5.3 Electrolyte Emergencies: Potassium, Sodium & Calcium

Electrolyte Emergencies: Potassium, Sodium & Calcium

Electrolyte disturbances are ubiquitous across acute hospital admissions. Because potassium, sodium, and calcium govern transmembrane action potentials, neuromuscular transmission, and osmotic fluid distribution, severe derangements precipitate lethal cardiac arrhythmias, seizures, and cerebral herniation unless treated systematically.

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1. Hyperkalaemia: Diagnostic Stratification & Emergency Management

Serum potassium is normally maintained within a narrow physiological range of 3.5–5.0 mmol/L by renal potassium excretion (driven by aldosterone in the cortical collecting tubule) and cellular buffering (Na+/K+-ATPase pump driven by insulin and beta-2 adrenergic stimulation).

Severity Classification (UK Kidney Association & Resuscitation Council UK / RCUK Guidelines)

• Mild Hyperkalaemia: 5.5–5.9 mmol/L
• Moderate Hyperkalaemia: 6.0–6.4 mmol/L
• Severe Hyperkalaemia: ≥ 6.5 mmol/L (OR any potassium elevation accompanied by electrocardiographic changes; this is a medical emergency!)

Electrocardiographic (ECG) Progression

As extracellular potassium rises, resting membrane potential partially depolarises, inactivating sodium channels and accelerating repolarisation. The ECG changes progress sequentially:

1. Tall, tented / peaked T waves: Narrow base, symmetrical, prominent in precordial leads (earliest sign).
2. P-wave flattening & PR prolongation: P waves widen and disappear; PR interval lengthens.
3. QRS complex widening: Intraventricular conduction delay; QRS widens and merges with the T wave.
4. Sine-wave pattern: Severe conduction block; pre-terminal rhythm.
5. Cardiac arrest: Degeneration into ventricular fibrillation (VF), pulseless electrical activity (PEA), or asystole.

The Three-Step Emergency Management Protocol

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2. Hypokalaemia: Pathophysiology & Safe Replacement

Hypokalaemia is defined as serum potassium < 3.5 mmol/L (severe if < 2.5–3.0 mmol/L).

• Aetiologies: Gastrointestinal loss (prolonged vomiting, diarrhoea, laxative abuse, VIPoma), renal wasting (loop or thiazide diuretics, primary hyperaldosteronism / Conn's syndrome, Cushing's syndrome, Renal Tubular Acidosis Types 1 and 2), transcellular shift (acute alkalosis, refeeding syndrome, excess insulin, salbutamol toxicity), and hypomagnesaemia.
• ECG Manifestations: Flattening or inversion of T waves, ST-segment depression, prominent U waves (positive deflection immediately following the T wave, prominent in leads V2–V4), prolonged PR interval, and ventricular arrhythmias (Torsades de Pointes).
• Replacement Protocol:
  • Mild Hypokalaemia (3.0–3.4 mmol/L, asymptomatic): Oral replacement with potassium chloride tablets (e.g. Sando-K, 2–4 tablets daily in divided doses with food, adjusted to plasma potassium; BNF).
  • Severe Hypokalaemia (< 3.0 mmol/L, symptomatic, or ECG changes): Intravenous potassium chloride (KCl) infusion.
  • Safe IV Infusion Limits: Never exceed 10 mmol/hour in a peripheral cannula (prevents chemical phlebitis and pain). Rates up to 20 mmol/hour require a central venous catheter and continuous cardiac monitoring in an HDU/ICU setting.
  • FATAL DANGER: NEVER administer an undiluted IV bolus or push of potassium chloride! Rapid boluses trigger immediate refractory cardiac arrest.
  • MANDATORY CLINICAL RULE: Correct Hypomagnesaemia! Magnesium is a necessary cofactor for the Na+/K+-ATPase pump and physiologically inhibits the renal outer medullary potassium (ROMK) channels. In hypomagnesaemia, unregulated potassium excretion into the urine occurs. Hypokalaemia is completely refractory to potassium replacement until co-existing hypomagnesaemia is corrected with IV magnesium sulphate.

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3. Hyponatraemia: Diagnostic Algorithm & Safe Correction Limits

Hyponatraemia is defined as a serum sodium < 135 mmol/L (severe if < 120–125 mmol/L). Because clinical manifestations are driven by brain cellular swelling (cerebral oedema), the speed of onset dictates severity.

Systematic Diagnostic Algorithm

                                [ Serum Sodium < 135 mmol/L ]
                                              │
                                 [ Check Serum Osmolality ]
                                              │
            ┌─────────────────────────────────┼─────────────────────────────────┐
            ▼                                 ▼                                 ▼
   [ High (>295 mOsm/kg) ]          [ Normal (275-295 mOsm/kg) ]      [ Low (<275 mOsm/kg) ]
   Hypertonic Hyponatraemia         Pseudohyponatraemia               True Hypotonic Hyponatraemia
   • Severe Hyperglycaemia          • Severe Hyperlipidaemia                        │
   • Mannitol Infusion              • Paraproteinaemia (Myeloma)                    │
                                                                      [ Assess Volume Status ]
                                              ┌─────────────────────────────────────┼─────────────────────────────────────┐
                                              ▼                                     ▼                                     ▼
                                      [ Hypovolaemic ]                        [ Euvolaemic ]                        [ Hypervolaemic ]
                                 Dry mucosa, low JVP, postural drop       Normal JVP, no oedema                Elevated JVP, oedema, ascites
                                              │                                     │                                     │
                                      [ Check Urine Na ]                    [ Check Urine Na & Osm ]              [ Heart Failure, Cirrhosis, ]
                                ┌─────────────┴─────────────┐                       │                             [ Nephrotic Syndrome        ]
                                ▼                           ▼                       ▼                                     │
                         [ Urine Na < 20 ]           [ Urine Na > 20 ]       [ Urine Na >30, Osm >100 ]            [ Fluid Restriction & ]
                         Extra-renal loss:           Renal loss:             SIADH                                 [ Loop Diuretics      ]
                         Vomiting, Diarrhoea         Diuretics, Addison's    • Small cell lung cancer
                                │                           │                • Stroke, Trauma, Meningitis
                         [ IV 0.9% Saline ]          [ IV 0.9% Saline ]      • SSRIs, Carbamazepine, PPIs
                                                                                    │
                                                                             [ Fluid Restriction 500-1000 mL ]

The Syndrome of Inappropriate Antidiuretic Hormone (SIADH)

SIADH is the most common cause of euvolaemic hyponatraemia. Excessive unsuppressed ADH (arginine vasopressin) acts on renal V2 receptors in collecting ducts, driving unregulated water reabsorption.

• Diagnostic Criteria: Hypotonic hyponatraemia (<275 mOsm/kg), inappropriately concentrated urine (urine osmolality > 100 mOsm/kg, typically >300), natriuresis (urine sodium > 30 mmol/L due to volume-expansion driven ANP release), clinical euvolaemia, and normal thyroid, adrenal, and renal function.
• Common Triggers: Malignancy (small cell lung carcinoma #1), chest disorders (pneumonia, tuberculosis, lung abscess), central nervous system disorders (stroke, subdural haematoma, meningitis), and drugs (SSRIs, carbamazepine, cyclophosphamide, PPIs).
• Management: Fluid restriction to 500–1000 mL/24 hours is first-line. Oral sodium chloride tablets, urea, or vasopressin receptor antagonists (vaptans, e.g. tolvaptan) are second-line for refractory cases.

Rate of Correction & Osmotic Demyelination Syndrome

When hyponatraemia develops chronically (>48 hours), cerebral astrocytes adapt to hypoosmolality by expelling intracellular organic osmolytes (glutamate, myo-inositol, taurine) to attenuate cellular swelling.

• Maximum Correction Rate: NEVER exceed 8–10 mmol/L in 24 hours (or 18 mmol/L in 48 hours). In high-risk patients (alcohol dependency, malnutrition, advanced liver disease), limit correction to ≤ 6–8 mmol/L in 24 hours.
• Osmotic Demyelination Syndrome (ODS / Central Pontine Myelinolysis): Rapid correction causes sudden extracellular hyperosmolality. Water rapidly rushes out of brain cells, collapsing astrocytes and precipitating demyelination of oligodendrocytes in the pons. Manifests 2–6 days post-correction with dysarthria, dysphagia, horizontal gaze paralysis, spastic quadriparesis, and irreversible "locked-in" syndrome.
• Severe Symptomatic Hyponatraemia (Seizures / Coma): Administer hypertonic 3% sodium chloride bolus (150 mL IV over 20 minutes; repeat once if needed) to achieve a rapid target rise of 4–6 mmol/L in serum sodium, reversing fatal brain herniation, and then immediately stop hypertonic infusions.

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4. Hypercalcaemia: Evaluation & Resuscitation Protocol

Normal serum adjusted calcium is 2.20–2.60 mmol/L (severe if > 3.0–3.5 mmol/L).

• Aetiology: Over 90% of cases are attributable to either primary hyperparathyroidism (80% of ambulatory cases; solitary parathyroid adenoma #1; elevated or inappropriately normal PTH, elevated calcium, low phosphate) or malignancy (most common inpatient cause; PTHrP production in squamous cell lung or renal cancer, osteolytic metastases in breast cancer or multiple myeloma; suppressed PTH).
• Clinical Presentation: Classically memorised as "bones, stones, abdominal groans, and psychiatric moans":
  • Bones: Bone pain, osteopenia, pathological fractures.
  • Stones: Nephrolithiasis, nephrocalcinosis, polyuria, and polydipsia (nephrogenic diabetes insipidus).
  • Abdominal Groans: Anorexia, nausea, severe constipation, peptic ulcer disease, acute pancreatitis.
  • Psychiatric Moans: Fatigue, depression, delirium, acute psychosis, coma.
  • Cardiac: Shortened QT interval on ECG, predisposing to fatal arrhythmias.

Acute Emergency Resuscitation

1. First-Line Intervention: Aggressive Intravenous Rehydration: Administer intravenous 0.9% normal saline at 3 to 4 litres over 24 hours (guided by cardiovascular status and urine output). Hypercalcaemic patients are profoundly dehydrated from polyuria and vomiting; rehydration restores renal perfusion and promotes urinary calcium excretion (calciuresis).
2. Second-Line Pharmacotherapy: Intravenous Bisphosphonates: Administer zoledronic acid 4 mg IV over 15 minutes (or pamidronate 30–90 mg IV). Bisphosphonates inhibit osteoclastic bone resorption. Exam Key: Bisphosphonates exhibit a delayed onset of action (takes 48 to 72 hours to lower calcium, with nadir effect at 4–6 days); they do not work acutely!
3. Adjunctive Therapies:
   • Calcitonin (SC/IM): Produces a rapid reduction in calcium within 2–4 hours; useful as an acute bridge while awaiting bisphosphonate efficacy, but tachyphylaxis occurs within 48 hours.
   • Glucocorticoids (oral prednisolone 20–40 mg daily): First-line for hypercalcaemia driven by calcitriol overproduction in sarcoidosis, lymphoma, or vitamin D toxicity.
   • Denosumab: Monoclonal antibody against RANKL, indicated in refractory hypercalcaemia of malignancy or when bisphosphonates are contraindicated by severe renal failure.