Persistent Hyponatremia in Burns Patient - Clinical Analysis

Step 1: Why is the Hyponatremia Persisting? - Identify the Underlying Cause(s)

A) Burns-Specific Sodium Loss (Hypovolemic Hyponatremia)

• Disruption of the Na-K ATPase (sodium pump) - leading to intracellular influx of sodium and water, reducing effective ECF sodium
• Massive transudation through the burn wound - sodium-rich fluid lost to the wound surface and interstitium (third spacing)
• Insensible losses from disrupted skin barrier are very high - partial-thickness wounds lose free water and Na+ continuously

"In hypovolemic patients, baroreceptors also stimulate the hypothalamus to retain water through ADH release because the homeostatic mechanism for maintaining intravascular volume is stronger than that for maintaining proper sodium concentration." - Sabiston Textbook of Surgery

"Nonrenal causes of hypovolemic hyponatremia include gastrointestinal loss and insensible loss (sweating, burns) of Na+-Cl- and water, in the absence of adequate oral replacement; urine Na+ concentration is typically <20 mM." - Harrison's Principles of Internal Medicine 22E

B) SIADH - Stress-Induced Inappropriate ADH Secretion

• The patient looks euvolemic clinically (but may have interstitial oedema masking true intravascular depletion)
• Urine Na+ is >20 mmol/L, urine osmolality >100 mOsm/kg (inappropriately concentrated)
• Serum osmolality is low (<270 mOsm/kg)

C) Hyperglycaemia-Related (Translational/Pseudo-Hyponatremia) - CRITICAL IN THIS DIABETIC PATIENT

• In severe hyperglycaemia, glucose (an osmotically active solute) draws intracellular water into the ECF, diluting sodium
• This is not true hyponatremia - total body sodium is not low, but the measured Na+ is artificially depressed
• Corrected sodium = Measured Na+ + 1.6 mEq/L for every 100 mg/dL glucose above 100 (Sabiston formula)

"In severe hyperglycemia, osmolality of the ECF rises... Serum sodium concentrations fall in proportion to the dilution caused by hyperglycemia. The measured sodium level is lowered by 1.6 mEq/L for every 100 mg/dL of glucose above 100. That phenomenon is referred to as transitional hyponatremia because no net change in body water occurs. No specific therapy is required other than treating the hyperglycemia." - Sabiston Textbook of Surgery

• Corrected Na+ = 128 + 1.6 × (400-100)/100 = 128 + 4.8 = 132.8 mEq/L

D) Over-Resuscitation with Hypotonic/Inappropriate Fluids

E) Additional Causes in This Patient Profile

Step 2: Diagnostic Workup to Find the Cause

1. Serum osmolality - Calculated vs measured gap (rules out pseudo-hyponatremia)
2. Urine Na+ and Cl- - The most important single test
   • <20 mmol/L = extrarenal loss / hypovolemic (burns losses, dehydration)

   • 20 mmol/L = renal loss or SIADH or diuretics

3. Urine osmolality - If <100 mOsm/kg = primary polydipsia; if >400 = SIADH or volume depletion
4. Blood glucose and serum osmolality - Calculate corrected Na+ (mandatory in this diabetic)
5. Volume status assessment - Clinically examine (skin turgor, JVP, mucous membranes, BP trend), bedside ECHO if available, urine output trend
6. TSH - Hypothyroidism causes euvolemic hyponatremia in elderly women
7. Serum cortisol ± ACTH stimulation test - Adrenal insufficiency (critical illness, burns)
8. Serum K+ - Hyperkalaemia suggests adrenal insufficiency; hypokalaemia suggests SIADH or diuretics
9. Fluid balance chart review - What fluids have been given? Are they appropriate?
10. Renal function (creatinine, urea) - Burns-associated AKI very common

Step 3: Treatment of Persistent Hyponatremia

Correction Rate - Safety First

"Overly rapid correction of hyponatremia (>8-10 mM in 24 h or 18 mM in 48 h) causes hypertonic stress in astrocytes within brain regions prone to ODS, leading to generalized protein ubiquitination and endoplasmic reticulum stress." - Harrison's 22E

Specific Treatments by Cause

Calculating Sodium Deficit (Sabiston Formula)

• TBW = 90 × 0.50 (use 50% for elderly female) = 45 L
• If Na+ = 125 mEq/L, target = 133 mEq/L (8 mEq rise in 24h)
• Sodium deficit = (133 - 125) × 45 = 360 mEq over 24 hours

Fluid Management in Burns (Parkland Formula Reminder)

• First 24 hours: 4 mL × 90 kg × 25% TBSA = 9,000 mL of Ringer's Lactate
• Half (4,500 mL) in first 8 hours from time of burn
• Half (4,500 mL) in next 16 hours

Key Clinical Decision Tree for This Patient

Persistent hyponatremia despite correction
             │
             ▼
    Check blood glucose first
      │                  │
  Hyperglycaemia     Normal glucose
  present?              │
      │           Check volume status
      ▼                  │
  Calculate          ┌──────────────────┐
  corrected Na+      │                  │
  Fix glucose        Hypovolemic    Euvolemic
                     (urine Na<20)  (urine Na>20)
                          │              │
                     IV isotonic    SIADH or
                     saline         adrenal insuff
                                    or hypothyroid
                                         │
                                   fluid restriction
                                   + rule out adrenal
                                   insuff (cortisol)

Special Considerations in This Patient

1. Elderly (67 years): Lower TBW (use 50% body weight), increased risk of ODS with rapid correction, higher risk of adrenal/thyroid dysfunction
2. Diabetic: Always calculate corrected sodium; hyperglycaemia is a very common "hidden" cause of persistent hyponatremia; osmotic diuresis depletes sodium continuously
3. 25% TBSA burns - both lower limbs: Massive ongoing sodium and water losses from wound surface; dressings leach sodium. Once wound starts closing/healing, these losses decrease
4. 90 kg: High resuscitation volumes; monitor for abdominal compartment syndrome if over-resuscitated
5. Hypermetabolic/catabolic state: Burns patients have very high ADH and aldosterone responses - this physiological state persists for weeks