A 50-year-old woman presents for parathyroidectomy. She has a history of hypertension, cholelithiasis, and nephrolithiasis. She denies seizures, syncope, palpitations, and diaphoresis. She underwent general anesthesia for repair of a fractured femur without complications. Her calcium concentration is 13 mg/dL.
Describe the physiology of calcium regulation.
Extracellular calcium concentrations are regulated by vitamin D and parathyroid hormone (PTH). Vitamin D increases calcium absorption from the gastrointestinal tract and augments the effects of PTH. PTH increases calcium release from bone, increases calcium absorption from intestines, enhances vitamin D production, and decreases renal clearance of calcium. Under normal circumstances, PTH levels are inversely related to ionized calcium concentrations. Calcitonin tends to decrease calcium levels. It is produced in the thyroid.
Calcium exists in two forms, bound and unbound. The bound portion is mostly attached to albumin. A small percentage is complexed with anions such as citrate and phosphate. The remainder is unbound. Unbound calcium is referred to as ionized or free calcium. Ionized calcium is the physiologically important form. Alkalosis decreases ionized calcium levels and predisposes to clinically significant hypocalcemia.
What are the clinical features of hypercalcemia?
Hypercalcemia occurs most commonly in association with hyperparathyroidism from single benign parathyroid adenomas. Other causes include malignant tumors, immobility, thyroid toxicity, Paget disease, renal failure, acquired immunodeficiency syndrome (AIDS), and adrenal insufficiency. Parathyroid hyperplasia can be related to pituitary adenomas and multiple endocrine neoplasia (MEN).
Hypercalcemia affects the cardiovascular, renal, gastrointestinal, hematologic, and central nervous systems. Calcium levels >13 mg/dL predispose to renal stones and other end-organ effects. Calcium concentrations >14 mg/dL are associated with uremia, coma, and cardiac arrest. Table 28-1 summarizes the clinical presentation of hypercalcemia.
Cardiac conduction abnormalities
|Central nervous||Seizures |
How is hypercalcemia treated?
The first step in treating hypercalcemia is to stop administration of calcium. Generally, this means eliminating calcium oral intake but could include intravenous administration. Simultaneous fluid administration with normal saline at 150 mL/hour and diuresis with furosemide are key points. Thiazide diuretics are contraindicated because they can increase calcium levels. This type of fluid management risks congestive heart failure, hypovolemic hypotension, hypokalemia, and hypomagnesemia. Dialysis may be needed for patients with preexisting heart failure or renal failure. Bisphosphonates such as pamidronate are reserved for life-threatening hypercalcemia. Salmon calcitonin, gallium nitrate, and glucocorticoids have also been used.