Clinical Study Macular Oedema
1,3Department of Medicine, Krishna Vishwa Vidyapeeth
Deemed to be University, Karad, Satara, Maharashtra, India.
2Department of Ophthalmology, Krishna Vishwa Vidyapeeth,
Deemed to be University, Karad, Satara, Maharashtra, India.
4Director, Akhildev IPR and Research Services, Greater Noida, UP, India.
5Associate Professor, Christ (Deemed to be University), India.
6Bharati Vidyapeeth College of Pharmacy, Palus, Maharashtra, India.
*Corresponding Author E-mail: vhkarambelkar@outlook.com
ABSTRACT:
Prior to the development of the ophthalmoscope, macular oedema remained mostly unknown. Macular oedema is caused by fluid buildup in the retinal layers around the fovea. It causes vision loss by changing the functional cell connection in the retina and stimulating an inflammatory reparative response. The clinical profile, aetiology, and varied types of Macular Oedema are hence the focus of research, and also to investigate the aetiology of macular oedema as well as the various forms of macular oedema in patients attending Krishna Hospital in Karad. The male to female ratio among the 60 participants was 2.53:1. Macular oedema is the major cause for loss in vision which is common vitreo retinal diseases, with diabetes being the most prevalent cause (35% of cases) in our study. Its early detection and treatment are critical for preventing blindness. It is consequently critical to understand the aetiology, pattern, and chronicity of macular oedema in order to customize treatment and monitor response to it.
KEYWORDS: Clinical Profile, Etiology, Macular Oedema, Retina Vision.
INTRODUCTION:
Macular oedema is a non-specific symptom or consequence of several intraocular and systemic illnesses that cause substantial vision loss. It is critical to identify the origin of vision loss because it can be a symptom of a variety of systemic disorders. In addition, prompt action is required to avoid irreversible vision loss1. Macular oedema is characterized by a cluster of localized swellings in the macular region that causes the central retina's thickness to expand. The Müller cells have also been shown to swell. The extracellular and/or intracellular retinal spaces might be affected by the collected fluid. It is an indiscriminate symptom or aftereffect of a wide range of intraocular and systemic disorders2.
Due to its distinct anatomical characteristics, the macula is the area that is most susceptible to the formation of edema. First, the macular framework's resistance prevents fluid from being forced into the retina from the vitreous cavity as a result of intraocular pressure (IOP)3. Second, the capillaries and retinal tissue's osmotic and hydrostatic forces balance one another. Thirdly, fluid from the sub-retinal space is drawn out by the significant choroidal osmotic pressure. Finally, the choroid is the final destination of fluid that the “retinal pigment epithelium (RPE)” actively pumps out of the subretinal region4.
Specifically, macular edema is linked to a gradual, permanent loss of eyesight. There are problems associated with each of the different therapy techniques. Accidental foveal burn is the most serious consequence linked to laser photocoagulation. Therefore, before activating the laser, a test burn should be applied to the disc3. The most terrifying consequence of intravitreal injections, endophthalmitis, is more common. Vitreous hemorrhage, cataracts from improper injection technique, central retinal artery blockage from an abrupt rise in intraocular pressure, and retinal tears are further risks5. For the treatment of macular edema, patient education is essential. Similar advice should be given to DME patients on the need to maintain rigorous metabolic control6. The ocular and systemic symptoms of diabetes can be prevented, delayed, and limited through patient education and appropriate behavior. Patients must be informed that diabetes might have an impact on many organ systems7,8.
DME patients should be given similar counseling about the importance of strict metabolic management. Diabetes ocular9 and systemic symptoms can be avoided, postponed, or restricted by patient education and proper behavior. Patients must be aware that diabetes can affect several organ systems10. The inner nuclear and plexiform layers of the retina as well as the outer plexiform (Henle's) layer of the retina exhibit fluid accumulation in this disease. An increase in the water content of the retinal tissue—which might be intracellular or extracellular—defines macular edema11.
Figure 1: Central retinal vein blockage detected via retinal imaging12
In a recent natural history cohort study, just 1% of patients with ischemia CRVO had baseline visual acuities of 20/100 or greater, compared to 78% of patients with no ischemic CRVO. Macular edema is the most frequent cause of visual loss associated with CRVO, while it can also result from macular ischemia, neovascular glaucoma, retinal neovascularization, or a combination of these issues. Figure 1 displays imaging from a patient with CRVO13. Diabetes is a complicated illness with systemic signs that are best addressed by a multidisciplinary team. It is vital to educate patients14. The nurses coordinate follow-up and keep the rest of the team informed of the patient's condition. Pharmacist can serve as patient’s advocate for diabetes management advances by providing pharmaceutical counseling and management, lifestyle counseling, and notifying clinicians as necessary. When patients comprehend the whole variety of symptoms of their underlying disease, their results improve15.
To examine the microvascular characteristics of various subtypes of “diabetic macular edema” (DME) using optical coherence tomography angiography (OCTA), Ghada A. Nassar et al. a cross-sectional study of treatment-naive DME patient. The morphology of the eyes was assessed using optical coherence tomography. The research comprised 52 eyes, 27 of which had CME and 25 of which had DRT. There were no significant changes in the VD of the SCP and DCP, the FAZ of the SCP, the FAZ of the DC), and the CF. According to linear regression analysis, DME morphology was the best predictor of BCVA. HbA1C and lipid levels were also significant predictors16. Di Zou et al. assess anti-VEGF therapy delivery in pseudophakic eyes getting anti-VEGF injections for DMO and investigate structural and functional effects. They examined the results of 81 pseudophakic eyes with DMO that had undergone at least six anti-VEGF injections. It took an average of 913±454.1 days to administer 11.1±4.7 anti-VEGF shots. The anti-VEGF medication employed to treat these DMO-treated eyes was poor, which is consistent with previous "real-world" results. There was a substantial propensity for patients to be shifted to a second anti-VEGF medication within the class17. Including William Rhoades, Eye loss may result from central retinal vein occlusion (CRVO). The etiology of CRVO involves the production of thrombi that cause an increase in vascular permeability, retinal capillary pressure, and perhaps even retinal neovascularization. Macular edema frequently contributes to CRVO-related vision loss. Macular edema has been treated using a variety of therapy techniques. Vascular endothelial growth factor (VEGF) intravitreal inhibition is now the most widely utilized treatment. Aflibercept, bevacizumab, and ranibizumab are the three most often utilized medications, and they are successful in inhibiting VEGF. Macular edema can also be treated using intraocular steroids. The treatment alternatives will be briefly covered in this review, and a more in-depth discussion of the effectiveness and safety of aflibercept will follow12.
Sermsiri Sangroongruangsri et al., study examined and evaluated the effectiveness of intravitreal bevacizumab, ranibizumab, and aflibercept for the treatment of macular edema caused by RVO. From their establishment until October 2017, PubMed, EMBASE, and the Cochrane Library were searched. There were 11 randomized controlled studies (18 publications; 1830 adult patients) found. This study and other meta-analyses showed that anti-VEGF medication had a therapeutic advantage over placebo, corticosteroids, laser therapy, and a favorable short-term safety profile for treating individuals with macular edema caused by RVO. When receiving short-term therapy, there was no discernible difference between IVA, IVB, and IVR in terms of BCVA improvement or CMT decrease18.
(a) Design: A cross-sectional case study on patients with macular edema and analysis of the various clinical patterns of macular edema depending on the etiology was conducted in the Department of Ophthalmology, Krishna Hospital Karad. The objectives of the study were to investigate the clinical characteristics, etiology, and different patterns of Macular Oedema, to investigate the cause of macular edema in patients attending Krishna Hospital in Karad and to investigate the various types of macular edema in patients visiting Krishna Hospital in Karad.
(b) Sample and Instruments: The research was carried out between December 2018 and May 2020. The study included all eligible macular edema patients who met the inclusion criteria and visited the Ophthalmology OPD or were receiving treatment at Krishna Hospital between December 2018 and May 2020. The study's protocol was described to the patients and informed written permission was obtained. A thorough history and examination of the patients were performed. Visual acuity was examined using Snellen's Distant Vision chart and Jaeger's Near Vision chart, Amsler's Grid, Ishihara's Chart, and Slit lamp 90D examination. Indirect and direct fundoscopy is used after dilating the eyes with 0.8% tropicamide and 5% phenylephrine eye drops (if not contraindicated). Using the Fundus camera, OCT, and FFA, the documentation and pattern of macular edema were assessed and then recorded. These instances were categorized based on etiology by comparing the patient's history, the examiner's clinical observations, and any related investigations.
RESULTS AND DISCUSSION:
The etiological categorization of all instances of Macular Oedema is presented in Table 3. The majority of the patients, 21 out of 60 (35%) had Diabetes Mellitus (DM), followed by Branch Retinal Vein Occlusion (BRVO) in 12 (20%) and Hypertension in 6 (10%). There were 39 cases of unilateral macular edema and 21 cases of bilateral macular edema. There was no significant relationship between gender and laterality of presentation (Chi-square statistic = 0.3978, p-value = 0.5282), Table 4. The distribution of the etiologies for unilateral instances with macular edema is shown in Table 5. Branch retinal vein occlusion (BRVO) affected 12 out of 39 patients (30.77%), diabetes mellitus was observed in 8 patients (20.51%), age-related macular degeneration in 4 patients (10.26%), and Irvine Gass syndrome in 2 patients (10.26%). The distribution of the etiologies for bilateral instances of macular edema is shown in Table 6. In all, 13 of the 21 bilateral instances (or 61.90% of the total) had diabetes mellitus as the predominant condition, followed by individuals with only hypertension and those with both hypertension and diabetes mellitus (14.29% each). In this study, 40 eyes (49.38%) had visual acuity ranging from 6/60-6/24, and 25 eyes had visual acuity of 6/60. In all, 16 eyes exhibited visual acuities ranging from 6/18 to 6/12, Table 7. However, 31 eyes were with near vision N36 (38.27%), 27 eyes with vision N36-N18 (33.33%), 19 eyes with vision N12-N10 (23.46%), and 4 eyes with vision N8 (8.16%), Table 8. Besides, type 2 diabetes was seen in 62.5% of diabetic macular edema patients on oral hypoglycemic medications and 29.17% of those taking insulin. On the insulin regimen given in Table 9, there were only 2 individuals with type 1 diabetes.
Table 3: Etiological categorization of all instances of macular oedema
|
Classification |
Number |
Percentage (%) |
|
Hypertension (HTN) |
6 |
10% |
|
DM |
21 |
35% |
|
HTN and DM |
3 |
5% |
|
Tuberculosis (TB) |
2 |
3.33% |
|
CRVO |
3 |
5% |
|
BRVO |
12 |
20% |
|
Age Related Macular Degeneration (ARMD) |
5 |
8.33% |
|
Central Serous Chorioretinopathy (CSCR) |
1 |
1.67% |
|
Retinitis Pigmentosa (RP) |
1 |
1.67% |
|
Berlins |
2 |
3.33% |
|
Irvine- Gass |
4 |
6.67% |
|
Total Number of patients |
60 |
100% |
Table 4: The number of instances that appear as unilateral/bilateral against gender
|
Gender |
Unilateral |
Bilateral |
Total |
|
Males |
29 (67.44%) |
14 (32.56%) |
43 |
|
Females |
10 (58.82%) |
7 (41.18%) |
17 |
|
Total |
39 (65%) |
21 (35%) |
60 |
Table 5: Unilateral case etiology distribution
|
Classification |
Males |
Females |
Total |
|
HTN |
2 |
1 |
10% |
|
DM |
7 |
1 |
35% |
|
TB |
1 |
1 |
3.33% |
|
CRVO |
3 |
0 |
5% |
|
BRVO |
7 |
5 |
20% |
|
ARMD |
4 |
0 |
8.33% |
|
CSCR |
1 |
0 |
1.67% |
|
Berlins |
1 |
1 |
2 (5.13%) |
|
Irvine- Gass |
3 |
1 |
4 (10.26%) |
|
Total number of patients |
29 |
10 |
39 |
Table 6: Bilateral case etiology distribution
|
Classification |
Males |
Females |
Total |
|
HTN |
2 |
1 |
3 (14.29%) |
|
DM |
11 |
2 |
13 (61.90%) |
|
HTN and DM |
1 |
2 |
3 (14.29%) |
|
ARMD |
0 |
1 |
1 (4.76%) |
|
RP |
0 |
1 |
1 (4.76%) |
|
Total |
14 |
7 |
21 |
Table 7: In situations of macular edema, visual acuity (far vision)
|
Distant Vision |
Right Eyes |
Left Eyes |
Total |
|
<6/60 |
13 |
12 |
25 (30.87%) |
|
6/60-6/24 |
26 |
14 |
40 (49.38%) |
|
6/18-6/12 |
10 |
6 |
16 (19.75%) |
|
Total |
49 |
32 |
81 |
Table 8: In situations of macular edema, visual acuity (near vision)
|
Near Vision |
Right Eyes |
Left Eyes |
Total |
|
<N36 |
19 |
12 |
31 (38.27%) |
|
N36-N18 |
17 |
10 |
27 (33.33%) |
|
N12-N10 |
9 |
10 |
19 (23.46%) |
|
N8 |
4 |
0 |
4 (4.94%) |
|
Total |
49 |
32 |
81 |
Table 9: Diabetes mellitus type and antidiabetic treatment
|
Type |
No. of patients |
Percentage |
|
Type 1 (Insulin dependent) |
2 |
8.33% |
|
Type 2 (Oral HGA) |
15 |
62.5% |
|
Type 3 (On Insulin) |
7 |
29.17% |
Data Analysis:
This cross-sectional research included macular edema patients. From December 2018 to May 2020, the research was carried out in the Department of Ophthalmology at Krishna Hospital in Karad. A total of 60 individuals with macular edema were included in the study. Patients with macular edema who visited the ophthalmology outpatient clinic or were hospitalized in the hospital were included in the study. All patients with challenging fundus (macular examination) such as central corneal opacities, thick central cataracts, media opacities (vitreous hemorrhage), and patients currently receiving macular edema therapy were excluded from the trial. The study was launched after receiving the necessary ethics approval and informed written permission from the patients. Patients' demographic profiles, histories, extensive ophthalmologic examinations, pertinent ophthalmological investigations such as FFA and OCT, and laboratory investigations such as blood sugar levels, lipid profiles, and so on were all obtained. In our study, 43 were men (71.67%) and 17 were females (28.33%), resulting in a male-to-female ratio of 2.53:1, which corresponds with the findings of the Wisconsin Epidemiological Study of Diabetic Retinopathy, which revealed a male-to-female ratio of 1.5:1.In our study, individuals were divided into seven groups with a ten-year age gap. The most prevalent age group was 61-70 years old, with 22 patients (36.67%). 11 patients (18.33%) between the ages of 51-60 years and 71-80 years, 10 patients (16.67%) between the ages of 41-50 years, and 2 patients (3.33%) between the ages of 21-30 years, 31-40 years, and 81-90 years. The mean age was 60 years, the average age was 62 years, and the age range was 23-85 years. According to the Wisconsin Epidemiological Study of Diabetic Retinopathy, middle-aged people are more impacted and have a greater prevalence of DR. Our findings are consistent with the findings of this investigation. Three patients had hypertension and diabetes (5%), three patients had CRVO (5%), two patients each had Berlin’s edema and tuberculosis (3.33%), and one patient had CSCR and RP (1.67%).
The current study examines the clinical profile and presentation patterns of macular edema patients. The male-to-female ratio among the 60 participants was 2.53:1. The average age was 60 years, with a range of 23 to 85 years. The most prevalent unilateral etiology was BRVO (31%), while the most common bilateral etiology was DM (62%). The majority of patients reported distant vision of 6/60-6/24 and close vision of N36. The most prevalent OCT pattern discovered (62%) was CYSTOID. DIABETES was the most prevalent cause of CYSTOID pattern in 22 eyes (44%). The male-to-female diabetes patient ratio was 3.8:1. 54.16% of diabetic macular edema patients had duration of 10-20 years.41.67% of diabetic macular edema patients had severe NPDR. Dyslipidemia was seen in 76% of eyes with clinically severe macular edema. MIXED was reported to be the most prevalent FFA pattern in 18 eyes (64.29%). The majority of cystoid macular edema cases (50% had Severe NPDR). The most common risk factor for retinal vein occlusion (93% of cases) was hypertension19. Traditionally, slit lamp assessment and stereo fundus photography are used to assess diabetic macular edema; however, many novel modalities are being employed and developed to assess diabetic macular edema20. Optical coherence tomography (OCT) is a high-resolution imaging method used to examine the retina and determine its thickness. OCT is less intrusive than FA and hence more tolerable21.
CONCLUSION:
Macular oedema is the major cause of vision loss in common vitreoretinal diseases, with diabetes being the most prevalent cause (35% of cases) in our study. Its early detection and treatment are critical for preventing blindness. There are several modifiable risk factors linked with diabetic macular edema that may be managed, such as poor glycemic control, hypertensive management, dyslipidemia, anemia, and nephropathy. Vasogenic alterations caused by hyperglycemia cause the “blood-retinal barrier” (BRB) to breach, triggering the macular edema cascade. However, the activation of a low-grade inflammation along with vasogenic alterations causes significant retinal injury and persistent macular abnormalities. Examining the retina with slit lamp bio microscopy and verifying the diagnosis with OCT is simple. OCT can assist identify persistent macular edema and distinct types of macular edema, which can help guide therapy. OCT has helped us comprehend and interpret macular edema and vitreoretinal interface diseases. It enables earlier, more exact diagnosis and better follow-up. OCT has become a standard, important tool for measuring treatment response and obtaining qualitative and quantitative data on the retinal thickness that can be correlated with visual acuity. FFA also aids in determining if macular edema will react to treatment, i.e. if it is ischemic and hence resistant to treatment.
REFERENCES:
1. Noma H., Yasuda K. and Shimura M. Involvement of cytokines in the pathogenesis of diabetic macular edema. International Journal of Molecular Sciences. 2021; 22(7): 3427. doi: 10.3390/ijms22073427.
2. Lobo C. Pseudophakic cystoid macular edema. Ophthalmologica. 2012; 227(2):61-67. doi: 10.1159/000331277.
3. Jia HQ et al. Diagnostic value of optical coherence tomography for diabetic macular edema. International Journal of Ophthalmology. 2008; 8(11):2248-50.
4. Cunha-Vaz J. Mechanisms of retinal fluid accumulation and blood-retinal barrier breakdown. Developments in Ophthalmology. 2017; 58:11-20, doi: 10.1159/000455265.
5. Koronis S. et al. Update in treatment of uveitis macular edema. Drug Design, Development and Therapy. 2019; 13: 667-680. doi: 10.2147/DDDT.S166092.
6. Soliman, W. et al. Local retinal sensitivity in relation to specific retinopathy lesions in diabetic macular oedema. Acta Ophthalmologica. 2012; 90(3):248-53 doi: 10.1111/j.1755-3768.2010.01912.x.
7. Schmidt-Erfurth U. et al. Guidelines for the management of diabetic macular edema by the European Society of Retina Specialists (EURETINA). Ophthalmologica. 2017; 237(4):185-222. doi: 10.1159/000458539.
8. Wu Q. et al. Detection of morphologic patterns of diabetic macular edema using a deep learning approach based on optical coherence tomography images. Retina, 2021; 41(5): 1110-1117. doi: 10.1097/IAE.0000000000002992.
9. Shirke DB et al.. Clinical study of paediatric ocular trauma and its assessment with paediatric ocular trauma score. Research Journal of Pharmacy and Technology 2023; 16(5):2359-3. doi: 10.52711/0974-360X.2023.00388
10. Rogers SL et al. Natural history of branch retinal vein occlusion: an evidence-based systematic review. Ophthalmology. 2010; 117(6): 1094-1101.e5. doi: 10.1016/j.ophtha.2010.01.058.
11. Bin Hwang H, Jee D, and Kwon JW. Characteristics of diabetic macular edema patients with serous retinal detachment. Medicine (United States), 2019; 98(51): e18333. doi: 10.1097/MD.0000000000018333.
12. Rhoades W. Management of macular edema due to central retinal vein occlusion - The role of aflibercept. Taiwan Journal of Ophthalmology. 2017; 7(2): 70–76. doi: 10.4103/tjo.tjo_9_17.
13. Shalchi Z. Anti-vascular endothelial growth factor for macular oedema secondary to branch retinal vein occlusion. Cochrane Database of Systematic Reviews. 2020; 7(7): CD009510. doi: 10.1002/14651858.CD009510.pub3.
14. Pande R. How diabetes affects your eyes. Ophthalmology Times, 2015.
15. Wang N. et al. Epidemiology of diabetic macular edema in patients with type 2 diabetes in the Beixinjing District of Shanghai. Chinese Journal. Ophthalmology. 2007; 43(7): 626-30.
16. Nassar GA. Macular vascular features of different types of diabetic macular edema using ocular coherence tomography angiography- a comparative study. International Journal of Retina and Vitreous. 2023; 9(1):1–11. doi: 10.1186/s40942-023-00469-6.
17. Zou D. Jawaid I and Amoaku WM. Retrospective analysis of treatment patterns in pseudophakic diabetic macular oedema eyes treated with anti-VEGF. Journal of Ophthalmology. 2021, 9967831. doi: 10.1155/2021/9967831.
18. Sangroongruangsri S. Comparative efficacy of bevacizumab, ranibizumab, and aflibercept for treatment of macular edema secondary to retinal vein occlusion: a systematic review and network meta-analysis. Expert Review of Clinical Pharmacology. 2018; 11(9): 903-916. doi: 10.1080/17512433.2018.1507735.
19. Singh L. Prevalence and pattern of macular edema in diabetes. Journal of Medical Science and clinical Research. 2016; 4(11): 13891-7, doi: 10.18535/jmscr/v4i11.63.
20. Lindner M. Association of periodontitis and diabetic macular edema in various stages of diabetic retinopathy. Clinical Oral Investigations. 2022; 26(1): 505–512. doi: 10.1007/s00784-021-04028-x.
21. Ichiyama Y. The effectiveness of vitrectomy for diffuse diabetic macular edema may depend on its preoperative optical coherence tomography pattern. Graefe's Archive for Clinical and Experimental Ophthalmology. 2016; 254(8): 1545-1551. doi: 10.1007/s00417-015-3251-4.
Received on 08.01.2024 Modified on 13.02.2024
Accepted on 22.03.2024 © RJPT All right reserved
Research J. Pharm. and Tech 2024; 17(3):986-990.
DOI: 10.52711/0974-360X.2024.00152