Electrolyte disturbances

Contents

Overview

Electrolyte disturbances are among the most common abnormalities in the ICU. They arise from disease processes, drug effects, and iatrogenic causes. Untreated or undertreated electrolyte abnormalities cause cardiac arrhythmias, neuromuscular dysfunction, seizures, and death. Systematic monitoring and correction are central to ICU care.

Sodium Disorders

Sodium is the primary determinant of serum osmolality and therefore water distribution between intracellular and extracellular compartments. Sodium disorders reflect abnormalities of total body water rather than sodium alone.

Hyponatraemia (Na <135 mmol/L)

Aetiology by volume status:

Hypovolaemic hyponatraemia: Sodium and water loss with relatively greater sodium loss. Causes: vomiting, diarrhoea, diuretics, Addison's disease. Urine sodium >20 mmol/L suggests renal loss; <20 mmol/L suggests extrarenal.

Euvolaemic hyponatraemia: Water retention with normal sodium. Causes: SIADH (most common — postoperative, CNS disease, pulmonary disease, drugs), hypothyroidism, primary polydipsia.

Hypervolaemic hyponatraemia: Sodium and water both increased, but water disproportionately. Causes: heart failure, hepatic cirrhosis, nephrotic syndrome.

SIADH (Syndrome of Inappropriate ADH): Diagnosed by serum osmolality <275 mOsm/kg, urine osmolality >100 mOsm/kg, urine sodium >30 mmol/L in a euvolaemic patient without hypothyroidism or hypoadrenalism. Causes: CNS disease, chest disease, drugs (SSRIs, carbamazepine, cyclophosphamide), pain, nausea, post-operative state.

Clinical features: Symptoms correlate with severity and rate of onset. Chronic mild hyponatraemia may be asymptomatic. Acute hyponatraemia or severe levels (<125 mmol/L): nausea, headache, confusion, seizures, cerebral oedema, and herniation.

Management:

  • Mild-moderate, asymptomatic: treat underlying cause; fluid restriction 1–1.5 L/day in SIADH.
  • Severe or symptomatic: hypertonic saline (3% NaCl). Target correction rate: 4–6 mmol/L in the first hour for seizures/herniation; no more than 8–10 mmol/L per 24 hours to prevent osmotic demyelination syndrome (ODS).
  • ODS (central pontine myelinolysis): caused by overly rapid correction of chronic hyponatraemia. Symptoms may be delayed 2–6 days: dysarthria, dysphagia, quadriplegia, altered consciousness.

Hypernatraemia (Na >145 mmol/L)

Almost always indicates free water deficit. Causes: inadequate water intake (unconscious patient, intubated), increased water loss (diabetes insipidus, osmotic diuresis, fever), hypertonic infusions.

Diabetes insipidus: Central (reduced ADH — TBI, pituitary surgery, hypothalamic disease) or nephrogenic (renal insensitivity to ADH — lithium, hypercalcaemia, hypokalaemia). Characterised by large volumes of dilute urine (urine osmolality <300 mOsm/kg) with rising serum sodium.

Central DI: treat with desmopressin (DDAVP) 0.5–4 micrograms SC/IV BD-TDS or 10–20 micrograms intranasal.

Management of hypernatraemia: Identify and treat the cause. Replace free water deficit: oral water preferred; IV 5% glucose or 0.45% NaCl. Correction rate: no faster than 0.5 mmol/L/hour to avoid cerebral oedema. Calculate free water deficit: FWD (L) = TBW × (Na/140 − 1), where TBW = 0.6 × lean body weight.

Potassium Disorders

98% of body potassium is intracellular. Small changes in extracellular potassium reflect large shifts in total body content or redistribution.

Hypokalaemia (K <3.5 mmol/L)

Causes: Gastrointestinal loss (diarrhoea, vomiting, NG drainage, fistula), urinary loss (diuretics, hyperaldosteronism, Cushing's syndrome, renal tubular acidosis, amphotericin, post-obstructive diuresis), transcellular shift (alkalosis, insulin, beta-2 agonists, refeeding), inadequate intake.

Clinical features: Muscle weakness (including respiratory muscle failure in severe hypokalaemia <2.5 mmol/L), constipation, polyuria (nephrogenic diabetes insipidus), cardiac arrhythmias (atrial and ventricular, including digoxin toxicity potentiation), ECG changes: flattened T waves, prominent U waves, ST depression, prolonged QU interval.

Management: Oral potassium chloride for mild-moderate cases. IV KCl for severe (<2.5 mmol/L) or symptomatic: up to 20–40 mmol/hour via a central line; maximum peripheral rate 10–20 mmol/hour in a large vein with dilution. Concurrent hypomagnesaemia impairs potassium retention — correct magnesium first.

Hyperkalaemia (K >5.5 mmol/L)

Causes: AKI and CKD, acidosis (hydrogen ions shift intracellularly, potassium shifts out), excessive intake (blood transfusion, potassium supplements), medications (ACE inhibitors, ARBs, potassium-sparing diuretics, heparin), rhabdomyolysis, haemolysis, TLS, adrenal insufficiency, pseudohyperkalaemia (prolonged tourniquet time, thrombocytosis, haemolysis in sample).

ECG changes (severity progression): Peaked T waves → PR prolongation → P wave flattening → wide QRS → sine wave pattern → ventricular fibrillation/asystole.

Management:

  1. Calcium gluconate 10 mL 10% IV over 2–3 minutes: membrane stabilisation — acts within minutes; does not lower potassium; repeat after 5 minutes if ECG changes persist. Use when ECG changes are present.
  2. Insulin-dextrose: 10 units rapid-acting insulin + 50 g glucose (50 mL 50% dextrose or 250 mL 20%): shifts K intracellularly. Onset 20–30 minutes, duration 4–6 hours. Monitor glucose.
  3. Salbutamol 10–20 mg nebulised or 0.5 mg IV: beta-2 agonist shifts K intracellularly. Acts within 30 minutes. Less predictable in ventilated patients.
  4. Sodium bicarbonate: effective in acidotic hyperkalaemia; shifts K intracellularly. 50 mmol IV over 20 minutes.
  5. Calcium resonium (polystyrene sulfonate) or patiromer: remove K from the GI tract. Slow onset (6–12 hours); used as maintenance, not emergency.
  6. Renal replacement therapy: definitive removal in refractory hyperkalaemia or renal failure.

Calcium Disorders

See the separate article on hypercalcaemia for detailed coverage of raised calcium. Key points on hypocalcaemia:

Hypocalcaemia (corrected Ca <2.1 mmol/L)

Causes: Hypoparathyroidism (post-thyroid or parathyroid surgery), vitamin D deficiency (dietary, malabsorption, reduced renal activation in CKD), hypomagnesaemia (impairs PTH release and action), hyperphosphataemia (precipitation of calcium), acute pancreatitis (calcium sequestration in fat saponification), massive blood transfusion (citrate chelation), sepsis (cytokine-mediated redistribution), alkalosis (reduces ionised calcium by increasing protein binding).

Clinical features: Paraesthesiae (perioral, fingertips), muscle cramps, tetany (Trousseau's sign — carpal spasm with inflated BP cuff; Chvostek's sign — facial muscle twitch with tapping the facial nerve). Laryngospasm. Seizures. Cardiac: prolonged QT, heart failure.

Management: Symptomatic or ionised Ca <0.9 mmol/L: IV calcium gluconate 10 mL 10% over 10 minutes (calcium gluconate preferred to calcium chloride for peripheral administration; calcium chloride causes tissue necrosis if extravasated). Follow with infusion if persistent. Correct concurrent hypomagnesaemia. Vitamin D supplementation and oral calcium once stable.

Magnesium Disorders

Magnesium is the second most abundant intracellular cation. Serum levels do not reflect total body stores reliably.

Hypomagnesaemia (Mg <0.7 mmol/L)

Causes: Poor intake (critical illness, prolonged starvation), GI loss (diarrhoea, vomiting, fistulae, PPI use — reduces intestinal Mg absorption), renal loss (loop diuretics, aminoglycosides, amphotericin, cisplatin, alcohol), DKA recovery, refeeding syndrome.

Clinical effects: Hypokalaemia (magnesium depletion impairs renal K reabsorption — correct Mg before K) and hypocalcaemia (impairs PTH release). Cardiac arrhythmias, particularly torsades de pointes. Neuromuscular excitability, tremor, seizures.

Management: IV magnesium sulphate 4–8 mmol (1–2 g MgSO4) over 20 minutes for acute severe hypomagnesaemia or torsades; then 20–40 mmol over 24 hours. Oral magnesium for mild/chronic.

Hypermagnesaemia (Mg >1.1 mmol/L)

Usually iatrogenic: excessive administration in pre-eclampsia, renal failure impairing excretion.

Features progress with rising level: nausea, flushing (>2 mmol/L) → loss of deep tendon reflexes (>3.5 mmol/L) → respiratory depression (>4.5 mmol/L) → cardiac arrest (>7.5 mmol/L).

Antidote: calcium gluconate 10 mL 10% IV antagonises magnesium at membranes. Supportive care; haemodialysis for life-threatening hypermagnesaemia in renal failure.

Phosphate Disorders

Hypophosphataemia (PO4 <0.8 mmol/L)

Causes: Refeeding syndrome (most important in ICU — see nutrition article), DKA treatment (insulin-driven intracellular shift), malabsorption, hyperparathyroidism, vitamin D deficiency, antacid binding, alcohol withdrawal.

Clinical effects: Impaired ATP synthesis (phosphate is essential for oxidative phosphorylation). Respiratory muscle failure and ventilator weaning failure, haemolytic anaemia, platelet dysfunction, immune impairment, cardiac dysfunction, seizures, neuromuscular dysfunction.

Management: Mild (0.6–0.8 mmol/L): oral phosphate supplements. Severe (<0.3 mmol/L) or symptomatic: IV potassium or sodium phosphate at 0.1–0.4 mmol/kg/hour via central line. Monitor for hypocalcaemia during IV replacement (phosphate can precipitate with calcium).

Hyperphosphataemia (PO4 >1.5 mmol/L)

Causes: renal failure (inability to excrete), rhabdomyolysis and TLS (cell lysis releases phosphate), hypoparathyroidism, vitamin D toxicity.

Consequences: metastatic calcification, hypocalcaemia, contributes to renal osteodystrophy.

Management: low-phosphate diet, phosphate binders (calcium carbonate, sevelamer), RRT in renal failure.

Viva Questions

How do you manage a patient with severe symptomatic hyponatraemia (Na 112 mmol/L, seizures)?

Severe symptomatic hyponatraemia with seizures is a neurological emergency requiring urgent correction. The immediate priority is to raise sodium sufficiently to stop seizures — a rise of 4–6 mmol/L is usually adequate and can be achieved with a 100–150 mL bolus of 3% hypertonic saline over 10–20 minutes. This can be repeated once or twice if seizures continue. Once seizures are controlled, the rate of sodium correction must be limited to no more than 8–10 mmol/L per 24 hours (some guidelines suggest 10–12 mmol/L in the first 24 hours in severe acute hyponatraemia). Correction faster than this risks osmotic demyelination syndrome — particularly in patients with chronic hyponatraemia (present for >48 hours), where the brain has adapted to the low-sodium environment and rapid correction causes osmotic injury to the myelin sheath of pontine neurones. Serum sodium should be monitored every 2–4 hours during active correction. The underlying cause should be identified and treated — most commonly SIADH in the ICU. Once the acute danger has passed, fluid restriction or demeclocycline (if appropriate) can be used to treat SIADH.

What are the ECG changes in hyperkalaemia and how do you manage it acutely?

Hyperkalaemia produces progressive ECG changes that correlate with severity. Early changes include peaked, symmetrical, narrow T waves — the most sensitive early sign. As potassium rises, PR interval prolongs, P waves flatten and disappear, and QRS widens. In severe hyperkalaemia, the QRS merges with the T wave to produce a sinusoidal pattern, which precedes ventricular fibrillation or asystole. Acute management follows a sequence of three aims: membrane stabilisation, driving potassium into cells, and removing potassium from the body. Membrane stabilisation is achieved with calcium gluconate 10 mL 10% IV over 2–3 minutes — this does not lower potassium but protects the heart against arrhythmia and should be given immediately when ECG changes are present. Driving potassium intracellularly requires insulin and dextrose (10 units rapid-acting insulin with 25 g glucose, monitored for hypoglycaemia), salbutamol nebulised at 10–20 mg, and sodium bicarbonate in acidotic patients. These measures buy time. Definitive potassium removal requires loop diuretics if urine output is maintained, calcium resonium or patiromer for GI binding, or renal replacement therapy in renal failure or refractory hyperkalaemia.

A ventilated ICU patient develops hypophosphataemia of 0.2 mmol/L and cannot be weaned from the ventilator. How are these related and how do you manage it?

Severe hypophosphataemia at this level causes profound impairment of cellular energy metabolism. Phosphate is essential for ATP synthesis via oxidative phosphorylation, and when it is depleted, high-energy phosphate production fails in metabolically demanding tissues. Respiratory muscles — already stressed by the work of ventilator weaning — are particularly sensitive. The diaphragm and intercostal muscles fatigue rapidly without adequate ATP, producing a failure to generate sufficient inspiratory force to sustain spontaneous breathing. At a phosphate level of 0.2 mmol/L, this mechanism is likely a significant contributor to ventilator weaning failure. Management requires IV phosphate replacement: potassium phosphate or sodium phosphate at 0.1–0.4 mmol/kg/hour via a central line, with the dose and rate guided by the severity and clinical status. Serum calcium must be monitored during replacement — intravenous phosphate can precipitate with calcium, causing hypocalcaemia and metastatic calcification. The underlying cause of hypophosphataemia should be identified and treated — in the ICU, the most common causes are refeeding after prolonged starvation, DKA treatment, and diuretic use. Phosphate should be monitored daily in all at-risk ICU patients and replaced proactively rather than waiting for symptomatic depletion.