6.2 Calcium, Thyroid, and Adrenal Disorders
Key Takeaways
- Early hypocalcemia occurs in the first 24-48 hours (preterm, IDM, asphyxia); late hypocalcemia typically appears around day 4-10 and is often phosphate- or PTH-related.
- Refractory hypocalcemia often will not correct until hypomagnesemia is treated, because magnesium is required for PTH secretion and action.
- Congenital hypothyroidism is usually silent at birth; newborn screening catches most cases, while delayed presentation includes prolonged jaundice, umbilical hernia, and macroglossia.
- Neonatal thyrotoxicosis follows transplacental TSH-receptor antibodies from maternal Graves disease, even if the mother is athyreotic after surgery or radioiodine.
- Salt-wasting 21-hydroxylase CAH produces shock, hyponatremia, and hyperkalemia that looks septic; 46,XX infants may have ambiguous genitalia, and 46,XY infants may look typical until crisis.
6.2 Calcium, Thyroid, and Adrenal Disorders
Quick Answer: Check calcium and magnesium whenever a neonate is jittery, seizing, or has a long QTc, and do not treat calcium in isolation if magnesium is low. Early hypocalcemia is a first 24-48 hour problem in preterm, IDM, and asphyxiated infants; late hypocalcemia clusters around day 4-10. Congenital hypothyroidism is a newborn-screen diagnosis; the classic face (macroglossia, umbilical hernia, prolonged jaundice) means treatment was late. Maternal Graves antibodies can cause neonatal thyrotoxicosis days after birth. Salt-wasting 21-hydroxylase CAH is shock with hyponatremia and hyperkalemia that looks like sepsis.
Fetal ionized calcium is kept high by active placental transport. After birth that pump disappears, PTH should rise, phosphate should fall, and vitamin D should help gut absorption. When any step fails, the NICU sees tetany, apnea, seizures, and arrhythmias that overlap with hypoglycemia. Always measure both glucose and calcium in an unexplained jittery or seizing neonate. OpenExamPrep independent teaching for this exam covers adrenal, calcium, and thyroid patient problems from AACN Certification Corporation's current Neonatal CCRN Test Plan; follow your unit's electrolyte and hormone protocols at the bedside.
Early versus late hypocalcemia
Early hypocalcemia occurs in the first 24-48 hours. Typical infants are preterm (limited stores, sluggish PTH, relatively high calcitonin), IDM (functional hypoparathyroidism and often low magnesium), and those with perinatal asphyxia or IUGR (phosphate load from cell injury, impaired PTH). The calcium drop is expected physiology pushed too far. Feeding helps, but symptomatic or very low ionized calcium needs intravenous calcium.
Late hypocalcemia typically appears around day 4-10 in a term infant who was discharged or was feeding well. Drivers include a high phosphate load from cow-milk or some formulas, hypoparathyroidism (including 22q11.2 / DiGeorge), hypomagnesemia, vitamin D disorders, and maternal hyperparathyroidism that suppressed the fetal parathyroid glands. Late disease should trigger a cause workup, not only a calcium bolus.
| Feature | Early hypocalcemia | Late hypocalcemia |
|---|---|---|
| Timing | First 24-48 hours | Typically day 4-10 |
| Typical infants | Preterm, IDM, asphyxia, IUGR | Term, high-phosphate feeds, hypoparathyroidism, low magnesium |
| Main driver | Loss of placental calcium; immature PTH | Phosphate load, PTH failure, magnesium, vitamin D |
| Exam trap | Treating only calcium when magnesium is low | Missing 22q11 or maternal hyperparathyroidism |
Signs include jitteriness, tetany, laryngospasm, stridor, apnea, seizures, and prolonged QTc. 10% calcium gluconate is given slowly intravenously with heart-rate monitoring because rapid infusion causes bradycardia. Never give calcium intramuscularly. Infiltration can destroy tissue the same way hypertonic dextrose can; use a reliable line and watch the site. Correct the ionized value and the cause.
Hypomagnesemia and hypercalcemia
Magnesium is required for PTH secretion and for PTH to work on bone and kidney. Hypomagnesemia with hypocalcemia is a classic trap: calcium infusions fail until you replete magnesium. IDM, IUGR, and some GI losses set this up. Check magnesium whenever hypocalcemia is unexpected or refractory.
Hypercalcemia is less common but not rare after therapeutic hypothermia or birth trauma when subcutaneous fat necrosis appears as firm, reddish-purple nodules days to weeks later. Other causes include Williams syndrome, idiopathic infantile hypercalcemia, excess vitamin D or calcium, phosphate depletion, and congenital hyperparathyroidism. Infants may have polyuria, hypotonia, constipation, dehydration, and later nephrocalcinosis. Stop extra calcium and vitamin D, hydrate, and involve endocrinology. Do not ignore a rising calcium in an infant who was cooled.
Congenital hypothyroidism
Most infants with congenital hypothyroidism (CH) look normal on day 1. That is why the newborn metabolic screen exists. Incidence is on the order of 1 in 2,000 to 4,000 live births. Thyroid dysgenesis is the most common cause in iodine-sufficient regions; dyshormonogenesis can present with a goiter. Screening programs use TSH-first or T4-first strategies depending on the state. Preterm infants may have a delayed TSH rise, so an early TSH-only screen can miss CH; many units repeat screening in very preterm babies.
If screening is missed or false-negative, delayed presentation includes prolonged jaundice (immature bilirubin conjugation), umbilical hernia, macroglossia, a large anterior fontanelle, hypotonia, constipation, a hoarse cry, hypothermia, poor feeding, and mottled or myxedematous skin. That phenotype is a failure of timely thyroxine, not a cute diagnostic silhouette. Confirm with free T4 and TSH and start levothyroxine promptly—typical term starting doses are often cited near 10-15 mcg/kg/day—without waiting for imaging. Imaging can come after treatment is started. Untreated CH damages neurodevelopment; hours and days matter more than a perfect scan.
Separate CH from transient hypothyroxinemia of prematurity (low T4 with a normal or low TSH in an ELBW infant). That pattern is not automatically treated as CH. Also separate CH from sick-euthyroid changes during critical illness. When in doubt, endocrinology owns the distinction; nursing owns getting the screen sent, chasing a critical TSH/T4 call, and not delaying the first levothyroxine dose once CH is confirmed.
Hyperthyroidism and thyrotoxicosis from maternal Graves
TSH-receptor antibodies (TRAb) of the IgG class cross the placenta. The mother may currently be hyperthyroid, euthyroid on medication, or athyreotic after thyroidectomy or radioiodine and taking replacement. Antibodies can still be present. Fetal clues include tachycardia, IUGR, goiter, and hydrops. The neonate may show tachycardia, hypertension, irritability, poor weight gain despite a good intake, diarrhea, stare, goiter, and high-output heart failure. Craniosynostosis is a longer-term risk of uncontrolled thyrotoxicosis.
Maternal antithyroid drugs can keep the newborn quiet for several days; thyrotoxicosis then appears around day 3-10 as those drugs clear. Do not discharge a Graves-exposed infant without a plan for heart rate, weight, and thyroid labs. Treatment is specialist-directed: beta blockade (often propranolol), methimazole, and iodine in severe cases. The CCRN-level recognition is: maternal Graves plus a tachycardic, failing-to-gain neonate is thyroid until proven otherwise, not only sepsis or congenital heart disease—though you still evaluate those.
Adrenal disorders
Congenital adrenal hyperplasia (CAH) from 21-hydroxylase deficiency accounts for most CAH. The block prevents cortisol (and, in the salt-wasting form, aldosterone) synthesis and shunts precursors into androgens. 46,XX infants may have ambiguous or virilized genitalia at birth—an immediate diagnostic clue. 46,XY infants often have typical male genitalia, so the first sign is a crisis. Salt-wasting crisis usually arrives in week 1-3: poor feeding, vomiting, weight loss, dehydration, shock, hyponatremia, hyperkalemia, metabolic acidosis, and sometimes hypoglycemia.
That picture looks septic. If you treat only with antibiotics and saline and miss glucocorticoid replacement and potassium management, the infant can arrest. 17-hydroxyprogesterone is elevated; sick and preterm infants can have intermediate elevations, so interpretation needs context. Newborn screening includes 17-OHP in U.S. programs, but crisis can precede the result. Immediate management is volume, glucose, hydrocortisone at stress doses (which also provides some mineralocorticoid effect), then fludrocortisone and sodium supplementation, plus hyperkalemia treatment. Do not wait for a genotype to give hydrocortisone in classic shock with this electrolyte pattern and genital clue.
Adrenal hemorrhage follows difficult delivery, macrosomia, breech extraction, asphyxia, or coagulopathy. Look for a flank mass, anemia, jaundice from resorbing blood, and scrotal discoloration if blood tracks downward. Unilateral hemorrhage may leave enough function; bilateral hemorrhage can cause insufficiency. Ultrasound confirms. Support hemodynamics and give steroids if adrenal function is inadequate.
Steroid-related adrenal suppression follows courses of dexamethasone (evolving BPD) or hydrocortisone (refractory hypotension). The hypothalamic-pituitary-adrenal axis can be suppressed. Do not stop chronic glucocorticoids abruptly. Use stress-dose hydrocortisone for surgery, sepsis, or acute critical illness in an infant recently on pharmacologic steroids. Cosyntropin testing is an endocrine decision; the nursing action is not to disappear the steroid bag overnight.
Putting the shock differential together
A 10-day-old with shock, hyponatremia, and hyperkalemia is sepsis until fluids, cultures, and antibiotics are in motion—and CAH until hydrocortisone and electrolytes are addressed. Ambiguous genitalia in a 46,XX infant should have already placed CAH on the admission problem list. A jittery IDM needs glucose, calcium, and magnesium, not only a bottle. A quiet 3-week-old with jaundice, a large tongue, and an umbilical hernia needs thyroid labs today, not a wait-for-the-classic-face approach. Adult CCRN material at /study-guides/ccrn does not replace these neonatal patterns; practice items for this exam sit at /practice/ccrn-neonatal.
A 10-day-old 46,XX infant with ambiguous genitalia presents in shock with sodium 118 mEq/L and potassium 7.4 mEq/L. Which diagnosis should be treated immediately alongside sepsis care?
An infant has persistent hypocalcemia despite an appropriate calcium infusion. Which electrolyte should be measured and corrected next to restore PTH action?
A 3-week-old whose newborn screen was missed is hypotonic with a large tongue, an umbilical hernia, and prolonged jaundice. Which endocrine diagnosis should be evaluated first?
A mother had thyroidectomy years ago for Graves disease and is now on levothyroxine. Her 5-day-old is tachycardic, irritable, and failing to gain. What is the most likely mechanism of neonatal thyrotoxicosis?