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Hypercalcemia can occur as a result of a vari-ety of disorders (Table 49–11). In primary hyper-parathyroidism, secretion of PTH is increased andis independent of [Ca2+]. In contrast, in second-ary hyperparathyroidism (chronic renal failureor malabsorption), the elevated PTH levels are in response to chronic hypocalcemia. Prolonged sec-ondary hyperparathyroidism, however, can occa-sionally result in autonomous secretion of PTH, resulting in a normal or elevated [Ca 2+] (tertiaryhyperparathyroidism).
Patients with cancer can present with hypercal-cemia whether or not bone metastases are present. Most often this is due to direct bony destruction, or secretion of humoral mediators of hypercalcemia (PTH-like substances, cytokines, or prostaglandins), or both. Hypercalcemia due to increased turnover of calcium from bone can also be encountered in patients with benign conditions such as Paget’s disease and chronic immobilization. Increased gastrointestinal absorption of calcium can lead to hypercalcemia in patients with the milk-alkali syn-drome (marked increase in calcium intake), hypervi-taminosis D, or granulomatous diseases (enhanced sensitivity to vitamin D).
Hypercalcemia often produces anorexia, nausea, vomiting, weakness, and polyuria. Ataxia, irritabil-ity, lethargy, or confusion can rapidly progress to coma. Hypertension is often present initially before hypovolemia supervenes. ECG signs include a shortened ST segment and a shortened QT interval. Hypercalcemia increases cardiac sensitivity to digi-talis. Pancreatitis, peptic ulcer disease, and kidney failure may also complicate hypercalcemia.
Symptomatic hypercalcemia requires rapid treatment. The most effective initial treatmentis rehydration followed by a brisk diuresis (urinary output 200–300 mL/h) utilizing intravenous saline infusion and a loop diuretic to accelerate calcium excretion. Premature diuretic therapy prior to rehy-dration may aggravate the hypercalcemia by exac-erbating volume depletion. Renal loss of potassium and magnesium usually occurs during diuresis, and laboratory monitoring and intravenous replacement as necessary should be performed. Although hydra-tion and diuresis may remove the potential risk of cardiovascular and neurological complications of hypercalcemia, the serum calcium level usually remains elevated above normal. Additional therapy with a bisphosphonate or calcitonin may be required to further lower the serum calcium level. Severe hypercalcemia (>15 mg/dL) usually requires addi-tional therapy after saline hydration and furosemide calciuresis. Bisphosphonates or calcitonin are pre-ferred agents. Intravenous administration of pami-dronate (Aredia) or etidronate (Didronel) is often utilized in this setting. Dialysis is very effective in correcting severe hypercalcemia and may be neces-sary in the presence of kidney or heart failure. Addi-tional treatment depends on the underlying cause of the hypercalcemia and may include glucocorticoids in the setting of vitamin D–induced hypercalcemia such as granulomatous disease states.
It is necessary to look for the underlying eti-ology and direct appropriate treatment toward the cause of the hypercalcemia once the initial threat of hypercalcemia has been removed. Approximately 90% of all hypercalcemia is due to either malignancy or hyperparathyroidism. The best laboratory test for discriminating between these two main categories of hypercalcemia is the PTH assay. The serum PTH concentration is usually suppressed in malignancy states and elevated in hyperparathyroidism.
Significant hypercalcemia is a medical emergency and should be corrected, if possible, before admin-istration of any anesthetic. Ionized calcium levels should be monitored closely. If surgery must be performed, saline diuresis should be continued intraoperatively with care to avoid hypovolemia; appropriate goal-directed hemodynamic and fluid management therapy should be utilized, especially for patients with cardiac impair-ment. Serial measurements of [K+] and [Mg2+] are helpful in detecting iatrogenic hypokalemia and hypomagnesemia. Responses to anesthetic agents are not predictable. Ventilation should be controlled under general anesthesia. Acidosis should be avoided so as to not worsen the elevated plasma [Ca2+].
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