6.2 DI, SIADH, Thyroid & Adrenal Crises

The Two ADH Disorders: DI vs SIADH

Antidiuretic hormone (ADH, vasopressin) is released by the posterior pituitary and tells the kidney to reabsorb free water. The two ADH disorders are mirror images, and the CCRN routinely tests the ability to separate them by sodium, serum osmolality, urine osmolality, and urine output.

Diabetes insipidus (DI)

Diabetes insipidus (DI) is a deficiency of ADH (central DI, from pituitary/hypothalamic injury, neurosurgery, or traumatic brain injury) or renal resistance to ADH (nephrogenic DI). Without effective ADH, the kidney cannot concentrate urine, so the patient produces massive amounts of dilute urine (often >200-300 mL/hr, sometimes >800 mL/hr) and loses free water. The result is hypernatremia, high serum osmolality, and low (dilute) urine osmolality with a low urine specific gravity (typically <1.005). A patient after pituitary surgery or traumatic brain injury with urine output of 800 mL/hr, serum sodium 152 mEq/L, high serum osmolality, and dilute urine has classic DI. Treatment of central DI is desmopressin (DDAVP), a synthetic ADH analog, plus careful free-water replacement to match ongoing losses. Nephrogenic DI — from lithium, chronic hypercalcemia, or hypokalemia — does NOT respond to desmopressin; management instead removes the offending cause and uses a low-solute diet with thiazides. Untreated DI leads to severe hypovolemia, hemodynamic instability, and hypernatremic encephalopathy, so meticulous strict intake-and-output, hourly urine measurement, and frequent sodium checks are essential nursing priorities.

Syndrome of inappropriate antidiuretic hormone (SIADH)

SIADH is the opposite: too much ADH, causing the kidney to retain free water. Causes include CNS disorders (subarachnoid hemorrhage, TBI, meningitis), pulmonary disease, malignancy (small-cell lung cancer), and many drugs. Water retention dilutes the serum, producing euvolemic or mildly hypervolemic hyponatremia with LOW serum osmolality and inappropriately CONCENTRATED (high-osmolality) urine. A subarachnoid hemorrhage patient with serum sodium 118 mEq/L, low serum osmolality, high urine osmolality, and signs of fluid overload has SIADH. First-line treatment is fluid restriction; hypertonic saline is reserved for severe symptoms.

DI vs SIADH at a glance

Correcting hyponatremia safely

Severe symptomatic hyponatremia (e.g., Na 112 mEq/L with seizures) is treated with 3% hypertonic saline, but the critical nursing concern is to avoid overly rapid correction. Raising sodium faster than about 8-10 mEq/L in 24 hours risks osmotic demyelination syndrome (ODS, formerly central pontine myelinolysis) — an often-irreversible injury causing quadriparesis and pseudobulbar palsy. Note that cerebral salt wasting (CSW), which can also follow SAH/TBI, produces hyponatremia but with hypovolemia and high urine output; it is treated with salt and volume, not fluid restriction — the key discriminator from SIADH.

Thyroid Emergencies

Thyroid storm

Thyroid storm is decompensated, life-threatening hyperthyroidism presenting with high fever, tachycardia (often >140-160), agitation or delirium, and high-output heart failure. Treatment layers several agents in a specific order: a beta-blocker (propranolol) for adrenergic symptoms; a thionamide (propylthiouracil/PTU or methimazole) to block new hormone synthesis; and then iodine given at least one hour AFTER the thionamide to block hormone release (giving iodine first would fuel hormone production). Add corticosteroids (which also block peripheral T4-to-T3 conversion) and active cooling. Avoid aspirin, which displaces thyroid hormone from protein.

Myxedema coma

Myxedema coma is decompensated severe hypothyroidism — essentially the opposite picture: hypothermia, bradycardia, hypoventilation (CO2 retention), hyponatremia, and altered mentation. Priority treatment is IV thyroid hormone replacement (levothyroxine), passive rewarming, ventilatory support, and stress-dose steroids (because coexisting adrenal insufficiency is common). Avoid beta-blockade, which worsens the bradycardia, and avoid active external rewarming, which can cause vasodilatory collapse.

Adrenal (Addisonian) Crisis

Adrenal crisis is acute deficiency of cortisol (and often aldosterone), triggered by abrupt steroid withdrawal, sepsis, or stress in a patient with adrenal insufficiency. The hallmark is refractory hypotension unresponsive to fluids and pressors, accompanied by hyponatremia, hyperkalemia, and hypoglycemia (aldosterone deficiency retains K+ and wastes Na+; cortisol deficiency impairs glucose and vascular tone). The priority treatment is IV hydrocortisone (stress-dose steroids) immediately, plus aggressive isotonic saline for the hypotension and hyponatremia and dextrose for hypoglycemia. Adrenal crisis is rapidly fatal without steroids — never delay hydrocortisone to complete diagnostic testing; a random cortisol level can be drawn but should not postpone treatment. In the ICU, a related concept is critical illness-related corticosteroid insufficiency (relative adrenal insufficiency), in which septic patients with refractory shock despite fluids and vasopressors may benefit from low-dose hydrocortisone. Nursing priorities include continuous hemodynamic monitoring, trending sodium/potassium/glucose, and teaching the chronic-steroid patient to "stress-dose" and never abruptly stop steroids, since abrupt withdrawal is a leading precipitant.

Rapid comparison of the four crises