What is diabetes? Ocolusystemic Disease Essen6als. Statistics, cont. Statistics. Statistics. The Diabetes Epidemic 9/5/12

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Edmund Lindsey
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1 What is diabetes? Ocolusystemic Disease Essen6als Steven Ferrucci, OD, FAAO Chief, Optometry Sepulveda VA Associate Professor, SCCO DM is a chronic disorder characterized by a lack of insulin or increased resistance to insulin Insulin is needed for proper uptake of glucose Clinical result is hyperglycemia retinopathy nephropathy neuropathy Statistics Statistics, cont. Approximately 23.6 million Americans with diabetes 8.3% of total population 11.3 % of adults 25-30% undiagnosed ( 7 million) Another 57 million Americans have prediabetes and are likely to develop diabetes if do not change habits 35% of adults age 20 or older Globally, Type 2 DM affects 5.9% of adult population 46% ages Highest percentage in Eastern Mediterranean and Middle East (9.2%) and North America (8.4%) Total Numbers: 246 million Worldwide India 40.9 million China 39.8 million Then USA, Russia, Germany, Japan, Pakistan, Brazil, Mexico and Egypt Statistics In 2007, medical expenditures for diabetes $116 billion $27 B direct care $58 B to treat diabetes related complications $31 B in excess general medical costs 2.3 x higher in diabetic vs non-diabetic pt Actual national burden of diabetes likely exceeds $174 B when indirect costs considered Seventh leading cause of death in 2006 The Diabetes Epidemic Incidence has increased 13.5% from 2005, and over 700% in last 40 years Improvements in diabetes care Pts living longer with diabetes Changes in way Diabetes is diagnosed 1

2 The Diabetes Epidemic Increased number or minority populations in US Rates of DM among minority populations are often 2-3 times greater Growth in elderly populations: 10% > 60 vs 16-20% > 80 Increasing prevalence of obesity which causes increased insulin resistance TYPE 1 Formerly IDDM or juvenile onset Prevalence: 0.2% 10% of all DM Most common age of onset < 30 Destruction of insulin producing B-cells in pancreas (auto-immune? viral?) Total lack of endogenous insulin Need to be on insulin to survive TYPE 2 Formerly NIDDM or adult onset Prevalence: 3.1% 90% of all DM Most frequent age of onset > 40 Often asymptomatic Characterized by insulin resistance Strong genetic predisposition Gestational Diabetes Affects 4% of all pregnancies High risk populations: Pregnant woman greater than age 25 Abnormal body weight Have first degree relatives with diabetes Hispanic, Asian, Native American, African American descent Screen in 24th to 28th week of pregnancy Gestational Diabetes Plasma glucose concentration at or above any 2 of 4 values on OGTT 1. Fasting, 95 mg/dl 2. 1 hour, 180 mg/dl 3. 2 hour, 155 mg/dl 4. 3 hour, 140 mg/dl May be treated with diet changes or insulin if needed At higher risk for developing type 2 later in life 5 fold increase at 5 yrs, 9 fold after 5 years Pre-Diabetes Blood sugar levels higher than normal, but not yet high enough to be diagnosed with DM ( mg/dl) ADA estimates 57 million Americans have pre-diabetes 30 minutes of exercise combined with 5-10% reduction in body weight resulted in 58% reduction in diabetes 2

3 Symptoms Risk Factors Often asymptomatic, especially Type 2 Classic symptoms polydipsia polyphagia polyurea Others: weight loss, delayed wound healing, dry mouth, dry skin, recurrent infections, refractive changes Family history Specific ethnic backgrounds African Americans Native Americans Hispanic Asian American Pacific islander Sedentary Lifestyle Pertinent medical history obesity cardiovascular disease HTN High cholesterol Polycystic ovarian syndrome Psychiatric illness Gestational DM IFG/IGT Traditional Diagnosis Criteria Fasting blood glucose > 126 mg/dl OGTT > 200 mg/dl (2 hour sample) Random testing > 200 mg/dl with symptoms very suggestive of DM Any random testing >200 mg/dl should be referred for further testing New Diagnosis Criteria Panel of experts at ADA annual meeting are recommending A1C be used for diagnosis of diabetes Glycosolated hemoglobin Tells blood sugar control over 3 months normal range 4% to 6% Recommended Criteria for Screening Asymptomatic Individuals for Type 2 DM All pts >45 yrs at 3 yr intervals Younger age or more frequently in pts who: are obese have a first-degree relative with diabetes are members of high-risk ethnic population gestational diabetes or delivered a baby > 9 lbs are hypertensive HDL < 35mg/dl or triglycerides > 250 mg/dl have impaired glucose regulation Treatment of Type 2 DM Goal: to produce desirable blood glucose levels with minimal adverse effects and maximal patient compliance Treatment begins with diet and exercise and ends with insulin Often, adequate control can be achieved with oral agents If not, insulin is utilized 3

4 Current recommendations for Treatment of Type 2 DM Control BS: HgbA1c < 7 Control HTN: <140/80 Control Cholesterol levels: Total cholesterol < 200 No smoking Exercise Normal BMI Yearly foot exams, dental exams, and dilated retinal exams Diabetic Retinopathy Leading cause of blindness year old 8-12% of all new cases of legal blindness 50,000 Americans legally blind Early diagnosis and treatment can decrease vision loss by 50-60% Factors which influence development of DR duration of disease control of BS Diabetic Retinopathy Duration of Disease: Type 2 <10 years 1% years 23% > 16 years 60% Control of BS (UKPDS) for every 1% decrease in HgbA1C there is a 35% reduction in risk for retinopathy Diabetic Retinopathy Non-proliferative Diabetic Retinopathy (NPDR) mild moderate severe very severe Proliferative Diabetic Retinopathy (PDR) Including high-risk Nonproliferative Diabetic Retinopathy (NPDR) Loss of retinal capillary pericytes Weakens capillary walls Causes non-perfusion in capillary beds and hypoxia Divided into mild, moderate, and severe Microaneurysms (ma) Dot/blot hemorrhages Mild NPDR 4

5 Mild NPDR Follow-up: annually 5-10% of pts with no retinopathy will progress to retinopathy within 1 year 5-10% with mild NPDR will also progress within 1 year Fundus photography helpful to document when there is a need to document baseline characteristics FA/laser not indicated Moderate NPDR Marked hemorrhages/ma Cotton wool spots (CWS) Venous beading (VB) Intra-retinal microvascular abnormalities to mild degree (IRMA s) Moderate NPDR Follow Up: 6 months as many as 16% of pts with mod NPDR can progress to proliferative disease within 4 years Fundus photography is helpful to document extent of retinopathy and to evaluate changes at subsequent visits FA/laser not indicated Severe/ Very Severe NPDR Rule: Marked hemes/ma in all 4 quadrants VB in 2 or more quadrants Marked IRMA s in one quadrant Very severe: 2 of the 3 above criteria Severe/Very Severe NPDR Follow-up: 3-4 months Between 10-50% of pts with this level progress to PDR within 1 year Laser is sometimes recommended Type 2 DM, associated with a 50% reduction in the rate of severe vision loss, vitrectomy and progression to high-risk PDR based on other factors including access to care, compliance, status of other eye, systemic control, and family history Severe/Very Severe NPDR FA generally not indicated although it may be useful in select cases to determine the presence/absence of non-perfusion and areas of occult neovascularization Fundus photos often helpful to document extent of retinopathy and to determine change at subsequent visits 5

6 Proliferative Diabetic Retinopathy (PDR) Hallmark is retinal neovascularization response to ischemia from capillary closure grow onto lattice of vitreous new vessels are fragile and easily rupture Neo divided into 2 categories NVD: on or within 2 DD of optic disc NVE: neovascularization elsewhere PDR Follow-up: Retinal consult within 2 weeks Most advocate PRP at this stage due to substantial lower risk of SVL and vitrectomy as noted previous If no laser, follow 2-3 months to look for HRC FA not indicated Color photos helpful High Risk PDR NVD >1/4 to 1/3 disc area Any NVD with a PRH or VH Moderate to severe NVE with VH or PRH Poses very high risk of severe VH and vision loss within 2 years High-risk PDR Immediate Retinal consult (24-48 hours) Prompt PRP is indicated FA usually not indicated unless concurrent CSME Fundus photography helpful to document extent of PDR and response to treatment If no response to PRP, possible need for vitrectomy Pan-Retinal Photocoagulation (PRP) Traditional treatment for proliferative disease Laser applied to retina, destroying parts Eliminates need for oxygen, thereby decreasing vasoproliferative stimulus Elimination of hypoxia causes regression of new vessel growth Not without complications: decreased VF, decreased night vision, CME ETDRS and DRS Proved benefit of immediate PRP Showed an overall reduction rate of severe vision loss (ie 5/200) of approximately 50% in treated vs. untreated eyes <4% chance of severe vision loss in 5 years w/ tx PRP in 2 to 3 sessions ( spots) Treat CSME first, if present 6

7 ETDRS and DRS 60-87% reduction in severe vision loss (5/200 or worse on 2 consecutive visits) after 3 years 97% reduction in bilateral SVL after 3 years 90% reduction in legal blindness after 5 years Clinically Significant Macular Edema(CSME) Characteristics retinal thickening at or within 500 microns (1/3 DD) of center of macula hard exudates at or within 1/3 DD if associated with thickening of adjacent retina thickening greater than 1 DD in size part of which is within 1 DD of center of macular May occur at any stage of retinopathy Treatment: retinal consult within 2 weeks CSME Focal Macular Laser (FML) Level of Retinopathy mild NPDR 3% incidence of DME moderate to severe NPDR 40% Proliferative 71% Type 2: Duration and Insulin no insulin 10 years 5% 20 years 15% on insulin 10 years 10% 20 years 30-35% Standard Treatment for CSME ETDRS: proved benefit of FML in improving vision Reduces the risk of moderate vision loss (doubling of the visual angle) from 30% to less than 15% so 50% reduction in MVL after 3 years Real goal is to prevent further loss, not to improve vision What is Hypertension? Affects 70 million Americans Essen6al HTN Malignant HTN Secondary HTN SYSTOLIC DIASTOLIC Normal <120 <80 Prehypertension Stage hypertension Stage 2 hypertension >160 >100 Essen6al HTN >140/90 Most common type of HTN 90-95% Family History common Risk Factors include: Sedentary lifestyle, smoking, stress, alcohol intake, obesity, high sodium intake, vitamin D deficiency, aging Usually controlled with 1 or 2 oral meds 7

8 Secondary HTN By defini6on results from an iden6fiable cause Cushings Syndrome Hypo/hyperthyroidism Kidney disease Pregnancy (pre- eclampsia) Coarcta6on of the aorta Certain prescrip6on and illegal dugs Ocular findings Papillidema Exudates CWS FSH AV changes Malignant HTN BP>210/130 Systemic Findings None HA s Vomi6ng Coma Malignant HTN Immediate referral for BP lowering ER or PCP MRI to r/o space occupying lesion MRA to r/o venous sinus thrombus LP if needed Malignant HTN 80% of pa6ents with malignant HTN die within 1 year 95% mortality within 3 years Hypertension Other Complications Retinopathy Left ventricular Hypertrophy Angina Myocardial infarction Heart Failure Stroke Peripheral vascular disease Chronic kidney disease Hypertension Risk Each increase of 20 mmhg systolic or 10 mmhg diastolic doubles risk of complications Risk reduction with treatment 35-40% reduction in stroke 20-25% reduction in myocardial infarction >50% reduction in heart failure 8

9 Hypertension Treatment Lifestyle Weight reduction BMI goal Diet Sodium restriction DASH diet Dietary Approaches to Stop Hypertension Physical activity Moderation of alcohol consumption DASH Diet Dietary Approaches to Stop Hypertension Proven to lower BP in as little as 14 days Best with moderate or less or pre-hypertension Includes whole grains, poultry, fish, and nuts and has reduced amounts of fats, red meats, sweets, and sugared beverages. Hypertension Treatment Medical management Thiazide diuretics (hydrochlorothiazide) Work by helping body reduce sodium and water thereby decreasing blood volume Beta blockers (atenolol) Reduce workload on heart, causing decreased heart rate Angiotensin-converting enzyme (ACE) inhibitors (lisinopril, captopril) Help relax blood vessels by blocking the formation of enzymes which narrow blood vessels Hypertension Treatment Medical management, cont Angiotensin II receptor blockers (losartan) Relax blood vessels by blocking action of the enzymes which narrow blood vessels Calcium Channel Blockers (verapamil, diltiazem) Help relax the smooth muscles of the arteries and heart, thereby decreasing blood pressure Renin inhibitors (aliskiren) Newer drug which works on renin, an enzyme produced in the kidneys which starts hypertensive cascade Pts with HTN retinopathy suffer (obviously) from systemic HTN However, at times, this may be first clue to pts underlying disease Pts are almost always asymptomatic, unless they have rare finding of edema or papilladema, which would cause decreased acuity Typically pts with HTN retinopathy are middle aged or older HTN more common in middle aged men- han women But more common in elderly woman than elderly men Much more prevalent in African-Americans than Caucasians 9

10 Clinical findings include Retinal artery narrowing and attenuation Retinal artery nicking and crossing changes Flame shaped hemes Cotton wool spots Rarely retinal or macula edema May have macular star Disc edema Keith Wagner Baker Classification System Grade 1 Hypertensive Retinopathy Retinal arterial narrowing and straightening Grade 2 AV Nicking Keith Wagner Baker Classification System Grade 3 Retinal hemorrhages Cotton wool spots Hard exudates Macular star Keith Wagner Baker Classification System Grade 4 Grade 3 with ONH edema Rare to have either macula edema or optic disc edema unless there is malignant HTN, where BP is elevated in 250/150 range However presentation of macular star and disc edema is almost pathognomonic for HTN crisis CWS typically do not appear until diastolic BP is > 110 Hypertensive Choroidopathy Choroid may also be affected by hypertension, esp when BP is elevated very rapidly Elschnig s Spots Patches of chorioretinal atrophy Siegrist s streaks Pigmented linear band or bands of chorioretinal atrophy 10

11 Monitor fundus q 12 months Sooner if severe Pt education Management involves appropriate tx of underlying HTN, with referral to primary care physician or internist If papilledema from HTN, consider medical emergency!! Immediate referral and/or trip to ER!! What is Obesity? Increased body weight caused by excessive accumulation of fat BMI defined as patient s weight (kg) divided by height (m 2 ) BMI categories of obesity Obesity Moderate obesity Extreme obesity over 40 Statistics 1/3 of US adults are obese 1 in 6 US children is overweight #2 modifiable risk factor for death (tobacco) May result in reduced life expectancy for the 1 st time in 200 years! Obese patients have 6.7 years less life expectancy than non-obese patients New England Journal of Medicine 300,000 Deaths Each Year (Directly Related) Obesity: Ocular Complications AMD Diabetic retinopathy Cataract Pseudotumor cerebri (papilledema) Floppy lid syndrome Ocular hypertension Exophthalmos/proptosis Obesity: Systemic Complications HTN Dyslipidemia Type 2 DM CAD Stroke Gall bladder disease Osteoarthritis Malignancies 11

Diabetic Retinopatathy

Diabetic Retinopatathy Jay M. Haynie, OD, FAAO Financial Disclosure I have received honoraria or am on the advisory board for the following companies: Carl Zeiss Meditec Arctic DX Macula Risk Advanced