Unformatted text preview: The Parathyroids
Vic V. Vernenkar, D.O.
St. Barnabas Hospital
Department of Surgery Functional Anatomy
Functional Anatomy Are characteristically located adjacent and posterior to the thyroid gland. Most individuals have 4 parathyroid glands (8090%), 2 on each side. Functional Anatomy
Functional Anatomy The paired superior glands arise from the 4th branchial pouch in close proximity to the origin of the thyroid gland. Functional Anatomy
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. Arterial Supply and Drainage
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. PTH Functions
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. PTH Functions
PTH Functions Directly inhibits phosphate reabsorption in proximal tubule. Stimulates 1,25 dihydroxyvitamin D and increasing gut absorption of calcium and phosphorus. Causes of Primary Causes of Primary Hyperparathyroidism Excessive, abnormally regulated secretion of PTH, resulting in hypercalcemia. Peaks between ages of 5060, with a female:male ration of 3:1. A small percentage have a history of radiation exposure as a child. Etiology and Pathology
Etiology and Pathology Adenomas, single in 8085% of patients. 24% incidence of multiple adenomas. Histologically, a proliferation in chief cells in a single focus with a compressed rim of surrounding normal tissue. Etiology and Pathology
Etiology and Pathology Diffuse hyperplasia of all 4 glands occurs in 15% of patients.
May be associated with MEN 1 in 2535%.
Histologically diffuse chief cell hyperplasia is seen with cords or sheets of chief cells.
Parathyroid carcinoma occurs in 0.51.0% of patients. Causes of Hypercalcemia
Causes of Hypercalcemia Malignancy
Familial hypocalciuric hypercalcemia
Granulomatous disease, Addisons disease
Vitamin D and A excess
Drugs thiazides, lithium Clinical Manifestations
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. Clinical Manifestations
Clinical Manifestations Neuromuscular: confusion, fatigue, coma, lethargy, weakness, depression, apathy. Renal: Stones most common manifestation of primary hyperparathyroidism. Clinical Manifestations
Clinical Manifestations Cardiovascular: HTN, short QT, heart block.
Skeletal: Bone pain, radiographic evidence (1
2%) is uncommon. Subperiosteal resorption middle phalanx of 23 finger. Salt and pepper pattern on skull xray.
GI: Nausea, vomiting, anorexia, constipation, PUD, pancreatitis. Diagnosis
Diagnosis Hypercalcemia and elevated PTH, >60mEq/mLare hallmarks of primary hyperparathyroidism. True hypercalcemia is characterized by decreased ionized calcium level, which accurately reflect functional extracellular calcium levels despite hypoalbuminemia. Diagnosis
Diagnosis For every 1 mg/dL drop in serum albumin, total serum calcium drops 0.8mg/dL. Hypophosphatemia occurs in 35% of patients. Diagnosis
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. Treatment of Primary Treatment of Primary Hyperparathyroidism Surgery is the only definitive treatment of symptomatic disease. Cure rate is 9095% at initial operation. Treatment of Primary 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. Treatment of Primary 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. Treatment of Adenomas
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. Multiglandular Hyperplasia
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%. Persistent or Recurrent Disease
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. Preoperative Localization
Preoperative Localization Recommended for recurrent disease. Adhesions make reoperation more difficult. Ectopic location of gland more likely in this setting. Preoperative Localization
Preoperative Localization US, CT& MRI (great for ectopic adenomas, deeper structures, mediastinum), Technetium99mSestamibi scan. Invasive localization with selective angiography, venous sampling with measurement of PTH can be combined with angiography. Surgical Reexploration
Surgical Reexploration 6080% success rate.
Increased risk of complications; nerve injury 5
10%, hypoparathyroidism 1020%.
Median sternotomy and mediastinal exploration is necessary in 12%.
The superior parathyroids may be posterior to the esophagus and as superior as the pharynx. Secondary Hyperparathyroidism
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. Secondary Hyperparathyroidism
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. Tertiary Hyperparathyroidism
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. Parathyroid Cancer
Parathyroid Cancer Younger, equal male:female ration when compared to adenomas. More frequently symptomatic, with elevated PTH, calcium and alkaline phosphatase. Capsular invasion, angioinvasion on path. Parathyroid Cancer
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. ...
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- Fall '11
- clinical manifestations, Differential diagnosis, Primary hyperparathyroidism, Secondary hyperparathyroidism, parathyroid cancer