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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4434_Библиотеки_им_академика_М_И_Перельмана.pdf
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- •Foreword
- •Foreword
- •Foreword
- •Preface
- •Acknowledgment
- •Contents
- •About the Editors
- •1.1 Introduction
- •1.6 Dissection Procedure
- •1.6.2 Dissection Guide
- •1.9 Conclusion
- •References
- •2.1 Introduction
- •1.5.3 Sentinel Lymph Node Biopsy
- •2.3.1 Oral Cavity Surgery
- •2.3.2 Pharyngeal Surgery
- •2.3.3 Transoral Robotic Surgery (TORS)
- •2.4 Laryngeal Surgery
- •2.6 Salivary Gland Surgery
- •2.7 Thyroid Gland Surgery
- •2.8 Neck Dissection
- •2.9.1 Paediatric Surgery
- •2.10 Anatomical Versus Surgical Landmarks
- •2.13 Conclusion
- •References
- •3.1 Introduction
- •3.6.1 Pharynx
- •3.6.2 Nasopharyngeal Surgery
- •3.6.6 Temporal Bone Surgery
- •3.7 Conclusion
- •References
- •4.2.1 Perineural Tumour Spread
- •4.2.2 Carotid Artery Involvement
- •4.3.1 Oral Cavity
- •4.3.2 Nasopharynx
- •4.3.3 Oropharynx
- •4.3.4 Hypopharynx
- •4.3.5 Larynx
- •4.4.1 Oral Cavity Squamous Cell Carcinoma
- •4.4.2 Oropharyngeal Squamous Cell Carcinoma
- •4.4.3 Nasopharyngeal Squamous Cell Carcinoma
- •4.4.4 Non-HPV Oropharyngeal Squamous Cell Carcinoma
- •4.4.5 Unknown Primary Tumours
- •4.5 Lymph Nodes
- •4.5.1 Introduction
- •4.5.2.1 Clustering
- •4.5.2.2 Morphology
- •4.5.2.3 Inhomogeneity
- •4.5.2.4 Size
- •4.5.2.5 Lymphatic Drainage
- •4.6 Advanced Imaging
- •4.6.1 Elastography
- •4.6.2 DWI-MRI
- •4.7.1 Introduction
- •4.11 Cross-Sectional Imaging
- •References
- •5: Approach Towards Oral Cavity Cancers
- •5.1 Introduction
- •5.3 Diagnostic Evaluation
- •5.8.2.1 Access-Incision Planning
- •5.8.3 Surgical Techniques
- •5.8.3.1 Anaesthesia Considerations
- •5.8.4.1 Peroral Wide Local Excision
- •5.8.5.1 Access Osteotomy Through Mandibulotomy
- •5.8.5.2 Surgical Steps
- •5.8.5.3 Pull-Through Approach
- •5.8.5.4 Oral Component
- •5.8.5.5 Neck Component
- •5.8.6.1 Peroral Wide Local Excision
- •5.8.6.2.1 Surgical Steps
- •5.8.11 Hard Palate (T1–T2 Lesion)
- •5.8.11.1 Upper Alveolectomy
- •References
- •6.1 Benign Oropharyngeal Tumours
- •6.1.1 Lingual Thyroid
- •6.1.2 Epidemiology
- •6.1.3 Clinical Presentation
- •6.1.4 Histology
- •6.1.5 Imaging
- •6.1.6 Blood Investigation
- •6.1.7 Treatment
- •6.1.8 Surgical Treatment
- •6.1.9 Non-surgical Treatment
- •6.2 Pleomorphic Adenoma
- •6.2.1 Diagnosis
- •6.4.8 Early Stage
- •6.4.9 Advanced Stage
- •6.4.10 Non-surgical Treatment
- •6.4.11 Case Illustration 1
- •6.4.12 Case Illustration 2
- •6.5 Benign Hypopharyngeal Tumours
- •6.5.1 Fibrolipoma
- •6.2.3 Treatment
- •6.2.4 Case Illustration 1
- •6.3 Papilloma
- •6.3.1 Epidemiology
- •6.3.2 Clinical Presentation
- •6.3.3 Histology
- •6.3.4 Treatment
- •6.4.1 Risk Factors
- •6.4.2 Clinical Presentation
- •6.4.3 Diagnosis
- •6.4.4 Histology
- •6.4.5 Imaging
- •6.4.6 Staging
- •6.4.7 Treatment
- •6.6.1 Epidemiology
- •6.6.2 Risk Factor
- •6.6.3 Clinical Presentation
- •6.6.4 Diagnosis
- •6.6.5 Blood Investigations
- •6.6.6 Imaging
- •6.6.8 Histology
- •6.6.9 Staging
- •6.6.9.1 Primary Tumour (T)
- •6.6.9.2 Regional Lymph Node (N)
- •6.6.9.3 Distant Metastasis (M)
- •6.6.9.4 Stage Groups
- •6.6.10 Treatment
- •6.6.10.1 Surgical
- •References
- •7.1 Introduction
- •7.2 Salvage Neck Dissection
- •7.3.2.1 Procedure
- •7.3.2.2 Advantages
- •7.3.2.3 Disadvantages
- •7.3.3.1 Procedure
- •7.3.3.2 Advantages
- •7.3.3.3 Disadvantages
- •7.4.1 Procedure
- •7.4.2 Advantages
- •7.4.3 Disadvantages
- •7.5.1 Procedure
- •7.5.2 Advantages
- •7.5.3 Disadvantages
- •7.6 Subtemporal-Preauricular Infratemporal Fossa Approach
- •7.6.1 Procedure
- •7.6.2 Advantages
- •7.6.3 Disadvantages
- •7.7 Facial Translocation
- •7.7.1 Procedure
- •7.7.2 Advantages
- •7.7.3 Disadvantages
- •7.8 Endoscopic Endonasal Transpterygoid Nasopharyngectomy (EETN)
- •7.8.1 Patient Selection
- •7.8.2 Surgical Technique
- •7.8.2.1 Nasoseptal Flap
- •7.8.2.2 Sinonasal Corridor
- •7.8.2.3 Posterior Septectomy
- •7.8.2.4 Inferior Sphenoidectomy
- •7.8.2.5 Transpterygoid Dissection
- •7.8.2.6 Tumour Extirpation
- •7.10 Miscellaneous
- •7.11 Conclusion
- •References
- •8.1 Introduction
- •8.6 Parotid Gland Surgery
- •8.6.1 Benign Parotid Tumour Surgery
- •8.6.2 Malignant Parotid Tumour Surgery
- •8.7.1.2 Skin Incision
- •8.7.1.4 Greater Auricular Nerve Preservation
- •8.7.1.8 Facial Nerve Branch Preservation
- •8.7.1.10 Homeostasis Control
- •8.7.1.12 Post-operative Follow-Up
- •8.7.2.1 Case Illustration 1
- •8.8 Complications Post Parotidectomy
- •8.9.2 Post-operative Assessment
- •8.12 Conclusion
- •References
- •9.1 Introduction
- •9.2.1 Recurrent Laryngeal Nerve
- •9.2.3 Berry’s Ligament
- •9.2.4 Parathyroid Gland Anatomy
- •9.2.5 Inferior Thyroid Artery
- •9.2.6 Zuckerkandl Tubercle
- •9.5 Retrosternal Thyroid Tumour
- •9.7 Intraoperative Neural Monitoring
- •9.9 Thyroid Lobectomy
- •9.9.1 Case Illustration 1: Completion Hemithyroidectomy
- •9.10 Conclusion
- •References
- •10.1 Introduction
- •10.2 Surgical Anatomy
- •10.3 Indications
- •10.4.1 Patient Preparation
- •10.4.2 Informed Consent
- •10.4.3 Preoperative Planning/Evaluation
- •10.4.4.1 Antibiotic
- •10.4.4.2 Systemic Corticosteroid
- •10.4.4.3 Topical Decongestants
- •10.4.4.4 Adrenaline
- •10.4.5 Anaesthesia
- •10.4.7 Image-Guided System (IGS)
- •10.5 Operative Techniques
- •10.5.1 Endoscopic Sinus Surgery
- •10.5.1.1 Uncinectomy
- •10.5.1.2 Middle Meatal Antrostomy (MMA)
- •10.5.1.3 Ethmoidal Bullectomy
- •10.5.1.4 Posterior Ethmoidectomy
- •10.5.1.5 Sphenoidotomy
- •10.5.1.6 Frontal Sinusotomy
- •10.6 Intraoperative Complication
- •10.6.1 Intranasal Complications
- •10.6.1.2 Arterial Injury
- •10.6.1.2.1 Sphenopalatine Artery
- •10.6.1.2.2 Anterior Ethmoidal Artery (AEA)
- •10.6.1.2.3 Posterior Ethmoidal Artery (PEA)
- •10.6.1.2.4 Internal Carotid Artery (ICA)
- •Call for Help
- •Interventional Radiologist/Endovascular
- •10.6.2 Intraorbital Complications
- •10.6.2.2 Orbital Emphysema (Grade I)
- •10.6.2.3 Intraorbital Haematoma (Grade I)
- •10.6.2.5 Extraocular Muscle Injury (Grade III)
- •10.6.2.6 Optic Nerve Injury (Grade III)
- •10.6.3 Intracranial Complications
- •10.6.3.1 CSF Leak
- •10.6.4 Post-operative Complication
- •10.6.4.1 Epistaxis
- •10.6.4.2 Nasal Synechia
- •10.6.4.3 Other Complications
- •References
- •11.1 Introduction
- •11.2 Anatomical Landmarks
- •11.3 Background
- •11.4 Patient’s Preparation
- •11.5 Equipment
- •11.6 Positioning
- •11.7 Preoperative Evaluation
- •11.8 Infrastructure Maxillectomy
- •11.9 Subtotal Maxillectomy
- •11.10 Total Maxillectomy
- •11.12 Transoral-Transnasal Endoscopic Maxillectomy
- •11.13 Endoscopic-Assisted Transfacial Maxillectomy
- •11.14 Conclusion
- •References
- •12.1 Introduction
- •12.3 Laryngeal Diseases
- •12.4 Supraglottic Carcinoma
- •12.5 Glottic Carcinoma
- •12.6 Subglottic Carcinoma
- •12.8 Surgical Treatment
- •12.9.1 Skin Incision
- •12.9.5 Larynx Skeletonization
- •12.10 Open Partial Horizontal Laryngectomy (OPHL)
- •12.10.1.1 Surgical Technique
- •12.10.2.1 Surgical Technique
- •12.10.3.1 Surgical Technique
- •12.11 Total Laryngectomy
- •12.11.1 Surgical Technique
- •12.12 Future Challenges
- •12.13 Conclusion
- •References
- •13.1 Introduction
- •13.5 Central Compartment Neck Dissection
- •13.6 Selective Neck Dissection
- •13.7.1 Selective Neck Dissection
- •13.7.2 Case Illustration 1
- •13.7.3 Case Illustration 2
- •13.7.4 Case Illustration 3
- •13.9 Radical Neck Dissection
- •13.11 Prognosis
- •13.12 Conclusion
- •References
- •14.1 Introduction
- •14.3 Endoscopic Assisted Surgical Access
- •14.3.1 Endoscopic Thyroidectomy
- •14.7 Clavicle Osteotomy
- •14.7.1 Case Illustration
- •14.7.1.1 Case 1
- •14.8 Base-of-Neck Tumour
- •14.11 Conclusion
- •References
- •15.1 Introduction
- •15.2 Orbital Exenteration
- •15.2.1 Surgical Steps
- •15.2.1.1 Lid-Sparing Exenteration
- •15.2.1.2 Total Exenteration
- •15.2.2 Case Illustrations
- •15.2.3 Complications
- •15.4 Conclusion
- •References
- •16.1 Introduction
- •16.2.1 Benign Pathology
- •16.4 Vestibular Disorders
- •16.4.1 Ménière’s Disease
- •16.4.2 Superior Semicircular Canal Dehiscence
- •16.5.3 Temporal Bone Paraganglioma
- •16.6 Malignant Neoplasms
- •16.7.1 Diagnostic Audiology
- •16.7.2 Vestibular Tests
- •16.7.3 Imaging
- •16.8.2 Postauricular Incision
- •16.8.3 Transmeatal Incisions
- •16.8.4 Endaural Incisions
- •16.9 Anterior Atticotomy
- •16.10 Transmastoid Approaches
- •16.10.3 Posterior Tympanotomy
- •16.11 Endolymphatic Sac Decompression
- •16.12 Subtotal Petrosectomy
- •16.13 Translabyrinthine Approaches
- •16.14 Transcochlear Approach
- •16.16 Middle Cranial Fossa
- •16.19 Endoscopic Ear Surgery
- •16.19.1 Protympanum
- •16.19.2 Epitympanum
- •16.19.3 Retrotympanum
- •16.19.4 Hypotympanum
- •16.21 Conclusion
- •References
- •17.1 Introduction
- •17.2.1 Vascular Lesions
- •17.2.2 Infantile Haemangioma
- •17.2.2.1 Introduction
- •17.2.2.2 Epidemiology
- •17.2.2.3 Pathogenesis
- •17.2.2.4 Phases
- •17.2.2.4.1 Proliferative Phase
- •17.2.2.4.2 Involution Phase
- •17.2.2.5 Diagnosis
- •17.2.2.6 Treatment
- •17.2.2.7 Medical Therapy
- •17.2.2.8 Laser Therapy
- •17.2.2.9 Surgical Therapy
- •17.2.3 Dermoid Cyst
- •17.2.3.1 Introduction
- •17.2.3.3 Clinical Presentation
- •17.2.3.4 Imaging
- •17.2.3.5 Treatment
- •17.2.3.5.1 Surgery
- •17.3 Thyroglossal Duct Cyst
- •17.3.1 Introduction
- •17.3.2 Embryology
- •17.3.3 Clinical Presentation
- •17.3.4 Diagnosis
- •17.3.4.1 Blood Investigation
- •17.3.4.3 Histology
- •17.3.4.4 Imaging
- •17.3.5 Treatment
- •17.3.5.1 Surgery
- •17.3.5.2 Sclerotherapy
- •17.4 Rhabdomyosarcoma
- •17.4.1 Introduction
- •17.4.3 General Characteristics
- •17.4.4 Histology
- •17.4.5 Diagnosis
- •17.4.5.1 Biopsy
- •17.4.6 Staging
- •17.4.7 Treatment
- •17.4.7.1 Chemotherapy
- •17.4.7.2 Radiation Therapy
- •17.4.7.3 Surgical Therapy
- •17.4.8 Prognosis
- •17.4.9 Recurrence
- •17.5.1 Introduction
- •17.5.2 Epidemiology
- •17.5.3 Aetiology
- •17.5.4 Pathogenesis
- •17.5.5 Presentation
- •17.5.6 Diagnosis
- •17.5.7 Imaging
- •17.5.8 Histology
- •17.5.9 Staging
- •17.5.9.1 Fisch Staging
- •17.5.9.2 Radkowski Staging
- •17.5.10 Treatment
- •17.5.10.1 Surgery
- •17.5.10.2 Outcome
- •17.5.10.3 Complications
- •17.5.10.4 Radiotherapy
- •17.5.10.5 Chemotherapy
- •17.5.10.6 Hormonal Therapy
- •17.5.10.7 Spontaneous Regression
- •17.6 Lymphatic Malformation
- •17.6.1 Introduction
- •17.6.2 Genetics
- •17.6.3 Clinical Presentation
- •17.6.4 Diagnosis
- •17.6.5 Treatment
- •17.6.5.1 Observation
- •17.6.5.2 Sclerotherapy
- •17.6.5.3 Surgery
- •17.6.5.4 Other Modalities
- •17.6.5.4.1 Novel Agents
- •17.7 Cystic Hygroma
- •17.8 Lymphoma
- •17.8.1 Hodgkin’s Lymphoma
- •17.8.2 Non-Hodgkin’s Lymphoma
- •17.8.4 Diagnosis
- •17.8.4.1 Haematology
- •17.8.4.2 Imaging
- •17.8.4.3 Surgery
- •17.8.7.1 Radiation Therapy
- •17.9 Langerhans Cell Histiocytosis
- •17.9.1 Epidemiology
- •17.9.2 Pathogenesis
- •17.9.3 Clinical Feature
- •17.9.4 Investigations
- •17.9.5 Treatment
- •17.9.5.1 Solitary or Single-System Involvement
- •17.9.5.2 Multisystem Involvement
- •17.9.5.3 Induction Chemotherapy
- •17.9.5.4 Continuation Chemotherapy
- •17.9.5.5 Post-treatment Follow-Up
- •17.9.5.6 Relapsed or Refractory Disease
- •References
- •18.1.1 Case Illustration 1
- •18.1.2 Surgical Steps
- •18.2 Case Illustration 2
- •18.3 Stomatoplasty
- •18.5.1 Case Illustration
- •18.6.1 Case Illustration
- •18.7 Deep Lobe Parotidectomy
- •18.8 Conclusion
- •References
- •19.1 Introduction
- •19.2.1 Cross-Sectional Imaging
- •19.2.2 Emerging Applications
- •19.2.6 PET-MR
- •19.2.8 Others
- •19.2.8.1 SPECT
- •19.2.8.2 Elastography
- •19.2.8.3 Fluoroscopy
- •19.2.8.4 Narrowband Imaging
- •19.2.9 Biochemical Investigations
- •19.2.10 Imaging Biomarkers
- •19.3.1 Neck Dissection
- •19.5 Oral Cavity Cancer (OCSCC)
- •19.7 Hypopharyngeal Cancer
- •19.8 Nasopharynx Carcinoma (NPC)
- •19.10 Salivary Gland Malignancy
- •19.10.1 Parotid Tumors
- •19.11 Intraoperative Facial Nerve Monitoring
- •19.12.1 Treatment
- •19.13 Parapharyngeal Space Tumors (PPS)
- •19.14.2 Diagnostic Controversy
- •19.14.5 Optimal Resection Margins
- •19.15.1 Nonsurgical Treatment
- •19.16.2 Induction Chemotherapy
- •19.19.1 Targeted Therapy
- •19.19.2 Immunotherapy
- •19.19.3 Cancer Stem Cells (CSCs)
- •19.20 Conclusion
- •References

18 Miscellaneous Head andNeck Surgery andtheSurgical Steps
18.5 Platysma-Based
RotationalFlap
Flap reconstruction plays critical roles in selected
cases of head and neck malignancy. In the majority
of cases, reconstruction is necessary for restoration of function and improving aesthetic outcomes.
In advanced cases of head and neck carcinoma,
several rotational aps may be performed to palliate the symptoms such as facial disgurement and
smelling discharge and lessen the pain.
447
18.5.1 Case Illustration
This is the case of a 60-year-old male who presented with an extensive right buccal carcinoma
(Fig. 18.36). He has no medical comorbidities.
CT scan imaging showed a heterogenous mass at
right buccal region with ulcerative mass and skin
involvement. There was no distant metastasis.
Intraoperatively, the skin incision is marked
around the mass. The mass has been excised with
1.0cm margin (Fig.18.37). The mass is removed
in total. The medial part at the buccinator muscle
is inltrated by the tumour. The tissue is sent to
pathology for HPE conrmation. The platysmabased skin ap is harvested, to be rotated superiorly and cover the surgical defect.
Fig. 18.36 Right buccal cancerous growth with everted
edges and central necrosis
Fig. 18.37 The mass has been excised with 1.0cm margin and platysma-based skin ap is harvested
Fig. 18.38 The platysma skin ap is measured to cover
the defect sufciently. The external jugular vein and the
greater auricular nerve cross supercial to sternocleidomastoid muscle
The platysma skin ap is measured meticulously to cover the defect sufciently. The external jugular vein and the greater auricular nerve
were observed to cross the supercial to sternocleidomastoid muscle (Fig.18.38). Subsequently,
the platysma skin ap is rotated and superimposed on the surgical defect (Fig. 18.39). The
skin is sutured with surgical stapler.
The ap is secured with surgical stapler
(Fig. 18.40). The exposed neck donor requires
skin graft. The diameter of the neck donor-site
wound is measured (Fig. 18.41). The measurement is necessary for accurate harvest of split
skin graft. This avoids unnecessary excess skin
graft. Then, the skin graft is placed in situ in the

448
N. Mat Lazim
Fig. 18.39 The platysma skin ap is superimposed on
the buccal surgical defect. The skin is sutured with surgical stapler
Fig. 18.40 The ap is secured. The neck donor site
requires skin graft
Fig. 18.41 The diameter of the neck donor-site wound is
measured. The measurement is necessary for accurate
harvest of split skin graft
Fig. 18.42 The skin graft has been placed in situ and the
sponge gauze is placed on the graft to promote healing
Fig. 18.43 The antibiotic cream is applied at the wound
edge. The drainage tube is secured in situ to promote
drainage post-operatively. This avoids seroma formation
that will impair the ap
surgical bed and the sponge gauze is placed on
the donor graft to promote healing (Fig.18.42).
The antibiotic cream is applied at the wound
edge, and the drain is secured in situ (Fig.18.43),
to promote drainage post-operatively. This avoids
seroma formation that can compromise the ap
and post-operative wound healing.
Post-operatively, the patient recovered uneventfully. He was on double antibiotics and local dressing daily. His drainage tube was removed at day 5
post-operatively. He was discharged home on day
12. On follow-up at the outpatient clinic, the
patient had wound breakdown. He was admitted
and managed conservatively. The patient however
succumbed to disease on day 3 of readmission.

18 Miscellaneous Head andNeck Surgery andtheSurgical Steps
18.6 Excision ofVagal
Schwannoma
Paraganglioma is a rare head and neck tumour. It
commonly occurs in young and middle-aged
patients [5]. The majority of paragangliomas in
the head and neck region are vagal schwannomas
and carotid body tumour. The glomus jugulare
that affects the surrounding structures near the
jugular foramen is rare. Notably, about 5% of
head and neck paragangliomas originate from the
vagus nerve. The vagus nerve is the dominant
nerve of the parasympathetic division of the autonomic nervous system, and a vagal paraganglioma is a prime example of an endocrine tumour
associated with the vagus nerve [6].
Vagal paraganglioma is mostly present with a
neck mass. The mass can be at level II or III neck
region. It mostly rms in consistence, and occasionally the palpation on the mass causes patients
to cough, because of stimulation of vagal nerve
and recurrent laryngeal nerve. A small tumour
with no symptoms can be observed. However, a
large tumour with compressive symptoms needs
a surgical removal.
Fig. 18.44 The landmarks are drawn on the patient; the
outline of the mass is in dotted lines. The angle of mandible is superior, and the medial border of sternocleidomastoid muscle is abutting the posterior border of the
mass
449
18.6.1 Case Illustration
This is the case of a young lady presented with
right-neck swelling for 2-year duration. On clinical examination, the mass was rm and mobile
and measured 3.0cm × 4.0cm at level II and III
neck (Fig.18.44). The CT scan reported that the
mass is a heterogenous mass and displaced the
carotid artery and internal jugular vein posteriorly. FNAC of the mass revealed a suspicion of
schwannoma. Patient was counselled about the
treatment, and she agreed for surgical removal of
the mass.
Intraoperatively, patient lies supine with neck
hyperextended. The recurrent laryngeal nerve
monitoring is applied to patients. The neck region
is cleaned with the diluted povidone iodine and
the surgical landmarks, which include the inferior border of mandible and anterior border of
sternocleidomastoid muscle drawn on the patient
(Fig.18.44). The margin of the mass is in dotted
Fig. 18.45 The skin incision is marked at the middle of
the mass following the curvilinear skin crease of the neck
lines. The angle of mandible is superior, and the
medial border of sternocleidomastoid muscle is
abutting the posterior border of the mass.
The skin incision is marked at the middle of
the mass following the curvilinear skin crease of
the neck (Fig.18.45). The skin incision is always
placed well below the inferior border of mandible
at 2.0–3.0 cm below so as to avoid the risk of
injury to marginal mandibular nerve.
Subsequently, after the skin incision is performed, inferior and superior subplatysmal skin
ap is raised (Fig. 18.46). The superior ap is
raised till mandible, whereas the inferior ap is
raised till the level of cricoid cartilage, just

450
N. Mat Lazim
a
Fig. 18.46 The skin incision is performed (a), and inferior and superior skin ap is raised (b)
b
Fig. 18.47 The mass is exposed and dissected away from
the vagus nerve
1–2 cm below the inferior margin of the mass.
This is to facilitate better dissection around the
mass. The dissection continues, and the carotid
artery and IJV are identied. The vagus nerve is
located in between the carotid artery and IJV.The
mass is exposed and dissected away from the
vagus nerve (Fig.18.47). As the mass arises from
the periphery of vagus nerve, i.e. the perineurium, the mass is able to be resected without transection of the vagal nerve (Fig. 18.48). The
carotid artery is located medially, and the IJV is
visualized laterally deep to the anterior border of
SCM (Fig. 18.49), which is preserved together
with vagal nerve. The excised mass measured
8.0 cm × 4.0 cm and had intact capsule
(Fig.18.50).
Fig. 18.48 The mass has been excised from the vagus
nerve (yellow vessel loupe). The carotid artery is located
medially (red vessel loupe), and the IJV is visualized laterally deep to the anterior border of SCM
Patient is doing well post-operatively, and the
sterile strip has been applied to the wound. The
drainage tube is placed in situ to prevent seroma
formation that could compromise wound healing
during post-operative period (Fig.18.51).
Indication for surgery of vagal paraganglioma
includes enlarging mass, the mass that causes
discomfort or neck pain or other compressive
symptoms like dysphagia, or a long-standing
mass which carries a high risk of malignant transformation. Meticulous dissection is necessary
when dissecting the mass as the carotid artery
and internal jugular vein are intimately closed to
the mass. Vessel branches from these two vessels
may be accidentally cut and it causes active

18 Miscellaneous Head andNeck Surgery andtheSurgical Steps
bleeding in the surgical eld, which impairs
effective dissection.
The mass can be carefully dissected from the
nerve if there is plane between the capsule of the
mass and the nerve. The perineurium and epineurium of the nerve can still be preserved in this
case as the mass arises from the lateral part of the
nerve. In case the mass engulfs the whole nerve,
the proximal and distal parts of the nerve can be
transected. A cable nerve graft can be performed
using greater auricular nerve or hypoglossal
nerve.
451
Fig. 18.49 All three critical neurovascular structures are
preserved, the vagus nerve (yellow vessel loupe), the
carotid artery (red vessel loupe) and the IJV (blue vessel
loupe)
Fig. 18.50 The mass excised measuring 8.0cm × 4.0cm,
with intact capsule
Fig. 18.51 The neck wound post-operatively on day 1.
The sterile strip has been applied to the wound. The drainage tube is in situ to prevent seroma formation that could
compromise wound healing
18.7 Deep Lobe Parotidectomy
Deep lobe parotidectomy is indicated for benign
tumours limited to deep lobe, small recurrent
tumours conned to deep lobe or metastases to
deep lobe.
The approach can be either transoral or transcervical depending on the nature of the mass. In
extensive cases, mandibulotomy is necessary.
This includes the size, exact location and patient’s
anatomy. Some patients might have trismus, so
this precludes the transoral approach.
This is a case of a middle-aged female
patient who was diagnosed with deep lobe
parotid pleomorphic adenoma. She was planned
for a deep lobe parotidectomy. As the tumour is
not large, she was planned for transcervical
approach. Intraoperatively, the standard modied Blair incision is used. The facial nerve
monitor is secured, and after the landmark has
been identied, the subplatysmal skin ap is
elevated superiorly and inferiorly (Fig.18.52).
The anterior border of sternocleidomastoid is
skeletonized, and the lower branches of facial
nerve are preserved. The dissection continues
to expose the posterior belly of digastric. The
dissection continues deep to the muscle, and
this allows access to the parapharyngeal space
where the mass is located. The mass is identied, and the capsular dissection allows the
removal of the mass fairly easily, with intact
capsule (Figs.18.53 and 18.54).

452
Fig. 18.52 The transcervical approach for removing a deep
lobe of parotid mass. The skin ap is elevated superiorly and
inferiorly. The branches of facial nerve are preserved. The
tissue over the posterior belly of digastric is dissected, and
this allows access to the parapharyngeal space
N. Mat Lazim
Fig. 18.54 The medial surface of the mass appears irregular; however, the capsule is maintained intact. This is
important for avoiding breach into tissue that can cause
tumour cell seedling and recurrence
Fig. 18.53 The mass is excised with intact capsule. It
measures 6.0cm×3.0cm
18.8 Conclusion
Selected head and neck surgery should be meticulously performed even though it is a minor head
and neck case, as most of these neck masses are
located adjacent to major vasculature of carotid
artery and IJV.Additionally, some cases of recur-

18 Miscellaneous Head andNeck Surgery andtheSurgical Steps
453
rent tumour for example need a good treatment
plan in order to avoid unnecessary repeated surgery if the surgical margin is positive and the
patient had received maximal radiation dose.
During the dissection, all critical structures
whether muscles, vessels or nerves need to be
addressed properly. This ensures a safe surgery
without serious sequelae to the patients. Hence,
optimal treatment outcomes can be achieved.
References
1. Grønlund S, Mey K, Andersen E, Rasmussen ER.The
true malignancy rate in 135 patients with preoperative
diagnosis of a lateral neck cyst. Laryngoscope Investig
Otolaryngol. 2016;1(4):78–82. Published 2016 Jun
21. https://doi.org/10.1002/lio2.23.
2. Gaszyńska E, Gaszyński T, Arkuszewski P.Diagnosis
and treatment of cervical branchial cleft cysts based
on the material from the Department of CranioMaxillofacial Surgery, Medical University in Łódź and
literature review. Pol Przegl Chir. 2012;84(11):547–
50. https://doi.org/10.2478/v10035- 012- 0091- 3.
3. Kadhim AL, Sheahan P, Colreavy MP, Timon
CV.Pearls and pitfalls in the management of branchial
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doi.org/10.1258/0022215042790637.
4. Bradley PT, Bradley PJ. Branchial cleft cyst carcinoma: fact or ction? Curr Opin Otolaryngol
Head Neck Surg. 2013;21(2):118–23. https://doi.
org/10.1097/MOO.0b013e32835cebde.
5. Mat LN. Challenges in managing a vagal schwannoma: lesson learnt. Int J Surg Case Rep. 2018;53:5–
8. https://doi.org/10.1016/j.ijscr.2018.10.025.
6. Kotsis T, Christoforou P.Vagal paraganglioma: surgical removal with superior laryngeal nerve preservation. Vasc Specialist Int. 2019;35(2):105–10. https://
doi.org/10.5758/vsi.2019.35.2.105.

Updates andControversies
intheManagement ofHead
andNeck Malignancy
BelayatHossainSiddiquee
19
19.1 Introduction
Since the early part of the last century, enrichment of knowledge about the cancer etiology and
pathogenesis has led to rapid evolution in the
treatment of HNSCC.Advances in different therapeutic modalities have a commendable impact
on locoregional cure and suppression, overall and
disease-free survival, and issues concerning the
quality of life. Relatively better consequences
contribute to shifting the therapeutic aim from
drastic ablation to organ conservation and functional revival. HNSCCs include mucosal carcinomas of the nose and paranasal sinuses, oral cavity,
nasopharynx, oropharynx, hypopharynx, and larynx and also salivary gland cancers. These
together constitute one of the most common cancers worldwide. The oncosurgical management
of these diseases is evolving, which is attributable to the advancement in anesthetic support,
emergence of efcient antibiotics and transfusion
and infusion technology, as well as development
of newer concepts and skills for reconstruction.
Drastic excision has changed into preservation of
function without compromising the ultimate aim
of cure.
In the early decades of the twentieth century,
radiotherapy had just been started, and outcomes
B. H. Siddiquee (*)
Head & Neck Surgery Division, Department of
ORLHNS, Bangabandhu Sheikh Mujib Medical
University, Dhaka, Bangladesh
of surgery were frustrating. These reasons drive
the concerned clinician to use radiotherapy (RT)
as the rst choice. From the middle of the same
century, improvements of perioperative care, and
recognizing frustrating result and side effects of
radiotherapy, led them to build up a combined
approach consisting of surgery followed by adjuvant radiotherapy for the majority of HNSCC
patients. Later modernization of radiotherapy
came up with increased cure rates and decreased
toxicities. Nowadays, radiotherapy is established
as a vital solitary option in early lesions and also
plays an imperative role as adjuvant therapy.
During the later decades of the last century,
emphasis revolved around organ-specic functional status following treatment and role of
emerging chemotherapy, which inuence both
nonsurgical and surgical organ-conservation tactics. In the last few decades, for advanced cancers, management concentrated on combining
chemotherapy and radiotherapy for both primary
and adjuvant treatment. Recently, the targeted
molecular therapies upcoming as a novel option
for managing head and neck cancers (HNSCCs)
have been claiming improved survival rate and
better functional results.
Previously, the concepts regarding etiopatho-
genesis, local invasiveness, regional and distant
metastasis, and also clinical behavior of HNSCC
were not mature enough. In 1948, Morton Levin
recognized the impact of sex in cancer formation of the upper aerodigestive tract [1]. Despite
© The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2022
N. Mat Lazim et al. (eds.), Head and Neck Surgery : Surgical Landmark and Dissection Guide,
https://doi.org/10.1007/978-981-19-3854-2_19
455

456
B. H. Siddiquee
providing information about age, socioeconomic status, chemical carcinogens, and radiation, the crucial etiological role of tobacco in
cancer formation had not been realized for long.
Ernst Wynder demonstrated the carcinogenic
effect of tobacco in mice in the late 1950s and
1960s [2–5]. Moreover, Wynder and coworkers
reported the causal relation of tobacco and alcohol in oral, laryngeal, and esophageal cancers
[6–8]. Subsequently, Vogler and associates also
linked tobacco to oral, pharyngeal, and laryngeal cancers [9]. Now, all forms of tobacco are
universally established as contributing elements
for HNSCC.Alcohol also raises the probability
of HNSCC, and it has been demonstrated that
the risk of consuming tobacco and alcohol
together has synergistic effect rather than simple additive effect [10, 11]. But the fact is that
all tobacco and alcohol consumers do not suffer
from HNSCC, signifying that individual disparity in genetic susceptibility is crucial [12].
Slaughter and associates in 1953 launched the
idea of “eld cancerization” in oral cavity squamous cell carcinoma (OCSCC) [13]. That thinking offered a validation for the synchronous or
metachronous second primary cancers in HNSCC
patients. Over 500,000 new cases of HNSCC
occur yearly in the world [14]. The US National
Cancer Institute’s report shows increased detection of oropharyngeal cancers (OPSCC) since
1973, although there has been a signicant
decrease in tobacco consumption [15]. Recent
trend is same in the majority of countries around
the globe.
Human papillomavirus (HPV) is stated as a
key risk factor for many HNSCCs. Reports recognizing the molecular link of HPV with HNSCC
have also been published [16]. Around 20% of
HNSCC samples have HPV genomic DNA,
mostly HPV type 16 and occasionally type 18
[17]. E6 and E7 viral oncoprotein expression
deactivates the tumor-suppressor proteins p53 and
Rb, respectively [18]. Oropharynx, especially the
tonsils, is the commonest site for HPV- related
tumors [19, 20]. Peculiar sexual performances
have been identied related to HPV transmission
in oral and oropharyngeal regions [21, 22].
Causative relation of HPV with OPSCC has posi-
tive effects on preventive and therapeutic management, and favorable prognosis. HPV association
is considered as a positive prognostic component
for OPSCC, particularly in patients who are nonconsumers of tobacco and/or alcohol and may be
related to increased radiosensitivity too [23–34].
HPV infections biologically relevant in laryngeal
carcinogenesis are also reported, but its clinical
impact on prevention and treatment is unclear
[25]. Oncogenic strains of Epstein-Barr virus
(EBV) are related to the development of nasopharyngeal carcinoma. Excitingly, some viruses own
the cancer- abolishing character and reovirus
(RV); a RNA virus is a noticeable one having
research interest [26].
The biological relationship of chronic inammation with cancers has been pronounced comprehensively as both inammation and cancer
are multifaceted processes under the inuence of
various stirring factors [27–29]. Bacteria, their
endotoxins, enzymes, and some other metabolic
by-products may bring genetic and epigenetic
alterations directly in adjacent epithelial cells
[30, 31]. They also raise the production of acetaldehyde and nitrosamine, which are carcinogenic [32, 33]. By all this relentless research
about etiology, pathogenesis, invention of newer
investigative tools especially radiological and
biological scans, and different biochemical tests
including tumor markers, clinicians and scientists are updating the treatment modules for
different HNSCCs by modication and improvisation. Despite this fact, overall disease-free
survival for HNSCCs is yet to be satisfactory.
Controversies are existing at intra- and interdisciplinary levels. Hopefully, this dynamicity will
get a new dimension in the twenty-rst century
to achieve the goal.
19.2 Investigations ofHead
andNeck Malignancy
19.2.1 Cross-Sectional Imaging
One major sector in the update management of
HNSCC is tremendous development and modernization of investigations in the later part of the

19 Updates andControversies intheManagement ofHead andNeck Malignancy
457
a
Fig. 19.1 (a–c) Cervical lymph node metastasis in different patients: (a) CT scan, (b) MRIT2W1, and (c) PET/CT
Table 19.1 Role of PET scan in the assessment of head and neck malignancy
1. Differentiate malignancy
from normal tissue and
benign lesions
2. Staging of HNSCC By determining the precise location of a tumor, its extension and whether the
3. Diagnosis and assessment
of residual or recurrent tumor
4. Assessment of therapeutic
response
5. Prognostic evidence Undetectable lesions on FDG- PET/CT 6months after nishing radiotherapy are
6. Tumor volume assessment
for radiotherapy scheduling
It shows a hypermetabolic state of tissue, which is a characteristic of malignant
tissue.
cancer has spread in regional or distal sites of the body.
FDG-PET/CT is a perfect noninvasive imaging, which can differentiate post-
therapeutic changes in cancer from residual or recurrent lesions [34].
FDG-PET/CT is competent to evaluate therapeutic response in HNSCC following
chemoradiation. FDG-PET should be advised 12weeks after the treatment is over
to minimize the false positivity created by radiation-induced inammation [35].
found to have higher control over locoregional and distant recurrence, longer
disease-free survival, and overall survival, when compared to the counterpart [36].
FDG-PET/CT is suitable for tumor volume contouring as the metabolic activity of
the lesion delineates the border between tumor and surrounding normal tissue [37].
FDG-PET also decreases inter-observer variations in tumor volume calculation,
ascertains lymph node involvement not detected by CT/MRI, and differentiates
tumor areas potentially requiring additional radiation dose [38].
cb
twentieth and early decades of the twenty-rst
century. Computerized tomography (CT) and
magnetic resonance imaging (MRI) have revolutionized the role of imaging in the diagnosis and
assessment of HNSCC.CT and MRI (with and
without contrast) have denite strengths and limitations. Thus, these are complementary to each
other in the assessment and treatment scheduling
(Fig.19.1).
The application of (18F-FDG) positronemission tomography (PET) in the later part of
1990s, use of a metabolic factor for imaging, and
fusion of functional (PET) and structural (CT)
imaging further facilitated disease management.
PET/CT fusion scan has the ability to provide an
inclusive evaluation of the patient with
HNSCC.The following role of PET/CT has been
explored and established (Table19.1).
19.2.2 Emerging Applications
Some applications make the biologic imaging
unique and an integral part of standard care for
HNSCC. Tumor hypoxia is a factor which can
inuence therapeutic response.
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