The Parathyroids

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The Parathyroids

• Vic V. Vernenkar, D.O.
• St. Barnabas Hospital
• Department of Surgery

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Functional Anatomy

• Are characteristically located adjacent and
  posterior to the thyroid gland.
• Most individuals have 4 parathyroid glands
  (80-90), 2 on each side.

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Functional Anatomy

• The paired superior glands arise from the 4th
  branchial pouch in close proximity to the origin
  of the thyroid gland.

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Functional Anatomy

• The paired inferior glands arise from the third
  branchial pouch along with the thymus (parathymus
  gland), migrate further, and thus are more likely
  to be found in ectopic locations such as the
  anterior mediastinum.
• Other potential sites include intrathyroid,
  posterior mediastinum, central compartment of
  neck.

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Arterial Supply and Drainage

• All the glands are supplied by the inferior
  thyroid artery. Occasionally, the superior glands
  are supplied by the superior thyroid artery.
• Venous drainage is via the superior, middle and
  inferior thyroid veins.
• The superior,middle thyroid veins drain directly
  into the IJ. The inferior into the innominate.

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PTH Functions

• Secreted in response to calcium levels, not under
  pituitary control.
• Increased mobilization of calcium and phosphate
  from bone by increasing osteoclastic activity.
• Directly promotes active calcium reabsorption in
  distal nephron.

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PTH Functions

• Directly inhibits phosphate reabsorption in
  proximal tubule.
• Stimulates 1,25 dihydroxyvitamin D and increasing
  gut absorption of calcium and phosphorus.

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Causes of Primary Hyperparathyroidism

• Excessive, abnormally regulated secretion of PTH,
  resulting in hypercalcemia.
• Peaks between ages of 50-60, with a femalemale
  ration of 31.
• A small percentage have a history of radiation
  exposure as a child.

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Etiology and Pathology

• Adenomas, single in 80-85 of patients.
• 2-4 incidence of multiple adenomas.
• Histologically, a proliferation in chief cells in
  a single focus with a compressed rim of
  surrounding normal tissue.

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Etiology and Pathology

• Diffuse hyperplasia of all 4 glands occurs in 15
  of patients.
• May be associated with MEN 1 in 25-35.
• Histologically diffuse chief cell hyperplasia is
  seen with cords or sheets of chief cells.
• Parathyroid carcinoma occurs in 0.5-1.0 of
  patients.

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Causes of Hypercalcemia

• Malignancy
• Primary hyperparathyroidism
• Familial hypocalciuric hypercalcemia
• Immobilization
• Granulomatous disease, Addisons disease
• Vitamin D and A excess
• Milk-Alkali syndrome
• Drugs- thiazides, lithium

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Clinical Manifestations

• Most are asymptomatic.
• Symptoms are related to the magnitude and rate of
  rise.
• Hypercalcemia of malignancy is often associated
  with a rapid rise and is frequently symptomatic.

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Clinical Manifestations

• Neuromuscular confusion, fatigue, coma,
  lethargy, weakness, depression, apathy.
• Renal Stones most common manifestation of
  primary hyperparathyroidism.

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Clinical Manifestations

• Cardiovascular HTN, short QT, heart block.
• Skeletal Bone pain, radiographic evidence (1-2)
  is uncommon. Subperiosteal resorption middle
  phalanx of 2-3 finger. Salt and pepper pattern on
  skull x-ray.
• GI Nausea, vomiting, anorexia, constipation,
  PUD, pancreatitis.

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Diagnosis

• Hypercalcemia and elevated PTH, gt60mEq/mL are
  hallmarks of primary hyperparathyroidism.
• True hypercalcemia is characterized by decreased
  ionized calcium level, which accurately reflect
  functional extracellular calcium levels despite
  hypoalbuminemia.

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Diagnosis

• For every 1 mg/dL drop in serum albumin, total
  serum calcium drops 0.8mg/dL.
• Hypophosphatemia occurs in 35 of patients.

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Diagnosis

• Elevated urinary cAMP and urinary calcium may be
  present in 35.
• Preoperative localization with ultrasound or
  nuclear medicine is rarely indicated for primary
  disease, but frequently needed for reoperation.

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Treatment of Primary Hyperparathyroidism

• Surgery is the only definitive treatment of
  symptomatic disease.
• Cure rate is 90-95 at initial operation.

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Treatment of Primary Hyperparathyroidism

• Location and number of glands may be highly
  variable.
• To rule out lesions in multiple glands, bilateral
  neck exploration may be required, with
  identification of all 4 glands.

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Treatment of Primary Hyperparathyroidism

• To confirm the presence or absence of parathyroid
  tissue, FS should be performed.
• FS is not helpful in differentiating normal from
  diseased tissue, only that it is gland.
• Intraoperative measurement of venous PTH also
  being done to confirm removal of functional
  parathyroid lesion.

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Treatment of Adenomas

• Single or multiple enlarged glands are removed
  leaving normal glands.
• If only three normal glands are identified, after
  a thorough exploration, ipsilateral thyroidectomy
  is often performed on the side of the missing
  gland.
• In this setting 96 are intrathyroidal.

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Multiglandular Hyperplasia

• Subtotal parathyroidectomy, or 3.5 glands
  removed.
• Total parathyroidectomy, is followed by auto
  transplantation of gland fragments to the
  nondominant forearm or sternocleidomastoid. Makes
  reoperation for recurrence easier.
• Permanent hypoparathyroidism in 5.

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Persistent or Recurrent Disease

• Occurs in less than 5 post op.
• Related to a single diseased gland remaining in
  the neck.
• Recurrent disease often related to regrowth of
  diseased tissue, inadvertent microscopic
  implantation during resection, parathyroid cancer
  must be part of differential.

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Preoperative Localization

• Recommended for recurrent disease.
• Adhesions make reoperation more difficult.
• Ectopic location of gland more likely in this
  setting.

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Preoperative Localization

• US, CT MRI (great for ectopic adenomas, deeper
  structures, mediastinum), Technetium-99m-Sestamibi
  scan.
• Invasive localization with selective angiography,
  venous sampling with measurement of PTH can be
  combined with angiography.

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Surgical Reexploration

• 60-80 success rate.
• Increased risk of complications nerve injury
  5-10, hypoparathyroidism 10-20.
• Median sternotomy and mediastinal exploration is
  necessary in 1-2.
• The superior parathyroids may be posterior to the
  esophagus and as superior as the pharynx.

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Secondary Hyperparathyroidism

• A consequence of chronic renal failure.
• These patients are unable to synthesize the
  active form of vitamin D, which results in
  hypocalcemia and a compensatory elevation of PTH.

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Secondary Hyperparathyroidism

• Untreated patients become symptomatic with bone
  demineralization, calcification of soft tissues,
  accelerated vascular calcification, pruritis,
  painful skin ulcerations from calcium deposition
  in skin calciphylaxis.
• Treatment is medical with dialysis with high
  calcium baths, phosphate binding antacids,
  calcium supplements.
• Surgical treatment is rarely indicated.

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Tertiary Hyperparathyroidism

• Associated with hypercalcemia and elevated PTH
  levels.
• Persistent disease in patients with secondary
  hyperparathyroidism despite renal transplant
  secondary to dysregulated parathyroid function.
• Treatment often requires surgical resection with
  subtotal parathyroidectomy.

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Parathyroid Cancer

• Younger, equal malefemale ration when compared
  to adenomas.
• More frequently symptomatic, with elevated PTH,
  calcium and alkaline phosphatase.
• Capsular invasion, angioinvasion on path.

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Parathyroid Cancer

• Often adherent to adjacent structures.
• Treatment is resection of the involved gland,
  ipsilateral thyroid lobe, regional lymph nodes.
• Recurrence is 50, prognosis poor, chemoradiation
  of no benefit.