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Parathyroidectomy

A parathyroidectomy is a surgical procedure involving the removal of one or more of the four small parathyroid glands located behind the thyroid in the neck, which regulate blood calcium levels by producing parathyroid hormone (PTH).^[1] It serves as the definitive treatment for hyperparathyroidism, a condition characterized by excessive PTH production leading to elevated blood calcium (hypercalcemia), and is typically indicated when medical management fails or symptoms are present.^[2] The primary indication for parathyroidectomy is primary hyperparathyroidism, most commonly caused by a benign adenoma in one gland (accounting for about 85% of cases), glandular hyperplasia, or rarely parathyroid carcinoma; surgery is recommended for symptomatic patients or asymptomatic individuals under age 50, with serum calcium more than 1 mg/dL above the upper normal limit, or those with complications like kidney stones, osteoporosis, or reduced kidney function.^[1]^[2] Secondary hyperparathyroidism, often due to chronic kidney disease or vitamin D deficiency, may also necessitate the procedure if symptoms persist despite treatments like phosphate binders or calcimimetics, while tertiary cases involve autonomous gland function post-secondary causes.^[2] Contraindications include familial hypocalciuric hypercalcemia (FHH), a genetic condition mimicking hyperparathyroidism but unresponsive to surgery.^[2] Preoperative localization of overactive glands is crucial and typically involves imaging such as sestamibi scans, neck ultrasounds, 4D computed tomography (CT), or PET-choline CT to guide the approach.^[1] The surgery can be performed under general or local anesthesia with sedation, often as an outpatient procedure lasting about one hour; options include minimally invasive parathyroidectomy (MIP) for single-gland disease via a small incision (around 2 inches) or traditional bilateral neck exploration to inspect all four glands if localization is unclear.^[3]^[2] Intraoperative PTH monitoring confirms successful removal by demonstrating a significant drop (over 50%) in hormone levels post-excision.^[2] While generally safe with a success rate exceeding 95% in curing hyperparathyroidism, potential risks include bleeding or hematoma (0.6% incidence), recurrent laryngeal nerve injury (1.1% permanent), hypocalcemia due to temporary gland stunning or hungry bone syndrome (up to 3.8% permanent), and infection; recurrence occurs in less than 2-5% of cases.^[3]^[2] Recovery typically involves monitoring for low calcium symptoms like numbness or muscle cramps, with calcium and vitamin D supplementation as needed, and most patients resume normal activities within days to weeks, though voice changes or low calcium may persist temporarily.^[1]^[3]

Background

Anatomy of the Parathyroid Glands

The parathyroid glands are a group of four small endocrine organs typically situated on the posterior aspect of the thyroid gland, with two superior glands positioned near the upper poles and two inferior glands near the lower poles. The superior parathyroids are located at the posterolateral aspect of the thyroid's superior pole, approximately 1 cm superior to the junction of the recurrent laryngeal nerve and inferior thyroid artery, and lie deep to the plane of the recurrent laryngeal nerve. In contrast, the inferior parathyroids are found near the inferior poles of the thyroid, within 1 to 2 cm of the inferior thyroid artery's insertion point, and are positioned superficial to the recurrent laryngeal nerve plane. These glands develop embryologically from the endoderm of the pharyngeal pouches, with the superior pair originating from the dorsal wings of the fourth pharyngeal pouches and the inferior pair from the dorsal wings of the third pharyngeal pouches; by the seventh week of gestation, the inferior glands undergo a longer caudal migration along the path of the thymus, contributing to their greater positional variability.^[4]^[5] Each parathyroid gland is oval or bean-shaped, measuring approximately 3 to 8 mm in length and weighing 30 to 40 mg, though dimensions can vary slightly between individuals. Their blood supply derives primarily from end branches of the inferior thyroid artery, with potential collateral contributions from the superior thyroid artery, thyroid ima artery, or vessels from the larynx, trachea, and esophagus; venous drainage occurs via the thyroid vein plexus into the internal jugular and innominate veins. A thin fibrous capsule separates the glands from the surrounding thyroid tissue, and they are highly vascularized to support their endocrine function.^[5]^[6]^[7] Anatomical variations are frequent and clinically significant, with supernumerary glands (more than four) identified in up to 13% of autopsy cases and fewer than four in some individuals, potentially totaling between three and eight glands overall. Ectopic locations occur in up to 16% of cases due to aberrant embryological descent, including intrathyroidal positioning, extension into the thymus or mediastinum, retroesophageal placement, or residence within the carotid sheath; the inferior glands are more prone to such variability owing to their extended migration path.^[5]^[4] Histologically, the parathyroid glands are composed predominantly of chief cells and oxyphil cells embedded in a stroma of adipocytes and connective tissue. Chief cells, the primary functional units, are polygonal with poorly defined borders, pale eosinophilic cytoplasm rich in secretory granules and mitochondria, and large round nuclei; they synthesize and secrete parathyroid hormone (PTH), which plays a key role in maintaining calcium homeostasis by regulating bone resorption, renal calcium reabsorption, and vitamin D activation. Oxyphil cells, larger and less numerous, form clusters with abundant eosinophilic cytoplasm due to numerous mitochondria and few secretory granules, along with smaller, densely staining nuclei; their function remains unclear, though they may contribute to PTH secretion in certain conditions and increase in prevalence with aging.^[6]

Physiology and Pathophysiology

The parathyroid glands, typically four small endocrine organs located posterior to the thyroid gland, play a central role in calcium homeostasis by secreting parathyroid hormone (PTH) in response to decreased serum ionized calcium levels detected by calcium-sensing receptors on chief cells. PTH acts primarily on three target organs: bones, kidneys, and intestines (via vitamin D). In bone, PTH stimulates osteoclast activity to promote calcium resorption and release into the bloodstream; in the kidneys, it enhances calcium reabsorption in the distal tubules while inhibiting phosphate reabsorption, leading to phosphaturia; and indirectly, it activates renal 1-alpha-hydroxylase to convert 25-hydroxyvitamin D to its active form, 1,25-dihydroxyvitamin D (calcitriol), which increases intestinal calcium and phosphate absorption. This integrated response maintains serum calcium within a narrow range of approximately 8.5–10.2 mg/dL, preventing hypocalcemia that could impair neuromuscular function and cardiac contractility.^[8]^[9] Primary hyperparathyroidism (PHPT) arises from autonomous overproduction of PTH due to intrinsic parathyroid gland abnormalities, most commonly a single parathyroid adenoma (accounting for 80–85% of cases), multigland hyperplasia (10–15%), or rarely parathyroid carcinoma (<1%). This excessive PTH secretion disrupts calcium balance, resulting in hypercalcemia (serum calcium >10.2 mg/dL) through enhanced bone resorption, renal calcium retention, and increased calcitriol-mediated absorption. Clinically, PHPT manifests with the classic tetrad of symptoms encapsulated by the mnemonic "stones, bones, groans, and moans": renal stones from hypercalciuria and nephrolithiasis, skeletal complications like osteitis fibrosa cystica and bone pain from accelerated resorption, abdominal groans due to peptic ulcers, pancreatitis, or constipation, and psychic moans from neuropsychiatric effects such as fatigue, depression, or cognitive impairment. Biochemical hallmarks include elevated PTH (>65 pg/mL), hypercalcemia, and hypophosphatemia (<2.5 mg/dL), often with increased urinary calcium excretion.^[10]^[11] Secondary hyperparathyroidism (SHPT) develops as a compensatory mechanism to chronic hypocalcemia or hyperphosphatemia, most frequently in chronic kidney disease (CKD) or vitamin D deficiency, where impaired renal function reduces calcitriol synthesis and phosphate clearance, stimulating PTH secretion to normalize calcium levels. In CKD, phosphate retention directly suppresses calcitriol production, leading to gut malabsorption of calcium and secondary hypocalcemia, which prompts parathyroid hyperplasia; PTH levels rise markedly (>65 pg/mL), but serum calcium remains normal or low, with elevated phosphate (>4.5 mg/dL). Vitamin D deficiency, common in up to 50% of the global population, similarly drives SHPT through reduced intestinal calcium absorption, though it is reversible with supplementation. Unlike PHPT, SHPT does not typically cause hypercalcemia unless it progresses.^[12]^[13] Tertiary hyperparathyroidism (THPT) represents an evolution of prolonged SHPT, particularly in end-stage renal disease, where chronic stimulation leads to parathyroid gland autonomy and nodular hyperplasia, resulting in unregulated PTH overproduction independent of serum calcium levels. This shift often occurs after years of CKD, with glands becoming resistant to negative feedback from calcium or calcitriol, causing hypercalcemia and severe hyperphosphatemia despite medical management. PTH levels are excessively high (>300–500 pg/mL), and complications include vascular calcification and bone disease; THPT is distinguished biochemically from SHPT by the emergence of elevated calcium alongside persistently high PTH and phosphate. Surgical intervention, such as parathyroidectomy, is frequently required to halt this autonomous state.^[13]^[14]

Indications

Primary Hyperparathyroidism

Primary hyperparathyroidism (PHPT) is the most common indication for parathyroidectomy, characterized by excessive parathyroid hormone (PTH) secretion leading to hypercalcemia, typically due to a single parathyroid adenoma in over 80% of sporadic cases.^[15] This condition arises from autonomous overproduction of PTH by the parathyroid glands, independent of serum calcium levels, distinguishing it from secondary forms.^[16] Parathyroidectomy is the definitive treatment, aiming to normalize calcium and PTH levels and prevent complications such as bone loss, kidney stones, and cardiovascular risks.^[17] Epidemiologically, PHPT affects approximately 1 in 1,000 adults, with an incidence of 66 per 100,000 person-years in women and 25 per 100,000 in men, rising with age and being three to four times more prevalent in postmenopausal women over 50 years.^[18] In the current era, over 80% of cases are asymptomatic at diagnosis, often detected incidentally through routine blood tests showing elevated serum calcium, though progression to symptomatic disease—including nephrolithiasis, osteoporosis, and neurocognitive impairments—occurs in a subset if untreated.^[15] The condition's prevalence has stabilized in regions with routine biochemical screening, but underdiagnosis remains common in underserved populations.^[19] According to the American Association of Endocrine Surgeons (AAES) guidelines, parathyroidectomy is indicated for all symptomatic patients with PHPT, including those with kidney stones, fractures, or reduced renal function, as surgery alleviates symptoms and halts disease progression.^[17] For asymptomatic patients, surgery is recommended if serum calcium exceeds 1 mg/dL above the upper normal limit (or >11.5 mg/dL in some contexts), the patient is younger than 50 years, bone mineral density T-score is ≤ -2.5 at the lumbar spine, hip, or forearm, a vertebral fracture is present, estimated glomerular filtration rate (eGFR) is <60 mL/min, or kidney stones are documented.^[17] These criteria prioritize intervention to mitigate anticipated complications, with observation reserved for those not meeting thresholds, involving annual monitoring of calcium, PTH, and bone density.^[17] In patients with multiple endocrine neoplasia (MEN), PHPT presents differently and influences surgical strategy. In MEN1, hyperparathyroidism affects over 95% of patients by age 50, typically as multiglandular hyperplasia, necessitating subtotal parathyroidectomy (removal of 3.5 glands) to address the high recurrence risk.^[17] MEN2A involves PHPT in 20-30% of cases, often as hyperplasia or adenoma, where resection of enlarged glands is preferred, sometimes combined with prophylactic thyroidectomy.^[17] Genetic counseling is advised for those under 40 or with multigland disease to guide family screening and timing.^[17] Successful parathyroidectomy for sporadic PHPT, particularly adenoma removal, normalizes serum calcium in over 95% of cases, with cure rates reaching 97-99% in experienced centers, leading to stabilization or improvement in bone density and reduced fracture risk within 1-2 years postoperatively.^[17] In MEN-associated PHPT, outcomes focus on delaying recurrence rather than permanent cure, with subtotal approaches achieving normocalcemia in 80-90% initially but requiring lifelong monitoring due to regrowth potential.^[17]

Secondary and Tertiary Hyperparathyroidism

Secondary hyperparathyroidism (SHPT) develops as a compensatory response to chronic kidney disease (CKD), where reduced renal phosphate excretion and impaired 1,25-dihydroxyvitamin D synthesis lead to hypocalcemia and hyperphosphatemia, prompting parathyroid gland hyperplasia and elevated parathyroid hormone (PTH) levels.^[12] This condition is prevalent among patients with end-stage kidney disease (ESKD) on dialysis, with global estimates indicating that approximately 30% to 54% of such individuals experience SHPT, and severe cases refractory to medical management affect 10% to 20% over time, particularly after 10 years of dialysis.^[20] The incidence of severe SHPT necessitating surgical intervention has risen alongside the increasing prevalence of CKD, driven by aging populations and higher dialysis rates.^[21] Parathyroidectomy is indicated for SHPT when medical therapies fail to control PTH elevation, typically defined as persistent intact PTH levels exceeding 800 pg/mL for more than six months despite optimized treatment with phosphate binders, vitamin D analogs, and calcimimetics such as cinacalcet or etelcalcetide.^[22] According to the National Kidney Foundation's Kidney Disease Outcomes Quality Initiative (KDOQI) guidelines, surgery is recommended for severe SHPT with PTH >800 pg/mL (88 pmol/L) that remains unresponsive, often accompanied by complications like vascular calcification, calciphylaxis, or refractory anemia.^[23] The Kidney Disease: Improving Global Outcomes (KDIGO) 2017 guidelines similarly suggest parathyroidectomy for CKD stages G3a–G5D patients with severe hyperparathyroidism refractory to pharmacological interventions, emphasizing cases with associated morbidity such as bone pain, fractures, or vascular disease.^[24] Calciphylaxis, a life-threatening condition involving cutaneous necrosis due to arteriolar calcification, serves as a critical indication for surgery when linked to uncontrolled SHPT, as parathyroidectomy can improve outcomes in these refractory scenarios.^[25] Surgical management of SHPT typically involves total parathyroidectomy with autotransplantation of parathyroid tissue into the forearm muscle or subtotal parathyroidectomy (leaving 30–60 mg of viable tissue) to minimize recurrence risk while avoiding permanent hypoparathyroidism.^[22] Total parathyroidectomy with autotransplantation is often preferred in dialysis patients to facilitate future access for graft removal if hyperparathyroidism recurs, reducing the need for reoperative neck surgery.^[2] These approaches effectively lower PTH levels and alleviate symptoms, with studies showing improved survival rates of 15%–57% post-surgery compared to medically managed cohorts.^[22] Tertiary hyperparathyroidism (THPT) emerges from prolonged SHPT, particularly in long-term dialysis or post-renal transplant patients, where parathyroid nodular hyperplasia becomes autonomous, leading to unregulated PTH secretion and hypercalcemia independent of calcium levels.^[26] This progression occurs in up to 10%–30% of renal transplant recipients within the first year, driven by persistent gland hyperplasia despite normalized renal function.^[27] Indications for parathyroidectomy in THPT focus on symptomatic or persistent hypercalcemia, with surgery recommended when serum calcium exceeds 11 mg/dL (2.75 mmol/L) or intact PTH surpasses 1,000 pg/mL despite medical optimization, alongside complications such as calciphylaxis, nephrocalcinosis, or severe bone disease.^[27] The KDIGO guidelines endorse parathyroidectomy for refractory cases post-transplant exhibiting autonomous PTH elevation and hypercalcemia, aiming to normalize calcium levels and prevent graft dysfunction.^[24] Calciphylaxis remains a key surgical trigger in THPT, as urgent parathyroidectomy can halt progression in medically resistant instances.^[25] The preferred surgical strategy mirrors that for SHPT, utilizing total parathyroidectomy with autotransplantation or subtotal resection to address diffuse hyperplasia while preserving some function and reducing recurrence, which can approach 10%–20% without autotransplantation.^[28] Medical alternatives, including calcimimetics like etelcalcetide, serve as first-line therapy for both SHPT and early THPT to suppress PTH and maintain calcium homeostasis, with parathyroidectomy reserved for failures where PTH remains >800–1,000 pg/mL or hypercalcemia persists.^[21]

Preoperative Evaluation

Localization Studies

Localization studies play a crucial role in the preoperative evaluation for parathyroidectomy, aiming to identify the location of abnormal parathyroid glands to guide surgical planning and improve outcomes in patients with hyperparathyroidism. These studies combine biochemical confirmation with imaging modalities to detect hyperfunctioning tissue, particularly adenomas, which account for the majority of cases in primary hyperparathyroidism. Accurate localization facilitates minimally invasive approaches and reduces operative time, though no single modality is infallible, and concordance between techniques is often sought for optimal results.^[29] Biochemical tests are essential for confirming the diagnosis and distinguishing primary hyperparathyroidism from mimics before proceeding to imaging. The intact parathyroid hormone (PTH) assay measures circulating PTH levels, which are typically elevated or inappropriately normal in the presence of hypercalcemia. Serum calcium levels are assessed to confirm hypercalcemia, a hallmark of the condition, while a 24-hour urine calcium collection helps rule out familial hypocalciuric hypercalcemia (FHH), a benign entity with low urinary calcium excretion despite elevated serum calcium and PTH. These lab evaluations establish the need for localization imaging without directly identifying gland position.^[30] High-resolution neck ultrasound serves as a first-line imaging modality due to its non-invasive nature, low cost, and lack of radiation exposure. It visualizes parathyroid adenomas as hypoechoic, well-circumscribed masses posterior to the thyroid, often with a vascular pedicle on color Doppler. The sensitivity for detecting single adenomas ranges from 70% to 90%, though it is operator-dependent and less effective for ectopic or posterior glands obscured by thyroid nodules.^[31]^[32] Technetium-99m (Tc-99m) sestamibi scintigraphy is another cornerstone first-line study, exploiting the differential uptake and washout of the radiotracer in hyperfunctioning parathyroid tissue compared to thyroid. Dual-phase imaging—early for thyroid and delayed for parathyroid—localizes adenomas with approximately 80% sensitivity, enhanced by single-photon emission computed tomography (SPECT)/CT for anatomic correlation. It is particularly useful for ectopic glands but can be confounded by thyroid pathology.^[31]^[33] When first-line studies are discordant or negative, advanced imaging such as four-dimensional computed tomography (4D-CT) is employed. This multiphase CT protocol captures arterial, venous, and delayed phases to assess perfusion and enhancement patterns characteristic of adenomas, offering high spatial resolution for precise localization. Sensitivities range from 79% to 92%, making it valuable for multigland disease or ectopic locations, though it involves higher radiation doses.^[34]^[31] Positron emission tomography/computed tomography (PET/CT) using tracers like 18F-choline or 18F-FDG provides functional imaging for challenging cases, such as persistent disease or hyperplasia. Choline PET/CT demonstrates superior sensitivity (up to 95%) for detecting small or ectopic adenomas due to rapid uptake in hypermetabolic parathyroid tissue, outperforming sestamibi in meta-analyses. FDG-PET/CT is less specific but useful in select scenarios like post-surgical recurrence. These modalities are reserved for non-localizing initial studies given their cost and availability.^[35]^[36] Combining ultrasound and sestamibi scintigraphy yields the highest concordance rates, localizing single adenomas in 85% to 95% of cases when both modalities agree, enabling focused surgical exploration. This dual-modality approach minimizes false positives and enhances preoperative confidence.^[37]^[31] Despite these advances, localization studies have limitations, particularly in multiglandular hyperplasia or small adenomas (<200 mg), where false negatives occur due to lower tracer avidity or subtle anatomic features. Sensitivity drops in secondary hyperparathyroidism or post-thyroidectomy scarring, necessitating selective use and surgical expertise.^[31]^[32]

Patient Preparation

Patient preparation for parathyroidectomy involves a comprehensive medical evaluation to optimize health and minimize perioperative risks. This includes assessing comorbidities, particularly cardiovascular disease in patients with chronic kidney disease (CKD) for secondary or tertiary hyperparathyroidism, and correcting nutritional deficiencies such as vitamin D insufficiency, which is common in up to 80% of patients with primary hyperparathyroidism (pHPT). Supplementation with vitamin D is recommended prior to surgery to prevent postoperative hypocalcemia, with a weak recommendation based on low-quality evidence from the American Association of Endocrine Surgeons (AAES) guidelines. Adequate hydration is essential, especially to manage elevated serum calcium levels, and may involve intravenous fluids in cases of severe hypercalcemia.^[2] Preoperative bone mineral density assessment via dual-energy X-ray absorptiometry at the lumbar spine, hip, and distal radius is advised to evaluate skeletal involvement. Voice quality evaluation is also performed to baseline for potential recurrent laryngeal nerve injury. Pharmacologic interventions focus on short-term control of severe hypercalcemia (serum calcium >14 mg/dL or symptomatic), using intravenous bisphosphonates such as pamidronate or zoledronic acid, or calcimimetics like cinacalcet, to stabilize patients before surgery.^[38] These agents lower calcium levels rapidly but should be used judiciously and not long-term.^[2] In patients with secondary hyperparathyroidism, calcimimetics may be continued briefly preoperatively but discontinued to avoid interference with intraoperative parathyroid hormone monitoring.^[39] Informed consent is obtained after discussing procedure-specific outcomes and risks, including a surgical cure rate exceeding 95% in experienced centers for pHPT and a low incidence of permanent recurrent laryngeal nerve injury (approximately 1-2%).^[40]^[2] Patients are informed of potential transient hypocalcemia and the benefits of normocalcemia restoration. Anesthesia planning typically involves general anesthesia for open procedures, though local anesthesia with sedation is suitable for select minimally invasive cases in low-risk patients.^[2] A multidisciplinary approach is crucial, particularly for patients with multiple endocrine neoplasia (MEN) syndromes or renal disease, involving endocrinologists for hormonal optimization and nephrologists for dialysis coordination in CKD cases.^[39] Preoperative localization studies, if positive, may guide minimally invasive techniques but are not detailed here.^[2]

Surgical Procedure

Conventional Open Parathyroidectomy

The conventional open parathyroidectomy represents the traditional surgical approach for treating hyperparathyroidism, involving a comprehensive exploration of the neck to identify and address all parathyroid glands. Performed under general anesthesia, this method ensures thorough visualization and is particularly suited for cases where preoperative imaging is inconclusive or multiple glands are affected.^[2]^[41] The procedure begins with a 2-4 cm transverse incision placed in a skin crease, approximately two fingerbreadths above the suprasternal notch, to minimize visible scarring while providing adequate access to the thyroid and parathyroid regions.^[41]^[3] The platysma muscle is divided, and the strap muscles are retracted to expose the thyroid gland, which is then mobilized for bilateral neck dissection. This systematic exploration identifies all four parathyroid glands, typically located posterior to the thyroid lobes, with removal of enlarged or hyperfunctioning ones; frozen section biopsy may be performed on excised tissue to confirm parathyroid origin if atypical features are noted.^[2]^[41] Intraoperative parathyroid hormone (PTH) monitoring is integral to confirming surgical success, with blood samples drawn pre-excision and at 10 minutes post-excision. According to the Miami criteria, a greater than 50% drop in PTH from the highest pre-incision or pre-excision level, reaching the normal range, indicates adequate removal and guides whether further exploration is needed.^[42]^[2] The operation typically lasts 1-2 hours, depending on the extent of exploration required.^[43]^[3] Patients generally experience a hospital stay of 1-2 days for monitoring and recovery before discharge.^[3]^[44] This approach is indicated for multigland disease, such as four-gland hyperplasia in secondary or tertiary hyperparathyroidism; reoperative cases for persistent or recurrent disease; and situations with failed preoperative localization studies.^[2]^[41] In contrast, minimally invasive techniques may be preferred for straightforward single-gland adenomas with clear localization.^[41]

Minimally Invasive Techniques

Minimally invasive techniques for parathyroidectomy have become the preferred approach for the majority of cases involving single-gland primary hyperparathyroidism, which accounts for 80-90% of patients, allowing for targeted removal with smaller incisions and reduced recovery time compared to conventional methods.^[45] These procedures rely on accurate preoperative localization studies, such as ultrasound and sestamibi scintigraphy, to identify the affected gland and minimize surgical exploration.^[46] Focused parathyroidectomy involves a small 1-2 cm incision directly over the localized adenoma, guided by imaging, and is suitable for single-gland disease without the need for extensive neck dissection. This technique achieves cure rates of 95-98% in appropriately selected patients, with operative times typically under 60 minutes and often performed as an outpatient procedure or with discharge the same day or next day.^[47]^[48]^[3] Endoscopic and video-assisted parathyroidectomy utilize a camera for visualization through small ports, often via transcervical or axillary approaches, which further reduce visible scarring and improve cosmetic outcomes. In minimally invasive video-assisted parathyroidectomy (MIVAP), a 1-2 cm central incision is combined with endoscopic tools in a gasless or insufflated field, yielding cure rates of approximately 98.6% and conversion to open surgery in about 12% of cases, primarily when multigland disease is unexpectedly found.^[49] These methods demonstrate shorter lengths of stay (mean 1.8 days) and high patient satisfaction with cosmesis scores around 8.8 out of 10, without increasing risks of bleeding (0.4%) or recurrent laryngeal nerve injury (1.3%).^[49] Radio-guided parathyroidectomy incorporates an intraoperative hand-held gamma probe to detect technetium-99m-sestamibi uptake in the abnormal gland, enabling precise excision through a minimal incision following preoperative injection. This approach reports success rates exceeding 95-98.7% in single-adenoma cases, with low-dose protocols maintaining high detection (>97%) and a conversion rate of 5-10% if additional glands are involved.^[50]^[51]^[52] Recent advancements in remote-access techniques, such as transaxillary, postauricular, and transoral endoscopic approaches, provide scarless options by avoiding neck incisions entirely, making them particularly suitable for young patients concerned with aesthetics. The transoral endoscopic parathyroidectomy vestibular approach (TOEPVA), for instance, uses intraoral ports and achieves comparable efficacy to focused open surgery, with no reported persistent hyperparathyroidism and success rates over 90% in selected cases from 2018-2022 data.^[53] Robotic-assisted transaxillary parathyroidectomy has also demonstrated feasibility and safety, with cure rates above 90% in preoperative localized disease as of 2023-2025 consensus guidelines.^[54]^[55] Overall conversion to open procedures across these minimally invasive methods remains low at 5-10%, typically due to multigland involvement.^[45]

Postoperative Care

Immediate Management

Immediate postoperative management following parathyroidectomy focuses on close monitoring to detect and address acute complications, particularly hypocalcemia, in the first 24-48 hours. Patients are typically observed in a recovery unit or surgical ward with continuous vital sign monitoring to identify issues such as cervical hematoma, which requires prompt intervention if compressive symptoms arise.^[56] Serum calcium levels are checked every 4-6 hours initially to assess for hypocalcemia, with parathyroid hormone (PTH) levels measured around 6 hours postoperatively to predict the risk of prolonged low calcium states.^[57]^[58] To prevent hypocalcemia, which occurs in 5-47% of cases due to transient parathyroid insufficiency, prophylactic oral calcium supplementation at 1-2 g of elemental calcium per day is initiated, often combined with calcitriol at 0.25-0.5 mcg per day.^[56] If symptoms of hypocalcemia such as perioral tingling, muscle cramps, or tetany develop, intravenous calcium gluconate is administered as a 10-20 mL bolus of 10% solution (equivalent to 100-200 mg elemental calcium) diluted in 50-100 mL of 5% dextrose over 5-10 minutes, followed by infusion if needed to maintain levels above 7.6-8 mg/dL.^[59] In patients with secondary hyperparathyroidism, hungry bone syndrome poses a higher risk, characterized by profound hypocalcemia from rapid skeletal uptake of calcium and phosphate after sudden PTH reduction, affecting 20-70% of cases.^[59] Management involves aggressive intravenous calcium replacement, potentially up to 4-6 g of elemental calcium per day via continuous infusion (e.g., 0.5-1.5 mg/kg/hour), alongside oral supplements and calcitriol, with serial monitoring of calcium, phosphate, and magnesium every 4-6 hours to guide titration.^[59]^[60] Pain at the incision site is generally mild and managed with acetaminophen at standard doses (up to 3-4 g per day), while nonsteroidal anti-inflammatory drugs (NSAIDs) are avoided to minimize potential renal strain in patients with underlying hyperparathyroidism-related kidney issues.^[61] Discharge typically occurs on postoperative day 1 if serum calcium is stable above 8 mg/dL (2 mmol/L), the patient is asymptomatic, and there are no signs of complications such as hematoma or ongoing hypocalcemia requiring intervention.^[56]

Long-Term Follow-Up

Following parathyroidectomy, patients undergo scheduled biochemical monitoring to confirm surgical cure and detect any persistent or recurrent hyperparathyroidism. Serum calcium and parathyroid hormone (PTH) levels are typically assessed at 6 months postoperatively to verify eucalcemia lasting at least this duration, which defines cure according to guidelines; subsequent annual evaluations of these markers are recommended to ensure ongoing normocalcemia.^[56] For patients with preoperative osteoporosis, a dual-energy x-ray absorptiometry (DXA) scan is advised at approximately 1 year post-surgery to evaluate improvements in bone mineral density (BMD), which often increase by 2-5% in the lumbar spine and femoral neck during the first year.^[62]^[63] Recurrence of hyperparathyroidism, defined as hypercalcemia after a normocalcemic interval exceeding 6 months, occurs in approximately 5-10% of cases, particularly in multiglandular hyperplasia where rates can reach 14.8% over 10 years.^[56]^[64] Rising serum calcium or PTH levels during follow-up prompt repeat localization studies, such as ultrasound or sestamibi scintigraphy, to identify residual or ectopic parathyroid tissue.^[65] Lifestyle modifications play a key role in long-term management to support bone health and calcium homeostasis. Patients are encouraged to maintain a daily calcium intake of 1000-1200 mg through diet, incorporating dairy, leafy greens, and fortified foods, alongside weight-bearing exercises like walking to enhance BMD recovery.^[56] In cases of secondary hyperparathyroidism due to chronic kidney disease, adjustments to dialysis regimens may be necessary to optimize phosphate control and prevent recurrent elevations in PTH.^[66] Quality of life typically improves substantially after successful surgery, with 80-90% of patients reporting resolution of symptoms such as fatigue, bone pain, and nephrolithiasis within 6 months, alongside enhancements in neurocognitive and musculoskeletal function as evidenced by validated scales.^[67]^[68] For patients with multiple endocrine neoplasia (MEN) syndromes, particularly MEN1, lifelong annual screening for recurrent hyperparathyroidism and associated tumors is essential due to the high risk of multigland disease and recurrence rates exceeding 50% over time.^[56]

Complications

Surgical Risks

Parathyroidectomy, like other neck surgeries, carries risks of mechanical and wound-related complications arising directly from the operative procedure. These include bleeding or hematoma formation, which occurs in approximately 0.3-1.5% of cases and may necessitate prompt evacuation to prevent airway compromise.^[69]^[70] The risk is notably higher in redo surgeries due to adhesions and altered anatomy, with reoperation rates for bleeding reaching up to 1.3% overall in combined thyroid and parathyroid procedures.^[71] Injury to the recurrent laryngeal nerve is another key concern, with permanent damage leading to hoarseness in 1-2% of patients.^[72]^[73] This injury typically results from dissection near the nerve's path along the inferior thyroid artery. Bilateral nerve injury, though rare at less than 5%, can result in significant airway compromise requiring urgent intervention.^[72] Surgical site infection is uncommon, affecting fewer than 1% of patients, and is generally managed with antibiotics; wound dehiscence remains a rare occurrence.^[74] Transient hypoparathyroidism, stemming from devascularization of remaining normal parathyroid glands during surgery, is common and usually resolves within weeks to months with supportive care.^[75] Scar-related issues, such as keloid formation, can arise, particularly in patients predisposed to hypertrophic scarring, with a higher propensity at minimally invasive incision sites due to tension and healing dynamics.^[76] These complications underscore the importance of intraoperative vigilance, though metabolic sequelae of nerve injury are addressed elsewhere.^[72]

Metabolic Disturbances

Hypocalcemia is the most common metabolic disturbance following parathyroidectomy, occurring transiently in 30-50% of patients due to the abrupt reduction in parathyroid hormone (PTH) levels after removal of hyperfunctioning glands.^[75] This condition arises from decreased bone resorption and increased renal calcium excretion, leading to symptomatic tetany, paresthesia, or cardiac arrhythmias in severe cases. Severe hypocalcemia may also result from hungry bone syndrome, where rapid bone remineralization following PTH reduction depletes serum calcium, often requiring extended supplementation.^[1] Patients with preoperative vitamin D deficiency experience more severe and prolonged hypocalcemia, as low 25-hydroxyvitamin D levels impair intestinal calcium absorption and exacerbate the PTH withdrawal effects.^[77] Persistent hypercalcemia affects approximately 5% of patients postoperatively, typically resulting from incomplete resection of adenomatous tissue, multigland disease missed during surgery, or underlying parathyroid carcinoma.^[78] This complication indicates surgical failure and may necessitate re-exploration or alternative therapies like cinacalcet to normalize serum calcium levels. In cases of secondary hyperparathyroidism, particularly in chronic kidney disease, parathyroidectomy induces phosphate shifts, including transient hyperphosphatemia due to reduced PTH-mediated phosphaturia and ongoing renal impairment.^[79] Long-term, permanent hypoparathyroidism is rare, occurring in less than 5% of patients, usually from inadvertent removal or devascularization of all parathyroid glands, requiring lifelong supplementation with calcium and active vitamin D to maintain normocalcemia.^[3]

Outcomes and Prognosis

Parathyroidectomy is highly effective for treating hyperparathyroidism, with success rates exceeding 95% in normalizing serum calcium levels and resolving symptoms in cases of primary hyperparathyroidism.^[3]^[1] Recurrence of hyperparathyroidism occurs in 2-5% of patients, often due to multigland disease or missed adenomas, and is less common with adequate preoperative localization and intraoperative PTH monitoring.^[2] Long-term prognosis is generally favorable, with most patients experiencing sustained symptom relief, including reduced bone pain, fatigue, and risk of complications such as kidney stones or osteoporosis. Studies indicate that surgery reduces fracture risk and may improve cardiovascular outcomes compared to conservative management.^[2] In secondary hyperparathyroidism associated with chronic kidney disease, parathyroidectomy has been linked to improved survival rates, with one cohort showing 90.4% overall survival at follow-up versus 67.4% in non-surgical groups.^[80] For tertiary hyperparathyroidism, cure rates are high, aiming for normocalcemia within 6 months post-surgery.^[2] Quality of life typically improves post-surgery, though a small subset may require ongoing calcium and vitamin D supplementation due to permanent hypoparathyroidism (0.5-3.8% incidence).^[2]^[1] Persistent or recurrent disease may necessitate reoperation in 4-10% of cases, particularly in complex presentations.^[81]

History and Advancements

Historical Development

The parathyroid glands were first identified in 1880 by Swedish medical student Ivar Sandström during his anatomical dissections of human and animal cadavers, marking a pivotal moment in endocrine anatomy after earlier hints from Richard Owen in 1860.^[82] However, the functional significance of these glands remained unclear until 1891, when French physiologist Eugène Gley demonstrated through experiments on animals that their removal led to fatal tetany, thereby establishing their role in calcium homeostasis and distinguishing them from the thyroid.^[83] The first parathyroidectomy was performed in 1925 by Austrian surgeon Felix Mandl on a patient with von Recklinghausen disease (osteitis fibrosa cystica), a severe manifestation of hyperparathyroidism, where he successfully removed a parathyroid adenoma, leading to clinical improvement.^[84] In the United States, Fuller Albright's diagnostic insights in the late 1920s facilitated the first successful parathyroidectomy in 1929, performed by surgeon James D. Barney on a patient with confirmed primary hyperparathyroidism, confirming the procedure's therapeutic potential and shifting focus toward surgical intervention for the condition.^[85] During the 1930s, Albright and collaborators further identified primary hyperparathyroidism as a distinct entity through metabolic studies on hundreds of cases, differentiating it from secondary forms and emphasizing skeletal and renal complications as key indicators for surgery.^[86] By the mid-20th century, surgical techniques evolved with routine bilateral neck exploration becoming standard, but challenges in localization persisted until the early 1990s, when George Irvin III developed the intraoperative parathyroid hormone (PTH) assay, enabling real-time confirmation of adenoma excision and reducing operative time.^[87] The 1990 National Institutes of Health (NIH) consensus conference established guidelines recommending parathyroidectomy for asymptomatic primary hyperparathyroidism in cases with serum calcium levels 1.0 mg/dL above the upper normal limit, young age, or complications, broadening surgical indications beyond overt symptoms.^[88] Subsequent updates by the American Association of Clinical Endocrinologists (AACE) and American Association of Endocrine Surgeons (AAES) in 2002 refined criteria to include bone density thresholds and kidney stone history, while the 2016 AAES guidelines emphasized preoperative imaging and minimally invasive approaches for improved outcomes.^[89]^[56] Key milestones in the 1990s included the introduction of technetium-99m sestamibi scintigraphy in 1992, which provided noninvasive preoperative localization of parathyroid adenomas with high sensitivity, facilitating targeted surgery.^[90] This imaging advance, combined with intraoperative PTH monitoring, spurred the development of minimally invasive parathyroidectomy techniques in the late 1990s, such as video-assisted and radioguided approaches, which minimized incisions and recovery time while maintaining cure rates above 95%.^[91]

Recent Advances

Recent advances in parathyroidectomy have focused on improving preoperative localization, surgical access, graft viability, medical management, and nerve protection, driven by technological integrations and refined protocols since 2020. Enhanced imaging modalities, particularly four-dimensional computed tomography (4D-CT), have evolved with machine learning applications to boost localization precision for parathyroid adenomas. A 2023 study comparing machine learning models for adenoma identification highlighted improved accuracies in distinguishing pathological glands on imaging datasets.^[92] By 2025, 4D-CT demonstrated superior sensitivity over ultrasound and sestamibi SPECT/CT, with localization rates exceeding 80% in challenging cases, particularly when initial scans were negative.^[93] Remote-access approaches, such as transaxillary parathyroidectomy, have gained traction for their cosmetic advantages and low complication profiles. A 2025 consensus from the Asia-Pacific Society of Thyroid Surgery affirmed that remote-access techniques, including transaxillary methods, yield complication rates comparable to conventional transcervical approaches, with low rates of transient hypoparathyroidism and rare permanent recurrent laryngeal nerve (RLN) injuries in experienced hands.^[94] These methods eliminate visible neck scars, enhancing patient satisfaction; studies report sustained cosmetic benefits and recurrence rates below 5% in single-gland disease.^[95] Parathyroid autotransplantation strategies have advanced to mitigate post-thyroidectomy hypoparathyroidism, with selective techniques showing promise in preserving function. In a 2025 analysis, selective autotransplantation of compromised glands during total thyroidectomy was linked to a reduced incidence of permanent hypoparathyroidism, dropping from 4.4% to 1.2% in studied cohorts.^[96] Recent protocols emphasize intraoperative viability assessment and optimized implantation sites, achieving graft survival rates of 93%, thereby limiting long-term calcium supplementation needs.^[97] Next-generation calcimimetics, including evocalcet, offer pharmacologic options to manage secondary hyperparathyroidism and potentially defer surgery. Approved for use in chronic kidney disease patients with secondary hyperparathyroidism, evocalcet effectively lowers parathyroid hormone and calcium levels with fewer gastrointestinal side effects than predecessors like cinacalcet.^[98] Clinical data from 2024 indicate that such agents can stabilize disease in cases resistant to vitamin D analogs, allowing surgical delay while preserving bone health.^[99] Intraoperative nerve monitoring has incorporated real-time electromyography (EMG) to safeguard the RLN during parathyroidectomy. Continuous intraoperative neuromonitoring (CIONM) with real-time EMG feedback, as validated in 2025 trials, facilitates early detection of traction injuries, reducing permanent RLN palsy rates to 1.1% in complex dissections.^[100] Advanced modes like NerveTrend enable dynamic signal trending, correlating with postoperative vocal outcomes and minimizing injury in reoperative or minimally invasive settings.^[101]

References

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404 Error
Insufficient relevant content. The provided URL (https://jamanetwork.com/journals/jamasurgery/fullarticle/2794606) returns a 404 error, indicating the page cannot be found. No information is available to extract or summarize the AAES guidelines on preoperative management for secondary and tertiary hyperparathyroidism surgery.
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Selective parathyroid autotransplantation prevent permanent ...
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Short and long-term impact of parathyroid autotransplantation on ...
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