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Residency Training Program

In Ophthalmology



Indications, Complications and Short versus Long-Term Outcome of Intravitreal Triamcinolone Acetonide Injection in Macular Edema

Prepared by:

Dr. Hattan Alkhiary

Supervised by:

Dr.Sawsan Nowilaty


Dr. Emad Abboud


  • Introduction.

  • Background:

- Diabetic Macular Edema

- Macular Edema in Retinal Vein Occlusion

- Post Surgical Macular Edema

- Intravitreal Triamcinolone Acetonide Injection:

- Pharmacokinetics

- Clinical uses

- Efficacy and duration of therapeutic effect:

- Complications

  • Patients and methods

  • Results:

- Visual acuity results

- Anatomic results: clinical appearance and OCT

- Complications results

  • Discussion

  • References

  • Introduction:

Macular edema is a common complication of diabetic retinopathy, retinal venous occlusions, intraocular surgery and variety of retinal diseases. It is a major cause for visual loss particularly in its diffuse or chronic form. Its treatment, primarily when it is diffuse in diabetic eyes or when it is due to retinal venous occlusions, is usually disappointing. Although in diabetic clinically significant macular edema (CSME) the benefit of focal macular laser photocoagulation was clearly demonstrated by the Early Treatment of Diabetic Retinopathy Study (ETDRS), 1 and laser treatment has since become and remains to date the “gold standard” for the treatment of diabetic macular edema, only 50% of laser-treated eyes in the ETDRS achieved stable vision at 3 years, while 12% of treated eyes continued to lose vision. Similarly, modified grid laser photocoagulation for diffuse macular edema was shown to have limited visual benefit in other studies where 60.9% of eyes had unchanged vision and 24.6% of eyes had worse following laser at 3 years (Lee and Olk).2 The clinical experience world-wide echoes the results of these studies. As for per­sistent macular edema due to central retinal vein occlusion (CRVO), to date there is no proven treatment. The Central Vein Occlusion Study Group did not find any signif­icant difference in visual acuity between laser-treated eyes and untreated eyes at any time point during follow­-up.3 Furthermore, although macular grid treatment with argon laser is the only proven therapy that results in a statistically significant improvement in vision in cases of macular edema secondary to branch retinal vein occlusion (BRVO), the clinical outcomes with this treatment are often disappointing.

The failure of laser to improve vision in a substantial subgroup of patients with macular edema in the above settings has created interest in other treatment methods. One such treatment, promoted in the late 1990’s, is intravitreal injection of steroids namely intravitreal triamcinolone acetonide injection (IVitTA) 35 . Although the exact mechanism of action of this treatment is unknown, there was a rationale behind the use of steroids namely their ability to inhibit the arachidonic acid pathway decreasing prostaglandin and their ability to down regulate the production of vascular endothelial growth factor (VEGF) and to reduce the breakdown of the blood-retinal barrier.4-8 Indeed, the reports on early clinical experience with intravitreal triamcinolone injections for the treatment of macular edema showed promising results with a substantial proportion of eyes gaining visual acuity associated a quasi disappearance of the macular edema. However, it became soon apparent that the beneficial effects were temporary as many eyes exhibited recurrences of the macular edema raising the need for further injections. Furthermore complications such as intraocular pressure elevations started to appear. The long term outcomes were rarely reported.

The purpose of the current retrospective study is to describe the short and long term visual and anatomical outcomes as well as the short and long term complications in eyes with macular edema due to diabetes, retinal venous occlusions or post intraocular surgery who were treated with intravitreal injections of 4mg of triamcinolone acetonide at the King Khaled Eye Specialist Hospital (KKESH) from 1/1/2002 to1/1/2006.


Diabetic Macular edema:

Diabetic retinopathy is a major cause of blindness worldwide. In the United States it is the leading cause of blindness in patients younger than 50 years of age.9 Approximately 29% of diabetic patients with disease duration of 20 years or more are affected with macular edema which is the main reason of reduced vision in this population. 9 The incidence of diabetic macular edema (DME) rises with the severity of retinopathy: macular edema is present in 3% of patients with mild non-proliferative diabetic retinopathy (NPDR), in 38% of patients with moderate to severe non-proliferative diabetic retinopathy, and in 71% of patients with proliferative diabetic retinopathy (PDR).10 The Early Treatment Diabetic Retinopathy Study (ETDRS), coined the term clinically significant macular edema (CSME) for macular edema involving or threatening the fovea and thus more likely to be associated with a risk of central visual loss. Macular edema is considered CSME if it presents with any of the following features:

  1. Retinal thickening at or within 500 microns of the center of the macula.

  2. Hard exudates at or within 500 microns of the center of the macula associated with thickening of the adjacent retina.

  3. Zone of retinal thickening >1 disk area in size, any part of which is within 1 disk diameter of the center of the macula. 1

Indeed, in the ETDRS the 3-year risk of moderate visual loss (defined as a doubling of the initial visual angle or a decrease of three lines or more on a logarithmic visual acuity chart) for diabetic patients with CSME was 30%.1 Effective treatment of CSME is therefore necessary.

Although the exact mechanism of diabetic macular edema is not fully understood, several mechanisms have been postulated and found to exist in clinical research. The pathophysiology of macular edema includes pericyte loss, microaneurysm formation, basement membrane thickening, focal closure of the capillary bed, and ultimately breakdown of the blood-retinal barrier with increased vascular permeability. 11 Furthermore, there are several factors that increase the risk for development of macular edema.

Risk Factors for Diabetic Macular Edema:

Risk factors for diabetic macular edema are hyperglycemia, hypertension, hyperlipidemia, longer duration of diabetes, control of blood sugar, adult-onset diabetes, pregnancy, and ophthalmic interventions such as panretinal photocoagulation and cataract extraction. 12

1) Increasing levels of hyperglycemia: Greater levels of HgbA1c result in greater rates of macular edema. In the Wisconsin Epidemiologic Study of Diabetic Retinopathy (WESDR) 13 the rate of diabetic macular edema (DME) in late-onset, long term (>15 years) diabetes increased from 18.1% in the lowest quartile HgbA1c level (6.8-9.7%) to 36.4% in the highest quartile HgbA1c level (13.2-19.2%) with an even greater relative risk in late-onset, short term diabetes. Furthermore, the Diabetes Control and Complications Trial (DCCT) 14 revealed that intensive treatment of diabetes to achieve near normal blood glucose levels (resulting in mean levels of 155 vs. 231 mg/dl) resulted in a 23% risk reduction in clinically significant macular edema.

2) Duration of diabetes: The prevalence of macular edema increases with the duration of diabetes. 13,15,16 In the WESDR, the rate of DME increased from 3% in patients with diabetes for 5 years to 28% in those with diabetes from more than 20years. 13

3) Hypertension: Systolic hypertension has been reported to increase the relative risk for DME from three to fourfold in both early and late-onset diabetes. 13

4) Hyperlipidemia: The WESDR13 and ETDRS1 reported a clear relationship between cholesterol levels and the presence of retinal hard exudates.

5) Renal disease: The presence of renal diseases as evidenced by proteinuria, may in crease the risk for DME from three to five-fold in early and late-onset diabetes 13,15

6) Pregnancy: It not only increases the overall progression of diabetic retinopathy but it may produce severe macular edema, especially if associated

with hypertension and proteinuria 19,20

7) Ophthalmic interventions: Panretinal photocoagulation (PRP) 21,22 and cataract extraction induce the development or progression of DME. Increased diabetic macular edema may occur transiently in up to 43% of diabetic patients treated with PRP, and the increase may persist in 25% of those treated.22 After phacoemulsification with intraocular lens implantation, 32% - 40% of patients with diabetes may acquire new macular edema immediately after surgery 23,24

Diagnosis of diabetic macular edema:

The diagnosis of macular edema is clinical. Slit lamp biomicroscopy with contact lens is the clinical “gold standard” for evaluation of macular thicknening and associated features of macular edema. Biomicroscopy with non-contact lenses (indirect 60, 78 and 90 diopters lenses) are also widely used for detection and assessment of macular edema Stereographic fundus photography may also be used although less commonly.

Clinically, diabetic macular edema may assume any one or a combination of the following forms:

  1. Focal macular edema. It refers to localized areas of retinal thickening caused primarily by focal exudative leakage from one or a cluster of microaneurysms, dilated retinal capillaries, and less commonly from intraretinal microvascular abnormalities. A partial or complete circinate ring of hard exudates deposition often surrounds these foci of edema 11. Clusters of microaneurysms are usually seen in the center of circinate exudates and are even better demonstrated on fundus fluorescein angiography. Individual leakage sites occasionally resolve spontaneously 25. This form of edema usually responds well to focal laser photocoagulation and carries a good prognosis when associated with good capillary perfusion around the fovea.

  1. Diffuse macular edema: It results from generalized breakdown of the blood-retinal barrier producing generalized leakage from dilated capillaries throughout the posterior pole. Occlusion of a considerable portion of the capillary bed leads to widening of the intercapillary spaces and compensatory dilation of the patent capillaries that tend to leak diffusely and cause edema. Hard exudates are less common in this form and edema is often chronic.25 Diffuse edema responds less well to laser treatment than focal edema and carries a poorer visual prognosis particularly if associated with extensive capillary non-perfusion.

  1. Cystoid macular edema is another common clinical variation of diabetic macular edema.26,27 The entire capillary bed exhibits diffuse leakage by fluorescein angiography and the prognosis for visual acuity remains generally poor despite good capillary perfusion and laser photocoagulation. It is worth mentioning that the ETDRS considered that cystoid macular edema is a factor for worse visual prognosis whereas two large prospective studies evaluating laser photocoagulation for diabetic macular edema found no difference in visual prognosis for eyes with cystoid features 2

  1. Extensive deposition of hard exudates plaques is another clinical presentation associated with diabetic macular edema. Although such plaques may resolve after months to years, photoreceptor degeneration often prevents visual recovery when the fovea is involved. Not infrequently a fibrous plaque may develop beneath the macula as a result of fibrous metaplasia of the retinal pigment epithelium (RPE) stimulated by the subretinal exudates 28-31.

Although the diagnosis of macular edema is clinical, the following ancillary tests have become extremely useful for the evaluation and/or the quantification of macular edema:

Fundus fluorescein angiography (FFA): This is clinically the most widely available and useful test. It permits study of the retinal circulation and identifies by the amount of fluorescein leakage the dysfunction of the retinal vascular endothelium. It is a significant diagnostic modality as it helps localize the sites of leakage and capillary non-perfusion, as well as the location and size of the perifoveal capillary network. It also also determines the type of leakage: “focal” secondary to leaking MA, or “diffuse” due to leakage from the capillary bed. Thus it improves the accuracy of planning treatment for macular edema 32.

Optical Coherence Tomography (OCT): Because slit lamp biomicroscopy and stereoscopic fundus photography are to some extent subjective, new imaging techniques for objective measurement of retinal thickness have been introduced to clinical use. Optical coherence tomography can provide diagnostically important information that complements standard fundus photography or fluorescein angiography. Optical coherence tomography images allow a direct visualization of retinal pathology and enable the visualization of internal retinal architectural structure, providing quantitative information of the retinal architecture. The morphometric measurements can be used to diagnose disease or to assess disease progression and response to therapy. Based on many studies, macular edema can be classified into three types as demonstrated by OCT: sponge-like retinal swelling, cystoid macular edema, and serous retinal detachment. Sponge-like retinal swelling is defined as increased retinal thickness with reduced intraretinal reflectivity. Cystoid macular edema is a type of edema where there are intraretinal cystoid spaces in the macular area. Serous retinal detachment is characterized by shallow foveal detachment with clear separation between the neurosensory retina and the retinal pigment epithelium due to accumulation of subretinal fluid.33-35 Brown et al 36 found excellent agreement between OCT and clinical contact lens examination for the absence or presence of foveal edema when OCT thickness was normal (300 microns). However, agreement was poor when foveal thickness was mildly increased on OCT (201-300 microns). Thus, OCT is capable of identifying the presence of mild macular edema better than the clinical examination alone and has hence become an essential ancillary test in the modern management of macular edema. Based on many studies, macular edema can be classified into three types as demonstrated by OCT: sponge-like retinal swelling, cystoid macular edema, and serous retinal detachment. Sponge-like retinal swelling was defined as increased retinal thickness with reduced intraretinal reflectivity. Cystoid macular edema is a type of edema where there are intraretinal cystoid spaces at the macular area. Serous retinal detachment is characterized by shallow foveal detachment with clear separation between the neurosensory retina and the retinal pigment epithelium due to accumulation of subretinal fluid.37

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