Diabetic Retinopathy is a common retinal disorder that is seen, managed, and followed up by not only a retina specialist but all ophthalmologists. It is a disease that is easy to diagnose, but often difficult to manage in a long run. For achieving optimal results besides the role of an ophthalmologist, one needs to have the involvement of a physician. The single most important factor for achieving a good outcome is patient compliance, as the disease, diabetes needs lifelong care. Here are few mistakes we need to avoid while managing a case of DR.

1. I can detect DME clinically, I don’t need OCT

OCT is not mandatory if there are no signs of DR, or in very mild retinopathy (<5 microaneurysms) and if the thickened retina is not seen on clinical examination. OCT is recommended in mild NPDR with visual impairment, and in moderate NPDR and beyond with/without visual improvement. It is advisable to get OCT in all diabetics at first presentation, irrespective of their clinical condition.

2. Neurosensory detachment in DME are very resistant, need multiple intravitreal injections

In situations when patients present with bilateral neurosensory detachment or unresponsive to intravitreal injections, one should rule out an underlying systemic disorder. Serous retinal detachments also may occur together with PEDs in patients receiving hemodialysis. Other disorders to keep in mind are anemia, malignancy such as multiple myeloma, or secondary uveal effusion syndromes. In such situations, therapy primarily will be directed to the underlying systemic disease.

3. Ignoring a worsening of DR severity on follow-up

Anemia and uncontrolled/poor glycemic control have been indicated as independent factors for the early progression of diabetes-related complications and considered to worsen DME. Studies have shown that Hb levels <12 g/dL and random blood sugar of > 200mg% results in doubling the risk of DR. The majority of these patients with anemia have an underlying renal dysfunction and affect erythropoietin production (EPO). For those with an underlying renal dysfunction and anemia , the DME improves from treatment with subcutaneous erythropoietin injections. However, there is often a worsening to DR severity level. Likewise, rapid control of glycemic status can lead to a sudden worsening of the DR status. This happens when a patient is switched from an oral hypoglycemic agent to insulin.

4. Asymmetric DR – Overlooked!

Epidemiological studies define asymmetric DR as none/mild DR in one eye and severe PDR in the other, a difference of two steps in the two eyes persisting for at least 2 years. Asymmetric presentation could result as a result of ocular ischemia caused by aortic arch atherosclerosis or by stenosis of the carotid arteries leading to neovascularization of the iris, disc, and peripheral retina. Other causes of asymmetric DR includes Myopia ≥5 D, Anisometropia >1 D, Amblyopia, Unilateral elevated intraocular pressure, Complete posterior vitreous detachment, Unilateral carotid artery stenosis, and Chorioretinal scarring

5. Ignoring a rapid progression of milder NPDR to PDR

A rapidly progressive NPDR to proliferative retinopathy in a span of a few months (4-6 months) is rare and therefore other underlying pathology that can cause further ischemia should be ruled out. Literature reports suspicion of chronic myeloid leukemia in such presentations. The plausible explanation might be the additional Ischemic angiogenic stimulus. Studies have shown angiogenesis and VEGF levels are also increased in bone marrow cells and the serum of patients with CML.

6. Any OCT thickening on OCT: Inject Intravitreal anti-VEGF:

Intravitreal anti-VEGF is the first-line treatment in Center-involving DME with vision less than 6/9. In a non-center involving DME, there is no role of intravitreal anti-VEGF, focal laser can be done. Likewise, in Center-involving DME with vision better than 6/9, it can be observed. DME should be classified using 300 μm thickness as the cutoff, into center involved DME, non-center involved.

7. My preference of treatment in DME is always Anti-VEGF

Some situations where intravitreal steroids can be used in the management of DME are;DME which are responding to anti-VEGF but there is difficulty in close follow up, Pseudophakic patients who have reached a plateau – persistent IRF / VA<6/12, Persistent edema which requires cataract surgery, Occurrence of a vascular event when on intravitreal anti-VEGF, Associated features such as extensive hard exudates, presence of hyperreflective spots on OCT, neurosensory detachment, Type I DME patient which was on anti-VEGF and had conceived. Pre-existing glaucoma is a relative contraindication to switching to steroids.

8. With the current standard of care, a good visual outcome can be achieved in nearly all patients with DME

Ominous clinical signs, that may portend a poor prognosis with therapy, are signs of macular ischemia such as a profuse number of hemorrhages, cotton-wool spots, and sclerosed vessels. Fundus fluorescein angiography (FFA) will help to confirm the same. An excess of foveal hard exudates, optic disc pallor, or associated retinal pigment epithelial degeneration also does not do well.

9. There is good evidence of managing PDR with intravitreal anti-VEGF alone. I practice this for all my PDR patients.

Over a period of 5 years, follow-up either anti-vascular endothelial growth factor therapy or PRP are viable treatments for patients with PDR. Patient-specific factors, including anticipated visit compliance, cost, and frequency of visits, should be considered when choosing treatment for patients with PDR. A patient with poor compliance is not a good candidate

10. With better instrumentations, a good visual outcome can be achieved in the majority of cases that undergo vitrectomy

Visual outcomes do not always correlate with the anatomical success rate and neither is there a dramatic improvement in the majority of cases. Besides macular detachment, preoperative rubeosis iridis, NVG, vitreopapillary traction, lack of panretinal photocoagulation, vitreous haemorrhage, fibrinoid syndrome, or anterior hyaloidal fibrovascular proliferation, poor preoperative visual acuity of <5/200, ischemic optic neuropathy, and macular ischemia are considered to carry poor prognosis even after surgery.