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Hypocalcemia 

Hypocalcemia
Chapter:
Hypocalcemia
Author(s):

Palak Choksi

, and Robert W. Lash

DOI:
10.1093/med/9780190862800.003.0077
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date: 18 September 2020

  1. A. Introduction

    1. a. Definition. Hypocalcemia is defined as a decreased level of calcium in the blood. Hypocalcemia often occurs in very ill, hospitalized patients.

    2. b. Because albumin binds calcium, it is important to make sure that hypocalcemia is real and not a reflection of a poor nutritional state or albumin loss from other reasons. For every 1 mg decrease in serum albumin (the normal albumin level is 4 mg/dL), you must correct the calcium by 0.8 mg/dL. For example, if the serum calcium is 7.5 mg/dL and the albumin is 2 mg/dL, then the corrected serum calcium is 9.1 mg/dL (and the patient is not hypocalcemic; see Chapter 76).

    3. c. In patients with respiratory alkalosis (such as hyperventilation), the total serum calcium is normal, but the ionized calcium is low. This may result in signs and symptoms of hypocalcemia.

  2. B. Clinical Manifestations of Hypocalcemia. Because hypocalcemia leads to enhanced excitation of the nervous system and muscle cells, the symptoms and signs primarily involve the neuromuscular and cardiovascular systems.

    1. a. Symptoms include paresthesias of the lips and extremities, muscle cramps, and in severe cases, tetany, laryngospasm with wheezing, or life-threatening stridor.

    2. b. Signs include hypotension, Chvostek’s sign (tapping the facial nerve at the angle of the jaw [over the masseter muscle] leads to contraction of the facial muscles), and Trousseau’s sign (occlusion of the brachial artery with a blood pressure cuff leads to carpal spasm). Cataracts and calcifications of the basal ganglia can occur if hypocalcemia is long-standing. The electrocardiogram (EKG) may show a prolonged QT interval or atrioventricular (AV) block.

  3. C. Causes of Hypocalcemia. There are many causes of hypocalcemia; the mnemonic “HIPOCAL” will help you remember the most important ones.

    • MNEMONIC: Causes of Hypocalcemia (“HIPOCAL”)

    • Hypoparathyroidism/Hungry bones

    • Infection

    • Pancreatitis/Packed red blood cells

    • Overload states

    • Chronic renal failure

    • Absorption abnormalities

    • Loop diuretics

      1. a. Hypoparathyroidism. The two major causes of hypoparathyroidism are neck surgeries such as thyroidectomy with damage to the parathyroid glands and autoimmune parathyroid destruction. Rare causes include DiGeorge’s syndrome and parathyroid injury as a result of infection or irradiation. Functional hypoparathyroidism (i.e., decreased secretion of parathyroid hormone [PTH]) may result from magnesium deficiency.

      2. b. Infection. Up to 20% of patients with gram-negative sepsis can be hypocalcemic due to abnormalities in the parathyroid–vitamin D axis. This hypocalcemia may cause hypotension, which (if due to hypocalcemia) is often responsive to calcium replacement.

      3. c. Pancreatitis. Serum calcium less than 8 mg/dL is one of Ranson’s criteria for severe pancreatitis. Calcium levels thus correlate with the severity of acute pancreatitis.

      4. d. Packed red blood cells. Massive blood transfusions can lead to metabolic alkalosis due to breakdown of citrate in the stored blood to bicarbonate. In addition, serum calcium may form complexes with citrate to induce hypocalcemia.

      5. e. Overload states. Occasionally, hypocalcemia can occur in the setting of rapid intravascular volume expansion.

      6. f. Chronic renal failure. Vitamin D is metabolized in the normal kidney to 1,25-dihydroxyvitamin D, which promotes intestinal calcium absorption. In patients with renal failure, intestinal calcium absorption decreases and patients become hypocalcemic.

      7. g. Absorption abnormalities. Patients with malabsorption of calcium, magnesium, or vitamin D will often have hypocalcemia.

      8. h. Loop diuretics. Unlike thiazide diuretics (which can cause hypercalcemia), furosemide and other loop diuretics lead to enhanced renal excretion of calcium and can cause hypocalcemia.

  4. D. Treatment

    1. a. If the patient has tetany, arrhythmias, laryngospasm, or seizures, immediate therapy with intravenous calcium gluconate is indicated. This is in addition to any other acute interventions necessary to treat a life-threatening complication. As a rule of thumb, every 1 g of calcium gluconate will raise the serum calcium by approximately 0.5 mg/dL.

    2. b. If the patient has asymptomatic hypocalcemia, oral calcium and vitamin D are usually sufficient.

    3. c. If the patient has hypomagnesemia, replacement of magnesium is required to correct hypocalcemia.

Suggested Further Readings

Hannan FM, Thakker RV. Investigating hypocalcaemia. BMJ 2013;346.Find this resource:

Hoffman E. The Chvostek sign: a clinical study. The American Journal of Surgery 1958;96:33–7. (Classic Article.)Find this resource:

Mannstadt M, Bilezikian JP, Thakker RV, et al. Hypoparathyroidism. Nat Rev Dis Primers 2017;3:17055.Find this resource:

Palmer BF, Clegg DJ. Electrolyte disturbances in patients with chronic alcohol-use disorder. N Engl J Med 2017;377:1368–77.Find this resource:

Shah M, Sharma A, Wermers RA, Kennel KA, Kellogg TA, Mundi MS. Hypocalcemia After Bariatric Surgery: Prevalence and Associated Risk Factors. Obes Surg 2017;27:2905–11.Find this resource: