Water excess refers to a pathological state in which excessive water intake or administration leads to water retention in the body, resulting in decreased serum osmolality and increased circulating blood volume. If the excess water enters cells, causing intracellular water excess, the condition is referred to as water intoxication. Both water excess and water intoxication are pathological manifestations of dilutional hyponatremia.
Etiology and Pathogenesis
These conditions often arise due to impaired water regulation mechanisms combined with unrestricted water intake or inappropriate fluid supplementation.
Compensatory Increased Secretion of Antidiuretic Hormone (ADH)
This condition is characterized by elevated capillary hydrostatic pressure and/or decreased colloid osmotic pressure. Although total fluid volume is excessive, the effective circulating blood volume decreases and fluid accumulates in the interstitial spaces. Common causes include right heart failure, constrictive pericarditis, inferior vena cava obstruction, portal vein obstruction, nephrotic syndrome, hypoproteinemia, and liver cirrhosis.
Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH)
SIADH is characterized by a significant increase in total body fluid, an increase in effective circulating blood volume and intracellular fluid, low serum sodium levels, and the absence of edema.
Impaired Renal Water Excretion
This is often seen during the oliguria phase of acute renal failure or acute glomerulonephritis, where reduced renal blood flow and glomerular filtration rate are present without water intake restrictions. Decreased water and sodium filtration rates, along with increased reabsorption in the proximal tubules, lead to reduced water and sodium delivery to the distal tubules. Water excretion difficulties arise, particularly with excessive water intake, although the effective circulating blood volume remains roughly normal.
Adrenal Insufficiency
Insufficient secretion of mineralocorticoids and glucocorticoids reduces glomerular filtration rates. When water intake is excessive, water retention occurs.
Reset Osmotic Threshold
Although renal excretion of water remains normal, the osmotic threshold for the stimulation of ADH secretion is lowered (e.g., during pregnancy), possibly due to increased secretion of human chorionic gonadotropin.
Excessive ADH Administration
This may occur in cases of improper treatment of central diabetes insipidus.
Clinical Manifestations
Acute Water Excess and Water Intoxication
This condition develops rapidly and features prominent neurological symptoms, such as headache, mental disturbances, disorientation, ataxia, seizures, alternating drowsiness and agitation, and even coma. Signs of increased intracranial pressure may also be present, including headache, vomiting, elevated blood pressure, respiratory depression, and bradycardia.
Chronic Water Excess and Water Intoxication
Mild water excess may present only as weight gain. When plasma osmolality drops below 260 mOsm/(kg·H2O) (serum sodium level ≤125 mmol/L), symptoms such as fatigue, a dull expression, nausea, decreased appetite, and subcutaneous tissue swelling may appear. If plasma osmolality falls to 240–250 mOsm/(kg·H2O) (serum sodium level 115–120 mmol/L), neurological symptoms such as headache, drowsiness, confusion, and delirium develop. At plasma osmolality levels of 230 mOsm/(kg·H2O) (serum sodium level 110 mmol/L), seizures or coma may occur. A rapid decrease in serum sodium levels to below 108 mmol/L within 48 hours can lead to permanent neurological damage or death.
Diagnosis and Differential Diagnosis
The diagnosis can be confirmed based on the patient’s medical history, clinical manifestations, and relevant laboratory tests.
Water excess and water intoxication should be differentiated from hyponatremia caused by sodium deficiency. In water excess and water intoxication, urinary sodium levels are typically greater than 20 mmol/L, whereas in sodium-deficient hyponatremia, urinary sodium levels are significantly reduced or undetectable.
Prevention and Treatment
Effective treatment of the underlying conditions, careful monitoring of 24-hour fluid balance, controlling fluid intake, and avoiding excessive fluid administration are measures to prevent the occurrence or worsening of water excess.
Mild Water Excess and Water Intoxication
Fluid intake can be restricted to ensure that intake is less than urinary output. Loop diuretics such as ethacrynic acid or furosemide can be used appropriately.
Acute and Severe Water Excess and Water Intoxication
Priority should be given to protecting cardiac and cerebral functions and correcting the hypotonic state.
Hypervolemic Syndrome
Dehydration is the primary approach to reduce cardiac load. Loop diuretics such as furosemide or ethacrynic acid are considered first-line treatments. Furosemide can be administered orally at 20–60 mg three to four times daily, or in severe cases, intravenously at 20–80 mg every 6 hours. Ethacrynic acid can be administered as 25–50 mg diluted in 40–50 ml of 25% glucose solution and injected slowly intravenously, with repeat doses possible every 2–4 hours as needed. In cases of inadequate effective circulating blood volume, restoring blood volume may be necessary. For critically ill patients, blood ultrafiltration therapy can be considered. Nitroprusside or nitroglycerin can also be used to reduce cardiac load. In confirmed cases of excessive antidiuretic hormone secretion, treatments may include diuretics, demeclocycline, or lithium carbonate alongside etiological management.
Hypotonic Hyponatremia (Especially with Neurological Symptoms)
The intracellular hypotonic state should be corrected promptly. In addition to fluid restriction and diuresis, hypertonic saline solutions (3%–5% sodium chloride) may be used. The typical dosage is 5–10 ml/kg, with close monitoring of cardiac and pulmonary function to adjust the dose and infusion rate. Fractionated administration is generally preferred. During treatment, attention should also focus on correcting abnormalities in potassium metabolism and managing acidosis.