DRG Category: 644
Mean LOS: 4.3 days
Description: Medical: Endocrine Disorders With Complication or Comorbidity
Syndrome of inappropriate antidiuretic hormone (SIADH), a disorder of the posterior pituitary gland, is a condition of excessive release of antidiuretic hormone (ADH) that results in excessive water retention and hyponatremia. Hyponatremia is the most common electrolyte imbalance that occurs while patients are in the hospital, and SIADH is a common cause. SIADH occurs when ADH secretion is activated by factors other than hyperosmolarity (increased concentration of solutes in the blood) or hypovolemia (decreased blood volume), which usually controls ADH secretion. The excess ADH secretion increases renal tubular permeability and reabsorption of water into the circulation, resulting in excess extracellular fluid volume, reduced plasma osmolality, decreased serum sodium levels, and increased glomerular filtration rates. The hyponatremia in this syndrome is not related to sodium loss but rather to water excess and the movement of water into the brain. In the process, brain cells lose potassium and amino acids. Without treatment, SIADH can lead to life-threatening complications. Water intoxication accompanied by sodium deficit and cerebral edema lead to complications such as seizures, coma, and death.
Several conditions contribute to SIADH. Central nervous system (CNS) responses to fear, pain, psychoses, and acute distress are known to increase the rate of ADH secretion by the posterior pituitary gland. Physiological conditions that increase intracranial pressure, such as acute CNS infections, brain trauma, anoxic brain death, stroke, and brain surgery, may lead to SIADH. Other conditions associated with SIADH include peripheral neuropathy, delirium tremens, and Addison disease. Certain medications, such as analgesics, anesthetics, thiazide diuretics, opiates, chlorpropramide, carbamezapine, vincristine, and nicotine, are also associated with SIADH. Some tumors have been associated with ADH production, such as cancer of the lungs, pancreas, and prostate as well as Hodgkin disease. Risk factors include head trauma, stroke, cardiopulmonary arrest, cancer of the lung, pneumonia, positive pressure ventilation, meningitis, alcohol withdrawal, low body weight, and certain medications (as listed previously).
Both children and adults are at risk, but being a hospitalized patient over age 30 years is a risk factor, as is low body weight, which may result in more women than men being affected. Women are also are more affected by drug-induced and exercise-induced hyponatremia than men, who are more prone to develop mild hyponatremia. Typical childhood conditions that can lead to SIADH include pneumonia, meningitis, head trauma, and subarachnoid bleeding. In adults, the condition is most commonly associated with CNS disorders. The very old and very young develop symptoms with smaller decreases in serum sodium levels than adults.
ASSESSMENT
History
Because SIADH is usually hospital acquired, the condition is noted because of hyponatremia found in laboratory testing. Given the serious nature of the related causes, often the patient will have urinary output monitored hourly. Ask if the patient has experienced alterations in urinary patterns. Question the patient about recent weight gain. Signs of sodium deficit generally occur slowly. Ask if the patient has experienced recent signs of hyponatremia such as fatigue, weakness, nausea, anorexia, or headaches.
The most common sign of SIADH is a dropping serum sodium level. Often no clinical signs are obvious, and the severity of symptoms does not always correlate with the degree of hyponatremia. Late signs include nausea, vomiting, muscle weakness, decreased reaction time, irritability, decreased level of consciousness, seizures, and even coma. Note that the most severe, life-threatening signs of SIADH are not fluid overload and pulmonary congestion but rather the CNS effects from acute sodium deficiency. Perform a neurological assessment to determine if the patient has experienced changes in the level of consciousness, which can range from confusion to seizure activity. Life-threatening symptoms such as seizures may indicate acute water excess, whereas nausea, muscle twitching, headache, and weight gain are more indicative of chronic water accumulation.
Psychosocial
The family and significant others may be fearful if the patient has experienced CNS changes that alter behavior and alertness. If the patient has had seizures, note that family members may have many questions. The patient's and family's responses to SIADH are often a reflection of their responses to these other conditions, which are important to consider in any evaluation of patient and family coping.
Test | Normal Result | Abnormality With Condition | Explanation |
---|---|---|---|
Urine osmolality (osmolality refers to a solution's concentration of solute particles per kilogram of solvent) | 200–1,200 mOsm/L | >100 mOsm/L | Excretion of inappropriately concentrated urine and hyponatremia caused by overproduction of ADH |
Blood osmolality | 275–295 mOsm/L | <275 mOsm/L | Sodium loss in urine and water intoxication lead to hemodilution |
Serum sodium | 135–145 mEq/L | <120 mEq/L | Sodium loss in the urine leads to hyponatremia and hemodilution |
Urine sodium | <20 mEq/L | >40 mEq/L | Sodium loss in the urine |
Other Tests: Blood urea nitrogen, urine specific gravity, serum electrolytes, plasma cortisol, computed tomography of head, radioimmunoassay of ADH
Diagnosis
DiagnosisExcess fluid volume related to retention of free water as evidenced by fatigue, weakness, nausea, anorexia, and/or headache
Outcomes
OutcomesFluid balance; Hydration; Electrolyte balance; Circulation status; Cardiac pump effectiveness; Knowledge: Disease process; Knowledge: Medication
PLANNING AND IMPLEMENTATION
Restoration of normal electrolyte and fluid balance and normal body fluid concentration are the treatment goals. Treatment involves correction of the underlying cause and correction of hyponatremia. If the patient's life is not in danger from airway compromise or severe hyponatremia, the physician often restricts fluids initially to 600 to 800 mL or less per 24 hours. With fluid restriction, the hormone aldosterone is released by the adrenal gland and the patient begins to conserve sodium in the kidneys. As serum sodium increases, SIADH gradually corrects itself. The patient needs assistance to plan fluid intake, and a dietary consultation is also required for consistency in fluid management.
If fluid restriction is unsuccessful, the physician may prescribe an IV infusion of a 3% to 4.5% saline solution. Correction of hyponatremia is done carefully, because fluid could move rapidly from the brain into the circulation by osmosis, causing damage to the brain. In complicated cases, consultation with a neurologist may be important because of the risk of neurological deficits if correction is not done carefully. Use caution in administering these hypertonic solutions and always place them on an infusion control device to regulate the infusion rate precisely. Correction of the serum sodium levels by 6 mEq/L in 24 hours is recommended by many experts, or if in an emergency, 6 mEq/L in 6 hours and then cease correction for the rest of the day. Monitor the patient carefully because sodium and water retention may also result, leading to pulmonary congestion and shortness of breath.
Diuretics to remove excess fluid volume may be used in patients with cardiac symptoms if they are symptomatic.
Pharmacologic Highlights
Medication or Drug Class | Dosage | Description | Rationale |
---|---|---|---|
Vasopressin receptor antagonists | Varies with drug | Conivaptan; tolvaptan | Block vasopressin receptors; used for hypervolemic and euvolemic (normal volume) hyponatremia when serum sodium level < 125 mEq/L, when hyponatremia is symptomatic, and when there has been inadequate response to fluid restriction |
Diuretics | Varies with drug | Thiazide diuretics; loop diuretics (furosemide) | Remove excess fluid volume (may be used in patients with cardiac symptoms) |
Other Drugs: Osmotic diuretics mannitol and urea; tetracycline derivative demeclocycine is no longer recommended because of its delayed mechanism of action and nephrotoxic side effects.
If the patient is at risk for airway compromise because of low serum sodium levels or seizure activity, maintaining a patent airway is the primary nursing concern. Insert an oral or nasal airway if the patient is able to maintain breathing or prepare the patient for endotracheal intubation if it is needed. If the patient is able to maintain airway and breathing, consider positioning the patient so that the head of the bed is either flat or elevated no more than 10 degrees. This position enhances venous return and increases left atria filling pressure, which, in turn, reduce the release of ADH.
Explore with the patient methods to maintain the fluid restriction. If thirst and a dry mouth cause discomfort, try alternatives such as hard candy (if the patient is awake and alert) or chewing gum. Allocate some of the restricted fluids for ice chips to be used throughout the day at the patient's discretion. Work with the patient to determine the amount of fluid to be sent on each tray so that fluid intake is spread equitably throughout the day. If the patient is receiving fluids in IV piggyback medications, consider those volumes as part of the 24-hour intake. Work with the pharmacy to concentrate all medications in the lowest volume that is safe for the patient.
Promote range-of-motion exercises for patients who are bedridden, and turn and reposition them every 2 hours to limit the complications of immobility. Initiate seizure precautions to ensure the patient's safety.
Evidence-Based Practice and Health Policy
Mentrasti, G., Scortichini, L., Torniai, M., Giamperi, R., Morgese, F., Rinaldi, S., & Berardi, R. (2020). Syndrome of inappropriate antidiuretic hormone secretion (SIADH): Optimal management. Therapeutics and Clinical Risk Management, 16, 663–672.
Be sure the patient and significant others understand the medication regimen, including the dosage, route, action, adverse effects, and need for follow-up laboratory tests (ADH level, serum sodium and potassium, blood urea nitrogen and creatinine, urine and serum osmolality). Instruct the patient to report changes in voiding patterns, level of consciousness, presence of edema, symptoms of hyponatremia, reduced neurological functioning, nausea and vomiting, and muscle cramping. If the patient is going home on fluid restriction, be sure to discuss methods of limiting fluid intake and encourage the patient to obtain weight daily to monitor for fluid retention.