Diabetic emergencies

1. Diabetic emergencies Monika Pitzele, M.D., Ph.D. Mt. Sinai Hospital Chicago, IL

2. Outline • Physiology of diabetes • Type I or Type II • New onset diabetics • Hyperglycemia • Diabetic ketoacidosis • Hyperosmolar hyperglycemic state • Pediatric population • Hypoglycemia

3. Physiology of diabetes

4. Insulin production

5. Insulin in glucose metabolism

6. When insulin is absent

7. Ketone body formation (fuel for brain, muscle)

8. Ketone bodies acetoacetate acidosis

9. Type I diabetes ● No circulating insulin ● Pancreatic βcells do not respond to insulinogenic stimuli ● 5-10% of cases ● Children and young adults

10. Type II diabetes • Insulin resistance, relative insulin deficiency or combination of both • 80-90% of cases • After age 40 • Obesity

11. Diagnostic criteria • Fasting plasma glucose ≥126mg/dLOR • Casual plasma glucose ≥200mg/dLand symptoms of hyperglycemia OR • During the oral glucose tolerance test 2h plasma glucose ≥200mg/dLOR • HbA1c≥6.5%

12. New onset diabetics • Up to 30% patients in DKA are new onset • If not in need of admission, very close follow up required • Ok to start therapy in ED • Insulin for Type I (extensive teaching required) • Metformin is a first line for Type II

13. Hyperglycemia

14. Hyperglycemia treatment • Insulin dose adjustment – communicate with primary physician • Supplemental dose of rapid-acting insulin: • 1 unit per 50mg/dL above the goal for type I • 1 unit per 30mg/dL above the goal for type II

15. DKA ● Life threatening complication of DM ● Cause of 24% of diabetic admissions ● Incidence among diabetics in US 15 episodes per 1000 patients ● Up to 20-30% of DKA cases are new onset diabetics

16. DKA triad From Kitabchi et al, Diabetic ketoacidosis, Med Clin North Am 1995;70(1):9-37

17. Diagnostic criteria for DKA

18. Nitroprusside reaction β– hydroxybutyrate Acetoacetate Acetone

19. Metabolic consequences of insulin deficiency Hyperglycemia →glycosuria→ osmotic diuresis → fluid loss →dehydration, electrolyte disturbances

20. Metabolic consequences of insulin deficiency Excess ketones→ketonuria, acidosis Β-hydroxybutyrate→ nausea and vomiting Acetone → fruity breath odor

21. Metabolic consequences of insulin deficiency Metabolic acidosis → respiratory compensation → Kussmaul respirations (rapid shallow breathing)

22. Clinical presentation of DKA patient ● Volume depletion ● Nausea, vomiting, abdominal pain ● Rapid shallow respirations ● Fruity breath ● Possibly AMS

23. Precipitating factors • Common presentation for new onset diabetic • Infection • MI • CVA • Cocaine use • Non-compliance

24. First look at the patient • ABC status (airway, breathing, circulation) • Mental status • Possible precipitating events • Volume status

25. Orders • Accucheck • BMP • CBC with diff • UA/urine dip • Plasma osmolality • Serum ketones (if urine dip positive) • VBG/ABG (if anion gap or urine ketones present) • +/- EKG

26. Is ABG necessary?

27. Is ABG necessary? • In patients who are hemodynamically stable and without respiratory failure there is reasonable evidence that venous and arterial pH are close to each other and could be clinically interchangeable • In several studies difference between venous and arterial pH ranged from 0.02-0.04

28. Anion gap Anion gap = Serum sodium – (Serum chloride + Serum bicarbonate) Normal gap 7-12 mEq/L In DKA >20

29. Electrolytes • Na (sodium) • Often mildly hyponatremic • Correct for hyperglycemia (for each 100mg/dL of glucose above 100mg/dL, add 1.6mEq of Na) • K (potassium) • Significant losses (osmotic diuresis) • Serum concentration normal/elevated (hyperosmolarity, acidosis, lack of insulin) • P (phosphorus) • Negative phosphate balance • Serum level normal or high

30. Regulation of potassium by insulin

31. ED treatment of DKA ● Fluid ● Insulin ● Potassium

32. Fluid replacement • Average fluid loss 3-6 liters • Losses should be corrected within 24h • Initial replacement with normal saline, if patient not in shock at 15-20 ml/kg/h (1-1.5 L during the first hour)

33. Fluid replacement • Subsequent rate of hydration should be guided by patient’s hemodynamic status, hydration levels, urinary output, serum electrolyte levels, urinary output • In hyponatremic patients use 0.9%NaCl at 250-500ml/h

34. Fluid replacement • If Na normal or high, use 0.45%NaCl at a similar rate • When plasma glucose is≤200mg/dL, use fluids with 5% glucose to prevent hypoglycemia while continuing insulin until ketonemia is resolved

35. Insulin

36. Insulin • Delayed only for hypokalemia (K<3.3) • Continuous infusion • If bolus, use 0.1 U/kg followed by 0.1U/kg/h, if no bolus, use 0.14U/kg/h

37. Insulin • Initial drop should be at least 10% during the first hour. If glucose does not fall by 10%, give 0.14U/kg bolus, then continue insulin at a previous rate • If serum glucose 200mg/dL, switch IVF to D5 ½ NS , decrease insulin drip to 0.02-0.05U/kg/h

38. Can subcutaneous insulin be used? • Rapid-acting insulin analogs (lispro, aspart and glulisine) can be used sq in uncomplicated mild/moderate DKA • Data from several randomized open label trial, findings have not been significantly incorporated into practice

39. Subcutaneous insulin dosing • Lispro/aspart: • 0.2 unit/kg as an initial dose, then 0.1 unit/kg q1h • 0.3 unit/kg initially, followed by 0.2 unit/kg q2h • Repeat until blood glucose <250mg/dL • Decrease dose to 0.05/0.1 unit/kg until DKA resolved

40. Subcutaneous insulin administration • The only difference in the studies was reduction of hospitalization costs by 30% • ACEP has no official guideline, but 2009 evidence review calls it “a reasonable alternative to IV insulin for uncomplicated DKA”

41. Electrolyte replacement

42. Potassium replacement • Initiate if level below 5.3 mEq/L • Add 20-30mEq to each liter of infused fluid • Delay insulin therapy in case of hypokalemia, replace until K>3.5mEq/L • Monitor for arrhythmias

43. Sodium replacement • After the initial bolus: • Low Na: use 0.9%NS • Normal or high Na: use 0.45%NS

44. Phosphate replacement • No indication for replacement in most patients • If needed, use 20-30mEq/L potassium phosphate in IVF • May replace K as 1/3 potassium phosphate and 2/3 potassium chloride

45. Is bicarbonate administration useful? • Studies have shown that administration of bicarbonate with pH above 6.9 made no difference in the treatment of DKA • Use with life-threatening hyperkalemia (K>6.0mEq/L and EKG changes)

46. Bicarbonate administration • In severe acidosis (pH<6.9) give 100mmol sodium bicarbonate (2 ampules) in 400ml sterile water with 20mEq KCl at 200ml/h until venous pH>7.0 • If pH<7.0 after the infusion, repeat infusion q2h until pH>7.0s

47. Patient monitoring ● Accucheck q 1h ● Chemistry, venous pH and serum osmolarity q2-4h

48. Goal of treatment • Serum glucose < 200 mg/dL • Serum anion gap < 12 mEq/L • Serum bicarbonate > 18 mEq/L • Venous pH > 7.3

49. DKA protocol “Hyperglycemic Crises in Adult Patients With Diabetes. A consensus statement from the American Diabetes Association”, A.E.Kitabchi, G.E.Umpierrez, M.B. Murphy, R.A.Kreisberg, Diabetes Care, 2006; 29(12):2739-48

50. Complications Cerebral edema - Rare in adults - Mortality up to 70%