DESCRIPTION

• Hyponatremia is defined as serum sodium (Na⁺) <135 mEq/L, and severity is graded according to the level:
  • Mild hyponatremia (130 to 134 mEq/L)
  • Moderate hyponatremia (120 to 129 mEq/L)
  • Severe hyponatremia (<120 mEq/L)
• Even mild hyponatremia 130 to 134 mEq/L has measurable effects on cognitive function, and severe hyponatremia can lead to seizures, brain edema, and death.
• Hyponatremia can be further divided into acute versus chronic hyponatremia:
  • Acute: develops over a period of <48 hours
  • Chronic: present for >48 hours
• Hyponatremia can be factitious in the setting of significantly elevated blood glucose.

EPIDEMIOLOGY

• Hyponatremia is common in the inpatient setting.
• The incidence for moderate to severe hyponatremia (<130 mEq/L) is 1% of hospitalized pediatric patients, and mild hyponatremia is present in up to 45% of pediatric patients admitted for community-acquired pneumonia.
• Levels <125 mEq/L are often associated with clinical symptoms.

ETIOLOGY

• Hyponatremia is usually divided into three classifications: (i) hypervolemic hyponatremia (e.g., nephrotic syndrome, cirrhosis, heart failure), (ii) euvolemic hyponatremia (e.g., syndrome of inappropriate antidiuretic hormone secretion [SIADH], primary polydipsia), and (iii) hypovolemic hyponatremia (e.g., gastrointestinal (GI) losses, diuretic use, intense exercise).
• Hyponatremia with increased tonicity: presence of endogenous (e.g., hyperglycemia and urea) and exogenous osmoles (e.g., mannitol, sorbitol); the measured serum Na1 is reduced by 1.6 mmol/L for every 100 mg/dL increase in blood glucose.
• Pseudohyponatremia: hyperlipidemia, hyperglycemia, and hyperproteinemia
• The most common reason for hyponatremia in hospitalized patients is SIADH.
• The most common cause in the general pediatric population is extrarenal losses including diarrhea and vomiting.

RISK FACTORS

• Conditions associated with SIADH including nausea, hypotension, hypovolemia, reduced circulatory volume (congestive heart failure [CHF], nephrosis, and cirrhosis), brain injury/infection, immobilization, asthma, pneumonia, mechanical ventilation, fever, stress, pain, and specific medications (narcotics, nonsteroidal anti-inflammatory drugs, serotonin reuptake inhibitors, chemotherapeutics, and antiviral medications)
• Excess sodium loss can be seen in disorders with increased renal (e.g., cerebral salt wasting or primary tubular disorders [Bartter or Gitelman syndrome]) or skin Na⁺ loss (e.g., cystic fibrosis) and salt loosing nephropathy such as obstructive uropathy or bilateral renal dysplastic kidneys.
• Conditions associated with increased stool losses (diarrhea, vomiting, loss of gastrointestinal fluids—surgical or tube drainage) increase the risk of developing hyponatremia.
• Excessive water intake such as in polydipsia or incorrectly mixed formula
• Decreased water excretion such as acute kidney injury
• Lipid emulsion administration may cause pseudohyponatremia due to lipemic blood sample which interferences with measurement of sodium level.
• Prematurity due to decreased tubular reabsorption of sodium in the setting of tubular immaturity and decreased responsiveness to aldosterone

GENERAL PREVENTION

Providing adequate Na⁺ intake and checking serum Na⁺ levels in high-risk patients (GI fluid losses and high risk for SIADH) is the most important step in prevention of severe hyponatremia.

PATHOPHYSIOLOGY

• Sodium is the major extracellular cation and is important osmole in the extracellular space.
  • A positive Na⁺ balance is required for growth.
  • Serum Na⁺ levels reflect extracellular Na⁺ and are tightly regulated within a narrow range (generally 135 to 145 mEq/L).
  • Approximately 2/3 of body mass is Na⁺-containing extracellular fluid space.
• There are three major mechanisms affecting serum Na⁺ levels: intake, excretion, and total body water. Hyponatremia can develop due to following reasons:
  • Reduced intake of Na⁺
  • Increased losses (Gl, renal, or skin)
  • Increased total body water or excess free water retention
• Hyponatremic encephalopathy results from hypoosmolality in the extracellular space and the influx of water into the intracellular space down the concentration gradient, resulting in parenchyma brain swelling and resulting symptoms.