Alcohol Withdrawal and Diabetes Mellitus Management October 20, 2014

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

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.

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) 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

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. American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). Arlington, VA: American Psychiatric Publishing. Retrieved September 30, 2014, from

(cont’d) DSM-V Diagnostic Criteria for Alcohol Use Disorder
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

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 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 88,0007 people (approximately 62,000 men and 26,000 women8) 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 NIAAA, 2014

Common, Fatal, Costly Problem
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

(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 Hoffman et al. (2013)

Office of Women’s Health at the U. S
Office of Women’s Health at the U.S. Department of Health and Human Services. (2013). Straight talk about alcohol. GirlsHealth.gov. Retrieved September 30, 2014, from

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 Hoffman et al. (2013)

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. Hoffman et al., 2013 National Institute on Alcohol Abuse and Alcoholism (NIAAA). (2014). Alcohol facts and statistics. Alcohol and Your Health. Retrieved September 30, 2014, from

Alcohol Withdrawal (If it doesn’t work, use this link: http://www

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. DSM-V

DSM-V Diagnostic Criteria for Alcohol Withdrawal
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.

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??) Hoffman et al. (2013)

Hoffman et al., 2013

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. Hoffman et al., 2013

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) Hoffman et al., 2013

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 Hoffman et al., 2013

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

Assessment: Clinical Institute Withdrawal Assessment (CIWA)
See Word Document for full CIWA and documentation sheet

Assessment: CIWA Calculation
Weed, 2011 MDCalc. (2014). CIWA-Ar for Alcohol Withdrawal. Retrieved September 20, 2014, from

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? Weed, 2011 Kosten, T.R., & O’Connor, P.G. (2003). Management of drug and alcohol withdrawal. New England Journal of Medicine, 348(18), personal experience of J.B.

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

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

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.

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 Weed, 2011 Hoffman et al., 2013 personal experience of J.B.

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

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 Weed, 2011 Hoffman et al., 2013 personal experience of J.B.

Interventions: Medications used at OSUWMC
Weed, H.G. (2011). Clinician’s Guide to Alcohol Withdrawal as a Secondary Diagnosis. 2nd Edition. From The Ohio State University Medical Center Evidence Based Practice Clinical Resources. Retrieved September 20, 2014, from

Evaluation Back to assessment – check CIWA score per the protocol
Re-assess Weed, 2011

Questions? National Institute on Alcohol Abuse and Alcoholism. (n.d.). What is a standard drink?. Alcohol and Your Health. Retrieved September 30, 2014, from

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), 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 National Institute on Alcohol Abuse and Alcoholism. (n.d.). What is a standard drink?. Alcohol and Your Health. Retrieved September 30, 2014, from Nurselabs.com (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. GirlsHealth.gov. Retrieved September 30, 2014, from Weed, H.G. (2011). Clinician’s Guide to Alcohol Withdrawal as a Secondary Diagnosis. 2nd Edition. From The Ohio State University Medical Center Evidence Based Practice Clinical Resources. Retrieved September 20, 2014, from

TAKE A BREAK (please)!

Diabetes

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! Diabetes is a huge problem in the United States today, and it is rapidly expanding. It is estimated that, by 2050, one in three Americans will have diabetes. Type 2 diabetes, which makes up 90 to 95% of the diabetes cases and was previously called “adult onset diabetes,” is affecting our children at younger ages than ever seen before; this is likely due to the obesity epidemic. Centers for Disease Control and Prevention (CDC). (2014). National Diabetes Statistics Report: Estimates of Diabetes and Its Burden in the United States, Atlanta, GA: U.S. Department of Health and Human Services.

From http://www. diabetes

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 In 2012, the cost of T2DM in the U.S. was estimated to be approximately $245 billion, a 41% increase from 2007 (ADA, 2013). The cost associated with T2Dm will continue to grow, as more individuals are diagnosed with diabetes every year; worldwide, diabetes incidence has doubled every 20 years since 1945 (King et al., 1999).

Diabetes Mellitus Definition Classifications
“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

American Diabetes Association (ADA). (2012)
American Diabetes Association (ADA). (2012). Standards of medical care in diabetes. Diabetes Care, 35(S1), S12, table 2. Retrieved October 14, 2014 from

Diabetes complications
This video demonstrates the complications from uncontrolled diabetes. Let’s watch.

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. To summarize what the video discussed …

… 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.

True or False? Diabetes is the leading cause of blindness, amputations, and kidney problems. FALSE! Poorly controlled diabetes is the leading cause of blindness, amputations, and kidney problems.

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. The best way to prevent diabetes-related complications is to have proper glycemic control, or normalized blood sugars. This can be achieved by eating the proper diet in the correct portion sizes, exercising regularly, and taking medications as prescribed, as well as checking blood sugars on a regular basis. Everyone’s treatment plan is different and determined in collaboration with one’s primary care provider.

Diabetes overview https://www.youtube.com/watch?v=MGL6km1NBWE
To summarize, the pancreas produces insulin in response to an increase in blood sugar, which occurs after eating food. The 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. Both result in high blood sugar levels, which leaves the cells starved of sugar.

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.

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!) Nordlie, R.C., Foster, J.D., & Lange, A.J. (1999). Regulation of glucose production by the liver. Annual Review of Nutrition, 19, University of California San Francisco (UCSF). (2014). The liver and blood sugar. Diabetes Education Online. Retrieved October 14, 2014 from

When BG level is low, less insulin is produced, and the pancreas’ alpha cells produce glucagon, which stimulates glucose release from the liver. The liver provides glucose any way that it can – first, through glycogenolysis (convert glycogen to glucose), then through gluconeogenesis, then ketogenesis. Decreased insulin in the body stimulates fat cells to break down into fatty acids and glycerol, as well as muscle cells to break down into amino acids. Glycerols and amino acids are converted into glucose by the liver and released into the blood stream, thereby increasing BG. GLUCOSE REGULATION BY THE LIVER (UCSF, 2014)

When BG level is low, less insulin is produced, and the pancreas’ alpha cells produce glucagon, which stimulates glucose release from the liver. The liver provides glucose any way that it can – first, through glycogenolysis (glycogen into glucose), then through gluconeogenesis, then through ketogenesis. In ketogenesis, low insulin level stimulates adipose tissue to break down fat cells into free fatty acids, which are taken up by the liver. The liver then breaks down these fatty acids into ketones to use as energy for less essential organs, reserving glucose for brain, RBCs, some of the kidneys. KETOGENSIS (UCSF, 2014)

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) Pessin, J.E., & Saltiel, A.R. (2000). Signaling pathways in insulin action: Molecular targets of insulin resistance. The Journal of Clinical Investigation, 106(2),

Insulin Functions Demonstrates glucose metabolism – from Below information from Pellico, L.H. (2013). Focus on Adult Health Medical Surgical Nursing. Lippincott Williams & Wilkins: Philadelphia, PA. Functions of insulin (Pellico, 2013): “Transports and metabolizes glucose for energy Stimulates storage of glucose as glycogen in the liver and muscle cells Signals liver cells to stop the release of glucose Enhances storage of dietary fat in adipose tissue Accelerates transport of amino acids into cells Facilitates the transport of potassium into cells Inhibits the breakdown of stored glucose, protein, and fat” (p. 817)

If blood sugar is too low, the pancreas secretes glucagon from the alpha cells of the islets of Langerhans, which stimulates glycogenolysis (glycogen into glucose) or gluconeogenesis (if no food for 8-12 hours, breakdown noncarbohydrates substances into glucose), which increases the blood sugar. In response to increased blood glucose levels, the pancreas secretes insulin from the beta cells of the islets of Langerhans, which transports glucose into the cells.

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 (> mg/dL) on two occasions Oral glucose tolerance test of mg/dL HbA1c % American Heart Association (AHA). (2014). About metabolic syndrome. American Heart Association. Retrieved October 14, 2014, from

Center for Disease Control and Prevention (CDC). (2014). Prediabetes
Center for Disease Control and Prevention (CDC). (2014). Prediabetes. Diabetes Public Health Resource. Retrieved October 14, 2014, from

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

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) Atkinson, M.A. (2012). The pathogenesis and natural history of type 1 diabetes. Cold Spring Harbor Perspectives in Medicine. American Diabetes Association (ADA). (2010). Diagnosis and classification of diabetes mellitus. Diabetes Care, 33(S1). Lightsey, R. (2011). Diagnosis and treatment of latent autoimmune diabetes in adults still evolving. ClinicalAdvisor. Retrieved October 13, 2014, from

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%) HbA1C is a measure of microvascular risk: The UKPDS, a longitudinal (from 1977 to 1997), multicenter (23 clinical sites), randomized controlled trial of 5,102 patients with T2DM who were treated with intensive therapy, demonstrated that every 1% decrease in HbA1C was correlated with a 37% decrease in relative risk for microvascular complications and a 21% decrease in relative risk of diabetes-related death (Boutati & Raptis, 2009; Stratton et al., 2000). HbA1c: Other conditions that influence HbA1C level include chronic renal failure, chronic liver disease, opiate use, antioxidant use, alcohol ingestion, and triclygeride level (Gallagher et al., 2009; NGSP, 2010a; Hinzmann et al., 2012). Any condition that increases the lifespan of erythrocytes will result in an elevated HbA1C, as the longer an erythrocyte survives, the longer the duration of glucose exposure and the more likely it is to become glyclated (NGSP, 2010a; Gallagher et al., 2009; Hinzmann et al., 2012). In addition, the number of reticulocytes influences HbA1C; increased numbers of reticulocytes decrease the erythrocyte mean age and therefore decreases HbA1C (Gallagher et al., 2009). Genetics influence HbA1C levels; studies have demonstrated that 62-9% of variance in HbA1C is genetic (Gallagher et al., 2009; Hinzmann et al., 2012). The average erythrocyte survives 117 days in men and 106 days in women, but a blood sample contains erythrocytes of various ages and therefore exposure to different levels of hyperglycemia. Plasma glucose levels from days prior to blood sample collection contribute a mere 10% to HbA1C, but levels from the most recent 30 days contribute 50% (Gallagher et al., 2009), so the HbA1C is actually a weighted average, with the plasma glucose levels from the most recent 30 days contributing more to the value, rather than a true mean (NGSP, 2010b).

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). JDRF. (n.d.). Type 1 Diabetes Facts. Retrieved October 15, 2014, from

From http://www. intechopen

T1DM Presenting Symptoms
DEHYDRATION Hyperglycemia Polydypsia Polyuria Polyphagia Glycosuria (if above renal reabsorption threshold of mg/dL) Blurred vision Weight loss Impaired growth Decreased immunity Diabetic Ketoacidosis (DKA) EVERYONE PRESENTS DIFFERENTLY – depends on how much beta cell function remains Glucose is an ostmotic agent = water follows it. Therefore, when spill glucose into urine, also secrete additional water, causing dehydration through osmotic diuresis. Atkinson, 2012; ADA, 2010

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 before meals and less than 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

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 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), doi: /JCI10533.

Saltiel, 2000, Figure 1

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%)

Obesity (especially visceral/trunk) – BMI >25 kg/m2 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 years) CDC, 2014; Pellico, 2013; and Longhurst, A.S. (2014). Type 2 Diabetes Statistics and Facts. Retrieved October 15, 2014, from

Impaired glucose metabolism HDL cholesterol <35mg/dL and/or triglyceride level >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

From http://www.ajmc.com/publications/supplement/2006/2006-11-vol12-n14Suppl/Nov06-2399ps369-s381/

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 Pellico, 2013, p. 820

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 before meals and less than 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

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 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 % of women with GDM develop T2DM in years. At risk for recurrent GDM with future pregnancies. Treatment: diet, exercise, insulin BG goals: < 95mg/dL pre-prandial < mg/dL 1 hour post-prandial < 120mg/dL 2 hours post-prandial CDC, 2014; Pellico, 2013

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

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

Neonatal Diabetes Mellitus
First 6 months of life Symptoms similar to that of T1DM Most commonly caused by mutations in the KCNJ11, ABCC8 or INS genes Management same as T1DM (need to replace insulin) National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). (2007). Monogenic forms of diabetes: Neonatal diabetes mellitus and maturity-onset diabetes of the young (NIH Publication No ). Bethesda, MD: National Diabetes Information Clearinghouse.

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 In addition to lifestyle management Stopped for pregnancy, illness, hospitalization

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 Faulds, E.R. (2014). Pharmacological Management of Type 2 Diabetes: Oral Medications and Noninsulin Injectables [Powerpoint slides]. Nursing 6111, May 2014.

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)

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

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)

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)

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)

http://www. pharmainfo
and

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 Dungan, K. (2014). Insulin in Inpatients and Outpatients [Powerpoint slides]. Presentation, May 2014.

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

Insulin Activity From

All charts are different!!!!!
From

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) INFORMATION FROM PELLICO, 2013: Intermediate acting have an onset of 2-4 hours, peak in 6-8 hours, and have a duration of hours. Usually taken after food. Long acting have an onset of 2 hours, no peak, and last for 24 hours; slight differences exist (see charts).

Bolus Insulin Rapid-acting Short-acting Lispro (Humalog)
Aspart (Novolog) Glulisine (Apidra) Short-acting Regular (Humulin R, Novolin R) FROM PELLICO, 2013: Rapid-acting have a 15 minute onset, peak in 60 minutes, and have a duration of 3-5 hours. Postprandial hyperglycemia, “mealtime insulin” Short-acting have a minute onset, peak in 2-3 hours, and have a duration of 4-6 hours. Administered minutes before a meal.

Multi- dose insulin using insulin analogs
Insulin Effect B L S Hs B Meals 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) Dungan, 2014 Pros: Better mealtime flexibility and coverage Less hypoglycemia Basal coverage throughout the day Better reproducibility of glycemic effects Cons: Multiple injections per day Cannot mix insulins More expensive

Combination Insulin Novolin 70/30 (Humulin 70/30) Humulin 50/50
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 Pre-mixed NPH have an onset of minutes, variable peak, and a duration of hours. Pre-mixed aspart have an onset of minutes, variable peak, and a duration of hours. Pre-mixed lispro have an onset of 5-15 minutes, variable peak, and a duration of hours. From WHY USE COMINBATION INSULIN?  simpler regimen, easier to use (for those with dexterity or vision problems) BUT need to have a consistent diet at set intervals (routine), may promote weight gain for T2DM

Twice-daily Split-mixed Regimens
Regular NPH Insulin Effect Dungan, 2014 “Not as flexible with this regimen – need to eat at consistent times May need a snack at bedtime to avoid overnight hypoglycemia – not good for T2DM due to goal of weight loss” (Dungan, 2014). B L S HS B 70/30 insulin: 70% NPH, 30% Regular 2/3 should be given before breakfast, 1/3 before supper

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

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

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 for instructions

Insulin Administration

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

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 CSII considerations: disruption of flow, change needle every 2-3 days, can be hooked up with a CGM, infection at needle sites, psychological implications, cost

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

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

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

Teaching: Medications

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 Pellico, 2013

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 mg/dL (affected by age and renal function) Keep a logbook/record There’s an (well, more than one!) app for that. Pellico, 2013

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 and 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 Pellico, 2013

Create Your Plate From

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 Drug interactions, variable absorption, often renal or liver dysfunction

Patient Predisposition
Pancreatic reserve Insulin resistance Treatment Illness Exogenous glucocorticoids Vasopressors Total parenteral nutrition Enteral nutrition Catecholamines HPA axis activation Inflammatory cytokines Lipotoxicity Hyperglycemia Dungan, 2014 Figure 2a: The etiology of hospital-related hyperglycemia is multi-factorial, incorporating patient-specific, illness-specific, and treatment-specific factors. Hyperglycemia may, in turn, exacerbate some illness-specific factors and increase the need for some treatment-specific factors, thus leading to a vicious cycle by which hyperglycemia begets further hyperglycemia. HPA=hypothalamic-pituitary-adrenal axis Etiology of Hospital Related Hyperglycemia

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, CO2 normal Attempt to correct low pH and low bicarbonate by “blowing off” CO2 = Kussmal respirations Pellico, 2013 Causes: lack of insulin (missed doses/administration issues, not enough prescribed, etc.), physical or emotional stress (counterregulatory hormones = glucagon, epinephrine, norepinephrine, cortisol = increase BG), illness or INFECTION (insulin resistance = increase BG)

DKA Signs/Symptoms Polyuria Polydypsia Diagnostic
pH 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 Pellico, 2013 Symptoms of dehydration: orthostatic hypotension, warm and dry skin, decreased skin turgor, flat neck veins, dry mucous membranes, weak and rapid pulse GI symptoms: anorexia, nausea, vomiting, abdominal pain, acetone breath HOW TO PREVENT: “sick days” rule – see BOX 30-7, page 843 – take insulin as prescribed or “sick day” dose, then retest frequently (every 3-4 hours)! Na low or normal, K low, Cl low

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: Initial K level high due to acidemia (from hydrogen movement into the cells) – hold K replacement until it declines. Insulin administration = push insulin into the cells. Also, rehydration = increased plasma volume = lower K concentration and urinary excretion of K

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, y.o., with or without T2DM Precipitating events: infection, acute or chronic illness, procedures such as dialysis or surgery, medications

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

HHNS Management Same as DKA, minus anion gap monitoring
Be very careful of fluid status (older patients)! See OSUWMC policy:

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? Pellico, 2013

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 Pellico, 2013, p

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 minutes (once symptoms resolve) Pellico, 2013

Hypoglycemia: Management
Glucagon 1 mg SQ or IM 25-50 mL ( g) of 50% D50W 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:

Have a great day! http://whatshouldwecallnursing.tumblr.com/
Have a wonderful semester!!!!! 

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 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, 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 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.

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, 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), Lightsey, R. (2011). Diagnosis and treatment of latent autoimmune diabetes in adults still evolving. ClinicalAdvisor. Retrieved October 13, 2014, from Longhurst, A.S. (2014). Type 2 Diabetes Statistics and Facts. Retrieved October 15, 2014, from 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 ). Bethesda, MD: National Diabetes Information Clearinghouse. National Institute of Diabetes, Digestive, and Kidney Diseases (NIDDK). (2011). National Diabetes Statistics, 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, 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), 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), doi: /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.). ChooseMyPlate.gov. Retrieved from May 27, 2014, from

Alcohol Withdrawal and Diabetes Mellitus Management October 20, 2014

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