DKA / HONK

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    Source: CDA 2013 Guidelines!  (HIGHLIGHTED PARTS)

    Glucose Emergencies

    Approach

    • This is a spectrum!
    • Sugar is VERY high --> little Insulin around --> HONK (enough insulin around to suppress ketosis)
    • Sugar is higher --> no insulin around --> KDA (ketosis causes acidosis)
    • Sugar is NORMAL --> no insulin around --> severe stress, high enough to cause fast lipolysis before hyperglycemia develops --> euglycemic DKA.
      • Euglycemic DKA also happens when EtOH + hepatic dysfunction (primary driver for hyperglycemia in DKA)

     

    Diabetic Ketoacidosis

    • Symptoms:
      • Initially:Polyuria, Polydypsia, Weight loss
      • Then: Neurologic symptoms eventually form (kussmaul breathing, lethargy, drowsy)
      • Eventually: Vomiting, nausea from acidosis. 
    • Causes 6 I's
      • Infection
      • Inflammation
      • Insulin dose missed
      • Iatrogenic - Steroids.
      • Intoxication
      • Ischemia
    • Physical
      • Low BP, high HR, high RR
    • Investigations
      • CBC, Creatinine, BUN, lactate, Extended Lytes, Osmolality, ABG, Lytes, Anion Gap (metabolic vs. mixed).
      • ECG (Hyperkalemia, triggers - ischemia).
      • Low potassium (buffered H+/K+ balance, low insulin, vomiting).
      • Urine + serum ketones.
      • Cultures, CXR
    • Similar to HONK, except have no insulin, so have ketones and metabolic acidosis.
    • Mechanism Points:
      • Patients lose +++ potassium through polyuria (can look falsely normal b/c cells shift potassium out).
    • Treatment:
      • PUT IN FOLEY CATHETER, MONITOR URINE OUTPUT q1H
      • FLUIDS (1L/h for adults, 10mL/kg kids)   (volume depleted, corrects acidosis - improves perfusion)
        • Give IV boluses 0.9%NS IV 500cc q30min
        • Goals: (All 3 of following:)
            1.  HR < 100 bpm
            2. SBP > 90 mmHg
            3.  Urinary Output >= 0.5 mL/kg/h
        • Once goals reached:
          • 0.9% NS IV 500 cc/h x4 hrs
          • THEN:  0.9% NS IV 250 cc/h x4 hrs
          • THEN:  0.9% NS IV 125 cc/h...... until R/A PO intake.
      • Insulin  (bolus 0.1 u/kg IV + infusion based on protocol.
        • DO NOT START unless serum K+ > 3.3 mmol/L
        • Start with Insulin R 0.1 U/kg/hr (bolus with 0.1U/kg initially if you want, but no benefit in one trial)
          • I.e. mix 100 u of Insulin R in 100 mL of 0.9% NaCl (=1 unit/mL) and run at 0.1 unit/kg/h.
        • Example Nomogram:
        • Capillary Glucose 100 units Insulin in 100mL of 0.9% NaCl
          Glucose < 4 mmol/L 0.5 mL/h
          Glucose 4.1-9 mmol/L 1 mL/h
          Glucose 9.1-13 mmol/L 2 mL/h
          Glucose 13.1-17 mmol/L 3 mL/h
          Glucose 17.1-28 mmol/L 4 mL/h
          Glucose >28 mmol/L 6 mL/h and notify MD
      • Glucose
        • Correction of anion gap will take longer than correction of hyperglycemia.
        • MUST keep insulin running to stop ketogenesis and continue closing gap, even if it means giving more glucose.
        • Once below 14mmol/L : Add D5W or D10W to IV fluids to keep glucose 12-14 mmol/L
      • Potassium
      •     (K+ will go down because patients pee out K+, and adapt by shifting K+ from cells, but now giving Insulin, which will shift K back and can rapidly cause hypokalemia)
        • Serum K+ Order
          If K+   < 3.3 mmol/L Notify MD STAT, and add 40 mEq KCl/L of IV fluid.
          If K+   3.3 - 5 (or 5.5) mmol/L Add or change to 20-40 mEq KCl/L of IV fluid
          If K+   > 5 (or 5.5) mmol/L Do not add KCl to IV fluid
      • Bicarbonate (controvercial)
        • If pH > 7.0, do NOT give bicarbonate
        • If pH 6.9-7.0 after first hour of hydration, give NaBicarb.
          • (Dissolve 1 amp (50 mmol) of sodium bicarbonate in 200 mL D5W (or sterile water, if available) over 1 hour, repeated every 1 to 2 hours until pH is ≥7.0)

    Common Mistakes

    • Assuming potassium is normal (but in fact low, b/c body compensating by shifting potassium out of cells)
      • Giving insulin shifts potassium back into cells, causing hypokalemia. 

    HyperOsmolar Non-Ketoic State (HONK) 

    • Hyperglycemic, Hyperosmolar, nonketotic coma
    • New name: NKHS (Nonketotic hyperosmolar syndrome)
    • Definition:
      • Lack of insulin causes high blood glucose levels.  Some insulin still present to prevent ketosis (differentiates from Diabetic Ketoacidosis).  Hyperglycemia causes massive osmotic diuresis (glycosuria), leads to obligatory water loss, and dehydration.  This causes hyperosmolality (>300 mOsm/L), which results in dehydration, altered mental status, and eventual coma.
    • Symptoms:
      • altered mental status (obtunded), focal neurological deficits, glucosuria, and clinical dehydration
    • Investigations:
      • typically blood glucose > 55 mmol/L (>1000 mg/dL)
      • Typically Serum Osm > 330 mosm
      • NOTE: adjust plasma sodium (for every 5.6 mmol/L of glucose, plasma Na drops by 1.6-2.4 mEq/L) due to water drawn in by hyperosolar state to dilute sodium.
    • Treatment:
      • FLUIDS (1L/h, often need up to 4-6L)
      • Electrolyte monitoring
      • Insulin (same regimen as DKA)
      • Potassium (insulin causes potassium shift). 

     

    Other 

    • Hyponatremia in Hyperglycemia

      • Extracellular glucose causes shift of free water into extracellular space.

      • 1.6 mmol/L Na drop for every 5.6 (100 mg/dL) increase in the plasma glucose above 5.6 mmol/L

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