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Electrolyte Disorders: Hypo/Hypernatremia & Hypo/Hyperkalemia

A complete MBBS-level guide based on Goldman-Cecil Medicine, Comprehensive Clinical Nephrology, Tietz Textbook of Laboratory Medicine, Medical Physiology (Boron & Boulpaep), and Ganong's Review.

PART 1: SODIUM (Na+) DISORDERS

Normal Values

Normal serum Na+: 135-145 mmol/L
Sodium is the primary determinant of plasma osmolality and ECF volume
Normal plasma osmolality: 280-295 mOsm/kg

HYPONATREMIA (Na+ < 135 mmol/L)

Definition & Epidemiology

Hyponatremia is the most common electrolyte disorder in hospitalized patients, with incidence as high as 15-30% in acutely and chronically hospitalized patients. A serum Na+ <135 mmol/L is associated with a ~45% relative increase in ICU admission rates.

Goldman-Cecil Medicine
Tietz Textbook of Laboratory Medicine, 7th Edition

First Step: Measure Plasma Osmolality

Hyponatremia is NOT always hypo-osmolar. It has THREE osmolar states:

Type	Plasma Osmolality	Cause
Hypo-osmolar	Low (<280 mOsm/kg)	True hyponatremia (most common)
Iso-osmolar	Normal (280-295)	Pseudohyponatremia (hyperlipidemia, hyperproteinemia)
Hyper-osmolar	High (>295)	Hyperglycemia, mannitol, uremia

Pseudohyponatremia is a lab artifact where excess lipid or protein displaces aqueous plasma volume - the true sodium in water is normal. Direct ion-selective electrodes (ISE) avoid this pitfall.

Diagnostic Algorithm for Hyponatremia

Hyponatremia Diagnostic Algorithm - Tietz Textbook of Laboratory Medicine

Algorithm for differential diagnosis of hyponatremia based on plasma osmolality and volume status. - Tietz Textbook of Laboratory Medicine, 7th Edition

Hypo-osmolar Hyponatremia: Classify by Volume Status

1. HYPOVOLEMIC Hyponatremia (Urine Na+ is the key)

Renal losses (Urine Na+ >20 mmol/L): Diuretics, mineralocorticoid deficiency (Addison's), metabolic alkalosis, salt-losing nephropathy (polycystic kidney, chronic interstitial nephritis), renal tubular acidosis
Extrarenal losses (Urine Na+ <10 mmol/L): Vomiting, diarrhea, burns, sweating

2. HYPERVOLEMIC Hyponatremia

Urine Na+ >20: Acute/chronic renal failure
Urine Na+ <10: Congestive heart failure, cirrhosis (with ascites), nephrotic syndrome
Mechanism: Reduced effective circulating volume activates ADH and RAAS, causing water retention

3. EUVOLEMIC Hyponatremia (most common cause = SIADH)

SIADH (Syndrome of Inappropriate ADH secretion)
Hypothyroidism, hypoadrenalism, reset osmostat
Diuretics

SIADH - Key Points

SIADH is characterized by:

Hypo-osmolar hyponatremia
Urine osmolality inappropriately high (>100 mOsm/kg)
Urine Na+ >20 mmol/L
No edema, no volume depletion
Causes: CNS disorders (meningitis, stroke, head trauma), pulmonary disease (TB, pneumonia, SCLC), drugs (SSRIs, carbamazepine, cyclophosphamide, NSAIDs), postoperative state

Clinical Features of Hyponatremia

Symptoms are due to cerebral edema from water moving into CNS cells:

Na+ 125-135: Nausea, malaise, headache
Na+ <125: Confusion, lethargy, generalized weakness
Na+ <120: Severe mental confusion
Na+ <105: Seizures, coma

The rapidity of onset determines severity - acute hyponatremia causes symptoms at higher Na+ levels (e.g., ~125 mmol/L) than chronic hyponatremia.

Treatment of Hyponatremia

Type	Treatment
Hypovolemic	Isotonic saline (0.9% NaCl) to restore volume
Hypervolemic	Fluid restriction + treat underlying cause
Euvolemic / SIADH	Fluid restriction; vasopressin receptor antagonists (tolvaptan, conivaptan); hypertonic saline for severe/symptomatic cases

CRITICAL WARNING - Osmotic Demyelination Syndrome (ODS): Correction must NOT exceed 8-10 mmol/L in 24 hours (or ~1-2 mmol/L/hour in symptomatic acute cases). Rapid correction causes osmotic demyelination (central pontine myelinolysis) - an irreversible, devastating neurologic injury.

HYPERNATREMIA (Na+ > 145 mmol/L)

Definition

Hypernatremia (plasma Na+ >144-145 mmol/L) always reflects hypertonicity - there is always an increased concentration of osmotically active solutes. It is considerably less common than hyponatremia because even a 1% increase in serum osmolality triggers thirst.

Goldman-Cecil Medicine

Mortality in critically ill patients with hypernatremia: 40-60%, with prolonged ICU stay.

Why Thirst is the Guardian

In any awake, alert person with a normal thirst mechanism and access to water, hypernatremia should not develop. Most cases occur in:

Patients with altered mental status
Infants
Elderly patients with impaired thirst (hypodipsia)
Hospitalized patients unable to access fluids

Causes Classified by Volume Status

Diagnostic Algorithm for Hypernatremia

Hypernatremia Diagnostic Algorithm - Tietz Textbook of Laboratory Medicine

Algorithm for differential diagnosis of hypernatremia based on volume status and urine Na+/osmolality. - Tietz Textbook of Laboratory Medicine, 7th Edition

Volume Status	Cause
Hypovolemic	Extrarenal: diarrhea, burns, sweating (Uosm >800, UNa <20)
Euvolemic	Diabetes insipidus (central or nephrogenic)
Hypervolemic	Hypertonic saline excess, Cushing syndrome, hyperaldosteronism, hypertonic NaHCO3

Diabetes Insipidus (DI) - Key Cause of Hypernatremia

	Central DI	Nephrogenic DI
Defect	Failure to release ADH	Failure of kidney to respond to ADH
Causes	Hypothalamic/pituitary tumor, head injury, surgery, hemorrhage	Lithium, demeclocycline, V2-receptor mutation, AQP2 mutation
Urine osmolality	Very low (100-150 mOsm/kg)	Low
Treatment	Desmopressin (synthetic ADH)	Treat cause; low-salt diet; thiazides

Daily urine output in DI can reach up to 20 liters.

Clinical Features of Hypernatremia

Primary neurologic symptoms due to shrinkage of CNS cells as water leaves cells:

Tremors, irritability, ataxia
Confusion
Coma
Seizures, focal neurologic deficits

Acute hypernatremia: symptoms at Na+ ~160 mmol/L. Chronic hypernatremia: symptoms may not appear until Na+ >175 mmol/L (brain adapts by generating "idiogenic osmoles").

Treatment of Hypernatremia

Goal: Correct the water deficit slowly.

Correction rate: No faster than 10 mmol/L/24 hours (0.5 mmol/L/hour).

Rapid correction of chronic hypernatremia causes dangerous cerebral edema because CNS cells still contain excess idiogenic osmoles and will absorb too much water.

Hypovolemic: 0.9% NaCl first to restore perfusion, then switch to 5% dextrose (D5W) or 0.45% NaCl
Euvolemic (DI): Free water replacement (oral or IV D5W)
Hypervolemic: Diuretics + free water replacement

Water deficit formula:

Water Deficit (L) = 0.6 × weight (kg) × [(serum Na / 140) - 1]

PART 2: POTASSIUM (K+) DISORDERS

Normal Values & Physiology

Normal serum K+: 3.5-5.0 mmol/L
>98% of total body K+ is intracellular (ICF concentration ~150 mmol/L)
Only ~2% is extracellular (ECF ~4 mmol/L)
Small shifts between ICF and ECF produce dramatic changes in serum K+

Regulators of K+ Distribution

Factor	Effect on Serum K+
Insulin	Drives K+ INTO cells (decrease)
Beta-2 agonists	Drives K+ INTO cells (decrease)
Acidosis	K+ moves OUT of cells (increase)
Alkalosis	K+ moves INTO cells (decrease)
Aldosterone	Increases renal K+ excretion (decrease)
Osmolarity increase	K+ moves OUT of cells (increase)

HYPOKALEMIA (K+ < 3.5 mmol/L)

Causes

1. Increased Renal Losses (most common cause)

Diuretics (loop diuretics, thiazides) - commonest cause
Hyperaldosteronism (primary - Conn's syndrome; secondary)
Cushing's syndrome / corticosteroid excess
Renal tubular disorders: Bartter syndrome, Gitelman syndrome, RTA
Amphotericin B, aminoglycosides

2. Extrarenal Losses

Severe diarrhea (intestinal secretions are K+-rich)
Vomiting (directly + aldosterone activation from volume loss)
Burns, excessive sweating

3. Transcellular Shift (K+ moves into cells)

Insulin administration (treatment of DKA) - large K+ influx into cells
Alkalosis - H+ leaves cells, K+ enters in exchange
Beta-2 agonists (salbutamol, in asthma treatment)
Catecholamine surge (acute MI, acute stress)

4. Inadequate Intake

Starvation, anorexia
IV fluids without K+ supplementation
Pica (clay ingestion - binds K+ in GI tract)

Clinical Features of Hypokalemia

Mild (3.0-3.5 mmol/L): Often asymptomatic; possible increased ventricular ectopy

Moderate (<3.0 mmol/L):

Muscle weakness, fatigue
Constipation, ileus
Muscle cramps
Palpitations
Polyuria (nephrogenic DI-like effect)

Severe (<2.5 mmol/L):

Generalized muscle weakness - can progress to paralysis
Rhabdomyolysis with potential AKI
Torsades de pointes (life-threatening arrhythmia)
Bradycardia, tachycardia, atrial/ventricular fibrillation
Metabolic alkalosis (K+/H+ exchange in cells)

ECG in Hypokalemia:

Flattened or inverted T waves
Prominent U waves (most characteristic)
ST segment depression
Prolonged QU interval

Treatment of Hypokalemia

Severity	Treatment
Mild (3.0-3.5)	Oral KCl supplementation; dietary K+ (bananas, oranges)
Moderate-severe (<3.0)	IV KCl infusion (max 10-20 mEq/hour via peripheral, 40 mEq/hour via central with monitoring)
Diuretic-induced	Add K+-sparing diuretic (spironolactone, amiloride)

Always check and correct magnesium! Hypomagnesemia causes refractory hypokalemia because Mg2+ is needed to maintain intracellular K+. Correcting K+ without correcting Mg2+ will fail.

Preferred salt: KCl (most cases), unless metabolic acidosis present (use potassium citrate).

HYPERKALEMIA (K+ > 5.0 mmol/L)

Severity Classification

Grade	Serum K+	ECG changes
Mild	5-6 mEq/L without ECG changes	None
Moderate	5-6 with ECG changes, or 6.1-6.5 without	Peaked T waves
Severe	>6.5, or 6.1-6.5 with ECG changes	Widened QRS, sine wave

Causes

1. Pseudohyperkalemia (MUST RULE OUT FIRST)

Traumatic hemolysis during blood draw (most common cause of "high K+")
Prolonged tourniquet time or fist clenching
Extreme leukocytosis (>70,000/cm3) or thrombocytosis (>500×10⁹/L) - K+ released during clotting
Diagnosed by: serum K+ >0.3 mmol/L higher than simultaneous plasma K+
Key clue: concomitant elevation of LDH suggests hemolysis

2. Transcellular Shift (K+ moves out of cells)

Acidosis - H+ enters cells, K+ exits (each 0.1 pH unit drop raises K+ by ~0.6 mEq/L)
Insulin deficiency (DKA) - combined with hyperosmolarity
Beta-blockers
Digitalis toxicity (inhibits Na-K ATPase pump)
Massive cell breakdown: crush injury, rhabdomyolysis, tumor lysis syndrome, massive hemolysis, burns, GI bleeding with intestinal K+ absorption

3. Decreased Renal Excretion (most common cause of sustained hyperkalemia)

Advanced renal failure (most common)
Adrenal insufficiency (Addison's disease) - low aldosterone
Hypoaldosteronism (type IV RTA, hyporeninemic hypoaldosteronism in diabetics)
Drugs: ACE inhibitors, ARBs, K+-sparing diuretics (spironolactone, amiloride, triamterene), NSAIDs, trimethoprim, heparin

ECG Changes in Hyperkalemia (Progressive - CRITICAL!)

ECG Changes in Hyperkalemia - Comprehensive Clinical Nephrology, 7th Edition

Progressive ECG changes with rising serum potassium. Ventricular fibrillation may occur at any stage of this progression. - Comprehensive Clinical Nephrology, 7th Edition

Sequence to memorize:

K+ 6-7: Peaked (tented) T waves - earliest change
K+ 7-8: Flattened P waves, prolonged PR interval, depressed ST segment
K+ 8-9: Atrial standstill (P waves disappear), widened QRS
K+ >9: Sine wave pattern - QRS merges with T wave
Terminal: Ventricular fibrillation, cardiac arrest

Note: ECG changes do NOT always correlate perfectly with K+ levels. A patient can jump from mild to severe cardiac effects unpredictably. ECG is MANDATORY for all hyperkalemic patients.

Clinical Features of Hyperkalemia

Often asymptomatic until severe
Muscle pain and weakness (skeletal muscle most sensitive)
Numbness, paresthesias
Severe: respiratory failure from diaphragm weakness
Nausea
Cardiac arrhythmias (see ECG above) - major mortality risk
In hyperkalemic periodic paralysis (rare AD disorder, prevalence 1:100,000): transient episodes of paralysis; resting membrane potential shifts from -90 mV to -60 mV, inactivating Na+ channels

Treatment of Hyperkalemia

The three-pronged approach: Stabilize - Shift - Remove

Step 1: Cardiac Membrane Stabilization (works in minutes)

IV Calcium gluconate (10% solution, 10 mL over 2-3 min)
Raises threshold for action potentials, reduces membrane excitability
Does NOT lower serum K+ - just protects the heart
Indicated when ECG changes are present
Effect lasts ~30-60 minutes - must follow with definitive treatment

Step 2: Shift K+ into Cells (works in 15-30 min)

IV Insulin (10 units) + Glucose (50 mL of 50% dextrose) - drives K+ into cells
Salbutamol (albuterol) nebulization - beta-2 agonist effect
IV sodium bicarbonate - useful if concurrent metabolic acidosis; promotes K+/H+ exchange

Step 3: Remove K+ from the Body (definitive)

Furosemide (loop diuretic) - increases renal K+ excretion (if kidneys functional)
Sodium polystyrene sulfonate (Kayexalate) or newer agents patiromer / sodium zirconium cyclosilicate - K+-binding resins in GI tract
Hemodialysis - fastest, most effective; indicated for renal failure or extreme hyperkalemia

Step 4: Low K+ diet + Treat underlying cause

Evaluation of Hyperkalemia (Algorithmic Approach)

Evaluation of Hyperkalemia Flowchart - Comprehensive Clinical Nephrology, 7th Edition

Workup of hyperkalemia - starting with ECG, ruling out pseudohyperkalemia, then systematic evaluation of cause. CKD = chronic kidney disease. - Comprehensive Clinical Nephrology, 7th Edition

QUICK COMPARISON TABLE

Feature	Hyponatremia	Hypernatremia	Hypokalemia	Hyperkalemia
Definition	Na+ <135	Na+ >145	K+ <3.5	K+ >5.0
CNS symptoms	Cerebral edema (confusion, seizures)	Brain shrinkage (confusion, coma)	Minimal	Muscle weakness
Cardiac	Rarely affected	Rarely affected	Flattened T, U waves, Torsades	Peaked T, widened QRS, VF
Commonest cause	Diuretics/SIADH	DI/dehydration	Loop/thiazide diuretics	Renal failure/pseudohyperkalemia
Correction rate	Max 8-10 mmol/L/24h	Max 10 mmol/L/24h	Oral KCl (mild), IV KCl (severe)	Ca-gluconate + insulin/glucose
Over-correction danger	Osmotic demyelination (ODS)	Cerebral edema	Hyperkalemia	Hypokalemia

MEMORY AIDS

For Hyponatremia causes (SIADH mnemonic):

Small cell lung cancer (most common malignancy)
Intracranial pathology
Addison's/Adrenal insufficiency (also causes hyponatremia + hyperkalemia)
Drugs (SSRIs, carbamazepine, opioids)
Hypothyroidism

ECG in Hyperkalemia - "PRST going wrong":

P - peaks (T waves), then P disappears
R - R/QRS widens
S - Sinusoid (terminal)
T - Tented (first sign)

Hypokalemia ECG - "T is Flat, U is Fat" - flattened T waves + prominent U waves

Sources: Goldman-Cecil Medicine, 26th Edition | Comprehensive Clinical Nephrology, 7th Edition | Tietz Textbook of Laboratory Medicine, 7th Edition | Medical Physiology (Boron & Boulpaep) | Ganong's Review of Medical Physiology, 26th Edition | National Kidney Foundation Primer on Kidney Diseases, 8th Edition

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