The causes of hypocalcemia in critically ill patients ( Table,.!) include primary hypoparathyroidism (rarely seen) and secondary hypoparathyroidism following neck surgery (common). These patients usually remain asymptomatic; however, patients may occasionally develop parasthesias, laryngeal spasm, or tetany. The hypocalcemia occurring in patients with sepsis has multiple etiologies. Some patients have dietary vitamin D deficiency, while others have acquired hypoparathyroidism, renal 1-hydroxylase deficiency, or peripheral resistance to calcitriol. Renal 1-hydroxylase deficiency usually occurs when renal insufficiency accompanies sepsis. A common finding in these patients is their impaired ability to mobilize skeletal calcium owing to PTH or vitamin D deficiency ( Za.!.o.g.a a..n.d
Vitamin D deficiency is being increasingly recognized as an important cause of hypocalcemia in patients in the ICU. Many of these patients are chronically ill, malnourished, and have minimal sunlight exposure. Although these vitamin-D-deficient patients usually have a normal serum calcium as out-patients, they are unable to maintain normal levels during critical illness. Hypocalcemia with hypophosphatemia are commonly associated with vitamin D deficiency.
Hyperphosphatemia may be a cause of hypocalcemia as a result of calcium precipitation and suppression of renal 1-hydroxylation of 25-hydroxyvitamin D. The most common causes of this syndrome include phosphorus administration (e.g. during treatment for diabetic ketoacidosis), rhabdomyolysis, and the tumor lysis syndrome following chemotherapy. This results from the massive and sudden release of phosphate from injured cells. Hypocalcemia secondary to hyperphosphatemia from an exogenous source is rare. It may be caused by excessive phosphate taken orally as a laxative or by a high-phosphate enema. Phosphorus burns may also cause hyperphosphatemia and hypocalcemia.
Hypocalcemia is occasionally seen in trauma patients with fat embolism. The hypocalcemia probably results from a combination of calcium chelation and increases in protein binding of calcium. Bone blood flow decreases to 10 to 20 per cent of control values during hypotension. Toxic shock syndrome may be associated with hypocalcemia. Although calcitonin levels are elevated, the exact pathogenesis of the hypocalcemia remains poorly defined.
Diagnosis of the various causes of hypocalcemia depends on measurements of the ionized calcium value. Patients with these diseases frequently have alterations in serum protein levels, acid-base status, free fatty acid concentrations, and received blood and albumin infusions. Hence estimation of ionized calcium based on serum total calcium and albumin levels is unreliable.
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