18.1 Diabetes Insipidus and SIADH

CPHON Test Content Outline (TCO) V.C.1–2 tests two water-and-sodium emergencies that look like “the child is peeing a lot” or “the sodium is wrong” until you name the hormone. Diabetes insipidus (DI) is too little antidiuretic hormone (ADH, vasopressin) effect. Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is too much ADH effect. Cerebral salt wasting (CSW) is the third map: hypovolemic hyponatremia treated with volume, not restriction. Get the volume status and the urine concentration right, or you will fluid-restrict a child who is already in shock or free-water-load a child who cannot make concentrated urine.

Pediatric hematology/oncology nurses see these syndromes after craniopharyngioma, Langerhans cell histiocytosis (LCH), central nervous system (CNS) germinoma, pituitary or hypothalamic surgery, vincristine, cyclophosphamide, and bulky CNS disease. The Oncology Nursing Certification Corporation (ONCC) uses generic drug names. The bedside job is strict intake and output (I&O), daily weights, paired serum and urine studies, seizure precautions when sodium is falling, and knowing when 3% hypertonic saline belongs in an intensive-care unit (ICU), not on a regular floor.

Central DI: the child who cannot hold water

Central DI is failure of the posterior pituitary or hypothalamus to release ADH. Without ADH, collecting ducts do not insert aquaporin water channels, and the kidney dumps large volumes of dilute urine. Serum sodium and serum osmolality rise. The child dehydrates.

Classic pediatric oncology settings:

• Craniopharyngioma and its resection or radiation field, because the tumor sits on the hypothalamic–pituitary axis.
• LCH with pituitary-stalk or hypothalamic involvement. New polydipsia and polyuria in a toddler with known LCH is DI until the sodium and urine specific gravity say otherwise.
• CNS germinoma, especially suprasellar, which can present with DI before anyone sees a mass on the waiting-room photograph.
• Pituitary or hypothalamic surgery, including biopsy, often with an immediate postoperative polyuria window that the night-shift nurse catches first.

Nephrogenic DI (kidney unresponsive to ADH) is a different problem and is not the usual CPHON craniopharyngioma script.

What you see: urine output that is inappropriately high for intake—often several milliliters per kilogram per hour of colorless urine—low urine specific gravity and low urine osmolality, thirst if the child can drink, dry mucous membranes, tachycardia, weight loss, and hypernatremia. An 8-year-old on the night of craniopharyngioma resection who puts out 9 mL/kg/hour of urine with specific gravity 1.002 and a sodium of 155 mEq/L is in central DI, not “just post-op diuresis” to ignore until morning. A 3-year-old with LCH who suddenly soaks diapers every hour and has a climbing sodium needs the same map.

Nursing actions:

• Strict I&O, hourly at first after pituitary surgery, plus daily or twice-daily weights. Do not skip overnight measurement so the child can “sleep through.”
• Replace free-water losses as ordered (often milliliter-for-milliliter urine replacement with hypotonic fluid, or enteral water once the gut is usable). Do not fluid-restrict DI.
• Give desmopressin (a synthetic ADH analog) or vasopressin as ordered. Intranasal, oral, subcutaneous, and intravenous routes exist; use the route the protocol specifies and watch the next sodium. Over-replacement turns DI into iatrogenic hyponatremia.
• Monitor serum sodium, osmolality, and urine specific gravity on a clock, not “when convenient.”
• Protect the unconscious, NPO, or developmentally unable child who cannot drink to thirst—those children dehydrate fastest.

Teach families that the tumor or the surgery injured the water hormone. The teaching is more useful than the abbreviation soup. A teenager after germinoma resection who sneaks ice water in the playroom because “I’m so thirsty” may be correcting DI the only way the hypothalamus still knows how; measure the sodium before you confiscate the cup as noncompliance.

SIADH: water in, sodium down, volume looks normal

SIADH is ADH release (or ADH-like activity) when it should be off. The kidney holds water, urine is concentrated, plasma is dilute, and hyponatremia develops. True SIADH is euvolemic or only slightly volume-expanded: moist mucous membranes, normal heart rate, no orthostatic collapse, no weight crash. Urine sodium is typically not low.

High-yield pediatric oncology triggers:

• Vincristine (and other vinca alkaloids) via neurohypophyseal effects.
• Cyclophosphamide, especially with the forced hydration already used for hemorrhagic-cystitis prevention. Water load plus ADH effect is a sodium trap. The mesna-and-hydration plan that protects the bladder can unmask SIADH if you are not watching the chemistry panel.
• CNS disease: brain tumors, intracranial pressure, meningitis, and surgery can all drive ADH release. Nausea and pain also stimulate ADH.

What you see: falling serum sodium and serum osmolality, high urine osmolality and high urine specific gravity for that low serum osmolality, lowish urine output compared with DI, and a child who looks volume-replete. A 4-year-old on vincristine whose sodium is 123 mEq/L, urine is concentrated, and weight is stable is SIADH until CSW is excluded by volume status. A school-age child who becomes confused, nauseated, or “just not herself” during cyclophosphamide hydration is a sodium check, not a lecture about hospital food.

Nursing actions:

• Fluid restriction is first-line for mild to moderate, minimally symptomatic SIADH once the team confirms the diagnosis. Teach families that “more juice for a low sodium” is the wrong instinct.
• Remove free-water sources (hypotonic intravenous fluids, excess oral water).
• Seizure precautions as sodium falls or if the child is already encephalopathic: suction, side rails, oxygen, a working intravenous line.
• Hypertonic saline (3% sodium chloride) for seizures or severe neurologic symptoms (coma, deep lethargy, repeated vomiting with a crashing sodium). That infusion belongs in an ICU with frequent sodium checks. The goal is to stop seizures and move sodium carefully, not to snap it to 140 mEq/L in an hour (osmotic demyelination risk with over-rapid correction of chronic hyponatremia).
• Stop or hold the offending chemotherapy only as the protocol and prescriber direct; nursing’s immediate job is water, sodium, and seizure safety, then notify.

CSW versus SIADH: volume is the fork

After CNS surgery or with CNS tumors, hyponatremia is not automatically SIADH. Cerebral salt wasting produces renal sodium loss, high urine output, hypovolemia, and hyponatremia. The child is tachycardic, has dry mucous membranes, is losing weight, and is making a lot of salty urine. CSW needs volume replacement (isotonic or hypertonic saline as ordered; mineralocorticoid support such as fludrocortisone on some pathways). Fluid restriction—the SIADH move—worsens hypovolemia.

Walk the 12-year-old after suprasellar germinoma surgery. If urine is pouring out dilute and sodium is 158 mEq/L, that is DI: desmopressin or vasopressin, replace losses, hourly I&O. If sodium is 122 mEq/L, urine is concentrated, and the child looks well filled, that is SIADH: restrict, seizure precautions, hypertonic saline in the ICU if the child seizes. If sodium is 122 mEq/L, urine output is high, and the child is tachycardic and losing weight, that is CSW: fill the tank. Those three pictures are the CPHON product for TCO V.C.1–2.