Hyponatraemia (Na <135 mEq/L)
Overcorrection of chronic hyponatraemia causes Osmotic Demyelination Syndrome (ODS/CPM) — irreversible pontine and extrapontine demyelination. Undercorrection of acute symptomatic hyponatraemia risks cerebral herniation. Duration determines safe correction rate.
Classification by Duration & Severity
| Type | Duration | Symptoms | Safe Correction Rate |
|---|---|---|---|
| Acute symptomatic | <48 hours | Seizures, coma, herniation signs | Raise Na 1–2 mEq/L/hr until symptoms resolve; then ≤10 mEq/L per 24h total |
| Chronic (or unknown) | >48h or unknown | Nausea, headache, lethargy, confusion | ≤8–10 mEq/L per 24h; ≤18 mEq/L per 48h |
Management by Type
Acute Symptomatic (Seizures/Coma) — Emergency
- 3% NaCl (hypertonic saline) — 150 ml IV over 20 minutes
- Repeat up to 3 times until acute symptoms resolve
- Check Na every 2h; slow the rate once Na rises 4–6 mEq/L or symptoms resolve
- Do NOT exceed 10 mEq/L rise in 24h total after acute phase
SIADH (most common cause in ICU)
| SIADH Diagnostic Criteria |
|---|
| Plasma osmolality <275 mOsm/kg + Urine osmolality >100 mOsm/kg + Urine Na >30 mEq/L + Euvolaemia + Normal thyroid and adrenal function |
- Fluid restriction: 800–1000 ml/day (first line; slow effect)
- 3% NaCl: If symptomatic or Na <125 despite fluid restriction
- Urea 0.25–0.5 g/kg PO/NGT daily: Effective but unpalatable; dissolve in OJ
- Tolvaptan (V2 antagonist): 15–60 mg PO OD for euvolaemic/hypervolaemic SIADH; do NOT use in liver disease (hepatotoxicity)
- Treat underlying cause (stop offending drugs, treat infection, etc.)
Hypovolaemic Hyponatraemia
Give 0.9% NaCl to correct volume depletion — Na will rise naturally as ADH suppressed. Monitor closely to avoid overcorrection.
If Na rises >10 mEq/L in 24h: give free water (PO, NGT, or D5W IV) to slow the rise. Desmopressin 2–4 mcg SC/IV q6–8h can be added to prevent further free water loss and slow correction rate.
Hypernatraemia (Na >145 mEq/L)
Almost always reflects free water deficit. Common causes in ICU: insensible losses, diabetes insipidus, inadequate free water in tube feeds, loop diuretics, osmotic diuresis.
Management
Free Water Deficit (FWD): FWD (L) = 0.6 × Weight (kg) × [(Na/140) − 1]
- Replace FWD over 24–48h with D5W or 0.45% NaCl IV, or free water via NGT
- Correct at ≤ 10–12 mEq/L per 24h (risk of cerebral oedema with rapid correction)
- Monitor Na q4–6h during correction
Diabetes Insipidus (DI)
- Central DI (low ADH): DDAVP 1–4 mcg SC/IV BD; desmopressin 10–40 mcg intranasal
- Nephrogenic DI (ADH resistance from lithium, hypercalcaemia, etc.): Thiazide diuretics + low-sodium diet; DDAVP less effective
- Replace ongoing urinary free water losses (large volume dilute urine) hourly with D5W or 0.45% saline
Hypokalaemia (K <3.5 mEq/L)
| Severity | K Level | Route | Replacement Rate | Monitoring |
|---|---|---|---|---|
| Mild | 3.0–3.5 mEq/L | Oral/NGT | KCl 40–80 mEq/day in divided doses | Recheck daily |
| Moderate | 2.5–3.0 mEq/L | IV + oral | 10–20 mEq/hr peripheral; 40 mEq/hr central | Continuous ECG; q6h K check |
| Severe / ECG changes | <2.5 or ECG changes | IV central line only | 20–40 mEq/hr central with max rate monitoring | Continuous ECG; q2h K; central line mandatory |
Hypokalaemia is refractory to K⁺ replacement if Mg²⁺ is low. Magnesium is essential for intracellular K⁺ retention via Na-K-ATPase. Check and correct Mg²⁺ before and alongside K⁺ replacement. Target Mg >0.8 mmol/L.
Concentration limits: Peripheral IV max 40 mEq/L (irritant — causes phlebitis); Central line max 80 mEq/L. NEVER give IV KCl as undiluted bolus — fatal arrhythmia.
Hyperkalaemia (K >5.5 mEq/L)
- Step 1 — Stabilise the Myocardium (if ECG changes): Calcium Gluconate 10 ml of 10% IV over 10 min; can repeat after 5 min. Duration: 30–60 min only. Does NOT lower K⁺.
- Step 2 — Shift K⁺ into Cells (works in 30–60 min):
- Insulin 10 units IV + 50 ml of 50% Dextrose (D50W) → lowers K by 0.6–1 mEq/L
- Salbutamol 10–20 mg nebuliser → lowers K by 0.5–1 mEq/L; max effect at 90 min
- NaHCO₃ 50 mEq IV if metabolic acidosis (pH <7.1) → modest effect
- Step 3 — Remove K⁺ from Body:
- Furosemide 40–80 mg IV (if urine output present)
- Sodium Polystyrene Sulfonate (Calcium Resonium) 15–30g PO/PR q4–6h
- Patiromer 8.4g PO OD (newer; better tolerated)
- Sodium Zirconium Cyclosilicate (ZS-9) 10g PO TDS × 48h
- Haemodialysis / CRRT (if anuric or refractory)
- Step 4 — Stop Causative Drugs: ACEi, ARBs, K-sparing diuretics, NSAIDs, heparin, TMP-SMX, calcineurin inhibitors
ECG Changes in Hyperkalaemia (Progressive)
Peaked T waves → PR prolongation → widened QRS → P wave loss → Sine wave → VF/PEA → Asystole
Any ECG change beyond peaked T waves → treat immediately with calcium + insulin/dextrose AND prepare for urgent dialysis.
Magnesium Disorders
Hypomagnesaemia (Mg <0.75 mmol/L)
Prevalence: 30–65% in ICU patients. Common causes: diarrhoea, loop/thiazide diuretics, aminoglycosides, amphotericin B, proton pump inhibitors (long-term), alcohol, refeeding syndrome.
Clinical Effects
- Refractory hypokalaemia and hypocalcaemia
- Cardiac arrhythmias: QTc prolongation, Torsades de Pointes, AF
- Neuromuscular: tremor, tetany, Trousseau/Chvostek signs, seizures
- Respiratory muscle weakness — may prevent extubation
Replacement Protocol
| Indication | Regimen |
|---|---|
| Asymptomatic, Mg 0.6–0.75 | Oral magnesium oxide 400–800 mg/day (poor absorption — causes diarrhoea; use as adjunct) |
| Symptomatic or Mg <0.6 mmol/L | MgSO₄ 2–4g (16–32 mEq) IV over 30–60 min; may repeat |
| Torsades de Pointes | MgSO₄ 2g IV push over 2–3 minutes; immediate effect on arrhythmia |
| Severe or ongoing losses | MgSO₄ 4–8g/day IV infusion; maintain with NGT supplementation |
Hypermagnesaemia (Mg >1.1 mmol/L)
Usually iatrogenic (over-replacement, especially in AKI). Effects: loss of DTRs (Mg >3.5), respiratory paralysis (Mg >5.0), cardiac arrest (Mg >7.5). Management: Stop Mg infusion; Calcium Gluconate 1–2g IV (antagonises cardiac/neuromuscular effects); dialysis for severe hypermagnesaemia in AKI.
Hypophosphataemia (PO₄ <0.8 mmol/L)
Severe hypophosphataemia (<0.3 mmol/L) causes respiratory muscle failure, cardiac dysfunction, rhabdomyolysis, haemolytic anaemia, and impaired oxygen delivery. A major cause of failure to wean from mechanical ventilation.
| Severity | PO₄ Level | Route | Dose |
|---|---|---|---|
| Mild | 0.65–0.8 mmol/L | Oral/NGT | Sodium/potassium phosphate 1.5–2.3g/day in divided doses |
| Moderate | 0.32–0.64 mmol/L | IV | Potassium phosphate 0.3–0.6 mmol/kg IV over 6–12h |
| Severe / symptomatic | <0.32 mmol/L | IV | Potassium/sodium phosphate 0.6–0.9 mmol/kg IV over 6–12h; repeat if needed |
Calcium Disorders
Hypocalcaemia (Total Ca <2.12 mmol/L; iCa <1.0 mmol/L)
Common causes: hypomagnesaemia (commonest in ICU), hypoparathyroidism, vitamin D deficiency, pancreatitis, citrate toxicity on CRRT, alkalosis.
- Acute symptomatic (tetany, seizures): Calcium Gluconate 10–20 ml of 10% IV over 10–20 min; follow with infusion 0.5–1 mg/kg/hr elemental Ca
- Asymptomatic: Oral calcium carbonate 1–3g/day; Vitamin D₃ (calcitriol 0.25–0.5 mcg/day)
- Always correct Mg²⁺ first — hypocalcaemia is refractory without Mg correction
Hypercalcaemia (Total Ca >2.65 mmol/L; severe >3.5 mmol/L)
Mnemonic: Bones, Stones, Groans, Moans, Psychic Overtones. Causes: PTH (hyperparathyroidism), PTHrP (malignancy), Vitamin D toxicity, sarcoidosis, thiazide diuretics, granulomatous disease.
- IV fluids: 0.9% NaCl 200–300 ml/hr (aggressive hydration) — first and most important step
- Furosemide: Only after adequate rehydration; 40–80 mg IV to promote calciuresis
- Zoledronic acid: 4 mg IV over 15 min — most potent; onset 48–72h, duration weeks. First-line for malignancy-related hypercalcaemia.
- Calcitonin: 4–8 IU/kg SC q12h — fastest acting (4–6h); tachyphylaxis within 48h; use as bridge to bisphosphonates
- Steroids: Prednisolone 40–60 mg/day — for sarcoidosis, lymphoma, vitamin D toxicity
- Denosumab: 120 mg SC — for bisphosphonate-refractory malignancy hypercalcaemia
- Dialysis: Severe refractory or with AKI — low-calcium dialysate
Refeeding Syndrome
Life-threatening electrolyte disturbances (primarily hypophosphataemia + hypokalaemia + hypomagnesaemia) occurring on re-introduction of nutrition after prolonged starvation. Caused by insulin-mediated cellular uptake of PO₄, K⁺, Mg²⁺, and thiamine.
High-Risk Patients
- BMI <18.5 or >15% weight loss in last 3–6 months
- Little/no nutritional intake for >5 days
- Chronic alcoholism
- Malabsorptive conditions (inflammatory bowel disease, bariatric surgery)
- Prolonged NPO in ICU
ASPEN/ESPEN Prevention Protocol
- Check and correct electrolytes BEFORE starting feeds
- Give IV Thiamine 200–300 mg/day BEFORE any glucose/carbohydrate
- Start feeds at 10–20 kcal/kg/day (25–50% of estimated needs); increase by 33% every 2 days
- Monitor PO₄, K⁺, Mg²⁺, Na⁺ and glucose daily for first week
- Replace aggressively if levels fall during refeeding
References
- Spasovski G, Vanholder R, Allolio B, et al. Clinical Practice Guideline on Diagnosis and Treatment of Hyponatraemia. Eur J Endocrinol. 2014;170(3):G1–G47.
- Sterns RH, Hix JK, Silver SM. Management of Hyponatremia in the ICU. Chest. 2013;144(2):672–679.
- Kovesdy CP. Management of Hyperkalaemia in Chronic Kidney Disease. Nat Rev Nephrol. 2014;10(11):653–662.
- Weisinger JR, Bellorín-Font E. Magnesium and Phosphorus. Lancet. 1998;352(9125):391–396.
- Stanga Z, Brunner A, Leuenberger M, et al. Nutrition in Clinical Practice — the Refeeding Syndrome: Illustrative Cases and Guidelines for Prevention and Treatment. Eur J Clin Nutr. 2008;62(6):687–694.
- Fong J, Khan A. Hypocalcaemia: Updates in Diagnosis and Management for Primary Care. Can Fam Physician. 2012;58(2):158–162.
- Bilezikian JP. Management of Acute Hypercalcaemia. N Engl J Med. 1992;326(18):1196–1203.
- National Institute for Health and Care Excellence (NICE). Nutrition Support for Adults: Oral Nutrition Support, Enteral Tube Feeding and Parenteral Nutrition. Clinical Guideline CG32. 2006 (Updated 2017).