The anatomy and physiology of the nose and sinuses

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Anatomy and physiology ....................................................................... 13

Paranasal sinuses 13
Functions 13
Development 13
Maxillary sinus 13
Ethmoid sinus 13
Anatomy of lateral nasal wall 14
Embryology 14
Bony part formed by 14
Cartilaginous part 14
Nasal turbinates 14
Paranasal sinus 14
Lateral wall opening 15
Osteomeatal complex 15
Middle turbinate 15
Basal lamella 15
Uncinate process 16
Agger Nasi 16
Bulla ethmoidalis 16
Hiatus semilunaris 16
Ethmoidal infundibulum 16
Supraorbital ethmoidal air cell 17
Haller cell (infraorbital ethmoid cell) 17
NLD 17
Frontal recess 17
Onodi cells (sphenoethmoidal cell) 17
Lamina papyracea 18
Blood supply 18
Venous drainage 18
Nerve supply 18
Clinical relevance 18
Frontal sinus 18
Sphenoid sinus 19
Olfactory groove Keros classification 19
Internal nasal valve 19
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External nasal valve 19
Pterygopalatine fossa............................................................................20
Contents 20
Passages 20
Endoscopic endonasal PPF/ ITF 20
Physiology .............................................................................................20
Anosmia ................................................................................................ 21
Definitions 21
Classification 21
Conductive 21
Neurosensory 21
Olfactory testing 21
Rhinitis .................................................................................................. 23
Allergic Rhinitis......................................................................................23
Definition 23
Symptoms 23
PE 24
Allergens 24
Clinical presentation 24
Impact 24
ARIA guidelines 24
Diagnostic tests 25
Skin Prick Test 25
Specific IgE 26
Treatment 26
Non allergic rhinitis ............................................................................... 28
Predisposing factors 28
Classification 28
Eosinophilic 28
Non-eosinophilic 28
Management 29
Rhinitis Medicamentosa ........................................................................ 29
Definition 29
Epidemiology 29
Autonomic innervation of nasal mucous membranes 29
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Indications for intranasal decongestants 29
Contraindications for intranasal decongestants 30
Pathophysiology of Rhinitis Medicamentosa 30
Clinical symptoms 30
Physical Examination 30
Histology 30
Causes 31
Management 31
Complications 31
Atrophic Rhinitis ....................................................................................31
Primary atrophic rhinitis (HERNIA) 31
Pathology 31
Clinical features 32
Treatment 32
Secondary atrophic rhinitis 32
Causes of CRS .....................................................................................33
Rhinosinusitis ........................................................................................ 33
Etiology 34
Predisposing factors 34
Pathology of sinusitis 34
Clinical Definition of RS 34
Bacteriology 35
(Acute RS) 35
(Chronic RS) 35
Indications for C&S 35
Acute bacterial sinusitis diagnosis (CPG) 36
Rhinosinusitis Task Force Criteria for diagnosis for ARS 36
Physical examination 36
Treatment: (Acute) 36
CRS 37
Pathophysiology 37
Hypothesis 38
Classification 38
Etiology ~ Acute sinusitis 39
History 39
PE 39
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Differential diagnosis 40
Investigations 40
Management 40
Complications of sinusitis ...................................................................... 45
DEFINITION 45
CLASSIFICATION 46
ORBITAL COMPLICATIONS 46
PATHOPHYSIOLOGY 47
COMMON PATHOGENS 47
FACTORS CONTRIBUTING TO DEVELOPMENT OF COMPLICATIONS IN SINUSITIS
48
MANAGEMENT OF ORBITAL COMPLICATIONS 48
Cavernous Sinus Thrombosis 50
Anatomy of cavernous sinus 50
Causes ‘softbed' 50
Microbiology 51
Pathophysiology 51
Investigation 52
Management 52
Imaging studies in CST 53
Orbital apex syndrome 53
BONY COMPLICATIONS 54
INTRACRANIAL COMPLICATIONS 55
Fungal sinusitis .....................................................................................55
Basic mycology 55
Definition 56
Acute invasive fungal sinusitis 56
Chronic invasive indolent disease 58
Granulomatous invasive fungal sinusitis 58
Fungal ball (mycetoma) 59
Allergic fungal rhino sinusitis 60
Nasal polyps.......................................................................................... 61
INTRODUCTION 61
INCIDENCE 61
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ETIOLOGY 62
ASSOCIATED CONDITIONS 62
HISTOLOGY 63
STAGING 63
CLINICAL FEATURES 63
INVESTIGATIONS 63
TREATMENT 64
DIFFERENTIAL 65
INDICATION FOR SURGERY FOR CRS 65
RECURRENCE 65
Unilateral nasal polyps 66
Evaluation of nasal polyposis 67
Management of nasal polyposis 67
Indication of surgery in nasal polyps ~ CRS 67
Ethmoidal polyp vs AC polyp (7) 68
AC Polyp 68
Cystic fibrosis ........................................................................................ 68
Definition 68
Pathogenesis 68
Essential abnormality 69
Diagnosis 69
Investigations 69
Features suggestive of diagnosis of CF 69
Management 70
Nasal polyposis in cystic fibrosis 70
Granulomatous disease of the nose ..................................................... 70
Granuloma 70
Causes 70
Wegener’s granulomatosis (Granulomatosis polyangiitis) 72
Eosinophilic Granulomatosis with polyangiitis (Churg Strauss syndrome) 74
Sarcoidosis 75
Sinonasal papilloma .............................................................................. 76
Inverted papilloma ................................................................................. 76
INTRODUCTION 76
EPIDEMIOLOGY 77
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PHYSICAL EXAMINATION 77
Diagnosis 77
HISTOLOGY 77
Histopathological Grading 78
STAGING 78
ETIOPATHOGENESIS 78
ORIGIN OF TUMOUR 78
INVESTIGATIONS 78
DIFFERENTIAL DIAGNOSIS 79
TREATMENT 79
FOLLOW UP 81
AREAS ASSOCIATED WITH HIGH RECURRENCE RATE 81
MALIGNANT TRANSFORMATION IN IP 81
Prognosis 82
ROLE OF RADIOTHERAPY 82
Epistaxis ................................................................................................ 82
DEFINITION 82
EPIDEMIOLOGY 82
PATHOPHYSIOLOGY 83
TYPES 84
SITES OF BLEEDING 84
MANAGEMENT 84
Olfactory neuroblastoma (Esthiosioneuroblastoma) .............................86
Introduction 86
Incidence 86
Macroscopic appearance 86
Microscopic appearance 86
Classification (stage) 87
Hyam's histological grading 87
Investigations 87
Treatment 88
Recurrence 88
Esthesioneuroblastoma vs differential diagnosis 88
Unilateral nasal obstruction 89
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Nasopharynx ......................................................................................... 89
Introduction 89
Surgical anatomy 89
Fossa of Rosenmuller 90
Epithelial lining of nasopharynx 90
Lymphatic drainage 91
Adenoids 91
WHO classification of NP tumours 91
NPC .......................................................................................................92
Epidemiology 92
Etiology 92
Molecular signalling pathways in NPC 94
Histopathology 94
Routes of tumour spread 95
Secondary malignancies 98
PE 98
Ix 98
Staging 99
Prognosis 99
Treatment 100
Non surgical 100
1. DXT 100
SE of radiotherapy 103
2. Chemotherapy 106
2. immunotherapy 107
Surgical 107
5 year survival rates for NPC 108
Locally recurrent NPC 108
Reirradiation 108
Brachytherapy 109
Stereotactic radiotherapy 109
External beam reirradiation 109
Surgery 109
NPC with mets 110
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NPC in paediatric and adolescent patients 111
Contraception 111
Nutritional support 111
Follow up 111
Juvenile Angiofibroma .........................................................................112
Epidemiology 112
Etiopathogenesis 112
Origin 112
Supply 112
Spread 113
Midfacial and anterior skull base tumours (differentials) 113
Diagnosis 113
Characteristic presentation 114
Additional findings 114
Gross examination 114
Staging (Fisch) 115
Treatment options 115
Changing technique 116
Surveillance 116
Recurrence 117
Summary 117
CSF Leak.............................................................................................117
CSF production 117
DEFINITION 117
CLASSIFICATION 118
SITES OF LEAKAGE 119
MANAGEMENT 119
TREATMENT 120
Unilateral nasal obstruction .................................................................122
Septal perforation ................................................................................123
ETIOLOGY TI4N 123
PATHOPHYSIOLOGY 124
INVESTIGATION 124
TREATMENT 125
Mucocele .............................................................................................125
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Definition 125
Properties 126
Epidemiology 126
Pathophysiology 126
Causes T(3)IAN 126
Management 127
Treatment 128
Medical treatment 129
Follow up 130
Management of Nasolacrimal duct obstruction ...................................130
Causes 130
History 131
PE 131
Tests 131
Management 132
EDCR 132
Unilateral proptosis ............................................................................. 133
Nasal bone fracture ............................................................................. 133
Epidemiology 133
Etiology 133
Pathophysiology 133
Clinical features, Ix, Tx 133
Classification 134
Surgical 134
Complications 134
Rhinolith .............................................................................................. 135
Definition 135
Types 135
Investigations 135
Treatment 135
Oroantral fistula ...................................................................................136
Etiology 136
Clinical presentation 136
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Diagnosis 136
Investigation 136
Treatment 136
Acoustic rhinometry............................................................................. 137
Septal Surgery ....................................................................................138
INDICATIONS 138
Contraindications 138
PRINCIPLE OF SEPTAL SURGERY 138
SMR 139
SEPTOPLASTY 139
POST-OP CARE 140
COMPLICATIONS 140
Anatomy of nose and paranasal sinus ................................................141
FESS ...................................................................................................141
Aim 141
Indications 141
Contraindication 141
Principles of FESS 142
Techniques 142
Complications 142
Lateral canthotomy 143
Maxillary sinus endoscopic procedures ..............................................143
Hemostasis in Endoscopic Sinus Surgery .......................................... 144
Approaches to Frontal Sinus ..............................................................145
Anatomy 145
Frontal recess 145
Ethmoidal infundibulum 145
Frontal recess cells 146
Indications 146
Surgical approach 146
Frontal sinus trephination 146
External frontoethmoidectomy 147
Draf I 147
Draf II 147
Draf III 147
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Axillary flap 148
Complications 148
Osteoclastic flap with frontal sinus obliteration 148
Cranialization of frontal sinus 149
Approaches to Sphenoid Sinus ........................................................... 149
Anatomy of sphenoid sinus 149
Endoscopic Transphenoidal Approach (ETA) ......................................151
Definition 151
- How to reduce bleeding for ESS 152
Endoscopic SPA ligation...................................................................... 153
Indications 153
Technique 153
Advantages 154
Limitations 154
Maxillectomy ....................................................................................... 154
Steps in maxillectomy 155
Endoscopic DCR .................................................................................155
Endoscopic orbital decompression .....................................................156
Intraorbital hemorrhage 156
Endoscopic orbital decompression 156
Surgical reduction of inferior turbinates...............................................157
Anatomy 157
Indications 158
Operative techniques 158
Total/ radical turbinectomy 159
Partial turbinectomy 160
SMR (turbinoplasty) 160
Nasal fracture reduction ...................................................................... 160
Overview 160
- Most common facial bone fracture (~50% facial bone fractures) 160
- Males 160
- 15-30 years 160
- In fight, MVA, fall 160
- Anatomy 160
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• Paired 160
• Fr. 160
- frontal process of maxilla 160
- Superiorly, nasal process of frontal bone 160
- a&b join in midline 160
- Quadrangular/ septal cartilage support nasal bones fr below 160
• 80% occur btw thicker proximal and thinner distal segments of nasal bones
160
• Lateral impacts more common depression of one nasal bone and lateral
displacement of contralateral nasal bone 161
Diagnosis 161
CLASSIFICATION (Hwang) 161
Indications 161
Anaesthesia 161
Equipment 162
. 162
- Good light source 162
- Frazier suction 162
- Nasal speculum 162
- Bayonet forceps 162
- Pledgets 162
- Merocel 162
- Elevators (goldman/boies/salinger/ballenger) 162
- Walsham forceps (2nd pic-for grasping nasal bones) 162
- Asch forceps (for septum reduction) 162
- External splint (thermoplast/aquaplast) 162
- Intranasal cocaine solution 162
- Infiltration lidocaine solution with epinephrine 162
- Needle, 27 gauge or smaller 162
- Syringe, 3 ml 162
Positioning 162
Technique 162
Complications 163
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Anatomy and physiology

Paranasal sinuses
Functions
1. Lightening of the head
2. Humidifying and heating inhaled air
3. increasing the resonance of speech
4. serving as a crumple zone to protect vital structures in the event of facial trauma
Development
Ethmoid and maxillary sinuses present at birth
- maxillary sinus 7-10 week intrauterine - first sinus to develop and largest
- ethmoid 9-10 week intrauterine
Sphenoid sinus pneumatize by 5 years & attains its mature size by the age of 14 years
Frontal sinus appear by age 7 and not completely developed until adolescence
- last paranasal sinus to develop
Maxillary sinus
- also known as antrum of high more
- pyramid shape
- base along nasal wall
- apex pointing lateral toward the zygoma
- capacity: 15-30 mls in an adult
- grows in a biphasic pattern: first phase 0-7 yrs, second phase 7-12 yrs
- Relations
- anterior wall: facial surface of maxilla and soft tissue cheek
- posterior wall: infra temporal and pterygopalatine fossa
- medial wall: middle meatus and inferior meatus
• thin + membranous-uncinate process, ant+post fontanels, inferior turbinate and inferior
meatus
- floor: alveolar + palatine process of maxilla
- roof: floor or orbit
- blood supply
- facial, maxillary, infraorbital, greater palatine nerves
- venous drainage
- anterior facial vein and pterygoid plexus
- Nerve supply
- infraorbital, superior alveolar and greater palatine nerves
- Lymphatic
- pterygopalatine fossa + submandibular LN
- Clinical importance
- oroantral fistula - extraction of molars
- dental infection - source of maxillary sinusitis
Ethmoid sinus
- situated in the anterior skull base
- complex bony labyrinth of thin walled cells
- anterior group → MM
- Posterior group superior meatus and SER
- few ethmoid cells at birth and 6-10 ethmoid cells in adult
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- Relations
- roof: anterior cranial fossa
- lateral: formed by the orbital plate of the ethmoid otherwise known as lamina papyracea
Anatomy of lateral nasal wall

- skeleton of lateral nasal wall is partly bony, partly cartilaginous and partly only soft tissue
Embryology
1. Ethmoturbinal ridges appear during 8th week of gestation
- First ET ridge
- Ascending portion: agger nasi
- Descending portion: uncinate
- Second ET ridge
- middle turbinate
- Third ET ridge
- Superior turbinate
- 4th and 5th ET ridges
- supreme turbinate
- Maxillo-turbinal ridge
- inferior turbinate
Bony part formed by

1. nasal
2. frontal process of maxilla
3. lacrimal
4. labyrinth of ethmoid
5. inferior concha
6. perpendicular plate of palatine bone
7. medial pterygoid bone
Cartilaginous part
1. Superior nasal cartilages
2. inferior nasal cartilages
3. 3-4 cartilages of the ala
Nasal turbinates
1. 3 turbinates
2. Sphenoethmoidal recess just above and
posterior and medial to superior turbinate
Paranasal sinus
1. Anterior group → drain into middle meatus
- frontal sinus
- maxillary sinus
- anterior ethmoidal
2. Posterior group
- posterior ethmoidal - into sup meatus
- sphenoid - into SER
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Lateral wall opening

Site Opening
Sphenoethmoidal recess (medial to superior meatus) Sphenoidal sinus
Superior meatus posterior ethmoidal sinus
middle meatus frontal sinus

anterior ethmoidal sinus
maxillary sinus
Inferior meatus NLD
Osteomeatal complex
- lateral to anterior 2/3 of middle turbinates
- represent final section of the common drainage and ventilation
pathway for anterior group of PNS
- Medial: middle turbinate
- Lateral: lamina papyracea
- posterior: basal lamella
- Anterior and inferior: open
Contents
1. Bone - uncinate, middle turbinate
2. Air cells - anger nassi, bulla ethmoidalis, infundibulum, anterior
ethmoid
3. Ostia of maxillary, anterior ethmoid and frontal recess
Middle turbinate
- 4cm in length
- 3 parts
- ant 1/3: attach sagittally to BOS
- middle 1/3: basal lamella, attach to LP
- Post 1/3: horizontal, attach along lamina papyrus as far as
perpendicular plate of palatine bone
Basal lamella
- middle portion of the middle turbinate
- important landmark separates ant & post air cells
- Boundaries
- superior: skull base
- lateral: lamina papyracea
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- Inferior: attachment 3rd part of MT to basal lamella
- Medial: attachment 1st part of MT to basal lamella
Uncinate process
- Thin bone, boomerang shaped, btw middle and inferior
turbinates
- Attachment
- Ant: post edge of lacrimal bone
- Inferior & posterior: ethmoid process of IT
- Lateral: lamina papyracea
- free poster superior border
- Superiorly, configuration of the ethmoidal infundibulum depends largely on the uncinate
process
• If uncinate attached to LP (50%), frontal sinus drain directly into MM, separate from
max sinus ostium
• If uncinate attached to skull base(10%) and to MT (40%), frontal sinus drain to MM with
max sinus
Agger Nasi
- Anterosuperior to the origin of MT
- Anterior most ethmoid air cells
- Boundaries
- Lat: lacrimal bone
- ant: frontal process of the maxilla
- Medial: uncinate process
- Post: ethmoid infundibulum
- Superiorly forms anterior boundary of frontal recess
- size of agger nasi cell contributes to size &
shape of frontal recess
Bulla ethmoidalis
- most prominent/largest anterior ethmoid cells
- posterior to uncinate process
- superior to infundibulum
- anterior to basal lamella
- pneumatized in 60-70%
Hiatus semilunaris
- 2 dimensional cleft btw posterior free border of
uncinate & anterior wall of bulla ethmoidalis
- opens into ethmoid infundibulum
Ethmoidal infundibulum
- Anterior end of hiatus semilunaris from a channel named
ethmoid infundibulum
- 3D space bounded
- medial: uncinate process
- post: ant wall of bulla ethmoidalis
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- Lat: lamina papyracea
- superiorly: frontal recess
- inferiorly: maxillary sinus ostium
- receives opening of
- anterior ethmoidal air cells - agger nasi & frontal
cell
- Maxillary sinus ostium
Supraorbital ethmoidal air cell

- arises from pneumatization of the orbital process of
the frontal bone
- located posterior to the frontal sinus ostium
- anterior ethmoid artery
- posterior to supraorbital cell
- anterior to suprabulla lamella
Haller cell (infraorbital ethmoid cell)

- Infraorbital ethmoid cell (belong to ant ethmoid group)
- inferior and lateral to ethmoidal bulla
- closely related to maxillary sinus ostium and infundibulum
- pneumatize into the maxillary sinus ostium just below the inferior orbital wall
NLD
- inferior to agger nasi cell and anterior to uncinate process
- 12mm in length
- opens in the inferior meatus, 15mm from the floor of the nose
Frontal recess
- communication btw frontal sinus and nasal cavity
- 3D cavity bounded
- medially: middle turbinate
- laterally: lamina papyracea
- superiorly: frontal ostium
- posteriorly: bulla ethmoidalis
- anteriorly: agger nasi & uncinate process
- inferiorly: ethmoidal infundibulum
Onodi cells (sphenoethmoidal cell)

- Post most of posterior group of ethmoid air cells
- 7-25% of patients and nearly 50% of patients from the Far
East
- superolateral to sphenoid sinus
- very often closely related to the optic nerve and ICA
- places the sphenoid sinus in a more medial and inferior
position
- increasing the risk of intracranial penetration if the surgeon
expect the sphenoid sinus to be behind the last posterior
ethmoid cell
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Lamina papyracea
- paper thin yellowish looking due to orbital fat
- medial rectus may be in close contact
- thickens towards the optic foramen
Blood supply
- AEA and PEA from ophthalmic
- SPA
Venous drainage
- corresponding veins
Nerve supply
- ant and post ethmoidal nerves
- orbital banches of pterygopalatine ganglion
Clinical relevance
- the common infections affecting the paediatric age group occur in the sinuses
- infections involving the ethmoid air cells may spread to the orbit through LP
- LP thin, can be breached during op
- Optic nerve in close relationship with posterior ethmoidal cells and is at risk during ethmoid
surgery
Frontal sinus
- originates from pneumatized frontal recess in anterosuperior direction into frontal bone
- may be absent on one/both sides or it may be very large
- if present, usually L shaped, inter sinus septum is usually present, but may be paramedian
and is partially dehiscent in 9%
- most variable in size and shape and regarded embryologically as anterior ethmoidal cells
- 4th week of gestation - development of frontal sinus out of the frontal recess can be seen
- At birth - small and from x ray cant be differentiated from anterior ethmoidal cells
- 5 y.o → pneumatization superiorly
- 12 y.o → large develop and may continue throughout adolescence
- Relations
- anterior wall - skin over forehead
- inferior wall - orbit and its contents
- posterior wall - meninges and frontal lobe of the brain
- Frontal sinus cells
- 4 types of frontal cells pneumatic above the anger nasi cell, therefore contributing to the
complexity of frontal recess anatomy
- Kuhn classification
• Type 1: above agger nasi cell
• Type 2: 2 cells stacked above agger nasi cell
• Type 3: large frontal sinus cell pneumatizes into frontal sinus
• Type 4: single isolated cell completely within the frontal sinus and has no connection to
the frontal recess
- Drainage
- through frontonasal duct into middle meatus
- Clinical relevance
- close proximally with the orbit and the brain, infections can cause serious complications,
examples include orbital cellulitis and brain abscess
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- obstruction to the frontal sinus drainage by the presence of a large agger nasi cell may
cause secretions within the frontal sinus
- large agger nasi cell can cause frontal mucocele
- Blood supply
- supraorbital and anterior ethmoidal artery
- Venous drainage
- accompanying veins
- Nerve
- supraorbital nerve (opthalmic division)
- Lymphatic
- submandibular gland
Sphenoid sinus
- a pair of large paranasal sinuses located posterior to the ethmoid sinus
- 2 sinuses are rarely symmetrical
- multiple complete and incomplete bony septations, with vertical, horrizontal and oblique
orientations
- ostium - situated in the upper part of its anterior wall and drain into SER
- Pneumatization
- concha (5%) - posterior extend of sphenoid sinus is well anterior to sella turcica
- preseller (23%) - posterior wall of sphenoid sinus reaches anterior face of sella turcica
- sellar (67%) - extends past the level of sella turcica to approach the pons posteriorly
- Blood supply (Art and vein)
- PEA/ PEV
- Nerve
- orbital branches from pterygopalatine ganglion
- Lymphatic
- retropharyngeal nodes
- Clinical relevance
- important to surgeon when doing transphenoidal
- infection of sphenoid sinus may involve the optic nerve if the canal of the optic nerve is
dehiscent
Olfactory groove Keros classification

Configurations of ethmoid roof, depends on the length of the lateral lamella of the cribriform plate
1. Type I 1-3mm
2. Type II 4-7mm
3. Type III 8-16mm
Internal nasal valve

- Superolateral - caudal border of upper lateral cartilage
- Median - septum
- inferior - floor of pyriform aperture
- posterior - head of inferior turbinate
- 10-150 - caucasian nose
- wider in African or Asian nose
- Angle < 100 - nasal obstruction
External nasal valve

Compartment caudal to INV
- Superolateral - caudal edge of lower lateral cartilage
- Laterally - nasal alar and bony pyriform aperture
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- Medially - medial crus of lower lateral cartilage, columella
Pterygopalatine fossa
lateral to nasal cavity and posterior to maxillary sinus
Ant wall: post surface of maxilla
Medial wall: lateral surface of palatine bone
Post wall and roof: parts of sphenoid bone
Contents
1. Terminal branches of maxillary artery
- Branches of max A
- 1st part: DAMAI
- 2nd part: muscular branches
- 3rd part: GP IS PT
2. Maxillary nerve
3. Pterygopalatine ganglion
Passages
1. Posteriorly
- → foramen rotundum → MCF
- → vidian canal → MCF/ foramen lacerum
- → palatovaginal canal → nasal cavity/
nasopharynx
2. Anteriorly → inferior orb fissure → orbit
3. Medially → SPA → nasal cavity
4. Laterally → pterygomaxillary fissure → ITF
5. Inferiorly → greater palatine canal → oral cavity
Endoscopic endonasal PPF/ ITF

1. Middle meatal transpalatine approach
- medial exposure of PPF contents
2. Middle meatal transantral approach
- lateral view of PPF
3. Inferior turbinatectomy transantral approach
- widest view and room for surgical manoeuvring of medial and lateral compartments of PPF
and ITF
Others
1. Trans-pterygopalatine fossa approach
2. Transmedial pterygoid plate approach
3. Trans lateral pterygoid plate approach
Physiology
1. Maxillary sinus flow originates in the antral floor, is directed centripetally toward primary ostium
2. Frontal sinus
- mucus flow up medial wall, lateral across roof, medially along floor, mucous exits through
primary ostium
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Anosmia
Definitions
1. Anosmia: absence of smell sensation
2. Partial anosmia: ability to perceive some, but not all
odorants
3. Hyposmia: deceased sensitivity to odorants
4. Hyperosmia: abnormally acute smell function
5. Dysosmia: distorted smell perception
6. Phantosmia: olfactory hallucination
7. Olfactory agnosia: inability to recognize an odor
Classification
1. Conductive loss
- obstruction of nasal passages (chronic
inflammation, polyps)
2. Sensorineural loss
- damage to neuroepithelium (viral infection, airborne toxin)
3. Central olfactory neural loss
- CNS damage (tumours, neurodegenerative disease)
Conductive
1. Inflammation of nasal mucosa
2. Tumours
3. Lack of nasal flow - laryngectomees, tracheostomy patients
Neurosensory
1. Infection
2. Inflammation - sarcoidosis, Wegener’s
3. Head trauma
4. Neurodegenerative disease - Alzheimer’s, Parkinsons, Huntinton’s
5. Tumour
6. Endocrine
7. Toxic/ drugs
8. Aging
9. Chronic medical illness
Olfactory testing
1. Psychophysical testing
- Quantitative test
- Olfactory threshold test
• finding the threshold
- Odour identification/ discrimination test
• supra-threshold test
- UPSIT (university of Pennsylvania smell identifiaaion test)
• normal 36-40
• partial anosmia 8-15
• total anosmia 8-15
• probable malingering 0-5
- Objective exploration methods
- electro-olfactogram
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2. Radiological evaluation
- CT scan - investigation of sinonasal diseases
- MRI - superior for detection of intracranial pathology
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Rhinitis
- Tissue inflammation & nasal hyper function which leads to symptoms or rhinorrhea, nasal
obstruction and sneezing/ itchiness, occurring > 1 hr/day
- Allergic vs non-allergic
- Allergic
- Intermittent vs persistent
- Mild vs moderate to severe
- Non-allergic
- Known causes: hormonal imbalance, infection, structural abnormality, rhinitis
medicamentosa, vasomotor
Allergic Rhinitis
- one of the most common chronic conditions
- Male= Female
- Passive smoking is a RF
Definition
- IgE mediated inflammation of the mucosal lining of the nose
- Characterized by sneezing, rhinorrhea, obstruction, itchiness
- common in children and adolescence
- Primary exposure
- body is first subjected to the allergen (antigen)
- No antibodies has been formed previously
- No symptoms of allergy are produced
- Secondary exposure and release of mediators
- subsequent exposure, and the antigen-antibody reaction develops (Type 1 hypersensitivity)
- Early phase: 5-30 mins. Due to release of vasoamine like histamine
• → allergen trigger plasma cells to produce IgE (regulated by T helper and T suppressor
cells) - increased T helper or decreased T suppressor cells will increase production of
plasma cells & increase IgE
• Mast cells release histamine and other mediators
• mast cells are the major source of mediators (histamines, cytokines, prostaglandins,
leukotrienes)
- Late or delayed phase: 2-8 hours - dt infiltration of inflammatory cells like eosinophils,
neutrophils, basophils, monocytes
- IgE has 2 portions
• Fc has high affinity to mast cells or basophils
• Fab has high affinity to allergens
Symptoms
1. Early
- itching
- sneezing
- rhinorrhea
2. Late
- congestion
- obstruction
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PE
- Transverse nasal crest (salute)
- Darken area under eyes (allergic shiner)
- Open mouth from nasal obstruction dt mouth breathing (allergic gape)
- Swollen IT, pale and edematous nasal mucosa
- Retracted TM, MEE
- Granular pharyngitis
- Hyperplasia of submucosal lymphoid tissue
- Prolonged mouth breathing due to adenoid hyperplasia
- Atopy: coexisting with asthma & eczema (an exaggerated IgE antibody response to
aeroallergens)
Allergens
- almost always low molecular weight proteins (airborne)
1. Indoor allergens/ irritants
- house dust mite
- animal dander
- insects
- tobacco smoke
2. Outdoor
- pollens
- molds/grass
Clinical presentation
1. Rhinorrhea
2. Obstruction
3. Itchiness
4. Sneezing
Impact
- affect daily life
- affect work performance
- associated with sleep complaints
- impact mood and feelings
ARIA guidelines
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Diagnostic tests
1. In-vivo tests
- Skin tests - skin prick test, intradermal test
- Patch test
- Provocation tests - bronchial provocation test and drug provocation test
2. In-vitro tests (serology)
- Total and specific IgE (RAST/ Unicap-RAST)
- CAST (cellular antigen stimulation test)
- FAST (flow-cytometric cellular antigen stimulation test)
3. Nasal smear:eosinophilia
Skin Prick Test

- A method for diagnosis of allergies that attempts to provoke a small, controlled allergic
response
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- A microscopic amount of an allergen is introduced to the skin for immediate hypersensitivity
towards the particular antigen (IgE antibodies to specific antigens)
- Clinical response - wheals and flare reactions
- Rapid and reliable test
- Sensitivity: 80-90%
- Specificity: 90-93%
- Indications
- Allergic patients
• AR
• Asthma
- Precautions
- C/I: recent episodes of bronchospasm, history of anaphylaxis, acute exacerbation of
bronchial asthma
- consent
- Ensure resuscitation trolley, defibrillator and oxygen available.
- Meds that interfere with allergy skin test
- First gen anti-histamine (chlorpheniramine, polaramine): 48-72 hours
- Cough syrup (Benadryl): 4 days
- Cetirizine, Zyrtec, aeries D, Telfast D: 5 days
- Non-sedating anti-histamine (clarityne, Aerius, Xyzal) - 7 days
- Antidepressants (Amitriptyline, doxepin) - 14 days
- Avoid topical steroid over the test area - 2-3 weeks
- Interpretation
- Positive: >3mm as compared to the negative control (saline)
- Histamine (positive control) must be positive during the test
- There should be presence of wheal and flare
- In the presence of pseudopod measure the largest wheal diameter
- Unreliable results
• If histamine control is negative
• If patient has dermatographism (can be detected by applying a linear pressure using a
blunt end of the pen)
• There will be a line of wheal and slight flare
Specific IgE
- Indications
- Children
- History of anaphylaxis
- History of acute exacerbation with bronchial asthma
- Eczema
- Dermatographism
Treatment
1. Avoidance of allergen
2. Medical therapy
- Topical corticosteroids
- MOA: bind to glucocorticoid receptors, affecting the production of various mediators →
reduce the number of mast cells, eosinophils, IL-4 and Th2 cells
• Reduce congestion, sneezing, itchiness and rhinorrhea
• Improve sleep, daytime fatigue and daytime sleepiness
• Safe drug with less systemic bioavailability
- Oral antihistamines
- H1 receptor antagonists
• Use for various types of allergies, e.g. AR, urticaria, pruritus
• 1st gen (sedating, thrice daily): chlorpheniramine, actifed, diphenhydramine, polaramine
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• 2nd generation (non-sedating, OD): loratadine (clarytyne), desloratadine (Aerius),
fexofenadine (Telfast), cetirizine (Zyrtec), levocetirizine (xyzal)
• SE of 1st gen anti-histamines
- CNS effects
• 1st gen affects the CNS, thus produces sedation, as a result of CNS depression
• Diminish alertness, slow reaction times and sleepiness
- Anti-cholinergic effects
• Dryness of mouth and throat
• Dryness of resp passages
• Urinary frequency
• Palpitations
- Oral and intranasal decongestants
- vasoconstriction effect (alpha receptor activation → vasoconstriction in nasal mucosa →
shrinkage of swollen mucosal membrane → nasal airway patent → drainage of sinus
secretions
- Relieve stuffy/ blocked nose
- Eg. Oral - pseudoephedrine, nasal sprays - oxymetazoline (Afrin), xylometazoline (Otrivine)
- Side effects
• Nervousness
• Sleeplessness
• Increase BP
• Palpitations
• Tachycardia
- Combination therapy (anti-histamine + decongestants)
• Clarinase (loratadine + pseudoephedrine)
• Telfast-D (fexofenadine + pseudoephedrine)
• Aerius-D (desloratadine + pseudoephedrine)
• Zyrtec-D (Cetirizine + Pseudoephedrine)
• Cirrus (cetirizine + pseudoephedrine)
• Actifed, Fedac (triprolidine + pseudoephedrine)
- Contraindications
• Hypersensitivity to any of the ingredients
- Precautions
• Rebound congestion if used for longer than 7 days
• Precaution: heart disease, high BP, thyroid disease, diabetes or difficulty in urination due
to prostate enlargement
- Oral corticosteroids
- Leukotriene receptor antagonist
- Monterleukast
• Reduce nasal congestion
• Reduce exacerbation of asthma
- Immunotherapy
3. Immunotherapy
- Increase the tolerability of the patient’s immune system to the allergens
- Decrease in the number of inflammatory cells in mucosa
- Reduce the frequency and severity of allergic rhinitis and asthma
- Treatment period: 3-5 years
- Role
- Allergen specific immunotherapy (via SPT/ Specific IgE)
- Indication
- patient with symptoms not well controlled by pharmacological therapy or avoidance
measures
- Type:
- Sublingual immunotherapy
• Allergen extract must be kept under the tongue for 2 mins then swallowed
• Treatment duration of 3 years
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• Advantages
- safer
- more comfortable for patients and clinicians
• Disadvantages of SLIT
- compliance
- Subcutaneous
4. Surgical intervention
- Inferior turbinate surgery
- Turbinoplasty
- Radio frequency ablation
- Submucosal diathermy
- Turbinectomy
- Septoplasty and FESS play little role, unless DNS or co-exist with rhinosinusitis
Non allergic rhinitis

- Inflammatory condition of nasal mucosa which is non-allergic & non-infective
- Related to autonomic imbalance/immunological abnormalities/ aspirin sensitivity
- Nasal itchiness and sneezing not seen in NAR
Predisposing factors
- Familial tendency
- Preceding infection
- Psychological or emotional
- Endocrine (preg/ puberty)
- Drugs (beta-blocker, methyl-dopa, aspirin, OCP)
- Pollution
- Alcohol/ smoking
Classification
1. Eosinophilic
2. Non Eosinophilic
Eosinophilic
- Characterized by marked nasal congestion, profuse rhinorrhea, hyposmia, ITH and mucoid
nasal secretion.
- Nasal polyposis frequently occurred
Non-eosinophilic
- Nasal obstruction is very mild, rhinorrhea is very severe.
- No significant mucosal swelling
- IT hypertrophy is not significant
- Tendency of nasal polyp formation is rare in this group
Eosinophilic Non-eosinophilic
Obstruction Marked Mild
Rhinorrhea Mild/moderate Severe
Sneezing/ pruritus Minimal Minimal
Hyposmia Usual Rare
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Eosinophilic Non-eosinophilic
Mucosal swelling Marked Mild
Inferior turbinate enlargement Marked Mild
Polyps Common Never
Sinus mucosal thickening Common Rare
Management
- Majority of patients benefit from medical management
- Only few require surgical intervention
- Eosinophilic type: steroids/ mast cell stabilisers
- Non-eosinophilic type: anti-cholinergic (ipatropium/ hyosine)/ sympatomimetic
(chlorpheniramine)
Rhinitis Medicamentosa
Definition
Chronic inflammatory condition of the nasal mucous membrane 20 to prolonged use of topical
vasoconstrictive agents
Epidemiology
Under-reported ~ 1%
Similar rate between man and woman
Peak incidence in young and middle aged adult
Autonomic innervation of nasal mucous membranes

Sympathetic
- Fr. preganglionic fibres in the thoracolumbar region → synapse on the neurons of the superior
cervical ganglion → post ganglionic fibres form the petrosal nerve which joins the greater
superficial nerve to form the vidian nerve
- Regulates catecholamine effects via alpha1,2, beta 1,2 receptors present on resistant blood
vessels and venous sinusoids
- Alphas: vasoconstrict
- Betas: vasodilator
- In normal physiology: Alphas> Betas
- Stimulation causes vasoconstriction and increase airway patency
Parasympathetic
- Originates from the facial nucleus of the brainstem and the superior salivatory nucleus→
fibres follow the greater superior petrosal nerve and the vidian nerve → Synapse on the
pterygopalatine ganglion and post ganglionic fibres innervates the nasal mucosa via branches
of posterior nasal nerve
- Regulates the cholinergic effects on muscarinic receptors, most profound is M3
- Stimulation causes glandular secretions and vasodilatation of vessels
Indications for intranasal decongestants

1. Short term relief of nasal congestion due to sinusitis, allergic rhinitis
2. Orbital complications of sinusitis
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3. Certain cases of MEE before M&G
4. Certain nasal surgery eg FESS
Contraindications for intranasal decongestants

1. Glaucoma
2. Advanced atherosclerotic disease
3. Angina pectoris
4. Patients on MAOI
5. Allergy
6. Children less than 6 y.o
7. Pregnancy FDA category C
Pathophysiology of Rhinitis Medicamentosa

- Precise mechanism unknown
- Theories
- Dysregulation of sympathetic/ parasympathetic tone by exogenous vasoconstricting
molecules
- Higher efficacy of sympatomimetic amines towards beta receptor
- Increased parasympathetic activity leading to increase vascular permeability, oedema, and
rebound congestion (vasomotor tone)
- Tissue hypoxia and reactive hyperemia
Clinical symptoms
- Nasal congestion without significant rhinorrhea and sneezing
- H/O overusage of topical decongestant (frequency, duration of relief)
- Snoring
- Dry mucous membranes of mouth and throat
- Chronic sinusitis
- Atrophic rhinitis
- Nasal polyposis
- Otitis media
Physical Examination
- Usually confined to the nasal cavity
- Cold spatula test maybe reduce bilaterally
- -ve Cottle’s test
- Anterior rhinoscopy
- Endoscopy
- Erythematous, granular, punctate bleeding
- Boggy and swollen mucosa
- Punctate bleeding
- Pale & anemic
Histology
→D5: Loss of ciliated cells
→ 1 wk: epithelial lesions
→ 2 wks: edema
→ 3 wks: epithelial hypertrophy with fibrosis
→ 5 wks: complete disorganisation of the mucosal architecture
→ 8 wks: squamous cell metaplasia of the resp mucosa with vascular sclerosis
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Causes
1. Intranasal decongestants (Amphetamine, ephedrine, phenylephrine)
2. Imidazolines (nap haze line, oxymetazoline, xylometazolline)
+ benzalkonium chloride (BKC) - preservative used in nasal spray → ciliostatic effect to nasal
mucosa
Management
1. Medical
- Patient education
- Discontinue or withdraw the usage of intranasal decongestant immediately
- Methods of withdrawal
- Combination with intranasal corticosteroid and wean intranasal decongestant slowly
- May need oral corticosteroid (start 15mg TDS taper over 5 days) & systemic decongestant
- Nasal irrigation
- Treat the underlying problem that triggered the usage of intranasal decongestant
2. Surgical
- Usually not recommended
- Done in cases of refractory to the withdrawal treatment
- Turbinate reduction procedure
- RFTVR
- Submucosal electrocautery
- Turbinoplasty
Complications
- Rare as usually it is self resolving with the intranasal decongestant
- Atrophic rhinitis
- Rhinosinusitis
- Septal perforation
Atrophic Rhinitis
Chronic inflammation of nose characterised by atrophy of nasal mucosa and turbinate bone
The nasal cavities are roomy and full of foul smelling crust
More in females
Usually starts at puberty, most common > 50 y.o
Primary vs secondary
Primary atrophic rhinitis (HERNIA)

Cause is not known
H: Hereditary
E: Endocrine disturbance: usually start at puberty, more in female, cease after menopause
R: racial factor
N: Nutritional deficiency: Def of vit A, D or iron
I: Infection
A: Autoimmune
Pathology
- ciliated columnar epithelium is lost and is replaced by stratified squamous type
- Atrophy of seromucious gland, venous blood, sinusoids and nerve element
- Arteries in the mucosa, periosteum and bone show obliterative endarteritis
- the bone of turbinates undergoes resorption causing widening of nasal chamber
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- paranasal sinuses are small due to their arrested development
Clinical features
- Foul smell from the nose
- Anosmia
- nasal obstruction due to large crust filling the nose
- epistaxis - when crust is remove
- after crust is removed, nasal cavity appeared roomy with atrophy of turbinates and nasal
mucosa is pale
- septal perforation and saddle deformity may be present
- hearing impairment maybe present due to obstruction of ET
Treatment
- Medical vs surgical
Medical
- aim at maintaining nasal hygiene by removal of crusts and the associated putrefying smell
- NaHCO3 nasal douche
- 25% glucose in glycerin
- inhibits the growth of proteolytic organisms which is responsible for the foul smell
- Local antibiotics
- eliminate secondary infection (klebsiella, staph, strep, diphteroids, E coli)
- Estradiol spray
- increase vascularity of nasal mucosa and regeneration of seromucinous glands
- placental extract injected submucosal into the nose
- systemic use of streptomycin 1g/day for 10/7
- reduce crusting and odor
- effective against klebsiella
- potassium iodide
- given by mouth, promote and liquefies nasal secretion
Surgical
- Young’s operation
- both the nostrils are closed completely just within the nasal vestibule by raising flaps
- opened aft 6/12
- body will revert back to normal function aft giving rest
- Modified Young’s operation
- aim to partially close the nose
- Narrowing the nasal cavities
- submucosal injection of Teflon paste
- Insertion of fat, cartilage, bone and teflon strips under the mucoperiosteum of the floor and
lateral wall of nose and the mucoperichondrium of the septum
- Section and medial displacement of the lateral wall of nose
- Whitmore operation
- trainer of stenson duct to max sinus
Secondary atrophic rhinitis

- Infection: syphilis, lupus, leprosy, rhinoscleroma
- cause destruction to the nasal structures leading to atrophic changes
- Long standing purulent sinusitis, RT or removal of turbinates
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Causes of CRS
Causes of CRS
Intrinsic causes Extrinsic causes
1. Gene4c
- mucociliary abnormali4es
- structural
- immunodeficiency 1. Infec4on
2. Acquired • viral
- Aspirin HS • bacterial
- anatomical dysregula4on • fungal
- hormonal 2. Non-infec4ous/ inflammatory
- pregnancy • allergic IgE mediated
- hypothyroid • non-IgE mediated
3. Structural • pharmacologic
- neoplasm • irrita4on
- reten4on cyst/ AC polyps 3. Disrup4on of normal ven4la4on
4. Autoimmune/ Idiopathic • Surgery
5. Immunodeficiency • infec4on
• trauma
Rhinosinusitis
Rhinosinusitis poses a major health problem.
Affects the quality of life, productivity and finances of its sufferers.
It is characterised by mucosal inflammation of the nose and paranasal sinuses
RS can be divided into 2 subtypes based on the duration of the symptoms
- Acute (Prevalence: 6-15%)
- Chronic (Prevalence: 5-15%)
Acute: worsening of Symptoms >5/7, persist aft 10 days and < than 12/52, with complete resolution
Chronic: Symptoms >12/52/ 3/12, without complete resolution
Acute on chronic - in between CRS
Common cold: Symptoms < 5 days
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Etiology
1. Infection
- Viral
- Bacterial
- Strep pneumonia, haemophilus influenza, staph aureus, moraxella catarrhalis (Paeds)
- Fungal
2. Local
- Craniofacial abnormalities (cleft)
- Anatomical variant - DNS, concha bullosa, haller’s cell, large agger nasi, paradoxical MT
- Nasal obstruction - AR, adenoid
- History of trauma
- Dental infection
- Previous sinus surgery
- Kartagener's syndrome
3. Iatrogenic
- surgery
- nasal packing
- NG tube
4. Systemic
- Asthma
- Cystic fibrosis
- Allergic fungal sinusitis
5. ID
- Congenital
- IgA/ IgG deficiency
- Acquired
- HIV/AIDS
- Organ transfusion
- Chemotherapy
- Steroids
6. Environmental
- Atmospheric pollution
- smoker
- dust
Predisposing factors
1. Positive family history
2. Asthma
3. Allergies, chronic bronchitis, emphysema
4. ARS
5. Chronic rhinitis
6. GERD
7. OSA
8. Adenotonsillitis
Pathology of sinusitis
Acute inflammation of sinus mucosa → hyperaemia , exudation of fluid, outpouring of PMN cells →
↑ activity of serous & mucous glands
Clinical Definition of RS
Inflammation of the nose and PNS characterised by 2 or more of the following, 1 of which
1. Blockage/ congestion
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2. Discharge/ PND
+/- hyposmia/ anosmia
+/- facial pain/ pressure
AND at least one of the following:

Endoscopic signs - polyps, mucopurulent discharge, oedema/mucosal obstruction
Or
CT changes - mucosal changes within OMC/ sinuses
Or
PMH of CRS (medically diagnosed)
Therefore, to diagnose RS - nasal endoscopy and CT is one of the requirements

Both tests are not readily available in primary health care, therefore PMH of CRS is therefore
sufficient to make a diagnosis of RS in primary health care
1. Nasoendoscopic examination
2. X ray - plain radiograph has no role in the routine management of rhinosinusitis
- Water’s view → opacity of fluid level
- role of X ray is ↓ now
3. CT PNS
- preferred imaging modality
- not to be done at 1st instance
- should be done after medical treatment had failed or with complications (immediate)
CT scan indication
I. Failed medication
II. Suspected neoplasm
III. Suspected complication
IV. Preoperative planning
V. Intracranial complications
Bacteriology
(Acute RS)
- most acute sinusitis start as viral infections followed by secondary bacterial infection
- Only 0.5-2% are complicated by bacteria infections
- common bacteria
- strep pneumonia
- haemophilus influenza
- moraxella catarrhalis
- strep progenies
- staph aureus
- Klebsiella pneumonia
- Anaerobic (odontogenic origin)
(Chronic RS)
- Staph Aureus
- Enterobacteraceia
- Pseudomonas
- Less common - strep pneumonia, hib, beta haemolytic strep
In Asian countries: pseudomonas > staph
Indications for C&S
- patients who do not respond to first & second line antibiotics
- Via
- Maxillary Sinus Tap - gold standard, but invasive and rarely performed
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- Endoscopic directed middle mental culture - less invasive and as accurate as MST -
recommended (comparable performance with CT scan in diagnosing acute bacterial RS)
- Nasal swab should not be performed
Acute bacterial sinusitis diagnosis (CPG)

At least 3 criteria
1. Discoloured (purulent greenish/ brownish) nasal discharge (with unilateral predominance)
2. Severe local pain (with unilateral predominance)
3. Fever >380C
4. Elevated ESR/ CRP
5. Double sickening (becoming worse again after initial recovery)
Rhinosinusitis Task Force Criteria for diagnosis for ARS

Not used now
Major Minor
Facial pain/ pressure Headache
Facial congestion/ fullness Fever (non-acute)
Post nasal drip/ rhinorrhea Halithosis
Nasal blockage Dental pain
Hyposmia/ Anosmia Fatigue
Purulence on endoscope Cough
Fever (Acute RS only) Ear fullness/ pain
Diagnosis:
2major/ 1 major + 2 minor
Physical examination
1. Anterior rhinoscopy (in primary care)
2. Rigid nasoendoscopy (in ORL center)
Treatment: (Acute)
1. Viral RS - self-limiting disease, symptomatic relief - analgesic/ antipyretic
2. Antibiotics - for ABRS
- Acute
- First line: Amoxycyllin, Augmentin (7-10 days)
- Second line: cephalosporin - zinnat, rocephin
- Third line: macrolides (azithromycin, clarithromycin), avelox
- Chronic
- Insufficient strong evidence to support routine use of antibiotics in CRS
- Macrolides administered by ORL specialists in CRS for its anti-inflammatory properties
3. nasal douching
4. Decongestants
- Topical - ARS - <2/52, followed by ICS
- Per oral - can give, with caution (glaucoma, BPH)
5. menthol inhalation
6. analgesia
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7. antihistamines - if hv allergy (may be
avoided, may dry up secretions too
much)
8. Monterleukast - a/w BA
9. Oral corticosteroids (30mg/day) for 7
days is significantly more effective than
placebo in improvement of symptoms
up to 12 days - but there is possibility
of exacerbation of bacterial infection
Patients requiring admission are patients

who have
1. ARS with complications
2. patients who are immunocompromised
- HIV, renal transplant, ESRF, steroids
3. severe rhinosinusitis
CRS
Pathophysiology
- Development of pathophysiology of CRS is multifactorial
Intrinsic and Extrinsic causes
Intrinsic
① Genetic
1. Mucociliary abnormalities
- Cystic fibrosis
- Primary ciliary dysmotility
2. Structural
3. Immunodeficiency
4. Autoimmune/ idiopathic
② Acquired
1. Infections
2. Inflammation
3. Post op/ trauma
4. Environmental
1. Anatomical abnormality
- OMC is an area of drainage from sinuses
- Inflammatory changes leads to obstruction by
a) microbes
b) allergens
c) chemical
d) pollutants
- anatomical changes that narrow OMC
a) concha bullosa
b) haller cell
c) large agger nasi cells
d) rotated uncinate
e) DNS
2. Allergy
- 15-80% patients has allergic rhinitis
- 80% CRS allergic to dust mites
- Allergen leads to inflammatory response & reflex sinus mucosal thickening
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- Allergic fungal sinusitis may also initiate allergic response
3. Mucociliary function
- In sinusitis, ciliary beat Hz ↓ thus ↓ mucociliary flow
- ↑ goblet cell disorder predispose to CRS
- Young’s syndrome
- Kartagener’s syndrome
- Cystic fibrosis
4. Mucous protein
- Contain IgG, IgM, complement for host defence
- reported ↓ antibody responses to
a) pneumococcal antigen 7
b) selective IgG2 or IGG3 deficiency
c) Defective response to H influenza
5. Autoimmune or idiopathic
- Granulomatous disorders
- Sarcoidosis
- Wegener’s
- Vasculitis
- SLE
- Churg-Strauss syndrome
6. Environmental
- ↑ incidence in urban/ industrial area
- tobacco smoke
- volatile organic compounds
- formaldehyde
- benzene
- toluene
7. Persistent infection
- early stage: viral infection
- small % develop bacterial infection (strep pneumonia, H. influenza, Moraxella catarrhalis)
- Initially 1 type of bacteria but may develop into mixed organism/ fungal (polymicrobial)
- most cases due to acute sinusitis either untreated or does not respond to treatment
Stasis of secretions inside sinuses dt

1. Mechanical obstruction at OMC dt anatomical factors
2. Mucosal edema caused by various aetiologies (e.g. acute viral or allergic rhinitis)
Hypothesis
1. Fungal hypothesis
2. Staphylococcus superantigen hypothesis
3. Immune barrier hypothesis
4. Eicosanoids and arachidonic pathway
Classification
1. CRS with nasal polyps (CRSwNP)
- defined above and bilaterally endoscopically visualised polyps in middle meatus
2. CRS without nasal polyps (CRSsNP)
- defined above and no visible polyps in middle meatus, if necessary after decongestant
CRS without nasal CRS with nasal polyps

polyposis
T helper cells Th1 cell-associated disease Th2 cell associated disease
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CRS without nasal CRS with nasal polyps

polyposis
Cytokines IL2, IFN gamma, IL5, IL4, IL13,eosinophils

IL-12,neutrophil
Superantigen effect
Subtypes 1. Allergic fungal CRS

2. Aspirin exacerbated resp ds
3. Eosinophilic mucin CRS
Familial Strong genetic component
Etiology ~ Acute sinusitis

*in nasal polyposis, other etiology is aspirin sensitivity
History
- duration
- Exacerbating relieving factors
- PMH
- PSH
- Allergy
- Medication history
- Social - smoking
- Intracranial symptoms
- Orbital symptoms
- Samster's triad - aspirin intolerance, polyps,
bronchial asthma
PE
- sinus palpation
- transillumination → lack sensitivity but may be
useful
- oral cavity/ oropharynx
- dentition
- cleft palate
- purulent PND/ inflammation
- Anterior rhinoscopy
- purulent rhinorrhea
- polyps
- nasal masses/ tumour
- DNS 
IT hypertrophy
- nasal endoscopy
- inflamed nasal mucosa
- purulent nasal discharge
- polyps
• Grading
- 0 no polyps
- 1 confined to middle meatus
- 2 beyond middle meatus but not blocking the nose completely
- 3 completely obstructing the nose
- DNS
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- anatomical variation
- complete head & neck (cervical LN)
- laryngeal examination (LPR)
- CN examination (underlying sinus malignancy)
Differential diagnosis
1. Allergic fungal sinusitis
2. Malignant tumour of nasopharynx, nasal cavity, sinuses
3. Non-allergic rhinitis
4. Allergic rhinitis
5. Rhinitis medicamentosa
6. Mucociliary
7. Wegener’s
8. Atrophic rhinitis
Investigations
- Endoscopically directed middle meatus culture
- maxillary sinus tap
- via inferior metal puncture
- moved away dt discomfort & better understanding of culture in CRS
- Plain X ray
- limited use
- CT PNS
- coronal view
- indicated after failure of medical tx or when neoplasm is suspected
- anatomical variation
- MRI
- only in neoplasm and intracranial complications
- Other tests
- RAST (radioallergosorbent assay test)
- SPT
- serum IgG
- HIV testing
- sweat test
Management
1. Aim
- to ↓ symptoms
- improve patient’s QOL
- Prevent progression & recurrence
2. Treatment modalities
- medical
- CRS without nasal polyposis
- Intranasal corticosteroid
- Nasal douching
- Oral antibiotics for acute on chronic cases - first line antibiotics
- Antihistamines for underlying AR
- Surgery if failed optimum medical therapy 3-6 months
Therapy Relevance
1. Antibiotics Yes, ABRS
2. Topical steroids Yes, post viral ABRS
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Therapy Relevance
3. Addition of topical corticosteroids to antibiotics Yes, in ABRS
4. Addition of oral corticosteroids to antibiotics Yes, in ABRS
5. Saline irrigation Yes
6. Antihistamines, analgesics, decongestant combo Yes, in viral ARS
7. Oral antihistamine added in allergic patients Yes
8. Paracetamol Yes, in viral and post viral ARS
9. Decongestants Yes
10. Mucolytics No
Antibiotics Amoxycyllin 250-500mg TDS x 5-10/7 Preferred antibiotics

Penicillin allergy, IM, renal impairment
Augmentin 625mg BD x 5-7/7 Preferred antibiotics
Zinnat 250-500mg BD x 5-10/7 Penicillin allergy

GI disease
Azithromycin 500mg OD Prolonged QT interval (torsades de

pointes, congenital long QT syndrome),
bradyarrythmias, uncompensated heart
failure, drugs that prolonged QT interval or
proarrtyhmic conditions), myasthenia
gravis, renal & hepatic impairment
Clarithromycin ABRS 250-500mg PO BD CAD, prolonged QT interval, myasthenia

x 7-14/7 gravis, severe renal and hepatic
CRS: 250mg PO BD impairment
For medical polypectomy:
Klacid MR 500mg OD x
2/52, then 250mg OD x
4/52
T. prednisone 20-30mg OD
x 1-2/52
Nasonex nasal spray 2p
BD
Intranasal Budesonide 64mcg/dose nasal spray For seasonal and perennial allergic
corticostero rhinitis, treatment and prevention of nasal
ids polyps
Adults 6 yrs and older
Rhinitis: 2p/nostril OD
Polyps: 2p/nostril BD
Fluticasone 50mcg/dose For seasonal and perennial allergic rhinitis

Treatment of associated sinus pain and
pressure
Adults/ adolescents (>12 years): 2 sprays
in each nostril once daily
Max daily dose: 4 sprays in each nostril
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Mometasone 50mcg aqueous nasal Symptomatic treatment associated ARS &

furoate sprays treatment of nasal polyps
AR (>12 y.o): 100mcg/day/ nostril OD,
max 200mcg (4 sprays) OD
Reduce to 50mcg OD when control
achieved
ARS:
- 2 sprays in each nostril BD (total
400mcg/day)
Nasal polyposis
- 2 sprays in each nostril twice daily
- Reduced to 2 sprays each nostril OD
when symptoms are adequately
controlled
- treat allergy
• avoidance of allergens
• nasal douching
• antihistamines (in patients with +ve atopy)
- systemic corticosteroids
• Short term oral corticosteroids (25mg/day for 2 weeks) is significantly more effective than
placebo in reduction of nasal polyp size & hyposmia
• ↓ circulating basophils, eosinophils & monocytes
• inhibit formation of arachidonic acid metabolites
• stabilise mast cells (hypersensitivity)
• short course esp in nasal polyps
• contraindicated in
- DM
- PUD
- Glaucoma
- advanced osteoporosis
• Causes transient suppression of adrenal function & increase bone turnover
- Topical corticosteroids
• Recommended
- In ARS: 14-21 days
- In CRS: 16-52 weeks
• reduced polyp recurrence, granulation and mucosal edema - improve OMC patency
• Immunomodulator
- Stabilise mast cells
- block formation of inflammatory mediators
- Inhibit chemotaxis of inflammatory cells
• Common SE
- Nasal irritation
- Mucosal bleeding & crusting
- Can lessen effects by
• Propylene glycol contained in the preparation
• Switching to a aqueous delivery system
• Concomitant nasal saline
• Compliance & correct technique
- Antihistamines
• limited in CRS - not recommended in CRS in non-allergic rhinitis patients
• however it has role in patients with underlying allergy/ atopy
• ineffective to relieve chronic nasal congestion
• first gen: Chlorphenarimine, diphenhydramine
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• Second gen: loratadine, cetirizine
• Third gen: fexofenadine, desloratadine, levocetirizine
- Antibiotics
• important in pre-op period to ↓ bacterial load
• ↓ edema & inflammation
• should be culture directed
• 1st line: augmentin, zinnat
• 3/52 - 6/52
• should observe improvement after 10/7
• Macrolides (clarithromycin)
- anti inflammatory effect
• accumulate in inflammatory cells > 100x, higher [ ]
- Immunomodulator effect
• target cytokine production
• altered & function of biofilm
• improve mucociliary clearance
- long term use 3-12 months
- Leukotriene antagonist
• inhibit formation/ action of leukotriene
• effective in chronic asthma/ AR
• ↓ mucosal inflammation in sinus disease
- Analgesics, decongestants, mucolytics, antiviral agents - insufficient recent evidence in tx of
RS
- Decongestants - in ARS - provide symptomatic relief - ability to prevent ABRS is unproven -
but it is used in ARS
• Should not be prescribed > 2/52 due to rebound phenomenon
• Cautiously prescribed in: DM, CVS, glaucoma, BPH patients
- Analgesic - symptomatic relief
- Nasal douching
• Facilitates mechanical removal of mucus, infective agents, & inflammatory mediators
• Decrease crusting
• Increases mucociliary clearance
• No difference btw isotonic and hypertonic saline irrigation
• Adverse effects: minor - nasal burning, irritation, nausea
- Mucolytics
• Guafenesin
• high dose req to obtain effect on mucus
• study showed: HIV infected patients reported less nasal congestion & thinner PND
- Line of treatment
• avoidance → decongestant (1/52), nasal douching, topical steroids, oral antibiotics →
review 6/52, if no improvement do CT PNS → consider oral steroids esp with polyps,
leukotriene antagonist (polyp)
- surgical
- ESS
• Indications for surgery (ESS)
- ARS with complications
- ARS - no clinical improvement aft 24-48 hours of IV antibiotics
- CRS with failed optimal medical treatment
- Fungal sinusitis
- Mucocele of fronto-ethmoid or sphenoid
- AC Polyp
- Recurrent acute bacterial sinusitis
- Control of epistaxis
• Types of surgery for CRS
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- Antral washout
- Inferior meatal antrostomy
- Caldwell Luc
• Indications
- chronic maxillary sinusitis with irreversible changes in sinus mucosa
- Removal of FB or root of tooth
- dental cyst
- oroantral fistula
- Recurrent antrochoanal polyp
- Approach to ethmoid (Horgan’s transantral ethmoidectomy)
- Approach to pterygopalatine fossa
- FESS
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Cranial nerve examination - CN 2,3,4,5,6

Superior orbital fissure syndrome - 6, 3,4, v1
Chemosis - edema of conjunctiva (ophthalmic vein obstructed)
Proptosis - increase retroorbital pressure
Diplopia - VI CN
Opthalmoplegia - 3,4,6 CN
Reduced visual acuity -Retinal haemorrhage... (Mr Kong's notes)
Complications of sinusitis
DEFINITION
Sinusitis → inflammation of sinus mucosa
Complication → inflammation extend into/ beyond bony wall of sinus
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CLASSIFICATION
Complication of
sinusitis
Acute
CHRONIC
• mucocele
• pyelocele
LOCAL • as part of other disease
1. orbital or descending
GENERAL/ DISTANT
2. intracranial inflammation into
1. Toxic shock syndrome
• abscess • tonsils
• rare
• intracerebral • pharynx
• staph aureus
• extradural • otitis media
• CF
• subdural • ET dysfunction
• fever
• meningitis • bronchiectasis
• rash
• encephalitis
• multisystem
• cavernous/
failure
sagittal sinus
thrombosis
3. Bony
• osteitis
• osteomyelitis
(pott’s puffy
tumour)
4. Dental
• abscess
ORBITAL COMPLICATIONS
Chandler’s classification (1 → 6)
I - Preseptal cellulitis
II - Orbital cellulitis without abscess
III - Orbital cellulitis with abscess (subperiosteum/ extra-periosteum)
IV - Orbital abscess
V - cavernous sinus thrombosis
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VI (modified) - orbital apex syndrome
osteomyelitis - diploic bone

osteitis - compact bone
Orbital septum (palpabral fascia) is a membranous sheet that

acts as the anterior boundary of the orbit. It extends from the
orbital rims to the eyelids.
PATHOPHYSIOLOGY
Mode of spread of infection
1. Bony dehiscent
- lamina papyracea
- floor of orbit
- infra-orbital canal
2. PNS development
- frontal sinus absent at birth
- most developed at birth
- ethmoid
- maxillary
- in children, ethmoiditis cause the complication but not the
frontal
3. through veins (thrombophlebitis)
- due to valveless venous network between nose, eyes &
intracranial
- communication between frontal sinus with intracranial via
diploid vein of Breschet
4. Dental
- 2nd premolar
- 1st molar
→intimate relation to maxillary sinus
COMMON PATHOGENS
Orbital pathogens
1. Orbital
- aerobes
- staph aureus
- h. influenza
- strep pneumonia
- anaerobes
- bactericides
2. Intracranial
- aerobes
- staph aureus
- strep pneumonia
- h. influenza
- Anaerobes
- others
- fungal
• aspergilloma
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FACTORS CONTRIBUTING TO DEVELOPMENT OF

COMPLICATIONS IN SINUSITIS
1. Patient
- Age
- immunocompromised
- congenital + acquired abnormalities of mucociliary clearance
- anat variation of nose + PNS
2. pathogen features
- viral URTI
- bacteria
- strep pneumonia
- h. influenza
- stap aureus
- fungal
- aspergilloma
- rhinospores
3. Treatment factors
- pt compliance
- poor control on prescribing antibiotics leading to bacterial resistance
MANAGEMENT OF ORBITAL COMPLICATIONS

1. History
2. Physical examination
3. Investigation
- PNS x-ray
- limited value
- shows opacification of affected sinus
- CT scan
- indicated when there is rapid deterioration or complication of clinical conditions and warrant
for surgical intervention
- MRI
- delineate intracranial involvement
4. Treatment
- Medical
- supportive
- monitoring V/S
- daily visual acuity
- daily eye examination
- IV antibiotics
• IV cefuroxime + metronidazole
• IV augmentin
- analgesia
- decongestants
- ?steroids
• will interfere with antibiotic penetrance
- Surgical
- indications
• failure of medical therapy in 48 hours
• reduced visual acuity in 2 consecutive readings (reduced colour vision first)
• increase in proptosis
• presence of abscess on ct scan
- MMA
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• maxillary sinusitis
- Proper surgical drainage
• middle meatus
- ESS
- MMA
• external approach
- modified lynch howard
- Frontal bone trephination
• frontal sinusitis
Chandler’s Investigations and Surgery

conservative Mx
I- preseptal - vast majority treated as CT: diffuse thickening of lid No

cellulitis outpatient and conjunctiva
- commonest pathogen
- strep, staph, H Medical therapy
influenza 1. Oral antibiotics
- Inflammation of the eyelid (outpatients)/ IV
and conjunctiva antibiotics
- Involvement of anterior 2. Facilitate sinus drainage
orbital sept - decongestant
- globe is completely - Mucolytics
unaffected - Saline irrigation
- no visual loss
- no limited eye refer Opthal
movement
- no tenderness
- upper eyelid - 20 frontal
sinusitis
- lower eyelid - 20 maxillary
sinusitis
- both eyelids - 20 ethmoid
sinusitis
II- orbital - oedema of adipose tissue IV antibiotics Yes, if no improvement

cellulitis - no visual loss within 72 hours
without - no limited eye movement
abscess - no tenderness
III - orbital - abscess forms between Same as above Yes,

cellulitis with periorbita and sinus wall - Yes if > 9 years old,
abscess extraconal CT: rim enhancing Expectant if < 9 years old
(subperiosteal/ - slow progression within hypodensity with mass
extra- 2/7 effect Approaches
periosteal) - external ethmoidectomy
- reduce vision (lynch)
- ophthalmoplegia - Endoscopic ideal for
- proptosed medial abscesses
- Transcaruncular approach
- frontal sinusitis - (transconjunctival, extend
displaces eyeball medially around lacrimal
downward and laterally caruncle)
- ethmoid sinusitis -
displaces forward ,
laterally and downward
- maxillary sinusitis -
displaces upwards and
forwards
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IV - orbital - Abscess forms within the Yes

cellultis with space defined by ocular IV antibiotics - Approach same as above
abscess muscles - Incise periorbita and drain
(intraperiostea - rapid/ acute deterioration intraconal abscess
l)
- reduced vision
- ophthalmoplegia
- proptosis
- increased pain
- involvement of cranial
nerve
V - Cavernous - spread of infection via the Poor venous enhancement IV heparin

Sinus valveless veins on CT IV antibiotics x 6/52
Thrombosis surrounding the paranasal Better visualisation on MRI Orbital decompression only
sinuses in patient with rapid
Bilateral deterioration in visual acuity
Mortality. Up to 30%
optic N can tolerate displacement up to 2cm

> than this can lead to rapid visual loss
Involvement of cranial nerve

- superior orbital fissure syndrome
- CN 3,4,6, V1 involved
- orbital apex syndrome/ sphenoidal ocular syndrome/ superior orbital syndrome
- CN 2, 3, 4, 6 v1
- usually 20 to sphenoid/ post ethmoid sinusitis with involvement of CN
- significant proptosis
- visual +/- ophthalmoplegia
- Causes
- bacteria
- sinusitis
- fungal
- neoplasm
Cavernous Sinus Thrombosis
Anatomy of cavernous sinus

1. venous vascular space
2. situated medial wall of MCF, lateral to pituitary fossa
3. lies in between 2 layers of duramater
4. Duramater
- outer (near periosteum) periosteal layer
- inner (facing the brain) meningeal layer - > dense
Causes ‘softbed'
1. Sinusitis
- posterior ethmoiditis
- sphenoiditis
2. Trauma
3. Furunculosis of nasal vestibule
- Facial vein → angular vein → nasofrontal vein → superior ophthalmic vein → cavernous sinus
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4. Bacteraemia
5. Ear infection → petrositis → through superior & inferior petrosal sinuses
6. Dental infection (maxillary tooth infection)
Microbiology
1. Most common: staph aureus (60-70%)
2. Others
- strep
- gram -ve bacilli
- anaerobes
- fungal infection
Blood culture commonly +ve in 70% of the cases

CSF culture +ve in 20% of cases
Pathophysiology
- Thrombophlebitis → extending posteriorly into cavernous sinus → cross basilar venous plexus
→ go opposite site → spread intracranially
Clinical features
- predominantly young patients in which 2/3 patients < 20 years old
- General
- high grade fever with chills
- Neurological
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- headache (progressive)
- reduced conscious level
- convulsion
- prostration
- meningeal sign
• Kernig’s sign (neck rigidity) for
- flexing hip 900 then extending the patient’s knee causes pain
• Brudzinki sign
- flexing the neck causes flexion of hips and knees
- Orbital features
- oedematous eyelid
- proptosis - due to ↑ retro-orbital pressure
- chemosis - due to obstruction of ophthalmic vein
- diplopia - due to 6th nerve involvement
- ophthalmoplegia - due to 3rd, 4th, 6th CN involvement
- Blindness - due to
• retinal haemorrhage
• ↑ IOP
• papilloedema
- RAPD
• optic nerve pathology
- 3rd nerve involvement
• ptosis
• mydriasis
• ophthalmoplegia
- Other features
- parasthesia, hyperesthesia in V1V2 distribution
Investigation
1. CT scan
- to confirm
- to be done once patient stable
- shows filling defect
2. Blood
- FBC
- BUSE
- RBS
- Blood C&S
Management
1. Medical
- Supportive
- IV line
- Resuscitation
- Serial visual activity
- High dose IV antibiotics (empirical) 4-6/52
- anaerobes - metronidazole
- sinus pathogen - 4th generation cephalosporin/ Rocephin - can cross BBB
- Furunculosis - staphylococcus - cloxacillin
- Steroids
- if no contraindication (dexa 8mg or 12mg)
- Anticoagulant
- controversial
- Follow CT scan aft completion of antibiotics
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2. Surgical
- only in patients with visual impairment, have to do urgent decompression
- endoscopic decompression
- external approach
• by modified Lynch Howarth incision
- underlying cause
- sinusitis
- dental infection
1. Orbital cellulitis
2. Other causes of meningitis
Orbital cellulitis Cavernous sinus thrombosis
Source Ethmoidal sinusitis More broader from nose, PNS,

ear
Onset Acute, abrupt slow progression
Laterality unilateral bilateral

if severe → bilateral
Other cranial nerve concurrent with complete Involved individually &

involvement opthalmoplegia sequentially
Imaging studies in CST

1. CT scan
- non-contrasted → thrombosis appreciated as increased density
2. Contrasted CT
- reveal filling defects within the cavernous sinus
- thickening of superior ophthalmic vein
- Nevertheless, CT scan findings may be subtle, negative CT scan cannot rule out CST reliably
when clinical suspicion is high
3. MRI with MRV - preferred imaging MRV will show the absence of flow in the affected
cavernous sinus
4. Carotid angiography
- demonstrable narrowing/ obstruction of inter cavernous segment of the carotid artery
Orbital apex syndrome

- also known as
- sphenoidal ocular syndrome
- supra-orbital syndrome
- posterior orbital cellulitis
- Usually secondary to sphenoid/ posterior ethmoid sinusitis
- significant proptosis
- CN palsies - CN 2,3,4,6, V1-2
- Visual loss +/- opthalmoplegia
- Cause
- bacterial sinusitis
- fungal
- neoplasm
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BONY COMPLICATIONS
1. Pott’s Puffy tumour
- described by Sir Percival Pott in 1760
- Def: osteomyelitis of frontal bone
- a manifestation of complication of frontal sinusitis in which both bony wall of frontal sinus
involved
- presented as “doughy” fluctuant swelling over the forehead
- not necessarily painful
- anterior and posterior frontal sinus walls are equally affected
- Anterior: cancellous bone
- Posterior: compact bone
- organisms
- staph aureus
- H. Influenza
- streptococci
- anaerobes
- Bacteroides
- ant→ forehead
- post → subdural abscess
- Investigations
- CT scan
• Erosion anterior table
• Collection at subperiosteum
• Concomitant Subdural abscess
- Management
- IV antibiotics
• 4-6/52 as penetration of antibiotics to bone is poor
- surgical excision → if failed medical treatment x 6/52
• Osteoclastic flap with removal of sequestrum
- incision
• full wing brow incision
• mid forehead incision
• bicoronal
- Cut out frontal sinus tracing from SXR
- elevate skin flap
- osteoclastic flap
• osteotome
• drill
• saw
- Remove ALL mucosa & drill inner surface bone
- obliterate the sinus (fat, muscle, bone)
- replacement of bone
- closure
• trephination & debridement of bone
• + reconstruction
Frontal mucocele Pott’s puffy tumour
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Mucous filled epithelium lined sac - doughy swelling on forehead

- dt obstruction to drainage channel of paranasal - caused by erosion of anterior sinus wall
sinuses secondary to frontal sinus osteomyelitis
- commonly frontal and ethmoidal sinuses - Bone infection via direct extension/ more
commonly by thromboplebitis of diploic veins
> cystic doughy

egg shall cracking forehead
superomedial not displacing eye ball
displaces eyeball
X-ray - eroding sinus, loss of scalloping x-ray - frontal sinus
Chronic infection Acute (20 to acute infection)
bone erosion ++ no bone erosion
not infection - due to obstructed sinus ostia osteomyelitis changes of frontal bone
Most common organism: staph aureus

seen commonly in adolescents and young adults
INTRACRANIAL COMPLICATIONS
- Less common
- incidence from 3.7-10%
- coexist with orbital complications
- adolescents and young adults, less in <10/12 and > 60 y.o
- > in males (55-75%)
- 2/3rd of brain abscess are 20 to sinus problems
- Types
1. Intracranial abscess
2. Extradural abscess
3. Subdural abscess
4. Meningitis
Management
- CT/ MRI
- IV antibiotics
- serial CT scans
- drainage
- burr hole
- mortality = 15-43%
- increases with age
- multiple subdural abscess with orbital thrombophlebitis
Fungal sinusitis
Basic mycology
Forms: Yeast/ mold
- Yeast: unicellular, reproduce asexually by budding
- Pseudohyphae - when bud doesn’t detach from yeast
- Mold: multicellular
- Grow by branching - hyphae
- Spore: reproductive structure produced in unfavourable conditions
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- If conditions favourable → growth
Definition
Inflammation or infection of paranasal mucosa by fungal organisms
Types depends on tissue + vessels involvement

Classification (Stammberger classification 2008)
1. Invasive - in immunocompromised (fungal hyphae in mucosa/ submucosa/ bone/ vessel)
- Acute invasive fungal sinusitis
- Chronic invasive fungal sinusitis (indolent)
- granulomatous invasive fungal sinusitis
2. Non invasive - immunocompetent - no fungal hyphae at mucosa
- fungal mycetoma (fungal ball/ aspergilloma)
- AFRS
Acute invasive fungal sinusitis

- almost always in immunocompromised patient, mortality 50-80%
- e.g.
• post transplant
• long term steroid
• DM
• CRF
• HIV
• Aspergillosis in the immunocompromised group
• Mucor in the poorly controlled dm group
- Pathophysiology
- fungal hyphae blocks vessels - causes necrosis
- HPE
- Fungal elements invading mucosa, submucosa, vessels, bone + extensive tissue necrosis
- inflammation of cells (no neutrophil infiltration)
- Organisms involved
- Aspergillosis sp - septated, branching 450
- mucor spp - non-septated with branching at 900
- Rhizomes
- Clinical features (Necrotic tissue + fast progressing symptoms)
- toxic looking
- fever (high grade)
- PND
- cough
- epistaxis
- fever
- proptosis
- headache
- mental status change
- seizures
- septal ulceration/ palatal ulcer
- necrotic tissue (black necrosis tissue)
- sinusitis
- rapid orbital and intracranial spread
- Investigations
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- Biopsy
- Fungal smear
• KOH (potassium hydroxide)
• Gomori methanamine silver stain
• PAS: periodic acid Shif
- Culture - saboraud dextrose agar
- CT PNS
• Mixed density - due to magnesium, calcium and iron (mixed density also seen in
chordoma/ IP/ ossifying fibroma)
• unilateral soft tissue thickening
• bony erosion
• spread along vessels with spread beyond the sinus with intact bony walls
• Intracranial spread: cavernous sinus thrombosis, carotid artery invasion, occlusion or
pseudo aneurysm
- MRI
• T1 variable (iso/hypointense), T2 hypointense
• intracranial and intraorbital extension
• obliteration of peri-antral fat is a subtle sign of extension
• meningeal enhancement suggestive of progression to cerebrum and abscess
- Treatment
- surgical debridement (endoscopic if early, open if invade orbit/ palate/ skin)+ systemic anti-
fungal (IV amphotericin, IV itraconazole) + correct the immunocompromised condition
- Aim of surgery: to
① reduce pathogen load,
② to remove devitalised tissue,
③ establish pathway for sinus drainage
Surgery - external/ endoscopic
- sometimes multiple procedures
- Topical Ampho B douching 0.05% 240ml - in ready to douche concentrations
- IV amphotericin B
• Conventional (deoxycholate)
- Requires regular renal & lipid profile monitoring
- Dose: 0.25-0.7mg/kg/day
- Start at low dose first, slowly increase if up if the renal profile not deranged
• Liposomal
- Non formulary (100mg/ ampoule)
- Invasive fungal infection refractory to conventional Ampho B/ there is renal impairment
or unacceptable toxicity
- IV Dose: 3-5mg/kg/day OD
- Voriconazole
• Indications: invasive aspergillosis, serious fungal infection
• Can be oral/ IV
- Itraconazole
• Adult: capsule 200mg TDS x 3/7, followed by 200mg BD or OD x 3/12
• Paeds: syrup
- Posaconazole
• Step down/ oral antifungal therapy
- Echinocandins
• No activity against mucormycosis
- Combination therapy has not been shown to be superior
- recovery of neutropenia is predictive of survival
- Involvement of intracranial is mortality related
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Chronic invasive indolent disease

- has a chronic course - months to years
- inhaled fungal organisms deposit in nasal passageways and paranasal sinuses
- surgery same as in CRSS + orbital apex syndrome (II, III, IV, V1, V2, VI)
- a/w immunocompetent patient
- common organisms
- aspergillus fumigatus, mucor, rhizopus, bipolairis, candida
- CF
- maxillofacial soft tissue swelling
- orbital invasion with proptosis
- cranial neuropathies
- decreased vision
- invasion of cribriform plate → headache, seizures, decreased mental status
- CT
- Hyperattenuating soft tissue mass in 1/> of the paranasal sinuses, bone involvement
(mottled appearance) +/- sclerosis
- May mimic malignancy
- MRI
- decreased signal on T1, markedly decreased signal on T2 weighted images
- HPE
- vascular invasion + mild inflammation
- Treatment
- surgical debridement + IV anti fungal + correct immunocompromised state
Granulomatous invasive fungal sinusitis

- AKA paranasal granuloma/ indolent fungal sinusitis
- > common in temperate climate (e.g. Sudan)
- Immunocompetent patients
- Duration ~ chronic invasive fungal sinusitis
- Surgery ~ CRSS + proptosis
- Organisms
- Aspergillus flavus (exclusively)
- tend to spread to
- orbit
- dura
- brain
- HPE
- fungal growth + local tissue invasion
- Hallmark microscopic: non-caseating granulomas
- Imaging and cf similar to chronic invasive
- Treatment
- Surgical debridement + itraconazole (systemic)
- Has high recurrence rate
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Acute invasive FS Chronic Invasive FS Chronic granulomatous FS
Fungi Aspergillus, zymocetes Aspergillus fumigatus Aspergillus flavus

(mucor, rhizopus)
Complications Orbit Orbit Orbit

Intracranial soft tissue soft tissue
Cavernous sinus
Treatment Surgery Surgery Surgery

Antifungal antifungal anti fungal
Non invasive
AFRS Fungal Balls Saprophytic
most common Mycetoma, aspergilloma Min/ no nasal symptoms

Allergic mucus Mucous crust with fungus
Behn and Kuhn criteria
Symp: ~ CRS Symp: ~ CRS
Scope: polyp/ mucopurulent

discharge
CT: single sinus opacification, no

bony erosion, rim of soft tissue
attenuation
Management: Surgical Managment: weekly nasal toilet
Fungal ball (mycetoma)

- non-invasive
- in immunocompetent patients
- almost exclusively in max sinus
- In older individuals
- Females > males
- usually unilaterally
- can occur in other cases
- concha bullosa
- C/F ~ CRSS
- asymptomatic or sometimes some pressure
- Cachosmia - sense of foul smell when no such odour exist
- HPE
- fungal element in thick matrix with low grade inflammatory response
- mucosa/ submucosa - no fungus seen
- Predisposing factors
- prolonged used of antibiotics
- post dental filling (dental filling has zinc oxide which can promote fungal growth)
- Diagnosis
- by CT scan findings
• homogenous bone opacity with punctate calcifications
- by MRI
• variable T1
• Hypointense T2 due to absence of free water
• calcification
- paramagnetic metals
• T2 no central enhancement to differentiate from neoplasm
- Treatment
- Surgical debridement/ cleaning - for sinus aeration
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• in the past - Caldwell Luc
• present - middle meatal antrostomy
• Antifungal unnecessary
Allergic fungal rhino sinusitis

Definition
- not infection of sinus but it is a allergic reaction to fungi colonising allergic
mucin (Ig E mediate hypersensitivity)
- allergic mucin - thick greasy mucin produce in nose which contain
eosinophils and non-invasive fungal hyphae (peanut butter like)
- Charcot-Leyden crystals - formed from breakdown of eosinophils and may
be seen in the stool or sputum of patients with allergic disease or parasitic
diseases. The crystals are slender and pointed and stain purplish red in
the trichrome stain
Epidemiology
- most common form of fungal sinusitis
- common in warm, humid climates
- Hypersensitivity reaction to inhaled fungal organisms in chronic non infectious inflammatory
reaction - IgE Type I immediate hypersensitivity and type III hypersensitivity are involved
Pathophysiology
- in atopic patient or host → exposed to fungi (airborne) → Type I (IgE) + Type III
hypersensitivity → release of eosinophils → release cytotoxic mediators → causes mucosa
oedema → trap the fungus
Organisms (non-specific)
- Aspergillus fumigatus
- bipolar spicifera
- curvularia
Clinical features
- young (3rd decade)
- immunocompetent
- atopic patient
- +/- CRSS but more subtle
- IgE often raised
Kuhn & Javer 1994 - major & minor criteria
Major (1spec) Minor
1. Type I hypersensitivity 1. Asthma

2. Nasal polyposis 2. unilateral predominance
3. characteristic CT scan 3. bone erosion/ CT
4. Positive fungal stain 4. + fungal culture
5. eosinophilic mucin 5. charcot-leyden crystals
6. serum eosinophils (if total IgE >1000, then if
become major criteria)
Diagnosis
- 2 major/ 1 major + 2 minor
CT scan findings by Kuhn + Javer 1994

1. Requires at least 1 opacified PNS (must!!) + any of below:
- unilateral/ asymmetrical of disease distribution
- heterogenous opacity - deposition of heavy metals (eg. iron & manganese)
- sinus expansion (medial + anterior wall of maxillary sinus)
- bony erosion
- remodelling and thinning of bony walls
- displacement of anatomic structure
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MRI
- variable T1
- Low T2 signal (attributed to high concentration of iron, magnesium and manganese
concentrated by fungal organisms and also due to a high protein, low free water content of
allergic mucin)
The fungal elements and allergic mucin always look hypointense on MRI - can be mistaken for
absence of disease
Treatment - surgery
- remove fungal load
- for sinus aeration
1. Surgical debridement
2. systemic steroid
- 0.5mg/kg daily x 2/52, then taper down then 5mg eod up to 6/12
3. Anti fungal - topical or systemic anti-fungals are not indicated
4. Immunotherapy
- not practical, why?
- because no specific fungal, it may be multiple
5. Local steroids
6. Anti-histamines
Topical or systemic antifungal not indicated, treat as u treat CRS
Risk factors for fungal-related rhino sinusitis

1. concurrent/ preceding viral/ bacterial infection
2. Immune response elicited by super Ag produced by micro-organisms
3. Biofilm formation
4. Allergy
5. Topical steroid therapy
6. antibiotic therapy
7. concentration of ambient mould
Nasal polyps
INTRODUCTION
1. Definition
- oedema of connective tissue stroma which contains inflammatory mediators
- histamine
- prostaglandins
- leukotrienes
- usually occurs at
- ethmoid sinus mucosa
- maxillary sinus mucosa
- frontal sinus mucosa
- sphenoid sinus mucosa
- usually bilateral
INCIDENCE
- 1-20/1000 population
- Male> female = 2-4:1
- Pt with asthma and polyps > in female
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ETIOLOGY
Unknown
5 theories BPVIA
1. Bernoulli’s phenomenon
- pressure drop next to constriction → mucosa gets suck into lumen
2. Polysaccharides changes
- alteration of polysaccharides in group substance
3. Vasomotor imbalance
- majority of cases are not atopy
4. Infection
- commonest commensal in nose - non encapsulated H. influenza
5. Allergy
- 3 factors
a) histologically > 90% of nasal polyps have eosinophilia
b) majority of patients have asthma
c) nasal finding in polyps mimic with nasal findings in allergic patients
• IL-5 has found to be significantly raised in NP compared with healthy controls
ASSOCIATED CONDITIONS
1. Asthma
- 20-40% of asthmatic patients have nasal polyposis and vice versa
- late onset asthma > a/w with nasal polyps than childhood asthma
2. Aspirin hypersensitivity
- 8% of patients with nasal polyposis have aspirin sensitivity and asthma
- SAMSTER’S TRIAD - asthma, nasal polyps, aspirin hypersensitivity
3. Cystic fibrosis
- autosomal recessive, multi systemic diseases affecting exocrine
- abnormalities in chromosome 7
- sweat test
- Na+ > 60mmol/L on 2 consecutive test
4. Young’s syndrome
- gland secretions abnormally thick and viscid
- Triad of
- azoospermia
- sinusitis
- bronchiectasis
5. Kartagener’s syndrome (immotile ciliary syndrome)
- Primary ciliary dyskinesia
- bronchiectasis
- sinusitis
- situs invertus
6. Chronic rhino sinusitis with/ without allergic rhinitis / non allergic rhinitis
- NARES is chronic rhinitis a/w/ polyps
7. Allergic fungal sinusitis
8. Age
- adult
- if found in < 2 y.0
- meningocele
- meningoencephalocele
- <10 y.o
- Cystic fibrosis
9. Churg Strauss syndrome
- characterised by
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- asthma
- fever
- eosinophilia
- vasculitis
- granuloma
HISTOLOGY
1. Macroscopic appearance
- smooth, round, soft, translucent, yellow/pale, glistening mass, asensate, do not bleed on
touch
2. Microscopic
- lined with respiratory ciliated columnar epithelium + goblet cells with oedematous submucosal
tissue with few capillaries and occasional nerve fibres
- Cellular infiltrate
- plasma cells
- lymphocytes
- macrophages
- eosinophils (almost 90%) (charcot leyden crystals - eosinophil breakdown product)
- if repeated trauma → squamous metaplasia occurs
STAGING
Lund and Mackay 1997
I - confined to middle meatus
II - extend beyond MT but not occupying nasal cavity
III - massive polyposis occupying nasal cavity
CLINICAL FEATURES
Symptoms
- nasal blockage, progressive, bilateral
- rhinorrhea
- sneezing
- hyposmia
- dysgeusia
- facial pain/ fullness
- vague pain - due to splaying of nasal bridge
- PND - mucus hyper secretion
- epistaxis - TRO sinister cause
- hearing impairment - ET blockage
- snoring
Signs
- mouth breather
- flaring of alar
- hyponasal voice
- obliterated nasomaxillary groove
- mass seen protruding from nostril
- cold spatula reduced
- no neurological deficit
- craniofacial abnormality
INVESTIGATIONS
- no specific blood investigations except skin prick test
- general workup prior to symptoms
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- if <10 y.o with nasal polyposis
- sweat test
- ciliary dysfunction
- immunodeficiency
- Imaging
1. Plain PNS
- show extent of disease
- AF level
- no role in management
- no value in diagnosing nasal polyposis
2. CT scan
- if plan for surgery
- allow assessment of anatomic variations
- confirm extent of pathology
- reduce radiolucency in nose
- B/L IT hypertrophy
- DNS
- mucosal thickening
- anatomical details
- CT scan for surgery → limited series of cuts of 4/5 coronal section at 5mm interval and 2 axial
cut through eye ball
TREATMENT
1. Medical
- Aim
- to relief the nasal obstruction
- Improve sinus drainage
- Restore olfaction and taste
- To prevent recurrence
a) intranasal steroid
• immunomodulator
• stabilise mast cell
• block formation of inflammatory mediators
• inhibit chemotaxis of inflammatory cells
• Topical or systemic
• Systemic
• Short courses of systemic corticosteroids to treat severe nasal mucosal congestion in
allergic patients
• pre op usage: reduces bleeding
• can only be used for short term, has side effects
• Topical
• reduces rhinitis symptoms, improves nasal breathing, reduces size of polyps and the
recurrence rate, negligible effect on smell and any other sinus pathology
b) douching
• alkaline medium leads to thinning of mucus
c) Oral antibiotics long term (Klacid)
• Anti-inflammatory
• Immunomodulatory
• inhibition of activation of pro-inflammatory genes
• inhibition of degranulation of neutrophils
• increased apoptosis of neutrophils
• increased mucociliary transport
• reduced goblet cell secretion
• short term antibiotics have little role in treating NP
d) trial of oral steroids
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- pre-op steroids (2/52 before surgery)
- to reduce size
- to reduce vascularity
2. Surgery
- failed optimum medical treatment
- grade 3 polyps
a) nasal polypectomy
b) intranasal ethmoidectomy
c) external ethmoidectomy
d) FESS
DIFFERENTIAL
1. Children
- meningoencephalocele
- meningocele
- encephalocele
- Cystic fibrosis
- AC polyp
2. Adults
- AC polyps
- inverted papilloma
- tumour
- angiofibroma
INDICATION FOR SURGERY FOR CRS

1. Primary indication
- nasal polyposis causes obstruction of most/ all tumours
- sinus mucocele/ pyocele
- fungal rhino sinusitis
- neoplasm/ suspected neoplasm causing rhino sinusitis
2. Additional indication
- continued chronic and/or recurrent sinusitis despite medical/surgical treatment
- recurrent sinusitis 20 nasal polyposis
- correction of anatomical variation predisposing to chronic and/or recurrent rhinosinusitis
RECURRENCE
Factors a/w recurrence
1. younger
2. asthmatic
3. aspirin hypersensitivity
4. Female > incidence of asthma
Role of plain PNS x ray in nasal polyps

Plain x ray has no role either in diagnosis of management
even in acute rhino sinusitis, the diagnosis is > clinically and medical management is the first line,
if failed medical treatment → AWO
Role of CT scan in nasal polyp

CT does not play a role in diagnosis of nasal polyp
It is indicated in surgical planning for
1. anatomical mapping
2. anatomical variations
The best view for CT PNS is coronal view
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Axial view can be reformatted
The ideal cut for PNS is 1.5mm cuts
Role of MRI in nasal polyps

If suspicious of malignancy/ intracranial complications
What are the information you get from CT scan?

1. Cribriform plate
- low anterior skull base
- one side low, another high
2. Fovea ethmoidalis
- lies just lateral to CP
- thick/thin/ dehiscent
3. UP attachment
- pneumatization
4. MT
- concha bulls
5. Different anatomical cells
- agger nasi
- ethmoidal bulla
- haller/ onodi cells
Why is coronal view more important than axial view in CT PNS?
1. coronal view visualise better OMC region (axial view > for post extension of mass and to see
anatomical variation e.g. Onodi cells)
2. Level of cribriform plate/ roof of ethmoid (Based on Krausse classification)
3. Anatomical variation
4. Extension of mass
5. Lamina papyracea intact/ not
WHY ETHMOIDAL SINUS MORE AFFECTED IN POLYPS

1. Ethmoidal air cells are smallest air cells among sinuses (4-6mm in size)
- the osmium is only 1-2mm only
- →more easily to get obstructed and infected (maxillary ostium is 4-6mm i.e. the size of
ethmoid air cells)
2. Relative poorly developed blood supply
3. Complex anatomy of ethmoid labyrinth
Pre-op oral steroids

1. All asthmatic patients
2. AFS
3. Massive polyposis
Importance of being younger with polyps?
1. > difficult for post op care
2. polyps > severe in younger age group
3. > chance of recurrence
Unilateral nasal polyps

Children Adults
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Developmental 1. AC polyp
1. Developmental (<3 y.o) 2. Inverted papilloma
• encephalocele 3. tumour
• meningocele 4. angiofibroma
• dermoid tumor
• gliomas
2. Acquired
• AC polyp
• Benign massive polyp
• NLD cyst
• hemangiomas
• papillomas
• Tumor
• JNA
• rhabdomyosarcoma
• lymphoma
• sarcoma
Evaluation of nasal polyposis

+ symptomas suggestive of NP
1. Essential
- Hx
- Nasal endoscopy
2. PE
- consider CT scan
3. Others (can consider)
- Allergy testing
- culture, biopsy, staining
- sweat test
- pulmonary function
- aspirin challenge
- exclude sinister pathology
- To differentiate allergic mucin, fungal sinusitis, rhino sinusitis → do culture & biopsy
Management of nasal polyposis

Indication of surgery in nasal
polyps ~ CRS
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Ethmoidal polyp vs AC polyp (7)

AC polyp Ethmoidal polyp
Age group Children Adult
Etiology Infection allergy/ + multifatoral
Multiplicity single multiple
Laterality unilateral bilateral
Origin max sinus near the ostium from ethmoid sinus, UP and MT
Lobulity Trilobed: antral, choanal, nasal grape-like
Recurrence uncommon (if completely common

removed)
AC Polyp
- Arises from - near accessory ostium
- Trilobed - antral, choanal, nasal
- Etiology - sinus infection + nasal allergy
- Unilateral
- In children & young adult
1. Angiofibroma
2. lymphoma
3. inverted papilloma
4. sinonasal tumour
- SNUC
- lymphoma
5. NPC with nasal cavity extension
6. Encephalocele
7. Fungal sinusitis
Treatment
1. ESS
2. Caldwell Luc approach if recurrent or revision ESS
Cystic fibrosis
Definition
A disease characterised by
1. chronic bronchopulmonary infection
2. Accompanied by
- airflow obstruction
- malabsorption
- failure to thrive (FTT)
3. High sweat sodium concentration
Pathogenesis
- CF is most common congenital cause of bronchiectasis
- CF is inherited as autosomal recessive disease
- It is due to gene mutation
- Gene responsible → produces protein (cystic fibrosis transmembrane regulator CFTR) →
function as chloride channel & regulated by cAMP
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Essential abnormality
1. ↑ electrical potential acoss airway epithelium
- in CF >35mV, Normal <30mV)
2. Chloride impermeability of luminal surface of airway
3. Na+ transport through airway epithelium ↑
- leading to relative deficiency of H2O in airway secretions
Lungs + upper airway become colonised by microorganisms which cause most of damage to
bronchial wall + surrounding lung
Diagnosis
- diagnosed in 1st of life by sweat test
- Sweat test: high sweat Na+ confirming the diagnosis
- Disadvantages of test - less reliable in adolescence + adults because sweat Na+ is higher
Clinical features
- Pulmonary function usually normal at birth & may remain so for many years
- by age of 5 years - 63% of cases will have resp disease
- By age of 21 years - resp disease is almost universal (bronchiectasis)
- Chronic pulmonary infection → bacterial colonisation → neutrophil recruitment to lung →
neutrophil release neutrophil elastase → cause further damage to lung → severe
bronchiectasis → respiratory failure
- Bacteria isolated
- Pseudomonas aeruginosa
- Staph aureus
- H. influenza
- Signs
- clubbing
- chest signs vary
Investigations
1. CXR
- thick bronchial walls esp upper zones
- later, ill defined nodule shadows with scattered areas of atelectasis
- increased signs of pulmonary hypertension
2. Lung function test
- gradually deteriorate
- FEV1 is a good indicator of prognosis
- Later in the disease
- resp failure
- spontaneous pneumothorax
- massive haemoptysis
- allergic bronchopulm aspergillosis
Features suggestive of diagnosis of CF
Major criteria Minor criteria
1. Bronchopulmonary infection 1. nasal polyps

2. FTT 2. *meconium lieus equivalent
3. Malabsorption 3. rectal prolapse
4. family history 4. intussusception
5. *Azoospermia 5. *biliary cirrhosis
6. *pancreatitis
7. *peptic ulcer
8. *DM
9. *Pneumothorax
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- *> common in adolescents, adults
Management
1. Physiotherapy BD
2. Postural drainage
3. Antibiotics - oral, IV
4. Bronchodilators + CS
Nasal polyposis in cystic fibrosis

- nasal polyposis occurs in 6-36% of CF patient
- Age 4-12 years old
- can also be seen in adults
- multiple
- bilateral
- recur frequently
- Etiology
- allergy
- infection
- Histology
- as patient without CF
- May cause RLN palsy + hoarseness
- due to pulmonary hypertension with severe dilatation pulmonary trunk in late CF
- may lead to OME/ glue ear (but incidence not higher without CF)
- SNHL due to antibiotic therapy with aminoglycosides
- Treatment
- like sinusitis
• antibiotics
• intranasal steroids
• surgical
- indicated in symptomatic nasal obstruction/ recurrence
- simple intranasal polypectomy + post op intranasal CS
- ESS - in recurrence
Granulomatous disease of the

nose
Granuloma
- Definition
• Organised collection of macrophages (which are referred to as epithelioid cells), which
tend to fuse to form multinucleated giant cells
Causes
1. Infective
- Bacterial
- Fungal
- Protozoal
- Viral
2. Unspecified (Autoimmune)
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- Wegener’s granulomatosis
- Sarcoidosis
3. Neoplasm - Lymphoma, histiocytosis
4. Others - rare
Bacterial
1. syphilis
- Primary
- Rare
- Manifests as primary chancre of the vestibule of nose
- Secondary
- Rarely recognised
- Manifests as simple rhinitis with crusting and fissuring in the nasal vestibule
- Diagnosis is suggested by presence of mucous patches in the pharynx, skin rash, fever and
lymphadenitis
- Tertiary
- Nose commonly involved
- Gumma on nasal septum
- Septum destroyed both in its bony and cartilaginous parts
- Hard palate perforation
- Offensive nasal discharge with crusts
- Bony or cartilaginous sequestra may be seen
- Bridge of nose collapses causing a saddle nose deformity
- Congenital
- Early
• First 3 months of life
• Manifests as snuffles
• Discharge become purulent
• Fissuring and excoriation of the nasal vestibule and of the upper lip
- Late form
• Manifests around puberty
• Clinical picture is similar to that seen in tertiary stage of acquire syphilis
• Other stigmata of syphilis such as corneal opacities, deafness and Hutchinson’s teeth are
also present
- Diagnosis
- serological tests
- biopsy of the tissue
- Treatment
- Benzathine penicillin 2.4 million units I.M. weekly for 3 weeks
- nasal crusts are removed by irrigation with alkaline solution
- bony and cartilaginous sequestra removed
- cosmetic disease corrected after disease becomes inactive
- Complications
- vestibular stenosis
- septal perf
- hard palate perf
- saddle nose deformity
2. Tuberculosis
- 10 TB nose is rare, often 20 to lung
- anterior part of nasal septum and anterior end of inferior turbinate is most common (septal
perf at cartilaginous part )
- Diagnosis
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- biopsy
- special staining of secretions for AFB
- culture of organisms
- Treatment
- anti-TB
3. Lupus
- low grade TB infection affecting nasal vestibule or the skin or nose and face
- Skin lesions: brown gelatinous nodules called “apple jelly” nodules
- vestibule: chronic vestibulitis
- nasal septum: perforation may occur in the cartilaginous part
- May be misdiagnosed as SCC
- Treatment: ~ TB nose
4. Leprosy
- very common in the tropics
- Etiology: Mycobacterium leprae
- Symp: excessive nasal discharge, red and swollen mucosa, late features: crusting and
bleeding
- PE: atrophic rhinitis, depressed nasal bridge, destruction of anterior nasal spine, extrusion of
the columella
- Dx: scrapings of nasal mucosa and biopsy
- Acid fast lepra bacilli can be seen in the foamy appearing histiocytes called lepra cells
- Treatment: dapsone, rifampicin and isoniazid
- Reconstruction procedures are required when disease inactive
5. Rhinoscleroma
- Org: Gr -ve bacillus called Klebsiella rhinoscleromatis or Frisch bacillus
- Endemic in certain parts of the world
- Starts in the nose and extends oropharynx, larynx, trachea and bronchi
- Stages of disease
- Atrophic: resembles atrophic rhinitis
- Granulomatous: nodules, subnormal infiltration, external nose and upper lip giving a
“woody” feel
- Cicatricial: stenosis of nares, distorted upper lip, adhesions in the nose, nasopharynx
oropharynx. There may be subglottic stenosis & respiratory distress
- Diagnosis
- biopsy shows infiltration of submucosa with plasma cells, lymphocytes, eosinophils,
Mikulicz cells and Russel bodies
• Mikulicz cells - large foam cells with a central nucleus and vacillated cytoplasm
containing bacilli
• Russel bodies - homogenous eosinophilic inclusion bodies found in the plasma cells
- The causative organisms can be cultured from the biopsy material
- Treatment
- streptomycin and tetracycline are given together for a 4-6 weeks and repeated, if necessary
aft 1 month
- Treatment is stopped only when two consecutive cultures from the biopsy material are
negative
- Steroids can be combined to reduce fibrosis
- Surgical treatment may be req to establish the airway and correct nasal deformity
Wegener’s granulomatosis (Granulomatosis polyangiitis)

Definition
- Systemic disorder of unknown etiology
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- Characterized by granulomatous inflammation of the resp tract
- With necrotising vasculitis of small and medium sized vessels
- And focal or proliferative glomerulonephritis
Site
- Classification affects nose, lungs, kidneys
- Can affect any organ
Epidemiology
- Average age of onset: 40-55 years old, but can occur at any age
- M:F=1:1
- Predominantly Caucasians
Clinical features
1. Nasal (60-90%)
- Obstruction
- Crusting
- Discharge
- Epistaxis
- Hyposmia/ Anosmia
- Pain
- Epiphora
- Change in shape of the nose
2. Otological (40%)
- Conductive
- SNHL
3. Airway and lung
- Subglottic stenosis
- Cough
- Hemoptysis
- SOB
4. Constitutional symptoms
- General systemic: anaemic, fatigue, night sweats, migratory arthralgia
- PE
- crusting
- granulations
- septal perf
- saddle nose
- MEE
Investigations
1. ANCA - strongly associated with 3 vasculitis
- GPA
- Eosinophilic granulomatosis with polyangiitis (Churg Strauss syndrome)
- Microscopic polyangiitis (MPA)
- Not 100% sensitive or specific for GPA
2. c-ANCA (cytoplasmic ANCA) specific for proteinase 3 (PR3)
- 90% sensitive and 98% specific for generalised GPA
- 10% of GPA will hv +ve test for perinuclear ANCA (p-ANCA) against myeloperoxidase
- 30% will hv negative ANCA test initially
3. Biopsy
- Difficult from nose
- Often higher yield from lung and renal biopsies
- Histological diagnosis: granulomatous inflammation + vasculitis + necrosis
4. Imaging
- CT: non-specific mucosal thickening (85%), bony destruction (75%) with new bone formation
(50%)
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- CXR: multiple cavity lesions
- Kidneys:
- UFEME: red cells, casts, albumin
- Serum creatinine raised
- Renal failure is the usual cause of death in these patients
5. ESR is raised
Management
European Vasculitis Study Group Classification - localised, early systemic, generalised disease
1. Localised (resp tract involvement only)
2. Early systemic
3. Generalised disease
- systemic steroids and cytotoxic drugs

- cyclophosphamide and azathioprine (steroid sparing agents)
- Monoclonal antibodies
• Rituximab
• Infliximab
Nose
- Nasal douching
- Topical steroids
- Sinus surgery - avoided - causes post-op scarring
- Surgical repair of septal perf - unlikely successful
- Recon of saddle nose - poor results if disease active - may consider if disease quiescent for a
year
Ear
- Grommets should be avoided
- HA for hearing loss
Subglottic stenosis
- Regular dilatation, intralesional steroid injection, endolaryngeal laser treatment
Mortality rates
- 5% despite immunosuppressant tx
- 10% for those who never enter remission
- Patients who enter remission - 50% will relapse
Eosinophilic Granulomatosis with polyangiitis (Churg Strauss

syndrome)
Definition
- Rare, potentially fatal systemic necrotising vasculitis of unknown etiology
- Affecting small to medium sized vessels
- Associated with asthma, eosinophilia, extravascular eosinophilic granuloma
- Asthma late onset
Epidemiology
- Mean age of onset: 50 y.o
- M:F = 1:1
- Causcasians mainly affected
Phases
1. Prodromal phase (few years)
- Nasal and pulmonary symptoms tend to worsen
2. Development of peripheral eosinophilia >10%
- Eosinophilic infiltrates of other organs
3. Onset of systemic vasculitis
- Peripheral nervous system symptoms - mononeuritis multiplex
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- Skin involvement - with purpura and nodules
- GI symptoms
- Renal disease
- Cardiac involvement
Physical examination
1. Nasal
- Obstruction
- Rhinorrhea
- Anosmia
- Sneezing
- Crusting
- Epistaxis
Diagnosis
At least 4 of the following (American College of Rheumatology 1990 criteria for Dx of EGPA)
1. Asthma
2. Fixed pulmonary infiltrates
3. Abnormalities of the paranasal sinuses
4. Eosinophilia > 10% differential
5. Extravascular eosinophilis on biopsy
Investigations
1. ANCA associated vasculitis, but p-ANCA only +ve in 30%
2. Eosinophilia
3. Acute phase proteins elevated
4. Biopsy - generally unhelpful
- But skin, nerve, muscle or lung tissue higher positive yield
5. CT
- Pan-opacification of paranasal sinuses on CT
Management
1. Immunosuppresion
- Corticosteroids
- Steroid sparing agents
2. Sinonasal symptoms
- Douching
- Intranasal steroids
- Surgery - polyps or mucociliary
Predictors of death
1. Cardiac involvement
2. Older age at diagnosis
3. ANCA -ve disease
Sarcoidosis
- granulomatous disease of unknown ethology
- non-casesting granulomatous
- Systemic disorder
- lungs
- lymph nodes
- eye
- Nose
- submucosal nodules involving septum or inferior turbinate with nasal obstruction, nasal pain
and sometimes epistaxis
- nasal vestibule, skin of face involvement
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- CXR
- diffuse pulmonary infiltrate with hilar adenopathy
- serum and urinary calcium levels are elevated
- Biopsy
- help establish the diagnosis
- Treatment
- systemic steroids
• for nasal symptoms: intranasal steroids
Sinonasal papilloma
- Benign tumour arising from ectodermally derived ciliated epithelium of the nasal cavity, termed
the “Scneiderian membrane”.
- 3 morphological types
1. Exophytic (fungiform) - septum/ vestibule
- 6-50%
- Male: Female 10:1
- 20-50 years old
- low anterior portion of nasal septum
- rarely involved lateral nasal wall
- HPV 6,11
- rarely in paranasal sinus and undergo malignant transformation
- bilateral uncommon
2. Inverted (Ringertz tumour)
- in nose and paranasal sinuses, upper
aerodigestive tract
- complex arborescent exoendophytic growth
pattern with ramifications into the underlying
stroma
- epithelium may be squamous, respiratory and
transitional cell like
- risk of malignant transformation → invasive
SCC, adenosquamous carcinoma,
adenocarcinoma
3. Cylindrical cell papilloma/ microcytic papillary
adenoma/ oncocytic Schneiderian papilloma)
- Rare
- No sex predilection
- > 50 y.o
- unassociated with HPV infection
- From lateral wall
- KRAS mutation
- exophytic fronds of bilayered, oncocytic epithelium supported by fibrovascular subintima
Inverted papilloma
Inverted Papilloma/ Scneiderian tumour/ Transitional cell papilloma
INTRODUCTION
- Benign epithelial sinonasal tumour composed of respiratory/ transitional/ squamous epithelium
which
① locally invade surrounding stromal tissue but basement membrane is intact &
② tends to recur & has
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③ potential for malignant transformation
- most common benign sinonasal tumour
- a/w HPV Type 6, 11, 16, 18
- exact cause is unknown
- Ectodermal in origin
EPIDEMIOLOGY
- incidence 0.5-4% of all nasal tumour
- Male > female = 4:1
- commonest age = 5th - 6th decade
- Site of origin
- 90% from lateral wall (middle meatus mucosa)
- PNS
- maxillary 60%
- ethmoid 30%
- sphenoid + frontal 10%
- nasal septum (rare)
- inferior turbinate/ meatus
- nasal vestibule
- How do they become malignant
- ab initio 1%
- synchronous 15%
- metachronous <10%
- usually unilateral
CLINICAL FEATURES
- unilateral nasal obstruction (majority) - progressive
- epistaxis
- rhinorrhea/ nasal discharge
- facial discomfort
- headache
- hearing impairment → impinges ET
PHYSICAL EXAMINATION
- unilateral mass polyp-like
- firm in consistency
- granular mulberry appearance
- red to pale pink colour
- bleeds on touch
- appearance more vascular
- probing - origin fr lat wall
- ? Punctate hemorrhages
Diagnosis
Biopsy
HISTOLOGY
most characteristic feature → invagination of neoplastic epithelium with intact base membrane into
underlying stroma
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Neoplastic epithelium may be
- resp type
- transitional type
- squamous type
1. orderly maturation
2. low mitotic rate
3. minimal atypia
Histopathological Grading
I: ciliated resp epithelium, early inversion of squamous metaplasia
II: partially ciliated respiratory epithelium, more inversion, involve seromucinous glands
III: near complete absence of resp epithelium, squamous metaplasia, dysplasia
IV: SCC, with grades II/III
STAGING
Krouse, 2000
I - confined to nasal cavity
II - involving OMC, ethmoid, medial wall of maxillary sinus
III - involved any wall except medial wall of max sinus, sphenoid and or frontal sinus
IV - extend beyond nasal cavity/ PNS, or a/w malignancy
ETIOPATHOGENESIS
Exact cause unknown
1. Viral etiology has been postulated
- HPV Type 6, 11, 16, 18
- →HPV is believed as tumour inducing + promoting agent involved in transformation of benign
to malignant upper aerodigestive tumour
- HPV interacts with p53 protein → leading to malignant transformation
- therefore p53 can be used as a prognostic marker
- 6,11 associated with benign papilloma
- 16,18 associated with malignant transformation
2. ↓ expression of CD4
3. EBV
ORIGIN OF TUMOUR
mucosa of sinonasal tract (Schneiderian membrane) which is formed by invaginating ectoderm of
olfactory plates during 4th week of life
INVESTIGATIONS
1. Diagnostic → biopsy
2. Imaging
- PNS X-ray - not useful except haziness of sinus involved
- CT scan (Ix of choice)
- homogenous opacity of affected sinus
- thinning of max wall/ bony erosion is due to pressure necrosis
- calcification within mass (due to entrapped or remodelled bone)
- post contrast enhance heterogeneously
- focal osteitis → site of origin of IP
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- MRI
- convoluted cerebriform pattern on T2 or enhanced T1 weighted images
- necrosis in a mass → suggest coexistent carcinoma
3. Blood investigations
DIFFERENTIAL DIAGNOSIS
1. AC Polyps
2. AFRS
3. Tumour of NPC
4. AdenoCA
5. Esthesioblastoma
6. Angiofibroma
TREATMENT
1. Medical - as adjunct to complications (e.g. sinusitis)
2. Surgical
① External approach
② Limited (Caldwell-Luc)
③ Radical (medical maxillectomy via lateral rhinotomy/ mid facial degloving)
- via lateral rhinotomy→ medial maxillectomy - GOLD STANDARD
- But endoscopic approach have facilitated a greater role in IP resection
• medial wall
• all 3 turbinates
• anterior ethmoid
- disadvantages/ complications
• scar
• epiphora
• dacrocystitis
• intermitted diplopia
• lid oedema
• crusting
• CSF leak
- through this approach, the recurrence rate reduces
(15-20%)
- mid facial degloving Approach

• for extensive benign nasal lesion
• 4 hidden incision made
- sublabial incision
- bilateral inter cartilaginous incision
- complete transfixation of columella from septum
- bilateral pyriform incision
• advantages
- no scar externally
- gives good exposure bilaterally
• disadvantages
- limited superior exposure
• tumour of lateral wall that extends to LP, supraorbital ethmoidal air cells & frontal
sinus might not be compromised
- Caldwell-Luc (limited external approach)
④ endoscopic approach (FESS)
- endoscopic endonasal medial maxillectomy
- grown in importance lately
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- Stepladder of surgical techniques: endonasal → mid facial degloving → sub cranial
approach (advantage: scar less)
- Lateral rhinotomy if exenteration of orbit needed simultaneously
• Key concepts:
- dissect involved mucosa along subperiosteal plane
- find the origin of the papilloma, bony removal of this region (very important to identify
site of attachment of the tumour pedicle in order to ensure full resection)
• Goal:
a) remove tumour completely,
b) identifying and adequately treating site of tumour attachment,
c) creating safe sinus cavity for long-term surveillance,
d) minimising patent morbidity
• Absolute contraindications
- massive skull base erosion
- intradural and intraorbital extension
- dissect the involved mucosa along the subperiosteal plane
- drill underlying bone → excise bony attachments
- Complete resection of bony attachment to the posterior, lateral and anterior maxillary
sinus walls requires special endoscopic techniques
• trans-septal through opposite nostril
• canine fossa puncture to introduce the debrider
• If tumour originate from anterior wall or has a large area of origin within the maxillary
sinus, an endoscopic medial maxillectomy is recommended for complete tumour
removal
- ENDOSCOPIC MEDIAL MAXILLECTOMY
• nasal packing
• LA
• Uncinectomy
- Maxillary antrum enlarged posteriorly until posterior wall of sinus is
encountered and medial wall of orbit is visualised
• Anteriorly up to lacrimal bone, sparing NLD
• Posteriorly up to posterior maxillary wall
• Superiorly up to skull base
• Inferiorly up to floor of nose
• Inferior turbinate is removed, middle turbinate is preserved
• Duct visualised and transected with a scalpel
• Type 1 resection
- Ip limited to middle meatus, anterior and posterior ethmoids, SER
- Anterior ethmoidectomy with clearance of frontal recess
- Posterior ethmoidectomy
- Large middle antrostomy
- Sphenoidotomy
- Partial/ middle turbinectomy
- lesion from MM into max sinus, originate from medial wall of max sinus
- Type 1 + medial matxillectomy +/- NLD section
- Lesion originate or involve posterolateral or inferior wall of max sinus
- Endonasal Denker op
• incision at anterior to inferior turbinate
• expose pyriform crest
• drill out anterior wall of max sinus
• Section NLD
• Preserve infraorbital nerve
- Anterior and posterior ethmoidec + sphenoid + Denker + complete inferior and middle
turbinectomy + frontal sinusotomy
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⑤ Combined approach
FOLLOW UP
1. Day 5 - remove pack
2. weekly x 6/52 → remove crusting, douching
3. Every 3/12 x 2 years
4. Every 6/12 up to 5 years
AREAS ASSOCIATED WITH HIGH RECURRENCE

RATE
1. Nasofrontal duct
2. supraorbital ethmoid cell
3. lacrimal fossa
4. infra-orbital recess of max sinus
WHY TEND TO RECUR?

1. Incomplete removal
2. Multicentric origin of tumour
- esp if attach over optic nerve/ carotid A within sphenoid sinus
3. Tumour location
- involve frontal/ maxillary sinus
4. Method of removal
5. underwent 2nd surgery
RECURRENCE RATE
1. External approach 20%
2. Intranasal approach 60%
- T1 - 0%
- T2 - 4%
- T3 - 20%
- T4 - 35%
3. Caldwell Luc 60%
mostly within first 2-3 years after initial treatment

mostly recur at site of original tumour
Threrefore, requires long term follow up
MALIGNANT TRANSFORMATION IN IP
- Predominant malignancy - synchronous or metachronous SCC
- Verrucuous and adenoca also reported
1. cancer + IP exist in same anatomic region without evidence that papilloma give rise to cancer
- SYNCHRONOUS TUMOUR (10-15%)
2. Small focus of cancer is found within papilloma
- AB INITIO (<1%)
3. Cancer develop in same anatomic region where a previously benign disease was resected
- METACHRONOUS TUMOUR (<10%)
Histological predictors of malignancy
1. Presence of bone invasion
2. Absence of inflammatory polyps
3. Increased ratio of neoplastic epithelium to stroma
4. Increased hyperkeratosis
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5. Presence of squamous epithelial hyperplasia
6. high mitotic index
7. Low number of eosinophils
8. Presence of plasma cells
9. HPV +ve
10. Overexpression of p53
Prognosis
1. Tumour size
- larger → higher recurrence
2. HPV
- 16,18 → more associated with malignancy
- 6,11 → benign pathology
ROLE OF RADIOTHERAPY
- usually reserved for those cases of IP a/w SCC
- pure IP → ineffective
- Furthermore → possible induction of malignancy (malignant transformation)
- Indication
- IP a/w SCC
- multiple recurrence
- incomplete resection
- moderate RT doses below 60 Gy can effectively prevent recurrence
Epistaxis
DEFINITION
Bleeding from inside the nose
usually a symptom/sign
EPIDEMIOLOGY
- affects all ages, but particular in:
- 2 peaks
- 15-25 years
- young patients - trauma/ arterial bleeding
- 45-65 years
- associated with hypertension/ atherosclerosis
- affects 10-12% of population
- male=female
- higher incidence in
- colder winter
- hot dry climates with reduced humidity
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Causes/ Ae)ology
Local
Systemic
Congenital Acquired -Blood disorder

glioma -idiopathic - from li;le’s area (85%) coagulopathies - haemophilia, DIVC
choana atresia -infec)ve platelet disorder - ITP, myeloprolifera)ve disease
meningocele acute - viral/ bacterial/fungal blood vessel disease - HHT
meningoencephalocele chronic - TB/ syphilis/ wegener’s Hyperfibrinolysis
-inflammatory -medical
nasal polyps/ CRSS HPT, atherosclerosis, liver failure, HIV
-neoplasia -drugs
benign - JNA, papilloma aspirin, an)coagulants, an)bio)cs (CMC,
malignant - SCC, adenoma methotrexate)
-Trauma
iatrogenic
FB
nose picking
facial trauma
-Drugs
rhini)s medicamentosa (topical decongestants/
cocaine)
PATHOPHYSIOLOGY
1. Progressive replacement of muscles layer in tunica media by connective tissue by fibrous/ scar
tissue
- reduces vascular ability to contract as in normal physiological response to bleeding e.g.
atherosclerosis/ HPT
2. Calcification within vessel wall
- monckerberg’s sclerosis
- affected larger vessels e.g. maxillary artery
- vessel is less elastic
3. Veins
- “Ballooning phenomenon” - weakening vein walls
- unknown case
- perhaps due to localised ischaemia and/or trauma
- bleeding from retrocolumellar vein
Spontaneous epistaxis
- contributing factors
- nose picking
- coughing
- sneezing
- straining
- pregnancy
- sinusitis
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TYPES
Anterior posterior
Incidence >common <common
Site Little’s area Posterosuperior part of nasal

cavity
Age Children Elderly

Young adult
Cause Trauma HPT/atherosclerosis
SITES OF BLEEDING
1. Little’s area/ Kieselbach plexus
- 90% of epistaxis
- Little’s area situated in area where exposure to airflow is more → prone for dryness
- Little’s area is highly vascular → arterial in origin
- Anastomosis of
- nasopalatine A - from ECA
- greater palatine A - from ECA
- Anterior ethmoidal A - from ICA
- Superior labial A - from ECA
- usually occurs in older age group
- duration: quite prolonged
2. Retrocolumellar vein
- occurs in age < 35 years
- duration: short lived
- situated behind columella & runs on floor of nose to lateral wall
- anterior to Little’s area
3. Woodruff’s plexus
- venous in origin
- situated at post end of of IT (1cm behind to IT and 1cm above floor in the lateral wall)
- treatment: tamponade
4. Haemorrhagic nodules → arterial origin
- an aneurysmal dilatation of artery
- can occur anywhere in nose
- usually associated with hypertensive changes in wall of arteries & turbinates/ haemorrhage in
adjacent connective tissue
5. Septal turbinates
- area of engorged vascular nasal mucosa on septum
- may be uni/bilateral
- Treatment: SMR
MANAGEMENT
1. History
- onset
- frequency of epistaxis, amount of bleeding
- drugs
- inhalants
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- easy bruising
- flexible
- rigid
3. In acute bleeding
- resuscitate
- IV line
- GXM
- Trotter’s method
- sit up
- lean forward
- open mouth
- pinch the nose
- ice fermentation
- establish site
- stop bleeding
- pack nose
• anterior
- ribbon gauze with vaseline/ cocaine 5/10%
- BIPP
- merocell
- kaltostat (calcium sodium alginate)
• inserted without LA
• relatively atraumatic
• absorbed locally
- nasal balloons
• posterior
- triple lumen epistat
• posterior balloon 10cc, anterior balloon 30cc, another lumen for breathing
- Foley’s catheter - 15ml of H2O/ air
- Post gauze pack
- Brighton’s balloon
- Simpson’s balloon
- avoid adrenaline packing → cause rebound bleeding while is difficult to control
• pack with 5% cocaine/ 10% cocaine → anaesthetic effect, vasoconstriction
• Principle of packing
- should not be left in nose >48 hours without antibiotic
- BIPP
• can use up to 5 days without antibiotics
• has antiseptic
- cauterisation
• silver nitrate
• electrocautery
SURGICAL INDICATION - failure of packing after 4-5 days (persistent oozing)
1. Arterial ligation
- ECA → ligate just above lingual art
- IMA → sublabial - Caldwell Luc’s - post lat wall
- Ant ethmoidal A/ Post ethmoidal A - Lynch Howarth’s - 2.4cm behind anterior lacrimal crest
2. SMR
3. Endoscopic cautery/ ligation of sphenopalatine Art
4. Angiography + embolisation
- failure to stop bleeding aft ligation of IMA
- ligation of non-dominant maxillary art
- failure to identify to max a in pterygomax space
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- blood flow through partially closed clips
- bleeding from post ethmoidal art
- revascularization of nasal blood supply
- ligation of IMA causes drop in local BP > through ligation of ECA
Olfactory neuroblastoma
(Esthiosioneuroblastoma)
Introduction
- First described by Berger and Luc 1924
- uncommon malignant neoplasm of nasal vault
- slow growing but with aggressive behaviour
- it is a neuroendocrine tumour rising from olfactory epithelium of neural crest origin (Jacobson's
vomero-nasal organ) of
- cribriform plate
- superior turbinate
- upper 1/3 of nasal septum
- = area lined with olfactory epithelium
Incidence
- 6% of nasal cavity neoplasm
- Age
- bimodal age
• 20-30 - less local recurrence, > mets
• 40-50 - > local recurrence, < mets
- can affect all ages
- case reported in child of 2 years old
- Sex: females more
Clinical features
1. Nasal
- nasal obstruction (70%) of cases
- epistaxis (50%) of cases
- Anosmia
2. orbital
- proptosis
- excessive lacrimation
- diplopia
3. Oral
- mobile tooth, non-healing tooth extraction site
4. headache/ facial pain
5. Neck
Macroscopic appearance
- lobulated
- soft, red to grey
- areas of necrosis + calcification
Microscopic appearance
- rests of small cells separated by fibrovascular septa with neurofibrillary intercellular matrix and
rosette formation
- Homer Wright rosettes- pseudo rosettes - cells mantling solid, fibrillary neuropil stroma
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- Flexner wintersteiner rosettes- true rosettes - cells surrounding an empty pseudolumen
- Immunochemistry definitive diagnosis
- positive for neuroendocrine marker
• chromogranin
• synaptophysin
• neuron specific enolase
• protein gene product
• S100 protein - stain sustenticular cells
Ki67 + signify poorer prognosis
Loss of lobulity signify poorer prognosis
Progressive Loss of s100 and nse indicate poorer prognosis
Classification (stage)
by Kadish et al, 1976
A - confined to nasal cavity
B - involved nasal cavity + PNS
C- extend beyond these limits
Kadish clinical staging with Morita's modification

A - limited to nasal cavity
B - involving nasal cavity and paranasal sinuses
C - extension beyond nasal and paranasal sinuses
D - distant metastasis
Metastasis (20-30%)
- bone
- lung
- abdomen
- pelvis
- CNS (rare)
Hyam's histological grading

Based on
1. Degree of differentiation
2. Tumour architecture
3. Mitotic index
4. Nuclear pleomorphism
5. Presence of rosettes
- Homer Wright - grade 1/2
- Flexner winter Steiner - grade 3/4
6. Fibrillary nature of matrix
7. Tumour necrosis
- ➗ into grade I, II, III, IV

- better differentiated (grade I, II)
Investigations
1. General - for op
2. Specific
- history - detailed
- PE - as mentioned
- Using VMA, HVA (homovanilic acid) - absent in ENB, but detectable in sympathetic
neuroblastoma (eg. MEN II)
3. Biopsy
- definitive
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4. CT scan
- dumb bell shaped mass extending across the cribriform plate
- Homogenous enhancing mass, with non enhancing area suggestive of area of necrosis
5. MRI
- T1 - hypointense to gray matter, T2 - iso/hyperintense, enhance with gado
- Involve olfactory bulb - pathognomonic
- intracranial extension
- intraorbital extension
6. Radio isotope scan
- technetium 99 - increased uptake
- Ethylcysteinate dimmer - specific for tumour of neural crest origin
Treatment
1. Surgical excision
- endoscopic
- external approach via craniofacial resection
- if involve cribriform plate
2. Dxt 5500-6500 cGy
- adjuvant therapy for low grade tumour
- residual/ recurrent
- all high grade tumours
3. Chemotherapy
- For recurrence and Metastatic disease
- cisplat + etoposide
- cyclophosphamide + vincristine +/- doxorubicin
Gold standard - CFR + Dxt
Recurrence
- Mayo clinic reported 42% local recurrence in 5 years post-op
- Other research - rate of 39-56%
- local recurrence ~30-40%, usually within 2 years
- metastasis - 20-30%
Esthesioneuroblastoma vs differential diagnosis

1. Sinonasal melanoma
- more aggressive
- in 5th-8th decade
- lack of HMB 45 immunopositivity
- pattern of S100 staining diffuse & strong
- chemo has no role
- Treatment: resection
2. SNUC
- absence of mitotic figures in ENB
- in SNUC, areas of necrosis, vascular invasion, glandular differentiation
- Cytokeratine antibodies staining +ve in SNUC
3. Lymphoma
- 6th-8th decades
- ♀:♂ 1:2
- ENB lacks common leukocyte antigen (LCA) immunostaining
4. Ewing’s sarcoma
- ENB lacks Myc-2 protein immunostaining
5. Rhabdomyosarc
6. Plasmacytoma
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Unilateral nasal obstruction Pterygopalatine fossa is a major crossroad within the

Based on anatomical position deep face, from where tumour infiltrates
1. Vestibule 1. V2 → foramen rotundum → intracranial cavity
- furuncle of hair follicle (furunculosis) 2. along vidian canal →posteriorly → foramen
- vestibulitis lacerum → pterygomaxillary fissure
- stenosis of nose(CNPAS) 3. laterally - pterygomaxillary fissure → masticator
- atresia space
- nasoalveolar cysts/ nasolabial cyst 4. Superiorly - inferior orbital fissure → orbital apex
- SCC → superior orbital fissure → intracranum
2. Nasal cavity
- FB/ rhinolith
- DNS 
Hypertrophic IT - compensatory/ paradoxical
- unilateral mass
- AC polyp
- Atrophic rhinitis
- Synechia
- Septal hematoma/ abscess
- Tumour
- benign
- malignant
3. Posterior choana
- posterior choana atresia
4. Nasopharynx
- NPC
- Angiofibroma
- Lymphoma
Nasopharynx
Introduction
- NP derived from primitive pharynx
- transitional zone between nasal cavity + oropharynx
- It is a space without many natural barriers to spread of tumour growth
Surgical anatomy
- inverted J-shaped muscular-aponeurotic sling suspended from the central skull base
- C1/C2 junction - level of demarcation btw nasopharynx and oropharynx
- average dimension of NP
- high 4cm
- wide 4cm
- AP 3cm
- Boundaries
- Anterior wall
• posterior choana orifice
• posterior margin of nasal cavity
- Floor
• Upper surface of soft palate
- Roof + post wall
• Roof
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- body of sphenoid (basi-sphenoid)
• Posteroinfeiorly
- basi-occiput/clivus
- C1-2 vertebra
- Lateral
• ET + tubal elevation
• FOR
Fossa of Rosenmuller
- situated between lateral & dorsal wall of NP
- in infants - not obvious
- In adults - recess measure up to 2.5cm depth
- Opens into NP at a point below foramen lacerum
- Anatomical relationship
- anteriorly: ET, levator palatini
- posteriorly: pharyngeal mucosa overlying pharyngobasilar
fascia, retropharyngeal space + node of Rouviere, superior
constrictor muscle, buccopharyngeal fascia
- medially: nasopharyngeal cavity
- Superiorly: foramen lacerum, floor of carotid canal
- posterolaterally: carotid canal opening, foramen lacerum (formed by posterior margin of
petrous apex and superior part of clivus), foramen ovale (lateral to foramen lacerum),
foramen spinosum
- laterally: tensor palatini muscle, mandibular nerve, prestyloid compartment of
parapharyngeal space
- inferiorly: upper edge of superior constrictor muscle, laterally: tensor veli palatini muscle
- Sinus of Morgagni - area of muscular deficiency in the upper nasopharynx where the
cartilaginous part of the ET and levator veli palatine muscle enter the pharyngeal wall
- Pharyngobasilar fascia - tough aponeurosis that connects the superior constrictor muscle to
the skull base
Epithelial lining of nasopharynx
- NP mucosa - serous & mucous gland in
submucosal layer
- during fetal life, there is gradual transition
of resp ciliated epithelium to squamous
type in lower & post part of NP
(Squamous metaplasia)
- true squamous metaplasia occurs only in
post-natal life & completed by 10 years of
age
- 60% of total epithelium surface is lined by
stratified squamous epithelium
- mucosa abutting choana + immediate NP
roof → ciliated epithelium
- rest of the roof + lateral walls →
transitional cell type (patches of
squamous + ciliated)
- post NP wall → squamous epithelium
- Subepithelial connective tissue is RICH in
lymphoid tissue
- small lymphocytes
- plasmacytes
- reticular cells
- fibroblasts
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Lymphatic drainage
- NP has extensive submucosal lymphatic plexus
- 1st order drainage/ 1st echelon → retropharyngeal group of Rouviere
- Node of Rouviere
- lies within the retropharyngeal space
• bounded anteriorly by pharyngeal constrictor muscles and posteriorly by prevertebral
fascia
-
lies anterior to lateral mass of atlas at lateral border of longus capitis muscle
-
situated anteromedial to ICA
-
Medial and lateral group
-
Medial group (near midline) - 1-2 lymph nodes
• →drains the roof and posterior border of the nasopharynx → lateral retropharyngeal node
of Rouviere
• may bypass this node → drain directly to JD/Level II node
- Lateral group (medial to carotid artery)
• can be found any level within the retropharyngeal space (skull base to C3)
• Most superior LN of lateral group - lymph node of Rouviere
• drains lateral nasopharynx, incl. FOR → directly into the deep nodes of the posterior
triangle (spinal accessory nodes or upper Level V nodes)
- NP is midline structure with rich lymphatic channels
- easily drain to contralateral & bilateral nodes
Adenoids
- Consist of B lymphocytes (mainly) & T lymphocytes
- poorly developed at birth
- not visible on plain radiograph in <1/12 old
- clinically identifiable by 4/12
- 50% infant < 6/12 - radiologically demonstrable
- 100% infant > 6/12 - radiologically demonstrable
- by 2 y.o - hypertrophy & hyperplasia of adenoids occur
- rapid growth from 3-5 years old
- involute after puberty
- if ↓ in size/ absent - indicate immunodeficiency
- If NP mass in infant < 1/12 - suspect encephalocele
WHO classification of NP tumours

1. Epithelial tumours
- benign
- papilloma
- pleomorphic adenoma
- oncocytoma
- Malignant
- NPC
- Adenocaricnoma
- adenoid cystic ca
- mucoepidermoid ca
2. Soft tissue tumour
- benign
- angiofibroma
- hemangioma
- neurofibroma
- malignant
- fibrosarcoma
- rhabdomyosarcoma
- angiofibrosarcoma
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3. Bone & cartilage tumour
- osteosarcoma/ osteoma
- chondrosarcoma/chondroma
4. Malignant lymphomas
- NHL, Hodkin’s lymphoma
- Plasmacytoma
5. Miscellaneous
- Meningioma
- teratoma
- malignant melanoma
NPC
A non lymphomatous SCC that occur in epithelial lining of NP which shows varying degree of
differentiation
Epidemiology
1. Geography & race
- incidence among Chinese + other south east Asian is 10-50x
- Highest incidence : 30-50/ 100000 (in Southern China)
- other parts: Southeast Asia, Eskimos from Arctic, inhabitants from North Africa and the
Middle East
- ↑ among Chinese
- Intermediate in Malay, natives of Sabah and Sarawak
- Lowest among Indians
- Highest in Xanthoderm, then Melanoderm, lowest in Caucasian
- 4th commonest ca in Malaysia
2. Sex
- ♂>♀ = 3:1
3. Age
- begins from 15-19 y.o
- remain most frequent CA in ♂ aged 15-34 y.0
- Reaches plateau btw 35-64 y.o
- declines after > 65
Etiology
Multifactorial
1. Genetic
- chinese have higher genetic susceptibility to NPC
- Chromosomal abnormalities
- chr 1-6, 9, 11, 13-14, 16-17, 22, X chromosome
- Early dysplastic changes → loss of allelic short arm chr 3+9 → inactivation
of tumour suppressor gene p14, p15, p16
- First degree relative - 2-15 times
- associated with chromosome 4, 3p21
- 3p21- where a cluster of tumour suppressor genes resided
2. EBV
- is a gamma herpes virus, member of the lymphocryptovirus genus natural
infection in childhood
- Acts as a carcinogen
- Lymphotropic action is restricted to B lymphocytes
- 10 infection of EBV takes place in childhood
- ALWAYS accompanied by seroconversion & remain dormant state for life
in B lymphocytes/ saliva
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- NPC is epithelial tumours, NOT related to endemicity of EBV
- Association of NPC with EBV is supported by
i) presence of humoral immune response against EBV antigens (e.g. VCA viral capsid
antigen, EA early antigen, NA, nuclear antigen)
ii) presence of EBV marker, EBV DNA in NPC cell tumour
- only Type III and I have a consistent immunological a/w EBV
- EBV serological marker
- IgA and Ig G to VCA
- Ig A and Ig G to EA
- Antibody to nuclear antigen (EBNA)
- Antibody dependent cellular cytotoxicity antibiotics
- Important in evaluating
a) Stage of disease at time of diagnosis
b) effect of & response to therapy
c) clinical course
d) survival • There is no prognostic
values of initial serology,
- using titre of IgA/ VCA and IgA/ EA including IgG and IgA
• if static/ ↓ in titre aft Tx → successful tx antibodies to VCA, EA, or
• if ↑ titre after tx → recurrence and/or metastasis EBNA
- If EBV serology +ve → multiple biopsy of NP • However, increasing titers of
- valuable in serological screening in endemic region EA-IgA, EA-IgG, one year
for NPC after completion of
- LMP 1 radiotherapy became highly
• integral membrane protein containing a significant for prediction of
cytoplasmic amino terminus, six transmembrane
relapse, regardless of the
domains, and a long cytoplasmic carboxy terminal
portion initial titers
• associated with poorer prognosis
- Plasma EBV DNA - highly sensitive and specific
• useful molecular marker in screening, monitoring, and prognostic prediction of NPC
• highly correlated with tumour burden
• tumour relapse cases had higher pretx plasma • Larger tumours → increased
concentration of EBV DNA number of tumour clonogens, as
• Plasma EBV DNA load before, during and at the well as other adverse radio biologic
end of neoadjuvant chemotherapy declined factors, including tumour hypoxia
significantly and thus their relative radio
• plasma EBV DNA remained persistently low or resistance
undetectable • 1cm3 increase in primary tumour
• Tumor relapse showed a rebound of plasma EBV volume → 1% increases in risk of
DNA concentrations, which might be detected 6 local control failure
months before clinical evidence of relapse supraclavicular node being the last
3. Environmental factors •
line of defence
- cigarette smoking - ↑ 3x (→more in keratinising SCC)
• failure of supraclavicular nodes to
- salted fish/ preserved vegetables (contain volatile contain the malignant cells →
nitrosamines) spilling into thoracic duct →
- Zinc and Cadmium - positively related with the genesis systemic circulation
of NPC
• Supraclavicular lymphadenopathy
- industrial fumes & chemicals (N3 disease) is therefore
- wood dust/ formaldehyde associated with a high risk of
- household smoke/ fumes systemic metastasis
- ↓ vit c, carotene, fibre diet
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Molecular signalling pathways in NPC

1. EGFR
- receptor tyrosine kinase (RTK)
- activation of this receptor → phosphorylation cascade (via tyrosine kinase pathway) cell
proliferation, apoptosis, invasion, angiogenesis, mets
- ↑ - indicated poor prognosis
- is a transcriptional factor as well as signal transducer in NPC
- over expression - negative prognostic factor for NPC as for other SCCHN
- higher expression - more advanced stage
- Targeting EGFR in NPC
① monoclonal antibodies (MAbs)
② tyrosine kinase inhibitors
2. Angiogenesis
- angiogenesis involves degradation of basement membranes, migration and proliferation of
endothelial cells, lumen formation and stabilisation of neovasculatures
3. Vascular Endothelial Growth Factors and Receptors
- VEGF - most cardinal vascular growth factor prompting tumour angiogenesis
- stimulate endothelial cell mitogenesis and migration
- It is also a vasodilator and increase microvascular permeability
Histopathology
- NPC arises from crypts & squamous or respiratory epithelium lining the nasopharynx
- It may be preceded by squamous metaplasia
- WHO classification of NPC (1978)
I - Keratinizing EBV radio- less worst produce keratin pearl,
SCC titre ↓ resistant aggressive prognosis presence of intercellular
bridges
- 25% in North
America
- 2% Chinese
II - Non keratinising ↓ ↑ varies in cell differentiation -

from mature to anaplastic
cells, does not produce
keratin
stratified or pavemented
arrangement with cell
borders being readily
discernible
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III - undifferentiated EBV radio- more better less differentiated,

most common titre ↑ sensitive aggressive prognosis highly variable cell types
(clear cell, spindle cell,
- most common anaplastic)
subtype vesicular or hyper chromatic
- 63% (95% from nuclei
China) prominent nucleoli
- most common scattered mitotic activity
type to affect
children
- detection of Epstein-Barr virus encoded early RNA (EBER) in situ hybridisation (ISH) or
EBER-ISH - useful histological ancillary technique -almost invariably positive
Routes of tumour spread

- from the 10 site, the tumour may spread in one/>
of the following directions
1. Anteriorly
- nasal cavity
- PNS
- Pterygopalatine fossa (via sphenopalatine
foramen) -
- apex of orbit
2. Posteriorly
- to retropharyngeal space
- Node of Rouviere
- pre vertebral muscles
- lateral mass of atlas
3. Laterally
i) into parapharyngeal space
- prestyloid
• mandibular nerve
• pterygoid muscles - trismus
• deep lobe of parotid
- post styloid - retroparotid syndrome of Villaret
• compression of vessels (IJV/ ICA)
• 9th, 10th, 11th, 12th CN invasion
• cervical sympathetic trunk invasion
- How tumour spread to parapharyngeal space?
• superior constrictor does not reach skull base
• lateral gap sinus of Morgagni is created
• this gap is bridged only by pharyngobasilar fascia
• Through this opening, the ET along with its 2
muscles enter into the nasopharynx
• tumour can easily breach this area and spread into
parapharyngeal space
ii) Otologic symptoms
4. Superiorly
- through sphenoid sinus & body → parasellar structures
(cavernous sinus)
- can also gain access via foramen ovale → MCF →
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cavernous sinus → petrous apex
- along carotid canal → cavernous sinus involving 3rd, 4th, 5th, 6th CN
- to brain via direct extension (not hematogenous)
- inferior orbital fissure → orbital apex
5. Inferiorly
- to oral cavity/ hard palate, oropharynx/ soft palate (may be submucosal)
- to retrotonsillar region/ pillars
Clinical features
1. Painless cervical LN 60%
- 1st echelon LN - retropharyngeal node of Rouviere (75-85%)
- 2nd echelon - JD nodes
- High risk nodes: bilateral RLNs, upper deep jugular LNs, Levels II-V LNs
- ipsilateral nodal spread - 85-90%
- bilateral and contralateral LN are common (60-70%)
- Isolated Level V LN - 10%
- Mets to Ia - rare
- Mets to Ib - clinically significant
- Isolated mets to levels I, III, IV and more distant lymph nodes - skip metastasis - uncommon in
NPC
- Features of malignant nodes
- Size: shortest axis >11mm in the JD regions, >10mm in the other cervical regions, >5mm in
lateral RLN, any visible medial RLN is abnormal
- Group of 3/> nodes
- Central necrosis
- Extracapsular extension (ECE)
2. Nasal symptoms
- epistaxis 40%
- advanced NPC with/without skull base erosion
- blood stained nasal discharge
- complete nasal obstruction late
- Ozaena - dt tumor necrosis in advanced NPC
3. audiological (tinnitus, otalgia, deafness) 30%
- insidious onset of OME
- tinnitus
- CHL dt ET obstruction
- presence of unilateral OME in adult should raise suspicion of NPC
- infiltration of glossopharyngeal nerve → unilateral otalgia
4. neurological (headache, CN palsy, Horner’s ) 20%
- either due to
- direct extension
- mets
- post- DXT
- most common CN palsies
- CN 5th, 6th, 9th, 10th (50% of all palsies)
- CN V first involved → CN 6 → CN3/4 → then 9th, 10th, 11th, 12th
- most common group CN 9& 10 → CN 3,4,6
- CN 5 & 6 - due to extension into the cavernous sinus (located inferiorly in the cavernous
sinus)
- CN 3 - may be affected in advanced cases - but isolated CN III will never occur alone
without associated involvement of CN 5/6
- CN 9,10,11 - jugular foramen syndrome (Vernet’s syndrome)
- CN 9,10,11,12 - Collet-Sicard syndrome
- Eye symptoms
- Diplopia - CN 6 - tumour infiltration of the cavernous sinus
- proptosis - tumor infiltration of the orbit through orbital fissures
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- Pain & headache
- hallmark of terminal disease - usually neuralgic - can be due to meningeal branch of the V2
- severe & excruciating pain & headache
- signify erosion of skull base & surrounding structures
- Trismus
- advanced disease
- involves pterygopalatine fossa/ pterygoid muscles
- Atypical facial pain
- Dermatomyositis
- skin lesions consist of distinctive hyperkeratotic, follicular, erythematous papules
- appear on the face and eyelids and eventually, neck shoulders, upper extremities
- 1-5% of the patients have distant metastasis at the time of first presentation
5. metastasis
- 3% at presentation
- locoregional
- distant
- mainly to bones (flat bone)
- thoracolumbar spine
- pelvis
- ribs/ sternum
- femoral head
- skull
- others
- lung
- liver
- approximately 5% of all patients have distant metastasis to these areas
- distant mets indicate median survival at 3/12
NEUROLOGICAL SYNDROMES CAUSED BY NPC
PETROSPHENOIDAL SYNDROME OF JACOD

Direct intracranial extension of the NPC with involvement of the II to the VI nerves (invade orbital
apex through optic canal and SOF)
- unilateral trigeminal type neuralgia
- unilateral ptosis (caused by III nerve involvement)
- complete ophthalmoplegia (caused by involvement of the III, IV, and VI nerves
- amaurosis (causes by involvement of the optic nerve)
SYNDROME OF RETROPAROTID SPACE OF VILLARET

- last 4 CN and cervical sympathetic nerve (invade post styloid parapharyngeal space)
- caused of lateral retropharyngeal LN metastasis in the retroparotid space
- difficulty in swallowing -involvement of 9th and 10th CN
- perversion of taste in the posterior 1/3 of the tongue - involvement of the 9th CN
- hyperesthesia/ hypoesthesia or anaesthesia of the mucous membrane of soft palate,
pharynx, and larynx, problems with respiration and salivation)
- paralysis and atrophy of the trapezius and SCM and unilateral weakness of the soft palate
(caused by involvement of the XI CN)
- unilateral paralysis and atrophy of the tongue (caused by involvement of the XII CN)
- cervical sympathetic nerves
• Horner’s syndrome
TROTTER’S TRIAD (NPC)
- indicates local invasion of 5th, 9th, 10th CN - invasion of FOR
1. Neuralgia (pain 1 side of head dt 5th CN involvement)
2. unilateral elevation & immobility of soft palate (Curtain’s sign)
3. Conductive hearing loss
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Secondary malignancies
- risk of developing synchronous second 10 or metachronous malignancy in upper aerodigestive
tract is about 4%
- Post treatment
- commonly
• SCC
• Sarcomas
- osteosarcoma
- malignant fibrous histiocytoma
- malignant schwannoma
- extra skeletal chondrosarcoma
- angiosarcoma
PE
- post nasal mirror - inadequate
- endoscopic examination with 00 rigid scope
- rigid nasoendoscope
- flexible endoscope
-
1. lymphoma - negative for CK, positive for leukocytes common antigen
2. small cell carcinoma - negative for EBER-ISH, +ve for neuroendocrine markers (Synaptophysin
and CD 56)
3. sinonasal undifferentiated carcinoma - negative for EBER-ISH
4. chordoma
5. salivary gland tumor
6. rhabdomyosarcoma - +ve for desmin and myoglobulin
7. melanoma - +ve for melanin, S100, HMB-45, melanin A
8. Olfactory neuroblastoma
9. Small blue cell neoplasm - sustenticular S-100 +ve
10. teratoma
11. fibrous tumor
Ix
1. Lab studies
- FBC - epistaxis (anaemia)
- ESR - ↑ in lymphoma
- Renal profile
- PTA/ Tymp - OME (CHL)
- ↑ titre for EBV capsid antigen (VCA)
2. Imaging
- CT scan (axial & coronal views)
- evidence of destruction of pterygoid plate
- destruction of foramen lacerum/ ovale/ spinosum/ jugular foramen
- tumour extension into ethmoid & sphenoid sinus
- enlarged deep impalpable LN esp node of rouviere
- isodense to muscle on non enhanced CT
- MRI
- modality of choice
- More sensitive for skull base,
- hypo to iso-intense and relatively hyperintense to muscle on T1-weighted and T2-weighted
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- defining intracranial spread
- Others
- CXR
- USS abdomen
- Bone scan
- PET scan
• detecting residual/ recurrent NPC
• detecting distant mets - most sensitive and specific is PET/CT (better than PET alone)
• useful in post DXT cases
3. Biopsy
- For definitive diagnosis
- perform ↓ GA but can be under LA
- even with obvious NP tumour, advisable to do full examination of upper aerodigestive tract
TRO second 10 tumour
4. FNAC of LN
- aid in diagnosis
- aid to initial tumour staging
- confirmation of recurrence of mets
- Prepared with conventionally stained Papanicolaou (alcohol fixed) and Giemsa (air-dried)
- Papanicolaou - highlight nuclear features
- Giemsa - delineates the cytoplasmic detail
Radiological preferred techniques for staging

- MRI - local and locoregional staging
- PET-CT - distant mets
- For re-staging - combination of PET-CT and MRI
- When MRI and PET CT not feasible, CT scan is an alternative imaging modality
Staging
TNM staging system most commonly used
- consist of clinical examination, pathological and radiological investigations
- T
- Tx: Primary tumour can’t be identified
- T0: No tumour identified, but EBV +ve cervical node
- T1: confined to nasopharynx, or extend to oropharynx/ nasal cavity WITHOUT PPS extension
- T2: extend to parapharyngeal space and/ or medial lat pterygoid muscles, and/or prevertebral
muscle
- T3: bony structures of skull base, cervical vertebra, pterygoid structures, and/or paranasal
sinus
- T4: intracranial, CN involvement, hypopharynx, orbit, parotid, and/or infiltration beyond the
lateral surface of pterygoid muscle
- HICOM - hypopharynx, intracranial, CN, orbit, masticator space
- N
- N1: unilateral cerv LN, unilateral or bilateral RPLN, <6cm, above caudal border of cricoid
cartilage
- N2: Bilateral cerv LN, <6cm, above caudal border of cricoid cartilage
- N3: Mets >6cm, and/or extend below caudal border of cricoid
- M
Prognosis
1. Patient factor
- Sex
- no significant difference of overall survival btw gender
- Age
- younger - better survival
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- Ethnic
- no significant difference - results divided
- Co-morbids
- Hb <11g/dl - low mid-radiation Hb - independent predictor of local disease recurrence and
malignancy-related death
2. Tumour factor
- Presenting stage
- T stage → local control
- N stage → predicts more for neck control
- distant mets
- CN involvement
- LN fixation
- Volume (larger than 64ml → unlikely to be controlled with total dose of 72 Gy) - according to
Willner et al
- Presence of circulating CK19 mRNA positive cells before treatment indicated occurrence of
micro metastasis and was a poor prognostic sign for NPC
- real time quantitative PCR - highly sensitive and specific
- plasma EBV DNA → highly sensitive and specific
- WHO - small number with WHO I - histological impact on survival still unknown
Other potential markers

1. macrophage inflammatory protein-3⍺
2. Endothelin 1
3. Cytoplasmic protein fragment
4. ℬ2 microglobulin
5. tissue polypeptide antigen
6. vascular endothelial growth factor
7. Osteopontin
Screening of NPC in general population could not be recommended due to insufficient evidence for
its effectiveness and safety
Treatment
Management of NPC is unique because
- relatively inaccessible making surgical removal
difficult & ↑ morbidity
- Tumour is radiosensitive
Radiotherapy is mainstay in Stage I
CCRT - Stage II, III, IVA and IVB NPC
IMRT is preferred radiation technique in NPC
Non surgical
1. DXT
- primary Tx modality
- Radiation field includes
① nasopharynx
② skull base
③ sphenoid sinus
④ cranial nerve foramina
⑤ post ethmoid sinus
⑥ post orbit
⑦ post maxillary sinus
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⑧ oropharynx
⑨ both neck should be radiated
• NP is midline structure with bilateral lymphatic drainage
• even in N0 neck (elective irradiation)
- Technique: 2 phase technique. WHY?
• so that the dose to spinal cord to be kept within tolerance to avoid transverse myelitis
- Phase I
- en-block treatment of nasopharynx & upper neck with parallel opposed lateral fields
- lower neck + supraclavicular fossa treated with anterior field
- delivered with 4-6 mV photons
- Give 40 Gy in 20 # x 4/52, 1# = 2 Gy
- Phase II
- ↓ field using electrons over posterior neck to keep spinal cord dose within tolerance
- immediately after completed Phase I
- to Include 10 tumour, any palpable LN
- delivered with 4-6mV photon
- give 26 Gy in 13# x 2-5/52
- Total dose Phase I + II - 66 Gy in 33# over 6.5 weeks
- In neck, total dose ~ 50-60 Gy (N0 neck)
- If residual bulky LN - receive additional small boost - taking total dose to 70Gy
- Conventional radiation
- universal intensity within each beam
- dose distribution determined by the density and depth of the tissue
- IMRT
- each radiation beam is subdivided into numerous small segments of beams (pencil beams)
- Different beams with different intensity → produce dose that conform to the required shape
of the target
- can deliver high-dose irradiation to defined tumour targets while minimising the doze to
surrounding organs and tissues → improving therapeutic ratio
- Patient setup and planning CT → influence planning target volume
• immobilisation
- head extended
- immobilisation device include neck and shoulder
• setup accuracy
- CT scan thickness 0.3cm or smaller
- MRI fusion with a treatment planning CT is highly recommended
- GTV
• all known gross disease, including abnormally enlarged regional LN
- CTV
• encompass GTV + regions considered to harbour potential microscopic disease
- PTV
• provides margin around CTV to allow for variation in treatment setup and other
anatomic motion during treatment
- Clinical Target Volume (CTV)
• tissue volume that contains a demonstrable GTV and/or subclinical malignant
disease that must be eliminated
• includes subclinical disease surrounding the GTV and regional lymphatics
• based on clinical knowledge and potential spread and pattern of failure aft tx
• no universal agreed guideline
- GTV-P (Primary tumour) & GTV-N (nodal disease) with a margin of >/=5mm → CTV
70-P and CTV 70-N respectively
• this margin can be reduced to 1mm for tumours in close proximity to critical
structures
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- High risk areas
• entire nasopharynx
• anterior 1/2 to 2/3 of the clivus
• skull base (including bilateral foramen ovale and rotundum in all cases)
• Pterygoid fossae
• Parapharyngeal space
• Inferior sphenoid sinus (in T3-T4 disease, entire sphenoid sinus)
• Posterior 4th to 3rd of the nasal cavity and maxillary sinuses (ensure
pterygopalatine fossa coverage)
• Cavernous sinus should be included in high-risk patients (T3, T4, bulky disease
involving the roof of the nasopharynx)
• LN drainage in NPC - follows orderly pattern
• High risk lymph nodal regions (CTV 59.4-N) include Level II, III, V and
retropharyngeal nodes
- Level Ib if ipsilateral level II are clinically involved
- Level IV and supraclavicular LN if III are involved
Nodal classification Levels to be included in the CTV
Ipsilateral neck Contralateral neck
N0 RP + II-III-Va RP + II-III-Va
N1 RP + Ib-II-III-IV-V RP+Ib-II-III-IV-V
N2 RP + Ib-II-III-IV-V RP + Ib-II-III-IV-V
N3 RP + Ib-II-III-IV-V +/- RP + Ib-II-III-IV-V

adjacent structures
based on clinical and
radiological findings
• CTV 59.4 - high risk subclinical disease
- recommended to treat these subclinical regions
- should be at least 10mm from the GTV
• CTV 54 - low risk CTV
- bilateral uninvolved lower neck nodal regions for N0
- PTV - should provide a margin around the CTVs to compensate for the variabilities of
treatment set up and internal organ motion
• minimum 3-5mm around the CTVs required in all directions to define each
respective PTV
- PTV: 70Gy in 33 # - 2.12Gy/ #
- High risk PTV 59.4 (CTV + margin): 59.4Gy in 33# at 1.7-1.8Gy/ #
- Once daily, 5 #/ week
- All targets should be treated simultaneously, using the simultaneous integrated boost
(SIB) technique
• other techniques
- segmental (‘step and shoot’) - carried out by superimposing many small pencil
beams using the multi leaf collimator
- dynamic - dynamic sliding window
- Organs at risk
• brain bilateral temporal lobes
• optic nerves and chiasma
• eyes
• lens
• pituitary
• brainstem
• spinal cord
• parotid glands
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• TMJ
• middle and inner ears
• skin
• oral cavity
• mandible
• glottic larynx
• brachial plexus
• oesophagus
- PRV of spinal cord - adding a 3D margin of at least 5mm to the delineated spinal cord
to ensure sufficient margins around the entire cord.
- PRV of brainstem and optic chiasma are defined by adding a 3D margin of at least
1mm around the delineated structures
- dose constraints of the parotid glands - 26Gy or less - should be achieved in at least
one parotid gland
• Treatment planning
- Inverse planning - result oriented paradigm
- both forward and inverse planning provide excellent target coverage with no
statistically significant differences. However, inverse planning provided improved
sparing a number of organs at risk.
- Altered fractionation
- Hyperfractionation (twice a day irradiation) - ↑ incidence of of neurological injury, temporal
necrosis, optic apparatus and brainstem
- Brachytherapy
- effective in early T-classification
- Radiosurgery
- dose to optic nerve, optic chiasm, brainstem and cavernous sinus should be kept under
8Gy
SE of radiotherapy
Can be divided into acute and late toxicities
1. Acute
① Radiation dermatitis
Grade 1: faint erythema or dry desquamation
Grade 2: moderate erythema, patchy moist desquamation, confined to skin fold and creases
Grade 3: bleeding induced by minor trauma or abrasion
Grade 4: skin necrosis or ulceration of full thickeness dermis
Grade 5: death
② Mucositis
WHO mucositis grading system
0 - normal
Mild 1 - painless ulcer, erythema, mood soreness
Moderate 2 - erythema, ulcer, able to eat solids
Severe 3 - oral ulcer, liquid diet only
Severe 4 - alimentation not possible
③ Dysphagia
④ Taste changes
⑤ Nausea and vomiting
⑥ Hematological toxicities (neutropenia)
⑦ Lethargy
2. Late
① Neurological complications
i) temporal lobe injuries
ii) cranial nerve palsies
iii) Lhemitte’s syndrome (shock-like sensation that occurs on flexion of the neck)
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iv) Spinal cord damage
v) Optic nerve atrophy
② Non neurological complications
i) Ear
• tinnitus
• hearing loss
• otorrhea
ii) Oral
• trismus
• dysphagia
• xerostomia
iii) Osteoradionecrosis
iv) Subcutaneous fibrosis
v) Endocrinopathies
• primary hypothyroidism
• Hypopituitarism (if dose > 40 Gy)
vi) Second cancer with radiation fields
XEROSTOMIA
- parotid serous acini cells - sensitive to ionising radiation → reversal uncommon
- begins soon aft initiation of radiotherapy → infection, dental decay
RTOG scoring for acute radiation-induced CTAE v 3.0 scoring criteria for xerostomia
salivary gland morbidity
Grade Criteria 0 None
0 No change over baseline 1 Symptomatic (dry or thick saliva) without

significant dietary alteration
Salivary flow >0.2ml/min
1 Mild dryness, slightly thickened 2 Symptomatic and significant oral intake

saliva alteration
slightly altered metallic taste Unstimulated saliva 0.1-0.2ml/min
2 moderate to complete dryness, 3 Symptoms leading to inability to

thick sticky saliva, markedly adequately aliment orally, IV fluids, tube
altered taste feedings or TPN indicated
3 Not defined for acute

xerostomia
4 acute salivary gland necrosis
- Treatment
• Symptomatic
- artificial saliva/ lubricants
- Cytoprotectant
• amifostine
- Salivary sparing radiotherapy
- Medical treatment
• Pilocarpine (muscarinic agonist)
• 5-10mg tds/qid
- S/E: perspiration, bowel and bladder irritation and hot sensation
- Sequelae
• Dental caries
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- Prevention
• oral hygiene
• smoking cessation
• low sugar diet
• avoiding caffeinated drinks
• frequent teeth brushing using soft bristle toothbrush
• antiseptic mouth wash
• Oral candidiasis
- oral rinse using Nystatin
- systemic anti fungal therapy: ketaconazole not indicated unless refractory
candidiasis is observed
HEARING LOSS
1. SNHL - cisplatin based chemotherapy - radiosensitizer
- typically in the high frequency range - related to the mean radiation dose exposure to the
cochlea and concurrent cisplatin
- can be chronic, progressive and irreversible.
- Due to vascular insufficiency
- can occur acutely, after a few days if cisplatin
- but if radiation induced - can have a latent period of 6-12 months
- Management
• Prevent
- limit radiation dose
- mean radiation dose > 48 Gy - ↑ risk of sensorineural deficit
• No standard therapy
• Steroids
• Hyperbaric oxygen therapy
• HA
• CI
OSTEORADIONECROSIS
- Tx: sequestrectomy combined with HBO2
- Long term antibiotics can be used but may not be sufficient
SOFT TISSUE FIBROSIS

- vascular/ microvascular damage → tissue hypoxia, nutritional depletion therapy → infection,
dental decay → tissue injury → activation of monocytes, macrophages, platelets → release
cytokines and growth factors → recruitment and proliferation of fibroblasts → increase
synthesis of extracellular matrix → decrease degradation of extracellular matrix
- Management
- Pentoxifylline +/- vitamin E
- Liposomal Cu/Zn
- Hyperbaric oxygen
- Physical therapy - jaw exercise
CRANIAL NEUROPATHY
- cranial nerves are a special group of the peripheral nerves in the cranium
- highly resistant to radiation damage
- Radiation
- →changes in electrophysiology and histochemistry
- cause changes in surrounding fibrotic structures and its embedded blood supply to the
nerve fibres
- XII, X, RLN commonly involved
- NG/ GT - CN palsy
- Laryngotracheal cavity - tracheostomy
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- 6th CN palsy - strabismus - Botox
TEMPORAL LOBE NECROSIS

- histopathologic changes limited to white matter
- focal coagulative and fibrinoid necrosis and demyelination
- dizziness
- memory impairment
- personality change
- temporal lobe epilepsy
- non-specific neurologic findings
- headache
- mental confusion
- general seizures
- CT
- small necrotic foci at the inferomedial aspect of each of the temporal lobes associated with
oedema
- “finger like” hypointense areas in the white matter
- MRI
- T1-weighted images - low intensity
- T2 - high signal intensity
- management
- surgical resection
- anticonvulsants - seizures
NEUROENDOCRINE DEFICITS
- latency period - 5 years
- most affected: growth hormone deficiency → gonadotropin → corticotrophin → thyrotropin
SECOND PRIMARY
1. Condemned mucosa syndrome
- synchronous transformation of multiple cells is rare, second primary tumour is caused by
widespread migration of cancer cells to other tissues or organs in the aerodigestive tract
2. Field cancerization
- mucosa accumulates genetic alterations that result in the induction of multiple and
independent, malignant lesions after repeated carcinogenic exposure
2. Chemotherapy
- can be before (neo-adjuvant), during (concurrent), after (adjuvant)
- standard of care for all patients with locally advanced NPC world wide
i. inherently cancericidal
ii. sensitize tumour to the effects of radiation therapy
- Major issue of neo-adjuvant
- may trigger the accelerated re-population and cross-resistance during subsequent radiation
therapy
- said to reduce loco regional relapse
- given as concurrent chemo-radiation
- 7-8 weeks (7-8 cycles)
- dose usually lower than neo-adjuvant or adjuvant chemotherapy
- usually use
• Platinum based chemotherapy (alkylating agents) - interfere with DNA repair - forming
DNA crosslinks and adducts
- cisplatin 100mg/m2
- carboplatin - used in renal and hearing impairment patients
- oxaliplatin
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• 5-FU 1000mg/m2 continuous infusion/day for 5/7

- Stage IIB, III, IVB
- Adjuvant chemotherapy
- poor compliance
- limited role for adjuvant chemotherapy in addition to definitive radiotherapy
- Palliative
- locoregional recurrence
- metastatic disease not amenable to potentially curative local therapies, such as irradiation
and nasopharyngectomy
- SE of chemo
- myelosuppression
- ototoxicity
- renal damage
- alopecia
- nausea, vomiting
- lethargy
3. immunotherapy
Surgical
1. Diagnostic
2. Therapeutic
① Radical neck dissection
- RND to control radioresistant nodes & post DXT cervical LN
- Indications
• persistent & recurrent cervical LN aft full course of XT in the absence of 10 disease
proven by endoscopic biopsy
② Nasopharyngectomy
- indication
• recurrent/ residual CA (<2cm)
• Tumour not eroding skull base
• no distant mets/ neck mets
• confined to NP
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- CT/ MRI to look for extent of disease
- Surgical technique impeded by
• Radiation fibrosis
• lack of adequate surgical margins of healthy tissue
③ Insertion of brachytherapy
- transnasal intracavity brachty with Iridium-192 to treat localized/ recurrent NPC
- brachytherapy of neck nodes
④ Treatment of complications
- OME - M&G
• M&G higher cure rate at the end of 2 year follow up compared to simple auripuncture
plus aspiration despite higher incidence of complications
- Advanced NPC with poor feeding
• feeding gastrostomy
⑤ Dental management
- dental clearance before start DXT to prevent osteoradionecrosis
5 year survival rates for NPC

Stage I - 90%
Stage II - 70%
Stage III - 60%
Stage IV - without distant mets 40%, with distant mets 0%
Locally recurrent NPC

rT1/T2 - endoscopic nasopharyngectomy/
brachytherapy/ IMRT, 3D-CRT
rT3/4 and nodal recurrence - nasopharyngectomy,
RND or re-irradiation
1. Reirradiation
2. Surgery
3. Targeted therapy
- tyrosine kinase inhibittor against EGFT
4. Photodynamic therapy
Reirradiation
Prognostic factors in NPC patients receiving salvage
reirradiation
1. Patient factors
- Age
- Performance score
- Disease factors
- Histology
- Recurrent T classification
- Persistent vs recurrent tumour
- Time interval from first course of radiation therapy
- Tumour volume
- Presence of synchronous nodal recurrence
- Prior local failure
- Epidermal growth factor receptor expression
2. Treatment factors
- Reirradiation dose
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Brachytherapy
Principle
- Application of the radiation source close to the tumour, radiation dosage is the highest at the
site of the radiation source, and decreases rapidly as the distances increases from the
radiation source towards the periphery
- Enables high dose of irradiation to be delivered to the residual or recurrent tumour, with the
surrounding tissue receiving a smaller dose
- Also delivers radiation at a continuous low dose rate
- Indications
- Tumour thickness <10mm
- No intracranial, paranasal sinus and oropharyngeal involvement
- No involvement of underlying bone or infra temporal fossa
- Absence of metastatic disease
- Expertise in nasopharyngeal intracavitary brachytherapy
① Intracavitary brachytherapy
• Radiation source is placed in a tube or a mould, and these devices are then inserted into
the nasopharynx for therapy
② Interstitial implantation
• Implanted into the tumour either transnasally or by endoscopic guidance
• ‘Radioactive gold grains’
Stereotactic radiotherapy
Principle
- technique in which a small target is stereotactically localised and irradiated by multiple
convergent beams using a large single dose of radiation
- useful for vascular malformations, benign intracranial/ skull base neoplasm, and cerebral
metastases
External beam reirradiation

- Reirradiation of NPC with curative intent is difficult due to the large numbers of important
structures situated in the vicinity of the target that was already irradiated
- Neurological tissues
- optic apparatus
- brain stem
- temporal lobe
- spinal cord
Surgery
1. Anatomy
- Slanting roof: body of sphenoid and anterior wall of sphenoid sinus
- Posterior wall: clivus, connected by ligaments of the arch of the atlas, then upper part of body
of the axis
- Lateral wall: superior constrictor muscle, ET opening
- Mucosal lining: stratified squamous epithelium (postero superior wall), pseudo stratified
columnar ciliated epithelium (near the posterior choana)
- epithelium → basement membrane → lamina propria → superior constrictor →
pharyngobasilar fascia → retropharyngeal space
2. Recurrence in the neck after radiotherapy
- neck recurrence following combined chemoradiation - <5%
- application of IMRT - isolated recurrence in the neck <1%
- Surgical salvage: MacFee incision is advisable
- parallel incisions placed at 7cm apart would provide adequate circulation and prevent
necrosis at the edge of the incisions
3. Recurrence in the Nasopharynx
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- Brachytherapy
- radiation dose highest at the source, declines gradually, proportional with increasing
distance from the tumour
- continuous rate
- radioactive gold grains
- Nasopharyngectomy
- remove tumour, mucosa, ET
- applicable for: small lesion localised in the
central part of the posterior wall or superior
wall, but not extending to FOR
- Open
• Anterior
- trans-antral mid facial degloving
- leFort 1 osteotomy
• Lateral
- Lateral infra temporal
- radical mastoidectomy
• hv to mobilze ICA, cranial nerve, floor
of MCF
• Inferior
- Transpalatal
- Transmaxillary
- Transcervical
• Antero-lateral approach
- maxillary swing
- Endoscopic
• Transnasal
• Trans-septal
- Complications
- Palatal fistula
- Submandibular necrosis
- Trismus
- ICA injury
- Significant poor prognostic factors on survival post-nasopharyngectomy
- Advanced T stage of disease at treatment
- LN mets
- invasion of skull base
- Invasion of parapharyngeal space
- +ve surgical margin
NPC with mets

M1 - options of treatment
- chemotherapy
- Radiotherapy
- Palliative care
Better overall 1 yr OS compared to those without treatment
1. Chemotherapy
- single agent response rates of cisplatin (28%) and carboplatin (22%)
- Augmented by 2nd active drug - 5-FU
- confers short term palliative benefit
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NPC in paediatric and adolescent patients

1. Undifferentiated histopathology associated with advanced loco regional disease at presentation
2. Propensity to systemic metastasis
3. Although highly sensitive to radiotherapy initially, high rate of distant and loco regional
recurrences might be observed
4. Radiation volume and doses adopted from adults have serious acute and late effects, including
second malignancies in young patients
5. Undifferentaiated NPC is highly chemosensitive
6. Preradiation chemotherapy minimises the risk of distant recurrence through eradication of
micrometers
7. Complete response or marked and rapid reduction in tumour volume can be achieved by
preradiation chemotherapy resulting in improvement in loco regional disease control
8. Preradiation chemotherapy may render to reduce radiation dose and volume in children by
decreasing the tumour volume
9. Concurrent administration of chemotherapy with radiation as a radiosensitizer may have a role
in improving DMFS, perhaps through better loco-regional control
10. Better OS and DFS by the integration of chemotherapy
Contraception
1. Intrauterine and implantable contraceptives - recommended for women treated for cancer
2. COCP/ POP - avoided in women with active cancer - risk of VTE
3. Cancer free for 6 months, no history of hormone-mediated cancers/ chest wall irradiation/
anaemia/ osteoporosis/ VTE - can use contraception
Nutritional support
- Oral
- Enteral
- Parenteral
- Nutritionally complete supplements
- Energy and protein supplements
- Carbohydrate supplements
- Protein supplements
- Fat supplements
Follow up
1. Clinical examination of nasopharynx including an endoscopic examination to detect superficial
tumours
2. Examination of neck and other systems (thorax and abdomen)
3. If radiotherapy cross sectional imaging is required , it should be offered no earlier than 3
months
4. Cross-sectioning, as needed, to detect deep infiltrating tumours not associated with mucosal
lesion during the initial 3-5 years post treatment
Year after completion of treatment Frequency of follow up
1st yr Every 1-2 months
Second year 2-3/12
Third year Every 3-5 months
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Fourth to 5th year Every 6 months
After 5th year Every 6-12 months
Juvenile Angiofibroma
- rare, benign, highly vascular tumour
- locally invasive, submucosa spread
- vascular supply mainly from maxillary artery
- also form ICA, ECA, CCA, Ascending pharyngeal arteries
Epidemiology
- up to 0.5% of H&N tumours
- Gender: Almost exclusively in males
- have been reported in children, elderly young women, pregnant women
- Age: 9-19 years
- Intracranial extension: 10-20%
- Recurrence rate: 50%
Etiopathogenesis
1. Hormonal theory
- Due to the lesion's occurence in adolescent males
2. Harmatomatous
- vascular nidus at sphenopalatine foramen
3. Embryonic fibrocartilage
- fibrocartilage at junction between basisphenoid + basiocciput
4. Paraganglionic
- paraganglionic cells at terminal branches of maxillary artery
5. Conjoint fascia theory
- origin from conjoined pharyngobasilar & buccopharyngeal fascia
Origin
- Superior lip of the Sphenopalatine foramen at the Jx of the pterygoid process of the sphenoid
bone and sphenoid process of the palatine bone
- Spread by: direct extension
- Superior: sphenoid sinus, orbit, intracranial
- Lateral: pterygopalatine fossa and infratemporal fossa
- Medial: nasopharynx
Supply
1. ECA
- IMAX (commonest)
- Vidian artery
- Ascending pharyngeal artery
- Pharyngeal artery - br of IMAX
(IMAX exits through palatovaginal canal)
2. ICA
3. CCA
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Spread
1. Medially
- JNAs are slow growing and initially expand intranasally into the nasopharynx and nasal cavity
and then into the pterygomaxillary space
2. Lateral
- Eventually erode bone and invade the infratemporal fossa & MCF (through superior orbital
fissure)
3. Superiorly
- orbit (through infraorbital foramen)
- intracranial via foramen rotundum and superior orbital fissure
4. Posterior: pterygopalatine fossa/ sphenoid sinus, sella turcica
5. Inferiorly: oropharynx
*infraorbital nerve is the endoscopic division of pterygopalatine fossa and infratemporal fossa
(medial is pterygopalatine fossa, lateral is infratemporal fossa)
Histology
- Large staghorn type vessels - thin walls and empty lumens (bcoz it lacks contractile elements)
- Myofibroblast is cell of origin
- Fibrous connective tissue with abundant endothelium-lined vascular spaces
- Pseudocapsule of fibrous tissue
- Blood vessels lack a complete muscular layer
Midfacial and anterior skull base tumours

(differentials)
1. JNA
2. Osteoma
3. Craniopharyngioma
4. Olfactory neuroblastoma
5. Chordoma
6. Chondrosarcoma
7. Rhabdomyosarcoma
8. NPC
Diagnosis
1. History
- Positive symptoms: epistaxis nose block, anaemia, hearing loss dt MEE
- Orbital symptoms
- Intracranial symptoms
- Negative symptoms: anosmia - to exclude olfactory neuroblastoma
- broadening of nasal bridge
- proptosis
- cheek swelling
- involvement of CN II, III, IV, VI
- sessile lobulated smooth mass, purplish, beefy red in nasopharynx
- MEE
3. Radiological study
- CT scan with contrast
- Excellent for bone detail
- Lesion enhances with CT
- Bone window:
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• Antral sign (Holman Miller sign) - anterior bowing of post wall of maxillary sinus
(remodelling of foramen and fissure)
• widening of left SP foramen
• Lesion fills left choanae
• Extends into sphenoid sinus
- Soft tissue window axial cut
• Homogenous enhancement
• Widening of left SP foramen
• Dumbbell
• Extend into nasopharynx/ pterygopalatine fossa
- MRI (supplement to CT)
- Axial T1
• Heterogenous intermediate signal
• bag of worms appearance
• Flow voids represent enlarged vessels
• Extension into
- Nasopharynx
- Masticator space
- orbit
- infratemporal fossa
- intracranial
- Angiogram - diagnostic and therapeutic role
- ECA Angiography
• Tumour blush for feeding vessel from IMA
• collateral
• balloon occlusion test can be done
• cerebral flow
• for embolization
4. When to biopsy
- NEVER BIOPSY IN CLINIC
- if rapid growth
- to differentiate between
- rhabdomyosarcoma
- olfactory neuroblastoma
NO NO ANSWER: no role for office biopsy

If in doubt: role of biopsy in controlled environment under GA, able to pack
Characteristic presentation
- Teenage or young adult male
- Recurrent epistaxis
- Nasal obstruction
Additional findings
- Conductive hearing loss
- Rhinolalia
- Hyposmia/ anosmia
- Swelling of cheek
- Dacrocystitis
Gross examination
- Sessile, lobulated, rubbery, red pink to tan gray in appearance
- Rarely: polypoidal or pedunculated
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- Usually encapsulated and composed of vascular tissue and fibrous stroma with coarse or fine
collagen fibres
Staging (Fisch)
I - tumours limited to nasal cavity, nasopharynx with no bony destruction
II - Tumours invading pterygopalatine fossa, paranasal sinuses with bony destruction
III - Tumours invading infratemporal fossa, orbit and /or parasellar region remaining lateral to
cavernous sinus
IIIA - without intracranial
IIIB - with intracranial
IV - invading cavernous sinus, optic chiasmal region, and/ or pit fossa (POC)
Medial - early
Lateral - advance
Superior - advance
Radkowski
IA - limited to nose or nasopharynx
IB - extension into 1 or more of PNS 
IIA - minimal extension into pterygomaxillary fossa
IIB - full occupation of pterygomaxillary fossa with/ without orbital bone erosion
IIC - extension into infra temporal fossa or posterior to pterygoid plates
IIIA - erosion skull base with minimal itnracrnail ext
IIIB - erosion skull base with extensive intracranial extension with/ without cavernous sinus
involvement
Andrew Classification - earliest classification for JNA
Treatment options
Symptomatic treatment - management of epistaxis, management of airway
1. Surgery
- Gold standard
- Approaches -endoscopic and open
- Endoscopic transnasal - up to Fisch IIIA
• Middle turbinectomy maybe performed for improved exposure
• MMA
• Posterior maxilla wall removed
• SPA ligation
• Tumour resection from pterygopalatine fossa
• can use coblator
- Endoscopic Denker’s
• Minimally invasive sublabial anterior maxillectomy
• Creates an endonasal anterior maxillotomy without the need for a separate sublabial
incision
- Transpalatal
• Soft palate is split and retracted
• Palatine bone and inferior aspect of pterygoid plate resected
• if lesion confined to nasopharynx
- Transantral
• Wide anterior antrostomy
• Removal of ascending process of maxilla
• Removal of inferior half of lateral nasal wall
- Facial translocation (midfacial devolving with or without LeFort I osteotomy)
• Gingivobuccal incision
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• Nasal intercartilaginous incision with transfixion incision
• Maxillary osteotomy EE's
• Sagittarius osteotomy
- Lateral rhinotomy/ medial macillectomy
• if lesion in nose, nasopharynx, pterygopalatine fossa

- Infratemporal fossa with or without craniotomy
- Maxillary swing
• Palatial flap, palatial slap little
• Anterior wall,
• Separating tuberosity from pterygoid plate
• Maxillary swing, nasal mass identification
• packing
• Specimen
2. Radiation therapy
- Reserved for unresectable, life threatening tumours
- External beam 30-55 Gy
- Local control 80%
- Recurrence rate of 15%
3. Chemotherapy
- Recurrent tumours with previous surgery and radiation
4. Hormone therapy
- Estrogen and antiandrogens (flutamide) used to decrease tumour size and vascularity
- unproven efficacy
- Complications
- feminisation
- CVS complications
Preoperative embolization
- 24-72 hours preoperative
- Gel foam or polyvinyl alcohol foam
- Gel foam: resorbed in approximately 2 weeks
- Polyvinyl alcohol: more permanent
- Efficacy
- Stage I patients reduced from 840cc to 275cc blood loss
- Complications
- Brain and ophthalmic artery embolization (stroke, visual loss)
- Facial nerve palsy
- Skin and soft tissue necrosis (facial pain, headache)
- SE
• fever
Changing technique
- Marked shift towards endonasal procedures
- Endonasal approach contraindicated in stage IV and some stage III cases
- May be used in conjunction with other approach in these cases
- Easier with midline tumours, more difficult with lateral tumours
Surveillance
Yearly CT scan/ MRI
Endoscopic surveillance
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Recurrence
- more likely in advanced disease
- younger patient
- invasion of basisphenoid
Summary
- Rare, benign, vascular tumour found almost exclusively in young males
- Surgery is a gold standard with a trend towards endoscopic approaches
- Frequent follow up after treatment is necessary
CSF Leak
CSF production
- 500mls produced a day by choroid plexus at 20mls/hour
- 140mls total volume actively circulating
- turned over 3 times a day
- CSF pressure 5-15cm H2O
Substance CSF Serum
Water (%) 99 93
Protein (mg/dL) 35 7000
Glucose (mg/dL) 60 90
Osmolarity (mOsm/L) 295 925
Sodium (mEq/L) 138 138
Potassium (mEq/L) 2.8 4.5
Calcium (mEq/L) 2.1 4.8
Magnesium (mEq/L) 0.3 1.7
Chloride (mEq/L) 102 119
pH 7.33 7.41
- Produced in choroid plexus of lateral, third and 4th ventricles

- lateral ventricle (interventricular foramen of Monroe) → third ventricle (cerebral aqueduct of
Sylvius) → 4th ventricle (foramen Magendie and Luschka) → subarachnoid space →
arachnoid villi in the superior sagittal sinus
DEFINITION
communication between subarachnoid space with extradural structures - rhinorrhea/ otorrhea
Incidence
- post-traumatic (80%)
- Iatrogenic (16%)
- spontaneous (<5%)
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Importance→ ascending infection causing meningitis → death
CLASSIFICATION
Omaya Classification - traumatic/ non-traumatic
1. Traumatic (75%)
- 2% H&N injury
- 5% skull base #
- accidental
- acute <3/52
- chronic >3/52
- iatrogenic
- acute <3/52
- chronic >3/52
- most common site

a) roof of ethmoid (fovea ethmoidalis) lateral lamella
b) post wall of frontal sinus
c) cribriform plate
d) sphenoid sinus
- Iatrogenic causes
- Neurosurgical procedures
• surgery for transphenoidal hypophysectomy
• surgery for acoustic neuroma
- surgery for meningocele
- Frontal craniotomy
- Other skull base procedures
- Rhinologic procedures
- surgery for FESS
- Other combined skull base procedures
- Septoplasty
2. Non-traumatic/ spontaneous (25%)
- > in Females 4:1, 40s
- aft sneezing/ coughing/ following URTI
a) High pressure leaks
- High ICP
- common in
- tumours
- hydrocephalus
- Benign intracranial hypertension
- 75% occurs in cribriform plate
- HPL acts as safety valve - closure of defect will worsen the condition if cause not treated
b) Normal pressure leaks
- no exact ethology
- 90% due to abnormal congenital pathway
- 10% due to direct erosion due to tumour
- NPC
- Sinonasal malignancy
- Mucocele
- Osteomyelitis
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SITES OF LEAKAGE
1. Anterior cranial fossa
- frontal
- ethmoid
- sphenoid
2. Middle cranial fossa
- sphenoid
- mastoid
3. Posterior cranial fossa
- sphenoid
- mastoid
MANAGEMENT
1. History
- persistent rhinorrhea
- salty taste
- associated symptoms
• increase flow with position of head, valsalva
- headache
• due to increased/ decreased ICP
• due to symp of meningitis
- repeated h/o meningitis/ fits
- anosmia → suggests olfactory trauma
- audiovestibular symptoms → in cases of otorhinorrhea
- h/o trauma/ surgery
- rhinorrhea → clear/ blood stained
- position & jugular pressure → increased flow
- Reservoir sign - a change in head position can cause a gush of CSF collected in sinus
- aft a period of lying down - upon upright position - chin to chest - gush of fluid
- Halo sign - blood centre, CSF periphery → due to differential sp gravity
- Handkerchief sign - CSF not stiffen the handkerchief
- Sniffing test
- Nasoendoscopy
- roof
- PNS
- ET
- Otoscope
- MEE
- Hemotympanum
- Hearing loss
- Battle’s sign
3. Investigation
- To confirm - through history and physical examination
- To localize - if history + physical not enough, if to go for surgical intervention
a) biochemistry
• glucose > 1.67mmol/L or > 30mg/dl ( it is invalid if mixed with blood)
• Glucose should be ~ 2/3rd of blood glucose
b) Pathognomonic (Electrophoresis) → Beta 2 transferrin (protein that involve in iron ferrous
transport) - 100% sensitive, 95% specific - can be found in CSF, perilymph, aqueous humor
• CSF has 2 bands - B1 and B2
• In other fluids, only B1 transferrin
c) Radiology
• HRCT (1mm slice ), coronal cut, bone window
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• CT cysternography - to give intra thecal contrast ad obtain CT scan
• MRI generally not used
d) Intrathecal dye injection
• skin test with 2% Na fluorocein intradermal 1/7 before op
• set lumbar drain on the day of surgery
• Then intrathecal Na fluorocein
• 0.5ml 10% Na fluorocein diluted in 10mls of CSF & given slow bolus over 10 mins (high
concentration → seizure, coma)
• Pt in trendelenburg position x 45-60 mins
• Put pt under GA → nasoendoscope
• will show yellow green fluid
• if not seen, use blue light filter or
• place cotton pledgets in
• olfactory slit → cribriform plate
• middle meatus → frontal/ ethmoid
• sphenoethmoidal recess → sphenoid
• ET → temporal bone/ mastoid
• SE of Na fluorescein
• allergy
• pulmonary edema
• seizures
• death
TREATMENT
Conservative/ Surgical
1. Medical (80% will resolve)

- head up
- RIB x 1-2/52, stool softener/ laxatives
- Reduce coughing, straining, blow nose, heavy lifting
- IV lasix, acetazolamide (to reduce CSF pressure)
- +/- antibiotics to reduce complications
- antibiotics ( that cross blood brain barrier) x 10-14/7 (Rocephin)
- lumbar drain 120-150ml 6 hourly (normal: 10-20mls/hour)
- controversial
- Indications
• Failed conservative management (can be consider if CSF leak does not resolve in 5-7
days)
• Spontaneous CSF rhinorrhea (aft 3-5 days) provided no identifiable cause)
• Traumatic CSF leak
• Recurrent leak
- continuous drainage is recommended over intermittent drainage - prevent spikes in CSF
pressure
- RF: headache, nausea, vomiting, ascending infection, pneumocephalus
- If failed localising → surgical intervention
2. Surgical - open/ endoscopic/ combined
- Indications
- failed medical treatment
- large high volume fistula
- prolonged leak regardless of etiology
- recurrent leak
- intraop recognition of leak
- Intracranial - by neursurg
- Open
- Bicoronal/ external ethmoidectomy
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- Anterior/middle/posterior fossa craniotomy
- Adv
• direct visualisation
• inspection of adjacent cerebral cortex
- Disadv2
• increased morbidity
• injury to brain dt retraction → seizure, anosmia, hematoma
• poor visualisation of sphenoid sinus
- Grafts
• fascia lata
• muscle plugs
• pedicle galeal flaps
- Extra cranial - by ORL
- Endoscopic (for <1.5cm defect)
• Adv: better magnification, no external scar, minimal morbidity
• Disadv:
- limited to lesion <1.5cm of fistula defect
- limited to medial wall of frontal sinus, ethmoid/ sphenoid sinus, cribriform plate
• Principles
- defect circumferentially visualised
- skull base circumferentially demucosalized around the defect size (5mm)
- no overlap btw in situ skull base mucosa and mucosal graft
- mucosal overlay graft lie flush with the skull base
• Grafting material
- fascia (temporalis, fascia lata, cadaveric fascia)
- muscle plugs
- autogenous fat
- septal mucoperisoteum
- cartilage grafts (nasal septum/ cartilaginous auricle)
- bone grafts (nasal septum, calvarium)
- acellular dermal allograft
- Flap
• nasoseptal flap - based on nasoseptal artery, terminal branch of SPA)
• middle turbinate
• inferior turbinate mucosa
• nasal floor
• Layers
A. Dura
B. fascial autograft/ acellular dermal allograft
C. bone or cartilage autograft
D. fascial autograft or acellular dermal allograft
E. mucosal free autograft
F. surgical sealant
- → packing
• Technique
- Overlay - graft placed over defect
- Underlay - graft between dura and defect
• autologous/ synthetic
- duragen/ dura patch/ dura repair
- autologous: hadad flap,
- Combined underlay and overlay
- Bath plug technique
• seal augmented by fibrin glue, gelfoam and nasal packing
- dura reduced
- mucosa around defect stripped at least 5mm around it
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- skull base defect measured using curette
- Harvest fat → suture it → push fat through defect →
pull in defect → suture through mucosal graft, suture
mucosa through fat
• Encephalocele → cauterize the stalk prior to reduction to
prevent intracranial hemorrhage, 2-5mm of bone exposed,
graft size 30% larger than defect
- Open
• depends on site of defect
- Frontal: craniofacial resection. external ethmoidectomy
- Sphenoid: Transethmoid sphenoidotomy
POST OP MANAGEMENT
bed rest 3-5 days, head up, avoid straining, heavy lifting, blowing nose,
maintain normal blood pressure
Antibiotics
If lumbar drain present - keep 3-5 days
Lumbar drain - to read
Differences between CSF & nasal secretions
CSF Nasal secretions
History nasal sinus surgery sneezing

head injury nasal stuffiness
intracranial tumour itchy nose
lacrimation
flow of discharge few drops/ fluid gusher when continuous, no effect on bending
bending forward forward
cannot be sniffed back
Discharge character thin, watery, clear mucoid/ clear
Taste sweet salty
sugar content >30mg/dl <10mg/dl
B2 transferrin Always present Always absent
Halo sign + _
Handkerchief sign not stiffened stiffens
Unilateral nasal obstruction

Based on anatomical
1. vestibule
- furuncle of hair follicle (furunculosis)
- vestibulitis
- stenosis of nose (CNPAS)
- atresia
- nasoalveolar cyst/ nasolabial cyst
- SCC
2. nasal cavity
- FB/ rhinolith
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- DNS
- Hypertrophic IT → compensatory/ paradoxical
- unilateral mass
- ac polyp
- atrophic rhinitis
- synechia
- septal haematoma/ abscess
- tumour
- benign
- malignant
3. post choanae
- post choanal atresia
4. nasopharynx
- NPC
- angiofibroma
- lymphoma
Septal perforation
Most common part - anterior cartilaginous part
Except syphilis in bony part
ETIOLOGY TI4N
1. Trauma
- iatrogenic
- SMR
- Septoplasty
- Cautery
- Injury
- MVA
- Sports injury
- Nose picking/ penetrating
- FB - battery (caustic)
2. Infection
- chronic inflammatory
- TB
- syphilis
- leprosy
3. Inflammatory disease
- Wegener’s
- SLE
- RA
- PAN
4. Inhalation of irritants
- occupational related
- cocaine
- arsenic
- mercury
- alkaline dust
- drugs
- cocaine
- topical steroids/ decongestants
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5. Idiopathic
6. Neoplasm
- SCC
- Basal cell ca
- T cell lymphoma
- adenoca
PATHOPHYSIOLOGY
- usually preceded by ulcer
- 1. mucosal congestion
- 2. followed shortly by mucosa becoming blanch and pale
- 3. mucosa necrosis → presence of adhered crust
- 4. crusting deepen → involve the cartilage → perforation
CLINICAL FEATURES
1. majority asymptomatic
2. symptomatic
- mucociliary function disturbed
- vicious cycle where there will be mucous stagnant due to mucociliary dysfunction → dried
crust & blood clot → obstruct nasal airflow → turbulent airflow → excessive drying of mucosa
→ mucociliary dysfunction
- Symptoms
- nasal obstruction due to large crust
- excessive crusting
- recurrent epistaxis → if crust separated
- dryness
- discomfort over nasal dorm
- whistling noise
- voice change → due to impaired resonance
- Severity of symptoms determined by
- site
- size
- larger the size - symptoms worse
- Site more anterior - worse
• anterior 1/3rd of nasal septum → has slower mucociliary function
INVESTIGATION
1. History
- trauma
- occupational hazard
2. Blood investigations
- FBC
- ESR
- VDRL/TPHA
3. CXR
- TRO TB
4. Urinalysis
- Wegener’s
- PAN
5. Biopsy
- TRO malignancy
- Wegener’s
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TREATMENT
- In general, if no symptoms → no treatment
Objective
1. To cure the causative disease process
2. For closure → to encourage natural healing by medical treatment → if fail → surgical repair
Medical treatment
1. Nose care, avoid trauma, nose blowing, nose picking
2. Ulcers → use cicatrix cream
3. Loosen the crust
- 25% glucose in glycerin drops
- Alkaline douching
4. If any bleeding granuloma → silver nitrate cauterisation
5. Treat cause of TB/ syphilis/ granuloma
Surgical closure
1. Obturator → in perforation < 3cm
- <1cm - small
- 1-2cm - medium
- >2cm - large
- usually silastic obturator → custom made is better
- ready made silastic → problem: not well fit to the perforation
- failed → surgical op
2. Surgical operation
- results unsatisfactory from obturator and perf >2cm
- closure by graft
- temporalis fascia
- fascia late
- pinna graft
- turbinate mucosa
- by mucosa flap
- from septum
- lateral nasal wall
- labial flap
- collapse nasal bridge → rhinoplasty
if
- surgery for neoplasm
- underlay technique
- Approaches
- alar-facial skin crease incision
• upper limit of perforation <2cm from floor
• external rhinoplasty
• mid facial degloving
Mucocele
Definition
A benign epithelial-lined, mucous containing sac completely filling the sinus capable of expansion
OR
A slowly expanding cystic lesion lined by pseudo stratified columnar epithelium and contains thick/
mucoid secretion
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10 mucocele - retention cyst

20 mucocele - sinus ostia obstruction
Properties
1. Slowly expand
- progressive
- rapid (if infected)
2. Expansion of bony structure
- cytokines (IL1, IL6) + TNF from lymphocytes + monocytes → fibroblast formation → it
secretes PG + collagenase → causes bone resorption → bone expansion
Epidemiology
1. Frontal sinus (commonest)
2. Ethmoid sinus
1+2 - 90%
3. Sphenoid sinus
4. Maxillary sinus
3+4 - 10%
- occurs at 4th - 7th decade, paeds are very rare

- usually unilateral, rarely bilateral
- in Paeds - usually a/w cystic fibrosis (diagnosed by sweat test)
- no gender predilection
Pathophysiology
- due to chronic obstruction of frontonasal duct/ obstruction to natural sinus drainage
- mucous retention cyst - single mucous gland causing obstruction
- Mucocele
- mucous gland secreting in a normal physiological manner
- obstruction of natural sinus drainage
- Mucus retention cyst - single mucous gland obstruction
Causes T(3)IAN
1. Anatomical variation
- frontal air cells
- supraorbital cells
- fibrous dysplasia
- osteoma
2. Neoplasia
- polyps
- osteoma
3. Infection (commonest)
- CRSS
4. Inflammation
- AR
5. Trauma
- 1st leading cause
6. Iatrogenic
- surgery
usually takes years to give symptoms
Pyocele
- forms when mucocele gets infected
- common pathogens
- staph aureus
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- H. Influenza
- strep pneumonia
Clinical features
any age, any gender
1. Asymptomatic - because it takes years to increase in size
2. If symptomatic
- due to mucocele expansion
- mucocele tends to grow/ follows the route of least resistance → the frontoethmoidal mucocel
tends to grow inferolaterally into the orbit
- >60% will present to ophthalmology before coming to ENT because of globe displacement
Frontoethmoidal mucocele
- orbital symptoms is commonest
- proptosis
- inferolateral displacement of eyeball
- ophthalmoplegia
- diplopia
- loss of visual acuity
- limited eye movement esp upwards &medial gaze
Anterior ethmoidal mucocele
- occur in young children
- epiphora → due to NLD obstruction
Posterior ethmoidal mucocele/ sphenoid mucocele
- retroorbital headache
- facial pain
- orbital symptoms
- diplopia
- proptosis
- ophthalmoplegia
- visual loss
Intracranial extension
- meningitis - due to subdural abscess etc
- ↑ ICP
- CSF fistula
vein of Breschet
- located on posterior wall of frontal sinus
- it drains into intracranial subdural venous system
- intracranial infection is caused by ascending infection from frontal pyocele e.g. subdural
abscess
other walls of frontal sinus drain into facial vein
Management
1. History
- “egg shell crackling” due to thinned overlying bone
3. Investigation
- plain PNS x ray
- frontal sinus (Caldwell view) OF view
- loss of scalloped margin
- pushed/ eroded inter sinus septum
- erosions of supraorbital ridge/ inferomedial floor of frontal sinus
- cloudiness of frontal sinus
- CT scan - homogenous lesion (CT>MRI)
- shows extension of mucocele
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-shows smooth clear cut margin of erosions of bone/ sclerosis
-sinus expansion, anatomical variant of sinuses
-3D CT scan - can show nasofrontal duct
-with contrast - shows no enhancement
• If pyocele - shows ring enhancement
- to look for involvement of posterior table of frontal bone
- MRI
- if intraorbital/ intracranial complication
• T1 with gad - low signal (hypointense)
• T2 - high signal (hyperintense)
Treatment
- surgery is a definitive treatment
- what are the issues
- option ?
- clear the mucosa ?
- obliterate the sinus ?
- stent the nasofrontal duct ?
Surgery
External Endoscopic
External
ethmoidectomy with/ Craniofacial resec7on Bicoronal/ Lothrop procedure
with/ without sinus hemicoronal - → Others – glabellar, (destruc7ve
without oblitera7on transcaruncular Marsupializa7on
oblitera7on osteoplas7c flap endonasal surgery)
(Lynch Howarth)
Endoscopic marsupialization
- Advantages
- No external scar
- Reduce morbidity
- Reduce hospital stay
- a/w with less diplopia
• rapid decompression of orbit cause post-op exacerbating of diplopia
• this approach will allow bone remodelling to occur, while the displaced globe may take
several months to resolve completely, this will reduce post op diplopia
- may not require stenting
- integrity of lamina papyracea is maintained
- prevent reaccumulation of mucus (reduce recurrence)
- C/I of endoscopic (when difficult to do endoscopic)
- laterally placed frontal mucocele
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- extensive sclerosis of bone
- large osteoma
Osteoclastic flap
- indication
- intracranial extension
- laterally placed mucocele
- failed complete external frontoethmoidectomy
Lothrop procedure (Draf III procedure)
- to provide enough access of endoscopic removal using burr
- remove intersinus septum & upper part of nasal septum _ frontal sinus floor to the orbital
laterally
- Indications: severe form of chronic frontal sinusitis where osteoplastic flap with obliteration is
the only alternative
- Modified Lathrop - widened the frontal recess area using a microdebrider
The decision making of type of surgery depends on

1. Surgeon option - surgeon preference/ experience
2. Extend of disease
3. CT scan
The primary goal of surgery

1. To eradicate mass with minimal morbidity
2. To prevent recurrence
Transcaruncular approach
- Incision made through caruncle to explore medial wall periosteum
- Periosteum opened + extended to provide adequate surgical field exposure
- Transnasal drainage tube inserted before closure of caruncle wound
Do we need to clear the mucosa?

- ideally should remove as much as possible
- should obliterate the sinus with e.g. fat, muscle, hydroxyapatite (must make sure remove all
mucosa), therefore no need stenting
- but in actual fact, it is difficult to clear all mucosa esp at the area of nasofrontal duct
- Stenting
- either rubber/ silicon - kept for 6/52 to 5/12
- to prevent stenosis
- to prevent medial collapse of orbit obstructing the drainage system
- can also use paediatric ett for stenting
Medical treatment
1. Antibiotics (if infected) x 2-4/52
2. Mitomycin C
- used to prevent stenosis of nasofrontal duct
- dose = 0.4mg/ ml x 4 units
Riedel approach
- radical approach to frontal sinus
- remove anterior and inferior walls of frontal sinus & collapsing forehead soft tissue down onto
posterior table of frontal sinus
- this leaves significant cosmetic deformity - indentation of forehead
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Follow up
- follow up for many years as recurrence often occurs after many years
- reassessment of osteal patency
- removal of debris/ crusting
- nasal douching
Retention cyst Mucoceles
1. common in maxillary sinus 1. common in frontal & ethmoidal sinuses

2. Due to obstruction of ducts of seromucous gland 2. due to obstruction of duct/ natural ostium of PNS
in sinus lining 3. Grows under periosteum
3. Grow under mucosa of sinus 4. thick + tough wall (sclerotic)
4. Thinned wall 5. expanding
5. Non-expanding (because grow under the 6. bony erosion +
mucosa)
6. No bony erosion
1. with bone expansion + destruction
- benign
- neurofibroma
- dermoid
- epidermoid
- malignant
- rhabdomyosarcoma
- lymphoma
2. In the absence of bone erosion
- retention cyst
- CRS
- AC Polyps
- Polyposis
Management of Nasolacrimal
duct obstruction
Lacrimation: watering that occurs secondary to excessive tear production in the presence of a
normal excretory system
Epiphora: watering that occurs secondary to abnormal excretory system in the presence of normal
tear secretion
Causes
1. Lacrimation
- ocular inflammation
- emotional distress
- irritation of the eyes
2. Epiphora
- malposition of lacrimal punta (ectropion)
- obstruction (anywhere along lacrimal drainage system)
- congenital
• NLDO
• Congenital dacryocele
- Acquired
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• punctual stenosis - infection
• canalicular obstruction - trauma, infection, irradiation)
• NLDO - trauma
• Dacryolithiasis
- lacrimal pump failure (lower lid laxity or weakness of orbicularis muscle)
History
1. Epiphora
- purulent discharge
- pain
- blood stain
- epistaxis
- trauma
2. Medical history
- prev surgery
- autoimmune disease
- malignancy
- radiation
PE
1. Eye examination
- position of eyelid, contour, function
- punctual opening
- palpation
- mass at medial cantonal region/ lacrimal sac region
2. Full nasal examination
Tests
1. Fluorescein disappearance test (no dye aft 3 mins)
2. Jones dye testing (primary and secondary test)
3. Lacrimal irrigation/ syringing
4. Probing (hard stop or soft stop)
5. Contrast dacrocystography
6. Nuclear lacrimal scintigraphy
7. Lacrimal endoscopy
1. Fluorescein disappearance test

- 1 drop of 2% fluorosceine at lower conjunctival fornix - 5 mins
- 0 to 4+: 0 - no dye remaining, 4+: representing all dye remaining
- little or no fluorescein remaining - indicates probable normal drainage outflow - no obstruction
2. Lacrimal irrigation/ syringing
- instil LA xylocaine 4%
- punctum dilated if narrow
- lacrimal cannula with 2mm saline filled syringe probed
- free passage of saline - patent lacrimal passage
- clear fluid from same puncta - same puncta block
- clear fluid from opposite puncta- common cannnalicular block
- mucoid fluid from opposite puncta - NLD block
3. Primary Jones Dye Test
- 2% fluorescein is instilled into the conjunctival sac + fine cotton-tipped applicator passed
beneath the inferior turbinate to the level of NLD ostium aft 2 mins and 5 mins
- +ve if dye recovered
- -ve = functional/ anatomic blockage
4. Secondary Jones Dye Test
- if primary test negative
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-
evaluates anatomic potency under increased hydrostatic pressure
-
clear saline into inferior canaliculus using syringe/ cannula
-
if +ve (presence of dye in irrigant): partial block
-
if -ve: block
5. Punctal dilatation and canalicular probing
- evaluate latency of proximal ductal system
- soft stop; canalicular obstruction
- hard stop - NLDO
6. Lacrimal scintilography - non invasive physiological test
- uses radio tracer technitium-99M pertechnitate
Management
1. Infants
- observe
- nasolacrimal duct stent
2. Adult
- Medical therapy - treat infection
- Surgery
- open DCR
- EDCR
- Endoscopic laser DCR
- Balloon catheter dilatation
- Stenting
EDCR
Contraindications
1. tumour
2. obstruction at level of canaliculi
3. Stone
Procedures
1. GA, throat pack, eye exposed
2. Pack nose
3. LA marcain adrenaline to axilla region
4. Mucoperiosteal flap
5. Removal of frontal processor maxilla by Kerrison punch and diamond drill
6. Dilate punctum followed by probing the lacrimal sac
7. Incision of lacrimal sac with sickle knife
8. Marsupialization of lacrimal sac
9. Stenting
Complications
1. Orbital emphysema/ hematoma
2. trauma to canaliculi by tubes
3. infection
4. synechia/scarring
5. tube cheese wiring or dislodged
6. hemorrhage
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Unilateral proptosis
1. with bone expansion & destruction
- benign
- neurofibroma
- dermoid
- epidermoid
- malignant
- rhabdomyosarcoma
- lymphoma
2. No bone erosion
- retention cyst
- CRS
- AC polyps
- polyposis
Nasal bone fracture

Epidemiology
- M:F = 2:1
Etiology
1. Assault (36%)
2. MVA (32%)
3. Fall (18%)
4. Sports (11%)
Pathophysiology
1. Biomechanics of force directed to mid face
- frontal
- lateral
- Children > likely to sustain cartilaginous injury (dt greater proportion of cartilage to bone)
Clinical features, Ix, Tx
1. Hx
- elicit detail hx of mechanism of injury
- swelling
- pain
- periorbita ecchymosis
- deformity
- epistaxis
- nasal blockage
- swelling of nose
- laceration
- ecchymosis
- deformity
- crepitus
- tenderness
- CSF rhinorrhea
- MUST RULE OUT septal haematoma
3. Investigations
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- blood
- FBC
- Coag
- GXM
- Plain X ray:
- lateral SXR
- Water’s view
4. Treatment
- Indications
1. Abnormal nasal function
2. Abnormal appearance
3. Presence of early post injury complications
Classification
Hwang
I - simple without displacement
II - simple with displacement/ without telescoping
IIA - unilateral
IIAs - unilateral with septal #
IIB - bilateral
IIBs - bilateral with septal #
III - comminuted with telescoping/ depression
Surgical
1. Closed reduction
- performed under LA/ GA
- Indication
- simple nasal bone #
- simple nasal septal complex #
- Impacted fragments require disimpaction with Walsham’s (disimpact) and Asche’s (septal
elevation)
- May be difficult once edema sets in (see nasal bone fracture reduction)
- Any septal hematoma req drainage
2. Open reduction
- Indications
- when close methods fail
- extensive # dislocation of nasal bone & septum
- # dislocation of caudal septum
- Open septal #
- Persistent deformity after close reduction
3. Medical treatment
- antibiotics
- decongestants
- analgesia
- NSAIDS
- douching
Complications
1. DNS
2. Nasal “hump”
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Rhinolith
Definition
- intranasal calcareous mass
- can be
- unilateral
- bilateral
- occurs more common in children (h/o FB ingestion)
- in adult → following H&N trauma
- Pathophysiology
- not fully understood
- Predisposing factors
- FB dislodgement (long standing) → acts as nucleus for encrustation → intense
inflammation with nasal secretion and stagnation → mineral salts precipitation (Ca, Mg,
Co3/ Po4)
Types
2 types (depends on origin of nucleus)
1. Exogenous (> common) - non-human in origin (e.g. bead, seeds, cotton wool, sand)
2. Endogenous (rare) - blood clot, tooth, bone fragment
Clinical features
- usually non-specific
- Hx
- epistaxis
- foul smelling discharge
- nasal obstruction
- fetor
- signs and symptoms of sinusitis
- septal perforation/ palatal perforation
- many of the symptoms are discovered incidentally
- Physical examination (by ARS/ endoscope)
- white yellowish mass in the nasal floor/ cavity
- hard + gritty
- surrounded by foul smelling pus discharge
- granulation, sometimes
Investigations
- rarely needed
- PNS x ray
• to confirm calcified mass done in patient with symptoms
- CT scan
• in very large rhinolith
• to identify the site, size, configuration
• co-existing sinus infection
Treatment
1. removal of rhinolith
- small - under LA
- Larga - under GA, need to be broken into pieces beyond removal
- sometimes require lateral
2. Antibiotics
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Oroantral fistula
Fistula - abnormal communication between 2 epithelial surface
OAF - abnormal communication between oral cavity + maxillary antrum
Etiology
1. Dental extraction
- usually upper 2nd premolar or 1st molar extraction due to longer roots which can protrude into
floor of maxillary sinus
- extraction of retained root
2. Following Calwell Luc op
- failure of incision to heal
3. Following trauma
- # maxilla
- following gunshot
4. Neoplasia
- due to bony erosion into oral cavity
Clinical presentation
1. Usually with signs and symptoms of maxillary sinusitis
- nasal discharge
- bad smell
2. Signs and symptoms of food entering the antrum via fistula in patients previously who had
inferior meatal antrostomy
3. On valsalva
- gush of air enter through fistula & causing gurgling
Diagnosis
can be clinically diagnosed by probing through the fistula into antrum
Investigation
1. PNS x ray
- retained root of teeth
- evidence of FB
- bony erosion by tumour
- signs of sinusitis
2. Pus C&S
3. Biopsy of suspicious wall (in case of neoplasm)
Treatment
1. Dental extraction
- immediate closure of mucosa
2. If fistula develop late post-op & patient developed infection & granulation tissue at fistula site
- send for pus C&S
- create inferior antrostomy sized 2x1cm for aeration of antrum
- follow up aft 4/52
- if no spontaneous healing - surgical closure
3. In chronic fistula - surgical closure
- trim bony edge
- the fistula is incised marginally & everted into the antral cavity
- the bare area is covered either with
- palatal flap - based on greater palatine artery
- buccal mucosa flap adjacent to fistular site (buccal advancement flap) - based on buccal
sulcus
- buccal fat pad flap
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Acoustic rhinometry
Nasal airway resistance constitutes about 50% of total airway resistance
3 methods for assessing nasal airway
1. Peak flow
- very subjective
- inspiratory flow
- does not tell the site of obstruction
- Physiological measure indicated the peak nasal airflow in litres per minute
- How to do
- Expire through mouth
- Close mouth
- Inspire forcefully through nose
- Limitation
- Patient cooperation
- Does not measure airflow during normal breathing
- Results may be compromised due to lower airway problem
2. Rhinomanometry
- it is a measurement of nasal airflow + nasal resistant of entire nostril
- either airflow/ pressure is measured
- pressure standardise and flow through each nostril measured or
- flow standardised and pressure measured
- measures nasal resistance + airflow
- R = airway pressure (p)/ nasal airflow (v) → Ohm’s law
- measures pressure of both nostril but not the volume
- 2 types
- Active - generation of nasal airway and pressure with normal breathing
• Anterior and posterior
- Passive - direction of an external flow of air through the nose and out of the mouth
- still non-specific
- difficult to do
- not reliable
3. Acoustic rhinometry
- measures nasal cross sectional area along the length of nasal passage
- measurement of nasal airway using sound wave
- 2D
- Can identify the narrowest portion
- Normal cross sectional area - 0.3 - 1.2 cm3
- can be done even in children
- Advantages
- Measures cross sectional area
- Plot cross sectional area against distance
- Study nasal volume changes
- cheap
- easy
- objective test
- no side effect
- can test each nostril separately
- can be done in children
- Disadvatanges
- operator dependent
- depth of nose play a role in accuracy of results - unrealiable in posterior part of nose
- Usage
- in allergic rhinitis - in pre & post treatment measurement
- In surgery
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• pre& post surgery
- TIT
- septoplasty
- rhinoplasty
- polyps
- Indications
- measurement of anatomical variation
- pre and post op quantitative measurement
- exclusion of functional disorder
- medicolegal
- determination of NP + velopharyngeal adequacy
- Aid in treatment of OSA
Comparison btw AR and RM

RM more sensitive and specific for patient with functional nasal obstruction such AF
AR more sensitive and specific when evaluating structural causes of nasal obstruction
Limitation of AR and RM
- accuracy of AR decrease as the distance from the nostril increases with the best accuracy at
5cm, breathing and swallowing not allowed during AR may affect outcome
- Compounding factors for both
- Age, height, nasal cycle, exercise, hyperventilation, breathing CO2, posture, medications and
smoking
4. Odiosoftrhino (OR)
Septal Surgery
INDICATIONS
1. Mechanical obstruction due to DNS
2. DNS causing recurrent sinus infection
3. As part of 1 stage septorhinoplasty
4. To gain access to nose, sinuses & pituitary fossa
Contraindications
1. large septal perforation
2. Wegener’s granulomatosis
3. T cell lymphoma
4. Cocaine abuse
PRINCIPLE OF SEPTAL SURGERY

1. Surgical point of view, the septum is divided into:
- anterior segment
- posterior segment
- by vertical line drawn between nasal mucosa of frontal bone & maxillary bone
2. Deviation posterior segment → SMR
3. Deviation of anterior segment → Septoplasty
4. If SMR done anterior to this line causes
- supra tip depression
- columella retraction
5. Immediate saddling is rare → occurs due to scar contraction in septum
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6. Septal surgery can be performed under GA/LA
7. Decongestants with cocaine x 10-15 mins before GA to reduce bleeding
8. Patient in Proetz position → the chin and EAM in vertical plane
9. Cocaine gravitate into superior part of middle meatus where it blocks both
- ethmoidal nerve
- sphenopalatine nerve
- kept in position x 10 mins
10. A small quantity of 2% lignocaine injected into columella
- lignocaine + adrenaline → risk of cardiac arrhythmia, but good activity in giving dry operative
field & shortened surgical duration
- Prilocaine + Felypresin → less risk
SMR
- High risk of septal perforation & external deformity
- Inability to correct anterior deviation
- Difficult to perform revision surgery
- Advantage
- easy to perform with satisfactory results
- Indications
- posterior septal deviation
- adults
- closure of septal perforation of other causes
- source of grafting material
- rhinoplasty/ tympanoplasty
- To obtain surgical access
- hypophysectomy
- vidian neurectomy
- Technique
- Killian incision through septal cartilage about 1cm above and parallel to its lower border
- Incision made through cartilage but NOT opposite perichondrium
- Mucoperichondrium of other side is elevated through this cartilaginous incision
- Dorsal and caudal strut of cartilage is left to maintain support of nasal dorsum + columella.
- Then elevate flap of maxillary crest and vomer, removed with hammer + gouge + bone
forceps
SEPTOPLASTY
- more conservative method
- Indications
- for anterior deviation
- children
- Technique
- Incision: Freer/ Cottle/ Hemitransfixation
- Incision made at caudal border of septal cartilage
- Exposure cartilaginous + bony septum by elevating mucosal flap on concave side
- difficulty of flap elevation at junction of septal cartilage above with anterior nasal spine, pre-
maxillary crest and vomer below (because perichondrium encloses cartilage in complete
envelope which does not fuse with periosteum)
- Tunnelling
- Anterior tunnelling → upwards + backwards above chondrovomerine junction
- Inferior tunneling → both side over pre-maxillary crest and vomer below chondrovomerine
junction
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SMR Septoplasty
more radical more conservative
Killian incision (oblique incision 5mm to 1cm above Freer/ Cottle/ Hemitransfixation
caudal border of septal cartilage) Advantages:
a) is placed in relatively avascular plane
b) Through and through mucosal edges which
reduced risk of tear
c) Provide easy access to whole septum including
anterior septal border
d) can be combined with rhinoplasty (easy to
extend incision to full transfixation incision)
Approach + elevation of flap Approach + elevation of flap

• from convex side • from concave side
• flap elevated from both sides of septum • flap elevated from 1 side only until reaches the
• incision of cartilage pathologic area
• Tunnel creation (Cottle’s max-premax approach)
Removal of cartilage + bone Removal of cartilage bone
• major portion of septal cartilage with bone • more tailored to specific pathologic where only
removed leaving the dorsal + caudal struts of specific deviation/ spur removed
cartilage to maintain support of nasal dorsum +
columella
complication ↑ complication ↓
POST-OP CARE
1. insert internal splint x 1/52
- pack to be removed after 24 hours
- problem
• post-op pain
• intranasal adhesion still occur
2. Nasal toilet/ douching
3. Antibiotics/ pain killers/ antihistamines
4. Toxic shock syndrome
- multi systemic disease caused by enterotoxin produced by staph aureus
- characterised by
• fever
• rash
• hypotension
• mucosal hyperaemia
• vomiting
• diarrhoea
COMPLICATIONS
1. Early
- hematoma
- infection
- haemorrhage
2. Late
- septal perforation
- external deformity
- columellar retraction
- supra tip saddling
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- Toxic shock syndrome
Anatomy of nose and paranasal

sinus
Medial boundary: superior and middle turbinate
Lateral: Orbit
Superior: Skull base
Back wall: Sphenoid sinus
Height of orbital floor is a safe distance from
Roof of maxillary sinuses is always below
FESS
Minimally invasive surgery done via endoscopic approach to improve sinus drainage & ventilation
& to restore normal mucociliary clearance
- 1st described by Kennedy, 1985
Aim
- eradicate OMC disease
- improve sinus drainage + ventilation
- restore normal mucociliary function
Indications
Absolute indications Relative indications Extended indications
1. Complications of RS 1. Epistaxis 1. Endonasal transphenoidal

2. Mucocele 2. Nasal polyps hypophysectomy
3. Fungal sinusitis 3. Recurrent acute sinusitis 2. Endoscopic DCR
4. Tumour (sinonasal) 4. CRS failed medical treatment 3. Optic nerve decompression
5. Encephalocele for 4/52 4. SPA ligation
6. CSF leak 5. Approach to pituitary 5. CSF leak repair
6. Lothrop’s procedure
7. Blow out # of orbit
Contraindication
1. ASA 3 or 4
2. Lateral frontal sinus disease (approach via bifrontal approach wiht osteoplastic flap)
3. osteomyelitis
4. extensive tumour
5. stenosed frontal sinus ostium
- to locate frontal sinus ostium that is tensed
- trephine frontal sinus
- put in dye
- locate dye endoscopically in nose (before the advent of IGS)
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Principles of FESS
1. Preservation of mucosa
2. Normal functional state
3. relief of obstruction
4. re-establish ventilation & drainage
Techniques
1. Messenklinger technique - anterior to posterior -done in normal anatomy
2. Wigan’s technique - posterior to anterior - when loss of anatomy/landmarks ( tumour/re do) -
safer - post skull base lower
Complications
1. Immediate
a) bleeding
- injury to vessels (SPA/ post septal branch of SPA)
- due to coagulation defect
- Tx
- nasal packing (non-adherent type)
- correct coagulopathy
b) orbital complications
i. periorbital
- after breach the LP
- subcutaneous emphysema, orbital cellulitis/ abscess
- Treatment
- post-op - avoid blowing the nose
- antibiotics
ii. intraocular muscles
- medial rectus + superior oblique muscles → lead to diplopia
- Treatment
- external medial cantal approach
iii. haemorrhage/ Retrobulbar hematoma
- sudden increase in intraorbital pressure → decreased visual acuity/ ocular pain
- Signs: ecchymosis, firm proptosis, differential globe compressibility compared to
contralateral eye, IOP > 40mmHg, RAPD
- Dt Arterial/ Venous
- Artery: commonly AEA 
Vein: Vein that lines the LP
- If artery - acute decompression
- If vein - slow ooze - loosen pack - refer opthal - meds - surgical decomp/
canthotomy
- acute emergency → can cause optic nerve/ retinal artery injury → permanent
blindness (60-90 mins) esp in sphenoid sinusitis/ sphenoehtmoidal cells
- Treatment
- immediate lateral canthotomy + cantholysis → endoscopic orbital decompression
- IV Dexamethasone 1mg/kg
- IV mannitol 1gm/ kg x 20 mins
- If orbital decompression failed → external ethmoidectomy
iv. optic N injury
- occur during removal of disease mucosa of Onodi cells
- Treatment
- refer opthalmologist, remove packing, steroids, orbital/ optic decompression
c) intracranial complications
i. internal carotid A injury
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- in sphenoid sinusitis
- dehiscence of ICA is 20%
- Dehiscence of optic nerve is 6%
- Treatment
- compress CCA against vertebra
- perform exploration for ligation
ii. CSF leakage
- may result from
- # cribriform plate during medialization of T
- lateral lamella of cribriform plate
- direct injury to posterior aspect of frontal recess/ at
region of sphenopalatine recess
- Treatment
- graft from nasal septum/ buccal mucosa/ temporals
fascia
- if persistent →lumbar drain
- Bath plug - fat from ear lobule + fibrin glue
d)injury to NLD
- Treatment
- avoid dissection anterior to anterior margin of MT
- avoid MMA too anteriorly
2. Delayed complications
- synechiae
- stenosis of maxillary osmium
- nasal crusting
- overlook disease → recurrence
- delayed bleeding can be due to mucosal infection, rupture of false aneurysm of carotid,
carotid cavernous fistula
Lateral canthotomy
- lateral canthus divided at its apex, on the bone of orbital rim
- eyelid retracted inferiorly
- lateral canthal tendon palpated and inferior crura transected
- inferior eyelid completely released
Maxillary sinus endoscopic

procedures
1. Middle metal antrostomy
- Boundaries
- Anterior: frontal process of maxilla
- post: Post fontanelle
- Superior: Orbital floor
- Inf: Inf Turb
- Indications
- CRS, AC polyp
2. Modified MMA
- Boundaries
- Anterior: frontal process of maxilla
- Post: Flushed with posterior wall of maxillary sinus
- Superior: Orbital flow
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- Inferior: post part of IT removed
- Indications
- Fungal sinusitis
- Some IP (small stalk, stalk reachable, 1st op, recurrent AC polyp
3. Modified/ partial medial maxillectomy
- Boundaries
- Ant: anterior wall of max sinus, remove lacrimal duct and ant IT
- Post: post wall of max sinus
- Sup: orbital floor, lacrimal sac
- Inf: floor of nasal cavity
- Indications: inverted papilloma (esp recurrent)
Hemostasis in Endoscopic Sinus

Surgery
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HISTORY
- Hereditary or acquired bleeding tendency

- Personal or family history of predisposition to bleeding
- Abnormal coagulation testing results
- Coexisting medical conditions
- Medication use (including herbal)
- Warfarin - stop 5/7 prior
- UFH - stop 4-6 hours prior
- Argatraban, dabigatran - stop 1-2 days prior
- Dipyridamole - stop 1-2 days prior
- Aspirin - stop 10/7 earlier - increase risk of surgical bleeding by 1.5x
- 4Gs - ginseng, garlic, ginger, and ginkgo biloba
• Affect platelet function - stop 10/7 prior
- Preop steroids
- Use of anti-thrombotic therapy
- Stop smoking/ alcohol
- URTI/fever
IINTRAOP
1. Controlled hypotension
- patient positioning - reverse trendelenburn 200
- normocapnia/ mild hypocapnia
- hypercapnia → vasodilatation
- MAP 65-70mmHg
2. Surgeon
- LA packing
- refer top
Boerzaart scoring
Approaches to Frontal Sinus

Anatomy
- Frontal bone: vertical, horizontal
- Frontal sinus: in btw anterior & post plates of vertical portion
- Anterior table: thick cancellous bone forms the forehead
- Posterior table: thin bone, direct contact with dura
Frontal recess
Anteriorly: UP and AG
Post: bulla, AEA 
Lat: lamina papyracea
Med: Hiatus semilunaris, MT
Inf: Ethmoidal infundibulum
Sup: Fovea ethmoidalis, supraorbital air cells, frontal ostium
Ethmoidal infundibulum
- 3D lumen btw anterior wall of ethmoid and posterior wall of UP
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- Anteriorly: UP
- Post: ant wall of bulla
- Lat: LP and fontanelle
INFUNDIBULUM
- Med: Hiatus semilunaris and UP
- Ant and Sup: frontal recess
- Post and Inferior: maxillary sinus
Frontal recess cells

1. Agger Nasi cells
2. Supraorbital ethmoid cells
3. Frontal cells (I-IV) Uncinate – skull base Uncinate – attached to middle Uncinate – attached to lamina
attachment causes frontal turbinate causes frontal sinus to papyracea causes frontal to
4. Frontal bulla cells sinus to drain into superior drain into ethmoidal infundibulum drain into superior aspect of
portion of ethmoidal middle meatus. Ethmoidal
5. Suprabulbar cells infundibulum infundibulum ends in terminal
6. recess
Interfrontal sinus septal cells
Indications
1. Chronic sinusitis unresolved with maximal medical therapy
2. Polyps of the sinus
3. AFRS
4. Periorbital and intracranial complications of sinusitis
5. Mucoceles and mucopyoceles
6. Benign neoplasms such as osteomas, inverted papillomas or fibrous dysplasia
Surgical approach
1. External approach
- frontal sinus trephination
- external frontoethmoidectomy
2. Endoscopic approach
- Simple drainage (DRAF 1)
- Extended drainage (DRAF 2)
- Endonasal median drainage (DRAF 3, modified Lothrop)
- Axillary flap approach
3. Integrated approach
- above and below approach
- trephine + endoscopic
- osteoclastic + endoscopic
Frontal sinus trephination

Indications
1. acute frontal sinusitis unresponsive to medical treatment
2. complication of acute frontal sinusitis
3. chronic frontal sinusitis - combined with endoscopic approach to assess potency of frontal
ostium esp in revision cases
Anaesthesia
- under LA/ GA
- ipsilateral tarsorrhaphy to protect globe
Incision
- superomedial aspect of orbital rim
- 1-2cm incision just under eye brow incision made through periosteum
- drill with a cutting burr - to create trephination
- If in complicated acute frontal sinusitis
- trephination made at floor of frontal sinus to reduce risk of acute osteomyelitis
- If in chronic frontal sinusitis
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- trephination made through anterior frontal wall to increase exposure + easy to move with
- The trephination can be enlarged using rongeur/ drill
- drainage tube can be placed
External frontoethmoidectomy
- danger of supraorbital and supratrochlear nerve injury
- 2/3 of bony margin of frontal recess is resected and replaced by scar tissue, may contract and
lead to formation of mucocele
Draf I
- Endoscopic frontal recess approach
- complete anterior ethmoidectomy +
uncinectomy surrounding the frontal recess to
frontal ostium
- obstructing frontal cells removed, if present
- Inferior part of Killian’s infundibulum and its
mucosa is not touched
Draf II
1. IIa - ethmoidectomy + resecting the floor of the
frontal sinus btw LP and MT
- Equivalent to nasofrontal approach (NFA) II
- Maximum diameter of neo-ostium gained 11mm
(normally5-6mm)
2. IIb - IIa + resecting the floor of the frontal sinus btw
LP and nasal septum anterior to the ventral margin
of the olfactory fossa
- Equivalent to nasofrontal approach (NFA) III
- Requires drill medially as nasal septum is
thick(diamond burr)
Draf III
- Modified lothrop procedure
- remove entire frontal sinus floor + superior nasal
septum and inter sinus septum
- Lamina to lamina
- Anterior to first olfactory fibre
- Frontal T (long crus - perpendicular plate of ethmoid, short limb - posterior frontal sinus
- Diameter about 1.5cm
Indications
Type I Acute sinusitis

- failure of conservative surgery
- Orbital and endocranial complications
Chronic sinusitis
- first time surgery
- No risk factors (aspirin intolerance, asthma triad)
- Revision after incomplete ethmoidectomy
Type IIa - Sinus complications of acute sinusitis
- Medial muco-pyocele
- Tumour surgery (benign)
- good quality mucosa
Type IIb - all indications of type IIa, if the resulting IIa is

smaller than 5x7mm, type type IIb, drill necessary
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Type III - difficult revision surgery

- Primarily in patients with prognostic risk factors
and severe polyposis particularly patients with
triad mucoviscidosis
- Mucoviscidosis
- Kartagener’s syndrome
- Ciliary immotility syndrome
- Benign and malignant tumour
Axillary flap
- overcome problems in ESS while surgical field is bloody, longer time
consumption for placing angled endoscopes in frontal recess before surgical
dissection takes place
- allows large part of dissection in frontal sinus with 0 degree telescope
- Method
- make incision 8mm above axilla of MT and 8mm forward, turned down
vertically up to axilla, turned back under axilla on to roof of MT
- Full thickness flap elevated with freer elevator
- Hajek koeffler punch remove ant wall of AG cell
- AG cell entered → probe passed in frontal drainage pathway and all
obstructing cells removed and flap repositioned back
- mucosal flap carefully kept to prevent scarring
Complications
1. Recurrent frontal sinusitis aft surgery
- remnant ethmoidal cells → recurrent sinusitis
- mechanical irritation of mucosa in frontal recess → severe
scarring over Killian’s infundibulum
Osteoclastic flap with frontal sinus

obliteration
1. bitemporal coronal incision
2. Scalp flap elevation up to bilateral supraorbital ridges and over
root of nose, avoid damage to supraorbital and supratrocheal
nerve damage
3. Indications
- failure of correctly performed Type 3 drainage
- Type 3 drainage not possible (AP diameter <8mm)
- Latearlly located mucopyocele
- Major destruction of posterior wall
- Inflammatory complications aft trauma (alloplastic material)
- Major benign tumour with and without obliteration (osteoma)
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- Problem frontal sinus sometimes in combination with complete endo nasal ethmoidectomy
Cranialization of frontal sinus

1. Indications
- comminuted fracture of frontal sinus
- incomplete removal of frontal sinus mucosa
- severe post traumatic edema of frontal lobe
- intracranial of foreign body
- destruction of posterior frontal sinus wall
2. Surgical steps ~ osteoclastic frontal sinus procedure + removal of remnant of posterior wall +
mucosa of frontal sinus floor + obliterate the drainage pathway + obliterate large dead space
btw ant wall and dura + recon ant wall with additional bone graft from temporal area
Lynch Howarth Incision

- A curvilinear incision is made just below the medial end of eyebrow. It is curved
medial to the medial canthus.
- The frontal process of maxilla and lamina papyracea is removed.
- Frontal sinus is entered via its floor and the lining mucosa is curetted.
- A stent is placed in the frontal sinus ostium to prevent stenosis. The stent is left
in place for a period of 4 weeks.
Transcaruncular approach
- Incision made through caruncle to explore medial wall periosteum
- Periosteum opened and extended to provide adequate surgical field exposure
- Transnasal drainage tube inserted before closure of caruncle wound
Approaches to Sphenoid Sinus

1. Indications for sphenoid sinus pathology
1. Sphenoid pathology (concomitant with ethmoid disease)
2. Isolated sphenoid pathology
• sphenoid sinusitis
• fungal sinusitis
• sphenoid mucocele
• inverted papilloma of sphenoid
3. Pathology of surrounding structures
• sella area - pituitary macro/micro adenoma
• clivus chroma
• 3rd ventricle decompression
Anatomy of sphenoid sinus

1. 3 types of pneumatization
- presellar (40%)
- concha - no pneumatization
- sellar - well pneumatized (65%)
2. Important relations in its lateral wall
- Optic nerve (postero superior) 6% dehiscent
- ICA (postero inferior) 20% dehiscent
- maxillary nerve
- vidian nerve
3. Ostium
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- at anterior wall of sphenoid (above inferior attachment of vomer + few mm lateral to the
rostrum)
4. 2 approaches
(1) External
I) Trans-ethmoid (external approach)
• Lynch incision
- midline between medial canthal + nasal bridge
- incision down to lower border of nasal bone
- posterior extension up to AEA (i.e. 2.4cm from anterior lacrimal crest)
- rarely done
• Advantages
- wider access
- better vision
• Disadvantages
- scar
- risk of bleeding to AEA
- does not give symmetrical view of sphenoid
- lacrimal sac injury
• Indications
- sinusitis
- mucocele
- CSF leaks
- biopsy
- optic nerve decompression
II) Trans-septal
• Killian’s incision
• Sublabial incision
• Advantages
- no scar
- gives symmetrical view of the sphenoid
- better view of sphenoid roof
• Disadvantages
- Longer route to pit fossa
- Vision obstructed by instrument
- Narrower access as compared to ll
III) Trans-pterygoid/ transantral
(2) Trans-nasal/ endonasal
- new approach - endoscopically
• 2 approaches
a) transethmoidal
• Bolger's parallelogram
- meidal limit: lateral aspect of superior turbinate
- lateral limit: lamina papyracea
- superior limit: skull base
- Inferior limit: horizontal portion of superior turbinate
b) transnasal
- can remove either inferior/ middle turbinate
- Advantages
• limited septal incision
• better lateral exposure
- Disadvantages
• compromised 3D exposure
• 1 handed surgery
• difficult with depth perception
• technically difficult in anatomical variation
- Indications
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• Hypophysectomy/ biopsy
• Sinusitis
• Mucoceles
- Equipment
• Endoscopes
- 4mm diameter
- 18/30cm length
- 00/300/450 lenses
- sheath with irrigation system
• Cable light source
- xenon cold light
• Camera/ monitor/ video recording system
- Removal of lesion
• remove segmentally
• initially inferior part, then lateral part
• Do not remove straight to superior part because it can cause prematurely delivery of
diaphragmatic sella into surgical field
• If superior part is hanging up, ask anaesthetist to do valsalva manoeuvre to ↑ ICP
- Reconstruction of sellar
• To ↓ dead space
• to prevent descend on chiasma into seller cavity
• can use fat/ fascia lata
- Post-op
• seawater douche
• post-op visual assessment
• post-op MRI
- Complications
• bleeding
- ICA
- sphenopalatine
- mucosa
• CSF leak
• pneumocephalus
• vision deterioration
-
Endoscopic Transphenoidal
Approach (ETA)
Definition
- Minimally invasive surgical technique for removal of sellar & parasellar region
- performed via anterior sphenoidotomy
- Sella turcica can be approached
- Transphenoidally
- Transcranially
- APPROACHES TO THE SPHENOID
- Trans-septal
- Trans-ethmoid
- Trans-nasal
- Trans-antral/ Transpterygoid
- EQUIPMENTS
- endosope
• rigid scope 4mm
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• 18mm/30cm in length
• 0/30/450 lenses
• sheath with irrigation system
- fibreoptic cable light source
• xenon cold light
• illumination whiter than lagoen
• spectral character are close to sunlight
- camera/monitor/ video recording systems
- POSITION
- Under GA
- Supine
- Trunk elevated 100
- Head turned 100 towards surgeon & fixed with head crest
- Reverse trendelenberg position
- ANAESTHESIA
- Nasal cavity packed with pledgets 10% cocaine
- Infiltrate with 1:80,000 marcain in advance
- Before starting
• hypotensive
• Adequate analgesia
- How to reduce bleeding for ESS
- Pre op
• stop smoking 1/52
• stop anticoagulant drugs
- aspirin
- warfarin
• r/o of URTI/ fever
• control DM/ HPT
• stop OCP for females
• short course of steroids x 1/52
• 1/7 before op give Affrin NS (make sure not HPT, C/I)
- Intra op
• give another dose of Affrin NS boring before op
• pack nose with Moffat’s solution (cocaine 10% 2cc, adrenaline 1:1000 2cc and H2O
injection 3cc
• can give steroid/ antibiotic as induction therapy
• hypotensive method
- 3 PHASES
• Nasal phase
• Sphenoid phase
• Sellar phase
- opening of sellar floor
• use micro drill with 4mm 00
• incision - cruciate/ midline/ linear rectangular
- remove lesion
• remove segmentally
• initially inferior part, then lateral part (if remove superior part 1st, can cause
premature delivery of diaphragm)
• If superior part hang up, ask anaes to do valsalva manoeuvre to increase ICP
• angled scope to visualize site
- Reconstruction of sella
• Aim
- protective barrier
- to reduce dead space
- prevent descent of chiasm into sellar cavity
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• use
- duragen
- tissel
- nasal septal flap
- tissel
- surgicell
- nasopore
- COMPLICATIONS
- intraop/post op
• bleeding from ICA, SPA branch, mucosal tear
• CSF leak
• DI/ panhypopituitarims
• pneumocephalus
• vision disturbances
• surgical technique complications
- sublabial approach - deformity of labial-septal-columellar complex
- anosmia
- stenosis of nasal vestibule
- synaechia/ crusting
- POST OP MANAGEMENT
• seawater douche tds
• post op with visual disturbances
- MRI of sellar with contrast
- visual field test
- TYPES OF TUMOUR REMOVED
- suprasellar craniopharyngioma
- tuberculum sellar meningioma
- macro adenoma of cavernous sinus
- clival chordoma
- pituitary micro/macroadenoma
- ADVANTAGES
- no facial scar
- shorter hospital stay
- no brain retraction
- improved visualization of suprasellar components of tumour by using angled 30 and 70
degree scope
- allow 4 handed technique which consists of 2 surgeons (neurosurgeon and rhinologist)
- DISADVANTAGES
- suprasellar extensions are difficult to address
- post op crusting can be significant
- DI is still a problem
- CSF leak
- trauma to optic nerve & ICA
- CONTRAINDICATIONS
- extensive tumour (lateral to ICA)p
- concha or presellar sphenoid sinus
Endoscopic SPA ligation

Indications
1. Surgical control of posterior epistaxis failed posterior packing
2. Recurrent posterior epistaxis
Technique
- Performed under GA using orotracheal intubation
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- usually patients already has posterior packing
- Greater palatine block to ↓ bleeding
- foramen palpated medial to 1st molar (junction of hard palate and alveolar ridge)
- wait at least 5 min to allow vasoconstriction
- pack removed & packed with Moffat’s solution
- 2 basic techniques
- technique 1
• direct approach
- identify posterior attachment of MT
- Incision made 1cm anterior to this point (IT to ethmoid sinus)
- mucosa elevated anterior to posterior
- identify SPA, ligate/ clip
- artery tends to lie directly posterior to ethmoid process of palatine bone
- Technique 2
• perform uncinectomy 1st step
• exposed bulla ethmoidalis & removed anterior posterior & inferior superior
• ground lamella identified & perforated inferomedially to enter posterior ethmoid sinus
• natural maxillary ostium identified
• Antrostomy enlarged to the posterior wall of maxillary sinus
• mucosa of the posterior edge of antrostomy elevated
• vessels identified immediately posterior to the antrostomy
• vessels followed to SP foramen
• bone of foramen removed using Kerrison’s rongeurs
• exposed main internal maxillary artery
• vascular clips applied to IMA and its branches
Advantages
over transantral ligation
1. no facial scar
2. avoid injury to infraorbital nerve
3. less likely to rebleed of cause ulceration
4. shorter hospital stay
5. no need prolonged nasal packing
6. relatively fast and easy
7. avoid external approach to control epistaxis
8. cheaper alternative to angiogram & embolisation
Limitations
1. may be technically difficult in acute bleeding esp with improper instruments
Maxillectomy
1. Partial
- medial maxillectomy
- en bloc resection of
• lateral wall of nose - MT, IT
• bone of lateral & superolateral of pyriform aperture
• medial 30% of orbital floor/ orbital rim
• Lamina papyracea
• lacrimal fossa
- palatal resection
- adjacent alveolus + hard palate
2. Total matxillectomy/ radical (indicated for tumour involving palate/ zygoma)
- en bloc resection of maxilla + lower 1/2 of ethmoid +/- pterygoid plate + muscles +/- orbital
content
3. Extended maxillectomy
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- indicated in tumour beyond upper jaw
- based on skull base approach involved in craniofacial resection
Steps in maxillectomy
1. Anaesthesia
- LA with moffat’s solution
- Hypotensive anaesthesia
- intranasal intubation/ tracheostomy
2. Incision
- Weber Ferguson + midline palatal incision + sublabial incision
3. 5 osteotomies
- frontal process of maxilla - use fissure burr
- body of zygoma - use of fissure burr
- midline palate - use fissure burr/ giggly saw
- pterygoid plate - this is the only blinded osteotome using curved osteotomy
- infraorbital rim - use fissure burr
Endoscopic DCR
- cannulate inferior canaliculi initially vertical
then horizontal
- hard stop = denting on lacrimal bone -
blockage at NLD
- soft stop = blockage at common/ inferior
canaliculi
- During syringing saline
- flow from inferior canaliculi - block at
inferior canaliculi
- flow from superior canaliculi - block at
common canaliculi
- pass through nose - either normal or hyper
secretions
- saline did not reach nose with hard stop
• block at NLD
• if saline purulent, dacrocystitis
- Technique
- first decongest nose
- infiltrate mucosa at area around axilla of MT
- incision made anterior to superior half of the uncinate process (sickle/ phaco knife)
- elevate mucosa
- identify frontal process of maxillae & lacrimal bone
- Identify Axilla, raise flap
- lacrimal bone removed with rongeur
- frontal process of maxilla removed with Hajek Koeffler punch
- may need to use drill to expose inferior part of lacrimal sac (thick bone
- also expose superior half of lacrimal duct
- cannulate inferior canaliculi with lacrimal probe to tent the wall to facilitate incision of the
sac
- sac marsupirlized using sickle blade
- end results is surgical window at inferior part of lacrimal sac
- silicone stent threaded through upper & lower canaliculi & through lacrimal window into
nasal cavity
- 2 ends of stent tied together or use ligar clip
- Post op stent kept 3-6/12
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- Advantages & limitations
- comparable results with open DCR
- no facial scar
- cannot be used in canaliculi obstruction
- can still preserve pumping action of NLD system
- can correct nasal pathology at same time with DCR
- Complications
- Intraop, early, late
• Bleeding dt branches of AEA ?
• Lacrimal sump - debris accumulate in the inferior part of lacrimal sac
• Canaliculi injury dt probing
• Restenosis
• Dislodged stent
• Keratitis
Endoscopic orbital
decompression
Indications
1. Intraorbital hemorrahge
2. For Grave’s ophthalmoplegia
3. For Subperiosteal abscess
Intraorbital hemorrhage
- loss of red colour discrimination, RAPD
- progressive ptosis, subconjunctival haemorrhage
- proposed globe hard on palpation
- Optic fundus - retinal artery circulation may be intermittent or pulsatile
Management
- Sit patient up
- Remove nasal packing
- Infiltrate lateral cants with LA and perform a lateral canthotomy and cantholysis
- to buy time to allow patient to be taken back to theatre for re-exploration
- need not be done with haemorrhage noticed intra-operatively
Surgical technique for lateral canthotomy of cantholysis
1. LA marcain adrenaline
2. Sharp scissors/ blade, horizontal incision through skin and soft tissue at lateral junction of
eyelids onto bone of the orbital rim
3. Eyelid draw outwards with forceps - tendon attaching inferior tarsal plate to bone exposed
4. Scissors turned vertically and tendon cut
5. Orbital fat should seen
6. If inadequate - cut superior tendon
7. Need not re-stitch, just dressing
8. Can be sutured aft 24 - 48 hours
9. Lateral cantonal tendon sutured to orbital periosteum
Endoscopic orbital decompression

1. Nasal packing
2. Infiltration
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3. Uncinectomy
4. Natural osmium of maxillary sinus identified and enlarged into posterior fontanelle (Blakesley
forceps and microdebrider)
- largest possible antrostomy, prevent prolapse of fat aft decompression obstructing antrostomy
5. Axillary flap - if frontal sinustomy to be done - if frontal sinusitis
6. sphenoehtmoidectomy performed - entire lamina papyracea viewable
7. Hard bone of frontal process of maxilla palpated and soft lacrimal bone identified
8. Junction of lacrimal bone and LP identified
- Lacrimal bone flaked off will reveal the lacrimal sac
9. Blunt end of Freer pushed through the LP → thin bone of LP flaked off
10. preserve orbital periosteum
- Tear with prolapse of orbital fat will obscure remaining LP and make removal difficult
- do not tear LP 1.5cm below frontal osmium - prolapse of fat here will obstruct frontal sinus
drainage
11. In subperiosteal abscess
- use curette with orbital periosteum intact, push the periorbita laterally → curette advances into
subperisoteal abscess → abscess drained
- Penrose drain inserted - left in place - removed aft 2/7
12. In Grave’s disease
- incise in series of horizontal incision/ removed entirely
- retention of medial strip may reduce incidence of post-op diplopia
- further decompression can be achieved by removal of posterior half of the orbital floor up to
infraorbital nerve
Surgical reduction of inferior

turbinates
Anatomy
1. Mucosa
- pseudo stratified columnar ciliated respiratory epithelium which contains goblet cells - produce
mucus layer (containing salts, glycoprotein, polysaccharides, lysozyme)
2. Submucosa
- contains a complex array of
- arteries
- AV anastomosis
- unique muscular veins
- venous sinusoids
3. Histologically
- IT composed of 3 layers
- medial mucosa layer - thicker then lateral due to increase size of lamina propria
- lateral mucosa layer
- central osseous layer
• Lamina propria contains venous sinusoids, lymphocytes, immunocompetent cells and
seromucous glands
4. Sinusoid engorgement
- chemical/ microbial irritants → cause rapid inflammation → activates mast cells, basophils,
other leucocytes → release histamines → swelling of turbinates
- Sympathetic (deep petrosal) and parasympathetic (vidian) venous systems
- Sympathetic
• regulates blood flow to nasal mucosa by regulating resistance vessels
• ↑ resistance - therefore less flow to nasal mucosa, therefore decongestant occur
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• Sympathetic tone to nasal vasculature is partially influenced by partial pressure of CO2
(pCO2) via carotid & aortic chemoreceptors)
- Parasympathetic
• regulates blood volume of nasal mucosa by regulating capacitance vessels
• relaxation of capacitance vessels
- allow congestion, oedema formation
5. Nasal valve
- area of greatly ↑resistance to nasal airflow
- consists of
- external nasal valve
- internal nasal valve
- External nasal valve
- formed by
• caudal edge of lateral crus of lower lateral cartilage
• soft tissue alar
• membranous septum
• sill of nostril
- seen in patients who have undergone rhinoplasty (e.g. pinched alar deformity)
- Internal nasal valve
- formed by
• medially - septum
• laterally - caudal end of upper lateral cartilage
• inferolateral - anterior end of IT
- located approximately 1.3cm from nares
- it is the narrowest segment of nasal airway
- accounts for 50% of total airway resistance
- IT exerts maximal role in airway resistance
Indications
1. relief of nasal obstruction (persistent despite optimal medical treatment)
2. Biopsy to confirm diagnosis of systemic disorder
- sarcoidosis
- ciliary dyskinesia
- Wegener’s granulomatosis
- OR to determine precise histological diagnosis of intranasal lesion
Contraindications
- relative contraindications in patients with bleeding disorders
Operative techniques
Mucosal preserving and non mucosal preserving
Mucosal preserving surgery Non mucosal perceiving
1. SMR 1. Cold steel partial/ total turbinectomy

2. Powered microdebrider 2. Cold steel turbinoplasty
3. Diathermy (electrocautery) 3. Powered microdebrider
4. cryosurgery
5. Radiofrequency ablation
6. Laser
7. Coblation
1. Trimming of inferior turbinates

- total/ radical turbinectomy
- partial turbinectomy
- anterior trimming
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- partial trimming
2. SMR (turbinoplasty)
- submucosal out fractures of IT bone
- with microdebrider
3. Electrocautery
- SMD
- surface diathermy/ mucosal cautery
4. Laser diathermy
- CO2
- YAG 
Argon
- KTP
- can be done under LA with less risk of bleeding, short term effect
5. Cryosurgery
- formation of intracellular ice crystal → denaturation of nuclear and cell membrane proteins →
bv thrombosis → tissue ischaemia → tissue destruction
- under LA with more side effects
- haemorrhage
- delayed mucosa sloughing
- damage external nose
6. Radio frequency ablation
- using unipolar/bipolar probe
- power setting at 10-12 watts
- probe withdrawn slowly at 0.5cm/second to deliver tissue energy of 500 Joules
- immediate results up to 1 year good
7. Steroid injection (intramucosally)
- triamcinolone acetone
- Side effects
- blindness due to accidental injection into vascular structure, can cause vasospasm/
occlusion of optic art supply
8. Coblation assisted
- bipolar configuration
- RF current through conductive solution
- not heat-driven
- molecular dissociation
- minimal thermal penetration
- low frequency - minimal collateral tissue damage, decreased tissue penetration
- control energy delivery
- short current path
- shrinks submucosal tissue, preserves mucosal and glandular architecture
9. Vivian neurectomy
- under GA
- effective in non-allergic/ VMR
Total/ radical turbinectomy

- clamping IT at its base (to achieve haemostasis)
- followed by use of nasal scissors/ turbinate scissors to resect entire turbinate along its base
- definitely widens nasal airway - predisposed to atrophic rhinitis, effective for long term nasal
patency
- ophir et al - 80% of 150 patients subjective reported improve in nasal breathing & 91% had
widely patent nasal airways at average follow up time of 2 1/2 years
- Complications
- haemorrhage
- nasal crusting
- synechiae
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- nasal discomfort
• because of exposed bone at lateral nasal wall - later leads to osteonecrosis
- atrophic rhinitis
- dysosmia/ anosmia - chronic crusting causes damage of olfactory cells
Partial turbinectomy
1. Anterior trimming
- remove anterior end of inferior turbinate
- it is directed at relieving obstruction at nasal valve while leaving a portion to continue its
function of air conditioning
2. Partial trimming
- only medial fleshy part is resected
- complication is similar to total but less severe
SMR (turbinoplasty)
- preserve mucosa of turbinate + maintain mucociliary clearance + maintain air conditioning
function
1. Submucosal out fractures of IT
- incision along inferior border
- medial and lateral submucosa flaps elevated
- anterior 2/3 bone of IT partially resected under flaps
- flap trimmed to redrape remaining bone
- Advantages
- as above immediate relief of symptoms
- Disadvantages
- long term improvement - poor
- symptom of rhinorrhea often persist
- SMR with microdebrider
- submucosal stroma resection
Nasal fracture reduction

Overview
- Most common facial bone fracture (~50% facial bone fractures)
- Males
- 15-30 years
- In fight, MVA, fall
- Anatomy
• Paired
• Fr.
- frontal process of maxilla
- Superiorly, nasal process of frontal bone
- a&b join in midline
- Quadrangular/ septal cartilage support nasal bones fr below
• 80% occur btw thicker proximal and thinner distal segments of nasal bones
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• Lateral impacts more common depression of one nasal bone and lateral
displacement of contralateral nasal bone
Diagnosis
History and Physical examination
1. History
- Trauma
- Epistaxis - resolved
- Ask patient how the external shape of the nose has changed since the fracture
- determine corrective maneuvers to restore patient’s appearance through reduction of the
nasal fracture
2. PE
- swelling over nasal bridge
- Difference in appearance or shape of nose
- Periorbital ecchymosis
- Plain radiographs
- No role in diagnosis or management of nasal fractures in isolated nasal injury
- Nasal bone CT
- Helpful if patient has associated facial fractures
CLASSIFICATION (Hwang)
I: simple without displacement
II: simple with displacement/ without telescoping
IIA - unilateral
IIAs - unilateral with septal #
IIB - bilateral
IIBs - bilateral with septal #
III: comminuted with telescoping/ depression
Indications
1. Simple fracture of the nasal bones/ nasal-septal complex
2. Nasal obstruction or airway compromise fr deviated nasal bones
3. Fracture of the nasal-septal complex with nasal deviation less than one half the width of the
nasal bridge
4. Reduction less than 3 hours aft injury in adults and children (if minimal edema is present)
5. Reduction 6-10 days aft injury in adults (aft oedema has resolved and before the setting of
fracture fragments)
6. Reduction 3-7 aft injury in children (aft oedema has resolved and before the setting of fracture
fragments)
Contraindications
1. Severe comminution of the nasal bones and septum
2. Associated orbital wall or ethmoid bone fractures
3. Nasal pyramid deviation that exceeds one half the width of the nasal bridge
4. Caudal septum fracture dislocation
5. Open septal fractures
6. Fractures examined 3 weeks or longer aft injury has occured.
Anaesthesia
Topical
1. Oxymetazoline + phenylephrine/ lidocaine 1-2% + epinephrine
2. Pack pledgets inside nasal cavity, along septum and on the floor of the nose
3. Remove pledgets aft 10-15 minutes
4. Local anesthetic infiltration
- 1-2% lidocaine + 1:100,000 epinephrine injected bilaterally in the following locations
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- Along and beneath the soft tissue of the nasal dorsum
- target infratrochlear nerves
- Into area of infraorbital foramen
- target infraorbital nerves
- Base of columella + along floor of nasal cavity
Equipment
.
- Good light source
- Frazier suction
- Nasal speculum
- Bayonet forceps
- Pledgets
- Merocel
- Elevators (goldman/boies/salinger/ballenger)
- Walsham forceps (2nd pic-for grasping nasal bones)
- Asch forceps (for septum reduction)
- External splint (thermoplast/aquaplast)
- Intranasal cocaine solution
- Infiltration lidocaine solution with epinephrine
- Needle, 27 gauge or smaller
- Syringe, 3 ml
Positioning
Sitting or recumbent position with head elevated
C-spine precautions take precedence over comfort
Technique
- Nasal pyramid fractures reduced first, followed by nasal septum reduction
- Explain risks, benefits and alternatives to the patient
- Obtain signed informed consent
- Deliver appropriate anaesthesia
- To reduce nasal pyramid
- measure distance fr alar rim to the depressed fragment externally
- Mark position with thumb
- Reduce depressed side of nose first
- Insert Boies or Salinger elevator into the nose under the depressed fragment
- Apply steady outward pressure on the posterior aspect of the nasal bone
- Control outward pressure with counter-pressure exteriorly with the other thumb, mould
fragment into position
- If fail, use Walsham forceps to directly grasp the nasal bone. Insert one blade beneath the
bone as the other blade is opposed on the outer skin surface. Manipulate the bone into
position
- Septal reduction - check whether reduced
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NOSE YXY
- If not, use Asch forceps to elevate the nasal pyramid while applying direct pressure to the
displaced portion of the septum until it is moved back into the proper position
- Check for septal haematoma
- Drain if present
- Stabilize reduction with internal packing
- vaseline gauze or 8cm merocel
- External splint (thermaplast, aquaplast)
- External splints require intense heat for activation and moulding, so nasal dorsal skin should
be protected with steri-strip bandage application prior to placement of the splint
- Remove packing in 5 days and removal nasal splint in 7 days
- Cover with oral antibiotics with adequate staph aureus coverage
- to prevent sinusitis and toxic shock syndrome
- Extra
- Routine radiography not necessary for diagnosis and management of nasal fracture
- Optimal timing
• Within 3 hours of injury with minimal edema - both adults and children
• If oedema significant - delay until edema resolved but before setting of bone fragments
- Adults - 6-10 days aft injury
- Children - 3-7 days aft injury
• Check for septal hematoma before and aft procedure
• Antibiotic prophylaxis necessary for intranasal packing
Complications
1. Inability to reduce
- Open reduction
- delay until 3 months aft injury - to allow complete resolution of swelling and settling of the
nasal and cartilaginous fragments
- Resolution allows more accurate evaluation of the pathology and therefore a better
cosmetic results after intervention such as open septorhinoplasty
2. Septal hematoma
- Bleeding in the subperichondrial plane of the septum lift the perichondrium off the
cartilage and disrupt its blood supply irreversible damage to the underlying nasal
cartilage within 3-4 days saddle nose deformity
- Drain with several small incisions in the mucoperichondrium
- Septal splints or intransal packing to prevent reaccumulation
- hemorrhage
- Pn: direct pressure/ intranasal packing
- KIV coag profile
- Dysesthesia
- Direct infiltration of LA - nerve damage dysesthesias/paraesthesias
- Infection
• Sinusitis
• Toxic shock like infection
• dt placement of intranasal packing
• Pn
- antibiotic prophylaxis
- Preprocedural prophylaxis - coronary valvular disease
163 of 163

The anatomy and physiology of the nose and sinuses

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The anatomy and physiology of the nose and sinuses

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NOSE YXY

Anatomy and physiology ....................................................................... 13

Anatomy and physiology

Anatomy of lateral nasal wall

Bony part formed by

Lateral wall opening

Sphenoethmoidal recess (medial to superior meatus) Sphenoidal sinus

Superior meatus posterior ethmoidal sinus

middle meatus frontal sinus

Inferior meatus NLD

Supraorbital ethmoidal air cell

Haller cell (infraorbital ethmoid cell)

Onodi cells (sphenoethmoidal cell)

Olfactory groove Keros classification

Internal nasal valve

External nasal valve

Endoscopic endonasal PPF/ ITF

Skin Prick Test

Non allergic rhinitis

Obstruction Marked Mild

Rhinorrhea Mild/moderate Severe

Sneezing/ pruritus Minimal Minimal

Hyposmia Usual Rare

Mucosal swelling Marked Mild

Inferior turbinate enlargement Marked Mild

Polyps Common Never

Sinus mucosal thickening Common Rare

Autonomic innervation of nasal mucous membranes

Indications for intranasal decongestants

Contraindications for intranasal decongestants

Pathophysiology of Rhinitis Medicamentosa

Primary atrophic rhinitis (HERNIA)

Secondary atrophic rhinitis

Intrinsic causes Extrinsic causes

AND at least one of the following:

Therefore, to diagnose RS - nasal endoscopy and CT is one of the requirements

Acute bacterial sinusitis diagnosis (CPG)

Rhinosinusitis Task Force Criteria for diagnosis for ARS

Facial pain/ pressure Headache

Facial congestion/ fullness Fever (non-acute)

Post nasal drip/ rhinorrhea Halithosis

Nasal blockage Dental pain

Hyposmia/ Anosmia Fatigue

Purulence on endoscope Cough

Fever (Acute RS only) Ear fullness/ pain

Patients requiring admission are patients

Intrinsic and Extrinsic causes

Stasis of secretions inside sinuses dt

CRS without nasal CRS with nasal polyps

T helper cells Th1 cell-associated disease Th2 cell associated disease

CRS without nasal CRS with nasal polyps

Cytokines IL2, IFN gamma, IL5, IL4, IL13,eosinophils

Subtypes 1. Allergic fungal CRS

Familial Strong genetic component

Etiology ~ Acute sinusitis

1. Antibiotics Yes, ABRS

2. Topical steroids Yes, post viral ABRS

3. Addition of topical corticosteroids to antibiotics Yes, in ABRS

4. Addition of oral corticosteroids to antibiotics Yes, in ABRS

5. Saline irrigation Yes

6. Antihistamines, analgesics, decongestant combo Yes, in viral ARS

7. Oral antihistamine added in allergic patients Yes

8. Paracetamol Yes, in viral and post viral ARS