Diabetes Care in the Elderly in Residential Care - a focus on hypoglycemic medications (Nursing In-Service)
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Provided to the nursing staff at Evergreen House, North Vancouver on September 9th and September 11th, 2013.
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Diabetes Care in the Elderly in Residential Care - a focus on hypoglycemic medications (Nursing In-Service)
- 1. Nursing In-Service: Diabetes Care in the Elderly in Residential Care focus on anti-hyperglycemic medications Evergreen House, Lion’s Gate Hospital September 9 & 11, 2013 Joan Ng, B. Sc. Pharm, Pharmacy Resident 1
- 2. Outline of Presentation 1. Pathophysiology 2. Diagnosis 3. Signs & Symptoms 4. Considerations in Elderly 5. Goals of Therapy & Treatment Targets 6. Treatment: non-drug measures & drug therapy 7. Insulin sliding scale vs. correctional insulin 8. Case Study: BT 9. Management of hypoglycemia 2
- 3. Pathophysiology of Diabetes • Diabetes Mellitus – Metabolic disorder characterized by hyperglycemia, due to defective insulin secretion, impaired insulin sensitivity, or both – T1DM (Insulin dependent) – T2DM (Non-insulin dependent) – Gestational Diabetes – Chronic hyperglycemia complications 3Reference: 1,2
- 5. Signs & Symptoms • Fatigue • Polyuria, polydipsia, weight loss • Complications: retinopathy, neuropathy, nephropathy, foot ulcers, erectile dysfunction • Diabetic ketoacidosis • Elderly: – Less glucosuria, polyuria, polydipsia – More confusion, incontinence 5Reference: 2, 3, 4
- 6. Considerations in Elderly • Most LTC patients are “frail elderly” – Multiple chronic illnesses with associated vulnerabilities (e.g. dementia, falls, polypharmacy) • Increased hypoglycemia risk with treatment – Diminished hypoglycemia counterregulation – More neuroglycopenic symptoms – Associated with poorer outcomes (CV events) – Leads to impaired cognition and function • Drug pharmacokinetics are changed 6Reference:
- 7. Goals of Therapy & Treatment Targets • Control symptoms • Glycemic control • Prevent/minimize complications • Reduce all CV risk factors • LTC Elderly: – HbA1c: 8-8.5% – Random BG: 7-14 mmol/L 7Reference: 1, 2, 6
- 8. Treatment: non-drug measures • Exercise: –Can improve insulin sensitivity –Encourage in those able to mobilize • Diet: –Caution against limiting caloric intake in LTC • Patients often already have insufficient caloric intake due to confusion, dysphagia, anorexia 8Reference: 1
- 9. Treatment: Metformin • Biguanide; hepatic glucose production, insulin sensitivity • 250-500mg qd 1g po bid (max 2550mg/day) • Elderly: should not be titrated to max dose • Pros: no hypoglycemia alone, good evidence • Cons: causes anorexia and weight loss, risk of lactic acidosis (renal/hepatic dysfunction), risk of B12 and folate deficiency long-term 9Reference: 2, 4, 5, 7, 10
- 10. Treatment: Sulfonylureas (Gliclazide, Glyburide) • Increases beta-cell insulin release, increases peripheral glucose utilization • Gliclazide: 40mg po bid 80mg po bid (regular release), 30mg MR qd 120mg MR qd • Pros: very effective, gliclazide less hypoglycemia than glyburide • Cons: hypoglycemia, needs consistent food intake, needs functioning beta-cells, weight gain 10Reference: 2, 4, 10
- 11. Treatment: Other Drugs Formulary: • Acarbose (brand: Glucobay, Prandase) • Thiazolidinendiones (pioglitazone) Non-formulary: • Meglitinides (repaglinide, nateglinide) • DPP-4 Inhibitors (sitagliptin, saxagliptin) • Incretin Mimetics (exenatide, liraglutide) 11
- 12. Treatment: Insulin - types • Rapid acting: insulin lispro, aspart, glulisine • Short acting: insulin regular • Intermediate acting: NPH • Long-acting: insulin detemir, glargine 12Reference: 2, 4, 8, 10 TYPE OF INSULIN TIME OF ONSET DURATION OF ACTION Basal insulin Glargine (Lantus) 1 to 2 hours 24 hours Detemir (Levemir) 1 to 2 hours 18 to 24 hours Isophane (NPH) 1 to 2 hours 10 to 20 hours Nutritional and correctional insulin Lispro (Humalog), aspart (Novolog), glulisine (Apidra) 5 to 15 minutes 3 to 6 hours Regular human insulin 1 to 02 hours 6 to 10 hours
- 13. Treatment: Insulin - regimens • Basal qhs insulin + oral hypoglycemics • Conventional regimens: qd – tid insulin • Intensive: basal + regular/rapid tid ac • Intensive continuous SC infusion • Acute: insulin sliding scale, correctional insulin • Pros: long-term safety and outcome evidence • Cons: hypoglycemia, weight gain, blood glucose monitoring imperative 13Reference: 2, 4, 8, 10
- 14. Insulin sliding scale vs. correctional: What is different? • Sliding Scale Insulin – Traditionally: regular/short-acting insulin to treat hyperglycemia after it has occurred – (now, almost always give basal insulin too) – Reactive, not proactive; possible insulin stacking • Physiological SC insulin protocol – Basal insulin (NPH or glargine) – Prandial/meal-time insulin (regular or short-acting) – Correctional-dose insulin (fine-tuning) 14Reference: 8, 9
- 15. SSI(+basal) vs physiologic insulin 15
- 16. Case Study: BT • 55yo female on EGH 3S • T2DM diagnosed 2005, previous poor control • alcoholic cirrhosis, history of IDU, BPD • Current drug therapy: – Insulin glargine (lantus) 18u q am, 15u q dinner – Insulin regular sliding scale at 0800, 1100, 1630 – Metformin 750mg bid 16
- 17. Case Study: BT- CBG control 17 Date Time Before breakfast Before Lunch Before Supper Bedtime Sliding Scale Given 9/1 0750 14.9 none 9/1 1155 23.1 10 units insulin regular 9/1 1600 28.1 14 units insulin given 9/1 2145 12.7 N/A 9/2 0730 21.5 10 units insulin regular 9/2 1130 21.6 none? 9/2 1645 17.1 5 units insulin regular • Suboptimal control • Nursing labour intensive: 3-4 times daily CBGs
- 18. Case Study: BT Recommendation: • change to regular tid prandial insulin + basal insulin at bedtime • Initially: 0.3-0.6 U/kg body weight total daily dose – ½ basal, ½ regular tid before meals • Measure BG more regularly in beginning, but when patient stabilizes, can decrease monitoring
- 19. Management of Hypoglycemia • Hypoglycemia: CBG <4.0 mmol/L • If patient is on acarbose, must give glucose • retest BG in 15 mins, re-treat with another 15 g carbohydrate if BG still <4.0 mmol/L 19Reference: 1
- 20. Questions? 20
- 21. References 1. Canadian Diabetes Association Clinical Practice Guidelines Expert Committee. Canadian Diabetes Association 2013 Clinical Practice Guidelines for the Prevention and Management of Diabetes in Canada. Can J Diabetes 2013;37(suppl 1):S1-S212. 2. Chau D, Edelman SV. Clinical Management of Diabetes in the Elderly. Clin Diabetes. 2001 Oct 1;19(4):172–5. 3. e-Therapeutics+ : Therapeutic Choices : Endocrine and Metabolic Disorders: Diabetes Mellitus [Internet]. [cited 2013 Sep 3]. Available from: https://www-e-therapeutics-ca. 4. Treatment of type 2 diabetes mellitus in the elderly patient [Internet]. [cited 2013 Sep 1]. Available from: https://uptodate.vch.ca/ 5. Laubscher T, Regier L, Bareham J. Diabetes in the frail elderly Individualization of glycemic management. Can Fam Physician. 2012 May 1;58(5):543–6. 6. American Diabetes Association. Diagnosis and Classification of Diabetes Mellitus. Diabetes Care. 2012 Dec 20;36(Supplement_1):S67–S74. 7. Lee M, Jensen B, Regier L. Oral Anti-Hyperglycemic Agents - Comparison chart. RxFiles drug comparison charts. 7th ed. Saskatoon, SK: Saskatoon Health Region; 2012. p. 25. Available from: www.RxFiles.ca. Accessed 2013 Sep 3. 8. Nau KC, Lorenzetti RC, Cucuzzella M, Devine T, Kline J. Glycemic control in hospitalized patients not in intensive care: beyond sliding-scale insulin. Am Fam Physician. 2010 May 1;81(9):1130–5. 9. Hirsch IB. SLiding scale insulin—time to stop sliding. JAMA. 2009 Jan 14;301(2):213–4. 10. Acarbose, Metformin, Gliclazide, Repaglinide, Sitagliptin, Exenatide, Liraglutide, Insulin. Lexi-Drugs Online [Internet]. Hudson (OH) : Lexi-Comp, Inc. 1978-2013 [cited 2013 Sep 5]. Available from: http://online.lexi.com. 21
- 22. Treatment: Acarbose • Alpha-glucosidase inhibitor in intestines – Delays digestion of complex carbs/disaccharides – Slower rise in postprandial glucose • 25mg qd 50-100mg tid cc • Not recommended if CrCl <25mL/min • Pros: safe, little hypoglycemia • Cons: less effective than other agents, GI side effects (flatulence, diarrhea) 22Reference: 2, 4, 10
- 23. Treatment: Meglitinides • Short-acting insulin secretagogues, stimulates beta-cell insulin release at meals • Repaglinide: 0.5mg tid ac 4mg po tid ac • Pros: less hypoglycemia than sulfonylureas, flexible with food intake • Cons: lack outcome data on morbidity/mortality 23Reference: 2, 4, 10
- 24. Treatment: Thiazolidinediones • Enhances insulin effects by activating PPAR- alpha receptor in cells • Pioglitazone: 15mg qd 45mg qd • Pros: no hypoglycemia • Cons: limited usefulness in elderly (fluid retention, CHF, MI, fractures) 24Reference: 2, 4
- 25. Treatment: DPP-IV Inhibitors • Dipeptidyl peptidase-4 inhibitors; increases insulin secretion by ↑incretin, ↓glucagon • Sitagliptin: 100mg qd; Saxagliptin: 2.5-5mg qd • Pros: no hypoglycemia, weight-neutral • Cons: no long-term safety data, expensive 25Reference: 2,4,7,10
- 26. Treatment: GLP-1 Therapies • Incretin mimetics, increases insulin secretion • Exenatide (Byetta): 5-10ug sc bid ac • Liraglutide (Victoza): 0.6-1.2mg sc daily • Pros: no risk of hypoglycemia • Cons: causes weight loss, nausea, diarrhea 26Reference: 4, 7, 10
Notes de l'éditeur
- Brief Pathophysiology: What is Diabetes? Diabetes Mellitus (DM) = Diabetes comes from a Greek word, meaning siphon (describes polyuria), and Mellitus comes from a Latin word, meaning honey (urine is sweet, high in sugars) = metabolic disorder characterized by presence of hyperglycemia, due to defective insulin secretion/action, or both (1) Type 1: Insulin Dependent DM Type 1 diabetes* encompasses diabetes that is primarily a result of pancreatic beta cell destruction and is prone to ketoacidosis. This form includes cases due to an autoimmune process and those for which the etiology of beta cell destruction is unknown. Often presents in young patients, but lean elderly diabetic patients can exhibit autoimmune changes, with islet cell antibodies and insulin deficiency (2) Type 2: Non-insulin dependent DM Type 2 diabetes may range from predominant insulin resistance with relative insulin deficiency to a predominant secretory defect with insulin resistance. Also Gestational diabetes Chronic hyperglycemia microvascular complications: retinopathy, nephropathy, neuropathy, and macrovascular complications (Cardiovascular disease) (1)
- Diabetes mellitus may present in a variety of settings:(3) asymptomatic; incidental discovery through routine laboratory screening nonspecific signs and symptoms such as fatigue, lassitude, weight changes presence of diabetic complications such as macrovascular or microvascular changes, neuropathy, kidney disease, erectile dysfunction acute metabolic symptoms such as polyuria, polydipsia, weight loss diabetic ketoacidosis Elderly: (2) age-related changes – affect clinical presentation of diabetes(2) renal threshold for glucose increases: glucosuria not seen at usual levels(2) tolerate relatively higher blood glucose levels before manifest osmotic diuresis (lower GFRs, lower glucose load delivered to tubules for reabsrption) (4) polydipsia absent because of decreased thirst with increased age dehydration common confusion, incontinence, and complications (e.g. neuropathy/retinopathy) are presenting symptoms complications: neuropathy, nephropathy, retinopathy, erectile dysfunction, foot ulcers, plus diabetic neuropathic cachexia, amyotrophy, malignant otitis externa, pappilary necrosis, osteoporosis Diabetic Ketoacidosis Diabetic ketoacidosis ( DKA ) is a potentially life-threatening complication in patients with diabetes mellitus . It happens predominantly in those with type 1 diabetes , but it can occur in those with type 2 diabetes under certain circumstances. DKA results from a shortage of insulin ; in response the body switches to burning fatty acids and producing acidic ketone bodies that cause most of the symptoms and complications. [1] DKA may be the first symptom of previously undiagnosed diabetes, but it may also occur in people known to have diabetes as a result of a variety of causes, such as intercurrent illness or poor compliance with insulin therapy . Vomiting , dehydration , deep gasping breathing , confusion and occasionally coma are typical symptoms. DKA is diagnosed with blood and urine tests ; it is distinguished from other, rarer forms of ketoacidosis by the presence of high blood sugar levels. Treatment involves intravenous fluids to correct dehydration, insulin to suppress the production of ketone bodies, treatment for any underlying causes such as infections, and close observation to prevent and identify complications. [1] [2] DKA is a medical emergency , and without treatment it can lead to death. DKA was first described in 1886; until the introduction of insulin therapy in the 1920s it was almost universally fatal. [3] It now carries a mortality of less than 1% with adequate and timely treatment. [4]
- Frail elderly (Definition): pts with accumulation of multiple chronic illnesses with associated vulnerabilities (dementia, functional decline, geriatric syndrome including falls, impaired mobility, and polypharmacy)(5) Increased hypoglycemia risk: (2) elderly patients glucose counterregulation (glucagon, epinephrine, growth hormone) to hypoglycemia is diminished reduced autonomic warning symptoms(2) autonomic neuropathy and decreased beta-receptor response also result in absense of typical hypoglycemic symptoms (5) more neuroglycopenic manifestations (dizziness, weakness, delirium, confusion) than adrenergic (tremors, sweating)(4) also delayed psychomotor responses to intervene in the correction of hypoglycemia associated with poorer outcomes – traumatic falls, exacerbation of comorbid conditions (4) lead to impaired cognition and function(4) **insulin secretagogues (sulfonylureas and meglitinides) and insulin should be used with caution in frail elderly (2) Can be severe, and precipitate cardiovascular events (5) Changes to PK of insulin and oral medications: (2) affect individual drug choices and dosing decisions
- Goals of Therapy (TC) Control symptoms Establish and maintain glycemic control, while avoiding hypoglycemia Prevent or minimize the risk of complications Achieve optimal control of associated risk factors such as hypertension, obesity and dyslipidemia Base on evaluation of functional status, life expectancy, social and financial support, own desires for treatment. (2) Reduce all CVD risk factors, smoking cessation, improvement in exercise, elimination of obesity, optimal control of hypertension. (2) HbA1c below 8-8.5% is reasonable, random BG between 7-14 mmol/L reasonable. (6) ACCORD, ADVANCE, VADT: confirmed the benefit of intensive glycemic control on microvascular outcomes (1) None of the above studies independently confirmed a significant benefit of tight glycemic control on macrovascular outcomes meta-analysis: those treated with more intensive therapy, compared to less intensive glycemic control, were found to have a 10% to 15% reduction in the risk of major CV events, primarily because of a 15% reduced risk of MI, but with no effect on stroke, CV death or all cause mortality Intensive glycemic control, associated with more than a 2-fold increase in the risk of severe hypoglycemia Increased mortality/lack of macro benefits: suggested factors: patient age, duration of diabetes, presence of CVD, history of severe hypoglycemic events, weight gain and the rapid decrease in A1C values
- Rxfiles: if CrCl <60, dose should be =< 850-1700mg/d Decreases morbidity and mortality Lactic acidosis is a physiological condition characterized by low pH in body tissues and blood ( acidosis ) accompanied by the buildup of lactate, especially D-lactate, and is considered a distinct form of metabolic acidosis. [1] The condition typically occurs when cells receive too little oxygen (hypoxia), for example, during vigorous exercise. In this situation, impaired cellular respiration leads to lower pH levels. Simultaneously, cells are forced to metabolize glucose anaerobically, which leads to lactate formation. Therefore, elevated lactate is indicative of tissue hypoxia, hypoperfusion, and possible damage. Lactic acidosis is characterized by lactate levels >5 mmol/L and serum pH <7.35 [U.S. Boxed Warning]: Lactic acidosis is a rare, but potentially severe consequence of therapy with metformin that requires urgent care and hospitalization. The risk is increased in patients with acute congestive heart failure, dehydration, excessive alcohol intake, hepatic or renal impairment, or sepsis. Symptoms may be nonspecific (eg, abdominal distress, malaise, myalgia, respiratory distress, somnolence); low pH, increased anion gap and elevated blood lactate may be observed. Discontinue immediately if acidosis is suspected. Lactic acidosis should be suspected in any patient with diabetes receiving metformin with evidence of acidosis but without evidence of ketoacidosis. Discontinue metformin in patients with conditions associated with dehydration, sepsis, or hypoxemia. The risk of accumulation and lactic acidosis increases with the degree of impairment of renal function.
- Discussing all the different types of regimens is beyond the scope of this presentation (insulin therapy itself can be its on presentation!) but briefly…
- Prospective observational studies have documented superior glycemic control with this three-pronged physiologic approach. Randomized Study of Basal Bolus Insulin Therapy in the Inpatient Management of Patients with Type 2 Diabetes Compared traditional SSI to new basal-bolus glargine + glulisine (and correctional) – basal-bolus better control (8) 3 components of insulin in physiologic subcutaneous insulin protocols: Basal insulin (usually NPH or glargine, inhibits hepatic glucose production overnight and between meals)(9) RCT of Lantus…bariatric surgery…superior glycemic control compared to SSI Prandial insulin (regular release or short-acting analogues, bolus or meal-time) (9) Correction-dose insulin (usually given in addition to the usual dose of mealtime insulin as a specific algorithm based on total daily dose of insulin or patient weight) Resembles SSI, but is actually only small fine-tuning therapy Initial dose: 0.3-0.6 U/kg body weight, ½ basal, ½ divided daily over 3 meals (8), plus correctional to provide final insulin adjustment based on preprandial glucose value Sliding Scale: different. Traditionally includes regular insulin or rapid-acting analogue to treat hyperglycemia after it had already occurred – often no insulin is given if premeal glucose levels are within target range (9) Reactive, not proactive(9) Does not take into account basal insulin needs, diet, personal characteristics, or insulin history (8) --now, basal insulin is often included in regimen Physicians only notified of extremes of hypoglycemia or hyperglycemia (8) Possibility of insulin stacking (PK of regular insulin given every 6 hours) (8) (Medscape: 8 hr duration) No way to anticipate nutritional status or illness-related changes in glucose levels roller coaster fluctuations in blood glucose (8) Not very effective: MEDLINE search of 52 trials from 1966-2003 – no report of benefit (9) Has been used for ~50 years because it is convenient and straightforward to administer(9)