Diabetic Ketoacidosis Irene N. Sills, MD Albany Medical Center Albany, NY

1. Diabetic Ketoacidosis Irene N. Sills, MD Albany Medical Center Albany, NY

2. Diabetic Ketoacidosis Presentation of new onset diabetes about 30% of the time Is a life-threatening emergency The metabolic abnormalities must be corrected in a careful, vigilant fashion

3. Diabetic Ketoacidosis • Pathophysiology • Diagnosis • Treatment • Complications of treatment • When the acidosis is resolved

4. Diabetic Ketoacidosis • Abnormal metabolic state • Due to insulin deficiency • In patient with type 1 diabetes • Characterized by hyperglycemia and acidosis

5. Hyperglycemia Ketone production Ketone utilization Osmotic diuresis HYPERKETONEMIA DEHYDRATION vomiting Decreased GFR Hydrogen ion production exceeds utilization ACIDOSIS

6. Endogenous Compensation for Acidosis • Chemical buffering by extracellular (bicarbonate) and intracellular buffers (protein, organic and inorganic phosphates, hemoglobin) • Control of CO2 levels by alveolar ventilation rate • Control of blood bicarbonate concentration by changes in H+ excretion (excretion of titrable acidity and ammonium) and reabsorption of bicarbonate

7. Failure to take insulin (total insulin deficiency) Relative insulin deficiency infection trauma surgery stress dehydration ** Hormones that lower glucose: INSULIN Hormones that raise glucose: catecholamines, cortisol, glucagon, growth hormone Diabetic Ketoacidosis

8. Physical Exam • Signs of dehydration • Kussmaul type breathing • Acetone odor • Blood pressure and pulse • Temperature • Ileus and gastric atony • State of consciousness

9. Laboratory 1 • Glucose 400-500 mg/dl, but may vary • Arterial pH less than 7.3; bicarbonate less than 15mM/L • Sodium usually normal, but may be low • Potassium initially elevated • Serum ketones positive • Serum osmolality elevated

10. Laboratory 2 • Anion gap elevated: Na- (Cl + HCO3) • Creatinine spuriously elevated • Hemoglobin and hematocrit elevated • WBC may be elevated

11. Therapy • 1. Correction of the dehydration (PRIORITY) • 2. Correction of the hyperglycemia

12. Dehydration • Immediately decreases levels of “anti-insulin” hormones • Insulin resistance exacerbates the insulin deficiency • Rehydration will decrease stress hormones • Rehydration will improve kidney perfusion

13. Dehydration • DKA is a hypertonic state and should be corrected over 36-48 hours • If clinically in shock, 10-20 cc/kg .9NS or plasma expander over 30-45 minutes • Fluids should be no more hypotonic than .45 NS • Maintenance fluid may be .9NS until serum glucose is less than 300 mg/dl when glucose containing solution is added

14. Dehydration • Deficit replacement should be given EVENLY over 36-48 hours • IV infusion rate usually calculates to one and a-half times maintenance • On-going losses should be replaced • Potassium should be added when patient voids • Bicarbonate is usually not needed

15. Insulin • Regular (novolog) insulin U100 • 0.05 - .1U/kg/hr • If glucose is <120-180 mg/dl and acidosis is persisting, it is better to increase the glucose in the infusion rather than decrease the insulin

16. Monitoring • Serum glucose hourly • Electrolytes, calcium, phosphorous every 2-4 hours • Flowsheet with accurate I’s and O’s, vital signs, insulin doses, mental status checks, and laboratory results

17. Complications of therapy • Hypokalemia • Inadequate rehydration • Hypoglycemia • Cerebral edema and other CNS catastrophes

18. Hypokalemia • Vomiting • Renal losses exacerbated by hyperaldosteronism • Insulin and pH correction moves potassium into the cells • Danger if the initial potassium is less than 3.6 meq/L

19. Inadequate Rehydration

20. Hypoglycemia

21. Cerebral edema • Paradoxical development of CSF and CNS acidosis • Altered CNS oxygenation • Unfavorable osmotic gradients • A decline in the true sodium

22. Cerebral Edema • Develops 4-12 hours after therapy begun • Biochemically all is well • If early mental status changes are not noticed, a child will develop neurologic changes leading to herniation and compromised cardiorespiratory status

23. Cerebral Edema • NEJM: Cerebral edema that was not clinically expected developed in a small group of children • CT scans while in DKA and after resolution • Ventricular narrowing during therapy • Perhaps, some degree of swelling in all children

24. Cerebral EdemaPrevention • Slow rehydration with slow changes in osmolality • Serum sodium should rise as serum glucose falls • Hourly mental status checks

25. After Resolution IV insulin until it is time for meal Twice daily short acting/intermediate acting insulin (or usual insulin dose) Approximately .75 units/kg 2/3’s in am; 1/3 in pm 2/3’s intermediate acting; 1/3 short acting Lunch: .2 units/kg short acting

26. Team Management • Physician • Certified diabetes educator • Dietician • Psychologist or social worker

27. Insulin • Rapid acting - Humalog or Novolog • Short acting - Regular • Intermediate acting - NPH, Lente • Long acting - Ultralente • New, peakless - Glargine (Lantus)

28. Prebreakfast Prelunch and dinner Prebedtime snack Younger child 70 - 120 mg/dl 70 - 150 mg/dl 90 - 180 mg/dl 80 - 180 mg/dl Target Blood Glucose Levels

29. Principles of Meal Planning • Meet nutritional requirements • Well balanced meals and • snacks • Healthful fat consumption • Avoid obesity • Incorporate social and cultural factors • Artificial sweeteners

30. Carbohydrate Protein Fat 50-60% calories 15-20% calories 25-35% calories Constituents of Meal Plan

31. Monitoring • Hemoglobin A1c • Home glucose monitoring • Glucowatch • Subcutaneous sensor

32. Havea good day! good day Have