received 30 September 2012; accepted 12 February 2013

Competing/conflicts of interest: No stated conflict of interest

Funding sources: No stated funding sources

This work has been presented in part at the Royal Australian and New Zealand Annual

Scientific Congress of Ophthalmology, 19-22 November 2011, Canberra, Australia.

This article has been accepted for publication and undergone full peer review but has not been through the

copyediting, typesetting, pagination and proofreading process, which may lead to differences between this

version and the Version of Record. Please cite this article as doi: 10.1111/ceo.12088 Acc

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ABSTRACT

Background: To report the incidence and risk factors for hypotony and estimate the risk of

sympathetic ophthalmia following diode laser trans-scleral cyclophotocoagulation (TSCPC).

Design: Retrospective study using data from a private tertiary glaucoma clinic and review of

the literature.

Participants: Seventy eyes of 70 patients with refractory glaucoma who received TSCPC

treatment.

Methods: Review of the records of consecutive patients who underwent TSCPC by a single

ophthalmic surgeon and review of the literature.

Main Outcome Measures: Hypotony (including phthisis bulbi), sympathetic ophthalmia.

Results: Seven eyes (10%; CI 5-19%) developed hypotony and included 4 eyes that

developed phthisis. Higher total energy delivered during TSCPC treatment was associated

with an increased risk of hypotony: eyes that developed hypotony received a mean total

energy of 192.5 ± 73.2 joules, compared to a mean of 152.9 ± 83.2 joules in hypotony-free

cases. The difference in mean energy delivered between the hypotony and non-hypotony

group was 38.53 (95% CI: -27.57 to 104.63). The risk of sympathetic ophthalmia estimated

from a review of the published literature and current series was one in 1512, or 0.07% (CI

0.03% - 0.17%).

Conclusions: Total laser energy is one of several risk factors that act in a sufficient

component cause-model to produce hypotony in an individual patient. The small sample size

precluded inference for other individual putative risk factors but titrating laser energy may

help decrease the occurrence of hypotony. The risk of sympathetic ophthalmia calculated

from the literature is likely an overestimate caused by publication bias.

Keywords: cyclophotocoagulation, diode laser, glaucoma, hypotony, total energy,

multifactorial, sympathetic ophthalmia.

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INTRODUCTION

Trans-scleral cyclophotocoagulation (TSCPC) using the diode laser is widely utilised as

treatment for high intraocular pressure (IOP) that is refractory to other medical and surgical

options.1-9

Reported success varies between 37% and 82%, but between study comparisons

are hampered by different treatment protocols, definitions of success, types of glaucoma

included and other uncontrolled factors.2-7,9-11

Recent reports used a combination of TSCPC

and intravitreal bevacizumab in the treatment of neovascular glaucoma (NVG). Whilst the

combination treatment provides rapid control of the anterior segment neovascularisation,12

there was no long term advantage in IOP lowering effect, compared to treatment with TSCPC

alone.13

In recent years, TSCPC has also been proposed for eyes with good visual

potential.4,14

Visually threatening complications of TSCPC treatment include hypotony, phthisis bulbi,

hyphaema, corneal oedema, vitreous haemorrhage and severe uveitis.2,9,15

The occurrence of

these complications is variable with overall occurrence in the larger TSCPC studies reported

to be around 3.3% - 12.2%.9,15

The reported frequency of hypotony in these studies varied

between 1.4% - 9.5%.9,15

Sympathetic ophthalmia has been reported as a “rare”

complication.16-18

These risks are comparable to the risks of visual loss reported with other

surgical options for end-stage glaucoma disease.14

Currently much variety exists in practice as to the ideal power settings to use in particular

cases of glaucoma and there are no standardised protocols for TSCPC that maximise success

and minimise the risk of complications.19

We report the incidence and risk factors for

hypotony following TSCPC in a single surgeon series, as well estimate the risk of

sympathetic ophthalmia based on published literature.

METHODS

This retrospective analysis included all consecutive patients who underwent primary TSCPC

treatment performed by one glaucoma specialist (GL) between January 2002 and February

2010. The data collected included patient demographics, medical and ocular history, ocular

medications (topical and oral), diagnostic category of glaucoma, IOP, best corrected visual Acc

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acuity (BCVA), TSCPC parameters (number, placement, power and duration of shots),

combination with intravitreal bevacizumab injection and complications. A minimum of 6

months follow up was required for inclusion in the study; reviews were performed by GL or

one other ophthalmic surgeon. Patients who had received previous TSCPC treatment with

another ophthalmic surgeon were excluded.

The indication for TSCPC was uncontrolled IOP on maximally tolerated medical therapy.

TSCPC with the laser (Iridex Corporation, CA, USA) was performed as an outpatient

procedure under peri-bulbar anaesthesia with ropivacaine 1% (Naropin, AstraZeneca, NSW,

Australia). Diode laser was applied with the G-probe using a power of 2000mW x 2000msec

evenly placed circumferentially around the limbus avoiding the 3 and 9 o’clock positions.

The burns were applied in an overlapping fashion 1-2 mm behind the limbus. The power of

diode laser was reduced by 200mW if more than two ‘pops’ from disruption of the ciliary

processes were observed. The number of burns was adjusted depending on the level of IOP

(IOP >40mmHg – 40 burns, 30-40mmHg – 30 burns and <30mmHg – 20 burns). If the

patient was on oral acetazolamide the number of burns was increased, usually by 10 shots for

those on 250 mg QID and 5 shots for 125 mg QID.

Prior to 2006, patients with NVG in whom medical treatment failed to control the IOP

underwent TSCPC alone. Following the availability of bevacizumab as a therapeutic option,

selected patients received combination therapy with TSCPC and intravitreal bevacizumab. In

eyes that underwent combination TSCPC and intravitreal bevacizumab, the eye was re-

prepared and draped after TSCPC, under the same peribulbar anaesthesia. A 0.05mL of

solution containing 1.25mg of bevacizumab was injected intra-vitreally 3.5 to 4.0mm

posterior to the limbus in the superotemporal quadrant. The injection was performed after the

TSCPC procedure to avoid any subconjunctival haemorrhage resulting in conjunctival burns.

Following the procedure, chloramphenicol ointment and a double eye pad were applied

overnight and oral analgesia was used as required. Prednisolone acetate1%/phenylephrine

HCl 0.12% (Prednefrin Forte, Allergan, NSW, Australia) QID was prescribed for 7 days and

glaucoma medications were maintained until the initial follow up visit at 3 weeks and then

adjusted according to the IOP. Additional TSCPC treatments were administered if adequate

IOP control was not achieved, following the above-mentioned protocol. Further follow up Acc

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was scheduled at 3 to 6 monthly intervals until stable and then annually. Hypotony was

defined as an IOP of ≤5 mmHg at final follow up that was considered to be responsible for

loss of vision. Phthisis bulbi was defined as visible shrinkage of the globe (assessed by GL)

associated with hypotony.

To analyse the effect of different treatment doses, total TSCPC energy (joules) was calculated

by multiplying the number of shots by the power delivered per shot (watts) and the duration

of each shot (seconds). Where multiple treatments were given, the total TSCPC energy was

the sum of the energy administered during each treatment episode. BCVA was arbitrarily

categorised into 3 levels, with level 1 being a BCVA of ≥6/12; level 2 <6/12 to 6/60; and

level 3 being a BCVA <6/60.

Statistical analysis was conducted using SPSS version 17.0. For patients who received

bilateral TSCPC (n = 2) only one eye (the eye with the worse visual outcome or presence of a

complication) was included for statistical analysis. Potential risk factors for hypotony such as

total energy delivered, type of glaucoma such as neovascular glaucoma, and previous surgery

were examined independently using the Chi-Square test, unpaired t-tests and Mann-Whitney

U Tests as appropriate after assessing normality. As the number of events was small, simple

linear regression was used to examine the relationship between variables of interest in the

pooled study analysis. P-values <0.05 were considered statistically significant.

RESULTS

Seventy eyes (34 Right and 36 Left) of 70 patients (36 Male:34 Female) with a mean age of

60 ± 21(standard deviation, SD) years (range 6-86 years) were eligible for inclusion in this

study. Five patients were under the age of 18 years. Thirty-four eyes (48.6%) had a history of

previous glaucoma surgery (excluding TSCPC). The mean follow up period was 29 ± 19

months (range 6-97 months). NVG 26 (37.1%) was the most common type of glaucoma

treated, followed by primary open angle glaucoma (POAG) 13 (18.6%). Less common types

included uveitic 6 (8.6%), traumatic 5 (7.1%), aphakic 4 (5.7%) and congenital glaucoma 3

(4.3%) (Table 1; Figure 1). Thirteen eyes (18.6%) with NVG received a combination of

TSCPC and intravitreal bevacizumab.

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The mean pre-treatment IOP was 36.5 ± 10.8 mmHg. The mean post-treatment IOP at final

follow up was 16.8 ± 9.1 mmHg, a mean reduction of 19.7mmHg. The post-treatment IOP at

6 months was 20.1 ± 9.4 mmHg. An average of 1.3 ± 0.6 treatment sessions per eye (range 1-

4) were used in the study, with 55 (78.6%) eyes receiving only a single treatment, 11 (15.7%)

eyes receiving 2 treatments, 3 (4.3%) eyes receiving 3 treatments and one (1.4%) eye

receiving 4 episodes of TSCPC. The mean total energy delivered per eye was 157.8 ± 83.4

joules, with an average of 43.2 ± 24.7 total shots, 1891 ± 180 mW of mean power and 1964 ±

124 ms mean duration per shot. The mean energy delivered per treatment session was 122.9 ±

31.5 joules.

The distribution of BCVA pre-TSCPC treatment was as follows: 14 (20.0%) eyes at level 1

(BCVA ≥6/12), 16 (22.9%) at level 2 (BCVA <6/12 to 6/60) and 40 (57.1%) at level 3

(BCVA <6/60). At final follow up post-TSCPC, the distribution was 10 (14.3%) eyes at level

1, twelve (17.1%) at level 2 and 48 (68.6%) at level 3. This represented a reduction in the

level of BCVA in 15 (21.4%) eyes, an improvement in 4 (5.7%) eyes and a stable level of

BCVA in the remaining 51 (72.9%) eyes during the period of follow up.

Hypotony occurred in 7 eyes (10.0%; CI: 5-19%) and phthisis developed in 4 of these eyes

(5.7%). Of the 7 eyes that developed hypotony, BCVA pre-TSCPC was hand movements or

worse in 5. The other 2 eyes had pre-TSCPC BCVA of 6/7.5 and 6/24 (with field loss to

within 5 degrees of fixation), which decreased to 6/20 and no light perception respectively at

final follow up.

Hypotony versus No Hypotony patient groups

The data was categorised based on the presence of hypotony (n = 7) or absence (n = 63)

arising from TSCPC treatment. The patient demographics and clinical data for each group are

summarised in Table 2. The ‘hypotony’ and ‘no hypotony’ groups were reasonably matched

for both age and gender.

There were no significant differences between the hypotony and the no hypotony groups with

respect to the number of TSCPC treatments, mean power delivered per TSCPC shot or mean

duration of TSCPC shots (p-values >0.05). Mean total energy of TSCPC delivered per eye

tended towards higher levels in the hypotony group (192.5 ± 73.2 joules) versus the no Acc

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hypotony group (154.0 ± 84.0 joules). The difference in mean energy delivered between the

hypotony and no hypotony group was 38.53 joules (95% CI: -27.57 to 104.63; p = 0.17)

(Table 2). The number of shots, 53.71 ± 18.88 in the hypotony group was higher compared to

42.06 ± 25.10 in the no hypotony group (p = 0.03).

There were no significant differences between the hypotony and no hypotony groups with

respect to any of the non-TSCPC variables, including; age, gender, pre-treatment BCVA, pre-

treatment IOP, glaucoma type or prior glaucoma surgery (p>0.05) (Table 2). Figure 1 shows

the distribution of patients according to the type of glaucoma and the proportion of each

group with post-treatment hypotony.

Of the 26 eyes with NVG, half (13 eyes) received concurrent intravitreal bevacizumab with

TSCPC. One (7.7%) patient of those who underwent TSCPC alone developed hypotony,

compared to two (15.4%) who received bevacizumab in addition. The 13 eyes that received

combination treatment however were delivered a significantly higher mean total energy of

TSCPC (183.8 ± 98.7 joules) versus the TSCPC alone group (121.9 ± 29.2 joules) (p = 0.04).

There was a significant difference in the IOP at final follow up (23.5 ± 13.6 mmHg versus

12.2 ± 7.5mmHg, combination and TSCPC alone groups, respectively; p = 0.02).

Other complications following TSCPC included uveitis, 3 (4.3%) and scleritis, 1 (1.4%). No

cases of sympathetic ophthalmia have been observed to date.

DISCUSSION

The overall hypotony rate of this study of 10% (CI 5-19%) was within the range (0-18%)

published in the literature,5 but is comparatively high when compared with larger TSCPC

studies (1.4 - 9.5%).9,15

Hypotony contributed in part to the observed loss in BCVA, however

these eyes are generally at an end stage and the natural history of the disease would almost

inevitably lead to loss of further vision and the eye overtime. Nonetheless, improvement of

the safety of TSCPC is of prime importance. Two factors of particular note are that the mean

energy delivered per treatment session and mean total energy in this study were amongst the

highest of the studies presented in Table 3. This allows us to compare the outcomes of a more

aggressive protocol against those previously published in the literature. Acc

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A review of the published literature conducted by Vernon et al investigating the incidence of

serious complications as a function of total diode laser energy during treatment, showed

protocols with less than 60 joules of energy per treatment session were free of these

complications.5 Above 60 joules of energy per treatment session revealed rates of persistent

hypotony ranging from 0-18%, and phthisis bulbi ranging from 0 - 5.3%.5,9,15,20-23

Murphy et

al investigated the predictive factors for developing hypotony and found the only associated

factors were high pre-treatment IOP and high mean treatment energy per episode; a

multivariable analysis was not conducted.15

In the current study, the difference in mean

energy between those who developed hypotony and those who did not was not statistically

significant (p = 0.17), however the point estimate of 38.53 joules with a confidence interval

around this difference of -25.57 to 104.63, would suggest a higher mean energy results in a

greater risk of hypotony. Our study also identified a greater number of shots of TSCPC

(related to total energy delivered) as a significant factor for developing hypotony (p = 0.03).

The occurrence of hypotony in an individual patient is likely to be multifactorial and a simple

deterministic approach to cause is not expected to reap dividends. A sufficient component

cause model can be useful in elucidating individual mechanisms of causation.24

The existing

literature combined with the biologic plausibility of the point estimate and the upper end of

the confidence interval, together implicate mean energy as part of the causal complement that

produces hypotony in an individual case. The fact that some patients who developed

hypotony received lower energy compared to the no hypotony group only support these

concepts. The lack of a statistically significant difference in mean energy between the two

groups is a function of sample size and not an argument against the possible causal role of

energy in hypotony.

Ramli et al, in a recently published study investigated the risk factors for hypotony after

TSCPC in an Asian population.25

With a comparatively high hypotony rate of 17.7%, they

identified NVG as a significant risk factor. This study delivered a mean of 83.3 joules of total

energy of TSCPC, increasing shot duration and power until ‘pops’ were heard throughout

50% of the procedure. Our study’s mean total energy of 157.8 joules is notably higher,

despite a lower hypotony rate of 10%. Our protocol limited ‘pops’ with reductions in power if

these were heard. The study population was also different, in that most of our population was

Caucasian, with less pigmentation and hence potentially lower absorption of laser energy per Acc

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shot than in the more pigmented Asian eye. The present study did not find type of glaucoma

or age to be associated with increased risk of hypotony, however it is difficult to form

definitive conclusions without larger sample sizes. A number of protocols suggest sparing

one quadrant may reduce the risk of hypotony,19

however other studies found it acceptable to

spare only the 2 clock hours at 3 and 9 o’clock positions to avoid the long posterior ciliary

vessels.

A literature search on PubMed was conducted in April 2012, using the search terms

“cyclodiode,” “cyclophotocoagulation” or “cycloablation”. All papers written in English

identified by this search were reviewed for data on the number of subjects, diagnostic

categories of glaucoma, pre-treatment IOP, post-treatment IOP, mean TSCPC total energy

delivered and complications, including hypotony and phthisis. Smaller studies with number

of subjects <40 were excluded, leaving 27 study groups (including results from this study)

with data available for a pooled analysis. A formal meta-analysis was not attempted.

The 27 TSCPC study groups included in the pooled analysis are summarised in Table 3.1-

7,9,14,15,20,21,23,25-37 The mean pooled pre-treatment IOP was 35.02 ± 6.11 (SD) mmHg (range

21 – 46 mmHg). This mean pre-treatment IOP was assigned as an arbitrary demarcation level

to examine the association between pre-treatment IOP and hypotony rate in the pooled data.

For the 13 studies with a mean pre-treatment IOP of less than 35 mmHg, the mean hypotony

rate was 1.02 ± 1.37%, compared to 7.23 ± 6.00% for the 14 studies with a pre-treatment IOP

of greater than 35 mmHg, (p = 0.01). Figure 2a shows the relationship of hypotony to mean

pre-treatment IOP in the pooled data sets (n = 27). Simple linear regression revealed a

positive correlation between pre-treatment IOP and hypotony rate (R2= 16%; p = 0.04). Also,

studies that reported no cases of hypotony had a mean pre-treatment IOP of 31.56 ± 3.98

mmHg, compared with 37.33 ± 5.26 mmHg for studies reporting cases of hypotony. Using

5% hypotony as the cut off yielded similar results. The confounding factor responsible for

this trend is that eyes with higher pre-treatment IOP likely to have received higher doses and

re-treatments of TSCPC, leading to a higher rate of hypotony.

Using the pooled data, there was a correlation between higher mean energy delivered per

treatment session and an increase in the rate of hypotony (R2 = 59%, p = 0.22) (Figure 2b).

For the studies in the pooled data that provided the information (n = 13), no statistically Acc

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significant association however was detected between mean total energy delivered and

hypotony rate. Due to inconsistent reporting of energy delivery among studies, we were

unable to further investigate this probability. The pooled analysis did not show a significant

relationship between the mean total energy delivered or energy per treatment session and

hypotony rate. This may be attributed to limitations of the analysis that could only be done on

the small number of studies reporting this data. Fourteen of the 27 study groups did not report

the total mean energy levels delivered per eye, with 8 studies neither reporting mean levels of

total energy or energy delivered per treatment session.

Our data corroborates the role of total energy delivered as an important factor in the causation

of hypotony. The R2 of 59% is significant and as discussed above mean energy is probably

one factor of a causal complement that produces hypotony in an individual case. It is

important to remember that there may be other such sufficient component causal models and

that “high” energy may not need to be present in each one of them; the level of energy used

as a cut off need not be a universally necessary cause.

Sympathetic ophthalmia is a rare complication of TSCPC but the actual incidence is not

known. While we did not encounter a case in this series, the incidence of sympathetic

ophthalmia following TSCPC with diode laser was estimated using data collected from an

extended literature search. A PubMed search (search terms as previous) was conducted in

September 2012. All identified papers written in any language (provided an abstract

translated into English was available) had their abstracts reviewed for data on the number of

cases of TSCPC with diode laser, and cases of sympathetic ophthalmia. Abstracts specifying

the use of diode laser TSCPC on human eyes were included.

Four cases of sympathetic ophthalmia have been reported following TSCPC.16-18

In the

extended literature search conducted, we identified 5979 eyes (6049 eyes including the

current study) that had undergone diode laser TSCPC.1-9,11-18,20-23,25-148

If we include all cases

of diode laser TSCPC reported in the literature (including the current study), the incidence is

estimated at one in 1512, or 0.07% (95% CI 0.03% - 0.17%). It must be emphasised that this

is likely to be an overestimate produced by reporting bias: only a minority of the TSCPC

performed worldwide are published but a remarkable adverse event like sympathetic Acc

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ophthalmia will likely selectively enter the literature. As long as this aspect is explained to

the patient, the above estimate may be useful for informed consent.

In summary, TSCPC is an established modality in the management of intractable glaucoma

but has potentially serious complications including hypotony, phthisis bulbi and sympathetic

ophthalmia. Our (aggressive) treatment protocol identified a greater total energy of TSCPC

delivered as a risk factor for hypotony. Higher pre-treatment IOP as suggested in the pooled

analysis and number of shots as identified in our study may also be related to the amount of

energy used. The cause of hypotony in an individual following cyclodiode treatment is likely

to be multifactorial; one way of elucidating individual mechanisms is in the framework of a

sufficient component cause-model. The complementary causes in such a framework could

include reported causes such as pre-treatment IOP, diagnostic category and laser energy used

and more than one such model may exist. Finally, based on available data the incidence of

sympathetic ophthalmia can be estimated to be about 0.07% (95% CI 0.03% - 0.17%); this is

likely an overestimate.

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TABLES

Table 1: Summary of eyes treated with cyclodiode

Diagnostic

category

Number of

eyes, n (%

total)

Pre-treatment

IOP (mmHg)

Post-treatment

IOP (mmHg)

Percentage

reduction in

IOP

Number of

treatment

episodes

Total energy

(J)

Hypotony n

(%)

All eyes 70 (100) 36.5 ± 10.8 16.8 ± 9.1 51 ± 28 1.3 ± 0.6 157.8 ± 83.7 7 (10)

NVG 26 (37) 43.0 ± 10.6 17.6 ± 12.0 56 ± 32 1.2 ± 0.5 152.8 ± 77.9 3 (12)

POAG 13 (19) 29.3 ± 5.8 14.4 ± 6.2 49 ± 23 1.2 ± 0.6 137.7 ± 67.5 1 (8)

Other

Secondary 9 (13) 32.4 ± 6.7 15.0 ± 5.3 53 ± 16 1.3 ± 0.5 138.6 ± 67.9 0 (0)

Uveitic 6 (9) 39.0 ± 8.8 18.2 ± 9.9 48 ± 32 1.3 ± 0.5 197.3 ± 90.5 1 (17)

Traumatic 5 (7) 43.0 ± 9.9 21.8 ± 7.0 44 ± 31 2.0 ± 1.2 260.3 ± 115.6 1 (20)

Aphakic 4 (6) 33.3 ± 12.0 15.8 ± 6.3 52 ± 19 1.5 ± 1.0 190.0 ± 114.9 0 (0)

Congenital 3 (4) 26.7 ± 5.8 18.7 ± 6.4 29 ± 19 1.0 ± 0 122.7 ± 40.3 0 (0)

CACG 2 (3) 26.0 ± 5.7 11.5 ± 10.6 50 ± 52 1.5 ± 0.7 126.5 ± 83.5 1 (50)

JOAG 2 (3) 24.0 ± 5.7 17.0 ± 12.7 34 ± 37 1.0 ± 0 85.0 ± 7.1 0 (0)

Data presented as mean ± SD unless stated otherwise Acc

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Table 2: Patient demographics and clinical data for groups categorised by ‘no hypotony’ and

‘hypotony’

Variable No hypotony

(n = 63)

Hypotony

(n = 7)

Unpaired group

comparison

(p-value)*

Age (years) 58.98 ± 20.23 64.86 ± 25.08 0.57

Gender (%, M:F) 54:46 29:71 0.15

Pre-treatment IOP (mmHg) 36.08 ± 11.00 40.14 ± 7.77 0.24

Level 1

(BCVA ≥ 6/12) 13 (20.6) 1 (14.3)

Level 2

(6/12 >BCVA ≥6/60) 15 (23.8) 1 (14.3)

Pre-

BCVA n

(%) Level 3

(BCVA < 6/60) 35 (55.6) 5 (71.4)

0.87

NVG 23 (36.5) 3 (42.8)

POAG 12 (19.0) 1 (14.3)

Glaucoma

Type

n (%)

Other 29 (46.0) 3 (42.9)

0.94

No

n-c

ycl

od

iod

e v

ari

ab

les

Prior glaucoma surgery n (%) 32 (51) 2 (29) 0.26

Number of treatments 1.27 ± 0.63 1.43 ± 0.53 0.20

Number of shots 42.06 ± 25.10 53.71 ± 18.88 0.03

Power (mW) 1898.76 ± 178.28 1822.43 ± 194.48 0.07

Duration (ms) 1963.49 ± 127.38 1964.29 ± 94.49 0.64

Total Energy (J) 153.98 ± 84.04 192.51 ± 73.19 0.17

Cy

clo

dio

de

vari

ab

les

Combination intravitreal

bevacizumab n (%) 11 (17) 2 (29) 0.27

Data presented as mean ± SD or n, percentage.

* counts/ratios examined with Chi Square, normally distributed data examined with unpaired

t-test, non-normally distributed data examined with independent samples Mann-Whitney U

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Table 3: Summary of studies included in retrospective pooled analysis

Study Number of

subjects (n)

Pre-treatment

IOP (mmHg)

Post-treatment

IOP (mmHg)

Total energy

(J)

Mean energy

per session (J) Hypotony (%)

Current study 70 36.5± 10.8 16.8± 9.1 157.8 122.9 10.0

Ramli et al. 201225

90 41.8 ± 12.9 17.8 ± 12.9 83.3 NA 17.8

Frezzotti et al. 20102 124 29.9 ± 8.4 20.8 ± 8.0 NA 36.7 0.0

Rotchford et al. 201014

49 28.0± 7.2 15.3 ± 5.8 99.7 57.6 0.0

Kaushik et al. 200826

66 36.4 ± 10.7 15.6 ± 6.6 87.8 NA 9.1

Ansari et al. 20074 74 40.3 21.1 124.1 NA 0.0

Illiev et al. 20073 131 36.9 ± 10.7 15.3 ± 10.4 133.9 86.8 17.6

Grueb et al. 20066 90 21 16 80 NA 1.1

Vernon et al. 20065 42 31.4 ± 8.8 15.6 ± 6.3 NA 56 0.0

Chang et al. 200431

A 73 36.9 ± 10.7 17.8 ± 11.0 140.4 NA 2.7

Chang et al. 200431

B 56 33.2 ± 10.0 19.0 ± 12.2 157.9 NA 1.8

Leszczynski et al. 200430

83 46.0 ± 12.6 18.0 ± 6.4 124.8 NA 3.6

Autrata et al. 200327

69 34.1 ± 7.13 20.8 ± 6.38 NA 105 0.0

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Murphy et al. 200315

263 40.7 ± 13.7 17.7 ± 10.9 155.2 104.1 9.5

Pucci et al. 20037 120 30.4 ± 3.1 20.3 ± 1.8 NA NA 0.0

Ataullah et al. 200237

55 35.8 ± 9.7 17.3 ± 7.7 91 52 3.6

Hauber et al. 20021 47 29.4 ± 10.9 15.7 ± 12.0 102.5 102.5 0.0

Kirwan et al. 200232

77 32.0 ± 6.4 NA NA NA 3.9

Kramp et al. 200228

193 24.6 ± 6.7 19.3 ± 5.7 NA NA 1.6

Egbert et al. 200129

79 29 ± 8.9 25.7 ± 10.3 NA NA 0.0

Gupta et al. 200033

52 44.7 ± 7.3 15.2 ± 8.2 NA NA 1.9

Rebolledaet al. 199935

43 45.6 ± 14.2 NA NA 58.4 2.3

Spencer et al. 199920

58 33.0 ± 10.7 16.7 ± 7.8 NA 55.5 3.5

Threlkeld et al. 199934

47 38.0 ± 11.0 16.0 ± 11.0 NA NA 14.9

Yap-Veloso et al. 199823

43 36.3 ± 13.9 17.7 ± 9.0 NA NA 2.33

Youn et al 199836

49 38.1 ± 14.3 16.8 ± 7.6 NA 74.5 6.12

Bloom et al. 19979 210 34.1 ± 10.6 20.1 ± 9.3 NA NA 1.43

Data presented as mean ± SD, unless stated otherwise. Studies presented without SD - data not available.

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FIGURES

Figure 1: Proportion of each diagnostic category of glaucoma with hypotony

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Figure 2: (a) Pre-treatment IOP, and (b) mean energy delivered per treatment session versus

occurrence of hypotony for the reviewed studies.

(a)

Studies included: n >40 reporting hypotony and pre-treatment IOP.1-7,9,14,15,20,23,25-37

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(b)

Studies included: n >40 reporting hypotony and mean energy delivered per treatment

session.1-3,5,14,15,20,27,35-37

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