Hypokalemia

• General
  • Most clinically affects the muscles/heart
  • K+ is readily absorbed, thus false hypokalemia is possible with large numbers of metabolically active cells
    • In hypokalemia, the kidneys should respond by secreting <20-25 mEq/day
  • Pseudohypokalemia
    • Insulin Excess
    • Epinephrine
• Main causes:
  • GI losses (Non-Renal) or Urinary losses (Renal) > Intracellular Shifting (insulin or beta-2 agonists (Albuterol), prednisone) > Decreased Intake
  • Meds: Terbutaline, Epinephrine, Piperacillin
  • Hypothermia
  • Alkalemia
  • Hypokalemic Periodic Paralysis
    • 1) Familial, onset <20 y/o
    • 2) Acquired in hyperthyroidism, Asian/Mexican Men
  • A) GI losses
    • Vomiting
    • Diarrhea (most rapid)
      • May see hypokalemia and hypomagnesemia
      • Typically with metabolic acidosis
      • May not normalize with potassium supplementation
      • Worsened by laxatives or enemas
    • Laxative abuse
      • NAGMA or metabolic Alkalosis
    • Gastroenteritis
      • Not refractory to potassium supplements
    • Tube drainage
    • Inability to absorb
  • B) Renal Losses
    • AKD/CKD
    • Hyperaldosteronism (aldosterone promotes excretion)
      • Hypertension and metabolic alkalosis
    • Uremia
    • DKA (Osmotic Diuresis)
    • Bicarb administration
    • Hypomagnesemia
    • Diuretic Abuse (Thiazide or Loop Diuretics)
      • MCly seen with carbonic Anhydrase Inhibitors, loop diuretics, and thiazides
      • Monitor in Athletes, or in 2 weeks after dose increase
    • Bartter Syndrome, Gitelman Syndrome, Liddle Syndrome
    • Hypokalemia + NAGMA
      • RTA Type 1 and 2
  • NSAIDs, Lithium, Foscarnet
  • Acetazolamide, Topiramate, Aminoglycosides, Tenofovir, Valproic Acid, Chemo
  • C) Intracellular Shifting
    • Medication Induced
      • MCly due to insulin, most typically seen after initial administration of insulin in a patient with DKA (give K+ if <3.3 + DKA prior to insulin)
      • Alkalemia: H+ is pushed out of cells to correct alkalemia while K+ is pushed in
      • B2 Activation: activation pushes K+ into cells
    • Total body potassium is normal and potassium replacement may cause rebound hyperkalemia
    • 0.5 mEq/L or more change
  • Refractory Hypokalemia + Alcoholic
    • Hypomagnesemia inhibits PTH release (Hypocalcemia too)
      • (Magnesium <1.6)
    • Decreased intracellular magnesium leads to excess potassium efflux from renal tubular cells into the lumen (renal potassium wasting)
  • May occur after B12 or folate replacement due to increased cell production
• Symptoms:
  • Mild: fatigue, myalgias, weakness, cramps, constipation
  • Moderate: Ileus
  • Severe: Cramps, Flaccid paralysis with hyporeflexia, hypoventilation
  • Cardiac arrhythmias (ST depression, T wave flattening, U waves, QT prolongation, Ventricular arrhythmias, Arrest)
  • Glucose intolerance
  • Renal impairment (rhabdomyolysis)
• W/U:
  • Potassium, Calcium, Magnesium, Urine K, Urine and Serum Osm
  • 1) Urine and Serum K and Osmolality
    • No longer recommended
    • TTKG (Transtubular potassium gradient) is calculated with
    • = (Urine K/Serum K)/ (Urine osm/Serum osm)
      • TTKG <2 suggests non-renal source
      • TTKG >4 suggests it is the result of inappropriate renal secretion of K+
  • 2) Urine K+
    • <20 mEq/L: Extrarenal K+ Loss
      • Get ABG
        • Normal
          • Decreased K+ Intake (rare)
          • Laxative Abuse
          • Copious perspiration
        • Metabolic Acidosis
          • GI Tract
          • Diarrhea
          • Villous Adenoma
          • Fistula

    • 20 mEq/L: Renal K+ Loss

      • Get ABG
        • Metabolic Acidosis
          • RTA
          • Carbonic Anhydrases
          • DKA
          • Ureterosigmoidostomy
        • Metabolic Alkalosis (Redistribution)
    • Other) FeK
      • <9.3%, Urine K+ < 13
        • Diarrhea, Transcellular shift, lack of intake

      • 9.3%, Urine K+ ≥13 (81% sensitive, 86% specific for renal wasting)

        • Hypertensive: Aldosterone effect
        • Not
          • Bicarb low: RTA
          • Bicarb not low:
            • Urine Na/Cl >1.6 or chloride <10: Emesis/Piperacillin
            • Urine Na/Cl 1 or chloride >20: Loops/Thiazides or genetic
• Treatment
  • Targets: 3.5-4.5 in most, >3 in renal failure, >5 in DKA with decent kidneys
  • CI to enteral K+: Severe, profound shock, NPO
  • Mild (3.0-3.5):
  • Moderate (2.5-2.9):
  • Severe (<2.5):
  • Oral > IV Potassium replacement
  • For every 10mEq of KCL given, serum K+ should rise by 0.1mEq/L
    • Give with saline, not dextrose (drives K+ into cells via insulin secretion)
    • KCL for metabolic alkalosis
    • KHCO3 or K citrate/acetate for metabolic acidosis (NAGMA)
  • IV KCL at a max of 20 mEq/hr via a central line if severe or worse
    • Two infusions of 10mEq/hr in two peripherals if no central
  • Treat concurrent hypomagnesemia
  • Cardiac Arrest/VT/VF
    • 20mEq IV over 2-3 minutes
  • Initiate PPI ± Amiloride