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HYPOCALCEMIA

HYPOCALCEMIA. MBBS 2011 BATCH 06/08/14. CALCIUM. Total body calcium content- 1-2 kg 99% of it is within the bone in the form of hydroxyapatite It is present both in ICF & ECF In blood total calcium concentration- 8.5-10.5 mg/dl It is present in two forms in blood- (both ≈ 50% each)

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HYPOCALCEMIA

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  1. HYPOCALCEMIA MBBS 2011 BATCH 06/08/14

  2. CALCIUM • Total body calcium content- 1-2 kg • 99% of it is within the bone in the form of hydroxyapatite • It is present both in ICF & ECF • In blood total calcium concentration- 8.5-10.5 mg/dl • It is present in two forms in blood- (both ≈ 50% each) 1. bound form- bound ionically to proteins and other anions 2. unbound form- free ionic form

  3. Normally ionic unbound form in the ECF is maintained within an exquisitely narrow range through a series of feedback mechanisms that involve PTH and active vitamin D metabolite. • Calcium is impotant for many physiological processes such as neuromuscular signaling, cardiac contractility, blood coagulation and hormone secretion. • Recommended dietary intake- 1000-1200 mg/day

  4. Calcium homeostasis

  5. HYPOCALCEMIA • Serum calcium < 8.4 mg/dl with a normal serum albumin. Or an ionized calcium < 4.2 mg/dl. • It must be differentiated from pseudohypocalcemia, in which total calcium is reduced due to hypoalbuminemia, but ionized (physiologically active) fraction remains within normal range. • An algorithm to correct for protein changes adjusts the total serum calcium (in mg/dL) upward by 0.8 times the deficit in serum albumin (g/dL) or by 0.5 times the deficit in serum immunoglobulin (in g/dL).

  6. CAUSES • Hypocalcemia associated with hypoparathyroidism • parathyroid agenesis • parathyroid destruction • reduced parathyroid function 2. Associated with high parathyroid hormone levels (secondary hyperparathyroidism) • Vit D deficiency or impaired action • Parathyroid hormone resistance syndromes • Drugs

  7. Clinical manifestations • May be asymptomatic (when mild and chronic) • Moderate to severe hypocalcemia is associated with paresthesias, usually of the fingers, toes, and circumoral regions, and is caused by increased neuromuscular irritability. • Chvostek's sign- twitching of the circumoral muscles in response to gentle tapping of the facial nerve just anterior to the ear. (may be present in 10% of normal individuals) • Trousseau's sign- Carpal spasm induced by inflation of a blood pressure cuff to 20 mmHg above the patient's systolic blood pressure for 3 min. • Severe hypocalcemia can induce seizures, carpopedal spasm, bronchospasm, and prolongation of the QT interval.

  8. Investigations • Total and ionic calcium • Serum albumin • Serum PTH • Serum Phosphorus • Vitamin D • Serum Mg • Serum alkaline phosphatase

  9. Approach to Hypocalcemia

  10. ECG manifestations • P wave, QRS complex unaffected. • Prolong QT interval (because of elongation of S-T segment) • The prolongation of QT interval is inversely proportional to the serum calcium level. • T wave is usually normal in duration, configuration and amplitude. • Hypocalcemia is the only condition which can prolong the ST segment without affecting the T wave.

  11. TREATMENT • Depends on the severity of the hypocalcemia, the rapidity with which it develops, and the accompanying complications. • Acute, symptomatic hypocalcemia is initially managed with i/v calcium gluconate (10% w/v) 1 ampul diluted in 50 mL of 5% D or NS given over 5 min. • Continuing hypocalcemia often requires a constant intravenous infusion ( i.e. 10 ampuls of calcium gluconatein 1 L of 5% D or normal saline over 24 h). • Accompanying hypomagnesemia, if present, should be treated with appropriate magnesium supplementation

  12. Chronic hypocalcemia due to hypoparathyroidism- treated with calcium supplements (1000–1500 mg/d in divided doses) and either vitamin D2 or D3 or calcitriol. • Vitamin D deficiency is treated using vitamin D supplementation, with the dose depending on the severity of the deficit and the underlying cause. • The treatment goal is to bring serum calcium into the low normal range and to avoid hypercalciuria, which may lead to nephrolithiasis. • When hypocalcemia is associated with severe hyperphosphatemia, reduction of phosphorus should precede aggressive calcium supplementation.

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