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160
ENDOCRINE SURGERY
substantial, making this an unappealing option for many patients. Single-agent regimens using doxorubicin, dacarbazine, capecitabine, and 5-fluorouracil have been reported with partial response rates up to 24–29% [30]. Newer che­motherapeutic agents, such as Irinotecan (a topoisomerase I inhibitor) and 17-AAG (heat shock protein 90 inhibitor), are currently being evaluated in phase II clinical trials.
Patients with metastatic disease can have sig­nificant symptoms from calcitonin excess including severe flushing, diarrhea, and weight loss. Patients with hormonal symptoms may benefit from medical treatment with somatosta­tin analogs. These patients may also benefit from cytoreductive surgery of unresectable disease. Procedures to decrease the tumor burden, including resection and ablation, may provide patients with significant symptomatic relief [27].
With the discovery of the RET protoonco­gene and its integral role in the pathogenesis of MTC, a new class of therapies have developed aimed at the molecular pathways central to the development and progression of MTC. RET is part of the receptor tyrosine kinase family. RET has been shown to signal through multiple downstream pathways including ERK, PI3K/ AKT, p38 MAPK, and JNK [4]. While present investigations and therapies aim to block the tyrosine kinase at the receptor level, there is significant potential for developing more focused therapies as we gain a better under­standing of the critical downstream targets of these receptors.
Recently, a new class of drugs has been dis­covered that act as tyrosine kinase inhibitors. The first commercially available receptor tyro­sine kinase inhibitor was imatinib mesylate (Gleevec), which has been used successfully in the treatment of chronic myelogenous leukemia and gastrointestinal stromal tumors. An initial phase II study with Gleevac in MTC has shown limited efficacy with no responses in 15 patients and significant toxicity [31].
Many of the tyrosine kinase inhibitors thatare now being investigated inhibit multiple recep­tors, including RET, EGFR, andVEGF. A tyrosine kinase inhibitor that show significant inhibition of the RET receptor tyrosine kinase has been identified and is currently in phase II clinical trials. This drug, initially labeled ZD6474 and now referred to as Vandetanib (Zactima), is available in an oral form and has been shown to
have efficacy in inhibiting the RET receptor. Vandetanib is currently being evaluated in a multicenter phase II clinical trial for patients with hereditary MTC. Preliminary results have been presented inabstract form and reveal a 20% partial response and a 30% stable response by CT imaging [32]. However, there was a much more dramatic decrease in tumor markers. Plans are underway to expand this trial to sporadic MTC as well.
Several other receptor kinase inhibitors are also undergoing evaluations in clinical trials, many of these trials have not been published but preliminary results have been presented and there appears to be some efficacy in patients with metastatic MTC. Motesanib diphosphate (AMG 706) is a multikinase inhibitor that is cur­rently in phase II clinical trials. AMG 706 targets VEGF, PDGF, RET, and Kit receptors. It is cur­rently being evaluated in both advanced differen­tiated thyroid cancer and advanced MTC. Results from the MTC portion of the trial are not avail­able yet, but some antitumor activity was seen in patients with differentiated cancer [33]. Sorafenib (BAY 43-9006), another RET kinase inhibitor currently in phase II trials, has been shown to cause a dramatic reduction in calcitonin levels and leads to marked symptomatic improvement in patients with metastatic disease. In addition, no patient on Sorafenib had progression of dis­ease [34]. Interestingly, many of these new thera­pies lead to dramatic reductions in calcitonin levels almost immediately, suggesting that tumor markers may not be a reliable way to monitor tumor response to therapy.
Future Therapies
Many of these tyrosine kinase inhibitors lack receptor specificity, therefore their true mechan­ism ofaction is not clearly known. Severalsignal­ing pathways, such as the phosphatidyl-inositol 3-kinase (PI3K)/Akt, mitogen-activated protein kinases (MAPKs), and Notch1/Hairy Enhancer of Split-1 (HES-1)/achaete-scute complex like-1 (ASCL1) signaling pathway, have also been shown to play important roles in regulating the growth of neuroendocrine tumors (NETs)[35–39] Thus, another potential therapeutic target could be manipulation of these various cellular signaling pathways.
Notch1 signaling is very minimal or absent in prostate cancer, and NETs such as small cell lung
161
MEDULLARY THYROID CANCER
cancer (SCLC), carcinoid, and MTC [35, 36, 40, 41]. Activation of Notch1 significantly reduced the growth of MTC (TT) cells and regulates cal­citonin levels in a dose-dependent manner. These observations support the hypothesis that Notch1 functions as a tumor suppressor in MTC tumors and cell lines. Recently, we and others have reported that Raf-1 activation in a MTC(TT) cell line results in growth suppression as well as reduction in NE hormones (such as calcitonin and serotonin) and levels of the RET protooncogene [42, 43, 39]. We have explored the possibility of pharmacologically activating raf-1 in MTC cells. Though the compound ZM336372 was originally identified as a small molecule inhibitor of Raf-1 [44], recently we have shown that it activates raf-1 pathway in NET[37,45].Recentlywehaveobservedthat treatment of MTC cells with ZM336372 resulted in growth inhibition suggesting that activation of raf-1 pathway is required for the antitumor pro­liferation effect (Kunnimalaiyaan et al., manu­script in submission). Given the important role of Notch1 and raf-1 in the regulation of growth of MTC, we hope that activating compounds for these signaling pathways will have novel and potent therapeutic value for the treatment of patients with MTC.
References
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2. Costante G, Meringolo D, Durante C, et al. Predictive value of serum calcitonin levels for preoperative diag­nosis of medullary thyroid carcinoma in a cohort of 5817 consecutive patients with thyroid nodules. J Clin Endocrinol Metab. 2007;92(2):450–5.
3. Machens A, Schneyer U, Holzhausen HJ, Dralle H. Pro­spects of remission in medullary thyroid carcinoma according to basal calcitonin level. J Clin Endocrinol Metab. 2005;90(4):2029–34.
4. Ball DW. Medullary thyroid cancer: therapeutic targets and molecular markers. Curr Opin Oncol. 2007;19(1): 18–23.
5. Cohen R, Campos JM, Salaun C, et al. Preoperative calcitonin levels are predictive of tumor size and postoperative calcitonin normalization in medullary thyroid carcinoma. Groupe d’Etudes des Tumeurs a Calcitonine (GETC). J Clin Endocrinol Metab. 2000; 85(2):919–22.
6. Machens A, Dralle H. Pretargeted anti-carcinoembryonic­antigen radioimmunotherapy for medullary thyroid car­cinoma. J Clin Oncol. 2006;24(20):e37; author reply e38.
7. de Groot JW,Kema IP, Breukelman H, et al. Biochemical markers in the follow-up of medullary thyroid cancer. Thyroid. 2006;16(11):1163–70.
8. Brandi ML, Gagel RF, Angeli A, et al. Guidelines for diagnosis and therapy of MEN type 1 and type 2. J Clin Endocrinol Metab. 2001; 86(12):5658–71.
9. Kouvaraki MA, Shapiro SE,Perrier ND, et al. RETproto­oncogene: a review and update of genotype-phenotype correlations in hereditary medullary thyroid cancer and associated endocrine tumors. Thyroid. 2005; 15(6): 531–44.
10. Ogilvie JB, Kebebew E. Indication and timing of thyroid surgery for patients with hereditary medullary thyroid cancer syndromes. J Natl Compr Canc Netw. 2006; 4(2):139–47.
11. Hundahl SA, Fleming ID, Fremgen AM, Menck HR. A National Cancer Data Base report on 53,856 cases of thyroid carcinoma treated in the U.S., 1985–1995 [see commetns]. Cancer. 1998; 83(12):2638–48.
12. Grozinsky-Glasberg S, Benbassat CA, Tsvetov G, et al. Medullary thyroid cancer: a retrospective analysis of a cohort treated at a single tertiary care center between 1970 and 2005. Thyroid. 2007; 17(6):549–56.
13. Brierley J, Tsang R, Simpson WJ, et al. Medullary thyr­oid cancer: analyses of survival and prognostic factors and the role of radiation therapy in local control. Thyr­oid. 1996; 6(4):305–10.
14. Barbet J, Campion L, Kraeber-Bodere F, Chatal JF. Prog­nostic impact of serum calcitonin and carcinoembryonic antigen doubling-times in patients with medullary thyr­oid carcinoma. J Clin Endocrinol Metab. 2005;90(11): 6077–84.
15. Skinner MA, Moley JA, Dilley WG, et al. Prophylactic thyroidectomy in multiple endocrine neoplasia type 2A. N Engl J Med. 2005;353(11):1105–13.
16. Moley JF, Shervin, N. Medullary thyroid cancer. In Clark OH, Duh, Q.Y., and Kebebew, E, editors. Textbook of endocrine surgery, Vol. 2. Philadelphia, PA:Elsevier Inc. , 2005. 129–141.
17. Moley JF, DeBenedetti MK. Patterns of nodal metastases in palpable medullarythyroid carcinoma: recommenda­tions for extent of node dissection. Ann Surg. 1999; 229(6):880–7; discussion 887–8.
18. Greenblatt DY, Elson D, Mack E, Chen H. Initial lymph node dissection increases cure rates in patients with medullary thyroid cancer. Asian J Surg. 2007;30(2): 108–12.
19. Machens A, Hauptmann S, Dralle H. Increased risk of lymph node metastasis in multifocal hereditary and sporadic medullary thyroid cancer. World J Surg. 2007; 31(10):1960–5.
20. Scollo C, Baudin E, Travagli JP, et al. Rationale for central and bilateral lymph node dissection in sporadic and hereditary medullary thyroid cancer. J Clin Endo­crinol Metab. 2003;88(5):2070–5.
21. Network NCC. Practice Guidelines for Thyroid Carci­noma: Medullary Carcinoma 2007.
22. Kebebew E, Greenspan FS, Clark OH, et al. Extent of disease and practice patterns for medullary thyroid cancer. J Am Coll Surg. 2005;200(6):890–6.
23. Machens A, Hofmann C, Hauptmann S, Dralle H. Locoregional recurrence and death from medullary thyroid carcinoma in a contemporaneous series: 5-year results. Eur J Endocrinol. 2007;157(1):85–93.
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24. Tisell LE, Hansson G, Jansson S, Salander H. Reopera­tion in the treatment of asymptomatic metastasizing medullary thyroid carcinoma. Surgery. 1986;99(1):60–6.
25. Moley JF, Wells SA, Dilley WG, Tisell LE. Reoperation for recurrent or persistent medullary thyroid cancer. Surgery. 1993;114(6):1090–5; discussion 1095–6.
26. Tung WS, Vesely TM, Moley JF. Laparoscopic detection of hepatic metastases in patients with residual or recur­rent medullary thyroid cancer. Surgery. 1995;118(6): 1024–9; discussion 1029–30.
27. Chen H, Roberts JR, Ball DW, et al. Effective long-term palliation of symptomatic, incurable metastatic medul­lary thyroid cancer by operative resection. Ann Surg. 1998;227(6):887–95.
28. Faik Erdogan M, Gursoy A, Erdogan G,Kamel N. Radio­active iodine treatmentin medullary thyroid carcinoma. Nucl Med Commun. 2006;27(4):359–62.
29. Martins RG, Rajendran JG, Capell P, et al. Medullary thyroid cancer: options for systemic therapy of meta­static disease? J Clin Oncol. 2006;24(11):1653–5.
30. You YN, Lakhani V, Wells SA, Jr, Moley JF. Medullary thyroid cancer. Surg Oncol Clin N Am. 2006;15(3):639–60.
31. de Groot JW, ZonnenbergBA, vanUfford-MannessePQ, et al. A phase II trial of imatinib therapy for metastatic medullary thyroid carcinoma. J Clin Endocrinol Metab. 2007; 92(9):3466–9.
32. Wells SA, Jr, Gosnell JE, Gagel RF, Moley JF, et al. Vandetanib in metastatic hereditary medullary thyroid cancer: follow-up results of an open-label phase II trial. J Clin Oncol. 2007;25(18S):6018.
33. Sherman SI, Schlumberger, MJ, Droz J, Hoffman M, et al. Initial results from a phase II trial of motesanib diphosphate (AMG 706) in patients with differen­tiated thyroid cancer (DTC). J Clin Oncol. 2007; 25(18S):6017.
34. Kober F, Hermann M., Handler A, Krotla G. Effect of sorafenib in symptomatic metastatic thyroid cancer. J Clin Oncol. 2007;25(18S):14065.
35. Kunnimalaiyaan M, TraegerK, Chen H.Conservation of the Notch1 signaling pathway in gastrointestinal carci­noid cells. Am J Physiol Gastrointest Liver Physiol. 2005;289(4):G636–42.
36. Kunnimalaiyaan M, Yan S, Wong F, et al. Hairy enhan­cer of split-1 (HES-1), a Notch1 effector, inhibits the
growth of carcinoid tumor cells. Surgery. 2005; 138(6):1137–42; discussion 1142.
37. Kunnimalaiyaan M,Chen H.The Raf-1pathway: a mole­cular target for treatment of select neuroendocrine tumors? Anticancer Drugs. 2006;17(2):139–42.
38. Chen H, Kunnimalaiyaan M, Van Gompel JJ. Medullary thyroid cancer: the functions of raf-1 and human achaete-scute homologue-1. Thyroid. 2005;15(6): 511–21.
39. Sippel RS, Carpenter JE, Kunnimalaiyaan M, Chen H. The role of human achaete-scute homolog-1 in medul­lary thyroid cancer cells. Surgery. 2003;134(6):866–71; discussion 871–3.
40. Nakakura EK, Sriuranpong VR, Kunnimalaiyaan M, et al. Regulation of neuroendocrine differentiation in gastrointestinal carcinoid tumor cells by notch signal­ing. J Clin Endocrinol Metab. 2005;90(7):4350–6.
41. Radtke F, Raj K. The role of Notch in tumorigenesis: oncogene or tumour suppressor? Nat Rev Cancer. 2003; 3(10):756–67.
42. Carson-Walter EB, Smith DP, Ponder BA, et al. Post­transcriptional silencing of RET occurs, but is not required, during raf-1 mediated differentiation of medullary thyroid carcinoma cells. Oncogene. 1998; 17(3):367–76.
43. Chen H, Carson-Walter EB, Baylin SB, et al. Differentia­tion of medullary thyroid cancer by C-Raf-1 silences expression of the neural transcription factor human achaete-scute homolog-1. Surgery. 1996;120(2):168–72; discussion 173.
44. Hall-Jackson CA, Eyers PA, Cohen P, et al. Paradoxical activation of Raf by a novel Raf inhibitor. Chem Biol. 1999;6(8):559–68.
45. Van Gompel JJ, Kunnimalaiyaan M, Holen K, Chen H. ZM336372, a Raf-1 activator, suppresses growth and neuroendocrine hormone levels in carcinoid tumor cells. Mol Cancer Ther. 2005;4(6):910–7.
46. Machens A, Niccoli-Sire P, Hoegel J, et al. Early malig­nant progression of hereditary medullary thyroid can­cer. N Engl J Med. 2003;349(16):1517–25.
47. Machens A, Dralle H. DNA-based window of opportu­nity for curative pre-emptive therapy of hereditary medullary thyroid cancer. Surgery. 2006;139(3): 279–82.
12

Technique of Thyroidectomy

He´le`ne Gibelin, Thibault Desurmont, and Jean-Louis Kraimps
Introduction
Thyroid surgery is the most common operation in endocrine surgery. Total extracapsular lobectomy with isthmusectomy (isthmolobect­omy) is the procedure of choice. The entire lobe and the isthmus, including the pyramidal lobe, must be removed.
Subtotal lobectomy should be avoided since reoperation to complete a lobectomy is asso­ciated with a greater risk of injury to the recur­rent laryngeal nerve (RLN) and parathyroid glands. Consequently, subtotal lobectomy is con­sidered an inadequate operation. Thyroid sur­gery can and should be a safe procedure with minimal morbidity and negligible mortality. An accurately performed operation on thyroid gland requires both experience and technical ability [1, 2]. This emphasizes the importance of skilled Departments in Endocrine Surgery, performing a great number of procedures and teaching the youngest surgeons and residents [3]. It is the best way to minimize incidence of complications.
The general rules of thyroid operation are as follows:
Good exposure (by conventional approach
or with the endoscope in mini-invasive
approaches). Excellent visualization is the
main way to avoid RLN or parathyroid
injury.
Systematic identification of anatomic struc-
tures and meticulous dissection [4]. Thyroid
operation without identification RLN or parathyroid glands does not make sense. Consequently, bleeding should be avoided; if the latter occurs, identification of these anatomic structures is absolutely required before hemostasis avoiding diathermy, even bipolar.
Before surgery, the patient should be informed about the reasons why an opera­tion is needed, the alternative methods of treatment that might be used, and the poten­tial risks and benefits of the procedure. Information about possible complications must be given to the patient and clearly explained before surgery.
The patient should undergo a thorough med­ical evaluation to be sure that he or she is euthyroid.
Isthmolobectomy
The patient is carefully positioned on the operat­ing table with the neck hyperextended. A rolled towel is placed under the shoulders which allows sufficient neck extension. A sponge ring isplaced under the occiput for adequate head support and to keep it from moving. The eyes should be care­fully taped shut to avoid corneal abrasions.
Disinfection is performed with an alcoholic agent without iodine, which might interfere with postoperative radionuclear scanning and ablative therapy.
J.G.H. Hubbard et al. (eds.), Endocrine Surgery, Springer Specialist Surgery Series, DOI 10.1007/978-1-84628-881-4_12, Ó Springer-Verlag London Limited 2009
163
164
ENDOCRINE SURGERY
Slight elevation of the head of the operating
table is helpful in decreasing venous congestion.
The surgical field is draped from below the sternal notch to the chin and laterally on poster­ior part of the sternocleidomastoid muscles.
Skin Incision
The standard Kocher’s incision must be used. It is a collar-type incision placed transversally along the Langer’s line of the skin. This yields an excellent cosmetic result. The length of the incision must be adapted to the thyroid size. Most often a 4- to 5-cm incision allows safe thyroidectomy, but a larger incision can be necessary in case of large goiters or short neck. The surgical incision should therefore be made about 1 cm caudal to the cricothyroid cartilage since it then will be centered directly over the thyroid gland.
The skin incision should be made perpen­dicular to the patient and carried down through the subcutaneous tissue and platysma muscle with preservation of the anterior jugu­lar veins.
The skin, subcutaneous fat, and platysma muscle should be mobilized as two flaps upward to the thyroid cartilage and downward to the sternal border (see Fig. 12.1). Once these flaps have been mobilized, skin towels are applied, as well as a self-retaining retractor.
Strap Muscles
The next step is the dissection in the midline of the neck between the strap muscles from the thyroid cartilage to the suprasternal notch. Sternohyoid and sternothyroid muscles are dis­sected and retracted using right-angle retractors. The middle thyroid vein is identified, ligatured,
Fig. 12.1. Mobilization of superior flap preserving the anterior jugular veins.
165
TECHNIQUE OF THYROIDECTOMY
and divided. Division of the strap muscles is rarely necessary in case of very large goiter or in reoperative cases.
Upper Pole
Lateral retraction using forceps allows the opening of the space between the lobe and the cricothyroid muscle, thus often exposing the external branch of the superior laryngeal nerve [5–7]. The external branch of the super­ior laryngeal innervates the cricothyroid mus­cle, the action of which is to increase the tension of the vocal cords. Injury can lead to an inability to achieve high notes during sing­ing or speaking. Furthermore, in about 15% of patients, the nerve accompanies the superior thyroid artery. The best way to avoid injury of this nerve is to open the space between thyroid lobe and cricothyroid muscle, to stay lateral to this muscle and to ligate and divide only the superior thyroid artery branches (see
Fig. 12.2).
The complete division of the superior ves­sels enables the surgeon to medially rotate and anteriorly mobilize the gland, which results in optimal exposure of superior parathyroid gland and RLN. In some cases, the posterior branch of the superior thyroid artery can be preserved for superior parathyroid gland supply.
Lower Pole
The inferior thyroid veins can be safely ligated and the trachea observed, allowing a better medial rotation of the lobe with a better expo­sure of the hilum of the gland.
Lateral Dissection
Lateral retraction of the carotid sheath and med­ial rotation of the thyroid lobe allows tension of the inferior thyroid artery and makes the RLN easier to identify, most often crossing under or occasionally over the inferior thyroid artery. At this step, RLN must be identified. A small vessel, the vasonervorum, is always observed on this nerve, confirming identification.
Dissection should be meticulous, with the aim of preserving as much of the inferior thyr­oid artery and its branches as possible, since it supplies the blood to the two parathyroid glands. Truncal ligation of inferior thyroid artery results most often in parathyroid necrosis and should not be done.
Dissection is carried out between the thyroid capsule and the last branches of the inferior thyr­oid artery [8, 9]. The branches are ligated or clipped individually directly on the surface of the thyroid gland. Dissection is continued from the bottom to the top, preserving parathyroid glands with their blood supply and RLN (see Fig. 12.3).
Fig. 12.2. Dissection of the upper pole. Elective division of the
superior thyroid artery. (1) Inter crico-thyroid space; (2) super­ior thyroid artery; and (3), left upper pole of the thyroid.
Fig. 12.3. Left superior parathyroid gland. (1) Left recurrent
laryngeal nerve and (2) left superior parathyroid gland.
166
ENDOCRINE SURGERY
Fig. 12.4. Left Berry ligament dissection. (1) Left thyroid lobe;
(2) trachea; and (3) left recurrent laryngeal nerve.
At the upper part of the dissection, the RLN is very close to the thyroid at the site of the ligament of Berry, just before the nerve enters to the cricoid muscle. It is at this site of the ligament of Berry that the RLN is the most vulnerable to injury [10] (see Fig. 12.4). The ligament of Berry is a dense group of vessels and connective tissue that attaches the thyroid to the trachea. Small vessels are often situated in it, posterior to the nerve and bleeding is parti­cularly dangerous in this site (see Fig. 12.5). Positive identification of the nerve must be made prior to ligature. The use of any cautery or other thermal dissection device should be avoided at this step due to the potential for
Fig. 12.5. Left Berry ligament dissection. (1) Insertion of
posterior part of left thyroid lobe at the Berry ligament; (2), trachea; and (3) left recurrent laryngeal nerve.
Fig. 12.6. View after left thyroid lobe resection. (1) Trachea;
(2) left recurrent laryngeal nerve; and (3) left superior para­thyroid gland.
thermal injury of the RLN, which is in close proximity (see Fig. 12.6).
After this step, the thyroid lobe may be quickly dissected free from the trachea. Near the midline, one should look for a pyramidal lobe, which is present in about 80% of indivi­duals and should be removed with the thyroid lobe.
Parathyroid Autotransplantation
Even in unilateral lobectomy, all identified parathyroid tissue should be preserved on its native blood supply. If a gland is devascularized during dissection, it should be transplanted [11]. Furthermore, it is sometimes impossible to preserve a parathyroid gland since it is under the thyroid capsulae.
It is recommended to systematically look at the parathyroid glands at the end of operation before closure. The gland can be congestive because of lack of veinous drainage. In this case, the parathyroid capsulae must be incised, and in a few seconds, the gland will recover a nice color.
Sometimes the gland is devascularized and autotransplantation is necessary. In this case, the gland is removed and cut into tiny cubes that are about 1 mm created by separating the muscle fibers of the sternocleidothyroid muscle, avoiding any bleeding. It is important to avoid bleeding since hematoma formation could compromise
3
in volume. A pocket is
167
TECHNIQUE OF THYROIDECTOMY
ab
Fig. 12.7. (a and b) Closure.
the parathyroid function of the graft. The minced tissue is then transplanted into the pocket, which is closed by titanium clip or non­absorbable suture as landmark.
Wound Closure
A drain is necessary only if a very large goiter has been removed with a large persisting space and can never replace accurate hemostasis. It is of little or no use if severe postoperative bleed­ing occurs [12, 13].
The sternothyroid and sternohyoid muscles are sutured on the midline, as the platysma with 4-0 absorbable suture. The skin is closed by an intradermal 5-0 absorbable suture. In addition, glue can also be used on the skin (see Fig. 12.7).
Reoperative Thyroid Surgery
The best approach is the identification of RLN in a previously undissected area.
A lateral or ‘‘back door’’ approach is recom­mended in case of reoperation. After standard collar incision, the anterior border of the ster­nocleidomastoid muscle is mobilized and retracted laterally to expose sternohyoid and sternothyroid muscles. The lateral border of the sternothyroid muscle, inferior to the omo­hyoid muscle, is mobilized off of the carotid artery and jugular vein. With a retractor, the sternothyroid muscle is reflected medially and the carotid artery laterally. The soft tissue at the inferolateral part of the thyroid lobe is exposed
and can be dissected. Dissection is performed in a straightforward manner with, first, identifica­tion of the RLN, then control of inferior pedicle, and then superior pedicle.
A second approach is to enter the thyroid bed similarly to the initial operation. Then one can choose either an inferior approach and search for the RLN in the paratracheal region inferior to the area of previous dissection or a superior approach to identify the RLN where it enters the larynx.
Substernal Goiter
Most intrathoracic goiters can be removed though a standard collar incision. A sternotomy is required in less than 10% of cases. In case of bilateral intrathoracic goiter, we recommend commencing the resection on the smaller side and in some cases dividing the isthmus. For intrathoracic goiter, we prefer the toboggan technique described by Charles Proye: the goiter should be mobilized from top to bottom. The first step is to divide and ligate the superior thyroid artery and veins with preservation of the superior parathyroid gland. Section of the head of the sternocleidomastoid muscle or of the straps muscles (sternothyroid or sterno­hyoid muscles) may help in some cases. The second step is to control middle thyroid veins and mobilise the lateral part of the lobe. It is necessary to identify the position of the RLN before trying to mobilize the intrathoracic part of the lobe. It is often easier to identify the nerve
168
ENDOCRINE SURGERY
close to the inferior horn of the thyroid cartilage where it enters the larynx and then to follow it caudally. The pedicle posterior to the nerve can then be controlled, and a space of dissection opened between the nerve and the posterior part of the thyroid. A finger is placed in cervi­cothoracic space, following the posterior part of the lobe. During this dissection, it is possible to control the location of the nerve in relation to the goiter. Adhesions surrounding the lobe are progressively liberated. With gentle traction on the thyroid lobe, to avoid fragmentation of the thyroid, it is progressively exteriorized with con­trol of the inferior thyroid vessels. When the entire lobe is extracted, it is important to check the absence of the inferior parathyroid gland at the posterolateral surface of the lobe. When a parathyroid gland is devascularized, it should be autotransplanted in the sternocleidomastoid muscle before the end of the procedure. The insertion of a closed suction drain is recom­mended because of the large remaining mediast­inal cavity.
Local or Regional Anesthesia
Local or regional anesthesia represents a safe alternative to general anesthesia in patients with amiodarone-induced thyrotoxicosis [14]. A regional C2-C4 superficial cervical and local field block is performed using a mixture of 0.5% lidocaine and 0.25% bupivacaine. To avoid excessive traction on the muscles, the skin inci­sion is higher on the neck, just inferior to the cricoid cartilage prominence.
intubation dose is recommended [17]. During the dissection, either the RLN or vagus nerve should be stimulated. A positive acoustic signal after stimulation of both the vagus nerve andthe RLN is an indication that the nerve conduction between the place of stimulation and the vocalis muscle is intact, so the vocal fold function is intact. If there is a positive signal after stimula­tion of only the RLN and not the vagus nerve, it means that there is usually a RLN paresis with a lesion distally located to the stimulation site.
However, neuromonitoring detects only neurogenic causes of RLN palsy and cannot predict a palsy induced by postoperative hema­toma or edema. Multicentric studies have demonstrated lower rates of transient and per­manent RLN palsy rates in comparison with conventional RLN identification [15–17]. The learning curve for an optimal use of this tech­nique is estimated to 100 operations.
Minimally Invasive Thyroidectomy
Endoscopic neck surgery was first described for parathyroidectomy by Gagner in 1996 [18], and subsequently proposed for thyroid surgery. Four techniques are currently per­formed: two complete endoscopic techniques and two video-assisted techniques. These tech­niques are safe and reproducible but indicated only in selected patients (see Table 12.1).
Intraoperative Neuromonitoring
In the literature, it is well demonstrated that identification of the RLN reduces the incidence of nerve palsy [15–17]. The principle of neuro­monitoring is based on instrumental testing of the reflex arc between the RLN or the vagus nerve and the vocalis muscle. The stimulating electrode is inserted in the vocalis muscle directly or placed at the surface of an endotra­cheal tube. To ensure the correct response, exact placement of the tube is necessary and no repe­titive administration of curare after the initial
Table 12.1. Relative indications of minimal invasive
thyroidectomy
Indications Nodule <3cmof
diameter
Thyroid estimated
volume <20 mL
Benign or low-
grade follicular lesion
Low-risk papillary
carcinoma
Absolute contraindications
Previous neck
surgery
Large goiter Hyperthyroidism
Locally advanced
cancer
Lymph node
metastases
Relative contraindications
Previous neck
irradiation
Thyroiditis
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TECHNIQUE OF THYROIDECTOMY
Complete Endoscopic Thyroidectomy
Gagner Technique
The patient under general endotracheal anesthe­sia is placed in the supine position with neck hyperextension. A 5-mm horizontal incision is performed above the sternal notch. The cervical fascia is opened and the space below the platysma is developed. A 5-mm trocar is inserted into the subplatysmal space and secured with a purse string suture. Pressure insufflation is limited to 10 mm Hg. Initial dissection along the anteromedial border of the ipsilateral sterno­cleidomastoid muscle (SCM) is performed by advancing a 08 endoscope. Once an adequate avascular space has been created, a 308 endo­scope is used. Additional trocars are inserted under direct vision: a 2- to 3-mm trocar at the midline, a 2- to3-mm trocar at the midportion of the ipsilateral SCM, and a 5- to 10-mm trocar along the anterior border of the SCM. The ster­nohyoid and sternothyroid muscles are retracted anteromedially after opening the linea alba with the hook. The thyroid lobe is mobilized without using cautery in the deeper tissue planes. The middle thyroid vein is ligated using 5-mm clips or the 5-mm harmonic scalpel. The RLN and the parathyroid glands are identified and carefully dissected from the thyroid gland. The inferior thyroid artery is identified, ligated with 5-mm clips as close as possible to the thyroid gland, and divided with the RLN in full view. The super­ior pole vessels are isolated, clipped, and divided when the superior laryngeal nerve has beeniden­tified. The inferior pole vessels are divided with the harmonic scalpel. The Berry’s ligament is divided with the harmonic scalpel after releasing the anteromedial attachments of the RLN. The specimen is then placed in a small bag (thumb portion of a surgical glove) and extracted through the superolateral trocar site. The skin is closed with adhesive strips [19, 20].
Cougard Technique
This technique is a variant of Gagner technique with central approach, which allows a bilateral exploration of the neck with three trocars. The patient is in the supine position with hyperex­tension of the neck. A 1.5-cm horizontal inci­sion is made above the sternal notch. The cervical fascia is opened and the linea alba is
divided. A space between superficial and deep strap muscles is developed. A 5-mm trocar is inserted into the subplatysmal space and secured with a purse string suture. Pressure insufflation is limited to 8 mm Hg. A 08 5-mm endoscope isinserted.A working space is created with the camera. One 3-mm trocar is inserted under direct vision, to avoid anterior jugular veins, on the left side and a 5-mm trocar on the right side. The sternohyoid and sternothyroid muscles are retracted anteromedially. After mobilization of the thyroid lobe, the inferior thyroid veins are first ligated by clips or 5-mm harmonic scalpel and divided, followed by the middle thyroid vein. The superior pole vessels are isolated after identification of the superior laryngeal nerve and ligated. The inferior thyroid artery is isolated and ligated after identification and preservation of the RLN and the parathyroid glands. Isthmus is divided using harmonic scal­pel and extracted by midline incision. The inci­sions are closed with surgical glue [21].
Video-Assisted Technique (MIVAT)
Lateral Approach: Henry Technique
The patient is in a supine position without hyperextension of the neck to avoid traction of the SCM and strap muscles. A 12- to 15-mm a transverse neck incision is made just above the isthmus. The anterior border of the SCM is liberated from the cervical fascia and the thyr­oid lobe to the carotid sheath up to the prever­tebral fascia. The superior limit of the dissection is the omohyoid muscle. To enlarge the space of dissection, a moist swab is stuffed upward and downward. Two 2.5-mm ports are inserted on the line of the anterior border of the SCM, 6 cm above and 3–4 cm below the first skin incision. These are inserted by passing a sharp trocar under direct vision, (from in to out) via the initial incision and then using this trocar as a guide stick to insert the working ports (from out to in). Then a 10-mm trocar is inserted through the incision. Pressure insufflation is limited to 8 mm Hg. All dissection is performed with 10-mm 08 endoscope and 2-mm graspers and scissors. The dissection starts with the identifi­cation of anatomic structures, particularly the RLN. The thyroid lobe is mobilized. Small ves­sels are cauterized. The branch of the inferior thyroid artery is isolated but not ligated. The