8.1 Introduction

Diabetic maculopathy (DM) causes gradual and largely irreversible loss 

of central vision. many patients with DM are elderly; thus assessment 

and treatment may be complicated by co-existing ocular pathology, 

such as cataract, glaucoma or a poor mydriasis response. Medico-social 

problems may also militate against optimal management.

.

Diabetic maculopathy is caused by oedema from leaking capillaries 

and/or ischaemia due to capillary loss. Diabetic changes to the choroidal 

vasculature may also worsen the ischaemia and contribute to the 

oedema by reducing retinal pigment epithelial function. Preventable 

visual loss is largely due to disruption of the fovea and perifoveal neuro-

retina by oedema. The ETDRS and the British Multi-centre Photo-

coagulation Study showed that appropriate macular photocoagulation 

was effective in preventing central visual loss due to macular oedema, 

in many cases, for up to seven years. Optimal management depends on 

detection and treatment by photocoagulation of oedema before the 

fovea is involved. The aim of treatment is to prevent further visual loss, 

since visual acuity rarely improves following treatment, best results are 

achieved by applying treatment before central vision deteriorates.

.

Loss of central vision due to macular ischaemia or generalized oedema 

cannot be prevented by photocoagulation. In young people visual acuity 

may be preserved despite macular ischaemia. Many cases of diabetic 

maculopathy involved co-existing macular oedema and ischaemia. In 

such cases, the prognosis depends on the extent of the oedema and 

the severity of the ischaemia. Central vision can remain surprisingly good, 

even with marked retinal capillary closure, provided coexisting oedema is 

treated before it involves the fovea.

.

8.2 Indications for treatment

Treatment is indicated when the maculopathy threatens the fovea or 

perifoveal area. Isolated microaneurysms around the fovea without 

clinical evidence of retinal thickening therefore do not merit treatment, 

but they should continue to be observed at regular intervals. Small 

localized areas of retinal thickening outside the central macula area 

do not require treatment, though such cases do require regular follow-up. 

Fluorescein angiographic evidence of retinal oedema in the absence of 

clinically obvious retinal thickening (Clinically Significant Macular Oedema, 

CSME in the ETDRS) is not normally regarded as an indication for 

treatment. 

.

8.3 Treatment protocols for diabetic maculopathy

The aim of treatment is resolution of retinal oedema before the fovea is 

involved. This is achieved using laser therapy to the macula. How laser 

therapy achieves this effect is unclear. There is either a direct effect on 

leaking microvascular complexes in the retinal circulation or an indirect 

effect mediated through the retinal pigment epithelium.

.

Safe treatment depends on accurate identification of the fovea and 

avoidance of excessively intense burns. The fovea can be difficult to 

identify if there is considerable oedema. Excessively intense burns can 

be avoided by starting treatment with very low powered burns, and 

gradually increasing the intensity until a satisfactory moderate blanching 

of the retina is achieved. Energy uptake varies, depending on the degree 

of the retinal oedema, so it is important to reduce power when treating 

less oedematous areas. 

.

Satisfactory results can be achieved with a number of different light 

wavelengths (see elsewhere in these guidelines). The most frequently 

used wavelengths are 514nm (the ‘Green’ component of the Argon 

Blue/Green laser) and 810nm (from the infra-red diode laser). The Argon 

blue/green laser should not be used for treatment of microaneurysms 

that are very close to the central area. This is because the blue light 

from this laser (487nm) is absorbed by xanthophylls pigment overlying 

the parafoveal area. this can cause nerve fibre layer damage and 

parafoveal scotomata (see section on lasers). 

In general, the blue laser waveband is not recommended due to its 

possible deleterious effects on the user (see Section 5.2).

.

8.3.1 Focal maculopathy

This type of maculopathy responds most readily to photocoagulation. 

Areas of focal leakage, usually a the centre of the exudative rings 

(identifiable if necessary by fluorescein angiography but only if doubt 

exists as to their precise location), are treated using a 50-100 micron 

beam at sufficient power level to obtain moderate blanching of the 

retina. When the microaneurysm is close to the fovea, a short 

superficial burn just sufficient to blanch it may be used.

However, the treatment of microaneurysms within 300 micron of the centre 

of the fovea should be undertaken with caution because of the significant 

risk of closure of the perifoveal arcade.

An alternative to direct treatment of focal leakage is to apply a gentle grid 

to the entire circinate ring, including the margin, in a fashion similar to that 

used for diffuse maculopathy.

.

Figure 26 Grid laser treatment  of diabetic maculopathy. a) Fundus  appearance b) Areas of laser therapy seen on fluorescein angiography  as spots of 'show-through' (arrow). Click on picture for a larger view.

.

8.3.2 Diffuse maculopathy

Diffuse maculopathy is a more difficult form of diabetic retinopathy to treat. 

However, grid laser photocoagulation offers the only available, validated 

therapy. The technique consists of applying 100-200 micron burns delivered 

at a power level sufficient to obtain a minimum blanching reaction the 

pigment epithelium in a grid pattern over the central macula avoiding the 

fovea itself (Figure 26a, b). Patients may visualize the grid entoptically.

.

8.3.3. Mixed maculopathy

Focal and diffuse areas of oedema should be identified and treated as above.
.

8.3.4 ischaemic maculopathy

Ischaemic maculopathy does not respond to laser therapy. However, if the 

degree of ischaemia is sufficiently large that it performs part of the pre-

proliferative retinopathy, then this of itself may warrant therapy.
.

8.3.5 Diffuse non-responsive macular oedema

Severe diffuse macula redeem which is non-responsive to grid laser 

photocoagulation or repeated grid laser photocoagulation, may benefit from 

vitrectomy with removal of the attached posterior hyaloid face. Cases likely 

to benefit have an appearance which may be very subtle, but presents as 

posterior hyoid face thickening, surface wrinkling and a detectable sheen, or 

abnormal reflex from the inner limiting lamina. The surgical goal should be the 

removal of all thickened posterior hyaloid and cortical gel material via a three 

port pars plana vitrectomy (see next section). Approximately 50% of patients 

may experience moderate improvement of vision, up to 2 lines or more. 

.

8.3.6 Diffuse maculopathy in the presence  of neovascularization

Occasionally maculopathy co-exists with disc or retinal neovascularization. 

Whether to treatment the new vessels with PRP or to treat the 

maculopathy first depends on the age of the patient and the relative 

severity of the retinopathy. In young patients with active new vessels it 

is generally recommended to treat the new vessels first with PRP since new 

vessels in these patients can advance rapidly with devastating consequences. 

In older patients with NIDDM, it is better to treat the maculopathy first or at 

least at the same time since PRP itself in these patients can hasten the 

progression of the maculopathy. Fractionating PRP into sessions of 700-800 

burns separated by 2-3 weeks reduces the risk of this progression.

.

8.4 Follow-up after treatment of diabetic maculopathy

Patients with diabetic maculopathy should be reviewed 3-4 months after 

treatment. If oedema persists, or if the visual acuity worsens, repeat 

fluorescein angiography may be helpful in identifying areas of residual 

focal leakage which should then be retreated. Treatment of leaking areas 

associated with exudates may cause regression of the exudates over 

many months.

Since focal maculopathy can recur, patients with treated maculopathy 

should be followed for a sufficient time to ensure that the condition is 

inactive. Patients with cataracts and treated diabetic retinopathy should 

have the maculopathy reassessed before cataract surgery since surgery 

can induce recurrence or advance of existing macular oedema. Any persistent 

areas of oedema should be re-treated either before or soon after surgery.

..............