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2. PATHOGENESIS BOTH : insulin deficiency + elevation of counterregulatory hormones (glucagon, catecholamines, cortisol, growth hormone) ↓ Increase hepatic & renal glucose production Impaired glucose utilization in peripheral tissues ↓ Hyperglycemia & increase plasma osmolality

3. PATHOGENESIS DKA : release of free fatty acids (lipolysis) ↓ Hepatic fatty acid oxidation to ketone bodies (β-hydroxybutyrate & acetoacetate) ↓ Ketonemia & metabolic acidosis

4. PATHOGENESIS HHS : Plasma insulin – inadequate for glucose utilization ‒ adequate to prevent lipolysis & ketogenesis DKA & HHS : ― magnitude of dehydration ― degree of ketosis (& acidosis)

5. PRECIPITATING FACTORS ● Infection ● Cerebrovascular accident ● Alcohol abuse ● Pancreatitis ● Myocardial infarction ● Trauma ● Drugs e.g. steroids, thiazides, sympathomimetic agents (dobutamine & terbutaline) ● Stop/inadequate insulin in DM type I ● Elderly with new-onset DM

7. DIAGNOSIS History & physical examination : Process : - HHS : over several days to weeks - DKA : much shorter (typically < 24 hr) 2) Classical clinical picture of both : - polyuria - polydipsia - polyphagia - weight loss - vomitting - abdominal pain (DKA) - dehydration - weakness - clouding of sensoria - coma

8. DIAGNOSIS 3) Physical finding : - poor skin tugor - Kussmaul respiration (DKA) - tachycardia - hypotension - alteration of conscious (lethargy  coma :HHS) - emesis (coffee-ground) - hypothermia (peripheral vasodilatation) - abdominal pain (DKA : Rx dehydration & metabolic acidosis)

9. LABORATORY FINDINGS : 1)Initial lab : - BS, BUN, Cr, serum ketone - electrolyte (with calculated anion gap) •pseudohypoNa : osmotic gradient from hypergly. • true hypoNa from severe hyperTG • hyperK from insulin deficiency,hypotonicity& acidemia(cell shift) - osmolality : ≥ 320 mOsm/kg  stupor/coma = 2 [measured Na (mEq/L) + BS (mg/dl)/18) - CBC with diff count (leukocytosisὰ serum ketone) - U/A, urine ketone

10. LABORATORY FINDINGS : 1)Initial lab: - EKG - HbA1C : acute or chronic poor control 2) Suspected infection : - bacterial cultures of urine,blood & throat ,etc - CxR - abdominal pain : pancreatitis  serum lipase (DKA : increase serum amylase & liver enz )

11. DIFFERENTIAL DIAGNOSIS : Ketoacidosis: - Starvation ketosis - Alcoholic ketoacidosis mildly elevation BS (rarely > 250 mg/dl) serum HCO3 not < 18 mEQ/L 2) High-anion gap metabolic acidosis : - Lactic acidosis (Ix : serum lactate) - drugs : • salicylate (Ix : serum salicylate), • methanol (Ix : serum methanol) • ethylene glycol (Ix : U/A-calcium oxalate &hippurate crystal),

12. DIFFERENTIAL DIAGNOSIS : 2) High-anion gap metabolic acidosis : - paraldehyde (strong odor breathing-osmolar gap- anion gap acidosis) - Chronic renal failure (hyperchloremic acidosis)

13. TREATMENT : Correction of dehydration, hyeprglycemia & E’lyte imbalance 2) Correct precipitating factor 3) Guideline for management

14. Fluid therapy : Adult patients : - initial fluid Rx in no cardiac compromise : 0.9%NaCl ≥ 15-20 ml/kg/hr in 1st hour ( ~ 1-1.5 L ) - subsequent choice for fluid depend on hydration, serum E’lyte & urine output • if N/↑serum Na  0.45% NaCl 4 – 14 ml/kg • if ↓ serum Na  0.9% NaCl - monitor BP; fluid input/output ; clinical exam ; sermoosmolality not > 3 mOsm/kg/H2O/hr - fluid replacement correct deficit in 24 hr

15. FLUID THERAPY : 2) Pediatric patients (< 20 yrs) : - 1st hr : 0.9%NaCl 10-20 ml/hr ( not > 50 ml/kg in first 4 hr of therapy ) - Continued fluid therapy = fluid deficit in 48 hr or 1.5 times of 24 hr maintenance or 5 ml/kg/hr • 0.45-0.9% NaCl rate • ↓ osmolality not > 3 mOsm/kg/hr - serum glucose = 250 mg/dl  change 5%DN/2 or 5%D/N/3 with potassium

17. INSULIN THERAPY : Not mild DKA : Rx of choice = regular insulin continuous IV infusion Exclude hypoK (< 3.3 mEq/l) Start regular insulin 0.15 units/kg iv bolus (iv bolus nit recommend in pediatric) Cont. infusion 0.1 units/kg/hr (5-7 units/hr in adult) Aim decrease BS 50-75 mg/dl/hr If in 1st hr BS not decrease > 50 mg/dl • check hydration • double dose insulin infusion every hr

18. INSULIN THERAPY : when BS = 250 mg/dl in DKA or = 300 mg/dl in HHS • ↓ insulin infusion rate = 0.05 - 0.1 unit/kg/hr (3-6 units/hr) • 5-10% Dextrose Keep until acidosis in DKA mental status hyperosmolarity in HHS  resolve

19. INSULIN THERAPY : Ketonemia • longer ot clear than hyperglycemia • monitor by measure serum β-OHB during Rx β-OHB  acetoacetic ȃ  worse ketosis then not use urine / serum ketone level for Rx During Rx : monitor serum E’lyte , BS, BUN, Cr, osmolality & venous pH (for DKA) q 2-4 hr ( venous pH < arterial pH = 0.03 units ) anion gap  resolution of acidosis

20. Mild DKA : Regular insulin SC or IM q 1 hr - priming dose of RI = 0.4 – 0.6 unit/kg • half  IV bolus • half  SC or IM - then RI 0.1 unit/kg/hr SC or IM

24. CRITERIA FOR RESOLUTION OF DKA : ● Glucose < 200 mg/dl ● Serum bicarbonate ≥ 18 mEq/l ● Venous pH > 7.3 When DKA resolve If NPO : • continue IV insulin & fluid replacement • RI sc q 4 hr (RI 5 unit / BS 50 mg/dl if BS > 150 mg/dl until RI 20 unit for BS ≥ 300 mg/dl)

25. When DKA resolve : 2) Patient is able to eat : - multiple-dose schedule : use combination of short/rapid-acting + intermediate/long-acting RI - continue IV insulin infusion for 1-2 hr after the spit-mixed regimen - DM : insulin dose = before the onset of DKA/HHS - new Dx DM : 0.5-1 units/kg/day divide two doses regimen of short + long-acting RI - type-2 DM : oral antihyperglycemic agent & diet

26. POTASSIUM : • Insulin Rx, correct ȃ & volume expansion  HypoK • Prevent hypoK : replace K < 5.5 mEq/l & adequate urine output • General 20-30 mEq K (2/3 KCl + 1/3 KPO4 ) in each liter of infusion fluid  keep serum K = 4-5 mEq/l • hypoK (< 3.3 mEq/l) : - K replacement begin with fluid Rx - insulin Rx delayed until K > 3.3 mEq/l

27. BICARBONATE : • controversial • keep pH > 7 for - reestrablish insulin activity blocks lipolysis - resolve ketoacidosis without add HCO3 • if pH < 6.9  100 mmol NaHCO3 in 400 ml sterile iv rate 200 ml/hr • if pH 6.9-7.0  50 mmol NaHCO3 in 200 ml sterile iv rate 200 ml/hr • if pH > 7.0  no NaHCO3 • mornitor venous pH q 2 hr until pH > 7.0 • caution : hypoK NaHCO3 in NaCl not Na > 155 mEq/l

28. PHOSPHATE : Whole-body phosphate deficit in DKA = 1 mmol/kg Serum phosphate decrease with insulin Rx I/C phosphate replacement • cardiac dysfunction • anemia • respiratory depression Serum phosphate < 1 mg/dl  20-30 mEq/l K2PO4 No Rx phosphate in HHS Over phosphate Rx  hypoCa without tetany

29. COMPLICATIONS : ● hypoglycemia : over insulin Rx ● hypoK : insulin Rx & Rx acidosis with NaHCO3 ● hyperglycemia : interrupt/stop iv insulin after recovery without subsequent sc insulin ● hyperchloremia : excessive saline for fluid & E’lyte replacement

30. COMPLICATION : ● transient non-anion gap metabolic acidosis (except acute renal failure or extreme oliguria) ● hypoxemia & noncardiogenic pulmonary edema be careful in widen A-a oxygen gradient

31. COMPLICATION : ● Cerebral edema from osmolality : - rapid alteration of consciousness - headache - seizure - incontinence - bradycardia - pupillary changes - rapid papilledema - respiratory arrest ☺ prevent by gradual replacement of Na & water deficit in hyperosmolality (max ↓ 3 mOsm/kg/hr) ☺ In HHS : keep BS 250-300 mg/dl until hyperosmolality & mental status improve

32. PREVENTION : Check up or F/U Pt education BS goals & use short-acting RI during illness self monitor  if BS > 300 mg/dl  be careful suppress fever & Rx infection 6)Early recovery : take easily digestible liquid diet (carbohydrate + salt)