Step 2 CK · Internal Medicine · Nephrology

Electrolyte Disorders (Clinical)

Name: Electrolyte Disorders (Clinical)
Creator: Veli Bakalov, MD

Volume-based algorithms, correction limits, and the ECG-driven emergencies

Nephrology·Fluids, Electrolytes & Acid-Base·4 min read·9 high-yield points·Reviewed by Veli Bakalov, MD @HemeOncBuddy

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Hyponatremia: check serum osmolality first (low = true hypotonic, normal = pseudohyponatremia, high = hyperglycemia or mannitol; add ~1.6 mEq/L Na per 100 mg/dL glucose above 100), then volume status.
SIADH = euvolemic, urine osm >100, urine Na >30–40, low uric acid, normal thyroid and adrenal function (SSRIs, carbamazepine, small cell lung cancer); fluid restriction first, and isotonic saline can worsen it.
Correct chronic hyponatremia by no more than ~8 mEq/L in 24 h; too fast causes osmotic demyelination 2–6 days later (dysarthria, dysphagia, quadriparesis).
Seizures or coma from hyponatremia: 3% saline to raise Na 4–6 mEq/L acutely, regardless of chronicity.
Hypernatremia is a water deficit: correct no faster than ~10–12 mEq/L per 24 h to avoid cerebral edema.
Central DI concentrates urine after desmopressin; nephrogenic DI (lithium, hypercalcemia, hypokalemia) does not; primary polydipsia concentrates with water deprivation.
Hyperkalemia: peaked T waves first; with any ECG change give IV calcium gluconate first, then insulin + glucose and albuterol, then remove K (diuretic, binder, dialysis).
Hypokalemia shows U waves and flat T waves; correct magnesium or the hypokalemia stays refractory.
Hypercalcemia: primary hyperparathyroidism (outpatient) vs malignancy (inpatient); IV saline first, then calcitonin and a bisphosphonate; hypermagnesemia (lost reflexes) is reversed with IV calcium.

Hyponatremia: osmolality, then volume

Step 1: serum osmolality. Low osmolality (<275 mOsm/kg) means true hypotonic hyponatremia. Normal osmolality means pseudohyponatremia from hyperlipidemia or paraproteinemia. High osmolality means hypertonic hyponatremia from hyperglycemia or mannitol; correct the measured sodium upward by ~1.6 mEq/L for every 100 mg/dL of glucose above 100.

Step 2: volume status, then urine studies. In hypotonic hyponatremia, examine volume, then use urine sodium and osmolality to separate renal from extrarenal causes and choose therapy: saline, restriction, or diuresis.

Hypotonic hyponatremia by volume status

Feature	Hypovolemic	Euvolemic	Hypervolemic
Causes	GI losses; diuretics (especially thiazides) or salt wasting	SIADH, hypothyroidism, adrenal insufficiency, primary polydipsia	Heart failure, cirrhosis, nephrotic syndrome
Urine Na	<20 if extrarenal; >20 with diuretics or salt wasting	>30 in SIADH	<20 (low effective circulating volume)
Treatment	Isotonic saline	Fluid restriction; treat the cause	Sodium and fluid restriction, loop diuretic

Primary polydipsia and low-solute diets (beer potomania, tea and toast) produce maximally dilute urine, osmolality <100.

SIADH and safe correction

SIADH. Euvolemic hypotonic hyponatremia with inappropriately concentrated urine (osmolality >100), urine Na >30–40, and low serum uric acid (<4 mg/dL, which helps separate it from hypovolemia), once thyroid and adrenal function are shown to be normal. Causes include SSRIs, carbamazepine, small cell lung cancer, CNS and pulmonary disease, and pain and surgery.

Treating chronic SIADH. Fluid restriction is first-line, with salt tablets and a loop diuretic if needed; vaptans (V2 receptor antagonists) or demeclocycline are for refractory cases. Isotonic saline can paradoxically worsen SIADH, because the kidney excretes the salt and keeps the free water.

Severe symptoms. Seizures or coma call for 3% hypertonic saline to raise sodium ~4–6 mEq/L quickly and stop herniation, regardless of chronicity. Aim for a small, controlled bump, not normalization, and recheck sodium frequently.

~8 mEq/Lmaximum hyponatremia correction per 24 h

4–6 mEq/Lacute rise with 3% saline for seizures or coma

10–12 mEq/Lmaximum hypernatremia correction per 24 h

Correcting chronic hyponatremia too fast causes osmotic demyelination syndrome (central pontine myelinolysis) 2–6 days later: dysarthria, dysphagia, spastic quadriparesis, even a locked-in state. Risk is highest with alcoholism, malnutrition, hypokalemia, and liver disease. If sodium overshoots, relower it with D5W and desmopressin.

Hypernatremia and diabetes insipidus

Always a water problem. Hypernatremia is always hypertonic and means a water deficit or impaired thirst or access to water: diabetes insipidus, osmotic diuresis, and GI or insensible losses. Restore perfusion with isotonic saline if the patient is hypotensive, then replace the free water deficit slowly, no faster than ~10–12 mEq/L per 24 hours, because rapid correction drives water into brain cells and causes cerebral edema.

Diabetes insipidus is polyuria with dilute urine. The water deprivation test, followed by desmopressin, separates the causes:

Polyuria with dilute urine

Feature	Central DI	Nephrogenic DI	Primary polydipsia
Defect	Low ADH (head trauma, pituitary surgery, tumor)	ADH resistance (lithium, hypercalcemia, hypokalemia)	Excess water intake
Water deprivation	Urine stays dilute	Urine stays dilute	Urine concentrates
After desmopressin	Urine concentrates	No response	Little further rise
Treatment	Desmopressin	Remove the cause; thiazide and low-salt diet (amiloride for lithium)	Limit water intake

Potassium

Hyperkalemia. Causes include CKD, ACE inhibitors and ARBs, potassium-sparing diuretics, tissue breakdown, and acidosis; exclude pseudohyperkalemia from a hemolyzed sample. The ECG progresses from peaked T waves (earliest) to PR prolongation and P-wave flattening, a widened QRS, then a sine wave and arrest. Any ECG change makes it an emergency.

StabilizeIV calcium gluconate first; it protects the myocardium but does not lower potassium.
ShiftInsulin plus glucose and albuterol; add bicarbonate if acidotic.
RemoveLoop diuretic, binders (patiromer, sodium zirconium cyclosilicate, or sodium polystyrene sulfonate), or dialysis.

Hyperkalemia emergency sequence

Hypokalemia. The ECG shows flattened T waves, U waves, and ST depression, with a higher risk of arrhythmia and digoxin toxicity. Causes are GI or renal losses and intracellular shifts (insulin, β-agonists, alkalosis). Replace potassium, orally when possible, and always correct hypomagnesemia, which causes refractory hypokalemia by increasing renal potassium wasting.

Calcium, magnesium, and phosphate

Correct for albumin. Add 0.8 mg/dL to the measured calcium for every 1 g/dL that albumin is below 4, or measure ionized calcium.

Calcium extremes

Feature	Hypercalcemia	Hypocalcemia
Clinical	Stones, bones, abdominal groans, psychiatric overtones; polyuria and dehydration	Perioral numbness, tetany, Chvostek and Trousseau signs, seizures
ECG	Short QT	Prolonged QT
Leading causes	Primary hyperparathyroidism (outpatients), malignancy (inpatients)	Hypoparathyroidism after neck surgery, vitamin D deficiency, CKD, hypomagnesemia
Treatment	IV isotonic saline first, then calcitonin and a bisphosphonate	IV calcium gluconate if symptomatic; fix magnesium

Thiazides worsen hypercalcemia; a loop diuretic is used only after volume repletion.

Hypercalcemia pacing. Calcitonin acts within hours but loses effect within about 2 days, while bisphosphonates take 2–4 days, so the two overlap. PTH sorts the cause: high or inappropriately normal in primary hyperparathyroidism, suppressed in malignancy.

Magnesium. Hypomagnesemia (alcohol use, diarrhea, diuretics, PPIs) causes refractory hypokalemia and hypocalcemia and torsades; replace magnesium. Hypermagnesemia (renal failure, magnesium sulfate for preeclampsia) causes loss of deep tendon reflexes and respiratory depression, reversed with IV calcium gluconate.

Phosphate. Refeeding syndrome drops phosphate as insulin drives it into cells, risking weakness, respiratory and heart failure, and rhabdomyolysis. Tumor lysis raises phosphate along with potassium and uric acid, and lowers calcium.