8/28/2017. Learning Objectives. Microvascular Complications

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1 Microvascular Complications: Implications for Providers and their Patients with Diabetes Eileen Egan, DNP, FNP C, CDE Chief Nurse Practitioner NYU Winthrop Endocrine, Diabetes and Metabolism Faculty Practice Stony Brook University, Adjunct Clinical Instructor Learning Objectives Define nephropathy, retinopathy, and neuropathy List at least 1 physical symptom of nephropathy, retinopathy, and neuropathy Identify diagnostic criteria for nephropathy, retinopathy, and neuropathy Identify 1 strategy to improve patient outcomes for nephropathy, retinopathy, and neuropathy List 1 treatment option for nephropathy, retinopathy, and neuropathy Microvascular Complications Nephropathy Diabetic kidney disease Retinopathy Diabetic eye disease Neuropathy Diabetic nerve disease Devastating impact on quality of life Incidence increases with duration of diabetes 1

Relative Risk Reduction with Enhanced Glycemic Control T1 DM DCCT 76% in retinopathy 50% in nephropathy

Relative Risk Reduction with Enhanced Glycemic Control T2 DM UKPDS 25% in microvascular complications 16%

cause mortality 18% in combined fatal & nonfatal MI Nephropathy Diabetic Kidney Disease Leading cause of

2 Relative Risk Reduction with Enhanced Glycemic Control T1 DM DCCT 76% in retinopathy 50% in nephropathy 60% in neuropathy EDIC 42% in any cardiovascular event 57% in nonfatal MI, stroke or death from CVD Relative Risk Reduction with Enhanced Glycemic Control T2 DM UKPDS 25% in microvascular complications 16% in fatal/nonfatal MI & sudden death For every 1% in A1C there was 25% in DM related deaths 7% in all cause mortality 18% in combined fatal & nonfatal MI Nephropathy Diabetic Kidney Disease Leading cause of end stage renal disease Strong relationship between DKD & CVD More prevalent in Blacks, Native Americans, & Hispanics 2

3 Diagnosis of Nephropathy Evaluate the serum estimated glomerular filtration rate (egfr) & the urine microalbumin/creatinine ration (ACR) egfr< 60 ml/min/ ACR> 30 mg/g creatinine Albuminuria is the 1 st clinical indicator Associated with risk of CVD, subsequent CVD events, & mortality Measure at least annually At diagnosis for patients w/ T2 DM At 5 years after diagnosis for patients w/ T1 DM Diagnosis of Nephropathy ACR can be influenced by several factors HTN, exercise, fever, infection, CHF, menses, marked hyperglycemia To make the diagnosis of DKD 2 elevated samples over a 6 month time span Achieving personal glycemic targets & BP control are essential in slowing progression Treatment of Nephropathy DKD w/ ACR >30mg/g creatinine Angiotensin converting enzyme inhibitor (ACE I) or an angiotensin receptor blocker (ARB) No data to support preventative use Combined use of an ACE I & ARB not recommended May increase hyperkalemia & acute kidney injury Review BMP periodically 3

Other considerations in Nephropathy Use of statins & fibrates Erythropoietin turnover & accuracy of A1C 66% risk of hypoglycemia w/ creatinine levels Re evaluation of medications Many DM medications

4 Other considerations in Nephropathy Use of statins & fibrates Erythropoietin turnover & accuracy of A1C 66% risk of hypoglycemia w/ creatinine levels Re evaluation of medications Many DM medications are dosed based on egfr Side effects of medications Stages of Kidney Disease Kidney damage is defines as abnormalities on pathologic, blood, urine, or imaging When to Refer Decline in egfr in the absence of albuminuria Heavy proteinuria, active urine sediment, & rapid decline in egfr IF DKD becomes difficult to manage due to comorbidities egfr<30 ml/min/ (stage 4 ) 4

Retinopathy Diabetic Eye Disease Leading cause of blindness Affects ~34% of people with DM worldwide/ 93 million people Risk Factors Duration of DM, HTN, pregnancy, nephropathy, & hyperglycemia

5 Retinopathy Diabetic Eye Disease Leading cause of blindness Affects ~34% of people with DM worldwide/ 93 million people Risk Factors Duration of DM, HTN, pregnancy, nephropathy, & hyperglycemia Increase risk for cataracts & glaucoma Diagnosis of Retinopathy Gold standards Dilated eye exam Stereoscopic 7 field fundus photography Fluorescein angiography pinpoints areas in need of intervention Early diagnosis & treatment can severe vision loss by 90% Clinical symptoms Often asymptomatic Spots, blank areas or floaters, cob web like strings, blurry, washed out colors Diagnosis of Retinopathy Type 2 diabetes Shortly after diagnosis T1 DM Within the first 5 years of diagnosis Annual exam May extend to every 2 years after 1 or more normal exam Pregnancy (if pre existing DM) Before conception otherwise 1 st trimester Every trimester For 1 year after delivery 5

Stages of Retinopathy Nonproliferative diabetic retinopathy (NPDR)

ischemia Staged as Mild, moderate, severe With or without macular edema Stages

retina narrow & close Neovascularization occurs Can affect both peripheral &

6 Stages of Retinopathy Nonproliferative diabetic retinopathy (NPDR) Microaneurysms Retinal hemorrhages Hard exudates Macular edema Macular ischemia Staged as Mild, moderate, severe With or without macular edema Stages of Retinopathy Proliferative Diabetic Retinopathy (PDR) Blood vessels in retina narrow & close Neovascularization occurs Can affect both peripheral & central vision Vitreous hemorrhage Tractional retinal detachment Neovascular glaucoma The Diabetic Eye 6

Treatment of Retinopathy Panretinal photocoagulation laser (PRP) Reduces risk of additional vision loss Shrinks vessels & reduces swelling Intraocular steroid & Intraocular vascular endothelial

7 Treatment of Retinopathy Panretinal photocoagulation laser (PRP) Reduces risk of additional vision loss Shrinks vessels & reduces swelling Intraocular steroid & Intraocular vascular endothelial growth factor (VEGF) Used alone or in supplement to PRP Superior to use of PRP alone in macular edema Vitrectomy Surgical removal of fibrous proliferation & hemorrhage Relieves tractional detachment of retina Neuropathy Diabetic Nerve Disease Most prevalent & chronic complication of DM Diabetic peripheral neuropathy (DPN) Diabetic autonomic neuropathy (DAN) cardiovascular autonomic neuropathy (CAN) most prevalent Heterogeneous group of conditions Impacts many organ systems & bodily functions Diverse clinical manifestations Diabetic Neuropathy Early recognition & management is vital diagnosis of exclusion Patients are often asymptomatic Treatment options exist for symptom relief No effective treatment to reverse underlying nerve damage Goal is to reduce sequelae and improve quality of life Optimize glucose control as early as possible 7

8 Relative Risk Reduction with Enhanced Glucose Control. T1 DM: 78% for DSPN 31 45% for CAN T2 DM: 5 9% for DSPN: comorbidities, polypharmacy, weight gain, undiagnosed T2 DM lead to inconsistent outcomes 60% for CAN with multifactorial approach: lifestyle, glucose, lipids DPN Small fiber Pain & dysthesias Large fiber Numbness & loss of protective sensation Up to 50% of patients have no symptoms Impact on quality of life Depression, social dysfunction, sleep altering pain Diagnosis of DPN Response to pinprick Light touch with a 10 g monofilament Ankle reflexes Vibration threshold with a 128 Hz tuning fork Michigan Neuropathy Screening Instrument & Michigan Diabetic Neuropathy Score 8

vibration Does the patient feel the vibration eyes are closed Does the perception of vibration fade before the vibration stops?

9 10 g Monofilament Test Place the device perpendicular to the skin, apply pressure until it buckles Hold in place for 1 second & release Place at highlighted siteswith the patient s eyes closed 128 Hz Tuning Fork Exam Assess for patient s perception of vibration Does the patient feel the vibration eyes are closed Does the perception of vibration fade before the vibration stops? Ankle Reflex Exam Support the ball of the foot Gently strike the Achilles tendon with a rubber hammer Watch for plantar flexion of the foot 9

When to Refer Neurology referral rarely needed Unless symptoms are unclear Do refer to podiatry in particular if loss of protective sensation exists Electrophysiological testing Nerve conduction

10 When to Refer Neurology referral rarely needed Unless symptoms are unclear Do refer to podiatry in particular if loss of protective sensation exists Electrophysiological testing Nerve conduction study Treatment of DPN FDA approved Pregabalin (Lyrica), duloxetine (Cymbalta) Not FDA approved, but options Capsaicin cream, gabapentin, tricyclic antidepressants, tramadol, venlafaxine, & carbamazepine Trial & error Symptom reduction Nothing reverses neuronal loss DAN Cardiovascular Reduced hear rate variability, resting tachycardia, orthostatic hypotension Gastrointestinal Gastroparesis, enteropathy, hypomotility Urogenital ED, female sexual dysfunction, neurogenic bladder Sudomotor dysfunction Gustatory sweating, hypohydrosis/anhidrosis Hypoglycemic unawareness 10

Cardiovascular Autonomic Neuropathy (CAN) Incidence of CAN increases with duration of DM 30% of those with T1DM after 20 years 60% of those witht2 DM after 15 years CAN is an independent risk factor

11 Cardiovascular Autonomic Neuropathy (CAN) Incidence of CAN increases with duration of DM 30% of those with T1DM after 20 years 60% of those witht2 DM after 15 years CAN is an independent risk factor for CV mortality, arrhythmia, silent ischemia, any major CV event, & myocardial dysfunction CAN includes: Orthostatic hypotension, Resting tachycardia, & Exercise intolerance CAN independently predicts the progression of DM Nephropathy & CKD in DM Clinical Signs of Cardiovascular Autonomic Neuropathy Impaired heart rate variability no change in HR noted with deep breathing, exercise, position changes Increased resting HR resting tachycardia >100bpm Orthostatic hypotension & orthostatic tachycardia or bradycardia Light headed, weak, faint, dizziness, palpitations, syncope upon standing, visual impairment Diagnosis of CAN EKG During 1 2 minutes of deep breathing As patient rises from seated position Orthostatic blood pressures in SBP or DBP by >20 or >10 respectively, upon standing, without an in HR despite hypotension If other microvascular complications exist, in particular hypoglycemic unawareness, evaluate for CAN Exclude drugs & co morbidities that may mimic symptoms: Beta blockers, diuretics, opioids, anticholinergics Anemia, dehydration, underlying arrhythmia, thyroid disease, adrenal insufficiency Smoking, alcohol, caffeine, recreational drugs 11

Treatment Options for CAN Symptom alleviation, nothing reverses it Midodrine (ProAmatine) Selective alpha1 adrenoreceptor agonist binds to noradrenalin receptors causing blood vessels to narrow & BP

12 Treatment Options for CAN Symptom alleviation, nothing reverses it Midodrine (ProAmatine) Selective alpha1 adrenoreceptor agonist binds to noradrenalin receptors causing blood vessels to narrow & BP to rise Droxidopa (Northera) Pro drug to norepinephrine increases levels of epinephrine in peripheral nervous system enabling body to maintain blood flow while standing Fludrocortisone (Florinef) Corticosteroid that can assist with volume repletion by causing the kidneys to retain sodium Gastroparesis Slowed/ delayed gastric emptying Direct effect on glycemic variability Impacts quality of life Impacts absorption of nutrients Not enough large clinical trials to indicate prevalence Seems to be more common in T1 DM Evaluate patients with long duration of DM and/or with other neuropathies Diagnosis of Gastroparesis time to refer Exclude other causes: opioids, GLPs, obstruction Gastric emptying study Measures gastric emptying w/ scintigraphy of digestible solids at 15 minute intervals for 4 hours after ingestion C octanoic acid breath test Meal w/ c octanoic acid is labeled with carbon 13 & breath is analyzed at intervals for carbon dioxide Barium study & esophagogastroduodenoscopy to r/o obstruction or peptic ulcer disease Acute changes in glucose can alter gastric emptying and/or be symptoms of altered gastric emptying 12

Treatment Options for Gastroparesis Metoclopramide (Reglan) Not recommended for more than 5 days due to potential side effects Extrapyramidal dystonia, tardive dyskinesia, Parkinson like Withdraw

13 Treatment Options for Gastroparesis Metoclopramide (Reglan) Not recommended for more than 5 days due to potential side effects Extrapyramidal dystonia, tardive dyskinesia, Parkinson like Withdraw drugs that may alter motility Benadryl, opioids, GLPs, tricyclic antidepressants, Parkinson's drugs Dietary modification Gastric electrical stimulation/ Gastric pacemaker Hypoglycemic Unawareness Inability to recognize impending hypoglycemia Effects up to 40% of people with T1 DM Effects up 10% of people with T2 DM Causes Chronic exposure to hypoglycemia/ tight control Hypoglycemia= <70mg/dl Clinically significant Hypoglycemia= <54mg/dl Recurrent severe hypoglycemia Longer duration of DM Alcohol Diagnosis of Hypoglycemic Unawareness There are no clinical symptoms for the patient!! The patient s unawareness of lows makes the diagnosis Person may become confused or disoriented, have a seizure, or lose consciousness Increase risk for: arrhythmia, cognitive impairment, fractures, mortality/death May result in: depression, fear of low, sleep disruption, decreased adherence with medications & quality of life Incidence of severe low often prompts the discussion Ask about symptoms of low at every appointment 13

14 Treatment Options for Hypoglycemic Unawareness Setting higher glycemic targets Home glucose monitoring A1C Continuous glucose monitoring Insulin pump therapy or insulin analogues Exclude drugs that will interfere with autonomic responses Beta blockers, SSRIs Question.? Mrs. T has had T1 DM for 30 years. She also has HTN. Her A1C is 8% and her BP is 150/90. Recent testing reveals a first time elevation of ACR at 65 mcg/mg. Does she have nephropathy? Should you initiate medication based on the ACR? What about the BP? Question? Mr. G was diagnosed with T2 DM last month. He got new glasses a few months ago at the mall because his vision was blurry. He sees well now. Does he need to see an eye doctor again this year? How often should he see the eye doctor and what type of exam does he need? 14

15 Case Study: DPN Mr. M presents in your office for follow up. He has had T2 DM for 25 years. He reports pain in his feet at night, especially when the sheets touch his skin. The discomfort is disrupting his sleep. During the day he complains of numbness and like his skin is tight. Do you think he has DPN? What diagnostic testing could you perform in the office? Does he need a referral? Case Study: CAN Mr. H returns for a follow up visit. He has had T2 DM x 20 yrs DSPN and stage 3 CKD for the past 5 yrs. He states he is struggling with trying to balance carbs, salt, and fluid intake. As he gets up from the chair in the waiting room he states that he feels dizzy and sees stars. He reports this happens all the time and he recently fell in the shower. Since he last saw you he also had a silent MI. He was started on a new medication by his cardiologist, but he cannot recall the name. Do you think he has CAN? What diagnostic testing could you do? What strategies can you recommend to improve/reduce symptoms and promote safety for Mr. H? Case Study: Hypoglycemic Unawareness Mrs. M is a 65 y/o female with T1 DM since age 3. She recently started CAPD. Her A1C is 6.2%. She administers insulin via injection & feels she has a good handle on adjustments surrounding her CAPD. She checks her glucose in your office, at your request, because she seems distracted. Her glucose is 39mg/dl & she states she feels fine & just drove. When you review her log for the past week, you see frequent values <70mg/dl. When you ask her about these low values, she states it s no problem because I feel fine. Do you think she has hypoglycemic unawareness? What strategies can you recommend to improve outcomes and promote safety for Mrs. M? 15

16 Thank you any questions? 16

Diabetic Retinopathy and Neuropathy: 2018 Clinical Practice Guidelines

Diabetic Retinopathy and Neuropathy: 2018 Clinical Practice Guidelines Richard Arakaki, M.D. Phoenix Area Diabetes Consultant August 9 th 2018 Disclose no conflict of interest Complications and Co-morbidities