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POSTOPERATIVE HYPOCALCEMIA

Overview

Transient postoperative hypocalcemia following total thyroidectomy, completion thyroidectomy, total laryngectomy, or level VI neck dissection is relatively common, occurring in up to 50% of patients depending on the procedure. The cause of this complication is related to compromised parathyroid gland function from direct parathyroid injury, ischemia, or unintentional removal; the latter resulting in permanent hypoparathyroidism. Importantly, hypoparathyroidism typically requires injury to more than three glands as one undisturbed gland is adequate to maintain calcium levels. Taken a step further, unilateral neck surgery such as thyroid lobectomy, which does not disturb parathyroid glands on the contralateral side, rarely causes hypoparathyroidism and hypocalcemia. However, hungry bone syndrome, a rare occurrence following surgery for severe primary hyperparathyroidism, may result in prolonged hypocalcemia and hypophosphatemia (differentiating it from postoperative hypoparathyroidism) secondary to the absorption of calcium by calcium-deprived bones and may occur even when leaving one or more functioning parathyroid glands undisturbed. Signs and symptoms associated with acute hypocalcemia range from asymptomatic to cramps, seizures, tetany, bronchospasm, laryngospasm, or cardiac arrythmia. Thus, at a minimum, serial postoperative calcium levels should be monitored closely in at-risk patients so early treatment can be initiated. Practice patterns vary by institution and among surgeons, although some advocate giving prophylactic calcium and vitamin D supplementation in the early postoperative period. At many institutions, postoperative parathyroid hormone (PTH) levels are frequently obtained following surgery to help predict the development of postoperative hypocalcemia.

Calcium in serum is bound to albumin; thus, serum calcium concentrations in patients with low or high serum albumin levels (normal range 3.5-5.4 g/dL) may not reflect ionized calcium concentrations – the physiologically active form. While ionized calcium (independent of albumin levels) remains the gold standard for evaluating calcium status, ionized calcium is not routinely performed because of higher cost and challenging sample handling requirements. For total serum calcium levels, consider using a calcium correction formula if albumin levels are abnormal. One commonly used formula for corrected total serum calcium (mg/dL) is serum calcium (mg/dL) + 0.8 x (4.0 − serum albumin [g/dL]).

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Signs and Symptoms

  • Chvostek sign: Contraction of ipsilateral facial muscles subsequent to percussion over the facial nerve, usually approximately 2 cm anterior to the tragus and 1 cm inferior to the zygoma. Not reliable as up to 30% of adults without hypocalcemia exhibit a positive Chvostek sign and 30% of adults with hypocalcemia do not exhibit this response.

  • Electrocardiogram: QT prolongation or prolongation of the QTc (corrected QT interval) secondary to a prolonged ST segment. If critically low hypocalcemia is not appropriately treated, this may lead to arrhythmias such as torsades de pointes, ventricular tachycardia, or complete heart block.

  • Paresthesias: Tingling or prickling sensation, often in the lips, tongue, fingers, and feet.

  • Tetany: Development of spontaneous muscle cramping and pain (e.g., carpopedal spasm).

  • Trousseau sign: Spasm of the forearm and hand occurring after placing a blood pressure cuff on the upper arm at a pressure greater than the systolic blood pressure for 3 minutes. May be present in up to 4% of adults without hypocalcemia and carries test sensitivity of 94%.

 

Management

  • Goals of therapy are to relieve symptoms, decrease risk of cardiac arrhythmias, and increase and maintain a serum calcium concentration in the low-normal range (e.g., 8.0-8.5 mg/dL).

  • Proactive monitoring of calcium levels and early treatment are important for at-risk patients. Most recommend obtaining total serum calcium levels (with albumin correction if applicable) every 6 hours after surgery until levels stabilize; more frequent testing should be obtained if calcium levels are trending downward, are concernedly low (e.g., serum calcium <7 mg/dL), or IV calcium is administered. Some centers also obtain early postoperative PTH levels, usually within the first couple of hours, to help predict impending hypocalcemia.

  • Hypocalcemia may not correct until magnesium is corrected. Hypomagnesemia causes hypocalcemia through impairment of PTH secretion and renal resistance to PTH, leading to decreased reabsorption of calcium in the kidney. Phosphate levels are commonly monitored along with calcium levels (hyperphosphatemia may precede hypocalcemia from acute hypoparathyroidism).

  • Promptly evaluate patient if concern for symptomatic hypocalcemia develops or if critically low calcium values are discovered.

  • If administering IV calcium gluconate:

    • Calcium gluconate infusion must be administered slowly to avoid complications including cardiotoxicity (e.g., bradycardia, asystole), hypotension, and peripheral vein sclerosis. Follow institutional protocol for rate of infusion.

    • Ideally given via central line (e.g., peripherally inserted central catheter [PICC]); intramuscular administration should be avoided because of risk of localized soft-tissue and skin necrosis with extravasation.

    • For symptomatic hypocalcemia requiring IV calcium gluconate, it may take time to establish a central line and consideration may be given to initiating IV calcium gluconate therapy via peripheral IV with a slow infusion (over 10-20 minutes) to treat symptoms acutely.

    • Monitor calcium levels closely; consider serial labs every 4 hours as well as ionized calcium levels with a blood gas if severe or requiring IV calcium administration.

    • Replenish potassium and magnesium levels when necessary.

    • If patient is taking medications PO, start oral calcitriol (activated form of vitamin D) and calcium carbonate concomitantly.

    • Exercise caution in patients with renal insufficiency or taking digitalis.

    • Ensure patient is on continuous telemetry and consider obtaining a 12-lead electrocardiogram if severe.

  • Management of acute postoperative hypocalcemia following thyroid surgery or level VI neck dissection varies among centers, and you should understand the preferred management algorithm at your center; promptly notify other senior members of your care team if critically low values develop and maintain a low threshold for consulting Endocrinology based on clinical context.

 

Example Treatment Protocols

  • Example of a traditional protocol:

    • If corrected serum calcium >7.5 mg/dL (or ionized calcium is >3 mg/dL): Start oral calcium and vitamin D supplementation with calcitriol (activated form of vitamin D).

    • If corrected serum calcium <7.5 mg/dL (or ionized calcium is <3 mg/dL): Start IV calcium gluconate supplementation.

    • If carpopedal spasm, tetany, seizures, or prolonged QT with hypocalcemia: Start IV calcium gluconate supplementation and consider continuous infusion.

  • Example of a protocol incorporating postoperative PTH testing:

    • If corrected serum calcium >7.0 mg/dL with detectable PTH: Start oral calcium and vitamin D supplementation.

    • If PTH is undetectable: Start oral calcium and vitamin D supplementation and follow calcium levels.

    • If corrected serum calcium <7.0 mg/dL: Obtain electrocardiogram, place central line, and start IV calcium gluconate supplementation.

 

References
1. Shindo, M.L. (2013). Hyperparathyroidism: Evaluation and Surgery. In Johnson, J.J., Rosen, C.A. (Eds.), Bailey’s Head and Neck Surgery-Otolaryngology 5e (pp. 2131-2146). Baltimore, MD: Lippincott Williams & Wilkins.
2. Kakava, K., Tournis, S., Papadakis, G., et al. (2016). Postsurgical hypoparathyroidism: A systematic review. In Vivo. 30(3):171-179.
3. Khan, M.I., Waguespack, S.G., Hu, M.I. (2011). Medical management of postsurgical hypoparathyroidism [published correction appears in Endocr Pract. 17(6):967. dosage error in article text]. Endocr Pract. 17 Suppl 1:18-25.
4. Witteveen, J.E., van Thiel, S., Romijn, J.A., et al. (2013). Hungry bone syndrome: Still a challenge in the post-operative management of primary hyperparathyroidism: A systematic review of the literature. Eur J Endocrinol. 168(3):R45-R53.