Dka presentation1

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Dka presentation1

  1. 1.
  2. 2. PATHOGENESIS <br />BOTH : <br />insulin deficiency <br />+ <br />elevation of counterregulatory hormones <br />(glucagon, catecholamines, cortisol, growth hormone)<br />↓<br />Increase hepatic & renal glucose production<br />Impaired glucose utilization in peripheral tissues<br />↓<br />Hyperglycemia & increase plasma osmolality<br />
  3. 3. PATHOGENESIS<br />DKA : <br />release of free fatty acids (lipolysis)<br />↓<br />Hepatic fatty acid oxidation to ketone bodies<br />(β-hydroxybutyrate & acetoacetate)<br />↓<br />Ketonemia & metabolic acidosis<br />
  4. 4. PATHOGENESIS<br />HHS : <br />Plasma insulin<br /> – inadequate for glucose utilization<br /> ‒ adequate to prevent lipolysis & ketogenesis<br />DKA & HHS : <br /> ― magnitude of dehydration<br /> ― degree of ketosis (& acidosis)<br />
  5. 5. PRECIPITATING FACTORS<br />● Infection<br />● Cerebrovascular accident<br />● Alcohol abuse<br />● Pancreatitis<br />● Myocardial infarction<br />● Trauma<br />● Drugs e.g. steroids, thiazides, sympathomimetic<br /> agents (dobutamine & terbutaline)<br />● Stop/inadequate insulin in DM type I<br />● Elderly with new-onset DM<br />
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  7. 7. DIAGNOSIS<br />History & physical examination :<br />Process : <br /> - HHS : over several days to weeks<br /> - DKA : much shorter (typically < 24 hr)<br />2) Classical clinical picture of both :<br /> - polyuria - polydipsia<br /> - polyphagia - weight loss<br /> - vomitting - abdominal pain (DKA)<br /> - dehydration - weakness<br /> - clouding of sensoria - coma <br />
  8. 8. DIAGNOSIS<br />3) Physical finding :<br /> - poor skin tugor<br /> - Kussmaul respiration (DKA)<br /> - tachycardia <br /> - hypotension<br /> - alteration of conscious (lethargy  coma :HHS)<br /> - emesis (coffee-ground)<br /> - hypothermia (peripheral vasodilatation)<br /> - abdominal pain <br /> (DKA : Rx dehydration & metabolic acidosis)<br />
  9. 9. LABORATORY FINDINGS :<br />1)Initial lab : <br /> - BS, BUN, Cr, serum ketone<br /> - electrolyte (with calculated anion gap) <br />•pseudohypoNa : osmotic gradient from hypergly. <br /> • true hypoNa from severe hyperTG<br /> • hyperK from insulin deficiency,hypotonicity& <br />acidemia(cell shift)<br /> - osmolality : ≥ 320 mOsm/kg  stupor/coma<br /> = 2 [measured Na (mEq/L) + BS (mg/dl)/18)<br /> - CBC with diff count (leukocytosisὰ serum ketone)<br /> - U/A, urine ketone<br />
  10. 10. LABORATORY FINDINGS :<br />1)Initial lab:<br /> - EKG <br /> - HbA1C : acute or chronic poor control<br />2) Suspected infection :<br /> - bacterial cultures of urine,blood & throat ,etc<br /> - CxR<br /> - abdominal pain : pancreatitis  serum lipase<br /> (DKA : increase serum amylase & liver enz )<br />
  11. 11. DIFFERENTIAL DIAGNOSIS :<br />Ketoacidosis: <br /> - Starvation ketosis<br /> - Alcoholic ketoacidosis<br /> mildly elevation BS (rarely > 250 mg/dl)<br /> serum HCO3 not < 18 mEQ/L<br />2) High-anion gap metabolic acidosis :<br /> - Lactic acidosis (Ix : serum lactate)<br /> - drugs : <br /> • salicylate (Ix : serum salicylate), <br /> • methanol (Ix : serum methanol)<br /> • ethylene glycol <br /> (Ix : U/A-calcium oxalate &hippurate crystal),<br />
  12. 12. DIFFERENTIAL DIAGNOSIS : <br />2) High-anion gap metabolic acidosis :<br /> - paraldehyde<br /> (strong odor breathing-osmolar gap-<br /> anion gap acidosis)<br /> - Chronic renal failure (hyperchloremic acidosis)<br />
  13. 13. TREATMENT :<br />Correction of dehydration, hyeprglycemia &<br />E’lyte imbalance<br />2) Correct precipitating factor<br />3) Guideline for management<br />
  14. 14. Fluid therapy :<br />Adult patients :<br /> - initial fluid Rx in no cardiac compromise : <br /> 0.9%NaCl ≥ 15-20 ml/kg/hr in 1st hour<br /> ( ~ 1-1.5 L )<br /> - subsequent choice for fluid depend on <br /> hydration, serum E’lyte & urine output <br /> • if N/↑serum Na  0.45% NaCl 4 – 14 ml/kg <br /> • if ↓ serum Na  0.9% NaCl<br /> - monitor BP; fluid input/output ; clinical exam ;<br />sermoosmolality not > 3 mOsm/kg/H2O/hr<br /> - fluid replacement correct deficit in 24 hr<br />
  15. 15. FLUID THERAPY :<br />2) Pediatric patients (< 20 yrs) :<br /> - 1st hr : 0.9%NaCl 10-20 ml/hr <br /> ( not > 50 ml/kg in first 4 hr of therapy ) <br /> - Continued fluid therapy = fluid deficit in 48 hr or<br /> 1.5 times of 24 hr maintenance or 5 ml/kg/hr <br /> • 0.45-0.9% NaCl rate<br /> • ↓ osmolality not > 3 mOsm/kg/hr<br /> - serum glucose = 250 mg/dl <br />  change 5%DN/2 or 5%D/N/3 with potassium<br />
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  17. 17. INSULIN THERAPY :<br />Not mild DKA : <br /> Rx of choice = regular insulin continuous IV infusion<br /> Exclude hypoK (< 3.3 mEq/l) <br /> Start regular insulin 0.15 units/kg iv bolus <br /> (iv bolus nit recommend in pediatric)<br /> Cont. infusion 0.1 units/kg/hr (5-7 units/hr in adult) <br /> Aim decrease BS 50-75 mg/dl/hr<br /> If in 1st hr BS not decrease > 50 mg/dl <br /> • check hydration<br /> • double dose insulin infusion every hr <br />
  18. 18. INSULIN THERAPY :<br />when BS = 250 mg/dl in DKA or<br /> = 300 mg/dl in HHS<br /> • ↓ insulin infusion rate = 0.05 - 0.1 unit/kg/hr<br /> (3-6 units/hr)<br /> • 5-10% Dextrose<br />Keep until acidosis in DKA <br /> mental status <br />hyperosmolarity in HHS  resolve<br />
  19. 19. INSULIN THERAPY :<br />Ketonemia<br /> • longer ot clear than hyperglycemia<br /> • monitor by measure serum β-OHB<br /> during Rx β-OHB  acetoacetic ȃ  worse ketosis<br /> then not use urine / serum ketone level for Rx<br />During Rx : monitor serum E’lyte , BS, BUN, Cr, <br />osmolality & venous pH (for DKA) q 2-4 hr<br /> ( venous pH < arterial pH = 0.03 units )<br /> anion gap  resolution of acidosis<br />
  20. 20. Mild DKA :<br />Regular insulin SC or IM q 1 hr <br /> - priming dose of RI = 0.4 – 0.6 unit/kg<br /> • half  IV bolus<br /> • half  SC or IM <br /> - then RI 0.1 unit/kg/hr SC or IM<br />
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  24. 24. CRITERIA FOR RESOLUTION OF DKA :<br />● Glucose < 200 mg/dl<br />● Serum bicarbonate ≥ 18 mEq/l<br />● Venous pH > 7.3<br />When DKA resolve <br />If NPO : <br /> • continue IV insulin & fluid replacement<br /> • RI sc q 4 hr <br /> (RI 5 unit / BS 50 mg/dl if BS > 150 mg/dl <br /> until RI 20 unit for BS ≥ 300 mg/dl)<br />
  25. 25. When DKA resolve :<br />2) Patient is able to eat :<br /> - multiple-dose schedule : use combination of<br /> short/rapid-acting + intermediate/long-acting RI<br /> - continue IV insulin infusion for 1-2 hr after the <br /> spit-mixed regimen<br /> - DM : insulin dose = before the onset of DKA/HHS<br /> - new Dx DM : 0.5-1 units/kg/day divide two doses <br /> regimen of short + long-acting RI <br /> - type-2 DM : oral antihyperglycemic agent & diet <br />
  26. 26. POTASSIUM :<br />• Insulin Rx, correct ȃ & volume expansion  HypoK<br />• Prevent hypoK : replace K < 5.5 mEq/l & <br /> adequate urine output<br />• General 20-30 mEq K (2/3 KCl + 1/3 KPO4 ) in each <br /> liter of infusion fluid  keep serum K = 4-5 mEq/l<br />• hypoK (< 3.3 mEq/l) : <br /> - K replacement begin with fluid Rx<br /> - insulin Rx delayed until K > 3.3 mEq/l<br />
  27. 27. BICARBONATE :<br />• controversial<br />• keep pH > 7 for <br /> - reestrablish insulin activity blocks lipolysis<br /> - resolve ketoacidosis without add HCO3 <br /> • if pH < 6.9  100 mmol NaHCO3 in 400 ml sterile<br /> iv rate 200 ml/hr <br /> • if pH 6.9-7.0  50 mmol NaHCO3 in 200 ml sterile<br /> iv rate 200 ml/hr <br /> • if pH > 7.0  no NaHCO3 <br /> • mornitor venous pH q 2 hr until pH > 7.0 <br /> • caution : hypoK<br />NaHCO3 in NaCl not Na > 155 mEq/l<br />
  28. 28. PHOSPHATE : <br />Whole-body phosphate deficit in DKA = 1 mmol/kg<br />Serum phosphate decrease with insulin Rx <br />I/C phosphate replacement <br /> • cardiac dysfunction <br /> • anemia<br /> • respiratory depression<br />Serum phosphate < 1 mg/dl  20-30 mEq/l K2PO4 <br />No Rx phosphate in HHS<br />Over phosphate Rx  hypoCa without tetany<br />
  29. 29. COMPLICATIONS :<br />● hypoglycemia : over insulin Rx<br />● hypoK : insulin Rx & Rx acidosis with NaHCO3 <br />● hyperglycemia : interrupt/stop iv insulin after <br /> recovery without subsequent sc insulin<br />● hyperchloremia : excessive saline for fluid & <br />E’lyte replacement<br />
  30. 30. COMPLICATION :<br />● transient non-anion gap metabolic acidosis <br /> (except acute renal failure or extreme oliguria)<br />● hypoxemia & noncardiogenic pulmonary edema<br /> be careful in widen A-a oxygen gradient<br />
  31. 31. COMPLICATION :<br />● Cerebral edema from osmolality : <br /> - rapid alteration of consciousness<br /> - headache - seizure <br /> - incontinence - bradycardia<br /> - pupillary changes - rapid papilledema<br /> - respiratory arrest<br />☺ prevent by gradual replacement of Na & water<br /> deficit in hyperosmolality<br /> (max ↓ 3 mOsm/kg/hr)<br /> ☺ In HHS : keep BS 250-300 mg/dl until <br />hyperosmolality & mental status improve<br />
  32. 32. PREVENTION :<br />Check up or F/U<br />Pt education <br /> BS goals & use short-acting RI during illness<br /> self monitor  if BS > 300 mg/dl  be careful<br />suppress fever & Rx infection<br />6)Early recovery : take easily digestible liquid diet<br /> (carbohydrate + salt)<br />

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