19.2 Electrolyte Disturbances

Electrolyte Disturbances

Why This Matters for the Exam

Sodium and potassium abnormalities are classic "numbers matter" questions on the ABHS Pediatrics Part 1 exam. Examiners test not just recognition of hyponatremia, hypernatremia, hypokalemia, or hyperkalemia, but the SAFE RATE of correction and the correct emergency-management sequence for life-threatening hyperkalemia.

Hyponatremia

Hyponatremia is a serum sodium concentration below 135 mEq/L (mmol/L). Symptoms — headache, nausea, lethargy, seizures, and coma — correlate with both the absolute sodium level (symptoms typically appear below 125 mEq/L, seizures below 120 mEq/L) and the speed of onset.

Causes

A Common Exam Trap: Pseudohyponatremia From Hyperglycemia

Before treating a low sodium result, check the glucose. Severe hyperglycemia (e.g., in diabetic ketoacidosis) pulls water osmotically out of cells and into the plasma, artificially lowering the measured sodium even though total body sodium is unchanged. A commonly used correction is: for every 100 mg/dL that glucose is above 100 mg/dL, add about 1.6–2.4 mEq/L back to the measured sodium to estimate the true (corrected) value. Treating the glucose, not the sodium, resolves this type of "hyponatremia."

Correction — Safety Limits

• Acute, symptomatic hyponatremia (seizures): give 3% hypertonic saline, 3–5 mL/kg IV over 10–15 minutes, aiming to raise serum sodium acutely by about 4–6 mEq/L — enough to stop seizures by reducing cerebral swelling.
• Overall correction rate: regardless of the acute bolus, the total rise in serum sodium should not exceed about 8 mEq/L in any 24-hour period (some protocols allow up to 10–12 mEq/L/day in lower-risk patients, but the safer teaching ceiling — especially for chronic or severe hyponatremia — is 8 mEq/L per 24 hours).
• Overcorrection risks osmotic demyelination syndrome (ODS), previously called central pontine myelinolysis: delayed (days later) dysarthria, dysphagia, and quadriparesis from destruction of the myelin sheath in the pons, caused by too-rapid osmotic shifts.
• Chronic hyponatremia (present more than 48 hours, or of unknown duration) must always be treated as chronic and corrected cautiously, even if the child is asymptomatic.

Hypernatremia

Hypernatremia is a serum sodium above 145 mEq/L, almost always reflecting a relative free-water deficit rather than true sodium excess.

Causes

Free-water loss exceeding sodium loss (diarrhea, diabetes insipidus — central or nephrogenic, inadequate breastfeeding in neonates, fever and insensible losses) or sodium gain (improperly mixed infant formula, excess sodium administration, salt poisoning).

Classic hypernatremic dehydration clues on exam: an irritable infant with a high-pitched cry, doughy (not tenting) skin turgor, hyperreflexia, and disproportionately severe neurologic signs relative to the degree of visible volume loss — because the brain has already adapted to the rising sodium.

Correction — Safety Limits

Rapid correction is dangerous because brain cells accumulate protective "idiogenic osmoles" during chronic hypernatremia; if serum sodium falls too quickly, water shifts INTO brain cells, causing cerebral edema, seizures, and permanent neurologic injury.

• Correct no faster than about 0.5 mEq/L per hour, and no more than roughly 10–12 mEq/L over 24 hours.
• Use hypotonic fluids (e.g., 5% dextrose in 0.2% saline) and, for hypernatremic dehydration, replace the fluid deficit over 48 hours rather than the standard 24 hours used for isonatremic dehydration.

Potassium Disorders

Hypokalemia

Hypokalemia (serum potassium below 3.5 mEq/L) results from gastrointestinal losses (vomiting, nasogastric suction, diarrhea), renal losses (diuretics, renal tubular acidosis types 1 and 2, Bartter or Gitelman syndromes), transcellular shift (insulin, beta-agonists, alkalosis), or poor dietary intake.

ECG changes: flattened or inverted T waves, prominent U waves, ST-segment depression, and a prolonged QU interval; severe hypokalemia can precipitate arrhythmias.

Management: oral potassium chloride for mild-to-moderate deficits; IV potassium (with continuous cardiac monitoring) for severe or symptomatic hypokalemia. IV potassium must never be given as a rapid push because of the risk of fatal arrhythmia.

Hyperkalemia

Hyperkalemia (serum potassium above 5.5 mEq/L, with higher reference thresholds often used in neonates) is caused by renal failure or acute kidney injury, tissue breakdown (hemolysis, rhabdomyolysis, tumor lysis syndrome), acidosis (which shifts potassium out of cells), adrenal insufficiency or salt-wasting CAH, certain medications, massive blood transfusion, or pseudohyperkalemia from a hemolyzed blood sample — always confirm an unexpected result with a fresh, non-hemolyzed sample.

ECG changes progress predictably as potassium rises:

Emergency Management of Severe Hyperkalemia

1. IV calcium gluconate 10% (0.5–1 mL/kg, maximum around 10 mL) over 5–10 minutes — stabilizes the cardiac membrane within minutes; it does NOT lower serum potassium, so repeat the dose if ECG changes persist.
2. Insulin plus glucose: regular insulin 0.1 unit/kg IV together with concurrent dextrose (to prevent hypoglycemia) — shifts potassium intracellularly, with onset in about 15–30 minutes.
3. Nebulized salbutamol (albuterol), 2.5–5 mg, as an additional temporizing intracellular-shift agent.
4. Sodium bicarbonate if concurrent metabolic acidosis is present.
5. Definitive potassium removal: potassium-binding resins (slow, enteral route), loop diuretics if renal function allows, or dialysis for refractory hyperkalemia or renal failure.
6. Identify and treat the underlying cause — for example, stress-dose hydrocortisone plus IV saline for a salt-wasting CAH adrenal crisis.