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L. Aljadeff and A. B. Morlandt
Oral Dysplasia: Risk ofMalignant Transformation
Although there is no way to denitively 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 signicant 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 etal., 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 etal. 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 modication, 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 etal. identied 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].

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Interestingly, articial 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 specically 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-specic 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 classication of potentially malignant disorders of the oral mucosa. J Oral Pathol Med. 2007;36:575–80.
3. Reibel J, Gale N, Hille J, etal. Oral potentially malignant disorders and oral epithelial dysplasia. In: El-Naggar AK, Chan JKC, Grandis JR, Takata T, Slootweg PPJ, editors. WHO classication 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 classication,
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 modications. 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, etal. 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, etal. 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 stratied 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. Denition 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: classications 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 classication
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, etal. 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, etal. 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, etal. 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, etal. 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, etal. 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, etal. 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. Articial 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, Walsh 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.
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Chapter 8
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Pharyngoesophageal Reconstruction
RayY.Wang, CaitlinM.Coviello, MohammadS.Jafferji, ShawnGroth,
andAndrewT.Huang
Introduction
Defects of the pharynx and cervical esophagus represent a signicant 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
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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
denitive 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 ofReconstruction
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.

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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
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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

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R. Y. Wang et al.
managed with primary closure in a single stage since the 1890s [12–14]. 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
1.5cm of residual mucosa has been described with functional swallow postoperatively [15]. Other authors have recommended primary closure when at least 3.5cm
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 signicant 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 [22–24]. 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 etal. 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%

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a
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b
Fig. 8.2 Various suture techniques in the primary repair of pharyngoesophageal deformities. (a)
Geometry. (b) Suture Techniques—Interrupted. (c) Suture Techniques—Continuous

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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 signicant 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
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