HyponatremiaEdit

Hyponatremia is a common and potentially serious electrolyte disorder characterized by a serum sodium concentration below 135 mmol/L. It reflects an imbalance between water and sodium in the body, usually due to excess water relative to sodium, impaired excretion of free water, or loss of sodium with relatively preserved water. Because brain cells are sensitive to shifts in osmolality, hyponatremia can range from subtle symptoms to life-threatening brain swelling and seizures if it is rapid or severe. It appears across a variety of clinical settings, from hospitalized patients and the elderly to athletes who overconsume fluids during endurance events or individuals taking medications that alter water handling Syndrome of inappropriate antidiuretic hormone secretion and diuretics.

Causes

Excess water intake relative to sodium. This is seen in psychogenic polydipsia, endurance sports, or situations where people drink large volumes of fluid without adequate electrolyte replacement. See Psychogenic polydipsia and Exercise-associated hyponatremia.
Impaired water excretion due to excess antidiuretic hormone activity. This includes the Syndrome of inappropriate antidiuretic hormone secretion and certain medications that promote water retention.
Loss of sodium with preserved or excessive water intake or reduced effective arterial blood volume. This occurs with heart failure, cirrhosis, kidney disease, or certain diuretic therapies, notably Thiazide diuretics.
Medication effects and interactions. Drugs such as Selective serotonin reuptake inhibitors (SSRIs), some Nonsteroidal anti-inflammatory drugs (NSAIDs), and other agents can contribute to hyponatremia in susceptible individuals.
Endocrine and other medical conditions. Adrenal insufficiency, hypothyroidism (less common as a sole cause), and certain renal disorders can predispose to low sodium by changing water handling.

Internal links: Hyponatremia, SIADH, Thiazide diuretics, SSRIs, NSAIDs, Polydipsia.

Pathophysiology

Hyponatremia arises when the body’s water balance dilutes the extracellular sodium. The brain is especially vulnerable to rapid drops in osmolality, which can cause swelling, intracranial pressure changes, and neurologic symptoms. The rate of sodium decline and the duration over which it occurs influence presentation and risk of complications such as osmotic demyelination syndrome with overly rapid correction. Clinicians assess the underlying physiology by evaluating serum osmolality, urine osmolality, and urine sodium to distinguish hypotonic hyponatremia from other forms and to identify the dominant mechanism (water excess, impaired excretion, or solute loss) Osmolality Urine osmolality Urine sodium.

Clinical presentation

Symptoms correlate with acuity and severity. - Mild or chronic: nausea, malaise, and mild confusion. - Moderate: headache, disorientation, lethargy. - Severe or rapidly evolving: vomiting, seizures, coma, or respiratory arrest due to brain edema. Athletes and hospitalized patients may present with different priority concerns, but the central risk remains the same: brain injury if the hyponatremia is corrected too quickly or is particularly severe.

Internal links: Hyponatremia, Seizure.

Diagnosis

A practical approach combines history, physical examination, and targeted laboratory testing: - Serum sodium concentration and serum osmolality to confirm hypotonic hyponatremia. - Assessment of volume status and medications to identify likely etiologies. - Urine studies (urine osmolality and urine sodium) help distinguish SIADH and renal salt handling from other causes. - Evaluation for contributing conditions such as heart failure Heart failure, liver disease Cirrhosis of the liver, and kidney disease. - Consideration of acute versus chronic hyponatremia to guide correction strategy. Internal links: Serum osmolality, Urine osmolality, Urine sodium.

Management

Management depends on symptoms, acuity, and the underlying cause, with a general emphasis on safety, effectiveness, and cost-conscious care. - Acute severe hyponatremia or symptomatic cases (seizures, coma): prompt administration of hypertonic saline (often 3% saline) under close monitoring to raise the serum sodium by a controlled amount, while guarding against overcorrection. - Less urgent or chronic hyponatremia: management focuses on correcting the underlying cause and avoiding rapid changes. This can include fluid restriction, careful salt and dietary management, and treating contributing conditions. - Specific etiologies: - SIADH-related hyponatremia may respond to fluid restriction; in selected cases, vasopressin receptor antagonists (vaptans) or other targeted therapies are considered, balancing efficacy with cost and safety considerations such as hepatotoxicity risk with some agents. - Hypovolemic hyponatremia due to sodium loss may require saline administration to restore volume and correct sodium. - Hypervolemic states (heart failure, cirrhosis) may use a combination of fluid restriction, salt management, diuretics, and treating the underlying disease. - Correction rate safety: aggressive correction can cause osmotic demyelination syndrome. A common guideline is to avoid increasing the sodium by more than roughly 8–12 mmol/L in the first 24 hours, with slower correction over subsequent days in chronic cases. In some high-risk situations, clinicians may use desmopressin to prevent unintended rapid rises during correction and to fine-tune the process. - Sports-related hyponatremia: management includes careful assessment of hydration status, electrolyte replacement, and avoidance of excessive water intake during events; prevention focuses on individualized hydration strategies and education for athletes and coaches.

Internal links: Hypertonic saline, Vasopressin receptor antagonists, Desmopressin, Hyponatremia treatment guidelines.

Controversies and debates

Rate of correction and chronicity. There is ongoing debate about the optimal correction rate for different patient populations. Critics of overly aggressive correction emphasize the risks of osmotic demyelination, while proponents argue for rapid correction in life-threatening presentations. The balance hinges on duration of hyponatremia, symptom severity, and comorbidities.
Use of vaptans. Vasopressin receptor antagonists can correct hyponatremia due to SIADH or euvolemic hyponatremia, but concerns about cost, modest long-term benefit, and rare adverse effects have tempered enthusiasm. Some clinicians reserve vaptans for select patients and fail to see them as a universal solution. See Vaptans for more detail.
Public health guidance versus clinician discretion. While guidelines aim to standardize care and reduce iatrogenic harm, some critics argue that rigid protocols can ignore individual patient contexts, comorbidities, and access-to-care issues. Advocates for physician-led decision-making emphasize tailoring treatment to risk, symptomatology, and patient preferences rather than applying one-size-fits-all rules.
Sports and hydration messaging. In endurance sports, there is debate about the balance between encouraging proper hydration and preventing overhydration that can lead to exercise-associated hyponatremia. Critics warn against overemphasizing extreme hydration protocols at the expense of practical, science-guided guidelines.

Internal links: Osmotic demyelination syndrome, Vaptans, Desmopressin.

Prognosis and outcomes

Hyponatremia is associated with increased morbidity and, in hospitalized patients, higher mortality risk when it is severe or rapidly progressive. Early recognition, accurate etiologic diagnosis, and careful correction tailored to the individual significantly improve outcomes. Prognosis depends on the underlying cause, the speed of onset, and the success of preventing neurological sequelae during treatment.

Internal links: Prognosis.