DIABETES MELLITUS AND DIABETIC EYE DISEASE
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Transcript of DIABETES MELLITUS AND DIABETIC EYE DISEASE
DIABETES MELLITUS AND DIABETIC EYE DISEASE
Dr Russell J Watkins
Diabetes Mellitus
During a meal, insulin is released from the beta-cells of the pancreatic islet cells
Insulin is a key hormone that regulates metabolism of triglycerides & carbohydrates
Diabetes mellitus is a group of metabolic disorders characterised by chronic hyperglycaemia resulting from relative insulin deficiency, insulin resistance or both.
Usually primary but may be secondary to pancreatic disease, acromegaly, Cushing’s disease, effect of drugs.
Also, impaired glucose tolerance as an entity
Diabetes Mellitus
Insulin deficiency results in impaired metabolism of carbohydrate, fat, protein, water & electrolytes
Death may result from Acute metabolic decompensation Longstanding metabolic derangements -
diabetic complications
Diabetes Mellitus
Primary DM is classified as Type I (insulin dependent - IDDM)
• Always need insulin• Younger
Type II (non-insulin dependent NIDDM)• Diet &/or oral antihyperglycaemics usual• May need insulin• Older
Diabetes Mellitus
Epidemiology Worldwide distribution Incidence of both type I & type II DM
• Prevalence of both types varies in different parts of the world
UK prevalence is 1-2% of population• 50% of type II remain undetected• Ratio of type II:type I is ~7:3
Diabetes Mellitus
Uncertain aetiology Environmental factors interact with genetic
factors• Variable clinical syndrome• Variable timing of onset
Pattern of inheritance & environmental factors differ in type I & type II
Diabetes Mellitus
Genetics of type I DM Polygenic Strongest genetic association = HLA-DQ ~36% concordance with identical twin
Genetics of type II DM no HLA linkage genetic factors must be important
• ~95% concordance in identical twins• genetic factors not yet identified
Diabetes Mellitus
Environmental factors in DM Type I
• Viral aetiology may be important• Diet (?Early introduction of cow’s milk)• Autoimmune - association with other AI
disease, HLA linkage, insulin autoantibodies detectable
Diabetes Mellitus
Environmental factors in DM Type II
• “Western diet” & obesity
• Age• Pregnancy
Diabetes Mellitus
Principles of treatment To alleviate symptoms of hyperglycaemia To avoid hypoglycaemia To limit complications
Diabetes Mellitus Complications of diabetes
Vascular• Atherosclerosis
(macrovascular)• Microvascular
(retina, kidney, nerve sheath)
Infections and poor wound healing
• Impaired PMNL function
Diabetes Mellitus
The current cost of DM in the UK 30% reduction in life expectancy Commonest cause of blindness in 20-65 yr
age group 600 patients reach ESRF per year Lower limb amputation rate 25-fold Use of hospital beds 6-fold 5% of total NHS budget
Diabetes Mellitus
Diabetes Control & Complications Trial (1993 onwards - NEJM 1993;329:1796) Published in NEJM, JAMA et al Diabetic complications are preventable The aim of treatment should be ‘near-normal’
glycaemia whilst avoiding hypoglycaemic episodes in insulin-treated patients (3-fold in such episodes in tightly controlled patients)
Diabetes Mellitus
Early Treatment of Diabetic Retinopathy Study (ETDRS) Published in mid 1980’s 12 published papers Current practice based on ETDRS guidelines Diabetic maculopathy (Report 1) reference
Arch Ophthalmol 1985;103:1796)
Diabetes Mellitus
The spectrum of diabetic eye disease Corneal hypoaesthesia & RES Cataract Vitreous degeneration Cranial neuropathy Arteriosclerotic retinopathy Vascular retinopathy (accelerated atherosclerosis) Diabetic papillopathy Diabetic retinopathy Advanced diabetic eye disease including retinal
detachment and rubeosis iridis
Arteriosclerotic Retinopathy Usually associated with hypertension;
accelerated by DM Signs
AV nipping (Salus’ sign) Dilated vein distal to AV crossing (bonnet’s
sign) Tapering of vein either side of AV crossing
(gunn’s sign) Right angle deflection of vein
Arteriosclerotic Retinopathy Signs (cont.)
Arteriolar “silver wiring” Ischaemic choroidal infarcts (elschnig bodies) Retinal arterial macroaneurysm Ischaemic optic neuropathy
Diabetic Retinopathy Prevalence of retinopathy at time of diagnosis:
1.5% age 20-40yrs 7% age 50-60yrs 10% age 60+
Diabetic retinopathy develops after >~8yrs duration of DM 79% of diabetics have retinopathy after 20yrs
Diabetic Retinopathy DR is the most common cause of blind & partial
sight registration in 30-60yr age group Blind diabetics
50% are dead within 3-4 yrs of registration Only 20% survive for 10 yrs
Diabetic Retinopathy Possible pathogenic mechanisms
Thickening of capillary basement membrane Capillary endothelial cell damage (aldose
reductase) Impaired RBC function O2 transport Stickiness & aggregation of platelets Loss of vascular pericytes (aldose reductase)
Diabetic Retinopathy Classification
Background Pre-proliferative Proliferative Maculopathy (can occur at any stage) Advanced
Background Retinopathy Signs of background diabetic retinopathy
Microaneurysms• First clinically detectable sign• INL
Hard exudates• OPL & INL
Haemorrhages• Flame shaped• Dot & blot
Pre-proliferative Retinopathy Pre-proliferative retinopathy
Cotton wool spots Venous dilatation & beading Arteriolar narrowing Large blot haemorrhages IRMA Capillary closure on FFA
Pre-proliferative Retinopathy
Risk of progression to proliferative retinopathy as predicted by ETDRS• Venous beading - >4x• Haemorrhages/microaneurysms - 4x• IRMA - 4x• CWS - 2x
Management is controversial - some would photocoagulate; others would monitor closely & treat NV
Proliferative Retinopathy Proliferative retinopathy
Overall Incidence of Proliferative Change Is 10-20% of Diabetics
Type I>type II Neovascularisation Is Pathognomonic of
Proliferative DR NVD & NVE Fibrovascular Epiretinal Membrane; Initially
Transparent, Becomes Opaque Vitreous traction with RD
Proliferative Retinopathy Results from
• Extensive capillary closure• Angiogenic factor causes friable NV at
watersheds• Endothelial buds from the venous end of
capillaries• Fibrovascular network adherent to vitreous
face• PVD may elevate vessels
Proliferative Retinopathy Management
• Photocoagulation• Good glycaemic control (DCCT)• Stop smoking & heavy alcohol intake• Treat systemic hypertension• Avoid physical exertion• Avoid direct trauma
Proliferative Retinopathy Risk of severe
visual loss in 2yrs Risk if treated
NVD + VH
40%
20%
NVD - VH
25%
5%
NVE + VH
30%
7%
NVE - VH
7%
7%
Diabetic Maculopathy Diabetic maculopathy
Retinopathy in the macula area Most common cause of visual loss in DM Type ii>type I Treatment based on ETDRS guidelines Classified as
• Exudative/focal• Oedematous/diffuse• Ischaemic• Mixed
Diabetic Maculopathy Exudative
Exudates in the macula area circinate Photocoagulation may be beneficial when
VA>6/60 Rx to centre of circinate ring or site of leakage
Oedematous Macular oedema (ECF in Henle’s layer) Rx with grid laser when VA>6/18
Diabetic Maculopathy Ischaemic
FFA reveals capillary non-perfusion No proven Rx 30% proceed to proliferative DR within 2yrs so
eventually require PRP
Mixed Exudates, oedema, ischaemia Laser may be of benefit
Diabetic Maculopathy ETDRS guidelines (CSME)
Thickening of retina at or within 500m of the fovea
Exudates at or within 500m of the fovea, if thickening of adjacent retina
A zone or zones of retinal thickening 1 disc area or larger, any part of which is within 1 disc diameter of the fovea
Advanced Diabetic Eye Disease Persistent vitreous haemorrhage Tractional retinal detachment Posterior hyaloid membrane Neovascular glaucoma with rubeosis iridis Patients will usually require vitrectomy, cutting
of traction membranes, epiretinal membrane peeling