Electrolyte Management


Sodium

  1. General Principles
    • plasma sodium concentration is regulated by changes in water intake and excretion (water balance), not by gain or loss of sodium
    • hyponatremia is primarily due to the intake of water that cannot be excreted
    • hypernatremia is primarily due to loss of water that has not been replaced
    • disorders of volume (sodium and water) often coexist with disorders of water balance

  2. Salt Exchange
    • daily salt intake varies from 50 - 90 mEq/day (3 to 5 grams)
    • USDA recommendation is < 2.3 gm/day
    • balance is maintained primarily by the kidneys
    • kidneys can reduce excretion of sodium to as little as 1 mEq/day

  3. Hyponatremia
    • defined as a sodium level < 135 mEq/L
    • mild = 130 - 134 mEq/l; moderate = 120 – 129 mEq/L; severe = < 120 mEq/L

    1. Etiology
      • usually indicates hypo-osmolality (excess water relative to solute)
      • an exception to this is when there is a very high concentration of an impermeant solute such as glucose or mannitol present, which draws water out from the ICF and dilutes other solutes in the ECF (pseudohyponatremia):   P(osm) = 2 x Na + (glucose / 18) + (BUN / 2.8)
      • may be associated with hypovolemia, euvolemia, or hypervolemia
      • impaired water excretion is most often due to the inability to suppress ADH secretion
      • the two major causes of persistent ADH secretion are reduced effective arterial volume and SIADH

      1. Hypovolemic Hyponatremia
        • volume loss results in nonosmotic stimulation of ADH and the retention of free water
        • very common in the immediate postop period
        • other causes include large GI losses or fluid sequestration (bowel obstruction, burn wounds)
        • urine sodium will be very low
        • treatment is directed towards correcting the volume deficit with isotonic saline

      2. Euvolemic Hyponatremia
        • most common cause on surgical services is SIADH as a result of head trauma
        • urine sodium and urine osmolality are elevated
        • treatment is free water restriction
        • if neurologic symptoms are present, then the sodium level can be slowly corrected with 3% NS (1 mEq/hour)
        • too rapid correction → central pontine myelinolysis

      3. Hypervolemic Hyponatremia
        • total body water is increased, but effective arterial blood volume is reduced
        • common causes include cirrhosis, congestive heart failure, and chronic renal disease
        • treat with a low salt diet and fluid restriction (1L/d)
        • in cirrhotics, spironolactone can be used to inhibit sodium reabsorption in the kidney
        • lasix is useful in patients with CHF

    2. Clinical Manifestations
      • reduction in plasma osmolality leads to water movement from the extracellular fluid into cells and the brain
      • symptomatic hyponatremia (Na < 125 mEq/L) is associated with CNS signs of cerebral edema: headache, confusion, lethargy, coma, seizures

  4. Hypernatremia
    • defined as a sodium level > 145 mEq/L
    • moderate = 146 - 159 mEq/L; severe = > 159 mEq/L

    1. Etiology
      • most commonly results from impaired thirst or lack of access to water
      • may also result from iatrogenic administration of hypertonic saline or sodium bicarbonate
      • CNS effects predominate because of water movement out of neurons
      • patients can be hypovolemic, euvolemic, or hypervolemic

      1. Hypovolemic Hypernatremia
        • results from loss of water in excess of salt from vomiting, diarrhea, fistulas, sweating, or fever
        • urine sodium concentration is low and osmolality is high
        • correct the volume deficit first with an isotonic fluid
        • correct the hypernatremia with free water once the volume deficit has been corrected
        • too rapid correction can lead to cerebral edema and herniation

      2. Euvolemic Hypernatremia
        • central diabetes insipidus results from a lack of ADH
        • although the urinary loss of free water may be extremely high, diabetes insipidus rarely results in hypovolemia because the majority of water is lost from the intracellular space
        • urine sodium is very low
        • treatment consists of free water and DDAVP

      3. Hypervolemic Hypernatremia
        • may result from the iatrogenic administration of large volumes of high sodium content fluids (3% NaCl, NaHCO3)
        • mineralocorticoid excess (Cushing’s syndrome, hyperaldosteronism) is a rare cause
        • patients may benefit from diuresis as well as hypotonic fluids

Chloride

  1. Hypochloremia
    • often associated with a metabolic alkalosis
    • gastric outlet obstruction, high N-G outputs, and high ileostomy outputs are all associated with large chloride (and sodium) losses
    • signs and symptoms are usually related to the volume loss

  2. Hyperchloremia
    • associated with hypernatremia in situations with a high free water loss
    • biliary and pancreatic fistulas are other important causes
    • may occur iatrogenically as a result of high volume 0.9 NaCl administration, which has a much higher chloride concentration (154 mEq/L) compared with plasma (97 – 107 mEq/L)

Potassium

  1. Potassium Exchange
    • average dietary intake is 50 – 100 mEq/day
    • excreted primarily in the urine
    • obligate loss of 20 mEq/day in the urine, even in absence of any intake
    • only 2% of K+ is located in the extracellular compartment
    • extracellular K+ is critical to cardiac and neuromuscular function since K+ is the primary determinant of resting membrane potential
    • intracellular and extracellular distribution of K+ is influenced by acidosis, injury, tissue catabolism
    • renin-angiotensin-aldosterone axis is the key regulator of K+ clearance

  2. Hyperkalemia (> 5.5 mEq/L)
    1. Etiology
      • pseudohyperkalemia: hemolysis of lab specimens
      • impaired excretion: renal insufficiency/failure
      • tissue injury: hemolysis, rhabdomyolysis, crush injuries, reperfusion of an ischemic extremity
      • blood transfusions
      • compartment shifts: acidosis, increased osmolality (glucose, mannitol)
      • succinylcholine use, especially in paraplegics, burn, or trauma patients
      • other common medications: beta blockers, digitalis, tacrolimus

    2. Clinical Manifestations
      • GI: nausea/vomiting, abdominal pain, diarrhea
      • neuromuscular: weakness, paralysis
      • cardiac conduction abnormalities occur when K+ ≥ 6.5 mEq/L: EKG changes (peaked T waves, widened QRS complex, prolonged PR interval), ventricular fibrillation, arrest

    3. Treatment
      1. K+ < 6.5 mEq/L
        • address the underlying cause
        • potassium removal: cation exchange resins, either orally or by retention enema (binds potassium in exchange for sodium), loop diuretics if renal function is preserved, dialysis

      2. Emergency Management
        • 1 amp D50, 10 units insulin, 1 amp bicarb to drive K+ intracellularly
        • 10 mL of 10% calcium gluconate to counteract the cardiac effects
        • potassium removal

  3. Hypokalemia (< 3.5 mEq/L)
    1. Etiology
      • inadequate intake
      • excessive renal excretion (diuretics)
      • GI loss: vomiting, high NG output, fistulas
      • compartment shifts: alkalosis, insulin therapy

    2. Clinical Manifestations
      • GI: ileus, constipation
      • neuromuscular: fatigue, weakness, diminished reflexes
      • cardiovascular: atrial arrythmias, flat T waves, arrest

    3. Treatment
      • oral repletion for mild cases
      • more severe cases (K+ < 3.0 mEq/L) require IV administration: 10 mEq/hr in an unmonitored setting; max of 40 mEq/hr via central line with continuous EKG monitoring
      • IV rates should be lower in patients with renal dysfunction
      • hypokalemia represents a large intracellular deficit, and replenishing total body levels can take days
      • magnesium levels must be monitored and corrected as well, since hypomagnesemia can produce refractory hypokalemia

Calcium

  1. Calcium Exchange
    • majority of the body’s calcium is contained within bone
    • only 0.1% of total body calcium is in the ECF
    • normal serum level is 8.5 to 10.5 mg/dL
    • calcium in the serum is found in three forms: ~ 40% is protein-bound, ~ 10% is complexed to phosphate and other anions, and ~ 50% exists in the ionized form
    • the ionized fraction is responsible for neuromuscular stability
    • concentration of serum calcium is dependent on the concentration of plasma proteins
    • a fall in serum albumin of 1 gm/dL is associated with a 0.8 mg/dL fall in total calcium concentration, yet the ionized calcium level may remain normal
    • normal daily intake of calcium is 1 to 3 grams
    • most of this is excreted via the GI tract; only 200 mg or less is excreted in the urine daily
    • parathyroid hormone and Vitamin D are the major regulators

  2. Hypercalcemia 10.5 mg/dL)i>
    1. Etiology
      • hyperparathyroidism in nonhospitalized patients
      • malignancy in hospitalized patients: bone metastases (breast cancer), multiple myeloma, ectopic PTH secretion (lung)

    2. Clinical Manifestations
      • GI: nausea/vomiting, abdominal pain, anorexia
      • neuromuscular: weakness, confusion, lethargy, coma
      • cardiac: hypertension, arrhythmias, A-V block, arrest
      • polyuria, polydipsia

    3. Treatment
      • critical level is 14 mg/dL
      • treat the volume deficit with normal saline, aiming for a urine output of 100 – 150 mL/hr
      • concurrent administration of calcitonin, which acts quickly by increasing urinary excretion and inhibiting bone resorption of calcium
      • bisphosphonates (Aredia) inhibit osteoclast-mediated bone resorption and are useful for long-term calcium control in patients with malignancy

  3. Hypocalcemia (< 8.5 mg/dL)
    1. Etiology
      • hypoparathyroidism following parathyroidectomy or thyroidectomy
      • pancreatitis, necrotizing fasciitis
      • renal failure
      • hypomagnesemia
      • malnutrition
      • acute alkalosis from hyperventilation
      • post resuscitation dilution

    2. Clinical Manifestations
      • neuromuscular: paresthesias of the face and extremities, muscle cramps, carpopedal spasm stridor, tetany, seizures
      • hyperreflexia: Chvostek’s sign (twitching of the facial muscles when tapping on the facial nerve)
      • cardiac: decreased cardiac contractility, heart failure, prolonged QT interval, ventricular arrhythmias

    3. Treatment
      • should be initiated if the total calcium < 7 mEq/L or in any symptomatic patient
      • IV 10% calcium gluconate
      • goal is a calcium concentration of 7 – 9 mg/dL
      • must also correct hypokalemia, hypomagnesemia, hyperphosphatemia, and acidosis, if present
      • mild post-op hypocalcemia may be managed with oral calcium and vitamin D

Magnesium

  1. Magnesium Exchange
    • 50% of the body’s magnesium is incorporated in bone and is only slowly exchangeable
    • the majority of the rest is intracellular, with < 1% in the extracellular space
    • < 1% is extracellular
    • essential for the proper function of many enzyme systems, cell division, and calcium and potassium homeostasis
    • serum concentration ranges between 1.5 to 2.5 mEq/L
    • normal dietary intake is 20 mEq (240 mg)
    • majority is excreted in the feces
    • kidneys have a remarkable ability to conserve magnesium: on a magnesium-free diet, renal excretion may be less than 1 mEq/day

  2. Hypomagnesemia (< 1.5 mEq/L)
    1. Etiology
      • poor intake: starvation, alcoholism
      • renal loss: diuretic use
      • GI loss: diarrhea, malabsorption, pancreatitis, fistulas

    2. Clinical Manifestations
      • symptoms resemble calcium deficiency: hyperactive reflexes, tremors, tetany, delirium, seizures
      • cardiac: EKG changes, arrhythmias, torsades de pointes
      • can produce hypocalcemia and lead to persistent hypokalemia

    3. Treatment
      • for severe deficits (<1.2 mEq/L) or symptomatic patients: IV magnesium sulfate 1 – 2 grams over 15 minutes
      • simultaneous administration of calcium gluconate to correct hypocalcemia
      • oral magnesium can be used for mild to moderate hypomagnesemia

  3. Hypermagnesemia (> 2.5 mEq/L)
    1. Etiology
      • occurs mainly in the setting of renal failure
      • antacids and laxatives can produce toxic levels in renal patients
      • may also occur in trauma and burn patients

    2. Clinical Manifestations
      • GI: nausea/vomiting
      • neuromuscular: weakness, lethargy, decreased reflexes
      • cardiac: EKG changes similar to hyperkalemia, arrest

    3. Treatment
      • eliminate exogenous sources
      • correct volume deficits
      • correct acidosis if present
      • IV calcium gluconate for cardiac protection
      • dialysis may be necessary

Phosphorus

  1. Phosphorous Exchange
    • 80% is stored in bone; <1% is in the extravascular space
    • involved in energy production (ATP)
    • serum levels are tightly controlled by renal excretion

  2. Hypophosphatemia (< 2.5 mg/dL)
    1. Etiology
      • poor GI uptake: phosphate binders, malabsorption, malnutrition
      • intracellular shift: respiratory alkalosis, refeeding syndrome, hungry bone syndrome
      • postoperative in liver resections

    2. Clinical Manifestations
      • related to a decrease in ATP production: muscle weakness, cardiac and respiratory dysfunction

    3. Treatment
      • PO or IV replacement

  3. Hyperphosphatemia
    1. Etiology
      • hypoparathyroidism or hyperthyroidism can lead to decreased urinary excretion
      • cell destruction: rhabdomyolysis, tumor lysis syndrome, hemolysis, sepsis, malignant hyperthermia
      • excessive phosphorous containing laxatives

    2. Clinical Manifestations
      • many cases are asymptomatic
      • hypocalcemia may occur from precipitation of calcium with excess phosphate ions in the serum
      • can cause deposition of soft tissue calcium-phosphorus complexes

    3. Treatment
      • phosphate binders
      • calcium when hypocalcemia is present
      • dialysis for patients with renal failure







References

  1. Schwartz, 10th ed., pgs 65 – 82
  2. Sabiston, 20th ed., pgs 85 - 94
  3. Cameron, 13th ed., pgs 1410 - 1417
  4. UpToDate. General Principles of Disorders of Water Balance (Hyponatremia and Hypernatremia) and Sodium Balance (Hypovolemia and Edema). Richard Sterns, MD, July 20, 2020. Pgs 1 – 36