It is also called free calcium. All cells need calcium in order to work. Calcium helps build strong bones and teeth. It is important for heart function. It also helps with muscle contraction, nerve signaling, and blood clotting. This article discusses the test used to measure the amount of ionized calcium in blood. A blood sample is needed. Most of the time blood is drawn from a vein located on the inside of the elbow or the back of the hand.
Your provider may order this test if you have signs of bone, kidney, liver or parathyroid disease. The test may also be done to monitor progress and treatment of these diseases.
Utilization Management Algorithms. Test Catalog. Download Test. Useful For Suggests clinical disorders or settings where the test may be helpful Assessing calcium states during liver transplantation surgery, cardiopulmonary bypass, or any procedure requiring rapid transfusion of whole blood in neonates and critically ill patients Second-order test in the evaluation of patients with abnormal calcium values. However, they may also cause negative health effects for many people. A urine calcium test is done to measure how much calcium is passed out of the body through urine.
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Ionized Calcium Test. Medically reviewed by Daniel Murrell, M. Why do I need an ionized calcium test? This is because the formulae do not, nor could they, take account of all the many factors that can affect calcium binding in particular patients. The limitations of the correction formulae have been exposed by a number of studies that have focused principally, although not exclusively, on the critically ill []. In common with other studies, "corrected" serum calcium was found to underestimate the prevalence of hypocalcemia and overestimate the prevalence of normocalcemia.
Given that hypoalbuminemia is a common feature of critical illness and that none of the correction factors applied to total calcium results are reliable in predicting ionized calcium concentration in this patient group [15], measurement of total calcium is considered an inappropriate measure of calcium status among the critically ill.
For this patient population, at least, the only reliable means of assessing calcium status is to measure ionized calcium directly. Blood pH is a major determinant of the proportion of total calcium that is bound to protein, principally because hydrogen ions compete with calcium ions for protein binding sites [17]. A decreased pH acidosis is associated with decreased calcium binding and therefore increased proportion of total calcium in the ionized state. To give some idea of the magnitude of this effect, each 0.
By the same mechanism, raised blood pH alkalosis causes reduction in serum ionized calcium concentration. Since this phenomenon is merely a shift of calcium from one fraction to another, total calcium concentration is not affected.
Despite what may well be a clinically significant change in calcium status, serum total calcium concentration remains unchanged. The most reliable way of assessing calcium status among patients with concomitant acid-base disturbance is to measure ionized calcium directly. Ionized calcium has been shown to be more reliable than total corrected calcium in some other patient groups, including those suffering mild hyperparathyroidism [19] and those with renal failure [20].
In health, plasma ionized calcium concentration is maintained between approximately 1. However, among certain patient groups, most notably the critically ill and neonates, hypocalcemia is the more common derangement.
The two most common causes of hypercalcemia are primary hyperparathyroidism and malignant disease cancer. In a tiny minority, excessive PTH is due to abnormal increase in size hyperplasia of all parathyroid glands or parathyroid cancer.
The condition can occur at any age and in both sexes, but postmenopausal women are the most commonly affected. Excessive PTH secretion leads to bone demineralization osteoporosis and chronic hypercalcemia that predisposes to urine-stone formation and renal damage.
In rare cases, the hypercalcemia is of sufficient severity to threaten life [22]. Surgical removal of the offending adenoma is curative. Hypercalcemia can be a complication of soft-tissue cancer, most commonly cancers of breast, lung and esophagus. Hypercalcemia is also a common feature of multiple myeloma, a hematological malignancy of plasma cells in bone marrow. Taken together, malignant disease is the second most common cause of hypercalcemia. One of the principal causes of hypercalcemia in these cases is uncontrolled excessive production by tumor cells of a protein called parathyroid hormone-related peptide PTHrP [23].
This is, as its name implies, similar to PTH in both structure and action. Like PTH, it increases plasma calcium by resorbing bone and decreasing calcium excretion.
The uncontrolled action of PTHrP inevitably results in abnormal loss of calcium from bone and consequent hypercalcemia. Direct destruction of bone tissue osteolysis by tumor cells that have metastasized to bone can also result in hypercalcemia; this is the principal mechanism of the hypercalcemia associated with multiple myeloma.
Generally speaking, hypercalcemia develops late in malignant disease and is a poor prognostic sign [24]. It is still important to detect because treatment aimed at normalizing calcium provides relief from symptoms of hypercalcemia, which in turn materially improves the quality of life of affected cancer patients [25].
Rare causes of hypercalcemia [26] include chronic renal failure, hyperthyroidism, sarcoidosis and tuberculosis. Some drugs, including thiazide diuretics and lithium, can precipitate hypercalcemia, as can ingestion of excessive vitamin D. Hypocalcemia is much less common than hypercalcemia [27] except in two patient groups: the critically ill and neonates.
The conditions most frequently associated with hypocalcemia in this patient group are sepsis, acute pancreatitis, acute renal failure, severe burns, trauma with rhabdomyolysis, alkalosis and massive blood transfusion. Hypocalcemia is relatively common in the neonatal intensive care unit.
The normal transition from an intrauterine environment to physiological independence at birth includes a rapid reduction in plasma calcium concentration. In some babies, most notably the premature, those with low birth weight and those born to diabetic mothers, this physiological reduction is exaggerated and transient hypocalcemia develops due to inadequate PTH response of immature parathyroid glands [29].
In general, the range and severity of symptoms associated with hypercalcemia reflect the severity of the increase. Mild hypercalcemia, roughly defined as ionized calcium in the range 1. These may include gastrointestinal nausea, vomiting, constipation and neuropsychiatric lethargy, depression, confusion ; psychosis, seizures and coma may ensue.
Cardiac arrest can occur if hypercalcemia is particularly severe. The effect of hypercalcemia on renal function is manifest acutely as polyuria and resulting polydipsia thirst. Long-standing chronic hypercalcemia, even if mild, predisposes to urine-stone formation and calcium-induced damage to renal tubule cells that can progress to renal failure. Mild hypocalcemia, roughly defined as ionized calcium in the range 0. Most common signs and symptoms associated with more severe hypocalcemia are manifestations of neuromuscular irritability, including paresthesia of peripheral extremities, muscle cramps, tetany and seizures.
Laryngeal spasm may restrict normal respiration and the effect on cardiac contractility may be evident as arrhythmias; ECG changes include prolonged QT interval and T-wave inversion.
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