Fundamentals of medical and surgical retina for cataract and refractive surgeons
Cataract extraction is one of the most commonly performed surgeries. Over the last years, it has benefited from consistent innovation in instrumentation, lens design and surgical technique that lead to improved outcomes following cataract surgery1. Phacoemulsification using small incision and implantation of a foldable intraocular lens (IOL) is currently the preferred technique among cataract surgeons. The procedure is efficient, and uneventful surgery is generally associated with good visual results. Nevertheless, cystoid macular edema (CME) may develop and can result in suboptimal postoperative vision. It can occur after uncomplicated surgery in patients with otherwise healthy eyes, after complicated surgery, or after surgery in patients with ocular diseases such uveitis or diabetic retinopathy2.
The specific etiology of aphakic and pseudophakic macular edema is not fully understood. Many factors are thought to contribute to its development such as the type of cataract surgery, light toxicity, vitreomacular traction, inflammatory mediators, and adrenergic drugs. Experimental and clinical evidence implicates inflammation mediated by prostaglandins. Prostaglandins released from the anterior segment of the eye that diffuse to the vitreous cavity and retina, stimulating the breakdown of the blood-ocular barrier (BRB) and subsequent leakage of fluids across the retinal vessel wall and through RPE into perifoveal retinal tissues resulting in macular edema3.
The inflammatory mediators play probably the essential initiating role in the development of inflammatory CME, but the exact factors and events responsible for further CME development and its chronicity have not yet been identified.
Though the rate of CME has been declining with decreasing surgical incision and use of microsurgical instrumentation, the high volume of cataract surgeries performed yearly makes this a common cause of poor vision in pseudophakic patients 4.
Determining the overall incidence of CME has been difficult because of variations in the patient populations evaluated (with varying risk factors) and the use of different methods for evaluating macular thickening. The risk factors most associated with CME are iris trauma, rupture of posterior capsule, vitreous loss or incarceration, dislocated IOL, use of iris fixed lenses, active uveitis and diabetes 2.
The diagnosis of CME can generally be made on clinical examination with evidence of perifoveal cystic spaces and can be confirmed with use of fluorescein angiography (FA) to document the classic petaloid pattern of leakage induced by inflammatory mediators that can lead to breakdown of the BRB.
Angiographic CME is diagnosed in patients who are otherwise asymptomatic with respect to visual acuity, but have detectable leakage from perifoveal capillaries on FA demonstrated by hyperfluorescence in the central macula and optic disc. Clinical CME is diagnosed in those patients who have detectable visual impairment as well as angiographic and/or biomicroscopic findings 4, 5 The actual incidence of clinical CME using modern techniques is likely in the range of 0.2 to 2% and the rate of angiographic CME is at least ten-fold higher in magnitude4.
Vitreous fluorometry, a more sensitive technique of measuring alterations in the BRB using fluorescein, shows an even higher incidence of alteration in the period immediately after cataract surgery. The Retinal Leakage Analyzer (RLA) and the Optical Coherence Tomography (OCT) are methodologies that can be used to objectively measure the disruption of the blood-retinal barrier and the increase in retinal thickness, respectively, leading to a quantitative evaluation of the macular edema 6. Although the FA is considered the diagnosis gold standard concerning the CME, the OCT, as a non-invasive technique, is now widely used in evaluation and follow-up 7.
Signs and symptoms of macular thickening typically develop four to six weeks postoperatively, resulting in temporary vision loss, responds to treatment with topical anti-inflammatory medications and usually resolves within 6 months. However, some cases respond poorly to conservative treatment, persist for more than six months and may develop permanent visual loss. Although the incidence of chronic CME is much less frequent, being reported at 1% to 2% of uncomplicated cases and about 8% after complicated cataract surgery, the associated vision loss makes it a serious complication.
Prophylaxis and Treatment:
Although the treatment options depend on the underlying cause of CME, the usually therapeutic approach as a prophylaxis and treatment of CME is directed towards blocking the inflammatory mediators, mainly the prostaglandins in the anterior segment of the eye, using topical steroids and non-steroidal anti-inflammatory drugs (NSAIDs). Corticosteroids are effective but they can cause an increase in intraocular pressure (IOP) in a small percentage of patients. Usually the medical treatment of uncomplicated cases can include first NSAIDs and in some cases addition of topical steroids. Clinical evidence suggests that combined use of NSAIDs and steroids is synergistic.
In patients with evidence of anterior segment inflammation or in those with chronic CME following posterior capsule trauma the steroids show to be effective and a stepwise plan may be undertaken starting with topical administration, followed by local injection, reserving high dose intravitreous for severe refractory cases. It can reduce macular edema and improve vision in eyes with CME that persists or recurs despite previous medical treatment. However, CME may recur in some cases even after more than one intravitreal injection of triamcinolone.
Carbonic anhydrase inhibitor – acetazolamide may help reduce the edematous component. It has the ability to stimulate the retinal pigment epithelium (RPE) to pump excess fluid out of the macula. In some specific cases of chronic CME, the vitrectomy appears also to be effective.
The actual guidelines for managing post-cataract surgery inflammation consider that the prevention of inflammation is the main goal, including a good patient selection, a correct preparation, a surgery taking care not to cause iris trauma, solving intraoperative complications, and treating post-operative inflammation 8.
It should be noted that diabetic patients with pre-surgical macular edema have a higher risk of worsening the macular edema after cataract surgery. Therefore, in these cases, it is useful the use of intravitreal triamcinolone (4mg) injected at the end of cataract surgery.