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Chronic Diseases of the Larynx | Foreign Bodies of the Airway & Esophagus | Intubation & Tracheostomy

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I. CHRONIC DISEASES OF THE LARYNX

A. Noninfectious Chronic Laryngitis

1. Reflux Laryngitis (Laryngopharyngeal Reflux — LPR)

• Gastric acid, pepsin, and bile refluxate contact the laryngeal mucosa, causing epithelial and stromal injury
• Classic symptoms: hoarseness, chronic throat clearing, globus sensation, chronic cough, laryngospasm
• Pepsin has been identified within intracellular vesicles of laryngeal epithelium as a direct injurious agent
• Diagnosis: pH monitoring (>90% sensitivity/specificity); empiric PPI trial is widely used
• Treatment: behavioral (head-of-bed elevation, dietary changes, avoid fatty/spicy foods, caffeine, alcohol), PPIs, H₂ blockers

2. Laryngeal Tuberculosis

• May occur with or without disseminated pulmonary TB; ~15% have isolated laryngeal involvement, ~47% have active pulmonary disease
• Symptoms: hoarseness is nearly uniform
• Laryngoscopic findings: granulomatous or ulcerative lesions of the true and false vocal folds
• Diagnosis: tissue biopsy showing acid-fast bacilli and granuloma formation
• Treatment: multi-drug anti-TB regimens for extended periods

3. Autoimmune and Granulomatous Diseases

4. Laryngeal Stenosis (Subglottic Stenosis)

• Congenital: due to cricoid malformation (elliptical cricoid); may present as stridor at birth, recurrent croup, or failure to extubate
• Acquired: most commonly from prolonged intubation; exacerbated by GERD, eosinophilic esophagitis, and MRSA infection
• Classification — Cotton-Myer Grading System:
  • Grade 1: 0–50% stenosis
  • Grade 2: 51–70% stenosis
  • Grade 3: 71–99% stenosis
  • Grade 4: 100% (complete) obstruction
• Diagnosis: rigid laryngoscopy and bronchoscopy
• Management:
  • Treat co-morbidities (GERD, EE, MRSA)
  • Endoscopic: scar division, balloon dilation, steroid injection
  • Open laryngotracheal reconstruction (LTR): anterior/posterior cricoid splits with costal cartilage grafts; cricotracheal reconstruction (CTR); cervical slide tracheoplasty
  • Staging: single-stage (no tracheotomy at end) vs. double-stage (tracheotomy removed later)

5. Laryngoceles

• Formed by increased intraglottic pressure (horn players, glass blowers) or obstruction of the laryngeal ventricle by inflammation or neoplasm
• Internal: tracks superiorly within paralaryngeal fat, causing supraglottic compromise
• Mixed/External: extends through the thyrohyoid membrane, presenting as a neck mass

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II. FOREIGN BODIES OF THE LARYNX, TRACHEA, BRONCHI, AND ESOPHAGUS

A. Epidemiology

• ~1,000 deaths/year in the United States from foreign body aspiration
• Most common cause of accidental death in children <1 year
• 25% of airway foreign bodies have been present for >2 weeks before diagnosis

B. Location (in decreasing frequency — airway)

The right main bronchus is preferred because it is more vertical, shorter, and wider than the left. This anatomical relationship persists from fetal life through adulthood.

1. Upper esophageal sphincter (cricopharyngeus) — most common
2. Level of the aortic arch
3. Level of the mainstem bronchus
4. Lower esophageal sphincter

C. Symptoms by Location

D. Diagnosis

• AP and lateral chest X-ray: radiopaque foreign body visible in <25% of cases; may show mediastinal shift away from the foreign body, elevated contralateral hemidiaphragm, obstructive emphysema, pneumomediastinum, pneumothorax, or post-obstructive collapse
• Inspiratory/expiratory films or lateral decubitus views: the dependent lung should collapse but appears hyperinflated if a bronchial foreign body is present (specific but only 50% sensitive)
• CT scan: more sensitive than plain X-ray; reserved for negative bronchoscopy when symptoms persist, to locate subsegmental objects
• Barium esophagram: definitive for esophageal foreign bodies; CT is a useful adjunct

Note: calcification of laryngeal cartilage or the stylohyoid ligament can mimic foreign bodies on plain films; oblique projections help distinguish them.

E. Management

1. Rigid laryngoscopy and bronchoscopy under general anesthesia with spontaneous ventilation — preferred approach
2. Foreign body, forceps, and bronchoscope are removed as a single unit
3. Sharp objects: grasp the sharp end and keep it within the bronchoscope tip during withdrawal to minimize mucosal injury
4. If complete obstruction: push the object further into one bronchus to restore ventilation
5. Repeat bronchoscopy after removal to confirm no additional foreign bodies
6. Flexible bronchoscopy: useful for distal airway objects but provides less airway control
7. Tracheotomy or thoracotomy: rarely required for large or embedded objects

• Sharp, caustic, or button battery foreign bodies: urgent endoscopic removal
• Children <1 year, symptomatic, or >24 hours: urgent endoscopic removal
• Healthy asymptomatic older child, smooth midesophageal/distal object <24 hours: may observe 8–16 hours for spontaneous passage; ~25–30% will pass spontaneously
• Rigid esophagoscopy under general anesthesia with endotracheal intubation

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III. INTUBATION AND TRACHEOSTOMY

A. Endotracheal Intubation

• Mucosal injury to the subglottis (most common site of acquired stenosis)
• Granuloma formation at the vocal processes
• Subglottic cysts (from blocked mucous glands)
• Acquired subglottic stenosis — worsened by GERD, eosinophilic esophagitis, MRSA

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B. Tracheostomy

Indications and Contraindications

Techniques

• Open (surgical) tracheostomy: performed in the operating room
• Percutaneous Dilatational Tracheostomy (PDT): first described by Ciaglia in 1985; widely adopted for elective tracheostomy at the bedside in the ICU
  • Advantages: decreased wound infection, less clinically relevant bleeding, more cost-effective
  • Periprocedural mortality: <0.1–0.2%
  • Major complication rate (bedside PDT): ~0.15%
  • Safety aids: bronchoscopic guidance or semi-open technique with blunt dissection; preprocedure ultrasound to identify anatomy, crossing veins, and thyroid lobe

Timing

• Early (≤7 days) vs. late (>7 days): controversial; most studies show no mortality difference
• One RCT showed significant reduction in mortality, pneumonia, and ICU stay with early tracheostomy (48h vs. 14–16 days) in patients predicted to require >2 weeks ventilation
• In the largest UK RCT (>900 patients): no mortality difference; notably, >50% of late tracheostomy patients were liberated from ventilation without needing the procedure

Complications

• Perioperative: peristomal bleeding (anterior jugular veins, thyroid isthmus), posterior tracheal/esophageal laceration, false tract, loss of airway
• Long-term: tracheal stenosis (~6% clinically significant; ~40% subclinical); subclinical stenosis usually occurs early in the subglottic position
• COVID considerations: aerosol-generating procedure requiring airborne/droplet precautions; tracheostomy after 10–14 days of MV associated with shorter MV duration and ICU stay

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Summary Table

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The Larynx — Complete Clinical Review

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1. Clinical Anatomy of the Larynx

Cartilaginous Framework

• Thyroid cartilage — largest; derived from 4th branchial arch
• Cricoid cartilage — the only complete cartilaginous ring in the entire airway
• Arytenoid cartilages — paired; bear the vocal processes (for cord attachment) and muscular processes (for muscle attachment)
• Epiglottis — leaf-shaped; attached to the inner thyroid angle
• Corniculate and cuneiform — small; in aryepiglottic folds
• All cartilages arise from the 4th and 6th branchial arches

Divisions

Key Spaces

• Paraglottic space: between thyroid ala, conus elasticus, and quadrangular membrane — critical pathway for tumour spread
• Preepiglottic space: bounded by vallecula, thyroid cartilage, thyrohyoid membrane, and epiglottis

Mucosa

• Stratified squamous epithelium: superior and medial surface of vocal folds
• Ciliated pseudostratified columnar (respiratory) epithelium: everywhere else
• Vocal fold lamina propria (the key to phonation):
  • Superficial layer: very loose, rich in hyaluronic acid — the "Reinke's space"
  • Middle layer: denser elastic fibres
  • Deep layer: cross-linked collagen — forms the vocal ligament with middle layer

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2. Functions of the Larynx

Respiratory Function

• Maintains a patent airway; the only complete cartilaginous ring (cricoid) keeps the subglottis open
• Regulates airflow; vocal folds abduct maximally during exercise (posterior cricoarytenoid is the sole abductor)

Protective Function

• Three-tier sphincteric mechanism during swallowing:
  1. Aryepiglottic folds (first tier)
  2. False vocal folds (second tier)
  3. True vocal folds (third tier, most important)
• Larynx elevates and moves anteriorly; epiglottis rotates to deflect food bolus laterally into pyriform fossae
• Cough reflex: forceful glottic closure followed by explosive opening expels foreign material
• Valsalva manoeuvre: closed glottis allows fixation of the thorax for effort

Vocal Function

• Phonation: exhalation drives air through adducted vocal folds → mucosal wave travels upward along the vocal fold (epithelium and superficial lamina propria vibrate over the vocal ligament)
• Pitch: determined by tension and length of vocal folds (cricothyroid lengthens/tenses; vocalis shortens/relaxes)
• Intensity: determined by subglottic air pressure
• Timbre: shaped by supraglottic resonators (pharynx, oral cavity, nasal cavity)

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3. Muscles of the Larynx

Extrinsic Laryngeal Muscles

• Sternohyoid (C2, C3), thyrohyoid (C1), omohyoid (C2, C3)

• Geniohyoid (C1), digastric (anterior belly CN V, posterior belly CN VII), mylohyoid (CN V), stylohyoid (CN VII)

• Inferior constrictor arises from the oblique line of the thyroid cartilage
• Cricopharyngeus: continuous circular muscle at the pharyngo-oesophageal junction

Intrinsic Laryngeal Muscles

The TA–LCA complex is functionally best considered a single adductor unit.

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4. Blood Supply of the Larynx

• Supraglottis → upper deep cervical (jugular) nodes; some contralateral crossover
• Subglottis/infraglottis → pretracheal and lower jugular nodes; contralateral crossover
• Glottis → very sparse lymphatics; ipsilateral only (explains low nodal spread from early glottic cancer)

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5. Innervation of the Larynx

Superior Laryngeal Nerve (SLN)

• Exits the vagus at the nodose ganglion; divides into:
  • Internal branch (sensory): pierces the thyrohyoid membrane; carries afferent sensation from the supraglottis and glottis down to the vocal folds
  • External branch (motor): supplies the cricothyroid muscle; also contributes to the human communicating nerve

Recurrent Laryngeal Nerve (RLN)

• Motor nucleus: nucleus ambiguus
• Supplies all intrinsic muscles of the larynx except the cricothyroid
• Sensory to the subglottis and trachea below the vocal folds
• Left RLN: loops under the aortic arch (ligamentum arteriosum) — longer course; more vulnerable to mediastinal pathology
• Right RLN: loops under the right subclavian artery
• Non-recurrent RLN (right side): associated with anomalous retrooesophageal subclavian artery

Intralaryngeal Nerves (important clinical detail)

• Galen's anastomosis: connects SLN and RLN (both motor and sensory)
• Human communicating nerve: from external branch of SLN, pierces cricothyroid membrane; provides additional laryngeal motor/sensory supply
• Interarytenoid nerve: from bilateral RLN branches — the only bilaterally innervated intrinsic muscle

Clinical pearl: Injury to the RLN causes ipsilateral vocal fold paralysis (paramedian position). Injury to the SLN external branch causes subtle pitch changes and loss of high-note projection (important for professional singers). Injury to the internal SLN branch impairs supraglottic sensation and increases aspiration risk.

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6. Methods of Examination of the Larynx

History and Symptoms

Indirect Laryngoscopy (Mirror Laryngoscopy)

• Technique: patient seated, tongue protruded; warmed laryngeal mirror placed against the soft palate at ~45°; light source directed; patient phonates "eee" for cord adduction
• Advantages: inexpensive, office-based, dynamic view
• Limitations: requires patient cooperation; gag reflex can prevent adequate visualisation; cannot see subglottis

Direct (Rigid) Laryngoscopy

• Performed under general anaesthesia (or topical local anaesthetic in cooperative adults)
• Direct-suspension microlaryngoscopy allows bimanual microsurgical technique
• Technique: rigid laryngoscope (Lindholm, Dedo, etc.) inserted to suspend the larynx, giving magnified view with operating microscope; topical lidocaine anaesthetises vocal folds
• Allows biopsy, microsurgery, foreign body removal

Flexible Nasopharyngolaryngoscopy

• Performed awake in the office with topical anaesthesia
• Excellent dynamic assessment of vocal fold mobility, arytenoid motion, swallowing
• Method of choice for laryngomalacia diagnosis (awake, to see dynamic collapse)
• Combined with stroboscopy for mucosal wave analysis in voice disorders

Rigid Stroboscopy

• Uses pulsed light matched to the fundamental frequency to create slow-motion illusion of vocal fold vibration
• Reveals mucosal wave abnormalities (stiffness, masses, scar)

Imaging

• CT neck with contrast: best for submucosal extension, cartilage invasion, nodal metastases; essential for airway emergency assessment
• MRI: superior soft tissue contrast; better for preepiglottic/paraglottic space
• Lateral neck X-ray: "thumbprint sign" in epiglottitis; "steeple sign" (subglottic pencilling) in croup

Electromyography (EMG)

• Laryngeal EMG via percutaneous needle into TA or PCA muscles
• Differentiates neurogenic paralysis from mechanical fixation (cricoarytenoid joint)
• Prognostic: absence of EMG activity or synkinesis predicts poor recovery

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7. Acute Stenosis of the Larynx

Definition

Causes of Acute Laryngeal Stenosis

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8. Stages of Acute Laryngeal Stenosis

Clinical rule: Stage I–II → medical management; Stage III → tracheostomy/intubation urgently; Stage IV → emergency cricothyrotomy/tracheostomy immediately.

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9. Acute Laryngeal Oedema — Aetiology, Clinic, Diagnosis, Treatment

Aetiology

• Allergic/Anaphylactic: most acute; food (nuts, shellfish), drugs (penicillin, NSAIDs, ACE inhibitors — bradykinin-mediated), insect venom
• Hereditary Angioedema (HAE): C1-esterase inhibitor deficiency; non-allergic, non-histamine mediated; life-threatening; triggered by trauma, stress, oestrogen
• Infectious: severe epiglottitis, retropharyngeal abscess
• Traumatic/Iatrogenic: post-intubation, post-irradiation, post-surgical
• Inflammatory: GPA (Wegener's), relapsing polychondritis
• Cardiovascular/Renal: fluid overload, hypoproteinaemia

Clinical Features

• Sudden onset dysphagia, odynophagia, "hot potato" muffled voice
• Progressive inspiratory stridor
• Drooling (cannot swallow)
• Dyspnoea progressing with stage of stenosis
• Tripod/sniffing position

Diagnosis

• Clinical diagnosis; do not delay treatment for imaging in severe cases
• Lateral neck X-ray: thickened, rounded epiglottis ("thumbprint sign"), distended hypopharynx
• Direct/indirect laryngoscopy: oedematous, pale/erythematous supraglottis
• Blood tests: C4 (low in HAE), C1-esterase inhibitor levels, tryptase (anaphylaxis)

Treatment

• Upright positioning; supplemental O₂; IV access
• Continuous monitoring; anaesthetic/ENT/surgical team standby

• Epinephrine (adrenaline) IM 0.5 mg (1:1000) — first-line; may repeat q5–15 min
• Nebulised (racemic) epinephrine — reduces local oedema
• IV corticosteroids: dexamethasone 8–10 mg or hydrocortisone 200 mg IV
• Antihistamines (H₁ + H₂): adjunct only, not sufficient alone
• Airway management: intubation early before complete obstruction; tracheostomy if intubation impossible

• C1-esterase inhibitor concentrate (preferred)
• Icatibant (bradykinin B₂ receptor antagonist) or ecallantide
• Fresh frozen plasma if specific agents unavailable
• Epinephrine and steroids are less effective
• Prophylaxis: tranexamic acid, danazol (long-term)

• Secure airway in controlled setting (OR with anaesthetist)
• IV cephalosporin (2nd/3rd generation) + anti-staphylococcal cover
• Intubation for 3–5 days; extubation when afebrile with regression of oedema on scope

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10. Acute Laryngitis — Clinic, Diagnosis, Treatment

Aetiology

• Viral (most common): parainfluenza (croup in children), influenza, rhinovirus, adenovirus, herpes simplex
• Bacterial: Moraxella catarrhalis, H. influenzae, S. pneumoniae, S. aureus
• Fungal: Candida albicans (immunocompromised)
• Non-infectious: vocal abuse/phonotrauma, noxious chemical exposure, allergy, angioedema, LPR

Clinical Features

• Sudden onset hoarseness — the cardinal symptom
• Dysphonia (rough, weak, breathy voice); increased vocal effort
• Sore throat, odynophonia
• Variable cough, low-grade fever (viral URI)
• No dyspnoea in uncomplicated acute laryngitis — dyspnoea suggests another diagnosis

Diagnosis

• Clinical: history of sudden hoarseness + URI or inciting factor
• Laryngoscopy: diffuse erythema, oedema of vocal folds; vessel injection; sometimes mucopus
• Check for: normal vocal fold mobility; absence of lesions; rule out other causes
• LPR signs: infraglottic oedema, interarytenoid swelling, thick mucus

Treatment (Symptomatic and Supportive)

• Vocal hygiene: voice rest (not absolute), reduced voice use
• Hydration: adequate fluid intake; avoid caffeine/alcohol (drying)
• Humidification
• Decongestants for nasal obstruction
• Cough suppression; mucolytics
• Avoid drying antihistamines
• PPIs / H₂ blockers if reflux suspected
• Antibiotics: only if bacterial cause confirmed or strongly suspected
• Steroids: reserved for urgent vocal demands (performers); not routine
• Natural history: resolves spontaneously in 1–2 weeks

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11. Chronic Laryngitis — Clinic, Diagnosis, Treatment

Definition / Concept

Aetiology

Clinical Forms

Chronic Hypertrophic (Hyperplastic) Laryngitis

• Chronic irritation (smoking, alcohol, vocal abuse) → chronic oedema and epithelial hyperplasia
• Diffuse thickening and redness of vocal folds; leukoplakia (white patches) possible
• Voice: hoarse, rough, low-pitched, effortful
• Risk: leukoplakia may harbour dysplasia or carcinoma in situ — requires biopsy
• Treatment: eliminate irritants; voice therapy; endoscopic removal of hyperplastic mucosa; PPI if LPR

Atrophic Laryngitis (Laryngitis Sicca)

• Atrophy of laryngeal mucous glands and submucosa → drying and crusting
• Often associated with ozaena (atrophic rhinitis) and atrophic pharyngitis ("atrophic pharyngolaryngitis")
• Voice: husky, dry, weak
• Symptoms: dry throat, sensation of a foreign body, chronic cough to clear crusts
• Laryngoscopy: pale, dry mucosa; thick dried crusts (yellowish-green); vocal folds thin
• Treatment: mucolytics, inhalation of saline/oils, alkaline laryngeal irrigations, vitamin A; treat underlying cause

Diagnosis of Chronic Laryngitis

• Laryngoscopy (flexible or direct) is mandatory
• Biopsy if any lesion suspicious for malignancy; many lesions mimic carcinoma
• 24-hour pH/impedance testing (gold standard for LPR — detects acid and non-acid reflux along entire oesophagus)
• Oesophageal manometry; allergy testing; microbiological culture

Treatment

• Culture-directed antimicrobials for proven infection
• LPR: PPIs + behavioural modification (head-of-bed elevation, diet, weight loss); consider Nissen fundoplication in refractory cases
• Smoking cessation (mandatory)
• Voice therapy for phonotrauma
• Immunotherapy for allergy
• Endoscopic surgery for obstructing or suspicious lesions

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12. False Croup (Viral Croup / Laryngotracheobronchitis)

Aetiology

• Most common cause of infectious upper airway obstruction in children
• Parainfluenza virus type 1 (most common); also parainfluenza 2 and 3, influenza A/B, RSV, adenovirus
• Age: 6 months – 3 years (peak ~2 years); more common in autumn

Pathophysiology

Clinical Features

• Prodromal URI (1–3 days) then sudden onset, often at night
• Barking ("seal-like") cough — hallmark
• Inspiratory stridor (subglottic level)
• Hoarse voice
• Low-grade fever
• Mild respiratory distress in most cases; rarely progresses to severe obstruction
• Child generally alert, not toxic; epiglottis is normal

Diagnosis

• Clinical diagnosis
• X-ray (AP neck/chest): "Steeple sign" — symmetric subglottic airway narrowing (pencilling of the subglottis); lateral view shows normal epiglottis
• Normal epiglottis on lateral X-ray differentiates croup from epiglottitis

Treatment

• Mild: cool mist humidification, reassurance
• Dexamethasone 0.15–0.6 mg/kg PO or IM (single dose) — reduces symptoms, hospitalisation, ED visits
• Moderate–severe: nebulised (racemic) epinephrine (L-epinephrine 5 mL of 1:1000) + dexamethasone; observe ≥2 hours post-nebulisation
• Hospitalisation for recurrent or persistent stridor at rest after treatment
• Intubation/tracheostomy: rarely needed

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13. True Croup (Laryngeal Diphtheria)

Aetiology

• Corynebacterium diphtheriae (gram-positive rod, toxin-producing)
• Now rare in immunised populations; still endemic in under-vaccinated regions

Pathophysiology

• Exotoxin (encoded by bacteriophage) inhibits protein synthesis via ADP-ribosylation of EF-2
• Causes superficial necrosis of the mucosa → formation of a tough greyish-white pseudomembrane that adherently covers the larynx, trachea, and pharynx

Clinical Features

• Insidious onset: low-grade fever, sore throat, malaise
• Progressive hoarseness and croupy cough
• Greyish-white membrane (pseudomembrane) on the pharynx/tonsils — cannot be removed without bleeding (pathognomonic)
• "Wet mouse" (mousy) odour
• Progressive airway obstruction (ascending croup) — the membrane spreads downward into the larynx and trachea
• Systemic toxicity: myocarditis, peripheral neuritis (palatal palsy, oculomotor palsy, peripheral neuropathy)
• "Bull neck" appearance from cervical lymphadenopathy and soft tissue oedema

Diagnosis

• Clinical picture + characteristic membrane
• Throat swab + Löffler's or tellurite medium culture (black colonies)
• Albert's stain: metachromatic granules (volutin)
• PCR for toxin gene (tox gene)

Treatment

1. Secure the airway — tracheostomy if airway compromised (intubation may dislodge membrane fragments)
2. Diphtheria antitoxin (DAT) — neutralises free toxin; administer early regardless of sensitivity test; IM or IV
3. Antibiotics: penicillin G IV or erythromycin × 14 days (eradicates organism, reduces transmission)
4. Isolation; cardiac monitoring; corticosteroids for airway oedema
5. Active immunisation after recovery (diphtheria does not confer immunity)

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14. Differential Diagnosis: False Croup vs. True Croup

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15. Acute Epiglottitis (Supraglottic Laryngitis)

Aetiology

• Classic: Haemophilus influenzae type b (Hib) — incidence dramatically reduced by Hib vaccine
• Post-vaccine era: now more common in adults and older children; also caused by other H. influenzae types (A, F), streptococci, S. aureus (including MRSA), N. meningitidis
• Non-infectious: thermal injury (hot liquids), caustic ingestion, allergic reactions, foreign body

Pathophysiology

Clinical Features (Classic — Young Child)

• Acute onset: high fever, severe sore throat, toxic appearance
• Drooling (cannot swallow due to pain and obstruction)
• Tripod / "sniffing" position: neck extended, jaw forward, leaning on hands
• Muffled ("hot potato") voice
• Stridor (inspiratory); absence of barking cough
• No cough (differentiates from croup)
• Rapid progression to respiratory failure

Diagnosis

• Do not examine the throat in a child with suspected epiglottitis outside a controlled setting — may trigger complete obstruction
• Lateral neck X-ray: "thumbprint sign" (rounded, thumb-like swelling of the epiglottis); thickened aryepiglottic folds; loss of air in the vallecula; distended hypopharynx
• However: up to 70% of epiglottitis cases have normal radiographic findings
• CT: not necessary; risks deterioration during transport
• Blood culture: often positive for causative organism
• Definitive: direct laryngoscopy/nasolaryngoscopy (in controlled setting only)

Treatment

1. Airway first: do not leave the child unattended; transport to OR with anaesthesiologist and ENT
2. Stable child: controlled intubation in OR (inhalational induction preferred) — remain intubated 3–5 days
3. Unstable/apnoeic: bag-valve-mask ventilation → intubation → needle cricothyrotomy or tracheostomy if intubation fails
4. IV antibiotics: 2nd/3rd generation cephalosporin (e.g., ceftriaxone) + cover for MRSA if suspected
5. Adults: may be managed in PICU without intubation if stable with close monitoring
6. Corticosteroids: used adjunctively to reduce oedema
7. Prophylaxis: rifampicin for close contacts; vaccination of unimmunised contacts

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16. Laryngomalacia (Congenital Laryngeal Stridor)

Aetiology and Pathophysiology

• Most common cause of neonatal/infantile stridor
• Aetiology: neurological or structural immaturity of the supraglottis (neuromuscular hypotonia); elevated laryngopharyngeal sensory thresholds; dysfunction of the laryngeal adductor reflex (LAR) — a vagally mediated reflex
• Flaccid supraglottis collapses during inspiration, obstructing the airway
• Premature Hispanic and Black infants at higher risk

Classification

• Type 1: short/tight aryepiglottic folds
• Type 2: redundant (prolapsing) supraglottic soft tissue (arytenoids, interarytenoid area)
• Type 3: posterior epiglottic collapse due to underlying neuromuscular disorder

Clinical Features

• Inspiratory stridor within first 2 weeks of life (usually within days 1–2)
• Better in prone position; worse when supine
• Worse with feeding, agitation, crying (in severe cases); mild LM often improves with crying (increased pharyngeal tone)
• Feeding difficulties; failure to thrive in severe cases
• Stridor usually low-pitched, not musical (cf. vocal fold paralysis which is higher-pitched and more musical)
• Spontaneous resolution by 12–18 months in the majority

Diagnosis

• Flexible laryngoscopy in the awake patient (gold standard):
  • Omega-shaped epiglottis falling backward during inspiration
  • Short aryepiglottic folds tethering the epiglottis posteriorly
  • Redundant arytenoid mucosa prolapsing into glottis with inspiration
  • Normal vocal fold mobility (distinguishes from vocal fold paralysis)
• Rigid operative endoscopy if other anomalies suspected or stridor is severe with cyanosis

Treatment

• Mild–moderate: observation and reassurance; resolves by 12–18 months
• Treat concurrent GERD (acid suppression) — reduces symptoms; may avoid surgery
• Severe (with stridor at rest, cyanosis, failure to thrive, apnoea, cor pulmonale):
  • Endoscopic supraglottoplasty (CO₂ laser or cold steel): division of aryepiglottic folds; removal of redundant supraglottic tissue
  • Tracheostomy: rarely required for extreme cases or failed supraglottoplasty

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17. Classification of Laryngeal Paralysis

Classification Scheme

• Unilateral: most common; variable clinical impact
• Bilateral: more severe; significant risk of airway compromise

• Median (adducted): vocal fold at or near midline → poor airway but adequate voice; occurs with RLN paralysis plus preserved adductor tone
• Paramedian: slightly lateral to midline — common position; voice often serviceable
• Cadaveric / lateral: complete flaccid paralysis; severe posterior gap → breathy voice, aspiration; worse airway with bilateral involvement

• High vagal lesion (above nodose ganglion): combined SLN + RLN dysfunction; more lateral fold position with less tone
• RLN alone: below the nodose ganglion; cricothyroid intact; fold in paramedian position

Aetiology

Clinical Features

• Dysphonia: breathy, weak, reduced projection, diplophonia, vocal fatigue
• Aspiration (especially liquids) if fold is lateralised
• Can be asymptomatic if fold in good paramedian position

• Medialized folds: stridor and dyspnoea but near-normal voice
• Lateralised folds: weak/aphonic voice; dysphagia; less airway distress

Treatment

• Unilateral paralysis: goal is glottic closure
  • Voice therapy; vocal fold injection augmentation (temporary — Gelfoam, fat, hydroxyapatite)
  • Medialization thyroplasty (Isshiki type I) — permanent implant
  • Arytenoid adduction — for large posterior gap
  • Laryngeal reinnervation (ansa cervicalis to RLN) — restores bulk and tone
• Bilateral paralysis: goal is adequate airway
  • Tracheostomy for acute respiratory compromise
  • Endoscopic arytenoidectomy / posterior cordotomy (enlarges glottis) — risks voice deterioration
  • Arytenoid abduction suture

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18. Laryngeal Tuberculosis

Aetiology

• Secondary to pulmonary TB in majority; ~47% have active pulmonary disease at diagnosis; ~33% have inactive pulmonary TB; ~15% have isolated laryngeal TB
• Causative agent: Mycobacterium tuberculosis

Clinical Features

• Hoarseness — nearly universal
• Odynophagia (painful swallowing)
• Chronic cough
• Weight loss, night sweats (systemic TB symptoms)
• Most commonly affected sites: true and false vocal folds

Laryngoscopy

• Granulomatous masses or ulcerative lesions (pale, irregular)
• Usually focal; may be bilateral
• Unilateral findings particularly in isolated laryngeal TB
• Mimics laryngeal carcinoma clinically and endoscopically — biopsy is essential

Diagnosis

• Tissue biopsy: acid-fast bacilli + caseating granulomas (Ziehl-Neelsen stain)
• Chest X-ray / CT for pulmonary TB
• Sputum culture and AFB smear
• Tuberculin skin test / IGRA (QuantiFERON)

Treatment

• Standard anti-TB multi-drug regimen: isoniazid, rifampicin, pyrazinamide, ethambutol × 2 months, then isoniazid + rifampicin × 4–7 months
• Laryngeal disease responds well to systemic treatment
• Airway protection if significant obstruction

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19. Foreign Bodies of the Bronchi and Trachea

Epidemiology

• ~1,000 deaths/year in the US; most common accidental death cause in children <1 year
• 80–90% of airway foreign bodies are in the bronchi
• Right main bronchus 60%; left 30%; trachea 3–12%; larynx 1–7%

Symptoms by Level

• Trachea: palpable "audible thud" on neck palpation; biphasic wheeze; "asthmatoid wheeze"
• Bronchus: cough, unilateral wheeze, post-obstructive emphysema/collapse/infection if chronic

Diagnosis

• AP + lateral chest X-ray (radiopaque <25% of aspirated FBs)
• Inspiratory–expiratory or lateral decubitus films: dependent lung with obstructed bronchus remains hyperinflated
• CT: more sensitive; used after negative bronchoscopy if symptoms persist
• Rigid bronchoscopy: gold standard for diagnosis and treatment

Treatment

• Rigid laryngoscopy + bronchoscopy under GA with spontaneous ventilation
• Foreign body + forceps + bronchoscope withdrawn as one unit
• Sharp objects: sharp end kept inside bronchoscope tip
• Flexible bronchoscopy: useful for distal airways
• Tracheostomy/thoracotomy: rare, for large/inaccessible objects
• Contraindicated: blind finger sweeping; chest physiotherapy; bronchodilators

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20. Foreign Bodies of the Oesophagus

Sites of Lodgement (Four Physiological Narrowings)

1. Upper oesophageal sphincter (cricopharyngeus) — most common
2. Level of the aortic arch
3. Level of the left mainstem bronchus
4. Lower oesophageal sphincter

Clinical Features

• Dysphagia, odynophagia, drooling
• Stridor and respiratory distress — from posterior tracheal/laryngeal compression by oesophageal foreign body
• Regurgitation, refusal to eat (especially children)
• Sharp objects: chest/back pain, risk of perforation, retropharyngeal abscess

Diagnosis

• AP + lateral neck/chest X-ray: coins lodge in coronal plane in oesophagus (visible on AP); in trachea on lateral
• Barium oesophagram: definitive
• CT: useful adjunct; identifies complications (perforation, abscess)
• Button batteries require urgent removal due to alkali liquefaction necrosis

Treatment

• Airway foreign body / complete obstruction: emergency; Heimlich manoeuvre if witnessed; rigid endoscopy
• Oesophageal foreign bodies: endoscopic removal under GA with endotracheal intubation
  • Sharp, caustic, button battery → urgent removal regardless of time
  • Asymptomatic smooth object <24 hours in healthy child → may observe 8–16 hours
• Complications: perforation → mediastinitis, tracheo-oesophageal fistula, retropharyngeal abscess

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21. Tracheostomy — Types, Technique, and Complications

Indications

1. Upper airway obstruction (tumours, angioedema, trauma, bilateral vocal fold paralysis)
2. Prolonged mechanical ventilation
3. Neurological condition preventing safe extubation (brain injury, spinal cord injury, severe agitation)

Types of Tracheostomy

Technique — Open Surgical Tracheostomy

1. Patient supine with shoulder roll; neck in moderate extension
2. Head of bed slightly elevated (reduces cervical venous pressure)
3. Identify landmarks: thyroid cartilage, cricoid cartilage, tracheal rings, sternal notch
4. Transverse incision 1 cm below the cricoid cartilage (not from sternal notch — larynx moves independently of sternum)
5. Divide platysma and strap muscles (sternohyoid, sternothyroid); retract laterally
6. Ligate/divide thyroid isthmus
7. Expose pretracheal fascia → trachea from cricoid to 4th ring
8. Cricoid hook to elevate tracheal rings
9. Tracheal incision: horizontal between 2nd and 3rd rings (or vertical); avoid 1st ring (subglottic stenosis risk)
10. ETT retracted to just proximal to lumen; insert tracheostomy tube under direct vision
11. Confirm placement: auscultation, CO₂, tidal volume
12. Secure with 3-0 Prolene sutures and tracheal tapes

Technique — Percutaneous Dilatational Tracheostomy (Ciaglia Technique)

1. Ideal anatomy: palpable thyroid cartilage, cricoid, and 1st–3rd tracheal rings without overlying vessels; use preprocedure ultrasound
2. Shoulder roll; neck extension; FiO₂ increased to 1.0
3. Midpoint of anesthesiologist bronchoscope positioned at distal ETT for continuous guidance
4. 1–1.5 cm horizontal/vertical skin incision; blunt dissection to trachea
5. 14-gauge needle inserted into the trachea (between 1st–2nd or 2nd–3rd rings) under bronchoscopic guidance; air aspiration confirms intraluminal placement
6. J-tipped guidewire advanced towards carina (Seldinger technique)
7. Serial dilatation with 14-F catheter then single tapered dilator
8. Tracheostomy tube (loaded on obturator) passed over wire; cuff inflated
9. Position confirmed by bronchoscopy through ETT, then through tracheostomy tube
10. Secure with tracheostomy tapes

Complications of Tracheostomy

• Haemorrhage: injury to anterior jugular veins or thyroid isthmus
• Posterior tracheal wall laceration (higher with PDT): tracheo-oesophageal fistula
• False tract / extraluminal placement
• Loss of airway / accidental decannulation
• Subcutaneous emphysema, pneumothorax, pneumomediastinum
• Hypoxia during procedure; cuff laceration

• Tracheal stenosis: clinically significant ~6%; subclinical ~40%; usually at the stoma or cuff site
• Tracheomalacia: softening of tracheal cartilages at cuff site
• Tracheo-innominate artery fistula: rare but catastrophic; occurs if tube placed too low or with high-riding innominate artery; presents as sentinel bleed → massive haemorrhage; emergency thoracotomy
• Tracheo-oesophageal fistula (late)
• Granuloma formation at stoma or tracheal wall
• Tube obstruction (most common cause of ED visits — blocked inner cannula)
• Tube dislodgement: in first 7 days, stoma can close rapidly; do not blindly reinsert; orotracheal intubation preferred

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22. Conicotomy (Cricothyrotomy / Cricothyroidotomy)

Anatomy

• Cricothyroid membrane: between the cricoid and thyroid cartilages; midline; ~9 mm high, ~30 mm wide; avascular central zone
• Structures at risk: cricothyroid arteries (superior portion); vocal folds (superior to membrane)

Indications

• Emergency "can't intubate, can't oxygenate" (CICO) situation
• Complete airway obstruction when orotracheal intubation is impossible or failed
• Temporising measure before definitive tracheostomy

Surgical Cricothyrotomy (Preferred in Adults)

1. Neck extension; identify cricothyroid membrane by palpation
2. Stabilise the larynx with non-dominant hand (laryngeal handshake)
3. Horizontal incision through skin and membrane in the lower third of the cricothyroid membrane (to avoid cricothyroid arteries above and vocal folds above)
4. Dilate with tracheal hook or haemostat
5. Insert size 6 cuffed tracheostomy or ETT tube; inflate cuff; confirm ventilation
6. Convert to formal tracheostomy within 24–72 hours (prolonged cricothyrotomy risks subglottic stenosis)

Needle Cricothyrotomy

• Preferred in infants and small children (surgical landmarks less defined; surgical cricothyrotomy risks subglottic stenosis and damage to cricoid)
• 14-gauge cannula-over-needle through the membrane; aspirate air; connect to jet ventilation
• Provides oxygenation but not adequate ventilation (CO₂ rises — time-limited)

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23. Tracheal Intubation — Indications and Technique

Indications

• Airway management in surgery (GA)
• Respiratory failure requiring mechanical ventilation
• Airway protection in obtunded patients (GCS ≤8)
• Anticipated prolonged ventilation (short-term; generally preferred over tracheostomy for <14 days)
• Facilitation of airway instrumentation (bronchoscopy, foreign body removal)
• Epiglottitis: controlled intubation in OR for 3–5 days

Technique (Rapid Sequence Intubation — RSI)

1. Pre-oxygenation: 100% O₂ via tight-fitting mask for 3–5 minutes (denitrogenation)
2. Pre-treatment: lidocaine (attenuates ICP rise), fentanyl (attenuates pressor response) — situational
3. Induction agent: ketamine (preferred if haemodynamically unstable), propofol, etomidate
4. Neuromuscular blockade: succinylcholine 1.5 mg/kg (rapid onset/offset; contraindicated if hyperkalaemia risk) or rocuronium 1.2 mg/kg
5. Cricoid pressure (Sellick manoeuvre): controversial; may prevent passive regurgitation
6. Laryngoscopy: Macintosh blade (curved, placed in vallecula) or Miller blade (straight, lifts epiglottis) — BURP manoeuvre if needed (Backward, Upward, Rightward Pressure on thyroid cartilage)
7. Tube insertion: cuffed ETT for adults; pass through vocal folds; cuff below vocal folds
8. Confirm placement: direct visualisation of tube through cords, bilateral chest auscultation, capnography (gold standard), CXR
9. Secure tube; inflate cuff to 20–25 cmH₂O to prevent aspiration while avoiding mucosal ischaemia

Complications of Intubation

• Failed intubation; oesophageal intubation (must exclude with capnography)
• Right mainstem bronchus intubation (tube advanced too far)
• Dental trauma; lip laceration; vocal fold trauma
• Subglottic stenosis (prolonged intubation → acquired subglottic stenosis)
• Vocal process granuloma
• Arytenoid dislocation (rare)
• Laryngospasm, bronchospasm on airway manipulation

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Summary Reference Table

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