HYPOPARATHYROIDISM
GENERAL FEATURES
• Primary hypoparathyroidism is a relatively uncommon condition that is characterized by inadequate parathyroid hormone (PTH) activity, resulting in hypocalcemia.
• Decreased secretion of PTH occurs following destruction or removal of the parathyroid glands, particularly in the treatment of hyperparathyroidism.
• Incidental destruction may occur during thyroid, laryngeal, or head or neck surgery or may result from extensive irradiation to the face, neck, or mediastinum.
• Hypoparathyroidism can also have an autoimmune etiology and is a common feature of polyglandular autoimmune syndrome type I, a familial disorder.
• Other rare causes include genetic defects or mutations and storage or infiltrative disease of the parathyroid glands.
CLINICAL ASSESSMENT
• Manifestations of hypoparathyroidism are primarily related to hypocalcemia (total serum calcium, 7.0-7.5 mg/dL).
• Acute disease causes neuromuscular irritability—circumoral tingling, extremity paresthesias, tetany, carpopedal spasm, laryngospasm, muscle cramps, and seizures.
• Some patients have only vague symptoms (fatigue, emotional instability, anxiety, or depression) with or without neuromuscular symptoms.
• Hyperactive deep tendon reflexes, Chvostek sign, and Trousseau sign may all be present.
• Chronic hypocalcemia may lead to mental status changes; cataracts; dry, coarse skin; brittle nails; and brittle, sparse hair and eyebrows.
DIAGNOSIS
• Low serum and urinary calcium levels. Since the calcium ion is highly bound to protein, a total calcium level cannot be interpreted without knowing the total protein or albumin level as well.
• Low parathyroid hormone and magnesium levels
• Low serum phosphate but normal alkaline phosphatase levels
• Measurement of 25-hydroxyvitamin D level is important to exclude vitamin D deficiency as a cause of hypocalcemia.
• CT of the skull may show dense bones and calcifications of the basal ganglia, especially with chronic hypocalcemia.
• Severe hypocalcemia may also cause prolonged QT intervals and abnormal T waves on ECG.
TREATMENT
• Emergency treatment for acute hypocalcemia includes airway management, IV calcium gluconate, vitamin D supplementation, and magnesium supplementation if levels are low.
• Intravenous calcium gluconate: Calcium infusion drips should be started at 0.5 mg/kg/hour and increased to 2 mg/kg/hour as needed, with an arterial line placed for frequent measurement of ionized calcium.
• Maintenance therapy includes oral calcium (500 mg to 2 g 2-4 times daily) and vitamin D supplements (1,25-dihydroxyvitamin D or
calcitriol).
• Monitor total serum calcium every 3 months, and maintain level at 8 to 8.6 mg/dL.
SUGGESTED READING
• Goltzman D. Clinical manifestations of hypocalcemia. UpToDate Web site. http://www.uptodate.com/contents/clinical-manifestations-of-hypocalcemia?source=search_result&selectedTitle=5%7E93. Updated October 15, 2008. Accessed December 6, 2011.
• Goltzman D. Etiology of hypocalcemia in adults. UpToDate Web site. http://www.uptodate.com/contents/etiology-of-
hypocalcemia-in-adults?source=searchresult&
selectedTitle=1%7E16. Updated March 18, 2011. Accessed December 6, 2011.
• Goltzman D. Treatment of hypocalcemia. UpToDate Web site.
http://www.uptodate.com/contents/treatment-of-
hypocalcemia?source=search_result&selectedTitle=
2%7E93. Updated July 27, 2010. Accessed December 6, 2011.
• Wallace DJ. Hypoparathyroidism in emergency medicine.
Medscape Web site. http://emedicine.medscape.com/article/767744-overview. Updated April 15, 2009. Accessed December 6, 2011.
QUESTION & ANSWER
1. A 42-year-old woman develops a tingling sensation in her hands on postoperative day 2 following a total thyroidectomy for papillary thyroid cancer. She appears anxious and complains of muscle cramps. Which of the following is the most appropriate initial step to manage this condition?
a. 75 µg of levothyroxine
b. 10 mL of 10% magnesium sulfate IV
c. Continuous infusion of calcium gluconate
d. Stat IM dose of synthetic parathyroid hormone
Answer: c
Explanation: Intravenous calcium gluconate is the appropriate treatment for severe, symptomatic hypocalcemia, although high-dose oral calcium supplementation (up to 1-2 g every 4 hours) may be sufficient for patients with mild symptoms. This patient is experiencing postthyroidectomy hypocalcemia, likely due to transient ischemia of the parathyroid gland. Unless the parathyroid glands were inadvertently excised during the procedure, the condition is likely to be self-limited and will resolve in a few days. If the hypocalcemia persists, calcium and vitamin D supplementation will be necessary. There is no role for thyroid hormone replacement in the treatment of hypocalcemia, and synthetic parathyroid hormone is a treatment for osteoporosis. Magnesium sulfate may be beneficial if magnesium levels are low but would not be the initial step.