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Year : 2006  |  Volume : 54  |  Issue : 2  |  Page : 133-137

Intravitreal injection of triamcinolone acetonide for diabetic macular edema: Principles and practice

Retina - Vitreous Service, Aravind Eye Hospital and Postgraduate Institute of Ophthalmology, Madurai, Tamilnadu, India

Correspondence Address:
Vasumathy Vedantham
Aravind Eye Hospital and Postgraduate Institute of Ophthalmology, 1, Anna Nagar, Madurai - 625 020, Tamilnadu
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0301-4738.25840

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Diabetic retinopathy is fast emerging as a leading cause of newly diagnosed legal blindness amongst the working population. Macular edema, as it is commoner, accounts for more vision impairment than neovascular proliferation in diabetic patients. Laser photocoagulation, which is the standard treatment of macular edema, is associated with significant complications and an improvement in visual acuity is unsatisfactory. Intravitreal injection of corticosteroids (especially triamcinolone acetonide) is an emerging treatment modality in the management of diabetic macular edema. This article presents an overview of the principles, technique and complications associated with this procedure.

Keywords: Corticosteroids, diabetic retinopathy, intravitreal injection, macular edema, triamcinolone acetonide.

How to cite this article:
Vedantham V, Kim R. Intravitreal injection of triamcinolone acetonide for diabetic macular edema: Principles and practice. Indian J Ophthalmol 2006;54:133-7

How to cite this URL:
Vedantham V, Kim R. Intravitreal injection of triamcinolone acetonide for diabetic macular edema: Principles and practice. Indian J Ophthalmol [serial online] 2006 [cited 2020 May 28];54:133-7. Available from: http://www.ijo.in/text.asp?2006/54/2/133/25840

Diabetic retinopathy is the most common cause of newly diagnosed legal blindness amongst the working population in the industrialized world today.[1] Although majority of diabetic patients have retinopathy of varying severity, approximately 25% of the diabetic patients have sight-threatening levels of retinopathy with legal blindness (best corrected visual acuity of 20/200 or worse) being 25 times more common in the diabetic when compared to the non-diabetic population.[2] The common causes of visual impairment in diabetic retinopathy include macular edema and complications due to proliferative retinopathy. The majority of diabetics have type II disease, wherein macular edema is commoner, it follows that overall, macular edema accounts for more vision impairment than proliferative retinopathy.[3] Laser photocoagulation of the macular region and parsplana vitrectomy greatly reduce visual loss from macular edema, however these procedures are associated with significant side-effects and complications. In addition, laser photocoagulation usually does not lead to improvement of visual acuity.[4] Intravitreal injection of corticosteroids (triamcinolone acetonide), constitutes a newer, less destructive treatment modality in the management of diabetic macular edema. However, this technique too has certain distinct complications that have to be borne in mind prior to institution of therapy. This article presents an overview of the principles, techniques and complications associated with this emerging treatment modality.

  Mechanism of Action Top

The rationale for the use of coticosteroids in the treatment of diabetic macular edema follows from the observation that the breakdown of the blood retinal barrier leads to the edema[5] and is in part mediated by Vascular endothelial growth factor (VEGF). Corticosteroids have been shown to inhibit VEGF and other cytokines and growth factors, thereby regulating endothelial cell tight junctions. In addition, they inhibit prostaglandin and leukotriene synthesis, which results in a local reduction of inflammatory mediators. The resultant anti-inflammatory effect contributes to the reduction of edema.[6] Increased diffusion by modulation of calcium channels[7] could also account for the efficacy of the corticosteroids in reducing macular edema.

  How best to administer the steroid? Top

As the eye comprises only 0.01% of the whole body volume, the best way to achieve optimal concentration of a drug in the eye would be a direct application to its site of action. Moreover, systemic steroids have several undesirable side effects, can worsen the diabetic status and are therefore undesirable.

The efficacy of various methods of ocular corticosteroid injection has always been a matter of debate.[8] Sub-Tenon's injections when compared to intravitreal injections have the disadvantage of probably a decreased drug penetration through the sclera and choroid and a rapid removal of the drug by the choroidal circulation after penetration with the resultant short duration of action. Probable placement at a site relatively far from the target zone such as the macula leading to "therapeutic failures" is also possible, following sub-Tenon's injections. This makes the sub-Tenon's route of injection of steroids less popular than the intravitreal route of steroid administration.[8] Intravitreal injection is currently the commonest mode of intraocular delivery of corticosteroids for diabetic macular edema.

  Outcome Top

There has been an increasing interest in the use of intraocular corticosteroids for diabetic macular edema after the significant observations of McCuen et al[9] and Young et al[10] on the lack of toxicity of intravitreally administered triamcinolone (9-fluoro-16-hydroxy prednisolone). Subsequently, there have been several studies documenting the antiangiogenic, antiproliferative and antiedematous effects of intravitreal triamcinolone acetonide (IVTA). The landmark study by Martidis et al,[11] was a prospective, noncomparative, interventional case series involving sixteen eyes with clinically significant macular edema (CSME) that failed to respond to at least two previous sessions of laser photocoagulation. At least 6 months after initial laser therapy, the response was measured by clinical examination and optical coherence tomography (OCT). Eyes with a residual central macular thickness of more than 300 microns (normal central macular thickness: 200 microns) and significant visual loss from the baseline were administered an intravitreal injection of 4 mg in 0.1 ml of triamcinolone acetonide. Mean improvement in visual acuity was 2.4, 2.4 and 1.3 Snellen lines at the 1, 3 and 6-months of follow-up respectively. The central macular thickness as measured by OCT decreased by 55%, 57.5% and 38%, respectively, over these same intervals from an initial pretreatment mean of 540.3 (± 96.3) microns. The researchers attributed more significant reduction in edema as compared to the improvement in visual acuity, which may be due to the injection being given after the chronic edema had already caused severe dysfunction. They hence suggested an early injection in severe cases. Massin et al[12] too, have found out that proportional improvement is there in the macular thickness than visual acuity, but the effect was only transient necessitating repeat injections. However, Jonas et al[13] have found an impressive improvement in visual acuity after IVTA injection, but they had used 25 mg of the drug. There was a significant albeit transient increase in the intraocular pressure (IOP) in the injected group. The maximum improvement in visual acuity was seen usually two to five months after injection and the visual acuity fell thereafter, coinciding with the disappearance of the triamcinolone crystals.[13] Significantly, the recent trend in tertiary eye care centers is towards an early primary intravitreal injection in eyes with diabetic cystoid macular edema (CME). The major concern has been the recurrence of macular edema approximately six months after the injection necessitating repeat injections. There is an ongoing multicentric clinical trial in the US (sponsored by the National Eye Institute) to test the efficacy of intravitreal triamcinolone in diabetic macular edema.

  Technique of IVTA Injection Top

The procedure should be carried out with meticulous aseptic precaution, preferably in the operating room. It is very easily carried out under topical anesthesia. A pre-injection single drop of Povidone-Iodine (5%) solution is applied to the eye followed by thorough cleaning of the eyelashes and application of a lid speculum. 0.5% proparacaine hydrochloride drops are applied topically. Alternatively, one could also apply cotton tip pledgets soaked in lignocaine hydrochloride (4%) to the injection site for a couple of minutes prior to the injection to decrease the discomfort. Triamcinolone acetonide in a single-use bottle (40 mg/ml, 1ml bottle), is drawn into a 1-cc tuberculin syringe after cleansing the top of the bottle with an alcohol wipe. A separate 27 or 26 gauge needle is placed onto the syringe, which is then inverted to remove air bubbles. The excess triamcinolone is discarded till 0.1 ml (4 mg) remains in the syringe. The injection site is usually the inferotemporal quadrant to avoid drug deposition in front of the visual axis. The stab is given 3 mm from the limbus (in aphakic and pseudophakic patients) and 3.5 mm from the limbus in phakic patients to ensure against passage of the needle through the vitreous base. The needle is usually not introduced all the way to the hub. Using a single, purposeful continuous maneuver, the steroid is injected into the eye. The needle is removed simultaneously with the application of a cotton tipped applicator over its entry site to prevent regurgitation of the injected material. Indirect ophthalmoscopy to check for central retinal artery (CRA) pulsation and paracentesis (if CRA pulsation is present or the globe feels very tense) are carried out, a drop of topical antibiotic solution is administered and the eye is patched. The patient is usually put on a post-injection course of topical antibiotic eye drops for a week.

Jonas et al recommended a slightly different preparation of IVTA.[14] They use 25 mg of triamcinolone acetonide in 0.2 ml of Ringer lactate solution. It is prepared by extracting 0.62 ml from the ampoule containing 40 mg per ml triamcinolone acetonide. The extracted volume is then placed into a tuberculin syringe and Ringer lactate solution is added to fill the syringe. A Millipore filter (pore size, 5 mm) is placed on top of the syringe and most of the contents of the syringe are pressed through the filter, resulting in the triamcinolone crystals left behind in the syringe due to its large size. The syringe is refilled with Ringer lactate solution and the same procedure is repeated three times. At the end, 0.2 ml of the solution is left in the syringe which is injected transconjunctivally into the vitreous cavity. Jonas et al used 25 mg, since they did not find impressive results with 4 mg of IVTA. They used 25 mg even for re-injections, with no signs of severe ocular toxicity.[14]

Interestingly, the 4 mg in 0.1 ml dose of triamcinolone is more popular basically, owing to convenience and the fact that a 0.1 ml volume of the drug in the vitreous cavity is well tolerated. There are no data that support this dosage over other alternative doses. There are ongoing studies to test the efficacy of 2 mg of IVTA.

[Figure - 1] A,B,C illustrate the steps involved in the procedure. The [Figure - 2] A and B are the pre and the 2 months post IVTA injection OCT pictures, respectively, of a 60-year-old diabetic patient with CME.

  Complications associated with the procedure Top

There are however certain serious complications that could occur due to the injection, such as glaucoma,[13],[14] cataract,[13],[14] endophthalmitis,[15] and pseudoendophthalmitis.[16] The last mentioned condition is caused if a 30-G needle is used instead of a 26 G needle, which causes a partial jamming due to the crystalline steroid in the barrel of the needle as the injection is given. This results in spraying of the drug into the vitreous at a high velocity, causing a pseudo-endophthalmitis like reaction.[16] This can be differentiated from true endophthalmitis by virtue of the immediate nature of visual loss, lack of pain, swelling and anterior segment reaction, as well as a spontaneous resolution without antibiotic therapy, all of which are not consistent with an infectious process.

An alternative hypothesis is that pseudo-endophthalmitis could be caused by an acute reaction to the vehicle of the drug.[17] This has been suggested since the vehicle contains 6.9 mg sodium chloride for isotonicity, 15 mg benzyl alcohol as a preservative, 7.5 mg carmellose sodium and 0.4 mg polysorbate 80. However, the vehicle is reported to be well tolerated by rabbit eyes.[9] This pseudo-endophthalmitis like reaction is commoner in vitrectomised and pseudophakic eyes wherein the relatively unicameral nature of the eye allows an easy access of the triamcinolone to the ocular structures leading to a brisk immune response.[17] In order to avoid ocular toxicity, some centers inject only 1 mg of triamcinolone with 4 mg which is reserved for reinjections.[17] All these complications are apart from the risks of retinal detachment and vitreous hemorrhage that are inherent to any intravitreal injection. Hence the risks and benefits of the procedure should be discussed with and written consent obtained from each patient prior to the injection.

  Precautionary measures and management of complications Top

In order to avoid these complications, one should follow certain precautions while performing this procedure:

1) The incidence of endophthalmitis following IVTA injection in one multicenter series was 0.87%.[15] The risk of endophthalmitis is increased due to the invasive nature of the procedure and the immunosuppressive effect of the injected corticosteroid. It is therefore important to use a fresh bottle for each patient to prevent endophthalmitis due to contaminants in the vial.[15] It would be worthwhile noting down the lot number of the steroid vial in a register to facilitate tracing and culturing the bottle for contaminants if endophthalmitis occurs. Prompt intravitreal injection of antibiotics following a vitreous tap at the first suspicion of endophthalmitis should be carried out.

2) Blepharitis is a risk factor for endophthalmitis[18] and hence an office-based procedure is discouraged and the injection is carried out after putting a lid speculum that adequately keeps the eyelids and lashes away from the field. Sterile draping would of course, be ideal.

3) It is also essential to ensure that the bevel of the needle faces anteriorly (with the needle aimed posteriorly and slightly inferiorly). This is done to avoid direct injection over the macula.

4) Indirect ophthalmoscopy to check for central retinal arterial pulsation, should be done at the end of the procedure. If the IOP is felt to be high after injection, a paracentesis should be done. Some surgeons aspirate 0.1 ml of vitreous to prevent the IOP rise and then remove the syringe alone with the needle still inside the eye. 0.1 ml of triamcinolone is then injected with another syringe introduced into the same needle.

5) One should make the patient sit up immediately after injection and continue maintaining an erect posture for the next six hours at least. This is to ensure that the drug assumes a dependant position and does not collect over the macula which would cause a transient visual loss. For the next few days the patient is instructed to sleep on his or her back which would prevent the anterior migration of the corticosteroid in aphakic and pseudophakic eyes due to the relatively unicameral nature of such eyes.[19] This is important since an anterior migration would result in an early increase in the IOP due to clogging of the trabecular meshwork.

6) The IOP should be checked at six and twenty-four hours after injection and at all the follow-up visits. This is especially important considering the fact that the peak of IOP elevations is seen about 3 to 5 months after injection.[14]

7) Two needle technique.[15] This is employed in cases where IVTA injection is contemplated in eyes with a filtering bleb, due to the increased risk of endophthalmitis. The sudden increase in the IOP following the intravitreal injection is presumed to cause microleaks within the bleb thereby allowing ingress to infectious microbes.[15] Here, one needle is used to inject the steroid and the other is placed in the anterior chamber for a simultaneous paracentesis in order to prevent a sudden change in the IOP.

  Follow-up care Top

Triamcinolone acetonide being a crystalline milky liquid, remains in the vitreous for a few days after injection as a discrete white cloud with little or no surrounding reaction. Prominent floaters might be therefore commonly encountered after treatment but these usually subside within a few days as the material drops out of the visual axis. The initial follow-up visits are usually scheduled at 1 to 7 days post injection. The patients should be instructed to adhere to their follow-up regimen and report at the first sign of worsening vision, pain and redness. At even the slightest suspicion of endophthalmitis, prompt intervention in the form of a vitreous specimen for culture and administration of intravitreal antibiotics should be carried out.

  Relative contraindications to IVTA injection Top

The following conditions are considered to be relative contraindications for IVTA injection and the procedure should be carried out only after a careful weighing of the risk-to-benefit ratio.

1) Decreased ocular barrier function such as blepharitis, dry eye, chronic nasolacrimal duct obstruction and presence of filtering bleb.

2) Glaucoma, glaucoma suspects and steroid responders.

3) Additional causes of systemic immunosuppression apart from diabetes mellitus, that would compound the risk of infectious endophthalmitis.

  The future Top

The main disadvantage of intravitreal corticosteroid injections is the short duration of efficacy. Steroid implants would perhaps obviate this. There are ongoing clinical trials to assess the efficacy of intravitreal steroid implants.[20] The most promising implant is one which contains Fluocinolone acetonide (fluocetonide), an insoluble and highly potent synthetic cortico-steroid which is also lipophilic and hence would be easily eliminated from the posterior compartment of the eye. It has a short systemic half life and would therefore have minimal side effects. The drug is concentrated into a 2 mm pellet, in order to deliver an adequate daily concentration that is inhibitory to the effects of the growth factors. An initial pilot study comprised 8 patients with refractory edema that did not respond to conventional therapy.[21] The consistently positive end results at one year prompted two larger ongoing multicentric trials, comparing steroid implants with conventional therapy. There is also recent interest on intravitreal dexamethasone implants.[20]

  Expanding indications of IVTA injection Top

Triamcinolone acetonide is increasingly being employed in pars plana vitrectomies, especially in complicated surgeries in diabetic eyes with recalcitrant macular edema.[22],[23] The vitreous gel in diabetic eyes is denser and more adherent than in non-diabetic eyes due to changes in its composition and cross-linkage. This in addition to the vitreoschisis that occurs, contributes to the residual posterior vitreous cortex (PVC) even after an apparent surgically complete posterior vitreous detachment (PVD). Sonada et al have found a diffuse pattern of PVC deposition in the macular area to be a common finding in diabetic eyes and have postulated it to represent the posterior wall of vitreoschisis hyaloid.[22]

IVTA is employed as a tool to identify the posterior hyaloid and/or the residual PVC. This is essential since one of the important goals of diabetic vitrectomy is the complete removal of the remaining islands of PVC that are thought to contribute to persistent edema (by the resultant incomplete release of vitreomacular traction).

Peyman et al have employed IVTA as a tool to ease the induction of PVD and have found it to considerably shorten the surgical time.[23] After core vitrectomy, 0.5 to 1 ml of triamcinolone acetonide is injected with a 20-gauge needle through one of the sclerotomies, which causes the granules to become trapped in the gel structure of the vitreous. Subsequently, the posterior hyaloid is separated from the optic disc with suction. Alternatively, it could be instilled after PVD to identify the residual PVC, which could then easily be removed with a surgical forceps or a silicone-tipped needle. [Figure - 3] A-D] illustrate the surgical steps involved in the usage of IVTA in parsplana vitrectomy in a diabetic patient.

IVTA is also increasingly being tried in various pilot studies for refractory macular edema (especially CME) in various conditions such as, central retinal vein occlusion, chronic uveitis, persistent pseudophakic CME and in other conditions such as exudative age-related macular degeneration, neovascular glaucoma, proliferative vitreoretinopathy, proliferative diabetic retinopathy, chronic pre-phthisical ocular hypotony, etc. Although the results are varied, intravitreal triamcinolone does seem to be beneficial in these situations in selected cases.

In order to define the safety profile and efficacy of IVTA and in order to explore the alternative doses, the results of the National Eye Institute sponsored multicentric randomized controlled clinical trial of intravitreal triamcinolone for the treatment of diabetic macular edema are eagerly awaited. More information can be obtained from the Diabetic Retinopathy Clinical Research Network website (www.drcr.net).

  References Top

National Diabetes Data Group. Diabetes in America , 2nd ed. NIH Publ. No.95-1468. US Govt. Printing Office: Washington; 1995.  Back to cited text no. 1
Kahn HA, Hiller R. Blindness caused by diabetic retinopathy. Am J Ophthalmol 1974;78:58-67.  Back to cited text no. 2
Klein R, Klein BE, Moss SE, Davis MD, DeMets DL. The Wisconsin epidemiologic study of diabetic retinopathy.IV. Diabetic macular edema. Ophthalmology 1984;91:1464-74.  Back to cited text no. 3
The early treatment diabetic retinopathy study research group. Photocoagulation for diabetic macular edema. Early treatment diabetic retinopathy study report no. 1. Arch Ophthalmol 1985;103:1796-806.  Back to cited text no. 4
Wilson CA, Berkowitz BA, Sato Y ando N, Handa JT, de Juan E Jr . Treatment with intravitreal steroid reduces blood-retinal barrier breakdown due to retinal photocoagulation. Arch Ophthalmol 1992;110:1155-9.  Back to cited text no. 5
Hood PP, Cotter TP, Costello JF, Sampson AP. Effect of intravenous corticosteroid on ex vivo leukotriene generation by blood leukocytes of normal and asthmatic patients. Thorax 1999;54:1075-82.  Back to cited text no. 6
Sze PY, Iqbal Z. Glucocorticoid actions on synaptic plasma membranes: Modulation of I125 calmodulin binding. J Steroid Biochem Mol Biol 1994;48:179-86.  Back to cited text no. 7
Vedantham V. Periocular corticosteroid therapy: comments. Br J Ophthalmol 2004;88:724-5.  Back to cited text no. 8
McCuen BW 2nd, Bessler M, Tano Y, Chandler D, Machemer R. The lack of toxicity of intravitreally administered triamcinolone acetonide. Am J Ophthalmol 1981;91:785-8.  Back to cited text no. 9
Young S, Larkin G, Branley M, Lightman S. Safety and efficacy of intravitreal triamcinolone for cystoid macular edema in uveitis. Clin Exp Ophthalmol 2001;29:2-6.  Back to cited text no. 10
Martidis A, Duker JS, Greenberg PB, Rogers AH, Puliafito CA, Reichel E, Baumal C. Intravitreal triamcinolone for refractory diabetic macular edema. Ophthalmology 2002;109:920-7.  Back to cited text no. 11
Massin P, Audren F, Haouchine B, Erginay A, Bergmann JF, Benosman R, et al . Intravitreal triamcinolone acetonide for diabetic diffuse macular edema: preliminary results of a prospective controlled trial. Ophthalmology 2004;111:218-24  Back to cited text no. 12
Jonas JB, Kreissig I, Sofker A, Degenring RF. Intravitreal injection of triamcinolone for diffuse diabetic macular edema. Arch Ophthalmol 2003;121:57-61.  Back to cited text no. 13
Jonas JB, Kreissig I, Hugger P, Sauder G, Panda-Jonas S, Degenring RF. Intravitreal triamcinolone acetonide for exudative age related macular degeneration. Br J Ophthalmol 2003;87:462-8.  Back to cited text no. 14
Acute endophthalmitis following intravitreal triamcinolone acetonide injection. Am J Ophthalmol 2003;136:791-6.  Back to cited text no. 15
Sutter FK, Gillies MC. Pseudo-endophthalmitis after intravitreal injection of triamcinolone. Br J Ophthalmol 2003;87:972-4.  Back to cited text no. 16
Roth DB, Chieh J, Spirn MJ, Green SN, Yarian DL, Chaudhry NA. Noninfectious endophthalmitis associated with intravitreal triamcinolone injection. Arch Ophthalmol 2003;121:1279-82.  Back to cited text no. 17
Bannerman TL, Rhoden DL, McAllister SK, Miller JM, Wilson LA. The source of coagulase-negative staphylococci in the Endophthalmitis Vitrectomy study: A comparison of eyelid and intraocular isolates using pulsed-field gel electrophoresis. Arch Ophthalmol 1997;115:357-61.  Back to cited text no. 18
Vedantham V. Intraocular pressure rise after intravitreal triamcinolone. Am J Ophthalmol 2005;139:575.  Back to cited text no. 19
Aiello LP, Cahill MT, Cavallerano JD. Growth factors and protein kinase C inhibitors as novel therapies for the medical management of diabetic retinopathy. Eye 2004;18:117-25.  Back to cited text no. 20
Pearson PE, data presented at the American Academy of Ophthalmology meeting, Dallas, TX: 2001.  Back to cited text no. 21
Sonada KH, Sakamoto T, Enaida H, Miyazaki M, Noda Y, Nakamura T, et al . Residual vitreous cortex after surgical posterior vitreous separation visualized by intravitreous triamcinolone acetonide. Ophthalmology 2004;111:226-30.  Back to cited text no. 22
Peyman GA, Cheema R, Conway MD, Fang T. Triamcinolone acetonide as an aid to visualization of the vitreous and the posterior hyaloid during parsplana vitrectomy. Retina 2000;20:554-5.  Back to cited text no. 23


  [Figure - 1], [Figure - 2], [Figure - 3]

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Mechanism of Action
How best to admi...
Technique of IVT...
Complications as...
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Relative contrai...
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Expanding indica...
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