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 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

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 mg/day

Calcium homeostasis

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).

CAUSES 1.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

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.

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

Approach to Hypocalcemia

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.

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 gluconate in 1 L of 5% D or normal saline over 24 h). Accompanying hypomagnesemia, if present, should be treated with appropriate magnesium supplementation

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.