VIVA NOTES

nd rd
2 – 3 YEAR
APRIL 2019

1
INDEX

TITLE PAGE
A. Basic ENT surgery
1. Functional Endoscopic Sinus Surgery (Nadzirah)……………………….………………………. 4
2. Septoplasty & turbinoplasty (Sui Teng)……………………………………………………………... 20
3. Cortical Mastoidectomy (Nana)…………..…………………………………………………………….. 27
4. Myringoplasty (Lee Lee)…………………………………………….………………………………………. 33
5. Neck dissection (Ikram)……………………………………………………………………………………… 36
6. Parotidectomy & Submandibulectomy (Mark Paul)……………………………………………. 48
7. Tracheostomy (Foong)………………………………………………….……………………………………. 57
8. DL Scopy, Oesophagoscopy, Bronchoscopy (Kai Jun)………………………………………….. 65

B. ENT Emergency
1. Epistaxis (Mark Paul)………………………………………………………………………………………….. 86
2. Stridor (Afidah)………………………………………………………....……………………………............ 90
3. Deep neck space infection (Hamizah)………………………………...………………………………. 107
4. Vertigo (Sui Teng)…………………………………………………....…………………………………………. 125
5. Foreign body (Nabila)…………………………………………………………………………………………. 134
6. SSNHL (Lee Lee)……………………………………………………….….....…………………………………. 136
7. Quinsy (Nasyat)………………………………………………………….………………………………………. 136
8. NOE with BOS OM (Ikram)………………………………………………………………………………….. 145
9. Laryngeal Trauma (Nana)……………………………………………………………………………………. 161

C. Daily ENT Clinic

1. Allergic Rhinitis (Nadzirah)………………………………………………………………………………….. 168
2. ARS & CRS (Nana)……………………………………………………………………………..................... 178
3. Recurrent tonsillitis (Firamir)……………………………………………….................................. 188
4. AOM & COM (Nabila)…………………………………………………………………………………………… 193
5. LPR (Hamizah)……………………………………………………………………………………………………... 205

2
 PART A:
Basic ENT Surgery

3
1.Functional Endoscopic Sinus Surgery (FESS)
Anatomical Basics in FESS
1.1 Nasal Turbinates
- Lateral nasal wall characterized by 3 nasal turbinates and meatus:
 Inferior turbinate (IT) and meatus (IM)
 Middle turbinate (MT) and meatus (MM)
 Superior turbinate (ST) and meatus (SM)

1.2 Paranasal Sinuses

- PNS is an air filled spaces located within bones of skull ant face
- Divided into 2 groups:
1) Anterior group (opens into middle meatus)
a. Maxillary
b. Frontal
c. Anterior ethmoid
2) Posterior group
a. Posterior ethmoid  opens into superior meatus
b. Sphenoid  opens into sphenoethmoidal recess (SER)

1.3 Osteomeatal Complex (OMC)

- OMC is a 3-dimesional space bounded by :
o Lateral : Lamina papyracea
o Medial : Middle turbinate
o Superior: Basal lamella
o Inferior : Maxillary sinus ostium
o Anterior: open
o Posterior: Basal lamella
- Provides a common drainage pathway.
- This space includes:
 Uncinate process (UP)  Bulla ethmoidalis (BE)
 Ethmoid infundibulum  Clefts between UP and MT
 Hiatus semilunaris  Clefts between BE and MT
 Maxillary ostium

4
1.4 Uncinate Process (UP)
- UP is a boomerang shaped, thin crescenteric bone forming the lateral nasal wall.
- Attachments:
 Inferior and posteriorly: Ethmoid process of IT
 Superior attachment of UP:
1. Lamina Papyracea  in this case, frontal recess opens direct into middle
meatus.

2. Skull base  this will cause frontal recess to open into ethmoid infundibulum.

3. Neck of MT  this configuration cause frontal recess to open into ethmoid

infundibulum.

 Laterally: Lamina Papyracea and frontanelle area.

5
1.5 Bulla Ethmoidalis (BE)
- BE is the most prominent and largest anterior ethmoidal air cells.
- Relations :
o Anterior: Uncinate process
o Posterior: Basal lamella
o Superior: Fovea ethmoidalis
o Inferior: Ethmoidal infundibulum
o Medial: Middle turbinate
- Basal lamella represent division between anterior and posterior ethmoid air cells.
- Anterior ethmoid air cells  via ethmoid infundibulum  drain into MM.
- Posterior ethmoid air cells  drain into superior meatus.

1.6 Ethmoid Infundibulum

- Ethmoid infundibulum is a 3D space that accept drainage from the maxillary, frontal, and
anterior ethmoid sinus leading to hiatus semilunaris
- Borders:
o Medial: UP
o Lateral: medial orbital wall (lamina papyracea)
o Superior: frontal recess
o Inferior: maxillary sinus ostium
o Anterior: lacrimal bone
o Posterior: BE

6
1.7 Lateral Sinus
- Lateral sinus is a 3D space and divided into :
1. Suprabullar recess
• Space bounded by BE (inferiorly) and fovea ethmoidalis (superiorly). Anteriorly
there is suprabullar lamella
2. Retrobullar recess
• Space bounded by BE (anteriorly) and basal lamella (posteriorly)

1.8 Hiatus Semilunaris

- Consist of:
1. Hiatus semilunaris superior
o Is a 2D passage way between BE (anterior and inferiorly) and skull base (superiorly)
and basal lamella (posteriorly) leading to a 3-dimensional lumen which is the lateral
sinus.
2. Hiatus semilunaris inferior
o Is a 2D passage way between BE and free edge of UP leading to a 3-dimensional
lumen which is the ethmoid infundibulum.

7
1.9 Maxillary sinus ostium
- Is formed by angle between BE and UP and is located at posterior and inferior.

1.10 Frontal recess

- Is a 3-dimensional cavity defined by:
 Anterior: UP and agger nasi cell
 Posterior: BE and suprabullar lamella
 Lateral: Lamina Papyracea
 Medial: Neck of MT
 Inferior: Ethmoid infundibulum
 Superior: Fovea ethmoidalis, supraorbital cell, anterior ethmoidal artery and frontal
ostium.

8
1.11 Supraorbital Ethmoid Air Cell
- Arises from penumatization of orbital process of frontal bone.

1.12 Anterior Ethmoidal Artery (AEA)

- Orbital branch of ophthalmic artery.
- Located just posterior to supraorbital cell and anterior to suprabullar lamella.

1.13 Agger Nasi Cell

- It is one of the anterior ethmoid air cell located medial to lacrimal sac and fossa, and
anterior to UP.

9
1.14 Frontal cell
- Frontal cell are anterior ethmoid air cells that pneumatize frontal recess above agger
nasi cell.
- According to KUHN CLASSIFICATION, frontal cells can be:
 Type I: Single small cell above agger nasi cell
 Type II: 2 stacked cells (or multiple) above agger nasi cell
 Type III: Single large cell above agger nasi cell extending to frontal sinus
 Type IV: Single small cell inside frontal sinus
- Significance?  A large frontal air cell can compromise nasofrontal pathway.

10
1.15 Middle Turbinate (MT)
- Consist of 3 parts:

MT Location Plane Attachment

First part Anterior Sagittal
Skull base, superiorly between cribriform
plate and lateral lamella
Second part Middle Frontal Lamina papyracea
Third part Posterior Horizontal Perpendicular plate of palatine bone

11
1.16 Basal Lamella
- Basal lamella of MT separates the anterior and posterior ethmoid air cells.
- Boundaries:
 Superior: skull base (fovea ethmoidalis)
 Lateral: Lamina Papyracea
 Inferior: attachment of third part of MT to basal lamella
 Medial: attachment of first part of MT to basal lamella

1.17 Roof of Ethmoi

- Composed of frontal bone superolaterally (termed as Fovea Ethmoidalis) and ethmoid
bone inferomedially (this part is termed as Lateral Lamella).
- Roof of anterior ethmoid has “step-ladder” appearance,
- Whereas roof of posterior ethmoid is flat.

1.18 Lateral lamella

- Is part of cribriform plate and thinnest at the location of anterior ethmoidal artery
passage. (common location for iatrogenic CSF leak)

1.19 Cribriform plate

- Perforated by olfactory nerve fibres.
- Attach to Crista Galli and perpendicular plate of ethmoid medially and neck of MT and
lateral lamella laterally.

1.20 Sphenoethmoidal air cell (Onodi cell)

- Is a hyperpneumatization of posterior ethmoidal air cell that pneumatize posterior,
lateral and superior to sphenoid sinus.
- Presence of Onodi cell displace sphenoid bone in more medial and inferior position
 Increase risk of intracranial penetration, optic nerve and ICA injury.

12
1.21 Infraorbital Ethmoid air cell (Haller cell)
- Is the anterior ethmoidal air cell that pneumatize into maxillary ostium just below the
inferior orbital wall.
- Haller cell cause  persistent maxillary sinus disease.

13
1.22 Posterior Ethmoid air cell
- Larger in size, fewer in number compare to anterior ethmoid air cell
- Relationship:
 Anterior: basal lamella of MT
 Posterior: anterior wall of sphenoid sinus
 Laterally: Lamina Papyracea
 Medically: ST and SM
 Superior: Fovea thmoidalis
 Inferior: 3rd part of MT

1.23 Olfactory Fossa

- Located between crista galli medially, cribriform plate inferiorly, and lateral lamella laterally
- Contain olfactory bulb.
- KEROS CLASSIFICATION (to determine the height of lateral lamella of cribriform plate) :
Type I : depth 1-3mm (26.3% of populations)
Type II : depth 4-7mm (73.3% of populations)
Type III : depth 8-16mm (0.5% of populations) high risk of potential damage to skull base!

1.24 Sphenoid Sinus

- Different types of pneumatisation (Congdon classifications) :
1. Choncal 5% - posterior extend of sphenoid sinus is anterior to sella turcica.
2. Presellar 23% - posterior extend of sphenoid sinus reaches anterior face of sella
turcica.
3. Sellar 67% - extend past level of sella turcica to approach pons posteriorly, allowing
sella to make superior indentation in the sinus.

14
FESS is a procedure to restore and establish ventilation and drainage, with preservation of nasal and
sinus mucosa and mucociliary clearance function.

Indications for FESS:

1. Chronic Rhinosinusitis
2. Recurrent Acute Rhinosinusitis
3. Nasal polyposis
4. Mucocele
5. Allergic fungal sinusitis and mycetoma

Preoperative preparation:
1. History
2. Clinical examination
3. Preop blood ix: FBC/coagulation profile, if more than 40years old, include RBS, CXR, ECG
4. Preoperative imaging: CT paranasal sinuses

Preoperative CT is essential prior to surgery for:

1. To look for normal anatomical landmark
2. To look for anatomical abnormality
3. To plan for surgical approach
4. To look for disease extend
5. To assist with the diagnosis

Preoperative CT evaluation:
1. Cribriform plate – Keros classification
2. Lamina papyracea

15
 3. Onodi cell
4. Sphenoid/ skull base
5. Anterior ethmoidal artery
6. Carotid artery
7. UP attachment
8. MT attachment

Anaesthesia – FESS can be done under LA or GA,

Options for LA :
1. 2% lignocaine (1:80,000) to MT, axilla of MT, IT, UP, septum (if septoplasty required)
2. Greater palatine artery block (via grater palatine foramen)

Intraoperative preparation:
1. Position: Reverse Trendelenburg; or supine with head flexed 15’
2. Throat pack inserted during intubation
3. Lubricate cornea and cover eyes
4. Clean with NS and drape using turban drape  make sure to expose half of medial part of
eyes bilaterally
5. Decongest nasal cavities with:
a. Adrenaline 1:100,000 soak with ribbon gauze/cottonoid/neuropatty and pack at
middle meatus and between IT and nasal septum
b. Moffet’s solution :
2mls 2% NaHCO3 + 2mls 10% cocaine + 1mls of 1:1000 adrenaline = 5mls
OR
4mls 8.4% NaHCO3 + 2mls 10% cocaine + 1mls of 1:1000 adrenaline + 13mls
NaCL = 20mls

*HUKM: Modified Moffet’s: 7-2-1

 7ml NS + 2ml 10% Cocaine + 1ml 1:1000 Adrenaline

c. Oxymetazoline or Co-phenylcaine

6. Inspect nasal cavity using 0’ nasoendoscope.

7. Infiltration of LA – option of LA as mention
8. Performing surgery

Messenklinger’s technique describes 5 lamella to be encounter in FESS surgery:

1. Uncinate process
2. Bulla ethmoidalis
3. Basal lamella of MT
4. Basal lamella of superior turbinate
5. Basal lamella of supreme turbinate

16
Step of FESS (important step from FESS dissection course HUKM)
1. Endoscopic examination of nasal cavity
2. Medialize the MT
3. Locate the maxillary ostium
4. Uncinectomy
5. Middle meatal antrostomy
6. Anterior ethmoidectomy
7. Remove the anteromedial wall of ethmoid sinus
8. Exposure of basal lamella of MT
9. Posterior ethmoidectomy
10. Transethmoid sphenodotomy/sphenoidectomy
11. Frontal sinosotomy

1.1 Uncinectomy
a. Retrograde uncinectomy
a. Identify free posterior edge of UP
b. Insert ball probe through hiatus semilunaris behind free edge of UP (where to insert?
through line transect lower border of BE and line at inferior aspect of UP).
c. Flip posterior free edge of UP anteriorly.
d. Use backbiter forceps and cut the junction between upper and lower limb of UP (2 bites,
why? To prevent injury to nasolacrimal duct and lacrimal sac)
e. Remove upper and lower limb of UP using through cutting instruments.
(To make sure resect all 3 layers; ie mucosa/bone/mucosa)

b. Anterograde uncinectomy
- Identify anterior attachment of UP and lacrimal bone.
- By using Freer elevator or sickle knife, release UP from its anterior attachment.
- Remove UP using through cutting instruments.

17
1.2 Middle Meatal Antrostomy (MMA)
- Identify natural maxillary ostium using curved ball probe
- Widened opening posteriorly and inferiorly using through cutting or backbiting forceps :
 Posterior: till posterior wall of maxillary antrum
 Inferior: inferior turbinate (at back)
 Anterior: lacrimal sac

1.3 Anterior Ethmoidectomy

- Open BE by using straight curette by moving the instruments towards yourself.
- Tissue or polyps is remove using Blakesley forceps by rotating and grasping.
Ccontinue till exposure of basal lamella.

1.4 Penetration of basal lamella

- Basal lamella is penetrated by using a straight curette at junction between a line drawn at
superior aspect of maxillary sinus that crosses the first part of MT. This junction is in line
with sphenoid ostium.
- Enlarge the opening using straight curette or Kerrison punch laterally towards lamina
papyracea.
- Then remove medial aspect of basal lamella using Kerrison punch until free edge of superior
turbinate, sphenoid ostium and posterior ethmoid air cells are visible

1.5 Posterior Ethmoidectomy

- Remove posterior ethmoid air cells using curette and Kerrison punch till sphenoid face and
skull base.
- Posterior limit of posterior ethmoidectomy is sphenoid face (at the level of sphenoid
ostium).

1.6 Frontal Sinusotomy

- to visualize frontal recess area, it is necessary to remove Agger nasi cell
- look for frontal recess using frontal sinus probe
- frontal recess is enlarge using frontal curette
- important landmark: Anterior Ethmoidal Artery, AEA (located posterior to frontal recess)
- once AEA identified, and frontal sinus has been entered, it is safe to
- remove remaining air cells anterior to that.

1.7 Sphenodotomy/ Sphenoidectomy

- sphenoid sinus can be open safely 10mm above the choana just lateral to midline septum at
rostrum of sphenoid
- identification of sphenoid ostium:
 Medial approach: via sphenoethmoidal recess, 10mm above the choana just lateral
to midline septum at rostrum of sphenoid
 Lateral approach: junction between line drawn at superior aspect of maxillary sinus
crossing first part of MT
- after identification of sphenoid ostium, opening is made using straight Blakesley forceps or
powered instruments like using diamond burr drill

18
Complications of FESS:
A. Local complication
- Bleeding
- Infection
- Nasal synechia/adhesion
- Hyposmia
B. Intracranial complication
- CSF leak
- Meningitis
C. Intraorbital complication
- Double vision/diplopia (due to injury to recti muscle)
- Reduce vision (due to retrobulbar hematoma)
- Proptosis
- Epiphora (due to injury to lacrimal duct)
- Periorbital hematoma/echymosis

Post-operative management
1. Pulse, BP monitoring
2. Regular analgesia
3. Observe for epistaxis, headache, orbital swelling, diplopia, reduce vision, CSF rhinorrhea
4. Removal of nasal pack – after 48 -72hour
5. Prophylactic Abx – not routinely prescribe (prescribe is patient has nasal pack)
6. Nasal douching after nasal pack removed – for 6/52
7. Nasal decongestion after nasal pack removed for 5/7
8. Intranasal steroid given for nasal polyposis
9. TCA patient in 7 - 10days, then 2 weekly till well healed
10. On each visit, nasal toilette should be done endoscopically

Post op advice
1. Avoid straining, heavy lifting, nasal blowing for 1-2weeks
2. Blood stained discharge is normal for first few days but profuse bleeding need urgent
attention
3. Nasal saline irrigation/douching as instructed by doctor to help cleanse nose
4. To consult doctor if there is high fever, constant clear watery nasal discharge, altered
vision/swollen eyes, severe headache/neck stiffness and profuse nose bleed.

19
2. Septoplasty
4 parts of nasal septum
1) Columellar septum
2) Membranous septum
3) Cartilaginous septum (quadrilateral cartilage): anterior 1/3
4) Bony septum (perpendicular plate of ethmoid, vomer): posterior 2/3

- Contribution from:
 sphenoidal crest and rostrum (posterior)
 nasal spine of the frontal bone(superior)
 Crest on maxillary and palatine crest (inferior)

20
 Septoplasty : reposition of the misplaced septum by freeing the quadrilateral cartilage from its
inferior and posterior attachement(anterior septum is hinging from the dorsum only-swinging
door technique)

Submucous resection of septum (SMR) : to remove the misplaced quadrilateral cartilage ,

except for a 1cm dorsal strut and 1 cm columella strut (to prevent columella retraction and
saddling).

Indications:
1) Symptomatic DNS
o functional nasal obstruction (especially id DNS is at the internal nasal valve area)
o recurrent epistaxis from septal spur
o Sluder’s neuralgia

2) Complications from DNS

o obstruction to the OMC/ impaired ventilation of PNS and middle ear cavity causing recurrent
otitis media/sinusitis.

3) Part of the cosmetic/reconstructive procedure

o Septorhinoplasty: to correct an external deviation of the nose especially the cartilaginous
dorsum.
o Repair of septal perforation.

4) Donor procedure to obtain cartilage

o augmentation of Saddle deformity

5) Preliminary step in skull base surgery

o Endoscopic transphenoidal surgery (TSS) for pituitary tumour (base of skull tumour)
o Vidian neurectomy

Surgical Procedures
Preparation:
1. Hypotensive anaesthetic is preferred, intubated with throat pack (tube anchored at the left
angle of the mouth)
2. Vibrissectomy: optional, depends on surgeon preference
3. Nasal mucosa is anaesthestized with a topical vasoconstricting solution.
Eg: Moffat’s solution (applied on ribbon gauze/sprayed into nasal cavity).
4. Elevate head 30 degrees up and slightly rotate towards surgeon side
5. Face cleaned, turban drape applied.
6. Nasal septal mucosa infiltrated with local anaesthetic agent (mucosal blanching -successful
infiltration).
- Why? to reduce bleeding and for raising mucoperichondrium flap with hydro-
dissection technique.

21
 Flap elevation:
2 types of incisions:
KILLIAN INCISION HEMITRANSFIXION INCISION (FREER’S INCISION)
 Mucosal incision, 1.5cm behind caudal  J-shaped vestibular incision at the
cartilage mucocutaneous junction starts from superior
extending to the floor of nasal cavity.
Advantage:
Relatively easy to get into correct plane (no  Superior incision must be away from the
fibrous tissue). external nasal valve(injury to ENV will cause
fibrosis and stenosisimpair the airflow into
Easier to raise an intact mucoperichondrial nasal cavity.
flap over the underlying cartilage with Freer
elevator Advantage :
- relatively avascular (compared to mucosal
incision)
Disadvantage: - provide easy access to whole septum
More posteriorly placed incision (behind the including anterior septal border
free edge of septum). - suitable for columellar dislocation/ anterior
nasal spine problem
Not suitable for addressing columellar - can combine with rhinoplasty incision
dislocation/ anterior nasal spine problem
Disadvantage :
Difficult to enter a plane of dissection
(mucoperichondrium is tightly bound to
underlying cartilage with dense fibrous tissue)

- Once correct avascular plane is reached, mucoperichondrium flap and mucoperiosteal flap easily
stripped off from the underlying bluish-white septal cartilage
- Depends on septal deformity, unilateral/ bilateral mucoperichondrial flap is raised,but bilateral
mucoperiosteal flap elevation is always performed.
- Difficult flap elevation at:
 Septovomerine, septoethmoidal junction required sharp dissection
 Previous fracture site
 Sharp septal spurto create inferior tunnel on the floor of the nasal cavity, which is
connected with the mucoperichondrial flap above.

Superior/ Anterior tunnel: Inferior tunnel:

Ant: mucocutaneous junction Ant: mucocutaneous junction
Inf: border of maxillary crest Inf: floor of nasal cavity
Sup: 1cm from base of skull Sup: upper border of maxillary crest
Post: rostrum Post: rostrum

22
Cartilage/bone/spur resection:
 Any tissue to be resected must be clearly visible and free from its overlying
mucoperichondrium and mucoperiosteum.

Septoplasty resection Submucous resection of septum

• After full exposure, blade is used to remove a  After full exposure
wedge shaped piece of cartilage inferiorly.  Quadrilateral cartilage is resected
• Posterior chondrotomy is performed. preserving:
• Cartilage and bone are removed posteriorly.  1cm columellar strut (for anterior nasal
• Once the quadrilateral cartilage has been spine) and
freed from its posterior and inferior  1cm dorsal strut.
attachment, it can be positioned in the
required position

 Additional resection of deviated posterior bony septum and prominent spurs may be
required if it is deemed symptomatic.

23
  If present of columella dislocation  create columella pocket in medial crura to reposition
septum into the pocket before closure.
 Is tearing of mucoperichondrium serious?
Unilateral: will not cause septal perforation, in fact it fascilitates drainage of blood to
prevent septal hematoma.
Bilateral: high risk of septal perforation.

Closure and packing:

 Hemitransfixion incision is closed with Vicryl.
 Killian incision - some surgeons may elect not to close
 Remaining flaps are approximated together with Quilting suture
o Can used Vicryl straight needle
To eliminate dead space, preventing hematoma/post op bleeding
 Silastic sheath is inserted to prevent synechae
 If there is tearing of mucoperichondrium flap in contact with turbinoplasty wound (keep
Silastic for 1-2 weeks).
 Nasal packing is indicated if there is excessive bleeding following closure.

Complications:
Early complications:
 Injury/infection to the septum:
- bleeding
- septal hematoma, septal perforation
- septal abscess
- persistent deviation

 Aggressive manipulation of the septum:

- skull base fracture CSF leak
- injury to the olfactory bulb Anosmia
- excessive chiseling of maxillary crest  Oronasal fistula
Late complication:
 Cosmetic defect: Saddle deformity or Columellar retraction

Septoplasty Vs Submucous resection of septum

Septoplasty SMR
Types of procedure More conservative More radical
Suitable age Paediatric Adult
Ideal for Anterior deviation Posterior deviation
Incision Freer’s incision Killian’s incision
Mucoperichondirum flap One side Both sides
Risk of tearing Low Low
Risk of septal perforation and Low Low
hematoma
Cosmetic deformity Uncommon Common
Rhinoplasty Can combine with rhinoplasty Cannot combine with
by extending the incision rhinoplasty

24
2.Inferior Turbinate Surgery

Indications:
1) Relief nasal obstruction (if persistent despite optimum medical tx)
2) Diagnostic procedure to confirm systemic disorder.
(Eg: Sarcoidosis, Wegener’s granulomatosis, Ciliary dyskinesia)
3) Part of other surgical procedure (Eg: Inf turbinectomy is part of Medial
Maxillectomy)

Non-mucosal preserving Mucosal preserving

 Turbinectomy  Turbinoplasty
 Trimming of inferior turbinate
- Preserve IT mucosa
- IT is fractured with hill’s elevator - Incision made over the inferior
- Pedicle of the turbinate is then crushed with border, medial and lateral
a straight clip for 1 minute, clip removed and submucosal flap elevated.
the crushed pedicle is cut with turbinectomy - Anterior 2/3 of the exposed
scissors. inferior concha bone resected
- Bleeding stump is cauterized. - Previous elevated flap folded
back to the remaining bone.
Advantage:
Widen nasal airway. Advantages:
Effective for long term nasal patency. Maintain mucocilliary clearance and air
conditioning function of IT
Potential complications: Less complication like:
1. Hemorrhage from the posterior stump. - bleeding, crusting, synechiae,
2. Exposed bone at lateral wall with Empty nose syndrome.
development of osteonecrosis:
nasal crusting, Disadvantages:
synechiae 1. Poor long term nasal patency
nasal discomfort 2. Persistent rhinorrhea (becoz
mucosa is preserved)
3. Dysomnia/anosmia (chronic crusting can
damage the olfactory cells)

4. Empty nose syndrome*

 Submucous diathermy  Radiofrequency Turbinate

- Anterior end of the IT is pierced with Volume Reduction(RFTVR)
monopolar diathermy needle  which is - RF  creates thermal lesion 
passed under the mucosal surface to the that induces fibrosis in erectile
posterior part of the IT. submucosa of the IT without
damaging the overlying mucosa.
- Mucosa is electrocauterized as the needle is - Preservation of the IT mucosa 
withdrawn. cause less crusting and less
postoperative bleeding.
- Maximum of 3 passess per turbinate, risk of
osteonecrosis.

25
*Empty nose syndrome:
 Secondary atrophic rhinitis post inferior turbinectomy resection
 Feelings of nasal obstruction, nasal dryness and crusting, and a sensation of being unable to
breathe.
 No sign of physical obstruction, the mucosa will be dry and pale, and may be signs of
secondary infection
 Causes: changes to the nasal mucous membrane and to the nerve endings in the mucosa
resulting from chronic changes to the temperature and humidity of the air flowing inside the
nose post turbinectomy.

26
3.Mastoidectomy

Mastoidectomy: Complete exenteration excessible mastoid air cells converting them into a single
cavity

Cortical mastoidectomy: mastoidectomy + preserving the posterior EAC wall

Atticotomy: Opening of the attic through transmeatal

Atticoantrostomy: Atticotomy + canal wall down to clean antrum (remove attic and aditus)

CAT: Cortical mastoidectomy + posterior tympanotomy (Intent to inspect & ventilate the ME)

Canal Wall Up (CWU) Canal Wall Down (CWD)

CAT MRM
Cortical mastoidectomy Radical mastoidectomy
Atticotomy Atticoantrostomy
Advantage: Advantage:
Rapid healing time No need second surgery
Easier long term care Recurrence low
Easier to fit hearing aid Residual disease easily detected
No water precaution

Disadvantage: Disadvantage
High recurrent rate Open cavity with lifetime maintenance
Possible need for second surgery due to Difficult to fit hearing aid
recurrence or disease not fully removed Long healing time
Residual disease difficult to detect Need water precaution
Long term follow up
Aesthetic concern dt enlarged meatus

Indications
To create a safe and dry ear
- Cholesteatoma
- Mastoid abscess
- Route for CI surgery
- Route for lateral skull base surgery
- AOM with complication
- Facial nerve decompression/repair

Contraindications
- Patient not fit for GA
- Patient with anticoagulants
- Patient in full blown sepsis
- No available facilities

In what patients do we perform transmeatal approach?

- Disease limited to the attic
- Sclerotic mastoid

27
What are the cause of persistent ear discharge post MRM?
Patient Disease
Default follow up High facial ridge
Uncontrolled comorbidities Inadequate meatoplasty
(DM) Large mastoid cavity
Patient with ET dysfunction Hidden areas for residual disease:
sinodural angle, facial recess, mastoid tip, sinus tympani,
peritubal, zygomatic, retrofacial, anterior and posterior
epitympanum
Infection
Petrositis
Cholesteatoma

Petrositis (inflammation of apical portion petrous part of temporal bone):

What is Gradenigo Triad?
Ear discharge
Diplopia (6th nerve palsy)
Retroorbital pain (5th nerve involvement)

Complications
Intraoperative Postoperative
Bleeding from sigmoid Conductive hearing loss: loss of bridging
sinus/emissary veins/ skin/ bone/ SNHL: labyrinth injury
jugular bulb Facial nerve palsy
Dura tear  CSF leak Vertigo
Facial nerve injury Meningitis
Labyrinthine fistula: vertigo Abscess
Toxic labyrinthitis (sterile Lateral sinus thrombosis
inflammation of inner ear) Temporal lobe abscess
Dislocation of ossicles Residual
Recurrence

What are the types of flap in MRM?

Causes of VERTIGO post mastoidectomy:

- Bone dust
- Labyrinthine toxicity
- Vibration
- Labyrinthine fistula

How do we prevent injury to the facial nerve?

1. Identify the structures related to FN (LSCC, SPI)
2. Use a diamond burr when nearing the area of the facial nerve
3. Irrigate generously to prevent heat transfer that may cause thermal injury to the nerve
4. Drill longitudinally in the direction of the FN to avoid transecting it
5. Use facial nerve monitor

28
Cortical Mastoidectomy

Complete exenteration of all the accessible mastoid air cells, converting them into a single cavity and
keeping the posterior meatal wall intact

Indications:
 Coalescent mastoiditis and masked mastoiditis
 AOM or acute on chronic OM refractory to antibiotics
 Initial stage of any transmastoid surgery
o Endolymphatic sac surgery
o Facial nerve decompression
o Vestibulocochlear nerve section
o Translabyrinthine approach for CP angle tumor
o CI surgery
o CAT

Limit of mastoid bowl:

- Superiorly: Superior temporal line/zygomatic root
- Anterior: post wall of EAC
- Posterior: Sigmoid sinus
- Inferior: Tangential line from tip of mastoid

29
Structures identified and relation to the facial nerve
1. LSCC: inferior to it
2. Short process of incus: pointes to second genu (medially)
3. Processus cochleariformis (anterior limit of the facial nerve): 1st genu is
posterosuperiormedially to it

30
Posterior tympanotomy:
1. Borders
 Anterolateral: chorda tympani
 Posteromedial: Facial nerve
 Superior: fossa incudes

2. Structures seen:
 Stapedial tendon
 Promontory
 Round window
 Round window niche
 Incudostapedial joint

3. Indications:
 Gain access to mesotympanum
 CI
 Part of CAT
 Cholesteatoma in mastoid bowl and mesotympanym

*In CI cases, how do we insert the electrode?

 Round window approach
 Cochleostomy approach: drill the cochlear at the anteroinferior aspect.
Both approaches enter the scala tympani.

31
32
 4.MYRINGOPLASTY
(Reference: Dhingra)

D(x): Closure of the perforation of Pars Tensa of the TM.

Advantages:
1. Restore hearing and in some cases tinnitus
2. Prevent repeated infection from EAC and ET
3. Prevent aeroallergens reaching the exposed middle ear mucosa, leading to persistent ear
discharge

Different from Tympanoplasty type 1 – repair TM with exposure of the middle ear to inspect the
middle ear and ossicular integrity.
 Myringoplasty + Ossicular reconstruction = Tympanoplasty

Contraindications
1. Acute discharge from middle ear
2. Nasal allergy which should be brought under control prior to surgery
3. Otitis externa
4. Ingrowth of squamous epithelium into the middle ear
5. When the other ear is dead or not suitable for HA rehab
6. Children below 3 yo

Anaesthesia: LA or GA

Position: Supine with face turned to one side; the ear to be operated is up.
Graft materials
1. Temporalis fascia (the commonest)
2. Areolar fascia overlying the temporalis fascia
3. Perichondrium from the tragus
4. Cartilage
5. Vein
6. Periosteum

Incision
1. Endomeatal
2. Endaural
3. Postaural

Technique
-Underlay or Overlay Technique
Underlay Overlay
1. Harvesting graft 1. Harvesting graft

2. Preparing the TM for grafting. 2. Preparing the TM for grafting.

-Incision is made along the edge of -Incision is made along the edge of
the perforation and the ring of the the perforation and the ring of the
epithelium is removed. epithelium is removed.

-Remove a strip of mucosal layer from -Remove a strip of mucosal layer

the inner side of perforation. from the inner side of perforation.

3. Inspecting the middle ear 3. Inspecting the middle ear

33
 - A stapes-type of incision is made and -A stapes-type of incision is made
the tympanomeatal flap is raised (LA and the tympanomeatal flap is raised(LA
given prior to this) to see the integrity given prior to this) to see the integrity and
and mobility of the ossicular chain, mobility of the ossicular chain,

- To ensure no squamous epithelium -To ensure no squamous epithelium has

has grown into the middle ear. grown into the middle ear.

4. Placing the graft 4. Placing the graft

-Middle ear is packed with gelfoam -Graft placed on the outer surface of
soaked with antibiotic. TM.(Over the anterior annulus)

- A proper sized graft is placed so that -A slit is made in the graft to tuck it under the
its edges extend under the margins of handle of malleus.
perforation all round (under the
anterior annulus)and also extends -Meatal skin removed earlier is now replaced,
over the posterior canal wall. covering the periphery of the graft.

-Tympanomeatal flap is replaced. -Ear canal packed with gelfoam and then
with a small antibiotic pack.
5. Closure of endomeatal/ endaural/ 5. Closure of endomeatal/ endaural/
postaural incision. postaural incision
6. Mastoid bandage. 6.Mastoid bandage
Advantage : Squamous epithelium is not Modification of the overlay technique is to
buried in the middle ear. place the anterior edge of the fascia graft
under the annulus after removing the
epithelium from its undersurface. This
prevents blunting of the anterior canal which
is seen as a complication of the overlay
technique.

Postop Care
1. Ear pack is removed after a week without disturbing the gelfoam.
2. Patient is seen at 2 to 6 weeks after the operation.
3. Complete epitheliazation of the graft takes 6-8 weeks

Complication
Underlay Overlay
Middle ear becomes narrow. Blunting of the anterior sulcus
Graft may get adherent to the promontory Epithelial pearls- There are epidermal cyst
when squamour epitherlium is buried under
the graft.
Anteriorly, graft may lose contact from the Lateralization of graft- Graft loose contact from
remnant of TM leading to anterior perforation the malleus handle resulting in conductive
hearing loss.
-It is prevented by tucking the graft under the
handle

34
Other procedures for closure of TM perforation:
1. Splintage
2. Cautery patching
3. Fat-graft Myringoplasty

35
5.NECK DISSECTION

Surgical Anatomy
Fascial layers of the neck
1. Superficial cervical fascia: platysma
2. Deep cervical fascia:
a. Superficial (investing)l layer: SCM, trapezius
b. Pretracheal:
i. Visceral: Thyroid, Trachea, Oesophagus
ii. Muscular: Strap muscles
c. Prevertebral fascia: Vertebral muscles, Phrenic nerve
d. Carotid sheath: ant from b. / post from c.

Platysma
• Origin – fascia overlying the pectoralis major and deltoid muscle
• Insertion:
1. depression muscles of the corner of the mouth
2. mandible
3. SMAS layer of the face
• Function:
1. wrinkles the neck
2. depresses the corner of the mouth
3. increases the diameter of the neck
4. assists in venous return

Surgical considerations:
i) Increases blood supply to skin flaps
ii) Absent in the midline of the neck
iii) Fibers run in an opposite direction to the SCM

SCM
• Origin: i) medial third of the clavicle (clavicular head)
ii) manubrium (sternal head)
• Insertion – mastoid process
• Nerve supply – spinal accessory nerve (CN XI)
• Blood supply:
i. occipital a. or direct from ECA
ii. superior thyroid a.
iii. transverse cervical a.

Omohyoid muscle
 Origin – upper border of the scapula
 Insertion: i) via the intermediate tendon onto the clavicle and first rib
ii) hyoid bone lateral to the sternohyoid muscle
 Blood supply – Inferior thyroid a.
 Functions: i) depress the hyoid
ii) tense the deep cervical fascia

36
 Surgical considerations:
• Absent in 10% of individuals
• Landmark demarcating level III from IV
• Inferior belly lies superficial to:
– The brachial plexus
– Phrenic nerve
– Transverse cervical vessels
• Superior belly lies superficial to IJV
 Landmark demarcating level III from IV
• Inferior belly – superficial to:
– Brachial plexus
– Phrenic nerve
– Transverse cervical vessels
• Superior belly lies superficial to IJV

Trapezius muscle
• Origin:
1) medial 1/3 of the sup. Nuchal line
2) external occipital protuberance
3) ligamentum nuchae
4) spinous process of C7 and T1-T12
• Insertion:
1) lateral 1/3 of the clavicle
2) acromion process
3) spine of the scapula
• Function – elevate and rotate the scapula and stabilize the shoulder

Surgical considerations
– Posterior limit of Level V neck dissection
– Denervation results in shoulder drop and winged scapula

Digastric muscle
• Origin – digastric fossa of the mandible (at the symphyseal border
• Insertion:
1) hyoid bone via the intermediate tendon
2) mastoid process

• Function:
1) elevate the hyoid bone
2) depress the mandible (assists lateral pterygoid)

Surgical considerations – “Residents friend”

- Posterior belly is superficial to: ECA, Hypoglossal nerve, ICA, IJV
- Anterior belly: landmark for identification of mylohyoid for dissection of the submandibular
triangle

37
Marginal Mandibular Nerve
• Should be preserved in neck dissections
• Most commonly injured in dissection level IB
• Can be found:
– 1cm anterior and inferior to angle of mandible
– At the mandibular notch
• Subplatysma
• Deep to fascia of the submandibular gland (superficial layer of deep cervical fascia)
• Superficial to adventitia of the facial vein
• More than one branch often present
• Travels with sensory branches that are sacrificed

Spinal Accessory Nerve

• Originates in the spinal nucleus – may extend to the fifth cervical segment
• Union of motor neurons
• Passes through two foramen
– Foramen Magnum: enters the skull posterior to the vertebral artery
– Jugular Foramen: exits the skull with CN IX, X and the IJV
• Crosses the IJV
• Crosses lateral to the transverse process of the atlas
• Occipital artery crosses the nerve
• Descends obliquely in level II (forms Level IIa and IIb ).
• Penetrates the deep surface of the SCM
• Exits posterior surface of SCM deep to Erb’s point
• Traverses the posterior triangle ensheathed by the superficial cervical fascia and lies on the
Levator scapulae
• Enters the trapezius approx. 5 cm above the clavicle

38
Pic: CN XI relationship with IJV

Phrenic Nerve
• Sole nerve supply to the diaphragm
• Supplied by nerve roots C3-5
• Runs obliquely toward midline on the anterior surface of anterior scalene
• Deep to prevertebral fascia
• Posterolateral to carotid sheath

Hypoglossal nerve
• Motor nerve to the tongue
• Cell bodies are in the Hypoglossal nucleus of the Medulla oblongata
• Exits the skull via the hypoglossal canal
• Lies deep to the IJV, ICA, CN IX, X, and XI
• Curves 90 degrees and passes between the IJV and ICA
• Surrounded by venous plexus (ranine veins)
• Extends upward along hyoglossus muscle and into the genioglossus to the tip of the tongue
 Lateral to hyoglossus
 Deep to mylohyoid

39
Thoracic Duct
 Conveys lymph from the entire body back to the blood
 Exceptions: Right side of head and neck, right upper oesophagus, right lung, right heart and
portion of the liver
 Begins at the cisterna chyle
• Enters posterior mediastinum between the azygous vein and thoracic aorta
• Courses to the left into the neck anterior to the vertebral artery and vein
• Enters the junction of the left subclavian vein and the IJV

40
Common Nodal Drainage Patterns

Level 1
o Submental triangle (Ia) – Anterior digastric – Hyoid – Mylohyoid
o Submandibular triangle (Ib) – Anterior and posterior digastric – Mandible.
o Marginal Mandibular: Most commonly injury dissection level Ib

Level II
• Upper Jugular Nodes
o Anterior Lateral border of sternohyoid, posterior digastric and stylohyoid
o Posterior Posterior border of SCM
o Skullbase
o Hyoid bone (clinicallandmark)
o Carotid bifurcation (surgical landmark)
• Level IIa anterior to XI
• Level IIb posterior to XI – Submuscular recess – Oropharynx > oral cavity and laryngeal mets

Level III
Middle jugular nodes
• Anterior: Lateral border of sternohyoid
• Posterior: Posterior border of SCM
• Inferior border of level II
• Cricoid cartilage lower border (clinical landmark)
• Omohyoid muscle (surgical landmark)
• Junction with IJV

41
Level IV
Lower jugular nodes
• Anterior: Lateral border of sternohyoid
• Posterior: Posterior border of SCM
• Cricoid cartilage lower border (clinical landmark)
• Omohyoid muscle (surgical landmark) - Junction with IJV
• Clavicle

Level V
Posterior triangle of neck
• Posterior border of SCM
• Clavicle
• Anterior border of trapezius
• Subdivided by level Va and Vb
• Separated by a horizontal plane defined by the lower border of the cricoid cartilage.
• Va  Spinal Accessory nodes
• Vb Transverse cervical artery nodes
• Supraclavicular nodes

Level VI
Anterior compartment
• Hyoid
• Suprasternal notch
• Medial border of carotid sheath
• Perithyroidal lymph nodes
• Paratracheal lymph nodes
• Precricoid (Delphian) lymph node

Subgroups
• Ia Submental
• Ib Submandibular
• IIa Upper jugular (Anterior to XI)
• IIb Upper jugular (Posterior to XI)
• III Middle jugular
• IV Lower jugular
• Va Posterior triangle (XI)
• Vb Posterior triangle (Transverse cervical)
• VI Central compartment

42
43
Staging
• Nx: Regional lymph nodes cannot be assessed.
• N0: No regional lymph node metastases.
• N1: Single ipsilateral lymph node, < 3 cm.
• N2a: Single ipsilateral lymph node 3 to 6 cm.
• N2b: Multiple ipsilateral lymph nodes < 6 cm.
• N2c: Bilateral or contralateral nodes < 6cm.
• N3: Metastases > 6 cm

Nasopharyngeal Carcinoma
– N1: Unilateral < 6cm
– N2: Bilateral < 6 cm
– N3a: >6cm
– N3b: Extension to supraclavicular fossa

Thyroid
– N1: Regional node mets
– N1a: Ipsilateral
– N1b: Bilateral, midline, contralateral cervical or mediastinal LN

Neck Dissection Classification

 Radical:
o Removal of all lymph nodes in Levels I-V including spinal accessory nerve (SAN),
SCM, and IJV
 Modified radical:
o Removal of all lymph nodes in Levels I-V with Preservation of non-lymphatic
structures
 Selective:
o Preservation of lymph node groups
 Extended
o Removal of all lymph nodes in Levels I-V with Removal of additional lymph node
groups or non-lymphatic structures

Radical Neck Dissection

• Removes
– Nodal groups I-V
– SCM, IJV, XI
– Submandibular gland, tail of parotid
• Indications:
o Extensive cervical involvement or matted lymph nodes with gross extracapsular spread
and invasion into the SAN, IJV, or SCM
o N3

44
Modified Radical Neck Dissection
• Removes: Nodal groups I-V
• Preserves: SCM, IJV, CN XI (any combination)
• Note according to which structures are preserved
o Type I: Preservation of SAN
o Type II: Preservation of SAN and IJV
o Type III: Preservation of SAN, IJV, and SCM (“Functional neck dissection”)
• Indication:
o Clinically obvious lymph node metastases
o SAN not involved by tumor
o Intraoperative decision
• Rationale: RND vs MRND Type I:
– Actuarial 5-year survival and neck failure rates for RND (63% and 12%) not statistically
different compared to MRND I (71% and 12%) (Andersen)
– No difference in pattern of neck failure

Indications for type II MRND

• Rarely planned
• Intraoperative tumor found adherent to the SCM, but not IJV and SAN

Indications for Type III MRND

• For N 0 neck (option: selective neck dissection ).
• Popular in Europe

Modified Radical Neck Dissection Rationale

• Reduce postsurgical shoulder pain and shoulder dysfunction
• Improve cosmetic outcome
• Reduce likelihood of bilateral IJV resection

Selective Neck Dissection

• Remove high risk lymph node groups based on tumor site.
• Supraomohyoid: Levels I-III
• Lateral: Levels II-IV
• Posterolateral: Levels II-V – Postauricular nodes – Suboccipital nodes
• Anterior: Level VI – RLN injury – Hyperparathyroidism
• Also known as an elective neck dissection
• Rate of occult metastasis in clinically negative neck 20-30%
• Indication: primary lesion with 20% or greater risk of occult metastasis

45
SND: Supraomohyoid type
• Definition: En bloc removal of cervical lymph node groups I - III
• Posterior limit is the cervical plexus and posterior border of the SCM
• Inferior limit is the omohyoid muscle overlying the IJV
• Indications:
 Oral cavity carcinoma with N0 neck
 Medina recommends SOHND with T2 - T4N0 or TxN1
(palpable node is <3cm, mobile, and in levels I or II)

Bilateral SOHND
• Anterior tongue
• Oral tongue and FOM that approach the midline

SOHND + parotidectomy
• Cutaneous SCC of the cheek
• Melanoma (Stage I: 1.5 to 3.99mm) of the cheek
• Byers does not advocate elective neck dissection for buccal carcinoma
• Adjuvant XRT given to patients with > 2- 4 positive nodes +/- ECS.

Lateral Neck dissection

• Definition: En bloc removal of the jugular lymph nodes including Levels II-IV
• Indications:
N0 neck in carcinomas of the oropharynx, hypopharynx, supraglottis, and larynx

SND: Posterolateral Type

• Definition:
En bloc excision of lymph bearing tissues in Levels II - V
and additional node groups: suboccipital and postauricular.
• Indications:
1. Cutaneous malignancies
2. Melanoma
3. Squamous cell carcinoma
4. Merkel cell carcinoma
5. Soft tissue sarcomas of the scalp and neck

46
SND: Anterior Compartment
• Definition: En bloc removal of lymph structures in Level VI
o Perithyroidal nodes
o Pretracheal nodes
o Precricoid nodes (Delphian)
o Paratracheal nodes along recurrent nerves
• Limits of the dissection are the hyoid bone, suprasternal notch and carotid sheaths
• Indications:
Selected cases of thyroid carcinoma
Parathyroid carcinoma
Subglottic carcinoma
Laryngeal carcinoma with subglottic extension
CA of the cervical esophagus

Extended Neck Dissection

• Definition: Removal of any structures that are routinely preserved in a neck dissection.
• Notated by naming the structure(s) removed.
• Indications:
 Carotid artery invasion
 Other examples:
a. Resection of the hypoglossal nerve resection or digastric muscle
b. Dissection of mediastinal nodes and central compartment for subglottic involvement
c. Removal of retropharyngeal LN for tumors originating in the pharyngeal walls.

47
6.PAROTIDECTOMY
Surgical Anatomy
 Parotid glands are situated anteriorly and inferiorly to the ear.
 Overlie the vertical mandibular rami and masseter, behind which they extend into the
retromandibular sulci.
 Superiorly from the zygomatic arches
 Inferiorly to below the angles of the mandible where they overlie the posterior bellies of the
digastric and SCM.
 Parotid duct exits the gland anteriorly, crosses masseter muscle, curves medially around its
anterior margin, pierces buccinato and enters the mouth opposite the 2 nd upper molar.

Superficial Muscular Aponeurotic System (SMAS) and Parotid Fascia:

 SMAS is a fibrous network that invests the facial muscles, and connects them with the
dermis.
 Continuous with platysma inferiorly; superiorly attaches to zygomatic arch.
 In the lower face, facial nerve courses deep to SMAS and platysma.
 Parotid glands are contained within two layers of parotid fascia, which extend from the
zygoma above and continue as cervical fascia below.

Structures that traverse, or are found within the parotid gland:

 Facial nerve and branches.
 ECA inside the gland  dividing into the IMax and the superficial temporal artery (STA).
 Maxillary and superficial temporal veins merge into the Retromandibular vein within the
parotid gland.
 Lymphatics: No of lymph nodes are present within the gland, principally in the superficial
lobe.

48
Relevant surgical relations:
 Posterior: Cartilage of external auditory meatus; tympanic bone, mastoid process, SCM.
 Deep: Styloid process, stylomandibular tunnel, parapharyngeal space, posterior
belly of digastric, SCM.
 Superior: Zygomatic arch, TMJ.

Intraoperative location of facial nerve:

 Posterior belly of digastric muscle:
The nerve runs at the same depth below the skin surface, and bisects the angle between the
muscle and the styloid process.
 Cartilage pointer:
Medial - most, pointed end of the cartilage of the external auditory meatus.
The nerve exits the foramen approximately 1cm deep and 1cm inferior to this point.
 Tympanic ring, mastoid process and tympanomastoid suture line:
Tympanomastoid suture line is the most precise landmark for the facial nerve as it leads
medially, directly to the stylomastoid foramen.
 Styloid process:
Facial nerve lateral to styloid process. Palpating the styloid process is therefore a useful
means to determine the depth and position of the facial nerve.

Types of Parotidectomy:
A. Partial parotidectomy: Resection of parotid pathology with a margin of normal parotid
tissue.  benign pathology.
B. Superficial parotidectomy: Resection of the entire superficial lobe of parotid and is
generally used for metastases to parotid lymph nodes e.g. from skin cancers, and for high
grade malignant parotid tumours.
C. Total parotidectomy.

49
Preoperative consent:
Scar.
Anaesthesia in the greater auricular distribution.
Facial nerve weakness: Temporary weakness common (<50%); permanent weakness rare.
Facial contour: loss of parotid tissue leads to a more defined angle of mandible, and
deepening of retromandibular sulcus.
Prominence of auricle: This is probably due to loss of innervation of the postauricular
muscles and preauricular scarring.
Frey’s syndrome (gustatory sweating).

Anaesthesia:
• General anaesthesia
• Short-acting muscle relaxation for intubation only
• Hyperextend the head, and turn to opposite side.

Partial/Superficial Parotidectomy:
 Lazy-S /Modified Blair incision: This is placed in preauricular and cervical skin creases.

 Raise superficial cervicofacial flap to the anterior border of parotid mass or of the
parotid gland in the plane between the SMAS and the parotid fascia with scalpel or
diathermy.

 Traction suture in the subcutaneous tissue of the ear lobule as well as securing the
anterior based skin flap to the

 Skeletonise anterior border of SCM

 Divide the EJV.

 Divide the greater auricular nerve as it crosses SCM posterior to the EJV.

 Attempt to preserve the posterior branch of the nerve to retain sensation of the skin of
the auricle.

 Identify and skeletonise the posterior belly of the digastric muscle.

 Skeletonise the cartilage of EAC up to the tragal pointer.

 Skeletonise the mastoid tip to the depth of the tragal pointer

 Locate the facial nerve trunk by blunt dissection.

50
 Tunnel and spread the tissues overlying the facial nerve and its branches, and divide the
parotid tissue overlying the nerve.

 Important to dissect directly on the nerve so as not to lose sight of it. Never divide
parotid tissue beyond exposed facial nerve.

 Dissect along the trunk to the pes anserinus.

 Divide the parotid fascia and parotid tissue superiorly and inferiorly to release the
parotid posteriorly and to permit anterior mobilisation of the gland/tumour.

 Dissect along, and strip the superficial lobe off the branches of facial nerve.

 Parotid dissection for deep lobe tumours by dissecting and free up the facial nerve from
the underlying deep lobe or tumour, to provide access to the deep lobe. This may
involve either a superficial parotidectomy (Figure 22), or

 simply reflecting the superficial lobe anteriorly.

 Deliver the tumour either between, or inferior to the facial nerve or its branches,
identifying the branches of the facial nerve around the tumour, and removing tumour
between the splayed facial nerve branches.

 Deep lobe of the parotid/tumour is bordered medially by the fat of the parapharyngeal
space, and can be delivered from the parapharyngeal space by blunt dissection.

 Divide the external carotid, deep transverse facial and superficial temporal arteries and
the retromandibular and superficial temporal veins if and when they are encountered
during dissection.

51
Facial nerve repair:
1. If transected, these nerves should be repaired with 9/0 nylon Prolene epineural sutures.
2. When primary nerve repair is not possible due to undue tension or nerve resection, then the
nerve can be grafted with great auricular nerve, or sural nerve.
3. The great auricular nerve is approximately the same diameter as the facial nerve trunk.
4. The sural nerve provides greater length and is better suited to bridging longer defects.
5. When the proximal end of the facial nerve is not available, e.g. with extensive proximal
perineural tumour extension, then a hypoglossal-facial nerve interposition graft can be used
to restore facial tone and movement. The nerve graft is sutured end to end to the distal
facial nerve, and end-to-side to the hypoglossal nerve.

52
6.SUBMANDIBULECTOMY
Surgical anatomy:
 SMG (submandibular gland) has both oral and cervical components.

 It passes around the posterior free margin of the mylohyoid muscle, which forms the
“diaphragm” of the mouth and separates the cervical and oral components of the gland.

 SMG is in the submandibular triangle (Level 1b) of the neck.

 The oral component extends some distance along the submandibular duct immediately deep
to the mucosa of the floor of the mouth.

 The duct opens close to the midline in the anterior floor of mouth.

 Cervical part of the gland is immediately deep to the platysma, and is encapsulated by the
investing layer of the deep cervical fascia.

 Digastric muscle forms the anteroinferior and posteroinferior boundaries of the

submandibular triangle. It is an important surgical landmark as there are no important
structures lateral to the muscle.

 The facial artery emerges from immediately medial to the posterior belly

 XII nerve runs immediately deep to the digastric tendon.

 Mylohyoid muscle attached to the mylohyoid line on the inner aspect of the mandible, the
body of the hyoid bone, and by a midline raphe to the opposite muscle.

 Of importance to the surgeon is that there are no important vascular or neurological

structures superficial to the mylohyoid; the lingual and XIIn are both deep to the muscle.

 Marginal mandibular nerve (M.M.) is at risk of injury as it runs within the investing layers of
deep cervical fascia overlying the gland, and may loop up to 3cms below the ramus of the
mandible.

 M.M. crosses over facial artery and vein before ascending to innervate the depressor anguli
oris.

 Lingual nerve runs in the lateral floor of mouth above the SMG, and sends secretomotor
nerve fibres to the submandibular ganglion which innervate the SMG. It comes into view
during SMG excision when the SMG is retracted inferiorly, and the mylohyoid is retracted
anteriorly.

53
  Hypoglossal nerve (XIIn) enters the submandibular triangle posteroinferiorly and medial to
the hyoid bone, crosses the submandibular triangle in an anterosuperior direction, and exits
into the mouth behind the mylohyoid muscle.

INDICATION:
1. Recurrent sialadenitis or obstructive sialodocholithiasis (salivary stones).

2. Malignancy.

3. Part of neck dissection.

CONSENT:
1. Describe procedure and incision.

2. Describe location of relationship of gland to marginal mandibular nerve, lingual nerve, and
hypoglossal nerve.

3. Describe Wharton's duct and its relationship to the floor of mouth, sublingual glands, lingual
and hypoglossal nerves.

4. Describe expected sequelae:

i. Numbness above incision.

ii. Potential for altered lower lip contour from transection of platysma muscle and
cervical branch of facial nerve.

5. Describe complications:

i. Bleeding, infection, reaction to anesthetic agents.

ii. Damage to adjacent structures: marginal mandibular nerve, lingual nerve,

hypoglossal nerve.

iii. Retained stone in distal stump of Wharton's duct

54
ANESTHETIC CONSIDERATIONS:
 Ensure only short active muscle relaxant used - facial nerve stimulator.

POSITIONING & DRAPING:

 Patient is placed in a supine position with neck extended and the head rotated to the
opposite side.

 Oral endotracheal intubation with tube secured to contralateral corner of mouth.

 The skin of the anterior neck and lower face is sterilised.

 Draping done in such a way that the lower lip, lower margin of the mandible, and upper neck
are exposed.

OPERATIVE PROCEDURE:
 Along the relaxed skin tension lines, a 4 cm horizontal incision is made at least 2
fingerbreadths below the mandible to ensure the marginal mandibular nerve is not
damaged.

 Subplatysmal flap raised to expose the anterior border of the SCM posteriorly and the
anterior belly of the digastric muscle.

 Posterior inferior aspect of the submandibular gland is identified immediately anterior to

the SCM where it overlays the posterior belly of the digastric muscle.

 Elevation of the fascia of the submandibular gland from an inferior to superior direction
(subcapsular dissection) that carries the marginal mandibular nerve superiorly away from
the gland.

 Elevation of the posterior facial vein (at angle of mandible) will draw the marginal
mandibular nerve superiorly away from the gland.

 Following flap elevation, the gland is exposed and retracted inferiorly, employing an Allis
clamp or Babcock for traction.

 Digastric muscle is identified along its course including the common tendon and the anterior
belly.

 Anterior aspect of the gland is mobilized posteriorly to expose the mylohyoid muscle.

 Posterior border of the mylohyoid retracted anterosuperiorly to expose the lingual nerve.

55
  Submandibular ganglion permitting separation of the gland from the lingual nerve.

 Duct of the gland traced anteriorly and transected after placement of a hemoclip as distal as
possible.

 Gland is dissected posteriorly to encounter the branch from the facial artery perfusing the
gland and ligated.

 Wound is irrigated with saline and closed in layers over a drain.

In a longer paragraph:
The patient was brought to the operating room and placed on the operating table in supine position.
Transorally intubated. A 4cm line extending anteriorly from the anterior border of the SCM and
parallel to the mandible was marked at 2 FBs below the angle of mandible in a pre-existing skin
crease. Epinephrine 1:100,000 was injected in the incision line in the left upper neck and the area
prepped with Betadine and draped in sterile fashion. The corner lip was exposed on the left side
during the resection.
The skin incision was carried straight down to the level of the digastric muscle without raising
subplatysmal flaps to prevent injury to the facial nerve branches. At this depth at the inferior edge
of the submandibular gland, the fascia of the submandibular gland was elevated off of the gland
from inferior to superior so that the marginal branch of the facial nerve was elevated off the gland
with the fascia and protected. This nerve was not encountered during the dissection. The facial
artery was identified going into and out of the gland and suture ligated on both sides. The gland was
dissected off the mylohyoid muscle which was then retracted anteriorly allowing unambiguous
identification of the lingual. The gland was dissected away from the lingual nerve and Wharton's
duct was identified and suture ligated. The specimen was then delivered from the operative field
and sent to pathology. The gland appeared inflamed but was otherwise without any appreciable
abnormalities.
The surgical site was copiously irrigated with sterile saline and hemostasis obtained with bipolar
cautery. The incision was closed over a 1/4-inch Penrose drain using deep 3-0 Vicryl stitches to
reapproximate the platysma and a running 4-0 nylon in skin. The patient was then turned over to the
care of the anesthesiology team, extubated uneventfully in the operating room and transferred to
the post-anesthesia care unit.

56
7.TRACHEOSTOMY

Definition:
Tracheotomy - a surgical opening in the trachea.
Tracheostomy - the creation of a stoma at the skin surface which leads into the tracheal
lumen.
A permanent or ‘end’ tracheostomy - elective procedure carried out as part of a surgical procedure
involving the removal of the larynx, such as a laryngectomy or pharyngolaryngectomy.

The effects of a tracheostomy

 laryngeal bypass – loss of cough and phonation;
 reduction in respiratory dead space- Reduce 30-50% --- improve resp effort by reducing
resistance to airway (normal dead space 150ml)
 loss of nasal mucosa filtration and humidification;
 increased risk of infection;
 tube acts as foreign body leading to local inflammation;
 sump above tracheostome and below larynx, when mucus collects.

Indications
 upper airway obstruction;
 removal of secretions (bronchial toilet);
 prolonged ventilation;
 part of another procedure.
Upper airway obstruction
 Congenital: SGS/ Tracheal stenosis/ laryngeal web/laryngeal cyst, web,
laryngo/tracheo/bronchomalacia, severe cervical kyphosis, hemangioma, cystic
hygroma, Craniofacial syndrome (severe micrognathia, macroglosia, generalized
oropharyngeal crowding)
 Trauma: laryngeal trauma/ maxillary or mandibular #/ Le Fort III
 Neoplasm: Ca larynx or hypopharynx,
 Infection: acute epiglottitis, croup
 Inflammation: edema secondary to corrosive agent, inhalation of smoke, allergic
reaction
 Neurological problem: Bilateral RLN palsy
 Foreign body in larynx

Removal of secretion (bronchial toilet)

 Accumulation of secretions in the lower respiratory tract is responsible for a reduction
in gas diffusion within the alveoli. This results in respiratory failure.
 easier to aspirate secretions with less upset to the patient.
 Severe head injury or coma, respiratory centre depression, not effective cough,
causing hypercarbia + hypoxic.
 Painful cough esp in chest injuries
 CCF/ pulmonary edema

Prolonged ventilation
 Reduced dead space, assists weaning off positive pressure ventilation
 Increased rate of subglottic stenosis if intubation continues for more than 10 days,
although there are those who would argue that intubation can be prolonged for up to
3 weeks.
 Resp failure/ insufficiency, Severe lung injury
 Resp paralysis (GB, tetanus, myasthenia gravis (severe), cervical spine injury)

57
 Part of another procedure.
 provide adequate surgical field for surgeon, while maintaining airway and prevent
aspiration
 temporary tracheostomy- major resections involving the oral cavity or pharynx, E.g.
hemiglossectomy/ total glossectomy/ total maxillectomy
 permanent tracheostomy- laryngectomy, pharyngolaryngectomy

Contraindication of tracheostomy
No absolute contraindication
Relative contraindication
- In laryngeal CA to avoid stomal recurrence
- RRP
- Ludwig angina/ deep neck infection

Type of tracheostomy
- Elective temporary
 Prior to H&N surgery/ prolonged intubation
- Elective permanent
 Laryngectomy
- Emergency tracheostomy
 Failed intubation
 Under LA
 Complication rate is 21%
- High tracheostomy
 Above thyroid isthmus
 It violates first tracheal ring
 Can cause perichondritis of cricoid & SGS
 Only indication --- ca larynx

Procedure
1. Head rest and shoulder bag.
2. Horizontal incision through skin, subcutaneous tissue, and deep cervical fascia midway between
cricoid and sternal notch.
3. Divide strap muscles in the midline.
4. Divide thyroid isthmus in midline and hemitransfix with 4/0 vicryl.
5. Warn the anaesthetist, and ensure a tracheostomy tube (3/4 of the diameter of the trachea) is
ready and the cuff has been tested and that a sucker is at hand.
6. A cricoid hook can be used to elevate the trachea into the wound.
7. Tracheotomy – vertical incision OR removing the anterior half of 3rd or 4th tracheal ring OR a
cruciate incision OR Bjork flap.
8. Ask anaesthetist to withdraw ETT.
9. Insert tracheostomy tube once tip of ETT has been withdrawn proximal to the stoma and inflate
cuff.
10. Secure tube with 2/0 silk sutures and tracheostomy tape (ensuring head is flexed).

58
Bjork flap
- Inverted U & inferiorly hinged tracheal flap sutured to inf edge of transverse skin incision
- Pro: Reduce incidence of accidental decannulation & make reinsertion easier
- Cons:
1. if the sutures in the flap cut out on the first tube change, the flap may prevent the
successful re-insertion of a tube.
2. The stoma, which involves exteriorisation of the trachea, may also need to be closed
surgically once the patient has been weaned-off of ventilatory support as it may not close
spontaneously.
3. higher degree of tracheal stenosis than other methods

Complications
Immediate complications
- Apnoea
 Loss of hypoxic drive, due to sudden wash out of CO2 which acts as resp stimulant
 More in children with chronic airway obstruction
 Avoid sedation
 Rx: administer 5% CO2 in O2 (carbogen) to assist ventilation
- Haemorrhage
 Cut edger from thyroid gland, ant jugular vein
- Air embolism
 Large neck vein maybe open and air sucked in
 Air enter right atrium --- cardiac tamponade + death
- Pneumothorax
 Result from direct injury to apical pleura/ lung cupola, esp in child due to low
tracheostomy
 High negative inspiratory pressure --- pt who are awake and distressed esp LA
 Rx: routine post-op CXR for paed, chest tube
 0.4% in adult, 10-17% in paed

- Surgical trauma to adjacent structures --- esophagus, RLN, great vessels

Intermediate complications
- Surgical exphysema
 Due to tight closure of trachy wound, tight packing material area tube, false passage
of tube into paratracheal tissue, pneumothorax

- Tube displacement 2%
 A serious cx during first 3 days
 Fistula tract still not well formed
 Rx: attempt recannulation, proceed intubation if fail

- Tube obstruction 3%
 Avoidable complication
 Potentially fatal
 Most common cause is accumulation of mucus & crust in the tube/ tracheal lumen.
Can also cause by granulation tissue
 Prevention: adequate humidification, suctioning, hydration. Use of double lumen
tube, easy cleansing
 Granulation at stoma and suprastoma (within the tracheal lumen)
 In preterm neonates: intermittent obstruction by baby’s chin (prevented by suitable
attachment to tube)

59
- Infection
 Cellulitis/ abscess is unlikely if incision is not closed tightly and drainage is allowed
o Rx: open wound and appropriate antibiotics
 Tracheitis is present in all pts with fresh trachy
o Rx: humidification, minimize fraction of O2 (high O2 exacerbate drying of
airway), minimize movement of trachy tube by stabilizing ventilatory circuit
to minimize torsion
 Pneumonia is possible

- Scabs and crusts

 Cold air in direct contact with trachea, which dry tracheal/ pulmonary secretion
 Interfere with ciliary clearance, produce thick tenacious mucus scab and crust which
lead to infection, obstruction, atelectasis, pneumonia
o Rx: humidification air, regular tracheal suction, instillation of NaHCO3 or
saline
- Dysphagia
 Tethering of trachea, larynx not able to move upward
 Pressure cuff compress on esophagus
o Rx: RT feeding, deflate cuff during feeding
- Tracheal necrosis <1%
 Focal pressure on trachea & secondary to infection
 Oversized trache/ Improper curve/ Tip impingement/ Cuff pressure
 Present as ulcer on wall of mid/lower cervical trachea
 Factors exaggerate it: previous irradiation, low grade infection, poor nutritional status

- TE fistula <1%
 Caused by friction fromposteriorly displaced trachy tube/ overinflated cuff/ rigid NG
tube/ traumatized during tracheal incision
 Presents with aspiration, chemical pneumonitis, violent coughing during eating,
chronic coughing a/w swallowing saliva
 Ix: plain x-ray --- air filled esophagus
 Endoscopic examination
o Mx: pre-op gastrostomy/ jejunosotmy. Arrange for surg repair with muscular
fap/ skin graft
- Trachea-arterial fistula 0.4%
 Mortality 80-90%
 Heralded by sentinel bleed
 Warning sign --- slight bleeding from trachea 3/7-3/52
 a/w improper tube position, improper curve and length of tube, secondary to
pressure from cuff > 30cmH2O
 Serious haemorrhage may occur dt erosion if innominate artery (brachiocephalic
artery)/ secondary infection/ erosion of tracheal wall by tip of malpositioned tube
o Rx: proper position of tube (change to a smaller size or putting gauze
underneath trachy tube to shift the pressure point), antibiotics for infection
 DDx for bloody secretion from TT suction
 Diffuse tracheitis
 Random bleeding from skin/ thyroid
 Ulceration from an ill-fitting tube
 Overzealous suctioning
 Granulation tissue

60
Late complications
- Laryngeal and tracheal stenosis
 Causes: Injury to cricoid cartilage/ Scar contracture by improper placed incision/
Repetitive incision/ Granulation (matures into fibrous scar)/ Tracheal infection
 Occurs at site of trachy where area irritated by cuff/ tip of tube
 Prevention: use high volume low pressure cuffs, do not overinflate cuffs
 Rx: laser incision, surgical resection + reconstruction

- Persistent trachea-cutaneous fistula

 Epithelization of tract from skin to trachea result in non-healing fistula
 Mx: coring out epith layer & allowing wound to granulate in. 3-layer closure can be
performed. Evaluate by direct laryngoscopy
- Scar
- Difficult decannulation
 Underlying problem not settled
Eg: Obstruction above trachy persist (bilateral VC palsy, subglottic stenosis)
 Obstructing granulation tissue suprastoma/ stoma
 Children
 Significant secretion need regular bronchial toilet
 Infractured cartilage/ tracheomalacia
 Anxiety

61
8.Paediatric Tracheostomy

Anatomy and Relations

 Overlying structure: thyroid isthmus covers rings 2,3,4.
 Tracheo-oesophageal grooves: Recurrent laryngeal nerves
 Laterally: CCA & IJV
 Posteriorly: cervical oesophagus, pre-vertebral fascia, vertebral bodies
 Inferiorly: brachiocephalic vein crosses trachea obliquely, Apex of pleura ascends into the
neck in infants and small children, Deep innominate artery

Few points in paediatric tracheostomy

- Significantly greater morbidity and mortality!
- Pediatric airway is smaller, soft, and pliable  Easy to cut thru
- Over retraction intraop may lead to  disorientation, lateral dissection, accidental injury to
the lung or major vessel.
- Higher in the neck than the adult larynx
- Poor pulmonary reserve, any temporary loss of airway patency may lead to severe cx
including death
- Neck extended but not hyper-extended, hyperextend neck will bring great vessels and lung
apex superiorly, atlanto-axial #, go straight to spine.
- DEFAT IS A MUST – s/c fat will occlude view.
- Cricoid cartilage is not easily palpable.
- Hyoid bone often overrides upper edge of thyroid cartilage  hence, notch difficult to
identify. You must feel the trachea rings with fingers or aspirate.
- Trachy size = (age + 16)/4 for children >2yo OR increase half size of ETT used
- Smallest cuffed tube available is size 5.
- STAY SUTURE:
o Serve to assist in elevation of the trachea
o Facilitate exposure of the tracheotomy incision intraoperatively
o Ease replacement due to blockage/dislodge / accidental decannulation esp in the
immediate postoperative period
- If trachy dislodge, cross the stay suture before intubate
- Prolonged intubation in paed --- 6/52 (1 -2 months). Risk of subglottic stenosis is lesser in
paed because it is pliable.
- CXR after op.

62
Procedure
Preparation and landmarks
 Select and check an age-appropriate and one-size smaller & larger tube prior to surgery.
 Size and position of the ETT and presence of air leak around the tube.

Landmarks
 Inspect for landmarks, excessive fat, central lines, scars from former vascular access or
surgery
 Soft cartilages, landmarks of laryngeal framework more difficult to feel.
 Mark midline, cricoid cartilage, suprasternal notch, and sternocleidomastoid muscles.

Positioning
 Avoid hyperextension to avoid mediastinal structures presenting in the neck; ensure head
taped in the midline.
 Use shoulder roll to extend the neck, bringing the trachea more anterior and superior but
avoid hyperextension.
 Tape the chin in midline position.

Surgery
1. Horizontal/vertical incision, midway between cricoid suprasternal notch
2. Remove excess SC fat with diathermy.
3. Retract straps in midline.
4. Divide isthmus with diathermy.
5. Identify tracheal rings and place two 4.0 Nylon or Prolene (non-absorbable monofilament)
stay sutures either side of midline.
(These are left uncut, labelled left and right, and taped to the child’s chest.)
6. Vertical tracheal incision 3 – 5 rings avoid removing cartilage to prevent later stenosis.
7. Place four 4.0 Vicryl sutures from edge of trachea to skin edge.
(This is an extra set of sutures that secures trachea to skin surface to reduce risk of
decannulation followed by incorrect re-insertion.)
- There is an argument that it renders the stoma more permanent but most paediatric
tracheostomies are inserted for mid- to long-term problems.
- The risk of tracheocutaneous fistula on subsequent extubation occurs, regardless of
technique, because a well-established tract will form around the tube over a few weeks.
8. Tracheostomy tube is inserted and position of distal tip above carina is checked with flexible
or rigid scope.
9. Tracheostomy tube is secured by suturing it to skin with 3.0 Nylon and with tapes.

63
Postoperative care
 CXR immediately post op to evaluate for pneumothorax and tube position
 Monitor closely and cared for by appropriately trained nursing staff (NICU/PICU)
 Observe for any bleeding, leaking, block or displacement of tube
 Clear secretions by frequent suctioning
(facilitated by the instillation of 0.5 ml sterile NS into the tube).
 Changed for the first time after 7 days.
 Timing of subsequent tube changes is variable
 May require more frequent changes if thick secretions, infection
 Immediate change if appears occluded.
 Patients should have the following items set up at the bedside
1. Emergency kit:
o A spare tracheostomy tube of the same size and one size smaller
o Round-ended scissors.
o Tracheostomy tapes and dressing.
o Water-based lubricant.
o Suction catheter that can be used to railroad in a new tracheostomy tube if
required.
2. Suction apparatus and sterile suction catheters

 Equipment required for tracheostomy change.

 Emergency Tracheostomy Box
 Oxygen – mask, self-inflating bag/mask
 Suction apparatus – checked and working
 Resus equipment available
 PPE – apron, gloves, goggles, face shield
 Dressing set
 Rolled towel – to place under the shoulders to extend the neck
 Good light

CANNOT INTUBATE  Procedure for immediate airway mx

- Do not PARALYSE!!
- Minimize attempts of intubation
- Start Steroids
- Consider: Jaw trust
Oropharyngeal airway
Nasopharyngeal airway
Laryngeal mask airway
Cricothyrotomy/ laryngotomy
Emergency tracheostomy

Prolonged cricothyrotomy lead to

- Perichondritis
- Subglottic edema
- Laryngeal stenosis

64
8.DL SCOPY, OESOPHAGOSCOPY & BRONCHOSCOPY

** All procedures must start with:

o Counselling of the patient regarding the procedure
o Time out in the operation theatre

DL SCOPY
1.Direct pharyngolaryngoscopy:
- A controlled and detailed examination of pharynx and larynx
- Should combined with palpation of the so-called ‘silent areas’ of the pharynx
(i.e. the tongue base, postnasal space, tonsil fossae, and where accessible, pyriform fossae)

2. Indications:
a) Diagnostic:
- To diagnosis, look for the extent of growth (staging) and biopsy of pharyngeal &
laryngeal lesions
- When IDL is not possible.
(Eg: in infants and young children with symptoms points to larynx or hypopharynx – ie:
hoarseness, dyspnoea, stridor and dysphagia)
- When IDL has not been successful
(Eg: Dt excessive gag reflex or overhanging epiglottis obscuring complete view of larynx)
- To examine hidden areas: Base of tongue, valleculae and lower part of pyriform fossa,
infrahyoid epiglottis, anterior commissure, ventricles and subglottic region.
- To guide difficult intubations & passage of the rigid bronchoscope, especially in
children.
- Identification of the oesophageal inlet for the passage of a nasogastric feeding tube.
- To identify opening of pharyngeal pouch prior to packing or for placing a fibre light in
order to facilitate the identification of the pouch of the neck.

b) Therapeutic:
- Remove benign lesions of larynx (Eg:papilloma, fibroma, vocal nodule, polyp or cyst.)
- Treatment of laryngeal lesions (Eg: laser, injection of VC)
- Removal of FB from pharynx, larynx and hypopharynx.
- Dilatation of laryngeal strictures
- To direct placement of a stomach tube.
- For guidance during upper oesophageal myotomy.
- Provide access for the endoscopic division of the common wall of the pouch and
pharynx in the Dohlmann’s procedure.

3. Contraindications:
o Cervical spine pathologies
o Resp distress unless airway has been protected by tracheostomy
o Recent coronary occlusion or cardiac decompensation.
Why? Becoz DL and rigid oesophagoscopy can result in profound vagal stimulation and
dysrhythmias)

65
4. Pre-operative check:
o Dentition.
o Neck mobility.
o Possibility of airway obstruction during intubation or post-op requiring tracheostomy.
o Close liaison with Anaesthetist:
Whether to intubate/not, type of tube, whether spontaneous/intermittent positive-pressure
or jet ventilation, type of the muscle relaxant.

5. Operative Technique
– Anaesthesia: GA is preferred
 Microlaryngeal tube (MLT): ETT anchored to the LEFT for right handed surgeon.
 Metal tube if laser required
 Jet Ventilation
– Prophylactic antibiotics/ steroid cover:
 Antibiotics unnecessary in the absence of intercurrent valvular heart disease
 Steroid cover in cases with likely to be instrumentation, lasering or intubation of
critically narrowed airway
– Position:
 Anaesthetic machine placed either at the patient’s feet or to the patient’s side
 Morning sniff/ barking dog position
 Head ring (Donut) applied, no need sandbag
 Neck is flexed on thorax; head is extended on atlanto-occipital joint.
(cervical spine necessary to align the oral, pharynx and laryngeal inlets along the
same axis for pharynolaryngoscopy)
– Gauze/tooth guard is placed on upper teeth
– Laryngoscope is lubricated with gel and held in left hand.
– Right hand is used to retract the lips and to handle instruments
– Laryngoscope is introduced by one side of the tongue which is pushed to the opposite side
till posterior third of the tongue is reached.
– Uvula is identified in the midline and scope directed laterally to inspect tonsillar fossa and
faucial pillars. Aspirate the saliva if necessary.
– It is then moved to the midline and advanced behind the epiglottis and lifted forward.
** following ETT can be helpful: keeping the ETT in view posteriorly, advance the tip of the
scope until the VC come into view, then inspect the posterior part of the larynx by directing
the tip of the scope behind ETT
– Different types of laryngoscope:
o Lindholm (standard, usually used) scope and place at epiglottis and lift it anteriorly
to visualize the larynx
– During the scope inspect:
o lateral and posterior pharyngeal pharyngeal wall
o tongue base, valleculae, epiglottis (the tip, lingual and laryngeal surface)
o both pyriform sinuses, aryepiglottic folds, arytenoids, postcricoid region
o both false cords, anterior and posterior commissure, right and left ventricles, right
and left vocal cords and subglottic area.
o mobility of VC should also be observed.

66
 – Proceed with microlaryngoscopy:
 Advantages
 Binocular vision and better illumination
 Magnification and precision.
 Documentation and recording of findings.
 Laser mountable.
 Two free hands for laryngeal procedures.
 Method
 Mayo table for support of suspension arm of laryngoscope.
 Select an operating microscope with 400mm focal-length lens or telescope for
magnification.
 Microlaryngeal instruments are used for manipulation, biopsy or excision.

For examination of ANTERIOR COMMISSURE:

 consider anterior commissure laryngoscope: can be advanced further bt the ventricular
bands to examine the ventricles & anterior commissure.
 Using VC spreader to visualize anterior commissure

For examination of VENTRICLES:

 Greatly assisted by application of laryngostat
 So operator can use 2 hands and can displace the false cord with biopsy forcep or laryngeal
hook and use a wide-angle 70 deg Hopkin’s rod scope to view ventricle.

For examination of SUBGLOTTIS:

 Use of anterior commissure laryngoscope: passed btw the VC to examine the subglottic
 A right angle telescope/30 deg Hopkins rod can be used to see the under-surface of VC and
the wall of the subglottis
 Subglottic scope rarely used

67
If patient is planned for TISSUE BIOPSIES of laryngeal or hypopharyngeal pathology  Do
oesophagoscopy and bronchoscopy before the biopsy to avoid the field becoming obscured with
blood.
 Biopsy a suspected tumour with long Blakesley - like forceps (Figure 21)
(using microinstruments may yield specimens that are too small and cause a pathologist to
understage an invasive cancer)
 Bleeding from mucosal trauma or biopsies settles spontaneously; only very rarely is
haemostasis with adrenaline – soaked (1:1000) gauze or with cautery required.

If patient proceed with MICROLARYNGEAL SURGERY:

 (ELMS)Microsurgical instrumentation: microscissors, different types of forceps, suction tips
 (ELLS) Laser: for CO2 laser, jet ventilation anaes may be used with essential safety
precautions (eye protection for both patient and OT personnel, wet drapes around the
patient’s face & lips and, if present, ET protection)

-After the procedure is completed, with draw the laryngoscope and lips and teeth examined for any
injury
- Examine the neck as well: for the injury and also cervical lymphadenopathy (if suspicious of CA)

6) Instruments involved:
Types of laryngoscope:

68
69
Other instruments:

handle
Benjamin clip

with chest support

70
 Blakesley foceps (for biopsy)

Vocal cord spreader/retractor

Microlaryngeal surgery instruments:

MICRO LARYNGEAL Set (Set Of 15 Instruments)

900 Straight Micro Laryngeal Forcep Serrated Jaw 25cm, 35cm

912 Micro Laryngeal Forcep Cup Jaw Straight 25cm

924 Micro Laryngeal Scissors Straight 25cm

939 Foreign Body Forcep 25,35,45,55cm

945 Biopsy Cup Forcep 25,35,45,55cm

957 Laryngeal Suction Tube 25cm, 35cm

960 Bronchoscope Suction Tube 35cm, 45cm, 55cm

963 Micro Laryngeal Round Knife 45̊

71
966 Micro Laryngeal Plaster Knife

972 Micro Laryngeal Probe 90̊

975 Micro Laryngeal Sickle Knife

Micro Laryngeal Swab Holder 984, 984A - Holder For Micro Laryngeal
984, 984A
Instrument

Anterior Commisure Laryngoscope With Fibre Optic Carrier

987
Small/Med/Large

999 Laryngoscope Holder And Chest Support

72
7. Post-op care
- Patient is kept in lateral position to prevent aspiration of blood or secretions.
- Patient's respiration should be watched for any laryngeal spasm and cyanosis.
- NBM for 6 hours
- Voice rest (for 48 hours if intervention performed)
- IV antibiotics if suspicious of infection
- IV dexamethasone if + oedema
- Antireflux medications if + findings of LPR.
- Drink plenty of fluids, avoid caffeine, avoid voice abuse.

8. Complications
- Injury to lip and tongue
- Injury to teeth, may dislodged and fall into pharynx
- Bleeding --- may cause aspiration
- Laryngeal edema --- cause resp distress

Oesophagoscopy
3 types: 1) Rigid oesophagoscopy
2) Flexible fibreoptic oscophagoscopy
3) Transnasal oesophagoscopy

Rigid Esophagoscopy
- Long scope 45cm (esp for pathology over distal esophagus)
- Shorter scope 25cm

1) Indications
a) Diagnostic:
- Metastatic neck dis with unknown primary (part of panendoscopy)
- TRO synchronous tumor in SCC oropharynx/ hypopharynx/ larynx
- Dysphagia --- CA esophagus, cardiac achalasia, strictures, esophagitis, diverticula
- Retrosternal burning --- reflux esophagitis and hiatus hernia
- Hematemesis eg esophageal varices

b) Therapeutic
- Removal of FB
- Dilatation in cases of esophageal strictures or cardia achalasia
- Endoscopic biopsy or removal of benign tumor
- Packing or passing NG in pharyngeal diverticulum
- Injection of esophageal varices
- Insertion of Soutar’s or Mousseau-Barbin tube in palliative Rx of esophageal CA

2) Contraindications
- Trismus --- technically difficult
- Disease of cervical spine --- cervical trauma, spondylosis
- Receding mandible
- Aneurysm of aorta for fear of ruptured & fatal haemorrhage
- Advanced heart, liver or kidney disease may be relative C/I.

73
3) Pre-operative:
- Barium swallow if chronic dysphagia.
(useful to exclude pouch and prevent perforation or if dysmotility expected).
- Lateral and PA plain soft tissue X-rays to assess site of FB.
- Be aware of the anatomical and physiological narrowing of the oesophagus as a distance from the
upper incisor teeth:
 Cricopharyngeus 15cm. (C6 level)
 Aortic arch 22.5cm. (T4 level)
 Left main bronchus 27.5cm. (T6 level)
 Diaphragm 40cm. (T10 level)

4) Technique
• Under GA
• Morning sniff position (same as DL scope)
• Gauze/tooth guard is placed over the upper teeth
• Oesophagoscope is lubricated and is held by its proximal end in a pen-like fashion and introduced
into mouth by the right side of the tongue and then towards the middle of its dorsum.
Advanced gently by left thumb & index finger.
 Use of thumb of non-dominant hand to act as fulcrum to protect the teeth.
 Make sure the bevel of the esophagoscope is pointing upwards.
 Follow down the right-hand side of ETT beyond the epiglottis.

4 basic steps
• Pass scope into right piriform sinus & then behind the ETT – identify arytenoids
• Passing the cricopharyngeal sphincter
 Keep the scope tip in the midline & behind the larynx, tip is lifted with movement of left
thumb to open the hypopharynx and puckled inlet at the cricopharygeus become visible.
*Scope may not advance due to: not enough muscle relaxant, large osteophytes causing
obstruction, cuff of ETT causing compression
• Crossing the aortic arch and left bronchus
 When crossing the aortic pulsation side, neck is slightly extended to keep scope in line with
the esophageal lumen
• Passing the cardia
 Maybe helpful to tilt the head of the operating table upward until the transition from
esophagus to gastric mucosa is observed
 Move patient’s head slightly to right and scope points to the left anterior-superior iliac spine

• Use a long metal sucker to clear oesophageal contents. Always keep the lumen in view while
advancing the esophagus. And also inspect the esophageal wall when scope is withdrawn.

74
5) Instruments

Rigid, open-ended
Esophagoscope
(with Hopkins rod lens
telescope) Figure 3

The esophagoscope is introduced, and once the foreign body is in view, the
Telescope (Figure 3) is removed from the sheath and a grasper with an
attached telescope is introduced into the sheath (Fig. 4). The foreign
body is grasped, and the sheath and telescope are removed together.

Suction port

For Hopkins rod telescope/

instrument to remove foreign bo

Paediatrics Esophagoscope
Light deflector

75
Prism light deflector

Handle (at the proximal end)

indicate the direction of the
bevel at the distal end

76
6) Post-operative:
- Sips of plain water followed by usual diet may be given in an uneventful oesophagoscopy.
- Patient is watched for pain in the interscapular region, surgical emphysema of neck, and
tachycardia, tachypneic, hypotension, ahrupt rise of temperature. They indicate oesophageal
perforation.

7) Complications
1. Injury to lips, teeth, arytenoids, pharyngeal mucosa
2. Mucosal tear/lacerations: minor – can be ignored, if in doubt – start antibiotics, NG tube and
monitor closely
3. Perforation of esophagus – most often occurs at site of Killian’s dehiscence
4. Compression of trachea --- in children, scope place on posterior tracheal wall causing
obstruction to respiration & cyanosis. Rx: Immediate withdrawal of scope.

8) Management of oesophageal perforation

* surgical emergency
- NBM,
- NG feed/ parenteral feeding
- Start broad spectrum IV antibiotics.
- Post-op CXR
- Gastrograffin swallow 10 days.
- Watch closely for pyrexia, tachycardia,or hypotension.
- Monitor closely for surgical emphysema in the neck, chest pain radiating to back, dyspnoea.

77
- Decision-making about the need for surgical intervention
 Conservative/non-operative mx may be considered in case of:
o highly selected perforations that have been promptly diagnosed,
o mainly of the cervical oesophagus,
o in stable patients with no evidence of systemic sepsis,
o with minimal extraoesophageal contamination

 Surgical options include:

o Simple external drainage to create a controlled fistula, allowing it to heal
spontaneously (only if there is no distal obstruction)
o Primary repair and external drainage of extraoesophageal contamination
o Primary repair with bolstering of the repair with a pedicled soft tissue flap
e.g.pectoralis major or infra-hyoid strap muscle
o Oesophageal diversion and drainage
o Oesophageal stenting
o Oesophagectomy
***Cardiothoracic consultation if perforation persists.

Flexible fibre-optic esophageoscopy

- With distal video chip, suction, irrigation, biopsy channel
- Transoral or transnasal
- Advantages over rigid oesophagoscopy
 Under LA
 Can be used in pt with abnormal spine or jaw
 Oesophagus, stomach, duodenum can be examined in one sitting

Bronchoscopy
Bronchoscopy is of two types:
1. Rigid
2. Flexible fibre optic

Rigid Bronchoscopy
1) Indications
- Diagnostic (examination of tracheobronchial tree)
 To find out the cause of wheezing, haemoptysis, or unexplained cough persist for 1/12
 When x-ray shows
o Atelectasis of a segment, lobe or entire lungs
o Opacity localized to a segment or lobe of lung
o Obstructive emphysema --- to exclude FB
o Hilar or mediastinal shadows
 Vocal cord palsy
 Collection of bronchial secretion for C+S, AFB, fungus, malignancy
 Large endobronchial biopsies

78
- Therapeutic
 Acute airway obstruction due to intra-luminal pathology; it is a quick procedure while
maintaining airway patency and ventilation
 FB removal
 Removal of retained secretions or mucus plug in cases of head injury, chest trauma, thoracic
& abd surg, or comatose pt
 Pathology requiring debulking, dilation or stenting
 Ablative surgery i.e. mechanical, laser, electrocautery, cryotherapy
 Stenting the airway for obstruction, tracheomalacia, tracheoesophageal fistulae
 Balloon tracheobronchoplasty

2) Pre-op preparation
- For children, choose an age-appropriate bronchoscope (Table 8.1).
- Ensure correct fittings to attach to the anaesthetic circuit (particularly important if the
bronchoscopy is required in an emergency situation) - refer to Instrument for bronchoscopy

3) Procedures
 Anaesthesia: GA
• Induction is via inhaled sevoflurane (usually in critical airway stenosis)
or by intravenous Agents (continuous IV propofol infusion)
• Ventilation
o Spontaneous-assisted ventilation
o Jet ventilation overcomes increased airway resistance associated with using a
telescope, but carries an increased risk of barotrauma if expiration iobstructed
 Position: same as DL scope
 Technique
 There are two methods to introduce bronchoscope:
1. Direct method. Here bronchoscope is introduced directly through the glottis.
2. Through laryngoscope. Here glottis is first exposed with the help of a spatula
type laryngoscop and then the bronchoscope is introduced through the
laryngoscope into the trachea. Laryngoscope is then withdrawn. This method
is useful in infants & young children & in adults who have short neck & thick
tongue.

79
  Procedure:
- Saline-soaked gauze/ tooth guard to protect upper teeth.
- For right handed surgeon: Bronchoscope (lubricated with gel) is held by the shaft in
surgeon’s right hand in a pen-like fashion. Fingers of left hand retract the upper lip and
guide the scope
- Introduce bronchoscope through the right side of the mouth which allow easier excursion
and minimal leverage.
- Look through the bronchoscope, keep the beak in the 12 0’clock and used to displace the
tongue forward and posterior pharyngeal wall. Then tip of epiglottis is identified and the
scope is passed behind it and lift up the epiglottis to expose the glottis. (avoid licking the
epiglottis repeatedly)
- Bronchoscope is rotated 90 degrees clockwise so that its longer edge of the beveled tip to
the right side and shorter edge against the left vocal cord (is in the axis of glottis to ease
its entry into trachea)

Once trachea is entered, scope is rotated 90 degrees anticlockwise back to the

original position
- Fit the anaesthetic system once in the trachea.
- Bronchoscope is gradually advanced correspond to axis of trachea and bronchi.
- The scope can be advanced while inspecting tracheal wall until distinct sharp edge of
carina is reached.

- It is more convenient to inspect the right main bronchus first as it is more vertical and easier
to enter. To achieve this, head and neck are flexed to the left when examining the right
bronchial tree and vice versa.
- Direct vision, 70 degree or right angled and retrograde telescope can be used for
magnification and details examination, and inspection of segmental and subsegmental
bronchi
- Telescopic forceps can be used for removal of foreign body.
- Carefully re-examine the airway while gently removing the bronchoscope

80
4) Instruments
- A rigid bronchoscope is a stainless steel tube through which a rigid telescope can be passed
(Figure 37).
- The distal end is bevelled to lift the epiglottis and to pass between the vocal cords; it can
also be used to core out tumour or to twist the scope through a tight stenosis (Figure 38).
- Slits in the distal wall of the bronchoscope allow ventilation of the contralateral lung while
one of the main bronchi is intubated (Figures 37, 38). Can examine airway up to main
bronchus.

- Bronchoscopes come in different lengths and diameters:

o Most commonly used in adult is size 6 - 9mm external diameter and 40 cm in length.
- Use a larger (>6.5mm) bronchoscope if possible as the optics are better with a larger
(5.5mm) telescope; when using a <6.0mm bronchoscope one has to use a 2.8mm telescope.

81
82
Accessories include a variety of forceps, scissors, suction catheters, caute-ry, injection needles and
stents (Figure 41).

5) Precautions during bronchoscopy:

- Select proper size according to patient’s age
- Do not force scope through closed glottis
- Repeated removal & introduction of bronchoscope should be avoided
- Procedure should not be prolonged >20min in infant & children, otherwise it may cause
subglottic edema in post-op period

83
6) Post-op Care
- Keep the patient in humid atmosphere.
- Watch for respiratory distress. This could be due to laryngeal spasm or subglottic oedema if
the procedure had been unduly prolonged or the bronchoscope introduced repeatedly.
Inspiratory stridor and suprasternal retraction will indicate need for tracheostomy.

7) Complications
- Injury to teeth & lips
- Laryngeal edema
- Haemorrhage from biopsy side
- Hypoxia and cardiac arrest

Flexible fibre-optic bronchoscope

- Has replaced rigid scope for diagnostic purpose in adult
- Provide magnification, better illumination, and permit examination of subsegmental/
tertiary bronchi
- Allow assessment in pt with neck & jaw abnormalities
- Allow bedside examination. Can pass through ETT or trachy
- Suction/ biopsy feasible
- Limited utility in children dt ventilation problem

References:
1) Oxford Handbook Otolaryngology And Head And Neck Surgery
2) Diseases of Ear, Nose and Throat PL Dhingra
3) The Open Access Atlas of Otolaryngology, Head & Neck Operative Surgery : RIGID
LARYNGOSCOPY, OESOPHAGOSCOPY & BRONCHOSCOPY IN ADULTS by Johan Fagan (Editor)
[email protected]
4) Textbook: Operative Otorhinolaryngology: Edited by Nigel Bleach, Chris Milford and Andrew
Van Hasselt
5) Esophageal Foreign Bodies. Eugene D. McGahren. Pediatrics in Review 1999;20;129 DOI:
10.1542/pir.20-4-129

84
 PART B:
ENT EMERGENCIES

85
1.EPISTAXIS
BLOOD SUPPLY OF NOSE:
• external and internal carotid systems, both on septum and the lateral walls.

Nasal septum:
Internal carotid system : (Branches of ophthalmic artery)
a) Anterior ethmoidal artery
b) Posterior ethmoidal artery
External carotid system :
a) Sphenopalatine artery (branch of maxillary artery)
b) Septal branch of greater palatine artery (Br. of maxillary artery).
c) Septal branch of superior labial artery (Br. of facial artery).

Lateral wall :
Internal carotid system: Branches of ophthalmic artery
a) Anterior ethmoidal A.
b) Posterior ethmoidal A.
External carotid system:
a) Posterior lateral nasal A.  From sphenopalatine artery.
b) Greater palatine artery A.  From maxillary artery.
c) Nasal branch of anterior superior dental A.  From infraorbital branch of maxillary artery
d) Branches of facial artery to nasal vestibule

Little’s area:
• situated in the anterior inferior part of nasal septum, just above the vestibule.
• 4 arteries- anterior ethmoidal, septal branch of superior labial, septal branch of sphenopalatine
and the greater palatine anastomosis  Kiesselbach’s plexus.
 This area is exposed to the drying effect of inspiratory current and to finger nail trauma, and
is the usual site for epistaxis in children and young adults.

86
CAUSES:
A. Local, in the nose or nasopharynx.
B. General
C. Idiopathic

A) Local causes:
Nose
1) Trauma
2) Infections
- Acute: viral rhinitis, acute sinusitis.
- Chronic: All crust-forming disease, e.g. atrophic rhinitis, rhinitis sicca.
3) Foreign bodies.
- Non-living: Any neglected foreign body, rhinolith.
- Living: Maggots leeches.
4) Neoplasms of nose and paranasal sinuses.
- Benign: Haemangioma, papilloma.
- Malignant: Carcinoma or sarcoma.
5) Atmospheric changes. High altitudes, sudden decompression.
6) Deviated nasal septum.

Nasopharynx :
1) Adenoiditis
2) Juvenile angiofibroma
3) Malignant tumours

87
B) General causes :
1) CVS: Hypertension, arteriosclerosis.
2) Disorders of blood and blood vessels.
3) Liver: Hepatic cirrhosis
4) Kidney:Chronic nephritis.
5) Drugs. Excessive use of salicylates and other analgesics anticoagulant therapy.
6) Mediastinal compression: Tumours of mediastinum (raised venous pressure in the nose).
7) Acute general infection.
8) Vicarious menstruation (epistaxis occurring at the time of menstruation).

C) Idiopathic :
• Many times the cause of epistaxis is not clear.

SITES OF EPISTAXIS :
1) Little’s area. In 90% cases.
2) Above the level of middle turbinate.
3) Below the level of middle turbinate.
4) Posterior part of nasal cavity.
5) Diffuse. Both from septum and lateral nasal wall.
6) Nasopharynx.

CLASSIFICATION OF EPISTAXIS :
A. Anterior epistaxis :
B. Posterior epistaxis :
• Blood flows back into the throat.
• “Coffee coloured” vomitus.

88
Management:
In any case of epistaxis, it is important to know:
1) Mode of onset.
2) Duration and frequency of bleeding.
3) Amount of blood loss.
4) Side of nose from where bleeding is occuring.
5) Whether bleeding is of anterior or posterior type.
6) Any known bleeding tendency in the patient or family.
7) History of known medical ailment (hypertension, leukaemias, mitral valve disease, cirrhosis,
nephritis).
8) History of drug intake (analgesics, anticoagulant, etc.)

First aid:
 Trotter’s method
 Cold compresses to the nose to cause reflex vasoconstriction.

Anterior nasal packing.

• Can be removed after 24 hours if bleeding has stopped.
• If it has to be kept for 2 to 3 days; systemic antibiotics should be given to prevent sinus
infection and toxic shock syndrome.

Posterior nasal packing.

Cauterisation: using silver nitrate or electrocautery.
Ligation of vessels :
1. SPA.

2. Anterior and posterior ethmoidal artery via medial canthotomy.

3. External carotid artery.

Management of the underlying systemic cause: HPT, coagulopathy.

89
2.STRIDOR

Definitions
1. Stridor (Latin: stridoris - “to creak”)
Harsh, grating, high-pitched sound produced by turbulent airflow due to partial obstruction
of the laryngotracheal airway.
A sign, not a symptom.
Tend to be worse when awake, feeding or upset.
Described typically in relation to breathing: inspiratory, expiratory OR both.

2. Stertor (Latin: stertere – “to snore”)

Noisy, low pitch inspiratory sound characterized by snoring or gasping sound due to
nasopharynx - oropharyngeal (supraglottis) obstruction.
Eg: -Mouth breather dt chronic nasal obstruction
-Paeds SDB due to tonsillar hyperplasia
-Epileptic pt during post-ictal phase

3. Wheezing
Continuous respiratory (insp/exp), high pitch, whistling sound dt turbulent airflow through
narrowed bronchial or smaller airways.
Eg: -Bronchial Asthma
-COPD

Types of Stridor

a) Inspiratory stridor
- Obstructive lesion at supraglottis or pharyngeal level
- Eg: Laryngomalacia

b) Expiratory stridor
- Lesion at thoracic trachea or bronchi
- Eg: tracheal stenosis

c) Biphasic stridor
- Lesion at glottis, subglottis or cervical trachea
- Eg: VC paralysis, subglottic stenosis

90
Differences between Adult & Paediatric airways

 ↓ radius of airway  will narrow airway significantly  ↑ resistance

(Pouseuille Law) Resistance = 1
radius4
 This Pouseuille law explains why even minor obstruction in child is more significant than in
adult.
 Bernoulli law states as velocity ↑, pressure on lumen wall ↓.

Table: Laryngeal inlet cross-section area in normal and in laryngeal edema

Cross section
Normal Edema 1mm Resistance
area

Infant 4 ↑ 16x ↓75%

m
m
m
Adolescent 8m ↑ 3x ↓44%
m
m

Adult 12 ↑2x ↓30%

mm

91
 PAEDIATRIC Criteria ADULT
Large occiput  neck in flexed position Normal size head in relation to thorax height
 achieved neutral position on supine
position without sandbag.

Head size

*Put folded towel under shoulder & neck

Neutral position.
Obligate nose breather (up to 2-3 mo) Nose Breath thru nose and mouth
Larger tongue Appropriate size
*Use proper size oropharyngeal airway device Tongue
drg mask ventilation!
Smaller Mandible Appropriate size
Higher Lower
More anterior (Difficult to view drg DL) 8yo - Adult:
Premature babies: C3 - C5-C6 (VC level)
Larynx
Birth: C1-C2/ Cricoid: C3 - Cricoid: C7
position
*Allow infant to suck, swallow & breath w/o
aspirate!
>2yo: C3-C4 at rest (VC level) / C1 at swallowing
Smaller diameter, Shorter length Larynx size Bigger & longer larynx
Funnel shape Cylinder shape

Airway
shape

*At 8yo  changed shape to cylinder.

Subglottis / Cricoid level
*Use uncuff ETT becoz narrowest part is
Narrowest
cricoid! Glottis/ VC level
part
*Tight fitting ETT will cause EDEMA 
STENOSIS!
Omega shape, long, floppy & narrow Leaf like
Epiglottis
*Use small, straight blade to intubate *Use long, curved blade
Large
*Covering significant portion of posterior Arythenoids Appropriate size
glottis
Vocal
Vocal process same length with vocal fold Vocal process 1/3, vocal fold 2/3
process
Soft and collapse easily Laryngeal
Firmer
*Tends to collapse on forced inspiration! cartilage
Flat, overlap cricoid Thyroid
Firmer
Overlapped by hyoid cartilage

92
 Thyrohyoid & cricothyroid space are
Space Larger
narrow
Submucosa loosely adhere to cartilage
Submucosa Closely adhered to cartilage
- Easily edema!
Laryngeal inlet lying less oblique/ angled Laryngeal
*Greater risk of aspiration! inlet

STRIDOR IN NEONATES & CHILDREN

Anatomic and physiologic considerations

Infant larynx:
- Softer & more pliable
- Larynx more superior and anterior
- Epiglottis is shorter & more angled over glottis
- VC is more slanted (Anterior Commisure is inferior)
- Narrowest part is cricoid ring (Subglottis)
- More prone to collapse, more sensitive to inhalational agents

Infant airway:
- Infant is obligate nasal breather < 2 months
- Tongue is relatively larger
- Trachea is highly compliant (risk of kinking), smaller & shorter:
o Neonates trachea length: 5cm
o 18 months’ trachea length: 7cm

Physiology - Neonate is at risk for RAPID 02 desaturation due to:

1. Higher metabolic rate
o O2 consumption in neonate = 2x adult (6ml/kg)
o Alveolar ventilation in neonate = 2x adult
2. Higher minute ventilation (Va)
o FRC = ERV + RV = 30ml/kg
o TV = 7ml/kg; Dead Space/RV = 2.2ml/kg
o Minute ventilation, Va
 Neonate = 100-150ml/kg/min
 Adult = 60-70ml/kg/min

3. Higher Va : FRC ratio

o Neonate = 5:1 vs Adult = 2:1
o To ↑ FRC:
1. Expiratory braking
- Use of active glottis narrowing during expiration
2.Ongoing active use of inspiratory muscles during expiration
3.Rapid respiratory rates
o Lack of these reflexes (Eg: VC palsy) → biphasic stridor → rapid decompensation 
req intubation/ CPAP.
4. Intercostal muscles and accessory muscles are immature
5. More reliant on diaphragm for inspiration
o Major muscles of ventilation is diaphragm  fatigue easier in resp distress

93
 6. Pliable rib cage  ↓ efficacy of neonate attempts to ↑ ventilation
o Adults can ↑ lungs volume by raising ribs + contracting diaphragm
o Infants ribcage & muscular attachment of diaphragm causes mechanical
disadvantage  because ribs already raised and diaphragm contraction only leads
to small ↑ thoracic cavity volume.
o Ribs are cartilaginous and more horizontal – reducing the effect of the ‘bucket
handle’ movement of the rib cage.

Aetiology of stridor in neonates and children

i. Congenital/ Acquired
ii. Febrile/ Afebrile
iii. Depends on age group, level of obstruction

Congenital Neck Mass

 Dermoid cyst
 Cystic teratoma
 Cystic hygroma
 Lymphangiomas
 Neurofibromas
 Lymphoma
 Hemangioma

Congenital Anomalies
 Choanal atresia
 Vocal Cord palsy
o Most will recover within 2-3 years
o Bilateral VC palsy – mb dt CNS problem
(Eg: Arnold-Chiari, Encephalocele, Myelomeningocele, Hydrocephalus)
o Tracheostomy if persistent stridor with chest recession
o Decision to treat VC surgically should be left for several years
 Laryngomalacia
o Start: 4-6 week
o Worsen: at 6 months to 8 months
o Resolve: by 2 years
 Supraglottic/ Subglottic cyst
 Laryngeal web
 Laryngeal cleft (posterior cleft)
o Type 1: supraglottic
o Type 2: partial cricoid
o Type 3: complete cricoid

94
 o Type 4: extensive up to carina
o Anterior cleft is RARE
o Need to exclude SGS as they may co-exist:
 same pathophysiology  failure decannalization of larynx
 Subglottic stenosis
 Tracheal stenosis
 Tracheoesophageal fistula (ToF)
 Tracheomalacia
 Vascular ring/ sling
o Abnormal formation of the aorta and/or its surrounding blood vessels that encircle
trachea and esophagus.
o Barium swallow: showed oesophageal narrowing
(worthwhile to do Ba swallow in neonate with no obvious cause for stridor)
o Endoscopy: shows pulsatile narrowing of trachea.
o After correction by cardiothoracic  narrowing may persist due to tracheomalacia

Congenital Syndromes
 Pierre-Robin
 Treacher Collin
 Downs Syndrome – Why?
o Big tongue impinges on epiglottis
o a/w laryngomalacia
o Subglottic stenosis
 Goldenhaar
 Cruozon
 Turner
 Apert
 Achondroplasia

ACQUIRED
1. IATROGENIC
- Intubation trauma
- VC palsy
- Subglottic stenosis
- Tracheomalacia

2. INFECTIOUS
- RRP
- Croup/ALTB (laryngotracheitis)
- Epiglottitis
- Tracheitis
- Retropharyngeal abscess

3. INFLAMMATORY
- GERD
- Eosinophilic esophagitis

4. TRAUMA
- Foreign body in airway
- Chemical ingestion
- Inhalational injury
- Laryngo-tracheal trauma (ie: intubation injury, sharp/blunt injury)

95
 5. NEOPLASTIC
- Subglottic hemangioma (PHACE)
o Asymptomatic until 3-6 months when tumor starts to ↑ size
 P - posterior fossa deformity (Dande Walker)
 H - head and neck
 A - arterial malformation (carotid)
 C - cardiac
 E - eyes

6. METABOLIC**
- Beckwith-Wiedemann
- Glycogen storage disease
- Hypocalcemia
- Mucopolysaccharidosis
- Congenital hypothyroidism  Stridor due to:
o Myxedema of larynx
o Thyroid enlarges  compresses trachea

Nasopharyngeal causes of airway obstruction

ACQUIRED
CONGENITAL
Neonates Children
Choana stenosis Syphilis AR
Choana atresia Neonatal rhinitis Adenoditis
Pyriform aperture stenosis FB
Nasal glioma Retropharyngeal abscess
Encephalocele
Meningocele

Laryngeal causes of airway obstruction:

ACQUIRED
CONGENITAL
Neonates Children
Vallecula cyst Intubation trauma Intubation trauma
Laryngomalacia Surgical trauma FB
Laryngeal cyst Laryngotracheal stenosis Fracture
Laryngeal web Arythenoid fixation Epiglottitis
Laryngeal atresia Reflux laryngitis Croup
Laryngotracheal stenosis Bact tracheitis
Posterior laryngeal cleft RRP
Arythenoid fixation Haemangiomas
VC palsy

96
Tracheal causes of airway obstruction:
ACQUIRED
CONGENITAL
Neonates Children
Tracheal stenosis Post intubation & FB
Tracheal atresia endoscopy injury Thyroid
Complete cartilage rings Reflux tracheitis Laryngotracheitis
- Eg: Pfeiffer Sd Tracheal stenosis Mediastinal tumors
Haemangiomas
Tracheobronchomalacia with
TE fistula
Vascular compression
Aberrant innominate artery
Pulmonary artery sling
Double aortic arch

Paediatric stridor can be:

ACUTE CHRONIC
 Croup  Laryngomalacia
 FB  SGS
 Tracheitis  VC palsy
 Retropharyngeal abscess  Laryngeal hemangioma
 Epiglottitis  RRP
 Allergic reaction  Web/ cysts
 Tracheomalacia/ stenosis

97
EVALUATION OF STRIDOR
History
1. Stridor:
a. Age of onset, duration, severity, progression
b. Aggravating & relieving factors & response to them, positioning
c. Quality of cry / voice (hoarseness)
2. Respiratory symptoms
a. Paroxysmal cough/ chronic cough OR choking
b. Cyanotic attack/ apnea
c. Respiratory effort
3. Associated symptoms
a. Feeding difficulties: aspiration, reflux, vomit, drooling
b. Fever
c. Sleep disordered breathing (SDB): snoring
4. Development history
a. Failure to thrive: weight gain, growth chart
b. Development
5. Birth history
a. Antenatal: Maternal condylomata (History of genital warts in pregnancy)
b. Perinatal: Prem/Term, SVD/ LSCS, ETT intubation & duration
6. Past medical history
a. Congenital anomalies
b. Birth marks
c. Cardiac surgery (Eg: PDA ligation)
d. Neurological disease
e. Recurrent pneumonias/ admission to hospital

Examination of a child with Stridor

1. General condition/ inspection:
a. level of consciousness
b. posture/ position
c. cyanosis, toxic/septic looking
d. severity of respiratory distress:
i. grunting
ii. nasal flaring
iii. usage of accessory muscles/ chest recession
- tracheal tug/ SSR, SCR, ICR: Severity
- *better indicator of airway compromise than degree of stridor!
iv. chest abnormality: pectus excavatum, pectus carinatum
e. craniofacial abnormality
i. dysmorphism
ii. jaw (Pierre-Robin) & tongue size (Down Sd)
iii. nasal & oral examination: nasal misting (choana atresia)
f. cutaneous hemangioma
2. Sound:

a. character of cry / voice / cough

b. stridor: type / stertor/ wheezing
3. Vital signs: RR, HR, SpO2, temperature (fever)
4. Palpate: neck mass
5. Auscultate: nose, neck and chest

98
Investigation in a child with Stridor
1) X-ray (neck: lateral & AP/ chest) – Eg; Steeple sign in ALTB

2) Awake fibreoptic assessment / FNPLS

a. Well tolerated outpt procedure  via nose/ mouth with simple restraint
b. Good view of upper airway, supraglottic & VC.
c. Provide dynamic assessment of larynx & VC mobility
d. BUT only allow supraglottic & glottis view, CANNOT exclude lower pathology

3) EUA
a. KIV secure airway (ETT/ Tracheostomy)
b. DLscopy Allow palpation of glottis &
c. Telescopic examination of lower airway visualization of subglottis-
d. Bronchoscopy
trachea
e. Tracheoscopy
f. +/- Oesophagoscopy

4) CT scan / MRI: vascular anomalies

5) ECHO: vascular compression

6) Barium swallow/ pH studies: aspiration in laryngeal cleft, check GERD/reflux

7) +/- swallowing assessment: FEES/ VSS

LARYNGOTRACHEOBRONCHOSCOPY
“… prior to endoscopy, there is no diagnosis.. only impression.. – Cotton”
 LTB is a gold standard, highly technical procedures requiring a team of surgeons,
anaesthetist and nurses.
 Anaesthesia required for airway endoscopy:
o IV induction - for older children
o Gas induction - for infants / poor venous access / those with precarious airway.
 Techniques:
o Intubation technique
 Allow passage of endoscope
 Laryngoscope adjusted
o Non- intubation technique
 Allow to view airway tht hasn’t been altered by passage of ETT
 Methods:
I. Spontaneous respiration
II. Intermittent apnea
III. Paralysis & Jet ventilation
- Short pulses of anaesthetic gas
- Risk of pneumothorax in neonates & smaller children
o Laryngeal mask
 Fibreoptic bronchoscopy
o Tracheostomy tube anaesthesia

99
INDICATIONS FOR ENDOSCOPY
1. Severe stridor
2. Worsening of airway obstruction
3. Airway obstruction  affect feeding, growth & causing failure to thrive
4. Radiological evidence suggests abnormalities
5. To make a diagnosis

COMPLICATIONS
1. Procedure & anaesthesia
2. Loss of airway control
3. Injury to teeth & gum
4. Injury to subglottis
5. Pneumothorax
6. Bleeding
7. Failure to recognize abnormalities

PREPARATION IN OT
1. Fully consented patient & parents
2. Adequate personnel & good communication with anaesthetist
3. Safety equipment: various airways prepared
4. Anaesthetist will ventilate/ intubate – liase to use MLT size 4 (Adult: size 5, 6)  anchored at
right angle of mouth.
5. Formula in airway intubation:
a. ETT size ( > 1 yo) = age/4 + 4 OR size of little’s finger (minus 1 if cuff tube)
b. Anchor at (in cm):
i. Oral intubation: depth from lower lip = age/2 + 12
ii. Nasal intubation: depth from nares = age/2 + 15

6. Laryngoscopes: Lindholm, Hinni (not laser safe, but has suction port), Stinus

7. Suspension set

8. Light source: Y-type, Benjamin light clip

9. Hopkins rod-lens telescope: short & long, diameter:

100
10. Microsurgery forceps:
a. crocodile, cup-forceps, micro-scissors
b. laryngeal probe, sickle-knife
c. laryngeal elevator & spreader
d. optic forceps

11. Bronchoscopes

12. Tracheostomy set with various sizes tube

13. Suction tubes

101
ALGORITHM FOR CHILD WITH STRIDOR

102
 APPROACH TO ADULT STRIDOR IN LARYNGEAL TRAUMA

I will attend to the pt immediately

Establish severity and do resuscitation:

1. Assess severity and pt’s condition (stable/x):
2. ABC:
a. Airway
b. Breathing
- Stridor, tachypneic, respiratory distress, cyanosis
- Huge neck swelling, open neck wound
- Give O2, Intubation or Cricoidotomy/Tracheostomy
c. Circulation
- GCS, Pulse volume (good, thread), V/S (↓BP, ↑/↓HR, Sp02)
3. While assessing, take quick history from medical staff/ family:
a. Mechanism of trauma: high impact/ collision, blunt/ sharp object used/
impact, gunshot, location & timing, onset of stridor.
b. Underlying comorbid: coagulopathy & meds (ie: Aspirin)
c. Allergy history

If patient is NOT stable:

1. Give oxygen supplement
2. IV Steroids
3. Tracheostomy
*If patient already intubated (in case intubated by casualty team), I will
convert to tracheostomy within 24 hours.
4. DL, EUA + KIV proceed

If the patient is stable, I will take further history:

1. Details on mechanism of injury, types of object causing the trauma
(blunt,sharp,penetrating)
2. Airway, respi sx: shortness of breath, noisy breathing (stridor)-onset, progressive
or not, hoarseness, odynophagia
3. Neck swelling: static or rapidly increasing, open wound, bleeding, neck pain.
4. Hemoptysis
5. Dirty surrounding- drain, soil
6. LOC, abdominal pain, chest pain
7. Is the patient just took/consume/inhale chemical, inhalant*
8. Did pt took any medication/food that may cause allergy*
9. History of intubation, thyroid surgery, any H&N malignancy or other malignancy

103
Proceed with examination:
1. Reassess general condition: GCS, pallor, repeat vital signs, any facial trauma/wound/ step
deformity.
2. Voice: hoarseness, stridor (biphasic, insp or exp - to locate site of obstruction).
3. Respiratory distress: unable to complete sentence, breathless, tracheal tug, use of
accessory muscle or chest recession.
4. Neck: swelling, ecchymosis, abrasion/laceration wound, sc emphysema - extension, thyroid
prominence: loss/intact, trachea: central/deviated, laryngeal crepitus: +/-
5. Oral cavity: trauma, bleeding, deformity of mandible, separated palate.
6. Proceed with FNPLS:
- See the supraglottic, glottis, look for presence of mucosal edema: site & severity,
hematoma, abrasion, any exposed cartilage, VC mobility, airway patency - that may
suggest laryngeal trauma, thus can classify according to Schaefer Classification.

Investigations:
1. X-ray: cervical/ chest/pelvic TRO other injury
- Cervical spine injuries must be ruled out in all cases of laryngeal trauma
- Chest: helpful to rule out a pneumothorax, tracheal deviation,or pneumoediastinum (suggesting
an airway injury)

2. CT Neck
(If patient stable, but suspecting laryngeal injury proceed with CT imaging)
- Identify laryngeal fractures and aid in operative planning for the repair and reconstruction of the
fractured larynx
- Detects mucosal edema, disruption of cricoaryteniod/cricothyroid joint, assessment of c-spine
- Reserved for patients in whom laryngeal injury is supected from either history or physical
examination without any indications for immediate surgery.
- Presence of massive edema or hematoma

104
 SCHAEFER GRADING OF LARYNGEAL INJURY
Group Symptoms Signs on FNPLS/ CT Management
1 Minor airway -Minimal hematoma Supportive Tx:
symptoms -Small laceration 1. Observe 48-72 hrs + voice rest
-No detectable fracture 2. Humidified air
3. IV Steroid & elevate head
4. Anti-reflux
5. Antibiotics
2 Airway -Edema/ hematoma Same as Group 1 + BUT often
compromise -Minor mucosal disruption require:
-No exposed cartilage 1. DL + Esophagoscopy
-Nondisplaced fracture on CT 2. Tracheostomy

*serial assessment sb done as

injuries may worsen with time.
3 Airway -Massive edema 1. Tracheostomy
compromise -Mucosa tears +
-Exposed cartilage 2. DL +Esophagoscopy
-Displaced fracture 3. Exploration/ repair
-Immobile VC 4. No stent needed
4 Airway -Same as Group 3 Same as Group 3
compromise + massive trauma to laryngeal +
mucosa Stent required
OR (min 3 months)
+ more than 2 fracture lines
5 Severe Complete laryngotracheal Same as Group 4
Respiratory separation (at cricoid level)
Distress -at Cricothyroid membrane
-at Cricotracheal junction

Indications for surgery:

1. Injuries involving the anterior commissure, exposed cartilage, multiple or displaced fracture of
thyroid cartilage, multiple fractures of cricoid cartilage
2. All injuries causing vocal fold paralysis +/- airway compromise till require intubation or
tracheostomy
3. Injury to neck requiring exploration-penetrating injury, dirty wound

Principles of surgery:
1. Exploration within 24hrs – maximizes airway & phonation results
2. Hemostasis
3. Evacuation of hematoma
4. Reconstruction of the laryngeal framework
5. Coverage of de-epithelialized surfaces

105
References:
1. Prof Dr Goh Bee See, UKMMC slides from 1st ORL-HNS PG Workshop 2013
2. Prof Dr Anura Michelle Manuel, UMMC slides
3. M Gleeson et al. Scott- Brown’s Otorhinolaryngology, Head and Neck Surgery, 2008 Great
Britain: Hodder Arnold.
4. MM Lesperance, PW Flint. Cumming’s Paediatric Otolaryngology, 2015 Canada: Elsevier
Saunders.
5. CD Bluestone, JP Simons, GB Healy. Bluestone and Stool’s Pediatric Otolaryngology, 2014
Connecticut: People’s Medical Publishing House – USA.
6. RT Colon, JS Reilly. Stridor and airway obstruction. Pediatric Otolaryngology 1st ed.
Philadelphia, PA: W.B. Sauders; 1983:1190-1214.
7. Notes from Dept of ORL-HNS, UKMMC’s Post Mortem Part II (Nov 2018)
8. GC Sahoo, Emergencies in Otorhinolaryngology 1st edition 2014, Chapter 2, Page 13

106
3.DEEP NECK SPACE INFECTIONS

ANATOMY
Cervical fascia — The muscles, vessels, and visceral structures of the neck are enveloped by the
cervical fascia, which has a superficial and deep component.

The superficial cervical fascia consists of the subcutaneous tissues of the neck, which completely
enclose the head and neck and is continuous with the platysma anteriorly.

Figure 1: (A) Sagittal section of the neck.

(B) Coronal section at the level of C7.
Adapted with permission from: Chow, AW. Life-threatening infections of the head, neck, and
upper respiratory tract. In: Principles of Critical Care, 2nd ed. Hall, JB, Schmidt, GA, Wood, LH
(Eds), McGraw-Hill, New York 1998. p.888. Copyright © 1998 McGraw-Hill.

107
The deep cervical fascia has 3 layers: superficial, middle, and deep (series of cylindrical
compartments that extend longitudinally from the base of the skull to the mediastinum) (figure 1):
1. Superficial or investing layer:
• encloses all of the deeper parts of the neck
• begin at the nuchal line and extending anteriorly, dividing to enclose the
trapezius, SCM, and strap muscles as well as the submaxillary and parotid
glands.
2. Middle or pretracheal fascia:
• encloses the cervical viscera including the pharynx, esophagus, larynx, trachea,
thyroid, and parathyroid glands.
3. Deep or prevertebral fascia:
• arises from the nuchal ligament and encloses the vertebral column and muscles
of the spine.

The prevertebral fascia originates posteriorly on the spinous processes and encircles the splenius,
erector spinae, and semispinalis muscles (figure 1 and figure 2).

Prior to completing its circle anterior to the vertebral bodies, it fuses to the transverse processes. At
this point, it is split into two layers: the alar fascia anteriorly and the prevertebral fascia posteriorly.

The "danger" space lies behind

the anatomic retropharyngeal
space. It is a potential space that
provides a path for
retropharyngeal infections to
extend into the mediastinum.

All three layers of the deep cervical fascia contribute to the carotid sheath, which forms a
neurovascular compartment that encloses the carotid artery, the internal jugular vein, and the vagus
nerve.

108
 Fascial spaces — 3 spaces between the planes of the deep cervical fascia that has major clinical
importance (9 spaces in total):
• The submandibular space
• The parapharyngeal space
• The retropharyngeal space

1. Submandibular space — lies within the submental and submandibular triangles between the
mucosa of the floor of the mouth and the superficial layer of the deep cervical fascia.
a. subdivided by the mylohyoid muscle:
i. sublingual space (contains the sublingual gland, hypoglossal nerve, part of the
submandibular gland, and loose connective tissue).
ii. the submylohyoid space (a.k.a the submaxillary space- contains the submandibular
salivary gland and lymph nodes)
b. the 2 divisions communicate posteriorly around the mylohyoid muscle.
c. It is this space that is primarily involved in Ludwig’s angina.
i. infection within the sublingual space results in gross swelling of the tongue that can
result in acute airway obstruction.
ii. Infection of the submylohyoid space may spread posteriorly along the styloglossus
muscle into the parapharyngeal space and continue to spread into the loose areolar
tissue of the retropharyngeal space, and then further inferiorly into the superior
mediastinum.

109
2. Parapharyngeal space — a.k.a the lateral pharyngeal or pharyngomaxillary space,
a. the space is in the lateral aspect of the neck, is shaped like an inverted cone, with its base at
the skull and its apex at the hyoid bone.

b. lies deep to the pharyngeal constrictor muscle and is contiguous medially with the pretracheal
fascia of the visceral compartment, and laterally with the superficial fascia (invests the parotid
gland), the internal pterygoid muscle, and the mandible.

c. The parapharyngeal space is divided into:

i. anterior (prestyloid or muscular) compartment.
ii. posterior (retrostyloid or neurovascular) compartment by the styloid process.

d. The anterior compartment contains no vital structures but rather only fat, lymph nodes,
connective tissue, and muscle.
i. most closely related to the tonsillar fossa and the internal pterygoid muscle

e. The posterior compartment contains the CN 9 to CN 12 superiorly and the CN 10 more

inferiorly, the carotid sheath and its contents, and the cervical sympathetic trunk.
i. the carotid sheath, which runs in the posterior aspect of the parapharyngeal space,
pierces the cone at its apex to enter the mediastinum.

f. Infection of the parapharyngeal space may result from pharyngitis, tonsillitis, parotitis, otitis,
or mastoiditis, as well as odontogenic infections, especially if the masticator space is involved.

110
3. Retropharyngeal space — The retropharyngeal space is bound (Figure 1):
a. anteriorly by the constrictor muscles of the neck
b. posteriorly by the alar layer of the deep cervical fascia.
c. It is situated behind the hypopharynx and the esophagus, and lies between the alar fascia
posteriorly and the posterior aspect of the pretracheal fascia anteriorly
d. It communicates with the parapharyngeal space laterally where the carotid sheaths reside.

4. Danger space — Posterior to the retropharyngeal space is the danger space (Figure 1).
a. bound by the alar fascia anteriorly and the prevertebral fascia
b. extends from the BOS and descends freely through the entire posterior mediastinum to the
level of the diaphragm (T1 to T2) where the two fascia layers fused.
c. the danger space provides the most important anatomic route for contiguous spread between
the neck and the chest**.

111
5. Prevertebral space — bound by the prevertebral fascia.
a. originates posteriorly on the spinous processes and encircles the splenius, erector spinae, and
semispinalis muscles (Figure 1).
b. Prior to completing its circle anterior to the vertebral bodies, it fuses to the transverse
processes.
i. At this point, it is split into two layers: the alar fascia anteriorly and the prevertebral
fascia posteriorly.
c. The prevertebral space extends from the BOS to the coccyx, thus allowing organisms to spread
as far down as the psoas muscle sheath.

6. Pretracheal space — comprises the anterior portion of the visceral compartment and completely
surrounds the trachea and esophagus (Figure 1).
a. It is contiguous with the carotid sheath laterally and with the superior mediastinum inferiorly.

7. Peritonsillar space — lies between the capsule of the palatine (faucial) tonsil medially, the superior
constrictor muscle laterally, and the tonsillar pillars anteriorly and posteriorly.
a. A dreaded complication of a peritonsillar abscess (Quinsy) is to rupture through the superior
constrictor muscle and extend directly into the parapharyngeal space, which lies posterior to
the tonsillar bed.

8. Parotid space — formed by the splitting of the investing fascia at the level of the stylomandibular
ligament to enclose the parotid gland within a superficial capsule and a deep capsule.
a. The superficial capsule is thick and strong, tightly adherent to the superficial pole of the
parotid gland.
b. The deep capsule adjacent to the dorsal lobe of the parotid gland, however, is thin and
infection in the gland can easily penetrate through this capsule and extend through the
stylomandibular tunnel into the parapharyngeal space.
c. The stylomandibular ligament effectively separates the parotid space from the submylohyoid
space.

112
9. The masticator space - lies lateral and anterior to the parapharyngeal space and consists of the
masseteric, pterygoid, and temporal spaces (not described in details in this note).
a. infection of the masticator space arises most frequently from molar teeth, particularly the
third molars (wisdom teeth).

113
Lymph nodes — The lymph nodes of the head and neck can be divided into 10 principal groups.
o Six of these (occipital, mastoid, parotid, facial, submandibular, and submental
nodes) form a collar at the junction of the head and neck.
o Within this collar, the sublingual and retropharyngeal nodes lie near the base of the
tongue.
 The anterior and lateral cervical nodes form a chain along the front and side of the neck,
respectively.
o The lateral cervical chain serves as a common root for drainage.
 The final conduit from all lymphatics in the head and neck is the large deep chain situated
along the carotid sheath.
 When inflamed, these nodes become adherent to the fascial sheath of the vessels; thus, a
suppurative infection of the cervical lymph nodes may frequently invade the bloodstream.

 The aggregation of lymphoid tissues surrounding the nasopharynx = Waldeyer's ring.

o comprises the palatine, lingual, adenoidal, and tonsillar lymphoid tissues.
o Acute inflammation such as acute tonsillopharyngitis, croup, otitis media,
retropharyngeal abscess or Epstein-Barr virus mononucleosis, may result in acute
airway compromise and constitutes a medical emergency.

Potential routes of spread — The deep cervical fascial spaces bound together by loose connective
tissue and intercommunicate to varied degrees.
 Figure below provides valuable information on the nature and extent of infection and also
suggests the optimal surgical approach for effective drainage.

114
115
MICROBIOLOGY
 Deep neck space infections are typically polymicrobial and normal flora
 Anaerobes > aerobes on all mucosal surfaces of the oral cavity by 10:1.
 The most common organisms:
o iridans streptococci (abundant in mouth).
 Staphylococcus aureus and facultative gram-negative rods like Pseudomonas aeruginosa and
extended-spectrum beta-lactamase (ESBL)-producing Enterobacteriaceae →patients with
risk factors (immunocompromised hosts, diabetes mellitus, postoperative infection, or
trauma).
 Infections arising from the pharynx frequently contain oral anaerobes and facultative
streptococci → Streptococcus pyogenes.
 Infections of the prevertebral space usually originate from contiguous spread of a cervical
spine infection (eg: discitis or vertebral osteomyelitis), by local instrumentation of the
trachea or esophagus, or by hematogenous spread.
o predominance of gram-positive organisms (most common- Staphylococcus aureus).
o less common organisms: facultative gram-negative bacilli, mycobacteria, and fungi.
o the microbiology of prevertebral space infections is quite different from that of
retropharyngeal or odontogenic deep neck infections.

GENERAL CLINICAL MANIFESTATIONS

 Because of the dense superficial layer of the deep cervical fascia and its musculofascial
planes, a fluctuant mass is not readily appreciated in deep neck space infections.
 Palpation of the oral cavity may help in identifying such a mass or focal tenderness.
o The characteristic signs of deep pus are pitting or a doughy feeling on firm deep
palpation.
 Specific sites of infection are often associated with characteristic clinical manifestations and
physical findings:
o Peritonsillar, parotid, parapharyngeal, and submandibular abscesses:
 sore throat and trismus (the inability to open the jaw).
 trismus indicates pressure or infection affecting the muscles of mastication
(the masseter and the pterygoids) or involvement of the motor branch of
the trigeminal nerve.
 findings on physical examination: swelling of the face and neck, erythema,
and purulent oral discharge. There may be pooling of saliva in the mouth
and asymmetry of the oropharynx. Lymphadenopathy is usually present.
o Dysphagia and odynophagia = inflammation of the cricoarytenoid joints.
o Dysphonia and hoarseness are late findings in neck infections = involvement of CN
10.
o Unilateral tongue paresis = involvement of the twelfth cranial nerve.
o Stridor and dyspnea = airway obstruction and may be manifestations of local
pressure or spread of infection to the mediastinum.

116
 IMAGING
 Computed tomography (CT) = imaging of choice for the diagnosis of deep neck space
infections.
o allows the critical evaluation of soft tissues and especially bone from a single
exposure
o can localize a process and define its extent, particularly extension into the
mediastinum or the cranial vault.
o for planning and guiding aspiration for culture or open drainage.

 Magnetic resonance imaging (MRI) = assessing the extent of soft tissue involvement and
for delineating vascular complications (not frequently done).
 Plain radiography = limited use.
o it is sometimes helpful for detecting retropharyngeal swelling or epiglottitis.

SPECIFIC DEEP NECK SPACE INFECTIONS

1. Peritonsillar abscess (quinsy)
 is a suppurative complication of acute tonsillitis with extension into the peritonsillar space.
 peritonsillar space consists of loose areolar tissue overlying the tonsil and is surrounded by
the superior pharyngeal constrictor muscle and the anterior and posterior tonsillar pillars.
 may affect patients of all ages but are most common among young adults between the ages
of 15 and 30 years.
 cellulitis →abscess formation (most commonly near the superior pole of the tonsil).
 c/o: high fever, odynophagia, unilateral sore throat, and otalgia.
 classic signs: muffled voice, trismus, unilateral deviation of the uvula towards the unaffected
side, and soft palate fullness or edema.
 oral airway may be compromised, and drooling may occur.
 often polymicrobial= predominantly Streptococcus pyogenes (group A streptococcus) and
oral anaerobes.

2. Parotid space infections

 acute suppurative parotitis = the sudden onset of unilateral induration and erythema that
extends from the cheek to the angle of the jaw.
 parotid gland swollen and extremely tender.
 purulent discharge when gentle compression around parotid duct (Stensen's duct).
 3 factors predispose to suppurative parotitis:
i) acutely diminished salivary flow.
ii) poor oral hygiene.
iii) increased susceptibility to infection
 typically seen in elderly, debilitated, and/or dehydrated patients who may be diabetic or
taking anticholinergic medications that decrease salivary flow.
 often polymicrobial
i) Staphylococcus aureus is commonest, but anaerobes are also common.

117
3. Submandibular space infections (Ludwig's angina)
 Ludwig's angina = bilateral infection of the submandibular space (which includes the
submylohyoid and sublingual spaces)
 begins in the floor of the mouth, most commonly related to the second or third mandibular
molar teeth.
 often polymicrobial infection involving the flora of the oral cavity.
 aggressive, rapidly spreading "woody" or brawny cellulitis without lymphadenopathy.
 airway compromise is a potential complication
 requires careful monitoring and rapid intervention to prevent asphyxia and aspiration
pneumonia.

4. Pretracheal space infections

 as a consequence of perforation of the anterior esophageal wall, occasionally through
contiguous extension from a retropharyngeal space infection, or as a consequence of
prolonged tracheostomy.
 Clinically = severe dyspnea, but hoarseness may be the first complaint. Swallowing may be
difficult, and fluids may be regurgitated through the nose.
 always serious because of impending airway obstruction and possible extension into the
mediastinum.

5. Prevertebral space infections

 predominance of gram-positive organisms (most common Staphylococcus aureus).
 less common organisms include various facultative gram-negative bacilli, mycobacteria, and
fungi.
 CT or MRI is helpful for differentiating a prevertebral space infection from a retropharyngeal
abscess.
 complications of prevertebral space infections arise from spinal epidural collections that
cause cord compression → irreversible paralysis.
 prevertebral space extends from the BOS to the coccyx and is contiguous with the psoas
muscle sheath, seemingly distant abscesses can form within the psoas muscle.

6. Parapharyngeal space infections

 potentially life-threatening if involve carotid sheath and its contents (eg: common carotid
artery, internal jugular vein, vagus nerve), airway impingement, and bacteremic
dissemination.
 dental infections are the most common underlying cause, followed by peritonsillar abscess,
and rarely parotitis, otitis, or mastoiditis (Bezold's abscess).
 infection of the anterior compartment is more common than the posterior compartment
 cardinal clinical features of parapharyngeal space infections are:
i) Trismus
ii) Induration and swelling below the angle of the mandible
iii) Medial bulging of the pharyngeal wall
iv) Systemic toxicity with fever and rigors.
 dyspnea may be prominent as edema and swelling involve the epiglottis and larynx.
 swelling of the pharyngeal wall will be behind the palatopharyngeal arch and is easily
missed.
 suppuration may advance quickly to other spaces, particularly to the retropharyngeal and
"danger" spaces, possibly reaching the mediastinum inferiorly or the BOS superiorly.

118
 abscess localized to the posterior neurovascular compartment of the parapharyngeal space
→ septicemia and neurologic signs (d/t cranial nerve involvement) (eg, Horner syndrome,
hoarseness, unilateral tongue paresis) but with minimal trismus.
 posterior tonsillar pillar is displaced.
 swelling and displacement of the parotid gland usually in infection of anterior or posterior
compartment.
 Diagnosis — CT or MRI.
 Complications
i) Carotid sheath involvement → potential for carotid artery erosion and suppurative
jugular thrombophlebitis. May be d/t spread from the parapharyngeal space,
submandibular space (Ludwig's angina), or suppuration of the deep cervical lymph
nodes.
 no characteristic symptoms or signs of a carotid sheath infection.
 may be a latent period of up to three weeks before obvious manifestations of a
deep neck space infection develop.
 presents either in a toxic condition or insidiously with a fever of undetermined
origin.
 trismus is absent, and signs of local suppuration may be subtle initially because of
the tight connective tissue around and within the carotid sheath.
 some patients, there is diffuse swelling along the sternocleidomastoid muscle with
marked tenderness and torticollis to the opposite side.
 erosion of the carotid artery arises from an arteritis due to contiguous inflammation,
resulting eventually in the formation of a false aneurysm, which may rupture.
(a) Erosion and rupture of the carotid artery may be heralded by recurrent small
hemorrhages from the nose, mouth, or ear ("herald bleeds").
(b) followed by hematoma formation in the surrounding tissues, a protracted
clinical course, and eventually the onset of shock.
(c) ligation of the carotid artery may be necessary in cases of major hemorrhage,
but the mortality rate remains high, and the risk of stroke is significant.
 Suppurative jugular thrombophlebitis a.k.a Lemierre's syndrome or postanginal
sepsis) should be suspected in patients with antecedent pharyngitis, septic
pulmonary emboli, and persistent fever despite antimicrobial therapy.
(a) caused most commonly by Fusobacterium necrophorum (often present in the
bloodstream).

119
7. Retropharyngeal and danger space infections
 among the most serious of deep space infections.
 can extend directly into the anterior or posterior regions of the superior mediastinum, or
into the entire length of the posterior mediastinum via the danger space (
 can occur in both children and adults.
 clinical features and diagnosis
i) Infection may reach the retropharyngeal space from either local or distant sites.
ii) Penetrating trauma (eg, from chicken bones or following instrumentation) →a sore
throat or difficulty in swallowing or breathing may be the first indication of infection.
iii) More distant sources of infection include odontogenic sepsis and peritonsillar abscess
(now a rare cause).
iv) differential diagnosis: cervical osteomyelitis, Pott's disease, meningitis, and calcific
tendonitis of the long muscle of the neck
v) CT scans and/or x-rays of the lateral neck → demonstrate cervical lordosis with swelling
and gas collections in the retropharyngeal space, causing anterior displacement of the
larynx and trachea.
 increased thickness of the prevertebral soft tissues (normal ~5mm deep), air or air-
fluid levels, and the presence of foreign bodies.
 pharynx or upper airway is displaced anteriorly by more than one half the width of
the C4 vertebral body.
 help to differentiate retropharyngeal from prevertebral space infection arising from
cervical vertebral osteomyelitis
 Complications
(a) Acute necrotizing mediastinitis (most feared).
(i) infection in the "danger" space between the alar and prevertebral fasciae
may drain by gravity into the posterior mediastinum, resulting in
mediastinitis and empyema
(ii) with the introduction of antibiotics, mediastinal extension has become
uncommon.
(iii) Clinically, the onset of acute necrotizing mediastinitis is rapid and is
characterized by the following:
1. Widespread necrotizing process extending the length of the posterior
mediastinum, occasionally into the retroperitoneal space.
2. Rupture of mediastinal abscess into the pleural cavity with empyema or
development of loculations.
3. Pleural or pericardial effusions, frequently with tamponade.
(iv) mortality of acute necrotizing mediastinitis in adults is high (25%), even
when appropriate antibiotics are administered.
(b) Aspiration pneumonia: result from impairment of swallowing or spontaneous
rupture of the abscess into the airway.

120
TREATMENT
1. Peritonsillar Abscess (PTA).
 Antibiotic therapy —
i) Parenteral — Empiric therapy include coverage for Group A streptococcus, Staphylococcus
aureus and respiratory anaerobes. Empiric regimens:
 Ampicillin-sulbactam intravenously (50 mg/kg per dose [maximum single dose 3 g]
every 6 hours in children; 3 g every 6 hours in adults).
Or
 Clindamycin intravenously (13 mg/kg per dose [maximum single dose 900 mg] every
8 hours in children; 600 mg every 6-8 hours in adults).
 IV vancomycin or linezolid should be added to empiric treatment if do not respond
to initial treatment or in those patients who present with moderate or severe
disease (eg, toxic appearance, temperature >39°C, drooling, and/or respiratory
distress), to provide optimal coverage for potentially-resistant Gram-positive cocci.
ii) Oral — Once patient is afebrile and clinically improved. Oral antibiotic given to complete
a 14-day course. Courses shorter than 10 days may be associated with recurrence.
 Amoxicillin-clavulanate (45 mg/kg per dose [maximum single dose 875 mg] every 12
hours in children; 875 mg every 12 hours in adults).
Or
 Clindamycin (10 mg/kg per dose [maximum single dose 600 mg] every 8 hours in
children; 300 to 450 mg every 6 hours in adults).

If empiric therapy is employed for presumed MRSA infection, regimens can include:
 Clindamycin (10 mg/kg per dose [maximum single dose 600 mg] every 8 hours in
children; 300 to 450 mg every 6 hours in adults), unless isolate is resistant.
 Linezolid (<12 years: 30 mg/kg per day in 3 doses; ≥12 years: 20 mg/kg per day in 2
doses in children; 600 mg twice per day in adults; maximum daily dose 1200 mg).

 Drainage — PTA usually requires surgical drainage through needle aspiration, incision and
drainage, or tonsillectomy.
i) Needle aspiration —performed in the outpatient setting with topical anesthesia.

ii) Incision and drainage —In older children, it may be performed in the outpatient setting
with topical anesthesia or procedural sedation; general anesthesia is usually required for
young children.

121
 iii) Tonsillectomy — Possible indications for tonsillectomy in patients with PTA:
 Significant upper airway obstruction or other complications.
 Previous episodes of severe recurrent pharyngitis or PTA (each of which predicts the
possible recurrence of PTA).
 Failure of the abscess to resolve with other drainage techniques.

2. Suppurative parotitis.
 For immunocompetent patients without risk factors for MRSA:
i) Nafcillin (1.5 g IV every 4 hours) or another antistaphylococcal penicillin or a first-
generation cephalosporin plus either:
 Metronidazole (500 mg IV every 6-8 hours) or clindamycin (600 mg IV every 6-8
hours).
 For immunocompetent patients with risk factors for MRSA:
i) vancomycin (15 to 20 mg/kg IV every 12 hours) or linezolid (600 mg orally or IV every 12
hours) be substituted for nafcillin.
 For immunocompromised patients:
i) Vancomycin (15 to 20 mg/kg IV every 8 to 12 hours, not to exceed 2 g per dose) or
linezolid (600 mg orally or IV every 12 hours) plus one of the following:
 Cefepime (2 g IV every 12 hours) plus metronidazole (500 mg IV every six to eight
hours) or
 Imipenem (500 mg IV every 6 hours) or
 Meropenem (1 g IV every 8 hours) or
 Piperacillin-tazobactam (4.5 g IV every 6 hours).
 Step-down to an oral regimen may be considered once the patient has improved and
surgical management is deemed unnecessary.
 The duration of therapy depends on the host immune status, severity and extent of
infection, and response to therapy.
 For uncomplicated suppurative parotitis, a total duration of 10 to 14 days is
reasonable.

3. Ludwig's angina.
 Immunocompetent hosts:
i) Ampicillin-sulbactam (3 g IV every 6 hours) or
ii) Penicillin G (2 to 4 MU IV every 4-6 hours) plus metronidazole (500 mg IV every 6-8
hours) or
iii) Clindamycin (600 mg IV every 6-8 hours)
 Immunocompetent patients with increased risk for MRSA
i) vancomycin (15 to 20 mg/kg IV every 8 to 12 hours, not to exceed 2 g per dose) or
ii) linezolid (600 mg orally or IV every 12 hours).
 Immunocompromised hosts:
i) Cefepime (2 g IV every 12 hours) plus metronidazole (500 mg IV every 6-8 hours) or
ii) Imipenem (500 mg IV every 6 hours) or
iii) Meropenem (1 g IV every 8 hours) or
iv) Piperacillin-tazobactam (4.5 g IV every 6 hours)
 Immunocompromised patients with increased risk for MRSA:
i) vancomycin (15 to 20 mg/kg IV every 8 to 12 hours, not to exceed 2 g per dose) or
ii) linezolid (600 mg orally or IV every 12 hours).

122
  Abx therapy should be continued for 2-3 weeks until clear evidence of clinical improvement
is present, and fever and leucocytosis have subsided.
 Longer courses are required when complications are present.
 If not responding adequately to antibiotics alone after this initial period, or if fluctuance is
detectable or a collection is observed on imaging, needle aspiration or a more formal
incision and drainage procedure under general anesthesia should be performed.

4. Prevertebral space infections.

 Immunocompetent host:
i) Nafcillin (1.5 g IV every 4 hours) or vancomycin (15 to 20 mg/kg IV every 8 to 12 hours,
not to exceed 2 g per dose), plus either:
 Gentamicin or tobramycin (1.7 mg/kg IV every 8 hours or 5 mg/kg IV every 24
hours), or
 Ciprofloxacin (400 mg IV q12h).
 Immunocompromised host:
i) Vancomycin (15 to 20 mg/kg IV every 8 to 12 hours, not to exceed 2 g per dose) or
linezolid (600 mg orally or IV every 12 hours) plus either:
 Cefepime (2 g IV every 12 hours) plus metronidazole (500 mg IV every 6-8 hours) or
 Imipenem (500 mg IV every 6 hours) or
 Meropenem (1 g IV every 8 hours) or
 Piperacillin-tazobactam (4.5 g IV every 6 hours).

 Duration:
i) For uncomplicated prevertebral space infections without evidence of discitis or
osteomyelitis: 2-3 weeks of therapy is adequate.
ii) When adjacent osteomyelitis is present, at least 6-8 weeks of IV antibiotics is necessary.

5. Parapharyngeal or retropharyngeal space infection.

 Drainage.
i) Open surgical drainage has been the traditional approach to abscess management.
 Well-defined deep neck space infections without airway compromise= ultrasound-
guided needle aspiration.
 In retropharyngeal space infection complicated by acute necrotizing mediastinitis,
surgical drainage of the mediastinum is required and may be performed by either
the cervico-mediastinal or the transthoracic approach.
 Antimicrobial selection.
i) Oral or odontogenic source:
 Ampicillin-sulbactam (3 g IV every 6 hours) or
 Penicillin G (2 to 4 MU IV every 4-6 hours) plus metronidazole (500 mg IV every 6-8
hours) or
 Clindamycin (600 mg IV every 6-8 hours).
ii) Rhinogenic or otogenic source:
 Ampicillin-sulbactam (3 g IV every 6 hours) or
 Ceftriaxone 1 g IV every 24 hours plus metronidazole 500 mg IV every 6-8 hours or
 Doxycycline (200 mg IV per day in 1 or 2 divided doses).
iii) Immunocompromised host:

123
  Cefepime (2 g IV every 12 hours) plus metronidazole (500 mg IV every six to eight
hours) or
 Imipenem (500 mg IV every 6 hours) or
 Meropenem (1 g IV every 8 hours) or
 Piperacillin-tazobactam (4.5 g every 6 hours).
 Duration — Therapy should generally be continued for 2-3 weeks for parapharyngeal or
retropharyngeal space infections until fever and leukocytosis have resolved and local
tenderness and swelling have subsided. Longer courses are required when complications are
present.

124
 4.Vertigo
Definitions:
 Balance: complex interaction between vestibular, ocular, proprioceptive and CNS to
maintain head and body position in relation to the environment
 Dizziness: nonspecific term which includes sense of imbalance, light-headedness, floating
sensation or vertigo
 Vertigo: a hallucination of movement which is either rotatory or translational, cardinal
symptom of vestibular disorder
 Nystagmus: an involuntary movement of the eyes due to the disturbance of vestibule-ocular
reflex

Dizziness

True vertigo Psychogenic

-hallucination of -lengthy story does not fit into any disease;
movement depressed, anxious patient

Vestibular cause

Non vestibular cause

Peripheral Central
 Acute peripheral vestibular  CVA
disorder:  CPA tumour
 Multiple  Medication
-Meniere’s disease
History taking:  Cardiovascular:
 neuronitis
-Vestibular Dizziness symptoms sclerosis
 Arnold Chiari postural hypotension,
-Labyrinthitis  Vertigo:
-Autoimmune inner ear dx Malformation ischaemic heart
-ototoxicity  Vestibular disease, arrhythmias
 Mechanical disturbance of migraine*  Haematological:
SCC anaemia
 Endocrine /metabolic:
-BPPV, perilymh fistula,
diabetes, thyroid
superior SCC dehiscience
disease, addison’s
 Chronic vestibular disorder
disease
 General medical: UTI,
AGE
 Obstetric: pregnancy
 Orthopaedic: cervical
vertigo

125
 Spontaneous Triggered

∗ internal vertigo, a false sensation of self motion – positional vertigo, occurring after a change
∗ external vertigo, a false sensation that the of head position,
visual surround is spinning or flowing – visually-induced vertigo, triggered by a
complex or large moving visual stimulus
– head motion-induced vertigo, occurring
during head motion

 Imbalance/unsteadiness

 History of the symptoms:

 description: spinning,presyncope, dysequilibrium
 onset: sudden/chronic
 duration: seconds, hours, days
 frequency: acute, episodic, persistent
 aggravating factors: position, loud sounds, coughing, stress, fatigue

 Ear symptoms- hearing loss, aural fullness, tinnitus, autophony ,otalgia/otorrhea

 Associated symptoms:
-Nausea/vomiting
-Headaches/heaviness
-Visual aura
-sensory amplification: photophobia/phonophobia/odour sensitivity/heat sensitivity
-neurological symptoms: visual disturbance, numbness, weakness, dysphagia/slurred speech

 Impact on ADLs and QOL-rated “moderate” when they interfere with but do not prohibit
daily activities and “severe” if daily activities cannot be continued.

 Past medical history

 Cardiovascular, endocrine, migraine, previous ontological/neurosurgical procedure

 Drug history
 Ototoxic medication: vestibulotoxicity(damage vestibular apparatus-cause vertigo)
or cochleotoxicity (damage to cochlear-cause hearing loss and tinnitus)
 CNS depressant: anti epileptic medication, transquilizer, alcohol
 Drug causing orthostatic hypotension: alpha /beta blockers

126
Physical examination
1)General examination:
 Blood pressure/pulse: irregular hear beat/arrhythmia
Postural hypotension: measured in supine position and again 1 minute after the patient
stands
-SBP drop of 20mmhg, DBP drop 10mmhg or pulse increase of 30 bpm indicative of
orthostatic hypotension
 Temperature
 Pallor

2)ENT examination:
Complete ENT examination (otoscopy, hearing assessment, cranial nerve examination)

3)Neuro-otology examination:

Test Peripheral Central

Spontaneous/gaze evoked nystagmus + +

Oculomotor test
a) fixation +
b) smooth persuit +
c) saccades +
d) convergence +

Special vestibular test (VOR)

a) Head shake test +
b) Halmagyi head thrust +

Test for vestibulospinal tract(VST) Fall towards + broad base gait in

a) Gait affected site cerebellar stroke
b) Romberg test

Cerebellar test
a) past pointing +
b) dysdiadokokinesia +

Test for mechanical disorder of SCC

a)dix hallpike +
b)fistula test +

127
 4) Peripheral nervous system: power, tone and reflexes

ALEXANDER’S LAW

Nystagmus of acute peripheral vestibular origin(vestibular neuronitis/MD/labyrinthitis) must

obey Alexander’s law
 Law 1
-direction of peripheral nystagmus away from hypofunction side(fast phase is always in one
direction irrespective of the gaze direction)
 Law 2
-peripheral nystagmus most intense when gaze is away from the hypofunction side(fast phase
is away from the lesion side)
 Law 3
-visual fixation will reduce intensity of peripheral nystagmus

*Alexander’s law does not apply to SCC lesion eg BPPV,Superior SCC dehiscent syndrome and
perilymph fistula

Degree of nystagmus

*nystagmus in acute peripheral vestibular lesion is initially observed in 3 directions of gaze(center

and eccentric position of both side with the most intense away from the hypofunction side)-3rd
degree nystagmus
Over time , it is sequentially observed in 2 directions (2nd degree)-midpoint and away
1st degree-away from the lesion side.

Drug associated with dizziness

Differences of peripheral and central spontaneous nystagmus

128
Differences in BPPV and Central nystagmus

Peripheral Central
Duration Temporary Permanent
Character Unidirectional Multidirectional/direction
changing with gaze

Conjugate(both eyes same Dysconjugate

direction)

Horizontal Vertical
Optic fixation Intensity reduced Unchanged
Removal of optic fixation Enhances Inhibits/unchanged
BPPV Central
Latency 2-20 seconds None, begins immediately
Duration Lasts up to 1 min persists
fatigability Yes No
Vertigo Present Absent
Direction of nystagmus Unidirectional, conjugate Variable ,direction changing

Features differentiating central from peripheral causes of vertigo

Central Peripheral
Imbalance Severe, mostly constant Mild to moderate, mostly
episodic
Neurologic symptoms Frequent Rare
Nystagmus Changes direction in different Unidirectional in all gaze
gaze positions positions

No change with visual fixation Decrease with visual fixation

Hearing loss Rare Frequent
Nausea Variable, may be absent Severe
Recovery by central Slow Rapid
compensation

129
Investigation:
 Blood invstigations:
 FBC
 Cardiac enzymes
 Renal profile
 FBS
 TFT
 VDRL
 Autoimmune screening
 ECG

 PTA

 MRI

 Special vestibular investigations

 Videonystafmography(VNG)/electronystagmography(ENG)
– assess oculomotor functions, allow objective assessment of eye movements
– able to differentiate between peripheral and central vestibular disorder.

 Video head impulse test (VHIT)

– computer based video assessment of eye movements with horizontal and
vertical head impulse test
– identify pathology affecting SCC and its nerve supply eg vestibular neuritis

 Vestibular Evoked Myogenic Potentials (VEMP)

– -evaluates inferior vestibular nerve which innervates saccule and posterior SCC
– -useful in diagnose superior SCC dehiscience/vestibular neuronitis(where there
is inferior vestibular nerve involvement),monitoring intratympanic gentamicin
therapy for MD.

 Caloric testing
– test for lateral SCC
– patient supine with head elevated 30 0 to bring horizontal SCC to vertical plane
– inspect the ear,irrigate water at 440C for 40 secs, wait for 5 minutes, then at
300C
– the direction of the fast phase of nystagmus follows the mnemonic:
o COWS: Cold Opposite Warm Same

 Electrocochleography (ECochG)
– variant of ABR, sound stimulation is provided but recording electrode is placed
closed to (AP) Action Potential (compound action potential of the auditory
nerve)
– (SP) Summating Potential (response of the cochlear to sound stimulation)
– used to diagnose Meniere’s Disease and endolymphatic hydrops where the
SP/AP ratio is greater than 0.5

130
Principles of Management:
 Acute management(symptomatic treatment)
– initially given to acutely vertiginous patient with nausea and vomiting
– vestibular suppressants and anti-emetics
– usually given for 3-5 days only as prolonged treatment can delay central compensation
Symptomatic (acute attacks)
Vestibular sedatives Benzodiasepines: diazepam, lorazepam
Antihistamine:dimenhydrinate
Anticholinergics : scopolamine
Anti-emetics Metoclopramide
Phenothiazines: prochlorperazine (stemetil)

 Anti-emetics medication can cause acute dystoniainvoluntary movements and

prolonged muscle contractures resulting in abnormal body motions and posture

Manifestation :
1. oculogyric crisis(fixed deviation of the eyes, upward and outward)
2. blephrospasm
3. painful jaw spasm
4. neck flexed backward or laterally
5. open mouth
6. tongue protrusion
7. ocular pain
8. restless, agitated, raised BP &tachycardia

Treatment:
Benztropine 1-2mg slow iv
Procyclidine (kemadrine) 5-10mg iv
Promethazine (phenargan) 25-50mg im/iv

 Specific treatment
Disease specific, depends on diagnosis

 Vestibular rehabilitation
– vertigo from peripheral vestibular disease normally improves 6-12 weeks from a
number of processes collectively known as cerebral compensation.
– mechanisms:
 Habituation response: allow central nervous system to adjust to changes in
labyrinthine signals (like ballet dancer)
 Sensory substitution: rely more heavily on visual / proprioceptive input

*vestibular rehabilitation aims at expediting and enhancing vestibular compensation and

rendering the dizzy patient asymptomatic

 Cawthorne Cooksey Exercise

131
 Surgical options
- indicated if failed medical treatment
Meniers’s disease Hearing preservation procedures
 Intratympanic medication(steroid
/gentamycin)
 Endolymphatic sac surgery
 Vestibular nerve section

Non-hearing preservation procedure

 labyrinthectomy
BPPV  Singular neurectomy(posterior
ampullary nerve section)
 Posterior semicircular canal
occlusion
Perilymph fistula  Middle ear exploration,defect sealed
with fascia ,fat or muscle
Superior SCC dehiscence syndrome  Plunging of superior SCC

132
Diagnostic criteria for vestibular migraine
Barany Society and the International Headache Society 2012

Vestibular Migraine
A. At least 5 episodes with vestibular symptoms of moderate or severe intensity, lasting 5
min to 72 hours
B. Current or previous history of migraine with or without aura according to the
International Classificationof Headache Disorders (ICHD)4
C. One or more migraine features with at least 50% of the vestibular episodes:
– headache with at least two of the following characteristics:
one sided location, pulsating quality, moderate or severe pain intensity, aggravation
by routine physical activity
– photophobia and phonophobia,
– visual aura
D. Not better
1. Vestibular accounted for by another vestibular disorder.
migraine
A. At least 5 episodes with vestibular symptoms1 o

Probable vestibular migraine

 At least 5 episodes with vestibular symptoms of moderate or severe intensity, lasting 5
min to 72 hours
 Only one off the criteria B and C for vestibular migraine is fulfilled(migraine history or
features during the episode)
 Not better accounted for by another vestibular disorder.

133
5. AERODIGESTIVE FOREIGN BODIES (Otolaryngology , Cummings ( 2017))

• Most common in boys under 3 years old

• Reliable history and witnessed aspiration or ingestion are most important for diagnosis
• AP/PA and lateral x rays are useful for initial studies
• Suspicion of airway foreign body mandates bronchoscopy
• Suspicion of aerodigestive battery foreign body mandates immediate removal
• Mid to distal oesophageal foreign bodies in asymptomatic older children may be observed for 8-
16 hours to see if object will pass

Anatomical area where oesophageal foreign bodies routinely lodged:

1. Upper oesophageal sphincter cricopharyngeus
2. Aortic arch
3. Left main stem bronchus
4. Lower oesophageal sphincter

OVERVIEW OF THE MANAGEMENT OF AERODIGESTIVE FOREIGN BODIES

Airway foreign body Oesophageal foreign body
History Witnessed aspiration Witnessed ingestion
• cough, • vomiting,
• dyspnea, • drooling,
• wheezing, • dysphagia,
• stridor • odynophagia,
• refractory asthma • food refusal
• chest pain
Physical examination o ↓ lung sound o Drooling
o Wheezing and crackles o Poor feeding
o Tachypnea o Choking
o hypoxemia

Imaging PA and lateral X-ray: PA and lateral X-ray:

• radiopaque FB • radiopaque FB
• unilateral emphysema • widened prevertebral
• hyperinflation shadow
• localized atelectasis or • loss of lordosis
infiltrate • air trapping
Treatment If adequate suspicion Young symptomatic children:
↓ FB present > 24 hours or sharp
proceed immediately to rigid metallic or caustic should undergo
bronchoscopy for removal endoscopic removal

Asymptomatic children : recent

ingestion < 24 hours and no
oesophageal disorders can be
observed for 8-16 hours

Source ; Cummings otolaryngology 2015

134
135
 6.SUDDEN SENSORINEURAL HEARING LOSS
(references from Scott Brown’s, protocol for Mx of ISSNHL using evidence based medicine and Harold
Ludman & Tony Wright))
D(X): Hearing loss more than 30dB in at least 3 contiguos frequencies within 3/7
 Usually unilateral
 <4% bilateral
 In less than 5% of cases is a specific cause found (> 95% - ISSNHL)

CAUSES EXAMPLE/MOA
Cochlear
Inflammatory Bacteria (AOM, Thyphoid fever), Spirochaetal
(syphlilis, Lyme Dz, Rickettsiae, Mycoplasmas,
Chlamydia), Virus (Mumps,Measles, Varicella,
Human spumaretrovirus, Infectious
mononucleosis, Lassa fever, HIV, AIDS),
Protozoa (Toxoplasmosis).
Traumatic Head injury, ear operations, noice trauma,
Barotrauma (-Membrane rupture,intracochlear
gas production)
Vascular Occlusion,Thrombosis, Hemorrhage, Spasm
Haematological Anemia, Embolism, Coagulation disorders,
polycythaemia vera.
Autoimmune/ Vasculitis Ab-Ag complex mediated destruction (SLE,
systemic vasculitides, Cogan’s syndrome,
relapsing polychondritis, Wegener’s
granulomatosis, polyarteritis nodosa, Kawasaki
Dz, Takayasu’s Dz, Bechet’s Dz)
Endolymphatic hydrops Meniere’s disease (intracochlear membrane
ruptured)
Metabollic disorders Renal failure (Alport’s syndrome, Renal
transplantation, Renal tubular acidosis, Ig A
nephropathy), Diabetes mellitus (peripheral
neuropathies), Phytanic acid storage Dz
(Refsum’s Dz), Hyperlipoproteinaemia
(hyperlipidaemia), Hypothyroidism
Skeletal system Otic capsule
Ototoxicity Destruction of cellular metabolism
Miscellaneous Scleroderma, Ulcerative colitis, sarcoidosis

Retrocochlear & CNS

Meningitis
Multiple Sclerosis
Friedreich’s ataxia
Amyotrophic lateral sclerosis
Vogt-Koyanagi-Harade Syndrome
Xeroderma pigmentosum
Tumour Vestibular Schwannoma (acoustic neuroma)-
Vascular compromise, Metastases in CPA,
Carinomatous neuropathy.
Central deafness

136
History
1. Is there a loss? Time of onset?
2. How long is the loss?
3. How severe is the loss?
4. How quickly is the loss occur?
5. Is there an identifiable cause? E.g: underlying medical illness, Trauma, noise induced,
undergone any surgery or procedure, taken any new drug?
6. Associatied Sx : Pain, Tinnitus, Vertigo?

Causes that can be excluded from Hx:

Noise trauma
Barotrauma
Direct temporal bone trauma
Medication related (occ)

Associated Sx: tinnitus & vertigo

Tinnitus:
 80% of the cases usually starting with this sx, alarmingly as, the deafness.
 Around 25% the tinnitus may presence the deafness.
 Does not affect the outcome.

Vertigo:
 The commonest in those with a probable vascular etiology.
 Poor prognosis indicator.
 Need to investigate thoroughly, the possibility of Vestibular Schwannoma should never be
overlooked.

137
Management:
1.Admission of the patient to hospital
2.Physical Examination:
-Complete head & neck examination:
• Ears: otoscopy, surgical scar
• Tunning fork test: Weber/ Rinne
• Neurological examination: cerebellar findings, cranial nerve
• Vestibular: Dix-Hallpike
3.Investigations
Blood Tests
 FBC, plasma viscousity
 Prothrombin time
 ESR
 BUSE/ creat
 Lipid profile
 Glucose
 Thyroid function
 VDRL/ TPHA
 Auto-antibodies

ECG, Chest X-ray

MRI brain, IAM, CPA (Contrast)
 Rule out CP angle tumor/ Multiple sclerosis/ Ischaemic changes
 3% vestibular schwannomas present with sudden deafness

CT (Contrast) if MRI unavailable

Audiometry
 PTA-Daily
 Acoustic Impedance measurement including Stapedius reflex threshold and decay
 Alternate binaural loudness balance (ABLB)
 Speech audiometry loudness discomfort levels
 Fistula test (electonystagmography + impedance ) if appropriate
 Brain stem auditory evoked response audiometry (Electocochleography)
 Promontory stimulation (IF no hearing present)
 Otoacoustic emissions

Lumbar puncture – for routine CSF examination

4.Empirical Medication (in ISSNHL)
5.Psychological help and rehabilitation

138
Known causes of SSNHL
• Trauma
• Autoimmune disease
• Neoplasia: acoustic neuroma
• Ototoxic drugs

Traumatic SNHL
1) Temporal bone fracture
 affecting the cochlea
 shearing injury affecting cranial nerve VIII.
 Perilymph fistula: rupture of the round or oval windows and the leakage of perilymph

- Surgery: stapedectomy

History usually elicit an inciting event

• blow to the head,
• lifting a heavy object
• exposure to sudden changes in barometric pressure (such as during flying
or diving)
• exposure to a loud noise

2) Perilymph fistula
• no definitive test other than intraoperative observation of leakage of
perilymph
• clinical history of sudden or rapidly progressive hearing loss
• Ruled out inflammation, granuloma, or neoplasia disorders that can
mimic a perilymph fistula (i.e. with MRI, ESR)

Autoimmune Disease
• Cogan’s syn, Wegener’s granulomatosis, polyarteritis nodosa, temporal
arteritis, Berger's, SLE
• Most often present as unexplained, bilateral, rapidly progressive hearing
loss
• 20-50 year old age group
• Otoscopy typically normal
• Audiogram variable
• May exhibit coexistent systemic immune disease

Pathogenesis
• vasculitis of vessels supplying the inner ear
• autoantibodies directed against inner ear antigenic epitopes
• Cross-reaction antibodies

Treatment
• Steroid is indicated in most cases
• Cytotoxic drugs (eg cyclophosphamide, methotrexate, azathioprine) may
be indicated when hearing loss progresses despite steroids.
• Plasmapheresis maybe indicated when hearing loss progresses despite steroids.

139
Neoplasia:
1.Acoustic neuroma
• 3% vestibular schwannomas present with sudden deafness
• MRI can detect tumors as small as 3mm
• Gold standard for diagnosis is MRI of IAM with gadolinium
• MRI in:
1) All patients with unilateral SNHL greater than 20dB difference from unaffected side
not explained by history
2) Word discrimination difference of 30% or greater from asymptomatic side

2.Metastases in the CPA

• From primary dz in the breast, bronchus and prostate

3.Carcinomatous neuropathy

• Peripheral neuropathy caused by malignant dz ranks second to the Guillain- Barre

syndrome.
• Unexplained peripheral neuropathy should be the signal to search for malignant dz.
• The highest incidence of this condition has been found in patient with lung ca, ovary
ca and stomach ca.

Ototoxic drugs
• Aminoglycoside, Cisplatin, Salicylate, Erythromycin, Diuretics
• Aminoglycoside – damage cochlear and vestibular hair cells
• Cisplatin – affect outer hair cells
• Diuretics – damage stria vascularis
• Carbon monoxide intoxication

Patient receives more than 1 ototoxic drug or with compromised renal function are at ↑ risk of HL.
First affect higher frequencies (basal turn) follows by lower frequencies (towards apex).
Typically, bilateral and can be permanent.

140
Idiopathic Sudden Sensorineural Hearing Loss (ISSNHL)
• Exclusion of specific cause on the basis of history, examination, basic
investigations +/- MRI

Postulated causes of ISSNHL (Pathogenesis)

• Viral infection
• Vascular occlusion
• Membrane break
• Immunological
• Activation of cochlear nuclear factor kappa B (NFkB)

1.Viral infection
• Incidence significantly higher for mumps, measles, varicella-zoster, influenza, and
CMV.

2.Vascular occlusion
• Thrombosis, embolus, reduced blood flow, or vasospasm causing reduction in
oxygenation of the cochlea
• The time course correlates well with a vascular event, a sudden or abrupt loss.
• However, histopathologic findings after permanent occlusion of the labyrinthine
vasculature include necrosis of the membranous labyrinth followed by ossification
and fibrosis - these findings are not consistent with those seen in most cases of SHL.
• There is no evidence that hyperviscosity is more common in pt with ISSNHL

3.Membrane break
• Simmons in 1968 proposed a double membrane break theory for SHL.
• Goodhill et al in 1973 discovered perilymph fistulas in three patients with sudden
hearing loss, thus establishing round and oval window breaks as accepted etiologies
for sudden hearing loss.
• Schuknecht and Donovan found no active or healed membrane breaks in the twelve
temporal bones they examined.

Treatment
• Treat the underlying cause
• It is known tht in the ISSNHL, there will be spontaneous improvement within 15 days
in 50-60% of cases.
• However it is inevitably lead to missed diagnosis and apportunity for tx if fail to
investigate patients.
• Evidence based medicine : short, reducing course of steroid +/- antivirals
• Controversial, lack of high quality evidence on the effectiveness of any specific
treatment.

Shotgun regime
- A: Acyclovir
- B: Betahisistine
- C: Carbogen
- D: Dextran,Dexa

141
Steroid
• Some study showed no significant difference btw steroid vs placebo. But all the studies in small
sample.
• As short duration of steroid wont gives much side effect, so better to give after discuss with
patient the risk and benefits of steroid.
• 75% of SSNHL resolved spontaneously within 2/52, so give steroid over 2/52.
• T. Prednisolone 1mg/kg (max of 60mg OD per day ( for 7 days and taper down over the
following week. (total of two weeks)
• Complications of steroid should not be overlooked.

Dextran
• Is a complex, branched glucan (polysacharride)
• Decrease blood viscosity and volume expander hence increase cochlear blood flow
• Contraindicated in pt with cardiac heart failure and bleeding disorders.
• IV dextran 2 bottles/ day for 3/7

Other Rx options
• Intra-tympanic steroid (For pt contraindicated for oral steroid (DM), failure of initial oral steroid
tx )- once weekly for three weeks followed by PTA.
• Inhalation of carbogen (5%CO2 +95% O2)
• Vasodilator drugs (IV histamine acid phosphate each day 2.75 mg in 500ml NS infused over 2H.
Risk of gastric bleed minimized by giving cimetidine 200mg tds and 400mg on)
• Hyperbaric oxygen
• Bed rest (in case of possibility of a membrane rupture); strenuous exertion should be avoided.
• Counsel patients about possibility of incomplete recovery of HL/ possible benefits of HAs and
other supportive measures (if required)

Recovery
EBM guide: 3 level scale
• Complete: recovery of hearing to within 10dB of prehearing loss speech reception
score or averaged pure-tone score
• Partial: > 50% recovery of hearing
• None: less than 50% recovery of hearing

Prognosis
• Spontaneous remission is common
• Patients received treatment 7 days or earlier after the onset of HL experienced significant greater
recovery
Poor prognostic factors:
• Elderly, age > 65yo
• Vertigo
-Improvement in 54% of pt with vertigo compared with 75% without vertigo.
• Severe hearing loss
• Downward sloping audiogram
-Improvement in 45% of pt with a downward sloping audiogram compared with 77%
with other types of audiogram

142
7.PERITONSILLAR ABSCESS (QUINSY)

– Most common complication of acute tonsillitis

– Definition: A collection of pus between the tonsil capsule and the superior pharyngeal
constrictor dt spread of infection from the superior pole of the tonsil into the potential space
between the pharyngeal muscle bed and the tonsillar capsule.
– Causative organism: Beta-Hemolytic Streptococcus
(anaerobes also common with periodontal disease)

Symptoms :
1) Usually unilateral
2) Adults >, rare in children
3) Severe worsening throat pain
4) Odynophagia
5) Dysphagia
6) Drooling of saliva
7) Trismus (d/t inflammation of the pterygoid musculature, esp. medial pterygoid)
8) Muffled and thick speech “hot potato voice”
9) Foul breath / halitosis
10) Referred otalgia – via CN IX

Signs:
– Generally unwell, dehydrated
– Unilateral swelling of the palate
– Tonsil medially displaced
– Uvula shifted to the opposite side
– Unilateral cervical lymphadenopathy
– Torticollis

Treatment:
1. Admission for intravenous fluids & antibiotics
2. Adequate analgesia
3. Needle aspiration
4. Incision & drainage
– Where? at point of maximum bulge; or above the upper pole of tonsil; or just lateral
to the point of junction of anterior pillar with a line drawn thru the base of uvula
– Using a guarded knife
– Small stab incision made
– Sinus forceps inserted to open the abscess
– If any reaccumulation during review – reopen
When we offer Tonsillectomy?
 recommended for recurrent peritonsillar abscess, preferably after acute infection has resolved

143
Complications:
1. Parapharyngeal abscess (spread through the superior constrictor muscle into a potential
space between the superior constrictor muscle and the deep cervical fascia)
2. Retropharyngeal abscess (spread in the retropharyngeal space)
3. Oedema of larynx
4. Septicaemia
5. Aspiration  pneumonitis, lung abscess
6. Jugular vein thrombosis
7. Spontaneous haemorrhage from carotid artery or jugular vein

144
8. NECROTISING OTITIS EXTERNA (NOE)
• Invasive infection of the external auditory canal and skull base, which typically occurs in
elderly patients with diabetes mellitus
• Serious, fatal skull base osteomyelitis with infection begins in bony EAC and spread along
skull base
• 1959- Meltzer & Kelemen presented the 1st case
• First described as ‘Pseudomonas osteomyelitis of temporal bone’
• 1979 - Chandler published a series of 13 cases 1968 – 1974, termed the condition as
‘Malignant otitis externa’ – propensity to cause complication
• NOE – reflect the disease is not neoplastic
• Invasive infection of EAC and skull base
• Elderly with diabetic, immunosuppressed

Epidemiology
• Mean age : 65-70 years old
• Male > female : 1.8:1 ~ 18:1
• Elderly diabetic – at risk population
• DM – important associated condition
-- > 90% patients are diabetics
– Review by Franco et al 2007 of 46 patients : 65% of patients had diabetes.
– Hypothesis :
• Microangiopathy, endarteritis of the ear canal
• Increased pH in diabetic cerumen  reduced concentration of of lysozyme
and loss its protective action
• Rare in children
– Immunocompromised
• Malnutrition
• Malignancy – AML, ALL, neutropenic post chemotheraphy, bone marrow
transplantation
– > toxic than adults
– FN involvement > frequent and rapid, usually complete and permanent – poor
recovery
• Mastoid process still underdeveloped
• The facial nerve is located near to EAC > susceptible
– Better prognosis compared to adult
– Common complications:
• necrosis of TM, EAC stenosis, auricular deformity , SNHL, CHL
• Other condition: HIV associated NOE
– Younger than average pt with DM
– High suspicious in OE with poor respond with appropiate therapy
– Lack of typical granulation tissue over EAC
– Pseudomonas NOE (CD4 counts< 100 cells /mm)
– Fungal NOE > common in this group esp with AIDS ( CD4 counts < 50 cells/mm)
• Recent ear surgery
• Chronic hearing aid irritation

145
Microbiology

• Pseudomonas Aeruginosa
– More virulent , mucoid surface layer protect from phagocytosis by macrophages
– Produce lytic enzymes – endotoxin, collagenase , elastase – invasion of surrounding
tissue
• Staphylococcus Aureus
• Staph epidermidis
• Proteus Mirabilis
• Klebsiella Oxytica
• Pseudomonas cepacia
• Fungal – Aspergillus fumigatus , A. flavus, A. niger and scedosporium apiospermum

Pathogenesis and mode of spread

146
Spread of infection:
1. Inferiorly through the stylomastoid foramen to involve the facial nerve.
2. Anteriorly to the parotid
3. Posteriorly to the mastoid and sigmoid sinus
4. Superiorly to the meninges and brain
5. Medially to the sphenoid
6. Spread through vascular channels are also common

Clinical Manifestations
• Purulent otorrhea
• Swollen tender EAC (hallmark)
• Granulation tissue or exposed bone over floor of canal at bony cartilaginous junction
– Maybe absent in atypical patient
• Periaural lymphadenopathy
• TM? Usually normal but view obscured by polyp
• Cranial neuropathies indicates spread of infection through skull base
• Look for signs to suggest complication – dural sinus thrombosis, meningitis and cerebral
abscess

Lab investigation :
• Elevated ESR
• Typically absent of leucocytosis – except in children with NOE
• Swab culture : pseudomonas is commonest

147
Criteria for diagnosis:

Imaging
• No single imaging modality sufficient to diagnose NOE
• CT scan
– Sensitive to bony erosion and decreased skull base density
– Sensitive in diagnosing abscess formation, mastoid involvement, TMJ joint,
infratemporal fossa, nasopharynx, petrous apex and carotid canal
– Inadequate to see intracranial extension and bone marrow involvement
– Not used for disease monitoring because all these changes persist despite resolution
of disease .
• MRI better shows changes of soft tissue
– Sensitive to see intracranial extension i.e dural enhancement, involvement of
medullary bone spaces
– Generally not recommended as first line diagnostic imaging modality given its lower
sensitivity for imaging bone erosion
– Not used for disease monitoring because all these changes persist despite resolution
of disease .
• Radionuclide scanning - useful as diagnosis tool, non spesific in outlining anatomic region
• Technetium Tc 99m methylene diphosphonate scintigraphy (bone scan) is +ve in almost
100% of NOE cases
– Technitium Tc 99m MDP radiotracer concentrates in areas with osteoblastic activity
(infection,trauma,neoplasm) – not spesific hence need biopsy to diagnose
malignancy
– Able to detect OM earlier than CT scan
– Poor value for disease monitoring – remain +ve indefinitely

148
 Modality Benefits Disadvantages

HRCT Demonstrate bony Evaluate the extent of Only appear after a week
destruction bony destruction & or more
abscess formation

MRI Demonstrate increase Evaluate intracranial Demonstrate late stage

signal of soft tissue extension and soft
beneath skull base tissue involvement

Tc-99m bone Absorbed by osteoblast Detect earliest changes Do not outline anatomic
scan in bony involvement (1- region; Remain positive
2 days) even when infection has
resolved and during bone
remodeling

Ga-67 Absorbed by leukocytes Quickly return to Do not outline anatomic

scintigraphy normal when infection region; Detect any
resolved - useful to inflammation - not useful
monitor resolution of as diagnostic tool
infection

SPECT Combine radioisotopes Good spatial Expensive, not widely

with CT localization of disease available
extent and anatomy

Management
• Frequent requires collaboration with endocrinologist,neurologist, radiologist & ID
• Aggressive diabetic control
• Reversal of acidosis
• Improvement of immunocompetencey where possible
• Aerobic, anaerobic and fungal culture – test for sensitivity
• Repeat culture is necessary if culture negative
• Witholding therapy until culture +ve is not recommended
• Tissue biopsy
– HPE TRO malignancy
– Microbiology for culture

149
Biopsy
• Definitive method – distinguish temporal bone SCC and NOE
• There are only two reports of simultaneous presentation of temporal bone cancer and
malignant external otitis [3].
• Radiological ix may not able to diff tumour from infection (NOE)
• How do we do it?
I. Biopsy in NOE case & suspicious tumour --> repeat if poor respond to medical treatment
II. Pseudomonas NOE far more common than temp bone SCC- biopsy reserve for cases of poor
medical respond.

Treatment
• Long term antibiotic therapy is mainstay of tx
• Culture directed therapy
• Antipseudomonal penicillins and aminoglycoside are abx of choice previously
– Combined therapy
– Required parenteral administration
– Prone ototoxicity and nephrotoxity
• Duration : 6-8 weeks

• Long term monotherapy with oral ciprofloxacin preferred ( high dose / adjusted dose in
renal insufficiency )
– Good bone penetration
– Excellent oral bioavalaibility
– Less significant side effect compared to combined therapy
• Newer generation oral fluoroquinolone abx other than ciprofloxacin may also be considered,
but none has been reported.
• Increased incidence of pseudomonal resistance to ciprofloxacin > reported – widespread use
quinolones in URTI/OM /OE
• Berenholz et al found 33% P aeruginosa in NOE resistant to ciprofloxacin [4].
• Use of topical abx is controversial – can change bacterial flora of EAC, making culture more
difficult + potential source of abx resistance.
• Used of concurrent Aminoglycosides also recommended in resistant and complicated case.
• Fungal NOE : Amphotericin B is the most commonly used but need to monitor toxicity effect.
Oral itraconazole has also been used after short course of Ampho B.

150
Any role of surgery ?
• Limited to superficial local debridement of granulation tissue or bony sequestrum and to
biopsy the granulation tissue
• Previously, major procedure eg deep debridement, mastoidectomy, facial nerve
decompression  mortality 50%
• Temporal bone surgery contraindicated because it was believed that it opens up new planes
for spread of disease.
• Illing E. et. al. Malignant otitis externa with skull base osteomyelitis. JSCR. 2011;5:6-6
• Surgical resection of diseased bone not recommended due to disease spread through fascial
and vascular planes
• Biopsies can be obtained
• Abscess can be drained
• Facial nerve decompression is not routinely performed

Hyperbaric Oxygen
• Role of hyperbaric oxygen – not well established
– Increase Po2 , improve hypoxia  oxidative killing
• Suggest to use in refractory skull base OM with intracranial involvement
• Side effects : oxygen toxicity/barotrauma/TM perforation
• Thorough review through cochrane database : no clear evidence to show the efficacy of HBO
compared to abx and surgical treatment

Disease Monitoring
• Clinical ( non spesific)
• Lab : ESR (non spesific inflammatory marker)
• Gallium Ga 67 citrate study :
– Poor anatomic resolution but complementary in diagnosis
– concentrate in areas of active inflammation through attaching to lactoferrin (
present in leucocytes ) / through binding to transferrin/ bacteria directly
– Positive in soft tissue and bone infection
• In practice , certain centres repeat CT/MRI 3/12ly after commencing treatment to monitor
response.

151
BASE OF SKULL OSTEOMYELITIS

Introduction
 First described by Meltzer and Kelemen in 1959
 Skull base osteomyelitis (SBO) is a serious, potentially life-threatening condition.
 Most commonly affecting the elderly, diabetics & the immuno-compromised.
 Most often presented as a complication of necrotizing otitis externa (NOE) secondary to
Pseudomonas aeruginosa infection or fungal infection.

Definition
 PROVEN (definite) SKULL BASE OSTEOMYELITIS
 Skull base infection in patients with localizing symptoms/signs, who at presentation, had :
1.Radiological or scintigraphic features indicative of bone erosion and/or infection , and
2.Isolation and/or visualization of the pathogen from the affected bone(s) and surrounding
tissue.

 PROBABLE SKULL BASE OSTEOMYELITIS

 Infection in patients with localizing symptoms/signs with evidence of SBO on imaging
studies,
- but from whom a pathogen was recovered from clinical specimens other than bone or
tissue (eg: ear swabs);
- or in whom a definite response to antimicrobial therapy was evident

Risk Factors
 Increasing age (elderly)
 Diabetes mellitus (poorly controlled DM)
 Microvascular disease
 Immunodeficiencies : primary or acquired
***Fungal SBO can occur in the absence of these risk factors

Anatomy of Central Skull Base

 Sphenoid bone is the foundation of the central skull base.
 Contains vital foramina, which transmit important neurovascular structures
 CN IX,X,XI and XII.
 Constitutes the floor of middle cranial fossa
 Contains the pituitary gland within sella turnica, and the parasellar cavernous sinuses.
 Sphenoid bone is the foundation of the central skull base.
 This anatomically complex structure contains vital foramina, which transmit important
neurovascular structures; constitutes the floor of middle cranial fossa , contains the pituitary
gland within sella turnica, as well as the parasellar cavernous sinuses.
 This Strategically located bone and its foramina are often involved in primary pathological
process ; extracranial disease that extends intracranially , and intracranial disease that
extends through the skull base.

152
Sphenoid
- Superior surface of sphenoid
 Anteriorly : cribiform plate of ethmoid bone
 Posteriorly : tuberculum sella
- Posterior to tuberculum sella : sella turnica
 Anterolateral to sella turnica : middle clinoid processes
 Posterior to sella turnica: dorsum sellae
 Dorsum sellae terminates laterally into posterior clinoid processes
- Sphenoid body
 Laterally: the greater wings and medial prerygoid plates.
 Anteriorly: the perpendicular plate of the ethmoid bones.
 contains sphenoid sinuses separated into 2 air cells by a septum.
 may extend laterally into the greater wing and into base of pterygoid plates.
 Anteriorly, both air cells communicates with the nasal fossa through an opening into the
sphenoiethmoidal recess

Basal Foramina
 Superior orbital fissure
- Medially : body of sphenoid
- Superiorly : lesser wing
- Inferiorly : greater wing
- Laterally : frontal bone (as the greater & lesser wings converged)
- Transmits : CN III , CN IV, CN V1 , orbital branch of middle meningeal artery, various
sympathetic filaments of internal carotid plexus , recurrent meningeal branches of
lacrimal artery, opthalmic veins

 Foramen rotundum
- A canal in the base of greater sphenoid wing
- Located infero-laterally to superior orbital fissure
- Transmits : CN V2, artery of foramen rotundum , emissary veins
- Best visualized on coronal CT

 Foramen ovale
- Located in the medial aspect of sphenoid body
- Endocranially : Postero-lateral to foramen rotundum
- Exocranially : base of lateral pterygoid plate
- Transmits : CN V3, emissary veins, accessory meningeal artery (from middle cranial fossa
to the infratemporal fossa)

153
  Foramen spinosum
- Found on the postero-medial aspect of greater sphenoid wing
- Endocranially : Postero-lateral to foramen ovale
- Exocranially : lateral to Eustachian tube
- Transmits : middle meningeal artery & vein , recurrent branch of CN V2
- Best visualized on axial CT

 Foramen lacerum
- Located at the base of medial pterygoid plate
- Exocranially : covered with fibrocartilage
- Carotid artery rests on the endocranial aspect of this fibrocartilag
- Contains : inconstant meningeal branch of scending pharyngeal artery , nerve of
pterygoid canal (they pierce through the cartilage)
- Foramen lacerum & carotid canal may be visualized both on axial & coronol CT / MRI

 Vidian (Pterygoid) canal

- Located in the base of pterygoid plates
- Inferior to the foramen rotundum
- Connects the pterygopalatine fossa (anterior) to foramen lacerum (posterior)
- Transmits :
o Vidian nerve (continuation of the GSPN)
o Vidian artery (branch of terminal portion of IMAX)
- Best visualized on axial and coronal CT

Pituitary Gland
 Lies in the hypophyseal fossa
 Covered by a circular fold of dura – diagphrama sellae
 Laterally: cavernous sinus

Cavernous sinus anatomy

 Located on each side of sphenoid bone, extending from superior orbital fissure (anteriorly)
to the petrous apex (posteriorly)
 Carotid artery, surrounded by a sympathetic plexus, courses through the sinus, and the
CN VI lies anterolateral to the carotid artery.
 Superior to inferior :
CN III – CN IV – CN V1 – CN V2
(contained within separate fibrous sheath at the lateral wall of the sinus)
 Medially : pituitary gland & sphenoid sinuses
 Meckel cave (enclosing the trigeminal ganglion) – located at postero-inferior of sinus
 Can be evaluated on coronal & axial CT/MRI

154
Clivus Anatomy
 Located between the foramen magnum and dorsum sellae
 Formed by basi-occipital bone and sphenoid body
 Anterolateral margin: Petro-occipital fissure
 Posterolateral margin: Synchondrosis between basioccipital and exoccipital bones
 Anterior: Blends into sphenoid sinus
 Posteroinferiorly: Forms the anterior aspect of foramen magnum

Central Skull Base

 Central skull base comprises of the clivus, bordered:
o anteriorly by the nasopharynx
o posteriorly by the foramen magnum
o anterolaterally by the petrous temporal bone
o posterolaterally by the jugular foramen.
 It is a conduit for passage of the CN IX, X, XI and XII.
 Osteomyelitis involving this is termed central base of skull osteomyelitis (CSBO) which is rare
and distinct from the widely reported typical temporal bone osteomyelitis secondary to
necrotizing otitis externa.

155
Typical VS Atypical SBO
 SBO typically presented as sequelae of (NOE) which primarily affecting the temporal bone
 Central or atypical SBO can be seen affecting the sphenoid & occipital bones, often centred
on the clivus
 Central SBO could also present as a late presentation of NOE originating from temporal bone
 Some authors concluded that central SBO originate from paranasal sinus inflammatory
disease or from hematogenous spread. (Malone et al., 1992)

Illustrates the routes of infectious spread after NOE

 Anteriorly (via fissureof Santorini): TMJ, masticator space and parotid gland
 Medial: ipsilateral paranasopharyngeal fatty tissue , encasing ICA and preclival soft tissue.
May spread to the contralateral side.
 Further extension through the osseous structures: venous sinus thrombosis and dural
extension
 Posteriorly: mastoid portion of the petrous bone

Atypical (central) SBO

 Central SBO is centered on the clivus , rather than the temporal bones
 Presumably arises from the paranasal sinuses inflammatory disease rather than otitis or
mastoiditis
 May also arise from hematological spread
 Risk factors: diabetics, immunocompromised
 Classic signs of infection: (fever, elevated WBC count, positive blood cultures) are usually
absent.
 They usually present with headache and cranial neuropathy with elevated ESR
 All will have clival and preclival abnormalities on MRI, best seen in T1-weighted images.

Presenting Symptoms
Presenting symptoms will depend on the precise location of infection
Presentation:
 Headache – initial complaint, often intractable.
 Cranial neuropathies : often a combination of CN VI and the lower CN (CN IX,X,XI,XII)

 dysphagia, dysarthria , hoarseness , diplopia
 Nasal symptoms : rhinorrhea, nasal blockage, facial pain, stooping headache, epistaxis ,
anosmia
 Elevated acute-phase reactants, in particular ESR

The diagnosis is difficult to make clinically, thus often delayed.

 Patients initially may have headache as the only symptoms, with cranial neuropathies
occurring later.
 The region in which this condition arises is an anatomical ‘minefield’ – dangerous zones
 Combination of CN VI + IX, X, XI should raise particular suspicion of clival pathology
 Ophthalmoplegia (most often CN VI paresis) + CN XII, in the past , is considered
pathognomonic of malignant neoplasm of nasopharynx (but now this combination has been
found not exclusive to NPC)

156
Radiological Investigations
1st line of radiological investigations: CT and MRI
Imaging findings:
 Bone erosions and marrow infiltration of the basi-occiput and or petrous apex
 Mass-like soft tissue swelling below the skull base
(Kimura et al.,1990; Erdman et al.,1991; Malone et al.,1992)
Typical findings of SBO is clival hypointensity on T1-weighted MRI and T2 hyperintensity – due to
bone marrow infiltrations.

Imaging of skull base in the setting of cranial neuropathy and probable infection is best
accomplished by MRI
MRI has the advantage of superior soft tissue discrimination without the beam-hardening artifacts of
CT and is particularly useful for assessing soft tissue planes around the skull base and abnormalities
of medullary cavity of bone
CT findings are generally unhelpful for monitoring reponse to treatment, because it may not even
abnormal initially, or if its abnormal, may remain abnormal for as long as 2 years post treatment.

Nuclear medicine Imaging Techniques:

 Gallium-67 scintigraphy
 Indium-111 white blood cell scans
 Technetium-99m methylene disphophonate (MDP) bone scans**
 Single-photon emission computed tomography (SPECT)**
** better than CT and MRI in detecting post-operative osteomyelitis and follow-up patients on
antibiotics
– marrow signal change may persist for up to 6 months after successful treatment.

 Combination of functional and anatomical imaging is needed to fully understand the spread
of disease and associated complications
1. High-resolution CT : assess the extent of bone erosion.
2. MRI : evaluate soft tissue extension
3. FDG-PET : assess the metabolic active disease and can be used in follow-up
4. Nuclear techniques – lack in anatomical details but aid in functional process imaging
 Gamma tracers ( Tc-99 m-MDP, Technetium-labelled leucocytes, Gallium-67-Citrate)
 Beta-emitting tracers (FDG : Fluor-2-Desoxy-Glucose)
5. Hybrid techniques PET-CT and PET-MRI are the newest modalities which combine imaging
strengths.
 PET- CT is advantageous : correlate with bone resorption and to a lesser extend soft tissue
involvement
 PET-MRI combines the superior soft tissue contrast of MRI and functional imaging of PET.

157
Follow-ups imagings
Proposed strategies: Intermittent imaging every 6 weeks until no infectious process can be viewed
1. The union of MRI and FDG-PET presents the best of both worlds
- Superb spatial resolution to detect subtle abnormalities in soft tissues and bone marrow
+strong evidence of altered bone metabolism

2. Since repetitive imaging is needed

- PET-MRI is more favourable compared to PET-CT (less radiation exposure)
- CT scan : measures bone remineralization
 doesn’t immediately occur after disease resolution
 less reliable imaging modality to evaluate (early) treatment response

- MRI : monitor soft tissue changes

o resolution of abnormalities often lags behind disease resolution.
o bone marrow signal can still be present for 6–12 months after successful treatment
o making MRI unreliable for distinguishing between resolved & ongoing SBO

- PET using fludeoxyglucose (FDG) is better suited for monitoring disease resolution
o FDG shows ongoing neutrophil activity in metabolically active tissues, and decreased
inflammation gives less signal intensity without much delay.

Follow-up:
CT scan:
- measured bone remineralization, however, this does not immediately occur after disease
resolution
- it is a relatively late phenomenon thus making CT a less reliable imaging modality to
evaluate (early) treatment response [1•, 5, 13].

MRI imaging:
- known to be a reliable imaging modality to monitor soft tissue changes in the diagnosis of
SBO, such as reduced fat planes or medullary bone abnormalities.
- Although abnormalities in soft tissues are easily depicted, resolution of abnormalities often
lags behind disease resolution.
- Furthermore, an abnormal bone marrow signal can still be present for 6–12 months after
successful treatment, making MRI unreliable for distinguishing resolved from ongoing SBO of
the bone marrow.
- Technetium-99 m is indicative of osteoblastic activity in damaged bone [9•, 26]. Because of
prolonged activities of osteoblasts in previously affected bone, Tc-99 m will continue to
demonstrate previously affected areas as hot spots for many years.

PET scan:
- using fludeoxyglucose is better suited for monitoring disease resolution, as FDG shows
ongoing neutrophil activity in metabolically active tissues, and decreased inflammation gives
less signal intensity without much delay.

158
Making The Diagnosis
 Tissue sampling procedure is often required for histopathological examination (HPE) to
establish diagnosis
- Because imaging appearance alone is highly suggestive but non-specific to SBO
- But this can cause delay in diagnosis
- Obtaining samples via CT-guided/MR-guided FNA of abnormal pre-clival tissue, during
endoscopic sphenoidotomy or open craniotomy
 Some authors advocate that with typical clinical presentation, imaging findings and a
positive response to Ciprofloxacin, diagnosis can be made without the need for biopsies.
(Cavel et al.,2007)
 Biopsy can ensure absence of malignancy and to aid subsequent microbiological advice.
(Clark et al., 2009)

Causative Pathogens
 Pseudomonas aeruginosa (most common bacterial SB0)
 Aspergillus (Invasive fungal skull base infection caused by Aspergillus infection, presumably
is secondary to underlying fungal sinus infection)
 Zygomycosis (Mucormycosis) (most common fungal SBO from invasive PNS infection)
 Gram-positive organisms (Staphylococcus aureus, MRSA)
 Mycobacterium
 Candida

Management
 Up to 6 weeks’ IV antimicrobial/ antifungal therapy followed by oral medication
 Hyperbaric oxygen therapy (adjuvant)
 Surgical debridement: performed more frequently in fungal SBO
 Bacterial SBO anti-microbial therapies
1. ticarcillin/clavulanic acid (anti-pseudomonal B-lactam penicillin)
2. ceftazidime (cephalosporin)
3. ciprofloxacin (quinolone) – 200mg/100mls infusion (severe infection: up to 400mg TDS)
4. vancomycin (glycopeptide)
 Fungal SBO anti-fungal therapies
i. amphotericin B formulation
ii. itraconazole
iii. voriconazole
iv. posaconazole
v. caspofungin

The bone infection unit in Oxford, UK, recommends up to 6 weeks of IV treatment followed by 6-12
months of oral antibiotics, guided by clinical response.

Adjuvant hyperbaric oxygen therapy may improve successful treatment by reversing tissue hypoxia,
enhancing phagocytic killing of aerobic microorganisms and stimulating neomicroangiogenesis

159
Keypoints
 Skull base osteomyelitis (SBO) is a serious, potentially life-threatening condition.
 Most commonly affecting the elderly, diabetics & the immunocompromised.
 Most often presented as a complication of NOE secondary to Pseudomonas aeruginosa
infection.
 Osteomyelitis involving the central skull based is termed central or atypical SBO which can
be seen affecting the sphenoid & occipital bones, often centred on the clivus
 Central SBO is thought to originate from paranasal sinus inflammatory disease or from
hematogenous spread but could also present as a late presentation of NOE originating from
temporal bone
 An elderly diabetic presenting with persistent headache warrants appropriate clinical and
radiological assessment , keeping the diagnosis of SBO in mind.
 Clinical presentation : headache , cranial neuropathies, acute or chronic nasal symptoms,
with/without history of chronic otitis externa (NOE), elevated ESR
 Radiological investigations
o MRI: accurately delineates soft tissue and marrow involvement
o CT: determines bony erosions
o Tc-99 m-MDP: excellent for early disease detection
o PET MRI : best modality for surveillance. Typical findings of SBO on MRI:
 Clival hypointensity on T1-weighted MRI
 T2 hyperintensity – due to bone marrow infiltrations
 Histopathology & Microbiology examination will substantiate the diagnosis of SBO, as well as
to exclude malignancy.
 Appropriate Antibiotics have to be started early and continued for at least 6 weeks.
 Pseudomonas aeruginosa infection predominates –initiation of anti-pseudomonal
therapy deems appropriate pending microbiological diagnosis.
 Zygomycetes responsible for more than 50% of fungal SBO – commencement of high
dose of Amphotericin B formulation is advised
 Early and aggressive surgical resection / debridement is recommended in fungal SBO & is
associated with improved survivals in patients with zygomycosis.

160
9.LARYNGEAL TRAUMA

Types of Laryngeal Trauma

External laryngeal trauma:
1. Blunt
- Crush: MVA; victim is thrust forward with a hyperextended neck, exposing larynx to anterior
crushing forces
- Clothesline injuries: high velocity impact of the larynx with stationary object, and large
amount of energy imparted over a small area = instant exsanguination from cricotracheal
separation or a crushed larynx
- Strangulation: hanging or strangulation by soft object = initial injury may be minor but can
subsequently lead to laryngeal oedema and compromised airway

2. Penetrating
- Gunshot wounds
o Low velocity: moderate damage to injured tissues
o High velocity: wide-field damage of laryngeal tissue and can extend beyond limit of
necrotic tissue
- Stab wounds: predictable course of injury and generally does not cause damage beyond entry
and exit path

Internal laryngeal trauma:

1. Inhalational injuries:
 Toxic gas or fires: oedema of airway (self limiting)
 Ingestion: full thickness airway burns —> morbidity
*High levels of thermal energy —> cause reflex closure of the glottis to limit thermal injury to the
supraglottic region only.

2. Iatrogenic injuries:
Can occur following airway management procedure

Pathophysiology of Laryngeal Trauma

Tissues involved: mucosa, nerves, soft tissue, cartilage and trachea

1.Acute: main concern is the airway

2.Chronic: progressive changes

 Healing by secondary intention —> scarring, subluxation, ankylosis of arytenoids and CA joints
 Fibrosis of muscle —> disrupts mucosal wave and appearance of non-vibrating segments
 Anterior and posterior glottis webbing
 Supra- and sub- glottis scarring
 Neural injury —> muscle palsy
 Cartilage # healed by secondary intention —> unstable #, mal-union or non-union
 Progressive shortness of breath and airway obstruction secondary to posterior vocal folds
drawn together due to maturation of granulation tissue
 Others: glottis incompetence, dysphonia, aspiration and dysphagia but chronic allows time for
glottis compensation

161
Schaeffer Classification Of Laryngeal Trauma

162
Sequelae of major laryngeal trauma:
Supraglottic, subglottic and/or posterior glottis level stenosis

Clinical Presentation

Symptoms Sign
Pain over the larynx Tachypnea
Voice change/hoarseness Stridor:
Odynophagia - Inspiratory: supraglottic obstruction maybe due
Dysphagia to oedema/hepatoma
Cough - Expiratory: subglottic; such as tracheal injury
Haemoptysis - Biphasic: injury at level of glottis
Shortness of breath Ecchymosis of overlying cervical skin
Aspiration Abrasions/open wound
Varying degrees of dysphonia Subcutaneous emphysema
Loss of normal thyroid prominence
Deviation of larynx
Loss of laryngeal crepitus

163
Airway evaluation
When airway is stable, further examination of larynx is possible
Flexible scope to evaluate any signs of compromise or impending airway
If airway worsens: tracheostomy

Imaging

Performed once airway is stabilised

CT scan: assess the larynx and its framework
Findings include: cartilage #, haematoma, oedema, cricoarythenoid joint dislocation or
subluxation, extra-tracheal subcutaneous air and airway stenosis
Used in conjunction with operative exploration
CT scan and MRI can identify missed laryngeal injuries in symptomatic patients with chronic sequelae
CTA used in penetrating trauma: to identify the location and trajectory of FB (bullets or shrapnel) and
integrity of vascular structures obtained

164
Management

Non-operative approach
Determined by type and extent of injury and coexisting illness
Usually done in group 1 and group 2 and undisplaced single # of laryngeal cartilaginous framework

Admission to ICU for 24H airway monitoring

Constant humidification
Head elevation
NBM
Voice rest
Blockade of gastric acid reflux
Corticosteroids and antibiotics

Operative approach
Aim:
Airway preservation
Prevention of secondary sequelae of healing
Restoration of function via repair of endogamy goal and other concomitant injuries
Stabilisation of # of the laryngeal framework

Indication:
All injuries involving anterior commiserate, exposed cartilage, multiple or displaced # of
thyroid cartilage, multiple # of cricoid cartilage
All injuries causing VFP +/- airway compromise to require intubation/tracheostomy
Injury to the neck requiring exploration

Principles:
Within 24H – maximise airway and phonation results
Hemostasis
Evacuation of hepatoma
Reconstruction of laryngeal framework
Coverage of de-epithelialized surfaces

165
Complications of Laryngeal Trauma

Immediate Long Term

Airway obstruction Voice compromise
A phobia Chronic obstruction
Dysphonia VC injuries (paralysis/fixation)
Odynophagia Fistula
Post op complications Cosmetic deformity
Chronic aspiration
Inability to decannulate
Subglottic stenosis

References:
 Scott-Brown
 Chai Notes
 Google drive PPUKM

166
 PART C:
DAILY ENT CLINIC

167
1.ALLERGIC RHINITIS
Rhinitis is defined as tissue inflammation & nasal hyperfunction which lead to symptom of
rhinorrhoea, nasal obstruction and sneezing/ itchiness (2 out of 3), occurring > 1hr/day.

Rhinitis :
1. Allergic
2. Non-allergic

Allergic Non-allergic
 Intermittent (seasonal)  Known cause: hormonal imbalance, infection,
 Persistent (perennial) structural abnormality, rhinitis medicamentosa
 Unknown cause (intrinsic): vasomotor

Allergic Rhinitis
IgE mediated hypersensitivity of mucous membrane of nasal airway following exposure to allergen
Characterized by sneezing, watery rhinorrhea and nasal obstruction.

Risk factor :
a. Family h/o allergy
b. Parental smoking
c. Chromosome induce atopy eg 5q chromosome where gene exist for IL4 & IL13 with high
serum IgE
d. Environment : more common in developed country, lifestyle changes, increased exposure to
allergen, pollutants or irritants, stress.

Pathogenesis :
Complex reaction composing of 4 phases :
1. Sensitization (armed mass cell)
2. Early phase (mediators)
3. Late phase (Inflammatory cells)
4. Systemic activation (eosinophil precursors)

168
Sensitization

Upon first exposure to allergen, antigen presenting cell (APC) will capture antigen and presents the
antigen to TH2 cell (causing activation of TH2 cell) and IgE-secreting B cell (causing production of IgE
from B cell). No allergic reaction occur during first exposure to allergen.
IgE has 2 portions
 Fc has high affinity to mast cells or basophils
 Fab has high affinity to allergens
Also activates B cell in local lymphoid tissue encouraging them to proliferate, migrate to nasal lining
and produce antibody IgE
Once produce, IgE is very rapidly and avidly taken up by local cell processing FcER1 mainly mast cell
Thus, armed mast cell are able to specifically response to subsequent allergen contact

What happen in atopy ?

In atopy, T cell mature into TH2 cell which secretes cytokines mainly IL-4,5,13

169
Early phase
Duration : 5-30min
Pathogenesis : due to release of vasoamine like histamine
Upon subsequent exposure to the same allergen, the sensitized mast cell is cross-linked by allergen.
This will activates the mast cell to release mediators in the form of :
a. Primary mediators (preformed) : Histamine, Heparin, Eosinophil chemotactic factor (ECF),
neutrophil chemotactic factor (NCF), Kinin, Tryptase
b. Secondary mediators (Newly synthesized) : Prostaglanding D2, Thromboxane A2, TNFα,
Leukotriene B4 C4 D4, Platelet activating factor
Regulated by T-helper and T-suppressor cells
Increased T-helper or decreased T-suppressor will increase production of plasma cells and increase
IgE
Role of histamine :
a. Vasodilator -> increase plasma exudate -> causing hyperactivity of gland (rhinorrhoea)
causing edema (nasal congestion)
b. On sensory nerve – cause itching and sneezing
c. Proinflammatory and immunomodulators
d. Bronchospasm

170
Late phase
Duration : 2-8 hrs
Pathogenesis : due to infiltration by inflammatory cells like eosinophil, neutrophils, basophils,
monocytes
Main symptoms includes nasal obstruction, hyperactivity

Systemic reaction
There is evidence of upregulation of production and release of precursors of eosinophil and basophil
from bone marrow in response of allergen contact  this is brought to reaction site and to other
respiratory site via selectin and adhesin molecules
Mast cell degranulation can also results in non IgE mechanism; eg : drug induce rhinitis like
morphine, codeine, aspirin

Clinical features
- Transverse nasal crest (salute)
- Darken area under eyes (allergic shiner)
- Open mouth from nasal obstruction due to mouth breathing (allergic gape)
- Dennie morgan line : prominent crease at inferior eyelids
- 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 aero-
allergens)

Classification (ARIA)
- Intermittent
 < 4/7 per week, or
 < 4 consecutive week
- Persistent
 > 4/7 per week & > 4 consecutive week
- Mild
 Normal sleep
 No impairment of daily activities, sport, leisure
 No impairment of work and school
 Symptoms present but not troublesome

171
 - Mod or severe AR must have at least one of the following
 Abnormal sleep
 Impairment of daily activity or sport
 Problem caused by work/ school
 Troublesome sx

Investigation
a. Skin prick test
- Simple, cheap, safe, specific and sensitive
- Principle: allergen introduce into skin cause degranulation of IgE sensitized mast cell,
mediator release leading to formation of wheal and flare
- How? A drop of standardized allergen placed on volar forearm, a prick made on the skin
by using lancet  cause formation of wheal and flare if there is reaction
- Read after 15-20 minutes by measuring the widest diameter
- Contraindication: patient on antihistamine, h/o life threatening anaphylaxis, severe
asthma, has dermographism
- Disadvantage: patient discomfort, non-standardized allergeo-extract, different
interpretation scale
b. Intradermal skin testing/Intradermal dilutional testing
- Using quantitative 1:5 serial dilution
- Antigen injected to produce a wheal of specific size
- Most sensitive method of skin testing
- Intradermal injection of 0.01ml of inert solution will form 4mm wheal, normally spread
to 5mm diameter (set end-point titration, SET)
- Intradermal testing utilizing serial dilution to quantify degree of sensitivity and
specificity of antigen
- Laborious and very uncomfortable for patient to be prick many times
- Wheal measure similar to intradermal testing
- First dilution cause wheal of 2mm, with progression of wheal by another 2mm
(confirmatory wheal)
- This type of test is important in determining the initial concentration of immunotherapy

172
c. Intradermal testing
- A diluted antigen extract is injected into dermal and superficial wheal forms
- After 10 minutes, the wheal is measured again to see if there is progression
- If diameter of wheal is greater than 2mm, then possible response has occur
- Cause relative minimal patient discomfort
- Disadvantages: high risk of anaphylaxis, time consuming, possible false positive
d. Modified quantitative testing
- A hybrid of skin prick and intradermal testing
- A skin prick test performed to determine the approximates range of sensitivity,
followed by single intradermal test to further identify the level of sensitivity and
quantify the allergic response.
e. Nasal smear
- To differentiate AR and NAR with eosinophilia (NARES) from other forms of rhinitis.
- Typically, there is eosinophilia but the absence does not exclude AR, may find
neutrophil as well.
f. RAST (Radioallergosorbent test)
- Measures antigen specific IgE
- Safe and highly sensitive
- Better for those patient on B-blocker, on antihistamine, children who cannot tolerate
skin testing, dermographism.
g. Modified RAST
- Soluble allergen bound to solid phase support (paper disc) to create a stable
immunosorbent media
- The paper disc is incubated with test sera, specific IgE antibody will bind to solid phase
allergen
- The paper disc is washed to remove all unbound sera and IgE
- The disc is then exposed to rabbit anti human IgE antibody which are radiolabelled. It
interacts with Fc determinant portion of human IgE bound to the solid phase allergen

173
 SPT RAST
Time for result immediate Days to weeks
Cost cheap expensive
Safety Safe – inhalant only Very safe
Sensitivity sensitive Slightly less sensitive
Affected by therapy yes no
Other requirement Training for performance and Trained operator and
interpretation interpreter requires
Treatment
1. Avoidance of allergen
2. Pharmacotherapy
3. Immunotheraphy
4. Surgical

Avoidance of allergen
i) Primary measures:
 Restriction to allergenic exposure to inhalant allergen in early life
 Avoid smoking during pregnancy or early life
ii) Secondary measures:
 Use washable curtain every 2weeks
 Dispose object that accumulate dust ie : thick dust accumulating carpet, curtains
 Replace air conditioning filters every 1 month
 Keep cat outside of bedroom, bathe cat every 1 month
 Increase house ventilation by opening windows

174
Pharmacotherapy
 Intermittent mild AR
 Oral H1-antihistamine or intranasal H1-antihistamine and/or decongestant or
LTRA (Leukotrience receptor antagonist --- montelukast)
 Intermittent moderate to severe AR
 Above + intranasal cortico-steroid
 Persistent mild
 Rx as intermittent mod-severe AR
 Persistent mod to severe
 Same as above
 If Rx failure, assess compliance, infection, and other causes. Consider short
course steroid or decongestant for nasal block, add ipratropium for
rhinorrhoea, antihistamine for itchiness
a. Antihistamine
H2-receptor antagonist To reduce nasal itchiness, sneezing and rhinorrhoea, less effect for
nasal congestion
Nasal antihistamine : rapid onset (<15-30min), only effective at site of administration,
require twice dosing, some intranasal antihistamine has bitter taste
Oral antihistamine : onset 1hour, has properties to relieves allergy at other site aside from
nasal site, may be use prior to exposure to allergen
First generation antihistamine : use is limited at it has sedatives and anticholinergic effect,
short lived, may impair cognitive function of children thus reduce performance in school, Eg
of 1st generation : Piriton
Second generation antihistamine : less undesirable CNS effect and anticholinergic effect
compare to 1st generation, have little or no sedative effect. Eg of 2nd generation : Loratadine,
desloratadine

b. Corticosteroid
Strong anti inflammatory properties by reducing cytokine and chemokine effect
Nasal corticosteroid : onset of action 6-12hours with maximum efficacy after 2/52, more
efficacious that antihistamine for relieve of nasal obstruction, aqeous preparation is
preferred as it is less irritative for nasal mucosa

175
 Oral corticosteroid : last resort when all other therapeutic agent is not effective, short
course (5-7days) for severe symptoms refractory to 1st line medication and nasal polyps,
avoid in young children.

c. Cromones (nasal)
Prevent release of inflammatory chemical eg :histamine release from mast cell
Less effective compare to antihistamine and corticosteroid
Poor compliance as need for frequent administration
Excellent safety profile, suitable options for children and pregnancy

d. Decongestant
Provoke vasoconstriction by acting upon adrenergic receptors thus relieving swelling of
nasal mucosa
Nasal decongestion : very effective in relieving nasal obstruction, usage for <5/7 to avoid
rebound vasodilatation (rhinitis medicamentosa) and atrophic rhinitis with prolonged usage
Oral decongestion : weaker effect that nasal decongestion but do not cause rebound
vasodilatation, combination with antihistamine is more effective

e. Anticholinergic
Block muscarinic receptor of seromucinous gland
Iptratropium bromide effectively control watery rhinorrhoea, but does not affect sneezing
or nasal congestion
Can be use with intranasal corticosteroid and antihistamine in patient with predominant
symptoms of rhinorrhoea or those not responding with other medication

f. Leukotriene receptor antagonist

Efficacy similar to oral antihistamine
Therapeutic use either alone or combination with antihistamine, eg: combination
antihistamine and montelukast more effective for nasal and ocular symptoms
Preferred in patient with co-existing asthma

176
Immunotherapy

Surgical
For those with persistent nasal block despite Rx
 Inferior turbinate surgery
 Turbinoplasty
 Radiofrequency ablation
 Submucosal diathermy
 Turbinectomy
 Septoplasty & FESS play little role, unless DNS or co-exist with rhinosinusitis

177
2.ACUTE & CHRONIC RHINOSINUSITIS

Rhinosinusitis in adults:
Inflammation of the nose and the PNS characterized by TWO or more symptoms, one of which
should either be:
– Nasal blockage/obstruction/congestion or nasal discharge (anterior/posterior nasal drip)
± facial pain/pressure
± reduction or loss of smell
AND at least one of the following:
– Endoscopic signs of
- Nasal polyps, and/or
- Mucopurulent discharge primarily from middle meatus and/or
- Oedema/mucosal obstruction primarily in middle meatus
– CT changes:
- Mucosal changes within the osteomeatal complex and/or sinuses
– Past history of CRS (medically diagnosed)

Rhinosinusitis in children:
Inflammation of the nose and the paranasal sinuses characterized by two or more
symptoms, one of which should be:

– Nasal blockage/obstruction/congestion or nasal discharge (anterior/posterior nasal drip)

± facial pain/pressure
± cough
AND at least one of the following:
– Endoscopic signs of
- Nasal polyps, and/or
- Mucopurulent discharge primarily from middle meatus and/or
- Oedema/mucosal obstruction primarily in middle meatus
– CT changes:
- Mucosal changes within the osteomeatal complex and/or sinuses
– Past history of CRS (medically diagnosed)

Phases:
Acute: <12 weeks complete resolution of symptoms
Chronic: ≥ 12 weeks without resolution of symptoms (may also be subjected to exacerbation)

178
Acute Rhinosinusitis
Increase in symptoms after 5 days of persistent symptoms after 10 days with less than 12
weeks duration

To assess severity, patient is asked to indicate on visual analogue score (VAS) score (0-10)
Mild: VAS 0-3
Moderate: VAS >3-7
Severe: VAS >7-10

Acute rhinosinusitis (ARS) in adults:

sudden onset of two or more of the symptoms:
• nasal blockage/obstruction/congestion
• or nasal discharge (anterior/posterior nasal drip)
• + facial pain / pressure
• + reduction or loss of smell
for < 12 weeks; with symptom free intervals if the problem is recurrent

Acute rhinosinusitis (ARS) in children:

sudden onset of two or more of the symptoms:
• nasal blockage/obstruction/congestion
• or discoloured nasal discharge
• or cough (daytime and night-time)
for < 12 weeks; with symptom free intervals if the problem is recurrent

Questions on allergic symptoms (i.e. sneezing, watery rhinorrhea, nasal itching, and itchy watery
eyes) should be included. ARS can occur once or more than once in a defined time period. This is
usually expressed as episodes/year but there must be complete resolution of symptoms between
episodes for it to constitute genuine recurrent ARS.

179
Common cold/ acute viral rhinosinusits:
Duration of symptoms for less than 10 days.

Acute post-viral rhinosinusitis:

Increase of symptoms after 5 days or persistent symptoms after 10 days with less than 12 weeks
duration.

Acute bacterial rhinosinusitis (ABRS):

presence of at least 3 symptoms/signs of
• Discolored discharge (with unilateral predominance) and purulent secretion in the
nasal cavity
• Severe local pain (with unilateral predominance)
• Fever (>38ºC)
• Elevated ESR/CRP
• ‘Double sickening’ (i.e. a deterioration after an initial milder phase of illness)

Chronic Rhinosinusitis (with or without NP)

presence of two or more symptoms one of which should be either nasal
blockage/obstruction/ congestion or nasal discharge (anterior/posterior nasal drip):
± Facial pain/pressure;
± reduction or loss of smell;
for ≥12 weeks.
Questions on allergic symptoms (i.e. sneezing, watery rhinorrhea, nasal itching, and
itchy watery eyes) should be included.

Chronic Rhinosinusitis with nasal polyps (CRSwNP):

CRS with bilateral, endoscopically visualised polyps in middle meatus.

Chronic Rhinosinusitis without nasal polyps (CRSsNP):

CRS with no visible polyps in middle meatus, if necessary following decongestant. **This
definition accepts that there is a spectrum of disease in CRS which includes polypoid change in the
sinuses and/or middle meatus but excludes those with polypoid disease presenting in the nasal
cavity to avoid overlap.

CRS Diagnosis
Symptoms present longer than 12 weeks
Two or more symptoms one of which should be either nasal blockage/obstruction/congestion or
nasal discharge (anterior/posterior nasal drip):
± facial pain/pressure,
± reduction or loss of smell
(In children ± cough)

Signs
• ENT examination, endoscopy;
• review primary care physician’s diagnosis and treatment;
• questionnaire for allergy and if positive, allergy testing if it has not already been done.

Treatment
Treatment should be based on severity of symptoms
• Decide on severity of symptomatology using VAS and endoscope.
** Acute exacerbations of CRS should be treated like acute rhinosinusitis.

180
181
182
183
184
185
186
187
3.RECURRENT TONSILLITIS: UPDATE, DEFINITION AND MANAGEMENT
Tonsillectomy and Post Tonsillectomy Bleeding.

Definition (CPG 2018)

Tonsillectomy: surgical procedure performed with or without adenoidectomy that completely
removes the tonsils, including it’s capsule by dissecting the peritonsillar space between the tonsil
capsule and the muscular wall.

Primary bleeding: bleeding that occurs within the first 24 hours after the procedure and is generally
attributed to surgical technique and the reopening of vessels.
Rate is 0.1% to 5.8%.

Secondary bleeding: occurs more than 24 hours following the procedure often between 5 and 10 days
and is usually caused by sloughing of the primary eschar as the tonsils bed heal by secondary intention.
Rate is 0.2% to 7.5%.

Recurrent tonsillitis
- need to established that the sore throat is due to tonsillitis
- frequency (CPG 2018) 7x in a year, or 5x for 2 consecutive years, or 3x for 3 consecutive years.
- History of more than 1x peritonsillar abscess

Definition (CPG 2018) of recurrent tonsillitis with documentation by GP must include more than 1 of
the following features:
1. Temperature of more than 38.3 degree celcius (101 F)
2. With cervical adenopathy
3. Tonsillar exudates
4. Swab positive for Group A beta hemolytic streptococcus (GABHS)

*Recurrent tonsillitis with modifying factors that do not fall to above criteria but is considered for
tonsillectomy are:
1. Patient with multiple antibiotic allergies or intolerence
2. PFAPA (periodic fever, aphthous stomatitis, pharyngitis and adenitis)

188
Contraindication for tonsillectomy:
1. Concurrent URTI
2. Coagulation disorder
3. H/o cleft repair
4. Epidemic of polio – predisposed to bulbar paralysis
5. Iatrogenic nerve injury

MANAGEMENT
A. Preoperative care
- Indication as per history, clinical examination
- Anaesthetist review for fitness of op
- Preoperative bloods
- Consent for op, explanation of procedure, risks and perioperative pain counselling to
patient and caregiver
- No need for antibiotic (CPG 2018)
- Arrange for ward admission
- NBM 6 hours preop

B. Operative technique
- Patient under GA via oral ETT
- Rose position: by keeping a sand bag under the supine patient’s shoulder blades
- Avoid over extension of neck due to risk of damaging the prevertebral muscle (as it brings
the odontoid peg and arch of the axis anteriorly impinging the prevertebral muscle)
- Standard clean with normal saline and draping
- Routine check of teeth, lips, buccal mucosa
- Insert Boyle Davis mouth gag into the mouth and suspended with Draffin Bipods
- Palate is palpated to exclude submucousal cleft and also to assessed the size of adenoid.
- Throat pack is inserted
- Single dose intraoperative intravenous dexamethasone to be given (CPG 2018)

189
Adenoidectomy
- St. Claire Thompson adenoid curette is inserted into the nasopharynx above the
superior extent of adenoid tissue.
- Curette is swept down the vault of the nasopharynx using the thumb as fulcrum.
- Hemostasis, check using mirror or palpate for any residual adenoid.
o Using swab wetted with hot water or 1:1000 adrenaline
o Bipolar diathermy
o Postnasal swab as last resort
Tonsillectomy
- Superior pole of one tonsil is held witH Dennis Browne tonsillar holding forceps and
pulled medially
- Mucosa is incised with Metzenbaum soft tissue scissor near the apex of the faucial
pillar. Incision is continued inferiorly towards the tongue base.
- Blunt dissection with scissor along the tonsillar capsule laterally to create a plane in
between the tonsil and pharyngeal musculature. Medial traction should be
maintained throughout the procedure.
- Blunt dissection now proceed with Gwynne Evans tonsil dissector.
- At the junction of the tonsil and tongue base, a snare is placed over the tonsil and
positioned at the lower extent of dissection to devide its final fibrous attachment.
- Alternatively, the lower pole can be clamped with a curved artery forcep and cut with
Metzenbaum leaving the earlier forcep in place to allow ligature using 2/0 silk.
- Once tonsil is removed, a swab is placed in the fossa and the second side is attended.
- Hemostasis
o Anterior pillar of the fauces may be reflected with a Mollison pillar retractor
and bleeding points visualised is controlled using a swab by dabbing rather
than wiping motion.
o Bipolar diathermy
o Vessel ligation. A bleeding vessel is clamped with a straight artery forceps,
taking care not to include the surrounding tissue.
o A curved clamp is then placed under the tip of the straight clamp, which is
removed and 2/0 linen or silk tie places under the curved clamp using Negus
knot pusher.
- Boyle Davis mouth gag released and lower poles checked again for bleeding.
- Massaging the masseter muscle
- Throat pack removed

190
 - Check for any injury sustained over teeth, lips, buccal mucosa and jaw.
- Patient is placed on their side, slightly head down and transferred to recovery area.

C. Postoperative Care
- Careful monitoring for early detection of haemorrhage
- Regular measurement of pulse rate
- Observation for excessive swallowing or any bleeding from mouth or nose.
- Adequate analgesia
- Antibiotic as preferred in each hospital setting.

191
EMERGENCY MANAGEMENT OF POST-TONSILLECTOMY BLEEDING
*Risks of bleeding:
- Increased patient’s age
- Male sex
- H/o recurrent acute tonsillitis
- H/o peritonsillar abscess

1. Secure large bore intravenous line

2. Bloods (FBC, Blood groups, RP..)
3. Arrange for OT. NBM with intravenous fluid maintanence.
4. OP (EUA with Hemostasis)
a. In the event of failed intubation d/t frank bleeding, tracheostomy need to be
considered.
b. Transoral compression of bleeding vessel with surgeons thumb and gauze.
c. Bipolar artery
d. Dabbing with swab wetted with diluted Hydrogen Peroxide
e. Ligate artery
i. Individual external carotid branches
ii. Or suture the pillars
iii. Or ligate external carotid (final resort)
5. Intravenous antibiotic
6. Adequate analgesia
7. Postop care similar for adenotonsillectomy procedure.

REFERENCES:
1. CPG TONSILLECTOMY IN CHILDREN 2018 (UPDATED VERSION FROM 2011)
2. Operative ORL- Nigel
3. A devastating outcome after adenoidectomy and tonsillectomy: Ideas to improve,
prevention and management 2009. (Journal of ORL)

192
4.ACUTE OTITIS MEDIA (AOM) & CHRONIC OTITIS MEDIA (COM)
(Diseases of the ear, 6th edition, Harold Ludman)

Definition:
OM is an inflammation of the middle ear without reference to etiology or pathogenesis

Classifications:
Myringitis :
inflammation of the tympanic membrane that occurs alone or in association with OE / ASOM.

OM without Effusion:
inflammation of the middle ear mucosa and TM without effusion in the tympanum. It presents as
early stage of AOM or in stage of resolution. Otoscopy may show inflamed TM with normal mobility
of the ear drum

AOM:
infectious disorder of the of the middle ear and TM with signs and symptoms of inflammation of the
tympanum.

Recurrent AOM:
3 or more acute infections of middle ear in 6 month OR 4 or more episodes in 12 months duration.

COM:
infections of the middle ear that lasted for more than 3 months with perforation of the TM

OME:
is a condition characterised by a collection of fluid within the middle ear without signs of acute
inflammation

Clinical features in middle ear disease ( CPG 2012)

*(CSOM is now known as COM)

193
Predisposing factors:
1. Age
 Frequent in age less than 7 years old. Why ?
a. the incidence of URTI is higher in young children
b. eustachian tube is short, straight ( in less than 1 year old )
c. the abundant and chronically infected lymphoid tissue in the nasopharynx
d. immature immune system

2. Breastfeeding
 Incidence is lower in breastfed infants due to :
presence of immunological factors in breastmilk
allergy to cows mill causes changes in the mucous membrane of the upper repiratory
tract
difference in the development of facial musculature in breastfed and bottle fed
-difference in position between bottle fed and breastfed

3. Underlying diseases
– Cleft palate/ patulous tube/ immune deficiency
– Presence of adenoid hypertrophy

194
Pathophysiology

There are five stages in ASOM and spontaneous healing can occur in any of them
Stages Descriptions Clinical manifestations
Hyperemia - Hyperemia of mucous membrane of the  Fullness of the ear
tympanic cavity, mastoid air cells and ET  Otalgia
- Changes in mucociliary transport
- Changes in the surfactant like substance
in ET

Exudation - Serum, fibrin, RBC and PMN from the  Marked otalgia
dilated capillaries of ME, antral and  CHL
mastoid mucus membranes fill the cavity  High fever
with exudates  Systemic sx (in small
- TM thicken and bulges under pressure of children)
exudates
Suppuration - Toxic factors from inflammatory cells +  Reduction of pain
pressure in the ME TM perforation and  Fever receeding
drainage of exudates.

Coalescence - < 5% of pt have persistent otorrhea thru  Fluctuating discharge

TM perforation for > 2. and otalgia
- Progressive thickening of the mucous  Low grade fever
membrane of ME  obstruct drainage of  Leucocytosis
mucopus in the smaller air cells around  CHL
antrum
- The small air cells undergo decalcification
and osteoclastic  leading to coalescence
into larger irregular cavities filled with
pus, hypertrophic mucosa and granulation
tissue
Complication - Osteoclastic erosion progresses to bony
limit  causing brain abscess, extradural
abscess, etc

195
Microbiology: Common pathogens are -
- Viruses : Rhinovirus and RSV
- Bacteria : Streptococcus pneumonia, hemophilus influenza, Moraxella catarrhalis

Culture :
- C&S of the discharge after spontaneous perforation is reliable in the first few hours only!
- Why? Because external ear canal flora contaminates the discharge
- If need to determine the causative agent in intact TM  can aspirate the ME fluid.
(Ind: toxic children, poor response to antimicrobial, presence of suppurative cxs and newborns
with AOM)
- To avoid culture commensal bacteria of the EAC  rinse EAC with instilled alcohol (70% ) for 1
minute  then aspirate back and proceed with tympanocentesis.

Treatment
1. Antimicrobial:
o Streptococcus pneumonia, Hemophilus influenza, Moraxella catarrhalis  all sensitive to
Amoxycilin and Ampicillin.
o But Hemophilus influenza and Moraxella catarrhalis have high beta lactamase activity 
causing resistant to beta lactam antibiotics
o Thus, drugs of choice have become:
 Amoxycilin (with or without clavulanate)
 Cefuroxime
 Others: Bactrim, azithromycin, clarithromycin
o Durations: 7 days

2. Adjunctive therapy: antipyretics, topical or oral decongestants

3. Surgery:
o How about myringotomy in AOM? Reserved only for special cases
o Indications:
o severe otalgia or high fever
o toxic child
o presence of suppurative complications
o poor response to antibiotic therapy
o newborns
o primary or secondary immunodeficiency

4. Preventions:
o Adenoidectomy (in chronically infected adenoid)
o Pneumococcal and H. influenzae vaccination

196
CHRONIC OTITIS MEDIA (MUCOSAL DISEASE)

Definition:
infections of the ME lasted > 3 months with perforation of the TM.

Perforation of the TM are described according to the location:

1. Central:
o perforation at the pars tensa, location is denoted by their relationship to handle of
malleus which are anterior, posterior, inferior and superior.
o Subtotal – a large defect surrounded by a completely intact annulus
2. Marginal: usually at the posterior TM with pathological loss of annulus.
3. Attic perforation: defects of pars flaccida

Other classifications are:

1. Tubotympanic disease:
- CP will expose the MEmucosa and ET orifice, hence the name

2. Atticoantral disease:
- marginal and attic defects exposed the attic, antrum and mastoid cells, hence the name.

Aetiology
What causes persistent of TM perforation in COM?
1. Persistent infection in the ME and mastoid results in continued otorrhea
2. Continued ET obstruction preventing spontaneous closure of the perforations
3. Some perforations are too large for spontaneous closure
4. At the margins of perforations, the squamous epithelium can overgrow and impinge on the
medial side of the TM

Histopathology
The changes occurring in com without cholesteatoma are:
a. Chronic inflammatory infiltrate with increased capillary permeability of lamina propria of the
ME mucosa
b. ME epithelium undergoes transformation resembles respiratory epithelium  increased in
goblet cells  produce the discharges seen in COM
c. Inflammatory granulation tissue developed during early stages of healing after destruction of
tissue.
- Florid granulation tissue will result in aural polyps.
- Aural polyps usually covered by ciliated columnar epithelium and some may undergo
metaplastic changes ; covered with squamous epithelium
d. Late stages characterized by fibrosis and sclerotic mastoid

Other changes occur in COM;

i. Ossicular chain prone to bony loss by avascular necrosis are:
 long process of incus
 stapes superstructure
ii. Cholesterol granuloma is foreign body granulomatous response to cholesterol crystal which
frequently formed in the submucosal tissue.
o The main etiological is haemorrhage into the middle ear mucosa.
o Macroscopically, appears as yellow-brown semisolid material that fill the middle
ear.
iii. Tympanosclerosis appears as dense white deposits laid down in the TM and within the
tympanomastoid cavity.

197
Common organisms: pseudomonas aeruginosa, proteus sp., staphylococcus aureus

Examination findings:
1. Perforated TM
2. Inactive: dry ear / Active: mucoid orpurulent discharge
3. Other ME structures that can be observed: ET orifice, niche of oval and round window

Medical treatment:
1. Aural toilet
2. Topical medications
3. Systemic antibiotics

COMPLICATIONS OF SUPPURATIVE OTITIS MEDIA

Route of infection spread;
1. Extension through pathological bony defect.

2. Spread of infected thrombus within small veins through bone and dura to adjacent venous
sinuses to intracranial structures lateral sinus cause cerebellar abscess and superior petrosal
sinus causes temporal lobe abscess.

3. Spread through normal anatomical pathway – oval window, round window, cochlear and
vestibular aquaduct.

4. Spread though non anatomical defect or iatrogenic such in oval window in stapedectomy

198
INRATEMPORAL COMPLICATIONS
Acute mastoiditis AOM  subclinical mastoid infection  mastoid empyema
acute coalesce mastoidtis  subperiosteal abscess  petrositis

Clinical features:
 Pain at the McEwen’s triangle
 Sagging of the posterosuperior meatal wall due to osteitis
 Tenderness at the mastoid cortex, mastoid tip, postauricular
groove and zygomatic root
 Swelling of the postauricular region does not occur until mastoid
cortex involved.
 Pinna pushed forward.

Subperiosteal Infection spread to soft tissue  subperiosteal abscess.

abscess & Most common site is postauricula (other sites can occur too)
Postauricular Luc abscess:
fistula tracking of infection through bony erosion of EAC resulting in
subtemporal abscess

Bezold’s abscess:
perforation over mastoid tip results in abscess in the SCM

FN paralysis Infection may spread from ME to the fallopian canal via congenital
dehiscence of the canal.
Commonly found in cholesteatoma due to:
 Osteitis and bony erosion
 Compression from oedema
 Direct infection to the nerve

Suppurative In AOM via round window or oval window niche.

labyrinthitis In COM, dt bony erosion of the otic capsule.
CM:
 severe rotatory vertigo with vomiting
 spontaneous horizontal nystagmus
 profound unilateral deafness.
Tx: Medical – vestibular sedatives, etc

Labyrinth fistula Most common  arch of lateral SCC.

It causes erosion of the bony covering of the labyrinth.
Principal diagnostic sign is positive FISTULA TEST:
 tragal pressure or pneumatic otoscope  ↑ pressure at EAC
 causing stimulation of exposed membranous labyrinth 
produce eye movement and vertigo.
Lateral canal fistula anterior to ampulla  deviation of eyes to
affected side
Posterior canal fistula causes vertical deviation.

199
Petrositis Gradenigo syndrome:
1. Retroorbital pain due to V3
2. Diplopia due to VI nerve palsy
3. Otorrhea

Tx:
1. Urgent treatment with high dose antibiotics
2. If failed abx, do surgical exploration
Cortical Mastoidectomy with skeletonization of SCC and any
pneumatized tracts sb followed along posterior superior route
to petrous apex.

INTRACRANIAL COMPLICATIONS
Extradural abscess Occurs after bone erosion adjacent to middle and posterior fossa
dura

Subdural abscess Spread of infection thru dura with granulation tissue formation at
subdural spaces  form subdural abscess
Lateral sinus Sigmoid and transverse sinuses together formed  Lateral sinuses
thrombosis
Infected clot in the lumen  results in bacteremia, septicemia and
septic embolization.

Clinical features:
 Headache, rigors, fever
 Spread to the neck results in tenderness along IJV
 Sagittal sinus thrombosis: papilloedema and visual loss
 Cavernous sinus thrombosis: proptosis and chemosis
 A rare findings of pitting oedema around the occiput caused
by thrombosis in large mastoid emissary vein –
GRIESINGER’S SIGN

Diagnosis : Delta sign on CT scan

200
CHOLESTEATOMA
Definition (by Abramson et al):
Cholesteatoma is a 3D epidermal and connective tissue structure usually in the form of sac and
frequently conforming to the architecture of the various spaces of the middle ear, attic and mastoid.

Classification:
1.Based on etiology:
a) Congenital cholesteatoma
b) Acquired cholesteatoma:
a. primary (no previous history of infection)
b. secondary (follow active middle ear infection)

2.Based on anatomical site:

a) Pars Tensa cholesteatoma: results from retraction pocket or perforation at posterosuperior
quadrant of the TM
b) Pars Flaccida cholesteatoma: results from retraction pocket or perforation of pars flaccida
c) Occults cholesteatoma: occurs deep to an intact TM and often congenital

Theories of Cholesteatoma:
1. Congenital cell rest
2. Metaplasia of the middle ear epithelium
3. Papillary ingrowth through an intact TM
4. Invagination of epthelium into pre pre existing retraction pocket or perforation of the TM

Epidemiology:
 Common in children 10 - 19 years old
 Common in children with cleft palate (due to ET dysfunction)

Histopathology
- Cholesteatoma capsule consist of fully differentiated stratified squamous epithelium resting
on connective tissue.
- Able to erode any bone in contact with squamous epithelium.
- The most susceptible to erosion are:
o long process of incus
o stapes superstructure.
- Its ability to erode bone due to activation of the osteoclasts.

Microbiology:
Common organism found in infected cholesteatoma are Pseudomonas aeruginosa and proteus
species.

How does the cholesteatoma developed ?

Pars tensa cholesteatoma:
 Chronic impairment of the ME ventilation  loss of fibrous layer of the TM at the
posterosuperior quadrant  retraction onto the incus long process, incudostapedial joint
and the promontory  repeated inflammation at the ME cleft leads to adhesion between
TM and medial wall of the ME and development of fixed retraction pocket

Pars flaccida cholesteatoma:

 Progressive enlargement of the attic retraction pocket  retention of the desquamated
keratin osteitis, granulation tissue and erosion of the scutum

201
Radiology:
Requirement for CT scan:
- To demonstrate underlying anatomical variation
- The extent and nature of the disease

Points that should take note when review the CT scan ;

1. Extend of mastoid pneumatization
2. Positions of the sigmoid sinus and the tegmen tympani
3. Characteristic bony erosion

202
SADE CLASSIFCATION for Pars Tensa Retraction

203
FREQUENTLY ASKED QUESTIONS

1. What is the name of the incision site in mastoidectomy? Why do you choose that incision?
Postauricular incision , which is 0.5 to 1 cm from the posterior auricular sulcus. However, we should
also takes into consideration of the age of the patient, as the pinna is smaller in younger age. The
incision may be exposed , thus for cosmetic reason, the outline of the incision site also depends on
the pinna size.

2. What are the landmarks for MRM? And WHY?

Mc ewen’s triangle – posterior wall of eac , mastoid tip , spine of henle and temporal line . it
indicates the mastoid anthrum

3. What are the common sites for recurrence of cholesteatoma?

Sinus tympani, sinodural angle, mastoid tip, eustachian tube ( need to find further references)

4. What are the boundaries of sinus tympani?

5. What is the first ossicles that commonly eroded FIRST in cholesteatoma? And WHY?
Long process of incus because it has a single blood supply (Cummings, 2017)

204
5. LPR (Laryngopharyngeal Reflux)
Definition:
Laryngopharyngeal reflux (LPR) is an inflammatory condition of the upper aerodigestive tract tissues
related to direct and indirect effect of gastroduodenal content reflux, which induces morphological
changes in the upper aerodigestive tract.
*Indirect effect: by neuroreflexive signaling and compensatory vagal responses

Epidemiology: Real incidence and prevalence are inaccurate and difficult to estimate worldwide
because of lack of diagnostic criteria.

Clinical presentation:

A. Symptoms (according to Reflux Symptom Index (RSI)).

 Hoarseness.
 Throat clearing.
 Postnasal drip.
 Dysphagia: difficulty in swallowing solids, fluids or tablets.
 Coughing after eating or lying down.
 Breathing difficulties or choking episodes.
 Annoying cough.
 Globus sensation.
 Burning, heartburn, chest pain, indigestion, or stomach acid coming up (reflux).
 Other symptoms (not on RSI): throat pain, odynophagia, ear pressure, eructation, or
halitosis.

B. Signs/ Findings (according to Reflux Finding Score (RFS)).

1) Subglottic edema (pseudosulcus).

205
 (A) Bilateral pseudosulcus vocalis (arrow).
Notice the subglottic edema extends
past the vocal process all the way to
the posterior larynx. Also present are:
a. posterior commissure hypertrophy
b. vocal fold edema
c. diffuse laryngeal edema
d. partial ventricular obliteration.

2) Ventricular obliteration.

Ventricular obliteration.
(A) Open laryngeal ventricles. Note
the sharp ventricular bands and the
open space between the true and
false vocal folds. Note small
prenodules.

(B) Ventricular obliteration. Both

the true and false vocal folds are
swollen, thus obliterating the
ventricles. Also present is mild
posterior commissure hypertrophy.

3) Erythema/hyperemia.
4) Vocal fold edema.
5) Diffuse laryngeal edema.
6) Posterior commissure hypertrophy.
7) Granuloma/granulation tissue.

206
 Reflux-Induced Granulomas and
Pseudosulcus

8) Thick endolaryngeal mucus.

9) Other findings (not on RFS): vocal fold erythema, leukoplakia, keratosis, posterior
pharyngeal wall inflammation, anterior pillars inflammation, coated tongue.

207
Pathogenesis of sign & symptoms:

MUCOSAL IRRITATION

- Inflammatory Stimulate mucosal Inflammation

reaction & chemoreceptor (at
- Dry (sticky) mucus distal esophagus)
Macroscopic & microscopic
hypersecretion histological changes in vocal
(dt pepsin ↓ fold mucosa.
mucin expression
& bicarbonate Mucus
secretion) hypersecretion Modifies biomechanical
properties of VF

Impair voice quality

Accumulation of subjectively and objectively:
sticky mucus Hoarseness

Dev symptoms: Dev symptoms:

- Post nasal drip - Dysphagia
- Globus sensation - Throat pain
- Throat clearing - Odynophagia
- Cough, Choking - Globus sensation

Sign and symptom prevalence

 75%: Globus sensation, throat clearing, hoarseness, excess throat mucus, and postnasal drip.
 Classical GERD symptoms eg: heartburn - less prevalent in LPR in comparison with GERD.
 LPR findings: thick endolaryngeal mucus, and laryngeal erythema (most prevalent).

Diagnosis

No gold standard (LPR diagnosis is probably the most controversial aspect of the disease).

1. Multichannel intraluminal impedance-pH metry.

a. Most reliable examination to perform the diagnosis.
b. Detects acid and non-acid reflux.
c. Probe placements:
i. proximal probe is usually placed 1cm below or 1–3cm above upper esophageal
sphincter (**remains controversial: intraesophageal vs hypopharyngeal).
ii. distal sensor at 5cm above lower esophageal sphincter.
d. Diagnostic criteria: 1 or more LPR events in proximal probe should be considered
abnormal in patients with LPR symptoms (**but still no international consensus).

208
 2. Empirical therapeutic trial.
a. utilization of some clinical scores such as RSI (RSI >13) and RFS (RFS >7) at baseline and
the prescription of proton pump inhibitors (PPIs) for a 3-month setup period.
b. improvement or not → titration of the PPI dose upwards (for three additional months).
c. LPR diagnosis is only considered if the patient responds after 3 or 6 months of treatment.
d. Diagnosis of nonresponder patients remains uncertain; requires additional examinations
(MII impedance-pHmetry).
e. definitions concerning the response to treatment:
i. improvement of 50%of symptom score after treatment.
ii. reduction of 5–10 points at RSI.
iii. the reduction of both RSI less than 13 and RFS less than 7 after 3 or 6 months of
treatment.

3. Pepsin and trypsin detection.

o analyses of pepsin or trypsin detection: on saliva, or in pharyngeal or laryngeal biopsies
(more sensitive but invasive) → detection using Peptest commercial kit (immunoassay),
ELISA or western blot.

4. Endoscopic Findings.
a. Endoscopic findings (RFS) in combination with symptoms (RSI).
b. Multiple studies done using digital image endoscopy to enhance endoscopic findings in
detecting mucosal changes in LP Reg: I-Scan (Pentax) and Narrow Band Imaging
(Olympus).

Treatment

1. First-line LPR treatment combines:

o Diet modification
o PPIs
o Sodium alginate (acid or mixed reflux)
 Alginate drugs make sense in case of nonacidic, mixed reflux, or in patients
with postprandial symptoms.
o Magaldrate anhydrous (biliary reflux)
 Combination of Magaldrate (after meals) + Alginate (bedtime) mb useful for
many patients.
o +/- Gastroprokinetic.
2. H2-receptor antagonists (at bedtime) are only recommended as second line treatment in
patients with LPR and GERD, or partial response to PPIs but physicians must keep in mind that
these molecules have a relatively short duration of action (4–8 h).

References:
1. Lechien JR, Saussez S, Karkos PD. Laryngopharyngeal reflux disease: clinical presentation, diagnosis and therapeutic
challenges in 2018. Curr Opin Otolaryngol Head Neck Surg. 2018;26(6):392-402.
2. Koufman JA, Aviv JE, Casiano RR, Shaw GY. Laryngopharyngeal reflux: position statement of the committee on speech,
voice, and swallowing disorders of the American Academy of Otolaryngology-Head and Neck Surgery. Otolaryngol Head
Neck Surg 2002; 127:32–35.
3. Belafsky PC, Postma GN, Koufman JA. The validity and reliability of the reflux finding score (RFS). Laryngoscope 2001;
111:1313–1317.
4. Belafsky PC, Postma GN, Koufman JA. Validity and reliability of the reflux symptom index (RSI). J Voice 2002; 16:274–
277.

209
210