Download Free Medical Ultimate Goals Of Diabetes Treatment PowerPoint Presentation

Ultimate Goals Of Diabetes Treatment PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : DKA usually evolves rapidly over a 24-hour period.

Tags : Diabetes Treatment,Diabetes,Glucose Control

Published on : Dec 23, 2021 | Views : 867 | Downloads : 3

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

Ultimate Goals Of Diabetes Treatment Sustained Normal Blood Glucose Control Lowest Incidence of DKA/HHS/Hypoglycemia No Long Term Diabetes Complications No Acute Diabetes Complications = = Best Quality of Life with a Chronic Disease
Slide 2-

DCCT 10% reduction in HbA1c 43% reduced risk of retinopathy progression 18% increased risk of severe hypoglycemia with coma and/or seizure DCCT Research Group, N Engl J Med 1993, 329:977-986.
Slide 3-

Classifying Diabetes 3 GADA, glutamic acid decarboxylase; HLA, human leukocyte antigen; IAA, autoantibodies to insulin; IA-2A, the tyrosine phosphatase insulinoma antigen; ZnT8A, zinc transporter 8; T1aD, type 1 (immune-mediated) diabetes; T1bD, type 1 (idiopathic) diabetes; T2D, type 2 diabetes. *Needs to be refined for nonwhite population groups. Rewers M. Diabetes Metab J. 2012;36:90-97.
Slide 4-

Etiologic Classification of Diabetes 4 APS1, autoimmune polyendocrine syndromes 1; HLA, human leukocyte antigen; IPEX, immunodeficiency, polyendocrinopathy, enteropathy, X-linked syndrome; LADA, latent autoimmune diabetes of adults; MODY, maturity-onset diabetes of the young; PNDM, permanent neonatal diabetes mellitus. Rewers M. Diabetes Metab J. 2012;36:90-97.
Slide 5-

ppt slide no 5 content not found
Slide 6-

Clinical Features DKA usually evolves rapidly over a 24-hour period. Common, early signs of ketoacidosis include nausea, vomiting, abdominal pain, and hyperventilation. The earliest symptoms of marked hyperglycemia are polyuria, polydipsia, and weight loss. As hyperglycemia worsens, neurologic symptoms appear and may progress to include lethargy, focal deficits, obtundation, seizure, and coma.
Slide 7-

Case Presentation #1 A 17-yr-old Hispanic woman, presented with DKA resulting from discontinuation of insulin therapy. She had been diagnosed with diabetes 10 yr previously, had always required multiple daily injections of insulin, and had experienced several previous episodes of DKA. There was a history of diabetes in her maternal grandmother and mother. Her (BMI) 24.3 kg/m2. The physical examination was unremarkable except for signs of volume depletion; The arterial pH was acidemic, anion gap 24, serum bicarbonate 12 mmol/liter, and serum glucose 344 mg/dl. The patient was admitted to the hospital and received standard treatment for DKA with iv fluids and insulin. She recovered uneventfully and was discharged on the third hospital day on a regimen of NPH insulin twice daily with insulin lispro before meals. Baseline biochemistry and serology. Glycosylated hemoglobin (HbA1c) at presentation was 13.8%. Autoantibodies to β-cell antigens were measured : Autoantibodies to glutamic acid decarboxylase (GAD) 65 and IA-2 were absent in the serum. β-Cell functional reserve was assessed 1 wk after resolution of DKA by serum C-peptide levels after an overnight fast and after stimulation with glucagon. The fasting C-peptide level was undetectable (<0.5 ng/ml) at baseline and did not change after glucagon stimulation.
Slide 8-

Case Presentation #1-2 Evolution of β-cell function. β-Cell functional reserve was assessed annually in our clinic. C-peptide secretion was consistently absent, both at baseline and after glucagon stimulation. Conclusion. This young, lean Hispanic patient with childhood-onset diabetes and a family history of relatively early-onset diabetes has no evidence of β-cell autoimmunity, was unable to come off insulin therapy without relapse of ketoacidosis, and has had difficulty achieving optimal glycemic control. Shortly after the index episode of DKA, she had virtually no β-cell functional reserve, and this has not improved over time with intensive insulin therapy. She has the phenotype of what we have recently defined as “A−β−” KPD.
Slide 9-

Case Presentation #2 A 56-yr-old African-American man with no prior history of diabetes, presented with DKA. He had the 3 Ps and 25-lb weight loss developing over the preceding 2 months. The past medical history was significant for hypertension. One brother was known to have diabetes and was being treated with an oral medication. Brother has Type 2 DM, on OHA. His weight was 198 lb, height 5 ft-11 in, and BMI 28 kg/m2. Mild acanthosis nigricans was present on the neck. The remainder of the physical examination was unremarkable. Labs: pH was 7.22, anion gap 35, bicarbonate 12 mmol/liter, and glucose 765 mg/dl. The patient was admitted to the hospital and received standard treatment for DKA with iv fluids and insulin. He recovered uneventfully and was discharged on the third hospital day on a regimen of NPH insulin twice daily with insulin lispro before meals. 2. Baseline biochemistry and serology. HbA1c at the time of hospital admission was 12%. Evaluation of β-cell autoantibodies as described above revealed GAD65 autoantibodies in high titer, but not IA-2 autoantibodies. β-Cell functional reserve assessed 2 wk after the acute episode of DKA revealed a fasting C-peptide level of 1.15 ng/ml and a peak C-peptide level after glucagon stimulation of 1.62 ng/ml.
Slide 10-

Case Presentation #2-1 Evolution of β-cell function. Fasting C-peptide levels and peak responses to glucagon increased over time, then reached a plateau. In early 2007, the fasting C-peptide was 2.6 ng/ml, and the peak postglucagon level was 5.2 ng/ml. Clinical course. Following a protocol described previously, we gradually withdrew insulin therapy and substituted oral diabetic medications with close monitoring for recurrence of ketoacidosis or decline in glycemic control. The patient tolerated the withdrawal without mishap, and insulin was totally discontinued. Pioglitazone was added to the regime. He has had no recurrence of DKA. HbA1c levels have ranged between 6.2 and 7.8%, and the most recent was 7.4%. His weight has ranged between 218 and 232 lb, and the current BMI is 30.8 kg/m2. Blood pressure and fasting lipid levels are within desired ranges. His current medications are pioglitazone 15 mg/d, glipizide XL 10 mg/d, metformin 1000 mg twice daily, simvastatin 40 mg/d, metoprolol XL 50 mg/d, candesartan 32 mg/d, hydrochlorothiazide 25 mg/d, and aspirin 81 mg/d.
Slide 11-

Case Presentation #2-1 Conclusion. This middle-aged, overweight African-American patient, presenting with DKA as the first manifestation of diabetes, has evidence of β-cell autoimmunity, is able to come off insulin therapy without relapse of ketoacidosis, and has experienced significant glycemic improvement. Shortly after the acute episode of DKA, he had partially preserved β-cell functional reserve, and this improved further while he was being treated with oral antidiabetic agents. He has the phenotype of A+β+ KPD.
Slide 12-

Case Presentation #3-1 A 35-year-old woman is admitted to the hospital with severe abdominal pain, nausea, and vomiting. The pain radiates to her back. She has no history of diabetes mellitus. On physical examination, her blood pressure is 110/60 mm Hg and pulse rate is 100 beats/min. Her temperature is 99.5ºF (37.5ºC). Her height is 60.5 in (153.7 cm), and weight is 198 lb (90 kg) (BMI = 38 kg/m2). She has truncal obesity and acanthosis nigricans at the base of the neck and in the axillae bilaterally. On abdominal examination, there is tenderness to deep palpation below the xiphoid process in the midline. There are minimal bowel sounds. Laboratory tests results (sample drawn at admission): Serum sodium = 132 mEq/L (136-142 mEq/L) (SI: 132 mmol/L [136-142 mmol/L]) Serum glucose = 480 mg/dL (70-99 mg/dL) (SI: 26.6 mmol/L [3.9-5.5 mmol/L]) Bicarbonate = 15 mEq/L (21-28 mEq/L) (SI: 15 mmol/L [21-28 mmol/L]) Potassium = 5.5 mEq/L (3.5-5.0 mEq/L) (SI: 5.5 mmol/L [3.5-5.0 mmol/L]) Phosphate = 3.5 mEq/L (2.3-4.7 mg/dL) (SI: 1.1 mmol/L [0.7-1.5 mmol/L]) Arterial blood pH = 7.20 (7.35-7.45) Anion gap = 22 Lipase = 450 U/L (10-73 U/L) (SI: 7.52 µkat/L [0.17-1.22 µkat/L]) Hemoglobin A1c = 12.0% (4.0%-5.6%) (108 mmol/mol [20-38 mmol/mol]) Qualitative hCG, negative
Slide 13-

Case Presentation #3-2 CT of the abdomen shows stranding around the pancreas and no fluid collection. The patient is currently being treated with intravenous insulin and fluids. On hospital day 2, her anion gap is starting to close and her serum glucose value is 280 mg/dL (15.4 mmol/L). Her pain is controlled by intravenous narcotics. Diet is restricted to nothing-by-mouth. Which of the following is the best next step in this patient’s care?
Slide 14-

ppt slide no 14 content not found
Slide 15-

ppt slide no 15 content not found
Slide 16-

ppt slide no 16 content not found
Slide 17-

Impaired glucose utilization in peripheral tissues Increased hepatic and renal gluconeogenesis Increased glycogenolysis
Slide 18-

ppt slide no 18 content not found
Slide 19-

 Stress Hormones cortisol, epinephrine  Glucose Production  Lipolysis FFAs FFAs +  Glucose Uptake Illness  Glucose  Fatty Acids Illness Leads to Stress Hyperglycemia 19
Slide 20-

Stress Hyperglycemia Exacerbates Illness  Stress Hormones cortisol, epinephrine  Glucose Production  Lipolysis FFAs FFAs +  Glucose Uptake  Glucose  Fatty Acids Hemodynamic insult Electrolyte losses Oxidative stress Myocardial injury Hypercoagulability Altered immunity  Wound healing  Inflammation  Endothelial function Illness 20
Slide 21-

Predisposing or Precipitating Factors For HHS Previously undiagnosed diabetes
Slide 22-

Predisposing or Precipitating Factors For DKA
Slide 23-

Evaluation and laboratory findings (1) Assess vital signs, cardiorespiratory status, and mental status. Assess volume status: vital signs, skin turgor, mucosa, urine output. Obtain the following studies: serum glucose, urinalysis and urine ketones, serum electrolytes, BUN and creatinine, plasma osmolality, mixed venous blood gas, electrocardiogram; add serum ketones if urine ketones present.
Slide 24-

Evaluation and laboratory findings (2) DKA is characterized by hyperglycemia, an elevated anion gap* metabolic acidosis, and ketonemia. Dehydration and potassium deficits are often severe. Serum glucose is usually greater than 250 mg/dL (13.9 mmol/L) and less than 800 mg/dL (44.4 mmol/L). Additional testing is obtained based on clinical circumstances and may include: blood or urine cultures, lipase, chest x-ray.
Slide 25-

Management Stabilize the patient's airway, breathing, and circulation. Obtain large bore IV (≥16 gauge) access; monitor using a cardiac monitor, capnography, and pulse oximetry. Monitor serum glucose hourly, and basic electrolytes and venous pH or bicarbonate every two to four hours until the patient is stable. Determine and treat any underlying cause of DKA (eg, pneumonia or urinary infection, myocardial ischemia).
Slide 26-

ppt slide no 26 content not found
Slide 27-

ppt slide no 27 content not found
Slide 28-

Protocol for the management of adult patients with DKA – IV Fluids EQUATION Corrected Sodium = Measured sodium + (((Serum glucose - 100)/100) x 1.6) Alternatively (equivalent equation): = Measured sodium + 0.016 x (Serum glucose - 100)
Slide 29-

Protocol for the management of adult patients with DKA – Insulin
Slide 30-

Protocol for the management of adult patients with DKA – Potassium Replacement
Slide 31-

Protocol for the management of adult patients with DKA – Bicarbonate
Slide 32-

Protocol for the management of adult patients with HHs – IV Fluids EQUATION Corrected Sodium = Measured sodium + (((Serum glucose - 100)/100) x 1.6) Alternatively (equivalent equation): = Measured sodium + 0.016 x (Serum glucose - 100) Water deficit = (0.5 females, 0.6 males)(body weight in kg) × (1–[corrected sodium/140]) Corrected sodium = serum sodium + (1.6[glu-100/100])
Slide 33-

Protocol for the management of adult patients with HHs – Insulin
Slide 34-

Protocol for the management of adult patients with HHs – Potassium
Slide 35-

Kavanagh BP, McCowen KC. N Engl J Med. 2010;363:2540-2546. Guidelines From Professional Organizations on the Management of Glucose Levels in the ICU 35
Slide 36-

AACE/ADA Recommendations: All Patients in Critical Care Blood glucose target: 140-180 mg/dL Intravenous insulin infusion prefered Hypoglycemia Reassess the regimen if blood glucose level is <100 mg/dL Modify the regimen if blood glucose level is <70 mg/dL Moghissi ES, et al. Endocr Pract. 2009;15:353-369. 36
Slide 37-

Indications for IV Insulin Therapy Diabetic ketoacidosis Nonketotic hyperosmolar state Critical care illness (surgical, medical) Postcardiac surgery Myocardial infarction or cardiogenic shock NPO status in type 1 diabetes Labor and delivery Glucose exacerbated by high-dose glucocorticoid therapy Perioperative period After organ transplant Total parenteral nutrition therapy ACE Task Force on Inpatient Diabetes and Metabolic Control. Endocr Pract. 2004;10:77-82. 37
Slide 38-

Components of IV Insulin Therapy Concentrations should be standardized throughout the hospital Regular insulin in concentrations of 1 U/mL or 0.5 U/mL Infusion controller adjustable in 0.1-U doses Accurate bedside blood glucose monitoring done hourly (every 2 hours if stable) Potassium should be monitored and given if necessary Clement S, et al. Diabetes Care. 2004;27:553-591. 38
Slide 39-

Achieving Glycemic Targets in the ICU a. Van den Berghe G, et al. N Engl J Med. 2001;345:1359-1367. b. Goldberg PA, et al. Diabetes Care. 2004;27:461-467. c. Davidson PC, et al. Diabetes Care. 2005;28:2418-2423; d. Finfer S, et al. N Engl J Med. 2009;360:1283-1297. 39
Slide 40-

Example: Updated Yale Insulin Infusion Protocol Insulin infusion: Mix 1 U regular human insulin per 1 mL 0.9% NaCl Administer via infusion pump in increments of 0.5 U/h Blood glucose target range: 120-160 mg/dL Use glucose meter to monitor blood glucose hourly Bolus and initial infusion rate: Divide initial BG by 100, round to nearest 0.5 U for bolus and initial infusion rates Example: Initial BG = 325 mg/dL: 325/100 = 3.25, round up to 3.5: IV bolus = 3.5 U + start infusion at 3.5 U/h Subsequent rate adjustments: Changes in infusion rate are determined by the current infusion rate and the hourly rate of change from the prior BG level Shetty S, et al. Endocr Pract. 2012;18:363-370. 40
Slide 41-

Shetty S, et al. Endocr Pract. 2012;18:363-370.
Slide 42-

YNHH ICU Insulin Infusion Protocol Target BG: 120-160 Begin IV insulin: BG ÷100 = ___ U/hr Shetty S, et al. Endocr Pract. 2012;18:363-370.
Slide 43-

Insulin Infusion Protocol Performance BG (mg/dL) Time (hours) Shetty S, et al. Endocr Pract. 2012;18:363-370.
Slide 44-

Results BG, blood glucose. Shetty S, et al. Endocr Pract. 2012;18:363-370.
Slide 45-

Bedside Glucose Monitoring Point-of-care measurement Most practical and actionable for guiding treatment But need to consider limitations in accuracy Strong quality-control program essential Specific situations rendering capillary tests inaccurate Shock, hypoxia, dehydration Extremes in hematocrit Elevated bilirubin, triglycerides Drugs (acetaminophen, dopamine, salicylates) Clement S, et al. Diabetes Care. 2004;27:553-591. Kanji S, et al. Crit Care Med. 2005;33:2778-85. 45
Slide 46-

IV Insulin Protocols Key Points Several published protocols for intravenous insulin infusions Each may be suitable for different patient populations Ideal protocol: one that will work in a given institution All protocol implementation will require multidisciplinary interaction and education Other protocols needed to make inpatient glucose management a success include Protocols to manage hypoglycemia Protocols to guide the transition from intravenous to subcutaneous therapy 46
Slide 47-

Transition from IV to SC Insulin 47
Slide 48-

Considerations for Transition From IV to SC Insulin Which patients on IV insulin will need a transition to scheduled SC insulin? Type 1 DM Type 2 DM on insulin prior to admission Type 2 DM (or new hyperglycemia) requiring ≥2 units/hour of insulin Umpierrez G, et al. J Clin Endocrinol Metab. 2012;97:16-38. 48
Slide 49-

Transition From IV Insulin to SC Insulin IV insulin should be transitioned to SC basal bolus insulin therapy When patient begins to eat and BG levels are stable Because of short half-life of IV insulin, SC basal insulin should be administered at least 1-2 hours prior to discontinuing the drip Umpierrez G, et al. J Clin Endocrinol Metab. 2012;97:16-38. 49
Slide 50-

Additional Questions to Consider When Converting to SC Insulin Is the patient eating? If so, what and when? What are the concomitant therapies? Glucocorticoids? Inotropes? Vasoconstrictors? Will resolution of the illness(es) or change in concomitant therapies reduce insulin needs? 50
Slide 51-

Calculating the SC Insulin Dose Establish the 24-hour insulin requirement by extrapolating from the average intravenous insulin dose required over the previous 6-8 hours (if stable) Take 60%-80% of the total daily dose (TDD) Give one-half as an intermediate-acting or long-acting insulin for basal coverage Give other half as a short-acting or rapid-acting insulin in divided doses before meal Umpierrez G, et al. J Clin Endocrinol Metab. 2012;97:16-38. 51
Slide 52-

Prevention of Hypoglycemia 52
Slide 53-

Potential Harm From Insulin Therapy The Joint Commission considers insulin to be 1 of the 5 highest-risk medicines in the inpatient setting Consequences of errors with insulin therapy can be catastrophic In 2008, insulin accounted for 16.2% of harmful medication errors, more than any other product, in an analysis of the USP MEDMARX reporting program data In 2008-2009, 2685 insulin medication error event reports were submitted to the Pennsylvania Patient Safety Authority 78.7% (n=2113) involved a patient (NCC MERP harm index = C to I); 1.8% (n=49) resulted in patient harm (harm index = E to I) Medical surgical units accounted for 22.3% (n=599) of events; pharmacy for 8.7% (n=234), and telemetry for 7.1% (n=191) Drug omission constituted the largest proportion of errors (24.7%, n=662), followed by wrong drug reports (13.9%, n=374), and wrong dose/overdosage (13%, n=348) Pennsylvania Patient Safety Advisory. Pa Patient Saf Advis. 2010;7:9-17. Available at: http://www.patientsafetyauthority.org/ADVISORIES/AdvisoryLibrary/2010/Mar7(1)/Pages/09.aspx#bm7. 53
Slide 54-

(Reference: Mean BG 100-110 mg/dL) Kosiborod M, et al. Circulation. 2008:117:1018-1027. Mean Glucose and In-Hospital Mortality in 16,871 Patients With Acute MI 54
Slide 55-

Common Features Increasing Risk of Hypoglycemia in an Inpatient Setting Advanced age Decreased oral intake Chronic renal failure Liver disease Beta-blockers ACE/ADA Task Force on Inpatient Diabetes. Endocr Pract. 2006;12:458-468. 55
Slide 56-

Factors Increasing Risk of Hypoglycemia in an Inpatient Setting Lack of coordination between dietary and nursing leads to mistiming of insulin dosage with respect to food Inadequate glucose monitoring Inadequate insulin dose adjustment Lack of coordination between transportation and nursing Unsafe work environment Indecipherable orders Garg R et al. J Hosp Med. 2009;4(6):E5-E7. ACE/ADA Task Force on Inpatient Diabetes. Endocr Pract. 2006;12:458-468. 56
Slide 57-

Factors Increasing Risk of Medication Errors With Insulin Use of “sliding scale” insulin in the absence of regularly scheduled insulin Use of “U” for units being misread as a number BG testing reporting and transcription errors Similar names of products, manufacturer’s labeling Accessibility as floor stock Nonstandard compounded IV solutions and infusion rates Pennsylvania Patient Safety Advisory. Pa Patient Saf Advis. 2010;7:9-17. Available at: http://www.patientsafetyauthority.org/ADVISORIES/AdvisoryLibrary/2010/Mar7(1)/Pages/09.aspx#bm7. 57
Slide 58-

Triggering Events for Hypoglycemia Transportation off ward causing meal delay New NPO status Interruption of any of the following: Intravenous dextrose TPN Enteral feedings Continuous renal replacement therapy ACE Task Force on Inpatient Diabetes and Metabolic Control. Endocr Pract. 2004;10:77-82. 58
Slide 59-

Summary Hyperglycemia Common in critically patients, both with and without diabetes Predictor of adverse outcomes, including mortality Significant improvements in mortality and morbidity with intensive glycemic management have been demonstrated In some randomized controlled trials In “before and after” comparisons Mixed Med-Surg ICU Good (140-180 mg/dL), but not stringent (80-110 mg/dL) glucose control most reasonable strategy for critically ill patients IV insulin infusion, using a validated protocol to minimize hypoglycemia, is the preferred approach in critical care setting 59