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Hyponatremia

Last updated: April 7, 2021

Summarytoggle arrow icon

Hyponatremia is a state of low sodium levels (< 135 mEq/L). Sodium is the most important osmotically active particle in the extracellular space and is closely linked to the body's fluid balance. Causes of hyponatremia include dehydration, excessive free water intake (e.g., primary polydipsia), and increased release of ADH causing reabsorption of free water in the kidneys (e.g., SIADH, CHF). The onset can be acute or chronic and symptoms are predominantly neurological and often nonspecific (e.g., nausea, headache, confusion). Investigating the cause of hyponatremia requires consideration of the patient's volume status and renal ability to retain sodium. Some conditions with very high protein (e.g., multiple myeloma) or glucose levels (e.g., DKA) in the blood may result in a laboratory artifact of falsely low serum sodium concentrations (pseudohyponatremia). Treatment involves careful correction of the sodium deficit and/or fluid imbalance. A rapid increase of the serum sodium concentration can have damaging osmotic effects, as seen in osmotic demyelination syndrome.

See the section “Core IM podcast 5 pearls on hyponatremia (episode 1: diagnosis)” for their show notes on this topic.

  • Hyponatremia: reduced serum sodium concentration (< 135 mEq/L)
  • Classification [1]
    • Severity [2]
      • Mild hyponatremia: 130–135 mEq/L
      • Moderate hyponatremia: 125–129 mEq/L
      • Severe hyponatremia (profound): < 125 mEq/L
    • Disease onset [2]
      • Acute hyponatremia: < 48 hours [3]
      • Chronic hyponatremia: ≥ 48 hours or duration unknown [2]
    • Plasma osmolality (see “Etiology”)

Hypotonic hyponatremia [1][4]

Causes of hypotonic hyponatremia
Hypovolemic hypotonic hyponatremia Euvolemic hypotonic hyponatremia Hypervolemic hypotonic hyponatremia
Description
Renal causes
Extrarenal causes

Exercise-associated hyponatremia (EAH) [6]

  • Definition: serum sodium level < 135 mmol/L that occurs during or up to 24 hours after prolonged, intense physical exercise
  • Pathophysiology
    • Excessive intake of water or hypotonic beverages
    • ADH secretion → ↑ solute-free water retention
    • Sodium loss via diaphoresis
  • Clinical features
  • Treatment: fluid restriction PLUS
  • Prevention
    • Limit fluid intake according to thirst
    • Education of individuals at risk (e.g., athletes)

Hypertonic hyponatremia [1][4]

Isotonic hyponatremia [1][4]

Isotonic hyponatremia should always be excluded as a cause of hyponatremia to avoid unnecessarily aggressive treatment.

Clinical features depend on the onset, duration, and severity of hyponatremia. Most patients with chronic hyponatremia are asymptomatic and symptoms typically only occur with serum sodium concentration < 120 mEq/L. [4][8]

Severely symptomatic hyponatremia [4]

Symptoms usually develop acutely (onset < 48 hours). The severity tends to correlate with the extent of cerebral edema.

Mild and moderately symptomatic hyponatremia [4]

Symptoms usually develop slowly (onset > 48 hours) and are typically nonspecific (patients can also be asymptomatic).

Clinical assessment of volume status [1][2]

Evaluation of the volume status is useful to further determine the cause. See also “IV fluids.”

Hypovolemic hyponatremia resulting from extrarenal causes typically manifests with oliguria due to hypovolemia while hypovolemic hyponatremia resulting from renal causes manifests with hypovolemia due to polyuria.

Diagnostic approach to hyponatremia [1][2][4][10]

  1. Confirm hyponatremia: Repeat BMP.
  2. Exclude hyperglycemia: Check serum glucose.
  3. Check the serum osmolality (SOsm): first step in the evaluation of confirmed hyponatremia
  4. Perform focused diagnostic evaluation based on serum osmolality.

If the patient has acute hyponatremia or severe symptoms, proceed directly to treatment.

After confirming hyponatremia, serum osmolality is the most appropriate initial laboratory test to assess the etiology.

Diagnostic evaluation based on serum osmolality

Hypotonic hyponatremia [2][4][10]

The distinction between hypovolemia and euvolemia is usually difficult to make on examination alone; examination findings have low sensitivity and specificity. Many authors recommend focusing on urinary sodium rather than clinical features to distinguish between the two. [1][2][10]

  • Interpretation of UNa and/or FENa : to determine if the cause is renal or extrarenal [10]
Interpretation of diagnostic evaluation in hypotonic hyponatremia [1][4][10]
Volume status Hypovolemic Euvolemic Hypervolemic
Urine sodium
  • < 20–30 mEq/L
  • ≥ 20–30 mEq/L
  • < 20–30 mEq/L
  • ≥ 20–30 mEq/L
  • < 20–30 mEq/L
  • ≥ 20–30 mEq/L
FENa
  • < 1%
  • ≥ 1%
  • < 1%
  • ≥ 1%
  • < 1%
  • ≥ 1%
Urine osmolality
  • > 100 mOsm/kg H2O
  • ≤ 100 mOsm/kg H2O
  • > 100 mOsm/kg H2O
  • > 100 mOsm/kg H2O
Causes (See “Etiology” for more information.)

In patients taking diuretics, urinary sodium concentrations should be interpreted with caution. A FEUa < 12 % can provide more diagnostic accuracy than UNa to differentiate hypovolemia from euvolemia. [10]

Additional tests [1][2][10]

Consider the following based on clinical suspicion:

Hypertonic hyponatremia [4]

Isotonic hyponatremia (pseudohyponatremia) [12][13]

If pseudohyponatremia is suspected, confirm or exclude hyponatremia using direct potentiometry.

Hyponatremia formulas [4]
Formula
Serum osmolality
  • (2 x Na+) + (glucose/18) + (BUN/2.8) + (ethanol/4.6)
Corrected serum sodium concentration for hyperglycemia [15][16]
  • Katz formula: measured Na+ concentration + [0.016 × (serum glucose concentration - 100)]
  • Hillier formula: measured Na+ concentration + [0.024 × (serum glucose concentration - 100)]
Fractional excretion of sodium (FENa) [10][11]
  • (SCreatinine × UNa)/(UCreatinine x SNa) × 100%
Fractional excretion of urea (FEUrea) [17]
  • (UUrea x SCreatinine)/(UCreatinine x SUrea) x 100%
Fractional excretion of uric acid (FEUA) ) [2][10][18]
  • (UUA × SCreatinine)/(UCreatinine × SUA) × 100%
Urine to serum electrolyte ratio [19]
  • (UNa + UK)/SNa
Total body water (TBW) [20]
  • Weight (kg) x k
    • k depends on the age and sex:
      • 0.6 in males
      • 0.5 in females and elderly males
      • 0.45 in elderly females
  • Watson formula
    • Males: 2.447 - 0.09156 x age (years) + 0.1074 x height (in cm) + 0.3362 x weight (in kg)
    • Females: -2.097 + 0.1069 x height (in cm) + 0.2466 x weight (in kg)
Change in sodium concentration [21]
  • Δ [Na+] = [(Sodium infusate + potassium infusate) - Serum Na+)]/(TBW + 1)
    • Sodium infusate is the amount of sodium present in 1 L of the given solution.
    • See “Crystalloid solutions” for the sodium (and potassium) mEq contained in each fluid.
IV fluid rate for correction of hyponatremia (mL/hour) [21]
  • 1000 x (Na+ correction rate in mEq/L/hr)/(change in sodium concentration)

General principles [1]

Alleviate Acute hyponatremia Aggressively and Correct Chronic hyponatremia Carefully!

Once specific treatment is given (e.g., discontinuation of diuretics, corticosteroids for hypocortisolism), there is a high risk of rapid autocorrection causing a dangerous increase in sodium.

Acute hyponatremia and severely symptomatic hyponatremia [1]

The goal of treating acute and/or severely symptomatic hyponatremia is the rapid correction of serum sodium with hypertonic saline to reverse neurological symptoms and prevent brain herniation. Early specialist consultation (intensive care, nephrology) is advised.

  • Indications [1]
  • Initial sodium goal: ↑ serum sodium 1–2 mEq/L/hour until an increase of 4–6 mEq/L has been reached within six hours [1]
  • Regimens for rapid correction
    • Severe symptomatic hyponatremia: hypertonic saline bolus (e.g., 3% NaCl ) [1]
    • Mild to moderate symptomatic hyponatremia: hypertonic saline infusion (e.g., 3% NaCl infusion ) [1]
    • Consider adding desmopressin to prevent overcorrection in patients with sodium < 120 mEq/L [23]
  • Further management and sodium goals: Once the acute sodium goal has been reached, start cause-specific treatment.
  • Monitoring
    • Serial serum sodium measurement
      • While receiving hypertonic saline bolus: every 20 minutes until symptoms resolve [10]
      • After the initial goal is reached: every 2–4 hours, then every 6–12 hours after stabilization [10][19]
    • Monitor urine output closely (e.g., every hour).

If there is any uncertainty about the chronicity of the hyponatremia, maximum sodium correction rates for chronic hyponatremia should not be exceeded in order to avoid the risk of ODS. [1]

Rapid sodium correction of 4–6 mEq/L should be achieved in the first 6 hours of therapy for patients with acute hyponatremia and/or severely symptomatic hyponatremia. [1]

Six in Six hours for Severe Symptoms and Stop [1]

Chronic hyponatremia without severe symptoms [1]

The goal of treating chronic hyponatremia is a slow correction of serum sodium levels to prevent overcorrection and subsequent osmotic cell damage. Treatment depends on the underlying cause (see “Cause-specific treatment” below).

  • Goal: The goal correction rate depends on the risk of ODS (see table).
  • Monitoring: Monitor patients closely for signs of overcorrection (see “Management of sodium overcorrection” below).
    • Monitor urine output closely (e.g., every hour): > 100 mL/hour is concerning for overcorrection. [1]
    • Check serum sodium frequently (at least every 4–6 hours until serum sodium is ≥ 125 mEq/L). [1]
Recommended sodium correction rates for chronic hyponatremia [1][2]
Patients at normal risk for ODS Patients with high-risk factors for ODS
Minimum correction rate (goal)
  • 4–8 mEq/L within 24 hours
  • 4–6 mEq/L within 24 hours
Maximum correction rate (limit)
  • 10–12 mEq/L within 24 hours
  • 18 mEq/L within 48 hours
  • 8 mEq/L within 24 hours

Rapid correction of chronic hyponatremia can cause osmotic demyelination syndrome! Do not exceed hourly or daily maximum correction limits.

In patients with chronic hyponatremia, urine output > 100 mL/hour suggests sodium overcorrection and risk of impending osmotic damage.

Cause-specific treatment [1]

Hypovolemic hyponatremia [1]

Euvolemic hyponatremia [1]

Serum sodium should be monitored every 6–8 hours in patients receiving vaptan therapy in order to identify overcorrection. [1]

Hypervolemic hyponatremia [1]

If hyponatremia persists after diuretic use has been stopped, consider other causes. [10]

Management of sodium overcorrection [1]

  • Initial serum Na+ ≥ 120 mEq/L: Management of overcorrection is probably not necessary. [1]
  • Initial serum Na+ < 120 mEq/L: If the increase in sodium exceeds sodium correction limits (e.g., > 8 mEq/L/24 hours in a patient at high risk for ODS), start treatment to lower serum sodium.
  • Monitor urine output and fluid balance closely (typically every hour).
  • Check serum sodium frequently (e.g., hourly) until sodium goals and limits are achieved. [1]

Correcting hyponatremia too rapidly may cause two complications: From low to high, your pons will die (osmotic demyelination syndrome); from high to low, your brain will blow (cerebral edema).

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

Correcting hyponatremia too rapidly can cause osmotic damage to the axonal myelin sheath in the CNS.

The symptoms and imaging findings of osmotic demyelination syndrome (ODS) first appear several days after the correction of hyponatremia!

AMBOSS has partnered with the popular Core IM podcast to bring you digestible internal medicine content on complex medical topics. In this section, you will find Core IM's 5 clinical pearls on the diagnosis of hyponatremia. Check out their website for the full show notes and listen to our coproduced episode on your favorite podcast platform.

  • Pearl 1: general approach
    • Hyponatremia is a significant clinical problem.
      • The most common electrolyte disorder, occurring in up to 30% of hospitalized patients [28]
      • May result from:
        • Underlying medical conditions
        • Medications
      • Mild chronic hyponatremia is associated with more frequent falls. [29]
    • Understand what each diagnostic test adds vs. rote dependence on algorithms.
    • Patient history and physical examination: may be helpful, but do not ignore other objective data that contradicts them!
      • History
        • Quickly assess for red flags (i.e., confusion, seizures) that require immediate intervention and ICU admission.
        • Ask about dietary history, fluid and alcohol intake, new medications, endocrine ROS, relevant comorbidities.
      • Physical examination
        • Volume status is theoretically helpful, as diagnostic algorithms depend on it, but error-prone. [30]
    • Our approach focuses on understanding what each diagnostic test adds rather than rote dependence on algorithms.
      • More helpful given that most cases of hyponatremia in the hospital are multifactorial [31]
      • Ask yourself where your patient with hyponatremia is located on a “Cartesian space” with:
    • What if we encounter a patient after intervention and with incomplete labs or urine studies?
      • Still obtain appropriate serum and urine studies to assess:
        • Response to interventions
        • Patient’s current ADH/EABV state
  • Pearl 2: serum osmolality
    • Patients with true hyponatremia are expected to have osmolality.
    • Serum osmolality can be thought of as a quality check to verify the hypothesis that low sodium is accompanied by low osmolality, as it should be.
    • Serum osmolality assessment prompts a consideration of effective and ineffective osmoles at play.
      • Effective osmoles do not cross the plasma membrane freely → shifts in water movement (impact tonicity)
      • Most of the clinical complications that arise as a result of hyponatremia (and its correction) are driven by the fact that sodium is an effective osmole that impacts tonicity and, therefore, cell size.
      • Ineffective osmoles cross the plasma membrane more readily and, therefore, do not cause shifts in water movement (do not change tonicity).
    • Serum osmolarity is not a serially measured lab! Measure it once, unless you are following clearance of an unmeasured osmole (such as a toxic alcohol) or if there is a significant sodium change that is difficult to contextualize.
  • Pearl 3: Urine osmolality (UOsm) acts as a window into ADH activity.
    • UOsm is the nearest to a direct measure of ADH activity in clinical practice. [2][35]
    • If ADH is not active, the result is dilute urine (↓ UOsm).
      • Low UOsm on presentation indicates:
        • Too little solute to keep up with normal fluid intake (“tea-toast syndrome”) [36]
        • Too much fluid despite normal solute intake (primary polydipsia) [37][38]
        • Some combination of low solute and high intake of hypoosmolar fluid (beer potomania) [39]
      • Low UOsm can also occur in the setting of acute illness, in which many patients will push large volumes of hypotonic fluids (i.e., sports drinks) in the setting of GI losses.
    • The story of hyponatremia is often the story of ADH activity. [40]
      • ADH activity is reflected by ↑ UOsm in patients with hyponatremia.
      • If ADH is present: Figure out if this is because of EABV, osmolality, or is independent of physiological stimulus (see “Pearl 4”).
    • Remember that renal insufficiency impacts our ability to maximally dilute urine. [41]
    • Changes in UOsm (and urine output) can be assessed serially to evaluate treatment response.
      • If urine osmolality gently declines with an intervention (e.g., volume resuscitation): Your intervention has resulted in suppression of ADH (proving the hypothesis).
      • Heads up! If urine output and UOsm change dramatically in response to an intervention, this may be an early indicator that a patient is correcting too quickly!
  • Pearl 4: Urine sodium (UNa), fractional excretion of sodium (FeNa), and fractional excretion of urea (FeUrea) reveal RAAS activity.
    • UOsm acts as a window into ADH activity at a given time; it does not tell us why ADH is activated.
      • Physiological (appropriate) ADH activity can occur in the following circumstances:
      • ADH activity that is not stimulated by one of the above mechanisms is by definition inappropriate. [44]
    • UNa provides a window into the activity of renin-angiotensin-aldosterone, which is more sensitive than ADH to EABV states. [45]
    • In patients with intermediate UNa , FeNa is more sensitive than UNa for reflecting EABV. [46]
      • ↓ FeNa: RAAS is active, EABV
      • Validated in oliguric patients; less reliable in patients producing large quantities of dilute urine
    • Caveats to UNa and FeNa use [2]
      • Use of diuretics (thiazide or loop) increases UNa, in which case, FeUrea is a reasonable surrogate (↓ FeNa PLUS FeUrea is better than either alone). [46]
      • CKD impairs Na reabsorption, making UNa less helpful in this patient group.
      • UNa will be low in patients with ↓ Na diets (rare in the US).
  • Pearl 5: A low serum uric acid can be helpful when considering SIADH (in order words, it points away from hypovolemic states)

Subscribe to the Core IM podcast below in “Tips and links.”

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