Rhinology Review [1 ed.] 3031087933, 9783031087936, 9783031087943

Table of contents :
Preface
Contents
About the Authors
1: Development of the Nose, Paranasal Sinuses
1.1 The Nasal Cavity
1.2 The Paranasal Sinuses
1.3 The Ethmoid Sinuses
1.4 The Maxillary Sinuses
1.5 Sphenoid Sinuses
1.6 Frontal Sinus
2: Anatomy of Nose and Sinuses
2.1 The External Nose
2.1.1 Surface Landmarks
2.1.2 Structural Anatomy
2.1.3 Blood Supply of the External Nose
2.1.3.1 Arterial Supply
2.1.3.2 Venous Drainage
2.1.3.3 Lymphatic Drainage
2.1.4 Nerve Supply
2.2 The Nasal Cavity
2.2.1 The Nasal Septum
2.2.2 Lateral Basal Wall
2.2.2.1 The Inferior Turbinate
2.2.2.2 The Middle Turbinate
2.2.2.3 The Superior Turbinate
2.2.2.4 The Uncinate Process
2.2.2.5 The Ostiomeatal Complex
2.2.2.6 Bony Lamellae Encountered during Endoscopic Sinus Surgery
2.2.3 Blood Supply of the Nasal Cavity
2.2.4 Nerve Supply of the Nasal Cavity
2.3 The Sinuses
2.3.1 The Ethmoid Sinuses
2.3.2 The Maxillary Sinus
2.3.3 The Frontal Sinus
2.3.4 The Sphenoid Sinus
2.4 Histology of the Nasal Mucosa
3: Nasal Physiology and Functions
3.1 Important Nasal Functions
3.2 Olfaction
3.3 Nasal Airflow and Conditioning
3.4 Defense Functions of the Nose
3.4.1 Mechanical Mechanisms
3.4.2 Humoral Mechanisms
3.4.3 Cellular Mechanisms
3.4.4 Reflex Mechanisms
3.5 Speech
4: Imaging of the Nose and Sinuses
4.1 Computed Tomography (CT)
4.2 Cone Beam CT
4.3 Magnetic Resonance Imaging
4.4 General Radiologic Findings of Inflammatory Lesions
4.5 General Radiologic Findings of Neoplastic Lesions
5: Investigative Rhinology
5.1 Allergy Tests
5.1.1 Skin Prick Tests
5.1.2 Tests for IgE
5.1.3 Nasal Smears
5.1.4 Blood Eosinophils
5.1.5 Nasal Provocation Test
5.2 Airway Tests
5.2.1 Rhinomanometry
5.2.2 Acoustic Rhinometry
5.2.3 Nasal Inspiratory Peak Flow
5.3 Olfactory Tests
5.3.1 Subjective Methods
5.3.2 Objective Methods
5.4 Tests of Mucociliary Transport
5.5 Other Objective Tests
5.5.1 Nitric Oxide Measurement
5.5.2 Nasal Lavage
5.6 Subjective Tests
5.6.1 SNOT 22
5.6.2 NOSE Scale
5.6.3 Visual Analog Scale (VAS)
5.6.4 Quality of Life (QOL) Questionnaires
6: Symptoms of Sinonasal Diseases
6.1 Epistaxis
6.1.1 Vascular Anatomy
6.1.2 The Sphenopalatine Artery (SPA)
6.1.3 The Anterior and Posterior Ethmoid Arteries
6.1.4 Definition and Classification
6.1.5 Primary (Idiopathic) Epistaxis
6.1.6 Secondary Epistaxis
6.1.6.1 Local Causes
6.1.6.2 General Causes
6.1.7 Management of Epistaxis
6.1.8 First-Aid Measures
6.1.9 General Measures
6.1.10 Control of Bleeding
6.1.10.1 Nasal Cautery
6.1.10.2 Nasal Packs
6.1.10.3 Nasal Balloons
6.1.10.4 Hot Water Irrigations
6.1.10.5 Tranexamic Acid
6.1.10.6 Arterial Control
6.1.11 Treatment of the Cause
6.1.12 Hereditary Hemorrhagic Telangiectasia (Osler–Weber–Rendu Disease)
6.1.12.1 Treatment
6.2 Nasal Obstruction
6.2.1 Classifications of Nasal Obstruction
6.2.2 Etiology of Nasal Obstruction
6.2.3 Causes of Nasal Obstruction in Children
6.2.4 Assessment of Nasal Obstruction
6.3 Olfactory Disorders
6.3.1 Classification of Olfactory Disorders
6.3.1.1 According to Etiology
6.3.1.2 According to Type
Quantitative Olfactory Disorders
Qualitative Olfactory Disorders
6.3.2 Causes of Olfactory Dysfunction
6.3.2.1 Conductive Olfactory Dysfunction
6.3.2.2 Sensory Olfactory Dysfunction
6.3.2.3 Neural Olfactory Dysfunction
6.3.2.4 Psychogenic (e.g., schizophrenia)
6.3.3 Assessment of Olfactory Function
6.3.3.1 Subjective Methods
6.3.3.2 Objective Methods
6.3.4 Treatment
6.4 Headache
6.4.1 Tension Headache
6.4.2 Migraine Headaches
6.4.3 Cluster Headaches
6.4.4 Neuralgias
7: Choanal Atresia and Congenital Nasal Masses
7.1 Choanal Atresia
7.1.1 Clinical Picture
7.1.1.1 Bilateral Choanal Atresia
7.1.1.2 Unilateral Choanal Atresia (Fig. 7.1)
7.1.2 Investigations
7.1.3 Differential Diagnosis
7.1.4 Management
7.2 Pyriform Aperture Stenosis
7.3 Congenital Nasal Masses
7.4 Meningoceles and Encephaloceles
7.5 Gliomas
7.6 Nasal Dermoids
8: Nasal Trauma
8.1 Foreign Bodies in the Nose
8.1.1 Clinical Picture
8.1.2 Investigations
8.1.3 Treatment
8.2 Fractures of the Nasal Bones
8.2.1 Types of Fracture of the Nasal Bones
8.2.2 Clinical Features
8.2.3 Investigations
8.2.4 Management
8.3 Septal Hematoma
8.4 Fractures of the Midface (Le Fort Fractures)
8.5 Frontal Sinus Fractures
9: Nasal Septum, Nasal Valves, and Turbinates
9.1 Septal Deviation
9.2 Septal Perforations
9.3 Nasal Valves
9.4 The Turbinates
9.4.1 Inferior Turbinates
9.4.2 Middle Turbinate
10: Rhinitis and Nasal Allergy
10.1 Classification of Rhinitis
10.2 Allergic Rhinitis
10.2.1 Classifications of Allergic Rhinitis
10.2.2 ARIA Classification
10.2.3 Pathophysiology
10.2.4 Comorbidities of Allergic Rhinitis
10.2.5 Clinical Picture
10.2.6 Investigations
10.2.7 Management
10.2.8 Aspirin-Exacerbated Respiratory Disease (AERD - Samter’s Triad)
10.2.8.1 Clinical Features
10.2.8.2 Investigations
10.2.8.3 Treatment
10.2.9 Rhinitis and Asthma
10.3 Non-Allergic Rhinitis
10.3.1 Etiology
10.3.2 Vasomotor Rhinitis (VMR)
10.3.3 Treatment
10.3.4 Non-Allergic Rhinitis with Eosinophilia Syndrome (NARES)
10.3.5 Non-Allergic Inhalant/Occupational Induced Rhinitis
10.3.6 Hormonal Rhinitis
10.3.7 Food-Induced Rhinitis
10.4 Infectious Rhinitis
10.4.1 Acute Viral Rhinitis (Coryza - Common Cold)
10.4.1.1 Clinical Picture
10.4.1.2 Treatment
10.4.2 Scleroma
10.4.2.1 Incidence
10.4.2.2 Pathology
10.4.2.3 Clinical Picture
10.4.2.4 Involvement of Other Regions
10.4.2.5 Investigations
10.4.2.6 Differential Diagnosis
10.4.2.7 Treatment
10.4.3 Rhinosporidiosis
10.5 Special Types of Rhinitis
10.5.1 Drug-Induced Rhinitis (Rhinitis Medicamentosa)
10.5.2 Atrophic Rhinitis
10.5.3 Primary Atrophic Rhinitis (Ozena)
10.5.3.1 Clinical Picture
10.5.3.2 Anterior Rhinoscopy Shows
10.5.3.3 Treatment
10.5.4 Secondary Atrophic Rhinitis
10.5.5 Rhinitis Sicca Anterior
11: Rhinosinusitis
11.1 Acute Rhinosinusitis
11.1.1 Etiology
11.1.2 Microbiology
11.1.3 Symptoms
11.1.4 Signs
11.1.5 Imaging
11.1.6 Treatment
11.2 Complications of Rhinosinusitis
11.2.1 Classification
11.2.2 Osteomyelitis of the Frontal Bone
11.2.3 Orbital Complications
11.2.3.1 Chandler Classification of Orbital Complications
11.2.3.2 Pre-Septal (Periorbital) Cellulitis
11.2.3.3 Orbital Cellulitis (Post-Septal Cellulitis)
11.2.3.4 Subperiosteal Abscess
11.2.3.5 Orbital Abscess
11.2.3.6 Treatment of Orbital Infections
11.2.4 Intracranial Complications
11.2.4.1 Meningitis
11.2.4.2 Epidural (Extradural) Abscess
11.2.4.3 Subdural Abscess
11.2.4.4 Frontal Lobe Abscess
11.2.4.5 Cavernous Sinus Thrombosis
11.2.4.6 Treatment of Intracranial Infections
11.2.4.7 Alarm Symptoms and Signs of Sinusitis
11.3 Chronic Rhinosinusitis
11.3.1 Diagnosis of CRS
11.3.2 Classification
11.3.3 CRS with Nasal Polyps (CRSwNP)
11.3.4 CRS without Nasal Polyps (CRSsNP)
11.3.5 Symptoms of CRS
11.3.6 Signs
11.3.7 Investigations
11.3.8 Treatment
11.3.9 Chronic Rhinosinusitis in Children
11.4 Sinonasal Polyposis
11.4.1 The Meltzer Clinical Scoring System
11.4.2 Medical Treatment of Sinonasal Polyposis
11.4.3 Surgical Treatment of Sinonasal Polyposis
11.4.4 Antrochoanal Polyp
11.5 Recalcitrant Sinusitis
11.5.1 Cystic Fibrosis (CF)
11.5.2 Primary Ciliary Dyskinesia or Kartagener Syndrome
11.5.3 Odontogenic Sinusitis
11.5.4 Aspirin-Exacerbated Respiratory Disease (AERD)
11.5.5 Wegener’s Granulomatosis (GPA—Granulomatosis with Polyangiitis)
11.5.6 Eosinophilic Granulomatous Polyangiitis (EGPA—Churg-Strauss Syndrome)
11.5.7 Sarcoidosis
11.5.8 Immunodeficiency
11.5.9 Laryngopharyngeal Reflux (LPR)
11.6 Fungal Sinusitis
11.6.1 Classification of Fungal Rhinosinusitis
11.6.2 Fungal Colonization
11.6.3 Fungal Ball (Mycelia Mass)
11.6.4 Allergic Fungal Rhinosinusitis (AFRS)
11.6.5 Eosinophilic Fungal Rhinosinusitis (EFRS)
11.6.6 Acute Invasive Fungal Sinusitis
11.6.7 Granulomatous Invasive Fungal Rhinosinusitis
11.6.8 Chronic Invasive Fungal Rhinosinusitis
11.7 Mucoceles
11.7.1 Clinical Picture
11.7.2 Radiologic Diagnosis
11.7.3 Treatment
12: Sinonasal Neoplasms
12.1 Fibro-Osseous Lesions
12.1.1 Osteomas
12.1.2 Ossifying Fibroma
12.1.3 Fibrous Dysplasia
12.2 Hemangioma
12.3 Inverted Papilloma
12.4 Juvenile Angiofibroma (JNA)
12.4.1 Clinical Picture
12.4.2 Extensions of the Tumor
12.4.3 Radiologic Evaluation
12.4.4 Radkowski Staging System
12.4.5 Treatment
12.5 Esthesioneuroblastoma
12.6 Nasopharyngeal Carcinoma
12.6.1 Clinical Picture
12.6.2 Investigations
12.6.3 Differential Diagnosis
12.6.4 Prognosis
12.6.5 Treatment
12.7 Sinonasal Carcinoma
12.7.1 Clinical Picture
12.7.2 Investigations
12.7.3 Treatment
12.8 Adenocarcinoma
12.9 Malignant Melanoma
12.10 Hemangiopericytoma
12.11 Lymphoma
13: Basic Endoscopic Sinus Surgery
13.1 Introduction to Basic Endoscopic Sinus Surgery
13.1.1 Concepts of Endoscopic Sinus Surgery (ESS)
13.1.2 Indications
13.1.3 Preoperative Preparation
13.1.4 Steps of Basic Stepwise ESS for Chronic Sinusitis (Figs. 13.1 and 13.2)
13.1.5 Postoperative Care
13.2 Endoscopic Frontal Sinus Approaches
13.2.1 General Principles
13.2.2 Draf Procedures (Figs. 13.3 and 13.4)
13.2.3 Wormald’s Classification of Frontal Sinus Procedures
13.2.4 The Axillary Flap Procedure
13.3 Endoscopic Maxillary Sinus Approaches
13.3.1 Indications of Endoscopic Surgery of the Maxillary Sinus
13.3.2 Canine Fossa Trephine
13.3.3 Middle Meatal Antrostomy
13.3.4 Endoscopic Inferior Meatal Antrostomy
13.3.5 Endoscopic Medial Maxillectomy
13.3.6 Prelacrimal Approach
13.4 Endoscopic Sphenoid Sinus Surgery
13.4.1 Endoscopic Approaches to the Sphenoid Artery
13.4.1.1 Steps of Sphenoidotomy
13.5 Complications of Endoscopic Sinus Surgery
13.5.1 Complications of Endoscopic Sinus Surgery (ESS)
13.5.2 Risk Factors for Complications
13.5.3 Cerebrospinal Fluid Leak
13.5.4 Orbital Complications
13.5.4.1 Orbital Fat Herniation
13.5.5 Extraocular Muscle Injury
13.5.6 Intraorbital Hematoma
13.5.7 Optic Nerve Injury
13.5.8 Damage to the Nasolacrimal Duct
13.5.9 Damage to the Internal Carotid Artery
13.5.10 Bleeding from the Posterior Nasal (Septal) Artery
13.5.11 Craniofacial Growth after ESS
13.5.12 Avoidance of ESS Complications
13.6 Revision ESS
13.6.1 Factors Indicative of Poor Outcome
13.6.2 Causes of Failure of Endoscopic Sinus Surgery
13.6.3 Important Landmarks in Revision Sinus Surgery
14: Advanced Endoscopic Sinus Surgery
14.1 Cerebrospinal (CSF) Rhinorrhea
14.1.1 Causes
14.1.2 Traumatic CSF Leaks
14.1.3 Spontaneous CSF Leaks
14.1.4 Clinical Presentation of CSF Leaks
14.1.5 Investigations
14.1.6 Treatment
14.2 Endoscopic Dacryocystorhinostomy (DCR)
14.2.1 Anatomy
14.2.2 Lacrimal tract obstruction may be:
14.2.3 Symptoms of Lacrimal Blockage
14.2.4 Diagnosis
14.2.5 Radiologic Evaluation
14.2.6 Endoscopic DCR
14.3 Endoscopic Anterior Skull Base Surgery
14.3.1 Sagittal Plane Approaches
14.3.1.1 Transcribriform Approach
14.3.1.2 Transplanum/Transtuberculum Approach
14.3.1.3 Trans-Sellar Approach
14.3.1.4 Transclival Approaches
14.3.1.5 Transodontoid Approach
14.3.2 Middle Coronal Plane Approaches
14.3.2.1 Transpterygoid Approach
14.3.2.2 Infratemporal Approach
14.3.2.3 Petrous Apex Approach
14.3.3 Flaps for Anterior Skull Base Reconstructions
14.4 Optic Nerve Decompression
14.5 Orbital Decompression
14.5.1 Indications of Orbital Decompression
14.5.2 Graves’ Ophthalmopathy
14.6 Approaches to the Sphenopalatine and Maxillary Arteries
14.6.1 Indications
14.6.2 Sphenopalatine Artery (SPA)
14.6.2.1 Surgical Approach
14.6.3 The Maxillary Artery (MA)
14.6.4 Transantral Approach to the Maxillary Artery
15: Rhinoplasty
15.1 Basic Facial Aesthetics
15.1.1 The Tripod Concept
15.1.2 Tip Support Mechanisms
15.1.3 Photography
15.2 Rhinoplasty Approaches
15.2.1 Closed Rhinoplasty
15.2.1.1 Advantages
15.2.1.2 Disadvantage
15.2.1.3 Basic Steps
15.2.2 Open Rhinoplasty
15.2.2.1 Advantages
15.2.2.2 Disadvantages
15.2.2.3 Indications
15.2.2.4 Basic Steps
15.2.3 Common Grafts in Rhinoplasty
15.2.3.1 Sources of Grafts
15.2.3.2 Commonly Used Grafts
16: External Sinonasal Approaches
16.1 Caldwell–Luc Operation (Sublabial Antrostomy)
16.2 External Ethmoidectomy
16.3 Frontal Sinus Trephination
16.4 Howard’s Eyebrow Approach
16.5 Frontal Osteoplastic Flap
16.5.1 Steps
16.5.2 Complications
16.6 Other External Approaches (Fig. 16.2)

Citation preview

Rhinology Review Samy Elwany Mohamed Askar

123

Rhinology Review

Samy Elwany • Mohamed Askar

Rhinology Review

Samy Elwany Department of Otolaryngology Alexandria University Alexandria, Egypt

Mohamed Askar Department of Otolaryngology Tanta Faculty of Medicine Tanta, Egypt

ISBN 978-3-031-08793-6    ISBN 978-3-031-08794-3 (eBook) https://doi.org/10.1007/978-3-031-08794-3 © The Editor(s) (if applicable) and The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 This work is subject to copyright. All rights are solely and exclusively licensed by the Publisher, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed. The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. The publisher, the authors, and the editors are safe to assume that the advice and information in this book are believed to be true and accurate at the date of publication. Neither the publisher nor the authors or the editors give a warranty, expressed or implied, with respect to the material contained herein or for any errors or omissions that may have been made. The publisher remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. This Springer imprint is published by the registered company Springer Nature Switzerland AG The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland

I dedicate this book to my small, lovely family: my wife, Maggie, my son Dino, and my daughter Nelly. I cannot express my love and gratitude to all of them for giving my life wonderful value and meaning. They are really the love of my life. I would also like to dedicate the book to all my students throughout my long career. Samy Elwany Special thanks to my backbone in my entire career of nasal surgery my wife Eman, my son Abdelrahman my daughters Bothyna and Alaa, my grandchildren Youssef, Mohamed, Ali, Layla, and Nelly. Special appreciation and respect to all my patients whom I believed I have helped to make them happier. Finally, I would like to thank my students and wish them a promising future. Mohamed Askar

Preface

The art and science of rhinology has greatly expanded during the last few decades. Several valuable well-written large textbooks are now available. While these textbooks provide plethora of useful information, they may not be the ideal tool for those preparing for exams or needing quick to-the-point information. This illustrated book was written to serve as a concise and to-the-point resource and trainee companion for postgraduates setting for their fellowship, diploma, board, and similar exams, and also as a quick compact reference and refresher for otolaryngologists in their everyday practice especially as the e-book will be available on smart phones and tablets. The book covers the full range of topics in the modern rhinology syllabus, as well as related important areas that may be encountered in today’s exams and practice. The topics of the book include basic sciences of rhinology, investigative rhinology, rhinologic symptoms and diseases, as well as office procedures and operations. The book also includes concise chapters on the basics of rhinoplasty and anterior skull surgery. All topics will be addressed in a comprehensive and comprehensible way to keep the book as a compact reference and revision aid. The book will distill key facts into bullet points for rapid access to essential information and will help otolaryngologists to better understand basic and clinical rhinology. Pictures, illustrations and videos were extensively used to complement the text. Each topic will be followed by MCQs with their answers for fast revisions. We hope the book will serve its purposes as a concise, time-saving resource detailing the essentials of rhinology and related topics for postgraduates and practicing otolaryngologists. Alexandria, Egypt Tanta, Egypt 

Samy Elwany Mohamed Askar

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Contents

1

 Development of the Nose, Paranasal Sinuses������������������������������������������   1 1.1 The Nasal Cavity��������������������������������������������������������������������������������   1 1.2 The Paranasal Sinuses������������������������������������������������������������������������   3 1.3 The Ethmoid Sinuses��������������������������������������������������������������������������   3 1.4 The Maxillary Sinuses������������������������������������������������������������������������   3 1.5 Sphenoid Sinuses��������������������������������������������������������������������������������   3 1.6 Frontal Sinus ��������������������������������������������������������������������������������������   4

2

 Anatomy of Nose and Sinuses ������������������������������������������������������������������   7 2.1 The External Nose������������������������������������������������������������������������������   7 2.1.1 Surface Landmarks ����������������������������������������������������������������   8 2.1.2 Structural Anatomy ����������������������������������������������������������������   9 2.1.3 Blood Supply of the External Nose����������������������������������������  11 2.1.4 Nerve Supply��������������������������������������������������������������������������  12 2.2 The Nasal Cavity��������������������������������������������������������������������������������  12 2.2.1 The Nasal Septum ������������������������������������������������������������������  12 2.2.2 Lateral Basal Wall ������������������������������������������������������������������  14 2.2.3 Blood Supply of the Nasal Cavity������������������������������������������  17 2.2.4 Nerve Supply of the Nasal Cavity������������������������������������������  17 2.3 The Sinuses ����������������������������������������������������������������������������������������  18 2.3.1 The Ethmoid Sinuses��������������������������������������������������������������  19 2.3.2 The Maxillary Sinus����������������������������������������������������������������  20 2.3.3 The Frontal Sinus��������������������������������������������������������������������  20 2.3.4 The Sphenoid Sinus����������������������������������������������������������������  24 2.4 Histology of the Nasal Mucosa����������������������������������������������������������  26

3

 Nasal Physiology and Functions ��������������������������������������������������������������  31 3.1 Important Nasal Functions������������������������������������������������������������������  31 3.2 Olfaction ��������������������������������������������������������������������������������������������  31 3.3 Nasal Airflow and Conditioning ��������������������������������������������������������  32 3.4 Defense Functions of the Nose ����������������������������������������������������������  33 3.4.1 Mechanical Mechanisms��������������������������������������������������������  33 3.4.2 Humoral Mechanisms ������������������������������������������������������������  34 3.4.3 Cellular Mechanisms��������������������������������������������������������������  34

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3.4.4 Reflex Mechanisms����������������������������������������������������������������  34 3.5 Speech ������������������������������������������������������������������������������������������������  34 4

 Imaging of the Nose and Sinuses��������������������������������������������������������������  37 4.1 Computed Tomography (CT)��������������������������������������������������������������  37 4.2 Cone Beam CT������������������������������������������������������������������������������������  39 4.3 Magnetic Resonance Imaging������������������������������������������������������������  40 4.4 General Radiologic Findings of Inflammatory Lesions����������������������  41 4.5 General Radiologic Findings of Neoplastic Lesions��������������������������  41

5

Investigative Rhinology ����������������������������������������������������������������������������  45 5.1 Allergy Tests ��������������������������������������������������������������������������������������  45 5.1.1 Skin Prick Tests����������������������������������������������������������������������  45 5.1.2 Tests for IgE����������������������������������������������������������������������������  46 5.1.3 Nasal Smears��������������������������������������������������������������������������  46 5.1.4 Blood Eosinophils������������������������������������������������������������������  46 5.1.5 Nasal Provocation Test������������������������������������������������������������  46 5.2 Airway Tests ��������������������������������������������������������������������������������������  46 5.2.1 Rhinomanometry��������������������������������������������������������������������  46 5.2.2 Acoustic Rhinometry��������������������������������������������������������������  47 5.2.3 Nasal Inspiratory Peak Flow ��������������������������������������������������  47 5.3 Olfactory Tests������������������������������������������������������������������������������������  47 5.3.1 Subjective Methods����������������������������������������������������������������  47 5.3.2 Objective Methods������������������������������������������������������������������  48 5.4 Tests of Mucociliary Transport ����������������������������������������������������������  48 5.5 Other Objective Tests��������������������������������������������������������������������������  48 5.5.1 Nitric Oxide Measurement������������������������������������������������������  48 5.5.2 Nasal Lavage��������������������������������������������������������������������������  48 5.6 Subjective Tests����������������������������������������������������������������������������������  48 5.6.1 SNOT 22 ��������������������������������������������������������������������������������   48 5.6.2 NOSE Scale����������������������������������������������������������������������������  49 5.6.3 Visual Analog Scale (VAS) ����������������������������������������������������  49 5.6.4 Quality of Life (QOL) Questionnaires������������������������������������  49

6

 Symptoms of Sinonasal Diseases��������������������������������������������������������������  51 6.1 Epistaxis����������������������������������������������������������������������������������������������  51 6.1.1 Vascular Anatomy ������������������������������������������������������������������  51 6.1.2 The Sphenopalatine Artery (SPA)������������������������������������������  52 6.1.3 The Anterior and Posterior Ethmoid Arteries ������������������������  53 6.1.4 Definition and Classification��������������������������������������������������  53 6.1.5 Primary (Idiopathic) Epistaxis������������������������������������������������  54 6.1.6 Secondary Epistaxis����������������������������������������������������������������  54 6.1.7 Management of Epistaxis��������������������������������������������������������  54 6.1.8 First-Aid Measures�����������������������������������������������������������������  55 6.1.9 General Measures�������������������������������������������������������������������  55 6.1.10 Control of Bleeding����������������������������������������������������������������  55

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6.1.11 Treatment of the Cause ����������������������������������������������������������  57 6.1.12 Hereditary Hemorrhagic Telangiectasia (Osler–Weber–Rendu Disease) ����������������������������������������������  57 6.2 Nasal Obstruction��������������������������������������������������������������������������������  58 6.2.1 Classifications of Nasal Obstruction��������������������������������������  58 6.2.2 Etiology of Nasal Obstruction������������������������������������������������  58 6.2.3 Causes of Nasal Obstruction in Children��������������������������������  59 6.2.4 Assessment of Nasal Obstruction ������������������������������������������  59 6.3 Olfactory Disorders����������������������������������������������������������������������������  59 6.3.1 Classification of Olfactory Disorders��������������������������������������  60 6.3.2 Causes of Olfactory Dysfunction��������������������������������������������  60 6.3.3 Assessment of Olfactory Function������������������������������������������  61 6.3.4 Treatment��������������������������������������������������������������������������������  62 6.4 Headache��������������������������������������������������������������������������������������������  62 6.4.1 Tension Headache ������������������������������������������������������������������  63 6.4.2 Migraine Headaches���������������������������������������������������������������  63 6.4.3 Cluster Headaches������������������������������������������������������������������  63 6.4.4 Neuralgias ������������������������������������������������������������������������������  63 7

 Choanal Atresia and Congenital Nasal Masses ��������������������������������������  67 7.1 Choanal Atresia����������������������������������������������������������������������������������  67 7.1.1 Clinical Picture�����������������������������������������������������������������������  67 7.1.2 Investigations��������������������������������������������������������������������������  68 7.1.3 Differential Diagnosis ������������������������������������������������������������  68 7.1.4 Management����������������������������������������������������������������������������  69 7.2 Pyriform Aperture Stenosis����������������������������������������������������������������  70 7.3 Congenital Nasal Masses��������������������������������������������������������������������  70 7.4 Meningoceles and Encephaloceles ����������������������������������������������������  70 7.5 Gliomas ����������������������������������������������������������������������������������������������  72 7.6 Nasal Dermoids����������������������������������������������������������������������������������  72

8

Nasal Trauma ��������������������������������������������������������������������������������������������  75 8.1 Foreign Bodies in the Nose����������������������������������������������������������������  75 8.1.1 Clinical Picture�����������������������������������������������������������������������  75 8.1.2 Investigations��������������������������������������������������������������������������  75 8.1.3 Treatment��������������������������������������������������������������������������������  77 8.2 Fractures of the Nasal Bones��������������������������������������������������������������  77 8.2.1 Types of Fracture of the Nasal Bones ������������������������������������  77 8.2.2 Clinical Features ��������������������������������������������������������������������  78 8.2.3 Investigations��������������������������������������������������������������������������  78 8.2.4 Management����������������������������������������������������������������������������  78 8.3 Septal Hematoma��������������������������������������������������������������������������������  79 8.4 Fractures of the Midface (Le Fort Fractures)��������������������������������������  79 8.5 Frontal Sinus Fractures ����������������������������������������������������������������������  79

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 Nasal Septum, Nasal Valves, and Turbinates������������������������������������������  83 9.1 Septal Deviation����������������������������������������������������������������������������������  83 9.2 Septal Perforations������������������������������������������������������������������������������  87 9.3 Nasal Valves����������������������������������������������������������������������������������������  88 9.4 The Turbinates������������������������������������������������������������������������������������  91 9.4.1 Inferior Turbinates������������������������������������������������������������������  91 9.4.2 Middle Turbinate��������������������������������������������������������������������  93

10 Rhinitis and Nasal Allergy������������������������������������������������������������������������  97 10.1 Classification of Rhinitis������������������������������������������������������������������  98 10.2 Allergic Rhinitis��������������������������������������������������������������������������������  98 10.2.1 Classifications of Allergic Rhinitis��������������������������������������  99 10.2.2 ARIA Classification������������������������������������������������������������  99 10.2.3 Pathophysiology������������������������������������������������������������������  99 10.2.4 Comorbidities of Allergic Rhinitis��������������������������������������  99 10.2.5 Clinical Picture�������������������������������������������������������������������� 100 10.2.6 Investigations���������������������������������������������������������������������� 100 10.2.7 Management������������������������������������������������������������������������ 101 10.2.8 Aspirin-Exacerbated Respiratory Disease (AERD - Samter’s Triad)���������������������������������������������������� 102 10.2.9 Rhinitis and Asthma������������������������������������������������������������ 102 10.3 Non-Allergic Rhinitis������������������������������������������������������������������������ 102 10.3.1 Etiology ������������������������������������������������������������������������������ 103 10.3.2 Vasomotor Rhinitis (VMR) ������������������������������������������������ 103 10.3.3 Treatment���������������������������������������������������������������������������� 103 10.3.4 Non-Allergic Rhinitis with Eosinophilia Syndrome (NARES)����������������������������������������������������������������������������� 104 10.3.5 Non-Allergic Inhalant/Occupational Induced Rhinitis�������� 104 10.3.6 Hormonal Rhinitis �������������������������������������������������������������� 104 10.3.7 Food-Induced Rhinitis �������������������������������������������������������� 105 10.4 Infectious Rhinitis���������������������������������������������������������������������������� 105 10.4.1 Acute Viral Rhinitis (Coryza - Common Cold)������������������ 105 10.4.2 Scleroma������������������������������������������������������������������������������ 106 10.4.3 Rhinosporidiosis������������������������������������������������������������������ 109 10.5 Special Types of Rhinitis������������������������������������������������������������������ 109 10.5.1 Drug-Induced Rhinitis (Rhinitis Medicamentosa)�������������� 109 10.5.2 Atrophic Rhinitis ���������������������������������������������������������������� 109 10.5.3 Primary Atrophic Rhinitis (Ozena)�������������������������������������� 109 10.5.4 Secondary Atrophic Rhinitis������������������������������������������������ 110 10.5.5 Rhinitis Sicca Anterior�������������������������������������������������������� 111 11 Rhinosinusitis �������������������������������������������������������������������������������������������� 115 11.1 Acute Rhinosinusitis ������������������������������������������������������������������������ 115 11.1.1 Etiology ������������������������������������������������������������������������������ 115 11.1.2 Microbiology ���������������������������������������������������������������������� 116 11.1.3 Symptoms���������������������������������������������������������������������������� 116

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11.1.4 Signs������������������������������������������������������������������������������������ 116 11.1.5 Imaging�������������������������������������������������������������������������������� 117 11.1.6 Treatment���������������������������������������������������������������������������� 117 11.2 Complications of Rhinosinusitis ������������������������������������������������������ 117 11.2.1 Classification ���������������������������������������������������������������������� 118 11.2.2 Osteomyelitis of the Frontal Bone�������������������������������������� 118 11.2.3 Orbital Complications �������������������������������������������������������� 118 11.2.4 Intracranial Complications�������������������������������������������������� 122 11.3 Chronic Rhinosinusitis���������������������������������������������������������������������� 124 11.3.1 Diagnosis of CRS���������������������������������������������������������������� 124 11.3.2 Classification ���������������������������������������������������������������������� 124 11.3.3 CRS with Nasal Polyps (CRSwNP)������������������������������������ 126 11.3.4 CRS without Nasal Polyps (CRSsNP)�������������������������������� 126 11.3.5 Symptoms of CRS �������������������������������������������������������������� 126 11.3.6 Signs������������������������������������������������������������������������������������ 126 11.3.7 Investigations���������������������������������������������������������������������� 127 11.3.8 Treatment���������������������������������������������������������������������������� 127 11.3.9 Chronic Rhinosinusitis in Children ������������������������������������ 127 11.4 Sinonasal Polyposis�������������������������������������������������������������������������� 128 11.4.1 The Meltzer Clinical Scoring System���������������������������������� 129 11.4.2 Medical Treatment of Sinonasal Polyposis ������������������������ 129 11.4.3 Surgical Treatment of Sinonasal Polyposis ������������������������ 130 11.4.4 Antrochoanal Polyp ������������������������������������������������������������ 131 11.5 Recalcitrant Sinusitis������������������������������������������������������������������������ 132 11.5.1 Cystic Fibrosis (CF)������������������������������������������������������������ 133 11.5.2 Primary Ciliary Dyskinesia or Kartagener Syndrome�������� 133 11.5.3 Odontogenic Sinusitis���������������������������������������������������������� 133 11.5.4 Aspirin-Exacerbated Respiratory Disease (AERD)������������ 135 11.5.5 Wegener’s Granulomatosis (GPA—Granulomatosis with Polyangiitis)������������������������������������������������������������������������ 136 11.5.6 Eosinophilic Granulomatous Polyangiitis (EGPA—ChurgStrauss Syndrome)�������������������������������������������������������������� 136 11.5.7 Sarcoidosis�������������������������������������������������������������������������� 137 11.5.8 Immunodeficiency �������������������������������������������������������������� 138 11.5.9 Laryngopharyngeal Reflux (LPR) �������������������������������������� 138 11.6 Fungal Sinusitis�������������������������������������������������������������������������������� 138 11.6.1 Classification of Fungal Rhinosinusitis ������������������������������ 139 11.6.2 Fungal Colonization������������������������������������������������������������ 139 11.6.3 Fungal Ball (Mycelia Mass)������������������������������������������������ 139 11.6.4 Allergic Fungal Rhinosinusitis (AFRS)������������������������������ 140 11.6.5 Eosinophilic Fungal Rhinosinusitis (EFRS)������������������������ 141 11.6.6 Acute Invasive Fungal Sinusitis������������������������������������������ 141 11.6.7 Granulomatous Invasive Fungal Rhinosinusitis������������������ 143 11.6.8 Chronic Invasive Fungal Rhinosinusitis������������������������������ 143

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11.7 Mucoceles ���������������������������������������������������������������������������������������� 143 11.7.1 Clinical Picture�������������������������������������������������������������������� 144 11.7.2 Radiologic Diagnosis���������������������������������������������������������� 145 11.7.3 Treatment���������������������������������������������������������������������������� 146 12 Sinonasal Neoplasms���������������������������������������������������������������������������������� 151 12.1 Fibro-Osseous Lesions���������������������������������������������������������������������� 151 12.1.1 Osteomas ���������������������������������������������������������������������������� 151 12.1.2 Ossifying Fibroma �������������������������������������������������������������� 152 12.1.3 Fibrous Dysplasia���������������������������������������������������������������� 153 12.2 Hemangioma ������������������������������������������������������������������������������������ 154 12.3 Inverted Papilloma���������������������������������������������������������������������������� 154 12.4 Juvenile Angiofibroma (JNA) ���������������������������������������������������������� 158 12.4.1 Clinical Picture�������������������������������������������������������������������� 158 12.4.2 Extensions of the Tumor������������������������������������������������������ 159 12.4.3 Radiologic Evaluation �������������������������������������������������������� 159 12.4.4 Radkowski Staging System ������������������������������������������������ 160 12.4.5 Treatment���������������������������������������������������������������������������� 161 12.5 Esthesioneuroblastoma �������������������������������������������������������������������� 163 12.6 Nasopharyngeal Carcinoma�������������������������������������������������������������� 165 12.6.1 Clinical Picture�������������������������������������������������������������������� 165 12.6.2 Investigations���������������������������������������������������������������������� 165 12.6.3 Differential Diagnosis���������������������������������������������������������� 166 12.6.4 Prognosis ���������������������������������������������������������������������������� 166 12.6.5 Treatment���������������������������������������������������������������������������� 166 12.7 Sinonasal Carcinoma������������������������������������������������������������������������ 167 12.7.1 Clinical Picture�������������������������������������������������������������������� 168 12.7.2 Investigations���������������������������������������������������������������������� 168 12.7.3 Treatment���������������������������������������������������������������������������� 168 12.8 Adenocarcinoma ������������������������������������������������������������������������������ 169 12.9 Malignant Melanoma������������������������������������������������������������������������ 169 12.10 Hemangiopericytoma������������������������������������������������������������������������ 169 12.11 Lymphoma���������������������������������������������������������������������������������������� 170 13 Basic  Endoscopic Sinus Surgery�������������������������������������������������������������� 173 13.1 Introduction to Basic Endoscopic Sinus Surgery������������������������������ 173 13.1.1 Concepts of Endoscopic Sinus Surgery (ESS)�������������������� 173 13.1.2 Indications �������������������������������������������������������������������������� 173 13.1.3 Preoperative Preparation������������������������������������������������������ 174 13.1.4 Steps of Basic Stepwise ESS for Chronic Sinusitis (Figs. 13.1 and 13.2)������������������������������������������������������������ 174 13.1.5 Postoperative Care �������������������������������������������������������������� 177 13.2 Endoscopic Frontal Sinus Approaches���������������������������������������������� 178 13.2.1 General Principles �������������������������������������������������������������� 178 13.2.2 Draf Procedures (Figs. 13.3 and 13.4)�������������������������������� 178 13.2.3 Wormald’s Classification of Frontal Sinus Procedures ������ 180 13.2.4 The Axillary Flap Procedure ���������������������������������������������� 180

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13.3 Endoscopic Maxillary Sinus Approaches ���������������������������������������� 181 13.3.1 Indications of Endoscopic Surgery of the Maxillary Sinus������������������������������������������������������������������������������������ 181 13.3.2 Canine Fossa Trephine�������������������������������������������������������� 181 13.3.3 Middle Meatal Antrostomy�������������������������������������������������� 182 13.3.4 Endoscopic Inferior Meatal Antrostomy ���������������������������� 182 13.3.5 Endoscopic Medial Maxillectomy�������������������������������������� 182 13.3.6 Prelacrimal Approach���������������������������������������������������������� 183 13.4 Endoscopic Sphenoid Sinus Surgery������������������������������������������������ 184 13.4.1 Endoscopic Approaches to the Sphenoid Artery ���������������� 185 13.5 Complications of Endoscopic Sinus Surgery������������������������������������ 187 13.5.1 Complications of Endoscopic Sinus Surgery (ESS)������������ 187 13.5.2 Risk Factors for Complications ������������������������������������������ 187 13.5.3 Cerebrospinal Fluid Leak���������������������������������������������������� 187 13.5.4 Orbital Complications �������������������������������������������������������� 190 13.5.5 Extraocular Muscle Injury�������������������������������������������������� 190 13.5.6 Intraorbital Hematoma�������������������������������������������������������� 191 13.5.7 Optic Nerve Injury�������������������������������������������������������������� 191 13.5.8 Damage to the Nasolacrimal Duct�������������������������������������� 192 13.5.9 Damage to the Internal Carotid Artery�������������������������������� 192 13.5.10 Bleeding from the Posterior Nasal (Septal) Artery�������������� 193 13.5.11 Craniofacial Growth after ESS�������������������������������������������� 193 13.5.12 Avoidance of ESS Complications���������������������������������������� 193 13.6 Revision ESS������������������������������������������������������������������������������������ 193 13.6.1 Factors Indicative of Poor Outcome������������������������������������ 194 13.6.2 Causes of Failure of Endoscopic Sinus Surgery������������������ 194 13.6.3 Important Landmarks in Revision Sinus Surgery���������������� 194 14 Advanced  Endoscopic Sinus Surgery������������������������������������������������������ 197 14.1 Cerebrospinal (CSF) Rhinorrhea������������������������������������������������������ 197 14.1.1 Causes���������������������������������������������������������������������������������� 197 14.1.2 Traumatic CSF Leaks���������������������������������������������������������� 198 14.1.3 Spontaneous CSF Leaks������������������������������������������������������ 199 14.1.4 Clinical Presentation of CSF Leaks������������������������������������ 201 14.1.5 Investigations���������������������������������������������������������������������� 201 14.1.6 Treatment���������������������������������������������������������������������������� 202 14.2 Endoscopic Dacryocystorhinostomy (DCR)������������������������������������ 206 14.2.1 Anatomy������������������������������������������������������������������������������ 206 14.2.2 Lacrimal tract obstruction may be:�������������������������������������� 206 14.2.3 Symptoms of Lacrimal Blockage���������������������������������������� 207 14.2.4 Diagnosis ���������������������������������������������������������������������������� 207 14.2.5 Radiologic Evaluation �������������������������������������������������������� 208 14.2.6 Endoscopic DCR ���������������������������������������������������������������� 208 14.3 Endoscopic Anterior Skull Base Surgery������������������������������������������ 210 14.3.1 Sagittal Plane Approaches �������������������������������������������������� 210 14.3.2 Middle Coronal Plane Approaches�������������������������������������� 212 14.3.3 Flaps for Anterior Skull Base Reconstructions ������������������ 214

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14.4 Optic Nerve Decompression ������������������������������������������������������������ 214 14.5 Orbital Decompression �������������������������������������������������������������������� 215 14.5.1 Indications of Orbital Decompression�������������������������������� 215 14.5.2 Graves’ Ophthalmopathy���������������������������������������������������� 215 14.6 Approaches to the Sphenopalatine and Maxillary Arteries�������������� 217 14.6.1 Indications �������������������������������������������������������������������������� 217 14.6.2 Sphenopalatine Artery (SPA)���������������������������������������������� 217 14.6.3 The Maxillary Artery (MA)������������������������������������������������ 218 14.6.4 Transantral Approach to the Maxillary Artery�������������������� 218 15 Rhinoplasty������������������������������������������������������������������������������������������������ 221 15.1 Basic Facial Aesthetics �������������������������������������������������������������������� 221 15.1.1 The Tripod Concept������������������������������������������������������������ 222 15.1.2 Tip Support Mechanisms���������������������������������������������������� 222 15.1.3 Photography������������������������������������������������������������������������ 223 15.2 Rhinoplasty Approaches ������������������������������������������������������������������ 223 15.2.1 Closed Rhinoplasty�������������������������������������������������������������� 223 15.2.2 Open Rhinoplasty���������������������������������������������������������������� 225 15.2.3 Common Grafts in Rhinoplasty������������������������������������������ 227 16 External Sinonasal Approaches���������������������������������������������������������������� 233 16.1 Caldwell–Luc Operation (Sublabial Antrostomy)���������������������������� 233 16.2 External Ethmoidectomy������������������������������������������������������������������ 234 16.3 Frontal Sinus Trephination���������������������������������������������������������������� 235 16.4 Howard’s Eyebrow Approach ���������������������������������������������������������� 236 16.5 Frontal Osteoplastic Flap������������������������������������������������������������������ 237 16.5.1 Steps������������������������������������������������������������������������������������ 237 16.5.2 Complications���������������������������������������������������������������������� 238 16.6 Other External Approaches (Fig. 16.2) �������������������������������������������� 238

About the Authors

Samy  Elwany  is a Professor of Otolaryngology at the Department of Otolaryngology, Alexandria University, Alexandria, Egypt. He is also the President of the Egyptian Society of Otolaryngology and the President of the Alexandria Society of Rhinology (Rhinoalex). He was the Chairman of the Department of Otolaryngology, Alexandria University from 2007 to 2010 and the head of the committee for promotion of Egyptian universities otolaryngology staff memebers from 2013–2016. He is a member of the CORLAS (Collegium Oto-Rhino-Laryngologicum Amicitiae Sacrum) and of the American Academy of Otolaryngology. He has published several papers in international journals and authored three books. He was the recipient of the Alexandria University and Egypt State awards. He serves on the editorial board of the Springer journal European Archives of Oto-Rhino-Laryngology and Head and Neck. Mohamed  Askar  is currently a Professor of Otolaryngology Head and Neck Surgery, Tanta Faculty of Medicine, Egypt. He received his medical degree from the Tanta Faculty of Medicine, Egypt, and a master’s degree in Otorhinolaryngology. He completed his training in Endoscopic Sinus Surgery in Glan Clwyd Hospital, Rhyl, UK, and obtained a PhD in Endoscopic Sinus Surgery. He was Secretary of both Egyptian and Pan Arab Rhinology Societies from 1998 to 2017. He serves as a board member of the Egyptian Society of Otorhinolaryngology Head and Neck Surgery.

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Development of the Nose, Paranasal Sinuses

1.1 The Nasal Cavity • The face develops from five processes: The unpaired frontonasal process, or frontonasal prominence and the paired maxillary prominences and mandibular prominences (Fig. 1.1). • During the fifth week of embryonic development, an area of thickened ectoderm (nasal placodes or olfactory placodes) develops on each side of the frontonasal process immediately under the forebrain. Fig. 1.1  Development of the nose and sinuses. FN frontonasal process, LN lateral nasal process, MN medial nasal process, NP nasal pit, MAX maxillary process, MAN mandibular process

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 S. Elwany, M. Askar, Rhinology Review, https://doi.org/10.1007/978-3-031-08794-3_1

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1  Development of the Nose, Paranasal Sinuses

• The nasal placodes later evaginate to form the nasal pits which indent the frontonasal prominence and divide it into medial and lateral nasal processes. • The nose is formed by the fusion of five prominences: the frontal process (bridge of the nose), the two medial nasal processes (tip and central portion of the lip), and the lateral nasal processes (the sides). • The ectodermal layer over the roof of the developing nasal fossa forms the olfactory epithelium. The axons of the olfactory cells form the olfactory nerves which continue into the olfactory bulb. • The nasolacrimal groove and duct are formed in the seventh week. • The ethmoturbinals appear as ridges along the lateral nasal wall at 8 weeks of gestation: • The ethmoturbinals give rise to several structures: –– First ethmoturbinal: ascending portion forms the agger nasi, and descending portion forms the uncinate process. –– Second ethmoturbinal: forms ethmoid bulla. –– Third ethmoturbinal: forms basal lamella of middle turbinate. –– Fourth ethmoturbinal: forms attachment of the superior turbinate to the lateral nasal wall. –– Fifth and sixth ethmoturbinals: usually degenerate but can form a supreme turbinate. • An additional ridge, the maxilloturbinal, arises inferior to the ethmoturbinals and ultimately forms the inferior turbinate. • The primitive nasal cavity is divided from the primitive pharynx by the oronasal membrane. • At 8 weeks gestation, the nasal septum arises as a midline growth of the frontonasal process. The descending septum merges with the fused palatine processes to create two distinct nasal cavities. • At 8 weeks gestation, a hypercellular mesenchymal capsule forms around the developing nasal structures and olfactory epithelium. • At 15–16  weeks gestation, the inferior, middle, and superior turbinates are formed. • At almost the same time, three furrows form between the ethmoturbinals: –– The first furrow forms between the first and second ethmoturbinals and forms the ethmoidal infundibulum, hiatus semilunaris, middle meatus, and part of the frontal recess. –– The second furrow forms between the second and third ethmoturbinals developing into the superior meatus. –– The third furrow forms between the third and fourth ethmoturbinals developing into the supreme meatus. • The growth of the lateral wall of the nose is nearly finished by the 24 week.

1.5  Sphenoid Sinuses

3

1.2 The Paranasal Sinuses • Development of the paranasal sinuses results from invagination and evagination from the furrows between between the developing turbinates. • The ethmoid sinuses are the first to fully develop, followed in order by maxillary, sphenoid, and frontal sinuses.

1.3 The Ethmoid Sinuses • The ethmoid sinuses are the most developed paranasal sinuses at birth having a complete number of cells in varying stages for development. • The ethmoid sinuses start development during the 11–12 weeks of gestation, and they reach their adult size by about 12 years of age. • Ossification of the ethmoid labyrinth occurs by 20–24 weeks gestation. • The ethmoid cells may extend into the frontal recess (frontal recess cells), sphenoid bone (sphenoethmoid or Onodi cell), and maxillary bone (infraorbital ethmoid or Haller cell).

1.4 The Maxillary Sinuses • The maxillary sinus first appears by 17–18 weeks gestation as an outgrowth in the lateral wall of the infundibulum of ethmoid. • Growth of the maxillary sinuses begins by approximately 3 years of age. • The sinus expands inferiorly at the time of eruption of the permanent dentition. • The floor of the maxillary sinus reaches the the inferior meatus at 8 years of age and reaches the level of the floor of the nose by 12 years of age. • Adult size is reached by mid-adolescence. • Ossification of the maxilla starts at 11–12 weeks gestation.

1.5 Sphenoid Sinuses • The sphenoid sinuses start development during the third to fourth months of gestation but does not begin clinically significant pneumatization until 4–6 years of age. • Sphenoid sinus pneumatization is typically completed by 12 years of age. • The sphenoid bone has two ossification centers separated by the canalis pharyngeus. • The Bertini bone is an ossified part of the anterior part of the cartilaginous capsule surrounding the sphenoid sinuses and becomes attached to the body of the sphenoid bone by 2–3 years of age.

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1  Development of the Nose, Paranasal Sinuses

1.6 Frontal Sinus • The frontal sinuses are usually not present at birth. • They are the last sinuses to start and complete development. • The sinus originates as an outgrowth of the middle meatus between the first and second ethmoturbinals in the frontal recess region. • Actual growth of the frontal sinuses begins during the fourth year of age and continues into early adulthood. • The frontal sinuses can usually be recognized on X-ray at about 7 years of age. MCQs 1. The ethmoturbinals give rise to all of the following structures except: (a) Uncinate process (b) Attachment of the superior turbinate (c) Crista ethmoidalis (d) Ethmoid bulla 2. The floor of the maxillary sinus reaches the level of the floor of the nose by: (a) 3 years of age (b) 12 years of age (c) 5 years of age (d) 18 years of age 3. The second furrow between the ethmoturbinals develop into: (a) Spheno-ethmoidal recess (b) Nasolacrimal duct (c) Superior meatus (d) Hiatus semilunaris 4. The first sinuses to fully develop are: (a) Frontal sinuses (b) Ethmoid sinuses (c) Maxillary sinuses (d) Sphenoid sinuses 5. The frontal sinuses can usually be recognized on X-ray: (a) At birth (b) At 2 years of age (c) At about 7 years of age (d) At puberty 6. The Bertini bone is a part of the cartilaginous capsule surrounding the: (a) Maxillary sinuses (b) Ethmoid sinuses (c) Sphenoid sinuses (d) Frontal sinuses 7. The number of ethmoid cells is complete: (a) At puberty (b) At 7 years of age (c) At 12 years of age (d) At birth

1.6  Frontal Sinus

8. The bridge of the nose is formed from: (a) Olfactory placodes (b) Medial nasal processes (c) Frontonasal process (d) Lateral nasal processes 9. The third ethmoturbinal forms: (a) Agger nasi cell (b) Uncinate process (c) Bulla ethmoidalis (d) Basal lamella 10. The number of furrows between the ethmoturbinals is: (a) Five (b) Two (c) Three (d) Six Answers 1. (c) 2. (b) 3. (c) 4. (b) 5. (c) 6. (c) 7. (d) 8. (c) 9. (d) 10. (c)

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Anatomy of Nose and Sinuses

2.1 The External Nose • The nose includes two functionally related parts: external nose and the nasal cavity. Each part includes different structural and histologic components. • The external nose has functional and aesthetic roles. The functional role is to control the passage of air into the nasal cavity. The aesthetic role is its prominent contribution to the shape of the face. • The facial skin over the external nose is continuous with the skin lining of the vestibule of the nasal cavity where it carries stiff hairs called vibrissae. • Beneath the skin and is an adherent fibrofatty layer which is thin over the dorsum of the nose and thick over the nasal tip. • Beneath the fibrofatty layer is the subcutaneous muscular aponeurotic system (SMAS) which is continuous with the SMAS of the entire face and includes the facial muscles. • The muscles of the external nose are divided into four groups and include: (a) The elevators: Procures and and levator labii superioris alaeque nasi. The action of these muscles is to shorten the nose and dilate the nostrils. (b) The depressors: Depressor septi and depressor alae. The actions of these muscles are to lengthen the nose. (c) The dilators: Alar portion of the nasalis and the dilator naris anterior. The action of these muscles is to dilate the nostrils. (d) The compressors: Transverse portion of the nasalis and the compressor narium minor is inconstant muscle. The action of these muscles is to narrow the nostrils.

Supplementary Information The online version contains supplementary material available at https://doi.org/10.1007/978-­3-­031-­08794-­3_2. © The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 S. Elwany, M. Askar, Rhinology Review, https://doi.org/10.1007/978-3-031-08794-3_2

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2  Anatomy of Nose and Sinuses

2.1.1 Surface Landmarks • For anatomical orientation, the terms ventral, dorsal, cephalic, and caudal are used instead of the terms anterior, posterior, superior, and inferior, respectively. • The radix is the uppermost limit of the nose. The nasion is the most posterior bony point at the top of the nose. The rhinion is the junction between the bony and cartilaginous dorsum (Fig. 2.1). • The glabella is the smooth prominence of the frontal bone above the nasion. • The external nose is divided into three thirds: (a) The upper third extends from the radix to the rhinion. (b) The middle third extends from the rhinion to the weak triangle which corresponds to the supratip depression. (c) The lower third includes everything below the supratip depression. • The upper two-thirds of the external nose form the nasal dorsum. The caudal third is made up of the lobule, columella, ala, and vestibule and is often referred to as the base of the nose. The nasal bridge is the bony part of the nose overlying the nasal bones. • The lobule is the area just caudal to the weak triangle. • The tip-defining point is formed by the domes of the lower lateral cartilages. • The tip of the nose is the midpoint of a line that connects the two tip-­ defining points. Fig. 2.1 Surface landmarks of external nose

Glabella Nasion Rhinion

Supratip Break

Subnasale

Nasolabial angle

2.1 The External Nose

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• The soft triangle corresponds to the angle between the medial and lateral crura. This area is characterized by absence of subcutaneous tissue between the skin of the outer and inner surfaces of the nostril rim. Trauma to the soft triangle can lead to difficult-to-correct scarring. • The supratip area extends from the supratip depression (weak triangle) to the tip-defining point. • The infratip area extends from the tip-defining point to the columella breakpoint. • The ala forms the soft convex portion on either side of the lobule and the lateral wall of the vestibule of the nose. • The junction of the lobule and ala forms the alar-lobular crease. The junction of the ala and the skin of the face forms the alar-facial crease. • The columella extends from the lobule to the upper lip, The subnasale is the junction between the columella and upper lip. • The nasolabial angle, formed by the upper lip and columella. It defines the projection of the tip of the nose. • The sill area is the medial extension of the ala that forms a shelf of skin that extends from the ala-facial crease to the columella.

2.1.2 Structural Anatomy • The framework of the external nose is composed of four paired components (Fig. 2.2): 1. Nasal bones. 2. Upper lateral cartilages (upper nasal cartilages). 3. Lower lateral cartilages (alar cartilage, major alar cartilages). 4. Minor alar cartilages. • The nasal septum is the pillar of the external nose. Loss of septal support leads to saddling of the external nose. • The nasal bones form the bony dorsum of the nose. The nasal bones are thicker superiorly than inferiorly and are fused in the midline. The thick superior border of the nasal bones articulates with the nasal process of the frontal bone forming the nasofrontal angle (120–130 degrees). The lower border of the nasal bones overlaps the upper lateral cartilage. The lateral borders of the nasal bones articulate with the ascending processes of the maxilla and form the superior edge of the pyriform aperture. • The upper lateral cartilages are the major component of the cartilaginous dorsum of the nose. The cephalic ends of the upper lateral cartilages are overlapped by nasal bones. The caudal ends of the upper lateral cartilage are overlapped by the cephalic edges of the lateral crus of the lower lateral cartilages. This overlap is called the scroll region. • The caudal edges of the upper lateral cartilages diverge away from the midline forming a small triangular space (the weak triangle) that marks the area of the supratip breakpoint.

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Fig. 2.2  Main structural components of the external nose. LLC lower lateral cartilage, MAC minor alar cartilages, NB nasal bone, ULC upper lateral cartilage

• The lower lateral cartilages are divided into three crura: medial, middle, and lateral. 1. The medial crus is composed of a footplate segment and a columellar segment and is connected to the other medial crus by dense fibrous tissue. 2. The middle crus connects the medial and lateral crura. The most anterior projecting point on the middle crus is called the tip-defining point. The tip of the nose is defined as the midpoint of a line extending from one tipdefining point to the other. The junction of the medial crus and the middle crus is the columellar breakpoint. 3. The lateral crus is the largest component of the lower lateral cartilage and is connected with its contralateral counterpart by the interdomal ligaments. Laterally, they articulate with the first of three or four lesser alar cartilages. • The caudal edge parallels the anterior half of the alar rim, and the cephalic edge interlocks with the upper lateral cartilage at the scroll area. • The keystone area defines the meeting of four structures: the upper lateral cartilages, the septal cartilage, the nasal bones, and the perpendicular plate of the ethmoid. It provides significant support for the nasal dorsum. • The pyriform aperture is a large, pyramidal-shaped opening that forms the bony entrance into the nasal cavity. It is bounded laterally and inferiorly by the premaxilla and maxilla and superiorly by the nasal bone.

2.1 The External Nose

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• The nasal spine is a small bony prominence, formed by the fusion of two halves of the premaxilla, in the midline. The nasal spine provides support strut for the septal cartilage which rests on a midline ridge of the premaxilla called the maxillary crest. • The dorsal border of the septal cartilage at its caudal end turns ventrally and makes acute angle (the anterior septal angle) to turn ventrally. Suspensory ligaments of the tip extend from the septal angle to the cephalic edges of the lower lateral cartilages.

2.1.3 Blood Supply of the External Nose 2.1.3.1 Arterial Supply • The arteries of the external nose run underneath the SMAS and send perforating vessels superficially to supply the overlying layers. • The external nose derives its blood supply from: 1. The facial artery, which is a branch from the external carotid artery. It gives rise to the lateral nasal artery, angular artery, infraorbital artery, and superior labial artery. 2. The ophthalmic artery, which arises from the internal carotid artery and gives rise to the dorsal nasal artery and supratrochlear artery. • The dorsal nasal artery, a terminal branch of the ophthalmic artery, is the main blood supply to the dorsum and side walls of the nose. The artery passes through the orbital septum above the medial canthus and descends along the dorsum of the nose. The dorsal nasal artery anastomoses with the lateral nasal branch of the angular artery, thus establishing communication between the external carotid and the internal carotid artery systems. • The supratrochlear artery, a branch of the ophthalmic artery supplies the root of the nose. • The lateral nasal artery anastomoses with the infraorbital artery to supply the side walls of the nose, and with the columellar artery (a branch from the superior labial artery) to supply nasal tip. • The septal branch of the superior labial artery supplies the anterior part of the nasal septum. 2.1.3.2 Venous Drainage The veins draining the external nose correspond to the arteries and drain the nose through the facial vein, retromandibular vein into the pterygoid plexus and through the ophthalmic veins into the cavernous sinus. 2.1.3.3 Lymphatic Drainage The external nose drains to the submandibular and upper deep cervical lymph nodes.

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2.1.4 Nerve Supply • Sensory innervation of the external nose is derived from the terminal branches of the trigeminal nerve: 1. The supraorbital and supratrochlear branches of the ophthalmic nerve supply the superior two-thirds. 2. The external nasal branch of the anterior ethmoid nerve innervates the lower dorsum and nasal tip region. 3. The infraorbital nerve supplies the lower third of the external nose. • The muscles of the external nose develop from the blastema of the second (hyoid) branchial arch and are supplied by the zygomatic and temporal branches of the facial nerve.

2.2 The Nasal Cavity • The nasal cavity is divided by the nasal septum into two main cavities. The anterior most part of the nasal cavity is called the vestibule, which is limited posteriorly by the internal nasal valve (limen nasi). The external nasal valves is the angle between the upper lateral cartilage and the nasal septum. Normally, it measure 15 degrees. • The nasal valve area includes the internal nasal valve and the anterior end of the inferior turbinate. It is the narrowest portion of the nasal cavity and influences the aerodynamics and resistance of nasal airflow. • The choanae are the paired posterior openings through which the nasal cavities communicate with the nasopharynx. • The roof of the nasal cavity is formed by the cribriform plate of the ethmoid bone. • The floor of the nasal cavity is formed mostly by the hard palate, which is formed in turn by the two palatine processes of the maxilla and the horizontal processes of the palatine bone. • The lateral wall of the nasal cavity formed by the ethmoid bone and maxilla anteriorly and by the palatine bone and the pterygoid process of the sphenoid bone posteriorly.

2.2.1 The Nasal Septum • The nasal septum provides support to the nasal tip and bridge and is also one of the regulators of nasal airflow. • The nasal septum is composed of three parts: membranous, cartilaginous, and bony (Fig. 2.3). • The membranous septum is the mobile part between the caudal end of the quadrangular cartilage and the columella. It consists of the vestibular skin and the subcutaneous tissue lying in between.

2.2 The Nasal Cavity

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Fig. 2.3  The nasal septum. CM crest of the maxilla, CP crest of the palatine bone, P perpendicular plate of ethmoid bone, SC septal cartilage, V vomer

• The columella consists of a pair of medial crura of the lower lateral cartilages connected together by fibrous tissue and covered by skin. • The cartilaginous septum is made up of the septal (quadrangular) cartilage which articulates with the perpendicular plate of the ethmoid bone, vomer, and the crest of the premaxilla. The cartilage is thicker anteriorly, and opposite turbinates. • The septal cartilage forms the internal nasal valve with the upper lateral cartilages. The nasal valve angle is about 10–15 degrees. The perichondrium of the septal cartilage is continuous with the periosteum of the maxillary crest and sharp dissection is needed in this area during septal surgery. • The bony septum is composed of the perpendicular plate of the ethmoid, the vomer, and small contributions from the sphenoid rostrum, the crest of the palatine bone, and the crest of the maxilla (premaxillary wings). • The most anterior part of the premaxilla is the anterior nasal spine which attaches to the lower edge of the septal cartilage and is important for the support of the tip of the nose. • The perpendicular plate of the ethmoid bone forms the upper part of the bony septum and is attached to the cribriform plate above. It is attached to the nasal bones at the upper midline, to the septal cartilage caudally, to vomer inferiorly, and to the rostrum (crest) of the sphenoid bone posteriorly.

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• The junction of the perpendicular plate, the nasal bones, the septal cartilage, and upper lateral nasal cartilages constitutes the keystone area of the nose. The stability of this area should be carefully maintained during rhinoplasty. • The vomer attaches to the septal cartilage, perpendicular plate of the ethmoid, and sphenoid rostrum superiorly, and to the crests of the palatine bone and the premaxilla inferiorly.

2.2.2 Lateral Basal Wall • The lateral nasal wall (Fig. 2.4) carries three scroll-like structures called the turbinates: inferior, middle, and superior. A rudimentary “supreme turbinate” may be rarely present above the superior turbinate.

Fig. 2.4  Lateral nasal wall. FS frontal sinus, IT inferior turbinate, LL lower lateral cartilage, MT middle turbinate, NB nasal bone, PP pterygoid process, SS sphenoid sinus, ST superior turbinate, UL upper lateral cartilage

2.2 The Nasal Cavity

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• The middle and superior turbinates are part of the ethmoid bone. The inferior turbinate includes a separate bone called the “concha.” • Each turbinate overhangs a corresponding space or air passage called meatus. In the case where a fourth, supreme nasal turbinate is present, there is a fourth supreme nasal meatus. • The superior meatus is the smallest of the three. It drains posterior ethmoid cells. • The middle meatus shows a curved fissure, the hiatus semilunaris, limited below by the edge of the uncinate process and above by the bulla ethmoidalis. –– The hiatus semilunaris communicates with a curved passage termed the infundibulum, which drains the anterior ethmoid cells and, in more than 50% of subjects, the frontal sinus. –– Below the bulla ethmoidalis and hidden by the uncinate process of the ethmoid is the ostium of the maxillary sinus. An accessory ostium is frequently present above the posterior part of the inferior nasal turbinate in the area called the posterior fontanelle in 30% of patients with chronic maxillary sinusitis and in 10 to 20% of normal individuals. • The inferior meatus is the largest of the three. The nasolacrimal duct opens near its anterior end and a valve may be present there (Hasner’s valve) to prevent air from being blown back from the nose into the lacrimal sac. • Above and posterior to the superior concha is the sphenoethmoidal recess which drains the sphenoid sinus.

2.2.2.1 The Inferior Turbinate • The inferior turbinate is the largest turbinate that extends horizontally along the lateral wall of the nasal cavity. It consists of a bony concha covering by a highly vascular connective tissue and respiratory epithelium. • The inferior concha is a separate lamina of a spongy bone is attached to the medial wall of the maxilla. • The inferior concha can be divided into three portions: –– The anterior portion articulates with the conchal crest of the maxilla. –– The middle portion presents three well-marked processes. –– The anterior or lacrimal process is articulated, with the descending process of the lacrimal bone, and, by its margins, with the groove on the back of the frontal process of the maxilla and shares in the formation of the canal for the nasolacrimal duct. –– The ethmoidal process ascends to join the uncinate process of the ethmoid. –– The maxillary process articulates with the maxilla. –– The posterior portion articulates with the conchal crest of the palatine bone. • The inferior turbinate consists of anterior end (head), body, and posterior end (tail). The anterior end is a part of the valve area of the nose. 2.2.2.2 The Middle Turbinate • The attachment of the middle turbinate to the lateral nasal wall and skull base is called the basal lamella that is divided into three segments: –– Anterior segment: oriented in the sagittal plane and attaches to the lateral wall of the nose posterior to the agger nasi anteriorly and the skull base at the junction of the cribriform plate with its lateral lamella superiorly.

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–– Middle segment: oriented in the coronal plane obliquely and attaches to the lamina papyracea. –– Posterior segment: oriented in the axial place (horizontal) and attaches to the lamina papyracea, maxilla, and perpendicular process of the palatine bone. • Anatomic variants: –– Concha bullosa: presence of large air cell within the middle turbinate. The cavity of the air cell is lined with thin epithelium. –– Paradoxical middle turbinate: the curvature of the turbinate projects laterally and may narrow or obstruct the nasal cavity, middle meatus, and infundibulum.

2.2.2.3 The Superior Turbinate • Superior turbinate attachment to sphenoid face (Parson ridge): –– Type A: sup turbinate attachment in medial 1/3 (40%). –– Type B: sup turbinate attachment in middle 1/3 (40%). –– Type C: sup turbinate attachment in lateral 1/3 (19%). –– Type D: sup turbinate attachment to orbit (1%). 2.2.2.4 The Uncinate Process • The uncinate process is the first structure encountered in the middle meatus. • It appears a sickle-shaped bone attached to the lateral nasal bone and runs from anterosuperior to posteroinferior. • The uncinate process has three types of attachments: –– Lateral attachment to lamina papyracea: this is the most common type resulting in a recessus terminalis. In this case, the frontal recess drains medial to the uncinate into the middle meatus. –– Superior attachment onto the skull base: frontal recess drains laterally into the infundibulum. –– Medial attachment to the middle turbinate; the frontal sinus drains into the infundibulum. 2.2.2.5 The Ostiomeatal Complex • The ostiomeatal complex is bounded medially by the middle turbinate and laterally by the lamina papyracea and includes the ethmoid bulla, hiatus semilunaris, ethmoid infundibulum, frontal recess, and uncinate process. • The ethmoid infundibulum is the space between the uncinate process, ethmoid bulla, and lamina papyracea of the ethmoid bone. The frontal recess is an hourglass-­like passage connecting the frontal sinus with the infundibulum. • The sinus terminalis is a blind pocket under the uncinate process when it attaches to the lamina papyracea. • Suprabullar recess is the space between the ethmoid bulla and the fovea ethmoidalis when the bulla does not extend up to the fovea. • The sinus lateralis/retrobullar recess is the space between the posterior surface of the ethmoid bulla and the vertical portion of the basal lamella.

2.2 The Nasal Cavity

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2.2.2.6 Bony Lamellae Encountered during Endoscopic Sinus Surgery 1. Uncinate process. 2. Ethmoid bulla. 3. Vertical portion of the basal lamella. 4. Vertical portion of the lamella of the superior turbinate. 5. Anterior wall of the sphenoid sinus.

2.2.3 Blood Supply of the Nasal Cavity • The arterial supply of the nasal cavity is provided by the branches of the external and internal carotid arteries. • The sphenopalatine artery (artery of epistaxis) is one of the terminal branches of the maxillary artery which is a branch of the external carotid artery and is the main blood supply to the nose. It provides the blood supply to a wide area on the lateral nasal wall and nasal septum. • The greater palatine artery supplies posterior part of the lateral nasal wall and the anterior septum by passing through the incisive canal. • The superior labial branch of the facial artery provides the blood supply to the nasal vestibule and the anterior and inferior portion of the septum. • The anterior and posterior ethmoid branches of the ophthalmic artery, which is a branch of the internal carotid artery, provide the blood supply to the superior and anterior part of the nasal septum and nose. • The Little’s area (Kiesselbach plexus) is a vascular area located at the anterior inferior part of the nasal septum. It is the site of anastomosis of the terminal branches of the sphenopalatine, anterior ethmoidal, the superior labial, and the greater palatine arteries. It is a frequent site of bleeding especially in children and adolescents. • The veins, accompanying the arteries, drain to the pharyngeal and pterygoid plexuses and the cavernous sinus. • The veins and venous sinuses of the nasal turbinates lack valves and anastomose with each other to form erectile tissue capable of congestion and decongestion. • Then lymphatic drainage of the nasal cavity goes to the retropharyngeal and upper deep cervical lymph nodes. The anterior part of the nasal cavity drains in the submandibular lymph node.

2.2.4 Nerve Supply of the Nasal Cavity • Sensory innervation of the nasal cavity is provided by the ophthalmic and maxillary branches of the trigeminal nerve (fifth cranial nerve). • The Inferior posterior nasal branches of greater palatine nerve are small nerves which largely supply the posterior aspect of the nasal cavity. • Autonomic innervation of the nasal cavity controls the vascular system of the nasal mucosa and the activity of the seromucinous glands.

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• The sympathetic nerve fibers originate from the lateral horn cells of the first and the second thoracic segments of the spinal cord and synapses in the superior cervical ganglion. • The parasympathetic fibers start from the superior salivatory nucleus in the brain stem to the geniculate ganglion. They leave ganglion as the greater superficial petrosal nerve which joins the postganglionic sympathetic branches from the superior sympathetic ganglion(deep petrosal nerve) at the foramen lacerum to form the vidian nerve inside the vidian canal. • The vidian nerve reaches the sphenopalatine ganglion where the parasympathetic fibers make synapses inside the ganglion. The sympathetic fibers pass without synapse in the ganglion. Fibers from the sphenopalatine ganglion are distributed to the nasal mucosa through several branches (posterior superior nasal nerves/short sphenopalatine nerves). The nasopalatine nerve (long sphenopalatine nerve) supplies the palate and part of the nasal septum.

2.3 The Sinuses • The paranasal sinuses (Fig. 2.5) are air-filled cavities around the nasal cavities. • The parental sinuses communicate with the nasal cavity through its ostia: the maxillary sinus, frontal sinus, and anterior ethmoid cells drain through the middle meatus. • The posterior ethmoid cells drain through the superior meatus. • The sphenoid sinus drains in the sphenoid-ethmoidal recess. a

b

Fig. 2.5 (a) Coronal CT scan showing the ostiomeatal complex. The lowermost portion of the uncinate process (red arrows) is seen covering the maxillary sinus ostium. Also, the bulla ethmoidalis (be), frontal sinus ostium (white arrow), and maxillary sinus (max) can be identified. Frontal sinus ostium shows the typical hourglass appearance. There is an interlamellar cell in the middle turbinate (lc). The orbit is separated from the ethmoid complex by thin lamina papyracea (blue arrow). (b) Coronal CT scan showing the suprabullar recess (sb) above the bulla ethmoidalis (be). The suprabullar recess is infected on the left side (white arrow) causing ipsilateral orbital pain

2.3 The Sinuses

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2.3.1 The Ethmoid Sinuses • The ethmoid sinuses are a collection of pneumatized air cells separated from one another by thin bony walls. • The air cells extend between the nasal cavity and the orbit posteriorly to reach the sphenoid sinus. • The ethmoid sinuses are separated from the orbit by the thin orbital plate of the ethmoid bone (lamina papyracea). . • There is an inverse relationship between maxillary sinus height and the height of the ethmoid cavity. • The ethmoid complex is divided by the basal lamella into the anterior and posterior ethmoid cells. • The posterior ethmoid cells are closely related to the optic nerve (Fig. 2.6). • The ethmoid roof (fovea ethmoidalis) and cribriform plate separate the ethmoid cells from the anterior cranial fossa. • The fovea ethmoidalis is a part of the frontal bone that closes the ethmoid cells superiorly and is continuous medially with the lateral lamina of the cribriform plate. • The lateral lamina of the cribriform plate is the continuation of the sagittal attachment of the middle turbinate and may be injured during endoscopic sinus surgery. • The anterior skull base is formed by the cribriform medially and the fovea ethmoidalis laterally and slopes downward posteriorly. It extends from the posterior wall of the frontal sinus anteriorly to the planum sphenoidale posteriorly. The bone is thinner medially along the lateral lamella of the cribriform plate. • The level of the ethmoid roof and cribriform plate varies considerably, even in the same patient, depending on the vertical dimension of the lateral lamina.

a

b

Fig. 2.6 (a) The posteriori ethmoid box (pe) bordered superiorly by anterior skull base, laterally by lamina papyracea, medially by the superior turbinate, and inferiorly by the basal lamella of the superior turbinate. (b) The optic nerve is close to the last posterior ethmoid air cell (yellow asterisk). This is considered the most common site of iatrogenic injury to the nerve. Sphenoid sinus (red asterisk)

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• Keros classification of the lateral lamella of cribriform plate. –– Type 1: cribriform plate 1–3 mm below the fovea. –– Type 2: cribriform plate 4–7 mm below the fovea. –– Type 3: cribriform plate 8–16 mm below the fovea (highest risk of skull base penetration). • The agger nasi cell (Fig. 2.7) is the most anterior of all ethmoid cells and is present in up to 98% of CT scans. It is a remnant of the first ethmoturbinal and is found superior, lateral, and anterior to the attachment of the middle turbinate. It defines the anterior aspect of the frontal recess. • The ethmoid bulla is the largest and most prominent ethmoid cell and it drains into the middle meatus. There may be a cleft behind the bulla (retrobulbar recess) or above the bulla (suprabullar recess, Fig. 2.5). • The ethmoid cells may pneumatize into the adjacent sinuses and affect their drainage: –– Infraorbital ethmoid or Haller cell into the maxillary sinus (Fig. 2.8). –– Supra bulla cell between the ethmoid bulla and skull base. –– Supraorbital ethmoid cell above the orbit and posterior and lateral to the frontal sinus. –– Frontal bullar cell adjacent to the posteriori wall of the frontal sinus (Fig. 2.9). –– Spheno-ethmoid or Onodi cell (Fig. 2.10) superior and lateral to the sphenoid sinus potentially placing the optic nerve and internal carotid artery at risk during surgery.

2.3.2 The Maxillary Sinus • The maxillary sinus (Fig.  2.5) is present at birth and borders the nasal cavity laterally and is separated from the orbit by the orbital floor. • The posterior wall of the maxillary sinus is related posteriorly to the pterygopalatine fossa, and its contents: the maxillary artery and branches of the trigeminal nerve/ y t. • The floor of the maxillary sinus is closely related to the roots of the second premolar and first molar teeth. • The medial wall of the maxillary sinus has two fontanelles where bone is absent. The anterior fontanelle is anterior to the uncinate process and the posterior fontanelle is posterior to it. • The natural ostium drains into the inferior aspect of the infundibulum at a 45-degree angle and is elliptically shaped. • Accessory ostia are round and present in the fontanelles in at least 30% of patients.

2.3.3 The Frontal Sinus • The frontal sinus originates embryologically from an anterior ethmoid cell. • The sinus is related inferiorly to the orbit and posteriorly to the anterior cranial fossa. • The mucociliary flow inside the frontal sinus goes up the intersinus septum across the frontal sinus roof laterally and then medially along the floor of the frontal sinus down to the frontal recess.

2.3 The Sinuses

a

c

21

b

d

Fig. 2.7 (a) Agger nasi (A) cell. (b) Frontal bulla cell (FB) pneumatizing above the bulla and ­extending along the skull base to attach to the posterior wall of the frontal sinus. (c) A huge infected left type 4 frontal air cell (arrow). (d) Infected type 4 frontal air cell. The red arrows delineate the outline of the cell

• The anterior ethmoid artery passes posterior to the frontal recess and occasionally without bony covering (Fig.  2.11). This should be taken in consideration during surgery. • The frontal recess (Fig. 2.7) is the hourglass outflow tract of the frontal sinus. Its narrowest part is the frontal ostium. The frontal sinus is directed anteromedially and drains through the frontal recess into the middle meatus or into the superior aspect of the infundibulum, depending on the site of attachment of the uncinate process. • Boundaries of the frontal recess: –– Anterior: posterior wall of the agger nasi. –– Posterior: ethmoid bulla. –– Medial: Middle turbinate. –– Lateral: lamina papyracea.

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Fig. 2.8  A huge Haller cell (hc) obstructing the maxillary sinus ostium (red arrow) and causing isolated maxillary sinusitis (white arrow)

a

c

b

d

Fig. 2.9  The supraorbital ethmoid cell is a pneumatization of the orbital plate of the frontal bone by an anterior ethmoid cell. It is almost always located posterior and lateral to the frontal sinus. It is the only frontal recess cell that can be better identified by axial CT scans. (a) Axial CT scan showing inflammation of right frontal sinus (F) and supraorbital cell (S). (b) Endoscopic view of the same case. The black arrow points to the frontal sinus and the white arrow points to the supraorbital cell. (c) An interesting case of right isolated disease supraorbital cell (red asterisk). The frontal sinus (yellow asterisk) is clear. (d) Transillumination at the end of surgery shows the two separate compartments: supraorbital cell(s) and frontal sinus (f)

2.3 The Sinuses

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a

b

c

Fig. 2.10  Onodi cell (sphenoethmoidal cell). (a) Onodi cell (white arrow) pneumatizing superior to the sphenoid sinus (red arrow) to come in direct contact with optic nerve, internal carotid canal, and opticocarotid recess (green arrow).The presence of a transverse septation within the sphenoid sinus indicates that the upper compartment is Onodi cell. (b) Onodi cell (white arrow) contacting the optic and internal carotid artery bony bulges. (c) Opening of the sphenoid sinus in the most inferomedial; portion of Onodi cell (white arrow)

• The frontal sinus and frontal recess are related to several air cells. • Bent and Kuhn classification of frontal air cells. –– Type I: a single frontal recess cell above the agger nasi. –– Type II: a tier of cells above the agger nasi projecting into the frontal recess. –– Type III: single massive cell arising above the agger nasi, pneumatizing into the frontal sinus. –– Type IV: single isolated cell within the frontal sinus.

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Fig. 2.11  The anterior ethmoid artery passing posterior to the frontal recess without bony covering. An unusual and serious surgical situation

• International Frontal Sinus Anatomy Classification (IFAC): –– Agger nasi cell anterior to the origin of the middle turbinate. –– Supra agger nasi cell located above the agger nasi cell and does not pneumatize into the frontal sinus. –– Supra agger frontal cell located superior to the agger nasi cell and extends into the frontal sinus. –– Supra bulla cell located above the bulla ethmoidalis but does not enter the frontal sinus. –– Supra bulla frontal cell is a supra bulla cell that pneumatizes along the skull base into the posterior wall of the frontal sinus. –– Supraorbital ethmoid cell (Fig. 2.9) is an ethmoid cell that pneumatizes over the roof of the orbit and often forms part of the posterior wall of a well pneumatized frontal sinus. It is usually located posterior and lateral to the frontal sinus. –– Frontal septal cell attached to or located in the interfrontal sinus septum.

2.3.4 The Sphenoid Sinus • The sphenoid sinus is bordered superiorly by the planum sphenoidal and sella turcica and pituitary gland. The sella turcica is located behind the tubercullum sellae at the inferior portion of middle cranial fossa. • Its posterior wall of the sinus is formed by the clivus. The clivus separates the sinus it from the posterior cranial fossa. • Pneumatization of the sphenoid sinus may be conchal (very small, 0.4%), presellar (25–30%), sellar (commonest type, 70–75%) and occasionally post-sellar exceeding the posterior limit of the sellar.

2.3 The Sinuses

a

25

b

Fig. 2.12  The sphenoid sinus. (a) The sphenoid sinus is related to several neurovascular structures including the optic nerve (white arrow), the carotid artery (red arrow), the maxillary nerve (orange arrow), and the vidian nerve (green arrow). (b) The intersinus septum (red arrow) is inserted into the bony covering of the carotid artery, thus increasing the risk of injury of carotid artery during surgery

• Relations of the lateral wall of the sphenoid sinus: (Fig. 2.12). –– Cavernous sinus. –– Internal carotid artery. –– Cranial nerves II to VI. • The optic nerve and internal carotid artery are closely related to the sphenoid sinus. The bulges produced by the optic nerve and the internal carotid artery depend upon the degree of pneumatization of the sphenoid sinus. If the anterior clinoid process of the lesser wing of the sphenoid bone is pneumatized, there might be a deep noticeable recess (infra opticocarotid recess) in the superior and lateral corner of the sphenoid sinus between the bulges of the optic nerve and internal carotid artery. • Carotid canal protrusion into the sphenoid sinus occurs in 24–36% of subjects, and dehiscence in carotid canal exists in 22–34% of cases. The intersinus septum may be inserted into the bony covering of the carotid artery with increased risk of injury of carotid artery during surgery. • Optic canal bulging into the sphenoid sinus occurs in 5–8% of subjects, and optic canal dehiscence may exist in about 10% of cases. • The vidian nerve usually runs in the floor of the sinus but occasionally may run within the sinus. • The ostium of the sphenoid sinus opens into the sphenoethmoidal recess halfway to two-thirds up to the anterior wall of the sinus medial to the posterior end of the superior turbinate.

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2  Anatomy of Nose and Sinuses

• The ostium is at an average of 6–8 cm from the anterior nasal spine, at an angle of 30 degrees from the floor of the nose and approximately 1–1.5  cm above the choana. • The posterior septal artery, which is a branch of the SPA, runs along the inferior face of the sphenoid sinus and may be injured while creating a sphenoidotomy.

2.4 Histology of the Nasal Mucosa • The nasal cavity includes three functional areas or regions: vestibular, respiratory, and olfactory. The limen nasi separates the vestibular and respiratory areas. • The vestibule of the nose is lined with stratified squamous epithelium which is continuous with the skin of the face. It is characterized by the presence of stiff hairs called vibrissae to entrap large-sized particles of larger size in the inspired air. • The respiratory region is lined with pseudostratified ciliated columnar epithelium with goblet cells (Fig. 2.13). The submucosa seromucinous acini. The cilia of the columnar cells moves the mucous blanket towards the pharynx. • Each cilium is composed of 2 central singlet microtubules and 9 peripheral doublet microtubules with inner and outer Dynein arms (Fig. 2.14). Cilia are attached to the cell at the basal bodies. • The nasal sinuses are lined with a thinner respiratory epithelium with few goblet cells and seromucinous acini especially near the ostia of the sinuses. • The olfactory epithelium is yellowish in color and measures about 9 cm2. With age, the olfactory diminishes in area and is replaced by respiratory epithelium. • The olfactory epithelium (Fig. 2.15) lies on the roof of the nasal cavity and is formed of:

Fig. 2.13 Scanning electron micrograph of the nasal mucosa. C cilia, GC goblet cell. Normally all cilia beat in the same direction (synchronous movement)

2.4 Histology of the Nasal Mucosa

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Fig. 2.14  Cross section of the cilia. Each cilium contains 2 central singlet microtubules and 9 peripheral doublet microtubules. C cilia

1. Olfactory cells: These are club-shaped bipolar cells. The dendrites of the cells are exposed to the outside while the axons travel through about 20 foramen in the cribriform plate and become encased by Schwann cells to form the olfactory filaments. The olfactory filaments synapse with the mitral cells in the olfactory bulbs at the base of the frontal lobe. 2. Basal cells: These are stem cells that lie near or on the basement membrane. The basal cells are capable of division and differentiation into either supporting or olfactory cells. 3. Supporting cells: There are two types of supporting cells in the olfactory epithelium: sustentacular cells and microvillous cells. –– The sustentacular cells function as metabolic support for the olfactory epithelium. –– The microvillous cells release acetylcholine and may have modulatory function. 4. Bowman’s glands: These are tubuloalveolar serous glands underneath the epithelium. Secretions of the glands dissolve odiferous substances for the bipolar cells. • The olfactory neurons are uniquely capable of regeneration. The human olfactory epithelium is renewed every 60 days by apoptosis, dead cells being replaced by basal cells.

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2  Anatomy of Nose and Sinuses

Fig. 2.15 Olfactory epithelium. BC basal cell, BG Bowman’s gland, D dendrites, OC bipolar olfactory cell, Sec secretion of Bowman’s glands, SC supporting cell

MCQs 1. All of the following structures are component of the keystone area except: (a) Upper lateral cartilage (b) Nasal bones (c) Septal cartilage (d) Lower lateral cartilages 2. The main blood supply of the nasal cavity is: (a) Greater palatine artery (b) Anterior ethmoid artery (c) Sphenopalatine artery (d) Facial artery 3. The dorsal nasal artery is a terminal branch of: (a) Ophthalmic artery (b) Facial artery (c) Infraorbital artery (d) Superior labial artery 4. The suspensory ligament of the nasal tip connects the lower lateral cartilage to: (a) Nasal spine (b) Septal angle (c) Upper lateral cartilage (d) Ala of the nose

2.4 Histology of the Nasal Mucosa

5. The weak triangle is located at: (a) Nasion (b) Subnasale (c) Supratip break point (d) Keystone area 6. The uncinate process may attach to any of the following structures except: (a) Lamina papyracea (b) Middle turbinate (c) Ethmoid bulla (d) Skull base 7. The Little’s area is located at: (a) Floor of the nose (b) Near the sphenopalatine foramen (c) In the inferior meatus (d) Anterior inferior aspect of the nasal septum 8. Frontal bulbar cell is: (a) Related inferiorly to the orbit (b) Adjacent to the auger Nasir cell (c) Adjacent to the posteriori wall of the frontal sinus (d) Called Haller cells 9. Type IV frontal air cell is: (a) The most constant frontal air cell (b) A single isolated cell within the frontal sinus (c) Located between the bulla ethmoidalis and skull base (d) Related to sinus terminales 10. The sphenoid sinus is related to all of the following cranial nerves except: (a) IV (b) V (c) III (d) IX 11. Bowman’s glands are: (a) Serous glands in the maxillary sinus mucosa (b) Mucous glands in the middle, meatus (c) Serous glands in the nasopharynx (d) Serous glands in the olfactory mucosa 12. The vibrissae are: (a) Stiff hairs in the vestibule of the nose (b) Specialized olfactory cilia (c) Specialized respiratory cilia (d) Located at the entrance of the nasopharynx

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Answers 1. (d) 2. (c) 3. (a) 4. (b) 5. (c) 6. (c) 7. (d) 8. (c) 9. (b) 10. (d) 11. (d) 12. (a)

2  Anatomy of Nose and Sinuses

3

Nasal Physiology and Functions

3.1 Important Nasal Functions • The nose and paranasal sinuses have six important functions: 1. Olfaction. 2. Respiration. 3. Air conditioning (filtering, warming, and humidification of inspired air). 4. Protection of the airway. 5. Speech. • The functions of the sinuses are less defined: 1. Resonating function. 2. Bumper (protective) function from accidental trauma.

3.2 Olfaction • Olfaction (the sense of smell) is fully mature at birth. However, the sense of smell in humans is much weaker than in most mammals. • Loss of smell (hyposmia or anosmia) is a common complaint in ENT practice and is on two main types: –– Sensory-neural anosmia or hyposmia due to damage to the olfactory organ or nerve fibers, e.g., viral infections or anterior skull base fracture. –– Conductive anosmia or hyposmia is more common and may occur due to partial or total obstruction of the nasal airway. • The olfactory mucosa is much thicker than the respiratory mucosa. • The olfactory mucosa contains about 20 million receptor cells and it lines the area of the olfactory cleft: the uppermost portion of the septum, the nasal side of the cribriform plate, and the medial surface of the upper turbinate. • The olfactory mucosa is composed of olfactory cells, supporting cells (sustentacular cells and microvillous cells), and basal cells. © The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 S. Elwany, M. Askar, Rhinology Review, https://doi.org/10.1007/978-3-031-08794-3_3

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• The olfactory lamina propria contains Bowman’s glands which produce a serous exudate to dissolve the odoriferous molecules. • The axons of the olfactory neurons synapse with the mitral cells in the olfactory bulb forming the olfactory (first) cranial nerve. • The second-order neurons, or mitral cells, project their fibers, mostly ipsilaterally, to several areas including olfactory tubercule, piriform cortex, amygdaloid nuclei, and the hypothalamus. • Only fat soluble or water-soluble odors are perceived. Sniffing intensifies the airflow and enhances olfaction. • Encoding olfactory information may be dependent upon odor binding proteins and/or receptor specialization and tonotopic arrangement. • Orthonasal olfaction refers to smelling through the nose. • Retronasal olfaction refers to perception of odors coming from the oral cavity and not through the nose. Retronasal olfaction contributes to the flavor of foods. Most patients with olfactory dysfunction complain of loss of both smell and taste. • Taste sensation is one of the chemical senses, that are stimulated by chemicals, like the sense of olfaction. The two systems provide complementary information. • The vomeronasal (Jacobson) organ is present as mucosal thickening on each side of the lower nasal septum. It secretes pheromones that perceived by another member of the same species and initiate physiologic and behavioral effects. The vomeronasal organ is well developed in animals but mostly rudimentary in humans.

3.3 Nasal Airflow and Conditioning • Breathing is the principal function of the nose. The total volume of air inhaled per day is about 10,000–12,000 L. Infants are obligate nasal breathers. • About 60% of the total resistance of the respiratory tract is provided by the nose especially by the nasal valve area to allow close contact and conditioning of the inspired air. At the end of inspiration, the air temperature in the nasopharynx is about 32 °C and the relative humidity is about 95%. • During mouth breathing, the resistance of the upper airways decreases to less than 20% of total airway resistance. • The nasal cavity consists of three segments with different airflow velocity and pattern: –– The inflow segment: the nostril, vestibule, and the valve area. –– The middle segment (air conditioning chamber): the irregular slit between the septum and lateral walls. –– The outflow segment: the sphenoethmoidal recess and the choana. • The nasal airflow is distributed between the middle meatus (50%), inferior meatus (35%), and olfactory cleft (15%). • The nasal valve is the angle (10–15°) between the nasal septum and the caudal part of the upper lateral cartilage.

3.4 Defense Functions of the Nose

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• The nasal valve area includes the nasal valve and the head of the inferior turbinate. The nasal valve area is the narrowest area of the nasal airway (flow-limiting segment). As the air passes through the nasal valve areas, its speed increases from about 3 m/s at the nostril to about 15 m/s (Bernoulli’s law) and the laminar airstream become turbulent (Venturi effect) to allow maximal contact between the inhaled air and the mucosa. • The vascular system of the nasal mucosa controls the nasal airflow. It is composed of five types of blood vessel types: precapillary resistance vessels, capillaries, veins, venous erectile tissue or sinusoids, and arteriovenous anastomoses. This vascular network includes capacitance and resistance vessels. • The α-adrenergic sympathetic innervation keeps continuous vasoconstrictor tone on the nasal vasculature. The cholinergic parasympathetic system enhances congestion and secretions. • The nasal cycle is the periodic changes in nasal resistance with reciprocal change of the resistance of both nasal cavities. • The importance of the cycle is believed to allow one side to perform more humidification and temperature changes, while the other side serves to maintain airflow to the lower respiratory tract. Normally we do not feel the nasal cycle but in pathological conditions the nasal cycle becomes more noticeable. • The nasal cycle occurs in a rhythm of 3–5 h and is controlled by the action of the adrenergic system on the capacitance vessels in the inferior turbinates. • Nasal resistance to airflow is affected by changes in body position. Changing from the erect or supine position to the lateral recumbent position results in the congestion of the dependent nasal cavity. • Cigarette smoke, estrogen, thyroxine, and other substances can cause congestion of nasal mucosa and increased nasal resistance to airflow.

3.4 Defense Functions of the Nose • Protective mechanisms of the nose are mechanical, humoral, and cellular.

3.4.1 Mechanical Mechanisms • The first line of nasal defense consists of the vibrissae at the nostril and the vestibule. • The second line of mechanical defense is the mucous blanket which entraps smaller particles and transport them to the nasopharynx. • The third barrier is the epithelial lining as a barrier between the nasal cavity and the nasal tissues. • The mucous layer actually consists of two layers: an upper, more viscous and sticky gel layer which entraps foreign particles, and a lower sol layer that allows ciliary movement. The mucous blanket is transported at a speed of 1.0–2.0 cm/ min towards the nasopharynx.

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3  Nasal Physiology and Functions

• Particles larger than 3 μm usually deposit in the anterior part of the nose. Particles smaller than 0.5 μm may pass into the lower airway. • Ostial patency required for adequate mucociliary clearance and gas exchange (nitric oxide). Low levels of nitric oxide may cause ciliary dysfunction.

3.4.2 Humoral Mechanisms • Humoral defense is provided by immunoglobulins (IgA and IgG) and other mediators including leukotrienes and interleukins.

3.4.3 Cellular Mechanisms • Cellular defense is mediated by several cells that can be recruited to counteract the effects of allergens, viruses, bacteria, and fungi. These cells include antigen presenting or dendritic cells, eosinophils, mast cells, plasma cells, neutrophils, as well as B- and T-lymphocytes.

3.4.4 Reflex Mechanisms • Sneezing (Naso–Nasal Reflex): The sneezing reflex is a strong important trigeminal reflex. It can be initiated by a wide range of physical and chemical nasal stimuli. Sneezing occurs in three steps: deep inflation, breath hold, and strong exhalation. It can be eliminated by local anesthesia. • Nasopulmonary Reflex (Nasotracheal Reflex): The nasopulmonary reflex induces slowing down of breathing and bronchial constriction following nasal stimulation, for example, by cold air. The afferent pathway is the trigeminal nerve, and the efferent pathway is the vagus nerve.

3.5 Speech • The nasal cavity and paranasal sinuses act as resonators. The term nasalance refers to the amount of nasal resonance. • Nasal speech sounds are produced by passage of the airstream through the nose. The amount of airflow is controlled by the soft palate. In the case of nasal consonants, such as English m, n, and ng, the mouth is closed and the airstream is expelled entirely through the nose. Nasalized vowels, on the other hand, are produced by expelling the air partly through the nose and partly through the mouth. • Rhinolalia clausa refers to decreased nasal resonance due to nasal obstruction. Rhinolalia aperta refers to increased nasal resonance and is observed in consonants requiring closure of the nasopharynx by the soft palate.

3.5 Speech

MCQs 1. The afferent nerve of the nasopulmonary reflex is the: (a) Vagus nerve (b) Olfactory nerve (c) Trigeminal nerve (d) Facial nerve 2. The second-order neurons of the olfactory pathway starts in the: (a) Olfactory mucosa (b) Pyriform cortex (c) Hypothalamus (d) Olfactory bulb 3. Increased sympathetic stimulation of the nasal mucosa: (a) Increases nasal resistance (b) Decreases nasal resistance (c) Increase nasal secretions (d) Decrease mucociliary velocity 4. The antigen presenting cells in the nasal mucosa are: (a) B-lymphocytes (b) Plasma cells (c) Mast cells (d) Dendritic cells 5. The inflow segment of the nose includes all of the following except: (a) Nostril (b) Nasal valve (c) Middle turbinate (d) Vestibule of the nose 6. Most of the nasal airflow passes through: (a) Middle meatus (b) Inferior meatus (c) Olfactory cleft (d) superior meatus 7. The nasal cycle is controlled by: (a) Adrenergic fibers (b) Cholinergic fibers (c) Jacobson’s organ (d) Humoral mediators 8. The internal nasal valve: (a) Changes turbulent flow to laminar flow (b) Decreases speed of inhaled airs (c) Changes laminar flow to turbulent flow (d) None of the above

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9. Nasal resistance may be increased by all of the following except: (a) Smoking (b) Hormones (c) Cold air (d) Pseudoephedrine 10. Particles smaller than 0.5 μm: (a) Usually pass to the lower passages (b) Usually deposit on the vibrissae (c) Usually deposit over the floor of the nose (d) Usually deposit in the middle meatus Answers 1. (c) 2. (d) 3. (b) 4. (d) 5. (c) 6. (a) 7. (a) 8. (c) 9. (d) 10. (a)

4

Imaging of the Nose and Sinuses

4.1 Computed Tomography (CT) • CT is the modality of choice to initially assess bony framework (Fig. 4.1), fissures, and foramina. It is also the best method to assess fibro-osseous lesions, osteomas, and other bony tumors. • CT scans typically obtained for visualizing the paranasal sinus should include coronal and axial (3-mm) cross sections. Soft tissue and bony windows facilitate evaluation of disease processes and the bony architecture. a

b

Fig. 4.1  CT scan is superior to MRI in assessing the bony frameworks and landmarks. (a) Iatrogenic left skull base defect (red arrow) following endoscopic sinus surgery. (b) A rare case of aneurysmal bone cyst of the maxilla (red arrows). This is a benign nonneoplastic rapidly expanding bony lesion characterized by the presence of cystic lesions filled with blood

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 S. Elwany, M. Askar, Rhinology Review, https://doi.org/10.1007/978-3-031-08794-3_4

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• With intravenous contrast, CT can also provide excellent soft tissue details, although it is inferior to the resolution provided by MRI. The use of intravenous contrast material just prior to scanning can help define soft tissue lesions and delineate vascularized structures, such as vascular tumors. • Coronal images (Fig. 4.2) represent the best plane for endoscopic correlation. Sagittal and axial planes are needed to assess other areas like the frontal sinuses and choana. A section thickness of 3 mm is adequate for rhinology. CT 1 mm cut sections can be both diagnostic and localizing the defects in CSF rhinorrhea. • Important anatomic areas to be examined by CT include the cribriform plate, the fovea ethmoidalis, the lamina papyracea, the bony framework of the sinuses, the turbinates, and the nasal septum. • Axial sections are helpful in certain situations, e.g., choanal atresia and evaluation of sphenoid sinus (Fig. 4.3). Sagittal images are important for evaluation of the frontal sinus. Fig. 4.2  A normal CT of the nose and sinuses. CP cribriform plate, EB ethmoid bulla, IO infraorbital nerve, IT inferior turbinate, MS maxillary sinus, MT middle turbinate, UP uncinate process. Notice the attachment of the uncinate process to the skull base

a

b

Fig. 4.3  Importance of axial scans. (a) Axial CT scan of the nose and sinuses showing atresia of the choana (black arrow) and bowing of the lateral nasal bone (white arrow). (b) Axial view showing isolated sphenoid sinusitis. MRI is needed to establish final diagnosis

4.2 Cone Beam CT

a

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b

Fig. 4.4  A case of allergic fungal sinusitis. (a) Bone window, (b) soft tissue window. Notice the electron dense opacities within the fungal mucin

• Soft tissue windows are usually requested to diagnose allergic or eosinophilic fungal sinusitis (Fig. 4.4). • CT angiography (CTA) combines a CT scan with intravenous injection of a contrast to “lights up” blood vessels and tissues that are being studied.

4.2 Cone Beam CT • Cone beam CT is an imaging technique that was used primarily in dentistry and has the advantage of lower radiation exposure compared to conventional CT. Cone beam CT provides detailed images of the bone and is used to assess the jaws, dentition, facial skeleton, nasal cavity, and sinuses (Fig.  4.5). However, it cannot be used reliably to assess soft tissues such as muscles, lymph nodes, glands, and nerves. It is especially useful for assessment of maxillo-facial trauma and the maxillary sinuses and the related teeth in cases of odontogenic sinusitis.

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a

4  Imaging of the Nose and Sinuses

b

c

Fig. 4.5  CBCT of left odontogenic maxillary sinusitis in coronal (a and b) and axial (c) CT scans. Note the clear delineation of the infraorbital nerve canal (arrows) in the axial cut

a

b

c

Fig. 4.6  MRI of a case of Juvenile angiofibroma (JNAI). (a) T1-weighted sequence, (b) T2-weighted sequence, (c) T1-weighted sequence with IV contrast

4.3 Magnetic Resonance Imaging • MRI provides excellent soft tissue contrast resolution with multiplanar capabilities. It does not involve ionizing radiation and therefore can be used for imaging children and women of childbearing age. • MRI is used to differentiate soft tissue masses from retained secretions and can also distinguish between the various soft tissue lesions (Fig. 4.6). • The standard sequences usually used in rhinology are a T1-weighted sequence, a T2 -weighed (fat-saturated) sequence, and a post-gadolinium sequence. • The T1- or “fat-weighted” sequence most effectively demonstrates the relationship of the tumor to fatty marrow in the skull base and the infiltration of fat pads in the pterygopalatine fossa and other areas. • The T2- or “fluid-weighted” sequence io differentiate retained secretions from actual tumor. Enhancement of inflammatory exudates depends upon its water and protein contents (Fig. 4.7).

4.5 General Radiologic Findings of Neoplastic Lesions

a

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b

Fig. 4.7 (a) Coronal CT showing supra orbital ethmoidal recess mucocele with intracranial extension (red arrow) and a Haller cell mucocele (white arrow). (b) T2-weighted MRI of the same patient showing variable enhancement of the inflammatory contents of the mucoceles as well as retained secretions in both maxillary sinuses. The degree of enhancement depends on the water and protein content of the mucin

• The post-gadolinium sequences delineate enhancing lesions and margins. It can also, with fat suppression, improve detection of perineural spread of tumor and intraorbital or intracranial invasion. • Magnetic resonance angiography (MRA) is a type of MRI that examines the blood vessels and is much less invasive than traditional angiography. Magnetic resonance angiography is used to evaluate arteries for occlusions, aneurysms, or other abnormalities.

4.4 General Radiologic Findings of Inflammatory Lesions • CT Scans –– Mucosal thickening and peripheral enhancement. –– Osteitis/bony thickening/bone expansion. • T1 MRI. –– Low signal. • T2 MRI. –– High signal. –– Mucosal thickening. –– Postcontrast T1 MRI. –– Homogenous enhancement of intact mucosa.

4.5 General Radiologic Findings of Neoplastic Lesions • CT Scans. –– Soft tissue mass. –– Bony erosion. –– Variable enhancement.

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4  Imaging of the Nose and Sinuses

• T1 MRI. –– Low signal. –– Obliteration of perineural fat. • T2 MRI. –– Low signal. –– Inhomogeneity of mucosal lining. • Postcontrast T1 MRI. –– Variable enhancement. –– Perineural spread and intraorbital invasion. MCQs 1. The imaging modality of choice to assess the bony walls of the sinuses is: (a) T1 MRI (b) CT (c) Plain X-rays (d) T2 MRI 2. Cone beam CT is good for examination of: (a) Soft tissues of the face (b) Contents of the orbit (c) Facial skeleton (d) Polyps and cysts 3. Axial CT scan sections are good for assessment of: (a) Choanal width (b) Maxillary sinus height (c) Ostiomeatal complex (d) Skull base 4. The best CT plane for endoscopic correlation is: (a) Axial plane (b) Coronal plane (c) Sagittal plane (d) None of the above 5. Cone beam CT has the advantage of: (a) Lower radiation exposure (b) Good delineation of soft tissues (c) Reliable detection of fungal sinusitis (d) All of the above 6. Sagittal CT scan sections are good for assessment of: (a) Sphenoid-ethmoidal recess (b) Roots of the teeth (c) Maxillary sinus (d) Frontal sinus 7. MRI is better than CT scan in assessing: (a) Bony boundaries (b) Tumor extension into pterygopalatine fossa (c) Fibro-osseous lesions (d) Blow out fractures

4.5 General Radiologic Findings of Neoplastic Lesions

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8. A suspected dental body in the maxillary sinus is best detected by: (a) CT with IV contrast (b) T1 MRI (c) Cone beam CT (d) T2 MRI 9. The MRI sequence that can demonstrate the relationship of the tumor to fatty marrow is: (a) T2 MRI (b) T1 MRI (c) T2 with contrast (d) None of the above 10. Osteitis of the bony wall of the sinuses can be best viewed by: (a) T1 MRI (b) T2 MRI (c) CTA (d) CT bone window Answers 1. (b) 2. (c) 3. (a) 4. (b) 5. (a) 6. (d) 7. (b) 8. (c) 9. (b) 10. (d)

5

Investigative Rhinology

• Apart from imaging, there are other tests that may be used for clinical and academic purposes. These tests include: A. Objective tests. (a) Allergy tests. (b) Airway tests. (c) Olfactory function tests. (d) Mucociliary clearance tests. B. Subjective test. (a) SNOT-22. (b) Nose scale. (c) Visual analog scale (VAS). (d) Quality of life questionnaires.

5.1 Allergy Tests 5.1.1 Skin Prick Tests • Skin prick tests are simple, cheap, and generally safe. However, they should not be performed if the patient has severe eczema or uses oral antihistamines. • The tests for food allergens are less reliable than inhalant allergens. • A drop of allergen extract is introduced into the skin by pricking with a lancet. • The test is read as the wheal diameter at 15 min. Reactions greater than 2 mm in children and 3 mm in adults are regarded as positive.

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 S. Elwany, M. Askar, Rhinology Review, https://doi.org/10.1007/978-3-031-08794-3_5

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5.1.2 Tests for IgE • Tests for IgE are unaffected with therapy contrary to skin prick tests. • Total IgE, although commonly performed, is not adequately reliable since it may be normal in 30–50% of patients with allergic rhinitis. • Specific IgE testing can be done with RAST or by ELISA (enzyme-linked immunosorbent assays). • Tests for specific IgE are generally more expensive, delayed and no more sensitive or specific than skin prick tests. • Tests for nasal IgE are helpful in diagnosing local allergic rhinitis.

5.1.3 Nasal Smears • Nasal smears for detection of eosinophils may be collected by Rhinoprobe or bronchial brush, and then stained with Wright–Giemsa stain. Nasal smears may be helpful in the differentiation of allergy from infections. The test is simple, noninvasive, and rapid and has moderate sensitivity.

5.1.4 Blood Eosinophils • Allergic rhinitis is uncommonly associated with blood eosinophilia unless it is associated with asthma, aspirin, or other systemic disorders.

5.1.5 Nasal Provocation Test • This is only needed in limited situations like testing for aspirin sensitivity. Allergen is introduced into the nose in graduated doses, and any reaction is measured and compared to placebo. The examiner should be ready to deal with unexpected reactions particularly severe bronchospasm.

5.2 Airway Tests 5.2.1 Rhinomanometry • Rhinomanometry measures nasal airway resistance by making quantitative measurements of nasal flow and pressure. • Rhinomanometry can be performed actively or passively, and by either anterior or posterior approaches. • Active anterior rhinomanometry is the most commonly used method. • The anterior rhinomanometer displays a flow curve which will be lowered when there is nasal obstruction. • Rhinomanometry is particularly useful when we compare pre- and post-­ treatment curves.

5.3 Olfactory Tests

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Disadvantages: –– Poor reproducibility –– No established threshold for the resistance at which symptomatic obstruction occurs –– Cannot be used when the nose is markedly obstructed. –– Cannot be used when there is a septal perforation

5.2.2 Acoustic Rhinometry • Acoustic rhinometry evaluates the dimensions of the nasal cavity with acoustic reflections and measures nasal cross-sectional areas and nasal volume. The test is usually done both before and after decongestion. • Acoustic rhinometry correlates well with subjective measures of airflow. • An audible sound pulse is generated and propagated in a sound probe. The reflected sound is picked up by a microphone, passed to a computer and analyzed. Changes in the nasal cross-sectional areas affect the acoustic impedance and the reflected sound.

5.2.3 Nasal Inspiratory Peak Flow • This test is done by peak flowmeter adapted with a nasal mask. • Normal flow rate is >120. Flow rate less than 50 denotes severe nasal obstruction. • Nasal expiratory peak flow is uncomfortable for the patient and may lead to accumulation of the mucus in the mask.

5.3 Olfactory Tests Olfactory function can be measured by subjective or objective methods.

5.3.1 Subjective Methods • Subjective tests are used for smell identification and threshold testing. The popular tests are: –– UPSIT (University of Pennsylvania Smell Identification Test) which is a scratch and sniff test that uses micro-encapsulated odorants. –– “Sniff ‘n sticks” which includes odor identification and threshold testing. The test can be used unilaterally.

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5  Investigative Rhinology

5.3.2 Objective Methods • Objective methods are not popular and need more validation: –– Olfactograms: Measurement of the electrical potentials of the olfactory epithelium after olfactory stimulation –– Olfactory bulb volumetry

5.4 Tests of Mucociliary Transport • Normal mucociliary clearance depends on normal mucus blanket and normal ciliary structure and motion (beating). • The saccharine test is an in vivo easy-to-perform test. Minimal saccharin transport time is less than 10 min. Transport times more than 20–30 min are considered abnormal. • Tests for research include electron microscopy, radioisotope transport test, ciliary beat frequency measurement, and nasal nitric oxide measurement.

5.5 Other Objective Tests These tests are being used primarily in for academic purposes:

5.5.1 Nitric Oxide Measurement • Nitric oxide was found to change in some ciliary disorders and inflammatory conditions. Currently nasal nitric oxide is not a clinically useful measure fors inonasal disease. Although sinus surgery may be associated with lowered nasal nitric oxide levels, there is no evidence that this may have any clinical consequences.

5.5.2 Nasal Lavage • Nasal lavage is used to sample nasal secretions for inflammatory mediators and cells. The osmolality, pH, and the viscosity of the fluid can be measured for research purposes. Eosinophil count from nasal irrigation has been shown to be a reliable marker of allergic rhinitis.

5.6 Subjective Tests 5.6.1 SNOT 22 • The 22-item Sinonasal Outcome Test (SNOT-22) is a validated patient-reported outcome measure for chronic rhinosinusitis. • The 20-question survey measures the physical impairments, functional limitations, disability, and societal limitations caused by the chronic rhinosinusitis.

5.6 Subjective Tests

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• SNOT 22 score of seven or less is considered normal. • SNOT-22 scores are used to classify chronic rhinosinusitis as mild (scores of 8–20), moderate (scores of more than 20–50), or severe (scores of more than 50).

5.6.2 NOSE Scale • NOSE scale is a reliable and validated tool to evaluate patients with nasal obstruction. • The scale measures the degree of nasal obstruction and its effect on sleep, work, and exercises. It can be used to assess of treatment and/or surgery. • The questionnaire is simple, short (five items), and can be easily completed by the patients with minimal or no assistance.

5.6.3 Visual Analog Scale (VAS) • Visual analog is a measurement instrument for subjective opinion of the patient about his symptoms or disease. • A scale from 0 to 10 is usually used. • Recently, the scale was used to follow up the condition of patients with allergic rhinitis.

5.6.4 Quality of Life (QOL) Questionnaires • There are several validated quality of life questionnaires that address the effect of a disease or a symptom on the quality of life of the patients. A good example of these questionnaires are SF-36 and its short form SF-12 questionnaires. MCQs 1. Which of the following tests is a subjective test: (a) Nasal prick test (b) SNOT-22 (c) RAST (d) None of the above 2. A test that can diagnose local allergic rhinitis is: (a) RAST (b) Nasal provocation test (c) Nasal IgE (d) All of the above 3. Acoustic rhinometry measures: (a) Nasal airflow (b) Nasal cross-sectional areas (c) Nasal resistance (d) All of the above

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4. The most used rhinomanometry technique is: (a) Anterior active (b) Posterior active (c) Posterior passive (d) Anterior passive 5. Nasal peak flowmetry measures: (a) Nasal volume (b) Nasal flow rate (c) Nasal resistance (d) All of the above 6. UPSIT is: (a) Subjective test of olfaction (b) Objective test of olfaction (c) Quality of life questionnaire (d) Objective test of airflow 7. Nasal mucociliary clearance can be measured by: (a) Expiratory nasal flowmetry (b) Active rhinomanometry (c) Saccharin test (d) Nasal lavage 8. NOSE scale is used to diagnose: (a) CSF leak (b) Deviated septum (c) Chronic rhinosinusitis (d) Olfactory loss 9. Patients with allergic rhinitis can be followed up by: (a) NOSE scale (b) SNOT-22 (c) VAS (d) None of the above 10. SNOT-22 includes: (a) 22 questions (b) 20 questions (c) 21 questions (d) 12 questions Answers 1. (b) 2. (c) 3. (b) 4. (a) 5. (b) 6. (a) 7. (c) 8. (b) 9. (c) 10. (a)

5  Investigative Rhinology

6

Symptoms of Sinonasal Diseases

6.1 Epistaxis 6.1.1 Vascular Anatomy • The nasal mucosa has rich blood supply (Fig. 6.1) from both the internal and external carotid arteries, and there are several anastomoses between the branches of both systems. • The upper part of the nose is supplied by branches from the internal carotid artery: anterior and posterior ethmoidal arteries which are branches of the ophthalmic artery. The rest of the nasal cavity is supplied by branches of the external carotid artery: –– The sphenopalatine artery (terminal branch of the maxillary artery). –– The greater palatine artery (a branch of the maxillary artery). –– The superior labial artery (a branch of the facial artery). • Little’s area (Kiesselbach plexus) is the commonest site of bleeding. In this area, four arteries anastomose to form a rich vascular network. These arteries are: 1. The anterior ethmoid artery. 2. The sphenopalatine. 3. The greater palatine. 4. The septal branch of the superior labial artery. • The Woodruff’s plexus is a venous plexus in the posterior part of the inferior meatus.

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 S. Elwany, M. Askar, Rhinology Review, https://doi.org/10.1007/978-3-031-08794-3_6

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6  Symptoms of Sinonasal Diseases

Fig. 6.1  Blood supply of the nose. aea anterior ethmoid artery, gpa greater palatine artery, L Little’s area, pea posterior ethmoid artery, sba sublabial artery, spa sphenopalatine artery

Fig. 6.2 Sphenopalatine artery and its branches (over the probe)

6.1.2 The Sphenopalatine Artery (SPA) • The sphenopalatine artery (SPA) is one of the terminal branches of the maxillary artery and is considered the main blood supply of the nose. It enters the nose through the sphenopalatine foramen close to the posterior end of the middle turbinate (Fig. 6.2). • The sphenopalatine artery is called the artery of epistaxis. • The SPA divides within the nose into lateral and medial branches: –– The lateral branch supplies the lateral wall of the nose and the inferior turbinate. –– The medial (septal) branch passes over the anterior sphenoid wall, 1 cm above the posterior choana, to the posterior septum, where it divides into several branches that travel anteriorly to anastomose in Kiesselbach plexus. • A branch of the SPA may run within the posterior maxillary fontanelle and may cause bleeding during surgery when wee large middle meatal antrostomy. • Division of the maxillary artery before the sphenopalatine foramen occurs in about 75% of cases. The number of branches varies from 2 to 10 branches.

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• The crista ethmoidalis of the palatine bone which is located anterior to the sphenopalatine foramen is a reliable landmark to the SPA. • Asymmetry of the maxillary and sphenopalatine arteries occurs in 3% of subjects only.

6.1.3 The Anterior and Posterior Ethmoid Arteries • The anterior and posterior ethmoidal arteries are branches from the ophthalmic artery (internal carotid system). • The anterior ethmoid artery is the larger and most constant one. • The posterior ethmoid artery may be absent in up to 30%. • The arteries exit the orbit through the frontoethmoid suture and travel medially usually in bony canals across the ethmoid sinus, entering the anterior cranial fossa through the lateral lamella of the cribriform plate. The anterior ethmoidal artery crosses the skull base in an anteromedial direction. The artery mesentery can run few millimeters below the fovea ethmoidalis in nearly 30% of individuals. This finding occurs more common in presence of supraorbital ethmoidal recess. While the posterior ethmoidal artery is located embedded into the fovea ethmoidalis running in a transverse direction. The middle ethmoidal artery exists in nearly 30% of population. • Terminal branches of the two arteries supply the dura of the anterior fossa and the upper part of the nasal cavity. • The 24–12–6 rule: the average distance from the orbital rim to the anterior ethmoid artery is 24  mm; from the anterior to the posterior ethmoidal artery is 12 mm; and the distance from the posterior ethmoid artery to the optic nerve is 6 mm. The anterior ethmoidal artery crosses the skull base in an anteromedial direction. The artery mesentery can run few millimeters below the fovea ethmoidalis in nearly 30% of individuals. This finding occurs more common in presence of supraorbital ethmoidal recess. While the posterior ethmoidal artery is located embedded into the fovea ethmoidalis running in a transverse direction. The middle ethmoidal artery exists in nearly 30% of population.

6.1.4 Definition and Classification • Epistaxis means bleeding from the nose. • Epistaxis may occur at any age with a bimodal distribution with two peaks: –– The first peak is during childhood usually from the Little’s area. –– The second peak is in the fifth or six decades and is frequently associated with hypertension. Epistaxis in older people is more likely to arise from the posterior part of the nasal cavity and is generally more severe than anterior epistaxis. • Epistaxis has been classified as anterior or posterior according to the bleeding site. The pyriform aperture or the middle turbinate may be used as arbitrary lines between anterior and posterior sites. Posterior bleeding is usually more severe and more difficult to control than anterior bleeding. • Epistaxis is either primary (idiopathic) in 70–75% of cases or secondary (due to a known cause) in the remaining 25–30%.

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6.1.5 Primary (Idiopathic) Epistaxis • Primary epistaxis is defined as spontaneous idiopathic bleeding from the nose in the absence of a definite cause. It usually occurs in children. • Primary epistaxis usually starts from the Little’s area since this area is easily accessible to digital trauma, as well as being susceptible to drying and exposure to irritants. • Primary epistaxis is usually mild and can be controlled easily.

6.1.6 Secondary Epistaxis Secondary epistaxis is epistaxis that is due to a known cause. There are numerous causes of secondary epistaxis:

6.1.6.1 Local Causes 1. Congenital:(Hereditary hemorrhagic telangiectasia, Osler–Weber–Rendu disease). 2. Trauma (nose picking, fractures, foreign bodies). 3. Inflammation (rhinitis, granulomatous diseases). 4. Neoplasms (bleeding polyps or angioma of the septum, juvenile angiofibroma, and malignant sinonasal neoplasms). 5. Septal deviations (particularly spur deviations). 6.1.6.2 General Causes 1. Hypertension: The association between hypertension and epistaxis, this remains controversial. Hypertension, however, is likely to prolong the duration of epistaxis. Hypertensive patients are frequently atherosclerotic, and it is believed that the state of the arterial wall in those patients may contribute to the severity and recurrence of epistaxis. 2. Anticoagulants (warfarin, aspirin). 3. Blood diseases (hemophilia, purpura, leukemia). 4. Environmental (high altitude, excessive dryness). 5. Endocrine (menstruation, pregnancy).

6.1.7 Management of Epistaxis The main lines of treatment are: A. First-aid measures. B. General measures. C. Control of bleeding. D. Treatment of the cause.

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6.1.8 First-Aid Measures • The patient is instructed to sit with the body tilted forward and the mouth open, and then to pinch the ala of the nose and hold for 10–15 min without releasing while breathing through the open mouth. • A piece of cotton soaked with decongestant solution may be inserted in the nose unless the patient is hypertensive. • Lying down should be avoided unless the patient feels faint.

6.1.9 General Measures • The patient is examined for signs of shock. • Respiration and circulation are secured, and intravenous access is established if necessary. • Investigations include a full blood count, bleeding and coagulation profile, and blood for group in severe cases.

6.1.10 Control of Bleeding • Controlling epistaxis with cautery, if a specific bleeding site can be identified, is preferred to nasal packing. • Bilateral cauterization is not recommended to avoid the possible risk of septal perforation.

6.1.10.1 Nasal Cautery • The bleeding point may be sealed with chemical cautery (silver nitrate stick), electrocautery, or bipolar diathermy. (a) Chemical cautery with silver nitrate sticks is patients, particularly children, with mild anterior epistaxis. Using silver nitrate solution is not recommended. (b) Electrocautery or diathermy (monopolar or bipolar) is the most precise way to control bleeding when the bleeding points can be identified preferably with the use of the endoscope. 6.1.10.2 Nasal Packs • Nasal packing (or tamponade) is indicated when cautery is not possible or effective. Several methods of packing are available.

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• Ribbon gauze impregnated with Vaseline, petroleum jelly, or bismuth iodoform paraffin paste (BIPP) that is inserted in layers. • Polyvinyl acetate (PVA) expandable polymer sponge (Merocel) or other non-­ absorbable packs. • Biodegradable dissolvable hemostatic packs such as oxidized cellulose and microfibrillar collagen. These packs have the advantage of achieving a better direct contact with the area of bleeding, and not needing to be subsequently removed. • Nasal packs may induce complications including sinusitis, toxic shock syndrome, airway compromise, missing a pack inside the nose, and recurrent bleeding after pack removal.

6.1.10.3 Nasal Balloons • These can be particularly useful for posterior bleeding from the nose or the  nasopharynx. Balloons have the advantage of keeping the nasal airway patent. 6.1.10.4 Hot Water Irrigations • Nasal irrigation with hot water at 50 °C (122 °F) has been reported as an effective means of stopping inaccessible or diffuse bleeding. It is assumed that edema of the mucosa may compress the bleeding capillaries. 6.1.10.5  Tranexamic Acid • The use of Tranexamic acid, which is antifibrinolytic agent, to slow the resolution of clotted blood is still controversial. Down. 6.1.10.6  Arterial Control • The choice of which arterial vessel to control depends on the likely source of the bleeding. In most cases, the target is the sphenopalatine artery. • The sphenopalatine artery (Fig. 6.3) can be exposed endoscopically by raising a posterolateral mucosal flap beneath the posterior end of the middle turbinate and identifying the ethmoidal crest of the palatine bone which points to the sphenopalatine foramen. The artery with all its branches can then be coagulated or clipped. • Clipping of the maxillary artery is nowadays only done as step of other surgical procedures to address posterior sinonasal tumors. • The anterior ethmoidal artery can be approached endoscopically, just behind the frontal recess, or through external approach through a medial orbital incision. The artery is usually located about 2.5 cm deep to the orbital rim just above the level of the medial canthus. • Selective arterial embolization technique, via catheterization of the maxillary artery, may be used in certain cases to occlude the feeding arteries within the nose.

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Fig. 6.3 Clipped sphenopalatine artery

6.1.11 Treatment of the Cause • Local or systemic causes of epistaxis, if present, should be managed in order to avoid recurrence of bleeding.

6.1.12 Hereditary Hemorrhagic Telangiectasia (Osler–Weber– Rendu Disease) • Hereditary hemorrhagic telangiectasia is an autosomal dominant genetic disorder caused by defects in a transforming growth factor-β (TGF-β) receptor. • The genetic defect causes loss of the muscularis layer and weakness of the elastic lamina of both venous and arterial vessels. • The disease causes recurrent epistaxis associated with telangiectasias on the skin and mucosal surfaces. • The four clinical diagnostic criteria are: 1. Epistaxis. 2. Telangiectasia. 3. Visceral lesions (lungs, gastrointestinal tract, liver, and brain). 4. First-degree relative with the disease.

6.1.12.1 Treatment • Cauterization (laser, bipolar, and radiofrequency). • Septodermoplasty. • Young’s procedure (complete anterior nasal occlusion from the raising of medial and lateral anterior nasal skin flaps). • In-office injected sclerotherapy or injected bevacizumab (a monoclonal antibody that inhibits vascular endothelial growth factor). • Oral tranexamic acid.

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6.2 Nasal Obstruction • Nasal obstruction is a common symptom that can affect the quality of life. • Nasal allergy and viral infections are the commonest causes of nasal obstruction. • Allergy and adenoids are common causes of nasal obstruction in children.

6.2.1 Classifications of Nasal Obstruction According to etiology: (a) Mucosal (e.g., rhinitis and allergy). (b) Structural (e.g., adenoids and septal deviation). (c) Mixed. According to duration: (a) Fluctuating. (b) Constant nasal is usually due to structural or mixed pathology. According to laterality: (a) Unilateral nasal obstruction usually points to structural abnormality or unilateral pathology (antrochoanal polyp, odontogenic pathology). (b) Bilateral. (c) Alternating nasal obstruction is actually a variety of bilateral nasal obstruction and is frequently position-related. D. According to position: (a) Position dependent (allergy, rhinitis, rhinosinusitis). (b) Non-position dependent (septal deviation, tumors). A. B. C.

6.2.2 Etiology of Nasal Obstruction A. B.

Nasal Obstruction due to Mucosal Pathology: 1. All forms of rhinitis. 2. Nasal allergy. 3. Acute rhinosinusitis. 4. Chronic rhinosinusitis. 5. Fungal rhinosinusitis. 6. Mucosal pathology due to systemic diseases. Nasal Obstruction due to Structural Abnormality. (a) Congenital. 1. Choanal atresia. 2. Pyriform fossa stenosis. (b) Acquired. 1. Adenoids. 2. Trauma. 3. Septal deviation. 4. Septal perforation. 5. Hypertrophy of the turbinates.

6.3 Olfactory Disorders



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6. Nasal valves dysfunction. 7. Nasal polyps. 8. Sinonasal and nasopharyngeal tumors and cysts.

6.2.3 Causes of Nasal Obstruction in Children 1. Choanal atresia/pyriform aperture stenosis. 2. Congenital masses and cysts. 3. Foreign bodies. 4. Adenoids. 5. Rhinitis and allergy. 6. Nasal polyps (cystic fibrosis). 7. Structural deformity.

6.2.4 Assessment of Nasal Obstruction A. B.

Subjective: 1. History taking (laterality, duration, other symptoms). 2. Validated questionnaire (NOSE scale, SNOT 22). Objective: 1. Clinical examination and nasal endoscopy. 2. Radiologic examination (CT scans, MRI). 3. Rhinomanometry and acoustic rhinometry (mostly of academic interest).

6.3 Olfactory Disorders • Normal olfaction (Normosmia) may be defined as the ability to detect most of tested odors in each olfactory test. • Some studies estimate up to 5% of people to have olfactory dysfunction without being aware of it. • Retronasal olfaction is the perception of odors emanating from the oral cavity during eating and drinking, as opposed to orthonasal olfaction, which occurs during sniffing. • Smell sensation is closely related to taste sensation. • Changes in olfaction may happen with age and may significantly impair quality of life. • Anosmia (total loss of smell) may expose the patients to dangerous situations like inability to recognize smoke and gas. Ageusia (complete loss of taste) is very rare due to multiple innervations of taste. Hypogeusia and dysgeusia are more common. • Olfactory disorders, in general, are more common in the geriatric population. • Loss of smell, and consequently taste alterations, is a frequent association with COVID 19 infections.

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• From a clinical point of view, it is important to distinguish between qualitative and quantitative olfactory disorders. • Malingering is not ruled out by ammonia test due to olfactory/trigeminal interactions centrally.

6.3.1 Classification of Olfactory Disorders 6.3.1.1 According to Etiology (a) Conductive: due to pathologies preventing air from reaching the olfactory area (e.g., polyps). (b) Sensory: due to damage of the olfactory mucosa (e.g., post covid). (c) Neural: due to damage of the olfactory neurons (e.g., neurodegenerative disorders). 6.3.1.2 According to Type Quantitative Olfactory Disorders • Quantitative olfactory disorders are defined as decreased or increased sensation without change in the character of the odor. (a) Hyposmia is decreased olfactory function. (b) Anosmia is total loss of olfactory function. (c) Specific anosmia is loss perception of only certain odors. (d) Hyperosmia is increased above average olfactory function. Qualitative Olfactory Disorders • Qualitative olfactory disorders are defined as abnormal perception of odors sensation: (a) Dysosmia is qualitative change or distortion of the perception of smell. (b) Parosmia is changed perception of odors that are usually into unpleasant ones. (c) Phantosmia is the perception of smells in the absence of an odor source usually in the form of unpleasant odors. (d) Olfactory agnosia: inability to detect and specify one odor. • Parosmia and phantosmia usually follow viral infections or head trauma and frequently improve spontaneously over months or years. They may also be due to some neurologic and psychiatric disorders.

6.3.2 Causes of Olfactory Dysfunction 6.3.2.1 Conductive Olfactory Dysfunction • Any cause of nasal obstruction may cause hyposmia/ anosmia. The extent of olfactory loss is proportionate to the degree of obstruction.

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6.3.2.2 Sensory Olfactory Dysfunction 1. Damage to the olfactory neuroepithelium. 2. Viral upper respiratory infections (particularly covid 19) due to damage of the olfactory receptors. 60–70% of patients may recover within 1–2 years after the viral infection. One-third of those patients suffer from dysosmia. 3. Primary atrophic rhinitis (ozaena). 4. Trauma the olfactory region can lead to anosmia. Patients may develop parosmia and phantosmia several months after the trauma. 5. Radiotherapy. 6. Exposure to noxious chemicals and vapors. 6.3.2.3 Neural Olfactory Dysfunction 1. Congenital anosmia due to hypoplasia or aplasia of the olfactory bulbs. 2. Old age. 3. Neurodegenerative disorders such as idiopathic Parkinson disease, Alzheimer disease. 4. Tumors: Olfactory groove meningiomas and Esthesioneuroblastoma. 6.3.2.4 Psychogenic (e.g., schizophrenia)

6.3.3 Assessment of Olfactory Function • Olfactory function can be assessed by subjective or objective methods:

6.3.3.1 Subjective Methods • Smell identification tests: An odorant is presented at supra-threshold concentration, and the patient has to identify the odor from a list of descriptions of odors. These tests are used to detect malingerers. • Threshold testing: The odorant is presented to the patient in ascending and descending concentrations, and the patient is asked to identify the least detectable concentration of the odorant. Examples of the currently available tests include: 1. UPSIT (University of Pennsylvania Smell Identification Test) which is a scratch and sniff test that uses patches impregnated with odorants. 2. Sniffin’ sticks test which combines threshold and odor identification. 6.3.3.2 Objective Methods • Objective measures are not validated so far and are usually used for research purposes: 1. Olfactory Bulb Volumetry. 2. Olfactograms: Measurement of the electrical potentials of the olfactory epithelium in response to olfactory stimulation. 3. Olfactory event-related potentials: EEG of olfaction with pleasant and unpleasant odors. If absent, suggest anosmia with bad prognosis.

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6.3.4 Treatment • The treatment of olfactory disorders mainly depends on the etiology. Some etiologies like age-related and congenital anosmia is permanent. • Spontaneous recovery may occur within 1–2  years with regeneration of the olfactory neuroepithelium. Recovery rates are much better in post-viral patients (up to 60%) than in post-traumatic patients (up to 20%). • There is no specific treatment for post-viral and post-traumatic olfactory anosmia or qualitative dysfunctions. The use of oral for topical steroids is not evidence based. • Olfactory training which means that patients regularly smell odorous substances may enhance recovery of smell in some patients.

6.4 Headache • The classification of headache is complex and often controversial. • Classification of the International Headache Society (HIS): –– Primary headaches: Migraine (seven groups, of which migraine with aura and migraine without aura are the commonest). Tension-type headache (episodic tension headache, chronic tension headache, and probable tension headache). Trigeminal autonomic cephalalgias (cluster headache and paroxysmal hemicrania). Other primary headaches. These include primary stabbing headache, primary cough headache, primary exertional headache, primary headache associated with sexual activity, hypnic headache, primary thunderclap headache, hemicrania continua, and new daily persistent headache. –– Secondary headaches: Secondary headaches include headache or facial pain attributed to disorders of nose, sinuses, teeth, mouth, eyes, ears, or other facial or cranial structures. It occurs due to stretching, compression, or inflammation of pain-sensitive structures the affected area. –– Painful cranial neuropathies (neuralgias and facial pain). • The term “rhinogenic headache” is debatable and controversial. In real life, most patients with headache visiting ENT clinics are actually suffering from primary headaches. • Facial plain is one of the major criteria of acute sinusitis. However, the association of chronic rhinosinusitis and headache is controversial and not evidence based so far. • “Contact headache” is another controversial category. It is assumed that pressure on the trigeminal nerve endings at the contact point by a deviated septum or spur will trigger facial pain or headache, and application of a local anesthetic with decongestant to the contact point will relieve the headache.

6.4 Headache

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6.4.1 Tension Headache • • • •

Most common type of primary headaches. More common in females. Common family history. Tightening or band-like sensation around forehead and temples—may spread to occiput usually, bilateral.

6.4.2 Migraine Headaches • More common in females (18%) than males (6%). • Age of onset: second to third decades. • May occur with or without aura. Aura, when present, immediately precedes headache and lasts less than 1 h. • Sudden onset. Frequently starts in the morning. May be triggered by stress. • Severe usually unilateral throbbing pain. May be bilateral in 40% of cases. • May last up to 72 h. • May be associated with nausea and vomiting, dizziness, photophobia, or phonophobia.

6.4.3 Cluster Headaches • Middle-aged patients. • Symptoms-free periods. • Severe or very severe unilateral orbital, supraorbital, and/or temporal pain lasting. • Up to 3 h if untreated. • May be associated with ipsilateral lacrimation, conjunctival injection, nasal congestion, facial sweating, ptosis, or miosis.

6.4.4 Neuralgias • Trigeminal neuralgia. –– Paroxysmal attacks of sudden pain lasting up to 2 min, affecting one or more divisions of the trigeminal nerve (usually maxillary or mandibular). –– More common in females. –– Age of onset >50 years. • Herpetic/post-herpetic neuralgia. • Glossopharyngeal neuralgia. • Tolosa-Hunt syndrome (painful ophthalmoplegia caused by nonspecific inflammation of the cavernous sinus or superior orbital fissure). • Gradenigo syndrome (Trigeminal neuralgia and VI nerve palsy due to petrositis complicating otitis media).

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MCQs 1. Parosmia is: (a) Perception of smells in the absence of an odor source usually in the form of unpleasant odors (b) Decreased olfactory function (c) Changed perception of odors that are usually into unpleasant ones (d) Quantitative change in the perception of smell 2. Crista ethmoidalis is a part of: (a) Ethmoid bone (b) Palatine bone (c) Basal lamella (d) Inferior concha 3. The distance between the anterior and posterior ethmoid arteries is: (a) 24 mm (b) 6 mm (c) 12 mm (d) 18 mm 4. The sphenopalatine foramen is located behind: (a) Uncinate process (b) Inferior concha (c) Crista ethmoidalis (d) Posterior end of superior turbinate 5. The nose scale is used to assess: (a) Nasal obstruction (b) Severity of headache (c) Olfactory function (d) Mucociliary clearance 6. Choanal atresia is an example of: (a) Mucosal nasal obstruction (b) Alternating nasal obstructions (c) Position-dependent nasal obstruction (d) Structural nasal obstruction 7. Olfactory function can be examined by all of the following tests except: (a) UPSIT (b) Sniffin’ sticks test (c) Saccharin test (d) Olfactometry 8. Primary epistaxis usually starts from: (a) Woodruff’s plexus (b) Little’s area (c) Posterior ethmoid artery (d) None of the above

6.4 Headache

9. The septal branch of sphenopalatine artery runs: (a) Across the floor of the choana (b) Below the ostium of sphenoid sinus (c) Behind the posterior fontanelle (d) Along the clivus 10. Specific anosmia is: (a) Perception of bad odors (b) Anosmia associated with change in taste (c) Decreased sense of smell (d) Loss perception of only certain odors Answers 1. (c) 2. (b) 3. (c) 4. (c) 5. (a) 6. (d) 7. (c) 8. (b) 9. (b) 10. (d)

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Choanal Atresia and Congenital Nasal Masses

7.1 Choanal Atresia • Congenital choanal atresia is due to persistence of the primitive bucconasal membrane, in the form of either a bony plate (10%), a fibrous membrane (30%), or both (60%). • Bilateral choanal atresia may cause respiratory distress since neonates are obligate nasal breathers. • Incidence: 1 in 8000 live births. • Females are more commonly affected than males. • Unilateral atresia is more common than bilateral (2:1). • About 20–25% of patients have other associated anomalies or syndromes including the CHARGE syndrome. • The CHARGE syndrome is an autosomal dominant genetic disorder including the following: –– Choanal atresia. –– Retarded growth. –– Cardiac anomalies such as atrial septal defect. –– Coloboma of the iris. –– Microphthalmos. –– Genitourinary hypoplasia and hydronephrosis. –– Ear abnormalities.

7.1.1 Clinical Picture 7.1.1.1 Bilateral Choanal Atresia • Bilateral atresia frequently presents as a respiratory emergency at birth since the newborn is an obligate nasal breather. • Cyclical respiratory distress with grunting, snorting, pallor, and cyanosis during closure of mouth or during feeding. The distress resolves with crying. © The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 S. Elwany, M. Askar, Rhinology Review, https://doi.org/10.1007/978-3-031-08794-3_7

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7  Choanal Atresia and Congenital Nasal Masses

Fig. 7.1 Unilateral choanal atresia in an adult. The atretic plate (black arrow) is mixed. Notice the bowing of the lateral nasal wall (white arrow)

• Feeding problems. • Retained nasal secretions. • Inability to pass a six-French catheter through the nose into the nasopharynx.

7.1.1.2 Unilateral Choanal Atresia (Fig. 7.1) • The primary symptoms of unilateral choanal atresia are unilateral nasal obstruction that may not be noticed until later in life. • Retained nasal secretions on the affected side. • No airway can be detected when holding a mirror (mirror test) below the nose after suctioning all secretions. • Inability to pass a catheter through the nose into the nasopharynx.

7.1.2 Investigations • A multislice computed tomography (CT) scan in the axial view is required to delineat: –– Location, thickness, and nature of atretic plate. –– Bowing of lateral nasal wall. –– Plain X-rays with instillation of radiopaque dye is obsolete and no longer used.

7.1.3 Differential Diagnosis 1. Pyriform aperture stenosis. 2. Midnasal stenosis.

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3. Neonatal rhinitis: neonatal rhinitis can mimic choanal atresia. Saline nose drops and in severe cases a short course of nasal steroid drops can be beneficial. 4. Nasal masses causing obstruction: meningoceles, encephaloceles, gliomas, dermoid cysts, and teratomas.

7.1.4 Management • Definitive treatment of choanal atresia is surgical. • Cases of unilateral atresia can be treated electively whenever appropriate. • In newborns with bilateral atresia, the priority is to insert and maintain an oropharyngeal airway. • Anesthetic considerations: –– Identification of associated anomalies especially cardiac anomalies. –– Avoidance of hypothermia. • Transnasal puncture: If the atresia is membranous, the patient may only require initial rupture of the atresia followed by serial dilations. • Endoscopic Transnasal repair (choanoplasty): In bony or mixed atresia, it is important to resect the plate as well as the posterior border of the nasal septum with a suitable burr or Kerrison′s forceps or curettes in order to create a wide choana. The surgery is performed with 2.7 or 4.0 mm endoscope (Fig. 7.2). • The use of flaps is controversial. • The use of stents is debatable. If stents are used, they are usual kept for 3–4 weeks. Care should be taken to avoid ulceration and necrosis of the ala of the nose and the columella. • Recurrent stenosis is the major problem of choanal atresia repair (10–45%) especially with bony or predominately bony atresia. It usually occurs during the first few months after surgery. It may be managed by a series of dilations of the choana every 4–8 weeks as needed or revision surgery and stunting. Fig. 7.2 Choanoplasty. The new choana (c) is widely open, and the uvula (v) is clearly seen

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Fig. 7.3  Pyriform fossa stenosis (double arrow)

7.2 Pyriform Aperture Stenosis • Congenital pyriform aperture stenosis (Fig. 7.3) is an uncommon cause of neonatal nasal obstruction. Its incidence is estimated to be 1/4th that of choanal atresia. • The stenosis may be associated with a single central incisor. • The usual presentation is cyclic respiratory distress similar to that of bilateral choanal atresia. • Surgical treatment is indicated when the condition is symptomatic in order to widen the pyriform fossa. The procedure (extramucosal pyriplasty) is performed via a sublabial incision. The stenotic bone is drilled out until sufficient nasal airway is established.

7.3 Congenital Nasal Masses • There are three important areas in the development of congenital nasal masses: (a) Fonticulus frontalis: this is the space between the frontal and nasal bones. It eventually fuses with foramen cecum to create a partition between the cranial cavity and the exterior. (b) Prenasal space: This is the space between the nasal bones and the nasal capsule (precursor of nasal cartilages). (c) Foramen cecum.

7.4 Meningoceles and Encephaloceles • These are extracranial herniations of the cranial contents through a defect in the skull (Fig. 7.4). They are classified as a neural tube defect and may be associated with other anomalies in 40% of cases.

7.4  Meningoceles and Encephaloceles

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a

b

c

d

e

f

Fig. 7.4 (a) Right meningoencephalocele in a child passing through a wide defect in the skull base. (b) CT of 2 years old baby showing left encephalocele herniating (M) through a skull base defect. (c) Resection of encephalocele (M) by bipolar cautery of its pedicle to separate it from its attachment to the skull base defect. (d) Endoscopic view of the skull base defect after ablation of the encephalocele. The white arrows points to the exposed bony rim after circumferential removal of the surrounding mucosa. (e) A piece of auricular cartilage (white arrow) was inserted in the epidural space. (f) A rotated mucoperiosteal flap from the nasal septum (white arrow) was used to cover the cartilage

• They may include meninges only (meningocele) or both brain and meninges (encephalocele/meningoencephalocele). • There are three types of encephaloceles:

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• • • •

(a) Sincipital encephaloceles (15%): The encephalocele herniates through a bony defect between the frontal and ethmoid bones anterior to the crista galli. (b) Basal encephaloceles (10%): The encephalocele herniates through a bony defect between the cribriform plate and the superior orbital fissure, presenting as an intranasal mass. (c) Occipital encephaloceles (75%): This is the most common form of this congenital disorder and is manifested as a swelling of different sizes over the occipital bone in the midline. Encephaloceles usually show positive Furstenberg’s test: applying pressure on the ipsilateral jugular vein elicits swelling or pulsation of the lesion. The diagnosis is radiologically confirmed by CT and/or MRI. MRI can also differentiate a meningocele from a meningoencephalocele. Early intervention in the first few months of life minimizes the risk of meningitis. Small lesions with minimal skull base defects may be managed endoscopically. Larger lesions require craniotomy/combined approach.

7.5 Gliomas • Gliomas are unencapsulated collections of glial cells situated outside the CNS. • About 5–20% of nasal gliomas have a fibrous stalk connection to the intracranial space. • Gliomas present as firm, non-compressible purple or gray mass. • Types: (a) Extranasal (60%). (b) Intranasal (30%). (c) Combined (10%). • Nasal gliomas appear hypo-or isointense on T1-weighted images and hyperintense on T2- weighted images. • The treatment of gliomas is by surgical excision. Intranasal gliomas can be excised with endoscopic techniques.

7.6 Nasal Dermoids • Dermoids are the most common congenital nasal mass. The incidence is estimated at 1:20,000 to 1:40,000 births. • Nasal dermoids develop due to incomplete obliteration of neuroectoderm in the developing frontonasal region. They constitute 1–3% of all dermoids and 10–12% of head and neck dermoids. • Congenital dermoids contain ectodermal and mesodermal embryonic elements. Mesodermal elements which include hair follicles, sebaceous glands, and sweat glands are found in the wall of the cyst and thus differentiate these masses from simple epidermoid cysts. Teratomas, on the other hand, contain all three embryonal germ layers.

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• The dermoids may have intracranial extension in 4–40% of cases. • Nasal dermoids manifest as a simple cyst, a cyst with a sinus tract, or a sinus tract alone. When there is a sinus tract, intermittent discharge or infection may occur. Protruding hair is seen in some patients and is pathognomonic. The cyst does not transilluminate, and Furstenberg test is negative. • CT and MRI have the gold standard in radiographic evaluation of nasal dermoid. Preoperative imaging should assess the anatomy of the sinonasal and cranial base with proper evaluation for intracranial extension. A bifid crista galli and an enlarged foramen cecum suggest intracranial extension. • Several extracranial approaches have been described for the excision of nasal dermoids including external rhinoplasty approach, midline vertical incisions, and medial paracanthal incision. The external rhinoplasty approach, when feasible, provides the best cosmetic result. MCQs 1. Positive Furstenberg’s test is one of the signs of: (a) Ethmoid mucocele (b) Dermoid with intracranial extension (c) Glioma (d) Encephalocele 2. The most common congenital nasal mass is: (a) Teratoma (b) Dermoids (c) Meningocele (d) Glioma 3. Neonatal cyclical respiratory distress is sign of: (a) Unilateral choanal atresia (b) Severe septal deviation (c) Bilateral choanal atresia (d) Adenoid hypertrophy 4. Choanal atresia can be best diagnosed by: (a) Axial CT scan (b) T1 MRI (c) T2 MRI (d) Sagittal CT scan 5. CHARGE syndrome may include all of the following except: (a) Choanal atresia (b) Cardiac anomalies (c) Diaphragmatic hernia (d) Genitourinary anomalies 6. Extramucosal pyriplasty is used for treatment of: (a) Unilateral choanal atresia (b) Bilateral choanal atresia (c) Pyriform aperture stenosis (d) Nasolacrimal duct stenosis

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7. Endoscopic choanoplasty usually includes resection of: (a) Posterior border of nasal septum (b) Posterior ends of inferior turbinates (c) Posterior ends of middle turbinates (d) All of the above 8. The most common type of encephaloceles is: (a) Sincipital (b) Occipital (c) Basal (d) Mixed 9. Which of the following lesions may be associated with a sinus: (a) Extranasal glioma (b) Dermoids (c) Sincipital encephalocele (d) None of the above 10. The percentage of nasal gliomas that have intracranial extension is: (a) 1–5% (b) 5–20% (c) 25–30% (d) 40–55% Answers 1. (d) 2. (b) 3. (c) 4. (a) 5. (c) 6. (c) 7. (a) 8. (b) 9. (b) 10. (b)

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Nasal Trauma

8.1 Foreign Bodies in the Nose • Foreign bodies in the nose are common in children. • Inert foreign bodies like beads and buttons may be asymptomatic and discovered only accidentally during an examination for an unrelated complaint. • Organic foreign bodies like peas, nuts, and rubber are irritants and usually become symptomatic. • Alkaline batteries (Fig. 8.1) are especially dangerous since they may leak into the nasal cavity causing mucosal ulcerations and even septal perforations. • If the foreign body is left in the nose for long time, calcium and magnesium carbonates and phosphates may deposit over it producing a “rhinolith” (Fig. 8.2). Rhinoliths usually become impacted and require removal under a general anesthetic.

8.1.1 Clinical Picture 1. Unilateral malodorous discharge which may be blood-stained. This is the diagnostic and most characteristic symptom. 2. Unilateral nasal obstruction. 3. The foreign body may be seen or felt with a probe and is frequently surrounded by thick offensive discharge.

8.1.2 Investigations • Plain X-rays can reveal a radiopaque foreign body (Fig. 8.1).

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 S. Elwany, M. Askar, Rhinology Review, https://doi.org/10.1007/978-3-031-08794-3_8

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76 Fig. 8.1  An alkaline battery within the right nasal cavity of a child. Alkaline batteries, if left in place, may leak and causes mucosal ulcerations and necrosis

Fig. 8.2  A small rhinolith in the left nasal cavity of a child. Rhinoliths form by deposition of calcium salts on neglected foreign bodies. Rhinoliths, if left in place, increase in size and become impacted in the nasal cavity. The discharge around the rhinolith is typically malodorous

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8.2  Fractures of the Nasal Bones

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8.1.3 Treatment • Removal of the foreign body after shrinking of the nasal mucosa by decongestant nasal drops. General anesthesia may be required in some cases.

8.2 Fractures of the Nasal Bones • The commonest causes of nasal bones fractures are assault, road traffic accident, and sports injuries. • Low-velocity trauma usually results in isolated nasal bones fracture. High-­ velocity trauma may result in additional facial fractures as well as fractures of the ethmoid labyrinth.

8.2.1 Types of Fracture of the Nasal Bones • There are four types according to the direction of trauma (Fig. 8.3): –– Type I fracture: Lateral trauma. –– Type II fracture: Fronto-lateral trauma. –– Type III facture: Frontal trauma. –– Type IV fracture: Caudal-frontal trauma. • Type I fractures may be associated with a horizontal (Jarjavay′s septal fracture) or C-shaped fracture of the septum. The fracture may displace the whole nose to the side opposite the blow. • Type II and III fractures may be associated with a vertical fracture of the septum (Chevallet′s septal fracture). Fig. 8.3  The direction of trauma determines the type of nasal fractures: (1): Lateral trauma. (2): Fronto-lateral trauma. (3): Frontal trauma. (4): Caudal-frontal trauma

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8.2.2 Clinical Features 1. Swelling, deformity, or deviation of the external nose. 2. Facial hematoma. 3. Septal hematoma or deviation. 4. Telecanthus and bruising under the eyes. 5. Associated injuries may coexist.

8.2.3 Investigations Plain radiographs of the nasal bones. Radiographs may also be needed for medicolegal purposes. 3D reconstructions for detailed information and more severe cases (Fig. 8.4).

8.2.4 Management • Treatment my not required in mild cases when there is no external deformity. • If there is external swelling, the patient should be reviewed again when the swelling has subsided. Evidence shows that nasal bone fractures may be mobile up to about 3 weeks post-injury. • Most fractures can be reduced preferably under general anesthesia after subsidence of external swelling. Disimpaction and realignment can usually be achieved with digital pressure and Walsham′s forceps, one blade in the nasal cavity and the other outside (with skin protection). Splinting is usually needed after correction. • Septal fractures do not need treatment unless there is septal deviation or hematoma. • Immobile healed nasal fractures will need rhinoplasty. Fig. 8.4 3D reconstruction of fractured nasal bones

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8.3 Septal Hematoma • Collection of blood beneath the mucoperichondrium of the nasal septum. • There is a unilateral or bilateral boggy nasal swelling that may completely occlude one nostril. • If septal hematoma is missed or become infected, a septal abscess will develop with further cartilage necrosis, and a saddle deformity may occur. • Aspiration alone is usually not enough, and blood will usually re-collect again unless the dead space is obliterated with quilting sutures. • Incision and drainage with quilt suturing (to obliterate the dead space) are the standard treatment and are required for most hematomas. • The patient should be given a course of antibiotics to reduce the risk of a secondary septal abscess.

8.4 Fractures of the Midface (Le Fort Fractures) Le Fort fractures are fractures of the midface, which involve separation of all or a portion of the midface from the skull base: • Le Fort type I –– Horizontal maxillary fracture, separating the teeth from the upper face. –– Fracture line passes through the alveolar ridge, lateral nose and inferior wall of the. It is also known as a Guerin fracture. • Le Fort type II –– A pyramidal fracture, with the teeth at the pyramid base, and nasofrontal suture at its apex. –– Fracture arch passes through the posterior alveolar ridge, lateral walls of maxillary sinuses, nasal bones, and inferior orbital rim. –– Uppermost fracture line can pass through the nasofrontal junction or the frontal process of the maxilla. • Le Fort type III –– It is called also craniofacial disjunction. –– Transverse fracture line passes through nasofrontal suture, maxillo-frontal suture, orbital wall, and zygomatic arch.

8.5 Frontal Sinus Fractures • Frontal sinus fractures (Fig.  8.5) may involve the anterior wall, the posterior wall, the nasofrontal recess, or they may be through and through. • The fracture lines may linear non-displaced, displaced, or compound. • Linear fractures may not need operative intervention. • Depressed or displaced fractures require elevation of fragments and excision of mucosa trapped between fragments. • Displaced posterior wall fractures—osteoplastic flap and fat obliteration. • Through and through fractures usually require a cranialization procedure at the time of anterior craniotomy.

80 Fig. 8.5  Multiple facial fractures following car accident. There is a depressed facture of the anterior wall of the left frontal sinus (black arrow), and multiple fractures involving the zygoma, maxilla, orbital floor, and nasal bones (white arrows). There is also Le Fort I facture on the right side (horizontal black arrow)

MCQs 1. Chevallet′s septal fracture is: (a) Transverse fracture (b) Vertical fracture (c) C-Shaped fracture (d) Comminuted fracture 2. Craniofacial disjunction refers to: (a) Le Fort I fracture (b) Le Fort II fracture (c) :e Fort III fracture (d) None of the above 3. Type III nasal bones fracture results from: (a) Frontal trauma (b) Fronto-lateral trauma (c) Lateral trauma (d) Any of the above 4. Guerin fracture refers to: (a) Le Fort II fracture (b) Le Fort I fracture (c) :e Fort III fracture (d) None of the above

8  Nasal Trauma

8.5  Frontal Sinus Fractures

5. Jarjavay′s septal fracture is a: (a) Transverse fracture (b) Vertical fracture (c) C-Shaped fracture (d) Comminuted fracture 6. A typical symptom of foreign bodies in the nose is: (a) Headache (b) Anosmia (c) Unilateral watery discharge (d) Unilateral malodorous discharge 7. Which of the following fractures is pyramidal in shape? (a) Le Fort I (b) Le Fort II (c) Chevallet′s fracture (d) Le Fort III 8. Nasal bone fractures may be mobile up to: (a) 1 week (b) 6 weeks (c) 3 weeks (d) 8 weeks 9. Linear non-displaced frontal bone fractures require: (a) Osteoplastic flap (b) Trephine procedure (c) Eyebrow incision (d) No intervention 10. Inert foreign bodies include (a) Beads (b) Peas (c) Beans (d) Alkaline batteries Answers 1. (b) 2. (c) 3. (a) 4. (b) 5. (a) 6. (d) 7. (b) 8. (c) 9. (d)

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9.1 Septal Deviation • Septal deviations are present in almost 50–75% of the general population without gender difference. In most cases, septal deviations are asymptomatic. • Septal deviations (Fig. 9.1) are present in about 20–30% of patients complaining from nasal obstruction. Fig. 9.1  The nasal septum is deviated to the left (arrows). There is also compensatory hypertrophy of the right inferior turbinate (RIT)

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• Etiology of Septal Deviations: 1. Congenital: During intrauterine life, due to compression of the facial structures of the fetus (maxillary molding theory). 2. Birth trauma: Septal deviation is more frequent in newborns delivered in the occipitoposterior position, and those who needed forceps deliveries. The trauma cause micro-fractures and unbalanced growth of the septum later on. 3. Accidental trauma: The nose is probably the organ most commonly exposed to accidental trauma which may result in septal fractures and/or deviations. • Types of Septal deviations: Several types of septal deviations have been commonly described (Figs. 9.2 and 9.3): 1. C-shaped deviations. 2. S-shaped deviations. 3. Spur deviations (acute angle deviations). 4. Anterior or caudal dislocation: Dislocation of the caudal edge of the septal cartilage. 5. Combinations of the above types. • Symptoms of Septal Deviations: 1. Nasal obstruction: This is the primary symptom of septal deviation. It may be unilateral or bilateral but it is characteristically constant. 2. External deformity as a part of a crooked nose. 3. Epistaxis due to the stretch and exposure of septal blood vessels. 4. Symptoms of associated sinusitis, e.g., headache. a

b

c

Fig. 9.2  Common types of septal deviations: (a) C-shaped deviation. (b) S-Shaped deviation. (c) Acute angle deviation

9.1 Septal Deviation

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Fig. 9.3  Dislocation of the caudal edge of septal cartilage (arrows)

• Surgery of Septal Deviations: –– There is no medical treatment for septal deviations. The indications of surgery are: 1. Symptomatic patients. 2. Presence of a complication, e.g., recurrent or chronic sinusitis. 3. The need of wider access to the posterior or superior nasal cavity during endoscopic surgery. 4. As a part of rhinoplasty (septorhinoplasty). –– The aim of surgery is to remove the obstructing components and at the same time preserve the integrity of the septum and the skeletal support of the external nose. –– In all septal surgeries, it is crucial to main the stability and strength of the L-strut in order to avoid saddle nose deformity or loss of tip support. –– Incisions for Septal Surgery: Two types of incisions can be utilized for septoplasty: 1. The classic Killian incision. This incision is done 0.5–1  cm behind the mucocutaneous junction. The incision is not suitable for patients with caudal dislocations or in association with rhinoplasty procedures. 2. Hemitransfixion incision or Cottle incision. This incision is specially used for patients with caudal deflections and in association with rhinoplasty procedures. The incision extends from the upper part of the caudal end of the septum to the area just anterior to the nasal spine along the caudal border of the septal cartilage. –– Submucous Resection Operation (SMR) 1. For many years, this was the original historic procedure for correction of septal deviation. 2. The concept of the procedure is to expose the deviated cartilage and bone bilaterally under the mucoperichondrium and mucoperiosteum, and then

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to resect them without sacrifice of mucosa and with maintenance of c­ audal and dorsal struts of septal cartilage (L-strut). The septal flaps are best approximated by a mattress suture. 3. Disadvantage of SMR procedure: (a) Not suitable for children. (b) Cannot address caudal deformities. (c) Higher risk of septal perforations. (d) Difficult revision surgery due to lack of cartilage or bone support. –– Septoplasty Procedures 1. The concept of all septoplasty procedures is conservative removal and/ or reconstruction of the deviated parts with preservation of skeletal support and restoration of normal physiologic nasal airway patency. 2. Submucosal tunnels are created on one or both sides of the septum between the cartilage and perichondrium to maintain the vascular supply of the septum. Deviated cartilage and spurs are resected. Pieces of the resected cartilage may be re-inserted to maintain skeletal support, and the septal flaps are approximated by a mattress suture. –– Endoscopic and Endoscopic Assisted Septoplasty (Fig. 9.4): 1. The advantages of using the endoscopes are: (a) Better visualization of the posterior and superior septum. (b) More conservative resection of isolated spurs. (c) Reduced risk of mucosal tears. –– Complications of Septal Surgery 1. Mucosa tears and septal perforations (Fig. 9.5). 2. Adhesions between the septum and lateral nasal wall. 3. Loss of tip support (droopy tip) due to loss of caudal support. 4. Saddle nose deformity or supratip depression due to failure to preserve the stability of the L-strut and keystone area (loss of skeletal support). 5. Trauma to the cribriform plate following aggressive manipulations of the perpendicular plate of ethmoid leading to anosmia and/or CSF rhinorrhea. 6. Residual deviations (incomplete surgery). 7. Recurrent deviations due to cartilage memory. a

c

b

0.0 0.2 0.4 0.6 0.8 1.0

Fig. 9.4  Endoscopic septoplasty. (a) Incision of septal cartilage (S). (b) Resection of septal cartilage (S). (c) Resection of posterior spur. LF left septal flap, RF right septal flap, SP spur, V vomer

9.2 Septal Perforations

a

87

b

Fig. 9.5  Septal perforations. (a) Anterior septal perforation (arrow). Lt left nasal cavity, RT right nasal cavity. (b) The posterior edge of huge septal perforation (*). LIT left inferior turbinate, LMT left middle turbinate, RIT right inferior turbinate, RMT right middle turbinate

• Hypertrophy of Inferior Turbinates with Septal Deviations –– Compensatory hypertrophy of the inferior turbinate is frequently seen with contralateral septal deviation (Fig. 9.1). –– Management of this compensatory hypertrophy is still controversial. –– Some authors found that spontaneous reversal of this hypertrophy eventually happens with no need to surgical intervention. –– Other authors reported that contralateral turbinoplasty enhanced subjective satisfaction of nasal airway patency.

9.2 Septal Perforations • Septal perforation (Fig.  9.5) is one of the challenging problems in rhinology. Most perforations are iatrogenic following septal surgery. • Etiology 1. Iatrogenic. The incidence of septal perforation after septoplasty is about 3% compared to 10–20% after submucous resection. 2. Trauma. 3. Cocaine and inhaled narcotics use. 4. Infected septal hematoma. 5. Septal abscess. 6. Infections, e.g., tertiary syphilis, mucormycosis, and tuberculosis. 7. Granulomatous disease, e.g., Wagener’s granulomatosis, Churg-­Strauss syndrome, and systemic lupus erythematosus. 8. Malignancy

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• Clinical Picture 1. Many patients remain asymptomatic until diagnosed in routine ENT examinations. 2. Nasal crusting. 3. Whistling (small perforations). 4. Nasal blockage. 5. Mild epistaxis or bloodstained discharge. 6. On examination: Septal perforations, unless very large, usually involve the cartilaginous septum. Huge septal perforation may create a single nasal cavity. 7. May be associated with saddling of the dorsum of the nose especially if the perforation is large. • Treatment –– Asymptomatic septal perforations do not require treatment. –– In the absence of clear etiology, laboratory investigations are essential to exclude granulomatous conditions. –– Non-surgical Treatment: Nasal hygiene and nasal washes and antibacterial or moisturizing ointments. Nasal septal buttons. These can bring some relief but are associated with crusting and are variably tolerated by the patients. –– Surgical Treatment: –– Surgical repair is challenging and is achieved through a variety of free grafts, pedicled flaps, or free flaps. Interposition grafts such as cartilage, temporalis fascia, periosteum, or acellular dermal allograft act as a scaffold and enhance healing. –– The surgical approach depends upon the size and location of the perforations: (a) Anterior perforation with size to 0.5 cm may be closed by the endonasal approach and advancement flaps. (b) Larger perforations up to 2 cm are better closed through external rhinoplasty approach with wide flaps and interposition grafts. Several type of flaps have described including septal flaps and inferior turbinate flaps. Some surgeons still prefer to use the endonasal approach for these perforations. (c) Other flaps have been described for larger perforations with limited success. These flaps include tunneled sublabial mucosal flap, facial artery musculomucosal flap, and microvascular free flaps.

9.3 Nasal Valves • There are two nasal valves: external and internal. Both of them are important in regulating nasal air flow. • The external nasal valve is bordered laterally by the alar sidewalls, medially by the columella, and inferiorly by the nasal floor (sill area).

9.3 Nasal Valves

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Fig. 9.6  The internal nasal valve (*) between the septal cartilage (SC) and the upper lateral cartilage (ULC)

• The internal nasal valve (Fig. 9.6) is the angle between the nasal septum and the upper lateral nasal cartilage. The angle normally measures about 15 degrees. The nasal valve area includes also the head of the inferior turbinate and the floor of the nose. • Function of the internal nasal valve: –– The internal nasal valve is the the narrowest part of the nasal airway, and it offers the highest resistance to the nasal air flow. –– As the air flows through the nasal valve, its pattern changes from laminar to turbulent. • Nasal valve dysfunction: Nasal valve dysfunction is commonly iatrogenic and less commonly due to accidental trauma. • Types of nasal valves dysfunction: (a) Dynamic (Fig. 9.7) due to weakening of the lower lateral nasal wall (alar collapse). (b) Static due to adhesions, fibrosis, and loss of cartilaginous support (Fig. 9.8). • Clinical diagnosis of nasal valve dysfunction: 1. Dynamic collapse of the external valve can be seen on inspiration. 2. Metal plate test: observing the condensation of exhaled air on a cold metal surface. 3. Cottle test: dragging the cheek laterally improves nasal air flow in cases of alar collapse or internal valve dysfunction. 4. Internal tenting test,or modified Cottle test, consists of intranasal insertion of a cotton bud at the point of the nasal valve weakness, and is more location specific than Cottle test. 5. Endoscopic examination of the nasal valve area.

90 Fig. 9.7  Alar collapse narrowing the left external nasal valve. The patency of the valve and the strength of the ala can be restored by a batten graft (*) as seen on the right side

Fig. 9.8 Extremely narrow right internal nasal valve (arrow). S septum, ULC upper lateral cartilage

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9.4 The Turbinates

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• Treatment of nasal valve dysfunction: –– Permanent treatment of nasal valves dysfunction requires surgery to restore the support, configuration, and function of the valve. Meanwhile, nasal appliances may be used as a temporary solution although they are frequently uncomfortable to the patient. –– Surgical techniques usually require the use of grafts: • External nasal valve: alar batten graft and lateral crural strut graft. These grafts can restore alar symmetry and increase tip projection. However, they may lead to loss of alar groove and thick alae. • Internal nasal valve: spreader grafts, spreader flaps, lateral flaring sutures, and butterfly grafts. Spreader grafts will widen the internal nasal valve and correct midvault collapse. A butterfly graft may cause supratip fullness.

9.4 The Turbinates 9.4.1 Inferior Turbinates • The inferior turbinate plays an important role in nasal airflow, and its head (anterior end) is part of the internal nasal valve area which accounts for about 50% of total airway resistance. • The inferior turbinate also contributes to warming, humidification, and filtering of inspired air. • Pathology of the inferior turbinates is common and is one of the most frequent causes of nasal obstruction. • Types of Turbinate Pathology (a) Pathologic hypertrophy: –– Pathologic hypertrophy is usually associated with chronic rhinitis and/or rhinosinusitis. A longstanding hypertrophied turbinate may exhibit polypoid or mulberry appearance. –– Hypertrophy of the turbinate should be differentiated from protrusion of the turbinate due to wide angle between the turbinate bone and the lateral nasal wall. (b) Compensatory hypertrophy: Compensatory hypertrophy occurs in patients with septal deviation (Fig. 9.1). It develops on the wide side of the nose as a physiological response to normalize its size and configuration. • Treatment of Turbinate Hypertrophy (a) Conservative Treatment –– Medical treatment is essentially treatment of the etiologic factor, e.g., allergy and chronic rhinitis. Local vasoconstrictor drops should be used intermittently for few days only. Patients who do not respond to proper medical treatment within 6 months should be considered for surgery. (b) Surgical Treatment –– Current indications for turbinate surgery are based on the patient’s symptoms and clinician assessment.

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–– The aim of turbinate surgery must be to reduce its size while preserving its structure and functions. Techniques that are unphysiological and unnecessarily destructive to the turbinate function should be abandoned. –– Excessive resection of the turbinate (Fig. 9.9) may lead to the development of the empty nose syndrome (excessively wide nasal cavity and decreased subjective perception of airflow by the patient). –– Types of Turbinate Reduction Procedures: (a) Resective procedures: These are cold procedures that reduce the size of the turbinates by resecting some of its tissues: 1. Turbinoplasty: This entails submucosal resection of the turbinate bone and surrounding tissues while preserving the whole mucosa. 2. Trimming of the turbinate by microdebrider or shaver usually in combination with an endoscope. This is better done submucosally (intraturbinally) in order to preserve the mucous membrane. (b) Restrictive procedures (Thermal turbinoplasty): The aim of these procedures is to induce submucosal fibrosis that will shrink the size of the turbinates and decrease its congestion: 1. High frequency submucosal diathermy. 2. Coblation surgery. 3. Laser turbinoplasty is no longer popular now. Fig. 9.9 Excessively resected right inferior turbinate (arrow). Note the air cell (concha bullosa) in the left middle turbinate (*). LIT left inferior turbinate

9.4 The Turbinates

93

9.4.2 Middle Turbinate • Abnormalities of the middle turbinate are classified into two types: (a) Anatomic variants. –– Concha bullosa. –– Paradoxically bent middle turbinate. (b) Pathological conditions. –– Polypoid middle turbinate. –– Mucocele of the middle turbinate (uncommon). • Concha Bullosa –– Concha bullosa (middle turbinate pneumatization) is an anatomical variant found in about 25% of the population (Fig. 9.10). A large concha bullosa may obstruct the osteomeatal complex and the infundibulum and predispose the development of sinusitis. –– When indicated, resection of the lateral wall of the air cell may be performed. –– Crushing of the middle turbinate (compression turbine-last) may be done in selected cases. • Paradoxically Curved Turbinate –– Paradoxically curved turbinate (Fig. 9.11) is a relatively uncommon anatomic variant that may compromise the ostiomeatal complex and the infundibulum. –– When indicated, limited resection of the paradoxical segment is performed. • Polypoid middle turbinate (Concha Polyposa) –– Polypoid middle turbinate is usually related to chronic rhinosinusitis and may add to ostial obstruction. –– When required, conservative trimming of the polypoid can be done preferably with a shaver. –– In all middle turbinate surgery, the stability of the middle turbinate should be maintained to prevent the occurrence of flail or lateralized middle turbinate. a

b

Fig. 9.10 (a) Right concha bullosa. CB concha bullosa, MM middle meatus, S septum. (b) Coronal CT scan showing bilateral concha bullosa (*)

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9  Nasal Septum, Nasal Valves, and Turbinates

Fig. 9.11  Left paradoxical middle turbinate (arrow)

MCQs 1. The internal nasal valve is the angle between: (a) The nasal bone and septal cartilage (b) The upper lateral cartilage and lower lateral cartilage (c) The upper lateral cartilage and septal cartilage (d) The ala of the nose and the columella 2. The primary symptom of deviation of the nasal septum is: (a) Epistaxis (b) Headache (c) Nasal obstruction (d) Mucoid nasal discharge 3. Dynamic external nasal valve dysfunction may happen due to: (a) S-shaped deviation of the nasal septum (b) Alar collapse or weakness (c) Hypertrophy of the anterior end of the inferior turbinate (d) Caudal dislocation of the nasal septum 4. A spreader graft may be used to: (a) Support the ala of the nose (b) Correct caudal dislocation (c) Widen a narrow internal nasal valve (d) Augment the anterior nasal spine

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5. The most common cause of septal perforation is: (a) Accidental trauma (b) Septal surgery (iatrogenic) (c) Wegener’s granulomatosis (d) Nasal tumors 6. Excessive resection of the inferior turbinates may lead to the development of: (a) Saddle nose (b) Alar collapse (c) Compensatory hypertrophy of the middle turbinates (d) Empty nose syndrome 7. Concha bullosa is a term used to describe: (a) Small ethmoid mucocele (b) Polypoid anterior end of the middle turbinate (c) Large agger nasi cell (d) Pneumatized middle turbinate 8. Advantages of endoscopic assisted septoplasty include all of the following except: (a) Better visualization of the posterior and superior septum (b) Easier correction of caudal dislocation of the septum (c) Conservative resection of isolated spurs (d) Less incidence of mucosal tears 9. High frequency submucosal diathermy of the inferior turbinate: (a) Induces submucosal fibrosis (b) Predisposes to empty nose syndrome (c) Is one of the resective turbinate procedures (d) Does not preserve the mucosa of the turbinate 10. Complications of submucous resection of the septum include all of the following except: (a) Septal perforations (b) Devitalization of roots of upper teeth (c) Supratip depression (d) Loss of nasal tip support 11. Which one of the following structures is a major component of the nasal septum? (a) Rostrum of the sphenoid bone (b) Vertical plate of the palatine bone (c) Vomer (d) Maxillary crest

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Answers 1. (c) 2. (c) 3. (b) 4. (c) 5. (b) 6. (d) 7. (d) 8. (b) 9. (a) 10. (b) 11. (c)

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• There is no universally accepted system for the definition, terminology, or the classification of rhinitis. • Rhinitis frequently affects patients’ quality of life and is commonly associated with sinusitis. The term “Rhinosinusitis” is frequently used. • Rhinitis is usually, and broadly, classified into infectious and non-infectious categories: –– The infectious category is the better-defined type. It may be viral, bacterial, or fungal in nature. –– The non-infectious category may be allergic or non-allergic in nature. • The diagnosis of viral or bacterial rhinitis is usually based on clinical grounds including the duration of the disease and the presence of purulent discharge I am and is not based on identification of specific organisms. • Allergic rhinitis is an IgE-mediated response to an antigen and occurs in genetically predisposed persons. • Non-allergic rhinitis (NAR) refers to a broad group of diverse nasal diseases that are not allergic in origin and not IgE-mediated. Some types of non-allergic rhinitis produce symptoms mimicking allergic rhinitis. • Generally speaking allergic rhinitis has a younger age of onset, a more positive family history, and a higher incidence of ocular symptoms. Female gender may be a risk factor for some types of allergic rhinitis.

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 S. Elwany, M. Askar, Rhinology Review, https://doi.org/10.1007/978-3-031-08794-3_10

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10.1 Classification of Rhinitis A. B.

Allergic Non-allergic (a) Infectious: (i) Viral (e.g., common cold). (ii) Bacterial (e.g., rhinoscleroma). (iii) Fungal (e.g., rhinosporidiosis). (b) Non-infectious: (i) Non-allergic rhinitis mimicking allergic rhinitis. 1. Vasomotor rhinitis. 2. Non-allergic rhinitis with eosinophilia (NARES). (ii) Occupational rhinitis. (iii) Gustatory rhinitis. (iv) Hormonal rhinitis. (v) Rhinopathy of pregnancy.

10.2 Allergic Rhinitis • Allergic rhinitis is an IgE-mediated type 1 hypersensitivity reaction of the nasal mucosa to allergens. Allergic rhinitis usually occurs in genetically predisposed persons. • Atopy means genetic predisposition to develop allergic IgE-mediated response to allergens. Patients with a family history of atopy have a higher risk of developing allergic diseases. • Allergic rhinitis has been estimated to affect 20–25% of the population. It is more common in children and younger age groups. It is not uncommon for children to “grow out of their allergies” due to environmental or immunologic changes. There is usually a decrease in the number of allergic individuals in the geriatric group. • Allergic rhinitis may be associated with allergic asthma, atopic eczema, and allergic conjunctivitis. • Allergic rhinitis may be over-diagnosed and/or under-treated, and it may significantly reduce quality of life. • Inhalant allergens are the principal triggers of allergic rhinitis. Food allergens are less frequent. • Another recently defined subtype of allergic rhinitis is “local allergic rhinitis” which is characterized by the presence of specific immunoglobulins (IgE) in nasal secretions only. Skin prick test and RAST test are characteristically negative. This is sometimes called “entopy.” Local allergic rhinitis is frequently misdiagnosed as vasomotor rhinitis. • Mixed allergic rhinitis refers to presence of both allergic and non-allergic elements in the same patient. • Recently, the visual analog scale (VAS) was recommended to follow up patients with allergic rhinitis.

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10.2.1 Classifications of Allergic Rhinitis A. Seasonal: Limited to definite season, e.g., hay fever. B. Perennial: Continuous or constant, sometimes with seasonal exacerbations.

10.2.2 ARIA Classification A. Intermittent: Symptoms are present fewer than 4 days a week or for fewer than 4 consecutive weeks. B. Persistent: Symptoms present for 4 or more days a week or for 4 or more consecutive weeks. Intermittent and persistent can each be subdivided into mild or severe: A. Mild: Symptoms are not troublesome and do not affect quality of life (sleep, work, education…. etc.) B. Moderate to severe: Symptoms are troublesome and do affect quality of life.

10.2.3 Pathophysiology • Sensitization to an allergen occurs in genetically predisposed people. Allergens are captured by dendritic allergen-presenting cells. This activates T-helper (Th) cells and these activated Th cells, called Th2 cells, release cytokines. • The most important cytokines are interleukin 4, interleukin 5 (IL-5), and interleukin 13 (IL-13). IL-4 drives B cells to produce allergen-specific IgE. This IgE binds through its high-affinity receptor, to effector cells especially mast cells and basophils. • On subsequent exposure to the same allergen, the allergen binds with two molecules of allergen-specific IgE on the surface of a mast cell and triggers the immediate release of inflammatory mediators such as histamine, leukotrienes, and prostaglandin. These mediators initiate the early-phase allergic reaction. • The cytokines also stimulate migration of leucocytes, particularly eosinophils and basophils to the sensitized mucosa. The leucocytes in turn release their mediators including the major basic protein leading to the late-phase allergic reaction usually occurring four to eight hours later and are associated with increased nasal congestion.

10.2.4 Comorbidities of Allergic Rhinitis 1. Allergic eye in up to 50% of patients. 2. Bronchial asthma. It is estimated that 30% of patients with allergic rhinitis suffer also from asthma, and up to 75% of asthmatic patients have also allergic rhinitis.

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10.2.5 Clinical Picture A.

Symptoms: 1. Sneezing 2. Nasal irritation and itching 3. Bilateral watery rhinorrhea 4. Nasal congestion and blockage 5. Eye symptoms (itching, lacrimation, red eye) in 40%–60% of patients due to allergic conjunctivitis which differentiates allergic rhinitis from other types of rhinitis 6. Itchy throat B. Signs: (a) Facial signs 1. Shiners: bluish discoloration and mild edema around the eyes. 2. Allergic gap (open mouth - mouth breathing). 3. Supratip crease (allergic salute). (b) Nasal signs 1. Pale, moist nasal mucosa with occasional blue hue. 2. Swollen inferior turbinates. 3. Signs of chronic rhinosinusitis may be present with or without nasal polyps.

10.2.6 Investigations • Skin prick test. –– A battery of common allergens are placed on the skin of the flexor aspect of the forearm. If the patient has an allergy to any of the allergens, then a wheal and flare will appear within 15–20 minutes. –– A negative control (carrier substance) and a positive control (histamine-­ containing solution) should be included to ensure accuracy of the results. • Allergen-specific IgE level (RAST test): RAST is a blood radioimmunoassay test that can detect specific IgE antibodies to suspected allergens. • Normal total serum IgE values are less than 100 IU/mL in adults, and less than 60 IU/ml in children. Total serum IgE levels (PRIST test): Total serum IgE may be elevated in type I allergies, and also in including helminthic infections and hyper-IgE syndrome. • Blood eosinophilia may occur in an acute allergic reaction but is unusual in chronic allergic rhinitis. • Nasal smears: An increase in eosinophils in a nasal smear may occur in allergic rhinitis but is not specific. • Measurements of local nasal IgE. • Nasal challenge A drop of the suspected allergen squeezed into the nose may cause rhinitis symptoms. The obstructive effect can be measured objectively by rhinomanometry pre-and post-challenge.

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10.2.7 Management A. Avoidance of the precipitating allergen. B. Pharmacotherapy: (a) Oral second-generation non-sedating oral antihistamines. These are fast acting and effective for rhinorrhea and sneezing but less so for nasal blockage. They will also reduce associated throat and eye symptoms. First generation antihistamines are no longer used for treatment of allergic rhinitis. (b) Topical steroid sprays are now considered to be the cornerstone in the treatment of allergic rhinitis. They act on both phases of nasal allergy and are effective for all nasal allergic symptoms including nasal congestion because of their anti-inflammatory effects. Systemic absorption or bioavailability is less than 2% and their main side effects are occasional crusting and minimal bleeding. These side effects can be easily managed by saline washes. (c) Topical antihistamines sprays have similar actions to oral antihistamines with the benefit of absent systemic side effects and higher concentrations in the nasal mucosa. (d) Combined steroid/antihistamine sprays are now increasingly to combine the advantages of both sprays. (e) Short courses of oral steroids for 7 to 10 days are very effective and may be used cautiously in poor responders and certain other situations. (f) Topical anticholinergic drugs (e.g., ipratropium bromide) may be used if watery rhinorrhea is a predominant symptom. They are more frequently used for treatment of geriatric and gustatory rhinitis. (g) Sodium cromoglycate stabilizes mast cell membranes and reduces the release of the allergic response mediators. It is a safe drug but needs to be used 4–6 times per day. It is especially useful in children. (h) Leukotriene receptor antagonists may be used in patients with asthma. C. Desensitization immunotherapy: Immunotherapy (injection or sublingual) involves exposure to regular small but increasing doses of an allergen to produce tolerance to the allergen by producing blocking IgG antibodies. It will only produce tolerance to the allergen presented. Immunotherapy is used for those do not respond to pharmacotherapy. Its main complication is anaphylaxis. D. Surgical treatment (a) Turbinate surgery to reduce the size of hypertrophied inferior turbinates in selected patients. (b) Surgical procedures to interrupt the parasympathetic supply to the nasal mucosal: vidian neurectomy, posterior nasal neurectomy, and application of botulinum toxin to the sphenopalatine foramen area. Recurrence of symptoms is common after these procedures. These procedures have been also used for vasomotor rhinitis.

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10.2.8 Aspirin-Exacerbated Respiratory Disease (AERD - Samter’s Triad) • About 10% of adults with asthma and 20–30% of patients with asthma and nasal polyps have AERD. • AERD develops usually between the ages of 20 and 50. The disease is due to intrinsic disorder of prostaglandin metabolism. Aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) inhibit an enzyme called cyclooxygenase. • Acetaminophen is usually safely tolerated at low doses (up to 500 mg at a time).

10.2.8.1 Clinical Features • Asthma. • Chronic rhinosinusitis with nasal polyps. • Sensitivity to aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs). 10.2.8.2 Investigations • Aspirin challenge test. • Examination of blood and nasal smears for eosinophils. 10.2.8.3 Treatment • Steroids (oral, intranasal, and inhalers) are the main treatment. • Non-steroid medications include drugs that inhibit the production of leukotrienes (zileuton) or block the function of leukotrienes (montelukast). • Endoscopic sinus surgery for obstructing nasal polyps. The recurrence rate after surgery is high. Nasalization procedures or reboot surgery may be needed in recalcitrant cases. • Aspirin desensitization as a steroid-sparing treatment in some patients.

10.2.9 Rhinitis and Asthma • Most asthmatic patients (70–80%) suffer also from rhinitis. • Both allergic and non-allergic rhinitis increase bronchial hyperreactivity and are risk factors for asthma. Allergic rhinitis may increase the risk of asthma about threefold. • Upper respiratory tract infections trigger exacerbations of asthma.

10.3 Non-Allergic Rhinitis • Non-allergic rhinitis includes diverse types of rhinitis and it is usually an under-­ estimated entity. • Literally speaking, the term non-allergic rhinitis can include many types of rhinitis, e.g., infectious, hormonal, occupational, gustatory, and geriatric rhinitis. Rhinopathy of pregnancy may be allergic, non-allergic, or mixed. • However, in clinical practice when we talk about non-allergic rhinitis, we usually mean the group that have similar symptoms to allergic rhinitis. It includes 2 main types:

10.3 Non-Allergic Rhinitis

• • • •

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(a) Idiopathic rhinitis (previously called vasomotor) (b) Non-allergic rhinitis with eosinophilia (NARES) Non-allergic rhinitis accounts for about half of perennial rhinitis cases. It becomes more common with increasing age. It has a multifactorial etiology and is a risk factor for the development of asthma. It is estimated that up to 40% of patients with allergic rhinitis were classified as also having some sort of non-allergic rhinitis. Itching and sneezing are less common with non-allergic rhinitis than with allergic rhinitis, but nasal congestion/ obstruction and anterior and posterior rhinorrhea are usually prominent. Non-allergic rhinitis is a diagnosis of exclusion, and the aim of investigations is to identify other causes of rhinitis.

10.3.1 Etiology 1. Changes in humidity and temperature. 2. Environmental pollution. 3. Active and passive smoking. 4. Occupational irritants and pollutants. 5. Nasal mucosal hyperreactivity following viral or bacterial rhinitis. 6. Emotional factors. 7. Endocrine factors: menstruation and pregnancy. 8. Drugs: ACE inhibitors, β-blockers, and oral contraceptives.

10.3.2 Vasomotor Rhinitis (VMR) • Vasomotor rhinitis is the most common type of non-allergic rhinitis especially in older patients. • Pathogenesis: Vasomotor rhinitis results from changes in vascular tone and permeability of the mucosal blood vessels due to stimulation of afferent sensory nerves which activate the parasympathetic nerves that supply the nasal mucosal glands and vasculature. The triggers for this neural stimulation include many factors such as cold air, temperature change, and anxiety. • Symptoms of vasomotor rhinitis are similar to those of allergic rhinitis. There is usually no ocular manifestations, but it may be associated with asthma. • Allergy tests are characteristically absent, and immunotherapy is not indicated.

10.3.3 Treatment • Intranasal steroids are the most effective treatment. The response to antihistamines is generally poor or modest. Anticholinergic nasal sprays (ipratropium bromide) can decrease the rhinorrhea. • Oral sympathomimetics (decongestants) can be used as a symptomatic treatment though they may produce side effects such as dry mouth, constipation, and

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e­ xcitability. They should not be used long term, in patients with hypertension, glaucoma or prostatic hypertrophy, or in children. • Local nasal decongestants can temporarily relieve nasal obstruction but the relief may be followed by rebound congestion (rebound phenomenon). Prolonged excessive use nasal decongestants lead to an aggravation of symptoms, which eventually become unresponsive to the decongestant, and rhinitis medicamentosa may develop. Saline washes and topical steroids can help to reverse these changes. • Surgical treatment: –– Sphenopalatine block with botulinum toxin: This usually result in short lived improvement of symptoms. –– Vidian neurectomy: Produces improvements for longer durations but there is risk of dry eye and frequent recurrence of symptoms. –– Posterior nasal neurectomy: Generally have the same results like vidian neurectomy but it spares normal lacrimation.

10.3.4 Non-Allergic Rhinitis with Eosinophilia Syndrome (NARES) • Allergic-like rhinitis with eosinophilia in nasal secretions (10–20% on nasal smear). Allergy testing is typically negative. • Generally speaking, patients with NARES have a higher tendency for nasal polyposis and a better response to topical steroids and second-generation antihistamines than patients with VMR. • Treatment is similar to that of vasomotor rhinitis. Occasionally short course of steroids are needed for stubborn cases.

10.3.5 Non-Allergic Inhalant/Occupational Induced Rhinitis • Pathogenesis: Stimulation of chemical irritant receptors of C sensory fibers leading to neuropeptide release, which produces the vasodilation and edema associated with inflammation independent of immune-mediated responses. Triggers are inhalants such as perfumes, cleaning agents, smoke, and other irritants. • Some high molecular weight inhalants, such as adhesives, paints, and insecticides, may also induce immunologic response . • The response to antihistamines is typically poor. • Topical nasal steroids are the main treatment.

10.3.6 Hormonal Rhinitis • • • •

Contraceptive bills. Pregnancy (multiple factors). Hypothyroidism. Acromegaly.

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10.3.7 Food-Induced Rhinitis • Food allergy rarely causes isolated rhinitis. • May be hyperreactivity to preservatives or additives. • Gustatory rhinitis is neurogenic in origin. Spicy foods (capsaicin) stimulate type C trigeminal nerve endings. • Oral allergy syndrome: irritation of oral cavity and nose due to association of food allergies with seasonal allergic rhinitis.

10.4 Infectious Rhinitis 10.4.1 Acute Viral Rhinitis (Coryza - Common Cold) • Acute viral rhinitis is one of the common causes of nasal obstruction. • The disease is more common in crowded poorly ventilated areas, in children and, during winter, and is attributed to one of a multitude of rhinoviruses transmitted from person to person in droplets and mists. • The disease is self-limiting, and spontaneous resolution usually takes place within 7–10 days unless secondary bacterial infection occurs. • The commonest secondary invaders include Streptococcus pneumoniae, Haemophilus influenzae, Staphylococcus aureus, and Moraxella catarrhalis.

10.4.1.1 Clinical Picture • After an incubation period of 1–3 days, the following stages can be recognized: –– Prodromal stage (stage of invasion): This lasts for few hours and is characterized by sneezing, burning sensation in the nasopharynx, nasal obstruction, and headache. –– Hyperemic stage (stage of secretion): This lasts for few days and is characterized by low grade fever, malaise, arthralgia, nasal obstruction, and profuse watery rhinorrhea. –– Resolution stage: This is the natural course of an uncomplicated disease and is characterized by resolution and gradual improvement of symptoms within 7–10 days. • Symptoms lasting beyond 7 days or worsening instead of improving suggest that secondary bacterial infection is being established (acute bacterial rhinosinusitis). • Complications: acute otitis media, lower respiratory infections. 10.4.1.2 Treatment • As the condition is self-limiting, only supportive treatment is required. This may include bed rest, analgesics, nasal decongestants (local, i.e., drops and systemic), and occasionally steam inhalations. • Antibiotics should be reserved for treatment of secondary bacterial infections since excessive unnecessary use of antibiotics in uncomplicated cases has significantly contributed to the surge in antibiotic resistance.

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10.4.2 Scleroma • Scleroma is a chronic specific inflammation of the upper respiratory tract caused by short gram-negative cocci called Frisch bacillus or Klebsiella rhinoscleromatis, and is characterized, in the typical case, with granulomatous lesions with characteristic hardness hence the name scleroma. • Scleroma was initially described by von Hebra (in 1870) as a lesion involving the nose (rhinoscleroma), but now it is known to also involve the larynx, trachea, and bronchi.

10.4.2.1 Incidence • Scleroma is present sporadically all over the world and is endemic in Egypt, Eastern Europe, Russia, and Central and South America (scleroma belt). • It is more common in adults and has a higher incidence among low socio-­ economic classes. The mode of transmission of infection is not yet known. 10.4.2.2 Pathology • Scleroma exists in 3 forms/stages that may overlap granulomatous, fibrotic, and atrophic. The granulomatous form is the most common one. • In the active granulomatous stage, the submucosa appears infiltrated by lymphocytes, plasma cells as well as two characteristic components: –– Mikulicz cells which are derived from histiocytes and appear as large vacuolated foam cells containing the scleroma bacilli. –– Russell bodies which are eosin-staining degenerated plasma cells. Electron microscopy showed a third type of cells called Mott cells. These are plasma cells with numerous inclusion bodies and are thought to be the precursors of Russell bodies. • In the fibrotic stage, the cellular infiltration is gradually replaced by fibroblasts and dense fibrous tissue giving the lesions its characteristic hardness. Contraction of the fibrous tissue may lead to narrowing or complete obliteration of the nasal cavity as well as external deformities. • In some cases, the pathological changes may be atrophic rather than granulomatous with atrophy of the epithelium and seromucinous glands. 10.4.2.3 Clinical Picture • Three clinical types or presentations have been described corresponding with the pathological features. These types are frequently intermixed together: –– Granulomatous type: This is the classical presentation (Fig. 10.1) where the nasal cavity shows firm pale pink granulomatous masses starting near the mucocutaneous junction of the nose and spreading posteriorly. The small

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Fig. 10.1  The typical granulomatous lesion of scleroma

masses coalesce together and may extend to the external nose and upper lip (Hebra nose). –– Fibrotic type: The nasal cavities are narrowed or may be obliterated by firm unyielding concentric fibrous stenosis and adhesions. External deformities are commonly present. –– Atrophic type: The mucosa appears pale, atrophic, and the nasal cavity appears roomy and contains crusts.

10.4.2.4 Involvement of Other Regions • Involvement of other regions is usually secondary to nasal involvement. Uncommonly, it is primary. Scleroma may also affect the following sites: –– The pharynx (pharyngoscleroma): This may cause stenosis of the nasopharynx and fibrosis of the soft palate (uvula sign). The tonsils also may be involved. –– The larynx (laryngoscleroma), trachea, and bronchi: Laryngoscleroma is more common in females, and it usually involves the subglottic region. In the granulomatous stage, the lesions usually appear as subglottic cushions. In the fibrotic stage, contraction of the fibrous tissue produces concentric subglottic stenosis.

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–– The lacrimal sac (dacryoscleroma). –– The middle ear (tympanoscleroma). –– The maxillary sinuses.

10.4.2.5 Investigations 1. Biopsy. 2. Scrapings and culture for bacilli. 3. Radiological evaluation: Usually CT scans showing soft tissue masses occupying and expanding the nasal cavity and external nose (Fig. 10.2). 10.4.2.6 Differential Diagnosis 1. Neoplastic lesions. 2. Other granulomata. 10.4.2.7 Treatment 1. Long course of antibiotics is the main treatment. The preferred antibiotic groups include the quinolones, aminoglycosides, and tetracyclines. Specific antibiotics may be also given after culture and sensitivity testing. 2. Surgery may be needed to open the nasal airway and to correct deformities.

a

b

Fig. 10.2  CT scan showing the granulomatous lesion of scleroma (s) expanding the external nose (a) and filling the nasal cavity (b). Note the perforation of the nasal septum

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10.4.3 Rhinosporidiosis • Rhinosporidiosis is a chronic granulomatous infection of the mucous membranes caused by Rhinosporidium seeberi. It manifests as vascular friable strawberry-­ like polyps that arise from the nasal mucosa. Pathologically, the polyps show pseudoepitheliomatous hyperplasia. The disease may involve also the conjunctiva and urethra. • The disease is endemic in in India, Sri Lanka, South America, and Africa. • The treatment of rhinosporidiosis is surgical excision. Recurrences may occur in a small percentage of cases.

10.5 Special Types of Rhinitis 10.5.1 Drug-Induced Rhinitis (Rhinitis Medicamentosa) • The most commonly known form is rebound congestion due to decreased vasomotor tone and refractoriness of sympathomimetic α receptors, following prolonged use of topical nasal decongestants. The preservatives such as benzalkonium chloride have also been considered as causative factors. • Some oral drugs may also cause drug-induced rhinitis including antihypertensives, erectile dysfunction drugs, female sex hormones, and psychotropic drugs. • The usual symptoms are nasal obstruction and dryness. The patients usually complain from progressively diminishing efficacy of nasal drops and persistent nasal obstruction. • Treatment: Discontinuation of topical decongestants, saline washes, and nasal steroid sprays. Short courses of oral corticosteroids may be needed nasal blockage.

10.5.2 Atrophic Rhinitis • Atrophic rhinitis is a chronic inflammation of the nasal mucosa characterized by atrophy of its epithelium and glands due to endarteritis and periarterial fibrosis. The functional ciliated respiratory nasal epithelium is replaced by a nonfunctional lining of non-ciliated squamous epithelium (squamous metaplasia), with a loss of mucosal glands and impairment of mucociliary clearance. • There are two types of atrophic rhinitis: Primary and secondary.

10.5.3 Primary Atrophic Rhinitis (Ozena) • Primary atrophic rhinitis is a clinical condition characterized by atrophy of the nasal mucosa, increased nasal patency, offensive odor, crust formation, and anosmia.

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• The disease is more common in females around the age of puberty. • The etiology of the disease is still unknown, and various theories (hormonal, infective…etc.) have been proposed. • Bacteriologic cultures from the nasal cavity frequently reveal bacillus foetidus-­ ozaenae which is thought to be responsible for the offensive odor that is not perceived by the anosmic patient.

10.5.3.1 Clinical Picture • The typical patient is a young adult female presenting with nasal obstruction, anosmia, and an offensive odor which is not perceived by the patient due to the associated anosmia. The presence of nasal obstruction in spite of the increase in volume of the nasal cavities (paradoxical nasal obstruction) is due to: • Accumulation of crusts. • Inability to sense the airflow due to atrophy of the trigeminal nerve endings in the nasal mucosa. • Occasionally, there is mild epistaxis due to separation of crusts. 10.5.3.2 Anterior Rhinoscopy Shows • Roomy nasal cavities. • Yellowish or greenish crusts. • Pale atrophic mucosa and small inferior turbinates. 10.5.3.3 Treatment • Frequent cleaning of the nose by saline washes is practically the safest and most effective symptomatic treatment. • Lubricant drops, e.g., menthol paraffin drops and 25% glucose in glycerin may be also used. • Surgical treatment is also of limited value: –– Submucosal implantation of inert materials to narrow the roomy nasal cavities. –– Young’s operation: Closure of the nasal cavity by mucocutaneous flaps. The flaps are sutured together in two layers. The nasal cavity is kept closed for a period of 6 months; then an examination is done—if the crusts have disappeared, a revision surgery is performed, and the nasal cavity is reopened. Recurrence of atrophic changes after reopening has been reported.

10.5.4 Secondary Atrophic Rhinitis • The most common cause is aggressive resection of the inferior turbinates (iatrogenic atrophic rhinitis). The extreme form of it has been coined the name “empty nose syndrome” (Fig. 10.3). • Other possible less common causes are: 1. Granulomatous diseases such as scleroma. 2. Chronic cocaine abuse. 3. Radiotherapy.

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Fig. 10.3 Excessive resection of both inferior turbinates resulting in very wide cavity. Only a small portion of the inferior turbinates is left (arrowheads)

• Treatment options are limited and may include irrigations, humidification to provide moisture, and experimental surgical procedures aiming at narrowing the nasal cavity with submucosal implants.

10.5.5 Rhinitis Sicca Anterior • An uncommon form of atrophic rhinitis characterized by dry thin mucosa of the anterior part of the nasal cavity and/or the nasal vestibule. • The disease is attributed to changes in temperature and/or humidity, nose picking, and frequent exposure to dust. • The symptoms include dryness, crusting, nasal blockage, and mild epistaxis. Treatment is with saline irrigation, topical antibiotics, and oil based nasal ointments. MCQs 1. Shiners refer to: (a) Black discoloration and mild edema around the eyes (b) Crease above the tip of the nose (c) Reddish decoration over the ala of the nose (d) Wet bluish lips 2. Mikulicz cells may be associated with: (a) Leprosy (b) Scleroma (c) Invasive fungal infections (d) None of the above 3. Posterior nasal neurectomy decreases: (a) Lacrimation (b) Parasympathetic activity of the nasal mucosa

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(c) Sensation of the nasal mucosa (d) Sympathetic supply to the olfactory area 4. AERD is associated with all of the following except: (a) Nasal polyps (b) Asthma (c) Decreased cyclooxygenase enzyme activity (d) Increased sensitivity to acetaminophen 5. Vidian neurectomy may lead to: (a) Dry eye (b) Change in taste sensation (c) Epiphora (d) Watery rhinorrhea 6. Rhinosporidiosis may involve: (a) Nasal mucosa (b) Urethra (c) Conjunctiva (d) All of the above 7. Scleroma usually starts in: (a) Subglottic area of larynx (b) Base of uvula (c) Anterior nasal cavity (d) Around Eustachian tube orifice 8. All the following cells are involved in the allergic reaction except: (a) Th2 cells (b) Th1 cells (c) Mast cells (d) B lymphocytes 9. Vasomotor rhinitis is associated with increased: (a) IgA (b) IgE (c) IgM (d) None of the above 10. Neuropeptides may be released in: (a) Hormonal rhinitis (b) Persistent allergic rhinitis (c) Non-allergic inhalant induced rhinitis (d) Intermittent allergic rhinitis

10.5 Special Types of Rhinitis

Answers 1. (a) 2. (b) 3. (b) 4. (d) 5. (a) 6. (d) 7. (c) 8. (b) 9. (d) 10. (c)

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Rhinosinusitis

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11.1 Acute Rhinosinusitis • Acute rhinosinusitis (ARS) is rhinosinusitis lasting 4 weeks or less. It usually follows viral upper respiratory infections. • Acute rhinosinusitis includes three distinct entities (in order of frequency): –– Acute viral rhinosinusitis (coryza): Symptoms last for 10 days or fewer. –– Acute post-viral rhinosinusitis: Symptoms still evident for more than 10 days in the absence of bacterial infection. –– Acute bacterial rhinosinusitis: Persistence of symptoms for more than 10 days with the presence of mucopurulent discharge, fever of 38 °C or above, facial pain and tenderness, and raised CRP level or ESR. It may happen after initial improvement (double sickening or worsening).

11.1.1 Etiology • The infection is usually rhinogenic (90%). Most cases follow viral upper respiratory infections. Spread of infections to the sinuses is encouraged by sneezing, blowing of the nose, and swimming. • Occasionally, the infection is dental in origin. The maxillary sinus is closely related to the upper second premolar, and first and second molar teeth. Infection of the maxillary sinuses may follow infection or extraction of any of these teeth.

Supplementary Information The online version contains supplementary material available at https://doi.org/10.1007/978-­3-­031-­08794-­3_11. © The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 S. Elwany, M. Askar, Rhinology Review, https://doi.org/10.1007/978-3-031-08794-3_11

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11.1.2 Microbiology • Viral: Rhinovirus, influenza virus, coronavirus, parainfluenza virus, and respiratory syncytial virus. • Bacterial: S. pneumoniae, H. influenzae, Moraxella catarrhalis, Staph. aureus, and Streptococcus pyogenes.

11.1.3 Symptoms • Facial pain/pressure. –– Pain develops due to accumulation of discharge and stretching of the nerve endings. It usually increases by straining or coughing. The distribution of pain depends upon the sinuses involved: Maxillary sinusitis: The pain is over the cheek and under the eye. The pain may radiate to the upper teeth especially on pending down and by straining. Frontal sinusitis: The pain of frontal sinusitis is usually over the forehead and above the eye. Occasionally, it shows morning periodicity (vacuum headache). Ethmoid sinusitis: The pain is usually felt over the bridge of the nose and between the eyes. It may be referred to the parietal region or behind the eyes. Sphenoid sinusitis: The pain is deep-seated pain and may be referred to the occipital region, behind the eyes, or to the vault of the head. • Nasal congestion/obstruction. • Nasal discharge with posterior drainage. The discharge is mucoid with viral infection and mucopurulent or purulent with bacterial infections. • Fever especially with bacterial infections. • Hyposmia. • Other symptoms: Headache, halitosis, fatigue, dental pain, and cough (especially in children).

11.1.4 Signs • External signs: –– External signs are more apparent in children, in severe infections, or when there is impending complication. –– Swelling over the affected sinus: In maxillary sinusitis, there may be swelling over the cheek and puffiness of the lower eyelids. In frontal and ethmoid sinusitis, there may be puffiness of the eyelids and swelling over the forehead or medial to the inner canthus.

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• • • •

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–– Tenderness. The point of tenderness depends upon the affected sinus: Maxillary sinusitis: Over the cheek. Frontal sinusitis: Over the upper inner angle of the orbit (floor of the sinus) and sometimes over the anterior wall of the sinus. Ethmoid sinusitis: Just medial to the inner canthus. Anterior rhinoscopy and endoscopic examination. Redness and edema of the nasal mucosa. Mucopurulent discharge especially in the middle meatus. Postnasal discharge trickling down the posterior wall of the pharynx.

11.1.5 Imaging • Imaging is not required for routine diagnosis of acute rhinosinusitis unless there is suspected complication.

11.1.6 Treatment • Treatment of acute rhinosinusitis is medical. Viral rhinosinusitis requires only supportive and symptomatic treatments. Antibiotics are reserved for bacterial infections.

11.2 Complications of Rhinosinusitis • Extension of infection into and beyond the bony wall of the paranasal sinuses occurs in about 3–5% of patients with sinusitis. The complications usually, but not always, occur during an acute exacerbation on top of longstanding chronic sinusitis. • Complicated rhinosinusitis accounts for: –– 10% of intracranial suppuration –– 10% of pre-septal orbital infection –– 90% of post-septal orbital infection. • Complications are more common in children than in adults. 1 per 12,000 ARS episodes in children compared to 1 per 36,000 ARS episodes in adults. • Predisposing factors: young age, immunodeficiency, debilitating diseases. • Pathways of spread of infection: –– Direct spread through a congenital or traumatic bony dehiscence. –– Spread of infection to the bony walls (osteitis or osteomyelitis). –– Vascular spread (retrograde thrombophlebitis). –– Spread along the perineural spaces around the olfactory nerves.

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11.2.1 Classification A. Local complications (5–10$). 1. Osteomyelitis. 2. Mucocele. B. Orbital complications (60–75%). 1. Pre-septal abscess. 2. Post-septal infection. 3. Subperiosteal abscess. 4. Orbital cellulitis/abscess. C. Intracranial complications (15–20%). 1. Extradural abscess. 2. Meningitis. 3. Subdural abscess. 4. Frontal lobe abscess. 5. Cavernous sinus thrombosis. D. Other complications: 1. Otitis media. 2. Recurrent pharyngitis and laryngitis. 3. Bronchitis, bronchopneumonia, bronchiectasis, and exacerbation of bronchial asthma.

11.2.2 Osteomyelitis of the Frontal Bone • Osteomyelitis usually involves the frontal bone, uncommonly it may involve the maxilla in children. • Osteomyelitis of the anterior wall leads to the formation of subperiosteal abscess and tender, may be fluctuant, forehead swelling called “Pott’s puffy tumor” (Fig. 11.1). • Osteitis of the posterior wall may be associated with extradural abscess, meningitis, or intracranial complications. • CT scans may show total opacification of the frontal sinus and sequestration of its anterior wall. • Treatment: Intravenous antibiotics, surgical drainage, and debridement of necrotic bone, and providing patent outflow tract of the involved sinus usually using appropriate Draf procedure.

11.2.3 Orbital Complications • Orbital complications arise most commonly from ethmoid sinusitis especially in children. • Routes of spread: Lamina papyracea, suture lines, and venous channels.

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Fig. 11.1  Pott’s puffy tumor (arrows) secondary to acute frontal sinusitis

• The orbital septum and tarsal plate may limit extension of the infection into the orbit.

11.2.3.1 Chandler Classification of Orbital Complications • Stage I: Pre-septal cellulitis. • Stage II: Orbital cellulitis. • Stage III: Subperiosteal abscess. • Stage IV: Orbital abscess. • Stage V: Cavernous sinus thrombosis. However, there are other orbital complications not mentioned by Chandler including: Orbital apex syndrome: It involves neuropathy of all cranial nerves passing through the optic canal and superior orbital fissure (II, III, IV, VI). The clinical presentation is visual loss, ptosis and complete ophthalmoplegia. The best example was in cases of acute invasive fungal rhinosinusitis in immunocompromised patients during Covid-19 pandemic. Superior orbital fissure syndrome causes dysfunction of III, IV, VI cranial nerves. Isolated optic nerve neuropathy can occur due to inflammatory (optic neuritis), ischemic and compressive optic neuropathy. The ischemic type if not managed within 100 minutes can lead to permanent visual loss.

11.2.3.2 Pre-Septal (Periorbital) Cellulitis • Eyelid edema and erythema. • Pain and tenderness over the eyelid. • Unrestricted normal eye movement. Normal vision.

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11.2.3.3 Orbital Cellulitis (Post-Septal Cellulitis) • Eyelid edema and erythema. • Orbital pain. • Chemosis. • Proptosis. • Limited eye movements. • Increased intraocular pressure. Decreased visual acuity. The color vision is usually affected first. 11.2.3.4 Subperiosteal Abscess • Eyelid edema and tenderness (Figs. 11.2 and 11.3). • Orbital pain. • Chemosis. • Proptosis. • limitation of, or pain with, eye movement.

a

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Fig. 11.2  Drainage of subperiosteal abscess. (a) Coronal CT showing large subperiosteal abscess (arrow) pushing the globe laterally and inferiorly. (b) Axial CT scan of the same case showing the abscess displacing the medial rectus muscle laterally (arrow). (c) Removal of the lamina papyracea (arrow) to drain the underneath abscess. (d) Drainage of the abscess (arrow)

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Fig. 11.3 (a) Left subperiosteal abscess. (b) Coronal CT scan of the case showing the abscess (arrow) penetrating the lamina papyracea. (c) Large left subperiosteal abscess. (d) CT scan showing the abscess (arrows) pushing the globe laterally and inferiorly. (e) The patient after endoscopic drainage of the abscess and treatment of infection. (f) Right intraconal orbital abscess (arrow). (g) Exposure of the periorbita (white arrow). (h) Evacuation of the orbital abscess through the periorbita and orbital fat. The incision was made in the superior aspect of the periorbita to avoid iatrogenic injury to the medial rectus muscle

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11.2.3.5 Orbital Abscess • Proptosis. • Orbital pain. • Chemosis. • Increased intraocular pressure. • Complete ophthalmoplegia (paralysis of cranial nerves III, IV, V, VI). • Visual impairment (central retinal artery occlusion, panophthalmitis, optic neuritis). 11.2.3.6 Treatment of Orbital Infections • Medical treatment with intravenous antibiotics for pre-septal cellulitis and for limited suppurations in the absence of visual loss or increased intraocular pressure. • Surgical drainage is indicated if medical treatment fails to improve the infection within 24–48 h, or if the patient has visual loss or increased intraocular pressure.

11.2.4 Intracranial Complications • Intracranial complications usually occur because of spread of infection from the frontal or, less commonly, the ethmoid sinuses. • Infections spread to intracranial structures through diploic veins (thrombophlebitis) or through bony dehiscence.

11.2.4.1 Meningitis • Headache. • neck stiffness, • High fever. • Positive Kernig’s sign: resistance, pain, or an inability to extend the knee when the hip is flexed at a 90-degree angle. • Positive Brudzinski’s sign: Severe neck stiffness causes a patient’s hips and knees to flex when the neck is flexed. 11.2.4.2 Epidural (Extradural) Abscess • Severe headache. • Pain and tenderness over the forehead. • May be altered mental status. • CT reveals collection in the epidural space. 11.2.4.3 Subdural Abscess • Severe headache. • High fever. • Meningismus. • Lethargy. • May be neurologic deficits.

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• Unenhanced CT reveals a hypodense collection over the frontal lobe and along the falx cerebri. • MRI reveals low signal on T1 and high signal on T2 images with peripheral contrast enhancement.

11.2.4.4 Frontal Lobe Abscess • General symptoms and signs: Slow full pulse, toxemia, and lethargy. The temperature is at first high then may become subnormal in terminal stages. • Symptoms and signs of increased intracranial pressure: Headache, vomiting, and papilledema. • Localizing signs: Memory defects, changes in mood and behavior, and upper motor neuron paralysis of the extremities. CT scans show the abscess cavity in the frontal lobe. • MRI demonstrates a cystic hypointense lesion with enhancing capsule on T2 images. 11.2.4.5 Cavernous Sinus Thrombosis • Occurs due to the spread of infection through the valveless veins between the orbit and the cavernous sinus. • High hectic fever with chills and rigors. • Bilateral orbital involvement on the form: • Orbital pain. • Chemosis. • Proptosis. • Complete internal and external ophthalmoplegia, fixed pupil, and ptosis. • Visual loss. • Increased intracranial pressure: Headache, projectile vomiting, and papilledema. • Hight mortality rate (up to 25%). 11.2.4.6 Treatment of Intracranial Infections • Intravenous antibiotics and metronidazole. • Supportive treatment and measures to lower intracranial pressure. • Drainage of purulent collections. • Management of the original sinus disease. • The use of anticoagulants for cavernous sinus thrombosis is controversial. 11.2.4.7 Alarm Symptoms and Signs of Sinusitis • Periorbital edema/erythema. • Proptosis. • Ophthalmoplegia or double vision. • Reduced visual acuity. • Severe headache. • Frontal swelling. • Signs of meningitis. • Neurological signs.

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11.3 Chronic Rhinosinusitis • Chronic rhinosinusitis (CRS) is inflammation of the mucosa of the nose and paranasal sinuses of at least 12 weeks’ duration, without complete resolution of symptoms or the pathology. • Recurrent rhinosinusitis is the occurrence of four or more annual episodes of rhinosinusitis, without persistent symptoms or permanent pathological changes in between them. • CRS is more common in adults than in children with an estimated prevalence of about 10–30%. • CRS is a multifactorial disease with many possible overlapping etiologies and is not just a persistent acute rhinosinusitis. • The relationship between nasal allergy and CRS is still controversial.

11.3.1 Diagnosis of CRS The European Position Paper on Rhinosinusitis and Nasal Polyps (EPOS) definition included: • At least two typical symptoms, one of which must be nasal blockage (obstruction and congestion) or rhinorrhea (anterior or postnasal). • Symptoms may also include: –– Facial pain. –– Hyposmia. • Confirmation by one or both of the following items: –– Endoscopic finding of edema, mucopurulent discharge, and nasal polyp formation in the middle meatus. –– CT revealing mucosal changes in the ostiomeatal complex.

11.3.2 Classification A. According to phenotypes (Fig. 11.4): (a) CRS without nasal polyps (CRSsNP). (b) CRS with nasal polyps (CRSwNP). B. According to endotypes: (a) Type 2 CRS: Type 2 inflammations characterized by cytokines IL-4, IL-5, and IL-13 as well as activation and recruitment of eosinophils and mast cells. (b) Non-Type: Non-type 2 inflammation is characterized by cytokines IL-6, IL-8, tumor necrosis factor, and interferon gamma (IFN-γ). Usually less associated with asthma or atopy than type 2 CRS.

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Fig. 11.4  Phenotypes of chronic rhinosinusitis. (a) CRSwNP (diffuse sinonasal polyposis). (b) Right CRSsNP. The ethmoid and maxillary sinuses are full of secretions

a

b C. According to phenotypes and endotypes. (a) Primary CRS: Patients have inflammatory disorder that is limited to their airway or respiratory system only. (i) Localized (unilateral). 1. Type 2: e.g., allergic fungal rhinosinusitis. 2. Non-type 2: e.g., isolated frontal or sphenoid sinusitis. (ii) Diffuse (bilateral). 1. Type 2: e.g., CRSwNP, eosinophilic rhinosinusitis, bilateral allergic fungal sinusitis, central compartment atopic disease. 2. Non-type 2: e.g., non-eosinophilic rhinosinusitis. (b) Secondary CRS: CRS that is part of another disease process. (i) Localized (unilateral). (ii) Local pathology: e.g., odontogenic sinusitis. (iii) Diffuse (bilateral).

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1. Mechanical (mucociliary): e.g., primary ciliary dyskinesia, cystic fibrosis. 2. Inflammatory: e.g., eosinophilic granulomatosis with polyangiitis (GPA), granulomatosis with polyangiitis (GPA) atopic disease. 3. Immunodeficiency: e.g., common variant immunodeficiency (CVID), IgA deficiency.

11.3.3 CRS with Nasal Polyps (CRSwNP) • CRSwNP (Fig. 11.4a) is usually associated with type 2 (Th2) inflammation, and its prevalence is about 3–6%. • CRSwNP may be associated with concomitant asthma or underlying conditions such as aspirin sensitivity, cystic fibrosis, primary ciliary dyskinesia, and granulomatous diseases.

11.3.4 CRS without Nasal Polyps (CRSsNP) • The more common form of CRS (Fig. 11.4b). • It usually starts with an obstruction of ostiomeatal complex followed by bacterial infection and frequent formation of bacterial biofilms. • Ostiomeatal obstruction may be triggered by anatomic variants, allergy, smoking, and pollutants. • Other predisposing factors include odontogenic infections, mucociliary disorders, and systemic diseases.

11.3.5 Symptoms of CRS • Symptoms of CRS are nonspecific. The more cardinal symptoms include: –– Nasal obstruction/ congestion. –– Nasal discharge/ postnasal drip. –– Hyposmia/ anosmia. –– Facial pressure. –– Cough especially in children.

11.3.6 Signs • Signs of CRS are nonspecific. • The common signs hyperemic mucosa and mucoid or mucopurulent nasal discharge in the middle meatus. • Frequently, there is a discrepancy between symptoms and nasal endoscopy findings.

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11.3.7 Investigations • Endoscopic guided middle meatus cultures for concurrent bacterial infection (>80% accuracy). • Allergy testing if concurrent allergic rhinitis is suspected. • CT scan of paranasal sinuses. • Other tests as required, e.g., sweat chloride test/genetic test if CF is suspected.

11.3.8 Treatment A.

Medical treatment. (i) Topical steroids: steroid sprays or steroid irrigations. (ii) Saline irrigations. (iii) Short-term (55%). • Three phases of the disease are seen in most but not in all patients, and with highly variable lengths and patterns: –– Allergic phase: Adult-onset asthma, rhinitis, and severely recurrent nasal polyps (several years). –– Eosinophilic phase: Pneumonia and gastroenteritis. –– Vasculitis phase: All other manifestations mentioned above.

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• Main cause of morbidity and mortality is cardiac involvement in up to 50% of patients. • The disease is associated with positive pANCA, blood eosinophilia (more than 10% in peripheral blood), and eosinophilic tissue infiltrates in the lungs and gastrointestinal tract. • Treatment: Oral steroids, and in severe cases, azathioprine or cytostatics or immunosuppressants such as cyclophosphamide.

11.5.7 Sarcoidosis • Sarcoidosis is a chronic noncaseating granulomatous affecting the airway and other organs. • Sinonasal involvement in about 1–5% of cases. • The nasal mucosa usually appears dry, erythematous, and with a strawberry-like appearance. Crusting is frequent and there may be septal perforation (Fig. 11.11). a

b

Fig. 11.11  A case of sarcoidosis. Note the erythematous granular appearance of the nasal mucosa (a) and the characteristic ocular manifestations (b)

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• Ocular manifestations include uveitis, lacrimal gland enlargement, and conjunctivitis. • Other extra nasal manifestations include night sweats, weight loss, erythema nodosum, and peripheral lymphadenopathy. • Plain chest radiograph typically shows showing bilateral hilar lymphadenopathy (butterfly pattern). • Angiotensin-converting enzyme (ACE) levels in serum are elevated. • Mucosal biopsies are diagnostic. • Treatment: oral steroids and immunosuppressants, such as methotrexate and azathioprine. • Surgery for sinonasal sarcoidosis is controversial and generally should be avoided.

11.5.8 Immunodeficiency • Refractory sinusitis is a common complication of local or systemic immunodeficiency especially human immunodeficiency virus (HIV) disease and bone marrow transplantation. • CRS occurs in 20–70% of HIV-infected patients. • The most frequently found organisms in HIV-positive patients with CRS are coagulase negative Staphylococcus aureus, Pseudomonas aeruginosa, and Aspergillus fumigates. • Both HIV and bone marrow transplantation patients may develop invasive fungal sinusitis (mostly mucormycosis) with high mortality rates. • Treatment: • General management of immunodeficiency. • Culture-specific antibiotics, nasal irrigations, and local corticosteroids. • Endoscopic sinus surgery ESS may be indicated in some cases if medical treatment fails.

11.5.9 Laryngopharyngeal Reflux (LPR) • There is no strong evidence so far that LPR is an important predisposing factor to CRS. However, LPR frequently gives the sensation of thick pharyngeal drainage, which is often wrongly attributed to sinusitis.

11.6 Fungal Sinusitis • Fungal rhinosinusitis includes different diseases, ranging from fatal acute infection to long-standing fungal balls and almost symptomless fungal colonization. • Fungi are found everywhere in the sinonasal area. Non-germinating spores of fungi are generally non-immunogenic. The adaptive immune response is triggered by fungal antigens of germinating spores and hyphae. • Important fungal genera:

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(a) Noninvasive: Alternaria, Aspergillus are the commonest and may cause IgEmediated sinusitis. (b) Invasive genera: Mucor, Rhinosporidium, and Cryptococci. These may cause potentially fatal fungal infections usually in immune-­compromised patients.

11.6.1 Classification of Fungal Rhinosinusitis A. B.

Noninvasive: (a) Fungal colonization. (b) Fungal ball. (c) Allergic fungal rhinosinusitis (AFRS). (d) Eosinophilic fungal rhinosinusitis (EFRS). Invasive: (a) Acute invasive fungal sinusitis. (b) Granulomatous invasive fungal sinusitis. Some authors denie this category and consider only acute and chronic types of invasive fungal sinusitis. (c) Chronic invasive fungal sinusitis.

11.6.2 Fungal Colonization • Nasal fungal colonization is usually found in patients having nasal crusts due to other diseases. Fungal colonization per se is symptomatic. Symptoms and treatment are those of the original disease.

11.6.3 Fungal Ball (Mycelia Mass) • Fungus balls (Fig. 11.12) are dense collections of fungal hyphae usually found in the maxillary sinus and less commonly in the sphenoid sinus. • Mainly Aspergillus species, e.g., Aspergillus fumigatus in immunocompetent patients. • Fungal balls usually occur unilaterally, and when they occur in the maxillary sinus they may be related to dental treatment. • Chronic nasal discharge, nasal obstruction, headache, facial pain, cacosmia. • Non-contrast CT scans show fungal balls as hyperdense material that occasionally shows calcifications. • Fungal balls usually appear hypointense on T1-weighted MRI. • T2-weighted images may show areas of signal void due to calcifications and paramagnetic metals, such as iron, magnesium, and manganese. • Treatment: Endoscopic removal of the fungus ball and clearing of the involved sinus. No medical treatment is required.

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b

Fig. 11.12  Fungal ball of the right sphenoid sinus (a) and a rare case of fungal ball of the frontal sinus (b). Note the hyperdensities characteristic of fungal infection of the sinuses

11.6.4 Allergic Fungal Rhinosinusitis (AFRS) • Allergic fungal rhinosinusitis is an IgE-mediated form of eosinophilic fungal rhinosinusitis. • Dematiaceous molds (e.g., Alternaria, Cladosporium, Bipolaris, Curvularia) and Aspergillus fumigatus in immunocompetent patients. • The hallmark of the disease is the presence of polypoid mucosa and highly viscid eosinophilic peanut butter-like mucus frequently with Charcot-Leyden crystals. • Non-contrast CT shows scattered hyperdensities more clearly seen in the soft tissue window due to presence of heavy metals, e.g., manganese in allergic mucin. • In advanced cases, bone remodeling and thinning are seen (Fig. 11.13). • MRI shows hyperintense signal on T1- and hypointense signal on T2-weighted images (signal void) due to its high protein and low water content. The inflamed mucosa is hypointense on T1 and hyperintense on T2 and shows gadolinium enhancement. • Bent-Kuhn criteria for diagnosis of AFRS: (a) Major criteria. 1. Type-1 hypersensitivity. 2. Nasal polyposis. 3. Characteristic CT scan signs like EFRS. 4. Positive fungal smear. 5. Eosinophilic mucin without tissue invasion. (b) Minor criteria. 1. Unilateral predominance. 2. Serum eosinophilia.

11.6 Fungal Sinusitis

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b

Fig. 11.13  Allergic fungal sinusitis. Note the characteristic hyperdensities in the coronal CT scan (a) and the thick mucoid eosinophilic mucin (b). Also note the encroachment of the fungal material on the left lamina papyracea

3. Radiographic bone erosion. 4. Asthma. 5. Charcot-Leyden crystals. 6. Fungal culture. Treatment: 1. Endoscopic surgery to reduce the antigenic load of the disease by removing the polyps and eosinophilic mucin. 2. Oral steroids are usually needed for preoperative preparation and during the postoperative period. 3. Steroid irrigations are used during the postoperative period until complete healing of the mucosa. 4. Oral and topical anti-fungal medications are not indicated.

11.6.5 Eosinophilic Fungal Rhinosinusitis (EFRS) • Eosinophilic fungal rhinosinusitis (known also as eosinophil-related fungal rhinosinusitis) is a noninvasive eosinophilic inflammation of the sinonasal mucosa usually associated with nasal polyps. • The fungi trigger cytokine driven eosinophilic inflammation in the sinuses independent from IgE-mediated allergy. • Treatment: Same as AFRS.

11.6.6 Acute Invasive Fungal Sinusitis • Acute invasive fungal rhinosinusitis (Fig.  11.14) most commonly occurs in immunocompromised patients and is characterized by fungal invasion of surrounding tissues, vascular thrombosis, tissue necrosis, and high mortality rates ranging up to 70%.

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Fig. 11.14  Mucormycosis. (a) Early case. Note the blackish areas in the nasal mucosa. (b) The typical black necrotic tissue inside the nasal cavity. (c) MRI showing he heterogenous appearance of the necrotic tissue and its extension into the left orbit. (d) large palatal defect surrounded by necrotic tissues

• Necrosis of nasal tissue and blackish appearance of the mucosa are early signs. • Involvement of the palate, orbit, and anterior cranial fossa is common. Meningitis, intracranial abscess, and cavernous sinus thrombosis may develop along the course of the disease. • Non-contrast CT shows bone destruction of sinus walls without bony expansion. • MRI shows variable T1-and T2-weighted signal intensity of the contents of the involved sinus depending upon the extent of thrombosis and necrosis. • Treatment: 1. Aggressive surgical debridement. 2. Systemic anti-fungal medications: 3. Polyenes (mainly amphotericin B deoxycholate).

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4. Liposomal preparations including triazoles (posaconazole and voriconazole) Liposomal preparations are less toxic than polyenes. 5. Itraconazole is indicated in patients with less severe Aspergillus infections. 6. Treatment of immune suppression.

11.6.7 Granulomatous Invasive Fungal Rhinosinusitis • Granulomatous invasive fungal rhinosinusitis is a noncaseating granulomas around few fungal hyphae. • The disease occurs mainly in hot humid countries. • A 5–20% mortality rate has been reported. • Treatment: same as acute invasive fungal sinusitis.

11.6.8 Chronic Invasive Fungal Rhinosinusitis • Chronic invasive fungal rhinosinusitis is a non-granulomatous, slowly destructive process with abundant hyphae. • Chronic invasive fungal rhinosinusitis occurs more commonly in diabetics and acquired immunodeficiency syndrome (AIDS). • The mortality rate is 20–40%. • Non-contrast CT usually shows soft tissue mass within one or more sinuses, bone destruction, and infiltration of surrounding tissues mimicking a malignancy. • T1-weighted MRI shows variable hypointensity. • T2-weighted MRI usually shows very low signal intensity. • Treatment: same as acute invasive fungal sinusitis.

11.7 Mucoceles • Paranasal sinus mucoceles are expansile cysts containing mucus. They may be secondarily infected, resulting in a mucopyocele. Mucoceles are lined with respiratory epithelium (Fig. 11.15). • Mucoceles constitute 3% of all sinus swellings and 2.7% of non-endocrine causes of exophthalmos. • There are two types of mucoceles: (a) Primary mucocele resulting from retention of secretions due to obstruction of the normal outflow tract of the sinuses (Fig. 11.16). (b)  Secondary mucoceles due to trauma, surgery, or another pathology (Fig. 11.17). • Mucocele formation is associated with bony remodeling secondary to the prolonged inflammatory reaction. Bony remodeling in combination with the mass effect of the retained mucus can result in expansion, and later resorption, of the bony wallow the sinus.

144 Fig. 11.15 (a) T2 weighted MRI showing the enhanced contents of a large right ethmoid mucocele. (b) The postoperative ethmoid cavity after marsupialization of the mucocele

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• Mucoceles develop most commonly in the frontal and ethmoid sinuses but may develop in other sinuses or even in aerated turbinate (Figs. 11.18 and 11.19). • Mucoceles are relatively uncommon in children. When present, the mucocele is usually associated with a persistent mucosal disease. (Fig. 11.20).

11.7.1 Clinical Picture • • • •

Cystic swelling above the medial canthus (ethmoidocele). Proptosis, diplopia, and eye pain. Headache especially with sphenoid sinus mucoceles. Large frontal sinus mucoceles may erode the anterior table of the sinus and cause external swelling.

11.7 Mucoceles Fig. 11.16 (a) Right frontal mucocele associated with osteoma and displacing the globe inferiorly. (b) Postoperative view of the widely opened frontal sinus. Notice the anterior ethmoid artery posterior to the frontal recess

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11.7.2 Radiologic Diagnosis • Computed tomography: Mucoceles appear in CT scan as well-circumscribed cysts with homogeneous attenuation, expanding the bony walls of the affected sinus. Bony dehiscence may be seen late. • Magnetic resonance imaging (MRI): The appearance of the mucocele depends upon protein concentration of the retained mucus. Mucoceles typically appear with low intensity on T1-weighted and with high intensity on T2-weighted images. As the mucocele gets older, the protein concentration of the retained mucus increases and the MRI characteristics of the mucocele change. A longstanding mucocele will eventually show an increased T1 signal intensity and a decreased T2 signal intensity that may totally drop out (signal void).

146 Fig. 11.17  A secondary fungal mucocele. (a) T2-weighed MRI showing mixed enhancement. (b) Operative view of the mucocele cavity showing the thick mud-like eosinophilic fungal mucin

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11.7.3 Treatment (a) Endoscopic marsupialization is the standard treatment in most cases. Marsuplization should ensure free gravitational drainage of the mucocele. All loculi of the mucocele should be widely opened. The mucosal lining of the mucocele should be left intact. (b) External approaches such as Lynch-Howarth front ethmoidectomy may be needed for few selected cases when the anatomy is markedly distorted or when there is a big defect in the anterior table of the frontal sinus.

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c

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Fig. 11.18 (a) frontal mucocele. Note type 4 frontal air cell within the frontal sinus. Failure or draining this cell will result in persistence of symptoms. (b) Opening of type 4 frontal air cell. (c) Mucocele of the sphenoid sinus. (d) Mucocele of the maxillary sinus. Maxillary sinus mucoceles usually attain large sizes

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Fig. 11.19  Unusual site of mucoceles (m). Mucocele of left concha bullosa (a) and inferior turbinate (b and c). Note the enhanced contents on T2-weighted MRI (b) and the lack of enhancement of T1-weighted MTI (c)

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Fig. 11.20  Coronal (a) and axial (b) views of a large ethmoid mucocele in a child. Mucoceles in the pediatric age groups are uncommon and usually associated with a persistent mucosal disease

11.7 Mucoceles

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MCQs 1. All of the following biologics may be used for treatment of nasal polyposis Except: (a) Anti-IL4 (b) Anti-IL9 (c) Ani-IgE (d) Anti-IL5 2. A positive Kerning’s sign is diagnostic of: (a) Meningitis (b) Extradural abscess (c) Frontal lobe abscess (d) Cavernous sinus thrombosis 3. An orbital subperiosteal abscess may be associated with all of the following except: (a) Orbital pain (b) Chemosis (c) Reduction of color vision (d) Proptosis 4. Lacrimal gland enlargement is a feature of: (a) Granulomatous polyangiitis (b) AERD (c) Hypothyroidism (d) Sarcoidosis 5. Positive cANCA is diagnostic of: (a) Mucormycosis (b) Wegener granulomatosis (c) EGPA (d) HIV 6. Causes of bilateral secondary CRS include all of the following except: (a) Odontogenic infection (b) Cystic fibrosis (c) Immunodeficiency (d) Ciliary dyskinesia 7. Type-2 sinonasal inflammation is associated with all of the following cytokines except: (a) IL-4 (b) IL5 (c) IL-6 (d) IL-13 8. Acute rhinosinusitis is sinusitis lasting for: (a) 1–4 weeks

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(b) 4–8 weeks (c) 8–12 weeks (d) More than 12 weeks 9. Scattered hyperdensities in the sinuses in CT scans may be diagnostic of: (a) Mucormycosis (b) Long-standing mucoceles (c) Sarcoidosis (d) Allergic fungal sinusitis 10. Major Bent-Kuhn criteria for diagnosis of allergic fungal sinusitis include all of the following except: (a) Type 1 hypersensitivity (b) Nasal polyposis (c) Serum eosinophilia (d) Eosinophilic mucin Answers 1. (b) 2. (a) 3. (c) 4. (d) 5. (b) 6. (a) 7. (c) 8. (a) 9. (d) 10. (c)

Sinonasal Neoplasms

12

12.1 Fibro-Osseous Lesions • Fibro-osseous benign lesions that affect the sinonasal tract are uncommon and include three entities: –– Osteoma. –– Fibrous dysplasia. –– Ossifying fibroma. • Osteoma is the most frequent entity.

12.1.1 Osteomas • Benign bony lesions are the most common sinonasal neoplasms. Of these neoplasms, the most common is osteoma. • Osteomas occur most commonly within the frontal (57%) and ethmoid sinuses and uncommonly within other sinuses. • Osteomas are frequently asymptomatic and are discovered accidentally. Occasionally they may cause headache, facial pain, nasal obstruction, proptosis, or facial deformity. • Osteomas may be complicated by secondary mucoceles due to obstruction of sinus drainage. • Osteomas can easily be diagnosed on CT scans (Fig. 12.1) and should be differentiated from other fibro-osseus lesions such as ossifying fibromas and fibrous dysplasia.

Supplementary Information The online version contains supplementary material available at https://doi.org/10.1007/978-­3-­031-­08794-­3_12. © The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 S. Elwany, M. Askar, Rhinology Review, https://doi.org/10.1007/978-3-031-08794-3_12

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Fig. 12.1  Big osteoma in the right ethmoid sinus. A small asymptomatic osteoma is seen in the left ethmoid sinus. The inset shows the osteoma which was resected endoscopically

• Gardner syndrome: multiple osteomas, soft tissue tumors, and colonic polyposis. • Osteomas, when symptomatic, can be resected or drilled endoscopically or via an external approach.

12.1.2 Ossifying Fibroma • Ossifying fibroma is a well-demarcated lesion with a central fibrous component that is peripherally surrounded by an osseous rim. • Ossifying fibromas occur more commonly found in the mandible and maxilla may also occur in the sinuses. • Histological classification of ossifying fibromas is controversial and several, sometimes overlapping. Types were described. Ossifying fibromas of the juvenile variant are believed to have more aggressive behavior and more tendency for recurrence. • CT scans of ossifying fibromas show a mixture of bone density and soft tissues with thick bony walls. The sharply defined outside margin of the lesion is the most important radiological sign for differential diagnosis with fibrous dysplasia and malignant tumors. Ossifying fibromas also lack the ground glass appearance of fibrous dysplasia on CT scans. • Treatment is by resection or, more frequently, drilling of the lesions through endoscopic or external routes.

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12.1.3 Fibrous Dysplasia • Fibrous dysplasia (FD) is a benign lesion that results from abnormality in bone metabolism. Although it is a benign disease, it may be locally destructive. • More common in females. • FD may be monostotic (Fig. 12.2) presenting as a solitary lesion (80%), or it may be polystotic presenting with multiple lesions. The monostotic form is the more common form (60%). • FD may be a part of McCune-Albright syndrome which includes endocrinopathy and café au lait spots in addition to polystotic fibrous dysplasia. • The usual age of onset is in childhood or early adulthood. • The disease commonly present with facial deformity or proptosis. • CT scans show fibrous dysplasia as a homogenous dense lesion with characteristic ground glass appearance. The lesions may, less frequently, have a sclerotic appearance. • In MRI, the lesion shows iso-to hypointensity in T1-weighted imaging with variable enhancement in T2. The lesion enhances with gadolinium. • Treatment is by resection or, more frequently, drilling of the lesions through endoscopic or external routes.

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Fig. 12.2  Monostotic fibrous dysplasia involving the ethmoid sinuses, bony nasal septum, and anterior skull base

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12.2 Hemangioma • • • • •

Usually presents as reddish polypoidal mass on nasal septum (bleeding polypus). More common in females, 20–50 years. Epistaxis is the typical presenting symptom. Soap-bubble appearance radiologically. Differential diagnosis: pyogenic granuloma (reddish brown hemorrhagic lesion that is more common in females and may be related to pregnancy,trauma, or nasal packing). • Treatment is by local excision.

12.3 Inverted Papilloma • Nasal cavity papillomas (Schneiderian papillomas) include three types: inverted (endophytic), fungiform (exophytic), and cylindrical (oncocytic). The inverted and cylindrical types usually originate from lateral nasal wall. The fungiform type usually originates from the nasal septum. • Exophytic papilloma arises from nasal septum and nasal vestibule and is associated with HPV types 6 and 11. • Inverted papilloma (IP) is benign neoplasms characterized by invagination of the neoplastic epithelium into the underlying stroma, without transgression of the basement membrane. • IP comprises 0.5–5% of primary nasal tumors. There may be a role for human papilloma virus in the etiology of inverted papillomas. • The peak age of presentation is the fifth and sixth decades with a male preponderance. • IP originates most commonly from the lateral nasal wall around the middle meatus (89%) and involves the medial wall of the maxillary sinus. The tumor, however, may involve other walls of the maxillary sinus and extend to other sinuses. Orbital and intracranial spread of the tumor has been reported (Fig. 12.3). Fig. 12.3  Coronal CT showing inverted papilloma with intracranial and orbital extensions (arrows)

12.3 Inverted Papilloma

•

• • • •

• •

a

155

The tumor may be multicentric with increased risk of leaving residual tumor tissue after surgery. Histologically, IP has an endophytic or inverted growth pattern consisting of thickened epithelium growing inward into the underlying connective tissue stroma to form large clefts, ribbons, and islands. The epithelium varies in cellularity and is composed of squamous, transitional, and columnar cells. IP is usually unilateral; bilateral involvement is rare. Although the tumor is benign, it may be locally destructive and they have tendency for recurrence (Fig. 12.4), with a recurrence rate of 5–25%. The incidence of being associated with malignancy (squamous cell carcinoma) or develop secondary malignancy is 5–20%. The rates of synchronous and metachronous malignancy are reported to be about 10.1% and 1.1%, respectively. The most common presenting symptom of inverted papillomas is unilateral nasal obstruction. On CT scans, inverted papilloma appears as soft tissue density. With contrast, the tumor enhances heterogeneously. Hyperdense areas may be observed within the tumor. Remodeling of the bony sinus walls is frequent. The site of origin of the tumor may be indicated by thickening and hyperostosis of the adjacent bone. Islands of tumor cells have been reported to exist within the bone at the site of origin of the tumor. On postcontrast, T1W MRI inverted papilloma shows a convoluted cerebriform enhancing pattern that differentiates it from other tumors. MRI also differentiates the tumor from secretions. Krause staging system. –– Stage T1: limited to one area of the nasal cavity. –– Stage T2: involvement of the medial wall of the maxillary or ethmoid sinuses and/or the ostiomeatal unit. b

Fig. 12.4 (a) CT scan showing recurrence of inverted papilloma following medial maxillectomy. (b) T2-weighted MRI of the same case showing the heterogenous enhancement. Of the mass and the typical convoluted cerebriform pattern with roughly alternating parallel layers of high and low signal intensity

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–– Stage T3: involvement of the superior, inferior, posterior, anterior, or lateral walls of the maxillary sinus. –– Stage T4: tumors with extra-sinonasal spread or malignancy. • Cannady staging system. –– Group A: confined to the nasal cavity, medial maxillary sinus, and ethmoid sinus (recurrence rate = 3%). –– Group B: involving the lateral maxillary sinus, sphenoid sinus, or frontal sinus (recurrence rate = 19%). –– Group C: extra-sinus extension (recurrence rate = 35%). • Treatment: –– The classic treatment of inverted papilloma is endoscopic medial maxillectomy and complete resection of the tumor (Fig.  12.5). It is important to a

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Fig. 12.5 (a) CT scan showing inverted papilloma filling the left nasal cavity and extending the left maxillary sinus. The inset shows the nasal mass. (b) T2-weighted MRI shows the heterogenous enhancement of the papilloma. (c) Endoscopic view of the papilloma inside the left maxillary sinus. (d) Postoperative CT scan showing complete resection of the mass via endoscopic medial maxillectomy

12.3 Inverted Papilloma

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remove all diseased mucosa and send it for histologic examination to exclude the presence of malignancy. It is also important to drill the bone at the site origin to decrease the chances of recurrence. Recurrence rate is about 12%. –– Frontal sinus inverted papilloma (Fig.  12.6) is more difficult to treat. It is important to differentiate between papillomas arising from the lateral nasal wall and extending into the frontal sinus and the more difficult-to-treat papillomas whose site of origin is within the frontal sinus. a

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Fig. 12.6 (a) Inverted papilloma extending to right frontal sinus. (b) T2-weighted MRI of the same case. (c) Endoscopic view of the papilloma inside the frontal sinus. (d) Draf IIb procedure was performed, and the papilloma was completely resected

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–– Resection of frontal sinus inverted papilloma usually requires Draf IIb or Draf III procedures. External approach through osteoblastic or eyebrow incisions may be needed for papilloma involving the extreme lateral frontal sinus. –– For papilloma with orbital or intracranial extensions, it is important to preserve the periorbita and the dura to prevent extension of the tumor into the orbit or beyond the dura.

12.4 Juvenile Angiofibroma (JNA) • Juvenile angiofibroma (JNA) is a sinonasal tumor, which almost exclusively affects adolescent males. The growth of the tumor is suggested to be provoked by testosterone stimulation during puberty in males. The finding of hormone receptors may explain the almost exclusive tumor occurrence in male adolescents. • 0.5% of all head and neck tumors. • Although histologically benign, JNA is potentially locally destructive. • JA originates from around the sphenopalatine foramen and grows as a polypoid vascular mass with rubbery consistence into the nasal cavity, nasopharynx, and other areas. • There is evidence supporting the theory that JNAs may be vascular malformations deriving from remnants of the first branchial arch artery, but currently, it is still included into tumor category. • Histologically, JNA is a biphasic tumor composed of stromal and vascular components. The stromal component is composed of variable number of fibroblast-­ like cells with different shapes (spindle, round, or stellate) and collagen. The vascular component is composed of thin walled differently sized and shaped vessels with patchy muscular layer. Older lesions tend to be more collagenous and have less vascularity. • Extra-nasopharyngeal angiofibromas are rare and may occur in an older age group or in females. The tumors have been described arising from the sinuses, nasal septum, turbinates as well as other sites. • The internal maxillary artery with its branches is the main blood supply of JNA. Larger tumors with extensions into the sphenoid sinus, the pterygopalatine fossa, the infratemporal fossa receive additional supply from the accessory meningeal, ascending pharyngeal, and ascending palatine arteries.

12.4.1 Clinical Picture • The characteristic early symptoms are recurrent epistaxis and nasal obstruction in a young adult male patient. . • Epistaxis is more pronounced in the younger age group. The patient may be anemic with low hemoglobin level.

12.4 Juvenile Angiofibroma (JNA)

159

• Nasal obstruction is initially unilateral. When the nasopharynx is totally occupied by the tumor, both sides of the nose will be obstructed. • Hearing loss may occur due to the obstruction of the Eustachian tube and development of serous otitis media. • Endoscopic examination does not usually give a true indication of the size and extent of the tumor.

12.4.2 Extensions of the Tumor • • • •

Anteriorly into the nasal cavity. Inferiorly below the level of soft palate into the oropharynx. Superiorly into the sphenoid sinus. Laterally into the pterygopalatine fossa and further into the infratemporal fossa through the pterygomaxillary fissure presenting clinically as fullness under the zygoma. JNA expands further under the zygoma and extends into the temporal fossa as a dumbbell-shaped mass above and below the zygomatic arch. As JNA expands in the pterygopalatine fossa, it causes anterior bowing of the posterior maxillary wall. • The tumor in the pterygopalatine fossa may extend superiorly to enter the inferior orbital fissure and then to the orbit causing proptosis. From the orbit, the tumor may enter the middle cranial fossa via superior orbital fissure. • The tumor also enters the cranial cavity by erosion of the bony greater wing of the sphenoid. Aggressive JNA may invade the cavernous sinus and may involve III, IV, V1, V2, and VI cranial nerves, or the internal carotid artery. JNA is typically extradural displacing the dura rather than infiltrating it. • The tumor may extend posterior to the medial pterygoid plate into the pterygoid fossa and parapharyngeal space.

12.4.3 Radiologic Evaluation • On CT, the tumor appears as lobulated mass with heterogenous density. The tumor enhances with contrast administration (Fig. 12.7a, b). • The lesion characteristically expands the skull base fissures and foramina, especially the sphenopalatine foramen, the vidian canal, the inferior orbital fissure, and the pterygomaxillary fissure. If the lesion extends into the pterygomaxillary fissure, it may produce forward bowing of the posterior maxillary wall (Holman-­ Miller sign). • On MRI, the lesions are isointense to hyperintense on T1- and T2-weighted scans. There may be multiple flow voids within the lesion related to the tumor vascularity. The tumor enhances intensely with gadolinium administration (Fig. 12.7c–f).

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Fig. 12.7 (a) CT scan showing large JNA extending to the infratemporal fossa. (b) Coronal CTA of the same case showing the large infratemporal extension. (c) T1-weighted MRI without contrast showing JNA as isointense mass. (d, e) Coronal and sagittal T1-weighted MRI showing the enhancement of JNA with contrast. (f) T2-weighted MRI showing variable enhancement of JNA and the flow void (arrow)

12.4.4 Radkowski Staging System The Radkowski system was based on modification of the sessions system: • Stage 1A: limited to nose or nasopharynx. • Stage IB: extension into at least one paranasal sinus. • Stage IIA: minimal extension through the sphenopalatine foramen; includes a minimal part of the medial pterygomaxillary fossa. • Stage IIB: full occupation of pterygomaxillary fossa with Holman-Miller sign (bowing of the posterior wall of the maxillary sinus on CT); lateral or anterior displacement of maxillary artery branches; may have superior extension with orbital bone erosion. • Stage IIC: extension through the pterygomaxillary fossa into the cheek, temporal fossa, or posterior to the pterygoids. • Stage IIIA: skull base erosion with minimal intracranial extension. • Stage IIIB: skull base erosion with extensive intracranial extension ± cavernous sinus.

12.4 Juvenile Angiofibroma (JNA)

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12.4.5 Treatment A. Embolization for Juvenile Angiofibroma • The aim of preoperative embolization of JNA is reduction of tumor vascularity and size with preservation of the normal arterial supply to surrounding tissues. • Embolization-induced changes improve the surgical conditions and contribute to radical tumor removal with minimal intraoperative blood loss. • Appropriately performed embolization carries a minimal risk for permanent neurologic morbidity and possibly a small risk of increasing recurrence rate after surgery. B. Surgical Procedures • Endoscopic resection of the tumor is the primary treatment of JNA (Fig. 12.8). • During endoscopic surgery, the posterior wall of the maxillary sinus is exposed and removed through a wide middle meatus antrostomy. The pterya

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Fig. 12.8 Two JNA case resected endoscopically. (a, b): stage IA. (c, d) stage IIA (Radkowski system)

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Fig. 12.9  A large JNA resected using the Denker’s approach. (a) Coronal CT showing the infratemporal extension. The arrow points to the bowing of the posterior maxillary wall (Holman-­ Miller sign). (b) T1-weighted MRI with contrast showing the enhanced mass. (c, d) Endoscopic view showing clipping of the internal maxillary artery and dissection of the mass. Note the smooth lobulated appearance of the mass. (e) Denker’s approach was used to completely resect the tumor

gopalatine fossa is entered, and the maxillary artery is identified and ­coagulated or clipped. The tumor is dissected and followed according to its extensions. Extended endoscopic approaches, e.g., Denker’s approach are needed to resect JNAs extending to other areas (Fig. 12.9).

12.5 Esthesioneuroblastoma

163

• Early identification and clipping of the maxillary artery are recommended to prevent its accidental injury. Also, drilling of basisphenoid and other bony areas is involved by the lesion to remove hidden microscopic tumor nests. • The basisphenoid is drilled to remove hidden microscopic nests of the tumor that may cause later recurrences. • In very selected cases, midfacial devolving or lateral skull base approaches may be needed to resect very large tumors. • In some cases, complete tumor excision is not always possible and residual tumor may be left in proximity to important structures. Not all residual tumors will grow and a “wait and watch” policy may be adopted, especially in late adolescence. If significant growth of the residual tumor is observed, additional surgery or radiation therapy may be needed.

12.5 Esthesioneuroblastoma • Esthesioneuroblastoma (olfactory neuroblastoma) is an uncommon neuroectodermal tumor of neural crest origin that arises from the olfactory epithelium lining the roof of the nasal cavity. It constitutes 2–7% of sinonasal tumors. • The age at presentation is bimodal in distribution in the second and sixth decades of life and without a gender predilection. • Esthesioneuroblastoma consists of lobular sheets with neurofibrillary fibers and rosettes. The tumor can be stained with neuroendocrine markers. • Hyams histopathological grades (I-V) are based on lobular architecture preservation, mitotic index, nuclear polymorphism, amount of the fibrillary matrix, rosette formation, and necrosis. Hyams classification is an important way of determining prognosis. • The tumors often display varying biologic activity ranging from indolent growth, with patient survival exceeding 20 years, to a highly aggressive neoplasm capable of rapid widespread metastasis, with survival limited to few months. • The Kadish staging: –– A: tumor confined to the nasal cavity. –– B: tumor extends into the paranasal sinuses. –– C: tumor extends beyond the nasal cavity and paranasal sinuses including involvement of the cribriform plate, skull base, orbit, or intracranial cavity. • The modified Kadish staging system includes a fourth stage for patients with nodal or distant metastases. • Esthesioneuroblastoma may present non-specifically with a combination of epistaxis, nasal obstruction, decreased olfactory function, diplopia, and proptosis, Endoscopic examination usually reveals large fleshy mass occupying one or both nasal cavities (Fig. 12.10a). • Local invasion occurs most frequently into the paranasal sinuses, orbits, and anterior cranial fossa. • Metastatic disease most frequently involves local lymph nodes (20–40%). Distant metastasis to the lungs, liver, and bone may occur.

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Fig. 12.10  A case of large esthesioneuroblastoma: (a) Endoscopic view of the large fleshy tumor. (b) Coronal CT scan showing the tumor with orbital and intracranial extensions. (c, d) T2-weighted MRI showing the enhancing tumor and the orbital extension

• On CT (Fig. 12.10b), the tumor does not have specific CT characteristics, presenting initially as a homogeneous soft tissue mass in the nasal vault. • MRI (Fig. 12.10c, d) differentiates entrapped secretions from tumor and offers a more accurate assessment of suspected intracranial, orbital, or perineural spread of tumor. MRI also may differentiate dural involvement from brain involvement. The rumor is usually hypointense on T1-weighted images and moderately hyperintense on T2-weighted sequences with occasional cysts or areas of necrosis. • Standard treatment involves surgical resection followed by postoperative ­radiation therapy and adjuvant chemotherapy very good local disease control and decreases the incidence of local or nodal recurrences. The transcribriform approach is the best approach for resection of these tumors. Because a high dose of radiation is required for the control of the tumor, there is a risk of retinopathy and optic neuropathy following radiotherapy.

12.6 Nasopharyngeal Carcinoma

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12.6 Nasopharyngeal Carcinoma • Nasopharyngeal carcinoma (NPC) is a squamous cell carcinoma with an incidence 40%). Treatment is by wide local excision (endoscopic or open-lateral rhinotomy). Recurrence rate is about 85%. Radiotherapy helps local and regional control.

12.10 Hemangiopericytoma • • • • • • • • • •

Rare vascular tumor. Occurs in ethmoid, nasal cavity, sphenoid sinus. More common in males (>50 years). Presents with epistaxis, nasal obstruction, facial swelling, proptosis. Painless gray or grayish blue polypoidal spongy hemorrhagic mass. 2.5% metastasis. Occasionally causes paraneoplastic syndromes. Treatment: preoperative embolization prior to wide local excision. High recurrence rate. 3% of patients die of disease.

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12.11 Lymphoma • Non-Hodgkin lymphoma. • More common in males, median age 50. • Sinonasal involvement is more common is Asia and South America (T or NK cell predominant) than in western countries (B cell dominant). • Epstein–Barr virus (EBV) is associated with Burkitt lymphoma and nasal NK-T lymphoma. • Poor prognostic factors: Asian ethnicity, old age, and advanced stage. •