Overview
Definition:
Electrolyte disturbances in preterm infants, particularly sodium balance, are common due to immature renal function, increased insensible water losses, and therapeutic interventions like diuretics
Sodium is critical for extracellular fluid volume, osmotic pressure, and acid-base balance
Diuretics, often used for conditions like patent ductus arteriosus (PDA) or fluid overload, can significantly impact sodium homeostasis.
Epidemiology:
Hyponatremia is the most frequent electrolyte abnormality in preterm infants, affecting up to 50% of very low birth weight (VLBW) neonates
Hypernatremia is less common but carries higher morbidity
Diuretic use, especially in VLBW infants for PDA or pulmonary edema, is associated with a higher incidence of both hyponatremia and hypernatremia.
Clinical Significance:
Improper management of sodium balance and diuretic therapy in preterms can lead to serious complications, including neurological deficits (seizures, cerebral palsy), growth restriction, renal injury, and increased mortality
Understanding these dynamics is vital for optimizing fluid and electrolyte management and improving outcomes for these vulnerable infants.
Sodium Balance In Preterms
Renal Immaturity:
Immature renal tubules have reduced capacity for sodium reabsorption, leading to significant sodium wasting, especially in early postnatal life
Glomerular filtration rate (GFR) and tubular function mature gradually.
High Insensible Losses:
Preterm infants have a large surface area to volume ratio and thin stratum corneum, resulting in high transepidermal water losses
This can lead to relative hypernatremia if fluid intake is insufficient to compensate for water losses.
Hormonal Influences:
Antidiuretic hormone (ADH) regulation is immature, affecting water balance
Aldosterone production is also less efficient, contributing to sodium loss.
Nutritional Factors:
Early enteral feeds may be low in sodium
Parenteral nutrition formulations require careful adjustment of sodium content to meet needs
Breast milk sodium content can vary.
Therapeutic Interventions:
Diuretics, fluid resuscitation, and certain medications can profoundly affect sodium levels, requiring close monitoring.
Hyponatremia In Preterms
Definition And Types:
Hyponatremia is defined as serum sodium < 135 mEq/L
It can be further classified as isotonic (rare), hypotonic (most common), or hypertonic
Hypotonic hyponatremia is typically due to excessive free water retention or sodium loss.
Causes:
Excessive free water intake
Renal sodium wasting (immature tubules, diuretic use)
Syndrome of Inappropriate Antidiuretic Hormone (SIADH) (rare in neonates but can be iatrogenic)
Vomiting or nasogastric losses without adequate sodium replacement.
Clinical Presentation:
Mild hyponatremia may be asymptomatic
Symptoms are often non-specific: lethargy
Irritability
Poor feeding
Hypotonia
Vomiting
Seizures (severe hyponatremia)
Cerebral edema with rapid correction.
Diagnostic Approach:
Review fluid intake and output
Assess for signs of dehydration or fluid overload
Serum electrolytes (sodium, potassium, chloride, bicarbonate)
Urine electrolytes and osmolality
Assess for underlying causes like PDA or infection.
Hypernatremia In Preterms
Definition And Types:
Hypernatremia is defined as serum sodium > 145 mEq/L
It is usually hypertonic and reflects a deficit of free water relative to sodium.
Causes:
Insensible water losses exceeding intake (high ambient temperature, radiant warmers, phototherapy, tachypnea)
Insufficient fluid intake
Diuretic therapy (especially thiazides or loop diuretics)
Osmotic diuresis (e.g., from excessive protein or glucose administration)
Inadequate sodium supplementation in preterm formula.
Clinical Presentation:
Irritability
High-pitched cry
Lethargy
Muscle twitching
Fever
Dry mucous membranes
Poor skin turgor
Fontanelle may be sunken
Severe hypernatremia can lead to lethargy, coma, seizures, intracranial hemorrhage, and death.
Diagnostic Approach:
Careful assessment of fluid balance (insensible losses, intake)
Review all fluid and electrolyte orders
Serum electrolytes
Urine specific gravity and osmolality
Assess for underlying conditions contributing to water loss.
Diuretics And Sodium Balance
Common Diuretics Used:
Furosemide (loop diuretic): inhibits Na-K-2Cl cotransporter in the thick ascending limb of Henle's loop, leading to significant sodium, potassium, and chloride excretion
Thiazide diuretics (e.g., hydrochlorothiazide): inhibit Na-Cl cotransporter in the distal convoluted tubule
less potent than loop diuretics but can cause significant sodium and potassium loss
Spironolactone (potassium-sparing): acts as an aldosterone antagonist
used cautiously due to risk of hyperkalemia and to counteract other diuretic-induced potassium losses.
Indications In Preterms:
Management of fluid overload (pulmonary edema, ascites)
Closure of PDA (primarily furosemide in conjunction with indomethacin/ibuprofen)
Treatment of respiratory distress syndrome (RDS) with severe atelectasis.
Impact On Sodium:
Furosemide and thiazides can exacerbate sodium wasting, leading to hyponatremia
They can also impair the kidney's ability to concentrate urine, potentially contributing to water retention and hyponatremia if free water intake is not carefully controlled
Paradoxically, in conditions of severe dehydration or excessive water intake, diuretics can unmask or worsen hypernatremia by promoting water loss.
Monitoring During Diuretic Therapy:
Frequent monitoring of serum electrolytes (sodium, potassium), renal function (BUN, creatinine), and fluid balance is essential
Monitor urine output and urine electrolytes
Assess for clinical signs of hyponatremia or hypernatremia.
Management Principles
General Approach:
Management is guided by the specific electrolyte disturbance, its severity, and the underlying cause
Gradual correction is crucial to prevent complications like osmotic demyelination syndrome (with rapid correction of hyponatremia) or cerebral edema (with rapid correction of hypernatremia).
Hyponatremia Management:
Mild, asymptomatic hyponatremia: Fluid restriction
Assess and correct underlying causes (e.g., optimize fluid intake if sodium wasting is the primary issue)
Symptomatic or severe hyponatremia: Careful, slow intravenous correction with hypertonic saline (e.g., 3% NaCl) targeting a rise of no more than 0.5 mEq/L/hr or 10-12 mEq/L over 24 hours
Avoid rapid correction to prevent central pontine myelinolysis
Consider oral salt supplementation if feeds are tolerated.
Hypernatremia Management:
Gradual free water replacement is key
Intravenous fluids with low sodium concentration (e.g., D5W or D10W) or hypotonic saline (e.g., 0.45% NaCl)
Target a reduction of no more than 10-12 mEq/L/day to prevent cerebral edema
Monitor neurological status closely
If due to excessive insensible losses, address the environmental factors (e.g., humidity, temperature).
Diuretic Adjustment:
Consider reducing the dose or discontinuing diuretics if electrolyte disturbances are severe and attributable to their use
If diuretics are essential, use the lowest effective dose and monitor electrolytes closely
Co-administration of potassium-sparing diuretics like spironolactone may sometimes be considered to mitigate potassium losses and potentially improve sodium retention, but requires careful monitoring for hyperkalemia.
Key Points
Exam Focus:
Preterm infants have immature kidneys predisposing to sodium wasting
Diuretics, particularly furosemide, are a major iatrogenic cause of electrolyte imbalances
Hyponatremia is common
hypernatremia is less common but more dangerous
Gradual correction of both hyponatremia and hypernatremia is paramount to avoid neurological complications.
Clinical Pearls:
Always calculate total fluid intake and output, including insensible losses, when assessing electrolyte status
Monitor urine sodium concentration to differentiate renal from extra-renal sodium losses
Consider the timing and type of fluid administration in relation to diuretic use
Be cautious with free water boluses in hypernatremic infants, especially if there is suspicion of rapid onset.
Common Mistakes:
Over-vigorous free water administration leading to hyponatremia or cerebral edema
Rapid correction of severe hyponatremia leading to osmotic demyelination syndrome
Failure to account for insensible water losses in preterm infants
Inadequate monitoring of electrolytes and fluid balance during diuretic therapy.