Macular edema: causes, symptoms, diagnosis, and modern treatment methods

Macular edema is not a specific condition, but a syndrome in which fluid accumulates in the macula. The macula is the central area of the retina responsible for sharp central vision, reading, facial recognition, and distinguishing fine details. When blood vessels in this area begin to leak fluid or the barrier between the blood and retinal tissue is compromised, the macula thickens, and images become blurred, distorted, or "wavy." [1]

Clinically, macular edema is most often associated with diabetic retinopathy, retinal vein occlusion, intraocular inflammation, neovascular age-related macular degeneration, the consequences of eye surgery, and a number of medications. Therefore, when edema is detected, it is important for the physician not only to confirm macular thickening but also to establish the underlying cause, as treatment strategies for diabetes, surgery, and inflammation will differ. [2]

The main complaints associated with this condition include blurred central vision, distortion of straight lines, fading colors, difficulty reading, and decreased contrast sensitivity. In some cases, the process develops gradually and remains undetected for a long time, especially if only one eye is affected. However, prolonged swelling increases the risk of permanent damage to the photoreceptors and irreversible vision loss, so an examination should be considered immediately. [3]

The following article is based on current guidelines, clinical recommendations, and official registration documents. Particular emphasis is placed on the causes, step-by-step diagnostics, modern injection regimens, the role of corticosteroid implants, laser treatment, and surgery. [4]

Table 1. Brief clinical guidelines for macular edema. The summary is based on materials from the US National Eye Institute and the StatPearls review. [5]

Parameter	What is important to know
What is this	Fluid accumulation in the macula with thickening of the central retina
Main complaints	Fogging, distorted lines, dull colors, central spot
Common causes	Diabetes, retinal vein occlusion, uveitis, surgery, neovascular macular degeneration
The main method of confirmation	Optical coherence tomography
Additional methods	Examination with pupil dilation, fluorescein angiography, Amsler grid
Basic treatment options	Injections, laser, drops, vitrectomy, therapy causes

Code according to ICD-10 and ICD-11

There's an important practical nuance to coding macular edema: in modern classifications, it's often coded not only as "retinal edema" but also as a manifestation of the specific disease that caused it. Therefore, two patients with identical optical coherence tomography findings may have different codes if one has diabetes, while the other has retinal vein occlusion or postoperative inflammation. [6]

The International Classification of Diseases, 10th Revision, code H35.81 for "retinal edema" is widely used in clinical documentation. In the International Classification of Diseases, 11th Revision, one of the most clearly defined variants is diabetic macular edema (9B71.02) as a subsection of diabetic retinopathy, although the system also requires an additional code for the type of diabetes mellitus. This underscores the modern approach: coding not only the edema but also its cause. [7]

Table 2. Practically used codes. The table reflects the principle of etiological coding, confirmed by classification resources. [8]

Situation	Code
International Classification of Diseases, 10th revision, general retinal edema	H35.81
International Classification of Diseases, 11th revision, diabetic retinopathy	9B71.0
International Classification of Diseases, 11th revision, diabetic macular edema	9B71.02
An important rule of the International Classification of Diseases, 11th revision	Additionally, the type of diabetes mellitus is coded.

Epidemiology

From an epidemiological perspective, macular edema is one of the key causes of central vision loss in working-age adults, particularly in diabetic retinopathy. In a large meta-analysis by the American Academy of Ophthalmology, the global prevalence of clinically significant macular edema among people with diabetes was 4.07%, corresponding to an estimated 18.83 million adults worldwide in 2020; by 2045, this number is projected to increase to 28.61 million. [9]

Looking beyond the general population, specifically at patients with diabetes, the risk increases with the duration of the disease and the severity of retinopathy. Reviews indicate that the incidence of diabetic macular edema increases with the duration of diabetes, and with advanced retinopathy, the likelihood of macular involvement becomes significantly higher. This makes regular ophthalmological screening a mandatory part of diabetes management, even when there are no symptoms yet. [10]

Another major group of cases is associated with retinal vein occlusion. Current guidelines consider macular edema to be the primary cause of vision loss in this vascular disorder, and the American Academy of Ophthalmology explicitly lists vascular endothelial growth factor-blocking agents as the first-line treatment for this condition. Broader epidemiological reviews describe retinal vein occlusion as one of the most common retinal vascular diseases worldwide. [11]

Postoperative cystoid macular edema remains a significant cause of visual impairment after cataract surgery. A 2025 meta-analysis estimated the overall incidence after uncomplicated surgery to be approximately 5%, although the risk is significantly higher in patients with diabetes, uveitis, epiretinal membrane, retinal vein occlusion, and complicated surgery. [12]

In uveitis, the incidence of macular edema depends on the anatomical type of inflammation. In a 2024 study, macular edema was detected significantly more frequently in patients with intermediate, posterior, and panuveitis than in those with anterior uveitis, explaining why macular monitoring with optical coherence tomography is necessary even for moderate complaints in inflammatory eye diseases. [13]

Table 3. Key epidemiological benchmarks. Values are based on major reviews and guidelines. [14]

Indicator	Landmark
Clinically significant macular edema among people with diabetes worldwide	4.07%
Estimated number of adults with clinically significant macular edema in 2020	18.83 million
Projected number of adults with clinically significant macular edema by 2045	28.61 million
Postoperative cystoid macular edema after uncomplicated cataract surgery	about 5%
Uveitic macular edema is more common in intermediate, posterior uveitis and panuveitis.	Yes

Reasons

The underlying pathogenetic principle is the same for most causes: vessels or adjacent tissues cease to retain fluid within the vascular bed, and it leaks into the retina. However, the pathway to this disorder varies. In diabetes, chronic microvascular damage predominates; in venous occlusion, venous congestion and ischemia; in uveitis, inflammation; after surgery, an inflammatory response and mediator release; and in neovascular macular degeneration, the growth of pathological vessels. [15]

The most common cause in everyday practice is diabetic retinopathy. Chronic hyperglycemia damages small retinal vessels, increases their permeability, and triggers plasma leakage into the macular region. The poorer the diabetes compensation and the longer the disease lasts, the higher the likelihood of macular involvement. [16]

The second major group of causes is retinal vein occlusion, both central and branch forms. When venous outflow is blocked, hydrostatic pressure increases, ischemia develops, the blood-retinal barrier is disrupted, and fluid begins to permeate the macula. This is why patients with sudden blurred vision due to vascular occlusion require urgent macular evaluation. [17]

The key non-vascular causes remain uveitis, post -cataract surgery, vitreomacular traction, epiretinal membrane, certain drug-induced conditions, and neovascular macular degeneration. The US National Eye Institute also specifically notes retinitis pigmentosa and drug-induced forms, including those associated with certain antiglaucoma medications. [18]

In practical terms, it's important for the physician to always answer two questions: "Why did the swelling occur?" and "Are there simultaneous ischemia, inflammation, or mechanical traction?" This influences the choice between injections of drugs that block vascular endothelial growth factor, corticosteroid therapy, laser treatment, and surgery. There is no universal treatment plan for all patients. [19]

Risk factors

The main risk factors for diabetic macular edema are long-term diabetes mellitus, poor glycemic control, severe diabetic retinopathy, hypertension, dyslipidemia, and chronic kidney disease. Recent studies have reaffirmed the link with renal impairment: the risk of diabetic macular edema is higher with more severe renal impairment. [20]

The American Diabetes Association's 2025 standards emphasize that ophthalmological examinations should be performed more frequently in patients with progressive retinopathy, diabetic macular edema, and failure to meet glycemic targets. This indirectly reflects not only the importance of early detection but also the role of systemic risk factors in worsening ocular prognosis. [21]

For retinal vein occlusions, the risk is increased by age, hypertension, atherosclerotic changes, diabetes, and other vascular factors. For postoperative cystoid macular edema, diabetes mellitus, uveitis, a history of retinal vein occlusion, epiretinal membrane, posterior capsule rupture, vitreous loss, and a more traumatic surgical procedure are important. [22]

In uveitis, the likelihood of macular edema is particularly increased by intermediate and posterior inflammation, as well as panuveitis. For tractional forms, the state of the vitreomacular interface, the presence of an epiretinal membrane, and incomplete posterior vitreous detachment are important. [23]

From a practical standpoint, the mere fact of having diabetes shouldn't be reassuring. If a person already has retinopathy, hypertension, impaired kidney function, or has had eye surgery, the risk of edema becomes significantly higher, and this requires active monitoring of the retina rather than waiting for symptoms. [24]

Table 4. Main causes and risk factors. Summary based on official reviews and clinical guidelines. [25]

Category	The most important positions
Common causes	Diabetic retinopathy, retinal vein occlusion, uveitis, postoperative inflammation
Additional reasons	Neovascular macular degeneration, vitreomacular traction, epiretinal membrane, drugs
Systemic risk factors	Long-term diabetes, high blood glucose, hypertension, dyslipidemia, chronic kidney disease
Ocular risk factors	Uveitis, retinal vein occlusion, previous surgery, epiretinal membrane
Postoperative risk factors	Posterior capsule rupture, vitreous loss, more traumatic surgery

Pathogenesis

Normally, the retina maintains a delicate balance between fluid intake and removal. This balance is maintained by tight junctions between the vascular endothelium, the retinal pigment epithelium, Müller cells, and other fluid transport mechanisms. When the blood-retinal barrier is damaged, proteins and solutes leak into the retinal tissue, osmotic pressure changes, and fluid retention in the macular region begins. [26]

In diabetes, the process develops against a background of thickening of the capillary basement membrane, loss of pericytes, increased vascular permeability, and tissue hypoxia. In response, the production of vascular endothelial growth factor and inflammatory mediators increases, further disrupting the barrier and maintaining chronic edema. This is why drugs that block vascular endothelial growth factor, and in some patients, corticosteroids, are so effective in the diabetic variant of the disease. [27]

In retinal vein occlusion, venous congestion, increased macular capillary pressure, and ischemia become the primary causes. These processes increase fluid leakage, and in ischemic forms, damage to photoreceptors and inner retinal layers develops more rapidly than in non-ischemic forms. Therefore, two patients with the same macular thickness may have different functional prognoses. [28]

In inflammatory and postoperative forms, prostaglandins, cytokines, and other inflammatory mediators play a key role. They make blood vessels more permeable and sometimes simultaneously impair pigment epithelium function and fluid drainage. If traction from the vitreous body or epiretinal membrane is added to the biochemical mechanism, the swelling becomes more persistent and may require surgical intervention. [29]

Symptoms

The most typical symptoms include blurred central vision, a gradual loss of clarity, distortion of straight lines, and a sensation that objects are "floating" or appearing wavy. In some patients, colors become less saturated, and some objects appear different sizes when viewed alternately with each eye. [30]

An important feature of macular edema is that peripheral vision can remain relatively intact for a long time. Therefore, a person often says they can "see generally," but they have difficulty reading, working with small print, recognizing faces, and driving in low-contrast conditions. If only one eye is affected, the other eye partially compensates for the problem, and seeking medical attention is delayed. [31]

If swelling develops rapidly, especially with retinal vein occlusion or active inflammation, visual impairment may be noticeable within hours or days. In the diabetic variant, the progression is often more gradual, although even here, a fairly rapid worsening of symptoms is sometimes observed. The absence of pain does not rule out serious damage to the macular area. [32]

With prolonged or recurrent edema, more persistent signs of functional impairment appear: decreased contrast sensitivity, a central spot, difficulty reading even with glasses, and poor perception of fine details. This indirectly indicates that the process has been going on for some time and requires not only prompt treatment but also an assessment of the prognosis using optical coherence tomography data. [33]

Table 5. Most common patient complaints. Guidelines based on data from the US National Eye Institute. [34]

Symptom	How does it feel?
Blurred central vision	text and faces become blurry
Metamorphopsia	straight lines appear wavy
Resizing objects	One eye sees an object differently than the other.
Fading of colors	the colors appear paler
Central spot	part of the image in the center "falls out"

Classification, forms and stages

Macular edema can be classified by cause, anatomical presentation, and the degree of involvement of the center of the macula. The following are categorized by cause: diabetic, post-occlusion, uveitic, post-surgical, neovascular, tractional, and drug-induced. From a practical standpoint, the etiologic classification is most important because it determines treatment. [35]

Optical coherence tomography data often reveals several morphological patterns: diffuse retinal thickening, a cystic variant with intraretinal cavities, the presence of subretinal fluid, and a traction component. Modern reviews emphasize that such patterns are not always distinct diseases, but they help to understand the underlying mechanism and predict treatment response. [36]

For diabetic macular edema, the concept of focal involvement is used separately. If the edema affects the foveal center, the risk of functional decline is higher, and these forms are more often the indication for active injection therapy. Guidelines also retain the distinction between focal and diffuse edema, although today, optical coherence tomography data and visual acuity play a decisive role in decision-making, rather than the old angiographic description. [37]

For retinal vein occlusion, assessing the ischemic and non-ischemic variants is crucial. The ischemic form is typically associated with a worse prognosis, a higher likelihood of irreversible functional impairment, and a higher risk of neovascular complications. Therefore, these patients typically require more intensive monitoring and examination. [38]

Table 6. Simplified clinical classification. The table combines the etiological and morphological approaches. [39]

Classification principle	Options
Because of	Diabetic, postocclusive, uveitic, postoperative, neovascular, traction, medicinal
According to optical coherence tomography data	Diffuse thickening, cystic variant, subretinal fluid, traction component
On the involvement of the center	With or without central involvement
According to the vascular profile in retinal vein occlusion	Ischemic, non-ischemic
With the flow	Acute, chronic, recurrent, persistent

Complications and consequences

The main complication is persistent loss of central vision. If fluid persists for a long time, the retinal architecture is disrupted, photoreceptors are damaged, the ellipsoid zone is destroyed, and even with anatomical reduction in macular thickness, vision restoration may be incomplete. Therefore, the severity of the edema and its duration are equally important. [40]

Certain causes carry additional risks. Retinal vein occlusion can lead to macular ischemia and neovascular complications. Diabetic retinopathy can also lead to progression of the underlying diabetic retinal disease. Inflammatory forms can lead to relapses due to recurrent uveitis. After cataract surgery, swelling regresses in some patients, but in high-risk groups, it can become persistent. [41]

The treatment itself can also cause complications. Intravitreal injections are associated with the risk of endophthalmitis, retinal detachment, retinal vasculitis, and a short-term increase in intraocular pressure, while corticosteroid implants further increase the risk of cataracts, glaucoma, and secondary infections. These risks do not negate the need for treatment, but they require careful patient selection and regular monitoring. [42]

When to see a doctor

You should consult an ophthalmologist as soon as possible if you experience any new blurring of central vision, the appearance of wavy lines, a sudden deterioration in reading, a sensation of a central spot, or color fading. Even if symptoms are mild and there is no pain, macular edema may already be reducing macular function and require injection treatment. [43]

People with diabetes, those with vision loss in at least one eye, those who have undergone cataract surgery, and those with a history of retinal vein occlusion or uveitis require a particularly urgent consultation. These groups are at higher risk for clinically significant edema, and early optical coherence tomography can make a real difference in management. [44]

If visual impairment occurs after an injection into the eye and is accompanied by pain, severe redness, photophobia, or rapidly increasing fog, this is a reason for an immediate re-examination. Official instructions for intravitreal medications specifically require immediate reporting of symptoms suspected of endophthalmitis or retinal detachment. [45]

Diagnostics

The basis for diagnosis remains a comprehensive fundus examination. First, the doctor assesses the patient's symptoms, measures visual acuity, performs biomicroscopy, dilates the pupil, and examines the retina. Even at this stage, macular thickening, hard exudates, hemorrhages, signs of inflammation, or vascular occlusion can be suspected. [46]

The primary confirmatory method today is optical coherence tomography. It allows for layer-by-layer visualization of the macular thickness, the presence of cystic cavities, subretinal fluid, traction, and epiretinal membrane, and a quantitative assessment of the response to treatment. Due to its high reproducibility, this method is considered the preferred method for diagnosing and monitoring edema. [47]

Fluorescein angiography is not necessary for everyone, but it remains crucial when it comes to understanding the source of a leak, distinguishing focal from diffuse processes, and assessing macular ischemia, peripheral nonperfusion, and inflammatory activity. This method is particularly useful for retinal vein occlusion, uveitis, and complex mixed cases where optical coherence tomography alone is insufficient. [48]

The Amsler grid is a simple aid for identifying central distortions and dynamic self-monitoring. It does not replace retinal imaging, but it helps document functional changes between visits, especially if the process is chronic or bilateral. [49]

Laboratory tests do not confirm macular edema itself, but are important for identifying the cause and risk factors. In diabetic cases, glycemic control and often renal function are assessed. In uveitis, the scope of testing depends on the suspected nature of the inflammation and is tailored individually. In other words, tests help understand the "why," not just "whether" there is edema. [50]

In complex cases, optical coherence tomography-angiography and wide-field imaging are additionally used, particularly if macular perfusion, peripheral ischemia, or vasculitis need to be assessed. However, for most patients, the starting point remains a clinical examination, optical coherence tomography, and, if indicated, fluorescein angiography. [51]

Table 7. Step-by-step diagnostics. The examination procedure reflects modern clinical practice. [52]

Step	What are they doing?	For what
1	Collection of complaints and visual acuity testing	understand the severity of the functional deficit
2	Examination with pupil dilation	see hemorrhages, exudates, signs of inflammation and vascular changes
3	Optical coherence tomography	confirm edema, measure thickness, see fluid type and traction
4	Fluorescein angiography as indicated	find the source of the leak, ischemia, nonperfusion, vasculitis
5	Tests by cause	assess diabetes, kidneys, and inflammatory background
6	Dynamic control	compare macular thickness and vision during treatment

Differential diagnosis

Differential diagnosis begins with determining whether the diagnosis is actually macular edema and not another macular condition. Optical coherence tomography must distinguish true fluid accumulation from foveoschisis, macular hole, severe epiretinal membrane, central serous chorioretinopathy, and the consequences of degenerative processes. Sometimes the structures appear similar, but the mechanisms are fundamentally different. [53]

Next, a distinction is made based on the cause. If microaneurysms, hard exudates, and other diabetic retinopathy are visible, the diabetic variant is most likely. If hemorrhages along the veins and venous dilation are predominant, retinal vein occlusion is considered. If there are cells in the vitreous, signs of chorioretinal inflammation, or vasculitis, uveitic edema is considered. If complaints arise after cataract surgery, a postoperative cystic form comes to the fore. [54]

Fluorescein angiography is particularly useful for distinguishing cystic edema with active leakage from conditions where fluid changes are present on imaging but classic leakage is absent. StatPearls specifically notes that the absence of typical angiographic leakage is possible in some inherited retinal diseases, foveoschisis, and drug-induced lesions. This helps avoid diagnostic error and inappropriate treatment. [55]

The vitreomacular interface is assessed separately. If a patient has significant traction or an epiretinal membrane, even a good anatomical response to injections may be incomplete until the mechanical component is addressed. Therefore, differential diagnosis involves not only identifying the underlying disease but also identifying the underlying mechanics of the process. [56]

Treatment

The first principle of treatment is to treat not only the swelling but also the underlying condition. In the diabetic form, glycemic, blood pressure, and lipid control are essential; in uveitis, inflammation suppression; in retinal vein occlusion, management of vascular risk factors; and in the postoperative form, anti-inflammatory therapy. Without addressing the underlying cause, even technically successful local treatment of the macula can only provide temporary relief. [57]

Vascular endothelial growth factor-blocking drugs remain the mainstay of treatment for many patients. The US National Eye Institute notes that such injections can slow or reverse the progression of macular edema, and the American Academy of Ophthalmology guidelines consider them first-line treatment for macular edema associated with retinal vein occlusion. For diabetic macular edema, these drugs also occupy a central place in current algorithms. [58]

Modern regimens have become more flexible. For faricimab, the official instructions allow for two strategies for diabetic macular edema: initial monthly injections followed by an extended interval depending on macular thickness and vision, or a fixed transition to an 8-week interval after the loading phase. This is important because some patients can reduce the frequency of visits without losing edema control. [59]

For aflibercept 8 milligrams, the official 2025 instructions for diabetic macular edema call for 3 monthly starting injections, then transitioning to 8-16 week intervals. For macular edema following retinal vein occlusion, the same formulation allows for a transition to once every 8 weeks after 3-5 monthly injections. This is no longer simply "monthly therapy," but a more personalized regimen based on the patient's response. [60]

Corticosteroid therapy is particularly important when the inflammatory component is pronounced, when the response to vascular endothelial growth factor-blocking drugs is insufficient, or when such drugs are not suitable for the patient. The UK National Institute of Health specifically recommends dexamethasone intravitreal implant for diabetic macular edema when the condition has not responded adequately to non-corticosteroid therapy or such therapy is not possible. [61]

For chronic diabetic macular edema that is poorly responsive to available treatments, the UK National Institutes of Health also recommends a fluocinolone intravitreal implant. The 2024 update emphasizes that this implant lasts longer than dexamethasone, potentially requiring less frequent replacement. This is especially important for patients with persistent macular edema and the high burden of frequent eye examinations. [62]

However, corticosteroids have well-known limitations. Official instructions for the dexamethasone implant warn of the risk of posterior subcapsular cataracts, increased intraocular pressure, glaucoma, and secondary infections. Therefore, for phakic patients, for patients with glaucoma, and for people who have difficulty tolerating increased intraocular pressure, the choice of this treatment requires particularly careful consideration. [63]

Laser treatment today often plays a supportive role. The US National Eye Institute notes that certain types of laser can be used for macular edema associated with diabetes or retinal vein occlusion, particularly if injections have failed or when additional leak control is required. Compared to the early research era, the role of laser has become more selective, but it has not disappeared from practice. [64]

Postoperative cystoid macular edema is often treated with topical anti-inflammatory drops. The National Eye Institute recommends using nonsteroidal anti-inflammatory drops alone or in combination with steroid drops, specifically in surgically associated forms. If topical therapy is insufficient, injections or concomitant traction may be required. [65]

Surgical treatment primarily consists of vitrectomy. It is considered when other methods have failed or when there is a significant vitreomacular traction component, epiretinal membrane, chronic persistent edema, or the need to install a system for more convenient long-term drug delivery. Vitrectomy is not a first-line treatment for most patients, but in properly selected cases, it offers the best chance of eliminating the mechanical cause of edema. [66]

Among the new methods, a continuous delivery system for ranibizumab via an implant is worth noting. In 2025, the US Food and Drug Administration approved this system for diabetic macular edema in patients who had previously responded to at least two intravitreal injections of a vascular endothelial growth factor inhibitor. This is not a universal option for everyone, but it is an important approach for patients who have difficulty maintaining a frequent injection schedule. [67]

Prevention

The best prevention of macular edema is not to wait for vision loss, but to proactively address the underlying causes. For people with diabetes, this means maintaining blood glucose levels within the target range, treating hypertension, correcting lipid imbalances, and having regular fundus examinations. The 2025 standards emphasize that screening allows for intervention before irreversible vision loss occurs. [68]

The National Eye Institute clearly states that in diabetic retinopathy, diabetes management helps prevent or delay vision loss, and that a comprehensive eye examination is necessary at least once a year. If retinopathy has already progressed or macular edema is confirmed, examinations should be more frequent. [69]

For patients undergoing cataract surgery, prevention includes a thorough assessment of risk factors before surgery and a rational anti-inflammatory regimen afterward. Particularly careful monitoring is required in patients with diabetes, uveitis, epiretinal membrane, and complications following surgery. [70]

For all groups, the behavioral component is also important: adherence to the injection schedule, follow-up examinations, and macular imaging. Inconsistent treatment is one of the common reasons why edema is only partially reduced anatomically or quickly returns after improvement. [71]

Forecast

The prognosis for macular edema depends on the cause, duration of the process, degree of ischemia, the state of the photoreceptor layers on optical coherence tomography, and the frequency of treatment. In general, early detection and timely initiation of treatment improve the chances of preserving central vision, while chronic and recurrent processes often leave functional deficits. [72]

In the diabetic variant, the prognosis is closely linked to the quality of systemic control and the response to injection therapy. Even good modern medications cannot fully compensate for prolonged, uncontrolled hyperglycemia and ongoing microvascular damage. Therefore, the ophthalmological prognosis here is always linked to the overall management of diabetes. [73]

In retinal vein occlusion, ischemia is considered a separate adverse factor. Both old and new data demonstrate that ischemic forms produce worse visual outcomes than non-ischemic forms, even if macular thickness can be reduced. This is due not only to fluid but also to impaired macular tissue perfusion. [74]

Postoperative and inflammatory forms often have a good prognosis with early recognition and proper treatment, but they can recur if the inflammatory background persists or the traction component is missed. Therefore, prognosis is not determined by a single visit or a single image, but by the results of consistent, dynamic observation. [75]

Table 8. Factors that influence vision prognosis. Summary based on reviews and guidelines. [76]

Factor	Impact on prognosis
Early initiation of treatment	improves the chances of preserving vision
Chronic long-term edema	impairs functional recovery
Macular ischemia	unfavorable sign
Good systemic control in diabetes	improves long-term outcome
Traction and epiretinal membrane	may worsen the response to injections
Compliance with the treatment schedule	critical for a lasting effect

FAQ

Can macular edema resolve on its own?
Sometimes mild cases do improve postoperatively, but spontaneous resolution is unthinkable. In diabetic, vascular, and inflammatory cases, waiting is dangerous, as prolonged fluid retention increases the risk of irreversible damage to the macula. [77]

Does macular edema always indicate diabetes?
No. Diabetes is the most common cause, but not the only one. Edema also occurs with retinal vein occlusion, uveitis, neovascular macular degeneration, after cataract surgery, with traction, and under the influence of certain medications. [78]

What test best identifies macular edema?
Optical coherence tomography is considered the best method for confirmation and monitoring. It shows macular thickness, the presence of cysts, subretinal fluid, and traction. Fluorescein angiography complements it when it is necessary to understand the source of the leak and the degree of ischemia. [79]

Are eye injections painful?
The procedure is performed under aseptic conditions with anesthesia of the ocular surface, so there is usually no significant pain, but short-term pressure or discomfort is possible. It is important to monitor for warning signs after the procedure, as rare but serious complications are still possible. [80]

Which is better – injections or laser?
It depends on the cause. For most clinically significant forms, injection therapy is now preferred, especially for diabetic and post-occlusive cases. Laser remains valuable as an adjunctive or selective method. [81]

When is a corticosteroid implant prescribed?
Most often, when the response to non-corticosteroid therapy is insufficient, when it is not suitable for the patient, or when there is a pronounced inflammatory component. For chronic diabetic macular edema, there are separate recommendations for the fluocinolone implant. [82]

Is it possible to fully restore vision?
Sometimes yes, especially if the edema is detected early and hasn't damaged the photoreceptors. However, in chronic cases, with ischemia and relapses, only partial restoration is possible, even if the macular thickness decreases. [83]

Is follow-up necessary if things improve?
Absolutely. Improved vision and reduced macular thickness do not mean the disease is completely cured. In diabetes, uveitis, and retinal vein occlusion, edema can recur, so dynamic monitoring remains part of treatment. [84]

Key points from experts

Below is a summary of key points from current guidelines from the American Academy of Ophthalmology and the UK National Institutes of Health, authored by Jennifer I. Lim, chief of retina services and vice chair for diversity and inclusion at the University of Illinois at Chicago; Jaclyn L. Kovach, ophthalmologist, Bascom Palmer Eye Institute, University of Miami Miller School of Medicine; and Christina J. Flaxel, Casey Eye Institute, Oregon Health and Science University. [85]

Jennifer I. Lim: In diabetic macular disease, the key is not a single injection, but a consistent monitoring strategy that assesses macular thickness, vision, and systemic risk factors. Otherwise, even an effective drug will not provide sustainable functional results. [86]

Jaclyn L. Kovach: Intravitreal vascular endothelial growth factor blocking agents should be considered as first-line treatment for retinal vein occlusion-associated macular edema because they are the basis of current treatment guidelines. [87]

Christina J. Flaxel: Early detection of retinopathy and macular edema through extensive examination and validated imaging remains the mainstay of preventing irreversible vision loss. The earlier macular edema is diagnosed, the greater the chance of preserving functional vision. [88]

The overall conclusion of expert groups is that modern treatment regimens have become more personalized. Today, physicians choose not simply "injection or laser," but a combination of etiologic therapy, monitoring regimen, type of injectable, the need for a corticosteroid implant, and, if necessary, surgery. [89]