Electrolyte imbalance

Electrolytes Imbalance

Dr. Eatimad Osheik

s p p c m

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Definition – Electrolyte Imbalance

Electrolyte imbalance refers to an abnormality in the concentration of serum electrolytes that disrupts normal physiological function.

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potassium calcium ±

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Major Electrolytes

• Sodium (Na⁺)
• Potassium (K⁺)
• Calcium (Ca²⁺)
• Magnesium (Mg²⁺)
• Chloride (Cl⁻)
• Bicarbonate (HCO₃⁻)

Normal Role

• Maintain fluid balance
• Regulate acid-base status
• Enable nerve conduction
• Support muscle contraction (including cardiac muscle)
• Maintain cellular homeostasis

Causes of Imbalance

Imbalance may occur due to:

• Renal disorders
• Gastrointestinal losses
• Endocrine diseases
• Medications
• Critical illness

Electrolyte disturbances are common, life-threatening, and reversible causes of morbidity and mortality.

Why It Is Important

• Can cause cardiac arrhythmias (especially potassium imbalance)
• Can lead to seizures and coma (severe sodium disorders)
• Common in hospitalised and ICU patients
• Frequently seen in:
  • Chronic kidney disease
  • Heart failure
  • Diabetes mellitus
• Influences drug safety (e.g., digoxin, diuretics)

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Sodium Imbalance

Physiology of Sodium Balance

Key Principles

• Sodium (Na⁺) is the major extracellular cation.
• Normal serum sodium: 135–145 mmol/L
• Determines plasma osmolality.

Plasma Osmolality Formula

$\text{Plasma osmolality}=2(\text{Na})+\text{Glucose}+\text{Urea}\text{(Units in mmol/L)}$

Sodium reflects water balance, not total body sodium alone.

Regulation

1. ADH (Vasopressin) – regulates water reabsorption
2. Thirst mechanism
3. Renin–angiotensin–aldosterone system (RAAS)
4. Natriuretic peptides

Hyponatraemia (Na <135 mmol/L)

Definition

Serum sodium <135 mmol/L

Severity	Range
Mild	130–134 mmol/L
Moderate	120–129 mmol/L
Severe	<120 mmol/L

Stepwise Diagnostic Approach

Step 1: Confirm True Hyponatraemia

Check serum osmolality.

A. Hypotonic hyponatraemia (most common)

• Low sodium + low osmolality

B. Isotonic (Pseudohyponatraemia)

• Hyperlipidaemia
• Hyperproteinaemia

C. Hypertonic hyponatraemia

• Hyperglycaemia
• Mannitol

Step 2: Assess Volume Status

1. Hypovolaemic Hyponatraemia

Loss of sodium > water

Causes:

• Vomiting/diarrhoea
• Thiazide diuretics
• Addison’s disease
• Third spacing

Urine sodium:

• <20 mmol/L → extrarenal loss
• >20 mmol/L → renal loss

2. Euvolaemic Hyponatraemia

No oedema, no dehydration

Most common cause: SIADH (Syndrome of Inappropriate ADH)

Causes of SIADH:

• CNS disease
• Lung pathology (e.g., pneumonia)
• Drugs (SSRIs, carbamazepine)
• Malignancy (classically Small-cell lung carcinoma)

Diagnostic criteria:

• Low plasma osmolality
• Inappropriately concentrated urine
• Urine Na >30 mmol/L
• Normal adrenal and thyroid function

Other causes:

• Hypothyroidism
• Glucocorticoid deficiency

3. Hypervolaemic Hyponatraemia

Water retention > sodium retention

Seen in:

• Heart failure
• Cirrhosis
• Nephrotic syndrome

Mechanism: Effective arterial blood volume ↓ → ADH

Clinical Features of Hyponatraemia

Depends on:

• Severity
• Speed of onset

Acute (<48 hrs):

• Headache
• Confusion
• Seizures
• Coma

Due to cerebral oedema

Chronic:

• Often asymptomatic

Management of Hyponatraemia

Key Principle: Correct Slowly

Overcorrection → Osmotic Demyelination Syndrome (Central Pontine Myelinolysis): dysphagia, dysarthria, paralysis, encephalopathy and coma

Severe symptomatic hyponatraemia:

• 3% hypertonic saline
• Raise Na by 4–6 mmol/L initially

Max correction:

• <10 mmol/L in 24 hrs
• <18 mmol/L in 48 hrs

By volume status:

• Hypovolaemic → 0.9% saline
• SIADH:
  • Fluid restriction (800–1000 mL/day)
  • Treat cause
  • Consider:
    • Demeclocycline
    • Tolvaptan (V2 antagonist)
• Hypervolaemic:
  • Fluid restriction
  • Loop diuretics
  • Treat underlying condition

Hypernatraemia (Na >145 mmol/L)

Definition

Serum sodium >145 mmol/L

Always indicates water deficit relative to sodium

Causes

1. Water Loss (most common)

A. Renal Loss:

• Osmotic diuresis
• Diabetes insipidus
  • Central DI: ↓ ADH production
  • Nephrogenic DI: Kidney resistant to ADH
  • Water deprivation test differentiates

B. Extrarenal Loss:

• Diarrhoea
• Burns
• Sweating

2. Sodium Gain:

• Hypertonic saline
• Sodium bicarbonate excess

Clinical Features

• Thirst
• Lethargy
• Irritability
• Seizures
• Coma

Due to cellular dehydration

Management of Hypernatraemia

Key Rule: Correct Slowly

Rapid correction → cerebral oedema

Calculate Water Deficit:

Water deficit = TBW × (current Na/140 − 1)

Where TBW:

• 0.6 × weight (men)
• 0.5 × weight (women)

Treatment:

• Free water orally if possible
• IV 5% dextrose
• 0.45% saline

Correct over 48–72 hours

Important Points – Sodium

• Symptoms depend on speed of change
• Always assess volume status
• Severe hyponatraemia → seizures, coma
• Correct slowly → prevent osmotic demyelination syndrome
• Hypernatraemia = usually water loss
• Correct hypernatraemia slowly → prevent cerebral oedema
• Confusion in elderly/on diuretics → check Na

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Potassium Imbalance

Physiology of Potassium

• Normal serum K⁺: 3.5–5.0 mmol/L
• 98% intracellular (mainly muscle)
• Major determinant of resting membrane potential
• Small changes → major cardiac effects

Regulation of Potassium

1. Renal excretion (most important)

   • Distal nephron
   • Influenced by:
     • Aldosterone
     • Sodium delivery
     • Acid-base status
     • Flow rate

2. Transcellular shifts

   • Insulin → shifts K⁺ into cells
   • β2 stimulation → shifts K⁺ into cells
   • Acidosis → shifts K⁺ out of cells
   • Alkalosis → shifts K⁺ into cells

Hypokalaemia (K⁺ <3.5 mmol/L)

Severity

Severity	Range
Mild	3.0–3.5 mmol/L
Moderate	2.5–3.0 mmol/L
Severe	<2.5 mmol/L

Causes of Hypokalaemia

1. Reduced Intake

• Rare alone

2. Transcellular Shift

• Insulin therapy
• β2 agonists
• Alkalosis
• Refeeding syndrome

3. Increased Loss (Most Common)

A. Gastrointestinal Loss:

• Vomiting
• Diarrhoea
• NG suction

Vomiting causes:

• Metabolic alkalosis
• Secondary hyperaldosteronism

B. Renal Loss:

Diuretics (commonest cause):

• Loop
• Thiazides

Hyperaldosteronism:

• Primary: Conn’s syndrome
• Secondary: Renal artery stenosis

Clinical Features of Hypokalaemia

Neuromuscular:

• Weakness
• Cramps
• Paralysis (severe)

Cardiac:

• Arrhythmias
• Digoxin toxicity risk

ECG Changes in Hypokalaemia

1. Flattened T waves
2. Prominent U waves
3. ST depression
4. Prolonged QT

Evaluation Approach

1. Confirm true value
2. Check acid-base status
3. Measure urine potassium

Urine K⁺:

• <20 mmol/day → extrarenal loss
• >20 mmol/day → renal loss

Management of Hypokalaemia

Mild (asymptomatic):

• Oral potassium chloride

Severe or symptomatic:

• IV potassium (careful!)

IV Rules:

• Max 10 mmol/hr (peripheral)
• Continuous ECG monitoring
• Never give as bolus

Correct magnesium if low

Hyperkalaemia (K⁺ >5.0 mmol/L)

Severity

Severity	Range
Mild	5.0–5.5 mmol/L
Moderate	5.5–6.5 mmol/L
Severe	>6.5 mmol/L

Causes of Hyperkalaemia

1. Pseudohyperkalaemia

Always exclude first:

• Haemolysis
• Thrombocytosis
• Difficult venepuncture

2. Reduced Renal Excretion (Most Common)

• Acute or Chronic Kidney Disease
• Hypoaldosteronism
• Addison’s disease
• ACE inhibitors
• ARBs
• Potassium-sparing diuretics

3. Transcellular Shift

• Acidosis
• Insulin deficiency (DKA)
• Tissue breakdown (rhabdomyolysis)
• Tumour lysis syndrome

4. Excess Intake

• Rare unless renal impairment

Clinical Features of Hyperkalaemia

• Muscle weakness
• Paraesthesia
• Life-threatening arrhythmias

ECG Changes in Hyperkalaemia

Progressive pattern:

1. Tall peaked T waves
2. Shortened QT
3. Prolonged PR
4. Wide QRS
5. Sine wave pattern
6. Ventricular fibrillation/asystole

ECG changes do not always correlate with potassium level.

Emergency Management of Hyperkalaemia

Indications for urgent treatment:

• K⁺ ≥6.5 mmol/L
• ECG changes
• Rapid rise

Stepwise Emergency Management:

1. Stabilize Cardiac Membrane

• IV Calcium gluconate
  • Acts within minutes
  • Does NOT lower potassium

2. Shift Potassium into Cells

• IV insulin + glucose
• Nebulised salbutamol
• Sodium bicarbonate (if acidotic)

3. Remove Potassium from Body

• Loop diuretics
• Potassium binders
• Dialysis (definitive)

Dialysis Indications:

• Severe renal failure
• Refractory hyperkalaemia
• Life-threatening ECG changes

Important Points – Potassium

• Think arrhythmia first
• Always do ECG in hyperkalaemia
• Peaked T waves → early sign
• Wide QRS → pre-arrest
• Hypokalaemia → weakness, ileus, arrhythmia
• Correct magnesium if low
• K⁺ >6.5 or ECG changes → IV calcium immediately

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Calcium Imbalance

Overview

Calcium is a vital extracellular cation essential for:

• Neuromuscular transmission
• Muscle contraction
• Blood coagulation
• Hormone secretion
• Enzyme activity
• Bone mineralization

Normal Values:

• Total serum calcium: 2.2–2.6 mmol/L (8.8–10.4 mg/dL)
• Ionized calcium: 1.1–1.3 mmol/L (physiologically active form)

Always interpret calcium in relation to serum albumin.

Corrected Calcium Formula

Corrected Calcium = Serum Calcium (mg/dL) + 0.8 × (4.0 − Serum Albumin (g/dL))

Calcium Homeostasis

Regulated by:

1. Parathyroid Hormone (PTH)

• ↑ Bone resorption
• ↑ Renal calcium reabsorption
• ↑ Phosphate excretion
• ↑ Vitamin D activation

2. Vitamin D (1,25-dihydroxyvitamin D)

• ↑ Intestinal calcium absorption
• ↑ Bone mineralization

Organs involved:

• Bone
• Kidney
• Gastrointestinal tract

Hypercalcaemia

Definition

Serum calcium > 2.6 mmol/L

Common Causes

1. Primary Hyperparathyroidism (Most common overall)

• Usually due to: Parathyroid adenoma

2. Malignancy (Most common inpatient cause)

• Mechanisms:
  • PTHrP secretion (e.g., lung, renal cancers)
  • Bone metastases
  • Myeloma

Other Causes:

• Vitamin D excess
• Thiazide diuretics
• Granulomatous disease (e.g., Sarcoidosis)
• Hyperthyroidism
• Immobilization
• Addison’s disease

Clinical Features

“Stones, Bones, Groans and Psychic Moans”

• Renal stones
• Bone pain
• Abdominal pain, constipation
• Depression, confusion
• Polyuria & polydipsia
• Shortened QT interval (ECG)

Severe hypercalcaemia (>3.5 mmol/L) → Medical emergency

Investigation

1. Repeat calcium
2. PTH level (key investigation)
   • High/inappropriately normal → Primary hyperparathyroidism
   • Suppressed → Malignancy or other causes
3. Urea & electrolytes
4. Vitamin D
5. Myeloma screen
6. CXR (malignancy, sarcoidosis)

Management

Acute Severe Hypercalcaemia:

1. IV 0.9% saline (first line)
2. IV bisphosphonates (e.g., zoledronic acid)
3. Calcitonin (short-term)
4. Steroids (if vitamin D-mediated)
5. Dialysis (if refractory)

Definitive Treatment:

• Parathyroidectomy (if primary hyperparathyroidism and symptomatic)

Indications for surgery:

• Symptomatic
• Ca >0.25 mmol/L above normal
• Osteoporosis
• Renal stones
• Age <50

Hypocalcaemia

Definition

Serum calcium < 2.2 mmol/L

Causes

1. Hypoparathyroidism

• Post-thyroidectomy (most common)
• Autoimmune
• Genetic

2. Vitamin D Deficiency

• Common in elderly and malnourished

3. Chronic Kidney Disease

• ↓ Vitamin D activation
• ↑ Phosphate retention

4. Acute Pancreatitis

5. Massive Blood Transfusion (citrate binding)

Clinical Features

Due to increased neuromuscular excitability:

• Perioral numbness
• Tetany
• Muscle cramps
• Seizures
• Laryngospasm

Classical Signs:

• Chvostek’s sign
• Trousseau’s sign

ECG: Prolonged QT interval

Investigation

1. Serum calcium (corrected)
2. PTH
3. Vitamin D
4. Magnesium (important!)
5. Phosphate

Trousseau’s Sign

How to test:

1. Place blood pressure cuff around the arm
2. Inflate the cuff for 1–4 mins
3. If hands & fingers go into spasm in palmar flexion = positive

Chvostek’s Sign

How to test:

1. Tap the face just below and in front of the ear
2. If facial twitching occurs of one side of the mouth, nose & cheek = positive

Management

Acute Symptomatic Hypocalcaemia:

• IV calcium gluconate (10%) slow infusion
• Cardiac monitoring

Chronic Management:

Depends on cause:

• Oral calcium supplements
• Vitamin D (cholecalciferol)
• Calcitriol in CKD
• Magnesium replacement if low

Secondary & Tertiary Hyperparathyroidism

Secondary Hyperparathyroidism

Due to chronic hypocalcaemia (usually CKD)

• High PTH
• Low/normal calcium

Tertiary Hyperparathyroidism

Autonomous PTH secretion after long-standing secondary hyperparathyroidism

• High PTH
• High calcium

Important Points – Calcium

• Correct calcium for albumin
• Hypocalcaemia → tetany, seizures, prolonged QT
• Hypercalcaemia → “bones, stones, groans, psychiatric overtones”
• Severe hypercalcaemia → dehydration + confusion
• First-line treatment (severe hypercalcaemia) → IV fluids

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Magnesium Imbalance

Overview

• Normal serum magnesium: 0.7–1.0 mmol/L
• 50–60% stored in bone
• Regulated mainly by:
  • Kidneys (primary regulator)
  • Gastrointestinal absorption

Magnesium is essential for:

• Neuromuscular stability
• ATP-dependent reactions
• Potassium and calcium homeostasis

Hypomagnesaemia (<0.7 mmol/L)

Causes

1. Reduced intake/absorption

• Malnutrition
• Chronic alcoholism
• Chronic diarrhoea
• Proton pump inhibitors (long-term)

2. Increased renal loss

• Diuretics (loop, thiazide)
• Uncontrolled diabetes
• Hypercalcaemia
• Aminoglycosides

Clinical Features

• Often associated with hypokalaemia and hypocalcaemia
• Neuromuscular hyperexcitability:
  • Tremors
  • Tetany
  • Seizures
• Cardiac arrhythmias (e.g., torsades de pointes)

Management

• Correct underlying cause
• Oral magnesium if mild
• IV magnesium sulfate if severe or symptomatic
• Always correct magnesium in refractory hypokalaemia

Hypermagnesaemia (>1.0 mmol/L)

Causes

• Renal failure (most common)
• Excess magnesium intake (e.g., antacids, laxatives)
• Iatrogenic (e.g., obstetric therapy)

Clinical Features (dose-dependent)

• Nausea, flushing
• Loss of deep tendon reflexes
• Hypotension
• Bradycardia
• Respiratory depression
• Cardiac arrest (severe)

Management

• Stop magnesium intake
• IV calcium gluconate (cardiac stabilisation)
• IV fluids + loop diuretics
• Dialysis if severe (especially in renal failure)

Important Points – Magnesium

• Hypomagnesaemia causes refractory hypokalaemia
• Always check magnesium in unexplained arrhythmias
• Loss of reflexes = early sign of hypermagnesaemia
• Renal failure is the commonest cause of hypermagnesaemia

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Chloride Imbalance

Overview

Chloride (Cl⁻) is the major extracellular anion.

Normal serum chloride: 98–106 mmol/L

It plays a key role in:

• Maintaining electroneutrality
• Acid-base balance
• Osmotic pressure

Clinically, chloride disorders are usually secondary to acid-base disturbances.

Hypochloraemia (Cl⁻ < 98 mmol/L)

Common Causes

1. Vomiting / Nasogastric suction — Loss of HCl → metabolic alkalosis
2. Diuretics (loop, thiazide)
3. Chronic respiratory acidosis (renal compensation)

Clinical Features

Usually due to associated alkalosis:

• Weakness
• Tetany (if alkalosis severe)
• Volume depletion

Management

• Treat underlying cause
• IV normal saline (chloride replacement)
• Correct potassium if low

Hyperchloraemia (Cl⁻ > 106 mmol/L)

Common Causes

1. Metabolic acidosis (normal anion gap) — Diarrhoea
2. Renal tubular acidosis
3. Excess IV normal saline (iatrogenic)
4. Renal failure

Clinical Features

Due to metabolic acidosis:

• Kussmaul breathing
• Weakness
• Confusion

Management

• Treat underlying cause
• Adjust IV fluids
• Correct acidosis if severe

Important Points – Chloride

• Vomiting → hypochloraemic metabolic alkalosis
• Diarrhoea → hyperchloraemic metabolic acidosis
• Always interpret chloride with bicarbonate
• Chloride abnormalities reflect acid-base disorders rather than primary disease

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Bicarbonate Imbalance

Overview

Bicarbonate (HCO₃⁻) is the major extracellular buffer.

Normal plasma bicarbonate: 22–28 mmol/L

It is regulated by:

• Kidneys (metabolic component)
• Lungs (via CO₂)

Changes in bicarbonate primarily reflect metabolic acid-base disorders.

Low Bicarbonate (Metabolic Acidosis)

Causes

A. High Anion Gap Metabolic Acidosis (HAGMA)

• Diabetic ketoacidosis
• Lactic acidosis
• Renal failure
• Toxins (e.g., salicylates)

B. Normal Anion Gap (Hyperchloraemic) Acidosis

• Diarrhoea
• Renal tubular acidosis

Clinical Features

• Kussmaul respiration
• Confusion
• Hypotension (severe cases)

Management

• Treat underlying cause
• IV fluids
• Insulin (DKA)
• Bicarbonate only if severe acidosis (pH < 7.1)

High Bicarbonate (Metabolic Alkalosis)

Causes

• Vomiting (loss of gastric acid)
• Diuretics
• Excess alkali intake
• Hyperaldosteronism

Clinical Features

• Weakness
• Tetany (due to ↓ ionized calcium)
• Arrhythmias (often with hypokalaemia)

Management

• Correct volume depletion (IV saline)
• Replace potassium
• Treat underlying cause

Important Points – Bicarbonate

• Low HCO₃⁻ = metabolic acidosis
• High HCO₃⁻ = metabolic alkalosis
• Always calculate anion gap
• Interpret alongside pH and PaCO₂ (ABG)
• Vomiting → metabolic alkalosis
• Diarrhoea → metabolic acidosis

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Phosphate Imbalance

Overview

• Normal serum phosphate: 0.8–1.5 mmol/L (2.5–4.5 mg/dL)
• 85% stored in bone (hydroxyapatite)
• Regulated by:
  • Kidney (primary regulator)
  • Parathyroid hormone (PTH)
  • Vitamin D
  • FGF-23

Phosphate balance depends on intestinal absorption, renal excretion, and bone exchange.

Hypophosphataemia (<0.8 mmol/L)

Causes

1. Reduced intake/absorption

• Malnutrition
• Alcoholism
• Vitamin D deficiency
• Antacids (phosphate binding)

2. Redistribution (intracellular shift)

• Refeeding syndrome
• Insulin therapy
• Respiratory alkalosis

3. Increased renal loss

• Hyperparathyroidism
• Fanconi syndrome
• Diuretics

Clinical Features

• Often asymptomatic (mild)
• Muscle weakness
• Rhabdomyolysis
• Respiratory failure
• Haemolysis
• Confusion, seizures (severe)

Management

• Treat cause
• Oral phosphate if mild
• IV phosphate if severe/symptomatic (monitor calcium closely)

Hyperphosphataemia (>1.5 mmol/L)

Causes

1. Reduced renal excretion (most common)

• Chronic kidney disease (CKD)

2. Increased load

• Tumour lysis syndrome
• Rhabdomyolysis
• Massive haemolysis

3. Endocrine causes

• Hypoparathyroidism

Clinical Features

• Usually asymptomatic
• Hypocalcaemia symptoms (tetany)
• Soft tissue and vascular calcification (chronic)

Management

• Treat underlying cause
• Dietary phosphate restriction
• Phosphate binders (e.g., calcium carbonate, sevelamer)
• Dialysis if severe (especially in CKD)

Important Points – Phosphate

• CKD = hyperphosphataemia
• Refeeding syndrome = hypophosphataemia
• Phosphate abnormalities often alter calcium levels inversely
• Severe hypophosphataemia can cause respiratory failure in ICU patients