Diabetic maculopathy for professionals
The treatment for diabetic macular oedema (DMO) is changing
- Laser has a role in circinate retinpoathy or if there is a small area of leakage.
- Anti-VEGF treatment is the primary treatment for diffuse or cystoid DME.
- It is not clear if laser will help diffuse or cystoid DME if anti-VEGF treatment available.
- We now carry out a maximum 2 grid laser sessions for such patients if not eligible for anti-VEGF or to supplement anti-VEGF.
- NICE is recommending anti-VEGF if oedema is >400µ, but most of us consider this is too late. Also, NICE is recommending Lucentis instead of Avastin (Avastin is much cheaper and we could treat many more patients for the same cost.) Eylea would be even better as this lasts twice as long as Lucentis.
- Laser probably helps in the long term,
- Anti-VEGF in the short term, and
- good blood glucose/blood pressure/lipid control is essential
- also, micropulse laser is probably helpful (units without this use subthreshold laser which is probably similar)
- PRP laser is carried out in addition if there is a lot of peripheral closure/ischaemia
- All our laser is now subthreshold
Many ophthalmologists have wondered why some patients who present with severe maculopathy do well and some do badly.
- If a patient presents with severe maculopathy but their diabetes is reasonably well controlled, (HbA1c < 9% and blood pressure reasonable) and it has been for some time, with laser/anit-VEGFs/further improvement of their diabetic control they may do very well, keeping central vision and be able to read, though often not good enough to drive.
- If a patient with similar severe retinopathy presents, and their HbA1c >11%, and their BP 200/120, they are likely to do very badly, even if their control is improved. Good control is essential in the long term, but nevertheless in the short term the retinopathy will get worse. see. Case 57
- An extremely low blood pressure will prevent some deterioration (as low as possible whilst the patient feels well, perhaps <115mmHg systolic.) BP & maculopathy see 2013
- Most patients will be in between, that is there will be some response to laser/anit-VEGFs, but their retinopathy may deteriorate a little as they improve their diabetic control.
- Smoking quadruples the retinopathy, and stopping will be extremely helpful.
- Statins are now recommended for nearly every type 2 diabetic patients, where well tolerated. They will help exudates disappear, but have much less effect on the oedema itself. (Exudates themselves can cause scarring and loss of sight.) Fibrates may be more effective than statins. Lipid lowering is essential BJO 2010.
- Massin (EASDec
2005 meeting) reported that macular oedema can be temporary.
It fluctuates during the day.
She presented a patient who had macular oedema after laser for proliferative retinopathy (type 1 diabetic, diabetic about 20 years. He did not look after himself..he overworked, ate a little too much, and took no exercise. One eye was treated with triamcinolone twice and improved temporarily each time. Whilst having these injections, he did start to exercise, and lose weight etc, and the macular oedema that was bilateral (despite the triamcinolone in one eye) resolved and his sight improved to 6/12, so he was able to read and drive. (anit-VEGFs would be the preferred treatment now.)
- Thus the key is to persuade patients and their professional carers not to allow the HbA1c to rise at any stage of the diabetes, and to aggressively treat blood pressure. In this way if retinopathy does develop it should respond better to laser.
- BJO 2011 Reduced renal function case 57.
- Increased macular thickness even in the absence of oedema Eye 2012
- sleep apneoa plays a significant role
- control of the HbA1c, BP, lipids, and so on is VERY VERY important: see targets
- see Planning laser for diabetic maculopathy; Laser settings for maculopathy
- Anti-VEGF (instead or in addition to grid laser) will reduce macular oedema
- The Restore Study used Lucentis, but Avastin should be similarly effective.
- Restore and other papers indicate anti-VEGF injections will often have to be continued long term to maintain sight.
- If oedema >400µ
- monthly injections until oedema stable...until there is no improvement in the oedema
- then contine monitoring with OCT offering injections if oedema increases again.
- So if there is 400µ central macular thickness, injections are carried out monthly until there is no extra response. In such a patient oedema may reduce to 250µ. If a further injection does not reduce the oedema, then 250µ would be considered the best that can be achieved. After that injections would be restarted if the thickness increases again. So if the thickness increases, perhaps to 300µ, injections would be restarted again so as to maintain 250µ.
- The drugs reduce macular oedema but will not improve sight if there is no oedema. Occasional patients will notice a deterioration in vision, and such eyes are more likely to have more macular ischaemiathan the eyes that benefit. Patiens with 'spongy' or diffuse oedema benefit most. Even with injections vision may not improve. As I remember vision improves only in 50% patients, but oedema reduces in most(?~80%). So vision is not a good indicator of whether anti-VEGF is needed.....macular thickness on the OCT must be used.
- examine the peripheral retina, and laser if ischaemic (PRP).
If the FAZ enlarges, vision is reduced, see & see. If vision is reduced and there is no oedema clinically, this is the likely cause: a fluorescein angiogram (FFA) will confirm this. Laser is not helpful. Laser is for macular oedema, seen with OCT or clinically with a slit lamp, or FFA. Avastin is less effective if the FAZ enlarges ('ischaemic maculopathy'). The ischaemia leads to foveal atrophy. Fundus autofluoresence is helpful in determining the degree of foveal damage (see 2002) , but is seldom available.
OCTs are very useful to determine which type of macular oedema is present. These are diagrams illustrating the text in a paper by Markomichelakis. There are 3 basic patterns, which often occur in combination: diffuse, cystoid, and serous detachment. This paper really examined uveitis patients, but reported similar findings in diabetic retinopathy.
Sponge type diabetic macular oedema responds better than cystoid Retina 2013. Response best sponge (=diffuse on this page) > cystoid > subretinal fluid, and best with short duration of diabetes (photo).
OCT is crucially important in deciding treatment, see see .and is the main guide for the use of anti-VEGF drugs (primarily Avastin)...if the oedema reduces the drug has worked and is a very useful guide.
Extra-foveal vitreous traction is linked to macular oedema. Ophir 2009 This is the case even in non-diabetics Fatum 2009. 33% of patients with diabetic mac. oedema have VMT (Vitreo-macular traction), Eye 2010.
Diffuse oedema responds best to anit-VEGFs. Cystoid usually has a very limited response, and serous detachment also has a poor response. The effect of treatment tis best in the first 6 months and thereafter depends on the injection frequency.
- classification BJO 14
- The protocol defined four categories
- subretinal fluid (category ‘S’)
- the planimetrically measured oedematous area (category ‘A’)
- vitreo-retinal interface abnormalities (category ‘V’)
- CSME aetiology (category ‘E’) defining the leakage source
- There is a relationship between macular oedema and visual acuity (Retina 2010), but atrophy of the photoreceptor layer is likely cause the most visual loss (Oxford MOS 2010).
- is there VMT (Vitreo-macular traction)? Eye 2010,
- diffuse oedema responds to treatment better than cystoid EYE 2013
- location: central/nasal temporal etc
- amount: thickness..amount with OCT
- type: diffuse/cystoid/foveal cyst
- +/- chronic (as above)
- +/- serous detachment;
- +/- epriretinal membrane;
- +/- VMT;
- +/-ma (microaneurysms);
- +/- exudates;
It is best used with OCT helps if there is vitreomacular traction (VMT), see, but not eyes with a PVD already (right), but some patients do get worse see. It is only really helpful if the diabetes (HbA1c/BP) is well controlled and the retinopathy is stable...no haemorrhages or exudates etc.
With vitrectomy with VMT. 50% patients gain 2 lines. 33% of patients with diabetic mac. oedema have VMT (Vitreo-macular traction), Eye 2010; vitrectomy may help in this group particularly.
On the other hand, this walled cysts and subretinal fluid as part of the VMT indicate sight will not be improved with vitrectomy. Nottingham 2011: vitrectomy reduces DMO in the short term, but then it recurs.
Left: VMT, vitrectomy may help. Right, a straightforward PVD, vitrectomy will not help reduce macular oedema.
If the 'wall' of the elevated retina
results will be poor as there is too much atrophy.
If there is subretinal fluid, surgery will not improve vision.
- This treatment has generally been replaced with intravitreal ant-VEGF treatment,especailly if the condition is chronic, and has little role in 2014.
- Intravitreal triamcinolone is really reserved ffor temporary problems such as post-cataract macular oedema
- It is likely intravitreal steroid implants are preferable and safer see see.
- there is a ~10% risk of severe glaucoma with the 4mg dose; most patients develop cataracts; 2mg is the commonest does used now; it can be extremely effective in some patients both reducing oedema and improving vision, but the effect does wear off after a few months.
- Intravitreal steroid implants
- if pseudophakic, approved by NICE, as part of the treatment of macular oedema secondary to retinal vein occlusion and diabetes
- They will be very helpful in certain cases of unilateral posterior uveitis macular oedema.