Translate

Search This Blog

الترجمة

Search This Blog

str

str

2

str

z

2

str

z

coinad

10/27/25

 


which the recurrent laryngeal or vagus nerves were at risk of injury, those with locally advanced cancer

and those with distorted anatomy due to large and/or substernal goiters.

The parathyroid glands are at risk during thyroid resection by virtue of their location which can be

firmly invested within the thyroid sheath or occasionally even within the thyroid capsule. Inferior

parathyroid glands are ultimately supplied by the ITA. Superior parathyroid glands are often served by

the ITA but may also have contributions from the superior thyroid artery. Ligation of the trunk of the

ITA proximal to the pedicle to the parathyroid glands must be avoided. Every attempt should be made

to mobilize the parathyroid glands away from the thyroid tissue while preserving the blood supply. If

the gland appears pale or dark and devascularized, the arterial supply is probably compromised. Such a

parathyroid gland is unlikely to survive after the operation and should be autotransplanted. This may be

done by mincing the gland into 1-mm pieces and inserting or injecting the pieces into well-vascularized

skeletal muscle (e.g., sternocleidomastoid, strap muscle, or pectoralis).84 With total thyroidectomy,

careful dissection is even more critical than with hemithyroidectomy. Temporary hypoparathyroidism is

relatively common and occurs in 20% to 40% of patients after total thyroidectomy and is due to mild

devascularization or venous congestion of parathyroid glands during mobilization. Symptoms of

hypocalcemia include paresthesias and numbness of the hands, feet, and lips which can be treated with

oral calcium with or without vitamin D supplements (e.g., calcitriol). Severe symptomatic hypocalcemia

can be treated with intravenous calcium gluconate. Temporary hypoparathyroidism complicating

thyroidectomy usually resolves over days to weeks, although occasionally it may take months to do so.

Hypoparathyroidism that persists longer than 6 months is usually destined to be permanent. The

transient hypocalcemia after total thyroidectomy may be worse in the patient with Graves disease

because of the increased bone turnover observed with hyperthyroidism; however, recovery is expected

and the incidence of permanent hypoparathyroidism should be no higher than in euthyroid patients.

Regardless of the specific extent or technique of thyroidectomy, these complications can largely be

avoided or ameliorated by delicate and deliberate surgical technique. A thorough understanding of the

function and anatomy, both normal and abnormal, of the thyroid gland, and of the rationale behind

various treatment options, is critical to ensure the best outcomes for our patients.

DISCLOSURES

The authors have nothing to disclose.

References

1. Gauger P, Delbridge LW, Thompson NW, et al. Incidence and importance of the tubercle of

Zuckerkandl in thyroid surgery. Eur J Surg 2001;167:249–254.

2. Sackett W, Reeve TS, Barraclough B, et al. Thyrothymic thyroid rests: incidence and relationship to

the thyroid gland. J Am Coll Surg 2002;195:635–640.

3. Bliss R, Gauger PG, Delbridge LW. Surgeon’s approach to the thyroid gland: surgical anatomy and

the importance of technique. World J Surg 2000;2:891–897.

4. Kandil E, Abdel Khalek M, Aslam R, et al. Recurrent laryngeal nerve: significance of the anterior

extralaryngeal branch. Surgery 2011;149:820–824.

5. Toniato A, Mazzarotto R, Piotto A. Identification of the nonrecurrent laryngeal nerve during

thyroid surgery: 20-year experience. World J Surg 2004; 28:659–661.

6. Cernea C, Ferraz AR, Nishio S, et al. Surgical anatomy of the external branch of the superior

laryngeal nerve. Head Neck 1992;14:380–383.

7. Carty SE, Cooper DS, Doherty GM, et al. American Thyroid Association. Consensus statement on the

terminology and classification of central neck dissection for thyroid cancer. Thyroid

2009;19(11):1153–1158.

8. Kupferman ME, Patterson M, Mandel SJ, et al. Patterns of lateral neck metastases in papillary

thyroid carcinoma. Arch Otolaryngol Head Neck Surg 2004;130:857–860.

9. Machens A, Holzhausen JJ, Dralle H. Skip metastases in thyroid cancer leaping the central lymph

node compartment. Arch Surg 2004;139:43–45.

10. Garber JR, Cobin RH, Gharib H, et al. Clinical practice guidelines for hypothyroidism in adults:

cosponsored by the American Association of Clinical Endocrinologists and the American Thyroid

2141

Association. Endocr Pract 2012; 18(6):88–1028.

11. Tan G, Gharib H. Thyroid incidentalomas: management approaches to nonpalpable nodules

discovered incidentally on thyroid imaging. Ann Intern Med 1997;126:226–231.

12. Cooper DS, Doherty GM, Haugen BR, et al. American Thyroid Association. Revised American

Thyroid Association guidelines for patients with thyroid nodules and differentiated thyroid cancer.

Thyroid 2009;19(11):1167–1214.

13. Chin B, Patel P, Cohade C, et al. Recombinant human thyrotropin stimulation of fluoro-D-glucose

positron emission tomography uptake in well-differentiated thyroid carcinoma. JCEM 2004;89:91–

95.

14. Shie P, Cardarelli R, Sprawls K, et al. Systemic review: Prevalence of malignancy incidental thyroid

nodules identified on fluorine-18 fluorodeoxyglucose positron emission tomography. Nucl Med

Commun 2008;30:742–748.

15. Kang BJ, O JH, Baik JH, et al. Incidental thyroid uptake on F-18 FDG PET/CT: correlation with

ultrasonography and pathology. Ann Nucl Med 2009;23:729–737.

16. Bertagna F, Treglia G, Piccardo A, et al. F18-FDG-PET/CT thyroid incidentalomas: a wide

retrospective analysis in three Italian centres on the significance of focal uptake and SUV value.

Endocrine 2013;43:678–685.

17. Bahn RS, Burch HD, Cooper DS, et al. Hyperthyroidism and other causes of thyrotoxicosis:

Management guidelines of the American Thyroid Association and the American Association of

Clinical Endocrinologists. Thyroid 2011;21:593–646.

18. Tallstedt L, Lundell G, Blomgren H, et al. Does early administration of thyroxine reduce the

development of Graves’ ophthalmopathy after radioiodine treatment? Eur J Endocrinol

1994;130:494–497.

19. Tallstedt L, Lundell G, Torring O, et al. Occurrence of ophthalmopathy after treatment for Graves’

hyperthyroidism. The Thyroid Study Group. N Engl J Med 1992;326:1733–1738.

20. Bartalena L, Marcocci C, Bogazzi F, et al. Use of corticosteroids to prevent progression of Graves’

ophthalmopathy after radioiodine therapy for hyperthyroidism. N Engl J Med 1989;321:1349–1352.

21. Sundaresh V, Brito JP, Wang Z, et al. Comparative effectiveness of therapies for Graves’

hyperthyroidism: a systematic review and network meta-analysis. J Clin Encocrinol Metab

2013;98:3671–3677.

22. van Soestbergen M, Van Der Vijver J, Graafland A. Recurrence of hyperthyroidism in multinodular

goiter after long-term drug therapy: a comparison with Graves’ disease. J Endocrinol Invest

1992;15:797–800.

23. Stoll SJ, Pitt SC, Liu J, et al. Thyroid hormone replacement after thyroid lobectomy. Surgery

2009;146:554–558

24. Tunbridge W, Brewis M, French JM, et al. Natural history of autoimmune thyroiditis. Br Med J Clin

Res 1981;282:258–262.

25. McManus C, Luo J, Sippel R, et al. Should patients with symptomatic Hashimoto’s thyroiditis

pursue surgery? J Surg Res 2011;170:52–55.

26. Smallridge R, DeKeyser FM, VanHerle AJ, et al. Thyroid iodine content and serum thyroglobulin:

cues to the natural history of destruction-induced thyroiditis. J Clin Endocrinol Metab 1986;62:1213–

1219.

27. Bartalena L, Brogioni S, Grasso L, et al. Treatment of amiodarone-induced thyrotoxicosis: a difficult

challenge: results of a prospective study. J Clin Endocrinol Metab 1996;81:2930–2933.

28. Violaris N, Windle-Taylor PC. Idiopathic fibrosis of the upper aero-digestive tract. J Laryngol Otol

1989;103:333–334.

29. Few J, Thompson NW, Angelos P, et al. Riedel’s thyroiditis: treatment with tamoxifen. Surgery

1996;120:998–999.

30. White ML, Doherty GM, Gauger PG. Evidence-based management of substernal goiter. World J Surg

2008;32:1285–1300.

31. Hughes DT, Haymart MR, Miller BS, et al. The most commonly occurring papillary thyroid cancer

in the United States is now a microcarcinoma in a patient older than 45 years. Thyroid 2011;21:231–

236.

32. Gupta A, Ly S, Castroneves L, et al. A standardized assessment of thyroid nodules in children

2142

confirms higher cancer prevalence than in adults. J Clin Endocrinol Metab 2013;98:3238–3245.

33. Leeman-Neill RJ, Brenner AV, Little MP, et al. RET/PTC and PAX8/PPARᵧ chromosomal

rearrangements in post-Chernobyl thyroid cancer and their association with iodine-131 radiation

dose and other characteristics. Cancer 2013;119:1792–1799.

34. Guglielmi R, Pacella CM, Bianchini A, et al. Percutaneous ethanol infection treatment in benign

thyroid lesions: role and efficacy. Thyroid 2004;14:125–131.

35. Baloch ZW, LiVolsi VA, Asa SL, et al. Diagnostic terminology and morphologic criteria for cytologic

diagnosis of thyroid lesions: a synopsis of the national cancer institute thyroid fine-needle

aspiration state of the science conference. Diagn Cytopathol 2008;36:425–437.

36. Kouniavsky G, Zeiger MA. The quest for diagnostic molecular markers for thyroid nodules with

indeterminate or suspicious cytology. J Surg Onc 2012;105:438–443.

37. Dedhia PH, Rubio GA, Cohen MS, et al. Potential effects of molecular testing of indeterminate

thyroid nodule fine needle aspiration biopsy on thyroidectomy volume. World J Surg 2014;38:634–

638.

38. Montone KT, Baloch ZW, LiVolsi VA. The thyroid Hürthle (oncocytic) cell and its associated

pathologic conditions: a surgical pathology and cytopathology review. Arch Pathol Lab Med

2008;132:1241–1250.

39. Lin JD, Chao TC, Chou SC, et al. Papillary thyroid carcinomas with lung metastases. Thyroid

2004;14:1091–1096.

40. Beninato T, Scognamiglio T, Kleiman DA, et al. Ten percent tall cells confer the aggressive features

of the tall cell variant of papillary thyroid carcinoma. Surgery 2013;154:1331–1336.

41. Ito Y, Miyauchi A, Inoue H, et al. An observation trial for papillary thyroid microcarcinoma in

Japanese patients. World J Surg 2010;34:28–35.

42. Ito Y, Miyauchi A, Kihara M, et al. Patient age is significantly related to the progression of

papillary microcarcinoma of the thyroid under observation. Thyroid 2014;24:27–34.

43. Yip L, Wharry LI, Armstrong MJ, et al. A clinical algorithm for fine-needle aspiration molecular

testing effectively guides the appropriate extent of initial thyroidectomy. Ann Surg 2014;260:163–

168.

44. Xing M, Alzahrani AS, Carson KA, et al. Association between BRAF V600E mutation and mortality

in patients with papillary thyroid cancer. JAMA 2013;309:1493–1501.

45. Callcut RA, Selvaggi SM, Mack E, et al. The utility of frozen section evaluation for follicular thyroid

lesions. Ann Surg Oncol 2004;11:94–98.

46. Kuo EJ, Roman SA, Sosa JA. Patients with follicular and Hürthle cell microcarcinomas have

compromised survival: a population level study of 22,738 patients. Surgery 2013;154:1246–1253.

47. Goffredo P, Cheung K, Roman SA, et al. Can minimally invasive follicular thyroid cancer be

approached as a benign lesion?: a population-level analysis of survival among 1,200 patients. Ann

Surg Oncol 2013;20:767–772.

48. Smallridge RC, Ain KB, Asa SL, et al. American thyroid association guidelines for management of

patients with anaplastic thyroid cancer. Thyroid 2012;22:1104–1039.

49. Sosa JA, Balkissoon J, Lu S, et al. Thyroidectomy followed by foxbretabulin (CA4P) combination

regimen appears to suggest improvement in patient survival in anaplastic thyroid cancer. Surgery

2012;152:1078–1087.

50. Hay I, Grant CS, Taylor WF, et al. Ipsilateral lobectomy versus bilateral lobar resection in papillary

thyroid carcinoma: a retrospective analysis of surgical outcome using a novel prognostic scoring

system. Surgery 1987;102:1088–1095.

51. Cady B, Rossi R. An expanded view of risk-group definition in differentiated thyroid carcinoma.

Surgery 1988;104:947–953.

52. Hay I, Bergstralh EJ, Goellner JR, et al. Predicting outcome in papillary thyroid carcinoma:

development of a reliable prognostic scoring system in a cohort of 1779 patients surgically treated

at one institution during 1940 through 1989. Surgery 1993;114:1050–1057.

53. Byar D, Green SB, Dor P, et al. A prognostic index for thyroid carcinoma: a study of the E.O.R.T.C.

thyroid cancer cooperative group. Eur J Cancer 1979;15:1033–1041

54. Moley JF, DeBenedetti MK. Patterns of nodal metastases in palpable medullary thyroid carcinoma.

Recommendations for extent of node dissection. Ann Surg 1999;229:880–887.

2143

55. Kloos RT, Eng C, Evans DB, et al. Medullary thyroid cancer: management guidelines of the

American Thyroid Association. Thyroid 2009;19:565–612.

56. Fialkowski E, Debenedetti M, Moley J. Long-term outcome of reoperations for medullary thyroid

carcinoma. World J Surg 2008;32:754–765.

57. Wells SA Jr, Robinson BG, Gagel RF, et al. Vandetanib in patients with locally advanced or

metastatic medullary thyroid cancer: a randomized, double-blind phase III trial. J Clin Oncol

2012;30:134–141.

58. Fersht N, Vini L, A’Hern R, et al. The role of radiotherapy in the management of elevated calcitonin

after surgery for medullary thyroid cancer. Thyroid 2001;11:1161–1168.

59. Skinner M, DeBenedetti MK, Moley JR, et al. Medullary thyroid carcinoma in children with

multiple endocrine neoplasia types 2A and 2B. J Pediatr Surg 1996;31:177–181.

60. Jonak C, Troch M, Mullauer L, et al. Rituximab plus dose-reduced cyclophosphamide,

mitoxantrone, vincristine and prednisolone are effective in elderly patients with diffuse large B-cell

lymphoma of the thyroid. Thyroid 2010;20:425–427.

61. Tsang RW, Gospodarowicz MK, Pintilie M, et al. Localized mucosa-associated lymphoid tissue

lymphoma treated with radiation therapy has excellent clinical outcome. J Clin Oncol

2003;21:4157–4164.

62. Mirallie E, Rigaud J, Mathonnet M, et al. Management and prognosis of metastases to the thyroid

gland. J Am Coll Surg 2005;200:203–207.

63. Choi JS, Chung WY, Kwak JY, et al. Staging of papillary thyroid carcinoma with ultrasonography:

performance in a large series. Ann Surg Oncol 2011;18:3572–3578.

64. Loh K, Greenspan FS, Gee L, et al. Pathological tumor-node-metastasis (pTNM) staging for papillary

and follicular thyroid carcinomas: a retrospective analysis of 700 patients. J Clin Endocrinol Metab

1997;82:3553–3562.

65. Stulak JM, Grant CS, Farley DR, et al. Value of preoperative ultrasonography in the surgical

management of initial and reoperative papillary thyroid cancer. Arch Surg 2006;141(5):494–496.

66. Kouvaraki MA, Shapiro SE, Fornage BD, et al. Role of preoperative ultrasonography in the surgical

management of patients with thyroid cancer. Surgery 2003;134(6):946–955.

67. Solorzano CC, Carneiro DM, Ramirez M, et al. Surgeon-performed ultrasound in the management of

thyroid malignancy. Am Surg 2004;70(7):580–582.

68. Bilimoria K, Bentrem DJ, Ko CY, et al. Extent of surgery affects survival for papillary thyroid

cancer. Ann Surg 2007;246(3):375–384.

69. Hughes DT, White ML, Miller BS, et al. Influence of prophylactic central lymph node dissection on

postoperative thyroglobulin levels and radioiodine treatment in papillary thyroid cancer. Surgery

2010;148:1100–1106.

70. Popadich A, Levin O, Lee JC, et al. A multicenter cohort study of total thyroidectomy and routine

central lymph node dissection for cN0 papillary thyroid cancer. Surgery 2011;150:1048–1057.

71. Mazzaferri EL, Kloos RT. Using recombinant human TSH in the management of well-differentiated

thyroid cancer: current strategies and future directions. Thyroid 2000;10(9):767–778.

72. Jonklaas J, Sarlis JN, Litofsky D, et al. Outcomes of patients with differentiated thyroid carcinoma

following initial therapy. Thyroid 2006;16:1229–1242.

73. Jung TS, Kim TY, Kim KW, et al. Clinical features and prognostic factors for survival in patients

with poorly differentiated thyroid carcinoma and comparison to the patients with aggressive

variants of papillary thyroid carcinoma. Endocr J 2007;54:265–274.

74. Ho AL, Grewal RK, Leboeuf R, et al. Selumetinib-enhanced radioiodine uptake in advanced thyroid

cancer. NEJM 2013;368:623–632.

75. Orita Y, Sugitani I, Toda K, et al. Zoledronic acid in the treatment of bone metastases from

differentiated thyroid carcinoma. Thyroid 2011;21:31–35.

76. Kloos RT, Ringel MD, Knopp MV, et al. Phase II trial of sorafenib in metastatic thyroid cancer. J

Clin Oncol 2009;27:1675.

77. Franko J, Kish KJ, Pezzi CM, et al. Safely increasing the efficiency of thyroidectomy using a new

bipolar electrosealing device (LigaSure) versus conventional clamp-and-tie technique. Am Surg

2006;72:132–136.

78. Siperstein A, Berber E, Morkoyun E. The use of the harmonic scalpel vs. conventional knot tying for

2144

vessel ligation in thyroid surgery. Arch Surg 2002;137:137–142.

79. Cardon C, Fajardo R, Ramirez J. A randomized, prospective, parallel group study comparing the

harmonic scalpel to electrocautery in thyroidectomy. Surgery 2005;137:337–3341.

80. Barczynski M, Konturek A, Stopa M, et al. Randomized controlled trial of visualization versus

neuromonitoring of the external branch of the superior laryngeal nerve during thyroidectomy.

World J Surg 2012;36:1340–1347.

81. Dralle H, Sekulla C, Haerting J, et al. Risk factors of paralysis and functional outcome after

recurrent laryngeal nerve monitoring in thyroid surgery. Surgery 2004;136:1310–1322.

82. Yarbrough D, Thompson GB, Kasperbauer JL, et al. Intraoperative electromyographic monitoring of

the recurrent laryngeal nerve in reoperative thyroid and parathyroid surgery. Surgery

2004;136:1107–1115.

83. Schlosser K, Zeuner M, Wagner M, et al. Laryngoscopy in thyroid surgery-essential standard or

unnecessary routine? Surgery 2007;142:858–864.

84. Gauger P, Reeve TS, Wilkinson M, et al. Routine parathyroid autotransplantation during total

thyroidectomy: the influence of technique. Eur J Surg 2000;166:605–609.

2145

Chapter 76

Parathyroid Glands

Gerard M. Doherty

Key Points

1 The normal parathyroid glands are flat, ovoid, and red-brown to yellow. Their dimensions are 5 to 7

mm × 3 to 4 mm × 0.5 to 2 mm, and they weigh between 30 and 50 mg each.

2 Parathyroid hormone (PTH) is the single most important hormonal regulator of calcium and

phosphate metabolism in humans with direct effects on the skeleton and kidney and indirect effects

on the intestine, mediated through vitamin D.

3 The demonstration of an elevated plasma PTH concentration alone does not establish the diagnosis

of hyperparathyroidism; with a simultaneous elevated serum calcium level, this finding is virtually

diagnostic.

4 A large proportion of patients with the diagnosis of hyperparathyroidism are minimally or

asymptomatic and the appropriate treatment for these patients remains controversial.

5 It is routinely possible to identify abnormal parathyroid glands prior to operation for most patients,

allowing the surgeon to know where to start the exploration; intraoperative PTH measurement can

be used to confirm removal of all hyperfunctioning parathyroid tissue, that is, when to stop the

operation.

ANATOMY

1 Typically, each person has four parathyroid glands – two superior and two inferior (Fig. 76-1).1 The

normal parathyroid glands are flat, ovoid, and red-brown to yellow. They measure 5 to 7 mm × 3 to 4

mm × 0.5 to 2 mm and weigh between 30 and 50 mg each. The lower glands are usually larger than

the upper glands. The superior glands are most often embedded in the fat on the upper posterior surface

of the thyroid lobe near the site where the recurrent laryngeal nerve enters the larynx. The inferior

glands are usually more ventral and lie close to or within the portion of the thymus gland that extends

from the inferior pole of the thyroid gland into the chest. Although this anatomy is fairly consistent,

substantial variations from the usual can occur, and it is essential that the surgeon have a thorough

understanding of these anatomic variations.

Variations in parathyroid gland anatomy are primarily caused by differences in patterns of

embryogenesis. During the fourth and fifth weeks of fetal development, a series of four pharyngeal

pouches develop (Fig. 76-2). The superior parathyroid gland arises from the fourth pharyngeal pouch in

conjunction with the lateral thyroid, and the inferior gland arises from the third pouch along with the

thymus. The derivatives of each pouch then migrate together so that the superior parathyroid gland

usually remains in close association with the upper pole of the thyroid, although it may occasionally be

loosely attached by a long vascular pedicle, migrating caudad along the esophagus into the posterior

mediastinum. Occasionally, a gland may be totally embedded in the thyroid parenchyma. The inferior

parathyroid gland descends with the thymus, but this migration is extremely variable. Inferior glands

can be found anywhere from the pharynx to the mediastinum. Regardless of their location, they usually

adhere to the thymus or are within the thyrothymic ligament. Supernumerary glands can be identified

in up to 15% of patients, most often in association with the thymus. Autopsy studies suggest that four

parathyroid glands are virtually always present.

The arterial supply to both the superior and inferior parathyroid glands is usually from the inferior

thyroid artery, although it may arise from the superior thyroid or thyroidea ima arteries or from the

rich anastomosis of vessels supplying the larynx, trachea, and esophagus. A mediastinal parathyroid

gland that descended during embryonic development usually receives its blood supply from either the

internal mammary artery or small arteries within the thymus; however, an enlarged parathyroid gland

that grows into the mediastinum usually carries with it the corresponding branch of the inferior thyroid

2146

artery. The inferior, middle, and superior thyroid veins, which drain the parathyroid glands, empty into

the internal jugular vein or the innominate vein.

Histologically, the normal adult parathyroid gland is about half parenchyma and half stroma,

including fat cells (Fig. 76-3). In children, the gland is almost entirely composed of parenchymal chief

cells. Beginning at puberty, adipocytes appear and, with age, occupy an increasing proportion of the

gland. Also with increasing age, acidophilic, mitochondria-rich oxyphil cells are present in increasing

numbers and are intermixed with the glycogen-laden, polygonal, water-clear cells. The functional

significance of the various cell types remains unclear, although the water-clear cells and oxyphil cells

are probably derived from the chief cells and secrete parathyroid hormone (PTH).

PHYSIOLOGY

The primary physiologic role of the parathyroid gland is the endocrine regulation of calcium and

phosphate metabolism. Average daily exchanges of these ions from the gastrointestinal tract, bone, and

kidney are shown in Figure 76-4.

Calcium

Calcium ion plays a critical role in all biologic systems. It participates in enzymatic reactions and is a

mediator in hormone metabolism. Calcium is intimately involved in the physiology of

neurotransmission, muscle contraction, and blood coagulation. It is the major cation in bone and teeth.

It represents about 2% of the average body weight, and almost all calcium is contained in the skeleton.

The normal range of serum calcium is 9 to 10.5 mg/dL (4.5 to 5.2 mEq/L), and the daily variation in a

normal person is generally less than 10%. About half of the total serum calcium is in an ionized,

biologically active form; 40% is bound to serum protein, mainly albumin, and 10% forms compounds

with organic ions, such as citrate. The total serum calcium concentration is a function of the serum

protein content, and because hydrogen ion competes with calcium for the same binding sites on

albumin, the body fluid pH is important. In general, for every change of 1 g/dL in the serum albumin

level, a direct alteration of 0.8 mg/dL occurs in the serum calcium concentration. Almost all the

physiologically important activity of calcium is represented by the unbound, or free, fraction.

2147

No comments:

Post a Comment

اكتب تعليق حول الموضوع