Hypocalcemia intravenous calcium

Severe hyperphosphatemia, presenting as hypocalcemia and tetany should be treated with hemodialysis and possibly careful intravenous calcium administration (see management of hypocalcemia)... 

Electrolyte disturbances that develop in patients with tumor lysis syndrome should be managed aggressively to avoid renal failure from hyperphosphatemia and hypocalcemia and cardiac signs from hyperkalemia. One exception pertains to the use of intravenous calcium for hypocalcemia. Adding calcium may cause further calcium phosphate precipitation in the presence of hyperphosphatemia and should be used cautiously. 

Hypoparathyroidism is treated primarily with vitamin D and calcium supplementation. In severe hypocalcemia, symptoms are best treated intravenously. Calcium chloride, calcium gluceptate, and calcium gluconate all can be administered intravenously the latter two are preferred because they are less irritating. The gluceptate salt also can be administered intramuscularly when the intravenous route is unavailable. 

B. Specific drugs and antidotes. If symptomatic hypocalcemia occurs after ingestion of a phosphate-containing product, administer intravenous calcium (see p 424). If methemoglobinemia occurs, administer methylene blue (p 466). 

Treat hypocalcemia with intravenous calcium gluconate or calcium chloride (see p 424). 

B. Specific drugs and antidotes. When clinically significant hypocalcemia is present, administer intravenous calcium gluconate (see p 424), 10-20 mL (children 0.2-0.3 mL/kg), and monitor ionized calcium levels and titrate further doses as needed. Treat hypomagnesemia with intravenous magnesium sulfate, 1-2 g given over 10-15 min (children 25-50 mg/kg diluted to less than 10 mg/mL). Treat hyperkalemia with intravenous calcium and other usual measures (p 37). 

Monitor the ECG and semm calcium and potassium levels give intravenous calcium (p 424 and see below) if there is evidence of hypocalcemia or severe hyperkalemia. 

A 37-year-old woman with suspected celiac disease was prepared for colonoscopy using sodium phosphate solution (Fleet Phospho-Soda ) 90 ml. About 12 hours later, she developed perioral paresthesia, Chvostek s sign, numbness in the limbs, and carpopedal spasm. Blood tests showed hypocalcemia and hyperphosphatemia. She was treated immediately with repeated doses of intravenous calcium gluconate and her electrolyte balance normalized over the next 2 days. 

Patients with chronic renal failure develop hyperphosphatemia, hypocalcemia, secondary hyperparathyroidism, and severe metabolic bone disease. The secondary hyperparathyroidism is thought to be due to hyperphosphatemia and decreased 1, 25-(OH)2 formation. Oral or intravenous l,25-(OH)2D3 (calcitriol) therapy along with oral phosphate-binding agents and calcium supplementation is effective in reducing the effects of renal osteodystrophy. 

Because of its toxicity, plicamycin (mithramycin) is not the drug of first choice for the treatment of hypercalcemia. However, when other forms of therapy fail, 25-50 mcg/kg given intravenously usually lowers serum calcium substantially within 24-48 hours. This effect can last several days. This dose can be repeated as necessary. The most dangerous toxic effect is sudden thrombocytopenia followed by hemorrhage. Hepatic and renal toxicity can also occur. Hypocalcemia, nausea, and vomiting may limit therapy. Use of this drug must be accompanied by careful monitoring of platelet counts, liver and kidney function, and serum calcium levels. 

Giving intravenous phosphate is probably the fastest and surest way to reduce serum calcium, but it is a hazardous procedure if not done properly. Intravenous phosphate should be used only after other methods of treatment (bisphosphonates, calcitonin, and saline diuresis) have failed to control symptomatic hypercalcemia. Phosphate must be given slowly (50 mmol or 1.5 g elemental phosphorus over 6-8 hours) and the patient switched to oral phosphate (1-2 g/d elemental phosphorus, as one of the salts indicated below) as soon as symptoms of hypercalcemia have cleared. The risks of intravenous phosphate therapy include sudden hypocalcemia, ectopic calcification, acute renal failure, and... 

There can be increases in calcium and phosphorus loss because of effects on both the kidney and the bowel, with increased excretion and reduced resorption (131). Tetany, which has been seen in patients receiving high-dose longterm intravenous glucocorticoids, has been explained as being due to hypocalcemia, and there are also effects on bone. Tetany has also been reported in a patient with latent hyperparathyroidism after the administration of a glucocorticoid (122). 

Phosphate An intracellular shift of phosphate occurs along with potassium as fluid rehydration commences.The phosphate deficit can also be worsened with correction of the metabolic acidosis. Controlled, randomized studies have shown that routine phosphate repletion is not necessary, but some practitioners think it prudent to provide supplemental phosphate if serum phosphate levels are less than 1 mEq/L, potentially reducing the risk of seizure or tissue ischemia. During intravenous phosphate administration, serum calcium concentrations should be monitored carefully to avoid hypocalcemia and tetany (Fisher and Kitabchi, 1983). 

Pseudo-hypocalcemia can occur in hemodialysis patients, particularly in those who have chylomicronemia before administration of heparin (120). This spurious hjrpocalce-mia is thought to result from lipolytic activity in vitro, sufficient to produce calcium soaps of fatty acid. This can be detected and eliminated by the analysis of blood samples immediately after venepuncture. During hemodialysis, there is a significant fall in plasma ionized calcium after intravenous administration of heparin (an average reduction of 0.03 mmol/1 after 10 000 lU) (121). 

Disodium edetate, trisodium edetate, and edetic acid readily chelate calcium and can, in large doses, cause calcium depletion (hypocalcemia) if used over an extended period of time, or if administered too rapidly by intravenous infusion. If used in preparations for the mouth, they can also leach calcium from the teeth. However, edetate calcium disodium does not chelate calcium. 

For symptomatic hypocalcemia, calcium may be administered intravenously. If hypocalcemia is secondary to hypoparathyroidism or pseudohypoparathyroidism, vitamin D and oral calcium supplements are administered. 

Vitamin D and its metabolites play an important role in the maintenance of extracellular calcium concentrations and in normal skeletal structure and mineralization. Vitamin D is necessary for the optimal absorption of calcium and phosphorus. On a worldwide basis, the most common cause of hypocalcemia is nutritional vitamin D deficiency. In malnourished populations, manifestations include rickets and osteomalacia. Nutritional vitamin D deficiency is uncommon in Western societies because of the fortification of miUc with ergocalciferol. " The most common cause of vitamin D deficiency in Western societies is gastrointestinal disease. Gastric surgery, chronic pancreatitis, small-bowel disease, intestinal resection, and bypass surgery are associated with decreased concentrations of vitamin D and its metabolites. Vitamin D replacement therapy may need to be administered by the intravenous route if poor oral bioavailability is noted. Decreased production of 1,25-dihydroxyvitamin D3 may occur as a result of a hereditary defect resulting in vitamin D-dependent rickets. It also can occur secondary to chronic renal insufficiency if there is insufficient production of the 1 -a -hydroxylase enzyme for the... 

Severe symptomatic hyperphosphatemia manifesting as hypocalcemia and tetany should be treated by the intravenous administration of calcium salts (see the discussion of hypocalcemia). Although this may seem counterintuitive in a patient with a phosphorus of 16 mg/dL and a calcium of 7 mg/dL (the calcium-phosphorus product is 112 mg /dL ), correction of severe hypocalcemia is of primary importance because of the critical nature of this disorder. In general, the... 

Parenteral phosphorus supplementation is associated with risks of hyperphosphatemia, metastatic soft tissue deposition of calcium-phosphate product, hypomagnesemia, hypocalcemia, and hyperkalemia or hypernatremia (caused by intravenous phosphorus salt) (Table 49-9). Inappropriate administration of large doses of parenteral phosphorus over relatively short time periods has resulted in symptomatic hypocalcemia and soft-tissue calcification. The rate of infusion and choice of initial dosage should therefore be based on severity of hypophosphatemia, presence of symptoms, and coexistent medical conditions. Patients should be closely monitored with frequent (every 6 hours) serum phosphorus determinations for 48 to 72 hours after starting intravenous therapy. It may be necessary to continue administration of intravenous phosphorus for several days in some patients, while other patients may be able to tolerate an... 

Conclusive evidence for the control mechanism of parathormone secretion has been obtained by experiments done on the thyroid-parathyroid preparation of the dog. In these experiments, the thyroid-parathyroid preparation is first perfused with calcium deficient blood, then the perfusate is injected intravenously to parathyroidectomized dogs. The injected dogs develop hypercalcemia and phosphaturia, indicating that perfusion of the parathyroids with low calcium levels stimulates parathormone secretion. It is not known whether the stimulated parathyroid synthesizes new hormone or releases existing parathormone. However, the crude parathyroid extracts of parathyroid-thyroid perfused with low calcium levels contained a new factor separable from the classical parathormone. The reciprocal experiment in which calcium-rich blood is used to perfuse the thyroid-parathyroid preparation leads to hypocalcemia in the animals injected with the perfusate. 

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