Management of diabetic ketoacidosis dka

A simplified approach to the DKA patient

1. MANAGEMENT OF DIABETIC KETOACIDOSIS (DKA) Dr./ Sahar H. Mostafa Consultant of Internal Medicine El-Mataria Teaching hospital-Cairo

2. Mechanism in DKA Counter-Regulatory Hormones GH Cortisol Catecholamines Glucagon Insulin deficiency ↑HGP( + gluconeogenesis & glycogenolysis )  HYPERGLYCEMIA ↓ Perpheral Glucose utilization  HYPERGLYCEMIA ↓FFAs( +lipolysis & ketogenesis )  KETONEMIA

3. HYPERGLYCEMIA  Glucosuria Osmotic diuresis ACIDOSIS Dehydration Mechanism in DKA

4. Blood glucose level > 250 mg/dl Arterial pH < 7.3 Serum HCO3 level < 15 mEq/l Moderate Ketonuria & Ketonemia Diagnostic Criteria for DKA

5. The clinical severity of DKA depends on the magnitude of acidosis > the degree of hyperglycemia Pearl

6. Initial Evaluation- Perform Immediately Good history and clinical examination , including vital signs, chest, heart, abdomen, neurological examination A flow sheet is essential: fluid intake and output, state of hydration are noted If coma or shock ---> urinary catheter, nasogastric tube It should be noted that management of DKA is individualized in every case

7. Initial Evaluation- Perform Immediately Obtain baseline blood glucose and acetone ABG Urine glucose and acetone Serum Electrolytes Blood urea and serum creatinine CBC, with differential Complete urine examination CXR ECG Cultures(as needed)

8. Remember that: There may be more than one cause of coma in the same patient: Diabetic coma and uremic coma, or D iabetic coma and Cerebrovascular accident

9. Remember that: Vascular thrombosis occurs more with hyperosmolar coma ( HNKC ) Abd pain (Periumbilical) may mimic pancreatitis (S. amylase is increased but not of pancreatic origin]

10. Remember that: A precipitating cause of coma may be more serious than DKA itself if neglected: Infection as UTI or chest infection, Myocardial infarction; so ECG is mandatory Mesenteric vascular occlusion/ intestinal obstruction Cerebrovascular insult; so neurological examination is essential

11. Fluid replacement Management

12. Fluid replacement Start with normal saline infusion as follows: 1000 -2000 ml in the 1st 1-2 Hrs, for a 70 kg man (15 – 20 ml/Kg/Hr) (until BP stabilized and urine flow established by 50-100 ml/hour)

13. Fluid replacement The patient can generally be viewed as being 10% dehydrated (TBW=60-63% body weight in male & 52-55% in female) ½ of total calculated deficit should be corrected over 1 st 8 hours plus the urine and any GIT loss. The second ½ over 16 hours

14. Fluid replacement Add 5% dextrose or dextrose in 0.45% saline to IV fluids when Bl. glucose reach  250 mg/dl at rate of 100-200ml/hour Fluid therapy depends upon degree of dehydration, age, weight, presence of cardiovascular diseases or other associated conditions

15. INSULIN Management

16. We are using only regular insulin The dose should be given by an insulin syringe matching the insulin bottle concentration

17. INSULIN An initial IV bolus 10-15 U may be given (0.15 U/Kg as bolus) ICU dose = 0.1 U / kg / Hr of R insulin Syringe pump: 50 ml saline + 7 Units /h = 10-15 Drops / min

18. INSULIN Another method, if ICU is not yet available: Bolus dose of R insulin = 0.3 U / Kg ( ½ of it IV & ½ IM ) {for a 70 kg man: 10 U IV and 10 U IM } Then  0.1 U/Kg/Hr {for a 70 kg man: 7 U/Hr OR 15 U / 2 Hs) IM U ntil disappearance of acetone from urine

19. INSULIN Then, after resolution of DKA :    Obtain blood Glucose every 4 hours and get the sliding scale of R Insulin SC in 5 in 5 units increments for every 50 mg blood glucose above 150 mg; to a max. of 20 U Overlap of IV and SC routes of R insulin may be done for 1-2 hours to avoid return of ketosis

20. INSULIN Rate of fall of Bl glucose should  50 - 80 mg/dl/1 st Hr If this doesn’t occurs, you can double infusion rate(if in ICU), OR you can give 10 U/Hr IV(In case ICU not available) The serum glucose level is better not to be allowed to fall to < 220 mg % during the first 4-5 Hs of ttt

21. POTASSIUM Management

22. POTASSIUM Initially, best to wait for results of admission of S . K+ levels Generally if anuria is present, hold off K+ until urine flow is established Check for signs of Hypokalemia: Ileus Hyporeflexia Muscle weakness, cramps Abnormal ECG: low T, or appearance of U wave

23. POTASSIUM If Serum K+ = 3.3 – 5.5 mEq/l  A dd 20 - 30 mEq K Cl / 6 Hs {or roughly for every one liter of IV Fluids} Usually 80-160 mEq is given in 1 st 12 hours in adults If Serum K+ <3.3 mEq/L Hold Insulin Give 40 mEq K Cl / Hr; until K+ level reach  3.3

24. POTASSIUM If Serum K+  5.5 mEq/L Don’t give K+ supplementation Only Check level / 2 Hrs O ral K+ supplementation is continued later on; because total body losses may reach up to 500 mEq / l { average urinary K+ loss of 3 - 7 mEq / kg occurs for Ds – Wks}

25. BICARBONATE Management

26. BICARBONATE HCO3 infusion is NOT needed in every case; because it can provoke ↓K+ and shift of O2-Hb dissociation curve to LEFT, impairing O2 delivery to Ts HCO3 infusion is given Only if: A rterial ph < 7.0, or S. HCO3 < 8 mEq/l, or T here is hyperventilation

27. BICARBONATE Why it is unnecessary to correct pH if  7 with HCO3 infusion ? It’s known that insulin will suppress lipolysis--> ↓FFAs delivered to the liver, thus --> blocking ketogenesis The remaining ketoacids are cleared &/or oxidized, thus --> regeneration of S. HCO3

28. BICARBONATE 50-100 mEq of HCO3 are infused over 2 Hs pH 6.9 --> give 44 mEq (1 amp) over 1 H ph < 6.9 --> give 88 mEq (2 amp) over 2 Hs Until ph  7.0 Both: S. HCO3 and S. K+ should be checked ever 4 hours until stability

29. PHOSPHATE / MAGNESIUM / CALCIUM Management

30. PHOSPHATE / MAGNESIUM / CALCIUM N= 2.5-4.5 mg/dl Initially PO4 levels are high(shift from ICF), then it drops during ttt to < 1 mg/dl with potential life threatening risk Manifestations of critical hypophosphatemia: Respiratory and skeletal muscle weakness Hemolytic Anemia Shift of O2-Hb dissociation curve to LEFT TTT: Give 1/3 of K+ supplements as K PO4 The remaining 2/3 as K Cl

31. PHOSPHATE / MAGNESIUM / CALCIUM N Ca+ = 4.4 - 5.2 mg/dl N Mg+ = 1.7 – 2.2 mg/dl Hypomagnesemia usually occurs due to intracellular shift (with K+ & Ph) following insulin ttt Hypercalcemia may be found in DKA (due to increase Ca + efflux from bone as a result of metabolic acidosis) Give calcium (if low) and magnesium supplementation to compensate for their loss

32. Electrolyte disturbance Heart failure due to: fluid overload acidosis (causing myocardiac depression) Shock due to: V olume depletion Acidosis MI S epticemia KEEP AN EYE ON:

33. Acute gastric dilatation or erosive gastritis Paralytic Ileus Cerebral edema (suspect if initial improvement occurs then patient deteriorates); Causes: Rapid fall of glucose (decrease of blood glucose should be by no more than 50-80 mg/dl/hour) Rapid infusion of IV fluid Too much HCO3 Hyponatremia KEEP AN EYE ON:

34. ARDS with hypoxemia in the absence of pneumonia or chronic pulmonary or heart disease, due to rapid ↓↓colloid osmotic pressure  ↑lung water with ↓of its compliance Disequilibrium (13%), esp. in children, due to correction with Hypotonic Solutions KEEP AN EYE ON:

35. DIC Hypoglycemia Acute renal failure Insulin resistance (try to increase insulin dose) KEEP AN EYE ON:

36. Associated lactic acidosis (due to hypoperfusion) Increased anion gap, due to the metabolic acidosis (N= 8-12 mEq/l) Anion Gap = Na – { Cl + HCO3} = 134 - { 108 +16 } = 10 KEEP AN EYE ON: