Hydroelectrolytic syndromes in neuroanesthesia and neurocritical care

Table 1 Hyponatremia syndromes and laboratory workup

Etiology	Volume status	Serum osmolality (mOsm/kg)	Urine osmolality	Urine Na+	Other features
SIADH	Euvolemic	↓ (< 280)	↑ (> 100 mOsm/kg, often > serum)	↑ (> 40 mEq/L)	↓ Serum uric acid; high FeUA before correction (> 11%) that normalizes after correction (4%-11%)
Cerebral salt wasting	Hypovolemic	↓ (< 280)	↑ (> 100, less concentrated than SIADH)	↑ (> 40 mEq/L)	↑ natriuretic peptides; persistent high FeUA (> 11%) even after Na+ correction
Diuretic-induced	Hypovolemic	↓ (< 280)	Variable (often ↑)	Variable (> 20 mEq/L)	History of loop or thiazide use; UNa interpretation may be confounded by recent diuretics
Excess hypotonic fluids	Euvolemic or hypervolemic	↓ (< 280)	↓ (< 100 mOsm/kg)	↓ (< 30 mEq/L)	Large-volume hypotonic IV fluids or low-solute intake (e.g., beer potomania)
Adrenal insufficiency	Euvolemic	↓ (< 280)	↑ (> 100 mOsm/kg)	↑ (> 40 mEq/L)	↓ Cortisol; hyponatremia resistant until glucocorticoid replaced

Confirm true hypotonic hyponatremia with serum osmolality < 280 mOsm/kg and rule out pseudohyponatremia. Volume status (clinical exam, hemodynamics) plus urine indices (osmolality, Na⁺) are essential to distinguish syndrome of inappropriate antidiuretic hormone secretion (euvolemic, concentrated urine, high urine Na) from cerebral salt wasting syndrome (hypovolemic, similar labs but with hypovolemia signs). Iatrogenic contributors (diuretics, hypotonic fluids) and endocrine causes (adrenal insufficiency) must always be considered. Continuous monitoring and tailored therapy (fluid restriction or vaptans for syndrome of inappropriate antidiuretic hormone secretion vs volume/sodium repletion for cerebral salt wasting syndrome) are critical. FeUA: Fractional excretion of uric acid; IV: Intravenous; SIADH: Syndrome of inappropriate antidiuretic hormone secretion; UNa: Urine Na.

Table 2 Hypernatremia syndromes and laboratory workup

Etiology	Volume status	Urine osmolality	Urine Na+	Key lab/clinical features
Extrarenal water losses	Hypovolemic	High (> 450 mOsm/kg)	Low (< 30 mEq/L)	↑ BUN/Cr ratio, hypotension/tachycardia, clinical signs of volume depletion
(Fever, hyperventilation, GI losses, drains, wounds)
Osmotic diuresis	Hypovolemic	High (> 300 mOsm/kg)	High (> 30 mEq/L)	Polyuria, osmotic diuresis; mannitol-induced free-water loss
(Mannitol, diuretics)
Central diabetes insipidus	Euvolemic	Low (< 200 mOsm/kg)	Low (< 30 mEq/L)	Polyuria (> 200 mL/hour), polydipsia, ↑ serum Na+, responds to desmopressin
Nephrogenic diabetes insipidus	Euvolemic	Low (< 200 mOsm/kg)	Variable (< 30 mEq/L)	Polyuria, ADH-resistance; no response to desmopressin
Hypertonic saline infusion	Hypervolemic	High (> 450 mOsm/kg)	High (> 30 mEq/L)	Positive fluid balance, volume overload, exogenous Na+ load (3%-23.4% NaCl)
Exogenous sodium load	Hypervolemic	High (> 450 mOsm/kg)	High (> 30 mEq/L)	Iatrogenic Na+ gain (bicarbonate drips, enteral salt), often with ↑ chloride
(NaHCO3, salt tablets)

Serum osmolality is invariably high (> 295 mOsm/kg) in true hypernatremia. Differentiation hinges on volume status (clinical exam, hemodynamics) and urinary indices (urine osmolality, urine Na⁺) to guide targeted therapy. ADH: Antidiuretic hormone; BUN: Blood urea nitrogen; Cr: Creatinine; GI: Gastrointestinal.

Table 3 Potassium disorders correction

Disorder	Treatment category	Agent	Dose/Route	Notes
Hypokalemia	Oral repletion	Potassium chloride	20-40 mEq per dose, 2-3 times/day	High bioavailability; GI side effects at higher doses
	IV repletion (peripheral)	Potassium chloride in D5W or NS	10 mEq in 100 mL, infused ≤ 10 mEq/hour	Must dilute to minimize phlebitis
	IV repletion (central)	Potassium chloride in D5W or NS	20 mEq in 100 mL, infused ≤ 20 mEq/hour (up to 40 mEq/hour in arrest)	ICU monitoring; higher rates only in life-threatening situations
Hyperkalemia	Membrane stabilization	Calcium gluconate (10% solution)	1 g IV over 5-10 minutes	Repeat every 5-10 minutes if ECG changes persist; central line preferred
	Intracellular shift	Insulin + dextrose	10 U regular insulin IV + 25 g dextrose	Lowers K+ in 10-20 minutes; monitor blood glucose
	Intracellular shift	Salbutamol (β2-agonist)	10-20 mg nebulized or 5-10 μg IV	Onset about 30 min; watch for tachycardia
	Intracellular shift	Sodium bicarbonate	50 mEq IV	Particularly if metabolic acidosis present
	Renal elimination	Furosemide	20-40 mg IV	Requires adequate renal function and volume status
	Dialytic removal	Hemodialysis or CRRT	-	Definitive in severe or refractory cases
	Gastrointestinal binding	SPS	15-30 g PO or PR	Erratic onset, GI side effects, risk of colonic necrosis
	Gastrointestinal binding	SZC	10 g PO	Onset about 1 h; better tolerated than SPS

GI: Gastrointestinal; D5W: 5% dextrose in water; NS: Normal saline; ICU: Intensive care unit; ECG: Electrocardiogram; CRRT: Continuous renal replacement therapy; SPS: Sodium polystyrene sulfonate; PO: By mouth; PR: Per rectum; SZC: Sodium zirconium cyclosilicate; IV: Intravenous.

Table 4 Magnesium disorders correction

Disorder	Treatment	Dose/route	Notes
Hypomagnesemia	IV magnesium sulfate	1-2 g IV over 1 hour, then 4-8 g IV over 12-24 h; in emergencies (e.g., torsades) 1-2 g IV over 15 min	Use central access for prolonged high-dose infusion; monitor serum Mg 2 h after start of infusion due to renal losses; faster infusion (e.g., in TdP) may be warranted
	Oral magnesium	Magnesium oxide or lactate 300-600 mg (12-25 mmol) PO 2-4 times daily	Use in mild, asymptomatic cases with intact GI tract; bioavailability limited; avoid if significant GI intolerance
Hypermagnesemia	Remove exogenous sources	Discontinue all magnesium-containing meds/infusions	Necessary first step; review all sources (IV fluids, TPN additives, supplements)
	Calcium gluconate	1-2 g IV over 5-10 min	Stabilizes cardiac membrane in severe elevations (> 4 mg/dL) or ECG changes; repeat PRN
	Loop diuretics + IV fluids	Furosemide 20-40 mg IV once, with isotonic saline bolus	Promotes renal Mg excretion; ensure adequate volume status; monitor electrolytes and renal function
	Hemodialysis	Standard-dialyze against low-Mg/zero-Mg bath	Reserved for refractory or life-threatening hypermagnesemia in renal failure

ECG: Electrocardiogram; GI: Gastrointestinal; IV: Intravenous; PO: By mouth; PRN: As needed; TPN: Total parenteral nutrition; TdP: Torsades de Pointes.

Table 5 Calcium disorders correction

Disorder	Medication	Dosing/infusion	Route	Key notes
Hypocalcemia	Calcium gluconate	1-2 g (10-20 mL of 10% solution) over 10-20 min; repeat as needed	IV	Preferred for mild-moderate hypocalcemia; monitor ECG during infusion
	Calcium chloride	1 g (10 mL of 10% solution) over 5-10 minutes	IV (central line preferred)	Reserved for severe/acute hypocalcemia (e.g., tetany, arrhythmias); risk of tissue necrosis if extravasated
	Oral calcium	1-4 g elemental calcium daily (e.g., calcium carbonate 500-1500 mg TID)	PO	For mild/asymptomatic hypocalcemia; combine with vitamin D in chronic cases
	Calcitriol	0.25-2 µg/day	PO/IV	Enhances intestinal calcium absorption; used in chronic hypocalcemia or renal failure
	Magnesium sulfate	1-2 g over 1 h (if hypomagnesemic)	IV	Corrects hypomagnesemia to restore PTH function
Hypercalcemia	Isotonic saline	1-2 L bolus, then 150-300 mL/hour	IV	First-line for volume resuscitation and calciuresis; avoid in heart failure
	Furosemide	20-40 mg every 4-6 h (after rehydration)	IV	Enhances calcium excretion; avoid in hypovolemia
	Zoledronic acid	4 mg over ≥ 15 min	IV	Bisphosphonate for malignancy or severe hypercalcemia; peak effect at 48-72 h
	Pamidronate	60-90 mg over 2-24 h	IV	Alternative bisphosphonate; adjust dose for renal impairment
	Calcitonin	4-8 units/kg every 6-12 h	SC/IM	Rapid calcium reduction (4-6 h); tachyphylaxis limits use to 48 h
	Denosumab	120 mg weekly × 1-3 doses	SC	For refractory hypercalcemia (e.g., malignancy); inhibits RANKL
	Prednisone	20-40 mg/day	PO	For hypercalcemia due to vitamin D toxicity or granulomatous diseases

ECG: Electrocardiogram; IM: Intramuscular; IV: Intravenous; PO: By mouth; PTH: Parathyroid hormone; SC: Subcutaneous; TID: Three times a day; RANKL: Receptor activator of nuclear factor kappa-B ligand.