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Clinical and Experimental Ophthalmology 2015; 43: 234–238 doi: 10.1111/ceo.12433
Original Article Severe intraocular pressure response to periocular or intravitreal steroid treatment in Australia and New Zealand: data from the Australian and New Zealand Ophthalmic Surveillance Unit Jude T Fitzgerald BMBS,1 Lynda Saunders MHA,1 Bronwyn Ridge BA(Psych),1 Andrew JR White FRANZCO,2 Ivan Goldberg FRANZCO,3,4,5 Ben Clark FRANZCO,6 Richard AD Mills FRANZCO1 and Jamie E Craig FRANZCO1 1
Department of Ophthalmology, Flinders University, Adelaide, South Australia, 2Save Sight and Westmead Millennium Institutes, Discipline of Ophthalmology, University of Sydney, 4Glaucoma Unit, Sydney Eye Hospital, 5Eye Associates, Sydney, New South Wales and 6Department of Ophthalmology, St John of God Hospital, Geelong, Victoria, Australia 3
ABSTRACT Background: Increase in intraocular pressure is a recognized complication of corticosteroid treatment via intravitreal or periocular injections for treatment of a range of conditions including macular oedema and retinal neovascularization. Design: This surveillance study was designed to determine the incidence and nature of severe intraocular pressure elevation as a complication of intravitreal or periocular corticosteroid injections in Australia and New Zealand. Participants: Seventeen cases meeting the defined criteria of severe intraocular pressure elevation, above 35 mmHg, following an intravitreal or periocular corticosteroid injection were included in the study. Methods: Over an 18-month period, ophthalmologists were invited to report cases to the Australian and New Zealand Ophthalmic Surveillance Unit. After reporting, further demographic and clinical information was sought via a follow-up questionnaire.
Main Outcome Measures: Intraocular pressure elevation above 35 mmHg. Results: Follow-up questionnaires were received for 20 cases of 34 initially reported to the unit. Seventeen met the defined criteria. Triamcinolone acetonide was used in all 17 cases, with 16 delivered as a 4-mg intravitreal injection. There was an absence of identified underlying risk factors in the majority of cases with personal history of glaucoma in 2 of 17 cases. No cases reported a positive family history of glaucoma. Trabeculectomy was performed in 8 of 17 patients (47%) for intraocular pressure management. Conclusions: Severe intraocular pressure elevation following intravitreal or periocular corticosteroid injection can occur in the absence of risk factors such as personal and family history of glaucoma. The severe intraocular pressure elevation may ultimately require trabeculectomy. Key words: intravitreal steroid injection, IVTA, steroid response, surveillance unit.
■ Correspondence: Dr Jude Fitzgerald, Department of Ophthalmology, Flinders University, Flinders Drive, Bedford Park, SA 5042, Australia. Email: jude.fitzgerald@flinders.edu.au Received 26 April 2014; accepted 24 August 2014. Competing/conflicts of interest: No stated conflict of interest. Funding sources: No stated funding sources. © 2014 Royal Australian and New Zealand College of Ophthalmologists
Steroid induced severe pressure rise
INTRODUCTION Raised intraocular pressure (IOP) is a recognized complication of corticosteroid treatment; it has been reported following topical and/or systemic corticosteroids and more recently intravitreal and periocular injections of corticosteroid.1–3 Intravitreal corticosteroid injections are used clinically for a range of retinal conditions including macula oedema and retinal neovascularization, for which they provide more efficacious and sustained treatment than other routes of administration.3 Intravitreal injections of triamcinolone acetonide (IVTA) have been shown to have a prolonged effect. The mean elimination half-life of 18.6 days following a 4-mg injection of triamcinolone means measurable quantities would be expected intraocularly for approximately 3 months post-injection.4 Although reported rates for IOP rise after corticosteroid administration vary depending on the definition of pressure response employed, a 2007 study showed over 60% of patients will have an IOP rise greater than 5 mmHg from baseline.5 In the same study, 32.5% of patients required topical glaucoma therapy for IOP control following intravitreal injection of 4 mg triamcinolone.5 A severe IOP elevation following corticosteroid injection is less common, with reported incidence between 5.5% and 12.3% for IOP > 35 mmHg following IVTA.6,7 The IOP rise following corticosteroid injection is usually seen around 4 to 8 weeks after treatment; however, severe pressure responses have been reported at greater than 6 months post-injection.8 Topical IOP lowering agents are adequate to control IOP in many cases of steroid response, yet some patients are not adequately controlled medically and require laser or surgical management, to prevent vision loss from glaucoma, which can lead to total blindness in the affected eye. Approximately 1% of patients will require laser or surgery to manage IOP following IVTA injection.7,9–11 Risk factors for IOP rise following steroid administration have been reported as increasing age, personal history of glaucoma, having a first-degree relative with primary open-angle glaucoma, high myopia, type 1 diabetes mellitus and some connective tissue disorders.12,13
235 1
2 3 4
5
The number of cases of severe IOP elevation after periocular and intraocular steroid treatment in Australia and New Zealand. The demographics of affected patients. The underlying risk factors in such patients. The time-course of periocular and intravitreal corticosteroid treatment responsible for the severe IOP elevation. The clinical management and outcomes of such patients.
Our study was run by the Department of Ophthalmology, Flinders University, Adelaide; it was registered with the Australian and New Zealand Ophthalmic Surveillance Unit (ANZOSU). ANZOSU is a newly established resource that facilitates national active surveillance of rare eye conditions that are either important for public health or whose natural history or management is of clinical or scientific interest. Ophthalmologists registered in Australia and New Zealand are sent a monthly report card by email listing conditions currently being studied through the ANZOSU. Any patients diagnosed in the study period with any of the conditions listed are reported by their treating ophthalmologist. Ophthalmologists responding to the monthly ANZOSU report card during an 18-month period, from May 2010 to January 2012, were asked to report instances of severe IOP elevation following steroid injection. This was defined as an IOP greater than or equal to 35 mmHg in an eye that had received a periocular or intraocular steroid injection within the past 12 weeks. The principal investigator was informed of all new cases that were reported to the ANZOSU and a brief questionnaire was sent to the reporting ophthalmologist requesting further de-identified information. Completed questionnaires were returned to the investigators via reply-paid envelopes. Information collated from the questionnaires included demographic details, presence of risk factors, dose and time-course of intravitreal treatment and presentation of severe IOP rise along with clinical management and its outcomes in accordance with the study objectives. The study was performed with ethics approval from Flinders University and was conducted in accordance with Declaration of Helsinki.
METHODS
RESULTS
We set out to establish prospectively the following factors involved in severe ocular hypertension following intravitreal or periocular use of steroids (triamcinolone acetonide, methylprednisolone acetate or dexamethasone):
ANZOSU recorded 34 eyes of 34 patients with severe IOP rise following administration of intravitreal, subconjunctival or periocular steroids, during the reporting period. Questionnaire responses with further clinical information regarding cases were
© 2014 Royal Australian and New Zealand College of Ophthalmologists
236
Fitzgerald et al.
received for 20 cases (59% follow-up response rate of initially reported cases). Of these 20 responses, three did not meet the specified IOP rise for the defined severe response. The reported data are on the 17 cases meeting the severe response definition.
Demographics of cases meeting the definition of severe response for which questionnaire was completed Responses were received from six different states of Australia and from New Zealand, with ages of steroid responders ranging from 8 to 76 years, with a mean of 57.5 ± 21.4 years. Females accounted for 53% of steroid responders.
Presence of underlying risk factors for steroid response A personal history of glaucoma was reported in 2 of 17 cases (11.8%). Of the 17 cases, 16 reported no known family history of glaucoma and 1 case had no family history information recorded.
Treatment type Triamcinolone acetonide was the steroid administered in all 17 cases, with 16 delivered via a 4-mg intravitreal injection. One case of severe IOP response was reported after a 40 mg subconjunctival dose of triamcinolone acetonide. No events of severe IOP rise were reported with injections of methylprednisolone acetate or dexamethasone implant products. A single dose of corticosteroid was
Table 1. Indication for intravitreal or periocular corticosteroid treatment Indication for steroid
Number of cases
Uveitis Diabetic maculopathy Maculopathy/cystoid macula oedema Retinal vein occlusion To visualize vitreous in posterior capsule rupture Not recorded
5 5 3 2 1 1
reported for 15 cases, while one case had a previous corticosteroid injection, and another had two previous orbital floor injections of methylprednisolone, but no previous intravitreal injections. Data were not collected regarding previous history of IOP response to corticosteroid or time delay between administrations. The indications for steroid treatment are listed in Table1, with the most common being uveitis and diabetic maculopathy.
Ocular hypertension characteristics and time-course The mean pre-steroid IOP and mean highest IOP post-steroid are shown in Table 2. The mean time to highest IOP was 50.3 days (7.2 weeks), with a large standard deviation due to a single outlier. The median time to rise was 42 days (6 weeks). The outlier, although outside the inclusion criteria for the study (IOP rise following steroid administration in the past 12 weeks) was included in analysis, and highlights the need for ongoing IOP surveillance long-term post-steroid injections.
Clinical management of ocular hypertension Topical treatment was recorded in 15 patients with a median of three agents required, ranging from two to four agents. Oral acetazolamide was also required in 13 cases. Surgical management (trabeculectomy) was ultimately performed in 8 of 17 patients (47%). In six of these cases, adjunctive mitomycin-C was recorded as being used, and in the remaining two cases, these data were not available. Laser trabeculoplasty was performed in one patient, for whom topical treatment and trabeculectomy were also performed.
Patient outcomes Referring ophthalmologists were asked whether optic disc damage or visual field damage had occurred as a result of the severe rise in IOP. Responses were sought as qualitative answers only,
Table 2. Ocular hypertension characteristics
Pre-steroid IOP Highest IOP post-steroid Time to rise
Average (mean)
Standard deviation
Range
18.3 mmHg 46.1 mmHg 50.3 days
±3.66 mmHg ±7.11 mmHg ±60.2 days
11–24 36–61 7–252 days
IOP, intraocular pressure. © 2014 Royal Australian and New Zealand College of Ophthalmologists
Steroid induced severe pressure rise and did not ask the referring ophthalmologist to quantify the damage if present. Five patients (29.4%) were reported to have suffered optic disc damage due to the IOP following steroid injection, nine cases were reported to have no disc damage and three did not know whether disc damage had occurred or not. Visual field damage was suffered by two patients (11.8%), who also had reported disc damage. Nine reported no visual field damage, and seven patients had visual field damage not reported or not known.
DISCUSSION This is the first reported data from the ANZOSU. Our low numbers of responses may represent underreporting of the true incidence. Of the 34 cases initially reported to the ANZOSU, follow-up clinical data were received for 20 cases (59%). The level of response to this surveillance unit in its early stages is similar to experience from other surveillance units, but does mean it is hard to understand the significance of the results. Response rate and acceptance by the practising community should improve over time.14 A similarly designed study by the British Ophthalmic Surveillance Unit (BOSU) had a national card return rate of 77% in 2009. The BOSU study differed from our study in its definition of severe steroid response, which was based on the requirement for laser or surgical treatment.11 Australian and New Zealand data on the incidence of severe steroid-induced ocular hypertension have not been reported previously. Similar studies using the same definition of IOP >35 mmHg have reported rates between 5.5% and 12.3%. Given the absence of available data on the total number of periocular and intraocular steroid injections in the testing period, we are unable to estimate prevalence data for this report. Of interest and importance for clinical practice are the small numbers with personal glaucoma history (11.8% of cases), and the lack of family history in the cases reported with IOP rise. This result was less than the figure of 20.7% of severe steroid responders with a personal history of glaucoma or ocular hypertension reported by the BOSU.11 Family and personal glaucoma history are wellrecognized risk factors for steroid response; however, our results show that an absence of these risk factors do not preclude a severe response that may require surgical management for control. This could be due to the ophthalmological community being more cautious with administration of steroids when these known risk factors are present. All patients receiving intravitreal or periocular corticosteroids need careful IOP monitoring.
237 Indications for corticosteroid treatment varied, most being for inflammatory eye disease or diabetic macula oedema. The underlying pathology did not seem to affect pressure response. The most common treatment was a 4 mg dose of triamcinolone acetonide delivered by intravitreal injection. This may represent the standard practice for steroid delivery in Australia at this time, rather than a tendency for IOP rise in this treatment regime compared with others. The need for trabeculectomy following IVTAinduced ocular hypertension has been reported as about 1%.7,9 The requirement for trabeculectomy within a severe response group would be expected to be higher. However, with the low rate of reporting of cases to ANZOSU, there is a strong likelihood of bias towards severe, treatment-resistant cases. Details of these cases are more likely to be recalled and therefore reported when the monthly report card and subsequent questionnaire are received. Conversely, cases in which a severe IOP rise was easily controlled with topical therapy may be less likely to be reported or the specific details recalled for the subsequent questionnaire. Severe ocular hypertension following IVTA in Australia and New Zealand occurs without previously described risk factors, in particular family history of glaucoma. The severity of these cases, which occurred up to 9 months post-injection, required trabeculectomy in almost half the population for whom details were provided. The reporting bias towards severe, treatment-resistant cases is acknowledged. Our low numbers of initial reported cases, and lack of responses to follow-up questionnaires suggest that the findings are an underrepresentation of the true number of cases. Further studies are needed to determine better epidemiological data within Australia and New Zealand of this severe treatment complication.
REFERENCES
© 2014 Royal Australian and New Zealand College of Ophthalmologists
1. Francois J. Corticosteroid glaucoma. Ann Ophthalmol 1977; 9: 1075–80. 2. Kalina RE. Increased intraocular pressure following subconjunctival corticosteroid administration. Arch Ophthalmol 1969; 81: 788–90. 3. Gillies MC, Simpson JM, Billson FA et al. Safety of an intravitreal injection of triamcinolone: results from a randomized clinical trial. Arch Ophthalmol 2004; 122: 336–40. 4. Beer PM, Bakri SJ, Singh RJ et al. Intraocular concentration and pharmacokinetics of triamcinolone acetonide after a single intravitreal injection. Ophthalmology 2003; 110: 681–6. 5. Kramar M, Vu L, Whitson JT, He YG. The effect of intravitreal triamcinolone on intraocular pressure. Curr Med Res Opin 2007; 23: 1253–8.
238
Fitzgerald et al.
6. Jonas JB, Degenring RF, Kreissig I, Akkoyun I, Kamppeter BA. Intraocular pressure elevation after intravitreal triamcinolone acetonide injection. Ophthalmology 2005; 112: 593–8. 7. Konstantopoulos A, Williams CPR, Newsom RS, Luff AJ. Ocular morbidity associated with intravitreal triamcinolone acetonide. Eye 2007; 21: 317–20. 8. Williams CP, Konstantopoulos A, Rowley SA, Luff AJ. Late intraocular pressure rise following intravitreal triamcinolone injection. Clin Experiment Ophthalmol 2007; 35: 385–6. 9. Rhee DJ, Peck RE, Belmont J et al. Intraocular pressure alterations following intravitreal triamcinolone acetonide. Br J Ophthalmol 2006; 90: 999–1003.
10. Jain S, Hurst JR, Thompson JR, Eke T. UK national survey of current practice and experience of intravitreal triamcinolone acetonide. Eye 2009; 23: 1164–7. 11. Jain S, Thompson JR, Foot B, Tatham A, Eke T. Severe intraocular pressure rise following intravitreal triamcinolone: a national survey to estimate incidence and describe case profiles. Eye 2014; 28: 399–401. 12. Razeghinejad MR, Katz LJ. Steroid-induced iatrogenic glaucoma. Ophthalmic Res 2012; 47: 66–80. 13. Kersey JP, Broadway DC. Corticosteroid induced glaucoma: a review of the literature. Eye 2006; 20: 407–16. 14. Foot B, Stanford M, Rahi J, Thompson J. The British Ophthalmological Surveillance Unit: an evaluation of the first 3 years. Eye 2003; 17: 9–15.
© 2014 Royal Australian and New Zealand College of Ophthalmologists
Copyright of Clinical & Experimental Ophthalmology is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
Clinical and Experimental Ophthalmology 2015; 43: 234–238 doi: 10.1111/ceo.12433
Original Article Severe intraocular pressure response to periocular or intravitreal steroid treatment in Australia and New Zealand: data from the Australian and New Zealand Ophthalmic Surveillance Unit Jude T Fitzgerald BMBS,1 Lynda Saunders MHA,1 Bronwyn Ridge BA(Psych),1 Andrew JR White FRANZCO,2 Ivan Goldberg FRANZCO,3,4,5 Ben Clark FRANZCO,6 Richard AD Mills FRANZCO1 and Jamie E Craig FRANZCO1 1
Department of Ophthalmology, Flinders University, Adelaide, South Australia, 2Save Sight and Westmead Millennium Institutes, Discipline of Ophthalmology, University of Sydney, 4Glaucoma Unit, Sydney Eye Hospital, 5Eye Associates, Sydney, New South Wales and 6Department of Ophthalmology, St John of God Hospital, Geelong, Victoria, Australia 3
ABSTRACT Background: Increase in intraocular pressure is a recognized complication of corticosteroid treatment via intravitreal or periocular injections for treatment of a range of conditions including macular oedema and retinal neovascularization. Design: This surveillance study was designed to determine the incidence and nature of severe intraocular pressure elevation as a complication of intravitreal or periocular corticosteroid injections in Australia and New Zealand. Participants: Seventeen cases meeting the defined criteria of severe intraocular pressure elevation, above 35 mmHg, following an intravitreal or periocular corticosteroid injection were included in the study. Methods: Over an 18-month period, ophthalmologists were invited to report cases to the Australian and New Zealand Ophthalmic Surveillance Unit. After reporting, further demographic and clinical information was sought via a follow-up questionnaire.
Main Outcome Measures: Intraocular pressure elevation above 35 mmHg. Results: Follow-up questionnaires were received for 20 cases of 34 initially reported to the unit. Seventeen met the defined criteria. Triamcinolone acetonide was used in all 17 cases, with 16 delivered as a 4-mg intravitreal injection. There was an absence of identified underlying risk factors in the majority of cases with personal history of glaucoma in 2 of 17 cases. No cases reported a positive family history of glaucoma. Trabeculectomy was performed in 8 of 17 patients (47%) for intraocular pressure management. Conclusions: Severe intraocular pressure elevation following intravitreal or periocular corticosteroid injection can occur in the absence of risk factors such as personal and family history of glaucoma. The severe intraocular pressure elevation may ultimately require trabeculectomy. Key words: intravitreal steroid injection, IVTA, steroid response, surveillance unit.
■ Correspondence: Dr Jude Fitzgerald, Department of Ophthalmology, Flinders University, Flinders Drive, Bedford Park, SA 5042, Australia. Email: jude.fitzgerald@flinders.edu.au Received 26 April 2014; accepted 24 August 2014. Competing/conflicts of interest: No stated conflict of interest. Funding sources: No stated funding sources. © 2014 Royal Australian and New Zealand College of Ophthalmologists
Steroid induced severe pressure rise
INTRODUCTION Raised intraocular pressure (IOP) is a recognized complication of corticosteroid treatment; it has been reported following topical and/or systemic corticosteroids and more recently intravitreal and periocular injections of corticosteroid.1–3 Intravitreal corticosteroid injections are used clinically for a range of retinal conditions including macula oedema and retinal neovascularization, for which they provide more efficacious and sustained treatment than other routes of administration.3 Intravitreal injections of triamcinolone acetonide (IVTA) have been shown to have a prolonged effect. The mean elimination half-life of 18.6 days following a 4-mg injection of triamcinolone means measurable quantities would be expected intraocularly for approximately 3 months post-injection.4 Although reported rates for IOP rise after corticosteroid administration vary depending on the definition of pressure response employed, a 2007 study showed over 60% of patients will have an IOP rise greater than 5 mmHg from baseline.5 In the same study, 32.5% of patients required topical glaucoma therapy for IOP control following intravitreal injection of 4 mg triamcinolone.5 A severe IOP elevation following corticosteroid injection is less common, with reported incidence between 5.5% and 12.3% for IOP > 35 mmHg following IVTA.6,7 The IOP rise following corticosteroid injection is usually seen around 4 to 8 weeks after treatment; however, severe pressure responses have been reported at greater than 6 months post-injection.8 Topical IOP lowering agents are adequate to control IOP in many cases of steroid response, yet some patients are not adequately controlled medically and require laser or surgical management, to prevent vision loss from glaucoma, which can lead to total blindness in the affected eye. Approximately 1% of patients will require laser or surgery to manage IOP following IVTA injection.7,9–11 Risk factors for IOP rise following steroid administration have been reported as increasing age, personal history of glaucoma, having a first-degree relative with primary open-angle glaucoma, high myopia, type 1 diabetes mellitus and some connective tissue disorders.12,13
235 1
2 3 4
5
The number of cases of severe IOP elevation after periocular and intraocular steroid treatment in Australia and New Zealand. The demographics of affected patients. The underlying risk factors in such patients. The time-course of periocular and intravitreal corticosteroid treatment responsible for the severe IOP elevation. The clinical management and outcomes of such patients.
Our study was run by the Department of Ophthalmology, Flinders University, Adelaide; it was registered with the Australian and New Zealand Ophthalmic Surveillance Unit (ANZOSU). ANZOSU is a newly established resource that facilitates national active surveillance of rare eye conditions that are either important for public health or whose natural history or management is of clinical or scientific interest. Ophthalmologists registered in Australia and New Zealand are sent a monthly report card by email listing conditions currently being studied through the ANZOSU. Any patients diagnosed in the study period with any of the conditions listed are reported by their treating ophthalmologist. Ophthalmologists responding to the monthly ANZOSU report card during an 18-month period, from May 2010 to January 2012, were asked to report instances of severe IOP elevation following steroid injection. This was defined as an IOP greater than or equal to 35 mmHg in an eye that had received a periocular or intraocular steroid injection within the past 12 weeks. The principal investigator was informed of all new cases that were reported to the ANZOSU and a brief questionnaire was sent to the reporting ophthalmologist requesting further de-identified information. Completed questionnaires were returned to the investigators via reply-paid envelopes. Information collated from the questionnaires included demographic details, presence of risk factors, dose and time-course of intravitreal treatment and presentation of severe IOP rise along with clinical management and its outcomes in accordance with the study objectives. The study was performed with ethics approval from Flinders University and was conducted in accordance with Declaration of Helsinki.
METHODS
RESULTS
We set out to establish prospectively the following factors involved in severe ocular hypertension following intravitreal or periocular use of steroids (triamcinolone acetonide, methylprednisolone acetate or dexamethasone):
ANZOSU recorded 34 eyes of 34 patients with severe IOP rise following administration of intravitreal, subconjunctival or periocular steroids, during the reporting period. Questionnaire responses with further clinical information regarding cases were
© 2014 Royal Australian and New Zealand College of Ophthalmologists
236
Fitzgerald et al.
received for 20 cases (59% follow-up response rate of initially reported cases). Of these 20 responses, three did not meet the specified IOP rise for the defined severe response. The reported data are on the 17 cases meeting the severe response definition.
Demographics of cases meeting the definition of severe response for which questionnaire was completed Responses were received from six different states of Australia and from New Zealand, with ages of steroid responders ranging from 8 to 76 years, with a mean of 57.5 ± 21.4 years. Females accounted for 53% of steroid responders.
Presence of underlying risk factors for steroid response A personal history of glaucoma was reported in 2 of 17 cases (11.8%). Of the 17 cases, 16 reported no known family history of glaucoma and 1 case had no family history information recorded.
Treatment type Triamcinolone acetonide was the steroid administered in all 17 cases, with 16 delivered via a 4-mg intravitreal injection. One case of severe IOP response was reported after a 40 mg subconjunctival dose of triamcinolone acetonide. No events of severe IOP rise were reported with injections of methylprednisolone acetate or dexamethasone implant products. A single dose of corticosteroid was
Table 1. Indication for intravitreal or periocular corticosteroid treatment Indication for steroid
Number of cases
Uveitis Diabetic maculopathy Maculopathy/cystoid macula oedema Retinal vein occlusion To visualize vitreous in posterior capsule rupture Not recorded
5 5 3 2 1 1
reported for 15 cases, while one case had a previous corticosteroid injection, and another had two previous orbital floor injections of methylprednisolone, but no previous intravitreal injections. Data were not collected regarding previous history of IOP response to corticosteroid or time delay between administrations. The indications for steroid treatment are listed in Table1, with the most common being uveitis and diabetic maculopathy.
Ocular hypertension characteristics and time-course The mean pre-steroid IOP and mean highest IOP post-steroid are shown in Table 2. The mean time to highest IOP was 50.3 days (7.2 weeks), with a large standard deviation due to a single outlier. The median time to rise was 42 days (6 weeks). The outlier, although outside the inclusion criteria for the study (IOP rise following steroid administration in the past 12 weeks) was included in analysis, and highlights the need for ongoing IOP surveillance long-term post-steroid injections.
Clinical management of ocular hypertension Topical treatment was recorded in 15 patients with a median of three agents required, ranging from two to four agents. Oral acetazolamide was also required in 13 cases. Surgical management (trabeculectomy) was ultimately performed in 8 of 17 patients (47%). In six of these cases, adjunctive mitomycin-C was recorded as being used, and in the remaining two cases, these data were not available. Laser trabeculoplasty was performed in one patient, for whom topical treatment and trabeculectomy were also performed.
Patient outcomes Referring ophthalmologists were asked whether optic disc damage or visual field damage had occurred as a result of the severe rise in IOP. Responses were sought as qualitative answers only,
Table 2. Ocular hypertension characteristics
Pre-steroid IOP Highest IOP post-steroid Time to rise
Average (mean)
Standard deviation
Range
18.3 mmHg 46.1 mmHg 50.3 days
±3.66 mmHg ±7.11 mmHg ±60.2 days
11–24 36–61 7–252 days
IOP, intraocular pressure. © 2014 Royal Australian and New Zealand College of Ophthalmologists
Steroid induced severe pressure rise and did not ask the referring ophthalmologist to quantify the damage if present. Five patients (29.4%) were reported to have suffered optic disc damage due to the IOP following steroid injection, nine cases were reported to have no disc damage and three did not know whether disc damage had occurred or not. Visual field damage was suffered by two patients (11.8%), who also had reported disc damage. Nine reported no visual field damage, and seven patients had visual field damage not reported or not known.
DISCUSSION This is the first reported data from the ANZOSU. Our low numbers of responses may represent underreporting of the true incidence. Of the 34 cases initially reported to the ANZOSU, follow-up clinical data were received for 20 cases (59%). The level of response to this surveillance unit in its early stages is similar to experience from other surveillance units, but does mean it is hard to understand the significance of the results. Response rate and acceptance by the practising community should improve over time.14 A similarly designed study by the British Ophthalmic Surveillance Unit (BOSU) had a national card return rate of 77% in 2009. The BOSU study differed from our study in its definition of severe steroid response, which was based on the requirement for laser or surgical treatment.11 Australian and New Zealand data on the incidence of severe steroid-induced ocular hypertension have not been reported previously. Similar studies using the same definition of IOP >35 mmHg have reported rates between 5.5% and 12.3%. Given the absence of available data on the total number of periocular and intraocular steroid injections in the testing period, we are unable to estimate prevalence data for this report. Of interest and importance for clinical practice are the small numbers with personal glaucoma history (11.8% of cases), and the lack of family history in the cases reported with IOP rise. This result was less than the figure of 20.7% of severe steroid responders with a personal history of glaucoma or ocular hypertension reported by the BOSU.11 Family and personal glaucoma history are wellrecognized risk factors for steroid response; however, our results show that an absence of these risk factors do not preclude a severe response that may require surgical management for control. This could be due to the ophthalmological community being more cautious with administration of steroids when these known risk factors are present. All patients receiving intravitreal or periocular corticosteroids need careful IOP monitoring.
237 Indications for corticosteroid treatment varied, most being for inflammatory eye disease or diabetic macula oedema. The underlying pathology did not seem to affect pressure response. The most common treatment was a 4 mg dose of triamcinolone acetonide delivered by intravitreal injection. This may represent the standard practice for steroid delivery in Australia at this time, rather than a tendency for IOP rise in this treatment regime compared with others. The need for trabeculectomy following IVTAinduced ocular hypertension has been reported as about 1%.7,9 The requirement for trabeculectomy within a severe response group would be expected to be higher. However, with the low rate of reporting of cases to ANZOSU, there is a strong likelihood of bias towards severe, treatment-resistant cases. Details of these cases are more likely to be recalled and therefore reported when the monthly report card and subsequent questionnaire are received. Conversely, cases in which a severe IOP rise was easily controlled with topical therapy may be less likely to be reported or the specific details recalled for the subsequent questionnaire. Severe ocular hypertension following IVTA in Australia and New Zealand occurs without previously described risk factors, in particular family history of glaucoma. The severity of these cases, which occurred up to 9 months post-injection, required trabeculectomy in almost half the population for whom details were provided. The reporting bias towards severe, treatment-resistant cases is acknowledged. Our low numbers of initial reported cases, and lack of responses to follow-up questionnaires suggest that the findings are an underrepresentation of the true number of cases. Further studies are needed to determine better epidemiological data within Australia and New Zealand of this severe treatment complication.
REFERENCES
© 2014 Royal Australian and New Zealand College of Ophthalmologists
1. Francois J. Corticosteroid glaucoma. Ann Ophthalmol 1977; 9: 1075–80. 2. Kalina RE. Increased intraocular pressure following subconjunctival corticosteroid administration. Arch Ophthalmol 1969; 81: 788–90. 3. Gillies MC, Simpson JM, Billson FA et al. Safety of an intravitreal injection of triamcinolone: results from a randomized clinical trial. Arch Ophthalmol 2004; 122: 336–40. 4. Beer PM, Bakri SJ, Singh RJ et al. Intraocular concentration and pharmacokinetics of triamcinolone acetonide after a single intravitreal injection. Ophthalmology 2003; 110: 681–6. 5. Kramar M, Vu L, Whitson JT, He YG. The effect of intravitreal triamcinolone on intraocular pressure. Curr Med Res Opin 2007; 23: 1253–8.
238
Fitzgerald et al.
6. Jonas JB, Degenring RF, Kreissig I, Akkoyun I, Kamppeter BA. Intraocular pressure elevation after intravitreal triamcinolone acetonide injection. Ophthalmology 2005; 112: 593–8. 7. Konstantopoulos A, Williams CPR, Newsom RS, Luff AJ. Ocular morbidity associated with intravitreal triamcinolone acetonide. Eye 2007; 21: 317–20. 8. Williams CP, Konstantopoulos A, Rowley SA, Luff AJ. Late intraocular pressure rise following intravitreal triamcinolone injection. Clin Experiment Ophthalmol 2007; 35: 385–6. 9. Rhee DJ, Peck RE, Belmont J et al. Intraocular pressure alterations following intravitreal triamcinolone acetonide. Br J Ophthalmol 2006; 90: 999–1003.
10. Jain S, Hurst JR, Thompson JR, Eke T. UK national survey of current practice and experience of intravitreal triamcinolone acetonide. Eye 2009; 23: 1164–7. 11. Jain S, Thompson JR, Foot B, Tatham A, Eke T. Severe intraocular pressure rise following intravitreal triamcinolone: a national survey to estimate incidence and describe case profiles. Eye 2014; 28: 399–401. 12. Razeghinejad MR, Katz LJ. Steroid-induced iatrogenic glaucoma. Ophthalmic Res 2012; 47: 66–80. 13. Kersey JP, Broadway DC. Corticosteroid induced glaucoma: a review of the literature. Eye 2006; 20: 407–16. 14. Foot B, Stanford M, Rahi J, Thompson J. The British Ophthalmological Surveillance Unit: an evaluation of the first 3 years. Eye 2003; 17: 9–15.
© 2014 Royal Australian and New Zealand College of Ophthalmologists
Copyright of Clinical & Experimental Ophthalmology is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
