Stage 1 Visit 1 - DR

Type 1 diabetes

• Auto-immune condition in which cells that produce insulin are destroyed

• 10% of Px with diabetes have this type

• Lifelong treatment with insulin is required to prevent death

• Tends to develop before 40 years old and usually in childhood

• Requires injections of insulin

Type 2 diabetes

• Body stops producing enough insulin for its needs or becomes resistant to the insulin produced

• 90% of diabetes cases

• Lifestyle management (diet and exercise) as is strongly correlated to obesity

• Requires oral drugs (tablets) or injections

Symptoms of Diabetes

• Urinating more often

• Thirst

• Tired

• Light headed/dizzy

• Weight loss

• Blurred vision - due to changes in the refractive index of the lens

Percentage of people with diabetes that will develop some DR?

• 50% of type 1 and 25% of type 2 have some DR

• If a Px has diabetes for 20 years almost all type 1 and 66% of type 2 will have DR

What is the leading cause of preventable sight loss?

• Diabetes - 5% of all sight loss is related to DED

What does insulin do?

• Regulates Blood glucose levels by stimulating glucose uptake from the blood which is stored as glycogen within the liver

What is HbA1c?

Chemical formed when glucose combines with haemoglobin

Blood HbA1c levels are an indirect measure of?

• Useful measure Blood glucose levels over a prolonged period - gets rid of any spikes that may alter results

• Non Diabetic levels - <36mmol/l

• In Diabetes - 48mmol/l is safe

What is the main modifiable risk factor for type 2 diabetes?

• Obesity - increases risk of type 2 by 13x for women, 6x for men

Non-modifiable risk factors for DR

• Duration of Diabetes - if diagnosed 20 years ago likely to have DR

• Ethnicity - Asians and Afro Caribbeans are 2x more likely to develop type 2

• Social Deprivation

• Gender - 56% men, 44% women

• Age

Modifiable Risk Factors of DR

• Glycaemia - control of diabetes = less likely to develop DR

• Blood Pressure

• Lipid levels - manage cholesterol levels = reduce risk of DR

Signs of Microangiopathy (Background) DR

• Pericyte loss

• Microaneurysms Formation

• Increased vascular permeability

• Capillary Occlusion

Pre-Proliferative DR

• Chronic Retinal Ischaemia - arteriolar perfusion is gradually reduced over months/years - leads to slow cell infarction

• Exudation

• CWS - sign of Retinal Ischaemia

• Intraretinal Microvascular Abnormalities

• Venous beading/looping

Signs of significant severe retinal Ischameia

• IRMA and Venous beading/looping are reliable

• CWS a sign but less reliable for significant ischaemia

Difference between IRMA and neo

• Neo sit on top of the retina, IRMA within the retina

• IRMA don’t leak

• No Exudation = IRMA

• Exudation = Neo

What does Chronic Ischaemia release

• VEGF - which stimulates angiogenesis and leads to retinal/iris neovascularisation

• Due to this = exudation

Pre-proliferative is indicated by

• >1 IRMA

• Venous beading

• Multiple deep dot or blot haemorrhages

Proliferative DR

• Presence of NEO + all the signs in pre-prof

• VEGF primary driver of neo

• Pre-retinal (between ILM and vitreous) and vitreous haemorrhages - urgent referral

• Can potentially lead to Vitreo-retinal traction

• Black circle = fibrovascular proliferation - forms around NV

Neovascularisation

• 2 forms;

  • NVD

  • NVE - in any of the 4 quadrants

• As NV proliferate, fibrous tissue forms around them - acts as scaffolding for developing NV

• OCT shows Neovasc that can extend into the vitreous

Vitreo-Retinal tractional detachment

• Fibrovascular material can be attached to both the ILM and vitreous

• The tension of the new vessels leads to tearing of the vessels which leads to haemorrhaging and elevation of the retina - T RD

• Can be relieved by vitrectomy surgery

Diabetic Maculopathy

• Can occur at any stage of DR

• Involves any of the following around the macula

  • Microaneurysms

  • Exudates

  • Dot and Blot

  • Oedema - can see with an OCT

How does DMO occur?

• Hyperglycaemia induces microvascular pathology

• BRB breakdown

• Exudation

• Release of VEGF

• Further increase in vascular permeability

Which layers are the fluid located in DMO

• Fluid build up is concentrated in INL and OPL

• Fluid forms cysts which increase retinal thickness

• Fluid causes disorganisation or retinal layers

Cataract in Diabetes

• Cortical and PSC are more common in diabetics and occur earlier in life

• 50% of type 2 have cataract

• Type 1 require surgery 20 years earlier than non-diabetics

Rx changes in Diabetes

• Poor glycaemic control changes osmotic pressure within the lens/cornea which changes the refractive index

• Most common myopic shift

• Can also be hyperopic shift, no proof of astigmatic

Pre-Proliferative DR screening

• Likely to be escalated to surveillance clinic - frequent supervision

• If Optom suspects; then should initiate their own referral to HES via GP requesting HES opinion within 6/52

  • Px is not in screening programme or missed their last appt.

  • Px had recent screening but DR has progressed

Diabetic Maculopathy referral

• Slow progression so routine referral

• If Px’s VA’s are reducing then refer 1/12

• DMO will be treated with anti-VEGF

Proliferative Retinopathy management/referral

• Px will be seen by ophthalmologist every 2-3 months

• If found Optom should call local HES and explain findings

• Urgent Referral - record details of the call on the px record card

Overall management of the different stages of DR

• DM px c no DR - one year recall - make sure px is enrolled on screening programme, if not write to GP to be enrolled

• Background DR e.g microaneurysms, haemorrhages

  • Confirm px is on screening programme

  • if in doubt ask px to contact their local screening programme / GP

  • Optom should write a letter to GP to confirm

  • NO REFERRAL to HES

• Pre-Proliferative DR - will likely be in surveillance clinic, ensure you ask px when they last had an appt etc. - if not on screening programme refer to HES via GP

• DMac - Refer to HES IF PX COMPLAINS OF BLURRED VISION - if vision remains stable no need for referral

• Proliferative DR - Urgent referral

• Complications of DR e.g Neovasc Glauc, pre-retinal/vitreous haemorrhage - emergency referral

HES management of Diabetic Eye Disease

• primary medical intervention is always to try and manage the systemic side of the disease e.g meds + lifestyle changes to bring the glucose levels under control which will reduce the severity of the disease.

What is Laser Photocoagulation Therapy?

• laser targetted at retinal tissue causing a small burn (500 microns)

• This laser destroys RPE cells alongside the overlying outer retinal layers

• e.g PR destroyed which reduces the metabolic demand of the outer layers

• Inner retinal layers are able to receive more oxygen supply from the choroid as the outer layers are no longer taking any oxygen

• Oxygen supply improved = reduced ischaemia = reduced VEGF production

What is the most common form of LPT and how does it work?

• Pan Retinal Photocoagulation (PRP)

• 1500 closely spaced burns to mid-peripheral retina

• Effective but induces permanent retinal scarring

• Preserves central vision

Side effects of PRP

• Reduced visual field

• Reduced night vision

• Reduced dark adaptation due to loss of rods

First line treatment for DMO?

• anti-VEGF drugs as intravitreal injections

• Ranibizumab and Aflibercept - require a central thickness of 400 microns

• Less effective the greater the initial VA reduction and the longer the duration of DMO

• Other options include intravitreal corticosteroids - supress inflammation e.g Dexamethasone

Does DR affect DV or NV more

• Changes results in DV more

Does DM affect DV or NV first

• Changes results in NV first

Grading scale