Diabetes 1: Diabetes & Diabetic Retinopathy PDF

Diabetes 1: DIABETES & DIABETIC RETINOPATHY Part 1 of 3 5LMS0069 Angela Gulati-Roy MSc., BSc. (Hons), MCOptom, AFHEA University of Hertfordshire  Online lecture etiquette… Schedule a time in your day to listen & review this content Turn off all other devices / remove distractions Don’...

Diabetes 1: DIABETES & DIABETIC RETINOPATHY Part 1 of 3 5LMS0069 Angela Gulati-Roy MSc., BSc. (Hons), MCOptom, AFHEA University of Hertfordshire  Online lecture etiquette… Schedule a time in your day to listen & review this content Turn off all other devices / remove distractions Don’t be PASSIVE  be inter-ACTIVE Note pad & pen (paper/electronic) Scheduled pauses for you to write notes / think about the answers ? What will I learn? Diabetes mellitus (DM) – Pathophysiology – Prevalence – Aetiology, classification & risk factors – Overview of control & management of DM Diabetic retinopathy (DR) – Histopathology – Risk factors – Retinopathy features, classification & grading – Diabetic screening & management Diabetes - definition Diabetes Mellitus (Greek, c1400-1600’s) ‘diabainein’ (syphon) ‘mellitus’ (like honey) A metabolic disorder Defective Insulin secretion, action OR both Systemic effects include long-term organ dysfunction & failure Diabetes Insipidus Rare, Similar presenting symptoms to diabetes mellitus Unrelated to glucose levels (‘insipidus’-un-tasty !) Pituitary Gland dysfunction affecting kidney function Diabetes - historical perspective Earliest known record of diabetes, 1550BC Pre-Buddhist Vedic Scriptures ‘Medh-Meah’- sweet urine – Indian physicians, 5th Century AD Pancreatomy - resulted in diabetes – Minkowski & von Mering (1889) Insulin, Meyer (1909) Insulin extraction, Banting, Best & Macleod (1921) Diabetes - facts & figures ref: International Diabetes Federation https://www.idf.org/aboutdiabetes/what-is-diabetes/f acts-figures.html Globally in 2019: ≈ 463 million adults (20-79 years) were living with diabetes – By 2045 this will rise to 700 million 1 in 5 of the people who are above 65 y/o have diabetes Diabetes caused 4.2 million deaths > 1.1 million children and adolescents are living with T1 diabetes > 20 million live births (1 in 6 live births) are affected by diabetes during pregnancy International diabetes federation, 2019 Global numbers are rising  Global predictions – the top 10 Adults age 20-79 with diabetes - IDF 2019 report U.K Statistics, diabetes.org.uk >1 in 15 people in UK have diabetes (diagnosed/undiagnosed) In 2018/19, 3.9 million diagnosed diabetics – ? A further 1 million un-diagnosed T2 diabetics By 2030, estimates > 5.5 million diagnosed cases DIABETES ANATOMY & PHYSIOLOGY RECAP Pancreas anatomy & function - recap Dual function: Exocrine (95% tissue) Aids digestion - secretes enzymes digest proteins, fats & carbohydrates Endocrine Regulates blood glucose Islet cells release hormones in to blood stream: Insulin (lowers blood sugar) Glucagon (raises blood sugar) Somastatin (controls sugar/salt) Pancreas - recap Islets of Langerhans (7mmol/L) This may occur if: >> Carbohydrates Stress Poor health/infection Absent/defective insulin Missing diabetic medication/insulin dose Symptoms of HYPER-glycaemia:  urination/thirst Fatigue hunger  Diabetic states (2): Hypo- glycaemia = Low blood glucose ( dose diabetic medication Symptoms of HYPO-glycaemia: Sweating, fatigue, dizzy Pale, weak, hunger Confusion Convulsions Coma (extreme) Diabetic States (3): Keto- acidosis Very raised blood glucose (>15mmol/L T1>>>T2) Insufficient insulin to allow glucose to enter cells Body burns own fatty acids, production of toxic ketone bodies This may occur: Prior to T1 diagnosis Missed insulin injections/faulty insulin pump or pen Infection, Alcohol, Drugs, extreme or prolonged stress Symptoms of keto-acidosis Vomiting, Dehydration, Sweet smelling breath (pear drops) Hyperventilation, Tachycardia Confusion, disorientation Coma & Death DIABETES – AETIOLOGY, CLASSIFICATION & RISK FACTORS Diabetes – general aetiology Primary causes: Mostly uncertain Genetic (current theories) Auto-immune response-exposure to viral/bacterial infection Risk factors-big role (?causative) Secondary causes: Pancreatic disease Cushing’s disease  increased production of cortisol Acromegaly Drug induced (steroid, think dosage/duration) Alzheimer’s disease (Diabetes t3 ??)  Diabetes classification & distribution Type 1 (T1) - usually early onset (approx. 8%) Type 2 (T2) - usually later onset (approx. 90%) (Gestational diabetes – up to 5%, may/not resolve during pregnancy) Others (2%): Maturity onset diabetes of the young (MODY), Neonatal diabetes, Wolfram Syndrome, Alström Syndrome, Latent Autoimmune diabetes in Adults (LADA), Type 3c diabetes, Steroid-induced diabetes ALSO: Pre-diabetes “borderline diabetes” 5-10% will progress to diabetes each year (The Lancet, Tabak et.al., 2012) Impaired glucose tolerance Impaired fasting glucose T1 diabetes: insulin deficiency ‘Juvenile’ (can occur later as latent auto-immune response) Destruction of pancreatic Beta cells  depletion of insulin stores – Variable rate of cell destruction – Deficient insulin production  total inability to produce insulin – symptoms often present only after majority of cells are destroyed No association with body weight Requires insulin management Cannot be prevented T1 diabetes: aetiology Multiple theories Susceptibility genes (the majority) Antigen complexes (chromosome 6) Rubella, Cytomegalovirus, Retrovirus – Virus has same antigens as beta cells  both destroyed? Diet (debated) Infant exposure to cows milk – body attacks foreign milk proteins – Over-production of t-cells  destroy beta cells High nitrate in water Low vitamin D T1 diabetes: risk factors Debated Viral exposure –  German measles, mumps Geography  northern climates – Colder climate  indoor lifestyle  > exposure to viruses Ethnicity – < China, > USA Caucasians Family history Other auto-immune conditions T1 diabetes: symptoms Ketones ‘may’ be present at diagnosis  highly symptomatic & rapid onset Frequent thirst/urination Fatigue Weight loss Recurrent yeast infections Slow wound healing Blurred vision T2 diabetes: insulin resistance ‘Adult’ onset (usually >35y/o, but not always) Inefficient response by the body to Insulin Results in increased demand for insulin production Increased insulin demand outweighs supply –  leads to eventual impaired insulin production Often weight associated Co-morbidities  High BP/cholesterol at diagnosis May be asymptomatic May be prevented (education) – May be controlled with diet/medication, some may need insulin T2 diabetes: aetiology Strong genetics – Overlaps as a risk factor? – Important to probe FH 50+ genes have been identified Diet – ? Causal/risk factor overlap Linked to medication: – Corticosteroids T2 diabetes: risk factors Family history (> both parents and/or if father is diabetic) Ethnicity (South Asian, African-Caribbean, Black-African) Age > 40y/o BMI > 30 (= obese classification) Poor diet Sedentary lifestyle Smoking High BP/Cholesterol Previous gestational diabetes or large baby Poly-cystic ovary syndrome (PCOS) – excess hormones  ? insulin resistance T2 diabetes: symptoms Can be asymptomatic OR milder version of T1: Polyuria Polydipsia Fatigue Weight loss (may be welcome) Blurred vision OVERVIEW OF DIAGNOSIS & MANAGEMENT OF DIABETES Control & continued management are key 1. MACRO-vascular disease Increased risk of CVD, M.I & Stroke Arterial wall chronic inflammation & damage General atherosclerosis (arterial narrowing) Lipid rich atheroma formation (prone to rupture) Increased platelet adhesionvascular occlusion BP control/aspirin/smoking cessation are key management strategies for DM & DR Control & continued management are key 2. MICRO-vascular disease Diabetic retinopathy Diabetic neuropathy  nerve fibre damage from disrupted vascular supply Diabetic nephropathy  changes in kidney structure affect function leakage of proteins in to urine Multi-disciplinary care & >> costs: Dedicated physicians & nurses for micro & macro- vascular care Including: ophthalmologists & optometrists  Criteria for medical diagnosis Symptoms and risk factor assessment Genetic tests (particularly in type 1 diagnosis) Children: Random plasma glucose (>11mmol/l) NICE guideline (18), 2015 Adults: use of HbA1c (amount of glycolated Haemoglobin in RBC) Reflects average plasma glucose over previous 8-12/52 – Avoids daily variations (>accurate) – Does not require fasting Cut-off for diagnosis, HbA1c = 6.5% Threshold based on reduced risk of developing complications (eyes/kidneys/heart disease & nerve damage) WHO, 2011 Treatment & aims (‘magic numbers’) Diet Activity levels: 60mins/day-children, 150 mins/week-adults Pharmacological agents (Type 2), Insulin therapy (Type 1&2) Glucose control aims (mmol/l): – Type 1; before meals: 4-7, after meals: 5-9 (NICE, 2015) – Type 2; before meals: 4-7 , 2hrs after meals: Prevalent in T2 3 types (may be a combination): – Focal – Diffuse – Ischaemic  Focal maculopathy Micro-aneurysms Surrounding hard exudate – complete or incomplete ring Circumscribed retinal thickening Focal oedema Often good VA prognosis Diffuse maculopathy Diffuse macula oedema Obscuration of RPE & choroid Leakage from vessels & micro-aneurysms Increased fluidmay show cystoid macula appearance VOLK is a MUST (3D) OCT Ischaemic maculopathy Capillary closure Features may vary – mild-severe Large blots haems. Multiple CWS Veneous changes IRMA Variable macula oedema Poor VA – Often disproportionate to visible signs Isolated features are rarely the norm… must be able to identify/classify & manage Diabetes 1: DIABETES & DIABETIC RETINOPATHY Part 3 of 3 5LMS0069 Angela Gulati-Roy MSc., BSc. (Hons), MCOptom, AFHEA University of Hertfordshire DIABETIC RETINOPATHY CLASSIFICATION & GRADING Classification of DR Rarely see isolated features Classify ‘stages’ of retinopathy – Type of feature – Location feature Retina and macula are considered as 2 separate zones Helps to determine speed of referral & degree of intervention Multiple classification systems exist – Early treatment of diabetic retinopathy study, ETDRS (1979-1989) – American academy of ophthalmology (2012) – Royal college of ophthalmologists, RCOphth (2012) Characteristic progression on the retina – dictates classification / stage of retinopathy Non (or pre-) proliferative phase – Leakage of vessels haemorrhage/exudate/oedema – As O2 supply reduces  signs of ischaemia >> haemorrhages, cotton wool spots, veneous changes IRMA Proliferative phase – Attempt by retina to re-vascularise – NVD/NVE/NVI & their 20 complications Pre-retinal / vitreous haemorrhage Retinal detachment Neovascular glaucoma Grade International Term Clinical features R0/M0 No features of DR or maculopathy R1 Mild, Non-Proliferative, Haemorrhages, Micro-aneurysms, BACKGROUND retinopathy Hard exudates R2 NON or PRE PROLIFERATIVE Extensive micro-aneurysms, Mod. (Moderate) retinopathy Intra-retinal haemorrhages, Hard exudates R2 R2 NON or PRE PROLIFERATIVE Large blot haemorhages, CWS Severe (Severe) Veneous changes IRMA R3A PROLIFERATIVE retinopathy NVD/NVE/NVI (active) Pre-retinal/vitreous haemorrhage, Pre-retinal fibrosis/traction Retinal detachment, Glaucoma R3S PROLIFERATIVE retinopathy No NEW haemorrhages, exudates or (stable) -treated & now stable new vessels. Signs of laser scarring evident M1 Diabetic maculopathy Exudates, oedema, retinal thickening within 1DD of fovea OR any haem or Adapted from National Diabetic Eye Screening micro-aneurysms (if VA> Dots & blots Cotton wool spots Veneous changes IRMA R2 and/or M1: management Check px still attending screening programme Last/next screening appointment? Change in VA’s/symptoms? – are these NEW changes? National screening outcome  R2 and/or M1 – within 13/52 from screening detection  early surveillance clinic/HES – triaged pending progression/severity Early surveillance clinic will review at 3, 6 or 12/12 pending progression of disease – Decide if HES referral for follow up tests/treatments (will be discharged from screening while under the care of HES) R3A (active) Dots, blots Cotton wool spots NVD R3A (active) NVD NVE Tractional fibriosis R3A (active) Dots Blots Pre-retinal haem. R3A (active): management Check px still attending screening programme Last/next screening appointment? Change in VA’s/symptoms? National screening outcome  R3  Early screening review clinic or HES – triaged pending progression/severity – **NVD/NVE within 1/52 from screening/optometrist detection – Optometrist detection referral protocol may vary – check local area R3A complications: management Optometrist detection of these features – warrants a SAME day referral: – Sudden loss of vision – Vitreous haemorrhage – Retinal detachment – High IOP > 30mmHg (NVI) R3S (stable treated) R3S: management Check px still attending screening programme – If HES deemed as stable & treated  annual re- screen Optometrist should still examine thoroughly & advise/manage appropriately – Check last/next screening appointment? – Check for changes in VA’s/symptoms/clinical signs? Optometric examination: Evaluation of DR – viewing the fundus ? Un-dilated  CoO = acceptable if being screened, but there are exceptions… ? Dilated (professionally must investigate all relevant Sx) Appropriate fundus viewing method – ✔ VOLK (optic disc, maculopathy, new vessels) – Red free (enhance vessels & haemorrhage view) – Systematic examination of all 8 retinal quadrants including macula (para-macula) ✔✔OCT (ideal) – retinal thickness – Assessment & monitoring of macula oedema – Vitreo-macula traction Image/fundus interpretation & recording - optometrist Document ALL ocular features seen & their location – Use disc diameters – Localise position relative to the optic disc or macula Draw pictures & annotate Grade retinopathy stage (R1, R2, M0, etc.) Consider retinal imaging, OCT Optometrist management - key points Probe SYMPTOMS – are these NEW &/or changed since last screening?) Probe HISTORY of medical condition(s) Change in clinical findings – e.g. VA, retinal appearance, Amsler ? Check last/next screening attendance – What was the outcome? – Has treatment been advised? If so, what, when ? Be aware of differentials – E.g. hypertensive retinopathy can appear similar AND can co-exist MUST AVOID DUPLICATION OF MANAGEMENT With any referral: consider to WHOM & HOW ictorial reminder  YOU have an important role to pl Further reading Clinical Ophthalmology, A Systematic Approach, 8th Ed., 2015, Kanski Atlas of Clinical Ophthalmology, Spalton et. al., 3rd Ed., 2004 Diabetic Retinopathy Guidelines, 2012, Royal College of Ophthalmologists Lee, R., Wong, T. Y., & Sabanayagam, C. (2015). Epidemiology of diabetic retinopathy, diabetic macular edema and related vision loss. Eye and vision (London, England), 2, 17 https ://doi.org/10.1186/s40662-015-0026-2 Useful websites: http://www.diabeticretinopathy.org.uk https://idf.org/