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Alcohol Withdrawal and Diabetes Mellitus Management October 20, 2014 Jennifer Bauman, RN, BA, PCCN PhD Student The Ohio State University College of Nursing.

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Presentation on theme: "Alcohol Withdrawal and Diabetes Mellitus Management October 20, 2014 Jennifer Bauman, RN, BA, PCCN PhD Student The Ohio State University College of Nursing."— Presentation transcript:

1 Alcohol Withdrawal and Diabetes Mellitus Management October 20, 2014 Jennifer Bauman, RN, BA, PCCN PhD Student The Ohio State University College of Nursing Nursing 6270 Autumn 2014

2 Objectives Define alcohol withdrawal. Discuss the CIWA scale. Describe nursing management of inpatient alcohol withdrawal. Define diabetes mellitus. Discuss nursing considerations for the hospitalized patient with diabetes mellitus. Describe medical and lifestyle (i.e., outpatient) management of diabetes mellitus.

3 Prevalence and Definition Estimated 8 million alcohol dependent individuals in the U.S. 500,000 episodes of alcohol withdrawal require pharmacological intervention Alcohol use disorder (DSM-V) As of September 17, 10/33 patients on 8PCU had a primary/admitting diagnosis of drug or alcohol intoxication/withdrawal (unknown number of patients had it listed as a secondary diagnosis) Estimated 15-20% of hospitalized patients afflicted by alcohol use disorder (Kosten et al., 2003)

4 DSM-V Diagnostic Criteria for Alcohol Use Disorder A problematic pattern of alcohol use leading to clinically significant impairment or distress, as manifested by at least two of the following, occurring within a 12-month period: Alcohol is often taken in larger amounts or over a longer period than was intended. There is a persistent desire or unsuccessful efforts to cut down or control alcohol use. A great deal of time is spent in activities necessary to obtain alcohol, use alcohol, or recover from its effects. Craving, or a strong desire or urge to use alcohol. Recurrent alcohol use resulting in a failure to fulfill major role obligations at work, school, or home. Continued alcohol use despite having persistent or recurrent social or interpersonal problems caused or exacerbated by the effects of alcohol. Important social, occupational, or recreational activities are given up or reduced because of alcohol use. Recurrent alcohol use in situations in which it is physically hazardous. Alcohol use is continued despite knowledge of having a persistent or recurrent physical or psychological problem that is likely to have been caused or exacerbated by alcohol. Tolerance, as defined by either of the following: – A need for markedly increased amounts of alcohol to achieve intoxication or desired effect. – A markedly diminished effect with continued use of the same amount of alcohol. Withdrawal, as manifested by either of the following: – The characteristic withdrawal syndrome for alcohol (refer to Criteria A and B of the criteria set for alcohol withdrawal). – Alcohol (or a closely related substance, such as a benzodiazepine) is taken to relieve or avoid withdrawal symptoms.

5 Specify if: In early remission: After full criteria for alcohol use disorder were previously met, none of the criteria for alcohol use disorder have been met for at least 3 months but for less than 12 months (with the exception that Criterion A4, “Craving, or a strong desire or urge to use alcohol,” may be met). In sustained remission: After full criteria for alcohol use disorder were previously met, none of the criteria for alcohol use disorder have been met at any time during a period of 12 months or longer (with the exception that Criterion A4, “Craving, or a strong desire or urge to use alcohol,” may be met). Specify if: In a controlled environment: This additional specifier is used if the individual is in an environment where access to alcohol is restricted (cont’d) DSM-V Diagnostic Criteria for Alcohol Use Disorder

6 Common, Fatal, Costly Problem Alcohol Use Disorders (AUDs) in the United States: – Adults (ages 18+): Approximately 17 million adults ages 18 and older (7.2 percent of this age group) had an AUD in 2012. This includes 11.2 million men (9.9 percent of men in this age group) and 5.7 million women (4.6 percent of women in this age group). 3 – Youth (ages 12–17): In 2012, an estimated 855,000 adolescents ages 12–17 (3.4 percent of this age group) had an AUD. This number includes 444,000 females (3.6 percent) and 411,000 males (3.2 percent). 5 Alcohol-Related Deaths: – Nearly 88,000 7 people (approximately 62,000 men and 26,000 women 8 ) die from alcohol related causes annually, making it the third leading preventable cause of death in the United States. 7 – In 2012, alcohol-impaired-driving fatalities accounted for 10,322 deaths (31 percent of overall driving fatalities). 9

7 Economic Burden: – In 2006, alcohol misuse problems cost the United States $223.5 billion. 10 – Almost three-quarters of the total cost of alcohol misuse is related to binge drinking. 10 Global Burden: – In 2012, 3.3 million deaths, or 5.9 percent of all global deaths (7.6 percent for men and 4 percent for women), were attributable to alcohol consumption. 11 – Alcohol contributes to over 200 diseases and injury-related health conditions, most notably alcohol dependence, liver cirrhosis, cancers, and injuries. 12 In 2012, alcohol accounted for 5.1 percent of disability adjusted life years (DALYs) worldwide. 11 – Globally, alcohol misuse is the fifth leading risk factor for premature death and disability; among people between the ages of 15 and 49, it is the first. 13 Family Consequences: – More than 10 percent of U.S. children live with a parent with alcohol problems, according to a 2012 study. 14 Common, Fatal, Costly Problem

8 (Ethyl) Alcohol = Ethanol Ethyl alcohol is the only type of consumable ethanol. Central nervous system (CNS) depressant Simultaneously enhances inhibitory tone via modulation of gamma-aminobutyric acid (GABA) activity and dampens excitatory tone via modulation of excitatory amino acid activity To keep the inhibitory and excitatory tones balanced (i.e., homeostasis), must have constant presence of ethanol. Abrupt cessation of ethanol creates an imbalance (i.e., interrupts homeostasis) = overactivity of CNS


10 Neurotransmitters Affected Remember that ethanol enhances inhibitory and dampens excitatory tones, resulting in CNS depression. GABA: major inhibitory neurotransmitter with very specific binding sites for ethanol. – Chronic ethanol use = insensitivity to GABA – More inhibitor is needed to maintain constant inhibitory tone = tolerance to large doses (think of the “functioning” alcoholic) Glutamate: one of the major excitatory amino acids – When glutamate binds to the N-methyl-D-aspartate (NMDA) receptor, calcium influx leads to neuronal excitation. – Ethanol dampens glutamate induced excitation. – Increasing sensitivity to glutamate = adaption, with the goal to maintain a normal state of arousal

11 Long term effects of Alcohol Misuse Liver disease – Cirrhosis “Among all cirrhosis deaths in 2009, 48.2 percent were alcohol related. The proportion of alcohol-related cirrhosis was highest (70.6 percent) among decedents ages 35–44”(NIAAA, 2014). However, only 5-10% of alcoholics develop cirrhosis – Fatty liver disease – Hepatitis – 1 in 3 liver transplants in 2009 were due to alcohol-related disease (NIAAA, 2014) Increased risk for cancer of mouth, esophagus, pharynx, larynx, liver, and breast Pancreatitis Malnutrition Wernicke’s Encephalopathy Higher risk for injury, especially falls Impaired judgment = high risk behavior = increased risk for STIs, sexual assault, etc.

12 Alcohol Withdrawal (If it doesn’t work, use this link:

13 DSM-V Diagnostic Criteria for Alcohol Withdrawal Cessation of (or reduction in) alcohol use that has been heavy and prolonged. Two (or more) of the following, developing within several hours to a few days after the cessation of (or reduction in) alcohol use described in Criterion A: – Autonomic hyperactivity (e.g., sweating or pulse rate greater than 100 bpm). – Increased hand tremor. – Insomnia. – Nausea or vomiting. – Transient visual, tactile, or auditory hallucinations or illusions. – Psychomotor agitation. – Anxiety. – Generalized tonic-clonic seizures.

14 The signs or symptoms in Criterion B cause clinically significant distress or impairment in social, occupational, or other important areas of functioning. The signs or symptoms are not attributable to another medical condition and are not better explained by another mental disorder, including intoxication or withdrawal from another substance. Specify if: With perceptual disturbances: This specifier applies in the rare instance when hallucinations (usually visual or tactile) occur with intact reality testing, or auditory, visual, or tactile illusions occur in the absence of a delirium. DSM-V Diagnostic Criteria for Alcohol Withdrawal

15 Symptoms of Withdrawal Insomnia Anxiety and/or Fear Restlessness Nausea and/or Vomiting Headache Seizures – may need CT scan, lumbar puncture Altered Sensory Perceptions, including visual (common), tactile (common), auditory Tremors Diaphoresis Tachycardia, which may/may not be accompanied by palpitations (why??)


17 Delirium Tremens (DT) “… hallucinations, disorientation, tachycardia, hypertension, fever, agitation, and diaphoresis in the setting of acute reduction or abstinence from alcohol.” Last up to 7 days, mortality rate of 5% Increased cardiac indices, oxygen delivery, and oxygen consumption Arterial pH rises due to hyperventilation (respiratory alkalosis) = decrease in cerebral blood flow Fluid and electrolyte status: Hypovolemic r/t diaphoresis, hyperthermia, vomiting, and tachypnea Hypokalemia r/t renal and extrarenal losses, alterations in aldosterone levels, and changes in potassium distribution across the cell membrane Hypomagnesemia r/t malnutrition; may predispose to dysrhythmia (torsades des pointes) and seizures Hypophosphatemia r/t malnutrition; may contribute to cardiac failure and rhabdomyolysis.

18 Who is at risk for DT? A history of sustained drinking A history of previous DT Over age 30 The presence of a concurrent illness The presence of significant alcohol withdrawal in the presence of an elevated alcohol level A longer period since the last drink (ie, patients who present with alcohol withdrawal more than two days after their last drink are more likely to experience DT than those who present within two days)

19 Other diagnoses to consider “A premature diagnosis of alcohol withdrawal can lead to inappropriate use of sedatives, which can further delay accurate diagnosis.” Infection (e.g., meningitis) Trauma (e.g., intracranial hemorrhage) Metabolic derangements Drug overdose Hepatic failure Gastrointestinal bleeding

20 Nursing Management: ADPIE Assessment Diagnosis Plan and Goals of Care Implementation Evaluation

21 Assessment: Clinical Institute Withdrawal Assessment (CIWA)

22 Assessment: CIWA Calculation withdrawal/ withdrawal/

23 Assessment – beyond CIWA Questions to ask: – CAGE questions (Kosten et al, 2003) Can you cut down on your drinking? Are you annoyed when asked to stop drinking? Do you feel guilty about your drinking? Do you need an eye opener drink in the morning when you wake up? – How long have you gone without alcohol in the past six months? – Has anyone ever advised that you cut down on your drinking? – When was the last drink (i.e., the most recent alcohol consumption)? – How much alcohol per day? – How long has the patient been dependent on alcohol? – Has he/she ever experienced withdrawal or delirium tremens before? If so, how many times has this occurred, and did he/she ever have seizures?

24 Continued assessment … Vital signs – what would you expect to find, and why? See “Symptoms” slide for signs/symptoms of withdrawal Risk for elopement, falls, aspiration Smoking status Blood sugar – Accu check Urine drug/toxicity screen Blood work to collect: – Chemistry – Complete Blood Count (CBC) with differential and platelet – Coagulation panel (PT, INR, PTT) – Liver Function Tests (LFT) – Uric acid – Alcohol, whole blood – Drug/toxicity screen – should be collected at the same time as the urine, if possible

25 Diagnosis Risk for Injury (especially falls!) r/t alcohol withdrawal Risk for Elopement r/t alcohol withdrawal Risk for Sensory-Perceptual Alterations r/t alcohol withdrawal Anxiety and/or Fear r/t alcohol withdrawal aeb restlessness, tachycardia, hypertension Risk for Aspiration (Ineffective Breathing Pattern) r/t alcohol withdrawal Risk for Seizures r/t alcohol withdrawal

26 Plan and Goals of Care The patient will remain free from falls during the hospital stay by using bed exit alarm and frequent monitoring by staff. The patient will not elope from the hospital during his/her stay through frequent monitoring, purple gown, security alert. The patient will not aspirate during his/her stay by keeping HOB > 30 degrees, monitoring during PO intake, staff evaluation for safe swallow.

27 Interventions IV access Administer medications (as ordered by LIP) Possible sitter/safety coach and/or to be closer to nurses’ station If at risk for elopement, place in special gown (at OSUWMC, it is bright purple), notify security of increased risk, and keep close to nurses’ station, away from elevators. Going off the unit is contraindicated, both due to risk for elopement and medication administration Avoid the use of restraints, especially LBB

28 Interventions Bed exit alarm Seizure pads on bedrails HOB at 30 degrees or greater, if no contraindications Quiet, dark, calm environment Fan or cool washcloths Nurse should present calm demeanor Limit setting Nicotine replacement Consults: social work, nutrition, psychiatry, nicotine dependence

29 Interventions: Medications Chlordiazepoxide (Librium) – long-acting benzodiazepine Diazepam (Valium) – long-acting benzo Lorazepam (Ativan) – short-acting benzo Flumazenil (Romazicon) – reversal agent for benzo Clonidine (Catapres) - centrally acting alpha-2 agonist, for severe DT, but may mask symptoms of worsening status Phenobarital – anticonvulsant, if severe DT or status epilecticus AVOID the routine use of anticonvulsants, beta blockers (mask symptoms) and antipsychotics (lower the seizure threshold) Vitamins, especially folic acid and thiamine Electrolytes, especially glucose, magnesium, phosphate, and potassium Intravenous fluids, if not contraindicated

30 Interventions: Medications used at OSUWMC

31 Evaluation Back to assessment – check CIWA score per the protocol Re-assess

32 Questions?

33 References American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). Arlington, VA: American Psychiatric Publishing. Retrieved September 30, 2014, from Hoffman, R.S., & Weinhouse, G.L. (2013). Management of moderate and severe alcohol withdrawal syndromes. In S.J. Traub & J. Grayzel (Eds.), UpToDate. Retrieved from Kosten, T.R., & O’Connor, P.G. (2003). Management of drug and alcohol withdrawal. New England Journal of Medicine, 348(18), 1786-95. MDCalc. (2014). CIWA-Ar for Alcohol Withdrawal. Retrieved September 20, 2014, from National Institute on Alcohol Abuse and Alcoholism (NIAAA). (2014). Alcohol facts and statistics. Alcohol and Your Health. Retrieved September 30, 2014, from consumption/alcohol-facts-and-statistics. National Institute on Alcohol Abuse and Alcoholism. (n.d.). What is a standard drink?. Alcohol and Your Health. Retrieved September 30, 2014, from alcohol-consumption/standard-drink. alcohol-consumption/standard-drink (n.d.). 5 Alcohol Withdrawal Nursing Care Plans. Retrieved September 30, 2014, from Office of Women’s Health at the U.S. Department of Health and Human Services. (2013). Straight talk about alcohol. Retrieved September 30, 2014, from Weed, H.G. (2011). Clinician’s Guide to Alcohol Withdrawal as a Secondary Diagnosis. 2 nd Edition. From The Ohio State University Medical Center Evidence Based Practice Clinical Resources. Retrieved September 20, 2014, from

34 TAKE A BREAK (please)!

35 Diabetes


37 Diabetes: A huge public health problem Diabetes affects 29.1 million people of all ages – Diagnosed: 21 million – Undiagnosed: 8.1 million That’s 9.3% of the U.S. population! About 1.7 million adults were newly diagnosed with diabetes in 2012 in the U.S. An estimated 86 million American adults have pre-diabetes By 2050, 1 in 3 Americans will have diabetes!


39 Why individuals with diabetes should be concern Medical expenses for people with diabetes are more than 2 times higher than for people without diabetes. The total annual cost of diabetes is $245 billion (CDC, 2014) – Direct medical: $176 billion – Indirect: $69 billion “In 2003–2006, after adjusting for population age differences, rates of death from all causes were about 1.5 times higher among adults aged 18 years or older with diagnosed diabetes than among adults without diagnosed diabetes” (CDC, 2014). INEQUALITIES – those in lower socioeconomic position and non- whites are more likely to develop T2DM

40 Diabetes Mellitus Definition – “Diabetes is a group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion, insulin action, or both” (ADA, 2010, S62). – “Deficient insulin action results from inadequate insulin secretion and/or diminished tissue responses to insulin at one or more points in the complex pathways of hormone action” (ADA, 2010, S62). Classifications – Prediabetes – Type 1 Diabetes Mellitus (T1DM) – Type 2 Diabetes Mellitus (T2DM) – Gestational Diabetes Mellitus – Monogenic Diabetes Mellitus – Other causes: surgery, medications, pancreatic disease


42 Diabetes complications

43 Diabetes is risky business for your heart Overall, the risk for death among people with diabetes is about twice that of people without diabetes. Poorly controlled diabetes is the 7th leading cause of death in the United States. Adults with diabetes have heart disease death rates about 2 to 4 times higher than adults without diabetes. The risk for stroke is 2 to 4 times higher among people with diabetes.

44 … and for your eyes, kidneys, nerves, mouth, and mental health … Poorly controlled diabetes is the leading cause of kidney failure, non-traumatic lower-limb amputations, and new cases of blindness among adults in the United States. Those with diabetes have about twice the risk of gum disease than those without diabetes. People with diabetes are more susceptible to many other illnesses. People with diabetes are twice as likely to have depression.

45 True or False? Diabetes is the leading cause of blindness, amputations, and kidney problems.

46 How to prevent complications Proper glycemic control can prevent or delay the micro- and macro-vascular complications that lead to poor outcomes (DCCT, 1993; Stratton et al., 2000). This can be achieved through adequate self- management (SM) (Atak et al., 2008; Chen et al., 2013; Aljasem et al., 2001; Osborn, Bains, & Egede, 2010). Regular follow-up with primary care providers is ESSENTIAL.

47 Diabetes overview

48 Pathophysiology Overview The pancreas produces insulin in response to an increase in blood sugar, which occurs after eating food Insulin functions as the “key” to let the sugar into the cells. Without the insulin, the sugar remains in the blood and cannot be used by the cell for daily functions. For those with Type 1 diabetes, the pancreas is unable to make insulin. For those with Type 2 diabetes, the cells have difficulty using the insulin, which happens when the cells become resistant to the insulin. After a while, the pancreas gets “tired” and produces less insulin. Both result in high blood sugar levels, which leaves the cells starved of sugar.

49 Glucose Regulation Glucose = major energy source BG level “regulated by rate of consumption and intestinal absorption of dietary carbohydrate, the rate of utilization of glucose by peripheral tissues and the loss of glucose through the kidney tubule, and the rate of removal or release of glucose by the liver” (Nordlie et al., 1999, p. 380). Liver regulates BG level through the following: – Glycogenesis: uptake of extra glucose, to store as glycogen – Glycogenolysis: release of glucose by turning glycogen into glucose – Gluconeogenesis: release of glucose by harvesting amino acids, waste products, fat byproducts – Ketogenesis: when glycogen and insulin levels are low, the liver breaks down fats into ketones to use as energy for less essential organs, reserving glucose for brain, RBCs, some of the kidneys (REMEMBER THIS FOR LATER!)




53 Insulin Discovered in 1922 by Banting and Best (Saltiel, 2000) Anabolic (i.e., storage) hormone Essential for appropriate tissue development, growth, and maintenance of whole-body glucose homeostasis Secreted by the β cells of the pancreatic islets of Langerhans in response to increased circulating levels of glucose and amino acids (after a meal) Regulates glucose homeostasis (i.e., balance) at many sites, reducing hepatic glucose output (via decreased gluconeogenesis and glycogenolysis) Increases the rate of glucose uptake, primarily into striated muscle and adipose tissue Affects lipid metabolism by increasing lipid synthesis in liver and fat cells and enhancing fatty acid release from triglycerides in fat and muscle Acts as the “key” to let glucose into the cells, via an insulin receptor on the outside of the cell (extracellular)

54 Insulin Functions


56 Pre-Diabetes and Metabolic Syndrome Metabolic Syndrome (AHA, 2014) – Affects approximately 1/3 of Americans – Increased risk for diabetes, stroke, heart disease – 3 of 5 criteria Fasting BG greater than 100 mg/dL Waist circumference greater than 35 inches for women, 40 inches for men (central obesity, indicating increased visceral adipose tissue) Hypertension (BP >130/85) Triglyceride level greater than 150mg/dL HDL less than 50mg/dL for women, 40mg/dL for men Pre-diabetes (CDC, 2014; ADA, 2012) – 15-30% of those with prediabetes will develop T2DM in 5 years – Elevated fasting BG (>100 -125 mg/dL) on two occasions – Oral glucose tolerance test of 140-199mg/dL – HbA1c 5.7-6.4%


58 Treatment of Prediabetes and Metabolic Syndrome LOSE WEIGHT Physical activity >150 minutes/week Dietary considerations Control BP, lipids, cholesterol levels Diabetes Prevention Program (DPP)


60 Type 1 Diabetes INSULIN DEPENDENT – no insulin is made by the pancreas 5-10% of total diabetes cases Genetic predisposition and environmental factors Autoimmune destruction of insulin-producing beta cells – Also at risk for other autoimmune diseases, such as Graves’, Hashimoto’s, Addison’s, vitiligo, celiac sprue, autoimmune hepatitis, myasthenia gravis, pernicious anemia (ADA, 2010). Minority do not exhibit autoimmune destruction = idiopathic 50-75% of cases diagnosed in childhood or adolescence 25-50% diagnosed in adulthood – Latent Autoimmune Disease of Adults (LADA) – Many misdiagnosed as type 2 diabetes (T2DM) – For LADA, typically only 1 antibody present (often GADA)

61 T1DM Testing Hemoglobin A1C = glycated hemoglobin = average BG over the past 8-12 weeks (lifespan of RBC) Can usually be confirmed by islet cell antibodies (ICA), glutamic acid decarboxylase antibodies (GADA), insulin antibodies (IAA), and/or insulinoma-2–associated antibodies (IA-2A) (ADA, 2010; Lightsey, 2011) 85-90% of patients have these antibodies (ADA, 2010) Genetics: strong HLA (human leukocyte antigen) associations, with linkage to the DQA and DQB genes, and it is influenced by the DRB genes (ADA, 2010) C-peptide level low – positive relationship to insulin (linked when proinsulin made by pancreas) – examines how much insulin the pancreas is producing Oral glucose tolerance test >200mg/dL Fasting BG > 126mg/dL For T1DM and T2DM: HbA1C >6.5% (some organizations state >7% - most say >6.5%)

62 Risk Factors/Demographics Onset at any age, but most are diagnosed when under age 30 Certain HLA types = 3-5x higher risk of T1DM (Pellico, 2013) Genetic predisposition PLUS environmental factors More than 15,000 children and 15,000 adults— approximately 80 people per day—are diagnosed with T1DM in the U.S. annually (JDRF) 85% of people living with T1DM are adults, and 15% children (JDRF) The prevalence of T1DM in Americans under age 20 rose by 23 percent between 2001 and 2009 (JDRF) The rate of T1DM incidence among children under age 14 is estimated to increase by 3% annually worldwide (JDRF).


64 T1DM Presenting Symptoms DEHYDRATION Hyperglycemia Polydypsia Polyuria Polyphagia Glycosuria (if above renal reabsorption threshold of 180- 200mg/dL) Blurred vision Weight loss Impaired growth Decreased immunity Diabetic Ketoacidosis (DKA) EVERYONE PRESENTS DIFFERENTLY – depends on how much beta cell function remains

65 T1DM Treatment New therapies: Vc-01 (beta cell encapsulation), islet cell transplant Medications: Insulin (discussed later in the presentation) Monitor blood sugars – Maintain your blood glucose within normal limits, usually 70-130 before meals and less than 180 1-2 hours after meals. – Keep your Hemoglobin A1C (Hgb A1C) below 7. (Hgb A1C is a blood test that shows what your blood glucose control has been over 2-3 months.) Lifestyle management – Reduce carbohydrate intake, especially simple carbohydrates (i.e., anything that ends in an “–ose”) … High-fiber, low glycemic index foods are best – Physical activity >150 minutes/week – Weight management – Mental health considerations

66 Type 2 Diabetes (T2DM) NON-INSULIN DEPENDENT Obesity, sedentary lifestyle, aging, genetic predisposition Increased insulin resistance  Relative insulin deficiency (i.e., insulin supply is less than the demand) – Resistance = “state of reduced responsiveness to normal circulating concentrations of insulin” (Saltiel, 2000). Pancreas compensates for insulin resistance by producing more insulin (hyperinsulinemia). After a while, the beta cells can no longer compensate, creating glucose intolerance and hyperglycemia. Hyperglycemia for many years prior to diagnosis = increased risk of micro- and macro-vascular complication development


68 T2DM Testing C-peptide level moderate to high – positive correlation with insulin Oral glucose tolerance test >200mg/dL Fasting BG > 126mg/dL HbA1C >6.5% (some organizations state >7% - most say >6.5%)

69 Risk Factors/Demographics Obesity (especially visceral/trunk) – BMI >25 kg/m 2 Poor dietary habits Men slightly more than women Sedentary lifestyle/physical inactivity Older age (>45 y.o.) Family history of diabetes – If either parent suffers from T2DM, a child’s risk of developing the disease is almost 15% If both parents have the condition, the risk of developing it is 75%. History of gestational diabetes or baby over 9lbs (10% of those with GD develop T2DM immediately; 35-60% within 10-20 years)

70 Risk Factors/Demographics Impaired glucose metabolism HDL cholesterol 250mg/dL Insulin resistance and hyperinsulinemia Race/ethnicity – Increased risk for African Americans, Hispanics/Latinos, American Indians (e.g., Pima Indians), some Asians, and Native Hawaiians or other Pacific Islanders – Asian Americans have a 9% higher risk of diabetes. Hispanics have a 12.8% higher risk, and non-Hispanic blacks have a 13.2% higher risk of diabetes than non- Hispanic white adults in the U.S. – In children and adolescents, diagnosed more frequently among American Indians, African Americans, Hispanics/Latinos, Asians, and Pacific Islanders


72 T2DM Presenting Symptoms Slow progression of glucose intolerance, so minimal to no symptoms (usually) May include – Irritability – Fatigue – Polydipsia – Polyuria – Polyphagia (sometimes) – Poor wound healing – Frequent infections – Vision changes

73 T2DM Treatment Medications: oral agents, then insulin in later stages (we’ll speak more about this later) Monitor blood sugars – Maintain your blood glucose within normal limits, usually 70- 130 before meals and less than 180 1-2 hours after meals. – Keep your Hemoglobin A1C (Hgb A1C) below 7. (Hgb A1C is a blood test that shows what your blood glucose control has been over 2-3 months.) Lifestyle management – Reduce carbohydrate intake, especially simple carbohydrates (i.e., anything that ends in an “–ose”) … High-fiber, low glycemic index foods are best – Physical activity >150 minutes/week – Weight management – lose 5-10% of body weight – Mental health considerations

74 Gestational Diabetes Mellitus (GDM) A form of glucose intolerance diagnosed during the second or third trimester of pregnancy. Placental hormones cause hyperglycemia and insulin resistance. In up to 14% of pregnancies (Pellico, 2013, p. 820). Usually glucose tolerance testing at 24-28 weeks, but do earlier if at increased risk. The risk factors for GDM are similar to those for T2DM. Within 1 year after pregnancy, 5% -10% of women with GDM continue to have high BG levels and are diagnosed as having diabetes, usually T2DM. 35-60% of women with GDM develop T2DM in 10-20 years. At risk for recurrent GDM with future pregnancies. Treatment: diet, exercise, insulin BG goals: – < 95mg/dL pre-prandial – < 130-140mg/dL 1 hour post-prandial – < 120mg/dL 2 hours post-prandial

75 Monogenic Diabetes Two forms: Maturity Onset Diabetes of the Young (MODY) and Neonatal Diabetes Mellitus 1-5% of U.S. diabetics have monogenic diabetes, usually MODY Due to mutations in a single gene – 20 genes have been implicated in the development of monogenic diabetes May happen spontaneously BUT has strong hereditary component Management depends on severity of disease Genetic testing of family members necessary

76 Maturity Onset Diabetes of the Young (MODY) More common than Neonatal Diabetes Often misdiagnosed as T1DM if found in adolescence or T2DM if later in life Presentation depends on severity; hyperglycemia may be discovered on routine lab work Each child has a 50% chance of inheriting the MODY gene Most commonly caused by mutations in the HNF1A gene or the GCK gene

77 Neonatal Diabetes Mellitus – First 6 months of life – Symptoms similar to that of T1DM – Most commonly caused by mutations in the KCNJ11, ABCC8 o r INS genes – Management same as T1DM (need to replace insulin)

78 Medications: Oral Agents Alone, only lower HbA1c 1-2% (Faulds, 2014) Can combine agents with different mechanisms of action (Faulds, 2014) – With combination, can only decrease HbA1c by 2-3% (Faulds, 2014) Insulin Secretagogues: action increases secretion of insulin by the beta cells – Sulfonylureas – Nonsulfonylurea insulin secretagogues (meglitinides and phenylalanine derivatives) Biguanides Alpha-glucosidase inhibitors Thiazolidinediones (glitazones) SEE TABLE 30-6 (pages 836-7) IN BOOK

79 Sulfonylureas Action: directly stimulate the pancreas to secrete insulin, increase insulin effectiveness at cellular level, decrease glucose production by the liver Lower HbA1c by 1-2% (Faulds, 2014) Must have a functioning pancreas, liver, kidneys Side effects: hypoglycemia; mild GI; sulfa allergy; weight gain; interact with NSAIDs, warfarin, sulfonamides Recommend not to take with beta blocker (mask symptoms of hypoglycemia) No alcohol Second-generation fewer side effects, drug interactions, excreted by liver and kidneys – Glipizide, glyburide, glimepiride

80 Non sulfonylurea Insulin Secretagogues Action: similar action as sulfonylureas Decrease HbA1c by 1-2% (Faulds, 2014) Rapid onset, short duration  must be taken with meals Side effects: hypoglycemia; weight gain (less than Sulf.); interactions with ketoconazole, fluconazole, erythromycin, rifampin, isoniazid repaglinide (Prandin), naglitinide (Starlix)

81 Biguanides Action: decreasing hepatic production of glucose, facilitate action of insulin on peripheral receptor sites Lower HbA1c 1-2% (Faulds, 2014) May be used with Sulf. to further lower BG Do not use if renal or liver impairment, respiratory insufficiency, infection, alcohol abuse Side effects: lactic acidosis, GI disruptions, drug interactions D/c use 2 days prior to contrast administration (renal) Metformin, metformin with glyburide

82 Alpha-Glucosidase Inhibitors Action: delay absorption of complex carbohydrates in intestine, slow entry of glucose into systemic circulation = lower post-prandial BG Decrease HbA1c 0.5-1% (Faulds, 2014) Side effects: hypoglycemia, GI side effects, drug interactions Take with first bite of food Monitor liver function Do not use if renal or GI dysfunction, cirrhosis acarbose (Precose), miglitol (Glyset)

83 Thiazolidinediones Action: Sensitize body tissue to insulin, stimulate insulin receptor sites Decrease HbA1c 0.5-1% (Faulds, 2014) May be used in combination with other meds Side effects: hypoglycemia, anemia, weight gain, edema, liver dysfunction, drug interactions, hyperlipidemia, impaired platelet function, decrease effectiveness of oral contraceptives pioglitazone (Actos), rosiglitazone (Avandia)

84 DPP-4 Inhibitors/Incretin Enhancers Action: stimulates release of insulin, prevents secretion of glucagon, slows postprandial gastric emptying Decrease HbA1c 0.5-1% (Faulds, 2014) Side effects: may promote weight loss, GI disturbances, hypoglycemia, pancreatitis Combination with metformin or Sulf. sitagliptin (Januvia), saxaglipton (Onglyza), exenatide (Byetta)


86 Who gets insulin? (Dungan, 2014) All T1DM Depending on severity, GDM (pregnancy) Eventually, most T2DM – At the time of diagnosis, approximately 50% of beta cell function is lost – Only a matter of time (average about 10 years) before require insulin HbA1c > 8% on two oral agents Unable to take oral agents HbA1c > 10% Symptomatic Other – Hospitalization – Corticosteroid administration – Infection – Cost


88 Medications: Insulin Onset, peak, duration, concentration, route See page 830, Table 30-4 for insulin regimens “Think like a pancreas!” Fast-acting (includes rapid- and short-acting), intermediate-acting, long-acting Basal and bolus coverage – Common basal insulin (long-acting) Detemir, Glargine, NPH – Common bolus insulin (fast- and intermediate-acting; sliding scale insulin for BG and carbohydrate coverage) Regular, lispro, aspart, glulisine

89 Insulin Activity



92 Basal Insulin Provides coverage throughout the day Syringe, pen, pump Intermediate acting – cloudy – NPH (Humulin N, Novolin N) Long acting – DO NOT MIX – Glargine (Lantus) – Detemir (Levemir)

93 Bolus Insulin Rapid-acting – Lispro (Humalog) – Aspart (Novolog) – Glulisine (Apidra) Short-acting – Regular (Humulin R, Novolin R)

94 Pros: Better mealtime flexibility and coverageBetter mealtime flexibility and coverage Less hypoglycemiaLess hypoglycemia Basal coverage throughout the dayBasal coverage throughout the day Better reproducibility of glycemic effectsBetter reproducibility of glycemic effectsCons: Multiple injections per dayMultiple injections per day Cannot mix insulinsCannot mix insulins More expensiveMore expensive BLSHsB Meals Insulin Effect Multi- dose insulin using insulin analogs Aspart: 50% of total daily dose divided over 3 meals (Ex. 5 unit SQ QAC) Glargine: 50% of total daily dose (Ex. 15 units QHS)

95 Combination Insulin Novolin 70/30 (Humulin 70/30) – 70% NPH – 30% Regular Humulin 50/50 – 50% each NPH and Regular Novolog Mix 70/30 – 70% Aspart protamine suspension – 30% Aspart Humalog Mix 75/25 – 75% Lispro protamine suspension – 25% Lispro Humalog Mix 50/50 – 50% each Lispro protamine suspension and Lispro

96 Twice-daily Split-mixed Regimens Regular NPH BSLHS Insulin Effect B 70/30 insulin: 70% NPH, 30% Regular 2/3 should be given before breakfast, 1/3 before supper

97 Medication calculation Carbohydrate count – 5 grams of CHO to 1 unit of insulin for tightest control – Can also be 10, 15, or 20 grams CHO: 1 unit Sliding scale insulin (SSI) for BG – Often 1 unit for every 50 mg/dL over 150 mg/dL – Different for every person

98 Calculation Practice Pre-lunch BG: 204 mg/dL – SSI order states to give 1 unit of aspart insulin for every 50 mg/dL over 150 mg/dL – How much to give? Planning to eat turkey sandwich with mustard (45 grams), unsweetened iced tea (0 grams), small apple (25 grams), and 1 cup carrots (12 grams) with ranch dressing (2 grams) = 84 grams total – Order states 10 grams CHO: 1 unit aspart insulin – How much to give?

99 Insulin Administration Store in refrigerator EXCEPT the current vial, which is stored at room temperature (good for 1 month) Inspect for clarity, precipitate, flocculation (frosted, whitish coating inside bottle) Check expiration date, opening date Roll vial between hands (do not shake) Pen versus syringe/needle Syringe selection – 1ml,.5ml,.3ml – 27 or 29 gauge needle, 0.5 inches long May draw up insulin up to 3 weeks early, store with needle in upright position Subcutaneous sites: posterior arms, anterior thighs, hips, abdomen Rotate sites to prevent lipodystrophy See page 832-3 for instructions

100 Insulin Administration

101 Insulin Administration Complications Insulin resistance Morning hyperglycemia Dawn phenomenon: relatively normal BG until 3am, due to nocturnal surges in growth hormone secretions Somogyi effect: nocturnal hypoglycemia with rebound hyperglycemia Insulin waning: progressive increase in BG from bedtime to morning Local allergic reaction 1-2 hours after administration Systemic allergic reaction (hives) – rare Lipodystrophy – Lipoatrophy: loss of subcutaneous fat, slight dimpling or pitting of subcutaneous fat – Lipohypertrophy: fibrofatty mass, raised and hardened tissue

102 Other Forms of Insulin Continuous Subcutaneous Insulin Infusion (CSII) pump U-500 insulin – Most insulin is 100 units/1 mL, this is 5 TIMES the normal concentration – High-risk medication – Used for those with poor absorption, insulin resistance, large doses

103 Other Forms of Insulin, cont. Inhaled insulin – Fast absorption – Not for those with lung disease – Pre-meal – Exubera 2006-2007 – Afrezza Peak 15-20 minutes, duration 2-3 hours Less weight gain Fewer episodes, less severe hypoglycemia

104 Patient Teaching Gerontologic Considerations – page2 821-22 (Box 30-4) Medications Physical activity Nutrition Self-monitoring of blood glucose (SMBG) Care for the following: – Feet – Eyes – Kidneys – Heart/brain – Mental health – Teeth – Also higher risk for fatty liver disease

105 Gerontologic Considerations Age-related changes make diabetes management difficult See Box 30-4 on page 822

106 Teaching: Medications

107 Teaching: Physical Activity Goal > 150 minutes per week Weight control, improve insulin utilization, ease stress, CVD risk factor improvement (i.e., lower lipids, increase HDL, decrease total cholesterol and triglycerides) Slow, gradual increase Consistent, daily exercise For those who take insulin, may need a snack after exercise to avoid hypoglycemia

108 Teaching: SMBG T2DM who are not on insulin  2-3 times per week, including a 2-hour post-prandial, also during medication changes or suspected hyper- or hypoglycemia If on insulin  before meals and at bedtime, suspected hyper- or hypoglycemia Continuous Glucose Monitoring (CGM) Urine Glucose Testing: renal threshold for glucose is 180-200 mg/dL (affected by age and renal function) Keep a logbook/record – There’s an (well, more than one!) app for that.

109 Teaching: Nutrition Consistent carbohydrate and caloric intake, at consistent intervals (especially for those who take insulin) – to prevent hypoglycemia Personalize care: consider lifestyle, preferences, culture, ethnicity, eating times Include skills such as reading labels, eating out, adjusting meal plan for special occasions/illness/exercise Exchange List for Meal Planning – see page 824-5 and htm htm Create Your Plate: fitness/food/planning-meals/create-your-plate/ fitness/food/planning-meals/create-your-plate/ 50-60% calories from carbohydrates, 20-30% from fat (cholesterol less than 200mg/day, saturated fat <7%), 10-20% from protein Fiber – Soluble: legumes, oats, fruits (help lower LDL and BG) – Insoluble: whole grains, cereals, vegetables

110 Create Your Plate

111 Inpatient Diabetes Management Usually hyperglycemia, but also hypoglycemia Typically discontinue oral agents, switch to bolus insulin (lispro and aspart are commonly used at OSUWMC) – why no oral agents? Acute illnesses = hyperglycemia Steroid administration NPO for procedure, etc. Electrolyte management

112 Treatment Patient Predisposition Illness Hyperglycemia Pancreatic reserve Insulin resistance Catecholamines HPA axis activation Inflammatory cytokines Lipotoxicity Exogenous glucocorticoids Vasopressors Total parenteral nutrition Enteral nutrition Etiology of Hospital Related Hyperglycemia

113 Complications requiring hospitalization: Diabetic Ketoacidosis (DKA) Caused by lack of insulin Results in hyperglycemia, ketosis, dehydration, electrolyte loss, acidosis No insulin = glucose does not enter cells but stays in plasma; liver releases glucose; kidneys attempt to get rid of extra glucose by osmotic diuresis = dehydration and electrolyte loss Breakdown of fat into free fatty acids and glycerol (see previous slides)  converted into ketone bodies by liver  metabolic acidosis – ABG: pH low, bicarbonate low, CO 2 normal – Attempt to correct low pH and low bicarbonate by “blowing off” CO 2 = Kussmal respirations

114 DKA Signs/Symptoms Polyuria Polydypsia Diagnostic – pH 6.8-7.3 – BG > 250 mg/dL – Serum bicarbonate low (0-15mEq/L0 – Serum and urine ketones – Glucose in urine – Na, K, Cl serum levels abnormal – how?!? – Anion gap Blurred vision (osmotic changes on the lens) SEE FIGURE 30-7 on page 842 Osmotic diuresis  Water and electrolyte loss  dehydration  circulatory failure Metabolic acidosis  CNS depression  coma

115 DKA Management Correct dehydration, electrolyte loss, acidosis – 6-10 L of IV fluids! (But not too quickly, due to risk for cerebral edema.) Start with NS, then to dextrose-containing fluids when BG < 250 mg/dL. – Frequent VS monitoring – respiratory, cardiac, neurological, intake/output balance. Ensure your patient is not fluid overloaded! – K and Cl replacement – most important to monitor K levels q2-4h – WHY DOES K SHIFT IN/OUT OF CELLS?! – Acidosis reversed by insulin administration Insulin gtt Do not lower BG too quickly! Hourly BG checks Dextrose when BG < 250mg/dL See OSUWMC policy: pe1Diabetes.pdf pe1Diabetes.pdf

116 Complications requiring hospitalization: Hyperglycemic Hyperosmolar (non-ketotic acidosis) Syndrome How is it different than DKA?  NO KETOSIS OR ACIDOSIS (insulin is still present) Mortality rate 10-40% Hyperosmolality (> 340mOsm/L) and hyperglycemia (> 600mg/dL) with minimal or no ketosis Older, 50-70 y.o., with or without T2DM Precipitating events: infection, acute or chronic illness, procedures such as dialysis or surgery, medications

117 HHNS Signs/Symptoms Hypotension Dehydration (more than DKA) Tachycardia Neurologic signs due to cerebral dehydration from hyperosmolality – Sensory alterations – Seizures – Hemiparesis

118 HHNS Management Same as DKA, minus anion gap monitoring Be very careful of fluid status (older patients)! See OSUWMC policy: uments/Guidelines/Type2Diabetes.pdf uments/Guidelines/Type2Diabetes.pdf

119 Complication requiring hospitalization: Hypoglycemia Causes: too much insulin or OHA, too little food, excessive PA Often prior to meals Think about insulin profiles – when does it peak?

120 Hypoglycemia: Symptoms DIFFERENT FOR EVERY PERSON Autonomic Nervous System (ANS) (onset) – Epinephrine, Norepinephrine released – Sweating, tremor, tachycardia, palpitations, anxiety, hunger Central Nervous System (CNS) (intermediate) – Brain cells do not have fuel – Impaired concentration, headache, lightheaded, dizzy, confusion, forgetful, numb lips/tongue, slurred speech, impaired coordination, labile emotions, irrational or combative behavior, double vision, drowsiness CNS (severe) – Disoriented, seizures, somnolence, LOC

121 Hypoglycemia: Management IF ABLE TO SWALLOW SAFELY, Give CHO – 15 grams of fast-acting carbohydrate PO 3-4 glucose tablets 4-6 oz fruit juice or soda (non-diet) 6-10 hard candies 2-3 TBL sugar/honey – Retest BG within 15 minutes; retreat if less than 0- 75 mg/dL – Plus snack with protein and starch within 30-60 minutes (once symptoms resolve)

122 Hypoglycemia: Management Glucagon 1 mg SQ or IM 25-50 mL (12.5-25 g) of 50% D 50 W via IVP at 10mL/min Be sure to evaluate if patient has insight to hypoglycemia, re-evaluate BG 15 minutes after intervention See OSUWMC policy for hypoglycemia management: uments/Hypoglycemia.pdf uments/Hypoglycemia.pdf

123 Have a great day! http://whatshouldwecallnursingschool.tumblr. com/ http://whatshouldwecallnursingschool.tumblr. com/ Have a wonderful semester!!!!!

124 References American Association of Diabetes Educators (AADE). (2014). Diabetes Tip Sheets. Retrieved May 27, 2014, from American Diabetes Association (ADA). (2013, March 6). American Diabetes Association Releases New Research Estimating Annual Cost of Diabetes at $245 billion. Retrieved December 1, 2013, from 2013.html?loc=cost-of-diabetes. 2013.html?loc=cost-of-diabetes American Diabetes Association (ADA). (2010). Diagnosis and classification of diabetes mellitus. Diabetes Care, 33(S1). American Diabetes Association (ADA). (2012). Standards of medical care in diabetes. Diabetes Care, 35(S1), S12, table 2. Retrieved October 14, 2014 from American Heart Association (AHA). (2014). About metabolic syndrome. American Heart Association. Retrieved October 14, 2014, from Aljasem, L.I., Peyrot, M., Wissow, L., & Rubin, R.R. (2001). The impact of barriers and self-efficacy on self-care behaviors in type 2 diabetes. Diabetes Educator, 27(3). Atak, N., Gurkan, T., & Kose, K. (2008). The effect of education on knowledge, self-management behaviors, and self-efficacy of patients with type 2 diabetes. Australian Journal of Advanced Nursing, 26(2), 66. Atkinson, M.A. (2012). The pathogenesis and natural history of type 1 diabetes. Cold Spring Harbor Perspectives in Medicine. Centers for Disease Control and Prevention (CDC). (2014). National Diabetes Statistics Report: Estimates of Diabetes and Its Burden in the United States, 2014. Atlanta, GA: U.S. Department of Health and Human Services. Center for Disease Control and Prevention (CDC). (2014). Prediabetes. Diabetes Public Health Resource. Retrieved October 14, 2014, from Chen, C-P., Peng, Y-S., Weng, H-H., Yen, H-Y., & Chen, M-Y. (2013). Health-promoting behavior is positively associated with diabetic control among type 2 diabetes patients. Open Journal of Nursing, 3, 274. Diabetes Control and Complications Trial Research Group (DCCT). (1993). The effect of intensive treatment of diabetes on the development and progression of long term complications in insulin-dependent diabetes mellitus. New England Journal of Medicine, 329, 977–986. Dungan, K. (2014). Insulin in Inpatients and Outpatients [Powerpoint slides]. Presentation, May 2014. JDRF. (n.d.). Type 1 Diabetes Facts. Retrieved October 15, 2014, from Faulds, E.R. (2014). Pharmacological Management of Type 2 Diabetes: Oral Medications and Noninsulin Injectables [Powerpoint slides]. Nursing 6111, May 2014.

125 References King, D.K., Glasgow, R.E., Toobert, D.J., Strycker, L.A., Estabrooks, P.A., Osuna, D., & Faber, A.J. (2010). Self-efficacy, problem solving, and social-environmental support are associated with diabetes self-management behaviors. Diabetes Care, 33, 751-753. King, P., Peacock, P., & Donnelly, R. (1999). The UK Prospective Diabetes Study (UKPDS): Clinical and therapeutic implications for type 2 diabetes. British Journal of Clinical Pharmacology, 48(5), 643-648. Lightsey, R. (2011). Diagnosis and treatment of latent autoimmune diabetes in adults still evolving. ClinicalAdvisor. Retrieved October 13, 2014, from evolving/article/203578/. Longhurst, A.S. (2014). Type 2 Diabetes Statistics and Facts. Retrieved October 15, 2014, from diabetes/statistics#1. Mercola, J. (2014). Sugar Consumption Accounts for a Big Chunk of Health Care Costs. Retrieved May 27, 2014, from National Institute of Diabetes, Digestive and Kidney Diseases (NIDDK). (2007). Monogenic forms of diabetes: Neonatal diabetes mellitus and maturity-onset diabetes of the young (NIH Publication No. 07-6141). Bethesda, MD: National Diabetes Information Clearinghouse. National Institute of Diabetes, Digestive, and Kidney Diseases (NIDDK). (2011). National Diabetes Statistics, 2011. Retrieved from May 27, 2014, from Nordlie, R.C., Foster, J.D., & Lange, A.J. (1999). Regulation of glucose production by the liver. Annual Review of Nutrition, 19, 379-406. Osborn, C.Y., Bains, S.S., & Egede, LE. (2010). Health literacy, diabetes self-care, and glycemic control in adults with type 2 diabetes. Diabetes Technology & Therapeutics, 12(11), 913. Pellico, L.H. (2013). Focus on Adult Health Medical Surgical Nursing. Lippincott Williams & Wilkins: Philadelphia, PA. Pessin, J.E., & Saltiel, A.R. (2000). Signaling pathways in insulin action: Molecular targets of insulin resistance. The Journal of Clinical Investigation, 106(2), 165-169. Saltiel, A.R. (2000). Series Introduction: The molecular and physiological basis of insulin resistance: Emerging implications for metabolic and cardiovascular diseases. Journal of Clinical Investigation, 106(2), 163-164. doi:10.1172/JCI10533. Stratton, I.M., Adler, A.I., Andrew, H., Neil, W., Matthews, D.R., Manley, S.E., Cull, C.A., Hadden, D., Turner, R.C., Holman, R.R. (on behalf of the U.K. Prospective Diabetes Study Group). (2000). Association of glycemia with macrovascular and microvascular complications of type 2 diabetes (UKPDS 35): Prospective observational study. British Medical Journal, 321, 405–412. University of California San Francisco (UCSF). (2014). The liver and blood sugar. Diabetes Education Online. Retrieved October 14, 2014 from United States Department of Agriculture (USDA). (n.d.). Retrieved from May 27, 2014, from

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