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 Table of Contents  
ORIGINAL ARTICLE
Year : 2021  |  Volume : 114  |  Issue : 1  |  Page : 13-20

Study of the efficiency and safety of subconjunctival triamcinolone acetonide in macular edema


Department of Ophthalmology, Med-V Military Hospital, Med-V University, Rabat, Morocco

Date of Submission30-Jul-2020
Date of Decision01-Aug-2020
Date of Acceptance01-Dec-2020
Date of Web Publication31-Mar-2021

Correspondence Address:
MD Abdellaoui Taoufik
Department of Ophthalmology, Med-V Military Hospital, Med-V University, Appt 4, Immeuble 48, Massira 1, Temara 10045
Morocco
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ejos.ejos_47_20

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  Abstract 

Purpose To evaluate through a prospective study the efficiency and safety of triamcinolone in subconjunctival injection on macular edema (ME), in the short and medium term.
Patients and methods All the patients included in the study underwent ophthalmologic examination and optic coherence tomography of the macula. The injection of 0.2–0.3 ml (8–12 mg) of triamcinolone was done in the subconjunctival space. We evaluated its efficiency by measuring the best-corrected visual acuity and the central macular thickness at 1, 3, and 6 months. Safety was evaluated by following up the intraocular pressure; the presence or absence of cataract and conjunctival complications at 1, 3, and 6 months; and the glycemic control.
Results A total of 44 eyes (36 patients) were included. The overall best-corrected visual acuity and central macular thickness improved after injection. Overall, 67% of diabetic patients required reinjection at the third month. In the cases of inflammatory ME (uveitis and Irvine–Gass), the evolution has remained stable for 6 months after a single injection. No significant variation in intraocular pressure was noted after 1 month (P=0.38), after 3 months (P=0.20), or after 6 months (P=0.13). However, four patients developed ocular hypertension (10 mmHg or more above baseline), which has been well controlled with local monotherapy. Overall, 9.5% of phakic patients developed a cataract at the control of the sixth month. The change in glycated hemoglobin before and after the injection was not significant (P=0.84).
Conclusion Subconjunctival triamcinolone acetonide seems to be an interesting and well-tolerated alternative therapy of ME in the short and medium term.

Keywords: cataract, intraocular pressure, macular edema, subconjunctival, triamcinolone


How to cite this article:
Taoufik A, Yassmine C, Yassine M, Yassine M, Fouad E, Karim R, Abdelbarre O. Study of the efficiency and safety of subconjunctival triamcinolone acetonide in macular edema. J Egypt Ophthalmol Soc 2021;114:13-20

How to cite this URL:
Taoufik A, Yassmine C, Yassine M, Yassine M, Fouad E, Karim R, Abdelbarre O. Study of the efficiency and safety of subconjunctival triamcinolone acetonide in macular edema. J Egypt Ophthalmol Soc [serial online] 2021 [cited 2021 May 7];114:13-20. Available from: http://www.jeos.eg.net/text.asp?2021/114/1/13/313079


  Introduction Top


Macular edema (ME) is defined as macular retinal thickening resulting from an accumulation of fluid in the retina surrounding the fovea. It is a common, nonspecific condition that should be considered as a response of the macular area to a change in the environment. It causes visual impairment, reversible to varying degrees, linked to the functional impairment of retinal cells. ME can be of multiple origins, dominated by diabetes, retinal venous occlusion (RVO), uveitis, postsurgical ME or Irvine–Gass syndrome, age-related macular degeneration, and vitreomacular interface anomalies.

For several decades, apart from the therapeutic modalities specific to the etiology, only laser treatments or pharmacological treatments with acetazolamide, steroidal, or NSAIDs were available. Advances in surgery then made it possible to offer vitrectomy for ME with vitreomacular interface anomalies. More recently, the advent of anti-vascular endothelial growth factor drugs (VEGF) has changed the therapeutic landscape of ME, but with a major drawback, that is, their short duration of efficacy, which is why research has focused on devices with extended duration of action. Corticosteroids are widely used in ophthalmology. Their anti-edematous [1],[2] and proven anti-inflammatory [3] properties are useful for treating the inflammatory side of many MEs. Furthermore, corticosteroids have a proven antiangiogenic effect owing to the inhibition of neovascular growth factors (including VEGF) and metalloproteinases [4], resulting in a reduction in the migration of endothelial cells. However, they are not devoid of adverse effects, both local, mainly the risk of glaucoma and cataracts, and general, particularly on carbohydrate metabolism.

Triamcinolone is a synthetic corticosteroid with moderate anti-inflammatory efficacy (four times stronger than hydrocortisone, and five times weaker than dexamethasone) but with a longer duration of action. The commercial form we used is called Kenacort retard (triamcinolone acetonide in the form of white crystals, along with an excipient) at 40 mg/ml. The triamcinolone injected subconjunctivally takes the form of a whitish deposit of crystals which gradually deliver the triamcinolone molecule, for 3 months on average, up to 13 months after the injection [5]. Triamcinolone has been used for a long time in the treatment of ME, in particular diabetic and uveitic, mainly in intravitreal or subtenon injections. Their use in subconjunctival is rarely described in the literature; all of the studies that have studied it have focused on the inflammatory (or surgical) ME. The objective of our study is to evaluate, by a prospective study, the efficacy and the tolerance of triamcinolone in subconjunctival injection on ME owing to different causes, in the short and medium term.


  Patients and methods Top


Study design

This is a prospective and monocentric study. It was conducted in the Ophthalmology Department of the Mohamed-V Military Hospital of Rabat, between January 2019 and January 2020. The study was conducted in accordance with the tenets of the Declaration of Helsinki. All participants provided informed consent.

Population

Inclusion criteria

We included in the study all eyes with ME of vascular origin (diabetic or on venous occlusion), never injected or having failed to respond to intravitreal injection of anti-VEGF drug (Bevacizumab), and eyes with inflammatory ME (uveitic or Irvine–Gass syndrome).

Exclusion criteria

We excluded from the study the following patients:

Patients with cataract.

Patients with intraocular pressure (IOP) more than or equal to 21 mmHg, or proven glaucoma.

Patients with active or old eye infection, or presumed herpetic manifestations.

Patients with proliferative diabetic retinopathy.

Patients with previous use of anti-VEGF drug, laser photocoagulation, or eye surgery within 3 months before administration of the study drug in the study eye.

Patients with previous injection of dexamethasone implant within 6 months before administration of the study drug in the study eye.

Data collection before injection

During the interrogation, we collected the data on age and sex of the patients; the cause of ME; type, age, and balance of diabetes; and the existence of prior treatment: retinal laser, macular laser, and intravitreal injection.

On ophthalmological examination, we noted the best-corrected visual acuity (BCVA), the state of the lens, and the IOP. The examination was supplemented by optic coherence tomography (OCT) of the macular (Zeiss Cirrus 4000 HD-OCT instrument, Jena, Germany, Software version 6.0.2.81) to confirm the ME, to measure the central macular thickness (CMT), and highlight an epimacular membrane (EMM). The glycated hemoglobin level was measured for diabetic patients before the injection.

The injection procedure

We used the commercial form called Kenacort retard (triamcinolone acetonide in the form of white crystals+excipient) at 40 mg/ml. After shaking the bottle to homogenize the solution, 0.2–0.3 ml (8–12 mg) of triamcinolone acetonide was injected in subconjunctival space, 6 mm from the lower or upper limbus. The injection was repeated at the same site in cases that required reinjection in the third month.

Patient follow-up

All patients were seen at the control consultation 1, 3, and 6 months after the injection. Patients who were reinjected in the third month were seen again in consultation 1 and 3 months after the second injection.

At each follow-up consultation, the patients underwent a complete examination with macular OCT. We assessed the following:

The effectiveness of the injection by measuring the BCVA and the CMT.

Its safety by measuring IOP, assessing the state of the lens in phakic patients, and the condition of the conjunctiva, as well as assessing the glycemic control for diabetic patients by measuring the glycated hemoglobin level 3 months after the injection.

Statistical analysis

SPSS version 23 (SPSS Inc., Chicago, Illinois, USA), was used for statistical analysis. Visual acuity (VA) measurements were converted using the logarithm of the minimum angle of resolution (logMAR), and in order to provide continuous numerical data for statistical analysis, the acuity ‘counting fingers’ was converted to 6/300, ‘hand motion’ to 6/600, and the ‘light perception’ to 6/1200. The Kolmogorov–Smirnov test was used to assess the normal distribution of the variables. The significance of the differences in the findings was determined by Student’s t test, Mann–Whitney U test, Wilcoxon test, Fisher’s exact test, χ2 test, and analysis of variance. A P value less than 0.05 was considered significant.


  Results Top


Population

The study included 44 eyes from 36 patients. The average age was 62 years. Women represented 61% of the population. The edema was of diabetic origin in 55% of cases, including 9% associated with an EMM, 18% of uveitic origin, 18% on RVO, and 9% on Irvine–Gass syndrome. Overall, 47% of the eyes were pseudophakic. Moreover, 67% of diabetic ME cases and 50% on RVO had previously benefited from intravitreal injection of anti-VEGF drug (Bevacizumab), with a median number of injections of 9 [3],[15] and 6 [3],[10], respectively. In addition, 72% of diabetics had previously had panretinal photocoagulation, and none had had a macular laser.

The initial BCVA was 0.84±0.49 logMAR. The lowest mean was observed in the ME on RVO: 1.20±0.70 logMAR, and the highest mean was in Irvine–Gass Syndrome: 0.76±0.45 logMAR. The mean initial CMT was 547±130 µm. The mean initial IOP was 14.38±3.15 mmHg. The mean baseline glycated hemoglobin level was 8.02±1.58%. The epidemiological and clinical characteristics of the patients according to the cause of the ME are shown in [Table 1].
Table 1 Initial epidemiological and clinical characteristics of the population studied depending on the cause of macular edema

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Efficiency

Evolution of visual acuity

All etiology combined, the overall VA improved in the first month and went from 0.84±0.49 to 0.59±0.54 (P=0.001). This was followed by a downward trend, the VA went to 0.72±0.52 in the third month (P=0.01) and 0.74±059 in the sixth month (P=0.1) ([Table 2]).
Table 2 Overall evolution of visual acuity, central macular thickness, and intraocular pressure

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This evolution is better explained when we study each etiology of ME separately ([Figure 1]):
Figure 1 Changes of the best-corrected visual acuity (BCVA) depending on different causes of macular edema.

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For diabetic ME, the VA improved significantly in the first month: it went from 1.24±0.68 to 0.67±0.41 logMAR (P=0.02) then tended to return at its initial value around the third month 1.03±0.62 logMAR (P=0.26). Overall, 67% of patients were reinjected in the third month, and the VA improved then to 0.80±0.52 (P=0.04), then tended toward its basic value in the sixth month at 1.10±0.58 logMAR (P=0.41).

For uveitic ME, the VA improvement was stable over the 6 months of follow-up: it went from 1.15±0.53 logMAR to 0.44±0.31 at 1 month (P=0.001), 0.38±0.30 logMAR at 3 months (P=0.001), and 0.54±0.40 logMAR at 6 months (P=0.01).

For ME on RVO, no improvement was noted. The VA went from 1.20±0.70 to 1.23±0.72 logMAR in the first month (P=0.90), and 1.25±0.73 logMAR at the third month (P=0.88). Other therapeutic alternatives were offered to patients.

For the Irvine–Gass ME, the evolution was good and stable. The VA went from 0.76±0.45 to 0.29±0.18 logMAR in the first month (P=0.01), and 0.30±0.21 logMAR in the third month (P=0.01), and 0.38±0.24 logMAR in the sixth month (P=0.04).

For diabetic ME with EMM, there was no improvement during follow-up. The acuity went from 0.99±0.62 to 0.92±0.58 logMAR at the first month (P=0.39), and 1.03±0.62 logMAR in the third month (P=0.40), and 1.05±0.64 logMAR in the sixth month (P=0.35).

Evolution of the central macular thickness

The variation of the CMT took a similar direction, with a maximum improvement in the first month. It went from 547±130 to 328±103 µm in the first month (P<0.001), then 371±94 µm in the third month (P=0.03), and 311±113 µm in the sixth month (P=0.01) ([Table 2]).

Changes of CMT according to the etiology of ME are presented in [Figure 2]:
Figure 2 Changes of the central macular thickness (CMT) depending on different causes of macular edema.

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For diabetic ME, the CMT went from 522±135 to 317±98 µm (P=0.02), then it increases in the third month to 461±128 µm (P=0.15). After reinjection in the third month, the CMT decreases again to 328±101 µm (P=0.05), then increases at the control of the sixth month to 412±139 (P=0.10).

For uveitic ME, the evolution of CMT was stable over the 6 months of follow-up: it went from 570±140 to 279±96 µm at 1 month (P<0.001), to 310±98 µm at 3 months (P=0.001), and 289±102 µm at 6 months (P<0.001).

For the ME on venous occlusion, no improvement was noted. The CMT went from 443±140 to 457±151 µm in the first month (P=0.72), and 460±138 µm in the third month (P=0.70).

For Irvine–Gass syndrome, the evolution was good and stable over the 6 months of follow-up: the CMT went from 466±123 to 243±74 µm in the first month (P=0.007), and 250±84 µm in the third month (P=0.01), and 265±98 µm in the sixth month (P=0.04).

For diabetic ME with EMM, the CMT went from 528±156 to 500±137 µm in the first month (P=0.29), and 538±148 µm in the third month (P=0.67), and 545±144 µm in the sixth month (P=0.42).

Safety

Evolution of intraocular pressure

The variation in mean IOP during the 6 months of follow-up was not overall statistically significant. It went from 14.38±3.15 mmHg initially to 14.85±3.49 the first month (P=0.38), to 15.21±3.91 the third month (P=0.20), and 15.26±3.99 the sixth month (P=0.13) ([Table 2]). On an individual scale, four patients developed high IOP: one case in the first month, two in the third month, and one in the sixth month ([Figure 3]). In all four cases, monotherapy was sufficient, and no case required surgical extraction of the triamcinolone deposits.
Figure 3 Individual variations in intraocular pressure (IOP).

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Evolution of the lens

The assessment of changes in the state of the lens during the study was carried out by the same doctor during follow-up. Among phakic patients, two (9.5%) developed a posterior subcapsular cataract in the sixth month control.

Evolution of the conjunctiva

The conjunctiva was assessed at the injection site using a slit lamp, with photographs of the deposits of triamcinolone at each visit. No patient has developed a local complication such as ulceration, ischemia, or conjunctival necrosis. It took between 6 and 9 months for the deposits to disappear completely.

Evolution of the glycemic control

There has been no effect on systemic glycemic control for diabetic patients. The average glycated hemoglobin level went from 8.02±1.58% initially to 8.04±1.55% after 3 months (P=0.84).


  Discussion Top


The subconjunctival injection is safer than the intravitreal way, if we compare the risks of the injection itself (particularly the possibility of endophthalmitis, intravitreal hemorrhage, and retinal detachment), and the probable retinal toxicity of triamcinolone. Compared with the subtenon injection, the subconjunctival injection offers the ease and the safety of the procedure, and allows a visual assessment of the amount of molecule remaining, as well as an effective surgical extraction of the crystals if needed.

In terms of effectiveness, our study shows that triamcinolone in the subconjunctival has satisfactory efficacy in diabetic ME, with a decrease in ME and a significant gain in VA during the first 3 months. After that, the gain in VA is no longer significant, hence the need for reinjections. In uveitic ME and Irvine–Gass syndrome, the efficacy is maintained until the sixth month. On the contrary, in ME on RVO and EMM, triamcinolone in subconjunctival has shown no effect.

Carbonniere and colleagues compared, for inflammatory ME, the efficacy and tolerance of subconjunctival injections of 8–12 mg of triamcinolone versus subtenon injections of 40 mg of triamcinolone and intravitreal injection of the 700 µg dexamethasone implant. They did not find any significant difference in terms of gain in VA and reduction in CMT between the three groups, although they observed a small delayed effect of the subconjunctival injection, and a longer recurrence delay for the dexamethasone implant [6]. On the contrary, a prospective multicenter study has shown that 4 mg of triamcinolone intravitreally gave similar efficacy to the intravitreal implant of dexamethasone, and better than 40 mg of triamcinolone in subtenon [7]. In another study of 31 cases of uveitic ME, Bleriot et al. [8] found a functional improvement after subconjunctival injection of triamcinolone, with significant gain in VA and reduction in CMT at 1 and 3 months, then a decrease in effectiveness at the sixth month.

For diabetic ME, we have not found an equivalent study in the literature. Several studies focused on comparing intravitreal versus subtenon triamcinolone in the diabetic ME. It seems that the intravitreal injection would be more effective [9],[10]. However, the two approaches allow an extended effect over 6 months [10]. In our study, the efficacy did not last more than 3 months. This could be explained by the higher dose injected in the subtenon (40 mg vs. 8–12 mg in our study), and by the molecule’s duration of effect, which is longer when injected intravitreally (estimated at 140±17 days) [11].

Likewise, we have not found an equivalent study for ME on RVO. It seems that intravitreal triamcinolone gives similar efficacy to bevacizumab [12], and to dexamethasone implant [13]. Subtenon triamcinolone appears to be ineffective in this indication [14]. The subconjunctival injection did not work in our study.

Overall, 10% of our patients developed an IOP elevation of more than 10 mmHg during the 6 months of follow-up. The data in the literature are very variable. Carbonniere et al. [6] found 14.3% elevation over 10 mmHg in the first month. Other studies did not find any increase in IOP during the 6 months of follow-up [8],[15]. The elevation of IOP after a periocular or intraocular injection of triamcinolone is indeed classically described in the literature, but its frequency is variable depending on the type of injection. The intravitreal route seems to be more responsible for IOP elevation. According to the Chuang et al. [16] study, 50% of the cases after injection of 4 mg and 38% after injection of 2 mg had secondary ocular hypertension. In addition, subtenon injection of 40 mg triamcinolone induced IOP elevation in 11% of the cases in the study by Byun and Park [17], which is comparable to 10% in our series after 8–12 mg in conjunctival space.

The IOP elevation can be discovered from 1 week to 10 months after subconjunctival triamcinolone injection [18],[19]. An eye drop test can be performed to detect the risk of this elevation. Bartlett et al. [20] found a 54% increase in IOP between 5 and 9 mmHg and 15% over 10 mmHg after four instillations of prednisolone per day for 6 weeks. This could be predictive of the risk of IOP elevation after periocular corticosteroid injection. In our study, we did not perform the eye drop test, and we did not observe severe ocular hypertension more than or equal to 30 mmHg. Monotherapy was sufficient, and no surgery was required. This is probably owing to the exclusion criteria: exclusion of patients with ocular hypertension or proven glaucoma. In case of uncontrolled hypertonia with maximum medical treatment, the subconjunctival route offers direct access and the possibility of easy extraction of triamcinolone deposits, which allows rapid normalization of the IOP [19],[21].

Cataract is also a classic complication of the periocular injection of triamcinolone. In our study, 12.5% of phakic patients developed a posterior subcapsular cataract. The frequency of cataracts is variable depending on the route of injection of triamcinolone; intravitreal injection seems to provide more cataracts with 35% of the cases 6 months after 4 mg intravitreal injection [22], 10% after 40 mg subtenon injection, and 3.1% after 20 mg subtenon injection [23]. Concerning the subconjunctival route, cataract was observed in 22% of cases with uveitic eyes [6], versus 9.5% in our study. Thus, the subconjunctival route seems to induce more cataract than the subtenon route, probably owing to the translimbic passage of the molecule when it is injected into the subconjunctival, which induces a higher concentration in the anterior segment [24],[25].

The amount of corticosteroid absorption in the systemic circulation after a subconjunctival injection is considerable, resulting in a higher relative systemic bioavailability compared with an oral administration. However, a lower dose is required to achieve equal intraocular corticosteroid concentrations when injected subconjunctivally, compared with peribulbar injection or oral administration, and therefore the absolute systemic concentration of corticosteroids is lower [24]. A subconjunctival corticosteroid injection is therefore not exclusively a local treatment and can cause systemic adverse effects. There are no data from the literature on the effect of periocular or intravitreal triamcinolone on glycemic control. A recent study did not find significant variations in blood glucose concentrations after intravitreal dexamethasone implant [26]. In our study, there was no significant change in glycated hemoglobin level before and after the injection.

Some authors have reported cases of ulceration [27], ischemia, or conjunctival necrosis [28], following subconjunctival injections of triamcinolone. These manifestations are rare, occurring after large doses (40 mg subconjunctival triamcinolone). The cause is not clearly identified. Cases of herpetic keratitis have also been described [29]. Another undesirable aesthetic effect is to be taken into consideration: the visibility of the crystals. Hence, the advantage of performing the injection in the inferior conjunctiva, where the deposits are then masked by the eyelid [6].

Despite being prospective, our study has certain limitations, namely, the small size of the study population, the relatively short average duration of follow-up, and the type of study that is not comparative with other treatment methods. Comparative prospective studies on larger cohorts of patients could support the results of our study.


  Conclusion Top


In conclusion, subconjunctival triamcinolone is an interesting therapeutic alternative in ME because it has many advantages. In addition to a low price, it avoids the complications of intravitreal and subtenon injections, its adverse effects are infrequent, and its extraction is easy in case of complications. It seems to be effective in inflammatory ME with a prolonged effect, and in diabetic ME with the need for quarterly reinjection. It is however ineffective in ME on RVO, and diabetic ME with EMM.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Antonetti DA, Wolpert EB, DeMaio L, Harhaj NS, Scaduto RCJr. Hydrocortisone decreases retinal endothelial cell water and solute flux coincident with increased content and decreased phosphorylation of occludin. J Neurochem 2002; 80:667–677.  Back to cited text no. 1
    
2.
Felinski EA, Cox AE, Phillips BE, Antonetti DA. Glucocorticoids induce transactivation of tight junction genes occludin and claudin-5 in retinal endothelial cells via a novel cis-element. Exp Eye Res 2008; 86:867–878.  Back to cited text no. 2
    
3.
Tamura H, Miyamoto K, Kiryu J, Miyahara S, Katsuta H, Hirose F et al. Intravitreal injection of corticosteroid attenuates leukostasis and vascular leakage in experimental diabetic retina. Investig Ophthalmol Vis Sci 2005; 46:1440–1444.  Back to cited text no. 3
    
4.
Wu WS, Wang FS, Yang KD, Huang CC, Kuo YR. Dexamethasone induction of keloid regression through effective suppression of VEGF expression and keloid fibroblast proliferation. J Invest Dermatol 2006; 126:1264–1271.  Back to cited text no. 4
    
5.
Kalina PH, Erie JC, Rosenbaum L. Biochemical quantification of triamcinolone in subconjunctival depots. Arch Ophthalmol 1995; 113:867–869.  Back to cited text no. 5
    
6.
Carbonniere C, Couret C, Bleriot A, Lebreton O, Masse H, Le Meur G et al. [Treatment of macular edema: comparison of efficacy and tolerability of subconjunctival triamcinolone injections, sub-tenon’s triamcinolone injections and intravitreal dexamethasone implant]. J Fr Ophtalmol 2017; 40:177–186.  Back to cited text no. 6
    
7.
Thorne JE, Sugar EA, Holbrook JT, Burke AE, Altaweel MM, Vitale AT et al. Periocular triamcinolone vs. intravitreal triamcinolone vs. intravitreal dexamethasone implant for the treatment of uveitic macular edema: the PeriOcular vs. INTravitreal corticosteroids for uveitic macular edema (POINT) trial. Ophthalmology 2019; 126:283–295.  Back to cited text no. 7
    
8.
Bleriot A, Couret C, Le Meur G, Lebranchu P, Weber M. Safety and efficacy of subconjunctival triamcinolone injections in the management of uveitic macular edema: retrospective study of thirty-one cases. J Fr Ophtalmol 2014; 37:599–604.  Back to cited text no. 8
    
9.
Yalcinbayir O, Gelisken O, Kaderli B, Avci R. Intravitreal versus sub-tenon posterior triamcinolone injection in bilateral diffuse diabetic macular edema. Ophthalmologica 2011; 225:222–227.  Back to cited text no. 9
    
10.
Tatsumi T, Oshitari T, Ando T, Takatsuna Y, Arai M, Baba T et al. Comparison of the efficacy of sub-tenon versus intravitreal triamcinolone acetonide injection during cataract surgery for diabetic macular edema. Ophthalmologica 2019; 241:17–23  Back to cited text no. 10
    
11.
Audren F, Tod M, Massin P, Benosman R, Haouchine B, Erginay A et al. Pharmacokinetic-pharmacodynamic modeling of the effect of triamcinolone acetonide on central macular thickness in patients with diabetic macular edema. Investig Ophthalmol Vis Sci 2004; 45:3435–3441.  Back to cited text no. 11
    
12.
Jin ZY, Zhu D, Tao Y, Wong IY, Jonas JB. Meta-analysis of the effect of intravitreal bevacizumab versus intravitreal triamcinolone acetonide in central retinal vein occlusion. J Ocul Pharmacol Ther 2013; 29:826–831.  Back to cited text no. 12
    
13.
Ozkok A, Saleh OA, Sigford DK, Heroman JW, Schaal S. THE OMAR STUDY: comparison of ozurdex and triamcinolone acetonide for refractory cystoid macular edema in retinal vein occlusion. Retina 2015; 35:1393–1400.  Back to cited text no. 13
    
14.
Ozdek S, Deren YT, Gurelik G, Hasanreisoglu B. Posterior subtenon triamcinolone, intravitreal triamcinolone and grid laser photocoagulation for the treatment of macular edema in branch retinal vein occlusion. Ophthalmic Res 2008; 40:26–31.  Back to cited text no. 14
    
15.
Lindholm JM, Taipale C, Ylinen P, Tuuminen R. Perioperative subconjunctival triamcinolone acetonide injection for prevention of inflammation and macular oedema after cataract surgery. Acta Ophthalmol 2020; 98:36–42.  Back to cited text no. 15
    
16.
Chuang LH, Yeung L, Wang NK, Chen HS, Ku WC, Lai CC. Secondary ocular hypertension after intravitreal injection with 2 mg or 4 mg of triamcinolone in retinal vein occlusion. J Ocul Pharmacol Ther 2010; 26:325–328.  Back to cited text no. 16
    
17.
Byun YS, Park YH. Complications and safety profile of posterior subtenon injection of triamcinolone acetonide. J Ocul Pharmacol Ther 2009; 25:159–162.  Back to cited text no. 17
    
18.
Herschler J. Increased intraocular pressure induced by repository corticosteroids. Am J Ophthalmol 1976; 82:90–93.  Back to cited text no. 18
    
19.
Mills DW, Siebert LF, Climenhaga DB. Depot triamcinolone-induced glaucoma. Can J Ophthalmol 1986; 21:150–152.  Back to cited text no. 19
    
20.
Bartlett JD, Woolley TW, Adams CM. Identification of high intraocular pressure responders to topical ophthalmic corticosteroids. J Ocul Pharmacol 1993; 9:35–45.  Back to cited text no. 20
    
21.
Aydin A, Akin T, Bilge AH. Management of persistent glaucoma secondary to depot methylprednisolone. Ophthalmic Surg Lasers Imaging 2007; 38:399–401.  Back to cited text no. 21
    
22.
Mishra SK, Gupta A, Patyal S, Kumar S, Raji K, Singh A et al. Intravitreal dexamethasone implant versus triamcinolone acetonide for macular oedema of central retinal vein occlusion: quantifying efficacy and safety. Int J Retina Vitreous 2018; 4:13.  Back to cited text no. 22
    
23.
Ogura Y, Shimura M, Iida T, Sakamoto T, Yoshimura N, Yamada M et al. Phase II/III clinical trial of sub-tenon injection of triamcinolone acetonide (wp-0508st) for diabetic macular edema. Ophthalmologica 2019; 241:161–169.  Back to cited text no. 23
    
24.
Weijtens O, Feron EJ, Schoemaker RC, Cohen AF, Lentjes EG, Romijn FP et al. High concentration of dexamethasone in aqueous and vitreous after subconjunctival injection. Am J Ophthalmol 1999; 128:192–197.  Back to cited text no. 24
    
25.
Weijtens O, Schoemaker RC, Lentjes EG, Romijn FP, Cohen AF, van Meurs JC. Dexamethasone concentration in the subretinal fluid after a subconjunctival injection, a peribulbar injection, or an oral dose. Ophthalmology 2000; 107:1932–1938.  Back to cited text no. 25
    
26.
Posch-Pertl L, Schwetz V, Michelitsch M, Rabensteiner J, Holler V, Gasser-Steiner V et al. Effect of dexamethasone intravitreal implant on blood glucose, hypothalamic-pituitary-adrenal axis function and vascular endothelial growth factor serum levels in patients with diabetic macular oedema. Acta Ophthalmol (Copenh) 2018; 96:e543–e544.  Back to cited text no. 26
    
27.
Agrawal S, Agrawal J, Agrawal TP. Conjunctival ulceration following triamcinolone injection. Am J Ophthalmol 2003; 136:539–540.  Back to cited text no. 27
    
28.
Ying-Jiun C, Chee-Kuen W, Shatriah I. Conjunctival necrosis following a subconjunctival injection of triamcinolone acetonide in a child. Middle East Afr J Ophthalmol 2015; 22:125–128.  Back to cited text no. 28
    
29.
Inoue H, Suzuki T, Joko T, Inoue T, Ohashi Y. A case of herpetic keratitis after subconjunctival triamcinolone acetonide injection. Case Rep Ophthalmol 2014; 5:277–280.  Back to cited text no. 29
    


    Figures

  [Figure 1], [Figure 2], [Figure 3]
 
 
    Tables

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