By the end of this note you will be able to recognise, investigate and initiate safe initial management of common sodium, potassium and calcium disturbances seen in Kenyan clinical rotations, while knowing which local guidelines and formulary references to consult for definitive therapy.
Definition
| Electrolyte | Normal serum range | Disorder definition |
|---|---|---|
| Sodium (Na⁺) | 135‑145 mmol/L | Hyponatraemia < 135 mmol/L; Hypernatraemia > 145 mmol/L |
| Potassium (K⁺) | 3.5‑5.0 mmol/L | Hypokalaemia < 3.5 mmol/L; Hyperkalaemia > 5.0 mmol/L |
| Calcium (Ca²⁺) (total) | 2.1‑2.6 mmol/L | Hypocalcaemia < 2.1 mmol/L; Hypercalcaemia > 2.6 mmol/L |
Disorders are further graded by severity (mild, moderate, severe) based on serum values and presence of symptoms.
Anatomy and physiology you need
- Sodium – principal extracellular cation; maintains plasma osmolality, extracellular fluid (ECF) volume, and drives water movement. Regulated by thirst, antidiuretic hormone (ADH), renin‑angiotensin‑aldosterone system (RAAS) and renal handling (proximal reabsorption, loop of Henle, distal nephron).
- Potassium – major intracellular cation; essential for membrane potential, nerve impulse transmission and muscle contraction. Renal excretion (principal cells of cortical collecting duct) is modulated by aldosterone, distal flow, and acid‑base status.
- Calcium – exists as ionised (physiologically active) and protein‑bound fractions. Controls neuromuscular excitability, cardiac contractility, coagulation and bone metabolism. Homeostasis involves parathyroid hormone (PTH), vitamin D, calcitonin and renal tubular reabsorption (proximal tubule, thick ascending limb, distal tubule).
Causes and risk factors
| Electrolyte | Common Kenyan causes | Tropical / infection‑related risk factors |
|---|---|---|
| Hyponatraemia | Excess free water intake, SIADH, heart failure, liver cirrhosis, nephrotic syndrome, thiazide diuretics, adrenal insufficiency | Severe malaria (SIADH), TB meningitis (SIADH), HIV‑associated adrenal disease, chronic diarrhoea from dysentery |
| Hypernatraemia | Water loss (vomiting, diarrhoea, fever), diabetes insipidus, inadequate water intake, high‑salt diet, osmotic diuresis | Malaria with high fever, sickle‑cell vaso‑occlusive crisis causing insensible loss, HIV‑related nephrogenic DI |
| Hypokalaemia | Diuretics, vomiting, diarrhoea, laxative abuse, insulin therapy, β‑agonists, renal tubular acidosis type 1 | Severe malaria with profuse sweating, TB treatment (rifampicin‑induced loss), HIV‑associated diarrhoea |
| Hyperkalaemia | Acute kidney injury, chronic kidney disease, ACE‑inhibitors/ARBs, potassium‑sparing diuretics, tissue breakdown (rhabdomyolysis) | Sickle‑cell crisis (muscle breakdown), severe malaria (haemolysis), HIV‑related nephropathy |
| Hypocalcaemia | Vitamin D deficiency, hypoparathyroidism, renal failure, acute pancreatitis, massive transfusion | HIV‑related malabsorption, TB meningitis (calcitonin dysregulation), chronic diarrhoea, malaria‑induced hypomagnesaemia |
| Hypercalcaemia | Primary hyperparathyroidism, malignancy (bone metastases, PTH‑rP), granulomatous disease (TB), excessive vitamin D | Disseminated TB (granulomatous production of 1‑α‑hydroxylase), HIV‑associated lymphoma, sickle‑cell osteonecrosis |
Pathophysiology
Hyponatraemia → excess water relative to Na⁺ → ↓ plasma osmolality → water shift into cells → cerebral oedema (if rapid) → symptoms (nausea, headache, seizures).
Hypernatraemia → water deficit relative to Na⁺ → ↑ plasma osmolality → cellular dehydration → neuronal shrinkage → thirst, confusion, seizures.
Hypokalaemia → ↓ extracellular K⁺ → hyperpolarisation of cell membranes → impaired cardiac repolarisation → arrhythmias; muscle weakness due to reduced excitability.
Hyperkalaemia → ↑ extracellular K⁺ → depolarisation → inactivation of Na⁺ channels → slowed conduction → peaked T waves → risk of ventricular fibrillation.
Hypocalcaemia → ↓ ionised Ca²⁺ → increased neuronal excitability → tetany, Chvostek/Trousseau signs; prolonged QT on ECG.
Hypercalcaemia → ↑ ionised Ca²⁺ → decreased neuronal excitability → polyuria, nephrogenic diabetes insipidus, renal calculi; shortened QT.
Arrows illustrate causal flow:
``` Excess ADH → water retention → hyponatraemia → cerebral oedema → seizures ↓ Renal loss of K⁺ (diuretics) → hypokalaemia → membrane hyperpolarisation → arrhythmia ↓ PTH excess or malignancy → ↑ bone resorption → hypercalcaemia → polyuria → dehydration → further hypercalcaemia
Clinical features
| Aspect | Questions to ask | Why it matters |
|---|---|---|
| Onset & tempo | “When did you first notice the symptoms? Did they appear suddenly or develop gradually?” | Acute changes suggest rapid shifts (e.g., hyper‑natremia from water loss, hyper‑kalemia from AKI) whereas chronic evolution points to endocrine or medication‑related disorders. |
| Fluid balance | “How much fluid do you drink each day? Any recent vomiting, diarrhoea, fever, sweating, or diuretic use?” | Excess loss → hyponatraemia, hypokalaemia, hypocalcaemia; inadequate intake or water excess → hypernatremia, hyperkalaemia, hypercalcaemia. |
| Medication & supplements | “What medicines, herbal remedies or over‑the‑counter supplements are you taking? Any recent changes?” | Loop/thiazide diuretics, ACE‑I/ARBs, potassium‑sparing agents, steroids, vitamin D, calcium tablets, antiretrovirals, anti‑TB drugs all alter electrolytes. |
| Renal & endocrine history | “Do you have known kidney disease, diabetes, hypertension, thyroid or adrenal problems?” | CKD, diabetic nephropathy, primary hyperaldosteronism, Addison’s disease, hyperparathyroidism are common causes. |
| Infectious & tropical context | “Recent malaria, TB, HIV infection or treatment? Any sickle‑cell crisis?” | Malaria‑induced hemolysis, TB drugs (rifampicin), HIV‑associated nephropathy, sickle‑cell vaso‑occlusion can precipitate electrolyte shifts. |
| Gastro‑intestinal losses | “Any recent laxative abuse, nasogastric suction, bowel surgery?” | Direct loss of Na⁺, K⁺, Ca²⁺ in stool or gastric secretions. |
| Neurological symptoms | “Weakness, cramps, paresthesias, confusion, seizures, altered consciousness?” | Hyper‑ or hypo‑natremia affect brain volume; hypo‑kalaemia and hypo‑calcaemia cause neuromuscular irritability; hyper‑kalaemia produces muscle weakness. |
| Cardiovascular signs | “Palpitations, chest pain, dyspnoea, syncope?” | Hyper‑kalaemia produces brady‑arrhythmias; hypo‑kalaemia predisposes to ventricular ectopy; hyper‑calcaemia can cause shortened QT. |
| Bone & renal stone history | “History of fractures, bone pain, kidney stones?” | Hyper‑calcaemia → stones, bone demineralisation; hypocalcaemia → tetany, osteomalacia. |
Examination findings and pathophysiologic basis
| Finding | Reason it occurs |
|---|---|
| Altered mental status (confusion, lethargy, seizures) | Cerebral oedema in hyponatraemia; cellular dehydration in hyper‑natremia. |
| Muscle weakness / cramps | Hypokalaemia → impaired Na⁺/K⁺‑ATPase; hyperkalaemia → membrane depolarisation; hypocalcaemia → increased neuronal excitability. |
| Tetany, Chvostek & Trousseau signs | Low ionised Ca²⁺ increases neuromuscular excitability. |
| Blood pressure changes (hypotension or hypertension) | Volume depletion (hyponatraemia) → hypotension; hyperaldosteronism or hyper‑calcaemia → hypertension. |
| Peripheral edema | Hypervolemic hyponatraemia (e.g., heart failure, cirrhosis) or hyper‑calcaemia‑induced nephrogenic diabetes insipidus causing polyuria then volume overload. |
| Cardiac rhythm abnormalities (peaked T waves, widened QRS, U waves) | Hyperkalaemia → peaked T, widened QRS; hypokalaemia → U waves, flattened T. |
| Dry mucous membranes, poor skin turgor | Dehydration leading to hypernatremia. |
| Abdominal tenderness, renal colic | Calcium stones from hyper‑calcaemia or hyperparathyroidism. |
| Signs of chronic disease (e.g., lymphadenopathy, oral thrush) | Underlying HIV or TB that may drive renal tubular dysfunction. |
Differential diagnosis
| Condition | Points to it | Distinguishing feature |
|---|---|---|
| Hypovolaemic hyponatraemia | Volume loss, low urine Na⁺, recent diarrhoea/vomiting | Urine Na⁺ <20 mmol/L, high BUN/Cr ratio |
| Euvolaemic hyponatraemia (SIADH) | Normal volume, recent drugs (SSRIs, carbamazepine), malignancy | Urine osmolality >100 mOsm/kg, urine Na⁺ >30 mmol/L |
| Hypervolemic hyponatraemia | Heart failure, cirrhosis, nephrotic syndrome | Edema, ascites, low serum albumin |
| Hypokalaemia | Diuretics, diarrhoea, vomiting, insulin therapy, β‑agonists | Urine K⁺ >20 mmol/L if renal loss; metabolic alkalosis |
| Hyperkalaemia | AKI, ACE‑I/ARB, potassium‑sparing diuretics, tissue breakdown (haemolysis, rhabdomyolysis) | ECG changes, serum K⁺ >5.5 mmol/L, reduced renal excretion |
| Hypocalcaemia | Post‑surgical neck, vitamin D deficiency, hypomagnesaemia, CKD | Low ionised Ca²⁺, prolonged QT, positive Chvostek |
| Hypercalcaemia | Malignancy, primary hyperparathyroidism, granulomatous disease, thiazide use | Serum Ca²⁺ >2.6 mmol/L, suppressed PTH in malignancy, elevated PTH in primary disease |
| Tubulopathies (e.g., Fanconi, Bartter, Gitelman) | Chronic polyuria, growth failure, metabolic alkalosis, hypokalaemia | Urine wasting of multiple solutes, normal BP |
| Endocrine disorders (Addison’s, Cushing’s, hyperaldosteronism) | Skin hyperpigmentation, striae, hypertension/ hypotension | Specific hormonal assays, renin‑aldosterone profile |
Investigations
| Test | What it answers | Interpretation |
|---|---|---|
| Serum Na⁺, K⁺, Ca²⁺ (total & ionised) | Current electrolyte status | Values outside reference define disorder severity |
| Serum osmolality | True vs. pseudo‑hyponatraemia | Low <275 mOsm/kg = hypotonic hyponatraemia |
| Urine Na⁺ & K⁺ | Renal vs. extrarenal loss | Urine Na⁺ <20 mmol/L → extrarenal; >30 mmol/L → renal |
| Urine osmolality | ADH activity in hyponatraemia | >100 mOsm/kg suggests inappropriate ADH |
| Renal function (creatinine, eGFR) | Ability to excrete K⁺/Ca²⁺ | Elevated creatinine → reduced excretion, risk of hyperkalaemia |
| ABG with electrolytes | Acid‑base status, effect on K⁺/Ca²⁺ | Metabolic alkalosis → hypokalaemia; acidosis → hyperkalaemia |
| PTH, 25‑OH vitamin D, phosphate | Calcium regulation | High PTH with high Ca²⁺ = primary hyperparathyroidism; low vitamin D = hypocalcaemia |
| ECG | Cardiac effect of K⁺/Ca²⁺ abnormalities | Peaked T, widened QRS (hyperkalaemia); U waves (hypokalaemia); QT changes (Ca²⁺) |
| Chest X‑ray / CT (if indicated) | Underlying malignancy or pulmonary TB causing SIADH | Mass lesions, infiltrates |
| Urinalysis (protein, glucose, sediment) | Tubular dysfunction, infection | Proteinuria → CKD; glucosuria with normal glucose → proximal tubulopathy |
Diagnosis and severity
| Disorder | Diagnostic criteria | Mild | Moderate | Severe |
|---|---|---|---|---|
| Hyponatraemia | Serum Na⁺ <135 mmol/L, confirmed hypotonic | 130‑134 | 125‑129 | <125 or symptomatic (seizure, coma) |
| Hypernatremia | Serum Na⁺ >145 mmol/L, hypertonic | 146‑150 | 151‑155 | >155 or neurologic signs |
| Hypokalaemia | Serum K⁺ <3.5 mmol/L | 3.0‑3.4 | 2.5‑2.9 | <2.5 or ECG changes |
| Hyperkalaemia | Serum K⁺ >5.0 mmol/L | 5.1‑5.5 | 5.6‑6.0 | >6.0 or ECG changes |
| Hypocalcaemia | Ionised Ca²⁺ <1.12 mmol/L | 1.0‑1.11 | 0.9‑0.99 | <0.9 or tetany/seizure |
| Hypercalcaemia | Corrected Ca²⁺ >2.6 mmol/L | 2.6‑2.9 | 3.0‑3.4 | >3.5 or renal failure, neuropsychosis |
Severity guides urgency: Severe disturbances demand immediate correction (IV fluids, calcium gluconate for hyperkalaemia, etc.) with continuous cardiac monitoring. Moderate cases allow slower correction, often oral/IV replacement or restriction. Mild disorders are managed with dietary advice and adjustment of offending drugs, with repeat labs in 24‑48 h.
Management
Immediate Stabilisation
- Hyperkalaemia with ECG changes:
- Membrane stabilisation: Intravenous calcium gluconate to restore the myocardial resting membrane threshold and prevent ventricular fibrillation (does not lower serum potassium). Avoid rapid boluses.
- Intracellular shift: Soluble insulin with hypertonic dextrose (dextrose prevents hypoglycaemia while insulin drives potassium into cells via Na+/K+-ATPase); nebulised salbutamol provides an adjunct shifting effect via beta-2 receptor activation.
- Elimination: Loop diuretics (furosemide) if urine output is preserved; gastrointestinal cation exchangers; emergency haemodialysis if refractory, anuric, or associated with severe uraemia/acidosis.
- Severe Hypokalaemia (paralysis or cardiac arrhythmias):
- Intravenous potassium chloride infused slowly in normal saline via an infusion pump (never bolus, never mix in dextrose initially as insulin release worsens hypokalaemia).
- Simultaneously identify and correct hypomagnesaemia; magnesium deficiency impairs the Na+/K+-ATPase pump and permits uninhibited renal potassium wasting.
- Severe, Symptomatic Hyponatraemia (seizures, coma):
- Hypertonic saline (3%) infusion to raise serum sodium promptly until acute neurological symptoms cease.
- Strict limits on correction rates to prevent osmotic demyelination syndrome (central pontine myelinolysis).
- Severe Hypernatraemia (hypovolaemic shock):
- Resuscitate intravascular volume first with isotonic saline (0.9% NaCl). Once hemodynamically stable, switch to hypotonic fluids (0.45% saline or 5% dextrose) to replace the calculated free water deficit gradually.
- Severe Symptomatic Hypocalcaemia (tetany, laryngospasm, seizures):
- Slow intravenous calcium gluconate (diluted, peripheral access preferred; extravasation causes tissue necrosis).
- Severe Hypercalcaemia (confusion, ECG shortening):
- Aggressive intravenous hydration with isotonic saline to restore intravascular volume and promote renal calcium excretion.
Definitive Management, Monitoring, and Safety
| Disorder | Definitive Therapy | Monitoring Parameters | Safety & Contraindications |
|---|---|---|---|
| Hyponatraemia | Fluid restriction (SIADH); 0.9% saline (hypovolaemic); stop thiazides | Serum sodium every 2–4 hours during acute correction | Max correction rate strict; avoid rapid shifts |
| Hypernatraemia | Enteral free water or 5% dextrose; treat diabetes insipidus | Strict fluid input/output, neurological checks | Avoid rapid drop to prevent cerebral oedema |
| Hypokalaemia | Oral potassium chloride; potassium-sparing diuretics | Serum potassium, magnesium, continuous ECG | Max peripheral infusion concentration limits; check renal output |
| Hyperkalaemia | Stop ACE inhibitors, ARBs, spironolactone; renal replacement | Serial ECGs, glucose, renal profile | Digoxin toxicity (calcium caution); never give IV push K+ |
| Hypocalcaemia | Oral calcium carbonate; active vitamin D (calcitriol) | Chvostek/Trousseau signs, corrected calcium, phosphate | Avoid extravasation; correct hypomagnesaemia first |
| Hypercalcaemia | Intravenous bisphosphonates (e.g., zoledronic acid); calcitonin | Hydration status, urine output, renal function | Bisphosphonates contraindicated in severe acute renal failure |
Complications and Prognosis
- Central Pontine Myelinolysis (Osmotic Demyelination): Occurs with over-rapid correction of chronic hyponatraemia; causes spastic quadriparesis, pseudobulbar palsy, and locked-in syndrome.
- Cerebral Oedema: Caused by overly rapid correction of chronic hypernatraemia, leading to brain swelling, herniation, and death.
- Cardiac Arrest: Asystole or ventricular fibrillation from severe potassium extremes (peaked T-waves degrading to sine-wave pattern, or severe U-waves predisposing to torsades de pointes).
- Tetany and Laryngospasm: Severe hypocalcaemia causing asphyxiation and neuromuscular irritability.
- Nephrocalcinosis and Renal Failure: Longstanding hypercalcaemia causing tubular damage and nephrogenic diabetes insipidus.
- Prognosis: Excellent if diagnosed early and corrected slowly; poor if severe neurological insults or irreversible arrhythmias supervene.
High-Yield Exam Points
- The Pseudohyperkalaemia Trap: Haemolysed blood samples, prolonged tourniquet time, or fist-clenching during phlebotomy falsely elevate potassium. Always check the sample integrity before acting, unless the ECG shows active hyperkalaemic changes.
- The "Calcium First" Rule: In hyperkalaemia with ECG changes, students often suggest insulin-dextrose first. The examiner expects calcium gluconate first to protect the heart against fatal arrhythmias.
- Corrected Calcium Calculation: Never interpret total calcium without checking serum albumin. Low albumin drops total calcium while leaving ionized (active) calcium normal.
- Hypomagnesaemia Block: If hypokalaemia or hypocalcaemia is refractory to replacement, the missing step is checking and replacing magnesium. Without magnesium, parathyroid hormone release is blunted, and renal potassium loss continues unabated.
- Thiazide vs. Loop Diuretics: Thiazides cause hyponatraemia, hypokalaemia, and hypercalcaemia (inhibit Na+/Cl- cotransporter in distal convoluted tubule). Loop diuretics cause hypokalaemia, hyponatraemia, and hypocalcaemia (inhibit Na+/K+/2Cl- transporter in the thick ascending limb).
Clinical Case
A 48-year-old male on treatment for pulmonary tuberculosis and advanced HIV infection presents to the emergency department with severe generalized weakness, nausea, dizziness on standing, and hyperpigmented palmar creases. His blood pressure is 85/50 mmHg with marked postural drop. Laboratory investigations reveal: Sodium 122 mmol/L, Potassium 6.2 mmol/L, Urea 14 mmol/L, Creatinine 160 µmol/L. ECG shows tall, peaked T-waves.
Questions and Model Answers
- What is the most likely unifying underlying diagnosis, and what triggered these electrolyte changes?
- Primary adrenal insufficiency (Addison's disease), likely secondary to adrenal destruction from tuberculosis, disseminated fungal infection, or CMV/HIV adrenalitis. The lack of aldosterone causes impaired renal sodium reabsorption and failure of potassium/hydrogen excretion in the distal tubule.
- What is the absolute immediate first step in medical management for this patient?
- Intravenous calcium gluconate to stabilize the cardiac myocyte membrane against hyperkalaemic arrhythmias, along with immediate isotonic fluid resuscitation (0.9% normal saline) to restore intravascular volume.
- Which definitive replacement therapy must be initiated once acute resuscitation is underway?
- Intravenous hydrocortisone (providing glucocorticoid and high-dose mineralocorticoid activity), followed by maintenance glucocorticoid and oral fludrocortisone once oral intake is tolerated.
Practice Questions
Question 1
A 34-year-old woman with severe vomiting from hyperemesis gravidarum is being treated on the ward. Her serum potassium is 2.2 mmol/L. She is started on an infusion of potassium chloride, but despite appropriate repletion over 48 hours, her repeat potassium is 2.3 mmol/L. What investigation should be ordered next to explain the treatment resistance?
A. Serum aldosterone level
B. Serum magnesium level
C. 24-hour urinary free cortisol
D. Arterial blood gas
Answer: B. Serum magnesium level
Explanation: Magnesium is an essential cofactor for the Na+/K+-ATPase pump; hypomagnesaemia causes uninhibited renal potassium excretion in the collecting duct, rendering hypokalaemia refractory to replacement until magnesium is corrected.
Question 2
A 58-year-old man who is chronic alcohol-dependent presents with confusion. His serum sodium is 108 mmol/L. Hypertonic saline is started. Twenty-four hours later, his sodium is 128 mmol/L. Two days later, he develops dysarthria, dysphagia, and flaccid quadriparesis with preserved alertness. What was the mechanism of this complication?
A. Cerebral cortical swelling and uncal herniation
B. Acute ischaemic stroke of the middle cerebral artery
C. Rapid cellular dehydration causing pontine demyelination
D. Wernicke encephalopathy from thiamine consumption
Answer: C. Rapid cellular dehydration causing pontine demyelination
Explanation: Over-rapid correction of chronic hyponatraemia causes brain cells (which had generated intracellular idiogenic osmoles) to rapidly lose water to the hypertonic extracellular space, leading to central pontine myelinolysis.
Question 3
A 62-year-old male with small cell lung carcinoma presents with lethargy, constipation, and thirst. Serum calcium is elevated, corrected for albumin. Electrocardiogram reveals a shortened QT interval. Intravenous normal saline rehydration is initiated. Which pharmacological agent is the most appropriate next step for durable reduction of his serum calcium?
A. Intravenous furosemide
B. Intravenous zoledronic acid
C. Oral calcium carbonate
D. Intravenous hydrocortisone
Answer: B. Intravenous zoledronic acid
Explanation: Intravenous bisphosphonates (such as zoledronic acid) inhibit osteoclastic bone resorption and represent the definitive medical therapy for hypercalcaemia of malignancy following initial saline rehydration.
Question 4
A bedside nurse notes a patient's serum potassium is reported as 6.8 mmol/L. The patient is sitting comfortably in bed eating breakfast, with an entirely normal ECG showing normal P-waves, normal PR intervals, and flat T-waves. What is the most appropriate next clinical step?
A. Administer intravenous soluble insulin with hypertonic dextrose
B. Administer intravenous calcium gluconate immediately
C. Repeat the blood draw without a tourniquet to exclude pseudohyperkalaemia
D. Refer immediately for emergent haemodialysis
Answer: C. Repeat the blood draw without a tourniquet to exclude pseudohyperkalaemia
Explanation: A completely normal ECG in an asymptomatic patient with marked hyperkalaemia strongly suggests pseudohyperkalaemia (frequently due to in vitro haemolysis or prolonged tourniquet application); repeating the sample avoids dangerous unnecessary treatment.
Question 5
A 45-year-old woman undergoes total thyroidectomy for a multinodular goitre. On postoperative day 1, she complains of tingling in her fingers and around her mouth. Inflating a blood pressure cuff on her arm induces carpal spasm. Why did this physical sign occur?
A. Hypomagnesaemia causing peripheral nerve axonal transport failure
B. Hypocalcaemia increasing neuronal sodium permeability and membrane excitability
C. Hyperphosphataemia directly blocking neuromuscular junction transmission
D. Acute surgical denervation of the recurrent laryngeal nerve
Answer: B. Hypocalcaemia increasing neuronal sodium permeability and membrane excitability
Explanation: Extracellular calcium normally stabilizes excitable membranes by blocking sodium channels; when hypocalcaemia occurs (from inadvertent parathyroid gland removal), sodium channels open more readily, resulting in spontaneous depolarization, tetany, and Trousseau sign.
Drafted with AI assistance from standard references and reviewed for structure. Check details against your lecture notes and the Kenya MoH guideline.