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SODIUM ABNOMALITIES

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HYPONATREMIA

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  • Serum sodium (SNa) < 135 mEq/L (mmol/L)

  • Prevalence: Up to 40% of pediatric inpatients, often iatrogenic from hypotonic IV fluid

    • Severe symptoms, morbidity, mortality with rapid SNa decline (>1 mEq/hr)

  • Pathophysiology: Osmolality of serum largely dependent on sodium, regulated by antidiuretic hormone (ADH), thirst mechanisms

    • In hyponatremia, normal regulatory mechanisms fail to maintain homeostasis

      • Resultant water/sodium imbalance results in hypotonic serum, regardless of total body water, sodium content

  • Etiology: Causes of abnormal sodium levels can be differentiated by the total body sodium level (high or low), the response of ADH, and the volume status of the patient (see Table 49-1)

    • Factitious, pseudohyponatremia

      • Hyperglycemia creates an osmotic gradient in plasma favoring extracellular water shift out of the cells

      • SNa “diluted” by ≈2 mEq/L for each 100 mg/dL rise in glucose

    • Normal body sodium

      • Syndrome of inappropriate antidiuretic hormone (SIADH): ADH inappropriately high , patient is typically euvolemic

        • Caused by many medications, pulmonary infections, increased intrathoracic pressure from mechanical ventilation, oncologic processes

      • Water intoxication (psychogenic polydipsia): ADH appropriately low , patient is typically euvolemic

    • Decreased body sodium

      • ADH appropriately elevated as the patient is hypovolemic from:

        • Gastrointestinal (GI) tract losses (vomiting, diarrhea)

        • Sepsis

        • Diuretics

        • Salt wasting: Kidney (renal tubule, concentrating defects), central nervous system (injury may alter sympathetic input to kidney), adrenal insufficiency (e.g., 21-hydroxylase deficiency)

        • Drain output (e.g., external ventricular drain [EVD])

    • Increased body sodium

      • ADH appropriately decreased as the patient is hypervolemic

        • Congestive heart failure, renal failure

        • Nephrotic syndrome

  • Clinical signs and symptoms:

    • Acute hyponatremia

      • Rate of decline dictates symptoms more than specific SNa

        • No time for compensation mechanisms to deploy

        • Cannot offset intracellular water shifts

      • Seizures, lethargy, headache, cerebral edema

    • Chronic hyponatremia

      • Hyponatremia for >24 hours and/or developing over days

      • Compensatory mechanisms change intracellular osmolality, can mitigate risk of cerebral edema

      • Vague neurological, GI symptoms (irritability, fatigue, vomiting)

  • Treatment:

    • Key elements: Tailor therapy to severity of symptoms, underlying cause(s)

    • Severe central nervous system (CNS) symptoms (seizures)

      • 3% NaCl to quickly raise SNa to ≈ 125 mEq/L (or lower if symptoms abate)

      • Rapid creation of osmolar gradient favors extracellular water reducing intracellular edema

    • Shock/hemodynamic instability

      • 0.9% NaCl to quickly expand intravascular volume, re-establish blood and oxygen delivery to vital organs

    • Factitious hyponatremia

      • Treat primary disease process (e.g. insulin infusion for diabetic ketoacidosis [DKA])

    • Normal total body sodium, euvolemia (SIADH)

      • Fluid restriction to ≈1/3 to 2/3 of hourly maintenance rate

      • Avoid hypotonic fluids

    • Decreased total body sodium, hypovolemia

      • Calculate sodium deficit

        (DesiredserumNaActualserumNa)×0.6×Weight(kg)

      • Must consider maintenance needs and any ongoing losses in calculations

        • Maintenance sodium needs ≈ 2 to 3 mEq/100 mL fluid

      • Replace with 0.9 normal saline (NS) (154 mEq/L) or 3% saline (513 mEq/L) depending on venous access and symptoms

      • Raise SNa by NO MORE THAN 0.5 to 1 mEq/hr

        • Correcting too rapidly can cause central pontine myelinolysis

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