Management of macular oedema in diabetic patients undergoing cataract surgery

Curr Opin Ophthalmol 2017, 28:23–28

In diabetic eyes, two different entities

1. a worsening of a preexisting DME : natural course is much more severe, with a tendency to progression
2. PME (Irvine Gass) onset – postsurgical : relatively benign natural history, with a peak incidence after 6 weeks and spontaneous resolution within 6 months in up to 68% of eyes

The medical history, the presence of signs of diabetic retinopathy, and particular features on fluorescein angiography (disc hyper-fluorescence), although revealing, are not always conclusive.

PREVENTION OF POSTSURGICAL MACULAR OEDEMA IN PATIENTS WITH DIABETES AND NO PREEXISTING DIABETIC MACULAR OEDEMA

1. Topical NSAIDs, administered twice or three times daily for several weeks after surgery, represent nowadays the most effective approach to prevent pseudophakic macular oedema (PME). NSAIDs inhibit the cyclo-oxygenase 2 pathway in the arachidonate cascade that leads to the production of
   prostaglandins and, consequently, to macular oedema
   1. Singh et al.  evaluated the efficacy of nepafenac ophthalmic suspension 0.1% [Nevanac; Alcon Laboratories (UK)] in 263 eyes of diabetic
      patients with no history of DME. These authors found a significantly lower incidence of macular oedema in the nepafenac group versus the control
      group treated with vehicle (3.2 versus 16.7%;P¼0.001)
   2. administered alone (Bromfenac sodium) or in combination with topical steroids (ketorolac tromethamine 0.4% and Dexamethasone 0.1%)
      , has been compared with topical steroid monotherapy. In both cases, topical NSAIDs appeared to be superior to topical steroids in terms of incidence of PME, postoperative anterior segment inflammation, and mean central foveal thickness (CFT) at the end of follow-up
   3. nonserious ocular adverse events: tworeports of punctate keratitis and a single report of  corneal epithelium defect.
2. anti-VEGF agents (Ranibizumab or Bevacizumab) administered intravitreally at the moment of cataract extraction.
   1. the CSME incidence at month 1 (25.9%) and at month 3 (22.2%) in the control group was significantly higher than that reported in the treated group at the same time of follow-up (3.7%)  Udaondo P, Garcia-Pous M, Garcia-Delpech S. Prophylaxis of macular edema with intravitreal ranibizumab in patients with diabetic retinopathy after cataract surgery: a pilot study. J Ophthalmol 2011; 2011:159436
   2. Chae et al.  found a significant difference inCSME incidence between treated and untreated eyes only at month 1 (10.3 versus 33.3%, P¼0.019) and a greater BCVA improvement in the Ranibizumab Group only at month 6 (0.046).
3. Triamcinolone acetonide : to reduce the breakdown of the BRB, inhibit the production of prostaglandins and downregulate production of VEGF
   1. Kim et al. [28] showed that subtenon triamcinolone acetonide injection, at the end of cataract surgery, can reduce the incidence of macular oedema, prevent central retinal thickness (CRT)increase (control group: +69μm; treated group: +10.5 μm; P=0.015) and promote a greater visual improvement, 1 month after surgery. No significant side effects have been reported
   2. Ahmadabadi et al. The mean CMT change was significantly lower in the treatment group than in the control group at month 1 (treatment: -8μm; control: +64.4 μm) and month 3 (treatment: -10μm; control: +34μm), with no longer significant difference at month 6 (treatment: -3.4μm; control +22μm). CSME occurred in foureyes (19%) in the control group and in zero eyes in the treatment group.
   3. A transient increase of intraocular pressure (IOP) in 14% of treated eyes was the only reported side effect. Ahmadabadi HF, Mohammadi M, Beheshtnejad H. Effect of intravitreal triamcinolone acetonide injection on central macular thickness in diabetic patients having phacoemulsification. J Cataract Refract Surg 2010; 36:917–922.

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