Hyponatremia Overview and Etiology

Hyponatremia

• Defined as a decreased sodium concentration in the blood, typically below 135 mEq/L.
• Inverse relationship between brain water and sodium concentration; higher brain water leads to lower sodium.
• Acute hyponatremia develops rapidly (hours), is dangerous, and can be fatal.
• Chronic hyponatremia develops over days or weeks, symptoms are less severe or may be absent.
• Brain adapts to chronic hyponatremia by losing organic solutes to maintain osmolality.
• Treatment depends on the type (acute vs. chronic). Acute needs prompt treatment, chronic needs careful correction to avoid osmotic demyelination.
• Maintaining constant plasma sodium concentration is crucial for cell volume, especially in the brain.
• Hyponatremia often results from water imbalance, related to AVP secretion and thirst.

Etiology of Hyponatremia

• Water retention: Abnormal renal water excretion.
• Sodium loss: Inability to reabsorb sodium.
  • Normal subjects: Water ingestion reduces plasma osmolality, lowering AVP, allowing excess water excretion.
  • Lack of AVP: Urine osmolality can drop to 40-100 mOsm/kg.
• High AVP levels: (without renal failure) can dilute sodium concentration. Common causes of sustained AVP release:
  • Effective circulating volume depletion: Congestive heart failure (CHF) can cause decreased cardiac output, despite potential volume overload.
    • Body senses low volume and releases hormones like renin, norepinephrine, and AVP increasing volume.
  • Syndrome of Inappropriate Antidiuretic Hormone (SIADH): Inappropriate AVP/ADH release.
    • Common with neurological disease, malignancy, post-major surgery, certain drugs.

Diagnosis of Hyponatremia

• Patient history, physical exam, and laboratory tests.
• Laboratory Tests:
  • Plasma sodium concentration to rule out kidney issues.
  • Adrenal and thyroid function to assess for endocrine problems.
  • Plasma osmolality, urine osmolality, and urine sodium concentration.

Plasma Osmolality

• True hyponatremia leads to a proportional reduction in plasma osmolality.
• Exceptions include conditions where plasma osmolality is normal or elevated but the patient still has hyponatremia. (e.g., uncontrolled diabetes where high glucose increases the overall osmolality, but sodium may still be low).

Treatment Considerations

• Other medical conditions need assessment and treatment, such as hyperglycemia.
• Normal plasma osmolality around 280-290 mOsm/kg. Hyponatremia is usually below 280 mOsm/kg.

Polyuria

• Excessive urine production.
• Causes:
  • Osmotic diuresis: Glucose pulling water into urine (e.g., uncontrolled diabetes).
  • Water diuresis: Urine osmolality less than plasma—AVP not working efficiently, so water is not reabsorbed.

Causes of Water Diuresis

• Decreased AVP production (central diabetes insipidus).
• Reduced renal response to AVP (nephrogenic diabetes insipidus).
• Other factors: Chronic lithium use, hypercalcemia, excessive water intake.

Hypernatremia

• Defined as a plasma sodium concentration above 145-147 mEq/L.
• Associated with hyperosmolality.
• Causes:
  • Water loss: Insensible/sweat losses (fever, respiration), urinary losses (diabetes insipidus, osmotic diuresis), GI losses, actual salt intake, hypertonic saline intake.
  • Impaired thirst mechanisms.
• Body's defense: Increased AVP and thirst.

Diabetes Mellitus and Hypernatremia

• Uncontrolled diabetes can lead to osmotic diuresis (causing hypernatremia).
• Hyperglycemia can trigger hyponatremia (water shifts from cells to blood).
• Both hyponatremia and hypernatremia are possible with uncontrolled diabetes, depending on the balance between water and sodium loss/gain.

Osmotic Diuresis

• Substances causing osmotic diuresis move water to the urine, lowering plasma volume and concentrating sodium, leading to hypernatremia.

Diagnosis of Hypernatremia

• Identify cause (too much salt, too little water, or water loss).
• History (infections, vomiting, diarrhea, diabetes status).
  • Plasma and urine glucose levels, urine osmolality measure AVP function.
• Normal response to hypernatremia: increased AVP, concentrated urine (1000-1200 mOsm/kg).
  • Low urine osmolality compared to plasma = AVP issues (central or nephrogenic).

Central vs. Nephrogenic Diabetes Insipidus

• Central: Brain does not produce AVP.
• Nephrogenic: Kidneys do not respond to AVP.
• Differentiate using synthetic AVP (DDAVP):
  • Increased urine osmolality with DDAVP = central problem.
  • No change in urine osmolality = nephrogenic problem.

Polyuria (Excessive Water Intake)

• Excessive water intake dilutes plasma sodium (hyponatremia).
• Inhibits AVP release, resulting in dilute urine.