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26 Deep Neck Space Infections
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4. Vieira F, Allen SM, Stocks RM, Thompson JW.Deep neck infection. Otolaryngol Clin North
Am. 2008;41(3):459–83.
5. Feldman DP, Picerno NA, Porubsky ES.Cavernous sinus thrombosis complicating odontogenic parapharyngeal space neck abscess: a case report and discussion. Otolaryngol Head Neck
Surg. 2000;123(6):744–5.
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Chapter 27
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Laryngology
ArashShahangian andC.KwangSung
Pearls
• The larynx has three main functions: to produce voice, to act as a conduit of air
to the lungs, and to protect the airway from aspiration
• The superior laryngeal nerve (SLN) has an internal branch (sensory to mucosa of
the TVFs, supraglottis, and hypopharynx) and an external branch (innervates
cricothyroid muscle)
Anatomy
Microscopic anatomy
• True vocal folds (TVFs)—ve layers
– Stratied squamous epithelium—no mucin glands
– Lamina propria—three layers
Supercial (Reinke’s space)
• consists of loose bers and matrix
• lowest concentrations of collagen and elastin
• most important for vocalization
A. Shahangian
Head and Neck Surgery, San Jose Medical Center, Kaiser Permanente, San Jose, CA, USA
C. K. Sung (*)
Department of Otolaryngology- Head and Neck Surgery, Stanford University School of
Medicine, Stanford, CA, USA
e-mail: kwangs@stanford.edu
© Springer Nature Switzerland AG 2023
F. Y. Lin, Z. M. Patel (eds.), ENT Board Prep,
https://doi.org/10.1007/978-3-031-26048-3_27
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Intermediate layer
• higher concentration of elastin and collagen
• together with deep layer forms the vocal ligament
• high concentration of macrophages; ready to ght pathogens translocating across the basement membrane
Deep layer
• highest concentration of collagen and elastin
– Thyroarytenoid muscle
• Vocal ligament
– Intermediate and deep layers of lamina propria
– Forms the upper most portion of conus elasticus
– Some bers insert into the vocalis muscle
• Broyle’s ligament (anterior commissure ligament)
– Condensation of bers with insertion into perichondrium of the laryngeal
cartilages
• Macula ava
– Thickened lamina propria along anterior and posterior membranous
vocal folds
– Serves as transition zone between pliable vocal fold and tougher anchoring
structures
A. Shahangian and C. K. Sung
Gross anatomy
• Intrinsic muscles
– Associated with quadrangular membrane
Thyroarytenoid (TA, vocalis)—shortens, tenses, thickens, and
adducts the TVF
Aryepiglottic—folds epiglottis posteriorly
Thyroepiglottic—widens the laryngeal inlet
– Associated with the arytenoid cartilages
Lateral cricoarytenoid (LCA)—adducts TVF
Posterior cricoarytenoid (PCA)—sole abductor of the TVF
Interarytenoid (IA)—adduct arytenoids, unpaired, bilateral innervation
• Extrinsic muscles
– Cricothyroid (CT)—lengthens TVF, increases tension, and changes pitch
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• Accessory muscles
– Sternohyoid, sternothyroid, and omohyoid—depressor of larynx
– Stylohyoid, thyrohyoid, digastric, mylohyoid, and geniohyoid—main eleva-
tors of larynx
• Laryngeal cartilages
– Thyroid, cricoid, and arytenoid cartilages are hyaline
– Corniculate—sits above arytenoid, broelastic cartilage
– Cuneiform—sits within aryepiglottic (AE) folds
• Laryngeal joints
– Cricothyroid—synnovial (diarthrosis)
– Cricoarytenoid—synnovial (diarthrosis)
Innervation ofLarynx
• Recurrent laryngeal nerve (RLN)
– Innervates all intrinsic muscles
– Sensory to mucosa of subglottis and trachea
– Loops around subclavian artery on the right and aorta on the left
– Nonrecurrent in 0.5% of cases on the right and less frequently on the left
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• Superior laryngeal nerve (SLN)
– Internal branch—sensory to mucosa of the TVFs, supraglottis, and
hypopharynx
Pierces through thyrohyoid membrane
– External branch—innervates cricothyroid muscle
Physiology ofvoice (Voice Production)
Required factors forproduction ofvoice
• Adequate intrathoracic pressure to generate air pressure
• Pliable membrane covering the vocal fold
• Vocal fold closure
• Favorable vocal fold shape
• Control of tension and length of vocal cord
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A. Shahangian and C. K. Sung
Glottal cycle
• Closed vocal folds and increased intrathoracic pressure increases subglottic air
pressure
• Vocal folds separate starting at inferior lip progressing superiorly
• Air ows through glottis and decreases subglottic air pressure
• TVF is pulled medially due to air ow (Bernoulli’s effect) and elastic recoil of
the vocal fold
• Inferior lips of TVF close rst as wave of contact moves from inferior to
superior
• Inferior–superior wave transmission is known as the mucosal wave
• Increase pitch and rate of vocal fold vibration
– Lengthening the vocal folds, increasing intrathoracic pressure, increased air
ow and contraction of laryngeal muscles → increase in fundamental
frequency
Vocal registers
• Falsetto or light voice— highest frequencies. Vibration only at the upper edge of
the vocal folds. Incomplete glottic closure
• Modal voice—mid range frequencies. Mucosa vibrates independently of the
underlying muscle
• Vocal (glottal) fry—closed phase of the vocal folds is longer compared to open
phase. Mucosa and muscle vibrate together. Low-frequency voice
Normal fundamental frequency
• Men 100–125Hz; increases with age
• Women 200–250Hz; decreases with age
Variables that affect voice frequency (Pitch)
• Vocal fold length
• Vocal fold tension
• Vocal fold mass
• Subglottic air pressure
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Clinical voice assessment
Components ofspeech
• Prosody—inection of speech consisting of putting the stress on syllables
• Phonation—production of voice dependent on VF closure, tension, pliable
mucosa, and adequate intrathoracic pressure
• Resonance—modication of sound generated from the VFs by the supraglottis,
pharynx, oral and nasal cavities, and sinuses
• Articulation—production of speech sounds dependent on musculature of the
tongue, lips, and teeth
• Pitch—subjective perception of VF vibration frequency
• Fundamental frequency—measured in vocal analysis
– Longer, thicker VFs in males yield an average fundamental frequency
of 128Hz
– Thinner shorter VFs in females yield a fundamental frequency of 256Hz
• Presbylarynx (aging of the VFs)— thinning VFs lead to increase in fundamental
frequency
• Timbre (quality)—relates to color and quality of a voice that makes it distinctive
Voice assessment instruments
• Used for subjective self-reporting of severity of vocal symptoms
• Voice Handicap Index (VHI)—measures impact of functional, physical, and
emotional aspects of vocal shortcomings
• Voice Related Quality of Life (VRQOL)—questionnaire of physical and social/
emotional functioning subscales combined to give a voice-related quality of life
assessment
• Reux Symptoms Index (RSI)—documents contribution of laryngopharyngeal
reux to symptoms
Vocal examination
• Auditory evaluation
– GRBAS—4-point scale scored by the clinician with 0 denoting no decit and
3 indicating a severe decit
Grade (overall quality)
Roughness
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Breathiness
Asthenia
Strain
– CAPE-V—Consensus Auditory-Perceptual Evaluation of Voice. Voice assess-
ment tool using sustained vowels, specic sentences, and running speech.
A. Shahangian and C. K. Sung
Objective voice measures
• Maximum phonation time (MPT)—longest of three trials measured
– Normal range (varies by source): females 15–25s; males 25–35s
• Subglottal air pressure
• Airow
• Laryngeal airway resistance
Acoustic measures
• Frequency—fundamental frequency and frequency range
• Intensity—loudness
• Variability measures
– Jitter—cycle to cycle variation in frequency
– Shimmer—cycle to cycle variation in amplitude (intensity)
Infectious andinammatory diseases ofthelarynx
Acute laryngitis
• Phonotrauma
– Vocal fold edema and possibly hemorrhage due to vocal misuse, overuse,
or abuse
• Viral—most common cause of acute laryngitis
– Supportive care—rehydration, voice rest, +/− steroids
– Croup—children <3 years, most commonly parainuenza virus
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• Bacterial
– Epiglottitis due to Haemophilus inuenzae
Decreased incidence with H. inuenzae B vaccine
Intubation in controlled setting or awake tracheostomy if respiratory
distress
• Fungal—most commonly Candida albicans
– Dysphonia with white plaques or speckles and erythema on the TVFs
– Immunocompromised patients
– Immunocompetent patients with use of recent use of broad-spectrum antibiot-
ics or inhaled corticosteroids
• Angioedema
– Inammatory reaction with vascular dilation and increased vascular
permeability
– Causes
Hereditary: C1 esterase inhibitor deciency
Non-hereditary causes: medications (ACE-I most commonly), food, insect
bites, transfusions, and infections
– Treatment: oxygenation, epinephrine, steroids, antihistamines
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Chronic Laryngitis
• Bacterial—superinfection of injured larynx; commonly Staphylococcus aureus
• Fungal
– Blastomycosis—endemic to southern USA
– Coccidioidomycosis—endemic to southwestern USA and Central and
South America
– Histoplasmosis—endemic to Ohio and Mississippi River valleys
pseudoepitheliomatous hyperplasia can mimic carcinoma
• Mycobacterial
– Tuberculosis (TB)—interarytenoid fold is most common site
Highly associated with active pulmonary TB
Granulomatous or ulcerative lesions
– Leprosy (Hansen’s Disease)—Mycobacterium leprae
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• Laryngopharyngeal reux (LPR) laryngitis—chronic inammation secondary to
back-ow of gastric contents
– Symptoms: hoarseness (92%), throat clearing (50%), cough (44%), globus
(33%), and dysphagia (27%). Over 50% deny heartburn.
– Laryngeal ndings:
Diffuse laryngeal edema
VF edema
Infraglottic edema with pseudosulcus
Erythema or hyperemia
Ventricular obliteration
Posterior commissure hypertrophy (pachydermia)
Granuloma
Thick endolaryngeal secretions
– Diagnosis:
Gold standard is 24-h dual-probe pH-metry and impedance
Reux Finding Score (RFS)>8 suggestive
Reux Symptom Index (RSI)>13 suggestive
– Treatment:
Diet and behavior modications with twice daily dosage of proton pump
inhibitor (PPI) for minimum 6 months
Laparoscopic Nissen fundoplication in refractory cases
A. Shahangian and C. K. Sung
• Immune diseases:
– Sarcoid—non-caseating granulomas usually of the supraglottis
5% of patients with pulmonary sarcoid have laryngeal disease
– Amyloidosis—rm, non-ulcerated, orange-yellow to gray submuco-
sal nodules
– Granulomatosis with polyangiitis (GPA or Wegner’s granulomatosis)
Diagnosis is conrmed on histology—necrotizing granulomatous inammation, multinucleated giant cells, and small vessel vasculitis
C-ANCA positive in active disease
Subglottic stenosis in 16% of patients
Vocal fold paralysis
• Etiologies:
– Trauma—iatrogenic (thyroid and anterior cervical spine surgery, carotid end-
arterectomy, neck dissection, cardiothoracic surgery, intubation), and
non-iatrogenic
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– Neoplasm
Malignant—thyroid cancer, lung cancer, and CNS tumors
Benign—vagal schwannoma, carotid body tumor, and glomus jugulare
– Neurologic—stroke, multiple sclerosis, ALS, myasthenia gravis, Parkinson’s,
and Guillain-Barre syndrome
– Idiopathic—suspected to be viral neuropathy
• Evaluation:
– History—breathy voice, diplophonia, aspiration, and dysphagia
– Flexible laryngoscopy and stroboscopy—assess symmetry, VF motion, VF
and arytenoid position, glottic gap, and pooled secretions in pyriform sinus
– Classic VF positions in VF palsy
Lateral VF position
• Suggests SLN and RLN injury, loss of cricothyroid with SLN injury
causes increased abduction
• Treated with type I thyroplasty and arytenoid adduction
Paramedian VF position
• Suggests RLN injury only, implies a lesion below the take-off of the SLN
Treated with type I thyroplasty
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– Guttman’s test
Test for SLN paralysis; normally, anterior thyroid cartilage pressure lowers
pitch, lateral thyroid cartilage pressure raises pitch; with SLN paralysis
this is reversed
– Laryngeal electromyography (LEMG)
Most useful 3 weeks to 6 months after nerve injury
Because of synkinesis, LEMG is more reliable for predicting poor prognosis of vocal recovery
• Medical management
– Voice and swallowing therapy
• Surgical management
– Injection laryngoplasty—awake or under general anesthesia
Gelfoam
Carboxymethylcellulose
Collagen
Hyaluronic acid
Micronized dermis
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