Cystoid macular oedema after cataract surgery - how is it treated?

Cystoid Macular Oedema After Cataract Surgery: Treatment and Incidence

Introduction

Cystoid macular oedema (CMO) is one of the most common causes of vision loss following cataract surgery. It occurs when fluid accumulates in the macula, leading to swelling and impaired visual function. The condition, also known as Irvine-Gass syndrome, is typically a result of post-surgical inflammation that increases vascular permeability in the macula. While most cases resolve spontaneously or with minimal intervention, persistent or severe cases may require targeted treatment. This article explores the incidence, pathophysiology, risk factors, and management of CMO after cataract surgery.

Incidence of Cystoid Macular Oedema After Cataract Surgery

The incidence of post-cataract surgery CMO varies based on factors such as diagnostic methods, patient comorbidities, and surgical techniques.

• Clinical CMO (symptomatic cases): Occurs in approximately 1-3% of cataract surgery patients.

• Subclinical CMO (detected via optical coherence tomography [OCT] but asymptomatic): Can occur in 10-30% of cases.

The incidence is higher in patients with predisposing conditions such as diabetes, uveitis, or retinal vein occlusion. Additionally, complicated surgeries (e.g., posterior capsule rupture or retained lens fragments) increase the risk of developing CMO.

Pathophysiology of CMO

CMO develops due to disruption of the blood-retinal barrier, leading to fluid accumulation in the macula. The process involves:

1. Surgical Trauma & Inflammation: Cataract surgery induces inflammation, triggering the release of inflammatory mediators such as prostaglandins and vascular endothelial growth factor (VEGF).

2. Breakdown of the Blood-Retinal Barrier: Inflammatory cytokines increase vascular permeability in the macular capillaries, allowing fluid leakage into the retinal layers.

3. Accumulation of Fluid in the Macula: The cystoid spaces seen on OCT are formed by fluid collecting within the outer plexiform and inner nuclear layers.

Risk Factors for CMO After Cataract Surgery

Several factors can increase the likelihood of developing CMO postoperatively:

Ocular Risk Factors

• Diabetic Retinopathy: Diabetic patients are at a higher risk due to pre-existing retinal vascular instability.

• Uveitis: Chronic inflammation predisposes the macula to postoperative swelling.

• Retinal Vein Occlusion: Eyes with prior venous occlusions have compromised retinal circulation.

• Epiretinal Membrane: Pre-existing macular pathology can exacerbate fluid accumulation.

• Previous Ocular Surgery: Patients with prior retinal detachment surgery or vitrectomy are at increased risk.

Surgical Risk Factors

• Complicated Surgery: Posterior capsule rupture, vitreous loss, or retained lens fragments increase inflammation.

• Use of Specific Intraocular Lenses (IOLs): Some IOLs, particularly those made of silicone, may have a slightly higher risk of CMO.

Systemic Risk Factors

• Diabetes Mellitus: Even in the absence of diabetic retinopathy, diabetes can increase susceptibility to CMO.

• Hypertension: Compromised vascular integrity may contribute to fluid leakage.

Diagnosis of CMO

CMO is diagnosed using a combination of clinical examination and imaging techniques.

1. Symptoms

• Blurred or distorted central vision

• Reduced contrast sensitivity

• Metamorphopsia (visual distortion)

• Mild visual loss (typically 20/40–20/100)

2. Clinical Examination

• Fundus examination may show thickening of the macula and cystic spaces.

• Fluorescein angiography (FA) can reveal petaloid leakage in the macula.

3. Optical Coherence Tomography (OCT)

• OCT is the gold standard for diagnosing and monitoring CMO.

• It detects retinal thickening, cystoid spaces, and subretinal fluid.

Treatment of CMO After Cataract Surgery

Most cases of CMO are self-limiting, resolving within 3–6 months. However, treatment is often required to hasten recovery and prevent permanent visual impairment.

1. First-Line Treatment: Anti-Inflammatory Therapy

The mainstay of treatment includes nonsteroidal anti-inflammatory drugs (NSAIDs) and corticosteroids.

• Topical NSAIDs

• Commonly used agents include ketorolac, bromfenac, nepafenac, and diclofenac.

• NSAIDs reduce prostaglandin-mediated inflammation and prevent fluid leakage.

• Typically used for 6–12 weeks.

• Topical Corticosteroids

• Prednisolone acetate 1%, dexamethasone, or loteprednol may be used.

• Steroids act by inhibiting inflammatory cytokines, reducing vascular permeability.

• Often used in combination with NSAIDs for better efficacy.

• Combination Therapy (NSAID + Steroid)

• Studies suggest that using both NSAIDs and corticosteroids reduces CMO recurrence and speeds up resolution.

2. Second-Line Treatment: Intravitreal Therapy

If topical therapy fails, intravitreal injections may be needed:

• Intravitreal Corticosteroids

• Triamcinolone acetonide (4 mg/0.1 mL) can be injected into the vitreous cavity.

• Used in refractory CMO cases or when systemic absorption of topical steroids is inadequate.

• Intravitreal Anti-VEGF Therapy

• Ranibizumab (Lucentis) or Aflibercept (Eylea) can reduce macular swelling in persistent cases.

• VEGF inhibitors are particularly useful in diabetic patients or those with retinal vein occlusion.

3. Systemic Therapy

• Oral Carbonic Anhydrase Inhibitors (CAIs)

• Acetazolamide (250 mg BD or TDS) can reduce macular oedema by enhancing fluid transport out of the retina.

• Used in refractory cases.

• Oral Corticosteroids

• Used in severe inflammation or when other treatments fail.

4. Surgical Intervention (Rare Cases)

• Pars Plana Vitrectomy (PPV)

• Considered in chronic, refractory CMO cases.

• Removes vitreous traction contributing to macular oedema.

• Posterior Sub-Tenon’s Steroid Injection

• Used for localized drug delivery in resistant cases.

Prevention of CMO After Cataract Surgery

Preventative strategies include:

1. Preoperative NSAID Use

• Initiating NSAIDs 1–3 days before surgery can reduce postoperative CMO risk.

2. Combination Therapy (NSAID + Steroid) Postoperatively

• Using both for 4–6 weeks after surgery improves outcomes.

3. Meticulous Surgical Technique

• Avoiding complications, such as posterior capsule rupture, reduces inflammation.

4. Managing Systemic Risk Factors

• Optimizing diabetes and hypertension control preoperatively lowers CMO incidence.

Conclusion

Cystoid macular oedema is a well-recognized complication following cataract surgery, though it is typically self-limiting and responsive to treatment. Most cases are managed effectively with topical NSAIDs and corticosteroids, while refractory cases may require intravitreal injections or systemic therapy. With early diagnosis and prompt intervention, the prognosis is generally good, and permanent vision loss is rare. Preventative measures, including preoperative NSAID use and careful surgical techniques, can further reduce the incidence of CMO in at-risk patients.