HypoCalcemia Flashcards
Causes of Hypocalcemia
Pseudohypocalcemia:
a. Acute respiratory alkalosis or severe metabolic alkalosis: clinically significant reduction in ionized Ca2+ may occur due to increased Ca2+ complexing to the increased levels of organic anions associated with alkalemia. Total SCa levels remain the same.
b. Hypoalbuminemia: low total SCa with normal ionized Ca2+ levels due to reduced albumin-bound calcium fraction.
Causes of Hypocalcemia
Differential diagnoses of true hypocalcemia may be categorized based on serum phosphate:
Hypocalcemia in association with normal to low phosphate:
a. Hungry bone syndrome: due to reduced bone resorption with acute surgical removal of PTH.
b. Magnesium deficiency reduces PTH synthesis/release and induces bone resistance to PTH (no release of bone calcium or phosphorus into circulation).
c. Malnutrition
d. Acute pancreatitis (likely due to compensatory hPTH and resultant phosphaturia)
e. Vitamin D deficiency (vitamin D 25 or calcitriol (1,25) deficiency or liver disease or anticonvulsants with associated reduced 25-hydroxylation)
f. Vitamin D resistance
Causes of Hypocalcemia
Differential diagnoses of true hypocalcemia may be categorized based on serum phosphate:
Hypocalcemia in association with hyperphosphatemia:
a. Kidney failure
b. Rhabdomyolysis (calcium is sequestered into injured tissue, thus hypocalcemia; intracellular phosphate is released from injured muscle cells, thus hyperphosphatemia)
c. Pseudohypoparathyroidism: resistance to PTH. PTH level is high.
d. Hypoparathyroidism (neck irradiation, amyloid infiltration of parathyroids, idiopathic, sporadic, or postoperative hypoparathyroidism)
Causes of Hypocalcemia
Differential diagnoses of true hypocalcemia may be categorized based on serum phosphate:
f. Autosomal dominant hypoparathyroidism:
1. Arises from activating mutation of CaSR
2. Renal effects: hypercalciuria, thus hypocalcemia
3. Parathyroid effects: PTH suppression, thus hyperphosphatemia and reduced 1,25 vitamin D. The latter leads to hypocalcemia.
Causes of Hypocalcemia
Differential diagnoses of true hypocalcemia may be categorized based on serum phosphate:
Treatment of rhabdomyolysis-induced hypocalcemia is not recommended unless neurologic symptoms or ECG changes (i.e., prolonged QT, tetany) because
a. Hypocalcemia associated with rhabdomyolysis is transient as Ca2+ sequestered in injured tissue will be released back into circulation with recovery.
b. PTH is stimulated during the initial hypocalcemic phase and can contribute to recovery phase “overshoot” hypercalcemia.
c. Calcium infusion in the presence of hyperphosphatemia may facilitate intravascular and soft-tissue calcifications.
Diagnosis of Hypocalcemia,
Notable Laboratory Findings
Urinary calcium excretion during treatment with calcium and vitamin D derivatives:
a. Increased in the treatment of hypoparathyroidism and may lead to nephrocalcinosis
b. Decreased in all other causes of hypocalcemia
Diagnosis of Hypocalcemia,
Notable Laboratory Findings
Calcium-to-creatinine-clearance ratio:
a. High, that is ratio > 0.020 in hPTH, post-AKI diuresis, diuretics (except thiazides and amiloride), and severe CKD
b. Low in all other etiologies of hypocalcemia.
Diagnosis of Hypocalcemia,
Notable Laboratory Findings
Urinary phosphate excretion:
a. High in vitamin D deficiency (due to increased PTH), steatorrhea, CKD, active phosphate infusion
b. Low in hypoparathyroidism (recall the opposite is true in primary hPTH, where phosphaturia and hypophosphatemia are observed), pseudohypoparathyroidism, magnesium deficiency
Diagnosis of Hypocalcemia,
Notable Laboratory Findings
Intracranial calcifications, particularly within basal ganglia, are observed more frequently in idiopathic hypoparathyroidism compared with other forms of hypoparathyroidism.
Management of Hypocalcemia
In the case of concurrent acidemia and clinically significant hypocalcemia, correct hypocalcemia FIRST. Do not correct acidemia prior to the correction of hypocalcemia. Alkalinization may acutely reduce circulating levels of ionized Ca2+ and induce life-threatening neurologic complications and/or arrhythmias.
Management of Hypocalcemia
Calcium CANNOT be given in the same IV line as sodium bicarbonate due to calcium precipitation as calcium carbonate.
Management of Hypocalcemia
Correct underlying etiology
Management of Hypocalcemia
Calcium supplement:
Calcium supplement:
a. Calcium gluconate is generally preferred over calcium chloride (CaCl2) because it is less irritating to tissue.
b. Calcium chloride may be used if there is central venous access.
Management of Hypocalcemia
Calcium supplement:
NOTE:
1 g of CaCl2 contains 272 mg (13.2 mEq) of elemental calcium, whereas 1 g of calcium gluconate contains 94 mg (4.7 mEq). THUS, 1 ampule of calcium chloride = 3 ampules of calcium gluconate in terms of elemental calcium content.
Management of Hypocalcemia
Calcium supplement:
In severe cases of hypocalcemia where there are neurologic complications (i.e., tetany, seizures, arhythmias), administer calcium gluconate as follows:
a. Intravenous bolus: 10 mL of 10% diluted in 50 mL of either 5% dextrose water or isotonic saline given over 5 to 10 minutes, followed by
b. Continuous infusion of a solution mixture containing 8 to 10 amps of calcium gluconate in 1 L of normal saline or 5% dextrose to run over the next 24 hours
