Sodium, Potassium, Calcium & Magnesium

• Hyponatraemia: treat severe neurological symptoms promptly with monitored 3% saline boluses. Correction limits: ≤10 mmol/L in the first 24 h, then ≤8 per 24 h, and ≤18 in 48 h; with high ODS risk, ≤8 in ANY 24 h. Aim below the limits.
• ECG changes from hyperkalemia: give calcium gluconate up front, shift potassium next (insulin+dextrose, salbutamol), and finally remove it (diuretics, dialysis).
• Hypercalcemia: volume first, then calcitonin (fast) then zoledronate (durable); symptomatic hypocalcemia gets IV calcium gluconate.
• Replace measured Mg and phosphate deficits by severity and kidney function, with monitoring; take extra care in refeeding. Do not give phosphate routinely in DKA without a real deficit or clinical reason.
• If hyponatremia overcorrects, rescue with DDAVP 1–2 µg IV; vaptans are not for acute correction; K⁺ binders (patiromer, sodium zirconium cyclosilicate) are guideline-recognized for hyperkalemia.

Workup of Hyponatremia

• Hyponatremia (Na <135 mmol/L): check symptoms — severe ones (seizures, coma) → emergent 3% saline treatment (see 52.2)
• Measure serum osmolality
• Serum osmolality below 275 mOsm/kg (hypotonic)?
• Yes
• Measure urine osmolality
• Is urine osmolality ≤100 mOsm/kg?
• Yes
• Urine Osm ≤100: too much water for the solute intake (primary polydipsia, low-solute diet or beer potomania). Dilute urine alone does not diagnose a reset osmostat.
• No
• Measure urine sodium
• Urine sodium ≤30 mmol/L? Read it alongside diuretics, kidney function and the clinical volume assessment.
• Yes
• Assess volume: hypovolemic (vomiting, diarrhea, remote diuretics) → normal saline; hypervolemic (CHF, cirrhosis) → water restriction + diuresis
• No
• Urine Na >30: assess volume, diuretics, kidney function and endocrine causes. Exclude adrenal insufficiency before calling it SIADH. Treat the cause; fluid restriction suits SIADH or overload, not everyone in this branch.
• No
• Osm 275–295: pseudohyponatremia (severe hyperlipidemia/protein); Osm >295: translocational (hyperglycemia, mannitol) — correct the underlying problem
• Correction limits: ≤10 mmol/L in the first 24 h, then ≤8 per 24 h, and ≤18 in 48 h. High ODS risk: ≤8 in ANY 24 h. Aim below these limits. While correcting, follow Na and urine output closely; if a limit is passed, stop and get specialist help with DDAVP/D5W rescue (Pathway 52.2 and the Treatment popup).

Treating Hyponatremia

• Hypotonic hyponatraemia (Na <135 mmol/L): urgency depends on symptoms and speed of onset, not the sodium value alone.
• Symptomatic? OR acute (<2 days)?
• Yes
• Severe symptoms: 3% saline 150 mL IV over 20 min, then check Na and symptoms. Repeat up to TWO more times if needed; stop when symptoms improve or Na has risen about 4–6 mmol/L. Moderate symptoms: usually one bolus, then reassess. Acute onset alone does not call for repeated boluses.
• Calculate fluid rate and composition by the Adrogué–Madias equation (change in serum sodium per 1 L infused): ([infused Na + K] − serum sodium) / (TBW + 1)
• Once symptoms are controlled, treat the cause and keep within the limits: ≤10 mmol/L in the first 24 h, then ≤8 per 24 h, and ≤18 in 48 h (≤8 in ANY 24 h with high ODS risk). If Na rises too fast, stop Na-raising treatment and get specialist help with DDAVP/D5W rescue.
• No vaptans for emergency correction. Persistent SIADH needs specialist, cause-specific treatment; avoid routine demeclocycline, especially with kidney risk. Any effective treatment can overcorrect — keep monitoring.
• No
• No significant symptoms and chronic or unknown duration: treat the cause and avoid unnecessary fast correction. Isotonic fluid for true hypovolaemia; fluid restriction for SIADH or overload. Watch for a sudden water diuresis once the cause is treated.
• Correction limits: ≤10 mmol/L in the first 24 h, then ≤8 per 24 h, and ≤18 in 48 h. High ODS risk: ≤8 in ANY 24 h. Aim below these limits.

Workup of Hypernatremia

• Hypernatremia
• Volume status?
• Yes
• Hypervolemic: hyperaldosteronism/Cushing's syndrome OR hypertonic sodium load — treatment: stop the saline infusion, give diuretics to prevent volume overload, consider free water
• No
• Hypovolemic or euvolemic — is ADH present?
• Urine osmolality?
• Yes
• Urine Osm >300 mOsm/kg: check urine volume, solute excretion and water losses. Values of 300–800 can occur with partial DI or osmotic diuresis and do not prove a normal ADH response. Ask endocrinology if DI is still possible.
• Low intake or insensible losses: restore perfusion with isotonic fluid if needed, then replace the water deficit plus ongoing losses by mouth/NG or with D5W. Chronic or unknown duration: usually ≤0.5 mmol/L/h and ≤10 mmol/L/day. Acute symptomatic cases need specialist-led correction.
• Osmotic diuresis: replace water and electrolyte losses, treat hyperglycaemia or the other solute load, and review feeds with the nutrition team. Give water by serial Na; do not cut nutrition when the real problem is too little water.
• No
• Urine Osm <300 mOsm/kg (ADH absent or ineffective) — ddAVP response?
• Response to ddAVP?
• Yes
• Known central DI with large volumes of dilute urine: desmopressin 1–2 µg IV/IM with close Na and urine checks; repeat when dilute polyuria returns, with endocrine advice. Intranasal 10–40 µg is the usual TOTAL daily maintenance dose, divided — not 10–40 µg three times a day.
• No
• Nephrogenic DI — treatment: low-sodium diet with thiazide diuretics, low-protein diet, NSAIDs, plus address the underlying cause if possible (renal tubular disease, chronic loop diuretics, electrolyte abnormalities, lithium toxicity)

Workup of Hypokalemia

• Low serum potassium
• Spurious cause: extreme leukocytosis (WBC >100,000/cm³)
• Transcellular shift: insulin excess · alkalemia · beta₂-adrenergic agonists/stress · hypothermia · theophylline · barium intoxication · thyrotoxicosis · hypokalemic periodic paralysis — consider during alcohol withdrawal, myocardial infarction, asthma attack
• Total body K⁺ decreased: low K⁺ intake OR increased K⁺ losses
• Look for renal K loss with a 24-h urine K or a spot K/creatinine ratio, read with acid–base status, intake and diuretics. Urine K concentration varies with dilution, and TTKG is unreliable on its own. Vomiting can cause secondary renal K loss.
• Renal losses plus hypertension — true aldosterone effects: primary hyperaldosteronism · renovascular or malignant hypertension
• Renal losses plus hypertension — aldosterone-like effects: apparent mineralocorticoid excess · Cushing's syndrome · congenital adrenal hyperplasia · Liddle's syndrome
• Renal losses, normotensive — secondarily elevated aldosterone (hypovolemia): Bartter's syndrome · aggressive diuretic use · Gitelman's syndrome

Treating Hypokalemia

• Hypokalemia
• Reverse correctable causes: stop diuretics · correct magnesium deficiency
• Severe hypokalaemia (K <2.5 mmol/L), arrhythmia, paralysis or marked weakness, or unable to take it enterally?
• Yes
• IV KCl by infusion pump, never as an IV push: usually ≤10 mEq/h peripherally or ≤20 mEq/h centrally with monitoring. Up to 40 mEq/h only for life-threatening cases in ICU, via a central line with continuous ECG and frequent K checks. Reduce in kidney impairment.
• No
• Acid–base status?
• Yes
• Metabolic acidosis (diarrhea or renal tubular acidosis) → give K⁺ citrate, K⁺ bicarbonate
• No
• Metabolic alkalosis or normal pH — normotensive: oral KCl · hypertensive: consider K⁺-sparing diuretic

Workup of Hyperkalemia

• High serum potassium
• Spurious cause: traumatic or ischaemic blood draw · marked leucocytosis (e.g. WBC >50,000/µL) · thrombocytosis (e.g. platelets >1,000,000/µL). Confirm with a careful repeat sample when safe — but do not delay emergency treatment for convincing severe hyperkalaemia.
• Transcellular shift — ICF-ECF exchange: insulin deficiency · hypertonicity · β₂-adrenergic blockade · succinylcholine · fluoride intoxication · digitalis intoxication · inorganic acidosis · hyperkalemic periodic paralysis || Cellular release: rhabdomyolysis · hemolysis · tumor lysis syndrome · intense exercise
• Impaired renal excretion — GFR decreased (<20 mL/min): exogenous administration (potassium-rich foods, K⁺ supplements, blood products) · endogenous retention of metabolic waste || Reduced aldosterone effect: potassium-sparing diuretics · ACE inhibitors · ARBs · type IV renal tubular acidosis (diabetes mellitus, interstitial nephritis, urinary tract obstruction) · NSAIDs · cyclosporine A · papillary necrosis (sickle cell disease, analgesic nephropathy) · heparin · ketoconazole, trimethoprim, pentamidine
• Abbreviations — GFR = glomerular filtration rate · ECF = extracellular fluid · WBC = white blood cell count · ICF = intracellular fluid

Workup of Hypocalcemia

• Confirm hypocalcaemia against the local reference range; measure ionised Ca in critically ill patients when you can. Albumin-corrected total calcium can mislabel ICU patients, especially with acid–base problems.
• PTH response?
• Yes
• PTH appropriately elevated — present but ineffective
• Vitamin D level?
• Yes
• Vitamin D normal → PTH RESISTANCE: bisphosphonates · uremic environment · CHELATION: hyperphosphatemia (rhabdomyolysis, tumor lysis syndrome, hemolysis, phosphosoda bowel preparation), pancreatitis, alkalemia, foscarnet therapy, citrate-containing infusions (blood products, plasmapheresis, CVVHD), ethylene glycol toxicity
• No
• Vitamin D low → VITAMIN D DEFICIENCY (25-OH vit D <15 ng/mL): severe liver disease · low dietary intake · P450 enzyme inducers (phenytoin, phenobarbital, isoniazid, rifampin)
• Advanced renal disease can reduce activation to the 1,25-form causing hypocalcemia, though 25-OH level may be normal
• No
• PTH low or inappropriately normal → HYPOPARATHYROIDISM: parathyroid injury or removal at surgery (tell apart from hungry-bone mineral uptake) · low or high magnesium · infiltration (haemochromatosis, Wilson's disease, malignant replacement) · autoimmune disease · radiation damage to the parathyroids · HIV infection (can also affect vitamin D activation)

Workup of Hypercalcemia

• Hypercalcemia: corrected calcium >10.3 mg/dL OR ionized calcium >5.2 mg/dL
• PTH response?
• Yes
• PTH high or inappropriately normal: consider primary or tertiary hyperparathyroidism, lithium or FHH. Use paired urine and serum tests and the calcium–creatinine clearance ratio, with specialist help. Low urine Ca supports FHH, but CKD, low vitamin D or intake and thiazides confuse it; a 200-mg/day cut-off alone does not diagnose it.
• No
• PTH appropriately low → PTH-independent mechanism; consider vitamin D level testing
• Vitamin D levels abnormally high?
• Yes
• EXCESS 1,25-OH: granulomatous disease (sarcoidosis) · lymphoma · calcitriol overdose · acromegaly · EXCESS 25-OH: vitamin D intoxication
• No
• PTH-RELATED PEPTIDE: humoral hypercalcemia of malignancy (elevated PTHrP) · DECREASED Ca²⁺ EXCRETION: volume depletion, thiazide diuretics, milk alkali syndrome · BONE RESORPTION: osteolytic malignancy, Paget's disease, immobilization, hyperthyroidism, adrenal insufficiency

Workup of Hypophosphatemia

• Hypophosphatemia (phosphorus <2.8 mg/dL) — interpret with PTH and serum calcium concentration
• FEPhos (%) = 100 × (urine phosphate × serum creatinine) / (serum phosphate × urine creatinine), all in the same units; read it with kidney function and serum phosphate.
• Yes
• RENAL LOSSES (FEPhos >5% OR urine phos >100 mg/day): chronic alcoholism · hyperparathyroidism · volume expansion · osmotic diuresis · theophylline use · corticosteroid use · Fanconi's syndrome · oncogenic osteomalacia (FGF-23)
• No
• GASTROINTESTINAL LOSSES (FEPhos <5% OR urine phos <100 mg/day): phosphate binders (including antacids) · malabsorption/malnutrition/diarrhea · vitamin D deficiency (reduced absorption)
• TRANSCELLULAR SHIFTS: refeeding syndrome · insulin administration · respiratory alkalosis · catecholamine release, beta-agonist therapy · post-parathyroidectomy ("hungry bone")
• OTHER REMOVAL — intensive continuous dialysis (CVVHD)

Workup of Hyperphosphatemia

• Hyperphosphatemia (phosphorus >4.5 mg/dL) — interpret with PTH and serum calcium concentration
• Too much phosphate taken in, absorbed or released from damaged cells? Check exposures, kidney function, calcium and PTH — no single urine phosphate cut-off gives the cause.
• Yes
• EXCESS LOAD OR ABSORPTION: phosphate-containing preparations, excess vitamin D or calcitriol, granulomatous disease, lymphoma. Check kidney function and exposures; urine phosphate >1500 mg/day is not required.
• TRANSCELLULAR SHIFTS: tumor lysis syndrome · rhabdomyolysis, hemolysis · relative insulin deficiency · metabolic acidosis
• No
• REDUCED EXCRETION: AKI or CKD, hypoparathyroidism, PTH resistance. In CKD, secondary hyperparathyroidism usually follows phosphate retention — read calcium, PTH and kidney function together.

Workup of Hypomagnesemia

• Hypomagnesemia
• 24-hr urine magnesium vs FEMag?
• Yes
• RENAL MAGNESIUM WASTING (24-hr urine magnesium >2 mEq OR FEMag >2%): hypercalcemia · osmotic diuresis · polyuric phase of resolving ATN · volume expansion · chronic alcoholism · Gitelman's syndrome (less commonly Bartter's syndrome) · diuretics (loop/thiazide) · aminoglycosides · amphotericin B · platinum-based chemotherapy · pentamidine · cyclosporine A · EGFR blockers (cetuximab)
• No
• REDUCED INTAKE OR EXTRARENAL LOSS (24-hr urine magnesium <2 mEq OR FEMag <2%): starvation · malabsorption · diarrhea · prolonged gastrointestinal drainage (nasogastric suction, intestinal fistulas, biliary drainage) · severe burns
• CHELATION: pancreatitis · alkalemia · hyperphosphatemia (rhabdomyolysis, tumor lysis syndrome, hemolysis, phosphosoda bowel preparation) · citrate-containing infusions (blood products, plasmapheresis, CVVHD) · foscarnet therapy · ethylene glycol toxicity

Workup and Treatment of Hypermagnesemia

• Hypermagnesemia
• ENDOGENOUS SOURCES: tumor lysis syndrome · diabetic ketoacidosis · adrenal insufficiency · theophylline intoxication · occasionally primary hyperparathyroidism
• EXOGENOUS ADMINISTRATION: magnesium-containing laxatives in renal failure · antacids in renal failure · overaggressive IV magnesium (treatment of preeclampsia/eclampsia)
• TREATMENT: stop further magnesium administration · with ECG changes or symptoms, give 1–2 g calcium gluconate IV over 10 min and consider hemodialysis, especially with renal insufficiency that is not easily reversible · if renal function is preserved, IV isotonic saline plus a loop diuretic may enhance magnesium excretion; use hemodialysis for severe or symptomatic hypermagnesemia, especially with renal failure

Treating Hyperkalemia

• Confirm the value and exclude a haemolysed or drip-arm sample — but never wait for the repeat in a patient with ECG changes. Send a blood gas potassium at the same time for a result in minutes, and put the patient on a cardiac monitor
• ECG changes (peaked T waves, flattened or absent P waves, a widening QRS, or a sine-wave pattern) or K⁺ ≥6.5 mmol/L?
• Yes
• ECG changes of hyperkalaemia: calcium gluconate 10% 30 mL IV over 10 min; in peri-arrest, calcium chloride 10% 10 mL over 5 min via secure access. Repeat the ECG and redose if changes persist. Calcium does not lower K. K ≥6.5 needs urgent K-lowering even with a normal ECG; give calcium without ECG changes only per local emergency guidance.
• Shift K into cells: soluble insulin 10 units with glucose 25 g IV over 15–30 min, plus nebulised salbutamol 10–20 mg. Check glucose at baseline, 15, 30, 60, 90 and 120 min, then hourly to 6 h. If baseline glucose is <7 mmol/L, follow with 10% glucose 50 mL/h for 5 h.
• Give sodium bicarbonate only where there is coexisting metabolic acidosis, and as a slow infusion rather than a bolus; on its own it is a weak and unreliable shifter
• No
• No ECG changes: K 5.5–5.9 → fix the cause, start removal and recheck. K 6.0–6.4 → consider insulin–glucose plus nebulised salbutamol, especially if acutely unwell or K is rising. A normal ECG does not mean low risk.
• Shifting is temporary — remove K too. Stop K supplements and infusions; review feeds, salt substitutes and contributing drugs, and hold the culprits where safe. Loop diuretic only if the patient passes urine and volume status allows. Sodium zirconium cyclosilicate or patiromer as add-ons; dialysis when indicated.
• Refractory, anuric, or with ongoing release from tissue breakdown (rhabdomyolysis, tumour lysis, massive haemolysis)?
• Yes
• Arrange urgent haemodialysis — this is an emergency indication for kidney replacement therapy. Expect a rebound as potassium redistributes after the session, and recheck within 1–2 hours
• No
• Recheck potassium at 1, 2, 4 and 6 hours, keep cardiac monitoring until K⁺ is below 6.0 mmol/L with a normal ECG, and treat the cause — AKI, adrenal insufficiency, drugs or tissue breakdown
• Hyperkalaemia with digoxin toxicity: digoxin-specific antibody fragments; give calcium slowly and only if needed. Avoid suxamethonium with hyperkalaemia, denervation, prolonged immobility, or major burns or trauma after the acute phase. Kidney failure alone does not rule out a single usual dose when K is normal and there is no neuropathy; avoid repeated or large doses.