Hypernatremia is defined as a serum sodium concentration >145 mmol/L. It represents a hyperosmolar state typically due to a net water deficit relative to sodium content, rather than excessive sodium accumulation.
🔑 Key Concept: Hypernatremia is fundamentally a “water problem”, not a sodium excess issue.
Classification
- Acute Hypernatremia: Develops in <24 hours.
- Chronic Hypernatremia: Persists for >48 hours.
- Correction must be cautious in chronic cases to avoid cerebral edema.
Etiology (Causes of Hypernatremia)
-
Water Losses
- Insensible Losses (Extrarenal):
- Excessive sweating, burns, fever, tachypnea, respiratory infections.
- Gastrointestinal Losses:
- Vomiting, infectious diarrhea, nasogastric suctioning.
- Transcellular Shifts:
- Conditions like rhabdomyolysis or seizures can shift water into cells, concentrating extracellular sodium.
- Insensible Losses (Extrarenal):
-
Renal Losses
- Diabetes Insipidus (DI):
- Central DI: Deficient ADH (vasopressin) secretion.
- Causes: Trauma, neurosurgery, tumors, infections, hypoxic brain injury, granulomatous disease.
- Nephrogenic DI: Renal unresponsiveness to ADH.
- Causes: Chronic kidney disease, hypercalcemia, hypokalemia, sickle cell disease, lithium, demeclocycline.
- Osmotic Diuresis:
- Seen in DKA, hyperosmolar hyperglycemic state (HHS), mannitol use, glycosuria, urea.
Clinical Presentation
Neurologic Symptoms
- Result from cellular dehydration in the CNS.
- Common signs and symptoms:
- Lethargy, weakness
- Irritability, confusion
- Seizures, coma (especially if Na+ >160 mmol/L)
⚠️ High-Risk Group: Elderly patients and those with impaired thirst or access to fluids.
Diabetes Insipidus Clue
- Patients with DI may report polyuria (3–20 L/day) and polydipsia.
- Urine is markedly dilute despite hypernatremia.
Diagnosis
Laboratory Evaluation
- Serum Sodium: >145 mmol/L
- Serum Osmolality: Elevated
- Urine Osmolality: Helps differentiate etiology:
- Low (<300 mOsm/kg): Suggests DI or primary polydipsia
- High (>600 mOsm/kg): Suggests extrarenal losses
- Urine Sodium and Potassium
- Glucose, Urea, Creatinine
- 24-hour urine volume
- Plasma Arginine Vasopressin (AVP) or copeptin levels (if available)
- Desmopressin (DDAVP) Test: Differentiates between Central and Nephrogenic DI
Management
General Principles
- Correct underlying cause
- Gradual correction of sodium to avoid cerebral edema
- Acute hypernatremia: Can correct faster (up to 1–2 mEq/L per hour in symptomatic cases)
- Chronic hypernatremia: Correct no more than 0.5 mEq/L per hour or 12 mEq/L per 24 hours
Fluid Replacement
- Initial resuscitation (if hypovolemic): Use isotonic fluids (0.9% saline)
- Free water replacement: Use 5% dextrose (D5W) or hypotonic saline (0.45%)
- Oral rehydration if mild and patient can drink
Specific Treatments
Central Diabetes Insipidus (CDI)
- Desmopressin (DDAVP): Intranasal, subcutaneous, IV, or IM
- Monitor sodium and fluid balance carefully
Nephrogenic Diabetes Insipidus (NDI)
- Address underlying cause (e.g., stop lithium)
- Low-sodium diet
- Thiazide diuretics (reduce polyuria via volume contraction)
- NSAIDs (e.g., indomethacin): Reduce prostaglandin-mediated inhibition of ADH
Complications
- Cerebral edema (from overly rapid correction)
- Seizures, permanent neurologic damage
- Coma if untreated severe hypernatremia
HIGH YIELD
- Hypernatremia = water deficit, not sodium excess.
- Always assess volume status first.
- Desmopressin test distinguishes CDI from NDI.
- Correct sodium slowly in chronic cases to avoid brain swelling.
- Elderly and neurologically impaired patients are at highest risk.
Mnemonic: "MODEL" for Hypernatremia Causes
Medications/Meals (high sodium)
Osmotic diuretics
Diabetes insipidus
Excessive water loss
Low water intake