History

Advances in parathyroid surgery have been colorful and international. Although the Swedish medical student Ivar Sandstrom is credited with first describing the “glandularae parathyrtreoidae” in 1880,¹ Sir Richard Owen made the original description in 1850.² Understanding of parathyroid function predated appreciation of the glands themselves; tetany was described in 1879 in a patient who underwent thyroidectomy (and incidental parathyroidectomy), and the connection between the parathyroids and tetany was identified in 1891.³ Famous patients with HPT include Albert Gahne, a Viennese tram car conductor who underwent two separate parathyroid resections in the 1920s by Felix Mandl for what was most likely parathyroid carcinoma,⁴ and Captain Charles Martell, a Merchant Marine captain who underwent seven operations and was eventually found to have a mediastinal parathyroid adenoma.⁵ Both men succumbed to their disease and the consequences of its treatment.

The relationship between chronic renal disease and HPT was first suggested by Albright and colleagues in 1934.⁶ Castleman and Mallory⁷ described the pathologic finding of parathyroid hyperplasia of chief cells with marked gland enlargement. Stanbury and associates⁸ described renal rickets, azotemic osteomalacia, and azotemic HPT and also performed the first subtotal parathyroidectomy as definitive therapy for renal osteitis fibrosa. Rasmussen and Craig⁹ and, independently, Berson and coworkers,¹⁰ extracted a stable homogeneous parathyroid polypeptide and demonstrated that hypercalcemia and phosphaturic properties reside in parathyroid hormone (PTH). Berson and Yalow won the Nobel prize in 1977 for developing an immunoassay for the measurement of PTH, and Reiss and Canterbury¹¹ developed an assay to measure the C-terminal and later the midmolecule portion of PTH.

Introduction of the serum channel autoanalyzer in the mid-1960s ushered in a new era of parathyroid surgery in that it facilitated earlier diagnosis of primary HPT. There was an increase in incidence of the disease and asymptomatic patients became commonplace. Additional technical advances have included improved preoperative localization with sestamibi scans, often using single-photon emission computed tomography (SPECT), the rapid intraoperative PTH assay, and the use of minimally invasive parathyroidectomy (MIP) with unilateral neck exploration through a small incision and regional anesthesia in the ambulatory setting.

Calcium Physiology

Calcium exists in extracellular plasma in a free ionized state, as well as bound to other molecules. So-called normal plasma levels of total calcium vary among laboratories, but the range of (bound and unbound) calcium is usually between 8.5 and 10.2 mg/dL (2.2 and 2.5 mmol/liter). The biologically inert bound fraction (55% of the total) binds to proteins. Changes in albumin alter total calcium levels significantly because most protein-bound calcium associates with albumin (80%). A small percentage of calcium is associated with other proteins, such as β-globulins, or with nonprotein molecules, such as phosphate and citrate. Mathematical formulas correcting for disparate albumin levels (e.g., corrected calcium = 0.8-mg/dL decrease for every 1.0-mg/dL decrease in albumin; [total calcium + 0.025] × [40 − albumin]) are notoriously inaccurate. Consequently, ionized calcium levels are measured when required. Forty-five percent of the total calcium is biologically active and exists in the ionized form, with a normal level of 4.5 to 5.0 mg/dL. Ionized calcium levels are inversely affected by the pH of blood; a 1-unit rise in pH will decrease the ionized calcium level by 0.36 mmol/liter.¹² Accordingly, patients who are hypocalcemic and hyperventilate can enhance their hypocalcemic symptoms, including perioral paresthesia, tingling in the fingers and toes, muscle cramping, and seizures.

Levels of calcium are highly modulated through a delicate interplay among PTH, calcitonin, and vitamin D acting on target organs such as bone, kidney, and the gastrointestinal (GI) tract (Table 39-1; Fig. 39-1). Chief cells in the parathyroid glands secrete PTH, an 84–amino acid protein, whenever serum calcium levels fall. PTH binds to its peripheral receptors and stimulates osteoclasts to increase bone resorption, to the kidney to increase calcium resorption and renal production of 1,25-dihydroxyvitamin D₃ (1,25[OH]₂D₃), and to the intestine to increase absorption of calcium and phosphate. Together, these processes raise the serum calcium level. The recently cloned calcium-sensing receptors (CaSRs) in the parathyroid glands detect changes in calcium levels, which results in a negative feedback loop that decreases PTH production.

Table 39-1 Actions of Major Calcium-Regulating Hormones

FIGURE 39-1 Calcium homeostasis and PTH.

Calcitonin is a 32–amino acid protein secreted by the parafollicular cells of the thyroid gland in response to high calcium levels. Its actions oppose those of PTH. Calcitonin rapidly inhibits bone resorption, thereby leading to a transient decrease in serum calcium levels. Although calcitonin plays a significant homeostatic function in other species, its effects on calcium metabolism in humans is not significant when a person is exposed to chronically elevated calcitonin levels. Accordingly, patients with extensive medullary carcinoma of the thyroid who have extraordinarily high serum calcitonin levels are usually eucalcemic.

Vitamin D is ingested or synthesized in precursor form, which then undergoes two hydroxylation steps before becoming biologically active. The first hydroxylation at carbon 25 occurs in the liver and the second hydroxylation at carbon 1 occurs in the kidney in response to increased PTH levels. 1,25(OH)₂D₃ increases calcium and phosphate resorption from the GI tract and stimulates bone resorption, which raises calcium levels. As a result, patients who are deficient in 1,25(OH)₂D₃ have an impaired ability to absorb calcium from their GI tract.

Anatomy

There are usually four parathyroid glands, which lie on the posterior surface of the thyroid. The superior glands are normally located on the posteromedial aspect of the thyroid near the tracheoesophageal groove, whereas the inferior parathyroids are more widely distributed in the region below the inferior thyroid artery (Fig. 39-2). Common sites for ectopic parathyroids are the thyrothymic ligament, superior thyroid poles, tracheoesophageal groove, retroesophageal space, and carotid sheath (Fig. 39-3).¹³ The percentage of individuals with supernumerary glands varies in published series from 2.5% to 22%.¹⁴ The average weight of a normal parathyroid gland is 35 to 40 mg; in adults, its color turns to yellow as the fat content increases. The inferior parathyroids originate from the third branchial pouch, whereas the superior parathyroids descend from the fourth branchial pouch. The superior and inferior parathyroid glands receive their blood supply from the inferior thyroid artery in 80% of cases. Each parathyroid gland generally receives a single end-artery blood supply that is vulnerable to injury during surgical manipulation. The glands are made up of chief and oxyphil cells, as well as fibrovascular stroma and adipose tissue.

FIGURE 39-2 Anatomic relationship of a left superior parathyroid adenoma to nearby structures, including the recurrent laryngeal nerve, carotid sheath, and its blood supply from the inferior thyroid artery. Aberrantly located parathyroid glands can be found behind the esophagus and in the carotid sheath, thymus, and mediastinum.

FIGURE 39-3 Possible locations of enlarged parathyroid glands in the neck and superior mediastinum with the use of an anteroposterior projection (A) and a lateral projection (B).

(From Udelsman R, Donovan PI: Remedial parathyroid surgery: Changing trends in 130 consecutive cases. Ann Surg 244:471–479, 2006.)

Primary HPT can be produced by three different pathologic lesions. A parathyroid adenoma is a benign encapsulated neoplasm responsible for 80% to 90% of cases. It usually affects a single gland, but 2% to 5% of patients with primary HPT have adenomas in two glands (double adenomas). Hyperplasia is a proliferation of parenchymal cells that affects all the parathyroid glands; it accounts for 10% to 15% of cases of primary HPT and all cases of secondary HPT. Most patients with primary HPT caused by multigland hyperplasia have sporadic disease. It is also associated with multiple endocrine neoplasia (MEN) type 1 (primary HPT combined with lesions of the pancreas and pituitary) and type 2A (primary HPT, medullary thyroid cancer, and pheochromocytoma) syndromes. Parathyroid carcinoma is a slow-growing, invasive neoplasm of parenchymal cells responsible for less than 1% of cases of primary HPT. Although fibrosis and mitotic activity are common, they are not specific for malignancy. The diagnosis of carcinoma is restricted to tumors that show invasion of blood vessels, perineural spaces, soft tissues, thyroid gland, or other adjacent structures, or to tumors with documented metastases. It is often difficult for the pathologist to make this diagnosis, especially if there is only a frozen section analysis of a resected parathyroid gland.

Diagnosis and Clinical Features

Primary HPT is the third most common endocrine disorder, after diabetes mellitus and thyroid disease. Middle-aged and older women are most commonly affected by the disease. It is characterized by hypersecretion of PTH, leading to hypercalcemia. Box 39-1 lists the differential diagnosis for hypercalcemia. The diagnosis is made by demonstrating elevated serum calcium and intact PTH (iPTH) levels and normal or increased urinary calcium levels in the setting of normal renal function. In up to 15% of patients, serum PTH levels fall within the upper normal range, but these levels are inappropriate relative to the elevated serum calcium levels. A 24-hour urine collection can help exclude the diagnosis of benign familial hypocalciuric hypercalcemia (BFHH), which results in mild increases in blood calcium and iPTH levels but low urinary calcium. Whereas the calcium-to-creatinine (Ca/Cr) clearance ratio is typically less than 0.01 in patients with BFHH, the ratio is usually more than 0.02 in primary HPT. BFHH is a generally benign condition transmitted in an autosomal dominant fashion that cannot be corrected by parathyroidectomy.

The clinical entity termed normocalcemic primary hyperparathyroidism has recently been described.¹⁵ It appears to be an early form of primary HPT in which patients have serum calcium levels in the high-normal range associated with an elevated serum PTH level. When these patients are symptomatic, surgical intervention is appropriate.

When HPT is seen in the setting of chronic renal failure, it is termed secondary HPT. This is a discrete clinical entity from primary HPT. Other less common causes of secondary HPT include malabsorptive and other metabolic disorders. Renal failure leads to hyperphosphatemia and decreased renal conversion of 25-hydroxycholecalciferol to 1,25-dihydroxycholecalciferol, thereby resulting in diminished intestinal calcium absorption. Both these effects lead to chronic hypocalcemia, which stimulates PTH secretion and parathyroid hyperplasia. As many as 90% of patients with chronic renal failure have evidence of secondary HPT. With prolonged stimulation of the parathyroids, a disorder termed tertiary HPT can develop in patients with chronic renal failure or those with long-standing secondary HPT who undergo kidney transplantation. Autonomous hyperfunction develops and the parathyroids no longer respond to calcium feedback inhibition, which results in hypercalcemia.

Before advent of the serum channel autoanalyzer, patients with primary HPT were typically seen with the clinical manifestations of hypercalcemia, including painful bones, kidney stones, abdominal groans, “psychic moans,” and fatigue overtones. Until the 1970s, 75% of patients presented with nephrolithiasis. Today, however, a biochemical diagnosis is usually made before the appearance of symptoms, and many patients are asymptomatic or minimally symptomatic. Less than 20% of primary HPT patients have renal symptoms and less than 5% have evidence of osteitis fibrosis cystica. Bone turnover is increased in up to 80% of patients with primary HPT, and serial measurements demonstrate a rapid fall in bone resorption within 2 weeks of parathyroidectomy.

Most contemporary series, however, demonstrate that at least 50% of patients today have a nonrenal nonosseous manifestation, and several series have demonstrated that 30% to 40% of patients are asymptomatic. Nonspecific complaints such as fatigue, lethargy, and depression are most commonly cited. Hypertension has been noted in approximately one third of patients with HPT, and a significant inverse relationship between mean arterial pressure and the glomerular filtration rate has been noted in these patients.

Hypercalcemic Crisis

Occasionally, patients with primary HPT are initially seen after symptoms and extremely high serum calcium levels have developed. Management of a so-called hypercalcemic crisis involves urgent medical and surgical strategies. Pharmacologic agents associated with or adversely affected by hypercalcemia need to be discontinued; specifically, digoxin potentiates arrhythmias in the setting of hypercalcemia. These patients are almost always severely dehydrated, and initial management requires hydration with normal saline. Medical management promotes the renal excretion of calcium. Once a patient with primary HPT is stabilized and serum calcium levels have been reduced to levels acceptable for induction of anesthesia (general or locoregional, if a minimally invasive surgical technique is anticipated), expedient efforts are made to localize the parathyroid disease in anticipation of urgent parathyroidectomy.

IV fluids, preferably normal saline, are administered at a rapid rate (200 to 300 mL/hr) to reverse the intravascular volume contraction and promote the renal excretion of calcium. Bedside vigilance to prevent fluid overload is essential. Loop diuretics are added to the regimen to reduce the risk for volume overload and inhibit calcium resorption in the loop of Henle. Patients with renal failure often cannot tolerate such large-volume resuscitation; instead, they undergo dialysis with a low-calcium dialysate.

Glucocorticoids lower calcium by inhibiting the effects of vitamin D. They also have been shown to decrease intestinal absorption of calcium, increase renal calcium excretion, and inhibit osteoclast-activating factor. Glucocorticoids are particularly effective in the setting of hypercalcemia secondary to granulomatous disease, in which the hypercalcemia stems from vitamin D toxicity. The initial dose of hydrocortisone is 200 to 400 mg/day IV for 3 to 5 days. Glucocorticoids are ineffective in most cases of hypercalcemia associated with malignancy.

Hypercalcemia of malignancy occurs by two mechanisms: (1) as a direct result of extensive osseous metastases; and (2) indirectly by release of parathyroid hormone–related peptide (PTHrP) by some tumors. Treatment of hypercalcemia of malignancy includes surgery, chemotherapy, or radiation therapy, or any combination of these, to treat the underlying cancer, as well as the administration of pharmacologic agents. Gallium nitrate, a compound that inhibits osteoclast resorption and lowers calcium levels, can be used at 200 mg/m² daily IV for 5 days. In this setting, gallium nitrate and pamidronate, a bisphosphonate (see later), have been equivalent in controlling hypercalcemia in small studies.

Calcitonin acts quickly (within 24 to 48 hours) to lower serum calcium levels and is more effective when used in combination with glucocorticoids. In a small, double-blind randomized trial of 50 cancer patients, however, calcitonin (up to 8 IU/kg SC or IM for 5 days) was less effective than gallium nitrate. Because preparations of calcitonin are extracted from salmon, patients with preformed antibodies or those with previous exposure to calcitonin can demonstrate an allergic reaction consisting of respiratory distress, flushing, nausea, vomiting, and tingling in the extremities.

Bisphosphonates are pyrophosphate analogues that have a high affinity for hydroxyapatite in bone. They potently inhibit osteoclast activity for up to 1 month. In hypercalcemia of malignancy, pamidronate (90 mg IV) or zoledronic acid (4 mg IV as initial treatment, 8 mg on retreatment) normalizes calcium levels in most patients. Although a single dose of pamidronate lowers calcium levels, evidence has suggested that zoledronic acid might become the bisphosphonate of choice because of its rapid onset of action and ability to lengthen the time to relapse by twofold. However, zoledronic acid also has been associated with compromised renal function.

Hypoparathyroidism

Hypoparathyroidism is an endocrine disorder in which hypocalcemia and hyperphosphatemia are the result of a deficiency in PTH secretion or action. The most common cause of hypoparathyroidism is damage to the parathyroid glands during thyroidectomy, but it can also occur after parathyroid exploration (see later, “Postoperative Complications”). The signs and symptoms of hypocalcemia are caused by neuromuscular excitability from reduced plasma ionized calcium. Early manifestations include perioral numbness and tingling in the fingers. Anxiety or confusion can follow, and it is important for the surgical team to reassure patients early to reduce psychiatric and neurocognitive symptoms. Anxiety often results in hyperventilation, which can then lead to respiratory alkalosis and a further reduction in the serum calcium level. Tetany, marked by carpopedal spasm, convulsions, or laryngospasm (or any combination of the three), may follow and can be fatal. Physical examination includes testing for a Chvostek sign, which is contraction of the facial muscles after tapping on the facial nerve anterior to the ear. Approximately 15% of normal individuals have a positive Chvostek sign, however.

There are also inherited forms of hypoparathyroidism. It can occur as part of a multiglandular endocrine deficiency syndrome (type 1), usually characterized by hypoparathyroidism, adrenal insufficiency, and mucocutaneous candidiasis. This syndrome generally develops in childhood, and not all patients express the classic triad. Idiopathic hypoparathyroidism also occurs sporadically in adults and is associated with antiparathyroid antibodies. Some cases might be related to incomplete penetrance of familial multiglandular syndrome type 1.

Disorders in which there is abnormal or absent formation of the parathyroid glands are associated with hypocalcemia. For example, DiGeorge’s syndrome occurs when the third and fourth branchial pouches develop abnormally. Transient neonatal hypocalcemia, a self-limited disorder, is more common than the genetic disorders that lead to permanent hypoparathyroidism. Parathyroid gland function can be impaired by infiltrative involvement of the glands in diseases such as hemochromatosis, Wilson’s disease, sarcoidosis, tuberculosis, or amyloidosis. Exposure to external radiation or very large doses of ¹³¹I for Graves’ disease or well-differentiated thyroid cancer has rarely been associated with hypocalcemia. Finally, abnormalities in magnesium levels are associated with a reversible abnormality of PTH secretion.

Pseudohypoparathyroidism is an uncommon metabolic disorder characterized by biochemical hypoparathyroidism, increased PTH secretion, and target tissue unresponsiveness to the biologic action of PTH. In addition to functional hypoparathyroidism, many of these patients exhibit a distinctive constellation of developmental and skeletal defects, collectively termed Albright’s hereditary osteodystrophy, including a round face, short stature, obesity, brachydactyly, heterotopic ossification, and mental retardation. Several forms of pseudohypoparathyroidism have been described and a diagnostic classification system has been developed (types 1a to 1c and 2).

Hyperparathyroidism

Primary Hyperparathyroidism

Effects of Surgery

Even though a National Institutes of Health (NIH) consensus conference was conducted in 1990, another workshop was held in 2002, and an international workshop was held in 2008 on the management of asymptomatic primary HPT, there is still no consensus among endocrinologists and endocrine surgeons about whether to administer nonoperative medical therapy and monitor patients or to refer them for early parathyroidectomy. Criteria for surgery have been established according to the best evidence to date (Box 39-2).¹⁶ To some extent, the role of parathyroidectomy in asymptomatic patients with mild to moderate hypercalcemia is debated because the natural history of the disease is still not well understood. Overall, rapid increases in the serum calcium level, progression of symptoms of complications, or both are uncommon in patients with borderline hypercalcemia. However, because of the long-term deleterious effects on bone mineralization, the pendulum has shifted to surgical intervention.¹⁷

Box 39-2 Adapted from Bilezikian JP, Khan AA, Potts JT Jr: Third International Workshop on the Management of Asymptomatic Primary Hyperthyroidism: Guidelines for the management of asymptomatic primary hyperparathyroidism: summary statement from the third international workshop. J Clin Endocrinol Metab 94:335–339, 2009.

Criteria for Surgical Referral

Serum calcium concentration >1 mg/dL (>0.25 mM/liter) above the upper limits of normal

Bone density at the lumbar spine, hip, or distal end of the radius that is >2 SD below peak bone mass (T-score <−2.5)

All individuals with primary hyperparathyroidism and <50 yr

Patients for whom medical surveillance is undesirable or impossible

Neuromuscular symptoms of primary HPT vary in expression and response to parathyroidectomy among series. However, proximal muscle weakness detected by examination of the isokinetic strength of knee extension and flexion appears to have a higher prevalence and good response to parathyroidectomy, as does respiratory muscle capacity. Psychiatric symptoms such as mental dullness, confusion, and depression are a focus of ongoing investigations. In a study by Roman and coworkers,¹⁸ 55 patients with primary HPT and benign euthyroid thyroid disease referred for surgery were evaluated preoperatively and postoperatively with validated psychometric and neurocognitive instruments. Patients with primary HPT reported more symptoms of depression preoperatively that improved postoperatively. Preoperatively, patients with primary HPT also showed greater delays in spatial learning. All subjects learned across the neurocognitive trials, but primary HPT patients were more delayed. After surgery, primary HPT patients improved and functioned at a level equivalent to that of patients with thyroid disease. The authors concluded that primary HPT may be associated with a deficit in spatial learning and processing that improves after parathyroidectomy. Several other studies have supported the possibility that patients with primary HPT may exhibit neurocognitive changes, and that these traits may show some improvement after parathyroidectomy.

Significant increases in bone mineral density in the lumbar spine and hip occur after parathyroidectomy, and these improvements are durable. Changes in bone remodeling and density are apparent within 6 months of surgery. Cohort studies have shown that fracture risk declines after parathyroidectomy. No effect of successful surgery has been noted on hypertension or renal impairment. Urinary calcium excretion and the incidence of nephrolithiasis are reduced by surgery. Currently, there are still no convincing data proving that surgical cure increases life expectancy. A Swedish case-control study conducted retrospectively demonstrated that 23 patients who underwent parathyroidectomy had a hazard ratio for death of 0.89 in comparison to matched controls in the normal population, but the numbers were too small to achieve statistical significance.¹⁹

Noninvasive Preoperative Localization

A major advance has been improvements in imaging techniques. This has led to the development of more localized surgery, with the opportunity for short operation times, the use of local or regional anesthesia, and limited or no hospital stay. There is now consensus—as marked by the recommendation of the 2002 NIH workshop and the 2008 international workshop—that preoperative localization is imperative before primary exploration if unilateral exploration is desired. Localization continues to be essential before all remedial parathyroidectomies (Table 39-2).

Table 39-2 Preoperative Imaging in Patients With Primary Hyperparathyroidism

Several noninvasive preoperative localization modalities are available, including technetium-99m (^99m Tc) sestamibi scintigraphy, ultrasonography, computed tomography (CT), magnetic resonance imaging (MRI), and thallous chloride-201(²⁰¹Tl) –^99mTc-pertechnetate subtraction scanning. Most recently, four-dimensional CT and positron emission tomography (PET)-CT fusion studies have also been used with success for parathyroid localization. There is general consensus that the single best study is sestamibi, especially when combined with SPECT, and it is now the most common nuclear medicine study performed. In 1989, ^99mTc, used for cardiac imaging, also was noted to be avidly taken up by parathyroid tissue. The study works by mitochondrial uptake of ^99mTc-sestamibi, and parathyroid cells typically have a large number of mitochondria. Sestamibi, a monovalent lipophilic cation, diffuses passively across cell membranes and concentrates in mitochondria. Hence, it is preferentially concentrated in adenomatous and hyperplastic parathyroid tissue because of increased blood supply, higher metabolic activity, and absence of P-glycoprotein on the cell membrane (Fig. 39-4). Sestamibi imaging can be performed preoperatively for MIP planning or on the morning of surgery in the operating room in conjunction with the use of a gamma probe to guide the surgeon during surgery.²⁰

FIGURE 39-4 Sestamibi scan demonstrating a left inferior parathyroid adenoma (arrow). Physiologic areas of increased tracer uptake include the thyroid, salivary glands, heart, and liver.

A meta-analysis of the sensitivity and specificity of sestamibi scanning in 6331 cases has demonstrated values of 91% and 99%, respectively, and suggested that 87% of patients with sporadic primary HPT would be candidates for unilateral exploration. Routine preoperative screening becomes cost-effective when more than 51% of patients are suitable for a unilateral operation. The sensitivity of sestamibi is limited in multiglandular disease. In one large study, scintigraphy localized at least one gland in all patients, but only 62% of the total number of hyperplastic glands. SPECT, which allows localization of structures in the anteroposterior plane, is particularly helpful in detecting smaller lesions and adenomas located behind the thyroid. The overall sensitivity for localizing adenomas smaller than 500 mg ranges considerably, from 53% to 92%.

A significant limitation of sestamibi scans is related to the coexistence of thyroid pathology or other metabolically active tissue (e.g., lymph nodes or thyroid cancer) that can mimic parathyroid adenomas by causing false-positive results on sestamibi scans. This limitation can be overcome in part by using the double-tracer subtraction technique of sestamibi, in which both thyroid and parathyroid nodular abnormalities can be diagnosed simultaneously, or in combination with neck ultrasonography to distinguish thyroid lesions and parathyroid adenomas preoperatively. Sestamibi scans are now being performed with simultaneous CT imaging to yield correlative functional and anatomic localization.

Ultrasound is effective, noninvasive, and inexpensive, but its limitations include operator dependency and restriction to application in the neck because it cannot image mediastinal parathyroid lesions (Fig. 39-5).²¹ It has a 48% to 74% true-positive rate. Ultrasound often is used in combination with sestamibi, in which case the combined true-positive rate rises to 90%. CT and MRI provide cross-sectional imaging and are useful for visualizing mediastinal tumors and glands within the tracheoesophageal groove. MRI does not involve the use of radiation, and parathyroid adenomas often appear intense on T2-weighted images. CT is less expensive and has a sensitivity of 70% and a specificity of nearly 100%. In a study of 42 surgical patients with primary HPT in which alternative preoperative localization strategies were compared, sensitivity was highest for sestamibi using the ^99mTc subtraction technique (95%), followed by ²⁰¹Tl-^99mTc subtraction (86%), CT (83%), and ultrasound (81%).²²

FIGURE 39-5 Ultrasound image of a hypoechoic parathyroid adenoma (with tumor perimeter marked).

Four-dimensional CT (4D-CT), a novel imaging modality similar to CT angiography, is derived from three-dimensional (3D)-CT scanning with an added dimension from the changes in perfusion of contrast over time. It generates detailed multiplanar images of the neck and allows the visualization of differences in the perfusion characteristics of hyperfunctioning parathyroid glands (i.e., rapid uptake and washout). Therefore, 4D-CT images provide anatomic and functional information (Fig. 39-6). In a study of 75 patients with primary HPT, 4D-CT demonstrated improved sensitivity (88%) over sestamibi (65%) and ultrasonography (57%) when the imaging studies were used to lateralize hyperfunctioning parathyroid glands to one side of the neck.²³

FIGURE 39-6 4D-CT showing increased uptake on delayed phase imaging of a parathyroid adenoma (arrow).

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