The Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) occurs when the body produces excessive antidiuretic hormone (ADH), also known as vasopressin. ADH regulates water balance, and its overproduction causes the kidneys to retain too much water. This excess water dilutes the body’s sodium, resulting in hyponatremia (low blood sodium concentration). Supportive therapy focuses on safely correcting this sodium imbalance and managing fluid retention, rather than curing the underlying cause. This management is essential because severe hyponatremia can lead to serious neurological symptoms like confusion, seizures, and coma.
The Cornerstone of SIADH Management: Fluid Restriction
Fluid restriction is the initial and most common supportive therapy for patients with mild to moderate SIADH. The goal is to reduce total water intake so the body can excrete retained water and correct dilutional hyponatremia. Typical restriction levels range from 800 to 1200 milliliters of total fluid intake per day, including all beverages.
Clinicians determine the appropriate level by assessing the patient’s sodium concentration and water excretion ability. This restriction forces the body into a negative water balance, where daily intake is less than water lost through urine and insensible losses. This strategy directly combats the water retention diluting the sodium level.
Patient adherence is a significant challenge, as restricting fluid intake below one liter per day can be difficult to tolerate long-term. Fluid restriction may not be sufficient alone to raise sodium levels to a safe range for many patients, often requiring additional measures.
Enhancing Sodium Levels Through Oral Supplementation
When fluid restriction alone does not adequately correct hyponatremia, increasing the patient’s solute load is the next step. This involves increasing the substances the body must excrete, obligating the kidneys to excrete more water. Solute increase can be achieved through dietary adjustments or oral supplements.
A simple method is encouraging a higher intake of dietary salt and protein, which contribute to the total solute load. A more direct approach uses oral sodium chloride tablets, providing a measured dose of sodium to raise blood concentration. Standard dosing is often around 100 milliequivalents three times daily, used as an adjunct to continued fluid restriction.
Oral supplementation is a non-invasive way to manage chronic SIADH, especially for elderly patients. Oral salt tablets safely increase serum sodium over time, but they must be combined with fluid restriction.
Pharmacological Interventions for Refractory SIADH
For severe or chronic SIADH that does not respond to fluid restriction and oral supplementation, pharmacological interventions are necessary. Specific treatments include Vaptans, such as Tolvaptan, which are vasopressin receptor antagonists. These medications block ADH action at the kidney’s V2 receptors, promoting free water excretion without significant electrolyte loss, a process called aquaresis.
Tolvaptan is an oral medication typically started at 15 milligrams daily and can be titrated for effect. When Vaptans are used, fluid restriction is often discontinued to prevent overly rapid sodium correction. Oral Urea is another option, acting as a non-toxic osmotic agent to increase solute load and induce water diuresis. Urea is usually administered around 30 grams daily and is effective for patients with chronic hyponatremia.
A third strategy combines a loop diuretic, such as Furosemide, with high salt intake. Loop diuretics increase free water excretion, and concurrent salt intake replaces sodium lost in the urine, avoiding net sodium loss. In acute, severe hyponatremia with neurological symptoms, patients may require intravenous 3% hypertonic saline solution. This concentrated salt solution is administered only in a hospital setting with close monitoring to rapidly raise the sodium level and prevent cerebral edema.
Essential Safety Measures During Treatment
The primary safety concern during SIADH treatment is correcting the serum sodium concentration too quickly. Rapid correction can lead to Osmotic Demyelination Syndrome (ODS), previously called central pontine myelinolysis. ODS results from the rapid shrinkage of brain cells as water moves out, causing demyelination and permanent neurological deficits.
Treatment protocols strictly limit the rate of sodium increase to a maximum of 8 to 10 milliequivalents per liter over any 24-hour period. For patients with risk factors, such as malnutrition or alcoholism, the correction rate may be limited further to 4 to 6 milliequivalents per liter per day. Strict monitoring is mandatory, especially in the first 24 to 48 hours, often requiring blood tests every four to six hours.
If the sodium level rises too quickly, corrective action must be taken immediately to slow the rate. This reactive strategy often involves administering free water, such as 5% dextrose in water, orally or intravenously to dilute the sodium concentration. Adherence to strict correction limits is essential for safely managing SIADH and preventing patient harm.