Syndrome of inappropriate antidiuretic hormone secretion (SIADH) and diabetes insipidus (DI) are two disorders that are challenging to understand and often get confused. These complex conditions centered on the activity of antidiuretic hormone (ADH) require immediate attention and treatment.
Antidiuretic hormone, or arginine vasopressin (AVP), is released by the pituitary gland in response to changes in volume, blood pressure and plasma osmolality. A key regulator of water absorption in the kidneys, ADH plays opposing roles in SIADH and DI. To put it simply, SIADH is exactly what it states, an inappropriate secretion of ADH. Too much ADH prevents the production of urine and leads to the retention of excess water in the body, hyponatremia, and hypo-osmolality (Lippincott Advisor, 2021a). SIADH may be caused by a central nervous system (CNS) disorder, cancer, mesothelioma, cardiopulmonary disorders such as asthma, atelectasis, myocardial infarction, vascular diseases, multiple sclerosis, Guillain-Barre syndrome, porphyria, myxedema, and psychosis. Complications are significant and include water intoxication, cerebral edema, noncardiogenic pulmonary edema, heart failure, seizures, coma, and death (Lippincott Advisor, 2021a).
The effect is reversed in diabetes insipidus. There are two types of DI: central (also known as pituitary, neurogenic or neurohypophyseal) and nephrogenic. In central DI, either the hypothalamus does not produce enough ADH, or the pituitary gland does not secrete enough ADH. Without vasopressin, filtered water is excreted in the urine instead of being reabsorbed. In nephrogenic DI, ADH production and secretion are normal, but the kidneys are resistant to the anti-diuretic effects of the hormone. The result in both subtypes is polyuria, greater than 3L/24 hours in adults and greater than 2L/24 hours in children. In severe cases of DI, 24-hour urine output can reach up to 10-20 L/day. These conditions may be caused by damage to the hypothalamus or pituitary gland, central nervous system malformation, certain drugs, kidney diseases, and genetic defects. Major complications of DI include hypovolemia, hyperosmolality, circulatory collapse, CNS changes, loss of consciousness, bladder distention and hydronephrosis (Lippincott Advisor, 2021b).
Since SIADH results in the retention of water, remember “SI” for “soaked inside.” For DI, excess fluid leaves the body, therefore think “dry inside.” Here’s a table outlining the main differences between SIADH and DI.
(Lippincott Advisor, 2021ab)
||Too much ADH prevents the production of urine and leads to the retention of excess water in the body.
||Not enough ADH or resistance to ADH leads to increased urine output and dehydration.
- Dilutional hyponatremia
- Moderate (Na+ 120-129 mEq/L)
- Severe (Na+ < 120 mEq/L)
- Poor concentration
- Speech difficulties
- Dizziness, gait disturbance
- Confusion, forgetfulness
- Sluggish deep tendon reflexes
- Tremor and asterixis
- Weight gain
- Cheyne-Stokes respirations (with severe or rapid onset)
- Cerebral edema
- Polyuria (more than 3L/24 hours)
- Polydipsia (extreme thirst)
- Urine osmolality less than serum osmolality
- Weight loss
- Weakness, fatigue
- Dry skin and mucous membranes
|Key Treatment Strategies
- Treat underlying condition
- Prevent further decrease in Na+ concentration, correct hyponatremia SLOWLY
- Fluid restriction 500 to 1,500 mL/day
- Loop diuretics (furosemide for fluid overload)
- 3% sodium chloride infusion if sodium less than 120 mEq/L or acute seizures
- Vasopressin receptor antagonists
- Institute seizure precautions
- Treat underlying cause
- IV fluids, (dextrose 5% water or hypo-osmolar IV) based on osmolality
- Administer desmopressin (DDAVP)
- Carbamazepine to help release ADH
- Thiazide diuretic and/or amiloride
- Low sodium, low-protein diet
- Prostaglandin synthesis inhibitors (indomethacin)
Monitoring will be similar for both SIADH and DI with a few differences. For both conditions, be sure to closely monitor vital signs, intake and output, as well as daily weight. Assess urine and serum electrolyte levels, particularly sodium, and observe for changes in neurologic status and level of consciousness. It is important to assess cardiac rate and rhythm, heart and lung sounds and evaluate your patient’s response to treatment. For DI, also check the blood urea nitrogen level, urine specific gravity and osmolality, and the 24-hour urine volume per your institution policies. In addition, for DI patients it is critical to monitor for signs and symptoms of hypovolemic shock.
I hope you find this brief outline helpful. For more detailed information, see NursingCenter’s pocket card Understanding Syndrome of Inappropriate Antidiuretic Hormone (SIADH) and Diabetes Insipidus (DI)