Pediatric emergency medicine trisk 2875 2875
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syndrome, a genetic disorder of the PTH receptor, renders the receptor
constitutively active. Children with Jansen syndrome present with
hypercalcemia, undetectable levels of PTH, and skeletal changes consistent
with hyperparathyroidism. Immobilization, particularly in rapidly growing
adolescents, may result in significant bone resorption and hypercalcemia.
Malignancy is a rare cause of hypercalcemia in children. Decreased renal
excretion occurs in familial hypocalciuric hypercalcemia (FHH), an
autosomal dominant disorder. FHH is characterized by mild, asymptomatic
hypercalcemia, increased tubular reabsorption of calcium, and
inappropriately normal PTH. Hypercalcemia may also be seen in patients
with Williams syndrome, and several metabolic disorders including
hypophosphatasia and Bartter syndrome. Medications associated with
hypercalcemia include thiazide diuretics and lithium.
The evaluation of hypercalcemia begins with a thorough assessment of
symptoms, diet, medications, medical history, and family history.
Laboratory evaluation should include ionized calcium, electrolytes,
phosphorus, magnesium, renal function, serum albumin, and acid–base
assessment. Review of previous laboratory studies, if available, should be
performed. Though results will not be available to the ED physicians, PTH
level is critical to ultimately determine the underlying cause. If the PTH is
not elevated, vitamin D metabolites should be obtained. Assessment of
urine calcium excretion via random urine calcium to creatinine ratio may
also be informative. Calcium excretion is high in hyperparathyroidism but
low in FHH and with thiazide therapy.
Clinical manifestations. Hypercalcemia is associated with a number of
signs and symptoms depending on the acuity and severity of the disorder.
Patients with mildly elevated calcium (less than 11.5 to 12 mg/dL) are often
asymptomatic, especially if the elevation is chronic in onset. Patients with
moderate hypercalcemia (12 to 14 mg/dL) may experience anorexia,
irritability, abdominal pain, constipation, and weakness. An important renal
manifestation of hypercalcemia is polyuria due to an inability to concentrate
urine, an acquired form of nephrogenic diabetes insipidus. Should polyuria
be associated with gastrointestinal symptoms and decreased fluid intake,
dehydration will ensue and aggravate the existing hypercalcemia by
reducing renal excretion of calcium. If hypercalcemia is severe, progressive
weakness, confusion, seizures, and coma may develop.
