• Clinical science

Sodium disorders

Abstract

Sodium is the most important extracellular cation and plays an important role in maintaining the body's extracellular fluid volume. Sodium imbalances typically reflect a dilution or concentration of extracellular fluid rather than an actual loss or gain of sodium. These changes in extracellular fluid volume are mainly due to an increase or decrease in ADH serum levels (which causes the retention and loss of free water respectively). In certain cases, however, sodium imbalances may be the direct result of sodium loss (e.g., following diarrhea, vomiting, or the use of antidiuretics) or excessive sodium intake. Treating sodium imbalances involves careful correction of the sodium deficit/excess and treating the underlying cause. A rapid correction of sodium imbalance can have damaging osmotic effects such as central pontine myelinolysis.

Definition

References:[1][2][3]

Etiology

Hyponatremia

Hypotonic hyponatremia (↓ serum osmolality)

Isotonic hyponatremia (↔ serum osmolality)

Hypertonic hyponatremia (↑ serum osmolality)

  • Hyperglycemia
  • Use of mannitol
  • Aldosterone
  • ADH
    • Effect: ADH causes water reabsorption and increases thirst.
    • Release of ADH
      • Primary stimulus: increase in serum osmolality (very sensitive even to a 1% change in serum osmolality).
      • Non-osmotic stimulus: A change in extracellular fluid volume by more than 10% (which is sensed by carotid baroreceptors) can also stimulate ADH release.
Types of hyponatremia Subtypes Serum osmolality Etiology
Urine Na+ < 20 mEq/L fractional excretion of sodium < 1% → Extrarenal mechanism Urine Na+ > 20 mEqL fractional excretion of sodium > 1%Renal mechanism
Hypotonic hyponatremia Hypovolemic hypotonic hyponatremia Decreased (↓ total body water, ↓↓ total body sodium)
  • GI loss1 (diarrhea hyponatremia can be worsened with the use of reduced osmolarity ORS, vomiting Patients who have had protracted bouts of vomiting may also present with a high level of urine sodium; Mechanism: severe vomiting may cause concomitant metabolic alkalosiskidneys try to correct alkalosis by eliminating HCO3- in the form of NaHCO3Urine Na+ > 20)
  • Insensible fluid loss1 (burns, sweating)
  • 3rd space fluid loss1 (peritonitis, ascites)
  • Bleeding

Clinical features: hypovolemia and oliguria

Urine osmolality: > 100 mOsmol/kg

Clinical features: hypovolemia + (paradoxical) polyuria

Urine osmolality: > 100 mOsmol/kg

Euvolemic hypotonic hyponatremia Decreased (total body water, ↔ total body sodium)
  • Decreased solute intake
  • Reset osmostat syndrome
  • Water intoxication:
    • Iatrogenic: excessive infusion of hypotonic (e.g., 0.45% NaCl) or sodium-free isotonic (e.g., RL) IV fluids
    • Primary (psychogenic) polydipsia
    • Beer potomania syndrome

Clinical features: minimal/no fluid overload + polyuria

Urine osmolality: < 100 mOsmol/kg

Clinical features: minimal/no fluid overload + oliguria

Urine osmolality: > 100 mOsmol/kg

Hypervolemic hypotonic hyponatremia Decreased (↑↑ total body water, ↑ total body sodium)

A high degree of correlation exists between mortality and hyponatremia in patients with CCF and/or cirrhosis

Mechanism of hyponatremia: The receptors of the renal afferent arteriole sense a decrease in effective arterial volume (due to decreased cardiac output in CCF, due to splanchnic vasodilation in the case of cirrhosis & due to volume contraction in the case of hypoproteinemia. This leads to RAAS activation which causes Na and water reabsorption. Additionally, ADH is released in response to non-osmotic stimuli which causes further water retention. The net effect is greater water retention in excess of sodium which results in hyponatremia.

Clinical features: fluid overload (edema) + oliguria

Urine osmolality: > 100 mOsmol/kg

Clinical features: fluid overload (edema) + oliguria

Urine osmolality: > 100 mOsmol/kg

Isotonic hyponatremia

Normal

Hypertonic hyponatremia

Increased
  • Hyperglycemia1 Na+ levels decrease in a nonlinear fashion in relation to blood glucose levels:
    • 100-250 mg/dL: ↓ of 1.6 mEq/L per 100 mg/dL rise in blood glucose level
    • 250-500 mg/dL: ↓ 4 mEq/L per 100 mg/dL rise
    • 500-1000 mg/dL: ↓ 8 mEq/L per 100 mg/dL rise
    • >1000 mg/dL: ↓ 16 mEq/L per 100 mg/dL rise
  • Use of mannitol1

1can also present with hypernatremia (see below); 2CRF and ARF may present with hypovolemic, euvolemic or hypervolemic hyponatremia

A urine osmolality of 100 mOsmol/L corresponds to a urine specific gravity of 1.003

The clinical presentation may not be so well defined if more than one cause for hyponatremia exists.

Hypernatremia

Hypovolemic hypernatremia

Euvolemic hypernatremia

Hypervolemic hypernatremia

Types of hypernatremia Pathophysiology Etiology

Urine osmolality > 800 mOsmol/kg of H2O or urine specific gravity > 1.025→ Extrarenal mechanism

Urine osmolality < 800 mOsmol/kg of H2O or urine specific gravity < 1.025 → Renal mechanism
Hypovolemic hypernatremia Loss of water in excess of sodium (hypotonic water loss)
  • GI loss1: diarrhea , vomiting, drainage from NG tubes and fistulas
  • ↑ Insensible fluid loss1 (sweating, burns)
  • 3rd space fluid loss1

Clinical features: oliguria + dehydration

Urine Na+: < 20 mEq/L

Clinical features: polyuria + dehydration

Urine Na+: > 20 mEqL

Euvolemic hypernatremia Unreplaced free water loss
  • Lack of access to water: altered mental status, patients in psychiatric wards who have been physically restrained, quadriparesis
  • Impaired thirst mechanism: primary hypodipsia

Clinical features: oliguria + dehydration

Urine Na+: variable

Clinical features: polyuria + dehydration

Urine Na+: variable

Hypervolemic hypernatremia Sodium gain
  • Iatrogenic: excessive infusion of NaHCO3 or hypertonic saline, hemodialysis
  • Drinking sea water

Clinical features:

  • Initially: polyuria + mild fluid overload
  • Later: dehydration

Urine Na+: > 20 mEq/L

Clinical features: normal urine output/mild polyuria + no fluid overload/no dehydration

Urine Na+: > 20 mEq/L

1 can also present with hyponatremia (see above)

References:[4][5][6][3][7]

Clinical features

  • Clinical features are primarily neurological and depend on the severity of the sodium imbalance.
    • Mild symptoms
    • Moderate symptoms
      • Muscle weakness
      • Lethargy
      • Confusion
    • Severe symptoms
  • Symptoms also depend on the onset of sodium imbalance
    • Acute onset (< 48 hours): usually symptomatic event even with mild sodium derangements
    • Subacute or chronic onset (> 48 hours): usually asymptomatic unless severe derangements are present

References:[8][3][7]

Diagnostics

  • Blood tests
  • Urine examination
    • Hyponatremia: urine sodium concentration
      • > 20 mEq/L implies renal sodium loss
      • < 20 mEq/L implies extrarenal sodium loss
        • An exception to this rule occurs when extrarenal sodium loss is present along with metabolic alkalosis (e.g., severe vomiting → loss of acidic gastric contents). In such patients, the kidneys try to correct metabolic acidosis by excreting bicarbonate ions in the form of sodium bicarbonate and the value of urine Na+ may thus be more than 20 mEq/L. In these cases, the following measurements are helpful:
          • Urine Cl-: Urine sodium values usually mirror urine chloride values. ; In the above-mentioned case, however, the value of urine Na+ will be markedly higher than urine Cl-.
          • Fractional sodium excretion (FENa): it remains unaffected (< 1% implies extrarenal cause)
    • Hypernatremia: urine osmolality
      • > 800 mOsmol/kg implies extrarenal water loss
      • < 800 mOsmol/kg implies renal water loss The kidneys continue to excrete water despite a water deficit.

References:[9][10][3][7]

Treatment

General principles

  • Treat underlying cause
  • Patients with serum sodium values < 120 mEq/L or >160 mEq/L require intensive care.
  • Careful correction of sodium levels: maximum correction within 24 hours is 10 mEq/L (rate of correction: 0.5–1 mEq/L per hour)
    • Effects of rapid correction
    • Exception: Faster correction rates (1-2 mEq/L per hour) without exceeding the daily correction limit of 10 mEq/L may be used in the case of:
  • The expected change in the serum sodium levels with the infusion of 1 L of a given solution is estimated by the formula: Δ [Na+] = (Sodium infusate + Potassium infusate - Serum Na+) / (Total body water + 1);
    • Sodium infusate is the amount of sodium present in 1 L of the given solution ;
    • Total body water is estimated by the formula: TBW = k x weight (kg)

Hyponatremia

Hypernatremia

The cornerstone of the management of hypernatremia is correcting the free water deficit.

Slow correction to prevent osmotic cell damage!

References:[3][7]

Complications

Osmotic myelinolysis

The symptoms of pontine myelinolysis and imaging findings appear 2 to 6 days after the correction of hyponatremia!; ; ;

Others

Intracranial hemorrhage

  • Encountered more commonly in the pediatric population
  • Causes (in relation to sodium imbalance):

Cerebral edema

Noncardiogenic pulmonary edema

Rhabdomyolysis

Bone fractures

Elderly people who have chronic hyponatremia are at an increased risk of bone fracture due to a combination of the following:

References:[11]

We list the most important complications. The selection is not exhaustive.