Larynx anatomy

• hollow musculoligamentous
structure with a
cartilaginous framework
• Location: C4-6
• Attachments
– Superiorly = hyoid bone
– Inferiorly = trachea
• Innervation = vagus
• Functions
– Voice production
– Airway
Laryngeal Cartilages
• 9 Cartilages connected by ligaments & membranes
– Single(Epiglottis, Thyroid, Cricoid),paired (Arytenoid,
Corniculate, Cuneiform)
• Superior part = stratified squamosal epithelium
• Below vocal cords= ciliated pseudostratified columnar
 epiglotis

arythenoid

thyroid
cricoid
Laryngeal joints
• Cricothyroid & crico-arytenoid joints
• Synovial joints
• important for abduction and adduction
movement of the vocal ligaments
 Laryngeal ligaments
• Extrinsic ligaments
 Thyrohyoid membrane
 cricotracheal ligament
 Hyoepiglttic ligament
• Intrinsic ligament
– vocal ligament
– vestibular ligament
 Vocal Cords
• Located in larynx
• Vocal ligaments run from arytenoid to thyroid
cartilages
• Elastic fibers covered by mucosa
• True vocal cords = Mucosal folds
– Exhaled air passes over them causing vibration
• “False” vocal cords = Vestibular folds
– lie superior to true pair, no role in voice production
Laryngeal cavity is divided into three compartments
by vestibular & vocal folds:
– Vestibule- above the vestibular folds
– Ventricle -b/n the vestibular& the vocal folds
– Subglottic space –below the vocal folds up to the
lower border of the cricoid cartilage
Muscles of the larynx divided in to :
1. extrinsic which attach the larynx to the neighboring structures
2. intrinsic which attach the various cartilages of the larynx
• Intrinsic muscles
– Adjust tension in the vocal ligaments,
– open and close the rima glottidis,
– control the inner dimensions of the vestibule,
– close the rima vestibuli, and
– facilitate closing of the laryngeal inlet.
Components of Speech
– Phonation: production of voice,
– determined by
• vocal fold position,
• expiratory force,
• vibratory capacity of vocal folds,
• vocal fold length and tension
– Resonation: oral/nasal speech balance, determined by
velopharyngeal musculature valving and by structure of the
chest, nasopharynx, nasal cavity, and oral cavity
– Articulation: production of speech sounds, determined by
actions of the lips, tongue, and jaw musculature activity
Examination of Larynx
• External examination
- External laryngeal
framework
- Evidence of perichondritis
- LNs in various triangles of
the neck
- Laryngeal crepitus
• Indirect laryngoscopy
- Opd procedure
- Local anesthesia( soft palate &
post pharyngeal wall)
- Mirrors of different size used
- Image seen in 2-D & inverted
- Ant commisure, ventricle &
subglottis not well visualized
Fiberoptic laryngoscopy
• Direct laryngoscopy
- OR procedure
- True 3-D image
- Good visualization of laryngeal structures
- Look for evidences for
- Polyps, intrachordal cysts, rienke edema
- VC nodules, granuloma, paralysis
- Papilloma, cancer…
• Bronchoscopy
- OR procedure
- Use bronchoscope
- Diagnostic/therapeutic
- Unexplained cough, hemoptysis, stridor & wheeze are the
usual indications
• Radiologic examination
- AP & lateral neck X ray
- FBs, growths, croup, supraglottitis…
- CXR
- Tuberculous lesions, mediastinal widening…
- Ba swallow
- Congental anomalies, esophageal & post cricoid tumors
- CT/MRI
 Diseases of the Larynx
Congenital Malformation
Inflammation
Tumors of the larynx
Laryngeal palsy
Laryngomalacia
• Laryngomalacia is the most common cause of stridor in infants.
• elongated omega-shaped epiglottis, short aryepiglottic fold,
pendulous mucosa
• caused by indrawing of supraglottis on inspiration
Clinical Features
• high-pitched crowing inspiratory stridor at 1 to 2 weeks
• constant or intermittent and more pronounced supine
• usually mild but when severe can be associated with feeding
difficulties, leading to failure to thrive
Diagnosis-direct or indirect laryngoscopy
Treatment
– observation is usually sufficient as symptoms usually
spontaneously subside by 12 to 18 months
– in the case of severe laryngomalacia, division of the
aryepiglottic folds provides relief
Subglottic Stenosis
 Congenital
• diameter of subglottis <4 mm in neonate (due to thickening of
soft tissue of subglottic space or maldevelopment of cricoid
cartilage)
 Acquired
• Acquired subglottic stenosis is now rare due to the use of smaller,
softer tubes and secure taping to prevent movement.
• following nasotracheal intubation due to
– long duration
– trauma of intubation
– large tube size
– Infection
Clinical Features
• biphasic stridor
• respiratory distress
• recurrent/prolonged croup
Diagnosis
• laryngoscopy
• CT
Treatment
• if soft tissue – laser and steroids
• if cartilage – laryngotracheoplasty (LTP)
 Acute Laryngotracheobronchitis (Croup)

• inflammation of tissues in subglottic space ±

tracheobronchial tree
• swelling of mucosal lining and associated with thick,
viscous, mucopurulent exudate which compromises
upper airway (subglottic space narrowest portion of
upper airway)
• normal function of ciliated mucous membrane impaired
Etiology
• viral: parainfluenzae I (most common), II, III, influenza A,
and B, RSV
Clinical Features
• age 4 months to 5 years
• preceded by URTI symptoms
• generally occurs at night
• biphasic stridor and croupy cough
(loud, sea-lion bark)
• appear less toxic than epiglottitis
• supraglottic area normal
• rule out foreign body and
subglottic stenosis
• “steeple-sign” on AP x-ray of neck
• if recurrent croup, think
subglottic stenosis
Treatment
• racemic epinephrine via nebulizer q1 to 2h, PRN
• systemic corticosteroids (e.g. dexamethasone, prednisone)
• adequate hydration
• close observation for 3 to 4 hours
• intubation if severe
• hospitalize if poor response to steroids after 4 hours and
persistent stridor at rest
• consider alternate diagnosis if poor response to therapy (e.g.
bacterial tracheitis)
Acute Epiglottitis
• acute inflammation causing swelling of
supraglottic structures of the larynx
without involvement of vocal cords
Etiology
• H. influenzae type B
• relatively uncommon condition due to HiB
vaccine
Clinical Features
• any age, most commonly 1 to 4 years
• rapid onset
• toxic-looking, fever, anorexia, restlessness
• cyanotic/pale, inspiratory stridor, slow
breathing, lungs clear with decreased air
entry
• prefers sitting up, open mouth, drooling,
tongue protruding, sore throat, dysphagia
Investigations
• investigations and physical examination may lead to complete
obstruction, thus preparations for intubation or tracheotomy must
be made prior to any manipulation
• Seek ENT/anesthesia consultation
• lateral neck radiograph – cherry-shaped epiglottic swelling (“thumb
sign”) – only if stable
• WBC (elevated), blood and pharyngeal cultures after intubation
Treatment
– secure airway & get IV access with hydration
– antibiotics – IV cefuroxime, cefotaxime, or
ceftriaxone
– moist air
– extubate when leak around tube and afebrile
– watch for meningitis
– When managing epiglottitis, it is important not to
agitate the child, as this may precipitate complete
obstruction.
Laryngitis
Acute Viral Laryngitis
• Pathogens:
– rhinovirus (most common), parainfluenza, respiratory syncytial virus,
adenovirus, influenza virus, pertussis
• SSx:
– dysphonia, low-grade fever, hoarseness, cough, rhinitis, postnasal
drip
• Dx:
– clinical history and exam
• Rx:
– conservative management required (hydration, pyretics, voice rest,
decongestants, humidification, smoking cessation),
– antibiotics not indicated unless suspect secondary bacterial
infection
Reflux-Induced Laryngitis
• Pathophysiology: • Laryngeal Findings:
– inflammatory response of
-erythema and edema of the
laryngeal mucosa from
posterior commissure,
Laryngopharyngeal Acid
arytenoids, superior surface of
Reflux (LPR)
the vocal folds, and laryngeal
• SSx: surface of the epiglottis;
– hoarseness (worse in the -diffuse supraglottic edema;
morning), -laryngeal pachydermia
– choking spells at night, (interarytenoid);
– regurgitation, postprandial -granulomas of the vocal process
heartburn (seen <50% of
the time in LPR)
– bitter taste in mouth,
– globus sensation, cough,
– chronic throat clearing,
Chronic Laryngitis
• Common Etiologies:
– smoking, pollution, vocal abuse, sinusitis, rhinitis,
laryngopharyngeal acid reflux
• SSx:
– hoarseness, pain, edema, dysphagia, respiratory compromise
• Dx:
– flexible nasopharyngoscopy, videostroboscopy, endoscopy
(thick erythematous vocal folds) with biopsy to rule out
malignancy
• Rx:
– address etiology (stop smoking, voice rehabilitation, treat
rhinosinusitis, reflux regimen), humidification, mucolytics,
consider short course of corticosteroids
TB Laryngitis
• typically secondary to pulmonary TB
• Histopathology: cellular inflammation,
granuloma in subepithelium, perichondritis
• Lesion: granulation and ulcerative tissue in
posterior glottis (posterior interarytenoids most
common, laryngeal surface of epiglottis, vocal
folds)
• Rx: Isoniazid, Rifampin, voice rest, narcotics for
pain
 Laryngeal polyp
• Usually pedenculated , less
Etiology
commonly sessile lesions – Idiopathic
involving mid to anterior half – VC hemmorage
of the VCs – Prior viral infections
• Unilateral in 90% of cases – The whole of the VC
• No sex predeliction, can occur becomes polypoid
at any age Risk factor
• Most common benign lesion – Smoking
of the adult larynx – Hypothyroidism
• Macroscopically – Reflux
– Mucoid – Chronic vocal misuse
– Angiomatous
Treatment is surgical
 Laryngeal cancer
• Most common malignant ca of H&N
• Incidence 8:100000/year M:F 5-10:1
• Peak 55th-65yrs
• Originates on the true VC(75%) ,supraglotis(25%) ,rarely in subglotis
• Hoarseness >2 weeks strong early warning
• Sites other than the VCs do not cause hoarseness leading to delay in
diagnosis
• Etiology
– Smoking
– Alcohol
– Previous radiation to neck
– Genetic factors
– Occupational exposure to asbestos ,mustard gas
• Clinical Presentation
- Hoarseness ,FB sensation ,dysphagia ,dyspnea
- Immobile or fixed VCs
- Verrucous, exophytic or infiltrative
• Diagnosis
– Palpation
– Indirect laryngoscopy
– Imaging-CT scan & MRI
Management
• Surgery with radiotherapy primary mode
• chemotherapy
 Unilateral V.C paralysis

• Result in ipsilateral paralysis of

intrinsic muscles except
cricothyroid
• Vc-median or paramedian
position
• C.F -1/3-asymptomatic ,change
in voice
• Mx –no treatment is required
 Bilateral paralysis
• Neuritis or surgical trauma (thyroidectomy) are
most important factor
• All intrinsic muscles are paralyzed
• VC –lie in median or paramedian position
• C.F- dyspnea & strider but has good voice
• Mx –tracheostomy
- surgical latealization of the cord
 Vocal cord paralysis
causes
Right Left both

•Neck trauma .trauma •Thyroid surgery

•Benign or malignant thyroid ds . Benign or malignant thyroid •Thyroid ca
•Thyroid surgery ds •Ca of cervical esophagus
•Cervical esophagus ca . Thyroid surgery •Cervical LAP
•Cervical LAP .Cervical esophagus ca
.Cervical LAP
•Aneurysm of subclavian aa
•Lung apex ca .bronchogenic ca
•TB of cervical pleura .ca of thoracic oesophagus
•idiopathic .aortic aneurysm
.mediastinal LAP
.intrathoracic surgery
.idiopathic
 Anatomy of the NECK
• Is a connecting tube b/n head & thorax
• Extends from
– Anteriorly-lower border of the mandible to upper surface of manubrium
– Posteriorly-from sup.nuchal lion to inter vertebral disk b/n CVll & TH1
– Laterally- from mastoid process to clavicle ,acromion process
• Skeletal framework is formed by cervical vertebrae
• In the tube 3 compartments provide longitudinal
organization
1. Visceral c.-anterior , contains part of digestive &
respiratory system ,several endocrine glands &LNs
2. Vertebral c. –posterior ,contains cervical v. ,spinal
cord, cervical nerves & muscles
3. Vascular c. –lateral ,two, contains-major BVs &
vagus N
• All these compartments are contained with in a
layer of cervical fascia
 Triangles of the Neck
Each half of the neck can be divided into 2 triangles:
Anterior and Posterior
Anterior triangle -Boundaries
Superior = Inferior margin of Mandible
Anterior = Midline of Neck
Posterior = Sternocleidomastoid muscle
anterior triangle
Posterior Triangle of the Neck
• Boundaries
– Anterior = Sternocleidomastoid muscle
– Posterior = Trapezius muscle
– Inferior = Clavicle
• Contents
– Nerves: Phrenic, Accessory, Cervical Plexus, Brachial Plexus
– Artery: Subclavian
– Vein: External Jugular
 Muscles of the neck
• Assists in the movement of head ,neck & its
skin ,
 in chewing & swallowing
 in movement of larynx during speech &
 in movement of the thorax during inspiration
• Are divided in to four groups
1. Superficial group
2. Hyoid (suprahyoid &infrahyoid)group
3. Scalene (lateral vertebral)group
4. Prevertebral (deep anterior vertebral)groups
 Superficial group
• Assists in the movement of head ,neck & its skin ,
 in chewing & swallowing
 in movement of larynx during speech &
 in movement of the thorax during inspiration
• Are divided in to four groups
1. Superficial group
2. Hyoid (suprahyoid &infrahyoid)group
3. Scalene (lateral vertebral)group
4. Prevertebral (deep anterior vertebral)groups
Hyoid group
Scalene group
Prevertebral group
 Fascia of the neck
• Neck is completely surrounded by skin &tethered to underlying deep F by a layer of
superficial fascia
• There are two fascia
1. Superficial fascia –is part of superficial fascia of the body
• Contains platysma ,subcutaneous branches of cervical plexus, external &
anterior jugular vein
• Is a subcutaneous layer of loose CT
1. Deep fascia-formed by condensations of CT
– Form fascial planes along which infection can spread &
divided in to 4layer
Neck spaces
- Entire length of the neck - Suprahyoid

- Prevertebral space - Parapharyngeal space

- Retropharyngeal space - Submandibular space

- Danger space - Parotid space

- Visceral vascular space - Masticator space

- Infrahyoid - Peritonsillar space

- Pretracheal space - Temporal space

Deep neck space infections
• Neck spaces by far the most complex anatomy
• Compartmentalization →prevent spread of infection
• Prevention & treatment based on anatomy
• Commonly arise from a septic focus of the mandibular teeth,
tonsils, parotid gland, deep cervical LNs, middle ear, or PNS
• Relatively uncommon in the post antibiotic era.
• Widespread use of ABs and profound immunosuppression in some,
the classic manifestations may be absent.
• Often rapid in onset and may progress to fatal complications.
 Causes
• Adults
- Odontogenic infections most common
- Salivary gland infections, FBs, trauma, instrumentation, URTI
- Iv drug use increasing cause
- 20% unknown
- Under diagnosed congenital anomalies may explain some
• Pediatrics
- Tonsillitis most common cause followed by odontogenic infn
Bacteriology
– Mixed infection, Average of 5 bacteria identified in each
– Usually reflect oropharyngeal flora
– Streptococci are the most commonly cultured organism
– Aerobic Gm –ves & staphylococci not common except in drug
abusers & seriously ill hospitalized patients
Diagnosis
Symptoms Signs
• Pain • Swelling
• Fever • Dental abn.
• Swelling • Flactuance
• Dys/odynophagia • Oropharyngeal abn.
• Trismus • Trismus
• Resp. difficulty • Laryngeal abn.
• Toothache
 Radiology
Plain films
PA & lateral neck X ray
- FB, tracheal deviation, subcut air, fluid in soft tissue, soft tissue edema
- Important in the diagnosis of pretracheal & retropharyngeal abscess
CXR
- Pulmonary edema, pnumothorax/pnumomediastinum, hilar LAP
- Mediastinal widening in mediastinitis
Panorex oral view
– Apices of 2nd & 3rd mandibular molars extend below myelohyoid line
• CT/MRI
• U/S
- Guides aspiration & supplement diagnosis, Operator dependent
Management
• Securing the airway is the 1st priority
- Humidified air & observation enough for most
- Intubation/cricothyrotomy/tracheostomy
• Fluid resuscitation often indicated
• Antibiotics
- Emperic pending culture result
- Immunocompetent
- Ampicillinsulbactam/clindamycin/ceftriaxone/cefoxitine
 - Compromised
- Ticarcillin clavulanate/piperacillin tazobactam +
aminoglycoside
- Clindamycin + ciprofloxacin/ceftazidime
- S. aureus suspected add vancomycin
- Necrotizing cervical fascitis
- Ceftriaxone + clindamycin/metronidazole
• Surgical management
– Tooth extraction if inciting tooth disease identified
– Incision & drainage
- Abscess
- Impending complications
- No improvement after 48 hrs of parentral antibiotics
Branchial Cleft Cysts/Fistulae
Embryology
• at 6th week of development, the 2nd branchial arch grows
over the 3rd and 4th arches and fuses with the neighbouring
caudal pre-cardial swelling forming the cervical sinus
• 3 types of malformations:
– 1) branchial fistula – persistent communication between
skin and GI tract
– 2) branchial sinus – blind-ended tract opening to skin
– 3) branchial cyst – persistent cervical sinus with no
external opening
Clinical Features
• 2nd branchial cleft malformations most common
– fistulas present in infancy as a small opening anterior to
the sternocleidomastoid muscle
• cysts present as a smooth, painless, slowly enlarging lateral neck
mass, often following an URTI
• 1st branchial groove malformations present as pre-auricular
pit/sinus
Treatment
• surgical removal of cyst or fistula tract
• if infected – allow infection to settle before removal
Thyroglossal Duct Cysts
• thyroid originates as ventral midline diverticulum of floor of
pharynx caudal to junction of 3rd and 4th branchial arches
(foramen cecum)
• thyroid migrates caudally along a tract then curves underneath
and down to cricoid; thyroglossal duct cysts are vestigial
remnants of tract
Clinical Features
• usually presents in the 2nd to 4th decades as a midline cyst that
elevates with swallowing and tongue protrusion
Treatment
• pre-operative antibiotics to reduce inflammation
• potential for neoplastic transformation so complete excision of
cyst and tract up to foramen cecum at base of tongue with
removal of central portion of hyoid bone (Sistrunk procedure)
Cystic Hygroma
• lymphangioma arising from vestigial
lymph channels of neck
Clinical Features
• usually presents by age 2
• thin-walled cyst extending from floor of mouth to
mediastinum, usually in posterior triangle or supraclavicular
area
• usually painless, soft, compressible
• infection causes a sudden increase in size
Treatment
• surgical excision if it fails to regress – difficult dissection due
to numerous cyst extensions
 Hemangioma
• Vascular lesion
• Soft redish-purple swelling
• Incidence-10% infancy
• Dx:-u/s
• Mgt:
– Conservative
– surgical
Otorhinolaryngology Emergencies
 Auricular hematoma
• Pathogenesis:
– Result from blunt force trauma, usually
from sports
– Blood accumulates in the sub‐
perichondrial spac
– result in decreased blood flow,
cartilaginous necrosis and infection.
• SSX
– Tender, fluctuant mass
• Mgt:
– Prompt evacuation within 7‐10 days
– Various techniques for compression
dressing to prevent re‐accumulation
– Cauliflower ear is the resulting deformity
due to a delay mgt
– Antibiotic prophylaxis
 Nasal hematoma

• Rare complication of NB fx
• Usually present with nasal
• obstruction and blue erythematous bulge from nasal septum
(bilateral)
• Prompt I&D and packing are crucial to prevent cartilaginous
necrosis of septum / saddle deformity*
 Nasal bone fracture
• Most common facial fracture
• 3rd most fractured bone
• High index of suspicion for fracture
• SSX:
– Change in appearance
– Epistaxis, Nasal obstruction
– Instability, Mobility, Crepitation
Lacerations, Septal hematoma
– Nasal X‐rays‐ variable reliability
– Early ENT referral (<5 days)
Mgt:
– Closed/ Open reduction‐ early
– Septorhinoplasty‐ late
Ccx:
– Septal hematoma
– Nasal obstruction
FB in the nose

Removal technique
• Parental puff technique
• Use Ambu-bag
• Cut foley catheter, use glue and suction
• Using PROPER instruments..
• Use local anaesthetic and decongestant
• GA may be necessary in children
• CONSIDER EARLY REFERRAL TO OTOLARYNGOLOGY
FBs in the ear

Syringing – don’t irrigate vegetables they swell!

Alkaline batteries – leak & necrosis
L- hook (beads)
Aligator forceps
Insects – kill first with oil or lidocaine
Wax – Visualization and proper technique
CONSIDER EARLY REFERRAL TO OTOLARYNGOLOGY
FB (inhaled & ingested)

Foreign body inhalation is the most common cause of accidental

death in children.
Ingested
• usually stuck at cricopharyngeus
• coins, toys
• presents with drooling, dysphagia, stridor if very large
Aspirated
• usually stuck at right mainstem bronchus
• peanuts, carrot, apple core, popcorn, balloons
• presentation
– stridor if lodged in trachea
– unilateral “asthma” if bronchial, therefore often
misdiagnosed as asthma
– if impacts to totally occlude airway: cough, lobar
pneumonia, atelectasis, mediastinal shift, pneumothorax
Diagnosis and Treatment
• inspiration-expiration chest x-ray (if patient is stable)
• bronchoscopy and esophagoscopy with removal
Epistaxis
Blood Supply to the Nasal Septum
1. Superior posterior septum -internal carotid --> ophthalmic A
2. Rest of the septum -external carotid --> internal maxillary , facial A
• All anastomose to form Kiesselbach’s plexus, located at Little’s
area (anterior portion of the cartilaginous septum), where 90% of
nose bleeds occur
• bleeding from above middle turbinate is internal carotid, and
from below is external carotid
Kiesselbach’s Plexus (Little’s area)
• confluence of arterial vessels at the anterior nasal septum
susceptible to bleeding due to the fragile mucosa and tightly
adherent to underlying mucosa affording little resistance to
mechanical stress
• Contributing Vessels: anterior ethmoidal, superior labial,
greater palatine, and sphenopalatine arteries
Etiology of Epistaxis
Local
• Trauma (most common)
– fractures: facial, nasal
– self-induced: digital, foreign body
– Iatrogenic: nasal, sinus, orbit surgery
– Barometric changes
– Nasal dryness: dry air, ± septal deformities
– Septal perforation
– Chemical: cocaine, nasal sprays, ammonia, etc.
• Tumours
– benign: polyps, inverting papilloma, angiofibroma
– malignant: squamous cell carcinoma, esthesioneuroblastoma
– Inflammation( rhinitis)
• infections: bacterial, viral, fungal
• Idiopathic
Systemic
• Coagulopathies
• meds: anticoagulants, NSAID
• hemophilias, von Willebrand’s
• hematological malignancies
• liver failure, uremia
• Vascular: hypertension, atherosclerosis...
Investigations
• CBC, PT/PTT (if indicated)
• x-ray, CT as needed
Treatment
• aim is to localize bleeding and achieve hemostasis
1. First-aid
• ABC’s
• patient leans forward to minimize swallowing blood
• constant firm pressure applied for 20 min on soft part of nose
2. Assess Blood Loss (can be potentially fatal hemorrhage)
• pulse, blood pressure, and other signs of shock
• IV NS, cross match for 2 units packed RBCs if significant
3. Determine Site of Bleeding
• insert cotton pledget of 4% topical lidocaine ± topical decongestant
cocaine, visualize nasal cavity with speculum and aspirate excess
blood and clots
4. Control the Bleeding
– first line topical vasoconstrictors (Otrivin™, cocaine)
– cauterize with silver nitrate
– anterior pack for 2-3 days
– posterior pack with a Foley catheter, gauze pack or Epistat™
balloon
– selective catheterization and embolization of branches of
external carotid artery
• ± septoplasty
• vessel ligation of
– anterior/posterior ethmoid artery
– internal maxillary
– external carotid
5. Prevention
– prevent drying of nasal mucosa with humidifiers, saline
spray, or topical ointments
– avoidance of irritants
– medical management of hypertension and
coagulopathies
Special Cases
• Adolescent male with unilateral recurrent epistaxis
consider juvenile nasopharyngeal angiofibroma (JNA).
This is the most common benign tumour of the
nasopharynx
• Thrombocytopenic patients – use resorbable packs to
avoid risk of re-bleeding caused by pulling out the
removable pack.
Airway management
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