Presentation on theme: "Alcohol Withdrawal and Diabetes Mellitus Management October 20, 2014"— Presentation transcript:
1 Alcohol Withdrawal and Diabetes Mellitus Management October 20, 2014 Jennifer Bauman, RN, BA, PCCNPhD StudentThe Ohio State University College of NursingNursing 6270Autumn 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 interventionAlcohol 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
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.American Psychiatric Association. (2013). Diagnostic and statistical manual of mentaldisorders (5th ed.). Arlington, VA: American Psychiatric Publishing. Retrieved September 30, 2014, from
5 (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
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 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).3Youth (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.7In 2012, alcohol-impaired-driving fatalities accounted for 10,322 deaths (31 percent of overall driving fatalities).9 NIAAA, 2014
7 Common, Fatal, Costly Problem Economic Burden:In 2006, alcohol misuse problems cost the United States $223.5 billion.10Almost three-quarters of the total cost of alcohol misuse is related to binge drinking.10Global 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.11Alcohol 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.11Globally, 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.13Family Consequences:More than 10 percent of U.S. children live with a parent with alcohol problems, according to a 2012 study.14
8 (Ethyl) Alcohol = Ethanol Ethyl alcohol is the only type of consumable ethanol.Central nervous system (CNS) depressantSimultaneously enhances inhibitory tone via modulation of gamma-aminobutyric acid (GABA) activity and dampens excitatory tone via modulation of excitatory amino acid activityTo 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 CNSHoffman et al. (2013)
9 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
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 GABAMore inhibitor is needed to maintain constant inhibitory tone = tolerance to large doses (think of the “functioning” alcoholic)Glutamate: one of the major excitatory amino acidsWhen 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 arousalHoffman et al. (2013)
11 Long term effects of Alcohol Misuse Liver diseaseCirrhosis“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 cirrhosisFatty liver diseaseHepatitis1 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 breastPancreatitisMalnutritionWernicke’s EncephalopathyHigher risk for injury, especially fallsImpaired judgment = high risk behavior = increased risk for STIs, sexual assault, etc.Hoffman et al., 2013National Institute on Alcohol Abuse and Alcoholism (NIAAA). (2014). Alcohol facts and statistics. Alcohol and Your Health. Retrieved September 30, 2014, from
12 Alcohol Withdrawal (If it doesn’t work, use this link: http://www
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.DSM-V
14 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.
15 Symptoms of Withdrawal InsomniaAnxiety and/or FearRestlessnessNausea and/or VomitingHeadacheSeizures – may need CT scan, lumbar punctureAltered Sensory Perceptions, including visual (common), tactile (common), auditoryTremorsDiaphoresisTachycardia, which may/may not be accompanied by palpitations (why??)Hoffman et al. (2013)
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 consumptionArterial pH rises due to hyperventilation (respiratory alkalosis) = decrease in cerebral blood flowFluid and electrolyte status:Hypovolemic r/t diaphoresis, hyperthermia, vomiting, and tachypneaHypokalemia r/t renal and extrarenal losses, alterations in aldosterone levels, and changes in potassium distribution across the cell membraneHypomagnesemia r/t malnutrition; may predispose to dysrhythmia (torsades des pointes) and seizuresHypophosphatemia r/t malnutrition; may contribute to cardiac failure and rhabdomyolysis.Hoffman et al., 2013
18 Who is at risk for DT? A history of sustained drinking A history of previous DTOver age 30The presence of a concurrent illnessThe presence of significant alcohol withdrawal in the presence of an elevated alcohol levelA 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
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 derangementsDrug overdoseHepatic failureGastrointestinal bleedingHoffman et al., 2013
20 Nursing Management: ADPIE AssessmentDiagnosisPlan and Goals of CareImplementationEvaluation
21 Assessment: Clinical Institute Withdrawal Assessment (CIWA) See Word Document for full CIWA and documentation sheet
22 Assessment: CIWA Calculation Weed, 2011MDCalc. (2014). CIWA-Ar for Alcohol Withdrawal. Retrieved September 20, 2014, from
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?Weed, 2011Kosten, 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.
24 Continued assessment … Vital signs – what would you expect to find, and why?See “Symptoms” slide for signs/symptoms of withdrawalRisk for elopement, falls, aspirationSmoking statusBlood sugar – Accu checkUrine drug/toxicity screenBlood work to collect:ChemistryComplete Blood Count (CBC) with differential and plateletCoagulation panel (PT, INR, PTT)Liver Function Tests (LFT)Uric acidAlcohol, whole bloodDrug/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 withdrawalRisk for Sensory-Perceptual Alterations r/t alcohol withdrawalAnxiety and/or Fear r/t alcohol withdrawal aeb restlessness, tachycardia, hypertensionRisk for Aspiration (Ineffective Breathing Pattern) r/t alcohol withdrawalRisk for Seizures r/t alcohol withdrawal
26 Plan and Goals of CareThe 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’ stationIf 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 administrationAvoid the use of restraints, especially LBBWeed, 2011Hoffman et al., 2013personal experience of J.B.
28 Interventions Bed exit alarm Seizure pads on bedrails HOB at 30 degrees or greater, if no contraindicationsQuiet, dark, calm environmentFan or cool washclothsNurse should present calm demeanorLimit settingNicotine replacementConsults: social work, nutrition, psychiatry, nicotine dependence
29 Interventions: Medications Chlordiazepoxide (Librium) – long-acting benzodiazepineDiazepam (Valium) – long-acting benzoLorazepam (Ativan) – short-acting benzoFlumazenil (Romazicon) – reversal agent for benzoClonidine (Catapres) - centrally acting alpha-2 agonist, for severe DT, but may mask symptoms of worsening statusPhenobarital – anticonvulsant, if severe DT or status epilecticusAVOID the routine use of anticonvulsants, beta blockers (mask symptoms) and antipsychotics (lower the seizure threshold)Vitamins, especially folic acid and thiamineElectrolytes, especially glucose, magnesium, phosphate, and potassiumIntravenous fluids, if not contraindicatedWeed, 2011Hoffman et al., 2013personal experience of J.B.
30 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
31 Evaluation Back to assessment – check CIWA score per the protocol Re-assessWeed, 2011
32 Questions?National Institute on Alcohol Abuse and Alcoholism. (n.d.). What is a standard drink?. Alcohol and Your Health. Retrieved September 30, 2014, from
33 ReferencesAmerican Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). Arlington, VA: American Psychiatric Publishing. Retrieved September 30, 2014, fromHoffman, R.S., & Weinhouse, G.L. (2013). Management of moderate and severe alcohol withdrawal syndromes. In S.J. Traub & J. Grayzel (Eds.), UpToDate. Retrieved fromKosten, 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, fromNational Institute on Alcohol Abuse and Alcoholism (NIAAA). (2014). Alcohol facts and statistics. Alcohol and Your Health. Retrieved September 30, 2014, fromNational Institute on Alcohol Abuse and Alcoholism. (n.d.). What is a standard drink?. Alcohol and Your Health. Retrieved September 30, 2014, fromNurselabs.com (n.d.). 5 Alcohol Withdrawal Nursing Care Plans. Retrieved September 30, 2014, fromOffice 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, fromWeed, 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
37 Diabetes: A huge public health problem Diabetes affects 29.1 million people of all agesDiagnosed: 21 millionUndiagnosed: 8.1 millionThat’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-diabetesBy 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 ItsBurden in the United States, Atlanta, GA: U.S. Department of Health and Human Services.
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 billionIndirect: $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 T2DMIn 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).
40 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).ClassificationsPrediabetesType 1 Diabetes Mellitus (T1DM)Type 2 Diabetes Mellitus (T2DM)Gestational Diabetes MellitusMonogenic Diabetes MellitusOther causes: surgery, medications, pancreatic disease
41 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
42 Diabetes complications https://www.youtube.com/watch?v=pQjWgOSFChIThis video demonstrates the complications from uncontrolled diabetes. Let’s watch.
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.To summarize what the video discussed …
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.FALSE! Poorly controlled 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.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.
47 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.
48 Pathophysiology Overview The pancreas produces insulin in response to an increase in blood sugar, which occurs after eating foodInsulin 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 glycogenGlycogenolysis: release of glucose by turning glycogen into glucoseGluconeogenesis: release of glucose by harvesting amino acids, waste products, fat byproductsKetogenesis: 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
51 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)
52 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)
53 Insulin Discovered in 1922 by Banting and Best (Saltiel, 2000) Anabolic (i.e., storage) hormoneEssential for appropriate tissue development, growth, and maintenance of whole-body glucose homeostasisSecreted 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 tissueAffects lipid metabolism by increasing lipid synthesis in liver and fat cells and enhancing fatty acid release from triglycerides in fat and muscleActs 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),
54 Insulin FunctionsDemonstrates glucose metabolism – fromBelow 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 energyStimulates storage of glucose as glycogen in the liver and muscle cellsSignals liver cells to stop the release of glucoseEnhances storage of dietary fat in adipose tissueAccelerates transport of amino acids into cellsFacilitates the transport of potassium into cellsInhibits the breakdown of stored glucose, protein, and fat” (p. 817)
55 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.
56 Pre-Diabetes and Metabolic Syndrome Metabolic Syndrome (AHA, 2014)Affects approximately 1/3 of AmericansIncreased risk for diabetes, stroke, heart disease3 of 5 criteriaFasting BG greater than 100 mg/dLWaist 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/dLHDL less than 50mg/dL for women, 40mg/dL for menPre-diabetes (CDC, 2014; ADA, 2012)15-30% of those with prediabetes will develop T2DM in 5 yearsElevated fasting BG (> mg/dL) on two occasionsOral glucose tolerance test of mg/dLHbA1c %American Heart Association (AHA). (2014). About metabolic syndrome. American Heart Association. Retrieved October 14, 2014, from
57 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
58 Treatment of Prediabetes and Metabolic Syndrome LOSE WEIGHTPhysical activity >150 minutes/weekDietary considerationsControl BP, lipids, cholesterol levelsDiabetes Prevention Program (DPP)
60 Type 1 Diabetes INSULIN DEPENDENT – no insulin is made by the pancreas 5-10% of total diabetes casesGenetic predisposition and environmental factorsAutoimmune destruction of insulin-producing beta cellsAlso 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 = idiopathic50-75% of cases diagnosed in childhood or adolescence25-50% diagnosed in adulthoodLatent 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
61 T1DM TestingHemoglobin 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 producingOral glucose tolerance test >200mg/dLFasting BG > 126mg/dLFor 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).
62 Risk Factors/Demographics Onset at any age, but most are diagnosed when under age 30Certain HLA types = 3-5x higher risk of T1DM (Pellico, 2013)Genetic predisposition PLUS environmental factorsMore 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
64 T1DM Presenting Symptoms DEHYDRATIONHyperglycemiaPolydypsiaPolyuriaPolyphagiaGlycosuria (if above renal reabsorption threshold of mg/dL)Blurred visionWeight lossImpaired growthDecreased immunityDiabetic Ketoacidosis (DKA)EVERYONE PRESENTS DIFFERENTLY – depends on how much beta cell function remainsGlucose 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
65 T1DM TreatmentNew therapies: Vc-01 (beta cell encapsulation), islet cell transplantMedications: Insulin (discussed later in the presentation)Monitor blood sugarsMaintain 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 managementReduce carbohydrate intake, especially simple carbohydrates (i.e., anything that ends in an “–ose”) … High-fiber, low glycemic index foods are bestPhysical activity >150 minutes/weekWeight managementMental health considerations
66 Type 2 Diabetes (T2DM) NON-INSULIN DEPENDENT Obesity, sedentary lifestyle, aging, genetic predispositionIncreased 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 developmentSaltiel, 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.
68 T2DM TestingC-peptide level moderate to high – positive correlation with insulinOral glucose tolerance test >200mg/dLFasting BG > 126mg/dLHbA1C >6.5% (some organizations state >7% - most say >6.5%)
69 Risk Factors/Demographics Obesity (especially visceral/trunk) – BMI >25 kg/m2Poor dietary habitsMen slightly more than womenSedentary lifestyle/physical inactivityOlder age (>45 y.o.)Family history of diabetesIf 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
70 Risk Factors/Demographics Impaired glucose metabolismHDL cholesterol <35mg/dL and/or triglyceride level >250mg/dLInsulin resistance and hyperinsulinemiaRace/ethnicityIncreased risk for African Americans, Hispanics/Latinos, American Indians (e.g., Pima Indians), some Asians, and Native Hawaiians or other Pacific IslandersAsian 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
71 From http://www.ajmc.com/publications/supplement/2006/2006-11-vol12-n14Suppl/Nov06-2399ps369-s381/
72 T2DM Presenting Symptoms Slow progression of glucose intolerance, so minimal to no symptoms (usually)May includeIrritabilityFatiguePolydipsiaPolyuriaPolyphagia (sometimes)Poor wound healingFrequent infectionsVision changesPellico, 2013, p. 820
73 T2DM TreatmentMedications: oral agents, then insulin in later stages (we’ll speak more about this later)Monitor blood sugarsMaintain 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 managementReduce carbohydrate intake, especially simple carbohydrates (i.e., anything that ends in an “–ose”) … High-fiber, low glycemic index foods are bestPhysical activity >150 minutes/weekWeight management – lose 5-10% of body weightMental 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 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, insulinBG goals:< 95mg/dL pre-prandial< mg/dL 1 hour post-prandial< 120mg/dL 2 hours post-prandialCDC, 2014; Pellico, 2013
75 Monogenic DiabetesTwo forms: Maturity Onset Diabetes of the Young (MODY) and Neonatal Diabetes Mellitus1-5% of U.S. diabetics have monogenic diabetes, usually MODYDue to mutations in a single gene20 genes have been implicated in the development of monogenic diabetesMay happen spontaneously BUT has strong hereditary componentManagement depends on severity of diseaseGenetic testing of family members necessary
76 Maturity Onset Diabetes of the Young (MODY) More common than Neonatal DiabetesOften misdiagnosed as T1DM if found in adolescence or T2DM if later in lifePresentation depends on severity; hyperglycemia may be discovered on routine lab workEach child has a 50% chance of inheriting the MODY geneMost commonly caused by mutations in the HNF1A gene or the GCK gene
77 Neonatal Diabetes Mellitus First 6 months of lifeSymptoms similar to that of T1DMMost commonly caused by mutations in the KCNJ11, ABCC8 or INS genesManagement 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.
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 cellsSulfonylureasNonsulfonylurea insulin secretagogues (meglitinides and phenylalanine derivatives)BiguanidesAlpha-glucosidase inhibitorsThiazolidinediones (glitazones)SEE TABLE 30-6 (pages 836-7) IN BOOKIn addition to lifestyle managementStopped for pregnancy, illness, hospitalization
79 SulfonylureasAction: directly stimulate the pancreas to secrete insulin, increase insulin effectiveness at cellular level, decrease glucose production by the liverLower HbA1c by 1-2% (Faulds, 2014)Must have a functioning pancreas, liver, kidneysSide effects: hypoglycemia; mild GI; sulfa allergy; weight gain; interact with NSAIDs, warfarin, sulfonamidesRecommend not to take with beta blocker (mask symptoms of hypoglycemia)No alcoholSecond-generation fewer side effects, drug interactions, excreted by liver and kidneysGlipizide, glyburide, glimepirideFaulds, E.R. (2014). Pharmacological Management of Type 2 Diabetes: Oral Medications and Noninsulin Injectables [Powerpoint slides]. Nursing 6111, May 2014.
80 Non sulfonylurea Insulin Secretagogues Action: similar action as sulfonylureasDecrease HbA1c by 1-2% (Faulds, 2014)Rapid onset, short duration must be taken with mealsSide effects: hypoglycemia; weight gain (less than Sulf.); interactions with ketoconazole, fluconazole, erythromycin, rifampin, isoniazidrepaglinide (Prandin), naglitinide (Starlix)
81 BiguanidesAction: decreasing hepatic production of glucose, facilitate action of insulin on peripheral receptor sitesLower HbA1c 1-2% (Faulds, 2014)May be used with Sulf. to further lower BGDo not use if renal or liver impairment, respiratory insufficiency, infection, alcohol abuseSide effects: lactic acidosis, GI disruptions, drug interactionsD/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 BGDecrease HbA1c 0.5-1% (Faulds, 2014)Side effects: hypoglycemia, GI side effects, drug interactionsTake with first bite of foodMonitor liver functionDo not use if renal or GI dysfunction, cirrhosisacarbose (Precose), miglitol (Glyset)
83 ThiazolidinedionesAction: Sensitize body tissue to insulin, stimulate insulin receptor sitesDecrease HbA1c 0.5-1% (Faulds, 2014)May be used in combination with other medsSide effects: hypoglycemia, anemia, weight gain, edema, liver dysfunction, drug interactions, hyperlipidemia, impaired platelet function, decrease effectiveness of oral contraceptivespioglitazone (Actos), rosiglitazone (Avandia)
84 DPP-4 Inhibitors/Incretin Enhancers Action: stimulates release of insulin, prevents secretion of glucagon, slows postprandial gastric emptyingDecrease HbA1c 0.5-1% (Faulds, 2014)Side effects: may promote weight loss, GI disturbances, hypoglycemia, pancreatitisCombination with metformin or Sulf.sitagliptin (Januvia), saxaglipton (Onglyza), exenatide (Byetta)
86 Who gets insulin? (Dungan, 2014) All T1DMDepending on severity, GDM (pregnancy)Eventually, most T2DMAt the time of diagnosis, approximately 50% of beta cell function is lostOnly a matter of time (average about 10 years) before require insulinHbA1c > 8% on two oral agentsUnable to take oral agentsHbA1c > 10%SymptomaticOtherHospitalizationCorticosteroid administrationInfectionCostDungan, K. (2014). Insulin in Inpatients and Outpatients [Powerpoint slides]. Presentation, May 2014.
92 Basal Insulin Provides coverage throughout the day Syringe, pen, pump Intermediate acting – cloudyNPH (Humulin N, Novolin N)Long acting – DO NOT MIXGlargine (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).
93 Bolus Insulin Rapid-acting Short-acting Lispro (Humalog) Aspart (Novolog)Glulisine (Apidra)Short-actingRegular (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.
94 Multi- dose insulin using insulin analogs Insulin EffectBLSHsBMealsAspart: 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, 2014Pros:Better mealtime flexibility and coverageLess hypoglycemiaBasal coverage throughout the dayBetter reproducibility of glycemic effectsCons:Multiple injections per dayCannot mix insulinsMore expensive
95 Combination Insulin Novolin 70/30 (Humulin 70/30) Humulin 50/50 70% NPH30% RegularHumulin 50/5050% each NPH and RegularNovolog Mix 70/3070% Aspart protamine suspension30% AspartHumalog Mix 75/2575% Lispro protamine suspension25% LisproHumalog Mix 50/5050% each Lispro protamine suspension and LisproPre-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.FromWHY 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
96 Twice-daily Split-mixed Regimens RegularNPHInsulin EffectDungan, 2014“Not as flexible with this regimen – need to eat at consistent timesMay need a snack at bedtime to avoid overnight hypoglycemia – not good for T2DM due to goal of weight loss” (Dungan, 2014).BLSHSB70/30 insulin: 70% NPH, 30% Regular2/3 should be given before breakfast, 1/3 before supper
97 Medication calculation Carbohydrate count5 grams of CHO to 1 unit of insulin for tightest controlCan also be 10, 15, or 20 grams CHO: 1 unitSliding scale insulin (SSI) for BGOften 1 unit for every 50 mg/dL over 150 mg/dLDifferent 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/dLHow 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 totalOrder states 10 grams CHO: 1 unit aspart insulin
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 dateRoll vial between hands (do not shake)Pen versus syringe/needleSyringe selection1ml, .5ml, .3ml27 or 29 gauge needle, 0.5 inches longMay draw up insulin up to 3 weeks early, store with needle in upright positionSubcutaneous sites: posterior arms, anterior thighs, hips, abdomenRotate sites to prevent lipodystrophySee page for instructions
101 Insulin Administration Complications Insulin resistanceMorning hyperglycemiaDawn phenomenon: relatively normal BG until 3am, due to nocturnal surges in growth hormone secretionsSomogyi effect: nocturnal hypoglycemia with rebound hyperglycemiaInsulin waning: progressive increase in BG from bedtime to morningLocal allergic reaction 1-2 hours after administrationSystemic allergic reaction (hives) – rareLipodystrophyLipoatrophy: loss of subcutaneous fat, slight dimpling or pitting of subcutaneous fatLipohypertrophy: fibrofatty mass, raised and hardened tissue
102 Other Forms of InsulinContinuous Subcutaneous Insulin Infusion (CSII) pumpU-500 insulinMost insulin is 100 units/1 mL, this is 5 TIMES the normal concentrationHigh-risk medicationUsed for those with poor absorption, insulin resistance, large dosesCSII considerations: disruption of flow, change needle every 2-3 days, can be hooked up with a CGM, infection at needle sites, psychological implications, cost
103 Other Forms of Insulin, cont. Inhaled insulinFast absorptionNot for those with lung diseasePre-mealExuberaAfrezzaPeak minutes, duration 2-3 hoursLess weight gainFewer episodes, less severe hypoglycemia
104 Patient Teaching Gerontologic Considerations – page2 821-22 (Box 30-4) MedicationsPhysical activityNutritionSelf-monitoring of blood glucose (SMBG)Care for the following:FeetEyesKidneysHeart/brainMental healthTeethAlso higher risk for fatty liver disease
105 Gerontologic Considerations Age-related changes make diabetes management difficultSee Box 30-4 on page 822
107 Teaching: Physical Activity Goal > 150 minutes per weekWeight control, improve insulin utilization, ease stress, CVD risk factor improvement (i.e., lower lipids, increase HDL, decrease total cholesterol and triglycerides)Slow, gradual increaseConsistent, daily exerciseFor those who take insulin, may need a snack after exercise to avoid hypoglycemiaPellico, 2013
108 Teaching: SMBGT2DM who are not on insulin 2-3 times per week, including a 2-hour post-prandial, also during medication changes or suspected hyper- or hypoglycemiaIf on insulin before meals and at bedtime, suspected hyper- or hypoglycemiaContinuous Glucose Monitoring (CGM)Urine Glucose Testing: renal threshold for glucose is mg/dL (affected by age and renal function)Keep a logbook/recordThere’s an (well, more than one!) app for that.Pellico, 2013
109 Teaching: NutritionConsistent carbohydrate and caloric intake, at consistent intervals (especially for those who take insulin) – to prevent hypoglycemiaPersonalize care: consider lifestyle, preferences, culture, ethnicity, eating timesInclude skills such as reading labels, eating out, adjusting meal plan for special occasions/illness/exerciseExchange List for Meal Planning – see page andCreate Your Plate:50-60% calories from carbohydrates, 20-30% from fat (cholesterol less than 200mg/day, saturated fat <7%), 10-20% from proteinFiberSoluble: legumes, oats, fruits (help lower LDL and BG)Insoluble: whole grains, cereals, vegetablesPellico, 2013
111 Inpatient Diabetes Management Usually hyperglycemia, but also hypoglycemiaTypically discontinue oral agents, switch to bolus insulin (lispro and aspart are commonly used at OSUWMC) – why no oral agents?Acute illnesses = hyperglycemiaSteroid administrationNPO for procedure, etc.Electrolyte managementDrug interactions, variable absorption, often renal or liver dysfunction
112 Patient Predisposition Pancreatic reserveInsulin resistanceTreatmentIllnessExogenous glucocorticoidsVasopressorsTotal parenteral nutritionEnteral nutritionCatecholaminesHPA axis activationInflammatory cytokinesLipotoxicityHyperglycemiaDungan, 2014Figure 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 axisEtiology of Hospital Related Hyperglycemia
113 Complications requiring hospitalization: Diabetic Ketoacidosis (DKA) Caused by lack of insulinResults in hyperglycemia, ketosis, dehydration, electrolyte loss, acidosisNo 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 lossBreakdown of fat into free fatty acids and glycerol (see previous slides) converted into ketone bodies by liver metabolic acidosisABG: pH low, bicarbonate low, CO2 normalAttempt to correct low pH and low bicarbonate by “blowing off” CO2 = Kussmal respirationsPellico, 2013Causes: 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)
114 DKA Signs/Symptoms Polyuria Polydypsia Diagnostic pHBG > 250 mg/dLSerum bicarbonate low (0-15mEq/L0Serum and urine ketonesGlucose in urineNa, K, Cl serum levels abnormal – how?!?Anion gapBlurred vision (osmotic changes on the lens)SEE FIGURE 30-7 on page 842Osmotic diuresis Water and electrolyte loss dehydration circulatory failureMetabolic acidosis CNS depression comaPellico, 2013Symptoms of dehydration: orthostatic hypotension, warm and dry skin, decreased skin turgor, flat neck veins, dry mucous membranes, weak and rapid pulseGI symptoms: anorexia, nausea, vomiting, abdominal pain, acetone breathHOW TO PREVENT: “sick days” rule – see BOX 30-7, page 843 – take insulin as prescribed or “sick day” dose, then retest frequently (every 3-4hours)!Na low or normal, K low, Cl low
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 q2-4hWHY DOES K SHIFT IN/OUT OF CELLS?!Acidosis reversed by insulin administrationInsulin gttDo not lower BG too quickly!Hourly BG checksDextrose when BG < 250mg/dLSee OSUWMC policy: https://onesource.osumc.edu/sites/ebm/Documents/Guidelines/Type1Diabetes.pdfInitial 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
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 ketosisOlder, y.o., with or without T2DMPrecipitating events: infection, acute or chronic illness, procedures such as dialysis or surgery, medications
117 HHNS Signs/Symptoms Hypotension Dehydration (more than DKA) TachycardiaNeurologic signs due to cerebral dehydration from hyperosmolalitySensory alterationsSeizuresHemiparesis
118 HHNS Management Same as DKA, minus anion gap monitoring Be very careful of fluid status (older patients)!See OSUWMC policy: https://onesource.osumc.edu/sites/ebm/Documents/Guidelines/Type2Diabetes.pdf
119 Complication requiring hospitalization: Hypoglycemia Causes: too much insulin or OHA, too little food, excessive PAOften prior to mealsThink about insulin profiles – when does it peak?Pellico, 2013
120 Hypoglycemia: Symptoms DIFFERENT FOR EVERY PERSONAutonomic Nervous System (ANS) (onset)Epinephrine, Norepinephrine releasedSweating, tremor, tachycardia, palpitations, anxiety, hungerCentral Nervous System (CNS) (intermediate)Brain cells do not have fuelImpaired concentration, headache, lightheaded, dizzy, confusion, forgetful, numb lips/tongue, slurred speech, impaired coordination, labile emotions, irrational or combative behavior, double vision, drowsinessCNS (severe)Disoriented, seizures, somnolence, LOCPellico, 2013, p
121 Hypoglycemia: Management IF ABLE TO SWALLOW SAFELY, Give CHO15 grams of fast-acting carbohydrate PO3-4 glucose tablets4-6 oz fruit juice or soda (non-diet)6-10 hard candies2-3 TBL sugar/honeyRetest BG within 15 minutes; retreat if less than 0-75 mg/dLPlus snack with protein and starch within minutes (once symptoms resolve)Pellico, 2013
122 Hypoglycemia: Management Glucagon 1 mg SQ or IM25-50 mL ( g) of 50% D50W via IVP at 10mL/minBe sure to evaluate if patient has insight to hypoglycemia, re-evaluate BG 15 minutes after interventionSee OSUWMC policy for hypoglycemia management: https://onesource.osumc.edu/sites/diabetes/Documents/Hypoglycemia.pdf
123 Have a great day! http://whatshouldwecallnursing.tumblr.com/ Have a wonderful semester!!!!!
124 ReferencesAmerican 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.
125 ReferencesKing, 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, fromLonghurst, A.S. (2014). Type 2 Diabetes Statistics and Facts. Retrieved October 15, 2014, fromMercola, J. (2014). Sugar Consumption Accounts for a Big Chunk of Health Care Costs. Retrieved May 27, 2014, fromNational 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, fromNordlie, 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 fromUnited States Department of Agriculture (USDA). (n.d.). ChooseMyPlate.gov. Retrieved from May 27, 2014, from