Pediatric emergency medicine trisk 1898 1898
Bạn đang xem bản rút gọn của tài liệu. Xem và tải ngay bản đầy đủ của tài liệu tại đây (103.11 KB, 1 trang )
Consider the diagnosis of hyperparathyroidism in a critically ill infant who presents
with hypercalcemia.
May present in adolescence with nonspecific symptoms including nausea and
constipation. The patient will have hypercalcemia.
Family history is important as hyperparathyroidism is associated with MEN I, II and
being an infant born to a mother with hypoparathyroidism.
Current Evidence
The parathyroid glands are derived from the third and fourth pharyngeal pouch and are usually
embedded in the posterior aspect of the thyroid gland. Occasionally, a gland may be found in
the anterior mediastinum. Parathyroid hormone (PTH) is the primary hormone produced by the
parathyroid glands. PTH is synthesized and released constitutively; its secretion is stimulated
by low, and suppressed by high, serum ionized calcium concentration. Prolonged
hypocalcemia, most commonly in the setting of renal failure, may lead to hypertrophy of the
parathyroid glands and secondary hyperparathyroidism. PTH acts on the kidney to decrease
the excretion of calcium, magnesium, and hydrogen, while increasing the excretion of
phosphate, sodium, and bicarbonate. Many of the effects are mediated by cyclic adenosine
monophosphate (cAMP), and an increased quantity of cAMP is present in the urine of patients
with hyperparathyroidism. PTH also increases the formation of 1,25-dihydroxyvitamin D in
the kidneys. PTH may increase intestinal absorption of calcium, although this effect is
primarily mediated by 1,25-(OH)2 D. Both PTH and 1,25-(OH)2 D affect bone mineralization.
PTH acts on bone to increase the release of calcium by increasing the number and activity of
the osteoclasts, whereas vitamin D decreases calcium use in bone formation by decreasing the
number of osteoblasts. The net effect of the actions of PTH and vitamin D is to increase serum
calcium by decreasing renal calcium excretion, decreasing new bone formation, increasing
bone resorption, and increasing intestinal absorption of calcium.
Clinical Considerations
Clinical Recognition
Hyperparathyroidism has two common presentations in children. The first presentation is the
critically ill infant who is found to have severe hypercalcemia during the course of diagnostic
investigations. The serum calcium level may be extremely high. The second presentation is a
child in the early- to mid-teens with nonspecific symptoms including nausea, constipation,
unexplained weight loss, personality changes, and headaches. Diffuse bone pain or renal colic
may be reported, although these symptoms are less common in children than in adults.
Triage
Consider hyperparathyroidism as a potential diagnosis in the critically ill neonate.
Initial Assessment/H&P
The physical findings of hypercalcemia are hypotonia, weakness, listlessness, anorexia,
constipation, and vomiting, and in the neonate, respiratory distress and apnea. There may be
hypertension, shortened QTc interval on ECG, polyuria (due to renal unresponsiveness to
