Hypoparathyroidism Postsurgical

Surgical destruction of the parathyroid glands is the most common cause of hypoparathyroidism. Hypoparathyroidism can occur after any surgical procedure that involves the anterior neck but is most commonly seen as a complication of parathyroid surgery or thyroid surgery, or after extensive resection for head and neck cancer. Trauma to the parathyroid vascular pedicles or inadvertent removal of the glands leads to either transient or permanent hypoparathyroidism. Estimates of the incidence of post-thyroidectomy hypoparathyroidism vary widely, ranging from 6.9% to 46% for transient and 0.4% to 33%' for permanent hypoparathyroidism. A survey by the American College of Surgeons reported an incidence of hypoparathyroidism following total thyroidectomy of 8%.2 A multicenter prospective trial of

5846 patients undergoing total thyroidectomy revealed an incidence of transient hypoparathyroidism of 7.3% and permanent hypoparathyroidism of 1.5%.' Characteristics of the surgical procedure associated with an increased risk of hypoparathyroidism were a greater extent of surgical resection and central rather than peripheral thyroid artery ligation, the latter of which is less likely to preserve the vascular supply to the parathyroid glands. Following total thyroidectomy, more experienced surgeons report fewer complications, including hypoparathyroidism.3

Surgical removal of hyperfunctioning parathyroid tissue often results in transient hypoparathyroidism because the remaining normal parathyroid tissue had been previously suppressed by hypercalcemia. Postsurgical hypoparathyroidism is usually manifest within the first 24 to 48 hours following surgery. Generally, calcium values and parathyroid responsiveness improve within 1 week after surgery. If the preexisting hyperparathyroidism resulted in excessive bone resorption, then a more severe, protracted form of post-parathyroidectomy hypocalcemia referred to as "hungry bones" may ensue. Once the PTH-stimulated bone resorption is halted by parathyroidectomy, then calcium and phosphorus are rapidly deposited into the bones, precipitating symptomatic hypocalcemia and hypophosphatemia. Patients with preoperative evidence of parathyroid bone disease such as osteitis fibrosa cystica, resorption of the distal phalanges, an elevated alkaline phosphatase, or those with renal osteodystrophy are at high risk for developing hungry bone syndrome and should be monitored carefully for the development of postoperative hypocalcemia and treated aggressively. Hungry bone syndrome is typically associated with more severe, symptomatic hypocalcemia and may require treatment for several weeks to months before biochemical parameters normalize. An elevated serum PTH level distinguishes hypocalcemia of hungry bones from other forms of post-parathyroidectomy hypocalcemia (Table 59-1).

The typical signs and symptoms associated with hypocalcemia are neuromuscular irritability, including perioral or acral paresthesias; muscle cramps that may progress to carpopedal spasm, laryngospasm, bronchospasm, or even

TABLE 59-1. Biochemical Characteristics oi Selected Hypocalcemic Disorders

Disorder

Calcium

Phosphorous

Hypoparathyroidism "Hungry bones" Pseudohypoparathyroidism Pseudo-pseudohypoparathyroidism

Low Low Low Normal

Low High High Normal

High Low High Normal

PTH = parathyroid hormone.

tetany; and central nervous system deficits as subtle as mood lability or as profound as stupor. Simple bedside maneuvers such as the Chvostek's sign and Trousseau's sign can reveal the presence of neuromuscular irritability. Chvostek's sign is described as circumoral twitching following tapping of the facial nerve. This sign is present in 10% to 30%4 of normal individuals; therefore, if it is to be used as a postoperative marker of hypocalcemia, it is important to verify that it is not present preoperatively. Trousseau's sign is carpal spasm that is elicited after inflation of a blood pressure cuff to 20 mm Hg above the patient's systolic blood pressure for 3 minutes. Severe hypocalcemia may also manifest as prolongation of the QT interval or nonspecific changes on an electrocardiogram.

Treatment decisions for postoperative hypoparathyroidism are based on the degree of hypocalcemia, the rapidity of its development, and severity of the symptoms. In severe cases (calcium level <7.5 mg/dL or severe symptoms), intravenous administration of calcium salts is required. A recommended approach includes using 10 ampules of calcium gluconate (90 mg of elemental calcium per 10-mL ampule) in 1 L of 5% dextrose with an initial infusion rate of 100 mL/hour. With frequent monitoring of serum calcium levels (usually every 1 to 2 hours), the infusion rate is titrated to keep the calcium level in the low-normal range. Once stabilized, the patient may be converted to a regimen of oral calcium and calcitriol as described later.

If the patient is asymptomatic with mild hypocalcemia (7.5 to 8.5 mg/dL), oral therapy consisting of up to 1000 mg of elemental calcium every 6 hours and 0.25 to 2.0 (Xg/day of calcitriol [l,25-(OH)2]vitamin D3 should be instituted. As with intravenous therapy, the oral doses can be titrated to keep the calcium in the low-normal range. Magnesium levels should be monitored and repleted because hypomag-nesemia results in both impaired PTH secretion and PTH resistance. In most cases, treatment with calcium and vitamin D is short term and necessary only until the residual parathyroid tissue begins to function.

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