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Hyperglycemic Emergencies DKA/HONC. William Harper, MD, FRCPC Endocrinology & Metabolism Assistant Professor of Medicine, McMaster University. DKA. A collection of severe and potentially life-threatening metabolic disturbances: Hyperglycemia  Osmotic diuresis

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Hyperglycemic emergencies dka honc

Hyperglycemic EmergenciesDKA/HONC

William Harper, MD, FRCPC

Endocrinology & Metabolism

Assistant Professor of Medicine, McMaster University


Hyperglycemic emergencies dka honc
DKA

A collection of severe and potentially life-threatening metabolic disturbances:

  • Hyperglycemia  Osmotic diuresis

    • Urinary loss of fluids & electrolytes

    • ECFv contraction

    • Depletion of total body K+ stores

      (even though may be hyperkalemic 2° to cell shift)

  • Ketone production  Metabolic acidosis

    • Compensatory Respiratory alkalosis (hopefully!)

  • Uncontrolled lipolysis  severe  TG



  • Dka pathophysiology

    fat cell

    TG

    DKA: Pathophysiology

    Insulin -

    Ketoacids

    Glucose

    HSL

    FFA

    Insulin

    + PFK

    Liver Cell

    Pyruvate

    Fatty

    Acyl-CoA

    Acetyl-CoA

    +

    Kreb’s

    Glucagon

    Insulin

    +

    VLDL (TG)


    Dka pathophysiology1

    fat cell

    TG

    DKA: Pathophysiology

    Insulin -

    Ketoacids

    Glucose

    HSL

    FFA

    Insulin

    + PFK

    Liver Cell

    Pyruvate

    Fatty

    Acyl-CoA

    Acetyl-CoA

    +

    Kreb’s

    Glucagon

    Insulin

    +

    VLDL (TG)


    Dka risk factors
    DKA risk factors

    • T1DM

      • 1st presentation

      • Acute-illness

      • Insulin omission (inappropriate sick-day management, noncompliance, Eating Disorders)

  • T2DM

    • During stress

    • Ethnicity: African-American, Hispanic

  • Extremes of age

  • Poor glycemic control

  • MDI with CSII


  • Dka precipitating factors
    DKA: Precipitating Factors

    Acute illness

    (MI, GIB, trauma,

    10-20%

    pancreatitis)

    20-38%

    New-onset DM

    5-39%

    Insulin omission

    33%

    Infections


    Dka diagnosis
    DKA: Diagnosis

    • Symptoms & Signs:

      • Polyuria, polydipsia, weight-loss

      • Fatigue

      • N/V, abdominal pain

      •  ECFv, Kussmaul’s, Acetone breath, mild impairment in cognition

  • Laboratory:

    • pH < 7.3, serum HCO3 < 15 mEq/L, AG > 14 mM

    • Raised serum ketones (and urine ketones)

    • BS > 14 mM (occasionally normal or only mild  BS)


  • Dka management
    DKA: Management

    • Monitoring

    • IV Fluid Resuscitation (3-9L deficit)

    • Potassium (“no pee no K”)

      • K+ deficit 3-5 mEq/Kg

  • IV insulin

  • Identify & Rx underlying cause

    • Noncompliance, infection, MI, etc.


  • Dka monitoring
    DKA: Monitoring

    • Consider ICU:

      • pH < 6.9, inadequate respiratory compensation

      • decreased LOC

      • Severe K+ disturbance (K+ < 3.0 or > 6.0 mEq/L)

  • Stepdown/Telemetry: all others

  • Ward:

    • Only very mild DKA!

    • pH > 7.2, serum HCO3 > 20, AG < 14

    • ECFv near normal

    • Not elderly, no hi-risk DKA precipitant (ex. MI)


  • Dka monitoring1
    DKA: Monitoring

    • CBG q1-2h on IV insulin gtt

    • q2h: Serum lytes, creatinine, glucose

    • q4-6h:

      • pH > 7.2, HCO3 > 20, AG < 15

      • ECFv stable and IV fluids @ maintenance rates

      • normal K+

  • Calcium profile:

    • Initially, then q12-24h unless abnormal

    • Phospate levels can be high at 1st but drop with Rx of DKA

  • Flowcharts to record biochemical parameters shown to be useful


  • Dka monitoring2
    DKA: Monitoring

    • EKG, cardiac enzymes: r/o ACS (silent MI)

    • Septic w/up: cultures, CXR, urinalysis, etc.

    • Consider pulmonary embolism?


    Dka iv fluids
    DKA: IV Fluids

    • IV NS 0.5-1L/h x 1-2h or longer so no more tachycardia, hypotension, orthostatic changes, low JVP.

    • Then change to 1/2 NS:

      • 200-500 cc/h over 12h in order to replace ½ estimated deficit

      • Then lower to 100-150 cc/h until deficit restored and eating/drinking well

  • If hypotension recalcitrant to fluids consider AI (Schmidt PGAS II) and send stat plasma cortisol and ACTH, then give solucortef 100 mg IV q8h.


  • Dka mortality
    DKA: Mortality

    • Adults 2-4%

      • Hypokalemia

      • MI, CVA, pneumonia, pulm. embolism, etc.

  • Kids 0.2-0.4%

    • Cerebral edema


  • Dka potassium
    DKA: Potassium

    • K+ defecit: 3-5 mEq/Kg (350 mEq for 70Kg)

    • Normal to high serum K+

    Ketoacidosis

    H+

    H+

    K+

    K+

    Insulin


    Dka potassium1
    DKA: Potassium

    • K+ deficit 3-5 mEq/kg (350 mEq 70kg)

    • Need K with initial IV fluid & insulin Rx unless:

      • Anuric

      • K > 5.5 mEq/L or hyperkalemic ECG changes

    > 20 mEq/h:

    Cardiac monitor

    > 60 mEq/L:

    Central line


    Dka iv insulin
    DKA: IV Insulin

    • Might delay starting IV insulin for a few hours if K+ severely low (< 3.0 mEq/L) and metabolic acidosis not severe (pH > 7.0)

    • Humulin R or Novolin Toronto

    • Bolus 0.1-0.2 U/kg IV

    • Then IV gtt @ 0.1-0.2 U/kg/h

      (50 U of regular insulin in 500cc D5W; 1U/10cc)

    • Aim is to demonstrate correction of Anion Gap (AG) and decrease in BS 4.4 mM/L/h

    • Monitoring serial serum ketones NOT useful as most assays measure Acetoacetate only:

      ßHß (not detected) DKA Rx Acetoacetate (detected)


    Dka iv insulin1
    DKA: IV Insulin

    • Using insulin to treat 2 different and separate metabolic disturbances in DKA:

      • Ketoacidosis

      • Hyperglycemia


    Dka iv insulin2
    DKA: IV Insulin

    • If AG not correcting and/or BS not decreasing then increase IV gtt rate 1.5-2X

    • If BS < 13 but AG still not corrected do NOT decrease insulin IV gtt.

    • Instead start IV glucose gtt:

      • D5W-D10W @ 100-200 cc/h

  • Once AG corrected than titrate IV insulin to BS

  • When BS < 13 and AG normal: reduce IV insulin gtt to 1-2 U/h and add IV glucose if not already done.


  • Dka switch to s c insulin
    DKA: Switch to S.C. insulin

    • Can consider switch to SC insulin when:

      • AG normalized

      • BS < 15 mM

      • Insulin IV gtt requirements < 2U/h

      • Patient able to eat

  • Overlap insulin IV gtt with 1st SC insulin by 2-4h to avoid recurrent ketosis

  • T2DM patients with DKA:

    • Don’t necessarily have to be d/c on insulin SC (I often do!)

    • Once acute stress resolved, many do well on OHA


  • Dka other rx
    DKA: Other Rx

    • Bicarbonate

      • May exacerbate hypokalemia

      • Only give if pH < 6.9 AND evidence of cardiovascular instability (arrythmia, CHF, hypotension)

      • 1-2 amps bicarb in 1L D5W IV with 10-20 mEq of added KCl given over 2h or until pH > 7.1

  • Phosphate

    • Routine IV not recommended

    • Rx symptomatic hypophosphatemia (rhabdo, unexplained CHF or respiratory failure, severe confusion)

    • 10cc K Phos soln (3.0mEq Pi and 4.4 mEq K/cc) in 1L NS IV over 8-12h


  • Dka other rx1
    DKA: Other Rx

    • Cerebral Edema

      • Usually only kids

      • Persistent decreased LOC despite standard Rx of DKA

      • CT scan to confirm diagnosis

      • Decadron 10 mg IV

      • Mannitol 25 mg IV


    Dka management1
    DKA: Management

    • Monitoring

      • ICU: pH < 6.9, severe K (< 3, > 6), decr LOC

  • IV Fluid Resuscitation (3-9L deficit)

  • Potassium (“no pee no K”)

  • IV insulin

  • Identify & Rx underlying cause

    • Noncompliance, infection, MI, etc.


  • Dka rx ebm
    DKA Rx: EBM

    • In patients not in shock, recovery is more rapid with slower rates of IV fluids (500 mL/h x 4h, then 250 mL/h)

      • RCT: Adrogue et al, 1989, JAMA: 262:2108-13

  • Low-dose insulin (0.1-0.2 U/Kg bolus, then rate of 0.1-0.2 U/Kg/h) has similar rate of recovery and less hypokalemia than high-dose insulin (50-150 U/h)

    • RCT: Kitabchi et al, 1976, Ann Intern Med: 84:633-8

    • RCT: Heber et al, 1977, Arch Intern Med: 137:1377-80

  • No clinical benefit to giving IV HCO3

    • RCT: Gamba et al, 1991, Rev Invest Clin: 43:234-48

  • No benefit to giving IV phosphate

    • RCT: Fischer et al, 1983, JCEM:57:177-80