Head & Neck, ENT Flashcards
What are the neck fascia?
A. Superficial cervical fascia
- lies between dermis and investing layer of deep cervical fascia
- contains the plastysma, and cutaneous vessels, nerves, lymphatics, fats
B. Deep cervical fascia
- *1) Investing layer of deep cervical fascia**
- contains SCM and trapezius
- arises from skull superiorly, attach to scapular spine, acromion, and clavicles inferiorly
- *2) Pretracheal fascia**
- anterior neck only
- extends inferiorly from hyoid bone into the thorax, merges with fibrous pericardium
- contains thyroid, trachea, esophagus
- *3) Prevertebral fascia**
- from base of skull to T3 vertebra
- contains vertebral column and associated muscles
- extends laterally as axillary sheath
4) Carotid sheath
How might deep fascia influence the spread of infection from the neck?
The neck fascia determines the direction in which a neck infection may spread:
- the investing layer of deep cervical fascia prevents the spread of abscesses
- if investing layer is breached, an infection between the investing and pre-tracheal layer can spread inferiorly to the thoracic cavity anterior to fibrous pericardium
- if abscess is located posterior to the pre-vertebral fascia, then it can extend laterally
What are the main neck muscles
i) innervation
ii) attachment
iii) function
- *1) Platysma**
i) innervated by CN VII (facial nerve)
ii) attach from mandible to pectoral muscle
iii) function: draws down corners of mouth - *2) Sternocleidomastoid (SCM)**
i) innervated by CN XI (accessory nerve)
ii) attach from mastoid to manubrium and clavicular head
iii) function: rotates head - *3) Trapezius**
i) innervated by CN XI (accessory nerve)
ii) Originates from occiput and spinous processes, cervical and thoracic vertebrae; inserts to scapular and clavicle
iii) function: elevates scapula
Where is the root of the neck?
- what is the boundaries
- what are the contents
Root of the neck refers to the junction between the thorax and neck, where structures pass from thorax to head:
- *Boundary:**
- anterior: manubrium
- posterior: body of T1
- lateral: 1st rib and costal cartilage
- *Contents:**
- Arteries: Brachiocephalic trunk (R), left CCA, left subclavian artery
- Veins: anterior jugular vein and IJV forms brachiocephalic vein, and EJV / subclavian vein
- Nerves: vagus nerve, RLN, phrenic nerve, sympathetic trunks, cervical sympathetic ganglia
What are the anatomical zones of the neck?
What is its clinical relevance?
Zone I
- from sternoclavicular notch to cricoid carilage
- vulnerable structures: cervcial pleura, lung apex, thyroid, trachea, esophagus, jugular vein, cervical vertebrae
Zone II
- from cricoid cartilage to angle of mandible
- vulnerable structures: larynx, pharynx, carotids, jugular vein, cervical vertebrae
Zone III
- from angle of mandible to base of skull
- vulnerable structures: oropharynx, oral cavity, nasal cavity
==================
It is used to describe penetrating trauma to neck:
-> Zone II is the most exposed zone, and is consequently the most likely to be injured; but best prognosis
-> Zone I and III has greatest morbidity and mortality, because:
i) may obstruct airway
ii) injured structures are difficult to visualise
iii) harder to control vascular damage by direct pressure in comparison to Zone II
Levels of neck LN
- *1a: Submental
1b: Submandibular** - *2: Upper jugular**
- from base of skull, to inferior border of the hyoid bone
- *3: Middle jugular**
- from inferior border of the hyoid bone, to inferior border of cricoid cartilage
- *4: Lower jugular**
- from inferior border of cricoid cartilage, to clavicles
- *5a: Posterior triangle
5b: Supraclavicular fossa** - *6: Anterior compartment**
- Pretracheal, paratracheal, precricoid (Delphian) and perithyroid nodes
7: Upper mediastinal
Drainage of neck lymph nodes
Level I
- Anterior nasal cavity
- Oral cavity
- FOM, tongue
Level II
- Nasal cavity, para-nasal sinus, nasopharynx
- Oral cavity, orophaynx
- Hypopharynx, supraglottic larynx
- Parotid and submanidbular glands
Level III
- oropharynx, hypopharynx, larynx
Level IV
- hypopharynx, larynx
- cervical esophagus
- thyroid
Level V
- oropharynx, nasopharynx
- posterior neck and scalp
Level VI
- thyroid
Anterior & posterior neck triangle borders
- *Anterior triangle:**
- Inferior aspect of mandible
- anterior border of SCM
- anterior midline
- *Posterior triangle:**
- Posterior border of SCM
- Anterior border of trapezius
- Clavicle
Content in the posterior neck triangle
“SEreBII”:
1) Subclavian artery
2) External jugular vein
3) Brachial plexus (trunk)
4) CN XI
Borders of Sub-triangles in Anterior neck triangle
- *1) Submental**
- inferior border of mandible
- anterior belly of digastric
- hyoid
- *2) Submandibular**
- inferior aspect of mandible
- anterior & posterior belly of digastric
- *3) Carotid**
- posterior belly of digastric
- superior belly of omohyoid
- anterior border of SCM
- *4) Muscular**
- superior belly of omohyoid
- anterior border of SCM
Content in the carotid triangle
- *1) Carotid sheath**
i) common carotid artery (medially)
ii) IJV (laterally)
iii) vagus nerve CN X (posteriorly at the middle) - *2) Ansa cervicalis**
- lies within the anterior wall of the sheath over the jugular vein
3) Hypoglossal nerve CN XII
Define Neck dissection terminologies
- *1) Radical Neck Dissection:**
- ipsilateral level 1-5
- SCM
- spinal accessory nerve
- internal jugular vein
- *2) Modified radical neck dissection**
- ipsilateral level 1-5
- preserve 1+ of (SCM, spinal accessory nerve, IJV)
- *3) Functional neck dissection**
- ipsilateral level 1-5
- preserve all of SCM, spinal accessory nerve, IJV
- *4) Selective Neck Dissection**
- preservation of 1 or more of level 1-5 LN
- Supraomohyoid SND (Level 1-3)
- Lateral SND (Level 2-4)
- Postero-lateral SND (Level 2-5)
- *5) Extended Neck Dissection**
- Radical neck dissection
- and 1+ additional LN groups or nonlymphatic structures
- *6) Central compartment dissection**
- dissection of level 6 only (usu for thyroid)
Selective neck dissection in HnN cancers
Oral cavity cancer:
- Selective 1-3 (aka supraomohyoid SND)
+ level 4 in tongue cancer because of skip lesion
- *Orophaynx, hypopharynx, larynx:**
- Selective 2-4 (aka lateral SND)
- *H&N skin cancer:**
- Selective 2-5 (aka posterolateral SND)
Drainage of pharyngeal cancer to cervical LN
- *1) Nasopharynx (NPC):**
- Level 2-5
- *2) Oropharynx:**
- Level 1-3
- *3) Laryngo-pharynx:**
- Level 2-6
General Mx approach to HnN cancers
- *1) Resection**
- preserve important organ functions
- oncologically clear margins
2) Reconstruction
3) ± Neck dissection
4) Rehabilitation
Margins of resection for skin tumours on head
Squamous cell carcinoma: 1-2cm
Basal cell carcinoma: 3-5mm
Melanoma: 5-50mm
Dermatofibrosarcoma protuberans: 3-5cm
Common histology of H&N cancer
90% is Squamous Cell carcinoma
Common sites of HnN cancers
1) Nasopharynx: fossa of Rosenmuller
- *2) Oral**
- tongue (most common)
- buccal mucosa, lips, floor of mouth, hard palate
- *3) Oropharyx**
- Tonsil (most common)
- tongue base > soft palate
- *4) Hypopharynx**
- Piriform fossa (most common)
- post cricoid > posterior pharyngeal wall
- *5) Larynx**
- glottic > supraglottic > subglottic
Risk factors for Head and Neck cancer (SqCC)
- *Environement factor**
1) Smoking
2) Spirits, alcohol
3) Sharp teeth
4) Betel nut chewing (嚼檳榔 in TW)
5) Previous H&N RT
Patient factor
1) Male Sex (M:F = 4:1)
2) Dental Sepsis
3) Syphilis, HPV
4) GERD
5) Primary H&N tumour (synchronous tumours)
6) Family history
________
think about 6S of oral cancer:
- smoking, spirits, sex, syphilia HPV, sharp teeth, sepsis dental
Ix in head and neck tumours
- *1) Incisional biopsy**
- NOT excisional
- *2) USG, FNAC**
- mass or LN
3) Pan-endoscopy ± biopsy
to look for SYNCHRONOUS tumours
- flexible rhinoscopy
- flexible laryngoscopy
- OGD
- bronchoscopy
- *4) CT, MRI of H&N**
- T, N staging
- look for boney erosion in skull base, orbit
- *5) PET/CT, Bone scan**
- for distant & bone met
Staging of H&N tumours
TNM staging is same except nasal cavity & nasopharynx
T (2-4)
T1: <2cm
T2: 2-4cm
T3: >4cm
T4: adjacent structure
N (3-6) based on size
N1: <3cm
N2: 3-6cm
a: single; b= multiple; c = bilateral
N3: >6cm
M
M1: met
history taking of symptoms Head and Neck cancer (pre-op)
1) Primary Symptoms
2) Symptoms suggestive of synchronous tumours (ask ALL)
Nose
- epistaxis; blood mixed in sputum
- nasal obstruction
- post nasal drip
Ear
- hearing loss
- tinnitis
- otalgia
Mouth
- mass, ulcers, pain
- blood in saliva
- trismus
- loose teeth
Throat
- sore throat
- hoarseness
- dyspnoea
- dysphagia
- haemoptysis
- *3) Metastatic symptoms**
- local: visual, headache, neurological
- lymph: lymph nodes
- distant: lung as SOB, bone pain
Additional aspects affected by H&N cancers
(ask these in history!)
As H&N is the most exposed area of body, will affect morphology & physiology:
- *1) Morphology**
- affects external appearance & aesthetics
- psycho-social complications
- *2) Physiology** (as large number of vital organs in small area):
- vision
- airway
- taste
- swallowing
- speech
Major functions requiring rehabilitation after HnN cancer surgery
- *1) Vision**
- reduced visual acuity from CNII infiltration or RT
- dry eyes (post RT)
- epiphora: lacrimal drainage onbstruction from surgery
- diplopia from muscle impingement
- dystopia from orbital floor invasion
- *2) Airway obstruction**
- temporary oedema
- permanent stricture
- *3) Taste**
- temporary loss of taste (chemo)
- permanent after RT or surgery
- *4) Swallowing**
- immediately dysphagia after glossectomy or pharyngectomy
- delayed dysphagia post RT
- *5) Speech**
- Loss of phonation (post laryngectomy)
- Loss of articulation (glossectomy, nasal, paranasal sinus surgery)
Function preservation Mx for HnN tumours
- *1) Vision**
- eye shield during RT
- chloramphenicol ointment for dry eyes
- tarsorrhaphy
- *2) Airway**
- tracheostomy
3) Taste… :(
- *4) Swallowing**
- anastomosis
- speech therapist
- *5) Speech**
- voice prosthesis
- speech therapy
Oral cavities spaces
1) Oral cavity proper: space medial or posterior to teeth
2) Vestibule: space between teeth and cheek
- *3) Oropharynx:**
- behind the glossopalatine arch (anterior pillars)
Arterial supply of oral cavity
- *External carotid artery branches:**
- Lingual artery
- Facial artery
- Maxillary artery
Nerve supply of oral cavity
- Sensation: V2, V3
- Muscle of mastication: V3
- Tongue: XII (except Palatoglossus which is pharyngeal plexus)
- Taste: VII (chorda tympani)
PE in oral lesions
Get gloves, penlight, tongue depressor:
0) General Examination
- *1) Ask patient to “AHH” open mouth, stick out tongue**
- note hoarseness of voice
- note trismus, ankyloglossia
- *2) Inspection of oral cavity**
- palate (roof)
- buccal mucosa (sides)
- floor of mouth (below tongue)
- vestibule using 2-prong technique
- tonsils
- anterior & posterior fallucial pillars
- oropharynx
- “comment on alveolar & gum health”
- “to complete by looking @ tongue base using indirect mirror”
- *3) Inspection of tongue**
- lateral border
- frenulum & inferior aspect
- look for movement
- *4) Palpation**
- try scraping white lesions
- characterise the mass
- BIMANUAL PALPATION
- *5) Neck exam, Cranial Nerve exam**
- for LN, facial nerve involvement
White oral lesions DDx
1) Leukoplakia
2) Lichem planus
3) Candidiasis, secondary syphilis, EBV hairy leukoplakia
4) Linea Alba
5) Leukoedema
6) Papilloma
7) Verrucous carcinoma, Squamous cell carcinoma
8) Geographic tongue
9) Hairy tongue
Presenation of oral infective white lesions:
- *1) Oral candidiasis**
- white, easily scrapped off white plagues
- shows hyphae in Gram stain
- *2) 2° syphilis**
- Snail track
- *3) EBV**
- hairy leukoplakia
Why are some oral lesion white?
White colour due to scattering of the light through an altered epithelial surface
Leukoplakia
- White patch firmly attached to oral mucosa which cannot be rubbed off
- Precancerous; 5% undergo malignant change
Lichen Planus
- Common chronic inflammation of oral mucosa (usually buccal mucosa)
- T cell mediated auto-immune
- “Wickham’s striae” (white striae around the lesion)
- Skin manifestations: pruritic papules on flexor surface
- Low malignant potential
What is this? Contributing factors?
- *Oral candidiasis**
- Creamy-white
- elevated, removable plaques
Risk factors:
Local
- poor oral hygiene, xerostomia, dentures
Systemic
- immunocompromised: steroids, antibiotics, radiation, HIV, haematological malignancy, neutropenia
- *Linea Alba**
- Normal linear elevation of the buccal mucosa extending from the corner of the mouth to the 3rd molars at the occlusal line
- *Leukoedema**
- Normal anatomic variant of the oral mucosa
- Bilateral, involves most of the buccal mucosa (rarely the lips and tongues)
- If streched, will become red again
- Increased thickness of epithelium and intracellular edema of prickle cell
Exophytic white mass in oral cavity
- *1) Papilloma**
- Exophytic, painless
- fingerlike projections forming cauliflower pattern
- usually solitary
- *2) Verrucous Carcinoma**
- Exophytic
- Low-grade variant of SCC
- HPV related
- *3) Squamous cell carcinoma**
- Early SCC looks like leukoplakia
- 6 Ss
Red intra-oral lesions DDx
Red due to thin epithelium, inflammation, dilatation of blood vessels, increased number of blood vessels, extravasation of blood:
1) Trauma
2) Infection (Stomatitis, Glossitis)
3) Lupus erythomatosus, Reactive arthritis (Reiter’s syndrome)
4) Erythroplakia (pre-malignant)
5) Hereditary hemorrhagic telangiectasia
Erythroplakia
- Red, non-specific, well-demarcated patch that cannot be classified under any other disease
- 15 times increased risk of SCC
- 90% CIS or SCC at time of diagnosis
Pigmented intra-oral lesions
1) Malignant melanoma
2) Lentigo
3) Pigmented naevi
4) Black hairy tongue
5) Smoker’s melanosis
6) Amalgam tattoo (from adj dental fillings)
7) Peutz-Jeghers syndrome
8) Addison disease
Malignant melanoma characters
ABCDE
A - Asymmetrical Shape
B - Border is irregular
C - Color is variegated
D - Diameter >6mm
E - Evolution
Oral ulcerative lesions DDx
1) Traumatic ulcers (Sharp tooth, dentures etc)
- *2) Aphthous ulcer** (major, minor, herpetiform)
- SLE
- Reiters syndrome
- *3) SqCC**
- Everted, irregular edge with dirty floor
- Indurated base
- Painless at first, then painful with nerve infiltrated
4) Infective ulcers
Infective oral ulcer causes
- HSV
- Herpangina by Coxsackie virus
- TB
- Syphilis – 1°, 2°, 3°
Intra-oral mass DDx
Benign vs Malignant:
MALIGNANT:
★ 1) SqCC, verrucous carcinoma
★ 2) Minor salivary gland adenocarcinoma
3) lymphoma
4) melanoma
5) Kaposi sarcoma
BENIGN:
- *1) Fibroma**
- hard nodule
- *2) Ranula**
- At Floor of mouth
- soft pseudocyst filled with saliva
- Due to Blocked sublingual duct
- *3) Lipoma**
- Soft mass
- *4) Torus palatini**
- at the hard palate
- Boney hard
- normal anatomical variation
How to investigate oral mass
(aka what to Ix when suspicious of oral cancer)
(actually same as H&N with additional Ix*)
- *1) Incisional biopsy**
- for oral lesions that persist for >3 weeks
- *2) USG, FNAC**
- for enlarged LN
3) Pan-endoscopy ± biopsy
to look for SYNCHRONOUS tumours
- flexible rhinoscopy
- flexible laryngoscopy
- OGD
- bronchoscopy
4*) Orthopantomogram (look for bone erosion)
- *5) CT, MRI of H&N**
- T, N staging
- look for boney erosion in skull base, orbit
- *6) PET/CT, Bone scan**
- for distant & bone met
Risk factors for oral cancer
- *Environement factor**
1) Smoking
2) Spirits, alcohol
3) Sharp teeth
4) Betel nut chewing (嚼檳榔 in TW)
5) Previous H&N RT
Patient factor
1) Male Sex (M:F = 4:1)
2) Dental Sepsis
3) Syphilis, HPV
4) GERD
5) Primary H&N tumour (synchronous tumours)
6) Family history
________
think about 6S of oral cancer:
- smoking, spirits, sex, syphilia HPV, sharp teeth, sepsis dental
Pre-malignant intra-oral lesion
- erythroplakia
- leukoplakia
- erythroleukoplakia
- proliferative verrucous leukoplakia
Common sites of oral cavity cancer
- *1) Tongue** (most common)
- lateral margin, middle third
- *2) Lips**
- lower half
- *3) Floor of mouth**
- anteriorly below tongue
4) Buccal mucosa
5) Alveolus & gingiva
6) Hard palate
Where to take biopsy in a tongue ulcer?
Ulcer edge, because:
- can compare with normal tissue
- easier to suture for haemostasis
Management of CA tongue
- *1) Resection of the tumour** with adequate margins
- partial glossectomy if T1 (<2cm)
- hemiglossectomy if T2 (2-4cm)
- total glossectomy (might need concommitant laryngectomy due to aspiration risk)
- *2) Adequate neck dissection**
- Selective neck dissection of I-IV (classically is I-III i.e. supraomohyoid neck dissection but can skip metastasis to level IV)
- *3) Reconstruction**
- ALT flap
4) Adjuvant RT
DDx of ulcer on tonsils
Tonsillar ulcer can be due to:
- *1) Infective**
- acute tonsillitis
- diptheria
- infectious mononucleosis
- *2) Neoplasm**
- orophayngeal SCC
- lymphoma
- salivary gland tumour
- *3) Blood disease**
- agranulocytosis
- leukaemia
- *4) Others**
- apthous ulcer
- Bechets disease
- AIDS
Boundaries of oropharynx
Roof: oral surface of soft palate & uvula
Lateral: anterior & posterior pillars (glossopalatine arch & pharyngopalatine arch), palatine tonsils
Anterior: posterior third of tongue & vallecula
Posterior: level of hard palate to aryepiglottic fold
Common sites of oropharyngeal cancer
- Tonsils 50%
- Tongue base 25%
- Soft palate 10%
- Posterior wall 5%
Risk factors for oropharyngeal cancer
6Ss:
1) Smoking
2) Spirits, alcohol
3) Sharp teeth
4) Male Sex (M:F = 4:1)
5) Dental Sepsis
6) Syphilis, HPV
7) Betel Nut chewing (嚼檳榔 in TW)
Important Hx to ask in suspected oropharyngeal cancer
(+ what are the symptoms of oropharyngeal cancer)
- *1) Symptoms**
- local ulcer, pain
- sore throat, muffled hot potato speech
- trismus
- dysphagia, odynophagia
- constitutional symptoms
- cervical lymphadenopathy
- *2) Risk factors**
- 6Ss (Smoking, spirits, sharp teeth, male sex, dental sepsis, syphilis, HPV, betel nut)
- *3) Other primary cancer** (VERY IMPORTANT)
- 30% synchronous primary
- 1.5% yearly cummulative risk of metachronous tumour
Investigation in suspected oropharyngeal cancer
(actually same as H&N with additional Ix*)
1*) EUA (examation under anaes), biopsy, tonsillectomy
- *2) USG, FNAC**
- for enlarged LN
3) Pan-endoscopy ± biopsy
to look for SYNCHRONOUS tumours
- flexible rhinoscopy
- flexible laryngoscopy
- OGD
- bronchoscopy
- *4) CT, MRI of H&N**
- T, N staging
- look for boney erosion in skull base, orbit
- *5) CXR, PET/CT, Bone scan**
- for distant & bone met
Management of oropharyngeal cancer
1) Resection
- *2) Lymph node clearance**
- Level II-IV (lateral selective neck dissection)
3) Reconstruction
- Soft palate, tonsillar fossa: radial forearm free flap
- Extensive palatomaxillary defects: prosthesis or vascularized bone-containing free flaps
4) Chemo-RT
Sites of Hypopharyngeal carcinoma
(where are hypophayngeal carcinoma?)
i.e. from the laryngopharynx (Level of hyoid to lower border of cricoid):
- 60% Piriform fossa
- 30% Postcricoid
- 10% Posterior pharyngeal wall
Hypopharyngeal carcinoma risk factors
- Smoking
- Alcohol
- Male predominance (exp in Postcricoid CA, more female than male)
- Irradiation for thyroid disease
- Plummer Vinson syndrome (aka Paterson-Kelly-Brown syndrome)
Clinical features of hypopharyngeal cancer
- Dysphagia
- Sore throat
- Hoarseness
- Otalgia
- LN 30% occult metastases
- Loss of laryngeal crepitus
Treatment of hypopharyngeal carcinoma
- *1) Surgical resection**
- Partial pharyngectomy
- Circumferential pharyngectomy + reconstruction
- Total pharyngo- laryngo- esophagectomy (PLO) with gastric pull up
- *2) Lymph node clearance**
- Level II-IV (lateral selective neck dissection)
- *3) Reconstruction**
- free flap (jejunal graft)
- regional flap (pectoralis major)
- (gastric pull-up for PLO)
4) RT
Larynx anatomy
1) Hyoid bone
- *2) Cartilages**
i) Cricoid cartilage
ii) Thyroid cartilage
iii) Epiglottis
iv) Arytenoids
v) Corniculate cartilage
vi) Cuneiform cartilage - *3) Ligaments**
- thyrohyoid ligament
- crico-thyroid ligament
- vestibular, vocal ligament
Nerves of the larynx (affected in surgery)
- *1) Recurrent Laryngeal Nerve**
- supplies all intrinsic muscles of larynx (except cricothyroid)
- *2) External** branch of Sup Laryngeal Nerve
- supplies cricothyroid muscle (tenses vocal cord)
- *3) Internal** branch of Sup Laryngeal Nerve
- sensation of vestibule
Causes of dysphonia
1) Organic
- *2) Functional**
- e.g. muscle tensional dysphonia
- *3) Psychiatric**
- Conversion disorder
Vocal cord nodules presentation and pathogenesis
aka Singer’s nodules
- *Presentation:**
- dysphonia, Breathy voice
- at junction of anterior and middle 1/3 of vocal folds
- always comes in pairs (bilateral & symmetrical), as chronic vocal trauma from vocalisation should symmetrically affect both sides of vocal folds
- *Pathogenesis:**
- Chronic vocal trauma (voice misuse) lead to local edema
- local edema causes fibrosis & nodules
Vocal cord nodules management
Speech therapy +/- excision
Vocal polyp (pathogenesis, presentation, management)
- *Pathogenesis**
- Acute vocal trauma creates haemorrhagic cyst
- becomes polyp
- *Presentation:**
- Dysphonia with breathy voice
- Unilateral protrusion
- *Management:**
- Excision
Vocal cord palsy causes
1) Idiopathic
2) Brainstem lesion
- *3) Recurrent laryngeal nerve palsy**
- CA thyroid, CA esophagus, CA lung
- Ortner syndrome in aortic stenosis
- *4) Aryteno-cricoid joint pathology:**
- intubation causing dislocation
- RA
- cancer infiltration
- *5) Iatrogenic**
- intubation
- H&N surgery
- thyroid, esophageal, cardiothoracic surgery
Management of vocal cord palsy in adults
- *1) Endoscopy**
- distinguish whether it is unilateral or bilateral
- if bilateral, whether in open or closed position
- *2) Assess airway adequacy and aspiration**
- bilateral open position -> aspiration risk
- bilateral close position -> airway obstruction
- *3) Rule out organic cause**
- CT/ MRI brain
- CT thorax
- *4a) For unilateral:**
- Vocal therapy
- Injection laryngoplasty (temporary)
- Medialization thyroplasty
- *4b) For bilateral**
- Tracheostomy for airway protection
History taking in Hoarseness
- *Onset, pattern**
- acute or chronic
- recurrent?
- acute vocal trauma e.g. screaming?
- *Occupation, vocal demand**
- singer? teacher?
- *Risk factors**
- smoking?
- GERD?
- hypothyroidism?
- neurological disorders?
- *Medical & Surgical Hx**
- CA mediastinum?
- H&N surgery?
- *Red flags for CA larynx**
- Bleeding
- Dyspnoea
- Dysphagia
- Constitutional symptoms
Ix in hoarseness
1) Cervical lymphadenopathy
2) Inspection of larynx
a) indirect laryngoscopy (DO NOT use direct layngoscopy which is for intubation)
b) Trans-nasal Flexible laryngoscopy
- less gag reflex
- inferior image quality
c) Trans-oral Rigid laryngoscopy with Stroboscopy
- Gag reflex
- better image quality
- Allows stroboscopy to detect subtle vocal cord lesions
Location of laryngeal tumour
1) Glottic 60%
2) Supraglottic 30%
3) Infraglottic 10%
CA laynx presentation
Depends on site:
- Glottic:*
- *1) Dysphonia, hoarseness of voice**
- progressive (>2 wks)
- non-resolving (>4 wks)
- Supraglottic:*
- *2) Sore throat
3) Odynophagia, dysphagia
4) Referred otalgia** - Subglottic*
- *5) Stridor, dyspnoea from airway obstruction**
- Others:*
- *6) Haemoptysis**
7) Cervical lymph node metastasis
8) Constitutional symptoms
CA larynx risk factors
1) Smoking
2) Alcohol
3) Radiation
4) Synchronous H&N cancer
5) Chronic laryngitis
6) GERD
7) Family history
HIV??
Important investigations when suspecting CA larynx
(actually same as H&N with additional Ix*)
- *1*) Flexible indirect laryngoscopy; microlaryngoscopy + Biopsy**
- assess extent of tumour
- histological diagnosis
- *2) USG, FNAC**
- for enlarged LN
3) Pan-endoscopy ± biopsy
to look for SYNCHRONOUS tumours
- flexible rhinoscopy
- flexible laryngoscopy
- OGD
- bronchoscopy
- *4) CT, MRI of H&N**
- T, N staging
- look for boney erosion in skull base, orbit
- *5) CXR, PET/CT, Bone scan, blood ALP**
- for distant & bone met
____
All of the above are for TNM stageing:
T = Local tumour stage (Endoscopy, CT/MRI)
N = Regional lymph node (USG neck + FNA)
M = Distant metastasis (CXR, Blood test, PET)
Appearance of neoplasm around vocal cord (see in indirect laryngoscope)
Requires biopsy:
- Leukoplakia
- Erythroplakia
- Mass (CA larynx)
Treatment options for CA larynx
Early stage (T1-T2)
- *1) Radiotherapy**, or
- *2) Endolaryngeal laser surgery** (preserve voice)
- *3) Partial laryngectomy** (rarely)
- e.g. vertical hemilaryngectomy; supraglottic laryngectomy
Late stage:
- *1) Resection**
- total laryngectomy
- *2) Lymph node management**
- modified radical neck dissection (or II-IV if possible)
- *3) Reconstruction**
- terminal tracheostomy + voice prosthesis
4) Adjuvant radiotherapy and chemotherapy
What are the voice prosthesis post-laryngectomy? Pros & Cons?
1) Esophageal speech
+ no prosthesis, no cost
- difficult to learn, difficult to understand
- Fragmented speech, hard to speak after eating
2) Tracheo-esophageal speech (valve prosthesis e.g. Provox)
+ good tone & understanding
- costly, unclean
- complication e.g. swallowing
3) Pneumatic device
+ tone is acceptable, cheap
- conspicuous
4) Electrolarynx
+ one-off cost, easy to learn
- monotonal robotic voice
- need battery
Cx of laryngectomy
General: bleeding, SSI, etc
- *Specific**:
1) pharyngo-cutaneous fistula
2) tracheostomal stenosis (from radiation, infection)
3) Neo-pharyngeal stricture (thus dysphagia)
4) Hypothyroidism ± Hypoparathyroidism
Histology type of NPC
1) Non-differentiated carcinoma (95%)
2) Non-keratinising carcinoma
3) Keratising SqCC
NPC location (and metastases)
- *Site: Fossa of Rosenmuller** of nasopharynx
- clinically obscure area
- thus clinically silent until widespread metastases occur
- *Metastasis:**
1) Local spread to parapharyngeal space - > base of skull
- > cranium via foramina
2) Distal spread
- > usually by lymphatics to H&N lymph nodes
- > may be hemat spread to organs
NPC risk factors
- *1) Genetics**:
- Cantonese
- Combination of HLA-A2 & BW-46
- *2) Infection**:
- EBV +ve
- *3) Diet**:
- High nitrosamine e.g. Salted fish, preserved food
NPC clinical presentation
0) Constitutional symptoms
_Primary symptoms (ENT!)_ **1) Ear**: conductive hearing loss, recurrent OME, tinnitus
2) Nose: obstruction, epistaxis, postnasal drip
3) Throat: sorethroat
- *4) Headache and facial pains**
- trigeminal nerve compression (test for corneal reflex)
- usu temporal headache
- *5) CN palsy** (2-6, 9-12)
- sphenoid sinus above nasopharynx, above that is cavernous sinus
- optic chiasm is also close
LN met, distant met:
- *6) Neck LN**
- level 2-4 (more common contralat; can be bilat)
Why hearing loss in NPC?
Conductive hearing loss due to:
- Obstruction of the eustachian tube
Ix for NPC
- *1) EBV testing**
- EBV DNA titre
- EBV VCA-IgA has the highest sensitivity
- EBV EA-IgA has the highest specificity
2) Flexible nasal endoscopy + biopsy
3) US + FNAC of neck LN
4) CT, MRI H&N
5) CXR, PET for met
NPC treatment and complication
1) Radiotherapy (best for undifferentiated carcinoma, SCC least)
+) Adjuvant chemotherapy
-
if relapsed:*
2) Surgical management i.e. Nasopharyngectomy - maxillary swing classically
- now have endoscopic methods
Follow-up after NPC RT
Routine follow up with plasma EBV DNA
- High recurrence in first 2 year and after 10 years -> use plasma EBV DNA to determine relapse
- Monitor for RT complications e.g. sarcomas, xerostomia, hypopituitarism
What are the symptoms and signs of mandible fracture?
Symptoms:
1) Gross disfigurement
2) Pain
3) Malocclusion
4) Drooling
Signs:
1) Trismus
2) Fragment mobility
3) Gingival laceration
4) Haematoma in floor of mouth
What are the complications of mandible fracture?
1) Malunion
2) Non-union
3) Osteomyelitis
4) TMJ ankylosis
Are mandibular fractures usually single or multiple?
They are usually multiple site
This is because the mandible forms an anatomic ring, thus >95% of mandible fractures have more than one fracture site
LeFort classification
For mid-face fracture:
Le Fort I
- transverse maxillary fracture, above dental apices
- also traverses the pterygoid plate
- thus palate necomes mobile, but nasal complex is stable
Le Fort II
- fracture through frontal process of maxilla
- through the orbital floor and pterygoid plate
- thus midface is mobile
Le Fort III
- fracture through the nasofrontal suture and fronto-zygomatic sutures
- thus complete craniofacial separation
What is a “tripod” fracture
i. e. zygomatico-maxillary complex fracture, involving 3 fractures:
1) Zygomatic arch fracture
2) Floor of orbit fracture (including maxillary sinus)
3) Lateral orbital rim and wall fracture
Symptoms / signs of tripod fracture
After facial trauma or deceleration injury:
1) Loss of cheek projection, increased width of face
- *2) Loss of sensation over cheek and upper lip**
- due to infra-orbital nerve injury (passes through orbital floor)
3) Facial bruising, swelling
- *4) Impingement**
- impingement of the temporalis muscle -> trismus
- impingement of extra-orbital muscles -> diplopia
Deviated nasal septum (etiology & presentation & management)
- *Etiology:**
- Trauma at birth
- Trauma (e.g. fighting)
- Unequal growth of nasal septum
- *Presentation & PE:**
- Unilateral nasal obstruction
- nose speculum can see deviation, sometimes even septal spur (sharp bone growth from severe trauma, see pic)
- If severe, the deviation can be observed directly
- *Management:**
- Septoplasty/SMR (submucous resection of septum)
What must be ruled out in a nasal fracture? Why?
Septal haematoma
Because septal haematoma will cause pressure-induced septal necrosis, and ultimately saddle nose deformity if unmanaged
This is because nasal septum & cartilage receive its nutrient from the nasal perichondrium. In septal hematoma, the two are separated, and septal necrosis will occur, causing deformity.
Septal hematoma (presentation & management)
- *Presentation:**
- bilateral nasal obstruction after nose trauma
- blood stain
- *Management:**
- Urgent drainage
Salivary glands in human
MAJOR GLANDS:
1) 2 parotids
2) 2 submanidbular
3) 2 sublingual
MINOR GLANDS:
- Hundreds
- Oral cavity, tongue base, larynx, NP
Parotid gland’s boundary and position
The parotid gland are bounded by:
- Superiorly – Zygomatic arch.
- Inferiorly – Inferior border of the mandible.
- Anteriorly – Masseter muscle.
- Posteriorly – External ear and sternocleidomastoid.
Inferiorly it wraps around the angle of the mandible. Its posterior border runs up behind the ramus of the mandible over the mastoid process.
Position:
- 80% overlies Masseter & Mandible
- 20% is retromandibular
Lobes of parotid gland
Superficial lobe & deep lobe, which is divided by:
- *Anatomically**
- Facial Nerve (anatomically)
- *Radiologically:**
- an imaginary line from mandible to mastoid
- the retromandibular vein might be used as surrogate of facial nerve (which cannot be visualised in MRI)
Structures that transverse parotid gland
Name them from superficial to deep
Superficial to deep:
- *1) Facial nerve & 5 branches (Tarzan big mac)**
- temporal
- zygomatic
- buccal
- marginal mandibular
- cervical
2) Retromandibular vein
- *3) External carotid artery**
- gives of last 2 branches: maxillary artery and superficial temporal artery (both supplies the parotid gland)
4) Parotid lymph nodes
Branching of facial nerve (and some muscles it innervate)
Facial nerve leaves stylomastoid foramen to enter Parotid gland, in which in forms bifurcates & further branches at the pes anserinus “TARZAN BIG MAC”:
- *1) Temporal-zygomatic**
- temporal (e.g. frontalis)
- zygomatic (obicularis oculi)
- *2) Cervical-facial**
- Buccal (Orbicularis oris, buccinator)
- Marginal mandibular (Depressor anguli)
- Cervical (Platysma)
Location of submandibular gland
1) In Submandibular Triangle, i.e. superior to the digastrics
- *2) Gland wraps around the mylohyoid**
- superficial lobe (larger) palpable between body of mandible and mylohyoid
- smaller deep lobe
3) Superficially covered by platysma
Duct of submandibular gland
- *Wharton’s duct (5cm):**
- arises from medial surface of deep gland of submandibular gland
- lies between mylohyoid and hypoglossus
- opens into the oral cavity via Wharton’s duct on either side of the lingual frenulum.
Sublingual gland anatomy
- *Sublingual glands location:**
- at FOM, between Mandible & Genioglossus
- separated from base of tongue by submandibular duct and lingual nerve
- bilateral gland merge to form horseshow around lingual frenulum
Drainge: It drains directly into the buccal floor
- *Characteristics:**
- No capsule
- Basically a collection of many small glands, thus sialogram is impossible
Where is the incision for submandibular gland excision?
Why?
Skin incision is made:
- around 3–4 cm below the mandible
- in order to avoid the marginal mandibular branch of facial nerve
- Note that the hypoglossal (CN XII) and lingual nerves are at risk during deeper dissection.
DDx of Enlarged salivary gland
Differentiate between infection (& inflammation), & neoplasm, & others
- *A. INFECTION, INFLAMMATION**
- Acute parotitis (S aureus)
- Viral sialadenitis (in childhood)
- Chronic sialoadenitis
- Sialolithiasis
- Sjogren’s syndrome
- *B. NEOPLASTIC** (usu unilateral)
- pleomorphic adenoma
- Warthin’s tumour
- Mucoepidermoid carcinoma
- Adenoid cystic carcinoma
- Acinic cell carcinoma
- Adenocarcinoma
- Malignant mixed tumour (e.g. Carcinoma ex-pleomorphic adenoma, Carcinosarcoma)
- Squamous cell carcinoma
- Lymphoepithelial carcinoma (Undifferentiated carcinoma)
- *C. OTHERS**
- Bulimia nervosa
- Alcoholism (sialadenosis)
- DM
- Drugs e.g. Phenytoin
- Cysts, lymphoepithelial cysts (e.g. HIV, post-transplant)
D) Mimics
- Pseudoparotidemegaly i.e. masseter hypertrophy caused by bruxism
- Skin lesions e.g. lipoma, sebaceous cyst
- Denal infection
Bilateral enlargement of salivary gland DDx
1) Pseudo-parotidemegaly, i.e. masseter hypertrophy from bruxism
- *2) Systematic disease**
- Bulimia nervosa
- Alcoholic cirrhosis (sialadenosis)
- DM
- Sjogren’s syndrome
3) Warthin tumour (10% is bilateral)
4) Benign lymphoepithelial cysts (e.g. in HIV)
Mimics of parotid and submandibular gland swelling
- *Parotid Gland Swelling:**
1) Masseter hypertrophy (e.g. due to bruxism)
2) Enlarged cervical LN (Upper level II)
- have to differentiate by imaging
3) Lipoma or other overlying skin / subcutaneous lesions
- subcutaneous in nature
4) Vascular malformation
- *Submandibular Gland Swelling**
1) Enlarged submandibular lymph node
2) Oral cavity mass (e.g. FOM Cancer) with direct extension to submandibular space
★ Important Hx in salivary gland enlargement
- *1) Is it Painful?**
- if pain, more likely inflammation (not necessarily)
- most salivary gland neoplasm are painless mass
- can still be high grade mucoepidermoid tumour, adenoid cystic carcinoma, adenocarcinoma (i.e. the aggressive ones)
- *2) Is the pain associated with meal?**
- if yes, more likely infection or inflamation
- *3) Swelling**
- acute onset or insidious onset?
- does it swell after meals? (if yes, more likely infection)
4) Presence of symptoms of acute infection (fever, tenderness, pus)
★ PE in salivary gland mass
- *1) Inspection**
- scars? esp BEHIND EAR!!
- Facial nerve palsy
- Swelling unilateral or bilareral? Symmetrical?
- Intraoral inspection of (Stensen’s duct, Wharton’s duct, FOM swelling, any pus in the duct openings?)
- *2) Palpation**
- Confirm lesion not arising from the skin (rule out e.g. lipoma)
- Palpate the ducts (for stones, to express pus)
3) Complete H&N ENT examination
4) Facial nerve examination
5) Palpation of neck lymph nodes
6) Endoscopy of the upper aerodigestive tract
Investigation of parotid mass
1) XR or sialogram for sialolithiasis
- *2) Ultrasound**
- Confirm mass from parotid or submandibular gland (differentiate from neck LN)
- Good for stones, dilated ducts
- *3) CT scan/ CT sialogram**
- good for inflammatory disease
- *4) MRI**
- Best soft tissue differentiation
- True multi-plane
- Better for tumour, accurate delineation of extent of invasion
- Differentiate other pathologies, e.g facial nerve schwannoma
- *±5) FNAC** (21 gauge or smaller)
- still performed for better patient prepare
- inaccurate & cannot note histology
- not for sole decision making
- *6) Biopsy**
- mainly excisional biopsy (i.e. Parotidectomy, submandibulectomy)
- incisional biopsy easily cause spillage
- core biopsy (Trucut) is not enough
Acute parotiditis
- causes
- presentation
- management
- *Causes:**
i) poor dental hygiene, with spread of bacteria via duct to gland -> may become parotid abscess
ii) mumps infection - *Presentation:**
- Tender swelling of parotid gland
- Pus from Stenson’s duct opening
- *Management:**
- Rehydration
- IV antibiotics
Acute sialoadenitis
Commonly presented in children due to viral infection:
- *1) Mumps**
- used to be common, now protected by vaccination
2) Coxsackievirus
3) CMV
4) Influenza
Chronic sialoadenitis (presentation, etiology)
Commonly presented in old age
- *Presentation**:
1) Mild pain, worsen after meal
2) Recurrent parotid or submandibular swelling after meal - *Etiology:**
1) Destruction of gland tissue from ascending duct infection related to dehydration and debilitation e.g in old age with thicker saliva
2) Secondary to ductal obstruction e.g. Stones (submandibular duct most likely)
3) Autoimmune (i.e. Sjogren)
Chronic sialoadenitis (treatment)
1) Hydration
2) Sialogogues, massage, heat, hydration, antibiotics during acute attacks
- *3) Remove stones**
- Spontaneous passage with assistance of massage
- Exploration of submandibular duct (transoral removal of stone with marsupialization or sialotomy)
- Sialoendoscopy
- *4) Excision of the gland**
- if stone is near hilum or refractory disease
Investigations in chronic sialoadenitis
- Serological test to r/o Sjogren syndrome (Anti-Ro SS-A; Anti-La SS-B, ANA, RF)
- Sialogram
- USG to r/o stones
Sialolithiasis (presentation, complication, management)
- *Presentation:**
- Recurrent chronic sialoadenitis (i.e. swelling esp after meal, pain esp after meal)
- usually in teenagers or young adults
- *Complication:**
- chronic sialoadenitis
- ductal ectasia
- duct strictures
- *Treatment:**
- Spontaneous passage with assistance of massage
- If near duct orifice, transoral removal of stone with sialotomy +/- marsupialization
- If near hilum, gland excision
Radiological findings of Sialolithiasis
- 80% in submandibular gland, 20% in parotid
- Usually only 1 stone
- Most submandibular stones are radio-opaque
- Most parotid stones are radiolucent
Sjogren’s syndrome clinical presentation
1) More female, 30-40yo
2) keratoconjunctivitis sicca, xerostomia
3) Injected cornea,conjunctivitis
4) Diffuse, tender enlargement of parotid and submandibular glands (Chronic sialoadenitis)
5) Features of associated autoimmune diseases
- fatigue, fever
- e.g. SLE
Diagnosis of Sjogren syndrome
1) Schirmer’s test
2) Raised ESR & CRP
- *3) Serology**
- ANA, RF
- Anti-Ro (SS-A), Anti-La (SS-B)
- should also check for ds-DNA antibody, Anti-CCP (or ACPA) to look for secondary Sjogren’s
- *4) Biopsy of sub-labial minor salivary glands**
- Gland destruction with lymphocytes infiltration
What physical exam findings may suggest malignant nature of parotid gland mas
1) Rapid growth and pain
2) Irregular surface, craggy
3) Tethering to skin and underlying muscles
4) Facial nerve palsy (suggestive of invasion)
Salivary gland neoplasms Sites
- *1) Parotid**
- most common site (80% overall)
- mostly benign (80% benign)
- mostly pleomorphic adenoma (80% of benign is PA)
- *2) Submandibular**
- 15% overall
- 50% benign
- *3) Sublingual/ Minor**
- 5% overall;
- 40% benign
Tumours of salivary gland
“Prince of Wales :) got MAAACS love”
- *Benign**:
- Pleomorphic adenoma
- Warthin’s Tumour
- *Malignant**:
- Mucoepidermoid carcinoma
- Adenoid cystic carcinoma
- Acinar cell carcinoma
- Adenocarcinoma
- Carcinoma ex-pleomorphic adenoma
- Squamous cell carcinoma
- Lymphoepithelial carcinoma (undifferentiated carcinoma)
Management of Salivary Gland malignancies
Influenced by site, stage, grade, histological subtype:
- *1) Surgical Excision**
- Complete local excision
- Radical excision for carcinoma ex-pleomorphic adenoma & SqCC
- *2) Control of invasions**
- Neck dissection for nodal metastasis (mucoepidermoid cancinoma, adenocarcinoma, carcinoma ex-pleomorphic adenoma)
- Extended neck dissection for SqCC
- Facial nerve sacrifice? (in Adenoid cystic carcinoma, due to tendency for perineural invasion)
- *3) Post-operative Radiotherapy**
- for high grade mucoepidermoid carcinoma, Adenoid cystic carcinoma, Acinic cell carcinoma, Carcinoma ex-pleomorphic adenoma, SqCC, Undifferentiated carcinoma aka lymphoepithelial carcinoma)
Pleomorphic adenoma presentation, site, complication
- *Presentation:**
- Slow-growing, painless mass
- *Site:**
1) 80% of Parotid tumours: mostly in superficial lobe, most in tail of gland
2) 50% of submandibular tumours
3) 45% of Minor salivary gland: lateral palate, submucosal mass
4) 6% of sublingual tumors
- *Complication:**
- Malignant degeneration risk in long term (e.g. Carcinoma ex-pleomorphic adenoma)
Pleomorphic adenoma surgical treatment
- *1) Complete surgical excision**
- Parotidectomy with facial nerve preservation
- Submandibular gland excision
- Wide local excision of minor salivary gland
- *2) Avoid enucleation and tumor spillage**
- if ruptured, cancer cells might be spread all over, causing seeding
- *3) Radiotherapy**
- for recurrent tumour
- prevention of recurrence in case of spillage
Warthin’s tumour presenation
aka Papillary Cystadenoma Lymphhmatosum
- *Presentation:**
- Old male
- Soft cystic mass
- slow-growing, painless mass
- Commonly parotid gland (10% bilateral); tail of parotid
Mucoepidermoid carcinoma presentation
Most common salivary gland cancer
Commonly seen in women from 30-80
- *Presentation:**
- Mostly parotid gland
- Low-grade: slow growing, painless mass
- High-grade: rapidly enlarging, +/- pain
- Ulcerates in later stage
Adenoid cystic carcinoma presentation
2nd most common salivary gland malignancy, in both sex around 50s
Site: common in submandibular, sublingual and minor salivary glands
- *Presentation:**
- enlarging mass
- Tendency of perineural spread (facial nerve), thus pain, paresthesias, facial weakness/ paralysis
- Common distant metastasis to lungs
Acinar cell carcinoma presentation
Commonly parotid gland, more common in women:
- *Presentation**:
- Solitary, slow-growing, often painless mass
- Bilateral parotid disease in 3%
Salivary gland Adenocarcinoma
Rare; affects parotid glands or minor salivary gland; more common in women from 50-80
Presentation:
– Enlarging salivary gland mass
– Aggressive, 25% with pain or facial weakness
What are some malignant mixed tumours of salivary gland
- *1) Carcinoma ex-pleomorphic adenoma**
- Carcinoma developing in the epithelial component of preexisting pleomorphic adenoma
- *2) Carcinosarcoma**
- Mixture of carcinomatous and sarcomatous components
- *3) Metastatic mixed tumor**
- Metastatic deposits of otherwise typical pleomorphic adenoma
Presentation of Carcinoma ex-pleomorphic adenoma
- *Presentation:**
1) Longstanding painless (usu parotid) mass i.e. pleomorphic adenoma, that undergoes sudden enlargement
2) Poorly circumscribed, Infiltrative
3) Hemorrhage and necrosis
What to consider when histology of salivary gland tumour shows squamous cell predominant
Consider Squamous cell carcinoma of salivary gland, after ruling out:
1) High-grade mucoepidermoid carcinoma
2) Metastatic SCC to intraglandular nodes, usually from scalp SCC
3) Direct extension of skin SCC
Lymphoepithelial carcinoma presentation
- Common in eskima (eskimoma) & Chinese
- EBV related, histology identical to NPC (i.e. undifferentiated):
- Always try to rule out it being a metastasis from NPC
Facial pain DDx
A. Local diseases around the face
1) Skin
- cellulitis (subcutaneous inflamm)
- erysipelas (cuticular lymphangitis)
- Facial Shingles
2) Sinus: acute or chronic sinusitis
3) Dental infections
4) Temporomandibular joint problems
B. Referred pain
5) NPC
C. Neurogenic pain
6) Trigeminal neuralgia
7) Post-herpetic neuralgia
8) Migraine
9) Cluster headache (retroorbital pain)
Facial pain investigations
- *1) Panendoscopy**
- bronchoscopy & esophagoscopy
- *2) Plain X-rays**
- paranasal sinus
- orthopantomography of upper & lower jaw
- *3) CT / MRI scanning**
- sinuses
- cerebellopontine angle
- brain
Facial nerve supplies
- *1) Somatic motor** for Facial musles
- consider the five branches
- *2) Special sensory**
- taste to anterior 2/3 of tongue, via chorda tympani
- *3) Secretomotor**
- via sphenopalatine ganglion to lacrimal glands and nose (greater petrosal nerve)
- via submandibular ganglion to submandibular and sublingual gland (chorda tympani)
Course of facial nerve
1) Starts from facial nucleus in pons
2) Goes through facial canal in the temporal bone
3) goes to geniculate ganglion
- greater petrosal nerve branches out; via sphenopalatine ganglion to supply lacrimal glands
4) Further branches
- motor branch to stapedius
- chorda tympani to tongue taste; as well as via submandibular ganglion to submandibular glands
5) Emerges from the stylomastoid foramen
6) Pierce the parotid gland, and bifrucates to:
a) Temporal-zygomatic
- temporal (e.g. frontalis)
- zygomatic (obicularis oculi)
b) Cervical-facial
- Buccal (Orbicularis oris, buccinator)
- Marginal mandibular (Depressor anguli)
- Cervical (Platysma)
Facial nerve palsy DDx
- *1) Supranuclear** (UMN lesion)
- usu stroke
- upper face spared
- *2) Lesion in the facial nucleus** (LMN lesion)
- usu stroke, tumour, demyelinating disease
- *3) Tumour in internal acoustic meatus**, or cerebropontine angle
- CP angle meningioma
- acoustic neuroma (rarely facial palsy due to slow growth)
4) Temporal bone fracture
- *5) Middle ear**
- AOM, CSOM, cholesteatoma
- Bell’s palsy (idiopathic swelling in facial canal)
- Ramsay Hunt Syndrome
- Middle ear tumour
- *6) Beyond stylomastoid foramen**
- Facial trauma (usu affect 1 branch)
- Parotid tumour
- Metastatic intraparotid lymph node
- *7) Others**
- Facial nerve schwannoma
- Iatrogenic from surgery
Localising facial palsy lesion site
- *1) Upper face spared**
- UMN lesion (thus lesion above facial nucleus)
- *2) Decrease in lacrimation and affects ipslateral taste**
- proximal to geniculate ganglion
- *3) Preserved lacrimation**
- distal to geniculate ganglion
- *4) hyperacusis present**
- proximal to stylomastoid foramen (stapedial reflex affected)
- *5) Only facial movments affected, normal stapedial reflex**
- dital to stylomastoid foramen
PE in facial nerve palsy
1) Cranial nerve examination
- especially facial nerve (but also try the other nerves)
2) External ear & middle ear exam
3) Parotid gland & intra-oral examination
4) Neck palpation
5) House & Brackmann facial paralysis grading system
Ix for facial nerve palsy
1) MRI brain – for suspected intracranial lesion
2) MRI temporal bone – if middle ear pathology is suspected
3) CT temporal bone – temporal bone trauma
4) MRI/CT parotid and USG FNA – if parotid lesion is suspected
- *5) Electrophysiological testing**
- electromyography (Determines the activity of the muscle itself)
- Electroneurography
Potential pathogenesis of Bell’s palsy and diagnosis
- *Pathogenesis**
- idiopathic
- Now identified as a herpes reactivation neuritis
- Nerve swollen in the facial nerve canal causing neuropraxia
Diagnosis:
Diagnosis by exclusion
Bell’s palsy management
- *1) Prednisolone** for 7-14 days
- reduce swelling
- use if not contraindicated (e.g. DM, TB)
2) Acylcovir or famciclovir for 5 days
- *3) Eye protection and eye drops**
- prevention of dry eyes from lack of blinking
- *4) Facial nerve physiotherapy**
- maintain muscle tone and hasten recovery
- prevent facial muscle dysuse atrophy
5) Rule out other cause if no improvement
Surgical CN VII decompression indications
– Traumatic cause
– Middle ear infection
– Iatrogenic injury (middle ear or parotid surgery)
Nose components
A. Skin
- *B. Bone**
- Nasal bones
- Nasal part of frontal bone
- Frontal process of maxilla
- *C. Cartilage**
- upper & lower lateral
- *D. Muscles**
1) Nasalis - transverse (compress nostril)
- alar (opens nostril)
2) Procerus
- pulls eyebrows down
3) Depressor septi nasi
- pulls nose down
Roof, medial wall, lateral wall, and floor of nasal cavity
- *Roof:**
- Cribiform plate (part of ethmoid bone)
Medial Wall:
Nasal septum which is partly cartilaginous (ant) & partly boney (post)
- Septal cartilage
- Vomer
- penpendicular plate of ethmoid bone
- *Lateral wall:**
- Superior, middle and inferior nasal conchae/ turbinates
- Superior, middle and inferior nasal meatus below the turbinates
- *Floor:**
- Palatine process of maxilla
- Horizontal plate of palatine bone
Vasculature of nasal cavity
From both external & internal carotid artery:
- *Artery (MFO) motherfucko:**
1) maxillary artery => sphenopalatine/ nasopalatine artery
2) facial artery => alar and nasal branches
3) ophthalmic artery => anterior and posterior ethmoidal artery
- *Venous drainage PIFO piperfucko**
1) Pterygoid venous plexus
2) infraorbital vein
3) facial vein
4) ophthalmic vein
What is the usual bleeding source in epistaxis?
Rupture of superficial mucosal vessels:
- Kiesselbach’s plexus (if anterior, which is most common 90%)
- Sphenopalatine artery (if posterior, which is more serious)
What is the management of epistaxis?
1) Direct pressure
- *2) Packing**
- anterior nasal packing with gauze strips
- posterior packing with Foley catheter
- packs must be removed in less than 5 days
- *3) Ligation or embolisation**
- of sphenopalatine artery (if posterior) or ethmoidal artery (if anterior)
What is a serious complication of nasal packing?
Toxic shock syndrome
- due to exotoxin released from Staph aureus
Inverted papilloma
- Common benign tumour
- Malignant potential (may turn into SCC in 1~2 decades)
- *Presentation:**
- Unilateral nasal obstruction
- *Diagnosis:**
- Histology (definitive)
- MRI (Convoluted Cerebriform Pattern)
- *Management:**
- Need complete removal
Juvenile angioma presentation
- Male in puberty (due to Vascular malformation)
- Unilateral nasal obstruction (looks like an “unilateral polyp”)
- Profuse, recurrent unilateral epistaxis
Paranasal sinus structure
Air filled extension of nasal cavity in:
1) frontal
- *2) ethmoid**
- divided by middle turbinate into anterior & posterior
- *3) sphenoid**
- require Lateral X-ray for visualisation
4) maxilla
Paranasal sinuses function and drainage site
For resonance of voice and drainage
_____
Drained by Osteomeatal Unit (OMU)
1) Frontal: Middle meatus via infundibulum
2) Ethmoid: Middle meatus via infundibulum (anterior); middle meatus on bulla ethmoidalis (middle); superior meatus (posterior)
3) Sphenoid: Sphenoethmoidal recess
4) Maxillary: Middle meatus via hiatus semilunaris
Examination & investigations for nasal cavity & nasophaynx
- *PE:**
1) Nasal speculum (inspection)
2) Mist Test aka Nasal Airflow Patency Test (using the metal tongue depressor)
3) Rigid endoscopy (rhinoscopy)
- *Ix:**
- *1) CT** (for extent of disease, bone erosion)
2) MRI (for soft tissue invasion e.g. eye, brain)
- *3) Tests for allergy** (for type I hypersentivity, i.e. allergic rhinitis)
- Blood test for Antigen specific IgE
- Skin prick test
4) Histology of mass
+ Resch) Rhinomanometry (calculates nasal airway resistance by measuring nasal flow and pressure)
+ Resch) Acoustic rhinometry (sends sound pulse into nose & measures reflected sound)
Otalgia DDx
- *Ear disease**
1) Otitis externa, furunculosis
2) Foreign body in ear
3) Herpes zoster external ear (Ramsay Hunt syndrome)
4) Erysipelas or other skin lesions of external ear
5) AOM
6) CSOM
7) Carcinoma of ear canal/middle ear
8) Cerebropontine angle tumour
- *Referred Pain**
1) Dental problems
2) Temporo-mandibular joint syndrome
3) Pharyngitis, tonsillitis, peritonsillar abscess
4) Parotitis (mumps, bacterial)
5) CA nasopharynx, oropharynx, hypopharynx, larynx
6) Cervical spondylosis C1,2,3
Otorrhoea DDx
- *1) Exudation in infection**
- Otitis Externa
- Chronic Suppurative Otitis Media
- Late stage of Acute otitis Media (i.e. with perforation)
- *2) CSF otorrhoea**
- Trauma, Skull base fracture
- *3) Blood**
- Trauma
- Barotrauma
- Tumours
Important History to ask in otorrhoea
1) Hearing
- *normal**: external ear disease e.g. otitis externa (rarely, might have temporary conductive hearing loss)
- *hearing loss**: middle ear disease
2) Otalgia?
painful: infection or neoplasm (note possibility of referred pain)
3) Nature of ear discharge
- blood? infection? CSF?
Otitis externa definition and presentation
Definition
aka Swimmer’s ear; an inflammation of the outer ear and external ear canal (EAC) skin
- *Presentation:**
- *1) Otalgia**
- directly related to the severity
- DIAGNOSTIC: worsened by pushing the tragus
2) Otorrhoea
3) Pruritus
- *4) Usually no hearing loss**
- might (though rarely) present with temporary conductive hearing loss
predisposing factors to otitis externa
A. Anatomical predisposition/ blockade
- *1) Narrow ear canal** (e.g. congenital meatal stenosis or post-traumatic)
- *2) Cerumen impaction
3) Foreign bodies, hearing aids, ear plugs**
B. High humidity of ear canal:
- *4) Swimming, shower, watersports** (high humidity)
- *5) Summer**
C. Skin lesions, immunosuppression:
- *6) Scratching and abrasion, post-RT
7) Skin disease e.g. Eczema
8) DM**
Pathogens of otitis externa
- *Bacterial**
- Pseudomonas aeruginosa (most common!!!)
- Strep epidermidis
- Staphylococcus aureus
- *Viral**
- Varicella Zoster Virus (Ramsay Hunt Syndrome)
- *Fungal**
- Candida albicans and Aspergillus spp.
- Usually due to overuse of topical antibiotics (e.g. in a patient with CSOM, or bacterial EOM)
Treatment of diffuse otitis externa
A. Non-pharmacological:
- *1) Local cleansing**
- remove wax/foreign body
- suction clearance
- dry mopping
2) Keep away from moisture esp NO swimming!
B. Pharmacological therapy
- *1) Local antibiotic eardrops** against skin flora
i) Choramphenicol 5% otic drops, 2-3 drops in affected ear, 3 times daily for 1 week
ii) Ofloxacin 0.3% otic drops, 10 drops in affected ear, 1 time daily for 1 week
2) Paracetamol for pain relief
What is ear furunculosis
A localised abscess (boil) in the external auditory canal (EAC); a form of otitis externa
- very painful
Treatment of furunculosis of EAC
- *1) Systemic antibiotics**
- e.g.cloxacillin against staphylococcus
- *2) Symptomatic treatment**
- Analgesics for pain relief
3) Drainage seldom required
Types of Hearing loss
- *1) Conductive Hearing Loss** (CDHL)
- Outer ear, middle ear
- *2) Sensorineural Hearing Loss** (SNHL)
- Inner ear, auditory nerve, central nervous system
3) Mixed Hearing Loss (CDHL + SNHL)
Hearing loss DDx in adults
A. CONDUCTIVE
EAC pathology
1) Cerumen impaction, foreign body
2) EAC stenosis
3) Otitis externa
4) Tumour
5) Exostosis, osteoma
<u>ME pathology</u>
6) CSOM, cholesteatoma
7) OME (Look out for NPC!!!)
7) Otosclerosis
8) Temporal bone fracture
9) Haemotympanum
- *B. SENSORINEURAL**
- *1) Presbyacusis
2) Ototoxicity
3) Transverse temporal bone fracture
4) Meniere’s disease
5) Ramsay hunt syndrome, syphilis
6) Hypothyroidism
7) Acoustic neuroma**
Sudden SNHL hearing loss definition
Rule of 3
- 30dB or more SNHL
- over 3 contiguous frequency
- within 3 days
Sudden SNHL hearing loss management
An otological emergencyt!!!
- *1) Steroid**
- Systemic or intratympanic
- Strong & immediate
2) Stop any possible ototoxic drugs
3) Perform MRI to rule out acoustic neuroma
Pathogenesis & Pathogens of otitis media
- *Pathogenesis:**
- Ascending infection of middle ear from the Eustachian tube. Usually in children.
- *Pathogens:**
- 1) Viral*
- RSV
- 2) Bacterial*
- Strep.pneumoniae
- H. influenzae
- Moraxella catarrhalis
Acute otitis media clinical presenation
1) Otalgia (unilateral)
2) Conductive deafness
- *3) Constitutional symptoms**
- fever
- *4) Otorrhoea**
- only when eardrum perforated (late stage)
AOM treatment
- *1) Oral antibiotics**
- Amoxiclav
- erythromycin
- 1 week to 10 days
- *2) Supportive treatment**
- Analgesics for pain relief
- *3) M&G**
- myringotomy and grommet insertion (occasionally)
- to relieve middle ear pressure
eardrum perforation DDx
- *1) Infection**
- acute otitis media (late stage)
- CSOM
- *2) Trauma**
- direct mechanical
- oatrogenic (e.g. Myrinectomy Grommet)
- barotrauma
- Blast injury
CSOM definition
Chronic or intermittent otorrhoea through a persistent perforated TM
CSOM presentation
- *1) Otalgia**
- chronic
- *2) Hearing loss**
- conductive or mixed
- *3) Chronic or recurrent Otorrhoea**
- Persistent, non-healing eardrum perforation
4) Vertigo
5) Constitutional symptoms
Ix in CSOM
- *1) Otoscopy**
- for diagnosis
- *2) Assess for active infection**
- Ear mopping
- Ear swab x bacterial culture
- Broad spectrum antibiotic eardrops (might not be a good idea due to potential sudden hearing loss)
- *3) Pure tone audiogram** (PTA)
- for both ears
CSOM pathogens
- *Bacterial:**
- Staphylococcus aureus
- Pseudomonas aeruginosa
- Escherichia coli
- Bacteroides fragilis
- Tuberculosis (rarely)
- *Fungal:**
- Candidiasis
- Aspergillosis
Types of CSOM
Depends on the site:
- *1) Central perforation**
- i.e. tubotympanic
- “safe” perforation
- *2) Marginal, or attic perforation**
- i.e. atticoantral
- “unsafe” perforation
Complications of Unsafe CSOM
i.e. Attico-antral perforation:
- *1) Cholesteatoma**
- Keratinizing squamous epithelium can be pushed back from EAC into middle ear via the marginal perforation
- *2) Extracranial Complications**
- facial nerve paralysis
- ossicular chain erosion
- Labyrinthitis (causing sudden hearing loss)
- Lateral semicircular canal fistula (cause vertigo)
- subcutaneous/subperiosteal abscess
- *3) Intracranial Complications**
- Meningitis, Brain abscess (usu temporal lobe, cerebellum)
- extradural abscess, subdural abscess
- Sigmoid sinus thrombophelbitis (posterior to mastoid)
- otitic hydrocephalus
Management of CSOM
Safe CSOM:
1) Hearing aid
2) Tympanoplasty to manage perforation
3) Antibiotics eardrops (? beware: SHL)
4) Aural toilet, ear ventilation
5) Avoid water sports, swimming
Unsafe CSOM:
1) Screen for complications
- *2) Mastoidectomy** (removal of mastoid, middle ear cavity, EAC walls)
- eradicate infection
- prevent complication
- not to improve hearing
3) Aural toilet, ear ventilation
4) Avoid water sports, swimming
What is the risk of using topical antibiotic eardrops?
Most of the topical antibiotics currently used are also ototoxic, esp aminoglycosides
Therefore, Sudden hearing loss (SHL) if long term antibiotic ear drops in CSOM / perforated ear drum patients; because antibiotics going into the middle and inner ear through the TM defect.
Otitis Media with Effusion definition
- *Definition**:
- Sterile effusion in middle ear for > 3months
- the presence of middle ear fluid for 6 weeks or more from the initial acute otitis media
- No perforation
- otitis media in inactive (no active inflammation)
Pathogenesis of OME
Once the eustachian tube is blocked, air is continuously drew in by the vasculatures (very much like the lungs), creating a space of negative pressure in the middle ear.
As a result, transudation of interstitial fluid -> forming the collection of Sterile effusion in middle ear
OME causes
Basically causes of blockade of Eustachian tube:
- *Congenital**
- Cleft palate
- Down’s syndrome
- Craniofacial abnormality
- Mucociliary dysfunction (e.g. Kartegener’s)
- IgG deficiency
- *Acquired**
- URTI
- AOM
- Nasal polyp
- NP mass (e.g. NPC)
OME presentation
1) Conductive Hearing loss
2) Otalgia
- *3) Speech delay, articulation problem**
- in children
OME Ix
1) Otoscopy
2) Tympanometry
3) Pure tone audiometry (PTA)
conductive hearing loss
OME – Treatment
1) Myringotomy + Grommet insertion
2) Do not swim
Otosclerosis pathogenesis
- Autosomal dominant, with incomplete penetrance
- Focal osseous dysplasia of bone derived from otic capsule:
i) Abnormal bone absorption & deposition
ii) Fibrous replacement & sclerosis
Otosclerosis presentation
Usu during pregnancy, around 20-30yo, present with:
1) Bilateral conductive hearing loss (80%)
2) Tinnitus
3) Vertigo
4) 50% Family Hx
Otosclerosis treatment
1) Conservative
2) Hearing aid
3) Stapedectomy
Vertigo causes by prevalence
- Benign paroxysmal positional vertigo
- Functional vertigo
- Central-vestibular vertigo
- Vestibular migraine
- Meniere’s disease
- Vestibular neuronitis
Important Hx to ask in “vertigo”
- *1) Symptom**
- confirm it is vertigo (cf. LOC, postural instability, nausea)
- ideally bystander interview
- *2) Time course**
- episodic vs acute sustained vs chronic sustained
- *3) Trigerring factors**
- loud noise? light? specific postures? URTI? Trauma? Ototoxic drugs?
- *4) Associated symptoms**
- headache? photophobia? Hearing loss?
PE in vertigo
1) Neurological examination, muscle power examination
- *2) Romberg test**
- if single leg is okay >5s, then Somatoform dizziness
- if Romberg failed, but HINTS & neurological exam normal, then motor weakness
- *3) HINTS (for stroke!)**
- Head Impulse (if abnormal, peripheral vertigo)
- Nystagmus
- Test of Skew (alternating cover uncover test; if abnoraml, then central vertigo)
- *4) Hallpike’s test**
- diagnostic for BPPV
Ix in vertigo
- *1) CT/MRI Brain & Brainstem**
- if suspects central causes
- *2) Audiological Test** (to confirm peripheral cause)
- Electronystagmography (using caloric reflex test or rotary chair)
- Posturography
Benign Paroxysmal positional vertigo aetiology
Due to canalolithiasis or cupulolithiasis:
BPPV is caused by presence of particulate/debris from from saccule/utricle affecting semicircular canal endolymph flow. It can be spontaneous or caused by head trauma
Usually lodged in posterior semiciruclar canal, bending the Posterior canal stereocilia
BPPV presentation
- *1) Vertigo**
- recurrent, last for about 3wk
- associated with a SPECIFIC position
- cause wakes in sleep
2) No hearing symptoms
BPPV management
Diagnosis:
Hallpike manoevre
- *Management:**
- *1) Reassurance & General measures**
- stop driving
- prop up or 2 high pillows
- Don’t sleep on side of bad ear
- Keep head vertical
2) Epley manoevre
3) Cawthorne-Cooksey exercises
- *4) Surgery** (not performed in HK)
- Posterior ampullary nerve section
- Posterior canal obliteration
Meniere’s Disease presentation
i.e. idiopathic endolymphatic hydrops (more common in women):
Triad of:
- *1) tinnitus
2) Vertigo** - *3) Progressive deafness** (esp low tone on audiometry)
+/-) aural fullness
+/-) each attack about a few hours
Meniere’s Disease Treatment
- *1) Long term:**
- Sodium restriction
- Thiazide diuretics (not loop as it causes vertigo too)
- Meniett Device
- Betahistine
- Intratympanic gentamicin injection (Medical labyrinthectomy)
- *2) Anti-vertigo & anti-nausea for attack**
- Betahistine
- Antihistamine (promethazine for vomit prevention)
- Anticholinergics antiemetic (Hyoscine)
- diazepam
- Phenothiazines?
3) Hearing aid for deafness
- *4) Occasionally surgery**
- endolymph sac decompression
- Vestibular neurectomy
- Labyrinthectomy
Presentation of upper airway obstruction (neonate)
- Dyspnea
- Feeding difficulties
- Choking, aspiration
- Coughing
- Voice change (noisy breathing, hoarseness, weak cry, not crying)
- Stridor
- Stertor
Upper airway obstruction DDx in children
- Croup (laryngotracheobronchitis)
- Acute Epiglottitis
- Retropharyngeal abscess
- Recurrent respiratory papillomatosis
- Foreign body (e.g. food, toy)
- Anaphylaxis
- Trauma
- OSA - adenotonsillar hypertrophy
Upper airway obstruction DDx in adults
- Tumours (pharyngeal tumours)
- Infection
- Trauma
- Foreign body (e.g. fish bone)
- Anaphylaxis
- OSA (e.g. obesity)
- Vocal cord palsy
Croup presentation & Ix
Young children of 3 months to 3 yo
- *Signs:**
- Fever, preceded by URTI
- Biphasic Stridor
- Barking cough, Tripod position
- Recurrent croup is associated with subglottic stenosis or subglottic hemangioma
XR neck: subglottic swelling - hourglass or steeple sign Nasopharyngeal aspirated (NPA) - viral antigens
Croup pathogens
Caused mainly by viral infection:
- Parainfluenza virus
- Influenza virus type A
- Respiratory syncitial virus
- Mycoplasma pneumoniae
Croup management
- *0) ABC, Close observation, 10% admitted**
- O2 therapy
- intubation needed for repeated adrenaline
- *1) PO/IM dexamathasone
2) nebulised budesonide
3) Nebulised adrenaline** (1:1000)
Must rule out underlying subglottic stenosis or hemangioma if recurrent croup
Acute epiglottitis presentation
Children 2-6 yo:
- *Presentation:**
- Fever
- Severe sore throat, rapidly worsening
- Inspiratory stridor
- Stertor, Hot potato voice
- Dysphonia, Drooling, not crying
- Tripod position
Ix are NOT indicated, but:
Laryngoscopy: cherry red epiglottis
XR neck: thumb sign
Blood culture: HIB
Acute epiglottitis pathogen
Mainly H. influenzae type B
but can be:
• Beta-hemolytic streptococcus
• Pneumococcus
• Staphylococcus
Acute epiglottits management
1) DO NOT attempt for throat exam (esp laryngoscopy), blood taking or IV access:
2) Diagnosis by history
3) Immediately OT for airway protection
- Inform senior pedi, ENT and anaesthetist
* *- Gaseous induction followed by intubation**
- *4) Antibiotics: IV Augmentin & Ceftaxime (Claforan)**
- also take blood for blood culture
5) Prophylactic Rifampicin for close contacts
Acute epiglottitis prophylaxis
1) Rifampicin
2) Prophylaxis HIB vaccination
Deep oropharyngeal fascial space infections (types and presentation)
All causes upper airway obstruction:
- *1) Peritonsillar abscess (Quinsy)**
- fever, stridor, sore throat, dysphagia, drooling
- Unilateral Peritonsillar swelling, medial tonsil deviation, deviation of uvula
- Trismus
- *2) Submandibular and sublingual** abscess (Ludwig’s agina)
- fever, stridor, sore throat, dysphagia, drooling
- Stertor, hot potato speech, trismus
- Board like floor swelling (Tender swelling at submental)
- Superior, posterior displacement of tongue
- Dental root abscess 50-90%
- *3) Parapharyngeal abscess**
- Commonest deep neck infection in adults
- fever, stridor, sore throat, dysphagia
- note neck stiffness, jaw angle swelling
- Great pain & trismus (if ant); great dyspnoea (if post)
- often Tonsillitis or Dental origin
- *4) Retropharyngeal abscess**
- Commonest deep neck infection in children < 4yo
- mimic croup, with fever, stridor, dysphagia, drooling
- Note neck stiffness & hyperextension
- Hx of URTI
- XR neck: increase retropharyngeal space
Deep oropharyngeal fascial space infections (management)
- *1) Peritonsillar abscess (Quinsy)**
- Airway protection
- Incision and drainage (trans-oral)
- Antibiotics with penicillin G + metronidazole
- Analgesics
- Consider elective tonsillectomy
- *2) Submandibular & submental abscess (Ludwig’s angina)**
- Airway protection (intubation)
- Antibiotics by penicillin G + metronidazole
- Soft tissue decompression
- Dental assessment
- *3) Paraphayngeal abscess**
- Airway protection (tracheostomy)
- Transcervical drainage
- CT/MRI (assess extent), blood culture, pus culture
- Antibiotics
- *4) Retropharngral abscess**
- Airway protection
- Drainage
- Antibiotics
Complications of deep neck fascia abscess (esp peritonsillar abscess & parapharyngeal abscess)
- *1) Jugular vein thrombophlebitis** aka Lemierre syndrome
- spiked fevers, rigors, swollen cervical lymph nodes, and a swollen, tender or painful neck
- abdominal pain, diarrhea, nausea and vomiting
- Pulmonary involvement
- Septic shock
2) Carotid artery erosion
Location of abscess in Quinsy
Paratonsillar abscess, i.e.:
Collection of pus between tonsillar capsule & superior constrictor
Quinsy pathogen
In peritonsillar abscess, most commonly GAS (strep pyogenes)
Can also be mixed oropharyngeal organisms:
- anaerobes
- viridans streptococcus
- Bacteroides, peptostreptococcus
What is Ludwig’s angina?
Infection begins in the floor of the mouth, leading to rapidly spreading indurated cellulitis, without abscess formation, involving the submandibular and sublingual spaces on both sides.
Ludwig’s angina pathogen and source
Pathogen:
Polymicrobial, but mainly:
- streptococcus
- anaerobes
- *Source:**
- Mostly dental source
Ludwig’s angina management
- Airway protection (intubation)
- IV Antibiotics by penicillin G + metronidazole
- Soft tissue decompression
- Dental assessment
Sore throat DDx
- *1) Infective**
- laryngitis, pharyngitis, tonsilitis, acute epiglottitis
- pertonsillar abscess (quinsy)
- croup
- Infective mononucleosis
- diptheria
- *2) Neoplastic**
- Orophayngeal tumour
- hypopharyngeal tumour
3) Allergy
4) Gastric Reflux
- *5) Inflammatory**
- e.g. post radiotherapy
Infective mononucleosis presentation
May persists for 1-3 months
- *1) Prodromal period 4-5 days
2) Malaise, headache**
Local
3) Sorethroat (pharyngitis)
4) Membranous tonsillitis (Inflammed tonsils, membranous slough, juicy-looking)
5) Petechiae on soft palate
->) can lead to upper airway obstruction
- *6) Lymphadenopathy
7) Palpebral conjunctivitis, puffy eyelids**
Complications:
- *8) Hepato splenomegaly
9) Sepsis
10) Rubelliform rash with amoxicillin, ampicillin**
Lab tests for glandular fever
- *1) CBC**
- Raised WBC
- mononuclear cells
- decreased platelet count
- *2) Peripheral Blood Smear**
- atypical lymphocytes
3) LFT
- deranged LFT
- increased clotting time
- *4) Positive monospot test**
- detection of heterophile antibodies
- *5) Serology**
- Seroconversion of IgM to IgG to EBV antigens
Management of infective mononucleosis
Supportive treatment only:
- *1) Bed Rest
2) Fluid replacement
3) Avoid ampicillin & amoxicillin**(due to rubelliform rash in children with EBV) - *4) Observe airway, Manage complications**
- corticosteroid if airway compromised
- consider penicillin if GAS cultured from tonsils
Clinical presentation of tonsilitis
Symptoms:
- Fever
- Sore throat
- Odynophagia, dysphagia, trismus
Oral cavity:
- Red Hyperaemic swollen tonsils (Always Bilateral), with whitish spots (i.e. exudates, pus)
- Red hyperaemic throat
- Swollen uvula
- Grey furry tongue
- Otalgia
Systemic:
- fever
- Cervical lymphadenopathy
- abdomimal pain, vomiting
Complications of tonsilitis
LOCAL:
1) Upper airway obstruction
- *2) Abscess formation**
- peritonsillar abscess (quinsy)
- parapharyngeal abscess
- retropharyngeal abscess
3) AOM
GENERAL:
- *1) Septicaemia
2) Acute rheumatic fever
3) Acute glomerulonephritis
4) Meningitis**
Acute tonsillitis pathogens
- *1) Virus (mainly)**
- Enterovirus
- Respiratory viruses e.g. Influenza ABC, Parainfluenza 1-4, adenovirus, rhinovirus, respiratory syncytial virus, metapneumovirus, coronavirus
2) Bacteria
- Strep pyogenes
- strep pneumoniae, H influenzae
- anaerobic
- *3) Others:**
- Corynebacterium diptheria
- Candida
- Syphilis
- TB
Tonsilitis management
- *Ix:**
- Throat swab for culture
- *General measures:**
- Bed rest
- Fluid replacement, IV line
- *Medical therapy:**
- Penicillin, Erythromycin
- Analgesics
- *Surgery:**
- Tonsillectomy if chronic & complicated (see “Indications for Tonsillectomy”)
Indications of Tonsillectomy
- *ABSOLUTE indicators**
1) Enlarged tonsils causing upper airway obstruction, severe dysphagia, sleep disorders, cardiopulmonary complication
2) Peritonsillar abscess unresponsive to medical treatment & drainage
3) Tonsillitis resulting in febrile convulsion
4) Tonsils requiring biopsy to define tissue pathology (e.g. unilateral swelling of tonsils)
- *RELATIVE indicators**
5) 3 or more tonsillitis per year
6) Halitosis
7) Recurrent tonsillitis in streptococcal carrier not responsive to antibiotics
8) Unilateral tonsil hypertrophy that is presumed to be neoplastic
Contraindications of tonsillectomy
1) Bleeding tendency
2) Acute infection within 2 weeks
3) Uncontrolled medical illness
- *4) Body Weight < 15kg**
- as the tonsillectomy may lead to significant proportion of bleeding
- relative contraindication: usually still perform but with monitor in pediatric ICU
Intra-operative complications of tonsillectomy
- *Intra-operative:**
1) Uncontrolled bleeding
2) Injury to teeth
3) Injury to posterior pharyngeal wall
4) TMJ dislocation (jaw dislocation)
5) Atlantoaxial subluxation e.g. Down’s syndrome
Post-op complications of tonsillectomy
- *Immediate (within 24 hours post-op)**
1) Reactionary haemorrhage
2) Aspiration
3) shock
4) bronchospasm - *Early**
1) Secondary haemorrhage D5-10 (due to infection)
2) Peritonsillar, parapharyngeal abscess
3) Pulmonary complication, pneumonia
4) Poor intake - *Late:**
1) Scarring of soft palate
2) Voice change
3) Recurrent infection (tonsil remnant)
Management of reactionary haemorrhage from tonsillectomy
An immediate complication post-op of tonseillectomy:
- *1) Resuscitation**
- ABC, may need intubation if airway compromise
- BP, capillary refill
- Fluid resuscitation
- 2 large bore IV access, ensure T&S
- *2) Inspect wound -> haemostasis procedure**
- if minor bleed: pack with adrenaline gauze, cauterisation, antibiotics
- if major bleed: haemostasis under GA, may need rapid sequence induction
Post-tonsillectomy reactionary haemorrhage signs
1) Frequent swallowing, gurgling sound in throat, vomiting
2) fresh blood in mouth
3) Pale skin, Cold periphery, poor capillary return
4) Restlessness
5) Tachycardia, orthostatic hypotension, Shock
