Добавил:
kiopkiopkiop18@yandex.ru t.me/Prokururor I Вовсе не секретарь, но почту проверяю Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз: Предмет: Файл:

Ординатура / Хирургия / @xirurgi_2025 / @xirurgi_2025 - 468 - файл

.pdf
Скачиваний:
0
Добавлен:
29.08.2026
Размер:
33 Мб
Скачать
130
https://t.me/medicina_free
L. Aljadeff and A. B. Morlandt
Oral Dysplasia: Risk ofMalignant Transformation
Although there is no way to denitively predict when an OPMD will undergo malignant transformation, some tools exist to stratify patients into risk categories.
Unfortunately, the malignant transformation rate of oral epithelial dysplasia var­ies widely in the literature, ranging from 0.13% to 36% [39]. This is, in large part, due to signicant differences in population risk factors, study design, inclusion cri­teria, and terminology. As discussed earlier in this chapter, the largest met analysis to date was conducted by Iocca etal., and they calculated an annual malignant transformation rate of 1.7% for mild dysplasia and 3.57% for severe dysplasia [11]. Furthermore, Speight has shown that while less than 5% of mild dysplasia will undergo malignant transformation, up to 50% of severe dysplasia will [37].
In 2018, Speight etal. published an excellent review of risk factors for malignant transformation of oral epithelial dysplasia and proposed an algorithm that incorpo­rates some of the most important clinical risk factors along with histopathologic grading to classify lesions as either high or low risk [4]. According to this algorithm, female gender, nonsmokers, high-risk subsites (tongue and oor of mouth), eryth­roplakia, nonhomogenous or speckled leukoplakia, PVL (that is persistent, recur­rent, or in multiple spots), and severe dysplasia all pose a high risk for malignant transformation. Meanwhile, homogenous leukoplakia that histopathologically dem­onstrates mild dysplasia is the only lesion that is considered low risk. However, risk stratifying patients must always be balanced against the reality that lesions without any evidence of epithelial dysplasia can still undergo malignant transformation and malignant transformation of high-risk lesions is not inevitable.
This conundrum highlights the urgent need for a data-driven method to distin­guish dysplastic lesions that will progress to cancer from those that will not. As the molecular underpinnings of the “hallmarks of cancer” have become better under­stood, molecular biomarkers of these critical processes have received a lot of atten­tion as potential predictors of malignant transformation [40, 41]. As Speight puts it, “The Holy Grail in terms of risk assessment is to discover a biomarker that can be used in a histologic or chairside test to predict malignant transformation of oral lesions” [4]. Some of the most investigated markers have been p53, S100A7, Ki67, survivin, MMP-9, and p16 [42]. Additionally, there is emerging data that genetic abnormalities such as loss of heterozygosity and aneuploidy, as well as epigenetic changes such as histone modication, post-transcriptional regulation of mRNA, and DNA methylation, are important in progression from dysplasia to carcinoma [4,
25]. However, although many molecular markers and genetic and epigenetic changes
have been shown to correlate with oral epithelial dysplasia and tumorigenesis, no single biomarker has been shown to reliably predict malignant transformation [4]. Unfortunately, the literature is full of poorly designed studies with little to no clini­cal application. A systematic review published by Smith etal. identied 2550 stud­ies published on molecular biomarkers for the malignant transformation of oral dysplasia. However, only 13 of them were longitudinal studies with adequate follow up that met their quality standards [42].
7 Oral Dysplasia
https://t.me/medicina_free
131
Interestingly, articial intelligence (AI) has shown some promise as a tool for integrating large amounts of data to estimate risk of malignant transformation [43]. The ability to digitize stained tissue specimens and develop machine learning tools in digital pathology have paved the way to a myriad of AI-based tests in oncology. One such test designed specically for oral dysplasia is Straticyte, marketed by Proteocyte AI (Toronto, ON). This prognostic test uses digitized immunohisto­chemical stains for a panel of biomarkers, including S100A7, to calculate a quanti­tative risk of malignant transformation [44]. Many molecular diagnostics are in use developed for breast cancer, prostate cancer, and brain cancer with encouraging preliminary results [43] and are commercially available. Historically, the manage­ment of dysplasia has been as diverse and variable as the opinions of all the clini­cians treating it; however, this exciting technology may allow standardization of treatment practices and afford new levels of sophistication in the management of dysplasia based on objective assessments of patient-specic histopathological data and molecular signatures. Ultimately, the management of dysplasia deserves increasingly standardized and customized practices, to limit the morbidity of unnec- essary and costly treatment for those patients whose OPMDs are unlikely to undergo malignant transformation, and discourage watchful waiting for those with aggres­sive lesions, which may ultimately progress to cancer.
References
1. Baillie S, Simms W.Queries and responses from the medical committee of the society for investigating the nature and cure of cancer. Edinb Med Surg J. 1806;2:382–9.
2. Warnakulasuriya S, Johnson NW, van der Waal I.Nomenclature and classication of poten­tially malignant disorders of the oral mucosa. J Oral Pathol Med. 2007;36:575–80.
3. Reibel J, Gale N, Hille J, etal. Oral potentially malignant disorders and oral epithelial dyspla­sia. In: El-Naggar AK, Chan JKC, Grandis JR, Takata T, Slootweg PPJ, editors. WHO clas­sication of head and neck tumours. 4th ed. Lyon: IARC; 2017. p.112–5.
4. Speight PM, Khurram SA, Kujan O.Oral potentially malignant disorders: risk of progression to malignancy. Oral Surg Oral Med Oral Pathol Oral Radiol. 2018;125(6):612–27.
5. Warnakulasuriya S, Kujan O, Aguirre-Urizar JM, Bagan JV, González-Moles MÁ, Kerr AR, Lodi G, Mello FW, Monteiro L, Ogden GR, Sloan P, Johnson NW.Oral potentially malignant disorders: a consensus report from an international seminar on nomenclature and classication, convened by the WHO Collaborating Centre for Oral Cancer. Oral Dis. 2021;27(8):1862–80.
6. Nikitakis NG.Special focus issue on potentially premalignant oral epithelial lesions: introduc­tion and perspective. Oral Surg Oral Med Oral Pathol Oral Radiol. 2018;125(6):575–6.
7. Van der Waal I.Historical perspective and nomenclature of potentially malignant or potentially premalignant oral epithelial lesions with emphasis on leukoplakia-some suggestions for modi­cations. Oral Surg Oral Med Oral Pathol Oral Radiol. 2018;125(6):577–81.
8. Chaturvedi AK, Udaltsova N, Engels EA, Katzel JA, Yanik EL, Katki HA, Lingen MW, Silverberg MJ.Oral leukoplakia and risk of progression to oral cancer: a population-based cohort study. J Natl Cancer Inst. 2020;112(10):1047–54.
9. Axell T, Pindborg JJ, Smith CJ, etal. Oral white lesions with special reference to precancer­ous and tobacco related lesions: conclusions of an international symposium held in Uppsala, Sweden, May 18-21, 1994. J Oral Pathol Med. 1996;25:49–54.
132
https://t.me/medicina_free
10. Hogewind WFC, van der Kwast WAM, van der Wall I. Oral leukoplakia, with emphasis on malignant transformation. J Craniomaxillofac Surg. 1989;17:128–33.
11. Iocca O, Sollecito TP, Alawi F, Weinstein GS, Newman JG, De Virgilio A, Di Maio P, Spriano G, Pardiñas López S, Shanti RM.Potentially malignant disorders of the oral cavity and oral dysplasia: a systematic review and meta-analysis of malignant transformation rate by subtype. Head Neck. 2020;42(3):539–55.
12. Waldron CA, Shafer WG.Leukoplakia revisited. Cancer. 1975;36:1386–92.
13. Reddi SP, Shafer AT.Oral premalignant lesions: management considerations. Oral Maxillofac Surg Clin North Am. 2006;18:425–33.
14. Abadie WM, Partington EJ, Fowler CB, Schmalbach CE.Optimal management of prolifera­tive verrucous leukoplakia: a systematic review of the literature. Otolaryngol Head Neck Surg. 2015;153:504–11.
15. Goette DK.Review of erythroplasia of queyrat and its treatment. Urology. 1976;8(4):311–5.
16. Cawson RA, Langdon JD, Eveson JW.Ertyroplasia (‘ertyroplakia’). In: Cawson RA, editor. Surgical pathology of the mouth and jaws. Oxford: Wright; 1996. p.180.
17. Pindborg JJ, Reichart PA, Smith CJ, etal. Histological typing of cancer and precancer of the oral mucosa. 2nd ed. Berlin: Springer; 1997.
18. Shafer WG, Waldron CA.Erththroplakia of the oral cavity. Cancer. 1975;36:1021–8.
19. Slaughter DP, Southwick HW, Smejkal W. “Field cancerization” in oral stratied squamous epithelium: clinical implications of multicentric origin. Cancer. 1953;6(5):963–8.
20. Califano J, van der Riet P, Westra W, Nawroz H, Clayman G, Piantadosi S, et al. Genetic progression model for head and neck cancer: implications for eld cancerization. Cancer Res. 1996;56:2488–92.
21. Smith C, Pindborg JJ.Histologic grading of oral epithelial atypia by the use of photographic standards. Copenhagen: C.Hamburgers Bogtrykkeri; 1969.
22. Pindborg JJ, Reichart PA, Smith CJ, van der Waal I.World Health Organization: histological typing of cancer and precancer of the oral mucosa. Berlin: Springer; 1997.
23. WHO, Collaborating Centre for Oral Precancerous Lesions. Denition of leukoplakia and related lesions: an aid to studies on oral precancer. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1978;46:518–39.
24. Brothwell DJ, Lewis DW, Bradley G, Leong I, Jordan RC, Mock D, Leake JL. Observer agreement in the grading of oral epithelial dysplasia. Community Dent Oral Epidemiol. 2003;31(4):300–5.
25. Ranganathan K, Kavitha L. Oral epithelial dysplasia: classications and clinical rele­vance in risk assessment of oral potentially malignant disorders. J Oral Maxillofac Pathol. 2019;23(1):19–27.
26. Abbey LM, Kaugars GE, Gunsolley JC, Burns JC, Page DG, Svirsky JA, Eisenberg E, Krutchkoff DJ, Cushing M.Intraexaminer and interexaminer reliability in the diagnosis of oral epithelial dysplasia. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1995;80(2):188–91.
27. Warnakulasuriya S, Reibel J, Bouquot J, Dabelsteen E.Oral epithelial dysplasia classication systems: predictive value, utility, weaknesses and scope for improvement. J Oral Pathol Med. 2008;37:127–33.
28. Kujan O, Oliver RJ, Khattab A, Roberts SA, Thakker N, Sloan P, etal. Evaluation of a new binary system of grading oral epithelial dysplasia for prediction of malignant transformation. Oral Oncol. 2006;42:987–93.
29. Nankivell P, Williams H, Matthews P, Suortamo S, Snead D, McConkey C, etal. The binary oral dysplasia grading system: validity testing and suggested improvement. Oral Surg Oral Med Oral Pathol Oral Radiol. 2013;115:87–94.
30. Lingen MW, Kalmar JR, Karrison T, etal. Critical evaluation of diagnostic aids for the detec­tion of oral cancer. Oral Oncol. 2008;44(1):10–22.
31. Downer MC, Moles DR, Palmer S, Speight PM.A systematic review of test performance in screening for oral cancer and precancer. Oral Oncol. 2004;40(3):264–73.
L. Aljadeff and A. B. Morlandt
7 Oral Dysplasia
https://t.me/medicina_free
32. Lane PM, Gilhuly T, Whitehead P, Zeng H, Poh CF, Ng S, etal. Simple device for the direct visualization of oral-cavity tissue uorescence. J Biomed Opt. 2006;11(2):024006.
33. Rashid A, Warnakulasuriya S.The use of light-based (optical) detection systems as adjuncts in the detection of oral cancer and oral potentially malignant disorders: a systematic review. J Oral Pathol Med. 2015;44(5):307–28.
34. Mashberg A.Final evaluation of tolonium chloride rinse for screening of high-risk patients with asymptomatic squamous carcinoma. J Am Dent Assoc. 1983;106(3):319–23.
35. Portugal LC, Wilson KM, Biddinger PW, etal. The role of toluidine blue in assessing mar­gin status after resection of squamous cell carcinomas of the upper aerodigestive tract. Arch Otolaryngol Head Neck Surg. 1996;122:517–9.
36. Field EA, McCarthy CE, Ho MW, Rajlawat BP, Holt D, Rogers SN, Triantafyllou A, Field JK, Shaw RJ.The management of oral epithelial dysplasia: the Liverpool algorithm. Oral Oncol. 2015;51(10):883–7.
37. Speight PM.Update on oral epithelial dysplasia and progression to cancer. Head Neck Pathol. 2007;1(1):61–6.
38. Awadallah M, Idle M, Patel K, Kademani D.Management update of potentially premalignant oral epithelial lesions. Oral Surg Oral Med Oral Pathol Oral Radiol. 2018;125(6):628–36.
39. Kademani D, Dierks E.Surgical management of oral and mucosal dysplasias: the case for surgical excision. J Oral Maxillofac Surg. 2007;65(2):287–92.
40. Hanahan D, Weinberg RA.Hallmarks of cancer: the next generation. Cell. 2011;144:646–74.
41. Nikitakis N, Pentenero M, Georgaki M, Poh C, etal. Molecular markers associated with devel­opment of potentially premalignant oral epithelial lesions: current knowledge and future impli­cations. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2008;125:650–69.
42. Smith J, Rattay T, McConkey C, Helliwell T, Mehanna H.Biomarkers in dysplasia of the oral cavity: a systematic review. Oral Oncol. 2009;45:647–53.
43. Bera K, Schalper KA, Rimm DL, Velcheti V, Madabhushi A. Articial intelligence in digital pathology—new tools for diagnosis and precision oncology. Nat Rev Clin Oncol. 2019;16(11):703–15.
44. Hwang JT, Gu YR, Shen M, Ralhan R, Walsh PG, Pritzker KP, Mock D.Individualized ve­year risk assessment for oral premalignant lesion progression to cancer. Oral Surg Oral Med Oral Pathol Oral Radiol. 2017;123(3):374–81.
133
Chapter 8
https://t.me/medicina_free
Pharyngoesophageal Reconstruction
RayY.Wang, CaitlinM.Coviello, MohammadS.Jafferji, ShawnGroth, andAndrewT.Huang
Introduction
Defects of the pharynx and cervical esophagus represent a signicant challenge for reconstructive surgeons due to the unique technical, functional, and outcome con­siderations involved. Reconstruction following ablative procedures for malignancy is the most common indication and is complicated by the need for expedient recov­ery to avoid delays in adjuvant therapy and additional technical challenges posted by prior treatment, particularly radiation. While the incidence of most head and neck cancers has decreased in recent years, presumably due to a decrease in tobacco use, an estimated 40,000 patients will be diagnosed annually with cancers of the laryngopharynx or esophagus [1, 2]. Historically, advanced laryngeal and hypopha­ryngeal cancers were treated with primary total laryngectomy with or without phar­yngectomy and/or adjuvant radiation [3]. Published in 1991, the landmark Department of Veteran Affairs Laryngeal Cancer Study Group trial demonstrated that an organ preservation approach with induction chemotherapy followed by radi­ation could achieve comparable overall survival with laryngeal preservation in 64% of patients [3]. Twelve years later, the RTOG 91-11 trial demonstrated superiority of concurrent chemotherapy with radiation for laryngeal preservation and locoregional control compared to induction chemotherapy and radiation or radiation alone, establishing concurrent chemoradiotherapy as the treatment of choice for
R. Y. Wang · C. M. Coviello · A. T. Huang (*) Department of Otolaryngology—Head and Neck Surgery, Baylor College of Medicine, Houston, TX, USA e-mail: ray.wang@bcm.edu; aitlin.coviello@bcm.edu; andrew.huang@bcm.edu
M. S. Jafferji · S. Groth Division of Thoracic Surgery, Michael E.DeBakey Department of Surgery, Baylor College of Medicine, Houston, TX, USA e-mail: mohammad.jafferji@bcm.edu; shawn.groth@bcm.edu
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 J. C. Melville et al. (eds.), Advancements and Innovations in OMFS, ENT, and Facial Plastic Surgery, https://doi.org/10.1007/978-3-031-32099-6_8
135
136
https://t.me/medicina_free
organ- sparing treatment of advanced laryngeal and hypopharyngeal cancers [4, 5]. Today, total laryngectomy is typically reserved for patients with very advanced (T4) local disease or in the salvage setting [6, 7]. Similarly, while surgery has historically been the primary curative modality for cancers of the esophagus, preoperative or denitive chemoradiation has been increasingly utilized in patients with locally advanced disease [8].
The choice of technique in pharyngeal reconstruction after surgery for advanced cancers of the larynx and hypopharynx is of particular importance as wound com­plications—particularly pharyngocutaneous stula (PCF)– carry considerable mor­bidity. When they occur in the primary setting, these complications can lead to delays in the initiation of adjuvant treatment, which have been shown to negatively impact survival [9]. Meanwhile, patients undergoing laryngectomy with or without pharyngectomy in the salvage setting have been demonstrated in multiple studies to be at increased risk of PCF and wound complications [7, 10]. In the RTOG 91-11 study, 59% of patients in the concurrent chemoradiation arm developed wound complications postoperatively with 30% developing PCF [11].
Furthermore, other functional outcomes such as the ability to tolerate oral nutri­tion, gastrostomy-tube dependence, stricture formation, and utilization of tracheo­esophageal puncture for phonation are impacted by the reconstructive technique and represent important considerations when approaching these patients.
In this chapter, we review fundamental principles of pharyngeal reconstruction after oncologic treatment and existing literature on the various techniques that have been described with regards to functional outcomes and complications.
R. Y. Wang et al.
Principles ofReconstruction
The pharynx is a funnel-shaped structure that serves dual functions as part of the upper respiratory and gastrointestinal tracts. It is divided into three components— the nasopharynx, which is bounded anteriorly by the choanae and inferiorly at the velum; the oropharynx, which is separated from the oral cavity anteriorly along the circumvallate papillae of the base of tongue to the anterior tonsillar pillars and soft palate and inferiorly by the larynx; and the hypopharynx, which comprises the pyri­form sinuses, post-cricoid, and esophageal inlet. A representative endoscopic view of the larynx and pharynx is demonstrated in Fig. 8.1. The pharynx serves as a conduit for air to the lower respiratory tract and for food and liquid bolus transit to the esophagus and stomach. As laryngectomy and pharyngoesophagectomy proce­dures result in opening of the alimentary tract to the neck and external environment, the goals of reconstruction are focused primarily on re-establishing a safe and func­tional passageway for the transit of food boluses that is robust enough to survive adjuvant therapy. In the primary setting, this closure must also be robust enough to withstand adjuvant radiation or chemoradiotherapy and heal quickly enough so as to not delay initiation of adjuvant treatment. Ideally, the pharyngeal reconstruction should also allow for a tracheoesophageal puncture to facilitate phonation while preventing leakage of saliva or food into the respiratory tract.
8 Pharyngoesophageal Reconstruction
https://t.me/medicina_free
Fig. 8.1 Laryngopharyngeal anatomy. (a) Greater cornu of thyroid cartilage, (b) Pyriform sinus, (c) Post­cricoid, (d) Glottic inlet, (e) Arytenoid, (f) Epiglottis, (g) Vallecula
137
Table 8.1
Reconstructive ladder
Microvascular free tissue transfer Regional tissue transfer Local tissue transfer Tissue expansion Skin graft Delayed primary closure Primary closure Secondary intention
The concept of the reconstructive ladder (Table 8.1) is well established within the reconstructive literature and describes a spectrum of reconstructive options that may be applied to a particular defect, ranging from healing by secondary intention to microvascular free tissue transfer (MVFTT). Selecting a reconstructive modality is a complex decision that depends on a variety of factors, including the patient’s anatomy, anticipated extent of the defect, and medical comorbidities. Depending on the extent of resection, the size of the defect may vary dramatically from small pharyngotomies in mucosa-sparing laryngectomy to total laryngopharyngectomy with total glossectomy or esophagectomy. There have been numerous algorithms described to guide pharyngeal reconstruction, and approaches are highly surgeon and institution-dependent. Ideally, the reconstruction would minimize risk of post­operative pharyngocutaneous stula and stenosis, allowing for as close to normal function as possible while minimizing donor site morbidity and operative complex­ity. A variety of techniques ranging from primary closure, skin grafting, local muco­sal ap, pedicled aps, abdominal-based enteric aps, and microvascular free tissue transfer (MVFTT) have been described.
Primary Closure
While the rst laryngectomy performed by Billroth in 1873 involved intentional creation of a pharyngocutaneous stula above the tracheostoma, pharyngeal defects following resection of laryngeal and hypopharyngeal malignancies have been
138
https://t.me/medicina_free
R. Y. Wang et al.
managed with primary closure in a single stage since the 1890s [1214]. With the advent of locoregional and MVFTT options and evidence of increased complica­tions rates with primary closure in the salvage setting, primary closure is predomi­nantly utilized in primary laryngectomy cases with limited pharyngeal resection. Primary closure may be utilized in cases of esophageal perforation or partial resec­tion, but total or subtotal esophagectomy defects require additional reconstruction. The exact amount of residual pharyngeal mucosa required to prevent stricture has not been clearly elucidated, although primary closure in patients with as little as
1.5cm of residual mucosa has been described with functional swallow postopera­tively [15]. Other authors have recommended primary closure when at least 3.5cm of residual mucosa remains, corresponding roughly to a 34Fr bougie catheter [16]. The decision to proceed with primary closure is largely based on surgeon preference and experience as data to delineate candidates for primary closure in both the pri­mary and the salvage setting is lacking [17]. In cases involving signicant resection of pharyngeal mucosa, a patch (interposition design) reconstruction sutured to the residual mucosa is often necessary to provide adequate circumference to avoid stricture.
The primary goal of pharyngeal closure is to obtain a water-tight, tension-free closure with care taken to avoid excessive tension resulting in strangulation of the mucosa. Multiple different suture techniques, including Lembert, Cushing, Connell, and Gambee sutures, have been utilized and are shown in Fig.8.2 [18]. The choice of suture technique varies greatly among surgeons and institutions, and there is little data to suggest superiority of one technique over another, though some studies have suggested that continuous sutures may have lower rates of pharyngocutaneous s­tula than interrupted suture [19, 20]. Meticulous technique is imperative as any gaps or tears in the mucosa can lead to a salivary leak and PCF.There is also considerable variation based on institutional and surgeon preference in the orientation of the closure (vertical, horizontal, or “T”-shaped). Due to its orientation, horizontal clo­sure may reduce likelihood of stricture and improve postoperative dysphagia and dysphagia-related quality of life, though this may not be suitable for larger defects [21]. The “T” closure is typically accomplished with a vertical suture line along the medial pyriform mucosa with a horizontal cross-bar at the base of tongue [22]. The “T”-shaped closure has been shown to reduce the incidence of pseudo-diverticula (pseudo-vallecula) separated from the neopharynx by a scar band (pseudoepiglot­tis); this has been suggested to reduce postoperative dysphagia in some studies although this relationship has not been consistently demonstrated [2224]. While the trifurcation of the “T”-shaped closure represents a theoretical weak point, which may increase the risk of pharyngocutaneous stula, there is limited data to support this assertion and retrospective studies have had mixed results [25, 26].
Described by Sofferman etal. in 2000, the mechanical stapling technique has also been advocated as an alternative method to manual suturing techniques, par­ticularly in the international literature [27, 28]. After the trachea has been transected, a linear stapler is clamped and red across the pyriform sinuses angling superiorly and again at the vallecula aiming inferiorly to separate the larynx from the pharynx [27]. A recent meta-analysis found a lower rate of pharyngocutaneous stula (13.7%
8 Pharyngoesophageal Reconstruction
https://t.me/medicina_free
a
139
b
Fig. 8.2 Various suture techniques in the primary repair of pharyngoesophageal deformities. (a) Geometry. (b) Suture Techniques—Interrupted. (c) Suture Techniques—Continuous
140
c
https://t.me/medicina_free
R. Y. Wang et al.
Fig. 8.2 (continued)
vs. 27.2%) and shorter mean hospital stay compared to conventional suture tech­nique [29]. However, because this is a closed technique with limited visualization of the pharynx, this technique is less suitable for tumors with signicant pharyngeal involvement as there is less control over the pharyngeal margins. Patients who had previously undergone radiation have also been found to have higher rates of pharyn­gocutaneous stula with this technique [28, 29]. While this technique is less com­monly used following oncologic resections, the mechanical stapler is commonly used with pharyngoesophageal diverticula with good outcomes [30].
Pedicled Flap Reconstruction
Prior to MVFTT, closure of large pharyngeal deformities not amenable to pri­mary closure was most often achieved using locoregional pedicled flap recon­struction. A variety of different flaps have been reported, with the most
Соседние файлы в папке @xirurgi_2025