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Dka presentation1
 

Dka presentation1

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    Dka presentation1 Dka presentation1 Presentation Transcript

    • 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
    • PATHOGENESIS
      DKA :
      release of free fatty acids (lipolysis)

      Hepatic fatty acid oxidation to ketone bodies
      (β-hydroxybutyrate & acetoacetate)

      Ketonemia & metabolic acidosis
    • PATHOGENESIS
      HHS :
      Plasma insulin
      – inadequate for glucose utilization
      ‒ adequate to prevent lipolysis & ketogenesis
      DKA & HHS :
      ― magnitude of dehydration
      ― degree of ketosis (& acidosis)
    • 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
    • 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
    • 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)
    • 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
    • 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 )
    • 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),
    • DIFFERENTIAL DIAGNOSIS :
      2) High-anion gap metabolic acidosis :
      - paraldehyde
      (strong odor breathing-osmolar gap-
      anion gap acidosis)
      - Chronic renal failure (hyperchloremic acidosis)
    • TREATMENT :
      Correction of dehydration, hyeprglycemia &
      E’lyte imbalance
      2) Correct precipitating factor
      3) Guideline for management
    • 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
    • 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
    • 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
    • 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
    • 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
    • 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
    • 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)
    • 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
    • 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
    • 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
    • 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
    • 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
    • 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
    • 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
    • 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)